[Federal Register Volume 63, Number 60 (Monday, March 30, 1998)]
[Notices]
[Pages 15195-15200]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 98-8208]


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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

[[Page 15198]]

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]
BILLING CODE 6560-50-F