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Methyl Ethyl Ketone
Methyl Ethyl Ketone SE Gad and DW Sullivan, Jr., Gad Consulting Services, Cary, NC, USA Ó 2014 Elsevier Inc. All rights reserved.
Chemical Abstracts Service Registry Number: 78-93-3 Synonyms: MEK, 2-Butanone, 2-Oxobutane, Ethyl methyl ketone Molecular Formula: CH3COCH2CH3 Chemical Structure:
is rapidly metabolized by microbes and mammals. MEK evaporates readily into the atmosphere and is subject to rapid photochemical decomposition. There is no evidence indicating the bioaccumulation of MEK.
Exposure and Exposure Monitoring
Background (Significance/History) Methyl ethyl ketone (MEK) is an organic compound. This colorless liquid ketone has a sharp, sweet odor reminiscent of butterscotch and acetone. It is produced industrially on a large scale, and also occurs in trace amounts in nature. It is soluble in water and is commonly used as an industrial solvent.
Uses MEK is used as a solvent for various coating systems, for example, vinyl, adhesives, nitrocellulose, and acrylic coatings. It is used in paint removers, lacquers, varnishes, spray paints, sealers, glues, magnetic tapes, printing inks, resins, rosins, cleaning solutions, and for polymerization. It is found in other consumer products, for example, household and hobby cements, and wood-filling products. MEK is used in dewaxing lubricating oils, the degreasing of metals, in the production of synthetic leathers, transparent paper and aluminum foil, and as a chemical intermediate and catalyst. It is an extraction solvent in the processing of foodstuffs and food ingredients. MEK can also be used to sterilize surgical and dental equipment. In addition to its manufacture, environmental sources of MEK include exhaust from jet and internal combustion engines, and industrial activities such as gasification of coal. It is found in substantial amounts in tobacco smoke. MEK is produced biologically and has been identified as a product of microbial metabolism. It has also been found in plants, insect pheromones, and animal tissues, and MEK is probably a minor product of normal mammalian metabolism. It is stable under ordinary conditions but can form peroxides on prolonged storage; these may be explosive.
Environmental Fate and Behavior MEK reacts to form a haloform that is more toxic than the original compound in water containing free halogens or hypohalites. MEK is expected to have very high mobility in soil. It does not accumulate in any environmental compartment and
Encyclopedia of Toxicology, Volume 3
Inhalation, ingestion, and dermal contact are all possible routes of exposure. MEK is a natural component in some foods. Indoor air pollution (and inhalation) can occur from volatilization of MEK from consumer and building products. Methyl ethyl ketone occurs as a metabolic byproduct of plants and animals and is released into the atmosphere by volcanoes and forest fires. Methyl ethyl ketone is emitted from pencil cedar, Zeravshan juniper, European firs, Evergreen Cyprus, blooming rape, and southern pea seeds. Methyl ethyl ketone’s production and use as a solvent for coatings, resins, rubbers, plastics, pharmaceuticals, adhesives, and rubber cements may result in its release to the environment through various waste streams. Its use as a starting material or intermediate in the manufacture of chemical products may also lead to its release to the environment.
Toxicokinetics MEK is rapidly absorbed by inhalation, skin contact, and ingestion, and transferred into the blood and other tissues. MEK is metabolized in the liver, mainly to 3-hydroxy-2-butanone and 2,3-butanediol that are eliminated in urine. Most MEK probably enters the general metabolism in the body and is converted to acetate that is eventually broken down to carbon dioxide and water that are then eliminated in exhaled air and urine. Small amounts of MEK itself are also eliminated in exhaled air and urine. MEK and its metabolites are mostly cleared from the body within 24 h, and MEK does not accumulate in the body.
Mechanism of Toxicity There is very limited information on the mechanisms of toxicity of MEK. Relatively high-inhaled concentrations of 1475–29 500 mg m 3 (500–10 000 ppm) caused pulmonary vasoconstriction and hypertension in cats and dogs. There are several human case reports of neurological effects resulting from high exposure to MEK in combination with other solvents, and animal studies have confirmed synergism between MEK and ethyl n-butyl ketone, methyl n-butyl ketone, n-hexane, carbon tetrachloride, 2,5-hexanedione, and chloroform. The main target organs involved in toxicological interactions are the nervous system and liver, and the lung has also been mentioned.
http://dx.doi.org/10.1016/B978-0-12-386454-3.00879-4
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Methyl Ethyl Ketone
Acute and Short-Term Toxicity (or Exposure) Animal MEK causes central nervous system depression in animals. The oral LD50 in rats is 6.86 ml kg 1 (2737 mg kg 1) and 4050 mg kg 1 in mice. Inhalation LC50 is 23 500 mg m 3 in rats and 32 mg m 3 in mice. The intraperitoneal LD50 is 607 mg kg 1 in rats, 616 mg kg 1 in mice, and 2 g kg 1 in guinea pigs. Animal studies indicate that MEK is a mild-to-moderate skin irritant, and a moderate-to-severe eye irritant.
Human The major acute toxicity of MEK is mucosal irritation, and MEK can irritate the eyes, nose, and respiratory system. No irritation was produced when 20% MEK in petrolatum was applied to volunteers for 48 h in a closed patch test; however, it can be irritating to the skin by defatting. It can cause dizziness, fatigue, memory alteration, dermatitis, headaches, nausea, and paresthesia of extremities, diminished vision, acidosis, and vomiting. Acute inhalation can cause central nervous system depression. MEK vapor is irritating to mucous membranes and conjunctivae at 200 ppm after 15 min, but the odor is noticeable at 25 ppm. The results from animal evidence suggest that MEK can be aspirated during ingestion or vomiting, and could result in severe lung damage (edema), respiratory failure, cardiac arrest, and death.
Chronic Toxicity (or Exposure) Animal Exposure to 5000 ppm for 13 weeks produced an exposurerelated effect on body and liver weights in rats, as well as a depression in brain weight in females. Guinea pigs and rats were exposed to 235 ppm for 12 weeks (5 days week 1, 7 h day 1). There were no deaths and no signs of toxicity. Extensive neurological studies with high exposures have shown no effects. In one study, rats were initially exposed to 10 000 ppm that was reduced to 6000 ppm due to severe irritation of the upper respiratory tract. Temporary signs of muscle incoordination and gait disturbances were observed. Exposures continued for only 7 of the planned 15 weeks because some animals died of bronchopneumonia; there were no neurological symptoms. In the other study, rats were exposed to 1125 ppm continuously for up to 55 days with no signs of neurotoxicity.
Human A mortality study of hundreds of workers who had worked at MEK dewaxing plants concluded that there was no evidence of a cancer hazard. The average follow-up was 14 years. This study is limited by the small size of the cohort and the relatively short follow-up period.
Immunotoxicity There is no evidence indicating that MEK is immunotoxic.
Reproductive Toxicity Pregnant rats were exposed by inhalation to up to 3000 ppm on days 6–15 of gestation; at 3000 ppm, there was a low but statistically significant increase in malformations. Sternebral and soft tissue anomalies were also increased. There was also a statistically significant increase in total skeletal anomalies at 1000 ppm. Maternal toxicity was not observed. In subsequent studies, pregnant rats and mice were exposed to up to 3000 ppm by inhalation during days 6–15 of gestation. There were no embryotoxic or teratogenic effects at any exposure level. There were fetotoxic effects (increased incidence of minor skeletal variations; delayed bone formation; reduced fetal weight) with very slight maternal toxicity at 3000 ppm.
Genotoxicity MEK was not mutagenic in Ames (Salmonella) and Escherichia coli tests, but induced aneuploidy in Saccharomyces cerevisiae. MEK was not found to be genotoxic in the mouse lymphoma assay, in Chinese hamster ovary cell, unscheduled DNA synthesis assay, or micronucleus assays.
Carcinogenicity The International Agency for Research on Cancer has not evaluated the carcinogenicity of MEK, the American Conference of Governmental Industrial Hygienists has not assigned a carcinogenicity designation for MEK, and the US National Toxicology Program has not listed MEK in its report on carcinogens. MEK is classified as a Group D chemical by the US Environmental Protection Agency, that is, it is not classifiable as to human carcinogenicity.
Clinical Management Remove from exposure in all cases. In case of dermal exposure, immediately wash all affected areas thoroughly. In the event of ingestion, vomiting should not be induced due to the risk of aspiration, if a large amount has been ingested, arterial blood gases should be monitored. In ocular exposure, irrigate the patient’s eye with 0.9% saline for 10–15 min. In all cases, administer additional symptomatic treatment.
Ecotoxicology The LC50 for MEK in bluegill ranges from 5640 to 1690 mg l 1. The LC50 values for Daphnia magna range from 1382 to 8890 mg l 1. MEK is produced by fungi in concentrations that affect the germination of some plants. The effect of MEK on the alarm behavior of social insects has been studied. It was considered inactive in producing alarm behavior in the ant Iridomyrmex preinosus.
Methyl Ethyl Ketone
Exposure Standards and Guidelines The (US) Occupational Safety and Health Administration permissible exposure limit, 8-h time-weighted average (TWA) is 200 ppm, and the (US) National Institute for Occupational Safety and Health (NIOSH) recommended exposure level, averaged over a 10-h work day is 200 ppm. The NIOSH shortterm exposure limit, for a 15-min exposure, is 300 ppm.
FIFRA Requirements Residues of MEK are exempted from the requirement of a tolerance when used as a surfactant in accordance with good agricultural practice as inert (or occasionally active) ingredients in pesticide formulations applied to growing crops only.
Acceptable Daily Intakes An Acceptable Daily Intake (ADI), defined as the amount of a chemical to which humans can be exposed on a daily basis over an extended period of time (usually a lifetime) without suffering a deleterious effect, for MEK is 3.2 mg day 1 for oral exposure.
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of this waste. Generators of small quantities of this waste may qualify for partial exclusion from hazardous waste regulations.
Atmospheric Standards This action promulgates standards of performance for equipment leaks of Volatile Organic Compounds (VOC) in the Synthetic Organic Chemical Manufacturing Industry (SOCMI). The intended effect of these standards is to require all newly constructed, modified, and reconstructed SOCMI process units to use the best demonstrated system of continuous emission reduction for equipment leaks of VOC, considering costs, nonair quality health, and environmental impact and energy requirements. Methyl ethyl ketone is produced, as an intermediate or final product, by process units covered under this subpart. It is listed as a hazardous air pollutant (HAP) generally known or suspected to cause serious health problems. The Clean Air Act, as amended in 1990, directs the EPA to set standards requiring major sources to sharply reduce routine emissions of toxic pollutants. The EPA is required to establish and phase in specific performance-based standards for all air emission sources that emit one or more of the listed pollutants. Methyl ethyl ketone is included on this list.
TSCA Requirements 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. Methyl ethyl ketone is included on this list.
CERCLA Reportable Quantities Persons in charge of vessels or facilities are required to notify the National Response Center (NRC) immediately when there is a release of this designated hazardous substance in an amount equal to or greater than its reportable quantity of 5000 lb or 2270 kg.
Federal Drinking Water Guidelines EPA 4000 mg l 1.
See also: Neurotoxicity.
Further Reading Noraberg, J., Arlien-Soborg, P., 2000. Neurotoxic interactions of industrially used ketones. Neurotoxicology 21, 409–418. Yang, R.S., 1986. The toxicology of methyl ethyl ketone. Residue Rev. 97, 121–143.
Relevant Websites RCRA Requirements U159: As stipulated in 40 CFR 261.33, when 2-butanone, as a commercial chemical product or manufacturing chemical intermediate or an off-specification commercial chemical product or a manufacturing chemical intermediate, becomes a waste, it must be managed according to Federal and/or State hazardous waste regulations. Also defined as a hazardous waste is any residue, contaminated soil, water, or other debris resulting from the cleanup of a spill, into water or on dry land,
http://ecb.jrc.it/esis/esis.php – European Chemicals Bureau; IUCLID Dataset, Methyl ethyl ketone (CAS # 78-93-3). Compilation of information provided to the EU by the European chemicals industry as of 2000. http://www.intox.org – International Programme on Chemical Safety. Methyl Ethyl Ketone. http://www.inchem.org – International Programme on Chemical Safety (IPCS). Methyl Ethyl Ketone (Environmental Health Criteria 143). http://www.hpa.org.uk/webc/HPAwebfile/ – HPAweb_C/1279889215207 – Methyl Ethyl Ketone Incidence Management, Health Protection Agency, 2010. http://www.epa.gov/iris/subst/index.html – U.S. Environmental Protection Agency's Integrated Risk Information System (IRIS) on Methyl ethyl ketone (MEK) (78-93-3).
Chemical Abstracts Service Registry Number: 78-93-3 Synonyms: MEK, 2-Butanone, 2-Oxobutane, Ethyl methyl ketone Molecular Formula: CH3COCH2CH3 Chemical Structure:
is rapidly metabolized by microbes and mammals. MEK evaporates readily into the atmosphere and is subject to rapid photochemical decomposition. There is no evidence indicating the bioaccumulation of MEK.
Exposure and Exposure Monitoring
Background (Significance/History) Methyl ethyl ketone (MEK) is an organic compound. This colorless liquid ketone has a sharp, sweet odor reminiscent of butterscotch and acetone. It is produced industrially on a large scale, and also occurs in trace amounts in nature. It is soluble in water and is commonly used as an industrial solvent.
Uses MEK is used as a solvent for various coating systems, for example, vinyl, adhesives, nitrocellulose, and acrylic coatings. It is used in paint removers, lacquers, varnishes, spray paints, sealers, glues, magnetic tapes, printing inks, resins, rosins, cleaning solutions, and for polymerization. It is found in other consumer products, for example, household and hobby cements, and wood-filling products. MEK is used in dewaxing lubricating oils, the degreasing of metals, in the production of synthetic leathers, transparent paper and aluminum foil, and as a chemical intermediate and catalyst. It is an extraction solvent in the processing of foodstuffs and food ingredients. MEK can also be used to sterilize surgical and dental equipment. In addition to its manufacture, environmental sources of MEK include exhaust from jet and internal combustion engines, and industrial activities such as gasification of coal. It is found in substantial amounts in tobacco smoke. MEK is produced biologically and has been identified as a product of microbial metabolism. It has also been found in plants, insect pheromones, and animal tissues, and MEK is probably a minor product of normal mammalian metabolism. It is stable under ordinary conditions but can form peroxides on prolonged storage; these may be explosive.
Environmental Fate and Behavior MEK reacts to form a haloform that is more toxic than the original compound in water containing free halogens or hypohalites. MEK is expected to have very high mobility in soil. It does not accumulate in any environmental compartment and
Encyclopedia of Toxicology, Volume 3
Inhalation, ingestion, and dermal contact are all possible routes of exposure. MEK is a natural component in some foods. Indoor air pollution (and inhalation) can occur from volatilization of MEK from consumer and building products. Methyl ethyl ketone occurs as a metabolic byproduct of plants and animals and is released into the atmosphere by volcanoes and forest fires. Methyl ethyl ketone is emitted from pencil cedar, Zeravshan juniper, European firs, Evergreen Cyprus, blooming rape, and southern pea seeds. Methyl ethyl ketone’s production and use as a solvent for coatings, resins, rubbers, plastics, pharmaceuticals, adhesives, and rubber cements may result in its release to the environment through various waste streams. Its use as a starting material or intermediate in the manufacture of chemical products may also lead to its release to the environment.
Toxicokinetics MEK is rapidly absorbed by inhalation, skin contact, and ingestion, and transferred into the blood and other tissues. MEK is metabolized in the liver, mainly to 3-hydroxy-2-butanone and 2,3-butanediol that are eliminated in urine. Most MEK probably enters the general metabolism in the body and is converted to acetate that is eventually broken down to carbon dioxide and water that are then eliminated in exhaled air and urine. Small amounts of MEK itself are also eliminated in exhaled air and urine. MEK and its metabolites are mostly cleared from the body within 24 h, and MEK does not accumulate in the body.
Mechanism of Toxicity There is very limited information on the mechanisms of toxicity of MEK. Relatively high-inhaled concentrations of 1475–29 500 mg m 3 (500–10 000 ppm) caused pulmonary vasoconstriction and hypertension in cats and dogs. There are several human case reports of neurological effects resulting from high exposure to MEK in combination with other solvents, and animal studies have confirmed synergism between MEK and ethyl n-butyl ketone, methyl n-butyl ketone, n-hexane, carbon tetrachloride, 2,5-hexanedione, and chloroform. The main target organs involved in toxicological interactions are the nervous system and liver, and the lung has also been mentioned.
http://dx.doi.org/10.1016/B978-0-12-386454-3.00879-4
297
298
Methyl Ethyl Ketone
Acute and Short-Term Toxicity (or Exposure) Animal MEK causes central nervous system depression in animals. The oral LD50 in rats is 6.86 ml kg 1 (2737 mg kg 1) and 4050 mg kg 1 in mice. Inhalation LC50 is 23 500 mg m 3 in rats and 32 mg m 3 in mice. The intraperitoneal LD50 is 607 mg kg 1 in rats, 616 mg kg 1 in mice, and 2 g kg 1 in guinea pigs. Animal studies indicate that MEK is a mild-to-moderate skin irritant, and a moderate-to-severe eye irritant.
Human The major acute toxicity of MEK is mucosal irritation, and MEK can irritate the eyes, nose, and respiratory system. No irritation was produced when 20% MEK in petrolatum was applied to volunteers for 48 h in a closed patch test; however, it can be irritating to the skin by defatting. It can cause dizziness, fatigue, memory alteration, dermatitis, headaches, nausea, and paresthesia of extremities, diminished vision, acidosis, and vomiting. Acute inhalation can cause central nervous system depression. MEK vapor is irritating to mucous membranes and conjunctivae at 200 ppm after 15 min, but the odor is noticeable at 25 ppm. The results from animal evidence suggest that MEK can be aspirated during ingestion or vomiting, and could result in severe lung damage (edema), respiratory failure, cardiac arrest, and death.
Chronic Toxicity (or Exposure) Animal Exposure to 5000 ppm for 13 weeks produced an exposurerelated effect on body and liver weights in rats, as well as a depression in brain weight in females. Guinea pigs and rats were exposed to 235 ppm for 12 weeks (5 days week 1, 7 h day 1). There were no deaths and no signs of toxicity. Extensive neurological studies with high exposures have shown no effects. In one study, rats were initially exposed to 10 000 ppm that was reduced to 6000 ppm due to severe irritation of the upper respiratory tract. Temporary signs of muscle incoordination and gait disturbances were observed. Exposures continued for only 7 of the planned 15 weeks because some animals died of bronchopneumonia; there were no neurological symptoms. In the other study, rats were exposed to 1125 ppm continuously for up to 55 days with no signs of neurotoxicity.
Human A mortality study of hundreds of workers who had worked at MEK dewaxing plants concluded that there was no evidence of a cancer hazard. The average follow-up was 14 years. This study is limited by the small size of the cohort and the relatively short follow-up period.
Immunotoxicity There is no evidence indicating that MEK is immunotoxic.
Reproductive Toxicity Pregnant rats were exposed by inhalation to up to 3000 ppm on days 6–15 of gestation; at 3000 ppm, there was a low but statistically significant increase in malformations. Sternebral and soft tissue anomalies were also increased. There was also a statistically significant increase in total skeletal anomalies at 1000 ppm. Maternal toxicity was not observed. In subsequent studies, pregnant rats and mice were exposed to up to 3000 ppm by inhalation during days 6–15 of gestation. There were no embryotoxic or teratogenic effects at any exposure level. There were fetotoxic effects (increased incidence of minor skeletal variations; delayed bone formation; reduced fetal weight) with very slight maternal toxicity at 3000 ppm.
Genotoxicity MEK was not mutagenic in Ames (Salmonella) and Escherichia coli tests, but induced aneuploidy in Saccharomyces cerevisiae. MEK was not found to be genotoxic in the mouse lymphoma assay, in Chinese hamster ovary cell, unscheduled DNA synthesis assay, or micronucleus assays.
Carcinogenicity The International Agency for Research on Cancer has not evaluated the carcinogenicity of MEK, the American Conference of Governmental Industrial Hygienists has not assigned a carcinogenicity designation for MEK, and the US National Toxicology Program has not listed MEK in its report on carcinogens. MEK is classified as a Group D chemical by the US Environmental Protection Agency, that is, it is not classifiable as to human carcinogenicity.
Clinical Management Remove from exposure in all cases. In case of dermal exposure, immediately wash all affected areas thoroughly. In the event of ingestion, vomiting should not be induced due to the risk of aspiration, if a large amount has been ingested, arterial blood gases should be monitored. In ocular exposure, irrigate the patient’s eye with 0.9% saline for 10–15 min. In all cases, administer additional symptomatic treatment.
Ecotoxicology The LC50 for MEK in bluegill ranges from 5640 to 1690 mg l 1. The LC50 values for Daphnia magna range from 1382 to 8890 mg l 1. MEK is produced by fungi in concentrations that affect the germination of some plants. The effect of MEK on the alarm behavior of social insects has been studied. It was considered inactive in producing alarm behavior in the ant Iridomyrmex preinosus.
Methyl Ethyl Ketone
Exposure Standards and Guidelines The (US) Occupational Safety and Health Administration permissible exposure limit, 8-h time-weighted average (TWA) is 200 ppm, and the (US) National Institute for Occupational Safety and Health (NIOSH) recommended exposure level, averaged over a 10-h work day is 200 ppm. The NIOSH shortterm exposure limit, for a 15-min exposure, is 300 ppm.
FIFRA Requirements Residues of MEK are exempted from the requirement of a tolerance when used as a surfactant in accordance with good agricultural practice as inert (or occasionally active) ingredients in pesticide formulations applied to growing crops only.
Acceptable Daily Intakes An Acceptable Daily Intake (ADI), defined as the amount of a chemical to which humans can be exposed on a daily basis over an extended period of time (usually a lifetime) without suffering a deleterious effect, for MEK is 3.2 mg day 1 for oral exposure.
299
of this waste. Generators of small quantities of this waste may qualify for partial exclusion from hazardous waste regulations.
Atmospheric Standards This action promulgates standards of performance for equipment leaks of Volatile Organic Compounds (VOC) in the Synthetic Organic Chemical Manufacturing Industry (SOCMI). The intended effect of these standards is to require all newly constructed, modified, and reconstructed SOCMI process units to use the best demonstrated system of continuous emission reduction for equipment leaks of VOC, considering costs, nonair quality health, and environmental impact and energy requirements. Methyl ethyl ketone is produced, as an intermediate or final product, by process units covered under this subpart. It is listed as a hazardous air pollutant (HAP) generally known or suspected to cause serious health problems. The Clean Air Act, as amended in 1990, directs the EPA to set standards requiring major sources to sharply reduce routine emissions of toxic pollutants. The EPA is required to establish and phase in specific performance-based standards for all air emission sources that emit one or more of the listed pollutants. Methyl ethyl ketone is included on this list.
TSCA Requirements 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. Methyl ethyl ketone is included on this list.
CERCLA Reportable Quantities Persons in charge of vessels or facilities are required to notify the National Response Center (NRC) immediately when there is a release of this designated hazardous substance in an amount equal to or greater than its reportable quantity of 5000 lb or 2270 kg.
Federal Drinking Water Guidelines EPA 4000 mg l 1.
See also: Neurotoxicity.
Further Reading Noraberg, J., Arlien-Soborg, P., 2000. Neurotoxic interactions of industrially used ketones. Neurotoxicology 21, 409–418. Yang, R.S., 1986. The toxicology of methyl ethyl ketone. Residue Rev. 97, 121–143.
Relevant Websites RCRA Requirements U159: As stipulated in 40 CFR 261.33, when 2-butanone, as a commercial chemical product or manufacturing chemical intermediate or an off-specification commercial chemical product or a manufacturing chemical intermediate, becomes a waste, it must be managed according to Federal and/or State hazardous waste regulations. Also defined as a hazardous waste is any residue, contaminated soil, water, or other debris resulting from the cleanup of a spill, into water or on dry land,
http://ecb.jrc.it/esis/esis.php – European Chemicals Bureau; IUCLID Dataset, Methyl ethyl ketone (CAS # 78-93-3). Compilation of information provided to the EU by the European chemicals industry as of 2000. http://www.intox.org – International Programme on Chemical Safety. Methyl Ethyl Ketone. http://www.inchem.org – International Programme on Chemical Safety (IPCS). Methyl Ethyl Ketone (Environmental Health Criteria 143). http://www.hpa.org.uk/webc/HPAwebfile/ – HPAweb_C/1279889215207 – Methyl Ethyl Ketone Incidence Management, Health Protection Agency, 2010. http://www.epa.gov/iris/subst/index.html – U.S. Environmental Protection Agency's Integrated Risk Information System (IRIS) on Methyl ethyl ketone (MEK) (78-93-3).