WHO/Food Add./68.30



    The content of this document is the result of the deliberations of the
    Joint Meeting of the FAO Working Party of Experts and the WHO Expert
    Committee on Pesticide Residues, which met in Rome, 4 - 11 December,
    1967. (FAO/WHO, 1968)

    Rome, 1968


    These pesticides were evaluated under the heading "Phenylmercury
    acetate (and other organomercury compounds)" by the 1966 Joint Meeting
    of the FAO Working Party and the WHO Expert Committee on Pesticide
    Residues (FAO/WHO, 1967a). Since the previous publication, the results
    of additional experimental work have been reported. This new work is
    summarized and discussed in the following monograph addendum.


    Chemical names

    The following organomercury compounds additional to those in the
    previous monograph are noted:

    Methylmercury compounds: MeHgX

    methylmercury acetate

    methylmercury nitrile

    methylmercury propionate

    methylmercury sulphate

    methylmercury p-chlorobenzoate

    methylmercury pentachlorphenate

    methylmercury oxinate

    methylmercury 2,3-dihydroxyprophyl mercaptide

    N-methylmercury 1,2,3,6-tetrahydro-3,6-endomethano-

    Ethylmercury compounds: EtHgX

    ethylmercury silicate

    ethylmercury oleate

    ethylmercury stearate

    ethylmercury hydroxide

    ethylmercury pentachlorophenate

    ethylmercury urea

    ethylmercury acetone

    ethylmercury 8-hydroxyquinolinate

    Alkoxyarylmercury compounds RO(CH2)MgX

    methoxyethylmercury dicyandiamide

    methoxyethylmercury benzoate

    methoxyethylmercury lactate

    ethoxymethylmercury silicate

    ethoxythylmercury hydroxide

    1-Carboxy-3-ethoxyethylmercury propanedicarboxylate-2,3
    Chlorometroxypropylmethyl acetate

    Arylmercury compounds: ArHgX

    phenylmercury hydroxide

    phenylmercury iodide

    phenylmercury benzoate

    phenylmercury lactate

    phenylmercury oleate

    phenylmercury propionate

    phenylmercury naphthenate

    phenylmercury pyrocatechinate

    phenylmercury triethanolammonium lactate

    phenylmercury formamide

    diphenylmercury dodecenyl succinate

    tolylmercury chloride

    N-tolylmercury p-toluenesulphamilide

    Other Organomercury Compounds

    Ethyl phenethynyl mercury


    Methyl bromide mercurimercaptide

    Methoxacetyl mercurychloride

    Cresol mercury naphthenate


    Biochemical aspects

    Groups of 15 rats were given drinking water containing 2g/ml of
    mercury as 203Hg-labelled methyl-, ethyl-, and propylmercury cyanide,
    hydroxide and propanediolmercaptide, for 3 weeks. One-third of the
    animals from each of the nine groups were killed at one, two and three
    weeks for tissue analysis. Activity was examined in kidney, blood,
    liver and brain, and concentrations were generally found to be
    distributed in that order, the greatest concentrations always found in
    the kidney. It was found that the tissue concentrations increased with
    time. No special affinity of alkyl mercury for the brain was found:
    the blood concentrations were generally 20 times brain levels, and the
    author felt that most or all of the brain activity could be accounted
    for on the basis of blood content. Relative tissue partitions were
    constant with time for each alkyl mercury cation regardless of anion,
    indicating marked stability of the alkyl-mercury bond (Ulfvarson,

    In similar subcutaneous injection studies with methyl- and
    phenylmercury hydroxide, methylmercury dicyandiamide,
    methoxyethylmercury hydroxide and mercuric nitrate, lasting 18 days,
    the body half-life of the methylmercury compounds was found to be
    about 20 days and no steady-state was achieved during the time of the
    experiment. In the case of the other three compounds, the half-life
    was found to be about 10 days and steady states were achieved. The
    renal concentration of the methylmercury compounds was relatively
    quite low and the blood and muscle concentration high. The principal
    route of excretion for all was via the faeces, even in the case of the
    latter three compounds, which were highly concentrated in the kidneys
    (Ulfvarson, 1962).

    In dogs given intravenous injections of 30-60 mg/kg of methylmercury
    thioacetamide, or of tracer doses labelled with 203Hg, the highest
    brain concentrations were found in the calcarine fissure and
    surrounding area; this was also the site of the greatest histological
    change. The distribution was nearly equal in the gray and white
    matter. In rats sacrificed 6-10 hours post-injection, the highest
    subcellular concentrations were found in the mitochondria; but in
    longer experiments, more equal distribution in these fractions was
    seen, except that the major part of the mercury in the nuclear
    fraction was accounted for by that carried in the erythrocytes
    (Yoshino et al., 1966).

    Short-term studies

    Chicken. Groups of 3-5 hens were fed 0 and approximately 3 and 4.5
    ppm of mercury as methylmercury dicyandiamide on dressed grain for 1-2
    months. Group average mercury consumptions were: 0, 2.8 and 3.5
    mg/bird/week of mercury. No mercury-attributed difference in general
    behaviour and egg production was seen between the groups, and gross
    and microscopic pathology were comparable. Mercury levels in whole
    eggs of the control birds averaged about 0.01 ppm while the mean in
    both treated groups after one month was about 8 ppm. Residues in whole
    eggs of the lower test level group rose to 11 ppm in the fifth and
    sixth weeks and those in the higher level group rose to 12 ppm in the
    seventh and eighth week. The first significant mercury residue was
    detected 3 days after beginning the trial. Mercury residues in the
    muscle of control hens ranged from 0.005 to 0.02 ppm, and in the test
    groups from 1.5 to 8.7 ppm. Residues in control livers were from nil
    to 0.1 ppm, and in test animals from 8.1 to 24.1 ppm (Smart & Lloyd,

    Observations in man

    A 16-month-old infant, apparently healthy-normal for his first 13
    months, fed probably almost daily from the ninth month of age porridge
    made from grain treated with methylmercury dicyandiamide, was found to
    have signs of extensive central nervous system motor disturbance and
    mental retardation, in addition to slight renal disease. The urine
    contained about 30-100 g/l of mercury. The EEG was essentially
    unremarkable. Treatment with BAL was not effective. Of the other
    members of the family, the father had undergone treatment for mercury
    poisoning from the same source; and the mother, although showing 64
    and 28 g/1 of mercury in two urine samples taken, remained
    asymptomatic, but gave birth to a baby girl who, although showing no
    other signs of mercurialism and a urinary content of less than 3 g/l,
    later showed marked mental retardation and neuromotor deficit. The
    authors also report four other cases of accidental methylmercury
    dicyandiamide poisoning in children. None showed a urinary mercury
    content greater than 3 g/l; two showed initial acute cerebral signs,
    excitement, dizziness, hallucinations and fever; and only one showed
    any EEG change, a slight dysrhythmia (Engleson & Herner, 1952).

    Eighty-nine cases of a severe neurological disorder from 1953 to 1965
    in the small Minamata Bay area of south-western Japan were attributed
    to ingestion of fish and shellfish from the bay, which has been
    contaminated with mercury from the effluent of a vinyl chloride
    manufacturing plant. The mercury was believed to be an alkylmercury
    salt. Fish-eating birds and animals in the area were also affected. In
    a few isolated instances, the person became ill after a definite
    latent period of a few weeks after ingestion of shellfish from the
    bay. Thirty-nine of the cases were fatal. No sex or age difference in
    incidence was observed. Clinical findings included incoordination,
    involuntary movements, upper motor neuron degeneration and often

    severe emotional and intellectual impairment. It was felt that the
    children were particularly liable to residual defects. Autopsies
    showed that the pathological changes were mostly confined to the
    central nervous system, with gross cerebral oedema and atrophy of the
    paracalcarine cerebral cortex and the cerebellum. Nerve-cell
    degeneration and gliosis was found in the granular layer of the
    cerebellum and, to a lesser degree, in the basal ganglia,
    hypothalamus, mid-brain and cerebral cortex (Kurland et al., 1960).

    In the same geographic area, from 1955 to 1960, seventeen cases of
    cerebral palsy have been observed in infants who had eaten no fish or
    shellfish from the area, born of mothers with generally no
    neurological disease. In two cases presented in detail, terminating
    fatally at 2-1/2 years and 6-1/4 years, clinical findings included
    spastic paralysis, upper motor neuron deficit, epilepsy and idiocy. At
    autopsy, lesions very similar in type and distribution to those seen
    in cases of "Minamata disease" were found. Although the disease had
    been reported in the families of these two infants, one of the mothers
    had remained asymptomatic and the other had only experienced
    occasional numbness of the fingers (Matsumoto et al., 1965).

    Mud from Minamata Bay showed mercury residues ranging from 19 to 59
    ppm and 2010 ppm in the town effluent channel. Oysters from the middle
    of the bay contained 38-69 ppm of mercury and mercury residues in
    samples of shellfish from three different areas showed residues
    ranging from 27 to 102 ppm. Shellfish from the bay were found to be
    toxic to laboratory animals, producing weight loss, neurological
    damage, convulsions, coma and death. Day-old chicks were affected 8-10
    days after beginning diets containing the seafood, whereas signs
    developed in cats only after 5-8 weeks. Total ingestion of only 20-80
    mg of mercury per animal from this source sufficed to produce
    intoxication in cats. Abnormal quantities of mercury were found in
    Minamata cats dying of the disease up to 62,36,19 and 70 ppm in liver,
    kidney, brain and hair, respectively, vs.4, 0.8, 0.1 and 3 ppm in
    the same tissues of "control" cats from the same area.

    Mercury residue ranges in eight patients who died within three months
    of development of the disease were: liver, 35-71 ppm; kidney, 29-144
    ppm; and brain, 5-21 ppm (Kurland et al., 1960)


    In view of the toxicity of organo-mercurial compounds, as well as the
    fact that mercury is present in nature at various levels, it is very
    important to know more about the overall intake of mercury from the
    environmental background, as well as its health hazards.

    It will also be helpful to know the nature of the mercurial compounds
    appearing in food.


    It is not possible to establish an acceptable daily intake on the
    basis of available information. Any use of mercury compounds that
    increases the level of mercury in food should be strongly discouraged.

    Further work required

    Information on the background level of mercury in the environment in
    different parts of the world as well as epidemiological observation in
    regions where the background level is known.


    This section draws particularly upon the paper on Organomercury
    Compounds prepared for the Codex Committee on Pesticide Residues by
    the UK Delegation to the Committee with assistance from the Swedish
    delegation (CCPR, 1967a) which at its meetings in the Hague 18-22
    September 1967 was referred by the Codex Committee to the Joint
    Meeting for a toxicological evaluation of the maximum residues therein
    suggested. These residues relate to crops or food stuffs treated with
    organomercury compounds in accordance with good agricultural practice
    and are:

              rice                     0.3 ppm (provisional)

              apples, tomatoes         0.1 ppm

              eggs, meat +             0.1 ppm

              potatoes                 0.05 ppm

              wheat, barley            0.03 ppm

              + except liver and kidney

    The Codex Committee (CCPR, 1967b) also commented that a permissible
    residue for organomercury, as distinct from inorganic mercury [or
    total mercury] could not be put forward on information then available;
    and added that the maximum level of mercury in sea water fish appeared
    from the limited evidence available to be 0.1 ppm although in a
    mercury-contaminated environment fish tended to accumulate mercury and
    very high residue levels could occur in these circumstances.


    Pre-harvest treatments

    Table I gives supplementary details of the rates of application of
    organomercurials for pre-harvest and seed treatments, and is taken
    from the Codex Committee paper, having been obtained by that Committee
    by means of a questionnaire to FAO Member Governments thought to be
    using significant quantities of mercury in agriculture.

        Table I  Rate of Application of Organomercurials

    Crop/Seed          Country            Rate of each application         Stage of
                                       g mercury/kg       g mercury/ha    application

    wheat              Australia                          0.1 - 6.0       seed
    barley                             1.6 - 2.5
    sorghum            Israel          0.01
    millet             Belgium         2
                       Sweden          0.02 - 0.04
                       Korea           0.4
                       Germany         0.04 - 0.06
                       U.S.A.          0.01 - 0.2
                       Bulgaria        0.02
                       Norway          1 - 2
                       Morocco         0.01 - 0.02
                       Hungary         0.5
                       Portugal        0.03
                       Austria         0.04
                       Spain           0.03 - 0.05
                       Denmark         0.01 - 0.1
                       N.Zealand       0.01 - 0.03
                       U.K.            0.01 - 0.03

    rice               Korea           0.4                                seed
                                                          10 - 20         up to tillering
                       U.S.A.                                             seed
                       India                              60              up to tillering

    flax               U.S.A           0.02 - 0.3                         seed

    cotton             Australia       0.08                               seed
                       Israel          0.2
                       U.A.R.          5
                       U.S.A.          0.03 - 0.3                         seed
                                                          11              soil treatment in furrow

    Table I  (cont'd)
    Crop/Seed          Country            Rate of each application         Stage of
                                       g mercury/kg       g mercury/ha    application

    potatoes           Australia                          0.1 - 0.2       seed tubers
                       U.K.                               20              foliar spray

    hops               Australia       0.1 - 0.2                          setts

    apples             Sweden          paint                              early spring
                       Australia                          40 - 280        up to early fruit growth
                       Germany                            100             pre-blossom
                       U.S.A.                             60 - 400        delayed dormant to petal fall
                       N. Zealand                         50 - 250        up to 8 weeks before harvest
                       U.K.                               15 - 90         up to 6 weeks before harvest
                       Denmark                            15

    pears              Australia                          250 - 800       dormant
                                                          45 - 250        bud burst to petal fall
                       U.S.A                              80              to petal fall

    tomatoes           U.K.            not more than
                                       40 mg mercury/
                                       1000 cu ft
                                       glasshouse                         on growing fruit

    vine               Australia                          1.3 kg          dormant

    sugar              Israel          0.14                               seed
    beet               Germany         0.12
                       Austria         0.12
                       Sweden          0.05

    beans/corn         U.S.A           0.3 - 0.7                          seed

    Table I  (cont'd)
    Crop/Seed          Country            Rate of each application         Stage of
                                       g mercury/kg       g mercury/ha    application

    cherries/peaches   U.S.A                              20 - 40         up to petal fall
    apricots/almonds                                      120 - 600       before buds swell to
                                                                          petal fall

    turf               Australia                          450g-10kg

    Other uses

    Widmark (1967) has indicated a number of other uses of organomercurial
    compounds which, whilst not agricultural in character, may have a
    bearing on the general situation of organomercury residues in food.
    These were reviewed at the 1967 Commission meetings arranged by IUPAC
    Pesticides Section and are summarized below:

    (i) Metallic mercury finds a variety of technical uses; during
    manufacture or especially in the disposal of worn or used products
    such as electrical relays, an unknown quantity of metallic mercury is
    introduced into the environment.

    (ii) Soluble inorganic salts of mercury are also used industrially on
    a reduced scale and thus some mercury will be introduced into sewage.

    (iii) In chemical industries electrodes of mercury are in use and
    vapours of mercury will accompany the waste gases through chimneys
    into the air. In Sweden it has been estimated that in 1964 the
    chlorine industry added approximately five tons of mercury into the
    air and another five tons to the water; this can be compared with 3.5
    tons of phenyl mercury as waste from the pulp industry (+ 0.5 tons
    from the burning of newspaper) and 4.5 tons of methyl mercury as seed
    dressing. (The use of alkyl and phenyl mercury is now banned in

    (iv) Since most minerals, fuels and soils contain trace amounts of
    mercury, heating of these materials on a large scale will serve as a
    source for the contamination of mercury in nature.

    (v) The same might be true for extraction processes, e.g. flotation of
    ore using reagents of complex forming properties.

    (vi) Non-mercury containing pollutants with complex forming properties
    may be able to convert mercurial minerals into a biologically
    receptable form.

    Regarding the widespread natural occurrence of traces of mercury,
    Widmark (1967) quotes atmospheric levels as approximately 20 nanograms
    per cubic metre and rainwater levels as about 200 nanograms per litre.

    Other aspects of mercury occurrence

    (i) In commenting on the geochemistry of mercury as applied to
    prospecting, Warren et al. (1966) say that British Columbia contains
    extensive mercury-bearing metallogenetic areas, but soils may be
    considered normal where they contain less than 0.05 ppm mercury. In
    the vicinity of the gold, molybdenum, and base metal deposits they
    have examined, soils may be expected to carry from 0.05 to 0.25 ppm
    reaching, in a few instances, as much as 2 ppm mercury. Varying
    amounts of humic material and clay in soil fractions modify the
    ability of a soil to accumulate mercury. Around mercury deposits there

    are usually from 1 to 10 ppm mercury in soils and in some cases much
    more. Different organs, and different species of plants vary widely in
    their ability to concentrate mercury. In medium and low ranges, plant
    sampling offers some advantages over soil sampling. If the calculated
    ash contents of vegetation runs more than 10 ppm mercury, there
    probably in mineralization in the vicinity. (In subsequent
    correspondence Professor Warren has said that he does not know the
    form in which mercury is present in vegetation. The above remarks
    presumably relate to mercury in the inorganic form).

    (ii) The following is extracted from the Tenth Report of the Joint
    FAO/WHO Expert Committee on Food Additives (FAO/WHO,p 1967b).

    Mercury occurs naturally in minute amounts in foods and beverages and
    as a contaminant from its uses as fungicides and in industry. Mercury
    is a particular cumulative-poison and not known to serve any essential
    function in man or animals. However, there is evidence that
    contamination of the environment with mercury is increasing.

    Average intakes of mercury from the diet were estimated some years ago
    to range from 0.00083 to 0.00033 mg/kg body-weight/day, with little
    accumulation at these levels of intake. Modern studies of the
    distribution of mercury in human foods and beverages and in human
    tissues in different environments and at different ages are urgently


    Pre-harvest treatments

    Residues in the case of cereals sown from dressed seed are
    insignificant: wheat normally dressed has been found to contain 0.01
    ppm Hg whilst barley contained 0.008 - 0.012 ppm whether dressed or
    not. Furutani and Osajima (1965) found 0.2 ppm for undusted rice and
    twice that level after treatment. Tomizawa (1966) found similar levels
    for untreated polished rice but 0.1 to 1.0 after field treatment with
    phenylmercury acetate.

    Smart and Hill (1967) have examined samples of rice imported into
    Britain and concluded that, in contrast to the position in Japan the
    mercury levels found were often negligible (mean 0.001 ppm) though an
    occasional sample might contain as much an 0.015 ppm Hg. Stone et al.
    (1957) have shown that phenylmercuric sprays applied to apples under
    commercial conditions do not give rise to residues in excess of 0.05
    ppm Hg when application is discontinued at closed calyx. Nardin (1965)
    found an average of 0.02 ppm Hg on treated apples over two seasons.
    Smart (1961) found residues well below 0.1 ppm five weeks or more
    after the last of eight commercial mercury applications. Limited data
    for treated pears gives 0.04 ppm (untreated), and 0.14 to 0.26 ppm
    two to four months after treatment.


    Westoo et al (1965) have examined eggs on the Swedish retail market
    and elsewhere: the mean value for Swedish eggs (79 samples) was
    0.029 ppm whilst elsewhere in Europe the mean value was less than
    0.010 ppm. Westoo (1966a) has also examined chicken (0.005 - 0.023
    ppm) and other meets from Denmark and Sweden: levels in Danish pork
    and beef were 0.003 - 0.005 (liver 0.009) ppm, and in Swedish pork
    and beef up to ten times higher. Mean values for fish in Sweden ranged
    from 0.031 to 1.30 ppm (25 samples of perch) with individual fish
    containing up to 5 ppm (Westoo, 1966b). The 1967 Codex paper (CCPR,
    1967a) suggested that, based on limited evidence, the maximum "normal"
    level in sea fish was 0.1 ppm.


    General considerations

    At meetings in August 1967 the IUPAC Commission on Terminal Pesticide
    Residues (IUPAC, 1967) recognised that recent work had shown that
    inorganic mercury can be transformed into methylmercury compounds in
    nature; this is a further complication in an already complex residue
    situation. Westoo (1966b) has examined gas and thin-layer
    chromatographic methods for the determination of methylmercury
    compounds in fish from Baltic and Swedish waters, with results varying
    from 0.07 to 4.45 ppm. Widmark (1967) concluded that contamination by
    mercury in nature seemed to be due to a complex series of factors of
    which organomercury pesticides was only one factor. A full scientific
    understanding of the complex is desirable and calls for the fullest
    cooperation of scientists in a variety of disciplines.


    These have been further reviewed by Widmark (1967). Only limited
    progress in the development of analytical residue methods specifically
    for alkyl, alkoxy and arylmercurials was reported. Of particular
    promise are methods based on chromatography as described by Westoo,
    (1966b), together with methods making use of ion exchanges
    electrophoresis and gel filtration.


    Existing tolerances (all of which refer to residue measured as Hg
    without distinction between the forms in which the metal may actually
    be present in the food) are as follows:-


              USA - zero on fruits and vegetables

              Brazil - 0.05 ppm

              Australia - 0.1 in S. Australia and Victoria, 0.01 ppm in
              Western Australia

              N. Zealand - zero, except fruit and vegetables (0.05 ppm)

              Benelux - 0.03 ppm

              Germany - zero (where derived from pesticide treatment)

    Guidance only (maximum acceptable levels)

              Denmark - 0.05 ppm

              Sweden - 0.05 ppm except for fish (1.0) and drinking water


    Since no acceptable daily intake level or temporary acceptable daily
    intake level can be given for mercury or for organomercurial
    compounds, it is not possible to recommend tolerances or temporary
    tolerances. Small natural concentrations of mercury appear to be
    widespread but the levels vary from area to area; it is also
    difficult, therefore, to suggest a practical residue limit for
    mercury. By way of guidance, however, practical residue limits of from
    0.02 ppm to 0.05 ppm mercury, according to local conditions, are
    suggested. Of the present uses of organomercurials reviewed, only
    those relating to the use on apples before and up to petal fall and to
    the treatment of cereal and other seeds do not appear to produce
    residues of mercury in the harvested crop significantly in excess of
    the natural background level of mercury. Surplus, waste or other seed
    which has been treated with organomercurial compounds should not be
    fed to poultry.


    Further work required

    Further work on the development on sensitive methods of analysis
    specifically for alkyl, alkoxy and arylmercurials is still required in
    order to study the occurrence of these forms of mercury in foodstuffs
    from different sources. Further work on the possible natural
    conversion of inorganic mercury to organically bound mercury is also

    The Codex Committee on Pesticide Residues (CCPR, 1967b) also
    considered the need for additional information on background levels of
    mercury in foods from a range of environments and on the nature,
    amounts and fate of mercury compounds in industrial effluents and the
    resultant levels of mercury likely to occur in fish, including
    shellfish. The Joint FAO/WHO Expert Committee on Food Additives
    (FAO/WHO 1967b) has also expressed the view that modern studies of the
    distribution of mercury in human food and beverages (and in human

    tissue) in different environments is urgently needed and has concluded
    that until the results of such studies are available it is not
    possible to set meaningful maximum permissible limits in dietary
    intakes for this element.


    Engleson, G. & Herner, T. (1952) Acts Ped., 41, 289

    Kurland, L.T., Paro, S.N. & Siedler, H. (1960) Wld Neurol, 1, 370

    Matsumoto, H., Koya, G. & Takeuchi, T. (1965)  J. Neuropathol.
    exper. Neurol., 24, 563

    Smart, N.A. & Loyd, M.K. (1963) J. Sci. Food Agric., 14, 734

    Ulfvarson, U. Int. Arch. Gewerbepathol. Gewerbepharmakol., 19, 12

    Yoshino, Y., Mozai, T. & Nakao, K. J. Neurochem., 13, 397


    CCPR. (1967a) Organomercury compounds. Paper prepared by the United
    Kingdom Delegation assisted by the Delegation of Sweden for
    presentation to the Second Session of the Codex Committee on Pesticide
    Residues. The Hague, The Netherlands. CCPR 67.13

    CCPR. (1967b) Report of the Second Session of the Codex Committee on
    Pesticide Residues. SF 10/115

    FAO/WHO. (1967a) Evaluation of some pesticide residues in food. FAO,
    PL:CP/15:WHOFood Add./67.32

    FAO/WHO. (1967b) Specifications for the identity and purity of food
    additives and their toxicological evaluation: some emulsifiers and
    stabilizers and certain other substances. (Tenth Report of the Joint
    FAO/WHO Expert Committee on Food Additives.) FAO Nutrition Mtg. Rept.
    43;WHO Tech. Rept. 373.

    Furutani, S., Osajima, Y. (1965) Residual components from agricultural
    chemicals in food. Kyusho Daigaku Nogakubu Gakugei Zasshi 21: 363-369;
    22: 45-48

    IUPAC. (1967) Proceedings of the Commission on Pesticide Residue
    Analysis. IUPAC Pesticides Section, Vienna.

    Nardin, H.F., (1965) An investigation of spray residues in apples and
    pears. N.S. Wales Dept. Agr. Chem. Bull. S.36

    Smart, N.A. (1961) Arylmercury spray residue in apples. Plant Pathol.
    10: 150-160

    Smart, N.A., Hill, A.R.C. (1967) Supplement to CCPR, 1967a

    Stone, H.M., P.J. Clark, Jacks, H. (1967) Mercury content of apples.
    N. Zealand J.Sci. Technol. 38: 843-848

    Tomizawa, C. (1966) Behaviour of mercury in rice plants treated with
    organomercury Hg-203 fungicides. Shokuhin Eiseigakn Zasshi 7 : 26

    Warren, H.V., Delavault, R.E., Barakso, J. (1966) Some observations on
    the geochemistry of mercury as applied to prospecting. Econ. Geog. 
    61 : 1010-1028.

    Westoo, G., Sjostrand, B., Westermark, T. (1965) (Mercury in hens
    eggs). Var Foda 17 : 1

    Westoo, G. (1966a) (Mercury in chicken and other meat). Var Foda 18 :

    Westoo, G. (1966b) Methylmercury compounds in fish: identification and
    determination. Acta Chem. Scand. 20 : 2131-2137.

    Widmark, G. (1967) Proceedings of the Commission on Pesticide Residue
    Analysis. IUPAC Pesticides Section. Appendix XIV.

    See Also:
       Toxicological Abbreviations