Methyl Ethyl Ketone; Toxic Chemical Release Reporting; Community Right-to-Know

ENVIRONMENTAL PROTECTION AGENCY

[OPPTS-400119; FRL-5752-6]

Methyl Ethyl Ketone; Toxic Chemical Release Reporting; Community

Right-to-Know

AGENCY: Environmental Protection Agency (EPA).

ACTION: Denial of petition.

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SUMMARY: EPA is denying a petition to remove methyl ethyl ketone (MEK)

from the list of chemicals subject to the reporting requirements under

section 313 of the Emergency Planning and Community Right-to-Know Act

of 1986 (EPCRA) and section 6607 of the Pollution Prevention Act of

1990 (PPA). EPA has reviewed the available data on this chemical and

has determined that MEK does not meet the deletion criterion of EPCRA

section 313(d)(3). Specifically, EPA is denying this petition because

EPA's review of the petition and available information resulted in the

conclusion that MEK meets the listing criteria of EPCRA section

313(d)(2)(B) and (C) due to its contribution to the formation of ozone

in the environment, which causes adverse human health and environmental

effects.

FOR FURTHER INFORMATION CONTACT: Daniel R. Bushman, Petitions

[[Page 15196]]

Coordinator, 202-260-3882 or e-mail: [email protected],

for specific information regarding this document or for further

information on EPCRA section 313, the Emergency Planning and Community

Right-to-Know Information Hotline, Environmental Protection Agency,

Mail code 5101, 401 M St., SW., Washington, DC 20460, Toll free: 1-800-

535-0202, in Virginia and Alaska: 703-412-9877, or Toll free TDD: 1-

800-553-7672.

SUPPLEMENTARY INFORMATION:

I. Introduction

A. Statutory Authority

This action is taken under sections 313(d) and (e)(1) of the

Emergency Planning and Community Right-to-Know Act of 1986 (EPCRA), 42

U.S.C. 11023. EPCRA is also referred to as Title III of the Superfund

Amendments and Reauthorization Act of 1986 (SARA) (Pub. L. 99-499).

B. Background

Section 313 of EPCRA requires certain facilities manufacturing,

processing, or otherwise using listed toxic chemicals in amounts above

reporting threshold levels, to report their environmental releases of

such chemicals annually. Beginning with the 1991 reporting year, such

facilities also must report pollution prevention and recycling data for

such chemicals, pursuant to section 6607 of the Pollution Prevention

Act of 1990 (PPA), 42 U.S.C. 13106. Section 313 established an initial

list of toxic chemicals that was comprised of more than 300 chemicals

and 20 chemical categories. MEK was included on the initial list.

Section 313(d) authorizes EPA to add or delete chemicals from the list,

and sets forth criteria for these actions. EPA has added and deleted

chemicals from the original statutory list. Under section 313(e)(1),

any person may petition EPA to add chemicals to or delete chemicals

from the list. Pursuant to EPCRA section 313(e)(1), EPA must respond to

petitions within 180 days, either by initiating a rulemaking or by

publishing an explanation of why the petition is denied.

EPCRA section 313(d)(2) states that a chemical may be listed if any

of the listing criteria are met. Therefore, in order to add a chemical,

EPA must demonstrate that at least one criterion is met, but does not

need to examine whether all other criteria are also met. Conversely, in

order to remove a chemical from the list, EPA must demonstrate that

none of the criteria are met.

EPA issued a statement of petition policy and guidance in the

Federal Register of February 4, 1987 (52 FR 3479), to provide guidance

regarding the recommended content and format for submitting petitions.

On May 23, 1991 (56 FR 23703), EPA issued guidance regarding the

recommended content of petitions to delete individual members of the

section 313 metal compounds categories. EPA has also published a

statement clarifying its interpretation of the section 313(d)(2) and

(3) criteria for adding and deleting chemical substances from the

section 313 list (59 FR 61432, November 30, 1994) (FRL-4922-2).

II. Description of Petition and Regulatory Status of Methyl Ethyl

Ketone

MEK is on the list of toxic chemicals subject to the annual release

reporting requirements of EPCRA section 313 and PPA section 6607. MEK

was among the list of chemicals placed under EPCRA section 313 by

Congress. MEK is subject to the Clean Air Act (CAA) as a volatile

organic compound (VOC) and a hazardous air pollutant. MEK is also on

the Hazardous Waste Constituents List under the Resource Conservation

and Recovery Act (RCRA).

On November 26, 1996, EPA received a petition from the Ketones

Panel of the Chemical Manufacturers Association (CMA), to delete MEK

from the list of chemicals reportable under EPCRA section 313 and PPA

section 6607. CMA had submitted a petition to delete MEK and methyl

isobutyl ketone (MIBK) from the EPCRA section 313 reporting

requirements in September 1988, but this petition was subsequently

withdrawn because the petitioner became aware of the Agency's concerns

for developmental toxicity and neurotoxicity. The current petitioner

states that since that time, EPA's concern for these effects has

decreased. Therefore, the petitioner argues that MEK does not meet any

of the listing criteria, and should be removed from the reporting

requirements of EPCRA section 313.

Specifically, the Panel believes that MEK is not known to cause,

nor can it reasonably be anticipated to cause, significant adverse

acute health effects at exposure levels that are likely to occur beyond

industrial site boundaries as a result of continuous or frequently

recurring releases. They also state that MEK ``is not known to cause

and cannot reasonably be anticipated to cause, significant chronic

health effects in humans.'' They state that EPA's Integrated Risk

Information System (IRIS) data base recognizes that MEK ``has little if

any neurotoxic potential.'' In addition, the Panel discusses in the

petition that based upon several developmental toxicity studies that

have been conducted, EPA should use a revised reference concentration

(RfC), based upon EPA modified guidance for conducting risk

assessments. The petitioner argues that MEK also does not cause the

type of adverse environmental effects that warrant reporting under

section 313.

Significant to the deliberations surrounding this petition review,

is MEK's status as a VOC. The petitioner argues for a revised

interpretation of the EPCRA section 313 VOC policy, contending that EPA

does not have the statutory authority to list chemicals based upon

``indirect'' toxicity. The petitioner further contends that: (1) There

are more effective ways to gather VOC emissions data; (2) EPA has

other, more efficient, tools than the Toxics Release Inventory (TRI)

for disseminating VOC emissions data; (3) TRI data are not used to

support VOC emissions control programs; (4) the act of including non-

toxic VOCs on the TRI may actually be counter productive, by providing

disincentives for switching to these less toxic VOCs; and, (5) releases

of MEK in ozone non-attainment areas do not justify a nationwide

reporting requirement (Ref. 1).

III. EPA's Technical Review of Methyl Ethyl Ketone

The technical review of the petition to delete MEK from the

reporting requirements of EPCRA section 313 included an analysis of the

available chemistry, health effects, ecological effects, and

environmental fate data for MEK.

A. Chemistry and Use

MEK, also known as 2-butanone, ethyl methyl ketone, and methyl

acetone, is the largest volume commercially produced ketone other than

acetone. It is a clear, colorless, stable, low-boiling (79.6 deg.C),

highly volatile (vapor pressure 90.6 torr at 25 deg.C) and highly

flammable (flash point 1 deg.C, autoignition temperature 515 deg.C)

liquid with an acetone-like odor. It is very soluble in water (240

grams per liter (g/l) at 20 deg.C), miscible with organic solvents,

and forms azeotropes with water and many organic liquids. MEK has

exceptionally high solvent power and is a good solvent for many natural

and synthetic resins. It is used as a solvent in the surface coatings

industry, specifically in vinyl lacquers, nitrocellulose lacquers, and

acrylics. It is used mainly in surface coatings and is also used as a

chemical intermediate. It is also used as a solvent for adhesives,

printing inks, degreasing and cleaning fluids, smokeless powder,

[[Page 15197]]

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

catalysts (Ref. 2).

Most MEK is produced by a two-step process from petroleum derived

butene/butane mixtures (Ref. 3). MEK is also available as a by-product

from liquid phase oxidation of butane to acetic acid and is produced by

direct oxidation of n-butenes.

There were 545 million pounds of MEK produced in the U.S. in 1994

and 16 million pounds were imported. Domestic production capacity is

projected to increase to 595 million pounds in 1997. Three producers,

Exxon Chemical, Hoechst-Celanese, and Shell Chemical, have been

identified. Domestic consumption was 388 million pounds in 1994. More

than half of the MEK consumed in the U.S. (60 percent) was used as a

solvent for protective coatings, as virtually all natural and synthetic

resins used in lacquers are soluble in MEK. The next largest use of MEK

(14 percent) was in solvent-based adhesives, such as rubber cement. MEK

was employed as a solvent in the manufacture of magnetic tapes (10

percent), and as a dewaxing agent in the refining of lubricating oil (5

percent). As a chemical intermediate (5 percent), MEK was used to

produce perfumes, antioxidants, catalysts, peroxides, and diacetal.

Three percent of the MEK consumed domestically was for printing ink,

while another three percent was used for miscellaneous purposes, such

as paint removal (Refs. 1 and 4).

Substitutes for MEK have been investigated by coating formulators

with mixed success. Alternative technologies include 100 percent

solvent products, water-based resins systems, and reformulated solvent

blends. Ethyl acetate in some cases is a drop-in substitute for MEK

with no significant change in properties. Butyl acetate and isobutyl

acetate can be used in many formulations as partial or full substitutes

for MEK. A blend of acetone and MIBK is also used as a MEK substitute.

Water-based and 100 percent solid coating systems may also be

substituted for MEK solvents. MEK is likely to remain in use,

particularly in high quality applications, unless alternative systems

are further developed (Ref. 4).

B. Metabolism and Absorption

MEK is well absorbed from the lung, gastrointestinal (GI) tract,

and skin. Pulmonary uptake in humans ranged from 41 percent to 56

percent. Case reports in humans and/or studies in rats demonstrate that

MEK is absorbed from the GI tract and the skin (Ref. 5).

C. Toxicological Evaluation

1. Acute toxicity. 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 (Ref. 6).

2. Subchronic and chronic toxicity. Available data indicate that

MEK has low chronic toxicity. Although no chronic exposure studies have

been found, several well-designed repeated-dose oral and inhalation

studies in laboratory animals demonstrate low systemic toxicity with

MEK. The Occupational Safety and Health Administration (OSHA)

Permissible Exposure Level (PEL) for MEK is 200 parts per million

(ppm), or about 589 milligrams per cubic meter (mg/m3).

EPA's current RfC of 1.0 mg/m3 (or approximately 968

milligrams per kilogram per day (mg/kg/day)) for MEK is based on a

developmental toxicity study in mice (Refs. 6 and 7).

a. Carcinogenicity. MEK is classified in EPA's IRIS data base (Ref.

8) as category D, not classifiable as to human carcinogenicity, based

on no human carcinogenicity data and inadequate animal data (Ref. 6).

b. Mutagenicity. There is a wealth of mutagenicity information on

MEK submitted pursuant to section 4 of the Toxic Substances Control Act

(TSCA). 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 UDS assay, for sister chromatid exchange (SCE's) in Chinese Hamster

Ovary (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 (Ref. 6).

c. Developmental toxicity. Not available at the time of the first

petition on MEK, is an inhalation developmental toxicity study in Swiss

mice. This is the key study, on which the RfC is based (Ref. 7). In the

study, four groups of 10 virgin and 33 pregnant mice were exposed to 0,

398, 1,010, or 3,020 ppm (0, 1,174, 2,978, or 8,906 mg/m3)

MEK for 7 hours per day (hr/day) during gestation days 6-15. Neither

maternal nor developmental toxicity was 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.

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

concern for developmental toxicity appears to be low. The Lowest

Observed Adverse Effect Level (LOAEL) is 3,020 ppm (approximately 2,898

mg/kg/day) and the No Observed Adverse Effect Level (NOAEL) is 1,010

ppm (968 mg/kg/day).

The two inhalation studies in rats that formed the basis of concern

at the time of the first petition were both conducted by the same group

of researchers and in the same laboratory. In the first study (Ref. 7),

animals were exposed to MEK at 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 LOAEL

from this study is 1,126 ppm.

The second study (Ref. 9) was conducted to determine the

repeatability of the above findings. Exposures to MEK were 0, 412,

1,002, or 3,005 ppm (0, 1,215, 2,955, or 8,861 mg/m3). 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 NOAEL from this study is 1,002 ppm, and the LOAEL is 3,005

ppm (Ref. 6).

d. Reproductive toxicity. Reproductive toxicity 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/sex/group) were

given 0, 0.3 percent, 1.0 percent, or 3.0 percent in drinking water

(Ref. 10). Because of significant toxicity seen in the high-dose group,

treatment of high-dose parents and offspring was reduced to 2.0

percent. The critical effect was decreased fetal birth weight at the

2.0 percent 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 percent (3,122 mg/kg/day) and the NOAEL is 1.0 percent

(1,771 mg/kg/day) (Ref. 6).

e. Neurotoxicity. According to the latest IRIS report on MEK, which

was updated in June 1993, ``at present, there is no convincing

experimental evidence

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that MEK is neurotoxic. . .other than possibly inducing central nervous

system depression at high exposure levels'' (Ref. 8). The prior

neurotoxicity concerns identified for MEK were based on enhancement of

the neurotoxicity of other solvents, such as n-hexane, by MEK (Ref.

11).

f. Toxicity related to ozone formation. MEK is a volatile organic

compound and, as such, has the potential to contribute to the formation

of ozone in the troposphere (i.e., the lower atmosphere). As EPA has

previously stated, ozone can affect structure, function, metabolism,

pulmonary defense against bacterial infection, and extrapulmonary

effects (Ref. 12). Among these extrapulmonary effects are: (1)

Cardiovascular effects; (2) reproductive and teratological effects; (3)

central nervous system effects; (4) alterations in red blood cell

morphology; (5) enzymatic activity; and (6) cytogenetic effects on

circulating lymphocytes.

3. Ecotoxicity. MEK is toxic to aquatic organisms at relatively

high concentrations. The fish 96-hour lethal concentration for 50

percent of the testing sample (LC50) range from 2,300 to

3,220 ppm; the daphnid 48-hour LC50s range from 2,200 to

5,091 ppm, and the green algal 96-hour effective concentration for 50

percent of the population (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. MEK's calculated

bioconcentration factor, 0.640, is low (Ref. 13).

As a VOC, MEK contributes to the formation of ozone in the

environment. As EPA has previously stated, ozone's effects on green

plants include injury to foliage, reductions in growth, losses in

yield, alterations in reproductive capacity, and alterations in

susceptibility to pests and pathogens (Ref. 12). Based on the known

interrelationships of different components of ecosystems, such effects,

if of sufficient magnitude, may potentially lead to irreversible

changes of sweeping nature to ecosystems.

D. Exposure Review

1. Exposure assessment. The available data indicate that MEK can

cause chronic developmental toxicity at moderately high to high doses.

Because there is a possibility that the developmental effects

associated with exposures to relatively high concentrations of MEK

could be caused by short-term exposures, an exposure assessment was

conducted. The exposure assessment was conducted only to determine the

potential for adverse chronic developmental effects to occur as a

result of concentrations of MEK that are reasonably likely to exist

beyond facility site boundaries as a result of continuous, or

frequently recurring, releases from facility sites (Ref. 14). For a

discussion of the use of exposure in EPCRA section 313 listing and

delisting decisions, refer to the Federal Register of November 30, 1994

(Ref. 12).

MEK releases were retrieved from the Toxics Release Inventory

System (TRIS) data base. There were 2,389 TRI reports submitted for MEK

in 1994. Most of the industrial releases are to air. Total quantities

released to air, water, and land in 1994 were 78,624,939 pounds,

108,163 pounds, and 51,794 pounds, respectively. Thus, since most

releases of MEK are to air, only airborne exposures were considered.

Furthermore, because the critical effect is developmental toxicity,

which can be initiated upon acute exposure, acute ambient

concentrations estimated by the Point Plume (PTPLU) model were the

exposure concentrations examined.

This procedure generates estimates of concentrations and exposures

under three different scenarios that include a variety of wind

conditions, one of which is a relatively stagnant situation. These

three scenarios have been labeled: (1) The typical scenario, (2) the

stagnant scenario, and (3) the maximum scenario. The model does not

consider decay of the chemical in the environment.

A combination of both conservative and non-conservative assumptions

were used to generate the exposure estimates with the PTPLU model. The

conservative assumptions include the use of weather station data known

to generate the highest concentrations and therefore potential

exposures, as well as the use of 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.

Estimates of acute ambient concentrations resulting from stack

releases from five discharging facilities range from 3.0 to 9.0 mg/

m3 for a ``typical'' scenario; 6.0 to 17.0 mg/m3

for a ``stagnant'' (no wind) scenario; and, 37 to 103 mg/m3

for the maximum scenario. Acute ambient concentrations resulting from

fugitive releases from five discharging facilities range from 5.0 to 12

mg/m3 for a typical scenario; 40.0 to 110 mg/m3

for a stagnant scenario; and, 100 to 240 mg/m3 for the

maximum scenario (Ref. 14).

2. Exposure evaluation. 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 for each type of release, fugitive and

stack. Release estimate data are evaluated as to whether they exceed an

Agency accepted RfC or reference dose (RfD), respectively, or when

appropriate, a Margin of Exposure (MOE).

The IRIS RfC for MEK is based on mild, but significant

developmental toxicity (decreased fetal body weight and misaligned

sternebrae). An RfC represents an estimate of a daily inhalation

exposure of the human population that is likely to be without

appreciable risk of deleterious effects during a lifetime. The RfC

makes adjustments to account for uncertainties about portal of entry

and long-term exposure effects. Because developmental effects are an

endpoint of concern for this chemical, it would not be appropriate to

use the RfC for assessing the potential risk of developmental toxicity

associated with acute exposure to MEK because the RfC is set for long-

term exposures. It would be appropriate to derive an RfCDT

and compare it to the estimated human exposure concentration; however,

there is no official Agency RfCDT. Therefore, a MOE approach

was used. The rationale for following this approach is that

developmental toxicity requires assessment of short-term exposures

(Ref. 6).

A MOE calculation is used in instances of non-cancer endpoints and

is essentially a ratio of the NOAEL and the estimated exposure to the

particular chemical, including any modifying factors on the exposure.

The resultant value is then compared to the product of the uncertainty

factors which are selected for the chemical of interest. Uncertainty

factors are generally factors of 10 with each factor representing a

specific area of uncertainty in the available data. For MEK, a factor

of 10 was used to account for the possible differences in

responsiveness between humans and animals in prolonged exposure

studies, and a second factor of 10 was used to account for variation in

susceptibility among individuals in the human population. The resultant

uncertainty factor of 100 was therefore used in this assessment (Ref.

6).

The calculated MOE includes the NOAEL (ca. 1,380 mg/kg/day) from

the mouse developmental study divided by the acute estimated Average

Potential

[[Page 15199]]

Dose Rates (APDRs). The MOE is greater than 100 for stack releases

under all three scenarios typical, stagnant, and maximum. The MOE is

greater than 100 for fugitive releases in all three scenarios except

one discharging facility under stagnant scenarios. 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 exposure characterization reflects

potential concerns engendered by estimated high exposures. Using these

assumptions, the assessment illustrated that exposure concentrations do

not exceed the MOE, except for one scenario (Ref. 6).

In summary, based on the concentrations likely to exist beyond

facility site boundaries and the resulting MOE calculations, there is

low concern for a potential for developmental effects for the general

population as a result of direct toxicity following acute inhalation

exposures to MEK. 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 developmental effects would be further

weakened, if not eliminated. Therefore, under the exposure conditions

described here, there appears to be low potential for developmental

effects associated with exposure to MEK (Ref. 6).

IV. Summary of Technical Review

The hazard assessment strongly indicates that, except for VOC

concerns, 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. The exposure assessment, conducted

only for developmental effects, indicates a low potential for these

effects to occur from reported releases of MEK from TRI facilities

under the conditions modeled. Thus, based on EPA's modeling, TRI

reported releases of MEK are not expected to be sufficient to cause the

type of high dose developmental effects associated with MEK. The

available data do indicate that MEK can enhance the neurotoxicity of

other solvents such as n-hexane; however, at this time EPA has not made

a final determination as to the significance of this effect with regard

to the EPCRA section 313(d)(2) criterion. MEK has low direct

environmental toxicity. MEK is however a high volume VOC that

contributes to the formation of tropospheric ozone which can cause

significant adverse effects to human health and the environment.

V. Rationale for Denial

EPA is denying the petition submitted by the Ketones Panel of the

CMA to delete MEK from the EPCRA section 313 list of toxic chemicals.

This denial is based on EPA's conclusion that VOCs, such as MEK,

contribute to the formation of tropospheric ozone which is known to

cause significant adverse effects to human health and the environment.

Therefore, EPA has concluded that MEK meets the listing criteria of

EPCRA section 313(d)(2)(B) and (C) because MEK contributes to the

formation of ozone which causes serious adverse human health and

environmental effects at relatively low doses. EPA has previously

stated that ozone meets the listing criteria of EPCRA section

313(d)(2)(B) and (C) (59 FR 61432, November 30, 1994). EPA has stated

in prior Federal Register notices (54 FR 4072, January 27, 1989; 54 FR

10668, March 15, 1989; 59 FR 49888, September 30, 1994; and 60 FR

31643, June 16, 1995) that because VOCs contribute to the formation of

tropospheric ozone they meet the criteria for listing under EPCRA

section 313. EPA has also stated (54 FR 4072, January 27, 1989 and 54

FR 10668, March 15, 1989) that while it is not EPA's intention to

include all VOC chemicals on the EPCRA section 313 list, those VOCs

whose volume of use or emissions are large enough to raise substantial

VOC concerns would be retained on the EPCRA section 313 list. MEK is a

VOC with both a high production volume and high air emissions.

Therefore, EPA has determined that MEK should remain on the EPCRA

section 313 list of toxic chemicals. EPA intends to provide further

clarification of its EPCRA section 313 VOC policy in a future Federal

Register notice.

EPA has previously determined (59 FR 61432, November 30, 1994) that

ozone has moderately high to high chronic toxicity and high

environmental toxicity. Therefore, in accordance with EPA's stated

policy on the use of exposure assessments (59 FR 61432, November 30,

1994), EPA does not believe that an exposure assessment is necessary to

conclude that MEK, since it contributes to the formation of ozone,

meets the toxicity criteria of EPCRA section 313(d)(2)(B) and (C).

EPA disagrees with the petitioner's contention that ``indirect

toxicity,'' such as that caused by VOCs, does not meet the EPCRA

section 313 listing criteria. The EPCRA section 313(d)(2) listing

criteria each state that EPA may list a chemical that it determines

``is known to cause or can reasonably be anticipated to cause'' the

relevant adverse human health or environmental effect. It further

provides that ``[a] determination under this paragraph shall be based

on generally accepted scientific principles.'' Ultimately, the crux of

the issue the petitioner raises lies in interpreting the phrase ``cause

or can reasonably be anticipated to cause,'' which Congress chose not

to define. In arguing that EPA lacks the statutory authority to base

its listing decisions on ``indirect toxicity,'' the petitioner would

have the Agency adopt an artificially narrow view of causation that

would require a single-step path between exposure to the toxic chemical

and the effect. Such a mechanistic approach confuses the mode or

mechanism of the chemical's action (i.e., the chain of causation) with

the fundamental question of whether, regardless of the number of

intervening steps, there is a natural and continuous line, unbroken by

any intervening causes, between exposure to the chemical and the toxic

effect. By contrast, EPA believes that Congress granted the Agency

broad discretion in making listing decisions and directed EPA to rely

on generally accepted scientific principles in making determinations to

implement this section of EPCRA.

It is a generally accepted scientific principle that causality need

not be linear, i.e., a one-step process (e.g., Proposed Guidelines for

Ecological Risk Assessment, September 9, 1996, 61 FR 47552 and 47586;

Proposed Guidelines for Carcinogen Risk Assessment, April 23, 1996, 61

FR 17960 and 17981). For purposes of EPCRA section 313, the distinction

between direct and indirect effects is technically an artificial one.

Whether the toxic effect is caused directly by a chemical by a one-step

process, or indirectly by a degradation product of the chemical or by a

second chemical that is created through chemical reactions involving

the first chemical, the toxic effect still occurs as a result of the

presence of the chemical in the environment. It makes no difference to

the affected organism whether the toxic agent was a result of chemical

reactions. Fundamentally, EPCRA section 313 is concerned with adverse

effects on humans and the environment, not the chain of causation by

which such effects occur. In fact, this type of ``indirect'' toxicity

is not unlike the effects of certain nonlinear carcinogens. Some

carcinogens induce

[[Page 15200]]

cancer through a two-step mechanism in which the chemical causes an

intervening pathological change, and this pathological change is the

direct cause of the cancer, but this does not mean that the chemical is

not known or reasonably anticipated to cause cancer. It is therefore

reasonable for EPA to consider such effects in light of the broad

statutory purpose to inform the public about releases to the

environment. Were EPA to exclude indirect effects from consideration,

it would dilute the purpose of the statute by precluding public access

to information about chemicals that cause a wide range of adverse

health and environmental effects.

VI. References

1. CMA. Petition of the Chemical Manufacturers Association Ketones

Panel to Delist Methyl Ethyl Ketone Under Section 313 of the Emergency

Planning and Community Right-to-Know Act of 1986. Chemical

Manufacturers Association. (November 27, 1996).

2. USEPA, OPPT. Tou, Jenny; ``Chemistry Report on Methyl Ethyl

Ketone, EPCRA 313 Delisting Petition.'' (March 10, 1997).

3. Kirk-Othmer Encyclopedia of Chemical Technology, 3rd. Edition,

Vol. 13 (1981), Vol. 21 (1983), and 4th Edition, Vol. 4 (1992), John

Wiley Sons, New York.

4. USEPA, OPPT. Wise, Sherry; ``Economic Analysis of the Proposed

Deletion of Methyl Ethyl Ketone from the EPCRA 313 List of Toxic

Chemicals.'' (February 10, 1997).

5. USEPA, OPPT. Keifer, Leonard; ``Absorption Review for Methyl

Ethyl Ketone (MEK).'' (January 22, 1997).

6. USEPA, OPPT. Hernandez, Oscar; ``Health Hazard Assessment:

Delist Petition for MEK.'' (June 1, 1997).

7. Schwetz, B.A., et al., ``Developmental Toxicity of Inhaled

Methyl Ethyl Ketone in Swiss Mice.'' Fund. and Appl. Toxicol. v. 16

(1991), pp. 742-748.

8. IRIS, 1993. U.S. Environmental Protection Agency's Integrated

Risk Information System file pertaining to methyl ethyl ketone.

9. Deacon, M.M., M.D. Pilny, J.A. John, et al., ``Embryo- and

Fetotoxicity of Inhaled Methyl Ethyl Ketone in Rats.'' Toxicol. Appl.

Pharmacol. v. 59. (1981), pp. 620-622.

10. Cox et al, 1975. ``Toxicity Studies in Rats with 2-Butanol

Including Growth, Reproduction and Teretologic Observations.'' Food and

Drug Research Laboratories, Inc. Rpt. 91MR-R 1673.

11. USEPA, OPPT. Memorandum from Lois Dicker, Ph.D., Chief,

Existing Chemicals Assessment Branch, Risk Assessment Division.

Subject: Review of the Interactive Effects of Methyl Ethyl Ketone (MEK)

with Neurotoxic Solvents: Response to OSHA/NIOSH Comments. (October 6,

1997).

12. USEPA. ``Addition of Certain Chemicals.'' Proposed rule, (59 FR

1788, January 12, 1994).

13. USEPA, OPPT. Nabholtz, J.V.; ``Delisting Petition for Methyl

Ethyl Ketone: Environmental Toxicity.'' (December 10, 1996).

14. USEPA, OPPT. Powers, Mary; ``Exposure Assessment for Methyl

Ethyl Ketone.'' (June 2, 1997).

VII. Administrative Record

The record supporting this decision is contained in docket control

number OPPTS-400119. All documents, including the references listed in

Unit VI. of this document and an index of the docket, are available to

the public in the TSCA Non-Confidential Information Center (NCIC), also

known as the Public Docket Office, from noon to 4 p.m., Monday through

Friday, excluding legal holidays. The TSCA NCIC is located at EPA

Headquarters, Rm. NE-B607, 401 M St., SW., Washington, DC 20460.

List of Subjects

Environmental protection, Community right-to-know, Reporting and

recordkeeping requirements, and Toxic chemicals.

Dated: March 19, 1998.

Lynn R. Goldman,

Assistant Administrator for Prevention, Pesticides and Toxic

Substances.

[FR Doc. 98-8208 Filed 3-27-98; 8:45 am]

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