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PREFACE
Health and Environmental Effects Documents (HEEOs) 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 In this document
and the dates searched are Included In "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
cover) reflect the date the document Is sent to the Program Officer (OSWER).
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 RfOs 1s the same as traditionally employed for chronic estimates,
except that subchronlc data are utilized when available.
In the case of suspected carcinogens, RfDs are not estimated. A
carcinogenic potency factor, or q-j* (U.S. EPA, 1980), 1s 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-
genlclty are derived. The RQ Is 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 toxldty and cardno-
genlcHy) represent two of six scores developed (the remaining four reflect
1gn1tab1l1ty, reactivity, aquatic toxldty, and acute mammalian toxlclty).
Chemical-specific RQs reflect the lowest of these six primary criteria. The
methodology for chronic toxldty and cancer-based RQs are defined In U.S.
EPA, 1983 and 1986a, respectively.
111
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EXECUTIVE SUMMARY
2-Chloropropane Is commonly known as Isopropyl chloride. It Is a color-
less, highly flammable liquid at room temperature (Hawley, 1981), which Is
mlsdble with ethanol and ethyl ether, but 1s almost Insoluble In water
(Wlndholz, 1983; Perry and Green, 1984). This compound 1s prepared by
refluxlng Isopropyl alcohol with concentrated hydrochloric acid In the
presence of a zinc chloride catalyst (Papa, 1982). The public portion of
the U.S. EPA TSCA Production File (U.S. EPA, 1977) reported that there were
four manufacturers and one Importer of 2-chloropropane during 1977. The
lack of available production data on 2-chloropropane suggests that this
compound 1s Imported and produced on a specialty chemical basis In the
United States. 2-Chloropropane Is used as a solvent and as an Intermediate
In the production of other chemicals (Hawley, 1981) and to some extent as an
anesthetic (Torkelson and Rowe, 1981).
In the atmosphere, 2-chloropropane 1s expected to exist almost entirely
In the vapor phase (Elsenrelch et al., 1981). Reaction with photochemically
generated hydroxyl radicals U1/2 ~8 davs) appears to be the primary
removal mechanism (U.S. EPA, 1987). Small amounts of this compound may be
removed from the atmosphere In wet precipitation; however, most of the
2-chloropropane removed by wet deposition Is likely to reenter the atmo-
sphere by volatilization. Reaction with ozone, reaction with atomic oxygen
and dry deposition are not expected to be environmentally relevant fate
processes (U.S. EPA, 1987; Herron and Hu1e, 1973). If 2-chloropropane Is
released to water, volatilization Is expected to be the dominant removal
mechanism. The volatilization half-life of this compound 1n a 1 m deep
waterway, flowing at 1 m/sec with a wind speed of 3 m/sec was estimated to
1v
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be 3 hours (see Section 2.2.5.). Chemical hydrolysis [t,/2 -38-40 days
(Kosklkalllo, 1976; Mabey and Mill, 1978)]; reaction with alkylperoxy
radicals [t1/2 of ~104 years (Hendry et al.t 1974)]; bloaccumulatlon 1n
aquatic organisms; and adsorption to suspended solids and sediments are not
predictably significant fate processes. In dry soil, 2-chloropropane Is
expected to undergo rapid volatilization. Volatilization from wet soils Is
expected to be significant. Available data on hydrolysis In water suggest
that chemical hydrolysis may be significant In the removal of this compound
from moist soil. Based on the estimated K , residual 2-chloropropane In
soil 1s expected to leach from soil Into groundwater.
There Is a potential for 2-chloropropane to be released to the environ-
ment from production and use facilities. It might also be released to the
atmosphere during chlorine disinfection of some wastewaters (Gould et al.,
1983). This compound was detected In the finished drinking water In one of
five selected cities In the United States (Coleman et al., 1976). It was
Identified as a volatile flavor component of Idaho Russet Burbank baked
potatoes (Coleman et al, 1981).
The only available Information concerning toxlclty of 2-chloropropane to
aquatic organisms was provided by Shell 011 Co. (1982), who reported that
140-280 mg/l was the range of concentrations that caused 0-100% mortalIHy
of five goldfish, Carasslus auratus.
In a Dow Chemical Company study (Torkelson and Rowe, 1981; Betso, 1987),
mice, rats, guinea pigs, rabbits and monkeys exposed by Inhalation to
2-chloropropane at 1000 ppm, 7 hours/day, 5 days/week developed liver and
kidney necrosis. Evidence of lung edema or pneumonltls was also observed 1n
female rabbits and monkeys. In rats, rabbits, guinea pigs and dogs exposed
to 2-chloropropane at 500 ppm, 7 hours/day, 5 days/week for 6 months, no
adverse effects were noted (Torkelson and Rowe, 1981). Extensive
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vacuolatlon and necrosis were observed In the livers of rats exposed to
2-chloropropane at 1000 ppm, 6 hours/day, 5 days/week for 4 weeks (Gage,
1970). No toxic signs or lesions were observed In rats exposed to 250 ppm.
Guinea pigs survived oral doses of 3 g/kg 2-chloropropane but not doses
of 10 g/kg (Torkelson and Rowe, 1981). Effects observed when 2-chloropro-
pane was tested for use as an anesthetic In dogs Include changes 1n blood
pressure and respiratory rate, damage to the heart muscle and decreased
coronary blood flow (Enders and Koner, 1952). Effects on the electrocardio-
gram and ventricular extrasystoles and unspecified cardiac Irregularities
were observed In humans (Elam and Newhouse, 1951; Buhr, 1953).
Tham et al. (1984) found that Infusion of 2-chloropropane Into rats at a
rate of 160 ymol/kg/m1nute resulted In a decreased vestibule-oculomotor
reflex. The threshold for the effect was a blood 2-chloropropane level of
1.9 mmol/l.
2-Chloropropane was mutagenlc In S. typhlmurlum strain TA100, both with
and without S-9 metabolic activation when tested In a desiccator (Simmon et
al., 1977).
Pertinent data regarding the cardnogenlclty, teratogenldty and other
reproductive effects of 2-chloropropane could not be located 1n the avail-
able literature as dted In Appendix A. Because of the lack of cardnogen-
lclty human or animal data, 2-chloropropane was assigned to EPA Group D, not
classifiable as to human cardnogenlclty.
Based on a NOAEL of 250 ppm (803 mg/m3) In the 4-week rat study (Gage,
1970), a subchronlc Inhalation RfD of 1 mg/m3 or 29 mg/day and a chronic
Inhalation RfD of 0.1 mg/m3 or 3 mg/day were derived. Data were
Insufficient for derivation of RfDs for oral exposure. An RQ of 1000 was
calculated for systemic toxldty based on hlstopathologlc lesions In rats at
1000 ppm (3212 mg/m3) In the 4-week Inhalation rat study (Gage, 1970).
v1
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TABLE OF CONTENTS
1. INTRODUCTION 1
1.1. STRUCTURE AND CAS NUMBER 1
1.2. PHYSICAL AND CHEMICAL PROPERTIES 1
1.3. PRODUCTION DATA 1
1.4. USE DATA 2
1.5. SUMMARY 2
2. ENVIRONMENTAL FATE AND TRANSPORT 4
2.1. AIR 4
2.1.1. Reaction with Hydroxyl Radicals 4
2.1.2. Reaction with Ozone 4
2.1.3. Reaction with Oxygen Atoms 4
2.1.4. Physical Removal Processes 5
2.2. WATER 5
2.2.1. Hydrolysis '. 5
2.2.2. Oxidation 5
2.2.3. B1oconcentrat1on 5
2.2.4. Adsorption 6
2.2.5. Volatilization 6
2.2.6. Blodegradatlon 6
2.3. SOIL 6
2.3.1. Hydrolysis 6
2.3.2. Leaching 6
2.3.3. Volatilization. .• 6
2.3.4. Blodegradatlon 7
2.4. SUMMARY 7
3. EXPOSURE 8
3.1. HATER 8
3.2. FOOD 8
3.3. SUMMARY 8
4. AQUATIC TOXICITY 9
4.1. ACUTE TOXICITY 9
4.2. CHRONIC EFFECTS 9
4.3. PLANT EFFECTS 9
4.4. SUMMARY 9
5. PHARMACOKINETCS 10
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TABLE OF CONTENTS (cont.)
Page
6. EFFECTS 11
6.1. SYSTEMIC TOXICITY 11
6.1.1. Inhalation Exposures 11
6.1.2. Oral Exposures 12
6.1.3. Other Relevant Information 12
6.2. CARCINOGENICITY 13
6.3. MUTAGENICITY 13
6.4. TERATOGENICITY 13
6.5. OTHER REPRODUCTIVE EFFECTS 13
6.6. SUMMARY 13
7. EXISTING GUIDELINES AND STANDARDS 15
7.1. HUMAN 15
7.2. AQUATIC 15
8. RISK ASSESSMENT 16
8.1. CARCINOGENICITY 16
8.1.1. Height of Evidence 16
8.1.2. Quantitative Risk Estimates 16
8.2. SYSTEMIC TOXICITY 16
8.2.1. Inhalation Exposure 16
8.2.2. Oral Exposure 18
9. REPORTABLE QUANTITIES 19
9.1. BASED ON SYSTEMIC TOXICITY 19
9.2. BASED ON CARCINOGENICITY 23
10. REFERENCES 24
APPENDIX A: LITERATURE SEARCHED 30
APPENDIX B: SUMMARY TABLE FOR 2-CHLOROPROPANE 33
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LIST OF TABLES
No. Title Page
1-1 Production and Import Volume Data for 2-Chloropropane
1n 1977 3
9-1 Inhalation Toxldty Summary for 2-Chloropropane 20
9-2 Inhalation Composite Scores for 2-Chloropropane 21
9-3 2-Chloropropane: Minimum Effective Dose (MED) and
Reportable Quantity (RQ) 22
1x
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LIST OF ABBREVIATIONS
BCF Bloconcentratlon factor
CAS Chemical Abstract Service
CS Composite score
Koc Soil sorptlon coefficient standardized
with respect to organic carbon
Kow Octanol/water partition coefficient
Kw Water-to-aIr ratio
MED Minimum effective dose
NOAEL No-observed-adverse-effect level
ppm Parts per million
RfD Reference dose
RQ Reportable quantity
RV
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1. INTRODUCTION
1.1. STRUCTURE AND CAS NUMBER
2-Chloropropane 1s also known as Isopropyl chloride and 2-propyl
chloride. The structure, molecular weight, empirical formula and CAS
Registry number of this compound are as follows:
CH3-CH-CH3
Cl
Molecular weight: 78.55
Empirical formula: C.H.C1
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(Papa, 1982). Production and Import data on 2-chloropropane are presented
In Table 1-1.
CMR (1986) lists Chemical Dynamics Corp., O&O Chemical, Fllo Chemical
and Jonas Chemical Corp. as suppliers of 2-chloropropane In the United
States. Additional data regarding chemical production and sales could not
be located 1n the available literature as cited In Appendix A. The lack of
Information concerning current domestic production of 2-chloropropane
suggests that this compound 1s Imported and produced on a specialty chemical
basis 1n the United States.
1.4. USE DATA
2-Chloropropane 1s used as a solvent and Intermediate for the production
of other chemicals (Hawley, 1981).
1.5. SUMMARY
2-Chloropropane Is commonly known as Isopropyl chloride. It Is a color-
less, highly flammable liquid at room temperature (Hawley, 1981)., which Is
mlsclble with ethanol and ethyl ether, but Is almost Insoluble In water
(Hlndholz, 1983; Perry and Green, 1984). This compound Is prepared by
refluxlng Isopropyl alcohol with concentrated hydrochloric acid 1n the
presence of a zinc chloride catalyst (Papa, 1982). The public portion of
the U.S. EPA TSCA Production File (U.S. EPA, 1977) reported that there were
four manufacturers and one Importer of 2-chloropropane during 1977. The
lack of available production data on 2-chloropropane suggests that this
compound 1s Imported and produced on a specialty chemical basis In the
United States. 2-Chloropropane Is used as a solvent and as an Intermediate
1n the production of other chemicals (Hawley, 1981) and to some extent as an
anesthetic (Torkelson and Rowe, 1981).
0066d -2- 09/24/87
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TABLE 1-1
Production and Import Volume Data for 2-Chloropropane In 1977a
Company
Eastman Kodak
Dow Chemical
Hlo Chemical
Columbia Organic;
Arapahoe Chemicals
Hooker Chemicals
Location
Rochester. NY
Freeport, TX
New York, NYb
Columbia, SC
Boulder, CO
Niagara Falls, NY
*
Production and Import Volume
(millions of pounds)
<0.001
1-10
small volume
0.001-0.010
0.001-0.010
(site- limited use)
nonec
aSource: U.S. EPA, 1977
blmporter
cTh1s company has Imported/produced 2-chloropropane In the past.
0066d -3- 06/17/87
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2. ENVIRONMENTAL FATE AND TRANSPORT
Limited data pertaining to the environmental fate and transport of
2-chloropropane were located 1n the available literature as cited In
Appendix A. Information concerning fate and transport of this compound was
derived from physical property data or the molecular structure of the
compound.
2.1. AIR
E1senre1ch et al. (1981) reported that organic; with vapor pressures
>10~4 mm Hg should exist almost entirely In the vapor phase In the atmo-
sphere. Therefore, 2-chloropropane, with a vapor pressure of 281 mm Hg at
20°C (BoubHk et al., 1984), 1s expected to exist primarily In the vapor
phase 1n the atmosphere.
2.1.1. Reaction with Hydroxyl Radicals. The estimated half-life for
2-chloropropane vapor reacting with photochemlcally generated hydroxyl
radicals Is -8 days. This estimation was made using an estimated reaction
rate constant of 1.3xlO~12 cmVmolecule-sec at 25°C and assuming an
ambient hydroxyl radical concentration of S.OxlO9 molecules/cm3 In a
typical atmosphere (U.S. EPA, 1987).
2.1.2. Reaction with Ozone. 2-Chloropropane Is not susceptible to oxida-
tion by ozone 1n the atmosphere (U.S. EPA, 1987).
2.1.3. Reaction with Oxygen Atoms. The reaction of 2-chloropropane with
atomic oxygen (OaP) In the atmosphere Is not expected to be environment-
ally significant (Herron and Hule, 1973), and the half-life for this reac-
tion 1s estimated to be >80 years. This estimation was made using a reac-
tion rate constant of 10~1S cmVmolecule-sec at 25°C (Herron and Hule,
1973) and an ambient (OaP) concentration of 2.5x10* molecules/cm3
(Graedel, 1978).
0066d -4- 09/24/87
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2.1.4. Physical Removal Processes. Since the water solubility of
2-chloropropane Is 3100 mg/l at 20°C (Perry and Green, 1984), It seems
likely that small amounts of the compound will be removed from the atmo-
sphere 1n precipitation. Nevertheless, most of the 2-chloropropane removed
from the atmosphere by wet deposition 1s likely to reenter the atmosphere by
volatilization (Section 2.2.5.). Dry deposition Is not expected to be a
significant removal process for 2-chloropropane.
2.2. WATER
2.2.1. Hydrolysis. Based on measured first-order reaction rate constants
of 2.30xlO'7 and 2.12xlO~7 sec"1, the half-life for the hydrolysis of
2-chloropropane at neutral pH and 25°C Is calculated to be 38 and 40 days,
respectively (Kosklkalllo, 1967; Mabey and Mill, 1978).
2.2.2. Oxidation. Reaction of 2-chloropropane with alkylperoxy radicals
In water 1s not expected to be environmentally relevant (Hendry et al.t
1974). The half-life for the reaction of 2-chloropropane with tert-butyl-
peroxy radicals 1s estimated to be ~104 years. This estimation was made
using a reaction rate constant of 0.6xlO~a l/mol-sec at 30°C (Hendry et
al., 1974) and an ambient alkylperoxy radical concentration of IxlO"9
mol/l (Mill et al., 1980).
2.2.3. B1oconcentrat1on. Pertinent data regarding the bloconcentratlon
of 2-chloropropane could not be located 1n the available literature as dted
In Appendix A. Therefore, the BCFs of 7 or 16 were estimated using a log
KQW of 1.90, a water solubility of 3100 mg/l at 20°C and the following
recommended linear regression equations (Lyman et al., 1982):
log BCF = 0.76 log KQW - 0.23 (2-1)
log BCF = 2.791 - 0.564 log S (2-2)
These values suggest that bloaccumulatlon of 2-chloropropane 1n aquatic
organisms 1s not a significant fate process.
0066d -5- 06/17/87
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2.2.4. Adsorption. Based on KQC values of 52-56 (Section 2.3.2.),
physical adsorption of 2-chloropropane to sediments and suspended solids \n
water 1s not expected to be significant.
2.2.5. Volatilization. The Henry's Law constant for 2-chloropropane was
estimated to be 1.6xlO"2 atm-mVmol at 25°C using a method of bond
contributions to Intrinsic hydrophlUc character of the compound (Hlne and
Mookerjee, 1975). Based on this value, the volatilization half-life of this
compound from water 1 m deep, flowing 1 m/sec with a wind speed of 3 m/sec
was estimated to be -3 hours, using the method of Lyman et al. (1982).
2.2.6. B1odegradat1on. Pertinent data regarding the blodegradatlon of
2-chloropropane 1n water could not be located In the available literature as
cited 1n Appendix A.
2.3. SOIL
2.3.1. Hydrolysis. Available data on the hydrolysis of 2-chloropropane
In water suggest that chemical hydrolysis may be significant In the removal
of this compound from moist soil, particularly 1f the reaction 1s catalyzed
by soil.
2.3.2. Leaching. A K of 56 was estimated for 2-chloropropane, using
the molecular topology and quantitative structure-activity analysis method
of Sabljlc (1984). A K of 52 was estimated, using a water solubility of
3100 mg/i at 20*C (Perry and Green, 1984) and the linear regression
equation, log KQC = -0.557 log S * 4.277 (Lyman et al., 1982), where S Is
1n ymol/i. These values suggest that 2-chloropropane 1s likely to be
highly mobile In soil (Swann et al., 1983).
2.3.3. Volatilization. The relatively high vapor pressure of 2-chloro-
propane [281 mm Hg at 20°C (BoubHk et al., 1984)] suggests that this
compound will volatilize rapidly from dry soil surfaces. Evaporation from
moist soils might also be significant, since this compound does not have a
0066d -6- 06/17/87
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tendency to adsorb significantly to soil and 1s expected to volatilize
rapidly from water (see Sections 2.2.5. and 2.3.2.).
2.3.4. B1odegradat1on. Pertinent data regarding the blodegradatlon of
2-chloropropane In soil could not be located In the available literature as
dted In Appendix A.
2.4. SUMMARY
In the atmosphere, 2-chloropropane 1s expected to exist almost entirely
In the vapor phase (E1senre1ch et al., 1981). Reaction with photochemically
generated hydroxyl radicals (t-i/o ~* days) appears to be the primary
removal mechanism (U.S. EPA, 1987). Small amounts of this compound may be
removed from the atmosphere 1n wet precipitation; however, most of the
2-chloropropane removed by wet deposition 1s likely to reenter the atmo-
sphere by volatilization. Reaction with ozone, reaction with atomic oxygen
and dry deposition are not expected to be environmentally relevant fate
processes (U.S. EPA, 1987; Herron and Hu1e, 1973). If 2-chloropropane Is
released to water, volatilization Is expected to be the dominant removal
mechanism. The volatilization half-life of this compound In a 1 m deep
waterway, flowing at 1 m/sec with a wind speed of 3 m/sec was estimated to
be 3 hours (see Section 2.2.5.). Chemical hydrolysis [t-,/2 -38-40 days
(Kosk1kall1o, 1976; Mabey and Mill, 1978)]; reaction with alkylperoxy
radicals [t,/2 of -10* years (Hendry et al., 1974)]; bloaccumulatlon 1n
aquatic organisms and adsorption to suspended sol Ids and sediments are not
predictably significant fate processes. In dry soil, 2-chloropropane 1s
expected to undergo rapid volatilization. Volatilization from wet soils 1s
expected to be significant. Available data on hydrolysis In water suggest
that chemical hydrolysis may be significant 1n the removal of this compound
from moist soil. Based on the estimated K , residual 2-chloropropane In
soil Is expected to leach from soil Into groundwater.
0066d -7- 06/17/87
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3. EXPOSURE
Monitoring data pertaining to human exposure to 2-chloropropane by
Inhalation or dermal contact could not be located In the available litera-
ture as dted 1n Appendix A. Potentially, this compound might be released
to the environment from production or use facilities. It might also be
released to the atmosphere during chlorine disinfection of some wastewaters
(Gould et al., 1983).
3.1. HATER
2-Chloropropane was qualitatively detected 1n the finished drinking
water of at least one of five selected cities In the United States (Coleman
et al., 1976).
3.2. FOOD
2-Chloropropane was Identified as a volatile flavor component of Idaho
Russet Burbank baked potatoes (Coleman et al., 1981).
3.3. SUMMARY
There 1s a potential for 2-chloropropane to be released to the environ-
ment from production and use facilities. It might also be released to the
atmosphere during chlorine disinfection of some wastewaters (Gould et al.,
1983). This compound was detected 1n the finished drinking water In one of
five selected cities In the United States (Coleman et al., 1976). It was
Identified as a volatile flavor component of Idaho Russet Burbank baked
potatoes (Coleman et al., 1981).
0066d -8- 06/17/87
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4. AQUATIC TOXICITY
4.1. ACUTE TOXICITY
The only available Information concerning tox1c1ty of 2-chloropropahe to
aquatic organisms was provided by Shell Oil Co. (1982), reporting that
140-280 mg/l was the range of concentrations that caused 0-100X mortalllty
of five goldfish, Carasslus auratus.
4.2. CHRONIC EFFECTS
Pertinent data regarding chronic toxlclty of 2-chloropropane to aquatic
organisms could not be located 1n the available literature as dted In
Appendix A.
4.3. PLANT EFFECTS
Pertinent data regarding effects of 2-chloropropane on aquatic plants
could not be located In the available literature as cited In Appendix A.
4.4. SUMMARY
The only available Information concerning toxlclty of 2-chloropropane to
aquatic organisms was provided by Shell Oil Co. (1982), reporting that
140-280 mg/l was the range of concentrations that caused 0-100X mortal 11ty
of five goldfish, Carasslus auratus.
0066d -9- 09/24/87
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5. PHARHACOKINETICS
According to Van Dyke and Wlneman (1971), 36Cl-2-chloropropane Is
enzymatlcally dechloMnated by rat liver mlcrosomes j_n vitro. The Incuba-
tion was done 1n the presence of a NADPH-generatlng system and 3*C1 Ion
release was measured. Other pertinent data regarding the pharmacoklnetlcs
of 2-chloropropane could not be located In the available literature as cited
1n Appendix A.
0066d -10- 09/24/87
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6. EFFECTS
6.1. SYSTEMIC TOXICITY
6.1.1. Inhalation Exposures.
6.1.1.1. SUBCHRONIC -- Torkelson and Rowe (1981) reported a Dow
Chemical Company study In which several species were exposed to 2-chloropro-
pane at 1000 ppm (3212 mg/m3), 7 hours/day, 5 days/week for 127 exposures
over 181 days. Further Information concerning this study, conducted 1n the
1950s, was obtained from Betso (1987). Groups of 10 female mice, 20 male
and 20 female rats, 8 male and 8 female guinea pigs, 2 male and 2 female
rabbits and 2 female monkeys were tested. Similar groups of animals,
exposed to air, were maintained as controls. No adverse effects on
behavior, appearance, growth, mortality, final average body weight, organ
weights and hematologlcal values occurred In any of the species examined.
Hlstologlcal examinations revealed necrosis of the parenchyma! cells In the
portal areas of the liver and degeneration of the tubular epithelium with
some necrosis 1n the kidneys. These effects were noted 1n all groups except
male rats. In addition, evidence of lung edema or pneumonltls was observed
1n female rabbits and monkeys.
Torkelson and Rowe (1981) also reported that Dow Chemical Company
exposed rats, rabbits, guinea pigs and dogs to 2-chloropropane at 500 ppm, 7
hours/day, 5 days/week for 6 months. At this exposure regimen, no adverse
effects were noted 1n appearance, growth, final organ and body weights,
hematologlcal and clinical studies or gross and hlstologlcal examinations.
Dow Chemical Company no longer has a record of this experiment (Betso, 1987).
In an Inhalation study, Gage (1970) exposed groups of four male and four
female Alderly Park SPF rats to 2-chloropropane at 250 or 1000 ppm (803 or
3212 mg/ma) for 20 6-hour exposures (5 days/week). No toxic signs were
0066d -11- 09/24/87
-------
noted during the exposure. At necropsy, the livers of the 1000 ppm exposed
rats showed extensive vacuolatlon and necrosis. The organs of the 250 ppm
exposed rats appeared normal. Further details of this study were not
available.
6.1.1.2. CHRONIC — Pertinent data regarding the chronic Inhalation
toxldty of 2-chloropropane could not be located In the available literature
as cited In Appendix A.
6.1.2. Oral Exposures. Pertinent data regarding the subchronlc and
chronic oral toxldty of 2-chloropropane could not be located In the avail-
able literature as dted In Appendix A.
6.1.3. Other Relevant Information. Torkelson and Rowe (1981) reviewed
unpublished data by Dow Chemical Company that Indicate that guinea pigs
survived oral doses of 2-chloropropane at 3 g/kg, but died after doses of
10 g/kg.
2-Chloropropane has been tested for use as an anesthetic. In a study
using dogs (Enders and Koner, 1952), 2-chloropropane at 0.8 ml/l (694
mg/i) was Inhaled for 3-5 minutes. The effects noted were a decrease 1n
arterial blood pressure, an Increase In venous blood pressure, an Increase
1n respiratory rate and a decrease In respiratory volume. In addition,
electrocardiograms showed significant damage to the heart muscle, and
coronary blood flow was decreased by 50%. In a human study (Elam and
Newhouse, 1951), patients anesthetized with nitrous oxide and then with
2-chloropropane showed effects on the electrocardiogram and ventricular
extrasystoles. In another study (Buhr, 1953), 12 patients were anesthetized
with 2-chloropropane for -12 minutes. Circulation was well maintained for
up to 8 minutes, but It was depressed thereafter. Unspecified cardiac
Irregularities were observed In two of the patients.
0066d . -12- 09/24/87
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Tham et al. (1984) studied the vestibule-oculomotor reflex 1n female
Sprague-Dawley rats dosed with 2-chloropropane by continuous Intravenous
Infusion for 60 minutes. Throughout the dosing period, the vestlbulo-
oculomotor reflex and blood 2-chloropropane concentration were measured.
Infusion of 2-chloropropane at 160 ymol/kg/mlnute resulted In a depression
of the vestibule-oculomotor reflex, with the threshold limit for the effect
at a blood level of 1.9 mmol/i.
6.2. CARCINOGENICITY
Pertinent data regarding the carclnogenlcHy of 2-chloropropane could
not be located In the available literature as cited 1n Appendix A.
2-Chloropropane has not been scheduled to be tested by the NTP (1987).
6.3. MUTAGENICITY
Simmon et al. (1977) reported that 2-chloropropane was mutagenlc In
Salmonella typhlmurlum strain TA100, both with and without S-9 metabolic
activation when the bacteria were exposed to 2-chloropropane vapor for 7-10
hours In a desiccator.
6.4. TERATOGENICITY
Pertinent data regarding the teratogenldty of 2-chloropropane could not
be located In the available literature as cited In Appendix A.
6.5. OTHER REPRODUCTIVE EFFECTS
Pertinent data regarding other reproductive effects of 2-chloropropane
could not be located 1n the available literature as cited In Appendix A.
6.6. SUMMARY
In a Dow Chemical Company study (Torkelson and Rowe, 1981; Betso, 1987),
mice, rats, guinea pigs, rabbits and monkeys exposed to 2-chloropropane at
1000 ppm, 7 hours/day, 5 days/week for 127 exposures over 181 days developed
liver and kidney necrosis. Evidence of lung edema or pneumonltis was also
0066d -13- 06/17/87
-------
observed 1n female rabbits and monkeys. In rats, rabbits, guinea pigs and
dogs exposed to 2-chloropropane at 500 ppm, 7 hours/day, 5 days/week for 6
months, no adverse effects were noted (Torkelson and Rowe, 1981). Extensive
vacuolatlon and necrosis were observed In the livers of rats exposed to
2-chloropropane at 1000 ppm, 6 hours/day, 5 days/week for 4 weeks (Gage,
1970). No toxic signs or lesions were observed In rats exposed to 250 ppm.
Guinea pigs survived oral doses of 3 g/kg 2-chloropropane but not doses
of 10 g/kg (Torkelson and Rowe, 1981). Effects observed when 2-chloropro-
pane was tested for use as an anesthetic In dogs Include changes 1n blood
pressure and respiratory rate, damage to the heart muscle and decreased
coronary blood flow (Enders and Koner, 1952). Effects on the electrocardio-
gram, ventricular extrasystoles and unspecified cardiac Irregularities were
observed 1n humans (Elam and Newhouse, 1951; Buhr, 1953).
Tham et al. (1984) found that Infusion of 2-chloropropane Into rats at a
rate of 160 ymol/kg/m1nute resulted In a decreased vestibule-oculomotor
reflex. The threshold for the effect was a blood 2-chloropropane level of
1.9 mmol/i.
2-Chloropropane was mutagenlc 1n S. typhlmuMuro strain TA100, both with
and without S-9 metabolic activation when tested In a desiccator (Simmon et
al., 1977).
Pertinent data regarding the carc1nogen1c1ty, teratogenldty and other
reproductive effects of 2-chloropropane could not be located In the avail-
able literature as cited In Appendix A.
0066d -14- 06/17/87
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7. EXISTING GUIDELINES AND STANDARDS
7.1. HUMAN
Pertinent guidelines and standards, Including EPA ambient water and air
quality criteria, drinking water standards, FAO/WHO ADIs, EPA or FDA toler-
ances for raw agricultural commodities or foods, and ACGIH, NIOSH or OSHA
occupational exposure limits could not be located 1n the available litera-
ture as dted In Appendix A.
7.2. AQUATIC
Guidelines and standards for the protection of aquatic organisms from
the effects of 2-chloropropane could not be located In the available litera-
ture as dted 1n Appendix A.
0066d -15- 06/17/87
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8. RISK ASSESSMENT
8.1. CARCINOGENICITY
Pertinent data regarding the cardnogenlclty of 2-chloropropane could
not be located 1n the available literature as cited In Appendix A.
8.1.1. Weight of Evidence. The cardnogenlclty of 2-chloropropane has
not been examined In humans or laboratory animals. Therefore, the compound
can be placed 1n EPA Group D (U.S. EPA, 1986b), not classifiable as to human
cardnogenlclty.
8.1.2. Quantitative Risk Estimates. The lack of data regarding the
cardnogenlclty of 2-chloropropane precludes the derivation of risk assess-
ment values based on cardnogenlclty.
8.2. SYSTEMIC TOXICITY
8.2.1. Inhalation Exposure.
8.2.1.1. LESS THAN LIFETIME EXPOSURES (SUBCHRONIC) -- In a Dow Chemi-
cal Company study reported by Torkelson and Rowe (1981) and Betso (1987),
necrosis 1n the liver and kidneys was observed 1n mice, rats, guinea pigs,
rabbits and monkeys exposed to 2-chloropropane at 1000 ppm (3212 mg/ma), 7
hours/day, 5 days/week for 127 exposures over 181 days. Evidence of lung
edema or pneumonltls was also noted 1n rabbits and monkeys. No effects were
noted 1n rats, rabbits, guinea pigs and dogs exposed to 2-chloropropane at
500 ppm (1606 mg/ma), 7 hours/day, 5 days/week for 6 months (Torkelson and
Rowe, 1981). Dow Chemical Company no longer has a record of the low dose
experiment (Betso, 1987).
Extensive vacuolatlon and necrosis of the liver was observed In rats
exposed to 2-chloropropane at 1000 ppm for 6 hours/day, 5 days/week for 4
weeks (Gage, 1970). No effects were observed In rats exposed to 250 ppm
(803 mg/m3).
0066d -16- 09/24/87
-------
Dow Chemical Company (Torkelson and Rowe, 1981) and Gage (1970) both
observed histopathologlcal lesions 1n laboratory animals exposed to 1000 ppm
2-chloropropane. In the 6-month study, Dow Chemical Company (Torkelson and
Rowe, 1981) Identified a NOAEL at 500 ppm, while In a 4-week study, Gage
(1970) Identified a NOAEL at 250 ppm. If additional data supporting the
NOAEL Identified at 500 ppm were available, the Dow Chemical Company study
(Torkelson and Rowe, 1981) would be suitable for risk assessment. Because
there are no data to support a NOAEL of 500 ppm, the more conservative NOAEL
of 250 ppm Identified 1n the 4-week study will be used for risk assessment.
Expanding the 250 ppm (803 mg/m3) dose level to continuous exposure by
multiplying by 6 hours/24 hours and 5 days/7 days, and by dividing by an
uncertainty factor of 100 (10 for Interspedes extrapolation and 10 to
protect sensitive Individuals) a human subchronlc Inhalation RfD concentra-
tion of 1 mg/m3 1s derived. Multiplying the exposure concentration by the
human breathing rate, 20 mVday, a subchronlc Inhalation RfD of 29 mg/day
for a 70 kg human 1s derived.
Confidence In the subchronlc RfD 1s low. The Gage (1970) study uses
only eight rats per dose group, and the rats were exposed for only 4 weeks.
The limited Information that showed no effects 1n the 6-month Dow Chemical
Company study at 500 ppm (Torkelson and Rowe, 1981) Indicates that longer
exposures at 250 ppm are likely to be safe. Confidence In the subchronlc
RfD 1s also low because 2-chloropropane has not been tested for
cardnogenlclty, teratogenldty or other reproductive effects.
8.2.1.2. CHRONIC EXPOSURES — The toxlclty of 2-chloropropane follow-
ing chronic Inhalation exposure has not been examined. A chronic Inhalation
0066d -17- 09/24/87
-------
RfO of 0.1 mg/m3 or 3 mg/day for a 70 kg human Is derived by dividing the
subchronlc RfD by an additional uncertainty factor of 10 to extrapolate from
subchronlc to chronic exposure.
Confidence In this RfD 1s low; the key study (Gage, 1970) was only 4
weeks long and only eight rats/dose group were examined. In addition,
2-chloropropane has not been examined In studies of cardnogenlcHy, terato-
genldty or studies of other reproductive effects.
8.2.2. Oral Exposure. Data were not available from which to derive sub-
chronic or chronic RfDs for oral exposure. NOAELs from available Inhalation
studies Include 500 ppm 1n the 6-month Dow Chemical Company study (Torkelson
and Rowe, 1981) and 250 ppm 1n the 4-week study by Gage (1970). Data from
the Dow Chemical Company study (Torkelson and Rowe, 1981; Betso, 1987) were
not available for evaluation, and the study 1s judged Inadequate for use In
quantitative risk assessment. The Gage (1970) study 1s too short for use 1n
deriving an RfD for oral exposure, especially where the additional
uncertainties of route-to-route extrapolation are Involved. Thus, no
subchronlc or chronic RfD for oral exposure to 2-chloropropane can be
derived.
0066d -18- 09/24/87
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9. REPORTABLE QUANTITIES
9.1. BASED ON SYSTEMIC TOXICITY
The toxlclty of 2-chloropropane Is discussed In Chapter 6. The toxldty
data suitable for deriving an RQ are presented In Table 9-1. The Dow
Chemical Company study (Torkelson and Rowe, 1981; Betso, 1987) that used
monkeys was omitted from the table because the species of monkey used In the
study was not provided, and therefore, a reasonable estimate of body weight
cannot be made.
The derivation of RQ values 1s presented In Table 9-2. In the studies
available for RQ derivation (Torkelson and Rowe, 1981; Betso, 1987; Gage,
1970), necrosis of the liver and the kidney was the only effect observed.
This effect, corresponding to an RV of 6, was observed 1n rats exposed to
2-chloropropane at 1000 ppm, 6 hours/day, 5 days/week for 4 weeks (Gage,
1970) and In all species exposed at 1000 ppm, 7 hours/day, 5 days/week for 6
months (Torkelson and Rowe, 1981; Betso. 1987). The lowest MED values at
which the effects were observed are from the Gage (1970) rat study, 438.9
mg/day, and the Dow Chemical Company mice study, 459.2 mg/day (Torkelson and
Rowe, 1981; Betso, 1987). Both MEDs correspond to an RV. of 1.5.
Multiplying the RVg by the RVd, a CS of 9 Is derived from both studies.
This CS corresponds to an RQ of 1000. Because the duration of exposure was
longer In the Dow Chemical Company study (Torkelson and Rowe; 1981; Betso,
1987) than 1n the study by Gage (1970). It was selected as the basis for the
RQ (Table 9-3).
0066d -19- 09/24/87
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TABLE 9-1
Inhalation ToxIcily Summary for 2-Chloropropane (Purity not reported)
o
I
Species/
Strain Sex
MIce/NR F
Rats/NR F
Guinea N.F
plgs/NR
Rabbits/ H.f
NR
Rats/ N.F
Alderly-
Park SPF
No. at Average
Start Height
(kg)
10 0.03b
20 0.35b
8/sex 0.84b
2/sex 3.8b
4/sex 0.2d
Vehicle/ Transformed Equivalent
Physical Exposure Animal Dose Human Dose3
State (mg/kg/day) (mg/kg/day)
air 1000 ppm 869. 9* 65.6
(3212 mg/m«).
7 hours/day.
5 days/week
for 181 days
air same as above 426. 4C 72.9
air same as above 318. 7C 73.0
air same as above 352. 2* 133.4
air 1000 ppm 441. 7* 62.7
(3212 mg/m«).
6 hours/day.
5 days/week
for 4 weeks
Response
Necrosis In the parenchymal
cells In the portal areas
of the liver; tubular degen-
eration of the epithelium
with some necrosis In kidneys
Same as above
Same as above
Necrosis In the parenchymal
cells In the portal areas
of the liver; tubular degen-
eration of the epithelium
with some necrosis In
kidneys; female rabbits
showed evidence of lung
edema or pneumonttls
Extensive vacuolatlon and
necrosis of the liver
Reference
Betso. 1987;
Torkelson and
Rowe. 1981
Betso. 1987;
Tor kelson and
Rowe. 1981
Betso. 1987;
Torkelson and
Rowe. 1981
Betso. 1987;
Torkelson and
Rowe. 1981
Gage. 1970
'Calculated by multiplying the animal transformed dose by the cube root of the ratio of the animal body weight to the human body weight (70 kg)
^Reference body weights (U.S. EPA. 1985)
Calculated by multiplying the concentration by the number of hours/day exposed, number days/week, by the Inhalation rates (0.039 m*/day
mice; 0.223 mVday rats; 0.40 mVday guinea pigs; 2 mVday rabbits) from U.S. EPA (1985) and by dividing by the animal body weight
dOata provided by Investigators
'Calculated by multiplying the concentration by 6 hours/24 hours by 5 days/7 days, by the Inhalation rate. 0.154 mVday [calculated from
I . 0.105 (w/0.113)"3 from U.S. EPA. 1985)] and dividing by the body weight.
-------
TABLE 9-2
Inhalation Composite Scores for 2-Chloropropane
Chronic
Species Animal Dose Human NED*
(mg/kg/day) (mg/day)
Rats 441.7 438.9
Nice 869.9 459.2
Rats 426.4 510.3
i
i
Guinea pigs 318.7 511
Rabbits 352.2 933.8
RVd Effects RVe CS
1.5 Extensive vacuolatlon and necrosis of 6 9
the liver
1.5 necrosis In the parenchymal cells In 69
the portal areas of the liver; tubular
degeneration of the epithelium with
some necrosis In the kidneys
1.4 necrosis In the parenchymal cells In • 6 8.4
the portal areas of the liver; tubular
degeneration of the epithelium with
some necrosis In the kidneys
1.4 necrosis In the parenchymal cells In 6 8.4
the portal areas of the liver; tubular
degeneration of the epithelium with
some necrosis In the kidneys
1 necrosis In the parenchymal cells In 66
the portal areas of the liver; tubular
degeneration of the epithelium with
some necrosis In the kidneys; female
rabbits showed evidence of lung edema
or pneumonltls
RQ Reference
1000 Gage. 1970
1000 Betso. 1987;
Torkelson and
Rowe. 1981
1000 Betso. 1987;
Torkelson and
Rowe. 1981
1000 Betso. 1987;
Torkelson and
Rowe. 1981
1000 Betso. 1987;
Torkelson and
Rowe. 1981
•The dose was divided by an uncertainty factor of 10 to approximate chronic exposure.
-------
TABLE 9-3
2-Chloropropane
Minimum Effective Dose (NED) and Reportable Quantity (RQ)
Route: Inhalation
Dose*: 459.2 mg/day
Effect: necrosis In the liver and kidneys
Reference: Torkelson and Rowe, 1981; Betso, 1987
RVd: 1.5
RVe: 6
Composite Score: 9
RQ: 1000
'Equivalent human dose
0066d -22- 06/17/87
-------
9.2. BASED ON CARCINOGENICITY
Pertinent data regarding the cardnogenldty of 2-chloropropane In
humans or animals could not be located In the available literature as cited
In Appendix A. The compound 1s assigned an EPA classification of 0 --
cannot be classified as to carclnogenldty to humans, which precludes hazard
ranking based on carclnogenldty.
0066d -23- 06/17/87
-------
10. REFERENCES
AldMch. 1984. Catalog/Handbook of Fine Chemicals. 1984-1985. Aldrlch
Chemical Co., Milwaukee, VII.
Betso, J. 1987. Dow Chemical Company. Personal communication to P.
Goetchlus, Syracuse Research Corp.
BoubHk, T., V. Fried and E. Hala. 1984. The Vapor Pressures of Pure
Substances. Selected Values of the Temperature Dependence of the Vapour
Pressures of Some Pure Substances In the Normal and Low Pressure Region.
Vol. 17. Elsevler Sc1. Publ., Amsterdam, Netherlands.
Buhr, G. 1953. Effect of Isopropyl narcosis on the human heart and circu-
lation. Der AnaesthesUt. 2: 180-183. (CA 48:6582h)
CHR (Chemical Marketing Reporter). 1986. 1987 OPD Chemical Buyers
Directory, 74th annual ed. Schnell Publ. Co., New York. p. 229.
Coleman, W.E., R.D. L1ngg, R.G. Melton, G. Kopfler and C. Frederick. 1976.
The occurrence of volatile or.ganlcs In five drinking water supplies using
gas chromatography/mass spectrometry. Identlf. Anal. Orga. Pollut. Water,
[Chem. Congr. North Am. Cont.], 1st, Meeting Date 1975, L.H. Keith, Ed. Ann
Arbor Science Publ., Ann Arbor, MI. p. 305-327.
Coleman. E.C.. C. Ho and S.S. Chang. 1981. Isolation and Identification of
volatile compounds from baked potatoes. J. Agrlc. Food Chem. 29: 42-48.
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Elsenrelch, S.J., B.B. Looney and J.D. Thornton. 1981. Airborne organic
contaminants of the Great Lakes ecosystem. Environ. Scl. Technol. 15(1):
30-38.
Elam, J.E. and M.L. Newhouse. 1951. The properties of Isopropyl chloride.
Br. Med. J. 1: 13-14. (CA 46:5714h)
Enders, A. and F.R. KSner. 1952. The Influence of Isopropyl chloride on
heart and circulation. Oer AngesthesUt. 1: 113-115. (CA 47:95071)
Gage, J.C. 1970. The subacute Inhalation toxlclty of 109 Industrial
chemicals. Br. J. Indust. Med. 27(1): 1-18.
Gould, J.P., R.E. Ramsey, M. Glabbal and F.G. Pohland. 1983. Formation of
volatile haloorganlc compounds In the chlorlnatlon of municipal landfill
leachates. Water Chlor1nat1on Environ. Impact Health Eff. 4: 525-539.
Graedel, T.E. 1978. Chemical Compounds In the Atmosphere. Academic Press,
New York, New York.
Hansch, C. and A.J. Leo. 1985. MedChem Project. Issue No. 26, Pomona
College, Claremont, CA.
Hawley, G.G. 1981. The Condensed Chemical Dictionary, 10th ed. Van
Nostrand Relnhold Co., New York. p. 583.
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Hendry, O.6., T. H111, L. Plszklewlcz, J.A. Howard and H.K. Elgenmann.
1974. A critical review of H-atom transfer 1n the liquid phase. Chlorine
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Chem. Ref. Data. 3: 937-978.
Herron, J.T. and R.E. Hu1e. 1973. Rate constant for the reactions of
atomic oxygen (03P) with organic compounds In the gas phase. J. Phys. Chem.
Ref. Data. 2: 467-518.
H1ne, J. and F.K. Mookerjee. 1975. The Intrinsic hydrophlUc character of
organic compounds. Correlations In terms of structural contributions. J.
Org. Chem. 40: 292-298.
Kosk1kall1ot J. 1967. Kinetics of the hydrolysis of alkyl ha Tides In
perchloric acid-water mixtures. Acta Chem. Scand. 21: 397-407.
Lyman, W.J., W.F. Reehl and D.H. Rosenblatt. 1982. Handbook of Chemical
Property Estimation Methods. McGraw H111 Book Co., New York. p. 4-9, 5-5,
15-13, 15-21, 15-27.
Mabey, W. and T. Mill. 1978. Critical review of hydrolysis of organic com-
pounds In water under environmental conditions. J. Phys. Chem. Ref. Data.
7: 383-415.
Mill, T., D.G. Hendry and H. Richardson. 1980. Free-radical oxldants In
natural waters. Science. 207: 886-887.
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NTP (National Toxicology Program). 1987. Management Status Report. Dated
1/9/87.
Papa, A.J. 1982. Propyl alcohols (Isopropyl). JJK Klrk-Othmer Encyclo-
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Ed. John Wiley and Sons, New York. p. 200.
Perry, R.H. and D. Green. 1984. Perry's Chemical Engineers' Handbook, 6th
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SablJIc, A. 1984. Predictions of the nature and strength of soil sorptlon
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243-246.
Shell 011 Co. 1982. BlodegradabllUy, BOO Inhibition and acute toxIcHy to
fish of chemical compounds with cover letter. TSCA 8(d) submission, F1cha
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Simmon, V.F., K. Kauhanen and R.G. Tardlff. 1977. Mutagenlc activity of
chemicals Identified 1n drinking water. Dev. Toxlcol. Environ. Sd. 2:
249-258.
Swann, R.L.. D.A. Laskowskl, P.J. McCall, K. Vander Kuy and H.J. Dlshburger.
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Tham, R., I. Bunnfors, B. Eriksson, B. Larsby, S. Undgren and L.M. Odkulst.
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Torkelson, T.R. and V.K. Rowe. 1981. Halogenated aliphatic hydrocarbons
containing chlorine bromine and Iodine, in: Patty's Industrial Hygiene and
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Wiley and Sons, Inc., NY. p. 3433-3601.
U.S. EPA. 1977. Computer print-out of non-confidential production data
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U.S. EPA. 1980. Guidelines and Methodology Used 1n the Preparation of
Health Effect Assessment Chapters of the Consent Decree Water Criteria
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U.S. EPA. 1984. Methodology and Guidelines for Reportable Quantity
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0066d -28- 09/24/87
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U.S. EPA. 1986a. Methodology for Evaluating Potential Carclnogenlclty In
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Prepared by the Office of Health and Environmental Assessment, Carcinogen
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U.S. EPA. 1986b. Guidelines for Carcinogen Risk Assessment. Federal
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U.S. EPA. 1987. Graphical Exposure Modeling System (GEMS). Fate of Atmo-
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Van Dyke, R.A. and L. Wlneman. 1971. Enzymatic dechlorlnatlon: DechloM-
natlon of chloroethanes and propanes J_n vitro. Blochem. Pharmacol. 20:
463-470.
Wlndholz, H., Ed. 1983. The Merck Index. 10th ed. Merck and Co., Inc.,
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0066d -29- 09/24/87
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APPENDIX A
LITERATURE SEARCHED
This HEED 1s 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
SRC Environmental Fate Data Bases
SANSS
AQUIRE
TSCAPP
NTIS
Federal Register
These searches were conducted In February, 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 Hyglenlsts).
1986. Documentation of the Threshold Limit Values and Biological
Exposure Indices, 5th ed. Cincinnati, OH.
ACGIH (American Conference of Governmental Industrial Hyglenlsts).
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. 3ohn 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.
0066d -30- 09/24/87
-------
Grayson, M. and 0. Eckroth, 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. L1eu, T.W. Chou and H.L. Johnson.
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 1n 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.
0066d -31- 09/24/87
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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, W.W. and M.T. Flnley. 1980. Handbook of Acute Toxldty
of Chemicals to F1sh and Aquatic Invertebrates. Summaries of
Toxldty Tests Conducted at Columbia National Fisheries Research
Laboratory. 1965-1978. U.S. Dept. Interior, F1sh 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.
Plmental, D. 1971. Ecological Effects of Pesticides on Non-Target
Spedes. 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.
0066d -32- 09/24/87
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APPENDIX B
Sumnary Table for 2-Chloropropane
Species
Inhalation Exposure
Subchronlc rat
Chronic rat
g Carclnogenlclty ID
Oral Exposure
Subchronlc ID
Chronic ID
Carclnogenlclty ID
REPORTABLE QUANTITIES
Exposure
250 ppra (803 rog/roa).
6 hours/day, 5 days/week,
for 4 weeks
250 ppra (803 rag/in*).
6 hours/day, 5 days/week,
for 4 weeks
ID
ID
ID
ID
Effect RfD Reference
NOAEL 1 mg/m»; Gage. 1970
29 rag/day
NOAEL 0.1 rag/ma; Gage. 1970
3 mg/day
ID ID ID
ID ID ID
ID ID ID
ID ID ID
S
Based on Chronic Toxlclty:
Based on Carclnogenlclty:
1000
ID
Torkelson and
Rowe. 1981;
Betso. 1987
ID
ID = Insufficient data
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