METHOMYL
HAZARDTEXT ®
Information to help in the initial response for evaluating chemical incidents
-IDENTIFICATION
SYNONYMS
Acetimidic acid, N-((methylcarbamoyl)oxy)thio-,methyl ester Acetimidothioic acid, methyl-, N-(methylcarbamoyl) ester Acetimidic acid, thio-N-((methylcarbamoyl)oxy)-, methyl ester CAS 16752-77-5 DUPONT 1179 DU PONT insecticide 1179 Ethanimidothioic acid, N-(((methylamino)carbonyl)oxy)-, methyl ester IN 1179 Insecticide 1,179 Lannate Lannate L Mesomile N-(((methylamino)carbonyl)oxy)ethanimidothioic acid methyl ester N-((methylcarbamoyl)oxy)thioacetimidic acid methyl ester Methyl N-(((methylamino)carbonyl)oxy)ethanimidothioate Methyl-N-((methylcarbamoyl)oxy)thioacetimidate S-methyl N-(methylcarbamoyloxy)thioacetimidate Methyl O-(methylcarbamoyl)thiolacethohydroxamate 1-(methylthio) acetaldehyde O-methyl carbamoyloxime 1-(methylthio) ethylideneamino methylcarbamate Metomil (Italian) NU-BAIT II Nudrin SD 14999 3-Thiabutan-2-one, o-(methylcarbamoyl)oxime WL 18236 Acetimidic acid, thio-N-(methylcarbamoyl)-oxy)-, methyl ester Methyomyl
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.
SYNONYM REFERENCE
- (RTECS , 1990; EPA, 1985)
USES/FORMS/SOURCES
Methomyl is a typical cholinesterase inhibitor and is used as an insecticide and nematocide on food crops, tobacco, and cotton (EPA, 1985; Lewis, 1993).
Methomyl is a carbamate compound. It occurs as a colorless or white crystalline solid with a slightly sulfurous odor (HSDB , 1996; ACGIH, 1992). Methanol is used as a solvent in many methomyl pesticide products (Gil et al, 2012). Please refer to "METHANOL" document for information on methanol toxicity.
-CLINICAL EFFECTS
GENERAL CLINICAL EFFECTS
- USES: Methomyl is a carbamate insecticide. Poisoning occasionally occurs from ingestion of contaminated crops or food.
- TOXICOLOGY: Carbamates 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 is common, but serious toxicity is unusual in the US. Common source of severe poisoning in developing countries. Toxicity is 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. 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 to 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
TOXICOLOGY: Carbamates 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 is common, but serious toxicity is unusual in the US. Common source of severe poisoning in developing countries. Toxicity is generally less severe than with organophosphates. EXPOSURE 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. 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 to 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.
METABOLIC ACIDOSIS, CASE REPORT: Metabolic acidosis (pH 7.25; bicarbonate 17) developed in a 25-year-old man who also experienced abdominal pain, coma, renal dysfunction, and fulminant hepatic failure after ingesting a half cup of a liquid containing 90% methomyl. Despite supportive care, he died 14 days after admission (Agha et al, 2009).
ATRIAL FIBRILLATION, CASE REPORT: A 26-year-old man presented with nausea and vomiting after exposure to methomyl dust. Cardiac examination showed an irregular heart rate, and ECG revealed atrial fibrillation with normal ventricular response. Following supportive care, his heart rhythm spontaneously returned to sinus rhythm 24 hours post-admission. He was discharged home without further sequela (Topacoglu et al, 2007). BRADYCARDIA: Muscarinic effects may commonly include bradycardia (Kudo et al, 2005; Park et al, 2000; Morgan, 1993). TACHYCARDIA: Nicotinic effects may include sinus tachycardia (Tracqui et al, 2001; Aaron & Howland, 1998). CONDUCTION DISORDER: T-wave changes including inversion were reported in a study of 22 spraymen with a 5-day exposure to methomyl (Saiyed et al, 1992). HYPOTENSION: Hypotension has been reported following carbamate insecticide poisoning due to weakened cardiac contractility (Park et al, 2000). ABNORMAL ECG: Sinus tachycardia with ST segment depression may occur early in the course of poisoning. Repolarization abnormalities may occur and are generally transient (Tracqui et al, 2001). HYPERTENSION: Nicotinic effects may include hypertension (Tracqui et al, 2001; Aaron & Howland, 1998).
DIAPHORESIS: Diaphoresis may commonly develop as a muscarinic effect (Waseem et al, 2010; Kudo et al, 2005; Park et al, 2000; Burgess et al, 1994; Morgan, 1993).
Nausea, vomiting, diarrhea, abdominal pain, and spontaneous defecation may occur (Agha et al, 2009; Topacoglu et al, 2007; Kudo et al, 2005). Nausea and vomiting were some of the most frequently reported symptoms in persons occupationally exposed to methomyl (Morse et al, 1979; South Dakota, 1971). SALIVATION: Salivation may occur as a cholinergic crisis effect following intentional ingestions (Waseem et al, 2010; Park et al, 2000; Flesch et al, 1999). PANCREATITIS: In a prospective case study of 17 children with documented organophosphate or carbamate insecticide poisoning, 5 were diagnosed with acute pancreatitis. All of the 5 had significantly elevated serum levels of immunoreactive trypsin and 4 had a significant increase in serum amylase levels. Clinical manifestations were mild. One case was a documented carbamate poisoning (Weizman & Sofer, 1992).
URINARY INCONTINENCE: Urinary incontinence has been reported following methomyl poisoning (Kudo et al, 2005). ABNORMAL RENAL FUNCTION TESTS: Renal biochemical abnormalities in a study of patients (n=84) following acute poisoning with carbamate insecticides or organophosphates included azotemia (BUN greater than 6.7 mmol/L) (21%), hematuria (17%), glycosuria (15%) and proteinuria (5%) (Saadeh, 2001).
MIOSIS: Miosis (pinpoint pupils) and blurred vision may be seen following exposure (ACGIH, 1991; Kudo et al, 2005). Miosis, a muscarinic effect, is characteristic of severe and moderately severe poisonings, but may appear late (Waseem et al, 2010; Hoffmann et al, 2008; Tsatsakis et al, 2001; Tracqui et al, 2001; Park et al, 2000; Flesch et al, 1999; Covaci et al, 1999). MYDRIASIS: Pupil dilation may occur as a nicotinic effect and may be present in up to 10% of patients (Aaron & Howland, 1998). LACRIMATION: Signs of acute toxicity may include lacrimation (Hayes, 1982). EXCESSIVE SALIVATION: Excessive salivation may occur (Hathaway et al, 1996; ACGIH, 1991).
CHOLINESTERASE INHIBITION: Methomyl reversibly inhibits serum pseudocholinesterase and erythrocyte acetylcholinesterase. In one case of exposure, up to 50% of the inhibition was seen within 40 minutes of exposure (Simpson & Bermingham, 1977). Recovery from methomyl inhibition is especially rapid, and in one case, recovery was essentially complete within 36 to 48 hours (Simpson & Bermingham, 1977). COAGULOPATHY: Disseminated intravascular coagulation caused by another carbamate, propoxur, has been reported (Misra et al, 1987).
HEPATIC FAILURE, CASE REPORT: Fulminant hepatic failure developed in a 25-year-old man who also experienced abdominal pain, coma, metabolic acidosis, and renal dysfunction after ingesting a half cup of a liquid containing 90% methomyl. Despite supportive care, including veno-venous hemofiltration, multiple fresh frozen plasma and albumin infusions, he died 14 days after admission (Agha et al, 2009). HYPERBILIRUBINEMIA: In a case series of 49 carbamate insecticide poisonings, 9 patients (11%) developed elevated serum bilirubin concentrations. Mean total serum bilirubin was reported to be 69.05 micromols/liter, while the mean indirect serum bilirubin concentration was 45.2 micromols/liter (Saadeh, 2001).
ENZYME INHIBITION: Methylcarbamates such as methomyl may inhibit a number of enzymes besides cholinesterases. Enzymes which have been inhibited by other methylcarbamates include alkaline phosphatase, aldolase, arginase, glucose-6-phosphate dehydrogenase (G-6PD), transaminase, and phosphofructokinase (Finkel, 1983).
MUSCLE FASCICULATIONS: Fasciculations, muscle weakness, involuntary twitching, and tremor are nicotinic effects that may occur following methomyl exposure (Hathaway et al, 1996) (ACGIH, 1991). MUSCLE WEAKNESS, CHRONIC EXPOSURE: Muscle weakness and fatigue were reported in persons occupationally exposed to methomyl (Morse et al, 1979).
Headache, blurred vision, miosis, tremor, paresis, and muscle twitching may be noted. Severe headache was the primary symptom in one case of acute methomyl poisoning (Smith, 1977). SEIZURE: In severe poisoning, respiratory depression and convulsions may occur (Hathaway et al, 1996). Seizure may occur following carbamate exposure, and children may be more susceptible to seizures than adults. In one series, 2 children poisoned by carbamates had seizures (Zweiner & Ginsburg, 1988). COMA: Unconsciousness and coma may occur in severe poisoning (Agha et al, 2009; Hathaway et al, 1996a). In one case series, 8 of 8 children with carbamate poisoning developed severe CNS depression with stupor and coma (Sofer et al, 1989). TREMOR: Tremor, paresis, and muscle twitching may be noted (Morgan, 1993). SEIZURES: In severe poisoning convulsions may occur. Children may be more susceptible to seizures than adults; in one series 2 children poisoned by carbamates had seizures (Zweiner & Ginsburg, 1988). In another series, 8 of 8 children with carbamate poisoning developed severe CNS depression with stupor and coma (Sofer et al, 1989). PERIPHERAL NEUROPATHY: NEUROPATHY: CASE REPORT: 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). MUSCLE WEAKNESS: Protracted malaise and weakness may occur after apparent recovery from carbamate poisoning (Garber, 1987). MUSCLE FASCICULATIONS: Muscle fasciculations may develop as a nicotinic effect (Waseem et al, 2010; Hoffmann et al, 2008; Ragoucy-Sengler et al, 2000; Flesch et al, 1999; Burgess et al, 1994; Ekins & Geller, 1994). HYPOTONIA: Hypotonia is a common nicotinic effect of carbamate insecticide poisoning (Ragoucy-Sengler et al, 2000; Tsatsakis et al, 2001). FATIGUE: Protracted malaise and weakness may occur after apparent recovery from carbamate poisoning (Garber, 1987).
MEMORY LOSS, CASE REPORT: A patient who had long-term excessive exposure to carbaryl 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).
DYSPNEA: Dyspnea is a common manifestation of carbamate insecticide exposure (Uludag et al, 2001; Ragoucy-Sengler et al, 2000). Chest tightness, bronchospasm, increased pulmonary secretions, and rales may develop secondary to muscarinic effects (Markowitz, 1992). RESPIRATORY DEPRESSION: Respiratory depression and rales may be noted. Dyspnea was reported in 7 of 8 children with carbamate poisoning (Sofer et al, 1989). Usual cause of death is respiratory failure as a result of respiratory muscle weakness and central depression of the respiratory drive (Aaron & Howland, 1998; Park et al, 2000). BRONCHOSPASM: Bronchospasm and chest tightness may occur (Morgan, 1993). ACUTE LUNG INJURY: Acute lung injury (pulmonary edema) is a potential clinical manifestation of severe carbamate poisoning and is attributed to the muscarinic action of the insecticide. Contributing factors to the development of pulmonary edema include bradycardia and weakened cardiac contraction from an accumulation of acetylcholine on the cardiovascular system. Hypoxia may develop due to increasing capillary permeability (Park et al, 2000; Tsatsakis et al, 2001). LARYNGEAL IRRITATION: Laryngeal irritation, violent coughing, and tachypnea occur frequently following inhalation of carbamate dusting powders and may not necessarily be associated with systemic signs and symptoms of carbamate poisoning (Alcorn & Hughes, 1980). ASPIRATION PNEUMONITIS: Aspiration pneumonitis may occur after ingestion of carbamates in hydrocarbon vehicles. A complication of prolonged intubation and mechanical ventilation following pulmonary effects of poisoning is aspiration pneumonia (Aaron & Howland, 1998).
TACHYPNEA: Tachypnea may occur following inhalation of carbamate dusting powders, but is not necessarily related to severity of ensuing symptoms (Alcorn & Hughes, 1980). HYPOTHERMIA: In a pediatric case series (n=54) of anticholinesterase (carbamate and organophosphate) poisonings, hypothermia was reported in 7% and hyperthermia was reported in 6% of the children (Verhulst et al, 2002).
CHRONIC CLINICAL EFFECTS
- Because it is rapidly metabolized to inactive products, methomyl might be predicted NOT to have cumulative toxicity with repeated exposures (ACGIH, 1992). Methomyl was less toxic following chronic exposure than with acute exposure in rats. No cumulative toxicity was seen with oral dosing in rats or dermal application in rabbits (Kaplan & Sherman, 1977).
- Occupational exposure to methomyl can produce clinical signs and symptoms in the absence of cholinesterase depression (Morse et al, 1979; South Dakota, 1971).
- Clinical symptoms which have been produced from occupational exposure to methomyl include, miosis, blurred vision, increased salivation, nausea, vomiting, fatigue, and muscle weakness (Morse et al, 1979; South Dakota, 1971).
- 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 organophosphate exposure, but have not been reported in methomyl exposures. Methomyl did not cause delayed neurotoxicity at a dose of 200 mg/kg in the standard atropinized hen assay (EPA, 1990).
- There was no cumulative toxicity when methomyl was administered to rats at an oral dose of 5.1 mg/kg/day over 14 days (ACGIH, 1992). No cumulative development of symptoms or cumulative inhibition of cholinesterase were seen in rats given methomyl at 9.9 mg/m(3) or 14.8 mg/m(3) for up to 3 months (Tanaka et al, 1987).
- No effects were seen at doses up to 250 ppm of methomyl in a 90-day feeding study in rats, but 200 and 400 ppm produced lower hemoglobin levels in females after 22 months (Kaplan & Sherman, 1977). No effects were seen in dogs given up to 400 ppm of methomyl in the diet for 2 years (Kaplan & Sherman, 1977).
- Two cases of contact sensitivity to methomyl have been reported in female nursery workers (Bruynzeel, 1991). Methomyl was not a sensitizer in guinea pigs (ACGIH, 1992).
-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.
- ANTIDOTE: 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.
ANTIDOTE: 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
- The actual lethal dose of a carbamate can vary widely and depends strongly on the route and rate of exposure and on the aggressiveness of the treatment used.
- Methomyl is considered one of the more toxic carbamates, with a rat LD50 of less than 50 mg/kg (Reigart & Roberts, 1999); however serious toxicity has not been reported after inadvertent exposure to commercial formulations.
- Ingestion of contaminated food resulted in three fatalities; the estimated lethal dose from this incident was 12 to 15 mg/kg (Liddle et al, 1979).
- Fatality resulted following inhalation and transdermal absorption of methomyl in a farmer who used this product with no self-protection. Blood concentration of methomyl on admission (prior to death) was 1.6 mg/dL (Tsatsakis et al, 2001).
- CASE REPORT: Fulminant hepatic failure developed in a 25-year-old man who also experienced abdominal pain, coma, metabolic acidosis, and renal dysfunction after ingesting a half a cup of a liquid containing 90% methomyl. Despite supportive care, including veno-venal hemodialysis, multiple fresh frozen plasma, and albumin infusions, he died 14 days after admission (Agha et al, 2009).
- CASE STUDY: Plasma cholinesterase (ChE) activity was measured in 105 healthy Thai children. The mean was 7,417 +/- 1,620 units/L. This was compared to the ChE activities (470 and 680 units/L) of two children intentionally poisoned with methomyl. The authors concluded that as little as a 10% decrease in plasma ChE levels in children may be a lethal anti-ChE poisoning (Ruangyuttikarn et al, 2001).
MAXIMUM TOLERATED EXPOSURE
The World Health Organization (WHO) has classified methomyl, technical grade, as pesticide class IB (highly hazardous) (World Health Organization, 2006).
Note that CHILDREN MAY EXHIBIT DIFFERENT PREDOMINANT SIGNS of poisoning from adults. In a study on 25 children poisoned by organophosphate or carbamate compounds, the major symptoms in most of them were CNS depression, stupor, flaccidity, dyspnea, and coma. Other classical signs of organophosphate poisoning, such as miosis, fasciculations, bradycardia, excessive salivation and lacrimation, and gastrointestinal symptoms, were infrequent (Sofer et al, 1989).
CASE REPORT: A 50-year-old man presented to the ED 1 hour after ingesting 30 mL of a nutrition supplement that contained methomyl (approximately 63 mg of methomyl). He complained of chest discomfort, sweating, and vomiting. Myosis, severe bradycardia, and urinary and fecal incontinence were also observed. He completely recovered after approximately 8 hours of emergency treatment. His blood concentration of 0.63 mcg/mL was considered toxic but not fatal (Kudo et al, 2005). In a retrospective review of 14 consecutive methomyl poisoning cases (volume: 5 mL inhalation and 50 to 200 mL oral), 11 patients developed myocardial injury. Other adverse effects included altered mental status (n=10; 71.4%), pneumonia (n=6; 42.9%), respiratory failure (n=6; 42.9%), and shock (n=2; 14.3%; systolic blood pressure less than 90 mmHg) (Lee et al, 2015).
Three workers at a pesticide-formulating plant developed symptoms of organophosphate poisoning associated with each worker wearing a uniform that was contaminated with 76 percent parathion and then laundered. The uniform had been laundered three times before the third worker wore it and he still developed nausea, vomiting, and red cell cholinesterase activity of 75 percent of normal (Clifford & Nies, 1989).
No effects were seen at doses up to 250 ppm of methomyl in a 90-day feeding study in rats, but 200 and 400 ppm produced lower hemoglobin values in females after 22 months (Kaplan & Sherman, 1977). No effects were seen in dogs given up to 400 ppm of methomyl in the diet for 2 years (Kaplan & Sherman, 1977).
- Carcinogenicity Ratings for CAS16752-77-5 :
ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A4 ; Listed as: Methomyl ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Methomyl EPA (U.S. Environmental Protection Agency, 2011): Not Assessed under the IRIS program. ; Listed as: Methomyl 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: Methomyl 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 CAS16752-77-5 (U.S. Environmental Protection Agency, 2011):
Oral: Inhalation: Drinking Water:
CALCULATIONS
CONVERSION FACTORS mg/m(3) = 6.63 x ppm
-STANDARDS AND LABELS
WORKPLACE STANDARDS
- ACGIH TLV Values for CAS16752-77-5 (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 CAS16752-77-5 (AIHA, 2006):
- NIOSH REL and IDLH Values for CAS16752-77-5 (National Institute for Occupational Safety and Health, 2007):
Listed as: Methomyl REL: IDLH: Not Listed
- OSHA PEL Values for CAS16752-77-5 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
- OSHA List of Highly Hazardous Chemicals, Toxics, and Reactives for CAS16752-77-5 (U.S. Occupational Safety and Health Administration, 2010):
ENVIRONMENTAL STANDARDS
- EPA CERCLA, Hazardous Substances and Reportable Quantities for CAS16752-77-5 (U.S. Environmental Protection Agency, 2010):
Listed as: Ethanimidothioic acid, N-[[(methylamino) carbonyl]oxy]-, methyl ester Final Reportable Quantity, in pounds (kilograms): Additional Information: Listed as: Methomyl Final Reportable Quantity, in pounds (kilograms): Additional Information:
- EPA CERCLA, Hazardous Substances and Reportable Quantities, Radionuclides for CAS16752-77-5 (U.S. Environmental Protection Agency, 2010):
- EPA RCRA Hazardous Waste Number for CAS16752-77-5 (U.S. Environmental Protection Agency, 2010b):
Listed as: Ethanimidothioic acid, N-[[(methylamino)carbonyl]oxy]-, methyl ester P or U series number: P066 Footnote: Listed as: Methomyl P or U series number: P066 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 CAS16752-77-5 (U.S. Environmental Protection Agency, 2010):
Listed as: Methomyl Reportable Quantity, in pounds: 100 Threshold Planning Quantity, in pounds: Note(s): d
- EPA SARA Title III, Community Right-to-Know for CAS16752-77-5 (40 CFR 372.65, 2006; 40 CFR 372.28, 2006):
- DOT List of Marine Pollutants for CAS16752-77-5 (49 CFR 172.101 - App. B, 2005):
- EPA TSCA Inventory for CAS16752-77-5 (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 CAS16752-77-5 (NFPA, 2002):
-HANDLING AND STORAGE
STORAGE
Containers: Glass jars, earthenware jars, composition jars, chipboard boxes, pasteboard boxes, fibre cartons, metal drums, wooden boxes (OHM/TADS , 1990). Keep containers tightly closed (OHM/TADS , 1990)
- ROOM/CABINET RECOMMENDATIONS
General Storage codes 1,2 for Carbamate pesticides (OHM/TADS , 1990). General Conditions: Keep away from heat and water (OHM/TADS , 1990). Do not subject or store liquid formulations at temperatures below 32 degrees F (EPA, 1985).
-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.
- Wear full protective clothing when working in the vicinity of spills or leaks or when fighting fires (AAR, 1987).
RESPIRATORY PROTECTION
- Wear a self-contained positive pressure breathing apparatus when working in the vicinity of spills or leaks or when fighting fires (AAR, 1987).
- 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 16752-77-5.
-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.
When heated to decomposition, Methomyl releases highly toxic fumes of oxides of carbon, nitrogen, and sulfur (Sax & Lewis, 1989).
- FLAMMABILITY CLASSIFICATION
- NFPA Flammability Rating for CAS16752-77-5 (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 CAS16752-77-5 (NFPA, 2002):
- Choose an extinguishing agent suitable for fires in surrounding material (AAR, 1987).
- Water may be used in flooding quantities as fog (AAR, 1987).
When heated to decomposition, Methomyl releases highly toxic fumes of oxides of carbon, nitrogen, and sulfur (Sax & Lewis, 1989).
DUST/VAPOR HAZARD
- When heated to decomposition, Methomyl releases highly toxic fumes of oxides of carbon, nitrogen, and sulfur (Sax & Lewis, 1989).
REACTIVITY HAZARD
- When heated to decomposition, methomyl releases highly toxic fumes of oxides of nitrogen and sulfur (Lewis, 1996).
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.
- Downwind evacuation should be considered if this material is involved in a fire or if a large discharge has occurred (AAR, 1987).
- AIHA ERPG Values for CAS16752-77-5 (AIHA, 2006):
- DOE TEEL Values for CAS16752-77-5 (U.S. Department of Energy, Office of Emergency Management, 2010):
Listed as Methomyl TEEL-0 (units = mg/m3): 2.5 TEEL-1 (units = mg/m3): 7.5 TEEL-2 (units = mg/m3): 10 TEEL-3 (units = mg/m3): 200 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 CAS16752-77-5 (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 CAS16752-77-5 (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.
DECONTAMINATION OF SPILLS No specific decontamination procedures were found for methomyl. The following procedures are for organophosphates. A variety of methods have been described for organophosphate spill decontamination, most of which depend on changing the pH to promote hydrolysis to inactive phosphate diester compounds (EPA, 1978). The rate of hydrolysis depends on both the specific organophosphate compound involved and the increase in pH caused by the detoxicant used (EPA, 1978) EPA, 1975a). Treatment of the spilled material with alkaline substances such as sodium carbonate (soda ash), sodium bicarbonate (baking soda), calcium hydroxide (slaked or hydrated lime), calcium hydroxide (lime or lime water, when in dilute solutions), and calcium carbonate (limestone) may be used for detoxification (EPA, 1975b). Alternatively, the material can be inactivated with strong detergent (Ford, 1989). While ammonia compounds have also been suggested as alternate detoxicants for organophosphate spills, UNDER NO CIRCUMSTANCES SHOULD AMMONIA EVER BE COMBINED WITH A CHLORINE-ACTIVE COMPOUND (BLEACH) AS HIGHLY IRRITATING CHLORAMINE GAS MAY BE EVOLVED. Other decontamination methods may be recommended by manufacturers of specific agents. Check containers, labels, or product literature for possible instructions regarding decontamination of spills.
Disposal of large quantities or contamination of large areas may be regulated by various governmental agencies and reporting may be required. Water spray may be used to reduce or knock down vapors (AAR, 1987).
Isolate and ventilate the area. Keep sources of fire away. Wear rubber or neoprene gloves and overshoes and an approved respirator. Get fire-fighting equipment ready. Contain any liquid spill around the edge and absorb with Zorb-All(R), soil, sweeping compound, sawdust, dry sand or similar material. Dispose of absorbed or dry material in disposable containers (Ford, 1989; EPA, 1975b). Scrub the spilled area with concentrated detergent such as TIDE(R), ALL(R), or similar material. Re-absorb scrubbing liquid and dispose as above (Ford, 1989). Several washes may be required for decontamination (EPA, 1978).
Isolate and ventilate the area. Keep sources of fire away. Wear rubber or neoprene gloves and overshoes and approved personal protection equipment. Get fire-fighting equipment ready (Ford, 1989). Treatment of the spilled material with alkaline substances such as sodium carbonate (soda ash), sodium bicarbonate (baking soda), calcium hydroxide (slaked or hydrated lime, lime or lime water when in dilute solutions), and calcium carbonate (crushed limestone) may be used for detoxification (EPA, 1975a). Contain any liquid spill around the edge and absorb with Zorb-All (R), soil, sweeping compound, sawdust, dry sand or similar material. Dispose of absorbed or dry material in disposable containers (Ford, 1989; EPA, 1975b). After the bulk of the material has been removed, further decontaminate spoiled surfaces with alkaline treatment as described above, or with concentrated alkaline detergent. Absorb and dispose of waste water as described above. Water spray may be used to reduce or knock down vapors (AAR, 1987). Disposal of large quantities or contamination of large areas may be regulated by various governmental agencies and reporting may be required. Consult the local Emergency Response Committee for guidance.
-ENVIRONMENTAL HAZARD MANAGEMENT
POLLUTION HAZARD
- SOIL: Clay loam soils were treated with the insecticides, carbaryl and methomyl, at up to 10 times the recommended field doses. The treatment produces an increase in the bacteria populations and the total soluble salt content of the soils (Elsayed et al, 1993).
- BIOACCUMULATION: The beet armyworm has a high resistance to many insecticides (eg, methomyl). The cause of this resistance is a detoxifying enzyme, carboxylamidase, located mainly (66.2%) in the armyworms midgut (Vanlaecke & Degheele, 1993).
ENVIRONMENTAL FATE AND KINETICS
ENVIRONMENTAL TOXICITY
- No specific environmental toxicity data were available at the time of this review.
1. LD50 (ORAL) DUCK: 15 mg/kg 2. LC50 (INHL) DUCK: 1890 ppm 3. LD50 (ORAL) PIGEON: 10 mg/kg 4. LD50 (ORAL) QUAIL: 23,700 mcg/kg 5. LC50 (INHL) QUAIL: 3680 ppm 6. LD50 (ORAL) WILD BIRD SPECIES: 10 mg/kg
-PHYSICAL/CHEMICAL PROPERTIES
MOLECULAR WEIGHT
DESCRIPTION/PHYSICAL STATE
- Methomyl is a white crystalline solid with a slight sulfurous smell (EPA, 1985)
VAPOR PRESSURE
- 5 X 10(-5) mmHg (at 25 degrees C) (ACGIH, 1986)
- 5 X 10(-5) mmHg (at 77 degrees F) (EPA, 1985)
DENSITY
- OTHER TEMPERATURE AND/OR PRESSURE
FREEZING/MELTING POINT
78-79 degrees C (Budavari, 1989) 172-174 degrees F (EPA, 1985)
SOLUBILITY
100 g/100 g of methanol (at 25 degrees C) (Budavari, 1996) 42 g/100 g of ethanol (at 25 degrees C) (Budavari, 1996) 22 g/100 g of isopropanol (at 25 degrees C) (Budavari, 1996) 73 g/100 g of acetone (at 25 degrees C) (Budavari, 1996)
HENRY'S CONSTANT
- 1.0 X 10(-10) atm-m(3)/mol (Ehrenfeld et al, 1986)
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