Hexachlorobenzene was first evaluated by the 1969 Joint Meeting
    (FAO/WHO 1970b) and recommendations were made for practical residue
    limits in a range of food commodities. The Meeting listed certain
    further work and information required.

         Since that time considerable interest has developed in HCB
    residues. There have been numerous problems in international trade as
    a result of the discovery of HCB residues in animal products and
    animal feeds. It is now recognized that HCB originates from industrial
    pollution as well as from agricultural practices.

         The realization that HCB is not biodegraded to any significant
    degree coupled with improved analytical methods has promoted extensive
    investigations which have revealed widespread contamination of animal
    feeds, animal products, people and other important components of the


         The 1969 Joint Meeting. on the basis of the results of a 13-week
    feeding study in rats, in which no adverse effects were detected at a
    daily dosage of 1.25 mg/kg, estimated a "tentative negligible daily
    intake" of 0-0.0006 mg/kg bw. The 1969 Meeting indicated that before
    an ADI could be established several toxicological studies would be

         The present Meeting decided that the term "tentative negligible
    daily intake" should not be used.

         Since the 1969 Joint Meeting no further work relevant to
    estimating an ADI has become available. It is known, however, that
    several laboratories are currently engaged in research that might
    provide a reasonable basis for the safety evaluation of HCB, and the
    Meeting urged that these data should be obtained for consideration by
    a future Joint Meeting.

         It was recognized that HCB residues in foods also arise from
    sources other than its proper use as a fungicide (e.g., industrial
    wastes from chlorination processes, and contamination of other
    chlorinated pesticides). Because of this, it will not be sufficient to
    attempt to control exposure merely by controlling the use of HCB as a
    fungicide. Notwithstanding the fact that residues of HCB stem less
    from its use as a pesticide than from other sources, the Meeting
    reaffirmed the recommendation made in 1969 that a suitable substitute
    for HCB as a seed fungicide should be sought. In addition the Meeting
    recommended that efforts should be made to reduce the level of HCB as
    an impurity in other pesticides. A specific recommendation to this
    effect was made in the case of quintozene.

         On the assumption that there is a level of HCB below which no
    significant toxicological effects can be expected, it was felt
    possible to give some provisional guidance. A daily intake of 0.0006
    mg/kg is considerably below any dosage rate known to be harmful, and
    the Meeting recommended that this value should be used as a guide for
    setting upper limits for residues until it was possible to establish
    an ADI based on the results of comprehensive toxicological studies.

         The Meeting considered the further work that was required for the
    establishment of an ADI and its recommendations are listed in the
    relevant section of this monograph addendum.


    Source of residues

         In the previous monograph (FAO/WHO 1970b) it was assumed that the
    only important source of HCB residues was contamination resulting from
    HCB seed dressings used to protect wheat from Bunt due to Tilletia
    foetide and T. caries against which HCB is spectacularly

         Since then it has been shown that HCB is present in significant
    amounts as a contaminant of the fungicides quintozene
    (pentachloronitrobenzene) and technazine (tetrachloronitrobenzene) and
    in the herbicide chlorthal-methyl (Daethal), (See also the monograph
    on quintozene). Analysis of 10 samples of commercial quintozene have
    shown HCB present in all 10, ranging from 0.1% to 10.8%. Of 12 samples
    of quintozene of European manufacture analysed in the Netherlands nine
    contained HCB at levels ranging from 0.8-5.3%. Three samples contained
    less than 0.1% HCR but these contained 3.6% pentachlorobenzene which
    is somewhat less intractable than HCB.

         HCB is also a by-product from the production of chlorinated
    solvents and as an intermediate for the preparation of
    pentachlorophenol. It has been shown that the commercial production of
    perchlorethylene gives rise to the formation of HCB which can be
    released unwittingly into the environment in quantities sufficient to
    contaminate large amounts of food commodities.

         In many instances the chlorination of hydrocarbons produces a
    heavy tarry residue. The tar contains a variety of highly chlorinated
    products, the two principal components being hexachlorobenzene and
    hexachlorobutadiene. These materials are not normally contaminants of
    the products of commerce produced by these reactions but if the tar is
    incinerated. dumped or discharged into municipal or industrial sewers
    the HCB quickly becomes dispersed in the environment. In some
    industrial processes it is possible to recycle the tar and thereby
    inhibit the formation of further quantities but there is no doubt a
    limit to such conservation. Any release of HCB into air or water must
    inevitably lead to accumulation of residues in human food. The
    predisposition which HCB possesses to accumulate in fatty bodies means

    that residues are detected in valuable components of the biosphere
    including people, animal fat. milk, birds, fish and wildlife.

    Evidence of residues in food in commerce or at consumption

         Since the previous review (FAO/WHO 1970b) considerable quantities
    of raw agricultural produce and food moving in trade within and
    between countries have been found to contain detectable quantities of

         The United States Food and Drug Administration Import Detection
    Reports issued each month indicate that substantial quantities of
    cheese and other dairy products from many different countries have
    been detained because of unacceptable residues in HCB.

         In a survey of pesticide residues in cheese imported into
    Australia in 1971, 68 of 184 samples were found to contain HCB at
    levels ranging from 0.03 to 4.06 ppm. More than 10% of the samples
    contained residues in excess of 0.3 ppm. Cheese from 16 countries was
    involved and HCB was found in samples from every country except two
    from which only single samples were examined. The incidence ranged
    from 10% to 75% for the remaining 14 countries.

         Results of a total diet study carried out in Australia (NHMRC
    1971) indicate that 46% of 240 samples of a total diet collected in
    six states over four seasons contained HCB at levels above 0.001 ppm.
    Of 10 food groups the ones with the highest incidence were meat
    dripping, meat and dairy produce. The highest concentration was found
    in meat dripping but this food represents only 1% of the total diet. A
    further survey has been conducted since the use of HCB seed dressings
    has been discontinued but the results are not yet available.

         There have been reports of significant residues of HCB in breast
    milk from the Netherlands (Tuinstra, 1971), Australia (Siyali, 1972)
    and Germany (Acker and Schulte, 1971). Swedish workers (Westoo et al.,
    1972) report significant levels of HCB in the breast milk of each of
    10 individual women selected at random. The level ranged from 0.07 to
    0.22 ppm expressed on the fat basis. In another survey of 18 samples,
    each a composite from 10-20 mothers, the level of HCB ranged from 0.06
    to 0.59 ppm (mean 0.19 ppm). This was slightly less than 8% of the
    level of DDT and metabolites and equal to the concentration of
    dieldrin in the same samples.

         An Australian study of occupationally exposed individuals showed
    levels in blood ranging from 0 to 0.41 ppm. A control group with no
    known exposure showed blood levels ranging from 0 to 0.095 ppm. HCB
    was detected in 95% of the people tested (the minimum level of
    detection being 0.00001 ppm) (Siyali, 1972).

         Another Australian study of a random selection of perirenal fat
    samples taken at autopsy revealed 106% of the samples positive with

    levels from "trace" to 8.2 ppm; 33% of the samples contained greater
    than 1 ppm. The mean of all samples was 1.25 ppm (Brady and Siyali,

         A German study detected residues of 6.3 ppm in human fat and 5.3
    ppm in the fat of human milk (Acker and Schulte, 1971). A recent
    Japanese study has shown levels in human adipose tissue to range from
    0.30 to 1.48 ppm (Curley et al., 1973).

         A survey of organochlorine residues in human fat in the United
    Kingdom (Abbott et al., 1972) showed that HCB residues occurred
    generally in the whole population ranging from 0.01 to 0.29 ppm with a
    mean of 0.05 ppm in 201 samples. Although this was the third such
    study carried out by the same investigators since 1963, HCB had not
    been detected or reported previously. The paper indicates some
    difficulty with identification and quantitation of the HCB.

         Swedish investigators (Westoo et al., 1971) report finding HCB in
    samples of local and imported breakfast cereals. The concentration
    ranged from 0.002 to 0.007 ppm which was considerably below the level
    of lindane. Lindane occurred in all samples at levels ranging from
    0.03 to 1.54 ppm.

         The Netherlands authorities in the course of inspecting imported
    animal foodstuffs found that certain milling fractions of raw cereals
    contained HCB residues ranging up to 3 ppm. These residues were the
    cause of considerable difficulties because of the magnification which
    occurs in animal fat, milk and eggs.

         Raw cereals and their milling fractions are not the only source
    of HCB residues which find their way into animal feeds. Import
    inspection in the Netherlands has revealed consistent and relatively
    high levels of HCB in bran, beans, clover seed. chicory root, copra
    press cake, cotton press cake, lespedasia meal, linseed, maize meal,
    peas, pollard pellets, potatoes, sorghum, soybean meal, sunflower
    press cake, vetch and wheat middlings. Rice was one of the few
    commodities examined which was consistently free of HCB. Commodities
    contaminated with HCB have been intercepted coming from Argentina,
    China, Indonesia, Morocco, Madagascar, Syria, South America, Turkey
    and United States of America. Although the level of HCB residues found
    in imported feed commodities entering the Netherlands was lower than
    that of DET residues, the frequency with which HCB residues occurred
    was much higher. It was reported to FAO (Swiss Federal Health Service
    (1973)) that residues of HCB had been detected in various commodities
    as follows:

         Meat fat            0.01-0.075 ppm
         Poultry fat         0.001-0.5 ppm
         Eggs (whole)        0.002-0.3 ppm
         Milk fat            0.002-0.04 ppm
         Milk products       0.04-0.5 ppm (1 sample
           (fat basis)          0.9 ppm)
         Raw cereals         0.001-0.05 ppm

         Swedish workers (Westoo and Noren, 1973) report finding small
    amounts of HCB in imported carrots, radishes and tomatoes, frequently
    in lettuce (up to 0.25 ppm) and in parsley. This appears to be the
    first occasion on which HCB had been reported from similar surveys
    carried out in Sweden and it is interesting to speculate whether it
    reflects improvements in methodology which enabled the detection of
    residues that have always occurred but have not been detected.

    Fate of residues

         There continues to be a lack of any experimental evidence to
    indicate that hexachlorobenzene is metabolized by plants, animals, or
    soil micro-organisms or that it is degraded into other products in the

         In a study resulting from accidental contamination of milk,
    (Goursaud et al., 1972) it was found that the source of the
    contamination appeared to be chicory roots used as cattle feed and
    which had been treated, prior to forcing, with the fungicide
    quintozene. The commercial 30% quintozene formulation contained 3%
    HCB. When milk cows were experimentally fed diets containing 2 mg/day
    of HCB and 25 mg/day of quintozene, progressive increases in the HCB
    content of the milk reached 2 ppm on the seventh day. Only traces of
    quintozene were found in the milk.

         In a series of feeding experiments involving sheep, laying hens,
    and growing chickens (Avrahami and Steele, 1972a, b, c) it was
    demonstrated that feeding dietary levels of HCB ranging from 0.1 to
    100 ppm resulted in rapid accumulation of HCB in omental fat (sheep),
    body fat (chickens and laying pullets), and egg yolk. Sheep stored HCB
    in body fat to the extent of seven to nine times the feed level at all
    levels tested. The half-life of HCB in fat appeared to be 10 weeks for
    sheep and 18 weeks in the case of chickens. For chickens and pullets,
    the fat: feed ratio ranged from 30:1 to 20:1 with increasing feed
    concentration. HCB concentration in egg yolk was about 25% of that in
    the corresponding fat of hens.

         Mention was made (Stijve, 1973) of some evidence for partial
    degradation of hexachlorobenzene in chicken fat samples during a
    survey of residues in cereals, fats, and dairy products using improved
    analytical methods. However, no controlled experiments were carried

         In a feeding study in the Netherlands (Verschuuren et al., 1973)
    young pigs were given a ration to which HCB had been added at the rate
    of 0.25 ppm. The pigs were fed for 14 weeks from the age of eight
    weeks. A sample of subcutaenous fat was taken by biopsy prior to the
    feeding of the fortified ration. At the end of 14 weeks feeding, the
    pigs were slaughtered. Vital organs were weighed. Liver and kidney
    were examined microscopically and samples of fat, brain, kidneys,
    liver and blood were taken for analysis. The total residue of HCB in
    the body of the pigs was estimated to approximate the total HCB

    administered in the feed indicating that little had been excreted. The
    residue in fatty tissue (1.6 ppm) was higher than an acceptable level.
    The ratio between the mounts of HCB in the diet and in the fat of the
    pig, in a period of 14 weeks was 8.3:1.

         Australian studies (McCray 1973) showed that sows receiving HCB
    in rations for a few weeks accumulated sufficient residue to transfer
    considerable quantities to the offspring at birth. They excreted
    substantial amounts in the milk so that the piglets acquired a body
    burden, sufficient to remain at significant levels even when they had
    grown to 100 kg bw. The awe investigator found that cows receiving HCB
    for a few days built up a reservoir in the fat which caused
    significant residues in milk at the end of the second subsequent

         Studies in the Netherlands (Vos et al., 1972) involving the
    feeding of from 0.05 ppm to 0.3 ppm of HCB in the rations to broiler
    chickens for seven weeks, showed that a plateau in the concentration
    of HCB in the fat was reached by the twentyninth day of feeding. The
    residue level in fat was directly proportional to the level of HCB in
    the ration, being approximately 12 times more concentrated.

         These investigators carried out parallel experiments using
    lindane, DOT, dieldrin, ondrin and heptachlor. They drew particular
    attention to the distinct difference between the properties and fate
    of lindane and HCB. HCB and heptachlor epoxide had the strongest
    tendency to accumulate of all the compounds tested. It was observed
    that relatively little lindane is accumulated in broiler fat when
    rations are contaminated with lindane.

         Other workers in the Netherlands (Wit et al., 1973) investigating
    the uptake of HCB from traces in foodstuffs set up an extensive trial
    involving the feeding of groups of pigs with prepared feeds containing
    varying amounts of pollard known to contain small quantities of HCB.
    They found it was impossible to obtain a ration that did not give rise
    to low levels of HCB in the fat of pigs fed for 15-16 weeks. Such
    animals showed 0.06-0.1 ppm HCB in fat. Pigs receiving rations
    containing 0.12 ppm HCB showed residues of 1.3 ppm in fat while those
    receiving 0.3 ppm in their dry ration had 2.3 ppm in their fat 15-16
    weeks later. The "concentrating factor" (the ratio of concentration in
    fat to that in feed) was estimated to range from 8 to 11 fold. This
    compared with 0.3 for lindane, 2 for dieldrin, 3 for alpha-BHC and 5
    for DDT. HCB is truly cumulative when fed to pigs.

    Methods of residue analysis

         Several papers have appeared on improvements in analytical
    techniques and these reveal that extraction and Clean-up procedures
    employed in typical multi-detection procedures give relatively poor
    recovery of HCB.

         Taylor and Keenan (1970) point out that in the method of Mills
    (1959) the exceptionally non-polar character of HCB results in it

    remaining preferentially in the hexane of the hexane/acetonitrile
    portion clean-up. In counter-current separations recovery is less than
    10%. Other methods using direct extraction with adsorption clean-up
    give acceptable recoveries from fatty substrates. (Onley and Mills
    1962; Moats, 1963; Langlois et al., 1963). The recovery from grain and
    cereal products where the levels of interest are much lower than
    animal products is unsatisfactory unless the sample is refluxed with
    hexane. The extract is then submitted to a Florisil clean-up.

         Taylor and Keenan (1970) developed a technique whereby the hexane
    extract was steam distilled to give recoveries of 95%-100%.
    Identification using TLC at the low concentrations found in cereal
    products is not sufficiently sensitive and the authors propose the use
    of two separate columns. The retention times relative to  dieldrin of
    a range of organochlorine pesticides on five stationary phases is
    given. The retention time for HCB is from 12 to 22% of the
    corresponding time for dieldrin. Some columns do not adequately
    separate HCB from alpha-BHC. A paper on the design of columns (Taylor,
    1970) provides useful guidance.

         Smythe (1972) outlines the difficulties in obtaining good
    recoveries of HCB from fatty substrates and proposes means to ensure
    adequate recoveries.

    Example of national tolerances

         Several countries have recently announced legal limits on
    administrative action levels for HCB residues in various commodities.
    These include:


    Switzerland           Meat fat                 0.5 ppm
                          Milk products            0.3 ppm (fat basis)
                          Raw wheat                0.05 ppm
                          Milled products
                            from wheat             0.01 ppm
                          Milk (whole)             0.01 ppm

    Germany               Meat fat                 0.5 ppm
                          Milk and milk
                            products               0.5 ppm (on fat basis)

    Netherlands           Meat fat                 0.5 ppm
                          Milk and milk
                            products               0.3 ppm (on fat basis)

    USA                   Milk fat                 0.5 ppm



         Since HCB was considered in 1969 information has become available
    to fulfil the requirements for residue information set out in the

         In addition, considerable data have been published indicating
    that HCB is a widespread contaminant of many food commodities, most
    particularly those of animal origin. Originally it appeared that the
    only source of contamination was the HCB seed-dressing fungicide used
    to disinfect wheat seed from bunt (Tilletia sp.). Steps have been
    taken to prohibit the use of HCB fungicides in several countries. It
    is now obvious that HCB occurs as an impurity in several other
    pesticides, particularly quintozene and technazine and possibly
    pentachlorophenol. More important still is the widespread occurrence
    of HCB as a by-product of industrial processes and the incineration of
    industrial wastes. The detection of HCB residues in many commodities
    used in animal feeds give rise to concern.

         Improved analytical techniques have become available recently and
    it is anticipated that their use will reveal that HCB occurs more
    frequently and at higher levels than is currently believed to be the

         The practical residue limits recommended by the 1969 Joint
    Meeting have been reviewed in the light of information that has since
    come to hand and the following comments are offered on the individual

    (1) Raw cereals (wheat) - 0.05 ppm

         In view of the evidence that cereals other than wheat are
    contaminated by HCB it would be wise to delete reference to (wheat)
    and to make the limit applicable to all cereals. The level 0.05 ppm
    still appears necessary to accommodate residues that appear from
    unknown sources. Such a limit will, however, discourage mis-use of
    treated seed. In due course it is hoped that the limit could be
    reduced to 0.01 ppm but much more data are required before such an
    amendment could be made.

    (2) Cereal products from wheat - 0.01 ppm

         It is considered that this definition is not sufficiently
    specific and that it should be changed to "flour". Milled products
    with a high bran content must inevitably contain higher amounts since
    the contamination is generally on the outside of the individual

    (3) Fat of cattle, sheep, goats, pigs and poultry - 1 ppm

         It would be desirable to aim at reducing this limit to 0.5 ppm
    within five years. However, it is known that breeding animals with

    residues pass a large proportion of the HCB residue to their offspring
    which retain the burden for many years. Pigs especially are prone to
    accumulate high levels. There is no known way to reduce the residue
    level once it has been built up in an animal as a result of any form
    of accidental exposure. To reduce the limit to 0.5 ppm at this stage
    would necessitate the destruction of highly valuable food and there is
    insufficient evidence that any or many countries could comply with
    such a level without severe losses.

    (4) Milk products (fat basis) - 0.3 ppm

         This limit can apparently be met only when the cows have adequate
    access to residue-free pasture or forage and that there is strict
    control over residues in feeding stuffs. The slightest contamination
    of dairy cows will result in residues in excess of 0.3 ppm. It is
    considered that 0.5 ppm would be a more realistic level until there is
    adequate data obtained by reliable analytical procedures.

    (5) Eggs (shell-free) - 1 ppm

         There is insufficient evidence from more than a few countries on
    which to decide whether such a limit could be reduced. More data are
    required from many countries.


         In the light of information considered it is recommended that
    action be taken to reduce the general environmental contamination by
    HCB especially from industrial sources not previously recognized as
    important in the emission of this intractable contaminant.

         Until such time as it is possible to reduce the contamination
    significantly, practical residue limits are required as a basis for
    uniform and reasonable administrative action. The recommendations made
    in 1969 have been reviewed in the light of new information and the
    limits have been amended as follows:

    Practical residue limits

         Fat of meat of cattle, sheep, pigs           1 ppm
         and poultry

         Eggs (shell-free)                            1 ppm

         Milk and milk products (fat basis)           0.5 ppm

         Raw grain                                    0.05 ppm

         Flour and similar milled cereal products     0.01 ppm

         At this stage it is not possible to propose limits for HCB
    residues in animal feedstuffs or compound feeds but such limits must
    of necessity be low if foods of animal origin are to conform to the
    above limits.


    Required (before an acceptable daily intake can be estimated).

    1. Long-term studies in suitable mammalian species to provide
    histologic data and biochemical data, particularly with respect to the
    known porphyrogenic action, and an assessment of tumorigenic

    2. Reproduction studies.

    3. Studies of teratogenic potential.

    4. Studies of pathways of metabolism and pharmacokinetics of HCB in
    rats and preferably in other species, including studies on tissue
    levels producing toxic effects.

    5. Information on HCB occurring in foods moving in commerce, using
    analytical procedures known to recover and determine the total of any
    such residues that may be present.

    6. Information on all possible sources of environmental contamination
    by HCB

    7. Information from many countries on residue levels in animal
    foodstuffs and compound feeds.


    Abbott, D. C., Collies, G. B. and Goulding, R. (1972) Organochlorine
    pesticide residues in human fat in the United Kingdom 1969-71. British
    Medical Journal: 553-556

    Acker, L. and Schulte, E. (1970) Uber das Vorkommen von chlorierten 
    Biphenylen and Hexachlorbienzol neben chlorierten Inseektiziden in
    Human milch und menschlicken Tettgevele. Naturwissenschaften, 57:

    Acker, L., and Schulte, E. (1971) Organochlorine compounds in the
    human body. Unschan 71(23): 848

    Avrahmi, M., Steele, R.T. (1972) Hexachlorobenzene 1,11,111. New
    Zealand J. Agr. Roe. 15(3): 476-488

    Brady, M.N. and Siyali, D.S. (1972) Hexachlorobenzene in human body
    fat. Mod. J. Aust. 1: 158-161

    Burke, J. A. and Holswade, W. (1966) J.A.O.A.C, 49: 374-385. (Quoted
    by Smyth and by Taylor)

    Collins, G.B., Holmes, D.C. & Wallen, M. (1972) Identification of HCB
    residues by gas-liquid chromatography. J. Chromatogr., 69: 198-200

    Curley, Boise, Jennings, Villaneuvor, Tamalis and Akazaki. (1973)
    Nature 242, 338-340

    FDA. (1969) Pesticide Analytical Manual Vol. 1 Food and Drug
    Administration, Washington, D.C. (Since transferred to the
    Environmental Protection Agency)

    Goursaud, J., Luquest, F. M. and Casalis, J. (1971) Sur la pollution
    des laits de feme par les residus do pesticides dens les departments
    du nord et du pas-de-Calais. Lait, 51(508), 559

    Langlois, B.E., Stomp, A.R., Liska, B.J. (1963) -J. Dairy Science
    46: 854-855

    Moats, W.A. (1963) J.A.O.A.C. 46: 172-176 (from review by Taylor and

    McCray, C.W. (1973) Preliminary report on study of excretion of HCB
    from pigs and cows - Report to Pesticides Co-ordinator - Australia

    Miller, G.J. and Fox, J.A. (1973) Chlorinated hydrocarbon pesticide
    residues in Queensland human milks, Medical Journal of Australia,

    Moubry, R.P., Myrdal, G.R. and Jensen, H.P. (1967) J.A.O.A.C, 50,
    885-888 (quoted by Smyth)

    Newton, K.G. and Greene, N.C. (1972) Organochlorine pesticide residue
    levels in human milk - Victoria, Australia - 1970. Pesticides
    Monitoring Journal 6(1): 4-8

    NHMRC. (1971) Report of pesticide residues in the total Australian
    diet - National Health and Medical Research Council, Canberra,

    Onley, J.H. and Mills, P.A. (1962) J.A.O.A.C. 45: 983-987 (From review
    by Taylor and Keenan)

    Siyali, D. (1972) Hexachlorobenzene and other organochlorine
    pesticides in human blood. Mod. J. Aust. (2): 1063-66

    Siyali, D.S. (1973) Polychlorinated biphenyls, hexachlorobenzene and
    other organochlorine pesticides in human milk. Med. J. Aust. p.

    Smythe, W. (1972) Detection of HCB residues in dairy produce meat and
    eggs. J.A.O.A.C. 55: 806-808

    Swiss Federal Health Service. (1973) Communication to FAO

    Taylor, I.S. (1970) Design of a column for the gas - chromatographic
    analysis of organochlorine pesticides. J. Chromatog., 52: 141-144

    Taylor, I.S. and Keenan. F.P. (1970) Studies on the analysis of
    hexachlorobenzene residues in foodstuffs. J.A.O.A.C. 53(6): 1293-5

    Tuinstra, L.G.N. (1971) Organochlorine insecticide residues in human
    milk in Leiden Neth. Milk Dairy J. 25: 24-32

    Westoo, G. and Noren, K. (1973) Residues of organochlorine and certain
    organophosphorus pesticides in fruits, berries, vegetables and roots
    1968-1972 Var Foda, 25 suppl. 1,6 (Stockholm)

    Wit, S.L. and van de Kamp, C.G. (1973) Stapeling van persistente
    bestrijdingsmidolden in varkers. Report No. 47/73 Tox. Report to
    Veterinary Inspector, Netherlands Ministry of Agriculture

    Zitco, V. and Choi, P.M.K. (1972) PCB and DET in eggs of cormorants,
    gulls and ducks from the Bay of Fundy, Canada. Bull. Fry. Cent. and
    Toxicol., 7(1)


    See Also:
       Toxicological Abbreviations