530SW87526
Environmental Protection
Agency
EPA Research and
Development
HEALTH AND ENVIRONMENTAL EFFECTS DOCUMENT
FOR CUMENE
Prepared for
OFFICE OF SOLID HASTE AND
EMERGENCY RESPONSE
Prepared by
Environmental Criteria and Assessment Office
Office of Health and Environmental Assessment
U.S. Environmental Protection Agency
Cincinnati, OH 45268
U-S. Environmental Protection Agency
Region V, Library
230 South Dearborn Street ~"
Chicago, Illinois 60604
DRAFT: DO NOT CITE OR QUOTE
NOTICE
This document Is a preliminary draft. It has not been formally released
by the U.S. Environmental Protection Agency and should not at this stage be
construed to represent Agency policy. It Is being circulated for comments
on Us technical accuracy and policy Implications.
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DISCLAIMER
This report 1s an external draft for review purposes only and does not
constitute Agency policy. Mention of trade names or commercial products
does not constitute endorsement or recommendation for use.
11
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PREFACE
Health and Environmental Effects Documents (HEEDs) are prepared for the
Office of Solid Waste and Emergency Response (OSWER). This document series
Is Intended to support listings under the Resource Conservation and Recovery
Act (RCRA) as well as to provide health-related limits and goals for emer-
gency and remedial actions under the Comprehensive Environmental Response,
Compensation and Liability Act (CERCLA). Both published literature and
Information obtained from Agency Program Office files are evaluated as they
pertain to potential human health, aquatic life and environmental effects of
hazardous waste constituents. The literature searched for 1n this document
and the dates searched are Included 1n "Appendix: Literature Searched."
Literature search material 1s current up to 8 months previous to the final
draft date listed on the front cover. Final draft document dates (front
cov«r) reflect the date the document 1s sent to the Program Officer (QSWER).
Several quantitative estimates are presented provided sufficient data
are available. For systemic toxicants, these Include Reference doses (RfDs)
for chronic and subchronlc exposures for both the Inhalation and oral
exposures. The subchronlc or partial lifetime RfO, 1s an estimate of an
exposure level that would not be expected to cause adverse effects when
exposure occurs during a limited time Interval, for example, one that does
not constitute a significant portion of the Hfespan. This type of exposure
estimate has not been extensively used, or rigorously defined as previous
risk assessment efforts have focused primarily on lifetime exposure
scenarios. Animal data used for subchronlc estimates generally reflect
exposure durations of 30-90 days. The general methodology for estimating
subchronlc RfDs 1s the same as traditionally employed for chronic estimates,
except that subchronlc data are utilized when available.
In the case of suspected carcinogens, RfOs are not estimated. A
carcinogenic potency factor, or q-j* (U.S. EPA, 1980), Is provided Instead.
These potency estimates are derived for both oral and Inhalation exposures
where possible. In addition, unit risk estimates for air and drinking water
are presented based on Inhalation and oral data, respectively.
Reportable quantities (RQs) based on both chronic toxlclty and cardno-
genldty are derived. The RQ 1s used to determine the quantity of a hazar-
dous substance for which notification 1s required In the event of a release
as specified under the CERCLA. These two RQs (chronic toxlclty and carclno-
genlclty) represent two of six scores developed (the remaining four reflect
1gn1tab1l1ty, reactivity, aquatic toxlclty, and acute mammalian toxlclty).
Chemical-specific RQs reflect the lowest of these six primary criteria. The
methodology for chronic toxlclty and cancer-based RQs are defined 1n U.S.
EPA, 1983 and 1986a, respectively.
111
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EXECUTIVE SUMMARY
Cumene Is a volatile, colorless liquid at room temperature and has a
characteristic, aromatic odor (Ward, 1979). It 1s soluble In many organic
solvents, but Is almost Insoluble Vn water (Wlndholz, 1983). Industrially,
It Is produced exclusively from the vapor phase reaction of benzene and
propylene 1n the presence of an add catalyst (Ward, 1979). Currently there
are eight domestic manufacturers of cumene (CMR, 1984). During 1985, 2.627
ml]lion pounds of this compound was produced In the United States {USITt,
1986). The use pattern for cumene 1s as follows (CHR, 1984): oxidation for
phenol/acetone production, 98%; polymerization of alpha-methylstyrene, 1.8%;
exports 0.2%.
In the atmosphere, cumene 1s expected to exist almost entirely 1n the
vapor phase (Elsenrelch et al., 1981). It appears tliat reaction with
photochemlcally generated hydroxyl radicals would be the primary degradation
pathway (t./2 1-2 days) (Ravlshankara et al., 1978; Lloyd et al., 1976).
Small amounts of cumene may be removed from the atmosphere In precipitation.
Reaction with ozone and direct photolysis are not expected to be Important
removal processes (U.S. EPA, 1987). In water, Important fate and transport
processes are expected to be volatilization (t,/2 * hours from a typical
river), aerobic blodegradatlon (Van der Linden, 1978; Kappelar and Wuhrmann,
1978a; Sasaki, 1978) and adsorption to suspended solids and sediments.
Measured and estimated BCF values suggest that bloconcentratlon In aquatic
organisms would not be significant. Chemical hydrolysis, oxidation and
photolysis are not expected to be Important fate processes In water (Mill et
al., 1978, 1979, 1980). In soil, 1t appears that cumene would blodegrade
fairly rapidly under aerobic conditions (Jamison et al., 1970; OrnoM et al.,
1v
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1975). This compound 1s expected to adsorb strongly to soil and have only
slight mobility. The relatively high vapor pressure of curaene suggests that
volatilization of this compound from dry soil surfaces would be significant.
Cumene Is a naturally occurring constituent of crude oil and as such Is
a minor component of finished hydrocarbon fuels. Curaene may be released to
the environment from a number of anthropogenic sources. Primary sources of
release Include wastewater effluents and fugitive emissions from manufactur-
ing and use facilities and petrochemical refineries, accidental spills of
finished fuel products during transport or processing and emissions from
gasoline stations and motor vehicles.
Given the available monitoring data, 1t appears that the general popula-
tion would be exposed to cumene primarily by Inhalation. Minor exposure may
result from the Ingestlon of foods and perhaps drinking waters. Monitoring
data for cumene In water, wastewater, food and air are summarized 1n Tables
3-1 through 3-6. Cumene has also been detected 1n a variety of plants
Including "oakmoss" (Evernla prunastrl (L.) Ach.) (Gavin et al., 1978) and
marsh grass (Mody et al., 1974a,b, 1975). Based on data given In Table
3-4, the average dally Intake of cumene by nonsmokers 1n urban locations was
estimated to be -300 vq and for rural locations the average dally Intake
has been estimated to be -5-50 yg. The average dally Intake of smokers Is
expected to be significantly higher than for nonsmokers because of the
cumene 1n tobacco smoke. The rate of cumene expiration from smokers and
nonsmokers was found to be 21.0 and 0.13 yg/hour, respectively (Conkle et
al., 1975).
Relatively IHtle Information Is available concerning toxic effects of
cumene on aquatic organisms. The lowest reported toxic concentration was
0.012 mg/l, the toxldty threshold for the dilate protozoan, Colpldlum
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colpoda {Rogerson et al., 1983). Because of the variability of data and
flawed experimental designs, the available environmental effects studies
have been judged Inadequate to assess the acute toxldty of cumene to
aquatic organisms (U.S. EPA, 1985a).
Data reported toy several Investigators Indicate that cumene Is absorbed
following oral, dermal and Inhalation exposure (Robinson et al., 1955;
Vallette and Cavler, 1954; Monsanto Co., 1984a; Senczuk and Lltewka, 1976;
Sato and Nakajltna, 1979). The results of tissue analyses 1n rats following
exposure to curoene vapors for periods up to 150 days Indicate that the com-
pound distributes mainly to endocrine organs, CNS components, bone marrow,
spleen and liver (Fabre et al., 1955). Gorban et al. (1978) and Gerarde and
Linden (1959) reported that cumene localized 1n tissues with a high llpld
content. Cumene 1s metabolized 1n a variety of species primarily to the
glucuronlde conjugates 2-phenyl-2-propanol, 2-phenyl-l-propanol and
2-phenylpropano1c add (Robinson et al., 1955; Senczuk and Lltewka, 1976;
Bakke and Schellne, 1970; Cl.ukraborty and Smith, 1967). Approximately 90%
of a single oral dose of cumene to rabbits was excreted within 24 hours as
glucuronlde conjugates of metabolites (Robinson et al., 1955). Humans
exposed to Inhalation doses of cumene showed blphaslc excretion of 2-phenyl-
2-propanol 1n the urine (Senczuk and Lltewka, 1976).
No data were available on the carcinogenic, reproductive, teratogenlc,
chronic oral or chronic Inhalation effects of cumene. Fabre et al. (1955)
reported passive congestion In the lungs, liver, spleen, kidney and adrenals
of rats and rabbits after subchronlc Inhalation exposure to cumene vapors at
500 ppm (2458 mg/m3), 8 hours/day, 6 days/week. Jenkins et al. (1970)
reported no compound-related effects on body weights or most hematologlcal
values 1n rats exposed to cumene vapors at 244 ppm (1200 mg/m3), 8 hours/
v1
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day, 5 days/week for 30 exposures or to 3.7 or 300 ppm (18 or 147 mg/rn3)
continuously for 90 days. A degree of leukocytosls was observed only 1n the
rats at the end of the experiment.
No compound-related effects were reported in male albino rats adminis-
tered cumene In the diet at up to 6000 ppm for 28 days (Cltoa-Selgy Co.,
1985). Wolf et al. (1956) reported Increased kidney weights In rats admin-
istered cumene orally at levels of 462 and 769 mg/kg/day for 139/194 days.
No hlstopathologlcal, pathological or hematologlcal effects were reported at
4ny dose level.
Acute oral LD5Q values reported for rats range from 1400-2900 mg/kg
(Koch Refining Co., 1984; Monsanto Co., 1984a; C1ba-Ge1gy Co., 1985; Union
Carbide Corp., 1985; Smyth et al., 1951). Acute dermal LD5Qs for cumene
applied undiluted to rabbit skin range from >3160 mg/kg (Monsanto, 1984a) to
>10,000 mg/kg (C1ba-Ge1gy Co., 1985). A 4-hour Inhalation LC5Q of 8000
ppm (39,329 mg/m3) was reported by several Investigators (Koch Refining
Co., 1984; Union Carbide Corp., 1985; Smyth et al., 1951).
Cumene was reported to be nonmutagenlc both In the presence and absence
of metabolic activation when tested by the Salmonella mlcrosome assay In
several strains (Monsanto Co., 1984b, 1985; Florin et al., 1980; Simmon et
al., 1977). Negative results were also reported In the Saccharomyces
cerevlslae D3 mltotlc recombination assay with and without S-9 activation
(Monsanto Co., 1985; Simmon et al., 1977). In addition, cumene failed to
elicit mlcronuclel formation 1n mouse bone marrow polychromatic erythrocytes
(Gulf 011, 1985a) and the CHO/HGPRT test for point mutations was also nega-
tive in both S-9 activated and nonactlvated treatments (Gulf 011, 1985b).
Positive results were obtained for UDS in rat hepatocytes and for cell
transformation 1n mouse embryo cells (Gulf 011, 1984a,b).
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A teratogenlc and embryolethal effect was reported 1n the offspring of
rats exposed bjf Inhalation to an unspecified concentration of camene for *
months (Serebrenlnlkov and Oglemev, 1978). Other data regarding terato-
genlclty or reproductive effects of cumene were not found.
A subthronlt Inhalation RfD of 0.3 ing/m3 or 6 wg/day and a chronic
Inhalation RfO of 0.03 mg/m3 or 0.6 mg/day were derived based on the NOAEL
of 3.7 ppra {18 rag/ro9) continuously for 90 days* at which guinea pigs had
no effects 1n the study by Jenkins et al, (1970). Uncertainty factors of
100 (10 for Interspedes extrapolation, 10 for the protection of sensitive
Individuals) for the subchronlc RfD and 10,00 (an additional factor of 10
for use of a subchronlc study) were used. Low confidence was placed 1n the
Inhalation RfOs. A subchronlc oral RfD of 1 mg/kg/day or 77 mg/day and a
chronic oral RfD of 0.1 mg/kg/day or 8 mg/day were derived based on the NOEL
In rats In the study by Wolf et al. (1956). At the LOAEL of 331 mg/kg/day,
rats had Increased kidney weight. Uncer- talnty factors of 100 (10 for
Interspedes extrapolation and 10 for the protection of the most sensitive
Individuals) for the subchronlc oral RfD and 1000 (an additional factor of
10 for the use of a subchronic study) for the chronic oral RfD were used.
Confidence 1n the oral RfDs 1s medium. An RQ of 1000 was derived based on
the dose-response data for leukocytosls In rats exposed by Inhalation 1n the
study by Jenkins et al. (1970). No carc1nogen1c1ty data were available;
therefore, cumene was classified as an EPA Group D chemical.
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TABLE OF CONTENTS
Page
1. INTRODUCTION 1
1.1. STRUCTURE AND CAS REGISTRY NUMBER 1
1.2. PHYSICAL AND CHEMICAL PROPERTIES 1
1.3. PRODUCTION DATA, ....... 1
1.4. USE DATA ....... 3
1.5. SUMMARY 3
2. ENVIRONMENTAL FATE AND TRANSPORT 6
2.1. AIR 6
2.1.1. Reaction with Hydroxyl Radicals 6
2.1.2. Reaction with Ozone ........ 6
2.1.3, Photolysis 6
2.1.4. Physical Removal Processes 6
2.2. WATER 7
2.2.1. Hydrolysis 7
2.2.2. Oxidation 7
2.2.3. Photolysis 7
2.2.4. Mlcroblal Degradation 7
2.2.5. Bloconcentratlon 8
2.2.6. Adsorption 9
2.2.7. Volatilization 9
2.3. SOIL 9
2.3.1. Mlcroblal Degradation 9
2.3.2. Adsorption 9
2.3.3. Volatilization 10
2.4. SUMMARY 10
3. EXPOSURE 12
3.1. WATER 12
3.2. FOOD 14
3.3. INHALATION 14
3.4. DERMAL 23
3.5. OTHER 23
3.6. SUMMARY 23
4. AQUATIC TOXICITY 25
4.1. ACUTE TOXICITY . 25
4.2. CHRONIC EFFECTS 25
4.3. PLANT EFFECTS 28
4.4. SUMMARY 28
1x
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TABLE OF CONTENTS (cont.)
Page
5. PHARHftCOKINETCS 29
5.1. ABSORPTION 29
5.2. DISTRIBUTION 30
5.3. METABOLISM 31
5.4. EXCRETION 33
5.5. SUMMARY. 33
6. EFFECTS 35
6.1. SYSTEMIC TOXICITY. ... ..... 35
6.1.1. Inhalation Exposures 35
6.1,2, Oral Exposures 36
6.1.3. Other Relevant Information 37
6.2. CARCINOGENICITY 39
6.3. MUTAGENICITY 40
6.4. TERATOGENICITY 42
6.5. OTHER REPRODUCTIVE EFFECTS 42
6.6. SUMMARY 42
7. EXISTING GUIDELINES AND STANDARDS 45
7.1. HUMAN 45
7.2. AQUATIC 45
8. RISK ASSESSMENT 46
8.1. CARCINOGENICITY 46
8.2. SYSTEMIC TOXICITY 46
8.2.1. Inhalation Exposure 46
8.2.2. Oral Exposure 47
9. REPORTABLE QUANTITIES 50
9.1. BASED ON SYSTEMIC TOXICITY 50
9.2. BASED ON CARCINOGENICITY 53
10. REFERENCES 55
APPENDIX A: LITERATURE SEARCHED 79
APPENDIX B: SUMMARY TABLE FOR CUMENE 82
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LIST OF TABLES
No. Title Page
1-1 Physical Properties of Cumene 2
1-2 Current Manufacturers of Cumene 1n the United States 4
1-3 Cumene Production 1n the United States 5
3-1 Summary of Monitoring Data for Cumene 1n Water 13
3-2 Cumene Levels In Various Industrial Effluents and
Contaminated Groundwaters 15
3-3 Cumene Concentrations 1n Various Industrial Discharges
to Receiving Streams 17
3*4 Sunnary of Monitoring Data for Cumene In Foods 18
3-5 Summary of Monitoring Data for Cumene 1n the Ambient
Atmosphere 19
3-6 Levels of Cumene Found 1n Air from Anthropogenic Sources. . . 21
4-1 Acute Toxldty of Cumene to Aquatic Organisms 26
6-1 Mutagen1c1ty Testing of Cumene 41
*
9-1 Toxldty Summary for Cumene 51
9-2 Composite Scores for Cumene Using the Ret 52
9-3 Cumene: Minimum Effective Dose (MED) and Reportable
Quantity (RQ) 54
x1
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LIST Of ABBREVIATIONS
BCF Bloconcentratlon factor
BOOT Biological oxygen demand, theoretical
CAS Chemical Abstract Service
CNS Central nervous system
CS Composite score
EC5Q Concentration effective to 50% of recipients
FHSA Federal Hazardous Substance Act
Koc Soil sorptlon coefficient standardized
with respect to organic carbon
OctanoVwater partition coeffi
Concentration lethal to 50% of recipients
K OctanoVwater partition coefficient
LD_0 Dose lethal to 50% of recipients
LOAEL Lowest-observed-adverse-effect level
MED Minimum effective dose
NOEC No-observed-effect concentration
NOEL No-observed-effect level
ppb Parts per billion .
ppm Parts per million
R0c0 Dose necessary to depress the respiratory rate by 50%
RfD Reference dose
RQ .Reportable quantity
RV. Dose-rating value
RVfi Effect-rating value
STEL Short-term exposed level
TLV Threshold limit value
TWA Time-weighted average
ThOD Theoretical oxygen demand
UDS Unscheduled DNA synthesis
UV Ultraviolet
v/v Volume per volume
w/w Weight per weight
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1. INTRODUCTION
1.1, STRUCTURE AND CAS REfilSTRY NUMBER
Cumene Is also known as (l-methylethyl)-benzene, 2-phenylpropane and
Isopropylbenzene. The structure, CAS Registry number, empirical formula and
nolecular weight of cunene Are as follows:
CH3
:H
CH3
V^ ^X"
CAS Registry number: 98-82-8
Empirical formula: C-H,-
Molecular weight: 120.2
1.2. PHYSICAL AND CHEMICAL PROPERTIES
Cumene 1s a colorless, volatile liquid at room temperature with a
characteristic aromatic odor (Ward, 1965). It 1s a member of the alky!
aromatic family of hydrocarbons, which Includes toluene and ethylbenzene
(Ward, 1965). Alkylbenzenes are susceptible to electrophlllc aromatic
substitution by nitric add, sulfurlc acid and alkyl halldes (Morrison and
Boyd, 1973). The alkyl side-chain (I.e., the Isopropyl group) may undergo
free-radical halogenatlon (Morrison and Boyd, 1973). Cumene 1s soluble In
alcohol and many other organic solvents {Wlndholz, 1983). Physical prop-
erties are listed 1n Table 1-1.
1.3. PRODUCTION DATA
Industrially, cumene 1s produced exclusively from the vapor phase
reaction of benzene and propylene 1n the presence of an add catalyst (Ward,
1979). The most common catalyst system Is solid phosphoric add on an
alumina support, although other catalyst systems such as boron tMfluoMde
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TABU 1-1
Physical Properties of Cumene
Property
Value
Reference
Melting point, °C
Boiling point, °C
Vapor pressure, 25°C
Water solubility, 25°C
Log Kow
Density, 20°C
20
Refractive Index (njj )
Flashpoint (Tag closed-cup)
Odor TLV
Conversion factor
-96.03
152.39
4.6 mm Hg
50 mg/l
3.66
0.8619 g/cm3
0.8450
35°C
0.088 ppm (v/v)
0.43 mg/m3
1 ppm =4.9 mg/m3
Ward, 1979
Ward, 1979
Hackay and Shul, 1981
Hackay and Shul, 1981
Hansch and Leo, 1985
Warr^. 1979
Ward, 1979
Ward, 1965
Amoore and Hautala,
1983
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and aluminum chloride may be used (Ward, 1979). Current domestic manufac-
turers of curaene are listed In Table 1*2. Domestic production volume data
for recent years are provided In Table 1-3.
1.4. USE DATA
The us* pattern for ctmene Is as follows (tMR, 1984): oxidation for
phenol/acetone production, 98%; polymerization of alpha-methylstyrene,
1,8%; exports 0.2%. Clark, Georgia-Gulf 1n Pasadena, TX, Texaco and Shell
1n Deer Park, TX, use cumene captlvely for the production of phenol and
Amoco uses cumene captlvely for the production of alpha-raethylstyrene (SRI,
1986).
1.5. SUMMARY
Cumene Is a volatile, colorless liquid at room temperature and has a
characteristic, aromatic odor (Ward, 1979). It Is soluble In many organic
solvents, but 1s almost Insoluble In water (Wlndholz, 1983). Industrially,
1t Is produced exclusively from the vapor phase reaction of benzene and
propyl^ne In the presence of an acid catalyst (Ward, 1979). Currently there
are eight domestic manufacturers of cumene (CMR, 1984). During 1985, 2.627
million pounds of this compound was produced In the United States (USITC,
1986). The use pattern for cumene Is as follows (CMR, 1984): oxidation for
phenol/acetone production, 98%; polymerization of alpha-methylstyrene, 1.8%;
exports 0.2%.
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TABU 1-2
Current Manufacturers of Cumene 1n the United States*
Company
Amoco Chemicals Corp.
Ashland 011
ChampUn Petroleum Co.
Clark Chemical Corp.
Georgia-Gulf Corp.
Chevron Corp.
Shell 011 Co.
Texaco Inc.
Location
Texas City, TX
Catlettsburg, KY
Corpus Chr1st1, TX
Blue Island,. IL
Pasadena, TX
Westvllle, NJ
Philadelphia, PA
Port Arthur, TX
Corpus Chrlstl, TX
Deer Park, TX
El Dorado, KS
Annual Capacity
{millions of
pounds per year)
30
400
400
no
750
140
450
450
550
720
135
*Source: SRI, 1986
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TABLE 1-3
Cmnene Production 1n the United States*
Year
1985
1984
1983
1982
1981
1980
Production Quantity
(thousands of pounds)
2,626,549
3,754,181
3,345,143
2,743,496
3,309,256
3,459,272
Sales Quantity
(thousands of pounds)
1,228,012
2,146,505
1,914,095
1,223,288
1,746,393
1,634,060
*Source: USITC, 1981, 1982, 1983, 1984, 1985, 1986
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2. ENVIRONMENTAL FATE AND TRANSPORT
2.1. AIR
Based on a vapor pressure of 4.-6 aw Hg at 25"C (Mackay and Shu1, 1981),
cumene Is expected to exist almost entirely In the vapor phase 1n the
ataosphere (Elsenretch et al., 1981).
2.T.I. Reaction with Hydroxyl Radicals. The estimated half-life for
cumene reacting with photochemically generated hydroxyl radicals In the
atmosphere Is 1.3 days at 25°C and 1.6 days at 32°C. These values are based
OR measured reaction rate constants of 7.79xlO~12 and 6.14x10'" cm3/
inolectfle-set, respectively, and an ambient hytJrwcyt radical concentration of
8.0x10= molecules/cm3 (Ravlshankara et al., 1978; Lloyd et al., 1976;
U.S. EPA, 1987).
2.1.2. Reaction with Ozone. Cumene 1s not susceptible to oxidation by
ozone 1n the atmosphere (U.S. EPA, 1987).
2.1.3, Photolysis. Cumene 1n cyclohexane does not adsorb UV light In the
environmentally -1gn1f1cant range (wavelengths >290 nm) (Sadtler, 1960),
which suggests that cumene would not be susceptible to direct photolysis.
Parlar et al. (1983) reported the results of a study 1n which a reduced
pressure photoreactor was used for the rapid determination of the photo-
products and the photolysis reaction rates of volatile chemicals. The
estimated photolytlc half-life of cumene In the natural atmosphere was -1500
years.
2.1.4. Physical Removal Processes. Based on a water solubility of 50
mg/l at 25°C (Mackay and Shu1, 1981), small amounts of cumene appear to
undergo dissolution Into clouds and subsequently be removed from the
atmosphere in precipitation.
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2.2. WATER
2.2.1. Hydrolysis. Cumene 1s not expected to hydrolyze under environ-
mental conditions since 1t contains no hydrolyzable functional groups {Lyman
et al., 1982).
2.2.2. Oxidation. The half-life for cumene reacting with alkyl peroxy
radicals 1n water was estimated to be ~2.2 years using an experimentally
determined rate constant of 10 M"1 sec"1 and an alkyl peroxy radical
concentration of 10"' M 1n natural water (Mill et al.. 1978, 1979, 1980).
The half-life for cumene reaction with photocheralcally generated hydroxyl
radicals 1n water was estimated to be -0.7 years using an experimentally
determined rate constant of 3xl09 fT1 sec"1 and a hydroxyl radical
concentration of 10~17 M 1n natural water (Mill et al., 1978, 1979, 1980).
2.2.3. Photolysis. Cumene 1n water does not adsorb UV light In the
environmentally significant range (wavelengths >290 nm) (Mill et al., 1979),
suggesting that this compound would not be susceptible to direct photolysis
In the environment.
2.2.4. M1crob1a1 Degradation. Mixed cultures of microorganisms collected
from various locations and depths In the Atlantic Ocean were all found to be
capable of degrading cumene (Walker et al., 1976). Van der Linden (1978)
extracted the water soluble fraction of gas oil and Incubated It for 10 days
at 25°C in North Sea coast water. The Initial cumene concentration was 5.4
wg/l, but after 10 days was reduced to 0.4 yg/a, (93% removal). In
contrast, when cumene was used as the sole carbon source In an artificial
seawater sample only 2% of the BOOT was consumed 1n 20 days (Price et al.,
1974). Kappelar and Wuhrmann (1978a) studied the blodegradatlon of the
water-soluble fraction of gas oil 1n a groundwater Inoculum percolating
through a soil column. Aerobic blodegradatlon of cumene proceeded after an
0034d -7- 05/27/87
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acclimation period of ~5 days and degradation to a concentration below the
detection limit (0.1 ppra organic carbon) occurred within 7 days (2 days
after acclimation). Results of this study show that groundwater mlcroflora
not previously exposed to gas oil are capable of rapidly degrading cumene
after a certain acclimation period (Kappelar and Wuhrmann, 1978a). After a
6-day lag period, curoene that was Incubated 1n nonaccllmated groundwater
underwent 50% degradation In -2.6 days (Kappelar and Wuhrmann, 1978b).
Mixed cultures of microorganisms obtained from on-contaminated and
rsJatlvely uncontao1nat«d estuary sediments readily degraded cuoene. The
culture obtained from the contaminated sediment was able to degrade cumene
faster than the uncontamlnated culture (Walker and Colwell, 1975). In an
aqueous batch system, Marlon and Malaney (1964) showed that activated sludge
from three different communities was able to blodegrade 50 mg/a. cumene, as
evidenced by oxygen uptake. Malaney and McKlnney (1966) expanded on the
preceding study by using activated sludge that had previously been
acclimated to 250 mg/8. benzene as Us sole carbon and energy source.
Cumene blodegraded with a ThOD of 37.8% after 192 hours of Incubation.
Activated sludge which had previously been acclimated to 500 mg/i aniline
as Its sole carbon and energy source, was also able to degrade cumene after
an acclimation period of -30 hours {Malaney, 1960). Cumene In an unaccll-
mated settled domestic wastewater Inoculum was found to consume 62% of Its
ThOD after 10 days and 70% of Us ThOO after 20 days (Price et al., 1974).
Results of the MITI test Indicate that cumene 1s easily biodegradable 1n
natural waters (>30% degraded In 2 weeks) (Sasaki, 1978).
2.2.5. B1oconcentrat1on. A BCF of 36 for cumene 1n goldfish has been
measured (Ogata et al., 1984). Using a measured log K value of 3.66
(Hansch and Leo, 1985) and the linear regression correlation equation, log
BCF = 0.76 log K - 0.23 (Lyman et al, 1982), a BCF of 356 was estimated.
0034d -8- 06/18/87
-------
Both the experimental and estimated BCF values Indicate that bloaccumulatlon
of cumene 1n aquatic organisms would not be significant.
2.2.6. Adsorption. Pertinent data regarding the adsorption of cumene to
suspended solids and sediments could not be located 1n the available litera-
ture as cited 1n Appendix A. An estimated K value of 2800 {Section
2.3.2.) suggests that physical adsorption of cumene to sediments and sus-
pended solids would be significant; however, (estuarlne) benthlc microorgan-
isms are capable of rapidly degrading cumene (Walker and Colwell, 1975).
Thus, cumene that 1s adsorbed to sediments nay be removed by blodegradatlon.
2.2.7. Volatilization. Henry's Law constant for cumene was estimated to
be 1.3xlO~a atm-mVmol at 25°C (Hackay and Shu1, 1981). Based on this
value, the volatilization half-life of this compound from a typical river
1 m deep, flowing 1 m/sec, with a wind speed of 3 m/sec was estimated to be
4 hours using the method of Lyman et al. (1982).
2.3. SOIL
2.3.1. H1crob1al Degradation. A number of microorganisms capable of
degrading cumene, Including Pseudomonas desmolytlca (Yamada et al., 1965),
Nocardla coralllna strain V-49 (Jamison et al., 1970) and Pseudomonas spp.
(OmoM et al., 1975), have been Isolated from soil. An Isolated culture of
£ desmolytlca and £_._ convexa was found to degrade cumene to 3-1sobutyl-
catechol and ( + )-2-hydroxy-8-methyl-6-oxononano1c add (J1gam1 et al.,
1975). Considering the available data regarding blodegradatlon of cumene by
mixed cultures of microorganisms obtained from natural water systems,
groundwater and sediments (see Section 2.1.4.), 1t Is expected that this
compound would blodegrade fairly rapidly under aerobic conditions 1n soil.
2.3.2. Adsorption. Pertinent data regarding the adsorption of cumene to
soil could not be located 1n the available literature as dted In Appendix A.
0034d -9- 06/18/87
-------
Using a measured log KQW value of 3.66 {Hansch and Leo, 1985) and the
linear regression correlation equation, log K = 1.00 log K - 0.21
(lyman et al., 1982), a K of 2800 was estimated. This K value
oc oc
Indicates that cumene would strongly adsorb to soil and would not be
significantly mobile 1n soil {Swann et al., 1983).
2.3.3. Volatilization. Experimental data pertaining to the volatiliza-
tion of cumene from soil could not be located 1n the available literature as
cited In Appendix A. The relatively high vapor pressure of cumene (4.6 mm
Hg at 25"C (Mackay and Shu1, 1981), and the estimated volatility data In
water (see Section 2.1.7.) suggest thai volatilization from soil surfaces
would be significant.
2.4. SUMMARY
In the atmosphere, cumene Is expected to exist almost entirely In the
vapor phase (E1senre1ch et al., 1981). It appears that reaction with
photochemically generated hydroxyl radicals would be the primary degradation
pathway (t-,,- 1-2 days) (Ravlshankara et al., 1978; Lloyd et al., 1976).
Small amounts of cumene may be removed from the atmosphere 1n precipitation.
Reaction with ozone and direct photolysis are not expected to be Important
removal processes (U.S. EPA, 1987). In water, Important fate and transport
processes are expected to be volatilization (t,/? 4 hours from a typical
river), aerobic blodegradatlon (Van der Linden, 1978; Kappelar and Wuhrmann,
1978a; Sasaki, 1978) and adsorption to suspended solids and sediments.
Measured and estimated BCF values suggest that bloconcentratlon 1n aquatic
organisms would not be significant. Chemical hydrolysis, oxidation and
photolysis are not expected to be Important fate processes 1n water (Mill et
al., 1978, 1979, 1980). In soil, It appears that cumene would blodegrade
fairly rapidly under aerobic conditions (Jamison et al., 1970; OmoM et al.,
0034d -10- 05/27/87
-------
1975). This compound 1s expected to adsorb strongly to soil and have only
slight wotonUjf. The relatively high vapor pressure of cunene suggests that
volatilization of this compound from dry -soil surfaces would be significant.
0034d -11- 06/18/87
-------
3. EXPOSURE
Cumene Is a naturally occurring constituent of crude oil and as such Is
a minor component of finished hydrocarbon fuels. Cumene may be released to
the environment from a number of anthropogenic sources. Primary sources of
release Include losses 1n wastewater and fugitive emissions from manufactur-
ing and use facilities and petrochemical refineries, accidental spills of
finished fuel products during transport or processing, and emissions from
gasoline stations and motor vehicles.
The National Occupational Exposure Survey estimated that 863 workers are
occupatlonally exposed to cumene (NIOSH, 1984). Based on the available
monitoring data It appears that the general population would be exposed to
cumene primarily by Inhalation. Minor exposure may result from contact with
refined petroleum products and Ingestlon of contaminated foods and perhaps
drinking waters. '
3.1. WATER
Table 3-1 provides a summary of monitoring data for cumene 1n water.
Only two reports of cumene quantification 1n drinking water were found In
the available literature. Keith et al. (1976) reported 0.01 wg/l cumene
1n finished drinking water of Terrebonne-PaMsh, LA, but found none In the
finished drinking waters of Cincinnati, OH; Miami, FL; Ottuma, IA; Seattle,
WA; New York, NY; Tucson, AZ; Grand Forks, NO; Lawrence, MA; or Philadel-
phia, PA. Coleman et al. (1984) detected cumene 1n Cincinnati, OH, drinking
water at a level of 14 ng/l. This 1s considerably below the 500 ng/i
detection limit reported by Westrlck et al. (1984), who found no cumene 1n
945 U.S. drinking water systems; however, 479 of the groundwater originated
systems were selected because of known contamination problems. Based on the
0034d -12- 05/27/87
-------
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0034d
-13-
05/27/87
-------
results of this study It may be concluded that cumene contamination >0.5
vg/l (ppb) 1s uncommon In drinking- waters originating from groundwater.
Burmaster (1982) and Burnham et al. (1972) reported unquantlfled levels of
cumene 1n drinking water obtained from groundwater.
Table 3-2 lists curaene concentrations In various Industrial effluents
and. contaminated groundwaters. Table 3-3 provides a summary of additional
monitoring data on cumene found 1n various Industrial discharges to receiv-
ing streams.
3.2. FOOD
flonltwrlntj tterta 1iwJ1tat« that ttie
-------
TABLE 3-2
Curoene Levels In Various Industrial Effluents
and Contaminated Groundwaters
Source
Cumene Concentration
Reference
Petroleum refinery
wastewater
Formation water {oil
field brine)
Underground coal
gasification
Underground coal
gasification
Coal gasification
Petrochemical plant
Wastewater from
styrene production
Wastewater from a
synthetic rubber factory
Wastewater from phenol
and acetone production
Liquid waste from
pharmaceutical produc-
tion
Textile finishing plant
effluent (untreated)
Paint manufacture
5 ng/g In dissolved air
flotation lagoon
140
19, 27 and -59 ppb In ground-
water from wells adjacent to
underground coal gasification
cavities
0.02^0.01 ppb (before jn. situ
gasification) 1HO ppb (after
J[n_ situ gasification)
26+5 ppb 1n process water
0.36 mg/j. In groundwater
from plant area
detected, NQ
detected, NQ
detected, NQ
0.06 and 2 mg/S.
detected, NQ
1581 ppb 1n contaminated
groundwater near underground
storage tanks
Snider and
Manning, 1982
Saner, 1981
Stuermer et a"l.,
1982
PelUzzarl
et al., 1979
Pell1zzar1
et al., 1979
Teply and
Dressier, 1980
Sokolowska and
Madejowskl, 1977
Chuevskaya and
Dudko, 1971
Dubrovlna et al.,
1977
Brooks et al.,
1983
Gordon and
Gordon, 1981
Botta et al.,
1984
0034d
-15-
06/18/87
-------
TABLE 3-2 (cont.)
Source Cusiene Concentration Reference
Drinking water from a detected, NQ Karrenbrock and
reservoir lined with Haberer. 1982
a chlorinated rubber
coating (concrete base)
Outboard motor opera- 0.1 pom aqueous concentration Hontz et al.,
tlon (cooling water for 7.0 HP motor operating 1982
discharge) for 30 minutes 1n 160 i water
0.7 ppm aqueous concentration
for 10.0 HP motor operating
for 30 minutes In 160 i. water
NQ = Not quantified
0034d -16- 05/27/87
-------
TABLE 3-3
Cumene Concentrations 1n Various Industrial
Discharges to Receiving Streams*
Concentrations
Industry
Timber products
Leather tanning
Iron and steel rofg.
Petroleum refining
Paving and roofing
Paint and Ink
Printing and publishing
Ore mining
Coal mining
Organlcs and plastics
Inorganic chemicals
Textile mills
Plastics and synthetics
Pulp and paper
Rubber processing
Auto and other laundries
Pesticide mfg.
Pharmaceuticals
Plastics mfg.
Electroplating
011 and gas extraction
Organic chemicals
Mechanical products
Transportation equipment
Publicly owned treat, works
No. of
Reports
6
1
2
12
1
28
7
1
9
14
9
1
3
5
2
11
5
2
6
1
13
7
5
1
42
High
(vg/D
6,319
192
18
1,316
48
2,621
739
42
1,646
17,933
606
112
57
341
867
3,925
1,753
24
1,576
3.8
334
328
1,766
21
1,258
Median
U«/D
228
192
18
91
48
168
41
42
50
.85
109
112
4
47
449
329
857
24
384
3.8
6.8
63
259
21
37
Low
(vg/D
36
192
17
13
48
8.0
25
42
4.0
4.9
14
112
1.2
8.4
32
35
217
24
112
3.8
3.1
21
44
21
1.6
*Source: U.S. EPA. 1983
0034d
-17-
05/27/87
-------
TABLE 3-4
Summary of Monitoring Data for Cumene 1n Foods
Source
Fried chicken
Tomatoes
Concord grape
Cooked Mce
Oat groats
Papaya
Baked potatoes
Beaufort cheese
Fried bacon
Australian honey
Dried legumes (beans,
split peas, lentils)
Southernpea seed
Cassava (Hanlhot
esculenta. Crantz)
Zlnfandel wine
Concentration
detected
detected
detected
detected
detected
trace
detected
detected
detected
trace*
detected
detected
detected
detected
Reference
Tang et a!., 1983
Schonuueller and Koclunaru 1969
Stern et al. , T967
Yajlma et al., 1978
Heydanek and HcGorrln, 1981
Flath and Forrey, 1977
Coleman et al., 1981
Dumont and Adda, 1978
Ho et al., 1983
Graddon et al., 1979
Lovegren et al., 1979
Fisher et al., 1979
Dougan et al., 1983
Stern et al., 1975
*Detect1on limit not specified
0034d
-18-
05/27/87
-------
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0034d
-19-
06/18/87
-------
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-------
TABLE 3-6
Levels of Curaene Found In A1r from Anthropogenic Sources
Source
Concentration
Reference
Shoe sole factory, air
T1re retreading factory,
air
Tire retreading factory,
air
Coal flyash (renoved by a
venturl scrubber)
Ambient air near
synthetic rubber plant
Building materials
Cigarette smoke
Tobacco
Gas from human waste
treatment (process not
specified)
Exhaust from gasoline
fueled vehicles
60-250 wg/m* 1n ambient
air of vulcanization area
2-200 wg/m3 1n ambient
air of vulcanization area
0-10 ng/m3 1n ambient
air of extrusion area
ISO ppi>
detected, NQ
0.06 mg/m3 average
cone. 1n Indoor air
7 jig/0.99 g cigarette
11 yg/1.15 g cigarette
14 yg/1.10 g cigarette
"2 ppb from the smoke of
one cigarette 1n a 60 m3
room
0.01% of the total
volatile composition of
Semols tobacco
0.02% of the total
volatile composition of
Appelterre tobacco
0.38 ppm (before
combustion)
0.085 (after combustion)
0.2% w/w of nonmethane
hydrocarbons
Cocheo et a!.,
1983
Cocheo et al.,
1983
Cocheo et al.,
1,983
Harrison
et al., 1985
AHverdleva and
Mlnchuk, 1973
Moelhave, 1979
Johnstone
et al., 1962
Holzer et al.,
1976
Olrlnck et al.,
1980
Tamashl, 1977
Nelson and
Qulgley, 1984
0034d
-21-
05/27/87
-------
TABLE 3-6 (cont.)
Source
Concentration
Reference
Motor vehicle emission gas detected, NQ
Jet engine
0.08-12.5 ppm
Hampton et al.,
1982
Katzman and
L1bby, 1975
NQ « Not quantified
0034d
-22-
05/27/87
-------
locations was estimated to be -5-50 jig. The average dally Intake of
smokers Is expected to be significantly higher than for nonsmokers because
of the cumene 1n tobacco smoke,.
3.4. DERMAL
Pertinent data regarding dermal exposure to cumene could not be located
In the available literature as cited In Appendix A.
3.5. OTHER
API (1984) reported that crude oils typically contain -0.1 wt% of
cumene, but that concentrations as high as 1.0 wt% have been reported.
Concentrations of cuaene In gasoline reportedly range from <0.05-0.51 vol%
(API, 1984). Measurements (24) of various grades of gasoline revealed that
cumene concentrations range from 0.14-0.51 vol% and that the average cumene
concentration was 0.3 vol% (API, 1984). Premium dlesel fuel contains 0.86
wt% of cumene; furnace oil (no.2) contains 0.60 wt% (API, 1984).
- *
Cumene has been detected In "oakmoss" [Evernla prunastrl (L.) Ach.]
(Gavin et al., 1978) and marsh grass (Mody et al., 1974a,b, 1975).
3.6. SUMMARY
Cumene Is a naturally occurring constituent of crude oil and as such Is
a minor component of finished hydrocarbon fuels. Cumene may be released to
the environment from a number of anthropogenic sources. Primary sources of
release Include wastewater effluents and fugitive emissions from manufactur-
ing and use facilities and petrochemical refineries, accidental spills of
finished fuel products during transport or processing, and emissions from
gasoline stations and motor vehicles.
Given the available monitoring data It appears that the general popula-
tion would be exposed to cumene primarily by Inhalation. Minor exposure may
result from the Ingestlon of foods and perhaps drinking waters. Monitoring
0034d -23- 06/18/87
-------
data for cumene In water, wastewater, food and air were summarized In Tables
3-1 through 3-6. Cumene has also been detected in a variety of plants
Including "oakmoss" (Evernla prunastM (L.) Ach.) (Gavin et al., 1978) and
marsh grass (Mody et al., 1974a,b, 1975). Based on data given 1n Table
3-4, the average dally Intake of cumene by nonsmokers 1n urban locations was
estimated to be -300 jig and for rural locations the average dally Intake
has been estimated to be -5-50 ng. The average dally Intake of smokers 1s
expected to be significantly higher than for nonsmokers because of the
cumene In tobacco smoke, . The rate of cumene expiration from smokers and
Aonsaokers was found to be 21.0 and 0.13 ytj/nour, respectively (Conkle et
al., 1975).
0034d -24- 06/18/87
-------
4. AQUATIC TOXICITY
4.1. ACUTE TOXICITY
Information concerning acute toxlclty of cumene to aquatic organisms Is
presented 1n Table 4-1. The lowest reported toxic concentration for fishes
was 20-30 mg/l. a LC.- for fathead minnows, Plmephales promelas (Dow
Chemical Co., 1985), one of two species for which there was Information.
Among Invertebrates, the lowest reported toxic concentration was 0.012
mg/l, the toxlclty threshold for the dilate protozoan, Colpl.dlum colpoda
(Rogerson et a!., 1983),
Th« available aquatic toxlclty data for cumen* are variable. Dulmke and
Luedemann (1978) reported 48-hour LC5Q values from two different labora-
tories for the golden orfe, Leudscus Idus. that differed by a factor of 4.
Some of this variability Is due to differences In experimental design that
affect the amount of cumene In solution. In static experiments or experi-
ments where test solutions are aerated, cumene volatilization will probably
result 1n actual cumene concentrations 1n solution that are much lower than
nominal concentrations. Incomplete reporting of experiments also compli-
cates data Interpretation. Several of the reported toxic concentrations 1n
Table 4-1 exceed the solubility of cumene In water, 50 mg/l (Hutchlnson et
a!., 1980). It Is not clear 1f carrier solvents were used to achieve these
high concentrations or If the data are based on nominal concentrations.
4.2. CHRONIC EFFECTS
Little Information 1s available concerning chronic toxlclty of cumene to
aquatic organisms. Le Roux (1977) found that concentrations up to 50 mg/l
did not significantly affect growth of mussel, Hytllus edulls. larvae
exposed for 27 days.
0034d -25- 06/18/87
-------
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4.3. PLANT EFFECTS
The only data that concern effects of cutnene on aquatic plants were
provided by Hutchlnson et al. (I960), who reported EC5Q values of 8.8 and
21.3 mg/l for Inhibition of photosynthesis 1n Chlamydomonas anqulosa and
Chlorena vulgar 1s. respectively.
4.4. SUMMARY
Relatively IHtle information is available concerning toxic effects of
cumene on aquatic organisms. The lowest reported toxic concentration was
0.012 mg/l, the tox1c1ty threshold for the dilate protozoan, Cololdlum
colpoda {Rogerson et al., 1983). Because of the variability of data and
flawed experimental designs, the available environmental effects studies
have been judged Inadequate to assess the acute toxlclty of cumene to
aquatic organisms (U.S. EPA, 1985a).
0034d -28- 06/18/87
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5. PHARMACOKINETICS
5.1. ABSORPTION
Absorption of cumene through the respiratory tract was reported by
Senczuk and LHewka (1976). Five male and five female volunteers were
exposed to 240. 480 or 720 nag/a3 cumene during three 8-hour exposure
sessions. The first two periods were for 2.5 hours and the third was 2
hours. Each period was separated by breaks of 30 minutes and each volunteer
was exposed every 10 days to one of the three concentrations of cumene. A
comparison of Inspired and expired air concentrations Indicated that mean
respiratory tract absorption ranged from 64% at the beginning of the
exposure period to 45% at the end of the sessions; the average retention was
-50%. The total amount of cumene absorbed during exposure was calculated
from retention, ventilation and exposure duration, and was nearly twice as
high at all exposure levels 1n the males (466-1400 mg) as 1n the females
« *
(270-789 mg).
Sato and Nakajlma (1979) determined the partition coefficients for some
aromatic hydrocarbons In water, blood, oil and air. The blood/air partition
coefficient for cumene (37) Indicates that the respiratory uptake of cumene
may be greater than benzene (7.8) or toluene (15.6), but less than styrene
(51.9).
Application of 0.2 m9. of cumene to shaved rat epidermis resulted 1n a
response of the sciatic nerve to electrical stimulation after 20 minutes,
which Indicates that cumene penetrated the skin. Dermal absorption In
rabbits was Indicated by CNS depression, gross pathological effects 1n the
viscera and death at higher doses after application of 2000-7940 mg/kg
cumene to the skin (Monsanto Co., 1984a).
0034d -29- 06/18/87
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Robinson et al. (1955) reported that cumene 1s absorbed following, oral
administration since 90% of an oral dose of 450 mg/kg to rabbits was
recovered as metabolites 1n the urine within 24 hours (Section 5.4.).
5.2. DISTRIBUTION
In a series of experiments, Fabre et al. (1955) examined the tissue
distribution of curoene In Wlstar rats exposed to the compound by Inhalation.
When rats were exposed to cumene vapor 8 hours/day for 10 days at 500 ppm
(2458 mg/ra3}, the highest concentrations were found 1n the spleen, bone
marrow and Hver, while lower concentrations were reported In the cerebellum
and kidneys. In a second experiment, rats exposed to cumene vapor at a
level of 500 ppm (2458 mg/m3), 8 hours/day for 2 months and sacrificed 24
hours after the last exposure had the highest concentration of the compound
1n the thyroid and adrenals. Lower concentrations occurred In the blood and
brain and,even lower concentrations occurred 1n the spleen, bone marrow and
liver. Cumene was detected In the blood of rats and rabbits 10 days follow-
ing vapor exposure to 500 ppm (2458 mg/m3) for 10 days and 1300 ppm (6391
mg/m3) for 150 days. WHh the exception of the adrenals, cumene was not
detected 1n any other organs In the rabbit.
In an abstract from the Russian literature, Gorban et al. (1978) studied
the tissue distribution of cumene In rats exposed by various routes to the
compound. After Intravenous administration of an unspecified level of
cumene, the highest concentrations of the compound were found In adipose
tissues, brain, adrenal glands, heart and lung. Maximum concentrations of
cumene were observed 1n adipose tissue at levels 15-20 times higher than 1n
adrenal glands and liver, when the tissues were evaluated 2-3 hours after
oral administration of the compound. Concentrations of cumene 1n the
tissues decreased sharply 2 days after oral dosing. Following Inhalation
0034d -30- 06/18/87
-------
exposure, levels of the compound 1n the tissues were found to be directly
correlated to level of exposure. Gerarde and Lltuten (1959) reported that
after absorption, cumene localized In tissues with a high I1p1d content.
5.3. METABOLISM
A single gavage dose of 450 mg/kg cumene was administered to Chinchilla
rabbits and -40, 25 and 25% of the dose was converted 1n 24 hours to the
glucuronlde conjugates of 2-phenyl-2-propanol, 2-phenyl-l-propanol and
2-phenylpropano1c acid, respectively (Robinson et a!., 1955), Bakke and
Schellne (1970) also Identified the glucuronlde conjugates of 2-phenyl-2-
propanol and 2-pheny1-1-propane! 1n the urine of albino rats given single
oral doses of 100 mg/kg cumene. The analytical method did not allow detec-
tion 1n rats of 2-phenylprop1on1c add, which was detected 1n the rabbit.
The same three metabolites (2-phenyl-2-propanol, 2-phenyl-l-propanol and
2-phenyl-propano1c add) were Identified after jm vitro Incubation with
cumene of enzymes from rat and rabbit livers, locust fat bodies and housefly
abdomens (Chakraborty and Smith, 1967). The main pathways of cumene metabo-
lism are summarized In Figure 5-1.
Senczuk and Lltewka (1976) Identified 2-phenyl-2-propanol 1n the urine
of humans exposed to cumene vapors at 240, 480 or 720 mg/m3 for 8-hour
exposure sessions (see Section 5.1.). Approximately 35% of the estimated
absorbed dose was converted Into the metabolite, as measured for a 48-hour
period following exposure. No attempt was made to Identify any other
metabolites.
Van Doom et al. (1981) reported an Increase 1n the urinary thlo com-
pounds following IntrapeMtoneal Injection of 125 mg/kg cumene Into male
Wlstar rats; 3.4% of the Injected dose was excreted as mercapturlc add,
which suggests that conjugation with glutathlone 1s not a major pathway for
cumene metabolism.
0034d -31- 06/18/87
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CHj-C-CH,
OH
I
CHj-CCH,
CH,-C-CH3
cumene 2-phenyH2-propanol excreted
glucuronide (40%)
n
2-phenyl-1 -pr opanol
2-phenylpropanoic
acid
H
i
CH,-C-CH:OG
I
H
'OG
excreted excreted
glucuronide (25%) glucuronide (25%)
= glucuronide
FIGURE 5-1
Main Pathways of Cumene Metabolism
Source: Williams, 1959
0034d
-32-
05/27/87
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Donahue and Harris (1945) reported an Increase 1n neutral sulfur and
ethereal sulfate compounds In the urine of dogs given oral doses of
0.43-0.86 g/kg cumene {0.5-1.0 cc/kgj. Amounts of metabolites excreted as a
percentage of dose were not reported.
5.4. EXCRETION
Approximately 90% of a single oral dose of 450 mg/lcg administered to
rabbits was excreted within 24 hours as glucuronlde conjugates of metabo-
lites (Robinson et a!., 1955). Humans exposed to Inhalation doses of curaene
at levels of 240, 480 or 720 rag/m3 for 8-hour sessions showed blphaslc
excretion of 2-piienyl-2-proj>anol 1n the urine after cessation of exposure
{Senczuk and tHewka, 1976). The half-lives of the two phases were reported
to be 2 and 10 hours, respectively.
5.5. SUMMARY
Data reported by several Investigators Indicate that cumene 1s absorbed
following oral, dermal and Inhalation exposure (Robinson et a!., 1955;
Vallette and Cavler, 1954; Monsanto Co., 1984a; Senczuk and Lltewka, 1976;
Sato and Nakajlma, 1979). The results of tissue analyses 1n rats following
exposure to cumene vapors for periods up to 150 days Indicate that the
compound distributes mainly to endocrine organs, CNS components, bone
marrow, spleen and liver (Fabre et al., 1955). Gorban et al. (1978) and
Gerarde and Linden (1959) reported that cumene localized 1n tissues with a
high I1p1d content. Cumene Is metabolized In a variety of species primarily
to the glucuronlde conjugates 2-phenyl-2-propanol, 2-phenyl-l-propanol and
2-phenylpropano1c add (Robinson et al., 1955; Senczuk and LHewka, 1976;
Bakke and Schellne, 1970; Chakraborty and Smith, 1967). Approximately 90%
of a single oral dose of cumene to rabbits was excreted within 24 hours as
0034d -33- 05/27/87
-------
glucuronlde conjugates of metabolites (Robinson et a!., 1955). Humans
exposed to Inhalation doses of cumene showed b1phasic excretion of 2-phenyl-
2-propanol 1n the urine (Senczuk and LUewka, 197%).
0034d -34- 05/27/87
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6. EFFECTS
6.1. SYSTEMIC TOXICITY
6.1.1. Inhalation Exposures.
6.1.1.2. SUBCHRONIC Fabre et al. (1955) exposed 36 Wlstar rats and
an unspecified strain of rabbits to a concentration of 500 ppra (2458
rag/m3) cumene vapor 8 hours/day, 6 days/week for 180 and 150 days, respec-
tively. Red and white blood cell counts and differential leukocyte counts
were made at 10-day Intervals during exposure and values for each species
were averaged. None of the blood parameters varied from the control values
In the rabbits, but the red blood cell counts were Increased slightly 1n the
rat. "Passive congestion" In the lungs, liver, spleen, kidney and adrenals
were observed from the hlstologlcal examination, although It was not clear
In which species this occurred. No other details were provided.
Jenkins et al. (1970) conducted two subchronlc Inhalation exposure
studies of cumene on groups of 15 Sprague-Dawley or Long-Evans rats, 15
Princeton derived guinea pigs, 2 beagle dogs and 2 squirrel monkeys (Salmlrl
sdurea). In the first study, the animals were exposed to 244 ppm (1200
mg/m3) cumene vapor 8 hours/day, 5 days/week for 30 exposures. In the
second study, the animals were exposed to 3.7 and 30 ppm (18 and 147
mg/m3) cumene vapor continuously for 90 days. Pre- and postexposure
values were obtained for body weight, leukocyte counts, hematocrlt and
hemoglobin content. The animals were sacrificed after the exposure period
and hlstopathologlcal examinations were performed on the heart, lung, liver,
spleen and kidneys of all species, and on the brain and spinal cord of the
dogs and monkeys. Normal values were compiled from preexposure data (encom-
passing the current study) from all experiments conducted 1n the reporting
laboratory. Treatment-related hlstopathologlcal effects were not found 1n
0034d -35- 06/18/87
-------
any of the organs or tissues at any exposure level. In addition, no com-
pound-related effects were observed 1n body weights or most hematologlcal
values; however, a degree of leukocytosls was observed only 1n the rats at
the end of the studies.
6.1.1.3. CHRONIC Pertinent data regarding the chronic Inhalation
toxldty of cumene to animals and humans could not be located In the avail-
able literature as cited 1n Appendix A.
6.1.2. Oral Exposures.
6,1.2.1. SU8CHSONIC in a 28-day study, groups of 10 male albino
rats were administered cwnene Vn ttw
-------
liver, kidney, spleen and testes. In addition, histopathologlcal examina-
tions were performed on the tissues examined grossly and the adrenals,
pancreas and femoral bone marrow. Examinations were conducted on rats that
were sacrificed when moribund or 18-22 hours after the last exposure. The
only treatment-related effect reported was Increased kidney weight* which
was slightly Increased at the 462 mg/lcg level and moderately Increased at
the 769 rag/kg level. No effect on kidney weight occurred at the low dose.
Insufficient data were provided to determine 1f the effect was significant.
No histopathologlcal, pathological or hematologlcal effects were reported at
any dose level.
6.1.2.1. CHRONIC Pertinent data regarding the chronic toxlclty of
orally administered cumene to animals and humans could not be located 1n the
available literature as cited 1n Appendix A.
6.1.3. Other Relevant Information. The oral LD5Q of cumene In rats was
reported to be 2700 mg/kg {Monsanto Co., 1984a) based on an assay using
Sprague-Oawley rats given single oral doses of cumene ranging from 2000-3980
mg/kg. The signs of Intoxication Included Increasing weakness, ocular
discharge, collapse and death. Hemorrhaglc lungs, liver discoloration and
acute gastrointestinal Inflammation were the pathological findings reported
1n the dead rats. Viscera appeared normal In the survivors sacrificed after
14 days of observation. An acute oral LD5Q of 2260 mg/kg was reported by
C1ba-Ge1gy Co. (1985) for male albino rats given oral doses of cumene rang-
ing from 1470-4640 mg/kg. Koch Refining Co. (1984) reported an acute oral
LD5Q of 1400 mg/kg In the rat. Based on data derived from a range finding
test. Union Carbide Corp. (1985) and Smyth et al. (1951) reported an oral
LD5Q for cumene of 2.91 g/kg when fed as a 20% dispersion 1n 1% Tergltol 7
to male albino Sherman strain rats, without previous withdrawal of feed.
0034d -37- 06/18/87
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The acute dermal LD5Q of cumene In New Zealand albino rabbits was
reported to be >3160 mg/kg when the compound was applied undiluted for 24
hours (Monsanto Co., 1984a). Hemorrhaglc areas 1n the lungs, Hver dis-
coloration, enlarged gall bladder, darkened kidney and spleen, and gastro-
intestinal Inflammation were the pathological findings reported In the dead
rabbits. The viscera of the survivors sacrificed after a 14-day observation
period appeared normal. The dermal ID of curaene was reported to be
>10,000 mg/kg 1n albino rabbits (dba-Gelgy Co., 1985). In a range finding
study. Union Carbide Corp. (1985) and Smyth et al. {1951) reported a dermal
LD5Q of 12.3 n."J-")9.*J) iWL/kg for skln penetration In ratblts after
application of the undiluted compound for 24 hours. Moderate to marked
erythema of the skin was noted at the end of the exposure period and the
principal damage at necropsy was to the kidney. Undiluted cumene applied to
the skin of New Zealand albino rabbits according to FHSA guidelines, at a
dose of 0.5 ml, produced slight defatting, which resulted In skin flaking
In 7-10 days. The FHSA Irritation score was 1.9 of a maximum of 8, which
does not classify cumene as a primary skin Irritant (Monsanto Co., 1984a).
Ciba-Geigy Co. (1985) reported a skin irritation score of 1.84/8 when 0.5
mi of undiluted cumene was applied to the skin of albino rabbits.
Application of 0.1 ma, undiluted cumene to the eyes of New Zealand
albino rabbits according to FHSA guidelines produced immediate discomfort,
followed by erythema and a copious discharge, which Improved after 48-72
hours and healed after 120 hours (Monsanto Co., 1984a). The FHSA Irritation
score was 7.6 of a maximum of 110, which classified cumene as an eye
irritant. Union Carbide Corp. (1985), however, reported that cumene was
harmless to rabbit eyes when applied undiluted at a dose of 0.5 ml.
C1ba-Ge1gy Co. (1985) reported an eye irritation score of 13/110 when 0.1
mi of undiluted cumene was applied to albino rabbits.
0034d -38- 06/18/87
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Nlelson and AlaMe (1982) found a dose-related decrease In the
respiratory rate In four male Swiss Webster alee exposed to 320-4450 ppm
(1570-21,880 mg/m3) cumene for 30 minutes. The RfD for cumene was deter-
mined to be 2490 ppm (12,240 mg/m3}. Werner et al. (1944) reported an
tC5Q of 10 wg/l {10,000 rag/m») In an unspecified strain of mice
exposed to curoene for 7 hours. A 4-hour LC5Q of 8000 ppm {39,329 mg/m3)
In rats was reported by Koch Refining Co. (1984) with effects of dizziness,
drowsiness, slight 1ncoord1nat1on and unconsciousness. Union Carbide Corp.
(1985) and Smyth et al. (1951) also reported a 4-hour Inhalation LC-0 of
8000 ppm (39,329 mg/m3) In rats. C1ba-Ge1gy Co. (1985) reported an acute
Inhalation LC5Q of >22.1 mg/l for a 1-hour exposure 1n male albino rats.
Signs of Intoxication such as excitation, lacrlmatlon, hyperpnea, tremors,
f1br1llary action, ataxla, prostration and sedation were noted. Monsanto Co.
(1984a) reported no toxic signs and no deaths In six Sprague-Dawley albino
male rats exposed by Inhalation to 17.6 mg/8, cumene for 6 hours. Fabre et
al. (1955) reported nervousness, Intoxication, disordered locomotion, loss
of balance, somnolence and death 1n Wlstar rats after 16 hours of continuous
exposure to cumene vapors at a concentration of 800 ppm (3933 mg/m3).
Deaths occurred between 1 and 16 hours from Initiation of exposures at a
concentration of 1322 ppm (6499 mg/m3).
6.2. CARCINOGENICITY
Pertinent data regarding the cardnogenlcHy of cumene could not be
located 1n the available literature as dted 1n Appendix A, and this chemi-
cal 1s not scheduled for testing by the NTP (1987).
0034d -39- 06/18/87
-------
6.3. MUTAGENICITY
Results of mutagetildty testing for cunrene are reported In Table 6-T.
Standard bacterial tests were conducted with the Ames Salmonella typhlmurlum
mlcrosomal assay, using plate Incorporation, spot test, vapor test and
sospetreloTi techniques on strains TA98, TA100, TA1535, TA1537 and TA1538.
Metabolic activation was provided by S-9 liver preparations from mice or
rats Induced with Aroclor 1254, Negative results were reported In all
assays by several Investigators up to dose levels that were toxic to the
tester bacteria {Monsanto Co,, 1984U, 1985; Florin *t a"L, 1980; S1im»n et
a!., 1977).
In addition, a negative response was also reported for cumene In the
Saccharomyces cerevlslae 03 mltotlc recombination assay with and without
metabolic activation (Monsanto Co., 1985; Simmon et al., 1977). Both of
these reports may have been derived from the same data since both studies
Involved the same principal Investigator.
Gulf 011 (1984a) reported positive results In the cell transformation
test when BALB/3T3 mouse embryo cells were exposed to cumene while growing
1n tissue culture. An Increase 1n transformations was observed at 60
jig/ml. Positive and vehicle controls Indicated proper functioning of
the assay system.
Cumene failed to elicit mlcronuclel formation 1n mouse bone marrow
polychromatic erythrocytes (Gulf 011, 1985a). A positive response for this
test 1s apparently Indicative of chromosomal damage.
A positive response for cumene was also reported by Gulf 011 (1984b) in
the DOS assay with rat hepatocytes from Fischer 344 rats. The expected
responses were achieved with both positive and negative controls. Cumene
was toxic to the hepatocytes at a dose level of 128 yg/m«, and UDS was
observed at doses of 16 and 32 jig/mi.
0034d -40- 06/18/87
-------
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Gulf 011 (1985b) also evaluated the mutagenlc activity of cumene 1n the
Chinese hamster ovary (CHO/HGPRT) cell system both 1t> the presence and
absence of metabolic activation. The test measures the mutation rate at the
HGPRT locus (HGPRT* -» HGPRT~). The results were considered negative
for both activated and nonactlvated treatments since there was no signifi-
cant Increase In mutant colonies at any dose level and no dose-related
response was observed,
6.4. TERATOGENICIPf
As reported 1n an anstratt from a Russian study (Seretrennlkov and
Ogleznev, 1978), pregnant rats were exposed by Inhalation to "maximum
permissible concentrations" of cumene for 4 months. The Incidence of
teratogenlc effects was reported to be Increased from 3-11% and the Inci-
dence of embryonal mortality from 7.5-39.3%. No additional Information was
provided and no other pertinent data regarding the teratogenldty of cumene
could be located In the available literature as cited In Appendix A.
6.5. OTHER REPRODUCTIVE EFFECTS
Pertinent data regarding other reproductive effects of cumene could not
be located In the available literature as cited 1n Appendix A.
6.6. SUMMARY
No data were available on the carcinogenic, reproductive, teratogenlc,
chronic oral or chronic Inhalation effects of cumene. Fabre et al. (1955)
reported passive congestion In the lungs, liver, spleen, kidney and adrenals
after subchronlc Inhalation exposure to cumene vapors at 500 ppm (2458
mg/m3), 8 hours/day, 6 days/week 1n rats and rabbits. Jenkins et al.
(1970) reported no compound-related effects on body weights or most hemato-
loglcal values 1n rats exposed to cumene vapors at 244 ppm (1200 mg/m3), 8
0034d -42- 05/27/87
-------
hours/day, 5 days/week for 30 exposures or to 3.7 or 300 ppm (18 or 147
fag/is3) continuously for 90 days. A degree of leukocytes is was observed
only In the rats at the end of the experiment.
No compound-related effects were reported 1n male albino rats adminis-
tered cumene 1n the diet at up to 6000 ppm for 28 days (C1ba-Ge1gy Co..
1985). Wolf et al, (1956) reported Increased kidney weights In rats admin-
istered cumene orally at levels of 462 and 769 mg/kg/day for 139/194 days.
No hlstopathologlcal, pathological or hematologlcal effects were reported at
any dose level.
Acute oral iD values reported for rats range from 1400-2900 mg/Vg
(Koch Refining Co., 1984; Monsanto Co., 1984a; C1ba-Ge1gy Co., 1985; Union
Carbide Corp., 1985; Smyth et al., 1951). Acute dermal LD5Qs for cumene
applied undiluted to rabbit skin range from >3160 mg/kg (Monsanto, 1984a) to
>10,000 mg/kg (C1ba-Ge1gy Co., 1985). A 4-hour Inhalation LC5Q of 8000
ppm (39,329 mg/m3) was reported by several Investigators (Koch Refining
Co., 1984; Union Carbide Corp., 1985; Smyth et al., 1951).
Cumene was reported to be nonmutagenlc both 1n the presence and absence
of metabolic activation when tested by the Salmonella mlcrosome assay In
several strains (Monsanto Co., 1984b, 1985; Florin et al., 1980; Simmon et
al., 1977). Negative results were also reported In the Saccharomyces
cerevlslae D3 mltotlc recombination assay with and without S-9 activation
(Monsanto Co., 1985; Simmon et al., 1977). In addition, cumene failed to
elicit micronuclel formation 1n mouse bone marrow polychromatic erythrocytes
(Gulf 011, 1985a) and the CHO/HGPRT test for point mutations was also nega-
tive In both S-9 activated and nonactlvated treatments (Gulf 011, 1985b).
Positive results were obtained for UDS 1n rat hepatocytes and for cell
transformation 1n mouse embryo cells (Gulf 011, 1984a,b).
0034d -43- 05/27/87
-------
A teratogenlc and embryolethal effect was reported 1n the offspring of
rats exposed by Inhalation to an unspecified concentration of curaene for 4
months (Serei>ren1n1kov ami Ogleznev, 1978). Other data regarding terato-:
genldty or reproductive effects of cumene were not found.
0034d -44- 05/27/87
-------
7. EXISTING GUIDELINES AND STANDARDS
7.1, HUMAN
ACGIH (19863,b) has recommended and adopted a TWA-TLV of 50 ppm (245
mg/m3) for exposure to cumene. In the absence of human data, the value
was recommended to prevent Induction of narcosis. The STEL (ACGIH, 1986b) of
75 ppm (365 rag/in3) was placed on the Notice of Intended Changes as a
deletion, with the TWA value retained. Deletion of the STEL was recommended
until adequate toxlcologlcal data become available to provide a better basis
for the STEL. The TLV 1s followed by a "skin" notation, since cumene Is
cons1
-------
8. RISK ASSESSMENT
8.1. CAfiCIHOfiENICITY
Since pertinent data regarding the carclnogenldty of cumene In humans
or animals were not located In the available literature, cumene Is classi-
fied as an EPA Group D chemical, i.e., not classifiable as to human carclno-
genldty.
8.2. SYSTEMIC TOXICITY
8.2.1. Inhalation Exposure.
8.2.1.1. LESS THAN LIFETIME EXPOSURES (SUBCHRONIC) - Data from two
subctironlc Inhalation studies were available for consideration of the RfO.
In one study, 36 Wlstar rats were exposed to cumene vapors at a concentra-
tion of 500 ppm (2458 mg/ma), 8 hours/day, 6 days/week for 180 days (Fabre
et a!., 1955). The authors reported "passive congestion" In the lungs,
liver, spleen kidneys and adrenals; however, the data were unclearly and
Imprecisely presented.
In the second study, Jenkins et al. (1970) exposed groups of 15 Sprague-
Dawley or Long Evans rats, 15 Princeton derived guinea pigs, 2 beagle dogs
and 2 squirrel monkeys to cumene vapors at 244 ppm (1200 mg/m3), 8 hours/
day, 5 days/week for 30 exposures and to 3.7 and 30 ppm (18 and 147 mg/m3)
continuously for 90 days. No treatment-related hlstopathologlcal effects
were found 1n any organ or tissue at any exposure level. In addition, no
compound-related effects were observed 1n body weight or most hematologlcal
values; however, 1n the rats a slight degree of leukocytosls was observed at
the end of the experiments. The 90-day continuous exposure level of 3.7 ppm
(18 mg/m3) (Jenkins et al., 1970) constitute a LOAEL for the rats and a
NOAEL for the guinea pigs. Reference Inhalation rates and body weights of
0.223 mVday and 0.35 kg for rats and 0.4 m3/day and 0.84 kg for guinea
pigs (U.S. EPA, 1985b) can be used to calculate transformed LOAEL of 11.5
0034d -46- 08/26/87
-------
mg/kg/day for the rats and NOAEL of 8.6 mg/kg/day for the guinea pigs. The
NOAEL 5s the more appropriate basis for an RfD. Dividing the NOAEL of 8.6
mg/kg/day by an uncertainty factor of 100' (10 for Interspecles extra-
polation, 10 for the range of sensitivities 1n humans and results In a
subchronlc Inhalation RfD of 0.09 mg/kg/day or 6 mg/day for a 70 kg man.
Assuming an Inhalation rate of 20 mVday for a human the RfO Is equivalent
to 0.3 mg/ra3. The level of confidence In the Jenkins et al. (1970) study
1s considered low since a NOEL could not be Identified and relatively few
animals were evaluated. Little supporting Inhalation data were available;
therefore, a low level of confidence In the RfD reflects the degree of
confidence In the study and the data base.
8.2.1.2. CHRONIC EXPOSURES -- Since no chronic Inhalation data were
available, the subchronlc Inhalation RfD derived from the Jenkins et al.
(1970) study could be used as the chronic Inhalation RFD, by using an
additional uncertainty factor of 10 to adjust for the extrapolation from
subchronlc to chronic exposure. Therefore, applying an uncertainty factor
of 1000 to the subchronlc NOAEL of 8.6 mg/kg/day results 1n a chronic
Inhalation RfD of 0.009 mg/kg/day or 0.6 mg/day (0.03 mg/m3). As
discussed In the above section, the confidence In the Inhalation RfD Is
considered low. Additional research 1s needed to support a more confident
RfD value.
8.2.2. Oral Exposures.
8.2.2.1. LESS THAN LIFETIME (SUBCHRONIC) Two subchronlc oral
exposure studies were available for consideration for the oral RfD. In a
study reported by Clba-Gelgy Co. (1985), diets that provided doses of 0,
22.8, 224.8 and 535.8 mg/kg/day were administered to rats for 28 days. A
significant Increase In the relative testls weight was reported only In the
group Ingesting 224.8 mg/kg/day, but no pathological lesions were noted upon
0034d -47- 08/26/87
-------
necropsy. No deaths occurred and no compound-related effects on behavior,
body weight, relative weights of the liver, kidney or adrenal or gross
pathology were reported.
Wolf et al. (1956) administered cumene 1n olive oil by stomach tube to
groups of 10 female Wlstar rats at dosages of 154, 462 and 769 mg/kg/day for
a total of 139 doses 1n 194 days. The TWA doses were 110, 331 and 551
mg/kg/day. No effects were observed at the 110 mg/kg/day dosage. The only
treatment-related effect reported was Increased kidney weight, which was
slightly Increased at the 331 mg/kg/day dosage and moderately Increased at
the 769 wgAg/day level. Tt» data from the Wolf et al. (1956) study was
chosen as the basis for the RfO since the study was longer than the
C1ba-Ge1gy (1985) study and a NOEL (110 mg/kg/day) and LOAEL (331 mg/kg/day)
could be Identified. Dividing the NOEL of 110 mg/kg/day by an uncertainty
factor of 100 (10 for Interspedes extrapolation and 10 to protect the
sensitive members of the population) yields a subchronlc oral RfD of 1
mg/kg/day or 77 mg/day for a 70 kg man.
The level of confidence In the Wolf et al. (1956) study Is considered
medium since both a NOEL and LOAEL were Identified by assessment of several
endpolnts, even though the group sizes were relatively small. Although two
subchronlc Inhalation studies with the same species provide supportive data,
there are no chronic studies; therefore, a low level of confidence 1n the
data base Is recommended. A medium to low level of confidence In the RfD
reflects the degree of confidence In the Wolf et al. (1956) study and the
data base.
8.2.2.2. CHRONIC EXPOSURES -- No studies are available concerning the
chronic oral administration of cumene. Therefore, the subchronlc oral RfD
derived from the Wolf et al. (1956) study can be used for the chronic oral
RfD with the use of an additional uncertainty factor of 10 to account for
0034d -48- 08/26/87
-------
extrapolation from subchronlc to chronic exposure. Thus, applying an
uncertainty factor of 1000 to the NOEL of 110 mg/kg/day results In an RfD of
0.1 mg/kg/day or 8 mg/day for a 70 kg man. The level of confidence 1n the
RfD Is considered medium to low, as discussed In the previous section.
0034d -49- 08/26/87
-------
9. REPORTABLE QUANTITIES
9.1. BASED OK SYSTEMIC TOXICITY
The toxlclty of cumene was discussed In Chapter 6 and the available
stadles are summarized 1n Table 9-1. No chronic toxlclty studies were
available; however, studies with exposure periods ranging from 28-194 days
were located. The 28-day oral exposure study using male rats reported by
C1ba-G«1gy Co. (1985) Is Inappropriate to consider for the RQ since the
exposure period was so short and the effect of Increased testlcular weight
was only observed at the middle dose level. Mo other effects at any dose
level were reported. Likewise, the 160-day Inhalation exposure study
reported by Fabre et al. (1955) should not be considered for the RQ since
the results of the study were not clearly presented.
Data used to calculate the CSs are presented In Table 9-2. Jenkins et
al. (1970) conducted both a 90-day continuous exposure and a 30-day Inhala-
tion exposure study using several different species. Leukocytosls was the
onli effect and was observed 1n the rats by both exposure regimens. The
lowest equivalent human dose In these experiments was 2.0 mg/kg/day. Multi-
plying by 70 kg and dividing by an uncertainty factor of 10 to approximate
chronic exposure yields the MED of 14 mg/day, which corresponds to an RV.
of 3.8. The RV& for leukocytosls 1s 3. Multiplying the RVrf by the
RV yields the CS of 11, which corresponds to an RQ of 1000.
The MED of 396 mg/day for the rat oral study reported by Wolf et al.
(1956) was calculated by multiplying the equivalent human dose of 56.6
mg/kg/day by 70 kg and dividing by an uncertainty factor of 10 to approxi-
mate chronic exposure. The corresponding RV, Is 1.6. The effect of
Increased kidney weight warrents an RV of 4. Multiplying the RV by
6 S
the RV. results 1n a CS of 6.4, which corresponds to an RQ of 1000.
0034d -50- 06/18/87
-------
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Data from both the Wolf et al. {1956} and Jenkins et al. (1970) studies
result 1n an RQ of 1000; however, the CS obtained from the Jen* 1ns et al.
(1970) data for Increased leukocytosls In rats exposed to cumene vapors
continuously for 90 days 1s higher than the CS' obtained from the oral
exposure data of Wolf et al. (1956), Therefore, the data reported by Jenkins
et al. (1970) Is recommended as the basis for the RQ for curoene (Table 9-3).
9.2. BASED ON CARCINOGENICITY
No pertinent data were available regarding the carclnogenldty of cumene
by oral or Inhalation routes. Therefore, the compound may be classified 1n
EPA Group D until the carclnogenldty of cutnene has been adequately
evaluated.
0034d -53- 05/27/87
-------
TABLE 9-3
Cumene
Effective Dose (MED) and Reportable Quantity (RQ)
Route:
Dose*:
Effect:
Reference:
RVd:
RVe:
Composite Score:
RQ:
inhalation
14 ing/day
leukocytosls
Jenkins et al., 1970
3.8
3
11
1000
*Equ1valent human dose
0034d
-54-
05/27/87
-------
10. REFERENCES
ACGIH (American Conference of Governmental Industrial Hyg1en1sts). 1986a.
Documentation of the Threshold Limit Values and Biological Exposure Indices,
5th ed. Cincinnati. OH. 5: 151.
ACGIH (American Conference of Governmental Industrial Hyg1en1sts), 1986b.
TLVs: Threshold limit values for chemical substances 1n the Work Environment.
Adopted by ACGIH with Intended changes for 1986-1987.
AHverdleva, S.S. and K.I. Mlnchuk. 1973. Atmospheric air pollution 1n the
Industrial area of a synthetic rubber plant. Tr. Azerb. Nauchno-Issled Inst.
G1g. Tr. Prof. Zabol. 8: 59-61. (Rus.) (CA 82:76697w)
Amoore, J.E. and E. Hautala. 1983. Odor as an aid to chemical safety: Odor
thresholds compared wUh threshold limit values and volatilities for 214
Industrial chemicals 1n air and water dilution. J. Appl. Toxlcol. 3(6):
272-290.
API (American Petroleum Institute). 1984. Letter and attachment from W.F.
O'Keefe to M. Grelf, TSCA Interagency Testing Committee, U.S. EPA (TS-792),
Washington, DC.
Arnts, R.R. and S.A. Meeks. 1980. B1ogen1c hydrocarbon contribution to the
ambient air of selected areas: Tulsa Great Smokey Mountains, R1o Blanco
County, CO. Office of Research and Development, U.S. EPA, Research Triangle
Park, NC. EPA 600/3-80-023.
0034d -55- 05/27/87
-------
Arnts, R.R. and S.A. Meeks. 1981. B1ogen1c hydrocarbon contribution to the
ambient air of s-elected areas. Aimos. Environ. 15(9): 1643-1651.
Bakke, O.M. and R.R. Schellne. 1970. Hydroxylatlon of aromatic hydrocarbons
In the rat- Toxlcol. Appl. Pharmacol. 16: 691-700.
Bobra. A.M., W.Y. Sh1u and 0. Mackay. 1983. A predictive correlation for
the acute toxlclty of hydrocarbons and chlorinated hydrocarbons to the water
flea (Daohnla manna). Oienosphere. 12(9,10): 1121-1129.
Botta, 0., L. Castellanl P1rr1 and E. Hantlca. 1984. Groundwater pollution
by organic solvents and their mlcroblal degradation products. Comm. Eur.
Communities (Rep) EUR, EUR 8518, Anal. Org. Mlcropollut. Water, p. 261-274.
BozzelH, J.W., B.B. Kebbekus and A. Greenburg. 1980. Analysis of selected
toxic and carcinogenic substances In ambient air 1n New Jersey. Office of
Cancer and Toxic Substances Research, New Jersey Department of Environmental
Protection. (CUed In U.S. EPA, 1985c)
Brlngmann, G. and R. Kuehn. 1982. Results of the toxic action of water
pollutants on Daphnla magna 1n an Improved standardized procedure. (Ger).
Z. Wasser Abwasser Forsch. 15(1): 1-16.
Brooks, J.M., D.A. Wlesenburg, G. Bodennec and T.C. Sauer, Jr. 1983.
Volatile organic wastes at the Puerto R1co dumpslte. In.: Wastes Ocean,
Vol. 1, I.W. Duedall, Ed. John WHey Publisher, New York, NY. p. 171-198.
0034d -56- 06/18/87
-------
Brown, D.W., A.J. Friedman, O.G. Burrows, et al. 1979. Investigation of
petroleum 1n the marine environs of the Strait of Juan de Fuca and northern
Puget Sound. EPA 600/7-79-164.
Burmaster, O.E. 1982. The new pollution: Groundwater contaalnation.
Environment. 24,(2): 7-36.
Burnham, A.K., G.V. Calder, J.S. Fritz, G.A. Junk, H.J. Svec and R. Willis.
1972. Identification and estimation of neutral organic contaminants In
potatl* water. Anal. Chan. 44{1): 139-142.
Chakraborty, J. and J.N. Smith. 1967. Enzymlc oxidation of some alkyl-
benzenes 1n Insects and vertebrates. Blochem. J. 102: 498-503.
Chuevskaya, A.I. and L.G. Dudko. 1971. Chromatographlc determination of
organic substances 1n waste waters from a synthetic rubber factory. Nauch
Tr. Omsk Med. Inst. 107: 13-14. (Rus). (CA 78:151312q)
Clba-Geigy Co. 1985. "Blofax" Toxicology Data Summary Sheet (undated-
unpublished). TSCA sec 8(d) submission 878215034. Office of Toxic Sub-
stances, U.S. EPA, Washington, DC.
CMR (Chemical Marketing Reporter). 1984. Chemical Profile: Cumene. July
23, 1984. Schnell Publishing Co., Inc., New York.
Cocheo, V., M.L. Bellomo and G.G. Bombi. 1983. Rubber manufacture: Sampl-
ing and identification of volatile pollutants. Am. Ind. Hyg. Assoc. J.
44(7): 521-527.
0034d -57- 05/27/87
-------
Coleman, E.G., C.T. Ho and S.S. Chang. 1981. Isolation and Identification
of volatn* compounds from .bated potatoes. 3. AgMc. Food Chetn. 29(1):
.42-48.
Coleman, W.E.. J.H. Munch, R.P. Stretcher. H.P. Rlnghand and f.C. Kopfler.
1984. The Identification and measurement of components In gasoline,
kerosene, and No. 2 fuel oil that partition Into the aqueous phase after
mixing. Arch. Environ. Contam. Toxlcol. 13: 171-178.
Conkle, 3.P., B.J. Camp and B.E. Welch. 1975. Trace composition of human
respiratory gas. Arch. Environ. Health. 30(6): 290-295.
CRCS, Inc. 1984. Information Review - Cumene. Prepared under EPA Contract
No. 68-OT-5789 for: TSCA Interagency Testing Committee. IR-464.
D1r1nck, P., J. Veys, M. Oecloedt and N. Schamp. 1980. Head-space enrich-
ment on tenax for characterization and flavor evaluation of some tobacco
types. Tob. Int. 182(26): 125-129.
Donahue, O.D. and M.R. Harris. 1945. The metabolism of cumene by the dog.
Fed. Proc. 4: 116.
Dougan, J., J.M. Robinson, S. Sumar, G.E. Howard and O.G. Coursey. 1983.
Some flavoring constituents of cassava and of processed cassava products.
J. Sc1. Food AgMc. 34(8): 874-884.
0034d -58- 06/18/87
-------
Dow Chemical Co. 1985. TSCA sec. 8(d) submission 878214937. Summary of
environmental data. Dow Item 1594. Office of Toxic Substances, U.S. EPA,
Washington, DC.
, V.A., V.A. Levs1vte1n. L.G. Strucnkova and £.1. Tslrenova. 1977.
Gas-chromatograph1c analysis of waste water from production of phenol and
acetone. Metody Anal. Kontrolya Proizvod Khlm Prom-stl. 9: 18-19. (Rus.)
(CA 88: 11 0095 j)
Dumont, 3. P. and 3. Adda. 1973. Occurrence of sesqulterpenes In mountain
cheese volatile*. 3. Agrlc. Food Chem. 26(2): 364-367.
E1senre1ch, S.3., B.B. Looney and 3.0. Thornton. 1981. Airborne organic
contaminants of the Great Lakes ecosystem. Environ. Sc1. Technol. 15(1):
30-38.
Erben, R. 1978. Effects of some petrochemical products on the survival of
Dlcranophorus fordpatus O.F. Mueller (RotatoMa) under laboratory condi-
tions. Verh-Int Ver Theor Angew Llmnol. 20(3): 1988-1991.
Erben, R. and B. Beader. 1983a. Effect of cumene, acetone, and acrylo-
nltMle on the crabs Asellus aquatlcus L. and Gammarus fossaMum Koch
(Isopoda, Amphlpoda). Poljopr Sumar. 29(2): 105-114. (CA 100:97766y)
Erben, R. and B. Beader. 1983b. Effect of some petrochemical products on
survival of the snails Lymnaea stagnalis L. and Radix peregra Mull.
(Pulmonata). Poljopr Sumar. 29(1): 29-36. (CA 100:97764w)
0034d -59- 06/18/87
-------
Fabre, R., R. Truhaut, T. Bernuchon and F. Lo1s1H1er. 1955. Toxlcologlc
studies of solvents to replace benzene. III. Study of Isopropylbenzene on
cumene. Arch. Mai. Prof. 16(4): 285-299.
Fisher, G.S,, H.G. Legendre, N.V. Lovgren, W.H. Schuller and 3.A. Wells.
1979. Volatile constituents of southernpea seed [Vlgna unqulculata (L.)
Walp.]. J. Agrlc. Food Chem. 27(1): 7-11.
Flath. fi,A. and fi.R. Forrey. 1977. Volatile components of papaya (Carljca
papaya 1.. solo variety). 3, Aqrlc. Food Chem. *25{1)' 103-109.
Florin, I., L. Rutberg, H. Curvall and C.R. Enzell. 1980. Screening of
tobacco smoke constituents for mutagenlclty using the Ames1 test.
Toxicology. 15(3): 219-232.
Gavin, J., G. N1coll1er and R. Tabacchl. 1978. Volatile constituents of
"oakmoss" (Evernla prunastrl (L.)). Part 3. Helv. Ch1m. Acta. 61(1):
352-357.
Gerarde, H.W. and N.J. Linden. 1959. Tox1colog1cal studies on hydrocarbons.
III. The blochemorphology of the phenylalkanes and phenylakenes. AMA Arch.
Ind. Health. 19: 403-418.
Gorban, G.H., G.I. Solomln, Y.P. B1z1n, et al. 1978. Study of the toxldty
and determination of the threshold of the acute Inhalation effect of
Isopropyl benzene. G1g. SanH. Issue. 10: 113. (Rus.) (Toxllne Abstract)
(Cited In CRCS, Inc., 1984)
0034d -60- 06/18/87
-------
Gordon, A.W. and H. Gordon. 1981. Analysis of volatile organic compounds
In a textile finishing plant effluent. Trans. Kentucky Acad. Science.
42(3-4): 149-157.
Sraddon. JLD., J.D. ftorrlson and 3.F. Smith. 1979. Volatile constituents
of some unlfloral Australian honeys. 0. Agrlc. Food Chem. 27(4): 832-837.
Grosjean, D. and K. fung. 1984. Hydrocarbons and carbonyls In Los Angeles
air. J, Air. Pollut. Control As&oc. 34: 537-543.
Gulf 011. 1984a. Gulf 011 Products Co. TSCA sec. 8(e) submission
8EHQ-11840536 88-8500694. Project No. 84-2131: Cell transformation test of
cumene. Office of Toxic Substances, U.S. EPA, Washington, DC. (Also Flche
No. OTS 0509712).
GiTf 011. 1984b. Gulf 011 Products Co. TSCA sec. 8(e) submission' 8EHQ-
11840536 88-8500694. Project No. 84-2130: Hepatocyte primary culture/DNA
repair test of cumene. Office of Toxic Substances, U.S. EPA, Washington,
DC. (Also Flche No. OTS 0509712)
Gulf Oil. 1985a. Gulf 011 Products Co. TSCA sec. 8(d) submission
878216011. Mlcronucleus test of cumene. Office of Toxic Substances, U.S.
EPA, Washington, DC.
Gulf 011. 1985b. Gulf 011 Products Co. TSCA sec. 8(d) submission
878216011. CHO/HGPRT test of cumene. 1985. Office of Toxic Substances,
U.S. EPA, Washington, DC.
0034d -61- 06/18/87
-------
Hampton, C.V., W.R. Plerson, T.H. Harvey. W.S. Updegrove and R.S. Harano.
1982. Hydrocarbon gases emitted from vehicles on the road. 1. A qualita-
tive gas chromatography mass/spectrometry survey. Environ. Sc1. Techno!.
16(5): 287-298.
Hansch, C. and A.J. Leo. 1985. Medchem Project. Issue No. 26. Pomona
College, Claremont, CA.
Harrison, F.L., O.J. Bishop aad B.J. Malion. 1985. Comparison of organic
combustion products In fly ash collected by a VentuM wet scrubber and an
electrostatic predpHator at a coal-fired power station. Environ. Sc1.
Technol. 19(2): 186-193.
Hawthorne, A.R., R.B. Gammage, C.S. Dudney, et al. 1983. Preliminary
results of a forty-home Indoor air pollutant monitoring study. In_: Spec.
Conf. Meas. Monlt. Non-Crlter. (Toxic) Contam. Air, E.R. Frederick, Ed. A1r
Pollut. Control Assoc., Pittsburgh, PA. p. 514-526.
Heydanek, M.G. and R.J. McGorrln. 1981. Gas chromatography-mass spectro-
scopy Investigations on the flavor chemistry of oat groats. J. Agrlc. Food
Chem. 29(5): 950-954.
Ho, C.T., K.N. Lee and Q.Z. Jin. 1983. Isolation and Identification of
volatile flavor compounds In fried bacon. J. Agrlc. Food Chem. 31(2):
336-342.
0034d -62- 06/18/87
-------
Holzer, 6., J. Oro and W. Bertsch. 1976. Gas chroroatographlc-mass spec-
troraetrlc evaluation of exhaled tobacco smoke. J. Chroa»ato
-------
Kappeler, T. and K. Wuhrmann. 1978t>. Mlcroblal degradation of the water-
soluble fraction of gas oil. II. Bloassays with pure strains. Water Res.
12: 335-342.
Karrenbrock F. and K. Haberer. 1982. Identification of organic solvents In
the water of a freshly coated drinking-water reservoir. Zentralbl.
Bakterlol. M1krob1al. Hyg., 1 Atot, Or1g. B. 176(5-6): 519-524. {Cited 1n
U.S. EPA, 1985c)
Katzman, H. and W.F. Llbby. 1975. Hydrocarbon emissions from jet engines
operated at simulated high-altitude supersonic flight conditions. Atmos.
Environ. 9(9): 839-842.
Keith, L.H., A.W. Garrison, F.R. Allen et al. 1976. Identification of
organic compounds In drinking water from thirteen U.S. cities, lr±: Identifi-
cation and Analysis of Organic Pollutant- 1n Water, L.H. Keith, Ed. Ann
Arbor Science, Ann Arbor, HI. p. 329-373.
Koch Refining Co. 1984. Material safety data sheet: Cumene-unpubllshed.
Corpus Chrlstl, TX.
Konasawlch D., W. Traversy and H. Zar. 1978. Great Lakes Water Quality
Board - Appendix E. Status report on organic and heavy metal contaminants
In the lakes Erie, Michigan, Huron and Superior basins. International Joint
Commission, Great Lakes Water Quality Board. Windsor, Ontario, p. 139.
(Cited In U.S. EPA, 1985c)
0034d -64- 06/18/87
-------
Kopfler, F.C., R.G. Melton, J.L. Mullaney and R.G. Tardlff. 1977. Human
exposure to water pollutants. In: Advances In Environmental Science and
Technology. Vol. 8. Fate of Pollutants 1n the A1r and Hater Environments.
Part 2. Chemical and Biological Fate of Pollutants In the Environment, I.H.
Suffet, £d. Symposium at the 165th National American Chemical Society
Meeting In the Environmental Chemistry Division, Philadelphia, PA, USA,
April, 1975. John WHey Publisher, New York. p. 419-433.
Krotoszynskl, B.Jt. and H.J. O'Melll. 1982. Involuntary feloactumilallon of
environmental pollutants In nonsmoking heterogeneous human population. J.
Environ. Sc1. Health Part A Environ. Sc1. Eng. 17(6): 855-883.
Le Roux, S. 1977. The toxlclty of pure hydrocarbons to mussel larvae.
Rapp P-V Reun Cons Int. Explor. Mer. 171: 189-190.
« *
Lloyd, A.C., K.R. Darnall, A.M. Winer and J.N. Pitts, Jr. 1976. RelaJve
rate constants for reaction of the hydroxyl radical with a series of
alkanes, alkenes, and aromatic hydrocarbons. J. Phys. Chem. 80(8): 789-794.
Lonneman, W.A., T.A. .Bellar and A.P. Altshuller. 1968. Aromatic hydro-
carbons 1n the atmosphere of the Los Angeles basin. Environ. Scl. Technol.
2(11): 1017-1020.
Lonneman, W.A., 6.R. Namle and J.J. Bufallnl. 1979. Hydrocarbons In Houston
air. Office of Research and Development, U.S. EPA, Research Triangle Park,
NC. EPA 600/3-79-018.
0034d -65- 06/18/87
-------
Lovegren, N.V., G.S. Fisher, H.G. Legendre and U.H. Schuller. 1979. Vola-
tile constituents of dried legumes. J. Agrlc. Food Chem. 27(4): 851-853.
lyman, W.J., W.F. Reehl and D.H. Rosenblatt. 1982. Handbook of Chemical
Property Estimation Methods. McBraw HT11 Book Co., New York. p. 4-9, 5-5,
7-4, 15-13, 15-21, 15-27.
Mackay, 0. and W.Y. Sh1u. 1381. A critical review of Henry's Law constants
for chemicals of environmental Interest. 3. Phys- Chem. Ref. Data, 19;
1175-1199.
Halaney, G.W. 1960. Oxldatlve abilities of aniline-acclimated activated
sludge. J. Water Pollut. Control Fed. 32: 1300-1311.
Malaney, G.W. and R.E. McKlnney. 1966. Oxldatlve abilities of benzene-
acclimated activated sludge. Water Sewage Works. 113(8): 302-3o9.
Mallns, D.C., B.8. McCain, O.W.-Brown, et al. 1984. Chemical pollutants In
sediments and disease of bottom-dwelling fish 1n Puget Sound, Washington.
Environ. Sc1. Technol. 18(9): 705-713.
Marlon, C.V. and G.W. Malaney. 1964. Ability of activated sludge micro-
organisms to oxidize aromatic organic compounds. Proc. Ind. Waste Conf.
18: 297-308.
McKnlght, O.M., W.E. Perelra, M.L. Ceazan and R.C. Wlssmar. 1982. Charac-
terization of dissolved organic materials In surface waters within the blast
zone of Mount St. Helens, Washington. Org. Geochem. 4(2): 85-92.
0034d -66- 06/18/87
-------
M111, T., H. Richardson and D.G. Hendry. 1978. Oxidation of organic com-
pounds In aquatic systems: The free radical oxidation of cumene. In: Aquatic
Pollutants: Transformation and Biological Effects. Proc. 2nd International
Symposium on Aquatic Pollutants, Noordwljkerhout (Amsterdam), The Nether-
lands, Sept. 26-28, 1977, 0. Hutzlnger, I.H. Van Lelyveld and B.C.J.
Zoeteman, Ed. Pergamon Press, New York, NY. p. 223-236.
Mill, T., D.G. Hendry, H. Richardson and A. Baraze. 1979. SRI Inter-
national. Chemical oxidation processes 1n aquatic systems: Oxidation of
cumene, pyMdlne and p-cresol. National Science Foundation Grant No.
ENV76-11153. NSF/RA-790085; NTIS PB-298088, 73 p.
Mill, T., D.G. Hendry and H. Richardson. 1980. Free-radical oxldants 1n
natural waters. Science. 207: 886-887.
k!}.F. and A.J. Alkezweeny. 1980. Aerosol formation In urban plumes
over Lake Michigan. Ann. NY Acad. Sc1. 338: 219-232.
Mody, N.V., E.J. Parish, 3. Bhattacharyya, D.H. Miles and P. A. Hedln. 1974a.
Constituents of marsh grass. IV. Essential oil In Sclrpus amerlcanus.
Phytochemlstry. 13(9): 2027-2029.
Mody, N.V., J. Bhattacharyya, D.H. Miles and P. A. Hedln. 19745. Con-
stituents of marsh grass. II. Survey of the essential oil In Spartlna
cynosuroldes. Phytochemlstry. 13(7): 1175-1178.
0034d -67- 06/18/87
-------
Hody, N.V., A.A. de la Cruz, O.H. Miles and P.A. Hedln. 1975. Constituents
of marsh grass. V. The essential oil of Dlstlchlls splcata. Phytochenlstry.
14{2): 599-601.
Moelhave, L. 1979. Indoor air pollution due to building materials. Proc.
First Int. Indoor CHra. Syrop. p. 89-110.
Monsanto Co. 1984a. Cumene health study Y-78-213: Acute toxldty, eye and
skin Irritation, 1978 TSCA sec. 8{d) submission 878215096. Office of Toxic
Substances, U.S. EPA, Washington, DC.
Monsanto Co. 1984b. Cumene health study ML-81-107: Ames/Salmonella
mutagenlclty assay of cumene, 1982. TSCA sec. 8(d) submission 878215097.
Office of Toxic Substances, U.S. EPA, Washington, DC.
Monsanto Co. 1985. Jji vitro microbiological mutagenldty assays of
Isopropyl benzene (cumene), 1978. TSCA sec. 8(d) submission 878215095.
Office of Toxic Substances, U.S. EPA, Washington, DC.
Montz, W.E., Jr., R.L. Puyear and J.D. Brammer. 1982. Identification and
quantification of water-soluble hydrocarbons generated by two-cycle outboard
motors. Arch. Environ. Contam. Toxlcol. 11(5): 561-565;
Morrison, R.T. and R.N. Boyd. 1973. Organic Chemistry, 3rd ed. Allyn and
Bacon, Inc., Boston, MA. p. 372-389.
0034d -68- 06/18/87
-------
Nellgan, R.E.. M.J. Leonard and R.J. Bryan. 1965. The gas chromatographlc
determination of aromatic hydrocarbons 1n the atmosphere. ACS Nat Meeting.
p. 118-121.
Nelson, P.f. and S.M. Qulgley. 1984. The hydrocarbon composition of
exhaust emitted from gasoline fueled vehicles. Atmos. Environ. 18(1):
79-87.
Nlelson, G.D. and Y. Alarie. 1982. Sensory Irritation, pulmonary Irrita-
tion, and respiratory stimulation by airborne benzene and alkylbenzenes:
Prediction of safe Industrial exposure levels and correlation with their
thermodynamlc properties. Toxlcol. Appl. Pharmacol. 65(3): 459-477.
NIOSH (National Institute for Occupational Safety and Health). 1984.
Current Awareness File. RTECS (Registry of Toxic Effects of Chemical
Substances).
NTP (National Toxicology Program). 1987. Management Status Report.
1/13/87.
Nutmagul, H.. D.R. Cronn and H.H. Hill, Jr. 1983. Photolonlzatlon/flame-
1on1zat1on detection of atmospheric hydrocarbons after capillary gas chroma-
tography. Anal. Chem. 55(13): 2160-2164.
Ogata, M., K. Fujlsawa, Y. Oglno and E. Mano. 1984. Partition coefficients
as a measure of bloconcentratlon potential of crude oil compounds In fish
and shellfish. Bull. Environ. Contain. Toxlcol. 33: 561-567.
0034d -69- 06/18/87
-------
Oldham, R.G., R.L. Spragglns, J.L. Parr and K.W. Lee. 1979. Analysis of
organic* 1n ambient air. Jjn: Proc. Spec. Conf. Control Specific (Toxic)
Pollut., E.R. Frederick, Ed. A1r Pollut. Control Assoc,, Pittsburgh, PA.
p. 130-149.
Oraorl, T., Y. Jlgatnl and Y. Mlnoda. 1975. Isolation, Identification and
substrate assimilation specificity of some aromatic hydrocarbons utilizing
bacteria. Agrlc. B1ol. Chera. 39; 1775-1779.
OSHA (Occupational Safety and Health Administration). 1985. Occupation
Standards. Permlssable Exposure Limits. 29 CFR 1910.1000.
Parlar, H., M. Coelhan, D. Vaughan, P. Czermak, U. Kohler and F. Korte.
1.983. Gas phase-mass analyzer system for the determination of the photo-
stabUHy of organic compounds under simulated tropospherlc conditions.
Fresenlus Z. Anal. Them. 315(7): 605-609.
Pell1zzar1, E.O., N.P. CastHo, S. Willis, D. Smith and J.T. Bursey. 1979.
Identification of organic components In aqueous effluents from energy-related
processes. ASTH Spec. Tech. Publ. 686 (Meas. Org. Pollut. Water Wastewater).
p. 256-274.
Price, K.S., G.T. Waggy and R.A. Conway. 1974. Brine shrimp bloassay and
seawater BOD of petrochemicals. J. Water Pollut. Control Fed. 46(1): 63-77.
Ravlshankara, A.R., S. Wagner, S. Fischer et al. 1978. A kinetics study of
the reaction of OH with several aromatic and oleflnlc compounds. Int. J.
Chem. Kinetics. 10: 783-804.
0034d -70- 06/18/87
-------
Robinson, 0., J.N. Smith and R.T. Williams. 1955. Studies In detoxlcatlon.
60. The metabolism of alkylbenzenes: Isopropylbenzene (cumene) and deriva-
tives of hydratroplc add. Blochem. J. 59: 153-159.
Rogerson A., W.Y. Sh1u, G.L. Huang, 0. Mackay and J. Berger. 1983. Deter-
mination and Interpretation of hydrocarbon toxtclty to dilate protozoa.
Aquat. Toxlcol. 3(3): 215-228.
Sadtler. 1960. Standard UV Spectra no. 95, Sadtler Research Lab. Phila-
delphia, PA.
Sasaki, S. 1978. The scientific aspects of chemical substances control law
1n Japan. In_: Aquatic Pollutants: Transformation and Biological Effects, 0.
Hutzlnger, L.H. Van Letyoeld, B.C.J. Zoeteman, Ed. Pergamon Press, Oxford.
p. 282-298.
Sato, A. and T. Nakajlma. 1979. Partition coefficients of some aromatic
hydrocarbons and ketones 1n water, blood and oil. Br. J. Ind. Med. 36(3):
231-234.
Sauer, T.C., Jr. 1981. Volatile liquid hydrocarbon characterization of
underwater hydrocarbon vents and formation waters from offshore production
operations. Environ. Sc1. Techno!. 15(8): 917-923.
Schormueller, J. and H.J. Kochmann. 1969. Analysis of volatile aroma
substances 1n tomatoes by gas chromatography and mass spectroscopy. Z.
Lebensm Unters. Forsch. 141(1): 1-9. (Ger). (CA 71:122582c)
0034d -71- 06/18/87
-------
Sella, R.L. 1979. Non-urban hydrocarbon concentrations 1n ambient air
nortJi of Houston, TX. Office of Research and Development, U.S. EPA,
Research Triangle Park, NC. EPA 600/3-79-010. NTIS PB 298-227.
Senczuk, W. and B. LUewka. 1976. Absorption of cumene through the
respiratory tract and excretion of d1methylphenylcarb1nol 1n urine. 8r. J.
Ind. Me
-------
SRI (Stanford Research Institute). 1986. 1986 Directory of Chemical
Producers: United States of America. SRI International, Menlo Park. CA.
p. 568-569.
Stern, O.J.. A. Lee, W.H. McFadden and K.L. Stevens. 1967. Volatile from
grapes: Identification of volatile* from Concord essence. J. Agrlc. Food
Chem. 15: 1100-1103.
Stern, D.J., D. Guadagnl and K.I. Stevens. 1975. Aging of wine: Qualitative
changes in tne volatile; of Iltifandcl wine during two years. Am. 3. fnol.
VH1c. 26(4): 208-213.
Stuermer, D.H., D.J. Ng and C.J. Morris. 1982. Organic contaminants In
groundwater near an underground coal gasification site In northeastern
Wyoming. Environ. Sc1. Techno!. 16(9): 582-587.
Swann, R.L., D.A. Laskowskl, P.J. McCall, K. Vander Kuy and H.J. Dlshburger.
1983. A rapid method for the estimation of the environmental parameters
octanol/water partition coefficient,, soil sorptlon constant, water to air
ratio and water solubility. Res. Rev. 85: 17-28.
Tamashl, Y. 1977. Deodorizing of gases from human waste treatment. Japan.
Kokal JP 52/66870 (77/66870) June 2, 1977. 6 p. (CA 88:11358r)
Tang, J., Q.Z. Jin, G.H. Shen, C.T. Ho and S.S. Chang. 1983. Isolation and
Identification of volatile compounds from fried chicken. J. Agrlc. Food
Chem. 31(6): 1287-1292.
0034d -73- 06/18/87
-------
Teply, J. and H. Dressier. 1980. Direct determination of organic compounds
In water using steam-solid chromatography. J. Chromatography. 191(0):
221-229.
Tsanl-Bazaca, E., A. Mclntyre, J. Lester and R. Perry. 1982. Ambient
concentrations and correlations of hydrocarbons and halocarbons In the
vicinity of an airport. Chemosphere. 11(1): 11-23.
Union Carbide Corp. 1S85. Range finding tests on cumene (Isopropylbenzene).
Unpublished data. Industrial fellowship 274*12. TSCA sec 8(d) suteUslon
878214980. Office of Toxic Substances, U.S. EPA, Washington, DC.
U.S. EPA. 1980. Guidelines and Methodology Used In the Preparation of
Health Effect Assessment Chapters of the Consent Decree Water Criteria
Documents. Federal Register. 45(231): 49347-49357.
U.S. EPA. 1983. Computer printout of monitoring data for various Indus-
tries. An evaluation of automated spectrum matching for survey Identifica-
tion of wastewater components by gas chromatography-mass spectrometry.
Anal. Ch1m. Acta. 146: 15-27.
U.S. EPA. 1984. Methodology and Guidelines for Reportable Quantity Deter-
minations Based on Chronic Tox1c1ty Data. Prepared by the Office of Health
and Environmental Assessment, Environmental Criteria and Assessment Office,
Cincinnati, OH for the Office of Solid Waste and Emergency Response,
Washington, DC.
0034d -74- 06/18/87
-------
U.S. EPA. 1985a. Cumene; Proposed Test Rule. Federal Register. 50(215):
46104-46121.
U.S. EPA. 1985b. Reference Values for Risk Assessment. Prepared by the
Office of Health and Environmental Assessment, Environmental Criteria and
Assessment Office, Cincinnati, OH for the Office of Solid Haste, Washington,
DC.
U.S. EPA. 1985c. Draft Final Test Rule Support Document Cumene. Office of
Toxic Substances, Washington, DC.
U.S. EPA. 1986a. Methodology for Evaluating Potential Cardnogenlclty In
Support of Reportable Quantity Adjustments Pursuant to CERCLA Section 102.
Prepared by the Office of Health and Environmental Assessment, Carcinogen
Assessment Group, Washington, DC for the Office of Solid Waste and Emergency
Response, Washington, DC.
U.S. EPA. 1986b. Guidelines for Carcinogen Risk Assessment. Federal
Register. 51(185): 33992-34003.
U.S. EPA. 1987. Graphical Exposure Modeling System (GEMS). Fate of Atmo-
spheric Pollutants (FAP). Office of Toxic Substances, U.S. EPA, Washington,
DC.
USITC (U.S. International Trade Commission). 1981. Synthetic Organic
Chemicals United States Production and Sales, 1980. USITC Publ. 1183,
Washington, DC. p. 25.
0034d -75- 06/18/87
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USITC (U.S. International Trade Commission). 1982. Synthetic Organic
Chemicals United States Production and Sales, 1981. USITC Publ. 1292,
Washington, DC. p. 25.
USITC (U.S. International Trade Commission). 1983. Synthetic Organic
Chemicals United States Production and Sales, 1982. USITC Publ. 1422,
Washington, DC. p. 27.
USITC (U.S. International Trade Commission). 1984. Synthetic Organic
Chemicals United States Production and Sales, T983. USITC Putrt. 1588,
Washington, DC. p. 27.
USITC (U.S. International Trade Commission). 1985. Synthetic Organic
Chemicals United States Production and Sales, 1984. USITC Publ. 1745,
Washington, DC. p. 25.
USITC (U.S. International Trade Commission). 1986. Synthetic Organic
Chemicals United States Production and Sales, 1985. USITC Publ. 1892,
Washington, DC. p. 29.
Vallette, G. and R. Cavler. 1954. Absorption percutanee et constitution
chlmlque; cas des hydrocarbures, des alcools et des esters. Arch. Int.
Pharmacol. 97: 232-240. (Fre.)
Van der Linden, A.C. 1978. Degradation of oil 1n the marine environment.
Dev. Blodeg. Hydrocarbons. 1: 165-200.
0034d -76- 06/18/87
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Van Doom, R., C.M. Leljdekkers, R.P. Bos, R. Brouns and P.T. Henderson.
1981. Alcohol and sulfate Intermediates In the metabolism of toluene and
xylenes to mercapturlc acids. J. Appl. Toxicol. 1(4): 236-242.
Walker, J.D. and R.R. Colwell. 1975. Degradation of hydrocarbons and mixed
hydrocarbon substrate by microorganisms from Chesapeake Bay. Prog. Water
Techno!. 7: 783-731.
Walker, J.D., J.J. Calom1r1s. T.L. Herbert and R.R. Colwell. 1976.
Petroleum hydrocarbons*. Degradation and growth potential for Atlantic Ocean
sediment bacteria. Mar. B1ol. 34(1): 1-9.
Ward, D.J. 1965. Cumene. .In.: K1rk-0thmer Encyclopedia of Chemical Tech-
nology, 2nd ed., Vol. 6, A. Standen, Ed. John WHey and Sons, New York.
p. 543-546.
Ward, O.J. 1979. Cumene. In.: Klrk-Othmer Encyclopedia of Chemical Tech-
nology, 3rd ed., Vol. 7, A. Standen, Ed. John Wiley and Sons, New York.
p. 286-290.
Werner, H.W., R.C. Dunn and W.F. von Oettlngen. 1944. The acute effects of
cumene vapors 1n mice. J. Ind. Hyg. Toxlcol. 26(8): 264-268.
WestMck, J.J., J.W. Hello and R.F. Thomas. 1984. The groundwater supply
survey. J. Am. Water Works Assoc. 76: 52-59.
0034d -77- 06/18/87
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Williams, R.T. 1959. Detox1cat1on Mechanisms, 2nd ed. Chapman and Hall,
London, p. 188-236.
Wlndholz, H.f Ed. 1983. The Merck Index, 10th ed. Merck and Co., Inc.,
Rahway, NJ. p. 375.
Wolf, M.A., V.K. Rowe, 0.0, McColHster, R.L. HolUngsworth and F. Oyen.
1956. Tox1colog1ca1 studies of certain alkylated benzene and benzenes. AMA
Arch. Jftd, Health. 14: 387-398.
Yajlma, I., T. Yanal, M. Nakamura, H. Sakaklbara and T. Habu. 1978. Vola-
tile flavor components of cooked' Mce. Agrlc. B1ol. Chem. 42(6): 1229-1233.
Yamada, K., S. Hor1guch1 and G. Takahashl. 1965. The utilization of hydro-
carbons by microorganisms. VI. Screening of aromatic hydrocarbon-assimilat-
ing microorganisms and cumlc add formation from p-cumene. Agrlc. B1ol.
Chem. 29(10): 943-948.
0034d -78- 06/18/87
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APPENDIX A
LITERATURE SEARCHED
This HEED is based on data Identified by computerized literature
searches of the following:
TSCATS
CASR online (U.S. EPA Chemical Activities Status Report)
TOXLINE
TOXBACK 76
TOXBACK 65
RTECS
OHM TADS
STORET
SAC Environmental fate Data Bases
SANSS
AQUIRE
TSCAPP
NTIS
Federal Register
These searches were conducted 1n January, 1987. In addition, hand searches
were made of Chemical Abstracts (Collective Indices 5-9), and the following
secondary sources should be reviewed:
ACGIH (American Conference of Governmental Industrial Hygienists).
1986. Documentation of the Threshold Limit Values and Biological
Exposure Indices, 5th ed. Cincinnati, OH.
ACGIH (American Conference of Governmental Industrial Hygienists).
1986-1987. TLVs: Threshold Limit Values for Chemical Substances in
the Work Environment adopted by ACGIH with Intended Changes for
1986-1987. Cincinnati, OH. Ill p.
Clayton, G.D. and F.E. Clayton, Ed. 1981. Patty's Industrial
Hygiene and Toxicology, 3rd rev. ed.. Vol. 2A. John Wiley and
Sons, NY. 2878 p.
Clayton, G.D. and F.E. Clayton, Ed. 1981. Patty's Industrial
Hygiene and Toxicology, 3rd rev. ed., Vol. 2B. John Wiley and
Sons, NY. p. 2879-3816.
Clayton, G.D. and F.E. Clayton, Ed. 1982. Patty's Industrial
Hygiene and Toxicology, 3rd rev. ed., Vol. 2C. John Wiley and
Sons, NY. p. 3817-5112.
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Grayson, M. and 0. EckToth, Ed. 1978-1984. Klrk-Othmer Encyclo-
pedia of Chemical Technology, 3rd ed. John Wiley and Sons, NY. 23"
Volumes.
Hamilton, A. and H.L. Hardy. 1974. Industrial Toxicology, 3rd ed.
Publishing Sciences Group, Inc., Littleton, MA. 575 p.
IARC (International Agency for Research on Cancer). IARC Mono-
graphs on the Evaluation of Carcinogenic Risk of Chemicals to
Humans. MHO, IARC, Lyons, France.
Jaber, H.M., W.R. Mabey, A.T. L1«u, T.VI. Cnou anil H.I. Oohnson,
1984. Data acquisition for environmental transport and fate
screening for compounds of Interest to the Office of Solid Waste.
SRI International, Menlo Park, CA. EPA 600/6-84-010. NTIS
PB84-243906.
NTP (National Toxicology Program). 1986. Toxicology Research and
Testing Program. Chemicals on Standard Protocol. Management
Status.
Ouellette, R.P. and J.A. King. 1977. Chemical Week Pesticide
Register. McGraw-Hill Book Co., NY.
Sax, I.N. 1984. Dangerous Properties of Industrial Materials, 6th
ed. Van Nostrand Relnhold Co., NY.
SRI (Stanford Research Institute). 1986. Directory of Chemical
Producers. Menlo Park, CA.
U.S. EPA. 1986. Report on Status Report In the Special Review
Program, Registration Standards Program and the Data Call In
Programs. Registration Standards and the Data Call In Programs.
Office of Pesticide Programs, Washington, DC.
U.S. EPA. 1985. CSB Existing Chemical Assessment Tracking System.
Name and CAS Number Ordered Indexes. Office of Toxic Substances,
Washington, DC.
USITC (U.S. International Trade Commission). 1985. Synthetic
Organic Chemicals. U.S. Production and Sales, 1984, USITC Publ.
1422, Washington, DC.
Verschueren, K. 1983. Handbook of Environmental Data on Organic
Chemicals, 2nd ed. Van Nostrand Relnhold Co., NY.
Wlndholz, M., Ed. 1983. The Merck Index, 10th ed. Merck and Co.,
Inc.. Rahway, NJ.
Worthing, C.R. and S.B. Walker, Ed. 1983. The Pesticide Manual.
British Crop Protection Council. 695 p.
0034d -80- 05/27/87
t
rO.S. Environmental Protection
Region V, Library
230 South Dearborn Street
Chicago, Illinois 60604
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In addition, approximately 30 compendia of aquatic toxldty data were
reviewed. Including the following:
Battelle's Columbus Laboratories. 1971. Water Quality Criteria
Data Book. Volume 3. Effects of Chemicals on Aquatic Life.
Selected Data from the Literature through 1968. Prepared for the
U.S. EPA under Contract No. 68-01-0007. Washington, DC.
Johnson, U.W. and H.T. Flnley. 1980. Handbook of Acute Toxlcity
of Cftenrtcals to Fish and Aquatic Invertebrates. Summaries of
Toxldty Tests Conducted at Columbia National Fisheries Research
Laboratory. 1965-1978. U.S. Dept. Interior, Fish and Wildlife
Serv. Res. Publ. 137, Washington, DC.
McKee, J.E. and H.W. Wolf. 1963. Water Quality Criteria, 2nd ed.
Prepared for the Resources Agency of California, State Water
Quality Control Board, Publ. No. 3-A,
Plawtrtal, D. 1371. tcolo^cal Effects of Pesticides on Non-Target
Species. Prepared for the U.S. EPA, Washington, DC. PB-269605.
Schneider, B.A. 1979. Toxicology Handbook. Mammalian and Aquatic
Data. Book 1: Toxicology Data. Office of Pesticide Programs, U.S.
EPA, Washington, DC. EPA 540/9-79-003. NTIS PB 80-196876.
4
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0034d -81- 05/27/87
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