| Section 1. Identification | |||
|---|---|---|---|
| Chemical Name | oxamyl | CAS No. | 23135-22-0 |
| Synonyms | methyl 2-(dimethylamino)-N-[[(methylamino)carbonyl]oxy]-2-oxoethanimidothioate | Chinese Name | 杀线威 |
| Molecular Formula | C7H13N3O3S | Molecular Weight | 219.261 |
| UN No. | 2588 | Data Source | PubChem (NIH/NLM) |
| GHS Hazard Classification | |
|---|---|
| Signal Word | DANGER |
| Pictograms | GHS06 · Acute Toxic GHS07 · Irritant GHS08 · Health Hazard GHS09 · Environmental Hazard |
| Hazard Statements | H300H312H330H411H311H336H400H410H361H370H372 |
| Precautionary Statements | P260P264P270P271P273P280P284P301+P316P302+P352P304+P340P316P317P320P321P330P362+P364P391P403+P233P405P501P261P262P319P361+P364P203P308+P316P318 |
| Contents | |||
|---|---|---|---|
| Section 2 | Hazards Identification | Section 4 | First-Aid Measures |
| Section 5 | Fire-Fighting Measures | Section 6 | Accidental Release Measures |
| Section 7 | Handling and Storage | Section 8 | Exposure Controls / Personal Protection |
| Section 9 | Physical and Chemical Properties | Section 10 | Stability and Reactivity |
| Section 11 | Toxicological Information | Section 12 | Ecological Information |
| Section 13 | Disposal Considerations | Section 14 | Transport Information |
H300: Fatal if swallowed [Danger Acute toxicity, oral]
H312: Harmful in contact with skin [Warning Acute toxicity, dermal]
H330: Fatal if inhaled [Danger Acute toxicity, inhalation]
H411: Toxic to aquatic life with long lasting effects [Hazardous to the aquatic environment, long-term hazard]
P260, P264, P270, P271, P273, P280, P284, P301+P316, P302+P352, P304+P340, P316, P317, P320, P321, P330, P362+P364, P391, P403+P233, P405, and P501 (click each P-code to see the statement)
H300+H330 (49.4%): Fatal if swallowed or if inhaled [Danger Acute toxicity, oral; acute toxicity, inhalation]
H300 (100%): Fatal if swallowed [Danger Acute toxicity, oral]
H311 (32.9%): Toxic in contact with skin [Danger Acute toxicity, dermal]
H312 (67.1%): Harmful in contact with skin [Warning Acute toxicity, dermal]
H330 (100%): Fatal if inhaled [Danger Acute toxicity, inhalation]
H336 (48.2%): May cause drowsiness or dizziness [Warning Specific target organ toxicity, single exposure; Narcotic effects]
H400 (49.4%): Very toxic to aquatic life [Warning Hazardous to the aquatic environment, acute hazard]
H410 (49.4%): Very toxic to aquatic life with long lasting effects [Warning Hazardous to the aquatic environment, long-term hazard]
H411 (98.8%): Toxic to aquatic life with long lasting effects [Hazardous to the aquatic environment, long-term hazard]
P260, P261, P262, P264, P270, P271, P273, P280, P284, P301+P316, P302+P352, P304+P340, P316, P317, P319, P320, P321, P330, P361+P364, P362+P364, P391, P403+P233, P405, and P501 (click each P-code to see the statement)
Aggregated GHS information provided per 85 reports by companies from 5 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.
Information may vary between notifications depending on impurities, additives, and other factors. The percentage value in parenthesis indicates the notified classification ratio from companies that provide hazard codes. Only hazard codes with percentage values above 10% are shown. For more detailed information, please visit ECHA C&L website.
H311: Toxic in contact with skin [Danger Acute toxicity, dermal]
H361: Suspected of damaging fertility or the unborn child [Warning Reproductive toxicity]
H370: Causes damage to organs [Danger Specific target organ toxicity, single exposure]
H372: Causes damage to organs through prolonged or repeated exposure [Danger Specific target organ toxicity, repeated exposure]
H400: Very toxic to aquatic life [Warning Hazardous to the aquatic environment, acute hazard]
H410: Very toxic to aquatic life with long lasting effects [Warning Hazardous to the aquatic environment, long-term hazard]
P203, P260, P262, P264, P270, P271, P273, P280, P284, P301+P316, P302+P352, P304+P340, P308+P316, P316, P318, P319, P320, P321, P330, P361+P364, P391, P403+P233, P405, and P501 (click each P-code to see the statement)
P260, P264, P270, P271, P284, P301+P316, P304+P340, P308+P316, P316, P319, P320, P321, P330, P403+P233, P405, and P501 (click each P-code to see the statement)
Signs and Symptoms of Acute Oxamyl Exposure: Acute exposure to oxamyl usually leads to a cholinergic crisis. Signs and symptoms may include increased salivation, lacrimation (tearing), perspiration, spontaneous defecation, and spontaneous urination. Pinpoint pupils, blurred vision, tremor, muscle twitching, mental confusion, convulsions, and coma may occur. Gastrointestinal symptoms include abdominal pain, diarrhea, nausea, and vomiting. Bradycardia (slow heart rate) is common. Dyspnea (shortness of breath) and pulmonary edema may also occur.
Emergency Life-Support Procedures: Acute exposure to oxamyl may require decontamination and life support for the victims. Emergency personnel should wear protective clothing appropriate to the type and degree of contamination. Air-purifying or supplied-air respiratory equipment should also be worn, as necessary. Rescue vehicles should carry supplies such as plastic sheeting and disposable plastic bags to assist in preventing spread of contamination.
Inhalation Exposure:
1. Move victims to fresh air. Emergency personnel should avoid self-exposure to oxamyl.
2. Evaluate vital signs including pulse and respiratory rate, and note any trauma. If no pulse is detected, provide CPR. If not breathing, provide artificial respiration. If breathing is labored, administer oxygen or other respiratory support.
3. Obtain authorization and/or further instructions from the local hospital for administration of an antidote or performance of other invasive procedures.
4. Transport to a health care facility.
Dermal/Eye Exposure:
1. Remove victims from exposure. Emergency personnel should avoid self- exposure to oxamyl.
3. Remove contaminated clothing as soon as possible.
4. If eye exposure has occurred, eyes must be flushed with lukewarm water for at least 15 minutes.
5. Wash exposed skin areas three times with soap and water.
6. Obtain authorization and/or further instructions from the local hospital for administration of an antidote or performance of other invasive procedures.
7. Transport to a health care facility.
Ingestion Exposure:
1. Evaluate vital signs including pulse and respiratory rate, and note any trauma. If no pulse is detected, provide CPR. If not breathing, provide artificial respiration. If breathing is labored, administer oxygen or other respiratory support.
2. Obtain authorization and/or further instructions from the local hospital for administration of an antidote or performance of other invasive procedures.
3. Vomiting may be induced with syrup of Ipecac. If elapsed time since ingestion of oxamyl is unknown or suspected to be greater than 30 minutes, do not induce vomiting and proceed to Step
4.Ipecac should not be administered to children under 6 months of age.Warning: Ingestion of oxamyl may result in sudden onset of seizures or loss of consciousness. Syrup of Ipecac should be administered only if victims are alert, have an active gag-reflex, and show no signs of impending seizure or coma. If ANY uncertainty exists, proceed to Step
4.The following dosages of Ipecac are recommended: children up to 1 year old, 10 mL (1/3 oz); children 1 to 12 years old, 15 mL (1/2 oz); adults, 30 mL (1 oz). Ambulate (walk) the victims and give large quantities of water. If vomiting has not occurred after 15 minutes, Ipecac may be readministered. Continue to ambulate and give water to the victims. If vomiting has not occurred within 15 minutes after second administration of Ipecac, administer activated charcoal.
4. Activated charcoal may be administered if victims are conscious and alert. Use 15 to 30 g (1/2 to 1 oz) for children, 50 to 100 g (1-3/4 to 3-1/2 oz) for adults, with 125 to 250 mL (1/2 to 1 cup) of water.
5. Promote excretion by administering a saline cathartic or sorbitol to conscious and alert victims. Children require 15 to 30 g (1/2 to 1 oz) of cathartic; 50 to 100 g (1-3/4 to 3-1/2 oz) is recommended for adults.
6. Transport to a health care facility. (EPA, 1998)
This is a solid carbamate pesticide. Move container from fire area. Fight fire from maximum distance. Dike fire control water for later disposal; do not scatter the material. Wear positive pressure breathing apparatus and special protective clothing.
Extinguish fire using agent suitable for type of surrounding fire, as the material itself does not burn or burns with difficulty. Use water in flooding quantities as a fog. Use alcohol foam, carbon dioxide or dry chemical. (EPA, 1998)
Excerpt from ERG Guide 131 [Flammable Liquids - Toxic]:
IMMEDIATE PRECAUTIONARY MEASURE: Isolate spill or leak area for at least 50 meters (150 feet) in all directions.
SPILL: Increase the immediate precautionary measure distance, in the downwind direction, as necessary.
FIRE: If tank, rail tank car or highway tank 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. (ERG, 2024)
If you spill this chemical, you should dampen the solid spill material with water,then transfer the dampened material to a suitable container. Use absorbent paper dampened with water to pick up any remaining material. Seal your contaminated clothing and the absorbent paper in a vapor-tight plastic bag for eventual disposal. Wash all contaminated surfaces with a strong soap and water solution. Do not reenter the contaminated area until the Safety Officer (or other responsible person) has verified that the area has been properly cleaned.
Generators of waste (equal to or greater than 100 kg/month) containing this contaminant, EPA hazardous waste number P194, must conform with USEPA regulations in storage, transportation, treatment and disposal of waste.
Oxamyl should be treated with alkali. Recommendable methods: Alkaline hydrolysis, adsorption.
The protective clothing should be kept in separate places where it cannot be contaminated with toxic chemicals. It should be forbidden to keep this clothing in living quarters. Protective clothing must be washed at least once a week and each time it is contaminated with pesticides. Before washing the clothing should be soaked for several hours in a calcium carbonate solution. /Pesticides/
Smoking, eating, and drinking before washing should be absolutely prohibited when any pesticide ... is being handled or used. /Pesticides/
This is a solid carbamate pesticide. Keep unnecessary people away; isolate hazard areas and deny entry. Stay upwind, keep out of low areas. Do not touch spilled material, or breathe the vapors, dusts or fumes from burning materials. Do not handle broken packages without protective equipment. Wash away any material that may have contacted the body with soap and water. (EPA, 1998)
You should protect this material from exposure to light and air, and store it under refrigerated temperatures.
Biological Exposure Indices (BEI) [ACGIH] - Acetylcholinesterase activity in red blood cells = 70% of individual's baseline; Butylcholinesterase activity in serum or plasma = 60% of individual's baseline; Sample at end of shift; [TLVs and BEIs]
AEGL 1: Notable discomfort, irritation, or certain asymptomatic non-sensory effects. However, the effects are not disabling and are transient and reversible upon cessation of exposure (Unit: mg/m3)
AEGL 2: Irreversible or other serious, long-lasting adverse health effects or an impaired ability to escape (Unit: mg/m3)
AEGL 3: Life-threatening health effects or death (Unit: mg/m3)
3.6 mg/m3
5.3 mg/m3
16 mg/m3
1.8 mg/m3
2.7 mg/m3
8.2 mg/m3
1.2 mg/m3
0.49 mg/m3
0.73 mg/m3
2.2 mg/m3
0.32 mg/m3
0.47 mg/m3
1.4 mg/m3
NOTE THAT VALUES ARE IN mg/m3, NOT ppm.
AEGLs Status: Proposed
0.15 [mg/m3]
1.7 [mg/m3]
2.5 [mg/m3]
Tolerances are established for the sum of the residues of the insecticide oxamyl (methyl N',N'-dimethyl-N-[methylcarbamoyl)-oxyl]-1-thiooxamimidate) and its oxime metabolite N,N-dimethyl-N-hydroxy-1-thiooxamimidate calculated as oxamyl in or on the following food commodities: apple, 2.0 ppm; banana, 0.3 ppm; cantaloupe, 2.0 ppm; celery, 3.0 ppm; cottonseed, 0.2 ppm; cucumber, 2.0 ppm; eggplant, 2.0 ppm; fruit, citrus, 3.0 ppm; melon, honeydew, 2.0 ppm; peanut, 0.2 ppm; peanut, 0.2 ppm; peanut, hay, 2.0 ppm; pear, 2.0 ppm; peppermint, hay, 10.0 ppm; pepper, bell, 3.0 ppm; pepper, non-bell, 5.0 ppm; pineapple, 1.0 ppm; potatoe, 0.1 ppm; pumpkin, 2.0 ppm; root crop vegetables, 0.1 ppm; soybean, 0.2 ppm; spearmint, hay, 10.0 ppm; squash, summer, 2.0 ppm; squash, winter, 2.0 ppm; tomatoe, 2.0 ppm, and watermelon, 2.0 ppm.
A tolerance of 6 ppm is established for residues of the insecticide oamyl (methyl N',N'-dimethyl-N- [(methylcarbamoyl)oxy]-1-thiooxamimidate) in pineapple, bran as a result of application of the insecticide to growing pineapples.
For emergency situations, wear a positive pressure, pressure-demand, full facepiece self-contained breathing apparatus (SCBA) or pressure- demand supplied air respirator with escape SCBA and a fully-encapsulating, chemical resistant suit. (EPA, 1998)
The current personal protective equipment required for all uses of oxamyl is short-sleeve shirt and short pants with coveralls, chemical resistant gloves, head gear for air blast, and an organic vapor respirator.
Oxamyl is a white, crystalline solid, with slight sulfurous odor. Used as an insecticide, nematicide and acaricide on many field crops, vegetables, fruits, and ornamentals. (EPA, 1998)
Colorless or white solid with sulfurous or garlic-like odor; [HSDB]
White crystalline solid
Colorless crystals
Slight sulfurous odor
Garlic-like odor
Decomposes on distillation
310 °C @760 [mm Hg]
212 to 216 °F Pure compound changes to different form upon melting, with a melting point of 226 to 230 °F. (EPA, 1998)
100-102 °C, changes to a different crystalline form, mp 108-110 °C
Soluble at 77.0 °F (280g/kg) (NTP, 1992)
Solubility (g/100 ml @ 25 °C): acetone, 67; ethanol, 33; 2-propanol, 11; methanol, 144; toluene, 1
In water, 280 g/l @ 25 °C
0.97 g/cu cm @ 25 °C
0.98 @25 °C
0.00023 mmHg at 77 °F (EPA, 1998)
0.00023 [mmHg]
0.00023 mm Hg @ 20-25 °C
0.00023 [mm Hg] @25 °C
log Kow = -0.47
Solid and formulations are stable... .
Decompostion is increased by aeration, sunlight, alkalinity and higher temperatures.
Decomposes to innocuous materials in natural waters and soil.
When heated to decomposition it emits very toxic fumes of /sulfur and nitric oxides/.
Aeration, sunlight, alkalinity, and higher temperatures increase the rate of decomposition.
DT50 >31 day (pH 5), 8 day (pH 7), 3 hr (pH 9)... .
Decomposes on distillation.
Non-corrosive
Positive
Agilent XCT
Electrospray ionization
formic acid (5.3nM)
MeCN (80%)
DOI:10.1038/s41598-020-62573-z
150.9 Ų [M+Na]+ [CCS Type: DT; Buffer gas: N2; Ionization: ESI+; Dataset: TOXCAST; Source Identifier: DTXSID6021086]
Solid and formulations are stable; aqueous solution decomposes slowly; half-lives: >31 days (pH 5); 8 days (pH 7); 3 hours (pH 9); accelerated by aeration and sunlight
Potential endocrine disrupting compound
Pesticide -> EPA IRIS
Insecticides, Nematicides
Active substance -> EU Pesticides database: Not approved
Decomposes to innocuous materials in natural waters and in soil. Aeration, sunlight, alkalinity, and higher temperatures increase the rate of decomposition. (NTP, 1992)
Amides and Imides
Carbamates
Sulfides, Organic
OXAMYL is a carbamate ester. Carbamates are chemically similar to, but more reactive than amides. Like amides they form polymers such as polyurethane resins. Carbamates are incompatible with strong acids and bases, and especially incompatible with strong reducing agents such as hydrides. Flammable gaseous hydrogen is produced by the combination of active metals or nitrides with carbamates. Strongly oxidizing acids, peroxides, and hydroperoxides are incompatible with carbamates.
Incompatible with alkaline materials.
Oxamyl is a cholinesterase or acetylcholinesterase (AChE) inhibitor. Carbamates form unstable complexes with chlolinesterases by carbamoylation of the active sites of the enzymes. This inhibition is reversible. A cholinesterase inhibitor suppresses the action of acetylcholine esterase. Because of its essential function, chemicals that interfere with the action of acetylcholine esterase are potent neurotoxins, causing excessive salivation and eye-watering in low doses. Headache, salivation, nausea, vomiting, abdominal pain and diarrhea are often prominent at higher levels of exposure. Acetylcholine esterase breaks down the neurotransmitter acetylcholine, which is released at nerve and muscle junctions, in order to allow the muscle or organ to relax. The result of acetylcholine esterase inhibition is that acetylcholine builds up and continues to act so that any nerve impulses are continually transmitted and muscle contractions do not stop.
2.5 x 10 ^-2 mg/kg-day
Pesticide
Smith, C.D. and Nowell, L.H., 2024. Health-Based Screening Levels for evaluating water-quality data (3rd ed.). DOI:10.5066/F71C1TWP
Cancer Classification: Group E Evidence of Non-carcinogenicity for Humans
No indication of carcinogenicity to humans (not listed by IARC).
Acute exposure to cholinesterase inhibitors can cause a cholinergic crisis characterized by severe nausea/vomiting, salivation, sweating, bradycardia, hypotension, collapse, and convulsions. Increasing muscle weakness is a possibility and may result in death if respiratory muscles are involved. Accumulation of ACh at motor nerves causes overstimulation of nicotinic expression at the neuromuscular junction. When this occurs symptoms such as muscle weakness, fatigue, muscle cramps, fasciculation, and paralysis can be seen. When there is an accumulation of ACh at autonomic ganglia this causes overstimulation of nicotinic expression in the sympathetic system. Symptoms associated with this are hypertension, and hypoglycemia. Overstimulation of nicotinic acetylcholine receptors in the central nervous system, due to accumulation of ACh, results in anxiety, headache, convulsions, ataxia, depression of respiration and circulation, tremor, general weakness, and potentially coma. When there is expression of muscarinic overstimulation due to excess acetylcholine at muscarinic acetylcholine receptors symptoms of visual disturbances, tightness in chest, wheezing due to bronchoconstriction, increased bronchial secretions, increased salivation, lacrimation, sweating, peristalsis, and urination can occur. Chronically high (>10 years) exposure leads to neuropsychological consequences including disturbances in perception and visuo-motor processing (A15321).
Inhalation (L793) ; oral (L793); dermal (L793)
As with organophosphates, the signs and symptoms are based on excessive cholinergic stimulation. Unlike organophosphate poisoning, carbamate poisonings tend to be of shorter duration because the inhibition of nervous tissue acetylcholinesterase is reversible, and carbamates are more rapidly metabolized. Muscle weakness, dizziness, sweating and slight body discomfort are commonly reported early symptoms. Headache, salivation, nausea, vomiting, abdominal pain and diarrhea are often prominent at higher levels of exposure. Contraction of the pupils with blurred vision, incoordination, muscle twitching and slurred speech have been reported. (L795)
Chemical: OXAMYL
Other Poison - Carbamate
Oral RfD: 0.025 mg/kg/day (UF: 100, MF: 1)
IRIS Current
LC50 (rat) = 170 mg/m3/1h
LD50: 2300 ug/kg (Oral, Mouse) (T14)
LC50: 170 mg/m3 over 1 hour (Inhalation, Rat) (T14)
LD50 Rat oral 5.4 mg/kg
LD50 Rabbit dermal 2,960 mg/kg
LC50 Rat inhalation 170 mg/cu m/ 1hr
LD50 Mouse oral 2300 ug/kg
For more Non-Human Toxicity Values (Complete) data for OXAMYL (13 total), please visit the HSDB record page.
If the compound has been ingested, rapid gastric lavage should be performed using 5% sodium bicarbonate. For skin contact, the skin should be washed with soap and water. If the compound has entered the eyes, they should be washed with large quantities of isotonic saline or water. In serious cases, atropine and/or pralidoxime should be administered. Anti-cholinergic drugs work to counteract the effects of excess acetylcholine and reactivate AChE. Atropine can be used as an antidote in conjunction with pralidoxime or other pyridinium oximes (such as trimedoxime or obidoxime), though the use of '-oximes' has been found to be of no benefit, or possibly harmful, in at least two meta-analyses. Atropine is a muscarinic antagonist, and thus blocks the action of acetylcholine peripherally.
The clinical approach to carbamate toxicity is similar to that for organophosphate poisoning; the major exception is that pralidoxime usually is not recommended. /Carbamates/
Stabilization: Assess the adequacy of the airway and ventilation and use oxygen, suction, intubation, artificial ventilation, intravenous lines, and cardiac monitors as needed. /Carbamates/
Elimination Enhancement: No methods are recommended, because of the short clinical effect of carbamates and the presence of an effective antidote (atropine). /Carbamates/
Emergency and supportive measures. Caution: rescuers and health care providers must take measures to prevent direct contact with the skin or clothing of contaminated victims, because secondary contamination and serious illness may result, especially with potent pesticides and nerve agents. 1. Maintain an open airway and assist ventilation if necessary. Pay careful attention to respiratory muscle weakness; sudden respiratory arrest may occur. If intubation is required, note potential interactions between neuromuscular blockers and cholinesterase inhibitors. Administer supplemental oxygen. 2. Treat hydrocarbon pneumonitis, seizures, and coma if they occur. 3. Observe patients for at least 6-8 hours to rule out delayed-onset symptoms resulting from skin absorption. /Organophosphates and carbamates/
For more Antidote and Emergency Treatment (Complete) data for OXAMYL (11 total), please visit the HSDB record page.
SRP: Workers should undergo an annual medical exam. Contraindications for work with organophosporous pesticides are organic diseases of the CNS, mental disorders and epilepsy, and pronounced endocrine disorders. Blood cholinesterase, both plasma and RBC, must be determined before work starts. In the event of prolonged work periods, this activity should be determined at intervals of 3-4 days. Persons exhibiting a fall in cholinesterase activity of 25% or more must be transferred to other work where they are not exposed until cholinesterase activity is restored. /Organophosphorous pesticides; Anticholinesterase pesticides/
Measurement of whole blood-AChE is the most widely adopted method for monitoring the effects of occupational exposure to organophosphorus insecticides. Physiological variations in blood ChE levels occur in a healthy person and are seen among a population. It has been estimated that the coefficient of variation for AChE activity in samples from an individual is 8-11%, and that a decrease of 23% below pre-exposure level may, therefore, be considered significant. If the average of several pre-exposure values were available, then a decrease of 17% would be significant. It has been recommended that, if measured activity is reduced by 30% or more of the pre-exposure value, AChE measurements should be repeated at appropriate intervals to confirm the results. Depressions of AChE or ChE in excess of 20-25% are considered diagnostic of exposure but not, necessarily, indicative of hazard. Depressions of 30-50% or more are considered indicators for removal of an exposed individual from further contact with pesticides until levels return to normal. /Organophosphorus pesticides; Anticholinesterase pesticides/
...Organophosphorus pesticides may undergo hydrolysis in vivo to yield substituted phosphoric acids that are subsequently excreted in urine. Advances in gas chromatography and combined gas chromatography/mass spectrometry (GC/MS) have made it possible to analyse the urine of exposed persons for the presence of appropriate metabolites. It is usually necessary to preserve the sample by the addition of chloroform, to concentrate or extract the metabolite(s), and to convert them to suitably-volatile derivatives that can be detected by GC. Obviously, access to a well-equipped analytical laboratory, capable of the quick processing of samples, is a necessary factor if monitoring by urine analysis is proposed. However, in some cases, simpler and sensitive colorimetric tests are available for screening the urine of exposed persons. Thus, 4-nitrophenol can be measured directly in the urine of workers exposed to parathion. Consideration of the concentration of metabolite(s) in the urine can be helpful in determining patterns of exposure, and these concentrations can be calibrated against the effects on AChE for a particular pesticide. However, the time-course and peak of excretion of metabolites appears to vary according to dose, so that serial sampling and analyses of urine are desirable. Levels of metabolite alone cannot be considered a guide to hazard. This is obvious when it is realized that pesticides that have very different toxicities may yield identical acidic metabolites. Thus, the level of metabolites in urine, after exposure to sufficient amounts of the very toxic parathion-methyl to depress blood-AChE to 50%, will be much lower than that of the identical metabolites, following exposure to the related fenitrothion, which is about 40 times less toxic. /Organophosphorus pesticides; Anticholinesterase pesticides/
/CASE REPORTS/ A 53 year old woman employed in transplanting tobacco plants apparently mistook a jug containing oxamyl for a water jar ... She drank a "swallow" of the clear liquid and within 10 min was semiconscious. Despite reasonably prompt attention in a university medical center, she died 12 hr later. ...The woman immediately realized her mistake and took some salt water, but apparently without benefit. When she reached the hospital, she was unconscious, incontinent of feces, apneic, and without detectable blood pressure, and her pupils were constricted. Autopsy revealed thrombotic and hemolytic crisis in sickle-cell disease, undoubtedly triggered by the oxamyl; this crisis may have been the cause of her death. The same hospital had a record of a 73 yr old man who ingested oxamyl by mistake but survived.
/EPIDEMIOLOGY STUDIES/ Cholinesterase activity measurements for 542 California agricultural pesticide applicators under medical supervision during the first 9 mo of 1985 were analyzed. Medical records of applicators were used if the subject had been exposed for over 3 hr in a 30 day period to category I and II organophosphate and carbamate pesticides. Employers of all workers with cholinesterase activity depressions that fell to 70% or less of the workers' plasma or RBC baselines were contacted to obtain a list of pesticides handled in the 2 wk interval preceding the greatest reported cholinesterase activity depression. In evaluating pesticide exposure data, it was not possible to distinguish listed pesticides primarily or cumulatively responsible for the noted cholinesterase activity depressions from those not responsible for the cholinesterase activity depression, but coincidentally used during the same period. The pesticides associated with plasma or RBC cholinesterase activity depression to 70% of baseline or lower are listed. Oxamyl (vydate) usage in California for 1985 was 25,200 lb. Twenty six workers, 4.8% of the sample, had cholinesterase values at or below the California action level value for removal from continued exposure to cholinesterase inhibiting pesticides. Eight of these 26 workers (31.5%) had pesticide related illnesses.
/SIGNS AND SYMPTOMS/ Principal effects /of anticholinesterases as toxic components of insecticides/ on eye, whether from local contact or systemic poisoning, are miosis and spasm of accommodation for near vision. /Anticholinesterases/
/SIGNS AND SYMPTOMS/ The clinical picture of carbamates intoxication results from accumulation of ACh at nerve endings. ...The signs and symptoms can be categorized into the following 3 groups: (a) Muscarinic manifestations - increased bronchial secretion, excessive sweating, salivation, and lachrymation; pinpoint pupils, bronchoconstriction, abdominal cramps (vomiting and diarrhea); and bradycardia. (b) Nicotinic manifestations - fasciculation of fine muscles (in severe cases, diaphragm and respiratory muscles also involved); and tachycardia. (c) Central nervous system manifestations- headache, dizziness, anxiety, mental confusion, convulsions, and coma; and depression of respiratory center. All these signs and symptoms can occur in different combinations and can vary in onset and sequence, depending on the chemical, dose, and route of exposure. The duration of symptoms is usually shorter than that observed in organophosphorus poisoning. Mild poisoning might include muscarinic and nicotinic signs only. Severe cases always show central nervous system involvement; the clinical picture is dominated by the respiratory failure sometimes leading to pulmonary edema due to the combination of the above mentioned symptoms. /Carbamate pesticides/
/LABORATORY ANIMALS: Acute Exposure/ The acute toxicity of oxamyl was assessed in rats, and both the rate of recovery and the dose response relationships for various biochemical parameters were determined. Male Sprague Dawley rats were given single acute oral doses of 1, 2.1, or 3.5 mg/kg. Weight gain was significantly decreased, and brain and blood acetylcholinesterase was significantly inhibited during the first few hours after exposure. After 7 and 4 days, liver glucose-6-phosphatase was inhibited when the animals were dosed with 2.1 and 3.5 mg/kg, respectively. After 1 day, the maximum inhibition of liver succinic-acid-dehydrogenase was noted at the 1 mg/kg dose level, and after 6 hours maximum inhibition was noted at dose levels of 2.1 or 3.5 mg/kg. Serum total lipids and glucose each revealed significant changes when oxamyl was given at the two higher dose levels. Serum protein was not affected at any dose level. /It was/ concluded that these findings are indicative of a reversible toxic effect of oxamyl on the investigated parameters.
/LABORATORY ANIMALS: Acute Exposure/ The effects of single acute oral doses of 1, 2.1 and 3.5 mg/kg oxamyl (a carbamate insecticide) on selected biochemical parameters in male Sprague-Dawley rats were investigated. The animals exhibited significantly decreased weight gain when compared to control animals. The compound inhibited brain and blood acetylcholinesterase significantly In the first few hours of exposure. Liver glucose-6-phosphatase was inhibited substantially after 7 and 4 days at the levels of 2.1 and 3.5 mg/kg. respectively. Maximum inhibition of liver succinic acid dehydrogenase was noted after 1 day at the level of 1 mg/kg and after 6 hr at the level of 2.1 and 3.5 mg/kg. Significant changes in serum total lipids and glucose were observed when oxamyl was given at 2.1 and 3.5 mg/kg, but serum protein was not affected at any dose level. However, the absence of statistically significant effects between Days 7 and 14 in most of the investigated parameters is indicative of an overall moderate degree of toxicity of oxamyl following acute oral administration of the selected doses.
/LABORATORY ANIMALS: Acute Exposure/ The acute toxicity of oxamyl an insecticide, and nematicide has been evaluated to establish proper handling guides. The material is highly toxic when given as a single oral dose; its LD50 is in fasted rats, 2.5 to 3.1 mg/kg 2.3 to 3.3 mg/kg in fasted mice and 7 mg/kg in glen pigs. A beagle dog given 30 mg/kg died, while 15 mg/kg was not lethal. In all species, clinical signs of cholinesterase inhibition (lacrimation, salivation, tremors) were observed. Cholinesterase activity was depressed in rats treated with a single oral dose. Atropine, when given immediately after oxamyl was antidotal. When given by intraperitoneal injection, oxamyl was highly toxic to rats, mice, and guinea pigs. The material is a mild eye irritant with the reaction limited to the conjunctiva and iris, but systemic absorption via eye contact makes use of protective equipment essential. Oxamyl produces mild skin irritation and the dermal absorption toxicity in rats (LD50 is > 1,200 mg/kg) and rabbits (740 mg/kg) is relatively high suggesting limited absorption. No sensitization was produced when tested in guinea pigs. Oxamyl is highly toxic via inhalation with the l-hr LC50 value in rats being 0.17 mg/liter (male) and 0.12 mg/liter (female). The corresponding 4-hr value is 0.064 mg/liter for male rats which indicates that concentration times time is roughly constant through the time periods tested. Repeated-dose studies orally in rats and dermally in rabbits showed oxamyl to be noncumulative with the target system being the nervous system mediated through cholinesterase inhibition. No specific tissue or organ pathology was seen in either species tested.
/LABORATORY ANIMALS: Acute Exposure/ In an acute nose only inhalation study, 10 Crl:(SD) IGS BR rats per sex per group were exposed to 0.0049 mg/L or 0.024 mg/L of aerosolized oxamyl dust for 4-hours. Test atmospheres were measured gravimetrically. Particle sizes generated had a /mass median aerodynamic diameter/ (MMAD) ranging from 0.85 to 1.2 um /geometric standard deviation/. Immediately following exposure, all rats were sacrifice and blood and brain samples were collected for cholinesterase analyses. No deaths in either sex or at either dose level were seen during or immediately after exposure prior to sacrifice. Tremors and lethargy was seen in most rats following exposure. Other clinical signs immediately following exposure were wet/stained fur, ocular/nasal discharge, and diarrhea. At the 0.0049 mg/L, these latter clinical signs were stated to be similar to control incidences, however, clinical signs by group or individual signs were not reported. Only initial body weights were determined, since animals were sacrifice immediately after exposure. Biologically and statistically significant plasma (PCHEI), erythrocyte (ECHEI) and brain cholinesterase inhibition (BCHEI) occurred in both sexes and dose levels, except PCHEI was not significant in females at the /lowest dose tested/ (LDT). In males at 0.0049 and 0.024 mg/L, PCHEI was 12% and 72%, ECHEI was 28% and 72%, and BCHEI was 15% and 68%, respectively. In females at 0.0049 and 0.024 mg/L, PCHEI was 6.5% and 76%, ECHEI was 29% and 73%, and BCHEI was 9% and 67%, respectively.
For more Non-Human Toxicity Excerpts (Complete) data for OXAMYL (26 total), please visit the HSDB record page.
LC50 Bobwhite oral 54 ppm/8 day
LC50 Mallard oral 369 ppm/8 day
LC50 Bobwhite oral 54 ppm/8 day
LC50 Mallard oral 369 ppm/8 day
LD50 Japanese quail (Coturnix coturnix japonica) oral 4.3 mg/kg body wt
LD50 Mallard (Anas platyrhynchos) oral 2.6 mg/kg body wt
For more Ecotoxicity Values (Complete) data for OXAMYL (11 total), please visit the HSDB record page.
/BIRDS and MAMMALS/ For avian species, reproductive effects include reduction in egg production and egg fertility based on the results of a mallard duck study. Chronic /levels of concern/ (LOC's) were exceeded for all use patterns for all-food items (except for seeds) using maximum and average /estimated environmental concentrations/ (EECs).
/OTHER TERRESTRIAL SPECIES/ Oxamyl is moderate to highly toxic to bees on an acute contact basis. Results of a residue on foliage study indicate that residues of oxamyl applied at 1.0 lb al/acre, may remain toxic to bees for as long as 6 days after treatment. Because oxamyl is moderate to highly toxic to honeybees, precautions with respect to spray drift to flowering plants should be followed.
/PLANTS/ Non-phytotoxic when used as directed. Some strawberry varieties may be injured.
/FIELD STUDIES/ New Zealand white rabbits maintained in outdoor pens were exposed to three simulated field-spray applications of oxamyl at 3.36 kg/ha. No clinical signs of toxicity, behavioral alterations, or gross pathologies were observed in any rabbits 5 days after the last treatment.
1.60e+03
2.10e+04
5.00e+02
2.00e+02
1.10e-01
4.40e-02
2.50e-02
Volatile
4.70e+03
6.20e+04
1.50e+03
Oxamyl's production may result in its release to the environment through various waste streams; its use as an insecticide, acaricide, and nematicide will result in its direct release to the environment. If released to air, a vapor pressure of 0.00023 mm Hg at 20-25 °C indicates oxamyl will exist solely as a vapor in the ambient atmosphere. Vapor-phase oxamyl will be degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals; the half-life for this reaction in air is estimated to be 1.4 days. If released to soil, oxamyl is expected to have very high mobility based upon Koc values ranging from 6 to 10. Volatilization from moist soil surfaces is not expected to be an important fate process based upon a Henry's Law constant of 2.37X10-10 atm-cu m/mole. Half-lives of oxamyl in soil ranged from 11 days in loamy sand to 415 days in fine sand under aerobic conditions, and 6 days in silt loam under anaerobic conditions. If released into water, oxamyl is not expected to adsorb to suspended solids and sediment based upon its Koc values. Volatilization from water surfaces is not expected to be an important fate process based upon this compound's Henry's Law constant. An estimated BCF of 3.1 suggests the potential for bioconcentration in aquatic organisms is low. Oxamyl was found to be stable at pH 4.7 for at least 11 days and hydrolyzed slowly in neutral solution; at pH 9, hydrolysis was rapid. Photolysis appears to be significant in acidic surface water, but not on soil. Occupational exposure to oxamyl may occur through inhalation and dermal contact with this compound at workplaces where oxamyl is produced or used. Monitoring data indicate that the general population may be exposed to oxamyl via ingestion of food. (SRC)
Oxamyl's production may result in its release to the environment through various waste streams; its use as an insecticide, acaricide, and nematicide(1) and will result in its direct release to the environment(SRC).
TERRESTRIAL FATE: Based on a classification scheme(1), Koc values ranging from 6 to 10(2), indicate that oxamyl is expected to have very high mobility in soil(SRC). Volatilization of oxamyl from moist soil surfaces is not expected to be an important fate process(SRC) given a Henry's Law constant of 2.37X10-10 atm-cu m/mole(SRC), derived from its vapor pressure, 0.00023 mm Hg(3) and water solubility, 2.8X10+5 mg/l(4). Oxamyl is not expected to volatilize from dry soil surfaces(SRC) based upon its vapor pressure(3). Half-lives of oxamyl in soil ranged from 11 days in loamy sand(5) to 415 days in fine sand (6) under aerobic conditions, and 6 days in silt loam under anaerobic conditions(5). Photolysis on soil does not appear to be significant(7).
AQUATIC FATE: Based on a classification scheme(1), Koc values ranging from 6 to 10(2), indicate that oxamyl is not expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is not expected(3) based upon a Henry's Law constant of 2.37X10-10 atm-cu m/mole(SRC), derived from its vapor pressure, 0.00023 mm Hg(4) and water solubility, 2.8X10+5 mg/l (5). According to a classification scheme(6), an estimated BCF of 3.1(SRC), from a log Kow of -0.48(7), suggests the potential for bioconcentration in aquatic organisms is low(SRC). The half-lives for the hydrolysis of oxamyl in sterile water-ethanol (99:1) phosphate buffers at 25 °C were 300 weeks, 17 weeks, 1.6 weeks, and 1.4 days at pHs of 4.5, 6.0, 7.0 and 8.0 respectively(8). Oxamyl was found to be stable at pH 4.7 for at least 11 days and hydrolyzed slowly in neutral solution (pH 6.9) with 3 and 9% hydrolysis occurring after 24 and 28 hours, respectively(9). At pH 9, hydrolysis was rapid with 30% conversion after 6 hours(9). Exposure to ultraviolet light was found to accelerate hydrolysis(9). An experimental value of the rate constant for the reaction of oxamyl with photochemically produced hydroxyl radicals in water has been determined to be 2.0X10+9 l/mol-s at 22 °C(10), which corresponds to a half-life of about 134 days(SRC), assuming a hydroxyl radical concentration of 3X10-17 molar(11). Photolysis appears to be significant in acidic surface water(12).
ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), oxamyl, which has a vapor pressure of 0.00023 mm Hg at 20-25 °C(2), is expected to exist solely as a vapor in the ambient atmosphere. Vapor-phase oxamyl is degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals(SRC); the half-life for this reaction in air is estimated to be 1.4 days(SRC), calculated from its rate constant of 2.3X10-11 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(3). Oxamyl is not expected to absorb light at wavelengths >290 nm, and would not be expected to be susceptible to direct photolysis by sunlight in air(SRC).
Using loamy sand (pH 6.8) from North Carolina and a sandy soil (pH 6.4) from Florida, half-lives for the degradation of oxamyl were 11 and 15 days, respectively, under aerobic conditions(1). Under anaerobic conditions, a half-life of 6 days was obtained with Keyport silt loam (pH 4.7)(1). The decomposition of oxamyl in soils followed first-order kinetics, the half-life ranging from 4-33 days in a Bet Dagan soil(2). Less than 5% of the oxamyl remained after one day in four water saturated, anaerobic subsoils at 10 °C(3). Half-lives in aerobic soils ranged from 21 days in loamy fine sand to 415 days in fine sand at 10 °C(3). Oxamyl in moist soils (Arrendondo sand, Cecil sandy loam, and Genada silt loam) was rapidly mineralized to CO2; mineralization half-lives for 14C oxamyl ranged from 23 to 46 days(4).
The rate constant for the vapor-phase reaction of oxamyl with photochemically-produced hydroxyl radicals has been estimated as 2.3X10-11 cu cm/molecule-sec at 25 °C(SRC) using a structure estimation method(1). This corresponds to an atmospheric half-life of about 1.4 days at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(1). The half-lives for the hydrolysis of oxamyl in sterile water-ethanol (99:1) phosphate buffers at 25 °C were 300 weeks, 17 weeks, 1.6 weeks, and 1.4 days at pHs of 4.5, 6.0, 7.0 and 8.0 respectively(2). The rate constant for the hydrolysis of oxamyl has been determined to be 169 L/min-mol(3). Oxamyl was found to be stable at pH 4.7 for at least 11 days and hydrolyzed slowly in neutral solution (pH 6.9) with 3 and 9% hydrolysis occurring after 24 and 28 hours, respectively(4). At pH 9, hydrolysis was rapid with 30% conversion after 6 hours(4). Exposure to ultraviolet light was found to accelerate hydrolysis(4). The half-life for the photodegradation of a thin film of oxamyl, thickness of 0.67 ug/sq-cm, was 55.38 hours(5). An experimental value of the rate constant for the reaction of oxamyl with photochemically produced hydroxyl radicals in water has been determined to be 2.0X10+9 l/mol-s at 22 °C(6), which corresponds to a half-life of about 134 days(SRC), assuming a hydroxyl radical concentration of 3X10-17 molar(7). Oxamyl underwent rapid and extensive degradation in solvents (methanol and hexane) and in the solid state as a thin film under a 300 nm light; half-lives were approximately 7 h and 2h, respectively(8). Photolysis appears to be significant in acidic surface water, but not on soil(9).
An estimated BCF of 3.1 was calculated for oxamyl(SRC), using a log Kow of -0.48(1) and a regression-derived equation(2). According to a classification scheme(3), this BCF suggests the potential for bioconcentration in aquatic organisms is low(SRC).
An experimental study using Arrendondo, Cecil, and Webster soils found Koc values of 8, 6, and 10, respectively(1). According to a classification scheme(2), these Koc values suggest that oxamyl is expected to have very high mobility in soil. Laboratory experiments show that oxamyl is fairly mobile in muck, loamy sand, and 2 silt loam soils (with movement faster in the loamy sand and slowest in the muck)(3). However, field leachate studies in silt loam, loamy sand, and fine sand show that movement is not that extensive even after 3 to 5 months with very little oxamyl below 15 inches(3). This difference may be attributed to oxamyl degradation losses being greater than movement through soil despite large rainfall levels(3).
The Henry's Law constant for oxamyl is 2.37X10-10 atm-cu m/mole(SRC), derived from its vapor pressure, 0.00023 mm Hg(1), and water solubility, 2.8X10+5 mg/l(2). This Henry's Law constant indicates that oxamyl is expected to be essentially nonvolatile from water surfaces(3). Oxamyl's Henry's Law constant indicates that volatilization from moist soil surfaces is not expected to occur(SRC). Oxamyl is not expected to volatilize from dry soil surfaces(SRC) based upon its vapor pressure(1).
GROUNDWATER: Oxamyl has been found in Long Island, NY and Rhode Island ground water at concentrations typically between 5 and 65 ppb(1). Oxamyl has also been detected in approximately 3 groundwater wells at a maximum concentration of 1.0 ug/L in Massachusetts(2). Oxamyl was not detected in 1003 wells (Jul 1994-Jun 1995) in 26 counties in California(3). According to the US Environmental Protection Agency Office of Pesticide Programs Pesticides in Groundwater Database, which complied monitoring studies for 1971-1991, oxamyl was detected in 904 of 23,305 total wells at concns ranging from 0.01 to 395.00 ug/l(4). Five of these were in Rhode Island (1984-1986), and 897 were in New York (1980-1991), one was in Massachusettes, with concns ranging from 1.0-2.0 ug/l and 0.01-395.00 ug/l respectively(4). One well in Massachusetts (1985)and one well in New Jersey (1987-1988) contained oxamyl at a concn of 0.1 and 1.4 ug/l, respectively(4). Three of the 904 wells exceeded the maximum contamination level of 200 ug/l(4).
SURFACE WATER: Oxamyl was found in 2% of samples with concentration >0.1 ug/l in estuaries and coastal waters in England and Wales in 1994(1).
In a study conducted from 1982-1984 sampling dietary intake of 25-30 yr old males, oxamyl was found in 2 of 201 adult foods sampled at a total of 0.012 ug; 83% of total the oxamyl intake was from cucumbers(1). Oxamyl was found in two ready-to-eat foods at an average concentration of 0.021 ug/g: once in cucumbers at 0.031 ug/g and once in raw sweet green pepper at 0.011 ug/g(2). Oxamyl was found in 4 out of 1219 samples of domestic (US) tomatoes at a maximum concentration of 0.12 ppm and twice in imported tomatoes at trace concentrations(3). Oxamyl has been detected as residues during the 1978-82, 1983-86, and 1994 US regulatory monitoring studies, however, concentrations were not reported(4,5,6). In a 1985-1991 US study of domestic foods which may be eaten by infants/children, oxamyl was found in one of 2464 samples of apples at a concentration of 0.06 ppm, and in 3 of 571 samples of pears at a maximum concentration of 0.38 ppm(7). Oxamyl was detected 8 times in imported agricultural commodities (cucumbers, grapes, sweet peppers, and strawberries) in Canada between Jan 1992-March 1994(8). Oxamyl residue was found 7 times at a maximum concentration of 0.26 in domestic (US) and imported apples in 1993-1994(9). Oxamyl residues were detected in various vegetables in Thailand during 1987-1989, at concentrations of 0.03 mg/kg(10).
Radioactive thiocyanate was the major metabolite identified in the milk... /of lactating goats orally administered five consecutive daily doses of 31 ppm oxamyl/.
Occupational exposure to oxamyl may occur through inhalation and dermal contact with this compound at workplaces where oxamyl is produced or used. Monitoring data indicate that the general population may be exposed to oxamyl via ingestion of food. (SRC)
Generators of waste (equal to or greater than 100 kg/month) containing this contaminant, EPA hazardous waste number P194, must conform with USEPA regulations in storage, transportation, treatment and disposal of waste.
Oxamyl should be treated with alkali. Recommendable methods: Alkaline hydrolysis, adsorption.
/GUIDE 131: FLAMMABLE LIQUIDS-TOXIC/ Health: TOXIC; may be fatal if inhaled, ingested or absorbed through skin. Inhalation or contact with some of these materials will irritate or burn skin and eyes. Fire will produce irritating, corrosive and/or toxic gases. Vapors may cause dizziness or suffocation. Runoff from fire control or dilution water may cause pollution. /Carbamate pesticide, liquid, flammable, poisonous; Carbamate pesticide, liquid, flammable, toxic; Carbamate pesticide, liquid, poisonous, flammable; Carbamate pesticide, liquid, toxic, flammable/
/GUIDE 131: FLAMMABLE LIQUIDS-TOXIC/ Fire or Explosion: HIGHLY FLAMMABLE: Will be easily ignited by heat, sparks or flames. Vapors may form explosive mixtures with air. Vapors may travel to source of ignition and flash back. Most vapors are heavier than air. They will spread along ground and collect in low or confined areas (sewers, basements, tanks). Vapor explosion and poison hazard indoors, outdoors or in sewers. Those substances designated with a "P" may polymerize explosively when heated or involved in a fire. Runoff to sewer may create fire or explosion hazard. Containers may explode when heated. Many liquids are lighter than water. /Carbamate pesticide, liquid, flammable, poisonous; Carbamate pesticide, liquid, flammable, toxic; Carbamate pesticide, liquid, poisonous, flammable; Carbamate pesticide, liquid, toxic, flammable/
/GUIDE 131: FLAMMABLE LIQUIDS-TOXIC/ Public Safety: CALL Emergency Response Telephone Number ... . As an immediate precautionary measure, isolate spill or leak area for at least 50 meters (150 feet) in all directions. Keep unauthorized personnel away. Stay upwind. Keep out of low areas. Ventilate closed spaces before entering. /Carbamate pesticide, liquid, flammable, poisonous; Carbamate pesticide, liquid, flammable, toxic; Carbamate pesticide, liquid, poisonous, flammable; Carbamate pesticide, liquid, toxic, flammable/
/GUIDE 131: FLAMMABLE LIQUIDS-TOXIC/ Protective Clothing: 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. /Carbamate pesticide, liquid, flammable, poisonous; Carbamate pesticide, liquid, flammable, toxic; Carbamate pesticide, liquid, poisonous, flammable; Carbamate pesticide, liquid, toxic, flammable/
For more DOT Emergency Guidelines (Complete) data for OXAMYL (16 total), please visit the HSDB record page.
IMO 6.1; Carbamate pesticides, solid, toxic, nos; carbamate pesticides, liquid, toxic, flammable, nos, flashpoint between 23 °C and 61 °C; carbamate pesticides, liquid, toxic, nos; carbamate pesticides, liquid, NOS
IMO 3.2; Carbamate pesticides, liquid, flammable, toxic, nos, flashpoint less than 23 °C
UN 2757; Carbamate pesticides, solid, toxic, nos; carbamate pesticides, liquid, nos
UN 2758; Carbamate pesticides, liquid, flammable, toxic, nos, flashpoint less than 23 °C
For more Shipping Name/ Number DOT/UN/NA/IMO (Complete) data for OXAMYL (6 total), please visit the HSDB record page.
No person may /transport,/ offer or accept a hazardous material for transportation in commerce unless that person is registered in conformance ... and the hazardous material is properly classed, described, packaged, marked, labeled, and in condition for shipment as required or authorized by ... /the hazardous materials regulations (49 CFR 171-177)./
The International Air Transport Association (IATA) Dangerous Goods Regulations are published by the IATA Dangerous Goods Board pursuant to IATA Resolutions 618 and 619 and constitute a manual of industry carrier regulations to be followed by all IATA Member airlines when transporting hazardous materials.
The International Maritime Dangerous Goods Code lays down basic principles for transporting hazardous chemicals. Detailed recommendations for individual substances and a number of recommendations for good practice are included in the classes dealing with such substances. A general index of technical names has also been compiled. This index should always be consulted when attempting to locate the appropriate procedures to be used when shipping any substance or article.
Marine pollutant
Poison Flammable Liquid