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    Primary use:    Insecticide
    Secondary use:  Nematocide
    Chemical Group: Carbamate
    Date issued:

         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
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    without the agreement of the       l'autorisation de l'Organisation
    Food and Agriculture               des Nations Unies pour
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    Nations or of the World Health     ou de l'Organisation Mondiale de
    Organization.                      la Sant.


    1.1  COMMON NAME: Carbofuran (ISO, BSI and ANSI)

    1.1.1 Identity:

          IUPAC: 2,3-dihydro-2,2-dimethylbenzofuran-7-yl methylcarbamate

          CAS No. 1: 2,3-dihydro-2,2-dimethyl-7-benzofuranyl 
          CAS Reg. No.: 1563-66-2 

          Molecular formula: C12H15NO3

          Molecular weight: 221.3

          Structural formula:
    Chemical Structure

    1.1.2 Synonyms: Bay 70143; Carbofuran; CuraterrR; ENT 27,164;   
          FMC 10242; FuradanR; Niagara 10242R; YaltoxiR. 

    1.2 SYNOPSIS: Carbofuran is a broad spectrum, non-cumulative carbamate 
        insecticide; a cholinesterase inhibitor with contact and stomach 
        action and highly toxic to mammals.  It is a systemic with no 
        phytotoxic action. 


    1.3.1 Physical characteristics - Carbofuran is a colourless (white) 
          crystalline solid.  It has a melting point of 150-152C, a 
          density (d204) of 1.180. The technical material contains 98.8% 
          active ingredient.  It is non-corrosive and non-flammable. 

    1.3.2 Solubility - Water                        700  mg/l,  25C
                       1-methyl-2-pyrrolidione      300  g/kg,  25C
                       Dimethylformamide            270  g/kg,  25C
                       Dimethylsufoxide             250  g/kg,  25C
                       Acetone                      150  g/kg,  25C
                       Acetonitrile                 140  g/kg,  25C
                       Methylene chloride           120  g/kg,  25C
                       Cyclohexanone                 90  g/kg,  25C
                       Benzene                       40  g/kg,  25C
                       Ethanol                       40  g/kg,  25C

          Carbofuran is virtually insoluble in conventional solvents of 
          agricultural formulations. 

    1.3.3 Stability - It is stable under neutral or acidic conditions but 
          unstable in alkaline media. 

    1.3.4 Vapour pressure - 2.66 x 10-6 kPa (2 x 10-5 mmHg), 33C

                            1.33 x 10-5 kPa (1 x 10-4 mmHg), 50C


    1.4.1 Common formulations - Flowables (100, 120, 300, 350, 480 g 
          a.i./l) granules (20, 30, 50, 100 and 150 g a.i./kg). 

    1.4.2 Pests controlled - Carbofuran is effective against a wide range 
          of foliar-feeding and soil pests including nematodes, corn 
          rootworm, rice water weevil, wireworms, sugar-cane borer, alfalfa 

          weevil, alfalfa snout beetle, armyworms, European corn borer, 
          flea beetle, aphids, thrips, hornworms and others. 

    1.4.3 Use pattern - Carbofuran may be applied to alfalfa, corn, 
          peanuts, peppers, strawberries, tobacco, bananas, sorghum, 
          potatoes, cottonwood trees, sugar-cane, and rice.  It may be 
          applied to foliage at 0.25-1.0 kg a.i./ha; in a 7 inch band or in 
          seed furrows at planting time at 0.5-4.0 kg/ha; and, as a soil 
          treatment incorporated into the top 1 inch of soil. On rice, 
          apply before or within 21 days after flooding.  It is compatible 
          with other non-alkaline pesticides and fertilizers. 

    1.4.4 Unintended effects - Carbofuran is not phytotoxic when used as 

    1.5  PUBLIC HEALTH USE - No recommended use.

    1.6  HOUSEHOLD USE - No recommended use.



    2.1.1 Absorption - Carbofuran may be absorbed from the gastrointestinal 
          tract; minimally through the intact skin; and, by inhalation of 
          spray mists or dusts. 

    2.1.2 Mode of action - Carbofuran is a reversible, direct inhibitor of 
          cholinesterases through carbamoylation of the esteratic site of 
          the enzyme.  Accumulation of acetylcholine at nerve synapses and 
          myoneural junctions causes the toxic effects.  The carbamoylated 
          enzyme undergoes spontaneous and rapid reactivation.  Carbofuran 
          and its ester metabolites are active. 

    2.1.3 Excretion products - The metabolism and excretion of carbofuran 
          have been well studied in rats, mice and lactating cows.  The per 
          oral dose is rapidly absorbed, degraded and eliminated.  In 
          mammals mixed function oxidases are chiefly responsible for 
          metabolism; 3-hydroxycarbofuran and 3-ketocarbofuran are the most 
          common carbamate metabolites. 3-Hydroxy-N-hydroxycarbofuran is 
          also produced to some extent in all the test animals except the 
          mouse.  Hydrolysis of the carbamoyl ester bond also occurs, 
          producing 3-ketocarbofuran phenol followed by carbofuran phenol 
          and 3-hydroxyphenol.  These degradation products are primarily 
          excreted as conjugates of glucuronic acid and sulfate. 

          In rats, 87% of the radioactivity from carbonyl 14C labelled 
          carbofuran (p.o.) is eliminated within 48 hours, 45% as C02 in 
          expired air, 38% in urine and 4% in faeces.  When ring-labelled 
          carbofuran is fed to cows and rats, nearly all of the 14C is 

          eliminated in urine (92% in 32 hours), none is exhaled and less 
          than 3% is found in faeces.  In milk cows, less than 3% is found 
          in milk following per oral and fistula administration. 

    2.1.4 Toxicity, single dose

          Oral LD50:

          Rat  (M,  F)               8.8   mg/kg  bw   (technical)
          Rat (weanling male)        8.06  mg/kg  bw   (technical)
          Rat (weanling female)      5.91  mg/kg  bw   (technical)
          Dog                      +15.38  mg/kg  bw   (technical)
          Mouse                     14.4   mg/kg  bw   (technical)
          Cat                    2.5-3.5   mg/kg  bw   (technical)
          Rabbit                     7.5   mg/kg  bw   (technical)
          Guinea-pig                 9.2   mg/kg  bw   (technical)

          Dermal LD50:

          Rat                      2 000   mg/kg  bw*  (technical)
          Rabbit                   2 000   mg/kg  bw*  (technical)

          Inhalation LC50:
          1 hour

          Rat   (M)                0.091-0.108    mg/l  (dust)
          Rat   (F)                      0.080    mg/l  (dust)

          4   hours

          Rat   (M,  F)                  0.120    mg/l  (50 W.P.)
          Rat   (M,  F)                  0.085    mg/l  (80 W.P.)
          Dog   (M)                      0.052    mg/l  (50 W.P.)
          Guinea-pig   (M, F)            0.053    mg/l  (75 W.P. aerosol)
          Guinea-pig   (M, F)            0.043    mg/l  (75 W.P. dust)

          I.P. LD50:

          Rat   (M)                      8.2      mg/kg  bw  (75% W.P.)
          Rat   (F)                      2.8      mg/kg  bw  (75% W.P.)
          * Manufacturer provided information.

          In an acute intubation study using female rats, it was found that 
          brain cholinesterase was more sensitive to carbofuran than plasma 
          and erythrocyte cholinesterase respectively. 

    2.1.5 Toxicity, repeated doses

          Oral: Groups of female rats were administered carbofuran by 

          gavage at a dosage level of 1.0 mg/kg/day for 28 days.  
          Cholinesterase activity was monitored at 1, 2, 6 and 24 hours 
          after administration on days 14 and 28.  Brain cholinesterase 
          activity was the most affected, reaching maximal depression by 
          six hours on both testing days; erythrocyte activity was least 
          affected.  The treatment activity values appeared comparable to 
          control values at 24 hours post treatment.  Similar results were 
          observed in a 90-day intubation study with male and female rats 
          receiving dosage levels of 0, 0.1, 0.3, 1.0 and 3.0 mg/kg bw/day.  
          In this study, maximum erythrocyte and plasma activity 
          depressions at the highest dosage level (3.0 mg/kg bw/day) 
          occurred within one hour of administration after three weeks of 
          treatment.  Normal activity was re-established within 24 hours.  
          No changes were observed at levels of 0.3  mg/kg bw or below.  
          These studies demonstrated the rapid and transient nature of 
          in vivo cholinesterase depression by carbofuran. 

          Dermal: Groups of male and female rabbits received dermal 
          applications of carbofuran 50% wettable powder at dosage levels 
          of 0, 0.5, 1.0 and 2.0 mg/kg bw/day for 20 successive days.  
          Mortality appeared to be dose-related.  Decreased body weights, 
          inflammatory skin lesions and decreased general activity were 
          observed in all treatment groups during the test period.  The 
          lesions disappeared within five days of cessation of treatment 
          and there were no treatment-related biochemical or 
          histopathological changes. 

          Inhalation: Groups of mice and female guinea-pigs were exposed to 
          carbofuran aerosol formulation at a concentration level of 0.01 
          mg/m3 (air) for four hours a day, five days a week for three 
          weeks.  There were no compound-related changes in mortality 
          rates, behaviour, haematology, biochemistry or histopathology. 

          Sensitization: No sensitization reactions were produced in 
          guinea-pigs following challenge doses administered two weeks 
          after daily subcutaneous injections of carbofuran. 

          Cumulation of compound:  Carbofuran is not accumulated in body 

          Cumulation of effect: Carbofuran did not produce any cumulation 
          of effect in several studies with multiple dosing. 

    2.1.6 Dietary studies

          Short-term:  Groups of male and female rats were offered varying 
          levels of carbofuran in the diet for 90 days.  Initially, 
          carbofuran was incorporated into the diet at dosages of 0, 0.1, 
          0.4, 2.0, 10 and 25 mg/kg diet.  Subsequently, the dietary levels 
          of carbofuran were progressively increased on days 22-35, 36-49 

          and 50-90 to yield final concentrations of 0, 1.6, 6.4, 32, 160 
          and 1600 mg/kg diet.  No mortality occurred during the study 
          period.  Intermittent tremors and episodes of incontinence were 
          observed among females receiving the 1600 mg/kg diet.  Depressed 
          growth rates were noted at dietary levels of 100 mg/kg and above 
          and persisted to the end of the test period at levels of 160, 400 
          and 1600 mg/kg diet.  However, this finding appeared to be 
          related to poor diet palatability.  Haematological and urological 
          values were unaffected and gross and microscopic pathological 
          findings were comparable. Cholinesterase activity was not 
          monitored.  No effects were observed among the three lowest 
          dosage groups. 

          A 14-day feeding study was conducted with carbofuran using 
          groups of male and female rabbits.  Dietary concentrations of 0, 
          70, 210 and 700 ppm did not produce mortality or untoward 
          behavioural effects.  Body weight reductions were observed within 
          the group receiving the 700 ppm diet. 

          Carbofuran was administered at dosages of 0, 0.025, 0.25, 1.25, 
          2.5 and 5.0 mg/kg/day by gelatin capsule to groups of male and 
          female dogs for 93 continuous days.  Clinical signs of 
          acetylcholine poisoning were observed within the groups receiving 
          either 2.5 or 5.0 mg/kg/day.  Plasma and erythrocyte 
          cholinesterase activities were within normal limits when 
          monitored four hours before and one hour after daily dosing.  At 
          5.0 mg/kg, some depression of plasma and erythrocyte 
          cholinesterase activities were observed when samples were drawn
          15, 30, 45 and 60 minutes following carbofuran administration 
          on day 72 and after extended dosing, again on day 113. 

          Long-term: In a two year study, groups of male and female rats 
          were offered diets containing 0, 10, 20 or 100 ppm of carbofuran.  
          Males exposed to 100 ppm exhibited slightly lower group mean 
          body weights.  Depressed plasma, erythrocyte and brain 
          cholinesterase activity values were noted for animals receiving 
          the 100 ppm diet; no effects were observed at the 10 or 20 ppm 
          levels.  There were no treatment-related effects on mortality, 
          food consumption, ophthalmology, haematology and clinical 
          chemistry parameters, urinalysis and histopathology.  The no-
          effect level (NOEL) was considered to be 20 ppm. 

          Groups of male and female mice were exposed to carbofuran at 
          dietary concentrations of 0, 20, 125 and 500 ppm for two years.  
          Decreased body weights were noted at the 500 ppm level during 
          weeks 1-65 for males and weeks 1-78 for females.  However, this 
          effect was not observed at study termination.  Brain 
          cholinesterase activity was depressed at the 6, 12 and 18 month 
          intervals and at termination for animals exposed to 125 or 500 
          ppm carbofuran.  No treatment-related effects were reported for 

          mortality, haematology and clinical chemistry parameters, 
          urinalysis and histopathology.  The no-effect level (NOEL) was 
          considered to be 20 ppm. 

          Carbofuran was administered to groups of male and female beagle 
          dogs via dietary inclusion for two years.  Initially, carbofuran 
          was incorporated into the diet at concentrations of 0, 1, 10, 50 
          and 100 ppm and a level to establish the maximum tolerated dose 
          (100 ppm for days 1-14 and 200 ppm during days 15-267).  The 50
          ppm diet was increased to contain 100 ppm of carbofuran on day 
          143 while all of the other dietary concentrations were fortified 
          on day 268 yielding dietary levels of 0, 2, 20, 100, 200 and 400
          ppm through termination.  Mortality was reported for one female 
          exposed to the 400 ppm diet; three males in the 400 ppm dietary 
          group were sacrificed in extremis after at least 518 days on 
          study.  At 100 ppm, occasional coughing and gagging were 
          observed; at 200 and 400 ppm, more severe signs of cholinergic 
          toxicity were observed daily.  Reduced mean body weights were 
          also exhibited at the 400 ppm level. There were no treatment-
          related effects associated with food consumption, haematology and 
          clinical chemistry parameters (cholinesterase activity was not 
          monitored), urinalysis and histopathology.  The no-effect level 
          (NOEL) was considered to be 50 ppm. 

    2.1.7 Supplementary studies of toxicity

          Carcinogenicity: In the long-term rat and mouse dietary studies 
          described in section 2.1.6, carbofuran did not demonstrate any 
          carcinogenic or tumorigenic potential at dietary levels up to and 
          including 100 ppm for rats and 500 ppm for mice.  No evidence of 
          carcinogenicity or tumorigenicity was observed in the dog at 
          dietary levels up to 400 ppm. 

          Teratogenicity: Carbofuran was administered daily by gavage to 
          groups of pregnant female rats at dosages of 0 (corn oil only), 
          0.25, 0.50 and 1.20 mg/kg/day on gestation days 6 through 15.  
          Caesarean sections were performed on all females on day 20 of 
          presumed gestation.  Foetuses were examined for soft tissue and 
          skeletal abnormalities.  Survival was 100% in all groups.  All 
          maternal and foetal parameters were comparable among the groups.  
          Carbofuran was not teratogenic when administered by gavage at a 
          dosage of 1.20 mg/kg/day. 

          Groups of pregnant female rabbits were administered carbofuran at 
          dosage levels of 0, 0.12, 0.50 and 2.0 mg/kg/day by gavage during 
          gestation days 6 through 18.  On gestation day 29, all surviving 
          dams were subjected to a Caesarean section and the foetuses were 
          examined for skeletal and soft tissue abnormalities. At the 2.0 
          mg/kg/day dosage group, one dam died on gestation day 11.  
          Depressed mean maternal body weight gains were also reported for

          the 2.0 mg/kg/day dosage group.  All other maternal and foetal
          parameters were comparable among the groups.  There was no 
          evidence of teratogenicity in this study at a dosage of 2.0 

          A teratology and postnatal dietary study was conducted with 
          carbofuran in the rat.  Carbofuran was incorporated into the diet 
          at concentrations of 0, 20, 60 and 160 ppm and administered to 
          pregnant female rats only during gestation days 6 through 19.  On 
          gestation day 20, approximately half of the dams from each dosage 
          group were submitted to Caesarean section and the foetuses were 
          examined for skeletal and visceral abnormalities.  The remaining 
          dams were allowed to deliver and care for the pups for 21 
          post-partum days.  At the end of the lactation period (post-
          partum day 21), the dams and pups were submitted to necropsy.
          Mean food consumption was slightly reduced in the 160 ppm group
          during the treatment period.  Apparent dose-related mean maternal
          body weight losses occurred in the 60 and 160 ppm groups during 
          the first two days of treatment (gestation days 6 and 7) and
          during the first 7 days of lactation. 

          A statistically significant (P < 0.05) reduction in mean pup body 
          weight for the 160 ppm group animals was reported on lactation 
          days 0, 4, 7, 14 and 21.  Examination of the foetuses and pups 
          did not reveal any teratogenic response in this study at a 
          dietary concentration of 160 ppm. 

          Mutagenicity: A dominant lethal test was conducted with groups 
          of male mice receiving intraperitoneal injections of carbofuran 
          suspended in corn oil at dosages of 0.25 and 0.50 mg/kg.  A 
          vehicle control group received corn oil only while a positive 
          control group was administered 100 mg/kg of methyl methane-
          sulfonate by the same route. Immediately following treatment, 
          each male was housed with three untreated, virgin females and 
          allowed to mate. This procedure was repeated weekly with a new 
          group of untreated, virgin females for a total of six consecutive 
          weeks.  Mated females were sacrificed in mid-gestation for 
          uterine examination.  Carbofuran did not affect mating ability, 
          frequency of pregnancy, the incidence of resorptions, 
          preimplantation losses or the number of embryos per dam.  
          Therefore, carbofuran was not considered to be mutagenic. 
          Carbofuran was evaluated for its mutagenic potential in a mitotic 
          recombination assay using Saccharomyces cervisiae D3.  
          Weight/volume concentrations of 0.1, 0.5, 1.0 and 5.0% were 
          tested in the presence and absence of metabolic activation; 
          1,2,3,4-diepoxybutane (positive control) and a negative control 
          were also tested.  Carbofuran was considered to be non-mutagenic 
          in this assay since it did not cause an increase in the number of 
          absolute or relative mitotic recombinants.  An Ames assay was 

          conducted with carbofuran using five tester strains of Salmonella 
          typhimurium.  Two trials were conducted with six concentrations 
          each, ranging between 1 and 1000 g/plate and 10 to 5000 
          g/plate, both in the presence and absence of metabolic 
          activation.  Positive controls (2-anthramine and N-methyl-N'-
          nitro-N-nitrosoguanidine) and a negative control were also 
          tested.  There was no increase in the number of revertants per 
          plate for any of the tester strains in the presence or absence of 
          metabolic activation.  These results indicate that carbofuran was 
          not considered to be mutagenic. 
          Escherichia coli WP2 was used in a reverse mutation assay with 
          carbofuran. Concentrations ranging between 1 and 1000 g/plate 
          and 10 to 5000 g/plate were tested in the presence and absence 
          of metabolic activation in two trials.  Positive controls (2-
          anthramine, AF-2 and N-methyl-N'-nitrosoguanidine) and a negative 
          control were also evaluated.  Carbofuran did not cause an 
          increase in the number of revertants in the presence or absence 
          of metabolic activation and was not considered to be mutagenic. 
          DNA repair assays were conducted using DNA repair-proficient and 
          repair-deficient strains of Bacillus subtilis (H17 and M45, 
          respectively) and Escherichia coli (W3110 and p3478, 
          respectively) to evaluate the mutagenic and genotoxic potentials 
          of carbofuran.  Concentrations of 0.01, 0.10, 1.0 and 5.0 mg/disc 
          were used in both bacterial assays.  Chloramphenicol was used as 
          the negative control, while 1-phenyl-3,3-dimethyltriazine served 
          as the positive control.  Carbofuran was not considered to be 
          mutagenic or genotoxic in either bacterial assay. 

          Carbofuran was tested to assess its ability to induce unscheduled 
          DNA synthesis in cultured human fibroblast cells (WI-38).
          Concentrations of 0.1, 1.0, 10, 100 and 1000 g carbofuran/ml 
          solvent were evaluated in the presence and absence of metabolic
          activation.  In addition to a negative (solvent) control, 
          dimethylnitrosamine and 4-nitroquinoline N-oxide were used as 
          positive contols in the presence and absence of metabolic 
          activation, respectively.  The rate of unscheduled DNA synthesis 
          was not increased in the presence or absence of metabolic 
          activation by carbofuran. 

          Reproduction: Groups of male and female rats were maintained on 
          diets containing concentrations of 0, 20 and 100 ppm of 
          carbofuran for three generations (two litters per generation).  
          Reproductive and general toxicological parameters were monitored.  
          Mean parental body weights and food consumption were consistently 
          lower within the 100 ppm dietary group.  Reduced survival of F1a, 
          F2a and F3a litters on lactation day 4 and consistently lower pup 
          body weights in all litters occurred within the 100 ppm group. 

          Dehydration was noted among some of the 100 ppm group F3a and F3b 

          Fertility, gestation time, general behaviour, appearance and 
          survival (parents only) were unaffected.  At the completion of 
          each generation, all parental animals and pups from the F2b and 
          F3b litters were sacrificed and necropsied.  No compound-related 
          gross or microscopic changes were reported.  Carbofuran did not 
          produce any adverse effects on reproduction.  The no-effect level 
          (NOEL) in this study was 20 ppm.  A one-generation reproduction 
          study in beagle dogs was conducted with carbofuran at dietary 
          levels of 0, 20 and 50 ppm.  Natural mating was allowed during 
          the second oestrus cycle.  Survival, behaviour, body weights, 
          food consumption, oestrus cycles, mating performance and 
          gestation and lactation parameters were monitored for the 
          parental animals.  At birth, litter size, pup viability, 
          survival, nursing ability, general behaviour and physical 
          appearance were reported for each litter.  Physical and 
          neurological examinations were also conducted on each of the pups 
          at birth.  After one week of age, the pups were examined by X-
          rays to evaluate skeletal structure and general development.  
          Gross pathological examinations were performed on one male and 
          female pup per litter. 
          Carbofuran did not affect reproductive performance.  There were 
          no adverse effects attributed to carbofuran in the parental 
          animals or progeny.  The no-effect level (NOEL) in this study was 
          50 ppm. 
          Neurotoxicity: Carbofuran was evaluated to determine its 
          potential to induce delayed neurotoxicity.  A group of mature 
          hens was orally administered 38.9 mg/kg (LD50) of carbofuran and 
          observed for signs of delayed neurotoxicity for 21 days.  A 
          positive control group received TOCP orally, at a dosage of 50 
          mg/kg.  The dosage and observation period were repeated in the 
          surviving birds since neurotoxicity was not observed during the 
          initial 21-day observation period.  The lack of neurotoxic effect 
          after the second administration and 21-day observation period 
          indicated that carbofuran does not induce delayed neurotoxicity. 

    2.1.8 Modification of toxicity - Equitoxic mixtures of carbofuran and 
          other anticholinesterase agents were administered orally to male 
          rats to determine if a potentiation effect on acute toxicity 
          would result.  The LD50 values were determined for carbofuran and 
          the other compounds (Systox, Guthion, Trithion, Ethion, 
          Phosphamidon, Dibrom, Diazinon, EPN, Delnau, Schradan, methyl 
          parathion, sevin, RE 5353 and Phosdrin).  The theoretical 
          additive LD50 value for each mixture was calculated and compared 
          to the value obtained in vivo.  The results of these trials 
          indicated that the acute oral toxicity of carbofuran was not 

          potentiated when administered in combination with other 
          anticholinesterase agents. 


    2.2.1 Absorption route - Carbofuran may be absorbed from the 
          gastrointestinal tract; through the intact skin;  and, by 
          inhalation of spraymist or dusts. 

    2.2.2 Dangerous doses

          Single: The acute oral LD50 is reported to be approximately 11 
          mg/kg bw, the dermal LD50 to be 10 000 mg/kg. The probable oral 
          lethal dose is reported to be 5-50 mg/kg bw. 

          Repeated: Not known; because of rapid metabolism it probably 
          differs little from the single dangerous dose. 

    2.2.3 Observations on occupationally exposed workers - Typical cases 
          involving blurred vision, nausea, excessive perspiration and a 
          sense of weakness have been reported among formulators and 
          applicators.  Uneventful recovery is reported to occur within a 
          few hours even without therapy but it was faster when atropine 
          was administered. 

    2.2.4 Observations on exposure of the general population - No 
          information available, if recommended agricultural practices are 
          followed, the general population will not be exposed to hazardous 
          amounts of carbofuran. 

    2.2.5 Observations on volunteers - No information available.

    2.2.6 Reported mishaps - In one episode, 142 boys and girls aged 13-16 
          were employed to remove tassles from corn the day after a field 
          had been erroneously sprayed with carbofuran (carbofuran is not 
          recommended for this purpose).  By early afternoon 74 teenagers 
          complained of symptoms of carbofuran poisoning, 40 of them were 
          treated with atropine, 28 remained in hospital for a few hours 
          and one patient remained overnight. The onset of symptoms was 
          rapid but mild, recovery was also rapid. 


    2.3.1 Fish - Carbofuran is very toxic to fish.

          LC50 (96 hours):  Bluegill        80  g/l
                            Yellow perch   147  g/l
                            Brown trout    280  g/l
                            Lake trout     164  g/l
                            Mosquito fish  300  g/l

                            Coho salmon    524  g/l
                            Steelhead      600  g/l

    2.3.2 Birds - Carbofuran is very toxic to birds and has been used as an 

          Oral LD50:  Domestic hen                6.0   mg/kg  bw
                      Bobwhite quail             5.04   mg/kg  bw
                      Ring-neck pheasant         4.15   mg/kg  bw
                      Japanese quail  (M)         1.9   mg/kg  bw
                      Japanese quail  (F)         1.7   mg/kg  bw
                      House sparrow               1.3   mg/kg  bw
                      Mallard duck 36 hours old   0.37  mg/kg  bw
                                    1 week old    0.63  mg/kg  bw
                                    4 weeks old   0.51  mg/kg  bw
                                    6 months old  0.42  mg/kg  bw
                      Quella                      0.42  mg/kg  bw
                      Red-wing blackbird          0.42  mg/kg  bw

     Dermal LD50:     House sparrow             100     mg/kg  bw
                      Quella                    100     mg/kg  bw

    Dietary:  The cumulative LD50 (10 days for pheasants) was 960 mg a.i.
    (as 10% granular)/kg of diet.

    2.3.3 Other species - Carbofuran is highly toxic to a variety of 
          beneficial invertebrates, the LD50 for honeybees is 0.16 g/bee. 



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

         Liquid formulations of 4% and over, Category 2

         Other liquid formulations, Category 3

         Solid formulations of 16% and over, Category 2

         Other solid formulations, Category 3


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

    3.3  HANDLING

         All formulations - Full protective clothing (see paragraph 4.3 in 
         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 the 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.  Special account should 
         be taken of the workers' mental ability to comprehend and follow 
         instructions. Training of workers in techniques to avoid contact 
         is 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 and be located 
         well away from the dropping zone. 

    3.7  LABELLING

         All formulations - "DANGER - POISON" (skull and cross-bones 
         insignia).  Carbofuran is a carbamate compound which inhibits 
         cholinesterase enzymes.  It is extremely toxic.  Contact with the 
         skin, inhalation of dust or spray, or swallowing should be 
         avoided.  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 and repeated doses may be necessary. Artificial 
         respiration may be needed. 


         Maximum residue levels - Maximum residue levels have been 
         recommended by the Joint FAO/WHO Meeting on Pesticides Residues. 



    4.1.1 General - Carbofuran is a carbamate pesticide of very high 
          toxicity.  It is an acute poison, absorbed by inhalation of dust 
          and spray mist; from the gastrointestinal tract; and, to a lesser 
          extent, through the intact skin.  Most formulations should be 
          handled by trained personnel wearing suitable protective 

    4.1.2 Manufacture and formulation - TLV - (ACGIH) 2.5 mg/m3.  
          Formulation should not be attempted without advice from the 
          manufacturer.  Although volatility is low, vapour and dusts 
          should be controlled preferably by mechanical means.  Protective 
          equipment for the skin and respiratory protection is necessary. 

    4.1.3 Mixers and applicators - When opening the container and when 
          mixing, protective impermeable boots, clean overalls, gloves and 
          a respirator should be worn.  Beware of possible positive 
          pressure build-up, especially with liquid formulations in metal 
          containers with inverted pour spouts.  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, 
          protective clothing, boots and gloves.  The applicator should 
          avoid working in spray mist and avoid contact with the mouth.  
          Particular care is needed when equipment is being washed after 
          use.  All protective clothing should be washed immediately after 
          use, including the inside of the gloves.  Splashes 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 (including flagmen in aerial operations) 
          - Persons exposed to carbofuran 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 agricultural 
          practice subject to 4.2  below, other populations should not be 
          exposed to hazardous amounts of carbofuran. 

    4.2  ENTRY OF PERSONS INTO TREATED AREAS - Unprotected persons should 
         be kept out of treated areas for at least one day. 

    4.3  SAFE DISPOSAL OF CONTAINERS AND SPILLAGE - Residues in containers 
         should be emptied in a diluted form into a deep pit taking care 
         to avoid contamination of 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 food and drink. 

         Spillage of carbofuran and its 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 headache, weakness, giddiness and nausea. Later there may 
          be perspiration, stomach pains, blurred vision, excessive 
          salivation, slurred speech, and muscle twitching, tremor, 
          diarrhoea and vomiting. 

    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 immediately if the person is conscious.  In the event of 
          collapse, artificial respiration should be given, preferably by 
          mechanical means.  If mouth-to-mouth resuscitation is used vomit 
          may contain toxic amounts of carbofuran.  If the eyes are 
          contaminated, flush them with water for at least 15 minutes.  If 
          carbofuran is inhaled, remove victim to fresh air immediately. 



    5.1.1 General information - Carbofuran is a carbamate insecticide of 
          very high toxicity.  It is absorbed from the gastrointestinal 
          tract and by inhalation, and only to a limited extent through the 

          intact skin.  Its mode of action is by reversible inhibition of 
          acetyl cholinesterase.  Erythrocyte cholinesterase is more 
          inhibited than plasma cholinesterase.  Symptoms of mild poisoning 
          are short lasting and in case of occupational over-exposure occur 
          without delay and at doses well below the fatal dose.  Because of 
          its rapid metabolism and excretion it does not accumulate in the 

    5.1.2 Symptoms and signs - Symptoms of poisoning include excessive 
          sweating, headache, chest tightness, weakness, giddiness, nausea, 
          vomiting, stomach pains, salivation, blurred vision, slurred 
          speech and muscle twitching. Paraesthesia and mild skin reactions 
          have also been reported.  Diagnosis can be based on a recent 
          history of activities and non-reactive pupils of the eyes. 

    5.1.3 Laboratory - Because carbofuran 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 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 carbofuran in 
          urine is also indicative of exposure. 

    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 isotonic saline or 
          water.  Since the symptoms of poisoning with carbofuran are of 
          short duration, atropine treatment is usually not necessary by 
          the time the patient reaches a place where this antidote is 
          available.  Where there are manifest symptoms 1-2 mg of atropine 
          sulfate (adult dose) may be given intramuscularly or even 
          intravenously and repeated as necessary.  Care should be taken to 
          avoid overdosage of atropine, especially when treating children.  
          In extreme cases, if the patient is unconscious or is in 
          respiratory distress, oxygen may be required.  Provide patient 
          support as required, including; suction of secretions, 
          maintenance of airways, intravenous fluids pro re nata and 
          bladder catheterization.  Morphine, aminophylline, 
          phenothiazines, reserpine, furosemide and ethacryoic acid are 
          condraindicated.  Pralidoxime chloride is of doubtful value but 
          if muscle weakness is severe a dilute solution may be given 
          cautiously intravenously.  If convulsions occur diazepam may be 
          given, the patient must be monitored for respiratory depression 
          and hypotensive reactions. 

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

    5.1.6 References of previously reported cases - Okeefe, M. & Pierse, C. 
          (1980), Bull. Environs Contam. Toxicol., 25, 777. 

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


    5.3.1 Detection and assay of compound - Chapman, R. A. & Robinson, J. 
          R, (1977) J. Chromatogr., 140, 209.  Cooke, R. F. et al. (1969) 
          J. Agric. Food Chem., 17, 277.  Cooke, R. F. (1973) Anal.
          Methods Pestic. Plant Growth Regul., 7, 187. 

    5.3.2 Other tests in cases of poisoning - Cholinesterase levels in 
          blood are unreliable as a routine test to detect poisoning by 
          carbofuran.  However, shortly after absorption inhibition of 
          erythrocyte cholinesterase may be demonstrated by an appropriate 
          method.  In plasma; Ellman, G. et al. (1961) Biochem.
          Pharmacol., 7, 88. In whole blood; Fleischer, J. et al. (1956) 
          Arch. Indust. Hyg., 14, 510; Wilheim, K. et al. (1973) Bull 
          Wld. Hlth, Org., 48, 235. 

See Also:
        Carbofuran (ICSC)