WHO/FOOD ADD./70.38



    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, 8 - 15 December 1969.



    Rome, 1970



    Chemical name

    dimethyl 3-methyl-4-nitrophenyl phosphorothionate


    0,0-dimethyl 0-(3-methyl-nitrophenyl) phosphorothioate, Sumithion(R),
    Folition(R), Accothion(R), Danathion(R) (Denmark), Metathion(R) 
    (Czechoslovakia), methylnitrophos (countries in Eastern Europe)

    Structural formula


    Other relevant chemical properties

    Properties of fenitrothion - melting point 0.3°C, boiling point
    109°C/0.1 mm Hg; d420 1.3084; yellowish-brown liquid with unpleasant
    odour; soluble in alcohols, ethers, ketones, aromatic hydrocarbons;
    insoluble in water; completely stable for 2 years, at 20-25°C; storage
    temperature should not exceed 40°C; unstable in alkaline media.

    Formulations - 95% concentrate, 50% emulsifiable concentrate, 40%
    wettable powder, 2.5% and 5% dust. Deburol(R) (Ciba) contains 15%
    fenitrothion and 62% mineral oil. One company indicates that their 95%
    concentrate contains 95% fenitrothion (minimum) and 0.5%
    3-methyl-4-nitrophenol (maximum).



    Absorption, distribution and excretion

    Various comprehensive studies in mouse, rat, and guinea-pig have dealt
    with the pharmacodynamic and biochemical aspects of fenitrothion and
    its metabolites (Nishizawa et al., 1961; Miyamoto, 1964a, 1964b, 1969;
    Miyamoto et al., 1963a; Vandanis and Crawford 1964; Hollingworth et
    al., 1967 Hladká and Nosál, 1967 and Douch et al., 1968).

    Fenitrothion is presumably rapidly absorbed from the mammalian
    intestinal tract as evidenced by the appearance of radioactivity in
    blood from guinea-pigs and rats administered phosphorus32 -labelled
    fenitrothion orally. The presence of the oxygen analogue was
    demonstrated in all tissues examined (brain, heart, lung, liver,
    kidney, spleen and muscle) and it was detectable in blood one minute
    after an intravenous injection of fenitrothion. This oxygen analogue
    (II of Fig. 1) is the important metabolite with respect to toxicity.
    It is formed in the microsomal fraction of the cell, the main organs
    responsible for the transformation being the liver and kidney.
    Fenitrooxon is further metabolized as indicated in Fig. 1. The major
    excretion product found is 3-methyl-4-nitrophenol (VII) which can
    further be oxidized to 3-carboxy-4-nitrophenol (VIII). Other
    metabolites are the demethyl-derivatives (V and VI) which, with
    increasing doses, are excreted in increasing amounts. A total of nine
    metabolites has been isolated, the majority of which can also be
    identified. In vitro studies showed that formation of the oxygen
    analogue (II) was dependent on the availability of reduced nicotine
    adenine dinucleotide phosphate (NADPH2) and oxygen. Liver slices
    incubated with fenitrothion did not produce measurable amounts of
    fenitrooxon, while liver homogenates and the supernatant fraction of
    such homogenates showed appreciable activation of added fenitrothion.
    No correlation between the toxicity and rate of formation of the
    oxygen analogue could, however, be demonstrated (Miyamoto et al.,
    1963a; Miyamoto, 1969).

    No observations are available in these studies on the distribution
    into fatty tissue: however, residue studies on milk, meat and fat from
    cattle indicate amounts of approximately 0.001 ppm in these samples
    (Miyamoto and Sato, 1969).

    Fenitrothion and its metabolites are excreted mainly in the urine
    (90-95 per cent). Up to 10 per cent was recovered in faeces. Within
    three days nearly complete recovery of an orally administered dose (15
    mg/kg) could be obtained. The metabolic, pattern of fenitrothion as it
    appears from these studies is shown in Fig. 1. The ratios between the
    amounts of metabolites was dependent upon the dose given, as is shown
    in Table 1, which gives the percentage distribution of metabolites in
    mouse urine after various doses of fenitrothion (Hollingworth et al.,

    Effect on enzymes and other biochemical parameters

    As with other organophosphorous compounds fenitrothion acts in the
    animal organism as a cholinesterase inhibitor, probably after
    conversion to the oxygen-analogue. Some evidence presented indicates
    that the cholinesterase inhibiting effect in brain depends more on the
    rate of penetration into the brain than on the rate of oxidation and
    decomposition of fenitrothion (Miyamoto, 1969).


        TABLE I

    Percentage distribution of metabolites of fenitrothion in mouse urine after
    administering various doses

           Metabolite                   Percentage of radioactive metabolite excreted
                                        in urine after giving P52 - labelled fenitrothion
                                        at the indicated dose levels in mg/kg body-weight

                                             3         17          200         850

    Phosphoric acid                         2.0        2.4         1.9         1.2

    Methylphosphoric acid                   1.5        2.5         2.4         1.1

    Dimethylphosphoric acid                32.2       21.4         5.8         3.0

    Dimethylphosphorothioic acid           12.8       20.3         8.7         6.6

    Phosphate analogue (II)                 2.7        1.6         3.3         2.5

    O-demethylphosphate analogue (VI)      26.1       28.4        24.6        17.1

    analogue (V)                           20.5       20.1        50.9        66.1

    Unknown                                 2.2        2.5         2.4         2.4

    Special studies on neurotoxicity


    Three hens protected against acute anti-cholinesterase effects with
    atropine and pralidoxime were given a single oral dose of 400 mg/kg
    body-weight of fenitrothion. No symptoms of paralysis occurred during
    an observation period of 28 days. Histologic examination of spinal
    cord and sciatic nerves revealed no pathological lesions in two hens
    and a few scattered degenerated fibres in the spinal cord of the third
    (Carshalton, 1962).

    Seven hens protected in the same way were given an oral dose of 250
    mg/kg body-weight of fenitrothion and three other hens were given 500
    mg/kg. Two of the 500 mg/kg group died within 1-2 days, while the
    remaining eight hens did not show any sign of paralysis during an
    observation period of six weeks (Kimmerle, 1962b).

    Special studies on potentiation


    Female rats were given intraperitoneal doses of a combination of
    fenitrothion and the following organophosphorus compounds: parathion,
    parathion-methyl, demeton, disulfoton, malathion, EPN,
    azinphos-methyl, carbophenothion, mevinphos, dioxathion, schraden,
    ethion, diazinon, Folex, coumaphos, and fenchlorphos as well as the
    carbamate carbaryl. No sign of a potentiating effect was demonstrated
    (DuBois and Kinoshita, 1963).

    When male rats were given acute oral doses of mixtures of fenitrothion
    and phosphamidon a marked potentiation of toxicity occurred as
    evidenced by increased mortality. In female rats a potentiation of
    toxicity occurred as evidenced by increased mortality. In female rats
    a potentiation occurred only in mixtures containing relatively low
    concentrations of fenitrothion, the potention effect diminishing as
    the concentration of fenitrothion was increased. It was concluded that
    potentiation is associated with a non-linear phosphorothioate
    conversion (Braid and Nix, 1968).

    Special studies on the metabolite fenitrooxon

    The metabolite fenitrooxon is more toxic than the parent compound (cf.
    Tables II and III).


    Acute toxicity of fenitrooxon

    Animal        Route      LD50 mg/kg     References

    Mouse         oral          90          Miyamoto, 1969

    Mouse         oral         120          Hollingworth et al., 1967

    Rat           oral          24          Miyamoto, 1969

    Rat           i.v.           3.3        Miyamoto, 1969

    Guinea-pig    oral         221          Miyamoto, 1969

    Guinea-pig    i.v.          32          Miyamoto, 1969

    Acute toxicity

    The symptoms of acute toxicity are the same as for other
    organophosphorus compounds, doses close to the LD50 producing
    symptoms which developed more rapidly after intravenous than after
    oral administration. The compound is considerably less toxic to
    mammals than its close structural analogue parathion-methyl (Miyamoto
    et al., 1963b). Table II gives the LD50 in several species:

        TABLE III

                                     LD50 mg/kg
    Animal                Route      body-weight    References

    Mouse       (M)       oral          1336        Carshalton, 1964

    Mouse       (F)       oral          1416        Carshalton, 1964

    Mouse       (M)       i.p.           115        DuBois and Puchala, 1960

    Mouse       (F)       i.p.           110        DuBois and Puchala, 1960

    Mouse                 i.v.           220        Miyamoto et al, 1963b

    Rat         (M)       oral           740        Gaines, 1969

    Rat         (F)       oral           570        Gaines, 1969

    Rat         (M)       i.p.           135        DuBois and Puchala, 1960

    Rat         (M)       i.p.           160        DuBois and Puchala, 1960

    Rat                   i.v.            33        Miyamoto et al, 1963b

    Guinea-pig  (M)       oral           500        DuBois and Puchala, 1960

    Guinea-pig            oral          1850        Miyamoto et al, 1963b

    Guinea-pig  (M)       i.p.           110        DuBois and Puchala, 1960

    Guinea-pig            i.v.           112        Miyamoto et al, 1963b

    Cat                   oral           142        Nishizawa et al, 1961
    Short-term studies


    In what was described as a preliminary test, groups of dogs, each
    comprising one male and one female animal, were given daily oral doses
    by capsule of 0, 2, 9 or 40 mg/kg body-weight of fenitrothion for
    periods up to 98 days. Body-weights, blood biochemistry,
    cholinesterase levels and haemograms were checked at intervals. At the
    2 mg/kg level there was no effect with respect to any other of the
    parameters mentioned. At 9 mg/kg a slight depression after 60 days and
    at 40 mg/kg a moderate depression after 29 days occurred in whole
    blood, plasma and red-cell cholinesterase. At 40 mg/kg there were also
    marked toxic symptoms typical of cholinergic stimulation, and the dogs
    in this group were sacrificed below the end of the 98-day period
    (Cooper, 1966).


    Groups of male rats (16 or 17 in number) were fed 0, 32, 63, 125, 250,
    and 500 ppm of fenitrothion in the diet for 90 days. Mortality, food
    intake, growth, general behaviour, urinalysis, average organ-weights
    and histpathology were comparable to the controls in the groups fed
    32, 63, 125, and 250 ppm. All the animals fed 500 ppm showed clinical
    symptoms of anti-cholinesterase poisoning and there were minimal
    symptoms in four animals in the 250 ppm group. In the 500 ppm group
    the average organ-weights of the testes and brain were increased in
    comparison with those of the control group. After interim sacrifice
    every month of four rats from each group, measurement of the
    cholinesterase activity of plasma, red cells, brain cortex, liver and
    kidney showed a dose-dependent depression, the lowest being in the
    brain. The cholinesterase activity in the 32 and 63 ppm groups
    generally increased after 60 days of dosing to a level within the
    normal limits, the beet recovery being in the plasma, kidney and
    brain, less in the red cells and the liver (Misu et al., 1966).

    Two groups, each of 20 male rats, were dosed by stomach tube on six
    days a week for six months with 10 mg/kg and 11 mg/kg body-weight of
    fenitrothion, respectively. During the first weeks the rats showed a
    temporary deterioration of general condition and loss of weight.
    Haematology and urinalysis during the experiment and gross and
    microscopic pathology at its termination did not reveal any
    abnormalities (Klimmer, 1961).

    Male rats were given daily oral doses of 13 mg/kg body-weight of
    fenitrothion for 28 days. Red-cell cholinesterase activity showed
    severe depression, but there was recovery 30 days after withdrawal of
    fenitrothion (Kimmerle, 1962a).

    Male rats were fed 5, 10, and 20 ppm of fenitrothion in the diet for
    an unspecified period. Brain and red cell cholinesterase activity was
    normal in the 5 ppm group, whereas the 10 ppm group showed a slight

    depression of red cell activity after five weeks with recovery two
    weeks after withdrawal.

    The 20 ppm group showed some depression of activity both in red cells
    and in brain and the recovery in the brain remained incomplete two
    weeks after withdrawal (Carshalton, 1964).

    Other reported studies with fenitrothion in the rat lasting 90 days
    indicate that the levels causing no appreciable effect on the
    cholinesterase activity of plasma, red-cells and whole blood were 20
    ppm in the diet and 10 ppm in drinking water. The only exception was a
    moderate inhibition of the activity in plasma among the male animals
    when given 10 ppm in drinking water. The above mentioned levels and
    higher, namely 92.8 ppm in the diet and 46.2 ppm and 215 ppm in
    drinking water, caused no effect on food or water intake, weight-gain,
    average organ-weights, haemogram and blood biochemistry. However, 92.8
    ppm of fenitrothion in the diet and 46.4 ppm in drinking water had a
    moderate effect on whole blood and red-cell cholinesterase and a more
    marked effect on plasma cholinesterase. The cholinesterase activity
    recovered between 30-40 days after withdrawal of fenitrothion. The
    levels of 430 ppm in the diet and 1000 ppm in drinking water caused a
    depression of body-weight gains (Cooper, 1966).

    Long-term studies


    An interim report on what appears to be a two-year feeding study in
    rats is available. Groups of nine or 10 male rats were fed 0, 25, 100
    or 400 ppm of fenitrothion in their diet and were sacrificed after
    feeding these levels for 63 weeks. As a positive control a group was
    also fed 800 ppm of malathion. At the 400 ppm level of fenitrothion,
    food intake and body-weight gain were increased and only a few animals
    survived the 63 week period. At this level there was a 100 per cent
    depression of red-cell cholinesterase. At the 100 ppm level a slight
    (10-30 per cent) cholinesterase depression occurred in the brain and a
    moderate depression (30-65 per cent) in the red blood cells and
    plasma. At 25 ppm there was no effect on cholinesterase nor was there
    any effect with regard to any other parameters evaluated (Ueda and
    Nishimura, 1966).


    In a field spraying operation in Southern Nigeria including a village
    using a five per cent spray of fenitrothion, examination of 18
    villagers one week later did not reveal any clinical symptoms of
    toxicity or plasma cholinesterase depression. The same was true of the
    three spraymen examined on the first, second and sixth day after
    spraying relative to a pre-spraying level (Vandekar, 1965).

    In another field spraying trial in Northern Nigeria, 10,000 huts in
    which about 16,500 people lived were sprayed. Field test
    cholinesterase determinations on whole blood did not show any
    appreciable difference in cholinesterase levels of 535 villagers
    tasted before spraying and 299 villagers tested 5-30 days after
    spraying. After one week of intensive spraying five out of 20 spraymen
    developed a 50 per cent depression of cholinesterase which returned to
    a stable level after a period of rest. One sprayman developed symptoms
    of toxicity which lasted only a few hours and disappeared without
    treatment (Wilford et al., 1965).

    Fenitrothion was given to a total of 24 human subjects in single oral
    doses of from 2.5 to 20 mg (0.042 to 0.33 mg/kg body-weight for a 60
    kg man). The excretion of the metabolite, 3-methyl-4-nitrophenol, in
    the urine was almost complete within 24 hours, the maximum excretion
    occurring in the first 12 hours. The percentage of the dose excreted
    during this time depended to a certain extent upon the size of the
    dose administered, being about 70 per cent of theoretical after a
    0.042 mg/kg dose and about 50 per cent after a 0.33 mg/kg dose. Both
    plasma and cholinesterase activity were not depressed below normal
    except possibly in one person given a 0.33 mg/kg dose, where some
    depression of plasma cholinesterase was apparent after six and 24
    hours (about 65 per cent of the pre-test level). When repeated doses
    of 2.5 or 5 mg approximately 0.04 to 0.08 mg/kg) were given to five
    individuals, four times at 24 hour intervals, most of the nitrocresol
    metabolite appeared in the urine within the interval 0 to 12 hours
    after administration. After receiving the third and fourth dose there
    was a trend towards a rise in red cell cholinesterase activity but in
    no cases was there any evidence of reduction below normal levels of
    the activity of this enzyme in either plasma or red cells (Nosal and
    Hladka, 1968).


    Adequate information is available on the toxicity, biochemistry and
    metabolism of fenitrothion, in three species of rodent. Information is
    also available in man including field spraying studies and a
    metabolism study. Only an interim report comprising a 63-week study in
    rats in available and there are no 1-2 year studies in a non-rodent
    mammalian species. The short-term studies in the rat, using
    cholinesterase inhibition criteria, provide a no-effect level. No
    reproduction or teratogenicity studies are available and in view of
    the similarity in the structure of fenitrothion to parathion-methyl,
    it is important that such studies be undertaken. For this reason and
    because no adequate long-term studies are available it was decided to
    give only a temporary acceptable daily intake to this compound.


    Level causing no toxicological effect

    Rat:  5 ppm in the diet, equivalent to 0.25 mg/kg body-weight/day


    0-0.001 mg/kg body-weight



    Fenitrothion is a broad-spectrum insecticide having a much lower acute
    mammalian toxicity than many similar organophosphorus insecticides.
    Its action is by direct contact or an a stomach poison. It can be
    applied as an emulsifiable concentrate, wettable powder, granular
    formulation or dust.

    It is toxic to bees and should not be sprayed on flowering crops.

    Fenitrothion can be combined with all conventional insecticides and
    fungicides except those having an alkaline reaction.

    The insecticide has been used throughout Europe, East Pakistan, East
    Africa, United Arab Republic, Japan, Republic of China, New Zealand,
    Canada, and Brazil. It is not registered for use in the United States.

    Pre-harvest treatments

    Fenitrothion is used on a wide variety of crops including fruits,
    field crops, vegetables, rice, cotton, cereals, cocoa, tea, and coffee
    for control of stem borers, hoppers, leaf miners, leaf rollers,
    whiteflies, fruit flies, mealybugs, mirids and bugs, thrips, aphids,
    mites, lady beetles, caterpillars, and soft scale insects.

    The recommended concentrations and rates of application vary for the
    different crops and pest species to be controlled. Concentrations of
    sprays range from 0.05 to 0.1%. active ingredient (a.i.) and rates of
    application from 0.5 to 2.0 kg a.i./hectare. The chemical is generally
    tolerated by most crops although high dosages may injure cotton, and
    phytotoxicity on Brassica crops and orchard fruits has been

    Safety intervals prior to harvest range from 10 to 21 days and differ
    depending on the country and the crop.

    Post-harvest treatments

    No post-harvest treatments are made in Europe. Admixture of 1 to 5 ppm
    of fenitrothion has been recommended to protect grains such as rice,
    wheat, and barley for months against various weevils and beetles. Bag
    treatment is acceptable in Brazil for protecting stored grains and
    post-harvest treatments are under development in various countries.

    Other uses

    Fenitrothion is used to control grasshoppers, locusts, and
    caterpillars on pastures and spruce budworm in forests. It also
    provides control of household and other pests, such as mosquitoes and
    their larvae, houseflies, cockroaches, lice, bedbugs, and poultry
    mites. Its action is rapid, and its residual activity is good.


    Typical maximum residues after treatment of a variety of crops are
    given in Table IV.
        TABLE IV

    Maximum residues after treatment of crops

                      Dosage                             residues at
                      active           Pre-harvest       harvest, ppm
    Crop              ingredient       interval, days    respectively     Reference

    Rice              1000 g/ha        41                0.005            Sumitomo 1969

    Rice              0.07% spray or                                      Miyamoto, Sato
                      5% granules      1-2 months        n.d.             1965

    Apple             0.05% spray      21                0.05             Sumitomo 1969

    Apple             0.2% spray       7 and 14          0.5 and 0.35     Bayer 1969

    Apple, Golden     0.15% spray      10 and 15         1.0 and 0.75     Bayer 1969

    cherry            0.2% spray       7 and 14          0.5 and 0.2      Bayer 1969

    Grape*            0.05% spray      10                0.50             Sumitomo 1969

    Tomato*           0.05% spray      7                 0.18             Sumitomo 1969

    Cocoa             0.1% spray       14                0.10             Miyamoto et al

    Red cabbage       0.15%; 1000      7                 Outside leaves
                      1/ha                               0.65
                                                         Cabbage less
                                                         outside leaves
                                                         0.25             Bayer 1969

    Sugar beets       0.15%; 1000      8                 n.d.             Bayer 1969

    TABLE IV (cont'd)

    Maximum residues after treatment of crops

                      Dosage                             residues at
                      active           Pre-harvest       harvest, ppm
    Crop              ingredient       interval, days    respectively     Reference

    Green tea         0.1% spray       14                0.27             Sumitomo 1969

    Cauliflower       0.1%; 1000       7                 n.d.             Bayer 1969

    Lettuce           0.1%; 1000       7 and 14          1.05 and 0.3     Bayer 1969

    Lettuce           0.05%; 600       1, 7, and 14      0.65, 0.06,      Möllhoff 1968
                      1/ha                               0.01

    Peas and pod      0.25%; 560       0 and 5           0.7 and <0.15    Bayer 1969

    *These green-house trials gave residues higher than those of field

    General comments

    Fenitrothion may be metabolized as shown in Figure 1. The major route
    in animals appears to be through splitting of the P-O-aryl bond to
    give the corresponding dimethyl esters of phosphorothioic and
    phosphoric acids. Another means of degradation is demethylation of the
    methoxy group to give desmethyl fenitrothion. Although formation of
    the oxygen analogue, fenitrooxon, is minor compared to products formed
    via hydrolysis, fenitrooxon must be taken into account because the
    mammalian toxicity of oxons is generally much higher than that of
    parent thiono pesticides. In plants the metabolism of fenitrothion
    appears to be similar to that in animals.

    In animals

    Orally administered 32P-labelled fenitrothion was readily absorbed
    from the digestive tract of guinea pigs or rats and the major portion
    of the radioactivity excreted in the urine. Neither fenitrothion nor
    fenitrooxon was detected and desmethyl fenitrothion, dimethyl
    phosphorothioic and dimethyl phosphoric acids were identified in the
    urine (Miyamoto et al., 1963a).

    Following intravenous injection of radioactive 32P fenitrothion into
    guinea pigs and rats, fenitrothion rapidly disappeared from the blood.
    Fenitrothion and fenitrooxon were found in the tissues, and their
    amounts decreased rapidly. The desmethyl compound and the dimethyl
    esters mentioned in the foregoing paragraph were found mostly in the
    liver and kidneys (Miyamoto, 1964a).

    Excretion of metabolic products is rapid and chiefly in the form of
    3-methyl-4-nitrophenol (the nitrocresol hydrolysis product) (Hladka
    and Nosal, 1967; Nosal and Hladka, 1968); the cresol methyl may be
    oxidized to COOH (Douch et al., 1968). The desmethyl compounds are
    also excreted (Hollingworth et al., 1967; Miyamoto et al., 1963b).
    Between 60 and 90% of the insecticide is excreted within two days,
    chiefly in the aforementioned forms. Only up to 10% is excreted in the
    feces. Detoxication via the desmethyl compounds is dose-dependent.

    After oral administration of up to 40 grams of fenitrothion per
    lactating cow, residues in the milk were as high as 0.4 ppm after 6
    hours and below the limit of detection after one day (Hais and Franz,
    1965). Detoxication in bovine rumens is rapid owing to reduction of
    fenitrothion to the amino compound (Miyamoto et al., 1967).

    Cows fed 3 mg/kg body weight of fenitrothion for seven consecutive
    days produced milk having up to 0.002 ppm residue of fenitrothion on
    the second day, and no residue one day after administration was
    stopped. Less than 0.003 ppm aminofenitrothion and about 0.1 ppm
    p-nitrocresol were detected during treatment, and no fenitrooxon was
    found (Miyamoto et al., 1967).

    Thirty calves (1-1.5 yr. av. wt. 243 kg) confined on a pasture sprayed
    with 375 g/ha of fenitrothion (11.8 ppm initial residue on grass) were
    periodically sacrificed and breast muscle and omental fat analysed. On
    the first day residues in the meat and fat were about 0.01 ppm. No
    residue of fenitrothion was found in the meat from the third day on
    and only 0.004-0.007 ppm was found in the fat on the third day; these
    amounts decreased almost to control levels by the seventh day
    (Republic of Argentina, 1968; Miyamoto and Sato, 1969).

    Lactating dairy cattle were fed 50 ppm of fenitrothion in the feed
    (dry basis) for 29 days. No residue of fenitrothion, fenitrooxon, or
    the cresol appeared in the milk. A maximum of 0.006 ppm of
    aminofenitrothion was found (Bowman, 1969).

    In plants

    About 50% of 32P-labelled fenitrothion sprayed on rice plants
    penetrated into the tissues in 24 hours; at the end of this period
    only 10% was left, indicating rapid decomposition. Some fenitrooxon
    formed but it disappeared from the tissues more rapidly than
    fenitrothion. Rice grains harvested 46 days after treatment contained
    0.0007 ppm fenitrothion and less than 1 ppm of p-nitrocresol and
    dimethyl phosphorothioic acid (Miyamoto and Sato, 1965).

    Fenitrothion does not appear to have much systemic action. After
    treatment of rice plants with fenitrothion, more residue is found in
    the bran than in the polished grains (Miyamato and Sato, 1965). Very
    little active ingredient passed from peel to fruit in stored bananas
    (Miyamoto et al., 1965a).

    The half-life of fenitrothion in green plants ranges between the
    values established for parathion and parathion-methyl, i.e. between
    one and two days; the half-life of the oxon is estimated to be only a
    few hours (Möllhoff, 1968).

    Although the oxon may form in plants it occurs only during the first
    few days after treatment and in proportions (ca. 1% smaller than those
    in animals (Miyamoto et al., 1963; Miyamoto and Sato 1965; Möllhoff,
    1968). Desmethyl compounds occur only in minor amounts in plants.

    Phytotoxicity of fenitrothion on cabbage was ascribed to high
    penetration of the insecticide and accumulation of the cresol
    hydrolysis product (Tomizawa and Kobayashi, 1964).

    In soil

    The soil bacteria Bacillus subtilis, converted more than half of
    radiolabelled 32P fenitrothion to the amino analogue under aerobic
    conditions at 37°C in 24 hours. The desmethyl derivatives of
    fenitrothion and aminofenitrothion as well as dimethyl phosphorothioic
    acid formed. None of the oxon or oxons of the degradation products
    were found (Miyamoto et al., 1966).

    Fenitrothion is gradually inactivated by other bacterial species
    including gram-positive and gram-negative rods, but not by fungi and
    yeasts (Yasuno et al., 1965).

    Fenitrothion is readily absorbed onto various kinds of soil and
    decomposed by alkalinity or microorganisms (Muramoto, 1967).
    Persistence in soil does not appear to be great.

    In storage and processing

    Fenitrothion shows promise for control of grain insects in storage.
    Applied at 2 and 1 ppm to barley, it decreased to 0.4 ppm after 15
    weeks' storage (Green and Tyler, 1966). On barley in silos the
    half-life of fenitrothion was about 100 days (Green and Tyler, 1966)
    and on stored bananas about 15 days (Miyamoto et al., 1965a). Applied
    to wheat 11% moisture) at rates of 1, 2 and 4 ppm, 0.2, 0.4., and 1.1
    ppm of fenitrothion remained, respectively, after 9 months of storage
    at 25°C and 60% relative humidity (Kane and Green, 1968).

    In extensive trials as a wheat protectant, fenitrothion levels
    steadied below 2 ppm after about 2 months regardless of application
    rate between 2.5 and 10 ppm. In one trial 6 ppm applied to grain
    decreased to 2.4, 1.7, and 1.1 ppm, respectively, after 1´, 4, and 6
    months. Flour made from the 2.4-ppm sample contained 0.3 ppm

    fenitrothion, while only traces were found in the flour and bread from
    the later samples (Cooper Technical Bureau, 1968).

    Evidence of residues in food in commerce or at consumption

    No report of residues of fenitrothion in food in commerce or at
    consumption has been found. Reference is made under "In storage and
    processing" to the finding of only "traces" of fenitrothion in flour
    and bread prepared from grain containing 1.7 and 1.1 ppm of the


    Metabolic studies on plants and mammals indicate that residues of
    fenitrooxon and aminofenitrooxon, when they do form, occur in small
    amount and are degraded or excreted more rapidly than the parent
    compound. Once pilot experiments establish that no more than traces of
    these compounds form on a given crop, there does not seem to be any
    need to analyse for these compounds on that crop in commerce. (For
    purposes of this discussion, a trace shall be considered less than 10%
    of the tolerance level of the parent compound).

    Analyses for the p-nitrocresol have been made and measurable amounts
    of the compound are found following good agricultural practice. A
    determination of the cresol is sometimes reported. However, if a pilot
    experiment on a given crop shows no excessive amount of the cresol to
    be present at harvest, there does not appear to be any need for its
    analysis on that crop in commerce. Other metabolites are generally
    rather polar and do not tend to be stored.

    In essence then, the analyst will be concerned with residues of
    fenitrothion itself unless pilot experiments indicate that other
    metabolites should be taken into account. This same view is expressed
    by Frehse and Möllhoff in a IUPAC report by Egan (1969).

    Fenitrothion in so similar to parathion and methyl parathion that
    analytical methods used for them may be used for fenitrothion.
    However, many of the earlier methods lack specificity. Numerous
    procedures for a wide variety of harvest products are based on
    thin-layer chromatography, spectroscopy and gas chromatography.
    Information relating to these analyses follow. No reference to
    inter-laboratory collaborative studies on analytical procedures was

    Extraction and partitioning

    It is not sufficient simply to wash the analytical samples since small
    amounts of the active ingredient penetrate into the plant. It is
    therefore important that complete extraction of the insecticide and
    metabolites (e.g. by exhaustive Soxhlet extraction) be compared
    against the extraction method used. Harvest products with a high
    content of water have been macerated with acetone (Horler, 1966;
    Möllhoff, 1967, 1968), acetonitrile (Coffin and Savary, 1964; Thier

    and Bergner, 1966), or ethanol (Fischer, 1968). Very good recoveries
    were obtained by Soxhlet extraction with chloroform-methanol (9:1 v/v)
    (Bowman and Beroza, 1969). For milk, a combination of polar and
    nonpolar extractants is required, e.g. acetone-methylene chloride
    (Bowman and Beroza, 1969), ethanol-hexane (Franz and Kovac, 1965).
    Extraction with methanol-acetonitrile also proved suitable for milk
    samples (Miyamoto et al., 1967). For oil-containing harvest products
    with a low water content, use is made of benzene (Dawson et al., 1964;
    Horler, 1966), petroleum ether (Kovac and Sohler, 1965), hexane
    (Horler, 1966), or chloroform (Yuen, 1966). On account of the
    favourable partition coefficients (Bowman and Beroza, 1965; Kovac,
    1963), fats and waxes are best removed by partitioning between hexane
    and acetonitrile (Franz and Kovac, 1965; Miyamoto et al., 1967;
    Möllhoff, 1967; Bowman and Beroza, 1969).

    Qualitative analysis

    Although no reports of fenitrothion being separated from similar
    residues by column chromatography have been noted, separation is
    possible with thin-layer or gas chromatography. Interfering active
    ingredients are parathion, parathion-methyl, malathion, and fenthion
    and the resolution is just sufficient for distinguishing fenitrothion
    from these active ingredients (see e.g. Möllhoff, 1968). By comparing
    gas chromatograms recorded with a phosphorus detector and an electron
    capture detector, fenitrothion can often be clearly differentiated
    from malathion and fenthion owing to differences in sensitivity.


    Colorimetric determinations are carried out by the method of Averell
    and Norris (1948) or by determination of the cresol after
    saponification of the active ingredient with alkali. The limits of
    determination are about 0.05 ppm.

    Thin-layer chromatography

    Thin-layer chromatography has been used for clean-up of the extracts
    with final determination by colorimetry after deleting the appropriate
    spot from the plate, or for direct determination on the plate after
    spraying. Quantitative evaluation is possible in the first instance;
    in the second, the evaluation is semiquantitative and more suitable
    for confirming identity. About 0.1 ppm of fenitrothion can be
    determined in most harvested products. Determination of lesser amounts
    is possible with procedures utilizing cholinesterase inhibition
    (Ackermann, 1966; Mendoza et al., 1968; Schutzmann and Barthel, 1969;
    Winterlin et al., 1968).

    Column chromatography

    For extract cleanup or separation of metabolites, columns are
    suitable, especially those packed with deactivated silica gel (Bowman
    and Beroza, 1969), deactivated Florisil (Möllhoff, 1967, 1968), or
    deactivated acid aluminum oxide (Horler, 1966). Columns packed with

    active Florisil (Beckman and Garber, 1969), magnesium oxide (Coffin
    and Savary, 1964), polyethylene-impregnated aluminum oxide (Coffin and
    Savary, 1964), and Sephadex LH-20 (Horler, 1968; Ruzicka, et al.,
    1968) have also been used.

    Gas chromatography

    The most reliable and highly sensitive methods for fenitrothion
    utilize gas chromatography with either the flame-photometric (Bowman
    and Beroza, 1969) or the thermionic detector (Miyamoto et al., 1967,
    Sato et al., 1968). These detectors respond to the phosphorus in the
    molecule with very high specificity. No cleanup is usually required
    with the flame-photometric detector when analysing for either
    fenitrothion or its oxygen analogue unless a fatty food is being
    analysed. In this case a simple hexane-acetonitrile partition is used.
    A cleanup was used with the thermionic detector but it may often be
    omitted. Limit of determination is usually 0.01-0.001 ppm.

    In the analysis for fenitrooxon a separation from fenitrothion on
    silica gel is used. The compound is then determined by gas
    chromatography (Bowman and Beroza, 1969) or enzymatically (Miyamoto et
    al., 1967). The cresol is determined by electron-capture gas
    chromatography (Bowman and Beroza, 1969) or colorimetrically (Miyamoto
    et al., 1967) after column separation. Analysis of fenitrothion,
    fenitrooxon, and the cresol by electron-capture gas chromatography is
    possible (Bowman and Beroza, 1969; Dawson et al., 1964; Horler, 1966;
    Möllhoff, 1967) but less specific; sensitivity, about 0.1 ppm, can be
    improved with a suitable cleanup.

    Determination of metabolites

    Gas chromatographic methods have been described for the simultaneous
    determination of fenitrothion, fenitrooxon (Bowman and Beroza, 1969;
    Möllhoff, 1968), 3-methyl-4-nitro phenol (Bowman and Beroza, 1969;
    Miyamoto et al., 1967) and the amino compound of fenitrothion
    (Miyamoto et al., 1967). As noted, for market controls determination
    of fenitrothion is generally sufficient (Möllhoff, 1968).

                                                                  Tolerance       Withholding
    Country                      Crop                               (ppm)        period (days)

    Austria                                                       2.0 proposed

    Belgium           Top fruits and vegetables                   0.5            14

    China,            Rice                                        -              21
    Republic of       Vegetables                                  -              10

    Denmark           Beets, apples, peas, clover                 -              15

                                                                  Tolerance       Withholding
    Country                      Crop                               (ppm)        period (days)
    East Africa       Mango, cereals                              -              7

    Germany,          Field crops, vegetables, fruits, and        -              10
    Eastern           special crops
                      Crops for Infant food and remedies          -              21

    Germany           Vegetables, root and field crops,           0.4            10
    (Fed. Rep.)       legumes, fruits, grapes

    Finland                                                       -              21

    France            Vegetables, fruits                          -              15

    Italy                                                         -              15

    Netherlands       Cereals, fruits                             0.5            21

    New Zealand                                                   -              14 (7 for

    Poland            Top fruits (except strawberries and         -              14

    Portugal          Vegetables, citrus, fruits, cocoa, coffee   -              21
                      Pasture grass                               -              10

    Spain             Vegetables, citrus, fruits                  -              15-21

    Sweden            Peas, rape, wheat, barley                   -              10

    Switzerland       Top fruits                                  0.2 in

    Fenitrothion is a broad spectrum insecticide with a much lower acute
    mammalian toxicity than many similar insecticides. It is not covered
    by patents and is produced by at least six companies. Use of
    fenitrothion is almost worldwide (excluding the U.S.A.) for such crops
    as rice, fruits, vegetables, cotton, cereals, soybeans, coffee and
    tea. Application rates are 0.5-2.0 kg a.i./ha. Waiting intervals are
    generally 10-21 days. It is used against spruce budworm (in forests),
    insects attacking man, and in some countries to protect stored
    products. Its use on pasture land (375 g/ha) results in almost no
    residues of fenitrothion in milk or meat (<0.01 ppm). The insecticide

    is available as a 95% concentrate, 50% emulsifiable concentrate, 40%
    wettable powder, 2.5 and 5% dusts. Composition of technical materials
    is not known and is apt to vary depending on manufacturer. Residue
    data are available mostly from Europe and Japan.

    Although several metabolites of fenitrothion are known to form
    (fenitrooxon, desmethyl fenitrothion, aminofenitrothion, and
    3-methyl-4-nitrophenol), they do not accumulate in significant amounts
    or they appear to be comparatively non-toxic. Unless experimental
    trials indicate otherwise, fenitrothion appears to be the only toxic
    residue to be determined in products in commerce.

    Many methods are available for residue analysis of fenitrothion. The
    best of these utilize gas chromatography with the flame photometric or
    thermionic detector. Some of these methods may also be used for
    analysis of metabolites. Sensitivity is usually better than 0.01 ppm.
    Evaluation of these procedures for regulatory purposes is suggested.
    Few data on residues in food in commerce or in diets have been


    TEMPORARY TOLERANCES (effective to June 1973)

    Apples, cherries, grapes, lettuce   0.5 ppm  )  Preharvest interval to 
                                                 )  be such that these
    Tomatoes                            0.2 ppm  )  tolerances are not
                                                 )   exceeded)

    Red cabbage, green tea              0.3 ppm

    Cocoa                               0.1 ppm

    The 3-methyl-4-nitrophenol is not included in the recommendations at
    this time but the Joint Meeting should review this aspect in due


    Milk (whole)                        0.002

    Meat or fat                         0.03


    REQUIRED (before 30 June 1973)

    1. Reproduction and teratogenicity studies in animals preferably in
       non-human primates.

    2. Adequate long-term studies in rodent and non-rodent mammalian

    3. Data on residue levels in raw agricultural commodities moving in
       commerce and in total diet studies.

    4. Data on disappearance of residues during storage, processing and

    5. Data on rate of residue decline in rice and pre-harvest interval.

    6. Before use as a grain protectant, data on persistence of residues
       in storage of the grains concerned and definitive data on residues 
       in bread are needed.

    7. Data on occurrence of 4-nitro-3-methylphenol residues and their
       significance toxicologically.

    8. Information on ingredients in technical products produced by
       several manufacturers.


    1. Observations in man.

    2. Evaluation of gas chromatographic methods for regulatory purposes.


    Ackermann, H. (1966) Enzymatischer Nachweis phosphororganischer 
    Insektizide nach dünnschicht-chromatographischer Trennung. Nahrung,

    Averell, P.R. and Norris, M.V. (1948) Estimation of small amounts of
    O,O-diethyl-O,p-nitro-phenyl thiophosphate. Anal. Chem. 20:753-6

    Bayer (1969) (Farbenfabriken Bayer AG.). Fenitrothion. Unpub. Rept.

    Beckman, H. and Garber, D. (1969) Recovery of 65 organophosphorus 
    pesticides from Florisil with a new solvent elution system. J. Ass.
    Offic. Anal. Chem. 52:286-93

    Bowman, M.C. and Beroza, M. (1965) Extraction p-values of
    pesticides and related compounds in six binary solvent systems.
    J. Ass. Offic. Agr. Chem. 48:943-52

    Bowman, M.C. and Beroza, M. (1969) Determination of Accothion, its
    oxygen analog, and its cresol in corn, grass and milk by gas
    chromatography. J. Agr. Food Chem. 17:271-6

    Bowman, M.C. (1969) Private communication

    Braid, P.E. and Nix, M. (1968) Potentiation of toxicity of Sumithion
    by phosphamidon in the rat. Canad. J. Physiol. Pharmacol. 46:145-9

    Carshalton (1962) WHO insecticide evaluation and testing programme
    - stage I. Mammalian toxicity report OMS 43=S5660, Test for neurotoxic
    effects in hens. Unpub. Rept. from the Toxicology Research Unit,
    Charshalton. Submitted by Farbenfabriken Bayer AG.

    Carshalton. (1964) OMS 43. Summary. OMS 43. Mammalian toxicity.
    Unpub. Rept. of the Toxicology Research Unit, Carshalton. Submitted
    by Farbenfabriken Bayer AG.

    Coffin, D.E. and Savary, G. (1964) Procedure for extraction and
    cleanup of plant material prior to determination of organophosphate
    residues. J. Ass. Offic. Agr. Chem. 47:875-81

    Cooper. (1966) Toxicity of Sumithion. Unpub. Rept. of the Cooper
    Technical Bureau. Submitted by Sumitomo Chemical Co., Ltd. Osaka

    Cooper. (1968) Technical Bureau. Sumithion as a grain protectant.
    Technical report by William Cooper and Nephews, Australia. Cited by
    Sumitomo, 1969

    Dawson, J.A., Donegan, L. and Thain, E.M. (1964) The determination of
    parathion and related insecticides by gas-liquid chromatography
    with special reference to fenitrothion residues in cocoa.
    Analyst, 89:495-6

    Douch, P.G.C., Hook, C.E.R. and Smith, J.N. (1968) Metabolism of
    Folithion (dimethyl-4-nitro-3-methylphenyl phosphorothionate).
    Australasian J. Pharm., 49: No.584. Suppl. Nr.66, 2.S.

    DuBois, K.P. and Puchala, E. (1960) The acute toxicity and
    anticholinesterase action of Bayer 41831. Unpub. Rept. from the
    Department of Pharmacology, University or Chicago. Submitted by
    Farbenfabriken Bayer AG.

    DuBois, K.P. and Kinoshita, F. (1963) The acute toxicity of Bayer
    41831 in combination with other anticholinesterase insecticides.
    Unpub. Rept. from the Department of Pharmacology, University of
    Chicago. Submitted by Farbenfabriken Bayer AG.

    Fischer, R. (1968) Nachweis und quantitative Bestimmung von
    Phosphor-Insektiziden in biologischem Material. III. Arch.
    Toxicol., 23:129-35

    Franz, J. and Kovac, J. (1965) Bestimmung toxischer Rückstände von
    O,O-Dimethyl-O-(3-methyl-4-nitrophenyl)-thiophosphat in Milch. Z.
    Anal. Chem. 210:354-8

    Frehse, H. and Möllhoff, E. (1969) Organophosphorus insecticide 
    residue analysis. Evaluation. (A) Metabolic products. In report of
    IUPAC Commission on the development, improvement, and standardization
    of methods of pesticide residue analysis. Egan, H. J. Ass. Offic.
    Anal. Chem. 52:306-9

    Gaines, T.B. (1969) Acute toxicity of pesticides. Toxicol. appl.
    Pharmacol., 14:515-34

    Green, A.A. and Tyler, P.S. (1966) A field comparison of malathion,
    dichlorvos and fenitrothion for the control of Oryzaephilus
    surinamensis (L) infesting stored barley. J. Stored Prod. Res.

    Hais, K. and Franz, J. (1965) On the problem of Metathione residues
    in milk after disinfestation. Cesk. Hyg. 10.205-8

    Hladká, A. and Nosál, M. (1967) The determination of the exposition
    to Metathion fenitrothion) on the basis of excreting its metabolite
    p-nitro-m-cresol through urine in rats. Internat. Arch.
    Gewerbepath. Gewerbehyg. 23:209-14

    Hollingworth, R.M., Fukuto, T.R. and Metcalf, R.L. (1967) Selectivity 
    of Sumithion Compared with Methyl Parathion. Influence of structure
    on anticholinesterase activity. Metabolism in the white mouse. J.
    Agric. Food Chem., 15:235-49

    Horler, D.F. (1966) Determination of fenitrothion on stored barley. J. Stored
    Prod. Res. 1:287-90

    Horler, D.F. (1968) Gel filtration on Sephadex LH-20. A general
    clean-up method for pesticides extracted from grain. J. Sci. Food Agr.

    Kane, J. and Green, A.A. (1968) The protection of bagged grain from 
    insect infestation using fenitrothion. J. Stored Prod. Res. 4 59.

    Kimmerle, G. (1962a) Toxikologische Untersuchungen mit dem Wirkstoff
    S 5660. Unpub. Rept. from Toxilkolisches und Gewerbehygienisches
    Laboratorium. Submitted by Farbenfabriken Bayer AG.

    Kimmerle, G. (1962b) S 5660. Unpub. Rept. on the neurotoxic effect
    on hens from Toxikologisches und Gewerbehygienisches Laboratorium.
    Submitted by Farbenfabriken Bayer AG.

    Klimmer, O.R. (1961) Opinion on the toxicity of the compound "S 5660"
    of Farbenfabriken Bayer AG., Leverkusen. Unpub. Rept. from
    Pharmakologisches Institut der Rheinischen
    Friedrich-Wilhelms-Universität, Bonn. Submitted by Farbenfabriken
    Bayer AG.

    Kovac, J. (1963) Bestimmung von
    O,O-Dimethyl-O-(3-methyl-4-nitrophenyl)-thiophosphat in technischen
    Produkten nach vorhergehender Abtrennung der Begleitstoffe mittels
    Dünnschichtchromatographie. J. Chromatogr. 11:412-3

    Kovac, J. and Sohler, E. (1965) Bestimmung von
    in Obst und Gemüse nach vorangegangener Abtrennung der mitextrahierten
    Farbstoffe durch Dünnschichtchromatographie. Z. Anal. Chem. 208.201-4

    Mendoza, C.E., Wales, P.J., McLeod, H.A. and McKinley, W.P. (1968)
    Thin-layer chromatographic-enzyme inhibition procedure to screen for
    organophosphorus pesticides in plant extracts without elaborate
    clean-up. Analyst 93:173-7

    Misu, Y., Segawa, T., Kuruma, I., Kojima, M. and Takagi, H. (1966)
    Subacute toxicity of O,O-dimethyl-O-(3-methyl-4-nitrophenyl)
    phosphorothioate (Sumithion) in the rat. Toxicol. appl.
    Pharmacol., 9:17-26

    Miyamoto, J., Sato, Y., Kadota, T., Fujinami, A. and Endo, M. (1963a)
    Studies on the mode of action of organophosphorus compounds. Part I.
    Metabolic Fate of p32 labeled Sumithion and Methylparathion
    in guinea-pig and white rat. Agric. Biol. Chem. (Tokyo), 27:381-9
    Miyamoto, J., Sato, Y., Kadota, T. and Fujinami, A. (1963b) Studies
    on the mode of action of organophosphorus compounds. Part II.
    Inhibition of mammalian cholinesterase in vivo following the
    administration of Sumithion and Methylparathion. Agric.
    Biol. Chem. (Tokyo), 27:669-76

    Miyamoto, J. (1964a) Studies on the mode of action of organophosphorus
    compounds. Part III. Activation and degradation of Sumithion
    and Methylparathion in vivo. Agric. Biol. Chem. (Tokyo),

    Miyamoto, J. (1964b) Studies on the mode of action of organophosphorus
    compounds. Part IV. Penetration of Sumithion, Methylparathion and
    their oxygen analogs into guinea pig brain and inhibition of
    cholinesterase in vivo. Agric. Biol. Chem. Tokyo), 28:422-30

    Miyamoto, J. and Sato, Y. (1965) Determination of insecticide residue
    in animal and plant tissues. II. Metabolic fate of Sumithion in rice
    plant applied at the preheading stage and its residue in harvested
    grains. Botyu-Kagaku, 30:45-9

    Miyamoto, J., Kawaguchi, Y. and Sato, Y. (1965a) Determination of
    insecticide residue in animal and plant tissues. I. Determination of
    Sumithion residues in bananas grown in Formosa. Botyu-Kagaku, 30:9-12

    Miyamoto, J., Sato, Y. and Fujikawa, K. (1965b) Determination of 
    insecticide residue in animal and plant tissues. III. Determination 
    of residual amount of Sumithion in cocoa beans grown in
    Nigeria. Botyu-Kagaku 30:49-51

    Miyamoto, J., Kitagawa, K. and Sato, Y. (1966) Metabolism of
    organophosphorus insecticides by Bacillus subtilis, with
    special emphasis on Sumithion. Jap. J. Exp. Med. 36:211-25

    Miyamoto, J., Sato, Y. and Suzuki, S. (1967) Determination of
    insecticide residue in animal and plant tissues. IV. Determination
    of residual amount of Sumithion and some of its metabolites in fresh
    milk. Botyu-Kagaku. 32:95-100

    Miyamoto, J. (1969) Mechanism of low toxicity of Sumithion toward
    mammals. Residue Reviews, 25:251-64

    Miyamoto, J. and Sato, Y. (1969) Determination of insecticide residue
    in animal and plant tissues. VI. Determination of Sumithion residue
    in cattle tissues. Botyu Kagaku 34:3-6

    Möllhoff, E. (1967) Gas chromatographic determination of residues of
    E605 products and Agritox in plants and soil samples.
    Pflanzenschutz-Nachrichten Bayer 20:557-74

    Möllhoff, E. (1968) Beitrag zur Frage der Rückstände und ihrer
    Bestimmung in Pflanzen nach Anwendung von Präparaten der E 605 - und
    Agritox - Reihe. Pflanzenschutz-Nachrichten Bayer 21:331-58

    Muramoto, N. (1967) Unpub. observations, cited by Sumitomo, 1969
    Nishizawa, Y., Fujii, K., Kadota, T., Miyamoto, J. and Sakamoto, H.
    (1961) Studies on the organophosphorus insecticides. Part VII.
    Chemical and biological properties of new low toxic organophosphorus
    insecticide. O,o-Dimethyl-O-(3-methyl-4-nitrophenyl) phosphorothioate.
    Agric. Biol. Chem. (Japan), 25:605-10
    Nosäl, M. and Hladkä, A. (1968) Determination of the exposure to
    fenitrothion [O,O-dimethyl-O-(3-methyl-4-nitrophenyl) thiophosphate]
    on the basis of the excretion of p-nitro-m-cresol by the urine
    of the persons tested. Internat. Arch. Gewerbepath. Gewerbehyg.

    Republic of Argentina (1968) - Unpub. Rept. prepared for Codex
    Committee on Pesticide Residues

    Ruzicka, J.H., Thomson, J., Wheals, B.B. and Wood, N.F. (1968) The
    application of gel chromatography to the separation of
    pesticides. I. Organophosphorus pesticides. J. Chromatogr.

    Sato, Y., Miyamoto, J., and Suzuki, S. (1968) Determination of
    insecticide residue in animal and plant tissues. V. A device to
    increase the sensitivity of the gas chromatography detector to
    organophosphorus insecticides. Bochu Kagaku 33:8-12

    Schutzmann, R.L. and Barthel, W.F. (1969) Indoxyl acetate spray
    reagent for fluorogenic detection of cholinesterase inhibitors in
    environmental samples. J. Ass. Offic. Anal. Chem. 52:151-6

    Sumitomo Chemical Company. (1969) Sumithion, Its toxicity, metabolism
    and residues. Unpub. Rept.

    Thier, H.P. and Bergner, K.G. (1966) Eine Schnellmethode zum Nachweis
    wichtiger Schädlings-bekämpfungsmittel in Ost und Gemüse. Deutsche 
    Lebensmittel-Rundschau 62:399-402

    Tomizawa, C. and Kobayashi, A. (1964) Relation between the behaviour 
    of parathion and Sumithion in cabbage leaves and their
    phytotoxicity. Noyaku Seisan Gijutsu 11:30-32; Chem. Abstr. 62,
    1387d (1965)

    Ueda, K. and Nishimura, M. (1966) Interim report. Chronic toxicity of
    Sumithion: two-year feeding study in rats. Unpub. Rept. from the
    Department of Hygiene and Toxicology, Tokyo Dental College.
    Submitted by Sumitomo Chemical Co., Ltd., Osaka.

    Vandanis, A. and Crawford, L.G. (1964) Comparative metabolism of O,
    O-dimethyl-O-p-nitrophenyl phosphorothioate (Methylparathion and
    O, O-dimethyl-O-(3-methyl-1-nitrophenyl) phosphorothioate
    (Sumithion) J. Econ. Entomol. 57:136-9

    Vandekar, M. (1965) Observations on the toxicity of carbaryl,
    Folithion and 3-isopropropyl-phenyl N-methylcarbamate in a
    village-scale trial in Southern Nigeria. Bull. Wld. Hlth Org.

    Wilford, K., Lietaert, P.E.A. and Foll, C.V. (1965) Toxicological
    observations during large scale field trial of OMS-43 in Northern
    Nigeria (preliminary report). WHO working paper 65/TOX/1 prepared
    for an informal meeting on toxicology of insecticides. Geneva,
    18-24 February 1965

    Winterlin, W., Walker, G. and Frank, H. (1968) Detection of
    cholinesterase-inhibiting pesticides following separation on
    thin-layer chromatograms. J. Agr. Food Chem. 16:808-12

    Yasuno, M., Hirakoshi, S. Sasa, M. and Uchida, M. (1965) Inactivation
    of some organophosphorus insecticides by bacteria in polluted water.
    Jap. J. Exp. Med. 35:545

    Yuen, S.H. (1966) Absorptiometric determination of fenitrothion 
    residues in cocoa beans. Analyst 91:811-3

    See Also:
       Toxicological Abbreviations
       Fenitrothion (EHC 133, 1992)
       Fenitrothion (HSG 65, 1991)
       Fenitrothion (ICSC)
       Fenitrothion (WHO Pesticide Residues Series 4)
       Fenitrothion (Pesticide residues in food: 1976 evaluations)
       Fenitrothion (Pesticide residues in food: 1977 evaluations)
       Fenitrothion (Pesticide residues in food: 1979 evaluations)
       Fenitrothion (Pesticide residues in food: 1982 evaluations)
       Fenitrothion (Pesticide residues in food: 1983 evaluations)
       Fenitrothion (Pesticide residues in food: 1984 evaluations)
       Fenitrothion (Pesticide residues in food: 1986 evaluations Part II Toxicology)
       Fenitrothion (Pesticide residues in food: 1988 evaluations Part II Toxicology)
       Fenitrothion (JMPR Evaluations 2000 Part II Toxicological)