[Federal Register Volume 64, Number 35 (Tuesday, February 23, 1999)]
[Proposed Rules]
[Pages 8769-8774]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 99-4320]
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ENVIRONMENTAL PROTECTION AGENCY
40 CFR Part 372
[OPPTS-400135; FRL-6050-3]
RIN 2070-AC00
Methyl Isobutyl 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 isobutyl ketone
(MIBK) 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 MIBK 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 MIBK meets the listing criteria of EPCRA section
313(d)(2)(B) 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
Coordinator, 202-260-3882 or e-mail: [email protected], for
specific information regarding this document or for further information
on EPCRA section 313, contact 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. General Information
A. Does This Notice Apply To Me?
This document does not make any changes to existing regulations,
however you may be interested in this document if you manufacture,
process, or otherwise use MIBK. Potentially interested categories and
entities may include, but are not limited to the following:
------------------------------------------------------------------------
Examples of Potentially
Category Interested Entities
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Chemical manufacturers Chemical manufacturers that
manufacture MIBK, use MIBK
as a chemical intermediate,
or use MIBK in the
manufacture of protective
coatings such as
nitrocellulose lacquers and
solvent-based vinyl and
acrylic coatings
------------------------------------------------------------------------
Chemical processors and users Facilities that use MIBK as
a process solvent
------------------------------------------------------------------------
This table is not intended to be exhaustive, but rather provides a
guide for readers regarding entities likely to be interested in this
document. Other types of entities not listed in this table may also be
interested in this document. Additional businesses that may be
interested in this document are those covered under 40 CFR part 372,
subpart B. If you have any questions regarding whether a particular
entity is covered by this section of the CFR, consult the technical
person listed in the ``FOR FURTHER INFORMATION CONTACT'' section.
B. How Can I Get Additional Information or Copies of This Document or
Other Support Documents?
1. Electronically. You may obtain electronic copies of this
document from the EPA Home Page at http://www.epa.gov/. On the Home
Page select ``Laws and Regulations'' and then look up the entry for
this document under the ``Federal Register - Environmental Documents.''
You can also go directly to the ``Federal Register'' listings at http:/
/www.epa.gov/fedrgstr/.
2. In person or by phone. If you have any questions or need
additional information about this action, please contact the technical
person identified in the ``FOR FURTHER INFORMATION CONTACT'' section.
In addition, the official record for this document, including the
public version, has been established under docket control number OPPTS-
400135, (including the references in Unit VII. of this preamble). This
record includes not only the documents physically contained in the
docket, but all of the documents included as references in those
documents. A public version of this record is available for inspection
from 12 noon to 4 p.m., Monday through Friday, excluding legal
holidays. The official record is located in the TSCA Nonconfidential
Information Center, Rm. NE-B607, 401 M St., SW., Washington, DC.
II. Introduction
A. Statutory Authority
This action is taken under sections 313(d) and (e)(1) of 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. Such facilities must also report pollution
prevention and recycling data for such chemicals, pursuant to section
6607 of the PPA of 1990, 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. MIBK 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, EPCRA section 313(d)(3)
requires EPA to find that none of the listing 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 in the
Federal Register of November 30, 1994 (59 FR 61432) (FRL-4922-2) a
statement clarifying its interpretation of
[[Page 8770]]
the section 313(d)(2) and (d)(3) criteria for modifying the section 313
list of toxic chemicals.
III. Description of Petition and Regulatory Status of Methyl
Isobutyl Ketone
MIBK is on the list of toxic chemicals subject to the annual
release reporting requirements of EPCRA section 313 and PPA section
6607. MIBK was among the list of chemicals placed under EPCRA section
313 by Congress. MIBK is also subject to Clean Air Act Amendments
(CAAA) and the Hazardous Waste Constituents List under the Resource
Conservation and Recovery Act (RCRA). MIBK is considered a volatile
organic compound (VOC) based on EPA's regulatory definition of a VOC
(57 FR 3941, February 3, 1992).
On April 23, 1997, EPA received a petition from the Ketones Panel
of the Chemical Manufacturers Association (CMA) to delete MIBK from the
list of chemicals reportable under EPCRA section 313 and PPA section
6607. CMA had submitted petitions to delete methyl ethyl ketone (MEK)
and MIBK from the EPCRA section 313 reporting requirements in September
1988, but these petitions were subsequently withdrawn because the
petitioner became aware of the Agency's concerns for various
toxicological effects of these chemicals. The petitioners state that
since that time, EPA's concern for the toxicity of MIBK has decreased.
Therefore, the petitioners argue that MIBK does not meet any of the
listing criteria, and should be removed from the reporting requirements
of EPCRA section 313.
Specifically, the petitioners believe that MIBK 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 MIBK is not known
to cause and cannot reasonably be anticipated to cause, significant
chronic health effects in humans. The petitioners argue that MIBK also
does not cause the type of adverse environmental effects that warrant
reporting under EPCRA section 313.
Significant to the deliberations surrounding this petition review,
is MIBK's status as a VOC. The petitioners argue for a revised
interpretation of the EPCRA section 313 VOC policy. The basis for this
argument is the petitioners contention that EPA does not have the
statutory authority to list chemicals based upon indirect toxicity. The
petitioners further contend 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 MIBK in ozone
non-attainment areas do not justify a nationwide reporting requirement
(Ref. 1).
IV. EPA's Technical Review Of Methyl Isobutyl Ketone
The technical review of the petition to delete MIBK from the
reporting requirements of EPCRA section 313 included an analysis of the
available chemistry, health effects, ecological effects, environmental
fate, exposure, and risk data for MIBK. Summaries of the technical
reviews are provided in Unit IV.A. through E. The docket for this
document contains additional information and more detailed discussions
concerning the data available for MIBK. The reader should consult the
support documents (Refs. 2, 3, 4, and 5) as well as the other studies
contained or referenced in the docket.
A. Chemistry and Use
MIBK, also known as, MIK, 4-methyl-2-pentanone, 2-methyl-4-
pentanone, and other names, is the second largest volume commercially
produced ketone. It is a clear, colorless, stable, moderately low
boiling, volatile, highly flammable liquid with a sweet, acetone-like
odor. It is moderately soluble in water (17 grams per liter (g/l) at 20
deg.C, is miscible with most organic solvents, and forms azeotropes
(i.e., mixtures that distill off in a fixed ratio) with water and many
organic liquids. MIBK has strong solvent power and is a good solvent
for many natural and synthetic resins (Ref. 2).
There were 163 million pounds of MIBK produced in the U.S. in 1996
and 25 million pounds were imported. Domestic production capacity is
projected to hold steady at 210 million pounds through 1999. Domestic
consumption was 148 million pounds in 1996. More than half of the MIBK
consumed in the U.S. (62 percent) was used as a solvent for protective
coatings. The next largest use of MIBK (18 percent) was as a chemical
intermediate for rubber antioxidants and acetylenic surfactants (Refs.
2 and 3).
B. Metabolism and Absorption
MIBK is well-absorbed from the lung, gastrointestinal (GI) tract,
and skin and is rapidly metabolized (Ref. 4).
C. Toxicological Evaluation
1. Acute toxicity. Available data indicate that MIBK has low acute
toxicity. In humans, short-term inhalation exposures up to 30 minutes
each day to concentrations as high as 500 parts per million (ppm)
produced irritation of the eyes and upper and lower respiratory system,
effects characteristic of solvent exposure (Ref. 4).
2. Subchronic and chronic toxicity. An assessment of direct
exposure systemic toxicity from available subchronic toxicity studies
on MIBK indicates that MIBK may cause liver and kidney toxicity.
However, without additional chronic data, the effects seen were not
considered to be serious or irreversible (Ref. 4).
i. Carcinogenicity. EPA was unable to identify any human or animal
carcinogenicity data on MIBK. Although MIBK was weakly positive in the
mouse lymphoma mutagenicity assay and in the mouse embryo cell
transformation assay, there is insufficient evidence to reasonably
extrapolate this information to anticipate that MIBK may cause cancer
in humans (Refs. 4 and 6).
ii. Mutagenicity. Studies indicate that MIBK is not a gene mutagen
in Salmonella typhimurium strains TA98, TA100, TA1535, and TA 1538
either with or without metabolic activation. MIBK is weakly positive in
mouse lymphoma cells in vitro without but not with activation, is not a
chromosome mutagen in vitro in Chinese hamster ovary and rat RL4 cells,
nor does it induce micronuclei in vivo in the mouse micronucleus assay
by intraperitoneal injection. MIBK does not induce DNA effects in the
Saccharomyces cerevisiae homozygosis and recombination assay, and it is
equivocal in the unscheduled DNA synthesis assay in rat hepatocytes in
vitro. MIBK induces morphological cell transformation in BALB/c 3T3
cell in culture without and possibly with metabolic activation. Thus,
in general, MIBK exposure does not appear to be associated with
genotoxicity in vitro or in vivo (Refs. 4 and 7).
iii. Developmental toxicity. MIBK was subject to testing under
section 4 of the Toxic Substances Control Act (TSCA). As part of the
testing requirements for MIBK, a developmental toxicity study in rats
and mice (Ref. 8) was previously submitted and reviewed by EPA (Ref.
4). EPA's 1985 review of the data concluded that MIBK caused
significant developmental toxicity (fetal death, reduced fetal body
weight, and delayed ossification) only at the high-dose of 3,000 ppm
(Ref. 9). No effects were observed at lower doses and a No
[[Page 8771]]
Observed Adverse Effect Level (NOAEL) of 1,000 ppm for both rats and
mice was derived. A Lowest Observed Adverse Effect Level (LOAEL) of
3,000 ppm was derived based on fetotoxicity in rats.
EPA's 1988 review of the same study concluded that in the rat study
there were statistically significant decreases in fetal body weight
(Ref. 10). In addition, it was noted that marginal decreases in fetal
body weight at the mid-dose of 1,000 ppm were observed when compared to
controls but they were not statistically significantly different and
were slightly higher than those in the low-dose group. It was concluded
in that review that MIBK induced developmental effects in rats with a
LOAEL of 300 ppm (the lowest dose tested). However, a statistical
evaluation of fetal body weight over the dose range tested concluded
that the significant reduction in fetal body weight per litter seen in
small litters at the low-dose group of 300 ppm was actually an artifact
of exceptionally heavy fetuses in two small litters in the control
group and therefore not treatment-related. The results of that
evaluation, coupled with the absence of effects at the mid-dose group
of 1000 ppm, argued against a dose-related decrease in fetal body
weight. Therefore, the LOAEL of 3,000 ppm and a NOAEL of 1,000 ppm
appear to be the more appropriate toxicity levels (Ref. 4).
iv. Reproductive toxicity. No reproductive/fertility studies
conducted with MIBK have been identified. The only information
available is from the 90-day inhalation toxicity study on MIBK (Ref.
11). In that study, organ weight and histological data in high-dose
rats and mice were comparable to controls for the ovaries, uterus,
oviducts, vagina, cervix, testis, epididymis, prostate, and seminal
vesicles. However, this is not sufficient information to characterize
the potential for reproductive toxicity of MIBK (Ref. 4).
v. Neurotoxicity. While MIBK alone appears to produce only
transient neurological effects at high doses, there is evidence that
MIBK enhances the neurotoxic effects of other compounds (Ref. 4). It
has been reported that simultaneous subchronic (90-days) exposure to
vapors of 1,000 ppm n-hexane and 100, 250, 500, or 1,000 ppm MIBK
markedly increased the neurotoxic action of n-hexane in hens (Ref. 12).
Another study also supports the suggestion that MIBK synergizes the
neurotoxic action of n-hexane by enhancing its metabolic activation
through induction of cytochrome P-450 enzymes (Ref. 13).
vi. Toxicity related to ozone formation. MIBK 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 (59 FR 1788, January 12, 1994), ozone can affect
structure, function, metabolism, pulmonary defense against bacterial
infection, and extrapulmonary effects. 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. MIBK is of low concern with respect to aquatic
toxicity based on measured toxicity data and quantitative structure
activity relationship (QSAR) analysis (Refs. 4 and 14). Measured
toxicity values include a fish 96-hour lethal concentration for 50
percent of the testing sample (LC50) of 780 milligrams per
liter (mg/L), a daphnid 24-hour LC50 of 4,300 mg/L and a
green algal 48-hour effective concentration for 50 percent of the
population (EC50) of 980 mg/L. Consistent with the measured
values, QSAR predicted acute toxicity resulted in a 96-hour
LC50 of 420 mg/L for fish and a 96-hour EC50 of
250 mg/L for green algal. The QSAR predicted chronic toxicity value for
fish is 47 mg/L, the daphnid chronic value is 15 mg/L, and the chronic
algal value is 16 mg/L. In addition, the 28-day bioconcentration factor
(BCF) of 0.5 is low.
As a VOC, MIBK contributes to the formation of ozone in the
environment. As EPA has previously stated (59 FR 1788, January 12,
1994), 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.
Based on 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. Toxicological Summary
The only toxicological studies that provide sufficient evidence
that MIBK can be reasonably anticipated to cause serious or
irreversible health effects from direct exposure are the developmental
toxicity studies. According to the EPA guidelines for developmental
toxicity risk assessment (1991), evidence of developmental toxicity in
a single animal study is sufficient to assume a potential hazard to
humans. These developmental studies indicate that MIBK has the
potential to cause developmental effects at moderately high to high
doses. Other types of health effects from direct exposure are not
considered either because the available data do not support a concern
that is consistent with the criteria, or the data are lacking. However,
as a VOC, MIBK contributes to the formation of tropospheric ozone which
can cause significant adverse effects to human health and the
environment.
E. Exposure Review
The available data indicate that MIBK can cause chronic
developmental toxicity at moderately high to high doses (i.e., MIBK has
low to moderately low toxicity). Because MIBK has low to moderately low
toxicity EPA believes it is appropriate to conduct an exposure
assessment. Since there is a possibility that the chronic developmental
effects associated with exposures to relatively high concentrations of
MIBK could be caused by short-term exposures, a short-term (i.e., acute
type) exposure assessment was conducted (Ref. 5). The exposure
assessment was conducted only to determine the potential for adverse
chronic developmental effects to occur as a result of concentrations of
MIBK that are reasonably likely to exist beyond facility site
boundaries. For a discussion of the use of exposure considerations in
modifying the EPCRA section 313 list of toxic chemicals, refer to the
Federal Register of November 30, 1994 (59 FR 61432).
1. Exposure assessment. Two exposure scenarios were considered,
ambient air exposures at or beyond the facility site boundary and
drinking water exposures due to releases to the surface water. The
estimates were derived through the use of 1994 annual release
information submitted under TRI and standard modeling techniques.
Releases reported for MIBK during 1994 were retrieved from the
Toxic Release Inventory System (TRIS) data base. According to TRIS,
more than 25,500,000 pounds of MIBK were released in 1994 from 1,031
sources nationwide. Of this amount, 27 percent was from fugitive or
nonpoint source emissions and 72 percent originated from stack or point
source emissions to the atmosphere (Ref. 5). In addition, lesser
amounts of MIBK (less than 1 percent) were released to surface waters,
underground injection of wastes, and the land.
The SCREEN3 and the Industrial Source Complex Short Term (ISCST3)
models were used to derive estimates of acute MIBK air concentrations
(Ref. 5). These acute models provided estimates
[[Page 8772]]
of concentrations of MIBK in the air for both 1 and 24 hours. The
ReachScan model was used to derive estimates of acute MIBK water
concentrations. These concentrations were used to calculate exposures
resulting from surface water releases to drinking water sources (Ref.
5).
The ambient air concentrations estimated are based on the
assumption that releases take place continuously over 365 days per
year; releases occurring over shorter periods will result in higher
concentrations. Ninety-nine percent of all MIBK released into the
environment is through stack (point) and fugitive (area) emissions into
the atmosphere (Ref. 5). The remaining one percent of releases go to
surface waters, landfill, and deep well injections.
Modeling data was used to estimate Average Potential Dose Rates
(APDRs) for MIBK. The inhalation APDRs range from 0.2 to 3.3
milligrams/kilogram/day (mg/kg/day) and the drinking water exposure
from the five facilities that result in the highest concentration in
surface waters ranged from 0.92 to 47 micrograms per liter (ug/L). The
resulting drinking water APDRs from these same sites ranged from 2.8
x 10-5 to 1.4 x 10-3 mg/kg/day.
2. Exposure evaluation. A margin of exposure (MOE) approach was
used in this assessment to describe potential risks associated with
exposure to MIBK (Ref. 4). The MOE is calculated as the ratio of the
NOAEL for developmental toxicity to the estimated exposure level. The
MOE does not provide an estimate of population risk, but simply
describes the relative distance between the exposuere level and the
NOAEL. The value of the MOE that is associated with a concern for toxic
effects is generally expressed as the product of the applicable
uncertainty and modifying factors; uncertainty factors that the Agency
considers for non-cancer effects are described in the Integrated Risk
Information System (IRIS) (1998). For consideration of developmental
toxicity, the applicable uncertainty factors are described in the
developmental toxicity guidelines (1991). These include two uncertainty
factors, one for consideration of intraspecies variation, and another
for interspecies variation. In accordance with EPA science policy, each
of these uncertainty factors is given a value of 10. Thus, for
developmental effects, an MOE greater than 100 would generally indicate
a low level of concern, whereas a value less than 100 is judged to be
of concern.
The rat NOAEL of 1,000 ppm from the inhalation developmental
toxicity study (6 hour exposures) was converted to an average daily
dose of 1,152 mg/kg/day. The NOAEL was then adjusted to a 24 hour
exposure duration (to achieve consistency with the exposure estimates,
which represent daily averages) and MOEs were calculated by dividing
the inhalation developmental toxicity NOAEL by the APDR estimates for
each of the top discharging facilities. MOEs for the highest single
hour of the year were not derived since the animal dose from the
inhalation developmental toxicity study was defined on a daily basis
and since there were uncertainties in the relevance of this scenario as
a descriptor of anticipated exposures. The relevant exposure scenario
for the pregnant female was defined in the exposure assessment as time
spent at home, 23.7 hours/day at exposures resulting from releases from
MIBK to air (stack and fugitive) for the highest single day of the
year. However, an exposure scenario duration of 23.7 hours/day spent
inside a residence may not characterize the target population. To
complement the analysis, an exposure duration of 16.4 hours spent
inside a residence was also evaluated. In addition, there were concerns
about the uncertainty introduced by comparing time spent indoors to
outdoor ambient air concentrations of MIBK. Therefore, the recommended
value of 2 hours/day spent outdoors at a residence was also evaluated
(Ref. 15). The MOEs for the exposure durations depicted were greater
than 100 for all of the top discharging facilities for exposure
estimates derived with the ISCST3 model, while corresponding MOEs based
on estimates obtained with the SCREEN3 model were lower than 100. The
ISCST3 model allows for the use of more site-specific data, in this
case wind speed, and therefore estimates of exposure obtained using
this model provide more relevant information.
The APDR estimates for acute exposures resulting from surface water
releases for the top five discharging facilities range from 2.8 x
10-5 to 1.4 x 10-3 mg/kg/day; the MOE values
for these estimates range from 1.7 x 108 to 3.3 x
106. Therefore, the MOE is greater than 100 for acute
exposures resulting from surface water releases for all of the top
discharging facilities (Ref. 4).
In summary, based on the concentrations likely to exist beyond
facility site boundaries and the resulting MOE calculations from the
exposure conditions described here, there is low concern for a
potential for developmental effects for the general population
following acute inhalation exposures to MIBK (Ref. 4).
V. Summary of Technical Review
The hazard assessment indicates that, except for VOC concerns, MIBK
has low acute and chronic (systemic) toxicity in that effects occur
only at high doses (3,000 ppm.). Based on information currently
available, all toxicity endpoints examined, except for developmental
toxicity, did not appear to meet the listing criteria for EPCRA section
313. A screening level risk assessment for developmental toxicity
indicated low risk based on modeled potential acute exposures to women
living in communities near release sites. Thus, based on EPA's
modeling, TRI reported releases of MIBK are not expected to be
sufficient to cause the type of high dose developmental effects
associated with MIBK. The available data do indicate that MIBK 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)
criteria. MIBK has low direct environmental toxicity. MIBK 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.
VI. Rationale for Denial
EPA is denying the petition submitted by the Ketones Panel of the
Chemical Manufacturers Association to delete MIBK from the EPCRA
section 313 list of toxic chemicals. This denial is based on EPA's
conclusion that VOCs, such as MIBK, 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
MIBK meets the listing criteria of EPCRA section 313(d)(2)(B) and
(d)(2)(C) because MIBK 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 (d)(2)(C) (59 FR
61432, November 30, 1994), and that because VOCs contribute to the
formation of tropospheric ozone they meet the criteria for listing
under EPCRA section 313 (54 FR 4072, January 27, 1989; 54 FR 10668,
March 15, 1989; 59 FR 49888, September 30, 1994; 60 FR 31643, FRL-4952-
7, June 16, 1995; and 63 FR 15195, FRL-5752-6, March 30, 1998). 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
[[Page 8773]]
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. MIBK is a VOC with both a
high production volume and high air emissions, therefore, EPA has
determined that MIBK should remain on the EPCRA section 313 list of
toxic chemicals.
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 appropriate
for determining that MIBK meets the toxicity criteria of EPCRA section
313(d)(2)(B) and (d)(2)(C) based on its contribution to the formation
of ozone.
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). And 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 cancer through a multiple-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.
VII. References
1. CMA, 1996. Petition of the Chemical Manufacturers Association
Ketones Panel to Delist Methyl Isobutyl Ketone Under Section 313 of the
Emergency Planning and Community Right-to-Know Act of 1986. Chemical
Manufacturers Association. (April 27, 1997).
2. USEPA, OPPT. Tou, Jenny; ``Chemistry Report on Methyl Isobutyl
Ketone, EPCRA 313 Delisting Petition.'' (August 10, 1997).
3. USEPA, OPPT. Rice, Cody, ``Economic Analysis of the Proposed
Deletion of Methyl Isobutyl Ketone from the EPCRA 313 List of Toxic
Chemicals.'' (May 20, 1997).
4. USEPA, OPPT. Anitole, Katherine; ``Hazard/Risk Assessment of
Methyl Isobutyl Ketone'' (November 24, 1997).
5. USEPA, OPPT. Brennan,Tom and Cinalli, Christina, ``Exposure
Assessment for Methyl Isobutyl Ketone.'' (August 14, 1997). Docket
control number OPPTS-400110 contains the references cited in this
document.
6. USEPA, OPPT. Memorandum from David Lai, Ph.D., Existing
Chemicals Assessment Branch, Risk Assessment Division, to Katherine
Anitole, Ph.D., Existing Chemicals Assessment Branch, Risk Assessment
Division. Subject: Hazard Assessment of Methyl Isobutyl Ketone (MIBK)
in Response to Petition for Delisting in TRI: Carcinogenicity. (June
27, 1997).
7. USEPA, OPPT. Memorandum from Michael C. Cimino, Ph.D., Science
Support Branch, Risk Assessment Division, to Katherine Anitole, Ph.D.,
Existing Chemicals Assessment Branch, Risk Assessment Division.
Subject: Delisting Petition for Methyl Isobutyl Ketone (MIBK):
Mutagenicity Hazard. (June 23, 1997).
8. Tyl, R.W., et al., ``Developmental Toxicity Evaluation of
Inhaled Methyl Isobutyl Ketone in Fischer 344 Rats and CD-1 Mice.''
Fund. Appl. Toxicol. v. 8, (1987), p. 310.
9. USEPA, OTS. Memorandum from Myron S. Ottley, Ph.D., Toxic
Effects Branch, Health and Environmental Review Division, to Jim
Kariya, Chemical Review and Evaluation Branch, Health and Environmental
Review Division. Subject: Review of Developmental Toxicity Data on
Methyl Isobutyl Ketone. (January 18, 1985).
10. USEPA, OTS. Memorandum from Marlissa Campbell, Toxic Effects
Branch, Health and Environmental Review Division, to Elbert Dage,
Chemical Review and Evaluation Branch, Health and Environmental Review
Division. Subject: Review of the Potential Developmental Toxicity of
methyl Isobutyl Ketone (MIBK). (1988).
11. Phillips, R.O., et al., ``A 14-Week Vapor Inhalation Study of
Methyl Isobutyl Ketone.'' Fund. Appl. Toxicol. v. 9, (1987), p.380.
12. Abou-Donia, M. et al., ``The Joint Neurotoxic Action of Inhaled
Methyl Butyl Ketone Vapor and Dermally Applied o-Ethyl-o-4-Nitrophenyl
Phenylphosphonothioate in Hens: Potentiating Effect.'' Toxicol. Appl.
Pharmacol. v. 79, (1985), pp. 69-82.
13. Habig, C., Abou-Donia, M., Lapadula, D., ``Cytochrome P-450
Induction in Chickens Exposed Simultaneously to N-Hexane and Methyl
IsoButyl Ketone.'' The Toxicologist v. 9, (1989), p. 194.
14. USEPA, OPPT. Memorandum from Jerry Smrcheck, Existing Chemicals
Assessment Branch, Risk Assessment Division, to Katherine Anitole,
Existing Chemicals Assessment
[[Page 8774]]
Branch, Risk Assessment Division. Subject: Ecological Hazard of MIBK.
(June 26, 1997).
15. USEPA, ORD. 1997. Exposure Factors Handbook, Office of Research
and Development, National Center for Environmental Assessment, U.S.
Environmental Protection Agency, Washington, DC, (1997): EPA/600/P-95/
002(Fa-Fc).
List of Subjects in 40 CFR Part 372
Environmental protection, Community right-to-know, Reporting and
recordkeeping requirements, and Toxic chemicals.
Dated: February 12, 1999.
Susan H. Wayland,
Acting Assistant Administrator for Prevention, Pesticides and Toxic
Substances.
[FR Doc. 99-4320 Filed 2-22-99; 8:45 am]
BILLING CODE 6560-50-F