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Dieldrin

1. NAME
   1.1 Substance
   1.2 Group
   1.3 Synonyms
   1.4 Identification numbers
      1.4.1 CAS number
      1.4.2 Other numbers
   1.5 Brand names, Trade names
   1.6 Main manufactures/main importers
2. SUMMARY
   2.1 Main risks and target organs
   2.2 Summary of clinical effects
   2.3 Diagnosis
   2.4 First-aid measures and management principles
3. PHYSICO-CHEMICAL PROPERTIES
   3.1 Origin of the substance
   3.2 Chemical structure
   3.3 Physical properties
      3.3.1 Colour
      3.3.2 Form
      3.3.3 Description (Worthing 1988; Windholz 1983;
   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 Occupational exposed populations
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
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 Dermatological
      9.4.9 Eye, ear, nose and throat: local effects
      9.4.10 Hematological
      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/specific 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)
    1.  NAME

        1.1  Substance

             Dieldrin

        1.2  Group

        1.3  Synonyms

             Common name
             HEOD;dieldrine;

        1.4  Identification numbers

             1.4.1  CAS number

                    60-57-1

             1.4.2  Other numbers

                    UN 1093
                    IUPAC

        1.5  Brand names, Trade names

             Dieldrin
             Alvit
             Octalox
             Panoram
             Quintox
             Cmpound-497
             ENT-16,225
             OMS-18
             To be completed by each centre.

        1.6  Main manufactures/main importers

             The manufacture and import of dieldrin has
             ceased. Formerly importer for Suriname:
             Shell Suriname Verkoopmaatschappij, Sir W.
             Churchillweg, Paramaribo, Suriname.

    2.  SUMMARY

        2.1  Main risks and target organs

             Dieldrin is highly hazardous by the oral and
             dermal routes. The most common form of human
             exposure occur through the ingestion of contaminated
             foodstuff or water, inhalation of vapor, or
             absorption through skin. The later being an
             important factor leading to occupational poisoning
             by dieldrin.
             Dieldrin is persistent in the environment and is not
             readily biodegradable.
             Dieldrin is a central nervous system stimulant.
             No data are available on the teratogenity
             risks.

        2.2  Summary of clinical effects

             Symptoms of poisoning are general malaise,
             headache, sweating, dizziness, nausea and vomiting,
             cardiac arrhythmias, muscular weakness, motor
             hyperexcitability, hyperreflexia, myoclonic jerking,
             and convulsions in severe poisoning. Convulsions may
             be delayed for 48 hours following exposure. Death
             may result from cardiac or respiratory arrest.
             Chronic poisoning may only produce convulsions.

        2.3  Diagnosis

              Clinical features
             Shortly after ingestion toxic doses of dieldrin will
             cause nausea and vomiting, followed by effects of
             neuronal hyperactivity: apprehension, excitability,
             parasthesias, dizziness, headache, disorientation,
             and tremor progressing to stupor, coma and
             convulsions in severe cases. Arrhythmias may occur
             owing to myocardial sensitivity to catecholamines.
             Signs of hepatitis or renal injury may develop.
             Intoxication from acute oral exposure generally
             begins within 45 minutes to several hours. Although
             convulsions may be delayed for 48 hours following
             exposure.
    
              Pharmacological criteria
             Not relevant
    
              Laboratory analysis
             The determination of the concentration of dieldrin
             in blood is useful for the confirmation of the
             diagnosis of dieldrin intoxication, but not of
             importance for clinical management.

        2.4  First-aid measures and management principles

             Treatment is symptomatic, aimed at controlling
             convulsions, coma, and respiratory depression.
             Cardio-circulatory function need to be observed.
    
             To control convulsions use clonazepam IV or diazepam
             IV or per rectum. Once convulsions are controlled
             further treatment with  Phenytoin or Sodium
              Valporate should be continued for a further two to
             four weeks.
              Do not give fats, oils or milk since these will
             assist absorption in the intestinal tract.
    
             If the patient is conscious perform gastric lavage
             for large ingestions, avoiding aspiration into the
             lungs. Followed by intragastic administration of a
             large amount of activated charcoal powder with water
             and a laxative.
             In the case of skin contact remove and discard
             contaminated clothing and wash exposed skin with
             (soap and) copious amounts of water, including hair
             and nails.
    
              Opiates and  adrenaline and nor-adrenaline 
             should only be given with extreme caution.
              Aminophylline, atropine or  oily laxatives 
             should not be administered.
    
             Rescuers must take precautions to avoid personal
             exposure.

    3.  PHYSICO-CHEMICAL PROPERTIES

        3.1  Origin of the substance

             Synthetic

        3.2  Chemical structure

             STRUCTURAL PICTURE:
    
             Molecular formula:C12H8Cl6O
    
             Molecular weight 380.93
    
             Structural names:
    
             (IUPAC)
             (1R,4S,4aS,5R,6R,7S,8S,8aR)-1,2,3,4,10,10-hexachloro-
             1,4,4a,5,6,7,8,8a-octahydro-6,7,-epoxy-1,4:5,8-
             dimehanonaphthalene
    
             (C.A.)
             (1a-alpha,2-beta,2a-alpha,3-beta,6-beta,6a-alpha,7-
             beta,7a-alpha)-3,4,5,6,9,9-hexachloro-
             1a,2,2a,3,6,6a,7,7a-octahydro-2,7:3,6-
             dimethanonaphth[2,3-b]oxirene(9CI)
    
             (Dieldrin is a stereoisomer of endrin and a
             metabolite of aldrin).

        3.3  Physical properties

             3.3.1  Colour

                    white

             3.3.2  Form

                    Solid-crystals

             3.3.3  Description (Worthing 1988; Windholz 1983;

                    Hayes and Laws 1991)
                    Melting point C: 176-177
                    Solubility in water: 0.17mg/L at 20 C:
                    soluble in aromatic and halogenated
                    solvents; moderately soluble in acetone;
                    slightly soluble in mineral oils, other
                    aliphatic hydrocarbons, and
                    alcohols.
                    Vapour Pressure: 400 Pa at 20 C
                    Density: 1.70 at 20 C
                    Stability: stable to alkali, mild acids and to light

                    Reactivity: react with concentrated
                    mineral acids, acid catalysts, acid
                    oxidizing agents, phenols and active
                    metals (iron, copper)
                    Flammability: nonflammable
    
                    Technical dieldrin contains 85% dieldrin
                    and 15% insecticidally active related
                    products. Minimum concentration is 95%
                    of the 85%/15% mixture (not less than
                    80.75% dieldrin).
                    Colour: buff to light brown
                    Melting point: C: 95

        3.4  Hazardous characteristics

             Combustion: with sufficient burning or
             external heat dieldrin will decompose whilst
             emitting toxic fumes. The smoke and fumes could
             be hazardous through inhalation, or absorption
             through the skin (Ellenhorn and Barceloux
             1988).
             Corrosiveness: noncorrosive 
    
             Environmental risks: dieldrin is persistent in
             the environment and is not readily
             biodegradable. Care must be taken in handling
             and use and particularly with waste disposal to
             avoid environmental contamination (Shell
             Agriculture 1990). Is should not be applied to
             any crops, and be kept away from animals and
             all forms of wild life (Shell Agriculture
             1990).
             Dieldrin is not readily decomposed chemically
             and waste material must be burned in a proper
             incinerator (minimum requirements: operating
             temperature of > 1000 C and residence time in
             the flame of at least 2 seconds) (3).

    4.  USES

        4.1  Uses

             4.1.1  Uses

             4.1.2  Description

                    Formerly used to control locusts
                    and tropical disease vectors, such as
                    Glossina spp. and mosquitoes (Worthing
                    1988).
                    Former industrial uses include timber
                    preservation, termite proofing of
                    plastic and rubber coverings of
                    electrical and telecommunications
                    cables, of plywood and building boards
                    and as termite barrier in building
                    construction (Worthing 1988).

        4.2  High risk circumstances of poisoning

             The most common form of human exposure
             occur through the ingestion of contaminated
             foodstuff or water, inhalation of vapor, or
             absorption through skin (Ellenhorn and
             Barceloux 1988). Undoubtedly, relatively
             extensive absorption by the dermal route has
             been an important factor leading to
             occupational poisoning by dieldrin (Hayes and
             Laws 1991).

        4.3  Occupational exposed populations

             Agriculture workers, structural insect
             control, and malaria control programs.

    5.  ROUTES OF EXPOSURE

        5.1  Oral

             Oral ingestion is the commonest route of
             poisoning, usually by the ingestion of
             contaminated foodstuffs or water.
             Oral ingestion may also occur through placing
             contaminated objects in the mouth during
             eating, drinking or smoking, or through
             violation of proper procedures, e.g. blowing
             out clogged spray nozzles by mouth.
             Intentional ingestion may also occur in suicide
             attempts.

        5.2  Inhalation

             Exposures occur through the inhalation of dust
             from powder concentrates, or aerosols from spray of
             liquid formulations while applying.

        5.3  Dermal

             Absorption through intact or damaged skin
             is a significant route of exposure, especially
             when applying.

        5.4  Eye

             Exposure to vapours, dust and aerosols is
             possible.

        5.5  Parenteral

             No data available.

        5.6  Others

             No data available.

    6.  KINETICS

        6.1  Absorption by route of exposure

             Dieldrin is absorbed from the
             gastrointestinal tract, the lungs and through
             intact skin (Windholz 1983, Ellenhorn and
             Barceloux 1988, Moffat 1986).
    
             Both dieldrin powder and solutions are readily
             absorbed after oral ingestion (Moffat 1986).
             Dieldrin is absorbed from the gastrointestinal
             tract via the hepatic portal vein in rats
             (Heath and Vandekar 1964).
             The intestinal absorption will be enhanced by
             the fat content of the diet. It is also
             influenced by the fibre content of the diet as
             well as by the total food intake. The
             absorption of dieldrin is enhanced by
             starvation in rats (Heath and Vandekar
             1964).
    
             Owing to the relatively low vapour pressure
             dieldrin seldom reaches levels in the air above
             those permitted. The extent of absorption by
             inhalation (dust or aerosol), depends on the
             appropriate particle size (Hayes and Laws
             1991).
    
             Dieldrin is readily and effectively absorbed
             through intact skin (Hayes and Laws 1991). Its
             high dermal toxicity does not depend on
             solution. Solid dieldrin, if very finely
             ground, is absorbed through the skin (Hayes and
             Laws 1991).
             Dermal penetration involves not only partition
             coefficients but also binding to various
             dermal, epidermal, and serum sites (Hayes and
             Laws 1991).

        6.2  Distribution by route of exposure

             Dieldrin is selectively stored in body fat
             (Moffat 1986), and may be found in fat of
             people in the general population (Hayes and
             Laws 1991). It persists in body fat for several
             year after cessation of exposure (Moffat 1986,
             Nair et al 1992). Dieldrin may also be found in
             blood and in various organs of people in the
             general population (Hayes and Laws 1991).
             The plasma: whole blood ratio is about 1.5, and
             the protein binding in plasma is more than 99 %
             (Moffat 1986).

             The storage of dieldrin is influenced by other
             chlorinated hydrocarbon insecticides (Hayes and
             Laws 1991). In starvation stored chlorinated
             hydrocarbon insecticides may be released into
             the circulation, sometimes with marked effects
             (Hayes and Law 1991).

        6.3  Biological half-life by route of exposure

             The reported half-life in blood is 50 to
             170 days (mean 97) (Moffat 1986).
             In chronic human exposure to dieldrin a
             half-life of about 1 year may be seen (Hunter
             et al 1969, Jager 1970).

        6.4  Metabolism

             Most organochlorines are metabolised
             slowly (Ellenhorn and Barceloux 1988). In
             common with other lipophilic xenobiotics,
             chlorinated hydrocarbon insecticides can be
             metabolised by the microsomal cytochrome P-450
             system in the liver to mainly unknown
             hydrophilic metabolites (Hayes and Laws 1991,
             Moffat 1986). At least one metabolite of
             dieldrin excreted in the feces has been
             identified (9-hydroxydieldrin) (Richardson and
             Robinson 1971).
             Hepatic enzyme induction can result from
             exposure to dieldrin (Ellenhorn and Barceloux
             1988).

        6.5  Elimination and Excretion

             Dieldrin is eliminated from humans in
             urine and faeces. In urine it is excreted as at
             least two neutral polar metabolites. In faeces
             it may be excreted unchanged, or metabolised.
             At least one metabolite has been identified
             (9-hydroxydieldrin) (Richardson and Robinson
             1971).
             Chlorinated hydrocarbon insecticides are
             excreted in milk, because of the lipid content
             of the milk and high bloodflow to breast tissue
             considerable concentration of these chemicals
             can be present compared to that in tissues.
             Contamination of both cow's and human milk is a
             form of excretion, but also an unique one that
             could lead to toxic effects in the recipient
             (Hayes and Laws 1991).

             Dieldrin or its metabolites are excreted
             rapidly in the bile of rats, with a rate of
             excretion three time greater in males than in
             females (Klevay 1970).
             When dieldrin is given orally to rats it is
             metabolised to compounds that are excreted in
             both faces and urine (respectively
             approximately 90 and 10 %) (Robinson and
             Roberts 1969).

    7.  TOXICOLOGY

        7.1  Mode of action

             Chlorinated hydrocarbon insecticides act
             by altering the electrophysiological and
             associated enzymatic properties of nerve cell
             membranes, causing a change in the kinetics of
             Na+ and K+ ion flow through the membrane.
             Disturbances of calcium transport or Ca2+
             - ATPase activity may also be involved, as well
             as phosphokinase activities (Hayes 1991). A
             major site of action of dieldrin appears to be
             at the synapse in the rat (Hayes and Laws
             1991).

        7.2  Toxicity

             7.2.1  Human data

                    7.2.1.1  Adults

                             The acute adult lethal
                             dose is approximately 1.5-5 g
                             (Steentoft 1979).
                             Although a clinical case is
                             published of a man who survived
                             drinking 9 g (120 mg/kg) of
                             dieldrin in toluene (Black
                             1974). An oral dosage of
                             0.21mg/person/day or 0.0031
                             mg/kg/day was tolerated by
                             volunteers (Hunter and Robinson
                             1967). The estimated absorbed
                             intake corresponding to the
                             safe threshold is 3.6
                             mg/person/day (Hayes and Law
                             1991).
                             A NOEL of 105-200 micrograms/L
                             has been reported (Hayes and
                             Curley 1968; Jager
                             1970).

                    7.2.1.2  Children

                             Toxic doses of approximately
                             29 mg/kg has been reported (Fry 1964).
                             A dosage of 23 mg/kg led to convulsion
                             in a child (Princi 1954).

             7.2.2  Relevant animal data

                    Acute oral LD50: for rats 24-167
                    mg/kg; for birds 10-500 mg/kg.
                    Acute percutaneous LD50: for rats
                    50-120 mg/kg.

             7.2.3  Relevant  in vitro data

                    Sufficient human data is available.

             7.2.4  Workplace standards

                    OSHA PEL, ACGIH TLV: Time Weighted
                    Average 0.25 mg/m3 (skin)
                    DFG MAK: 0.25 mg/m3
                    In Great Britain: 0.25 mg/m3 (long
                    term), 0.75 mg/m3 (short term).

             7.2.5  Acceptable daily intake (ADI)

                    Dieldrin was last reviewed at the
                    FAO/WHO JMPR 1977 when 0-0.0001 mg/kg
                    was confirmed as the estimate of the ADI
                    in man (Worthing 1988).
                    RfD 0.00005mg/kg/day.

        7.3  Carcinogenicity

             Dieldrin has been reviewed by the IARC. Orally
             given to the mouse dieldrin can produce liver tumors
             (Hayes and Law 1991). The significance of the
             marginal increase in incidence of hepatic tumors in
             mice, following lifetime exposure to dieldrin, is
             doubtful (Worthing 1988). In the rat, dog and monkey
             dieldrin is respectively negative and inconclusive
             for the oral hepatocarcinogenicity. The IARC has not
             stated that dieldrin pose no carcinogenic risk to
             humans (Hayes and Law 1991).

        7.4  Teratogenicity

             No data available

        7.5  Mutagenicity

             Chlorinated hydrocarbon insecticides are,
             in general, negative in mutagenicity tests
             (Wildemauwe et al 1983).

        7.6  Interactions

             With chronic exposure, hepatic enzyme
             induction can result (Hayes and Law 1991).

    8.  TOXICOLOGICAL ANALYSES AND BIOMEDICAL INVESTIGATIONS

    9.  CLINICAL EFFECTS

        9.1  Acute poisoning

             9.1.1  Ingestion

                    Toxic doses of dieldrin will
                    cause nausea and vomiting, shortly after
                    ingestion, followed by effects of
                    neuronal hyperactivity: apprehension,
                    excitability, parasthesias, dizziness,
                    headache, disorientation, and tremor
                    progressing to stupor, coma and
                    convulsions in severe cases. Convulsions
                    may be delayed for 48 hours following
                    exposure (Shell Agriculture 1990).
                    Arrhythmias may occur owing to
                    myocardial sensitivity to catecholamines
                    (Olsen 1994). (The solvent for dieldrin
                    may also contribute to these symptoms).
                    Prolonged or repeated exposure may cause
                    convulsions without earlier symptoms
                    (Shell Agriculture 1990).

             9.1.2  Inhalation

                    Dieldrin is well absorbed, the
                    extent depends on the appropriate
                    particle size. Symptoms are basically
                    the same as by ingestion.

             9.1.3  Skin exposure

                    Is a significant route of
                    exposure. Symptoms are basically the
                    same as by ingestion.

             9.1.4  Eye contact

                    Irritation may result. No further
                    data available.

             9.1.5  Parenteral exposure

                    No data available.

             9.1.6  Other

                    No data available.

        9.2  Chronic poisoning

             9.2.1  Ingestion

                    Chronic intoxication may produce
                    convulsions and muscular jerking alone,
                    without prominent signs of poisoning.
                    Headache, dizziness, hyperexcitability,
                    psychological disorders, chest pains,
                    arthralgia, ataxia and incoordination
                    (especially in the Romberg and other
                    tests), nystagmus, tremor of hands,
                    sweating, dermatographia, loss of recent
                    memory, tachycardia and severe
                    impairment of spermatogenesis, may be
                    detected in some patients (Hayes and Laws
                    1991; Cassertt and Doull`s 1996).

             9.2.2  Inhalation

                    No data available.

             9.2.3  Skin exposure

                    Skin rashes may occur.

             9.2.4  Eye contact

                    Irritation may result. No further
                    data available.

             9.2.5  Parenteral exposure

                    No data available.

             9.2.6  Other

                    No data available.

        9.3  Course, prognosis, cause of death

             Intoxication from acute oral exposure
             generally begins within 45 minutes to several
             hours. In mild poisoning headache, dizziness
             and nausea occur. Severe poisoning progresses
             to vomiting, muscular weakness, coma and
             convulsions.
             Since chlorinated hydrocarbons are highly
             lipid-soluble, the duration of toxicity may be
             prolonged.

             Recurrent or delayed-onset seizures have been
             reported. Also severe poisoning producing coma
             without observed convulsions has been reported.
             Signs of hepatitis or renal injury may develop
             without earlier symptoms. Death may result from
             cardiac arrest.
             Chronic intoxication may produce convulsions alone
             (Shell Agriculture 1990; Ellenhorn and Barceloux 1988;
             Olsen 1994).

        9.4  Systemic description of clinical effects

             9.4.1  Cardiovascular

                    Arrhythmias (eg tachycardia) may occur
                    owing to myocardial sensitivity to
                    catecholamines (Olsen 1994).

             9.4.2  Respiratory

                    No data available.

             9.4.3  Neurological

                    9.4.3.1  Central Nervous System

                             Dieldrin is a CNS
                             stimulator resulting in
                             apprehension, excitability,
                             parasthesia, dizziness,
                             disorientation, tremor, and
                             convulsions in severe
                             cases.
                             A temporary change of
                             personality characterised by 
                             fear, weeping, difficulty in
                             sleeping, bad dreams, mania, or
                             other inappropriate behaviour
                             has been reported in a few
                             accidental and occupational
                             cases.
                             Abnormal performance of various
                             psychological tests
                             administered to sprayers has
                             been reported (Ibanez-Peterson
                             and DeFranzanetti 1957).

                    9.4.3.2  Peripheral nervous system

                             Paraesthesia. No further
                             data available.

                    9.4.3.3  Autonomic nervous system

                             No data available.

                    9.4.3.4  Skeletal and smooth muscle

                             Some persons poisoned
                             by dieldrin have experienced
                             sudden contraction of a major
                             muscle, sometimes sufficient to
                             move a part of the body or
                             cause a person to fall. In
                             extreme cases, these movements
                             were accompanied by momentary
                             loss of consciousness (Hayes
                             and Laws 1991).

             9.4.4  Gastrointestinal

                    The only, non specific clinical
                    effects, reported shortly after acute
                    ingestion are nausea and vomiting.

             9.4.5  Hepatic

                    It is still inconclusive if
                    dieldrin can induce hepatocellular
                    carcinoma in humans (Hayes and Laws
                    1991).
                    After ingestion, signs of hepatitis may
                    develop (Olsen 1994).

             9.4.6  Urinary

                    9.4.6.1  Renal

                             After ingestion signs
                             of renal injury (haematuria and
                             albuminuria) may develop (Olsen
                             1994).

                    9.4.6.2  Others

                             No data available.

             9.4.7  Endocrine and reproductive systems

                    No data available.

             9.4.8  Dermatological

                    Dieldrin may cause a nonspecific
                    dermatitis. Persons with chronic skin disease
                    may be in special danger from occupational
                    exposure to dieldrin (Hayes and Laws 1991).

             9.4.9  Eye, ear, nose and throat: local effects

                    No data available.

             9.4.10 Hematological

                    Aplastic anaemia.

             9.4.11 Immunological

                    A rare case of an autoimmune
                    haemolytic anaemia cured by splenectomy,
                    with the presence of antidieldrin IgG
                    antibodies in the serum and on the red
                    cell membrane is reported (Hayes and
                    Laws 1991).

             9.4.12 Metabolic

                    9.4.12.1 Acid-base disturbances

                             Metabolic acidosis.

                    9.4.12.2 Fluid and electrolyte disturbances

                             No data available.

                    9.4.12.3 Others

                             No data available.

             9.4.13 Allergic reactions

                    Dieldrin may cause a dermagrapghia and
                    dermatitis.

             9.4.14 Other clinical effects

                    A case resembling radiculomyelitis 
                    was attributed to dieldrin. It's the only 
                    case described and so far reported
                    (Urbanska-Bonenberg and Langauer-Lewowicka 1966).
                    Case report also exists were the temperature has
                    reduced.

             9.4.15 Special risks

                    Pregnancy: No data available.
    
                    Breast feeding: Chlorinated hydrocarbon
                    insecticides are excreted in milk. The
                    lipid content of the milk and high
                    bloodflow to breast tissue can lead to
                    considerable concentration of these
                    chemicals compared to that in tissues.
                    Infants in countries with a large use of
                    insecticides can be at particular risk,
                    especially since breast feeding is
                    recommended by the WHO and other
                    agencies (Hayes and Laws 1991).
    
                    Enzyme deficiencies: No data available.

        9.5  Others

             No data available.

        9.6  SUMMARY

    10. MANAGEMENT

        10.1 General principles

             Whether first attention is given in a
             particular case to removal of the poison or to
             sedation must depend on the condition of the
             patient at the time.
    
             Treatment is symptomatic, aimed at controlling
             convulsions, coma, and respiratory
             depression.
             Cardiovascular function needs to be observed.
             If ingested, gastric lavage may be indicated,
             followed by activated charcoal powder.
    
              Opiates should only be administered with
             extreme caution because of their depressive
             effects on the respiratory centre.  Adrenaline
              and nor-adrenaline should only be
             administered with extreme caution, because they
             may sensitise the myocardium and thus provoke
             serious cardiac arrhythmias.  Aminophylline,
             atropine or  oily laxatives should not be
             administered.

        10.2 Life supportive procedures and symptomatic/specific
             treatment

             Make a proper assessment of airway,
             breathing, circulation and neurological status
             of the patient.
    
             Maintain a clear airway. Support ventilation
             using appropriate mechanical device. Administer
             oxygen.
    
             Control convulsions with appropriate drug
             regimen. Drugs of choice are clonazepam IV or
             diazepam IV or per rectum.
    
             Monitor blood pressure and ECG. Control cardiac
             dysrrhythmias with proper drug regimen (proper
             means).

        10.3 Decontamination

             Skin contact:
             Remove and discard contaminated clothing.
             Wash exposed skin with (soap and) copious
             amounts of water, including hair and nails.
    

             Eye contact:
             Irrigate exposed eyes with copious amounts of
             water (or saline).
    
             Ingestion:
             Emesis is contraindicated because of the risk
             of abrupt onset of seizures. If the patient is
             conscious perform gastric lavage for large
             ingestion, avoiding aspiration into the lungs.
             This should be followed by intragastric
             administration of a large amount of activated
             charcoal powder (50-200g) with water and a
             water soluble cathartic. Do not give fats, oils
             or milk as these will assist absorption in the
             intestinal tract.
             Gastric lavage is indicated if patient seen
             within 4 hours of ingestion.
             In the case of ingestion of a solution, or an
             emulsifiable concentrate, a risk of chemical
             pneumonitis following aspiration exist.

        10.4 Enhanced Elimination

             Enhanced elimination is not indicated
             because of the large volume of distribution of
             chlorinated hydrocarbon insecticides.

        10.5 Antidote treatment

             10.5.1 Adults

                    There is no specific antidote.

             10.5.2 Children

                    There is no specific antidote.

        10.6 Management discussion

             The use of activated charcoal in the
             treatment of an acute dieldrin intoxication is
             fully established. Repeated dosing may be
             beneficial as it partially interrupts the
             entero-hepatic circulation (Hayes and Laws
             1991).
    
             If clonazepam or diazepam are not available,
             barbiturates administered slowly by intravenous
             or intramuscular injection can be used, eg
             phenobarbitone (Shell Agriculture 1990). Major
             side effects of the treatment with barbiturates
             are sedation, respiratory depression,
             hypotension, shock, apnoea and laryngospasm
             (KNMP 1996).
    

             When convulsions are under control and do not
             recur it is recommended that treatment is
             continued with  Phenytoin (or Sodium
              Valporate), for 2 to 4 weeks (Shell
             Agriculture 1990).

    11. ILLUSTRATIVE CASES

        11.1 Case reports from literature

             A man who attempted suicide by drinking 9
             g (120 mg/kg) of dieldrin in toluene did not
             regain full consciousness until 5 days later;
             headache and disturbance of short-term memory
             persisted for several weeks, and there was
             evidence of mild liver damage. Convulsions were
             so severe and persistent in spite of
             conventional treatment that it seems unlikely
             that the patient would have survived without
             heroic treatment, including profound muscular
             paralysis induced by pancuroniumbromide,
             intermittent positive pressure ventilation, and
             -sympathetic blockade (Black 1974).
    
             A foodborne outbreak affecting a large number
             of people by dieldrin-contaminated rice in
             Mali, of whom 79 were studied epidemiologically
             was reported by the WHO. In most cases onset
             was 0.5-1.5 hr after the rice was eaten, and
             the delay never exceeded 6 hr. Signs and
             symptoms included convulsions aching muscles,
             vomiting, vertigo, and fainting. Contamination
             of the rice was attributed to the use of
             dieldrin to kill rats and insects in the
             building where the grain had been stored (WHO
             1977).

    12. ADDITIONAL INFORMATION

        12.1 Specific preventive measures

             Rescuers must take precautions to avoid
             personal exposure.

             The manufacture of dieldrin has ceased.
             Disposal of any remaining stocks should be done
             with care to avoid contamination of the
             environment. Disposal can be done by burning
             the remaining stock in a proper incinerator
             designed for chlorinated hydrocarbon
             insecticides waste disposal. Seek further
             advice from the local distributor or poisons
             centre.

        12.2 Other

             No data available

    13. REFERENCES

        1.   Worthing CR (1988) The Pesticide Manual, 8th ed, 4580.
        2.   Windholz M ed (1983) The Merck Index: an encyclopaedia
             of chemicals, drugs, and biologicals, 10th ed. Rahway,
             New Jersey, Merck and Co., Inc.
        3.   Shell agriculture (1990) Safety guide, Shell
             International Chemical Company Limited Crop
             Protection Division Shell Centre London, 35-36,
             71-75.
        4.   Ellenhorn MJ and Barceloux DG (1988) Medical Toxicology:
             Diagnosis and treatment of human poisoning, Elsevier,
             Amsterdam, 1078-1080.
        5.   Hayes WJ jr. and Laws ET jr. eds. (1991) Handbook of
             Pesticide Toxicology, Academic Press Inc., San
             Diego, 732-735, 741, 828, 832, 836-840.
        6.   Moffat AC (1986) Clarke's Isolation and
             Identification of drugs 2nd ed., The Pharmaceutical
             Press London, 536-537.
        7.   Heath DF and Vandekar M (1964) Toxicity and
             metabolism of dieldrin in rats. Br J Ind
             Med, 21:269-279.
        8.   Robinson J & Roberts M (1969) Estimation of the exposure
             of the general population to dieldrin (HEOD). Food
             Cosmet Toxicol, 7:501-514.
        9.   Hunter CG, Robinson J & Roberts M (1969)
             Pharmacodynamics of dieldrin (HEOD). Ingestion by
             human subjects for 18 to 24 months and postexposure
             for eight months. Arch Environ Health, 18:12-21.
        10.  Jager KW ed (1970) Aldrin, Dieldrin, Endrin and
             Telodrin, Am. Elsevier, New York.
        11.  Richardson A and Robinson J (1971) The
             identification of a major metabolite of HEOD
             (dieldrin) in human feces. Xenobiotica,
             1:213-219.
        12.  Klevay LM (1970) Dieldrin excretion by the isolated
             pefused rat liver: A sexual difference. Toxicol Appl
             Pharmacol, 17:813-815.
        13.  Steentoft A (1979) A case of fatal dieldrin
             poisoning. Med Sci Law, 19:268-269.
        14.  Black AMS (1974) Self poisoning with dieldrin: A
             case report and pharmacokinetic discussion.
             Anaesthesiol Intens Care, 2:369-374.
        15.  Hunter CG & Robinson (1967) J Pharmacodynamics of
             dieldrin (HEOD) I. Ingestion by human subjects for
             18 months. Arch Environ Health, 15:614-626.
        16.  Fry DR (1964) Human dieldrin poisoning. Lancet,
             1:764.
        17.  Wildemauwe C, Lontie J-F, et al. The mutagenicity in
             procaryocytes of insecticides, acaricides, and
             nematicides. Residue Rev 1983; 89:129-178 (Hayes
             735)

        18.  Olson KR ed. (1994) Poisoning and Drug Overdose, 2nd
             ed. Appleton & Lange Connecticut, 129-130.
        19.  Ibaez-Peterson EH & DeFranzetti RP (1957)
             Psychometric studies and their clinical value in
             dieldrin spraymen. Bol Of Sanit Panam 43:531-533 (in
             Spanish).
        20.  Urbanska-Bonenberg L & Langauer-Lewowicka H (1966)
             Polyorganic toxic action of dieldrin. Med Pr 17:
             336-339.
        21.  KNMP (1996) Informatorium Medicamentorum 1996 deel 1,
             Koninklijke Nederlandse Maatschappij ter bevordering der
             Pharmacie's-Gravenhage.
        22.  World Health Organization (WHO) (1977) Outbreak of food
             poisoning of chemical origin. Wkly Epidemiol Rec,
             52:217.
             Nair A., Dureja P., and Pillai MKK. Aldrin and Dieldrin
             Residues in Human Fat, Milk and Blood Serum Collected
             from Delhi. Human & Experimental Toxicology. 
             11;43-45.
             Princi 1954 from Hayes and Law 1991
             Casarett and Doull's Toxicology: The basic science
             of poisons. Ed. Klaassen CD. 1996

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

        Author:     J.F.M. de Kom
                    Drug and Poisons Information Centre
                    Diakonessen Hospital
                    Zinniastraat/Bodegravenlaan
                    Paramaribo
                    Suriname
    
        Telephone:  597 499644
        Fax:        597 499224
        E-Mail:     dekomj@sr.net
    
        Date:       March 1996
    



    See Also:
       Toxicological Abbreviations
       Dieldrin (ICSC)
       Dieldrin (FAO Meeting Report PL/1965/10/1)
       Dieldrin (FAO/PL:CP/15)
       Dieldrin (FAO/PL:1967/M/11/1)
       Dieldrin (FAO/PL:1968/M/9/1)
       Dieldrin (FAO/PL:1969/M/17/1)
       Dieldrin (AGP:1970/M/12/1)
       Dieldrin  (IARC Summary & Evaluation, Supplement7, 1987)
       Dieldrin (IARC Summary & Evaluation, Volume 5, 1974)