Provisional Peer-Reviewed Toxicity Values for Aroclor 5460 (CASRN 11126-42-4)


4%	United States
iPjif'	Environmental Protectio
m »Agency
EPA/690/R-14/001F
Final
2-3-2014
Provisional Peer-Reviewed Toxicity Values for
Aroclor 5460
(CASRN 11126-42-4)
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 MANAGERS
Evisabel A. Craig, PhD
National Center for Environmental Assessment, Cincinnati, OH
Q. Jay Zhao, PhD, DABT
National Center for Environmental Assessment, Cincinnati, OH
PRIMARY INTERNAL REVIEWERS
Paul G. Reinhart, PhD, DABT
National Center for Environmental Assessment, Research Triangle Park, NC
Ambuja Bale, PhD, DABT
National Center for Environmental Assessment, Washington, DC
Questions regarding the contents of this document may be directed to the U.S. EPA Office of
Research and Development's National Center for Environmental Assessment, Superfund Health
Risk Technical Support Center (513-569-7300).
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TABLE OF CONTENTS
COMMONLY USED ABBREVIATIONS AND ACRONYMS	iii
PROVISIONAL PEER-REVIEWED TOXICITY VALUES FOR AROCLOR 5460
(CASRN 11126-42-4)	1
BACKGROUND	1
DISCLAIMERS	1
QUESTIONS REGARDING PPRTVs	1
INTRODUCTION	2
REVIEW OF POTENTIALLY RELEVANT DATA (CANCER AND NONCANCER)	5
Human Studies	8
Oral Exposures	8
Inhalation Exposures	8
Animal Studies	8
Oral Exposures	8
Other Data (Short-Term Tests, Other Examinations)	10
Developmental Studies in Chickens	13
Short-term-Duration Studies	14
Metabolism/Toxicokinetic Studies	14
Mode of Action/Mechanistic Studies	15
DERIVATION 01 PROVISIONAL VALUES	15
Derivation of Oral Reference Doses	17
Derivation of Inhalation Reference Concentrations	17
CANCER WEIGHT-OF-EVIDENCE (WOE) DESCRIPTOR	17
Derivation of Provisional Cancer Potency Values	18
APPENDIX A. PROVISIONAL SCREENING VALUES	19
APPENDIX B. DATA TABLES	22
APPENDIX C. BMD OUTPUTS	29
APPENDIX D. REFERENCES	30
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COMMONLY USED ABBREVIATIONS AND ACRONYMS
a2u-g
a2u-globulin
LOAEL
lowest-observed-adverse-effect level
ACGIH
American Conference of Governmental
MN
micronuclei

Industrial Hygienists
MNPCE
micronucleated polychromatic
AIC
Akaike's information criterion

erythrocyte
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
POD[Adj]
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
FEV1
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
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PROVISIONAL PEER-REVIEWED TOXICITY VALUES FOR
AROCLOR 5460 (CASRN 11126-42-4)
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 flittp://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 (www.epa.eov/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.
QUESTIONS REGARDING PPRTVs
Questions regarding the contents and appropriate use 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).
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INTRODUCTION
Aroclor 5460 (CASRN 11126-42-4) belongs to a class of chlorinated aromatic
compounds known as polychlorinated terphenyls (PCTs), which are structurally and chemically
similar to polychlorinated biphenyls (PCBs). Currently, the production and use of PCTs are
banned in the United States and Canada. PCTs are also severely restricted in 12 European
countries where only preparations with a PCT content <0.01% by weight are permitted (FAQ.
1992). However, between 1959 and 1972, the Monsanto Company was a major producer of
millions of pounds of various PCT blends in the United States, including the ones termed "pure"
PCT aroclors (aroclor 5460, aroclor 5442, and aroclor 5432). Among these, aroclor 5460 was
the predominant PCT produced (Jensen and Jorgensen, 1983). Aroclor 5460 was manufactured
for use as a paint additive, sealant, wax, hot-melt adhesive, fire retardant, plasticizer, hydraulic
fluid, and lubricant. Aroclor 5460 is a mixture of polychlorinated terphenyl molecules in
multiple configurations (orthometa-, or para-) with 60% chlorination by weight in contrast to
aroclor 5442 with 42% chlorination. The chemical formula of aroclor 5460 can be given as
Ci8Hi4-nCln, in which "n" is the number of chlorine atoms that can range from 1-14. The general
chemical structure of aroclor 5460 is presented in Figure 1. A table of physicochemical
properties for aroclor 5460 is provided below (see Table 1).

Figure 1. General Chemical Structure of Aroclor 5460
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Table 1. Physicochemical Properties of Aroclor 5460 (CASRN 11126-42-4)a
Property (unit)
Value
Distillation range (ASTM D-20 [Mod.] Corr.)
280-335°C at 5 mmHg
Pour point (ASTM D-97)
46°C
Specific gravity (25°C)
1.470
Vaporization rate at 100°C and 760 mm Hg
0.000004 g/cm2/hr
Acidity-maximum (mg KOH/g)
0.05
Solubility in water (mg/L at 25 °C)
Insoluble
Relative vapor density (air =1)
ND; heavier than air
Molecular weight (g/mol)
ND; dependent on mixture composition
"Source: Monsanto (19601. A roc lor 5460 is a stable, nonflammable, yellow- to amber-colored resin that is
insoluble in water and in low molecular weight alcohols. It is also nonoxidizing, noncorrosive, thermoplastic,
and of low volatility.
ND = no data
A summary of available toxicity values for aroclor 5460 from EPA and other
agencies/organizations is provided in Table 2.
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Table 2. Summary of Available Toxicity Values for Aroclor 5460
(CASRN 11126-42-4)a
Source/Parametera'b
Value
(Applicability)0
Notes'1
Reference
Date Accessed
Noncancer
ACGIH
NV
NA
ACGIH (2013)
NA
ATSDR
NV
NA
ATSDR (2013)
NA
Cal/EPA
NV
NA
Cal/EPA (2013a.
b>
9-11-2013e
NIOSH
NV
NA
NIOSH (2010)
NA
OSHA
NV
NA
OSHA (2011.
2006)
NA
IRIS/RID, RfC
NV
NA
U.S. EPA
9-11-2013
Drinking Water
NV
NA
U.S. EPA (2012a)
NA
HEAST/RfD
NV
NA
U.S. EPA (2011a)
NA
CARA HEEP
NV
NA
U.S. EPA (1994b)
NA
WHO
NV
NA
WHO
9-11-2013
Cancer
IRIS/WOE, OSF
NV
NR
U.S. EPA
9-11-2013
HEAST
NV
NR
U.S. EPA (2011a)
NA
IARC
NV
NR
IARC (2013)
NA
NTP
NV
NR
NTP (2011)
NA
Cal/EPA
NV
NR
Cal/EPA (2013b.
2009)
NA
aSources: American Conference of Governmental Industrial Hygienists (ACGIH); Agency for Toxic Substances
and Disease Registry (ATSDR); California Environmental Protection Agency (Cal/EPA); National Institute for
Occupational Safety and Health (NIOSH); Occupational Safety and Health Administration (OSHA); Integrated
Risk Information System (IRIS); Health Effects Assessment Summary Tables (HEAST); Chemical Assessments
and Related Activities (CARA); Health and Environmental Effects Profile (HEEP); World Health Organization
(WHO); International Agency for Research on Cancer (IARC); National Toxicology Program (NTP).
Parameters: weight of evidence (WOE); reference dose (RfD); reference concentration (RfC); oral slope factor
(OSF).
°NV = not available.
dNA = not applicable; NR = not relevant.
eThe Cal/EPA Office of Environmental Health Hazard Assessment (OEHHA) Toxicity Criteria Database
(http://oeMia.ca.gov/todb/index.asp) was also reviewed and found to contain no information on aroclor 5460.
Literature searches were conducted on sources published from 1900 through
September 2013 for studies relevant to the derivation of provisional toxicity values for
aroclor 5460, using CASRN 11126-42-4. The following databases were searched by chemical
name, synonyms, or CASRN: ACGIH, ANEUPL, AT SDR, BIOSIS, Cal EPA, CCRIS, CD AT,
ChemlDplus, CIS, CRISP, DART, EMIC, EPIDEM, ETICBACK, FEDRIP, GENE-TOX,
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HAPAB, HERO, HMTC, HSDB, IARC, INCHEM IPCS, IP A, ITER, IUCLID, LactMed,
NIOSH, NTIS, NTP, OSHA, OPP/RED, PESTAB, PPBIB, PPRTV, PubMed (toxicology
subset), RISKLINE, RTECS, TOXLINE, TRI, U.S. EPA IRIS, U.S. EPAHEAST, U.S. EPA
HEEP, U.S. EPA OW, and U.S. EPA TSCATS/TSCATS2. The following databases were
searched for relevant health information: ACGIH, ATSDR, Cal EPA, U.S. EPA IRIS, U.S. EPA
HEAST, U.S. EPA HEEP, U.S. EPA OW, U.S. EPA TSCATS/TSCATS2, NIOSH, NTP,
OSHA, and RTECS.
REVIEW OF POTENTIALLY RELEVANT DATA
(CANCER AND NONCANCER)
Table 3 provides an overview of the relevant database for aroclor 5460 and includes all
potentially relevant repeated-dose short-term-, subchronic-, and chronic-duration studies via the
oral and inhalation routes. The phrase "statistical significance," used throughout the document,
indicates ap-value of <0.05.
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Table 3. Summary of Potentially Relevant Data for Aroclor 5460 (CASRN 11126-42-4)
Category
Number of Male/Female,
Strain, Species, Study
Type, Study Duration,
(Concentration)
Dosimetry"
Critical Effects
NOAEL'
BMDL/
BMCLa
LOAEL'
Reference
(Comments)
Notesb
Human
1. Oral (mg/kg-d)a
Acute0
ND
Short-termd
ND
Long-term6
ND
Chronicf
ND
2. Inhalation (mg/m3)a
Acute0
ND
Short-termd
ND
Long-term0
ND
Chronicf
ND
Animal
1. Oral (mg/kg-d)a
Subchronic
10/10, Albino rat, diet,
7 d/wk, 95 d, (0; 100;
300; and 1,000 ppm)
M: 0,7.13,
21.6.65.6
(ADD)
HED: 0,1.71,
5.18.15.7
F: 8.06,23.5,
77.8 (ADD)
HED: 0,1.93,
5.64,18.7
Increased absolute and relative liver weights
M: 7.13
(ADD)
F: 23.5
(ADD)
NC
M: 21.6
(ADD)
F: 77.8
(ADD)
Industrial
Bio-Test
Laboratories
(1983b)
NPR,
PS
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Table 3. Summary of Potentially Relevant Data for Aroclor 5460 (CASRN 11126-42-4)
Category
Number of Male/Female,
Strain, Species, Study
Type, Study Duration,
(Concentration)
Dosimetry3
Critical Effects
NOAEL3
BMDL/
BMCL3
LOAEL3
Reference
(Comments)
Notesb
Subchronic
6/0 (4 controls), Rhesus,
monkey, diet, 7 d/wk,
12 wk, (0 and 5,000 ppm)
0, 690 (ADD)
HED: 0, 311
Decreased body weight, alopecia, liver
hypertrophy, swollen eyelids and lips,
progressive generalized subcutaneous edema,
purulent discharge from the eyes, acne-like
lesions, and hypertrophy, hyperplasia, and
dysplasia of the gastric mucosa
NI
NC
690
(ADD)
Allen and
Norback
(1973)
PR
Developmental
ND
Reproductive
ND
Carcinogenicity
ND
2. Inhalation (mg/m3)a
Subchronic
ND
Chronic
ND
Developmental
ND
Reproductive
ND
Carcinogenicity
ND
""Dosimetry: NOAEL and LOAEL values are presented as an adjusted daily dose (ADD in mg/kg-d) and a human equivalent dose [HED in mg/kg-d, as calculated
according to U.S. EPA (2011b') Recommended Use of Body Weight3/4 as the Default Method in Derivation of the Oral Reference Dose] for oral noncancer effects. All
long-term exposure values (4 wk and longer) are converted from a discontinuous to a continuous (daily) exposure.
ADD = adjusted daily dose; ADD = dose in ppm x (daily food consumption body weight).
HED = human equivalent dose; HED = animal dose (mg/kg-d) x (BWa ^ BWh)14.
bNotes: PS = principal study; PR = peer reviewed; NPR = not peer reviewed; NA = not applicable.
" Acute = exposure for <24 hr (U.S. EPA. 2002).
'Short-term = repeated exposure for >24 hr < 30 d (U.S. EPA. 2002).
"Long-term = repeated exposure for >30 d < 10% lifespan (based on 70-yr typical lifespan) (U.S. EPA. 2002).
'Chronic = repeated exposure for >10% lifespan (U.S. EPA. 2002).
NC = not calculated; ND = no data; NI = not identified.
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HUMAN STUDIES
Oral Exposures
No studies were identified.
Inhalation Exposures
No studies were identified.
ANIMAL STUDIES
Oral Exposures
The effects of oral exposure of animals to aroclor 5460 were evaluated in two
subchronic-duration studies (Industrial Bio-Test Laboratories. 1983b; Allen and Norback. 1973).
Subchronic-Duration Studies
Industrial Bio-Test Laboratories (1983b)
In the subchronic-duration toxicity study performed for the Monsanto Company by
Industrial Bio-Test Laboratories (1983b). 10 Albino rats/sex/dose were exposed to aroclor 5460
in the diet continuously for 95 days. There is an inconsistency in the study report in which the
study authors indicated that the animals were sacrificed after 90 days (page 4 of the report);
however, body-weight data were provided through 95 days (page 7 of the report). Therefore, the
study is considered to be 95 days in duration. The animals were treated with aroclor 5460 (purity
not reported) at concentrations of 0; 100; 300; or 1,000 ppm. Adjusted daily doses are calculated
for this PPRTV assessment based on body weights and food intake rates reported by the authors.
Adjusted daily doses1 were 0, 7.13, 21.6, and 65.6 mg/kg-day for males and 0, 8.06, 23.5, and
77.8 mg/kg-day for females. Animals were housed individually in steel, wire-bottomed cages.
Pulverized Wayne Lab-Blox rat ration (Allied Mills, Chicago, IL) was provided ad libitum for
most of the study. For the last 5 weeks of feeding, pulverized Purina Labena Chow
(Ralston-Purina Co., St. Louis, MO) was provided. Dose formulations were prepared by
blending appropriately weighed amounts of aroclor 5460 with a preweighed portion of the stock
diet. No further information was reported concerning the animals, husbandry, and dosing. Body
weights were determined prior to treatment, weekly during treatment, and at necropsy. Overall
body-weight gain (Days 0-95) was calculated for each dose group and statistically analyzed.
Food consumption was measured weekly. Clinical observations on mortality and abnormal
behavior were made daily. Hematology, clinical chemistry, and urinalysis were conducted prior
to the beginning of treatment, on treatment Day 34, and prior to the conclusion of treatment on
Day 89 on five rats/sex from the control and 1,000-ppm groups. Hematological analyses
included hemoglobin concentration, erythrocyte count, hematocrit value, and total and
differential leukocyte counts. Clinical chemistry was limited to determining blood urea nitrogen
concentrations and serum alkaline phosphatase activity. Urinalyses included determination of
glucose, albumin, microscopic elements, urinary pH, and specific gravity. At the scheduled
termination, all animals were necropsied, and selected tissues (not specifically listed by the study
authors) were excised, processed, and examined microscopically. The liver, kidney, spleen,
gonads, heart, and brain were weighed. This study was not subjected to peer review and was
performed before EPA Good-Laboratory-Practice (GLP) guidelines became effective in 1984.
Adjusted daily dose = dose in ppm x (daily food consumption body weight). For 100 ppm in male rats: Adjusted
daily dose = 100 ppm x (0.0261 mg/day ^ 0.366 kg) = 7.13 mg/kg-day.
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No treatment-related effects were noted on mortality or behavior. Also, there were no
effects on hematology, clinical chemistry, or urinalysis (see Tables B-l through B-4). Though
not statistically significant, absolute body weight in the high-dose group was decreased by
approximately 10% throughout the treatment period in both sexes. A smaller decrease of
approximately 5% was also observed in most of the weekly body-weight measurements in both
sexes of the mid-dose group (see Table B-5). Total food consumption was decreased by 17% in
males and 8% in females in the high-dose group (see Table B-6). As shown in Table B-7, males
in the mid-dose group showed biologically significantly increased absolute (10%, not statistically
significant) and relative liver weights (14%, liver-to-body weight ratio). Additionally, males in
the high-dose group exhibited an increase in absolute liver weight (29%), liver-to-body weight
ratio (40%>), and liver-to-brain weight ratio (31%). Females in the high-dose group showed a
statistically significant increase in absolute, liver-to-body, and liver-to-brain weight
measurements (16—24%>). Also, females in the low-dose group showed statistically significant
decreases in relative spleen weight, but these changes were not dose dependent. No other
treatment-related effects on organ weight were observed (see Tables B-8 through B-12). Gross
and histopathological findings among treated animals were comparable to controls. The authors
did not report a NOAEL or a LOAEL for the study. However, based on biologically
significantly increased absolute and relative liver weights in the mid-dose male rats, a LOAEL of
21.6 mg/kg-day is identified, with a corresponding NOAEL of 7.13 mg/kg-day.
Allen and Nor back (1973)
Allen and Norback (1973) conducted a peer-reviewed, subchronic-duration study in
which aroclor 5460 (purity not reported) was administered in the diet to 6 male rhesus monkeys
at 5,000 ppm for 12 weeks. An adjusted daily dose of 690 mg/kg-day is calculated for this
PPRTV assessment utilizing the average body weight (2.9 kg) and daily food consumption
(0.4 kg) provided in the study report. Four male rhesus monkeys served as untreated controls.
All animals were provided 400 g of commercial feed (brand not stated) on a daily basis.
Throughout the course of the study, the general appearance of the animals was evaluated daily.
Blood was drawn biweekly for hematological and biochemical analysis of hemoglobin,
hematocrits, differential white count, serum glutamic oxaloacetic transaminase (SGOT), serum
glutamic pyruvic transaminase (SGPT), total protein, and serum electrophoresis. Additional
parameters assessed included body weight, histological examination of the liver and
gastrointestinal tract, and electron microscopy of the liver. Histopathological evaluation of other
tissues was not described.
The study authors reported an average decrease in body weight of 19% in the treated
group; however, raw body-weight data were not provided. Within 6 weeks, all of the
aroclor 5460-fed animals had alopecia. Hematocrit, lymphocytes, and total serum protein levels
were decreased after 12 weeks in the treated group (statistical significance not reported), but
information on hematological measurements was not provided for the control group. Findings at
necropsy included a purulent discharge exuded from the eyes, and isolated acneiform lesions
present on skin areas devoid of hair. A progressive, generalized, subcutaneous edema of the face
was manifested as swollen eyelids and lips. Liver weight was increased in the treated animals
(2.3%) of the body weight in controls versus 5.6% in the treatment group). Electron microscopy
analysis showed that the hypertrophic state of the liver in treated animals was due to an increase
in lipid droplets and proliferation of the smooth endoplasmic reticulum. Edematous thickening
of the stomach wall, marked hypertrophy of the pyloric and fundic regions, and ulceration of the
gastric mucosa were also noted in the aroclor 5460-treated animals. The study authors stated that
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the gastric submucosa contained large cystic areas that occasionally ruptured and led to necrosis.
However, the actual incidences of the clinical and pathological observations were not reported.
A NOAEL or LOAEL for this study was not specified by the authors. However, based on the
effects listed above, the 690 mg/kg-day dose is considered the LOAEL. Identification of a
NOAEL is precluded.
Chronic-Duration Studies
No studies were identified.
Developmental Studies
No studies were identified.
Inhalation Exposures
No inhalation studies were found on the subchronic-duration, chronic-duration,
developmental, or reproductive toxicity or on the carcinogenicity of aroclor 5460 in animals.
OTHER DATA (SHORT-TERM TESTS, OTHER EXAMINATIONS)
Table 4 summarizes other studies conducted with aroclor 5460 that are not appropriate
for selection of a point of departure (POD) for derivation of a provisional RfD (p-RfD) but
provide supportive data.
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Table 4. Other Studies
Test
Materials and Methods
Results
Conclusions
References
Developmental
White Leghorn chickens (4 males/20 females per dose
except 8 males at the high dose) were administered
aroclor 5460 in the diet at concentrations of 0; 500; 1,000;
or 2,000 ppm for 18 wk. Mortality, food consumption,
behavioral reaction, body weight, egg production, and
gizzard color were some of the parameters examined.
Maternal: Mortality as a frank
effect was observed at the high
dose in both sexes.
Fetal: Ambiguous results as
presented.
Confounding factors in this study
precluded conclusions on fetal
toxicity.
Industrial Bio-
Test Laboratories
(1983c. d)
Developmental
Twelve White Leghorn chicks (sex unspecified) were
administered aroclor 5460 in the diet at doses of 0, 50,
200, or 400 ppm for 21 d. Chicks were examined for
mortality, clinical signs of toxicity, body weight, and
pericardial fluid volume.
No effects observed.
Aroclor 5460 was not
developmentally toxic to chickens
at dose levels up to 400 ppm for
21 d.
Industrial Bio-
Test Laboratories
(1983a*)
Short-term
LD50 tests in rats
Oral LD50 in rats was
19,200 mg/kg.
The short-term toxicity of
aroclor 5460 in rats appeared
minimal.
Fishbein (1974)
as cited in Jensen
and Joreensen
(1983)
Short-term
Dermal minimum lethal dose (MLD) tests in rabbits
MLD in rabbits was 7,940 mg/kg.
The short-term toxicity of
aroclor 5460 in rabbits appeared
minimal.
Fishbein (1974)
as cited in Jensen
and Joreensen
(1983)
Metabolism/
toxicokinetic
Wistar rats (6 males/dose) were treated with 0; 10; 100;
or 1,000 ppm aroclor 5460 in the diet for 7 d. Tissue
distribution, weights, and microsomal activity (aniline
hydroxylase, aminopyrine .Y-dcmethvlasc and
cytochrome P450), protein, and phospholipid levels were
measured in the liver.
Liver weights were increased.
Residues were found in all tissues
analyzed but were highest in the
liver. Increased levels of enzyme
activity, microsomal protein, and
phospholipids were observed.
Aroclor 5460 has an inductive
effect on the hepatic microsomal
enzyme system.
Sosa-Lucero et
al. (1973 s)
Mode of action/
mechanistic
Four male S-D rats received daily intraperitoneal
injections of 0 or 300 mg/kg-d aroclor 5460 for 4 d and
sacrificed on Day 5. Livers were weighed and
microsomes prepared and analyzed using gel
electrophoresis and microsomal enzyme assays.
Increases were observed in
microsomal protein and
cytochrome P450 levels. No
changes in body or liver weight
were observed.
Aroclor 5460 has an inductive
effect on the hepatic microsomal
enzyme system.
Nilsen and
Tofteard (1981)
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Table 4. Other Studies
Test
Materials and Methods
Results
Conclusions
References
Mode of action/
mechanistic
CD-I mice (5/sex/dose) were given a single gavage dose
of 0; 50; 100; 250; 500; or 1,000 mg/kgbw aroclor 5460.
The mice were sacrificed 7 d after dosing. Intestines
were examined microscopically, and intestinal sacs were
prepared for the measurement of D-glucose absorption
and fluid transfer.
Aroclor 5460 treatment reduced
D-glucose absorption but not fluid
transfer.
Malabsorption of D-glucose
occurred and may have been
attributed to intracellular metabolic
effects of aroclor 5460.
Madge (1911)
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Developmental Studies in Chickens
Three developmental studies were conducted in chickens (Industrial Bio-Test
Laboratories. 1983a. c, d). EPA guidelines for acceptable developmental toxicity studies
(870.3700) require testing in the "most relevant species." The preferred species for
developmental toxicity studies are rats and rabbits. No evidence was presented in the available
studies to support the chicken as a relevant species for the assessment of the developmental
toxicity of aroclor 5460 as it pertains to humans. Furthermore, these studies did not evaluate
sufficient parameters for consideration as acceptable developmental toxicity studies. Other
study-specific deficiencies include inadequate presentation of methods and inadequate number of
dose groups. For these reasons, these studies are not considered acceptable developmental
toxicity studies suitable for establishing reference toxicity values.
Two separate reports were issued by Industrial Bio-Test Laboratories (1983c. d) to
Monsanto that describe different endpoints from what appears to be a single study. These studies
were performed before EPA GLP guidelines were established. Although somewhat illegible,
both reports appear to have the same study designation, IBT No. J5314. The report for the
longer-term study. Industrial Bio-Test Laboratories (1983c). was designated as a chicken toxicity
study with aroclor 5460. In this study, 12-week-old White Leghorn chickens were administered
aroclor 5460 (purity not reported) in the diet at concentrations of 0; 500; 1,000; or 2,000 ppm
(adjusted daily doses calculated for this PPRTV assessment are 0, 30.2, 62.6, and 126 mg/kg-day
for males and 0,40.9, 67.7, and 154.7 mg/kg-day for females).2 Each group had 4 males and
20 females; however, all four males at 2,000 ppm died at early time points (cause of death not
reported) and were replaced by four additional males. The duration of treatment was not
specified, although it is assumed that the dosing formulations were administered throughout the
evaluation period of 18 weeks. The chickens were weighed weekly beginning at Week 1 of the
experiment (when chickens were 12 weeks of age) through Week 18, and observed daily for
mortality and behavioral reaction. Food consumption measurements were made periodically and
reported in weekly intervals (average grams/chicken/day) through Week 16; however, food
consumption was not reported separately for each sex. As females in each group began laying
eggs, the eggs were collected twice a day, numbered, and weighed. No treatment-related effects
were observed on body weight, food consumption, or behavioral reaction (type of reaction
assessed not specified). Increased mortality was observed at 2,000 ppm in males (7/8 treated
versus 0/4 controls) and females (12/20 treated versus 4/20 controls), therefore, mortality
confounded the interpretation of the data as reported. Egg production was decreased at 1,000
and 2,000 ppm; however, the average number of eggs per chicken per week was not presented.
The content of the gizzard in many of the birds was green in color, but the significance of this
finding is unclear. No other treatment-related pathological findings were reported.
The second report, Industrial Bio-Test Laboratories (1983d). was designated as an egg
hatchability and chick viability study following aroclor 5460 treatment. The duration of
treatment was not stated, but chick viability data were only reported for 4 weeks. In this study,
12-week-old White Leghorn chickens were administered aroclor 5460 (purity not reported) in the
diet at concentrations of 0; 500; 1,000; or 2,000 ppm. At each dose, there were 4 males and
20 females; however, all 4 males at 2,000 ppm died (cause of death not reported) and were
replaced by 4 other males. The weight and food consumption of these animals were not
2Adjusted daily dose = dose in ppm x (daily food consumption body weight). For 500 ppm in male chickens:
Adjusted daily dose = 500 ppm x (0.117 mg/day ^ 1.94 kg) = 30.2 mg/kg-day.
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reported, thus adjusted daily doses could not be calculated. It was stated that food and water
were offered ad libitum to the chicks and that they were observed for 30 days prior to sacrifice
and necropsy to evaluate gross pathology. However, whether chicks were directly exposed to
aroclor 5460 is unclear. Hatchability, behavior, and chick viability were reported. Although a
treatment-related decrease in hatchability was observed, the lack of a clear understanding of the
dosimetry and treatment duration precludes the identification of a NOAEL and LOAEL.
In a separate study performed for Monsanto by Industrial Bio-Test Laboratories (1983a).
12 single-comb White Leghorn chicks (cockerels)/group were administered aroclor 5460 in the
diet at concentrations of 0, 50, 200, or 400 ppm ad libitum for 21 days. Adjusted daily doses
could not be calculated because daily food consumption data were not available for this study.
The chicks were received a day after hatching and were allowed a 48-hour acclimation period.
Chicks were examined daily for mortality and evidence of toxicity. Body weights were
measured prior to treatment and each week of treatment (Days 7, 14, and 21). After 21 days, the
chicks were sacrificed and necropsied. Pericardial fluid was collected and the volume measured.
Statistical analyses were focused on pericardial, subcutaneous, and peritoneal edema, and gross
liver and kidney damage. There was no evidence of pericardial edema or adverse effects on
mortality, behavioral reactions, body weight, or gross pathology. Based on the lack of observed
effects, the highest concentration tested (400 ppm) is considered the NOAEL.
Short-term-Duration Studies
Jensen and toraensen (1983) reported data from Fishbein (1974) that showed that the oral
LD50 in rats was 19,200 mg/kg for aroclor 5460. Additionally, the dermal minimum lethal dose
in rabbits was determined to be 7,940 mg/kg. Thus, the lethality of a single dose of aroclor 5460
is minimal.
Metabolism/Toxicokinetic Studies
Sosa-Lucero et at. (1973) evaluated the distribution of aroclor 5460 in rat tissues and its
effect on hepatic microsomal mixed function oxidase. Six male Wistar Albino rats/dose group
were sacrificed after treatment with 0; 10; 100; or 1,000 ppm (equivalent to adjusted daily doses
of 0, 0.7, 6.5, and 64.7 mg/kg-day)3 aroclor 5460 in the diet for 7 days. Blood, liver, brain,
kidney, spleen, testes, heart, and omental fat were taken, weighed, and analyzed by electron
capture gas chromatography to determine the concentration of aroclor 5460 found in each tissue.
Microsomes were isolated from the liver and enzyme assays were conducted. No macroscopic
manifestation of toxicity was observed, and body weights were not affected. Aroclor 5460
residues were found at dose-dependent concentrations in all tissues analyzed, with the greatest
concentration in the liver and the least in the brain. In animals administered 1,000 ppm, the
following statistically significant findings were observed: (1) absolute and relative liver weights
were increased by 15-18%; (2) microsomal protein and phospholipids were increased by
28-36%; (3) cytochrome P450 was increased by 72%; (4) aniline hydroxylase activity was
increased by 12%; and (5) aminopyrine A'-demethylase activity was increased by 63%. Although
glucose levels were decreased by 26%, these changes were not statistically significant. The
3Adjusted daily dose = dose in ppm x (daily food consumption body weight), where a default daily food
consumption value of 0.02 kg CU.S. EPA. 19881 was used and body weight information was obtained from Sosa-
Lucero et al. (19731.
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increased levels of drug-metabolizing enzyme activities and the parallel increase in the content
of microsomal protein, phospholipids, and cytochrome P450 indicated an inductive effect of
aroclor 5460 on the hepatic microsomal enzyme system in the male rat.
Mode of Action/Mechanistic Studies
In a study by Nilsen and Toftaard (1981). four male Sprague-Dawley rats were injected
intraperitoneally with aroclor 5460 (purity not reported) in corn oil at doses of 0 or 300 mg/kg
body weight each day for 4 days. Animals were killed on the morning of the fifth day following
a 24-hour fast. Livers were collected and weighed, and microsomes were prepared. Microsomes
were subjected to SDS-polyacrylamide gel electrophoresis and microsomal enzyme assay
analyses. Aroclor 5460 significantly increased (30%) the concentration of total microsomal
cytochrome P450 protein content, although no changes in body or liver weights were observed.
When the various forms of liver microsomal cytochrome P450 were analyzed separately,
increases were noted in cytochrome P450 RLvMc P450s5 (275%), RLvMc P450s4 (40%), and
RLvMc P45050 (83%). The in vitro capacity of liver microsomes to metabolize biphenyl,
benzo(a)pyrene, and androstene-3,17-dione was also increased (7- to 19-fold). These findings
indicate that aroclor 5460 increased the metabolic activity of the liver in rats.
Madge (1977) evaluated in vitro intestinal absorption of different substrates in the CD-1
mouse (five/sex/dose) following single gavage doses of aroclor 5460 in corn oil at doses of 0; 50;
100; 250; 500; or 1,000 mg/kg bw. Seven days after dosing, the mice were sacrificed. The
intestines were excised, examined microscopically, and in vitro inverted intestinal sacs were
prepared to measure D-glucose absorption. The histology of the small intestine was unchanged,
as was the wet intestinal weight. D-glucose absorption, but not fluid transfer, was significantly
decreased following treatment with 250; 500; or 1,000 mg/kg body weight of aroclor 5460.
Absorption of D-galactose, L-arginine, and L-histidine remained unaltered. When D-mannose, a
compound known to diffuse through intestinal tissues, was added to the serosal fluid to provide
absorptive cells with an added source of energy, differences in D-glucose absorption were not
found between aroclor 5460-treated animals and controls. The study author concluded that
malabsorption of D-glucose probably resulted from intracellular metabolic effects of
aroclor 5460 and not malfunctions of the D-glucose carrier at the mucosal membrane.
DERIVATION OF PROVISIONAL VALUES
Tables 5 and 6 present summaries of noncancer and cancer reference values, respectively.
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Table 5. Summary of Noncancer Reference Values for Aroclor 5460 (CASRN 11126-42-4)
Toxicity Type (units)
Species/Sex
Critical Effect
p-Reference
Value
POD Method
PODhed
UFC
Principal Study
Screening Subchronic p-RfD
(mg/kg-d)
Rat/M
Increased absolute and
relative (liver-to-body)
liver weight
6 x 1(T3
NOAEL
1.71
300
Industrial Bio-Test
Laboratories (1983b)
Screening Chronic p-RfD
(mg/kg-d)
Rat/M
Increased absolute and
relative (liver-to-body)
liver weight
6 x 1(T4
NOAEL
1.71
3,000
Industrial Bio-Test
Laboratories (1983^
Subchronic p-RfC (mg/m3)
NDr
Chronic p-RfC (mg/m3)
NDr
NDr = not determined.
Table 6. Summary of Cancer Values for Aroclor 5460 (CASRN 11126-42-4)
Toxicity Type
Species/Sex
Tumor Type
Cancer Value Principal Study
p-OSF
NDr
p-IUR
NDr
NDr = not determined.
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DERIVATION OF ORAL REFERENCE DOSES
No studies investigating the effects of aroclor 5460 are considered appropriate for the
derivation of p-RfDs. The database for aroclor 5460 oral toxicity studies includes two
subchronic-duration studies conducted in rats and monkeys (Industrial Bio-Test Laboratories.
1983b; Allen and Norback. 1973). The subchronic-duration monkey study by Allen and
Norback (1973) was peer reviewed and identified a LOAEL of 690 mg/kg-day based on skin,
liver and stomach effects. However, this study is limited because incidences of the findings were
not reported, only the liver and stomach were histopathologically analyzed, only young male
monkeys were used, and only a single high dose was tested. Benchmark dose modeling of the
data could not be performed due to the presence of a single treatment group.
From the subchronic-duration rat study by Industrial Bio-Test Laboratories (1983b) ,a
NOAEL of 7.13 mg/kg-day and a LOAEL of 21.6 mg/kg-day are identified for male rats based
on increased absolute and relative liver weight. Female rats were less sensitive, with a NOAEL
of 23.5 mg/kg-day and a LOAEL of 77.8 mg/kg-day for the same liver effects. No
histopathological changes in either sex were reported in the liver. This study was not peer
reviewed, and it was performed before EPA GLP guidelines were established. Additionally,
there are misgivings about the quality of the data presented because this study was performed
during a time where critical errors were committed at Industrial Bio-Test Laboratories.
Benchmark dose modeling was not possible because the study authors presented only mean
values without standard deviation (SD) or individual data.
Liver changes, such as increased liver weight and liver hypertrophy, were commonly
observed endpoints in several studies in multiple animal species treated with aroclor 5460
(Industrial Bio-Test Laboratories. 1983b; Shirai et al.. 1978; Allen and Norback. 1973). These
changes were associated with enhanced proliferation of liver cell smooth endoplasmic reticulum
and liver enzyme induction (Nilsen and Toftaard. 1981; Allen and Norback. 1973; Sosa-Lucero
et al.. 1973). Similar liver toxicity was also seen in monkeys chronically exposed to the related
PCB compound aroclor 1254. For example, animals treated with aroclor 1254, a compound
similar in chlorination to aroclor 5460, exhibit increased liver weights and hepatocellular
hypertrophy accompanied by progressive necrosis (U.S. EPA. 1994a). This observation further
supports the liver as a target organ for aroclor 5460 toxicity.
From the available database for oral exposure to aroclor 5460, the rat study by (Industrial
Bio-Test Laboratories. 1983b) is the only one that examines an adequate number of subjects of
both sexes, and provides the most sensitive LOAEL for liver effects (LOAEL = 21.6 mg/kg-day
for increased absolute and relative liver weight in male rats). However, because the report was
not peer reviewed or published, the data were not clearly presented, and there are concerns
regarding the quality of studies performed by Industrial Bio-Test Laboratories, this study is
considered unsuitable for the derivation of p-RfDs. Instead, screening p-RfDs are derived in
Appendix A.
DERIVATION OF INHALATION REFERENCE CONCENTRATIONS
No suitable published studies investigating the effects of subchronic- or chronic-duration
inhalation toxicity of aroclor 5460 in humans or animals were identified.
CANCER WEIGHT-OF-EVIDENCE (WOE) DESCRIPTOR
Table 7 identifies the cancer WOE descriptor for aroclor 5460.
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Table 7. Cancer WOE Descriptor for Aroclor 5460
Possible WOE
Descriptor
Designation
Route of Entry
(oral, inhalation, or
both)
Comments
"Carcinogenic to
Humans "
NS
NA
No human carcinogenicity data were
identified.
"Likely to Be
Carcinogenic to Humans"
NS
NA
No animal carcinogenicity studies were
identified.
"Suggestive Evidence of
Carcinogenic Potential"
NS
NA
No animal carcinogenicity studies were
identified.
"Inadequate Information
to Assess Carcinogenic
Potential"
Selected
Both
This descriptor is selected due to the lack
of any information on the carcinogenicity
of aroclor 5460.
"Not Likely to Be
Carcinogenic to Humans"
NS
NA
Although the genotoxicity studies were
negative or equivocal, there are no data to
indicate that aroclor 5460 is not
carcinogenic.
NA = not applicable; NS = not selected.
DERIVATION OF PROVISIONAL CANCER POTENCY VALUES
The lack of data on the carcinogenicity of aroclor 5460 precludes the derivation of
quantitative estimates for either oral (p-OSF) or inhalation (p-IUR) exposure.
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APPENDIX A. PROVISIONAL SCREENING VALUES
For the reasons noted in the main document, subchronic and chronic provisional
reference doses (p-RfDs) for aroclor 5460 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
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 Health Risk Technical Support Center.
DERIVATION OF SCREENING PROVISIONAL RfDs
The report by Industrial Bio-Test Laboratories (1983b) is selected as the principal study
for derivation of the screening p-RfD. The critical effect is increased absolute and relative liver
weight in male rats following exposure to aroclor 5460. Although this is an unpublished,
non-peer-reviewed sub chronic-duration rat study and there are misgivings regarding the quality
of studies performed by Industrial Bio-Test Laboratories historically, this particular study did
utilize an adequate number of animals and examined relevant tissues and parameters. Liver
effects are further supported by the similar response observed in female rats in the same study
and in monkeys in the only other subchronic-duration study ( Allen and Norback. 1973).
Although limited by their short-term duration and lack of comprehensive examination of tissues,
two other studies also support the liver as a target organ of aroclor 5460 toxicity, with observed
effects including increased liver weight, enhanced proliferation of liver cell smooth endoplasmic
reticulum, and liver enzyme induction (Mlsen and Toftgard. 1981; Allen and Norback. 1973;
Sosa-Lucero et al.. 1973). The monkey study is limited because it utilized only young males, did
not present quantitative histopathological information, and tested a single dose of aroclor 5460
(690 mg/kg-day), which is considerably higher than all doses tested in the rat study (Industrial
Bio- Test Laboratories. 1983b). Thus, the NOAEL of 7.13 mg/kg-day identified from the report
by Industrial Bio-Test Laboratories (1983b) constitutes the lowest point of departure (POD)
among available studies and is used as the POD in the derivation of screening p-RfDs.
Derivation of Screening Subchronic p-RfD
The screening subchronic p-RfD for aroclor 5460, based on the NOAEL of
7.13 mg/kg-day (Industrial Bio- Test Laboratories. 1983b). is derived as follows:
The U.S. EPA endorses body-weight scaling to the 3/4 power (BW3 4) 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. 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 or developmental endpoints.
Thus, following the U.S. EPA (2011b) guidance, the POD for increased absolute and relative
liver weight in male rats is converted to a human equivalent dose (HED) through an application
of a dosimetric adjustment factor (DAF) as follows:
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DAF =	(BWa1/4 - BWh1/4)
Where:
DAF =	dosimetric adjustment factor
BWa	=	animal body weight
BWh =	human body weight
Using a BWa of 0.25 kg for rats and a default BWh of 70 kg for humans (U.S. EPA.
201 lb), the resulting DAF is 0.24. Applying this DAF to the NOAEL identified in the rat
subchronic-duration study yields a NOAELhed as follows:
PODhed =	NOAEL (mg/kg-day) x DAF
=	NOAEL (mg/kg-day) x 0.24
=	7.13 (mg/kg-day) x 0.24
=	1.71 mg/kg-day
Screening Subchronic p-RfD = NOAELhed ^ UFc
= 1.71 mg/kg-day -^300
= 6 x 10~3 mg/kg-day
Table A. 1 summarizes the uncertainty factors for the screening subchronic p-RfD for
aroclor 5460.
Table A.l. Uncertainty Factors for the Screening Subchronic p-RfD for Aroclor 5460
UF
Value
Justification
ufa
3
A UFa of 3 (10°5) has been applied to account for uncertainty in characterizing the
toxicodynamic differences between rats and humans following oral aroclor 5460
exposure. The toxicokinetic uncertainty has been accounted for by calculation of a HED
through application of a DAF as outlined in the EPA's Recommended Use of Body
Weisht3/4 as the Default Method in Derivation of the Oral Reference Dose (U.S. EPA,
2011W.
ufd
10
A UFd of 10 has been applied because there are no acceptable two-generation
reproductive toxicity or developmental toxicity studies via the oral route.
UFh
10
A UFh of 10 has been applied for inter-individual variability to account for human-to-
human variability in susceptibility in the absence of quantitative information to assess
the toxicokinetics and toxicodynamics of aroclor 5460 in humans.
ufl
1
A UFl of 1 has been applied for LOAEL-to-NOAEL extrapolation because the POD is a
NOAEL
UFS
1
A UFS of 1 has been applied because a subchronic-duration study was selected as the
principal study.
UFC
300
Composite UF.
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Derivation of Screening Chronic p-RfD
Based on the same database and similar considerations, and utilizing the NOAELhed of
1.74 mg/kg-day (Industrial Bio-Test Laboratories. 1983b) as the POD, the screening chronic
p-RfD for aroclor 5460 is derived as follows:
Screening Chronic p-RfD = NOAELhed ^ UFc
= 1.71 mg/kg-day ^ 3,000
= 6 x 10~4 mg/kg-day
Table A.2 summarizes the uncertainty factors for the screening chronic p-RfD for
aroclor 5460.
Table A.2. Uncertainty Factors for the Screening Chronic p-RfD for Aroclor 5460
UF
Value
Justification
ufa
3
A UFa of 3 (10°5) has been applied to account for uncertainty in characterizing the
toxicodynamic differences between rats and humans following oral aroclor 5460
exposure. The toxicokinetic uncertainty has been accounted for by calculation of a
HED through application of a DAF as outlined in the EPA's Recommended Use of
Body Weight3'4 as the Default Method in Derivation of the Oral Reference Dose (U.S.
EPA. 201 lbl
ufd
10
A UFd of 10 has been applied because there are no acceptable two-generation
reproductive toxicity or developmental toxicity studies via the oral route.
UFh
10
A UFh of 10 has been applied for inter-individual variability to account for human-to-
human variability in susceptibility in the absence of quantitative information to assess
the toxicokinetics and toxicodynamics of aroclor 5460 in humans.
ufl
1
A UFl of 1 has been applied for LOAEL-to-NOAEL extrapolation because the POD
is a NOAEL.
UFS
10
A UFS of 10 has been applied to account for the extrapolation from less than chronic
exposure because no chronic-duration toxicity studies are available to evaluate
chronic systemic toxicity.
UFC
3,000
Composite UF.
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APPENDIX B. DATA TABLES
Table B-l. Hematologic Data from Albino Rats Exposed to Aroclor 5460 in the Diet for
95 Daysa b
Dose
(ppm)
Adjusted
Daily
Dose
(mg/kg-d)
Sex
Total Leukocyte Count (103/mm3) on
Day
Erythrocyte Count
(106/mm3) on Day
0
33
89
0
33
89
0
0
0
M
F
15.6
14.5
18.7
14.6
16.6
8.1
5.90
5.78
6.66
6.78
7.73
6.94
1,000
65.6
77.8
M
F
13.6 (-13)
13.6 (-6)
21.2(13)
21.4 (47)
16.3 (-2)
13.5 (67)
6.16(4)
6.46 (12)
6.34 (-5)
6.09 (-10)
6.87 (-11)
6.27 (-10)
Dose
(ppm)
Adjusted
Daily
Dose
(mg/kg-d)
Sex
Hemoglobin Concentration
(g/100 mL) on Day
Hematocrit Value (%) on Day
0
33
89
0
33
89
0
0
0
M
F
12.5
12.9
14.2
14.2
14.4
14.4
47
47
48
47
50
47
1,000
65.6
77.8
M
F
12.8 (2)
14.5 (12)
12.4 (-13)
12.2 (-14)
12.8 (-11)
12.7 (-12)
48	(2)
49	(4)
43 (-10)
42 (-11)
44 (-12)
43 (-9)
'Values were obtained from Industrial Bio-Test Laboratories (198351 from Table IV on page 11.
bData are presented as mean values (absolute % change from controls); % change is calculated.
Table B-2. Additional Hematologic Data from Albino Rats Exposed to Aroclor 5460 in the
Diet for 95 Daysa'b
Dose
(ppm)
Adjusted
Daily Dose
(mg/kg-d)
Sex
Differential Leukocyte Count (# cells/100)
Lymphocytes on Day
Neutrophils on Day
Monocytes on Day
0
33
89
0
33
89
0
33
89
0
0
0
M
F
87.6
90.0
92.8
94.4
85.0
92.8
9.8
6.2
6.6
4.8
14.4
6.2
2.4
3.2
0.2
0.0
0.4
0.2
1,000
65.6
77.8
M
F
87.6 (0)
84.8 (6)
79.0
(-15)
93.6(1)
84.2 (-1)
81.6
(-12)
8.8 (-10)
11.6 (87)
18.4
(179)
4.6 (-4)
15.0 (4)
17.4
(181)
3.2(33)
3.0 (-6)
0.2 (0)
0.0 (0)
0.4 (0)
1.0 (400)
Dose
(ppm)
Adjusted
Daily Dose
(mg/kg-d)
Sex
Eosinophils on Day
Basophils on Day
0
33
89
0
33
89
0
0
0
M
F
0.2
0.4
-t \o
© ©
0.2
1.0
0.0
0.2
0.0
0.2
o o
© ©
1,000
65.6
77.8
M
F
0.4 (100)
0.6 (50)
2.0 (400)
1.6(167)
0.4 (100)
0.0 (-100)
0.0 (0)
0.0 (-100)
0.4
0.2 (0)
0.0 (0)
0.0 (0)
'Values were obtained from Industrial Bio-Test Laboratories (1983b') from Table V on page 12.
bData are presented as mean values (absolute % change from controls); % change is calculated.
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Table B-3. Clinical Blood Chemistry Data from Albino Rats Exposed to Aroclor 5460 in the
Diet for 95 Daysa'b

Adjusted
Daily Dose
(mg/kg-d)

Serum Alkaline Phosphatase Activity
(King-Armstrong Units) on Day
Blood Urea Nitrogen Concentration
(mg Urea N/100 mL) on Day
Dose (ppm)
Sex
0
33
89
0
33
89
0
0
0
M
F
39
40
40
29
12
12
18
24
19
23
17
21
1,000
65.6
77.8
M
F
28 (-28)
27 (-33)
36 (-10)
25 (-14)
13(8)
12 (0)
18(0)
18 (-25)
20	(5)
21	(-9)
21 (24)
26 (24)
"Values were obtained from Industrial Bio-Test Laboratories (1983b) from Table VI on page 14.
bData are presented as mean values (absolute % change from controls); % change is calculated.
Table B-4. Urinalysis Data from Albino Rats Exposed to Aroclor 5460 in the Diet for 95 Days"



Glucose
Albumin






Examination of

Adjusted

Concentration
Concentration
Specific



Microscopic
Dose
Daily Dose

on Day
on Day
Gravity on Day
pH on Day
Elements on Day
(ppm)
(mg/kg-d)
Sex
0
33
89
0
33
89
0
33
89
0
33
89
0
33
89
0
0
M
n
n
n
n
n
t
1.015
1.031
1.037
6
7
7
N
N
N

0
F
n
n
n
n
n
n
1.020
1.034
1.033
6
7
6
N
N
N
1,000
65.6
M
n
n
n
n
n
t
1.026
1.027
1.022
7
7
7
N
N
N

77.8
F
n
n
n
n
n
t
1.015
1.035
1.028
6
7
6
N
N
N
'Values were obtained from Industrial Bio-Test Laboratories (1983b) from Table VII on page 16.
n = negative; N = normal; t = trace: less than 10 mg albumin/100 mL.
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Table B-5. Body Weight and Weight Gain Data from Albino Rats Exposed to Aroclor 5460
in the Diet for 95 Days"

Adjusted

Body Weight (g)b on Day
Dose (ppm)
Daily
Dose
(mg/kg-d)
Sex
0
7
14
21
28
35
42
49
0
0
M
109
163
218
280
311
341
372
394

0
F
107
146
171
200
205
223
227
239
100
7.13
M
110(1)
171 (5)
222 (2)
286 (2)
312 (0)
353 (4)
365 (-2)
400 (2)

8.06
F
107 (0)
148 (1)
170 (-1)
198 (-1)
206 (0)
219 (-2)
224 (-1)
242 (1)
300
21.6
M
109 (0)
166 (2)
218 (0)
269 (-4)
292 (-6)
327 (-4)
343 (-8)
374 (-5)

23.5
F
107 (0)
143 (-2)
163(—5)
190 (-5)
203 (-1)
216 (-3)
221 (-3)
234 (-2)
1,000
65.6
M
110(1)
159 (-2)
200 (-8)
254 (-9)
280 (-10)
309 (-9)
328 (-12)
357 (-9)

77.8
F
107 (0)
143 (-2)
161 (-6)
189 (-6)
196 (-4)
208 (-7)
214 (-6)
221 (-8)

Adjusted

Body Weight (g)b on Day
95-Day
Weight
Gains (g)
Dose (ppm)
Daily
Dose
(mg/kg-d)
Sex
56
63
70
77
84
91
95
0
0
M
431
444
452
488
503
510
516
407

0
F
251
257
254
274
280
276
282
175
100
7.13
M
424 (-2)
440 (-1)
442 (-2)
476 (-2)
487 (-3)
496 (-3)
501 (-3)
391 (-4)

8.06
F
247 (-2)
259 (1)
263 (4)
279 (2)
283 (1)
285 (3)
289 (2)
182 (4)
300
21.6
M
396 (-8)
423 (-5)
433 (-4)
462 (-5)
480 (-5)
491 (-4)
494 (-4)
385 (-5)

23.5
F
240 (-4)
256 (0)
258 (2)
267 (-3)
272 (-3)
270 (-2)
278 (-1)
171 (-2)
1,000
65.6
M
387 (-10)
406 (-9)
417 (-8)
446 (-9)
463 (-8)
463 (-9)
474 (-8)
364 (-11)

77.8
F
230 (-8)
238 (-7)
243 (-4)
252 (-8)
257 (-8)
259 (-6)
262 (-7)
155 (-11)
"Values were obtained from Industrial Bio-Test Laboratories (1983b) from Table II on page 7.
bData are presented as mean values (absolute % change from controls); % change is calculated.
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Table B-6. Food Consumption Data from Albino Rats Exposed to Aroclor 5460 in the Diet




for 95 Days
a



Dose
Adjusted Daily
Dose (mg/kg-d)

Food Consumed (g/rat/week) on Week
(ppm)
Sex
1
2
3b
4C
5d
6
7
0
0
M
127
153
215
174
82
229
209

0
F
99
112
177
138
62
139
138
100
7.13
8.06
M
F
130 (2)
104 (5)
158(3)
124(11)
231 (7)
164 (-7)
182 (5)
125 (-9)
109 (33)
70(13)
199 (-13)
121 (-13)
184 (-12)
133 (-4)
300
21.6
23.5
M
F
135 (6)
101 (2)
158(3)
117(4)
218(1)
158 (-11)
178 (2)
121 (-12)
105 (28)
72 (16)
182 (-21)
112 (-19)
181 (-13)
122 (-12)
1,000
65.6
77.8
M
F
97 (-24)
100 (1)
126 (-18)
113(1)
181 (-16)
154 (-13)
151 (-13)
119 (-14)
72 (-12)
54 (-13)
142	(-38)
143	(-3)
177 (-15)
114 (-17)



Food Consumed (g/rat/week) on Week
Total Food
Dose
(ppm)
Adjusted Daily
Dose (mg/kg-d)
Sex
8
9
10
ir
12
13
Consumption
(g/rat)
0
0
M
221
213
234
146
198
195
2,393

0
F
134
133
157
93
120
115
1,617
100
7.13
8.06
M
F
170 (-23)
141 (5)
184 (-14)
144 (8)
213 (-9)
169 (8)
132 (-10)
98 (5)
179 (-10)
133 (11)
177 (-9)
127 (10)
2,346 (-2)
1,653 (2)
300
21.6
23.5
M
F
190 (-14)
129 (-4)
187 (-12)
134(1)
231 (-1)
161 (3)
144 (-1)
91 (-2)
188 (-5)
121(1)
186 (-5)
116 (1)
2,283 (-5)
1,555 (-4)
1,000
65.6
77.8
M
F
163 (-26)
108 (-19)
185 (-13)
124 (-7)
218 (-7)
149 (-5)
131 (-10)
86 (-8)
173 (-13)
116 (-3)
173 (-11)
104 (-10)
1,989 (-17)
1,484 (-8)
"Values were obtained from Industrial Bio-Test Laboratories (1983b) from Table III on page 9.. Data are presented
as mean values (absolute % change from controls); % change is calculated.
bValues represent a 9-d period.
0Values represent an 8-d period.
dValues represent a 4-d period.
eValues represent a 6-d period.
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Table B-7. Liver and Body Weight Data from Albino Rats Exposed to Aroclor 5460 in the Diet for 95 Daysa'b
Dose (ppm)
Adjusted
Daily Dose
(mg/kg-d in
M/F)
Terminal body weight (g)
Absolute Liver Weight (g)
Liver/Body Weight Ratio
(g/100 g)
Liver/Brain Weight Ratio
(g/g)
Males
Females
Males
Females
Males
Females
Males
Females
0
0/0
516
282
22.6
11.7
4.39
4.16
11.8
5.98
100
7.13/8.06
501 (-3)
289 (2)
22.7 (0)
12.4 (6)
4.52 (3)
4.29 (3)
11.1(6)
6.08 (2)
300
21.6/23.5
494 (-4)
278 (-1)
24.8 (10)
11.7 (0)
5.02(14)*
4.23 (2)
12.3 (4)
6.07 (2)
1,000
65.6/77.8
474 (-8)
262 (-7)
29.1 (29)**
13.6(16)**
6.14(40)**
5.16(24)**
15.5 (31)**
7.06 (18)**
'Values were obtained from Industrial Bio-Test Laboratories (1983b') from Table VIII on page 18.
bData are presented as mean values (absolute % change from controls); % change is calculated.
*p < 0.05; **p < 0.01
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Table B-8. Kidney Weight Data from Albino Rats Exposed to Aroclor 5460 in the Diet for
95 Daysab
Dose (ppm)
Adjusted
Daily Dose
(mg/kg-d in
M/F)
Absolute Kidney Weight
(g)
Kidney/Body Weight
Ratio (g/100 g)
Kidney/Brain Weight
Ratio (g/g)
Males
Females
Males
Females
Males
Females
0
0/0
3.95
2.17
0.766
0.770
2.06
1.10
100
7.13/8.06
3.70 (-6)
2.21 (2)
0.738 (-4)
0.767 (0)
1.81 (-12)
1.09 (-1)
300
21.6/23.5
3.87 (-2)
2.36 (9)
0.785 (2)
0.848 (10)
1.92 (-7)
1.22(11)
1,000
65.6/77.8
3.70 (-6)
2.19(1)
0.782 (2)
0.833 (8)
1.97 (-4)
1.14(4)
"Values were obtained from Industrial Bio-Test Laboratories (1983b') from Table IX on page 19.
bData are presented as mean values (absolute % change from controls); % change is calculated.
Table B-9. Spleen Weight Data from Albino Rats Exposed to Aroclor 5460 in the Diet for
95 Daysab
Dose
(ppm)
Adjusted Daily Dose
(mg/kg-d in M/F)
Absolute Spleen Weight
(g)
Spleen/Body Weight Ratio
(g/100 g)
Spleen/Brain Weight
Ratio (g/g)
Males
Females
Males
Females
Males
Females
0
0/0
0.773
0.627
0.151
0.222
0.402
0.320
100
7.13/8.06
0.684 (-12)
0.498 (-21)
0.137 (-9)
0.172
(-23)**
0.336 (-16)
0.24 (-25)**
300
21.6/23.5
0.695 (-10)
0.546 (-13)
0.14 (-7)
0.196 (-12)
0.344 (-14)
0.282 (-12)
1,000
65.6/77.8
0.701 (-9)
0.563 (-10)
0.148 (-2)
0.214 (-4)
0.373 (-7)
0.293 (-8)
'Values were obtained from Industrial Bio-Test Laboratories (1983b') from Table X on page 20.
bData are presented as mean values (absolute % change from controls); % change is calculated.
**p < 0.01
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Table B-10. Gonad Weight Data from Albino Rats Exposed to Aroclor 5460 in the Diet for
95 Daysab
Dose
(ppm)
Adjusted Daily Dose
(mg/kg-d in M/F)
Absolute Gonad
Weight (g)
Gonad/Body Weight Ratio
(g/100 g)
Gonad/Brain Weight
Ratio (g/g)
Males
Females
Males
Females
Males
Females
0
0/0
3.35
0.125
0.651
0.0444
1.74
0.0638
100
7.13/8.06
3.48 (4)
0.126(1)
0.698 (7)
0.0438 (-1)
1.70 (-2)
0.0622 (-3)
300
21.6/23.5
3.53 (5)
0.110 (-12)
0.719(10)
0.0398 (-10)
1.75(1)
0.0571 (-11)
1,000
65.6/77.8
3.36 (0)
0.130(4)
0.713 (10)
0.0494 (11)
1.80 (3)
0.0675 (6)
"Values were obtained from Industrial Bio-Test Laboratories (1983b) from Table XI on page 21.
bData are presented as mean values (absolute % change from controls); % change is calculated.
Table B-ll. Heart Weight Data from Albino Rats Exposed to Aroclor 5460 in the Diet for
95 Daysab
Dose
(ppm)
Adjusted Daily Dose
(mg/kg-d in M/F)
Absolute Heart Weight
(g)
Heart/Body Weight Ratio
(g/100 g)
Heart/Brain Weight Ratio
(g/g)
Males
Females
Males
Females
Males
Females
0
0/0
1.54
1.00
0.301
0.357
0.803
0.513
100
7.13/8.06
1.56(1)
0.981 (-2)
0.313 (4)
0.341 (-4)
0.767 (-4)
0.485 (-5)
300
21.6/23.5
1.57 (2)
0.965 (-4)
0.318(6)
0.348 (-3)
0.778 (-3)
0.499 (-3)
1,000
65.6/77.8
1.55 (1)
0.930 (-7)
0.328 (9)
0.355 (-1)
0.827 (3)
0.485 (-5)
'Values were obtained from Industrial Bio-Test Laboratories (1983b) from Table XII on page 22.
bData are presented as mean values (absolute % change from controls); % change is calculated.
Table B-12. Brain Weight Data from Albino Rats Exposed to Aroclor 5460 in the Diet for


95 Days"


Dose
Adjusted Daily Dose
(mg/kg-d in M/F)
Absolute Brain Weight (g)
Brain/Body Weight Ratio (g/100 g)
(ppm)
Males
Females
Males
Females
0
0/0
1.92
1.96
0.375
0.699
100
7.13/8.06
2.04 (6)*
2.13 (9)
0.410 (9)
0.742 (6)
300
21.6/23.5
2.02 (5)
1.94 (-1)
0.411 (9.6)
0.699 (0)
1,000
65.6/77.8
1.88 (-2)
1.92 (-2)
0.399 (6)
0.735 (5)
"Values were obtained from Industrial Bio-Test Laboratories (1983b) from Table XIII on page 23.
bData are presented as mean values (absolute % change from controls); % change is calculated.
*p < 0.05
28
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APPENDIX C. BMD OUTPUTS
BMD analysis is not performed for this assessment.
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APPENDIX D. REFERENCES
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31
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