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


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

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





    Chemical name

    2,2-dichlorovinyl dimethyl phosphate




    Biochemical aspects

    Dichlorvos inhibits cholinesterase activity and thus causes
    parasympathomimetic effects. It requires no metabolic conversion, but
    inhibits the enzyme directly. Dichlorvos is broken down rapidly in the
    liver (Tracy, 1960; Tracy et al., 1960). Thus, the onset of poisoning
    is rapid, and if recovery occurs, it is prompt (Klotzsche, 1956;
    Durham et al., 1957; Gaines, 1960, Yamashita, 1962).

    In blood from a human female with pseudocholinesterase deficiency,
    0.185 µg of dichlorvos caused 50 per cent inhibition of the
    erythrocyte esterase activity. The erythrocyte esterase activity in
    normal blood was inhibited by only 15 per cent by 0.3 µg of dichlorvos
    (Vigliani, 1966). Assays of whole blood from a cow given 1.0 mg/kg of
    dichlorvos either orally or subcutaneously did not show any
    cholinesterase inhibition; however, intravenous administration of the
    same dose produced 29 per cent inhibition after 1-2 hours with rapid
    recovery. In a goat given 1.52 mg/kg subcutaneously there was 44 per
    cent inhibition in 1/4 hour; 46 per cent in 1/2 hour; 41 per cent in 1
    hour and 35 per cent in 2 hours, followed by rapid recovery (Casida et
    al., 1962).

    The compound is not stored in the body nor excreted in the milk to any
    appreciable extent in cows or rats, even when administered in doses
    that produced severe poisoning (Tracy, 1960; Tracy et al. 1960).

    With whole homogenates of liver, kidney, spleen and adrenals from rat
    and rabbit, the principal labelled metabolite of dichlorvos-35P was
    dimethylphosphate, 50-85 per cent, with the remaining radioactivity
    appearing in demethyl-dichlorvos, monomethyl phosphate and inorganic
    phosphate. In the plasma of both species, dimethyl phosphate accounted
    for 98 to 100 per cent of the dichlorvos hydrolyzed. When dimethyl
    32P-phosphate was incubated with rat plasma or liver homogenate, all

    the radioactivity was recovered as unchanged dimethyl phosphate.
    Dichlorvos was hydrolyzed by the soluble and mitochondrial fractions
    of rat liver but not by the microsomes. Demethyl-dichlorvos was
    hydrolyzed by the soluble fraction only. In rat liver homogenate, 2-3
    times more dichloroacetaldehyde than inorganic phosphate was produced
    from demethyl-dichlorvos. Inorganic phosphate was produced from
    monomethyl phosphate in both plasma and liver homogenate. The reaction
    was very slow. In soluble rat liver preparations, the
    dichloroacetaldehyde released by the hydrolysis of dichlorvos was
    reduced in the presence of DPNH to dichloroethanol. A very small
    amount may have appeared as dichloroacetate. It is possible that a
    pathway exists for conjugation of dichloroethanol with glucuronic acid
    (Hodgson & Casida, 1962).

    In rats given dichlorvos-32P, 10 mg/kg orally, rapid absorption,
    distribution and hydrolysis took place. Female rats treated every 1/2
    hour with 4 mg/kg of dichlorvos-32P for 2 hours and sacrificed 1/2
    hour after the last dose showed mainly hydrolysis products in the
    tissues. In mice given 4 doses of 10 mg/kg every 15 minutes, 95 per
    cent of the dichlorvos administered was hydrolyzed in the liver,
    kidney and small intestine. In male rats given
    dimethyl-32P-phosphate, 500 mg/kg orally, necropsy 90 hours after
    dosing indicated that almost the entire dose had been eliminated. The
    urine contained only unmetabolized dimethyl-32P-phosphate, which
    accounted for about 50 per cent of the radioactivity administered. The
    tissues were almost devoid of radioactivity. In a rat given
    demethyl-dichlorvos-32P, 500 mg/kg orally, about 14 per cent of the
    dose was eliminated in the urine in 90 hours, and the tissue
    distribution was similar to that of the rat which had received
    dichlorvos. A very high proportion of the radioactivity was found in
    bone, indicating rapid degradation to phosphoric acid. Metabolites in
    the urine were 86 per cent, phosphoric acid and 14 per cent
    demethyl-dichlorvos. From 67 to 100 per cent of the administered
    radioactivity was recovered with 1 week in the combined urine and
    faeces of cows, rats and a goat given various doses of
    dichlorvos-32P. Excretion of radioactivity in the faeces accounted
    for 11-15 per cent of the dose, except in cows treated orally, where
    about 50 per cent of the radioactivity was excreted. The excreted
    metabolites appeared to be demethyl-dichlorvos, dimethyl phosphate,
    monomethyl phosphate and inorganic phosphate. Most of the
    radioactivity in the milk of the cows and goat was due to hydrolysis
    products. The level of organosoluble radioactivity was significantly
    above background only within the first 2 hours. The highest excretion
    level was found at 12 hours in the cows (Casida, McBride &
    Niedermeier, 1962).

    Both single and repeated large doses cause a stress-attributed
    reduction in the eosinophil count of the peripheral blood of rats
    (Klotzsche, 1956).

    Experiments in rats showed that the liver is highly efficient in
    detoxicating dichlorvos (Gaines, 1966) and that the compound is
    absorbed from the gastrointestinal tract by the blood of the hepatic
    portal system (Laws, 1966).

    Acute toxicity

    Animal            Route         LD50                   References
                                    mg/kg body-weight

    Mouse             Oral          124                    Yamashita, 1962

    Mouse             i.p.          28*                    Casida et al., 1962

    Rat               Oral          73                     Klotzsche, 1956

    Rat, male         Oral          80                     Durham et al., 1957
                                                           Gaines, 1960
                                                           Mattson et al., 1955

    Rat, female       Oral          56**                   Durham et al., 1957
                                                           Gaines, 1960
                                                           Mattson et al., 1955

    Rat, female       Oral          80***                  Durham et al., 1957

    Chick, male       Oral          14.8                   Sherman & Ross, 1961

    * Technical grade; purity not stated.
    ** Based on 99 per cent pure material.
    *** Result of 2 tests on a technical preparation (90 per cent pure).
    Rat. Under laboratory conditions it was possible to produce
    concentrations ranging from 31 to 118 µg/l in an exposure chamber.
    Under the severest conditions of respiratory exposure, rats showed
    signs of poisoning within 2 hours and died in 4.5-17.5 hours (Durham
    et al., 1957).

    Domestic animals. Horses tolerated a single dose of 50 mg/kg
    dichlorvos in feed, but showed moderate acute poisoning when the
    insecticide was given by stomach-tube at 25 mg/kg (Jackson et al.,
    1960). An almost identical dose (27 mg/kg) given by stomach-tube
    caused severe but non-fatal poisoning in a cow (Tracy et al., 1960).

    Dichlorvos does not produce either immediate or delayed paralysis in
    hens (Durham et al., 1957).

    Man. Men withstood brief exposure (30-60 minutes) to concentrations
    as high as 6.9 µg/l without depression of cholinesterase activity or
    any other observed effect (Durham et al., 1959; Hayes, 1961). A single
    exposure for 8 hours at a concentration ranging from 0.9 to 3.5 µg/l
    produced slight inhibition of plasma cholinesterase activity in man
    (Witter et al., 1961). Slightly higher concentrations or longer
    periods of exposure, or both, produce measurable reduction of both the
    red cell and plasma enzyme activity in men, monkeys and rats (Hayes,

    Short-term studies

    Rat. Relatively small repeated doses lower the blood cholinesterase
    activity but much larger doses are required to produce illness. Thus,
    Durham et al. (1957) found that a dietary concentration of only 50 ppm
    soon produced detectable lowering of plasma and red cell
    cholinesterase activity in female rats, but a dietary level of 1000
    ppm (about 50 mg/kg/day) was tolerated for 90 days without any
    diminution of growth or sign of intoxication. Male and female rats
    reproduced as well as controls when maintained on a dietary level of
    100 ppm (Gaines, 1964).

    When dichlorvos is given by stomach-tube it is not so well tolerated
    as when the same dosage is absorbed from the diet gradually throughout
    the day. Female rats tolerated doses of 10 and 20 mg/kg in the diet
    but suffered severe, acute poisoning when given single doses of 30
    mg/kg. Even at 30 mg/kg, the rats survived and the red cell
    cholinesterase activity and growth of their litters were normal (Tracy
    et al., 1960).

    Reproduction studies in rats fed 0, 0.1, 1.0, 10.0, 100 or 500 ppm in
    the diet through three successive generations did not show any
    significant effect on numbers, and sizes of litters, survival of young
    or growth of young being suckled while dichlorvos was still being fed
    to the dams. Dichlorvos appeared to be without teratogenic effect
    (Witherup et al., 1965).

    Dog. Dichlorvos given to dogs by capsule at rates equivalent to
    dietary levels of 5 and 15 ppm (0.13-0.37 mg/kg/day) produced no
    detectable effect; levels equivalent to 25 ppm and 50 ppm depressed
    brain cholinesterase activity to 88 and 33 per cent of control,
    respectively, and led to some increase in the activity and
    aggressiveness of the dogs (Blucher et al., 1962).

    Monkey. A dermal dose of 50 mg/kg produced cholinergic signs in a
    monkey 20 minutes after administration, and it died after 8 daily
    doses at this rate. Higher dosage rates produced even more rapid onset
    of illness, even though a single dose of 100 mg/kg was not fatal
    (Durham et al., 1957).

    Monkeys tolerated continuous exposure to concentrations ranging from
    0.1-0.5 µg/l for 22 days without a definite change in cholinesterase
    activity. They showed a definite depletion by the 50th day of exposure
    (Durham et al., 1959), but the concentration of dichlorvos may have
    exceeded 0.5 µg/l sometime between the 22nd and 50th day (Hayes,

    Horse. Horses showed mild depression of red cell but not plasma
    cholinesterase activity when exposed continuously to concentrations
    ranging from 0.24-1.48 µg/l, but they returned to normal in spite of
    continuing exposure (Tracy et 1960).

    Man. Men showed no change in cholinesterase activity when exposed
    for 8-10 half-hour intervals, 4 nights per week, for 11 weeks to
    concentrations from 0.07 to 0.66 µg/l (average 0.25 µg/l). They did
    show a small but statistically significant depression of plasma enzyme
    activity, but not of red cell enzyme activity, when the schedule of
    dosing was maintained but the concentration increased to 0.40-0.55
    µg/l (average 0.51 µg/l). The other parameters studied, including
    complex reaction time, airway resistance and vision, remained normal,
    (Rasussen et al., 1963). The tolerated inhaled dosage averaged 0.5 
    mg/man/day while the dosage that caused a slight fall of plasma
    cholinesterase was 1.1 mg/man/day. The compound produced no decrease
    in whole blood cholinesterase activity and no other indication of
    injury when used for malaria control (Funckes et al., 1963; Gratz et
    al., 1962).

    When 15 subjects were exposed for 8 months to concentrations of 0.1
    mg/M3 and higher of dichlorvos in the air, 5 showed a slight
    reduction in plasma cholinesterase activity. When 36 subjects were
    exposed to concentrations of less than 0.1 mg/M3, none showed any
    reduction in plasma cholinesterase activity (Vigliani, 1966).

    Long-term studies

    No really long-term studies have been made of dichlorvos, nor do they
    appear indicated because of the rapid action and excretion of the


    Dichlorvos is rapidly metabolised in mammalian tissues to relatively
    non-toxic metabolites which are rapidly excreted. From the data
    available to date, the maximum level causing no significant
    toxicological effect in man is 0.01 mg/kg/day by inhalation.
    Continuous exposure of man to 0.1 mg/M3 caused some depression of
    plasma cholinesterase activity without clinical signs. It would be
    desirable to determine the maximum oral dose causing no inhibition of
    cholinesterase activity in man. In short-term experiments in dogs, the
    oral no-effect level was 0.37 mg/kg/day.


    Level causing no toxicological effect

    Rat: 10 ppm in the diet equivalent to 0.5 mg/kg/day.

    Dog: 0.37 mg/kg/day.

    Estimate of acceptable daily intake for man

    0-0.004 mg/kg body-weight


    Use pattern

    (a) Pre-harvest treatment

    No information was available on the use of dichlorvos treatments
    applied to food crops prior to harvest. Its potentialities in this
    field seem limited by its lack of systemic properties and its short
    persistence. It is used on beef and dairy cattle and on goats, sheep
    and swine and in and around the buildings which house these animals.

    (b) Post-harvest treatments

    Strong & Spur (1961) showed that dichlorvos was active against a range
    of insect pests of stored produce. Experimental work has since been
    carried out on its application for the protection of cereals and
    cereal products during storage and for the control of insects in
    facilities where foods are stored, processed, handled or shipped.
    Trials have shown that 4 micrograms of dichlorvos vapour per litre of
    air for six hours will control common stored product insects. Durham
    et al. (1959) found that the tightness of the warehouse and the
    temperature influences the amount required to obtain the desired
    concentration in the air; but in fairly tight warehouses the necessary
    concentration can be obtained by releasing dichlorvos at 50 mg/m3.
    Dichlorvos was dispensed by Gillenwater & Harein (1964) from a
    specially designed heat volatilizer containing impregnated resin
    pellets. However, it could be applied as a pressurized aerosol
    formulation although higher levels of residues might result from such
    use, particularly in any foodstuffs situated close to the aerosol

    Some tests have been conducted recently on dichlorvos impregnated
    resin strips which show considerable promise for future extension of
    its use in the control of insects in stored produce (Green et al.,

    (c) Uses other than on food

    For the control, primarily, of flies and, mosquitos dichlorvos is
    being used both inside and outside of agricultural premises such as
    barns, feed lots, milk rooms, poultry houses, stables, corrals,
    holding pens and poultry pens and yards. It has been used for a number
    of years for the control of Ephestia elutella (Hübner) and
    Lasioderma serricorne (Fabricius) in tobacco warehouses and in
    processing areas. The insecticide is applied into the air spaces after
    working hours. Dichlorvos is also being used in the United States in
    sprays (0.5 per cent for the control of insect pests such as ants,
    bedbugs, cockroaches, flies, silverfish, spiders, ticks and wasps.


    The use of dichlorvos in ways which might possibly leave residues in
    food is quite recent. There appear to be no legal or other tolerances.

    Residues resulting from supervised trials

    There is only a limited amount of data available on residues in food
    produced by dichlorvos. In a series of warehouse tests conducted in
    the United States packaged noodles, raisins, beans, peanuts, flour and
    sugar were exposed to 21 weekly treatments of dichlorvos applied as a
    vapour at the rate of 50 mg/m3 per treatment. In each treatment, the
    insecticide was vaporized slowly over a period of six hours. The
    highest residue found after 21 applications in composite samples of
    the various foods was 1.68 ppm in peanuts contained in burlap bags.
    The residues in the other foods were well below 1 ppm (Unpublished
    information received from US Department of Agriculture).

    Following the work of Strong & Spur (1961) which showed that
    dichlorvos was toxic to stored-product insects at very low
    concentrations, preliminary tests were conducted in the United Kingdom
    to assess its value for rapid disinfestation of grain where a long
    residual life is unnecessary or undesirable. Feed barley was treated
    with an emulsifiable formulation of dichlorvos as the grain was turned
    from one bin into another. A deposit of 4 ppm appeared effective in
    controlling the insects present but the insecticide disappeared very

    Resin strips measuring about 2-1/2" × 10" × 1/4" and containing about
    18.6 per cent of dichlorvos by weight are under test to determine
    their effectiveness in providing continuous control of flying and
    crawling insects. The initial generation of dichlorvos by these strips
    is approximately 40 mg/hr/strip and will produce a dichlorvos
    concentration in the air of 1 mg/l at 30 per cent R.H. The emission
    rate falls and after 30 days an almost constant rate of 3.0-4.0 mg of
    dichlorvos is emitted producing a concentration of the insecticide in
    the air of 0.075-0.1 µg/l of air. About 0.1 µg/l of dichlorvos is
    produced for about two-thirds of the active life of the strips.

    Residues in food moving in commerce

    No information was available.

    Fate of residues

    Fragmentary data indicate that dichlorvos residues appearing in foods
    from good agricultural practices are of a very low level and they
    disappear quite rapidly when the treated foods are aired.

    Green & Tyler (1966) found barley sprayed with dichlorvos at the rate
    of 4 ppm while being turned from one bin to another had 1.9 ppm
    (average) by analysis during treatment, 0.93 ppm after one week, 0.25
    ppm after six weeks, 0.22 ppm after 10 weeks, and none could be
    detected 15 weeks later.

    A variety of foods were exposed in a room in which were hung
    dichlorvos resin strips at the rate of 1 strip/1000 cu. ft for seven
    weeks. The dichlorvos concentration in the air reached 0.33 µg/l after
    24 hours and decreased to 0.03 µg/l after eight weeks. Residues of
    dichlorvos in the various foods increased to maximum levels ranging
    from 3.4 ppm for whole apples after 28 days' exposure down to 0.03 ppm
    in sugar after 56 days. Whole apples, bacon and cheese had dichlorvos
    residues greater than 1 ppm; banana (skin), currants (covered with
    paper), dried milk (polyethylene bag) and surface samples of wheat,
    cocoa beans and flour in hessian sacks had residues of 0.1-1 ppm; and
    eggs, oranges, sugar, banana (edible part) had dichlorvos residues
    below 0.1 ppm. On removal to an insecticide-free room, 20-70 per cent
    of the residue was lost after four days, and 60-100 per cent after 10
    days (Unpublished information).

    Dichlorvos was added to rice at levels of 4.5 ppm and 19 ppm, and to
    flour at 4.5 ppm and 14 ppm. Then the food was placed in sealed
    containers and stored for 65 hours at room temperature. As in home
    practice, the rice was washed with cold water and then cooked for
    20-30 minutes until edible. There was 98 per cent less dichlorvos in
    the rice after washing and cooking. The biscuits made from the treated
    flour had 80 per cent and 60 per cent less dichlorvos, respectively
    (Unpublished information).

    Residues in meats were followed by exposure to dichlorvos labelled
    with P32: the effects of cooking on such residues were investigated.
    Dichlorvos penetrated only into the surface layers of the samples and
    the residues in fat were generally lower than in the other samples.

    Following the frying and boiling of steak containing dichlorvos
    residues, the latter were completely destroyed and it was possible to
    detect only products of hydrolysis (Miller & Aitken, 1965). Also after
    the usual conservation of plums by thermalsterilization, dichlorvos
    residues disappeared completely (Benes, personal communication).
    Geisabühler & Haselbach (1963) concluded that the milling process does
    not result in any considerable decrease of residues in wheat treated

    with dichlorvos. During storage however the decomposition of the
    residues proceeds much more quickly in milled wheat products than it
    does in whole grains. No dichlorvos could be detected in samples of
    white flour after one month of storage at room temperature.

    Methods of residue analysis

    The method which has been used for determining dichlorvos residues in
    foods was developed by Shell Development Company. It is a
    spectrophotometric method based on enzyme inhibition. It has a
    sensitivity 0.10 ppm of dichlorvos.

    Gas-liquid-chromatographic methods have been developed for
    orgophosphorus compounds. It appears promising that this type of
    analysis could be perfected for the determination of dichlorvos


    No tolerances are recommended at this time because of insufficient
    information on the specific uses of dichlorvos on foods and the
    resulting residues. Recommendations for tolerances should be
    considered at the next joint meeting.

    Further work or information

    Information is required on:

    (a)  range of commodities likely to be treated,

    (b)  occurrence of residue levels resulting from good pest control

    (c)  rate of disappearance through normal aging, processing, cooking,


    (d)  chemical nature of terminal residues occurring in foods from good
         pest control practices.


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    Loquvam, G. L., Powers, M. T. & Riggs, C. W. (1962) Unpublished report
    from the Hine Laboratories, San Francisco, California

    Casida, J. E., McBride, L. & Niedermeier, R. P. (1962) J. Agr. Food
    Chem., 10, 370

    Durham, W. F., Gaines, T. B., McCauley, R. H., Sedlak, V. A., Mattson,
    A. M. & Hayes, W. J., jr (1957) A. M. A. Arch. industr. Hlth, 15,

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    Org., 29, 243

    Gaines, T. B. (1960) Toxicol. Appl. Pharmacol., 2, 68

    Gaines, T. B. (1964) Unpublished report

    Gaines, T. B. (1966) Nature (Lond.) 209, 88

    Gratz, N. G., Bracha, P. & Carmichael, A. G, (1962) WHO/Vector

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    Hodgson, E. & Casida, J. E. (1962) J. Agr. Food Chem., 10, 208

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    econ. Ent., 53, 602

    Klotzsche, C. (1956) Z. Angew. Zool., 1, 87

    Mattson, A. M., Spillane, J. T. & Pearce, G. W. (1955) J. Agr. Food
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    Rasmussen, W. A., Jensen, J. A., Stein, W. J. & Hayes, W. J., jr
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    Sherman, M. & Ross, E. (1961) Toxicol. Appl. Pharmacol., 3, 521

    Tracy, R. L. (1960) Soap Chem. Spec., 36, 74

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    Vigliani, E. C. (1966) Unpublished report to Shell Chemical Co.

    Witherup, S., Caldwell, J. S. & Hull, L. (1965) Unpublished report
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    Yamashita, K. (1962) Industr. Med. Surg., 31, 170


    Durham, W. F., Hayes, W. J. & Mattson, A. M. (1959) Toxicological
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    Geissbühler, H. & Haselbach, C. (1963) On the behaviour of DDVP upon
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    CIBA, Basle) Battelle Inst. Geneva, 30 October

    Gillenwater, H. B. & Harein, P. K. (1964) A dispenser designed to
    provide large quantities of insecticide vapor. J. Econ. Ent., 57
    (5): 762-3

    Green, A. A., Kane, J. & Gradidge, J. M. G. (1966) Experiments in the
    Control of Ephestia elutella using Dichlorvos Vapour. J. Stored
    Proc. Res., 2: 147-157

    Green, A. A. & Tyler, P. S. (1966) A field comparison of malathion,
    dichlorvos and fenitrothion for the control of Oryzaephilus infesting
    stored barley. J. Stored Prod. Res., 1: 273-295

    Millar, K. R. & Aitken, W. M. (1965) Residues in meat following
    exposure to P32 labelled dichlorvos vapour in an enclosed space.
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    Strong, H. G. & Spur, D. E. (1961) Evaluation of Insecticides as
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    See Also:
       Toxicological Abbreviations
       Dichlorvos (EHC 79, 1988)
       Dichlorvos (HSG 18, 1988)
       Dichlorvos (ICSC)
       Dichlorvos (FAO Meeting Report PL/1965/10/1)
       Dichlorvos (FAO/PL:1967/M/11/1)
       Dichlorvos (FAO/PL:1969/M/17/1)
       Dichlorvos (AGP:1970/M/12/1)
       Dichlorvos (WHO Pesticide Residues Series 4)
       Dichlorvos (Pesticide residues in food: 1977 evaluations)
       Dichlorvos (Pesticide residues in food: 1993 evaluations Part II Toxicology)
       Dichlorvos (IARC Summary & Evaluation, Volume 53, 1991)