[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

[[Page 65656]]

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

[[Page 65657]]

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