[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
------------------------------------------------------------------------
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