United States
Environmental Protection
1=1 m m Agency
EPA/690/R-16/006F
Final
9-28-2016
Provisional Peer-Reviewed Toxicity Values for
Mixtures of l,2,3,4,5-Pentabromo-6-Chlorocyclohexane
(CASRN 87-84-3)
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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AUTHORS, CONTRIBUTORS, AND REVIEWERS
CHEMICAL MANAGER
Chris Cubbison, PhD
National Center for Environmental Assessment, Cincinnati, OH
DRAFT DOCUMENT PREPARED BY
SRC, Inc.
7502 Round Pond Road
North Syracuse, NY 13212
PRIMARY INTERNAL REVIEWER
Anuradha Mudipalli, MSc, PhD
National Center for Environmental Assessment, Research Triangle Park, NC
This document was externally peer reviewed under contract to
Eastern Research Group, Inc.
110 Hartwell Avenue
Lexington, MA 02421-3136
Questions regarding the contents of this PPRTV assessment should 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).
ii l,2,3,4,5-Pentabromo-6-Chlorocyclohexane

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TABLE OF CONTENTS
COMMONLY USED ABBREVIATIONS AND ACRONYMS	iv
BACKGROUND	1
DISCLAIMERS 	1
QUESTIONS REGARDING PPRTVs	1
INTRODUCTION	2
REVIEW OF POTENTIALLY RELEVANT DATA (NONCANCER AND CANCER)	4
HUMAN STUDIES	11
Oral Exposures	11
Inhalation Exposures	11
ANIMAL STUDIES	11
Oral Exposures	11
Inhalation Exposures	18
OTHER DATA (SHORT-TERM TESTS, OTHER EXAMINATIONS)	18
Genotoxicity	19
Acute Toxicity Studies	19
Metabolism/Toxicokinetic Studies	22
DERIVATION 01 PROVISIONAL VALUES	22
DERIVATION OF ORAL REFERENCE DOSES	23
DERIVATION OF INHALATION REFERENCE CONCENTRATIONS	24
CANCER WEIGHT-OF-EVIDENCE DESCRIPTOR	24
DERIVATION OF PROVISIONAL CANCER POTENCY VALUES	25
APPENDIX A. SCREENING PROVISIONAL VALUES	26
APPENDIX B. DATA TABLES	32
APPENDIX C. BENCHMARK DOSE MODELING RESULTS	43
APPENDIX D. REFERENCES	57
iii l,2,3,4,5-Pentabromo-6-Chlorocyclohexane

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COMMONLY USED ABBREVIATIONS AND ACRONYMS
a2u-g
alpha 2u-globulin
MN
micronuclei
ACGIH
American Conference of Governmental
MNPCE
micronucleated polychromatic

Industrial Hygienists

erythrocyte
AIC
Akaike's information criterion
MOA
mode of action
ALD
approximate lethal dosage
MTD
maximum tolerated dose
ALT
alanine aminotransferase
NAG
N-acetyl-P-D-glucosaminidase
AST
aspartate aminotransferase
NCEA
National Center for Environmental
atm
atmosphere

Assessment
ATSDR
Agency for Toxic Substances and
NCI
National Cancer Institute

Disease Registry
NOAEL
no-observed-adverse-effect level
BMD
benchmark dose
NTP
National Toxicology Program
BMDL
benchmark dose lower confidence limit
NZW
New Zealand White (rabbit breed)
BMDS
Benchmark Dose Software
OCT
ornithine carbamoyl transferase
BMR
benchmark response
ORD
Office of Research and Development
BUN
blood urea nitrogen
PBPK
physiologically based pharmacokinetic
BW
body weight
PCNA
proliferating cell nuclear antigen
CA
chromosomal aberration
PND
postnatal day
CAS
Chemical Abstracts Service
POD
point of departure
CASRN
Chemical Abstracts Service Registry
PODadj
duration-adjusted POD

Number
QSAR
quantitative structure-activity
CBI
covalent binding index

relationship
CHO
Chinese hamster ovary (cell line cells)
RBC
red blood cell
CL
confidence limit
RDS
replicative DNA synthesis
CNS
central nervous system
RfC
inhalation reference concentration
CPN
chronic progressive nephropathy
RfD
oral reference dose
CYP450
cytochrome P450
RGDR
regional gas dose ratio
DAF
dosimetric adjustment factor
RNA
ribonucleic acid
DEN
diethylnitrosamine
SAR
structure activity relationship
DMSO
dimethylsulfoxide
SCE
sister chromatid exchange
DNA
deoxyribonucleic acid
SD
standard deviation
EPA
Environmental Protection Agency
SDH
sorbitol dehydrogenase
FDA
Food and Drug Administration
SE
standard error
FEVi
forced expiratory volume of 1 second
SGOT
glutamic oxaloacetic transaminase, also
GD
gestation day

known as AST
GDH
glutamate dehydrogenase
SGPT
glutamic pyruvic transaminase, also
GGT
y-glutamyl transferase

known as ALT
GSH
glutathione
SSD
systemic scleroderma
GST
glutathione-S-transferase
TCA
trichloroacetic acid
Hb/g-A
animal blood-gas partition coefficient
TCE
trichloroethylene
Hb/g-H
human blood-gas partition coefficient
TWA
time-weighted average
HEC
human equivalent concentration
UF
uncertainty factor
HED
human equivalent dose
UFa
interspecies uncertainty factor
i.p.
intraperitoneal
UFh
intraspecies uncertainty factor
IRIS
Integrated Risk Information System
UFS
subchronic-to-chronic uncertainty factor
IVF
in vitro fertilization
UFd
database uncertainty factor
LC50
median lethal concentration
U.S.
United States of America
LD50
median lethal dose
WBC
white blood cell
LOAEL
lowest-observed-adverse-effect level


iv l,2,3,4,5-Pentabromo-6-Chlorocyclohexane

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PROVISIONAL PEER-REVIEWED TOXICITY VALUES FOR
l,2,3,4,5-PENTABROMO-6-CHLOROCYCLOHEXANE (CASRN 87-84-3)
BACKGROUND
A Provisional Peer-Reviewed Toxicity Value (PPRTV) is defined as a toxicity value
derived for use in the Superfund Program. PPRTVs are derived after a review of the relevant
scientific literature using established Agency guidance on human health toxicity value
derivations. All PPRTV assessments receive internal review by a standing panel of National
Center for Environment Assessment (NCEA) scientists and an independent external peer review
by three scientific experts.
The purpose of this document is to provide support for the hazard and dose-response
assessment pertaining to chronic and subchronic exposures to substances of concern, to present
the major conclusions reached in the hazard identification and derivation of the PPRTVs, and to
characterize the overall confidence in these conclusions and toxicity values. It is not intended to
be a comprehensive treatise on the chemical or toxicological nature of this substance.
The PPRTV review process provides needed toxicity values in a quick turnaround
timeframe while maintaining scientific quality. PPRTV assessments are updated approximately
on a 5-year cycle for new data or methodologies that might impact the toxicity values or
characterization of potential for adverse human health effects and are revised as appropriate. It is
important to utilize the PPRTV database (http://hhpprtv.ornl.gov) to obtain the current
information available. When a final Integrated Risk Information System (IRIS) assessment is
made publicly available on the Internet (http://www.epa.gov/iris). the respective PPRTVs are
removed from the database.
DISCLAIMERS
The PPRTV document provides toxicity values and information about the adverse effects
of the chemical and the evidence on which the value is based, including the strengths and
limitations of the data. All users are advised to review the information provided in this
document to ensure that the PPRTV used is appropriate for the types of exposures and
circumstances at the site in question and the risk management decision that would be supported
by the risk assessment.
Other U.S. Environmental Protection Agency (EPA) programs or external parties who
may choose to use PPRTVs are advised that Superfund resources will not generally be used to
respond to challenges, if any, of PPRTVs used in a context outside of the Superfund program.
This document has been reviewed in accordance with U.S. EPA policy and approved for
publication. Mention of trade names or commercial products does not constitute endorsement or
recommendation for use.
QUESTIONS REGARDING PPRTVs
Questions regarding the content of this PPRTV assessment should 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).
1 l,2,3,4,5-Pentabromo-6-Chlorocyclohexane

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INTRODUCTION
l,2,3,4,5-Pentabromo-6-chlorocyclohexane (PBCC), CASRN 87-84-3, is a discontinued
flame retardant. The empirical formula for PBCC is CeHeBrsCl (see Figure 1). PBCC is a solid
at room temperature and is expected to have low solubility in water (Dow Chemical Co, 1978).
A table of physicochemical properties for PBCC is provided below (see Table 1).
CI
Br.. J-, .Br
IT
Br "y ""Br
Br
Figure 1. l,2,3,4,5-Pentabromo-6-Chlorocyclohexane Structure
Table 1. Physicochemical Properties for PBCC (CASRN 87-84-3)
Property (unit)
Value
Boiling point (°C)
ND
Melting point (°C)
204a
Specific gravity (water = 1)
ND
Vapor pressure (mm Hg at 25 °C)
1.16 x 10 3 (calculated)13
Solubility in water (mg/L)
1.2-7.0 ±0.8b
Relative vapor density (air = 1)
ND
Molecular weight (g/mol)
513.09a
aLide (2005).
bDow Chemical Co (1978).
ND = no data.
Table 2 provides a summary of available toxicity values for PBCC. The Health Effects
Assessment Summary Tables (HEAST) (U.S. EPA, 2011a) report an oral slope factor (OSF) of
2.3 x 10 2 (mg/kg-day) 1 for PBCC, based on tumors of the intestinal tract in rats exposed via the
diet for 2 years (Dow Chemical Co. 1981).
2 l,2,3,4,5-Pentabromo-6-Chlorocyclohexane

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Table 2. Summary of Available Toxicity Values for PBCC (CASRN 87-84-3)
Source (parameter)ab
Value (applicability)
Notes
Reference
Noncancer
IRIS
NV
NA
U.S. EPA (2016)
HEAST
NV
NA
U.S. EPA (201 la)
DWSHA
NV
NA
U.S. EPA (2012)
ATSDR
NV
NA
ATSDR (2016)
Cal/EPA
NV
NA
Cal/EPA (2014): Cal/EPA
(2016a): Cal/EPA (2016b)
WHO
NV
NA
WHO (2016)
NIOSH
NV
NA
NIOSH (2015)
OSHA
NV
NA
OSHA (2006); OSHA
(2011)
ACGIH
NV
NA
ACGIH (2015)
Cancer
IRIS
NV
NA
U.S. EPA (2016)
HEAST (OSF)
2.3 x 10 2 (mg/kg-d) 1
Route: oral, diet; species, rat;
duration, 2 yr
U.S. EPA (2011a)
DWSHA
NV
NA
U.S. EPA (2012)
NTP
NV
NA
NTP (2014)
IARC
NV
NA
IARC (2015)
Cal/EPA
NV
NA
Cal/EPA (2011): Cal/EPA
(2016a): Cal/EPA (2016b)
ACGIH
NV
NA
ACGIH (2015)
"Sources: ACGIH = American Conference of Governmental Industrial Hygienists; ATSDR = Agency for Toxic
Substances and Disease Registry; Cal/EPA = California Environmental Protection Agency; DWSHA = Drinking
Water Standards and Health Advisories; HEAST = Health Effects Assessment Summary Tables;
IARC = International Agency for Research on Cancer; IRIS = Integrated Risk Information System;
NIOSH = National Institute for Occupational Safety and Health; NTP = National Toxicology Program;
OSHA = Occupational Safety and Health Administration; WHO = World Health Organization.
Parameters: OSF = oral slope factor.
NA = not applicable; NV = not available.
Literature searches were conducted on sources published from 1900 through July 2016
for studies relevant to the derivation of provisional toxicity values for PBCC, CASRN 87-84-3.
Searches were conducted using EPA's Health and Environmental Research Online (HERO)
database of scientific literature. HERO searches the following databases: PubMed, TOXLINE
(including TSCATS1), and Web of Science. The following databases were searched outside of
HERO for health-related values: ACGIH, ATSDR, Cal/EPA, U.S. EPA IRIS, U.S. EPA HEAST,
U.S. EPA Office of Water, U.S. EPA TSCATS2/TSCATS8e, NIOSH, NTP, and OSHA.
3 l,2,3,4,5-Pentabromo-6-Chlorocyclohexane

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REVIEW OF POTENTIALLY RELEVANT DATA
(NONCANCER AND CANCER)
Most of the data pertinent to the toxicity of this compound are from studies of
commercial formulations that contained PBCC as the primary constituent. The nature of the
mixtures and the results of the studies are described below. The available literature includes only
one study (of genotoxicity) in which purified PBCC was tested (although purity of the test
material was not reported). This genotoxicity study (Zeiger et aL 1992) is described in the Other
Studies section (below). Unless otherwise noted, all references to pentabromochlorocyclohexane
and PBCC refer to a commercial mixture of PBCC and related hexahalogenated cyclohexanes.
Commercially prepared formulations of PBCC included SE-651, which was the prototype
formulation (manufactured by an unknown process), and FR-651, which was manufactured via
ultraviolet bromination (Dow Chemical Co, 1980b, c). FR-651 existed in alpha, beta, or gamma
steric configurations. Available toxicological data on these mixtures consist of unpublished
studies on SE-651 as well as studies of various formulations of FR-651 containing
predominantly the alpha isomer (FR-651 A), gamma isomer (FR-651G), and an FR-651 "slurry
dried" formulation. Table 3 compares the compositions of these formulations from available
reports. Toxicological data were also found on formulations labelled FR-651C [Keyes et al.
(1982) as cited in U.S. EPA (1985)1 and FR-65 1P (Dow Chemical Co, 1986); however, the
compositions of these formulations were not provided in the available reports, therefore they are
not included in Table 3.
Table 3. Compositions of Commercial Formulations of PBCC
Compound
Percent in Formulation3
SE-651b
SE-651, Japanese-
produced0
FR-651Gd
FR-65 lAe
FR-651
"Slurry Dried'*
Pentabromochlorocyclohexane
65
85.3
50.3
77.25
70.7
T etrabromodichlorocyclohexane
25
9.7
30.8
19.0
24.2
T ribromotrichlorocyclohexane
10
1.2
14.7
3.5
5.1
Dibromotetrachlorocyclohexane
-
-
4.3
0.25
0.8
Hexabromocyclohexane
-
3.8
(tentatively identified)
-
-
-
"Percentages may not total 100% because of unstated impurities or rounding error. Other mixtures of PBCC exist
(FC-651C, FR-65 IP), but the compositions are unknown (Dow Chemical Co. 19861.
bDow Chemical Co (1980a. 1980b. 1980c. 1980d. 1979a) reported that a detailed analysis of SE-651 was not available
but that the available composition data indicated these percentages.
°Dow Chemical Co (1973).
dDow Chemical Co (1980d).
eDow Chemical Co (1980b. 1980c).
fDow Chemical Co (1975).
4 l,2,3,4,5-Pentabromo-6-Chlorocyclohexane

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Tables 4 A and 4B provide overviews of the relevant noncancer and cancer databases for
PBCC, respectively, and include all potentially relevant, repeated-dose, short-term-, subchronic-,
and chronic-duration studies of mixtures containing this compound. No developmental or
reproductive toxicity studies of PBCC were located in the available literature. Principal studies
are identified in the table in bold font. The phrase "statistical significance," used throughout the
document, indicates ap-walue of < 0.05, unless otherwise noted.
5 l,2,3,4,5-Pentabromo-6-Chlorocyclohexane

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Table 4A. Summary of Potentially Relevant Noncancer Data for PBCC (CASRN 87-84-3)

Number of Male/Female,








Strain, Species, Test








Material3, Study Type,



BMDL/

Reference

Category
Study Duration
Dosimetryb
Critical Effects
NOAELb
BMCLb
LOAELb
(comments)
Notes0
Human
1. Oral (mg/kg-d)
ND
2. Inhalation (mg/m3)
ND
Animal
1. Oral (mg/kg-d)b
Short-term
5 M/5 F, F344 rat,
0, 10, 30,
Increased absolute liver
10
NA
30
TRl, (1987);
NPR

FR-651A, diet, 29 d
100, 300,
weight in female rats



Dow Chemical



1,000




Co f1979b)



ADD: 0, 10,




(Mechanical



30, 100, 300,




problems with



1,000




scale affected








consumption








measurements;








thus, the doses








estimated by








study authors








are uncertain.)

Short-term
5 M/5 F, F344 rat,
0, 10, 30,
Increased absolute liver
10
NA
30
Dow Chemical
NPR

FR-651G, diet, 29 d
100, 300,
weight in female rats



Co (1979a)



1,000








ADD: 0, 10,








30, 100, 300,








1,000






6
l,2,3,4,5-Pentabromo-6-Chlorocyclohexane

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Table 4A. Summary of Potentially Relevant Noncancer Data for PBCC (CASRN 87-84-3)
Category
Number of Male/Female,
Strain, Species, Test
Material3, Study Type,
Study Duration
Dosimetryb
Critical Effects
NOAELb
BMDL/
BMCLb
LOAELb
Reference
(comments)
Notes0
Subchronic
10 M/10 F, unspecified
strain, rat, SE-651, diet,
90 d
0,10,30,
100,300,
1,000
ADD: 0,10,
30,100, 300,
1,000
Increased relative liver
and kidney weights in
both sexes;
centrilobular
degeneration and
necrosis in livers of
males at doses
>100 mg/kg-d
30
DUB (organ
weights
reported as
means only;
lesion
incidences not
reported)
100
Dow Chemical
NPR
PS
Co (1990.
1960)
(Study authors
reported dose
associated with
histopathology
of liver, but not
incidences.)
Subchronic
10 M/10 F, F344 rat,
FR-651A, diet, 91 d
0, 600
ADD: 0, 600
Liver and kidney lesions
in treated males and
females
NDr
DUB (single
dose; dose
uncertain)
600
Dow Chemical
Co (1980b.
1980c)
(Mechanical
problems with
scale affected
consumption
measurements;
thus, the doses
estimated by
study authors is
uncertain.)
NPR
7
l,2,3,4,5-Pentabromo-6-Chlorocyclohexane

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Table 4A. Summary of Potentially Relevant Noncancer Data for PBCC (CASRN 87-84-3)
Category
Number of Male/Female,
Strain, Species, Test
Material3, Study Type,
Study Duration
Dosimetryb
Critical Effects
NOAELb
BMDL/
BMCLb
LOAELb
Reference
(comments)
Notes0
Subchronic
10 M/10 F (treated) and
15 M/15 F (control), CDF
F344 rat, FR-651G, diet,
91 d
0, 10, 30,
100
ADD:0, 10,
30, 100
Liver changes
(hepatocellular swelling
and decreased staining
intensity) in males at
100 mg/kg-d
30
DUB (doses
uncertain; liver
change
incidences are
0% at 30 and
100% at 100)
100
Dow Chemical
Co fl980d)
(Mechanical
problems with
scale affected
consumption
measurements;
thus, the doses
estimated by
authors are
uncertain.)
NPR
Subchronic
10 M/10 F (treated) and
15 M/15 F (control), CDF
F344 rat, FR-651 "slurry
dried", diet, 92 d
0, 90, 260,
780
ADD:0, 90,
260, 780
Liver changes
(hepatocellular swelling
and decreased staining
intensity)
90
DUB (doses
uncertain; liver
change
incidences are
0% at 90 and
100% at 260)
260
Dow Chemical
Co (1980a)
(Mechanical
problems with
scale affected
consumption
measurements;
thus, the doses
estimated by
authors are
uncertain.)
NPR
8
l,2,3,4,5-Pentabromo-6-Chlorocyclohexane

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Table 4A. Summary of Potentially Relevant Noncancer Data for PBCC (CASRN 87-84-3)

Number of Male/Female,








Strain, Species, Test








Material3, Study Type,



BMDL/

Reference

Category
Study Duration
Dosimetryb
Critical Effects
NOAELb
BMCLb
LOAELb
(comments)
Notes0
Chronic
50 M/50 F (treated) and
0,1,15,
Svstemic effects:
Svstemic
20 for
Svstemic
Dow Chemical
NPR, PS

86 M/86 F (control),
50 (M);
Hepatocellular
effects:
intestinal
effects:
Co (1983a.

F344 rat, FR-651A, diet,
hypertrophy and
15 (M) 20 (F)
lesions in male
50 (M)
1983b)
HEDs not

2 yr
0,1,20,
altered staining

rats at
70(F)

calculated


70(F)
properties of

termination;

(histopathology
for



hepatocytes, as well as

45 for

at termination
portal-of-


ADD: 0,1,
increased severity of

intestinal

limited to
entry


15, 50 (M);
age-related,

lesions in

gastrointestinal
effects—



chronic-duration,

female rats

tract)
intestinal


0,1,20,
progressive glomerulo




lesions


70(F)
nephropathy (at








interim sacrifice)(at








highest dose)








Portal-of-entrv effects:
Portal-of-

Portal-of-





Lesions of the large
entrv effects:

entrv





intestine at termination
15 (M) 20 (F)

effects:





(at highest dose)


50 (M)








70 (F)


2. Inhalation (mg/m3)
ND
aSee Table 3 for test material composition information.
bDosimetry: NOAEL, BMDL/BMCL, and LOAEL values are presented as ADDs (mg/kg-day) for oral noncancer effects.
°Notes: PS = principal study; NPR = not peer reviewed.
ADD = adjusted daily dose; BMCL = benchmark concentration lower confidence limit; BMDL = benchmark dose lower confidence limit; DUB = data
unamenable to Benchmark Dose Software; F = female(s); FEL = frank effect level; HED = human equivalent dose; LOAEL = lowest-observed-adverse-effect
level; M = male(s); NA = not applicable; ND = no data; NDr = not determined; NOAEL = no-observed-adverse-effect level.
9
l,2,3,4,5-Pentabromo-6-Chlorocyclohexane

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Table 4B. Summary of Potentially Relevant Cancer Data for PBCC (CASRN 87-84-3)

Number of








Male/Female Species,








Test Material3, Study



BMDL/

Reference

Category
Type, Study Duration
Dosimetryb
Critical Effects
NOAELb
BMCLb
LOAELb
(comments)
Notes0
Human
1. Oral (mg/kg-d)
ND
2. Inhalation (mg/m3)
ND
Animal
1. Oral (mg/kg-d)a
Chronic/
50 M/50 F (treated)
0,1,15,
Increased incidences of
NA
5.9 for
NA
Dow
NPR, PS
carcinogenicity
and 86 M/86 F
50 (M);
polypoid adenomas plus

adenomas or

Chemical
Portal-of-entry

(control), F344 rat,
0,1, 20,
adenocarcinomas of the

adenocar-

Co (1983a)
effect—intestinal

FR-651A, diet, 2 yr
70(F)
large intestine in males

cinomas in


tumors



and females at the high

females






dose





Chronic/
50 M/50 F (treated) and
0, 1, 15,
Increased incidence of
NA
DUB (primary
NA
Keyes et al.
NPR
carcinogenicity
86 M/86 F(control),
50 (M);
polypoid adenomas or

report not

(1982) as
Portal-of-entry

F344 rat, FR-651C,
0, 1, 20,
adenomas plus

available)

cited in
effect-intestinal

diet, 2 yr
70(F)
adenocarcinomas of the



U.S. EPA
tumors



large intestine in high-dose



(1985)




females





2. Inhalation (mg/m3)
ND
aSee Table 3 for test material composition information.
bDosimetry: NOAEL, BMDL/BMCL, and LOAEL values for oral systemic exposures are expressed as HEDs (mg/kg-day); HED = ADD (mg/kg-day) x default
DAF (U.S. EPA. 2011b').
°Notes: PS = principal study; NPR = not peer reviewed.
ADD = adjusted daily dose; BMCL = benchmark concentration lower confidence limit; BMDL = benchmark dose lower confidence limit; BW = body weight;
DAF = dosimetric adjustment factor; DUB = data unamenable to Benchmark Dose Software; HED = human equivalent dose;
LOAEL = lowest-observed-adverse-effect level; NA = not applicable; ND = no data; NOAEL = no-observed-adverse-effect level.
10
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HUMAN STUDIES
Oral Exposures
No studies have been identified.
Inhalation Exposures
No studies have been identified.
ANIMAL STUDIES
Oral Exposures
Overview of Animal Oral Exposure Studies
Potentially relevant data for noncancer effects come from unpublished studies of rats
exposed to SE-651 for 90 days (Dow Chemical Co, 1990, 1960); to FR-651A in the diet for
29 days, 13 weeks, or 2 years (TRI.. 1987; Dow Chemical Co. 1983a, b, 1980b, c, 1979b);
FR-651G in the diet for 29 days or 13 weeks (Dow Chemical Co. 1980a, 1979a); and FR-651
"slurry dried" in the diet for 92 days (Dow Chemical Co. 1980a).
Short-Term-Duration Studies
TRL (1987); Dow Chemical Co (1979b)
Groups of five/sex F344 rats received FR-651 A (77% PBCC) in the diet for 29 days at
doses of 0, 10, 30, 100, 300, or 1,000 mg/kg-day FR-651 A. The study evaluated clinical signs,
body weight, serum chemistry, liver and kidney weights, and gross necropsy. No deaths nor
clinical signs of toxicity were reported. Isolated occurrences of body-weight aberrations in
individual treated females were reported, which the study authors suggested may have been due
to a malfunction in the weighing system. Body weights of treated males did not differ from
controls. A statistically significant decrease in blood urea nitrogen (BUN) was observed in
females given 1,000 mg/kg-day, and a statistically significant decrease in alanine
aminotransferase (ALT) occurred in males exposed to 300 or 1,000 mg/kg-day (see Table B-l);
however, the toxicological significance of the decreases in BUN and ALT is uncertain. There
were no treatment-related gross necropsy findings. Statistically significant increases in absolute
and relative liver weights were observed in males (21 and 19%, respectively) and females
(26 and 11%, respectively) treated with 1,000 mg/kg-day (see Table B-l). In addition,
biologically significant elevations of absolute liver weight (>10%) were also observed in female
rats exposed to 30 or 300 mg/kg-day. Considering that biologically significant increases in
absolute liver weight started at 30 mg/kg-day in female rats, a lowest-observed-adverse-effect
level (LOAEL) of 30 mg/kg-day is identified. The no-observed-adverse-effect level (NOAEL) is
10 mg/kg-day.
Dow Chemical Co (1979a)
Groups of F344 rats five/sex received FR-651G (50.3% PBCC) in the diet for 29 days at
doses of 0, 10, 30, 100, 300, or 1,000 mg/kg-day FR-651G. Evaluations and statistical analyses
were the same as in the FR-651 A study (TRL. 1987; Dow Chemical Co. 1979b). except that food
consumption was also measured. No deaths nor clinical signs of toxicity were reported. In
males exposed to 1,000 mg/kg-day, body weight was statistically significantly decreased from
Day 12 onward; terminal body weight was 21% lower than in controls. A statistically significant
decrease in ALT was seen in males exposed to >300 mg/kg-day and in females exposed to
100 and 1,000 mg/kg-day (see Table B-2), while alkaline phosphatase (ALP) was statistically
significantly decreased in females at >100 mg/kg-day and in males at all treatment doses except
100 mg/kg-day. The BUN was not altered in males at any dose, but BUN was statistically
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significantly reduced at >30 mg/kg-day in females. However, the toxicological significance of
decreases in BUN and the two liver enzymes is uncertain. As shown in Table B-2, absolute and
relative liver and kidney weights in male rats were significantly (statistically and/or biologically)
increased at doses >300 mg/kg-day (>20% higher than controls). In female rats, absolute liver
weights were significantly (statistically and/or biologically) increased (>10% higher than
controls) at doses >30 mg/kg-day, while relative liver weights were statistically significantly
increased at doses >100 mg/kg-day. Absolute kidney weights in female rats were biologically
significantly increased (>16% higher than controls) at doses >100 mg/kg-day, while relative
kidney weights were statistically significantly increased (12% higher than controls) at a dose of
1,000 mg/kg-day. Livers appeared darkened in 5/5 males and in 4/5 females at 1,000 mg/kg-day;
4/5 males exposed to 300 mg/kg-day also exhibited this effect (see Table B-2). A dose-related
increase in the incidence of pale appearance of kidneys was reported in males exposed to
>100 mg/kg-day (as shown in Table B-2, incidences were 2/5, 5/5, and 5/5 at the top three doses,
while this effect was not observed in any control or lower dose animals). A LOAEL of
30 mg/kg-day is identified for this study based on a significant increase in absolute liver weights
in females. The NOAEL is 10 mg/kg-day.
Subchronic-Duration Studies
Dow Chemical Co (1990, 1960)
SE-651was administered to groups of 10 male and 10 female rats (strain not specified) in
the diet for 90 days (Dow Chemical Co, 1990, 1960). Although this report did not include the
chemical composition of SE-651, a composition of 65% pentabromochlorocyclohexane,
25% tetrabromodichlorocyclohexane, and 10% tribromotrichlorocyclohexane has been ascribed
to this formulation in other reports (Dow Chemical Co. 1980b. c). Dietary concentrations were
reported as 0, 0.01, 0.03, 0.1, 0.3, and 1.0% pentabromochlorocyclohexane; the study authors
estimated the doses as 0, 10, 30, 100, 300, and 1,000 mg/kg-day SE-651. The animals were
examined "frequently" for clinical signs of toxicity. Food consumption was recorded for the first
month (frequency not reported), and body weights were measured twice weekly for the first
month and then weekly thereafter. Blood was collected from five females/group in the control
group and the two highest dose groups for analysis of hematocrit (Hct), hemoglobin (Hb), and
total and differential white blood cell (WBC) counts. The animals were sacrificed at study
termination or when moribund. At sacrifice, the lungs, heart, liver, kidneys, spleen, and testes
were weighed, and together with the pancreas and adrenal glands, examined microscopically.
There were no treatment-related effects on survival, clinical appearance, food
consumption, or hematology at any dose (Dow Chemical Co. 1990, 1960). Male rats exhibited a
statistically significant reduction in body weight (12% less than controls at termination;
see Table B-3) at 1,000 mg/kg-day. No statistically or biologically significant reductions in body
weight were observed in females or lower dose males. Relative liver weights (see Table B-3)
were statistically significantly increased at doses >100 mg/kg-day in males (>7% increase over
controls) and at doses >300 mg/kg-day in females (>13% increase over controls). As shown in
Table B-3, relative kidney weights were also statistically significantly increased at all doses
except 30 mg/kg-day in males (>10% increase over controls) and at doses >300 mg/kg-day in
females (>18% increase over controls). Absolute organ weights were not reported.
Histopathology findings were noted in the liver and kidneys of both sexes; however, incidences
of lesions were not reported. The study authors noted that male rats exposed to >100 mg/kg-day
exhibited centrilobular granular degeneration and necrosis, and that females exposed to
>300 mg/kg-day exhibited bile duct epithelium proliferation, round cell infiltration periportally,
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and fatty degeneration in the mid-zonal area of the liver. Fatty degeneration was also noted in
the livers of male rats at 1,000 mg/kg-day. Kidney lesions consisted of interstitial and tubular
nephritis at doses >300 mg/kg-day in both sexes, and hyaline casts (in males) or marked
hydronephrosis (in females) at 1,000 mg/kg-day. A LOAEL of 100 mg/kg-day is identified for
increased relative liver and kidney weights in male rats, as well as centrilobular degeneration and
necrosis of the liver in males. The NOAEL is 30 mg/kg-day.
Dow Chemical Co (1980b, 1980c)
Groups of 10 CDF F344 rats/sex were fed FR-651A in the diet at target doses of 0 or
600 mg/kg-day FR-651 A for 13 weeks (Dow Chemical Co. 1980b. c). Analysis of the test
material indicated the composition shown in Table 5.
Table 5. Composition of FR-651A Used in Dow Chemical Co (1980b, 1980c)
Compound
Percent Composition
Percent Alpha Isomer
Pentabromochlorocyclohexane
77.25
100
T etrabromodichlorocyclohexane
19.0
99.3
T ribromotrichlorocyclohexane
3.5
97.3
Dibromotetrachlorocyclohexane
0.25
NR
NR = not reported.
The test material was shown to be stable in the diet for at least 1 week, so diets were
prepared weekly. Twice-weekly observations for clinical signs of toxicity were made, and body
weight and food consumption were measured weekly. Blood samples were collected from
five animals/sex/dose on Day 26, and from all animals at sacrifice, and were analyzed for BUN,
ALT, and ALP. In addition, blood samples collected on Day 85 were analyzed for Hct, Hb, red
blood cells (RBCs), and total and differential WBC counts. Urine was collected on Day 85 for
analysis of specific gravity, pH, sugar, protein, ketones, bilirubin, and occult blood. Prior to
sacrifice, the rats were subjected to ocular exams. At necropsy, the brain, heart, liver, kidneys,
and testes were weighed. Additionally, most tissues (>30, including those that were weighed as
well as the gastrointestinal tract and ovaries) were examined microscopically.
There were no deaths nor clinical signs of toxicity among the rats (Dow Chemical Co.
1980b, c). Treated males exhibited higher body weights than controls, with correspondingly
higher food consumption rates after the fourth week on study, while body weights of treated
females did not differ from controls (see Table B-4). The authors noted that "recurrent
mechanical weighing problems were encountered during the study that resulted in numerous
errant values." Thus, the food consumption values were examined visually and outlier values
were omitted prior to statistical analysis. Whether these mechanical problems also affected
body- and organ-weight measurements is uncertain because the study authors did not specifically
address this question. At termination, the treated males' mean body weight was 11% higher
(p < 0.05) than that of controls. Clinical chemistry findings in treated males and females
consisted of decreases in BUN, ALP, and/or ALT (see Table B-4), but only the BUN in females
and the ALP in males reached statistical significance. The toxicological significance of
decreases in these parameters is uncertain. The absolute liver and kidney weights were higher in
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treated animals (23 and 18%, respectively, in males; 17 and 10%, respectively, in females) than
in controls; in addition, the relative liver and kidney weights were increased in males (10 and
6%, respectively), and relative liver weight was increased in females (12%). As shown in
Table B-4, all treated males and females exhibited liver lesions (hepatocellular hypertrophy and
decreased staining intensity of cytoplasm) that the study authors considered to be "very slight" in
severity. In addition, 7/10 males exhibited "slight" hepatocellular necrosis. Kidney lesions,
consisting of focal tubular degeneration and inflammation, were seen in 9/10 tested males (but
not in females or controls). The only dose tested in this study, 600 mg/kg-day, is a LOAEL for
liver lesions in males and females, as well as for kidney lesions in males. A NOAEL could not
be identified. The effect level in this study is uncertain; as noted earlier, mechanical problems
affecting food consumption measurements were reported, rendering the dose estimated by the
authors uncertain.
Dow Chemical Co (1980d)
Dow Chemical Co (1980d) exposed groups of 10 CDF F344 rats/sex (15/sex controls) to
FR-651G in the diet at target doses of 0, 10, 30, or 100 mg/kg-day FR-651G for 13 weeks.
Analysis of the test material indicated the composition shown in Table 6.
Table 6. Analysis of FR-651G Used in Dow Chemical Co (I980d)
Compound
Percent Composition
Percent Gamma Isomer
Pentabromochlorocyclohexane
50.3
55.9
T etrabromodichlorocyclohexane
30.8
67.9
T ribromotrichlorocyclohexane
14.7
57.1
Dibromotetrachlorocyclohexane
4.3
53.5
"Percent composition: Column totals over 100.0 due to rounding.
The protocol of the Dow Chemical Co O980d) study of FR-651G was the same as
described above for Dow Chemical Co (1980b. 1980c). with minor alterations. Specifically,
15 controls/sex were used (instead of 10/sex); blood samples for hematology were collected from
7 rats/sex/dose (instead of 5) on Day 84; and comprehensive histopathology examinations were
limited to the control and high-dose groups. The liver was examined microscopically in all
animals; in addition, reproductive organs (ovaries and uterus) of 10 females in the 30-mg/kg-day
group were examined.
There were no deaths, signs of systemic toxicity, or treatment-related ocular effects
among the rats following pathologic examination in the Dow Chemical Co (1980d) study. The
study authors noted that mechanical malfunctions were experienced with the weighing apparatus
that affected body weight and food consumption measurements, and reported that the apparent
differences between treated and control animals were not attributable to treatment because the
differences reflected implausible measurements (e.g., a 136-g weight gain in 2 weeks). It is
possible these malfunctions also affected the organ-weight measurements. Decreases in BUN,
serum ALT, and serum ALP were seen in both sexes of rat; however, the toxicological
significance is uncertain. No treatment-related hematological changes were observed at any dose
or in either sex. Urine specific gravity was significantly decreased (<1%) in high-dose males
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compared with controls, but there were no other urinalysis findings. Increases in absolute and
relative liver weight, observed in both sexes, were not biologically significant (<10%), but the
increase in relative liver weight of high-dose females was statistically significant
(see Table B-5); however, the mechanical malfunctions with weight measurements (as noted by
the study authors) limit the confidence in organ-weight measurements. Significant
histopathology findings were restricted to the liver, and consisted of statistically significant
hepatocellular swelling and decreased staining intensity in the centrilobular or central and
mid-zonal portions of the liver in 10/10 high-dose males and a statistically nonsignificant
increase (3/10) in high-dose females (see Table B-5). One high-dose male also exhibited very
slight focal hepatocellular necrosis and inflammation. None of the other organs showed
dose-related effects. Based on the liver lesions, a LOAEL of 100 mg/kg-day is identified for this
study; the NOAEL is 30 mg/kg-day. The effect levels in this study are uncertain because
mechanical problems affecting food consumption and body-weight measurements were reported,
rendering the doses estimated by the study authors uncertain.
Dow Chemical Co (1980a)
Dow Chemical Co (1980a) exposed groups of 10 CDF F344 rats/sex (15/sex controls) to
FR-651 "slurry dried" in the diet for 92 days. Due to an error in preparation of the premix used
in the study (discovered after the study was completed), dietary concentrations during the last
month of the study were approximately twice the levels used in the first 2 months. The study
authors estimated time-weighted average (TWA) doses of 0, 90, 260, or 780 mg/kg-day FR-651
for 92 days. In the available copy of the report, the composition of the test material was
redacted; a handwritten sheet in the Dow Chemical Co (1975) Toxic Substances Control Act
(TSCA) submission indicated the FR-651 "slurry dried" composition shown in Table 7.
Table 7. Composition of FR-651 "Slurry Dried"
Compound
Percent Composition
Pentabromochlorocyclohexane
70.7
T etrabromodichlorocyclohexane
24.2
T ribromotrichlorocyclohexane
5.1
Dibromotetrachlorocyclohexane
0
The Dow Chemical Co (1980a) study of FR-651 "slurry dried" was conducted under the
same protocol as (Dow Chemical Co. 1980b. c), with minor alterations. Specifically,
15 controls/sex were used (instead of 10/sex); blood samples for hematology were collected from
7 rats/sex/dose (instead of 5) on Day 84; and comprehensive histopathology examinations were
limited to the controls (10/sex) and high-dose groups. The liver, kidneys, and brain were
examined microscopically in all animals.
No rats died, and no signs of toxicity were noted (Dow Chemical Co. 1980a).
Statistically significantly decreased terminal body weight (see Table B-6) was seen in high-dose
males and females (17 and 8% less than controls, respectively). Decreased food consumption
was also reported in males (but not females) at this dose during the final month of the study
when test material concentrations were doubled (see Table B-6). The study authors noted
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"recurrent" mechanical problems with the weighing apparatus. While the authors' discussion
pertained to food consumption values, it is possible other weight measures (body and organ
weights) were also affected by the malfunctions. Serum chemistry parameters (ALT, BUN, and
ALP) were decreased in treated males and females (see Table B-6), but the toxicological
significance of these declines is uncertain. Significant hematology findings consisted of
increased Hct and Hb in high-dose males only (increases were 3 and 6%, respectively, compared
with controls). However, the study authors noted that the Hct value was skewed by an aberrant
value in a single animal, and the Hb values were within the normal range for this strain of rat.
Urinalysis findings were unremarkable. Relative liver weights were increased (>10%) in all
male treatment groups and in females exposed to 260 or 780 mg/kg-day; absolute liver weights
were increased (>10%) in males exposed to 260 mg/kg-day and in females exposed to 260 or
780 mg/kg-day (see Table B-6). Other organ-weight changes, including increased relative (but
not absolute) kidney weights and decreased absolute brain and heart weights (data not shown),
were attributed to lower fasted body weights in the affected dose groups. All animals of the
260- and 780-mg/kg-day dose groups exhibited liver changes consisting of very slight or
slight-to-moderate hepatocellular hypertrophy and altered appearance and staining intensity in
the central and mid-zonal areas of the cytoplasm (homogenous eosinophilia) is evident in males
dosed with 780 mg/kg-day (see incidences in Table B-6). A LOAEL of 260 mg/kg-day is
identified based on liver histopathology in males and females; the NOAEL is 90 mg/kg-day.
Statistically significant increases were observed in relative, but not absolute, liver weight in
males at all doses. As with the other subchronic-duration studies conducted by this laboratory,
the effect levels in this study are uncertain due to mechanical problems affecting food
consumption measurements, thus rendering the doses estimated by the authors uncertain.
Chronic-Duration Studies
Dow Chemical Co (1983a. 1983b)
In the study by (Dow Chemical Co, 1983a, b), FR-651A was administered in the diet to
groups of 50 male and 50 female F344 rats for 2 years. Dietary concentrations were formulated
to yield daily doses of 0, 1, 15, or 50 mg/kg-day FR-651A in males and 0, 1, 20, or,
70 mg/kg-day FR-651A in females. Stability tests indicated that the material was stable in the
dietary mixture for up to 30 days. The test material exhibited the composition shown in Table 8.
Table 8. Analysis of FR-651A in 2-vear Study by Dow Chemical Co (1983a)
Compound
Percent Composition
Pentabromochlorocyclohexane
76.5
T etrabromodichlorocyclohexane
19.5
T ribromotrichlorocyclohexane
4.0
Dibromotetrachlorocyclohexane
-
Control groups consisted of 86 male and 86 female rats receiving untreated diets.
Additional groups of 15 rats/sex were treated with 0 or 15 mg/kg-day (males) or 0 or
20 mg/kg-day (females) and sacrificed (three/sex) on study Days 10, 30, 45, 90, and 540 for
analysis of bromine levels in serum and in adipose and liver tissue. In addition, satellite groups
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of 10 rats/sex were administered all doses and sacrificed at 1 year for interim evaluations and
histopathology.
All animals were observed twice per week during the first year and daily during the
second year for clinical signs of toxicity. Body weights and food consumption were measured
weekly for the first 3 months on 20 rats/sex/dose (for use in dietary concentration adjustments to
meet target doses) and monthly for all animals (Dow Chemical Co. 1983a. b). Blood samples for
hematology (Hct, Hb, RBC count, and total and differential WBC count) and serum chemistry
(BUN, ALP, and ALT) were collected from 10 rats/sex/dose prior to euthanasia in both the
interim (high-dose and control groups only) and terminal (all dose groups, including
18-20 rats/sex/dose for clinical chemistry) sacrifices. Urine samples were collected from the
same groups and analyzed for specific gravity, pH, protein, glucose, ketones, bilirubin, occult
blood, and urobilinogen. All animals received gross necropsy at death or scheduled sacrifice.
The following organs were weighed: liver, kidneys, brain, heart, and testes. At interim sacrifice,
a comprehensive histopathology examination was performed on all rats of the control and
high-dose groups. Examination for gross lesions and histopathological examination of the liver
were also performed on the low-dose group. At terminal sacrifice, all remaining rats received
histology examination of the oral cavity, tongue, esophagus, stomach, small and large intestines,
and cecum; the study authors indicated that these tissues were selected based on gross necropsy
findings.
Survival to the 2-year study termination was similar in both the control and treated
groups of rats (Dow Chemical Co. 1983a. b). In addition, clinical observations did not indicate
any differences between treated and control rats. Statistically significant decreases in body
weight were observed consistently in male rats exposed to 50 mg/kg-day FR-651A from Day 533
to study termination and in female rats exposed to 70 mg/kg-day during the final 3 months of the
study; these decreases were not accompanied by reductions in food consumption. Terminal body
weights in high-dose males and females were statistically significantly lower than controls, but
the decrements compared with controls were <10% (see Table B-7). No body-weight changes
attributable to treatment were observed in the lower dose groups. Statistically significant serum
chemistry changes (data not shown) were not dose related and not considered to be related to
treatment. Hematology analyses at both the interim and terminal sacrifices showed significant
increases in total WBC in males receiving 50 mg/kg-day, but the differential counts did not
suggest alterations in the proportions of neutrophils or lymphocytes. There were no statistically
significant hematology changes in females (data not shown in Table B-7).
Selected organ weights are shown in Table B-7. At the interim sacrifice, absolute liver
weights were statistically significantly increased (>10% higher than controls) in the male rats
receiving 15 or 50 mg/kg-day; relative liver weight was increased only at the high dose (11%).
Relative liver weight was statistically significantly increased (7-8%) over controls in females
receiving 20 or 70 mg/kg-day at the interim sacrifice, but absolute liver weight was not
significantly different from controls (Dow Chemical Co. 1983a. b). Relative liver weight
changes in the high-dose groups may have been impacted by decreases in body weight in both
males and females in these groups. There were no significant differences in liver weight among
the exposed and control groups at the terminal sacrifice. At the interim sacrifice, histopathology
findings consisted of "very slight" altered tinctorial (staining) properties and "very slight,"
multifocal hepatocellular hypertrophy in high-dose males (see Table B-8), and "slightly"
increased severity of age-related chronic progressive glomerulonephropathy (incidence not
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reported) in high-dose males and females. At terminal sacrifice, the incidences of lesions
(dilatation, hypercellularity, and aggregates of cellular debris) in intestinal crypts of the colon
were significantly (p < 0.05) increased in high-dose males (8/49 vs. 0/84 controls) and females
(11/50 vs. 1/86 controls), as shown in Table B-8. A LOAEL of 50 mg/kg-day in male rats is
identified based on liver and kidney histopathology at the 1-year interim sacrifice and lesions of
the large intestine at termination. TheNOAELis 15 mg/kg-day. The lack of histopathology
examination of the liver at the terminal sacrifice is an important limitation of this study.
The incidences of primary polypoid adenoma and/or adenocarcinoma of the colon
(see Table B-9) were statistically significantly higher in high-dose animals (5/49 males and
9/50 females) compared with controls (1/84 males and 1/86 females) (Dow Chemical Co. 1983a.
b). The tumor incidences were not different from controls at lower doses. As noted above,
histopathology examination at termination was restricted to the gastrointestinal tract, limiting the
confidence in the carcinogenicity information from this study.
Keyes et al. (1982) as reported in U.S. EPA (1985)
U.S. EPA (1985) summarized the results of a chronic-duration dietary study of FR-65 1C
conducted by Keyes et al. (1982). The primary study report was not available for review.
Available information included the study protocol (Dow Chemical Co. 1977). a letter reporting
the preliminary results (Dow Chemical Co. 1981). and a summary of the study reported by U.S.
EPA (1985). The composition of the test material was not characterized in any of the available
literature. FR-651C was administered for 2 years to groups of 50/sex F344 rats in the diet at
concentrations intended to yield doses of 1, 15, or 50 mg/kg-day FR-651C in males and 1, 20, or
70 mg/kg-day FR-651C in females; groups of 86 rats/sex served as controls [Keyes et al. (1982)
as reported in U.S. EPA (1985)1. In addition, satellite groups of 10 rats/sex were administered
all doses and sacrificed at 1 year for interim evaluations and histopathology. All rats were
subjected to necropsy and comprehensive histopathology examination at the end of 2 years.
According to U.S. EPA (1985). there was no difference in survival between controls and treated
animals. The results provided by U.S. EPA (1985) are considered to represent the final results,
as the document cited a more recent report than Dow Chemical Co (1981). The only
treatment-related finding reported by U.S. EPA (1985) was a significant increase in the incidence
of polypoid adenomas of the large intestine in female rats exposed to 70 mg/kg-day;
8/50 females exhibited these tumors, compared with 2/85 controls (see Table B-10). One
additional female exhibited a polypoid adenocarcinoma. The tumor incidence in treated male
groups was not significantly different from controls. A NOAEL and LOAEL cannot be
determined from this study due to the lack of data on non-neoplastic endpoints.
Inhalation Exposures
No studies examining effects of PBCC in animals exposed via inhalation have been
identified.
OTHER DATA (SHORT-TERM TESTS, OTHER EXAMINATIONS)
The genotoxicity database for PBCC is limited to a single study discussed below.
Table 9 provides an overview of other supporting studies on PBCC, which include an acute oral
lethality study, skin and eye irritation tests, and a skin sensitization test. No studies of PBCC
metabolism, toxicokinetics, mechanism, or mode of action have been identified. Data on
bromine levels in the tissues of animals exposed to mixtures containing PBCC are discussed
below.
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Genotoxicity
A single study examining the genotoxicity of PBCC (purity not reported) was identified
in the available literature. Zeiger et al. (1992) reported inconclusive results for this compound in
Ames assays using Salmonella typhimurium strains TA100, TA1535, TA97, and TA98, both
with and without metabolic activation. The tests were hampered by precipitation of the test
material; precipitates were evident at doses >100 [j,g/plate (doses up to 10,000 [j,g/plate PBCC
were tested). Results at lower doses were negative.
Acute Toxicity Studies
The acute oral lethality of FR-651P (composition not reported) administered via a single
gavage dose was estimated to be >5,000 mg/kg FR-651P in male F344 rats and
>2,500 mg/kg FR-65 1P in female F344 rats (Dow Chemical Co. 1986). In the Dow Chemical
Co (1958) study, investigators dosed two rats (strain and sex not specified) with
2,000 mg/kg PBCC (specific mixture not reported) by gavage. No mortality (0/2) was observed
and the authors reported that PBCC caused no skin or eye irritation. The Dow Chemical Co
(1973) study indicated that the acute oral lethality of PBCC (identified as Japanese-produced
SE-65 1) was low, but provided no supporting information. Likewise, Dow Chemical Co (1975)
reported that the LD50 in rats was >2 g/kg for a sample characterized only as
pentabromochlorocyclohexane; no further details were given.
Dow Chemical Co (1959a. 1959b) reported anecdotally that plant personnel handling
SE-651 had experienced eye irritation or "general eye discomfort" and corneal burns; these
findings led to animal testing for skin and eye irritation. No information on exposure conditions
in the plant(s), or other supporting information, was provided. Tests of SE-651 for eye irritation
in the rabbit were equivocal. Dow Chemical Co (1959b) observed that a saturated solution of
SE-651 appeared "discomforting," but concluded that the test material was essentially
nonirritating. Dow Chemical Co (1964) applied several different samples of undiluted SE-65 1 to
rabbit eyes and observed slight conjunctival redness that cleared within 24 hours, and concluded
that the test material may be slightly irritating to the eyes.
Skin irritation tests using SE-651 (also described as FR-651) applied to intact or abraded
skin of rabbits indicated that SE-651 was slightly irritating in a saturated solution in Dowanol
DPM (dipropylene glycol methyl ether), but not irritating in undiluted form (Dow Chemical Co.
1979c. d, 1959b). Dow Chemical Co (1973) reported that regular contact of J apanese-produced
SE-651 with skin would likely induce slight erythema, but the study authors provided no
supporting information.
Dow Chemical Co (1979c. 1979d) reported that SE-651 (also described as FR-651) was a
potential skin sensitizer based on erythema seen in male guinea pigs treated with SE-651 in
Dowanol DPM: Tween 80 (9:1); however, other details of the methods used were not reported.
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Table 9. Other Studies
Test
Materials and Methods
Results
Conclusions
References
Human studies
ND
Animal toxicity studies
Acute studies
FR-651P (composition not reported)
administered as a 25% suspension in
corn oil via single gavage dose to
three male and three female F344 rats.
Mortality, clinical signs, and body
weights were monitored during a 14-d
post-treatment observation period.
0/3 male rats died at 5,000 mg/kg;
0/3 female rats died at 2,500 mg/kg.
Clinical signs were limited to diarrhea.
One male rat was lethargic with palpebral
closure.
Oral LD50 of FR-65 IP may be
>5,000 mg/kg in male rats and
>2,500 mg/kg in female rats;
limited basis to draw conclusion.
Dow Chemical Co
(1986)
Acute studies
Test material, characterized as
pentabromochlorocyclohexane, was
administered orally as 10% solution in
corn oil to two rats.
0/2 rats died at 2,000 mg/kg. Liver
damage (no further details) was observed
at autopsy.
Inadequate information to draw
a conclusion.
Dow Chemical Co
(1958)
Acute studies
A single dose of test material,
characterized as PBCC, was
administered orally in corn oil to rats by
gavage. PBCC was also applied to the
eyes and skin of rabbits.
No mortality at the highest dose
(2,000 mg/kg); slight effect on kidneys
(pale color and edematous).
PBCC may be slightly irritating to eyes;
no evidence of skin irritation.
Oral LD50 may be
>2,000 mg/kg. PBCC may be
slightly irritating to the eyes.
PBCC not irritating to rabbit
skin but may be irritating to
humans after prolonged contact.
Dow Chemical Co
(1975. 1958)
Acute studies
other than
oral/inhalation
SE-651 applied to rabbit eye as powder
or as saturated solution in propylene
glycol.
The study authors reported that saturated
solution appeared "discomforting" but
conjunctivae and corneas were
undisturbed.
SE-651 in solution is not
considered an eye irritant.
Dow Chemical Co
(1959b)
Acute studies
other than
oral/inhalation
Several different samples of undiluted
SE-651 applied to rabbit eyes.
Very slight to slight conjunctival redness
observed; eyes cleared in 24 hr.
Undiluted SE-651 may be
slightly irritating to the eyes.
Dow Chemical Co
(1964)
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Table 9. Other Studies
Test
Materials and Methods
Results
Conclusions
References
Acute studies
other than
oral/inhalation
"Fire retardant for styrofoam" (80%
PBCC with other ingredients) applied
daily for 3 or 10 d to intact and abraded
skin of rabbits (ear or belly), undiluted
or as saturated solution in
Dowanol DPM.
When applied undiluted, no irritation
occurred. When applied in solution to
either intact or abraded skin, slight
hyperemia and slight exfoliation observed;
skin normal at 14 d.
Test material in undiluted form
is considered nonirritating to
skin; in solution, it is slightly
irritating to skin.
Dow Chemical Co
(1959b)
Acute studies
other than
oral/inhalation
Several different samples of wetted
SE-651 applied daily for 3 or 10 d to
intact and abraded skin of rabbits (ear or
belly), undiluted.
No sample produced more than slight
irritation to intact skin, observed as
redness, exfoliation, and occasional
swelling. Repeated exposure of abraded
skin to some samples resulted in slight
skin burns.
SE-651 is slightly irritating to
intact skin, and may cause burns
to abraded skin.
Dow Chemical Co
(1964)
Acute studies
other than
oral/inhalation
SE-651 (Japanese-produced, 85.3%
PBCC) tested for eye and skin irritation;
methodological details not reported.
Test material characterized as essentially
nonirritant to eye, and regular contact with
skin likely to induce slight erythema. No
details provided.
Inadequate information to draw
a conclusion.
Dow Chemical Co
(1973)
Acute studies
other than
oral/inhalation
FR-651 applied repeatedly to skin of
male New Zealand albino rabbits. No
further details of methods provided.
Authors reported no perceptible primary
irritation.
FR-651 is not considered a skin
irritant.
Dow Chemical Co
(1979c. 1979d)
Acute studies
other than
oral/inhalation
FR-651 applied as 10% solution in
Dowanol DPM: Tween 80 (9:1) to skin
of 10 male Hartley guinea pigs to test
skin sensitization. No further details of
methods provided.
Authors reported very slight to moderate
redness in 8/10 guinea pigs. No further
details were provided.
FR-651 is considered a potential
skin sensitizer.
Dow Chemical Co
(1979c. 1979d)
ND = no data
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Metabolism/Toxicokinetic Studies
No studies examining the toxicokinetic behavior of PBCC in humans or animals have
been identified.
In the subchronic-duration studies of FR-651A, FR-651G, and FR-651 "slurry dried"
described above (Dow Chemical Co. 1980a. b, c), bromine content of the adipose tissue, liver,
and kidney of treated and control rats was measured at termination. In all three studies,
increased bromine levels were detected in treated animals relative to controls. Bromine
concentrations were higher in the kidney than liver or adipose (kidney > liver > adipose tissue).
Concentrations increased across dose groups in a dose-related manner. No sex differences in
bromine concentrations were evident. The authors estimated that about 1-2% of the total
bromine ingested was in these tissues at termination (Dow Chemical Co. 1980a. b, c).
In the chronic-duration toxicity study of FR-65 1A described above (Dow Chemical Co.
1983a. b), groups of three/sex of the control and mid-dose rats (15 mg/kg-day FR-651 A in males
and 20 mg/kg-day FR-651 A in females) were sacrificed for measurement of bromine in the
adipose tissue, liver, and serum on Days 10, 30, 45, 90, 365, 540, and 734 of the study. Bromine
content in control and high-dose animal tissues was measured at the interim (1 year) and terminal
sacrifices. Increased bromine levels were detected in treated animals (relative to controls) at
every time point. The highest concentrations of bromine were in the serum
(serum > liver > adipose tissue); bromine content of the kidneys was not analyzed in this study.
Table 10 provides information on the bromine concentrations after 10 and 734 days of exposure
to FR-651 A. As the table shows, concentrations in these tissues increased over the 2-year study
period, reaching final concentrations slightly more than twofold higher than the concentrations at
Day 10 of the study.
Table 10. Bromine Concentration in F344 Rats Exposed to FR-651A in the Diet
for 2 Years"

Mean Concentration of Bromine (ppm)
Males
Females
Tissue (days)
10
734
10
734
Serum
93
242
111
276
Liver
31
73
38
74
Adipose
12
24
17
33
'Dow Chemical Co (1983a. 1983b).
DERIVATION OF PROVISIONAL VALUES
Tables 11 and 12 present summaries of noncancer and cancer reference values,
respectively.
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Table 11. Summary of Noncancer Screening Reference Values for PBCC
(CASRN 87-84-3)
Toxicity Type
(units)
Species/Sex
Critical Effect
p-Reference
Value3
POD
Method
PODa
UFc
Principal
Study
Screening
subchronic p-RfD
(mg/kg-d)
Rat (strain not
specified)/female s
Elevated liver weight;
centrilobular
degeneration and
necrosis
2 x 10-2
(as SE-651)
NOAEL
30
HED:
7.3
300
Dow
Chemical
Co (I960)
Screening
chronic p-RfD
(mg/kg-d)
F344 rat/males
Portal-of-entry effect:
Intestinal lesions
(dilatation, hyper-
cellularity, and
aggregates of cellular
debris)
2 x 1(T2
(as FR-651A
)
BMDLio
20
1,000
Dow
Chemical
Co (1983a.
1983b)
Subchronic
p-RfC (mg/m3)
NDr
Chronic p-RfC
(mg/m3)
NDr
aPortal-of-entry effects not converted to HED.
BMDLio = 10% benchmark dose lower confidence limit; HED = human equivalent dose; NDr = not determined;
NOAEL = no-observed-adverse-effect level; p-RfC = provisional reference concentration; p-RfD = provisional
reference dose.
Table 12. Summary of Cancer Screening Reference Values for PBCC (CASRN 87-84-3)
Toxicity Type (units)
Species/Sex
Tumor Type
Cancer Value3
Principal Study
Screening
p-OSF (mg/kg-d) 1
Rat/females
Portal-of-entry effect:
Polypoid adenomas and
adenocarcinomas of the
large intestine
2 x 1CT2 (as FR-651A)
Dow Chemical Co
(1983a. 1983b)
p-IUR (mg/m3)-1
NDr
"Portal-of-entry effects not converted to HED.
NDr = not determined; p-IUR = provisional inhalation unit risk; p-OSF = provisional oral slope factor.
DERIVATION OF ORAL REFERENCE DOSES
There are no in vivo toxicological data on pure PBCC. Information on the oral toxicity
of PBCC is available from several unpublished studies of commercial mixtures containing this
compound. These include two 29-day experiments in rats CTRL. 1987; Dow Chemical Co.
1979a. b), four sub chronic-duration (90-92 day) experiments in rats (Dow Chemical Co. 1990.
1980a. b, c, d, 1960). and two 2-year chronic-duration toxicity and carcinogenicity studies in rats
[Keyes et al. (1982) as cited in U.S. EPA (1985); Dow Chemical Co (1983a. 1983b)l.
The available information is not considered sufficiently reliable for use in deriving
provisional subchronic and chronic reference doses (p-RfDs) for several reasons. First, the
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studies tested mixtures containing between 50.3 and 85.3% PBCC with variable concentrations
of other congeners (see Table 3). Second, the available studies were unpublished and conducted
by the same laboratory, the Dow Chemical Co., using the same species (rat) and strain (F344).
Third, three of the four sub chronic-duration studies (Dow Chemical Co. 1980a. b, c) reported
mechanical problems with the weighing apparatus, which the study authors indicated could have
affected food consumption measurements (and in one case, body-weight measurements). Thus,
the doses and body weights estimated by the authors are uncertain. Fourth, two chronic-duration
studies are available, but the primary report for the chronic-duration study of FR-651C mixture is
not available for review, and the chronic-duration study of the FR-651A mixture did not include
a comprehensive histopathology examination at termination. Importantly, the tissues examined
microscopically at termination in the study of FR-651A did not include the liver, which was
identified as a primary target tissue in all of the short-term-, subchronic- and chronic-duration
studies (Dow Chemical Co. 1990. 1983a. b, 1980a. b, c, d, 1979a. b, 1960) of the various
formulations and at the interim sacrifice of the chronic-duration study of FR-651A. Although
the liver weights of PBCC-treated rats were statistically (p < 0.05) and biologically significantly
elevated (10-13% at the two highest doses) at the 1-year interim sacrifice, the rat liver weights
were not statistically or biologically significantly elevated at the 2-year termination. Because the
liverweight increases appeared to resolve over time, they are not considered further as a potential
point of departure (POD) for chronic-duration exposures.
Due to the uncertainties in the available data for PBCC, subchronic and chronic p-RfDs
were not derived. Instead, screening subchronic and chronic p-RfDs are derived in Appendix A.
DERIVATION OF INHALATION REFERENCE CONCENTRATIONS
No studies of humans or animals exposed to PBCC (alone or as a mixture) via inhalation
have been identified in the available literature, precluding derivation of provisional inhalation
reference concentrations (p-RfCs).
CANCER WEIGHT-OF-EVIDENCE DESCRIPTOR
Table 13 provides the cancer weight-of-evidence (WOE) descriptor for PBCC. Under the
2005 Guidelines for Carcinogen Risk Assessment (U.S. EPA. 2005). PBCC exhibits "Suggestive
Evidence of Carcinogenic Potential" based on evidence of carcinogenicity in orally treated male
and female rats. This descriptor is based on the occurrence of adenomas and adenocarcinomas of
the large intestines in male and female F344 rats at the highest dose (FR-651 A) tested in Dow
Chemical Co (1983a, 1983b) and also on the occurrence of adenomas and adenocarcinomas of
the large intestines in female F344 rats at the highest dose of a related PBCC mixture (FR-651C)
[Keyes et al. (1982) as cited in U.S. EPA (1985)1.
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Table 13. Cancer WOE Descriptor for PBCC
Possible WOE Descriptor
Designation
Route of Entry
(oral, inhalation,
or both)
Comments
"Carcinogenic to Humans "
NS
NA
There are no data to support this conclusion.
"Likely to Be Carcinogenic to
Humans "
NS
NA
There are no suitable animal studies to support
this conclusion. Tumors observed in only one
strain (F344) of one species (rat), in only one
organ, and a dose response was not
demonstrated.
"Suggestive Evidence of
Carcinogenic Potential"
Selected
Oral
Two chronic-duration studies of F344 rats
orally exposed to mixtures in which PBCC
was the primary constituent have shown
increased incidences of intestinal tumors
IKeves et al. (1982) as cited in U.S. EPA
(1985): Dow C hemical Co (1983a. 1983M1.
"Inadequate Information to
Assess Carcinogenic Potential"
NS
NA
Available studies are sufficient to assess
carcinogenic potential.
"Not Likely to Be Carcinogenic
to Humans "
NS
NA
There are no suitable animal studies to support
this conclusion.
NA = not applicable; NS = not selected; WOE = weight of evidence.
DERIVATION OF PROVISIONAL CANCER POTENCY VALUES
Data on the oral carcinogenicity of PBCC are available in two 2-year carcinogenicity
studies of mixtures in rats [Keyes et al. (1982) as cited in U.S. EPA (1985); Dow Chemical Co
(1983a. 1983b}]. The available information is not considered sufficiently reliable for use in
deriving provisional cancer potency values for several reasons. First, both of the available
studies are unpublished and conducted by or for the Dow Chemical Co. Second, the primary
report for the carcinogenicity study of FR-651C is not available for review, and the
carcinogenicity study of FR-651A did not include comprehensive histopathology examination at
termination, based in part on the findings of the study of FR-651C. The tissues examined after
2 years in the study of FR-651A did not include the liver, which was identified as the primary
target tissue in sub chronic-duration studies of the various formulations and at the 1-year interim
sacrifice in the 2-year study of FR-651A (Dow Chemical Co. 1983a. b). The presence of other
tumors associated with PBCC exposure cannot be determined in this study because the
histopathological examination at the 2-year termination was limited to the gastrointestinal tract.
Due to the uncertainties in the available data for PBCC, provisional cancer potency
values were not derived; however, a "screening value" for oral cancer potency of the FR-651A
PBCC mixture is provided in Appendix A.
No carcinogenicity studies of humans or animals exposed to PBCC (alone or as a
mixture) via inhalation have been identified in the available literature, precluding derivation of
inhalation cancer potency values.
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APPENDIX A. SCREENING PROVISIONAL VALUES
For the reasons noted in the main document, provisional toxicity values for
l,2,3,4,5-Pentabromo-6-chlorocyclohexane (PBCC) could not be derived. However, information
is available for this chemical, which although insufficient to support derivation of a provisional
toxicity value under current guidelines, may be of limited use to risk assessors. In such cases,
the Superfund Health Risk Technical Support Center summarizes available information in an
appendix and develops a "screening value." Appendices receive the same level of internal and
external scientific peer review as the main documents to ensure their appropriateness within the
limitations detailed in the document. Users of screening toxicity values in an appendix to a
provisional peer-review toxicity value (PPRTV) assessment should understand that there is
considerably more uncertainty associated with the derivation of an appendix screening toxicity
value than for a value presented in the body of the assessment. Questions or concerns about the
appropriate use of screening values should be directed to the Superfund Heath Risk Technical
Support Center.
DERIVATION OF SCREENING ORAL REFERENCE DOSES
The screening toxicity values derived in this document apply only to the specific
mixtures of PBCC tested in the principal studies (i.e., SE-651 for the screening subchronic
provisional reference dose [p-RfD] and FR-651A for the screening chronic p-RfD and screening
provisional oral slope factor [p-OSF]). Dose adjustment may be necessary before extrapolating
to other mixtures of PBCCs.
The 90-day rat study of PBCC (SE-651) conducted by the Dow Chemical Co (1960) is
selected as the principal study for derivation of a screening subchronic p-RfD. Of the four
available subchronic-duration studies available (see Table 4A), only the Dow Chemical Co
(1960) study did not report malfunctions in the weighing system, which rendered body weights
and food consumption estimates unreliable. In the principal study, male and female F344 rats
(10/sex/dose) were dosed for 90 days with 0, 10, 30, 100, 300, or 1,000 mg/kg-day (human
equivalent doses [HEDs]: 0, 2.4, 7.2, 24.4, 73.3, or 244.5 mg/kg-day). Relative liver and kidney
weights were elevated at statistically significant levels in males and females at 300 mg
PCBB/kg-day and higher. Histopathological examination confirmed the elevated organ weights
seen at higher doses and showed central lobular granular degeneration and necrosis in the liver
and interstitial and tubular nephritis of the kidney at 100 mg/kg-day. The organ-weight results
were reported as group means without a standard deviation (SD) and the histopathology results
were qualitatively described without incidence data. As a result, benchmark dose (BMD)
modeling was not possible. A no-observed-adverse-effect level (NOAEL) of 30 mg/kg-day is
based on male histopathological liver effects at 100 mg/kg-day which is confirmed by
statistically significantly elevated relative liver weight at 300 mg/kg-day in the absence of
significant body weight (BW) reduction. Selection of liver alterations as the critical effect is
supported by the Dow Chemical Co. that consistently found the liver to be a target organ in
short-term-, subchronic-, and chronic-duration exposures to PBCC mixtures.
The NOAEL of 30 mg/kg-day based on liver effects in male rats identified in Dow
Chemical Co (1960) is the selected point of departure (POD) for derivation of the screening
subchronic p-RfD. In Recommended Use of Body Weight 3/4 as the Default Method in
Derivation of the Oral Reference Dose (U.S. EPA. 201 lb), the Agency endorses a hierarchy of
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approaches to derive human equivalent oral exposures from data from laboratory animal species,
with the preferred approach being physiologically based toxicokinetic modeling. Other
approaches may include using some chemical specific information, without a complete
physiologically based toxicokinetic model. In lieu of chemical specific models or data to inform
the derivation of human equivalent oral exposures, EPA endorses body weight scaling to the
3/4 power (i.e., BW3/4) as a default to extrapolate toxicologically equivalent doses of orally
administered agents from all laboratory animals to humans for the purpose of deriving an RfD
under certain exposure conditions. More specifically, the use of BW3 4 scaling for deriving an
RfD is recommended when the observed effects are associated with the parent compound or a
stable metabolite, but not for portal of entry effect endpoints.
A validated human physiologically based toxicokinetic model for PBCC is not available
for use in extrapolating doses from animals to humans. Furthermore, the selected liver
alterations in male rats are not portal of entry effects. Therefore, scaling by BW3/4 is relevant for
deriving an HED for these effects.
Following U.S. EPA (2011b) guidance, the POD (30 mg/kg-day) from the Dow Chemical
Co (1960) study is converted to an HED through the application of a dosimetric adjustment
factor (DAF)1 derived as follows:
DAF = (BWa1/4 - BWh1/4)
where
DAF = dosimetric adjustment factor
BWa = animal body weight
BWh = human body weight
Using a reference BW„ of 0.25 kg for rats and a reference BWh of 70 kg for humans (U.S.
EPA, 1988). the resulting DAF is 0.24. Applying this DAF to the POD identified in the Dow
Chemical Co (1960) study yields a POD (HED) as follows:
POD (HED) = NOAEL (mg/kg-day) x DAF
= NOAEL (mg/kg-day) x 0.24 = 30 mg/kg-day x 0.24
= 7.2 mg/kg-day
The screening subchronic p-RfD for PBCC (SE-651) is derived as follows:
Screening Subchronic p-RfD = POD (HED) UFc
= 7.2 mg/kg-day -^300
= 2 x 10"2 mg/kg-day
Table A-l summarizes the uncertainty factors for the screening subchronic p-RfD for
mixtures containing PBCC described in this PPRTV document.
4As described in detail in Recommended Use of Body Weight4 as the Default Method in Derivation of the Oral
Reference Dose (U.S. EPA. 201 lb), rate related processes scale across species in a manner related to both the direct
(BW11) and allometric scaling (BW3'4) aspects such that BW3'4 ^ BW1'1 = BW converted to a
DAF = BWa"4 - BWi,1'4.
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Table A-l. Uncertainty Factors for the Screening Subchronic p-RfD for Mixtures
Containing PBCC
UF
Value
Justification
UFa
3
A UFa of 3 (10°5) is applied to account for uncertainty in characterizing the toxicokinetic
or toxicodynamic differences between rats and humans following PBCC exposure. The
toxicokinetic uncertainty has been accounted for by calculation of an HED through
application of a DAF as outlined in the EPA's Recommended Use of Body Weight4 as the
Default Method in Derivation of the Oral Reference Dose (TJ.S. EPA. 2011b).
UFh
10
A UFh of 10 is applied to account for human variability in susceptibility, in the absence of
information to assess toxicokinetic and toxicodynamic variability of PBCC in humans.
UFd
10
A UFd of 10 is applied to account for deficiencies and uncertainties in the database,
specifically the lack of data on reproductive or developmental toxicity and the lack of data
in a second species.
UFl
1
A UFl of 1 is applied because the POD is a NOAEL, not a LOAEL.
UFS
1
A UFS of 1 is applied because the POD comes from a subchronic-duration study of rats.
UFC
300
Composite UF = UFA x UFH x UFD x UFL x UFS.
DAF = dosimetric adjustment factor; HED = human equivalent dose; LOAEL = lowest-observed-adverse-effect
level; NOAEL = no-observed-adverse-effect level; POD = point of departure; UF = uncertainty factor.
Derivation of a Screening Chronic Provisional Reference Dose
The 2-year rat study of PBCC (FR-651A) conducted by Dow Chemical Co (1983a.
1983b) is selected as the principal study for derivation of a screening chronic p-RfD. The
principal study dosed male and female F344 rats (50/sex/dose) with controls of 86 rats/sex for
2 years with one of four doses: 0, 1, 15, or 50 mg/kg-day in males and 0, 1, 20, or 70 mg/kg-day
in females. HEDs for systemic effects are 0, 0.2, 3.7, or 12.2 mg/kg-day in males and 0, 0.2, 4.9,
or 17.1 mg/kg-day in females. As shown in Table 4A, the lowest-observed-adverse-effect level
(LOAEL) of the available studies (50 mg/kg-day in males and 70 mg/kg-day in females) is
identified in the Dow Chemical Co (1983a. 1983b) chronic-duration study of PBCC (FR-65 1 A).
In addition, FR-651A contains the highest proportion of PBCC (77%) among the mixtures with
toxicological data (see Table 3); thus, it provides the best data for screening levels for PBCC.
Finally, no mechanical problems with weight measurements were reported in the
chronic-duration study (Dow Chemical Co, 1983a. b).
Effects seen at the LOAEL in the Dow Chemical Co (1983a. 1983b) included
(1) increased absolute and/or relative liver weight in males and females at the interim (but not
terminal) sacrifice; (2) increased incidences of hepatocellular hypertrophy and altered tinctorial
(staining) properties of hepatocytes in males at the interim sacrifice; (3) increased severity of
age-related chronic progressive glomerulonephropathy in males and females at the interim
sacrifice; and (4) lesions of the large intestine at termination. The incidence of histopathology
findings in the large intestines of male and female rats is selected for BMD modeling to identify
a POD for screening chronic p-RfD derivation. Liver-weight measures are not considered for
use in deriving the screening chronic p-RfD because the liver-weight changes seen at the interim
sacrifice were no longer apparent at the terminal sacrifice.
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Liver histopathology endpoints observed at the interim sacrifice were considered as a
potential POD because the liver is a target organ in all of the studies conducted by the Dow
Chemical Co. rDow Chemical Co (1990. 1983a. 1983b. 1980a. 1980b. 1980c. 1980d. 1979a.
1979b. 1960); Keyes et al. (1982) as cited in U.S. EPA (1985)1. The histopathological
examination (Dow Chemical Co. 1983a. b) reported 34 non-neoplastic liver parameters at the
1-year interim sacrifice (10 rats/sex/dose). Only two parameters, altered multifocal
hepatocellular tinctorial (staining) properties (9/10) and multifocal hepatocellular hypertrophy
(9/10), demonstrated a statistically significant (p < 0.05) dose-related increase above the control
rats. Both effects were observed only in males (0/10 in females) and only at the highest dose
(50 mg/kg-day). These effects were not observed at lower doses or in the control animals (0/10).
The severity of both effects was reported in the study as "very slight." The severity of the
remaining 32 liver parameters was reported to be "slight" or "very slight," and none
demonstrated a statistically significant dose-related trend. The study authors did not conduct a
histopathological exam of the liver at the 2-year terminal sacrifice, but they did conduct a gross
pathological exam of major organ systems and tissues. In the livers, pathologists looked at
22 parameters and reported no dose-related changes. Because of the low severity and the
uncertain toxicological significance of the liver effects reported at the interim histopathological
exam, coupled with the lack of evidence for liver damage in the gross pathological exam, the
liver was not considered suitable as a target organ for deriving a screening chronic p-RfD.
Finally, the incidences of age-related chronic progressive glomerulonephropathy were not
reported, so this endpoint is not considered as the basis for screening p-RfD derivation.
As described in Appendix C, BMD modeling was performed on the incidence of dilation,
hypercellularity, and aggregates of cellular debris in intestinal crypts in male and female rats in
the principal study (Dow Chemical Co. 1983a. b). The lower benchmark dose lower confidence
limit 10% (BMDLio) of 20 mg/kg-day in males was selected as the POD for chronic p-RfD
derivation. The liver histopathology effects (hepatocellular hypertrophy and altered staining
properties of hepatocytes) and intestinal lesions were reported at the same LOAEL
(50 mg/kg-day) in the principal study (Dow Chemical Co. 1983a. b); therefore, it is presumed
that the (BMDLio) of 20 mg/kg-day for histopathological findings in the large intestines is also
protective against any potential liver effects.
The critical effect for the screening chronic p-RfD (intestinal lesions) may represent a
portal-of-entry effect. Because available dosimetric scaling approaches may not be appropriate
for portal-of-entry effects, a dosimetric adjustment of the POD to an HED was not used (U.S.
EPA, 2011b); instead, the default interspecies UF \ of 10 was used to extrapolate from the POD
in animals to the POD in humans.
The screening chronic p-RfD for FR-651A is derived as follows:
Screening Chronic p-RfD =	POD UFc
=	BMDLio UFc
=	20 mg/kg-day ^ 1,000
=	2 x 10"2 mg/kg-day
Table A-2 summarizes the uncertainty factors for the screening chronic p-RfD for
mixtures containing PBCC described in this PPRTV document.
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Table A-2. Uncertainty Factors for the Screening Chronic p-RfD for
Mixtures Containing PBCC
UF
Value
Justification
UFa
10
A UFa of 10 is applied to account for uncertainty associated with extrapolating from
animals to humans in the absence of data with which to perform interspecies dose scaling.
UFh
10
A UFh of 10 is applied to account for human variability in susceptibility, in the absence of
information to assess toxicokinetic and toxicodynamic variability of PBCC in humans.
UFd
10
A UFd of 10 is applied to account for deficiencies and uncertainties in the database,
specifically the lack of data on reproductive or developmental toxicity and the lack of data
in a second species.
UFl
1
A UFl of 1 is applied because the POD is a BMDL, not a LOAEL.
UFS
1
A UFS of 1 is applied because the POD comes from a chronic-duration study of rats.
UFC
1,000
Composite UF = UFA x UFH x UFD x UFL x UFS.
BMDL = benchmark dose lower confidence limite; LOAEL = lowest-observed-adverse-effect level; POD = point
of departure; UF = uncertainty factor.
DERIVATION OF SCREENING PROVISIONAL CANCER POTENCY VALUES
Two studies examined the carcinogenic potential of mixtures containing PBCC
administered orally to rats for 2 years [Keyes et al. (1982) as cited in U.S. EPA (1985); Dow
Chemical Co (1983a. 1983b)l. A detailed report of the design and results was available only for
the Dow Chemical Co (1983a. 1983b) study of FR-651A; results of the Keyes et al. (1982) as
cited in U.S. EPA (1985) study of FR-651C were obtained from secondary sources (U.S. EPA,
1985; Dow Chemical Co. 1981). Both studies used the same doses, and the tumor types seen in
both studies were the same (polypoid adenomas and adenocarcinomas of the intestines).
Statistically significant increases in incidence (in pairwise comparisons) were seen in males and
females exposed to FR-651A and in females exposed to FR-651C. According to information
provided by U.S. EPA (1985), incidences of tumors in females exposed to FR-651C were
slightly lower than the incidences in females exposed to FR-651A at the same doses
(see Tables B-9 and B-10). For this reason and because the full results were only available from
the Dow Chemical Co (1983a, 1983b) study, the cancer data from study of FR-651A were
subjected to BMD modeling, but data from the study of FR-651C were not. Furthermore,
confidence in the principal study is limited because organs and tissues outside of the
gastrointestinal (GI) tract were not examined histopathologically at the terminal sacrifice.
Derivation of a Screening p-OSF
The screening p-OSF for PBCC is based on the incidences of intestinal tumors in female
rats exposed to FR-651A for 2 years (Dow Chemical Co, 1983a, b) and was derived as follows:
Prior to dose-response modeling, doses administered in the study by Dow Chemical Co
(1983a, 1983b) were converted to HEDs according to the equation below:
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Dose (HED) = Dose x (BWa/BWh)14
where:
Dose = average daily animal dose
BWa = TWA rat body weight in study (Dow Chemical Co. 1983a. b)
BWh = 70 kg, reference human body weight (U.S. EPA. 1988)
BMD modeling of the data on incidences of polypoid adenomas and adenocarcinomas of
the intestines in both male and female rats exposed to FR-651A yielded BMDLio (HED)
estimates of 11 and 5.9 mg/kg-day, respectively. The lower BMDLio (HED) of 5.9 mg/kg-day,
obtained from data on female rats, was selected as the POD for calculation of the screening
p-OSF. Because the Dow Chemical Co (1983a. 1983b) study was conducted for the full lifetime
of the rats (2 years), no adjustment for less-than-lifetime observation was necessary.
The screening p-OSF of 2 x 10"2 (mg/kg-day)"1 was derived as follows:
Screening p-OSF = BMR BMDLio (HED)
= 0.1^-5.9 mg/kg-day
= 2 x 10"2 (mg/kg-day)"1
The screening p-OSF should not be used with exposure exceeding the POD
(5.9 mg/kg-day) because at doses higher than this value, the fitted dose-response model better
characterizes the dose-response relationship. Further, the screening p-OSF should not be
extrapolated to PBCC mixtures with compositions differing greatly from that of FR-651A
because there are no data to support such extrapolation.
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APPENDIX B. DATA TABLES
Table B-l. Selected Effects on Male and Female CDF F344 Rats Exposed to FR-651A in
Food for 29 Days"
Endpoint
Exposure Group (mg/kg-d)
0
10
30
100
300
1,000
Males
Number of animals
5
5
5
5
5
5
BUN (mg/100 mL)
18 ± 2b
18 ±3
17 ±2
17 ±2
19 ±2
17 ± 1
Serum ALT (mU/mL)
59 ±4
52 ±6
46 ±4*
55 ± 11
45 ±5*
45 ±3*
Terminal body weight (g)
201 ±24
194 ±34
(-3.5%)
204 ± 18
(1.5%)
207 ±21
(3.0%)
188 ±22
(-6.5%)
206 ± 14
(2.5%)
Absolute liver weight (g)
6.39 ± 1.00
5.85 ±0.88
(-8.5%)
6.61 ±0.85
(3.4%)
7.02 ±0.85
(9.9%)
6.37 ±0.91
(-0.3%)
7.74 ±0.36*
(21.1%)
Relative liver weight (g/100 g)
3.16 ± 0.13
3.03 ±0.13
(-4.1%)
3.23 ±0.18
(2.2%)
3.39 ± 0.11*
(7.3%)
3.38 ± 0.17
(7.0%)
3.77 ±0.19*
(19.3%)
Absolute kidney weight (g)
1.60 ±0.18
1.47 ±0.21
(-8.1%)
1.62 ±0.13
(1.3%)
1.63 ±0.11
(1.9%)
1.52 ±0.12
(-5.0%)
1.57 ±0.12
(-1.9%)
Relative kidney weight (g/100 g)
0.79 ±0.01
0.76 ±0.04
(-3.8%)
0.79 ±0.01
(0%)
0.79 ±0.04
(0%)
0.81 ±0.04
(2.5%)
0.76 ± 0.06
(-3.8%)
Females
Number of animals
5
5
5
5
5
5
BUN (mg/100 mL)
21 ±4
18 ± 1
18 ±2
17 ± 1
18 ±4
16 ±3*
Serum ALT (mU/mL)
49 ±4
40 ±2*
42 ±6
49 ±6
41 ±3
45 ±4
Terminal body weight (g)
124 ±8
129 ±8
(4.0%)
133 ± 11
(7.3%)
133 ±3
(7.3%)
129 ± 13
(4.0%)
140 ±4*
(12.9%)
Absolute liver weight (g)
3.61 ±0.35
3.77 ±0.17
(4.4%)
4.11 ± 0.37
(13.9%)
3.96 ±0.09
(9.7%)
4.01 ±0.49
(11.1%)
4.54 ±0.13*
(25.8%)
Relative liver weight (g/100 g)
2.91 ±0.17
2.92 ±0.14
(0.3%)
3.09 ±0.07
(6.2%)
2.99 ±0.10
(2.7%)
3.11 ± 0.13
(6.9%)
3.24 ±0.09*
(11.3%)
Absolute kidney weight (g)
1.0 ±0.08
1.03 ±0.04
(3.0%)
1.08 ±0.10
(8.0%)
1.10 ±0.04
(10.0%)
1.05 ±0.12
(5.0%)
1.17 ±0.04*
(17.0%)
Relative kidney weight (g/100 g)
0.80 ±0.03
0.80 ±0.03
(0%)
0.81 ±0.04
(1.3%)
0.83 ± 0.02
(3.7%)
0.81 ±0.02
(1.3%)
0.83 ±0.01
(3.7%)
aDow Chemical Co (1979b): TRL (1987).
bMean ± standard deviation.
* Significantly different from control using Dunnett's test (p < 0.05), as reported by study authors.
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Table B-2. Selected Effects on Male and Female CDF F344 Rats Exposed to FR-651G in
Food for 29 Days3
Endpoint
Exposure Group (mg/kg-d)
0
10
30
100
300
1,000
Males
Number of animals per group
5
5
5
5
5
5
Final body weight (g)
243 ± 23b
223 ± 29
(-8.2%)
221 ± 19
(-9.1%)
239 ±38
(-1.6%)
227 ± 17
(-6.6%)
193 ± 14*
(-20.6%)
BUN (mg/100 mL)
18 ± 1
18 ±2
18 ±2
17 ±2
17 ± 1
17 ±2
Serum ALT (mU/mL)
53 ±7
46 ±4
51 ± 9
45 ±4
32 ± 1*
36 ±5*
Serum ALP (mU/mL)
247 ± 25
201 ±22*
210 ±24*
217 ± 19
133±13*
208±15*
Absolute liver weight (g)
6.99 ±0.73
6.31 ±0.80
(-9.7%)
6.64 ±0.79
(-5.0%)
7.37 ± 1.46
(5.4%)
9.11 ±0.68*
(30.3%)
8.04 ±0.89
(15.0%)
Relative liver weight (g/100 g)
3.16 ± 0.16
3.16 ± 0.16
(0%)
3.35 ± 0.15
(6.0%)
3.39 ±0.27
(7.3%)
4.49 ±0.11*
(42.1%)
4.47 ±0.14*
(41.5%)
Absolute kidney weight (g)
1.68 ±0.16
1.63 ±0.22
(7.9%)
1.60 ±0.18
(6.6%)
1.77 ±0.26
(7.9%)
1.84 ±0.15
(19.7%)
1.64 ±0.16
(21.1%)
Relative kidney weight (g/100 g)
0.76 ±0.05
0.82 ±0.03
(7.9%)
0.81 ±0.03
(6.6%)
0.82 ±0.02
(7.9%)
0.91 ±0.01*
(19.7%)
0.92 ±0.05*
(21.1%)
Slight darkened appearance of
liver
o
Di
o
0/5
0/5
0/5
4/5
5/5
Pale appearance of kidneys
Equivocal
0/5
0/5
0/5
2/5
0/5
1/5
Slight
0/5
0/5
0/5
0/5
5/5
4/5
Females
Number of animals per group
5
5
5
5
5
5
Final body weight (g)
140 ±4
141 ± 16
(0.7%)
141 ±5
(0.7%)
154 ± 12
(10.0%)
152 ±11
(8.6%)
137 ± 16
(-2.1%)
BUN (mg/100 mL)
22 ±2
20 ±2
17 ± 1*
16 ±2*
16 ± 1*
15 ± 1*
Serum ALT (mU/mL)
54 ± 12
42 ±2
41 ±4
32 ± 13*
40 ±5
32 ±6*
Serum ALP (mU/mL)
188 ± 16
190 ± 18
176 ± 26
148±18*
138±15*
117 ±18*
Absolute liver weight (g)
3.60 ±0.23
3.78 ±0.46
(5.0%)
3.96 ±0.19
(10.0%)
4.49 ±0.49*
(24.7%)
5.12 ±0.43*
(42.2%)
5.49 ±0.62*
(52.5%)
Relative liver weight (g/100 g)
2.91 ±0.11
3.00 ±0.09
(3.1%)
3.15 ± 0.11
(8.2%)
3.23 ±0.14*
(11.0%)
3.74 ±0.22*
(28.5%)
4.49 ±0.23*
(54.3%)
Absolute kidney weight (g)
1.00 ±0.06
1.06 ±0.12
(9.6%)
1.06 ±0.04
(6.0%)
1.16 ± 0.12
(16.0%)
1.18 ± 0.10
(18.0%)
1.11 ± 0.16
(11.0%)
Relative kidney weight (g/100 g)
0.81 ±0.03
0.84 ±0.03
(3.7%)
0.84 ±0.02
(3.7%)
0.83 ± 0.02
(2.5%)
0.86 ±0.04
(6.2%)
0.91 ±0.04*
(12.3%)
33 1,2,3,4,5 -Pentabromo-6-Chlorocyclohexane

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Table B-2. Selected Effects on Male and Female CDF F344 Rats Exposed to FR-651G in

Food for 29 Days3




Exposure Group (mg/kg-d)
Endpoint
0
10
30
100
300
1,000
Females
Darkened appearance of liver
Equivocal
0/5
0/5
0/5
0/5
2/5
0/5
Slight
0/5
0/5
0/5
1/5
1/5
4/5
Diffuse
0/5
0/5
0/5
0/5
1/5
0/5
"Dow Chemical Co (1979a).
bMean ± standard deviation.
°Number affected/number examined.
* Significantly different from control using Dunnett's test (p < 0.05), as reported by study authors.
Table B-3. Mean Body and Organ Weights of Male and Female Ratsa
Exposed to SE-651 in Food for 90 Daysb
Endpoint
Dose (mg/kg-d)
0
10
30
100
300
1,000
Males
Number of animals
10
9
10
10
10
10
Average body weight (g)
321
301
(-6.2%)
309
(-3.7%)
304
(-5.3%)
297
(-7.5%)
281*
(-12.5%)
Relative liver weight (g/100 g)
2.69
2.75
(2.2%)
2.66
(-1.1%)
2.87**
(6.7%)
3.21**
(19.3%)
3.24**
(20.4%)
Relative kidney weight (g/100 g)
0.69
0.76**
(10.1%)
0.70
(1.4%)
0.76**
(10.1%)
0.80**
(15.9%)
0.77**
(11.6%)
Females
Number of animals
10
10
10
10
9
10
Average body weight (g)
190
197
(3.7%)
194
(2.1%)
193
(1.6%)
184
(-3.2%)
182
(-4.2%)
Relative liver weight (g/100 g)
2.82
2.84
(0.7%)
2.94
(4.3%)
3.04
(7.8%)
3.18**
(12.8%)
3.36**
(19.1%)
Relative kidney weight (g/100 g)
0.83
0.77
(-7.2%)
0.83
(0%)
0.83
(0%)
0.98*
(18.1%)
0.93*
(12.0%)
aUnspecified strain.
bDow Chemical Co (1990. 1960).
* Significantly different from control (p = 0.01-0.05), statistical methods not reported by study authors.
**Significantly different from control (p < 0.01), statistical methods not reported by study authors.
34 l,2,3,4,5-Pentabromo-6-Chlorocyclohexane

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Table B-4. Selected Effects on Male and Female CDF F344 Rats Exposed to FR-651A in
Food for 13 Weeksa'b
Endpoint
Exposure Group (mg/kg-d)
0
600
Males
Number of animals
10
10
Terminal body weight (g)
281 ±31°
312 ± 23*
(11.0%)
Terminal food consumption rate (g/day)
15 ±2
18 ± 1*
Serum ALP (mU/mL)
88 ±8
75 ±4*
Serum ALT (mU/mL)
28 ±2
27 ±2
BUN (mg/100 mL)
23 ±8
17 ±2
Absolute liver weight (g)
7.23 ±0.99
8.87 ±0.71*
(22.7%)
Relative liver weight (g/100 g)
2.82 ±0.15
3.11 ± 0.21*
(10.3%)
Absolute kidney weight (g)
1.79 ±0.24
2.12 ± 0.18*
(18.4%)
Relative kidney weight (g/100 g)
0.70 ±0.03
0.74 ±0.04*
(5.7%)
Incidence of hepatocellular hypertrophy (very slight)
0/10d
10/10**
Decreased staining intensity of hepatocellular cytoplasm (very slight)
0/10
10/10**
Centrilobular hepatocellular necrosis with microfocal aggregates of RE
cells (very slight to slight)
0/10
7/10**
Focal renal tubular degeneration and inflammation with or without
fibrosis (very slight to slight)
3/10
9/10**
Females
Number of animals
10
10
Terminal body weight (g)
202 ± 17
208 ± 17
(3.0%)
Food consumption rate (g/day)
12 ± 1
14 ± 1*
Serum ALP (AP; mU/mL)
55 ± 12
41 ± 17
Serum ALT (mU/mL)
26 ±4
22 ±4
BUN (mg/100 mL)
20 ±4
15 ± 1*
Absolute liver weight (g)
5.01 ±0.51
5.88 ±0.58*
(17.4%)
Relative liver weight (g/100 g)
2.72 ±0.14
3.05 ±0.18*
(12.1%)
Absolute kidney weight (g)
1.35 ±0.09
1.48 ±0.13*
(9.6%)
Relative kidney weight (g/100 g)
0.74 ±0.05
0.77 ± 0.04
(4.1%)
35 l,2,3,4,5-Pentabromo-6-Chlorocyclohexane

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FINAL
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Table B-4. Selected Effects on Male and Female CDF F344 Rats Exposed to FR-651A in
Food for 13 Weeksa'b
Endpoint
Exposure Group (mg/kg-d)
0
600
Females
Incidence of hepatocellular hypertrophy (very slight)
0/10
10/10**
Decreased staining intensity of hepatocellular cytoplasm (very slight)
0/10
10/10**
Centrilobular hepatocellular necrosis with microfocal aggregates of RE
cells (very slight to slight)
0/10
0/10
Focal tubular degeneration and inflammation with or without fibrosis
(very slight to slight)
1/10
0/10
aDow Chemical Co (1980b. 1980c).
bThe study authors noted recurrent mechanical problems with weighing apparatus used for food consumption
measurements; thus, the doses estimated by the authors are uncertain. It is possible that body- and organ-weight
measurements were also affected.
°Mean ± standard deviation.
dNumber affected/number examined.
* Significantly different from control (p < 0.05) based on Dunnett's test, as reported by study authors.
**Significantly different from control (p < 0.05) based on Fisher's exact test performed for this review.
RE = reticuloendothelial.
36 1,2,3,4,5 -Pentabromo-6-Chlorocyclohexane

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Table B-5. Selected Effects on Male and Female CDF F344 Rats Exposed to FR-651G in
Food for 13 Weeksa'b
Endpoint
Exposure group (mg/kg-d)
0
10
30
100
Males
Number of animals
15
10
10
10
Urine specific gravity
1.056 ±0.006c
ND
ND
1.049 ±0.003*
Absolute liver weight (g)
8.33 ±0.80
7.90 ± 1.04
8.07 ± 0.64
9.11 ±0.95
Relative liver weight (g/100 g)
3.01 ±0.54
2.80 ±0.15
2.87 ±0.09
3.12 ± 0.11
Absolute kidney weight (g)
2.05 ±0.11
1.98 ±0.20
2.02 ±0.17
2.13 ±0.23
Relative kidney weight (g/100 g)
0.75 ±0.15
0.70 ±0.03
0.72 ±0.03
0.73 ±0.04
Liver swelling and decreased staining intensity of
hepatocytes (very slight to slight)
0/10d
0/9
0/10
10/10**
Focal hepatocellular necrosis and inflammation (very
slight)
0/10
0/9
0/10
1/10
Females
Number of animals
15
10
10
10
Urine specific gravity
1.051 ±0.008
ND
ND
1.054 ±0.006
Absolute liver weight (g)
5.06 ±0.57
5.04 ±0.70
5.02 ±0.45
5.48 ±0.52
Relative liver weight (g/100 g)
2.67 ±0.14
2.67 ±0.13
2.75 ±0.21
2.90 ±0.11*
Absolute kidney weight (g)
1.38 ± 0.13
1.37 ±0.15
1.37 ±0.13
1.43 ± 0.11
Relative kidney weight (g/100 g)
0.73 ±0.04
0.73 ± 0.04
0.76 ±0.05
0.76 ±0.04
Liver swelling and decreased staining intensity of
hepatocytes (very slight to slight)
0/10
0/11
0/10
3/10
Focal hepatocellular necrosis and inflammation (very
slight)
0/10
0/11
0/10
0/10
aDow Chemical Co (1980d).
bThe study authors noted recurrent mechanical problems with weighing apparatus used for food consumption
measurements; thus, the doses estimated by the authors are uncertain. It is possible that body- and organ-weight
measurements were also affected.
°Mean ± standard deviation.
dNumber affected/number examined.
* Significantly different from control (p < 0.05) based on Dunnett's test, as reported by study authors.
**Significantly different from control (p < 0.05) based on Fisher's exact test performed for this review.
ND = no data.
37 1,2,3,4,5 -Pentabromo-6-Chlorocyclohexane

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Table B-6. Selected Effects on Male and Female CDF F344 Rats Exposed to FR-651
"Slurry Dried" in Food for 92 Daysa'b
Endpoint
Exposure Group (mg/kg-d)
0
90
260
780
Males
Number of animals per group
15
10
10
10
Terminal body weight (g)
324 ± 38°
302 ± 25
(-6.8%)
307 ± 20
(-5.2%)
269±19*
(-17.0%)
Food consumption, Days 85-92 (g/day)
17 ±2
17 ± 1
18 ± 1
15 ± 1*
Serum ALT (mU/mL)
33 ±4
32 ±6
28 ±4
28 ±6
Serum ALP (mU/mL)
90 ± 10
78 ±9*
75 ± 10*
70 ±6*
BUN (mg/100 mL)
19 ±2
17 ±2
16 ±2*
17 ±3
Fasted body weight (g)
298 ± 38
277 ± 24
(-7.0%)
282 ± 19
(-5.4%)
247±19*
(-17.1%)
Absolute liver weight (g)
8.12 ±0.83
8.57 ±0.64
(5.5%)
9.46 ±0.84*
(16.5%)
8.51 ±0.54
(4.8%)
Relative liver weight (g/100 g)
2.73 ±0.15
3.10 ± 0.21*
(13.6%)
3.35 ±0.12*
(22.7%)
3.45 ±0.14*
(26.4%)
Absolute kidney weight (g)
2.05 ±0.17
2.02 ±0.15
(-1.5%)
2.08 ±0.13
(1.5%)
1.94 ±0.13
(-5.4%)
Relative kidney weight (g/100 g)
0.69 ±0.05
0.73 ±0.03
(5.8%)
0.74 ±0.02*
(7.2%)
0.79 ±0.04*
(14.5%)
Hepatocellular hypertrophy (very slight to
slight)
0/10d
0/10
10/10**
0/10
Hepatocellular hypertrophy (slight to moderate)
0/10
0/10
0/10
10/10**
Altered appearance and staining intensity of
hepatocellular cytoplasm (very slight to slight)
0/10
0/10
1/10
0/10
Altered appearance and staining intensity of
hepatocellular cytoplasm (slight to moderate)
0/10
0/10
0/10
9/10**
Focal hepatocellular necrosis and inflammation
(very slight)
0/10
0/10
0/10
1/10
Females
Number of animals per group
15
10
10
10
Terminal body weight (g)
203 ± 17
200 ± 15
(-1.5%)
207 ± 15
(2.0%)
187 ± 10*
(-7.9%)
Food consumption, Days 85-92 (g/day)
13 ± 1
14 ±2
14 ± 1
13 ± 1
Serum ALT (mU/mL)
26 ±4
21 ± 3
22 ±6
15 ±2*
Serum ALP (mU/mL)
51 ± 12
47 ± 10
35 ± 11*
36 ±7*
BUN (mg/100 mL)
17 ±2
18 ± 12
14 ±2
16 ±2
Fasted body weight (g)
185 ± 16
189 ± 15
(2.2%)
190 ± 14
(2.7%)
170 ±9*
(-8.1%)
38 l,2,3,4,5-Pentabromo-6-Chlorocyclohexane

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FINAL
09-28-2016
Table B-6. Selected Effects on Male and Female CDF F344 Rats Exposed to FR-651
"Slurry Dried" in Food for 92 Daysa'b
Endpoint
Exposure Group (mg/kg-d)
0
90
260
780
Females
Absolute liver weight (g)
4.93 ±0.50
5.02 ±0.44
(1.8%)
5.82 ±0.39*
(18.1%)
5.86 ±0.28*
(18.9%)
Relative liver weight (g/100 g)
2.66 ±0.16
2.67 ±0.26
(0.4%)
3.08 ±0.18*
(15.8%)
3.45 ±0.14*
(29.7%)
Absolute kidney weight (g)
1.30 ± 0.11
1.34 ±0.10
(3.1%)
1.39 ±0.08
(6.9%)
1.38 ±0.07
(6.2%)
Relative kidney weight (g/100 g)
0.71 ±0.05
0.72 ± 0.06
(1.4%)
0.74 ±0.04
(4.2%)
0.81 ±0.04*
(14.1%)
Hepatocellular hypertrophy (very slight to
slight)
0/10
0/10
10/10**
10/10**
Hepatocellular hypertrophy (slight to moderate)
0/10
0/10
0/10
0/10
Altered appearance and staining intensity of
hepatocellular cytoplasm (very slight to slight)
0/10
0/10
2/10
3/10
Altered appearance and staining intensity of
hepatocellular cytoplasm (slight to moderate)
0/10
0/10
0/10
0/10
Focal hepatocellular necrosis and inflammation
(very slight)
0/10
0/10
0/10
0/10
aDow Chemical Co (1980a).
bThe study authors noted recurrent mechanical problems with weighing apparatus used for food consumption
measurements; thus, the doses estimated by the authors are uncertain. It is possible that body- and organ-weight
measurements were also affected.
°Mean ± standard deviation.
dNumber affected/number examined.
* Significantly different from control (p < 0.05) based on Dunnett's test, as reported by study authors.
**Significantly different from control (p < 0.05) based on Fisher's exact test performed for this review.
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Table B-7. Selected Effects on Male and Female F344 Rats Exposed to FR-651A in Food
for 2 Years"
Males
Endpoint
Exposure Group (mg/kg-d)
0
1
15
50
Number of animals
86
50
50
50
Terminal body weight (g)
423 ± 25b
416 ±25
(-1.7%)
417 ±33
(-1.4%)
405 ± 20*
(-4.3%)
Urine specific gravity
1.051 ±0.011
1.047 ±0.009
1.043 ±0.008
1.037 ±0.007*
Interim sacrifice (10 rats/group)
Absolute liver weight (g)
8.88 ±0.55
9.42 ± 0.67
(6.1%)
9.80 ±0.67*
(10.4%)
10.01 ± 1.18*
(12.7%)
Relative liver weight (g/100 g)
2.36 ±0.10
2.47 ±0.11
(4.7%)
2.48 ±0.12
(5.1%)
2.63 ± 0.26*
(11.4%)
Absolute kidney weight (g)
2.57 ±0.10
2.58 ±0.12
(0.4%)
2.70 ±0.17
(5.1%)
2.70 ±0.13
(5.1%)
Relative kidney weight (g/100 g)
0.68 ±0.03
0.68 ±0.02
(0%)
0.68 ±0.02
(0%)
0.71 ±0.02
(4.4%)
Terminal sacrifice (18-20 rats/group)
Absolute liver weight (g)
11.65 ± 1.90
11.28 ±0.87
(-3.2%)
11.84 ± 1.25
(1.6%)
12.28 ± 1.73
(5.4%)
Relative liver weight (g/100 g)
2.94 ±0.50
2.89 ±0.45
(-1.7%)
2.93 ±0.32
(-0.3%)
3.15 ±0.44
(7.1%)
Absolute kidney weight (g)
3.04 ±0.24
2.91 ±0.15
(-4.3%)
3.12 ±0.32
(2.6%)
3.04 ±0.19
(0%)
Relative kidney weight (g/100 g)
0.77 ±0.08
0.74 ±0.09
(-3.9%)
0.77 ±0.09
(0%)
0.78 ±0.05
(1.3%)
Females
Endpoint
Exposure Group (mg/kg-d)
0
1
20
70
Number of animals
86
50
50
50
Terminal body weight (g)
300 ± 25
297 ± 27
(-1.0%)
299 ± 20
(-0.3%)
284 ± 27*
(-5.3%)
Urine specific gravity
1.040 ±0.004
1.038 ±0.011
1.047 ±0.008
1.044 ±0.017
Interim sacrifice (10 rats/group)
Absolute liver weight (g)
5.70 ±0.43
5.93 ±0.43
(4.0%)
6.16 ±0.57
(8.1%)
6.20 ±0.54
(8.8%)
Relative liver weight (g/100 g)
2.62 ±0.09
2.69 ±0.10
(2.7%)
2.84 ±0.25*
(8.4%)
2.81 ±0.09*
(7.3%)
Absolute kidney weight (g)
1.69 ±0.09
1.73 ±0.09
(2.4%)
1.72 ±0.09
(1.8%)
1.78 ±0.16
(5.3%)
Relative kidney weight (g/100 g)
0.78 ±0.03
0.79 ±0.03
(1.3%)
0.79 ±0.04
(1.3%)
0.81 ±0.34
(3.8%)
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Table B-7. Selected Effects on Male and Female F344 Rats Exposed to FR-651A in Food

for 2 Years"


Females
Terminal sacrifice (18-20 rats/group)
Absolute liver weight (g)
8.01 ± 1.03
7.99 ±0.79
8.61 ± 1.46
8.48 ± 1.24


(-0.2%)
(7.5%)
(5.9%)
Relative liver weight (g/100 g)
2.86 ±0.59
2.89 ±0.43
3.06 ±0.64
3.17 ±0.48


(1.0%)
(7.0%)
(10.8%)
Absolute kidney weight (g)
2.25 ±0.30
2.18 ± 0.19
2.35 ±0.43
2.31 ±0.33


(-3.1%)
(4.4%)
(2.7%)
Relative kidney weight (g/100 g)
0.81 ±0.19
0.79 ±0.12
0.84 ±0.23
0.86 ±0.11


(-2.5%)
(3.7%)
(6.2%)
aDow Chemical Co (1983a. 1983b).
bMean ± standard deviation.
* Significantly different from control (p < 0.05) based on Dunnett's test, as reported by the study authors.
Table B-8. Incidences of Selected Histopathological Observations (Non-neoplastic Lesions)
of Male and Female F344 Rats Exposed to FR-651A in Food for 2 Years3
Males
Endpoint
Exposure Group (mg/kg-d)
0
1
15
50
Interim sacrifice
Altered tinctorial properties of hepatocytes, multifocal
0/10b
0/10
0/10
9/10**
Multifocal hepatocellular hypertrophy
0/10
0/10
0/10
9/10**
Terminal sacrifice0
Dilatation, hypercellularity, and aggregates of cellular
debris in intestinal crypts
0/84
0/50
2/50
8/49*
Females
Endpoint
Exposure Group (mg/kg-d)
0
1
20
70
Interim sacrifice
Altered tinctorial properties of hepatocytes, multifocal
0/10
0/10
0/10
0/10
Multifocal hepatocellular hypertrophy
0/10
0/10
0/10
0/10
Terminal sacrifice0
Dilatation, hypercellularity, and aggregates of cellular
debris in intestinal crypts
1/86
0/49
1/50
11/50*
aDow Chemical Co (1983a. 1983b).
bNumber affected/number examined.
°Histopathology examination at terminal sacrifice was limited to tissues of the gastrointestinal tract.
* Significantly different from control (p < 0.05), by Fisher's exact test as reported by the study authors.
**Significantly different from control (p < 0.05), by Fisher's exact test conducted for this review.
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Table B-9. Incidences of Neoplastic Lesions of Large Intestine in Male and Female
F344 Rats Exposed to FR-651A in Food for 2 Years"
Males
Endpoint
Exposure Group (mg/kg-d)
0
1
15
50
Polypoid adenoma
1/84
1/50
0/50
5/49*
Polypoid adenocarcinoma
0/84
0/50
0/50
1/49
Polypoid adenoma and/or adenocarcinoma
1/84
1/50
0/50
5/49*
Females
Endpoint
Exposure Group (mg/kg-d)
0
1
20
70
Polypoid adenoma
1/86
0/49
3/50
8/50*
Polypoid adenocarcinoma
0/86
0/49
0/50
1/50
Polypoid adenoma and/or adenocarcinoma
1/86
0/49
3/50
9/50*
aDow Chemical Co (1983a. 1983b).
* Significantly different from control (p < 0.05), by Fisher's exact test as reported by the study authors.
Table B-10. Incidences of Neoplastic Lesions of Large Intestine in Male and Female
F344 Rats Exposed to FR-651C in Food for 2 Years"
Males
Endpoint
Exposure Group (mg/kg-d)
0
1
15
50
Polypoid adenoma
1/83
0/49
1/50
2/48
Polypoid adenocarcinoma
0/83
0/49
1/50
0/48
Polypoid adenoma and/or adenocarcinoma
1/83
0/49
2/50
2/48
Females
Endpoint
Exposure Group (mg/kg-d)
0
1
20
70
Polypoid adenoma
2/85
0/50
2/50
8/50*
Polypoid adenocarcinoma
0/85
0/50
0/50
1/50
Polypoid adenoma and/or adenocarcinoma
2/85
0/50
2/50
9/50*
"Keyes et al. (1982) as cited in U.S. EPA (1985).
* Significantly different from control (p < 0.05), by Fisher's exact test (one sided) as reported by the study authors.
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APPENDIX C. BENCHMARK DOSE MODELING RESULTS
MODELING PROCEDURE FOR DICHOTOMOUS DATA
Benchmark dose (BMD) modeling of dichotomous data was conducted with the EPA's
BMD software (BMDS, Version 2.5). For these data, the gamma, logistic, log logistic,
log-probit, multistage, probit, and Weibull dichotomous models available within the software
were fit using a benchmark response (BMR) of 10% extra risk. Adequacy of model fit was
judged based on the %2 goodness-of-fitp-value (p > 0.1), magnitude of scaled residuals in the
vicinity of the BMR, and visual inspection of the model fit. Among all of the models providing
adequate fit, the benchmark dose lower confidence limit (BMDL) from the model with the
lowest Akaike's information criterion (AIC) was selected as a potential point of departure (POD)
when BMDL values were within a factor of 2-3. When BMDL values from models providing
adequate fit varied more than two or threefold, the lowest BMDL was selected as a potential
POD.
Model Predictions for Lesions of the Intestinal Crypts in F344 Rats Given FR-651A in the
Diet for 2 Years
All available quantal models in BMDS (Version 2.5) were fit to the data on lesions of the
intestinal crypts (dilatation, hypercellularity, and aggregates of cellular debris) in male and
female rats (Dow Chemical Co, 1983a, b) (see Table C-1). BMD modeling was performed using
the doses administered in the study. A default BMR of 10% extra risk was used in the BMD
modeling.
Table C-l. Incidences of Intestinal Lesions in Male and Female F344 Rats Exposed to
FR-651A in Food for 2 Years3
Males
Endpoint
Exposure Group (mg/kg-d)
0
1
15
50
Terminal sacrifice
Dilatation, hypercellularity, and aggregates of
cellular debris in intestinal crypts
0/84b
0/50
2/50
8/49*
Females
Endpoint
Exposure Group (mg/kg-d)
0
1
20
70
Terminal sacrifice
Dilatation, hypercellularity, and aggregates of
cellular debris in intestinal crypts
1/86
0/49
1/50
11/50*
aDow Chemical Co (1983a. 1983b).
bNumber affected/number examined.
* Significantly different from control (p < 0.05), as reported by the study authors.
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For male rat data, all of the available models provided adequate fit (p > 0.1;
see Table C-2), and scaled residuals at the dose closest to the BMR were acceptable for all
models. BMDLs from all models were within a factor of three, so the model with the lowest
AIC was selected. The 1-degree multistage model exhibited the lowest AIC (see Table C-2).
The BMDio and BMDLio values from this model were 32 and 20 mg/kg-day, respectively. The
BMDLio from this study was selected as the POD for deriving the screening chronic p-RfD.
Figure C-l shows the model fit to the data.
Table C-2. BMD Model Results from Incidence of Dilation, Hypercellularity, and
Aggregates of Cellular Debris in Intestinal Crypts in Male F344 Rats"
Model
DF
x2
X2 Goodness-of-Fit
/j-valucb
Scaled
Residuals0
AIC
BMDio
(mg/kg-d)
BMDLio
(mg/kg-d)
Gammad
2
0.07
0.97
-0.05
64.52
32.91
20.35
Logistic
2
2.44
0.30
-0.13
67.22
42.16
35.20
Log-logistice
2
0.06
0.97
-0.04
64.52
32.72
19.58
Log-probite
3
1.43
0.70
-0.53
63.58
33.00
24.63
Multistage (l-degree)fg
3
0.29
0.96
-0.27
62.86
31.92
19.76
Multistage (2-degree/
2
0.12
0.94
-0.03
64.63
34.08
20.16
Multistage (3-degree/
2
0.12
0.94
-0.03
64.63
34.08
20.16
Probit
2
2.06
0.36
-0.17
66.79
40.49
32.95
Weibulld
2
0.07
0.96
-0.04
64.53
33.11
20.33
aDow Chemical Co (1983a. 1983b).
bValues <0.1 fail to meet conventional goodness-of-fit criteria.
°Scaled residuals for dose group near BMD.
dPower restricted to >1.
"Slope restricted to >1.
fBetas restricted to >0.
gSelected model. All models provided adequate fit to the data. BMDLs for models providing adequate fit were
sufficiently close (differed by less than two- to three-fold), so the model with the lowest AIC was selected
(1-degree multistage).
AIC = Akaike's information criterion; BMD = maximum likelihood estimate of the dose associated with the
selected benchmark response; BMDL = 95% lower confidence limit on the BMD (subscripts denote benchmark
response [i.e., io = dose associated with 10% extra risk]); DF = degree(s) of freedom.
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Multistage Model, with BMR of 10% Extra Risk for the BMD and 0.95 Lower Confidence Limit for the B
Multistage
0.3
0.25
0.2
0.15
0.05
BMDL
BMD
0
10
20
30
40
50
dose
15:28 07/02 2014
Figure C-l. Fit of Selected Model to Data on Intestinal Lesions in Male F344 Rats
Multistage Model. (Version: 3.4; Date: 05/02/2014)
Input Data File:
C:/USEPA/PTV/FR651A/intestinalcrypts/male/mst_intestinalcrypts_male_multil. (d)
Gnuplot Plotting File:
C:/USEPA/PTV/FR651A/intestinalcrypts/male/mst_intestinalcrypts_male_multil.pit
Wed Jul 02 15:28:45 2014
BMDS Model Run
The form of the probability function is:
P[response] = background + (1-background)*[1-EXP(
-betal*doseAl) ]
The parameter betas are restricted to be positive
Dependent variable = Effect
Independent variable = Dose
Total number of observations = 4
Total number of records with missing values = 0
Total number of parameters in model = 2
Total number of specified parameters = 0
Degree of polynomial = 1
Maximum number of iterations = 5 00
Relative Function Convergence has been set to: le-008
Parameter Convergence has been set to: le-008
Default Initial Parameter Values
Background =	0
Beta(1) = 0.00361031
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the user,
Beta(1)
Asymptotic Correlation Matrix of Parameter Estimates
( *** The model parameter(s) -Background
have been estimated at a boundary point, or have been specified by
and do not appear in the correlation matrix )
Beta(1)
1
Interval
Variable
Limit
Background
Beta(1)
Estimate
Parameter Estimates
95.0% Wald Confidence
Std. Err.	Lower Conf. Limit Upper Conf.
0
0.00330101	*
* - Indicates that this value is not calculated.
Analysis of Deviance Table
Model
Full model
Fitted model
Reduced model
AIC:
Log(likelihood)
-30.2044
-30. 4323
-41.2668
62.8645
# Param's	Deviance	Test d.f.	P-value
4
1	0.455702	3	0.9285
1	22.1248	3	<.0001
Dose
Est. Prob.
Goodness of Fit
Expected Observed	Size
Scaled
Residual
0.0000
1.0000
15.0000
50.0000
0.0000
0.0033
0.0483
0.1521
Chi^2 = 0.29	d.f. = 3
Benchmark Dose Computation
0.000 0.000 84.000	0.000
0.165 0.000 50.000	-0.407
2.415 2.000 50.000	-0.274
7.455 8.000 49.000	0.217
P-value = 0.9624
Specified effect
Risk Type
Confidence level
BMD
BMDL
BMDU
0.1
Extra risk
0. 95
31.9176
19.7645
56.4295
Taken together, (19.7645, 56.4295) is a 90
interval for the BMD
two-sided confidence
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For female rat data, all of the available models provided adequate fit (p > 0.1;
see Table C-3), and scaled residuals at the dose closest to the BMR were acceptable for all
models. BMDLs from all models were within a factor of three, so the model with the lowest
AIC was selected. The logistic model exhibited the lowest AIC (see Table C-3). The BMDio
and BMDLio values from this model were 54 and 45 mg/kg-day, respectively. Figure C-2 shows
the model fit to the data.
Table C-3. BMD Model Results from Incidence of Dilatation, Hypercellularity, and
Aggregates of Cellular Debris in Intestinal Crypts in Female F344 Ratsa
Model
DF
X2
X2 Goodness-of-Fit
/j-valueb
Scaled
Residuals0
AIC
BMDio
(mg/kg-d)
BMDLio
(mg/kg-d)
Gammad
1
0.57
0.45
0
80.30
47.87
30.99
Logistic6
2
0.61
0.74
0.003
78.34
53.53
44.84
Log-logisticf
1
0.57
0.45
0
80.30
48.47
30.64
Log-probitf
1
0.57
0.45
0
80.30
45.77
32.73
Multistage (1-degree)8
2
2.73
0.25
-1.20
80.95
37.77
23.93
Multistage (2-degree)8
2
0.7
0.71
0.07
78.39
46.73
31.88
Multistage (3-degree)8
1
0.57
0.45
0
80.30
49.97
32.24
Probit
2
0.7
0.70
0.02
78.38
50.61
41.44
Weibulld
1
0.57
0.45
0
80.30
49.22
31.18
"Dow Chemical Co (1983a. 1983b).
bValues <0.1 fail to meet conventional goodness-of-fit criteria.
°Scaled residuals for dose group near BMD.
dPower restricted to >1.
Selected model. All models provided adequate fit to the data. BMDLs for models providing adequate fit were
sufficiently close (differed by less than two- to three-fold), so the model with the lowest AIC was selected
(Logistic).
fSlope restricted to >1.
gBetas restricted to >0.
AIC = Akaike's information criterion; BMD = maximum likelihood estimate of the dose associated with the
selected benchmark response; BMDL = 95% lower confidence limit on the BMD (subscripts denote benchmark
response [i.e., io = dose associated with 10% extra risk]); DF = degree(s) of freedom.
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Logistic
0.4
0.35
0.3
0.25
T3
0)
-t—'
o
£	0.2
<
c
o
'¦£	0.15
LL
0.1
0.05
0
0	10	20	30	40	50	60	70
dose
15:35 07/02 2014
Figure C-2. Fit of Selected Model to Data on Intestinal Lesions in Female F344 Rats
Logistic Model. (Version: 2.14; Date: 2/28/2013)
Input Data File:
C:/USEPA/PTV/FR651A/intestinalcrypts/female/log_intestinalcrypts_female_Log-BMR10.(d)
Gnuplot Plotting File:
C:/USEPA/PTV/FR651A/intestinalcrypts/female/log_intestinalcrypts_female_Log-BMR10.pit
Wed Jul 02 15:35:01 2014
BMDS Model Run
The form of the probability function is:
P[response] = 1/[1+EXP(-intercept-slope*dose)]
Dependent variable = Effect
Independent variable = Dose
Slope parameter is not restricted
Total number of observations = 4
Total number of records with missing values = 0
Maximum number of iterations = 5 00
Relative Function Convergence has been set to: le-008
Parameter Convergence has been set to: le-008
Logistic
BMDL
Model, with BMR of 10% Extra Risk for the BMD and 0.95 Lower Confidence Limit for the BM
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Default Initial Parameter Values
background =	0 Specified
intercept =	-4.35077
slope = 0.0443347
Asymptotic Correlation Matrix of Parameter Estimates
the user,
intercept
slope
( *** The model parameter(s) -background
have been estimated at a boundary point, or have been specified by
and do not appear in the correlation matrix )
intercept
1
-0. 93
slope
-0.93
1
Parameter Estimates
Interval
Variable
Limit
intercept
0.822186
slope
0.0776384
Model
Full model
Fitted model
Reduced model
Estimate
-4.92187
-6.53333
0.0522159
Std. Err.
-3.31042
0.0129709
95.0% Wald Confidence
Lower Conf. Limit Upper Conf.
0.0267935
Analysis of Deviance Table
Log(likelihood)	# Param's	Deviance Test d.f.	P-value
-36.6959	4
-37.1683	2	0.944869 2	0.6235
-50.2639	1	27.136 3	<.0001
AIC:
78.3366
Dose
Est. Prob.
Goodness of Fit
Expected Observed	Size
Scaled
Residual
0.0000
1.0000
20.0000
70.0000
0.0072
0.0076
0.0203
0.2198
Chi^2 = 0.61	d.f. = 2
Benchmark Dose Computation
0.622 1.000	86	0.481
0.373 0.000	49	-0.613
1.014 1.000	50	-0.014
10.991 11.000	50	0.003
P-value = 0.7380
Specified effect
Risk Type
Confidence level
BMD
BMDL
0.1
Extra risk
0. 95
53.5272
44.8415
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Model Predictions for Polypoid Adenomas and Adenocarcinomas in F344 Rats Given
FR-651A in the Diet for 2 Years
BMD modeling of the incidences of polypoid adenoma or adenocarcinoma of the
intestines in male and female rats exposed to FR-651A for 2 years was performed using the
procedure outlined above, with a slight modification: only the multistage model is applied to
cancer data sets. The incidences of intestinal tumors are shown in Table C-4 below. A default
BMR of 10% extra risk was used in the BMD modeling.
Table C-4. Incidences of Intestinal Tumors in Male and Female F344 Rats Exposed to
FR-651A in Food for 2 Years"


Males

Animal Dose (mg/kg-d)
Endpoint
0
1
15
50
Polypoid adenoma and/or adenocarcinoma
1/84
1/50
0/50
5/49*
Females

Animal Dose (mg/kg-d)
Endpoint
0
1
20
70
Polypoid adenoma and/or adenocarcinoma
1/86
0/49
3/50
9/50*
aDow Chemical Co (1983a. 1983b).
* Significantly different from control (p < 0.05), as reported by study authors.
For the data in female rats, all of the available models provided adequate fit (p > 0.1;
see Table C-5), and scaled residuals at the dose closest to the BMR were acceptable for all
models. The 1-degree multistage model exhibited the lowest AIC (see Table C-5). The
BMDio (FLED) and BMDLio (FLED) values from this model were 9.5 and 5.9 mg/kg-day,
respectively. The BMDLio (FLED) of 5.9 mg/kg-day was selected as the POD for deriving the
screening cancer potency value. Figure C-3 shows the model fit to the data.
50 l,2,3,4,5-Pentabromo-6-Chlorocyclohexane

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Table C-5. BMD Model Results from Incidence of Polypoid Adenoma and/or


Adenocarcinoma in Female F344 Rats3






X2 Goodness-of-Fit
Scaled

BMDio
BMDLio
Model
DF
X2
/>-valucb
Residuals0
AIC
(mg/kg-d)
(mg/kg-d)
Multistage (l-degree)de
2
0.68
0.71
0.03
85.86
9.46
5.93
Multistage (2-degree)d
1
0.68
0.41
0.10
87.85
9.69
5.93
Multistage (3-degree)d
1
0.68
0.41
0.10
87.85
9.69
5.93
aDow Chemical Co (1983a 1983b).
bValues <0.1 fail to meet conventional goodness-of-fit criteria.
°Scaled residuals for dose group near BMD.
dBetas restricted to >0.
Selected model All models provided adequate fit to the data. BMDLs for models providing adequate fit were
nearly identical, so the model with the lowest AIC was selected (1-degree multistage).
AIC = Akaike's information criterion; BMDio = maximum likelihood estimate of the dose associated with the
selected benchmark response; BMDL = 95% lower confidence limit on the BMD (subscripts denote benchmark
response [i.e., h> = dose associated with 10% extra risk]); DF = degree(s) of freedom.
n=
<
Multistage Cancef Model, with BMR of 10% Extra Risk fof the BMD and 0.95 Lower Confidence Limit for the BMDL
0.35
0.3
0.25
0.2
0.15
0.1
0.05
Multistage Canoef
Linear extrapolation
B M C L
3MC
10
12
14
16
15:37 07/03 2014
dose
Figure C-3. Fit of Selected Model to Data on Intestinal Tumor Incidences in Females
51 l,2,3,4,5-Pentabromo-6-Chlorocyclohexane

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Multistage Model. (Version: 3.4; Date: 05/02/2014)
Input Data File:
C:/USEPA/PTV/FR65lA/polyploid_adeno_adenocarc/female/msc_neoplasm_female_Mscl-
BMR10.(d)
Gnuplot Plotting File:
C:/USEPA/PTV/FR65lA/polyploid_adeno_adenocarc/female/msc_neoplasm_female_Mscl-
BMR10.pit
Thu Jul 03 15:37:18 2014
BMDS Model Run
The form of the probability function is:
P[response] = background + (1-background)*[1-EXP(
-betal*doseAl) ]
The parameter betas are restricted to be positive
Dependent variable = Effect
Independent variable = Dose
Total number of observations = 4
Total number of records with missing values = 0
Total number of parameters in model = 2
Total number of specified parameters = 0
Degree of polynomial = 1
Maximum number of iterations = 5 00
Relative Function Convergence has been set to: le-008
Parameter Convergence has been set to: le-008
Default Initial Parameter Values
Background = 0.0053994
Beta(1) = 0.0113803
Asymptotic Correlation Matrix of Parameter Estimates
Background	Beta(l)
Background	1	-0.55
Beta (1)	-0.55	1
Parameter Estimates
Interval
Variable
Limit
Background
Beta(1)
Estimate
0.00746827
0.0111378
Std. Err.
95.0% Wald Confidence
Lower Conf. Limit Upper Conf.
* - Indicates that this value is not calculated.
Analysis of Deviance Table
Model
Full model
Fitted model
Reduced model
Log(likelihood)	# Param's	Deviance Test d.f.	P-value
-40.3666	4
-40.9294	2	1.12573 2	0.5696
-50.2639	1	19.7946 3	0.0001872
52 l,2,3,4,5-Pentabromo-6-Chlorocyclohexane

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AIC:	85.8589
Goodness of Fit
Scaled
Dose	Est._Prob. Expected Observed	Size	Residual
0.448
-0.692
0. 026
0. 024
Benchmark Dose Computation
Specified effect =	0.1
Risk Type	=	Extra risk
Confidence level =	0.95
0.0000
0.2000
4.8000
17.0000
Chi^2 = 0.68
0.0075
0.0097
0.0591
0.1787
d.f.
0.642
0.474
2.957
8.934
1.000
0.000
3.000
9.000
¦value =
86.000
49.000
50.000
50.000
.7115
BMD =	9.45977
BMDL =	5.93052
BMDU =	17.0663
Taken together, (5.93052,	17.0663) is a 90	% two-sided confidence
interval for the BMD
Cancer Slope Factor =	0.0168619
For the data in male rats, all of the available models provided adequate fit (p > 0.1;
see Table C-6), and scaled residuals at the dose closest to the BMR were acceptable for all
models. The 3-degree multistage model exhibited the lowest AIC (see Table C-6). The
BMDio (HED) and BMDLio (HED) values from this model were 15 and 11 mg/kg-day,
respectively. Figure C-4 shows the model fit to the data.
53 l,2,3,4,5-Pentabromo-6-Chlorocyclohexane

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Table C-6. BMD Model Results from Incidence of Polypoid Adenoma and/or


Adenocarcinoma in Male F344 Rats3






X2 Goodness-of-Fit
Scaled

BMDio
BMDLio
Model
DF
X2
/>-valucb
Residuals0
AIC
(mg/kg-d)
(mg/kg-d)
Multistage (l-degree)d
2
2.20
0.33
0.59
60.67
20.61
9.86
Multistage (2-degree)d
2
1.34
0.51
0.20
59.15
15.37
10.73
Multistage (3-degree)de
2
1.06
0.59
0.06
58.60
14.55
11.09
aDow Chemical Co (1983a. 1983b).
bValues <0.1 fail to meet conventional goodness-of-fit criteria.
°Scaled residuals for dose group near BMD.
dBetas restricted to >0.
Selected model. All models provided adequate fit to the data. BMDLs for models providing adequate fit were
sufficiently close (differed by less than two- to three-fold), so the model with the lowest AIC was selected
(3-degree multistage).
AIC = Akaike's information criterion; BMDio = maximum likelihood estimate of the dose associated with the
selected benchmark response; BMDL = 95% lower confidence limit on the BMD (subscripts denote benchmark
response [i.e., h> = dose associated with 10% extra risk]); DF = degree(s) of freedom.
Multistage Cancer Model, with BMR of 10% Extra Risk for the BMD and 0 95 Lower Confidence Limit for the BMDL
025
Multistage Cancer
Linear extrapolation
02
0 15
1
005
0
BMC
BMDL
0
2
4
6
8
10
12
14
dose
15:27 07/03 2014
Figure C-4. Fit of Selected Model to Data on Intestinal Tumor Incidences in Males
54 l,2,3,4,5-Pentabromo-6-Chlorocyclohexane

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Multistage Model. (Version: 3.4; Date: 05/02/2014)
Input Data File:
C:/USEPA/PTV/FR65lA/polyploid_adeno_adenocarc/male/msc_neoplasm_male_Msc3-BMR10.(d)
Gnuplot Plotting File:
C:/USEPA/PTV/FR65lA/polyploid_adeno_adenocarc/male/msc_neoplasm_male_Msc3-BMR10.pit
Thu Jul 03 15:27:45 2014
BMDS Model Run
The form of the probability function is:
P[response] = background + (1-background)*[1-EXP(
-betal*dose/sl-beta2*dose/s2-beta3* doseA3)]
The parameter betas are restricted to be positive
Dependent variable = Effect
Independent variable = Dose
Total number of observations = 4
Total number of records with missing values = 0
Total number of parameters in model = 4
Total number of specified parameters = 0
Degree of polynomial = 3
Maximum number of iterations = 5 00
Relative Function Convergence has been set to: le-008
Parameter Convergence has been set to: le-008
Default Initial Parameter Values
Background = 0.00996563
Beta(l) =	0
Beta(2) =	0
Beta(3) = 3.546e-005
Asymptotic Correlation Matrix of Parameter Estimates
( *** The model parameter(s) -Beta(l) -Beta(2)
have been estimated at a boundary point, or have been specified by
the user,
and do not appear in the correlation matrix )
Background	Beta(3)
Background	1	-0.45
Beta (3)	-0.45	1
Parameter Estimates
95.0% Wald Confidence
Interval
Variable	Estimate	Std. Err.	Lower Conf. Limit Upper Conf.
Limit
55 1,2,3,4,5 -Pentabromo-6-Chlorocyclohexane

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Background	0.0109438	*
Beta(l)	0	*
Beta(2)	0	*
Beta(3)	3.41808e-005	*
Indicates that this value is not calculated.
Model
Full model
Fitted model
Reduced model
Analysis of Deviance Table
#
Log(likelihood)
-26.4745
-27.2999
-31.4297
Param's
4
2
1
Deviance Test d.f.
1.65086
9.91044
P-value
0. 438
0.01934
AIC:
58.5998
Goodness of Fit
Scaled
Dose	Est._Prob. Expected Observed	Size	Residual
0.0000	0.0109	0.919
0.3000	0.0109	0.547
4.1000	0.0133	0.664
14.0000	0.0995	4.875
Chi^2 = 1.06 d.f.	=2	P
1.000 84.000	0.085
1.000 50.000	0.615
0.000 50.000	-0.820
5.000 49.000	0.060
value = 0.58 80
Benchmark Dose Computation
Specified effect =	0.1
Risk Type	=	Extra risk
Confidence level =	0.95
BMD =	14.5534
BMDL =	11.0934
BMDU =	33.3989
Taken together, (11.0934, 33.3989) is a 90	% two-sided confidence
interval for the BMD
Cancer Slope Factor = 0.00901439
56 l,2,3,4,5-Pentabromo-6-Chlorocyclohexane

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