UKPID MONOGRAPH
SELENIUM HEXAFLUORIDE
ST Beer BSc
SM Bradberry BSc MB MRCP
JA Vale MD FRCP FRCPE FRCPG FFOM
National Poisons Information Service
(Birmingham Centre),
West Midlands Poisons Unit,
City Hospital NHS Trust,
Dudley Road,
Birmingham
B18 7QH
This monograph has been produced by staff of a National Poisons
Information Service Centre in the United Kingdom. The work was
commissioned and funded by the UK Departments of Health, and was
designed as a source of detailed information for use by poisons
information centres.
Peer review group: Directors of the UK National Poisons Information
Service.
SELENIUM HEXAFLUORIDE
Toxbase summary
Type of product
Used as a gaseous electric insulator.
Toxicity
Selenium hexafluoride is a gas so toxicity is associated primarily
with inhalation.
Features
Topical
- Selenium compounds may produce local irritation, burning,
erythema and pain.
Inhalation
Brief/minor inhalation:
- Mucous membrane irritation with cough, coryzal symptoms and
a bitter metallic taste.
Moderate/substantial inhalation:
- In addition to mucous membrane irritation there may be a
garlic odour on the breath, hoarseness, dyspnoea, nausea,
vomiting, headache and dizziness.
- Chemical pneumonitis may complicate severe cases.
- An inflammatory response with granuloma formation has been
attributed to pulmonary selenium accumulation following
chronic inhalation (Diskin et al, 1979).
Management
Topical
1. Irrigate with copious volumes of water.
2. Other symptomatic measures as required.
Inhalation
1. Remove from exposure.
2. Establish a clear airway.
3. Administer supplemental oxygen as necessary.
4. Treat symptomatically.
5. Parenteral steroids may be considered if pulmonary oedema is
present but there is no evidence that their use influences
outcome; discuss with an NPIS physician.
References
Diskin CJ, Tomasso CL, Alper JC, Glaser ML, Fliegel SE.
Long-term selenium exposure.
Arch Intern Med 1979; 139: 824-26.
Köppel C, Baudisch H, Beyer KH, Klöppel I, Schneider V.
Fatal poisoning with selenium dioxide.
Clin Toxicol 1986; 24: 21-35.
Wilber CG.
Toxicology of selenium: a review.
Clin Toxicol 1980; 17: 171-230.
Substance name
Selenium hexafluoride
Origin of substance
Produced by passing gaseous fluorine over finely divided selenium
in a copper vessel. (CSDS, 1991)
Synonyms
Selenium fluoride (CSDS, 1991)
Chemical group
A compound of selenium, a group VI A element.
Reference numbers
CAS 7783-79-1 (CSDS, 1991)
RTECS VS 9450000 (RTECS, 1997)
UN 2194 (CSDS, 1991)
HAZCHEM CODE NIF
Physicochemical properties
Chemical structure
SeF6 (DOSE, 1994)
Molecular weight
192.95 (DOSE, 1994)
Physical state at room temperature
Gas (CSDS, 1991)
Colour
Colourless (CSDS, 1991)
Odour
NIF
Viscosity
NIF
pH
NIF
Solubility
Insoluble in water. (CSDS, 1991)
Autoignition temperature
NA
Chemical interactions
Selenium, nitrogen and hydrogen fluoride are produced following
reaction with ammonia gas at 200°C. (MERCK, 1996)
Major products of combustion
When heated to high temperatures, may decompose to emit toxic
fluoride and selenium fumes. (HSDB, 1997)
Explosive limits
NA
Flammability
Non-flammable (HAZARDTEXT, 1997)
Boiling point
-34.5°C (CSDS, 1991)
Density
3.25 at -25°C (CSDS, 1991)
Vapour pressure
8.68 x 103 Pa at -48.7°C (MERCK, 1996)
Relative vapour density
Vapour density 6.7 (HSDB, 1996)
Flash point
NA
Reactivity
Selenium hexafluoride hydrolyzes slowly in cold water.
(HAZARDTEXT, 1997)
Uses
Selenium hexafluoride is used as a gaseous electric insulator and
in transformers. (CSDS, 1991; HUNTER, 1994)
Hazard/risk classification
Selenium compounds, except cadmium sulphoselenide.
Index no. 034-002-00-8
Risk phrases
T; R23/25-33 - Toxic by inhalation and if swallowed. Danger of
cumulative effects.
Safety phrases
S(1/2-)20/21-28-45- keep locked up and out of the reach of
children. When using do not eat, drink or smoke. After contact
with skin, wash immediately with plenty of .... (to be specified
by the manufacturer). In case of accident or if you feel unwell,
seek medical advice immediately (show label where possible).
EEC no. NIF (CHIP2, 1994)
INTRODUCTION AND EPIDEMIOLOGY
The metalloid selenium occurs naturally in four oxidation states:
elemental selenium (0), selenite (+4), selenide (-2) and selenate
(+6). Selenium is an essential trace element with a narrow therapeutic
index. It functions as an essential micronutrient at less than 1 ppm
and is likely to exhibit metabolic toxic effects at systemic
concentrations of 10 ppm (Oldfield, 1987). Selenium is closely related
to sulphur in its chemical behaviour (Wilber, 1980). It is a component
of selenocysteine, the active site of the antioxidant enzyme
glutathione peroxidase and is required for free radical detoxification
in conjunction with vitamin E. Selenium is also a component of the
deiodinase which catalyzes hepatic T4 to T3 conversion (Hofbauer et
al, 1997).
Although animal studies have suggested a potential role for selenium
in the treatment of heavy metal poisoning and chemical carcinogenesis,
there is insufficient evidence and experience to advocate any
therapeutic use in man (Whanger, 1992).
Two endemic diseases associated with selenium have been described in
China. Chronic selenium intoxication with hair and nail loss, skin
lesions and dental caries occurred in Enshi County, Hubei Province of
China (Yang et al, 1983; Whanger, 1989) and was most severe in the
1960's. The major source of selenium in this case was thought to be
selenium rich coal (containing up to 5000 µg selenium/g) used for
heating and cooking.
The second disease "Keshan" is a cardiomyopathy associated with low
dietary selenium intake (less than 17 µg selenium/day) (Whanger, 1989;
Parízek, 1990). "Kashin Beck" disease, an osteoarthropathy, has also
been associated with selenium deficiency but this has not been
confirmed (Whanger, 1989; Parízek, 1990).
Selenium toxicity can be a common problem in livestock. Cattle
ingesting large amounts of plants containing high selenium residues
may develop "blind staggers", characterized by gastrointestinal
stasis, partial blindness and paralysis. Chronic ingestion may result
in "alkali disease" with emaciation, hair loss and hoof deformities.
Selenium hexafluoride is a colourless gas which is insoluble in water.
It is used in industry primarily as a gaseous electric insulator.
Thus, the main route of exposure is inhalation, though skin contact
may lead to features of poisoning. Exposure to selenium hexafluoride
may also occur during production of selenium hydroxide and
hydrofluoric acid (HSDB, 1997).
There is evidence that selenium intake by man is declining globally
and selenium deficiency is considered a greater clinical problem than
selenium toxicity (Rayman, 1997).
MECHANISM OF TOXICITY
Selenium inactivates cellular oxidative processes by catalyzing
oxidation of sulphydryl groups on co-factors such as glutathione.
Sulphur and selenium are readily exchanged during amino acid
metabolism resulting in selenium incorporation into amino acids such
as cysteine. Selenium competes with sulphur for sites at which sulphur
normally plays a role in cellular respiration (Schellman et al, 1986;
Ahmed et al, 1990). In addition, mitosis is inhibited by selenium at
metaphase.
TOXICOKINETICS
Absorption
Selenium hexafluoride is absorbed by the lungs (Högberg and Alexander,
1986). As selenium hexafluoride is a gas and insoluble in water,
gastrointestinal absorption does not occur to any significant extent.
Distribution
There are no specific data concerning the metabolism and distribution
of selenium hexafluoride. There is evidence from human studies that
selenium binds to plasma lipoproteins (Sandholm, 1975) and some is
present in erythrocytes, partly as a component of glutathione
peroxidase (Högberg and Alexander, 1986).
Animal studies suggest that following exposure to many different
selenium compounds, selenium accumulates in all major organs
particularly the liver and kidneys (Glover, 1970; Civil and McDonald,
1978; Diskin et al, 1979). By contrast the lung appears to be an
important target organ of systemic selenium toxicity in man. Diskin et
al (1979) suggested blood-borne selenium made a significant
contribution to high lung selenium concentrations resulting in
pulmonary granuloma formation.
Excretion
Animal studies suggest that excretion of selenium compounds during
short-term exposure occurs chiefly via the kidneys as methylated
derivatives (such as the trimethylselenonium ion) with faecal
excretion playing a minor role (Diskin et al, 1979; Högberg and
Alexander, 1986; Wilber, 1980).
After substantial or prolonged exposure it is likely that elimination
of the hepatic selenium metabolite dimethylselenide in expired air is
important; dimethylselenide has a characteristic garlic odour (Diskin
et al, 1979; Högberg and Alexander, 1986; Magos et al, 1987).
CLINICAL FEATURES: ACUTE EXPOSURE
Specific data regarding the toxicity of selenium hexafluoride are
scarce, and there are no human case reports.
Dermal exposure
Topical exposure to selenium compounds produces local irritation with
pain, burning and erythema (Wilson, 1962; Fan and Kizer, 1990).
Ocular exposure
Selenium hexafluoride is an eye irritant. Ocular exposure to selenium
dusts or fumes has produced "rose eye" characterized by swollen pink
eyelids (Glover, 1970) and conjunctival burns within hours of exposure
(Wilson, 1962).
Inhalation
It is known from animal studies that selenium hexafluoride is a
pulmonary irritant (Proctor et al, 1978) and inhalation of other
selenium compounds by man has caused pulmonary toxicity. The
likelihood of systemic selenium uptake following selenium hexafluoride
inhalation is likely to be only modest since it is insoluble in water.
Pulmonary toxicity
Selenium compounds may cause immediate irritation of the mucous
membranes, hoarseness, coughing and coryzal symptoms (Motley et al,
1937; Wilson, 1962; Schecter et al, 1980; Fan and Kizer, 1990). An
acute sore throat and mild bronchitis of two weeks duration were
described in laboratory technicians following dimethylselenide
exposure (Motley et al, 1937).
A 24 year-old male who accidentally inhaled hydrogen selenide
immediately developed cough and wheeze and was admitted to hospital 18
hours later with progressive dyspnoea. Examination and investigations
revealed pneumomediastinum (but no other chest X-ray abnormalities),
hypoxia (pO2 9.2 kPa) and a severe obstructive ventilatory defect.
Substantial improvement ensued during the next five days with
conventional therapy (Schecter et al, 1980).
Workers exposed to selenium oxide fumes developed symptoms and signs
of a chemical pneumonitis between 10 hours and three days later.
Features included dyspnoea, cyanosis, chest pain and wheeze, with
radiological evidence of bilateral consolidation (Wilson, 1962).
Non-cardiogenic pulmonary oedema has been described particularly
following inhalation of high concentrations of inorganic selenium
compounds (such as hydrogen selenide or selenium dioxide) (Glover,
1970; Waldron and Scott, 1994).
Gastrointestinal toxicity
A bitter metallic taste, nausea and vomiting have followed inhalation
of selenium compounds (Fan and Kizer, 1990). These features developed
immediately following inhalation of selenium oxide fumes and
temporarily resolved within three hours (Wilson, 1962). Several hours
later the 28 affected workers complained of nausea, vomiting and
diarrhoea in association with malaise, headache and pulmonary
complications (Wilson, 1962).
A garlic odour on the breath is widely reported in selenium poisoning
(Carter, 1966; Civil and McDonald, 1978; Schellman et al, 1986) and
may occur in acute inhalational selenosis (Fan and Kizer, 1990).
Cardiovascular toxicity
An undefined transient fall in blood pressure associated with
tachycardia was reported among workers exposed to selenium oxide fumes
during a fire (Wilson, 1962).
Acute severe selenium poisoning by ingestion has been associated with
circulatory collapse (Carter, 1966) but this has not been reported
following inhalation. Transient T-wave inversion, Q-T interval
prolongation (Civil and McDonald, 1978) and increased cardiac enzyme
activities (Nantel et al, 1985) have also been reported in selenium
poisoning but again only following ingestion.
Nephrotoxicity
Acute nephrotoxicity has not been reported following selenium
hexafluoride (or other selenium salt) inhalation, although transient
haematuria and proteinuria have complicated selenium ingestion (Nantel
et al, 1985).
Hepatotoxicity
Transient increases in hepatic enzyme activities have complicated
acute selenium ingestion but have not occurred following inhalation
(Nantel et al, 1985).
Neurotoxicity
Headache, malaise and dizziness may accompany the respiratory features
(Wilson, 1962; Fan and Kizer, 1990). Workers exposed to selenium have
complained of lassitude and irritability resolving on removal from
exposure (Glover, 1970).
Ingestion
Selenium hexafluoride is a gas at room temperature; there are no
reports of ingestion.
CLINICAL FEATURES: CHRONIC EXPOSURE
Dermal exposure
Skin irritation has been reported in workers exposed to selenium fumes
(Glover, 1970).
A selenium refiner, employed for 50 years, was noted to have red hair
and fingernails following daily dermal contact with selenium (Diskin
et al, 1979).
Ocular exposure
Conjunctivitis developed in a student exposed to hydrogen selenide gas
once a week for a year (Alderman and Bergin, 1986).
Inhalation
Pulmonary toxicity
A 71 year-old selenium refiner died from an acute myocardial
infarction after 50 years employment. At post-mortem non-caseating
pulmonary granulomas were noted in association with very high selenium
concentrations in the peribronchial nodes and lung parenchyma (26 and
109 ppm respectively; normal values for peribronchial nodes 0.1 ppm,
lungs 0.15-0.21 ppm). The authors proposed a selenium-induced
inflammatory response. Normal tracheal selenium concentrations and the
absence of alveolar changes suggested a significant contribution from
blood-borne selenium (Diskin et al, 1979).
Dimethylselenide, excreted by the lungs following chronic or
substantial selenium exposure, is itself a primary respiratory tract
irritant. "Rose cold" with sore throat, cough, coryzal symptoms and
bronchitis is thought to occur secondary to pulmonary dimethylselenide
excretion (Diskin et al, 1979).
Gastrointestinal toxicity
A 21 year-old student exposed to hydrogen selenide gas at least once a
week for a year gave a six month history of diarrhoea and abdominal
pain, a bitter taste and garlic breath. Six dental caries developed
over the same period (Alderman and Bergin, 1986). Blood and urine
selenium concentrations were not measured but symptoms resolved on
removal from exposure.
Dermal toxicity
Red hair and fingernails were noted in association with abnormally
high hair (213 ppm, normal 0.36-0.74 ppm) and nail (178 ppm, normal
not reported) selenium concentrations in a worker exposed by
inhalation to selenium fumes for 50 years (Diskin et al, 1979).
Transverse fingernail ridges have been described following
occupational hydrogen selenide gas inhalation over some 12 months
(Alderman and Bergin, 1986).
MANAGEMENT
Dermal exposure
Decontamination with copious lukewarm water is the priority. Glover
(1983) suggested topical thiosulphate relieved selenium dioxide burns
and pain caused by selenium dioxide trapped under the nails but there
are no controlled data to substantiate this view.
Ocular exposure
Remove from exposure and irrigate with lukewarm water for at least 10
minutes. A topical anaesthetic may be required. Glover (1983) proposed
that the stinging associated with "rose eye" may be relieved by the
application of 10 per cent sodium thiosulphate ointment to the eyelids
but there is insufficient evidence to advocate this routinely. Seek an
ophthalmic opinion for those with persisting symptoms or abnormal
examination findings.
Inhalation
Immediate management involves removal from exposure, establishment of
a clear airway and administration of supplemental oxygen as necessary.
Parenteral steroids may be considered if laryngeal or pulmonary oedema
are present but there is no evidence that their use influences
outcome. Mechanical ventilation may be required. Wilson (1962)
suggested ammonia inhalation could relieve the burning associated with
acute selenium inhalation but this recommendation is unsupported by
other studies.
Antidotes
Animal studies
Selenium-intoxicated (sodium selenite, 10 mg/kg intramuscularly) rats
were administered intraperitoneal sodium calciumedetate, 0.5 g/kg, at
intervals of 15, 30 and 60 minutes post selenium poisoning (n=30 in
each group). Selenium poisoned rats given no antidote served as
controls. The 30 day survival ratio was increased substantially (from
9/30 in controls to 20/30 in selenium-treated rats) only if the
antidote was administered within 15 minutes of selenium intoxication.
Treatment with sodium calciumedetate was of little benefit at 15
minutes post selenite poisoning at a dose of 12.5 mgSe/kg (Sivjakov
and Braun, 1959).
Paul et al (1989) investigated the effect of potential antidotes on
sodium selenate (2.24 mg/kg subcutaneously)-induced weight loss.
Groups of rats (n=4) were administered an antidote by intraperitoneal
injection 15 minutes following selenium dosing. DMPS (sodium
dimercaptopropanesulphonate) 60 mg/kg, DMSA (dimercaptosuccinic acid)
50.9 mg/kg and sodium calciumedetate 500 mg/kg had no protective
effect and dimercaprol 15 mg/kg increased selenium-induced weight
loss. Diethyldithiocarbamate (DDC) 70 mg/kg significantly (p<0.05)
reduced weight loss but only for the first 48 hours post antidote
administration.
In further experiments, DDC 70 mg/kg reduced selenium-associated
weight loss but did not affect tissue selenium distribution when
administered 15 minutes, three hours or six hours after sodium
[75Se]selenite (50 µCi, 17.4 µgSe/kg subcutaneously) (Paul et al,
1989).
A protective effect of linseed oil in selenium-poisoned animals has
been suggested via selenium binding to tissues in a less toxic form
(Levander, 1972).
Levander and Morris (1970) claimed that in rats fed a diet containing
10 ppm selenium, supplementation with methionine and vitamin E offered
protection against selenium-induced macroscopic liver damage. The
authors suggested that vitamin E and other fat-soluble antioxidants
may make the methyl group of methionine more available for selenium
detoxification with subsequent excretion via the lungs and kidneys
(Levander and Morris, 1970). Diets high in choline or betaine
supplements also have been claimed to offer protection against chronic
selenosis (Klevay, 1976).
Clinical studies
Following ingestion of 22.3 mg/kg selenium (as sodium selenate), a 15
year-old female underwent gastric lavage within one hour then was
treated with vitamin C 1 g intramuscularly, (4 g/day orally
thereafter) and forced diuresis. Dimercaprol therapy was commenced:
150 mg qds on day one, 75 mg tds on day two, and 50 mg tds on day
three. The 24 hour urine selenium concentration on day two was 680
µg/L (urine volume not stated). Dimercaprol did not enhance urine
selenium elimination, though the patient recovered fully (Civil and
McDonald, 1978).
Antidotes: Conclusions and recommendations
1. Clarke et al (1996) suggest that no chelating agents have proven
effective in removing significant amounts of selenium; we concur
with this view.
2. Chelation therapy cannot currently be advocated in selenium
poisoning.
Haemoperfusion
As the majority of blood selenium is located in erythrocytes or bound
to plasma proteins (Köppel et al, 1986) haemoperfusion is unlikely to
be effective.
MEDICAL SURVEILLANCE
The possibility of pulmonary toxicity should be considered in those
occupationally exposed to selenium hexafluoride, especially in
individuals with pre-existing respiratory disease (HSDB, 1997).
Urinary selenium excretion is a useful indicator of recent exposure
(Wilber, 1980) with 24 hour excretion a more reliable parameter than
random samples (Robberecht and Deelstra, 1984; Alaejos and Romero,
1993). Dietary intake, age, sex, pregnancy, energy consumption,
selenium status, and any underlying pathological conditions which may
influence selenium excretion must be considered when interpreting
results.
Formation of metal-selenium complexes in heavy metal workers exposed,
for example, to mercury, cadmium and lead will result in raised
urinary selenium concentrations (Alaejos and Romero, 1993).
Increased blood selenium concentrations may be observed following
acute exposure (Högberg and Alexander, 1986). Whole blood
concentrations remain elevated longer than serum concentrations since
most blood selenium is located in alpha and beta globulins and
erythrocytes (Alderman and Bergin, 1986; Clark, 1996). However, blood
concentrations alone do not accurately reflect the total body selenium
burden (Wilber, 1980). As a result of serum protein binding, serum
selenium concentrations decrease less rapidly than urine selenium
concentrations (Sánchez-Ocampo et al, 1996).
Platelet glutathione peroxidase activity and hair selenium
concentrations have been suggested as indicators of human selenium
status (Högberg and Alexander, 1986). It must be noted, however, that
selenium is added to many antidandruff shampoos and is adsorbed onto
hair.
Normal selenium concentrations in biological fluids
Plasma: 70-130 µg/L.
24 hour urine excretion: less than 300 µg.
OCCUPATIONAL DATA
Occupational exposure standard
Selenium and compounds: Long-term exposure limit (8 hour TWA reference
period) 0.1 mg/m3 (Health and Safety Executive, 1997).
OTHER TOXICOLOGICAL DATA
Carcinogenicity
There is no conclusive evidence to link exposure to selenium compounds
with an increased incidence of cancer in humans. Some epidemiological
studies have proposed an inverse relationship between blood selenium
concentrations and cancer mortality (Wilber, 1980).
Gerhardsson et al (1986) stated "selenium might have a protective
effect in occupational exposure against at least certain carcinogens
causing lung cancer". Willett and Stampfer (1988) discuss the possible
protective effect of selenium but conclude that insufficient evidence
exists to recommend dietary selenium supplementation in humans.
Reprotoxicity
There are no reprotoxicity data regarding selenium hexafluoride
exposure. Selenium is essential for reproduction and is selectively
maintained in the testes during selenium deficiency (Reprotext, 1997).
Selenium salts have been found to cross the placenta and selenium is
normally excreted in breast milk (Reprotox, 1997).
Robertson (1970) reported a cluster of spontaneous abortions among
laboratory staff occupationally exposed to selenium where it was used
as a culture medium component. However, it is not clear what other
chemicals these staff were exposed to chronically.
Genotoxicity
There is experimental evidence of selenium genotoxicity mediated via
active oxygen species formation (Kitahara et al, 1995).
Fish toxicity
NIF
EC Directive on Drinking Water Quality 80/778/EEC
Selenium: maximum admissible concentration 10 µg/L (DOSE, 1994).
WHO Guidelines for Drinking Water Quality
Guideline value 10 µg/L, as selenium (WHO, 1993).
AUTHORS
ST Beer BSc
SM Bradberry BSc MB MRCP
JA Vale MD FRCP FRCPE FRCPG FFOM
National Poisons Information Service (Birmingham Centre),
West Midlands Poisons Unit,
City Hospital NHS Trust,
Dudley Road,
Birmingham
B18 7QH
UK
This monograph was produced by the staff of the Birmingham Centre of
the National Poisons Information Service in the United Kingdom. The
work was commissioned and funded by the UK Departments of Health, and
was designed as a source of detailed information for use by poisons
information centres.
Date of last revision
28/1/98
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