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 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. 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: 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 98-100°C; and a specific gravity of 1.195 at 25/20°C. Aldicarb is non-corrosive to most metals and plastics. The technical product is 94.7-97.7% pure aldicarb. 1.3.2 Solubility - (30°C) 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 (20°C) 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 100°C, 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 25°C. 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 µg/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 µg/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)