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




    Velsicol 104(R), E-3314


    Residues from the use of heptachlor mostly occur as heptachlor
    epoxide. As conversion to the latter rapidly occurs in the animal
    body. It is considered here alongside the parent compound.

    Chemical names

    Heptachlor: 1,4,5,6,7,10,10-heptachloro-4,7,8,9,-tetrahydro-4,7-
    endomethyleneindene (British interpretation of IUPAC rules of
    nomenclature) and
    (USA Interpretation).

    Heptachlor epoxide:




    Biochemical aspects

    In plants and soil, heptachlor is converted to its epoxide which is
    more persistent on plants than the parent heptachlor (Gannon & Bigger,
    1958; Gannon & Decker, 1958).

    Rat liver microsomes have been proved to epoxidize heptachlor in
    vitro. The extent of epoxidation in vivo was about 10 times
    greater in males than in females (Wong & Terriere, 1965).

    Heptachlor epoxide is stored in the fat of dogs add rats. Some storage
    occurs in the liver, kidney and muscles but none in the brain. The
    metabolite was found in dogs after feeding heptachlor in a
    concentration of 1-3 mg/kg body-weight. When heptachlor was fed at
    high dosage levels to dogs, small amounts of unmetabolized heptachlor
    were also found in the fat, but this was not the case in the rat
    regardless of the level fed (Davidow & Radomski, 1953).

    In the rat, the maximum amount of the metabolite appeared after
    feeding 1, 5, 15 and 30 ppm heptachlor for two weeks. At 0.3 ppm,

    storage occurred in females but not in males, and at 0.1 ppm no
    storage occurred in either sex. Female rats accumulate about 6 times
    as much epoxide as males. Twelve weeks were required for complete
    disappearance of the metabolite from the fat after discontinuing
    heptachlor feeding (Radomski & Davidow, 1953).

    When cows were fed 3 mg/kg body-weight (in corn oil) daily for 14
    days, the epoxide level in the milk rose to a maximum of 1.8 ppm,
    equivalent to 44 ppm in butter fat. Residues could be detected in milk
    51 days after feeding ceased (Davidow et al., 1953). Mixtures of
    heptachlor and heptachlor epoxide were fed daily to 4 dairy cows for
    20 days (2 at 5 ppm and 2 at 10 ppm daily). Three days after feeding
    commenced, the minimum levels of heptachlor epoxide in the milk were
    0.26 and 0.34 ppm in the 2 cows fed 5 ppm, and 0.23 and 0.65 ppm in
    the 2 cows fed 10 ppm; the maximum levels after 15 days' feeding were
    0.63 and 0.80 ppm, and 1.51 and 1.66 ppm respectively (Storherr et
    al., 1960).

    Investigations on heptachlor storage in human fat in several parts of
    the world have recently been reported. The average ranged between 0
    and 0.24 ppm; it tended to be lower in those countries in which a high
    storage of DDT was recorded (Dale et al., 1965; Hayes et al., 1965;
    Robinson et al., 1965; Zavon et al., 1965).

    Heptachlor and its epoxide are included among the chlorinated
    hydrocarbon insecticides that stimulate the metabolism of drugs by
    microsomal enzymes (Remmer, 1964).

    Disturbance of the acid-base balance seems to be of great significance
    in the mechanism of action of heptachlor (Spynu & Osetrov, 1957).

    Acute toxicity

    Animal         Route       LD50                    References
                               mg/kg body-weight

    Rat            Oral        60-142*                 Velsicol Corporation, 1959
    Chick          Oral        63                      Sherman & Ross, 1961

                                  Heptachlor epoxide
    Animal         Route       LD50                    References
                               mg/kg body-weight
    Rat            Oral        34-88*                  Velsicol Corporation, 1959
    Mouse, male    Oral        32-48                   Velsicol Corporation, 1959
    * Sex differences.
    Intravenous lethal doses for heptachlor and heptachlor epoxide in the
    mouse are given as 40 and 10 mg/kg body-weight respectively (Radomski
    & Davidow, 1953). In the rabbit, the lethal dose of epoxide is 5-10
    mg/kg body-weight. The acute effects are neurotoxic disturbances like
    those observed with other chlorinated hydrocarbons (Velsicol, 1959).

    Short-term studies

    Rat. The addition of heptachlor (up to 45 ppm) or its epoxide (up to
    60 ppm) or both to diet of rats for 140 days produced liver
    microscopical changes, i.e. enlarged centrolobular cells showing big
    nuclei with prominent nucleoli, cytoplasmic fat accumulation and
    occasional aggregation of granules (Stemmer & Jolley, 1963). In an
    experiment involving 269 rats, it was demonstrated that these changes
    regress after withdrawal of the pesticide. It has also been suggested
    that these changes are produced indirectly, through the autonomic
    nervous system and the adrenal medulla. Electron microscopic studies
    demonstrated an increase of rough and smooth endoplasmic reticulum
    (Stemmer & Hamdi, 1963).

    In a reproduction study covering 3 generations, a group of 80 rats was
    given 6.9 mg/kg body-weight of heptachlor daily for 3 months before
    mating. Cataracts were found in 6.8 per cent of the young and became
    obvious between the 19th and 26th day. Among the parents, 15.2 per
    cent of the animals were affected and the lesions appeared after 4-9
    months. The only effect on reproduction was decrease of litter size
    (Mestitzova, 1966).

    The continuous exposure of rats to doses of over 7 ppm of either
    heptachlor or its epoxide increased the mortality of the pups during
    the suckling period. 10 ppm fed to 3 generations of rate showed no
    adverse effects on reproductive capacity, growth or survival (Witherup
    et al., 1955; Kettering Laboratory, 1959).

    Dog. When heptachlor was fed orally, dissolved in corn oil, to
    groups of 2 and 4 dogs at levels of 5 mg/kg and 1 mg/kg body-weight
    respectively, all the animals at the higher dose level died within 21
    days. At the lower dose level 3 out of 4 dogs died within 424 days but
    one was living at 455 days. No pathological data are available from
    this experiment (Lehman, 1952).

    Three dogs given heptachlor epoxide orally in dosages of 2, 4 and 8
    mg/kg a day for 5 days a week died after 22, 10 and 3 weeks
    respectively. Daily oral doses of 0.25 and 0.5 mg/kg body-weight did
    not produce any sign of illness during 52 weeks, but 0.25 mg/kg,
    estimated to be equivalent to 6 ppm in the diet, was reported as the
    minimal dose producing a pathological effect (Velsicol, 1959).

    Diets containing 0.5, 2.5, 5.0 and 7.5 ppm of heptachlor epoxide were
    given to groups of 5 dogs (2 males and 3 females, 23 to 27 weeks of
    age) for 60 weeks. No deaths attributable to heptachlor epoxide

    occurred. The weights of the male dogs tended to be inversely
    proportional to the concentration of the compound in the diet. The
    female dogs had normal weights. The liver weights were increased at 5
    ppm and above. Degenerative liver changes were seen in only 1 dog at
    7.5 ppm (Velsicol, 1959).

    Long-term studies

    Rat. Groups of rats (usually 10 males or 10 females) were fed diets
    containing 5, 10, 20, 40, 80, 160 and 300 ppm of heptachlor epoxide
    for 2 years. Concentrations of 80 ppm or higher resulted in 100 per
    cent mortality in 2-20 weeks. All the female animals given 40 ppm died
    within a period of 54 weeks. This concentration had no effect on the
    mortality of the male animals up to 104 weeks. Diets containing 20 ppm
    or less produced no signs of illness in male or female rats during a
    2-year period but an increase in liver weight was observed in diets
    containing more than 10 ppm (males) and 5 ppm (females) (Velsicol,

    Groups of 20 rats of strain CFW fed heptachlor epoxide at 10, 20 and
    40 ppm for 2 years showed significant increases in mortality only in
    females at 40 ppm. Liver weights in the females were slightly
    increased. Tumour incidence was lower in the experimental groups than
    in the controls and was independent of the content of heptachlor
    epoxide in the diet (Velsicol, 1959).

    CFN rats were fed heptachlor epoxide in concentrations of 0.5, 2.5, 5,
    7.5 and 10 ppm. No differences have been observed among the five
    experimental groups and their results can be considered together. The
    incidence of tumour-bearing animals was 8/23 (34 per cent) and 13/24
    (54 per cent) in the control males and females respectively; it was
    65/111 (58 per cent) and 92/114 (80 per cent) in the experimental
    males and females respectively. Again, many tumours were located in
    endocrine organs. Liver tumours were observed in 7 males and 12
    females in the experimental groups only (over-all incidence 19/225
    (8.4 per cent), but only two of them were malignant (Kettering
    Laboratory, 1959).

    Heptachlor dissolved in ethanol was added to the diet of CF rats as
    1.5, 3, 5, 7 and 10 ppm for 110 weeks. Each group, as well as an
    untreated control, included 40 animals (20 of each sex). Mortality was
    comparable in all groups. The number of tumour-bearing animals was
    16/40 at 0 ppm, 9/40 at 1.5 ppm, 13/40 at 3 ppm, 12/40 at 5 ppm, 15/40
    at 7 ppm and 12/40 at 10 ppm. Most tumours were found in the pituitary
    and other endocrine organs. No liver tumours were recorded. No
    preferential tumour site in any particular group was observed but all
    the 4 thyroid tumours observed were in the 7 and 10 ppm groups
    (Witherup et al., 1955).

    In a recent experiment carried out on a total of 154 female rats, a
    mixture of heptachlor/heptachlor epoxide 3:1 was added to the diet at
    0, 5, 7.5, 10 and 12.5 ppm for two years. Pituitary and mammary
    tumours were seen at all dose levels, including the controls; their

    incidence varied from group to group but not in relation to the dose
    of heptachlor. At the end of the two years, all groups including the
    controls showed liver histological changes, i.e. cell enlargement in
    centrolobular parts, loss of cytoplasmic granules and appearance of
    lipid vacuoles. No quantitative differences could be detected between
    rats given 0 and 5 ppm, whereas in the other groups the severity of
    the changes was related to the dose. At 12.5 ppm, regenerative liver
    changes were present (Kettering Laboratory, 1966).


    It is well established that heptachlor and its epoxide accumulate in
    body fat and persist there for long periods. The formation of epoxide
    is relatively rapid in the animal, plants and in the soil.

    The epoxide is more persistent than the parent compound and
    calculations of toxicity should perhaps be based on the data obtained
    with the epoxide rather than heptachlor, particularly since most
    reports indicate that the epoxide is the more toxic of the two

    A sex difference in toxicity has been observed, particularly in the
    rat, females accumulating heptachlor and its epoxide more than males.
    The toxic dose for female rats is lower than that for males.

    The changes observed in the liver cells are difficult to explain. A
    possible relation with tumour formation has not been demonstrated,
    while evidence has been presented that the change is reversible.

    Some suspicion of carcinogenicity could arise from one of the
    long-term experiments with heptachlor epoxide, since in both males and
    females the total number of tumour-bearing animals was higher than in
    the controls and liver tumours were only found in the experimental
    group. However, the interpretation of this finding is debatable: in
    the first place it concerns only one experiment among several
    long-term studies. In addition to this, the over-all incidence of
    liver tumours was low, most of them were histologically benign and no
    dose-response relationship was observed among the different
    experimental groups. For these reasons the carcinogenicity of
    heptachlor epoxide appears doubtful.


    Level causing no toxicological effect

    Rat. 5 ppm in the diet, equivalent to 0.25 mg/kg/day.

    Dog. 2.5 ppm in the diet, equivalent to 0.0625 mg/kg/day

    Estimate of acceptable daily intake for man

    0-0.0005 mg/kg body-weight*

    Further work required

    Elucidation of the significance of the finding that heptachlor and its
    epoxide are 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 these compounds, with a view to removing doubts
    which may remain as to their safety in use.


    Use pattern

    (a) Pre-harvest treatments

    The pattern of use for heptachlor has been evolving since it was
    introduced to agriculture in the 1950's. Up until 1960, it had a broad
    scale of use on forage, cereal, oil seed, vegetable, sugar beet and
    some nut crops, such as peanuts. There has been a gradual reduction of
    scale and pattern of use of this insecticide for various reasons
    including a desire to reduce the unintentional contamination of milk
    and animal products.

    The present trend in Canada, the USA and Western Europe is towards
    restricting its use to vegetable and cereal seed and to applications
    to the soil against insects therein. In certain countries it is also
    applied to young pasture plants that will not be grazed or fed in the
    season of use, to transplant water for seedlings and to ground cover
    under a restricted number of orchard trees. In each case there are
    restrictions concerning the access of livestock. In Japan, up until at
    least 1963, large quantities of heptachlor dust have been used on
    upland wheat, barley and rice.

    Dosages vary between countries. The average recommended dose is 2
    kilos of actual heptachlor per hectare for use on soil prior to or at
    planting on cereals and legumes, including barley, green beans, lima
    beans, corn, oats, rice, soybeans and wheat. To cereal seeds it is
    sometimes used as a slurry at 30-45 grams per 100 kilos applied prior
    to planting.

    (b) Post-harvest treatments

    No post-harvest use that has been reported.

    * Sum of heptachlor and heptachlor epoxide by weight.


    Canada 0.1 ppm (combined heptachlor and heptachlor epoxide) on beans,
    cabbage, lettuce, rutabagas (yellow turnips). (Heptachlor is scheduled
    under the Feeds Act as a compound that should not be present in
    commercial feed. In 1965 the tolerance for cereals was eliminated.)

    USA 0.1 in cabbage, lettuce, rutabagas and snap beans; zero for many
    other foods.

    Netherlands 0.1 ppm.

    In Canada and USA administrative "actionable levels" have also been
    established for residues of heptachlor and heptachlor epoxide in milk
    and other animal products. (It was the impression of the FAO Working
    Party that this practice was also in vogue in other countries, but
    reliable information was not available.)

    Residues resulting from supervised trials

    There is a large amount of information but much of it needs reviewing
    in the light of developments in analytical methods since about 1961.
    Although some of the earlier work has recently been reviewed in N.
    America, reliable recent results are scarce. The published literature
    in languages other than English is difficult to obtain. For example,
    Ishikura (personal communication, 1965) reports a large scale of use
    on cereals in Japan, but information does not appear to be available
    on the resulting residues.

    Lichtenstein & Polvika (1959), Young & Rawlins (1958) and many other
    authors publishing prior to 1961, suggested that no residues of
    heptachlor would persist in soil, and that none would be translocated
    from soil to plants, especially in forage crops. More reliable
    analytical methods have since showed that heptachlor and its epoxide
    persist in soil and can result in residues in some species of plants.
    The early investigations suggested that heptachlor could be used
    effectively on a wide range of vegetables, root crops, potatoes,
    forage and peanuts, with residues that would in many instances not
    exceed 0.1. ppm in the harvested product. Dawsey, Woodham & Lofgren
    (1961) stated that no residues were detected in 14 of 16 crops tested,
    but radishes and onions showed significant amounts when grown in plots
    treated with 0.25 of 0.5 lb of heptachlor per acre. However,
    Lichtenstein & Schulz (1965) found some build up, over a three-year
    period in soil from annual application of heptachlor at useful rates.
    Residues found in various crops grown in such soil were carrots up to
    0.69 ppm, potatoes up to  0.27, radishes up to 0.21 and beets up to

    Information from Burrage & Saha (1976) however suggests that the use
    of heptachlor for seed and soil treatments for certain cereals may be
    without fear of residues occurring on harvested grain, but the
    possible need for restrictions on the use of straw for animal feed and
    the significance of soil residues in crop rotations require further
    evaluation. Investigations on the relationships between residues in
    oil seeds and certain forage crops to their oil contents, recently
    reported by Bruce & Decker (1966), have been less reassuring.

    It would be most useful to have the results of similar investigations,
    with reliable analytical procedures from other countries. Information
    pertaining to residues in successive crops grown in rotation over a
    period of years after the initial treatment would be of particular

    Residues in food moving in commerce

    Information is slowly becoming available on residues in food moving in
    commerce. Some indirect information also is available from total diet
    studies, particularly in Canada and the USA. The occurrence of
    residues is broadly related to the scale of use in the respective
    countries. Residues have varied from traces to 1.0 ppm in up to 10
    per cent of the sample diets studied. A six-month average in one USA
    study indicated highest residues in these <10 per cent of diets as
    meat 0.05 ppm, dairy products (fat basis) 0.025 ppm and other food
    0.005 ppm, after processing for consumption.

    Canadian investigations of residues in commercial lots of sugar beet
    pulp suggest that heptachlor and heptachlor epoxide residues can occur
    in this animal feed, which if fed in too large a quantity can result
    in undesirable levels of residues occurring in animal products.
    Consequently, the feeding of contaminated sugar beet pulp is
    restricted to stated levels in the animals' diet. No heptachlor
    residues were found in a recent survey of meat and dairy products in
    Britain (Lewis, 1965).

    The Members of the FAO Working Party on Pesticide Residues, were aware
    that information is being obtained on residues in milk and animal
    products, commercial feeds, cannery wastes and other agricultural
    by-products moving in commerce but these data were not available for
    evaluation. Information of this kind is important in the evaluations
    of this compound and the co-operation of Member countries of FAO and
    WHO is requested in making it available for review.

    Fate of residue

    (a) In soil

    A body of information is becoming available in Canada and the USA.

    The persistence of residues in soil appears to be related to soil
    type, climate, soil management and cropping practices (Harris, 1966;
    Duffy & Wong, 1966; Lichtenstein & Schulz, 1960, 1965a; Harris &
    Lichtenstein, 1961; Wilkinson et al., 1964; Saha & Stewart, 1966).
    Similar information in other countries is relatively scarce (Weise,
    1964). Recent work suggests that low level soil residues may be
    contributing directly to residues in animal products, particularly in
    arid and semi-arid zones. In these areas, livestock are known to
    ingest some soil in foraging, resulting in residues in animal products
    that cannot be accounted for on the basis of residues in plants alone.

    It is possible that heptachlor and heptachlor epoxide residues can be
    dissipated from soil more rapidly than dieldrin or DDT (Harris &
    Lichtenstein, 1961).

    Bowman et al. (1965) suggested from laboratory evidence that
    heptachlor was changed to 1-hydroxychlordene in dry soils with low
    organic content and that no conversion of heptachlor to heptachlor
    epoxide was detected in these soils. In another study under field
    conditions, the same authors detected a small amount of
    1-hydroxychlordene in fine sandy loam. Duffy & Wong (1966) have
    reported the presence of 1-hydroxychlordene in some Canadian Atlantic
    provinces soils, but Harris (personal communication) has not been able
    to confirm its presence in Ontario soils. This degradation product has
    not been reported as a component of residues in food. (Its presence
    would be of interest since the LD50 to rats is only of the order of
    2400 mg/kg.) Gamma-chlordane is also a component of residues in soil.

    (b) In plants

    The conversion of heptachlor to heptachlor epoxide was first reported
    by Gannon & Decker (1958a, 1958b). The parameters that control the
    rate of epoxidation are still obscure, but several reports suggest
    that living tissue, even if only that of micro-organisms, is required
    (Davidow & Radomski, 1953). The exact mechanisms by which plants
    acquire residues of these compounds are are not understood either.
    Evidence for translocation by plants has been produced by Gannon &
    Decker (1958), Lichtenstein & Schulz (1960), Dawsey (1961),
    Lichtenstein et al. (1965), etc. Special attention has been given
    recently to the mechanisms of contamination and the location of these
    residues within plants and their stability (Byrne & Steinhauer, 1966;
    Burrage & Saha, 1966; King, Clark & Hemken, 1966; Saha & Stewart,
    1966). These data are all from Canada and USA. It would be useful to
    have comparable information from other sources.

    Some information is also becoming available on the relationship
    between the residues in soil, the oil content of plants and the
    residues that can be expected in them (Bruce & Decker, 1966). This
    type of information will have a special bearing on future evaluations
    of residues in oil seed crops or fibre crops (soybeans, cotton,
    peanuts, rape, etc.) whose by-products become animal food and may thus
    lead to residues in human food.

    (c) In animals

    Residues in animal products have attracted special interest. Low level
    residues have been detected and measured recently, in milk and dairy
    products using analytical methods that were not previously available
    (USA six-month average in up to 10 per cent of diets 0.025 ppm on a
    fat basis, in dairy products) and in meat (USA six-month average in 10
    per cent diets, 0.05 ppm). It has been suggested that loads of DDT
    already stored in the body fat of animals are partially responsible
    for the prevention of storage of heptachlor and heptachlor epoxide
    (Street, 1966, in press) and their degradation without storage, which
    could account for the observation that the loads of heptachlor epoxide
    in human body fat are lower in those parts of the world in which a
    higher rate of storage of DDT is recorded (Dale et al., 1965; Hayes et
    al., 1965; Robinson et al., 1965; Zavon et al., 1965).

    (d) In storage and processing

    If tolerances are to be based on amounts ingested by consumers,
    information on the behaviour of residues during storage and processing
    is needed. Although residues from heptachlor have often been regarded
    as stable, various data indicate that some disappearance takes place
    in storage and processing. This was found in work relating to the
    stability of residues in silage (unpublished information from USDA).
    Work of Saha & Stewart (1966) indicates that cooking peeled turnips
    results in complete disappearance of residues of heptachlor and
    heptachlor epoxide in turnip flesh, using an analytical method
    sensitive to 0.2 ppm. Similar results have been reported by
    Lichtenstein et al. (1965) for carrots. Gooding (1966) suggested that
    the normal processes of alkali-refining, bleaching, dehydrogenation
    and deodorization will remove all traces from edible vegetable oils,
    but definite proof has not been published. Residues do not appear in
    sugar or molasses when residues occur in sugar beets, but remain in
    the pulp. More information is needed on the fate of residues during

    Methods of analysis

    A number of multidetection systems are available for the detection and
    determination of residues 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 used and the residues
    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. (1964) using dimethylformamide, and other
    methods of confirmation of identity, e.g. using infra-red
    spectrophotometry, are also available. The methods are in general
    sensitive to 0.002 ppm of heptachlor or heptachlor epoxide in milk and
    0.02 ppm in most other foods, though under favourable conditions
    greater sensitivity can, if appropriate, be obtained.


    The potential hazard resulting from the use of heptachlor in food
    production has recently been reduced. The pesticide is now only being
    used on seeds and in soil employed in cereal and vegetable production.
    Present evidence indicates that soil and seed treatments can be
    continued without residues resulting in harvested grain. (The present
    evidence pertains to wheat. It may well extend to a wider range of

    Since the Temporary ADI is very small (0.0005 mg/kg/day), it is
    recommended that a Temporary Tolerance of 0.1 ppm be established, from
    uses of the insecticide in the soil and on to seed, only for raw root
    vegetables (other than potatoes), cole crops, head lettuce, spinach
    and other leafy vegetables. In this recommendation residues of both
    heptachlor and heptachlor epoxide are to be combined within the total
    of 0.1 ppm. This recommendation is based on the assumption that there
    will be no losses of residue in storage and processing, including

    In addition "practical residue limits" are recommended for potatoes at
    0.05 ppm; whole milk 0.002 ppm, dairy products 0.025 ppm on a fat
    basis; meat 0.05 ppm (fat basis).

    Additional data pertaining to these recommendations should be reviewed
    at an early date.

    Further information

    1. Many of the measurements undertaken prior to about 1961 of residues 
       after treatments of crops or of soil need to be repeated with the 
       aid of the more sensitive analytical techniques that have since 
       become available.

    2. More evidence is needed on the extent to which heptachlor is used
       in various countries and on the residues which occur in foods in
       international commerce; also on the fate of such residues during 
       the normal course of storage and processing, including cooking, 
       to which such foods are subjected before consumption.

    3. Investigations are desirable on the fate of low levels of
       heptachlor in feeds consumed by animals. This is because 
       information on commercial samples suggest that animal feeds may be 
       the sources of some of the albeit fairly low residues found in
       products from animals.


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    See Also:
       Toxicological Abbreviations
       Heptachlor (EHC 38, 1984)
       Heptachlor (HSG 14, 1988)
       Heptachlor (ICSC)
       Heptachlor (PIM 578)
       Heptachlor (FAO Meeting Report PL/1965/10/1)
       Heptachlor (FAO/PL:1967/M/11/1)
       Heptachlor (FAO/PL:1968/M/9/1)
       Heptachlor (FAO/PL:1969/M/17/1)
       Heptachlor (AGP:1970/M/12/1)
       Heptachlor (WHO Pesticide Residues Series 4)
       Heptachlor (WHO Pesticide Residues Series 5)
       Heptachlor (Pesticide residues in food: 1991 evaluations Part II Toxicology)
       Heptachlor (CICADS 70, 2006)