SM Bradberry BSc MB MRCP
    ST Beer BSc

    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 in nuclear reactors, electrical insulators and resistors, spark
    plugs, microwave tubes, the aerospace industry, photographic equipment
    and many tools.


    The lung is the main target organ of beryllium toxicity.

    Beryllium lung disease is classified as acute or chronic dependant on
    the duration of disease rather than the duration of exposure. The
    acute illness does not persist beyond one year.

    Chronic beryllium disease is a cell-mediated (delayed)
    hypersensitivity reaction characterized by granuloma formation and
    pulmonary fibrosis which may be fatal.



         -    Beryllium compounds may cause contact dermatitis.
         -    Beryllium ulcers occur where a beryllium crystal penetrates
              the skin at a site of previous trauma.
         -    Beryllium chloride, fluoride, nitrate or sulphate are acute
              eye irritants.


         -    Gastrointestinal beryllium absorption is poor and systemic
              toxicity via this route does not occur.


    Mild inhalation:
         -    Metallic taste, cough, breathlessness.

    Substantial inhalation:
         -    Cough, chest pain, metallic taste, exertional
              breathlessness, nasopharyngitis, tracheobronchitis,
              conjunctivitis, pneumonitis, epistaxis and fever.
         -    Additional features seen in chronic beryllium disease
              include fever, anorexia, arthralgia, nausea, vomiting,
              haemoptysis, palpitation, convulsions, renal calculi,
              corneal calcification, hepatosplenomegaly (secondary to cor
              pulmonale) and systemic granulomas causing lymphadenopathy
              and parotid gland enlargement.

         -    Chest X-ray may show upper zone nodules and fibrosis and
              there may be a restrictive ventilatory defect.



         -    Skin nodules from subcutaneous implantation of beryllium
              metal or its salts are best managed by local excision.


    -    Beryllium salt ingestion is not a significant toxicological
    1.   Management is entirely supportive.
    2.   Gastrointestinal decontamination is not necessary.


    -    Most cases are occupational.
    1.   Occupational hygiene is paramount.
    2.   If pulmonary toxicity is suspected remove from exposure.
    3.   Symptoms of acute and chronic beryllium disease respond well to
         oral steroids.
    4.   Experimental studies to assess the value of chelators in
         beryllium poisoning are underway, but there are insufficient data
         currently to recommend their use in man.Urine beryllium
         concentrations allow assessment of beryllium absorption but
         chronic beryllium disease is not excluded by a low urine
         beryllium concentration.


    Haberman AL, Pratt M, Storrs FJ.
    Contact dermatitis from beryllium in dental alloys.
    Contact Dermatitis 1993: 28: 157-62.

    Hooper WF.
    Acute beryllium lung disease.
    N C Med J 1981; 42: 551-3.

    Izumi T, Kobara Y, Inui S, Tokunaga R, Orita Y, Kitano M, Jones
    Willams W.
    The first seven cases of chronic beryllium disease in ceramic factory
    workers in Japan.
    Ann NY Acad Sci 1976 ; 278: 636-53.

    Jones Williams W.
    Diagnostic criteria for chronic beryllium disease (CBD) based on the
    UK Registry 1945-1991.
    Sarcoidosis 1993; 10: 41-3.

    Kriebel D, Brain JD, Sprince NL, Kazemi H.
    The pulmonary toxicity of beryllium.
    Am Rev Respir Dis 1988; 137: 464-73.

    Monie RDH, Roberts GH.
    Chronic beryllium pneumonitis: First case accepted by UK register from
    Scott Med J 1991; 36: 185-6.

    Substance name


    Origin of substance

         Occurs in the minerals beryl, phenacite, bertrandite, bromellite
         and chrysoberyl.                        (DOSE, 1992)


         Glucinium                               (CSDS, 1989)

    Chemical group

         A group II A element

    Reference numbers

         CAS            7740-41-7                (CSDS, 1989)
         RTECS          DS1750000                (RTECS, 1996)
         UN             1567 (Be powder)         (CSDS, 1989)

    Physicochemical properties

    Chemical structure
         Beryllium, Be                           (DOSE, 1992)

    Molecular weight
         9.01                                    (DOSE, 1992)

    Physical state at room temperature
         Solid                                   (CSDS, 1989)

         Greyish-white                           (CSDS, 1989)

         Odourless                               (HSDB, 1996)



         Insoluble in cold water (or mercury), slightly soluble in hot
         water. Soluble in dilute acids and alkalis.
                                                 (HSDB, 1996)

    Autoignition temperature

    Chemical interactions
         Beryllium reacts readily with some strong acids, producing
         hydrogen.                               (NFPA, 1996)
         Powdered beryllium mixed with carbon tetrachloride or
         trichloroethylene will flash on heavy impact.
                                                 (HSDB, 1996)
         Warm beryllium incandesces in fluorine or chlorine.
                                                 (HSDB, 1996)
         Molten lithium at 180C will attack beryllium severely.
                                                 (NFPA, 1996)

    Major products of combustion
         Combustion yields beryllium oxide fume which is toxic if inhaled.
                                                 (HSDB, 1996)

    Explosive limits

         Flammable                               (HSDB, 1996)

    Boiling point
         2970C                                  (CSDS, 1989)

         1.85 at 20C                            (CSDS, 1989)

    Vapour pressure

    Relative vapour density

    Flash point



         Beryllium is an important component of nuclear reactors as a
         neutron source with low neutron-absorbing capacity.
         Beryllium oxide is used in the electronics industry in
         insulators, resistors, spark plugs and microwave tubes.
         Beryllium-copper alloys are used in the aerospace, electronic,
         mechanical and other industries as constituents of aircraft
         engine parts, switches, circuit breakers, fuse clips, springs,
         bearings, gear parts, camera shutters and many tools and are the
         major source os occupational beryllium exposure.
         Other important beryllium alloys are beryllium-aluminium,
         beryllium-copper-cobalt and beryllium-nickel alloys.
                                       (IPCS, 1990; Jones Williams, 1994)

    Hazard/risk classification

    Index no. 004-001-00-7
    Risk phrases
         Carc. Cat.2; R49 - May cause cancer by inhalation.
         T+; R26 - Very toxic by inhalation.
         T; R25-48/23 - Also toxic if swallowed. Toxic: danger of serious
         damage to health by prolonged exposure through inhalation.
         Xi; R36/37/38 - Irritating to eyes, respiratory system and skin.
         R43 - May cause sensitization by skin contact.

    Safety phrases
         S53-45 - Avoid exposure - obtain special instruction before use.
         In case of accident or if you feel unwell, seek medical advice
         immediately (show label were possible).

    EEC no.                                      (CHIP2, 1994)


    Beryllium is a brittle metal which forms compounds in the divalent
    state. It has a high affinity for oxygen such that a surface film of
    beryllium oxide forms when the metal is exposed to air. This provides
    resistance to corrosion which, with low density and high electrical
    and thermal conductivity, make beryllium an important constituent of
    many alloys; approximately 72 per cent of all beryllium produced is
    used in this way (IPCS, 1990).

    In the general population tobacco smoking is a major source of
    beryllium exposure but beryllium toxicity is predominantly an
    occupational disease via exposure to beryllium dust or fumes in the
    industries listed above. Historically beryllium poisoning occurred
    also during the production of fluorescent and neon lamps when
    beryllium was used to coat their inner surface. In these circumstances
    secondary cases of occupational beryllium poisoning occurred in the
    families of workers via dust carried home in clothing (Hardy, 1965).
    Non-occupational beryllium contact-sensitivity has been reported in
    individuals fitted with beryllium-containing dental prostheses.

    Table 1 lists the main beryllium salts by solubility.

    Table 1. Solubility1 of beryllium compounds


    Soluble beryllium compounds        Insoluble beryllium compounds

      Beryllium chloride                 Beryllium acetate
      Beryllium fluoride                 Beryllium hydroxide
      Beryllium nitrate                  Beryllium oxide
      Beryllium sulphate tetrahydrate2   Beryllium sulphate
                                                   (after IPCS, 1990)
    1 In cold water
    2 Formed from beryllium sulphate in hot water


    Beryllium has been shown experimentally to disrupt phosphate and
    nucleic acid metabolism with subsequent inhibition of enzyme activity
    and cell replication (IPCS, 1990). Beryllium also impairs
    reticuloendothelial cell function (Dinsdale et al, 1981).

    As discussed below beryllium is immunogenic and capable of initiating
    a type IV hypersensitivity reaction (Vilaplana et al, 1992) via
    mechanisms which are, at least in part, genetically determined (Barna
    et al, 1984; McConnochie et al, 1988).



    Beryllium is absorbed mainly by inhalation of dust or fumes; dermal
    and gastrointestinal absorption are poor. The rate of beryllium
    absorption from the alveolar space depends on the solubility and
    particle size of the salt with greater absorption of small particles
    of soluble salts (IPCS, 1990).


    Beryllium is transported in blood and lymph protein-bound or as
    colloidal beryllium phosphate (Aller, 1990). The small amount of
    beryllium absorbed following ingestion is deposited primarily in bone.

    By contrast, the distribution of beryllium following inhalation
    depends on the solubility of the salt. Beryllium oxide, which is
    poorly soluble (Table 1), is stored mainly in lung tissue, pulmonary
    lymph nodes and bone whereas more soluble beryllium compounds (e.g.
    beryllium chloride; Table 1) will also be found in the liver,
    abdominal lymph nodes, spleen, muscle, kidney, skin and heart (IPCS,

    Beryllium is taken up by cellular lysosomes and may be found
    subsequently in the nucleus, nucleolus and cytoplasm (Aller, 1990).


    Lung clearance of inhaled beryllium is usually rapid during the first
    few days after exposure, followed by a second slower phase (IPCS,
    1990). The initial rapid elimination is explained partly by
    mucociliary clearance of particulate matter with subsequent
    gastrointestinal elimination and partly by beryllium uptake by
    alveolar macrophages. The slow phase may be contributed to by
    precipitation to a more insoluble form and embedding in pulmonary
    tissues (Aller, 1990).

    Beryllium which reaches the systemic circulation is eliminated mainly
    in the urine, probably via active tubular secretion since most plasma
    beryllium is colloidally bound and therefore does not pass through the
    glomerulus (Reeves, 1986). The total body half-life of beryllium in
    man is approximately 180 days (ICRP, 1960).


    Dermal exposure

    Beryllium compounds may cause contact dermatitis. The beryllium source
    is usually occupational although non-occupational hypersensitivity has
    occurred in individuals wearing beryllium-containing dental prostheses
    (Haberman et al, 1993). There is usually a latent period of one to two
    weeks before the development of erythematous, macular, sometimes
    blistering lesions which resolve when exposure ceases. Once
    sensitization has occurred reactivation of the inflammatory response
    requires only minimal beryllium contact and in this respect beryllium
    skin disease is a chronic condition (VanOrdstrand et al, 1945)
    although beryllium contact sensitivity is not usually associated with
    systemic toxicity (Haberman et al, 1993). Beryllium ulcers occur where
    a beryllium crystal penetrates the skin at a site of previous trauma
    (VanOrdstrand et al, 1945; Jones Williams, 1988). Treatment by
    excision and curettage usually promotes complete healing (VanOrdstrand
    et al, 1945).

    Ocular exposure

    Dust of beryllium chloride, fluoride, nitrate and sulphate are acute
    eye irritants (Grant and Schuman, 1993).


    This may follow the inhalation of beryllium fluoride, -sulphate, -
    oxide, -hydroxide or beryllium metal dust (Eisenbud et al, 1948).
    Clinical features are dose-related and usually occur within days but
    can be delayed for several weeks. Beryllium lung disease manifests in
    acute and chronic forms, classified depending on the duration of
    disease rather than the duration of exposure. Acute beryllium lung

    disease is a true chemical pneumonitis which may occur during
    beryllium extraction processes. It is now largely of historical
    interest due to improved occupational working conditions (Markham,

    Pulmonary toxicity

    A single beryllium salt inhalation may cause irritation of the nose,
    pharynx and eyes. Depending on the magnitude of exposure there may be
    a nasal discharge and mild epistaxis (Jones Williams, 1994). More
    substantial inhalation of soluble bismuth salts (Table 1) will result
    in rhinitis, tracheitis and bronchitis (Jones Williams, 1994). By
    contrast, less soluble beryllium salts can reach the alveoli and
    moderate to severe exposure may precipitate a chemical pneumonitis,
    usually within 72 hours, with cough, chest pain, exertional
    breathlessness and possibly fever, hypoxia and inspiratory crackles on
    auscultation of the lung fields (Kriebel et al, 1988a; Jones Williams,
    1994). A subacute presentation is also recognised with more gradual
    onset of respiratory symptoms, often accompanied by constitutional
    upset and progression to chronic beryllium lung disease.

    In patients who develop moderate or severe respiratory symptoms, chest
    radiographic findings typically lag behind clinical signs for up to
    three weeks (Jones Williams, 1994). In those with pneumonitis initial
    diffuse shadowing may progress to widespread, poorly defined opacities
    which take months to clear (Jones Williams, 1994). There are no
    characteristic histological features. Restrictive spirometry may be
    present but usually resolves along with radiological improvement
    (Hooper, 1981).

    Most patients recover from acute beryllium lung disease when removed
    from exposure but fatalities have occurred (VanOrdstrand et al, 1945)
    and a minority develop late complications including chronic
    bronchitis, bronchiectasis, emphysema, asthma or progression to
    chronic beryllium lung disease (Rees, 1979; Jones Williams, 1993). The
    latter may occur after a symptom free interval of several years
    (Hardy, 1965; IPCS, 1990).

    Gastrointestinal toxicity

    Following acute beryllium inhalation some patients complain of a
    metallic taste, usually in association with symptoms of constitutional
    upset including anorexia and fatigue (VanOrdstrand et al, 1945).
    Diarrhoea has also been reported (Hooper, 1981).


    Dermal exposure

    Beryllium exposure from soil on abraded skin of bare feet has been
    implicated in the aetiology of non-filarial elephantiasis in Ethiopia
    (Frommel et al, 1993).


    Chronic beryllium disease is a hypersensitivity response to beryllium
    which occurs in susceptible individuals. There may be a latent period
    of several weeks or years between exposure (which may have been only a
    few hours) and the onset of symptoms. Inhalation of poorly soluble or
    insoluble beryllium compounds (e.g. beryllium oxide; Table 1) or
    beryllium dust are usually responsible and cases have been reported in
    fluorescent lamp plants (now historical) (Hardy and Tabershaw, 1946),
    ceramic factories (Izumi et al, 1976), the electronics and atomic
    energy industries (Jones Willliams, 1988), those involved in the
    refining of beryllium or its alloys (Cullen et al, 1987), welders
    (Monie and Roberts, 1991) or manufacturers of beryllium-containing
    dental prostheses (Kotloff et al, 1993).

    Although the lungs are the main target organ in chronic beryllium
    disease, unlike the acute illness, there are frequently widespread
    systemic manifestations, many secondary to granuloma formation as
    discussed below.

    Pulmonary toxicity

    Chronic beryllium disease manifests primarily as pneumonitis with
    exertional dyspnoea, cough (which may be productive), chest pain
    (Stoeckle et al, 1969; Hasan and Kazemi, 1974; Monie and Roberts,
    1991) and possibly fever, haemoptysis, wheeze and hoarseness (Hasan
    and Kazemi, 1974). Respiratory symptoms are frequently accompanied by
    systemic upset with general malaise, anorexia and weight loss (see

    The most frequently observed clinical signs in the respiratory system
    are finger clubbing, central cyanosis and inspiratory crackles on
    auscultation of the lung fields (Stoeckle et al, 1969; Hasan and
    Kazemi, 1974; Monie and Roberts, 1991; Jones Williams, 1994).

    Death has occurred following massive haemoptysis in a patient with
    bilateral upper lobe mycetomas (probably related to steroid therapy)
    (O'Brien et al, 1987).

    In chronic beryllium disease a diffuse reticular pattern, more
    prominent in the upper zones, is seen on chest x-ray with nodules of
    varying size and sometimes bilateral (possibly calcified) hilar
    adenopathy (Andrews et al, 1969; Stoeckle et al, 1969; Hasan and
    Kazemi, 1974). There may be progression to upper zone fibrosis with
    relative emphysema in adjacent lobes, pleural thickening,
    pneumothoraces (usually from ruptured bullae) and evidence of
    pulmonary hypertension (Stoeckle et al, 1969; Hasan and Kazemi, 1974).
    Pulmonary function tests typically show a restrictive, or isolated
    diffusion defect, but obstructive lesions have been reported (Andrews
    et al, 1969). A probable "dose-related" decrease in FVC and FEV1
    without chest x-ray abnormalities has also been described (Kriebel et
    al, 1988b).

    Lung biopsy in chronic beryllium disease usually shows a chronic
    inflammatory response with non-caseating granulomas, diffuse fibrosis
    and smooth muscle hypertrophy (Andrews et al, 1969; Hasan and Kazemi,
    1974). The presence of beryllium in tissue sections can be confirmed
    using laser microprobe mass spectrometry (LAMMS) analysis (Jones
    Williams and Wallach, 1989; Monie and Roberts, 1991).

    In 124 cases of chronic beryllium disease, Freiman and Hardy (1970)
    found a clear relation between the histological appearance of the lung
    (at lung biopsy or autopsy) and disease prognosis. Only 26 of 95
    patients with histological evidence of diffuse pulmonary cell
    infiltration were alive at the time of the study with a mean disease
    duration of 8.3 years for the entire group. Follow-up of 43 patients
    in the UK Beryllium Case Registry 1945-91 (Jones Williams, 1993)
    reported 25 deaths, 21 from cor pulmonale, though nearly half had
    survived more than 20 years from the original diagnosis.

    Lung damage in chronic beryllium disease may be partly reversible. In
    a survey of 214 workers at a beryllium plant Sprince et al (1978)
    demonstrated that beryllium-induced hypoxemia and radiographic
    abnormalities were reduced over three years following improved
    workplace ventilation and engineering processes with a significant
    reduction in the air beryllium concentration.

    Chronic beryllium disease reflects a cell-mediated (delayed)
    hypersensitivity reaction as evidenced by the ability of beryllium to
    activate proliferation of beryllium-specific helper T cells (Deodhar
    et al, 1973). This property forms the basis of the lymphocyte
    transformation test (LTT) which was shown by Rossman et al (1988) to
    have high sensitivity and specificity in the diagnosis of chronic
    beryllium disease using bronchoalveolar lavage fluid cells. In
    patients with compatible lung pathology Mroz et al (1991) found that
    an abnormal LTT in peripheral blood cells also could diagnose chronic
    beryllium disease reliably.

    The current diagnostic criteria for chronic beryllium disease
    therefore are a positive blood beryllium lymphocyte transformation
    test in the presence of a history of beryllium exposure, consistent
    clinical and radiological features plus granulomas and beryllium
    deposits in tissues (Jones Williams, 1988).

    It should be remembered that a positive beryllium LTT alone is not
    diagnostic of chronic beryllium disease; it reflects beryllium
    exposure but may be reversible when exposure is reduced (Rom et al,

    Reports that chronic beryllium disease shows a familial tendency
    probably reflect the role of histocompatibility antigens in beryllium
    hypersensitivity (McConnochie et al, 1988; Saltini et al, 1989;
    Deodhar and Barna 1991). It is also likely that the observed
    precipitation of chronic beryllium disease by pregnancy or infection
    (Hardy and Tabershaw, 1946) is related to altered immunological

    The main differential diagnosis in chronic beryllium disease is
    sarcoidosis although the presence of beryllium in tissues and a
    positive beryllium lymphocyte transformation test allow clarification
    (Jones Williams and Wallach, 1989). The Kveim test is negative in
    beryllium disease (Jones Williams and Wallach, 1989).

    Dermal toxicity

    Chronic pulmonary beryllium toxicity may be complicated by cutaneous
    granulomas (Jones Williams, 1994).

    Gastrointestinal toxicity

    Patients with chronic beryllium disease often experience anorexia,
    weight loss, nausea and vomiting (Hasan and Kazemi, 1974; Jones
    Williams, 1994). Parotid gland enlargement is due to granuloma
    formation (Hasan and Kazemi, 1974).


    Hypercalciuria is common in chronic beryllium disease and renal
    calculi have been reported (Hardy and Tabershaw, 1946; Stoeckle et al,
    1969). Granulomata may be seen on renal biopsy (Jones Williams, 1994)

    Cardiovascular toxicity

    Patients with severe untreated chronic beryllium lung disease may
    develop cor pulmonale with orthopneoa, palpitation (Hasan and Kazemi,
    1974), hepatomegaly and/or splenomegaly (Hall et al, 1959; Stoeckle et
    al, 1969; Jones Williams, 1993).


    Central nervous system granulomas may cause seizures (Hasan and
    Kazemi, 1974).


    Extrapulmonary lymph node granulomata may cause generalised
    lymphadenopathy (Hasan and Kazemi, 1974). Granulomas may be found also
    in the spleen and bone marrow (Stoeckle et al, 1969; Jones Williams,

    Musculoskeletal toxicity

    Arthralgia may be a feature of chronic beryllium disease (Hasan and
    Kazemi, 1974).

    Ocular toxicity

    Corneal calcification and band keratopathy have been described in
    chronic beryllium disease (Grant and Schuman, 1993). A positive
    Schirmer's test (indicating reduced tear secretion) is recognized
    (McConnochie et al, 1988; Monie and Roberts, 1991).


    Dermal exposure

    Skin nodules developing from subcutaneous implantation of beryllium
    metal alloy or its salts, particularly in machinists and ceramic
    workers with skin lacerations, are best managed by local excision.
    This is usually curative although chronic beryllium disease has
    developed in isolated cases (Jones Williams, 1988).


    Occupational hygiene

    Beryllium toxicity is only likely to occur following occupational
    exposure, usually by inhalation of beryllium containing dusts or
    powders. In these circumstances cessation of exposure is the priority.
    Adequate skin protection and hygiene to avoid unnecessary beryllium
    exposure are essential.

    Supportive measures

    Symptoms of acute and chronic beryllium disease respond well to oral
    prednisolone (20-80 mg daily) and in the chronic form treatment is
    usually lifelong (Izumi et al, 1976; Jones Williams, 1994).


    DMPS and DMSA

    In animal studies oral DMPS or DMSA (50 mg/kg bd for five days)
    increased faecal but not urinary beryllium excretion in rats
    administered 0.5 mg/kg intraperitoneal beryllium nitrate daily for
    five days/week for three weeks (Flora et al, 1995). Chelation therapy
    with both agents reversed the hepatotoxic effect of beryllium as shown
    by liver alkaline phosphatase activity and DMPS caused a significant
    reduction in the liver and spleen beryllium content in association
    with an increased blood beryllium concentration (Flora et al, 1995).

    There are no data regarding the use of DMPS or DMSA in human beryllium

    HEDTA and EDTA

    In beryllium-poisoned rats (treated for 18 days with parenteral
    beryllium nitrate 1 mg/kg daily) the administration of intraperitoneal
    HEDTA (N-(2-hydroxyethyl)ethylenediamine triacetic acid) or calcium
    disodium EDTA (ethylenediamine tetraacetic acid) prevented
    beryllium-induced hepatotoxicity (as indicated by hepatic alkaline
    phosphatase activity) but neither chelating agent significantly
    reduced blood or tissue beryllium concentrations (Mathur et al, 1993).


    In animal studies intraperitoneal ferric ammonium citrate (40 mg/kg
    body weight daily) commenced three days prior to beryllium exposure
    and continued until death or recovery, protected against
    beryllium-induced mortality in rats exposed to intravenous beryllium
    sulphate (6 mg/kg). (Lindenschmidt et al, 1986) or an aerosol of
    beryllium sulphate (30 per cent w/v) (Sendelbach and Witschi, 1987)
    via increased ferritin production with subsequent faecal elimination
    of ferritin-bound beryllium. There are no human data regarding iron
    therapy in the management of beryllium poisoning.


    Health surveillance is necessary for those potentially exposed to
    beryllium fumes or dust. Pre-employment clinical examination and chest
    x-ray are recommended. Those with an history of atopy are particularly
    susceptible to beryllium lung disease (Hooper, 1981). Regular
    monitoring of the beryllium concentration in workplace air, with
    provision of protective respiratory equipment if required, is
    mandatory (Health and Safety Executive, 1994).

    Urine beryllium concentrations allow assessment of beryllium
    absorption (Health and Safety Executive, 1994) but chronic beryllium
    disease is not excluded by a low urine beryllium concentration (IPCS,

    The identification of beryllium in affected tissues remains important
    in establishing the diagnosis (Jones Williams and Wallach, 1989; Jones
    Williams, 1994). Kreiss et al (1989) demonstrated that subclinical
    chronic beryllium disease could be detected via a positive lymphocyte
    proliferation test but recent studies suggest this has a limited role
    in screening (Stokes and Rossman, 1991).

    Since there may be a substantial latency period between beryllium
    exposure and the onset of beryllium disease, retired workers should be
    kept under medical supervision for up to 20 years.

    The UK Beryllium Case Registry provides important information on the
    incidence and clinical course of beryllium disease (Jones Williams et
    al, 1980). By 1994 it included 59 cases of whom 47 manifest the
    chronic form (Jones Williams, 1994).


    Maximum exposure limit

    Long-term exposure limit (8 hour TWA reference period)

    0.002 mg/m3 (Health and Safety Executive, 1995b).



    In a cohort mortality study of 689 patients included in a North
    American beryllium disease case registry mortality from lung cancer
    (standardised mortality ratio (SMR) = 2.0) and non malignant beryllium
    disease were significantly increased, with deaths from lung cancer
    occurring more frequently in those with acute rather than chronic
    beryllium disease (Steenland and Ward, 1991).

    Ward et al (1992) similarly found a significantly increased SMR for
    lung cancer in workers at two beryllium plants in operation before
    1950 although the overall slightly increased SMR for the 9225 cohort
    of workers from seven plants was not significant.

    The International Agency for Research on Cancer (IARC) Working Group
    on the carcinogenicity of beryllium has concluded that there is
    "sufficient evidence in humans for the carcinogenicity of beryllium
    and beryllium compounds" (IARC, 1993) although their conclusions have
    been disputed (MacMahon, 1994; Kotin, 1994a and b).

    By 1993 there were no known cases of beryllium-associated lung cancer
    in the UK registry (Jones Williams, 1993).


    There are no data confirming that beryllium is a reprotoxin in man
    (Reprotox, 1996).


    Escherichia coli, HeLa cells and Ehrlich ascites tumour cells, DNA
    cell binding assays positive

    Chinese hamster ovary and rat lung epithelial cells, 20 hr exposure,
    positive cytotoxic effects

    Oral rat (6 month) in drinking water, caused cytotoxicity at the toxic
    dose level and induced chromosomal aberrations, but was negative in
    dominant lethal assays (DOSE, 1992).

    Fish toxicity

    Acute toxicity range to fish (24-96 hr) (species unspecified) in fresh
    water 87-0.97 g/L

    LC50 (96 hr) fathead minnow 150 g/L (DOSE, 1992).

    EC Directive on Drinking Water Quality 80/778/EEC



    SM Bradberry BSc MB MRCP
    ST Beer BSc

    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


    Aller AJ.
    The clinical significance of beryllium.
    J Trace Elem Electrolytes Health Dis 1990; 4: 1-6.

    Andrews JL, Kazemi H, Hardy HL.
    Patterns of lung dysfunction in chronic beryllium disease.
    Am Rev Respir Dis 1969; 100: 791-800.

    Barna BP, Deodhar SD, Chiang T, Gautam S, Edinger M.
    Experimental beryllium-induced lung disease. I. Differences in
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