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UNITED STATES ENVIRONMENTAL PROTECTION AGENCY

WASHINGTON, D .C. 20460

'4L PR03*- 602o

OFFICE OF

PREVENTION, PESTICIDES AND

TOXICSUBSTANCES

JUN

HEMORAND

Subject : Hazard and Risk Assessment of Methyl Ethyl Ketone

From : Oscar Hernandez, Ph .D ., Chief (Acting

Existing Chemicals Assessment Branc h 041tv

Risk Assessment Division (7403)

To : Maria Doa, Ph .D ., Chie f

Toxic Release Inventory Branch

Environmental Assistance Division (7408 )

Attached is the final hazard assessment of Methyl Ethyl

Ketone (MEK), CAS No . 78-93-3, following RAD disposition of this

chemical on May 21, 1997 . The assessment conclusion is that,

overall, there is low potential risk associated with exposure to

MEK under the release scenarios described in the assessment .

All items discussed at disposition have been

incorporated into this final version . These include the

following :

0 The estimated acute potential dose rates have been adjusted

based on an average human female body weight of 65 kg, as

provided by Mary Katherine Powers of EETD .

0 The original study used to derive the IRIS RfC (Schwetz et

al ., 1991), was examined in order to determine the body

weight of the adult mice tested . There was no indication of

body weight and therefore the standard default of 25 g for

mice was used in converting concentrations into dose

equivalents . This body weight is consistent with that

reported in other toxicity studies for the same strain

(Swiss Albino) of mice .

0 The use of an uncertainty factor of 100 for MEK to compare

to the MOE was maintained .

Recycled/Recyclable

Printed with Soy/Canole Ink on paper that

63980000335

contains at least 50% recycled fiber
p. 2

HAZARD ASSESSMENT OF METHYL ETHYL KETON E

(in response to Section 313 delisting petition of

the Chemical Manufacturers Association, Arlington, VA)

11 .13ACKGROUN D

On November 29, 1996, the Chemical Manufacturers Association (CMA)

repetitioned the Agency to delete methyl ethyl ketone (MEK) from the list of chemicals

subject to the reporting requirements of Section 313 of the Emergency Planning and

Community Right-To-Know Act of 1986. CMA had submitted a petition to delete MEK

and methyl isobutyl ketone from Section 313 in September 1988, but this petition was

withdrawn based on the Agency's concerns for developmental toxicity and

neurotoxicity. Since that time, as a result of new information or a reevaluation of

existing information, the level of concern for these effects has decreased (IRIS 1993) . This is CIVIA's basis for resubmitting the petition.

MEK (CH3COCH2CH3) is a clear, colorless, organic liquid with a sharp sweet

odor. It is miscible with water and a variety of organic solvents. Its greatest use is as a

solvent in the surface coatings industry, specifically vinyl lacquers, nitrocellulose

lacquers, and acrylics . It is also used as a solvent for adhesives, printing inks,

degreasing and cleaning fluids, smokeless powder, and the hard wood pulping industry

and as an intermediate in the production of antioxidants, perfumes, and catalysts .

Currently, MEK is produced in the US by three companies: Exxon Chemical CO.,

Hoechst Celanese, and Shell Chemical . Estimated total domestic capacity in 1995 was

ca. 595 million pounds .

In humans, inhalation of high doses produces irritation of the eyes and upper

and lower respiratory system, effects characteristic of solvent exposure . (USEPA(b),

HE RD memorandum dated January 30, 1997) . Likewise, animal data indicates that

MEK has toxic effects only at high doses . For example, in acute oral toxicity studies,

the LD 50 in rats and mice ranges from 2.5-5.6 g/kg and in subchronic inhalatio n

studies, decreases in body weight, increases in liver weight and liver weight to body

weight ratios, and increases in enzyme activity, were observed only at high doses

(5,000 ppm) (IRIS 1993) . The NOAEL and LOAEL were 1,010 and 3,020 ppm,

respectively, based on the developmental study used to derive the IRIS RfC(IRIS,

1993) . The RfC for MEK is 1 .0 mg1m', or ca . 0.3 ppm. The OSHA PEL for MEK is

200 ppm, or ca. 589 Mg/M3

. Because of the low hazard (low intrinsic toxicity) for MEK,

the Environmental Assessment Division (EAD) requested that the Risk Assessment
p. 3

Division (RAD) perform a risk assessment .

2. HAZARD SUMMARY

2 .1 Absorption and Metabolism

[E MEK is well-absorbed from the lung, GI tract, and skin. Pulmonary uptake in

humans ranged from 41% to 56% . (USEPA(a), HERD memorandum dated January 22,

1997) .

2.2 Acute Toxicity

[E] Available data indicate that MEK has low acute toxicity . In humans, inhalation of

high doses produces irritation of the eyes and upper and lower respiratory system,

effects characteristic of solvent exposure. (USEPA(b), HERD memorandum dated

January 30, 1997) . In acute oral toxicity studies, the LD 50 in rats and mice ranges

from 2.5-5.6 g/kg.

2.3 Carcinogenicity

[E] MEK is classified in IRIS as D, not classifiable as to human carcinogenicity,

based on no human carcinogenicity data and inadequate animal data . (IRIS, 1993).

2.4 Mutagenicity

IE MEK was negative in the Ames assay with and without activation . It induced

chromosome mutations (aneuploidy) in yeast cells . It also induced cell transformation

in BALB/c cells . It was also negative in the following : in the UDS assay, for SCE's in

CHO cells, in the mouse micronucleus assay, for gene mutations in E. coli, in the

mouse lymphoma assay, and for chromosome aberrations in CHO cells. (USEPA(c),

HERD memorandum dated January 24, 1989).

2.5 Systemic Toxicity from Repeated Doses

B Available data indicate that MEK appears to have low systemic toxicity and is,

therefore, of low health concern . Although no chronic studies have been found, several

well-designed repeated-dose oral and inhalation studies in laboratory animals

demonstrate low systemic toxicity with MEK (USEPA(b), HERD memorandum dated

January 30, 1997). For example, in subchronic inhalation studies, decreases in body

weight, increases in liver weight and liver weight to body weight ratios, and increases i n

2
p. 4

enzyme activity, were observed only at high doses (5,000 ppm) (IRIS 1993) .

2.6 Developmental Toxicity

B The key study, on which the RfC is based, is an inhalation developmental

toxicity study in Swiss mice (Schwetz et al . 1991, as cited in attached assessment) . This study was not available at the time of the first petition . Four groups of 10 virgin

and 33 pregnant mice were exposed to 0, 398, 1, 010, or 3,020 ppm (0, 1, 1 74, 2,978, or 8,906 Mg/M3) MEK 7 hr/day during gestation days 6-15.

Neither maternal nor developmental toxicity were observed at the low or mid

doses . At 3,020 ppm, there was a decrease in fetal body weight that was significant

only in males and a significant trend in the incidence of misaligned sternebrae when

measured on a fetus but not litter basis . At this dose there was also an increase in

maternal relative liver and kidney weight, but the biological significance of this effect is

not known (IRIS 1993).

E Based on the dose level at which these effects were observed, the concern for

developmental toxicity appears to be low. The LOAEL is 3,020 ppm and the NOAEL

is 1,010 ppm .

[E] The two inhalation studies that formed the basis of concern for the first petition

were conducted in rats by the same group of researchers and in the same laboratory .

In the first study (Schwetz et al . 1974, as cited in IRIS 1993), animals were exposed to

0, 1, 126, or 2,618 ppm (0, 3,320, or 7,720 Mg/M3 ). At the low dose, there was a

decrease in fetal body weight and crown :rump length ; these effects were not seen at

the high dose . There was also a significant increase in total number of litters

containing fetuses with skeletal anomalies. At the high dose, there was a significant

increase in number of fetuses and litters having gross anomalies . Maternal toxicity was

not observed . The apparent LOAEL is 1,126 ppm .

The second study (Deacon et al . 1981, as cited in the IRIS 1993) was conducted

to determine the repeatability of the above findings . Exposures were to 0, 412, 1,002,

or 3,005 ppm (0, 1,215, 2,955, or 8,861 Mg/M). No effects were seen at the low or mid

dose. At the high dose, there was delayed ossification of bones in the skull and

cervical centra and an increase in the incidence of extralumbar ribs . There was also

decreased maternal body weight gain and increased water consumption at the high

dose. The apparent NOAEL is 1,002 ppm, and the LOAEL is 3,005 ppm .

2.7 Reproductive Toxicity

3
p. 5

[E] Data on MEK could not be found . There is a two-generation rat study with 2-

butanol (a metabolic precursor to MEK) in which Wistar rats (30/sextgroup) were given

0, 0.3%, 1 .0%, or 3 .0% in drinking water. Because of significant toxicity seen in the

high-dose group, treatment of high-dose parents and offspring was reduced to 2.0% .

The critical effect was decreased fetal birth weight at the 2 .0% dose. Based on the

dose level at which these effects were observed, the concern for reproductive toxicity

appears to be low. The LOAEL for 2-butanol is 2.0% (3,122 mg/kg1day) and the

NOAEL is 1 .0% (1,771 mg/kg/day). (USEPA(b), HERD memorandum dated January

30, 1997) .

2.8 Neurotoxicity

ME According to the latest IRIS report on MEK, which was updated 6/93, "at present,

there is no convincing experimental evidence that MEK is neurotoxic in either

experimental animals or humans other than possibly inducing CNS depression at high

exposure levels ." Prior concerns were based on enhancement by MEK of neurotoxicity

seen with other solvents .

2.9 Environmental Effects

FR MEK is of low concern with respect to aquatic toxicity based on measured

toxicity data and SAR analysis . The fish 96-hr LC50 values range from 2,300 to 3,220

ppm; the daphnid 48-hr LC50 values range from 2,200 to 5,091 ppm, and the green

algal 96-hr EC50 is 1,200 ppm. The fish chronic values range from 220 to 300 ppm,

the daphnid chronic value is 52 ppm, and the algal chronic value is 45 ppm. In

addition, the bioconcentration factor is low, 0.640. (USEPA(d), HERD memorandum

dated December 10, 1997) .

3 . EXPOSURE SUMMARY (USEPA(e), EETD memorandum dated January 28,1997)

Most of the industrial releases of MEK are to air . According to the SIDS Initial

Assessment Report [LISEPA(f) 1995], the concentrations of MEK in the environment

are low, because MEK is manufactured in totally enclosed continuous processes, and

significant emission reductions have been made over the past few years . The SIDS

Report, however, did not present monitoring data for MEK levels at the fenceline of

MEK facilities .

In addition, the Ketones panel had submitted an exposure report for MEK

performed by ENSR Corporation as part of the petition for delisting . It appears that an

extensive amount of work has been done (in many cases using EPA models) . However, insufficient site-specific information was included for an adequate evaluatio n

4
p. 6

of their results. In addition, some debatable assumptions were made, such as th e

statement that "airborne concentrations are likely to be highest around facilities with the

highest emission rates". This is not necessarily true. Airborne concentrations depend

on weather conditions as well as emission rates . For these reasons, exposur e

estimates based on the concentrations in air presented in the petition are not included

in this report.

Concentrations and exposures resulting from the fugitive and stack air releases

in the TRIS download were estimated using equations developed based on PTPLU, a

single source Gaussian dispersion algorithm . The PTPLU model provides ground-level

concentrations which are hourly average values .

The scenarios modeled assume that there is no treatment of these stack and

fugitive releases, and therefore no reduction in the amount released to the

environment. These concentrations can be expected to occur up to 250 meters from

the source, which may be beyond the facility fenceline .

Estimated concentrations are based on the assumption that releases take place

continuously over 365 days per year; releases occurring over shorter periods will result

in higher concentrations. This will be true no matter what short-term model is

employed. There is no way to determine the number of release days from reports to

the TRIS database . It is safe to assume, however, that acute estimated concentrations

can occur at points beyond facility fencelines .

A combination of both conservative and non-conservative assumptions were

used to generate these equations. The conservative assumptions include the use of

weather station data known to generate the highest concentrations and therefore

potential exposures, as well as a 24-hour exposure duration . Non-conservative

assumptions include the assumption that TRI releases are spread over 365 days per

year, 24 hours a day, and a 24-hour averaging time for concentration estimates . Given

a shorter release period, estimated exposures could be significantly higher . '

This procedure generates estimates of concentrations and exposures under

three different scenarios including a variety of wind conditions, including relatively

stagnant situations . These three scenarios have been labeled 1) the typical scenario,

2) the stagnation scenario, and 3) the maximum scenario. The model does not

consider decay of the chemical in the environment.

I Some short-term concentrations are outside the scope of PT?LU, due to either release fluctuations,

geography, or combinations of source geometry and atmospheric conditions . Concentrations with durations of several

minutes can significantly exceed hourly averages modeled here .

5
p. 7

The environmental assumptions applied to each scenario are summarize d

below. The wind speeds for the scenarios occur at a height of ten meters, and the runs

used wind speeds varying with height .

Typical scenario: wind speed of five meters per second, and a 24-hour duration .

Stagnation scenario : wind speed of 2 meters per second, and a 24-hour

duration. It was designed to model an outdoor stagnation episode exceeding 24 hours .

This scenario does not mean closed-room conditions ; it is a relative term to indicate

calm outdoor conditions with low wind dilution.

Maximum scenario: wind speed of 0.5 meters per second, and a two-hour

duration . It models the least air dilution during stagnant conditions .

Using PTPLU, concentrations were modeled at 50-meter intervals beginning at

50 meters downwind from the source. Model output reported results across stability

classes for a range of wind speeds effective at the stack top . The runs used wind

speeds varying with height.

The assumptions used in estimating acute potential dose rates (APDRs) are as

follows:

Typical: An inhalation rate of 11 .3 m'/day, a body weight of 65 kg2 , and a twentyfour-hour averaging period .

Stagnation : An inhalation rate of 11 .3 m'/day, a body weight of 65 kg, and a

twenty-four-hour averaging period.

Maximum: An inhalation rate of 0.47 M3 /hr, a body weight of 65 kg, and a twohour averaging period .

The inhalation rates and body weights cited above are average values for adult

females . Data for pregnant women as a group are not available . An inhalation rate of

0.47 M3 /hr was used in the maximum scenario . This value was generated by dividing

the daily inhalation rate of 11 .3 M3 by 24 hours.

2 The female average body weight is based on a mean value for adults age 18-75 of 65.4 kg based on a single

study cited in the Department of Health and Human Services Publication No . (PHS) 87-1688.

6
p. 8

Estimated concentrations in air and APDRs resulting from stack releases are

shown in Table 1 . Estimated concentrations and APDRs resulting from fugitive

releases are shown in Table 2.

Due to a lack of more specific information, these exposure estimates are based

on "what-if' scenarios . A "what-if' scenario is defined by EPA:s 1992 EL(posure

Assessment Guidelines as one which answers the question, "What potential dose rates

result if the following exposure conditions are assumed?" Assumptions are then made

about representative conditions. Please note that a "what-if' scenario contains no

estimate of the probability of the estimated exposures .
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P. 10

4. RISK ASSESSMENT

This assessment focuses on the potential risk associated with estimated exposures to MEK at or

beyond the facility site boundary . The exposure estimates illustrated in this assessment utilize release

information submitted under TRI and standard modeling techniques to derive ambient air concentrations

of MEK under three release scenarios (typical, stagnant, and maximum or peak) for the top releasing

facilities in each category - stack and fugitive- of air emissions .

The IRIS RfC of 1 .0 mg1m3 for MEK is based on mild, but significant developmental toxicity

(decreased fetal body weight and misaligned sternebrae) at 3,030 ppm in the inhalation developmenta l

3

toxicity study in mice (Schwetz et al . 1991, as cited in IRIS 1993). An RfC by definition represents an

"estimate (with uncertainty spanning an order of magnitude) of a daily inhalation exposure of the human

population (including sensitive subgroups) that is likely to be without appreciable risk of deleterious effects

during a lifetime". As such, the RfC incorporates adjustments to account for uncertainties about portal of

entry and long-term exposure effects . Because of emphasis on developmental effects, it would not be

appropriate to use the RfC for assessing the potential risk of developmental toxicity associated with acute

exposure to MEK. It would be more appropriate to derive a RfCDTand compare it with the estimated

human exposure concentration. There is, however, no official Agency RfCDT . Instead, a margin of

exposure (MOE)4 approach was used . The rationale for following this approach was that the effect of

concern for MEK is developmental toxicity, which requires assessment of short-term exposures .

Most releases of MEK are to air ; thus, only airborne exposures were considered . Furthermore,

because the critical effect is developmental toxicity, which can be initiate d

upon acute exposure, acute ambient concentrations estimated by the Point Plume (PTPLU) model were

the exposure concentrations selected.

3The RfC was set with an uncertainty factor of 1000: 10 for interspecies extrapolation, 10 for sensitive

individuals, and 10 for incomplete database including a lack of chronic and reproductive toxicity studies ; and with a

modifying factor of 3 for lack of unequivocal data for the respiratory tract (portal-of-entry) effects, for a total

adjustment factor of 3000. Confidence in the RfC is low due to medium confidence in the principal study and low

confidence in the database. (IRIS, 1993). Furthermore, developmental effects in rats were not consistent between

studies.

4 The MOE is the ratio of the NOAEL of the critical toxic effect to the estimated human exposure levels . When the MOE is equal or greater than the product of applicable uncertainty and modifying factors (see footnote 1),

the chemical is likely to be of low concern . For MEK, this uncertainty factor is 100.

9
P.

Table 3 : Acute MOE Calculations for Stack Releases a

Discharging Facilffy- Typical Stagnant maximum

690 4W 1380

Gencorp

1380 690 1380

O'Sullivan Corp.

1380 690 1380

IPC Corinth Div . Inc.

2760 1380 2760

Resilite Sports

Products, Inc .

2760 1380 2760

3M Middleway Plan t

'The MOE is the ratio of the NOAEL in the mouse developmental study (1380 mg/kg/day) to

APDR estimates in Table 1 .

Table 4: Acute MOE Calculations for Fugitive Releases'

Discharging Facilffy- Typical Stagnant maximum

690 ............. . . . . . . . . .. . .......................................... ..... ............... .. 460

.......... .................. .. ... .............................. Mobile Oil Beaumont ....

..................................

...

....

...

....

...

....

...

....

................... .... .. . . . . . .

...............................

.................................................

...

.....

1380 138 690

Texas Recreation Corp.

1380 138 690

Sun Refining and

Marketing

1380 172 1380

Shell Oil Deer Par k

Manufacturing Complex

1380 197 1380

Amoco Oil Co. Whiting

Refinery

'The MOE is the ratio of the NOAEL in the mouse developmental study (11380 mg/kg/day) to

APDR estimates in Table 2.

MOE calculations for acute ambient exposures for stack and fugitive releases

from the top ten discharging facilities are summarized in Tables 3 and 4. In each case,

the NOAEL (ca 1380 mg/kg/day)5 from the mouse developmental toxicity study was

divided by the acute estimated average potential dose rates (APDRs) . The default

assumptions for the mouse ventilation rate and mouse body weight were based on

values given in USEPA (g). These appear to be consistent with the strain of mouse

(Swiss Albino) tested in the developmental toxicity study by Schwetz, et al . (1991).

As can be seen in Tables 3 and 4, the MOE is greater than 100 for stack releases

under all three exposure scenarios ; typical, stagnant, and maximum (peak) . For

5 ppm - mg/kg/day = [ppm x (molecular weight/24.5) x mouse ventilation rate (m'/day) x duration of

exposure (hr/day) - mouse body weight (kg) = mg/kg/day

[1010 ppm x (72.1/24.5) x 0.040 m'/day x 7 hr/24 hours] - 0.025 kg = 1380 mg/kg/day

10
p. 12

fugitive releases, the MOE is greater than 100 for all three exposure scenarios, except

one discharging facility under stagnant scenarios .

Conclusions

Overall, the assessment supports low potential risk for developmental effects to

individuals exposed to MEK. This conclusion is based on MOE values greater tha n

100 for the top releasing facilities with one exception . A potential risk is indicated by an

MOE value lower than 100 for one facility under exposure conditions characterized by

fugitive releases under a stagnant scenario . It should be noted that the exposure

estimates are based on facility release estimates, which generally are not the result of

monitoring studies. Also, the APDRs assume that the target population is exposed to

ambient (outdoor) air continuously. Thus, the risk characterization reflects potential

concerns engendered by estimated high exposures . The hazard assessment strongly

indicates that MEK has low acute and chronic (systemic) toxicity in that effects occur

only at high doses. Specifically, developmental toxicity for MEK is characterized by

high dose effects and lack of consistency between studies for one species .

Furthermore, based on the developmental effects observed, if the MOE were calculated

on the basis of a benchmark dose instead of the apparent NOAEL from the

developmental toxicity study, the concern for potential risk would be further weakened,

if not eliminated. Therefore, under the exposure conditions described here there

appears to be low potential risk associated with exposure to MEK.

&REFERENCES

IRIS . 1993. Integrated Risk Information System Database . Washington, DC: USEPA,

USEPA(a) . 1997. EPCRA Section 313 Delisting Petition : Absorption Review for

Methyl Ethyl Ketone (MEK) . Memorandum dated January 22, 1997, from Leonard

Keifer, Health Effects Branch, HERD to Lorraine Randecker, Analysis and Information

Management Branch, CSRAD . Washington, DC : USEPA.

USEPA(b). 1997. Health Hazard Assessment: Delist Petition for MEK. Memorandum

dated January 30, 1997, from Katherine Anitole and Nicole Paquette, Health Effects

Branch, HERD to Lorraine Randecker, Analysis and Information Management Branch,

CSRAD . Washington, DC: USEPA.

USEPA (c) . 1989 . Delisting Petitions for Methyl Ethyl Ketone (MEK) and Methyl

Isobutyl Ketone (MIBK) : Mutagenicity Hazard . Memorandum dated January 24, 1989

from Michael Cimino, Health Effects Branch, HERD to E. Dage, Analysis and

Information Management Branch, CSRAD . Washington, DC : USEPA.

USEPA(d) . 1997 . Delisting Petition for Methyl Ethyl Ketone : Environmental Toxicity.

Memorandum dated December 10, 1996, from J .V. Nabholz, Ecological Effects Branch,

HERD to Dan Bushman, Environmental Assistance Division . Washington, DC : USEPA.

USEPA(e). 1998. Exposure Assessment for Methyl Ethyl Ketone in Response t o

I I
p. 13

Delisting Petition. Memorandum dated January 28, 1997, from Mary Katherine Powers,

EETD. Washington, DC :USEPA.

USEPA(f). 1995. OECD-SIDS: Review of US Initial Assessment Reports . Methyl ethyl

ketone . Memorandum dated April 30, 1995, from Oscar Hernandez, Chief, Risk

Analysis Branch, CSRAD, to Angela Auletta, Chief, Health Effects Branch, HERD . Washington, DC : USEPA.

USEPA(g). 1987 . Recommendations for and Documentation of Biological Values for

Use in Risk Assessment. Environmental Criteria and Assessment Office, Office of

Health and Environmental Assessment, Office of Research and Development, USEPA,

Cincinnati, OH . NTIS # PB 88-179 874/AS, EPA # 600/6-87/008 .

National Center for Health Statistics (NCHS) 1987. Anthropometric reference data and

prevalence of overweight, United States, 1976-1980. Data from the National Health and

Nutrition Examination Survey, Series 11, No. 238. Hyattsville, MD : US Department of

Health and Human Services, Public Health Service, National Center for Healt h

Statistics . DHHS Publication No . (PHS) 87-1688.

12