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Aldrin

1. NAME
   1.1 Substance
   1.2 Group
   1.3 Synonyms
   1.4 Identification numbers
      1.4.1 CAS number
      1.4.2 Other numbers
   1.5 Main brand names/main trade names
   1.6 Main manufacturers/main importers
2. SUMMARY
   2.1 Main risks and target organs
   2.2 Summary of clinical effects
   2.3 Diagnosis
   2.4 First-aid measures and management principles
3. PHYSICO-CHEMICAL PROPERTIES
   3.1 Origin of the substance
   3.2 Chemical structure
   3.3 Physical properties
      3.3.1 Colour
      3.3.2 State/from
      3.3.3 Description
   3.4 Hazardous characteristics
4. USES
   4.1 Uses
      4.1.1 Uses
      4.1.2 Description
   4.2 High risk circumstance of poisoning
   4.3 Occupationally exposed populations
5. ROUTES OF ENTRY
   5.1 Oral
   5.2 Inhalation
   5.3 Dermal
   5.4 Eye
   5.5 Parenteral
   5.6 Others
6. KINETICS
   6.1 Absorption by route of exposure
   6.2 Distribution by route of exposure
   6.3 Biological half-life by route of exposure
   6.4 Metabolism
   6.5 Elimination 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 ANALYSIS AND BIOMEDICAL INVESTIGATIONS
   8.1 Material sampling plan
      8.1.1 Sampling and specimen collection
         8.1.1.1 Toxicological analyses
         8.1.1.2 Biomedical analyses
         8.1.1.3 Arterial blood gas analysis
         8.1.1.4 Haematological analyses
         8.1.1.5 Other (unspecified) analyses
      8.1.2 Storage of laboratory samples and specimens
         8.1.2.1 Toxicological analyses
         8.1.2.2 Biomedical analyses
         8.1.2.3 Arterial blood gas analysis
         8.1.2.4 Haematological analyses
         8.1.2.5 Other (unspecified) analyses
      8.1.3 Transport of laboratory samples and specimens
         8.1.3.1 Toxicological analyses
         8.1.3.2 Biomedical analyses
         8.1.3.3 Arterial blood gas analysis
         8.1.3.4 Haematological analyses
         8.1.3.5 Other (unspecified) analyses
   8.2 Toxicological Analyses and Their Interpretation
      8.2.1 Tests on toxic ingredient(s) of material
         8.2.1.1 Simple qualitative test(s)
         8.2.1.2 Advanced qualitative confirmation test(s)
         8.2.1.3 Simple quantitative method(s)
         8.2.1.4 Advanced quantitative method(s)
      8.2.2 Tests for biological specimens
         8.2.2.1 Simple qualitative test(s)
         8.2.2.2 Advanced qualitative confirmation test(s)
         8.2.2.3 Simple quantitative method(s)
         8.2.2.4 Advanced quantitative method(s)
         8.2.2.5 Other dedicated method(s)
      8.2.3 Interpretation of toxicological analyses
   8.3 Biomedical investigations and their interpretation
      8.3.1 Biochemical analysis
         8.3.1.1 Blood, plasma or serum
         8.3.1.2 Urine
         8.3.1.3 Other fluids
      8.3.2 Arterial blood gas analyses
      8.3.3 Haematological analyses
      8.3.4 Interpretation of biomedical investigations
   8.4 Other biomedical (diagnostic) investigations and their interpretation
   8.5 Overall interpretation of all toxicological analyses and toxicological investigations
9. CLINICAL EFFECTS
   9.1 Acute poisoning
      9.1.1 Ingestion
      9.1.2 Inhalation
      9.1.3 Skin exposure
      9.1.4 Eye contact
      9.1.5 Parenteral exposure
      9.1.6 Other
   9.2 Chronic poisoning
      9.2.1 Ingestion
      9.2.2 Inhalation
      9.2.3 Skin exposure
      9.2.4 Eye contact
      9.2.5 Parenteral exposure
      9.2.6 Other
   9.3 Course, prognosis, cause of death
   9.4 Systematic description of clinical effects
      9.4.1 Cardiovascular
      9.4.2 Respiratory
      9.4.3 Neurological
         9.4.3.1 Central Nervous System (CNS)
         9.4.3.2 Peripheral nervous system
         9.4.3.3 Autonomic nervous system
         9.4.3.4 Skeletal and smooth muscle
      9.4.4 Gastrointestinal
      9.4.5 Hepatic
      9.4.6 Urinary
         9.4.6.1 Renal
         9.4.6.2 Other
      9.4.7 Endocrine and reproductive systems
      9.4.8 Dermatological
      9.4.9 Eye, ears, nose, throat: local effects
      9.4.10 Haematological
      9.4.11 Immunological
      9.4.12 Metabolic
         9.4.12.1 Acid-base disturbance
         9.4.12.2 Fluid and electrolyte disturbance
         9.4.12.3 Others
      9.4.13 Allergic reactions
      9.4.14 Other clinical effects
      9.4.15 Special risks
   9.5 Other
   9.6 Summary
10. MANAGEMENT
   10.1 General principles
   10.2 Life support 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)
    ALDRIN

    International Programme on Chemical Safety
    Poisons Information Monograph 573
    Chemical

    1.  NAME

        1.1  Substance

             Aldrin

        1.2  Group

             Diene-organochlorine or chlorinated 'cyclodiene' insecticide

        1.3  Synonyms

             Common names: 

             Aldrin; 
             Aldrine;
             HHDN;
             Compound 118;
             Octalene;
             OMS 194.

             Chemical names: 

             Hexachloro-hexahydro-endo-exo-dimethanonaphthalene;
             1,2,3,4,10,10-hexachloro-1,4,4a,5,8,8a-hexahydro-1,4:5,8-
             dimethanonapthalene

        1.4  Identification numbers

             1.4.1  CAS number

                    309-00-2

             1.4.2  Other numbers

                    NIOSH RTECS:         IO2100000
                    EPA hazardous waste: P004
                    OHM/TADS:            7215090
                    DOT/UN/NA/IMCO:      IMO6.1NA2762
                    HSDB (1992):         199
                    NCI:                 C00044

        1.5  Main brand names/main trade names

             Aldrex; Altox; Drinox; Octalene; Toxadrin

        1.6  Main manufacturers/main importers

             1948-1974:    J Hyman & Co., Denver, CO, USA
             1954-1990:    Shell Chemical Corporation, Pernis, The
                           Netherlands

    2.  SUMMARY

        2.1  Main risks and target organs

             The CNS seems to be the primary site with resultant
             seizures. Toxic exposures produce tremors, giddiness,
             hyperexcitability, seizures, and coma.  Few case reports of
             fatalities exist. Poisoning occurs mainly through absorption
             through the skin. Epidemiological studies do not show any
             carcinogenic risk.

        2.2  Summary of clinical effects

             Absorption can occur by inhalational, dermal, and
             gastrointestinal routes.  Clinical toxicity from aldrin
             actually is due to its rapid metabolism in the body to
             dieldrin. Symptoms reflect CNS toxicity due to GABA
             neurotransmission inhibition:  headache, tremors, giddiness,
             hyperexcitability, seizures and coma.  Most deaths are
             intentional or accidental exposures to concentrated amounts.
             Aldrin is used in various formulations which include
             emulsifiable concentrates, wettable powders, granules, dusts
             and solutions in hydrocarbon liquids (deJong, 1991).

        2.3  Diagnosis

             The diagnosis is based on the history of exposure
             (dermal, inhalational or gastrointestinal) and signs of CNS
             hyperexcitability including seizures.
    
             Blood levels of dieldrin (as aldrin is rapidly metabolized to
             dieldrin) help confirm the exposure (to aldrin or dieldrin)
             where available, although treatment will be determined by
             clinical status.  Background levels of dieldrin in the
             general population is in the order of 1 ng/mL.

        2.4  First-aid measures and management principles

             Skin decontamination should occur when dermal absorption
             is suspected, along with protection of healthcare
             workers.
    
             Because of the potential for seizures, do not induce
             vomiting. Gastric lavage can be performed after adequate
             airway protection, in cases where large amounts (greater than
             1 mg/kg) of concentrated product has been ingested and the
             patient presents early.

    
             Standard supportive care is recommended in severe
             cases.

    3.  PHYSICO-CHEMICAL PROPERTIES

        3.1  Origin of the substance

             Manufactured by the Diels-Alder condensation of
             hexachlorocyclopentadiene with 
             bicyclo[2.2.1]-2,5-heptadiene.

        3.2  Chemical structure

             C12H8Cl6
    
             MW:    364.91

        3.3  Physical properties

             3.3.1  Colour

                    Pure aldrin is a white crystalline solid.
                    Technical grade aldrin is tan in colour.

             3.3.2  State/from

                    Crystalline solid.

             3.3.3  Description

                    Aldrin has a mild chemical odor, and is very
                    soluble in most organic solvents (aromatics, esters,
                    ketones, paraffins, halogenated solvents).
    
                    Density: 1.7 g/L at 20C
    
                    Conversion factor: 1 ppm = 14.96 mg/m3 at 25C, 1 atm
    
                    (ATSDR, 1993)

    3.4  Hazardous characteristics

             Melting point:            104C (pure), 40 to 60C
                                       (technical grade)
    
             Boiling point:            145C
    
             Impurities of aldrin include octachlorocyclopentene  (0.4%),
             hexachloro-butadiene (0.5%), toluene (0.6%), a complex
             mixture of compounds formed by polymerization during the
             aldrin reaction (3.7%) and carbonyl compounds (2%) (FAO/WHO,
             1968).

    4.  USES

        4.1  Uses

             4.1.1  Uses

             4.1.2  Description

                    Aldrin is a very effective soil insecticide and
                    has been used to treat seed also.  It has been used to
                    control termites, corn rootworms, seed corn beetle,
                    seed corn maggot, wireworms, rice water weevil,
                    grasshoppers, and Japanese beetles.  It also is used,
                    in an emulsifiable concentrate or wettable powder, to
                    protect wooden structures from termite destruction
                    both pre- and post-construction in building exteriors. 
                    It is also used to coat and protect rice.  Additional
                    use includes soil treatment for non-food crops (de
                    Jong, 1991).

        4.2  High risk circumstance of poisoning

             In countries where aldrin is used for treating crops and
             grain, severe acute poisoning (accidental or intentional) may
             occur. Higher rates of exposure may occur in homes treated
             with aldrin for termite control.  Air concentrations of
             dieldrin were elevated in home interior areas (Dobbs &
             Williams, 1983). However, the concentration that was measured 
             (0.3 to 75 mg/m3 ) in crawl spaces and in slab houses during
             application was less than most threshold limit values, time
             weighted average (Marlow et al., 1982).  This seems to imply
             that workers may not be seriously exposed as long as they are
             wearing appropriate equipment; household members may get low
             level, long term exposure contributing to their overall body
             burden.  In public buildings contamination may occur, and in
             one school building hard surfaces and carpets had the highest
             concentrations of aldrin (Calder et al., 1993).
    
             Persons living near hazardous waste sites may potentially be
             exposed to dieldrin (as aldrin would be expected to decompose
             to dieldrin) from contamination of water supplies.  In one
             community built over contaminated soil, Acceptable Dietary
             Intake (ADI) limits were exceeded (Van Wijnen & Stijkel,
             1988).

        4.3  Occupationally exposed populations

             Since aldrin is no longer manufactured, production
             workers are currently not exposed.  However, aldrin is still
             used in certain countries and pest control operators and
             field workers may have significant exposures.  Hazardous
             waste site clean-up workers potentially may be exposed
             (ATSDR, 1993).

    5.  ROUTES OF ENTRY

        5.1  Oral

             Aldrin is readily absorbed after ingestion.

        5.2  Inhalation

             Aldrin vapor is absorbed by inhalation.

        5.3  Dermal

             Aldrin is readily absorbed after dermal contact, and is
             variable depending on the type of solvent used.

        5.4  Eye

             No data available.

        5.5  Parenteral

             No data available.

        5.6  Others

             Not applicable.

    6.  KINETICS

        6.1  Absorption by route of exposure

             Skin absorption rate not available (ATSDR, 1993). 
             Gastrointestinal absorption rate not available.  Respiratory
             absorption occurs; expiratory aldrin concentrations are
             decreased compared to inspired concentrations. However,
             dieldrin blood concentrations remained below 1 ng/L (de Jong,
             1991; Bragt et al., 1984; Beyermann & Eckrich, 1973).

        6.2  Distribution by route of exposure

             Oral
    
             Aldrin is rapidly converted to dieldrin primarily in the
             liver.  Consequently little aldrin is found in the blood or
             tissues. Dieldrin is found in a ratio of 156:1
             (adipose:blood) in the body (Hunter & Robinson, 1967). 
             Autopsy cases show dieldrin levels in brain (0.0061 mg/kg
             white matter, 0.0047 mg/kg grey matter), liver (0.03 mg/kg)
             and adipose tissue (0.13 to 0.36 mg/kg) (Adeshina & Todd,
             1990; Ahmad et al., 1988; Holt et al., 1986; DeVlieger et
             al., 1968).

        6.3  Biological half-life by route of exposure

             After chronic, oral human exposure, blood dieldrin
             concentration decreases exponentially following first order
             kinetics with an estimated half-life of 369 days (Hunter et
             al., 1969).  No information is available for other routes of
             exposure.

        6.4  Metabolism

             Aldrin is quickly metabolized to dieldrin, mediated by
             the mixed-function mono-oxygenases. Liver tissue has the
             largest activity but several other organs such as the lung
             and skin also have this enzymatic process. Dieldrin is then
             metabolized at a much slower rate to hydrophilic metabolites
             (de Jong, 1991; ATSDR, 1993).

        6.5  Elimination and excretion

             Elimination occurs primarily through the feces via the
             bile. 9-Hydroxydieldrin seems to be the major metabolite
             excreted. Dieldrin is also excreted in breast milk (ATSDR,
             1993; Richardson & Robinson, 1971). Small amounts (3 to 8%)
             of dieldrin metabolites are excreted in the urine after
             either topical or intravenous administration (Feldman &
             Maibach, 1974). Dieldrin metabolites may also be found in the
             urine after ingestion.

    7.  TOXICOLOGY

        7.1  Mode of action

             Aldrin and dieldrin may have several modes of action.
             First, it may increase pre-synaptic neurotransmitter release.
             In addition, aldrin and dieldrin may inhibit  GABA (gamma
             aminobutyric acid) mediated neuroinhibition  (ATSDR, 1993;
             Obata et al., 1988;  Gant et al., 1987; Abalis et al., 1986;
             Cole & Casida, 1986; Bloomquist et al., 1986; Bloomquist &
             Soderlund, 1985; Lawrence & Casida, 1984).

        7.2  Toxicity

             7.2.1  Human data

                    7.2.1.1  Adults

                             An acute convulsive episode may
                             occur without, or with minor, development of
                             warning symptoms when the dieldrin blood
                             concentration reaches 200 g/L or higher.
                             Repetitive, small dose exposures to aldrin
                             may cause dieldrin to  accumulate and cause
                             symptoms of intoxication (de Jong, 1991).

                             Concentrations of dieldrin in the blood
                             correlate with toxicity.  Asymptomatic people
                             had concentrations in the blood ranging from
                             0.5 to 2 g/L (IPCS, 1989a).  Blood levels
                             greater than 105 g/L are needed to develop
                             toxicity; this corresponds to a daily intake
                             of 0.02 mg dieldrin/kg/day (IPCS, 1989a).
                             Dieldrin concentrations in adipose tissue
                             range from 0.1 to 0.3 mg dieldrin per kg body
                             fat (IPCS, 1989a)  Exposure may occur through
                             only one route or through a combination of
                             dermal, inhalational or gastrointestinal
                             absorption (de Jong, 1991). Acute ingestion
                             of 25.6 mg/kg with resulting severe toxicity
                             has been reported with survival (Smith,
                             1991).

                    7.2.1.2  Children

                             There have been few cases of aldrin
                             toxicity (accidental) in children with
                             resulting signs of CNS stimulation similar to
                             adults.  Death has occurred after acute
                             ingestion of 8.2 mg/kg (Smith,1991).
                             Theoretically the very young are at risk
                             because of their smaller rates of glucoronide
                             conjugation and subsequent excretion
                             (Calabrese, 1978).  The fetus concentrates
                             dieldrin, and the possibility of contaminated
                             breast milk consumption increase the risk of
                             CNS effects in the very young (IPCS, 1989a;
                             Polishuk et al., 1977).  However, based on
                             average breast milk dieldrin concentrations
                             (up to 6 /L) and a child drinking
                             approximately 150 mL milk/kg body weight, the
                             estimated daily intake would be 0.15 to 0.9
                             g dieldrin/kg body weight (IPCS, 1989a).
                             Other estimates place this estimated daily
                             intake at 0.65 to 0.70 g/day for the first
                             four months of breast feeding (Acker et al.,
                             1984).  Because of these small levels, the
                             presence of dieldrin in the blood is
                             considered clinically
                             insignificant.

             7.2.2  Relevant animal data

                    Oral LD50 (rats) is 39 to 64 mg/kg (Gaines,
                    1960; Treon et al., 1952).  Chronic exposure for six
                    weeks showed an increase in rat mortality at doses of
                    8 mg/kg/day (NCI, 1978).

                    Inhalation exposure to aldrin in several species
                    resulted in death in at least some of each species at
                    levels greater than 108 mg/m3 (Treon et al., 1957).
                    Single dermal applications (in xylene) produce death
                    in 50% of animals given 98 mg/kg/day (Gaines, 1960).

                    Oral administration of aldrin to rats causes
                    convulsions like in humans, at doses of 10 mg/kg/day
                    (Mehrotra et al., 1989).

             7.2.3  Relevant in vitro data

                    Aldrin (1 to 1000 mol/L) induced unscheduled
                    DNA synthesis in SV-40 transformed human fibroblast
                    cells (VA-4) both in the presence and absence of rat
                    liver  microsomes (Ahmed et al., 1977; Zelle & Lohman,
                    1977).
    
                    The DNA breakage rates in an Escherichia coli plasmid
                    after treatment with aldrin or dieldrin did not 
                    differ from those in untreated plasmid DNA, suggesting
                    that, at least in these studies, the compounds did not
                    interact directly with DNA (Griffin & Hill, 1978).
    
                    The effects of aldrin and dieldrin (both at 100 g/mL)
                    on the uptake of tritiated thymidine by cultured rat
                    thymocytes and human lymphocytes were tested under
                    different experimental conditions. Both compounds
                    appeared to have marginal effects on thymidine uptake,
                    suggesting inhibition of DNA synthesis (Rocchi et al.,
                    1980).
    
                    Aldrin  (100 mmol/L)  and  dieldrin  (500 mmol/L) did
                    not induce unscheduled DNA synthesis in primary
                    cultures of Fischer 344 rat hepatocytes (Probst et
                    al., 1981). Williams (1982) reported the results of
                    the  hepatocyte  primary  culture/DNA  repair  test,
                    using freshly isolated  hepatocytes  of  high
                    metabolic  capability  to  monitor the production of
                    DNA damage by measuring DNA repair synthesis.  Aldrin
                    and dieldrin gave equivocal results concerning DNA
                    repair, but there was no damage to DNA. Aldrin (0.3
                    to 3 mmol/L) induced DNA strand breaks in an alkaline
                    elution/rat hepatocyte assay (Sina et al., 1983).
    
                    Both aldrin and dieldrin inhibited gap junctional
                    intercellular communication between
                    6-thioguanine-sensitive and 6-thioguanine-resistant
                    human teratocarcinoma cells in culture (Zhong-Xiang et
                    al., 1986).

             7.2.4  Workplace standards

                    Argentina
                    Max. permiss. conc. TWA        0.25 mg/m3
                    STEL                           0.75 mg/m3
    
                    Australia
                    TLV-TWA                        0.25 mg/m3
    
                    Belgium
                    TLV-TWA                        0.25 mg/m3
    
                    Finland
                    Max. permis. conc. TWA         0.25 mg/m3
                    STEL                           0.75 mg/m3
    
                    Germany
                    Max. work-site conc.(MAK) TWA  0.25 mg/m3
                    STEL (30 min)                  2.5 mg/m3
    
                    Netherlands
                    Max. limit TWA                 0.25 mg/m3
    
                    Poland
                    Max. permis. conc. CLV         0.01 mg/m3
    
                    Romania
                    Max. permis. conc. TWA         0.20 mg/m3
                    Ceiling value (CLV)            0.25 mg/m3
    
                    Switzerland
                    MAK-TWA                        0.25 mg/m3
    
                    Thailand
                    Max. permiss. conc.            0.25 mg/m3
    
                    UK (recommended)
                    TWA                            0.25 mg/m3
                    STEL (10 min)                  0.75 mg/m3
    
                    USA
                    OSHA PEL-TWA (skin)            0.25 mg/m3(OSHA, 1989)
                    ACGIH TLV-TWA (skin)           0.25 mg/m3(ACGIH, 1993)
                    NIOSH REL-TWA (skin)           0.25 mg/m3(NIOSH, 1992)
    
                    USSR
                    MAC-CLV                        0.01 mg/m3
    
                    Yugoslavia
                    MAC-TWA                        0.25 mg/m3
    
                    (IPCS, 1989b)

             7.2.5  Acceptable daily intake (ADI)

                    WHO (diet)              0.1 g/kg (IPCS, 1989a)
                    WHO (water)             0.03 mg/L recommended
                                            (IPCS, 1989b)

        7.3  Carcinogenicity

             No increased incidence of malignant neoplasms has been
             found in several studies (de Jong, 1991; Ribbens, 1985; Van
             Raalte, 1977).  In animal assays however, an increased
             incidence of hepatic tumors including hepatocellular adenomas
             was found (Davis & Fitzhugh, 1962; NCI, 1978).  The data does
             not allow any conclusions to be made concerning an increased
             risk of cancer development with aldrin or dieldrin (IARC,
             1974a; IARC, 1974b).

        7.4  Teratogenicity

             No human studies were identified.  In animals an
             increase in fetal mortality, increased incidence of cleft
             palate and webbed foot  and a decreased postnatal survival
             have been reported (Ottolenghi et al., 1974; Virgo &
             Bellward, 1975; Treon et al., 1954).

        7.5  Mutagenicity

             Increased sister chromatid exchanges and exchange-type
             chromosome aberrations were noted in floriculturists after
             exposure to several pesticides including aldrin (Dulout et
             al., 1985).

        7.6  Interactions

             Possible additive effects with other organochlorine
             pesticides have been postulated (ATSDR, 1993).

    8.  TOXICOLOGICAL ANALYSIS AND BIOMEDICAL INVESTIGATIONS

        8.1  Material sampling plan

             8.1.1  Sampling and specimen collection

                    8.1.1.1  Toxicological analyses

                    8.1.1.2  Biomedical analyses

                    8.1.1.3  Arterial blood gas analysis

                    8.1.1.4  Haematological analyses

                    8.1.1.5  Other (unspecified) analyses

             8.1.2  Storage of laboratory samples and specimens

                    8.1.2.1  Toxicological analyses

                    8.1.2.2  Biomedical analyses

                    8.1.2.3  Arterial blood gas analysis

                    8.1.2.4  Haematological analyses

                    8.1.2.5  Other (unspecified) analyses

             8.1.3  Transport of laboratory samples and specimens

                    8.1.3.1  Toxicological analyses

                    8.1.3.2  Biomedical analyses

                    8.1.3.3  Arterial blood gas analysis

                    8.1.3.4  Haematological analyses

                    8.1.3.5  Other (unspecified) analyses

        8.2  Toxicological Analyses and Their Interpretation

             8.2.1  Tests on toxic ingredient(s) of material

                    8.2.1.1  Simple qualitative test(s)

                    8.2.1.2  Advanced qualitative confirmation test(s)

                    8.2.1.3  Simple quantitative method(s)

                    8.2.1.4  Advanced quantitative method(s)

             8.2.2  Tests for biological specimens

                    8.2.2.1  Simple qualitative test(s)

                    8.2.2.2  Advanced qualitative confirmation test(s)

                    8.2.2.3  Simple quantitative method(s)

                    8.2.2.4  Advanced quantitative method(s)

                    8.2.2.5  Other dedicated method(s)

             8.2.3  Interpretation of toxicological analyses

        8.3  Biomedical investigations and their interpretation

             8.3.1  Biochemical analysis

                    8.3.1.1  Blood, plasma or serum

                    8.3.1.2  Urine

                    8.3.1.3  Other fluids

             8.3.2  Arterial blood gas analyses

             8.3.3  Haematological analyses

             8.3.4  Interpretation of biomedical investigations

        8.4  Other biomedical (diagnostic) investigations and their
             interpretation

        8.5  Overall interpretation of all toxicological analyses and
             toxicological investigations

             Sample collection
    
             Blood collection for aldrin and dieldrin levels may be done.
             However, aldrin may not be found as it is metabolized quickly
             to dieldrin. Keep containers and any remaining product for
             further identification. Typically collect 1 to 5 mL of serum
             (preferred) or whole blood in an anticoagulant free evacuated
             tube, which has an uncoated interior.
    
             Biomedical analysis
    
             Measurement of aldrin and dieldrin levels may be done.
             However, aldrin may not be found as it is metabolized quickly
             to dieldrin.  Another problem is that few laboratories are
             capable of determining dieldrin levels.
    
             Remember that management is not dependent on levels and is
             supportive and symptomatic.

    9.  CLINICAL EFFECTS

        9.1  Acute poisoning

             9.1.1  Ingestion

                    Case reports describe the onset of symptoms
                    within 15 minutes after oral exposure (Garrettson &
                    Curley, 1969; Spiotta, 1951; Black, 1974).  Central
                    nervous system hyperirritability is the most common
                    manifestation attributable to aldrin.  Symptoms may
                    include headache, dizziness, hyperirritability,
                    malaise, nausea and vomiting, anorexia, muscle
                    twitching, and myclonic jerking prior to the
                    development of seizures (Jager, 1970).  Seizures may

                    be prolonged and signs of hyperirritability may last
                    several days (Spiotta, 1951; Black, 1974).  Renal
                    dysfunction followed an acute ingestion of aldrin.
                    This resulted in an elevated blood urea nitrogen,
                    gross hematuria, and albuminuria (Spiotta,
                    1951).

             9.1.2  Inhalation

                    This route of exposure usually occurs in
                    workers manufacturing or spraying the insecticide.
                    However, no acute poisoning cases were identified by
                    this exposure route.  Most of these cases probably
                    represent multiple subacute and asymptomatic exposures
                    with a sudden unexpected seizure episode being the
                    first clinical effect  (see chronic poisoning
                    below).

             9.1.3  Skin exposure

                    This route of exposure is difficult to separate
                    from inhalation, and both may be occurring
                    simultaneously (ATSDR, 1993)  Like inhalation
                    exposures, dermal absorption primarily occurs in
                    workers.  If the exposure is severe one would expect a
                    progression of symptoms similar to oral exposure.
                    However, many exposures in workers involve multiple
                    subacute contacts which remain asymptomatic until a
                    seizure was the first observed clinical
                    effect.

             9.1.4  Eye contact

                    No 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

                    No neurological, hepatic or hematological
                    effects are noted in humans at levels under 0.003
                    mg/kg/day (Hunter & Robinson, 1967).

             9.2.2  Inhalation

                    Convulsions may appear suddenly and without
                    early signs and may be due to the accumulation of
                    aldrin (and its metabolite dieldrin) over several days
                    (Jager, 1970).  Hemolytic anemia (dieldrin) and
                    aplastic anemia (aldrin) has been described after
                    prolonged exposure (Muirhead et al., 1959; Pick et
                    al., 1965; de Jong, 1991).

             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

             After an acute ingestion (or possibly through dermal or
             inhalational methods) signs of CNS hyperirritability develop
             as soon as 15 minutes after exposure.  Seizures soon follow
             and may last for several hours before being controlled with
             medication. Motor hyperexcitabiltiy and restlessness may
             persist for several days.  The course may be mild or severe
             depending on the amount ingested and any efforts to limit
             absorption.  The outcome may be fatal if complications from
             seizures develop.  Survivors recover completely; irreversible
             effects have not been described in humans (IPCS,
             1989a).

        9.4  Systematic description of clinical effects

             9.4.1  Cardiovascular

                    No specific cardiovascular toxicity effect has
                    been described. Blood pressure fluctuations and
                    tachycardia have been described after overdose, but
                    these occurred in the presence of  (and presumably due
                    to) CNS excitation and seizures (Spiotta, 1951; Black,
                    1974).

             9.4.2  Respiratory

                    No data available.

             9.4.3  Neurological

                    9.4.3.1  Central Nervous System (CNS)

                             Central nervous system excitation is
                             the primary adverse effect seen in humans.
                             Convulsions can occur suddenly after a
                             massive ingestion or after multiple, subacute
                             exposures.  Typically a prodrome precedes 
                             development of seizures and consists of
                             headache, dizziness, hyperirritability,
                             malaise, nausea and vomiting, and myoclonic
                             twitching (Patel & Rao, 1958; Jager
                             1970).
    
                             Persistent effects consisting of motor
                             hyperexcitability and restlessness for
                             several days have been reported (Spiotta,
                             1951).

                    9.4.3.2  Peripheral nervous system

                             An increased incidence of PNS
                             diseases was noted in pesticide workers. 
                             However this increase was due to a higher
                             incidence of cervicobrachial and lumbosacral
                             syndromes; syndromes associated with manual
                             labor in a plant, not insecticide exposure
                             (de Jong, 1991).

                    9.4.3.3  Autonomic nervous system

                             No data available.

                    9.4.3.4  Skeletal and smooth muscle

                             No data available.

             9.4.4  Gastrointestinal

                    Nausea, vomiting and anorexia may occur.

             9.4.5  Hepatic

                    No data available with aldrin.  Few case
                    reports with dieldrin which showed transient
                    transaminase elevation for several days, although the
                    effects of solvents (such as toluene) could not be

                    discounted (Garrettson & Curley, 1969; Black,
                    1974).

             9.4.6  Urinary

                    9.4.6.1  Renal

                             Only one case report mentions an
                             elevation of blood urea nitrogen, gross
                             hematuria and albuminuria for several days
                             after an acute overdose although causality
                             was not established (Spiotta,
                             1951).

                    9.4.6.2  Other

                             None.

             9.4.7  Endocrine and reproductive systems

                    Although aldrin levels in blood and placental
                    tissues were higher in women with premature labor or
                    spontaneous abortion than in women with normal
                    deliveries, other organochlorine pesticide levels were
                    also higher and therefore assigning causality to
                    aldrin is not possible.  In addition other confounders
                    were not addressed in that study such as smoking or
                    alcohol consumption (Saxena et al., 1980).

             9.4.8  Dermatological

                    No evidence of dermatitis was seen in pesticide
                    manufacturing workers (Jager, 1970).

             9.4.9  Eye, ears, nose, throat: local effects

                    No data available.

             9.4.10 Haematological

                    Normal haematological parameters were noted in
                    pesticide manufacturing workers during at least four
                    years of follow up (Jager, 1970).  No increased
                    relative risk in pesticide workers has been noted (de
                    Jong, 1991).  However a worker developed haemolytic
                    anaemia after working in an area sprayed with aldrin,
                    although it was not shown to be directly responsible
                    because other chemicals were in use also (Pick et al.,
                    1965).

             9.4.11 Immunological

                    Although no data was found on aldrin, dieldrin
                    was associated with the development of
                    immunohaemolytic anaemia after eating contaminated
                    food (Hamilton et al., 1978).

             9.4.12 Metabolic

                    9.4.12.1 Acid-base disturbance

                             May be observed in seizure states.

                    9.4.12.2 Fluid and electrolyte disturbance

                             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

                    There was no increased incidence of malignant
                    neoplasm in pesticide workers (de Jong,
                    1991).

             9.4.15 Special risks

                    Theoretically the very young are at risk
                    because of their smaller rates of glucuronide
                    conjugation and subsequent excretion (Calabrese,
                    1978). The fetus concentrates dieldrin, and the
                    possibility of contaminated breast milk consumption
                    increase the risk of CNS effects in the very young
                    (IPCS, 1989a; Polishuk et al., 1977). However, based
                    on  average breast milk dieldrin concentrations (up to
                    6 g/L) and a child drinking approximately 150 mL
                    milk/kg body weight, the estimated daily intake would
                    be 0.15 to 0.9 g dieldrin/kg body weight (IPCS,
                    1989a). Other estimates place this estimated daily
                    intake at 0.65 to 0.70 g/day for the first four
                    months of breast feeding (Acker et al., 1984). Because
                    of these small levels, the presence of dieldrin in the
                    blood is considered clinically insignificant.

        9.5 Other

            No data available.

        9.6 Summary

    10. MANAGEMENT

        10.1 General principles

             Clinical observation after appropriate decontamination,
             and symptomatic treatment is usually sufficient.

        10.2 Life support procedures and symptomatic/specific treatment

             Make a proper assessment of airway, breathing,
             circulation and neurological status of the patient. Maintain
             a clear airway. Aspirate secretions from airway. Administer
             oxygen. Perform endotracheal intubation and support
             ventilation using appropriate mechanical device when
             necessary. Control convulsions with benzodiazepines or
             phenobarbital. Open and maintain at least one intravenous
             route. Perform cardio-respiratory resuscitation when
             necessary. Monitor vital signs. Correct hypotension as
             required. Monitor blood pressure and ECG. Monitor fluid and
             electrolyte balance. Monitor acid-base balance.(de Jong,
             1991; Ellenhorn & Barceloux, 1988).

        10.3 Decontamination

             Remove and discard contaminated clothing. Irrigate
             exposed eyes with copious amounts of water (or saline). Wash
             skin with copious amounts of water. Emesis is
             contraindicated. If the patient is obtunded, convulsing or
             comatose, or since aldrin may induce these conditions
             rapidly, insert an oro- or a naso-gastric tube and lavage
             after endotracheal intubation. Administer activated charcoal.
             If an oro- or naso-gastric tube is in place, administer after
             lavage through the tube. Administer a cathartic unless
             already given with activated charcoal.

        10.4 Enhanced elimination

             No data is available as to whether haemodialysis or
             haemoperfusion are effective.  However the large molecular
             weight and lipophylic nature of aldrin would seem to indicate
             that haemodialysis would not be effective. Forced diuresis,
             alkalinization, acidifiction are not effective.

        10.5 Antidote treatment

             10.5.1 Adults

                    There is no antidote.

             10.5.2 Children

                    There is no antidote.

        10.6 Management discussion

             Additional data is needed to identify differences in
             toxicity from different routes of exposure.  Also information
             on less subtle forms of CNS effects is lacking (ATSDR, 1993).
             The metabolism of aldrin may include some element of
             enterohepatic recirculation, although this has not been
             demonstrated.

    11. ILLUSTRATIVE CASES

        11.1 Case reports from literature

             No cases of poisoning with aldrin were identified. The
             following two cases reflect poisoning with dieldrin which
             would be expected to be similar to aldrin poisoning.
    
             Two siblings aged 2 and 4 years apparently ingested dieldrin 
             (5% solution) and within 15 minutes were noticed to be
             salivating heavily when generalized convulsions started. By
             the time a physician arrived the younger child was dead, and
             the four year old male was treated with mechanical
             respirator, anticonvulsants (phenobarbital, paraladehyde and
             phenytoin) and general supportive care. He recovered
             completely and was discharged (Garettson and Curley,
             1969).
    
             A 21-year-old male ingested 9 g (120 mg/kg) of dieldrin in a
             15% solution with toluene. Within 20 minutes he was frothing
             at the mouth, cyanotic and semi-conscious. En route to the
             hospital he lost consciousness and had a grand mal seizure. 
             He was treated with an endotracheal tube, gastric lavage,
             catharsis (with mannitol), anticonvulsants (diazepam,
             phenobarbital, phenytoin and muscular paralysis), beta
             blockers for tachycardia and hypertension and general
             supportive treatment (Black, 1974).

    12. ADDITIONAL INFORMATION

        12.1 Specific preventive measures

             The substance is not produced in most countries to our
             knowledge, and is banned in many countries.Caution in using
             this product with appropriate protective gear to prevent
             absorption (dermal, inhalational, or gastrointestinal) is

             imperative.  Workers should be educated as to the proper
             handling and use (IPCS, 1989a).
    
             Use in the treatment of termite control for buildings as long
             as it is used appropriately appears safe for the
             occupants.

        12.2 Other

             Infants and toddlers appear to have higher dietary
             intake of aldrin (and dieldrin) compared to adults. However,
             the rates of intake have been decreasing over time as use of
             aldrin and dieldrin have decreased (Gartell et al., 1986a,
             1986b).

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

        Author:     John G. Benitez, M.D.
                    Toxicology Treatment
                    University of Pittsburgh Medical Center
                    Room NE 583, MUH
                    200 Lothrop Street
                    Pittsburgh, PA  15213
                    U.S.A.
    
                    Tel:     412-257-2142
                    Fax:     412-648-6855
    
        Date:       September 1995
    
        Peer
        review:     Berlin, Germany, October 1995
    

        Finalized:  IPCS, September 1996
    
        Editor:     Mrs J. Dumnil
                    International Programme on Chemical Safety
    
        Date:       June 1999
    
    
    
    



    See Also:
       Toxicological Abbreviations
       Aldrin (ICSC)
       Aldrin (FAO Meeting Report PL/1965/10/1)
       Aldrin (FAO/PL:CP/15)
       Aldrin (FAO/PL:1967/M/11/1)
       Aldrin  (IARC Summary & Evaluation, Supplement7, 1987)
       Aldrin (IARC Summary & Evaluation, Volume 5, 1974)