United States
Environmental Protection
1=1 m m Agency
EPA/690/R-09/021F
Final
9-30-2009
Provisional Peer-Reviewed Toxicity Values for
Endosulfan
(CASRN 115-29-7)
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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COMMONLY USED ABBREVIATIONS
BMD
Benchmark Dose
IRIS
Integrated Risk Information System
IUR
inhalation unit risk
LOAEL
lowest-observed-adverse-effect level
LOAELadj
LOAEL adjusted to continuous exposure duration
LOAELhec
LOAEL adjusted for dosimetric differences across species to a human
NOAEL
no-ob served-adverse-effect level
NOAELadj
NOAEL adjusted to continuous exposure duration
NOAELhec
NOAEL adjusted for dosimetric differences across species to a human
NOEL
no-ob served-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
RfC
inhalation reference concentration
RfD
oral reference dose
UF
uncertainty factor
UFa
animal to human uncertainty factor
UFC
composite uncertainty factor
UFd
incomplete to complete database uncertainty factor
UFh
interhuman uncertainty factor
UFl
LOAEL to NOAEL uncertainty factor
UFS
subchronic to chronic uncertainty factor
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PROVISIONAL PEER-REVIEWED TOXICITY VALUES FOR
ENDOSULFAN (CASRN 115-29-7)
Background
On December 5, 2003, the U.S. Environmental Protection Agency's (U.S. EPA) 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)	U.S. EPA's Integrated Risk Information System (IRIS).
2)	Provisional Peer-Reviewed Toxicity Values (PPRTVs) used in U.S. 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 U.S. EPA's 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 U.S. EPA IRIS Program. All provisional toxicity values receive internal
review by two U.S. EPA scientists and external peer review by three independently selected
scientific experts. PPRTVs differ from IRIS values in that PPRTVs do not receive the
multiprogram consensus review provided for IRIS values. This is because IRIS values are
generally intended to be used in all U.S. EPA programs, while PPRTVs are developed
specifically for the Superfund Program.
Because new information becomes available and scientific methods improve over time,
PPRTVs are reviewed on a 5-year basis and updated into the active database. 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 documents conclude that
a PPRTV cannot be derived based on inadequate data.
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 Resource Conservation and Recovery Act (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.
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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 document and understand the strengths
and limitations of the derived provisional values. PPRTVs are developed by the U.S. EPA
Office of Research and Development's National Center for Environmental Assessment,
Superfund Health Risk Technical Support Center for OSRTI. Other U.S. 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 U.S. EPA Office of Research and Development's National Center for Environmental
Assessment, Superfund Health Risk Technical Support Center (513-569-7300), or OSRTI.
INTRODUCTION
Endosulfan (CASRN 115-29-7) is a mixture of two stereoisomers: approximately
70% endosulfan I (endosulfan a; CASRN 959-98-8) and 30% endosulfan II (endosulfan P;
CASRN 33213-65-9). A chronic reference dose (RfD) of 6 x 10"3 mg/kg-day for endosulfan is
available on IRIS (U.S. EPA, 1994b). The RfD is based on reduced body weight gain in
females, and increased incidence of marked progressive glomerulonephrosis and blood vessel
aneurysms in males, in a 2-year rat feeding study (Hoechst Celanese Corp., 1989a), as well as
decreased weight gain in males and neurologic findings in both sexes in a 1-year dog feeding
study (Hoechst Celanese Corp., 1989b). In both studies, a NOAEL of approximately
0.6 mg/kg-day was identified. Uncertainty factors of 10 each for interspecies extrapolation and
protection of sensitive humans were applied to the NOAEL to derive the RfD. No source
document other than the IRIS record is given. The Drinking Water Standards and Health
Advisories list (U.S. EPA, 2006) does not include an RfD for endosulfan. The HEAST
(U.S. EPA, 1997) reports a subchronic RfD of 0.006 mg/kg-day for endosulfan, adopting the
chronic RfD from IRIS as the subchronic RfD. In a Toxicological Profile for Endosulfan,
ATSDR (2000) derived intermediate- and chronic-duration oral Minimal Risk Levels (MRLs)
for endosulfan based on immunological and hepatic effects, respectively. The
intermediate-duration oral MRL is based on a 6-week immunotoxicity study in rats exposed via
the diet (Banerjee and Hussain, 1986). Uncertainty factors of 10 each for interspecies and
intraspecies variability were applied to the NOAEL of 0.45 mg/kg-day to derive the
intermediate-duration oral MRL of 0.005 mg/kg-day. The chronic duration oral MRL is based
on the same dog-feeding study as the IRIS RfD (Hoechst Celanese Corp., 1989b). However,
ATSDR selected 0.6 mg/kg-day as a LOAEL and 0.18 mg/kg-day as a NOAEL based on
increased serum alkaline phosphatase levels. Uncertainty factors of 10 each for interspecies and
intraspecies variability were applied to the NOAEL of 0.18 mg/kg-day to derive the
chronic-duration oral MRL of 0.002 mg/kg-day.
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Neither IRIS (U.S. EPA, 2009) nor the HEAST (U.S. EPA, 1997) reports an RfC for
endosulfan. ATSDR (2000) has not derived any inhalation MRLs for endosulfan. ACGIH
(2007), NIOSH (2005), and OSHA (2009) have all adopted the same occupational exposure limit
(time-weighted average) of 0.1 mg/m3. ACGIH cites liver damage, CNS impairment, and kidney
damage as potential effects in exposed workers (ACGIH, 2007).
An assessment of the carcinogenicity of endosulfan is not available on IRIS (U.S. EPA,
2009), in the HEAST (U.S. EPA, 1997), or in the Drinking Water Standards and Health
Advisories list (U.S. EPA, 2006). The CARA list (U.S. EPA, 1991a, 1994a) includes a Health
Effects Assessment for a- and P-endosulfan (U.S. EPA, 1987) that assigned endosulfan to cancer
weight-of-evidence Group D (under U.S. EPA 1986 Guidelines for Carcinogen Risk
Assessment), "Not classifiable as to human carcinogenicity," based on inconclusive animal data.
A subsequent draft Health and Environmental Effects Document (U.S. EPA, 1991b) also
assigned endosulfan to Group D. Based on more recent negative studies, the Office of Pesticide
Programs has classified endosulfan in Group E: "Evidence of noncarcinogenicity for humans"
(U.S. EPA, 1999). Endosulfan has not previously been evaluated under the U.S. EPA (2005)
Guidelines for Cancer Risk Assessment. NCI (1968, 1978) has conducted carcinogenicity
bioassays of endosulfan. Endosulfan is not included in the 11th Report on Carcinogens (NTP,
2005). IARC (2009) has not evaluated endosulfan for potential carcinogenicity.
Review documents by ATSDR (2000), WHO (1984, 1989), and U.S. EPA (1999, 2000,
2001) were consulted for relevant information. To identify toxicological information published
since the ATSDR (2000) Toxicological Profile for Endosulfan, update literature searches were
conducted in December 2007 using the following databases: MEDLINE, TOXLINE, BIOSIS
DART/ETIC (each searched from 1998-December 2007), TSCATS1/2, CCRIS, GENETOX,
HSDB, RTECS (not date-limited), and Current Contents (searched from June 2007-December
2007). A final search of the published literature was conducted for endosulfan (December
2007-August 2009).
A Notice of Availability for the Reregi strati on Eligibility Decision (RED) for Endosulfan
is being published in the Federal Register. To obtain a copy of the RED document, please
contact the OPP Public Regulatory Docket (7502C), U.S. EPA, Ariel Rios Building,
1200 Pennsylvania Avenue NW, Washington, DC 20460, telephone (703) 305-5805. Electronic
copies of the RED and all supporting documents are available on the Internet at
http://www.epa.gov/pesticides/reregistration/status.htm.
REVIEW OF THE PERTINENT LITERATURE
Human Studies
Case control studies of 261 patients with breast cancer (Ashengrau et al., 1998) and
30 patients with gall bladder carcinoma (Shukla et al., 2001) did not find associations between
serum levels of endosulfan and cancer.
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Animal Studies
The available carcinogenicity studies for endosulfan following oral exposure have been
reviewed previously (see U.S. EPA, 1987, 1991b, 1999; AT SDR, 2000; WHO, 1984). There
was no evidence of carcinogenicity in male or female NMRI mice fed endosulfan in the diet at
concentrations up to 18 ppm (2.5 mg/kg-day) for 2 years (Hoechst Celanese Corporation, 1988;
Hack et al., 1995), in male or female Sprague-Dawley rats fed up to 75 ppm (3.25 mg/kg-day)
for 2 years (Hoechst Celanese Corporation, 1989a; Hack et al., 1995), or in male or female
Wistar rats fed up to 100 ppm (8 mg/kg-day) for 2 years (Keller, 1959).
Oral exposure (gavage followed by diet) of male and female B6C3F1 and B6AKF1 mice
to 1.0 or 2.15 mg/kg-day of endosulfan for 73-76 weeks produced some suggestive findings
including statistically significant (p < 0.05) elevations in total tumor incidence and pulmonary
adenomas in all treatment groups combined., These findings, however, are not considered
biologically relevant because no significant differences were apparent for individual endosulfan
treatment groups, and because no pulmonary carcinomas were diagnosed in endosulfan-treated
animals (Innes et al., 1969; NCI, 1968). Low survival in all treated B6C3F1 mice and high-dose
B6AKF1 mice complicates interpretation of this study.
The results of a subsequent NCI (1978) study do not support the assessment of
carcinogenicity by endosulfan. No evidence of carcinogenicity was observed in male or female
B6C3F1 mice fed up to 6.9 or 3.9 ppm (1.3 or 0.76 mg/kg-day), respectively, for 78 weeks,
female Osborne-Mendel rats fed up to 445 ppm (39 mg/kg-day) for 71 weeks, or male
Osborne-Mendel rats fed up to 952 ppm (75 mg/kg-day) for 72-82 weeks. The maximum
tolerated dose was clearly exceeded, as evidenced by high mortality in male rats and mice and
other serious nonneoplastic effects (weight loss, kidney, and testicular damage) in all treated rat
groups. A reevaluation of the histology slides (Reuber, 1981) reported statistically significant
(p < 0.05) increases in certain types of tumors grouped across tissues in female rats (total
neoplasia, malignant tumors, sarcomas, lymphosarcomas, and reproductive system tumors) and
male rats (endocrine organ tumors). The incidence of parathyroid adenomas in male rats was
also reported to be increased. In mice, the reevaluation found a marginally significant increase
in the incidence of liver carcinomas in low-dose females—but not in high-dose females or males.
Reuber (1981) failed to report details regarding definitions of neoplasia used, tissue occurrence
of neoplasia observed, and how his data compare with data from the original study (NCI, 1978).
The conclusions of the reevaluation have not been independently confirmed.
Other Studies
Evidence of hepatic tumor-promoting activity was observed in one of two studies in male
Sprague-Dawley rats initiated by partial hepatectomy and nitrosodiethylamine treatment.
Flodstrom et al. (1988) did not observe an increase in hepatic foci positive for
y-glutamyltranspeptidase in rats exposed to a-endosulfan, P-endosulfan, or technical endosulfan
for 10 weeks at doses up to 5 mg/kg-day. In contrast, Fransson-Steen et al. (1992) observed
statistically significant increases in the number and volume of hepatic foci positive for
y-glutamyltranspeptidase in larger test groups of male rats fed a-endosulfan, P-endosulfan, or
technical endosulfan for 20 weeks up to 15 mg/kg-day. Based on observations that endosulfan
has exhibited activity as an endocrine disruptor (U.S. EPA, 1999) and induced proliferation in
hormone-responsive human (endometrial and breast) cancer cell lines (Coumoul et al., 2001;
Soto et al., 1994; Vonier et al., 1996; others), a hypothesis was suggested that endosulfan may
promote cancer formation in humans through a mode-of-action involving endocrine disruption.
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However, other studies have produced conflicting results (e.g., Arcaro et al., 1998;
Newbold et al., 2001) and insufficient data are available to evaluate the hypothesis.
Reviews generally consider endosulfan to be genotoxic (U.S. EPA, 1991b, 1999;
ATSDR, 2000; WHO, 1984). Extensive mutagenicity testing in Salmonella typhimurium and
Escherichia coli strains reported both positive and negative results with and without metabolic
activation. Conflicting positive and negative results have also been seen in assays for mutation,
gene conversion, and chromosome aberrations in Saccharomyces cerevisae—although no
mutations were seen in Schizosaccharomycespombe. Similarly, both positive and negative tests
for gene mutation have been observed in cultured mouse lymphoma cells with and without
metabolic activation. Endosulfan did not induce unscheduled DNA synthesis in primary rat
hepatocytes. Endosulfan induced micronuclei in cultured sheep lymphocytes and sister
chromatid exchange in both preimplantation embryos of hybrid mice and human lymphoid cells
in vitro. Endosulfan also induced chromosome aberrations in bone marrow cells of Syrian
hamsters. Both positive and negative results were seen in assays measuring the formation of
micronucleated polychromatic erythrocytes in mice. Endosulfan induced sex-linked recessive
lethal mutations and sex-chromosome loss in Drosophila. Both positive and negative results
have been observed in dominant lethal mutation studies in male mice. A cluster of four women
living near endosulfan-contaminated areas in Florida produced five children born with global
developmental delay, hypotonia, carnitine deficiency, and P-hydroxy butyrate anomalies
suggestive of mitochondrial DNA damage (Thrasher, 2000). However, it is not clear that these
effects can be attributed to endosulfan exposure.
Additional information, not summarized in this document, is available from the
U.S. EPA, Office of Pesticide Programs (OPP). Because endosulfan is a currently registered
pesticide, many potentially useful toxicity studies have been submitted to the OPP as confidential
business information (CBI). This information is unpublished and is unavailable for use in this
assessment. The OPP maintains its own program for developing health-based values (e.g. RfDs
and RfCs) for pesticides. Consequently, no values are developed here.
DERIVATION OF PROVISIONAL SUBCHRONIC AND CHRONIC
ORAL p-RfD VALUES FOR ENDOSULFAN
A provisional oral RfD for endosulfan is not derived because an RfD is available on IRIS.
DERIVATION OF PROVISIONAL SUBCHRONIC AND CHRONIC
INHALATION p-RfC VALUES FOR ENDOSULFAN
A provisional inhalation reference concentration (p-RfC) is not derived because
endosulfan is a currently registered pesticide. Additional information can be obtained by
contacting the U.S. EPA, Office of Pesticide Programs.
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PROVISIONAL CARCINOGENICITY ASSESSMENT FOR ENDOSULFAN
Weight-of-Evidence Descriptor
Under the 2005 Guidelines for Carcinogen Risk Assessment (U.S. EPA, 2005), the lack
of available evidence suggests that there is "Inadequate Information [to] Assess the Carcinogenic
Potential' of endosulfan.
Quantitative Estimates of Carcinogenic Risk
Oral Exposure
A provisional oral slope factor (p-OSF) is not derived because endosulfan is a currently
registered pesticide. Additional information can be obtained by contacting the U.S. EPA, Office
of Pesticide Programs.
Inhalation Exposure
A provisional inhalation unit risk (p-IUR) is not derived because endosulfan is a currently
registered pesticide. Additional information can be obtained by contacting the U.S. EPA, Office
of Pesticide Programs.
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