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Bromine

1. NAME
   1.1 Substance
   1.2 Group
   1.3 Synonyms
   1.4 Identification numbers
      1.4.1 CAS number
      1.4.2 Other numbers
   1.5 Main brand names, main trade names
   1.6 Main manufacturers, main importers
2. SUMMARY
   2.1 Main risks and target organs
   2.2 Summary of clinical effects
   2.3 Diagnosis
   2.4 First-aid measures and management principles
3. PHYSICO-CHEMICAL PROPERTIES
   3.1 Origin of the substance
   3.2 Chemical structure
   3.3 Physical properties
      3.3.1 Colour
      3.3.2 State/form
      3.3.3 Description
   3.4 Hazardous characteristics
4. USES
   4.1 Uses
      4.1.1 Uses
      4.1.2 Description
   4.2 High risk circumstance of poisoning
   4.3 Occupationally exposed populations
5. ROUTES OF ENTRY
   5.1 Oral
   5.2 Inhalation
   5.3 Dermal
   5.4 Eye
   5.5 Parenteral
   5.6 Others
6. KINETICS
   6.1 Absorption by route of exposure
   6.2 Distribution by route of exposure
   6.3 Biological half-life by route of exposure
   6.4 Metabolism
   6.5 Elimination by route of exposure
7. TOXICOLOGY
   7.1 Mode of Action
   7.2 Toxicity
      7.2.1 Human data
         7.2.1.1 Adults
         7.2.1.2 Children
      7.2.2 Relevant animal data
      7.2.3 Relevant in vitro data
      7.2.4 Workplace standards
      7.2.5 Acceptable daily intake (ADI) and other guideline levels
   7.3 Carcinogenicity
   7.4 Teratogenicity
   7.5 Mutagenicity
   7.6 Interactions
8. TOXICOLOGICAL ANALYSES AND BIOMEDICAL INVESTIGATIONS
   8.1 Material sampling plan
      8.1.1 Sampling and specimen collection
         8.1.1.1 Toxicological analyses
         8.1.1.2 Biomedical analyses
         8.1.1.3 Arterial blood gas analysis
         8.1.1.4 Haematological analyses
         8.1.1.5 Other (unspecified) analyses
      8.1.2 Storage of laboratory samples and specimens
         8.1.2.1 Toxicological analyses
         8.1.2.2 Biomedical analyses
         8.1.2.3 Arterial blood gas analysis
         8.1.2.4 Haematological analyses
         8.1.2.5 Other (unspecified) analyses
      8.1.3 Transport of laboratory samples and specimens
         8.1.3.1 Toxicological analyses
         8.1.3.2 Biomedical analyses
         8.1.3.3 Arterial blood gas analysis
         8.1.3.4 Haematological analyses
         8.1.3.5 Other (unspecified) analyses
   8.2 Toxicological analyses and their interpretation
      8.2.1 Tests on toxic ingredient(s) of material
         8.2.1.1 Simple qualitative test(s)
         8.2.1.2 Advanced qualitative confirmation test(s)
         8.2.1.3 Simple quantitative method(s)
         8.2.1.4 Advanced quantitative method(s)
      8.2.2 Tests for biological specimens
         8.2.2.1 Simple qualitative test(s)
         8.2.2.2 Advanced qualitative confirmation test(s)
         8.2.2.3 Simple quantitative method(s)
         8.2.2.4 Advanced quantitative method(s)
         8.2.2.5 Other dedicated method(s)
      8.2.3 Interpretation of toxicological analyses
   8.3 Biomedical investigations and their interpretation
      8.3.1 Biochemical analysis
         8.3.1.1 Blood, plasma or serum
         8.3.1.2 Urine
         8.3.1.3 Other fluids
      8.3.2 Arterial blood gas analyses
      8.3.3 Haematological analyses
      8.3.4 Interpretation of biomedical investigations
   8.4 Other biomedical (diagnostic) investigations and their interpretation
   8.5 Overall interpretation of all toxicological analyses and toxicological investigations
9. CLINICAL EFFECTS
   9.1 Acute poisoning
      9.1.1 Ingestion
      9.1.2 Inhalation
      9.1.3 Skin exposure
      9.1.4 Eye contact
      9.1.5 Parenteral exposure
      9.1.6 Other
   9.2 Chronic poisoning
      9.2.1 Ingestion
      9.2.2 Inhalation
      9.2.3 Skin exposure
      9.2.4 Eye contact
      9.2.5 Parenteral exposure
      9.2.6 Other
   9.3 Course, prognosis, cause of death
   9.4 Systematic description of clinical effects
      9.4.1 Cardiovascular
      9.4.2 Respiratory
      9.4.3 Neurological
         9.4.3.1 Central Nervous System (CNS)
         9.4.3.2 Peripheral nervous system
         9.4.3.3 Autonomic nervous system
         9.4.3.4 Skeletal and smooth muscle
      9.4.4 Gastrointestinal
      9.4.5 Hepatic
      9.4.6 Urinary
         9.4.6.1 Renal
         9.4.6.2 Others
      9.4.7 Endocrine and reproductive systems
      9.4.8 Dermatological
      9.4.9 Eye, ears, nose, throat: local effects
      9.4.10 Haematological
      9.4.11 Immunological
      9.4.12 Metabolic
         9.4.12.1 Acid-base disturbances
         9.4.12.2 Fluid and electrolyte disturbances
         9.4.12.3 Others
      9.4.13 Allergic reactions
      9.4.14 Other clinical effects
      9.4.15 Special risks
   9.5 Others
   9.6 Summary
10. MANAGEMENT
   10.1 General principles
   10.2 Life supportive procedures and symptomatic treatment
   10.3 Decontamination
   10.4 Enhanced elimination
   10.5 Antidote treatment
      10.5.1 Adults
      10.5.2 Children
   10.6 Management discussion
11. ILLUSTRATIVE CASES
   11.1 Case reports from literature
12. ADDITIONAL INFORMATION
   12.1 Specific preventive measures
   12.2 Other
13. REFERENCES
14. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES), COMPLETE ADDRESS(ES)
    BROMINE

    International Programme on Chemical Safety
    Poisons Information Monograph 080
    Chemical

    1.  NAME

        1.1  Substance

             Bromine

        1.2  Group

             Halogen

        1.3  Synonyms

             Brom (German);
             Brome (French);
             Bromo (Italian);
             Broom (Dutch).

        1.4  Identification numbers

             1.4.1  CAS number

                    7726-95-6

             1.4.2  Other numbers

                    DOT:  1744 59 (designated corrosive material)
                    IMIS: 0390
                    NIOSH RTECS:  EF 9100000
                    UN:   1744

        1.5  Main brand names, main trade names

        1.6  Main manufacturers, main importers

             United States Manufacturers (Weiss, 1980):
    
             Arkansas Chemicals Inc., El Dorado, Arkansas 71730
             Bromet Company, Magnolia, Arkansas 71753
             Dow Chemical Company, Midland, Michigan 48640

    2.  SUMMARY

        2.1  Main risks and target organs

             Inhalation of the irritant bromine vapours and/or direct
             contact (liquid or vapour) with skin and mucous membranes
             will produce direct tissue injury.  Injury may occur at
             various levels of the respiratory tract depending on the

             concentration of bromine and duration of exposure.  Target
             organs include the upper and lower respiratory tract, skin,
             and eyes.
    
             In theory, although never demonstrated in the literature, the
             potential exists for bromine to accumulate in body tissues as
             bromide after an inhalation or direct skin contact. If
             accumulated to sufficiently high concentrations, bromide
             would subsequently produce neurotoxic and acne-like effects
             as seen with the ingestion of bromide compounds or the
             chronic inhalation of methyl bromide.  However, due the
             extreme irritant nature of bromine, the duration of exposure
             is generally severely limited, reducing any likely body
             burden of bromide.

        2.2  Summary of clinical effects

             Acute
    
             Dermal:  Pure bromine (liquid or vapour) is extremely
             irritating to the skin.  Unlike most other chemical agents,
             there is no immediate visible skin reaction after contact. 
             The delay before initial signs of injury become apparent
             often results in more extensive damage.  The most common
             local effects are blister formation, brownish discoloration
             of the skin and slow-healing ulcers (Sagi et al., 1985).
    
             Mucous Membranes:  Exposure to low concentrations produces
             lacrimation, rhinorrhoea, eye irritation with mucous
             secretions from the oropharyngeal and upper airways,
             coughing, dyspnoea, choking, wheezing, epistaxis, and
             headache.  A brownish discoloration of the tongue and buccal
             mucosa may occur and be accompanied by a characteristic
             breath odour.  Inflammatory lesions of the upper airway,
             photophobia and blepharospasm are seen with higher
             concentrations (Parmeggiani, 1983). Upper and lower
             respiratory tract:  Initial irritant symptoms of bromine
             vapour inhalation include: dyspnoea, coughing, choking, and
             wheezing. In addition, immediate or delayed
             bronchoconstriction and the development of laryngeal spasm,
             glottal oedema, asthma and cheobronchitis. With increased
             parenchymal penetration, there may be associated
             peribronchiolar abscesses, pulmonary infiltrates consistent
             with chemical pneumonitis, bronchiolitis obliterans and
             pulmonary oedema (Edelman, 1991; Rom & Barkman, 1983).  Acute
             obstructive ventilatory impairment may lead to severe
             hypoxaemia, metabolic acidosis, measles-like rash and
             subsequent death.  It should be noted that more severe
             respiratory symptoms may be delayed for several hours after
             the exposure (Lossos et al., 1990; Kraut & Lilis, 1988).
    

             Central nervous system:  The bromide ion is a central nervous
             system depressant producing ataxia, slurred speech, tremor,
             nausea, vomiting, lethargy, dizziness, visual disturbances,
             unsteadiness, headaches, impaired memory and concentration,
             disorientation and hallucinations.  This has only been
             documented in the literature with reference to overdoses of
             bromide-containing medications and the inhalation of
             bromide-containing fumigants. Although theoretically
             possible, this has not been reported in the medical
             literature from acute (or chronic) exposure to bromine.
    
             Respiratory:  There are few reports about the chronic
             complications of an acute exposure to bromine.  However, the
             literature has described the chronic manifestations of
             chlorine inhalation.  Bromine is potentially capable of
             extensive damage to the lower respiratory tract.  Limited
             studies have reported diffuse interstitial pulmonary
             fibrosis, emphysema and/or airway hyperreactivity secondary
             to acute exposure to bromine (Lossos et al., 1990; Kraut &
             Lilis, 1988).
    
             Dermal:  There is a rare cutaneous manifestation of bromide
             accumulation known as bromoderma tuberosum, which progresses
             from red papules to pustules that enlarge and develop into
             indurated lesions with a central ulcer (Sticht & Kaferstein,
             1988).  This effect is related to the ingestion of bromides
             formerly used in medications and, in theory, to chronic
             inhalation of low-level concentrations of bromine (Sax,
             1984).
    
             Other:  Most available data come from studies involving
             chronic exposure to bromides in the form of oral medications.
             This type of exposure has lead to depression, ataxia and
             psychoses (bromism).  Chronic exposure to methyl bromide has
             caused peripheral neuropathy.  Soviet literature has
             described loss of corneal reflexes, joint pain, vegetative
             disorders, thyroid dysfunction and depression of bone marrow
             (Sticht & Kaferstein, 1988).  However, there is no published
             evidence that these chronic occur effects with the inhalation
             and/or dermal absorption of bromine liquid or vapour.

        2.3  Diagnosis

             Signs characteristic of acute bromine poisoning include:
    
             *  after exposure of skin, delayed onset of burns
             *  brownish discolouration of tongue and buccal mucosa
             *  characteristic odour on the breath
    
             Bromine gas blood concentrations are not clinically useful. 
             Bromine is generally unmeasurable since it changes directly
             to hydrobromic and bromic acid.  No specific laboratory

             studies are needed unless otherwise indicated by the severity
             of symptoms (see Section 2.4.)

        2.4  First-aid measures and management principles

             Acute contact with bromine liquid or vapour requires
             removal from the source of the bromine contamination.
    
             Eye:  The eye(s) should be irrigated with copious amounts of
             water for at least 15 minutes.  If irritation, pain,
             swelling, lacrimation or photophobia persist, further medical
             evaluation is recommended.
    
             Dermal:  Remove contaminated clothing and wash affected area
             thoroughly with copious volumes of water for 20 minutes. 
             Since effects may be delayed, close observation for
             blistering and discoloration of the skin is required for the
             next 24 hours (Sagi et al., 1985). 
    
             Inhalation:  Respiratory support in accordance with
             symptomatology, including: maintenance of an adequate airway,
             oxygen, antibronchospasm therapy (beta adrenergic agonist,
             aerosols, aminophylline and/or short course of
             corticosteriods) and antibiotics if there is evidence of
             infection.  Initial testing should include: chest x-ray to
             view inflammatory changes in the parenchyma, spirometry
             (flow-volume loop with and without bronchodilator) to
             determine air flow capacity and reversibility, diffusing
             capacity (DLco) to assess changes in the alveolar-capillary
             permeability, arterial blood gases to evaluate blood
             oxygenation (Po2) and ventilation (Pco2), and complete white
             blood count.  Repeat chest radiograph and spirometry are
             recommended to determine the progression or resolution of
             residual effects.  Ventilation-perfusion scanning does not
             usually provide significant additional information, except to
             rule out other processes, such as pulmonary emboli.  Careful
             examination is important to detect pathology (fine wheezes in
             subtle or early asthma and fine crackles in early pulmonary
             oedema) not revealed by the studies noted above.
    
             Ingestion: Not relevant

    3.  PHYSICO-CHEMICAL PROPERTIES

        3.1  Origin of the substance

             Bromine occurs naturally in the earth's crust as a
             non-metallic element. Like other halogens, it is very
             reactive and principally found in the form of inorganic
             bromides (Na, K, NH4, Ca and Mg) and as a component secondary
             to chlorine in minerals and biological systems (humans and
             animals).  A pure bromine-containing mineral, bromite (AgBr)

             is found in Mexico (Sticht & Kaferstein, 1988).  Bromine is
             derived from sea water and naturally occurring brines.
    
             Most sources outside of the United States (United Kingdom,
             France, Japan Israel and Soviet Union) recover bromine from
             salt lakes and sea water (Stokinger, 1981).  The bromine
             concentration in sea water averages about 0.0065%, while the
             Dead Sea contains an average concentration of 1.5% (Sticht &
             Kaferstein, 1988).
    
             Before the bromine can be steamed out of the sea water, the
             bromine is concentrated by vaporization and the addition of
             sulphur dioxide.  Water is then added to the resultant
             hydrogen bromide to produce a concentrated bromide solution. 
             The remainder of the process is similar to bromine recovery
             from brines.  The by-products of hydrochloric and sulfuric
             acid are recycled to the incoming water to reduce the pH
             sufficiently to promote efficient chlorination. 
    
             Most production in the United States is limited to naturally
             occurring brines in Michigan and Arkansas and accounts for
             about two-thirds of the world's annual production (Sticht &
             Kaferstein, 1988).  The oil-field brines in Arkansas are more
             concentrated (5000 ppm) than in Michigan and represent the
             principal area of bromine production in the United States
             (Leddy, 1983).  The brine (bromine-containing carnallite) is
             oxidized with elemental chlorine to liberate the bromine
             which is then condensed, distilled and dried.  The bromine is
             stored and shipped in glass bottles with lead caps and
             lead-lined metal barrels, drums and tanks.  Steam and
             chlorine are emitted from steaming-out towers and the spent
             brine is neutralized and pumped back into the subterranean
             strata  (Leddy, 1983).  In some cases, the debrominated brine
             is processed further to produce calcium and magnesium brine
             chemicals (Meyer, 1977).

        3.2  Chemical structure

             Bromine (Br):  Atomic Weight 79.904; Atomic Number 35;
             Valences 1 to 7; Elemental State Br2, molecular weight
             159.82; two stable isotopes 79Br and 81Br (Budivari,
             1996).

        3.3  Physical properties

             3.3.1  Colour

                    Dark reddish brown.

             3.3.2  State/form

             3.3.3  Description

                    Boiling Point:          -59.47C
                    Melting Point:          -7.25C
                    Flash Point:            -7.3C
                    Autoignition
                    Temperature:            Not found
                    Specific Gravity:       Liquid = 3.12 at 20C
                                            Vapour = 5.5 at 20C
                    Vapour Pressure:        175 mmHg at 20C, 3.385 psia
                                            (0.2303 atm)
                    Solubility
                    (g/100 mL at 20C):     Water 3.55g; Freely soluble in
                                            alcohol, ether, CHCl3, CCl4
                                            and CS2.
                    Explosive Limits:       Not combustible, but may cause
                                            fire on contact with
                                            combustibles
                    pH:                     Not found
                    Viscosity:              Not found
    
                    (Sax, 1984; Sticht & Kaferstein, 1988; OSHA, 1989;
                    Budivari, 1996; Meyer, 1977; Weiss, 1980)

        3.4  Hazardous characteristics

             Bromine is a dark reddish-brown, volatile, diatomic
             liquid with a suffocating odour at room temperature.  It is
             the only liquid non-metallic element.  Because the vapour
             pressure is so high, the dark red vapours are immediately
             detectable when a container is opened.
    
             The corrosive property of bromine is considered a major
             hazard by the United States Department of Transportation.
             Bromine is capable of dissolving metals and non-metals and
             spontaneously combines with aluminum, titanium copper,
             phosphorus, arsenic, gold and antimony.  It will not corrode
             platinum, lead or nickel.  The corrosive reaction results in
             a non-hazardous bromide. (Sittig, 1985; Budivari, 1996;
             Meyer, 1977) 
    
             As an oxidizer, bromine will react with inorganic matter,
             such as wood or sawdust; tremendous heat is produced
             increasing the risk of combustion following bromine spills.  
             Bromine spills should be neutralized with a 5 to 10% solution
             of sodium thiosulphate.  Sawdust should never be used to
             absorb bromine.  Explosions are also possible if ammonium
             hydroxide is used in an attempt to neutralize a spill (Meyer,
             1977).
    
             Bromine is slightly soluble in water, producing hydrogen
             bromide.  Hydrogen bromide is a corrosive colourless gas with
             a pungent odor that is extremely soluble in water.  In the
             presence of sunlight and humid air or hot water, it forms

             hydrobromic acid with concentrations up to about 60% (Sticht
             & Kaferstein, 1988).  Although less toxic than bromine, it
             has all the irritant qualities of bromine.
    
             Bromine should be stored in its original container, separated
             from combustible, organic or other readily oxidizable
             materials and protected against physical damage and sunlight. 
             Bromine should be kept above 20F (- 6.6C) to prevent
             freezing but heating above atmospheric temperatures should be
             avoided as raised vapour pressure could rupture the container 
             (OSHA, 1989).
    
             When handling bromine in significant quantities, full body
             protection (constructed of resistant material) should be
             worn.
    
             Bromine will readily dissolve in alcohol, ether and other
             organic solvents. 
    
             When elemental chlorine is used in the treatment of waste
             water, it releases free bromine and bromine chloride from the
             bromide solution. Acute toxicity of bromine and chlorine have
             been studied in fish; however, no US drinking water limits
             have been set for bromine (Calabrese & Kenyon, 1991). 
             Although bromine has been used as a water disinfectant for
             swimming pools, it is not recommend for this purpose in
             drinking water due to its cumulative neurotoxicity and the
             lack of sufficient research (NAS, 1977).

    4.  USES

        4.1  Uses

             4.1.1  Uses

             4.1.2  Description

                    Pure bromine is used in the synthesis of a
                    variety of bromine-containing substances.  In the
                    early 1970s, about 75% of the production of bromine
                    went into the making of ethylene dibromide (EDB) as an
                    antiknock agent in leaded gasoline.  With the United
                    States' mandate to reduce vehicle exhaust emissions,
                    EDB use significantly declined in the 1980s.  Export
                    of EDB has maintained production in the US at about
                    40% (Leddy, 1983).
    
                    Fumigant production in the form of methyl bromide and
                    ethylene dibromide account for about 10% of the total
                    bromine marketed, while high density bromine fluids
                    account for about 25%.  The high density bromine
                    fluids (calcium bromide and zinc bromide) are used
                    around the world as completion fluids in oil wells

                    (Leddy, 1983).  The remaining market for bromine is in
                    the manufacture of various organic compounds including
                    tetrabromobisphenol A, decarbromodiphenyl oxide,
                    hexabromocyclododecane and
                    pentabromocholorocyclohexane which are blended with
                    various polymeric materials to modify the finished
                    products.
    
                    Other uses for bromine include flame retardants,
                    cleaning agents, dyestuffs, photography, water
                    sanitation, pharmaceuticals, bleaching fibers and
                    silk, and chemical warfare gas (Sticht & Kaferstein,
                    1988; Sittig, 1985).

        4.2  High risk circumstance of poisoning

             Because of bromine's high reactivity with other
             elements, the forms of inorganic bromides found in the
             environment pose no danger of poisoning.  Primary risk of
             poisoning is through industrial sources during bromine
             recovery and/or when bromine is applied to the synthesis of
             bromine-containing substances noted above.  It is estimated
             that 20,000 workers in the US have the potential for
             occupational exposure to bromine (Broderick & Schwartz,
             1992)

        4.3  Occupationally exposed populations

             Professions that would be potentially at risk of
             exposure include:
    
             Drug Makers
             Dye Makers
             Gold Extractors
             Gasoline Additive Makers
             Organic Chemical Synthesizers
             Petroleum Refinery Workers
             Photographic Chemical Makers
             Silk and Fibre Bleachers
             (NIOSH, 1977)

    5.  ROUTES OF ENTRY

        5.1  Oral

             Unknown

        5.2  Inhalation

             During an accidental spill or leak during transportation
             or manufacturing.

        5.3  Dermal

             During an accidental spill or leak during transportation
             or manufacturing and/or improper handling or use of
             protective equipment.

        5.4  Eye

             During an accidental spill or leak during transportation
             or manufacturing and/or improper handling or use of
             protective equipment.

        5.5  Parenteral

             Unknown.

        5.6  Others

             No data available.

    6.  KINETICS

        6.1  Absorption by route of exposure

             The reactivity of bromine in biological systems makes it
             difficult to study the pharmacokinetics and to separate the
             effects of the bromine from those of the bromine compounds
             and metabolites.
    
             Inhalation
    
             Absorption of bromine vapours by other routes is usually
             minimal compared with the dose delivered by inhalation.  The
             physical characteristics of the bromine are extremely
             important in determining the site and depth of lung
             penetration and systemic absorption, as well as the local
             effects of the exposure.  The appearance or odour of bromine
             are usually adequate to alert the person to the presence of
             the material and afford time for escape.
    
             The toxic effects of the bromine vapour on the respiratory
             tract are primarily due to its water solubility.  Bromine is
             slightly more water soluble than chlorine and will produce
             immediate irritation of the upper airways (Broderick &
             Schwartz, 1992).  However, when the person is caught in a
             confined space or in an overwhelming vapour cloud, inhalation
             may cause irritation to the lower airways.

        6.2  Distribution by route of exposure

             No data available.

        6.3  Biological half-life by route of exposure

             The biological half-life for bromide through ingestion
             is 12 to 30 days; however, there are no data available on the
             inhalation of bromine (Sticht & Kaferstein, 1988).

        6.4  Metabolism

             Due to its reactivity, bromine does not persist as an
             element in living tissue but quickly forms bromide.   In this
             form, it may be deposited in the tissues, displacing other
             halogens (Sticht & Kaferstein, 1988).  However, there are no
             data available regarding the metabolism of inhaled
             bromine.

        6.5  Elimination by route of exposure

             No data available.

    7.  TOXICOLOGY

        7.1  Mode of Action

             The injurious effects of bromine are generally felt to
             be similar to those of chlorine (Rom & Barkman, 1983;
             Broderick & Schwartz, 1992; Schwartz, 1987).  Due to its
             potent oxidatising action, bromine liberates nascent oxygen
             or oxygen free radicals from the water present in mucous
             membranes.  Nascent oxygen is a potent oxidizer, capable of
             producing tissue damage.  The extent of the damage is
             dependent on the dose of bromine and the availability of
             water to react with it. In addition, the formation of
             hydrobromic and bromic acids will result in secondary
             irritation during the reaction.  Contact with the respiratory
             epithelium produces initial alveolar capillary congestion
             followed by focal and confluent patches of high-fibrinogen
             oedematous fluid.  The fluid is interstitial at first but can
             fill the alveoli.  Once this occurs, copious frothy, 
             blood-tinged sputum is seen.  A granulocyte response may occur
             several hours after inhalation.  Hyaline membrane formation
             can occur later resulting in clinical deterioration at a time
             when signs of improvement have occurred.  Poor oxygen
             diffusion, hypoxia and hypercapnia result from development of
             atelectasis, emphysema and membrane formation.  Acute
             obstructive ventilatory impairment leads to severe
             hypoxaemia, metabolic acidosis and death usually due to
             cardiac arrest secondary to the hypoxaemia.

        7.2  Toxicity

             7.2.1  Human data

                    7.2.1.1  Adults
                                                                      
                             Exposure Effects Levels (ppm)
                                                                      
                             0.05 to 3.5       Odour Threshold
                             0.1               TLV-TWA Limit
                             >1.0             Irritation Level
                             40 to 60          Toxic pneumonitis &
                                               pulmonary oedema
                             1000              Fatal within a few
                                               minutes
                                                                      
                             (Calabrese & Kenyon, 1991; Fazzalari,1978)

                    7.2.1.2  Children

                             No data available.

             7.2.2  Relevant animal data

                    Post mortem on guinea pigs and rabbits exposed
                    to bromine at 300 ppm for three hours revealed the
                    presence of pulmonary oedema; pseudomembranous deposit
                    on the trachea; and bronchi and haemorrhage of the
                    gastric mucosa (Stokinger, 1981).

                    The mortality of mice exposed to 240 or 750 ppm
                    bromine was dependent on the duration of exposure
                    (Bitron & Aharonson, 1978).

             7.2.3  Relevant in vitro data

                    Not relevant.

             7.2.4  Workplace standards

                    TLV-TWA: 0.1 ppm (approximately 0.66 mg/m3)
                    adopted in 1986 (ACGIH, 1991).
    
                    TLV-STEL: 0.3 ppm (approximately 2.0 mg/m3) adopted
                    in 1986 (ACGIH, 1991).
    
                    OSHA PEL: TWA 0.1ppm (approximately 0.7 mg/m3); STEL
                    0.3 ppm (approximately 2.0 mg/m3) (ACGIH, 1991)
    
                    NIOSH REL: TWA 0.1 ppm (approximately 0.7 mg/m3);
                    STEL 0.3 ppm (approximately 2.0mg/m3) (ACGIH,
                    1991)
    

                                                                        
                    Country/         TWA              STEL
                    Organization
                                     ppm     mg/m3    ppm       mg/m3
                                                                        
                    Australia        0.1     0.7      0.3       2
                    Belgium          0.1     0.66     0.3       2
                    Denmark          0.1     0.7      -         -
                    Finland          -       -        0.1       0.7
                    France           -       -        0.1       0.7
                    Germany          0.1     0.7      "I"       "I"
                    Hungary          -       -        -         0.7
                    Japan            0.1     0.65     -         -
                    Poland           -       0.7      -         -
                    Sweden           0.1     0.7      0.3       2
                    Switzerland      0.1     0.7      0.2       1.4
                    United Kingdom   0.1     0.7      0.3       2
                    US: ACGIH        0.1     0.66     0.3       2
                    US: NIOSH/OSHA   -       0.7      -         2
                    USSR             0.1     -        -         0.5
                                                                        
                    (ILO, 1991)
                    "I" = Local Irritant

             7.2.5  Acceptable daily intake (ADI) and other guideline levels

                    Acceptable Daily Intake (ADI)
    
                    Oral: 1 mg bromide/kg body weight (Sticht & 
                    Kaferstein, 1988).

        7.3  Carcinogenicity

             No data have been found implicating bromine as a
             carcinogen (Calabrese & Kenyon, 1991; Alderson, 1986).

        7.4  Teratogenicity

             No data have been found implicating bromine as a
             teratogen (Calabrese & Kenyon, 1991).

        7.5  Mutagenicity

             No data have been found implicating bromine as a mutagen
             (Calabrese & Kenyon, 1991).

        7.6  Interactions

             No data available.

    8.  TOXICOLOGICAL ANALYSES AND BIOMEDICAL INVESTIGATIONS

        8.1  Material sampling plan

             8.1.1  Sampling and specimen collection

                    8.1.1.1  Toxicological analyses

                    8.1.1.2  Biomedical analyses

                    8.1.1.3  Arterial blood gas analysis

                    8.1.1.4  Haematological analyses

                    8.1.1.5  Other (unspecified) analyses

             8.1.2  Storage of laboratory samples and specimens

                    8.1.2.1  Toxicological analyses

                    8.1.2.2  Biomedical analyses

                    8.1.2.3  Arterial blood gas analysis

                    8.1.2.4  Haematological analyses

                    8.1.2.5  Other (unspecified) analyses

             8.1.3  Transport of laboratory samples and specimens

                    8.1.3.1  Toxicological analyses

                    8.1.3.2  Biomedical analyses

                    8.1.3.3  Arterial blood gas analysis

                    8.1.3.4  Haematological analyses

                    8.1.3.5  Other (unspecified) analyses

        8.2  Toxicological analyses and their interpretation

             8.2.1  Tests on toxic ingredient(s) of material

                    8.2.1.1  Simple qualitative test(s)

                    8.2.1.2  Advanced qualitative confirmation test(s)

                    8.2.1.3  Simple quantitative method(s)

                    8.2.1.4  Advanced quantitative method(s)

             8.2.2  Tests for biological specimens

                    8.2.2.1  Simple qualitative test(s)

                    8.2.2.2  Advanced qualitative confirmation test(s)

                    8.2.2.3  Simple quantitative method(s)

                    8.2.2.4  Advanced quantitative method(s)

                    8.2.2.5  Other dedicated method(s)

             8.2.3  Interpretation of toxicological analyses

        8.3  Biomedical investigations and their interpretation

             8.3.1  Biochemical analysis

                    8.3.1.1  Blood, plasma or serum

                    8.3.1.2  Urine

                    8.3.1.3  Other fluids

             8.3.2  Arterial blood gas analyses

             8.3.3  Haematological analyses

             8.3.4  Interpretation of biomedical investigations

        8.4  Other biomedical (diagnostic) investigations and their
             interpretation

        8.5  Overall interpretation of all toxicological analyses and
             toxicological investigations

             Biomedical Analysis
    
             Initial testing should include: chest x-ray to view
             inflammatory changes in the parenchyma, spirometry 
             (flow-volume loop with and without bronchodilator) to
             determine air flow capacity and reversibility, diffusing
             capacity (DLco) to assess changes in the alveolar-capillary
             permeability, arterial blood gases to evaluate blood
             oxygenation (Po2) and ventilation  (Pco2) and complete white
             blood cell count.  Repeat chest radiographs and spirometry
             are recommended to determine the progression and resolution
             of residual effects.  Careful examination is important to
             detect pathology (fine wheezes in subtle or early asthma and
             fine crackles in early pulmonary oedema) not evident from the
             studies noted above.

    9.  CLINICAL EFFECTS

        9.1  Acute poisoning

             9.1.1  Ingestion

                    Not relevant.

             9.1.2  Inhalation

                    Upper and Lower Respiratory Tract:  Initial
                    symptoms due to irritation by bromine vapour
                    inhalation include:  dyspnoea, coughing, choking, and
                    wheezing; immediate or delayed bronchoconstriction;
                    and the development of laryngeal spasm, glottal
                    oedema, asthma and tracheobronchitis.  With increased
                    parenchymal penetration, there may be associated
                    peribronchiolar abscesses, pulmonary infiltrates
                    consistent with chemical pneumonitis, bronchiolitis
                    obliterans and pulmonary oedema (Edelman, 1991; Rom &
                    Barkman, 1983).  Acute obstructive ventilatory
                    impairment may lead to severe hypoxaemia, metabolic
                    acidosis, measles-like rash and subsequent death.  It
                    should be noted that more severe respiratory symptoms
                    may be delayed for several hours after the exposure
                    (Lossos et al., 1990; Kraut & Lilis, 1988).

             9.1.3  Skin exposure

                    Pure bromine (liquid or vapour) is extremely
                    irritating to the skin.  Unlike most other chemical
                    agents, there is no immediate visible skin reaction
                    with contact.  Lack of action due to the delay in
                    initial signs of injury often re4sults in more
                    extensive damage.  The most common local effects are
                    blister formation, brownish discoloration of the skin
                    and slowly healing ulcers (Sagi et al., 1985).

             9.1.4  Eye contact

                    Exposure to low concentrations produce
                    irritation of the eye with lacrimation.  Photophobia
                    and blepharospasm are seen with higher concentrations
                    (Parmeggiani, 1983).

             9.1.5  Parenteral exposure

                    Not relevant.

             9.1.6  Other

                    Not relevant.

        9.2  Chronic poisoning

             9.2.1  Ingestion

                    Not relevant.

             9.2.2  Inhalation

                    There are few reports on the chronic
                    complications of acute exposure to bromine.  However,
                    the literature has described the chronic
                    manifestations of chlorine inhalation.  Bromine is
                    potentially capable of extensive damage to the lower
                    respiratory tract.  Limited studies have reported
                    diffuse interstitial pulmonary fibrosis, emphysema
                    and/or airway hyperreactivity secondary to acute
                    exposure to bromine (Lossos et al., 1990; Kraut &
                    Lilis, 1988).

             9.2.3  Skin exposure

                    There is a rare cutaneous manifestation of
                    bromide accumulation known as bromoderma tuberosum,
                    which progresses from red papules to pustules that
                    enlarge and develop into indurated lesions with a
                    central ulcer (Sticht & Kaferstein, 1988).  This
                    effect is related to the ingestion of bromides
                    formerly used in medications and may, in theory, occur
                    after chronic inhalation of low concentrations of
                    bromine (Sax, 1984).

             9.2.4  Eye contact

                    No data available.

             9.2.5  Parenteral exposure

                    No data available.

             9.2.6  Other

                    No data available.

        9.3  Course, prognosis, cause of death

             The course and prognosis of a bromine exposure is 
             depends on the concentration and duration of the exposure.
             Effects may vary from mild irritation of mucous membranes 
             to severe damage of the skin and lung parenchyma.  Death
             is secondary to severe hypoxaemia/metabolic acidosis due to
             acute obstructive ventilatory impairment.

        9.4  Systematic description of clinical effects

             9.4.1  Cardiovascular

                    In an acute bromine exposure, significant
                    hypoxaemia and hypercapnia secondary to marked
                    respiratory obstruction and/or restriction are
                    responsible for the cardiovascular changes.  Initial
                    sinus tachycardia and cardiac arrhythmias may progress
                    to cardiac arrest with progressive pulmonary
                    obstruction.

             9.4.2  Respiratory

                    Initial irritant symptoms of bromine vapour
                    inhalation include:  dyspnoea, coughing, choking, and
                    wheezing, in addition, immediate or delayed
                    bronchoconstriction and the development of laryngeal
                    spasm, glottal oedema, asthma and tracheobronchitis. 
                    With increased parenchyma penetration, there may be
                    associated peribronchiolar abscesses, pulmonary
                    infiltrates consistent with chemical pneumonitis,
                    bronchiolitis obliterans and pulmonary oedema
                    (Edelman, 1991; Rom & Barkman, 1983).  Acute
                    obstructive ventilatory impairment may lead to severe
                    hypoxaemia, metabolic acidosis, measles-like rash and
                    subsequent death.  It should be noted that the onset
                    of severe respiratory symptoms may be delayed for
                    several hours after the exposure (Lossos et al., 1990;
                    Kraut & Lilis, 1988).

                    There are few reports on the chronic complication of
                    acute exposure to bromine.  However, the literature
                    has extensively described the chronic manifestations
                    of chlorine inhalation.  Bromine is potentially
                    capable of extensive damage to the lower respiratory
                    tract.  Limited studies have reported diffuse
                    interstitial pulmonary fibrosis, emphysema and/or
                    airway hyperreactivity secondary to acute exposure to
                    bromine (Lossos et al., 1990; Kraut & Lilis,
                    1988).

             9.4.3  Neurological

                    9.4.3.1  Central Nervous System (CNS)

                             The bromide ion is a central nervous
                             system depressant producing ataxia, slurred
                             speech, tremor, nausea, vomiting, lethargy,
                             dizziness, visual disturbances, unsteadiness,
                             headaches, impaired memory and concentration,
                             disorientation and hallucinations.  This has
                             only been documented in the literature with

                             reference to overdoses of bromide-containing
                             medications and the inhalation of
                             bromide-containing fumigants.

                    9.4.3.2  Peripheral nervous system

                             Chronic exposure to methyl bromide
                             has caused peripheral neuropathy; however,
                             there are no data on pure bromine
                             exposure.

                    9.4.3.3  Autonomic nervous system

                             No data available.

                    9.4.3.4  Skeletal and smooth muscle

                             No data available.

             9.4.4  Gastrointestinal

                    Not relevant.

             9.4.5  Hepatic

                    No data available.

             9.4.6  Urinary

                    9.4.6.1  Renal

                             No data available.

                    9.4.6.2  Others

                             No data available

             9.4.7  Endocrine and reproductive systems

                    No data available.

             9.4.8  Dermatological

                    Pure bromine (liquid or vapour) is extremely
                    irritating to the skin.  Unlike most other chemical
                    agents, there are no immediate visible skin reaction
                    with contact.  Lack of action due to the delay in
                    initial signs of injury often results in more
                    extensive damage.  The most common local effects are
                    blister formation, brownish discoloration of the skin
                    and slowly healing ulcers (Sagi et al., 1985).

                    There is a rare cutaneous manifestation of bromide
                    accumulation known as bromoderma tuberosum, which
                    progresses from red papules to pustules that enlarge
                    and develop into indurated lesions with a central
                    ulcer (Sticht & Kaferstein, 1988).  This effect is
                    related to the ingestion of bromides formerly used in
                    medications and, in theory, to chronic inhalation of
                    low level concentrations of bromine (Sax,
                    1984).

             9.4.9  Eye, ears, nose, throat: local effects

                    Exposure to low concentrations produce
                    irritation of the eye with lacrimation, rhinorrhoea,
                    choking and burning sensation of the throat. With
                    higher concentrations, there may be photophobia and
                    blepharospasm, epistaxis, hoarseness, stridor and
                    laryngeal oedema.

             9.4.10 Haematological

                    No data available.

             9.4.11 Immunological

                    No data available.

             9.4.12 Metabolic

                    9.4.12.1 Acid-base disturbances

                             With severe exposure to bromine,
                             metabolic acidosis may follow acute
                             respiratory acidosis secondary to acute
                             pulmonary obstruction and pulmonary oedema. 
                             With poor pulmonary function, inadequate
                             ventilation leads to excess carbonic
                             acid.

                    9.4.12.2 Fluid and electrolyte disturbances

                             No data available.

                    9.4.12.3 Others

                             No data available

             9.4.13 Allergic reactions

                    No data available.

             9.4.14 Other clinical effects

                    No data available.

             9.4.15 Special risks

                    There is one report of neonatal bromism
                    (neurological depression and hypotonia) secondary to
                    maternal exposure to bromides at a photographic
                    laboratory.  However, no data are available on pure
                    bromine exposure.

        9.5  Others

             No data available.

        9.6  Summary

    10. MANAGEMENT

        10.1 General principles

             Acute contact with bromine liquid or vapour requires
             removal from the source of the bromine contamination.
    
             Eye:  The eye(s) should be irrigated with copious amounts
             of tepid water for at least 15 minutes.  If irritation, pain,
             swelling, lacrimation or photophobia persist, further medical
             evaluation is recommended.
    
             Dermal:  Remove of contaminated clothing and thoroughly
             wash the affected area with copious volumes of water for 20
             minutes.  Since the effects may be delayed, close observation
             for blistering and discoloration of the skin is required for
             the next 24 hours (Sagi et al., 1985). 
    
             Inhalation:  Respiratory support in accordance with
             symptomatology, including: maintenance of an adequate airway,
             oxygen, antibronchospasm therapy (inhaled beta adrenergic
             agonist, aminophylline and/or short course of
             corticosteriods) and antibiotics if there is evidence of
             infection.  Assisted or supported ventilation with tracheal
             intubation and positive pressure ventilation may be
             needed.

        10.2 Life supportive procedures and symptomatic treatment

             Acute contact with bromine liquid or vapour requires
             removal from the source of the bromine contamination.
    
             Eye:  The eye(s) should be irrigated with copious amounts
             of water for at least 15 minutes.  If irritation, pain,

             swelling, lacrimation or photophobia persist, further medical
             evaluation is recommended.
    
             Dermal:  Remove contaminated clothing and wash affected
             area thoroughly with copious volumes of water for 20 minutes. 
             Since effects may be delayed, close observation for
             blistering and discoloration of the skin is required for the
             next 24 hours (Sagi et al., 1985).
    
             Inhalation:  Respiratory support in accordance with
             symptomatology, including: maintenance of an adequate airway,
             oxygen, antibronchospasm therapy (beta adrenergic agonist,
             aerosols, aminophylline and/or short course of
             corticosteriods) and antibiotics if there is evidence of
             infection.  Initial testing should include: chest x-ray to
             view inflammatory changes in the parenchyma, spirometry
             (flow-volume loop with and without bronchodilator) to
             determine air flow capacity and reversibility, diffusing
             capacity (DLco) to assess changes in the alveolar-capillary
             permeability, arterial blood gases to evaluate blood
             oxygenation (Po2) and ventilation (Pco2), and complete white
             blood count.  Repeat chest radiograph and spirometry are
             recommended to determine the progression or resolution of
             residual effects.  Ventilation-perfusion scanning does not
             usually provide significant additional information, except to
             rule out other processes, such as pulmonary emboli.  Careful
             examination is important to detect pathology (fine wheezes in
             subtle or early asthma and fine crackles in early pulmonary
             oedema) not revealed by the studies noted above.
    
             Ingestion:  Not relevant

        10.3 Decontamination

             Acute contact with bromine liquid or vapour requires
             removal from the source of the bromine contamination.
    
             Eye:  The eye(s) should be irrigated with copious amounts
             of tepid water for at least 15 minutes.
    
             Dermal:  Removal of contaminated clothing and thorough
             washing of affected area with copious volumes of water for 20
             minutes.
    
             Inhalation:  Maintain adequate fresh air source.

        10.4 Enhanced elimination

             Contaminated clothing should be discarded.  When
             bromide-containing medications are ingested; the compounds
             are degraded to bromide and excreted in the urine over a
             period of weeks (biological half-life of 12-20 days). 
             Bromide also occurs naturally in the urine (Schaller, 1985).

             However, there are no data on excretion of bromide after a
             bromine exposure (inhalation or dermal).

        10.5 Antidote treatment

             10.5.1 Adults

                    No data available.

             10.5.2 Children

                    No data available.

        10.6 Management discussion

             No data available.

    11. ILLUSTRATIVE CASES

        11.1 Case reports from literature

             Burns caused by bromine and some of its compounds:
    
             Three cases of exposure to bromine-containing compounds were
             reviewed which emphasise the significance of the delay in the
             appearance of clinical signs and symptoms.  Prompt first aid,
             including copious irrigation with water, reduced the extent
             and depth of the injury (Sagi et al., 1985).
    
             Accidental Bromine Exposure in an Urban Population:  An
             Acute Epidemiological Assessment:
    
             In 1984, a large number of people in Geneva, Switzerland, was
             exposed to bromine gas for several hours at concentrations
             above the short-term exposure limit (0.3 ppm);  91 exposed
             individuals were evaluated.  The main symptoms were:  acute
             conjunctivitis (90%); upper respiratory tract irritation
             (68%); cough (47%); and headache (46%).  Follow-up one month
             later revealed that, in all cases, the moderate eye and upper
             airway irritation was self-limiting (Morabia et al.,
             1988).
    
             Pneumomediastinum:  Complication of exposure to bromine
    
             A maintenance technician in a chemical company developed a
             cough with severe bronchospasm and spontaneous
             pneumomediastinum following an accidental exposure to
             bromine.  The chest radiograph on admission was normal and
             only a surveillance chest x-ray taken a few hours later
             demonstrated the presence of eumomediastinum.  This indicates
             the need for vigilance and serial chest radiographs after an
             exposure (Lossos et al., 1990).

    
             Chemical Pneumonitis Due to Exposure to Bromine Compounds

             A laboratory technician developed chemical pneumonitis
             following an accidental exposure to bromide compounds
             (hydrogen bromide and phosphorus tribromide).  The patient's
             course was protracted with recurrent pulmonary infiltrates
             despite having no subsequent exposures.  The case illustrated
             the importance of close medical follow-up after an irritant
             respiratory exposure (Kraut & Lilis, 1988).

    12. ADDITIONAL INFORMATION

        12.1 Specific preventive measures

             Although bromine is not combustible, it may react with
             other chemicals causing fire and explosion.  Good
             ventilation, local exhaust or breathing protection are
             recommended; also protective gloves and clothing, face-shield
             or eye protection in combination with breathing protection
             (Chemical Safety Sheets, 1991).

        12.2 Other

             An International Chemical Safety Card (ICSC), produced
             by the IPCS, exists - No. 0107.

    13. REFERENCES

        ACGIH (American Conference of Governmental Industrial
        Hygienists) (1991) Guide to Occupational Exposure Values 1991.
        Cincinnati, ACGIH.
    
        Alderson M  (1986)  Occupational Cancer.  London,  Butterworth &
        Company Ltd, 48.
    
        Bitron MD & Aharonson EF  (1978)  Delayed mortality of mice
        following inhalation of acute doses of CH2O, SO2, Cl2, and Br2. 
        American Industrial Hygiene Association Journal 39:129-138.
    
        Broderick A & Schwartz DA (1992)  Halogen Gases, Ammonia, and
        Phosgene. In: Sullivan JB and Krieger GR, Eds.   Hazardous
        Materials Toxicology.  Baltimore,  Williams & Wilkins, 791-796.
    
        Budvari S (ed) (1996)  The Merck Index: An Encyclopedia of
        Chemicals, Drugs, and Biologicals.  Merck & Co. Inc., Whitehouse
        Station, NJ, USA, pp 228-229.
    
        Calabrese EJ & Kenyon EM  (1991)  Air Toxics and Risk Assessment. 
        Chelsea,  Lewis Publishers Inc., 173-175.

    
        Chemical Safety Sheets (1991), Samson Chem.  Publishers,
        Dordrecht, The Netherlands
    
        Edelman PA  (1991)  Irritant Gas Inhalation.  In: Hardwood-Nuss A
        et al,  Eds.  The Clinical Practice of Emergency Medicine. 
        Philadelphia,  J.B. Lippincott Company, 516-519.
    
        Fazzalari FA (1978) Compilation of Odor and Taste Threshold Values
        Data. Philadelphia, American Society for Testing and Materials.
        
    
        Kraut A & Lilis R  (1988)  Chemical Pneumonitis due to Exposure to
        Bromine Compounds.  Chest 94(1): 208-210.
    
        ILO (International Labour Office) (1991)  Occupational Exposure
        Limits for Airborne Toxic Substances.  Geneva,  ILO Publications,
        54-55.
    
        Leddy JL  (1983)  Salt, Chlor-Alkali and Related Heavy Chemicals.
        In: Kent JA, ed. Riegel's Handbook of Industrial Chemistry.  New
        York,  Van Nostrand Reinhold Company, 232-233.
    
        Lossos IS et al (1990)  Pneumomediastinum:  a complication of
        exposure to bromine.  British Journal of Industrial Medicine
        47:784.
    
        Meyer E  (1977)  Chemistry of Hazardous Materials.  Englewood
        Cliffs, Prentice-Hall Inc., 109-117.
    
        Morabia A et al  (1988)  Accidental Bromine Exposure in an Urban
        Population:  An Acute Epidemiological Assessment.  International
        Journal of Epidemiology 17(1): 148-152.
    
        NAS (National Academy of Sciences) (1977) Advisory Center on
        Toxicology. Drinking Water and Health. Washington, National
        Academy of Sciences.
    
        NIOSH (National Institute for Occupational Safety and Health)
        (1977) In: Key MM et al. (eds)  Occupational Diseases. Washington
        D.C.
    
        OSHA (Occupational Safety and Health Administration) (1988) 
        Chemical Information Manual.  Rockville,  Government Institutes
        Inc., II-40 - II-43.
    
        OSHA (1989) Industrial Exposure Control Technologies for OSHA
        Regulated Hazardous Substances. Rockville, US Department of
        Labor.
    
        Parmeggiani L (1983) Encyclopedia of Occupational Health and

        Safety.  Geneva, Publication of the International Labour Office
        326-327.
    
        Rom WN & Barkman HW  (1983)  Respiratory Irritants.  In: Rom WN,
        ed. Environmental and Occupational Medicine.  Boston,  Little,
        Brown and Company, 273-283.
    
        Sagi et al. (1985)  Burns caused by bromine and some of its
        compounds.  Burns 11:343-350.
    
        Sax NI, ed. (1984)  Dangerous Properties of Industrial Materials.
        New York, Van Nostrand Reinhold Company, 518.
    
        Schaller KH, ed. (1985)  Analyses of Hazardous Substances in
        Biological Materials, Volume 1.  Weinheim (Federal Republic of
        Germany),  VCH, 67-68.
    
        Schwartz DA (1987)  Acute Inhalation Injury. Occupational
        Medicine: State of the Art Reviews 297-318.
    
        Sittig M (1985)  Handbook of Toxic and Hazardous Chemicals and
        Carcinogens. Park Ridge,  Noyes Publications, 144-145.
    
        Sticht G & Kaferstein H (1988)  Bromine.  In: Seiler H, Sigel H,
        Sigel A, eds.  Handbook on Toxicity of Inorganic Compounds. New
        York,  Marcel Dekker Inc., 143-154.
    
        Stokinger HE (1981)  The Halogens and the Nonmetals, Boron and
        Silicon.  In: Clayton GD, Clayton FE,  eds.  Patty's Industrial
        Hygiene and Toxicology.   New York:  John Wiley & Sons Inc.,
        2965-2971.
    
        Weiss G, ed. (1980)  Hazardous Chemicals Data Book. Park Ridge,
        Noyes Data Corporation.

    14. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES), COMPLETE
        ADDRESS(ES)

        Author:     Dr O.M.J. Kasilo
                    Drug and Toxicology Information Service
                    University of Zimbabwe Medical School
                    P.O.Box A178, Avondale
                    Harare
                    Zimbabwe
    
                    Tel: 263-4-290233 direct/89163172
                    Fax: 263-4-732828/795019
    
        Date:       April 1990
    
        Co-Author:  P.A. Edelman, M.D.
                    Regional Poison Center

                    University of California, Irvine
                    1310 W. Stewart Dr. 306
                    Orange, CA 92668
                    USA
    
                    Tel: 1-714-6395006
                    Fax: 1-714-9974377/5325097
    
        Date:       January 1992
    
        Peer
        Review:     Strasbourg, France, April 1990
                    Newcastle-upon-Tyne, United Kingdom, February 1992
    
        Editor:     Mrs J. Dumnil
                    International Programme on Chemical Safety
    
        Date:       July 1999
    
        
    



    See Also:
       Toxicological Abbreviations
       Bromine (ICSC)