820K87113
March 31, 1987
METHYL ETHYL KETONE
Health Advisory
Office of Drinking Water
U.S. Environmental Protection Agency
I. INTRODUCTION
The Health Advisory (HA) Program, sponsored by the Office of Drinking
Water (ODW), provides information on the health effects, analytical method-
ology and treatment technology that would be useful in dealing with the
contamination of drinking water. Health Advisories describe nonregulatory
concentrations of drinking water contaminants at which adverse health effects
would not be anticipated to occur over specific exposure durations. Health
Advisories contain a margin of safety to protect sensitive members of the
population.
Health Advisories serve as informal technical guidance to assist Federal,
State and local officials responsible for protecting public health when
emergency spills or contamination situations occur. They are not to be
construed as legally enforceable Federal standards. The HAs are subject to
change as new information becomes available.
Health Advisories are developed for One-day, Ten-day, Longer-term
(approximately 7 years, or 10% of an individual's lifetime) and Lifetime
exposures based on data describing noncarcinogenic end points of toxicity.
Health Advisories do not quantitatively incorporate any potential carcinogenic
risk from such exposure. For those substances that are known or probable
human carcinogens, according to the Agency classification scheme (Group A or
B), Lifetime HAs are not recommended. The chemical concentration values for
Group A or B carcinogens are correlated with carcinogenic risk estimates by
employing a cancer potency . (unit risk) value together with assumptions for
lifetime exposure and the consumption of drinking water. The cancer unit
risk is usually derived from the linear multistage model with 95% upper
confidence limits. This provides a low-dose estimate of cancer risk to
humans that is considered unlikely to pose a carcinogenic risk in excess
of the stated values. Excess cancer risk estimates may also be calculated
using the One-hit, Weibull, Logit or Probit models. There is no current
understanding of the biological mechanisms involved in cancer to suggest that
any one of these models is able to predict risk more accurately than another.
Because each model is based on differing assumptions, the estimates that are
derived can differ by several orders of magnitude.
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II. GENERAL INFORMATION AND PROPERTIES
CAS No. 78-93-3'
Structural Formula
O
I!
CH3-CH2-C-CH3
Synonyms
2-Butanone, butan-2-one, ethyl methyl ketone, MEK.
Uses
0 As a solvent in processes involving gums, resins, cellulose acetate,
and cellulose nitrate
0 Used extensively in the synthetic rubber industry
0 In production of paraffin wax and high grade lubricating oil
0 In household products such as surface coating compounds (lacquer and
varnishes), paint remover, and glues.
Properties
Chemical Formula C^gO
Molecular Weight 72.10
Physical State liquid
Boiling Point 79.68C
Melting Point
Density
Vapor Pessure 100 mm Hg at 25°C
Water Solubility 295 mg/L at 25°C
Log Octanol/Water Partition
Coeffficient
Taste Threshold
Odor Threshold
Conversion Factor 1 ppm = 2.95 mg/m3
Occurrence
0 Methyl ethyl ketone (MEK) is a synthetic organic chemical which does
not occur naturally. Production of MEK in 1980 was approximately 600
million Ibs (U.S. ITC, 1981).
0 No information on the environmental fate of MEK has been identified.
Based upon its reported vapor pressure and solublity, MEK is expected
to slowly volatilize from soil and water. Due to MEK's relatively
high solublity in water MEK is expected to be mobile in soil.
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Methyl Ethyl Ketone March 31, 1987
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0 MEK has not been included in Federal and State surveys of drinking
water. However, a number of studies have reported that MEK does
occur in surface water systems (Scheiman et al., 1974; U.S. EPA,
1976; Coleman et al., 1976).
III. PHARMACOKINETICS
Absorption
0 Munies and Wurster (1965) studied the dermal absorption of MEK in
humans under normal, hydrated and dehydrated skin conditions. MEK
was applied at 1 00 ml to the forearm using an absorption cell; the
duration of exposure was 8 hours. MEK was detected in the expired
air at 3.6 mg/L 15 minutes after exposure. A steady-state level of
6.5 to 6.6 mg/L in the expired air was attained within 2 to 3 hours
after exposure.
0 DiVincenzo and coworkers (1974) reported that levels of 11% of admini-
stered MEK and metabolites were found in the serum 1 hour following
a single intraperitoneal dose of 450 mg/kg in guinea pigs.
Distribution
0 Dietz and Traiger (1979) determined the blood concentrations of
2-butanol, 2,3-butanediol and 3-hydroxy-2-butanone in rats after
a single oral dose of 355 mg/kg MEK. The blood concentrations of
MEK and metabolites 4 hours after dosing were as follows: MEK
(94.1 mg/100 ml), 2-butanol (3.2 mg/100 ml), 3-hydroxy-2-butanone
(2.4 mg/100 ml), and 2,3-butanediol (8.6 mg/100 ml).
Metabolism
0 No information was found in the available literature on the metabolism
of methyl ethyl ketone.
Excretion
Insufficient pharmacokinetic data for MEK are available to assess
distribution and elimination of MEK in animals.
IV. HEALTH EFFECTS
Humans
Data regarding the effects of oral exposure to MEK on humans were not
located in the available literature. However, Smith and Mayers
(1944) reported that two young women exhibited signs of severe intoxi-
cation, including convulsions and loss of consciousness, after exposure
to MEK and acetone (298 to 560 and 330 to 495 ppm, respectively).
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Animals
Short-term Exposure
0 The acute LDso and LDsg of MEK have been determined for several routes
of exposure:
Species Route LDgp Reference
rat oral 2.9 g/kg Kimura et al., 1971
rat inhalation 5.9 g/m3 Carpenter et al., 1949
(2,000 ppm/4 hr)
rabbit dermal >8 g/kg Smyth et al., 1962
0 Kimura and co-workers (1971) also have determined the oral LD5Q values
for weanling and newborn rats to be 2.5 and 0.8 g/kg, respectively.
0 Patty and co-workers (1935) studied the toxic effects of MEK inhalation
in the guinea pig. The animals were exposed to high concentrations
of vapor: 3,300 ppm (9.7 g/m3) , 10,000 ppm (29.5 g/m3) , 33,000 ppm
(97.3 g/m3) or 100,000 ppm (295 g/m3) for various durations up to
14 hours. Pathologic examination was done on animals that died during
exposure, on those immediately sacrificed after exposure and on
animals sacrificed 4 and 8 days after termination of exposure. At
levels of 10,000 ppm (29.5 g/m3), 33,000 ppm (97.3 g/m3) and 100,000
ppm (295 g/m3), MEK exposure produced irritation of the nose and
eyes, tearing, respiratory distress, incoordination and narcosis.
Exposure to MEK vapor at a concentration of 100,000 ppm (295 g/m3) to
guinea pigs for 30 minutes or more resulted in corneal opacity. This
condition improved gradually in guinea pigs that lived 4 and 8 days
following exposure; at the end of 8 days, the eyes were nearly
normal. This condition was not observed in animals exposed to lower
concentrations. The pathologic findings in animals that died during
exposure or were sacrificed immediately after exposure to MEK (at all
levels except 3,300 ppm) were congestion of the liver, kidney, lung
and brain congestion and emphysema. Congestion of the visceral
organs was not observed in the animals sacrificed 4 and 8 days after
termination of MEK exposure.
0 Studies have assessed the hepatotoxic effect of MEK after acute
exposure (DiVincenzo and Krasavage, 1974). Guinea pigs were admini-
stered a single intraperitoneal dose of MEK (750, 1,500 or 2,000
mg/kg). Twenty-four hours after exposure, blood samples of animals
were analyzed for orni thine carbamyl transf erase (OCT) activity and
liver tissues were examined for histopathological changes. Liver
effects observed were increased lipid content and elevated serum
ornithine carbamyl transferase activity, a sensitive enzymatic assay
for liver injury (Davidsohn and Wells, 1965). Elevated serum OCT
activity was observed 24 hours after administration of 2,000 mg/kg of
MEK. Lipid accumulation in cells of the animal was present at the
two higher doses (1,500 and 2,000 mgAg)«
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Long-term Exposure
0 LaBelle and Brieger (1955) compared the longer-term exposure of
composite solvent, containing 235 ppm (0.693 g/m^) MEK and seven
other solvents (total of 226 ppm) to MEK alone. In each case, 25
rats were exposed to the composite solvent vapors, MEK vapors or air
alone for 7 hours per day, 5 days per week for 12 weeks. There were
no deaths or sign of toxicity observed in the animals. There were
also no significant gross or microscopic pathological changes observed
at autopsy upon examination of control or exposed animals.
0 Cavender et al. (1983) exposed rats of both sexes to methyl ethyl
ketone at concentrations of 0, 1,250, 2,500 or 5,000 ppm, 6 hours/day,
5 days/week, for 90 days. No animals died during the study. The
90-day exposures had no adverse effect on the clinical health or
growth of male or female rats except for a depression of mean body
weight in the 5,000 ppm exposure group. However, at necropsy,
increases in liver weight were noted in the 1,250 and 2,500 ppm group
of female rats. Increases in liver weight, liver weight/body weight
ratios and liver weight/brain weight ratios were observed in both
male and female rats at the dose level of 5,000 ppm methyl ethyl
ketone. In the male rats at the dose level of 5,000 ppm, kidney
weight/body weight ratios also were elevated. Spleen and brain
weights, and brain weight/body weight ratios were elevated in the
5,000 ppm female rats. Urine volumes in the 5,000 ppm male rats were
higher than control values. Mean corpuscular hemoglobin values in
male and female rats at the dose level of 5,000 ppm were elevated.
Serum glutamic-pyruvic transaminase activity in female rats at the
dose level of 2,500 ppm of MEK was elevated while female rats at the
dose level of 5,000 ppm MEK exhibited significantly decreased SGPT
activity. In addition, alkaline phosphatase, potassium and glucose
values for female rats at the dose level of 5,000 ppm were increased
relative to controls. While some of these changes were statistically
significant, they were considered incidental findings, without
toxicological significance.
8 Inhalation exposure of rats to methyl ethyl ketone at a level of 200
ppm, 12 hours/day, 7 days/week for 24 weeks resulted in slight neuro-
logical effects visible only at 4 months of treatment (Takeuchi et al.,
1983), but exposure of rats to 1,125 ppm continuously for 5 months
did not result in neuropathy (Saida et al., 1976). In both studies,
only a single toxicological endpoint, either motor nerve conduction
velocity, mixed nerve conduction velocities, or distal motor latency
(Takeuchi et al., 1983) or paralysis (Saida et al., 1976), was
examined. It was interesting to note in the study by Saida et al.
(1976) that rats exposed to the combination of methyl ethyl ketone
and methyl n-butyl ketone developed paralysis after 25 days, and
exposure to 225 ppm methyl n-butyl ketone alone produced paralysis
after 66 days (suggesting that methyl ethyl ketone shortened the
latency period for the onset of methyl n-butyl ketone-induced neuro-
pathy.
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Reproductive Effects
0 Data reported by Schwetz and co-workers (1974) implicate MEK to be an
embryotoxic, fetotoxic and teratogenic agent in the rat. Pregnant
rats (Sprague-Dawley) were exposed to MEK vapor at a concentration of
1,126 ppm (3.3 g/m3) or 2,618 ppm (7.7 g/m3) for 7 hours/day on days
6 through 15 of gestation. The following parameters were evaluated:
maternal mortality, liver weight and behavior, number of corpora
lutea/dam, number of resorptions, number of implantations, fetal
mortality, fetal weight and size, and skeletal and visceral anomalies
among the fetuses. MEK exposure at either dose level did not appear
to affect adversely the number of implantation sites, the number of
live fetuses/litter, or the number of corpora lutea/dam. There was
evidence of fetotoxicity as indicated by a marked decrease in fetal
body weights following exposure to 1,126 ppm (3.3 g/m3). Decreased
fetal weight was not observed after exposure to 2,618 ppm (7.7 g/m3)
of MEK. Skeletal and visceral anomalies were noted after exposure to
MEK. The total incidence of skeletal anomalies (skull, vertebral,
and sternebral) was increased significantly (P<0.05) in the 1126 ppm
exposure group compared to the controls. A significant difference
(P <0.05) also was observed in the incidence of skeletal defects of
the sternum of the high-dose group and controls. The occurrence of
visceral anomalies, including dilated ureters and subcutaneous edema,
was significantly (P<0.05) increased in the offspring of rats treated
at the high level (2,618 ppm, 7.7 g/m3).
Developmental Effects
0 The results of another study of embryo- and fetotoxicity of inhaled
MEK in rats were reported by Deacon and co-workers (1981). In this
study, pregnant Sprague-Dawley rats were exposed to 0, 400 ppm
41.2 g/m3), 1,000 ppm (2.9 g/m3) or 3,000 ppm (8.8 g/m3) MEK for
7 hours/day on days 6 through 15 of gestation. Maternal toxicity, as
evidenced by decreased body weight gain and increased food consump-
tion, was observed among rats exposed to 3,000 ppm (8.8 g/m3); slight
fetotoxicity was observed among litters of rats exposed to this level
as evidenced by an increased incidence of two minor skeletal variants.
The results of this study verify the observation of an increased
incidence of skeletal variants observed in the earlier study by
Schwetz and co-workers (1974).
Mutagenicity
0 The mutagenic potential of MEK was investigated in a testing of
microbial mutagenicity of pesticides (Smirasu, 1976). In this study,
MEK was used as one of several solvents for the mutagenicity screening.
The test systems used were Escherichia coli WP2 and Salmonella typhi-
murium strains TA1535, TA1537, TA1536 and TA1538 to detect base-pair
substitutions and frameshift mutations. There was no increase in the
number of revertants observed in any of the test systems following
exposure to MEK. However, it should be noted that MEK was tested as
a solvent control at a single concentration.
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Methyl Ethyl Ketone
Carcinogenicity
March 31, 1987
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No information was found in the available literature on the carcino-
genic effects of MEK exposure to humans or animals.
V. QUANTIFICATION OF TOXICOLOGICAL EFFECTS
Health Advisories (HAs) are generally determined for One-day, Ten-day,
Longer-term (approximately 7 years) and Lifetime exposures if adequate data
are available that identify a sensitive noncarcinogenic end point of toxicity.
The HAs for noncarcinogenic toxicants are derived using the following formula:
HA = (NOAEL or LOAEL) x (BW) = mg/i, ( ug/L)
(UF) x ( L/day)
where:
NOAEL or LOAEL = No- or Lowest-Observed-Adverse-Effeet-Level
in mg/kg bw/day.
BW = assumed body weight of a child (10 kg) or
an adult (70 kg).
UF = uncertainty factor (10, 100 or 1,000), in
accordance with NAS/ODW guidelines.
L/day = assumed daily water consumption of a child
(1 L/day) or an adult (2 L/day).
One-day Health Advisory
A One-day HA for MEK is calculated based upon findings reported by
DiVincenzo and Krasavage (1974). Guinea pigs were administered MEK at a
single intraperitoneal dose of 750, 1,500 or 2,000 mgAg» Hepa to toxicity
in guinea pigs was measured in terms of increased serum ornithine carbamyl
transferase activity and lipid accumulation in the liver. Elevated serum
ornithine carbamyl transferase activity was observed 24 hours after admini-
stration of 2,000 mg/kg of MEK. Lipid accumulation in liver cells of animals
was noted also at the two higher doses (1,500 and 2,000 mg/kg). Therefore,
in view of demonstrated hepatotoxicity in terms of increased serum enzyme
activity (at dose level of 2,000 mg/kg) and lipid accumulation in the liver
cells at dose levels of 1,500 and 2,000 mgA
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Methyl Ethyl Ketone March 31, 1987
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10 kg = assumed body weight of a child.
100 = uncertainty factor, chosen in accordance with NAS/ODW
guidelines for use with a NOAEL from an animal study.
1 L/day = assumed daily water consumption of a child.
Ten-day Health Advisory
There are no data from which to derive a Ten-day HA directly. Therefore,
it is recommended that the HA can be determined by dividing the One-day HA by
10, resulting in a HA of 7500 ug/L for a 10 kg child.
Longer-term Health Advisory
Adequate duration-specific oral data are not available from which to
derive the Longer-term HA. However, the LaBelle and Brieger (1955) inhalation
study in rats may be considered for a longer-term HA. In this study, a group
of 25 rats was exposed to 235 ppm (693 mg/m3) MEK for 7 hours/day, 5 days/week
for 12 weeks. Without indicating the specific organs examined, the authors
reported that no significant pathological changes were observed either macro-
scopically or microscopically. The Longer-term HA is derived as follows:
Step 1: Determination of the Total Absorbed Dose (TAD)
3
TAD = (693 mq/nr»)(1 mj/hr)(7 hr/day) (5/7) (0.5) = 24<7 Bg/kg/day
where:
693 mg/m3 = NOAEL of 235 ppm based on absence of pathological change
in rats.
1 m^/hr = respiratory rate of adult human (pulmonary rate/body weight
ratio) assumed to be the same for humans and test animals.
7 hr/day * exposure duration.
5/7 » conversion from 5 days exposure to 7 days exposure.
0.5 - assumed fraction of MEK absorbed.
70 kg « assumed body weight of an adult.
Step 2s Determination of the Longer-Term HA
Longer-term HA for a 10-kg childs
(24.7 mg/kg/day) (10 kg) . 2.5 mg/L (or 2500 ug/L)
(100) (1 L/day)
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Methyl Ethyl Ketone March 31, 1987
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where:
24.7 mgAg/day « TAD.
10 kg = assumed body weight of a child.
100 » uncertainty factor, chosen in accordance with NAS/ODW
guidelines for use with a NOAEL from an animal study.
1 L/day = assumed daily water consumption of a child.
Longer-term HA for a 70-kg adult:
(24.7 mg/kg/day) (70 kg) = 8.6 mg/L (or 860o ug/L)
(100) (2 L/day)
where:
24.7 mg/kg/day = TAD.
70 kg = assumed body weight of an adult.
100 = uncertainty factor, chosen in accordance with NAS/ODW
guidelines for use with a NOAEL from an animal study.
2 L/day = assumed daily water consumption of an adult.
Lifetime Health Advisory
The Lifetime HA represents that portion of an individual's total exposure
that is attributed to drinking water and is considered protective of noncar-
cinogenic adverse health effects over a lifetime exposure. The Lifetime HA
is derived in a three step process. Step 1 determines the Reference Dose
(RfD), formerly called the Acceptable Daily Intake (ADI). The RfD is an esti-
mate of a daily exposure to the human population that is likely to be without
appreciable risk of deleterious effects over a lifetime, and is derived from
the NOAEL (or LOAEL), identified from a chronic (or subchronic) study, divided
by an uncertainty factor(s). From the RfD, a Drinking Water Equivalent Level
(DWEL) can be determined (Step 2). A DWEL is a medium-specific (i.e., drinking
water) lifetime exposure level, assuming 100% exposure from that medium, at
which adverse, noncarcinogenic health effects would not be expected to occur.
The DWEL is derived from the multiplication of the RfD by the assumed body
weight of an adult and divided by the assumed daily water consumption of an
adult. The Lifetime HA is determined in Step 3 by factoring in other sources
of exposure, the relative source contribution (RSC). The RSC from drinking
water is based on actual exposure data or, if data are not available, a
value of 20% is assumed for synthetic organic chemicals and a value of 10%
is assumed for inorganic chemicals. If the contaminant is classified as a
Group A or B carcinogen, according to the Agency's classification scheme of
carcinogenic potential (U.S. EPA, 1986), then caution should be exercised in
assessing the risks associated with lifetime exposure to this chemical.
Lifetime HA for MEK may be derived based on LaBelle and Brieger (1955)
inhalation study in rats for 12 weeks. In this study, a NOAEL of 693 mg/m3
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Methyl Ethyl Ketone March 31, 1987
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was identified. Animals were exposed to MEK for 7 hours/day, 5 days/week for
12 weeks. The Lifetime HA is derived as follows:
Total absorbed dose (TAD) of 24.7 mg/kg/day was determined as described
under Longer-term HA.
Step 1: Determination of the Reference Dose (RfD)
RfD = 24.7 mg/kg/day = 0.0247 mgAg/<3ay
(1,000) y
where:
24.7 mg/kg/day = TAD (NOAEL) based on absence of pathological changes.
1,000 = uncertainty factor, chosen in accordance with NAS/ODW
guidelines for use with a NOAEL from an animal study
of less-than-lifetime duration.
Step 2: Determination of the Drinking Water Equivalent Level (DWEL)
DWEL = (0.0247 mg/kg/day) (70 kg) = 0.86 mg/L or 860 ug/L
2 L/day
where:
0.0247 mgAg/<3ay = RfD.
70 kg = assumed body weight of an adult.
2 L/day - assumed daily water consumption of an adult.
Step 3: Determination of the Lifetime Health Advisory
Lifetime HA - 0.86 mg/L x 20% =0.17 mg/L (170 ug/L)
where:
0.86 mg/L = DWEL.
20% » assumed relative source contribution from water.
Evaluation of Carcinogenic Potential
0 No studies on the carcinogenic effects in animals to MEK have been
found in the available literature.
0 IARC has not made an assessment of MEK's carcinogenic potential.
0 Applying the criteria described in EPA's guidelines for assessment
of carcinogenic risk (U.S. EPA, 1986), methyl ethyl ketone may be
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Methyl Ethyl Ketone March 31, 1987
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classified in Group D: Not classified. This category is for agents
with inadequate animal evidence of carcinogenicity.
VI. OTHER CRITERIA, GUIDELINES AND STANDARDS
0 An occupational threshold limit value (TLV) of 200 ppm was set by
ACGIH (1980).
VII. ANALYTICAL METHODS
0 There is no standardized method for the determination of methyl ethyl
ketone in drinking water samples. However, methyl ethyl ketone may be
determined by purge and trap gas chromatographic-mass spectrometric
(GC-MS) procedure used for determination of volatile organic compounds
in industrial and municipal discharges (U.S. EPA, 1984). In this
method, a 5 mL water sample is spiked with an internal standard of an
isotopically stable analog of methyl ethyl ketone and purged with an
inert gas. The volatile compounds are transferred from the aqueous
phase into the gaseous phase where they are passed into a sorbent
column and trapped. After purging is completed, the trap is backflushed
and heated to desorb the compounds on to a gas chromatograph (GC).
The compounds are separated by the GC and detected by a mass spectro-
meter (MS). The labeled compound serves to correct the variability
of the analytical technique. The method detection limit is dependent
upon the nature of interferences, but it is estimated to be 50 ug/L.
VIII. TREATMENT TECHNOLOGIES
9 Because of its polarity and resulting miscibility in water, MEK is a
difficult compound to remove from contaminated potable water. The
conventional water treatment techniques of coagulation and sand
filtration are ineffective in MEK removal (McGuire et al., 1978).
8 Chlorination does cause some oxidative degradation of MEK. Treatment
with 100 mg/L chlorine for 12 hours reduced MEK by 5% (McGuire et al.,
1978). However, such treatment leads to the formation of trihalo-
methanol which makes chlorination an undesirable treatment. Oxidative
treatment with 100 mg/L potassium permanganate for 3 hours was com-
pletely ineffective in reducing MEK concentrations (McGuire, 1978).
8 MEK also is not a good candidate for removal by air stripping. It has
a low Henry's Law Constant of 3.4 x 10~5 atm m3/roole (McGuire et al.,
1978).
8 Adsorption to granular activated carbon (GAG) offers the best potential
for MEK removal. McGuire et al. (1978) reported a 95% removal effi-
ciency using a 1.1 min detention time over a 1.2 hr treatment period.
However, in another laboratory investigation of removal of MEK (7.2
. mg/L) by Filtrasorb 400, breakthrough occurred after 3 hours of
'treatment at a flow rate of 23 ml/min and a detention time of 2.1 min
(McGuire et al., 1978).
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Methyl Ethyl Ketone March 31, 1987
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McGuire et al. (1978) also attempted laboratory isotherm studies using
GAG and 0.2 mm ortho-phosphate buffered glass distilled water as a
solvent for the MEK. These results also indicate that treatment with
GAG can be used to remove MEK.
Treatment with powdered activated carbon (PAG) however, does not seem
to be as effective (McGuire et al., 1978; Kuo et al., 1977).
Treatment technologies for the removal of methyl ethyl ketone from
water are available and have been reported to be effective. Selection
of individual or combinations of technologies to achieve methyl ethyl
ketone reduction must be based on a case-by-case technical evaluation,
and an assessment of the economics involved.
Positioning the chlorina*-ion step in water treatment so that it occurs
after MEK removal also should be considered since MEK can serve as a
precursor for THM formation.
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• Methyl Ethyl Ketone March 31, 1987
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IX. REFERENCES
ACGIH. 1980. American Conference of Governmental Industrial Hygienists.
TLVs - Threshold limit values for chemical substances in workroom air,
adopted by ACGIH for 1980. Cincinnati, OH.
Carpenter, C.P., H.F. Smyth and U.C. Pozzani. 1949. The assay of acute
vapor toxicity, and the grading and interpretation of results on 96
chemical compounds. J. Ind. Hyg. Tox. 31(6):343-346.
Cavender, F.L., H.W. Casey, H. Salem, J.A. Swenberg and E.J. Gralla. 1983.
A 90-day vapor inhalation toxicity study of methyl ethyl ketone. Fund.
Appl. Toxicol. 3:264-270.
Chain, E.S.K. 1982. Oxidation of particular organics. Personal communication.
Coleman, W.E., R.D. Lingg, R.G. Melton and F.C. Kopfler. 1976. The occur-
rence of volatile organics in five drinking water supplies using gas
chromatography/mass spectrometry. Chapter 21. In; L.H. Keith, ed.
Identification and analysis of organic pollutants in water. Ann Arbor,
MI: Ann Arbor Science Publications, Inc.
Deacon, M.M., M.D. Pilny, J.A. John, B.A. Schwetz, F.J. Murray, H.O. Yakel
and R.A. Kuna. 1981. Embryo- and fetotoxicity .of inhaled methyl ethyl
ketone in rats. Toxicol. Appl. Pharmacol. 59:617-619.
Dietz, F.K., and G.J. Traiger. 1979. Potentiation of CCL4 of hepatotoxicity
in rats by a metabolite of 2-butanone: 2,3-butanediol. Toxicology.
14:209-215.
DiVincenzo, G.D., and N.J. Krasavage. 1974. Serum ornithine carbamyl trans-
ferase as a liver response test for exposure to organic solvents. Am.
Ind. Hyg. Assoc. J. 35:21-29.
Duckett, S., N. Williams and S. Francis. 1974. Peripheral neuropathy associ-
ated with inhalation of methyl n-butyl ketone. Experientia. 30:1283.
Hites, R.A., G.A. Jungclaus, V. Lopez-Avila and L.S. Sheldon. 1979. Poten-
tially toxic organic compounds in industrial wastewater and river systems:
two case studies. ACS Symp. Ser. 94:63-90. D. Schuetzle, ed., Moni-
toring Toxic Substances.
Kimura, E.T., D.E. Ebert and P.W. Dodge. 1971. Acute toxicity and limits
of solvent residue for sixteen organic solvents. Toxicol. Appl. Pharmacol.
19:699-704.
Kuo, P.P.K., E.S.K. Chain, F.B. DeWalle and J.H. Kim. 1977. Gas stripping,
sorption, and thermal desorption procedures for preconcentrating volatile
polar water-soluble organics from water samples for analysis by gas
chromatography. Analytical Chemistry. 6:1023-1029.
LaBelle, C.W., and H. Brieger. 1955. The vapor toxicity of a composite
solvent and its principal components. Arch. Ind. Health. 12:623-627.
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Methyl Ethyl Ketone March 31, 1987
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Love, O.T., and R.G. Eilers. 1981. Treatment for the control of trichloro-
ethylene and related industrial solvents in drinking water. U.S. Environ-
mental Protection Agency, Drinking Water Research Division. Cincinnati,
Ohio.
McGuire, M.J., I.H. Suffet and J.V. Radziul. 1978. Assessment of unit
processes for the removal of trace organic compounds from drinking water.
JAWWA. 10:565-572.
Munies, R., and D.E. Wurster. 1965. Investigation of some factors influ-
encing percutaneous absorption. Absorption of methyl ethyl ketone.
J. Pharm. Sci. 54:1281-1284.
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