CARBOFURAN
HAZARDTEXT ®
Information to help in the initial response for evaluating chemical incidents
-IDENTIFICATION
SYNONYMS
BAY 70143 7-BENZOFURANOL, 2,3 DIHYDRO-2,2-DIMETHYL-,METHYLCARBAMATE BRIFUR C2292-59A CARBAMIC ACID, METHYL-, 2,2-DIMETHYL-2,3-DIHYDROBENZOFURAN-7-YL ESTER CARBOFURAN CARBOFURANE CHINUFUR CRISFURAN CRISTOFURAN CURATERR D 1221 2,3-DIHYDRO-2,2-DIMETHYLBENZOFURANYL-7-N-METHYLCARBAMATE 2,3-DIHYDRO-2,2-DIMETHYLBENZOFURAN-7-YL METHYLCARBAMATE 2,3-DIHYDRO-2,2-DIMETHYL-7-BENZOFURANYL METHYLCARBAMATE 2,2-DIMETHYL-7-COUMARANYL N-METHYLCARBAMATE 2,2-DIMETHYL-2,3-DIHYDRO-7-BENZOFURANYL N-METHYLCARBAMATE FMC 10242 FURACARB FURADAN FURADAN G FURADAN 3G FURADAN 4F FURADAN 75 WP FURADANE FURODAN KARBOFURANU (Polish) KENOFURAN METHYLCARBAMATE METHYL CARBAMIC ACID 2,3-DIHYDRO-2,2-DIMETHYL-7-BENZOFURANYL ESTER ME F248 N-METYLOKARBAMINIAN 2,3-DWUWODORO-2,2-DWUMETYLOBENZOFURANYLU-7 (Polish) NIA 10242 NIA 10242 75 WP NIAGARA 10242 NIAGARAL 242 NIAGARA NIA-10242 OMS 864 PILLARFURAN YALTOX CARBOFURAN MIXTURE, LIQUID
IDENTIFIERS
Editor's Note: This material is not listed in the Emergency Response Guidebook. Based on the material's physical and chemical properties, toxicity, or chemical group, a guide has been assigned. For additional technical information, contact one of the emergency response telephone numbers listed under Public Safety Measures.
BEILSTEIN HANDBOOK REFERENCE:5-17-04-00048 BEILSTEIN REFERENCE NUMBER:1428746 IMO CLASSIFICATION:3.2 IMO CLASSIFICATION:6.1 STANDARD INDUSTRIAL TRADE CLASSIFICATION NUMBER:59110
SYNONYM REFERENCE
- (CHRIS , 2000; Hayes & Laws, 1991; Hartley & Kidd, 1987; HSDB , 2000; OHM/TADS , 2000; RTECS , 2000)
USES/FORMS/SOURCES
Carbofuran is used as a broad-spectrum systemic insecticide, miticide, acaricide, and nematocide (ACGIH, 1991a; Budavari, 2000; Lewis, 1998; OHM/TADS, 2000). Carbofuran is used as an agricultural systemic insecticide on sunflowers, fruits (such as strawberries and bananas), tobacco, beet, sorghum, oilseed rape, peanuts, potatoes, lucerne, groundnuts, soya beans, sugar cane, rice, cotton, coffee, cucurbits, lavender, mushrooms, corn, alfalfa, and other field crops. It is also used on ornamentals and forest trees (ACGIH, 1991a; Hartley & Kidd, 1987a; Lewis, 1997). Carbofuran is also used as a pesticide in household products (Lewis, 1998).
Pure carbofuran is a white crystalline solid. It is available in a technical grade (98% pure, in the form of a tan crystalline solid), as granules (at 2%, 3%, 5%, or 10%), as a wettable powder (at 50%, 75% or 80%), as a flowable paste (at 4 lb/gal or 48%) (Baron, 1991; CHRIS, 2000; Hayes, 1982a; Hayes & Laws, 1991a). Carbofuran can be dissolved in a liquid carrier to form a water emulsifiable liquid. It is available in a seed treater form (AAR, 1998a; Baron, 1991; CHRIS, 2000).
It can be produced by the reaction of o-nitropehnol, methyallyl chloride, and methyl isocyanate, involving steps of dehydrochlorination, nitro reduction, diazotisation, hydration, and isocyanate addition (Ashford, 1994). It can be prepared by cyclization and rearrangement of 2-methallyloxyphenol to form 7-hydroxybenzofuran, followed by esterification to from the carbamate (HSDB, 2000). It can be generated by Claisen rearrangement and cyclization of 2-methallyloxy-1-nitrobenzene to 2,3-dihydro-2,2-dimethyl-7-nitrobenzofuran, followed by reduction, diazotiation, and concentration to form the phenol (HSDB, 2000).
-CLINICAL EFFECTS
GENERAL CLINICAL EFFECTS
- The following are symptoms from carbamate insecticides in general, which are due to the anticholinesterase activity of this class of compounds. All of these effects may not be documented for carbofuran, but could potentially occur in individual cases.
- USES: Carbofuran, a carbamate insecticide, is used as a systemic carbamate acaricide, insecticide, and nematicide. It is applied to soil to control insects and nematodes in ornamental plants, trees, and crops.
- TOXICOLOGY: Carbamate insecticides competitively inhibit pseudocholinesterase and acetylcholinesterase, preventing hydrolysis and inactivation of acetylcholine. Acetylcholine accumulates at nerve junctions, causing malfunction of the sympathetic, parasympathetic, and peripheral nervous systems and some of the CNS. Clinical signs of cholinergic excess develop.
- EPIDEMIOLOGY: Exposure to carbamate insecticides is common, but serious toxicity is unusual in the US. Common source of severe poisoning in developing countries. Toxicity generally less severe than with organophosphates.
MILD TO MODERATE POISONING: MUSCARINIC EFFECTS: Can include bradycardia, salivation, lacrimation, diaphoresis, vomiting, diarrhea, urination, and miosis. NICOTINIC EFFECTS: Tachycardia, hypertension, mydriasis, and muscle cramps may develop. SEVERE POISONING: MUSCARINIC EFFECTS: Bronchorrhea, bronchospasm, and acute lung injury. NICOTINIC EFFECTS: Muscle fasciculations, weakness, and respiratory failure. CENTRAL EFFECTS: CNS depression, agitation, confusion, delirium, coma, and seizures. Hypotension, ventricular dysrhythmias, metabolic acidosis, pancreatitis, and hyperglycemia can also develop. CHILDREN: May have different predominant signs and symptoms than adults (more likely CNS depression, stupor, coma, flaccidity, dyspnea, and seizures). Children may also have fewer muscarinic and nicotinic signs of intoxication (ie, secretions, bradycardia, fasciculations, and miosis) as compared with adults. INHALATION EXPOSURE: Vapors rapidly produce mucous membrane and upper airway irritation and bronchospasm, followed by systemic muscarinic, nicotinic, and central effects if exposed to significant concentrations.
- POTENTIAL HEALTH HAZARDS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 131 (ERG, 2004)
TOXIC; may be fatal if inhaled, ingested or absorbed through skin. Inhalation or contact with some of these materials will irritate or burn skin and eyes. Fire will produce irritating, corrosive and/or toxic gases. Vapors may cause dizziness or suffocation. Runoff from fire control or dilution water may cause pollution.
ACUTE CLINICAL EFFECTS
- Carbofuran can be fatal by any route of exposure in small doses, with an estimated lethal human oral dose between 7 drops and 1 teaspoon for a normal adult (HSDB , 1996). Exposure by inhalation is unlikely because of the nature of its commercial formulations; however, the dust and aerosols can be highly toxic (Hayes & Laws, 1991). It is similar to CARBARYL in its toxicological properties (HSDB , 1996).
- Symptoms occur rapidly after overexposure to carbofuran; depending on the dose, they may begin within minutes to an hour (ACGIH, 1991; Hayes & Laws, 1991). Recovery from nonfatal doses occurs spontaneously within 1 to 4 hours (Hayes & Laws, 1991). Cholinergic symptoms reported from nonfatal exposures to carbofuran include headache, weakness, nausea, light-headedness, miosis, blurred vision, abdominal cramps, excessive perspiration and salivation, diarrhea and vomiting (Hayes & Laws, 1991).
- Symptoms of cholinesterase inhibition in general are nausea, vomiting, abdominal cramps, diarrhea, profuse salivation, chest tightness, blurring or dimness of vision, miosis, tearing, muscle spasms, eye pain, slurred speech, fasciculations, muscle twitching, difficulty breathing, frothing at the nose and mouth, pulmonary rales, hypertension, seizures, incontinence, coma, and death from respiratory arrest, paralysis, or intense bronchoconstriction (HSDB).
- With carbofuran poisoning cholinesterase inhibition is rapidly reversible; in this sense it is less dangerous than the organophosphate pesticides. It was much less toxic by the dermal route than following oral exposure in rats; a dose of 1000 mg/kg on the skin produced only minimal symptoms (ACGIH, 1991).
- Pre-treatment of rats with memantine at 18 mg/kg and atropine sulfate at 16 mg/kg completely protected against the central and peripheral neurological effects of carbofuran. This pre-treatment also prevented changes seen in various marker enzymes (creatine kinase, lactic dehydrogenase, transaminases, and acetylcholinesterase) (Gupta & Dettbarn, 1993).
- Carbofuran was more toxic than several of its N-methyl carbamate derivatives in decreasing the activity of human erythrocyte acetylcholinesterase and serum butyrylcholinesterase, and Drosophila nervous system cholinesterase. Human erythrocyte acetylcholinesterase was more sensitive than butyrylcholinesterase to carbofuran inhibition (Loewenstein et al, 1993).
- Pre-treatment with tetraisopropylpyrophoshoramide (iso-OMPA) potentiated the toxicity of carbofuran in rats (Gupta & Dettbarn, 1993).
CHRONIC CLINICAL EFFECTS
- In general, cholinesterase inhibitors are of concern because of potential cumulative toxicity. However, because inhibition due to carbofuran is rapidly reversible, cumulative toxicity may not be of as great a concern.
- Rats given 10 or 25 ppm in the diet had no cumulative effect (Rotaru et al, 1981). Carbofuran decreased hemoglobin, clotting factors, red blood cell counts, and hematocrit, and prolonged clotting time when injected into mice (HSDB). It had no effect in rats when given in the diet at a dose of 25 mg/kg for 2 years, or in dogs at dietary doses of 20 mg/kg for 2 years or at 50 mg/kg for 1 generation (HSDB).
-FIRST AID
FIRST AID AND PREHOSPITAL TREATMENT
- PREHOSPITAL: Activated charcoal is contraindicated because of possible respiratory depression, seizures, and risk of aspiration. Remove contaminated clothing and wash skin with soap and water. Universal precautions and nitrile gloves to protect personnel. Vomiting should be contained and treated as hazardous material. Rescue personnel should avoid dermal exposure to vomiting because of the risk of intoxication.
- There are two primary classes of antidotes: ATROPINE (muscarinic antagonist); OXIMES (pralidoxime in the US, or obidoxime in some other countries) to reverse neuromuscular blockade. Use of oximes is generally indicated for patients with severe toxicity and are used in conjunction with atropine.
-MEDICAL TREATMENT
LIFE SUPPORT
- Support respiratory and cardiovascular function.
SUMMARY
- FIRST AID - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 131 (ERG, 2004)
Move victim to fresh air. Call 911 or emergency medical service. Give artificial respiration if victim is not breathing. Do not use mouth-to-mouth method if victim ingested or inhaled the substance; give artificial respiration with the aid of a pocket mask equipped with a one-way valve or other proper respiratory medical device. Administer oxygen if breathing is difficult. Remove and isolate contaminated clothing and shoes. In case of contact with substance, immediately flush skin or eyes with running water for at least 20 minutes. Wash skin with soap and water. Keep victim warm and quiet. In case of burns, immediately cool affected skin for as long as possible with cold water. Do not remove clothing if adhering to skin. Effects of exposure (inhalation, ingestion or skin contact) to substance may be delayed. Ensure that medical personnel are aware of the material(s) involved and take precautions to protect themselves.
PREHOSPITAL DECONTAMINATION/NOT RECOMMENDED PERSONNEL PROTECTION Universal precaution should be followed by all individuals (i.e., first responders, emergency medical, and emergency department personnel) caring for the patient to avoid contamination. Nitrile gloves are suggested. Avoid direct contact with contaminated clothing, objects or body fluids. Vomiting containing carbamates should be placed in a closed impervious containers for proper disposal.
DERMAL EXPOSURE EYE EXPOSURE DECONTAMINATION: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, the patient should be seen in a healthcare facility.
INHALATION EXPOSURE INHALATION: Move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with an inhaled beta2-adrenergic agonist. Consider systemic corticosteroids in patients with significant bronchospasm.
There are two primary classes of antidotes: ATROPINE (muscarinic antagonist); OXIMES (pralidoxime in the US, or obidoxime in some other countries) to reverse neuromuscular blockade. Use of oximes is generally indicated for patients with severe toxicity and are used in conjunction with atropine.
-RANGE OF TOXICITY
MINIMUM LETHAL EXPOSURE
A suicidal ingestion of 155 grams of carbofuran proved fatal to a 26-year-old man. Death was attributed to anoxia due to respiratory paralysis (Ferslew et al, 1992). Between 7 drops and 1 teaspoon of carbofuran may be fatal to humans. It is considered extremely toxic (OHM/TADS , 2000).
The 30-day empirical minimum lethal dosage is 0.2 mg/kg/day for mallards and 4.2 mg/kg/day for pheasants (HSDB , 2000). After 17 g/kg of carbofuran was applied to the skin of rabbits for 20 days intermittently, death occurred (RTECS , 2000). After 1960 mg/kg of carbofuran was administered orally to chickens for 2 weeks continuously, death occurred (RTECS , 2000). Although carbofuran is not irritating to rabbit eyes, ocular exposure has caused death in rabbits (Hayes & Laws, 1991).
MAXIMUM TOLERATED EXPOSURE
Workers exposed to a concentration of nearly 0.1 mg/m(3) per day have not demonstrated adverse effects (ACGIH, 1986). Workers wearing respirators in areas with air concentrations of 0.007 to 0.642 mg/m(3) did not report any symptoms (Tobin, 1970). A woman developed acetylcholinesterase activity inhibition of 50% to 80% of normal following oral exposure to 60 mg of carbofuran. All symptoms resolved and complete recovery was noted within 72 hours (Izmirova et al, 1981). A 23-year-old man was admitted to the hospital in a coma, and with respiratory failure, miosis, tachycardia, and hypertension a few hours after ingesting approximately 100 mL carbofuran. He survived, but he exhibited carbofuran-induced delayed sensorimotor neuropathy which continued for 4 months after exposure (Yang et al, 2000). Grain farmers exposed dermally to 1,262 mcg/kg of carbofuran exhibited no acute adverse effects during the exposure and for 4 days post-exposure. The farmers were reported to excrete approximately 28 mcg/kg of carbofuran in their urine. No ChE inhibition was reported (Hussain et al, 1990). Twenty-five pesticide industry workers exposed acutely to airborne carbofuran concentrations ranging from 0.018 to 1.115 mg/m(3) experienced acute toxicity, with onset ranging from 0.5 to 3 hours (mean, 1.5 hours). Most recovered within 2 to 3 hours following removal from exposure. In 24 cases, blood ChE activities were inhibited (Huang et al, 1998).
4.5 mg/kg of carbofuran is the minimum toxic dose for cattle and sheep (Lewis, 1998). In Rhesus monkeys, slight cholinesterase depression occurred with exposure to 0.86 mg/m(3) of carbofuran in the form of 75% wettable powder (ACGIH, 1991). Dogs ingesting 500 ppm of carbofuran in their diet for 1 year showed a loss in body weight (which was associated with food retension), loose stools, testicular degeneration, weight reduction of the brain and heart, inflammation in the lungs, and depression of plasma acetylcholinesterase activity, hematocrit, hemoglobin, and erythrocyte count, with concurrent changes in electrolyte values (Hayes & Laws, 1991). Rats given carbofuran in their diet at 100 ppm for 2 years showeda loss in body weight and a moderate reduction of acetylcholinesterase activities in plasma, erythrocytes, and brain (Hayes & Laws, 1991). In rats, carbofuran inhibits acetylcholinesterase in maternal tissues to a lesser degree than the fetal tissues (HSDB , 2000). Dermal application of carbofuran at 1000 mg/kg caused minimal symptoms in rats with no deaths (HSDB , 2000). Rats ingesting 100 ppm of carbofuran through their diet were reported having no increase in birth defects in their offspring; however, the offspring survival rate decreased (HSDB , 2000). Mice treated with multiple IP doses of carbofuran at 0.25 mg/kg caused significant decrease in lymphocyte count hemoglobin content, red blood cells total count, platelet count, erythrocyte sedimentation rate, and hematocrit value; increase in white blood cells total count, neutrophil count, and basophil count; bone marrow depression; and splenic hyperplasia (HSDB , 2000).
- Carcinogenicity Ratings for CAS1563-66-2 :
ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A4 ; Listed as: Carbofuran EPA (U.S. Environmental Protection Agency, 2011): Not Assessed under the IRIS program. ; Listed as: Carbofuran IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): Not Listed NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: Carbofuran MAK (DFG, 2002): Not Listed NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed
TOXICITY AND RISK ASSESSMENT VALUES
- EPA Risk Assessment Values for CAS1563-66-2 (U.S. Environmental Protection Agency, 2011):
Oral: Slope Factor: RfD: 5x10(-3) mg/kg-day
Inhalation: Drinking Water:
References: ACGIH, 1991 EPA, 1988 Hartley & Kidd, 1987 Hayes, 1982 HSDB, 2000 ) OHM/TADS, 2000 RTECS, 2000 LC50- (INHALATION)DOG: LC50- (INHALATION)GUINEA_PIG: 53 mg/m(3) -- in the form of 75% wettable powder (ACGIH, 1991) 43 mg/m(3) for 4H 32 mg/m(3) for 4H (OHM/TADS, 2000)
LC50- (INHALATION)RAT: Male, 108 mg/m(3) -- in the form of 50% wettable powder (ACGIH, 1991) Female, 133 mg/m(3) -- in the form of 50% wettable powder (ACGIH, 1991) 85 mg/m(3) 0.017 - 0.047 mg/L for 4H (EPA, 1988)
LD50- (ORAL)CAT: LD50- (ORAL)CHICKEN: LD50- (ORAL)DOG: 19 mg/kg -- in the technical grade (Hayes, 1982) 15-18.9 mg/kg (EPA, 1988)
LD50- (ORAL)GUINEA_PIG: LD50- (ORAL)HUMAN: LD50- (SKIN)HUMAN: LD50- (INTRAVENOUS)MOUSE: LD50- (ORAL)MOUSE: 14.4 mg/kg (EPA, 1988) 2 mg/kg
LD50- (SKIN)RABBIT: 10,200 mg/kg (HSDB, 2000) 3400 mg/kg -- in the form of 75% wettable powder (ACGIH, 1991; Hayes, 1982) 885 mg/kg -- in the technical grade (HSDB, 2000)
LD50- (INHALATION)RAT: >0.026 mg/L for 1H (EPA, 1988) 0.075 - 0.108 mg/L for 4H (EPA, 1988)
LD50- (OCULAR)RAT: 21.5 mg/kg -- in the form of 25% wettable powder (HSDB, 2000) 18 mg/kg -- in the form of 75% wettable powder (HSDB, 2000)
LD50- (ORAL)RAT: Male, 8.7 mg/kg (ACGIH, 1991) Female, 8 mg/kg (ACGIH, 1991) 132 mg/kg -- in the form of 10% granule (Hayes, 1982) 19 mg/kg -- in the form of 75% wettable powder (ACGIH, 1991; Hayes, 1982) 8.2 - 14.1 mg/kg -- in the technical grade (Hartley & Kidd, 1987; Hayes, 1982) 5.3 mg/kg (OHM/TADS, 2000) 5 mg/kg 3.8 - 34.5 mg/kg (EPA, 1988)
LD50- (SKIN)RAT: TDLo- (ORAL)HUMAN: Female, 1200 mcg/kg -- caused hallucinations, distorted perceptions, dyspnea, and sweating Male, 6200 mcg/kg for female multigeneration -- caused delayed effects on newborn
TDLo- (INTRAPERITONEAL)MOUSE: TDLo- (ORAL)MOUSE: Female, 210 mcg/kg at 1-21D of pregnancy -- caused biochemical and metabolic changes in newborn Female, 10,500 mcg/kg at 1-21D of pregnancy -- caused immune and reticuloendothelial system abnormalities and other changes in newborn Female, 220 mg/kg at 6-16D of pregnancy -- caused musculoskeletal system abnormalities in newborn Female, 110 mg/kg at 6-16D of pregnancy -- caused fetotoxicity and fetal death
TDLo- (SKIN)RABBIT: TDLo- (ORAL)RAT: Male, 86 mg/kg at 60D prior to mating -- caused paternal effects Female, 70 mg/kg at 6-19D of pregnancy -- caused preimplantation and postimplantation mortality 21 mg/kg for 30 D-intermittent -- caused biochemical changes and induced degenerative effects in the brain
CALCULATIONS
OTHER When two fields were treated with 0.5 pound per acre of carbofuran by aerial spraying, no local concentrations exceeded 3.3 mcg/m(3). The calculated dermal doses for an individual directly under the spraying operation was 44 mcg/kg and in a nearby area the calculated exposure was 100 mcg/kg (Draper et al, 1981).
-STANDARDS AND LABELS
WORKPLACE STANDARDS
- ACGIH TLV Values for CAS1563-66-2 (American Conference of Governmental Industrial Hygienists, 2010):
Editor's Note: The listed values are recommendations or guidelines developed by ACGIH(R) to assist in the control of health hazards. They should only be used, interpreted and applied by individuals trained in industrial hygiene. Before applying these values, it is imperative to read the introduction to each section in the current TLVs(R) and BEI(R) Book and become familiar with the constraints and limitations to their use. Always consult the Documentation of the TLVs(R) and BEIs(R) before applying these recommendations and guidelines.
- AIHA WEEL Values for CAS1563-66-2 (AIHA, 2006):
- NIOSH REL and IDLH Values for CAS1563-66-2 (National Institute for Occupational Safety and Health, 2007):
Listed as: Carbofuran REL: IDLH: Not Listed
- OSHA PEL Values for CAS1563-66-2 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
- OSHA List of Highly Hazardous Chemicals, Toxics, and Reactives for CAS1563-66-2 (U.S. Occupational Safety and Health Administration, 2010):
ENVIRONMENTAL STANDARDS
- EPA CERCLA, Hazardous Substances and Reportable Quantities for CAS1563-66-2 (U.S. Environmental Protection Agency, 2010):
Listed as: 7-Benzofuranol, 2,3-dihydro-2,2-dimethyl-, methylcarbamate Final Reportable Quantity, in pounds (kilograms): Additional Information: Listed as: Carbofuran Final Reportable Quantity, in pounds (kilograms): Additional Information:
- EPA CERCLA, Hazardous Substances and Reportable Quantities, Radionuclides for CAS1563-66-2 (U.S. Environmental Protection Agency, 2010):
- EPA RCRA Hazardous Waste Number for CAS1563-66-2 (U.S. Environmental Protection Agency, 2010b):
Listed as: 7-Benzofuranol, 2,3-dihydro-2,2-dimethyl-, methylcarbamate P or U series number: P127 Footnote: Listed as: Carbofuran P or U series number: P127 Footnote: Editor's Note: The D, F, and K series waste numbers and Appendix VIII to Part 261 -- Hazardous Constituents were not included. Please refer to 40 CFR Part 261.
- EPA SARA Title III, Extremely Hazardous Substance List for CAS1563-66-2 (U.S. Environmental Protection Agency, 2010):
Listed as: Carbofuran Reportable Quantity, in pounds: 10 Threshold Planning Quantity, in pounds: Note(s): Not Listed
- EPA SARA Title III, Community Right-to-Know for CAS1563-66-2 (40 CFR 372.65, 2006; 40 CFR 372.28, 2006):
- DOT List of Marine Pollutants for CAS1563-66-2 (49 CFR 172.101 - App. B, 2005):
- EPA TSCA Inventory for CAS1563-66-2 (EPA, 2005):
Listed as: 7-Benzofuranol, 2,3-dihydro-2,2-dimethyl-, methylcarbamate
SHIPPING REGULATIONS
- DOT -- Table of Hazardous Materials and Special Provisions (49 CFR 172.101, 2005):
- ICAO International Shipping Name (ICAO, 2002):
LABELS
- NFPA Hazard Ratings for CAS1563-66-2 (NFPA, 2002):
-HANDLING AND STORAGE
SUMMARY
For normal handling, adequate ventilation must be assured and workers must wear protective coverall clothing, chemical goggles, and a chemical cartridge respirator. Prohibition of eating and smoking in the working area and compulsory bathing after each work day should be mandated (Plunkett, 1976).
STORAGE
-PERSONAL PROTECTION
SUMMARY
- RECOMMENDED PROTECTIVE CLOTHING - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 131 (ERG, 2004)
Wear positive pressure self-contained breathing apparatus (SCBA). Wear chemical protective that is specifically recommended by the manufacturer. It may provide little or no thermal protection. Structural firefighters' protective clothing provides limited protection in fire situations ONLY; it is not effective in spill situations where direct contact with the substance is possible.
- Protective coverall clothing, and a chemical cartridge respirator should be worn since carbofuran is toxic through all routes of contact (OHM/TADS , 2000; Plunkett, 1976).
Skin and inhalation exposures are rated at a lower danger than if exposed orally (ACGIH, 1991). Although it may be poorly absorbed by the skin, based on animal studies, skin absorption can occur (CHRIS , 2000; OHM/TADS , 2000). In case of contact with skin, wash area first with soap and water, then with alcohol, and finally with soap and water again (CHRIS , 2000).
EYE/FACE PROTECTION
- It is an eye irritant; therefore, chemical goggles should be worn (CHRIS , 2000; Plunkett, 1976).
RESPIRATORY PROTECTION
- Refer to "Recommendations for respirator selection" in the NIOSH Pocket Guide to Chemical Hazards on TOMES Plus(R) for respirator information.
PROTECTIVE CLOTHING
- CHEMICAL PROTECTIVE CLOTHING. Search results for CAS 1563-66-2.
-PHYSICAL HAZARDS
FIRE HAZARD
Editor's Note: This material is not listed in the Emergency Response Guidebook. Based on the material's physical and chemical properties, toxicity, or chemical group, a guide has been assigned. For additional technical information, contact one of the emergency response telephone numbers listed under Public Safety Measures. POTENTIAL FIRE OR EXPLOSION HAZARDS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 131 (ERG, 2004) HIGHLY FLAMMABLE: Will be easily ignited by heat, sparks or flames. Vapors may form explosive mixtures with air. Vapors may travel to source of ignition and flash back. Most vapors are heavier than air. They will spread along ground and collect in low or confined areas (sewers, basements, tanks). Vapor explosion and poison hazard indoors, outdoors or in sewers. Those substances designated with a "P" may polymerize explosively when heated or involved in a fire. Runoff to sewer may create fire or explosion hazard. Containers may explode when heated. Many liquids are lighter than water.
Carbofuran is not flammable but will support combustion if ignited (CHRIS , 2000). Irritating and poisonous fumes of nitrogen oxide are produced when heated or if on fire (CHRIS , 2000).
- FLAMMABILITY CLASSIFICATION
- NFPA Flammability Rating for CAS1563-66-2 (NFPA, 2002):
- FIRE CONTROL/EXTINGUISHING AGENTS
- FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 131 (ERG, 2004)
- SMALL FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 131 (ERG, 2004)
- LARGE FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 131 (ERG, 2004)
Water spray, fog or alcohol-resistant foam. Move containers from fire area if you can do it without risk. Dike fire control water for later disposal; do not scatter the material. Use water spray or fog; do not use straight streams.
- TANK OR CAR/TRAILER LOAD FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 131 (ERG, 2004)
Fight fire from maximum distance or use unmanned hose holders or monitor nozzles. Cool containers with flooding quantities of water until well after fire is out. Withdraw immediately in case of rising sound from venting safety devices or discoloration of tank. ALWAYS stay away from tanks engulfed in fire. For massive fire, use unmanned hose holders or monitor nozzles; if this is impossible, withdraw from area and let fire burn.
- NFPA Extinguishing Methods for CAS1563-66-2 (NFPA, 2002):
- Do not attempt to extinguish fire unless the flow of carbofuran is stopped/contained. Positive pressure self-containing breathing apparatus should be worn when fighting fires involving carbofuran (AAR, 1998).
- Water should be used in flooding quantities as fog to fight fires involving carbofuran or as spray or fog to knock down fumes or vapors and to cool containers exposed to the heat of a fire. Run-off water should be kept out of sewers and water sources. In addition, uninvolved carbofuran should be covered with plastic sheets to prevent contacting with run-off water (AAR, 1998).
- Use dry chemical, foam, or carbon dioxide to fight fire. Solid streams of water may not be effective to extinguish fires (AAR, 1998).
DUST/VAPOR HAZARD
- Irritating and poisonous fumes of nitrogen oxide are produced when heated or if on fire (CHRIS , 2000).
- Irritating and poisonous fumes of nitrogen oxide are produced when heated or if on fire (CHRIS , 2000).
EVACUATION PROCEDURES
- Editor's Note: This material is not listed in the Table of Initial Isolation and Protective Action Distances.
- SPILL - PUBLIC SAFETY EVACUATION DISTANCES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 131 (ERG, 2004)
Increase, in the downwind direction, as necessary, the isolation distance of at least 50 meters (150 feet) in all directions.
- FIRE - PUBLIC SAFETY EVACUATION DISTANCES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 131 (ERG, 2004)
If tank, rail car or tank truck is involved in a fire, ISOLATE for 800 meters (1/2 mile) in all directions; also, consider initial evacuation for 800 meters (1/2 mile) in all directions.
- PUBLIC SAFETY MEASURES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 131(ERG, 2004)
CALL Emergency Response Telephone Number on Shipping Paper first. If Shipping Paper not available or no answer, refer to appropriate telephone number: MEXICO: SETIQ: 01-800-00-214-00 in the Mexican Republic; For calls originating in Mexico City and the Metropolitan Area: 5559-1588; For calls originating elsewhere, call: 011-52-555-559-1588.
CENACOM: 01-800-00-413-00 in the Mexican Republic; For calls originating in Mexico City and the Metropolitan Area: 5550-1496, 5550-1552, 5550-1485, or 5550-4885; For calls originating elsewhere, call: 011-52-555-550-1496, or 011-52-555-550-1552; 011-52-555-550-1485, or 011-52-555-550-4885.
ARGENTINA: CIQUIME: 0-800-222-2933 in the Republic of Argentina; For calls originating elsewhere, call: +54-11-4613-1100.
BRAZIL: PRÓ-QUÍMICA: 0-800-118270 (Toll-free in Brazil); For calls originating elsewhere, call: +55-11-232-1144 (Collect calls are accepted).
COLUMBIA: CISPROQUIM: 01-800-091-6012 in Colombia; For calls originating in Bogotá, Colombia, call: 288-6012; For calls originating elsewhere, call: 011-57-1-288-6012.
CANADA: UNITED STATES:
For additional details see the section entitled "WHO TO CALL FOR ASSISTANCE" under the ERG Instructions. As an immediate precautionary measure, isolate spill or leak area for at least 50 meters (150 feet) in all directions. Keep unauthorized personnel away. Stay upwind. Keep out of low areas. Ventilate closed spaces before entering.
- AIHA ERPG Values for CAS1563-66-2 (AIHA, 2006):
- DOE TEEL Values for CAS1563-66-2 (U.S. Department of Energy, Office of Emergency Management, 2010):
Listed as Carbofuran TEEL-0 (units = mg/m3): 0.1 TEEL-1 (units = mg/m3): 0.3 TEEL-2 (units = mg/m3): 0.43 TEEL-3 (units = mg/m3): 0.5 Definitions: TEEL-0: The threshold concentration below which most people will experience no adverse health effects. TEEL-1: The airborne concentration (expressed as ppm [parts per million] or mg/m(3) [milligrams per cubic meter]) of a substance above which it is predicted that the general population, including susceptible individuals, could experience notable discomfort, irritation, or certain asymptomatic, nonsensory effects. However, these effects are not disabling and are transient and reversible upon cessation of exposure. TEEL-2: The airborne concentration (expressed as ppm or mg/m(3)) of a substance above which it is predicted that the general population, including susceptible individuals, could experience irreversible or other serious, long-lasting, adverse health effects or an impaired ability to escape. TEEL-3: The airborne concentration (expressed as ppm or mg/m(3)) of a substance above which it is predicted that the general population, including susceptible individuals, could experience life-threatening adverse health effects or death.
- AEGL Values for CAS1563-66-2 (National Research Council, 2010; National Research Council, 2009; National Research Council, 2008; National Research Council, 2007; NRC, 2001; NRC, 2002; NRC, 2003; NRC, 2004; NRC, 2004; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; United States Environmental Protection Agency Office of Pollution Prevention and Toxics, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; 62 FR 58840, 1997; 65 FR 14186, 2000; 65 FR 39264, 2000; 65 FR 77866, 2000; 66 FR 21940, 2001; 67 FR 7164, 2002; 68 FR 42710, 2003; 69 FR 54144, 2004):
- NIOSH IDLH Values for CAS1563-66-2 (National Institute for Occupational Safety and Health, 2007):
CONTAINMENT/WASTE TREATMENT OPTIONS
SPILL OR LEAK PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 131 (ERG, 2004) Fully encapsulating, vapor protective clothing should be worn for spills and leaks with no fire. ELIMINATE all ignition sources (no smoking, flares, sparks or flames in immediate area). All equipment used when handling the product must be grounded. Do not touch or walk through spilled material. Stop leak if you can do it without risk. Prevent entry into waterways, sewers, basements or confined areas. A vapor suppressing foam may be used to reduce vapors.
RECOMMENDED PROTECTIVE CLOTHING - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 131 (ERG, 2004) Wear positive pressure self-contained breathing apparatus (SCBA). Wear chemical protective that is specifically recommended by the manufacturer. It may provide little or no thermal protection. Structural firefighters' protective clothing provides limited protection in fire situations ONLY; it is not effective in spill situations where direct contact with the substance is possible.
Quick action can recover most of the material and limit hazard (OHM/TADS , 2000). This material may be dangerous if it enters water intakes. Local health, wildlife, and pollution control officials as well as operators of water intakes in the vicinity should be notified of water spills (CHRIS , 2000). LAND SPILL Contain material using a holding area by digging a pit, pond, or lagoon (AAR, 1998). Cover carbofuran with plastic sheets to prevent dissolving in rain (AAR, 1998).
WATER SPILL Use constructed sand bag barriers, excavated lagoons, or natural deep water pockets to trap the material on the bottom. Mechanical dredges or lifts may be used to remove immobilized material and precipitates (AAR, 1998). If more than 10 ppm of carbofuran is dissolved in water, add activated carbon at 10 times the amount of the spilled material (AAR, 1998). Close beach and shore to the public until the material has been removed. Clean up should be done by scraping the beach at low tide with a mechanical scraper. Avoid human contact with the spilled carbofuran (OHM/TADS , 2000).
AIR SPILL
Alkaline hydrolysis, using calcium oxide, sodium hydroxide, and/or sodium carbonate, is the recommended mode of disposal for carbofuran (HSDB, 2004; Sittig, 1991). Carbofuran can be buried in chemical waste landfills, but may require biological treatment at a municipal sewage treatment plant prior to disposal. It can also be incinerated in a pesticide incinerator (OHM/TADS , 2000). Waste management activities associated with material disposition are unique to individual situations. Proper waste characterization and decisions regarding waste management should be coordinated with the appropriate local, state, or federal authorities to ensure compliance with all applicable rules and regulations.
-ENVIRONMENTAL HAZARD MANAGEMENT
POLLUTION HAZARD
- Carbofuran is fouling to shorelines (CHRIS , 2000).
- This material may be dangerous if it enters water intakes. Contact local health, wildlife, and pollution control officials as well as operators of nearby water intakes in the event of a water spill (CHRIS , 2000).
- Air emissions from the material's manufacture consisted of 1.5 kg of hydrocarbons and 0.5 kg of carbofuran per metric ton of pesticide produced (HSDB, 2004).
ENVIRONMENTAL FATE AND KINETICS
Carbofuran exists in both the vapor and the particulate phases in the ambient atmosphere. Photooxidation (reaction with hydroxyl radicals) appears to be the most important degradation process in the vapor phase. Carbofuran in the particulate phase may be physically removed by wet and dry deposition. Direct photolysis may also be an important removal process in the atmosphere (HSDB, 2004). Carbofuran reacts with the vapor-phase hydroxyl radicals at the estimated half-life of 4.6 hours (Howard, 1991). Carbofuran reacts with the vapor-phase hydroxyl radicals at the estimated half-life of 13 hours in an atmosphere containing 5x10(5) hydroxyl radicals per cubic meter at 25 degrees C. This is based on the rate constant for the vapor phase reaction with hydroxyl radicals, estimated at 2.9x10(-11) cm(3)/molecule-sec (HSDB, 2004).
SURFACE WATER Chemical hydrolysis, photolysis, photooxidation, and microbial degradation appear to be the important degradation processes in the water. In fact, degradation in natural water can be 30-50% faster in sunlight as compared to dark due to the presence of hydroxyl radicals in sunlit water. Volatilization, adsorption, or bioconcentration are not expected to be significant (Howard, 1991). Hydrolysis results in the generation of 3-hydroxy carbamate and 7-phenol products, which are less toxic than the parent compound (EPA, 1988). Direct photolysis and photooxidation by reaction with hydroxyl radicals may contribute to removal from natural water. This may become increasingly important as acidity increases and the hydrolytic half-life increases (Howard, 1991). Carbofuran persistence in vitro after 8 weeks in capped bottles, at 21 degrees C, in darkness (% remaining from initial concentration of 5 ppm) (Verschueren, 2001):
GROUND WATER
TERRESTRIAL Chemical hydrolysis and microbial degradation appear to be the important degradation process in the soil (with 3-hydroxycarbofuran, 3-ketocarbofuran, and carbofuran phenol as degradation products). Although some evaporation from plants may occur, volatilization from soil is not expected to be significant (even at temperatures up to 35 degrees C) (Howard, 1991). Less than 1% volatilized from sandy loam soil after 60 days, while 36% volatilized from sandy soil (at 25 degrees C; laboratory testing). (Verschueren, 2001). Carbofuran degrades 7 to 10 times faster in alkaline soil (pH 7.9) than in acid and neutral soils (pH 4.3 to 6.8). It may hydrolyze to its phenol, which immediately binds to soil constituents and is slowly metabolized by microorganisms (OHM/TADS , 2000). High soil water content, high soil temperatures, high pH, low clay content, or heavy soil texture can accelerate degradation of carbofuran (HSDB, 2004; OHM/TADS , 2000). Carbofuran is highly mobile and has the potential to leach (EPA, 1988). It is degraded by soil fungi to hydroxycarbofuran (OHM/TADS , 2000). The soil half-life related to hydrolysis ranged from 21 to 227 days, as influenced by soil type and conditions of soil incubation (Verschueren, 2001). The disappearance of 95% of carbofuran followed first-order kinetics and varied between 145 to 434 days as a function of temperature, pH, moisture, and initial amount applied to soil (Verschueren, 2001; HSDB, 2004). The photodegradation rate increases in the presence of soil particles (HSDB, 2004). Calculated half-lives in soil with known history of insecticide use (pH 6.5) (Verschueren, 2001): Technical grade: 11-13D Granular form: 60-75D
ABIOTIC DEGRADATION
- Carbofuran in soil is primarily hydrolyzed and degraded by soil microorganisms. Degradation is enhanced by lower clay content, increased soil moisture, higher soil temperature, and higher soil pH. It is highly mobile and can leach to groundwater, where it may persist under low pH and low temperature conditions. Organic content of the soil (greater than 65% carbon) limits leaching from soil. Volatilization from soil is not significant, although evaporation from plant surfaces may occur (HSDB, 2004; OHM/TADS , 2000; Howard, 1991; EPA, 1988)
- In the atmosphere, vapors are photooxidized by reaction with hydroxyl radicals. Wet and dry deposition removes particulate carbofuran from the air. Direct photolysis also occurs (HSDB, 2004).
- Carbofuran undergoes hydrolysis, photolysis, photooxidation, and biodegradation in aquatic systems. Direct photolysis and photooxidation are more important in acidic waters. Adsorption, volatilization, and bioconcentration are not important (Howard, 1991).
BIODEGRADATION
- Fungi in soil degrades carbofuran to its toxic metabolite, hydroxycarbofuran (OHM/TADS , 2000).
- The rate of biodegradation in soil is greatly increased by pretreatment with carbofuran. This does not appear to be the result of any increase in the microbial population (Howard, 1991; HSDB, 2004).
In four soils with known insecticide use, carbofuran had the following calculated half-lives: 11 to 13 days at pH 6.5 for the technical grade, and 60 to 75 days for the granular formation. The time of disappearance from the soil at 3.1 to 5.6 kg/hectare was 145 to 434 days (HSDB, 2004).
- Soils used to grow muskmelon were evaluated for their ability to develop enhanced rates of biodegradation of carbofuran. Previously treated and untreated soil samples were tested for microbial action against the chemical. The results showed that the uptake and microbial breakdown of the pesticide were enhanced in soils that had a history of carbofuran use (Buhler et al, 1992).
BIOACCUMULATION
OTHER Although toxic, carbamates (which carbofuran is one) in general do not persist in biological systems. They are readily metabolized and excreted (Clayton & Clayton, 1994; OHM/TADS , 2000).
34, based on the octanol/water partition coefficient (Howard et al, 1991). 15, based on the water solubility (Howard, 1991).
ENVIRONMENTAL TOXICITY
Carbofuran exposure at 7.66 mg/L for 6D disrupted protein and carbohydrate metabolism in Clarius batrachus (linn). Liver and muscle tissue were examined after 1 ,3, and 6 days from exposed, recovery, and control fish in two scenarios, a 6D exposure period and a 6D recovery period. Protein, amino acids, ammonia, glycogen, aminotransaminases, glycogen phosphorylase (a and ab), and glutamate dehydrogenase levels were estimated from tissue samples (Begum, 2004). Total protein content in liver tissue decreased significantly during the exposure period. Levels decreased in the early part of the recovery period, but recovery occurred after 6D in clean water. Muscle tissue levels decreased similarly. The return in protein content may indicate tissue recovery to the toxic effects of carbofuran. Amino acids effects were variable and not significant. Ammonia content increased in liver and muscle tissue, and remained high in the liver more than the muscle after removal from treatment. Liver levels did not recover after transfer to clean water. Elevated ammonia concentrations may have been due to increased ammoniagenesis. Glycogen levels dropped markedly in liver tissue during treatment and into the early part of the recovery period. Slight decreases occurred in muscle tissue during treatment. The recovery period allowed levels to recover in both tissues. Acute exposure caused marked glycogenolysis likely because of stress-induced increases in catecholamines and glucocorticoids. Adverse effects occurred to transaminases, phosphorylases (a and ab), and glutamate dehydrogenase in liver and muscle tissues. ALAT activity was elevated and recovered in the liver. Muscle ALAT activity was also enhanced, although effects were observed later than in the liver and persisting after transfer to clean water. Observed increases in ammonia were linked to these metabolic effects. Increases in phosphorylase a activity in muscle and liver tissue confirmed glycogen breakdown in the tissues. This may have been due to the increased energy demand associated with the toxic stress of carbofuran exposure. GDH activity was enhanced in liver and muscle tissue, indicating increases to glutamate oxidation. This increased ammonia production and alpha-ketoglutarate formation.
Carbofuran may affect the Biological Oxygen Demand, but it does not concentrate in the food chain (CHRIS , 2000). A study was done to examine the short term changes in bacterial populations due to application of carbofuran. The largest population changes occurred about 7 to 15 days after application. The population response was small and short-lived, and was not measurable after 20 days (Edwards et al, 1992). Carbofuran is characterized as very highly toxic to cold and warm water fish. It is highly toxic to freshwater invertebrates (EPA, 1988). LC50 - FRESHWATER FISH (acute): 94 to 2859 ppb (EPA, 1988) Acute freshwater invertebrates toxicity ranges from 9.8 to 38.6 ppb (EPA, 1988).
It is very highly toxic to birds. The subacute avian oral LD50 ranges from 16 to 1104 ppm (EPA, 1988). In particular, the granular form is highly toxic to birds regardless of application rate or methods employed. In fact, carbofuran poses the greatest risk to birds as compared with other granular pesticides, including alternatives to carbofuran (EPA, 1988).
It is toxic to bees (Hartley & Kidd, 1987). Low concentrations are harmful to aquatic life (CHRIS , 2000).
Aquatic Toxicity: TLm - CHANNEL CATFISH: 0.21 ppm for 96H (OHM/TADS , 2000) TLm - CHANNEL CATFISH: 0.24 ppm for 96H (OHM/TADS , 2000) LC50 - BLUEGILL: 0.24 ppm for 96H -- static test environment (CHRIS , 2000) LC50 - BLUEGILL, wt 0.8 g: 240 mcg/L for 96H -- at 18 degrees C; with static bioassay; in the form of 50% wettable powder (HSDB, 2004) LC50 - BLUEGILL SUNFISH: 0.64 ppm for 96H (OHM/TADS , 2000) LC50 - BROWN TROUT, wt 0.5 g: 560 mcg/L for 96H -- at 12 degrees C; with static bioassay in the technical grade (HSDB, 2004) LC50 - COHO SALMON, wt 0.6 g: 530 mcg/L for 96H -- at 12 degrees C; with static bioassay; in the technical grade (HSDB, 2004) LC50 - CHANNEL CATFISH: 0.21 ppm for 96H -- static test environment (CHRIS , 2000) LC50 - CHANNEL CATFISH, wt 1.0 g: 248 mcg/L for 96H -- at 20 degrees C; with static bioassay; in the technical form (HSDB, 2004) LC50 - FATHEAD MINNOW, wt 1.3 g: 872 mcg/L for 96H -- at 17 degrees C; with static bioassay; in the technical grade (HSDB, 2004) LC50 - GREEN SUNFISH: 0.16 mg/L for 72H; with static bioassay (HSDB, 2004) LC50 - LAKE TROUT, wt 0.5 g: 164 mcg/L for 96H -- at 12 degrees C; with flow-through bioassay; in the technical grade (HSDB, 2004) LC50 - MOSQUITO FISH: 0.52 mg/L for 72H -- with static bioassay (HSDB, 2004) LC50 - PINK SHRIMP: 0.0046 ppm for 48H (OHM/TADS , 2000) LC50 - RAINBOW TROUT: 0.28 ppm for 96H-- static test environment (CHRIS , 2000) LC50 - RAINBOW TROUT, wt 1.5 g: 380 mcg/L for 96H -- at 12 degrees C; with static bioassay; in the technical grade (HSDB, 2004) LC50 - SHEEPSHEAD MINNOW: 386 mcg/L for 96H -- with flow-through bioassay (HSDB, 2004) LC50 - YELLOW PERCH, wt 0.6 g: 147 mcg/L for 96H -- at 12 degrees C; with static bioassay; in the technical material (HSDB, 2004)
Avian Toxicity: LC50 - (ORAL) JAPANESE QUAIL, 14 days old: 438 ppm -- with 5-day diet ad libitum in the technical grade (HSDB, 2004) LC50 - (ORAL) JAPANESE QUAIL: 746 ppm -- with 5 day diet ad libitum, technical grade (HSDB, 2004) LC50 - (ORAL) MALLARD, 36 hours old: 0.370 mg/kg (CHRIS , 2000) LC50 - (ORAL) MALLARD, 10 days old: 190 ppm with 5-day diet ad libitum in the technical grade (HSDB, 2004) LC50 - (ORAL) RING-NECKED PHEASANT, 10 days old: 573 ppm -- with 5-day diet ad libitum in the technical grade (HSDB, 2004) LD50 - (ORAL) BOBWHITE QUAIL, Female, 3 months old: 5.04 mg/kg -- technical grade (HSDB, 2004) LD50 - (ORAL) FULVOUS WHISTLING DUCK, Female, 3 - 6 months old: 0.238 mg/kg -- in the technical grade (HSDB, 2004) LD50 - (ORAL) MALLARD, Female, 3 - 4 months old: 0.397 mg/kg -- technical grade (HSDB, 2004) LD50 - (ORAL) MALLARD, Female, 12 months old: 0.510 mg/kg -- in the technical grade (HSDB, 2004) LD50 - (ORAL) MALLARD, Male, 12 months old: 0.480 mg/kg -- technical grade (HSDB, 2004) LD50 - (ORAL) MALLARD: 190 ppm for 10D (CHRIS , 2000) LD50 - (ORAL) MALLARD, 7 days old: 0.628 mg/kg (CHRIS , 2000) LD50 - (ORAL) MALLARD, 30 days old: 0.5510 mg/kg (CHRIS , 2000) LD50 - (ORAL) MALLARD, 6 months old: 0.415 mg/kg (CHRIS , 2000) LD50 - (ORAL) PHEASANT: 960 mg/kg for 10D -- using 10% granule (HSDB, 2004) LD50 - (ORAL) RING-NECKED PHEASANT, Female, 3 months old: 4.15 mg/kg -- technical grade (HSDB, 2004)
-PHYSICAL/CHEMICAL PROPERTIES
MOLECULAR WEIGHT
DESCRIPTION/PHYSICAL STATE
- Pure carbofuran is a white crystalline solid. It is available in a technical grade (98% pure, in the form of a tan crystalline solid), as granules (at 2%, 3%, 5%, or 10%), as a wettable powder (at 50%, 75% or 80%), and as a flowable paste (at 4 lb/gal or 48%) (Baron, 1991; CHRIS , 2000; Hayes, 1982; Hayes & Laws, 1991).
- Carbofuran can be dissolved in a liquid carrier to form a water emulsifiable liquid. It is also available in a seed treater form (AAR, 1998; Baron, 1991; CHRIS , 2000).
- Pure carbofuran is odorless; however, it can have a slight phenolic odor in various commercial forms (HSDB , 2000).
VAPOR PRESSURE
- 4.85x10(-6) mmHg (at 19 degrees C) (HSDB , 2000)
- 0.031 mPa (at 20 degrees C) (HSDB , 2000)
- 0.072 mPa (at 25 degrees C) (HSDB , 2000)
- 8.3x10(-6) mmHg (at 25 degrees C) (Howard, 1991)
- 3.4x10(-6) mmHg (at 25 degrees C) (HSDB , 2000)
- 0.2x10(-4) mmHg (at 33 degrees C) (ACGIH, 1991; EPA, 1988; Lewis, 2000; OHM/TADS , 2000)
- 2.7 mPa (at 33 degrees C) (Hartley & Kidd, 1987)
- 1.1x10(-4) mmHg (at 50 degrees C) (Hayes & Laws, 1991)
- 3x10(-6) mmHg (at 77 degrees F) (NIOSH , 2000)
SPECIFIC GRAVITY
- OTHER TEMPERATURE AND/OR PRESSURE
DENSITY
- OTHER TEMPERATURE AND/OR PRESSURE
FREEZING/MELTING POINT
Pure Material: 153-154 degrees C (Baron, 1991; Hartley & Kidd, 1987; Baron, 1991) Technical material: 150-152 degrees C (ACGIH, 1986; Hartley & Kidd, 1987; Baron, 1991; Lewis, 2000; Sittig, 1991) 151 degrees C (HSDB , 2000) 150-153 degrees C (ACGIH, 1991; Budavari, 2000; Howard, 1991; OHM/TADS , 2000)
SOLUBILITY
It "mixes and sinks in water" (CHRIS , 2000) 320 mg/L (at 20 degrees C) (HSDB , 2000) 700 ppm (at 25 degrees C) (Budavari, 2000; HSDB , 2000) 700 mg/L (at 25 degrees C) (Hartley & Kidd, 1987) 0.07% (at 25 degrees C; 77 degrees F) (Hayes & Laws, 1991; NIOSH , 2000)
Acetone: 15% (w/w) (ACGIH, 1991; Hartley & Kidd, 1987) Acetonitrile: 14% (w/w) (ACGIH, 1991; Hartley & Kidd, 1987) Benzene: 4% (w/w) (EPA, 1988; Hartley & Kidd, 1987; Hayes & Laws, 1991) Cyclohexanone: 9% (w/w) (ACGIH, 1991; Hartley & Kidd, 1987; Hayes & Laws, 1991) Dichloromethane: 120 g/kg (Hartley & Kidd, 1987) Dichloromethane: >200 g/L (at 20 degrees C) (HSDB , 2000) Dimethyl formamide: 25-30% (w/w) (Tobin, 1970) Dimethyl formamide: 27% (w/w) (at 25 degrees C) (Hayes & Laws, 1991) Dimethyl sulfoxide: 25-30% (w/w) (Tobin, 1970) Dimethyl sulfoxide: 25% (w/w) (at 25 degrees C) (Hayes & Laws, 1991) Ethanol: 4% (w/w) (Hartley & Kidd, 1987; Hayes & Laws, 1991) Isopropanol: 20-50 g/L (at 20 degrees C) (HSDB , 2000) Kerosene: <1% (Hayes & Laws, 1991) Methylene chloride: 12% (EPA, 1988) N-methyl-2-pyrrolidone: 25-30% (w/w) (Tobin, 1970) N-methyl-2-pyrrolidone: 30% (w/w) (at 25 degrees C) (Hayes & Laws, 1991) Petroleum ether: Barely soluble (Hartley & Kidd, 1987) Petroleum ether: <1% (Hayes & Laws, 1991) Toluene: 10-20 g/L (at 20 degrees C) (HSDB , 2000) Xylene: Barely soluble (Hartley & Kidd, 1987) Xylene: <1% (Hayes & Laws, 1991) Carbofuran is slightly soluble to insoluble in most common solvents (Tobin, 1970). "It essentially is insoluble in conventional formulation solvents used in agriculture" (Hayes, 1982).
OCTANOL/WATER PARTITION COEFFICIENT
- log Kow = 2.32 (Howard, 1991)
HENRY'S CONSTANT
- 3.9x10(-9) atm-m(3)/mol (calculated) (Howard, 1991)
- 4.4x10(-9) atm-m(3)/mole (estimated) (HSDB , 2000)
OTHER/PHYSICAL
-REFERENCES
GENERAL BIBLIOGRAPHY- 40 CFR 372.28: Environmental Protection Agency - Toxic Chemical Release Reporting, Community Right-To-Know, Lower thresholds for chemicals of special concern. National Archives and Records Administration (NARA) and the Government Printing Office (GPO). Washington, DC. Final rules current as of Apr 3, 2006.
- 40 CFR 372.65: Environmental Protection Agency - Toxic Chemical Release Reporting, Community Right-To-Know, Chemicals and Chemical Categories to which this part applies. National Archives and Records Association (NARA) and the Government Printing Office (GPO), Washington, DC. Final rules current as of Apr 3, 2006.
- 49 CFR 172.101 - App. B: Department of Transportation - Table of Hazardous Materials, Appendix B: List of Marine Pollutants. National Archives and Records Administration (NARA) and the Government Printing Office (GPO), Washington, DC. Final rules current as of Aug 29, 2005.
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