Methyl ethyl ketoxime

87.1204

87.12

202-496-6|406-930-7

1993

DTXSID1021821

Liquid|Colorless liquid

29280090

32.59

1.2465

Transparent liquid

0.9232 g/cm³ @ Temp: 80 °C

-29.5 °C

152.5 °C

140 °F

n20/D 1.442(lit.)

H2O: 114 g/L (20 ºC)

Store in a cool, dry place. Keep container closed when not in use.

<8 mm Hg ( 20 °C)

3 (vs air)

Henry's Law constant = 1.22X10-6 atm-cu m/mol at 20 °C (est)

pKa = 12.45 at 25 °C

Hydroxyl radical reaction rate constant = 1.48X10-12 cu cm/molecule-sec at 25 °C (est)

Highly flammable. Water soluble.

Oximes

Highly Flammable

METHYL ETHYL KETOXIME is sensitive to heat. Has exploded at least twice when heated in the presence of acidic impurities [Chem. Eng. News, 1974, 52(35), 3]. Reacts with oxidizing agents. Mixtures with strong acids may explode. Reacts with sulfuric acid to form an explosive product (NTP, 1992).

III

3

UN 1993 3/PG 3

1

R21; R40; R41; R43

S13-S23-S26-S36/37/39-S61-S45-S36/37-S25

EL9275000

Xn

Stable. Combustible. Incompatible with strong oxidizing agents. May react with strong acids to form an explosive material.

P280-P305 + P351 + P338

H312-H317-H318-H351

SRP: The most favorable course of action is to use an alternative chemical product with less inherent propensity for occupational harm/injury/toxicity or environmental contamination. Recycle any unused portion of the material for its approved use or return it to the manufacturer or supplier. Ultimate disposal of the chemical must consider: the material's impact on air quality; potential migration in soil or water; effects on animal and plant life; and conformance with environmental and public health regulations.

This chemical is combustible. (NTP, 1992)

|Danger|H312: Harmful in contact with skin [Warning Acute toxicity, dermal]|P201, P202, P261, P272, P280, P281, P302+P352, P305+P351+P338, P308+P313, P310, P312, P321, P322, P333+P313, P363, P405, and P501|H312 (61.05%): Harmful in contact with skin [Warning Acute toxicity, dermal]|P201, P202, P260, P261, P264, P270, P272, P273, P280, P281, P302+P352, P305+P351+P338, P308+P313, P310, P312, P314, P321, P322, P333+P313, P363, P405, and P501|Aggregated GHS information provided by 95 companies from 9 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.|H312 (100%): Harmful in contact with skin [Warning Acute toxicity, dermal]|Aggregated GHS information provided by 2517 companies from 17 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.|H302: Harmful if swallowed [Warning Acute toxicity, oral]|P201, P202, P260, P261, P264, P270, P272, P280, P281, P301+P312, P302+P352, P305+P351+P338, P308+P313, P310, P312, P314, P321, P322, P330, P333+P313, P361, P363, P405, and P501

Fires involving this material can be controlled with a dry chemical, carbon dioxide or Halon extinguisher. A water spray may also be used. (NTP, 1992)

Excerpt from ERG Guide 128 [Flammable Liquids (Water-Immiscible)]: As an immediate precautionary measure, isolate spill or leak area for at least 50 meters (150 feet) in all directions. LARGE SPILL: Consider initial downwind evacuation for at least 300 meters (1000 feet). FIRE: 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. (ERG, 2016)

SMALL SPILLS AND LEAKAGE: If you should spill this chemical, use absorbent paper to pick up all liquid spill material. Seal the absorbent paper, as well as any of your clothing which may be contaminated, in a vapor-tight plastic bag for eventual disposal. Wash any surfaces you may have contaminated with a 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. STORAGE PRECAUTIONS: You should store this chemical under freezer conditions, and keep it away from all oxidizing materials. (NTP, 1992)

RECOMMENDED RESPIRATOR: Where the neat test chemical is weighed and diluted, wear a NIOSH-approved half face respirator equipped with an organic vapor/acid gas cartridge (specific for organic vapors, HCl, acid gas and SO2) with a dust/mist filter. (NTP, 1992)

The mean concentration of 2-butanone oxime detected in three alkyd enamel paints purchased from retail outlet stores was 0.92, 2.93 and 1.34 mg/g respectively(1); in two-week chamber studies using these paints, an average of 84% of the 2-butanone oxime in the paints initially was recovered in the volatile emissions(1).

LD50 Rat sc 2700 mg/kg body weight|LD50 Mouse ip 521 mg/kg body weight|LD50 Rabbit dermal 1000-2000 mg/kg body weight|LC50 Rat inhalation 20 mg/L/4 hours|LD50 Rat 2528 mg/kg body weight

Toxicity studies of methyl ethyl ketoxime (greater than 99% pure) were carried out in male and female F344/N rats and B6C3F1 mice. The compound was administered in drinking water for 14 days or 13 weeks. In addition, the genetic toxicity of methyl ethyl ketoxime was evaluated by determining mutagenicity in Salmonella typhimurium and induction of sister chromatid exchanges and chromosomal aberrations in cultured Chinese hamster ovary cells in vitro, with and without S9 activation. The frequency of micronucleated normochromatic erythrocytes in the peripheral blood of mice from the 13-week study was also determined. In the 14-day studies, groups of five male and five female rats and mice were given drinking water containing 0, 106, 312, 625, 1,250, or 2,500 ppm methyl ethyl ketoxime. The mean body weight gain of male rats in the 2,500 ppm group was significantly less than that of the controls; the final mean body weight of male mice in the 2,500 ppm group was also less than that of the controls. Spleen weights were increased in male and female rats in the 1,250 and 2,500 ppm groups. No chemical-related gross lesions were observed. Microscopic tissue evaluations were not performed. In the 13-week studies, groups of 10 male and 10 female rats were given drinking water containing 0, 312, 625, 1,250, 2,500, or 5,000 ppm and groups of 10 male and 10 female mice were given drinking water containing 0, 625, 1,250, 2,500, 5,000, or 10,000 ppm. Mean body weights and body weight gains of 2,500 and 5,000 ppm male rats and 10,000 ppm male and female mice were less than those of the controls; mean body weight gains of male rats in the 1,250, 2,500 and 5,000 ppm groups and females in the 2,500 and 5,000 ppm groups were also less than those of the controls. Hematology results of this drinking water study indicate that methyl ethyl ketoxime induces a methemoglobinemia and a responsive Heinz body anemia. Liver and spleen weights were generally significantly greater than those of the controls in male and female rats exposed to 1,250 ppm or greater; spleen weights were also increased in male and female mice in the 10,000 ppm groups. Kidney weights were significantly greater in male rats in the 5,000 ppm group and in female rats exposed to 1,250 ppm or greater than those of the controls. Microscopically, there were exposure-related increases in the incidences and severities of hematopoietic cell proliferation in the spleen at exposure concentrations of 625 ppm or greater in male and female rats and at 5,000 and 10,000 ppm in male and female mice. A significant increase in the incidence of hematopoietic proliferation in the bone marrow was observed in rats exposed to 625 ppm or greater. Liver Kupffer cell erythrophagocytosis and hemosiderin pigmentation, as well as renal tubule hemosiderin pigmentation, occurred in exposed rats and mice. Other lesions observed include hyperplasia of the transitional epithelial lining of the urinary bladder in male and female mice exposed to 2,500 ppm or greater and degeneration of the nasal olfactory epithelium in male and female rats in the 2,500 and 5,000 ppm groups, male mice in the 5,000 and 10,000 ppm groups, and female mice exposed to 2,500 ppm or greater. Methyl ethyl ketoxime is extensively metabolized and does not accumulate in tissues. Single gavage doses of 2.7, 27, or 270 mg/kg administered to rats were primarily converted to carbon dioxide, mostly in the first 24 hours after dosing. After intravenous administration, less radioactivity on a percentage basis was excreted as carbon dioxide than in the gavage study, and more of the administered dose was excreted in urine and as volatiles. Following dermal administration, significantly greater amounts of volatiles were excreted than after gavage or intravenous administration. The 270 mg/kg gavage dose may result in saturation of a metabolic pathway(s). There is some evidence that the ketoxime is metabolized to the ketone and, presumably, hydroxylamine. Methyl ethyl ketoxime was mutagenic in Salmonella typhimurium strain TA1535 when tested in the presence of hamster liver S9 activation enzymes; results of mutagenicity testing were negative in strains TA97, TA98, and TA100, with and without exogenous metabolic activation. No induction of sister chromatid exhanges or chromosomal aberrations was observed in cultured Chinese hamster ovary cells treated with methyl ethyl ketoxime, with or without S9, and no increase in the frequency of micronucleated erythrocytes was noted in peripheral blood obtained from male and female mice administered methyl ethyl ketoxime in drinking water for 13 weeks. In summary, the major target of methyl ethyl ketoxime is the erythrocyte; the no-effect level for erythrotoxicity is 625 ppm in male rats and 312 ppm in female rats based on erythrocyte counts after 13 weeks of exposure. The no-effect level for hematopoietic toxicity is 312 ppm in rats based on erythroid cell hyperplasia in bone marrow and 2,500 ppm in mice based on hematopoietic cell proliferation in the spleen. Hematology results of this drinking water study indicate that methyl ethyl ketoxime induces a methemoglobinemia and a responsive Heinz body anemia. Methyl ethyl ketoxime was at most weakly genotoxic; it induced mutations in S. typhimurium under very specific conditions and increased the frequency of sister chromatid exchanges in cultured Chinese hamster ovary cells, but it did not induce sister chromatid exchanges or chromosomal aberrations in cultured Chinese hamster ovary cells in vitro or increase the frequency of micronucleated erythrocytes in mice treated in vivo.

2-Butanone oxime's production and use as an anti-skinning agent in paints and lacquers, as a blocking-agent for isocyanate in polyurethanes, and in the manufacture of oxime silanes for use as a crosslinking agent for silicone sealants(1) may result in its release to the environment through various waste streams(SRC).

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 116(SRC), determined from a structure estimation method(2), indicates that 2-butanone oxime is expected to have high mobility in soil(SRC). Volatilization of 2-butanone oxime from moist soil surfaces is expected to occur(SRC) given a an estimated Henry's Law constant of 1.22X10-6 atm-cu m/mole(SRC), estimated from its vapor pressure, 1.06 mm Hg at 20 °C(3), and water solubility, 1X10+5 mg/L(4). 2-Butanone oxime is expected to volatilize from dry soil surfaces based upon its vapor pressure(SRC). A 14-19.6% theoretical BOD over a 2-week period(5) and a 24.7% theoretical BOD over a 4-week period(6) using activated sludge in the Japanese MITI test(3,6) suggests that biodegradation may occur in soil(SRC). [|AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 116(SRC), determined from a structure estimation method(2) indicates that 2-butanone oxime is not expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is expected to occur(3) based upon an estimated Henry's Law constant of 1.22X10-6 atm-cu m/mole(SRC), derived from its vapor pressure, 1.06 mm Hg(4), and water solubility, 1X10+5 mg/L(5). Using this Henry's Law constant and an estimation method(3), volatilization half-lives for a model river and model lake are 28 and 208 days, respectively(SRC). According to a classification scheme(6), an observed BCF range of 0.5 to 5.8 in catfish over a 6-week test period(7), suggests the potential for bioconcentration in aquatic organisms is low. A 14-19.6% theoretical BOD over a 2-week period(8) and a 24.7% theoretical BOD over a 4-week period(7) using activated sludge in the Japanese MITI test(7-8) suggests that biodegradation may occur in water(SRC).|ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), 2-butanone oxime, which has a vapor pressure of 1.06 mm Hg at 20 °C(2) is expected to exist solely as a vapor in the ambient atmosphere. Vapor-phase 2-butanone oxime 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 11 days(SRC), calculated from its rate constant of 1.48X10-12 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(2).

The rate constant for the vapor-phase reaction of 2-butanone oxime with photochemically-produced hydroxyl radicals has been estimated as 1.48X10-12 cu cm/molecule-sec at 25 °C(SRC) using a structure estimation method(1). This corresponds to an atmospheric half-life of about 11 days at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(1).

5.01|Using 2-butanone oxime concentrations of 0.2 and 2.0 mg/L, a BCF range of 0.5 to 5.8 was measured in catfish over a 6-week exposure period(1).

Using a structure estimation method based on molecular connectivity indices(1), the Koc of 2-butanone oxime can be estimated to be 116(SRC). According to a classification scheme(2), this estimated Koc value suggests that 2-butanone oxime is expected to have high mobility in soil.

The Henry's Law constant for 2-butanone oxime is estimated as 1.22X10-6 atm-cu m/mole(SRC) derived from its vapor pressure, 1.06 mm Hg at 20 °C(1), and water solubility, 1X10+5 mg/L(2). This Henry's Law constant indicates that 2-butanone oxime is expected to volatilize slowly from water surfaces(3). Based on this Henry's Law constant, the volatilization half-life from a model river (1 m deep, flowing 1 m/sec, wind velocity of 3 m/sec)(3) is estimated as 28 days(SRC). The volatilization half-life from a model lake (1 m deep, flowing 0.05 m/sec, wind velocity of 0.5 m/sec)(3) is estimated as 208 days(SRC). 2-Butanone oxime's Henry's Law constant indicates that volatilization from moist soil surfaces may occur(SRC). 2-Butanone oxime expected to volatilize from dry soil surfaces(SRC) based upon its vapor pressure(SRC). In two-week chamber studies using paints containing 2-butanone oxime, an average of 84% of the 2-butanone oxime in the paints initially was recovered in the volatile emissions(4).

According to the 2006 TSCA Inventory Update Reporting data, the number of persons reasonably likely to be exposed in the industrial manufacturing, processing, and use of 2-butanone oxime is 1000 or greater; the data may be greatly underestimated(1).|NIOSH (NOES Survey 1981-1983) has statistically estimated that 313,185 workers (25,609 of these were female) were potentially exposed to 2-butanone oxime in the US(1). Occupational exposure to 2-butanone oxime may occur through inhalation and dermal contact with this compound at workplaces where 2-butanone oxime is produced or used(SRC). The U.S. Consumer Product Safety Commission's Chemicals in Products database lists 764 products that contain 2-butanone oxime (methyl ethyl ketoxime); all but 16 of these products are in the paints and coatings category; other products containing methyl ethyl ketoxime included a glass cleaner and a skin soap(2). The general population will exposed to 2-butanone oxime through inhalation of vapors and dermal contact from consumer products containing the compound (especially paints and coatings)(SRC).

Pregnant mice were administered a single oral dose of 14(C)-2 butanone oxime on day 14 of gestation. In addition, a male mouse was administered a single oral dose of (14)C-2-butanone oxime. It appears that the substance is rapidly absorbed via the oral route, and distributed intact through the body. Urine and bile contained significant activity throughout the study. Intestinal activity was minimal. This suggests that the substance is primarily excreted via the kidneys.|The disposition of 14(C)-methyl ethyl ketoxime (MEKO) was determined in the male F344 rat following oral, iv and dermal administration. Oral doses of 2.7, 27 and 270 mg/kg were primarily excreted as CO2 (71-49%) in decreasing percentage as the dose increased. Excretion in urine (13-26%) and as volatiles (5-18%) increased as the dose increased. Five to 6% of the dose remained in the major tissues after 72 hr. An iv dose of 2.7 mg/kg was also principally excreted as CO2 (48.8%) with excretion in urine and as expired volatiles accounting for 21.4 and 11.4%, respectively. About 7% of the administered radioactivity remained in the tissues after 72 hr. Following dermal administration, 13 and 26% of a 2.7 and 270 mg/kg dose, respectively, were absorbed. Volatilization from the dose site prior to placement in the metabolism cage may account for the low absorption. MEKO was biotransformed to at least five polar metabolites that could only be partially resolved by anion exchange chromatography. Incubation with glucuronidase, but not sulphatase, changed the urinary metabolic profile. Methyl ethyl ketone was a major component in the volatiles.|...Methyl ethyl ketoxime is extensively metabolized and does not accumulate in tissues. Single gavage doses of 2.7, 27, or 270 mg/kg administered to rats were primarily converted to carbon dioxide, mostly in the first 24 hours after dosing. After intravenous administration, less radioactivity on a percentage basis was excreted as carbon dioxide than in the gavage study, and more of the administered dose was excreted in urine and as volatiles. Following dermal administration, significantly greater amounts of volatiles were excreted than after gavage or intravenous administration. The 270 mg/kg gavage dose may result in saturation of a metabolic pathway(s). There is some evidence that the ketoxime is metabolized to the ketone and, presumably, hydroxylamine...

The substance /2-butanone oxime/ can be metabolized in vivo in animals to 2-butanone and hydroxylamine.|...Methyl ethyl ketoxime is extensively metabolized and does not accumulate in tissues. Single gavage doses of 2.7, 27, or 270 mg/kg administered to rats were primarily converted to carbon dioxide, mostly in the first 24 hours after dosing. After intravenous administration, less radioactivity on a percentage basis was excreted as carbon dioxide than in the gavage study, and more of the administered dose was excreted in urine and as volatiles. Following dermal administration, significantly greater amounts of volatiles were excreted than after gavage or intravenous administration. The 270 mg/kg gavage dose may result in saturation of a metabolic pathway(s). There is some evidence that the ketoxime is metabolized to the ketone and, presumably, hydroxylamine...

0.05 Days

Both oximes and hydroxylamine (HYAM) are compounds with known oxidative capacity. We tested in vitro whether acetaldoxime (AAO), cyclohexanone oxime (CHO), methyl ethyl ketoxime (MEKO) or HYAM affect haemoglobin oxidation (into HbFe3+), formation of thiobarbituric acid reactive substances (TBARS), and glutathione (GT) depletion in human haemolysate, erythrocytes or blood. All these parameters are known to be related to oxidative stress. Glutathione S-transferase (GST) activity was measured as it may be affected by oxygen radicals. All three oximes caused a low degree of HbFe3+ accumulation in erythrocytes. This was higher in haemolysates indicating that membrane transport may be limiting or that protective mechanisms within erythrocytes are more effective. HbFe3+ accumulation was lower for the oximes than for HYAM. AAO and HYAM caused TBARS formation in blood. For HYAM this was expected as free radicals are known to be generated during HbFe3+ formation. Free radical generation by AAO and HYAM in erythrocytes was confirmed by the inhibition of GST. For the other two oximes (CHO and MEKO) some special effects were found. CHO did inhibit erythrocyte GST while it did not cause TBARS formation. MEKO was the least potent oxime as it caused no TBARS formation, little HbFe3+ accumulation and little GST inhibition in erythrocytes. However, GT depletion was more pronounced for MEKO than for the other oximes, indicating that glutathione conjugation occurs. TBARS formation, GT depletion and GST modulation caused by the oximes and HYAM were also tested in rat hepatocytes. However, no effects were found in hepatocytes. This suggests that a factor present in erythrocytes is necessary for free radical formation. Studies with proposed metabolites of the oximes (i.e. cyclohexanone, acetaldehyde or methylethyl ketone) and addition of rat liver preparations to the erythrocyte incubations with oximes, suggest that metabolism is not a limiting factor in erythrocyte toxicity.|Acetoxime and methylethyl ketoxime (MEKO) are tumorigenic in rodents, inducing liver tumors in male animals. The mechanisms of tumorigenicity for these compounds are not well defined. Oxidation of the oximes to nitronates of secondary-nitroalkanes, which are mutagenic and tumorigenic in rodents, has been postulated to play a role in the bioactivation of ketoximes. In these experiments, we have compared the oxidation of acetoxime and methylethyl ketoxime to corresponding nitronates in liver microsomes from different species. The oximes were incubated with liver microsomes from mice, rats, and several human liver samples. After tautomeric equilibration and extraction with n-hexane, 2-nitropropane and 2-nitrobutane were quantitated by GC/MS-NCI (limit of detection of 250 fmol/injection volume). In liver microsomes, nitronate formation from MEKO and acetoxime was dependent on time, enzymatically active proteins, and the presence of NADPH. Nitronate formation was increased in liver microsomes of rats pretreated with inducers of cytochrome P450 and reduced in the presence of inhibitors (n-octylamine and diethyldithiocarbamate). Rates of oxidation of MEKO (Vmax) were 1.1 nmol/min/mg (mice), 0.5 nmol/min/mg (humans), and 0.1 nmol/min/mg (rats). In addition to nitronates, several minor metabolites were also enzymatically formed (two diastereoisomers of 3-nitro-2-butanol, 2-hydroxy-3-butanone oxime and 2-nitro-1-butanol). Acetoxime was also metabolized to the corresponding nitronate at rates approximately 50% of those observed with MEKO oxidation in the three species examined. 2-Nitro-1-propanol was identified as a minor product formed from acetoxime. No sex differences in the capacity to oxidize acetoxime and MEKO were observed in the species examined. The observed results show that formation of sec-nitronates from ketoximes occurs slowly, but is not the only pathway involved in the oxidative biotransformation of these compounds. Due to the lack of sex-specific oxidative metabolism, other metabolic pathways or mechanisms of tumorigenicity not involving bioactivation may be involved in the sex-specific tumorigenicity of ketoximes in rodents.

SYMPTOMS: Symptoms of exposure to this compound may include slight eye and skin irritation. It may interfere with alcohol metabolism resulting in the formation of acetaldehyde, blotchy red marks, red eyes, tiredness and visible veins. ACUTE/CHRONIC HAZARDS: This compound may be harmful if swallowed, inhaled or absorbed through the skin. When heated to decomposition it emits toxic fumes of carbon monoxide, carbon dioxide and nitrogen oxides. (NTP, 1992)

EYES: First check the victim for contact lenses and remove if present. Flush victim's eyes with water or normal saline solution for 20 to 30 minutes while simultaneously calling a hospital or poison control center. Do not put any ointments, oils, or medication in the victim's eyes without specific instructions from a physician. IMMEDIATELY transport the victim after flushing eyes to a hospital even if no symptoms (such as redness or irritation) develop. SKIN: IMMEDIATELY flood affected skin with water while removing and isolating all contaminated clothing. Gently wash all affected skin areas thoroughly with soap and water. If symptoms such as redness or irritation develop, IMMEDIATELY call a physician and be prepared to transport the victim to a hospital for treatment. INHALATION: IMMEDIATELY leave the contaminated area; take deep breaths of fresh air. If symptoms (such as wheezing, coughing, shortness of breath, or burning in the mouth, throat, or chest) develop, call a physician and be prepared to transport the victim to a hospital. Provide proper respiratory protection to rescuers entering an unknown atmosphere. Whenever possible, Self-Contained Breathing Apparatus (SCBA) should be used; if not available, use a level of protection greater than or equal to that advised under Protective Clothing. INGESTION: DO NOT INDUCE VOMITING. If the victim is conscious and not convulsing, give 1 or 2 glasses of water to dilute the chemical and IMMEDIATELY call a hospital or poison control center. Be prepared to transport the victim to a hospital if advised by a physician. If the victim is convulsing or unconscious, do not give anything by mouth, ensure that the victim's airway is open and lay the victim on his/her side with the head lower than the body. DO NOT INDUCE VOMITING. IMMEDIATELY transport the victim to a hospital. (NTP, 1992)

/SRP:/ Immediate first aid: Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial respiration, preferably with a demand valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR if necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on the left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain medical attention. /Poisons A and B/|/SRP:/ Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if needed. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock and treat if necessary ... . Anticipate seizures and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with 0.9% saline (NS) during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 mL/kg up to 200 mL of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool ... . Cover skin burns with dry sterile dressings after decontamination ... . /Poisons A and B/|/SRP:/ Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in severe respiratory distress. Positive-pressure ventilation techniques with a bag valve mask device may be beneficial. Consider drug therapy for pulmonary edema ... . Consider administering a beta agonist such as albuterol for severe bronchospasm ... . Monitor cardiac rhythm and treat arrhythmias as necessary ... . Start IV administration of D5W /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Watch for signs of fluid overload ... . Treat seizures with diazepam or lorazepam ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Poisons A and B/

2-butanone oxime

Adhesive manufacturing|2-Butanone, oxime: ACTIVE|The U.S. Consumer Product Safety Commission's Chemicals in Products database lists 764 products that contain 2-butanone oxime (methyl ethyl ketoxime); all but 16 of these products are in the paints and coatings category; other products containing methyl ethyl ketoxime included a glass cleaner and a skin soap.