IPCS INCHEM Home


    AGP:1970/M/12/1

    WHO/FOOD ADD/71.42

    1970 EVALUATIONS OF SOME PESTICIDE RESIDUES IN FOOD

    THE MONOGRAPHS

    Issued jointly by FAO and WHO

    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
    Group on Pesticide Residues, which met in Rome, 9-16 November, 1970.

    FOOD AND AGRICULTURE ORGANIZATION OF THE UNITED NATIONS

    WORLD HEALTH ORGANIZATION

    Rome, 1971

    DIQUAT

    IDENTITY

    Chemical name

    9,10 - Dihydro - 8a, 10a - diazoniaphenanthrene ion

    1,1' - Ethylene - 2,2' - bipyridylium ion

    6,7 - Dihydrodipyridol (1, 2a : 2', 1' - c) - pyrazidinium ion

    Synonyms

    FB 2(R), Reglone(R), Aquacide(R), Dextrone(R)

    Structural formula

    CHEMICAL STRUCTURE 

    Other relevant chemical properties

    Diquat is available only as a salt, generally as the dibromide. The
    cationic portion of the molecule is the active ingredient. Diquat
    dibromide exists as the monohydrate and forms white to yellow crystals
    which decompose above 300C. The technical material is available only
    as a dark reddish-brown aqueous solution. Solubility in water at 20C
    is 700 g/litre: it is slightly soluble in alcoholic and hydroxylic
    solvents and practically insoluble in non-polar organic solvents,
    stable in acid or neutral solutions and unstable under alkaline
    conditions. One electron reduction by zinc or sodium dithionite yields
    the green free-radical which in the presence of atmospheric oxygen
    reverts to diquat. The single electron reduction is completely
    reversible, and the redox potential of - 349 mV is independent of pH.
    Further reduction yields polyhydrobipyridyl derivatives.

    Solutions of the free radical exhibit a sharp absorption peak at 379
    nm which has a greater intensity than that of the unreduced diquat at
    310 nm. Concentrated aqueous solutions corrode steel, tinplate,
    galvanised iron and aluminium.

    Purity

    Technical, 95 percent

    EVALUATION FOR ACCEPTABLE DAILY INTAKE

    BIOCHEMICAL ASPECTS

    Absorption, distribution and excretion

    Dogs administered orally 10-15 mg 14C-labelled diquat dibromide
    excreted 29-32 percent in the urine and 51-62 percent in the faeces in
    72 hours. In the first 24 hours, 25-28 percent of the dose was
    excreted in the urine (Swan, 1960).

    Following oral doses of 5-10 mg/kg to rats, diquat dibromide was
    eliminated entirely with 96-101 percent recovery within four days, the
    levels in the urine were 4-6 percent and in the faeces 90-96 percent
    (Daniel and Gage, 1966). Following subcutaneous doses of 5 or 6 mg/kg
    to rats, diquat dibromide was eliminated again within four days with
    90-98 percent recovery-in urine 88-98 percent and in faeces 0-2
    percent. In all studies, the bulk of the residues excreted following
    oral administration was in the faeces, whereas after a subcutaneous
    dose most was in the urine, indicating that absorption from the gut
    was relatively poor. Studies where chemical rather than radiological
    measurements were made showed that following an oral dose of 30-40
    mg/kg to rats, only 4-7 percent of the dose was recovered in the urine
    and 11-42 percent in the faeces after 48 hours (Swan, 1960).

    The percentage excretion of an oral dose in the urine, calculated from
    a chemical method of analysis, was lower than that obtained from a
    radio-analytical method of analysis, suggesting that a proportion of
    the dose appeared in a form other than diquat. Following a
    subcutaneous dose, the radiochemical and chemical analyses gave
    results which were closer than the values following an oral dose,
    indicating possible absorption from the gut of microbial degradation
    products following oral administration, rather than actual animal
    metabolism (Swan, 1960).

    In vitro experiments using suspensions of gut material suggested
    that microbial breakdown of diquat was responsible for the low
    recoveries by the chemical assay where only the parent ion was
    measured (Swan, 1960).

    Effects on enzymes and other biochemical parameters

    Although there is no direct evidence in mammals to support the view,
    it is tempting to assume that the ability of bipyridyls to be reduced
    and re-oxidized with the production of free radicals is linked with
    their toxic effects, as has been suggested to be the case in plants.
    Gage (1968) has shown that free radicals can be produced from diquat
    incubated anaerobically in the presence of NADPH and microsomes
    derived from rat liver. Diquat also increased the respiration of liver

    mitochondrial fragments. This action has been related to the activity
    of flavo-protein dehydrogenases. Purified lipoamide dehydrogenase from
    pig heart was able to reduce diquat to the free radical in the
    presence of NADH. Rees (1969) has shown that a fresh extract of bovine
    lens, incubated anaerobically with diquat, can catalyze similar
    reactions. From these experiments, there can be little doubt that
    flavo-proteins of animal tissues in the presence of their
    co-substrates can reduce the bipyridyls, although aerobically the
    equilibrium concentration of the free radical is probably extremely
    low.

    The property that diquat has of undergoing cyclic reduction and
    oxidation might suggest that it could interfere in electron-transport
    processes, diverting electrons from the system and reducing oxygen to
    water. Gage (1968) found that the resting respiration of mitochondria
    was almost unaffected by diquat, probably because of its inability to
    penetrate the mitochondrial membrane.

    TOXICOLOGICAL STUDIES

    Special studies on reproduction

    Rat

    Six groups of rats (ten males or ten females) were examined for
    reproduction and teratogenic effects of diquat dichloride at 0, 125
    and 500 ppm in the diet (Griffiths et al., 1966). This experiment
    examined the effects of dietary feeding of diquat to males only,
    females only and both males and females at 500 ppm and males and
    females at 125 ppm. Growth of the parent rats was moderately retarded
    at 500 ppm, and all parents developed cataracts. No effect on
    reproduction or occurrence of terata was observed. At 125 ppm, no
    effect on the growth of parents was noted. Lens opacities did not
    occur. Of all offspring produced (1637), one female at 500 ppm had a
    unilateral cataract.

    A single intraperitoneal injection of diquat (7 mg/kg from day six
    through 14 of gestation) produced a high incidence of retarded growth
    of sternum and auditory ossicles, as well as marked weight reduction
    in rat embryos. A higher dose of 14 mg/kg interrupted most
    pregnancies, and in the rats that reached term, the embryonic effects
    were more pronounced (Khera and Whitta, 1968).

    Special studies for mutagenicity

    Diquat was screened for mutagenic activity in Drosophila
    melanogaster using the Muller-5 test to detect recessive lethality
    on the X chromosome. Compared to a spontaneous mutation rate of 0.14
    percent, the rate was 0.11 percent after treatment with diquat, which
    is comparable with the control value (Benes and Sram, 1969).

    Special studies on cataractogenicity

    The initial cataractogenic effects in rats of diquat appear to be
    reversible, as was noted in a study where rats were fed a diet
    containing 500 ppm diquat. This dose was shown to produce cataracts in
    three to six months. After feeding continuously for periods of several
    days to eight weeks, the rats were given a normal diquat-free diet for
    the remainder of one year. Cataracts did not develop in any of these
    rats, indicating that continuous prolonged exposure to diquat was
    necessary for the formation of cataracts in the rat. Temporary
    exposure to this known cataractogen does not lead to irreversible
    damage (Clark and Hurst, 1970).

    Since it is known that some forms of cataract are influenced by light
    and that the toxicity of diquat to plants is dependent upon light,
    experiments were undertaken to study the effect of light on cataract
    formation in rats. Rats were fed 500 ppm diquat in the dark for three
    months and controls were fed the same diet under light conditions.
    After three months feeding on these diets, both groups of animals
    showed an equal number of cataracts, suggesting that light does not
    influence the development of cataract formation (Clark and Hurst,
    1970).

    Ascorbic acid (200 mg/ml) in the drinking water of rats receiving
    diquat (500 ppm) in the diet did not influence the development of
    cataracts (Clark and Hurst, 1970.)

    See also "Short" and "Long-term Studies" and "Reproduction". LD50
    values for diquat in various species are summarized in Table I.

    A level of 90 ppm diquat at 18C killed 50 percent of a population of
    rainbow trout within 48 hours. At 70 ppm, 50 percent mortality was
    observed in 48 hours (Swan, 1960).

    A single dermal application of 10 or 20 mg of diquat to rats as an
    aqueous solution produced a slight reversible erythema in the treated
    area (Cooke and Gage, 1956).

    Acute dermal administration of diquat at doses of 500 and 1000 mg/kg
    to rabbits resulted in toxic signs within 48-72 hours at 1000 mg/kg
    and no abnormalities at 500 mg/kg (Swan, 1963b).

    Installation of 10 mg diquat of a 10 percent aqueous solution into the
    conjuctival sac of rabbits produced no effect (Cook and Gage, 1956).

    Short-term studies

    Rat

    Three groups of rats (four males and four females) were exposed to
    diquat in aerosol form at levels of 0.5, 1.06 and 2 g/litre for 15
    daily six-hour exposure periods. At the 2 g/litre level, weight gain
    was slightly reduced. No such effect was noted at the 1.06 and 0.5

    g/litre levels. Histopathological examination of the lungs showed
    slight irritation with peribronchial lymphoid hyperplasia,
    perivascular oedema and macrophages in the alveoli at the 2 g/litre
    level (Gage, 1967).

        TABLE I

    LD50 values of diquat in various species
                                                                             

                            Salt    LD50
    Species        Route    Form    (mg           Reference
                                    cation/kg)
                                                                             

    Mouse          Oral     Cl      125           Swan, 1963a
                            Br      125           Clark and Hurst, 1970

    Rat            Oral     Cl      302           Swan, 1962
                            Br      215-235       Clark and Hurst, 1970
                                                  Swan, 1960
                   s.c.     Cl      11            Clark and Hurst, 1970
                            Br      11-20         Clark and Hurst, 1970
                                                  Cook and Gage, 1956

    Guinea Pig     Oral     Br      100           Clark and Hurst, 1970

    Rabbit         Oral     Br      100           Swan, 1960
                                                  Clark and Hurst, 1970

                   Dermal   Br      400           Swan, 1963b
                                                  Cookson and McElligott, 1966
                   i.p.     Br      15               "            "         "

    Hen            Oral     Br      215-430       Swan, 1960
                            Br      200-400       Clark and Hurst, 1970

    Dog            Oral     Br      100-200       Clark and Hurst, 1970

    Cow            Oral     Br      approx. 30    Walley, 1962
                                                  Clark and Hurst, 1970
                                                                             
    
    Subcutaneous administration of 1 mg diquat/kg body-weight to rats for
    21 days produced no toxic effects; post-mortem examination showed no
    organic damage (Cooke and Gage, 1956).

    Rabbit

    Groups of rabbits (three males and three females) were administered
    diquat percutaneously at doses of 0, 20, 40, 80 and 160 mg diquat

    ion/kg body-weight for 20 days. At 20 mg/kg, no deaths occurred,
    whereas, at 40 mg/kg and above, from 66 to 100 percent of the animals
    died.

    Microscopic examination revealed vacuolar changes in the distal
    convoluted renal tubules with occasional necrosis of cells. These
    changes were preceded by weight loss and muscular weakness (Cookson
    and McElligott, 1966).

    Groups of five female and five male rabbits were administered up to 20
    daily percutaneous doses of diquat at O, 3.13, 6.25, 12.5 and 25
    mg/kg. The calculated LD50 was 7.9 mg/kg (5.7 mg ion/kg). Signs of
    poisoning included: local hyperaemic and subcutaneous oedema;
    increasing sloughing of surface layers of skin followed by scab
    formation. These effects were reversible at the 6.25 mg/kg dose after
    treatment was concluded. Other signs included weakness, incoordination
    and lethargy. In many animals, ulceration of the gastric mucosa was
    observed at post-mortem indicating that oral contamination had
    presumably occurred (Swan, 1963b).

    Dog

    Groups of dogs (three males and three females) were fed diets
    containing 0, 16, 32, 68, 200 and 600 ppm diquat dichloride for
    periods up to four years. At dosages of 600 and 200 ppm, bilateral
    opacities of the lens were observed at ten and 15 months,
    respectively. Dietary levels of 68 ppm did not affect the lens within
    the four year interval tested. No effects were observed on growth,
    tumour formation, food consumption, blood chemistry and gross and
    microscopic pathology. The dose of 68 ppm (equivalent to 50 ppm diquat
    ion) is the no-effect level in dogs with regard to cataract formation
    (Hurst, 1966).

    Sheep and calf

    Five groups of two sheep (one male and one female, eight months old)
    and three groups of one calf each were given diquat at doses of 0, 1,
    5, 10 and 20 ppm and 0, 5 and 20 ppm, respectively, in their drinking
    water for one month. These levels caused no toxicological effect over
    the trial period as evidenced by growth, food consumption and visual
    observation (Sarfaty, 1963).

    Cow

    Oral administration of diquat for five days at 10 mg/kg body-weight to
    a cow resulted in death within 15 days preceded by severe signs of
    poison, including dullness, inappetence anaemia, increased heart rate.
    At post-mortem, heart and kidney infarcts and intestinal catarrh were
    found. Administration of 5 mg diquat/kg daily for fourteen days to a
    cow (in the diet for two days, then drenched) resulted in increased
    inappetence after two days, slight haemorrhage as noted by blood in
    the faeces and temporary impairment of vision (Walley, 1962).

    Comparative

    Groups of four male and four female mice and guinea pigs, two female
    rabbits and a male dog, exposed to 15 daily six-hour treatments with
    diquat in aerosol form at 1.06 mg/litre, showed no adverse effects
    (Gage, 1967).

    Long-term studies

    Rat

    Groups of rats (25 males and 25 females per group) were fed diquat
    dichloride for two years at doses of 0.125, 250, 500 or 1000 ppm in
    the diet. After 56 days, the 1000 ppm level was discontinued because
    of lack of growth and mortality in males and females. At 125 ppm, a
    partial lens opacity (cataract) was seen at 207 days. All males and 19
    out of 21 females were affected by 657 days. At 250 and 500 ppm, lens
    opacities were produced in all animals within 155 and 124 days,
    respectively. At 500 ppm, a reduction of female body-weight was
    apparent after 20 weeks and in males after five weeks. No such effects
    were noted at 250 and 125 ppm. No adverse effects were reported in
    survival, blood chemistry, tumour, incidence and gross and microscopic
    pathology (Swan, 1962; Goater et al., 1964).

    Seven groups of rats (25 males and 25 females/group; controls had 75
    and 75 females) were fed diquat dichloride at levels of 0,10, 50, 100,
    250, 500 or 1000 ppm for two years. Growth depression was observed in
    the males at 1000 ppm. Lens opacity was observed at doses of 50 ppm
    and above in both males and females (no such effect was noted at the
    10 ppm level). Growth, food consumption survival, tumour formation,
    behaviour, haematological and urine analyses and gross and microscopic
    examination revealed no effects differing from the controls. A
    no-effect level based upon cataract formation is 10 ppm, equivalent to
    7.2 ppm diquat cation (Kohn et al., 1965a, b and c).

    OBSERVATIONS IN MAN

    Damage and discolouration of fingernails caused by exposure to
    concentrated solutions of diquat were observed in three instances. The
    cause of the damage is unknown but presumably is of a local nature.
    All three patients had frequent exposure to the concentrated chemical
    without taking precautions to prevent contamination of the skin. The
    cause of the nail damage was unknown, but it seemed probable that the
    chemical reached the nail matrix by entering the nail fold and
    stimulated infection, interfering with the formation of the nail from
    the matrix. The damage is presumed to be local and not as result of
    ingestion because of asymmetry of the lesions and the fact that the
    toenails were unaffected. A curious colour change and softening of the
    nail at the base are characteristic. In some instances, the nail was
    shed and was not regrown (Samman and Johnston, 1969).

    Of 42 reported exposures of man varying from one to 75 individual
    exposures, four incidents of dermal abnormalities were reported. These
    include rashes, blisters and a transient skin discolouration. In
    almost all instances, these incidents were attributable to the
    concentrated commercial preparation (Anonymous, 1966).

    Poisoning cases in humans with bipyridyl compounds have demonstrated
    the acute toxic effects of these compounds. In one case, the
    accidental ingestion of a small quantity of diquat led to diarrhoea
    and oral ulceration. After forced diuresis, the man recovered and was
    released from care. It was observed that the urine contained traces of
    diquat as long as eleven days after ingestion (Oreopoulos, 1969).

    COMMENT

    In biochemical studies in rats and dogs, it has been observed that
    after oral administration, the major part of the dose is excreted in
    the faeces. Following a subcutaneous dose, most residue was found in
    the urine, indicating that absorption from the gut was relatively
    poor. A small proportion of the material found in urine after oral
    administration was other than the parent compound, due possibly to
    absorption of microbial degradation products rather than actual animal
    metabolism.

    Diquat is a cataractogenic compound, as has been demonstrated in
    lont-term rat and in dog experiments at relatively low levels of 2.5
    and 5 mg/kg body-weight, respectively. Transient exposure of rats to
    diquat does not lead to the formation of cataracts.

    Intraperitoneal administration of 7 mg/kg diquat to pregnant rats
    resulted in embryotoxic effects. In a three-generation rat
    reproduction study, 500 ppm diquat resulted in no effect on
    reproduction.

    In man, the acute and dermal problems associated with accidental or
    suicidal ingestion and dermal contamination appear to be of primary
    concern. Cataract formation has not been observed in man as a result
    of exposure to diquat, nevertheless studies in the prophylaxis and
    treatment of diquat-induced cataracts in mammals were considered
    urgent.

    Non-reversible cataractogenic effects in rats and dogs at relatively
    low oral levels, 50 ppm (2.5 mg/kg) and 200 ppm (5
    mg/kg),reapectively, and a potential embryonic effect make it
    advisable to establish only a temporary acceptable daily intake for
    man.

    TOXICOLOGICAL EVALUATION

    Level causing no toxicological effects

    Rat:  10 ppm in the diet, equivalent to 0.5 mg/kg body-weight/day
          (corresponds to 0.36 mg diquat ion/kg body-weight/day)

    Dog:  68 ppm in the diet, equivalent to 1.7 mg/kg body-weight/day
          (corresponds to 1.22 mg diquat ion/kg body-weight/day)

    ESTIMATE OF TEMPORARY ACCEPTABLE DAILY INTAKE IN MAN

    0-0.0025 mg/kg body-weight as diquat dichloride (0-0.002 mg/kg
    body-weight expressed as diquat ion)

    RESIDUES IN FOOD AND THEIR EVALUATION

    USE PATTERN

    Diquat is used world wide for the following purposes; desiccation of
    beans, peas, sugar beet, sorghum, maize, rice etc; potato haulm
    destruction; pre-emergence weed control in carrots, onions, hops,
    vines and sugar-cane flower control; control of submerged and some
    floating weeds in still water or streams, defoliant and desiccant for
    cotton; desiccation of red and white clover, sunflower, linseed and
    rape for seed; desiccant for barley and wheat for stock feed purposes.

    FATE OF RESIDUES

    Photodecomposition

    The photodecomposition of diquat resulted in disappearance of
    radioactivity with both the ring and ethylene bridge radioactivity
    labelled indicating the occurrence of volatile breakdown products.
    Approximately 75% of the material was lost with 96 hours of sunlight
    exposure. The photo-chemical breakdown of diquat gives
    1,2,3,4-tetrahydro-1-oxo-pyridyl 1,2-a-5-pyrazinium bromide.

    CHEMICAL STRUCTURE 

    Further degradation of the molecule occurs in the presence of sunlight
    presumably to volatile products (Funderburk and Bozarth, 1967; Slade
    and Smith, 1967).

    In soil

    One of the most striking features of diquat is its rapid and complete
    inactivation by soil. This inactivation results from a reaction
    complex formed between the positively charged diquat cation and the
    negatively charged sites on the clay minerals present in the soils.

    In animals

    Silage made from grass desiccated with diquat (13 ppm) was fed to farm
    animals over long periods; no residues were detected in the animal
    tissue or milk secreted during this time (Black et al., 1966). The
    fate of 14C-diquat administered orally to cattle has been studied.
    Three cows received single oral doses of 5 mg diquat dibromide/kg
    body-weight and one cow received a single dose of 20 mg/kg. Milk
    residues after seven days amounted to 0.001 to 0.015% of the
    administered dose with the major residues occurring in three days of
    dosing at the lower levels. At the higher dose levels, residues were
    evident at all sampling intervals (seven days) with the major amounts
    recovered within six days. Residues in urine varied from 0.4 to 2.6%
    of the administered dose. Tissue residues, 24 hours after an oral
    administration of 11.5 mg diquat dibromide/kg, were found primarily in
    kidney (0.7 ppm) and liver (0.2 ppm) with slight residues in several
    other tissues (<0.1 ppm). Chemical analysis of the liver and kidney
    resulted in 0.01 and less than 0.03 ppm diquat, indicating that major
    residues were not diquat but metabolic conversion products (Stevens
    and Walley, 1966). Traces of metabolites found in the milk were
    believed to arise from breakdown in the gut or in the rumen; Daniel
    and Gage (1966) found similar breakdown in the rat. After dosing a
    calf with 14C-diquat (5 ppm), less than 0.01 ppm of diquat or its
    metabolites were found in the muscle tissue. Because of its use for
    aquatic weed control, the fate of diquat in fish has been studied.

    Radiotracer studies of the distribution of diquat in fish following
    treatment of water indicated that the major residues occurred in the
    digestive system, and the only residue was diquat (Funderburk and
    Bozarth, 1967).

    After exposure of rainbow trout to 1 ppm, diquat residues were found
    in the viscera and skin but none in the flesh (Calderbank, 1968).

    In plants

    The uptake by foliage and extent of subsequent movement are critically
    dependent on the environmental conditions. Traces of diquat were
    detected in potato tubers after the tops had been killed with the
    chemical (Calderbank et al., 1961; Headford et al., 1967). By means of
    14C-labelled diquat, it has been shown that this transfer occurs in
    the xylem. Smith et al., (1966) confirmed that darkness increased this
    long-distance transport of diquat. Experiments with potato plants and
    tubers have shown that even if metabolism occurred in the plant no
    degradation products were transported to the tubers (Smith, 1967). No
    significant loss of diquat residues was found after storage of potato
    tubers for up to seven months. It has been assumed that since the
    plants die rapidly in bright sunlight, significant quantities of the
    breakdown products formed on the surface of dead tissues should not
    move from these dead leaves to edible parts of the plant. This has
    been partially demonstrated with potatoes, where it has been shown
    that diquat residues in tubers from sprayed plants appear as the
    unchanged diquat and not the photoderivative.

    Diquat taken up from nutrient solution into plants was not metabolized
    but remained as the parent compound (Funderburk and Lawrence, 1964).

    In water

    Diquat applied to water for aquatic weed control purposes quickly
    disappears due to uptake by weeds, absorption by soil, silt and
    particulate suspended matter, and, to a slight extent, by
    photochemical degradation (Calderbank, 1968). No information is
    available on the ultimate fate of the chemical in this environment.
    The rate of disappearance is very variable, depending on the movement
    of the water, the presence of mud or suspended matter, and the
    strength of sunlight, but treatments within the range of 0.5 - 4
    mg/litre in the water have resulted in less than 0.1 mg/litre being
    detected in from four to 14 days after application. Decomposition of
    the killed weed is rapid, any remaining residue of diquat thus
    liberated being subsequently absorbed on the bottom mud. Such residues
    in the largely organic muds may be more readily available to bacterial
    degradation than when absorbed to clay minerals in soils.

    Evidence of residues in food in commerce or at consumption

    A summary of the diquat residues in food crops, raw and processed in
    wheat, flour and bread and also in barley, malt and beer is given in
    Tables II, III and IV: (Calderbank, 1968).

    METHODS OF RESIDUE ANALYSIS

    The residue analysis of diquat is usually carried out colorimetrically
    after extraction of the plant or animal tissue with boiling dilute
    sulphuric acid, isolation by ion exchange column, elution, reduction
    and the absorption of the derived coloured free radical measured at
    377 nm. This method of Calderbank et al. (1961), was modified by
    Kirston (1966), simplified by Calderbank and Yuen (1966) and adapted
    by Black et al. (1966). Limit of sensitivity is about 0.01 ppm, and
    the procedure should be suitable for regulatory purposes. Engelhardt
    and McKinley (1966) determined the compound by polarography:

    Coha and Koljcojic (1969) used a combination of TLC and ring oven.
    Funderburk and Lawrence (1963) developed a sensitive bioassay
    technique for residues in water using the lesser duckweed (Lemna
    minor L.) and also Funderburk et al. (1966) used a thin-layer
    chromatographic procedure for examining the photochemical
    decomposition products of diquat in solution. Faust and Hunter (1965)
    determined diquat in natural surface waters by absorptiometric
    measurements at the wavelength of maximum absorption of the unreduced
    herbicide (310 nm) following clean-up by ion-exchange.

        TABLE II

    Summary of residues in food crops (dessiccation uses)

                                                                             

                                                           Average Residues
                                                           3-21 days after
                                          Rate of          application,
    CROP                                  Application      mg/kg
                                          lb/acre          DIQUAT
                                                                             

    Barley                                0.5-1.0          0.5-4.0

    Wheat, rape seed                      0.5-1.0          ND-1.3

    Maize                                 0.5-1.2          ND

    Rice (with husk)                      0.15-0.54        0.7-5.0

    Rice (dehusked or polished)           0.15-0.54        ND

    Peas, beans, sunflower seed           0.35-1.2         ND-0.2

    Sorghum seed                          0.25-1.0         0.2-0.8

    Cotton (as picked)                    0.5-1.0          0.05-0.5

    Onions                                0.5-2.0          0.02-0.05

    Potatoes                              0.5-1.5          ND-0.04

    Sugar cane juice                      0.5-2.0          ND

    Seed oils (sesame, sunflower,
    rape, cotton)                         up to 1.2        ND
                                                                             

    ND - not detected
    
    TABLE III

    Residues in wheat, flour and bread
                                                                

    (Wheat desiccated with diquat at 0.7 lb/acre)

    Sample                                  Residues of diquat
                                            (mg/kg)
                                                                

    Wheat (at harvest)                      1 (approx)

    Wheat (cleaned for milling)             0.6-0.7

    White flour                             0-0.1

    Bread                                   0.1

    Bran                                    1.2-2.4
                                                                

    TABLE IV

    Residues in barley, malt and beer
                                                                       

    Intervals between                         Diquat residues found,
    application and harvest                          mg/kg
    (0.68 lb diquat/acre applied)      Barley         Malt           Beer
                                                                       

    4 days                             4.24           2.05           0.12

    5 days                             2.35           1.07           0.04

    10 days                            0.94           0.61           0.02
                                                                       

    NATIONAL TOLERANCES

    Country                            Crop                 Tolerance (ppm)

    United States of America           Sugarcane              0.05
                                                             (negligible
                                                              residue)

    APPRAISAL

    Diquat is very widely used as a desiccant - e.g. for rice, clover,
    rape, linseed, peas, beans, maize, potato haulm, etc. and as a
    pre-emergence herbicide in carrots, onions, hops, vines, etc.; it is

    also used for aquatic weed control. Residues are very unlikely to
    accrue from soil or pre-emergence applications but can occur following
    use for desiccation purposes. Residues in seed from such desiccated
    crops vary from negligible in such well-protected seeds as maize to
    about 5 ppm in rice (husk). Barley and wheat for stock feed or seed
    purposes can contain up to 5 and 2 ppm, respectively, of diquat
    following desiccation uses. Residues often occur in treated oil seeds,
    such as sunflower, sesame and cotton, but no residues are observed in
    the expressed oil. The spectrophotometric procedure should be suitable
    for regulatory purposes.

    RECOMMENDATIONS

    TEMPORARY TOLERANCES

    Rice (with husk)                                          5 ppm

    Rape seed, sorghum seed                                   2 ppm

    Peas, beans, sunflower seed                               0.5 ppm

    Onions, potatoes, maize, rice (polished)                  0.1 ppm

    Sesame, sunflower, rape, cotton seed oils                 0.1 ppm

    Information given also on:

    Cotton (as picked)                                        1 ppm

    In cereal grains for stock feed or seed purposes only, the following
    levels should also be accepted:

    Barley                                                    5 ppm

    Wheat                                                     2 ppm

    FURTHER WORK OR INFORMATION

    REQUIRED (before June 1973)

    1. Further studies on the mechanism of cataractogenesis in animals.

    2. A three-generation reproduction study where there is exposure to
       diquat during the entire duration of the experiment.

    DESIRABLE

    Clinical studies on factory workers and users of diquat in order to
    detect the extent of cataractogenic risk.

    REFERENCES

    Anonymous. (1966) Unpublished report 29 December 1966 from ICI Ltd.
    through Chevron Chemical Co. to FDA

    Benes, V. and Sram, R. (1969) Mutagenic activity of some pesticides in
    Drosophila melanogaster. Industr. Med Surg., 38: 442-444

    Black, W.J.M., Calderbank, A., Douglas, G. and McKenna, R.H.J. (1966)
    Residues in herbage and silage and feeding experiments following the
    use of diquat as a desiccant. J.Sci.Fd. Agr., 17: 506-509

    Calderbank, A., Morgan, C.B. and Yuen, S.H. (1961) Determination of
    diquat residues in potato tubers. Analyst, 86: 569-579

    Calderbank, A. and Yuen, S.H. (1966) An improved method for
    determining residues of diquat. Analyst, 91: 625-629

    Calderbank, A. (1968) The bipyridylium herbicides. Advances in pest
    control research, 8: 127-235

    Clark, D.G. and Hurst, E.W. (1970) The toxicity of diquat. Brit. J.
    Ind. Med., 27: 51-55

    Coha, F. and Koljcojic, R. (1969) Combination of thin-layer
    chromatography and the ring oven method for the semi-quantitative
    estimation of some herbicides. J. Chromatog., 40: 304-307

    Cooke, E. and Gage, J.C. (1956) Toxicological report. Unpublished
    report TR/35 15 March 1956 for ICI Ltd. through Chevron Chemical Co.
    to FDA

    Cookson, J.H. and McElligott. (1966) The dermal toxicity of diquat.
    Unpublished report IHR. 200 from ICI Ltd. through Chevron Chemical Co.
    to FDA 

    Daniel, J.W. and Gage, J.C. (1966) Absorption and excretion of diquat
    and paraquat in rats. Brit. Indust. Med. J., 23: 133-136

    Engelhardt, J. and McKinley, W.P. (1966) Bypyridylium herbicides.
    Polarography of 1,1'-ethylene-2,2'-bipyridylium dibromide. J. Agr. Fd.
    Chem., 14: 377-380

    Faust, S.D. and Hunter, N.E. (1965) Chemical methods for the detection
    of aquatic herbicides. J. Am. Water Works Assoc., 57: 1028-1037

    Funderburk, H.H. and Lawrence, J.M. (1963) A sensitive method for
    determination of low concentrations of diquat and paraquat. Nature,
    199: 1011-1012

    Funderburk, H.H. and Lawrence, J.M. (1964) Mode of action of diquat
    and paraquat. Weeds, 12: 259-264

    Funderburk, H.H., Negi, N.S. and Lawrence, J.M. (1966) Photochemical
    decomposition of diquat and paraquat. Weeds, 14: 240-243

    Funderburk, H.H. and Bozarth. (1967) Review of the metabolism and
    decomposition of diquat and paraquat. J. Agr. Fd. Chem., 15: 563-567

    Gage, J.C. (1967) The toxicity of diquat aerosols. Unpublished report
    IHR/212 (March 1967) from ICI Ltd. through Chevron Chemical Co. to FDA

    Gage, J.C. (1968) The action of paraquat and diquat on the respiration
    of liver cell fraction. Biochem. J., 109: 757-761

    Goater, T.O., Kenyon, A.J. and Hurst, E.W. (1964) The two-year test
    with diquat dichloride monohydrate in rats. Unpublished report IHR/165
    (Nov. 1964) ICI Ltd.

    Griffiths, D., Ponsford, D.C. and Hurst, E.W. (1966) A study of
    reproduction in rats treated with diquat monohydrate in the diet.
    Unpublished report IHR/188 (Jan. 1966) from ICI Ltd. through Chevron
    Chemical Co. to FDA

    Headford, D.W.R. and Douglas, G. (1967) Tuber necrosis following the
    desiccation of potato foliage with diquat. Weed Res., 7: 131-144

    Hurst, E.W. (1966) A long-term toxicity test with diquat dichloride
    monohydrate in dogs. Unpublished report IHR/195 (May 1966) from ICI
    Ltd. through Chevron Chemical Co. to FDA

    Kirston, W.J. (1966) The determination of diquat residues in potato
    tubers. Analyst, 91: 732-738

    Khera, K.S. and Whitta, L.L. (1968) Embryopathic effects of diquat and
    paraquat in the rat. Ind. Med. Surg., 37: 553

    Kohn, F.E., Kay, J.H. and Calandra, J.C. (1965a) Two-year chronic oral
    toxicity of diquat - albino rats 1000, 500 and 250 ppm (27 February
    1965). Unpublished report from Industrial Bio-Test Lab. Inc. through
    ICI Ltd. and Chevron Chemical Co. to FDA

    Kohn, F.E., Kay, J.H. and Calandra, J.D. (1965b) Two-year chronic oral
    toxicity of diquat - albino rats 100 and 10 ppm (27 February 1965).
    Addendum report -  Unpublished report from Industrial Bio-Test Lab.
    Inc. through ICI and Chevron Chemical Co. to FDA

    Kohn, F.E., Kay, J.H. and Calandra, J.C. (1965c) Two-year chronic oral
    toxicity of diquat - albino rats, 50 ppm (27 February 1965). Addendum
    report. Unpublished report from Industrial Bio-Test Lab. Inc. through
    ICI Ltd. and Chevron Chemical Co. to FDA

    Oreopoulos, D.G. and McEvoy, J. (1969) Diquat poisoning. Post-Grad.
    Med. J., 45: 635-637

    Rees, J.R. (1969) Reaction between lens constituents and substances
    which cause cataracts. Thesis for B.Sc. Degree, University of Oxford
    cited by Conning et al. (1969)

    Samman, P.D. and Johnston, E.K. (1969) Nail damage associated with
    handling of paraquat and diquat. Brit. Med. J., 1: 818-819

    Sarfaty, A.B. (1963) Observational trials on toxicity to sheep and
    cattle. Unpublished report from ICI Ltd. through Chevron Chemical Co.
    to FDA

    Slade, P. and Smith, A.E. (1967) Photochemical degradation of diquat.
    Nature, 213: 919-920

    Smith, J.M. and Sagar, G.R. (1966) Re-examination of the influence of
    light and darkness on the long distance transport of diquat in
    Lycopersicon esculentum. Weed Res., 6: 314-321

    Smith, A.E. (1967) Residues in potato tubers following haulm
    desiccation with 14C-diquat. Bull. Environ. Contam. Toxicol., 169-177

    Stevens, M.A. and Walley, J.K. (1966) Tissue and milk residues arising
    from the ingestion of single doses of diquat and paraquat by cattle.
    J. Sci. Fd. Agric., 17: 472-475

    Swan, A.A.B (1960) Toxicological report. Unpublished report TR/35
    Supplement (7 June 1960) from ICI Ltd. through Chevron Chemical Co. to
    FDA

    Swan, A.A.B. (1962) Unpublished interim toxicological report No:
    TR/375 (5 July 1962) from ICI Ltd. through Chevron Chemical Co. to FDA

    Swan, A.A.B. (1963a) Diquat-oral toxicity to mice. Unpublished report
    (24 January 1963) from ICI Ltd. through Chevron Chemical Co. to FDA

    Swan, A.A.B. (1963b) The dermal toxicity of diquat dichloride.
    Unpublished report TR/540 (20 June 1963) from ICI Ltd. through Chevron
    Chemical Co. to FDA

    Walley, J.K. (1962) Diquat toxicity in cattle. Unpublished report
    IHR/167 (Nov. 1962) from ICI Ltd. through Chevron Chemical Co. to FDA
    


    See Also:
       Toxicological Abbreviations
       Diquat (HSG 52, 1991)
       Diquat (PIM 580F, French)
       Diquat (WHO Pesticide Residues Series 2)
       Diquat (Pesticide residues in food: 1976 evaluations)
       Diquat (Pesticide residues in food: 1977 evaluations)
       Diquat (Pesticide residues in food: 1978 evaluations)
       Diquat (Pesticide residues in food: 1993 evaluations Part II Toxicology)