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                                         ORIGINAL:   ENGLISH




    Primary use: Insecticide
    Secondary use: Acaricide
    Chemical group: Organophosphorus compound

         It must be noted that the issue of a Data Sheet for a
    particular pesticide does not imply endorsement of the pesticide by
    WHO or FAO for any particular use, or exclude its use for other
    purposes not stated. While the information provided is believed to
    be accurate according to data available at the time when the sheet
    was compiled, neither WHO nor FAO are responsible for any errors or
    omissions, or any consequences therefrom.

    The issue of this document does    Ce document ne constitue pas une
    not constitute formal              publication. Il ne doit faire
    publication. It should not be      l'objet d'aucun compte rendu ou
    reviewed, abstracted or quoted     résumé ni d'aucune citation sans
    without the agreement of the       l'autorisation de l'Organisation
    Food and Agriculture               des Nations Unies pour
    Organization of the United         l'Alimentation et l'Agriculture
    Nations or of the World Health     ou de l'Organisation Mondiale de
    Organization.                      la Santé.


    1.1  COMMON NAME: Azinphos-methyl (ISO, BSI; exception - USSR; 

    1.1.1 Identity:

          IUPAC: S-(3,4-dihydro-4-oxobenzo (d)-(1,2,3)-triazin-3-
                   ylmethyl-O,O-dimethyl phosphorodithioate 

          CAS No. 1: Phosphorodithioic acid, O,O-dimethyl ester, S-ester 
                       with 3(mercaptomethyl)-1,2,3-benzotriazin-4(3H)-one 

          CAS Reg. No: 86-50-0

          Molecular formula: C10H12N3O3PS2

          Molecular weight: 317.1

          Structural formula:

    Chemical Structure

    1.1.2 Synonyms: Azinfos-methyl; Azinophos-methyl; Azinphos methyl; 
          Azinphosmetile; Bay 9027; Bay 17 147; CarfeneR; CotneonR; 
          CotnionR; Cotnion-methylR; CrysthionR; CrysthyonR; DBDR;
          Ent 23,233; GothnionR; GusathionR; GuthionR, Methyl GusathionR; 
          Methyl GuthionR; Metiltriazotion; NCI-CO0066; R 1582. 

    1.2  SYNOPSIS: Azinphos-methyl is a broad spectrum, non-cumulative, 
         non-systemic organophosphorus insecticide/acaricide; an 
         irreversible cholinesterase inhibitor with good contact and 
         stomach action.  It has good residual activity and is highly toxic 
         to mammals and some wildlife.  It is toxic to some ornamental and 
         fruit trees.  Toxicity is increased following metabolism. 


    1.3.1 Physical characteristics - Azinphos-methyl forms colourless 
          crystals melting at 73-74°C.  It has a density (d2O/4) of 1.44
          and a refractive index n76/D) of 1.6115. 

    1.3.2 Solubility - In water, 33 mg/l at room temperature; it is soluble 
          in most organic solvents except aliphatics. 

    1.3.3 Stability - Azinphos-methyl is unstable at temperatures above 
          200°C and is rapidly hydrolysed by cold alkali and acid.  
          Solutions in ethanol and propylene glycol are stable for at least 
          3 weeks. 

    1.3.4 Vapour pressure - Less than 3.8 x 10-4 mmHg at 20°C.


    1.4.1 Common formulations - These include emulsifiable concentrates, 
          200 g a.i./l; wettable powders, 200-500 g a.i./kg; dust 
          preparations, 25 and 50 g a.i./kg; ULV preparations, 150-200 g/l. 

    1.4.2 Pests controlled - These include aphids, mites, codling moths, 
          lygusbugs, bollworms, armyworms, bollweevils, thrips, 
          grasshoppers, stinkbugs, spittle bugs, plum curculio, pear 
          psylla, scale and the European brown snail. 

    1.4.3 Use pattern - Azinphos-methyl is used on alfalfa, almonds, 

          apricots, apples, artichokes, beans, barley, caneberries, 
          blueberries, broccoli, brussel sprouts, cabbage, cauliflower, 
          celery, cherries, citrus, clover, coffee, cotton, crabapples, 
          cranberries, cucumbers, eggplant, filberts, grapes, melons, 
          nectarines, oats, onions, peaches, pears, pecans, plums, peppers, 
          potatoes, prunes, quinces, rice, rye, soybeans, spinach, 
          strawberries, sugar cane, sugar beets, tobacco, tomatoes, trees, 
          walnuts, watermelons, wheat, ornamentals and others.  It is 
          applied at a rate of 4.5-6.5 kg/ha. 

    1.4.4 Unintended effects - Azinphos-methyl is toxic to Hawthorn and 
          American Linden trees at high concentrations and the EC has 
          caused russetting to some fruit varieties. 

    1.5  PUBLIC HEALTH USES - No recommended use.

    1.6  HOUSEHOLD USE - No recommended use.



    2.1.1 Absorption route - Azinphos-methyl is absorbed from the 
          gastrointestinal tract; through the intact skin; and, by 
          inhalation of fine spray mist or dusts. 

    2.1.2 Mode of action - Azinphos-methyl is an inhibitor of 
          cholinesterase activity in vitro mammalian, avian and piscene 
          studies have shown, however, that it is a poor inhibitor of brain 
          cholinesterase.  The oxygen analogue, gutoxon is a more potent 
          anticholinesterase agent in brain tissue.  After cessation of 
          treatment it usually takes several weeks for normal enzyme 
          activities to resume. 

    2.1.3 Excretion products - Azinphos-methyl is readily absorbed and 
          metabolised in mammals.  Dimethylphosphorothioic and 
          dimethylphosphoric acids, desmethyl azinphosmethyl and azinphos-
          methyloxon are principal metabolites as demonstrated in in vitro 
          mouse tissue studies.  The benzotrianzine moiety is rapidly 
          excreted without degradation, less than 0.1% of the radioactivity 
          of peroral or intraperitoneal doses (0.1-0.2 mg/kg bw) of 14C-
          labelled azinphos-methyl is eliminated as CO2.  Approximately 65% 
          of the radioactivity of these doses was eliminated in urine, 
          about 25% in faeces.  In studies with dairy cows no residues of 
          azinphos-methyl or gutoxon appeared in milk, four unidentified 
          non-phosphorus containing metabolites were present in low 

    2.1.4 Toxicity, single dose:

          Oral LD50:

          Rat  (M)                  16    (13-25)   mg/kg bw
          Rat  (F)                  13.5  (11-16.4) mg/kg bw
          Mouse  (M)                 7.15 mg/kg bw
          Guinea-pig (M)            80    mg/kg bw

          Dermal LD50:

          Rat  (M)                 455    mg/kg bw
               (F)                 220    mg/kg bw
          Mouse                     65    mg/kg bw

          I.P. LD50:

          Rat  (M)                  11.6  mg/kg bw
          Rat  (F)                   5.1  mg/kg bw
          Mouse   (M)                5.4  mg/kg bw
          Mouse   (F)                3.4  mg/kg bw
          Guinea-pig (M)            40.0  mg/kg bw

          I.V. LD50:

          Rat (M & F)                7.5  mg/kg bw

          I.V. LD50:

          Mouse   (M)                8.0  mg/kg bw

          Inhalation LC50

          Rat  (M)                  69.0  mg/kg bw
               (F)                  79.0  mg/kg bw

          Most susceptible species - Females, in all species tested, appear 
          to be more sensitive than males, the mouse appears to be the 
          most susceptible species. 

    2.1.5 Toxicity, repeated doses:

          Oral: See Dietary studies, section 2.1

          Dermal: In animals given 2 or 20 mg/kg bw doses five times a 
          week for three weeks there was a slight depression of 
          cholinesterase activity at the highest dose only.  The no-
          observed-effect level was reported to be 2.0 (mg/kg bw)/day. 

          Inhalation: Male and female rats exposed to 4.72 mg/m3 for 6 
          hours a day, 5 days a week for 12 weeks showed depressed 
          erythrocyte and plasma cholinesterase activity, males showed 

          depression growth rates. Concentrations of 0.195 and 1.24 mg/m3 
          produced no ill effects. 

    2.1.6 Dietary studies:

          Short term: Groups of male rats were fed azinphos-methyl at 
          dosage levels of 0, 5, 10, 20, 50 or 100 mg/kg (diet) for 9 
          weeks.  At the two highest dose levels clinical signs of toxicity 
          and decreased body weight gains were observed.  Whole blood 
          cholinesterase activity was depressed in all treatment groups. 

          Groups of male and female rats were fed azinphos-methyl at dosage 
          levels of 0, 2, 5, and 20 mg/kg (diet) for 120 days.  No clinical 
          or laboratory evidence of toxicity was evident at 60 days.  At 
          the highest dose, at 120 days, there was some inhibition of brain 
          and erythrocyte cholinesterase (10 and 30 per cent respectively).  
          There were no observed treatment related changes in gross or 
          microscopic anatomy. 

          Weanling male rats fed 50 or 100 mg/kg (diet) for 16 weeks showed 
          increased mortality rates (50%), severe clinical signs of 
          toxicity, which stabilized after 30 days, and showed a dose 
          dependent decrease in body weight gain.  All cholinesterase 
          activities were markedly depressed throughout the dosing period.  
          Brain and erythrocyte activities were not fully restored to 
          normal 30 days after cessation of treatment.  No evidence of 
          testicular atrophy was evident in the survivors. 

          Groups of male and female dogs given azinphos-methyl in 5, 10, 20 
          or 50 mg/kg diets for 12 weeks showed no treatment related 
          depression of weight gain or clinical signs of toxicity.  At 50 
          mg/kg cholinesterase activity was significantly decreased by the 
          end of the 12 weeks. 

          In a second experiment male and female dogs were given azinphos-
          methyl in 0, 20, 50, 100, 200 or 400 mg/kg diets for 19 weeks.  
          Cholinesterase activity was slightly depressed in the 20 and 50 
          mg/kg groups after four weeks, reactivation occurred after 6 and 
          9 weeks respectively.  On the 100 mg/kg diets and above, 
          cholinesterase activity was depressed to 50% of control level.  
          Slight though unequivocal reactivation occurred in the 100 mg/kg 
          group only, after 17 weeks. 

          Long term: In a 2 year rat study, both sexes were given azinphos-
          methyl at 0, 2.5, 5 or 20 mg/kg (diets), an additional group was 
          given 50 mg/kg (diet) for 47 weeks followed by a 100 mg/kg (diet) 
          for the remainder of the study period.  In the highest dosage 
          groups, severe clinical signs of toxicity were observed in over 
          10% of the females.  There were no treatment induced changes in 
          mortality, body weight gain, food consumption, or haematology.  

          In males at 20 mg/kg (diet) and above erythrocyte and plasma 
          cholinesterase activities were significantly depressed; at 5 
          mg/kg (diet) the plasma activity was inhibited up to the 39th 
          week.  In females these activities were consistently depressed at 
          the highest dosage level only; at 20 mg/kg (diet) the plasma 
          activity was depressed up to week 65; at 5 mg/kg (diet) 
          erythrocyte activity was depressed up to week 10 only.  Brain 
          cholinesterase activity was depressed in the highest dosed 
          animals only which also experienced some increase in liver 
          weight.  There was no indication that tumour incidence was 
          increased by azinphos-methyl treatment. 

          Groups of male and female dogs were fed azinphos-methyl at both 
          constant and progressively increasing dosage levels: 5 mg/kg 
          (diet) for 2 years; 20 mg/kg (diet) for 36 weeks increased to 50 
          mg/kg (diet) for 15 months; 50 mg/kg (diet) for two years; 50 
          mg/kg (diet) for 36 weeks, followed by 100 mg/kg (diet) for 21 
          weeks, 150 mg/kg (diet) for 27 weeks and, finally 300 mg/kg 
          (diet) for 21 weeks.  In males at 300 mg/kg (diet) severe 
          clinical signs of toxicity with slight weight loss were observed. 

          Fewer females showed severe signs of toxicity at the highest 
          dosage level and there was a slight reduction in food consumption 
          at both highest dosages.  Erythrocyte cholinesterase activity was 
          slightly decreased at 20 mg/kg (diet), markedly at 50 mg/kg 
          (diet) and higher.  In the second year, all dogs showed a 
          decrease in plasma cholinesterase activity at dosage levels of 50 
          mg/kg (diet) and above.  There were no treatment related changes 
          in mortality rates, laboratory parameters or in gross or 
          histopathological incidences. 

          The no-effect-levels have been demonstrated in the rat and dog to 
          be approximately 0.125 (mg/kg bw)/day. 

    2.1.7 Supplementary studies of toxicity

          Carcinogenicity:  Azinphos-methyl has been classified as a 
          tumorogen with no carcinogenic potential.  Azinphos-methyl was 
          given at time weighted average dietary levels of 78 and 156 mg/kg 
          (diet) to male rats, 62.5 and 125 mg/kg (diet) to female rats, 
          3.13 and 62.5 mg/kg (diet) for male mice, and 62.5 and 125 mg/kg 
          (diet) for female mice.  Compound related tumours of the pancreas 
          and of thyroid follicle cells were observed.  Mutagenicity 
          studies have also provided no clear support of a carcinogenic 
          potential for azinphos-methyl. 

          Mutagenicity:  Results of a dominant lethal mutation study in 
          which male mice received 1.125 or 1.25 mg/kg bw doses (i.p.) were 
          negative.  In a Chinese hamster cell culture study, azinphos-
          methyl was mutagenically active only at doses of 600 ppm or more. 

          Similar results, at high doses, were observed in human cell 
          culture studies.  Azinphosmethyl was inactive in several 
          microbial pre-screening tests for mutagenicity. 

          Teratogenicity: There was no evidence of teratogenic potential 
          for azinphos-methyl in several mammalian reproductive studies 
          including a mouse dominant lethal mutagenicity test.  It was also 
          inactive in a chick embryo study (1 mg/egg); though embryotoxic 
          (66% mortality), the survivors showed no morphologic abnormality. 

          Reproduction: In a rat 3-generation study, 0, 5, 10, 25 or 50 
          mg/kg (diet) doses were continuously fed to males and females 
          from thirty days prior to first mating of the FO generation.  A 
          high mortality rate among females forced the elimination of the 
          highest dose group after the first mating; poor weanling survival 
          was also observed at this dosage level.  In the remaining groups 
          no treatment related adverse effects were observed relative to 
          reproductive behaviour and success, and no embryotoxic or fetal 
          toxic effects were observed.  Gross and microscopic anatomy of 
          the F3b weanlings were normal. 

          Azinphos-methyl was fed to pregnant rabbit does from day 8 to day 
          16 of pregnancy at dosage levels of 5 or 25 mg/kg (diet).  No 
          treatment related changes were observed in litter size, number of 
          stillbirths, sex ratios, fetal weight, fetal development, or pup 
          survival to 30 days. 

          Neurotoxicity: There was no evidence of demylenation in rats fed 
          azinphos-methyl at dosage levels up to 20 mg/kg (diet) for 120 
          days.  Azinphos-methyl is a neuroactive agent with immediate 
          neurotoxic action and no known delayed neurotoxic effect. 

    2.1.8 Modification of toxicity - No information available.


    2.2.1 Absorption route - Azinphos-methyl may be absorbed from the 
          gastrointestinal tract, through the intact skin; and by 
          inhalation of fine spray mist or dusts. 

    2.2.2 Dangerous doses:

          Single: Azinphos-methyl has a toxicity rating 5 - extremely 
          toxic, the probable lethal oral dose for humans is from 5 to 50 
          mg/kg bw, approximately seven drops or one teaspoon (0.2 g) for 
          a 70 kg person. 

          Repeated: No information available.

    2.2.3 Observations of occupationally exposed workers - Cholinesterase 

          activity in 15 male agricultural field workers was only slightly. 
          lower than in controls.  No clinical signs of toxicity were 
          observed in the workers exposed to the pesticide.  One spray-
          aircraft pilot experienced severe symptoms of azinphos-methyl 
          poisoning while flying his craft. Probable source of the 
          contamination was a concentrate spill on his hands and a spray 
          directly onto his face. He was able to land safely and was 
          treated in hospital; his recovery was uneventful. 

    2.2.4 Observations on exposure of the general population - No 
          information available. 

    2.2.5 Observations of volunteers - In several experimental exposure 
          studies male volunteers were given peroral doses ranging from 4 
          to 20 (mg/man)/day for 30 days.  No clinical signs of toxicity 
          were observed and there was significant depression of 
          cholinesterase levels only at the highest dose levels (18 and 20 

          In a second study, 2 male volunteers received 16 mg of azinphos-
          methyl for 30 days.  Neither subject showed any depression of 
          blood cholinesterase during treatment.  Excretion of the 
          degradation products reached maximum level 24 hours after the 
          initial treatment and continued at that level until the day 
          following cessation of treatment. 

    2.2.6 Reported mishaps - No information available.


    2.3.1 Fish - Azinphos-methyl is quite toxic to fish.

          LC50 (48 hour):

          Channel cat fish             9.0  mg/l
          Sunfish                    0.025  mg/l
          Golden shiner                0.1  mg/l
          Large mouth bass           0.025  mg/l
          Bluegills                  0.025  mg/l
          Goldfish                     2.0  mg/l

          Median tolerance limits:

          TL50 (96 hour):

          Rainbow trout             0.0032
          Chinook salmon            0.0043
          Coho salmon               0.0042
          Guppies                   0.12
          Fathead minnow            0.093

          Stickleback               0.012; (0.5% salinity)
          Stickleback               0.005; (2.5% salinity)

    2.3.2 Birds - Both laboratory and field tests have shown that birds 
          have a significantly high tolerance to azinphos-methyl regardless 
          of the route of absorption. 

          Acute LD50:

          Chicken         277 mg/kg bw

          The 100 day cumulative LD50, 250 mg/kg (diet):

          Juvenile bobwhite quail     5500 mg/kg bw

          Juvenile ringneck pheasant  2000 mg/kg bw

          Bobwhite quail showed no adverse effects after exposure to 6 
          spray applications (0.83-0.89 kg a.i./ha) at 6 day intervals over 
          a two month period.  Ringneck pheasants similarly exposed to 
          spray applications of 5.5 kg a.i./ha showed no ill effects and 
          their reproductive success was not affected. 

    2.3.3 Other species - Azinphos-methyl is acutely toxic to a variety of 
          wildlife species including amphibians, crustaceans, molluscs, and 
          many beneficial insects such as honey bees.  There is no evidence 
          however that it is accumulative in aquatic environments and it is 
          not persistent on plants. 



         (For definition of categories see the Introduction to Data Sheets) 

         Liquid formulations of 8% and over, Category 2

         Other liquid formulations, Category 3

         Solid formulations of 32% and over, Category 2

         Other solid formulations, Category 3


         All formulations - Should be transported and stored in clearly 
         labelled impermeable containers under lock and key, secure from 
         access by unauthorized persons and children.  No food or drink 
         should be stored in the same compartment. 

    3.3  HANDLING

         All formulations - Full protective clothing (see 4.3, part 4) 
         should be used by those handling the compound. Adequate washing 
         facilities should be available at all times during the handling 
         and should be close to site of handling.  Eating, drinking and 
         smoking should be prohibited during handling and before washing 
         after handling. 


         All formulations - Container must either be burned or crushed and 
         buried below topsoil. Care must be taken to avoid subsequent 
         contamination of water sources.  Decontamination of containers in 
         order to use them for other purposes should not be permitted. 


         All formulations - Pre-employment medical examination of workers 
         necessary.  Workers suffering from active hepatic or renal disease 
         should be excluded from contact.  Pre-employment and periodic 
         cholinesterase test for workers desirable.  A periodic urinary p-
         nitrophenol test may be used as an alternative.  Special account 
         should be taken of the workers' mental ability to comprehend and 
         follow instructions.  Training of workers in techniques to avoid 
         contact essential. 


         All formulations - Pilots and loaders should have special 
         training in application methods and early symptoms of poisoning, 
         and must wear a suitable respirator.  Use of flagmen not 
         recommended.  Flagmen, if used, should wear protective clothing, a 
         broad brimmed hat and be located well away from the dropping zone. 

    3.7  LABELLING

         Minimum cautionary statement - All formulations.  "DANGER - 
         POISON" (skull and cross-bones insignia). Azinphos-methyl is an 
         organophosphorus compound of very high toxicity, which inhibit 
         cholinesterase activity.  Contact with the skin, inhalation of 
         dust or spray, or swallowing may be fatal.  Wear protective 
         gloves, clean protective clothing and a respirator of the organic-
         vapour type when handling this material. Bathe immediately after 
         work.  Ensure that containers are stored under lock and key.  
         Empty containers must be disposed of in such a way as to prevent 
         all possibility of accidental contact with them.  Keep the 
         material out of reach of children and well away from foodstuffs, 
         animal feed and their containers. 

         In case of contact, immediately remove contaminated clothing and 
         wash the skin thoroughly with soap and water; for eyes, flush with 
         water for 15 minutes.  If poisoning occurs, call a physician.  
         Atropine sulfate is a specific antidote, repeated doses may be 
         necessary.  Artificial respiration also may be needed. 


    3.8.1 Maximum residue levels - The Joint FAO/WHO Meeting on Pesticide 
          Residue recommended maximum residue levels. 



    4.1.1 General - Azinphos-methyl is a highly toxic organophosphorus 
          pesticide.  It penetrates the intact skin and is also absorbed by 
          inhalation and via the gastrointestinal tract.  Most formulations 
          should be handled by trained personnel wearing protective 

    4.1.2 Manufacture and formulation - T.L.V. - 0.2 mg/m3, STEL - 0.6 
          mg/m3.  Closed systems and forced ventilation may be required to 
          reduce, as much as possible, the exposure of workers to the 

    4.1.3 Mixers and applicators - When opening the container and when 
          mixing, protective impermeable boots, clean overalls, gloves and 
          respirator should be worn.  Mixing, if not mechanical, should 
          always be carried out with a paddle of appropriate length.  When 
          spraying tall crops or during aerial application, a respirator 
          should be worn as well as an impermeable hood, clothing, boots 
          and gloves.  The applicator should avoid working in spray mist 
          and avoid contact by mouth.  Particular care is needed when 
          equipment is being washed after use.  All protective clothing 
          should be washed immediately after use, including the insides of 
          gloves. Splashes must be washed immediately from the skin and 
          eyes with large quantitites of water.  Before eating, drinking or 
          smoking, hands and other exposed skin should be washed. 

    4.1.4 Other associated workers (including flagmen in aerial operations)
          - Persons exposed to azinphos-methyl and associated with its 
          applications should wear protective clothing and observe the 
          precautions described above in 4.1.3 under "Mixers and 

    4.1.5 Other populations likely to be affected - With good application 
          practice subject to 4.2 below, other populations should not be 
          exposed to hazardous amounts of azinphos-methyl. 

    4.2  ENTRY OF PERSONS INTO TREATED AREAS - Unprotected persons should 
         be kept out of tall crops for four days and out of other crops for 
         24 hours after application. 

         containers should be emptied in a diluted form into a deep pit, 
         taking care to avoid ground waters.  The empty container may be 
         decontaminated by rinsing two or three times with water and 
         scrubbing the sides.  An additional rinse should be carried out 
         with 5% sodium hydroxide solution which should remain in the 
         container overnight.  Impermeable gauntlets should be worn during 
         this work, and a soakage pit should be provided for the rinsings.  
         Decontaminated containers should not be used for other purposes.  
         Spillage of the compound or formulations should be removed by 
         washing with 5% sodium hydroxide solution and then rinsing with 
         large quantities of water. 


    4.4.1 Early symptoms of poisoning - Early symptoms of poisoning may 
          include excessive sweating, headache, weakness, giddiness, 
          nausea, vomiting, hypersalivation, stomach pains, blurred vision, 
          slurred speech and muscle twitching.  Later there may be 
          convulsions and coma. 

    4.4.2 Treatment before person is seen by a physician, if these symptoms 
          appear following exposure - The person should stop work 
          immediately, remove contaminated clothing and wash the affected 
          skin with soap and water, if available, and flush the area with 
          large quantities of water.  If swallowed, vomiting should be 
          induced if the person is conscious.  In the event of collapse, 
          artificial respiration should be given, bearing in mind that if 
          mouth-to-mouth resuscitation is used vomit may contain toxic 
          amounts of azinphos-methyl. 



    5.1.1 General information - Azinphos-methyl, an organophosphorus 
          pesticide of very high mammalian toxicity, is active against a 
          variety of agricultural and public health pests.  It is readily 
          absorbed from the gastrointestinal tract; through the intact 
          skin; and, by inhalation.  It is converted in vivo to the oxygen 
          analogue guthionoxon which inhibits cholinesterase.  It does not 
          accumulate in body tissues. 

    5.1.2 Symptoms and signs - Initial symptoms of poisoning may include 
          excessive sweating, headache, weakness, giddiness, nausea, 
          hypersalivation, vomiting, stomach pains, blurred vision, slurred 

          speech and muscle twitching. More advanced symptoms of poisoning 
          may be convulsions, coma, loss of reflexes and loss of sphincter 

    5.1.3 Laboratory - The most important finding is reduction of blood 
          cholinesterase activity.  Urinary levels of organophosphorus 
          metabolites may also be used as a measure of exposure.  Neither 
          method is specific for the compound. 

    5.1.4 Treatment - If the pesticide has been ingested, unless the 
          patient is vomiting, rapid gastric lavage should be performed 
          using 5% sodium bicarbonate, if available.  For skin contact, the 
          skin should be washed with soap and water.  If the compound has 
          entered the eyes, they should be washed with large quantities of 
          isotonic saline or water.  Persons without signs of respiratory 
          inefficiency but with manifest peripheral symptoms should be 
          treated with 2-4 mg of atropine sulfate by intravenous injection 
          and 1000 mg of pralidoxime chloride or 250 mg of toxogonin (adult 
          dose) by slow intravenous injection.  More atropine may be given
          as needed. Persons with severe intoxication, respiratory 
          difficulties, convulsions or unconscious should immediately be 
          given atropine and a reactivator.  In such severe cases 4-6 mg of 
          atropine sulfate should be given initially followed by repeated 
          doses of 2 mg at 5-10 minute intervals.  Diazepam may be given to 
          control convulsions.  The patient's condition including 
          respiration, blood pressure, pulse frequency, salivation, and 
          convulsions should be carefully observed as a guide to further 
          administration of atropine.  If the patient is cyanotic, oxygen 
          should be given at the same time as atropine sulfate.  The 
          airways should be kept free and artificial respiration should be 
          applied, if required, preferably by mechanical means.  If 
          necessary, intubation should be performed. 

          Contraindications are morphine, barbiturates, phenothiazine 
          tranquillizers and central stimulants of all kinds. Pralidoxime 
          and toxogonin alone are not regarded as effective antidotes in 
          organophosphorus poisoning.  In cases of severe poisoning, when 
          administered early, pralidoxime may be used to relieve nicotinic 

    5.1.5 Prognosis - If the acute toxic effect is survived and adequate 
          artificial respiration has been given, if needed, the chances of 
          complete recovery are good.  However, in very severe cases, 
          particularly if artificial respiration has been inadequate, 
          prolonged anoxia may give rise to permanent brain damage. 

    5.1.6 Reference of previously reported cases - No information 


    5.3  LABORATORY METHODS - References are given only,

          Test                       Normal     Action     Symptomatic
                                     level*     level*     level*

          Cholinesterase             100%       50%        variable

          Whole Blood or Erythro-
          cyte Cholinesterase        100%       70%        usually 40%

          *  Expressed at percentage of pre-exposure activity.

    5.3.1 Detection and assay of compound - Abbot D. C. et al. (1967) 
          Analyst, 92 171.  Bowman M. C. & Beroza M. (1967),
          J. Assoc. Off. Anal. Chem., 50, 1228.  Burke J. A. & 
          Holswade W. (1966) J. Assoc. Off. Anal. Chem., 49, 377.  Getz M. 
          E. & Wheeler H. G. (1968) J. Assoc. Off. Anal. Chem., 51, 
          1101. MacDougall D. (1964) Anal. Methods Pestic., Plant Growth 
          Regul., 2, 231. ibid, (1972) Anal. Methods Pestic., Plant Growth 
          Regul., 6, 397.  Meager W. R. et al. (1960) J. Agric. Food Chem., 
          8, 282.  Norris M. U. et al. (1954) J. Agric. Food Chem., 2, 

    5.3.2 Other tests in case of poisoning - Levels of cholinesterase in 
          the blood, particularly plasma, provide the most useful diagnosis
          of poisoning.  Michel, N.O. (1949) J. Lab. Clin. Med., 34, 1564-
          1568.  Ellman, G.L. et al. (1961) Biochem. Pharmacol., 7, 88-95 

          Measurements of urine metabolites may also be determined in order 
          to give an indication of exposure for methods.  See section 
          5.3.1, Detection and Assay. 

See Also:
        Azinphos methyl (PIM 739)