Chemistry Reference
In-Depth Information
brain as a compartment on its own, because of its role as
a target organ and because thallium ions penetrate into
it more slowly. He found the brain concentration to be
always lower than the mean concentration in the organ-
ism calculated from body load and body weight. There
are not enough data to estimate the biological half-time
in humans, but observations on a single case of thallium
poisoning—on the basis of urinary excretion of thallium
over a 3-month interval—were consistent with a half-
time of 30 days (Clinical Conferences at the Johns Hop-
kins Hospital, 1978).
range of 0.1-76.5
g/L. From a questionnaire, a clear
dose-response relationship was identifi ed between thal-
lium concentrations in urine and the prevalence of tired-
ness, weakness, sleep disorder, headache, nervousness,
paraesthesia, and muscle and joint pain, with a similar
dose-response relationship when thallium in hair was
taken as an indicator of exposure (WHO, 1996).
From these limited studies, it has been suggested
that an approximately 15-fold increase in urinary thal-
lium excretion above the mean unexposed level of 0.3-
0.4
µ
g/L may be related to subjective symptoms that
could possibly be considered as early adverse effects.
The Task Group (WHO, 1996) considered that expo-
sures with urinary thallium concentrations <5
µ
6 BIOLOGICAL MONITORING
g/L are
unlikely to cause adverse health effects. In the range
of 5-500
µ
Few data are available on levels of thallium in nor-
mal subjects. In a study on six people of various ages
dying from unrelated causes, Weinig and Zink (1967)
estimated tissue concentrations of thallium by mass
spectroscopy. The highest values were found in hair,
with concentrations ranging from 4.8-15.8
g/L, the magnitude of risk and severity of
adverse effects are uncertain, whereas exposures with
urinary thallium concentrations >500
µ
µ
g/L have been
associated with clinical poisoning.
Extensive data on thallium levels in persons from
the general population is available from the NHANES
studies in the United States. Thallium levels in urine,
blood, and hair are useful biomarkers of exposure to
thallium.
µ
g/kg. Con-
centrations in nails ranged from 0.72-4.93
µ
g/kg, and
in the wall of the colon from 0.56-5.40
g/kg wet tis-
sue. The mean tissue concentration was calculated as
1.2
µ
g/kg, from which it was derived that the thallium
content in a 75-kg person would be on the order of
0.1 mg. The same investigators found the thallium con-
centration in early-morning urine samples in nine sub-
jects to range from 0.13-1.69
µ
7 EFFECTS AND DOSE-RESPONSE
RELATIONSHIPS
g/L. Johnson (1976), in
a study in New Zealand on 11 subjects with no known
exposure to toxic metals, found a mean thallium con-
centration in liver of 0.47 mg/kg dried tissue, with
a range of 0.4-0.9 mg/kg.
The concentration of thallium in whole blood in a
population of 320 children in New Jersey was meas-
ured by AAS. Values ranged between nondetectable
(<5
µ
7.1 Laboratory Animals
In acute poisoning, the principal effects are seen in
the digestive and nervous systems with, in addition, a
necrotizing renal papillitis. In chronic poisoning, the
most striking feature is loss of hair. This phenomenon,
so characteristic of thallium poisoning, is probably the
result of cessation of cell proliferation in the hair folli-
cles (Cavanagh and Gregson, 1978) and is thus closely
similar to the hair loss caused by X-irradiation and
radiomimetic chemicals.
In mammalian species, the acute LD
50
for thallium
compounds for all routes of administration ranges
between approximately 5 and 70 mg/kg (Adamson
et al
., 1975; Hart
et al
., 1971; Truhaut, 1959).
In chronic poisoning, the daily ingestion of thallium
acetate added to the diet of male and female rats was
tolerated at the 10 mg/kg level but was lethal in male
rats at the 30 mg/kg level by 15 weeks (Downs
et al
.,
1960). Rats given 10-20 mg thallium acetate followed
by weekly subcutaneous injections of 5 mg/kg devel-
oped irritability, diarrhea, alopecia, and poor weight
gain. Abnormalities, in particular degenerative changes
in the mitochondria (Herman and Bensch, 1967), were
seen in kidney, liver, and intestinal epithelial cells by
electron microscopy. Kennedy and Cavanagh (1977)
µ
g/L) and 80
µ
g/L, with a mean concentration of
3.0
g/L. Approximately 80% of the children showed
no detectable thallium in the blood, whereas 17.5%
had between 5 and 20
µ
g/L. Five children (1.6% of the
total group) had blood thallium levels between 40 and
80
µ
g/L, but all were without evidence of thallium tox-
icity (Singh
et al
., 1975).
In three carefully controlled population-based stud-
ies involving a total of 686 unexposed subjects, the
range of urinary thallium concentrations was 0.06-
1.2
µ
g/L, with a mean thallium urinary concentration
of 0.3-0.4
µ
g/L. With a short biological half-life and an
assumed steady state in such population-based sam-
ples, the urinary excretion value can be considered
as an indicator of total dose after inhalation and total
dietary intake (WHO, 1996).
In a population sample living in the vicinity of thal-
lium emission into the atmosphere, the mean urinary
thallium concentration was 5.2
µ
µ
g/L ± 8.3
µ
g/L, with a
