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Zinc and salts

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 Brand names, Trade names
   1.6 Manufacturers, 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
   3.4 Other characteristics
4. USES/CIRCUMSTANCES OF POISONING
   4.1 Uses
   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
   8.6 References
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 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 Relevant laboratory analyses and other investigations
      10.2.1 Sample collection
      10.2.2 Biomedical analysis
      10.2.3 Toxicological analysis
      10.2.4 Other investigations
   10.3 Life supportive procedures and symptomatic treatment
   10.4 Decontamination
   10.5 Elimination
   10.6 Antidote treatment
      10.6.1 Adults
      10.6.2 Children
   10.7 Management discussion
11. ILLUSTRATIVE CASES
   11.1 Case reports from literature
   11.2 Internally extracted data on cases
   11.3 Internal cases
12. ADDITIONAL INFORMATION
   12.1 Availability of antidotes
   12.2 Specific preventive measures
   12.3 Other
13. REFERENCES
14. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES), COMPLETE ADDRESSES
    CHEMICAL SUBSTANCES
    1. NAME
     1.1 Substance
       Zinc
     1.2 Group
       Non-ferrous metal
     1.3 Synonyms
       zinc salts
       zinc chloride
       zinc sulphate
       zinc acetate
     1.4 Identification numbers
       1.4.1 CAS number
             7440-66-6
       1.4.2 Other numbers
             557-34-6
             5970-45-6
             7446-20-2 
             7646-85-7
             7733-02-0
     1.5 Brand names, Trade names
     1.6 Manufacturers, Importers
    2. SUMMARY
     2.1 Main risks and target organs
       Oral, Inhalation:  Nausea, dyspnoea and chest pains.
       Target organs: Liver, kidney and heart.
     2.2 Summary of clinical effects
       Inhalation:  Zinc chloride inhalation has caused fatal 
       poisoning in individuals exposed during the generation of 
       chemical smoke.  Severe respiratory inflammation was observed 
       in these patients, who developed fever and a pale cyanotic 
       colour.  Death is due to acute pulmonary oedema, 
       bronchopneumonia or interstitial pulmonary fibrosis.
       
       Oral:  Poisoning following oral ingestion of zinc salts such 
       as zinc chloride is characterised by corrosion and 
       inflammation of the mucous membrane of the mouth and stomach, 
       which usually becomes white; ulceration of the stomach may 
       occur, often followed by perforation.  Symptoms include 
       burning pains in the oesophagus and stomach, nausea and 
       vomiting, diarrhoea, hypotension, cold sweats and cramps in 
       the legs.  Oesophageal or gastrointestinal stricture may 
       follow (Reynolds, 1982).
     2.3 Diagnosis
       The diagnosis depends on the history and the clinical 
       presentation.  Blood and urine should be collected for 
       biomedical analysis, including serum measurements for 
       elemental zinc.
     2.4 First-aid measures and management principles
       Decontamination by emesis, gastric aspiration and lavage and 
       chelation with calcium disodium edetate. Seek medical 
       attention immediately and transfer patient to hospital.
    3. PHYSICO-CHEMICAL PROPERTIES
     3.1 Origin of the substance
       Zinc is widely distributed and appears in almost all igneous 
       rocks.   Occurs in calamine or zinc spar, sphalerite or zinc 

       blende, zincite, willemite, franklinite, zinc spinel or 
       gahnite.  Zinc constitutes about 0.02% of the crust of the 
       earth.
     3.2 Chemical structure
       Chemical name: Zinc (metal)
       
       Atomic weight: 65.37
       Atomic number: 30
       Valency: 2
       Isotopes: 64 (48.89%) 
                 66 (27.81%)
                 67 (4.11%)
                 68 (18.57%) 
                 70 (0.62%)
       
       Chemical name: Zinc chloride       MW: 136.3
       
       Chemical name: Zinc sulphate       MW: 287.5 (Heptahydrate)
       
       Chemical name: Zinc acetate        MW: 219.5 (dihydrate)
       
       (Budivari, 1989)
     3.3 Physical properties
       Zinc metal
       
       Description: bluish-white, lustrous metal stable in dry 
       air; becomes coated with a white layer of basic 
       carbonate on exposure to moist air.  Malleable when 
       heated to 100 to 150C, at 210C it becomes brittle and 
       pulverisable.   Burns in air with a bluish-green flame.
       
       Boiling Point: 906.1C
       
       Melting point: 419.4C
       
       Moh's hardness: 2.5.
       
       Relative density: 7.14 (Water = 1)
       
       Solubility: water, insoluble; dilute acids or alkalis in 
       all proportions at 20C
       
       Zinc chloride 
       
       Description:   White or almost white, odourless, 
       deliquescent, caustic, crystalline powder or granules or 
       opaque white masses or sticks.
       
       Melting point: about 260C
       
       Solubility:  water          1 in 0.5
                    alcohol        1 in 1.5
                    glycerol       1 in 2
       
       Zinc sulphate
       

       Description:   Odourless, colourless, transparent, 
       efflorescent crystals or white crystalline powder with 
       an astringent metallic taste.  It is efflorescent in dry 
       air and loses 5 molecules of water of crystallisation 
       when slowly heated to 50C, and a further molecule at 
       100C.
       
       Solubility:    water          1 in less than 1
                      alcohol        practically insoluble
                      glycerol       1 in 2.5
       
       Zinc acetate
       
       Description:   Colourless or white crystals or granules 
       with a faint acetous odour and a sharp disagreeable 
       metallic taste. It effloresces slowly to form a basic 
       salt.
       
       Melting point:      237C
       
       Relative density:   1.735
       
       Solubility:    water,    1 in 2.5
                      alcohol   1 in 30
     3.4 Other characteristics
       Zinc metal
       
       Normal state of zinc (metal) at room temperature: solid
                 
       Colour: bluish - silvery metallic
                      
       Odour: odourless
       
       Dangers associated with zinc powder:  Powdered zinc presents 
       an explosion hazard. If it is stored in damp places, there is 
       a danger of spontaneous combustion.  Residues from reduction 
       reactions may start a fire if thrown into combustible waste.
       
       Possible chemical reactions in air: None.
       
       Possible chemical reactions with other agents:  Strong and 
       weak alkalis, forms hydrogen.
       
       Electrical and thermal conductivity with possible 
       consequences:  No data available. 
       
       Environmental risks:  Affects microbial soil organisms, 
       reduces the synthetic activity of plant enzymes.  Zinc 
       affects marine life, poisoning both plants and animals.  Zinc 
       can cause a reduction in growth of certain aquatic plants; 
       this toxicity varies over several orders of magnitude for 
       aquatic plants dependent on their ability to concentrate zinc. 
       Because of the low toxicity of zinc, man-made emissions 
       probably do not present a serious environmental hazard unless 
       they are accompanied by more toxic metals such as cadmium.
       

       Pure zinc is very slowly attacked by dilute sulphuric or 
       hydrochloric acid;  the presence of a small amount of another 
       metal eg. copper, tin, lead, accelerates the action of the 
       acids.  Slowly soluble in acetic acid; soluble in nitric 
       acid. Slowly soluble in ammonia water; readily soluble in 
       solutions of fixed alkali hydroxides with evolution of 
       hydrogen.  Zinc has a standard electrode potential of +0.761 
       and is thus electropositive to most structural metals except 
       aluminium and magnesium, which is the basis for its use in 
       batteries and electrogalvanising of steel.  
                                     
       Zinc chloride
       
       Normal state of zinc chloride at room temperature: solid
                           
       Colour: white or almost white
       
       Odour: odourless
       
       Dangers associated with zinc chloride: see Metal Fume Fever 
       monograph
       
       Possible chemical reactions in air: none.
       
       Electrical and thermal conductivity with possible 
       consequences:  No data available 
       
       Environmental risks: as for metal.
       
       Zinc sulphate
       
       Normal state of zinc sulphate at room temperature: solid
       
       Colour: colourless, transparent
       
       Odour: odourless
       
       Possible chemical reactions in air: none.
       
       Electrical and thermal conductivity with possible 
       consequences:  No data available.
       
       Environmental risks: As for metal.
       
       Zinc acetate
       
       Normal state of zinc acetate at room temperature: solid
       
       Colour: colourless or white
       
       Odour: faint acetous odour
       
       Possible chemical reactions in air: none.
       
       Possible chemical reactions with other agents: No data 
       available. 

       
       Electrical and thermal conductivity with possible 
       consequences: No data available. 
       
       Environmental risks: As for metal.
    4. USES/CIRCUMSTANCES OF POISONING
     4.1 Uses
       As an ingredient or reagent in chemical processing and 
       the manufacture of household goods. Zinc sulphate is 
       used in agriculture and zinc phosphide as a rodenticide 
       (the toxic effects of zinc phosphide are principally due 
       to the release of phosphine). Zinc sulphate is also used 
       medicinally as a mineral supplement and the acetate and 
       sulphates are used as astringents and topical agents in 
       the treatment of skin ulcers (Simkin, 1976; IRPTC, 
       1985).
     4.2 High risk circumstance of poisoning
       Associated hazards in the metallurgy of zinc arise from the 
       presence of arsenic, cadmium, manganese, lead and possibly 
       copper and silver.
     4.3 Occupationally exposed populations
       Zinc plant workers, galvanisers, metal workers, farm workers, 
       paint workers, cosmetic workers.
    5. ROUTES OF ENTRY
     5.1 Oral
       Zinc and its salts are poorly absorbed from the 
       gastrointestinal tract;  only a small proportion of dietary 
       zinc is absorbed.  Zinc is distributed widely throughout the 
       body and is excreted in the faeces with only traces appearing 
       in the urine, since the kidneys have little or no role in 
       regulating the content of zinc in the body.  Ingestion of 
       soluble salts may cause nausea, vomiting and purging.  
       
       In one case, a 6 year-old child died after ingesting a zinc 
       chloride soldering solution.
     5.2 Inhalation
       Inhalation of fumes or dust may result in a sweet taste, dry 
       throat, cough, weakness, generalised aching, chills, fever, 
       nausea and vomiting.   Zinc chloride fumes may be irritant to 
       skin and mucous membranes. Zinc phosphide may cause dyspnoea 
       and diarrhoea following inhalation of the dust.
     5.3 Dermal
       In various species, more than 2.5% of a topical dose is 
       absorbed through the skin. Chronic poisoning due to 
       occupational exposure to zinc chloride has been associated 
       with leg pains, fatigue, loss of appetite and loss of weight. 
       The patient's condition improved following removal from the 
       zinc source (du Bray, 1937).
     5.4 Eye
       Zinc dust and fine machinings are irritant and abrasive to the 
       eye.   Many zinc salts, for example the chloride, are 
       extremely corrosive to ophthalmic tissues.
     5.5 Parenteral
       Accidental intravenous administration of 7.4 g of zinc 
       sulphate to a 72 year-old woman resulted in death after 47 
       days (Brocks et al., 1977).

     5.6 Others
       Dialysis: a 32 year old woman suffered severe nausea, vomiting 
       and fever on six occasions after home dialysis using water 
       which had been stored in a galvanised tank (Gallery et al, 
       1972).  
       
       Zinc phosphide introduced per vagina was followed by death 
       from renal failure after 92 hours (Santini, 1955).
    6. KINETICS
     6.1 Absorption by route of exposure
       About 20 to 30% of the zinc ingested from the diet is absorbed 
       from the gastrointestinal tract.  The amount absorbed from 
       foods can be influenced by the presence of phytic acid, which 
       makes zinc unavailable; and possibly by the intake of calcium,
        although this is uncertain in man.
     6.2 Distribution by route of exposure
       Zinc is distributed widely throughout the body, and is 
       deposited relatively slowly in the skeleton, where it is 
       bound for long periods.   Approximately 98% of the zinc in 
       normal human plasma is protein bound.  The principal carrier 
       protein is albumin which binds about 80-85% of plasma zinc; 
       approximately 15% is bound to 2-macroglobulin, less than 2% 
       to retinol-binding protein and less than 1-2% of zinc is 
       free or ultrafiltrable (Giroux & Henkin, 1972; Whitehouse et 
       al., 1983; Chivers, 1984; Foote & Delves, 1984).  Zinc is 
       found in high concentrations in the choroid plexus, prostate, 
       kidney, liver, lung, spleen, and brain (particularly the 
       cerebellum and hippocampus).  Only small amounts are found in 
       the CSF, urine and serum.  Reports of zinc concentration after 
       parenteral administration of a single dose indicate 
       substantial accumulation in the brain (Brocks, 1977). 
       
       Serum zinc concentrations in 17 healthy volunteers ranged from 
       0.566 to 1.02 mg/l, averaging 0.83 mg/l; plasma 
       concentrations did not significantly differ from those of 
       serum, although erythrocyte zinc concentrations averaged 
       12.25 mg/l in normal volunteers (Kosman & Henkin, 1979).  Low 
       plasma zinc levels have been observed in dietary zinc 
       deficiency as well as in various other disease states (Prasad,
        1979).  
       
       The mean plasma concentration of zinc is 960 g/L in healthy 
       adults and 890 g/L in healthy children.  
       
       In adults representative of industrial workers, the average 
       zinc concentration of eight organs and tissues were (g/g of 
       ash):
       
                 kidney                   4900  140
                 liver                    3800  110
                 heart                    2800  67
                 pancreas                 2400  70
                 aorta                    1900  70
                 lung and spleen (each)   1400  35, 29
                 brain                    820  34 
       

                 (Schroeder & Nason, 1967)
       
       There are few data on normal values of zinc in blood and 
       urine. Vallee (1962) reported values in human serum of 109 to 
       130 g/100 ml, similar to those of iron; whole blood zinc, 
       880  200 g/100 mL; and red cell zinc, 1440  270 g/100 mL. 
        This value for whole blood is in fair agreement with the 
       value of 580 g/100 mL obtained by mass spectrometry.  
       
       The normal or therapeutic value in blood is 68 to 136 
       microgram/100 ml and, in the CSF, 20 to 60 g/kg/litre.
       
       Similarly, Schroeder et al. (1967) estimated urinary excretion 
       estimated at less than 500 g/day, close to the 150 g/L 
       obtained by mass spectroscopy. 
                 
       Whole blood and plasma zinc concentrations in healthy brass 
       foundry workers were noted to be 46% and 22% higher, 
       respectively, than in healthy control subjects; the 
       investigator concluded that excess zinc that is not 
       immediately excreted is stored in erythrocytes (Hamdi, 1969). 
       
       The volume of distribution has not been not fully established. 
       Serum levels of zinc are modified by many diseases, including 
       cancer, wound healing and atherosclerosis.
     6.3 Biological half-life by route of exposure
       5 to 16 months (whole body) (IRPTC, 1985)
     6.4 Metabolism
       Zinc occurs in the body in two different protein combinations:
       
       i) as a metalloenzyme in which Zn is an integral part of an 
       important enzyme system, such as carbonic anhydrase for the 
       regulation of CO2 exchange, and 
       
       ii) as a metal - protein complex in which Zn is loosely bound 
       to a protein, which acts as its carrier and transport 
       mechanism in the body (metallothionine).
     6.5 Elimination by route of exposure
       In man, most of the average dietary intake of 10 - 15 mg Zn is 
       excreted in the faeces.  Of the amount absorbed, about 20% is 
       excreted in the daily urine and up to 60% is excreted in the 
       faeces (Prasad, 1979).  The kidneys have little or no role in 
       the regulation of zinc content in the body.  Normal urine 
       zinc concentrations are from 0.3 to 0.4 mg/24 hours (231 to 
       641 gs/day), but may increase to as much as 2.1 mg/24 hours 
       in patients with albuminaemia (Vallee, 1957), or up to 22-fold 
        with chelation therapy.  Intestinal excretion appears to 
       regulate body zinc content under normal conditions. Urinary 
       zinc concentrations of 0.6 to 0.7 mg/l were observed in 
       workers exposed to zinc oxide at levels of 3 to 5 mg/m3 
       (ACGIH, 1971).  Healthy brass foundry workers exposed to zinc 
       fumes excreted zinc in the urine at an average rate of 0.4 
       mg/24 hours (range 0.3 to 0.6), and increase of only 14% over 
       normal control subjects (Hamdi, 1969).  Sweat can represent a 
       sizeable route of zinc excretion, according to Prasad et al 
       (1963); depending on climatic conditions, zinc loss in sweat 

       can range from 1150  300 microgram/L in temperate climates to 
       2300 to 12, 700 microgram in 2 to 11 litres/day in hot 
       climates.
    7. TOXICOLOGY
     7.1 Mode of Action
       Zinc is an essential trace element, however an excessive 
       exposure of the body to zinc leads to disturbances of the 
       functional state of individual organs and systems.  
       Intoxication is manifested by the reduction in the content of 
       free -SH- groups in serum; reduced activity of hepatic 
       arginase; and reduced prothrombin index (IRPTC, 1985).
     7.2 Toxicity
       7.2.1 Human data
             7.2.1.1 Adults
                     Inhalation
                     
                     The minimum concentration of zinc dust that is 
                     toxic after exposure for 30 minutes is 4,800 
                     mg/3. 
                     
                     Metal fume fever caused by zinc oxide fumes is 
                     covered in a separate monograph.
                     
                     Parenteral
                     
                     When zinc chloride is administered parenterally, 
                     zinc depresses the central nervous system, 
                     causing tremors and paralysis in the 
                     extremities.  
                     
                     Ingestion
                     
                     Zinc chloride:  The lethal dose of the various 
                     zinc salts have not been defined, but a few 
                     grams of the chloride have been lethal in an 
                     adult, although recovery has occurred after 
                     ingestion of 90 grams.  
                     
                     Zinc sulphate:  Fatalities have been reported 
                     following the ingestion of 10 to 30 g of zinc 
                     sulphate. Intravenous infusion of 7.4 g of zinc 
                     sulphate over 60 hours was fatal in a 72 year-
                     old woman (Brocks et al, 1977).  
                     
                     Zinc phosphide:  Systemic toxicity is 
                     principally due to the release of phosphine. 
                     Ingestion of 4 to 5 grams of zinc phosphide has 
                     caused death on two occasions (Frketic et al., 
                     1957; Gilli, 1948), but patients have survived 
                     ingestion of 25 grams (Paszko, 1961) and 50 
                     grams (Simonovic, 1954).  Doses in the region 
                     of 100 mg daily appear to be harmless, 
                     (Phillips, 1882), but as little as 30 mg causes 
                     nausea (British Pharmaceutical Codex, 1979).
             7.2.1.2 Children
                     As for adults.

       7.2.2 Relevant animal data
             Acute oral toxicity:
             
             Zinc sulphate heptahydrate, LDLO (rat, oral)
             2200 mg/kg 
             
             Zinc acetate dihydrate, LDLO (rat, oral) 2460 mg/kg 
             
             Zinc phosphide, LD50 (rat, oral) 40 mg/kg 
             Acute toxicity parenteral route: 
             
             (inorganic zinc salts are highly toxic)
             
             zinc sulphate heptahydrate, LD50 (IV) 40 mg/kg; and LDLO 
             49 mg/kg
             
             zinc chloride LD50 (IV) 30 mg/kg.
             
             The acute toxicity of zinc salts administered 
             subcutaneously appears to be intermediate between that 
             following intravenous and oral administration: 
             
             zinc sulphate heptahydrate LDLO (rat, s/c) 330 mg/kg.
             
             No experimental data are available on zinc oxide, which 
             accounts for most industrial exposure.  
             
             The acute toxicity of organic derivatives of zinc are 
             similar to those of the inorganic compounds. 
             
             LD50 (rat, oral) 1400 mg/kg
             LD50 (rat, i/p) 23 mg/kg
             
             The lethal intravenous dose for rats is 60 to 90 mg/kg.
       7.2.3 Relevant in vitro data
             No data available.
       7.2.4 Workplace standards
             Current threshold limit value for exposure to fumes of 
             zinc chloride is 1 mg/m3.  A zinc content of more than 
             15 ppm markedly impairs the potability of drinking 
             water (WHO, 1963). 
             Zinc chloride fumes:
              
             TLV-TWA: 1 mg/m3  (ACGIH, 1989).
             TLV-STEL: 2 mg/m3  (ACGIH, 1989).
             
             Zinc sulphate: 
             
             2 mg/m3 (Dreisbach, 1987).
       7.2.5 Acceptable daily intake (ADI) and other guideline levels
             A dietary intake of 15 to 20 mg/day has been recommended 
              (Vallee, 1957).
     7.3 Carcinogenicity
       Zinc metal and dust are carcinogenic (IRPTC, 1985).  Zinc 
       appears to be potentially carcinogenic only when a high 
       concentration of insoluble material has caused necrosis and 

       is followed by a regenerative response (Walters & Roe, 1975). 
       No indication exists that occupational exposure to zinc 
       increases the incidence of any type of cancer.  Zinc may, 
       however, sustain tumour growth (Lonard et al., 1986).
     7.4 Teratogenicity
       Zinc appears not to be teratogenic except perhaps at very high 
       doses, but it can modify the teratogenic potential of other 
       metals.  Teratogenicity in animals varies according to the 
       species (Lonard et al., 1986).
       
       Zn pyrithione [1-hydroxy-2-(1H)-pyridinethione] is a broad 
       spectrum antifungal and antimicrobial agent found in 
       formulations that come into contact with skin, and in 
       shampoos and hairdressings as an anti-dandruff agent.  
       Because more than 2.5% is absorbed through the skin in various 
        species, its teratogenicity has been evaluated in the pig 
       (Wedig et al., 1976) and in the rabbit (Nolen et al., 1975).  
       There was no evidence of any teratogenic or embryotoxic 
       effect was observed in either case. The relevance of this to 
       other zinc compounds uncertain.
     7.5 Mutagenicity
       Studies on the mutagenicity of zinc strongly suggest that 
       zinc does not represent a mutagenic risk.  Zinc chloride does 
       not affect DNA synthesis in vitro.  In bacterial mutagenicity 
       tests, zinc sulphate is not mutagenic (Lonard et al., 1986).
     7.6 Interactions
       It has been suggested that concurrent administration of a zinc 
       salt might diminish the effect of penicillamine (Lyle, 1976).
    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
             No data available 
       8.3.3 Haematological analyses
             Complete blood count
             Blood film
             Haematocrit
             Prothrombin time
             Liver function tests
       8.3.4 Interpretation of biomedical investigations
     8.4 Other biomedical (diagnostic) investigations and their 
       interpretation
       High levels of zinc lead to microcytic anaemia with a reduced 
       prothrombin time. The excretion of zinc is increased in 
       patients with albuminaemia. Serum concentrations of zinc can 
       be used in the diagnosis of poisoning. Urinalysis may reveal 
       haematuria and proteinuria.  Urine volume may be reduced.  
       Blood urea nitrogen and creatinine levels are elevated in the 
       presence of renal damage.
     8.5 Overall Interpretation of all toxicological analyses and 
       toxicological investigations
     8.6 References
    9. CLINICAL EFFECTS
     9.1 Acute poisoning
       9.1.1 Ingestion
             Zinc salts of strong mineral acids are irritating to the 
              gastrointestinal tract, and when ingested they act as 
             emetics.  The emetic concentration in water is 675 to 
             2280 ppm.  The onset of symptoms occurs within half to 
             one hour.  Zinc ion, however, is ordinarily too poorly 
             absorbed to induce acute systemic effects.  
             
             Ingestion of soluble salts may cause nausea, vomiting 
             and purging.   After large doses have been ingested, 
             fatal collapse may occur as a result of serious damage 
             to the buccal and gastroenteric mucous membranes.  
             Residual nephritis, and strictures of the oesophagus 
             and pyloric end of the stomach may occur.  Zinc sulphate 
             also produces a burning pain in the mouth and throat, 
             and hyperglycaemia has been reported in one fatal case. 
             Mass poisonings from drinking acidic beverages made in 
             galvanised containers have been recorded.  Fever, nausea,
             vomiting, stomach cramps, and diarrhoea occurred 3 to 
             12 hours following ingestion (Callender & Gentkow, 
             1988).  
             
             The threshold concentration of taste for zinc salts is 

             15 ppm. 
             
             Except for their irritant action, inorganic zinc 
             compounds are relatively non-toxic by mouth.
       9.1.2 Inhalation
             Inhalation of fumes may result in a sweet taste, dry 
             throat, cough, weakness, generalised aching, chills, 
             fever, nausea and vomiting.  Zinc chloride fumes damage 
             mucous membranes and are irritant to skin. 
             
             Metal fume fever is a brief, self-limiting illness 
             characterised by fever, chills, myalgia, vomiting and 
             prostration which is usually due to inhaling fumes of 
             zinc oxide.  This syndrome should be distinguished from 
             the severe necrotising bronchitis and bronchopneumonia 
             which can follow inhalation of bronze powder (70% 
             copper, 30% zinc stearate), and from the severe and 
             often lethal damage to the mucosa of the respiratory 
             tract produced by zinc chloride fumes.  
       9.1.3 Skin exposure
             Zinc salts of strong mineral acids are astringent, 
             corrosive to the skin, and irritating to the 
             gastrointestinal tract if swallowed. Skin contact, 
             especially with zinc dichromate can cause 
             papulovesicular lesions with exfoliation.  Zinc chloride 
             has been implicated in contact dermatitis (IRPTC, 
             1985).
       9.1.4 Eye contact
             Corneal damage results in epithelial erosion and stromal 
              opacification of the cornea sometimes accompanied by 
             anterior subcapsular lens changes.  These effects are 
             due to the precipitation of protein caused by zinc.  
             Lens opacities can result from exposure to high 
             concentrations of zinc salt, and may be associated with 
             reduced intraocular pressure and deposition of pigment 
             on the posterior surface of the cornea.  Symptoms 
             sometimes resemble severe acute attacks of closed-angle 
             glaucoma.
       9.1.5 Parenteral exposure
             Inorganic zinc salts are highly toxic after parenteral 
             administration.  Following accidental intravenous 
             administration of 7.4 g of zinc sulphate to a 72-year-
             old woman, the serum zinc concentration was 41.8 mg/l; 
             hypotension, pulmonary oedema, vomiting, diarrhoea, 
             jaundice, and renal failure developed and she died 
             after 47 days (Brocks et al., 1977).  
       9.1.6 Other
             No data available. 
     9.2 Chronic poisoning
       9.2.1 Ingestion
             Chronic ingestion of low doses of zinc salts is 
             associated with anaemia (Chunn, 1973), including 
             hypochromic (Porter et al., 1977) and sideroblastic 
             anaemia (Broun et al., 1990). Treatment was ineffective 
             until zinc ingestion was stopped.
             

             After ingestion of 660 mg zinc sulphate daily for over a 
             year, profound hypochromic macrocytic anaemia, 
             associated cardiac failure, and copper deficiency 
             developed.  Treatment consisted of slow transfusion of 
             packed cells, copper sulphate 4 mg daily, and the 
             withdrawal of the zinc sulphate.  The blood picture was 
             normal four weeks later (Porter et al., 1977).  
             
             Chronic anaemia unresponsive to iron in three children 
             was attributed to zinc poisoning, resulting from the 
             children chewing metal toys of a zinc alloy. When the 
             toys were withdrawn, the children responded to 
             conventional treatment with iron (Chunn, 1973).
             
             Broun et al. (1990) reported on two cases on 
             sideroblastic anaemia from chronic ingestion of zinc 
             salts.  In the first case, a 31-year-old man who had 
             been ingesting coins for the past 12 years on the basis 
             of a delusional belief that they would protect him from 
             harm.  In the second case, a 48-year-old man had been 
             taking zinc supplements daily for the past two years.  
             The anaemia in both patients resolved, with improvement 
             of their presenting symptoms once the zinc cause was 
             removed (Broun et al., 1990).
       9.2.2 Inhalation
             Inhalation is associated with zinc fume fever (see 
             separate monograph).
             
             Within 4 to 12 hours after exposure to freshly formed 
             fumes, the first sign is an unusual metallic taste, or 
             some alteration of familiar tastes such as tobacco 
             smoke.  This is accompanied by dryness and irritation 
             of the throat, with coughing and dyspnoea, feelings of 
             weakness and fatigue, pains in the muscles and joints, 
             and general malaise, similar to the prodromal syndrome 
             of influenza.  Fever then drops, associated with 
             alternating chills.   Body temperature is usually around 
             102 F, but may reach 104 F, with febrile shivering or 
             rigors, accounting for the trade terms of "brass 
             founders ague," "brass chills," spelter shakes," and 
             "zinc chills".  The subject sweats profusely while the 
             body temperature begins to fall, occasionally 
             associated with convulsions.  Severe pain in the chest, 
             aggravated by difficult breathing, has been described.  
             Clinical and symptomatic recovery is usually complete 
             in 24 to 48 hours.  Rapid development of tolerance is 
             another characteristic feature of Zinc Fume Fever, but 
             it is lost equally quickly: a zinc or brass worker may 
             experience fume fever on his first day back at work 
             rather than during subsequent consecutive days of 
             exposure but re-exposure even on consecutive days may 
             lead to repeated attacks (McCord, 1960).
             
             Extensive fibrosis of the lung, resulting in the death, 
             of a worker who had been employed for 29 years in a 
             zinc stearate factory has been reported (Uotila & Noro, 

             1957).  The exposure must have been extremely high, 
             because in the long years of exposure of workers to 
             zinc stearate in a large US rubber factory, no adverse 
             effects of any kind were experienced (McCormick, 1971). 
             
             
             Gastrointestinal disturbances consisting of pressure in 
             the stomach region, nausea, and weakness, suggestive of 
             gastric or duodenal ulcers, have occurred in workers 
             employed for years in galvanising; in torch cutting of 
             galvanised metal parts (Kapp, 1934); in welding 
             galvanised iron sheets; and in brass foundry work (Hamdi,
              1969).  
       9.2.3 Skin exposure
             Repeated applications of zinc solutions to the skin may 
             cause erythematous, papular and granulomatous reactions 
             in susceptible individuals. One case of exposure to 
             zinc chloride has been associated with leg pains, 
             fatigue, weight loss and anorexia; the symptoms 
             resolved after removal from the source of contamination.
       9.2.4 Eye contact
             No data available. 
       9.2.5 Parenteral exposure
             No data available. 
       9.2.6 Other
             A 32-year-old woman developed severe nausea, vomiting 
             and fever on six occasions after home dialysis using 
             water which had been stored in a galvanised tank.  The 
             plasma zinc concentration 36 hours after the sixth home 
             dialysis was 7 mg/l and fell slowly after dialysis for 
             six weeks in hospital to 1.58 mg/l.  The red cell zinc 
             concentrations were respectively 35 and 12.3 mg/l 
             (normal 10 to 14 mg/l). No further episodes occurred 
             when the domestic water was deionised before use.  
             (Gallery et al., 1972).
     9.3 Course, prognosis, cause of death
       Death usually occurs within 6 to 12 hours following ingestion 
       (IPRTC, 1985), and is due to pulmonary oedema and cardiac, 
       respiratory and hepatic failure.  There are no recorded 
       studies of death following acute inhalation but the time 
       course would be similar to that after oral ingestion.  If the 
       patient is asymptomatic at the end of 72 hours, recovery is 
       likely.  However, death may occur up to one week after 
       poisoning.
     9.4 Systematic description of clinical effects
       9.4.1 Cardiovascular
             Cardiac failure due to anaemia, hypotension, cardiac 
             arrhythmias, shock, circulatory collapse, premature 
             atrial beats.
       9.4.2 Respiratory
             Cyanosis, severe retrosternal pain, widespread 
             consolidation of the lungs, pulmonary oedema, areas of 
             haemorrhaging, and extensive necrosis and numerous 
             punctate cysts, adult Respiratory Distress Syndrome 
             (Hjortso et al., 1988), severe respiratory failure, 
             severe coughing and dyspnoea, asthma, metal fume fever, 

             decrease in FEV1.
       9.4.3 Neurological
             9.4.3.1 CNS
                     CNS depression, lethargy, somnolence, 
                     depression.
             9.4.3.2 Peripheral nervous system
                     Myalgias
             9.4.3.3 Autonomic nervous system
                     No data available. 
             9.4.3.4 Skeletal and smooth muscle
                     Leg pains have been reported following possible 
                     transdermal absorption of zinc chloride.
       9.4.4 Gastrointestinal
             Gastroenteritis, nausea and vomiting, corrosion of 
             gastric mucosa, diarrhoea, haemorrhagic gastric erosion 
             (Moore, 1978), substernal pain, strictures of the 
             oesophagus and pyloric end of the stomach.  Zinc 
             sulphate produces a burning pain in the mouth and 
             throat, with severe burns.
       9.4.5 Hepatic
             Jaundice, alkaline phosphatase, amylase, lipase and 
             hepatic metallo-thionein elevation.
       9.4.6 Urinary
             9.4.6.1 Renal
                     Oliguria, residual nephritis
             9.4.6.2 Others
                     No data available. 
       9.4.7 Endocrine and reproductive systems
             Hyperglycaemia has been noted in one fatal ingestion; 
             hyperamylasaemia.
       9.4.8 Dermatological
             Zinc dichromate and other salts may cause 
             papulovesicular lesions with exfoliation.
       9.4.9 Eye, ears, nose, throat: local effects
             Epithelial erosion, stromal opacification, anterior 
             subcapsular lens changes, lens opacities, reduced
             intraocular pressure, taste disturbances, erythematous 
             uvula.
       9.4.10 Haematological
              Hypochromic macrocytic anaemia, copper deficiency, 
              thrombocytopenia, sideroblastic anaemia.
       9.4.11 Immunological
              No data available. 
       9.4.12 Metabolic
              9.4.12.1 Acid-base disturbances
                       Metabolic acidosis and hypocalcemic tetany.
              9.4.12.2 Fluid and electrolyte disturbances
                       Dehydration, pallor, weakness
              9.4.12.3 Others
                       Circulatory collapse, impaired copper 
                       absorption
       9.4.13 Allergic reactions
              Contact allergic dermatitis.  Fume fever on repeated 
              exposure.
       9.4.14 Other clinical effects
              No data available. 

       9.4.15 Special risks
              There is a suggestion that low serum zinc 
              concentrations during pregnancy might be a sign of 
              zinc deficiency with associated risks to mother and 
              child.  Zinc crosses the placenta and can accumulate 
              in foetal brain and liver (IRPTC, 1985).
     9.5 Others
       No data available. 
     9.6 Summary
    10. MANAGEMENT
      10.1 General principles
         From inhalation:  Treat pulmonary oedema.  Give prednisone 
         25 to 50 mg orally per day, or an equivalent dose of 
         another oral corticosteroid, to reduce tissue response to 
         inhaled metal fumes.  Gradually decrease the dose as the 
         patient improves. Treat metal fume fever by bed rest and 
         give aspirin for fever and pain.
         
         Except for zinc chloride, which is corrosive, gastric 
         decontamination by emesis, aspiration or gastric lavage 
         should be considered after ingestion of zinc salts unless 
         contraindicated. Demulcents may be given provided mucosal 
         damage is not present. Activated charcoal should then be 
         administered.
         
         Absorbed zinc may be removed by chelation by dimercaprol or 
         calcium disodium edetate. Management is otherwise 
         symptomatic, with particular emphasis on monitoring cardiac 
         function since myocardial damage is the principal cause of 
         death.
                   
         Fluid replacement 
         Replace fluid loss with 5% glucose in saline, treat the 
         metabolic acidosis and hypocalcemic tetany if present.
         
         Pain 
         Relieve pain with meperidine or morphine sulphate.
                   
         Anuria 
         Observe for and treat anuria and liver damage.
                   
         Cardiac damage 
         Death is probably due to cardiac damage.
      10.2 Relevant laboratory analyses and other investigations
         10.2.1 Sample collection
                Usual blood and urine sampling for biomedical 
                analysis (zinc serum levels are clinically useful).  
                Collect in plastic where possible, keep cool and 
                tightly closed, until analysed.   Traditional vacuum 
                tubes not specifically labelled for trace element 
                analysis can contain substantial amounts of 
                extraneous zinc.  During treatment urine samples may 
                be clinically useful.   Clean, unused plastic 
                containers are appropriate for the collection and 
                storage of urine and tissue samples prior to zinc 
                determinations (Breitschwerdt et al, 1986).

         10.2.2 Biomedical analysis
                Routine blood and urine analysis should be performed.
                
                Hepatic function tests.
                
                Blood glucose.
         10.2.3 Toxicological analysis
                Hepatic function tests.
                
                Blood glucose (for hypoglycaemia).
         10.2.4 Other investigations
                Monitor FEV1, other pulmonary function tests
      10.3 Life supportive procedures and symptomatic treatment
         Following respiratory exposure, move patient to fresh air.  
         Monitor for respiratory distress.  Emergency airway support 
         and 100% humidified supplemental oxygen with assisted 
         ventilation may be needed.  If a cough or difficulty in 
         breathing develops, evaluate for respiratory tract 
         irritation, bronchitis, pneumonitis.  All patients: support 
         respiratory and cardiovascular function.
         
         Exposed eyes should be irrigated with copious amounts of 
         water at room temperature for at least 15 minutes.  If 
         irritation, pain, swelling and lacrimation occur after 15 
         minutes of irrigation, an ophthalmologic examination should 
         be performed. Rinsing with 0.05 M neutral sodium edetate 
         may help prevent or reverse a portion of the protein 
         precipitation caused by zinc salts in the eye. 
         
         Skin exposure: wash the exposed area thoroughly with soap 
         and water.  A physician may need to examine the area if 
         irritation or pain persists after washing.
      10.4 Decontamination
         Zinc chloride is highly corrosive and emesis or gastric 
         lavage should be avoided after oral ingestion. Zinc 
         sulphate is much less corrosive.
         
         After ingestion of zinc sulphate, the stomach should be 
         emptied by emesis, aspiration and lavage, unless the 
         patient is already vomiting, or if there is evidence of 
         oral mucosal burns, and demulcents such as milk or white of 
         egg should be given freely.  
         
         With more corrosive salts, dilute rapidly with water or 
         milk. Immediately dilute with 4 to 8 ounces (120 to 240 mL) 
         of milk or water (not to exceed 15 mL/kg in a child).  
         Emesis may be indicated in substantial recent ingestions of 
         zinc sulphate unless the patient is obtunded, comatose or 
         convulsing, or is at risk of doing so based on the history. 
          Emesis is most effective if initiated within 30 minutes of 
         ingestion.  
         
         If emesis is unsuccessful following two doses of ipecac, the 
         decision to lavage or otherwise attempt to decontaminate 
         the gut should be made on an individual basis.  In zinc 
         phosphide poisoning, it has been suggested that 0.5 grams 

         of copper sulphate (as a 1% aqueous solution) may be 
         administered: this has the theoretical benefit of 
         preventing absorption by forming insoluble copper phosphide 
         but evidence of efficacy is lacking (Gosselin et al, 1984) 
         and the administration of copper salts may be hazardous.  
         
         Whole bowel irrigation successfully removed 50 tablets each 
         containing 500 mg zinc sulphate from the bowel of a 16 year-
         old (Burkhart et al, 1990).   The patient was asymptomatic 
         throughout the procedure, and stool guaiac tests were 
         negative.  The only adverse effect associated with whole 
         bowel irrigation was an increase in serum chloride 
         concentration from 105 to 127 mEq /L.
         
         For total cover/immersion, use copious amounts of 
         water/detergent to remove surface metal dust.  
                        
         Eye Contact
              
         Flood affected eye(s) with copious amounts of lukewarm, 
         gently running water for at least 15 minutes.  During this 
         time hold apart occasionally the upper and lower eyelid(s). 
          Obtain medical attention immediately.
         
         Skin Contact
         
         Rinse the affected area(s) with copious amounts of lukewarm, 
         gently running water for at least 15 minutes.  Remove 
         contaminated clothing and shoes.   Wash/thoroughly clean all 
         clothing before re-using or discard.  If skin irritation 
         exists, seek medical attention.
      10.5 Elimination
         See 10.6 Antidote treatment; diuresis may be required if 
         renal failure occurs.
      10.6 Antidote treatment
         10.6.1 Adults
                Administration of sodium calcium edetate by mouth and 
                 intravenously has been suggested.  
                
                Dimercaprol 2.3 mg/kg bodyweight intramuscularly 
                every four hours for four doses, then daily for 6 
                days (Murphy, 1970) was effective in a 16 year old 
                boy (see case study).  
                
                Injury due to splashes of zinc chloride in the eye 
                can be treated by immediate irrigation with neutral 
                disodium edetate solution 0.05M.
         10.6.2 Children
                Administer calcium disodium edetate or dimercaprol to 
                 symptomatic patients suspected to have excess body 
                zinc burden.
                
                A 13 month-old boy was given calcium disodium edetate 
                180 mg (15 mg/kg) intravenously following accidental 
                ingestion of 30 mL of a moss killer solution 
                containing 13% zinc chloride.  The serum zinc 

                concentration decreased from 10,020 micrograms/l 
                prior to chelation to 1,450 micrograms/l after 
                chelation.  A marked improvement of his mental 
                status was also noted after chelation therapy (Hedtke 
                et al, 1989).
                
                In a 16 month-old boy who swallowed soldering flux, 
                chelation with calcium EDTA and dimercaprol starting 
                75 hours after ingestion was ineffective in 
                enhancing zinc clearance. Dimercaprol (12 mg/kg) and 
                calcium EDTA (1 g/m2) were given daily divided into 
                four doses for 5 days.  Blood zinc levels had 
                declined from 10,199 to 1,600 micrograms/l prior to 
                chelation and decreased only from 1,600 to 870 
                micrograms/l after chelation (McKinney et al, 1991).
                
                Calcium EDTA lowers serum zinc to normal levels 
                (Chobanian, 1981; Potter, 1981) and, in the rat, 
                EDTA has been shown to increase urinary excretion 
                greatly (Millar et al, 1954).
      10.7 Management discussion
         Gastric lavage may be beneficial in patients exposed to non-
         corrosive salts of zinc but it should not be used for 
         corrosive salts such as zinc chloride.  Activated charcoal 
         is useful to adsorbing zinc.
    11. ILLUSTRATIVE CASES
      11.1 Case reports from literature
         A 16 year-old boy ingested 12 g of elemental zinc in an 
         attempt to promote wound healing.  Lethargy occurred 3 days 
         after ingestion, and blood zinc concentrations were 
         elevated. Treatment with dimercaprol 2.3 mg/kg body weight 
         intramuscularly every four hours for 4 injections, then once 
         daily for 6 days, resulted in clinical improvement and a 
         fall in zinc concentrations.  (Murphy, 1970).
                             
         A 13 month-old boy accidentally ingested 30 mL of a moss 
         killer solution containing 13% zinc chloride, and developed 
         spontaneous vomiting, erythematous uvula, lethargy, 
         somnolence, frequent premature atrial beats, hyperglycaemia,
          elevated alkaline phosphatase, oliguria, hyperamylasemia, 
         and a large superficial burn to the greater curvature of the 
         stomach.  He was treated with intravenous fluids and 15 
         mg/kg of calcium disodium edetate.  His mental status 
         improved dramatically and he was discharged after a day of 
         additional observation. (Hedtke et al, 1989).
         
         Two persons survived the acute ingestion of zinc chloride 
         after developing serum levels of 1.46 and 19.4 mg/l; 
         symptoms included lethargy, nausea, vomiting and erosion of 
         the gastrointestinal mucosa.  Administration of calcium 
         EDTA reduced the serum zinc concentration to normal 
         (Chobanian, 1981; Potter, 1981).  
         
         A six year old child died of corrosive gastritis and hepatic 
         necrosis 9 days after ingesting a zinc chloride soldering 
         solution (Jacobziner and Raybin, 1962).  Hyperglycaemia has 

         been reported after a dose of zinc sulphate from which the 
         patient subsequently died (Dreisbach, 1987).
                             
         A 31 year-old man presented to the Emergency Department with 
         nausea, vomiting and abdominal pain.  The patient was a 
         chronic paranoid schizophrenic who admitted to ingesting 
         coins for the past 12 years on the basis of a delusional 
         belief that they would protect him from harm.   Coin-like 
         structures in his stomach and abdomen were noted on X-ray.  
         He was hospitalised and given intravenous fluids and 
         analgesics.  At admission he had a haemoglobin of 9.3 g/dl; 
         over the next 8 days it fell to a low of 6.6 g/dl at which 
         time he was given a transfusion.  The rest of his blood 
         results indicated sideroblastic anaemia. A gastroscopy was 
         performed on the 14th day, at which time a large number of 
         coins were found and removed from his stomach. The serum 
         zinc level preoperatively was greater than 45.9 micromol/l 
         (normal 9.2 to 23.0 micromol/l).  Both the zinc level and 
         the anaemia returned to normal over the next four months 
         (Broun et al, 1990).
                   
         A 48 year-old man presented with a 6-month history of 
         chronic fatigue, and a blood screen notable for 
         sideroblastic anaemia. The patient reported taking zinc 
         supplements daily for the past two years.  His serum zinc 
         level was 36.4 micromol/l.  Two weeks after stopping the 
         zinc, his anaemia had resolved (Broun et al, 1990).
      11.2 Internally extracted data on cases
         To be added by the centre.
      11.3 Internal cases
         To be added by the centre.
    12. ADDITIONAL INFORMATION
      12.1 Availability of antidotes
      12.2 Specific preventive measures
         Respiratory Protection: Use self contained breathing 
         apparatus (in fire).
         
         Gloves: Rubber or plastic.
         
         Protective clothing: suitable to prevent repeated or 
         prolonged skin contact, e.g., coveralls, etc.
         
         Eyes: Wear suitable eye protection.
      12.3 Other
         No data available 
    13. REFERENCES
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    ACGIH (1989)  Threshold Limit Values and Biological Exposure 
    Indices for 1989 - 90.  American Conference of Governmental 
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    Allen RE, Pierce JO, & Yeager D (1968) Determination of zinc in 
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    Assoc J, 29: 469-473.
    
    Breitschwerdt EB, Armstrong PJ, Robinette CL et al. (1986) three 
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    Broun ER, Greist A, Tricot G, Hoffman R (1990) Excessive zinc 
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    Callender GE, Gentkow CJ (1988) Milt. Surg, 80, 67, 1939.  Cited 
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    Dreisback RH, Robertson WO (1987) Handbook of Poisoning: 
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    du Bray ES (1937) Chronic zinc intoxication.  An instance of 
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    14. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES), COMPLETE 
    ADDRESSES
    Authors: Peter Hayes, MPharm, BPharm, MRPharmS, MCPP, MBIM.
              Trudi Patricia Martin, BPharm, MPharm, MPS.
              Department of Pharmacy
              University of Queensland
              Brisbane QLD 4072
              Australia

    
              Tel: 61-7-3653191
              Fax: 61-7-3653194
    
    Date:     February, 1994




    See Also:
       Toxicological Abbreviations