2-Butanone oxime

0.9232 at 68 °F (NTP, 1992) - Less dense than water; will float

0.9232 g/cu cm at 20 °C

0.923 @ 20°C

Liquid

Colorless liquid

greater than or equal to 100 mg/mL at 72 °F (NTP, 1992)

In water, 100,000 mg/L at 25 °C

Soluble in chloroform; miscible with ethanol and ether

306 °F at 760 mmHg (NTP, 1992)

152.5 °C

152 °C @760 [mm Hg]

-21.1 °F (NTP, 1992)

-29.5 °C

-29.5 °C

22.6 mmHg at 73 °F ; 50.9 mmHg at 118 °F (NTP, 1992)

0.9 [mmHg]

VP: 7.6 mm Hg at 50 °C

1.06 mm Hg at 20 °C

Danger

H301: Toxic if swallowed [Danger Acute toxicity, oral]

P203, P260, P261, P264, P264+P265, P270, P271, P272, P280, P301+P316, P302+P352, P304+P340, P305+P354+P338, P308+P316, P317, P318, P319, P321, P330, P332+P317, P333+P317, P362+P364, P403+P233, P405, and P501 (click each P-code to see the statement)

This chemical does not meet GHS hazard criteria for < 0.1% (2 of 4723) of reports.

Danger

H312 (> 99.9%): Harmful in contact with skin [Warning Acute toxicity, dermal]

Chemical: 2-Butanone, oxime

Hazard Traits - Carcinogenicity

2-Butanone, oxime is listed on the EPA's Chemical Data Reporting (CDR) system. Manufacturers and importers of 2-Butanone, oxime are required to report information about their production and use of this chemical to the EPA under the Toxic Substances Control Act (TSCA). (40 eCFR Part 711)

Status: Active Update: 23-01-2023 https://echa.europa.eu/registration-dossier/-/registered-dossier/14908

2-Butanone, oxime: HSNO Approval: HSR001191 Approved with controls

A skin sensitizer; [Quick CPC] Dermal sensitization, hemolytic anemia, and CNS depression reported in animal studies; Hemolytic effects were seen in a 4-week inhalation study at 533 ppm, but not at 283 ppm; MEKO has been produced since 1958, and no adverse effects in workers have been reported; Painters using alkyd paints containing MEKO were exposed at levels <1-2 ppm; [AIHA] 8-hour exposure of 12 rats to saturated atmosphere caused no mortalities; Hematological changes (increased methemoglobin and reticulocytes and decreased hemoglobin) observed in 4-week inhalation study of rats at 400 ppm; In a 13-week oral neurotoxicity study of rats, transient neurobehavioral changes were observed immediately following administration, but reversed by the next day; No progressive long term neurotoxicity observed; [IUCLID]

Pursuant to section 8(d) of TSCA, EPA promulgated a model Health and Safety Data Reporting Rule. The section 8(d) model rule requires manufacturers, importers, and processors of listed chemical substances and mixtures to submit to EPA copies and lists of unpublished health and safety studies. 2-Butanone, oxime is included on this list. Effective date: 12/15/86; Sunset date: 12/19/95.

All persons who manufacture (including import) or process or intend to manufacture or process MEKO, including persons who manufacture or process or intend to manufacture or process MEKO as a byproduct, or who import or intend to import products which contain MEKO, after the date specified in paragraph (e) of this section to the end of the reimbursement period, shall submit letters of intent to conduct testing, submit study plans, conduct tests and submit data, or submit exemption applications, as specified in this section, subpart A of this part, and parts 790 and 792 of this chapter for single-phase rulemaking.Methyl ethyl ketoxime is included on this list. Required testing: health effect testing.

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).

Acute Tox. 4 (> 99.9%)

Acute toxicity (ingestion) - category 3

Acute toxicity (Oral) - Category 4

Hazardous to the aquatic environment (Acute) - Category 3

Acute toxicity (Oral) - Category 4

Carc. 1B

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.

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.

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.

8.0 [ppm]

150 [ppm]

880 [ppm]

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)

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 following link will take the user to the National Toxicology Program (NTP) Test Agent Search Results page, which tabulates all of the "Standard Toxicology & Carcinogenesis Studies", "Developmental Studies", and "Genetic Toxicity Studies" performed with this chemical. Clicking on the "Testing Status" link will take the user to the status (i.e., in review, in progress, in preparation, on test, completed, etc.) and results of all the studies that the NTP has done on this chemical.[Available from, as of June 21, 2012: http://ntp-apps.niehs.nih.gov/ntp_tox/index.cfm?fuseaction=ntpsearch.searchresults&searchterm=96-29-7]

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.

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).

AEROBIC: 2-Butanone oxime, present at 30 mg/L, reached 24.7% of its theoretical BOD in 4 weeks using an activated sludge inoculum at 100 mg/L in the Japanese MITI test(1). 2-Butanone oxime, present at 30 mg/L, reached 14-19.5% of its theoretical BOD in 2 weeks using an activated sludge inoculum at 100 mg/L in the Japanese MITI test(2).

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).

/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ Male CD-1 mice were exposed 6 hr/day, 5 days/wk, for 1, 2, 4, or 13 wk via whole-body inhalation exposures to MEKO vapor concentrations of 0, 3 +/- 0.1, 10 +/- 0.3, 30 +/- 1, or 100 +/- 2 ppm (10 mice/group/interval). Satellite animals were removed after 1, 2, 4, or 13 wk of exposure and allowed to recover for 4 or 13 wk (5 mice/group/interval). After termination, the nasal turbinates were evaluated microscopically, and cross-sectional nasal maps of the lesions were prepared. At the end of the 1-, 2-, 4-, and 13-wk exposure periods, degeneration of the olfactory epithelium lining the dorsal meatus was seen in the anterior region of the nasal cavity. In a few instances, the olfactory epithelium covering the tips of the nasoturbinal scrolls projecting into the dorsal region of the nasal cavity was also degenerated. Large areas of olfactory epithelium lying laterally and posteriorly were unaffected. In general, approximately 10% or less of the total olfactory tissue was affected. In several instances, the degenerated olfactory epithelium was reepithelialized by squamous/squamoid and/or respiratory types of epithelium. Degeneration, which was dose related in incidence and severity, was seen in mice exposed to 30 and 100 ppm after 1 wk of exposure and in several mice exposed to 10 ppm after 13 wk of exposure. The incidence and severity of the degeneration present after 1 wk of exposure did not increase with the longer exposures. The olfactory degeneration was reversible. Recovery was complete within 4 wk following exposures at 10 ppm and nearly complete within 13 wk after exposures at 30 and 100 ppm. A no-observed-effect level (NOEL) for the olfactory degeneration was considered to be 3 ppm.

/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ /Fischer 344/ rats were exposed by inhalation to MEKO vapor /for 3 hours a day, 5 days a week for 4 weeks at doses of 25, 100, and 400 ppm. Exposure levels were analyzed and particle size distribution measured. Ten animals/sex/group were used. At 100 ppm increased methemoglobin was observed in female rats. At 400 ppm significant alterations in most hematological parameters (increased methemoglobin, increased reticulocytes, increased platelets, increased MCW and MCH, increased total leucocytes and erythrocytes and MCHC) were observed for both male and female rats. At 400 ppm remarkable erythrocyte morphology included increased numbers of nucleated erythrocytes and polychromia, were seen in male and female rats. At 400 ppm increased absolute and relative organ weights of liver and spleen in males and females were seen.

/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ /Fischer 344 rats were dosed once daily by gavage for 28 days at doses of 0, 250, 500 mg/kg/day. Control animals (15/group) received distilled water (negative control), 0.5% methylcellulose (vehicle control) or clofibric acid, 250 mg/kg (positive control), at the same dose volume as administered to the treated animals. Under the conditions of this study, MEKO did not produce any significant hepatic peroxisome proliferation in the rate, as indicated by a lack of effect on palmitoyl-CoA oxidation and by electron microscopy. The potential responsiveness of the animals used in this study was confirmed by the marked induction of palmitoyl-CoA in the rats treated with clofibric acid. While MEKO was not a peroxisome proliferator in the rat, significant increase in the levels of hepatic glutathione (primarily reduced glutathione) were observed in rats given 250 and 500 mg/kg/day MEKO for 14 days. This lack of an effect after 7 days of dosing correlated with the hepatocellular hypertrophy which was seen microscopically after 14 and 28 but not 7 days of treatment.

/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ In this study /Sprague-Dawley rats were administered butanone oxime by gavage at 25, 75, and 225 mg/kg/day 5 days a week for 13 weeks./ Ten animals/sex/group were used. No mortality occurred. Dose related effects on hematological parameters and effects on organ weights of spleen and liver, no neurological effects. The primary target of the substance is the blood system with hemolytic anemia and compensatory hematopoiesis. Also, extramedullary hemosiderosis (iron-accumulation) in the spleen was observed.

For more Non-Human Toxicity Excerpts (Complete) data for 2-Butanone oxime (9 total), please visit the HSDB record page.

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).

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).

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).

Pursuant to section 8(d) of TSCA, EPA promulgated a model Health and Safety Data Reporting Rule. The section 8(d) model rule requires manufacturers, importers, and processors of listed chemical substances and mixtures to submit to EPA copies and lists of unpublished health and safety studies. 2-Butanone, oxime is included on this list. Effective date: 12/15/86; Sunset date: 12/19/95.

All persons who manufacture (including import) or process or intend to manufacture or process MEKO, including persons who manufacture or process or intend to manufacture or process MEKO as a byproduct, or who import or intend to import products which contain MEKO, after the date specified in paragraph (e) of this section to the end of the reimbursement period, shall submit letters of intent to conduct testing, submit study plans, conduct tests and submit data, or submit exemption applications, as specified in this section, subpart A of this part, and parts 790 and 792 of this chapter for single-phase rulemaking.Methyl ethyl ketoxime is included on this list. Required testing: health effect testing.

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.

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...

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...

Used as an anti-skinning agent in alkyd paints; Also used as a blocking agent (urethane polymers) and a corrosion inhibitor (boilers); [AIHA]

Painting (Pigments, Binders, and Biocides) [Category: Paint]

Antiskinning agent in lacquers.

2-Butanone oxime is widely used as a blocking agent in coatings such as isocyanate urethane coatings for wire and in magnetic tape coatings and resins

Catalyst, oxygen scavenger in steam generation, extraction of silver

Used primarily as an antiskinning agent in alkyd coating resins to prevent formation of a solid or gelatinous skin in the container.

2023: 2,500,000 - <4,000,000 lb

2-Butanone, oxime is listed as a High Production Volume (HPV) chemical (65FR81686). Chemicals listed as HPV were produced in or imported into the U.S. in >1 million pounds in 1990 and/or 1994. The HPV list is based on the 1990 Inventory Update Rule. (IUR) (40 CFR part 710 subpart B; 51FR21438).

Production volumes for non-confidential chemicals reported under the Inventory Update Rule.[Table#8032]

Production volume for non-confidential chemicals reported under the 2006 Inventory Update Rule. Chemical: 2-Butanone, oxime. Aggregated National Production Volume: 10 to < 50 million lbs.

Machinery 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.