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    METHAMIDOPHOS

    EXPLANATION 

    First draft prepared by Dr E.M. den Tonkelaar,
    National Institute of Public Health and Environmental Protection, 
    Bilthoven, The Netherlands

         Methamidophos toxicity was evaluated by the JMPR in 1976, 1982
    and 1985 (Annex 1, FAO/WHO 1977ab, 1983ab and 1986ac).  In 1985 the
    Meeting allocated an ADI of 0-0.0006 mg/kg bw, based on a complete
    data package which replaced invalid IBT (Industrial Biotest) data. 
    Because methamidophos is a metabolite of acephate, for which an ADI
    had been established based on a study in humans, it was decided to re-
    evaluate methamidophos.  This study was considered at the present
    Meeting as well as new data on in vitro cholinesterase inhibition
    and on delayed neuropathy.

    EVALUATION FOR ACCEPTABLE DAILY INTAKE 

    BIOLOGICAL DATA 

    Biochemical aspects 

    Effect on cholinesterase activity 

         The cholinesterase inhibition of methamidophos, acephate and
    paraoxon (a known strong anticholinesterase) were determined on human
    erythrocytes and on brain samples of rats, mice and rainbow trout in
    an in vitro experiment. In all cases, except trout brain
    cholinesterase, acephate and methamidophos were found to be six and
    three orders of magnitude weaker than paraoxon, respectively (see
    Table 1) (Hussain et al., 1985). 

        Table 1.  Concentrations of acephate, methamidophos and paraoxon required
              to inhibit 50% of the activity (I50) of cholinesterases from human
              erythrocyte, rat, mouse and trout brain in vitro.

                                                                             
    Chemical         Human           Rat brain      Mouse brain    Trout brain
                     erythrocyte
                                                                             

    Acephate 
    (x 10-2M)        1.9  0.1       0.7  0.008    6.0  2.0      2.8  0.3

    Methamidophos
    (x 10-5M)        2.3  0.3       2.0  0.2      2.0  0.2      5.6  0.9

    Paraoxon
    (x 10-8M)        3.3  0.5       2.3  0.3      5.0  0.8      2200  100
                                                                             
    
         Sprague-Dawley rats (5/sex/group) received single topical
    applications of analytical grade methamidophos (purity 99.1%) and
    methamidophos technical (purity 74.7%) at dose levels of 0, 1.0, 2.5,
    6.25 or 15.6 mg a.i./rat on a shaved dorsal area ranging from 6.6% to
    8.7% of the total body surface area.  The rats were sacrificed 24 or
    72 hours following application of the test material.  Animals were
    observed daily for toxic signs and mortality; body weight was measured
    prior to dosing and at sacrifice on day 1 or day 3.  Gross pathology
    and histopathology were performed at sacrifice and plasma, RBC and
    brain ChE activities were determined. 

         Three-fifths and 2/5 of female rats died during the 24 hour
    exposure to methamidophos analytical grade and methamidophos technical
    in the 15.6 a.i./rat dose groups, respectively.  After 72-hour

    exposure to methamidophos technical 1/5 females in the high dose group
    died.  No clinical signs of toxicity were observed at the lowest dose
    group (1.0 mg a.i./rat).  No compound related gross pathological
    changes were noted at necropsy and no histopathological changes in the
    skin were found.  Dose-dependent significant cholinesterase inhibition
    was observed in both males and females following treatment with both
    test materials.  For calculation of the dose the amount of active
    ingredient was determined per cm2 total body surface area.  ID50
    values were determined to compare the relative sensitivities of each
    tissue to cholinesterase inhibition.  The lowest ID50 values were
    observed in each tissue after 24 hours for both males and females. 
    RBC and plasma ChE were inhibited to a greater extent by the test
    materials than brain ChE (see Table 2).  No consistent difference in
    cholinesterase inhibition was observed to be produced by either
    methamidophos technical or analytical grade (Easter and Rosenberg,
    1987). 

    Table 2.  ID50 (g a.i./cm2 total body surface area) 24 hrs. 
              after administration. 

                                                                       
               Test material        RBC ChE    Brain ChE   Plasma ChE
                                                                       

    males      methamidophos
               (analytical grade)      6.98        23.40         9.51

               methamidophos
               (technical)            10.00        18.55         5.85

    females    methamidophos
               (analytical grade)      4.94        14.04         1.61

               methamidophos
               (technical)             5.41         8.33         0.57
                                                                       

    Special study on pharmacokinetics 

         Male Wistar rats were given atropine sulfate (100 mg/kg i.p.) 10
    to 15 minutes prior to i.v. dosing with 10 mg/kg methamidophos (purity
    74%) in propylene glycol.  At various time intervals after dosing
    blood was taken and methamidophos values in plasma were analysed. 
    Pharmacokinetic values were calculated using a one compartment model:
    t1/2 = 1.5 hr; Vd(volume of distribution)=0.81 L/kg; C1(clearance)=
    5.8 mL/min/kg;  kel(elimination constant)=0.45 hr-1.  The volume of
    distribution of 0.81 L/kg indicates that methamidophos is not highly
    tissue bound (Eigenberg et al., 1983). 

    Toxicological studies 

    Acute toxicity studies

    The acute toxicity of methamidophos is presented in Table 3. 

    Short-term studies 

         In a range finding study, groups of Wistar rats (10/sex/group)
    were exposed to aerosols containing methamidophos (purity 75.7%) at
    mean concentrations of 0 (vehicle=polyethylene glycol/ethanol), 1.4,
    5.4 or 33.1 mg/m3 6 hours per day for 5 days.  

         The only effects observed were cholinergic signs and a
    significant depression of cholinesterase activity in plasma and brain
    as well as a reduced male body weight gain on day 5 occuring at 33.1
    mg/m3 only.  The NOAEL in this study was 5.4 mg/m3 (Pauluhn, 1987a).


         Groups of Wistar rats (10/sex/group) were exposed to aerosols
    containing methamidophos (purity 73%) at mean concentrations of 0
    (air), 0 (vehicle=polyethylene glycol/ethanol), 2.6, 12.0 or 48.4
    mg/m3 6 hours per day, 5 days per week over a period of 3 weeks
    (head/nose exposure).  Cholinergic symptoms were observed at 48.4
    mg/m3. Body weight was slightly reduced in high dosed rats.  Reduced
    ALAT, urea and creatinine values were observed at 48.4 mg/m3. 
    Cholinesterase activities were significantly depressed in plasma
    (35-88%), erythrocytes (20-25%) and in brain (20-74%) at 12.0 and 48.4
    mg/m3.  In the urine, acidification was observed at 48.4 mg/m3. 
    Relative adrenal weight was increased and relative thymus, liver and
    spleen weight were decreased in high dose male rats. There were no
    signs of specific organ damage or local damage to the respiratory
    tract. The NOAEL in this study was 2.6 mg/m3 (Pauluhn, 1987b). 

         Groups of Wistar rats (10/sex/group) were exposed to 0 (air), 0
    (vehicle=polyethylene glycol/ethanol), 1.1, 5.4 or 23.1 mg
    methamidophos (purity 73.4%)/m3 6 hours per day, 5 days a week for 3
    months.  Two additional satellite groups (10/sex/group), of which one
    was exposed to the vehicle aerosol and the other to 23.1 mg
    methamidophos/m3, served as recovery groups with a 6-week exposure-
    free recovery period.  Observations included clinical signs, body
    weight, haematology, biochemistry, urinalysis, cholinesterase
    inhibition in plasma, erythrocytes and brain, lung function tests,
    acetylcholine (ACH) provocation test, ophthalmoscopy, gross pathology,
    organ weights and histopathology. 


        Table 3.  Acute toxicity of methamidophos in animals.

                                                                                                      
    Species   Sex       Route     LD50           LC50       Purity        Reference
                                  (mg/kg b.w.)   (mg/m3)
                                                                                                      

    Rat       M**       oral      161                       95.3%         Flucke, 1990a
                                  142                       98.5%
                                  163                       97.8%

              M, F      Inhal.                   213        75.7%         Pauluhn, 1987a
                        (4 hr)

    Hen       F         oral      48                        72.5%         Pauluhn and Kaliner, 1984
                                  180*

                        oral      251#                      95.3%         Flucke, 1990b
                                  432#                      98.5%
                                  823#                      96.5%

                        dermal    50                        74%           Flucke, 1985

    Turkey    F         Oral      15*                       72.5%         Pauluhn and Kaliner, 1984
    Hen

                                                                                                      

    1  test compound: ()-methamidophos
    2  test compound: (+)-methamidophos
    3  test compound: (-)-methamidophos
    *  50 mg atropine sulphate/kg b.w. was administered i.m. 5 min. before the test
       compound. 
    ** unfasted rats
    #  The enantiomers also differed in that the symptoms and recovery period lasted
       longer, and mortalities occurred later with (-)-methamidophos that in the case
       of (+)-methamidophos.
    

         Cholinergic symptoms were observed at 23.1 mg/m3.  In the same
    dose group body weight as well as food consumption were significantly
    reduced in both male and female rats.  Ophthalmoscopy, haematology and
    urinalysis  were unremarkable.  At 23.1 mg/m3 ASAT and LDH
    concentrations were significantly increased in males.  Protein,
    cholesterol and glucose were significantly decreased in both high dose
    male and female rats.  Creatinine was significantly decreased at 5.4
    and 23.1 mg/m3 in both sexes.  Significant cholinesterase inhibition
    (>30%) was observed in plasma and brain in rats at 5.4 and 23.1
    mg/m3.  Liver N-demethylase was significantly decreased in rats at
    the highest dose level.  The lung function tests performed at the end
    of the exposure period gave no indications of functional lung damage. 
    In an acetylcholine provocation test, basal lung function parameters
    were not changed but an increased reactivity of the bronchial
    musculature to an acetylcholine aerosol was observed at dose levels of
    5.4 mg/m3 and higher.  In rats at 23.1 mg/m3, absolute and
    relative spleen weight were significantly decreased, and relative
    brain, and absolute and relative adrenal weight were increased, at the
    same dose level.  At gross pathology and histopathology no evidence of
    treatment related organ damage or of local damage to the respiratory
    tract was observed.  A dose related increase in reticulum cells and an
    increase in neutrophilic myelocytes in both male and female rats were
    observed at 5.4 and 23.1 mg/m3 at the bone marrow morphological
    examinations.  At the end of the recovery period, changes in
    biochemical parameters and cholinesterase returned to normal.  The
    NOAEL in this study is 1.1 mg methamidophos/m3  (Pauluhn, 1988).

    Special studies on delayed neurotoxicity 

    Chickens 

         Acute neurotoxicity was studied in 30 adult Leghorn hens after
    the simultaneous oral administration of 75 mg methamidophos and 400 mg
    trimethylphosphate (TMPO)/kg bw, followed after 21 days by 50 mg
    methamidophos and 264 mg trimethylphosphate/kg bw (both under atropine
    protection).  Two independent positive control groups of 5 hens were
    administered 375 mg triorthocresylphosphate (TOCP)/kg bw once.  The
    negative control group received the solvents (water and polyethylene
    glycol/ethanol for TMPO) under atropine protection twice at an
    interval of 21 days.  After the first administration of the
    combination 15/30 hens died.  No mortalities were observed after the
    second administration.  From the 27th post-observation day onwards,
    7/15 surviving hens exhibited an incipient uncoordinated gait, but
    progression was not observed.  Delayed paralysis was not observed and
    after morphological examination of the nerve tissues no indication for
    induced neuropathy was provided.  All hens in the positive control
    group showed delayed paralysis and morphological nerve damage (Pauluhn
    and Kaliner, 1984).

     
         Groups of 3 hens received single oral doses of 0 (corn oil), 27.5
    or 55 mg/kg bw methamidophos EC 63.3%.  After 24 hours blood samples
    were taken and the birds were killed and then brain, blood, liver,
    heart, spleen and kidney tissues were collected for enzyme assays.  No
    effects were observed on the activity of glutathione-S-transferase
    (GST) and brain neurotoxic esterase (NTE).  Blood and heart
    cholinesterase were inhibited, but acid phosphatase (AP) was increased
    in brain, blood and liver tissues of the treated hens. 

         Another group of 10 hens received daily doses of 5.5 mg/kg
    methamidophos EC 63.3% for 60 days, under atropine protection with an
    observation period of 72 days.  A control group received corn oil for
    60 days.  The hens were observed for any abnormalities in the ability
    to walk or any clinical delayed neuropathic symptoms. Treated hens had
    signs of cholinergic toxicity, especially in the first week of
    treatment.  Two and 3 hens died after 5 and 11 doses, respectively. 
    None of the surviving 5 hens showed signs of leg weakness or ataxia
    throughout 60 days of the experiment or after 72 days (El-Sebae
    et al., 1987). 

         The effect on neurotoxic esterase (NTE) was studied after dermal
    application of 200 mg methamidophos (73.0%)/kg b.w. to 9 Leghorn
    chickens under atropine protection.  This dose represented 4 x the
    LD50 without atropine protection.  A positive control group and a
    negative control group (9/group) received 100 mg TOCP/kg b.w. orally
    and 5 ml Cremophor EL (2% v/v)/kg b.w. in demineralized water,
    respectively.  NTE activity in the nerve tissue (brain and spinal
    cord) was determined after 24 and 48 hours and seven days post-
    application in 3 chickens/group. 

         A mean inhibition of approximately 60% occurred in the brain
    after 24 and 48 hours and approximately 46% in the spinal cord after
    24 hours.  An inhibition of over 80% in all cases in both nerve
    tissues was observed in the positive controls at these times. 
    According to the authors an inhibition of 70-80% within 1-40 hours
    after administration is necessary for induction of delayed neuropathy.
    This threshold value was not reached after a dose of methamidophos
    which was about 4 x the LD50 for dermal exposure (Flucke and Eben,
    1988). 

         The effect on NTE in the nervous tissues and lymphocytes of hens
    was also studied after the oral administration of 50 mg/kg b.w.
    racemic methamidophos (purity 95.5%) and the enantiomers (+)- and (-)-
    methamidophos (dose levels: 50, 100 or 400 mg/kg b.w. and 50, 200 or
    400 mg/kg b.w., respectively) under atropine protection.  The highest
    doses of the (+) and (-) enantiomers were about 10 and 5 times the
    LD50 respectively.  NTE activity in brain, spinal cord, sciatic nerve
    and lymphocytes was determined 24 and 48 hours and 7 days after
    administration.

         About 60-85% inhibition occurred in the brain and spinal cord
    after administration of racemic methamidophos, which could be
    reactivated.  (+)- Methamidophos showed greater inhibition (up to 100%
    in brain at 400 mg/kg b.w.) but nearly complete reactivation (>80%)
    of the inhibited NTE occurred, whereas at 400 mg/kg bw (-)-
    methamidophos up to 58 and 84% inhibition in brain after 24 and 48
    hours, respectively, was observed, of which only a small fraction
    could be reactivated.  Irreversible NTE inhibition levels of nearly
    90% to almost 100% were observed with TOCP, which was used as a
    positive control, at oral doses of 100 and 300 mg/kg b.w. (Flucke and
    Eben, 1990).

         Two hundred mg/kg b.w. methamidophos (purity 74%) was dermally
    applied twice at an interval of three weeks to 30 chickens under
    atropine protection.  A control group of 6 animals and a positive TOCP
    group of 5 animals were also used.  Ten of 30 chickens died after the
    first treatment and one died after the second treatment.  No delayed
    neurotoxic damage was observed as confirmed by a negative clinical
    test for neurotoxicity (forced movement) and the absence of basic
    histomorphological variations between the chickens treated with
    methamidophos and those in the negative control group.  The TOCP group
    developed neuropathy (Flucke and Kaliner, 1985). 

         Groups of white Leghorn hens (16/group) were orally administered
    by gavage 0, 0.3, 1.0 or 3.0 mg methamidophos (purity 76%)/kg bw 5
    days a week for 3 months.  Ten hens/group were examined for delayed
    neurotoxicity and plasma cholinesterase activity; NTE activities in
    the brain and spinal cord were determined in 6 hens/group. 

         Two hens in the control group and 2 hens in the high dose group
    died during the study (deaths were not considered to be
    treatment-related).  Somnolence and slight emaciation as well as a
    decreased mean body weight were observed in hens at 3 mg/kg b.w., but
    there were no signs of ataxia.  Plasma cholinesterase (after 4 weeks)
    and NTE activity in the spinal cord (after 12 weeks) were inhibited at
    1 mg/kg bw (23 and 22%, respectively) and 3 mg/kg bw (48% and 41%,
    respectively). NTE activity in the brain was only inhibited (17%) in
    the highest dose group.  No dose related effects including
    neuropathological changes were observed grossly or microscopically. 
    The NOAEL for general toxicity and plasma cholinesterase and NTE
    inhibition was 0.3 mg/kg bw/day (Sachsse et al., 1987). 

    Special studies on genotoxicity 

         The results of a cytogenetic assay in Chinese hamster ovary cells
    and an unscheduled DNA synthesis test in rat primary hepatocytes are
    described in Table 4.

     
        Table 4.  Results of genotoxicity assays on methamidophos.

                                                                             
    Test system    Test object    Concentration     Results       Reference
                                                                             

    Cytogenetics   Chinese        3150,4200 and     equivocal8    Murli, 1990
    assay 1        hamster        5250 g/ml2
                   ovary cells    (without
                                  action3) 

                                  1250,2500,        negative
                                  3750 and 4990
                                  g/ml (with
                                  action4)

    UDS assay      Rat            0.001 to 10       negative      Curren, 1988
                   hepatocytes    l/ml5,6,7
                                                                             

    1  Both with and without rat liver S9 fraction
    2  Test article purity = 74.5%
    3  Mitomycin was used as positive control
    4  Cyclophosphamide was used as positive control
    5  Test article: Monitor technical (purity 71.2%)
    6  Dose levels > 3.0 l/ml were too toxic to be evaluated for UDS.
    7  7,12-dimethylbenz(a)anthracene was used as a positive control 
    8  Slight increases in chromosome aberations were found at cytotoxic doses
    
    Special studies on skin sensitization 

         Repeated application (via a modified Buehler method) of
    methamidofos technical (purity 73.8%) at a concentration of 25% w/w in
    distilled water to the shaven backs of Hartley guinea pigs did not
    cause allergic sensitization (Cushman, 1984). 

    Observations in humans 

    Cholinesterase inhibition

         In an oral dosing study, human volunteers were given combinations
    of acephate and methamidophos.  Groups of 3 males and 3 females
    received 0.1, 0.2, or 0.3 mg/kg bw/day of a methamidophos/acephate
    combination (1:9) for 21 days followed by a 7-day recovery period
    after which the dose for each group was increased to 0.4 mg/kg bw/day
    (females only) for 10 days.  Groups of 2 males and 2 females received
    0.1 or 0.2 mg/kg bw/day of a methamidophos/acephate combination (1:4)
    for 21 consecutive days. In none of the groups was any effect noted on

    erythrocyte cholinesterase.  Plasma cholinesterase activity was
    affected in the 1:9 groups in males at 0.3 mg/kg bw/day and only
    slightly in females at 0.4 mg/kg bw/day.  Plasma cholinesterase
    inhibition in the 1:4 group was observed at 0.2 mg/kg bw/day.  The
    NOAEL in this study was 0.3 mg/kg bw/day for the combination 1:9 and
    0.2 mg/kg bw/day for the combination 1:4, with methamidophos
    concentrations of 0.03 and 0.04 mg/kg bw/day, respectively (Garofalo,
    1973).  The raw data were validated and support the above conclusions
    regarding cholinesterase activities.  Acephate and methamidophos were
    detected in urine and blood from the subjects, but urine samples were
    only collected periodically and excretion data were not calculated
    (Cavalli, 1978). 

         Information was obtained from the manufacturer concerning 36
    cases of intoxication by methamidophos in the Federal Republic of
    Germany during 1978-1982.  These were mainly the result of misuse of
    the compound (painting hop poles).  Efficient warnings prevented
    further accidents.  These cases could not be used for evaluation of a
    delayed haemotoxic potential because not enough information was
    available (Machemer, 1988).

    COMMENTS 

         An in vitro experiment found that methamidophos inhibited
    cholinesterase at a much higher rate than acephate. The I50 for human
    erythrocyte cholinesterase and rat brain cholinesterase were  of the
    same order of magnitude.

         Delayed neurotoxicity has been studied in hens following oral and
    dermal exposures.  Methamidophos inhibited NTE and elicited signs of
    delayed neuropathy at dose levels which were higher than the LD50,
    indicating that the potential to induce delayed neuropathy was low. 
    A NOAEL of 0.3 mg/kg bw/day was demonstrated in a 90-day oral
    neurotoxicity study in hens.

         Inhibition of erythrocyte cholinesterase was not found in a
    short-term study in humans in which dose levels up to 0.3 mg/kg bw/day
    of a combination of one part methamidophos with nine parts acephate or
    0.2 mg/kg bw/day of a combination of one part methamidophos with four
    parts acephate were given.  The estimations of the NOAEL for
    methamidophos in this study were 0.03 and 0.04 mg/kg bw/day,
    respectively.  These data from humans were used in allocating the ADI. 
    In allocating the ADI it was assumed that the effects observed after
    administration of the mixture were due solely to methamidophos.

    TOXICOLOGICAL EVALUATION

    Level causing no toxicological effect 

         Rat:      2 ppm in the diet, equal to 0.1 mg/kg bw/day 
         Dog:      2 ppm in the diet, equal to 0.06 mg/kg bw/day 
         Chicken:  0.3 mg/kg bw/day
         Human:    0.04 mg/kg bw/day 

    Estimate of acceptable daily intake for man 

         0-0.004 mg/kg b.w.

    Studies which will provide information valuable in
    the continued evaluation of the compound 

         Further observations in humans. 

    REFERENCES 

    Cavalli, R.D. (1978) Data validation Industrial Bio-Test report no.
    636- 02498.  A study on the effects of orthene and monitor on plasma
    and erythrocyte cholinesterase activity in human subjects during
    subacute oral administration.  Submitted to WHO by Chevron Chemical
    Company, Richmond, CA, USA. 

    Curren, R.D. (1988) Unscheduled DNA synthesis in rat primary
    hepatocytes. Test article: Monitor technical.  Unpublished report no.
    1119, from Microbiological Associates, Inc.  Submitted to WHO by Bayer
    AG, Leverkusen, Germany. 

    Cushman, J.R. (1984) Modified Buehler test for the skin sensitization
    potential of methamidophos technical (SX-1490). Unpublished
    toxicological report no. 596 from Chevron Environmental health Center,
    Richmond, California, USA. Submitted to WHO by Bayer AG. 

    Easter, M.D. and Rosenberg, D.W. (1986) The cholinesterase inhibition
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    California, USA.  Submitted to WHO by Bayer AG. 

    Eigenberg, D.A., Pazdernik, T.L. and Doull, J. (1983) Haemoperfusion
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    El-Sebae, A.H., Ahmed, N.S., El-Gendy, K.S., El-Bakary, A.S. and
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    Flucke, W. (1985) SRA 5172 TA (Tamaron TA) (c.n. methamidophos) Study
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    Flucke, W. (1990a) Methamidophos (Tamaron):  Racemate and Enantiomers. 
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    Flucke, W. (1990b) Methamidophos (Tamaron): Racemate and enantiomers. 
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    Flucke, W. and Eben, A.  (1990) Methamidophos:  racemate and
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    Flucke, W. and Kaliner, G. (1985) SRA 5172 TA (Tamaron TA) (c.n.
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    Garofalo, M. (1973) A study on the effects of orthene and monitor on
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    and methamidophos. J. Environ. Sci. Health. B20(1), 129-147. 

    Machemer, L. (1988) Expertise on the question: Does methamidophos
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    AG. 

    Murli, H.  (1990) Mutagenicity test on SRA 5172 in an in vitro
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    Pauluhn, J. (1988) SRA 5172 (Common name methamidophos, the active
    ingredient of MonitorR) Study of the subchronic inhalation toxicity
    to rats in accordance with OECD guideline no. 413.  Unpublished report
    no. 16578 from Bayer AG Fachbereich toxikologie, Wuppertal. Submitted
    to WHO by Bayer AG. 

    Pauluhn, J. and Kaliner, G. SRA 5172 and trimethylphosphate (TMPO)
    (c.n. methamidophos) Study for the combination's acute neurotoxicity
    to hens and turkey hens.  Unpublished report no. 13056 from Bayer AG
    Institute of toxicology, Wuppertal.  Submitted to WHO by Bayer AG. 

    Pauluhn, J., Machemer, L and Kimmerle, G. (1987) Effects of inhaled
    cholinesterase inhibitors on bronchial tonus and on plasma and
    erythrocyte acetylcholine esterase activity in rats. Toxicology 46,
    177-190.

    Sachsse, K., Oharek, A., Zbinden, K., Madoerin, K., Luetkemeier, H.,
    Wilson, J., Terrier, Ch. and Vogel, W. (1987) 3-Month subchronic
    delayed neurotoxicity study with SRA 5172 (c.n. methamidophos) in the
    hen.  Unpublished report no.: R 4106 from RCC AG, Switzerland. 


    See Also:
       Toxicological Abbreviations
       Methamidophos (HSG 79, 1993)
       Methamidophos (ICSC)
       Methamidophos (JMPR Evaluations 2002 Part II Toxicological)
       Methamidophos (Pesticide residues in food: 1976 evaluations)
       Methamidophos (Pesticide residues in food: 1979 evaluations)
       Methamidophos (Pesticide residues in food: 1981 evaluations)
       Methamidophos (Pesticide residues in food: 1982 evaluations)
       Methamidophos (Pesticide residues in food: 1984 evaluations)
       Methamidophos (Pesticide residues in food: 1985 evaluations Part II Toxicology)