Methyl Ethyl Ketone; Toxic Chemical Release Reporting; Community
Right-to-Know
[Federal Register: March 30, 1998 (Volume 63, Number 60)]
[Notices]
[Page 15195-15200]
From the Federal Register Online via GPO Access [wais.access.gpo.gov]
[DOCID:fr30mr98-78]
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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: bushman.daniel@epamail.epa.gov,
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/m<SUP>3</SUP>).
EPA's current RfC of 1.0 mg/m<SUP>3</SUP> (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/m<SUP>3</SUP>)
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/m<SUP>3</SUP> ). 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/m<SUP>3</SUP>). 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 (LC<INF>50</INF>) range from 2,300 to
3,220 ppm; the daphnid 48-hour LC<INF>50</INF>s range from 2,200 to
5,091 ppm, and the green algal 96-hour effective concentration for 50
percent of the population (EC<INF>50</INF>) 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/
m<SUP>3</SUP> for a ``typical'' scenario; 6.0 to 17.0 mg/m<SUP>3</SUP>
for a ``stagnant'' (no wind) scenario; and, 37 to 103 mg/m<SUP>3</SUP>
for the maximum scenario. Acute ambient concentrations resulting from
fugitive releases from five discharging facilities range from 5.0 to 12
mg/m<SUP>3</SUP> for a typical scenario; 40.0 to 110 mg/m<SUP>3</SUP>
for a stagnant scenario; and, 100 to 240 mg/m<SUP>3</SUP> 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 RfC<INF>DT</INF>
and compare it to the estimated human exposure concentration; however,
there is no official Agency RfC<INF>DT</INF>. 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