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    WORLD HEALTH ORGANIZATION             FOOD AND AGRICULTURE
                                          ORGANIZATION
    ORGANISATION MONDIALE DE LA SANTE     ORGANISATION POUR L'ALIMENTATION
                                          ET L'AGRICULTURE
                                                                             
                                          VBC/DS/83.53
                                          ORIGINAL:   ENGLISH
                                                                            
    DATA SHEET ON PESTICIDES No.  53
                                                                             
    ALDICARB


                                                                             
    CLASSIFICATION:
                                                                             
    Primary use:  Insecticide
    Secondary use:   Acaricide, nematicide
    Chemical group:   Carbamate


         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     rsum 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 Sant.

    1.   GENERAL INFORMATION

    1.1  COMMON NAME:   Aldicarb  (BSI,  ISO, ANSI,  exception - Germany)

    1.1.1 Identity:

          IUPAC: 2-methyl-2-(methylthio)propionaldehyde O-(methylcarbamoyl)
                 oxime 

          CAS No. 1: Propionaldehyde,2-methyl-2-(methylthio)-,O-
                     (methylcarbamoyl)oxime

          CAS Reg. No.: 116-06-3

          Molecular formula: C7H14N2O2S  
 
          Structural formula:

    Chemical Structure

          Molecular weight:   190.29

    1.1.2 Synonyms: Aldicarb, aldicarbe, carbanolate, Ent 27093, NCI 
          08640, OMS 771, TernicR, TemikR, UC-21149 

    1.2  SYNOPSIS - Aldicarb is a broad spectrum carbamate pesticide; a 
         fast-acting cholinesterase inhibiting agent with effective direct 
         contact and stomach action; and, a plant systemic of extremely 
         high acute toxicity to mammals.  It is non-cumulative and rapidly 
         metabolized in both plants and animals, the initial degradation 
         products are also highly toxic to mammals.  Aldicarb is a
         persistent carbamate compound with excellent residual and
         knock-down properties. 

    1.3  SELECTED PROPERTIES

    1.3.1 Physical characteristics - The pure compound is a white 
          crystalline solid with a slight sulfurous odour; a melting point 
          of 98-100C; and a specific gravity of 1.195 at 25/20C. 
          Aldicarb is non-corrosive to most metals and plastics. The 
          technical product is 94.7-97.7% pure aldicarb.

    1.3.2 Solubility - (30C)   9.0 g/kg water
                              430.0 g/kg acetone
                              240.0 g/kg benzene
                               50.0 g/kg carbon tetrachloride
                              440.0 g/kg chloroform
                              240.0 g/kg methyl isobutyl ketone
                              120.0 g/kg toluene
                       (20C) 250.0 g/kg ethanol
                              200.0 g/kg methanol

    1.3.3 Stability - Aldicarb is a relatively stable compound, it is 
          heat labile and decomposes above 100C, it is stable in acidic 
          aqueous solution but rapidly decomposes in alkaline media. 

    1.3.4 Vapour pressure - 0.133 x 10-4 kPa (1 x 10-4 mm Hg) at 25C.

    1.4  AGRICULTURE, HORTICULTURE AND FORESTRY

    1.4.1 Common formulations - To reduce handling hazards aldicarb is 
          prepared in granular formulations only; on corn cob grits at 50,
          100 and 150 g a.i./kg; on coal at 100 g a.i./kg; and, on gypsum 

          at 100 and 150 g a.i./kg. 

    1.4.2 Susceptible pests - Aldicarb is effective against various 
          insects (especially aphids, whiteflies, leaf miners, flea 
          beetles and ground beetles), mites and nematodes on field 
          crops, some vegetable and fruit crops, cotton and 
          ornamentals in commercial plantings. 

    1.4.3 Use pattern - Aldicarb is applied only as a soil dressing at 
          rates of 0.56-11.25 kg a.i./ha depending upon the crop.  For 
          most effective use, aldicarb should be incorporated into the 
          soil 2.5-5.0 cm below the surface.  It may be applied 
          in the seed furrow, in band or broadcast applications; 
          preplanting, at planting or after crop emergence.  
          Formulated aldicarb may be used concurrently with many 
          fertilizers or other pesticides.  It should not be applied 
          at the same time with alkaline compounds nor mixed with 
          fertilizers or other pesticides prior to application.  The 
          active ingredient is released from the granules by water 
          action, for best effect the soil moisture content should be 
          increased immediately following application.  Aldicarb 
          should not be used on stored crops or products. 

    1.4.4 Unintended effects - Applied as directed aldicarb is not 
          phytotoxic. 

    1.5  PUBLIC HEALTH PROGRAMMES (NO RECOMMENDED USAGE REPORTED)

    1.6  HOUSEHOLD USE (NO RECOMMENDED USAGE REPORTED)

    2.   TOXICOLOGY AND RISKS

    2.1  TOXICOLOGY MAMMALS

    2.1.1 Absorption route - Aldicarb may be absorbed from the 
          gastrointestinal tract; through moist, intact skin; and, by 
          inhalation of dust.  The presence of a binding agent in the 
          granular product, the only formulation available, reduces the 
          inhalation hazard in normal use. 

    2.1.2 Mode of action - Toxicity is primarily due to inhibition of 
          cholinesterase activity which is spontaneously reversible. 

    2.1.3 Excretion products - Within 48 hours of administration of 
          carbonyl-14C labelled aldicarb rats eliminated over 60% of the 
          14C as carbondioxide, less than 30% was found in the urine.  In 
          other 14C-studies rats excreted more than 80% of the degradation 
          products in urine and less than 10% in faeces (an excretion 
          pattern favoured by enterohepatic cycling of glucuronides which 
          may also serve to extend the systemic activity of the toxic 

          metabolites).  The major urinary metabolites were aldicarb 
          sulfoxide (40% of the dose), its oxime and nitrile forms (over 
          30%); the sulfone and related oxime and nitrile; and, the 
          aldehyde and acid analogues.  Aldicarb is not commonly found in 
          the excreta.  Bound residues of ingested plant tissues are not 
          absorbed and therefore are found in the faeces. In single dose 
          and short-term diet studies, lactating cows eliminated aldicarb 
          metabolites as rapidly as rats and in the same array of 
          metabolites.  Approximately 1% of the dose was excreted in the 
          milk, sulfone and sulfoxide were the major metabolites at 15 and 
          4% of the total milk residue content respectively. 

    2.1.4 Toxicity, single doses

          Oral LD50:

          technical material, Rat (M),    0.67-1.23 mg/kg b.w. (corn oil)
                              Rat (F),    0.62-1.07 mg/kg b.w. (corn oil)
                              Rat (F),         1.0  mg/kg b.w. 
                              (glycerol formal:  ethanol 9:1)
                              Mouse (M),  0.38-0.50 mg/kg b.w. (corn oil)
                              Mouse (F),       1.5  mg/kg b.w. (cotton seed 
                                                                oil)
                              Guinea-pig,      1.0  mg/kg b.w. (corn oil)
                              Rabbit           1.3  mg/kg b.w. (propylene 
                                                               glycol)
          formulated product, Rat (M),         0.81 mg/kg b.w. (50% W.P., 
                                                               water)
                              Rat (M),    0.67-1.23 mg/kg b.w. (50% W.P., 
                                                               corn oil)
                              Rat (M),         7.07 mg/kg b.w. (10% on 
                                                               gypsum, 
                                                               neat)
                              Rat (M),         7.9  mg/kg b.w. (5.5% with
                                                               fungicides, 
                                                               corn oil)
                              Rat (F),         0.62 mg/kg b.w. (50% W.P.,
                                                               water)
                              Rat (F),    0.77-1.07 mg/kg b.w. (50% W.P.,
                                                               corn oil)
                              Rat (F),         6.7  mg/kg b.w. (5.5% with 
                                                               fungicides,
                                                               corn oil)
                              Rabbit (F), 7.9-17.8  mg/kg b.w. (10% on 
                                                               gypsum, 
                                                               neat)
                              Rabbit (F), 5.3-10.6  mg/kg b.w. (15% on 
                                                               gypsum,
                                                               neat)
                              Rabbit (F),     8.4   mg/kg b.w. (15% on corn

                                                               cob grits, 
                                                               neat)

          Dermal LD50:

          technical material, Rat (M),    38.1-44.9 mg/kg b.w. (water)
                              Rat (M),        >10   mg/kg b.w. (corn oil)
                              Rat (M),     3.2-7.0  mg/kg b.w. (DMP)
                              Rabbit (M),  144-200  mg/kg b.w. (corn oil)
                              Rabbit (M),       20  mg/kg b.w. (water)
                              Rabbit (M),      5.0  mg/kg b.w. (propylene 
                                                               glycol)
                              Rabbit (M),     10.0  mg/kg b.w. (corn oil)
                              Guinea-pig (M), 24.0  mg/kg b.w. (organic
                                                               solvent)
          formulated product, Rat (M,F), 2100-5000  mg/kg b.w. (10% gypsum,
                                                               dry)
                              Rat (M,F),  283- 673  mg/kg b.w. (10% gypsum, 
                                                               water)
                              Rat (M,F), 1980-6320  mg/kg b.w. (15% gypsum, 
                                                               dry)
                              Rat (M,F),  283-1010  mg/kg b.w. (15% gypsum, 
                                                               water)
                              Rabbit (M),     4800  mg/kg b.w. (10-15% 
                                                               gypsum, dry)
                              Rabbit (M,F),   2000  mg/kg b.w. (5.5% with 
                                                               fungicide,
                                                               neat)
          Intraperitoneal    LD50:

          technical material, Rat (M,F),  0.44-7.1  mg/kg b.w. (corn oil)
                              Rat (M),    0.28-0.44 mg/kg b.w. (PEG 400)
                              Rat (M),         0.57 mg/kg b.w. (ethanol)
                              Mouse (F),       0.3  mg/kg b.w. (cotton seed
                                                               oil)

          Intravenous LD50:

          technical material, Rat (M),         0.47 mg/kg b.w. (water)

          Inhalation - Aldicarb does not produce toxic fumes, all test rats 
          survived an eight-hour exposure to aldicarb granules (no direct 
          contact) showing no acute or delayed ill effects.  Inhalation of 
          aldicarb dust has been shown to be lethal at high concentrations 
          or with prolonged exposure to low levels.  All test rats, mice 
          and guinea-pigs died from exposure to 200 mg/m3 for five minutes, 
          five of six female rats died from exposure, to 6.7 mg,/m3 for 30 
          minutes whereas all test animals survived 15 minutes of 6.7 mg/m3 
          of aldicarb dust. See section 2.2.1. 


    2.1.5 Toxicity, repeated doses

          Oral - See sections 2.1.6 and 2.1.7.

          Dermal - Aldicarb applied to male rabbits on abraded skin, with 
          moist dressings for six hours a day in a three-week study 
          produced reduced body weight gains and clinical signs of toxicity 
          at the lowest dose (5(mg/kg b.w.)/day) and depressed plasma 
          cholinesterase activity at the two highest doses only (10 and 
          20(mg/kgb.w.)/day).  There were no mortalities, and no 
          histopathologic or haematologic signs of toxicity.  Adverse 
          effects were rapidly reversed when the treatment stopped.  
          Aldicarb similarly applied to non-abraded skin with dry dressings 
          produced no adverse effects at 20 mg/kg b.w. 

          Dermal irritation and sensitization - Aldicarb applied to shaved 
          intact skin of rabbits produced no signs of irritation at the 20 
          mg/kg level of treatment.  Wet preparations were absorbed more 
          readily than dry preparations but they were not more effective.  
          Multiple subdermal applications of 0.7 mg/kg b.w. did not 
          sensitize the animals. 

          Cumulation of compound - Aldicarb does not acclumulate in body 
          tissues, it is rapidly metabolized rnd excreted. 

          Cumulation of effect - Repeated exposure to sublethal amounts
          does not produce a cumulation effect. 

    2.1.6 Dietary studies

          Short-term - In several studies male and female rats were fed 
          aldicarb in diets for one week at dose levels ranging from 0.3 to 
          16.0 mg/kg b.w. Treatment related mortality was 100% and 40% 
          among males and females respectively at the 16.0 mg/kg level and 
          20% of the females only, at 8.0 mg/kg b.w. Growth rates were 
          depressed in both sexes at 3.2 mg/kg and above.  There were 
          treatment related depressions gross organ weights and organ to 
          body weight ratios in both males and females at 1.6 mg/kg and 
          above.  Plasma and erythrocyte cholinesterase activities were 
          depressed at 1.5 mg/kg and above in both sexes. 

          In several studies of one week to six months duration, aldicarb 
          sulfoxide and sulfone were fed to rats of both sexes at dosage 
          levels of 0.4-1.6 mg/kg b.w. and 0.4-20.0 mg/kg b.w. 
          respectively.  There were no treatment related deaths, changes in 
          gross organ weights or organ to body weight ratios.  The 
          sulfoxide metabolite significantly reduced growth at 0.8 mg/kg
          b.w. and above in both sexes, the sulfone at 5.0 mg/kg and above 
          in males and, 0.6 mg/kg and above in females.  The sulfoxide 
          depressed plasma and erythrocyte cholinesterase activity at 0.8 

          mg/kg level, the sulfone at 5.0 mg/kg and above.  Brain 
          cholinesterase activity was depressed by sulfone at 20 mg/kg b.w. 

          The rat no-adverse-effect dose of aldicarb was estimated to be 
          0.125 (mg/kg)/day. 

          Mice fed dietary aldicarb at dosage levels ranging from 0.1 to 
          1.2 mg/kg b.w. for seven days showed no treatment related signs 
          of toxicity among the survivors, treatment related mortalities 
          occurred at the 1.2 mg/kg level only. Mice fed a 1:1 ratio of 
          aldicarb and aldicarb sulfone at dose levels from 2 to 36 mg/kg  
          b.w. showed no treatment related mortality.  Growth rates were 
          depressed in both sexes at 18 and 36 mg/kg levels, liver weights
          were lower in males at 18 and 36 mg/kg and in females at the 36
          mg/kg dose, kidney weights were depressed in both sexes at 36 
          mg/kg dose.  Male mice showed severe cholinergic signs at the 36
          mg/kg level. 

          No adverse effects were observed in male and female beagles fed 
          aldicarb in diets at dosage levels of 0.2, 0.3 and 0.7 mg/kg b.w. 
          for seven-day and 100-day studies.  In both studies the animals 
          were returned to the control diet for 24 hours at the end of the 
          study, therefore no useful cholinesterase information was 
          obtained.  Beagles fed sulfoxide and sulfone metabolites at diet 
          dosage levels of 0.0625-0.5 mg/kg and 0.2-5.4 mg/kg respectively 
          showed no ill-effects attributable to treatment. 

          Long-term - No significant treatment related ill-effects were 
          observed in several two-year studies of rats fed aldicarb in 
          diets at dose levels of 0.005-0.3 mg/kg b.w.

          No significant treatment related ill-effects were observed in 
          two-year studies of dogs on diets containing aldicarb at 0.025, 
          0.05 and 0.1 mg/kg b.w. dose levels. 

          In a two-year study of mice fed aldicarb in the diet at dosages 
          of 0.10 and 0.30 mg/kg b.w., no adverse effects were observed.
          In a similar mouse study mortalities occurred among the males at 
          the 0.4 mg/kg dose and above, among the females at the 0.2 mg/kg 
          dose and above. 

          In CD-1 mice fed aldicarb at 0.7 mg/kg b.w. for 18 months, the 
          incidence of hepatomas among the surviving treated males was 
          significantly higher than among the surviving controls or the 
          dead males. Among the treated dead males the increase of lymphoid 
          neoplasms was significant.  However, the incidence of both 
          hepatomas and lymphoid neoplasms among controls was unusually 
          high and in a similar follow-up study there was no significant 
          increase in carcinogenic response among the treated animals. 


    2.1.7 Supplementary studies of toxicity
          
          Carcinogenicity - Aldicarb is classified as a tumorogen with no 
          carcinogenic potential (NCI-GI-TR-136, 7-).  In the dietary 
          studies described in section 2.1.6 neither aldicarb nor its 
          metabolites were implicated in the development of neoplastic 
          lesions.  It was also found to be carcinogenically negative in a 
          transplacental host-mediated hamster cell culture assay and a 
          mouse dermal application study. 

          Nitrosoaldicarb on the other hand, was found to be strongly
          carcinogenic in rats following oral administration of cumulative 
          doses of 40 mg/kg b.w. over two weeks and 90 mg/kg b.w. over nine 
          weeks.  It produced carcinoma and/or benign tumours of the non-
          glandular stomach tissue of all survivors.  It was also active in 
          a transplacental host-mediated hamster cell culture assay. There 
          is no evidence that the n-nitrosamide derivative of aldicarb is a 
          naturally occurring product. 

          Teratogenicity - No evidence of teratogenicity was presented in 
          the literature surveyed.  Aldicarb injected into hen's eggs at a 
          dose of 1.0 mg/egg produced no teratogenic effects.  Aldicarb 
          given to pregnant rats at doses of 0.4-1.0 mg/kg b.w. for the 
          duration of pregnancy, for the first seven days, or from day five 
          to day 15 produced no changes in the standard indices of 
          reproductive behaviour or performance and no teratogenic 
          manifestations in the pups. 

          Mutagenicity - No evidence of mutagenicity was presented in the 
          literature surveyed.  Aldicarb was found to be a weak mutagen in 
          only one of several microbial pre-screening tests for 
          mutagenicity, in all other tests it was negative.  It was also 
          found to be negative in two DNA alteration tests with human skin 
          fibroblast cultures; in an ICR mouse micronucleus assay; and, in 
          a rat dominant lethal study.  Metabolism of aldicarb by rat liver 
          microsomal enzyme systems did not activate aldicarb mutagenicity. 

          Reproduction - No evidence of modifaction of reproductive 
          behaviour or performance was presented in the literature 
          surveyed. (See also the sections above.) Single oral doses of 
          aldicarb as low as 1.0 g/kg b.w. given to pregnant rabbits on 
          day 18 of gestation had a greater effect on the foetuses than the 
          dams.  Foetal blood cholinesterase activity was significantly 
          decreased by aldicarb, there was evidence of a rapid and 
          prolonged placental transfer of the compound and/or its 
          metabolites. Foetal brain cholinesterase activity was depressed 
          at the 100 g/kg level.  In a three-generation study, rats fed 
          1.0 and 2.0 mg/kg diets for 90 days showed no treatment-related 
          adverse changes in standard reproduction indices when mated.  
          There were no observed treatment-related adverse changes in 

          standard reproductive indices or in gross and microscopic 
          abnormalities in the pups. In another three-generation study, 
          rats fed 4, 6 and 14 mg/kg diets for 100 days prior to mating 
          showed no ill-effects of treatment save a significant decrease in 
          growth rate at the highest dose. There were no observed 
          treatment-related adverse changes in standard reproductive 
          indices, gross or microscopic abnormalities in the foetuses. 

          Neurotoxicity - No ataxia, hind limb paralysis or delayed 
          neurotoxicity was observed in hens given a single dose of 
          aldicarb (45 mg/kg b.w.) or, in the diet (0, 2.25 and 4.5
          mg/kg b.w.) for 30 days.  A positive control study (TOCP) 
          was carried out for comparison.  In the dietary study, a dose-
          related weight loss occurred and acute clinical signs of toxicity 
          were observed on days 2 and 3 of treatment. 

          Behaviour - In a study of rats trained and evaluated in standard 
          avoidance tests, the lowest behaviourally effective aldicarb dose 
          was found to be 0.266 mg/kg b.w. (i.p.) suggesting that the level 
          required to produce significant alteration in behaviour is close 
          to the fatal dose and unlikely to be achieved in suggested use 
          patterns. 

    2.1.8  Modifications of toxicity - Aldicarb showed no synergistic 
           effects when used in combination with a number of 
           organophosphorus pesticides. 

    2.2  TOXICOLOGY - MAN

    2.2.1 Absorption route - Aldicarb may be absorbed from the 
          gastrointestinal tract; through moist, intact skin; and by 
          inhalation of dust. 

    2.2.2 Dangerous doses

          Single - The lowest lethal dose of aldicarb is unknown.  However, 
          human volunteer studies indicate that an oral dose of 0.1 mg/kg 
          b.w. will induce mild, transient clinical signs of toxicity, 0.26 
          mg produced acute poisoning requiring atropine treatment. 

          Repeated - No published information available.

    2.2.3 Observations of occupationally exposed workers - There has been 
          only one reported fatality involving aldicarb since its 
          introduction.  A field worker in California became ill after a 
          day's work in fields treated with aldicarb and an organophosphate 
          pesticide; he died en route to the hospital. 

          Between 1966 and 1982 over 108 incidences of confirmed and/or 
          suspected aldicarb poisonings were reported in the literature.  

          Illnesses resulting from exposure during loading, application and 
          handling of treated plants and soils were the result of gross 
          misuse of the product.  Carelessness, failure to wear protective 
          clothing or premature entrance into the treated areas were the 
          causes cited in most incidents.  Most cases involved systemic 
          illness, some with skin or eye irritation. The signs and symptoms 
          were cholinergic and recovery was rapid when the symptomatic 
          patients vere treated with atropine.  Blood cholinesterase was 
          depressed and toxic degradation products were detected in urine.  
          There were no reports of chronic effects. 

    2.2.4 Observations on exposure of the general public - See section 
          2.2.6. With good agricultural practices exposure of the general 
          public to harmful quantities of aldicarb is unlikely. 

    2.2.5 Observations of volunteers - Male volunteers were given an 
          aqueous solution of aldicarb orally at dose levels of 0.025, 
          0.05, 0.1, and 0.25 mg/kg b.w. Acute signs of toxicity were 
          observed at the two highest doses one hour after administration, 
          blood cholinesterase activity was depressed at all dose levels.  
          The clinical and cholinesterase effects diminished within six 
          hours of atropine treatment. Approximately 10% of the dose was 
          excreted in the urine within eight hours of administration, toxic 
          residues were present. 

    2.2.6 Reported mishaps - A report of two episodes of aldicarb poisoning 
          a year apart, in a small community in Nebraska, United States of 
          America, demonstrates the difficulties encountered in successful 
          diagnosis and etiologic investigation.  Each incident of 
          poisoning immediately followed ingestion of locally grown 
          hydroponic cucumbers.  Although collectively the clinical signs 
          and symptoms were typically cholinergic, their similarity to 
          those of influenza and food allergy reaction led to incorrect 
          diagnoses in some cases.  Neither vomitus nor urine were analysed 
          for toxicity potential or metabolite content.  Also, although the 
          rapid onset and recovery patterns suggested an anticholinesterase 
          agent, the time lapse between onset of illness and blood analysis 
          precluded finding cholinesterase depression.  It was this absence 
          of cholinesterase depression in a total review of clinical 
          evidence that eventually indicated carbamate involvement.  The 
          suspect cucumbers had been either completely consumed or the 
          remaining portions were too small and aged to permit specific 
          identification.  However, aldicarb was found in the water and 
          gravel (1.8 mg/l and 0.6 mg/kg respectively), of the hydroponic 
          system, and in cucumbers (6.6-0.7 mg/kg), produced in that 
          system.  The contamination was deemed to be accidental and 
          represents a gross misuse of the product. 

    2.3  TOXICITY TO NON-MAMMALIAN SPECIES


    2.3.1 Fish - Toxic to fish.

          LC50:  (24 h) Channel catfish, 1.6 mg/l
                     (96 h) Rainbow trout, 8.8 mg/l

          The sequence of toxic signs is hyperactivity, lethargy, body 
          paralysis, scoliosis, loss of equilibrium, opercular and mouth 
          paralysis followed by death. 

    2.3.2 Birds - Toxic to birds.

          Oral LD50:  Peking duck,     3.4 mg/kg b.w.
                      Japanese quail,  6.0 mg/kg b.w.
                      Domestic hen,    9.0 mg/kg b.w.
                      Pigeon,         12.5 mg/kg b.w.
                      Pheasant,       15.2 mg/kg b.w.

          Dietary LD50:  Bob-white quail, 2400 mg/kg diet of seven days 
          duration. 

    3.   FOR REGULATORY AUTHORITIES - RECOMMENDATIONS ON REGUIATION OF 
         COMPOUND 

    3.1  RECOMMENDED RESTRICTIONS ON AVAIIABILITY (For definition of 
         categories, see the Introduction to Data Sheets) - Only granular 
         formulations are available.  All formulations are placed in 
         Category 2. 

    3.2  TRANSPORTATION AND STORAGE

         Formulations in Category 2 - Should be transported or stored in 
         clearly labelled containers and away from containers of food and 
         drink.  Storage should be under lock and key and secure from 
         access by unauthorized persons and children. 

    3.3  HANDLING

         Fomulations in Category 2 - Protective clothing (see part 4) 
         should be provided for workers.  Adequate washing facilities 
         should be available close at hand.  Eating, drinking and smoking
         should be prohibited during handling and before washing after
         handling. 

    3.4  DISPOSAL OF CONTAINER - Do not reuse containers.  Container must 
         be either burned or buried below topsoil.  Care must be taken to 
         avoid subsequent contamination of water sources. 

    3.5  SELECTION, TRAINING AND MEDICAL SUPERVISION OF WORKERS

         Formulations in Category 2 - Pre-employment medical examination 

         for workers desirable.  Workers suffering from active hepatic or 
         renal diseases should be excluded from contact.  Pre-employment 
         and periodic cholinesterase tests for workers desirable.  Training 
         of workers in techniques to avoid contact is essential. 

    3.6  ADDITIONAL REGULATIONS RECOMMENDED IF DISTRIBUTED BY AIRCRAFT -
         Not to be applied by aircraft. 

    3.7  LABELLING - "DANGER - POISON" (skull and cross bones insignia).

         Precautionary statements - Hazard to Humans and Domestic Animals. 
         - Poisonous if swallowed.  May be fatal or harmful by skin or eye 
         contact or by breathing dust.  Rapidly absorbed through skin or 
         eyes.  Do not get on skin or eyes.  Do not breathe dust.  Antidote 
         is atropine sulfate.  See statement of practical treatment and 
         other detailed warnings on the package.  Read the entire label 
         before using this pesticide. Wear long-sleeved clothing and 
         protective gloves when handling.  Wash hands and face before 
         eating or smoking.  Bathe at the end of work day, washing entire 
         body and hair with soap and water.  Change contaminated clothing 
         daily and wash in strong washing soda solution and rinse 
         thoroughly before reusing. 

    3.8  RESIDUES IN FOOD - Maximum residue levels have been recommended by 
         the joint FAO/WHO Meeting on Pesticide Residues. 

    4.   PREVENTION OF POISONING IN MAN AND EMERGENCY AID

    4.1  PRECAUTIONS IN USE

    4.1.1 General - Aldicarb is a carbamate insecticide of extremely high 
          acute toxicity which is quickly metabolized and therefore acts 
          only as an acute poison.  It can be absorbed by inhalation of the 
          dust and also through the intact skin. It is important that 
          formulations be washed immediately from the skin and eyes. 

    4.1.2 Manufacture and formulation - Aldicarb is available only as a 
          formulated product.  The manufacturer does not sell concentrates 
          for formulation. 

    4.1.3 Applicators - When opening the container, care should be taken to 
          avoid contact with the mouth, eyes and skin.  If necessary a 
          facial visor and gloves should be worn.  The applicator should 
          avoid contact with the mouth, eyes and skin.  Granules must be 
          washed immediately from the skin or eyes with large quantities of 
          water.   Before eating, drinking or smoking, hands and other 
          exposed skin should be washed. 

    4.1.4 Other associated workers - Persons exposed to aldicarb and 
          associated with its application should observe the precautions 

          described in 4.1.3 under "applicators". 

    4.1.5 Other populations likely to be affected - With correct use in 
          agriculture, the general population should not be exposed to 
          hazardous amounts of aldicarb. 

    4.2  ENTRY OF PERSONS INTO TREATED AREAS - No re-entry restrictions 
         have been established for agricultural uses. 

    4.3  DISPOSAL OF SPILLAGE - If a container is broken, handle with 
         rubber gloves.  Do not get dust or granules on the skin or in the 
         eyes.  Do not breathe dust.  Sweep up and bury any small spills or 
         excess aldicarb formulation at least 45 cm deep in the soil 
         isolated from water supplies and food crops.  Spillage of aldicarb 
         formulations should be removed by cleaning up granules, washing 
         with 5% sodium hydroxide solution and then rinsing with large 
         quantities of water. 

    4.4  EMERGENCY AID

    4.4.1 Early symptoms of poisoning - Early symptoms may include 
          excessive sweating, headache, weakness, nausea, vomiting, stomach 
          pains, salivation, tightness of the chest, blurred vision, 
          slurred speech and muscle twitching. 

    4.4.2 Treatment before a person is seen by a physician, if these 
          symptoms appear following exposure - The person should stop work 
          immediately, remove contaminated clothing, 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. 

    5.   FOR MEDICAL AND LABORATORY PERSONNEL

    5.1  MEDICAL DIAGNOSIS AND TREATMENT IN CASES OF POISONING

    5.1.1 General information - Aldicarb is a carbamate insecticide of 
          extremely high toxicity.  It is absorbed from the 
          gastrointestinal tract and through the intact skin.  Its mode of 
          action is by reversibly inhibiting acetyl cholinesterase.  
          Erythrocyte cholinesterase is more inhibited than plasma 
          cholinesterase.  Symptoms of poisoning are short lasting and in 
          the case of occupational overexposure, occur without delay at a 
          dose well below the fatal dose.  Because of its rapid metabolism 
          and excretion it does not accumulate in the tissues. 

    5.1.2 Symptoms and signs - Symptoms of poisoning include excessive 
          sweating, headache, chest tightness, weakness, nausea, vomiting, 
          stomach pains, salivation, blurred vision, slurred speech, and 
          muscle twitching. Paraesthesia and mild skin reaction have also 

          been reported. 

    5.1.3 Laboratory - Because aldicarb is a reversible inhibitor of 
          cholinesterase, measurements of cholinesterase activity should be 
          made by a method which minimizes the reactivation of inhibited 
          enzyme. 

          Erythrocyte cholinesterase determination is more informative than 
          measuring either plasma or whole blood cholinesterase, but the 
          enzyme will only be inhibited for a short time (few hours) after 
          exposure.  The presence of metabolites of aldicarb in urine is 
          also indicative of exposure. 

    5.1.4 Treatment and information for physician - This product is a 
          carbamate pesticide containing 2-methyl-2-
          (methylthio)propionaldehyde O-(methyl-carbamoyl)oxime.  It is a 
          spontaneously reversible cholinesterase inhibitor causing 
          parasympathetic nerve stimulation.  Preferred treatment of 
          poisoning in adults is atropine sulfate given intravenously.  As 
          much as 2-4 mg may be needed every 10-12 minutes until the 
          patient is fully atropinized.  Dosage for children is 
          appropriately reduced.  Atropinization should be maintained for 
          12 hours by intramuscular administration of atropine in lower 
          doses given at appropriate time intervals.  Do not administer 
          opiates or cholinesterase inhibiting drugs.  Artificial 
          respiration or oxygen may be necessary. Observe the patient 
          continuously for at least 24 hours.  Allow no further exposure to 
          any cholinesterase inhibitors until cholinesterase level is 
          normal by blood test. 

    5.1.5 Prognosis - If the acute effects are survived, the chances of 
          complete recovery are very good. 

    5.1.6 References of previously reported cases

          Goses, E. A. et al. (1980) American Jour. Epidemiology, 111 (2), 
          254.  Peoples, S. A. et al. (1978) Calif. Dept. Food Agric. Sci.
          Rep., pp. 321-324 

    5.2  SURVEILLANCE TESTS - Due to the rapid reactivation of inhibited 
         enzyme, determination of blood cholinesterase level is of little 
         if any practical value in detemining when workers should be 
         withdrawn to prevent overexposure.  Minor complaints, such as 
         headache and nausea, cause the worker to stop work and thus 
         prevent further overexposure.  The worker quickly recovers, 
         particularly if appropriate decontamination procedures are 
         followed. 

    5.3  LABORATORY METHODS


    5.3.1 Detection and assay of compound - Aaronson, M. J. et al. (1980) 
          Jour. Food Safety, 2, 171.  Davies, R. D. (1979) Jour. of 
          Chromatography, 1970, 453.  Galoux, M. (1979) Jour. of 
          Chromatography, 177, 245.  Johnson, D. P. et al. (1966) J. Assoc.
          Off. Anal. Chem., 49, 399.  Lee, D. F. & Rougham, J. A. (1971) 
          Analyst (London), 96, 798. Maitland, J. C. et al. (1968) J. 
          Agric. Food Chem., 16, 549.  Romine, R. R. et al. (1973) Anal.
          Methods Pestic. Plant Growth Regul., 7. 143.  Tewari, S. N. & 
          Singh, R. (1979) Jour. of Chromatography, 1972, 528.  Tewari, S. 
          N. & Singh, R. (1979) Fresenius Z. Anal. Chem., 294, 287.
          Woodham, D. W. et al. (1973) J. Agric. Food Chem., 21 (4), 604. 

    5.3.2 Other tests in cases of poisoning - Cholinesterase levels in 
          blood are unreliable as a routine test to detect poisoning by 
          aldicarb.  However, shortly after absorption, inhibition of 
          erythrocyte cholinesterase may be demonstrated by an appropriate 
          method.  Plasma cholinesterase activity: Ellman, G. L. et al. 
          (1969) Biochem. Pharmacol., 7, 88. 

          Whole blood cholinesterase activity: Fleischer, J. et al. (1956) 
          Arch. Indust. Hyg., 14, 510; Wilhelm, K. et al. (1973) Bull.
          Wld Hlth Orig., 48, 235 




    Note: This data sheet was drafted in the Bureau of Chemical Standards, 
         Environmental Health Directorate, Health and Welfare, Canada, and 
         subsequently underwent medical, scientific, and industrial review. 

See Also:
        Aldicarb (EHC 121, 1991)
        Aldicarb (IARC Summary & Evaluation, Volume 53, 1991)
        Aldicarb (ICSC)