United States Pollution Prevention February 1995
Environmental Protection and Toxics EPA 749-F-95-003a
Agency (7407)
vvEPA OPPT Chemical Fact Sheets
1,1'-Biphenyl Fact Sheet: Support Document
(CAS No. 92-52-4)
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 These sources include online databases, unpublished EPA information, government publications, review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 1995. No attempt has been
made to verify information in these databases and secondary sources.
I. CHEMICAL IDENTITY AND PHYSICAL/CHEMICAL PROPERTIES
The chemical identity and physical and chemical properties of biphenyl are summarized in Table 1.
TABLE 1. CHEMICAL IDENTITY AND CHEMICAL/PHYSICAL PROPERTIES OF BIPHENYL
Characteristic/Property Data Reference
CAS No. 92-52-4
Common Synonyms diphenyl; bibenzene; Budavari et al. 1989
phenylbenzene
Molecular Formula C12H10 Budavari et al. 1989
Chemical Structure
Physical State Colorless leaflets Budavari et al. 1989
Molecular Weight 154.20 Budavari et al. 1989
Melting Point 69-71 °C Budavari et al. 1989
Boiling Point 254-255°C Budavari et al. 1989
Water Solubility (mg/L) insoluble Budavari et al. 1989
7.5mg/L@25°C Vershueren 1983
Density 1.041g/mL Budavari et al. 1989
Koc 1.40 x103 (calculated) CHEMFATE1994
Log Kom 4.09 CHEMFATE1994
Vapor Pressure 9.64 x 10'3 mm Hg @ 25 "C CH EM FATE 1994
Reactivity incompatible with oxidizers Keith and Walters 1985
Flash Point 109°C closed cup Keith and Walters 1985
Henry's Law Constant 3 x 10'4 atm-m3/mol CH EM FATE 1994
Fish Bioconcentration Factor 436 (static test, CHEMFATE1994
rainbow trout)
Odor Threshold 0.06 mg/m3 Vershueren 1983
pleasant, peculiar odor Budavari et al. 1989
Conversion Factors 1 ppm = 6.5 mq/m3 ACGIH 1991
1 ppm = 6.5 mg/m
1 mg/m3 = 0.154 ppm
-------
II. PRODUCTION, USE, AND TRENDS
A. Production
USITC (1994) identified three companies in the United States that made biphenyl in 1992; these companies,
along with the other identified (TRI92 1994) domestic producer, are listed in Table 2. The production
capacities of these plants are not available. U.S. production of biphenyl was 53 million pounds in 1990 (Table
3). This was a 23 percent increase from the production volume of 43 million pounds in 1989.
TABLE 2. U.S. PRODUCERS OF BIPHENYL AND THEIR LOCATIONS
Producer
Chevron Corporation, Chevron Chemical Company
Koch Chemical Company, a division of Koch Refining
Company, Specialties Group
Monsanto Chemical Company
Sybron Chemicals Company
Plant Location
Baytown, TX
Corpus Christi, TX
Anniston, AL
Wellford, SC
TOTAL
Sources: USITC 1994, EPA TRI Database.
B.
Uses
The primary use of biphenyl is in the formulation of dye carriers for textile dyeing (HSDB 1994). Biphenyl is
used as an intermediate for poly chlorinated biphenyls (HSDB 1994) and as a paper impregnant for citrus fruit
where it acts as a fungicide (Gray son 1985). In the past, a major use of biphenyl has been as a component of
heat-transfer fluids (Grayson 1985). Table 3 provides a list of applicable SIC Codes for biphenyl use. No
estimates of percentages of domestic end use patterns are available.
-------
c.
Trends
Production of poly chlorinated biphenyls (PCB's) was once the most important use of biphenyl. Recently,
however, the use of PCB's in liquid-filled transformers and as dielectric fluids has been restricted by the U.S.
Environmental Protection Agency. They are being replaced by liquids containing halogen and silicone (The
Freedonia Group, Inc. 1995). U.S. demand associated with other uses of biphenyl are expected to remain
constant.
TABLE 3. END USE PATTERN OF BIPHENYL-1992 ESTIMATE
Derivative
(Typical Standard Industrial Classification
(SIC) Code)1
Dye Carrier
(SIC 2865)
Intermediate for Manufacture of Polychlorinated
Biphenyls
(SIC 2865)
Fungicide
(SIC 2879)
Heat Transfer Agent
(SIC 2899)
Percentage of U.S.
Use
N/A
N/A
N/A
N/A
1 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.
N/A Not available
ENVIRONMENTAL FATE
A. Environmental Release
Biphenyl is released to the atmosphere as a fume during its use as a heat transfer fluid and, to a lesser
extent, by volatilization from soil and water (U.S. EPA 1984). Atmospheric levels of biphenyl
measured 20-1500 ng/m3 in Kingston, RI, an industry-free urban area (CHEMFATE 1994).
Biphenyl enters the aquatic environment in wastewater effluents from textile mills that use it as a dye
carrier; from industrial processes; and from leaking heat exchangers (U.S. EPA 1984).
Because of its use as a fungicide, residues of biphenyl have been detected in tangerines (0.01-0.085
mg/kg, whole fruit), grapefruits (0-150 mg/kg, peel or whole fruit), oranges (0-0.012 mg/kg, edible
portion), and lemons (0.02-0.12 mg/kg, edible portion) (U.S. EPA 1984). One investigator reported
airborne concentrations of 3.2-250 pg biphenyl/m3 from diesel exhaust (U.S. EPA 1984). In
monitoring studies, biphenyl was detected at the following sites: in the Tennessee River (2
micrograms/L), in a roadside ditch in Kentucky (5000 mg/kg), in Lake Michigan at the mouth of the
Galien River (4 micrograms/L), in effluent from industrial and water treatment facilities (0-130
micrograms/L), in Great Lakes Municipal drinking water (0.3-31.9 nanograms/L), in Athens, GA,
drinking water (1-5 nanograms/L), and in groundwater at the site of an inactive underground coal
gasification process (25-43 micrograms/L) (U.S. EPA 1984).
In 1992, environmental releases of biphenyl, as reported to the Toxic Chemical release inventory by
-------
certain types of U.S. industries, totaled about 885 thousand pounds, including approximately 820
thousand pounds to the atmosphere, 50 thousand pounds to underground injection sites, 10 thousand
pounds to surface water, and 5 thousand pounds to land (TRI92 1994).
B. Transport
No information was found in the secondary sources searched regarding the transport of biphenyl in
air. Volatilization and sorption are important in the transport of biphenyl in water. The Henry's Law
constant for biphenyl (3 x 10"4 atnrmVmol) suggests that the chemical could undergo volatilization.
The volatilization half-life of 4.3 hours was estimated for biphenyl in a stream 1 meter deep, flowing
1 meter/second, with an air current of 3 meters/second (U.S. EPA 1984). The log octanol/water
partition coefficient of 4.09 for biphenyl suggests that the chemical has potential for sorption to
particulate matter (U.S. EPA 1984). One study demonstrated that 50% of the biphenyl applied to
activated sludge in water remained as nonextractable residue (U.S. EPA 1984).
The high octanol/water partition coefficient and the low water solubility of biphenyl would probably
preclude significant leaching of the chemical through soil (U.S. EPA 1984). However, soil
microorganisms may metabolize biphenyl to the more polar hydroxy biphenyls and dihydroxy
biphenyls which may leach into groundwater (U.S. EPA 1984). The volatilization of biphenyl from
soil is not likely to be significant. Less than 2% of the applied radioactivity from (14C)-biphenyl,
incorporated into wet sand, loam, and humus, evaporated in 2 hours (U.S. EPA 1984).
C. Transformation/Persistence
1. Air — In the air, biphenyl reacts with hydroxyl radicals and undergoes photolysis (U.S. EPA
1984). The calculated half-life for the reaction of biphenyl with OH" is 2.2 days at 25 °C,
assuming an OH concentration of 5 x 105 molecule/cm3 (CHEMFATE 1994).
In a photolysis experiment, biphenyl was impregnated into paper and exposed to UV
irradiation (>300 nanometers) in the presence of NOX. The chemical underwent
"considerable" photodegradation, yielding 2- and 4-nitrobiphenyl as reaction products (U.S.
EPA 1984). The half-life of biphenyl was ~2 hours. In another study, 80 ppb of 14C-
biphenyl was irradiated on silica gel for 17 hours at a wavelength of >290 nm (U.S. EPA
1984). Photodecomposition products included 9.5% 14CO2 and <0.1% organic fragments.
Biphenyl also reacts slowly with ozone. The calculated half-life for the reaction is 57.3 days
at 25°C, assuming an ozone concentration of 7 x 1011 molecule/cm3 (CHEMFATE 1994).
2. Soil — The main removal process for biphenyl in soil appears to be biodegradation. The
following organisms have been shown to degrade biphenyl: Saccharomyces cerevisiae
(with the production of benzoic acid), Streptomyces sp.,Achromobacter, Pseudomonas
putida, Oscillatoria sp., gram negative bacteria, Acaligenes sp. 559,Acaligenes Y42 and
Acinetobacter P6 (U.S. EPA 1984). Bacteria generally oxidize biphenyl via cytochrome P-
450 to 2,3-dihydroxybiphenyl (U.S. EPA 1984). Fungi metabolize biphenyl to 4-hydroxy- or
2-hydroxybiphenyl and 4,4'-dihydroxybiphenyl (U.S. EPA 1984). In one study, 9.1% of the
biphenyl was degraded by activated sludge in 2 days (U.S. EPA 1984).
3. Water — The main environmental fate processes for biphenyl in water are photolysis and
microbial degradation (U.S. EPA 1984). Biphenyl in solution, irradiated with a germicidal
UV lamp (UV spectra of -250 nm), underwent 50% degradation in ~40 hours (U.S. EPA
1984).
The biodegradation of biphenyl by aquatic microorganisms proceeds via aromatic
hydroxylation to 2-, 3-, and 4-hydroxybiphenyl, with further hydroxylation to 2,3-
dihydroxybiphenyl (U.S. EPA 1984). The degradation rates for biphenyl under various
conditions were: 74% in 14 days (activated sludge), 100% in 7 days (anaerobic digester),
100% in 8 hours (aerated lagoon), 100% in 96 hours (retention pond), 79% in 5 days
(domestic wastewater), 87% in 24 hours and 100% in 5 days (industrial wastewater)
(CHEMFATE 1994).
4. Biota — The bioconcentration factors of biphenyl (436 for the rainbow trout, 540 for algae
-------
[Chlorella fusca], and 282 for the orfe [Leuciscus idus melanotus] [U.S. EPA 1984])
suggest a moderate potential for the accumulation of the chemical in aquatic organisms. The
octanol/water partition coefficient of 4.1 (CHEMFATE 1994) suggests that the chemical has
an affinity for lipids.
IV. HEALTH EFFECTS
A. Pharmacokinetics
1. Absorption — The detection of urinary metabolites in animals following oral administration
of biphenyl indicate the chemical is absorbed by this route (see section IV.A.4) (U.S. EPA
1984). Systemic effects in rabbits, rats, and mice, observed following repeated inhalation
exposure to biphenyl-impregnated celite dust, indicate that the chemical is also absorbed by
this route (U.S. EPA 1984). Similarly, repeated application of biphenyl to the depilated
backs of rabbits resulted in systemic effects, indicating dermal absorption (U.S. EPA 1984).
2. Distribution — Little information was found in the secondary sources searched regarding the
distribution of biphenyl. Following absorption, biphenyl is transported to the liver where it
undergoes hydroxylation and conjugation, and becomes more polar (U.S. EPA 1984). In rats
given 14C-biphenyl orally, about 85, 7, 0.1, and 0.6% of the administered radioactivity was
detected in the urine, feces, expired air (as CO2), and tissues, respectively, within 96 hours
of dosing (U.S. EPA 1984). Bile collected for 96 hours after the oral administration of
biphenyl to rats contained 12 metabolites of biphenyl, accounting for 5.2% of the
administered dose (U.S. EPA 1984). The octanol/water partition coefficient of 4.1
(CHEMFATE 1994) suggests that the chemical has an affinity for lipids, but no information
was found to demonstrate this.
3. Metabolism — In the liver, biphenyl undergoes hydroxylation and conjugation (U.S. EPA
1984). More than 10 mono-, di-, and tri-hydroxybiphenyl metabolites have been identified
in the urine of animals (U.S. EPA 1984). These metabolites may occur as conjugates of
mercapturic acid and glucuronide. A major metabolite in the rat, mouse, guinea pig, rabbit
and pig is 4-hydroxybiphenyl; other major metabolites include 4,4-dihydroxybiphenyl in the
pig and rat and 2-hydroxybiphenyl in the mouse (U.S. EPA 1984). There is evidence to
suggest that the metabolism of biphenyl is mediated by a cytochrome P-450 system and that
an arene oxide intermediate capable of binding to biomacromolecules may be formed (U.S.
EPA 1984).
4. Excretion — Following the hydroxylation and conjugation of biphenyl in the liver, the
chemical is excreted mainly in the urine as mercapturic acid or glucuronide conjugates (U.S.
EPA 1984). Small amounts have also been detected in the feces, in expired air as CO2, and
in the tissues (see section IV.A.2) (U.S. EPA 1984). Rabbits, guinea pigs, and pigs given
biphenyl by gavage excreted at least 20% of the administered dose in the urine within 24
hours; rats administered 14C-biphenyl orally excreted 75-80% of the dose in 24 hours (U.S.
EPA 1984).
B. Acute Effects
Workers exposed acutely to biphenyl in air have experienced nausea, vomiting, bronchitis, and
irritation of the eyes and mucous membranes.
1. Humans — Workers exposed to biphenyl fumes experienced irritation to the eyes and
mucous membranes at concentrations of 3-4 ppm or 19-25 mg/m3 (Sandmeyer 1981). The
concentration of 3-4 ppm is roughly equivalent to 2-3 mg/kg over an 8-hour exposure
period1. Others, exposed (concentrations not available) during paper impregnation, had
transient nausea, vomiting, and bronchitis (ACGIH 1991). At concentrations below 1 mg
biphenyl/m3 there were no differences between exposed and unexposed workers in a
For dose comparison purposes this has been calculated by multiplying 19-25 mg/m3 by 0.143 (the occupational
standard breathing rate, 10 m3, divided by the assumed adult body weight, 70 kg, and assuming 100% absorption) to
obtain the dose in mg/kg/day (U.S. EPA 1988).
-------
comparison of blood pressure, pulmonary function tests, serum creatinine values, urinary
protein levels, and standard blood cell counts (ACGIH 1991).
2. Animals — Oral LD50 values for biphenyl are 3280 mg/kg for the rat and 2410 mg/kg for the
rabbit (U.S. EPA 1984)).
C. Subchronic/Chronic Effects
The EPA has derived a chronic oral reference dose (RfD2) of 0.05 mg/kg/day for biphenyl, based on
kidney damage in rats. Workplace exposure to biphenyl has caused the death of one worker and
adverse effects on the liver and nervous system (see section IV.G) of others. In animals, oral doses
of large amounts of biphenyl produced adverse effects on the kidneys, the liver, the blood and spleen,
and growth and longevity. Subchronic inhalation exposure of animals to biphenyl-impregnated dust
produced lesions of the respiratory tract.
1. Humans — A Finnish paper mill worker died in 1969, following 11 years of "heavy
exposure" to biphenyl (ACGIH 1991). The cause of death was reported as "yellow atrophy"
of the liver. During the 11 years, average concentrations of biphenyl in the workplace air
ranged from 0.6 to 128 mg/m3 (0.09 to 19.7 ppm;
0.086 to 18.3 mg/kg/day). Eight other workers experienced signs of toxicity that were
characterized by damage to the liver and nervous system (see section IV.G).
2. Animals — The following study was the basis for EPA's derivation of the chronic oral RfD
for biphenyl, 0.05 mg/kg/day (U.S. EPA 1994). Albino rats (15/sex/group) received diets
containing biphenyl concentrations of 0.0, 0.001, 0.005, 0.01, 0.05, 0.1, 0.5 or 1% for 700
days (U.S. EPA 1984; 1994). Growth retardation, reduced hemoglobin levels, decreased
food intake, kidney damage (that included irregular scarring, lymphocytic infiltration,
tubular atrophy and patchy tubular dilation), and decreased longevity were observed in rats
given 2:0.5% biphenyl (2:250 mg/kg/day; the lowest-observed-adverse-effect level
[LOAEL]). Sporadic effects were noted at lower doses (2 male rats receiving 0.1 and 0.05%
biphenyl had disintegrated blood cells in the renal pelvis and two others had small basophilic
concretions in the renal medullas); 0.1% biphenyl (50 mg/kg/day) was selected as the no-
observed-adverse-effect level (NOAEL) for the study (U.S. EPA 1994). In the calculation of
the RfD the EPA applied a modifying factor of 10 to account for intraspecies variability
demonstrated by uncertainty in the threshold of the study, in addition to the uncertainty
factor of 100 (U.S. EPA 1984; 1994). Another study from the same laboratory demonstrated
that the renal damage occurring in rats fed >0.5% could be reversed by placing animals on a
control diet (U.S. EPA 1984).
Supporting the results of the critical study for the RfD, a 0.1% NOAEL was also found in a
subchronic feeding study and in a 3-generation reproduction study; both studies were
conducted in rats and were unpublished (U.S. EPA 1994).
Another study investigated the effect of dietary biphenyl on the induction of poly cystic renal
lesions in the rat. Rats fed biphenyl in commercial rat chow for 21 days exhibited increased
kidney weight, urine volume, and urine specific gravity at 2:500 mg/kg body weight/day and
poly cystic renal changes at 1000 mg/kg/day. The no-effect level for renal effects was 300
mg/kg/day. When a semisynthetic diet was substituted for the commercial chow, increased
kidney weight occurred at 50 mg/kg/day (the lowest dose tested) and polycystic changes and
other renal effects occurred at 2:150 mg/kg/day (U.S. EPA 1984).
In an inhalation study, three albino rabbits and 10 Sprague-Dawley rats inhaled biphenyl-
impregnated celite dust (300 mg biphenyl/m3), 7 hours/day, 5 days/week over a period of 90
days (U.S. EPA 1985a). Similarly, 3 rabbits and 6 rats were exposed to 40 mg biphenyl/m3
over 64 days. Control information was not available. All animals had severe
bronchopulmonary lesions characterized by emphysema, lobular pneumonia, bronchitis and
multiple abscesses of the lungs. Minor liver and kidney damage also occurred (U.S. EPA
The RfD is an estimate (with uncertainty spanning perhaps an order of magnitude) of the daily exposure level for
the human population, including sensitive subpopulations, that is likely to be without an appreciable risk of
deleterious effects during the time period of concern.
-------
1985a). The concentration of 40 mg/m3 is roughly equivalent to 7.43 mg/kg over the 7-hour
exposure period3. In the same study, mice exposed to 5 mg/m3 for 64 days exhibited
respiratory difficulty, whereas rats exposed similarly did not (ACGIH 1991). In the absence
of control data, the pulmonary effects could not be attributed solely to biphenyl (U.S. EPA
1985a).
Rabbits exposed by dermal application to 0.5 g biphenyl/kg, 2 hours/day for 5 days exhibited
growth depression; slight cardiac, hepatic, and renal changes; and follicular atrophy,
necrosis, and leukocytic infiltration of the spleen; and there were "some" deaths (Sandmeyer
1981). Repeated application of 25% biphenyl in olive oil to the skin of rabbits did not
produce irritation, but resulted in the death of 1 animal after 8 applications, and produced
weight loss in 3 others after 20 applications (ACGIH 1991).
D. Carcinogenicity
Based on no information on humans and inadequate studies in rats and mice, the EPA has classified
biphenyl as D, not classifiable as to human carcinogenicity. There is some evidence that biphenyl
may be a tumor promoter.
1. Humans — No information was found in the secondary sources searched for the
carcinogenicity of biphenyl in humans.
2. Animals — Treatment-related tumors were not found under the following conditions: (1) in
B6AKF[ and B6C3F[ mice (18/sex/strain) treated with 215 mg/kg biphenyI/day by gavage
from day 7 to day 28 of age, then with 517 ppm dietary biphenyl for the subsequent 18
months (U.S. EPA 1994); (2) in albino rats given <500 mg/kg bipheny I/day in the diet for
700 days (U.S. EPA 1994); and (3) in groups of 12 male and 12 female Sprague-Dawley rats
given < 1% dietary biphenyl for 2 years. Several deficiencies limit the validity of the last
study (U.S. EPA 1994).
Groups of 25 male F344 rats were given 0.05% N-butyl-N-(4-hydroxybutyl)nitrosamine
(BBN) in drinking water for 4 weeks followed by a basal diet or a diet containing 0.5%
biphenyl for 32 weeks (U.S. EPA 1994). A group of 5 rats received only 0.5% biphenyl. In
the 18 surviving rats treated with BBN and biphenyl, the incidences of hyperplasia,
papillomas and carcinomas in the urinary bladder were 94, 83 and 61%, respectively. These
were statistically significant in comparison to incidences of 25, 12, and 0%, respectively, in
animals treated with BBN alone (there were no signs of hyperplasia, papillomas and
carcinomas in the rats fed biphenyl alone). The results of this study suggest that 1,1-
biphenyl is a tumor promoter (U.S. EPA 1994).
E. Genotoxicity
Biphenyl induced forward mutations in mouse lymphoma cells and sister chromatid exchanges (SCE)
in Chinese hamster cells; however, a dose-response relationship was not observed in the SCE assay
(U.S. EPA 1994). Biphenyl did not induce reverse mutations in Salmonella typhimurium and
Escherichia coli, DNA repair in E. coli, chromosomal aberrations in Chinese hamster cells, or
unscheduled DNA synthesis in rat hepatocy tes (the presence or absence of metabolic activation was
not specified) (U.S. EPA 1994).
F. Developmental/Reproductive Toxicity
Limited information indicates that biphenyl is not teratogenic and does not produce significant fetal
toxicity, even at maternally toxic doses.
1. Humans — No information was found in the secondary sources searched regarding the
For dose comparison purposes, this has been calculated by multiplying 40 mg/m by 0.186 (the 7-hour breathing
rate, 0.065 m3 [standard 24-hour breathing rate, 0.223 m3] divided by the assumed adult rat body weight, 0.350 kg,
and assuming 100% absorption) to obtain the dose in mg/kg/day (U.S. EPA 1985b).
-------
developmental/reproductive toxicity of biphenyl in humans.
2. Animals — Pregnant Wistar rats received biphenyl in oral doses of 0, 125, 250, 500 or 1000
mg/kg/day on days 6-15 of gestation (U.S. EPA 1994). No fetal or maternal toxicity
occurred in animals receiving doses <500 mg/kg. There was some (but not statistically
significant) evidence of toxicity in both dams (death) and fetuses (reduced fetal weights,
decreased number of live fetuses, and increased resorptions) at 1000 mg/kg (U.S. EPA
1994). In one study, no significant effects occurred in rats given 0, 0.1, or 0.5% dietary
biphenyl from 60 days before mating through weaning of their offspring (U.S. EPA 1994);
however, in a 3-generation study on rats, 1% dietary biphenyl produced "unspecified adverse
effects" (U.S. EPA 1994).
G. Neurotoxicity
Workers exposed chronically to concentrations of biphenyl ranging from low to high developed
persistent damage to the central and peripheral nervous systems.
1. Humans — In a Finnish paper mill, levels of biphenyl in the workplace air ranged from 0.6
to 128 mg/m3 from 1959 to 1970 (ACGIH 1991). Central and peripheral nerve damage was
observed in workers who were exposed in this plant. Neurological findings in 24 workers
were as follows: (1) electroencephalographic abnormalities (10 workers) of a generally
diffuse nature, persisting for 1 to 2 years; and (2) electromyographic abnormalities (9
workers), including fibrillation of muscles (7 of the 9 workers) and long rhythmic series of
fasciculations resembling that in infantile spinal muscular atrophy (1 worker). These
abnormalities also persisted upon reexamination (ACGIH 1991).
2. Animals — No information was found in the secondary sources searched on the
neurotoxicity of biphenyl in animals.
V. ENVIRONMENTAL EFFECTS
In laboratory studies, biphenyl is highly toxic to aquatic organisms; an acute toxicity value of <1 mg/L has
been reported. EPA has requested chronic aquatic toxicity testing for biphenyl under Section 4 of the Toxic
Substance Control Act (TSCA). Results of chronic tests in fish and invertebrates suggest low chronic toxicity
for biphenyl.
A. Toxicity to Aquatic Organisms
Acute toxicity values as low as 0.36 mg/L (for daphnids) and 1.3 mg/L (for rainbow trout) have been reported
(Fenner-Crisp 1988). Other ninety-six-hour LC50 values for biphenyl in fish are as follows: 1.5 mg/L for
Oncorhynchus mykiss (rainbow trout); 4.7 mg/L for Lepomis macrochirus (bluegill); 4.6 mg/L for
Cyprinodon variegatus (sheepshead minnow); 6 mg/L for Pimephales promelas (fathead minnow) (this
concentration is near the water solubility of biphenyl) (U.S. EPA 1984). Other estimated 48-hour LC50 values
for biphenyl inDaphnia magna are 4.7 and 2.1 mg/L (U.S. EPA 1984).
The growth of Chlorella autotrophica (green algae) was slightly inhibited (4 mm zone of inhibition at 1.0 mg
biphenyl/plate) and totally inhibited (36 mm zone of inhibition) at 10 mg/plate (U.S. EPA 1984).
Results from aquatic chronic toxicity testing in rainbow trout and daphids suggest low chronic toxicity for
biphenyl (Fenner-Crisp 1988). Chronic toxicity values were 230 micrograms/L and 275 micrograms/L for fish
and daphnids, respectively. Chronic values greater that 100 micrograms/L are indicative of low toxicity.
B. Toxicity to Terrestrial Organisms
No information was found in the secondary sources searched regarding the toxicity of biphenyl to
terrestrial organisms; however, studies with experimental animals have demonstrated low acute
toxicity and low to moderate chronic toxicity. Biphenyl is not expected to be toxic to terrestrial
organisms at levels normally found in the U.S. U.S. environment.
C. Abiotic Effects
-------
No information was found regarding the abiotic effects of biphenyl.
VI. EPA/OTHER FEDERAL/OTHER GROUP ACTIVITY
The Clean Air Act Amendments of 1990 list biphenyl as a hazardous air pollutant. Occupational exposure to
biphenyl is regulated by the Occupational Safety and Health Administration (OSHA). The OSHA permissible
exposure limit (PEL) is 0.2 parts per million of air (ppm) as an 8-hour time-weighted average (TWA) (29 CFR
1910.000). 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 biphenyl.
TABLE 4. EPA OFFICES AND CONTACT NUMBERS FOR INFORMATION ON BIPHENYL
EPA Office Statute Contact Number
Pollution Prevention & Toxics PPAa (202)260-1023
EPCRA(§313/TRI)b (800)535-0202
TSCA (§4, §8A, §8D, §12B)C (202) 554-1404
Pesticides FIFRAd (800) 858-7378
Air Clean Air Act (§111, §112B)e (919)541-0888
Solid Waste & CERCLA' (800) 535-0202
Emergency Response
"PPA = Pollution Prevention Act
bEPCRA = Emergency Planning and Community Right to Know Act of 1986
CTSCA = Toxic Substances Control Act
dFIFRA = Federal Insecticide and Rodenticide Act. Biphenyl is a list "B" pesticide (as of 1989), according to IRIS (U.S. EPA 1994) (54 FR
22706 [5/25/89]).
'Listed as hazardous air pollutant under §111 and §112 of Clean Air Act [42 U.S.C. 7401 etseq.]
'CERCLA = Comprehensive Environmental Response, Compensation, and Liability Act of 1980, as amended.
-------
TABLE 5. OTHER FEDERAL OFFICES/CONTACT NUMBERS FOR INFORMATION ON BIPHENYL
Other Agency/Department/Group
Contact Number
Agency of Toxic Substances & Disease Registry3
American Conference of Governmental Industrial Hygienists
(TLV-TWA, 0.2 ppm)b
Consumer Product Safety Commission
Food & Drug Administration
National Institute for Occupational Safety & Health
(TWA, 0.2 ppm; IDLH, 300 ppm)c
Occupational Safety & Health Administration (TWA, 0.2 ppm)d
(Check local phone book for phone number under Department of Labor)
(404) 639-6000
(513)742-2020
(301) 504-0994
(301)443-3170
(800) 356-4674
"Newly listed hazardous substance subject to Toxicological Profile (55 FR 46131, Nov. 1, 1990)
bTLV-TWA: Time-weighted-average concentration for a normal 8-hour workday and a 40-hour workweek to which nearly all workers may be
repeatedly exposed without adverse effects (ACGIH 1994-1995).
CTWA: Time-Weighted-Average concentration for up to a 10-hour workday during a 40-hour workweek. IDLH: immediate danger to life and
health.
dTWA: 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).
-------
VII. CITED REFERENCES
ACGIH. 1991. American Conference of Governmental Industrial Hygienists. Biphenyl. Documentation of
Threshold Limit Values and Biological Exposure Indices, 6th ed. ACGIH, Cincinnati, OH, pp. 137-138.
ACGIH. 1994-1995. American Conference of Governmental Industrial Hygienists. Threshold Limit Values for
Chemical Substances and Physical Agents and Biological Exposure Indices. ACGIH, Cincinnati, OH.
Budavari S, O'Neil MJ, Smith A, Heckelman PE (Eds.). 1989. The Merck Index, 11th ed. Merck & Co., Inc.,
Rahway, NJ, p. 3312.
CHEMFATE. 1994. Syracuse Research Corporation's Environmental Fate Data Bases. Syracuse Research
Corporation, Syracuse, NY.
Fenner-Crisp P. 1988. Memorandum from Penelope Fenner-Crisp, Health and Environmental Review Division,
to Richard Troast, Existing Chemicals Division. Subject: Review of Final Reports on Biphenyl: Daphnia Chronic
and Rainbow Trout Early Life Stage Tests. August 10, 1988.
Freedonia Group, Inc. "Electric Power Equipment to 1998." September 1994.
Grayson, M. (ed.). Kirk-Othmer Concise Encyclopedia of Chemical Technology, Third edition. New York: John
Wiley and Sons, 1985.
Hazardous Substances Data Bank (HSDB), 1994.
Keith LH, Walters DB. 1985. Compendium of Safety Data Sheets for Research and Industrial Chemicals, Part
III. VCH Publishers, Inc., pp. 186-187.
NIOSH. 1990. National Institute for Occupational Safety and Health. 1990. NIOSH Pocket Guide to Chemical
Hazards. NIOSH, Cincinnati, OH, pp. 100-101.
NIOSH. 1992. National Institute for Occupational Safety and Health. 1992. NIOSH Recommendations for
Occupational Safety and Health. Compendium of Policy Documents and Statements. NIOSH, Cincinnati, OH,
p. 77.
OSHA. 1993. Occupational Safety and Health Administration. Air Contaminants. Final rule. 29 CFR 1910.
Fed. Reg. 58:35338-35351.
Sandmeyer EE. 1981. Aromatic hydrocarbons. In: Clayton GD and Clayton FE, Eds. Patty's Industrial
Hygiene and Toxicology, 3rd ed., Vol. 2B., pp. 3325-3330.
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 Toxic Chemical Release Inventory. Office of Pollution Prevention and Toxics, U.S.
Environmental Protection Agency, Washington, D.C., P. 86.
U.S. EPA. 1984. U.S. Environmental Protection Agency. Health and Environmental Effects Profile for 1,1'-
Biphenyl. Environmental Criteria and Assessment Office, Cincinnati, OH, 36. pp.
U.S. EPA. 1985a. U.S. Environmental Protection Agency. Reportable Quantity Document for 1,1'-Biphenyl.
Environmental Criteria and Assessment Office, Cincinnati, OH.
U.S. EPA. 1985b. U.S. Environmental Protection Agency. Reference values for Risk Assessment.
Environmental Criteria and Assessment Office, U.S. EPA, Cincinnati, OH, Table 1-2.
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. 1994. Integrated Risk Information System (IRIS) Online. Coversheet for 1,1'-Biphenyl. Office of
Health and Environmental Assessment, U.S. EPA, Cincinnati, OH, Retrieved 11/94.
United States International Trade Commission (USITC). 1994. Synthetic Organic Chemicals: United States
Production and Sales, 1992, 76th edition. USITC Publication 2720, February 1994.
Verschueren K. 1983. Handbook of Environmental Data on Organic Chemicals, 2nd ed. Van Nostrand
Reinhold Co., New York, pp. 582-584.
-------
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. Asamended. 42 U.S.C. 7412.
GENETOX. 1994. U.S. EPA GENETOX Program, computerized database.
IARC. International Agency for Research on Cancer. IARC Monographs on the Evaluation of Carcinogenic Risk of Chemicals to Man. Lyon:
IARC.
Howard, P.H., Ed. 1989. Handbook of Environmental Fate and Exposure Data. Lewis Publishers, Chelsea, Ml.
IPCS. International Programme on Chemical Safety. Environmental Health Criteria. World Health Organization, Geneva, Switzerland.
Keith LH, Walters DB. 1985. Compendium of Safety Data Sheets for Research and Industrial Chemicals, Part III. VCH Publishers, Inc.
NIOSH (National Institute for Occupational Safety and Health). 1992. NIOSH Recommendations for Occupational Safety and Health.
Compendium of Policy Documents and Statements. Cincinnati, OH: NIOSH.
NTP. National Toxicology Program. Toxicology and Carcinogenesis Studies. Tech Rep Ser.
NTP. National Toxicology Program. Management Status Report. Produced from NTP Chemtrack system. Aprils, 1994. National
Toxicology Program, Research Triangle Park, NC.
OSHA. 1993. Occupational Safety and Health Administration. Table Z-2. Limits for Air Contaminants.
TSCATS. 1994 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.
Verschueren K. 1983. Handbook of Environmental Data on Organic Chemicals, 2nd ed. Van Nostrand Reinhold Co., New York.
A-1
------- |