Methyl Ethyl Ketone Concentration Research Articles

Biological monitoring of occupational exposure to methyl ethyl ketone in Japanese workers

The relationship between occupational exposure to methyl ethyl ketone (MEK) and its concentration in urine and blood was studied in a group of 72 workers in a printing factory. Personal exposure monitoring was carried out with passive samplers during the workshifts. The time weighted average (TWA) concentration of MEK ranged from 1.3 to 223.7 ppm, with a mean concentration of 47.6 ppm. In addition to MEK, toluene, xylene, isopropyl alcohol, and ethyl acetate were detected as the main contaminants in all samples. At the end of the workshift, urine samples were collected to determine the urinary MEK, hippuric acid (HA), and creatinine, and blood samples were also collected at the same time for determination of MEK. The concentrations of urinary MEK ranged from 0.20 to 8.08 mg/L with a mean of 1.19 mg/L and significantly correlated with TWA concentrations of MEK in the air with a correlation coefficient of 0.889 for uncorrected urine samples. The concentration of MEK in the blood was also significantly correlated with the TWA concentration of MEK with a correlation coefficient of 0.820. From these relationships, MEK concentrations in urine and blood corresponding to the threshold limit value-TWA (200 ppm; ACGIH 1992) were calculated to be 5.1 mg/L and 3.8 mg/L as a biological exposure index (BEI), respectively. Although the BEI for urinary MEK obtained from the present study was higher than that of previous reports and ACGIH's recommendation (2.0 mg/L), the BEI agreed well with a previous study in Japan.(ABSTRACT TRUNCATED AT 250 WORDS)

Biological exposure indices of organic solvents for Korean workers.

Biological exposure indices (BEIs) of toluene, perchloroethylene (PCE) and methyl ethyl ketone (MEK) for Korean workers were studied respectively. Exposure in workplace to organic solvents were measured by personal sampling. Blood toluene, blood PCE, urinary trichloroacetic acid and urinary MEK were determined by headspace GC. Urinary hippuric acid was determined by HPLC and corrected for creatinine. BEIs for Korean workers were calculated with the levels of the determinants corresponding to permissible exposure limits in Korea which were the same with TLV of ACGIH. Blood toluene level of 2.2 mg/l and urinary hippuric acid level of 1.7 g/g creatinine corresponded to exposure of 100 ppm toluene. Blood PCE concentration of 1.6 mg/l and urinary trichloroacetic acid concentration of 2.9 mg/l corresponded to exposure to 50 ppm PCE. Urinary MEK concentration of 1.4 mg/l corresponded to exposure to 200 ppm of MEK. In conclusion, BEIs for Korean workers determined in this study were different to ACGIH's BEI as urinary determinants were lower and blood determinants were higher than ACGIH's BEI.

Sensory Irritation Effects of Methyl Ethyl Ketone and its Receptor Activation Mechanism

The burning and painful effect in nose and eyes, termed sensory irritation, of methyl ethyl ketone vapours was investigated in a mouse bioassay. Sensory irritation is mediated via the trigeminal nerves and results in a reflexively induced decrease in respiratory rate in mice. Methyl ethyl ketone was used as a model substance for ketones. At the lower exposure concentrations a partial fading (desensitization) of the response was seen. Little desensitization was seen at higher concentrations. n-Propanol, a model substance for alcohols, desensitized the receptor at all exposure levels. Preexposure to propanol did not influence the response at high methylethyl ketone concentrations. This suggests that the two substances bind to different receptive sites with different properties, if the ketone response is due to a high exposure concentration. A decrease in tidal volume was also mediated from the upper respiratory tract. The tidal volume effect is mediated by nerves different from those mediating the frequency response, as the time-response relationship, the desensitization pattern, the maximum response and the apparent dissociation constants were different for the two types of effect. Neither the location nor the perceived response related to the volume response is known.

Biological monitoring of occupational exposure to methyl ethyl ketone

This study was conducted to evaluate the usefulness of three commonly used methods of biological monitoring for worker exposed to methyl ethyl ketone (MEK) under field conditions using blood, breath and urine. Environmental MEK exposures were measured by personal sampling with carbon-felt dosimeters. The correlation coefficient (r) between the time-weighted average (TWA) MEK concentration in air and the MEK concentration in blood collected at the end of the work shift was 0.85. The correlation coefficient between the TWA MEK level in air and the concentration exhaled in the breath of workers at the end of the work shift was 0.71. The end-of-shift urinary MEK excretion correlated best with the environmental concentration (r = 0.89). Correlations became lower after urine samples had been corrected for urinary creatinine (r = 0.83) or specific gravity (r = 0.73). After 8 h exposure to 200 ppm MEK, the corresponding end-of-shift urinary excretion was 5.1 mumol/l or 4.11 mg/g creatinine. This value is higher than that previously found in some studies, the difference probably being due to the physical activities of the present workers and their extensive skin contact with the solvent. The kinetics of inhaled MEK was also studied in eight subjects. Breath and urine samples were collected during the 8-h work shift on 2 consecutive Mondays. The results showed that urinary MEK excretion rose steadily until the end of exposure, whereas the MEK concentration in exhaled air varied markedly throughout the day.(ABSTRACT TRUNCATED AT 250 WORDS)

Developmental toxicity of inhaled methyl ethyl ketone in Swiss mice

Methyl ethyl ketone (MEK) is a widely used industrial solvent to which there is considerable human exposure. To assess the potential for MEK to cause developmental toxicity in rodents, groups of Swiss (CD-1) mice were exposed to 0, 400, 1000, or 3000 ppm MEK vapors 7 hr/day on Days 6–15 of gestation. Groups consisted of about 30 bred females each. Exposure of pregnant mice to these concentrations of MEK did not result in overt maternal toxicity although there was a slight, treatment-related increase in relative liver weight which was statistically significant in the 3000 ppm group. Mild developmental toxicity was observed in the 3000 ppm group in the form of a reduction in mean fetal body weight. This reduction was statistically significant for the males only, although the relative decrease from the control values was the same for both sexes. There was no increase in the incidence of resorptions or the number of litters with resorptions among mice exposed to MEK. There was no significant increase in the incidence of any single malformation, but several malformations which were not observed in the concurrent control group or the controls of contemporary studies were present at a low incidence—cleft palate, fused ribs, missing vertebrae, and syndactyly. There was also a significant trend for increased incidence of misaligned sternebrae, a developmental variation. In summary, pregnant Swiss (CD-1) mice were relatively insensitive to the toxic effects of MEK at the inhaled concentrations used in this study. However, the offspring of the mice exhibited significant signs of developmental toxicity at the 3000 ppm exposure level. Neither maternal nor developmental toxicity was observed at 1000 ppm MEK or below.

Developmental Toxicity of Inhaled Methyl Ethyl Ketone in Swiss Mice

Developmental Toxicity of Inhaled Methyl Ethyl Ketone in Swiss Mice. Schwetz, B. A., Mast, T. J., Weigel, R. J., Dill, J. A., and Morrissey, R. E. (1991). Fundam. Appl. Toxicol. 16, 742–748. Methyl ethyl ketone (MEK) is a widely used industrial solvent to which there is considerable human exposure. To assess the potential for MEK to cause developmental toxicity in rodents, groups of Swiss (CD-1) mice were exposed to 0, 400, 1000, or 3000 ppm MEK vapors 7 hr/day on Days 6–15 of gestation. Groups consisted of about 30 bred females each. Exposure of pregnant mice to these concentrations of MEK did not result in overt maternal toxicity although there was a slight, treatment-related increase in relative liver weight which was statistically significant in the 3000 ppm group. Mild developmental toxicity was observed in the 3000 ppm group in the form of a reduction in mean fetal body weight. This reduction was statistically significant for the males only, although the relative decrease from the control values was the same for both sexes. There was no increase in the incidence of resorptions or the number of litters with resorptions among mice exposed to MEK. There was no significant increase in the incidence of any single malformation, but several malformations which were not observed in the concurrent control group or the controls of contemporary studies were present at a low incidence—cleft palate, fused ribs, missing vertebrae, and syndactyly. There was also a significant trend for increased incidence of misaligned sternebrae, a developmental variation. In summary, pregnant Swiss (CD-1) mice were relatively insensitive to the toxic effects of MEK at the inhaled concentrations used in this study. However, the offspring of the mice exhibited significant signs of developmental toxicity at the 3000 ppm exposure level. Neither maternal nor developmental toxicity was observed at 1000 ppm MEK or below.

Effects of ethanol on the kinetics of methyl ethyl ketone in man.

The kinetics of inhaled methyl ethyl ketone (MEK) at a concentration of 200 ppm for four hours were studied in volunteers after swallowing ethanol at a dose of 0.8 g/kg. Ethanol was given either before or at the end of the exposure to MEK. The blood concentrations of MEK, 2-butanol, and 2,3-butanediol were monitored during and after the exposure. MEK concentrations in exhaled air and MEK and 2,3-butanediol concentrations in urine were also measured. Ethanol inhibited the primary oxidative metabolism of MEK and caused an increase in the blood concentrations of MEK and 2-butanol after ingestion. Ethanol ingestion, through higher blood MEK concentrations, also increased the elimination of MEK in the urine and exhaled air. Ethanol taken before exposure to MEK reduced the serum concentration of 2,3-butanediol initially but there was an increase about eight hours after the exposure. Urinary excretion of 2,3-butanediol followed the same pattern. Prior ingestion of ethanol thus seemed to interfere with the metabolism of 2,3-butanediol during and after exposure to MEK.

Changes in urinaryn-hexane metabolites by co-exposure to various concentrations of methyl ethyl ketone and fixedn-hexane levels

To make clear how the n-hexane metabolism is modified by co-exposure with MEK, rats were exposed to various concentrations of MEK mixed with a fixed concentration of n-hexane. Twenty-four male Wistar rats were divided into four equal groups. Each group was exposed for 8 h to 2000 ppm n-hexane, 2000 ppm n-hexane plus 200 ppm MEK, 2000 ppm n-hexane plus 630 ppm MEK and 2000 ppm n-hexane plus 2000 ppm MEK, respectively. Free metabolites and the sum of free and conjugated metabolites of n-hexane were analyzed by gas chromatography. The main metabolite was 2-hexanol during the exposure and 2,5-hexanedione (2,5-HD) after the exposure in any group. The main metabolites, 2-hexanol and 2,5 HD, decreased in inverse proportion to the co-exposed MEK concentrations. The results suggest that augmentation of n-hexane neurotoxicity by MEK co-exposure could not be explained only by 2,5-HD. In addition, 2,5-HD is recommended as an index for biological monitoring of n-hexane exposure. However, one should be careful to evaluate the exposed n-hexane concentration by urinary 2,5-HD, because n-hexane metabolism could be largely modified by co-exposure with MEK.

Dose-dependent kinetics of inhaled methylethylketone in man

Physiologically based stimulation of earlier human inhalation exposure to methylethylketone (MEK) at a concentration of 200 ppm for 4 h suggested that the kinetics were dose-dependent. Two male volunteers were therefore exposed to MEK for 4 h at 3 exposure concentrations: 25, 200 and 400 ppm. Blood MEK concentrations were monitored during and after exposure. The results showed clearly that the kinetics of MEK were dose-dependent at higher exposure concentrations. Simulated exposure to MEK for 8 h suggests that saturation kinetics are reached at an exposure concentration of 50–100 ppm, depending on the physical work load.

Coexposure of man to m-xylene and methyl ethyl ketone. Kinetics and metabolism.

In a study of the kinetics and metabolic interaction of xylene and methyl ethyl ketone (MEK) eight male volunteers were exposed to m-xylene (100 ppm) and MEK (200 ppm). The exposures to the two compounds were carried out both separately and in combination. Respiratory uptake and blood concentration, as well as urinary metabolites (methyl hippuric acid and 2,3-butanediol), were monitored. Coexposure to xylene and MEK resulted in inhibited xylene metabolism. The xylene concentration in blood increased significantly, and the urinary excretion of methyl hippuric acid decreased. The combined exposure did not cause any change in the concentration of MEK in the blood or the excretion of 2,3-butanediol in the urine. Exposure to MEK 20 h before the m-xylene exposure had no detectable effect on the kinetics of m-xylene.

Determination of methyl ethyl ketone and its metabolites in urine using capillary gas chromatography

A method is described for the determination of the concentration of methyl ethyl ketone and its metabolites: 2-butanol, 3-hydroxy-2-butanone and the meso- and d,l-isomers of 2,3-butanediol in urine. The analytes were isolated from urine by solid-phase extraction and analysed by capillary gas chromatography. The recovery rates were 50–70% for the 2,3-butanediol isomers and 88–96% for the other analytes. The precision of the method ranged from 5 to 12% (S.D.%). The detection limit was 1.0 and 1.4 mg/l for meso- and d,l-2,3-butanediol, respectively, and ranged from 0.1 to 0.15 mg/l for the other analytes.

Kinetics of methyl ethyl ketone in man: absorption, distribution and elimination in inhalation exposure.

The kinetics of inhaled methyl ethyl ketone (MEK) in human volunteers was studied in an exposure chamber. Relative pulmonary uptake was about 53% throughout a 4-h exposure period at 200 ppm. Blood MEK concentration rose steadily until the end of exposure. Repeated bicycle exercise increased the overall blood MEK level markedly in comparison to sedentary activity, with transient peaks in association with cycling; thus blood MEK concentration depended both on the rate of uptake and the amount taken up. Only 3% of the absorbed dose was excreted unchanged by exhalation. A well-known metabolite of MEK, 2,3-butanediol, was detected in the urine with maximum rates of excretion at about 6 to 12 h from the beginning of exposure. About 2% of the MEK dose taken up by the lungs was excreted in the urine as 2,3-butanediol. The main part of inhaled MEK is supposedly metabolized in the intermediary metabolism. Elimination of MEK in blood appeared to exhibit two phases: the initial alpha-phase (T1/2 = 30 min; kel alpha = 0.023) over the first post-exposure hour, followed by the terminal beta-phase (T1/2 = 81 min; kel beta = 0.009).

Oxidation of methyl ethyl ketone to diacetyl on V 2O 5-P 2O 5 catalysts

A V 2O 5-P 2O 5 catalyst with a P V atomic ratio of 1.6 prepared by using oxalic acid as a reducing agent was found to be effective for the synthesis of diacetyl in the vapor-phase air-oxidation of methyl ethyl ketone (MEK). The selectivity to diacetyl was about 40 mol% at MEK conversions of up to 70%, and it decreased slightly with a further increase in the conversion. The selectivity for the oxidative CC fission to form acetic acid and acetaldehyde varied from 58 to 56 mol% with an increase in the conversion. The rate was nearly proportional both to the oxygen concentration up to 20 vol% and to the MEK concentration up to 10 vol%, even at the low temperature of 140 °C. The apparent activation energy was 7.6 kcal/mol. The addition of water vapor favors the oxidative fission against the diacetyl formation. The effects of reaction variables on the selectivity was also studied. A peroxide-like reaction mechanism was proposed.

Methyl ethyl ketone exposure in industrial workers. Uptake and kinetics.

Exposure to methyl ethyl ketone (MEK) was studied in workers occupationally exposed in industrial workplaces. Alveolar concentrations of MEK were compared with environmental exposure and with blood MEK concentrations. Urinary excretion of MEK and its metabolite, acetylmethylcarbinol , were compared with environmental exposure. The solubility of MEK was also studied in human body tissues which allowed us to estimate the distribution and kinetics of MEK by means of data computing on a multicompartimental mathematic model. The alveolar MEK concentration was correlated with the environmental MEK concentration and corresponded to 30% of it. Blood MEK concentration was correlated with alveolar MEK concentration and corresponded to 104-116 times the alveolar concentration and 31-35 times the environmental concentration. Urinary MEK excretion was correlated with environmental MEK exposure and the urinary excretion of acetylmethylcarbinol . The mean urinary MEK concentration was 4.8 times the mean environmental MEK concentration. The MEK solubility in the human tissues (brain, kidney, lung, fat, heart, muscles and liver) turned out to be similar to that found in blood (blood/air = 183). The amount of MEK and its metabolite, acetylmethylcarbinol , eliminated by the kidney corresponded together to 0.1% of the alveolar MEK uptake.

An evaluation of a water purification system for use in animal facilities.

A commercially available water purification system was evaluated for its ability to minimize chemical and microbial contaminants. The reduction or removal of these impurities from the drinking water of experimental animals would reduce experimental variability. 3 strains of bacteria were collected from the processed water. An increase in the total number of bacteria was observed the longer the filters remained in use. Determinations of heavy metals in water samples before and after processing were made for lead, zinc, copper, nickel, manganese, iron, arsenic and mercury. Calcium and magnesium levels were also determined. The concentrations of these inorganic chemicals were reduced by the purification process except at 2 time points in which desorption of the chemical could have occurred. Bacterial colonization and desorption of these chemicals were controlled by installing new filter cartridges. Volatile halocarbon concentrations were determined for water samples before and after purification. All volatile halocarbons analyzed were less than 10 ppb before and after purification at all time points. Other organic chemicals were greatly reduced by the purification process. In a study of contaminants associated with installation of the unit, it was found that flushing the unit for 8 days reduced lead and methyl ethyl ketone concentrations to insignificant levels. The purification system was found to be effective in providing high quality drinking water as verified by a microbial and chemical testing program.

Investigation of Some Factors Influencing Percutaneous Absorption III: Absorption of Methyl Ethyl Ketone

The percutaneous absorption of methyl ethyl ketone (MEK) was followed for a period of 8hr. under normal, dehydrated, and hydrated skin conditions. Data are presented showing a delay in absorption when the skin is pretreated with a strong desiccant; however, the final steady-state concentration of MEK in expired air was of the same magnitude as that obtained under normal skin conditions. Hydration, as noted previously, continued to enhance absorption. Apparent first-order expired air elimination rates following percutaneous absorption were determined and compared to those obtained after oral ingestion of MEK.

Factors Influencing Percutaneous Absorption II: Absorption of Methyl Ethyl Ketone

A method is described for following the percutaneous absorption process with a vapor-phase chromatography technique. Data showing the absorption of methyl ethyl ketone (MEK) from a forearm surface of 91.5cm.² under both normal and hydrous conditions of the stratum corneum are presented. Hydration of the stratum corneum enhanced the percutaneous absorption rate of methyl ethyl ketone, but this penetrant subsequently partially dehydrated the stratum corneum. The resulting steady-state concentration of MEK in expired air, however, was still higher than that obtained with normal skin.

Heat transfer to boiling water-methylethylketone mixtures

An apparatus has been designed for determination of heat transfer to boiling mixtures of water-methylethylketone under atmospheric pressure, using the central portion of a horizontal platinum heating wire at the same time as a resistance thermometer, according to the method of M cA dams [5]. A hysteresis effect observed in mixtures containing an excess of methylethylketone was avoided by keeping the annealed wire immersed in the liquid for a sufficiently long time at room temperature. The reference value of the resistance thermometer was aso measured with immersed wire at the boiling temperature of the liquid. The entire region of heat transfer up to the maximum of nucleate boiling was measured for some mixtures including the pure components (0, 4·2, 20, 52, 88·5, and 100% wt of methylethylketone). With increasing concentration of methylethylketone a gradual shift of the curves to lower heat transfer occurred, except for the 4·2% and 20% mixtures, where a noticeably high maximum heat flux of 2·5 and 2·0 times that of water was found. Since it was also observed with heating wires of different metals and alloys, this peculiar behaviour can be considered to be a characteristic property of the liquid mixtures themselves.

THE HYDROLYSIS OF ACETIC ANHYDRIDE IN WATER AND IN THE SYSTEM WATER: METHYL ETHYL KETONE

The rate of hydrolysis of acetic anhydride at 25 °C. in water (I), in solutions of methyl ethyl ketone (MEK) in water (II), and in solutions of water in MEK (III) have been studied. In I the observation of previous investigators that the velocity constant varies linearly with the initial concentration of acetic anhydride, but for any given initial concentration of acetic anhydride the reaction is pseudomonomolecular, was confirmed and extended. In II the velocity constant is lower than in I and decreases linearly with increasing concentration of MEK, but, again, the reaction is pseudomonomolecular for any given initial concentration of acetic anhydride. An equation and a nomogram that relate the velocity constant to the initial concentration of acetic anhydride, MEK, and water are presented. In III the second-order rate equation must be modified to compensate for the presumed catalytic effect of the hydrogen ion produced by hydrolysis.