[Federal Register Volume 68, Number 225 (Friday, November 21, 2003)]
[Proposed Rules]
[Pages 65648-65663]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 03-28787]
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ENVIRONMENTAL PROTECTION AGENCY
40 CFR Part 63
[OAR-2003-0188; FRL-7587-5]
RIN A2060-0013
List of Hazardous Air Pollutants, Petition Process, Lesser
Quantity Designations, Source Category List
AGENCY: Environmental Protection Agency (EPA).
ACTION: Proposed rule.
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SUMMARY: The EPA proposes to amend the list of hazardous air pollutants
(HAP) contained in section 112(b)(1) of the Clean Air Act (CAA) by
removing the compound ethylene glycol monobutyl ether (EGBE) (2-
Butoxyethanol) (Chemical Abstract Service (CAS) No. 111-76-2) from the
group of glycol ethers. Today's action is being taken in response to a
petition to delete EGBE from the HAP list submitted by the Ethylene
Glycol Ethers Panel of the American Chemistry Council (formerly the
Chemical Manufacturers Association) on behalf of EGBE producers and
consumers. Petitions to delete a substance from the HAP list are
permitted under section 112(b)(3) of the CAA.
The proposed rule is based on EPA's evaluation of the available
information concerning the potential hazards and projected exposures to
EGBE. We have made an initial determination that there are adequate
data on the health and environmental effects of EGBE to determine that
emissions, ambient concentrations, bioaccumulation, or deposition of
EGBE may not reasonably be anticipated to cause adverse human health or
environmental effects. Today's action includes a detailed rationale for
removing EGBE from the glycol ethers group of HAP under section
112(b)(1) list of HAP.
DATES: Comments. Written comments on the proposed rule must be received
by January 20, 2004.
Public Hearing. A public hearing will be held if requests to speak
are received by the EPA on or before December 8, 2003. If requested, a
public hearing will be held on December 19, 2003.
ADDRESSES: Comments. Comments may be submitted electronically, by mail,
or through hand delivery/courier. Electronic comments may be submitted
on-line at http://www.epa.gov/edocket/. Written comments sent by U.S.
mail should be submitted (in duplicate if possible) to: Air and
Radiation Docket and Information Center (Mail Code 6102T), Attention
Docket ID Number
[[Page 65649]]
OAR-2003-0188, Room B108, U.S. EPA, 1200 Pennsylvania Avenue, NW.,
Washington, DC 20460. Written comments delivered in person or by
courier should be submitted (in duplicate if possible) to: Air and
Radiation Docket and Information Center (Mail Code 6102T), Attention
Docket ID Number OAR-2003-0188, Room B102, U.S. EPA, 1301 Constitution
Avenue, NW., Washington, DC 20460. The EPA requests a separate copy
also be sent to the contact person listed below (see FOR FURTHER
INFORMATION CONTACT).
Public Hearing. If a public hearing is requested by December 8,
2003 the public hearing will be held at the new EPA facility complex,
Research Triangle Park, NC December 19, 2003. Persons interested in
presenting oral testimony should contact Ms. Kelly A. Rimer, Risk and
Exposure Assessment Group, Emission Standards Division (C404-01), U.S.
EPA, Research Triangle Park, North Carolina 27711, telephone number
(919) 541-2962 at least two days in advance of the hearing.
FOR FURTHER INFORMATION CONTACT: Ms. Kelly A. Rimer, Risk and Exposure
Assessment Group, Emission Standards Division (C404-01), U.S. EPA,
Research Triangle Park, NC 27711, telephone number (919) 541-2962,
electronic mail address [email protected].
SUPPLEMENTARY INFORMATION:
Regulated Entities. Entities potentially affected by today's action
are those industrial facilities that manufacture or use EGBE. Today's
action proposes to amend the list of HAP contained in section 112(b)(1)
of the CAA by removing the compound EGBE.
Docket. The EPA has established an official public docket for this
action under Docket ID Number A-99-24 and Electronic Docket ID Number
OAR-2003-0188. The official public docket is the collection of
materials that is available for public viewing at the EPA Docket Center
(Air Docket), EPA West, Room B-108, 1301 Constitution Avenue, NW.,
Washington, DC 20004. The Docket Center is open from 8:30 a.m. to 4:30
p.m., Monday through Friday, excluding legal holidays. The telephone
number for the Reading Room is (202) 566-1744, and the telephone number
for the Air Docket is (202) 566-1742. All items may not be listed under
both docket numbers, so interested parties should inspect both docket
numbers to ensure that they have received all materials relevant to the
proposed rule.
Electronic Access. An electronic version of the public docket is
available through EPA's electronic public docket and comment system,
EPA Dockets. You may use EPA Dockets at http://www.epa.gov/edocket/ to
submit or view public comments, access the index of the contents of the
official public docket, and access those documents in the public docket
that are available electronically. Once in the system, select
``search'' and key in the appropriate docket identification number.
Certain types of information will not be placed in the EPA dockets.
Information claimed as confidential business information (CBI) and
other information whose disclosure is restricted by statute, which is
not included in the official public docket, will not be available for
public viewing in EPA's electronic public docket. The EPA's policy is
that copyrighted material will not be placed in EPA's electronic public
docket but will be available only in printed paper form in the official
public docket. Although not all docket materials may be available
electronically, you may still access any of the publicly available
docket materials through the EPA Docket Center.
For public commenters, it is important to note that EPA's policy is
that public comments, whether submitted electronically or in paper,
will be made available for public viewing in EPA's electronic public
docket as EPA receives them and without change unless the comment
contains copyrighted material, CBI, or other information whose
disclosure is restricted by statute. When EPA identifies a comment
containing copyrighted material, EPA will provide a reference to that
material in the version of the comment that is placed in EPA's
electronic public docket. The entire printed comment, including the
copyrighted material, will be available in the public docket.
Public comments submitted on computer disks that are mailed or
delivered to the docket will be transferred to EPA's electronic public
docket. Public comments that are mailed or delivered to the docket will
be scanned and placed in EPA's electronic public docket. Where
practical, physical objects will be photographed, and the photograph
will be placed in EPA's electronic public docket along with a brief
description written by the docket staff.
Comments. You may submit comments electronically, by mail, by
facsimile, or through hand delivery/courier. To ensure proper receipt
by EPA, identify the appropriate docket identification number in the
subject line on the first page of your comment. Please ensure that your
comments are submitted within the specified comment period. Comments
submitted after the close of the comment period will be marked
``late.'' The EPA is not required to consider these late comments.
Electronically. If you submit an electronic comment as prescribed
below, EPA recommends that you include your name, mailing address, and
an e-mail address or other contact information in the body of your
comment. Also include this contact information on the outside of any
disk or CD ROM you submit and in any cover letter accompanying the disk
or CD ROM. This ensures that you can be identified as the submitter of
the comment and allows EPA to contact you in case EPA cannot read your
comment due to technical difficulties or needs further information on
the substance of your comment. The EPA's policy is that EPA will not
edit your comment and any identifying or contact information provided
in the body of a comment will be included as part of the comment that
is placed in the official public docket and made available in EPA's
electronic public docket. If EPA cannot read your comment due to
technical difficulties and cannot contact you for clarification, EPA
may not be able to consider your comment.
Your use of EPA's electronic public docket to submit comments to
EPA electronically is EPA's preferred method for receiving comments. Go
directly to EPA Dockets at http://www.epa.gov/edocket, and follow the
online instructions for submitting comments. Once in the system, select
``search'' and key in Docket ID No. OAR-2003-0188. The system is an
``anonymous access'' system, which means EPA will not know your
identity, e-mail address, or other contact information unless you
provide it in the body of your comment.
Comments may be sent by electronic mail (e-mail) to [email protected], Attention Docket ID No. OAR-2003-0188. In contrast to
EPA's electronic public docket, EPA's e-mail system is not an
``anonymous access'' system. If you send an e-mail comment directly to
the docket without going through EPA's electronic public docket, EPA's
e-mail system automatically captures your e-mail address. E-mail
addresses that are automatically captured by EPA's e-mail system are
included as part of the comment that is placed in the official public
docket and made available in EPA's electronic public docket.
You may submit comments on a disk or CD ROM that you mail to the
mailing address identified in this document. These electronic
submissions will be accepted in WordPerfect or ASCII file
[[Page 65650]]
format. Avoid the use of special characters and any form of encryption.
By Mail. Send your comments (in duplicate, if possible) to: EPA
Docket Center (Air Docket), U.S. EPA West, (MD-6102T), Room B-108, 1200
Pennsylvania Avenue, NW., Washington, DC 20460, Attention Docket ID No.
OAR-2003-0188.
By Hand Delivery or Courier. Deliver your comments (in duplicate,
if possible) to: EPA Docket Center, Room B-108, U.S. EPA West, 1301
Constitution Avenue, NW., Washington, DC 20004, Attention Docket ID No.
OAR-2003-0188. Such deliveries are only accepted during the Docket
Center's normal hours of operation.
By Facsimile. Fax your comments to: (202) 566-1741, Docket ID No.
OAR-2003-0188.
CBI. Do not submit information that you consider to be CBI through
EPA's electronic public docket or by e-mail. Send or deliver
information identified as CBI only to the following address: Kelly
Rimer, c/o Roberto Morales, Office of Air Quality Planning and
Standards (OAQPS) Document Control Officer (C404-02), U.S. EPA, 109 TW
Alexander Drive, Research Triangle Park, NC 27709, Attention Docket ID
No. OAR-2003-0188. You may claim information that you submit to EPA as
CBI by marking any part or all of that information as CBI (if you
submit CBI on disk or CD ROM, mark the outside of the disk or CD ROM as
CBI and then identify electronically within the disk or CD ROM the
specific information that is CBI). Information so marked will not be
disclosed except in accordance with procedures set forth in 40 CFR part
2.
Worldwide Web (WWW). In addition to being available in the docket,
an electronic copy of today's proposed rule will also be available on
the WWW through the Technology Transfer Network (TTN), on the TTN's
policy and guidance page for newly proposed or promulgated rules at
http://www.epa.gov/ttn/oarpg. The TTN provides information and
technology exchange in various areas of air pollution control. If more
information regarding the TTN is needed, call the TTN HELP line at
(919) 541-5384.
Outline. This preamble is organized as follows:
I. Background
II. Criteria for Delisting
III. EPA Analysis of the Petition
A. Background
B. Exposure Assessment
C. Human Health Effects of EGBE
D. Human Health Risk Characterization and Conclusions
E. Ecological Risk Characterization and Conclusions
F. Transformation Characterization
G. Public Comments
H. Conclusions
IV. Statutory and Executive Order Reviews
A. Executive Order 12866: Regulatory Planning and Review
B. Paperwork Reduction Act
C. Regulatory Flexibility Act (RFA)
D. Unfunded Mandates Reform Act
E. Executive Order 13132: Federalism
F. Executive Order 13175: Consultation and Coordination With
Indian Tribal Governments
G. Executive Order 13045: Protection of Children From
Environmental Health Risks and Safety Risks
H. Executive Order 13211: Actions Concerning Regulations That
Significantly Affect Energy Supply, Distribution, or Use
I. National Technology Transfer and Advancement Act
I. Background
Section 112 of the CAA contains a mandate for EPA to evaluate and
control emissions of HAP. Section 112(b)(1) includes a list of 188
specific chemical compounds and classes of compounds that Congress
identified as HAP. The EPA must evaluate the emissions of substances on
the HAP list to identify source categories for which the Agency must
establish emission standards under section 112(d). We are required to
periodically review the list of HAP and, where appropriate, revise the
list by rule. In addition, under section 112(b)(3), any person may
petition us to modify the list by adding or deleting one or more
substances. A petitioner seeking to delete a substance must demonstrate
that there are adequate data on the health and environmental effects of
the substance to determine that emissions, ambient concentrations,
bioaccumulation, or deposition of the substance may not reasonably be
anticipated to cause any adverse effects to human health or the
environment. A petitioner must provide a detailed evaluation of the
available data concerning the substance's potential adverse health and
environmental effects and estimate the potential exposures through
inhalation or other routes resulting from emissions of the substance.
On August 29, 1997, the American Chemistry Council's Ethylene
Glycol Ethers Panel submitted a petition to delete EGBE (CAS No. 111-
76-2) from the HAP list in CAA section 112(b)(1), 42 U.S.C.,
7412(b)(1). Following the receipt of the petition, we conducted a
preliminary evaluation to determine whether the petition was complete
according to Agency criteria. To be deemed complete, a petition must
consider all available health and environmental effects data. A
petition must also provide comprehensive emissions data, including peak
and annual average emissions for each source or for an appropriately
selected subset of sources, and must estimate the resulting exposures
of people living in the vicinity of the sources. In addition, a
petition must address the environmental impacts associated with
emissions to the ambient air and impacts associated with the subsequent
cross-media transport of those emissions. After receiving additional
submittals through December 21, 1998, we determined the petition to
delete EGBE to be complete. We published a notice of receipt of a
complete petition in the Federal Register on August 3, 1999 and
requested information to assist us in technically reviewing the
petition.
We received eight submissions in response to our request for
comment and information which would aid our technical review of the
petition. The comments made general statements encouraging EPA to
delist EGBE. None of the comments included technical information.
II. Criteria for Delisting
Section 112(b)(2) of the CAA requires us to make periodic revisions
to the initial list of HAP set forth in section 112(b)(1) and outlines
criteria to be applied in deciding whether to add or delete particular
substances. Section 112(b)(2) identifies pollutants that should be
listed as:
* * * pollutants which present, or may present, through inhalation
or other routes of exposure, a threat of adverse human health
effects (including, but not limited to, substances which are known
to be, or may reasonably be anticipated to be, carcinogenic,
mutagenic, teratogenic, neurotoxic, which cause reproductive
dysfunction, or which are acutely or chronically toxic) or adverse
environmental effects whether through ambient concentrations,
bioaccumulation, deposition, or otherwise * * *
Section 112(b)(3) of the CAA establishes general requirements for
petitioning the Agency to modify the HAP list by adding or deleting a
substance. Although the Administrator may add or delete a substance on
his or her own initiative, the burden is on a petitioner to include
sufficient information to support the requested addition or deletion
under the substantive criteria set forth in section 112(b)(3)(B) and
(C).
The Administrator must either grant or deny a petition to delist a
HAP within 18 months of receipt of a complete petition. If the
Administrator decides to deny a petition, the Agency publishes a
written explanation of the basis for denial in the Federal Register.
[[Page 65651]]
A decision to deny a petition is final Agency action subject to review.
If the Administrator decides to grant a petition, the Agency publishes
a written explanation of the Administrator's decision, along with a
proposed rule to add or delete the substance. The proposed rule is open
to public comment and public hearing, and all additional substantive
information received is considered prior to the issuance of a final
rule.
To delete a substance from the HAP list, section 112(b)(3)(C)
provides that the Administrator must determine that:
* * * there is adequate data on the health and environmental effects
of the substance to determine that emissions, ambient
concentrations, bioaccumulation of deposition of the substance may
not reasonably be anticipated to cause any adverse effects to the
human health or adverse environmental effects.
We do not interpret CAA section 112(b)(3)(C) to require absolute
certainty that a pollutant will not cause adverse effects on human
health or the environment before it may be deleted from the list. The
use of the terms ``adequate'' and ``reasonably'' indicate that the
Agency must weigh the potential uncertainties and likely significance.
Uncertainties concerning the risks of adverse health or environmental
effects may be mitigated if we can determine that projected exposures
are sufficiently low in relation to levels where adverse effects may
occur to provide reasonable assurance that such adverse effects will
not occur. Similarly, uncertainties concerning the magnitude of
projected exposures may be mitigated if we can determine that the
levels which might cause adverse health or environmental effects are
sufficiently high to provide reasonable assurance that exposures will
not reach harmful levels. However, the burden remains on a petitioner
to demonstrate that the available data support an affirmative
determination that emissions of a substance may not be reasonably
anticipated to result in adverse effects on human health or the
environment. The EPA will not remove a substance from the list of HAP
based merely on the inability to conclude that emissions of the
substance will cause adverse effects on human health or the
environment. As a part of the requisite demonstration, a petitioner
must resolve any critical uncertainties associated with missing
information. We will not grant a petition to delete a substance if
there are major uncertainties that need to be addressed before we would
have sufficient information to make the requisite determination.
III. EPA Analysis of the Petition
A. Background
The broad category of glycol ethers (GE) are general solvents, also
known as cellosolves. In 2000, ethylene glycol monobutyl ether made up
an estimated 45 percent of the total GE production in the U.S. (or
325,000-350,000 tons). It is a colorless liquid with a mild, rancid
odor. It is soluble in most organic solvents and mineral oil. It mixes
with acetone, benzene, carbon tetrachloride, ethyl ether, n-heptane and
water, and it is miscible with many ketones, ethers, alcohols, aromatic
paraffin, and halogenated hydrocarbons.
Ethylene glycol monobutyl ether is used in hydraulic fluids and as
a coupling agent for water-based coatings. It is used in vinyl and
acrylic paints and varnishes and as a solvent for varnishes, enamels,
spray lacquers, dry cleaning compounds, textiles, and cosmetics.
Ethylene glycol monobutyl ether is a solvent for grease and grime in
industrial cleaning. It is also used as a freeze-thaw agent in latex
paints and emulsions, and as an intermediate in the production of
esters, ethers, alkoxy alkyl halides, polyether alcohols, hemiacetals
and acetals.
The petition states that EGBE released to the air has a half life
of 3 to 33 hours. However, the California Air Resources Board (CARB)
reports an EGBE half-life of 14 to 22 hours. The midpoint in these
ranges of both these half-lives is 18 hours, and we used this value in
our analysis as it represents a reasonable estimate of the half-life of
EGBE. The petition identifies the principal oxidation products of EGBE
as n-butyl formate, 2-hydroxyethyl formate, propionaldehyde, 3-
hydroxybutyl formate, and several isomeric forms of an organic nitrate
compound. Only one of these compounds (i.e., propionaldehyde) is a
listed HAP. However, the formate esters are known to transform in the
atmosphere into formaldehyde, which is another listed HAP. In addition,
propionaldehyde undergoes further transformation to formaldehyde and
acetaldehyde (which is also a HAP).
The portion of EGBE that does not degrade to secondary products in
the air, rapidly partitions to soil and water. Once in soil, EGBE is
further decomposed through biotic processes, but it has been estimated
that as much as 35 percent of the EGBE deposited on soil can eventually
move to water. Due to its low volatility, high solubility, low vapor
pressure, and minimal tendency to bind to sediments, once in surface
water EGBE tends to remain dissolved until it biodegrades (half life =
1 to 4 weeks). It has a low bioconcentration factor, therefore, it is
not anticipated to accumulate in the environment or in food stuffs.
Its relatively rapid biodegradation in water indicates that humans
are unlikely to be exposed to significant amounts of EGBE in drinking
water. However, the fact that EGBE released to the air preferentially
partitions to water does raise a question concerning the risk from EGBE
ingestion originating from air releases. Based on our review of the
available information on EGBE, we have concluded that inhalation and
ingestion are the important routes of nonoccupational exposures
resulting from EGBE emissions, and consider these two routes of
exposure in evaluating this petition.
B. Exposure Assessment
As a first step in evaluating the petition's inhalation risk
assessment, we reviewed the petitioner's emissions inventory upon which
the modeling was based. The petitioner used the 1993 Toxics Release
Inventory (TRI) as a starting point to identify emissions of GE,
including EGBE. To locate facilities emitting EGBE which were not
included in the TRI, the petitioner searched EPA's TTN to identify
regulatory documentation that might contain EGBE emissions data. This
documentation includes information on recently promulgated maximum
control technology (MACT) standards, information on area sources, and
consumer and commercial product Volatile Organic Compounds (VOC) rules.
The petitioner searched the National Air Toxics Clearinghouse which
contains a database of State air toxic programs identifying those
States with active air toxics programs and those that collected
chemical specific data and contacted the State agencies for data. The
petitioner also contacted 12 trade associations concerned with the use
of EGBE to obtain data regarding industry use of EGBE and/or GE.
Lastly, the petitioner contacted facilities known to be large EGBE
emission sources to obtain specific modeling data, such as emission
rates, stack height, distance to fence line.
After reviewing the petitioner's inventory, we have concluded that
the methods used to identify sources of EGBE emissions are adequate and
provide a reasonable representation of the EGBE emissions. To evaluate
the overall completeness of the inventory, we compared the petition's
list of EGBE emission sources to EPA's 1996 National Toxics Inventory
(NTI), which is now called the National Emissions Inventory (NEI). We
found the
[[Page 65652]]
petitioner's inventory to be comparable to the NTI. Therefore, we
conclude that the petitioner's emissions inventory provides an adequate
basis for dispersion modeling and the exposure assessment and is
acceptable for that purpose.
The petitioner used a modification of the air dispersion modeling
approach described in EPA's ``Tiered Modeling Approach for Assessing
Risk due to Sources of Hazardous Air Pollutants'' (EPA-450/4-92-001)
(Tiered Approach) to develop predictions of the maximum annual
concentrations for the EGBE emission sources identified in its
inventory. The petitioner's modifications of the Tiered Approach first
consisted of conducting an ``inverted tier 1'' assessment before the
petitioner conducted a standard tier 1 analysis. The EPA's tier 1
conservatively predicts the air concentration from a facility when few
data are available. The required inputs are: Estimates of annual
emission rate, distance to fence line and whether the release is from a
point or area source. The result of tier 1 is a maximum annual
concentration for the pollutant assessed. The petitioner used the
inverted tier 1 approach in order to identify an emission rate that
would result in a specified maximum annual concentration. The
petitioner could then estimate, for a large number of facilities, what
emission rates would result in the specified maximum concentration. All
facilities who emitted EGBE in amounts that resulted in the specified
maximum concentration would then be brought forth to the next level of
analysis. In our review of this approach, we have determined that it is
reasonable, and would tend to overestimate rather than underestimate
maximum annual ambient average concentrations. This is because the
petitioner used a combination of a ground level emission release and a
50 meter distance to fence line, which are assumptions that would tend
to overstate impacts. Also, the petitioner chose to use a maximum
annual ambient average concentration of 3 milligrams per cubic meter
(mg/m\3\) as the cut-off for a facility to be brought forward to a more
detailed analysis. The value the petitioner chose as a cut-off is far
below the EPA inhalation reference concentration, which is a peer-
reviewed value defined as an estimate (with uncertainty spanning
perhaps an order of magnitude) of a daily inhalation exposure to the
human population (including sensitive subgroups) that is likely to be
without appreciable risk of deleterious noncancer effects during a life
time. Given that the current EPA Inhalation Reference Concentration
(RfC) is 13 mg/m\3\, using 3 mg/m\3\ as a cutoff resulted in a greater
number of facilities being brought into the more detailed analysis.
This increases our confidence that the exposure assessment will likely
over-rather than under-estimate the actual maximum annual ambient
average concentrations of EGBE.
All 3,439 sources in the inventory went through the inverted tier 1
analysis. Of those, 286 showed maximum annual ambient average
concentrations of EGBE of 3 mg/m\3\ or greater. The petitioner included
these 286 sources in the next level of analysis, the standard tier 1
analysis described above.
Upon review, we determined the petitioner appropriately applied the
tier 1 analysis and correctly identified 64 sources as showing a
maximum annual ambient average concentration of 3 mg/m\3\ or greater.
These sources moved on to the next phase of the analysis.
This next phase is the petitioner's second modification to the
standard EPA Tiered Approach. It includes a probabilistic modeling
exercise along with a decision analysis method (CARTSCREEN). The
petitioner employed these methods as an additional screening tool for
sources whose maximum annual average ambient concentrations of EGBE
that, according to the tier 2 analysis, are predicted to exceed 3 mg/
m\3\, but that may not warrant a tier 2 or 3 analysis. The petitioner
first constructed a distribution of values of additional source
parameters, for example, stack diameter, exit temperature and velocity.
The model randomly selected a value for each input from that
distribution of values, constructing a hypothetical facility, before
running SCREEN3. This procedure was repeated a total of 25,000 times.
The results of this probabilistic modeling exercise were imported into
the decision tool CARTSCREEN along with data from actual facilities, in
order to complete the data set. The results of CARTSCREEN showed which
facilities would emit EGBE in amounts that result in maximum annual
average ambient concentrations of 3 mg/m\3\ or greater. Of the 64
facilities for which this analysis was conducted, 41 sources moved on
to the tier 2 analysis.
We have determined that the assumptions and parameter selection
underlying this modification are consistent with the objectives of the
EPA tiered approach. The modeling component of this approach used
SCREEN3, which is a regulatory model developed and used by the EPA. In
addition, we have determined that CARTSCREEN uses well established
decision tree methods which are appropriately applied here.
The petitioner brought forth the 41 sources from the previous
iteration, and added 29 sources back into the tier 2 analysis because
there were enough data to do so. The petitioner added these 29
facilities back into the analysis in order to be conservative, even
though these facilities produce hazards below the 3 mg/m\3\ cutoff
established by the petitioner. The petitioner used EPA's SCREEN3 model
and followed EPA's Guidance on Air Quality models (40 CFR part 51,
appendix W), the EPA's Tiered Modeling Guidance, and SCREEN3
documentation. The tier 2 analysis required the following information
for each facility: annual EGBE emission rate; release type (point,
area, volume) release height; inside stack diameter; stack gas exit
velocity and temperature; horizontal distance across area or volume
sources; terrain, land use (urban or rural); and building dimensions.
The petitioner included the raw data for the dispersion model analysis
and the model outputs. The results showed that maximum predicted annual
average ambient concentration of EGBE ranged from near 0 mg/m\3\ to 37
mg/m\3\.
We reviewed the data, verified the appropriateness of the model and
facility input parameters, and evaluated the model outputs for several
emissions sources selected at random. Our evaluation confirmed that the
petitioner applied appropriate EPA guidelines in the dispersion
modeling analysis and that the predicted maximum annual EGBE
concentrations were consistent with the objective of the tier 2
analysis.
Two sources had predicted concentrations over 3 mg/m\3\. However,
the petitioner included five facilities in the tier 3 analysis, in
order to include the two largest EGBE emissions sources identified in
the inventory. The analysis used EPA's Industrial Source Complex Short
Term Model, Version 3 (ISCST3) model and followed EPA's Guidance on Air
Quality models, the EPA's Tiered Modeling Guidance, and ISCST3
documentation. In addition to the release inputs used in tier 2, the
ISCST3 model requires emissions information for all emission points,
(SCREEN3 makes the simplifying assumption that all emissions come out
of 1 stack), fence line data, 5 years of meteorological data, and a
receptor grid. The petitioner used the regulatory default mode. The
results showed that the maximum annual average ambient concentration
(regardless of fence line) resulting from a single major source's
emissions of EGBE is 0.3 mg/m\3\. (A major source is a source that
emits greater than 10 tons
[[Page 65653]]
per year (tpy) of EGBE or 25 tpy of EGBE combined with other HAP.)
We have determined that the petitioner performed the dispersion
modeling analysis following appropriate modeling guidance. Based on our
technical review of the various emission modeling components, we have
confirmed that the highest predicted maximum annual average off-site
concentration (i.e., the maximum annual level occurring over 5 years)
of EGBE for any individual major source facility does not exceed 0.3
mg/m\3\. We judge that these estimates are more likely to over predict
than under predict actual exposures due to the health-protective
assumptions made in the analysis. Based on the information provided in
the petition on EGBE emissions, we evaluated the potential impact of
emission sources within close proximity to each other. First, we looked
at the emissions from closely located major sources. Based on our
evaluation, we concur with the petitioner that the maximum annual EGBE
concentration from closely located major sources is expected to be no
greater than 0.07 mg/m\3\.
Next, we evaluated the petitioner's modeling approach for closely
located area sources (i.e., sources emitting less than 10 tpy EGBE
located 500 meters from each other). We determined that the assumptions
underlying the petitioner's model were conservative, and that the
maximum estimated annual concentration of EGBE from area sources is
likely to be no greater than 0.5 mg/m\3\. We note that this
concentration is higher than the maximum annual ambient average
concentration predicted from either a major source or a group of
closely located major sources. This is not unexpected as smaller
sources can have emission release characteristics that can result in
higher impacts to the surrounding communities. For example, while
smaller sources may emit less EGBE, they may also have shorter stack
heights, or fence lines that are closer to the emission points. Also,
people may live closer to a smaller facility.
We reviewed the literature and various EPA databases to assess the
potential contribution of the ambient background EGBE to the maximum
annual concentration of EGBE. Subsequently, we determined that EGBE
monitoring data that could be used to determine the background EGBE
level are not available. We, therefore, proceeded to evaluate the
petitioner's background estimation approaches. Based on our evaluation,
we have determined that both approaches provide acceptable, yet
conservative estimates. Therefore, we have concluded that the ambient
background concentration of EGBE is not likely to have a significant
influence on maximum annual exposures to EGBE.
To summarize the air quality modeling component of the inhalation
exposure assessment, the petitioner provided a tiered modeling analysis
of EGBE emissions using EPA guidelines and models. The analysis was
performed following acceptable modeling guidance. Based on a detailed
technical review of the analyses, it is our conclusion that model
inputs, assumptions, and results provide a conservative representation
of EGBE sources. The modeling analysis demonstrated that the maximum
annual concentration of EGBE was no greater than 0.3 mg/m\3\ from a
single major source, 0.07 mg/m\3\ from a cluster of major sources, and
0.5 mg/m\3\ from a cluster of area sources.
We judge the petition's overall approach to exposure assessment to
be acceptable. The use of the maximum annual average ambient
concentration for each emission source to characterize the exposed
population provides a conservative approach to chronic exposure
modeling. Furthermore, based on our experience, we judge that a refined
exposure assessment estimating exposures for actual people living near
these facilities would result in maximum individual exposures
significantly lower than the maximum annual average ambient approach.
Given the likely proximity of inhabitable areas and the variability of
human activity patterns over an annualized time period, it is our
expectation that actual maximum individual exposure would be at least a
factor of 2 less than predicted by the models and at least an order of
magnitude below EPA's RfC.
After evaluating the petitioner's ingestion exposure scenarios, we
determined that the scenarios were acceptable and that the human
exposure parameters used to calculate a person's average daily intake
were conservative. However, as a part of our assessment of potential
ecological risk due to EGBE emissions, we had previously derived an
independent estimate of the concentration of EGBE in a water body
situated at the point of the maximum annual average EGBE concentration
from the largest emission source in the petitioner's inventory. This
estimate was approximately 28 times greater than that presented in the
petition. Therefore, based on this estimate, we were concerned that the
petitioner's estimation method was not sufficiently conservative, and
we carried out the following analysis described below.
Our estimation of EGBE in surface water was a worst-case estimate.
It was derived using a Mackay Level III fugacity model to estimate the
steady state equilibrium concentration of a known volume (i.e., 1,000
kilograms per hour (kg/h) of EGBE released to the atmosphere in each of
four environmental media: Air, soil, sediment, and water. The EGBE
concentration predicted in air was then ratioed with the maximum
concentration predicted for a single major source from the petitioner's
ISCST3 model (i.e., 0.3 mg/m\3\) of the largest emission source to
develop a scaling factor. The EGBE concentration in water as predicted
by the Mackay model was then multiplied by the scaling factor to
predict EGBE concentrations in a water body situated at the point of
the maximum annual average EGBE concentration. The results yielded an
estimated concentration of 3.6 milligrams per liter (mg/L) of EGBE in
the water body.
We consider these results to be very conservative (i.e., worst
case) because numerous variables were not taken into consideration
that, if considered, were likely to reduce estimates of EGBE in water.
For example, we did not consider degradation in the water, nor did we
consider that the body of water would have to be continuously exposed
at the fence line concentration across its entire surface to approach
this predicted concentration. Therefore, we do not anticipate surface
water concentrations greater that 3.6 mg/L to occur as a result of
airborne deposition of EGBE.
Even though we do not feel that surface water concentrations would
approach 3.6. mg/L, we used this worst case estimate, to recalculate
the average daily intake for each of the age groups in each exposure
scenario. For the Residential Scenario involving the ingestion of EGBE
in drinking water, we calculated an average daily intake of 0.1
milligram per kilogram per day (mg/kg/day) for adults and 0.2 mg/kg/day
for children of both age groups. For the Residential Scenario involving
dermal contact with EGBE during bathing and showering, we determined an
average daily intake of 0.00003 mg/kg/day for adults, 0.0004 mg/kg/day
for older children, and 0.0005 mg/kg/day for younger children. For the
Recreational Scenario involving incidental ingestion of EGBE in surface
water while swimming, we calculated an average daily intake of 0.0007
mg/kg/day for adults, 0.04 mg/kg/day for older children, and 0.03 mg/
kg/day for younger children. Lastly, for the
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Recreational Scenario involving dermal contact with EGBE in surface
water, we calculated an average daily intake of 0.0003 mg/kg/day for
adults, 0.0002 mg/kg/day for older children, and 0.0006 g/kg/day for
younger children.
Combining the Residential and Recreational Scenarios for each of
the age groups provided a worst-case exposure scenario. The average
daily intake for the combined worst case are: Adults 0.1 mg/kg/day,
older children 0.3 mg/kg/day, and younger children 0.3 mg/kg/day. Based
on this analysis, we have concluded that exposures to EGBE arising from
the ingestion of surface water exposed may not reasonably be
anticipated to exceed 0.3 mg/kg/day, and would be significantly less.
C. Human Health Effects of EGBE
The petitioner used the 1997 draft Integrated Risk Information
System (IRIS) assessment as the basis for their human health effects
evaluation of EGBE. Since then, the IRIS assessment has been completed
(in 1999) and more recent toxicological information on EGBE has become
available. Therefore, rather than evaluating the information presented
in the petition, we focus our evaluation of EGBE's health effects on
the more recent data.
We used the IRIS toxicological database to evaluate the human
health effects associated with exposures to EGBE, and to identify an
appropriate human health criterion for the risk characterization (IRIS,
1999). Specifically, we used the toxicological data presented in
support of the IRIS RfC and Inhalation Reference Concentration and
reference dose (RfD) which is contained in The Toxicological Review of
Ethylene Glycol Monobutyl Ether (EGBE). This document is electronically
available via EPA's IRIS Page at http://www.epa.gov/iris. The IRIS is
the Agency's official repository of consensus human health risk
information. It was created and is maintained by the Agency to provide
assistance to Agency decision makers on the potential adverse human
health effects of particular substances. In addition, EPA scientists
have investigated and analyzed information on the human carcinogenic
potential of EGBE that was published after the IRIS assessment was
final. We had our evaluation of the new information peer reviewed by
experts external to the agency, and we use this evaluation to help us
draw conclusions about the potential for EGBE to cause cancer in humans
(see docket for EPA's August, 2003 Interim Final Report, ``An
evaluation of the Human Carcinogenic Potential of Ethylene Glycol Butyl
Ether''). Based on these reviews, we have determined that adequate data
concerning the potential health effects of EGBE are available and are
of sufficient quality to use as the basis for deciding whether or not
to delete EGBE.
The IRIS reports that the reproductive toxicity of EGBE has been
studied in a variety of well conducted oral and inhalation studies
using rats, mice, and rabbits. In addition, several developmental
studies have addressed EGBE toxicity from conception to sexual maturity
including toxicity to the embryo and fetus, following oral and dermal
exposures to rats, mice, and rabbits. Ethylene glycol monobutyl ether
was not found to cause adverse effects in any reproductive organs in
any study. In a two generational reproductive toxicity study, fertility
was reduced in mice only at very high (maternally toxic) doses.
Maternal toxicity related to the adverse effects on red blood cells
(called hematologic effects) due to exposure to EGBE and relatively
minor developmental effects have been reported in developmental
studies. We conclude from these studies that EGBE is not significantly
toxic to reproductive organs of parents, male or female. In addition,
no teratogenic toxicities were noted in any of the studies. Therefore,
we also conclude that EGBE is not significantly toxic to developing
fetuses of laboratory animals.
Our review of the IRIS assessment confirmed that hemotologic
effects is the primary response in sensitive species following
inhalation, oral, or dermal administration of EGBE. The reported
sensitivities range from that of the guinea pig which displays no
hemolytic effects from EGBE at exposures levels as high as 1,000 mg/kg
(oral) or 2,000 mg/kg (dermally) to the rat which displays increased
sensitivity at single-inhalation exposures below 100 parts per million
(ppm) (483 mg/m\3\) and single oral exposures below 100 mg/kg. No
hemolysis has been observed in controlled laboratory acute inhalation
exposures of human volunteers up to 195 ppm (941.9 mg/m\3\) and
reversible hemolytic effects have been observed in a case where humans
consumed single oral doses of 400 to 1,500 mg/kg of EGBE.
Data considered in the IRIS toxicological review, primarily from
acute and in vitro studies, indicate that humans are significantly less
sensitive to the hemolytic toxicity of EGBE than typical laboratory
species such as mice, rats, or rabbits. While studies of chronically
exposed humans are lacking, several laboratory animal studies have
demonstrated this, as have in vitro studies using either whole blood or
washed red blood cells. In addition, blood from potentially sensitive
individuals, including the elderly and those persons with congenital
hemolytic disorder such as sickle-cell anemia or hereditary
spherocytosis, does not show an increased hemolytic response when
incubated with EGBE's active metabolite, 2-butoxyacetic acid (BAA).
The principal study used to determine the EGBE RfC is a 2-year
bioassay that involved groups of F344 rats exposed to 0, 31, 125, and
500 ppm EGBE in air for 12 months (6 hours/day, 5 days/week). Female
rats exposed to the three highest concentrations at all exposure
durations developed clinical signs consistent with hemolytic effects
associated with EGBE exposures. A Lowest Observed Adverse Effects Level
(LOAEL) of 31 ppm (149.7 mg/m\3\) was identified in this study for
hematologic and histopathologic effects in female rats.
The human equivalent concentration (HEC) was calculated using the
standard RfC approach, a physiologically based pharmacokinetic (PBPK)
approach, a benchmark concentration (BMC) approach, and a PBPK/BMC
approaches combined. The PBPK/BMC approach was determined by the IRIS
Peer Review Panel to provide the best estimate of a HEC because it
incorporated much of the mechanistic information available for EGBE,
best characterized the dose-response relationship for EGBE-induced
hematologic effects, and reduced the potential uncertainties to the
greatest extent. The HEC as determined by the PBPK/BMC method was then
reduced by a series of uncertainty factors to derive the RfC. An
overall uncertainty factor (UF) of 30 was applied to account for
extrapolation from an adverse effect (UF = 3) and to account for the
variation in the sensitivity within the human population (UF = 10).
The principal study for the ingestion Rfd involved groups of 10
female F344 rats exposed to 750, 1,500, 3,000, 4,500, and 6,000 ppm of
EGBE via drinking water for 13 weeks. Decreases in body weight were
observed in female rats exposed to the two highest dose levels. The
study results show hematologic changes at all dose levels after 13
weeks that were indicative of mild to moderate anemia. Using this
study, EPA calculated human equivalent doses (HED) using all four
approaches. We selected the PBPK/BMD approach for the derivation of the
RfD because it incorporated much of the mechanistic information
available for EGBE, best characterized the dose-response relationships
for EGBE-induced hematologic effects, and reduced the potential
uncertainties to the greatest extent. Using the HED from the PBPK/
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BMC model, and a total UF of 10 to account for variation in sensitivity
within the human population (UF = 10), the EPA determined that the IRIS
RfD was 0.5 mg/kg/day.
The IRIS review states that EGBE has been adequately tested in
conventional genotoxicity tests for its potential to induce gene
mutations in in vitro systems and cytogenetic damage in both in vitro
and in vivo systems. The available data do not support a mutagenic or
clastogenic potential for EGBE. The EPA's Toxicological Review of EGBE,
available at http://www.epa.gov/iris/toxreviews/0500-tr.pdf#page=68,
states that one laboratory has reported weak genotoxicity responses at
toxic doses, though these data are considered to be questionable, may
be a result of impurities in the test material.
In addition, the 1999 IRIS describes structure-activity
relationship (SAR) analyses that have been conducted to provide insight
into EGBE's potential carcinogenicity to humans. These analyses have
been found to be useful for agents that are believed to initiate
carcinogenesis through Deoxyribonucleic Acid (DNA) reactive mechanisms.
Based on chemical structure, EGBE does not resemble any known chemical
human carcinogens and is not expected to have electrophilic or DNA
reactive activity. The IRIS review states that there are no reliable
epidemiologic studies available that address the potential
carcinogenicity of EGBE.
The IRIS review utilized a draft report of the results of a 2-year
inhalation bioassay performed by the National Toxicology Program (NTP,
1998) using rats and mice that had recently become available. The NTP
(1998) report indicates no evidence of carcinogenic activity in male
F344/N rats, and equivocal evidence of carcinogenic activity in female
F344/N rats based on increased combined incidences of benign and
malignant pheochromocytoma (mainly benign) of the adrenal medulla. They
also reported some evidence of carcinogenic activity in male B6C3F1
mice based on increased incidences of hemangiosarcoma of the liver, and
some evidence of carcinogenic activity in female B6C3F1 mice based on
increased incidences of forestomach squamous cell papilloma or
carcinoma (mainly papilloma).
The IRIS discusses the relevance of these tumors to humans. For
example, the phenochromocytoma in the female rats were indicated as
only a marginally significant trend. Further, these types of tumors are
difficult to distinguish from non-neoplastic adrenal medullary
hyperplasia, and therefore need to be interpreted with caution. The
hemangiosarcoma in livers of male mice appear to be exposure related.
However, the increases were slight and, like the forestomach lesions in
female mice, were not observed in any other sex or species. There is
also evidence to suggest that these cancer lesions in mice are
associated with unique aspects of mouse physiology (i.e., the known
increased sensitivity of mice to oxidative stress and the existence of
a forestomach), and are secondary to noncancer (i.e., hemolysis and
forestomach irritation) effects.
The IRIS concludes that because of the uncertain relevance of these
tumor increases to humans, the fact that EGBE is generally negative in
genotoxic tests, and the lack of human data to support the findings in
rodents, the human carcinogenic potential of EGBE, in accordance with
the recently proposed Guidelines for Carcinogen Risk Assessment (U.S.
EPA, 1996a), cannot be determined at this time, but suggestive evidence
exists from rodent studies. Therefore, under existing EPA guidelines,
EGBE is judged to be a possible human carcinogen.
Since the publication of NTP's draft report (NTP, 1998) on their 2-
year inhalation bioassay of EGBE, and since the IRIS update of December
1999, there has been continued discussion among scientists from
government, industry, and academia concerning the human carcinogenic
potential of EGBE. The NTP (2000a) finalized their study results
without changing their original determination of equivocal evidence of
carcinogenic activity in female rats, some evidence of carcinogenic
activity in male mice, and some evidence of carcinogenic activity in
female mice. These findings by NTP, along with the EPA's conclusion in
the 1999 IRIS assessment that the carcinogenic potential of EGBE
``cannot be determined at this time, but suggestive evidence exists
from rodent studies'', prompted scientists from academia and industry
to design research projects aimed at determining the mode of action for
the formation of the forestomach and liver tumors observed in mice. We
report here on recent findings in scientific publications, from
scientific meetings and in the EPA (1999b) draft cancer guidelines, to
provide an up-to-date evaluation of the mode of action involved in the
origin of these tumors in mice and their human relevance.
Establishing the mode of action is critical for determining an
effect's relevance to humans and for choosing the approach most
appropriate for dose-response modeling (i.e., whether to use a linear
or nonlinear approach). As is extensively discussed in the Agency's
interim and draft cancer guidelines (U.S. EPA. 1999b; 2003), in order
to determine a chemical's mode of action, one must consider the full
range of key influences a chemical or its metabolites might have as an
initiator or promoter of the complex carcinogenic process. With this in
mind, we evaluated EGBE's role in the formation of female mouse
forestomach and male mouse liver tumors that were observed following
two-years of inhalation exposure (National Toxicology Program, 2000a).
Our August 2003 interim final report provides details of this
evaluation.
With regard to forestomach papillomas and carcinoma in female mice,
the NTP study (NTP 2000a) shows that at the highest exposure level, 250
ppm, the 10 percent incidence of squamous papilloma and 12 percent
combined incidence of squamous cell papillomas or carcinomas were
significantly increased over study controls and exceeded the ranges for
historical controls of 0-2 percent and 0-3 percent, respectively. This
study reports that 8 percent is the highest incidence of forestomach
neoplasms that has been observed in contemporary historical controls.
NTP (2000a) did not observe significant increases in forestomach
papillomas and carcinomas at any other exposure levels in female mice,
nor at any exposure level in male mice or either sex of rats.
Recent reviews of available in vitro and in vivo genotoxicity
assays are in agreement that EGBE is not likely to be genotoxic
(Commonwealth of Australia, 1996; Elliot and Ashby, 1997; U.S. EPA,
1999a; NTP, 2000a). The NTP (2000a)) suggested that EGBE caused chronic
irritation leading to forestomach injury including penetrating ulcers
and that the observed ``neoplasia (papillomas and one carcinoma) was
associated with a continuation of the injury/degeneration process.''
The Agency believes that EGBE is not genotoxic and that a nonlinear
mode of action is principally responsible for the increased forestomach
tumor incidence reported by NTP (2000a). However, reports of weak
positive effects by EGBE at high concentrations in some in vitro assays
(see discussion in full report located in the docket under ``Other
Possible Modes of Action for Forestomach Tumor Development in Female
Mice'') indicate the potential for contribution from direct interaction
of butoxyacetaldehyde (BAL), an EGBE metabolite, with DNA. While these
weak positive findings may be due to study design artifacts (e.g.,
changes in
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pH or osmolarity associated with high EGBE concentrations), they may
indicate contribution from BAL which has caused clastogenic changes in
Chinese hamster lung (v79) and human lymphocyte cells (Elliot and
Ashby, 1997). As we discuss in the full report, available evidence from
a published EGBE PBPK model that has been modified to include kinetics
for the metabolism of the BAL intermediate (Corley, 2003) suggests that
the conditions of these in vitro assays (e.g., no metabolic activation;
high, cytotoxic concentrations of BAL) are of little relevance to
expected target organ (forestomach) environment (e.g., high metabolic
activity; low concentrations of BAL). However, additional research
(e.g., verification of these PBPK modeling results and further
genotoxicity research using more appropriate assays and currently
accepted test protocols) would be beneficial to provide a more
definitive determination regarding the role of BAL in the formation of
forestomach tumors in female mice.
We conclude that the available data establish a plausible
nonlinear, nongenotoxic mode of action for the moderate increase
observed by NTP (2000a) in the incidence of forestomach tumors in
female mice following chronic inhalation exposure to EGBE. Forestomach
tissue irritation caused by constant exposure to EGBE and its
metabolites and subsequent cell proliferation appear to be key
precursor events in the mode of action for these tumors. While certain
dosimetric processes and morphological aspects of the forestomach make
rodents particularly susceptible to these events, we judge this mode of
action to be of qualitative relevance to humans. However, due to the
lack of a comparable organ for storage and the long term retention of
EGBE, the exposure concentrations that would be necessary to cause
hyperplastic effects and tumors in humans, if attainable, are likely to
be much higher than the concentrations necessary to cause forestomach
effects in mice. In fact, our analysis indicates that the exposure
concentrations necessary to cause hyperplastic effects in humans would
be much higher than the existing RfD and RfC for EGBE. Given that
humans, including potentially sensitive subpopulations such as
children, have no known organ for the retention of a comparable target
dose of EGBE or its metabolites, we feel it is reasonable to conclude
that the RfC and RfD developed for EGBE (EPA, 1999a) are sufficient for
the prevention of hyperplasia and associate tumors in humans.
With respect to liver tumors in male mice, scientists have placed
particular focus on hemangiosarcomas of the liver reported by NTP
(2000a) because this was the only tumor type that was increased over
both concurrent and historical controls, and because one study proposed
a mode of action involving EGBE for this tumor (Sascha et al., 2002).
A metabolite of EGBE, butoxyacetic acid, has long been known to
cause hemolysis in rodents (Carpenter et al, 1956). This hemolysis
leads to the accumulation of hemosiderin (iron) in phagocytic Kupffer
cells of the liver of both rats and mice (NTP, 2000a). Recent research
in mice and rats indicates that the increased iron levels associated
with EGBE-induced hemolysis can produce oxygen radicals which produce
oxidative damage in the liver that is more severe in mice than in other
species, and increased DNA synthesis in both cells that line blood
vessels and liver cells that is unique to mice (Sascha et al., 2002).
This research hypothesizes that these events can contribute to the
transformation of the endothelial cells to hemangiosarcomas (and
hepatocytes to hepatocellular carcinomas) in male mice. Given the high
background rate of these tumors in male mice relative to female mice
and rats (NTP, 2000b; Klaunig, 2002), we feel it is reasonable to
hypothesize that the endothelial cells and hepatocytes in the livers of
male mice are more susceptible to oxidative stress resulting from iron
buildup in local Kupffer cells. While additional research would be
informative with respect to mechanistic issues such as the relative
susceptibility of endothelial cells and hepatocytes to oxidative stress
caused by the hemolytic effects of EGBE and the apparent resistance of
female mice to the development of hemangiosarcomas despite experiencing
similar hemolytic effects, there is enough evidence at this time to
support an EPA determination that events associated with hemolysis
could have contributed to the increased incidence of these tumors in
male mice exposed to EGBE.
Available data establish a plausible nonlinear, nongenotoxic mode
of action for the moderate increase observed by NTP (2000a) in the
incidence of liver tumors in male mice following chronic inhalation
exposure to EGBE. The proposed mode of action suggests that the
endothelial cells and hepatocytes of male mice are sensitive to the
formation of the subject neoplasms (as evidenced by the relatively high
background rate of these tumors in male mice) and that excess iron from
EGBE-induced hemolysis can result in sufficient iron-induced oxidative
stress to cause the observed, marginal increase in the incidence of
liver hemangiosarcomas and hepatocellular carcinomas in these animals
(NTP, 2000a). Given the relatively low sensitivity of humans, including
subpopulations such as children, to the hemolytic effects of EGBE, we
feel it is reasonable to conclude that the EGBE RfC and RfD (EPA,
1999a) are sufficient for the prevention of hemolysis and associate
tumors in humans.
We anticipate additional research may be completed in the near
term. We will review those results and peer review our findings at the
earliest opportunity.
D. Human Health Risk Characterization and Conclusions
We used a Hazard Quotient (HQ) approach to characterize the
noncancer risk associated with the exposures to EGBE. In this case, the
HQ is developed by comparing the level of exposure to the IRIS RfC or
RfD for EGBE. If the HQ is less than 1, the reference level is not
exceeded, and the adverse health effects are unlikely.
Based on our assessment of the information provided in the
petition, it is possible to derive a quantitative evaluation of an
inhalation HQ for EGBE. Based on our evaluation of the modeling data,
we judge that maximum ambient annual average exposures to EGBE are not
likely to exceed 0.3 mg/m3 for a single major source, or 0.5
mg/m3 for a group of closely located area sources. The
reference level to be used in the determination of EGBE's HQ is the RfC
of 13 mg/m3. This criterion addresses the health effect of
concern due to chronic inhalation exposures to EGBE. In addition, the
criterion includes the margins of safety built into the IRIS RfC (i.e.,
any needed uncertainty factors to address sensitive subpopulations and
other factors) and is, therefore, protective of sensitive
subpopulations.
Using this approach, we calculate an HQ for the maximum annual
ambient concentration of EGBE from a single major source to be 0.02. In
other words, the EGBE air concentration is 2 percent of the RfC. For
closely located area sources, the HQ is 0.04, or 4 percent of the RfC.
To be extremely conservative, we might assume that the single major
source is located among the group of area sources. In this case, the
maximum annual ambient average concentration would be 0.8 mg/
m3 and the HQ would be 0.06, or 6 percent of the RfC. All HQ
are well below the health criterion of an HQ of 1. Further, we judge
that the
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exposures to EGBE of actual persons living in the immediate vicinity of
EGBE emission sources would be significantly less than the
concentrations estimated by the model. Considering such things as human
activity patterns and that predicted ambient concentrations fall
significantly from those predicted by the models, we expect that the HQ
for most of the surrounding population would be several orders of
magnitude less than one.
We also use a Hazard Index (HI) approach to characterize the
potential for EGBE exposures to cause adverse effects when combined
with typical exposures to pollutants that also affect the circulatory
system. In this case, we rely on the 1996 National Air Toxics
Assessment (NATA) which estimates risks to certain HAP by census
blocks. The NATA results indicate that more than 99 percent of the
census blocks have circulatory system HI below 0.1. As such, even when
combined with other exposures to circulatory system toxicants, EGBE
exposures would results in HI that are well below 1.0 and, therefore,
would not be associated with risk of adverse effects.
The reference level we used to determine EGBE's ingestion HQ is the
IRIS RfD of 0.5 (mg/kg/day). Based on our analysis, we judge that
maximum exposures to EGBE via ingestion of water contaminated with EGBE
from air releases is not likely to exceed 0.28 mg/kg/day. The resulting
HQ is 0.6. In other words the concentration in the environment is 60
percent of the RfD. Given the conservative nature of the parameters
used to derive the average daily intake, we conclude that the actual HQ
will be significantly less than 0.6.
Therefore, based on information presented in the petition, EPA's
evaluation of data made available after the submission of the petition,
and our own supplemental analyses, we have made an initial
determination that emissions, ambient concentrations, bioaccumulation
or deposition of EGBE may not reasonably be anticipated to cause any
adverse effects to human health.
E. Ecological Risk Characterization and Conclusions
We developed an independent ecological risk assessment (ERA) to
evaluate the potential environmental impacts of EGBE emissions. We
organized our analysis according to EPA's framework for ecological risk
assessment and followed a two tiered approach. Under this approach, the
tier 1 analysis used conservative point estimates of exposure (maximum
possible concentration in the environment) and effect (e.g., national
ambient water quality criterion). If the tier 1 analysis indicated that
a conservative estimate of exposure would not exceed a very sensitive
effects threshold (i.e., quotient <1), the analysis was terminated. If
the tier 1 analysis indicated the potential for effect (i.e, quotient
1), the analysis proceeded to tier 2. In tier 2, more
realistic assumptions were made about exposure and effects. If the tier
2 quotients were less than one, the analysis was terminated. However,
if one or more of the tier 2 quotients were greater than one, the risk
assessment would proceed to a probabilistic risk assessment.
Because EGBE concentrations will be the highest close to the
emission source and because it is unlikely to be transported widely due
to its short half-life in air and its propensity to partition from air
to soil and water, we decided that the appropriate spatial modeling
scale for the analysis was local. Using the petitioner's dispersion
modeling analysis, we selected the single facility from the inventory
that was the source of the largest maximum predicted annual
concentration of EGBE as predicted by the ISCST3 model. This maximum
annual average concentration was then used in conjunction with a Mackay
Level I fugacity model to determine a steady state equilibrium
concentration of EGBE in soil, water, and sediment in a simulated
environment situated at the fence line. (Due to the relatively short
distance from the source to the fence line, we assumed EGBE to disperse
in the atmosphere as a passive tracer, not subject to removal through
deposition or chemical reaction during transport.)
We developed exposure scenarios for small mammals and aquatic
species and derived a quotient to characterize the potential ecological
risk. The tier 1 ERA suggested that EGBE may have the potential to
cause adverse effects to small mammals and to sensitive aquatic biota
residing close to and downwind of the largest emitting source. This
determination was, at least in part, due to the conservatism of tier 1
analysis, and the fact the decision criterion for these quotients were
derived from very minor effects which were unlikely to be ecologically
significant at the population level of ecological organization.
The tier 2 analysis combined a Level III Mackay Model and the
ISCST3 outputs for the largest source. The Level III fugacity model
takes into account reaction, advection and intermedia exchange after
emission to the atmosphere. Based on the fugacity/ISCST3 approach, the
estimated EGBE concentrations in air, soil, and water were determined
to be 0.3 mg/m3, 0.07 mg/kg, and 3.64 mg/L, respectively.
The lowest aquatic acute toxicity value available was for the
protozoan Endosiphon sulcatum which experienced a 5 percent inhibition
of cell multiplication at 91 mg/L following a 72-hour exposure. Due to
the relatively minor effect reported and because the protozoa were
exposed over several generations during the 72-hour period, we applied
an acute/chronic adjustment factor of 10 to derive a safe level (i.e.,
toxicity reference value (TRV)) of 9 mg/L for aquatic biota in water.
The TRV for small mammals was based on the critical mammalian
studies identified by IRIS for inhalation and oral exposure. Hemolysis
was the critical endpoint of concern. A TRV of 20 mg/kg/day was derived
by dividing the most sensitive LOAEL for female rats (59 mg/kg/day) by
an uncertainty factor of three to adjust for the absence of a NOAEL.
Exposure scenarios were developed for each species and a quotient
was calculated. In both cases, the quotient for aquatic invertebrates
and small mammals was determined to be less than one. This suggested
that both aquatic organisms and small mammals are not likely to be
adversely affected by EGBE emissions to the atmosphere.
Based on our review of these data supplemented by additional
environmental modeling, we have made an initial determination that
there are adequate data on environmental effects of EGBE to determine
that ambient concentrations, bioaccumulation, or deposition of EGBE are
not reasonably anticipated to cause adverse environmental effects.
F. Transformation Assessment
Ethylene glycol monobutyl ether is one of many VOC that transform
into other HAP after emission into the ambient air. The petition
identifies the principal oxidation products of EGBE as n-butyl formate,
2-hydroxyethyl formate, propionaldehyde, 3-hydroxybutyl formate, and
several isomeric forms of an organic nitrate compound. Only one of
these compounds (i.e., propionaldehyde) is a listed HAP. However, the
formate esters are known to transform in the atmosphere into
formaldehyde, which is another listed HAP. In addition, propionaldehyde
undergoes further transformation to formaldehyde and acetaldehyde
(which is also a HAP). Both formaldehyde and acetaldehyde are probable
human carcinogens and
[[Page 65658]]
have been identified by the EPA as among the 33 HAP of greatest concern
under the Integrated Urban Air Toxics Strategy published in the Federal
Register on July 19, 1999 (64 FR 38706).
The petitioner concluded that insignificant amounts of these
compounds are formed as a result of secondary transformation of EGBE.
After reviewing the petitioner's analysis, we concluded that it was a
reasonable effort to determine whether EGBE transformation products are
likely to be of concern. However, there were data gaps and additional
questions which we judged to need further attention. Consequently, we
undertook an independent analysis to estimate typical urban ambient air
concentrations of formaldehyde, acetaldehyde, and propionaldehyde due
to EGBE transformation. Our evaluation, summarized below, indicates
that atmospheric transformation of EGBE emissions may not reasonably be
anticipated to cause adverse effects to human health. The full
transformation assessment is contained in the docket.
A large percentage of ambient formaldehyde and acetaldehyde is due
to atmospheric transformation of VOC. In fact, the State of California
has estimated that as much as 88 percent of the ambient formaldehyde
and 41 to 67 percent of the ambient acetaldehyde arise from atmospheric
transformation from VOC. The remainder is attributed to direct
emissions. A previous analyses carried out as part of the EPA's
Cumulative Exposure Project (CEP) in the mid-1990s suggests that EGBE
transformation is not among the most significant contributors to
ambient formaldehyde and acetaldehyde. The CEP analysis identified two
pollutants (propene and ethene) as major contributors to ambient
concentrations of formaldehyde, and two pollutants (propene and 2-
butene) as the major contributors to acetaldehyde. Several other VOCs
including EGBE were considered only minor precursors to formaldehyde
and acetaldehyde in the CEP analysis.
Secondary formaldehyde is formed from EGBE via a two step process.
First, EGBE with an average half-life of approximately 18 hours and a
life time of about 25 hours transforms into intermediate compounds,
such as formate esters and proprionaldehyde. Second, these compounds
transform into formaldehyde. Based on the information contained in the
petition, formate esters have half-lives ranging from 21 hours to 55
hours. Proprionaldehyde has a half-life of about 12 hours. Due to the
relatively long time required to complete the process, and the
resulting large dilution of the EGBE reaction products in the
atmosphere, we do not anticipate elevated concentrations of
formaldehyde formation due to EGBE transformation near EGBE emissions
points that will cause adverse effects to human health.
We have estimated that the half-life for EGBE to convert to
formaldehyde through the two step process is approximately 37 hours.
Assuming the average wind speed is about 3 miles per hour (mph), a
plume from any given EGBE emission will travel about 111 miles in a 37-
hour period. A conservative dispersion calculation at this point in
time indicates that the plume is well dispersed such that EGBE
concentrations are decreased by at least 300-fold from the predicted
maximum fence line concentrations. Considering dispersion alone and the
maximum fence line concentration for the largest EGBE emission source
presented in the petition of approximately 330 micrograms per meter
cube (ug/m3) (i.e., 0.3 mg/m3), we can
conservatively estimate that EGBE levels in typical urban areas might
be as high as 1 ug/m3. Concurrent with this dispersion, EGBE
emissions transform relatively slowly into formaldehyde which, in turn,
decomposes much more quickly. We estimate that the concentrations of
formaldehyde due to EGBE transformation at this point would be roughly
0.06 ug/m3.
Based on available ambient monitoring data for 82 urban area
monitoring sites in 17 States, we determined that the ambient average
concentration of formaldehyde in urban areas is about 2.8 ug/
m3. Therefore, we estimate that roughly 2 percent (i.e.,
0.06 ug/m3) of the ambient formaldehyde could be due to EGBE
transformation. However, due to the conservatism built into the
estimation procedure, we feel this is an overestimate. We feel that the
actual contribution of EGBE to formaldehyde levels is much less than 2
percent.
We also considered the risk to human health posed by ambient
formaldehyde. Using EPA default exposure and risk assumptions (such as
the assumption that there is no threshold for the carcinogenic effect
and that the dose-response relationship is linear at low doses), the
increased risk of cancer for people assumed to be exposed for a
lifetime to the ambient concentration can be calculated by multiplying
the ambient concentration by the cancer Unit Risk Estimate (URE). The
URE is an upper bound estimate of the increased risk of cancer per unit
of exposure for a lifetime. (The IRIS glossary defines upper-bound as
``a plausible upper limit to the value of a quantity. This is usually
not a true statistical confidence limit''.) The current URE for
formaldehyde, as listed by IRIS, is 1.3 x 10-5 per microgram
per cubic meter (per ug/m3). (Note: The EPA periodically
reviews and updates the toxicological information for chemicals on
IRIS. Currently we are reviewing formaldehyde. As such, the URE may
change, but based on currently available information, it is not likely
to become higher than what is currently on IRIS.) This means that if
people are exposed to 1 microgram of formaldehyde per cubic meter of
air (1 ug/m3) for a lifetime, we estimate that they would
have an estimated upper bound increased risk of cancer of 1.3 x
10-5 or 13 in a million. Therefore, if we assume people are
exposed to the average ambient concentration of formaldehyde (i.e., 2.8
ug/m3) for a lifetime, we calculate the upper bound
increased cancer risk for these people to be about 30 in a million, or
3 x 10-5. Thus, while the total level of risk from ambient
levels of formaldehyde is greater than one in a million (or 1 x
10-\6\), a relatively small portion of these ambient levels
is likely to be attributable to EGBE transformation.
Given the level of risk from formaldehyde generally, and because
EGBE is likely to contribute less than 2 percent to the total ambient
concentration of formaldehyde, we do not anticipate that formaldehyde
from EGBE transformation will have an adverse impact on human health.
We also assessed the potential for adverse health effects other
than cancer. No EPA RfC is available for formaldehyde for an assessment
of noncancer risks. Therefore, we compared ambient levels to the
minimal risk level (MRL) for formaldehyde, produced by the Agency for
Toxics Substances and Disease Registry. The MRL for formaldehyde is 10
ug/m\3\. The ambient outdoor levels of formaldehyde used for this
analysis are less than the MRL, which suggests that adverse noncancer
effects are not likely to result from exposures to these ambient
outdoor concentrations.
Propionaldehyde is also produced by the secondary transformation of
EGBE. The half-life of propionaldehyde is about 1.4 times shorter than
the half-life of EGBE, which indicates that propionaldehyde degrades
about 1.4 times faster than it is formed from EGBE. Assuming steady
state, we have determined that the concentration of propionaldehyde (in
ug/m\3\) is expected to be roughly 2.8 times lower than the
concentration of EGBE. Assuming that 1
[[Page 65659]]
ug/m\3\ is representative of the ambient EGBE concentrations expected
in typical urban areas, based on monitoring data, we estimate that
propionaldehyde concentrations resulting from degradation of these EGBE
levels would be roughly 0.4 ug/m\3\.
Based on available monitoring data from 23 sites, the mean ambient
air concentration of propionaldehyde is 0.94 ug/m\3\. The 95th
percentile of the ambient monitoring data is 2.3 ug/m\3\. Since the
ambient average concentration of propionaldehyde in urban areas is
about 0.94 ug/me, we estimated that as much as 40 percent
(i.e., 0.4 ug/m\3\) of the ambient propionaldehyde could be due to EGBE
transformation.
Propionaldehyde is not classified as a carcinogen, and we were not
able to locate data that indicated carcinogenic properties.
Consequently, cancer risks due to the ambient levels of propionaldehyde
were not evaluated. There are, however, very limited data on noncancer
effects of propionaldehyde; but there are no RfCs or MRLs available.
The only noncancer benchmark found on propionaldehyde is a draft
Preliminary Evaluation Concentration (PEC) of 9 ug/m\3\, developed in
1994 and presented in a draft EPA report titled: Non-Cancer Benchmarks
for Screening Hazardous Air Pollutants for the Urban Area Source
Program. Draft for Peer Review. (April 1994). The draft PEC is an
interim screening level value and has not undergone peer review. It is
based on the assumption that propionaldehyde exhibits toxic effects
similar to acetaldehyde, but is less toxic than acetaldehyde. In
deriving the PEC, several uncertainty factors were applied to account
for various uncertainties and data limitations. Based on the approach
to derivation, we believe that the PEC is probably protective, and that
exposures to propionaldehyde at levels below 9 ug/m\3\ are not likely
to pose significant risk of adverse noncancer health effects.
Using the PEC as a decision criterion, the mean ambient
concentrations for propionaldehyde (about 0.94 ug/m\3\) and the 95th
percentile (about 2.3 ug/m\3\) are well below the PEC of 9 ug/m\3\.
Although we estimate EGBE transformation to contribute as much as 40
percent of the ambient concentration of propionaldehyde, we judge that
adverse noncancer health effects are not likely to result due to
transformation of EGBE to propionaldehyde.
Acetaldehyde is also formed from EGBE via a two step process. In
this process, EGBE transforms to propionaldehyde which then further
converts to one of 3 compounds: formaldehyde, acetaldehyde or
peroxypropionly nitrate. As described previously in this section, we
assumed that each EGBE molecule is converted to one propionaldehyde
molecule in 25 hours and that half of the propionaldehyde converts into
acetaldehyde in 12 hours. Based on these assumptions, we estimated that
in approximately 37 hours, one half of the available EGBE molecules in
the ambient air is convert to acetaldehyde molecules. The half-life of
acetaldehyde is about 2.5 times shorter than the half-life of EGBE's
conversion to acetaldehyde through the two step process, which
indicates that acetaldehyde degrades about 2.5 times faster than it is
formed from EGBE. Therefore, assuming steady state, the concentration
of acetaldehyde is predicted to be roughly 6.7 times lower than the
concentration of EGBE. Assuming that 1 ug/m\3\ is representative of the
ambient EGBE concentrations that would be expected in typical urban
areas, we estimate that acetaldehyde concentrations resulting from
degradation of these EGBE levels would be roughly 6.7 times lower, or
0.15 ug/m\3\.
Since the ambient average concentration of acetaldehyde in urban
areas is about 2.5 ug/m\3\ (based on available ambient monitoring data
for urban areas), we estimated that roughly 6 percent or 0.15 ug/m\3\
of the ambient acetaldehyde could be due to EGBE transformation. We
think this is a conservative estimate, and that the actual contribution
of EGBE to acetaldehyde levels in typical urban areas is likely to be
less than 6 percent.
To evaluate the potential risks for public health, the increased
cancer risks can be estimated. The URE for acetaldehyde is 2 x
10-\6\ per ug/m\3\. (Note: As with formaldehyde, the URE for
acetaldehyde is currently being reviewed by EPA and is likely to
change. However, based on currently available information, the URE for
acetaldehyde is not likely to become significantly higher, and may be
much lower than the current value.) This means that if people are
exposed to 1 microgram of acetaldehyde per cubic meter of air (1 ug/
m\3\) for a lifetime, we estimate that they would have an estimated
upper bound increased risk of cancer of 2.2 x 10-\6\, or 2.2
in 1 million. Therefore, if we assume people are exposed to the average
ambient concentration of acetaldehyde (i.e., 2.5 ug/m\3\) for a
lifetime, we calculated the upper bound increased cancer risk for these
people to be about 6 in 1 million, or 6 x 10-\6\. As with
formaldehyde, the total risk level from ambient levels of acetaldehyde
is greater than 1 in 1 million. However, only a relatively small
portion of these ambient levels is attributable to EGBE transformation.
Because EGBE is likely to contribute less than 6 percent of the total
ambient concentration of acetaldehyde, we do not anticipate that
acetaldehyde from EGBE transformation will have an adverse impact on
human health.
We also evaluated the potential for noncancer hazards. The RfC for
acetaldehyde is 9 ug/m\3\, which is higher than the reported ambient
concentrations, therefore, we do not expect adverse noncancer effects
to occur due to exposures to these outdoor ambient concentrations.
Based on our analyses, as well as information presented in the
petition, we feel that EGBE transformation to HAP is not a significant
concern for public health. Since EGBE transformation products are
likely to pose relatively low risks in typical urban ambient air, and
since EGBE emissions are not expected to result in elevated levels of
formaldehyde, proprionaldehyde, or acetaldehyde near EGBE emission
sources that pose significant risks to human health, we have made an
initial determination that the available data indicate that atmospheric
transformation of EGBE emissions to other HAP is not reasonably
anticipated to cause significant human health risks.
The quantitative estimates and the associated risk estimates
presented above have some uncertainty associated with the estimates.
This is due to the simplified approach, assumptions made, and
incomplete knowledge of the atmospheric chemistry, and toxicity of the
chemicals. However, we generally used conservative assumptions
including: lifetime exposures; linear non-threshold dose-response
relationship; conservative estimate of formaldehyde that would be
formed per mole of EGBE transformed; and that the EGBE concentrations
are 1 ug/m\3\. Therefore, we judge that the estimates of risk due to
the transformation of EGBE to formaldehyde, proprionaldehyde, and
acetaldehyde as presented in this analysis are more likely to be
overestimated rather than underestimated. Overall, this analysis
suggests that the fractions of formaldehyde, proprionaldehyde, and
acetaldehyde in typical urban ambient air resulting from transformation
of EGBE emissions are not likely to pose significant risks to human
health.
The EPA also recognizes that EGBE is a potential tropospheric ozone
precursor. However, we feel that it is inappropriate to include a
substance on the HAP list under CAA section 112(b)
[[Page 65660]]
due entirely to its tendency to form ozone. Section 112(b)(2) of the
CAA provides that no air pollutant which is listed under CAA section
108(a), such as ozone, may be added to the HAP list. It further
provides that a pollutant that is a precursor to a pollutant listed
under section 108(a), such as EGBE, may not be included on the HAP list
unless it ``independently meets'' the HAP list criteria. As explained
in this preamble, we feel that the petitioner has demonstrated that
EGBE does not independently meet the criteria for listing as a HAP
under section 112 of the CAA.
The CAA established requirements for reducing the emission of air
pollutants, and deals separately with HAP (which are to be listed and
regulated under CAA section 112) and criteria air pollutants (which are
to be listed under CAA section 108 and regulate under various other
sections of the CAA). Precursors of criteria air pollutants, such as
VOC, are regulated for their contribution to ambient levels of criteria
pollutants under statutory provisions that do not apply to HAP. This
structure would lose its significance if EPA were to include substances
on the HAP list solely as a result of their contribution to
concentrations of criteria air pollutants.
G. Public Comments
We requested public comment as a part of the Federal Register
notice announcing the receipt of a complete petition to delist EGBE (64
FR 42125-27). The comments contained no technical information or data
which was relevant to our review of this petition. Copies of the
comments have been included in the docket for the proposed rule.
H. Conclusions
Uncertainty is an inherent part of risk assessment. It arises
because risk assessment is a complex process, requiring the integration
of multiple factors, and because it involves predictions of risk that
are not directly observable. In the analysis, uncertainty arises for
the following reasons. The IRIS database, used as the source of the
human health effects decision criteria, is imperfect and leads to
uncertainty in the RfC. We also recognize that there is uncertainty in
the computer models used to predict the fate and transport of EGBE in
the environment. These models are simplifications of reality and some
variables are excluded.
For decisions which are based largely on risk assessments, some
degree of uncertainty is acceptable. Such is the case for this proposed
delisting decision. We do not interpret CAA section 112(b)(3)(C) to
require absolute certainty that a pollutant will not cause adverse
effects on human health or the environment before it may be deleted
from the list. The use of the terms ``adequate'' and ``reasonably''
indicate that the Agency must weigh the potential uncertainties and
their likely significance. To this end, the assessment applies
conservative assumptions to bias potential error toward overstating
human and ecological health effects. Thus, EPA is confident that even
when we consider the uncertainties in the petition's initial assessment
and in the additional analyses, the results are more likely to over-
estimate rather than under-estimate true exposures and risks.
Based on our evaluation of the petition and the subsequent
analyses, we judge that the potential for adverse human health and
environmental effects to occur from projected exposures is sufficiently
low to provide reasonable assurance that such adverse effects will not
occur. For example, the petitioner appropriately applied EPA's model
guidelines and EPA's tiered dispersion modeling approach which we
designed to be conservative. Also, the petitioner used sound analytic
principles in modifying the standard assessments described in the
Tiered Approach, the inverted tier 1 and the CARTSCREEN analyses. In
addition, the petition did not apply a formal exposure assessment to
the predicted ambient air concentrations. Instead, the petition used
the maximum annual ambient average air concentrations alone as a
surrogate for exposure. Based upon the likely proximity of inhabitable
areas and knowledge of human activity patterns, we feel that actual
exposures will be far less than predicted exposures that were derived
from the dispersion analysis. Further, when modeling clusters of EGBE
sources, the petition showed that concentrations resulting from both
closely located major and area sources are not likely to adversely
affect health. Finally, the petition's analysis using available data
from monitors suggest that ambient concentrations of EGBE in urban
areas are over two orders of magnitude lower than the modeled maximum
concentrations.
With regard to toxicity, the information available to the Agency at
this time indicates that nonlinear modes of action are likely
responsible for the increased incidence of tumors observed by the NTP
(2000) in mice following chronic EGBE exposure. Application of
nonlinear quantitative assessment methods indicate that the noncancer
RfD of 0.5 mg/kg/day and the RfC of 13 mg/m3, which EPA
developed for EGBE, are adequately protective of these carcinogenic
effects. This determination assumes a nonlinear mechanism that requires
exposure levels to be high enough to cause certain lesions that are
precancerous. Information is currently inadequate to dismiss the
potential contribution of a linear mechanism associated with the
possible mutagenic metabolite BAL. Additional research (e.g.,
verification of existing physiologically based pharmaco kinetic
modeling results and improved genotoxicity assays) would assist the
Agency in making a more certain decision concerning the potential for
BAL to contribute to the adverse effects seen in animals following EGBE
exposure and use of the proposed nonlinear assessment approach. If
additional information on BAL becomes available between the proposal
and the final action on the delisting decision, EPA will evaluate and
peer review such information. We may or may not determine that any new
information would be relevant to our analysis of EGBE emissions.
As described above, EPA's proposed decision to remove EGBE from the
list of HAP is based on the results of a risk assessment demonstrating
that emissions of EGBE may not reasonably be anticipated to result in
adverse human health or environmental effects. In addition to the
analyses presented and the uncertainties inherent in risk assessment,
we have considered other information related to EGBE in making this
decision, namely the transformation of EGBE into other HAP as it
decomposes in the ambient air. We conclude that ambient concentrations
of the transformed HAP are very small, and that they decompose rapidly.
Therefore, we do not anticipate that EGBE transformation will be
significant enough to have an adverse impact on human health.
We also considered the fact that EGBE is reported to the Toxics
Release Inventory (TRI) as part of the group of glycol ethers. The 2000
TRI shows the air emissions of the class of chemicals ``Certain Glycol
Ethers'' to be ranked number 12 by volume. Under the proposed rule, it
would no longer be regulated as a HAP, but it will continue to be
reported in the TRI, as part of the group ``Certain Glycol Ethers'' and
regulated under EPA's criteria pollutant (ozone) program.
In conclusion, EPA has made an initial determination, after careful
consideration of the petition and after completing additional analyses,
that there are adequate data on the health and environmental effects of
EGBE to determine that emissions, ambient concentrations,
bioaccumulation of
[[Page 65661]]
deposition of EGBE may not reasonably be anticipated to cause any
adverse effects to the human health or adverse environmental effects.
IV. Statutory and Executive Order Reviews
A. Executive Order 12866: Regulatory Planning and Review
Under Executive Order 12866 (58 FR 51735, October 4, 1993), EPA
must determine whether the regulatory action is ``significant'' and,
therefore, subject to Office of Management and Budget (OMB) review and
the requirements of the Executive Order. The Executive Order defines
``significant regulatory action'' as one that is likely to result in a
rule that may:
(1) Have an annual effect on the economy of $100 million or more or
adverse affect in a material way the economy, a sector to the economy,
productivity, competition, jobs, the environment, public health or
safety, or state, local or tribal governments or communities;
(2) Create a serious inconsistency or otherwise interfere with an
action taken or planned by another agency;
(3) Materially alter the budgetary impact of entitlements, grants,
user fees, or loan programs, or the rights and obligation of recipients
thereof; or
(4) Raise novel legal or policy issues arising out of legal
mandates, the President's priorities, or the principles set forth in
the Executive Order.
Pursuant to the terms of Executive Order 12866, it has been
determined that the proposed action does not constitute a ``significant
regulatory action'' and is, therefore, not subject to OMB review.
B. Paperwork Reduction Act
This action does not impose an information collection burden under
the provisions of the Paperwork Reduction Act, 44 U.S.C. 3501 et seq.
The proposed action will remove EGBE from the CAA section 112(b)(1) HAP
list and, therefore, eliminate the need for information collection
under the CAA. Burden means the total time, effort, or financial
resources expended by persons to generate, maintain, retain, or
disclose or provide information to or for a Federal agency. This
includes the time needed to review instructions; develop, acquire,
install, and utilize technology and systems for the purposes of
collecting, validating, and verifying information, processing and
maintaining information, and disclosing and providing information;
adjust the existing ways to comply with any previously applicable
instructions and requirements; train personnel to be able to respond to
a collection of information; search data sources; complete and review
the collection of information; and transmit or otherwise disclose the
information. An Agency may not conduct or sponsor, and a person is not
required to respond to a collection of information unless it displays a
currently valid OMB control number. The OMB control numbers for EPA's
regulations are listed in 40 CFR part 9 and 48 CFR chapter 15.
C. Regulatory Flexibility Act
The Regulatory Flexibility Act (RFA) generally requires an agency
to prepare a regulatory flexibility analysis of any rule subject to
notice and comment rulemaking requirements under the Administrative
Procedure Act or any other statute unless the agency certifies that the
rule will not have a significant economic impact on a substantial
number of small entities. Small entities include small business, small
organizations, and small governmental jurisdictions. For the purposes
of assessing the impacts of today's proposed rule on small entities,
small entity is defined as: (1) A small business that meets the
definitions for small business based on the Small Business Association
(SBA) size standards which, for this proposed action, can include
manufacturing (NAICS 3999-03) and air transportation (NAICS 4522-98 and
4512-98) operations that employ less 1,000 people and engineering
services (NAICS 8711-98) operations that earn less than $20 million
annually; (2) a small governmental jurisdiction that is a government of
a city, county, town, school district or special district with a
population of less than 50,000; and (3) a small organization that is
any not-for-profit enterprise which is independently owned and operated
and is not dominant in its field.
After considering the economic impact of today's proposed rule on
small entities, I certify that this proposed action will not have a
significant economic impact on a substantial number of small entities.
In determining whether a rule has significant economic impact on a
substantial number of small entities, the impact of concern is any
significant adverse economic impact on small entities, since the
primary purpose of the regulatory flexibility analysis is to identify
and address regulatory alternatives ``which minimize any significant
economic impact of the proposed rule on small entities.'' (5 U.S.C. 603
and 604). Thus, an agency may certify that a rule will not have a
significant economic impact on a substantial number of small entities
if the rule relieves regulatory burden, or otherwise has a positive
economic effect on all of the small entities subject to the rule. The
proposed rule will eliminate the burden of additional controls
necessary to reduce EGBE emissions and the associated operating,
monitoring and reporting requirements. We have, therefore, concluded
that today's proposed rule will relieve regulatory burden for all small
entities. We continue to be interested in the potential impacts of the
proposed rule on small entities and welcome comments on issues related
to such impacts.
D. Unfunded Mandates Reform Act
Title II of the Unfunded Mandates Reform Act of 1995 (UMRA), Public
Law 1044, establishes requirements for Federal agencies to assess the
effects of their regulatory actions on State, local, and tribal
governments and the private sector. Under section 202 of the UMRA, EPA
generally must prepare a written statement, including a cost-benefit
analysis, for proposed and final rules with ``Federal mandates'' that
may result in expenditures to State, local, and tribal governments, in
the aggregate, or to the private sector, of $100 million or more in any
1 year. Before promulgating an EPA rule for which a written statement
is needed, section 205 of the UMRA generally requires EPA to identify
and consider a reasonable number of regulatory alternatives and adopt
the least costly, most cost-effective or least burdensome alternative
that achieves the objectives of the rule. The provisions of section 205
do not apply when they are inconsistent with applicable law. Moreover,
section 205 allows EPA to adopt an alternative other than the least
costly, most cost-effective or least burdensome alternative if the
Administrator publishes with the final rule an explanation why that
alternative was not adopted. Before EPA establishes any regulatory
requirements that may significantly or uniquely affect small
governments, including tribal governments, it must have developed under
section 203 of the UMRA a small government agency plan. The plan must
provide for notifying potentially affected small governments, enabling
officials of affected small governments to have meaningful and timely
input in the development of EPA regulatory proposals with significant
Federal intergovernmental mandates, and informing, educating, and
advising small governments on compliance with the regulatory
requirements.
Today's proposed rule contains no Federal mandates for State,
local, or
[[Page 65662]]
tribal governments or the private sector. The proposed rule imposes no
enforceable duty on any State, local or tribal governments or the
private sector. In any event, EPA has determined that the proposed rule
does not contain a Federal mandate that may result in expenditures of
$100 million or more for State, local, and tribal governments, in the
aggregate, or the private sector in any 1 year. Because the proposed
rule removes a compound previously labeled in the CAA as a HAP, it
actually reduces the burden established under the CAA. Thus, today's
proposed rule is not subject to the requirements of sections 202 and
205 of the UMRA.
E. Executive Order 13132: Federalism
Executive Order 13132 (64 FR 43255, August 10, 1999) requires EPA
to develop an accountable process to ensure ``meaningful and timely
input by State and local officials in the development of regulatory
policies that have federalism implications.'' ``Policies that have
federalism implications'' is defined in the Executive Order to include
regulations that have ``substantial direct effects on the States, on
the relationship between the national government and the States, or on
the distribution of power and responsibilities among the various levels
of government.''
Under Executive Order 13132, EPA may not issue a regulation that
has federalism implications, that imposes substantial direct compliance
costs, and that is not required by statute, unless the Federal
government provides the funds necessary to pay the direct compliance
costs incurred by State and local governments, or EPA consults with
State and local officials early in the process of developing the
proposed regulation. The EPA also may not issue a regulation that has
federalism implications and that preempts State law unless the Agency
consults with State and local officials early in the process of
developing the proposed regulation.
Today's proposed rule removes the substance EGBE from the list of
HAP contained under section 112(b)(1) of the CAA. It does not impose
any additional requirements on the States and does not affect the
balance of power between the States and the Federal government. Thus,
the requirements of section 6 of the Executive Order do not apply to
the proposed rule.
F. Executive Order 13175: Consultation and Coordination With Indian
Tribal Governments
Executive Order 13175 (65 FR 67249, November 9, 2000) requires EPA
to develop an accountable process to ensure ``meaningful and timely
input by tribal officials in the development of regulatory policies
that have tribal implications.'' The proposed rule does not have tribal
implications, as specified in Executive Order 13175.
A review of the available emission inventory does not indicate that
tribal EGBE emissions sources are subject to control under the CAA,
therefore, the proposed rule is not anticipated to have tribal
implications. In addition, the proposed action will eliminate control
requirements for EGBE and, therefore, reduces control costs and
reporting requirements for any tribal entity operating a EGBE source
subject to control under the CAA which we might have missed. Thus,
Executive Order 13175 does not apply to the proposed rule.
G. Executive Order 13045: Protection of Children From Environmental
Health Risks and Safety Risks
Executive Order 13045 (62 FR 19885, April 23, 1997) applies to any
rule that: (1) Is determined to be ``economically significant'' as
defined under Executive Order 12866, and (2) concerns an environmental
health or safety risk that EPA has reason to believe may have a
disproportionate effect on children. If the regulatory action meets
both criteria, the Agency must evaluate the environmental health or
safety effects of the planned rule on children, and explain why the
planned regulation is preferable to other potentially effective and
reasonably feasible alternatives considered by the Agency.
The EPA interprets Executive Order 13045 as applying only to those
regulatory actions that are based on health or safety risks, such that
the analysis required under section 5-501 of the Executive Order has
the potential to influence the regulation. The proposed rule is not
subject to Executive Order 13045 because it is not economically
significant as defined in Executive Order 12866, and because the Agency
does not have reason to believe the environmental health or safety
risks addressed by this action present a disproportionate risk to
children. This determination is based on the fact that the RfC is
determined to be protective of sensitive sub-populations, including
children.
H. Executive Order 13211: Actions Concerning Regulations That
Significantly Affect Energy Supply, Distribution, or Use
The proposed rule is not subject to Executive Order 13211 (66 FR
28355, May 22, 2001) because it is not a significant regulatory action
under Executive Order 12866.
I. National Technology Transfer and Advancement Act
Section 112(d) of the National Technology Transfer and Advancement
Act of 1995 (NTTAA), Public Law No. 104-113, section 12(d) 915 U.S.C.
272 note, directs all Federal agencies to use voluntary consensus
standards instead of government-unique standards in their regulatory
activities unless to do so would be inconsistent with applicable law or
otherwise impractical. Voluntary consensus standards are technical
standards (e.g., material specifications, test method, sampling and
analytical procedures, business practices, etc.) that are developed or
adopted by one or more voluntary consensus standards bodies. Examples
of organizations generally regarded as voluntary consensus standards
bodies include the American Society for Testing and Materials (ASTM),
the National Fire Protection Association (NFPA), and the Society of
Automotive Engineers (SAE). The NTTAA requires Federal agencies like
EPA to provide Congress, through OMB, with explanations when an agency
decides not to use available and applicable voluntary consensus
standards. The proposed rule does not involve technical standards.
Therefore, EPA is not considering the use of any voluntary consensus
standards.
List of Subjects in 40 CFR Part 63
Environmental protection, Air pollution control, Hazardous
substances, Reporting and recordkeeping requirements.
Dated: November 4, 2003.
Marianne Lamont Horinko,
Acting Administrator.
For the reasons set out in the preamble, title 40, chapter 1, part
63, of the Code of Federal Regulations is proposed to be amended as
follows:
PART 63--[AMENDED]
1. The authority citation for part 63 continues to read as follows:
Authority: 42 U.S.C. 7401, et seq.
Subpart C--[Amended]
2. Subpart C is amended by adding Sec. 63.61 to read as follows:
Sec. 63.61 Deletion of ethylene glycol monobutyl ether (CAS number
111-76-2) from the list of hazardous air pollutants.
The substance ethylene glycol monobutyl ether (EGBE) (2-
Butoxyethanol) (CAS No. 111-76-2) is deleted from the list of hazardous
air
[[Page 65663]]
pollutants established by 42 U.S.C. 7412(b)(1).
[FR Doc. 03-28787 Filed 11-20-03; 8:45 am]
BILLING CODE 6560-50-P