ALDICARB
HAZARDTEXT ®
Information to help in the initial response for evaluating chemical incidents
-IDENTIFICATION
SYNONYMS
ALDECARB ALDICARBE (French) CARBAMIC ACID, METHYL-, 0-((2-METHYL-2-(METHYLTHIO) PROPYLIDENE)AMINO) DERIV. CARBAMYL 2-METHYL-2-(METHYLTHIO)PROPANAL, O-((METHYLAMINO) CARBONYL) OXIME 2-METHYL-2-(METHYLTHIO)PROPIONALDEHYDE O- (METHYLCARBAMOYL)OXIME 2-METHYL-2-METHYLTHIO-PROPIONALDEHYD-O-(N-METHYL- CARBAMOYL)-OXIM (German) 2-METIL-2-TIOMETIL-PROPIONALDEID-O-(N-METIL- CARBAMOIL)-OSSIMA (Italian) PROPANAL, 2-METHYL-2-(METHYLTHIO)-, O-((METHYLAMINO) CARBONYL)OXIME PROPIONALDEHYDE, 2-METHYL-2-(METHYLTHIO)-, O- (METHYLCARBAMOYL)OXIME SULFONE ALDOXYCARB TEMIC TEMIK TEMIK G TEMIK G10 TEMIK 10 G UC-21149 UNION CARBIDE 21149 UNION CARBIDE UC-21149 AMBUSH CARBANOLATE OMS-771
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.
4921627 - Carbamate pesticide, solid, nos, (compounds and preparations) (insecticides, nec) 4921626 - Carbamate pesticide, solid, nos, (compounds and preparations) (insecticides, other than agricultural, nec) 4921625 - Carbamate pesticide, liquid, nos (compounds and preparations) (agricultural insecticides, nec liquid) 4921624 - Carbamate pesticide, liquid, nos (compounds and preparations) (insecticides, other than agricultural, nec) 4910528 - Carbamate pesticide, liquid, nos (compounds and preparations) (agricultural insecticides, nec) 4910527 - Carbamate pesticide, liquid, nos (compounds and preparations) (insecticides, other than agricultural, nec)
SYNONYM REFERENCE
- (HSDB , 1999; RTECS , 1999)
USES/FORMS/SOURCES
Aldicarb 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 (Ashford, 1994; Budavari, 1996a; Lewis, 1997a; Lewis, 1998; Hartley & Kidd, 1987a; Hayes, 1982a).
It is formulated as granules (10-15% active ingredient) or in mixed formulations with lindane, PCNB, and ethazol(Hartley & Kidd, 1987a; Hayes, 1982a; Hayes & Laws, 1991a).
-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 aldicarb, but could potentially occur in individual cases.
- USES: Aldicarb, 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 151 (ERG, 2004)
Highly toxic, may be fatal if inhaled, swallowed or absorbed through skin. Avoid any skin contact. Effects of contact or inhalation may be delayed. Fire may produce irritating, corrosive and/or toxic gases. Runoff from fire control or dilution water may be corrosive and/or toxic and cause pollution.
ACUTE CLINICAL EFFECTS
- Based on its acute oral LD50 of 650 MICROGRAMS/kg in rats (RTECS , 1993), aldicarb is an EXTREMELY TOXIC substance (Morgan, 1989). It is hazardous by the dermal, oral, or subcutaneous exposure routes, and possibly by other routes (EPA, 1985; Sax & Lewis, 1989). There has been at least one occupational fatality in which exposure to aldicarb was a contributing factor (Lee & Ransdell, 1984).
- The largest reported episode of foodborne pesticide illness occurred in California in the summer of 1985, when 1,376 persons became ill from eating watermelons contaminated with aldicarb. At least 50% of affected persons exhibited signs of abdominal pain, nausea, vomiting, diarrhea, salivation, blurred vision, sweating, disorientation, and muscle twitching or weakness (Anon, 1986; Goldman et al, 1990a). A total of 61 definite cases amongst 264 reports were also noted approximately one week earlier in Oregon (Green et al, 1987).
- General symptoms of exposure to carbamate insecticides include nausea, vomiting, abdominal cramps, diarrhea, salivation, sweating, lassitude, weakness, rhinorrhea, chest tightness, blurring or dimness of vision, pinpoint pupils, tearing, eye pain, loss of coordination, slurring of speech, muscle twitching, breathing difficulty, cyanosis, hypertension, jerking movements, incontinence, convulsions, coma, and death due to paralysis of respiratory muscles, respiratory arrest, or bronchoconstriction (HSDB , 1993).
- Cardio-pulmonary arrest developed in 2 hours and acute necrotic hemorrhagic pancreatitis on the second day after intentional ingestion of TEMIK G(R), an insecticide containing 10% aldicarb. Pseudocholinesterase activity returned to normal after 77 days (Droy et al, 1994).
- The effects of acute exposure to carbamates may occasionally be long-lasting. Protracted malaise and weakness may occur after apparent recovery from carbamate poisoning (Garber, 1987). Delayed axonal peripheral neuropathy, similar to that seen with organophosphates, has been described in one patient who ingested 500 mg/kg of carbaryl (Dickoff et al, 1987).
- Carbamates cause rapid reversible inactivation of cholinesterases by formation of carbamylated enzymes. Reversal of inhibition is relatively rapid, with a half-life of hours. In known cases of aldicarb poisoning, symptoms have been rapidly reversible, sometimes within a few hours (National Research Council, 1977).
- The rapid reactivation of cholinergic activity with carbamate insecticide poisoning often results in less severe symptoms than those seen in organophosphate poisoning; however, it should be assumed that severe and even fatal anticholinergic effects can occur with exposure to any carbamate if the dose is sufficiently high. Respiratory depression and acute pulmonary edema are usually the immediate causes of death from acute exposures to N-methyl carbamates, such as aldicarb (Morgan, 1989).
- Carbamate insecticides are direct-acting cholinesterase inhibitors. Metabolism results in detoxification. Anticholinergic effects of carbamates are thus usually milder and more short-lived than those caused by organophosphates (Finkel, 1983). Carbamates are rapidly excreted in rats.
- Methylcarbamates inhibit a number of enzymes besides cholinesterases. Enzymes which have been inhibited by methylcarbamates include alkaline phosphatase, aldolase, arginase, glucose-6-phosphate dehydrogenase (G-6-PD), transaminase, and phosphofructokinase (Finkel, 1983).
CHRONIC CLINICAL EFFECTS
- There were 38 cases of occupational illness involving acute exposure to aldicarb during 1974 to 1975 in the state of California (Peoples, 1978). Chronic exposures are expected to produce effects similar to those seen in acute poisoning.
- Because carbamate insecticides generally have rapid inactivation and reversal of cholinesterase activity, cumulative toxicity is less likely with these compounds than with the organophosphates.
- Neurological effects have been reported with long-term exposure to carbaryl, a related compound. One patient developed a progressive debilitating syndrome, including headaches, memory loss, proximal muscle weakness, muscle fasciculations, muscle cramps, and anorexia with marked weight loss (Branch & Jacqz, 1986). These effects are similar to those seen with chronic organophosphate exposure. Persons who were exposed to aldicarb in ground water in Suffolk County, New York, reported symptoms of peripheral neuropathy in responses to a preliminary questionnaire (Sterman & Varma, 1983).
- Abnormalities in T-cell subsets were seen in a group of 23 women exposed to ground water contaminated with aldicarb in the less than 60 ppb range (Fiore et al, 1986).
-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 151 (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. For minor skin contact, avoid spreading material on unaffected skin. Keep victim warm and quiet. 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
- Aldicarb can be fatal if swallowed; at very low exposure levels, it causes reversible cholinesterase inhibition (EPA, 1990; HSDB , 1999).
- Aldicarb is the most toxic of the carbamate pesticides; it causes cholinesterase inhibition at very low exposure levels. Unlike other carbamates, aldicarb is extremely toxic by the oral, dermal, and inhalation routes of exposure (EPA Toxicity Category I). When it is applied in solutions of oil or other organic solvents, it is rapidly absorbed through the skin; its skin toxicity is roughly 1000 times that of other carbamates. After ingestion, it is rapidly and almost completely absorbed from the gut. Signs and symptoms of aldicarb poisoning include the sudden onset of diarrhea, nausea and vomiting, abdominal pain, excessive perspiration, blurred vision, headache, muscular fasciculations, temporary paralysis of the extremities, and dyspnea (EPA, 1990) EXTOXNET, 1999; (Hayes, 1982; Hayes & Laws, 1991).
- Based on its acute oral toxicity in rats, aldicarb would be in the SUPER TOXIC group of carbamates, with a probable lethal oral dose in humans of less than 5 mg/kg (less than 7 drops for a 150-pound person) (EPA, 1985).
MAXIMUM TOLERATED EXPOSURE
- In humans, the primary exposure route is oral, by way of food or water that is contaminated. Aldicarb is excreted in urine, primarily, and is quickly metabolized (EXTOXNET, 1999).
FOOD CONTAMINATION/CALIFORNIA: Illnesses were detected in patients receiving a dose of 0.0011 to 0.06 milligram/kilogram. This amounted to 1/4 to 1 cucumber and 1/2 slice to 5 slices of melon (Goldman et al, 1990). FOOD CONTAMINATION/CALIFORNIA: Illnesses were detected in patients receiving a dose of 0.0011 to 0.06 milligram/kilogram. This amounted to 1/4 to 1 cucumber and 1/2 slice to 5 slices of melon (Goldman et al, 1990). FOOD CONTAMINATION/NEBRASKA: Illnesses at doses of 0.025 to 0.041 milligram/kilogram of body weight (Jackson & Goldman, 1986; Goes et al, 1980). Severe poisoning requiring hospital treatment only occurred with exposures to more than 0.01 milligram/kilogram (Goldman et al, 1990). FOOD CONTAMINATION/LOUISIANA: Of 16 persons who ate an aldicarb-contaminated salad, 14 became ill, with predominantly gastrointestinal and neurological symptoms. It was estimated that a 6 gram portion of the salad contained 272.6 parts per million, or approximately 17 milligrams of aldicarb. Thus, a 70-kg adult would have consumed 0.2 milligrams of aldicarb per kilogram of body weight. All the victims recovered following symptomatic therapy (Anon, 1999). FOOD CONTAMINATION/GREENHOUSES: Two epidemics of poisoning from eating contaminated cucumbers grown in a hydroponic greenhouse have been recorded (Hayes, 1982b) with victims becoming ill between 1/2 and 12 hours after ingestion. All recovered without treatment. A woman consumed 0.5-1.0 g of a mint plant growing near a treated rosebush 24 days after the bush was treated with a 10% granular aldicarb formulation. Signs and symptoms of poisoning were maximal 2 hours after onset; after atropine treatment, the patient was resting comfortably three and a half hours after onset (Hayes, 1982). FAO/WHO estimated that the acceptable daily intake (ADI) of aldicarb is 0-0.005 mg/kg body weight; EPA set the ADI at 0.001 mg/kg body weight (Hayes & Laws, 1991).
- Occupational exposure to aldicarb may occur after product handling; most poisonings occur after loading and application. All confirmed occupational overexposures to aldicarb have occurred after improper handling or misuse of the product (EXTOXNET, 1999; (Hayes & Laws, 1991).
- Carcinogenicity Ratings for CAS116-06-3 :
ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed EPA (U.S. Environmental Protection Agency, 2011): D ; Listed as: Aldicarb 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): 3 ; Listed as: Aldicarb 3 : The agent (mixture or exposure circumstance) is not classifiable as to its carcinogenicity to humans. This category is used most commonly for agents, mixtures and exposure circumstances for which the evidence of carcinogenicity is inadequate in humans and inadequate or limited in experimental animals. Exceptionally, agents (mixtures) for which the evidence of carcinogenicity is inadequate in humans but sufficient in experimental animals may be placed in this category when there is strong evidence that the mechanism of carcinogenicity in experimental animals does not operate in humans. Agents, mixtures and exposure circumstances that do not fall into any other group are also placed in this category.
NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed 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 CAS116-06-3 (U.S. Environmental Protection Agency, 2011):
Oral: Slope Factor: RfD: 1x10(-3) mg/kg-day
Inhalation: Drinking Water:
LC50- (INHALATION)RAT: LD50- (ORAL)CHICKEN: LD50- (SKIN)GUINEA_PIG: LD50- (ORAL)LABORATORY_QUAIL: LD50- (ORAL)MOUSE: LD50- (SUBCUTANEOUS)MOUSE: LD50- (SKIN)RABBIT: LD50- (INTRAPERITONEAL)RAT: LD50- (INTRAVENOUS)RAT: LD50- (ORAL)RAT: LD50- (SKIN)RAT: LD50- (SUBCUTANEOUS)RAT: LD50- (UNASSIGNED)RAT: LDLo- (ORAL)GOAT: TCLo- (ORAL)HUMAN:
-STANDARDS AND LABELS
WORKPLACE STANDARDS
- ACGIH TLV Values for CAS116-06-3 (American Conference of Governmental Industrial Hygienists, 2010):
- AIHA WEEL Values for CAS116-06-3 (AIHA, 2006):
- NIOSH REL and IDLH Values for CAS116-06-3 (National Institute for Occupational Safety and Health, 2007):
- OSHA PEL Values for CAS116-06-3 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
- OSHA List of Highly Hazardous Chemicals, Toxics, and Reactives for CAS116-06-3 (U.S. Occupational Safety and Health Administration, 2010):
ENVIRONMENTAL STANDARDS
- EPA CERCLA, Hazardous Substances and Reportable Quantities for CAS116-06-3 (U.S. Environmental Protection Agency, 2010):
Listed as: Propanal, 2-methyl-2-(methylthio)-, O-[(methylamino)carbonyl]oxime Final Reportable Quantity, in pounds (kilograms): Additional Information: Listed as: Aldicarb Final Reportable Quantity, in pounds (kilograms): Additional Information:
- EPA CERCLA, Hazardous Substances and Reportable Quantities, Radionuclides for CAS116-06-3 (U.S. Environmental Protection Agency, 2010):
- EPA RCRA Hazardous Waste Number for CAS116-06-3 (U.S. Environmental Protection Agency, 2010b):
Listed as: Aldicarb P or U series number: P070 Footnote: Listed as: Propanal, 2-methyl-2-(methylthio)-, O-[(methylamino)carbonyl]oxime P or U series number: P070 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 CAS116-06-3 (U.S. Environmental Protection Agency, 2010):
Listed as: Aldicarb Reportable Quantity, in pounds: 1 Threshold Planning Quantity, in pounds: Note(s): b
- EPA SARA Title III, Community Right-to-Know for CAS116-06-3 (40 CFR 372.65, 2006; 40 CFR 372.28, 2006):
- DOT List of Marine Pollutants for CAS116-06-3 (49 CFR 172.101 - App. B, 2005):
- EPA TSCA Inventory for CAS116-06-3 (EPA, 2005):
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 CAS116-06-3 (NFPA, 2002):
-HANDLING AND STORAGE
SUMMARY
Aldicarb is highly toxic, systemic carbamate compound. Do not get aldicarb on the skin or in the eyes. Do not ingest or inhale aldicarb dust. It should only be used, handled, and stored in a regulated, marked area. Personnel should wash immediately after exposure to aldicarb and again at the end of their shift. Static electrical charges can build up when aldicarb powders are subjected to friction that results from sliding, conveying, or mixing. When aldicarb is used near flammable materials, proper precautions (inert atmospheres, electrical grounding) should be taken in order to prevent fires (Lewis, 1998; (Hartley & Kidd, 1987; Rhone-Poulenc , 1999; Sittig, 1991). Other Preventative Measures (HSDB , 1999): Change clothing that has become contaminated each day. Before re-use, wash the clothing in a strong soda solution and rinse thoroughly. After working with aldicarb, wash hands before smoking or eating. At the end of each work day, personnel should bathe, ensuring that the entire body and hair are thoroughly cleansed with soap and water.
HANDLING
- Wear appropriate protective clothing when using or handling aldicarb; wash immediately after exposure to it (Hartley & Kidd, 1987; Sittig, 1991).
STORAGE
- ROOM/CABINET RECOMMENDATIONS
Aldicarb should be stored in a regulated, marked area, out of reach of children and animals, and away from food, feedstuffs, fertilizers, and seed. Aldicarb is not stable at 50 degrees C (HSDB , 1999; Sittig, 1991).
Under normal storage conditions and in acidic media, aldicarb is stable; however, it decomposes rapidly in alkaline media and at temperatures above 100 degrees C. Store away from strong alkalis (such as sodium hydroxide and sodium bicarbonate) and strong bases (Hayes & Laws, 1991; Sittig, 1991).
-PERSONAL PROTECTION
SUMMARY
- RECOMMENDED PROTECTIVE CLOTHING - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 151 (ERG, 2004)
Wear positive pressure self-contained breathing apparatus (SCBA). Wear chemical protective clothing 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.
- Aldicarb is extremely toxic by the oral, dermal, and inhalation routes of exposure (EPA Toxicity Category I). Ingestion, inhalation, and skin contact should be prevented by use of appropriate protective clothing, gloves and footwear. Consideration must be given to durability as well as to permeation resistance. Thoroughly wash immediately after exposure to aldicarb and at the end of all work shifts (EPA, 1990) EXTOXNET, 1999; (Hayes, 1982; Hayes & Laws, 1991; Sittig, 1991).
EYE/FACE PROTECTION
- Prevent contact with the eyes; wear appropriate eye protection (HSDB , 1999).
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 116-06-3.
-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 151 (ERG, 2004) Non-combustible, substance itself does not burn but may decompose upon heating to produce corrosive and/or toxic fumes. Containers may explode when heated. Runoff may pollute waterways.
Aldicarb will ignite only with extreme difficulty. Once ignited, it may burn. Fight fire from a long distance and remain upwind. All personnel should keep away from low areas and ensure that closed areas are well-ventilated. If little risk is involved, move aldicarb containers out of the hazard area (Sittig, 1991).
- FLAMMABILITY CLASSIFICATION
- NFPA Flammability Rating for CAS116-06-3 (NFPA, 2002):
- FIRE CONTROL/EXTINGUISHING AGENTS
- SMALL FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 151 (ERG, 2004)
- LARGE FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 151 (ERG, 2004)
Water spray, fog or regular 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 151 (ERG, 2004)
Fight fire from maximum distance or use unmanned hose holders or monitor nozzles. Do not get water inside containers. 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 CAS116-06-3 (NFPA, 2002):
- Fight large fires involving aldicarb with water spray, fog, or foam. Fight small fires with dry chemical, carbon dioxide, water spray, or foam (Sittig, 1991).
DUST/VAPOR HAZARD
- Aldicarb is a very toxic inhalation hazard (EPA, 1990).
- Static electrical charges can build up when aldicarb powders are subjected to friction that results from sliding, conveying, or mixing. When aldicarb is used near flammable materials, proper precautions (inert atmospheres, electrical grounding) should be taken in order to prevent fires (Rhone-Poulenc , 1999).
REACTIVITY HAZARD
- Under normal storage conditions and in acidic media, aldicarb is stable; however, it decomposes rapidly in alkaline media and at temperatures above 100 degrees C. Store away from strong alkalis (such as sodium hydroxide and sodium bicarbonate) and strong bases (Hayes & Laws, 1991; Sittig, 1991).
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 151 (ERG, 2004)
Increase, in the downwind direction, as necessary, the isolation distance of at least 25 to 50 meters (80 to 160 feet) in all directions.
- FIRE - PUBLIC SAFETY EVACUATION DISTANCES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 151 (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 151 (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 in all directions for at least 50 meters (150 feet) for liquids and at least 25 meters (75 feet) for solids. Keep unauthorized personnel away. Stay upwind. Keep out of low areas.
- Evacuate and isolate the area; evacuate residents who are downwind. Deny entry to the isolated hazard area. Stay upwind (Sittig, 1999).
- AIHA ERPG Values for CAS116-06-3 (AIHA, 2006):
- DOE TEEL Values for CAS116-06-3 (U.S. Department of Energy, Office of Emergency Management, 2010):
Listed as Carbanolate; (Aldecarb; Methyl-2-(methylthio)propionaldehyde oxime, 2-) TEEL-0 (units = mg/m3): 0.0001 TEEL-1 (units = mg/m3): 0.0003 TEEL-2 (units = mg/m3): 0.3 TEEL-3 (units = mg/m3): 100 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 CAS116-06-3 (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):
Listed as: Aldicarb Proposed Value: AEGL-1 10 min exposure: 30 min exposure: 1 hr exposure: 4 hr exposure: 8 hr exposure:
Definitions: AEGL-1 is the airborne concentration of a substance above which it is predicted that the general population, including susceptible individuals, could experience notable discomfort, irritation, or certain asymptomatic non-sensory effects. However, the effects are not disabling, are transient, and are reversible upon cessation of exposure.
Listed as: Aldicarb Proposed Value: AEGL-2 10 min exposure: 30 min exposure: 1 hr exposure: ppm: mg/m3: 0.087 mg/m(3)
4 hr exposure: ppm: mg/m3: 0.053 mg/m(3)
8 hr exposure: ppm: mg/m3: 0.027 mg/m(3)
Definitions: AEGL-2 is the airborne concentration 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.
Listed as: Aldicarb Proposed Value: AEGL-3 10 min exposure: 30 min exposure: 1 hr exposure: 4 hr exposure: 8 hr exposure: ppm: mg/m3: 0.081 mg/m(3)
Definitions: AEGL-3 is the airborne concentration of a substance above which it is predicted that the general population, including susceptible individuals, could experience life-threatening health effects or death.
- NIOSH IDLH Values for CAS116-06-3 (National Institute for Occupational Safety and Health, 2007):
CONTAINMENT/WASTE TREATMENT OPTIONS
SPILL OR LEAK PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 151 (ERG, 2004) Do not touch damaged containers or spilled material unless wearing appropriate protective clothing. Stop leak if you can do it without risk. Prevent entry into waterways, sewers, basements or confined areas. Cover with plastic sheet to prevent spreading. Absorb or cover with dry earth, sand or other non-combustible material and transfer to containers. DO NOT GET WATER INSIDE CONTAINERS.
RECOMMENDED PROTECTIVE CLOTHING - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 151 (ERG, 2004) Wear positive pressure self-contained breathing apparatus (SCBA). Wear chemical protective clothing 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.
If aldicarb is spilled, keep unnecessary people away from the spill area. Ensure that personnel remain upwind and out of low areas; ventilate closed spaces before entering. Wear appropriate protective clothing including respiratory protection; do not touch spilled aldicarb unless wearing appropriate protective clothing. Remove and isolate contaminated clothing at the site (Sittig, 1991).
Small Spills: "Take up with sand or other noncombustible absorbent material and place into containers for later disposal." (Sittig, 1991) Small Dry Spills: "With clean shovel, place material into clean, dry container and cover; move containers from spill area." (Sittig, 1991)
It is recommended that aldicarb be incinerated (followed by effluent gas scrubbing) (Sittig, 1991). 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
- Aldicarb is released to the environment as a result of its manufacture and use as a systemic insecticide, acaricide, and nematocide (Howard, 1991).
ENVIRONMENTAL FATE AND KINETICS
Aldicarb released into air will react with hydroxyl radicals with an estimated vapor phase half-life of 0.24 days. However, it may also be partially absorbed into airborne particulate matter where it will not react with hydroxyl radicals (Howard, 1991).
SURFACE WATER Aldicarb in water will not adsorb to sediments. Based on an octanol/water coefficient of 5 it will not bioconcentrate in aquatic organisms. It will hydrolyze, but based on the Henry's Law Constant, volatilization will not be an important fate process (EPA, 1990) EXTOXNET, 1999; (Howard, 1991). The scientific judgment of the half-life of aldicarb in surface water ranges from 20 days (480 hours) to 361 days (8664 hours) based on estimated aqueous aerobic biodegradation (Howard et al, 1991). The scientific judgment of the half-life of aldicarb in ground water ranges from 40 days (960 hours) to 635 days (15,240 hours) based on estimated aqueous aerobic biodegradation and anaerobic ground water grab sample data (Howard et al, 1991). Half-lives in water vary with pH and temperature (EXTOXNET, 1999; (Howard, 1991): 131 days at pH 3.95 and 20 degrees C 170 days at pH 8.5 and 15 degrees C 175 days at pH 4.5 and 22 degrees C 245 days at pH 7.0 and 25 degrees C 266 days at pH 8.0 and 25 degrees C 324 days at pH 7.96 and 20 degrees C 1900 days at pH 7.5 and 15 degrees C 3240 days at pH 5.5 and 15 degrees C
TERRESTRIAL Aldicarb is is moderately persistent when released to soil, but will sorb only a very small amount. Based on the soil type, it will hydrolyze and oxidize (both chemically and biologically) to form the sulfoxide and sulfone at various rates. Subsurface soils oxidize aldicarb more slowly than near surface soils. Aldicarb is mobile in fine to coarse textured soils, even those soils with high organic matter content, and will migrate to ground water; however, it is not expected to move horizontally from a bare, sloping field (EPA, 1990) EXTOXNET, 1999; (Howard, 1991). The scientific judgment of the half-life of aldicarb in soil ranges from 20 days (480 hours) to 361 days (8664 hours) based on unacclimated aerobic soil grab sample data (Howard et al, 1991). The degradation and movement of aldicarb residues was measured in soil and groundwater in potato fields. The average half-life in groundwater was found to be less than 1 year (Jones et al, 1992). Aldicarb residues degraded at a rate corresponding to a half-life of about 1.1 months in soils (Jones et al, 1992). Generally, in-furrow applications of aldicarb result in greater residue movement than aldicarb applied at the early-plant-emergence stage (Jones et al, 1986). The half-life times for total toxic residue disappearance in groundwater-saturated subsoils in Indian River County, Florida, was estimated to range from 10-26 days, suggesting a resumption of faster aerobic degradation rates in the upper soil layers after having undergone slow degradation in unsaturated subsoils. It was estimated that toxic residues in aldicarb-contaminated groundwaters in Indian River County would migrate only short distances (1-17 ft) before conversion of toxic residues to non-toxic residues was completed (Dierberg FE, 1984).
ABIOTIC DEGRADATION
- "The hydrolysis reactions of aldicarb are both acid and base catalyzed." Generally, the rate of hydrolysis in water by itself is slower than the rate when soil is present. "While aldicarb is susceptible to photolysis when irradiated in acetonitrile at 254 nm, no data were found that indicate that it is photolyzed at environmentally important wavelengths" (Howard, 1991).
"Scientific judgment of the photooxidation half-life of aldicarb in air": range - 1 hour to 9.5 hours based on the estimated rate constant for vapor phase reaction with hydroxyl radicals (Howard et al, 1991). A first order hydrolysis half-life is 12.5 years (4580 days) based on a first order rate constant of 1.5 x 10(-4) day(-1) at pH 5 and 5 degrees C (Howard et al, 1991). Another first order hydrolysis half-life is 55 days (1320 hours) based on a first order rate constant of 1.3 x 10(-2) day(-1) at pH 8.85 and 20 degrees C (Howard et al, 1991).
BIODEGRADATION
- Studies on aldicarb biodegradation rarely focus on the distinction between biological and chemical degradation. Occasionally, it is reported that aldicarb oxidation is mediated biologically (Howard, 1991).
The scientific judgment of the aerobic half-life of aldicarb ranges from 20 days (480 hours) to 361 days (8664 hours) "based on unacclimated aerobic soil grab sample data" (Howard et al, 1991). "The scientific judgment based upon anaerobic half-life of aldicarb": range - 62 days (1488 hours) to 635 days (15,240 hours) based on anaerobic ground water grab sample data (Howard et al, 1991).
BIOACCUMULATION
AQUATIC Aldicarb and its metabolites are absorbed by plants from the soil and translocated into the roots, stems, leaves, and fruit. Aldicarb residues have been reported in citrus fruit and leaves, sugar beets, and grape leaves and fruit (EPA, 1990; Howard, 1991).
ENVIRONMENTAL TOXICITY
- Aldicarb is highly toxic to mammals, birds, estuarine/marine, and freshwater organisms (EPA, 1990) EXTOXNET, 1999).
It is very toxic to birds; their greatest exposure is through eating "unincorporated granules" and "contaminated earthworms" (EXTOXNET, 1999). "Aldicarb is not toxic to bees, even when applied directly" (EXTOXNET, 1999).
- ECOTOXICITY VALUES (HSDB , 1999):
LC50 - (ORAL) Phasianus colchicus (ring-necked pheasant, age 10 days): >300 ppm in 5D diet ad libitum (no mortality to 300 ppm), technical material, 99.0% LC50 - (ORAL) Anas platyrhynchos (mallard duck, age 10 days): <1000 ppm in 5D diet ad libitum (70% mortality at 1000 ppm), technical material, 99.0% LC50 - (ORAL) Anas platyrhynchos (mallard duck, age 5 days): 594 ppm in 5D diet ad libitum (95% confidence limit 507-695 ppm), technical material, 99.0% LC50 - (ORAL) Coturnix japonica (Japanese quail, age 14 days): 381 ppm in 5D diet ad libitum (95% confidence limit 317-453 ppm), technical material, 99.0% LC50 - (ORAL) Bobwhite quail, age 56 days: 2400 mg/kg for 7D LC50 - Rainbow trout: 8.8 mg/L for 96H, conditions of bioassay not specified LC50 - Paramecium multimicronucleatum: 145 ppm for 9H; 122 ppm for 13H; 104 ppm for 17H; 93 ppm for 24H; static bioassay LC50 - Pimephales promelas (Fathead minnow): 1370 mcg/L for 96H, flow-through bioassay LC50 - (ORAL) Anas platyrhynchos (mallard duck, 3-4M females): 3.40 mg/kg (95% confidence limit 2.70-4.28 mg/kg) LC50 - (ORAL) Callipepla californica (California quail, 10M males): 2.58 mg/kg (95% confidence limit 1.96-3.40 mg/kg) LC50 - (ORAL) Callipepla californica (California quail, 10M females): 4.67 mg/kg (95% confidence limit 3.32-6.56 mg/kg) LC50 - (ORAL) Phasianus colchicus (pheasant, 3-4M females): 5.34 mg/kg (95% confidence limit 3.85-7.40 mg/kg) LC50 - (ORAL) Coturnix japonica (Japanese quail): 387 ppm in 5D diet ad libitum (95% confidence limit 336-445 ppm), technical grade, 99% active ingredient
-PHYSICAL/CHEMICAL PROPERTIES
MOLECULAR WEIGHT
DESCRIPTION/PHYSICAL STATE
- Aldicarb forms colorless to white crystals which are odorless or have a slightly sulfurous odor (Budavari, 1996; Hartley & Kidd, 1987; Hayes, 1982; Hayes & Laws, 1991; Lewis, 1997) Lewis, 1998; (Verschueren, 1983).
VAPOR PRESSURE
- 1 x 10(-5) mmHg (at 0 degrees C) (Hayes & Laws, 1991)
- 0.05 mmHg (at 20 degrees C) (Hayes, 1982)
- 13 mPa (at 20 degrees C) (Hartley & Kidd, 1987)
- 1 x 10(-4) mmHg (at 25 degrees C) (Hayes & Laws, 1991; Howard, 1991; Verschueren, 1983)
- 7 x 10(-4) mmHg (at 50 degrees C) (Hayes & Laws, 1991)
- 4 x 10(-3) mmHg (at 75 degrees C) (Hayes & Laws, 1991)
SPECIFIC GRAVITY
- OTHER TEMPERATURE AND/OR PRESSURE
DENSITY
- NORMAL TEMPERATURE AND PRESSURE
BOILING POINT
- Aldicarb decomposes quickly above 100 degrees C (Hayes & Laws, 1991; Howard, 1991).
FLASH POINT
AUTOIGNITION TEMPERATURE
EXPLOSIVE LIMITS
SOLUBILITY
OCTANOL/WATER PARTITION COEFFICIENT
HENRY'S CONSTANT
- 1.0 x 10(-10) atm-m(3)/mol (Ehrenfeld et al, 1986)
- 4.17 x 10(-9) atm-m(3)/mole (Howard, 1991)
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