FINAL DRAFT
United States • FrAn_niil fifl?ft
Environmental Protection L I ,;!:!
Aaency Harch, 1988
SEPA Research and
Development
HEALTH AND ENVIRONMENTAL EFFECTS DOCUMENT
FOR P-CHLORO-M-CRESOL
Prepared for
OFFICE OF SOLID WASTE AND
EMERGENCY RESPONSE
Prepared by
Environmental Criteria and Assessment Office
Office of Health and Environmental Assessment
U.S. Environmental Protection Agency
Cincinnati, OH 45268
DRAFT: DO NOT CITE OR QUOTE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 Its 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.
U,S. Environmental Protection
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11
0
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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 for 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 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
cover) reflect the'date the document 1s 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 RfD, Is an estimate of an
exposure level that would not be expected to cause adverse effects when
exposure occurs during a limited time Interval I.e., for an Interval that
does not constitute a significant portion of the Ufespan. 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 Is 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. Instead,
a carcinogenic potency factor, or q-j* (U.S. EPA, 1980a) Is , provided.
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 carclno-
genlclty are derived. The RQ 1s used to determine the quantity of a
hazardous substance for which notification 1s required 1n the event of a
release as specified under the Comprehensive Environmental Response, Compen-
sation and Liability Act (CERCLA). These two RQs (chronic toxlclty and
carclnogenlclty) 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, 1984 and 1986a, respectively.
111
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EXECUTIVE SUMMARY
p-Chloro-m-cresol 1s a white to slightly pinkish crystalline compound
that Is odorless when very pure, but usually has a phenolic odor (Wlndholz,
1983; Hawley, 1981). It 1s freely soluble 1n common organic solvents, but
only very slightly soluble (3850 ppm at 20"C) 1n water {Wlndholz, 1983).
p-Chloro-m-cresol Is not currently manufactured In the United States on an
Industrial scale; however, H 1s Imported (U.S. EPA, 1986b). It 1s used as
an external germicide, antiseptic and disinfectant and as a preservative for
glues, gums, paints, Inks, textile and leather goods (Hawley, 1981;
Wlndholz, 1983).
The dominant environmental fate process for p-chloro-m-cresol In the
atmosphere Is expected to be vapor-phase photooxldatlon with hydroxyl
radicals. In a typical ambient atmosphere, the p-chloro-m-cresol hydroxyl
radical reaction half-life has been estimated to be 1.1 days (U.S. EPA,
1987). If released to water, photooxldatlon and blodegradatlon appear to be
the major removal processes. Based on an estimated rate constant and
natural water radical concentrations (Jaber et al., 1984; Mabey et al..
1981), the half-life of p-chloro-m-cresol with respect to reaction with
peroxy radicals In sunlit natural water has been estimated as 0.8 days.
Various screening tests have demonstrated that p-chloro-m-cresol 1s signifi-
cantly biodegradable under aerobic conditions, but resistant to blodegrada-
tlon under anaerobic conditions (Tabak et al., 1964, 1981; Voets et al.,
1976; Chambers et al., 1963; Paull and Franke, 1971; Johnson and Young,
1983). If released to soil, leaching 1s likely to occur along with aerobic
blodegradatlon. Two laboratory studies have concluded that p-chloro-m-
cresol will be mobile In soil systems (Zullel, 1981; Hudson-Baruth and
1v
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SeHz, 1986). In various subsurface soil regions or groundwaters where
aerobic degradation 1s not viable and other degradation processes cannot
occur, p-chloro-m-cresol may be relatively persistent. :
The greatest potential for human exposure to p-chloro-m-cresol may occur
In occupational settings that formulate products (glues, gums, paints, Inks,
textile or leather goods) or use products that have been formulated with
p-chloro-m-cresol. With the exception of effluent monitoring data,
published environmental monitoring data are very limited. p-Chloro-m-cresol
has been detected 1n drinking well water 1n areas of China that are Irri-
gated with sewage effluents (Tu et al., 1986) and In an unspecified finished
drinking water (Kool et al., 1982). Uastewater effluents from various
Industries and from municipal sewage treatment have been found to contain
p-chloro-m-cresol (U.S. EPA, 1981; BourquVn and Gibson, 1978; Bulsson et
al., 1984; Shackelford and Keith, 1976; Bursey and Pelllzzarl, 1982).
Halogenated organic compounds (such as p-chloro-m-phenol) can be released to
the environment from Inadvertent formation In waters (potable water, waste-
water, cooling water) that have undergone chlorlnatlon procedures (Bourquln
and Gibson, 1978).
The limited data regarding the aquatic toxlclty of p-chloro-m-cresol
Indicate that freshwater plants may be less sensitive to p-chloro-m-cresol
than fish and Invertebrate species. No data for saltwater species were
found 1n the available literature.
The toxldty data concerning p-chloro-m-cresol are limited. In a 28-day
gavage study, decreased body weight was observed In rats treated at 400
mg/kg/day, with no effects noted at 200 mg/kg/day (Madsen et al., 1986). In
a single dose study, hlstopathologlcal effects were observed In the livers
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of rats treated with p-chloro-m-cresol at 400 mg/kg by gavage or by subcuta-
neous Injection (Robenek et al., 1980). Subcutaneous and IntraperUoneal
dosing of rats and rabbits has resulted In kidney and liver hlstopathology
(W1en, 1939).
In humans, sensUlzatlon has been reported In Individuals exposed to
chlorocresols (Guy and Jacob, 1941; Hancock and Naysmlth, 1975; Alnley et
al., 1970).
The only mutagenldty study available reported negative results 1n S.
typhlmurlum strains TA100, TA1535, TA1537 and TA98, both with and without
metabolic activation (Madsen et al., 1986). Pertinent data regarding the
cardnogenlclty, teratogenlcHy and the toxldty of p-chloro-m-cresol
following subchronlc or chronic Inhalation exposure, and chronic oral
exposure were not located 1n the available literature cited 1n Appendix A.
The lack of Inhalation data precluded the derivation of Inhalation RfDs.
Using the 28-day study by Madsen et al. (1986), a human subchronlc RfD of 2
mg/kg/day or 140 mg/day for a 70 kg human was calculated. Confidence 1n
this RfO 1s very low. A chronic oral RfD was not calculated, because the
only subchronlc study available (Madsen et al., 1986) was of Insufficient
duration for the derivation of a chronic RfO. A provisional RQ for systemic
toxldty of 1000 pounds was calculated on the basis of decreased body weight
1n rats 1n the Madsen et al. (1986) study. Because of the lack of data, an
RQ based on cardnogenlclty could not be calculated.
A 90-day oral study 1s available 1n the FIFRA CBI literature. The RfD
and RQ calculations will be reviewed when this study Is available.
v1
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TABLE OF CONTENTS
Page
1. INTRODUCTION 1
1.1. STRUCTURE AND CAS NUMBER 1
1.2. PHYSICAL AND CHEMICAL PROPERTIES 1
1.3. PRODUCTION DATA 2
1.4. USE DATA 2
1.5. SUMMARY 4
2. ENVIRONMENTAL FATE AND TRANSPORT 5
2.1. AIR '. 5
2.2. WATER 5
2.2.1. Hydrolysis 5
2.2.2. Oxidation 5
2.2.3. Photolysis 6
2.2.4. Mlcroblal Degradation 6
2.2.5. Volatilization 7
2.2.6. Adsorption 7
2.2.7. Bloconcentratlon 7
2.3. SOIL 7
2.3.1. Mlcroblal Degradation 7
2.3.2. Adsorption. ..... 8
2.4. SUMMARY 8
3. EXPOSURE 10
3.1. WATER 10
3.2. FOOD 11
3.3. INHALATION 12
3.4. DERMAL 12
3.5. SUMMARY 12
4. AQUATIC TOXICITY 13
4.1. ACUTE TOXICITY 13
4.2. CHRONIC EFFECTS 13
4.3. PLANT EFFECTS 13
4.4. SUMMARY 13
5. PHARMACOKINETCS 14
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TABLE OF CONTENTS (cont.)
Page
6. EFFECTS 15
6.1. SYSTEMIC TOXICITY 15
6.1.1. Inhalation Exposures 15
6.1.2. Oral Exposures 15
6.1.3. Other Relevant Information 15
6.2. CARCINOGENICITY 17
6.3. MUTAGENICITY 17
6.4. TERATOGENICITY 17
6.5. OTHER REPRODUCTIVE EFFECTS 17
6.6. SUMMARY 17
7. EXISTING GUIDELINES AND STANDARDS 19
7.1. HUMAN 19
7.2. AQUATIC 19
8. RISK ASSESSMENT 20
8.1. CARCINOGENICITY 20
8.1.1. Weight of Evidence 20
8.1.2. Quantltatlve'RIsk Estimates . . . 20
8.2. SYSTEMIC TOXICITY 20
8.2.1. Inhalation Exposure ... 20
8.2.2. Oral Exposure 20
9. REPORTABLE QUANTITIES 22
9.1. BASED ON SYSTEMIC TOXICITY 22
9.2. BASED ON CARCINOGENICITY 22
10. REFERENCES 26
APPENDIX A: LITERATURE SEARCHED 34
APPENDIX B: SUMMARY TABLE FOR p-CHLORO-m-CRESOL 37
V111
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LIST OF TABLES
No. Title Page
1-1 1977 U.S. Production Data for p-Chloro-m-cresol 3
9-1 Oral Toxlclty Summary for p-Chloro-m-cresol Using the Rat . . 23
9-2 Oral Composite Scores for p-Chloro-m-cresol Using the Rat . . 24
9-3 p-Chloro-m-cresol: Minimum Effective Dose (MED) and
Reportable Quantity (RQ) 25
1x
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LIST OF ABBREVIATIONS
BCF Bloconcentratlon factor
CS Composite score
Kow Octanol/water partition coefficient
Concentration lethal to 50% of recipients
Dose lethal to 50% of recipients
MED Minimum effective dose
NOAEL No-observed-adverse-effect level
ppb Parts per billion
ppm Parts per million
RfD Reference dose
RQ * Reportable quantity
RVj Dose-rating value
RVe Effect-rating value
UV Ultraviolet
v/v Volume per volume
WS Water solubility
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1. INTRODUCTION
1.1. STRUCTURE AND CAS NUMBER
p-Chloro-m-cresol Is a common chemical name for the compound currently
referenced by Chemical Abstracts Service (CAS) as phenol, 4-chloro-3-methyl-.
It Is also known by the chemical synonyms 4-chloro-m-cresol, 4-chloro-3-
cresol, 2-chloro-5-hydroxytoluene, 4-chloro-5-methylphenol and 4-chloro-3-
methylphenol (SANSS, 1987). Tradename products containing p-chloro-m-cresol
Include Aptal, Baktol, Baktolan, Candaseptlc, Ottafact, Parmetol, Parol,
Perltonan, Preventol, Raschlt and Rasen-Anlcon (SANSS, 1987). The
structure, molecular weight, empirical formula and CAS Registry number for
p-chloro-m-cresol are as follows:
OH
Molecular weight: 142.59
Empirical formula: C?H7C10
CAS Registry number: 59-50-7
1.2. PHYSICAL AND CHEMICAL PROPERTIES
p-Chloro-m-cresol 1s a white to slightly pinkish crystalline compound
that Is odorless when very pure, but usually has a phenolic odor (Ulndholz,
1983; Hawley, 1981). It Is freely soluble In alcohol, benzene, chloroform,
ether, acetone, petroleum ether, fixed oils, terpenes and aqueous alkaline
solutions (Wlndholz, 1983). Selected physical properties are listed below:
Melting point:
Boiling point:
66-68°C
235°C
Ueast, 1985
Ueast. 1985
0076d
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Water solubility:
at 20°C 3850 ppm Wlndholz, 1983
at 25°C 4000 ppm Hawley, 1981
Vapor pressure:
at 25°C 0.0116 mm Hg Jaber et al., 1984
Log Kow: 3.10 Hansch and Leo, 1985
Air conversion
factors at 20°C: 1 mg/m3 = 0.166 ppm
1 ppm =6.04 mg/m3
p-Chloro-m-cresol 1s volatile with steam. Aqueous solutions turn yellow
on exposure to light and air (Wlndholz, 1983).
1.3. PRODUCTION DATA
p-Chloro-m-cresol 1s not currently manufactured In the United States on
an Industrial scale; however, It 1s Imported (U.S. EPA, 1986b). Imports
through principal United States customs districts In recent years have been
reported as follows (USITC, 1982, 1983, 1984):
Imports
Year (millions of pounds)
1983 0.293
1982 0.260
1981 0.274
Production data cited In the U.S. EPA TSCA Production File for 1977 are
presented In Table 1-1. p-Chloro-m-cresol can be prepared by the chlorlna-
tlon of m-cresol (Wlndholz, 1983).
1.4. USE DATA
p-Chloro-m-cresol 1s used as an external germicide, antiseptic and
disinfectant and as a preservative for glues, gums, paints, Inks, textile
and leather goods (Hawley, 1981; Wlndholz, 1983). It has been used as a
topical antiseptic for both humans and animals (Wlndholz, 1983).
0076d -2- 02/01/88
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TABLE 1-1
1977 U.S. Production Data for p-Chloro-m-cresol*
Producer
(Location)
Key Chemical Co.
(Greensboro, NC)
Gallard-Schleslnger Chemical
(Carle Place, NY)
Mobay Chemical Corp.
(Plttsburg, PA)
Aceto Chemical Co.
(Flushing, NY)
Agfa-Gevaett Inc.
(Teterboro, NJ)
Struktol Co.. of America
(Akron, OH)
3M Company
(St. Paul, MN)
Hercules Inc.
(Wilmington, DE)
The Frank Herzl Corp.
(New York, NY)
Cosan Chemical Corp.
(Clifton, NJ)
Type of Producer
Importer
Importer
Importer
Importer
Importer
Importer
Importer
Importer
Importer
Importer
Production Range
(pounds)
<1000
1-10 thousand
confidential
10-100 thousand
<1000
confidential
none
confidential
none
confidential
*Source: U.S. EPA, 1977
007 6 d
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1.5. SUMMARY
p-Chloro-m-cresol 1s a white to slightly pinkish crystalline compound
that 1s odorless when very pure, but usually has a phenolic odor (Wlndholz,
1983; Hawley, 1981). It 1s freely soluble 1n common organic solvents, but
only very slightly soluble (3850 ppm at 2(TC) In water (Wlndholz, 1983).
p-Chloro-m-cresol Is not currently manufactured In the United States on an
Industrial scale; however. 1t 1s Imported (U.S. EPA, 1986b). It Is used as
an external germicide, antiseptic and disinfectant and as a preservative for
glues, gums, paints, Inks, textile and leather goods (Hawley, 1981;
Wlndholz, 1983).
0076d -4- 02/01/88
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2. ENVIRONMENTAL FATE AND TRANSPORT
2.1. AIR
p-Chloro-m-cresol has a vapor pressure of 0.0116 mm Hg at 25°C {Jaber et
al., 1984). Organic compounds having vapor pressures of this magnitude are
expected to exist almost entirely 1n the vapor phase In the ambient
atmosphere (Elsenrelch et al., 1981).
The dominant environmental fate process for p-chloro-m-cresol In the
atmosphere Is probably the vapor phase reaction with hydroxyl radicals that
are photochemlcally formed by sunlight. The half-life of this reaction 1n a
typical ambient atmosphere has been estimated to be 1.1 days based on an
estimated reaction rate constant of 9.1xlO~12 cmVmolecule-sec at 25°C
and an atmospheric hydroxyl radical concentration of 8xl05 molecules/cm3
(U.S. EPA, 1987). p-Chloro-m-cresol absorbs UV light >290 nm, which
suggests a potential for direct photolysis; however, kinetic rate data are
not available, to assess the relative Importance of photolysis (Callahan et
al., 1979).
The relative Importance of physical removal from the atmosphere by
processes such as rainfall cannot be predicted accurately from the available
data.
2.2. WATER
2.2.1. Hydrolysis. p-Chloro-m-cresol 1s not expected to hydrolyze
significantly 1n environmental waters {Mabey et al., 1981; Callahan et al.,
1979).
2.2.2. Oxidation. Rate constants for the reaction of p-chloro-m-cresol
with peroxy radicals and singlet oxygen have been estimated to be IxlO4
and IxlOVM-sec, respectively (Jaber et al., 1984). Assuming the concen-
trations of peroxy radicals and singlet oxygen In sunlit natural water are
0076d -5- 12/14/87
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-TO"9 and 10"12 M (Mabey et a!., 1981), respectively, the half-life with
respect to peroxy radicals would be 0.8 days and the half-life with respect
to singlet oxygen would be 80 days.
2.2.3. Photolysis. The UV absorption spectrum of p-chloro-m-cresol
exhibits absorption at >290 nm, which suggests potential direct photolysis
(Callahan et al., 1979). Similar compounds (chlorophenol, dlch'lorophenol)
have been shown to photodegrade In sunlight or UV light (>290 nm), but the
rate at which photolysis may occur In the environment has not been deter-
mined (Callahan et al., 1979; U.S. EPA, 1980b).
2.2.4. M1crob1al Degradation. Various screening tests have demonstrated
that p-chloro-m-cresol Is significantly biodegradable under aerobic
conditions, but resistant to blodegradatlon under anaerobic conditions. A
static-culture flask-screening procedure using settled domestic wastewater
as the mlcroblal Inoculum found p-chloro-m-cresol to degrade significantly
with rapid adaptation, as 100% of Initial concentrations (5 and 10 ppm)
blodegraded within 14 days (Tabak et al., 1981). Screening tests similar to
detergent blodegradabHlty studies determined 30-100% p-chloro-m-cresol
degradation under aerobic conditions and 0% degradation under anaerobic
conditions (Voets et al., 1976). Significant degradation of p-chloro-m-
cresol has been observed using Warburg resplrometer tests with phenol-
adapted bacteria (Chambers et al., 1963; Tabak et al., 1964). Sapromat
apparatus procedures using activated sludge Inocula have determined 85-100%
blodegradatlon of p-chloro-m-cresol with Initial concentrations as high as
100 ppm (Paull and Franke, 1971). p-Chloro-m-cresol has been found,
however, to have small Inhibitory effects on anaerobic digestion of test
chemicals (Johnson and Young, 1983).
0076d -6- 02/01/88
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2.2.5. Volatilization. Based on a vapor pressure of 0.0116 ram Hg and a
water solubility of 4000 ppm at 25°C (see Section 1.2.}. the Henry's Law
constant for p-chloro-m-cresol can be estimated to be 5.44xlO~7
atm-m3/mol. This value of Henry's Law constant Indicates that volatili-
zation from water Is very slow (Lyman et a!., 1982). Using the method
outlined In Lyman et al. (1982), the volatilization half-life of p-chloro-m-
cresol from a model river (1 m deep flowing 1 m/sec with a wind velocity of
3 m/sec) has been estimated to be 80.5 days. This rate of removal Is not
competitive with rates of removal by photooxldatlon or, perhaps, blodegra-
datlon.
2.2.6. Adsorption. Based on the soil adsorption data presented 1n
Section 2.3.2., p-chloro-m-cresol Is not expected to significantly partition
from the water column to sediment.
2.2.7. B1oconcentrat1on. Estimation of the BCF of an organic chemical
can be made from the following recommended regression-derived equations
(Lyman et al., 1982):
log BCF = 0.76 log KQW - 0.23 (2-1)
log BCF = 2.791 - 0.564 log WS (In ppm) (2-2)
For p-chloro-m-cresol, the BCF values calculated from Equations 2-1 and 2-2
are 134 and 6, respectively, based on a log K of 3.10 and a water
solubility of 3850 ppm at 20°C (see Section 1.2.). Bloconcentratlon does
not appear to be a major fate process based on these estimated BCF values.
2.3. SOIL
2.3.1. H1crob1al Degradation. Experimental data pertaining to the
mlcroblal degradation of p-chloro-m-cresol In soil were not located. As
noted In Section 2.2.4., various screening tests have demonstrated that
p-chloro-m-cresol blodegrades significantly under aerobic conditions, but
0076d -7- 02/01/88
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resists blodegradatlon under anaerobic conditions. It Is possible,
therefore, that blodegradatlon will occur under aerobic soil conditions.
2.3.2. Adsorption. The results of two experimental studies Indicate that
p-chloro-_m-cresol will be mobile In soil and susceptible to significant
leaching. Zullel (1981) found p-chloro-m-cresol to have significant
mobility 1n an activated carbon-sand filter system, which was considered
Indicative of a low adsorption potential 1n soil systems. Hudson-Baruth and
Seltz (1986) determined that only minor adsorption of p-chloro-m-cresol
occurred 1n dolomite systems and suggested that leaching would occur In
dolomite groundwater aquifers. The detection of p-chloro-m-cresol 1n well
water In China (Section 3.1.) has demonstrated that leaching can occur In
the environment.
2.4. SUMMARY
The dominant environmental fate process for p-chloro-m-cresol In the
atmosphere Is expected to be vapor-phase photooxldatlon with hydroxyl
radicals. In a typical ambient atmosphere, the p-chloro-m-cresol hydroxyl
radical reaction half-life has been estimated to be 1.1 days (U.S. EPA,
1987). If released to water, photooxldatlon and blodegradatlon appear to be
the major removal processes. Based on an estimated rate constant and
natural water radical concentrations (Jaber et al., 1984; Mabey et al.,
1981), the half-life of p-chloro-m-cresol with respect to reaction with
peroxy radicals 1n sunlit natural water has been estimated to be 0.8 days.
Various screening tests have demonstrated that p-chloro-m-cresol Is signifi-
cantly biodegradable under aerobic conditions, but resistant to blodegrada-
tlon under anaerobic conditions (Tabak et al., 1964, 1981; Voets et al.,
1976; Chambers et al., 1963; Paull and Franke, 1971; Johnson and Young,
1983). If released to soil, leaching 1s likely to occur along with aerobic
0076d -8- 02/01/88
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blodegradatlon. Two laboratory studies have concluded that p-chloro-m-
cresol will be mobile 1n soil systems (Zullel, 1981; Hudson-Baruth and
Seltz, 1986). In various subsurface soil regions or groundwaters where
aerobic degradation 1s not viable and other degradation processes cannot
occur, p-chloro-m-cresol may be relatively persistent.
0076d -9- 12/14/87
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3. EXPOSURE
Occupational exposure to p-chloro-m-cresol through Inhalation and dermal
contact may be possible at facilities that formulate products (glues, gums,
paints, Inks, textile or leather goods) or use products that have been
formulated with p-chloro-m-cresol. Consumer exposure may be possible
through use of these products; however, no data regarding actual human
exposure to p-chloro-m-cresol were located 1n the literature cited 1n the
Appendix.
Exposure of p-chloro-m-cresol to the general population may occur
through oral consumption of drinking water that has been contaminated by
Inadvertent formation during chlorlnatlon treatment or by leaching Into well
water.
3.1. WATER
p-Chloro-m-cresol detection In a finished drinking water sample has been
reported (source or concentration were not reported) (Kool et al., 1982).
Groundwater from 11 drinking water wells 1n areas of China that are
Irrigated with sewage effluents have been found to contain p-chloro-m-cresol
(Tu et al., 1986). Monitoring of surface waters at various locations of the
Lake Erie or Lake Michigan ecosystems did not detect any positive concentra-
tions of p-chloro-m-cresol (Great Lakes Hater Quality Board, 1983).
p-Chloro-m-cresol has been detected 1n a number of wastewater effluents.
Positive detections have been reported for raw and treated wastewaters from
the following Industries (U.S. EPA, 1981): Iron and steel manufacturing,
aluminum forming, foundries, metal finishing, photographic equipment and
supplies, pharmaceutical manufacturing, organic chemicals and plastics
manufacturing, paint and Ink formulation, soap and detergent manufacturing,
0076d -10- 12/14/87
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textile mills, and auto and other laundries. Reported mean concentrations
1n the raw wastewaters ranged from 0.01 ppb (organic chemical and plastics
manufacturing) to 100 ppm (metal finishing). Reported mean concentrations
1n the treated wastewaters ranged from 0.01 ppb (organic chemical and
plastics manufacturing) to 36 ppb (foundries). Chlorinated municipal
effluents have been reported to contain p-chloro-m-cresol levels of ~2 ppb
(Bourquln and Gibson, 1978). p-Chloro-m-cresol levels of 73 ng/l, 154
ng/i and 0.22 mg/kg (dry wt) were detected 1n a final effluent from a
treatment works, 1n a soil leachate and 1n a wastewater sludge, respec-
tively, from the United Kingdom (Bulsson et al., 1984). Effluents from
chlorinated domestic sewage (Shackelford and Keith, 1976) and from mechani-
cal products and transportation equipment Industries (Bursey and PelUzzarl,
1982) have also been found to contain positive levels of p-chloro-m-cresol.
The gross analysis of the water monitoring data contained In the U.S.
EPA STORET Data Base cites 7667 reporting stations with a minimum, maximum
and mean concentration of 0.0, 101, 331 and 78.5 ppb, respectively.
Halogenated organic compounds (such as p-chloro-m-phenol) can be
released to the environment from Inadvertent formation In waters (potable
water, wastewater, cooling water) that have undergone chlorlnatlon proce-
dures (Bourquln and Gibson, 1978). p-Chloro-m-cresol may potentially occur
1n the environment as a metabolite of the soil degradation of herbicides
such as 4-chloro-2-methylphenoxyacetate, although this supposition has never
been demonstrated experimentally (U.S. EPA, 1980b).
3.2. FOOD
Pertinent food monitoring data were not located 1n the available
literature cited In the Appendix.
0076d -11- 02/03/88
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3.3.- INHALATION
p-Chloro-m-cresol has been detected In the stack effluent from a
municipal waste Incinerator (James et al., 1985).
3.4. DERMAL
Pertinent dermal monitoring data were not located In the available
literature cited In the Appendix.
3.5. SUMMARY
The greatest potential for human exposure to p-chloro-m-cresol may occur
In occupational settings that formulate products (glues, gums, paints. Inks,
textile or leather goods) or use products that have been formulated with
p-chloro-m-cresol. With the exception of effluent monitoring data,
published environmental monitoring data are very limited. p-Chloro-m-cresol
has been detected In drinking well water 1n areas of China that are Irri-
gated with sewage effluents (Tu et al., 1986) and In an unspecified finished
drinking water (Kool et al., 1982). Wastewater effluents from various
Industries and from municipal sewage treatment have been found to contain
p-chloro-m-cresol (U.S. EPA, 1981; Bourquln and Gibson, 1978; Bulsson et
al., 1984; Shackelford and Keith, 1976; Bursey and Pell1zzar1, 1982).
Halogenated organic compounds (such as p-chloro-m-phenol) can be released to
the environment from Inadvertent formation In waters (potable water, waste-
water, cooling water) that have undergone chlorlnatlon procedures (Bourquln
and Gibson, 1978).
0076d -12- 12/14/87
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4. AQUATIC TOXICITY
4.1. ACUTE TOXICITY
Gerslch and Hayes (1986) reported a 48-hour LC5Q of 2.0 mg/a. for
Daphnla magna exposed to p-chloro-m-cresol . The test was conducted at a pH
of 7.5-8 at 19.6-20.8°C under static conditions.
Hattula et al. (1981) reported a 24-hour LC5Q of 1.3 ppm In trout,
Sal mo trutta. exposed to p-chloro-m-cresol. The test was conducted at 5°C
under static conditions. The static 96-hour LC5_ for p-chloro-m-cresol 1n
the fathead minnow, Plmephales promelas. was reported as 30 yg/i (U.S.
EPA, 1972).
4.2. CHRONIC EFFECTS
Pertinent data regarding effects on aquatic organisms following chronic
exposure were not located In the available literature cited 1n Appendix A.
4.3. PLANT EFFECTS
Blackman et al. (1955) reported an LC5Q of 95,488 yg/l for
duckweed, Lemna minor, exposed to p-chloro-m-cresol.
4.4. SUMMARY
The limited data regarding the aquatic toxldty of p-chloro-m-cresol
Indicate that freshwater plants may be less sensitive to p-chloro-m-cresol
than fish and Invertebrate species. No data for saltwater species were
found In the available literature.
0076d -13- 12/14/87
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5. PHARMACOKIMETICS
The only data regarding the pharmacoklnetlcs of p-chloro-m-cresol
located 1n the literature concerns excretion. Zondek and Shapiro (1943)
recovered 15-20% of an -1000 rag/kg dose 1n the urine of rabbits (wt. ~1 kg)
given a single subcutaneous Injection of p-chloro-m-cresol. In humans given
an unspecified dose of p-chloro-m-cresol by Intramuscular Injection, the
compound was not recovered In the urine In appreciable amounts (Zondek and
Shapiro, 1943).
0076d -14- 03/08/88
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6. EFFECTS
6.1. SYSTEMIC TOXICITY
6.1.1. Inhalation Exposure. Pertinent data regarding the toxlclty of
p-chloro-m-cresol following subchronlc or chronic Inhalation exposure were
not located In the available literature cited In Appendix A.
6.1.2. Oral Exposure.
6.1.2.1. SUBCHRONIC — Hadsen et al. (1986) treated groups of 10 male
and 10 female rats by gavage with p-chloro-m-cresol In soybean oil at doses
of 0, 50, 200 or 400 mg/kg/day. Compared with controls, a significant
decrease 1n weight gain (p<0.05 males, p<0.01 females) was observed In rats
treated at 400 mg/kg/day during the last week of treatment. No effects on
hematology or clinical chemistry were noted. At necropsy, no significant
alterations 1n relative organ weights were observed. Without providing any
details, the authors stated that no pathological changes were noted In the
kidneys, spleen, brain, .adrenals, liver, testes, stomach, small Intestine,
pancreas, lung, aorta, heart, thymus, thyroid and parathyroid.
6.1.2.2. CHRONIC — Pertinent data regarding the toxlclty of
p-chloro-m-cresol following chronic oral exposure were not located 1n the
available literature cited 1n Appendix A.
6.1.3. Other Relevant Information. Hlen (1939) reported subcutaneous
LD5Qs of 400 and 360 mg/kg for p-chloro-m-cresol In rats and mice, respec-
tively. An Intravenous ID™ In mice was 70 mg/kg. p-Chloro-m-cresol
treatment resulted 1n muscle tremors, and death occurred In a few hours as a
result of respiratory failure. Damage to renal tubules was observed at high
doses.
Robenek et al. (1980) found alterations 1n the livers of rats sacrificed
60 hours after being given a single oral or subcutaneous dose of p-chloro-m-
cresol 1n peanut oil at 400 mg/kg. Control rats were treated with peanut
0076d -15- 02/01/88
-------
oil. The observed liver effects were similar following both oral and subcu7
taneous exposure. Electron micrographs showed a considerable Increase In
mitochondria, and freeze fracturing revealed Irregularities In bile
canallcull. Numerous vacuoles were observed In the cytoplasm of cells that
are presumably hepatocytes (Increase In mitochondria, vacuoles In cytoplasm,
etc.). Light microscopy revealed dilation of the sinusoids and activation
of Kupffer cells In both groups of rats.
In a 14-day study conducted by Wlen (1939), groups of five young rats
(sex unspecified) were treated by subcutaneous Injection with p-chloro-m-
cresol at 0 or 80 mg/kg/day. Growth was not affected, and lesions were not
observed In the kidney, liver or spleen. H1ld Inflammation was reported at
the Injection site. W1en (1939) also treated three rabbits with subcuta-
neous Injections of p-chloro-m-cresol at 12.5 mg (5 ml of a 1/400 (v/v)
solution) dally for 4 weeks. No changes In hematology, or hlstologlcal
changes In the liver or kidney were noted. Controls were not used In this
study.
In an l£ vitro study, W1en (1939) found that 1/1000 p-chloro-m-cresol
solution decreased the magnitude of the heart beat of Isolated hearts from
rabbits. Similar effects were observed with phenol.
Guy and Jacob (1941) reported that a 1.5% aqueous solution of p-chloro-
m-cresol can cause vesicular dermatitis 1n sensitive humans. The symptoms
occur within 4 hours and regress within 1 week.
Hancock and Naysmlth (1975) and Alnley et al. (1970) reported sensltlza-
tlon reactions In humans treated with heparln preserved with chlorocresol.
Testing with heparln without chlorocresol Indicated that chlorocresol was
the cause of the reaction. The specific chlorocresol Involved was not
stated.
0076d -16- 03/10/88
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6.2. CARCINOGENICITY
Pertinent data regarding the cardnogenldty of p-chloro-m-cresol
following any route of exposure were not located 1n the available literature
cited In Appendix A.
6.3. MUTAGEMICITY
p-Chloro-m-cresol tested negative for reverse mutation In Salmonella
typhlmurlum strains TA100, TA1535, TA1537 and TA98 {Madsen et al., 1986).
The tests were conducted both with and without metabolic activation (rat
S-9) at concentrations of 1.28, 6.4, 32, 160 or 800 jig/plate.
6.4. TERATOGENICITY
Pertinent data regarding the teratogenlclty of p-chloro-m-cresol were
not located In the available literature In Appendix A.
6.5. OTHER REPRODUCTIVE EFFECTS
Pertinent data regarding other reproductive effects of p-chloro-m-cresol
were not located In the available literature cited 1n Appendix A.
6.6. SUMMARY
The toxldty data concerning p-chloro-m-cresol are limited. In a 28-day
gavage study, decreased body weight was observed In rats treated at 400
mg/kg/day, with no effects noted at 200 mg/kg/day (Madsen et al., 1986). In
a single dose study, hlstopathologlcal effects were observed In the livers
of rats treated with p-chloro-m-cresol at 400 mg/kg by gavage or by subcuta-
neous Injection (Robenek et al., 1980). Subcutaneous and Intraperltoneal
dosing of rats and rabbits has resulted 1n kidney and liver hlstopathology
(Wlen, 1939).
In humans, sensltlzatlon has been reported In Individuals exposed to
chlorocresols (Guy and Jacob, 1941; Hancock and Naysmlth, 1975; Alnley et
al., 1970).
0076d -17- 03/10/88
-------
The only mutagenlclty study available reported negative results In S.
tvphlmuMum strains TA100, TA1535, TA1537 and TA98, both with and without
metabolic activation {Madsen et al., 1986). Pertinent data regarding the
carclnogenlclty, teratogenlclty and the toxlclty of p-chloro-m-cresol
following subchronlc or chronic Inhalation exposure, and chronic oral
exposure were not located 1n the available literature cited 1n Appendix A.
0076d -18- 03/10/88
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7. EXISTING GUIDELINES AND STANDARDS
7.1. HUMAN
U.S. EPA (1980b) recommended an ambient water quality criterion of 3000
yg/l, which was based on an odor threshold of 3000 vg/ft. for
p-chloro-m-cresol 1n water {Deltz and Traud, 1978). U.S. EPA (1980b) stated
that data on human health effects must be developed as a more substantial
basis for recommending a criteria to protect human health.
The RQ for p-chloro-m-cresol 1s 5000 pounds (U.S. EPA, 1985a).
7.2. AQUATIC
Acute toxldty 1n aquatic species has been shown to occur at concentra-
tions as low as 30 yg/i, (U.S. EPA, 1980b).
0076d -19- 02/01/88
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8. RISK ASSESSMENT
8.1. CARCINOGENICITY
Pertinent data regarding the cardnogenlclty of p-chloro-m-cresol were
not located In the available literature cited In Appendix A.
8.1.1. Weight of Evidence. The lack of data concerning the cardno-
genlclty of p-chloro-m-cresol 1n either humans or animals Indicates that the
compound should be classified as an EPA Group D chemical {U.S. EPA, 1986c),
not classifiable as to human carclnogenlclty.
8.1.2. Quantitative Risk Estimates. The lack of carclnogenlclty data for
p-chloro-m-cresol precludes the derivation of a potency factor.
8.2. SYSTEMIC TOXICITY
8.2.1. Inhalation Exposure. The lack of data concerning the toxlclty of
p-chloro-m-cresol following Inhalation exposure precludes the derivation of
subchronlc or chronic Inhalation RfDs.
8.2.2. Oral Exposures.
8.2.2.1. LESS THAN LIFETIME EXPOSURES — The only subchronlc study
available Is the 28-day study by Madsen et al. (1986). In this study, no
effects were observed 1n rats treated by gavage with p-chloro-m-cresol 1n
soybean oil at doses of 50 or 200 mg/kg/day. A significant decrease 1n
weight gain (p<0.05 males, p<0.01 females) was observed In rats treated at
400 mg/kg/day during the last week of treatment. No other effects were
noted. The parameters examined Included hematology and clinical chemistry.
Detailed descriptions of the experimental protocol were not provided. The
lowest NOAEL found 1n this study (200 mg/kg/day) can be used to derive a
subchronlc RfD for p-chloro-m-cresol. A human subchronlc RfD of 2 mg/kg/day
or 140 mg/day for a 70 kg human Is calculated by dividing the rat NOAEL by
an uncertainty factor of 100 (10 for Interspecles extrapolation and 10 to
protect sensitive Individuals).
0076d -20- 03/08/88
-------
Confidence 1n this RfD 1s very low. The study used for the basis of the
RfD 1s only 28 days 1n duration; there are no supporting subchronlc studies
and a single dose study (Robenek et a!., 1380) found liver lesions at 400
mg/kg, a dose resulting In only decreased body weight 1n the 28-day study
(Madsen et al., 1986). In addition, p-chloro-m-cresol has not been
evaluated for teratogenldty or carclnogenlclty and no pharmacoklnetlc data
were available.
8.2.2.2. CHRONIC EXPOSURES -- No chronic oral studies of p-chloro-m-
cresol are available. The only subchronlc study available was 28 days long
(Madsen et al., 1986), a duration Insufficient for the derivation of a
chronic RfD.
0076d -21- 03/08/88
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9. REPORTABLE QUANTITIES
9.1. BASED ON SYSTEMIC TOXICITY
The tox1c1ty of p-chloro-m-cresol was discussed In Chapter 6. The only
study suitable for the derivation of an RQ 1s summarized In Table 9-1. In
the 28-day rat study (Madsen et al., 1986), decreased body weight gain was
observed 1n rats treated by gavage at 400 mg/kg/day. The derivation of the
RQ 1s presented 1n Table 9-2. A human MED of 478.8 mg/day Is calculated by
multiplying the equivalent human dose of 68.4 mg/kg/day by 70 kg and divid-
ing by 10 to extrapolate from subchronlc exposure. This MED corresponds to
an RV of 1.5. The effect, decreased body weight, corresponds to an RV,
of 4. Multiplying the RV& by the RVd, a CS of 6 1s derived.
The CS of 6 derived from the 28-day rat study (Madsen et al., 1986)
corresponds to an RQ of 1000 pounds. This RQ 1s presented 1n Table 9-3.
Because this RQ 1s based on a study only 28 days 1n duration. It should be
considered provisional until 'longer-term studies are available.
9.2. BASED ON CARCINOGENICITY
The lack of data precludes the derivation of a carclnogenldty based RQ.
0076d -22- 02/01/88
-------
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0076d
-23-
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-------
TABLE 9-2
Oral Composite Score for p-Chloro-m-cresol Using the Rata
Chronic
Animal Dose Human MEDb RVd Effect RVe CS RQ
(mg/kg/day) (mg/day)
400 478.8 1.5 decreased body 4 6 1000
weight gain
aSource: Madsen et al.. 1986
bThe dose was divided by an uncertainty factor of 10 to approximate chronic
exposure.
0076d -24- 12/14/87
-------
TABLE 9-3
p-Chloro-m-cresol
Minimum Effective Dose (MED) and Reportable Quantity (RQ)
Route: oral
Dose*: 478.8 mg/day
Effect: decreased body weight gain
Reference: Madsen et al., 1986
RVd: 1.5
RVe: 4
Composite Score: 6
RQ: 1000
*Equ1va1ent human dose
0076d -25- 12/14/87
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10. REFERENCES
Alnley, E.J.. et al. 1970. Adverse reaction to chlorocresol-preserved
heparln. Lancet. 1803: 705. (Cited In U.S. EPA, 1980b)
Blackman, G.E., et al. 1955. The physiological activity of substituted
phenols. I. Relationships between chemical structure and physiological
activity. Arch. Blochem. Blophys. 54: 45. (Cited In U.S. EPA, 1980b)
Bourquln, A.M. and D.T. Gibson. 1978. Mlcroblal Degradation of Halogenated
Hydrocarbons. In: Water Chlorlnatlon Environmental Impacts and Health
Effects, Vol. 2. Ann Arbor Science, Ann Arbor, MI. p. 253-264.
Bulsson, R.S.K, P.W.W. Kirk and 3.N. Lester. 1984. Determination of
chlorinated phenols 1n water, wastewater and wastewater sludge by capillary
GC/ECD. J. Chromat. Sc1. 22: 339-342.
Bursey, J.T. and E.O. Pelllzzarl. 1982. Analysis of Industrial Wastewater
for Organic Pollutants In Consent Degree Survey. U.S. EPA, Environ. Res.
Lab., Athens, GA. p. 79, 80.
Callahan, M.A., SLImak, M.W.. N.W. Gabel, et al. 1979. Water-Related
Environmental Fate of 129 Priority Pollutants - Volume II. U.S. EPA,
Washington, DC. EPA 440-79-029B.
Chambers, C.W., H.H. Tabak and P.W. Kabler. 1963. Degradation of aromatic
compounds by phenol-adapted bacteria. 3. Water Pollut. Control Fed. 35:
1517-1528.
0076d -26- 02/01/88
-------
Deltz, F. and J. Traud. 1978. Odor and taste threshold concentrations of
phenol bodies. Guf-wasser/abwasser. 119: 318. (Cited In U.S. EPA, I980b)
Elsenrelch, S.J., B.B. Looney and O.J. Thornton. 1981. Airborne organic
contaminants 1n the Great Lakes ecosystem. Environ. Scl. Techno!. 15:
30-38.
Gerslch, P.M. and M.A. Hayes. 1986. Acute toxlclty tests with Daphnla
magna and Plmephales promelas 1n support of national pollutant discharge
elimination permit requirements. Water Res. 29(7): 939-941.
Great Lakes Water Quality Board. 1983. An Inventory of Chemical Substances
Identified 1n the Great Lakes Ecosystem. Report, Volume 1 - Summary. Great
Lakes Water Quality Board, Windsor Ontario, Canada, p. 59.
Guy, W.H. and P.M. Jacob. 1341. Occupational dermatitis due to para-
chloro-meta-cresol. 3. Am. Med. Assoc. 116: 2258. (Cited In U.S. EPA,
1980b)
Hancock, B.W. and A. Naysmlth. 1975. HypersensHlvlty of chlorocresol
preserved heparln. Br. Med. 3. p. 746. (Cited In U.S. EPA, 1980b)
Hansch, C. and A.J. Leo. 1985. Hedchem Project. Issue No. 26. Pomona
College, Claremont, CA.
Hattula, M.L., V.H. Wasenlus, H. Reunanen and A.U. Arstlla. 1981. Acute
toxlclty of some chlorinated phenols catechols and cresols to trout. Bull.
Environ. Contam. Toxlcol. 27(3): 295-298.
0076d -27- 02/01/88
-------
Hawley, 6.G. 1981. The Condensed Chemical Dictionary, 10th ed. Van
Nostrand Relnhold Co., New York. p. 238.
Hudson-Baruth, B.A. and M.G. SeHz. 1986. Adsorption of Select Phenol
Derivatives by Dolomite. Environ. Pollut. Ser. B. 11(1): 15-28.
Jaber, H.M., W.R. Mabey, A.T. L1u, T.W. Chou and H.L. Johnson. 1984. Data
Acquisition for Environmental Transport and Fate Screening. SRI Inter-
national, p. 239. EPA 600/6-84-009. NTIS PB84-243906, PB84-243955.
James, R.H., R.E. Adams, J.H. Flnkel, H.C. Miller and L.D. Johnson. 1985.
Evaluation of analytical methods for the determination of POHC In combustion
products. J. Air Pollut. Control Assoc. 35(9): 959-961.
Johnson, L.O. and J.C. Young. 1983. Inhibition of anaerobic digestion by
organic priority pollutants. J. Water Pollut. Control Fed. 55: 1441-1449.
Kool, H.J., C.F. Van Kreljl and B.C.J. Zoeteman. 1982. Toxicology assess-
ment of organic compounds In drinking water. Cr1t. Rev. Env. Contr. 12:
345.
Lyman, U.J., W.F. Reehl and D.H. Rosenblatt. 1982. Handbook of Chemical
Property Estimation Methods. McGraw-Hill Book Co., New York. p. 5-4, 5-10,
15-16 to 15-29.
Mabey, W.R., J.H. Smith, R.T. Podoll, et al. 1981. Aquatic Fate Process
Data for Organic Priority Pollutants. U.S. EPA, Washington, DC. p. 273,
274. EPA 440/4-81-014.
0076d -28- 12/14/87
-------
Madsen C., P.M. Andersen, 0. Meyer and G. Wurtzen. 1986. 4-Chloro-3-
methylphenol: Salmonell a/mamma 11 an-ml crosome mutagenldty test and subacute
toxIcHy test 1n rats. Bull. Environ. Contam. Toxlcol. 37(5): 651-654.
Paull, 0. and G. Franke. 1971. Behavior and Degradation of Technical
Preservatives 1n the Biological Purification of Sewage. In: Proc. 2nd Symp.
Int. Blodeter. Mater, p. 52-60.
Robenek, H., R. Melss, J. Gehllng and H. Themann. 1980. Alterations In the
rat liver Induced by p-chloro-m-cresol with emphasis on the Intercellular
junctions: A thin-section and freeze-fracture study. 0. SubmTcrosc. Cytol.
12(4): 635-646.
SANSS (Structure and Nomenclature Search System). 1987. Chemical Informa-
tion System (CIS) computer data base. Online.
Shackelford, W.M. and L.H. Keith. 1976. Frequency of Organic Compounds
Identified 1n Water. U.S. EPA, Athens, GA. EPA 600-4-76-062. p. 194.
Tabak, H.H., C.W. Chambers and P.M. Kabler. 1964. Mlcroblal metabolism of
aromatic compounds. I. Decomposition of phenolic compounds and aromatic
hydrocarbons by phenol-adapted bacteria. J. BacteMol. 87-910-919.
Tabak, H.H.. S.A. Quave, C.I. Mashnl and E.F. Barth. 1981. B1odegradab1l-
Ity studies with organic priority pollutant compounds. J. Water Pollut.
Control Fed. 53: 1503-1518.
0076d -29- 12/14/87
-------
Tu, J., D. Chen, X. Shu and M. Heng. 1986. Organic pollutants In drinking
water wells within an area Irrigated with sewage water. Huanjlng Huaxue.
5: 60-74. (CA 106:22946x)
U.S. EPA. 1972. The effect of chlorlnatlon on selected organic chemicals.
Water Pollut. Control Res. Series 12020. (Cited In U.S. EPA, 1980b)
U.S. EPA. 1977. Computer print-out of non-confidential production data
from the TSCA Production File for 1977. U.S. EPA, Washington, DC.
U.S. EPA. 1980a. Guidelines and Methodology Used 1n the Preparation of
Health Effect Assessment Chapters of the Consent Decree Water Criteria
Documents. Federal Register. 45(31): 49347-49357.
U.S. EPA. 1980b. Ambient Water Quality Criteria Document for Chlorinated
Phenols. Prepared by the Office of Health and Environmental Assessment,
Environmental Criteria and Assessment Office, Cincinnati, OH for the Office
of Water Regulations and Standards, Washington, DC. EPA-440-5-80-032. NTIS
PB81-117434.
U.S. EPA. 1981. Treatablllty Manual - Volume 1. U.S. EPA, Washington, DC.
EPA 600/2-82-OOla. p. 1.8.12-1 to 1.8.12-4.
0076d -30- 02/01/88
-------
U.S. EPA. 1984. Methodology and Guidelines for Reportable Quantity
Determination 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.
U.S. EPA. 1985a. Notification requirements; reportable quantity adjust-
ments; final rule and proposed rule. 40 CFR Parts 117 and 302. Federal
Register. 50(65): 13456-13522.
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 Waste, Washington,
DC.
U.S. EPA. 1986a. Methodology for Evaluating Carc1nogen1c1ty 1n Support of
Reportable Quantity Adjustment. 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. The Verification of the Production of 41 Chemicals. Test
Rules Dev. Branch, Existing Chem. Assess. D1v., OTS, U.S. EPA, Washington,
DC. p. 1, 2, 4.
U.S. EPA. 1986c. Guidelines for Carcinogen Risk Assessment. Federal
Register. 51(185): 33992-34003.
0076d -31- 02/01/88
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U.S. EPA. 1987. Graphical Exposure Modeling System (GEMS). Fate of Atmo-
spheric Pollutants (FAP) computer data systems. PCGEMS Version April 1987.
U.S. EPA, Research Triangle Park, NC.
USITC (U.S. International Trade Commission). 1982. Imports of Benzenold
Chemicals and Products 1981. USITC Publ. 1272, Washington, DC, p. 13.
USITC (U.S. International Trade Commission. 1983. Imports of Benzenold
Chemicals and Products 1982. USITC Publ. 1401, Washington, DC. p. 12.
USITC (U.S. International Trade Commission. 1984. Imports of Benzenold
Chemicals and Products 1983. USITC Publ. 1548, Washington, DC. p. 13.
Voets, 3.P., P. P1pyn, P. Van Lancker and W. Verstraete. 1976. Degradation
of mlcroblcldes under different environmental conditions. 0. Appl.
Bacterlol. 40(1): 67-72.
Weast, R.C., Ed. 1985. CRC Handbook of Chemistry and Physics, 66th ed.
CRC Press, Boca Raton, FL. p. C-219.
W1en, R. 1939. The toxlclty of parachlorometacresol and of phenylmercurlc
nitrate. Quart. J. Yearbook Pharm. 12: 212.
Wlndholz, M., Ed. 1983. The Merck Index, 10th ed. Merck and Co., Rahway,
NJ. p. 299.
0076d -32- 02/01/88
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Zondeck, 8. and 8. Shapiro. 1943. Fate of halogenated phenols In the
organism. Blochem. J. 37: 592-595.
Zullel, N. 1981. Behavior of disinfectants (chlorophenols) during under-
ground passage. Sc1. Total Environ. 21: 215-220.
0076d -33- 02/01/88
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• APPENDIX A
LITERATURE SEARCHED
This HEED 1s based on data Identified by computerized literature
searches of the following:
CHEHLINE
TSCATS
CASR online (U.S. EPA Chemical Activities Status Report)
TOXLINE
TOXLIT
TOXLIT 65
RTECS
OHM TADS
STORET
SRC Environmental Fate Data Bases
SANSS
AQUIRE
TSCAPP
NTIS
Federal Register
CAS ONLINE (Chemistry and Aquatic)
HSDB
These searches were conducted 1n October 1987. and the following secondary
sources were reviewed:
ACGIH (American Conference of Governmental Industrial Hyg1en1sts).
1986. Documentation of the Threshold Limit Values and Biological
Exposure Indices, 5th ed. Cincinnati, OH.
ACGIH (American Conference of Governmental Industrial Hyg1en1sts).
1987. TLVs: Threshold Limit Values for Chemical Substances 1n the
Work Environment adopted by ACGIH with Intended Changes for
1987-1988. Cincinnati, OH. 114 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 WHey and
Sons, NY. p. 3817-5112.
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Grayson, N. 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. IARC, WHO, Lyons, France.
Jaber, H.M., W.R. Mabey, A.T. Lieu, 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.
EPA 600/6-84-010. NTIS PB84-243906. SRI International, Menlo
Park, CA.
NTP (National Toxicology Program). 1987. 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). 1987. Directory of Chemical
Producers. Menlo Park, CA.
U.S. EPA. 1986. Report on Status Report 1n the Special Review
Program, Registration Standards Program and the Data Call 1n
Programs. Registration Standards and the Data Call 1n Programs.
Office of Pesticide Programs, Washington, DC.
USITC (U.S. International Trade Commission). 1986. Synthetic
Organic Chemicals. U.S. Production and Sales, 1985, USITC Publ.
1892, Washington, DC.
Verschueren, K. 1983. Handbook of Environmental Data on Organic
Chemicals. 2nd ed. Van Nostrand Relnhold Co., NY.
Worthing, C.R. and S.B. Walker, Ed. 1983. The Pesticide Manual.
British Crop Protection Council. 695 p.
Wlndholz, M., Ed. 1983. The Merck Index, 10th ed. Merck and Co.,
Inc., Rahway, NJ.
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In addition, approximately 30 compendia of aquatic toxlclty 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 Toxlclty
of Chemicals to F1sh and Aquatic Invertebrates. Summaries of
Toxlclty Tests Conducted at Columbia National Fisheries Research
Laboratory. 1965-1978. U.S. Dept. Interior, F1sh and Wildlife
Serv. Res. Publ. 137, Washington, DC.
McKee. O.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
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.
U.S. environmental Protection Agenqr
Region 5, Library (PU-12J)
77 West Jackson Boulevard, IZUi
Ch»c»go, It 60604-3S90
0076d -36- 02/01/88
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