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DISCLAIMER
This report Is an external draft for review purposes only and does not
constitute Agency policy. Mention of trade names or commercial products
does not constitute endorsement or recommendation for use.
11
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PREFACE
Health and Environmental Effects Documents (HEEDs) are prepared for the
Office of Solid Waste and Emergency Response (OSHER). This document series
Is Intended to support listings under the Resource Conservation and Recovery
Act (RCRA) as well as to provide health-related limits and goals for emer-
gency and remedial actions under the Comprehensive Environmental Response,
Compensation and Liability Act (CERCLA). Both published literature and
Information obtained from Agency Program Office files are evaluated as they
pertain to potential human health, aquatic life and environmental effects of
hazardous waste constituents. The literature searched for 1n this document
and the dates searched are Included 1n "Appendix: Literature Searched."
Literature search material 1s current up to 8 months previous to the final
draft date listed on the front cover. Final draft document dates (front
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 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, for example, one that does
not constitute a significant portion of the llfespan. This type of exposure
estimate has not been extensively used, or rigorously defined as previous
risk assessment efforts have focused primarily on lifetime exposure
scenarios. Animal data used for subchronlc estimates generally reflect
exposure durations of 30-90 days. The general methodology for estimating
subchronlc RfDs 1s the same as traditionally employed for chronic estimates,
except that subchronlc data are utilized when available.
In the case of suspected carcinogens, RfDs are not estimated. A
carcinogenic potency factor, or q-j* (U.S. EPA, 1980), Is provided Instead.
These potency estimates are derived for both oral and Inhalation exposures
where possible. In addition, unit risk estimates for air and drinking water
are presented based on Inhalation and oral data, respectively.
Reportable quantities (RQs) based on both chronic toxldty and cardno-
genlclty are derived. The RQ 1s used to determine the quantity of a hazar-
dous substance for which notification Is required In the event of a release
as specified under the CERCLA. These two RQs (chronic toxldty and carclno-
genlclty) represent two of six scores developed (the remaining four reflect
1gn1tab1l1ty, reactivity, aquatic toxldty, and acute mammalian toxldty).
Chemical-specific RQs reflect the lowest of these six primary criteria. The
methodology for chronic toxldty and cancer-based RQs are defined 1n U.S.
EPA, 1984 and 1986a, respectively.
111
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EXECUTIVE SUMMARY
p-Chlorobenzo1c add (74-11-3) 1s a crystalline solid at room tempera-
ture (Hlndholz, 1983). It Is soluble In ethanol and ethyl ether but Is
sparingly soluble 1n water (Hlndholz, 1983; Perry and Green, 1984). It may
undergo reactions Involving the aromatic nucleus or the chlorine substHu-
ent, as well as reactions typical of the carboxyl group (Mu1r, 1963). This
compound may be prepared by the oxidation of p-chlorotoluene (Gelfand, 1979;
Mu1r, 1963). The 1987 OPD Chemical Buyers Directory lists eight suppliers
of p-chlorobenzolc add; however, The Directory of Chemical Producers (SRI,
1986) and recent U.S. International Trade Commission publications on
chemical production and sales (USITC, 1985, 1986) contain no production data
for this compound. The limited amount of production data on p-chlorobenzo1c
add suggests that this compound may be Imported or produced on a specialty
chemical basis 1n the United States. p-Chlorobenzolc acid has been used 1n
plastldzers, as a dye carrier, and as a fungicide and dye Intermediate; Us
esters have potential for use as Insecticides and plant growth regulators
(Williams, 1978).
p-Chlorobenzolc add 1s an acidic compound that Is expected to Ionize
significantly under environmental conditions (pH 5-9) and to form salts that
are much more water soluble than the parent compound. Variations 1n the
behavior of p-chlorobenzolc add may result from 1on1zat1on. Because of the
lack of pertinent data, the fate of this compound In the atmosphere cannot
be predicted. Data by Korte and Klein (1982) Indicate that direct photoly-
sis may not be a dominant removal mechanism In the atmosphere. p-Chloroben-
zolc vapor reacting with photochemlcally generated hydroxyl radicals In the
atmosphere has an estimated half-life of ~7 days (U.S. EPA, 1987). This
1v
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compound Is not expected to react significantly with atmospheric ozone (U.S.
EPA, 1987). If released to water, blodegradatlon of p-chlorobenzo1c acid
under aerobic conditions Is expected to be the dominant fate process.
Screening studies suggest that the aerobic blodegradatlon half-life of this
compound In natural water systems should range from 2 weeks to <1 month
(Horvath, 1973; Haller, 1978; D1Geron1mo et al., 1979; Freltag et al.,
1985). 4-D1hydroxybenzoate, procatechuate and ds-d1hydrod1ol have been
Identified as products of p-chlorobenzolc acid metabolism (Harks et al.,
1984; Karasevlch and Zaltsev, 1984; Gibson, 1977). Chemical hydrolysis,
reaction with photochemlcally generated hydroxyl radicals In water (t,/?
of 1.1 years) (Anbar et al., 1966; Mill et al., 1980), photolysis (Crosby
and Le1t1s, 1969), bloconcentratlon In aquatic organisms (Freltag et al.,
1985), adsorption to suspended solids and sediments, volatilization and
anaerobic blodegradatlon (Gibson and Sufllta, 1986; Horowitz et al., 1962)
are not expected to be significant fate processes. If released to soil,
aerobic blodegradatlon may be an Important fate process. Results of one
blodegradatlon screening study Indicated that p-chlorobenzo1c add at an
Initial concentration of 25 mg/a was completely degraded by a soil
Inoculum 1n 64 days (Alexander and Lustlgman, 1966). p-Chlorobenzo1c acid
has the potential to leach Into groundwater; mobility may Increase with
Increasing pH because of greater 1on1zat1on. Volatilization from moist soil
surfaces Is not expected to be significant. p-Chlorobenzo1c acid Is pre-
dicted to be resistant to blodegradatlon In soil under anaerobic conditions.
p-Chlorobenzo1c add has been positively Identified 1n drinking water
samples from Poplarvllle, MS, and Cincinnati, OH, and tentatively Identified
In drinking water samples from New Orleans, LA, and Philadelphia, PA (Lucas,
1984). The occurrence of p-chlorobenzo1c add 1n drinking water and waste-
water samples may be the result of chlorlnatlon of humlc and fulvlc adds.
-------
Qulmby et al. (1980) have tentatively Identified this compound as a
chlorlnatlon product of humlc and fulvlc adds In aqueous solution.
Monitoring data regarding exposure to p-chlorobenzolc add by Inhalation,
dermal contact or Ingestlon of food could not be located In the available
literature as cited In Appendix A.
Information regarding the toxldty of p-chlorobenzolc add to aquatic
organisms was limited. Trabalka and Burch (1978) reported that no mortality
occurred In Daphnla pulex exposed to p-chlorobenzolc add at concentrations
of <100 mg/i for 96 hours under static conditions. Caslda (1955) reported
an LC5Q of 8.7 mM (1362 mg/l) for mosquito, Aedes aeqyptll. larvae
exposed for an unspecified period.
The only pharmacoklnetlc study of p-chlorobenzolc add showed that
nearly all the radioactivity of a 50 mg dose of neutralized labeled
p-chlorobenzolc acid was recovered In the urine within 24 hours (Lang and
Lang, 1956) Small amounts of radioactivity were recovered 1n the feces and
Insignificant levels remained In the tissues. Kleckebusch et al. (1960)
state that the main metabolite of p-chlorobenzolc acid Is p-chloroh1ppur1c
acid.
Rats fed p-chlorobenzolc add 1n the diet at 0.1 or 0.2% did not develop
toxic effects, and no differences 1n the number of litters or the develop-
ment of the young were noted (Kleckebusch et al., 1960). D'eng et al.
(1983) observed that a single oral LD5Q dose produced a transient stimula-
tion of protein synthesis whereas dally dosing with 1/10 LD5Q and 1/50
LDcQ resulted In Inhibition of protein synthesis 1n the liver of rats.
Kaulla (1962) reported that p-chlorobenzolc add has in vitro flbrlnolytlc
activity. The rat Intraperltoneal L05Q for p-chlorobenzolc acid 1s 100
mg/kg (NIOSH, 1986).
v.1
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Pertinent data regarding the cardnogenlcHy, mutagenldty, teratogen-
IcUy and toxldty of p-chlorobenzolc add following subchronlc and chronic
Inhalation exposure and chronic oral exposure could not be located In the
available literature as cited tn Appendix A.
A subchronlc RfD for oral exposure of 121 mg/day was derived from the
NOAEL of 0.2% of the diet (173 mg/kg/day) 1n the 5-month rat dietary study
by application of an uncertainty factor of 100 {Kleckebusch et al., 1960).
An RfO of 12 mg/day for chronic oral exposure was derived by application of
an additional uncertainty factor of 10. Confidence 1n the chronic RfD 1s
very low. The RfD 1s based on a freestanding NOAEL found 1n a subchronlc
oral study (Kleckebusch et al., I960), and no supporting studies are
available. Data were Insufficient for derivation of RfDs for Inhalation
exposure or for derivation of a tox1c1ty-based RQ. p-Chlorobenzolc add was
assigned to EPA Group D. Data were Insufficient for quantitative estimation
of cancer potency or hazard ranking based on cardnogenlclty.
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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 2
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. Photolysis 5
2.2. WATER 5
2.2.1. Hydrolysis 5
2.2.2. Oxidation 5
2.2.3. Photolysis 5
2.2.4. M1crob1al Degradation 5
2.2.5. B1oconcentrat1on 7
2.2.6. Adsorption 7
2.2.7. Volatilization 7
2.3. SOIL . . 7
2.3.1. M1crob1al Degradation 7
2.3.2. Leaching 8
2.3.3. Volatilization 9
2.4. SUMMARY 9
3. EXPOSURE 11
3.1. WATER •. 11
3.2. SUMMARY 11
4. AQUATIC TOXICITY 13
4.1. ACUTE TOXICITY 13
4.2. CHRONIC EFFECTS 13
4.3. PLANT EFFECTS 13
4.4. SUMMARY 13
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TABLE OF CONTENTS (cont.)
Page
5. PHARMACOKINETCS 14
5.1. ABSORPTION 14
5.2. DISTRIBUTION . . 14
5.3. METABOLISM 14
5.4. EXCRETION 14
5.5. SUMMARY 14
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 16
6.3. MUTAGENICITY 16
6.4. TERATOGENICITY 16
6.5. OTHER REPRODUCTIVE EFFECTS 16
6.6. SUMMARY 16
7. EXISTING GUIDELINES AND STANDARDS 18
7.1. HUMAN 18
7.2. AQUATIC 18
8. RISK ASSLSSMENT 19
8.1. CARCINOGENICITY . 19
8.1.1. Height of Evidence 19
8.1.2. Quantitative Risk Estimates 19
8.2. SYSTEMIC TOXICITY 19
8.2.1. Inhalation Exposure 19
8.2.2. Oral Exposure 19
9. REPORTABLE QUANTITIES 21
9.1. BASED ON SYSTEMIC TOXICITY 21
9.2. BASED ON CARCINOGENICITY 21
10. REFERENCES 23
APPENDIX A: LITERATURE SEARCHED 30
APPENDIX B: SUMMARY TABLE FOR p-CHLOROBENZOIC ACID 33
1x
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LIST OF ABBREVIATIONS
BCF Bloconcentratlon factor
Koc Soil sorptlon coefficient standardized
with respect to organic carbon
Kow Octanol/water partition coefficient
LC5Q Concentration lethal to 50% of recipients
(and all other subscripted dose levels)
1059 Dose lethal to 50% of recipients
NOAEL No-observed-adverse-effect level
RfD Reference dose
RQ Reportable quantity
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1. INTRODUCTION
1.1. STRUCTURE AND CAS NUNBER
p-Chlorobenzo1c acid 1s also known as 4-chlorobenzo1c add, chloro-
dracyllc add and p-carboxychlorobenzene (NIOSH, 1987). The structure,
molecular weight, empirical formula and CAS Registry number are as follows:
Q
-OH
Molecular weight: 156.57
Empirical formula: C7H.C102
CAS Registry number: 74-11-3
1.2. PHYSICAL AND CHEMICAL PROPERTIES
p-Chlorobenzo1c add 1s a crystalline solid at room temperature
(Wlndholz, 1983). This compound may undergo reactions Involving the
aromatic nucleus or the chlorine substHuent, as well as reactions typical
of the carboxyl group (Mu1r, 1963). It 1s freely soluble In ethanol and
ethyl ether (Hlndholz, 1983). Relevant physical properties are as follows:
Melting point (°C): 243 Mulr. 1963
Boiling point (°C): sublimes Mu1r, 1963
Vapor pressure: not available
Water solubility (25°C): 80 mg/l Perry and Green, 1984
Log Kow: 2.65 Hansch and Leo, 1985
pKa (25°C): 3.98 Mulr, 1963
Specific gravity: 1.541 (24/4) MuU. 1963
0070d -1- 09/09/87
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1.3. PRODUCTION DATA
p-Chlorobenzok add Is prepared by the oxidation of p-chlorotoluene
(Gelfand, 1979; Mu1r, 1963). The public portion of the U.S. EPA TSCA
Production File (U.S. EPA, 1977) reports that one company manufactured
p-chlorobenzo1c add 1n 1977 In the United States; however, the Identity of
the company and Us production volume are confidential. U.S. EPA (1977)
Indicated that Tenneco Chemicals Inc. and Riches-Nelson Inc. Imported/manu-
factured this compound before 1977. The 1987 OPD Chemical Buyers Direc-
tory (Van, 1986) lists AldMch Chemical Co., Chugal International, Conray
Chemicals, Maypro Industries, M1k1 Sangyo (USA), Mobay Corp., Niagara
Technology and Wall Chemical Corp. as current suppliers of this compound.
The Directory of Chemical Producers (SRI, 1986) and recent U.S. Inter-
national Trade Commission publications on chemical production and sales
(USITC, 1985, 1986) contain no production data for p-chlorobenzolc add.
The lack of data regarding current domestic production of this compound
suggest that 1t may be Imported or produced on a specialty chemical basis In
the United States.
1.4. USE DATA
p-Chlorobenzo1c add has been used In plastldzers, as a dye carrier,
and as a fungicide and dye Intermediate (Williams, 1978). Its esters have
potential for use as Insecticides and plant growth regulators (Williams,
1978).
1.5. SUMMARY
p-Chlorobenzo1c add (74-11-3) 1s a crystalline solid at room tempera-
ture (Wlndholz, 1983). It 1s soluble In ethanol and ethyl ether but Is
sparingly soluble In water (Wlndholz, 1983; Perry and Green, 1984). It may
0070d -2- 09/09/87
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undergo reactions Involving the aromatic nucleus or the chlorine substltu-
ent, as well as reactions typical of the carboxyl group (Mu1r, 1963). This
compound may be prepared by the oxidation of p-chlorotoluene (Gelfand, 1979;
Mulr, 1963). The 1987 OPD Chemical Buyers Directory lists eight suppliers
of p-chlorobenzolc add; however, The Directory of Chemical Producers (SRI,
1986) and recent U.S. International Trade Commission publications on
chemical production and sales (USITC. 1985, 1986) contain no production data
for this compound. The limited amount of production data on p-chlorobenzolc
acid suggest that this compound may be Imported or produced on a specialty
chemical basis In the United States. p-Chlorobenzolc acid has been used In
plast1c1zers, as a dye carrier, and as a fungicide and dye Intermediate; Us
esters have potential for use as Insecticides and plant growth regulators
(U1ll1ams, 1978).
0070d -3- 09/09/87
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2. ENVIRONMENTAL FATE AND TRANSPORT
Limited data pertaining to the environmental fate and transport of
p-chlorobenzo1c add could be located 1n the available literature as cited
In Appendix A. When possible, Information concerning the fate and transport
of this compound was derived from Its physical properties or Its molecular
structure.
Based on a pKa of 3.98 (Mu1r, 1963), p-chlorobenzolc acid 1s expected to
Ionize significantly under environmental conditions (pH 5-9) and to form
salts, that are much more water soluble than the parent compound.
Ion1zat1on can alter the behavior of a compound 1n water or soil (e.g., by
decreasing volatilization or by Increasing or decreasing adsorption to soil,
sediments or suspended solids 1n water).
2.1. AIR
2.1.1. Reaction with Hydroxyl Radicals. The estimated half-life for
p-ch1orobenzo1c add vapor reacting with photochemlcally generated hydroryl
radicals In the atmosphere Is -1 days, using an estimated reaction rate
constant of 1.5xlO~12 cm3/molecule-sec at 25°C and an average hydroxyl
radical concentration of 8.0x10* molecules/cm3 1n a typical atmosphere
(U.S. EPA, 1987). This reaction rate, however, will be different If
p-chlorobenzolc add Is present In partlculate phase In the atmosphere. The
physical state of a compound (solid, vapor, etc.) 1n the atmosphere can be
predicted from Us equilibrium vapor pressure (E1senre1ch et al., 1981).
Since the vapor pressure value for p-chlorobenzolc acid Is not known, Us
physical state 1n the atmosphere cannot be predicted.
2.1.2. Reaction with Ozone. p-Chlorobenzo1c add 1s not susceptible to
oxidation by ozone 1n the atmosphere (U.S. EPA, 1987).
0070d -4- 09/09/87
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2.1.3. Photolysis. When Irradiated with light from a photoreactor at
wavelengths >290 nm for 17 hours (Korte and Klein, 1982), 50 ppb [14C]-p-
chlorobenzolc add adsorbed onto silica gel underwent 6.3X photomlnerallza-
tlon. Korte and Klein (1982) were attempting to relate photomlnerallzatlon
to atmospheric degradation. Their results, however, Indicate that direct
photolysis will not be a dominant removal mechanism 1n the atmosphere.
2.2. WATER
2.2.1. Hydrolysis. Halogenated aromatic compounds and carboxyllc acids
are generally resistant to hydrolysis under environmental conditions (Lyman
et al., 1982). Therefore, p-chlorobenzolc add 1s not expected to be
susceptible to chemical hydrolysis.
2.2.2. Oxidation. The estimated half-life for the reaction of p-chloro-
benzolc add with photochemical 1y generated hydroxyl radicals In water Is
-1.1 years using an experimentally determined reaction rate constant of
1.92x10* l/mol-sec (Anbar et al., 1966) and an ambient hydroxyl radical
concentration of lxlO~17 mol/l (Mill et al., 1980). Experimental data
concerning the reaction of p-chlorobenzolc acid with alkylperoxy radicals or
singlet oxygen were not available.
2.2.3. Photolysis. p-Chlorobenzolc acid appeared to be unaffected when
an aqueous solution of Us sodium salt was Irradiated with outdoor sunlight
1n a period of <14 days (Crosby and Le1t1s, 1969).
2.2.4. Nlcroblal Degradation. When 47 and 0.47 mg/l radlolabeled
p-chlorobenzolc acid (ring U-14C) was Incubated In stream water samples at
29°C for 12 days, the loss of Initial 14C as 14C02 was found to be 5.9
and 79%, respectively (Boethllng and Alexander, 1979). No measurable loss
of 14C was observed when 4.7xlO~3 mg/l p-chlorobenzolc add was
Incubated 1n autoclaved samples of stream water for 2 days (Boethllng and
0070d -5- 06/25/87
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Alexander, 1979). It was concluded from this Investigation that blodegrada-
tlon occurs more readily at low concentrations of substrate. Results of
blodegradatlon screening studies using activated sludge as Inoculum Indicate
that this compound Is likely 'to blodegrade under aerobic conditions by mixed
mlcroblal populations found 1n natural water systems (Horvath, 1973; Mailer,
1978; D1Geron1mo et al., 1979; Freltag et al., 1985). It appears that the
rate of blodegradatlon may be enhanced by mlcroblal adaptation or by the
presence of a co-substrate (Thorn and Agg, 1975; Mailer, 1978; Horvath,
1973). For example, 25 mg/i p-chlorobenzoate Incubated with an activated
sludge Inoculum was decomposed after an Initial 4-day lag period and was 50%
degraded after 24 days (Horvath, 1973). In the presence of a co-substrate
(glucose), the lag period was essentially eliminated; 50% degradation
occurred In 12 days and 100% degradation took place 1n 28 days (Horvath,
1973). Hetabollsm of p-chlorobenzo1c add by an Isolated culture of Alcall-
genes eutrophus under aerobic conditions resulted In the formation of c1s-
dlhydrodlol (Gibson, 1977). Further degradation of dlhydrodlols has been
found to Involve dehydration to ortho-dlhydroxy derivatives (catechols)
before ring cleavage (Gibson, 1977). Other mlcroblal Isolates have been
found to metabolize p-chlorobenzoate by Initial dehalogenatlon to p-hydroxy-
benzoate followed by further degradation to protocatechuate (Marks et al.,
1984; Karasevlch and ZaHsev, 1984).
When p-chlorobenzo1c acid was Incubated under anaerobic conditions with
digester sludge, anoxlc pond sediment, mlcroflora from a methogenlc aquifer
and mlcroflora from a sulfate-redudng aquifer, loss of Initial substrate
was 17, 6, 14 and 11%, respectively, after 3 months (Gibson and SufUta,
1986). This loss, however, was not attributed to blodegradatlon since
substrate disappearance did not exceed loss observed In sterile controls.
0070d -6- 09/09/87
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No mineralization was observed when this compound was Incubated under
anaerobic conditions for 65 weeks In an aqueous solution Inoculated with
anoxlc sediment taken from a hypoeutrophlc lake (Horowitz et al., 1982).
Likewise, no mineralization was observed when this compound was Incubated
for 8 weeks In aqueous solution amended with sludge taken from an anaerobic
digester (Horowitz et al., 1982).
2.2.5. B1oconcentrat1on. The BCF of p-chlorobenzo1c add was determined
to be 63 1n green alga, Chlorella fusca. and 3.4 1n the golden orfe,
Leuclscus Idus melanotus (FreHag et al., 1985). These BCF values suggest
that bloconcentratlon of p-chlorobenzolc add In aquatic organisms would not
be significant.
2.2.6. Adsorption. Based on the low K values (Section 2.3.2.),
p-chlorobenzolc add Is not expected to adsorb significantly to sediments or
suspended sol Ids In water.
2.2.7. Volatilization. Volatilization from water surfaces 1s not
expected to be significant because p-chlorobenzolc add Is present
predominantly In the 1on1c state under most environmental conditions.
2.3. SOIL
2.3.1. M1crob1al Degradation. The degradation period for a 25 rug/a.
p-chlorobenzolc add Inoculated with a mixed culture of microorganisms
obtained from soil was found to be 64 days (Alexander and Lustlgman, 1966).
No significant loss In p-chlorobenzolc add, at an Initial concentration of
16 mg/i, was observed after 25 days Incubation with a soil Inoculum
(Haller, 1978). Microorganisms Isolated from soil samples taken from a
landfill site (previously used to dispose of chlorinated organlcs) showed
growth when Incubated with p-chlorobenzolc acid for 72 hours at 25°C, which
was attributed to the presence of plasmlds In the Isolated cells that were
0070d -7- 09/09/87
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capable of transferring the trait to nonadopted cells (Vandenbergh et al.,
1981). These results suggest that p-chlorobenzolc add will blodegrade In
son after a lag period. Data pertaining to the blodegradatlon of p-chloro-
benzolc acid 1n aqueous media suggest that aerobic blodegradatlon may be an
Important fate process 1n soil as well. Cells of one Pseudomonas sp. and
one Bacillus sp. Isolated from soil and grown on benzoate were found to
cooxldlze p-chlorobenzoate, but other microorganisms Isolated from soil and
grown on benzoate (two Pseudomonas sp., three Nocardla sp. and one Achromo-
bacter sp.) did not cooxldlze p-chlorobenzoate (Spokes and Walker, 1974). A
Nocardla sp. Isolated from soil metabolized p-chlorobenzolc add to
p-hydroxybenzo1c add (Klages and Llngens, 1979). Based on available data
pertaining to the anaerobic blodegradatlon of p-chlorobenzolc add In
aqueous media, this compound Is expected to resist blodegradatlon In soil
under anaerobic conditions.
2.3.2. Leaching. A K of 390-660 has been estimated for p-chloro-
benzolc add using a water solubility of 80 mg/l at 25°C (Perry and Green,
1984) and the following linear regression equation (Lyman et al., 1982):
log KQC = -0.55 log S * 3.64 (2-1)
This K value suggests that p-chlorobenzolc add would be moderately
mobile In soil (Swann et al., 1983); however, 1on1zat1on can have a signifi-
cant effect on the behavior of this compound 1n soil. In general, neutral
species of a compound adsorb much more strongly than Us Ionic species when
the sorptlon mechanisms depend on organic carbon content of soil (Lyman et
al., 1982). Based on a pKa of 3.98 (Mu1r, 1963), the ratio of Ionized to
unionized p-chlorobenzolc add In natural waters with relatively low Ionic
strength has been estimated to be 10:1 at pH 5, 105:1 at pH 6, 1050:1 at pH
7 and so forth. This Information suggests that p-chlorobenzolc add may
0070d -8- 06/25/87
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have a greater tendency to leach through soil than would be predicted from
Us K value and that the mobility of this compound would Increase with
Increasing pH 1f such sorptlve mechanisms are operative.
2.3.3. Volatilization. Volatilization from moist soil surfaces Is not
expected to be significant because p-chlorobenzo1c add 1s Ionized under
environmental conditions.
2.4. SUMMARY
p-Chlorobenzolc add Is an acidic compound that Is expected to Ionize
significantly under environmental conditions (pH 5-9) and form salts that
are much more water soluble than the parent compound. Variations In the
behavior of p-chlorobenzo1c add may result from 1on1zat1on. Lack of
pertinent data precludes determination of the fate of this compound In the
atmosphere. Data by Korte and Klein (1982) Indicate that direct photolysis
may not be a dominant removal mechanism In the atmosphere. p-Chlorobenzolc
vapor reacting with photochemically-generated hydroxyl radicals 1n the
atmosphere has an estimated half-life of -7 days (U.S. EPA, 1987},. This
compound Is not expected to react significantly with atmospheric ozone (U.S.
EPA, 1987). If released to water, blodegradatlon of p-chlorobenzolc add
under aerobic conditions 1s expected to be the dominant fate process.
Screening studies suggest that the aerobic blodegradatlon half-life of this
compound In natural water systems should range from 2 weeks to <1 month
(Horvath, 1973; Haller, 1978; 01Geron1mo et al., 1979; Freltag et al.,
1985). 4-D1hydroxybenzoate, procatechuate and ds-d1hydrod1ol have been
Identified as products of p-chlorobenzo1c add metabolism (Marks et al.,
1984; Karasevlch and Zaltsev, 1984; Gibson, 1977). Chemical hydrolysis,
reaction with photochemlcally generated hydroxyl radicals 1n water (t,,~
of 1.1 years) (Anbar et al., 1966; Mill et al., 1980), photolysis (Crosby
0070d -9- 09/09/87
-------
and LeIUs, 1969), bloconcentratlon In aquatic organisms (Freltag et al.,
1985), adsorption to suspended solids and sediments, volatilization and
anaerobic blodegradatlon (Gibson and SuflHa, 1986; Horowitz et al., 1982)
are not expected to be significant fate processes. If released to soil,
aerobic blodegradatlon may be an Important fate process. Results of one
blodegradatlon screening study Indicate that p-chlorobenzo1c add at an
Initial concentration of 25 mg/i was completely degraded by a soil
Inoculum 1n 64 days (Alexander and Lustlgman, 1966). p-Chlorobenzolc add
has the potential to leach Into groundwater; mobility may Increase with
Increasing pH because of greater lonlzatlon. Volatilization from moist soil
surfaces Is not expected to be significant. p-Chlorobenzo1c add Is
predicted to be resistant to blodegradatlon In soil under anaerobic
conditions.
0070d -10- 09/11/87
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3. EXPOSURE
Pertinent monitoring data regarding exposure to 4-chlorobenzolc add by
Inhalation, dermal contact or Ingestlon of food could not be located In the
available literature as cited In Appendix A.
3.1. WATER
p-Chlorobenzolc add has been positively Identified 1n drinking water
obtained from Poplarvllle, MS, during 1979 and Cincinnati, OH, during 1978,
and It has been tentatively Identified 1n drinking water obtained from New
Orleans, LA, and Philadelphia, PA, during during 1976 (Lucas, 1984).
p-Chlorobenzo1c add has been positively Identified In samples of advanced
waste treatment water taken from facilities 1n Lake Tahoe during 1974,
Pomona, CA, during 1975, Escondldo, CA, during 1975 and Dallas, TX, during
1974 (Lucas, 1984). The occurrence of p-chlorobenzo1c acid In drinking
water and wastewater samples may be the result of chloMnatlon of humlc and
fulvlc adds. Qulmby et al. (1980) have tentatively Identified this
compound as a chlorlnatlon product of humlc and fulvlc acids In aqueous
solution.
3.2. SUMMARY
p-Chlorobenzo1c add has been positively Identified 1n drinking water
samples from Poplarvllle, MS, and Cincinnati, OH, and tentatively Identified
In drinking water samples from New Orleans, LA. and Philadelphia, PA (Lucas,
1984). The occurrence of p-chlorobenzo1c acid In drinking water and waste-
water samples may be the result of chlorlnatlon of humlc and fulvlc adds.
Qulmby et al. (1980) have tentatively Identified this compound as a
chlorlnatlon product of humlc and fulvlc adds In aqueous solution.
0070d -11- 09/09/87
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Monitoring data regarding exposure to p-chlorobenzo1c add by Inhalation,
dermal contact or Ingestlon of food could not be located In the available
literature as cited 1n Appendix A.
0070d -12- 09/09/87
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4. AQUATIC TOXICITY
4.1. ACUTE TOXICITY
Information regarding the toxlclty of p-chlorobenzo1c add to aquatic
organisms was limited. Trabalka and Burch (1978) reported that no mortality
occurred In Daphnla pulex exposed to p-chlorobenzo1c acid at concentrations
of <100 mg/i for 96 hours under static conditions. Caslda (1955) reported
an LC50 of 8.7 mM (1362 mg/i) for mosquito, Aedes aeqyptll. larvae
exposed for an unspecified period.
4.2. CHRONIC EFFECTS
Pertinent data regarding chronic toxlclty of p-chlorobenzo1c add to
aquatic organisms could not be located 1n the available literature as cited
In Appendix A.
4.3. PLANT EFFECTS
Pertinent data regarding effects of p-chlorobenzolc add on aquatic
plants could not be located In the available literature as cited In
Appendix A.
4.4. SUMMARY
Information regarding the toxlclty of p-chlorobenzo1c add to aquatic
organisms was limited. Trabalka and Burch (1978) reported that no mortality
occurred In Daphnla pulex exposed to p-chlorobenzo1c add at concentrations
<100 mg/l for 96 hours under static conditions. Caslda (1955) reported an
LC_n of 8.7 mM (1362 mg/l) for mosquito, Aedes aeqyptll. larvae exposed
for an unspecified period.
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5. PHARMACOKINETICS
5.1. ABSORPTION
Pertinent data regarding the absorption of p-chlorobenzo1c acid could
not be located 1n the available literature as cited In Appendix A.
5.2. DISTRIBUTION
Lang and Lang (1956) found Insignificant levels of radioactivity In the
organs of rats 1-23 days after they were given 1ntraper1toneal Injections of
50 mg [carboxy-14C]p-chlorobenzo1c acid that had been neutralized with
NaOH. The abstract from which these data were taken stated that there was
no storage In the body.
5.3. METABOLISM
Kleckebusch et al. (1960) reported that p-chlorobenzolc acid Is metabo-
lized In a manner similar to benzole add, with p-chloroh1ppur1c acid as the
major metabolite.
5.4. EXCRETION
Nearly all of the radioactivity of a 50 mg dose of neutralized [14C]p-
chlorobenzolc add administered to rats by 1ntraper1toneal Injection was
recovered 1n the urine within 24 hours (Lang and Lang, 1956). Small amounts
of radioactivity were also recovered In the feces.
5.5. SUMMARY
The only pharmacoklnetlc study of p-chlorobenzo1c add showed that
nearly all the radioactivity of a 50 mg l.p. dose of neutralized labeled
p-chlorobenzolc add was recovered 1n the urine within 24 hours (Lang and
Lang, 1956) Small amounts of radioactivity were recovered In the feces and
Insignificant levels remained In the tissues. Kleckebusch et al. (1960)
state that the main metabolite of p-chlorobenzolc acid 1s p-chlorohlppurlc
acid.
0070d -14- 09/09/87
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6. EFFECTS
6.1. SYSTEMIC TOXICITY
6.1.1. Inhalation Exposures. Pertinent data regarding the toxlclty of
p-chlorobenzolc add following subchronlc or chronic Inhalation exposure
could not be located 1n the available literature as cited 1n Appendix A.
6.1.2. Oral Exposures.
6.1.2.1. SUBCHRONIC — In a study by Kleckebusch et al. (1960),
groups of 20 male and 20 female young (40-50 g) Elberfleld rats were fed
diets containing p-chlorobenzolc acid at 0, 0.1 or 0.2% for 5 months. Feed
Intake was measured dally. The approximate dally doses determined by the
authors were 13 and 26 mg for the low and high dose groups, respectively.
Near the end of the experiment, a 24-hour urine sample was analyzed for
protein and sugar content, and the sediment was examined microscopically.
While urine samples were being taken, the rats were fasted. At the end of
the experiment, the rats were sacrificed, organ weights were determined and
the livers and kidneys were examined hlstologlcally. The results of the
study showed no adverse effects 1n any of the parameters examined.
6.1.2.2. CHRONIC — Pertinent data regarding the chronic oral toxlc-
lty of p-chlorobenzolc add could not be located 1n the available literature
as cited 1n Appendix A.
6.1.3. Other Relevant Information. D'eng et al. (1983) showed an eleva-
tion of two hepatic enzymes In the serum 0.5-5 hours after the administra-
tion of an L05Q dose. Dally oral administration of 1/10 the LD5Q dose
produced an Inhibition of hepatic protein synthesis within 2 weeks. The
significance of this study Is difficult to evaluate because 1t was available
only In abstract form.
0070d -15- 09/09/87
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In an abstract reported by Kaulla (1962), p-chlorobenzok add has been
shown to have substantial Jin vitro MbMnolytlc activity.
NIOSH (1986) lists the rat 1ntraper1toneal LO.- for p-chlorobenzo1c
add as 1000 mg/kg.
6.2. CARCINOGENICITY
Pertinent data regarding the cardnogenldty of p-chlorobenzo1c add
following any route of exposure could not be located In the available
literature as cited 1n Appendix A.
6.3. MUTAGENICITY
Pertinent data regarding the mutagenldty of p-chlorobenzo1c add could
not be located In the available literature as cited In Appendix A.
6.4. TERATOGENICITY
Pertinent data regarding the teratogenldty of p-chlorobenzo1c acid
could not be located 1n the available literature as dted 1n Appendix A.
6.5. OTHER REPRODUCTIVE EFFECTS
In the study by Kleckebusch et al. (1960), no differences 1n the number
of litters or the development of the young were noted 1n rats fed p-chloro-
benzolc add 1n the diet at 0.1 or 0.2X. The rats were mated 8 weeks and ~4
months after the beginning of the experiment. A delay In sexual maturation
of females at both exposure levels was noted; however, the authors judged
the difference not to be significant.
6.6. SUMMARY
Rats fed p-chlorobenzo1c add 1n the diet at 0.1 or 0.2% did not develop
toxic effects, and no differences 1n the number of Utters or the develop-
ment of the young were noted (Kleckebusch et al., 1960). D'eng et al.
(1983) observed that a single oral ID,- dose produced a transient stimula-
tion of hepatic protein synthesis whereas dally dosing with 1/10 LD5Q and
0070d -16- 11/10/87
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1/50 LD5Q resulted 1n Inhibition of protein synthesis 1n the liver of
rats. Kaulla (1962) found that p-chlorobenzo1c add has in. vitro flbrlno-
lytlc activity. The rat IntraperHoneal LD5Q for p-chlorobenzo1c acid Is
1000 mg/kg (NIOSH, 1986).
Pertinent data regarding the cardnogenlclty, mutagenldty and terato-
genlclty of p-chlorobenzolc add following subchronlc and chronic Inhalation
exposure and chronic oral exposure could not be located 1n the available
literature as dted In Appendix A.
0070d -17- 11/10/87
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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 1n Appendix A.
7.2. AQUATIC
Guidelines and standards for the protection of aquatic organisms from
the effects of p-chlorobenzo1c add could not be located In the available
literature as cited 1n Appendix A.
0070d -18- 09/09/87
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8. RISK ASSESSMENT
8.1. CARCINOGENICITY
Pertinent data regarding the cardnogenlclty of p-chlorobenzo1c add
could not be located In the available literature as cited In Appendix A.
8.1.1. Height of Evidence. The lack of data concerning the cardnogen-
lclty of p-chlorobenzo1c add 1n either humans or animals Indicates that the
compound should be classified as an EPA Group D chemical (U.S. EPA, 1986b),
not classifiable as to human cardnogenlclty.
8.1.2. Quantitative Risk Estimates. The lack of cardnogenlclty data
precludes the derivation of cardnogenlclty-based quantitative risk assess-
ment values.
8,,2. SYSTEMIC TOXICITY
8.2.1. Inhalation Exposure. The lack of data concerning the toxldty of
p-chlorobenzolc add following Inhalation exposure precludes the derivation
of Inhalation risk assessment values.
8.2.2. Oral Exposure.
8.2.2.1. LESS THAN LIFETIME EXPOSURES (SUBCHRONIC) -- In the study by
Kleckebusch et al. (1960), no adverse effects were noted In rats fed diets
containing p-chlorobenzolc add at 0.1 or 0.2% (13 or 26 mg/day) for 5
months. Despite the lack of an effect level, this study can be used to
derive a subchronlc RfD. Dividing the dally dose of 26 mg provided by the
author by 0.15 kg rat body weight, estimated from rat body weights at the
start and end of the study, a rat dose of 173.3 mg/kg/day Is estimated.
Dividing the rat NOAEL by an uncertainty factor of 100 (10 for Interspecles
extrapolation and 10 to protect sensitive Individuals), a human subchronlc
oral RfD of 2 mg/kg/day, or 121 mg/day for a 70 kg human, 1s derived.
0070d -19- 09/09/87
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Confidence In this RfD Is very low. The RfD Is based on a freestanding
NOAEL, so that It Is likely that the value 1s unnecessarily conservative.
On the other hand, the study by Kleckebusch et al. (1960) was marginally
adequate because an effect level was not defined and hlstopathologlcal
examinations of only the liver and kidneys were completed. In addition,
there are no supporting studies; no other subchronlc or chronic studies are
available, and p-chlorobenzolc add has not been studied for carclnogen-
1c1ty, mutagenldty or developmental toxlclty.
8.2.2.2. CHRONIC EXPOSURES — No chronic oral studies of p-chloroben-
zolc acid are available. A chronic oral RfD of 0.2 mg/kg/day, or 12 mg/day
for a 70 kg human, can be derived by dividing the subchronlc oral NOAEL by
an additional uncertainty factor of 10 to extrapolate from subchronlc to
chronic exposure.
Confidence In the chronic RfO 1s very low. The RfD Is based on a free-
standing NOAEL found 1n a subchronlc oral study (Kleckebusch et al., 1960),
and no supporting studies are available.
0070d -20- 09/09/87
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9. REPORTABLE QUANTITIES
9.1. BASED ON SYSTEMIC TOXICITY
The only toxlclty study of p-chlorobenzolc acid (Kleckebusch et al.,
1960) did not Identify any adverse effects. Therefore, as Indicated 1n
Table 9-1, an RQ value cannot be derived.
9.2. BASED ON CARCINOGENICITY
No data were located regarding the cardnogenlcUy of p-chlorobenzolc
acid 1n humans or animals, and the compound was placed 1n EPA Group D.
Hazard ranking based on cardnogenlcUy 1s not possible for EPA Group D
substances.
0070d -21- 09/09/87
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TABLE 9-1
p-Chlorobenzolc Acid
Minimum Effective Dose (MED) and Reportable Quantity (RQ)
Route:
Dose:
Effect:
Reference:
RVd:
RVe:
Composite Score:
RQ: Data are not sufficient for deriving an RQ
0070d -22- 09/09/87
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Caslda, J.E. 1955. Toxlclty of aromatic adds to the larvae of mosquito
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Crosby, O.G. and E. Le1t1s. 1969. Photodecomposltlon of chlorobenzolc
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D'eng, B., A.I. Nlkolaev, P.X. Khaslgov, N.V. Ukhacheva and N.A. Zaltsev.
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DIGeronlmo, H.J., M. N1ka1do and M. Alexander. 1979. Utilization of
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0070d -23- 09/09/87
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Freltag, 0., L. Ballhorn, H. Geyer and F. Korte. 1985. Environmental
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Gelfand, S. 1979. Chlorocarbons - Hydrocarbons (Toluenes). In.: K1rk-
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Gibson, D.T. 1977. Blodegradatlon of aromatic petroleum hydrocarbons, in:
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Haller, H.D. 1978. Degradation of mono-substituted benzoates and phenols
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Horowitz, A., O.R. Shelton, C.P. Cornell and J.M. Tledje. 1982. Anaerobic
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0070d -24- 09/09/87
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0070d -25- 09/09/87
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Property Estimation Methods. McGraw-Hill Book Co., New York. p. 7-4, 4-9,
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0070d -26- 09/09/87
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Perry, R.H. and 0. Green, Ed. 1984. Perry's Chemical Engineer's Handbook,
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i
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APPENDIX A
LITERATURE SEARCHED
This HEED Is based on • data Identified by computerized literature
searches of the following:
TSCATS
CASR online (U.S. EPA Chemical Activities Status Report)
TOXLINE
TOXBACK 76
TOXBACK 65
RTECS
OHM TADS
STORET
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 Hyg1en1sts).
1986. Documentation of the Threshold Limit Values and Biological
Exposure Indices, 5th ed. Cincinnati, OH.
ACGIH (American Conference of Governmental Industrial Hyg1en1sts).
1986-1987. TLVs: Threshold Limit Values for Chemical Substances 1n
the Work Environment adopted by ACGIH with Intended Changes for
1986-1987. Cincinnati, OH. Ill p.
Clayton, G.D. and F.E. Clayton, Ed. 1981. Patty's Industrial
Hygiene and Toxicology, 3rd rev. ed., Vol. 2A. John Wiley and
Sons. NY. 2878 p.
Clayton, G.D. and F.E. Clayton, Ed. 1981. Patty's Industrial
Hygiene and Toxicology, 3rd rev. ed., Vol. 2B. John Wiley and
Sons, NY. p. 2879-3816.
Clayton, G.D. and F.E. Clayton, Ed. 1982. Patty's Industrial
Hygiene and Toxicology, 3rd rev. ed., Vol. 2C. John Wiley and
Sons, NY. p. 3817-5112.
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Grayson, M. and 0. Eckroth, Ed. 1978-1984. KUk-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, HA. 575 p.
IARC (International Agency for Research on Cancer). IARC Mono-
graphs on the Evaluation of Carcinogenic Risk of Chemicals to
Humans. WHO, IARC, Lyons, France.
Jaber, H.H., W.R. Habey, 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, Nenlo 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 Re1nhoId 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 Standard? Program and the Data Call In
Programs. Registration Standards and the Data Call In Programs.
Office of Pesticide Programs, Washington, DC.
U.S. EPA. 1985. CSB Existing Chemical Assessment Tracking System.
Name and CAS Number Ordered Indexes. Office of Toxic Substances,
Washington, DC.
USITC (U.S. International Trade Commission). 1985. Synthetic
Organic Chemicals. U.S. Production and Sales, 1984, USITC Publ.
1422, Washington. DC.
Verschueren, K. 1983. Handbook of Environmental Data on Organic
Chemicals, 2nd ed. Van Nostrand Relnhold Co., NY.
Wlndholz, M., Ed. 1983. The Merck Index, 10th ed. Merck and Co.,
Inc., Rahway, NJ.
Worthing, C.R. and S.B. Walker, Ed. 1983. The Pesticide Manual.
British Crop Protection Council. 695 p.
0070d -31- 09/09/87
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In addition, approximately 30 compendia of aquatic toxldty data were
reviewed, Including the following:
Battelle's Columbus Laboratories. 1971. Hater 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, Fish and Wildlife
Serv. Res. Publ. 137, Washington, DC.
NcKee, 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, 0. 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.
0070d -32- 09/09/87
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o
o
APPENDIX B
Summary Table for p-Chlorobenzolc Acid
Species
Inhalation Exposure
Subchronlc ID
Chronic ID
Carclnogenlclty ID
, Oral Exposure
CO
CO
1 Subchronlc rat
Chronic rat
Carclnogenlclty ID
REPORTABLE QUANTITIES
Based on chronic toxlclty: ID
Based on Carclnogenlclty: ID
o
to
Exposure Effect RfD or q-|* Reference
ID ID ID ID
ID ID ID ID
ID ID ID ID
0.2% In the diet NOAEL 121 mg/day Kelckebusch
for 5 months et al., 1960
0.2% In the diet NOAEL 12 mg/day Kelckebusch
for 5 months et al.. 1960
ID ID ID ID
ID
ID
^ ID = Insufficient data
GO
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