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Dibutyltindichloride

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
   2.3 Diagnosis
   2.4 First-aid measures and management principles symptomatic treatment.
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
   4.2 High risk circumstance of poisoning
   4.3 Occupationally exposed populations
5. ROUTES OF EXPOSURE
   5.1 Oral
   5.2 Inhalation
   5.3 Dermal
   5.4 Eye
   5.5 Parenteral
   5.6 Other
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)
   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
      8.5.1 Sample collection
      8.5.2 Biomedical analysis
      8.5.3 Toxicological analysis
      8.5.4 Other 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 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 Other
      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)
    DIBUTYLTINDICHLORIDE

    International Programme on Chemical Safety
    Poisons Information Monograph 586
    Chemical

    1.  NAME

        1.1  Substance

             dibutyltindichloride

        1.2  Group

             organotin compounds

        1.3  Synonyms

             di-n-butyltin dichloride,
             dibutyldichlorostannane,
             dibutyldichlorotin,
             dibutyltin chloride,
             dichlorodibutylstannane,
             dichlorodibutyltin,

        1.4  Identification numbers

             1.4.1  CAS number

                    683-18-1

             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

             After skin and eye contact, local irritation and
             inflammation will occur after 1-8 hours, without workers
             being aware of it at the moment of exposure.In vitro and in
             vivo experiments immunosuppressive properties were
             observed
    

             Summary of clinical effects
    
             Local skin and eye irritation and inflamation my occur after
             a latent period of 1-8 hours.Lymphocytoxic and
             immunosupressive properties are only observed in in vitro and
             in vivo animal experiments up to now.

        2.3  Diagnosis

             irritation of skin and eyes.

        2.4  First-aid measures and management principles
             symptomatic treatment.

    3.  PHYSICO-CHEMICAL PROPERTIES

        3.1  Origin of the substance

             The reaction between HCl and the stabilizer dibutyltin
             most probably produces dibutyltin dichloride (Boyer,
             1989)

        3.2  Chemical structure

             (C4H9)2SnCl2

        3.3  Physical properties

             3.3.1  Colour

             3.3.2  State/Form

             3.3.3  Description

                    Molecular weight.: 303.83
                    Crystalline form: white needles
                    Index of refraction: 1.499
                    Specific gravity:1.36
                    Melting point: 142C
                    Boiling point: decomposes 113.6C
                    Solubility:
                    - decomposes in cold water 
                    - decomposes in hot water
                    - soluble in ether.  benzene, and alcohol.(Weast &
                    Selby, 1967)

        3.4  Hazardous characteristics

             No data available.

    4.  USES

        4.1  Uses

             4.1.1.  Uses

                    <4.1.1.>Description

                    The presence of 0.5-3% of a dibutyltin stabilizer
                    prevents the degradation of plastics by combining with
                    the HCl liberated from the polymer during
                    manufacturing  processes which require high
                    temperatures (Frey et al.1964).

        4.2  High risk circumstance of poisoning

             No data available.

        4.3  Occupationally exposed populations

             Process workers in contact with butytin compounds.

    5.  ROUTES OF EXPOSURE

        5.1  Oral

             In animal experiments

        5.2  Inhalation

             No data vailble.

        5.3  Dermal

             Occupationally and in volunteers

        5.4  Eye

             Irritation of the eye

        5.5  Parenteral

             No data available

        5.6  Other

             No data available

    6.  KINETICS

        6.1  Absorption by route of exposure

             No data available

        6.2  Distribution by route of exposure

             After dibutyltin intravenously the highest concentration
             was found in the liver with a small amount in the kidneys
             (Barnes & Magee, 1958)

        6.3  Biological half-life by route of exposure

             No data available

        6.4  Metabolism

             No data available

        6.5  Elimination by route of exposure

             No data available

    7.  TOXICOLOGY

        7.1  Mode of Action

             The ations of homologous series of di-substituted
             orgaNotin compounds from dimethyl to dioctyltin are
             inhibiting of  mitochondrial respiration by preventing the
             oxidation of keto- acids, presumaly via the inhibition of
             alpha-keto oxidase activity, leading to the accumulation of
             pyruvate (Aldridge, 1976; Piver 1973).

        7.2  Toxicity

             7.2.1  Human data

                    7.2.1.1  Adults

                             No data available

                    7.2.1.2  Children

                             No data available

             7.2.2  Relevant animal data

                    LD50 rat orally in oil solution 100 mg/kg
                    (Klimmer 1969)

             7.2.3  Relevant in vitro data

                    In vitro dibutyltin dichloride is extremely
                    cytotoxic.  Blast transformation of human as well as
                    rat thymocytes was already inhibited at concentrations
                    as low as 0.02 microgram dibutyltindichloride ml
                    medium (Seinen et al., 1979).

             7.2.4  Workplace standards

                    Maximum allowable concentration value
                    (calculated as tin) has been issued for organotin
                    compounds at 0.1 mg/m3 (Zuckerman et al 1978). To
                    avoid local irritation momentary (5 minutes) values
                    should not exceed 0.2 mg/m3 (MAK 1987).

             7.2.5  Acceptable daily intake (ADI)

                    Once incorporated into final consumer products,
                    the potential for tin compound is not likely to pose a
                    major human health hazard.  The daily intake should
                    not exceed 15 ng (normally 1-5 ng (Merian
                    1991).

        7.3  Carcinogenicity

             No data available.

        7.4  Teratogenicity

             No data available.

        7.5  Mutagenicity

             No data available.

        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

                    Small quantities of dialkyltin are extractable
                    from PVC bottles into biological fluids (Piver, 1973). 
                    The Food and Drug Administration has permitted the use 
                    a.o.  dioctyl maleate, dioctyl-S,S'-bis (isooctyl 
                    mercapto acetate) at levels not to exceed 3% in
                    resin,to  stabilize plastic bottles and films which
                    contact food.  These long-chained organotin compounds
                    were though to be less toxic than the dibutyltin
                    derivates because they are relatively insoluble in
                    bodt fluids and poorly  absorbed from the gastro
                    intestinal tract (Barnes &  Stoner 1958).

        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

             8.5.1  Sample collection

             8.5.2  Biomedical analysis

             8.5.3  Toxicological analysis

             8.5.4  Other investigations

        8.6  References

    9.  CLINICAL EFFECTS

        9.1  Acute poisoning

             9.1.1  Ingestion

                    No data available

             9.1.2  Inhalation

                    Irritation of the respiratory tract.

             9.1.3  Skin exposure

                    No visible changes occured for 1-8 hours after
                    exposure,  thereafter irritation and on the second day
                    the  development of sterile inflamation.  After one
                    week the lesions had practically disappeared.

             9.1.4  Eye contact

                    Irritation of the eyes.

             9.1.5  Parenteral exposure

                    No data available

             9.1.6  Other

                    No data available

        9.2  Chronic poisoning

             9.2.1  Ingestion

                    No data available

             9.2.2  Inhalation

                    Irritation of the respiratory tract

             9.2.3  Skin exposure

                    Irritation and inflammation of the skin

             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

             No data available.

        9.4  Systematic description of clinical effects

             9.4.1  Cardiovascular

                    No data available.

             9.4.2  Respiratory

                    Pulmonary oedema occured in rats after a single
                    i.v.injection of dibutyltin dichloride 10 mg/kg
                    (Barnes  & Stoner 1958).

             9.4.3  Neurological

                    9.4.3.1  Central Nervous System (CNS)

                             No data available

                    9.4.3.2  Peripheral nervous system

                             No data available.

                    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

                    No data availabe.

             9.4.5  Hepatic

                    Alkyltin-induced damage to the bile duct is
                    specific to animal species which, unlike man, have
                    common bile duct systems (Kimbrough 1976).  A single
                    dose of dibutyltin dichloride of 30 mg/kg by gavage
                    produced distal bile  duct necrosis and papillary
                    regeneration proliferation  in hamsters within 7 days
                    after administration.  In contrast rabbits, guinea
                    pigs, hens and cats, all of  which have separate bile
                    ducts and pancreatic duct  systems, do not exhibit
                    bile duct injury after dibutyltin dichloride treatment
                    (Barnes & Stoner, 1959;  Barnes & Magee,
                    1958).

             9.4.6  Urinary

                    9.4.6.1  Renal

                             No data available.

                    9.4.6.2  Other

                             No data available.

             9.4.7  Endocrine and reproductive systems

                    No data available.

             9.4.8  Dermatological

                    After application, no visible changes occured
                    for 2h to 3h, although a swelling of the mouth of the
                    hair  follicles was noticeble.  The follicular
                    inflammation  progressed during the following 8h with
                    only slight  visible irritation of the skin between
                    the openings of the follicles.  On the second day,
                    sterile pustules  developed over the follicular
                    openings, but remained  small during the next 3 to 4
                    days.  After one week, the  lesions had practically
                    disapeared (Lyle, 1958).  Dibutyltin dichloride at 335
                    nmol/cm2 produced epidermal  necrosis and dermal
                    inflammation within 24  hours.[Tributyltin chloride
                    produced the same effect  already at 23
                    nmol/cm2].

             9.4.9  Eye, ears, nose, throat: local effects

                    Lacrimation and severe suffusion of the
                    conjunctivae appeared within a few minutes and
                    persisted for 4 days. Immediate lavage of the eye
                    did not prevent development  of the signs (Lyle,
                    1958).

             9.4.10 Haematological

                    Since dibutyltin compounds induce
                    immunosupression selectively, T-lymphocytes are
                    predominantly involved (Seinen et al., 1979).

             9.4.11 Immunological

                    Dibutyltin dichloride is lymphocytotoxic and
                    immunosuppressive. Dietary levels of dibutyltin
                    dichloride as low as 20 ppm produced thymus atrophy in
                    rats within 2 weeks (Seinen et al., 1977a).  Immune
                    responses were diminished in weaning rats fed 50-150
                    ppm dibutyltin dichloride or 150 ppm dioctyl tin
                    dichloride in the diet for 6 weeks, corresponding to
                    the decrease in the weight and number of cells of the
                    thymus (Seinen et al., 1977b).  The functional
                    disturbance was manifested by an inhibition in
                    cell-reaction to tuberculin, skin allograft rejection,
                    graft-vs-host reactivity and cells, and peripheral
                    lymphe-nodes.  The E-rossette formation was inhibited
                    at very low levels (Seinen et al., 1977b;  1979a; 
                    1979b).

             9.4.12 Metabolic

                    9.4.12.1 Acid-base disturbances

                             No data available.

                    9.4.12.2 Fluid and electrolyte disturbances

                             No data availble.

                    9.4.12.3 Others

                             No data available.

             9.4.13 Allergic reactions

                    No data availble.

             9.4.14 Other clinical effects

                    No data availabe.

             9.4.15 Special risks

                    No data available.

        9.5  Others

             No data available.

        9.6  Summary

    10. MANAGEMENT

        10.1 General principles

             Decontamination of the exposed skin and clothes.

        10.2 Life supportive procedures and symptomatic treatment

             Not applicable.

        10.3 Decontamination

             Skin contact with the colorless dibutyltin chlorides
             does  not immediately give any symptom or sign.  Although
             prevention of later effects may not be effective, washing 
             with water and soap is indicated.  Clothes that have been
             moistened by vapour or liquid compounds must be immediately 
             taken off.

        10.4 Enhanced elimination

             No data available.

        10.5 Antidote treatment

             10.5.1 Adults

                    2.3.dimercapto propanol (BAL) prevents the
                    accumulation of alpha-keto acids produced by the
                    dialkyltins in animal experiments.  BAL proved to be
                    an effective antidote (Stoner at al., 1955).

             10.5.2 Children

                    No data availble.

        10.6 Management discussion

             2.3 dimercapto propanol (BAL) prevents the accumulation
             of alpha-keto acids produced by the dialkyltins in animal 
             experiments.  BAL proved to be an effective antidote (Stoner 
             et al., 1955).

    11. ILLUSTRATIVE CASES

        11.1 Case reports from literature

             A single dermal application of undiluted dibutyltin
             diacetate,dibutyltin dilaurate,dibutyltin oxide, dibutyltin
             maleate  on the back of the hands of volunteers was not
             irritating.  Incontrast,exposed areas of the skin reddened
             within 8 hours  after a single application of dibutyltin
             dichloride.  This effect was accompanied by follicular
             inflammation and  pruritus (Lyle, 1958).

    12. ADDITIONAL INFORMATION

        12.1 Specific preventive measures

             No data available

        12.2 Other

             No data available

    13. REFERENCES

        Aldridge WN (1976) The influence of organotin compounds on
        mitochondrial functions.  In: Zuckerman JJ,ed Organotin
        compounds:New chemistry and applications,Washington DC American
        Chemical Society, pp.186-196.
    
        Barnes JM, Magee PN (1958) The biliary and hepatic lesion produced
        experimentally by dibutyltin salts.  J Pathol Bacteriol
        75:267-279.
    
        Barnes JM, Stoner HB (1959) The toxicology of tin compounds. 
        Pharmacol Rev 11:211-231.
    
        Boyer IJ (1989) Toxicity of dibutyltin,tributyltin and other
        organotin compounds to humans and to experimental animals. 
        Toxicology 55:253-298.
    
        Frey AH, Horst RW, Paliobagis MA (1964) The chemistry of
        poly(vinyl)chloride stabilization.J Polym Sci 2:1765 
    

        Kimbrough RD (1976) Toxicity and health effects of selected
        organotin compounds; A review.  Environ Health Perspect
        14:51-56.
    
        Klimmer OR (1969) [The application of organotin compounds reviewed
        by the experimental toxicologist] Arzneim Forsch 19:934-939 (in
        German).
    
        Lyle W (1958) Lesions of the skin in process workers caused by
        contact with butyltin compounds.  Br J Ind Med 15:193-196.
    
        MAK (1987) Maximum Concetrations at the Workplace,Report No.XXIII
        DFG.  VCH Verlagsgesellschaft,Weinheim-Basel-Cambrige-New
        York.
    
        Merian E ed. (1991) Metals and Their Compounds in the Environment
        VCH Verlagsgesellschaft,Weinheim-Basel-Cambridge-New York.
    
        Piver WT (1973) Organotin compounds: Industrial applications and
        biological investigation.  Environ Health Perspect 4:61-79.
    
        Seinen W, Vos JG, van Spanje I, Snoek M, Hooykaas H (1977a)
        Toxicity of organotin compounds II Comparative in vivo and in
        vitro studies with various organotin and organolead compounds in
        different animal species with special emphasis on lymphocyte
        cytotoxicity.  Toxicol Appl Pharmacol 42:179-212.
    
        Seinen W, Vos JG, van Krieken R, Penninks A, Brands R, Hooykaas H
        (1977b) Toxicity of organotin compounds III Supression of
        thymus-dependent immunity in rats by di-n-butyltin dichloride and
        di-n-octyltin dichloride.  Toxicol Appl Pharmacol 42:213-224.
    
        Seinen W, Penninks A (1979a) Immune supression as a consequence of
        a selective cytotoxic activity of certain organometallic compounds
        in thymus and thymus-dependent lymphocytes.  Ann NY Acad Sci
        320:499-517
    
        Seinen W, Vos JG, Brands R, Hooykaas H (1979b) Lymphocytotoxicity
        and immunosuppression by organotin compounds: Suppression of GVH
        -activity; blast transformation and E-rosette formation by
        di-n-butyltin dichloride and di-n-octyltin dichloride. 
        Immunopharmacology 1:343-355.
    
        Stoner HB, Barnes JM, Duff JI (1955) Studies on the toxicity of
        alkyltin compounds.  Br J Pharmacol 10:16-25.
    
        Weast RC, Selby SM (1967) Handbook of Chemistry and Physics 48ed. 
        pg C-677, The Chemical Rubber Co.  Cleveland, Ohio.
    

        Zuckermann JJ, Reisdorf RP, Ellis III HV, Wilkinson RR (1978) ACS
        Symp.Ser.82:388-424.

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

        Author:              Prof.Dr.A.N.P.van Heijst
                             Baarnse weg 42 A
                             3735 MJ Bosch en Duin
                             The Netherlands.
    
                             Telephone (30)287178 
    
        Date:                August 1993.
    
        Peer Review:         PIM Peer Review Group in Cardiff:  Besbelli,
                             O.Kasilo, L.Lefebre, J.Szajewski, W.Temple,
                             A.N.P.van Heijst.
    
        Date:                February 1994
    


    See Also:
       Toxicological Abbreviations