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DDT

1. DDT
   1.1 Substance
   1.2 Group
   1.3 Synonyms
   1.4 Identification numbers
      1.4.1 CAS
      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
      3.3.1 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 circumstances of poisoning
   4.3 Occupationally Exposed Population
5. ROUTES OF EXPOSURE
   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 and excretion
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)
         8.2.2.3 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 Systemic description of clinical effects
      9.4.1 Cardiovascular
      9.4.2 Respiratory
      9.4.3 Neurological
         9.4.3.1 Central nervous system
         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 Dermatologic
      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 the literature
12. ADDITIONAL INFORMATION
   12.1 Specific preventive measures
   12.2 Other
13. REFERENCES
14. AUTHOR(S), REVIEWER(S), DATE (INCLUDING EACH UP-DATE), COMPLETE ADDRESSES
    DDT

    International Programme on Chemical Safety
    Poisons Information Monograph 127
    Chemical

    1.  DDT

         1.1  Substance

              Dichlorodiphenyltrichloroethane (DDT)

         1.2  Group

         1.3  Synonyms

              Alpha,alpha-bis(p-chlorophenyl)beta, beta,
              beta-Trichlorethane;
              2,2-Bis(p-chlorophenyl)-1,1,1-Trichloroethane;
              Clofenotane (INN);
              Chlorinated diphenyloxide;
              Chlorophenothane (USP);
              p,p'-DDT;
              Dicophane (BP);
              ENT - 1506;
              Klorfenoton (Swedish);
              1,1,1,Trichloor2,2-bis(4-chloor-fenyl)-Ethaan(Dutch);
              1,1,1,Trichlor-2,2 bis(4-chlor-phenyl)aethan(German);
              1,1,1,Trichloro,2,2-Di(4-chlorophenyl)ethane;
              1,1-(2,2,2-trichloroethylidene)-bis (4-chlorobenzene) (CAS);
              1,1,1-trichloro-2,2-bis (4-chlorophenyl) ethane (IUPAC);
              OMS-16;

         1.4  Identification numbers

              1.4.1  CAS

                     50-29-3

              1.4.2  Other numbers

                     UN transportation number    2761
                     RTECS                       KJ 3325000
                     NCI                         C 00464

        1.5  Brand names/Trade names

             Anofax;
             Cezarex;
             DinozideGesarol;
             Guesapan;
             Guesarol;
             Gyron;
             Ixodex;
             Neocide;
             Neocidol;
             Zerdane;

        1.6  Manufacturers, importers

             To be added by the poison control centre.
    

    2.  SUMMARY

        2.1  Main risks and target organs

             DDT has a wide margin of safety when used
             judiciously, and few if any adequately documented cases of
             DDT poisoning in man have been fatal.  It appears that the
             main toxicity to humans is related more to the solvent
             vehicle rather than the DDT itself.
    
             DDT is a central nervous system stimulant, acting chiefly
             on the cerebellum and motor cortex.  The liver is the only
             other organ significantly affected by DDT.

        2.2  Summary of clinical effects

             The earliest symptom of poisoning by DDT is
             hyperaesthesia of the mouth and lower part of the face. 
             This is followed by paraesthesia of the same area and of
             the tongue and then by dizziness, an objective disturbance
             of equilibrium, paraesthesia and tremor of the
             extremities, confusion, malaise, headache, fatigue, and
             delayed vomiting (probably centrally mediated). 
             Convulsions only occur in severe poisoning.  It is not
             clear whether cardiac arrhythmia might be a possible cause
             of death in acute poisoning.  In most instances of
             fatalities following ingestion of DDT solutions, the signs
             and symptoms were predominantly or exclusively those of
             poisoning by the solvent vehicle.

        2.3  Diagnosis

             Clinical diagnosis may be difficult as symptoms are
             not specific and are dose related. The clinical effects of
             DDT may be modified by the vehicle or co -ingredients.  A
             single dose of DDT at the rate of 10 mg/kg may produce
             illness in some but not all subjects; smaller doses
             generally produce no illness.
    
             Blood levels are not clinically useful.
    
             There are both simple qualitative and recommended
             qualitative (involving thin layer chromatography) tests
             for biological samples (stomach contents or suspect
             fluids).  Gas liquid chromatography can be performed on
             blood and urine within 72 hours.  The urine can be
             examined for the presence of DDA when the diagnosis is
             uncertain.
    
             Hyperlipoproteinaemia can be tested for if chronic
             exposure is suspected.

        2.4  First-aid measures and management principles

             In the event of exposure to DDT, contaminated
             clothing and contact lenses should be removed to prevent
             further absorption.  In the case of skin contact, the
             affected area should be washed carefully with soap and
             water. Wash eyes for 10 to 15 minutes with clean running
             water. First aid personnel should wear rubber or plastic
             gloves and avoid contamination.
    
             Ingestions of small amounts of DDT do not constitute a
             significant risk, and may be managed by dilution with
             water.
    
             The management of large quantities of ingested DDT should
             be primarily directed towards decontamination and
             supportive care, as there is no specific antidote.  The
             use of gastric lavage for recent large ingestions and
             activated charcoal are indicated.
    

    3.  PHYSICO-CHEMICAL PROPERTIES

        3.1  Origin of the substance

             A synthetic product, DDT can be manufactured by the
             condensation of chlorobenzene with trichloroacetaldehyde 
             (Worthing & Walker, 1987).

        3.2  Chemical Structure

             The chemical name for DDT is:
    
             1,1,1-trichloro-2,2-bis(4-chlorophenyl)ethane
    
             The empirical formula is C14H9Cl5
    
             The relative molecular mass is 354.50

        3.3  Physical properties

             3.3.1  Colour

                    White

             3.3.2  State/Form

                    Solid-crystals

             3.3.3  Description

                    At room temperature DDT is a white,
                    tasteless, almost odourless crystalline solid
                    (Hayes & Laws, 1991).
    
                    Solubility:             Practically insoluble in water
                                            2g/100mL ethanol
                                            28g/100mL ether
                                            Highly soluble in apolar
                                            organic solvents
    
                    Boiling point:          185C
    
                    Melting point:          108.5C to 109.0C
    
                    Flash point:            162-171 F 
    
                    Density (20C):         1.016 kg/L
    
                    Specific gravity:       1.55
    
                    Vapour pressure (20C)  2.53  10-5 Pa

        3.4  Hazardous characteristics

             The term DDT is generally understood to refer to para
             para'-DDT.  However, the compound's structure permits
             several different isomeric forms including ortho para-DDT
             and meta para-DDT.  Technical DDT consists predominantly
             of para para'-DDT with smaller amounts of other compounds
             such as ortho para-DDT, para para'-TDE, ortho para-DDE
             (WHO, 1989).  These other isomeric forms may add to the
             action of DDT as it is known that ortho para-DDT is of
             insecticidal value (Worthing & Walker, 1987).
    
             DDT is resistant to destruction by light and oxidation
             (Budavari et al., 1989).
    
             para para'-DDT is dehydrochlorinated, at temperatures
             above its melting point, to DDE which has no insecticidal
             properties.  This reaction is catalysed by iron(III) or
             aluminium chlorides, UV light and in solution by alkalis
             (Worthing & Walker, 1987).  As such, DDT should not be
             stored in iron containers and should not be mixed with
             iron and aluminium salts or with alkaline solutions.
    
             High temperatures should also be avoided (Budavari et al.,
             1989).
    
             The environmental distribution and effects of DDT arise
             from its unusual chemical stability and hence its
             persistence.  DDT and some of the breakdown products of
             DDT, principally DDE, are highly persistent in soil,
             sediment and biota as they are relatively resistant to
             breakdown by the enzymes and higher organisms found in the
             soil (WHO, 1979).  Thus, contamination by materials can
             last long after cessation of DDT use.
    
             DDT and its metabolites are highly toxic to fish and,
             besides their lethal effects, they affect development,
             behaviour and biochemical processes.  DDT and its
             metabolites, should be regarded as hazardous to fish
             productivity and distribution and, hence, to human food
             supplies.  Accumulated DDT and its metabolites are further
             transferred from aquatic organisms to consumers, including
             birds, mammals, and, ultimately, humans (WHO, 1979).
    
             When exposed to simulated atmospheric conditions DDT
             decomposes to carbon dioxide and hydrochloric acid (WHO,
             1979).
    

             Fires involving DDT may produce irritating or poisonous
             gases.  Fire fighters should wear self contained breathing
             apparatus and chemical protective clothing. For small
             fires, use dry chemical, CO2, halon, water spray or
             standard foam extinguishment.  For larger fires, water
             spray, fog or standard foam is recommended.  For spills,
             take up with sand or other non-combustible absorbent
             material and place into containers for later disposal
             (DOT, 1987).
    

    4.  USES

        4.1  Uses

             4.1.1  Uses

                    Pesticide For Use Against Invertebrate Animals
                    Insecticide

             4.1.2  Description

                    DDT is a potent non-systemic stomach and
                    contact insecticide.  It is persistent on solid
                    surfaces, in soil, sediment and biota (Worthing &
                    Walker, 1987).
    
                    DDT has had a wide usage, particularly in
                    agriculture and vector control, and as such has
                    been formulated in almost every conceivable form. 
                    These include solutions in xylene and petroleum
                    distillates, emulsifiable concentrates, water-
                    wettable powders, granules, aerosols, smoke
                    candles, and charges for vaporisers (Hayes & Laws,
                    1991).
    
                    For its use as a topical medication it has also
                    been formulated as lotions, dusting powders and
                    shampoos (Reynolds, 1989).
    
                    The use of DDT is restricted or banned in some
                    countries except when it is needed for the
                    protection of health.

        4.2  High risk circumstances of poisoning

             Accidental poisoning of children by DDT present in
             the home or garage (mostly a problem when in non aqueous
             solution, and the vehicle is often more of a problem than
             the DDT).
    
             Accidental exposure among adult farm workers and secondary
             exposure to their children.
    
             Suicide attempts.
    
             Exposure of the general population may occur through the
             consumption of foodstuffs treated incorrectly with DDT or
             harvested prematurely before residues have declined to
             acceptable levels, from contact with treated areas or from
             domestic use.
    

             Use and contact with DDT formulated with oils, fats and
             lipid solvents.

        4.3  Occupationally Exposed Population

             Factory workers involved in synthesising DDT.
    
             Workers involved in formulating and dispensing DDT.
    
             Agricultural spray workers.
    
             Crop harvesters during disease vector control periods.
    
             Public health workers involved in vector control.
    

    5.  ROUTES OF EXPOSURE

        5.1  Oral

             Ingestion occurs through accidental or deliberate
             ingestion and ingestion via contaminated foodstuffs.

        5.2  Inhalation

             DDT is relatively non volatile and, although
             inhalation of spray drift may occur during occupational
             use, respiratory exposure is a less significant
             route.

        5.3  Dermal

             DDT is poorly absorbed via the dermal route and as
             such is a less important route of entry.  Dermal
             absorption increases when DDT is formulated in oily
             solutions.

        5.4  Eye

             Exposure to vapours, dust and aerosols.

        5.5  Parenteral

             Accidental or intentional.

        5.6  Others

             No data available
    

    6.  KINETICS

        6.1  Absorption by route of exposure

             In inhalation, most DDT dust is of such large
             particle size that any that is inhaled is deposited in the
             upper respiratory tract and eventually is swallowed (Hayes
             & Laws, 1991).
    
             Absorption of DDT from the gastrointestinal tract is slow. 
             Studies based on toxicity indicate that DDT dissolved in
             animal or vegetable fats is absorbed from the
             gastrointestinal tract about 1.5- to times more
             effectively than is undissolved DDT.  Convulsions occur
             only after 2 hours when DDT is administered orally at a
             rate of 2 or more times the oral LD50 value (Hayes &
             Laws, 1991).
    
             Intravenous injection at the rate of 50 mg/kg produces
             convulsions in rats in 20 minutes (Hayes & Laws,
             1991).
    
             Dermal absorption of DDT is very limited (Hayes & Laws,
             1991).

        6.2  Distribution by route of exposure

             DDT is stored in all tissues.  Storage of the
             compound in blood, liver, kidney, heart and the central
             nervous system (CNS) has been reported.  Higher
             concentrations of DDT are usually found in adipose tissue
             than in other tissues (Hayes & Laws, 1991).
    
             In the general population DDT and some of its metabolic
             derivatives can be stored in the tissues and excreted in
             urine and milk (Hayes & Laws, 1991).
    
             DDT and one of its major metabolic products, DDE, have
             high fat: water partition coefficients and, therefore,
             tend to accumulate in adipose tissue.  Studies in both
             humans and laboratory animals indicate that there is a
             log-log relationship between the daily intake and the
             residues of both DDT and DDT-derived material in adipose
             tissue.  At a constant rate of intake, however, the
             concentration of insecticide in adipose tissue reaches an
             equilibrium and remains relatively constant (Klaassen et
             al., 1986).

        6.3  Biological half-life by route of exposure

             In a study of volunteer adult males who ingested
             between 3.5 and 35 mg DDT/person/day, the storage of DDT
             was proportional to dosage.  DDT was slowly lost from
             storage in fat after dosing was stopped.  The
             concentration remaining following 25.5 months of recovery
             was from 32 to 35% of the maximum stored for those who had
             received 35 mg DDT/person/day but was 66% for those who
             received only 3.5 mg DDT/person/day. This indicated that
             a slower loss occurred at lower storage levels (Hayes &
             Laws, 1991).

        6.4  Metabolism

             DDT is converted to a slight extent to the much less
             toxic DDE by dehydrochlorination; DDE apparently does not
             undergo further biotransformation, but it is stored for an
             indefinite period of time in adipose tissues.  Most of the
             para, para-DDE present in human fat represents  preformed
             dietary DDE rather than endogenously produced DDE.  The
             major detoxification pathway of DDT is via dechlorination
             to DDD, an active insecticide which readily degrades to
             DDA, a water soluble, rapidly excreted detoxification
             product (Baselt, 1982).

        6.5  Elimination and excretion

             DDT is slowly eliminated from the body.  Elimination
             has been estimated at a rate of approximately 1% of stored
             DDT per day (Klaassen et al., 1986).

             Urinary DDA presents about 47% of ingested precursor
             material during low exposure, but DDA excretion becomes
             quantitatively less important as DDT intake increases.
             Urinary DDA concentrations correlate reasonably well with
             DDT storage levels in body fat. DDA was undetectable in
             the urine of members of the general population and ranged
             from 0.01 to 2.67 mg/L in workers with low to high
             exposure to DDT.  By contrast, urine concentrations of
             DDT, DDE and DDD in healthy unexposed persons averaged
             0.007, 0.016 and 0.003 mg/L respectively, and 0.011, 0.021
             and 0.006 mg/L respectively in occupationally exposed
             workers (Baselt, 1982).

             DDT is also excreted in human milk and transferred through
             the placenta (Hayes & Laws, 1991).
    

    7.  TOXICOLOGY

        7.1  Mode of action

             DDT is a central nervous system stimulant acting
             chiefly on the cerebellum and motor cortex.  Its action
             produces hyperexcitability, tremor and muscular weakness. 
             Convulsions and myocardial sensitivity may occur
             (Dreisbach & Robertson, 1987).

        7.2  Toxicity

             7.2.1  Human data

                    7.2.1.1  Adults

                             DDT has a wide margin of safety
                             when used judiciously, and few if any
                             adequately documented cases of DDT
                             poisoning in man have been fatal
                             (Gosselin et al., 1984).  It appears that
                             the main toxicity to humans is related
                             more to the solvent vehicle rather than
                             the DDT itself.
    
                             10 mg/kg is the single oral dose of DDT
                             necessary to produce illness in some but
                             not all subjects even though no vomiting
                             may occur (Hayes & Laws, 1991).
    

                             Convulsions have occurred in cases when
                             the dosage level was 16 mg/kg or greater
                             and no effective treatment was undertaken
                             (Hseih, 1954).
    
                             Amounts at least as high as 285 mg/kg
                             have been ingested without fatalities.
                             However, the amount retained is unknown
                             as these doses lead promptly to vomiting
                             (Hayes & Laws, 1991).
    
                             Considerable individual variation is
                             recognized with DDT toxicity.  Woodward
                             et al. (1944) described the generally
                             accepted acute mean lethal dose (LD50) in
                             rats as 250 mg/kg and Gosselin et al.
                             (1984) suggest that this is a reasonable
                             estimate for man.  Baselt (1982) states
                             that in general, DDT is relatively safe
                             with an estimated lethal dose of 30 g in
                             an adult.
    

                             Fats and oils enhance the toxicity of DDT
                             by promoting absorption.  In many
                             instances of alleged poisoning with DDT
                             the principal symptoms have been due to
                             the commercial vehicle that the DDT is
                             formulated with.  This vehicle has often
                             been kerosene (Reingold & Lasky,
                             1947).

                    7.2.1.2  Children

                             From studies in the young of
                             animal species it has been suggested
                             (Hayes & Laws, 1991) that the young are
                             at no greater risk than an
                             adult.

             7.2.2  Relevant animal data

             Animal     Formulation     Oral      Dermal     IV
                                        LD50      LD50       LD50
                                        mg/kg     mg/kg      mg/kg
    
             Rat        Water           500       1000       -
                        suspension      to 2500
                        or powder
    
                        Oil solution    113       250 to     47
                                        to 450    3000
    
             Mouse      Water           300 to    375        -
                        suspension      1600
                        or powder
    
                        Oil solution    100 to    250 to     -
                                        800       500
    
             (Hayes & Laws, 1991)

             7.2.3  Relevant in vitro data

                    No data available.

             7.2.4  Workplace standards

                    STEL ACGIH              3 milligram per cubic metre 
                                            (Parmeggiani, 1983)
    
                    TLV-TWA                 1 milligram per cubic metre
                                            (ACGIH, 1989)
    
                    OSHA PEL-TWA            1 milligram per cubic metre
                                            (skin designation) (OSHA,
                                            1989)
    

                    Odour threshold         not pertinent as is odourless
                                            (CHRIS, 1985)

             7.2.5  Acceptable daily intake (ADI)

                    0.02 mg/kg body weight  (provisional tolerable
                    daily intake, WHO 1995) [sum of p,p'DDT, o,p'DDT,
                    p,p'DDE and p,p'TFE(DDD)]
    
                    Other Guideline Levels:
                    WHO guideline value for drinking water:
                    1 microgram/L (total isomers) (WHO, 1984)

        7.3  Carcinogenicity

             DDT has been evaluated by the International Agency for
             Research on Cancer (IARC, 1987,1991).  It was concluded that
             the human evidence from several epidemiological studies was
             not adequate to indicate that DDT was carcinogenic.
    
             Many experiments have been conducted in rodents. Liver
             tumours were introduced in most of the mouse and in two of
             the rat experiments (IARC, 1991).
    
             Some risk of lymphoma, leukemia, pancreatic cancer, and
             breast cancer was found in humans exposed to DDT. Animal
             studies showed a significant association between DDT
             administration and lymphoma, respiratory cancer, liver
             cancer, and estrogenic effects on mammary tissue. On the
             basis of epidemiological principles, human studies were
             deficient in adequate sample sizes and were not exempt from
             such confounding factors as multiple chemical exposure,
             lifestyle factors, genetic, and other environmental
             influences (Jaga and Brosius, 1999).

        7.4  Teratogenicity

             The effects of DDT on reproduction parameters have been
             summarised by IARC (1991).  One human study has suggested
             that there may be a weak relationship between DDT levels in
             cord blood and low birth weight.  Studies in rodents and
             rabbits have not demonstrated any teratogenic potential, but
             exposure of rodents to DDT impaired reproductive function
             (e.g., spermatogenesis, neonatal survival) in some
             studies.

        7.5  Mutagenicity

             IARC (1991) reported one study in which chromosomal
             aberrations were observed in the peripheral lymphocytes of
             workers with increased plasma DDT levels. This finding is not
             supported by studies on bone-marrow cells of rodents.  In
             most studies, DDT did not induce genetoxic effects in
             cultured rodent or human cell systems and was not mutagenic
             to fungi or bacteria.

        7.6  Interactions

             DDT is known to interfere with the metabolism and
             function of steroid hormones.  One such mechanism is by the
             induction of hepatic microsomal enzymes which results in an
             increased conversion of oestrogens, androgens, and
             glucocorticoids to more polar metabolites.  Increased urinary
             excretion of the more polar metabolites is usually
             compensated for by increased steroid biosynthesis (Gosselin
             et al., 1984).
    
             Individuals on chronic drug therapy with phenobarbitol and/or
             phenytoin have increased hepatic microsomal enzymes activity. 
             Watson et al. (1972) suggest that this increased activity
             accelerates the metabolism of some DDT to DDA by the slow
             series of dehydrohalogenation reactions.
    
             Fat and oils increase the absorption of DDT from the
             intestine.
    

    8.  TOXICOLOGICAL ANALYSES AND BIOMEDICAL INVESTIGATIONS

        8.1  Material sampling plan

             8.1.1  Sampling and specimen collection

                    8.1.1.1  Toxicological analyses

                             Sample should be drawn into a vial
                             or tube filter with a teflon or foil lined
                             screw cap. Polyethylene or rubber caps must
                             be used. Sample size: 7 to 10 mL. Use
                             whole blood without added anticoagulant 
                             (EPA, 1982).

                    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

                             If an analysis cannot be run
                             immediately, place in refrigerator at 2 to
                             5C for periods of up to 24 hours before
                             analysis. If time interval to analysis
                             exceeds 24 hours, sample (serum) should be
                             stored in a deep-freeze at -15 to -25C. 
                             Stored in this manner, analysis may be
                             delayed up to a month. (EPA, 1982).

                    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)

                             Nitric-sulphuric acid colour test:
    
                             The reagent:
                             Mix 1 mL nitric acid with 30 mL sulphuric
                             acid
    
                             Method:
                             Dissolve the sample in 1 mL Ethanol, and add
                             a pellet of potassium hydroxide.  Evaporate
                             to dryness at 100C in a waterbath.  To the
                             residue, add 0.5 mL water and 1 mL carbon
                             tetrachloride.  Shake, allow to separate,
                             decant the lower carbon tetrachloride layer
                             and shake it with 1 mL reagent.
    
                             Indications:
    
                             A RED colour in the acid layer suggests the
                             presence of DDT or its metabolite DDE.  The
                             red colour changes to ORANGE then to GREEN. 
                             A RED colour is also given by DDD but the
                             colour does not change (Moffat, 1986).

                    8.2.2.2  Advanced Qualitative Confirmation Test(s)

                             Thin Layer chromatography:
                             Recommended qualitative for biological sample
                             (stomach contents or suspect fluids).
    
                             Sampling:
                             10 to 20 mL stomach content
    

                             Chemical and reagents:
                             *Petroleum ether (40 to 60C boiling
                             fraction)
                             *Aqueous sodium hydroxide (20 g/L)
                             *Sodium sulphate (anhydrous)
                             *Organochlorine standards (DDT, HCH, Lindane,
                             HCB, heptachlor, aldrin, endrine) (all in 1
                             g/L) in methanol, Silica gel.
    
                             Equipment:
                             TLC plates (20  20 cm), pipettes, spray
                             bottle.
    
                             Method:
    
                             10 mL of sample is extracted twice with 5 mL
                             portions of petroleum ether.  Extracts are
                             combined and washed with 5 mL portions of
                             purified water and sodium hydroxide solution. 
                             The extract is dried over sodium sulphate and
                             evaporated to dryness under stream of
                             compressed air.
    
                             The extract is reconstituted in 100 mg
                             methanol and 20 mg is spotted on TLC plate. 
                             Standard mixture is spotted on a second
                             column.  The chromatogram is developed using
                             petroleum ether (saturated tank) and allowed
                             to dry.  The plate is sprayed with silver
                             nitrate solution and after drying in ambient
                             temperature, is exposed to UV light (254 nm,
                             15 min).
    
                             Organochlorine compounds give a BROWN-GREY
                             reaction and identification is made by
                             comparison with the standard
                             chromatogram.

                    8.2.2.3  Simple Quantitative Method(s)

                    8.2.2.3  Advanced Quantitative Method(s)

                             Recommended quantitative test for
                             biological sample (blood).
    

                             Principle of test:
                             A 2 mL aliquot of serum is extracted with 6
                             mL of hexane in a round bottom tube.  The
                             extraction is conducted for 2 hours on a slow
                             speed rotating mixer.  If emulsion forms,
                             centrifugation may be used to effect
                             separation.  A 5 mL aliquot of the hexane
                             layer is quantitatively transferred to an
                             evaporative concentrator tube to which a
                             micro-snider column is affixed.  The extract
                             is concentrated in a water bath, and the
                             final volume is adjusted to correspond to the
                             expected concentration of the pesticide
                             residue.  A suitable aliquot is analysed by
                             electron capture gas chromatography.
    
                             Sampling:
    
                             7 to 10 mL blood drawn, is transferred to a
                             vial or tube fitted with a teflon or foil
                             lined screw.  Whole blood sample is placed in
                             the refrigerator for about 30 minutes for
                             setting and centrifuged  for 10 minutes for
                             the separation of at least 3 mL of clear
                             serum 2 mL of serum is used for
                             extraction.
    
                             Chemicals and reagents:
                             Hexane, distilled in glass, pesticide grade.
    
                             Equipment:
                             1.  A rotatory mixer, designed to accommodate
                                 the 16 mm culture tubes and which may be
                                 operated at a rotary speed of 50 rpm.
                             2.  Gas chromatograph, fitted with electron
                                 capture detector.
                             3.  Tubes, culture, 16 125 mm, fitted with
                                 screw caps with teflon-faced rubber
                                 liners.
                             4.  Micro-snider column.
                             5.  Concentrator tube.
                             6.  Syringe, 100 mL, Hamilton.
                             7.  Vortex mixer.
                             8.  Pipette, Mohr type, 1 mL grad in 0.01 mL
                                 increments.
                             9.  Pipettes, transfer, 2,5 and 6 mL.
                             10. Beads solid, glass, 3 mm.
                             11. Water bath capable of holding temperature
                                 of 95 to 100C.
                             12. Centrifuge, capable of speed of 2000 rpm.
    

                             Specimen preparation:
                             No special preparation required.
    
                             Procedure:
                             Mix blood serum sample thoroughly and, with a
                             volumetric pipette, transfer 2 mL to a 15 mL
                             round bottom culture tube.  In case of the
                             presence of any flocculent or sedimentary
                             material, centrifuge in 5 min 2000 rpm before
                             pipetting, in order to avoid poor
                             reproducibility of replicated analyses of the
                             same sample.
    
                             Add 6 mL hexane from a volumetric pipette. 
                             Tightly stopper the culture tube.  Place on
                             rotator for 2 hours of 50 rpm speed. In the
                             case of emulsion formation centrifuge at 2000
                             rpm 4 to 5 minutes. Transfer 5 mL of the
                             hexane extract to a 10 mL grad. concentrator
                             tube, add one 3 mm glass bead and attach a
                             modified micro - Snider column. Evaporate the
                             extract in a steam or hot bath at 100C. 
                             (When working with blood from high exposure
                             donors, the 5 mL aliquot may require dilution
                             rather than concentration) allow the tube to
                             cool 3 to 5 minutes, remove the micro -
                             Snider column an rinse down the sides of the
                             tube and the column joint with hexane. 
                             Stopper the concentrator tube and hold on the
                             Vortex mixer, set for high speed for 30
                             seconds  for volumes of 6 mL or less. For
                             larger volumes mix for 1 minute. Proceed with
                             electron capture GLC.
    
                             p.p.b = \f(a b x, c y)  0.6
    
                             Where:
    
                             a =   nanograms of pesticide in standard peak
                             b =   height of sample peak
                             c =   height of standard peak
                             x =   total volume of final extract in
                                   microlitres
                             y =   microliters of extract injected
    
                             e.g.: nanograms in standard peak = 0.3
                             height of sample peak = 80 mm
                             height of standard peak = 90 mm
                             total volume of final extract = 1000
                             microlitre

                             volume of final extract injected = 5
                             microlitre
                             p.p.b = \f(0.3  80  1000,90  5)  0.6 = 32
                             ppb
                             Quality Control:
    
                             Composition of standard mixture:
    
              a HCH 20 pg/mL       HCB 20 pg/mL             pp DDT 80 pg/mL
    
              b HCH 40 pg/mL       Heptachlor 20 pg/mL      pp DDE 60 pg/mL
    
              g HCH 20 pg/mL       op DDT 50 pg/mL          pp DDD 50 pg/mL
    
                             Specificity:
                             It is group specific
    
                             Detection Limit:
                             b-HCH, lindane, heptachlor, heptachlor
                             epoxide, o,p-DDE, dieldrin:-1 ppb
                             endrin, op-DDT,pp-DDD,pp-DDT:-2 ppb

                    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

                             Blood levels are not clinically useful.
    
                             Biochemical tests to detect liver and kidney
                             dysfunction should be performed although the
                             results are expected to be negative (Gosselin
                             et al., 1984).
    
                             Determination of blood sugar and sugar
                             tolerance levels are desirable (Gosselin et
                             al., 1984).

                    8.3.1.2  Urine

                             "Basic analyses"
    
                             "Dedicated analyses"
    
                             "Optional analyses"

                    8.3.1.3  Other fluids

             8.3.2  Arterial blood gas analyses

             8.3.3  Haematological analyses

                    "Basic analyses"
    
                    "Dedicated analyses"
    
                    "Optional 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

             Relevant laboratory analyses and other investigations:
             Laboratory analysis may indicate prolonged exposure to DDT
             but has little relation to acute exposure management as
             decontamination needs to be undertaken before laboratory
             results are available.
    
             Sample collection:
             Analysis of blood and urine is required within 72 hours to
             detect high DDT levels.
    
             Biomedical analysis:
             Blood levels are not clinically useful.
             Biochemical tests to detect liver and kidney dysfunction
             should be performed although the results are expected to be
             negative (Gosselin et al., 1984).
    
             Determination of blood sugar tolerance levels are desirable
             (Gosselin et al., 1984).
    
             Toxicological analysis:
             Gas liquid chromatography can be performed on blood and urine
             within 72 hours.
    
             The urine can be examined for the presence of DDA when the
             diagnosis is uncertain (Gosselin et al., 1984).
    
             Other investigations:
             Hyperlipoproteinaemia can be tested for if chronic exposure
             is suspected (Gosselin et al., 1984).

        8.6  References
    

    9.  CLINICAL EFFECTS

        9.1  Acute poisoning 

             9.1.1  Ingestion

                    Onset of signs and symptoms depends on the
                    dose. Onset may be as soon as 30 minutes after
                    ingestion of a large dose or as late as 6 hours after
                    smaller but still toxic doses.
    
                    Large doses are followed promptly by vomiting due to
                    local gastric irritation. Delayed emesis and/or
                    diarrhoea may occur.
    
                    Onset of signs and symptoms are characterised by
                    paraesthesia of the tongue, lips and face. In more
                    severe poisonings paraesthesia may also involve the
                    extremities. The patient suffers from a sense of
                    apprehension, dizziness, an objective disturbance of
                    equilibrium, and ataxia. Confusion may develop,
                    malaise, headache, fatigue and sore throat may also be
                    present. Tremor is a characteristic manifestation,
                    usually involving first the neck and head and
                    particularly the eyelids. Convulsions both clonic and
                    tonic may develop and alternate with periods of coma
                    and paresis. In the absence of convulsions, the vital
                    signs are essentially normal, but in severe poisoning
                    the pulse may be irregular and abnormally slow. 
                    Because DDT sensitises the heart to endogenous
                    adrenaline, ventricular fibrillation and sudden death
                    may occur at any time during the acute phase of
                    poisoning. Complicating pulmonary signs suggesting a
                    pulmonary oedema are probably due to concomitant
                    solvent intoxication.  Death, if it occurs, is usually
                    due to respiratory failure from medullary paralysis
                    (Gosselin et al., 1984; Dreisbach & Robertson, 1987;
                    Hayes & Laws, 1991).

             9.1.2  Inhalation

                    Inhalation of fine DDT aerosol or dust into the
                    lung produces moderate irritation of nose, throat and
                    eyes with no other detectable ill effects (Hayes &
                    Laws, 1991).

             9.1.3  Skin exposure

                    Dermal exposure to DDT is usually associated
                    with no illness and usually no irritation. 
                    Formulations of DDT involving solvents have been shown
                    to cause a slight transient dermatitis. These effects
                    have usually been shown to be related to the solvent
                    (Hayes & Laws, 1991).

             9.1.4  Eye contact

                    Contact with the eyes may cause ocular irritation. 
                    Further effects may be due to the solvent present.

             9.1.5  Parenteral exposure

                    Intravenous administration in animals has
                    resulted in ventricular fibrillation and death. This
                    could be extrapolated to mean something similar in
                    humans.

             9.1.6  Other

                    No data available.

        9.2  Chronic poisoning

             9.2.1  Ingestion

                    No data available.

             9.2.2  Inhalation

                    No data available.

             9.2.3  Skin exposure

                    No data available.

             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

             There have been no accidents or suicides involving
             respiratory or dermal exposure leading to recognised signs
             and symptoms of DDT poisoning.
    
             Onset of acute poisoning may be as soon as 30 minutes after
             ingestion of a large dose or as late as 6 hours after smaller
             but still toxic doses.  Recovery from mild poisoning is
             essentially complete in 24 hours, but recovery from severe
             poisoning requires several days.
    
             The earliest symptom of poisoning by DDT is hyperaesthesia of
             the mouth and lower part of the face.  This is followed by
             paraesthesia of the same area and of the tongue and then by
             dizziness, an objective disturbance of equilibrium,
             paraesthesia and tremor of the extremities, confusion,
             malaise, headache, fatigue, and delayed vomiting (probably
             centrally mediated).  Convulsions only occur in severe
             poisoning.  It is not clear whether cardiac arrhythmia might
             be a possible cause of death in acute poisoning. In most
             instances of fatalities following ingestion of DDT solutions,
             the signs and symptoms were predominantly or exclusively
             those of poisoning by the solvent vehicle (Hayes & Laws,
             1991).

        9.4  Systemic description of clinical effects

             9.4.1  Cardiovascular

                    Cardiac arrhythmias have been associated with
                    death following DDT poisoning in some species of
                    laboratory animals, but this may not be the case in
                    acute human poisonings.  Palpitations, tachycardia and
                    irregular heart action have been noted in some cases
                    of acute poisonings (Hayes & Laws, 1991).

             9.4.2  Respiratory

                    The effects of DDT on the respiratory system
                    are secondary to the effects on the nervous system
                    (Hayes & Laws, 1991).

             9.4.3  Neurological

                    9.4.3.1  Central nervous system

                             Dizziness, an objective disturbance
                             of equilibrium, confusion, malaise, headache,
                             fatigue, and delayed vomiting (probably
                             centrally mediated) may occur following
                             ingestion of DDT.  Convulsions only occur in
                             severe poisoning (Hayes & Laws,
                             1991).

                    9.4.3.2  Peripheral nervous system

                             The earliest symptom of poisoning by
                             DDT is hyperaesthesia of the mouth and lower
                             part of the face. This is followed by
                             paraesthesia of the same area and of the
                             tongue, then paraesthesia of the extremities
                             (Hayes & Laws, 1991).

                    9.4.3.3  Autonomic nervous system

                             Increased salivation has been
                             reported in persons who ingested
                             DDT-contaminated food (Hayes & Laws,
                             1991).

                    9.4.3.4  Skeletal and smooth muscle

                             Tremor of the extremities has been
                             reported in persons who ingested
                             DDT-contaminated food (Hayes & Laws,
                             1991).

             9.4.4  Gastrointestinal

                    Except for vomiting, which is probably
                    centrally mediated, the gastrointestinal system has
                    not been affected in acute poisoning (Hayes & Laws,
                    1991).

             9.4.5  Hepatic

                    DDT is a hepatic enzyme inducer. Involvement of
                    the liver has been mentioned in only a small
                    proportion of cases of accidental DDT poisoning (Hayes
                    & Laws, 1991).

             9.4.6  Urinary

                    9.4.6.1  Renal

                             There is no indication of renal damage 
                             in people accidentally poisoned by DDT or 
                             in workers heavily exposed to it (Hayes &
                             Laws, 1991).

                    9.4.6.2  Others

             9.4.7  Endocrine and reproductive systems

                    The effects of DDT on reproduction parameters
                    have been summarised by IARC (1991).  One human study
                    has suggested that there may be a weak relationship
                    between DDT levels in cord blood and low birth weight. 
                    Studies in rodents and rabbits have not demonstrated
                    any teratogenic potential, but exposure of rodents to
                    DDT impaired reproductive functions (e.g.,
                    spermatogenesis, neonatal survival) in some
                    studies.
    
                    DDT is known to interfere with the metabolism and
                    function of steroid hormones.  One  such mechanism is
                    by the induction of hepatic microsomal enzymes which
                    results in an increased conversion of oestrogens,
                    androgens, and glucocorticoids to more polar
                    metabolites.  Increased urinary excretion of the more
                    polar metabolites is usually compensated for by
                    increased steroid biosynthesis (Gosselin et al.,
                    1984).

             9.4.8  Dermatologic

                    Skin irritation results from extensive contact
                    with organochlorine pesticides or with the white
                    petroleum distillate vehicles.

             9.4.9  Eye, ears, nose, throat: local effects

                    Eyes-Acute
    
                    DDT has not been demonstrated to have a selective
                    effect on the eyes.  Pure DDT dissolved in purified
                    kerosene was tested in a concentration of 0.01% on a
                    human eye and caused no discomfort or irritation; it
                    also proved non-irritating at 4% concentration on
                    rabbit eyes.  Rare instances have been reported of
                    ocular irritation following contamination of the eye
                    by powders containing DDT (Grant, 1986).
    

                    Eyes - Chronic
                    In one instance chronic superficial punctate keratitis
                    was associated with fatal poisoning from long exposure
                    to DDT dust, but it was possible that constituents
                    other than DDT were responsible, or that there was
                    hypersensitivity (Grant, 1986).
    
                    Nose and throat-acute
    
                    Volunteers exposed to DDT dispersed into the air
                    either by volatilising units or by continuously or by
                    intermittently operated aerosol dispensers in some
                    instances reported some dryness of the throat, but
                    otherwise the results were negative (Hayes & Laws,
                    1991).

             9.4.10 Haematological

                    In acute poisoning a slight decrease in
                    haemoglobin and a moderate leukocytosis without any
                    constant deviation in the differential white count
                    have been observed in volunteers.  These findings are
                    considered secondary to the neurological
                    effects.

             9.4.11 Immunological

                    DDT appears to have a depressant effect on the
                    immune system although the evidence is by no means
                    conclusive (Hayes & Laws, 1991).

             9.4.12 Metabolic

                    9.4.12.1 Acid base disturbances

                             No data available

                    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

                    Pregnancy
                    The effect of DDT on reproduction parameters have been
                    summarised by IARC (1991).  One human study has
                    suggested that there may be a weak relationship
                    between DDT levels in cord blood and low birth weight. 
                    Studies in rodents and rabbits have not demonstrated
                    any teratogenic potential, but exposure of rodents to
                    DDT impaired reproductive function (e.g.,
                    spermatogenesis, neonatal survival) in some
                    studies.
    
                    Breast feeding
                    Concentrations of DDT in the milk of women in various
                    populations have been reported. Values reported from
                    Guatemala (0.48 to 4.07 ppm total DDT, 1970-1974) and
                    early values from the USSR (1.22 to 4.88 ppm total
                    DDT, 1964) were much higher than those of other
                    countries, and yet there was no indication of illness
                    among babies fed such milk (Hayes & Laws, 1991).
    
                    Enzyme deficiencies
                    DDT is known to interfere with the metabolism and
                    function of steroid hormones.  One such mechanism is
                    by the induction of hepatic microsomal enzymes which
                    results in an increased conversion of oestrogens,
                    androgens, and glucocorticoids to more polar
                    metabolites.  Increased urinary excretion of the more
                    polar metabolites is usually compensated for by
                    increased steroid biosynthesis (Gosselin et al.,
                    1984).
    
                    Individuals on chronic drug therapy with phenobarbitol
                    and/or phenytoin have increased hepatic microsomal
                    enzyme activity.  Watson et al. (1972) suggest that
                    this increased activity accelerates the metabolism of
                    some DDT to DDA by the slow series of
                    dehydrohalogenation reactions.

        9.5  Others

             No data available

        9.6  Summary
    

    10. MANAGEMENT

        10.1 General principles

             Management should be directed towards decontamination
             of the patient especially where hydrocarbon solvents are
             involved.  Care must be taken to minimise further problems,
             due to aspiration of solvents that may follow spontaneous
             emesis or treatment.  Other solvent effects should also be
             monitored.  The patient should be observed carefully
             especially for central nervous system effects such as
             convulsions. Convulsions, hypoxaemia and resultant acidosis
             are the immediate life-threatening emergencies. Diazepam is
             the anticonvulsant of choice.  Moderate to severely poisoned
             patients should have intravenous lines and a cardiac monitor
             in place as DDT also sensitises myocardial tissue.
    
             Affected skin must also be decontaminated.  Wash the area
             well with soap and water.
    
             Oils and fats should not be given.  Do not administer
             adrenaline, other adrenergic amines or stimulants, because of
             the enhanced myocardial sensitivity induced by DDT these may
             induce ventricular fibrillation.

        10.2 Life supportive procedures and symptomatic treatment

             Make a proper assessment of airway, breathing,
             circulation and neurological status of the patient.
    
             Control convulsions with appropriate drug regimen.
    
             Monitor blood pressure and ECG.
    
             Control cardiac dysrhythmias with proper drug regimen (proper
             means).
    
             Monitor acid-base balance.
    
             Where spontaneous emesis has occurred monitor respiratory
             functions and watch for signs of pulmonary aspiration.

        10.3 Decontamination

             Oral exposure:
    
             Emesis is contra indicated.
    
             Perform gastric lavage for recent large ingestions.
    
             Administer activated charcoal. If an oro- or naso-gastric tube
             is in place, administer after lavage through the tube.
    

             If the patient is obtunded, convulsing or comatose, or if the
             poison involved may induce these conditions rapidly, insert
             an oro- or naso-gastric tube and lavage after endotracheal
             intubation.
    
             Inhalation:
    
             Move patient to fresh air and monitor respiratory function.
    
             Eye exposure:
    
             Irrigate exposed eyes with copious amount of water.
             Remove contact lenses. 
    
             Dermal exposure:
    
             Remove and discard contaminated clothing.
             Wash skin with soap and copious amounts of water.

        10.4 Enhanced Elimination

             Elimination techniques such as dialysis, diuresis and
             haemoperfusion have not been shown to be effective due to
             extensive tissue binding and large volume of distribution.

        10.5 Antidote treatment

             10.5.1 Adults

                    No specific antidote is available.

             10.5.2 Children

                    No specific antidote is available.

        10.6 Management discussion

             As body stores diminish, the elimination half-life of
             DDT for the remaining store increases dramatically.  This is
             probably due to complex lipoprotein binding, wherein
             different bound forms exhibit different association
             characteristics. This requires further research and
             clarification in order to understand the mechanism
             sufficiently to be able to successfully mobilise DDT from
             adipose tissue.
    

    11. ILLUSTRATIVE CASES

        11.1 Case reports from the literature

             Oral (food contamination), male, adults
    
             In three men who ate pancakes made with DDT and who ingested
             5 to 6 g each, slight jaundice appeared after 4 to 5 days and
             lasted 3 to 4 days (Hayes & Laws, 1991).
    
             Oral, child
    
             A 2-year-old child drank an unknown quantity of flyspray,
             which 5% was DDT, but the nature of the other active
             ingredients or the solvent was unknown.  About one hour after
             taking the material, the child became unconscious and had a
             generalised, sustained convulsion.  Convulsions were present
             when the child was hospitalised 2 hours post-ingestion, and
             these were controlled by barbiturates and other sedatives. 
             Convulsions re-occurred on Day 4, and again on Day 21, but
             responded to treatment.  On day 12, it was noted that the
             patient was deaf. Hearing began to improve about Day 24 and
             was normal, as were other neurological findings, when the
             patient was seen at 2.5 months after the accident (Hayes &
             Laws, 1991).
    

    12. ADDITIONAL INFORMATION

        12.1 Specific preventive measures

             It is essential that persons intending to use DDT be
             provided with adequate health precautions and other safety
             instructions prior to usage.  This information should be
             provided by the manufacturer in the form of either an
             information leaflet or on a label attached to the DDT
             container.
    
             Protective clothing is important.  Protective measures may
             include wearing a long-sleeved shirt, long trousers or
             overalls, and a hat of some sort.  Respiratory protection
             should be considered.  The label should give these
             details.
    
             Clothing worn during spraying should be washed daily after
             use. Contaminated clothing should be washed separately from
             the general wash to avoid cross-contamination.  When working
             with liquids, there is often a danger of a splash in the
             eyes.  This may damage the eyes. Simple goggles or a face
             shield will protect against this. Eye protection is most
             important if wearing contact lenses, because DDT may get in
             behind the lenses. They must be removed before the eyes are
             washed.
    
             Greater precautions are necessary when mixing the
             concentrated material than when spraying. Measurements should
             be accurate and spillages should be cleaned up promptly.  Mix
             the chemical carefully using a stick or paddle. Ensure there
             is minimal skin exposure by he use of gloves. If any
             concentrate is spilled on the skin, wash it off as soon as
             possible.
    
             The hazards of spraying increase dramatically on a windy day,
             as there is an increased risk of inhaling spray drift or
             contaminating the skin.
    
             Always wash hands before eating, drinking, or smoking.  After
             spraying, shower and change clothing.
    
             By preference, DDT should be stored in a locked shed, safely
             out of reach of children and animals. DDT should also be kept
             away from work areas and separate from other stored materials
             such as animal foods.  Always leave DDT in its original
             containers, or if it must be transferred to another container
             ensure that this is one not normally used for food or drink. 
             This secondary container should be well labelled and of a
             variety that is not likely to leak.
    

             Empty containers must be disposed of carefully, so as to
             ensure that rivers, streams, and other water sources are not
             polluted, and that unsuspecting people or animals are not
             exposed to residues of concentrate.  Crushing or burning,
             followed by burial, is generally the best method.

        12.2 Other

             No data available
    

    13. REFERENCES

        ACGIH (1981) Documentation of the Threshold limit value, 4th
        Ed, American Conference of Governmental Industrial Hygienists,
        Cincinnati, Ohio.
    
        Baselt RC (1982) Disposition of Toxic Drugs and Chemicals in Man
        pp. 220-222, 2nd Edition.  Biomedical Publications, Davis,
        California, USA.
    
        Budavari S, O'Neil MJ, Smith A & Heckleman PE (1989) The Merck
        Index: An encyclopedia of chemicals, drugs and biologicals.  446pp
        11th ed. Merck & CO., Inc, Rahway, N.J., USA.
    
        Chris (1985) Chris hazardous chemical data. US Department of
        Transportation, US Coast Guard, Washington, DC,.
    
        Dot (1987) US Department of Transportation 1987 Emergency Response
        Guide Book.  Office of Hazardous Materials Transportation.
        Research and Special Programs Administration, Washington DC, Guide
        Number 55.
    
        Dreisbach RH & Robertson WO (1987) Handbook of Poisoning:
        Prevention, Diagnosis & Treatment.  Appleton & Lange, Connecticut,
        99-100 pp.
    
        EPA (1982) Manual of analytical methods for the analysis of
        pesticide residues in human and environmental samples.
    
        EPA (1982) Management of Pesticide Poisoning.
    
        Gosselin RE, Smith RP & Hodge HC (1984) Clinical toxicology of
        commercial products, Williams & Wilkins, Baltimore 134-136 pp.
    
        Grant WM (ed) (1986)  Toxicology of the eye, pp. 305-306, 3rd
        edition.  Charles C Thomas, Springfield, Illinois, USA.
    
        Hayes WJ (Jr) & Laws ER (Jr) (eds) (1991) Handbook of pesticide
        toxicology, Academic Press, Inc. 743-780 pp.
    
        Hsieh HC (1954) DDT intoxication in a family of southern Taiwan. 
        Arch. Ind. Hyg. Occup. Med.  10:3 44-346.
    
        IARC (1991) IARC Monograph: Occupational Exposures in Insecticide
        Application and Some Pesticides. Vol. 53 179-248 pp.
    
        IARC (1987) IARC Monographs: An updating of IARC Monographs Vol. 2
        to 42 Supplement 7 440 pp.
    
        Jaga K &  Brosius D (1999) Pesticide exposure: human cancers on
        the horizon. Reviews on Environmental Health.  14(1):39-50
    

        Klaassen CC, Amdur MO & Doull J (eds) (1986) Casarett & Doull's
        Toxicology: The basic science of poisons. 3rd ed. Macmillan
        Publishing Co., New York, pp.  543-549.
    
        Moffat AC (ed) (1986) Clarke's Isolation and Identification of
        Drugs.  2nd Edition The Pharmaceutical Press, London, pp. 143.
    
        OSHA (1989) Department of Labour, Occupational Safety and Health
        Administration: 29 CFR Part 1910; Air contaminants; final rule. 
        Federal register  54(12):2332-2983.
    
        Parmeggiani L. (ed) (1983) Encyclopedia of Occupational Health and
        Safety.  592-593 pp Vol. 1, 3rd (revised) edition. International
        Labour Office, Geneva.
    
        Reingold I & Lasky II (1947) Acute fatal poisoning following
        ingestion of a solution of DDT. Ann. Intern. Med. 26:945-947.
    
        Reynolds JEF (ed) (1989) Martindale: The Extra Pharmacopoeia 29th
        ed, Pharmaceutical Press, London, 1347-1348 pp.
    
        Watson M, Gabica J & Benson WW (1972) Serum organochlorine
        pesticides in mentally retarded patients on differing drug
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        WHO (1979) DDT and its derivatives. Environmental Health Criteria
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        WHO (1984) Guidelines for drinking water quality Vol. 2 Health
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        WHO (1989) DDT and its derivatives - environmental aspects. 
        Environmental Health Criteria 83.  WHO, Geneva 12 pp.
    
        WHO (1995) Pesticide residues in food-1994. Report of the Joint
        meeting of the FAO Panel of Experts on Pesticide Residues in Food
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        FAO Plant Production and Protection paper, 127, 1995. 
    
        Woodward G, Nelson AA & Calvery HO (1944) Acute and sub-acute
        toxicity of DDT (2,2-bis(p-chlorophenyl)-1,1,1-trichloroethane) to
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        Worthing CR & Walker SB (eds) (1987) The pesticide manual: A World
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        pp.
    

    14. AUTHOR(S), REVIEWER(S), DATE (INCLUDING EACH UP-DATE), COMPLETE
        ADDRESSES

        Author:
    
        Dr Nida Besbelli
        Poison Centre
        Refik Saydam Hygiene Institute
        Cemal Grsel Cad. No. 18 Sihhiye
        06100 Ankara
        Turkey
    
        Prepared: February 1990
    
        Reviewers:
    
        Dr Wayne A. Temple
        National Toxicology Group
        University of Otago Medical School
    
        Dr Nerida A. Smith
        Pharmacy School
        University of Otago Medical School
    
        P.O. Box 913
        Dunedin, New Zealand
        Telephone   64 3 4797244
        Facsimile   64 3 4770509
    
        Reviewed:   August 1992
    
        Updated and Peer Reviewed,  Sao Paulo INTOX-11, October 21,1999.
    
        Drs W. Temple, New Zealand- co-ordinator; B. Groszek, Poland; J.
        de Kom, Surinam; J.C. Rios Bustamante, Chile; J.C. Piola,
        Argentina.
    



    See Also:
       Toxicological Abbreviations
       Ddt (ICSC)
       DDT (PDS)
       DDT (JECFA Evaluation)
       DDT (FAO Meeting Report PL/1965/10/1)
       DDT (FAO/PL:CP/15)
       DDT (FAO/PL:1967/M/11/1)
       DDT (FAO/PL:1968/M/9/1)
       DDT (FAO/PL:1969/M/17/1)
       DDT (Pesticide residues in food: 1979 evaluations)
       DDT (Pesticide residues in food: 1980 evaluations)
       DDT (Pesticide residues in food: 1984 evaluations)
       DDT (JMPR Evaluations 2000 Part II Toxicological)