United States
Environmental Protection
1=1 m m Agency
EPA/690/R-06/013F
Final
3-01-2006
Provisional Peer Reviewed Toxicity Values for
1,3-Dichloropropane
(CASRN 142-28-9)
Superfund Health Risk Technical Support Center
National Center for Environmental Assessment
Office of Research and Development
U.S. Environmental Protection Agency
Cincinnati, OH 45268

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Acronyms and Abbreviations
bw	body weight
cc	cubic centimeters
CD	Caesarean Delivered
CERCLA	Comprehensive Environmental Response, Compensation and Liability Act
of 1980
CNS	central nervous system
cu.m	cubic meter
DWEL	Drinking Water Equivalent Level
FEL	frank-effect level
FIFRA	Federal Insecticide, Fungicide, and Rodenticide Act
g	grams
GI	gastrointestinal
HEC	human equivalent concentration
Hgb	hemoglobin
i.m.	intramuscular
i.p.	intraperitoneal
i.v.	intravenous
IRIS	Integrated Risk Information System
IUR	inhalation unit risk
kg	kilogram
L	liter
LEL	lowest-effect level
LOAEL	lowest-observed-adverse-effect level
LOAEL(ADJ)	LOAEL adjusted to continuous exposure duration
LOAEL(HEC)	LOAEL adjusted for dosimetric differences across species to a human
m	meter
MCL	maximum contaminant level
MCLG	maximum contaminant level goal
MF	modifying factor
mg	milligram
mg/kg	milligrams per kilogram
mg/L	milligrams per liter
MRL	minimal risk level
MTD	maximum tolerated dose
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MTL
median threshold limit
NAAQS
National Ambient Air Quality Standards
NOAEL
no-observed-adverse-effect level
NOAEL(ADJ)
NOAEL adjusted to continuous exposure duration
NOAEL(HEC)
NOAEL adjusted for dosimetric differences across species to a human
NOEL
no-observed-effect level
OSF
oral slope factor
p-IUR
provisional inhalation unit risk
p-OSF
provisional oral slope factor
p-RfC
provisional inhalation reference concentration
p-RfD
provisional oral reference dose
PBPK
physiologically based pharmacokinetic
PPb
parts per billion
ppm
parts per million
PPRTV
Provisional Peer Reviewed Toxicity Value
RBC
red blood cell(s)
RCRA
Resource Conservation and Recovery Act
RDDR
Regional deposited dose ratio (for the indicated lung region)
REL
relative exposure level
RfC
inhalation reference concentration
RfD
oral reference dose
RGDR
Regional gas dose ratio (for the indicated lung region)
s.c.
subcutaneous
SCE
sister chromatid exchange
SDWA
Safe Drinking Water Act
sq.cm.
square centimeters
TSCA
Toxic Substances Control Act
UF
uncertainty factor
Hg
microgram
|j,mol
micromoles
voc
volatile organic compound
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PROVISIONAL PEER REVIEWED TOXICITY VALUES FOR
1,3-DICHLOROPROPANE (CASRN 142-28-9)
Background
On December 5, 2003, the U.S. Environmental Protection Agency's (EPA's) Office of
Superfund Remediation and Technology Innovation (OSRTI) revised its hierarchy of human
health toxicity values for Superfund risk assessments, establishing the following three tiers as the
new hierarchy:
1.	EPA's Integrated Risk Information System (IRIS).
2.	Provisional Peer-Reviewed Toxicity Values (PPRTV) used in EPA's Superfund
Program.
3.	Other (peer-reviewed) toxicity values, including:
~	Minimal Risk Levels produced by the Agency for Toxic Substances and Disease
Registry (ATSDR),
~	California Environmental Protection Agency (CalEPA) values, and
~	EPA Health Effects Assessment Summary Table (HEAST) values.
A PPRTV is defined as a toxicity value derived for use in the Superfund Program when
such a value is not available in EPA's Integrated Risk Information System (IRIS). PPRTVs are
developed according to a Standard Operating Procedure (SOP) and are derived after a review of
the relevant scientific literature using the same methods, sources of data, and Agency guidance
for value derivation generally used by the EPA IRIS Program. All provisional toxicity values
receive internal review by two EPA scientists and external peer review by three independently
selected scientific experts. PPRTVs differ from IRIS values in that PPRTVs do not receive the
multi-program consensus review provided for IRIS values. This is because IRIS values are
generally intended to be used in all EPA programs, while PPRTVs are developed specifically for
the Superfund Program.
Because science and available information evolve, PPRTVs are initially derived with a
three-year life-cycle. However, EPA Regions or the EPA Headquarters Superfund Program
sometimes request that a frequently used PPRTV be reassessed. Once an IRIS value for a
specific chemical becomes available for Agency review, the analogous PPRTV for that same
chemical is retired. It should also be noted that some PPRTV manuscripts conclude that a
PPRTV cannot be derived based on inadequate data.
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Disclaimers
Users of this document should first check to see if any IRIS values exist for the chemical
of concern before proceeding to use a PPRTV. If no IRIS value is available, staff in the regional
Superfund and RCRA program offices are advised to carefully review the information provided
in this document to ensure that the PPRTVs used are appropriate for the types of exposures and
circumstances at the Superfund site or RCRA facility in question. PPRTVs are periodically
updated; therefore, users should ensure that the values contained in the PPRTV are current at the
time of use.
It is important to remember that a provisional value alone tells very little about the
adverse effects of a chemical or the quality of evidence on which the value is based. Therefore,
users are strongly encouraged to read the entire PPRTV manuscript and understand the strengths
and limitations of the derived provisional values. PPRTVs are developed by the EPA Office of
Research and Development's National Center for Environmental Assessment, Superfund Health
Risk Technical Support Center for OSRTI. Other EPA programs or external parties who may
choose of their own initiative to use these PPRTVs are advised that Superfund resources will not
generally be used to respond to challenges of PPRTVs used in a context outside of the Superfund
Program.
Questions Regarding PPRTVs
Questions regarding the contents of the PPRTVs and their appropriate use (e.g., on
chemicals not covered, or whether chemicals have pending IRIS toxicity values) may be directed
to the EPA Office of Research and Development's National Center for Environmental
Assessment, Superfund Health Risk Technical Support Center (513-569-7300), or OSRTI.
This document has passed the STSC quality review and peer review evaluation indicating
that the quality is consistent with the SOPs and standards of the STSC and is suitable for use by
registered users of the PPRTV system.
INTRODUCTION
The 1997 HEAST (U.S. EPA, 1997) does not list subchronic or chronic RfD or RfC
values for 1,3-dichloropropane (1,3-DCP), noting that data were inadequate for quantitative risk
assessment, or any cancer assessment for the chemical. A Health and Environmental Effects
Profile (HEEP) for Dichloropropanes (U.S. EPA, 1985), which was listed in the HEAST as a
reference for subchronic and chronic toxicity, reported no pertinent data regarding the subchronic
or chronic toxicity or carcinogenicity of the chemical. 1,3-DCP is not listed on IRIS (U.S. EPA,
2002), or the Drinking Water Standards and Health Advisories list (U.S. EPA, 2000). No
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relevant documents, other than the previously mentioned HEEP, were located in the CARA list
(U.S. EPA, 1991, 1994). ACGIH (2002), NIOSH (2002), and OSHA (2002a,b) have not
assessed the toxicity of 1,3-DCP. Neither ATSDR (2002), IARC (2002), nor the WHO (2002)
have written a toxicological review document on 1,3-DCP. 1,3-DCP is not included in the NTP
Management Status Report (2002). Literature searches were conducted from 1985 thru 2001 for
studies relevant to the derivation of provisional toxicity values for 1,3-DCP. Databases searched
included: TOXLINE, MEDLINE, CANCERLIT, TSCATS, RTECS, CCRIS, DART,
EMIC/EMICBACK, HSDB and GENETOX.
REVIEW OF PERTINENT DATA
Human Studies
No studies were located regarding the subchronic or chronic toxicity or carcinogenicity of
1,3-DCP in humans.
Animal Studies
A single study investigated subchronic oral toxicity of 1,3-DCP in the rat (Terrill et al.,
1991). 1,3-DCP dissolved in corn oil was administered by oral gavage at doses of 0 (corn oil
vehicle only), 200, 600 or 1800 mg/kg-day, 7 days/week, for 14 days and, based on results of the
14-day study, at 50, 200 or 800 mg/kg-day, 7 days/week, for 90 days to male and female
Sprague-Dawley-derived rats (10/sex/group). Signs of toxicity, body weight, and food
consumption were monitored. Ophthalmoscopic examinations (90-day study only) and
hematological and clinical chemistry determinations were performed on all animals at
termination. All animals underwent gross necropsy. Histopathological examinations were
performed on the liver and kidney of all animals, and on a comprehensive collection of tissues,
including stomach, from all mid- and high-dose animals and from 5 control animals per sex.
In the 14-day range-finding study, all high-dose, but no animals in other treatment groups,
died within the first week (Terrill et al., 1991). Clinical signs in the high-dose group included
languid behavior, salivation and tremors after dosing. No clinical signs were reported for the
other treatment groups. Because of the early deaths of high-dose animals, no comparisons for
body weight, food consumption, hematology, clinical chemistry, organ weights or histopathology
were made between the high-dose and control animals. For mid-dose and low-dose animals, no
treatment-related differences were apparent in body weight, food consumption or hematological
data. Organ weight, clinical chemistry and urinalysis data point toward the liver and kidney as
target organs of 1,3-DCP toxicity. The most notable findings were statistically significant
increases in absolute and relative liver weights (>21%) in mid-dose males and females and
absolute and relative kidney weights (>11%) in mid-dose males. Other potentially relevant
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findings were small, statistically significant decreases in urine pH in low- and mid-dose males
and mid-dose females, and small, statistically significant increases in serum albumin (mid-dose
group) and total protein (low- and mid-dose groups) in females. No gross or microscopic lesions
attributable to treatment were found in either males or females.
In the 90-day study, no treatment-related deaths occurred (Terrill et al., 1991). The only
clinical observation was urine-stained fur in high-dose females. Food consumption was
comparable in treated and control animals. Body weight data were unremarkable in treated
females and low- and mid-dose males. In high-dose males, however, body weight was
progressively reduced throughout the study, with the deficit from controls reaching a statistically
significant 17% at termination. Ophthalmoscopic and hematologic evaluations did not reveal any
treatment-related effects. Clinical chemistry changes of note included significant increases in
alkaline phosphatase (high-dose males and females) and slight, but statistically significant,
increases in alanine aminotransferase and bilirubin (high-dose males), albumin (mid- and high-
dose males and mid-dose females) and protein (mid-dose females). Urine pH was significantly
decreased in mid- and high-dose males, but not in females. Absolute and/or relative liver
weights were significantly increased in a dose-related fashion in mid- and high-dose males and
low-, mid- and high-dose females. Absolute and/or relative kidney weights were significantly
increased in high-dose males and in relation to dose in mid- and high-dose females. Other
statistically significant organ weight changes, which occurred primarily in high-dose males where
they were secondary to significantly reduced body weight, were not considered related to
treatment. Postmortem evaluations did not reveal any gross treatment-related lesions.
Microscopic examination revealed minimal-to-slight centrilobular hypertrophy of the
liver in mid- (1/10) and high-dose (10/10) males and high-dose (9/10) females, but not in
controls or lower-dose animals (Terrill et al., 1991). The lesion was characterized by decreased
eosinophilia and cytoplasmic enlargement of hepatocytes surrounding the central vein. Early
chronic progressive kidney nephropathy, characterized by multifocal tubular cell regeneration
and minimal mononuclear cell infiltration, was found in 0/10, 0/10, 3/10 and 7/10 males and
0/10, 1/10, 0/10 and 3/10 females in the control, low-, mid- and high-dose groups, respectively.
In a few cases, tubules were slightly dilated and contained proteinaceous casts. While chronic
progressive nephropathy is a common finding in mature Sprague-Dawley rats, the early
appearance of this lesion in this study was considered treatment-related by the researchers. No
stomach abnormalities were noted, indicating a lack of portal-of-entry adverse effects. This
study identifies the liver and kidney as the critical target organs of 1,3-DCP toxicity, based on
histopathological lesions and increased weights in both organs, and potentially related urinalysis
and serum chemistry changes, including small increases in serum alkaline phosphatase, alanine
aminotransferase, bilirubin, albumin and protein, and decreased urine pH. These effects were
seen primarily in males and females of the mid- and high-dose groups, and generally increased in
severity in relation to dose. The only observations in the low dose group were increased
absolute, but not relative, liver weight in females, and minimal nephropathy in 1/10 females. It is
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not clear, however, that nephropathy in this individual was related to treatment: 1) none of the 10
females at the next higher dose were affected and no males at the same dose were affected, even
though males overall appeared to be more sensitive for this endpoint, and 2) although not present
in any controls in this study, this is a spontaneously occurring lesion in aging rats. The increase
in absolute liver weight at the low dose appears to have been a treatment-related effect, but was
not of sufficient magnitude to increase relative liver weight and was not accompanied by lesions
or other evidence of toxicity; therefore, the increase in liver weight at the low dose level is not
considered to be adverse. It is concluded that the low dose of 50 mg/kg-day represents a
NOAEL, and the mid-dose of 200 mg/kg-day a LOAEL, for hepatic and renal effects in this
study.
One other relevant toxicity study was located. In a study to assess the acute toxicity of
1,3-DCP with respect to testicular changes, the chemical was administered by oral gavage in
arachis oil vehicle to male albino Wistar rats (10/treated group, 20 in vehicle control group) at
dose levels of 0, 100 or 400 mg/kg-day for 14 days (Shell Oil, 1979a). Macro- and microscopic
examinations revealed no significant differences between treated and control animals in the
testes, epididymides, ductuli efferentes, vasa deferentes or kidneys.
Genotoxicity studies of 1,3-DCP have produced mixed results. 1,3-DCP did not show
any mutagenic potential in selected Escherichia coli strains or in the Ames assay in Salmonella
typhimurium frameshift strains TA98, TA1537 and TA1538, or base-pair strain TA100, with or
without metabolic activation; in base-pair strain TA1535, 1,3-DCP produced weak positive
results only in the presence of S9 (Dean et al., 1985; Granville et al., 2001; Shell, 1979b;
Stolzenberg and Hine, 1980). 1,3-DCP was weakly mutagenic without S9 in the E. coli
prophage-induction assay (Granville et al., 2001). 1,3-DCP was inactive in SOS chromotests
with E. coli (von der Hude et al., 1988; Mersch-Sundermann et al., 1994), but active in the
Bacillus subtilis microsome rec-assay with, but not without, S9 (Matsui et al., 1989). 1,3-DCP
did not induce mitotic gene conversion in the yeast Saccharomyces cerevisiae with or without S9
(Dean et al. 1985), and did not increase mitotic chromosome segregation rates in the fungus
Aspergillus nidulans (Crebelli et al., 1995). 1,3-DCP produced negative results in an assay for
forward mutations in mouse lymphoma cells (Henry et al., 1998). 1,3-DCP did not induce an
increase in the frequency of chromosome aberrations in rat liver RL4 cells without S9 (Shell Oil,
1979b), but did induce an increase in sister chromatid exchange in Chinese hamster V79 cells in
vitro with or without S9 (von der Hude et al., 1987). In isolated human lymphocytes, 1,3-DCP
exhibited clastogenic activity in the micronucleus and Comet assays (Tafazoli and Kirsch-
Volders, 1996; Tafazoli et al, 1998). 1,3-DCP induced significant increases in micronuclei in
selected, but not all, human B lymphoblastoid cell lines; protection was apparently provided by
the activities of various cytochrome P450 isoenzymes and/or microsomal epoxide hydrolase
(Doherty et al., 1996). In vivo, 1,3-DCP was mutagenic in the eye w/w+ assay in Drosophila
melanogaster (Rodriguez-Arnaiz, 1998), but was inactive in a sex-linked recessive lethal assay in
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D. melanogaster when administered by inhalation for 6 hours at 2400 mg/m3 or 96 hours at 990
mg/m3 (Kramers et al., 1991).
DERIVATION OF PROVISIONAL SUBCHRONIC AND CHRONIC
ORAL RfD VALUES FOR 1,3-DICHLOROPROPANE
The subchronic rat study by Terrill et al. (1991) identified the liver and kidney as critical
targets for 1,3-DCP. Effects included histopathological lesions (minimal-to-slight centrilobular
hypertrophy in the liver, minimal chronic progressive nephropathy in the kidney) and increased
weights in both organs, and potentially related urinalysis and serum chemistry changes, including
small increases in serum alkaline phosphatase, alanine aminotransferase, bilirubin, albumin and
protein, and decreased urine pH. The NOAEL for these effects was 50 mg/kg-day, and the
LOAEL was 200 mg/kg-day. Support for these findings comes from the associated 14-day
range-finding study, which found similar effects (increased liver and kidney weights, increased
serum albumin and protein, and decreased urine pH), primarily at 600 mg/kg-day. Subchronic
and chronic p-RfD values for 1,3-DCP can be derived from the subchronic study, as detailed
below.
A subchronic p-RfD of 0.2 mg/kg-day is derived by applying an uncertainty factor of
300 (10 to extrapolate from rats to humans, 10 to protect sensitive individuals and 3 for database
limitations, including lack of reproductive or developmental studies) to the NOAEL of 50 mg/kg-
day, as follows:
subchronic p-RfD = NOAEL / UF
= 50 mg/kg-day / 300
= 0.2 mg/kg-day or 2E-1 mg/kg-day
A chronic p-RfD of 0.02 mg/kg-day is similarly derived by applying to the NOAEL of
50 mg/kg-day an uncertainty factor of 3000 (10 for use of a subchronic study, 10 to extrapolate
from rats to humans, 10 to protect sensitive individuals and 3 for database limitations, including
lack of reproductive or developmental studies), as follows:
p-RfD = NOAEL / UF
= 50 mg/kg-day / 3000
= 0.02 mg/kg-day or 2E-2 mg/kg-day
Confidence in the principal study is medium. The study provided sufficient detail of
methods and results, examined an adequate array of endpoints (including portal-of-entry tissues),
and identified sensitive target organs and critical effect levels. Group sizes, however, were only
minimally adequate, limiting the power of the study to detect treatment-related changes.
Confidence in the oral database is low. The only supporting data come from the 14-day range-
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finding experiment associated with the key study. Chronic, developmental and reproductive
studies are lacking. Low-to-medium confidence in the subchronic and chronic p-RfDs results.
DERIVATION OF PROVISIONAL SUBCHRONIC AND CHRONIC
INHALATION RfC VALUES FOR 1,3-DICHLOROPROPANE
Subchronic or chronic inhalation p-RfC values for 1,3-DCP cannot be derived because
human and animal toxicity data following subchronic or chronic inhalation exposure to 1,3-DCP
are lacking.
DERIVATION OF A PROVISIONAL CARCINOGENICITY ASSESSMENT
FOR 1,3-DICHLOROPROPANE
There are no human or animal carcinogenicity data for 1,3-DCP. Genotoxicity assays of
1,3-DCP have yielded mixed responses in bacteria, fruit flies and mammalian cells. Under the
proposed U.S. EPA (1999) cancer guidelines, the available data are inadequate for an assessment
of human carcinogenic potential.
Derivation of quantitative estimates of cancer risk for 1,3-DCP is precluded by the
absence of carcinogenicity data for 1,3-DCP.
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