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    NICKEL CARBONYL




    SM Bradberry BSc MB MRCP
    ST Beer BSc
    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.


    NICKEL CARBONYL

    Toxbase summary

    Type of product

    An intermediate in nickel refining and used as a catalyst in the
    petroleum, plastic and rubber industries.

    Toxicity

    Vapourised nickel carbonyl is highly toxic; inhalation may be fatal.

    Features

    Topical

         -    Nickel carbonyl is a potential skin irritant but
              transcutaneous absorption is poor.

    Inhalation

    Minor inhalation:
         -    Dry sore throat, cough, dizziness and headache.

    Substantial inhalation:
         -    Sore throat, cough, chest tightness and dyspnoea occur
              within minutes, often associated with dizziness, nausea,
              headache and muscle cramps.
         -    A chemical pneumonitis may develop in severe cases,
              sometimes after a latent period of a few days.  Anorexia,
              abdominal pain, jaundice and diarrhoea are also reported and
              rarely myocarditis, delirium, convulsions or coma.  Death
              may occur due to pulmonary haemorrhage, pulmonary or
              cerebral oedema or toxic myocarditis.
         -    Investigations may show increased hepatic transaminase
              activities and a neutrophil leukocytosis.  There may be
              diffuse opacifications and/or a pleural effusion on chest x-
              ray in those with symptoms or signs of pneumonitis.  ECG
              changes include ventricular ectopic beats in mild poisoning
              or ST and T wave changes and QT interval prolongation
              (suggesting a toxic myocarditis) in more severe cases.

         -    Chronic low-level occupational nickel carbonyl inhalation
              may cause an obstructive airways defect.  EEG abnormalities
              and reduced monoamine oxidase activities are also reported.

    Management

    Topical

    1.   Remove from exposure and treat symptomatically.

    Inhalation

    1.   Remove from exposure.
    2.   Patients who are asymptomatic following minimal exposure are not
         at risk of developing a delayed pneumonitis and can be released
         if clinical assessment is normal.
    3.   Administer supplemental oxygen by face mask.
    4.   Intravenous hydrocortisone may be beneficial for severe pulmonary
         complications but this is not confirmed.
    5.   Collect urine for nickel concentration estimation.
    6.   Perform a chest X-ray, ECG, biochemical profile and blood count.
    7.   Chelation therapy with oral (or intravenous in severely ill
         patients) diethyldithiocarbamate (DDC), if available, or oral
         disulfiram should be considered in symptomatic cases.
    8.   Although the urine nickel concentration in the first eight hours
         after exposure correlates with poisoning severity, these results
         are unlikely to be available acutely and treatment must be guided
         by symptoms.  Discuss with NPIS.
    9.   Alcohol should be avoided for at least 48 hours following
         treatment with DDC or disulfiram.

    References

    Jones CC.
    Nickel carbonyl poisoning.  Report of a fatal case.
    Arch Environ Health 1973; 26: 245-8.

    Kurta DL, Dean BS, Krenzelok EP.
    Acute nickel carbonyl poisoning.
    Am J Emerg Med 1993; 11: 64-6.

    Shi Z.
    Acute nickel carbonyl poisoning: a report of 179 cases.
    Br J Ind Med 1986; 43: 422-4.

    Shi Z.
    Long-term effects of exposure to low concentrations of nickel carbonyl
    on workers' health.  In: Nieboer E, Nriagu JO, eds.  Nickel and human
    health - current perspectives.  Vol 25.
    New York: John Wiley & Sons, Inc, 1992; 273-9.

    Shi Z, Lata A, Yuhua H.
    A study of serum monoamine oxidase (MAO) activity and the EEG in
    nickel carbonyl workers.
    Br J Ind Med 1986; 43: 425-6.

    Sunderman Sr FW.
    Use of sodium diethyldithiocarbamate in the treatment of nickel
    carbonyl poisoning.
    Ann Clin Lab Sci 1990; 20: 12-21.

    Substance name

         Nickel carbonyl

    Origin of substance

         Nickel carbonyl is produced by passing carbon monoxide over
         finely divided nickel.             (CSDS, 1991)

    Synonyms

         Tetracarbonyl nickel               (CSDS, 1991)
         Nickel tetracarbonyl               (DOSE, 1994)

    Chemical group

         A compound of nickel, a transition metal (d block) element.

    Reference numbers

         CAS            13463-39-3          (DOSE, 1994)
         RTECS          QR6300000           (RTECS, 1996)
         UN             1259                (DOSE, 1994)
         HAZCHEM CODE   NIF

    Physico-chemical properties

    Chemical structure
         Nickel carbonyl, Ni(CO)4           (DOSE, 1994)

    Molecular weight
         170.75                             (DOSE, 1994)

    Physical state at room temperature
         Liquid                             (CSDS, 1991)

    Colour
         The liquid is colourless, the solid is white.
                                            (CSDS, 1991)

    Odour
         Musty, sooty odour.                (HSDB, 1996)

    Viscosity
         0.212 cP at 25C                   (HSDB, 1996)

    pH
         NIF

    Solubility
         Sparingly soluble in water: 0.18 g/L at 9.8C.
                                            (MERCK, 1989; HSDB,1996)

         Soluble in alcohol, benzene, chloroform, acetone and carbon
         tetrachloride.                     (DOSE, 1994)

    Autoignition temperature
         <93C (vapour)                     (HSDB, 1996)

    Chemical interactions
         Nickel carbonyl reacts violently with dinitrogen tetroxide, and
         may explode when mixed with bromine, or a butane-oxygen mixture.
         A shock-sensitive explosive is formed following reaction with
         tetrachloropropadiene.             (CSDS, 1991)

    Major products of combustion
         NIF

    Explosive limits
         Vapour explodes in air or oxygen at 20C, partial pressure 15mm,
         liquid explodes at 60C.           (HSDB, 1996)

    Flammability
         Flammable - burns with yellow flame.  In direct sunlight, both
         the liquid and gas will flash.     (HSDB, 1996)

    Boiling point
         43C                               (CSDS, 1991)

    Density
         1.32 at 17C (liquid)              (CSDS, 1991)

    Vapour pressure
         53329 Pa at 25.8C                 (CSDS, 1991)

    Relative vapour density
         5.95 at 50C (gas)                 (HSDB, 1996)

    Flash Point
         <-20C (closed cup)                (CSDS, 1991)

    Reactivity
         On exposure to atmospheric oxygen, a deposit is produced on
         nickel carbonyl which may ignite.  Mixtures with air or oxygen at
         low partial and total pressures explode after an induction
         period.

         The vapour forms an explosive mixture with air.  It is highly
         flammable and may explode if heated to 60C or above.
                                            (CSDS, 1991)

    Uses

         Nickel carbonyl is an intermediate in the Mond process of nickel
         refining.

         It is used in organic synthesis, the manufacture of catalysts and
         nickel vapour plating.             (CSDS, 1991; DOSE, 1994)

    Hazard/risk classification

    Index no.     028-001-00-1

    Risk phrases
         F; R11, Carc. Cat. 3; R40, Repr. Cat. 2; R61, T+; R26  - Highly
         flammable.  Possible risk of irreversible effects.  May cause
         harm to the unborn child.  Very toxic by inhalation.

    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 where possible).

    EEC no.      236-669-2                  (CHIP2, 1994)

    INTRODUCTION

    Gaseous nickel carbonyl is formed in the Mond process of nickel
    purification by the reaction of elemental nickel with carbon monoxide. 
    Most exposures are occupational via inhalation. The gas can be
    condensed into a liquid which boils at 43C.

    MECHANISM OF TOXICITY

     In vitro studies demonstrate that nickel causes crosslinking of
    amino acids to DNA, alters gene expression, induces gene mutations and
    the formation of reactive oxygen species (Costa et al, 1994a and b;
    Haugen et al, 1994; Huang et al, 1994; Shi et al, 1994).  Nickel also
    suppresses NK cell activity and interferon production (Shen and Zhang,
    1994).

    TOXICOKINETICS

    Absorption

    Nickel carbonyl can be absorbed by inhalation and ingestion, the
    former being more important occupationally.  Significant percutaneous
    absorption does not occur. Vapourised nickel carbonyl is the most
    readily absorbed form of inhaled nickel.

    Distribution and excretion

    Following nickel carbonyl inhalation, nickel is transported in the
    blood bound principally to albumin.  High  concentrations are found 
    in the kidneys, liver, lungs and brain.  Nickel is excreted primarily
    in the urine with a half-life following acute  inhalation of up to 50
    hours although some absorbed nickel is retained in body stores and
    excreted over several months (IPCS, 1991; Sunderman, 1992b).

    Nickel crosses the placenta and is passed to the child in maternal
    milk (Fairhurst and Illing, 1987; IPCS, 1991).

    CLINICAL FEATURES: ACUTE EXPOSURE

    Inhalation

    Pulmonary toxicity

    The clinical features observed following acute nickel carbonyl
    exposure have been classified as immediate and delayed although such a
    distinction may not be clear (Sunderman and Kincaid, 1954). 
    Individuals who are moderately poisoned typically will develop a dry
    sore throat, cough, chest tightness and dyspnoea within minutes often
    associated with dizziness, nausea, headache, and muscle cramps
    (Vuopala et al, 1970; Shi, 1986).

    In more severe cases a chemical pneumonitis may develop sometimes
    after a latent period of a few days (Brandes, 1934).  These patients
    may exhibit features of generalised systemic upset (muscle pains,
    fatigue) in addition to gastrointestinal and neurological symptoms
    (see below) (Sunderman and Kincaid, 1954; Jones, 1973; Sunderman,
    1989).  Haemoptysis has also been described (Shi, 1986).

    Clinical signs include hyperaemia of the conjunctivae and throat,
    cyanosis, tachycardia and tachypnoea with wheeze and crackles on
    auscultation of the lung fields (Shi, 1986).  There may be diffuse
    opacifications and/or a pleural effusion on chest x-ray (Shi, 1986).

    Death may occur in cases with severe pulmonary manifestations
    (Anonymous, 1903; Brandes, 1934; Sunderman and Kincaid, 1954; Jones,
    1973) with post-mortem evidence of pulmonary nickel deposition,
    pulmonary consolidation or  haemorrhage, pleural thickening, a
    fibrinoid alveolar infiltrate and/or pulmonary or cerebral oedema
    (Brandes, 1934; Sunderman and Kincaid, 1954; Jones, 1973).

    Gastrointestinal toxicity

    The respiratory effects of mild nickel carbonyl exposure are
    associated frequently with nausea (Vuopala et al, 1970; Shi, 1986). 
    More substantial exposures cause anorexia, vomiting, abdominal pain
    and diarrhoea which usually accompany development of a chemical
    pneumonitis (Vuopala et al, 1970; Shi, 1986).

    Neurotoxicity

    Dizziness and headache are very common following mild or moderate
    nickel carbonyl exposure (Anonymous, 1903; Shi, 1986).  In more severe
    cases there may be dysphoria, somnolence, blurred vision (Shi, 1986)
    and rarely delirium, convulsions (Sunderman and Kincaid, 1954;
    Sunderman, 1989) or coma (Brandes, 1934).  Exaggerated limb reflexes
    have also been reported (Brandes, 1934).  Nickel particles have been
    identified in the brain of fatal cases (Brandes, 1934).

    Hepatotoxicity

    Patients with nickel carbonyl poisoning may have transiently raised
    hepatic transaminase activities (Shi, 1986), hepatic tenderness
    (Vuopala et al, 1970) and/or hepatomegaly (Brandes, 1934).  Jaundice
    has been reported in more severely poisoned patients (Sunderman and
    Kincaid, 1954).

    Haemotoxicity

    A leukocytosis is common in moderate to severe acute nickel carbonyl
    poisoning (Sunderman and Kincaid, 1954; Shi, 1986).

    Cardiotoxicity

    Electrocardiographic changes have been reported following acute nickel
    carbonyl exposure and vary from a sinus tachycardia or ventricular
    ectopic beats in mild cases (Shi, 1986) to ST and T wave changes and
    QT interval prolongation (suggesting a toxic myocarditis), in those
    more significantly exposed (Shi, 1986).  Post mortem findings from
    early nickel carbonyl fatalities described "fatty" (Anonymous, 1903)
    and dilated (Anonymous, 1903; Brandes, 1934) heart chambers.

    CLINICAL FEATURES: CHRONIC EXPOSURE

    Inhalation

    Chronic exposure to low concentrations of nickel carbonyl may result
    in an obstructive airways defect (low FEV1 and PEFR) (Shi, 1992; Shi,
    1994). Pulmonary eosinophilia (Loeffler's syndrome) due to a type III
    hypersensitivity reaction to nickel has been described (Sunderman and
    Sunderman, 1961).

    EEG abnormalities and reduced monoamine oxidase activity are also
    reported in those subject to repeated occupational exposure (Shi et
    al, 1986).

    MANAGEMENT

    Inhalation

    Patients who are completely asymptomatic following suspected nickel
    carbonyl inhalation are not at risk of developing delayed sequelae and
    can be discharged if clinical assessment is normal.  Symptomatic
    patients require a full assessment including collecting urine for
    nickel concentration estimation, checking a biochemical profile and
    blood count and performing a chest x-ray and ECG.

    Acute severe nickel carbonyl inhalation requires prompt supportive
    treatment. Intravenous hydrocortisone may be beneficial in the
    management of severe pulmonary complications but its value has not
    been confirmed in controlled clinical trials.  The role of chelation
    therapy is discussed below.

    Antidotes

    Calcium EDTA

    Parenteral calcium disodium EDTA did not protect mice or rabbits
    against the lethal effects of nickel carbonyl (West and Sunderman,
    1958b).

    There are no human data.

    Diethyldithiocarbamate and disulfiram

    Diethyldithiocarbamate (DDC) has been advocated in the treatment of
    acute nickel carbonyl poisoning (Sunderman, 1992a; Kurta et al, 1993). 
    DDC forms a chelate with Ni2+ such that 2(DDC) + Ni2+ ---- nickel
    bis(DDC) which is renally excreted.  DDC is not available as a
    pharmaceutical preparation in many countries although disulfiram
    (Antabuse), which is metabolised to DDC (two molecules of DDC from
    each of disulfiram) has been employed.

    All rats exposed to lethal concentrations of nickel carbonyl vapour
    survived if treated immediately with 50 or 100 mg/kg parenteral DDC
    (West and Sunderman, 1958a).  A similar degree of protection was
    observed when DDC was administered at eight hours, but this benefit
    was at least partially lost at 24 hours.  In the same study immediate
    oral administration of the antidote offered some protection against
    nickel carbonyl poisoning but was less effective than parenteral DDC,
    especially at higher nickel carbonyl concentrations (West and
    Sunderman, 1958a).

    Baselt and Hanson (1982) compared the effect of oral disulfiram, DDC
    and d-penicillamine in the treatment of rats acutely exposed to nickel
    carbonyl vapour (1.4 mg/L) for 15 minutes.  Disulfiram was not an
    effective antidote in these circumstances and although d-penicillamine
    protected against death at a nickel carbonyl concentration of 1.4

    mg/L, only DDC was effective following exposure to a nickel carbonyl
    concentration of 1.7 mg/L (Baselt and Hanson, 1982).

    Well documented clinical studies involving DDC in nickel carbonyl
    poisoning are scarce.  Sunderman and Sunderman (1958) reported the
    first clinical case of acute nickel carbonyl poisoning treated
    effectively with oral DDC.  A 25 year-old male was accidentally
    sprayed with nickel carbonyl and immediately developed dizziness,
    nausea, tachypnoea, cyanosis and chest pain (Sunderman and Sunderman,
    1958).  He was administered 95 per cent oxygen, 2 g oral DDC and 2 g
    oral sodium bicarbonate within minutes, then 1 g oral DDC twice daily
    for ten days.  The urine nickel concentration on the day of exposure
    was 2000 g/L (normal <30 g/L).  He made a full recovery.  This and
    other individual case reports involving the use of DDC and disulfiram
    in nickel carbonyl poisoning are summarised in Table 1.

    Table 1.  Case reports of DDC and disulfiram in nickel carbonyl
    poisoning

                                                                        

    Max urine     Treatment                  Outcome        Study
    [Ni] g/L
                                                                        

    2000          2g oral DDC daily from     Survived       Sunderman
                  day 1 - 11                                & Sunderman,
                                                            1958

    535           4 g oral DDC on day 2      Died (day 4)   Jones, 1973

    1720          0.75 - 2.25 g oral         Survived       Kurta et al,
                  disulfiram daily days                     1993
                  1, 2, 9-11
                  1.2 - 2.8 g oral DDC
                  daily days 2 - 8
                                                                        

    The patient described by Jones (1973) presented the day following
    exposure to nickel carbonyl, had a maximum urine nickel concentration
    of 535 g/L 24 hours post exposure, received 4 g oral DDC on day two
    and died from respiratory complications on day four.  Another patient
    with severe nickel carbonyl poisoning survived despite the development
    of a chemical pneumonitis requiring 60 per cent oxygen and continuous
    positive airways pressure (CPAP) ventilation for four days (Kurta et
    al, 1993).  The maximum urine nickel concentration was 1720 g/L and
    the patient received 0.75 - 2.25 g oral disulfiram daily on days one,
    two and 9-11 with 1.2 - 2.8 g oral DDC daily on days two to eight.

    Sunderman (1990) reported that more than 375 persons exposed to nickel
    carbonyl vapour over 30 years had been treated successfully with DDC. 
    No deaths occurred in those who received "adequate" doses of DDC
    within four days of exposure.  However data for only 23 of these cases
    have been published (Sunderman and Sunderman, 1958; Sunderman, 1979;
    Sunderman, 1990; Table 2).

    Although the details of these cases are scarce and the data are
    uncontrolled, it is noteworthy that 75-100 per cent recovered.  Only
    three of the four nickel carbonyl poisoned patients described by
    Sunderman (1979) received treatment; the fourth (untreated) patient
    died.

    There is experimental evidence that disulfiram and DDC promote the
    accumulation of bivalent nickel ions in the brain (Jasim and Tjlve,
    1984; Belliveau et al, 1985; Tjlve and Borg-Neczak, 1994; Nielsen and
    Andersen, 1994) and this may limit the use of these agents as nickel
    antidotes (Tjlve and Borg-Neczak, 1994).

    Antidotes: Conclusions and recommendations

    1.   Well documented clinical studies using DDC (or disulfiram) in
         nickel carbonyl poisoning are scarce.
    2.   Sunderman (1992a) has recommended a treatment protocol for DDC in
         acute nickel carbonyl poisoning (Table 3), variations of which
         are advocated widely (Poisindex, 1996).  This is based on urine
         nickel concentrations in the first eight hours following exposure
         and makes no allowance for urine volume.  These treatment doses
         have no firm scientific rationale and, moreover, the analytical
         results are unlikely to be available in the necessary time
         course. However, it is reasonable to consider treatment with DDC
         (where available) in life-threatening nickel carbonyl poisoning.
    3.   Disulfiram is a therapeutic alternative but clinical experience
         with this antidote is very limited.  Although theoretically the
         dose of disulfiram required should be approximately half that of
         DDC (Poisindex, 1996) this is not borne out in animal studies in
         which disulfiram is less effective than DDC and higher doses are
         required.

    MEDICAL SURVEILLANCE

    Prior to employment involving nickel carbonyl exposure special
    consideration should be given to those with a history of respiratory
    disease.

    Monitoring of nickel concentrations in 'spot' samples of blood and
    urine is not indicated routinely as these concentrations do not
    reflect the total body nickel burden in those exposed to nickel
    carbonyl.  Furthermore, urine nickel concentrations vary considerably
    and should be interpreted as groups of 24 hour samples rather than
    individual urine specimens (Sunderman et al, 1986; Nickel Producers
    Environmental Research Association and the Nickel Development
    Institute, 1994).


        Table 2.  Case series of DDC in nickel carbonyl poisoning

                                                                                                             
            Mean  SD                   DDC treatment
                                                                      
            max urine      Day started       Daily         Duration           %
    n=      [Ni] g/L      mean  SD         dose g        days            Recovery      Study
                                                                                                             

      6     935  610      5.7  3.9         1 - 2         ?               100           Sunderman &
                                                                                         Sunderman, 1958

      4     450 - 580      2.0  0           ?             ?                75           Sunderman, 1979
            ("Range")      (n = 3)

    13      638  656      ?                 2             "2 - 14"        100           Sunderman, 1990 
                                             "average"
                                                                                                             

    Table 3.  DDC in nickel carbonyl poisoning: Sunderman's treatment protocol (Sunderman, 1992a)

                                                                                                 

       ->  Mild exposure (initial 8 h urine nickel concentration < 100g/L)

                               Oral DDC     1.0 g       (0.2 g every 2 min for 5 doses)

       ->  Moderate or severe exposure (initial 8 h urine nickel concentration > 100g/L)*

               First day:      Oral DDC     1.0 g        0 h
                                            0.8 g        4 h
                                            0.6 g        8 h
                                            0.4 g       16 h

               Thereafter:     Oral DDC     0.4 g       tds (until urine nickel concentration
                                                        normal)

       ->  Consider parenteral DDC (25 mg/kg) if urine nickel concentration >500 g/L
                                                                                                 

    *  In very severe poisoning (initial 8 h urine nickel concentration >500 g/L) an initial
       intravenous DDC dose of 25 mg/kg (dissolved in phosphate buffer) is suggested.
    
    Following acute nickel carbonyl exposure the urine nickel
    concentration in an initial eight hour urine collection is a useful
    guide to the severity of poisoning although this analysis is not
    widely available; a concentration greater than 500 g/L indicates
    substantial intoxication (Sunderman, 1992a).

    OCCUPATIONAL DATA

    Occupational exposure standard

    Short-term exposure limit (15-minute reference period) 0.24 mg/m3
    (Health and Safety Executive, 1995).

    OTHER TOXICOLOGICAL DATA

    Carcinogenicity

    Epidemiological studies have shown a significant increase in deaths
    from carcinoma of the lung and nasal sinuses among nickel refinery
    workers (Morgan, 1958; Roberts et al, 1992; Anderson, 1992; Morgan and
    Usher, 1994).  The excess risk of death continues for several years
    after leaving employment (Muir et al, 1994).

    The exact aetiological agent is unknown.  Although animal data suggest
    nickel carbonyl may be carcinogenic there is insufficient human
    evidence to confirm this (IARC, 1990).

    In a study of respiratory tract cancer among nickel refinery workers,
    Morgan (1958) proposed that nickel-containing dusts, copper sulphate
    or arsenic-contaminated sulphuric acid were more likely causative
    agents than nickel carbonyl.

    Fortunately, measures to improve industrial hygiene have greatly
    reduced the occupational hazard of nickel carbonyl exposure (Doll et
    al, 1977) but respiratory tract malignancies among employees in the
    nickel industry remain notifiable diseases in the UK (Seaton et al,
    1994).

    Reprotoxicity

    Occupational exposure of fertile women to nickel carbonyl is avoided
    in some industries although there are no conclusive human data
    regarding its reprotoxicity (Reprotox, 1996).

    Genotoxicity

    NIF

    Fish toxicity

    NIF

    EC Directive on Drinking Water Quality 80/778/EEC

    Nickel: Maximum admissible concentration 50 g/L (DOSE, 1994).

    AUTHORS

    SM Bradberry BSc MB MRCP
    ST Beer BSc
    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
    7/10/96

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    New York: John Wiley & Sons, Inc., 1992; 621-7.

    Anonymous.
    Nickel carbonyl poisoning.
    Lancet 1903: 1; 268-9.

    Baselt RC, Hanson VW.
    Efficacy of orally-administered chelating agents for nickel carbonyl
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    Res Commun Chem Pathol Pharmacol 1982; 38: 113-24.

    Belliveau JF, O'Leary GP, Cadwell L, Sunderman FW.
    Effect of diethyldithiocarbamate on nickel concentrations in tissues
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    Ann Clin Lab Sci 1985; 15: 349-50.

    Brandes WW.
    Nickel carbonyl poisoning.
    JAMA 1934; 102: 1204-6.

    CHIP2/Chemicals (Hazard Information and Packaging for Supply)
    Regulations 1994.
    Health and Safety Commission.
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    Costa M, Salnikow K, Cosentino S, Klein CB, Huang X, Zhuang Z.
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    Environ Health Perspect 1994b; 102: 127-30.

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    Toxicology 1984; 32: 297-313.

    Jones CC.
    Nickel carbonyl poisoning.  Report of a fatal case.
    Arch Environ Health 1973; 26: 245-8.

    Kurta DL, Dean BS, Krenzelok EP.
    Acute nickel carbonyl poisoning.
    Am J Emerg Med 1993; 11: 64-6.

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    Budavari S, ed.
    New Jersey: Merck and Co., Inc., 1989.

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    Ann Occup Hyg 1994; 38: 189-98.

    Muir DCF, Jadon N, Julian JA, Roberts RS.
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    See Also:
       Toxicological Abbreviations
       Nickel carbonyl (ICSC)