Selenium - Toxicology of Metals - page 777

Blood pressure and pulse rate were increased. Symp-
tomatic treatment was performed by parenteral fl uid
administration. The plasma Se concentration was
increased to 20 times normal 5 hours after ingestion.
Erythrocyte Se exceeded plasma Se 24 hours after
intoxication. Urinary Se excretion decreased parallel
to the plasma Se concentration. Ten weeks later, the Se
content in her hair had risen to 10 times normal. The
child fully recovered (Lombeck et al ., 1987).
A patient died 8 days after ingesting selenious acid
in the form of gun blueing. The patient's clinical course
demonstrated hypotension, respiratory distress, severe
myopathy that contributed to respiratory failure, and
a garlicky odor to the breath. Four days after inges-
tion, the serum selenium concentration was 20 times
normal and urinary excretion 70 times normal. Tissue
selenium concentrations were up to 40 times normal
(Pentel et al ., 1985).
One patient ingested a mouthful of selenic acid (30 g/
L); he only suffered mild gastrointestinal disturbances;
3 hours after ingestion, the plasma concentration was
the highest (931

exposed to “selenium oxide” during a fi re in a rectifi er
plant. Bronchial spasm was followed by chills, nausea
and vomiting, headache, fever, and bronchitis. Chemi-
cal pneumonia also developed in some of the cases
(Wilson, 1962).
Hydrogen selenide inhalation may also cause acute
intoxication at concentrations as low as 0.7 mg/m 3
(Buchan, 1947). Signs of toxicity include irritation of
the respiratory tract, pulmonary edema, severe bron-
chitis, and bronchial pneumonia (Glover, 1970).
A well-documented case of subacute selenite intoxi-
cation has been reported. A 57-year-old woman took
daily doses of tablets that accidentally contained
approximately 31 mg selenium (probably the major
amount in the form of selenite). After approximately
11 days, she noted marked hair loss that eventually
developed into alopecia. Two weeks later, she noted
white horizontal streaking on her fi ngernails, ten-
derness and swelling of the fi ngertips, and purulent
discharge. Over a 3-week period, all fi ngernails were
affected, and one fi ngernail was lost. She had periodic
episodes of nausea and vomiting, a sour-milk breath
odor, and felt increasing fatigue. Altogether, she con-
sumed 77 tablets. Four days after the last tablet, her
serum selenium level was 0.528

g/L). A second patient ingested 1.7 g
of sodium selenite. He had severe gastroenteritis, tran-
sient electrocardiographic changes, and developed a
slight elevation of serum bilirubin; 3 hours after inges-
tion, the selenium level was 2.716

µ

g/mL. Excessive
simultaneous intake of vitamin C might have reduced
selenite to elemental selenium and thus alleviated the
toxic reaction (Jensen, 1984).
A 48-year-old woman took 2000 mg of selenium
dioxide. She presented with mildly altered conscious-
ness and hematemesis and mucosal damage through-
out the oral cavity, esophagus, and stomach. After
intubation and gastric lavage, hemodialysis was per-
formed. The patient was discharged uneventfully on
the 16th day (Kise et al ., 2004).
In another case report, a woman used selenium
sulfi de-containing shampoo two or three times weekly
for 8 months to cure excoriations of the scalp. One hour
after the last wash, she developed tremor, abdominal
pain, and occasionally vomited. She had garlic odor on
her breath, and the urinary level of selenium 5 days
later was 32

µ

µ g/L (Gasmi et al .,

1997).
A 44-year-old worker neutralized 450 liters of
selenic acid with caustic soda. Boiling occurred, and
the mixture was spread all over the room. He suffered
skin burns and died 90 minutes later with pulmonary
edema, unstable blood pressure, and garlic breath
(Schellmann et al ., 1986).
A 15-year-old girl drank a selenate solution that
contained 1160 mg selenium (Civil and McDonald,
1978). She was forced to vomit after 20 minutes and
was treated with vitamin C and dimercaprol. She
developed only slight symptoms (minor aches, irrita-
bility, and garlic breath). Nevertheless, the initial serum
level was 3.1

µ g/mL. After 2 days, the serum level was

0.21 g/mL. There were also minor ECG changes, and

tests showed slightly abnormal liver function.
A 3-year-old boy swallowed an unknown amount
of a liquid containing 1.8% selenious acid and other
poisons. He rapidly became comatose with unrecorda-
ble blood pressure and peripheral pulse and died after
1.5 hours. There was garlic odor of the breath (Carter,
1966).
There are also reports on acute intoxication after
exposure through inhalation. A group of workers
briefl y and accidentally exposed to high concentra-
tions of “selenium fume” complained of intense irrita-
tion of the eyes, nose, and throat, followed by headache
(Clinton, 1947). In another incident, 37 men were

µ

µ g/mL (Ransone et al ., 1961).

7.2 Chronic Toxicity
7.2.1 Laboratory Animals

There are several early reports on the adverse effects
of diets containing 5 mg Se/kg, usually given as selenite,
in several laboratory animal species (Moxon, 1943). In
rats, a 5 mg Se/kg diet may result in growth reduction
(Ip, 1981). At a dietary level of 6.4 mg Se/kg (given as
selenite), there were liver changes and splenomegaly.
At 8 mg Se/kg, anemia, pancreatic enlargement, and