FAO, PL:CP/15
    WHO/Food Add./67.32


    The content of this document is the result of the deliberations of the
    Joint Meeting of the FAO Working Party and the WHO Expert Committee on
    Pesticide Residues, which met in Geneva, 14-21 November 1966.1

    1 Report of a Joint Meeting of the FAO Working Party and the WHO
    Expert Committee on Pesticide Residues, FAO Agricultural Studies, in
    press; Wld Hlth Org. techn. Rep. Ser., 1967, in press




    HEOD, Octalox (R)


    Dieldrin is a technical product containing 85 per cent of the chemical
    known as HEOD of which the composition is as follows:

    Chemical name





    Biochemical aspects

    When 14C-dieldrin was applied to growing cultures of Aspergilllus
    and Penicillium species, no metabolites could be detected in the
    culture medium or in the mycelium. Mosquito larvae (Aedes aegypti)
    cultivated in an aqueous medium to which 14C.-dieldrin was added,
    converted this compound to hydrophilic metabolites (Ludwig et al.,

    A greater toxicity was found in rats kept on a low protein diet than
    in rats on a high protein diet (Lee et al., 1964).

    After stimulation of rat liver microsomal enzymes with phenobarbital,
    the dieldrin content in fat was decreased in comparison with
    non-stimulated rats (Cueto & Hayes, 1965).

    In experiments with 14C-dieldrin it was demonstrated that dieldrin
    in the blood is carried mainly in the erythrocyte contents and plasma,
    not in the erythrocyte stroma, leucocytes or platelets. Haemoglobin is
    largely but not entirely responsible for the intraerythrocytic
    binding. In the plasma, dieldrin binds with soluble proteins (Moss &
    Hathway, 1964).

    In studies on the urine of individuals exposed to dieldrin, 2 neutral
    polar metabolites of dieldrin were found by paper and column
    chromatography. No dieldrin could be detected with this method, but
    dieldrin or a material having the same retention time was found by gas
    chromatography (Cueto Hayes, 1962).

    In dogs fed 3 ppm of dieldrin 45.5 ppm were found in the fat, and in
    dogs fed 1 ppm, 3.4 ppm were found in the fat. In other organs,
    concentrations ranging from 2.9 ppm (liver) to 0.05 ppm (brain) were
    found (Borgmann et al., 1952).

    14C-dieldrin is preferentially excreted in the bile with its
    metabolites. Dieldrin and a hydrophilic metabolite were found in the
    bile fifteen minutes after an intravenous injection (Mörsdorf et al.,

    Studies with 36Cl-dieldrin have shown that the initial distribution
    is general, but within a few hours of injection it concentrates more
    in the fat. Excretion of 36Cl averages about 5 per cent per day and
    is markedly increased by a restriction of diet, which reduces the body
    fat. Excretion from the cannulated bile duct accelerates as the rat
    loses weight, exceeding 10 per cent per day after a few days. Only 3
    per cent of the 36Cl is excreted as dieldrin unless the bile is
    cannulated, when up to 10 per cent may be excreted. The remainder of
    36Cl, is found in the metabolites and these are excreted to 90 per
    cent in the faeces and 10 per cent in the urine. The most important
    metabolite, containing about 60 per cent of the total 36Cl, is
    excreted in the bile (Heath & Vandekar, 1964).

    Rats were fed 1 or 25 ppm dieldrin for 120 days. Two metabolites were
    found in the urine, one of which was much more abundant in males than
    in females. In the same study, small amounts of aldrin were found in
    the urine of rats fed dieldrin (Datta et al., 1965).

    Experiments with rats and rabbits showed that 14C-dieldrin given
    intravenously was converted in 24 hours mainly into hydrophilic
    metabolites. After 48 hours the presence of unconverted dieldrin and
    the hydrophilic metabolites could be demonstrated in most organs and
    tissues. A higher percentage of hydrophilic metabolites were found in
    the kidney and liver. It was found that within one hour after
    intravenous injection of 14C-dieldrin in rats, radioactive products
    appeared in the bile. In 4 hours 13 per cent of the radioactivity was
    excreted in the bile. Most of the radioactivity was found in
    hydrophilic metabolites. After oral administration of 14C-dieldrin to
    rabbits, six metabolites were isolated from the urine, all more
    hydrophilic than the original compound. The main metabolite (86 per
    cent of the total radioactivity in the urine) could be identified as
    one of the two enantiomorphs of 6,7-trans-dihydroxy-dihydroaldrin. The
    oral LD50 of this compound in mice is 1250 mg/kg body-weight, and
    the intravenous LD50 is 51 mg/kg body-weight (Ludwig et al., 1966).

    After the feeding of dieldrin to animals it is stored in the adipose
    tissues. Although small amounts of dieldrin are found in liver, kidney
    and muscle tissues, the greatest amount of storage is in the fat,
    where dieldrin is stored unchanged (Bann et al., 1956; Butcher et al.,
    1957; Heath & Vandekar, 1964; Ivey et al., 1961; Lehmann, 1956; Street
    et al., 1957). It is lost slowly from the body fat (Butcher et al.,
    1957; Heath & Vandekar, 1964). It is stored in human fat in
    significant amounts (Hunter et al., 1963).

    Acute toxicity
    Animal              Route          LD50                    References
                                       mg/kg body-weight

    Mouse               Oral           38                      Borgmann at al., 1952

    Rat (new-born)      Intragastric   168                     Lu et al., 1965

    Rat (pre-weaning)   Oral           25                      Lu et al., 1965

    Rat                 Oral           37-87                   Borgmann et al., 1952
                                                               Gaines, 1960
                                                               Heath & Vandekar, 1964
                                                               Lehmann, 1951
                                                               Lu at al., 1965
                                                               Treon & Cleveland, 1955

    Guinea-pig          Oral           49                      Borgmann at al., 1952

    Rabbit              Oral           45-50                   Borgmann et al., 1952

    Dog                 Oral           56-80                   Borgmann at al., 1952

    Sheep               Oral           50-75                   Borgmann at al., 1952
    Short-term studies

    Rat. In a 90-day feeding study, groups of 12 rats (6 male and 6
    female) were fed diets containing 25, 50 and 125 ppm of dieldrin; an
    increased mortality rate was observed at 125 ppm. In another
    experiment groups of 10 male and 10 female rats were given, 2, 5, 10,
    50, 100 and 150 ppm dieldrin. All rats on 150 ppm died. Histological
    liver changes were observed in rats on 10 ppm and above (Borgmann et
    al., 1952).

    Groups of 12 rats, 6 females and 6 males, were fed 2.5 and 25 ppm of
    technical dieldrin. The rats were killed after 2, 4, 6 and 8 months.
    Food intake and growth were normal. No change in liver weight was
    found. Cytoplasmic alteration of the liver cells was found at both
    concentrations in males and females (Ortega et al., 1957).

    Rabbit. In a 90-day study, groups of 20 rabbits (10 female and 10
    male) were given dieldrin orally at dosage levels of 0.625, 1.25, 2.5,
    5 and 10 mg/kg body-weight per day. Survival rates were affected at
    all levels. At 2.5 mg/kg and above, all animals died (Borgmann et al.,

    Dog. Dogs (1-4 animals per group) were given diets containing 1, 3,
    10, 25 and 50 ppm dieldrin, six days per week. The animals on 25 and
    50 ppm died after 5 and 33 days respectively. Dogs on 10 ppm survived
    for 9 months and on 1 and 3 ppm for 15 months. In the groups on 1 and
    3 ppm the livers were significantly larger than those of the controls.
    Histological changes were noted in brain, liver and kidney. Groups of
    4 dogs (2 male and 2 female) were given 1 and 3 ppm of dieldrin in
    their diet for 68 weeks. The concentration of 3 ppm increased the
    liver/body-weight ratio and produced renal damage in 1 female. With 1
    ppm of dieldrin, livers were enlarged but no histopathological changes
    were found (Treon & Cleveland, 1955).

    Dogs (both sexes) in groups of 3 or 4 were given dosage levels of 0.2,
    0.6 and 2.0 mg/kg per day by mouth for a maximum time of 313 days. The
    highest dosage killed all the dogs. Two of the 4 dogs died when given
    0.6 mg/kg body-weight per day (Borgmann et al., 1952).

    Three groups of 3 dogs were given orally 0.2 and 0.6 mg per day of
    recrystallized dieldrin per kg of body-weight for one year; 3 of them
    produced litters but none of the pups of the group given 0.6 mg
    survived, probably because of high quantities of dieldrin in the milk
    of the dams. Histological changes were found in the liver and/or
    kidneys of adult dogs (Kitselman, 1953).

    A group of 14 dogs was given dieldrin orally for 25 months at the
    following daily doses: 0.2 mg/kg (2 dogs), 0.5 mg/kg (4 dogs), 1, 2, 5
    and 10 mg/kg (2 dogs in each group). All the dogs given 2, 5 or 10
    mg/kg died in 35 days. All those given 1 mg/kg or 0.5 mg/kg (with one
    exception) died in one year. Convulsions and fatty liver changes were
    frequently seen. At 0.2 mg/kg no effects were observed (Fitzhugh et
    al., 1964).

    Long-term studies

    Mouse. Groups of approximately 200 young C3HeB/Fe mice, with equal
    numbers of each sex, were fed a diet containing 10 ppm of dieldrin for
    their life-span (maximum 2 years). The dieldrin shortened their
    average life-span by 2 months, as compared with an equal number of
    controls, and significantly increased the incidence of hepatic tumours
    (Davis & Fitzhugh, 1962).

    Rat. Groups of 40 rats (20 male and 20 female) were fed diets
    containing 2.5, 12.5 and 25 ppm dieldrin for 2 years. The
    liver/body-weight ratio increased and characteristic histological
    liver damage was seen at all dosages (Treon & Cleveland, 1955).

    With groups of 16 female rats each, dieldrin was incorporated in the
    diet for three generations at 2.5, 12.5 and 25 ppm. Two litters of
    offspring were taken from each generation of these groups. The
    presence of dieldrin in the diet at 2.5 and 12.5 ppm initially
    reduced the number of pregnancies but this effect tended to disappear
    with continued feeding of the diet. All doses increased the mortality
    among the suckling young. The effect on survival during suckling was
    severe at 12.5 and 25 ppm dieldrin (Treon & Cleveland, 1955).

    In a 2-year experiment, groups of 24 rats (12 male and 12 female) were
    given 0.5, 2, 10, 50, 100 and 150 ppm dieldrin. Concentrations of 50
    ppm and above increased the mortality rate in a dose-response
    relationship. The liver/body-weight ratio increased and characteristic
    histological lesions occurred in the liver at all levels; these were
    minimal at 0.5 ppm but increased in severity with increasing dose.
    There was an increase in the number of tumours in the experimental
    groups, especially at the lower levels of feeding, in contrast to the
    control group (Fitzhugh et al., 1964).

    In other experiments, 40 males and 40 females were given dieldrin in
    the diet at a concentration of 75 ppm for 440 days. Twenty animals of
    each sex were used as controls. All the females and 22 males of the
    experimental group, and 5 control males died spontaneously before the
    end of the treatment. Seven males were killed in good condition
    between 300 and 440 days and the last 11 males were killed after 440
    days. The liver/body-weight, ratio was markedly increased in the rats
    killed during exposure, but was found to be normal in later
    sacrifices. "Lesions of the hepatic parenchyma that have been
    considered typical of exposure to the organochlorine insecticides in
    rats" were observed only, in healthy animals killed during the
    treatment. Rats dying spontaneously or killed after withdrawal of the
    insecticide did not show such changes (Hunter et al., 1964).

    Ewes. Thirty-six ewes were given 0, 1, 5 or 25 ppm of dieldrin in
    their diets for a period of 40 months including 4 gestation periods.
    At 25 ppm lambs died shortly after birth. Liver function as well as
    other physiological tests on the ewes did not show any changes related
    to the treatment with dieldrin (Shell, 1963).

    Observations on man

    In one study, a total of 13 men was divided into 4 groups receiving 0,
    11, 57 and 211 µg dieldrin/man/day. No effects on body-weight, blood
    cell counts, haemoglobin, total plasma protein, blood urea and serum
    alkaline phosphatase, cholinesterase and transaminases were recorded
    during the first 35 weeks. At the highest dose level, the average
    concentration of dieldrin in the fat was 2.26 ppm. Ratios of fat

    concentration at 35 weeks to fat concentration at 0 week ranged from
    0.8-1.6 for men exposed to no dieldrin to 2.1-5.2 for those exposed to
    11 µg/day; 2.5-6.0 for those exposed to 57 µg/day and 8.1-14.5 for
    those exposed to 211 µg/day (Shell, 1966).

    Several reports are now available on the storage of dieldrin in human
    fat in the general population for several countries (Dale & Quinby,
    1963; Dale et al., 1965; Egan et al., 1965; Hoffman et al., 1964;
    Hunter et al., 1963; Robinson et al., 1965; Zavon, 1965). The average
    concentration ranged between 0.03 and 0.30 ppm. It appears that in
    those countries in which a higher DDT storage was recorded, this was
    associated with a low dieldrin storage and vice-versa. In the United
    States of America the amount of dieldrin stored in the fat increased
    from 1950 to 1958 and then remained constant (USFDA Advisory
    Committee, 1965). In the United Kingdom, from the above-mentioned
    references, it appears that comparable figures were obtained in 1961
    and 1965.

    In one study, dieldrin was found in human milk at an average
    concentration of 0.006 ppm (Egan et al., 1965).


    The primary site of action of dieldrin is the central nervous system.
    CNS stimulation is the cause of death in acute poisoning. Signs of CNS
    stimulation are also seen after repeated high doses. Repeated doses at
    lower levels give rise to liver damage.

    In one long-term rat-feeding experiment, there was a general increase
    in tumour production in the experimental animals at the lower dosage
    levels as compared to the controls, but the liver was not particularly
    affected. Liver tumours, however, were significantly increased at a
    dose level of 10 ppm in one strain of mice susceptible to the
    development of these tumours.


    Levels causing no toxicological effect

    Dog.    1 ppm equivalent to 0.025 mg/kg/day produced liver changes.

    Rat.    0.5 ppm in the diet equivalent to 0.025 mg/kg/day produced
            minimal liver changes.

    Estimate of acceptable dally intake for man

    0-0.0001 mg/kg/day*

    * Sum of aldrin and dieldrin by weight.

    Further work required

    Elucidation of the significance of the finding that dieldrin is one of
    the compounds which affect liver cellular metabolism (p. 3).

    Development of methods of toxicological investigation aimed at
    defining and clarifying the various biological changes seen in the
    reported studies of this compound, with a view to removing doubts
    which may remain as to its safety in use.


    Use pattern

    (a) Pre-harvest treatments

    Aldrin and dieldrin are used for soil treatment against various soil
    insects (1.5-5 kg/ha), for seed treatment on grains, sugar beets,
    beans (0.5-2.5 g/kg seed), leeks and onions (37-50 g/kg seed for 
    bulb- or root-dip), and for foliar application on various agricultural
    crops, fruits, nursery stocks and ornamental plants.

    The use pattern has recently changed considerably due to restrictions
    in many countries. In the United States of America and Canada, aldrin
    and dieldrin may not be used on any crop that is likely to be fed to
    animals; the use in soil for sugar beets has been withdrawn, whereas
    the use in soil where other root crops are grown in rotation is under
    review. In Canada, the registration of aldrin and dieldrin in
    fertilizer mixtures has been withdrawn. Soil and seed treatment is
    recommended only for use in grain production. In Britain, the use for
    treatment of cereal seeds sown in the spring and the use in fertilizer
    mixtures has been withdrawn. In Germany, the prohibition of uses on
    agricultural crops is being considered. In Austria, uses for
    vegetables are forbidden. In the Netherlands, Belgium and Luxembourg,
    aldrin and dieldrin may not be used on carrots and carrots may not be
    grown in treated soil in the year of application. Furthermore, to
    prevent edible crops obtaining too high residues, the soil used in
    rotation for growing food crops, such as lettuce under glass, may not
    be treated. In Belgium, seed treatment of grain-seed and pulses is
    forbidden in order to avoid poisoning of seed-eating birds, and
    subsequently of predatory birds and mammals.

    (b) Post-harvest treatments

    The use of dieldrin in food storage practice for treatment of empty
    warehouses, etc., is decreasing, and is prohibited in many countries
    (e.g. the Netherlands, Belgium). In Britain, there is a limited use
    under strict precautions. Aldrin and dieldrin are not used for direct
    treatment of stored commodities or for treatment of containers, etc.,
    which may come into contact with foodstuffs.

    (c) Other uses

    The use of aldrin and dieldrin in sheep dips or cattle sprays is no
    longer allowed in many countries (e.g. the United States of America,
    Canada, Britain, Australia, New Zealand, the Netherlands and Belgium).
    Dieldrin is used in many sub-tropical and tropical regions for the
    control of mosquito larvae, adult mosquitos, chiggers, fleas, ticks,
    reduviid bugs, tsetse-flies and other disease vectors. These
    applications usually are carried out under supervision of trained
    personnel of public health agencies or pest control operators.

    Aldrin and dieldrin are used in various countries for termite control
    in basements of buildings during construction and for spot treatment
    against other domestic pests. In the Netherlands and Belgium, the use
    for household purposes is no longer allowed. Dieldrin as a 0.05 per
    cent solution is used for wood preservation to prevent attack by
    wood-boring insects. In many countries, it is also used for
    mothproofing of wool at a dosage of about 0.05 per cent dieldrin on
    the weight of wool during the dyeing operation.

    (d) Tolerances

    The many countries and the great variety of crops in question make it
    impossible to present a complete survey of all tolerances, established
    or considered. The following table, therefore, is only intended to
    serve as a rough guide to current levels. (The figures usually refer
    to totals of aldrin plus dieldrin).

    Residues resulting from supervised trials

    (a) In crops grown in treated soils

    Various factors influence the residues remaining in soil and in or on
    the crop at harvest. Retention in soil has been greatest when the
    organic matter has been high (Bowman, Schechter & Carter, 1965). Low
    moisture content (Harris, 1964; Lichtenstein & Schulz, 1961) and dense
    coverage of crops (Harris & Lichtenstein, 1961; Lichtenstein et al.,
    1962) have also been found to favour retention. Water leaching through
    the soil does not appear to play an important role in the decrease of
    the residue (Lichtenstein, 1958).

    After two yearly applications to soil of 2 kg/ha of aldrin and
    dieldrin, Lichtenstein & Schulz (1965) found residues in carrots and
    radishes in excess of 0.1 ppm, whereas in potatoes 0.1 ppm was
    reached. Continued soil treatment has eventually led to residues in
    potatoes, turnips, beet roots and chicory roots in excess of
    tolerances (0.1-0.55 ppm) in the Netherlands (unpublished information
    from Netherlands Government).

    Country                        Food                         Tolerance
                                                                (parts per million)

    United States of America       fruits, vegetables               0.1-0.25
                                   potatoes                         0.1
                                   animal feed                      0

    Canada                         fruits, vegetables               0.1-0.25
                                   potatoes                         0.1

    Netherlands                    fruits, vegetables               0.1

    Sweden                         fruits, vegetables               0.1

    Switzerland                    potatoes                         0.1

    Germany (Federal)              all edible crops             Limit of sensitivity of
                                                                analytical method
                                                                (under consideration)

    Germany (DDR)                  all edible crops                 0
                                                                (under consideration)

    Translocation of aldrin and dieldrin from the soil to the aerial parts
    of the crop has been demonstrated by several investigators, although
    in the case of cereal crops, Morley & Chiba (1965) and Saha & McDonald
    (1966) found no detectable amounts in the grains, residues were found
    in the leaves.

    (b) After direct application to growing crops

    In several experiments carried out in the United States of America on
    various fruits and vegetables at practical dosage levels, the residues
    in the edible part of the plant varied from <0.01-0.2 ppm when the
    recommended safety interval was observed (unpublished information from
    Shell Company).

    (c) In meat and meat products

    Various workers have measured residues in the bodies of cattle dipped
    in or sprayed with dieldrin, or receiving the insecticides in their
    diet. For example, Ivey, Claborn & Mann (1961) measured residues in
    various body tissues of animals which had received aldrin. The
    residues have been highest in the fat; Egan (1965), for example, found
    up to about 9 ppm in the fat of sheep slaughtered 4 1/2 weeks after an
    experimental dipping.

    Residues in raw food moving in commerce

    In 1965, analyses were carried out in the Netherlands on glasshouse
    lettuce grown in soil treated with aldrin (2.5 kg/ha) against
    cutworms. A total of 105 samples from lettuces going on to the market
    was examined, Seventy-eight per cent of the examinations showed a
    residue of less than the tolerance (0.1 ppm), 11 samples contained
    0.1-0.2 ppm, 7 samples contained 0.2-0.3 ppm, 3 samples contained
    0.3-0.4 ppm, and 2 samples contained 0.4-0.55 ppm (unpublished

    Residues at time of consumption

    Although losses or residues are likely to occur from some foods
    through mechanical means (cleaning, trimming, etc.), substantial
    losses during cooking are not to be expected. In recent total diet
    studies in the United States of America, where, during the months of
    June, August, October and December 1965, and February and April 1966,
    a total of 317 samples of total diet was analysed for the presence of
    aldrin and dieldrin residues, aldrin was found in 13 samples at levels
    varying between traces to 0.07 ppm; whereas in 76 samples, dieldrin
    was found at levels varying between traces to 0.20 ppm (unpublished
    communication from the United States Food and Drug Administration).
    Analyses carried out in Britain during the years 1962-1965 showed
    dieldrin residues in home-produced butter of 0.03-0.07 ppm, and in
    home-produced milk of 0.002-0.003 ppm (Lewis, 1963, 1964, 1965).

    Studies have been made in various countries of the dieldrin content of
    human fat. In measurements undertaken between 1962 and 1965 in
    Britain, the average residues were of the order of 0.25 ppm (Egan et
    al., 1965). In a similar investigation carried out in the Netherlands
    since 1963, the average residue in 15 samples of human fat was 0.15
    ppm, with a range of 0.06 to 30 ppm (direct communication). However,
    although it is likely that these residues mainly arise from food, the
    extent to which other routes have been responsible, such as the
    inhalation of contaminated atmosphere (Abbott et al., 1965, 1966) or
    the wearing of treated clothing, has not been clearly demonstrated.

    Methods of residue analysis

    A number of multidetection systems are available for the detection and
    determination of residues of aldrin and dieldrin, together with
    residues of a number of other compounds. An example is the AOAC system
    (1966) in which acetonitrile partition and Florisil column clean-up
    are employed, and the residues are identified and measured by gas
    chromatography coupled with thin layer or paper chromatography.
    Alternative clean-up systems, e.g., that of de Faubert Maunder et al.
    (1965) using dimethylformamide, and other methods of confirmation of
    identity, using infra-red spectrophotometry, are also available. The
    methods are sensitive to about 0.002 ppm of aldrin or dieldrin in milk
    and 0.02 ppm in most other foods, though under favourable conditions
    greater sensitivity can, if appropriate, be obtained.


    In view of the exceptionally low acceptable daily intake of aldrin and
    dieldrin, and the occurrence of unintentional residues, the meeting
    came to the conclusion that no allowance could be made for a finite
    tolerance figure as a result of agricultural use.

    Total diet studies have revealed the presence of dieldrin in the human
    food as consumed. Furthermore, aldrin and dieldrin have been shown to
    persist for long periods in the soil after soil treatment, and to
    occur quite widely in human fat, in aquatic and terrestrial wild life,
    and in the abiotic environment. Consequently, it is recommended that
    the use of these compounds should be reduced, and, as far as possible,
    restricted to those usages which cannot result in residues in food or
    in the biotic and abiotic environment.

    Although various agricultural uses of aldrin and dieldrin have already
    been restricted or prohibited in many countries, some foods moving in
    international trade may continue to contain residues (e.g., resulting
    from earlier soil treatments). It is, therefore, suggested that a
    "practical residue limit" be established for such foods on the
    following basis: vegetables, 0.05 ppm; fat in products of animal
    origin (excluding milk), 0.2 ppm, or in whole milk, 0.003 ppm. The
    above figures should be kept under review.

    Further Information

    Further information is required on the results of total diet studies
    carried out in different countries.

    More information is needed on the residence occurring in crops grown
    in soils which were treated in previous years and on the possible
    occurrence of residues in cereal crops grown in treated soil or from
    treated seeds under conditions of extensive monoculture (i.e., no
    other crops grown in rotation) such as prevail in certain countries.

    Attention is also needed to residues present in products used for
    animal feed which are moving in international trade.


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    See Also:
       Toxicological Abbreviations
       Dieldrin (ICSC)
       Dieldrin (PIM 575)
       Dieldrin (FAO Meeting Report PL/1965/10/1)
       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)