United States
Environmental Protection
1=1 m m Agency
EPA/690/R-12/027F
Final
11-01-2012
Provisional Peer-Reviewed Toxicity Values for
Thallium and Compounds
Metallic Thallium (7440-28-0), Thallium (I) acetate (563-68-8),
Thallium (I) carbonate (6533-73-9), Thallium (I) chloride (7791-12-0),
Thallium (I) nitrate (10102-45-1), and Thallium (I) sulfate (7446-18-6)
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
Nina Ching Y. Wang, PhD
National Center for Environmental Assessment, Cincinnati, OH
CONTRIBUTORS
Michael Griffith, PhD
National Center for Environmental Assessment, Cincinnati, OH
Jon Reid, PhD, DABT
National Center for Environmental Assessment, Cincinnati, OH
DRAFT DOCUMENT PREPARED BY
ICF International
9300 Lee Highway
Fairfax, VA 22031
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	iii
BACKGROUND	1
HISTORY	1
DISCLAIMERS	2
QUESTIONS REGARDING PPRTVS	2
INTRODUCTION	2
REVIEW OF POTENTIALLY RELEVANT DATA (CANCER AND NONCANCER)	3
HUMAN AND ANIMAL STUDIES	10
Carcinogenicity Studies	10
Inhalation Exposures	10
DERIVATION 01 PROVISIONAL VALUES	10
DERIVATION OF PROVISIONAL ORAL REFERENCE DOSES	10
DERIVATION OF INHALATION REFERENCE CONCENTRATIONS	11
CANCER WEIGHT-OF-EVIDENCE DESCRIPTOR	11
DERIVATION OF PROVISIONAL CANCER POTENCY VALUES	11
APPENDIX A. PROVISIONAL SCREENING VALUES	12
APPENDIX B. DATA TABLES	17
APPENDIX C. REFERENCES	20
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COMMONLY USED ABBREVIATIONS
BMC
Benchmark Concentration
BMD
Benchmark Dose
BMCL
Benchmark Concentration Lower bound 95% confidence interval
BMDL
Benchmark Dose Lower bound 95% confidence interval
HEC
Human Equivalent Concentration
HED
Human Equivalent Dose
IRIS
Integrated Risk Information System
IUR
inhalation unit risk
LOAEL
lowest-observed-adverse-effect level
LOAELadj
LOAEL adjusted to continuous exposure duration
LOAELhec
LOAEL adjusted for dosimetric differences across species to a human
NOAEL
no-ob served-adverse-effect level
NOAELadj
NOAEL adjusted to continuous exposure duration
NOAELhec
NOAEL adjusted for dosimetric differences across species to a human
NOEL
no-ob served-effect level
OSF
oral slope factor
p-IUR
provisional inhalation unit risk
p-OSF
provisional oral slope factor
p-RfC
provisional reference concentration (inhalation)
p-RfD
provisional reference dose (oral)
POD
point of departure (oral)
RfC
reference concentration (inhalation)
RfD
reference dose
UF
uncertainty factor
UFa
animal to human uncertainty factor
UFC
composite uncertainty factor
UFd
incomplete to complete database uncertainty factor
UFh
interhuman uncertainty factor
UFl
LOAEL to NOAEL uncertainty factor
UFS
subchronic to chronic uncertainty factor
WOE
weight of evidence
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PROVISIONAL PEER-REVIEWED TOXICITY VALUES FOR THALLIUM AND
COMPOUNDS: METALLIC THALLIUM (7440-28-0),
THALLIUM (I) ACETATE (563-68-8), THALLIUM (I) CARBONATE (6533-73-9),
THALLIUM (I) CHLORIDE (7791-12-0), THALLIUM (I) NITRATE (10102-45-1),
THALLIUM (I) OXIDE (1314-12-1), THALLIUM (III) OXIDE (1314-32-5),
THALLIUM (I) SELENITE (12039-52-0), AND THALLIUM (I) SULFATE (7446-18-6)
BACKGROUND
HISTORY
On December 5, 2003, the U.S. Environmental Protection Agency's (EPA) Office of
Superfund Remediation and Technology Innovation (OSRTI) revised its hierarchy of human
health toxicity values for Superfund risk assessments, establishing the following three tiers as the
new hierarchy:
1)	EPA's Integrated Risk Information System (IRIS).
2)	Provisional Peer-Reviewed Toxicity Values (PPRTVs) used in EPA's Superfund
Program.
3)	Other (peer-reviewed) toxicity values, including
~	Minimal Risk Levels produced by the Agency for Toxic Substances and Disease
Registry (ATSDR),
~	California Environmental Protection Agency (CalEPA) values, and
~	EPA Health Effects Assessment Summary Table (HEAST) values.
A PPRTV is defined as a toxicity value derived for use in the Superfund Program when
such a value is not available in EPA's IRIS. PPRTVs are developed according to a Standard
Operating Procedure (SOP) and are derived after a review of the relevant scientific literature
using the same methods, sources of data, and Agency guidance for value derivation generally
used by the EPA IRIS Program.
This PPRTV assessment was developed using only information provided in the
Toxicological Review of Thallium and Compounds (CAS No. 7440-28-0) (U.S. EPA. 2009). All
of the information provided in this document was available to peer reviewers according to the
standard IRIS peer review process.
No toxicity values were posted on the IRIS database (U.S. EPA. 2009) for thallium
because of limitations in the database of toxicological information. However, the Toxicological
Review presents information which could be used for development of an RfD. In this document,
an appendix with a "screening subchronic and chronic p-RfD" is provided, recognizing the
quality decrements, which may be of value under certain circumstances, described later in this
document.
Because new information becomes available and scientific methods improve over time,
PPRTVs are reviewed on a 5-year basis and updated into the active database. Once an IRIS
value for a specific chemical becomes available for Agency review, the analogous PPRTV for
that same chemical is retired. It should also be noted that some PPRTV documents conclude that
a PPRTV cannot be derived based on inadequate data.
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DISCLAIMERS
Users of this document should first check to see if any IRIS values exist for the chemical
of concern before proceeding to use a PPRTV. If no IRIS value is available, staff in the regional
Superfund and Resource Conservation and Recovery Act (RCRA) program offices are advised to
carefully review the information provided in this document to ensure that the PPRTVs used are
appropriate for the types of exposures and circumstances at the Superfund site or RCRA facility
in question. PPRTVs are periodically updated; therefore, users should ensure that the values
contained in the PPRTV are current at the time of use.
It is important to remember that a provisional value alone tells very little about the
adverse effects of a chemical or the quality of evidence on which the value is based. Therefore,
users are strongly encouraged to read the entire PPRTV document and understand the strengths
and limitations of the derived provisional values. PPRTVs are developed by the EPA Office of
Research and Development's National Center for Environmental Assessment, Superfund Health
Risk Technical Support Center for OSRTI. Other EPA programs or external parties who may
choose of their own initiative to use these PPRTVs are advised that Superfund resources will not
generally be used to respond to challenges of PPRTVs used in a context outside of the Superfund
Program.
QUESTIONS REGARDING PPRTVS
Questions regarding the contents of the PPRTVs and their appropriate use (e.g., on
chemicals not covered, or whether chemicals have pending IRIS toxicity values) may be directed
to the EPA Office of Research and Development's National Center for Environmental
Assessment, Superfund Health Risk Technical Support Center (513-569-7300), or OSRTI.
INTRODUCTION
An IRIS Toxicological Review of Thallium and Compounds was previously developed
and posted (http ://www. epa. gov/iri s/toxreviews/1012tr. pdf). However, due to study and data
quality limitations as stated in the IRIS Toxicological Review, an RfD was not derived.
Although these limitations precluded the derivation of an RfD, there are dose-response data that
may be used in the derivation of screening subchronic and chronic p-RfDs (see Appendix A).
This PPRTV for Thallium and Compounds is based mostly on the IRIS Toxicological Review;
all relevant text and tables were either reproduced or adapted from the IRIS Toxicological
Review.
Metallic thallium (Tl) is insoluble in water; however, the majority of the thallium salts
are soluble in water with the exception of thallium (III) oxide. Thallium compounds and their
chemical and physical properties are listed in Table 1. Thallium occurs naturally in the earth's
crust. It is used in industry, but is also released due to combustion of fossil fuels, refinement of
oil fractions, smelting of ores, and by some other industrial processes such as cement production
and brickworks (Kazantzis. 2007; IPCS. 1996). A summary of past uses and possible health
effects of thallium (I) sulfate as cited in the IRIS Toxicological Review is provided as follows:
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Due to its ability to remove hair, thallium (I) sulfate was used in the past
as a depilatory agent. Thallium (I) sulfate was once used in medicine to treat
infections, such as venereal diseases, ringworm of the scalp, typhus, tuberculosis,
and malaria. It was also used in the past as a pesticide for various rodents and
insects but has been bannedfor this use in the U.S. since 1972. Currently,
thallium is used in the semiconductor industry and the manufacture of optic
lenses. When thallium is alloyed with mercury, it is used on switches and
closures, which can operate at subzero temperatures. Thallium compounds are
also used to manufacture low-melting glass, low-temperature thermometers,
alloys, electronic devices, mercury lamps, fireworks, and imitation gems.
Thallium radioisotopes are used in medicine for scintigraphy of certain tissues
and the diagnosis of melanoma (Ibrahim et al., 2006; National Library of
Medicine [NLM], 1998; IPCS, 1996; Agency for Toxic Substance and Disease
Registry [ATSDR], 1992; U.S. EPA, 1991).
Table 1. Chemical and Physical Properties of Thallium
and Selected Thallium Compounds"
Name
CASRN
Chemical
Formula
Molecular
Weight
Melting Point
(C)
Boiling Point
(C)
Solubility in Water
(g/L)
Metallic thallium
7440-28-0
T1
204.38
303.5
1457
Insoluble
Thallium (I) acetate
563-68-8
T1C2H302
263.43
131
No data
Very soluble
Thallium (I) carbonate
6533-73-9
ti2co3
468.78
273
No data
40.3 (15.5C)
Thallium (I) chloride
7791-12-0
T1C1
239.84
430
720
Very soluble (20C)
Thallium (I) nitrate
10102-45-1
T1N03
266.39
206
430
95.5 (20C)
Thallium (I) oxide
1314-12-1
T120
424.77
596
No data
Soluble
(as TIOH)
Thallium (III) oxide
1314-32-5
ti2o3
456.76
717
875
Insoluble
Thallium (I) selenite
12039-52-0
Tl2Se03
535.72
No data
No data
No data
Thallium (I) sulfate
7446-18-6
T12S04
504.82
632
Decomposes
48.7 (20C)
"Sources: IPCS (1996); Downs 0993); ATSDR CI9921. Table was obtained directly from Table 2-1 in U.S. EPA (2009).
REVIEW OF POTENTIALLY RELEVANT DATA
(CANCER AND NONCANCER)
Table 2 provides a summary of studies of thallium toxicity in humans. Table 3 provides
a summary of oral toxicity studies of thallium (and compounds) in animals. No inhalation
studies in animals or human were identified. A literature search through May 2009 was
conducted in support of the IRIS Toxicological Review of Thallium and Compounds (U.S. EPA.
2009); an updated literature search was not conducted in developing the PPRTV for Thallium
and Compounds. All pertinent data on thallium and related compounds have been reviewed by
IRIS, and a Toxicological Review is available (U.S. EPA. 2009). Tables 2 and 3 are adapted
from the Toxicological Review with minor clarifications (U.S. EPA (2009), Tables 4-1 and 4-5,
respectively).
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Table 2. Thallium Toxicity In Humans Following Oral Exposure
Reference
Sex
Age
Dose
Symptoms"
Final Outcome
Males-Adult
Gefel et al.
(1970)
Male
41 years
Unknown but chronic;
urine thallium
0.15 mg/100 mL
High blood pressure; lower back pain; vomiting; severe pain in the feet;
weakness of the calf muscle; alopecia; slurred speech; atrophic lower limbs;
limited vision
Death
Cavanagh
et al. (1974)
Male
60 years
0.93 g thallium (I)
acetate in 2 divided
doses
Diarrhea; vomiting; dizziness; back pain; paresthesia of the feet and lower legs;
high blood pressure; facial weakness; dysphagia; difficulty breathing
Death within a week of
symptoms
Cavanagh
et al. (1974)
Male
56 years
0.93 g thallium (I)
acetate in 3 divided
doses
Abdominal pain; diarrhea; vomiting; paresthesia; photophobia, nystagmus,
visual impairment; facial weakness; bilateral ptosis
Death within 3 weeks of
symptoms
Cavanagh
et al. (1974)
Male
26 years
0.31 g thallium (I)
acetate
Paresthesia in both feet; chest pain; tenderness over the sternum; vomiting,
weakness, pain in the knees and ankles that inhibited walking; alopecia
Recovery
Davis et al.
(1981)
Male
19 years
5-10 g thallium (I)
nitrate
Nausea; vomiting; slurred speech; paresthesia of hands and feet; respiratory
weakness
Death
Limos et al.
(1982)
Male
56 years
Unknown
Visual disturbances; alopecia; elevated aspartate aminotransferase (AST) and
alanine aminotransferase (ALT); high blood glucose and creatine kinase;
decreased myelinated fibers; denervated Schwann cell clusters
Bedridden; could not speak
Limos et al.
(1982)
Male
26 years
Unknown
Visual disturbances; alopecia; elevated AST and ALT; high blood glucose and
creatine kinase; decreased myelinated fibers; denervated Schwann cell clusters
Residual tremors of the
extremities and muscle
weakness of the lower
limbs
Roby et al.
(1984)
Male
45 years
Unknown; urine
thallium:
2000 ng/L
Burning pain in feet; inability to walk; alopecia; acute fibrillation
Continued neurological
dysfunction
Heyl and
Barlow
(1989)
Male
"Five
young
men"
Unknown
Follicular plugging of the skin (nose, cheeks, and nasolabial folds) by keratinous
material; crusted eczematous lesions and acneiform eruptions on the face; dry
scaling on palms and soles; and alopecia (scalp, eyelashes, lateral eyebrows,
arms, and legs). Skin biopsies (scalp and cheek): disintegrating hair shafts, gross
follicular plugging, and eosinophilic keratohyalin granules in the epidermis;
necrotic sebaceous glands; pustular lesions on the face: folliculitis and necrosis
of the follicles; (feet) marked hyperkeratosis and hypergranulosis
4/5 recovered; 1/5
experienced permanent
neurological damage
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Table 2. Thallium Toxicity In Humans Following Oral Exposure
Reference
Sex
Age
Dose
Symptoms"
Final Outcome
Yokoyama
etal. (1990)
Male
31 years
Unknown; urine
thallium:
3.5 mg/L
Nausea, vomiting; leg pain; alopecia; abnormal behavior; decreased conduction
velocity of fast nerve fibers
Recovery
Hantson et
al. ^1997^
Male
48 years
200 mg thallium (I)
sulfate
No overt symptoms within 24 hours; increase in binucleated cells with
micronuclei 15 days after exposure
Recovery
Hirata et al.
(1998)
Male
29 years
Unknown; hair
thallium: 20 ng/g
(32 months after
possible exposure)
Alopecia; abdominal pain; diarrhea; tingling in extremities; neuropathy
Recovery
Atsmon et
al. (2000)
Male
40 years
Unknown; urine
thallium: 7 mg
Weakness of the limbs; vomiting; severe neurological symptoms; alopecia; high
blood pressure; increased ALT and AST; Mees lines; decreased visual acuity;
bilateral foot drop
Recovery
Sharma et
al. (2004)
Male
48 years
Unknown; serum
thallium:
870 ng/100 mL urine
thallium: 5000 |ig/mL
Painful peripheral neuropathy; decreased consciousness
Death
Females-Adult
Roby et al.
(1984)
Female
51 years
Unknown; serum
thallium:
50 ng/100 mL; urine
thallium: 5000 |ig/L
Numbness and weakness of the legs and hands; alopecia; fluctuating pulse and
blood pressure; bradycardia; hypotension
Persistent ventricular
ectopy and neurological
dysfunction, necessitating
placement at a nursing
home
Roby et al.
(1984)
Female
61 years
Unknown; serum
thallium:
740 (ig/100 mL
Burning chest pain; paresthesia; difficulty speaking and swallowing; inability to
walk; hypotension; acute respiratory distress syndromeb (ARDS)
Death
Roby et al.
(1984)
Female
80 years
Unknown; serum
thallium:
422 ng/100 mL; urine
thallium: 21,600 |ig/L
ARDS
Death
Hoffman
(2000)
Female
Pregnant;
ages not
specified
150-1350 mg thallium
(I) sulfate
Paresthesia; abdominal pain; muscle weakness; lethargy; alopecia; Mees lines
[lines of discoloration across the nails of the fingers and toes]
None specified
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Table 2. Thallium Toxicity In Humans Following Oral Exposure
Reference
Sex
Age
Dose
Symptoms"
Final Outcome
Saha et al.
(2004)
Female
26 years
Unknown; serum
thallium:
12 ng/100 mL
Headache; lethargy; abdominal pain; muscle cramps; joint pain; backache;
numbness of fingers; alopecia; erosion of nails
Not specified
Both Sexes-Adult
Brockhaus
et al. (1981)
Both
Not
reported
Unknown
Sleep disorders; tiredness; weakness; nervousness; headache; other psychic
alterations; neurological and muscular symptoms
Not reported
Schoer
(1984);
Gosselin et
al. (1984)
Both
Adult
10-15 mg/kg thallium
None specified
Death (average lethal dose)
Rusyniak et
al. (2002)
Both
Various
Unknown; various
levels were detected in
urine
Myalgia; arthralgia; paresthesia; dysesthesia; joint stiffness; insomnia; alopecia;
abdominal pain
Recovery in seven adults;
five had ongoing
psychiatric problems
Tsai et al.
(2006)
Both
48-year
old
female;
52-year
old male
1.5-2.4 g
Confusion; disorientation; hallucination; anxiety; depression; memory
impairment; peripheral neuropathy; erythematous skin rashes; diarrhea;
tachycardia; alopecia
Impairment of memory and
verbal fluency remained at
six months;
neuropsychological
impairment persisted at
nine months
Lu et al.
(2007); Kuo
et al. (2005)
Both
48 and 52
years
I.5	and 2.3 g/person
(estimated); serum
thallium:
950-2056 |ig/L; Urine
thallium:
II,325-14,520	(ig/L
Nausea, vomiting; general aching muscle pain; numbness of tongue and mouth
within a few hours; severe paresthesia and dysesthesia in hands and feet (one day
post exposure); erythematous rash; diarrhea; urine retention; hyporeflexia;
muscle weakness; hypoesthesia; acneiform eruptions; alopecia (1-3 weeks);
Mees lines (2-3 months).
Skin biopsy: parakeratosis; dilated hair follicles filled with keratin and necrotic
sebaceous materials; mild epidermal atrophy; vacuolar degeneration of the basal
layer.
Cutaneous nerve biopsy: axonal degeneration; loss of epidermal nerves
indicating involvement of the small sensory nerves (2 months).
At 1-year follow-up,
persistent paresthesia,
dysesthesia, and
impairment of small
sensory nerve fibers in skin
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Table 2. Thallium Toxicity In Humans Following Oral Exposure
Reference
Sex
Age
Dose
Symptoms"
Final Outcome
Children
Reed et al.
(1963)
Both
1-11
years
Unknown
Alopecia; lethargy; ataxia; abdominal pain; vomiting; abnormal reflexes;
neuropathy; muscle weakness; coma; convulsion
Neurological abnormalities;
retardation; psychosis;
death
Feldman
and
Levisohn
(1993s)
Male
10 years
Unknown; serum
thallium: 296 |ig/L:
urine thallium:
322 ng/24 hours
Alopecia; leg paresthesia; abdominal pain; seizures
Recovery
Hoffman
(2000)
Both
Trans-
placental
Unknown
Premature birth; low birth weight; alopecia
None specified
Ammendola
et al. (2007)
Male
16 years
1.3 g thallium sulfate;
urine thallium:
3400 ng/L
Acute stage: gastrointestinal disturbances; alopecia; clinical and
electrodiagnostic signs of severe polyneuropathy
3 years postpoisoning:
neurological symptoms
making progress;
electrophysiological signs
of peripheral neuropathy
mainly confined to lower
limbs. 6 years
postpoisoning: persistent
weakness and sensory
disturbances of distal lower
extremities; neurological
and electrodiagnostic
abnormalities affecting
mainly the feet.
"ALT = alanine aminotransferase; AST = aspartate aminotransferase
bARDS = acute respiratory distress syndrome
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Table 3. Thallium Toxicity in Animals Following Oral Exposure3
Reference
Species
Age
Sex
Route
Dose and Duration
NOAEL
LOAEL
Effect
Acute studies
Leloux et al.
(1987)
Rat
3/sex
Adult
Both
Oral (gavage)
20 mg/kg thallium (I)
nitrate; single dose
NIb
15 mg/kg Tl
Difficulty breathing; rough coat; increased
absolute kidney, adrenal weights; death
Leloux et al.
(1987)
Rat
10/sex/
group
Adult
Both
Oral (gavage)
0, 1 mg/kg thallium (I)
nitrate; once daily for
4 days
NI
0.77 mg/kg Tl
Alopecia; diarrhea; increased absolute
kidney, eye weights; death
Mourelle et
al. (1988)
Rat
10/group
NS
Male
Oral (gavage)
0, 10 mg/kg thallium
(I) sulfate; single dose.
Sacrificed at 24 hours
to 2 days after dosing
NI
8.1 mg/kg Tl
Liver changes: increased triglycerides and
lipid peroxidation; decreased glutathione
and glycogen; increased alkaline
phosphatase in serum and liver cell
membranes
Subchronic studies
Downs et al.
(1960)
Rat/
5/sex/
group
NS
Both
Oral (feed)
0, 5, 15, or 50 ppm
thallium (I) acetate
(corresponding to 0,
0.4, 1.2, or
3.9 mg/kg-day Tl);
15 weeks
0 or 30 ppm
(corresponding to 0 or
2.4 mg/kg-day Tl);
9 weeks
0.4 mg/kg-day
Tl*
1.2 mg/kg-day Tl*
Alopecia; increased kidney weight;
mortality in treated and control groups.
*The NOAEL and LOAEL are for alopecia.
Because of reported mortality in the control
and treated groups, a study NOAEL and
LOAEL cannot be reliably determined.
Downs et al.
(1960)
Rat
5/sex/
group
Weanling
Both
Oral (feed)
0, 20, 35, 50, 100, and
500 ppm thallium (III)
oxide (corresponding
toO, 1.8,3.1,4.5,9.0,
and 44.8 mg/kg-day
Tl); 15 weeks
NI
1.8 mg/kg-day Tl
(20 ppm)
Reduced body weight; alopecia; increased
mortality; increased absolute and relative
kidney weights
El-Garawany
et al. (1990)
o
cd II
04 s:
NS
Male
Orald
0.8 mg/kg thallium (I)
sulfate; 90 days
NI
0.65 mg/kg-day Tl
Increased blood urea; serum creatinine;
serum bilirubin; serum ALT
Manzo et al.
(1983)
o
00
cd II
04 s:
NS
Female
Oral (DWe)
10 mg/L Tl as
thallium (I) sulfate;
36 weeks
NI
1.4 mg/kg-day Tl
Nerve histopathology; alopecia; mortality
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Table 3. Thallium Toxicity in Animals Following Oral Exposure3
Reference
Species
Age
Sex
Route
Dose and Duration
NOAEL
LOAEL
Effect
MRI (1988)
Rat
20/sex/
group
45 days
Both
Oral (gavage)
0,0.01, 0.05, or
0.25 mg thallium (I)
sulfate/kg
(corresponding to 0,
0.008, 0.04, or
0.20 mg/kg-day Tl);
90 days
NI
0.008 mg/kg-day
Tlf
Increased incidence of alopecia and other
observations related to coat (rough coat,
piloerection, shedding); lacrimation,
exophthalmos, and miosis; and various
behavioral observations; statistically
significant increases in AST, LDH, and
sodium levels; decreased blood sugar levels.
The study authors identified 0.2 mg/kg-day
Tl as the NOAEL.
Reproductive and developmental toxicity
Formigli et al.
(1986);
Gregotti et al.
(1985)
Rat
10/group
Adult
Male
Oral (DW)
0, 10 ppm thallium (I)
sulfate; 30 or 60 days
NI
0.7 mg/kg-day Tl
Testicular effects: tubular epithelium
disarrangement; cytoplasmic vacuolation;
reduced sperm motility; distention of
smooth endoplasmic reticulum of Sertoli
cells; reduced p-glucuronidase activity
Wei (1987)
Mouse
NS
Male
Oral (DW)
0,0.001,0.01,0.1,
1.0, and 10 mg/L
thallium (I) carbonate
(corresponding to 0,
0.0003, 0.003, 0.03,
0.3, and 3 mg/kg-day
Tl); 6 months
NI
0.0003 mg/kg-day
Tl
Decreased sperm motility and counts;
increase in deformed sperm; decrease in live
fetuses.
Dose estimated from an assumed average
body weight of 20 g and drinking water
ingestion rate of 6 mL/day.
Rossi et al.
(1988)
Rat
Perinatal
Both
[Oral
(Mother's,
then pup's
DW)]
0, 1 mg/dL of thallium
(I) sulfate
Day 1 of gestation to
weaning then thru
60 days
NI
NI
Prenatal and postnatal exposure caused a
delay in the development of the pilus
apparatus [the formation of hair] by 50 days;
reduction of the a- and (^-adrenergic and
muscarinic vasomotor reactivity noted.
aU.S. EPA (2009) Table 4-5.
I:'NI = not identified.
NS = not specified.
Presumably via gavage.
eDW = drinking water.
fSee discussion of the NOAEL and LOAEL determination in Section 5.1.1 of U.S. EPA (20091.
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HUMAN AND ANIMAL STUDIES
Refer to the IRIS Toxicol ogical Review (U.S. EPA. 2009) for summaries of human and
animal studies. The principal study selected for derivation of screening subchronic and chronic
p-RfDs (Midwest Research Institute. 1988) is summarized in Appendix A.
Carcinogenicity Studies
No studies of the carcinogenicity of thallium or thallium compounds were identified in
the IRIS Toxicological Review (U.S. EPA. 2009).
Inhalation Exposures
No studies were identified in the IRIS Toxicological Review (U.S. EPA. 2009) regarding
the effects of subchronic or chronic inhalation exposure of animals to thallium or thallium
compounds.
DERIVATION OF PROVISIONAL VALUES
DERIVATION OF PROVISIONAL ORAL REFERENCE DOSES
Although there are substantial data available on human exposure to thallium, the majority
are case reports of poisonings, suicide attempts, or accidental ingestion of rodenticides. There
are two population surveys with oral thallium exposure through contaminated homegrown foods
(Dolgner et al.. 1983; Brockhaus et al.. 1981). However, these studies are limited by the lack of
objective tests for toxicity, reliance on the incidence of symptoms obtained from questionnaires,
and characterization of chronic thallium exposure by measuring the levels in urine and hair at a
single point in time (U.S. EPA. 2009). In addition, three occupational exposure studies (Ludolph
et al.. 1986; Marcus. 1985; Schaller et al.. 1980) provide no conclusive associations between
thallium exposure and any specific health effects, possibly due to the small study populations
and study design limitations. Therefore, the available human studies are not suitable for
derivation of a p-RfD.
There are numerous animal studies on the effects of thallium; however only four
repeat-dose oral toxicity studies with more than one dose level were identified (Midwest
Research Institute. 1988; Wei. 1987; Zasukhina et al.. 1983; Downs et al.. 1960). Wei (1987).
Zasukhina et al. (1983). and Downs et al. (1960) were not considered adequate for RfD
derivation (see U.S. EPA (2009) for details). The MRI (1988) 90-day study in rats was
evaluated in the IRIS Toxicological Review as a candidate principal study as the most
comprehensive of the available thallium studies. Histopathological changes in the skin (hair
follicle atrophy in high-dose female rats with alopecia) and clinical observations, including those
related to animal coat (rough coat, piloerection, shedding, and alopecia), eyes (including
lacrimation, exophthalmos, and miosis), and behavior were considered as possible endpoints for
POD derivation.
The conclusion reached in the IRIS Toxicological Review of Thallium and Compounds
(U.S. EPA. 2009) was that the available toxicity database for thallium contains studies that are
generally of poor quality. The MRI (1988) study that was selected as a candidate principal study
for RfD derivation suffers from certain critical limitations (e.g., high background incidence of
alopecia, lack of histopathological examination of skin tissue in low- and mid-dose groups, and
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inadequate examination of objective measures of neurotoxicity), and there are particular
difficulties in the selection of appropriate endpoints. Therefore, a RfD for soluble thallium salts
was not derived.
However, Appendix A of this document contains Screening Values (screening subchronic
and chronic p-RfD) that may be useful in certain instances. See the attached Appendix A.
DERIVATION OF INHALATION REFERENCE CONCENTRATIONS
As reviewed in the Toxicological Review of Thallium and Compounds (U.S. EPA. 2009)
no subchronic or chronic p-RfC values can be derived because there are no suitable studies of
inhalation exposures.
CANCER WEIGHT-OF-EVIDENCE DESCRIPTOR
The Cancer WOE descriptor for thallium is provided in the Toxicological Review of
Thallium and Compounds (U.S. EPA, 2009) as "Inadequate Information to Assess Carcinogenic
Potential (both oral and inhalation)"
DERIVATION OF PROVISIONAL CANCER POTENCY VALUES
The lack of data on the carcinogenicity of any thallium compound as indicated in the
IRIS Toxicological Review (U.S. EPA. 2009) 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, it is inappropriate to derive a subchronic or
chronic p-RfD for thallium. However, information is available 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. 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 a supplemental 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 PROVISIONAL ORAL REFERENCES DOSES
The 90-day study by MRI (1988) is selected as the principal study for derivation of the
screening subchronic and chronic p-RfD. This study was summarized in the Toxicological
Review (U.S. EPA. 2009) as follows:
In a study performed by Midwest Research Institute (Midwest Research
Institute, 1988) for EPA 's Office of Solid Waste, male andfemale Sprague-
Dawley rats (45 days old, 20/sex/group) were administered 0 (untreated and
vehicle controls), 0.01, 0.05, or 0.25 mg/kg-day of an aqueous solution of thallium
(I) sulfate (approximately 0, 0.008, 0.04, or 0.20 mg/kg-day Tl) by gavage for
90 days. The study was conducted in compliance with EPA good laboratory
practice (GLP) mandates. The MRI (1988) study is an unpublished study;
accordingly, an external peer review was initiated by EPA in November 2006.
Body weight, food consumption, hematologic and clinical chemistry parameters,
ophthalmologic examinations, gross pathological observations, and organ
weights (liver, kidneys, brain, gonads, spleen, heart, and adrenals) were recorded
for all animals. Neurotoxicological examinations (three times/week) were
performed on six rats/sex/group; these examinations were apparently
observational (further details were not provided in the study report). Tissues
from three rats/sex/group were prepared for neuropathologic examination.
Complete histopathologic examinations (including neuropathologic
examinations) were conductedfor the vehicle control and 0.2 mg/kg-day Tl
groups only; for the other three groups, only the livers, lungs, kidneys and gross
lesions were examined histopathologically. Neuropathologic examinations
included the following: dorsal and ventral root fibers of the spinal nerves, dorsal
root ganglia, spinal cord at C3-C6 andLl-L4, and six sections of the brain.
There were no statistically significant differences in body weight, food
consumption, or absolute and relative organ weights among control groups and
groups receiving thallium (I) sulfate (Midwest Research Institute. 1988). The
study authors concluded that the histopathologic examination did not reveal any
treatment-related effects.
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Lacrimation (secretion of tears), exophthalmos (abnormalprotrusion of
the eyeball), and miosis (contraction of the pupil) were observed at higher
incidences in the treated male and female rats compared with both untreated and
vehicle controls (see Table B.l;Midwest Research Institute. 1988).
Ophthalmologic examination and gross and histopathologic examination of the
eyes, however, revealed no treatment-related abnormalities. The incidence of
clinical observations related to the coats (including rough coat, piloerection,
shedding, and alopecia) and behavior (including aggression, tension/agitation,
hyperactivity, vocalization, and self-mutilation) were also elevated in male and
female rats at the higher doses (see Table B.l; Midwest Research Institute. 1988).
As noted above, the incidence of alopecia was increased, particularly in
female rats (see Table B.2; Midwest Research Institute, 1988). Examination of
individual animal clinical observation data for female rats from the MRI (1988)
study showed that alopecia was first observed in control and treated groups
anywhere from study day 44 to 60. Based on a statistical analysis performed by
the U.S. EPA, the incidence of alopecia (total number of cases in each dose
group) was statistically significantly elevated relative to controls in mid-dose
males and mid- and high-dose females. Most instances of alopecia in females
were attributed to barbering behavior (where fur was present but cropped short).
Of the 12 high-dose females with alopecia, 5 instances were not totally attributed
to barbering behavior. Histopathologic examination revealed atrophy of the hair
follicles in two high-dose female rats. Because the skin was examined for
histopathologic changes only in the vehicle control and high-dose groups, no
information on dermal histopathology was available for the low- and mid-dose
groups. The two high-dose females with atrophy of the hair follicles also had
alopecia; whether the hair follicle atrophy and alopecia occurred at the same
location on the rats could not be determinedfrom the study report. The study
authors concluded that the alopecia was attributable to the cyclic pattern of hair
growth in rodents. Consequently, the authors did not consider these findings to
be toxicologically significant.
Subtle but statistically significant changes were observed in several blood
chemistry parameters that the investigators considered probably treatment
related (Midwest Research Institute. 1988). Specifically, dose-related increases
in AST, lactate dehydrogenase (LDH), and sodium levels and decreases in blood
sugar levels were detected in male andfemale rats after 30 and 90 days of
exposure. Reported values for the selected blood chemistry parameters are
summarized in Table B.3. Other changes in blood chemistry parameters were
less consistent across species, dose groups, and exposure durations.
At 90 days, the differences in AST, LDH, sodium, and blood sugar levels
in dosed male andfemale rats were no greater than +31, +38, +4, and -21%,
respectively, of the vehicle control group values (Midwest Research Institute.
1988). The investigators observed that the increases in AST and LDH levels
could indicate a possible effect of treatment on cardiac function, that increases in
LDH coupled with subtle changes in electrolytes could indicate an effect on renal
function, and that, in rare instances, a decrease in blood sugar coupled with an
increase in sodium occurs as a defense mechanism for maintaining cellular
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integrity. The investigators concluded that none of the changes observed in the
blood chemistries of male or female rats during the study were of sufficient
magnitude to significantly affect the health status of the animals. Further,
histopathologic evaluation did not confirm any cellular damage suggested by the
clinical chemistry findings.
The authors concluded that the minor dose-related changes in this study did not affect the
health status of the treated animals and therefore were not toxicologically significant and
identified the highest dose, 0.25 mg/kg-day thallium (I) sulfate (0.20 mg/kg-day T1 [2 moles of
soluble thallium (I) in one mole of the soluble thallium salt, TI2SO4]), as a no-observed-effect
level (NOEL). However, after review, EPA (2009) came to different conclusions as indicated
below:
Several candidates for critical effects were considered, but ultimately EPA (2009)
considered that only two endpoints were appropriate for RfD development: (1) hair follicle
atrophy in female rats that also had alopecia and (2) clinical observations; those related to animal
coat (rough coat, piloerection, shedding, and alopecia), eyes (including lacrimation,
exophthalmos, and miosis) and behavior. Endpoint (2) was not selected as the critical effect in
this PPRTV because there is a high background occurrence of alopecia in control animals and
the potential for misclassification. As a result, there is some uncertainty about the incidence of
treatment-related alopecia in the treated animals. In addition, the underlying basis for other
clinical observations is unknown. Endpoint (1) was selected as the critical effect because
atrophy of hair follicles is consistent with the atrophic changes observed in the cases of human
thallium poisoning (e.g., follicular plugging of the skin including alopecia) and may be the best
indicator for human response to thallium exposure. For this PPRTV, hair follicle atrophy is
selected as the critical effect because it may serve as a better indicator of alopecia resulting from
thallium exposure.
The high dose (0.25 mg/kg-day thallium [I] sulfate or 0.2 mg/kg-day soluble Tl) was
characterized as a LOAEL. Because skin tissue from rats in the low- and mid-dose groups was
not examined for histopathologic changes, the NOAEL for this endpoint cannot be determined
with certainty. Given the low incidence of hair follicle atrophy in females in the high dose group
and absence of cases of hair follicle atrophy in male rats, the mid-dose can reasonably be
assumed to approximate a NOAEL for skin histopathology. Thus, an estimated NOAEL of
0.05 mg/kg-day thallium (I) sulfate (TI2SO4) or 0.04 mg/kg-day Tl (soluble form) was used as
the POD for hair follicle atrophy from the MRI (1988) study.
The screening subchronic p-RfD was derived using a composite UF of 1000 as follows:
Screening Subchronic p-RfD
(Thallium [I] Sulfate)
NOAEL -h UFc
0.05 mg/kg-day T12S04 - 1000
5 x 10"5 mg/kg-day Thallium (I) Sulfate
Screening Subchronic p-RfD
(Soluble Thallium)
NOAEL -h UFc
0.04 mg/kg-day Tl 1000
4 x 10" mg/kg-day Tl
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The calculation of the NOAEL for soluble T1 being:
2 moles TT	204.3 8 g (MW TT)
0.04 mg/kg-day = 0.05 mg/kg-day x
x
1 mole T12S04 504.82 g (MW T12S04)
An interspecies UFa of 10 is applied for extrapolation from laboratory animals to humans
since no information is available to characterize the toxicokinetic or toxicodynamic differences
between experimental animals and humans.
An intraspecies UFH of 10 is applied to account for variation in human susceptibility in
the absence of information on the variability of response to thallium in the human population.
A database UFD of 10 is applied to account for a lack of adequate developmental toxicity
studies and a two-generation reproductive study, and additional uncertainty associated with the
limited data available on neurotoxicity.
An UFs of 1 applied for extrapolation from subchronic studies since the principal study is
considered a subchronic study.
An UFl of 1 is applied to account for extrapolation from LOAEL to NOAEL, because a
NOAEL was utilized.
The screening chronic RfD was derived using a composite UF of 3000 as follows:
An interspecies UFA of 10 is applied for extrapolation from laboratory animals to humans
since no information is available to characterize the toxicokinetic or toxicodynamic differences
between experimental animals and humans.
An intraspecies UFh of 10 is applied to account for variation in human susceptibility in
the absence of information on the variability of response to thallium in the human population.
A database UFd of 10 is applied to account for a lack of adequate developmental toxicity
studies and a two-generation reproductive study, and additional uncertainty associated with the
limited data available on neurotoxicity.
An UFS of 3 is applied to account for extrapolation from subchronic to chronic exposure
duration. As explained in the IRIS Toxicological Review, "Oral toxicity data for thallium
suggest that an UF of 10 would overestimate the difference in response following subchronic and
chronic oral exposures. Effects on the coat/skin as well as other clinical observations occur
Screening Chronic p-RfD
(Thallium [I] Sulfate)
NOAEL -h UFC
0.05 mg/kg-day T12S04 - 3000
2 x 10" mg/kg-day Thallium (I) Sulfate
Screening Chronic p-RfD
(Soluble Thallium)
NOAEL -h UFC
0.04 mg/kg-day T1 3000
1 x 10"5 mg/kg-day T1
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within weeks of exposure to thallium (i.e., these sensitive effects do not require chronic exposure
in order to manifest)."
An UFl of 1 is applied to account for extrapolation from LOAEL to NOAEL, because a
NOAEL was utilized.
Based on molecular weight (MW) adjustments and stoichiometric calculations, a
summary of screening subchronic and chronic p-RfDs for other soluble thallium salts is
presented in Table A.l.
Table A.l. Screening Subchronic and Chronic p-RfDs for Other Thallium Salts
Thallium Salt
(Formula; MW)
Screening Subchronic p-RfD
(mg/kg-day)
Screening Chronic p-RfD
(mg/kg-day)
Thallium (I) acetate
(T1C2H302; 263.43)
5 x 10"5a
1 x 10"5b
Thallium (I) carbonate
(T12C03; 468.78)
5 x 10"5c
2 x 10"5d
Thallium (I) chloride
(T1C1; 239.84)
5 x 10"5a
1 x 10"5b
Thallium (I) nitrate
(T1N03; 266.39)
5 x 10"5a
1 x 10"5b
aBased on the screening subchronic p-RfD for soluble thallium and the molecular weight conversion as follows:
screening subchronic p-RfD of (1:1) thallium salt = screening subchronic p-RfD of soluble thallium x (Molecular
weight of (1:1) thallium salt ^ Molecular weight of thallium), rounded to one significant figure. For example, for
the screening subchronic p-RfD of thallium (I) acetate = 4 x 10"5 mg/kg-day T1 x MW(T1C2H302) ^ MW(T1) =
4 x 10"5 mg/kg-day x (263.43 204.38) = 5 x 10"5 mg/kg-day.
bBased on the screening chronic p-RfD for soluble thallium and the molecular weight conversion as follows:
screening chronic p-RfD of (1:1) thallium salt = screening chronic p-RfD of soluble thallium x (Molecular weight
of (1:1) thallium salt ^ Molecular weight of thallium), rounded to one significant figure. For example, for the
screening chronic p-RfD of thallium (I) acetate =1 x 10"5 mg/kg-day T1 x MW(T1C2H302) ^ MW(T1) =
1	x 10"5 mg/kg-day x (263.43 204.38) = 1 x 10"5 mg/kg-day.
Based on the subchronic screening p-RfD for thallium (I) sulfate and the molecular weight conversion as follows:
screening subchronic p-RfD of (2:1) thallium salt = screening subchronic p-RfD of thallium (I) sulfate x
(Molecular weight of (2:1) thallium salt Molecular weight of thallium [I] sulfate), rounded to one significant
figure. For the screening subchronic p-RfD of thallium (I) carbonate = 5 x 10"5 mg/kg-day T12S04 x MW(T12C03)
- MW(T12S04) = 5 x 10"5 mg/kg-day x (468.78 - 504.82) = 5 x 1 () s mg/kg-day.
dBased on the chronic screening p-RfD for thallium (I) sulfate and the molecular weight conversion as follows:
screening chronic p-RfD of (2:1) thallium salt = screening chronic p-RfD of thallium (I) sulfate x (Molecular
weight of (2:1) thallium salt ^ Molecular weight of thallium [I] sulfate), rounded to one significant figure. For the
screening chronic p-RfD of thallium (I) carbonate = 2 x 10"5 mg/kg-day T12S04 x MW(T12C03) MW(T12S04) =
2	x 10"5 mg/kg-day x (468.78 504.82) = 2 x 10"5 mg/kg-day.
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APPENDIX B. DATA TABLES
Table B.l. Selected Clinical Observations in Sprague-Dawley Rats Treated

with Thallium Sulfate for 90 Days"


Observation1"
Untreated Control
Vehicle Control
0.008 mg/kg-day
0.04 mg/kg-day
0.2 mg/kg-day
Male
Coat/skin
Rough coat
1/20
3/20
11/20
16/20
19/20
Piloerection
0/20
0/20
1/20
4/20
13/20
Shedding
0/20
0/20
4/20
10/20
8/20
Alopecia
2/20
1/20
4/20
9/20
4/20
Eyes
Lacrimation
1/20
6/20
19/20
20/20
20/20
Exophthalmos
1/20
5/20
12/20
20/20
20/20
Miosis
0/20
1/20
5/20
7/20
15/20
Behavior0
3/20
0/20
7/20
6/20
7/20
Female
Coat/skin
Rough coat
1/20
0/20
1/20
5/20
11/20
Piloerection
0/20
0/20
0/20
3/20
8/20
Shedding
0/20
0/20
2/20
3/20
13/20
Alopecia
4/20
1/20
4/20
9/20
12/20
Eyes
Lacrimation
7/20
6/20
20/20
20/20
20/20
Exophthalmos
5/20
6/20
19/20
20/20
20/20
Miosis
2/20
3/20
1/20
11/20
8/20
Behavior0
2/20
2/20
0/20
1/20
7/20
'MRI (19881. Table was obtained directly from Table 4-2 in U.S. EPA (20091.
''Listed as number of animals with the sign observed at least once during the 90-day study.
0 Animals exhibiting one or more behavioral observations at least once during the 90-day study, including the
following: aggression, tension/agitation, hyperactivity, vocalization, self-mutilation.
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Table B.2. Incidence of Alopecia in Rats"
Dose
(mg/kg-day Tl)
Males
Females
Alopeciab'c
Hair follicle atrophy0
Alopeciab'c
Hair follicle atrophyd
0 (untreated control)
2/20
e
4/20
e
0 (vehicle control)
1/20
0/20
1/20
0/20
0.008
4/20
e
4/20
e
0.04
9/20f
e
9/208
e
0.2
4/20
0/20
12/20f
2/20
aMRI (19881. Table was obtained directly from Table 4-3 in U.S. EPA (20091.
dumber of animals with alopecia at least once during the 90-day study based on clinical observations.
Of the animals with alopecia, the following are the numbers of cases in each dose group that the study authors stated
are not totally attributed to "barbering behavior":
Males: untreated control, 1; vehicle control, 0; 0.008 mg/kg-day, 2; 0.04 mg/kg-day, 4; 0.2 mg/kg-day, 1.
Females: untreated control, 0; vehicle control, 0; 0.008 mg/kg-day, 1; 0.04 mg/kg-day, 3; 0.2 mg/kg-day, 5.
dBased on histopathologic observation.
eSkin was not examined for histopathologic lesions.
incidence of alopecia (total number of cases) was statistically significantly elevated (p < 0.05) relative to incidence in
vehicle control, incidence in untreated control, and pooled incidence of vehicle and untreated control, based on
Fisher's exact test performed by EPA.
incidence of alopecia (total number of cases) was statistically significantly elevated (p < 0.05) relative to incidence in
vehicle control and pooled incidence of vehicle and untreated control, based on Fisher's exact test performed by
EPA.
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Table B.3. Selected Blood Chemistry Values3

Study
Untreated
Vehicle
0.008
0.04
0.2
Endpoint
Day
Control
Control
mg/kg-day
mg/kg-day
mg/kg-day
Malesb
AST (I.U.)
30
91 26.5
108  18.6
128  24.5
134  29.0'd
152  20.1'd

90
77  19.7
87  17.8
99  20.4
113 27.0c,d
114  31.1cd
LDH (I.U.)
30
795  322
1206  424
1333  340
1396  407
1802  341'd

90
587 305
856  385
1003  363
1071 507
1119  477
Na (meq/L)
30
148  1.3
149 2.4
152  4.0
154  2.5'd
153  2.1'd

90
144  1.6
147  2.0
147  1.9
149  2.0'd
151  2.2'd
Blood sugar
30
100 22.1
97  18.1
93  10.0
90  18.3
62  14.8'd
(mg/100 mL)
90
158  15.6
138  16.8
131  17.6
121  15.7
113 22.4c'd
Femalesb
AST (I.U.)
30
95 22.8
115 30.3
127  27.8
149  26.8'd
154  18.2'd

90
77  19.2
90  19.1
93 33.1
111 30.7
112  31.0
LDH (I.U.)
30
1047 335
1277  495
1402 501
1763  370'd
1764  361'd

90
745  320
881 273
823  354
1044  436
1219  338b
Na (meq/L)
30
148  1.7
150  1.9
153  4.10 d
154  2.8'd
155  2.5'd

90
146  1.8
146  1.0
148  1.80 d
150  2.0'd
152  1.0o d
Blood sugar
30
103 23.9
80  13.3
80  9.0
67  20.0
50  11.8'd
(mg/lOOmL)
90
110 28.7
89  15.9
103  19.9
88  20.4
70  18.0
aMRI (19881. Table was obtained directly from Table 4-4 in U.S. EPA (20091.
''Mean  standard deviation of 7-10 rats.
Significantly different (p <0.05) from the untreated control group.
dSignificantly different (p < 0.05) from the vehicle control group.
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APPENDIX C. REFERENCES
Ammendola. A; Ammendola. E; Argenzio. F; Tedeschi. G. (2007). Clinical and
electrodiagnostic follow-up of an adolescent poisoned with thallium. Neurol Sci 28: 205-
208. http://dx.doi.org/10.1007/sl0072-007-Q822-0
AT SDR (Agency for Toxic Substances and Disease Registry). (1992). Toxicological profile for
thallium [ATSDR Tox Profile], Atlanta, GA: U.S. Department of Health and Human
Services, Public Health Service.
http://www.ntis.gov/search/product.aspx?ABBR=PB93110856
Atsmon. J: Taliansky. E; Landau. M; Neufeld. MY. (2000). Thallium poisoning in Israel. Am J
Med Sci 320: 327-330.
Brockhaus. A: Dolgner. R; Ewers. U: Kramer. U: Soddemann. H; Wiegand. H. (1981). Intake
and health effects of thallium among a population living in the vicinity of a cement plant
emitting thallium containing dust. Int Arch Occup Environ Health 48: 375-389.
http://dx.doi.org/10.1007/BF0Q378686
Cavanagh. JB; Fuller. NH; Johnson. HR; Rudge. P. (1974). The effects of thallium salts, with
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