ST Beer BSc
    SM Bradberry BSc MB MRCP

    National Poisons Information Service
    (Birmingham Centre),
    West Midlands Poisons Unit,
    City Hospital NHS Trust,
    Dudley Road,
    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


    Toxbase summary

    Type of product

    Used as a gaseous electric insulator.


    Selenium hexafluoride is a gas so toxicity is associated primarily
    with inhalation.



         -    Selenium compounds may produce local irritation, burning,
              erythema and pain.


    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).



    1.   Irrigate with copious volumes of water.
    2.   Other symptomatic measures as required.


    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.


    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)


         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)

    Physicochemical properties

    Chemical structure
         SeF6                                    (DOSE, 1994)

    Molecular weight

         192.95                                  (DOSE, 1994)

    Physical state at room temperature
         Gas                                     (CSDS, 1991)

         Colourless                              (CSDS, 1991)




         Insoluble in water.                     (CSDS, 1991)

    Autoignition temperature

    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

         Non-flammable                           (HAZARDTEXT, 1997)

    Boiling point
         -34.5°C                                 (CSDS, 1991)

         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

         Selenium hexafluoride hydrolyzes slowly in cold water.
                                                 (HAZARDTEXT, 1997)


         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)


    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).


    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



    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.


    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.


    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).


    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).


    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.


    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).


    Transient increases in hepatic enzyme activities have complicated
    acute selenium ingestion but have not occurred following inhalation
    (Nantel et al, 1985).


    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).


    Selenium hexafluoride is a gas at room temperature; there are no
    reports of ingestion.


    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).


    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).


    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.


    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.


    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

    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,

    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


    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.


    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

    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

    Normal selenium concentrations in biological fluids

    Plasma: 70-130 µg/L.
    24 hour urine excretion: less than 300 µg.


    Occupational exposure standard

    Selenium and compounds: Long-term exposure limit (8 hour TWA reference
    period) 0.1 mg/m3 (Health and Safety Executive, 1997).



    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.


    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.


    There is experimental evidence of selenium genotoxicity mediated via
    active oxygen species formation (Kitahara et al, 1995).

    Fish toxicity


    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).


    ST Beer BSc
    SM Bradberry BSc MB MRCP

    National Poisons Information Service (Birmingham Centre),
    West Midlands Poisons Unit,
    City Hospital NHS Trust,
    Dudley Road,
    B18 7QH

    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


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    See Also:
       Toxicological Abbreviations
       Selenium hexafluoride (ICSC)