Methyl ethyl ketone exposure

Ten Berg K, Hoogeboom AJ, Wesby-van Swaaij E, et al Maternal occupational methyl ethyl ketone exposure and multiple congenital anomalies. Teratology 65(6) 326, 2002... 

Membranes and Osmosis. Membranes based on PEI can be used for the dehydration of organic solvents such as 2-propanol, methyl ethyl ketone, and toluene (451), and for concentrating seawater (452—454). On exposure to ultrasound waves, aqueous PEI salt solutions and brominated poly(2,6-dimethylphenylene oxide) form stable emulsions from which it is possible to cast membranes in which submicrometer capsules of the salt solution ate embedded (455). The rate of release of the salt solution can be altered by surface—active substances. In membranes, PEI can act as a proton source in the generation of a photocurrent (456). The formation of a PEI coating on ion-exchange membranes modifies the transport properties and results in permanent selectivity of the membrane (457). The electrochemical testing of salts (458) is another possible appHcation of PEI. 

Table 3 shows the toxicological properties of selected ketones. A detailed review of the physiological effects of exposure to methyl ethyl ketone and methyl isobutyl ketone has been documented (6). 

Methyl Isopropenyl Ketone. Methyl isopropenyl ketone [814-78-8] (3-methyl-3-buten-2-one) is a colorless, lachrymatory Hquid, which like methyl vinyl ketone readily polymerizes on exposure to heat and light. Methyl isopropenyl ketone is produced by the condensation of methyl ethyl ketone and formaldehyde over an acid cation-exchange resin at 130°C and 1.5 MPa (218 psi) (274). Other methods are possible (275—280). Methyl isopropenyl ketone can be used as a comonomer which promotes photochemical degradation in polymeric materials. It is commercially available in North America (281). 

Solvents acetone, methyl ethyl ketone (MEK), toluene, xylene, glycol, ethers, alcohol defats and dries skin some may be absorbed may carry other components through skin high volatility, exposure possible irritation central nervous system depression (e.g. dizziness, loss of coordination) low to high toxicity, longterm effects... 

Toxicity. Breathing moderate amounts of methyl ethyl ketone (MEK) for short periods of time can cause adverse effects on the nervous system ranging from headaches, dizziness, nausea, and numbness in the fingers and toes to unconsciousness. Its vapors are irritating to the skin, eyes, nose, and throat and can damage the eyes. Repeated exposure to moderate to high amounts may cause liver and kidney effects. 

Exposure to other chemicals can influence the metabolism of -hexane. The effect of oral pretreatment with methyl ethyl ketone (MEK) on the metabolism of inhaled -hexane was investigated in male Fischer 344 rats (Robertson et al. 1989). Groups of 2-4 rats were given MEK (1.87 mL/kg, approximately 1,500 mg/kg) by gavage for 4 days prior to a single 6-hour inhalation exposure to w-hexane (1,000 ppm). Animals were sacrificed at 0, 1, 2, 4, 6, 8, and 18 hours after exposure ended, and samples of blood, liver, testis, and sciatic nerve were obtained and analyzed for -hexane, MEK, and their metabolites. Significant increases in the levels of the neurotoxic metabolite 2,5-hexanedione and 2,5-dimethylfuran (derived from 2,5-hexanedione) were found in blood and sciatic nerve of rats pretreated with MEK. Levels of 2,5-hexanedione in blood were approximately 10-fold higher than control immediately after -hexane exposure in rats and fell rapidly to approximately 2-fold after 6 hours. In sciatic nerve, increases in 2,5-hexanedione were approximately 6-fold at 2 hours and 3-fold at 4 hours. Similar patterns were found with 2,5-dimethylfuran. 2,5-Hexanedione was not detected in the testis of non-pretreated rats levels were measurable but very low in pretreated rats (0.3-0.6 g/g compared to... 

The potentiation of -hexanc neurotoxicity by co-exposure to methyl ethyl ketone may be duration-dependent, as suggested by an experiment in volunteers (Van Engelen et al. 1997). Simultaneous exposure to 60 ppm n-hexane and either 200 or 300 ppm methyl ethyl ketone for 15.5 minutes had no effect on exhaled n-hexane concentrations, and actually lowered 2,5-hexanedione serum concentrations... 

Photoacid generator. D1 (4 wt%) was mixed with poly(glycidyl methacrylate) (PGMA) (20 wt%) in ethyl cellosolve acetate. The mixture was spin-coated on a silicon wafer and baked at 80V for 1 minute. Exposure was performed with a 600-W Xe-Hg lamp in conjunction with a UVD2 filter. The resist was developed in a mixture of methyl ethyl ketone to ethanol (7/1 w/w). 

Dick RB, Setzer JV, Taylor BT, et al Neurobehavioral effects of short duration exposures to acetone and methyl ethyl ketone. BrJ Ind Med 46 111-121, 1989... 

Solvents used as nonreactive diluents include acetone, cellosolve, methyl ethyl ketone, methyl isobutyl ketone, methylene chloride, 1,1,1-trichloroethane, toluene, and xylene. Skin and eye irritation and, in higher concentrations, CNS depression and respiratory irritation may result ftom exposure to these solvents as diluents for epoxy resin... 

The neurotoxic properties of -hexane are potentiated by exposure to methyl ethyl ketone (qv). Because other compounds may also have this effect, human exposure to mixed solvents containing any neurotoxic hexacarbon compound should be minimized. ... 

Hexanedione was found to be a major metabolite of MBK in several animal species peripheral neuropathy occurred in rats after daily subcutaneous injection of 2,5-hexanedione at a dose of 340mg/kg 5 days/ week for 19 weeks.Nonneurotoxic aliphatic monoketones, such as methyl ethyl ketone, enhance the neurotoxicity of MBK. In one rat study, the longer the carbon chain length of the nonneurotoxic monoketone, the greater the potentiating effect on MBK. It is expected that exposure to a subneurotoxic dose of MBK, plus high doses of some aliphatic monoketones, would also produce neurotoxicity. In addition, MBK itself potentiates the toxicity of other chemicals. ... 

In humans, short-term exposure to 300 ppm was objectionable, causing headache and throat irritation 2 00 ppm caused mild irritation of eyes 100 ppm caused slight nose and throat irritation. No significant neurobehav-ioral effects (as determined by a series of psychomotor tests) were found in volunteers from 4-hour exposures to methyl ethyl ketone at 200 ppm significant odor and irritant effects were reported. ... 

Dick RB, Krieg EF Jr, Setzer J, et al Neurobehavioral effects from acute exposures to methyl isobutyl ketone and methyl ethyl ketone. Fundam Appl Toxicol 19 453M-73, 1992... 

Mitran E, Callender T, Orha B, et al Neurotoxicity associated with occupational exposure to acetone, methyl ethyl ketone, and cyclohexanone. Environ Res 73(l/2) 181-8, 1997... 

Ong CN, Sia GL, Ong HY, et al Biological monitoring of occupational exposure to methyl ethyl ketone. Int Arch Occup Environ Health 63 319-324, 1991... 

Numerous studies have been conducted in which animals were exposed to 2-hexanone via inhalation. However, the purpose of many of these studies was to assess the potential effects of combined exposure to 2-hexanone and another substance (usually chloroform or methyl ethyl ketone [MEK]). Study design has consequently involved exposure to only one concentration of 2-hexanone as a control exposure. A single high dose of 2-hexanone was used in several other studies in order to elicit and study histopathological changes in the affected nervous tissue. In addition, the grade or purity of the 2-hexanone administered was not stated in many studies, or in some cases, hexanone with purity as low as 70% was used. As a result of these various complications, the usefulness of the available data is limited. 

Interaction of 2-hexanone with EPN (Abou-Donia 1985a) and methyl ethyl ketone (Saida et al. 1976) may occur through the potentiation of the production of 2,5-hexanedione. An effective method of reducing the neurotoxic effects of combined exposures to these compounds would be to pharmacologically block the metabolic pathways that lead to the production of 2,5-hexanedione, given the same caveats presented for interference with metabolic pathways presented above. Increasing the breakdown or clearance of 2,5-hexanedione might also be effective. 

Chromosomal aberrations in peripheral lymphocytes were also reported in a study of about 40 workers who had been occupationally exposed to trace quantities of 2-butanone (methyl ethyl ketone), butyl acetate, toluene, cyclohexanone and xylene in addition to dimethylfonnamide. Blood samples were taken at two Ibur-nionth intervals, when exposure was to an average of 180 and 150 mg/nr dimethylformamide, respectively. The frequencies of chromosomal aberrations were 3.82% and 2.74% at these two sampling times. Subsequent sampling at tliree six-month intervals, when average dimethylformamide exposures were to 50, 40 and 35 mg/m- , gave lower aberration frequencies of 1.59%, 1.58% and 1.49%. Aberration frequencies in two control groups were 1.61% and 1.10% (Koudela Spazier, 1981). 

Carpenter et al. (1988) carried out a nested case-control study of cancer of the central nervous system among workers at two nuclear facilities located in Tennessee (United States). They identified 89 cases (72 males and 17 females) who had died between 1943 and 1979. Four controls, living at the time the case was diagnosed, were matched to each case. Job history records were scrutinized by an industrial hygienist to assess potential exposure to each of 26 chemicals or chemical groups. Toluene, xylene (see this volume) and 2-butanone (methyl ethyl ketone) were evaluated as one chemical group the matched relative risk was 2.0 (95% confidence interval (Cl), 0.7-5.5 n = 28) in comparison with unexposed workers. Almost all cases had had low exposure, according to the classification used and there was no dose-response trend. The authors stated that the relative risks w ere adjusted for internal and external exposure to radiation. 

Walker et al. (1993) conducted a cohort mortality study among 7814 shoe-manufacturing workers (2529 males and 5285 females) from two plants in Ohio (United States) that have been in operation since the 1930s. The workers, men and women, were potentially exposed to solvents and solvent-based adhesives. It was thought that toluene may have been a predominant exposure, but a hygiene survey in 1977-79 showed that, in addition to toluene (10 measurements ranged from 10 ppm to 72 ppm [38-270 mg/m3]), there were also 2-butanone (methyl ethyl ketone), acetone, hexane and... 

Fig. 97. Solvent retained by nitrocellulose films (50/i thickness) after exposure to air at 25°C (Baelz [48]). I—Cyclohexenyl acetate, II—methyl cyclohexanone, III—diacetone alcohol, IV—cyclohexanone, V—cellosolve acetate, VI—amyl acetate-ethyl alcohol I 1, VII—amyl acetate, VIII— methyl cellosolve acetate, IX—amyl acetate-toluene 1 1, X—butyl acetate-ethyl alcohol 1 1, XI—butyl acetate, XII—cellosolve, XIII—methyl-ethyl ketone, XIV—cellosolve-toluene 1 1, XV—methyl cellosolve, XVI—ethyl acetate, XVII—acetone.

Exposure to the hydrophobic organic solvent Using more hydrophilic solvents such as ethyl acetate and methyl ethyl ketone. 

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