Document ID: EPA-HQ-OAR-2005-0172-12813
Agency: epa
Document Type: Supporting & Related Material
Title: 
Posted Date: 2010-04-07T04:00Z

6560-50-P

ENVIRONMENTAL PROTECTION AGENCY

40 CFR Part 50

[EPA-HQ-OAR-2005-0172; FRL-         ]

RIN 2060-   this # has not been assigned yet

            

	National Ambient Air Quality Standards for Ozone

AGENCY:  Environmental Protection Agency (EPA).

ACTION:  Proposed rule.

SUMMARY:  Based on its reconsideration of the primary and secondary
national ambient air quality standards (NAAQS) for ozone (O3) set in
March 2008, EPA proposes to set different primary and secondary
standards than those set in 2008 to provide requisite protection of
public health and welfare, respectively.  With regard to the primary
standard for O3, EPA proposes that the level of the 8-hour primary
standard, which was set at 0.075 ppm in the 2008 final rule, should
instead be set at a lower level within the range of  0.060 to 0.070
parts per million (ppm), to provide increased protection for children
and other “at risk” populations against an array of O3-related
adverse health effects that range from decreased lung function and
increased respiratory symptoms to serious indicators of respiratory
morbidity including emergency department visits and hospital admissions
for respiratory causes, and possibly cardiovascular-related morbidity as
well as total non-accidental and cardiopulmonary mortality.  With regard
to the secondary standard for O3, EPA proposes that the secondary O3
standard, which was set identical to the revised primary standard in the
2008 final rule, should instead be a new cumulative, seasonal standard
expressed as an annual index of the sum of weighted hourly
concentrations, cumulated over 12 hours per day (8:00 am to 8:00 pm)
during the consecutive 3-month period within the O3 season with the
maximum index value, set at a level within the range of 7 to 15
ppm-hours, to provide increased protection against O3-related adverse
impacts on vegetation and forested ecosystems.

DATES:  Written comments on this proposed rule must be received by
[insert date 60 days after date of publication in the Federal Register].

Public Hearings:  Three public hearings are scheduled for this proposed
rule.  Two of the public hearings will be held on February 2, 2010 in
Arlington, Virginia and Houston, Texas.  The third public hearing will
be held on February 4, 2010 in Sacramento, California.

ADDRESSES:  Submit your comments, identified by Docket ID No.
EPA-HQ-OAR-2005-0172, by one of the following methods:

  HYPERLINK "http://www.regulations.gov"  www.regulations.gov :  Follow
the on-line instructions for submitting comments.

Email:   HYPERLINK "mailto:a-and-r-Docket@epa.gov" 
a-and-r-Docket@epa.gov .

Fax:  202-566-9744.

Mail:  Docket No. EPA-HQ-OAR-2005-0172, Environmental Protection Agency,
Mail code 6102T, 1200 Pennsylvania Ave., NW, Washington, DC  20460. 
Please include a total of two copies.  

Hand Delivery:  Docket No. EPA-HQ-OAR-2005-0172, Environmental
Protection Agency, EPA West, Room 3334, 1301 Constitution Ave., NW,
Washington, DC.  Such deliveries are only accepted during the Docket’s
normal hours of operation, and special arrangements should be made for
deliveries of boxed information.

Public Hearings:  Three public hearings are scheduled for this proposed
rule.  Two of the public hearings will be held on February 2, 2010 in
Arlington, Virginia and Houston, Texas.  The third public hearing will
be held on February 4, 2010 in Sacramento, California.  The hearings
will be held at the following locations:

Arlington, Virginia – February 2, 2010

Hyatt Regency Crystal City @ Reagan National Airport

Washington Room (located on the Ballroom Level)

2799 Jefferson Davis Highway

Arlington, Virginia  22202

Telephone: 703-418-1234

Houston, Texas – February 2, 2010

Hilton Houston Hobby Airport

Moody Ballroom (located on the ground floor)

8181 Airport Boulevard

Houston, Texas  77061

Telephone: 713-645-3000

Sacramento, California – February 4, 2010

Four Points by Sheraton Sacramento International Airport

Natomas Ballroom

4900 Duckhorn Drive

Sacramento, California  95834

Telephone:  916-263-9000

See the SUPPLEMENTARY INFORMATION under “Public Hearings” for
further information.

Instructions:  Direct your comments to Docket ID No.
EPA-HQ-OAR-2005-0172.  The EPA’s policy is that all comments received
will be included in the public docket without change and may be made
available online at   HYPERLINK "http://www.regulations.gov" 
www.regulations.gov , including any personal information provided,
unless the comment includes information claimed to be Confidential
Business Information (CBI) or other information whose disclosure is
restricted by statute.  Do not submit information that you consider to
be CBI or otherwise protected through   HYPERLINK
"http://www.regulations.gov"  www.regulations.gov  or email.  The  
HYPERLINK "http://www.regulations.gov"  www.regulations.gov  website is
an “anonymous access” system, which means EPA will not know your
identity or contact information unless you provide it in the body of
your comment.  If you send an email comment directly to EPA without
going through   HYPERLINK "http://www.regulations.gov" 
www.regulations.gov , your email address will be automatically captured
and included as part of the comment that is placed in the public docket
and made available on the Internet.  If you submit an electronic
comment, EPA recommends that you include your name and other contact
information in the body of your comment and with any disk or CD-ROM you
submit.  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.  Electronic files should avoid the use of special
characters, any form of encryption, and be free of any defects or
viruses.  

Docket:  All documents in the docket are listed in the   HYPERLINK
"http://www.regulations.gov"  www.regulations.gov  index.  Although
listed in the index, some information is not publicly available, e.g.,
CBI or other information whose disclosure is restricted by statute. 
Certain other material, such as copyrighted material, will be publicly
available only in hard copy.  Publicly available docket materials are
available either electronically in   HYPERLINK
"http://www.regulations.gov"  www.regulations.gov  or in hard copy at
the Air and Radiation Docket and Information Center, EPA/DC, EPA West,
Room 3334, 1301 Constitution Ave., NW, Washington, DC.  The Public
Reading Room is open from 8:30 a.m. to 4:30 p.m., Monday through Friday,
excluding legal holidays.  The telephone number for the Public Reading
Room is (202) 566-1744 and the telephone number for the Air and
Radiation Docket and Information Center is (202) 566-1742. 

FOR FURTHER INFORMATION CONTACT:  Ms. Susan Lyon Stone,  Health and
Environmental Impacts Division, Office of Air Quality Planning and
Standards, U.S. Environmental Protection Agency, Mail code C504-06, 
Research Triangle Park, NC 27711; telephone: 919-541-1146; fax:
919-541-0237; email:    HYPERLINK "mailto:stone.susan@epa.gov" 
stone.susan@epa.gov .

SUPPLEMENTARY INFORMATION:

General Information

What Should I Consider as I Prepare My Comments for EPA?

1.  Submitting CBI.  Do not submit this information to EPA through  
HYPERLINK "http://www.regulations.gov"  www.regulations.gov  or email. 
Clearly mark the part or all of the information that you claim to be
CBI.  For CBI information in a disk or CD ROM that you mail to EPA, 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 claimed as CBI.  In addition to one complete version of the comment
that includes information claimed as CBI, a copy of the comment that
does not contain the information claimed as CBI must be submitted for
inclusion in the public docket.  Information so marked will not be
disclosed except in accordance with procedures set forth in 40 CFR part
2.

	2.  Tips for Preparing Your Comments.  When submitting comments,
remember to:

Identify the rulemaking by docket number and other identifying
information (subject heading, Federal Register date and page number).

Follow directions – The Agency may ask you to respond to specific
questions or organize comments by referencing a Code of Federal
Regulations (CFR) part or section number.

Explain why you agree or disagree, suggest alternatives, and substitute
language for your requested changes.

Describe any assumptions and provide any technical information and/or
data that you used.

Provide specific examples to illustrate your concerns, and suggest
alternatives.

Explain your views as clearly as possible, avoiding the use of profanity
or personal threats.

Make sure to submit your comments by the comment period deadline
identified.

Availability of Related Information

A number of documents relevant to this rulemaking are available on EPA
web sites.  The Air Quality Criteria for Ozone and Related Photochemical
Oxidants (2006 Criteria Document) (two volumes, EPA/ and EPA/, date) is
available on EPA’s National Center for Environmental Assessment web
site.  To obtain this document, go to   HYPERLINK
"http://www.epa.gov/ncea"  http://www.epa.gov/ncea , and click on Ozone
in the Quick Finder section.  This will open a page with a link to the
March 2006 Air Quality Criteria Document.  The 2007 Staff Paper, human
exposure and health risk assessments, vegetation exposure and impact
assessment, and other related technical documents are available on
EPA’s Office of Air Quality Planning and Standards (OAQPS) Technology
Transfer Network (TTN) web site.  The updated final 2007 Staff Paper is
available at:   HYPERLINK
"http://epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_sp.html" 
http://epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_sp.html  and the
exposure and risk assessments and other related technical documents are
available at   HYPERLINK
"http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_td.html" 
http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_td.html .  The
Response to Significant Comments Document is available at:   HYPERLINK
"http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_rc.html" 
http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_rc.html .  These
and other related documents are also available for inspection and
copying in the EPA docket identified above.

Public Hearings

	The public hearings on February 2, 2010 and February 4, 2010 will
provide interested parties the opportunity to present data, views, or
arguments concerning the proposed rule.  The EPA may ask clarifying
questions during the oral presentations, but will not respond to the
presentations at that time.  Written statements and supporting
information submitted during the comment period will be considered with
the same weight as any oral comments and supporting information
presented at the public hearing.  Written comments must be received by
the last day of the comment period, as specified in this proposed
rulemaking.

	The public hearings will begin at 9:30 a.m. and continue until 7:30
p.m. (local time) or later, if necessary, depending on the number of
speakers wishing to participate.  The EPA will make every effort to
accommodate all speakers that arrive and register before 7:30 p.m.  A
lunch break is scheduled from 12:30 p.m. until 2:00 p.m.

	If you would like to present oral testimony at the hearings, please
notify Ms. Tricia Crabtree (C504-02), U.S. EPA, Research Triangle Park,
NC 27711.  The preferred method for registering is by e-mail ( 
HYPERLINK "mailto:crabtree.tricia@epa.gov"  crabtree.tricia@epa.gov ). 
Ms. Crabtree may be reached by telephone at (919) 541-5688.  She will
arrange a general time slot for you to speak.  The EPA will make every
effort to follow the schedule as closely as possible on the day of the
hearing.

	Oral testimony will be limited to five (5) minutes for each commenter
to address the proposal.  We will not be providing equipment for
commenters to show overhead slides or make computerized slide
presentations unless we receive special requests in advance.  Commenters
should notify Ms. Crabtree if they will need specific audiovisual (AV)
equipment.  Commenters should also notify Ms. Crabtree if they need
specific translation services for non-English speaking commenters.  The
EPA encourages commenters to provide written versions of their oral
testimonies either electronically on computer disk, CD-ROM, or in paper
copy.

	The hearing schedules, including lists of speakers, will be posted on
EPA’s web site for the proposal at   HYPERLINK
"http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_fr.html" 
http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_fr.html  prior to
the hearing. Verbatim transcripts of the hearings and written statements
will be included in the rulemaking docket.

Children’s Environmental Health  

Consideration of children’s environmental health plays a central role
in the reconsideration of the 2008 final decision on the O3 NAAQS and
EPA’s decision to propose to set the 8-hour primary O3 standard at a
level within the range of 0.060 to 0.070 ppm.  Technical information
that pertains to children, including the evaluation of scientific
evidence, policy considerations, and exposure and risk assessments, is
discussed in all of the documents listed above in the section on the
availability of related information.  These documents include: the Air
Quality Criteria for Ozone and Other Related Photochemical Oxidants; the
2007 Staff Paper; exposure and risk assessments and other related
documents; and the Response to Significant Comments.  All of these
documents are available on the Web, as described above, and are in the
public docket for this rulemaking.  The public is invited to submit
comments or identify peer-reviewed studies and data that assess effects
of early life exposure to O3.

Table of Contents

	The following topics are discussed in this preamble:

I.	Background

	A.	Legislative Requirements 

	B.	Related Control Requirements

C.	Review of Air Quality Criteria and Standards for O3

	D.	Reconsideration of the 2008 O3 NAAQS Final Rule

		1.	Decision to Initiate a Rulemaking to Reconsider

		2.	Ongoing Litigation

	

II.	Rationale for Proposed Decision on the Level of the Primary Standard

	A.	Health Effects Information

		1.	Overview of Mechanisms

		2.	Nature of Effects

		3.	Interpretation and Integration of Health Evidence

		4.	O3-Related Impacts on Public Health

	B.	Human Exposure and Health Risk Assessments

		1.	Exposure Analyses

		2.	Quantitative Health Risk Assessment

	C.	Reconsideration of the Level of the Primary Standard

		1. 	Evidence and Exposure/Risk-Based Considerations

		2.	CASAC Views Prior to 2008 Decision

		3.	Basis for 2008 Decision on the Primary Standard

		4. 	CASAC Advice Following 2008 Decision

		5.	Administrator’s Proposed Conclusions

	D.	Proposed Decision on the Level of the Primary Standard

Communication of Public Health Information

Rationale for Proposed Decision on the Secondary Standard

A.	Vegetation Effects Information

	1.	Mechanisms

	2.	Nature of Effects

	3.	Adversity of Effects

B.	Biologically Relevant Exposure Indices

C.	Vegetation Exposure and Impact Assessment

	1.	Exposure Characterization

	2.	Assessment of Risks to Vegetation

D.	Reconsideration of Secondary Standard

1.	Considerations Regarding 2007 Proposed Cumulative Seasonal Standard

	2.	Considerations Regarding 2007 Proposed 8-Hour Standard

	3.	Basis for 2008 Decision on the Secondary Standard

	4.	CASAC Views Following 2008 Decision

	5.	Administrator’s Proposed Conclusions

E.	Proposed Decision on the Secondary O3 Standard

Revision of Appendix P -- Interpretation of the NAAQS for O3 and
Proposed Revisions to the Exceptional Events Rule

A.	Background

B.	Interpretation of the Secondary O3 Standard

C.	Clarifications Related to the Primary Standard

D.	Revisions to Exceptions from Standard Data Completeness Requirements
for the Primary Standard

E.	Elimination of the Requirement for 90 Percent Completeness of Daily
Data across Three Years

F.	Administrator Discretion to Use Incomplete Data

G.	Truncation versus Rounding

H.	Data Selection

I.	Exceptional Events Information Submission Schedule

Ambient Monitoring Related to Proposed O3 Standards

A.	Background

B.	Urban Monitoring Requirements

C.	Non-Urban Monitoring Requirements

D.	Revisions to the Length of the Required O3 Monitoring Season

Implementation of Proposed O3 Standards

A.	Designations

B.	State Implementation Plans

C.	Trans-boundary Emissions

VIII.	Statutory and Executive Order Reviews

	A.	Executive Order 12866: Regulatory Planning and Review

B.	Paperwork Reduction Act

C.	Regulatory Flexibility Act

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 and Safety Risks

H.	Executive Order 13211: Actions that Significantly Affect Energy
Supply, Distribution or Use

I.	National Technology Transfer and Advancement Act

J.	Executive Order 12898: Federal Actions to Address Environmental
Justice in Minority Populations and Low-Income Populations

 

References

I.	Background

	The proposed decisions presented in this notice are based on a
reconsideration of the 2008 O3 NAAQS final rule (73 FR 16436, March 27,
2008), which revised the level of the 8-hour primary O3 standard to
0.075 ppm and revised the secondary O3 standard by making it identical
to the revised primary standard.  This reconsideration is based on the
scientific and technical information and analyses on which the March
2008 O3 NAAQS rulemaking was based.  Therefore, much of the information
included in this notice is drawn directly from information included in
the 2007 proposed rule (72 FR 37818, July 11, 2007) and the 2008 final
rule (73 FR 16436).

A.	Legislative Requirements

Two sections of the Clean Air Act (CAA) govern the establishment and
revision of the NAAQS.  Section 108 (42 U.S.C. 7408) directs the
Administrator to identify and list “air pollutants” that in her
“judgment, cause or contribute to air pollution which may reasonably
be anticipated to endanger public health or welfare” and satisfy two
other criteria, including “whose presence . . . in the ambient air
results from numerous or diverse mobile or stationary sources” and to
issue air quality criteria for those that are listed.  Air quality
criteria are intended to “accurately reflect the latest scientific
knowledge useful in indicating the kind and extent of all identifiable
effects on public health or welfare which may be expected from the
presence of [a] pollutant in the ambient air . . . .”

Section 109 (42 U.S.C. 7409) directs the Administrator to propose and
promulgate “primary” and “secondary” NAAQS for pollutants for
which air quality criteria are issued.  Section 109(b)(1) defines a
primary standard as one “the attainment and maintenance of which in
the judgment of the Administrator, based on such criteria and allowing
an adequate margin of safety, are requisite to protect the public
health.”  A secondary standard, as defined in section 109(b)(2), must
“specify a level of air quality the attainment and maintenance of
which, in the judgment of the Administrator, based on such criteria, is
requisite to protect the public welfare from any known or anticipated
adverse effects associated with the presence of such air pollutant in
the ambient air.” 

The requirement that primary standards include an adequate margin of
safety was intended to address uncertainties associated with
inconclusive scientific and technical information available at the time
of standard setting.  It was also intended to provide a reasonable
degree of protection against hazards that research has not yet
identified.  Lead Industries Association v. EPA, 647 F.2d 1130, 1154
(D.C. Cir 1980), cert. denied, 449 U.S. 1042 (1980); American Petroleum
Institute v. Costle, 665 F.2d 1176, 1186 (D.C. Cir. 1981), cert. denied,
455 U.S. 1034 (1982).  Both kinds of uncertainties are components of the
risk associated with pollution at levels below those at which human
health effects can be said to occur with reasonable scientific
certainty.  Thus, in selecting primary standards that include an
adequate margin of safety, the Administrator is seeking not only to
prevent pollution levels that have been demonstrated to be harmful but
also to prevent lower pollutant levels that may pose an unacceptable
risk of harm, even if the risk is not precisely identified as to nature
or degree.  The CAA does not require the Administrator to establish a
primary NAAQS at a zero-risk level or at background concentration
levels, see Lead Industries Association v. EPA, 647 F.2d at 1156 n. 51,
but rather at a level that reduces risk sufficiently so as to protect
public health with an adequate margin of safety.

In addressing the requirement for an adequate margin of safety, EPA
considers such factors as the nature and severity of the health effects
involved, the size of the population(s) at risk, and the kind and degree
of the uncertainties that must be addressed.  The selection of any
particular approach to providing an adequate margin of safety is a
policy choice left specifically to the Administrator’s judgment.  Lead
Industries Association v. EPA, 647 F.2d at 1161-62; Whitman v. American
Trucking Associations, 531 U.S. 457, 495 (2001).

In setting standards that are “requisite” to protect public health
and welfare, as

provided in section 109(b), EPA’s task is to establish standards that
are neither more nor

less stringent than necessary for these purposes.  Whitman v. America
Trucking

Associations, 531 U.S. 457, 473.  In establishing “requisite”
primary and secondary

standards, EPA may not consider the costs of implementing the standards.
 Id. at 471.  

	Section 109(d)(1) of the CAA requires that “not later than December
31, 1980, and at 5-year intervals thereafter, the Administrator shall
complete a thorough review of the criteria published under section 108
and the national ambient air quality standards . . . and shall make such
revisions in such criteria and standards and promulgate such new
standards as may be appropriate . . . .”  Section 109(d)(2) requires
that an independent scientific review committee  “shall complete a
review of the criteria . . . and the national primary and secondary
ambient air quality standards . . . and shall recommend to the
Administrator any new . . . standards and revisions of existing criteria
and standards as may be appropriate . . . .”  This independent review
function is performed by the Clean Air Scientific Advisory Committee
(CASAC) of EPA’s Science Advisory Board.

B.	Related Control Requirements

 States have primary responsibility for ensuring attainment and
maintenance of ambient air quality standards once EPA has established
them.  Under section 110 of the Act (42 U.S.C. 7410) and related
provisions, States are to submit, for EPA approval, State implementation
plans (SIPs) that provide for the attainment and maintenance of such
standards through control programs directed to emission sources.  

The majority of man-made nitrogen oxides (NOx) and volatile organic
compounds (VOC) emissions that contribute to O3 formation in the United
States come from three types of sources: mobile sources, industrial
processes (which include consumer and commercial products), and the
electric power industry.  Mobile sources and the electric power industry
were responsible for 78 percent of annual NOx emissions in 2004.  That
same year, 99 percent of man-made VOC emissions came from industrial
processes (including solvents) and mobile sources.  Emissions from
natural sources, such as trees, may also comprise a significant portion
of total VOC emissions in certain regions of the country, especially
during the O3 season, which are considered natural background emissions.

The EPA has developed new emissions standards for many types of
stationary sources and for nearly every class of mobile sources in the
last decade to reduce O3 by decreasing emissions of NOx and VOC.  These
programs complement State and local efforts to improve O3 air quality
and meet the 0.084 ppm 8-hour national standards.  Under title II of the
CAA, 42 U.S.C. 7521-7574), EPA has established new emissions standards
for nearly every type of automobile, truck, bus, motorcycle, earth
mover, and aircraft engine, and for the fuels used to power these
engines.  EPA also established new standards for the smaller engines
used in small watercraft, lawn and garden equipment.  In March 2008, EPA
promulgated new standards for locomotive and marine diesel engines and
in August 2009, proposed to control emissions from ocean-going vessels. 

Benefits from engine standards increase modestly each year as older,
more-polluting vehicles and engines are replaced with newer, cleaner
models.  In time, these programs will yield substantial emission
reductions.  Benefits from fuel programs generally begin as soon as a
new fuel is available.

The reduction of VOC emissions from industrial processes has been
achieved either directly or indirectly through implementation of control
technology standards, including maximum achievable control technology,
reasonably available control technology, and best available control
technology standards; or are anticipated due to proposed or upcoming
proposals based on generally available control technology or best
available controls under provisions related to consumer and commercial
products.  These standards have resulted in VOC emission reductions of
almost a million tons per year accumulated starting in 1997 from a
variety of sources including combustion sources, coating categories, and
chemical manufacturing.  EPA has also finalized emission standards and
fuel requirements for new stationary engines.   In the area of consumer
and commercial products, EPA has finalized new national VOC emission
standards for aerosol coatings and is working toward amending existing
rules to establish new nationwide VOC content limits for household and
institutional consumer products and architectural and industrial
maintenance coatings.  The aerosol coatings rule took effect in July
2009; the compliance date for both the amended consumer product rule and
architectural coatings rule is anticipated to be January 2011.  These
actions are expected to yield significant new VOC reductions – about
200,000 tons per year.  Additionally, in ozone nonattainment areas, we
anticipate reductions of an additional 25,000 tons per year as States
adopt rules this year implementing control techniques recommendations
issued in 2008 for 4 additional categories of consumer and commercial
products, typically surface coatings and adhesives used in industrial
manufacturing operations.    These emission reductions primarily result
from solvent controls and typically occur where and when the solvent is
used, such as during manufacturing processes.  

The power industry is one of the largest emitters of NOx in the United
States. Power industry emission sources include large electric
generating units (EGU) and some large industrial boilers and turbines. 
The EPA’s landmark Clean Air Interstate Rule (CAIR), issued on March
10, 2005, was designed to permanently cap power industry emissions of
NOx in the eastern United States.  The first phase of the cap was to
begin in 2009, and a lower second phase cap was to begin in 2015.  The
EPA had projected that by 2015, the CAIR and other programs would reduce
NOx emissions during the O3 season by about 50 percent and annual NOx
emissions by about 60 percent from 2003 levels in the Eastern U.S. 
However, on July 11, 2008 and December 23, 2008, the U.S. Court of
Appeals for the D.C. Circuit issued decisions on petitions for review of
the CAIR.  In its July 11 opinion, the court found CAIR unlawful and
decided to vacate CAIR and its associated Federal implementation plans
(FIPs) in their entirety.  On December 23, the court granted EPA’s
petition for rehearing to the extent that it remanded without vacatur
for EPA to conduct further proceedings consistent with the Court’s
prior opinion.  Under this decision, CAIR will remain in place only
until replaced by EPA with a rule that is consistent with the Court’s
July 11 opinion.  The EPA recognizes the need in our CAIR replacement
effort to address the reconsidered ozone standard, and we are currently
assessing our options for the best way to accomplish this.   It should
also be noted that new electric generating units (EGUs) are also subject
to NOx limits under New Source Performance Standards (NSPS) under CAA
section 111, as well as either nonattainment new source review or
prevention of significant deterioration requirements.

With respect to agricultural sources, the U.S. Department of Agriculture
(USDA) has approved conservation systems and activities that reduce
agricultural emissions of NOx and VOC.  Current practices that may
reduce emissions of NOx and VOC include engine replacement programs,
diesel retrofit programs, manipulation of pesticide applications
including timing of applications, and animal feeding operations waste
management techniques.  The EPA recognizes that USDA has been working
with the agricultural community to develop conservation systems and
activities to control emissions of O3 precursors. 

These conservation activities are voluntarily adopted through the use of
incentives provided to the agricultural producer.  In cases where the
States need these measures to attain the standard, the measures could be
adopted.  The EPA will continue to work with USDA on these activities
with efforts to identify and/or improve the control efficiencies,
prioritize the adoption of these conservation systems and activities,
and ensure that appropriate criteria are used for identifying the most
effective application of conservation systems and activities. 

The EPA will work together with USDA and with States to identify
appropriate measures to meet the primary and secondary standards,
including site-specific conservation systems and activities.  Based on
prior experience identifying conservation measures and practices to meet
the PM NAAQS requirements, the EPA will use a similar process to
identify measures that could meet the O3 requirements.  The EPA
anticipates that certain USDA-approved conservation systems and
activities that reduce agricultural emissions of NOx and VOC may be able
to satisfy the requirements for applicable sources to implement
reasonably available control measures for purposes of attaining the
primary and secondary O3 NAAQS.

C.	Review of Air Quality Criteria and Standards for O3

	In 1971, EPA first established primary and secondary NAAQS for
photochemical oxidants (36 FR 8186).  Both primary and secondary
standards were set at a level of 0.08 parts per million (ppm), 1-hr
average, total photochemical oxidants, not to be exceeded more than one
hr per year.   In 1977, EPA announced the first periodic review of the
air quality criteria in accordance with section 109(d)(1) of the Act. 
The EPA published a final decision in 1979 (44 FR 8202).  Both primary
and secondary standard levels were revised from 0.08 to 0.12 ppm.  The
indicator was revised from photochemical oxidants to O3, and the form of
the standards was revised from a deterministic to a statistical form,
which defined attainment of the standards as occurring when the expected
number of days per calendar year with maximum hourly average
concentration greater than 0.12 ppm is equal to or less than one.  In
1983, EPA announced that the second periodic review of the primary and
secondary standards for O3 had been initiated.  Following review and
publication of air quality criteria and a supplement, EPA published a
proposed decision (57 FR 35542) in August 1992 that announced EPA’s
intention to proceed as rapidly as possible with the next review of the
air quality criteria and standards for O3 in light of emerging evidence
of health effects related to 6- to 8-hr O3 exposures.  In March 1993,
EPA concluded the review by deciding that revisions to the standards
were not warranted at that time (58 FR 13008).

	In August 1992 (57 FR 35542), EPA announced plans to initiate the third
periodic review of the air quality criteria and O3 NAAQS.  On the basis
of the scientific evidence contained in the 1996 CD (U.S. EPA 1996a) and
the 1996 Staff Paper (U.S. EPA, 1996b), and related technical support
documents, linking exposures to ambient O3 to adverse health and welfare
effects at levels allowed by the then existing standards, EPA proposed
to revise the primary and secondary O3 standards in December 1996 (61 FR
65716).  The EPA proposed to replace the then existing 1-hour primary
and secondary standards with 8-hour average O3 standards set at a level
of 0.08 ppm (equivalent to 0.084 ppm using standard rounding
conventions).  The EPA also proposed, in the alternative, to establish a
new distinct secondary standard using a biologically based cumulative
seasonal form.  The EPA completed the review in July 1997 (62 FR 38856)
by setting the primary standard at a level of 0.08 ppm, based on the
annual fourth-highest daily maximum 8-hr average concentration, averaged
over three years, and setting the secondary standard identical to the
revised primary standard.

	The EPA initiated the most recent periodic review of the air quality
criteria and standards for O3 in September 2000 with a call for
information (65 FR 57810; September 26, 2000) for the development of a
revised Air Quality Criteria Document for O3 and Other Photochemical
Oxidants (henceforth the "2006 Criteria Document").  A project work plan
(EPA, 2002) for the preparation of the Criteria Document was released in
November 2002 for CASAC and public review.  The EPA held a series of
workshops in mid-2003 on several draft chapters of the Criteria Document
to obtain broad input from the relevant scientific communities.  These
workshops helped to inform the preparation of the first draft Criteria
Document (EPA, 2005a), which was released for CASAC and public review on
January 31, 2005; a CASAC meeting was held on May 4-5, 2005 to review
the first draft Criteria Document.  A second draft Criteria Document
(EPA, 2005b) was released for CASAC and public review on August 31,
2005, and was discussed along with a first draft Staff Paper (EPA,
2005c) at a CASAC meeting held on December 6-8, 2005.  In a February 16,
2006 letter to the Administrator, CASAC provided comments on the second
draft Criteria Document (Henderson, 2006a), and the final 2006 Criteria
Document (EPA, 2006a) was released on March 21, 2006.  In a June 8, 2006
letter to the Administrator (Henderson, 2006b), CASAC provided
additional advice to the Agency concerning chapter 8 of the final 2006
Criteria Document (Integrative Synthesis) to help inform the second
draft Staff Paper.  

A second draft Staff Paper (EPA, 2006b) was released on July 17, 2006
and reviewed by CASAC on August 24-25, 2006.  In an October 24, 2006
letter to the Administrator, CASAC provided advice and recommendations
to the Agency concerning the second draft Staff Paper (Henderson,
2006c).   A final 2007 Staff Paper (EPA, 2007a) was released on January
31, 2007.  In a March 26, 2007 letter (Henderson, 2007), CASAC offered
additional advice to the Administrator with regard to recommendations
and revisions to the primary and secondary O3 NAAQS. 

	The schedule for completion of the 2008 rulemaking was governed by a
consent decree resolving a lawsuit filed in March 2003 by a group of
plaintiffs representing national environmental and public health
organizations, alleging that EPA had failed to complete the review
within the period provided by statute.  The modified consent decree that
governed the 2008 rulemaking, entered by the court on December 16, 2004,
provided that EPA sign for publication notices of proposed and final
rulemaking concerning its review of the O3 NAAQS no later than March 28,
2007 and December 19, 2007, respectively.  That consent decree was
further modified in October 2006 to change these proposed and final
rulemaking dates to no later than May 30, 2007 and February 20, 2008,
respectively.  These dates for signing the publication notices of
proposed and final rulemaking were further extended to no later than
June 20, 2007 and March 12, 2008, respectively.  The proposed decision
was signed on June 20, 2007 and published in the Federal Register on
July 11, 2007 (72 FR 37818).

	Public hearings on the proposed decision were held on Thursday, August
30, 2007 in Philadelphia, PA and Los Angeles, CA.  On Wednesday,
September 5, 2007, hearings were held in Atlanta, GA, Chicago, IL, and
Houston, TX.  A large number of comments were received from various
commenters on the 2007 proposed revisions to the O3 NAAQS.  A
comprehensive summary of all significant comments, along with EPA’s
responses (henceforth “Response to Comments”), can be found in the
docket for the 2008 rulemaking, which is also the docket for this
reconsideration rulemaking.

The EPA’s final decision on the O3 NAAAQS was published in the Federal
Register on March 27, 2008 (73 FR 16436).  In the 2008 rulemaking, EPA
revised the level of the 8-hour primary standard for O3 to 0.075 parts
per million (ppm), expressed to three decimal places.  With regard to
the secondary standard for O3, EPA revised the 8-hour standard by making
it identical to the revised primary standard.  The EPA also made
conforming changes to the Air Quality Index (AQI) for O3, setting an AQI
value of 100 equal to 0.075 ppm, 8-hour average, and making proportional
changes to the AQI values of 50, 150 and 200.  

D.	Reconsideration of the 2008 O3 NAAQS Final Rule

Consistent with a directive of the new Administration regarding the
review of new and pending regulations (Emanuel memorandum, 74 FR 4435;
January 26, 2009), the Administrator reviewed a number of actions that
were taken in the last year by the previous Administration.  The 2008
final rule was included in this review in recognition of the central
role that the NAAQS play in enabling EPA to fulfill its mission to
protect the nation’s public health and welfare.  In her review, the
Administrator was mindful of the need for judgments concerning the NAAQS
to be based on a strong scientific foundation which is developed through
a transparent and credible NAAQS review process, consistent with the
core values highlighted in President Obama’s memorandum on scientific
integrity (March 9, 2009).

1.	Decision to Initiate a Rulemaking to Reconsider

In her review of the 2008 final rule, several aspects of the final rule
related to the primary and secondary standards stood out to the
Administrator.  As an initial matter, the Administrator noted that the
2008 final rule concluded that the 1997 primary and secondary O3
standards were not adequate to protect public health and public welfare,
and that revisions were necessary to provide increased protection.  With
respect to revision of the primary standard, the Administrator noted
that the revised level established in the 2008 final rule was above the
range that had been unanimously recommended by CASAC.  She also noted
that EPA received comments from a large number of commenters from the
medical and public health communities, including EPA’s Children’s
Health Protection Advisory Committee, all of which endorsed levels
within CASAC’s recommended range.

With respect to revision of the secondary O3 standard, the Administrator
noted that the 2008 final rule differed substantially from CASAC’s
recommendations that EPA adopt a new secondary O3 standard based on a
cumulative, seasonal measure of exposure.  The 2008 final rule revised
the secondary standard to be identical to the revised primary standard,
which is based on an 8-hour daily maximum measure of exposure.  She also
noted that EPA received comments from a number of commenters
representing environmental interests, all of which endorsed CASAC;s
recommendation for a new cumulative, seasonal secondary standard.  

Subsequent to issuance of the 2008 final rule, in April 2008, CASAC took
the unusual step of sending EPA a letter expressing strong, unanimous
disagreement with EPA’s decisions on both the primary and secondary
standards (Henderson, 2008).  The CASAC explained that it did not
endorse the revised primary O3 standard as being sufficiently protective
of public health because it failed to satisfy the explicit stipulation
of the Act to provide an adequate margin of safety.  The CASAC also
expressed the view that failing to revise the secondary standard to a
cumulative, seasonal form was not supported by the available science. 
In addition to CASAC’s letter, the Administrator noted a recent
adverse ruling issued by the U.S. Court of Appeals for the District of
Columbia Circuit on another NAAQS decision.  In February 2009, the DC
Circuit remanded the Agency's decisions on the primary annual and
secondary standards for fine particles (PM2.5).  In so doing, the Court
found that EPA had not adequately explained the basis for its decisions,
including why CASAC’s recommendations for a more health-protective
primary annual standard and for secondary standards different from the
primary standards were not accepted.  American Farm Bureau v. EPA, 559
F.3d. 512 (D.C. Cir. 2009).  

Based on her review of the information described above, the
Administrator is initiating a rulemaking to reconsider parts of the 2008
final rule.  Specifically, the Administrator is reconsidering the level
of the primary standard to ensure that it is sufficiently protective of
public health, as discussed in section II below, and is reconsidering
all aspects of the secondary standard to ensure that it appropriately
reflects the available science and is sufficiently protective of public
welfare, as discussed in section IV below.  Based on her review, the
Administrator has serious cause for concern regarding whether the
revisions to the primary and secondary O3 standards adopted in the 2008
final rule satisfy the requirements of the CAA, in light of the body of
scientific evidence before the Agency.  In addition, the importance of
the O3 NAAQS to public health and welfare weigh heavily in favor of
reconsidering parts of the 2008 final rule as soon as possible, based on
the scientific and technical information upon which the 2008 final rule
was based.  

Also, EPA conducted a provisional assessment of “new” scientific
papers (EPA, 2009) of scientific literature evaluating health and
ecological effects of O3 exposure published since the close of the 2006
Criteria Document upon which the 2008 O3 NAAQS were based.  The
Administrator notes that the provisional assessment of “new” science
found that such studies did not materially change the conclusions in the
2006 Criteria Document.  This provisional assessment is supportive of
the Administrator’s decision to reconsider parts of the 2008 final
rule at this time, based on the scientific and technical information
available for the 2008 final rule, as compared to foregoing such
reconsideration and taking appropriate action in the future as part of
the next periodic review of the air quality criteria and NAAQS, which
will include such scientific and technical information.

The reconsideration of parts of the 2008 final rule discussed in this
notice is based on the scientific and technical record from the 2008
rulemaking, including public comments and CASAC advice and
recommendations.  The information that was assessed during the 2008
rulemaking includes information in the 2006 Criteria Document (EPA,
2006a), the 2007 Policy Assessment of Scientific and Technical
Information, referred to as the 2007 Staff Paper (EPA, 2007b), and
related technical support documents including the 2007 REAs (U.S. EPA,
2007c; Abt Associates, 2007a,b).  Scientific and technical information
developed since the 2006 Criteria Document will be considered in the
next periodic review, instead of this reconsideration rulemaking,
allowing the new information to receive careful and comprehensive review
by CASAC and the public before it is used as a basis in a rulemaking
that determines whether to revise the NAAQS.  

2.	Ongoing Litigation

In May 2008, following publication of the 2008 final rule, numerous
groups, including state, public health, environmental, and industry
petitioners, challenged EPA's decisions in federal court.  The
challenges were consolidated as State of Mississippi, et al. v. EPA (No.
08-1200, D.C. Cir. 2008).  On March 10, 2009, EPA filed an unopposed
motion requesting that the Court vacate the briefing schedule and hold
the consolidated cases in abeyance.  The Agency stated its desire to
allow time for appropriate officials from the new Administration to
review the O3 standards to determine whether they should be maintained,
modified or otherwise reconsidered.  The EPA further requested that it
be directed to notify the Court and all the parties of any actions it
has taken or intends to take, if any, within 180 days of the Court
vacating the briefing schedule.  On March 19, 2009, the Court granted
EPA's motion.  Pursuant to the Court's order, on September 16, 2009 EPA
notified the Court and the parties of its decision to initiate a
rulemaking to reconsider the primary and secondary O3 standards set in
March 2008 to ensure they satisfy the requirements of the CAA  In its
notice to the Court, EPA stated that this notice of proposed rulemaking
would be signed by December 21, 2009, and that the final rule will be
signed by August 31, 2010.

II.	Rationale for Proposed Decision on the Level of the Primary Standard

	As an initial matter, the Administrator notes that the 2008 final rule
concluded that the 1997 primary O3 standard was “not sufficient and
thus not requisite to protect public health with an adequate margin of
safety, and that revision is needed to provide increased public health
protection” (73 FR 16472).  The Administrator is not reconsidering
this aspect of the 2008 decision, which is based on the reasons
discussed in section II.B of the 2008 final rule (73 FR 16443-16472). 
The Administrator also notes that the 2008 final rule concluded that it
was appropriate to retain the O3 indicator, the 8-hour averaging time,
and form of the primary O3 standard (specified as the annual
fourth-highest daily maximum 8-hour concentration, averaged over 3
years), while concluding that revision of the standard level was
appropriate.  The Administrator is not reconsidering these aspects of
the 2008 decision, which are based on the reasons discussed in sections
II.C.1-3 of the 2008 final rule, which address the indicator, averaging
time, and form, respectively, of the primary O3 standard (73 FR
16472-16475).  For these reasons, the Administrator is not reopening the
2008 decision with regard to the need to revise the 1997 primary O3
standard nor with regard to the indicator, averaging time, and form of
the 2008 primary O3 standard.  Thus, the information that follows in
this section specifically focuses on a reconsideration of level of the
primary O3 standard.

This section presents the rationale for the Administrator’s proposed
decision that the O3 primary standard, which was set at a level of 0.075
ppm in the 2008 final rule, should instead be set at a lower level
within the range from 0.060 to 0.070 ppm.  As discussed more fully
below, the rationale for the proposed range of standard levels is based
on a thorough review of the latest scientific information on human
health effects associated with the presence of O3 in the ambient air
presented in the 2006 Criteria Document.  This rationale also takes into
account:  (1) staff assessments of the most policy-relevant information
in the 2006 Criteria Document and staff analyses of air quality, human
exposure, and health risks, presented in the 2007 Staff Paper, upon
which staff recommendations for revisions to the primary O3 standard in
the 2008 rulemaking were based; (2) CASAC advice and recommendations, as
reflected in discussions of drafts of the 2006 Criteria Document and
2007 Staff Paper at public meetings, in separate written comments, and
in CASAC’s letters to the Administrator both before and after the 2008
rulemaking; and (3) public comments received during the development of
these documents, either in connection with CASAC meetings or separately,
and on the 2007 proposed rule.

In developing this rationale, the Administrator recognizes that the CAA
requires her to reach a public health policy judgment as to what
standard would be requisite to protect public health with an adequate
margin of safety, based on scientific evidence and technical assessments
that have inherent uncertainties and limitations.  This judgment
requires making reasoned decisions as to what weight to place on various
types of evidence and assessments, and on the related uncertainties and
limitations.  Thus, in selecting standard levels to propose, and
subsequently in selecting a final level, the Administrator is seeking
not only to prevent O3 levels that have been demonstrated to be harmful
but also to prevent lower O3 levels that may pose an unacceptable risk
of harm, even if the risk is not precisely identified as to nature or
degree.

	In developing this rationalethis proposed rule, EPA has drawn upon an
integrative synthesis of the entire body of evidence, published through
early 2006, on human health effects associated with the presence of O3
in the ambient air.  As discussed below in section II.A, this body of
evidence addresses a broad range of health endpoints associated with
exposure to ambient levels of O3 (EPA, 2006a, chapter 8), and includes
over one hundred epidemiologic studies conducted in the U.S., Canada,
and many countries around the world.  In reconsidering this evidence,
EPA focuses on those health endpoints that have been demonstrated to be
caused by exposure to O3, or for which the 2006 Criteria Document judges
associations with O3 to be causal, likely causal, or for which the
evidence is highly suggestive that O3 contributes to the reported
effects.  This rationale also draws upon the results of quantitative
exposure and risk assessments, discussed below in section II.B.  Section
II.C focuses on the considerations upon which the Administrator’s
proposed conclusions on the level of the primary standard are based. 
Policy-relevant evidence-based and exposure/risk-based considerations
are discussed, and the rationale for the 2008 final rulemaking on the
primary standard and CASAC advice, given both prior to the development
of the 2007 proposed rule and following the 2008 final rule, are
summarized.  Finally, the Administrator’s proposed conclusions on the
level of the primary standard are presented.  Section II.D summarizes
the proposed decision on the level of the primary O3 standard and the
solicitation of public comments.

Judgments made in the 2006 Criteria Document and 2007 Staff Paper about
the extent to which relationships between various health endpoints and
short-term exposures to ambient O3 are likely causal have been informed
by several factors.  As discussed below in section II.A, these factors
include the nature of the evidence (i.e., controlled human exposure,
epidemiological, and/or toxicological studies) and the weight of
evidence, which takes into account such considerations as biological
plausibility, coherence of evidence, strength of association, and
consistency of evidence.

In assessing the health effects data base for O3, it is clear that human
studies provide the most directly applicable information for determining
causality because they are not limited by the uncertainties of dosimetry
differences and species sensitivity differences, which would need to be
addressed in extrapolating animal toxicology data to human health
effects.  Controlled human exposure studies provide data with the
highest level of confidence since they provide human health effects data
under closely monitored conditions and can provide exposure-response
relationships.  Epidemiological data provide evidence of associations
between ambient O3 levels and more serious acute and chronic health
effects (e.g., hospital admissions and mortality) that cannot be
assessed in controlled human exposure studies.  For these studies the
degree of uncertainty introduced by potentially confounding variables
(e.g., other pollutants, temperature) and other factors affects the
level of confidence that the health effects being investigated are
attributable to O3 exposures, alone and in combination with other
copollutants. 

	In using a weight of evidence approach to inform judgments about the
degree of confidence that various health effects are likely to be caused
by exposure to O3, confidence increases as the number of studies
consistently reporting a particular health endpoint grows and as other
factors, such as biological plausibility and strength, consistency, and
coherence of evidence, increase.  Conclusions regarding biological
plausibility, consistency, and coherence of evidence of O3-related
health effects are drawn from the integration of epidemiological studies
with mechanistic information from controlled human exposure studies and
animal toxicological studies.  As discussed below, this type of
mechanistic linkage has been firmly established for several respiratory
endpoints (e.g., lung function decrements, lung inflammation) but
remains far more equivocal for cardiovascular endpoints (e.g.,
cardiovascular-related hospital admissions).  For epidemiological
studies, strength of association refers to the magnitude of the
association and its statistical strength, which includes assessment of
both effects estimate size and precision.  In general, when associations
yield large relative risk estimates, it is less likely that the
association could be completely accounted for by a potential confounder
or some other bias.  Consistency refers to the persistent finding of an
association between exposure and outcome in multiple studies of adequate
power in different persons, places, circumstances and times.  For
example, the magnitude of effect estimates is relatively consistent
across recent studies showing association between short-term, but not
long-term, O3 exposure and mortality.

	Based on the information discussed below in sections II.A.1 – II.A.3,
judgments concerning the extent to which relationships between various
health endpoints and ambient O3 exposures are likely causal are
summarized below in section II.A.3.c.  These judgments reflect the
nature of the evidence and the overall weight of the evidence, and are
taken into consideration in the quantitative exposure and risk
assessments, discussed below in section II.B.

	To put judgments about health effects that have been demonstrated to be
caused by exposure to O3, or for which the 2006 Criteria Document judges
associations with O3 to be causal, likely causal, or for which the
evidence is highly suggestive that O3 contributes to the reported
effects into a broader public health context, EPA has drawn upon the
results of the quantitative exposure and risk assessments.  These
assessments provide estimates of the likelihood that individuals in
particular population groups that are at risk for various O3-related
physiological health effects would experience “exposures of concern”
and specific health endpoints under varying air quality scenarios (i.e.,
just meeting various standards), as well as characterizations of the
kind and degree of uncertainties inherent in such estimates.

	In the 2008 final rulemaking and in this reconsideration, the term
“exposures of concern” is defined as personal exposures while at
moderate or greater exertion to 8-hour average ambient O3 levels at and
above specific benchmark levels which represent exposure levels at which
O3-related health effects are known or can reasonably be inferred to
occur in some individuals, as discussed below in section II.B.1.  The
EPA emphasizes that although the analysis of “exposures of concern”
was conducted using three discrete benchmark levels (i.e., 0.080, 0.070,
and 0.060 ppm), the concept is more appropriately viewed as a continuum
with greater confidence and less uncertainty about the existence of
health effects at the upper end and less confidence and greater
uncertainty as one considers increasingly lower O3 exposure levels.  The
EPA recognizes that there is no sharp breakpoint within the continuum
ranging from at and above 0.080 ppm down to 0.060 ppm.  In considering
the concept of exposures of concern, it is important to balance concerns
about the potential for health effects and their severity with the
increasing uncertainty associated with our understanding of the
likelihood of such effects at lower O3 levels.  

	Within the context of this continuum, estimates of exposures of concern
at discrete benchmark levels provide some perspective on the public
health impacts of O3-related health effects that have been demonstrated
in controlled human exposure and toxicological studies but cannot be
evaluated in quantitative risk assessments, such as lung inflammation,
increased airway responsiveness, and changes in host defenses.  They
also help in understanding the extent to which such impacts have the
potential to be reduced by meeting various standards.  These O3-related
physiological effects are plausibly linked to the increased morbidity
seen in epidemiological studies (e.g., as indicated by increased
medication use in asthmatics, school absences in all children, and
emergency department visits and hospital admissions in people with lung
disease).  Estimates of the number of people likely to experience
exposures of concern cannot be directly translated into quantitative
estimates of the number of people likely to experience specific health
effects, since sufficient information to draw such comparisons is not
available -- if such information were available, these health outcomes
would have been included in the quantitative risk assessment.  Due to
individual variability in responsiveness, only a subset of individuals
who have exposures at and above a specific benchmark level can be
expected to experience such adverse health effects, and susceptible
subpopulations such as those with asthma are expected to be affected
more by such exposures than healthy individuals.  The amount of weight
to place on the estimates of exposures of concern at any of these
benchmark levels depends in part on the weight of the scientific
evidence concerning health effects associated with O3 exposures at and
above that benchmark level.  It also depends on judgments about the
importance from a public health perspective of the health effects that
are known or can reasonably be inferred to occur as a result of
exposures at and above the benchmark level.  Such public health policy
judgments are embodied in the NAAQS standard setting criteria (i.e.,
standards that, in the judgment of the Administrator, are requisite to
protect public health with an adequate margin of safety).

	As discussed below in section II.B.2, the quantitative health risk
assessment conducted as part of the 2008 final rulemaking includes
estimates of risks of lung function decrements in asthmatic and all
school age children, respiratory symptoms in asthmatic children,
respiratory-related hospital admissions, and non-accidental and
cardiorespiratory-related mortality associated with recent ambient O3
levels, as well as risk reductions and remaining risks associated with
just meeting the then current 0.084 ppm standard and various alternative
O3 standards in a number of example urban areas.  There are two parts to
this risk assessment:  one part is based on combining information from
controlled human exposure studies with modeled population exposure, and
the other part is based on combining information from community
epidemiological studies with either monitored or adjusted ambient
concentrations levels.  This assessment provides estimates of the
potential magnitude of O3-related health effects, as well as a
characterization of the uncertainties and variability inherent in such
estimates.  This assessment also provides insights into the distribution
of risks and patterns of risk reductions associated with meeting
alternative O3 standards.

	As discussed below, a substantial amount of new research conducted
since the 1997 review of the O3 NAAQS was available to inform the 2008
final rulemaking, with important new information coming from
epidemiologic studies as well as from controlled human exposure,
toxicological, and dosimetric studies.  The research studies newly
available in the 2008 final rulemaking that were evaluated in the 2006
Criteria Document and the exposure and risk assessments presented in the
2007 Staff Paper have undergone intensive scrutiny through multiple
layers of peer review and many opportunities for public review and
comment.  While important uncertainties remain in the qualitative and
quantitative characterizations of health effects attributable to
exposure to ambient O3, and while different interpretations of these
uncertainties can result in different public health policy judgments,
the review of this information has been extensive and deliberate.  In
the judgment of the Administrator, this intensive evaluation of the
scientific evidence provides an adequate basis for this reconsideration
of the 2008 final rulemaking.

A.	Health Effects Information

	This section outlines key information contained in the 2006 Criteria
Document (chapters 4-8) and in the 2007 Staff Paper (chapter 3) on known
or potential effects on public health which may be expected from the
presence of O3 in ambient air.  The information highlighted here
summarizes:  (1) new information available on potential mechanisms for
health effects associated with exposure to O3; (2) the nature of effects
that have been associated directly with exposure to O3 and indirectly
with the presence of O3 in ambient air; (3) an integrative
interpretation of the evidence, focusing on the biological plausibility
and coherence of the evidence; and (4) considerations in characterizing
the public health impact of O3, including the identification of “at
risk” populations.

	The decision in the 1997 review focused primarily on evidence from
short-term (e.g., 1 to 3 hours) and prolonged ( 6 to 8 hours)
controlled-exposure studies reporting lung function decrements,
respiratory symptoms, and respiratory inflammation in humans, as well as
epidemiology studies reporting excess hospital admissions and emergency
department (ED) visits for respiratory causes.  The 2006 Criteria
Document prepared for the 2008 rulemaking emphasized the large number of
epidemiological studies published since the last review with these and
additional health endpoints, including the effects of acute (short-term
and prolonged) and chronic exposures to O3 on lung function decrements
and enhanced respiratory symptoms in asthmatic individuals, school
absences, and premature mortality.  It also emphasized important new
information from toxicology, dosimetry, and controlled human exposure
studies.  Highlights of the evidence include:

	(1)  Two new controlled human-exposure studies are now available that
examine respiratory effects associated with prolonged O3 exposures at
levels below 0.080 ppm, which was the lowest exposure level that had
been examined in the 1997 review.

	(2)  Numerous controlled human-exposure studies have examined
indicators of O3-induced inflammatory response in both the upper
respiratory tract (URT) and lower respiratory tract (LRT), and increased
airway responsiveness to allergens in subjects with allergic asthma and
allergic rhinitis exposed to O3, while other studies have examined
changes in host defense capability following O3 exposure of healthy
young adults.

	(3)  Animal toxicology studies provide new information regarding
mechanisms of action, increased susceptibility to respiratory infection,
and the biological plausibility of acute effects and chronic,
irreversible respiratory damage.

	(4)  Numerous acute exposure epidemiological studies published during
the past decade offer added evidence of ambient O3-related lung function
decrements and respiratory symptoms in physically active healthy
subjects and greater responses in asthmatic subjects, as well as
evidence on new health endpoints, such as the relationships between
ambient O3 concentrations and asthma medication use and school
absenteeism, and between ambient O3 and cardiac-related physiological
endpoints.

	(5)  Several additional studies have been published over the last
decade examining the temporal associations between O3 exposures and
emergency department visits for asthma and other respiratory diseases
and respiratory-related hospital admissions.

	(6)  A large number of newly available epidemiological studies have
examined the effects of acute exposure to PM and O3 on mortality,
notably including large multicity studies that provide much more robust
and credible information than was available in the 1997 review, as well
as recent meta-analyses that have evaluated potential sources of
heterogeneity in O3-mortality associations.

1.	Overview of Mechanisms

	Evidence on possible mechanisms by which exposure to O3 may result in
acute and chronic health effects is discussed in chapters 5 and 6 of the
2006 Criteria Document.   Evidence from dosimetry, toxicological, and
human exposure studies has contributed to an understanding of the
mechanisms that help to explain the biological plausibility and
coherence of evidence for O3-induced respiratory health effects reported
in epidemiological studies.  More detailed information about the
physiological mechanisms related to the respiratory effects of short-
and long-term exposure to O3 can be found in section II.A.3.b.i and
II.A.3.b.iii, respectively.  In the past, however, little information
was available to help explain potential biological mechanisms which
linked O3 exposure to premature mortality or cardiovascular effects.  As
discussed more fully in section II.A.3.b.ii below, since the 1997 review
an emerging body of animal toxicology and controlled human exposure
evidence is beginning to suggest mechanisms that may mediate acute O3
cardiovascular effects.  While much is known about mechanisms that play
a role in O3-related respiratory effects, additional research is needed
to more clearly understand the role that O3 may have in contributing to
cardiovascular effects.

	With regard to the mechanisms related to short-term respiratory
effects, scientific evidence discussed in the 2006 Criteria Document
(section 5.2) indicates that reactions of O3 with lipids and
antioxidants in the epithelial lining fluid and the epithelial cell
membranes of the lung can be the initial step in mediating deleterious
health effects of O3.  This initial step activates a cascade of events
that lead to oxidative stress, injury, inflammation, airway epithelial
damage and increased alveolar permeability to vascular fluids. 
Inflammation can be accompanied by increased airway responsiveness,
which is an increased bronchoconstrictive response to airway irritants
and allergens.  Continued respiratory inflammation also can alter the
ability of the body to respond to infectious agents, allergens and
toxins.  Acute inflammatory responses to O3 in some healthy people are
well documented, and precursors to lung injury are observed within 3
hours after exposure in humans.  Repeated respiratory inflammation can
lead to a chronic inflammatory state with altered lung structure and
lung function and may lead to chronic respiratory diseases such as
fibrosis and emphysema (EPA, 2006a, section 8.6.2).  The severity of
symptoms and magnitude of response to acute exposures depend on inhaled
dose, as well as on individual susceptibility to O3, as discussed below.
 At the same O3 dose, individuals who are more susceptible to O3 will
have a larger response than those who are less susceptible; among
individuals with similar susceptibility, those who receive a larger dose
will have a larger response to O3.

The inhaled dose is the product of O3 concentration (C), minute
ventilation or ventilation rate, and duration of exposure (T), or (C ×
ventilation rate × T).  A large body of data regarding the
interdependent effect of these components of inhaled dose on pulmonary
responses was assessed in the 1986 and 1996 O3 Criteria Documents.  In
an attempt to describe O3 dose-response characteristics, acute responses
were modeled as a function of total inhaled O3 dose, which was generally
found to be a better predictor of response than O3 concentration,
ventilation rate, or duration of exposure, alone, or as a combination of
any two of these factors (EPA 2006a, section 6.2).  Predicted O3-induced
decrements in lung function have been shown to be a function of exposure
concentration, duration and exercise level for healthy, young adults
(McDonnell et al., 1997).  A meta-analysis of 21 studies (Mudway and
Kelly, 2004) showed that markers of inflammation and increased cellular
permeability in healthy subjects are associated with total O3 dose.

	The 2006 Criteria Document summarizes information on potentially
susceptible and vulnerable groups in section 8.7.  As described there,
the term susceptibility refers to innate (e.g., genetic or
developmental) or acquired (e.g., personal risk factors, age) factors
that make individuals more likely to experience effects with exposure to
pollutants.  A number of population groups and lifestages have been
identified as potentially susceptible to health effects as a result of
O3 exposure, including people with existing lung diseases, including
asthma, children and older adults, and people who have larger than
normal lung function responses that may be due to genetic
susceptibility.  In addition, some population groups and lifestages have
been identified as having increased vulnerability to O3-related effects
due to increased likelihood of exposure while at elevated ventilation
rates, including healthy children and adults who are active outdoors,
for example, outdoor workers, and joggers.  Taken together, the
susceptible and vulnerable groups are more commonly referred to as
"at-risk" groups, as discussed more fully below in section II.A.4.b.

	Based on a substantial body of new evidence from animal, controlled
human exposure and epidemiological studies, the 2006 Criteria Document
concludes that people with asthma and other preexisting pulmonary
diseases are likely to be among those at increased risk from O3
exposure.  Altered physiological, morphological and biochemical states
typical of respiratory diseases like asthma, COPD and chronic bronchitis
may render people sensitive to additional oxidative burden induced by O3
exposure (EPA 2006a, section 8.7).  Children and adults with asthma are
the group that has been studied most extensively.  Evidence from
controlled human exposure studies indicates that asthmatics may exhibit
larger lung function decrements in response to O3 exposure than healthy
controls.  As discussed more fully in section II.A.4.b.ii below,
asthmatics present a differential response profile for cellular,
molecular, and biochemical parameters (EPA, 2006a, section 8.7.1) that
are altered in response to acute O3 exposure.  They can have larger
inflammatory responses, as manifested by larger increases in markers of
inflammation such as white bloods cells (e.g., PMNs) or inflammatory
cytokines.  Asthmatics, and people with allergic rhinitis, are more
likely to mount an allergic-type response upon exposure to O3, as
manifested by increases in white blood cells associated with allergy
(i.e., eosinophils) and related molecules, which increase inflammation
in the airways.  The increased inflammatory and allergic responses also
may be associated with the larger late-phase responses that asthmatics
can experience, which can include increased bronchoconstrictor responses
to irritant substances or allergens and additional inflammation.  In
addition to the experimental evidence of lung function decrements,
respiratory symptoms, and other respiratory effects in asthmatic
populations, two large U.S. epidemiological studies as well as several
smaller U.S. and international studies, have reported fairly robust
associations between ambient O3 concentrations and measures of lung
function and daily symptoms (e.g., chest tightness, wheeze, shortness of
breath) in children with moderate to severe asthma and between O3 and
increased asthma medication use (EPA, 2007a, chapter 6).  These
responses in asthmatics and others with lung disease provide biological
plausibility for the more serious respiratory morbidity effects observed
in epidemiological studies, such as emergency department visits and
hospital admissions.

	Children with and without asthma were found to be particularly
susceptible to O3 effects on lung function and generally have greater
lung function responses than older people.  The American Academy of
Pediatrics (2004) notes that children and infants are among the
population groups most susceptible to many air pollutants, including O3.
 This is in part because their lungs are still developing.  For example,
eighty percent of alveoli are formed after birth, and changes in lung
development continue through adolescence (Dietert et al., 2000). 
Moreover, children have high minute ventilation rates and relatively
high levels of physical activity which also increases their O3 dose
(Plunkett et al., 1992).  Thus, children are at-risk due to both their
susceptibility and vulnerability.

65 years of age) O3-mortality effect estimates to that of the elderly
population (>65 years) indicates that, in general, the elderly
population is more susceptible to O3 mortality effects.    SEQ CHAPTER
\h \r 1 There is supporting evidence of age-related differences in
susceptibility to O3 lung function effects.  The 2006 Criteria Document
(section 7.6.7.2) concludes that the elderly population (>65 years of
age) appear to be at greater risk of O3-related mortality and
hospitalizations compared to all ages or younger populations, and
children (<18 years of age) experience other potentially adverse
respiratory health outcomes with increased O3 exposure.  

	Controlled human exposure studies have also indicated a high degree of
interindividual variability in some of the pulmonary physiological
parameters, such as lung function decrements.  The variable effects in
individuals have been found to be reproducible, in other words, a person
who has a large lung function response after exposure to O3 will likely
have about the same response if exposed again to the same dose of O3
(EPA 2006a, section 6.1).  In controlled human exposure studies, group
mean responses are not representative of this segment of the population
that has much larger than average responses to O3.  Recent studies,
discussed in section II.A.4.b.iv below, reported a role for genetic
polymorphism (i.e., the occurrence together in the same population of
more than one allele or genetic marker at the same locus with the least
frequent allele or marker occurring more frequently than can be
accounted for by mutation alone) in observed differences in antioxidant
enzymes and genes involved in inflammation to modulate pulmonary
function and inflammatory responses to O3 exposure.  These observations
suggest a potential role for these markers in the innate susceptibility
to O3, however, the validity of these markers and their relevance in the
context of prediction to population studies needs additional
experimentation.

	Controlled human exposure studies that provide information about
mechanisms of the initial response to O3 (e.g., lung function
decrements, inflammation, and injury to the lung) also inform the
selection of appropriate lag times to analyze in epidemiological studies
through elucidation of the time course of these responses (EPA 2006a,
section 8.4.3).  Based on the results of these studies, it would be
reasonable to expect that lung function decrements could be detected
epidemiologically within lags of 0 (same day) or 1 to 2 days following
O3 exposure, given the rapid onset of lung function changes and their
persistence for 24 to 48 hours among more responsive human subjects in
controlled human exposure studies.  Other responses take longer to
develop and can persist for longer periods of time.  For example,
although asthmatic individuals may begin to experience symptoms soon
after O3 exposure, it may take anywhere from 1 to 3 days after exposure
for these subjects to seek medical attention as a result of increased
airway responsiveness or inflammation that may persist for 2 to 3 days. 
This may be reflected by epidemiologic observations of significantly
increased risk for asthma-related emergency department visits or
hospital admissions with 1- to 3-day lags, or, perhaps, enhanced
distributed lag risks (combined across 3 days) for such morbidity
indicators.  Analogously, one might project increased mortality within
0- to 3-day lags as a possible consequence of O3-induced increases in
clotting agents arising from the cascade of events, starting with cell
injury described above, occurring within 12 to 24 hours of O3 exposure. 
The time course for many of these initial responses to O3 is highly
variable.  Moreover these observations pertain only to the initial
response to O3.  Consequent responses can follow.  For example, Jörres
et al., (1996) found that in subjects with asthma and allergic rhinitis,
a maximum percent fall in FEV1 of 27.9% and 7.8%, respectively, occurred
3 days after O3 exposure when they were challenged with of the highest
common dose of allergen.  

2.	Nature of Effects

	The 2006 Criteria Document provides new evidence that notably enhances
our understanding of short-term and prolonged exposure effects,
including effects on lung function, symptoms, and inflammatory effects
reported in controlled exposure studies.  These studies support and
extend the findings of the previous Criteria Document.  There is also a
significant body of new epidemiological evidence of associations between
short-term and prolonged exposure to O3 and effects such as premature
mortality, hospital admissions and emergency department visits for
respiratory (e.g., asthma) causes.  Key epidemiological and controlled
human exposure studies are summarized below and discussed in chapter 3
of the 2007 Staff Paper, which is based on scientific evidence
critically reviewed in chapters 5, 6, and 7 of the 2006 Criteria
Document, as well as the Criteria Document’s integration of scientific
evidence contained in chapter 8.    Conclusions drawn about O3-related
health effects are based upon the full body of evidence from controlled
human exposure, epidemiological and toxicological data contained in the
2006 Criteria Document.  

a.	Morbidity

	This section summarizes scientific information on the effects of
inhalation of O3, including public health effects of short-term,
prolonged, and long-term exposures on respiratory morbidity and
cardiovascular system effects, as discussed in chapters 6, 7 and 8 of
the 2006 Criteria Document and chapter 3 of the 2007 Staff Paper.  This
section also summarizes the uncertainty about the potential indirect
effects on public health associated with changes due to increases in
UV-B radiation exposure, such as UV-B radiation-related skin cancers,
that may be associated with reductions in ambient levels of ground-level
O3, as discussed in chapter 10 of the 2006 Criteria Document and chapter
3 of the 2007 Staff Paper.

i.	Effects on the Respiratory System from Short-term and Prolonged O3
Exposures 

Controlled human exposure studies have shown that O3 induces a variety
of health effects, including:  lung function decrements, respiratory
symptoms, increased airway responsiveness, respiratory inflammation and
permeability, increased susceptibility to respiratory infection, and
acute morphological effects.  Epidemiology studies have reported
associations between O3 exposures (i.e., 1-hour, 8-hour and 24-hour) and
a wide range of respiratory-related health effects including:  pulmonary
function decrements; respiratory symptoms; increased asthma medication
use; increased school absences; increased emergency department visits
and hospital admissions.

(a)	Pulmonary Function Decrements, Respiratory Symptoms, and Asthma
Medication Use

(i)	Results from Controlled Human Exposure Studies

	A large number of studies published prior to 1996 that investigated
short-term O3 exposure health effects on the respiratory system from
short-term O3 exposures were reviewed in the 1986 and 1996 Criteria
Documents (EPA, 1986, 1996a).  In the 1997 review, 0.50 ppm was the
lowest O3 concentration at which statistically significant reductions in
forced vital capacity (FVC) and forced expiratory volume in 1 second
(FEV1) were reported in sedentary subjects.  During exercise,
spirometric (lung function) and symptomatic responses were observed at
much lower O3 exposures.  When minute ventilation was considerably
increased by continuous exercise (CE) during O3 exposures lasting 2 hour
or less at > 0.12 ppm, healthy subjects generally experienced decreases
in FEV1, FVC, and other measures of lung function; increases in specific
airway resistance (sRaw), breathing frequency, and airway
responsiveness; and symptoms such as cough, pain on deep inspiration,
shortness of breath, throat irritation, and wheezing.  When exposures
were increased to 4- to 8-hours in duration, statistically significant
lung function and symptom responses were reported at O3 concentrations
as low as 0.08 ppm and at lower minute ventilation (i.e., moderate
rather than high level exercise) than the shorter duration studies.

	The most important observations drawn from studies reviewed in the 1996
Criteria Document were that:  (1) young healthy adults exposed to O3
concentrations > 0.080 ppm develop significant, reversible, transient
decrements in pulmonary function if minute ventilation or duration of
exposure is increased sufficiently; (2) children experience similar lung
function responses but report lesser symptoms from O3 exposure relative
to young adults; (3) O3-induced lung function responses are decreased in
the elderly relative to young adults; (4) there is a large degree of
intersubject variability in physiological and symptomatic responses to
O3 but responses tend to be reproducible within a given individual over
a period of several months; (5) subjects exposed repeatedly to O3 for
several days show an attenuation of response upon successive exposures,
but this attenuation is lost after about a week without exposure; and
(6) acute O3 exposure initiates an inflammatory response which may
persist for at least 18 to 24 hours post exposure.

	The development of these respiratory effects is time-dependent during
both exposure and recovery periods, with great overlap for development
and disappearance of the effects.  In healthy human subjects exposed to
typical ambient O3 levels near 0.120 ppm, lung function responses
largely resolve within 4 to 6 hours postexposure, but cellular effects
persist for about 24 hours.  In these healthy subjects, small residual
lung function effects are almost completely gone within 24 hours, while
in hyperresponsive subjects, recovery can take as much as 48 hour to
return to baseline.  The majority of these responses are attenuated
after repeated consecutive exposures, but such attenuation to O3 is lost
one week postexposure. 

Since 1996, there have been a number of studies published investigating
lung function and symptomatic responses that generally support the
observations previously drawn.  Recent studies for acute exposures of 1
to 2 hours and 6 to 8 hours in duration are compiled in the 2007 Staff
Paper (Appendix 3C).  As summarized in more detail in the 2007 Staff
Paper (section 3.3.1.1), among the more important of the recent studies
that examined changes in FEV1 in large numbers of subjects over a range
of 1-2 hours at exposure levels of 0.080 to 0.40 ppm were studies by
McDonnell et al. (1997) and Ultman et al. (2004).  These studies
observed considerable intersubject variability in FEV1 decrements, which
was consistent with findings in the 1996 Criteria Document.

	For prolonged exposures (4 to 8 hours) in the range of 0.080 to 0.160
ppm O3 using moderate intermittent exercise and typically using
square-wave exposure patterns (i.e., a constant exposure level during
time of exposure), several pre- and post-1996 studies (Folinsbee et al.,
1988,1994; Horstman et al., 1990; Adams, 2002, 2003a, 2006) have
reported statistically significant lung function responses and increased
symptoms in healthy adults with increasing duration of exposure, O3
concentration, and minute ventilation.  Studies that employed triangular
exposure patterns (i.e., integrated exposures that begin at a low level,
rise to a peak, and return to a low level during the exposure) (Hazucha
et al., 1992; Adams 2003a, 2006) suggest that the triangular exposure
pattern can potentially lead to greater FEV1 decrements and respiratory
symptoms than square-wave exposures (when the overall O3 doses are
equal).  These results suggest that peak exposures, reflective of the
pattern of ambient O3 concentrations in some locations, are important in
terms of O3 health effects.

	McDonnell (1996) used data from a series of studies to investigate the
frequency distributions of FEV1 decrements following 6.6 hour exposures
and found statistically significant, but relatively small, group mean
decreases in average FEV1 responses (between 5 and 10 percent) at 0.080
ppm O3.  Notably, about 26 percent of the 60 exposed subjects had lung
function decrements > 10 percent, including about 8 percent of the
subjects that experienced large decrements (>20 percent) (EPA, 2007b,
Figure 3-1A).  These results (which were not corrected for exercise in
filtered air responses) demonstrate that while average responses may be
relatively small at the 0.080 ppm exposure level, some individuals
experience more severe effects that may be clinically significant. 
Similar results at the 0.080 ppm exposure level (for 6.6 hours during
intermittent exercise) were seen in more recent studies of 30 healthy
young adults by Adams (2002, 2006).   In Adams (2006), relatively small
but statistically significant lung function decrements and respiratory
symptom responses were found (for both square-wave and triangular
exposure patterns), with 17 percent of the subjects (5 of 30)
experiencing > 10 percent FEV1 decrements (comparing pre- and
post-exposures) when the results were not corrected for the effects of
exercise alone in filtered air (EPA, 2007b, Figure 3-1B) and with 23
percent of subjects (7 of 30) experiencing such effects when the results
were corrected (EPA, 2007b, p. 3-6).

	These studies by Adams (2002, 2006) were notable in that they were the
only controlled exposure human studies available at the time of the 2008
rulemaking that examined respiratory effects associated with prolonged
O3 exposures at levels below 0.080 ppm, which was the lowest exposure
level that had been examined in the 1997 review.  The Adams (2006) study
investigated a range of exposure levels (0.000, 0.040, 0.060, and 0.080
ppm O3) using square-wave and triangular exposure patterns.  The study
was designed to examine hour-by-hour changes in pulmonary function
(FEV1) and respiratory symptom responses (total subjective symptoms
(TSS) and pain on deep inspiration (PDI)) between these various exposure
protocols at six different time points within the exposure periods to
investigate the effects of different patterns of exposure.  At the 0.060
ppm exposure level, the author reported no statistically significant
differences for FEV1 decrements nor for most respiratory symptoms
responses.  Statistically significant responses were reported only for
TSS for the triangular exposure pattern toward the end of the exposure
period, with the PDI responses being noted as following a closely
similar pattern (Adams, 2006, p. 131-132).  EPA’s reanalysis of the
data from the Adams (2006) study addressed the more fundamental question
of whether there were statistically significant differences in responses
before and after the 6.6 hour exposure period (Brown, 2007), and used a
standard statistical method appropriate for a simple before-and-after
comparison.  The statistical method used by EPA had been used previously
by other researchers to address this same question.  EPA’s reanalysis
of the data from the Adams (2006) study, comparing FEV1 responses pre-
and post-exposure at the 0.060 ppm exposure level, found small group
mean differences from responses to filtered air that were statistically
significant (Brown, 2007). 

	Further examination of the post-exposure FEV1 data and mean data at
other time points and concentrations also suggest a pattern of response
at 0.06 ppm that is consistent with a dose-response relationship rather
than random variability.  For example, the response at 5.6 hours was
similar to that of the post-exposure 6.6 hour response and appeared to
also differ from the FA response.  At the 0.08 ppm level, the subjects
in this study did not appear to be more responsive to O3 than subjects
in previous studies, as the observed response was similar to that of
previous studies (Adams, 2003a,b; Horstman et al., 1990; McDonnell et
al., 1991).  Although of much smaller magnitude, the temporal pattern of
the 0.06 ppm response was generally consistent with the temporal
patterns of response to higher concentrations of O3 in this and other
studies.  These findings are not unexpected because the previously
observed group mean FEV1 responses to 0.08 ppm were in the range of 6-9%
suggesting that exposure to lower concentrations of O3 would result in
smaller, but real group mean FEV1 decrements, i.e., the responses to
0.060 ppm O3 are consistent with the presence of a smooth
exposure-response curve with responses that do not end abruptly below
0.080 ppm.

	Moreover, the Adams studies (2002, 2006) also report a small percentage
of subjects experiencing moderate lung function decrements (> 10
percent) at the 0.060 ppm exposure level.  Based on study data (Adams,
2006) provided by the author, 7 percent of the subjects (2 of 30
subjects) experienced notable FEV1 decrements (( 10 percent) with the
square wave exposure pattern at the 0.060 ppm exposure level (comparing
pre- and post-exposures) when the results were corrected for the effects
of exercise alone in filtered air (EPA, 2007b, p. 3-6).  Furthermore, in
a prior publication (Adams, 2002), the author stated that, “some
sensitive subjects experience notable effects at 0.06 ppm,” based on
the observation that 20% of subjects exposed to 0.06 ppm O3 (in a face
mask exposure study) had greater than a 10% decrement in FEV1 even
though the group mean response was not statistically different from the
filtered air response.  The effects described by Adams (2002), along
with the reanalysis of the Adams (2006) data as described above,
demonstrate considerable inter-individual variability in responses of
healthy adults at the 0.060 ppmlevel with some individuals experiencing
greater than 10% decrements in FEV1.  The observation of statistically
significant small group mean lung function decrements in healthy adults
at 0.060 ppm O3 lowers the lowest-observed-effects level found in
controlled human exposure studies for lung function decrements and
respiratory symptoms.  

Of potentially greater concern is the magnitude of the lung function
decrements in the small group of healthy subjects who had the largest
responses (i.e., FEV1 decrements > 10%).  This is a concern because for
active healthy people, moderate levels of functional responses (e.g.,
FEV1 decrements of > 10% but < 20%) and/or moderate symptomatic
responses would likely interfere with normal activity for relatively few
responsive individuals.  However, for people with lung disease, even
moderate functional or symptomatic responses would likely interfere with
normal activity for many individuals, and would likely result in more
frequent use of medication (see section II.A.4 below).    

(ii)	Results of Epidemiological and Field Studies

	A relatively large number of field studies investigating the effects of
ambient O3 concentrations, in combination with other air pollutants, on
lung function decrements and respiratory symptoms has been published
over the last decade that support the major findings of the 1996
Criteria Document that lung function changes, as measured by decrements
in FEV1 or peak expiratory flow (PEF), and respiratory symptoms in
healthy adults and asthmatic children are closely correlated to ambient
O3 concentrations.  Pre-1996 field studies focused primarily on children
attending summer camps and found O3-related impacts on measures of lung
function, but not respiratory symptoms, in healthy children.  The newer
studies have expanded to evaluate O3-related effects on outdoor workers,
athletes, the elderly, hikers, school children, and asthmatics. 
Collectively, these studies confirm and extend clinical observations
that prolonged (i.e., 6-8 hour) exposure periods, combined with elevated
levels of exertion or exercise, increase the dose of O3 to the lungs at
a given ambient exposure level and result in larger lung function
effects.  The results of one large study of hikers (Korrick et al.,
1998), which reported outcome measures stratified by several factors
(e.g., gender, age, smoking status, presence of asthma) within a
population capable of more than normal exertion, provide useful insight.
 In this study, lung function was measured before and after hiking, and
individual O3 exposures were estimated by averaging hourly O3
concentrations from ambient monitors located at the base and summit. 
The mean 8-hour average O3 concentration was 0.040 ppm (8-hour average
concentration range of 0.021 ppm to 0.074 ppm O3).  Decreased lung
function was associated with O3 exposure, with the greatest effect
estimates reported for the subgroup that reported having asthma or
wheezing, and for those who hiked for longer periods of time.

	Asthma panel studies conducted both in the U.S. and in other countries
have reported that decrements in PEF are associated with routine O3
exposures among asthmatic and healthy people.  One large U.S. multicity
study, the National Cooperative Inner City Asthma Study or NCICAS,
(Mortimer et al., 2002) examined O3-related changes in PEF in 846
asthmatic children from 8 urban areas and reported that the incidence of
> 10 percent decrements in morning PEF are associated with increases in
8-hour average O3 for a 5-day cumulative lag, suggesting that O3
exposure may be associated with clinically significant changes in PEF in
asthmatic children; however, no associations were reported with evening
PEF.  The mean 8-hour average O3 was 0.048 ppm across the 8 cities. 
Excluding days when 8-hour average O3 was greater than 0.080 ppm (less
than 5 percent of days), the associations with morning PEF remained
statistically significant.  Mortimer et al. (2002) discussed potential
biological mechanisms for delayed effects on pulmonary function in
asthma, which included increased nonspecific airway responsiveness
secondary to airway inflammation due to O3 exposure.  Two other panel
studies (Romieu et al., 1996, 1997) carried out simultaneously in
northern and southwestern Mexico City with mildly asthmatic school
children reported statistically significant O3-related reductions in
PEF, with variations in effect depending on lag time and time of day. 
Mean 1-hour maximum O3 concentrations in these locations ranged from
0.190 ppm in northern Mexico City to 0.196 ppm in southwestern Mexico
City.  While several studies report statistically significant
associations between O3 exposure and reduced PEF in asthmatics, other
studies did not, possibly due to low levels of O3 exposure.  EPA
concludes that these studies collectively indicate that O3 may be
associated with short-term declines in lung function in asthmatic
individuals and that the Mortimer et al. (2002) study showed
statistically significant effects at concentrations in the range below
0.080 ppm O3.

	Most of the panel studies which have investigated associations between
O3 exposure and respiratory symptoms or increased use of asthma
medication are focused on asthmatic children.  Two large U.S. studies
(Mortimer et al., 2002; Gent et al., 2003) have reported associations
between ambient O3 concentrations and daily symptoms/asthma medication
use, even after adjustment for copollutants.  Results were more mixed,
meaning that a greater proportion of studies were not both positive and
statistically significant, across smaller U.S. and international studies
that focused on these health endpoints.

	The NCICAS reported morning symptoms in 846 asthmatic children from 8
U.S. urban areas to be most strongly associated with a cumulative 1- to
4-day lag of O3 concentrations (Mortimer et al., 2002).  The NCICAS used
standard protocols that included instructing caretakers of the subjects
to record symptoms (including cough, chest tightness, and wheeze) in the
daily diary by observing or asking the child.  While these associations
were not statistically significant in several cities, when the
individual data are pooled from all eight cities, statistically
significant effects were observed for the incidence of symptoms.  The
authors also reported that the odds ratios remained essentially the same
and statistically significant for the incidence of morning symptoms when
days with 8-hour O3 concentrations above 0.080 ppm were excluded.  These
days represented less than 5 percent of days in the study.

	Gent and colleagues (2003) followed 271 asthmatic children under age 12
and living in southern New England for 6 months (April through
September) using a daily symptom diary.  They found that mean 1-hour max
O3 and 8-hour max O3 concentrations were 0.0586 ppm and 0.0513 ppm ,
respectively.  The data were analyzed for two separate groups of
subjects, those who used maintenance asthma medications during the
follow-up period and those who did not.  The need for regular medication
was considered to be a proxy for more severe asthma.  Not taking any
medication on a regular basis and not needing to use a bronchodilator
would suggest the presence of very mild asthma.  Statistically
significant effects of 1-day lag O3 were observed on a variety of
respiratory symptoms only in the medication user group.  Both daily
1-hour max and 8-hour max O3 concentrations were similarly related to
symptoms such as chest tightness and shortness of breath.  Effects of
O3, but not PM2.5, remained significant and even increased in magnitude
in two-pollutant models.  Some of the associations were noted at 1-hour
max O3 levels below 0.060 ppm.  In contrast, no effects were observed
among asthmatics not using maintenance medication.  In terms of
person-days of follow-up, this is one of the larger studies currently
available that address symptom outcomes in relation to O3 and provides
supportive evidence for effects of O3 independent of PM2.5.  Study
limitations include the post-hoc nature of the population stratification
by medication use.  Also, the study did not account for all of the
important meteorological factors that might influence these results,
such as relative humidity or dew point. 

	The multicity study by Mortimer et al. (2002), which examined an
asthmatic population representative of the United States, and several
single-city studies indicate a robust association of O3 concentrations
with respiratory symptoms and increased medication use in asthmatics. 
While there are a number of well-conducted, albeit relatively smaller,
U.S. studies which showed only limited or a lack of evidence for symptom
increases associated with O3 exposure, these studies had less
statistical power and/or were conducted in areas with relatively low
1-hour maximum average O3 levels, in the range of 0.03 to 0.09 ppm.  The
2006 Criteria Document concludes that the asthma panel studies, as a
group, and the NCICAS in particular, indicate a positive association
between ambient concentrations and respiratory symptoms and increased
medication use in asthmatics.  The evidence has continued to expand
since 1996 and now is considered to be much stronger than in the 1997
review of the O3 primary standard.

	School absenteeism is another potential surrogate for the health
implications of O3 exposure in children.  The association between school
absenteeism and ambient O3 concentrations was assessed in two relatively
large field studies.  The first study, Chen et al. (2000), examined
total daily school absenteeism in about 28,000 elementary school
students in Nevada over a 2-year period (after adjusting for PM10 and CO
concentrations) and found that ambient O3 concentrations with a
distributed lag of 14 days were statistically significantly associated
with an increased rate of school absences.  The second study, Gilliland
et al. (2001), studied O3-related absences among about 2,000 4th grade
students in 12 southern California communities and found statistically
significant associations between 8-hour average O3 concentrations (with
a distributed lag out to 30 days) and all absence categories, and
particularly for respiratory causes.  Neither PM10 nor NO2 were
associated with any respiratory or nonrespiratory illness-related
absences in single pollutant models.  The 2006 Criteria Document
concludes that these studies of school absences suggest that ambient O3
concentrations, accumulated over two to four weeks, may be associated
with school absenteeism, and particularly illness-related absences, but
further replication is needed before firm conclusions can be reached
regarding the effect of O3 on school absences.  In addition, more
research is needed to help shed light on the implications of variation
in the duration of the lag structures (i.e., 1 day, 5 days, 14 days, and
30 days) found both across studies and within data sets by health
endpoint and exposure metric.

(b)	Increased Airway Responsiveness

	As discussed in more detail in the 2006 Criteria Document (section 6.8)
and the 2007 Staff Paper (section 3.3.1.1.2), increased airway
responsiveness, also known as airway hyperresponsiveness (AHR) or
bronchial hyperreactivity, refers to a condition in which the propensity
for the airways to bronchoconstrict due to a variety of stimuli (e.g.,
exposure to cold air, allergens, or exercise) becomes augmented.  This
condition is typically quantified by measuring the decrement in
pulmonary function after inhalation exposure to specific (e.g., antigen,
allergen) or nonspecific (e.g., methacholine, histamine)
bronchoconstrictor stimuli.  Exposure to O3 causes an increase in airway
responsiveness as indicated by a reduction in the concentration of
stimuli required to produce a given reduction in FEV1 or increase in
airway obstruction.  Increased airway responsiveness is an important
consequence of exposure to O3 because its presence means that the
airways are predisposed to narrowing on exposure to various stimuli,
such as specific allergens, cold air or SO2.  Statistically significant
and clinically relevant decreases in pulmonary function have been
observed in early phase allergen response in subjects with allergic
rhinitis after consecutive (4-day) 3-hour exposures to 0.125 ppm O3
(Holz et al., 2002).  Similar increased airway responsiveness in
asthmatics to house dust mite antigen 16 to 18 hours after exposure to a
single dose of O3 (0.160 ppm for 7.6 hours) was observed.  These
observations, based on O3 exposures to levels much higher than the 0.084
ppm standard level suggest that O3 exposure may be a clinically
important factor that can exacerbate the response to ambient
bronchoconstrictor substances in individuals with preexisting allergic
asthma or rhinitis.  Further, O3 may have an immediate impact on the
lung function of asthmatics as well as contribute to effects that
persist for longer periods.  

	Kreit et al. (1989) found that O3 can induce increased airway
responsiveness in asthmatic subjects to O3, who typically have increased
airway responsiveness at baseline.  A subsequent study (Jörres et al.,
1996) suggested an increase in specific (i.e., allergen-induced) airway
reactivity in subjects with allergic asthma, and to a lesser extent in
subjects with allergic rhinitis after short-term exposure to higher O3
levels; other studies reported similar results.  According to one study
(Folinsbee and Hazucha, 2000), changes in airway responsiveness after O3
exposure resolve more slowly than changes in FEV1 or respiratory
symptoms.  Other studies of repeated exposure to O3 suggest that changes
in airway responsiveness tend to be somewhat less affected by
attenuation with consecutive exposures than changes in FEV1 (EPA, 2006a,
section 6.8).

	The 2006 Criteria Document (section 6.8) concludes that O3 exposure is
linked with increased airway responsiveness.  Both human and animal
studies indicate that increased airway responsiveness is not
mechanistically associated with inflammation, and does not appear to be
strongly associated with initial decrements in lung function or
increases in symptoms.  As a result of increased airway responsiveness
induced by O3 exposure, human airways may be more susceptible to a
variety of stimuli, including antigens, chemicals, and particles. 
Because asthmatic subjects typically have increased airway
responsiveness at baseline, enhanced bronchial response to antigens in
asthmatics raises potential public health concerns as they could lead to
increased morbidity (e.g., medication usage, school absences, emergency
room visits, hospital admissions) or to more persistent alterations in
airway responsiveness (EPA 2006a, p. 8-21).  As such, increased airway
responsiveness after O3 exposure represents a plausible link between O3
exposure and increased hospital admissions. 

(c)	Respiratory Inflammation and Increased Permeability

	Based on evidence from the 1997 review, acute inflammatory responses in
the lung have been observed subsequent to 6.6 hour O3 exposures to the
lowest tested level --0.080 ppm -- in healthy adults engaged in
moderately high exercise (section 6.9 of the 2006 Criteria Document and
section 3.3.1.3 of the 2007 Staff Paper).  Some of these prior studies
suggest that inflammatory responses may be detected in some individuals
following O3 exposures in the absence of O3-induced pulmonary decrements
in those subjects.  These studies also demonstrate that short-term
exposures to O3 also can cause increased permeability in the lungs of
humans and experimental animals.  Inflammatory responses and epithelial
permeability have been seen to be independent of spirometric responses. 
Not only are the newer lung inflammation and increased cellular
permeability findings discussed in the 2006 Criteria Document (section
8.4.2) consistent with the 1997 review, but they provide better
characterization of the physiological mechanisms by which O3 causes
these effects.  

	Lung inflammation and increased permeability, which are distinct events
controlled by different mechanisms, are two commonly observed effects of
O3 exposure observed in all of the species studied.  Increased cellular
permeability is a disruption of the lung barrier that leads to leakage
of serum proteins, influx of polymorphonuclear leukocytes (neutrophils
or PMNs), release of bioactive mediators, and movement of compounds from
the airspaces into the blood.  

	A number of controlled human exposure studies have analyzed
bronchoalveolar lavage (BAL) and nasal lavage (NL) fluids and cells for
markers of inflammation and lung damage (EPA, 2006a, Annex AX6). 
Increased lung inflammation is demonstrated by the presence of
neutrophils found in BAL fluid in the lungs, which has long been
accepted as a hallmark of inflammation.  It is apparent, however, that
inflammation within airway tissues may persist beyond the point that
inflammatory cells are found in the BAL fluid.  Soluble mediators of
inflammation, such as cytokines and arachidonic acid metabolites have
been measured in the BAL fluid of humans exposed to O3.  In addition to
their role in inflammation, many of these compounds have
bronchoconstrictive properties and may be involved in increased airway
responsiveness following O3 exposure.  An in vitro study of epithelial
cells from nonatopic and atopic asthmatics exposed to 0.010 to 0.100 ppm
O3 showed significantly increased permeability compared to cells from
normal persons. This indicates a potentially inherent susceptibility of
cells from asthmatic individuals for O3-induced permeability.  

	In the 1996 Criteria Document, assessment of controlled human exposure
studies indicated that a single, acute (1 to 4 hours) O3 exposure (>
0.080 to 0.100 ppm) of subjects engaged in moderate to heavy exercise
could induce a number of cellular and biochemical changes suggestive of
pulmonary inflammation and lung permeability (EPA, 2006a, p. 8-22). 
These changes persisted for at least 18 hours.  Markers from BAL fluid
following both 2-hour and 4-hour O3 exposures repeated up to 5 days
indicate that there is ongoing cellular damage irrespective of
attenuation of some cellular inflammatory responses of the airways,
pulmonary function, and symptom scores (EPA, 2006a, p. 8-22).  Acute
airway inflammation was shown in Devlin et al. (1990) to occur among
adults exposed to 0.080 ppm O3 for 6.6 hours with exercise.   McBride et
al. (1994) reported that asthmatic subjects were more sensitive than
non-asthmatics to upper airway inflammation for O3 exposures that did
not affect pulmonary function (EPA, 2006a, p. 6-33).  However, the
public health significance of these changes is not entirely clear.  

	The studies reporting inflammatory responses and markers of lung injury
have clearly demonstrated that there is significant variation in
response of subjects exposed, especially to 6.6 hours O3 exposures at
0.080 and 0.100 ppm.  To provide some perspective on the public health
impact for these effects, the 2007 Staff Paper (section 3.3.1.1.3) notes
that one study (Devlin et al., 1991) showed that roughly 10 to 50
percent of the 18 young healthy adult subjects experienced notable
increases (i.e., > 2 fold increase) in most of the inflammatory and
cellular injury indicators analyzed, associated with 6.6-hour exposures
at 0.080 ppm.  Similar, although in some cases higher, fractions of the
population of 10 healthy adults tested saw > 2 fold increases associated
with 6.6-hour exposures to 0.100 ppm.  The authors of this study
expressed the view that “susceptible subpopulations such as the very
young, elderly, and people with pulmonary impairment or disease may be
even more affected” (Devlin et al., 1991).  

	Since 1996, a substantial number of human exposure studies have been
published which have provided important new information on lung
inflammation and epithelial permeability.  Mudway and Kelly (2004)
examined O3-induced inflammatory responses and epithelial permeability
with a meta-analysis of 21 controlled human exposure studies and showed
that an influx in neutrophils and protein in healthy subjects is
associated with total O3 dose (product of  O3 concentration, exposure
duration, and minute ventilation) (EPA, 2006a, p. 6-34).  Results of the
analysis suggest that the time course for inflammatory responses
(including recruitment of neutrophils and other soluble mediators) is
not clearly established, but there is evidence that attenuation profiles
for many of these parameters are different (EPA, 2006a, p. 8-22).

	The 2006 Criteria Document (chapter 8) concludes that interaction of O3
with lipid constituents of epithelial lining fluid (ELF) and cell
membranes and the induction of oxidative stress is implicated in injury
and inflammation.  Alterations in the expression of cytokines,
chemokines, and adhesion molecules, indicative of an ongoing oxidative
stress response, as well as injury repair and regeneration processes,
have been reported in animal toxicology and human in vitro studies
evaluating biochemical mediators implicated in injury and inflammation. 
While antioxidants in ELF confer some protection, O3 reactivity is not
eliminated at environmentally relevant exposures (2006 Criteria
Document, p. 8-24).  Further, antioxidant reactivity with O3 is both
species-specific and dose-dependent.

(d)	Increased Susceptibility to Respiratory Infection

	As discussed in more detail in the 2006 Criteria Document (sections
5.2.2, 6.9.6, and 8.4.2), short-term exposures to O3 have been shown to
impair physiological defense capabilities in experimental animals by
depressing alveolar macrophage (AM) functions and by altering the
mucociliary clearance of inhaled particles and microbes resulting in
increased susceptibility to respiratory infection.  Short-term O3
exposures also interfere with the clearance process by accelerating
clearance for low doses and slowing clearance for high doses.  Animal
toxicological studies have reported that acute O3 exposures suppress
alveolar phagocytosis and immune system functions.  Impairment of host
defenses and subsequent increased susceptibility to bacterial lung
infection in laboratory animals has been induced by short-term exposures
to O3 levels as low as 0.080 ppm.  

	A single controlled human exposure study reviewed in the 1996 Criteria
Document (p. 8-26) reported that exposure to 0.080 to 0.100 ppm O3 for
6.6 hours (with moderate exercise) induced decrements in the ability of
AMs to phagocytose microorganisms.  Integrating the recent animal study
results with human exposure evidence available in the 1996 Criteria
Document, the 2006 Criteria Document concludes that available evidence
indicates that short-term O3 exposures have the potential to impair host
defenses in humans, primarily by interfering with AM function.  Any
impairment in AM function may lead to decreased clearance of
microorganisms or nonviable particles.  Compromised AM functions in
asthmatics may increase their susceptibility to other O3 effects, the
effects of particles, and respiratory infections (EPA, 2006a, p. 8-26).

(e)	Morphological Effects

The 1996 Criteria Document found that short-term O3 exposures cause
similar alterations in lung morphology in all laboratory animal species
studied, including primates.  As discussed in the 2007 Staff Paper
(section 3.3.1.1.5), cells in the centriacinar region (CAR) of the lung
(the segment between the last conducting airway and the gas exchange
region) have been recognized as a primary target of O3-induced damage
(epithelial cell necrosis and remodeling of respiratory bronchioles),
possibly because epithelium in this region receives the greatest dose of
O3 delivered to the lower respiratory tract.  Following chronic O3
exposure, structural changes have been observed in the CAR, the region
typically affected in most chronic airway diseases of the human lung
(EPA, 2006a, p. 8-24).

Ciliated cells in the nasal cavity and airways, as well as Type I cells
in the gas-exchange region, are also identified as targets.  While
short-term O3 exposures can cause epithelial cell profileration and
fibrolitic changes in the CAR, these changes appear to be transient with
recovery occurring after exposure, depending on species and O3 dose. 
The potential impacts of repeated short-term and chronic morphological
effects of O3 exposure are discussed below in the section on effects
from long-term exposures.  Long-term or prolonged exposure has been
found to cause chronic lesions similar to early lesions found in
individuals with respiratory bronchiolitis, which have the potential to
progress to fibrotic lung disease (2006 Criteria Document, p. 8-25).

Recent studies continue to show that short-term and sub-chronic
exposures to O3 cause similar alterations in lung structure in a variety
of experimental animal species.  For example, a series of new studies
that used infant rhesus monkeys and simulated seasonal ambient exposure
(0.5 ppm 8 hours/day for 5 days, every 14 days for 11 episodes) reported
remodeling in the distal airways; abnormalities in tracheal basement
membrane; eosinophil accumulation in conducting airways; and decrements
in airway innervation (2006 Criteria Document, p. 8-25).  Based on
evidence from animal toxicological studies, short-term and sub-chronic
exposures to O3 can cause morphological changes in the respiratory
systems, particularly in the CAR, of a number of laboratory animal
species (EPA, 2006a, section 5.2.4).

(f)	 Emergency Department Visits/Hospital Admissions for Respiratory
Causes

	Increased summertime emergency department visits and hospital
admissions for respiratory causes have been associated with ambient
exposures to O3.  As discussed in section 3.3.1.1.6 of the 2007 Staff
Paper, numerous studies conducted in various locations in the U.S. and
Canada consistently have shown a relationship between ambient O3 levels
and increased incidence of emergency department visits and hospital
admissions for respiratory causes, even after controlling for modifying
factors, such as weather and copollutants.  Such associations between
elevated ambient O3 during summer months and increased hospital
admissions have a plausible biological basis in the human and animal
evidence of functional, symptomatic, and physiologic effects discussed
above and in the increased susceptibility to respiratory infections
observed in laboratory animals.  

	In the 1997 review of the O3 NAAQS, the Criteria Document evaluated
emergency department visits and hospital admissions as possible outcomes
following exposure to O3 (EPA, 2006a, section 7.3).  The evidence was
limited for emergency department visits, but results of several studies
generally indicated that short-term exposures to O3 were associated with
respiratory emergency department visits.  The strongest and most
consistent evidence, at both lower levels (i.e., below 0.120 ppm 1-hour
max O3) and at higher levels (above 0.120 ppm 1-hour max O3), was found
in the group of studies which investigated summertime daily hospital
admissions for respiratory causes in different eastern North American
cities.  These studies consistently demonstrated that ambient O3 levels
were associated with increased hospital admissions and accounted for
about one to three excess respiratory hospital admissions per million
persons with each 0.100 ppm increase in 1-hour max O3, after adjustment
for possible confounding effects of temperature and copollutants. 
Overall, the 1996 Criteria Document concluded that there was strong
evidence that ambient O3 exposures can cause significant exacerbations
of preexisting respiratory disease in the general public.  Excess
respiratory-related hospital admissions associated with O3 exposures for
the New York City area (based on Thurston et al., 1992) were included in
the quantitative risk assessment in the 1997 review and are included in
the current assessment along with estimates for respiratory-related
hospital admissions in Cleveland, Detroit, and Los Angeles based on more
recent studies (2007 Staff Paper, chapter 5).  Significant uncertainties
and the difficulty of obtaining reliable baseline incidence numbers
resulted in emergency department visits not being used in the
quantitative risk assessment in either the 1997 or the 2008 O3 NAAQS
review.

	In the past decade, a number of studies have examined the temporal
pattern associations between O3 exposures and emergency department
visits for respiratory causes (EPA, 2006a, section 7.3.2).  These
studies are summarized in the 2006 Criteria Document (chapter 7 Annex)
and some are shown in Figure 1 (in section II.A.3).  Respiratory causes
for emergency department visits include asthma, bronchitis, emphysema,
pneumonia, and other upper and lower respiratory infections, such as
influenza, but asthma visits typically dominate the daily incidence
counts.  Most studies report positive associations with O3.  Among
studies with adequate controls for seasonal patterns, many reported at
least one significant positive association involving O3. 

	In reviewing evidence for associations between emergency department
visits for asthma and short-term O3 exposures, the 2006 Criteria
Document (Figure 7-8, p. 7-68) notes that in general, O3 effect
estimates from summer only analyses tended to be positive and larger
compared to results from cool season or all year analyses.  Several of
the studies reported significant associations between O3 concentrations
and emergency department visits for respiratory causes, in particular
asthma.  However, inconsistencies were observed which were at least
partially attributable to differences in model specifications and
analysis approach among various studies.  For example, ambient O3
concentrations, length of the study period, and statistical methods used
to control confounding by seasonal patterns and copollutants appear to
affect the observed O3 effect on emergency department visits.    

	Hospital admissions studies focus specifically on unscheduled
admissions because unscheduled hospital admissions occur in response to
unanticipated disease exacerbations and are more likely than scheduled
admissions to be affected by variations in environmental factors, such
as daily O3 levels.  Results of a fairly large number of these studies
published during the past decade are summarized in 2006 Criteria
Document (chapter 7 Annex), and results of U.S. and Canadian studies are
shown in Figure 1 below (in section II.A.3).  As a group, these hospital
admissions studies tend to be larger geographically and temporally than
the emergency department visit studies and provide results that are
generally more consistent.  The strongest associations of respiratory
hospital admissions with O3  concentrations were observed using short
lag periods, in particular for a 0-day lag (same day exposure) and a
1-day lag (previous day exposure).   Most studies in the United States
and Canada indicated positive, statistically significant associations
between ambient O3 concentrations and respiratory hospital admissions in
the warm season.  However, not all studies found a statistically
significant relationship with O3, possibly because of very low ambient
O3 levels.  Analyses for confounding using multipollutant regression
models suggest that copollutants generally do not confound the
association between O3 and respiratory hospitalizations. Ozone effect
estimates were robust to PM adjustment in all-year and warm-season only
data.  

	Overall, the 2006 Criteria Document concludes that positive and robust
associations were found between ambient O3 concentrations and various
respiratory disease hospitalization outcomes, when focusing particularly
on results of warm-season analyses.  Recent studies also generally
indicate a positive association between O3 concentrations and emergency
department visits for asthma during the warm season (EPA, 2006a, p.
7-175).  These positive and robust associations are supported by the
controlled human exposure, animal toxicological, and epidemiological
evidence for lung function decrements, increased respiratory symptoms,
airway inflammation, and increased airway responsiveness. Taken
together, the overall evidence supports a causal relationship between
acute ambient O3 exposures and increased respiratory morbidity outcomes
resulting in increased emergency department visits and hospitalizations
during the warm season (EPA, 2006a, p. 8-77).

ii.	Effects on the Respiratory System of Long-term O3 Exposures

	The 1996 Criteria Document concluded that there was insufficient
evidence from the limited number of studies to determine whether
long-term O3 exposures resulted in chronic health effects at ambient
levels observed in the U.S.  However, the aggregate evidence suggested
that O3 exposure, along with other environmental factors, could be
responsible for health effects in exposed populations.  Animal
toxicological studies carried out in the 1980’s and 1990’s
demonstrated that long-term exposures can result in a variety of
morphological effects, including permanent changes in the small airways
of the lungs, including remodeling of the distal airways and CAR and
deposition of collagen, possibly representing fibrotic changes.  These
changes result from the damage and repair processes that occur with
repeated exposure.  Fibrotic changes were also found to persist after
months of exposure providing a potential pathophysiologic basis for
changes in airway function observed in children in some recent
epidemiological studies.  It appears that variable seasonal ambient
patterns of exposure may be of greater concern than continuous daily
exposures. 

	Several studies published since 1996 have investigated lung function
changes over seasonal time periods (EPA, 2006a, section 7.5.3).  The
2006 Criteria Document (p. 7-114) summarizes these studies which
collectively indicate that seasonal O3 exposure is associated with
smaller growth-related increases in lung function in children than they
would have experienced living in areas with lower O3 levels.  There is
some limited evidence that seasonal O3 also may affect lung function
growth in young adults, although the uncertainty about the role of
copollutants makes it difficult to attribute the effects to O3 alone.

	Lung capacity grows during childhood and adolescence as body size
increases, reaches a maximum during the twenties, and then begins to
decline steadily and progressively with age.  Long-term exposure to air
pollution has long been thought to contribute to slower growth in lung
capacity, diminished maximally attained capacity, and/or more rapid
decline in lung capacity with age (EPA, 2006a, section 7.5.4). 
Toxicological findings evaluated in the 1996 Criteria Document
demonstrated that repeated daily exposure of rats to an episodic profile
of O3 caused small, but significant, decrements in growth-related lung
function that were consistent with early indicators of focal
fibrogenesis in the proximal alveolar region, without overt fibrosis. 
Because O3 at sufficient concentrations is a strong respiratory irritant
and has been shown to cause inflammation and restructuring of the
respiratory airways, it is plausible that long-term O3 exposures might
have a negative impact on baseline lung function, particularly during
childhood when these exposures might be associated with long-term risks.

	Several epidemiological studies published since 1996 have examined the
relationship between lung function development and long-term O3
exposure.  The most extensive and robust study of respiratory effects in
relation to long-term air pollution exposures among children in the U.S.
is the Children’s Health Study carried out in 12 communities of
southern California starting in 1993.  One analysis (Peters et al.,
1999a) examined the relationship between long-term O3 exposures and
self-reports of respiratory symptoms and asthma in a cross sectional
analysis and found a limited relationship between outcomes of current
asthma, bronchitis, cough and wheeze and a 0.040 ppm increase in 1-hour
max O3 (EPA, 2006a, p. 7-115).  Another analysis (Peters et al., 1999b)
examined the relationship between lung function at baseline and levels
of air pollution in the community.  They reported evidence that annual
mean O3 levels were associated with decreases in FVC, FEV1, PEF and
forced expiratory flow (FEF25-75) (the latter two being statistically
significant) among females but not males.  In a separate analysis
(Gauderman et al., 2000) of 4th, 7th, and 10th grade students, a
longitudinal analysis of lung function development over four years found
no association with O3 exposure.  The Children’s Health Study enrolled
a second cohort of more than 1500 fourth graders in 1996 (Gauderman et
al., 2002).  While the strongest associations with negative lung
function growth were observed with acid vapors in this cohort, children
from communities with higher 4-year average O3 levels also experienced
smaller increases in various lung function parameters. The strongest
relationship with O3 was with PEF.  Specifically, children from the
least-polluted community had a small but statistically significant
increase in PEF as compared to those from the most-polluted communities.
 In two-pollutant models, only 8-hour average O3 and NO2 were
significant joint predictors of FEV1 and maximal midexpiratory flow
(MMEF).  Although results from the second cohort of children are
supportive of a weak association, the definitive 8-year follow-up
analysis of the first cohort (Gauderman et al., 2004a) provides little
evidence that long-term exposure to ambient O3 at current levels is
associated with significant deficits in the growth rate of lung function
in children.  Avol et al. (2001) examined children who had moved away
from participating communities in southern California to other states
with improved air quality.  They found that a negative, but not
statistically significant, association was observed between O3 and lung
function parameters.  Collectively, the results of these reports from
the children’s health cohorts provide little evidence to support an
impact of long-term O3 exposures on lung function development.

	Evidence for a significant relationship between long-term O3 exposures
and decrements in maximally attained lung function was reported in a
nationwide study of first year Yale students (Kinney et al., 1998;
Galizia and Kinney, 1999) (EPA, 2006a, p. 7-120).  Males had much larger
effect estimates than females, which might reflect higher outdoor
activity levels and correspondingly higher O3 exposures during
childhood.  A similar study of college freshmen at University of
California at Berkeley also reported significant effects of long-term O3
exposures on lung function (Künzli et al., 1997; Tager et al., 1998). 
In a comparison of students whose city of origin was either Los Angeles
or San Francisco, long-term O3 exposures were associated with
significant changes in mid- and end-expiratory flow measures, which
could be considered early indicators for pathologic changes that might
progress to COPD.  

	There have been a few studies that investigated associations between
long-term O3 exposures and the onset of new cases of asthma (EPA, 2006a,
section 7.5.6).  The Adventist Health and Smog (AHSMOG) study cohort of
about 4,000 was drawn from nonsmoking, non-Hispanic white adult Seventh
Day Adventists living in California (Greer et al., 1993; McDonnell et
al., 1999).  During the ten-year follow-up in 1987, a statistically
significant increased relative risk of asthma development was observed
in males, compared to a nonsignificant relative risk in females (Greer
et al., 1993).  In the 15-year follow-up in 1992, it was reported that
for males, there was a statistically significant increased relative risk
of developing asthma associated with 8-hour average O3 exposures, but
there was no evidence of an association in females.  Consistency of
results in the two studies with different follow-up times provides
supportive evidence of the potential for an association between
long-term O3 exposure and asthma incidence in adult males; however,
representativeness of this cohort to the general U.S. population may be
limited (EPA, 2006a, p. 7-125).

	In a similar study (McConnell et al., 2002) of incident asthma among
children (ages 9 to 16 at enrollment), annual surveys of 3,535 children
initially without asthma were used to identify new-onset asthma cases as
part of the Children’s Health Study.  Six high-O3 and six low-O3
communities were identified where the children resided.  There were 265
children who reported new-onset asthma during the follow-up period. 
Although asthma risk was no higher for all residents of the six high-O3
communities versus the six low-O3 communities, asthma risk was 3.3 times
greater for children who played three or more sports as compared with
children who played no sports within the high-O3 communities.  This
association was absent in the communities with lower O3 concentrations. 
No other pollutants were found to be associated with new-onset asthma
(EPA, 2006a, p. 7-125).  Playing sports may result in extended outdoor
activity and exposure occurring during periods when O3 levels are
higher.  It should be noted, however, that the results of the
Children’s Health Study were based on a small number of new-onset
asthma cases among children who played three or more sports.  Future
replication of these findings in other cohorts would help determine
whether a causal interpretation is appropriate.

	In animal toxicology studies, the progression of morphological effects
reported during and after a chronic exposure in the range of 0.50 to
1.00 ppm O3 (well above current ambient levels) is complex, with
inflammation peaking over the first few days of exposure, then dropping,
then plateauing, and finally, largely disappearing (EPA, 2006a, section
5.2.4.4).  By contrast, fibrotic changes in the tissue increase very
slowly over months of exposure, and, after exposure ceases, the changes
sometimes persist or increase.  Epithelial hyperplasia peaks soon after
the inflammatory response but is usually maintained in both the nose and
lungs with continuous exposure; it also does not return to pre-exposure
levels after the end of exposure.  Patterns of exposure in this same
concentration range determine effects, with 18 months of daily exposure,
causing less morphologic damage than exposures on alternating months. 
This is important as environmental O3 exposure is typically seasonal. 
Long-term studies by Plopper and colleagues (Evans et al., 2003;
Schelegle et al., 2003; Chen et al., 2003; Plopper and Fanucchi, 2000)
investigated infant rhesus monkeys exposed to simulated, seasonal O3 and
demonstrated: 1) remodeling in the distal airways, 2) abnormalities in
tracheal basement membrane; 3) eosinophil accumulation in conducting
airways; and 4) decrements in airway innervation (EPA, 2006a, p. 5-45). 
These findings provide additional information regarding possible
injury-repair processes occurring with long-term O3 exposures suggesting
that these processes are only partially reversible and may progress
following cessation of O3 exposure.  Further, these processes may lead
to nonreversible structural damage to lung tissue; however, there is
still too much uncertainty to characterize the significance of these
findings to human exposure profiles and effect levels (EPA, 2006a, p.
8-25).

	In summary, in the past decade, important new longitudinal studies have
examined the effect of chronic O3 exposure on respiratory health
outcomes.  Limited evidence from recent long-term morbidity studies have
suggested in some cases that chronic exposure to O3 may be associated
with seasonal declines in lung function or reduced lung function
development, increases in inflammation, and development of asthma in
children and adults.  Seasonal decrements or smaller increases in lung
function measures have been reported in several studies; however, the
extent to which these changes are transient remains uncertain.  While
there is supportive evidence from animal studies involving effects from
chronic exposures, large uncertainties still remain as to whether
current ambient levels and exposure patterns might cause these same
effects in human populations.  The 2006 Criteria Document concludes that
epidemiological studies of new asthma development and longer-term lung
function declines remain inconclusive at present (EPA, 2006a, p. 7-134).
 

iii. 	Effects on the Cardiovascular System of O3 Exposure

	At the time of the 1997 review, the possibility of O3-induced
cardiovascular effects was largely unrecognized.  Since then, a very
limited body of evidence from animal, controlled human exposure, and
epidemiologic studies has emerged that provides evidence for some
potential plausible mechanisms for how O3 exposures might exert
cardiovascular system effects, however further research is needed to
substantiate these potential mechanisms.  Possible mechanisms may
involve O3-induced secretions of vasoconstrictive substances and/or
effects on neuronal reflexes that may result in increased arterial blood
pressure and/or altered electrophysiologic control of heart rate or
rhythm.  Some animal toxicology studies have shown O3-induced decreases
in heart rate, mean arterial pressure, and core temperature.  One
controlled human exposure study that evaluated effects of O3 exposure on
cardiovascular health outcomes found no significant O3-induced
differences in ECG or blood pressure in healthy or hypertensive subjects
but did observe a significant O3-induced increase the
alveolar-to-arterial PO2 gradient and heart rate in both groups
resulting in an overall increase in myocardial work and impairment in
pulmonary gas exchange (Gong et al., 1998).  In another controlled human
exposure study, inhalation of a mixture of PM2.5 and O3 by healthy
subjects increased brachial artery vasoconstriction and reactivity
(Brook et al., 2002).

	The evidence from a few animal studies also includes potential direct
effects such as O3-induced release from lung epithelial cells of
platelet activating factor (PAF) that may contribute to blood clot
formation that would have the potential to increase the risk of serious
cardiovascular outcomes (e.g., heart attack, stroke, mortality).  Also,
interactions of O3 with surfactant components in epithelial lining fluid
of the lung may result in production of oxysterols and reactive oxygen
species that may exhibit PAF-like activity contributing to clotting and
also may exert cytotoxic effects on lung and heart muscle cells.  

	Epidemiological panel and field studies that examined associations
between O3 and various cardiac physiologic endpoints have yielded
limited evidence suggestive of a potential association between acute O3
exposure and altered heart rate variability (HRV), ventricular
arrhythmias, and incidence of heart attacks (myocardial infarction or
MI).  A number of epidemiological studies have also reported
associations between short-term exposures and hospitalization for
cardiovascular diseases.  As shown in Figure 7-13 of the 2006 Criteria
Document, many of the studies reported negative or inconsistent
associations.  Some other studies, especially those that examined the
relationship when O3 exposures were higher, have found robust positive
associations between O3 and cardiovascular hospital admissions (EPA,
2006a, p. 7-82).  For example, one study reported a positive association
between O3 and cardiovascular hospital admissions in Toronto, Canada in
a summer-only analysis (Burnett et al., 1997b).  The results were robust
to adjustment for various PM indices, whereas the PM effects diminished
when adjusted for gaseous pollutants.  Other studies stratified their
analysis by temperature (i.e., by warms days versus cool days). Several
analyses using warm season days consistently produced positive
associations. 

The epidemiologic evidence for cardiovascular morbidity is much weaker
than for respiratory morbidity, with only one of several U.S. and
Canadian studies showing statistically significant positive associations
of cardiovascular hospitalizations with warm-season O3 concentrations. 
Most of the available European and Australian studies, all of which
conducted all-year O3 analyses, did not find an association between
short-term O3 concentrations and cardiovascular hospitalizations. 
Overall, the currently available evidence is inconclusive regarding an
association between cardiovascular hospital admissions and ambient O3
exposure (EPA, 2006a, p. 7-83).

	In summary, based on the evidence from animal toxicology, controlled
human exposure, and epidemiological studies, from the 2006 Criteria
Document (p. 8-77) concludes that this generally limited body of
evidence is suggestive that O3 can directly and/or indirectly contribute
to cardiovascular-related morbidity, but that much needs to be done to
more fully integrate links between ambient O3 exposures and adverse
cardiovascular outcomes.

b.	Mortality

i.	Mortality and Short-term O3 Exposure

	The 1996 Criteria Document concluded that an association between daily
mortality and O3 concentration for areas with high O3 levels (e.g., Los
Angeles) was suggested.  However, due to a very limited number of
studies available at that time, there was insufficient evidence to
conclude that the observed association was likely causal.  

	The 2006 Criteria Document included results from numerous
epidemiological analyses of the relationship between O3 and mortality. 
Additional single city analyses have also been conducted since 1996,
however, the most pivotal studies in EPA’s (and CASAC’s) finding of
increased support for the relationship between premature mortality and
O3 is in part related to differences in study design – limiting
analyses to warm seasons, better control for copollutants, particularly
PM, and use of multicity designs (both time series and meta-analytic
designs).  Key findings are available from multicity time-series studies
that report associations between O3 and mortality.  These studies
include analyses using data from 90 U.S. cities in the National
Mortality, Morbidity and Air Pollution (NMMAPS) study (Dominici et al.,
2003) and from 95 U.S. communities in an extension to the NMMAPS
analyses (Bell et al., 2004).  

	The original 90-city NMMAPS analysis, with data from 1987 to 1994, was
primarily focused on investigating effects of PM10 on mortality. A
significant association was reported between mortality and 24-hour
average O3 concentrations in analyses using all available data as well
as in the warm season only analyses (Dominici et al., 2003).  The
estimate using all available data was about half that for the
summer-only data at a lag of 1-day.  The extended NMMAPS analysis
included data from 95 U.S. cities and included an additional 6 years of
data, from 1987-2000 (Bell et al., 2004).  Significant associations were
reported between O3 and mortality in analyses using all available data. 
The effect estimate for increased mortality was approximately 0.5
percent per 0.020 ppm change in 24-hour average O3 measured on the same
day, and approximately 1.04 percent per 0.020 ppm change in 24-hour
average O3 in a 7-day distributed lag model (EPA, 2006a, p. 7-88).  In
analyses using only data from the warm season, the results were not
significantly different from the full-year results.  The authors also
report that O3-mortality associations were robust to adjustment for PM
(EPA, 2006a, p. 7-100).  Using a subset of the NMMAPS data set, Huang et
al. (2005) focused on associations between cardiopulmonary mortality and
O3 exposure (24-hour average) during the summer season only.  The
authors report an approximate 1.47 percent increase per 0.020 ppm change
in O3 concentration measured on the same day and an approximate 2.52
percent increase per 0.020 ppm change in O3 concentration using a 7-day
distributed lag model.  These findings suggest that the effect of O3 on
mortality is immediate but also persists for several days.  

	As discussed below in section II.A.3.a, confounding by weather,
especially temperature, is complicated by the fact that higher
temperatures are associated with the increased photochemical activities
that are important for O3 formation.  Using a case-crossover study
design, Schwartz (2005) assessed associations between daily maximum
concentrations and mortality, matching case and control periods by
temperature, and using data only from the warm season.  The reported
effect estimate of approximately 0.92 percent change in mortality per
0.040 ppm O3 (1-hour maximum) was similar to time-series analysis
results with adjustment for temperature (approximately 0.76 percent per
0.040 ppm O3), suggesting that associations between O3 and mortality
were robust to the different adjustment methods for temperature.

	An initial publication from APHEA, a European multicity study, reported
statistically significant associations between daily maximum O3
concentrations and mortality in four cities in a full year analysis
(Toulomi et al., 1997).  An extended analysis was done using data from
23 cities throughout Europe (Gryparis et al., 2004).  In this report, a
positive but not statistically significant association was found between
mortality and 1-hour daily maximum O3 in a full year analysis.  Gryparis
et al. (2004) noted that there was a considerable seasonal difference in
the O3 effect on mortality; thus, the small effect for the all-year data
might be attributable to inadequate adjustment for confounding by
seasonality.  Focusing on analyses using summer measurements, the
authors report statistically significant associations with total
mortality, cardiovascular mortality and respiratory mortality (EPA,
2006a, p. 7-93, 7-99).

	Numerous single-city analyses have also reported associations between
mortality and short-term O3 exposure, especially for those analyses
using warm season data.  As shown in Figure 7-21 of the 2006 Criteria
Document, the results of recent publications show a pattern of positive,
often statistically significant associations between short-term O3
exposure and mortality during the warm season.  In considering results
from year-round analyses, there remains a pattern of positive results
but the findings are less consistent.  In most single-city analyses,
effect estimates were not substantially changed with adjustment for PM
(EPA, 2006a, Figure 7-22).  

	In addition, several meta-analyses have been conducted on the
relationship between O3 and mortality.  As described in section 7.4.4 of
the 2006 Criteria Document, these analyses reported fairly consistent
and positive combined effect estimates ranging from approximately 1.5 to
2.5 percent increase in mortality for a standardized change in O3 (EPA,
2006a, Figure 7-20).  Three recent meta-analyses evaluated potential
sources of heterogeneity in O3-mortality associations (Bell et al.,
2005; Ito et al., 2005; Levy et al., 2005).  The 2006 Criteria Document
(p. 7-96) observes common findings across all three analyses, in that
all reported that effect estimates were larger in warm season analyses,
reanalysis of results using default convergence criteria in generalized
additive models (GAM) did not change the effect estimates, and there was
no strong evidence of confounding by PM.  Bell et al. (2005) and Ito et
al. (2005) both provided suggestive evidence of publication bias, but
O3-mortality associations remained after accounting for that potential
bias.  The 2006 Criteria Document concludes that the “positive O3
effects estimates, along with the sensitivity analyses in these three
meta-analyses, provide evidence of a robust association between ambient
O3 and mortality” (EPA, 2006a, p. 7-97). 

	Most of the single-pollutant model estimates from single-city studies
range from 0.5 to 5 percent excess deaths per standardized increments. 
Corresponding summary estimates in large U.S. multicity studies ranged
between 0.5 to 1 percent with some studies noting heterogeneity across
cities and studies (EPA, 2006a, p. 7-110).

	Finally, from those studies that included assessment of associations
with specific causes of death, it appears that effect estimates for
associations with cardiovascular mortality are larger than those for
total mortality.  The meta-analysis by Bell et al. (2005) observed a
slightly larger effect estimate for cardiovascular mortality compared to
mortality from all causes.  The effect estimate for respiratory
mortality was approximately one-half that of cardiovascular mortality in
the meta-analysis.  However, other studies have observed larger effect
estimates for respiratory mortality compared to cardiovascular
mortality.  The apparent inconsistency regarding the effect size of
O3-related respiratory mortality may be due to reduced statistical power
in this subcategory of mortality (EPA, 2006a, p. 7-108).

	In summary, many single- and multicity studies observed positive
associations of ambient O3 concentrations with total nonaccidental and
cardiopulmonary mortality.  The 2006 Criteria Document finds that the
results from U.S. multicity time-series studies provide the strongest
evidence to date for O3 effects on acute mortality.  Recent
meta-analyses also indicate positive risk estimates that are unlikely to
be confounded by PM; however, future work is needed to better understand
the influence of model specifications on the risk coefficient (EPA,
2006a, p. 7-175).  A meta-analysis that examined specific causes of
mortality found that the cardiovascular mortality risk estimates were
higher than those for total mortality.  For cardiovascular mortality,
the 2006 Criteria Document (Figure 7-25, p. 7-106) suggests that effect
estimates are consistently positive and more likely to be larger and
statistically significant in warm season analyses.  The findings
regarding the effect size for respiratory mortality have been less
consistent, possibly because of lower statistical power in this
subcategory of mortality.  The 2006 Criteria Document (p. 8-78)
concludes that these findings are highly suggestive that short-term O3
exposure directly or indirectly contribute to non-accidental and
cardiopulmonary-related mortality, but additional research is needed to
more fully establish underlying mechanisms by which such effects occur.

ii.	Mortality and Long-term O3 Exposure

	Little evidence was available in the 1997 review on the potential for
associations between mortality and long-term exposure to O3.  In the
Harvard Six City prospective cohort analysis, the authors report that
mortality was not associated with long-term exposure to O3 (Dockery et
al., 1993).  The authors note that the range of O3 concentrations across
the six cities was small, which may have limited the power of the study
to detect associations between mortality and O3 levels (EPA, 2006a, p.
7-127).   

	As discussed in section 7.5.8 of the 2006 Criteria Document, in this
review there are results available from three prospective cohort
studies: the American Cancer Society (ACS) study (Pope et al., 2002),
the Adventist Health and Smog (AHSMOG) study (Beeson et al., 1998; Abbey
et al., 1999), and the U.S. Veterans Cohort study (Lipfert et al., 2000,
2003).  In addition, a major reanalysis report includes evaluation of
data from the Harvard Six City cohort study (Krewski et al., 2000).  
This reanalysis also includes additional evaluation of data from the
initial ACS cohort study report that had only reported results of
associations between mortality and long-term exposure to fine particles
and sulfates (Pope et al., 1995).  This reanalysis was discussed in the
2007 Staff Paper (section 3.3.2.2) but not in the 2006 Criteria
Document.

	In this reanalysis of data from the previous Harvard Six City
prospective cohort study, the investigators replicated and validated the
findings of the original studies, and the report included additional
quantitative results beyond those available in the original report
(Krewski et al., 2000).  In the reanalysis of data from the Harvard Six
Cities study, the effect estimate for the association between long-term
O3 concentrations and mortality was negative and nearly statistically
significant (relative risk = 0.87, 95 percent CI: 0.76, 1.00).

	The ACS study is based on health data from a large prospective cohort
of approximately 500,000 adults and air quality data from about 150 U.S.
cities.  The initial report (Pope et al., 1995) focused on associations
with fine particles and sulfates, for which significant associations had
been reported in the earlier Harvard Six Cities study (Dockery et al.,
1993).  As part of the major reanalysis of these data, results for
associations with other air pollutants were also reported, and the
authors report that no significant associations were found between O3
and all-cause mortality.  However, a significant association was
reported for cardiopulmonary mortality in the warm season (Krewski et
al., 2000).  The ACS II study (Pope et al., 2002) reported results of
associations with an extended data base; the mortality records for the
cohort had been updated to include 16 years of follow-up (compared with
8 years in the first report) and more recent air quality data were
included in the analyses.  Similar to the earlier reanalysis, a
marginally significant association was observed between long-term
exposure to O3 and cardiopulmonary mortality in the warm season.  No
other associations with mortality were observed in both the full-year
and warm season analyses. 

	The Adventist Health and Smog (AHSMOG) cohort includes about 6,000
adults living in California.  In two studies from this cohort, a
significant association has been reported between long-term O3 exposure
and increased risk of lung cancer mortality among males only (Beeson et
al., 1998; Abbey et al., 1999).  No significant associations were
reported between long-term O3 exposure and mortality from all causes or
cardiopulmonary causes.  Due to the small numbers of lung cancer deaths
(12 for males, 18 for females) and the precision of the effect estimate
(i.e., the wide confidence intervals), the 2006 Criteria Document (p.
7-130) discussed concerns about the plausibility of the reported
association with lung cancer. 

 	The U.S. Veterans Cohort study (Lipfert et al., 2000, 2003) of
approximately 50,000 middle-aged males diagnosed with hypertension,
reported some positive associations between mortality and peak O3
exposures (95th percentile level for several years of data).  The study
included numerous analyses using subsets of exposure and mortality
follow-up periods which spanned the years 1960 to 1996.  In the results
of analyses using deaths and O3 exposure estimates concurrently across
the study period, there were positive, statistically significant
associations between peak O3 and mortality (EPA, 2006a, p. 7-129).

	Overall, the 2006 Criteria Document (p. 7-130) concludes that
consistent associations have not been reported between long-term O3
exposure and all-cause, cardiopulmonary or lung cancer mortality.  TC
\l4 "3.3.1.2	Mortality and Long-term PM Exposure 

c.	Role of Ground-level O3 in Solar Radiation-related Human Health
Effects

	Beyond the direct health effects attributable to inhalation exposure to
O3 in the ambient air discussed above, the 2006 Criteria Document also
assesses potential indirect effects related to the presence of O3 in the
ambient air by considering the role of ground-level O3 in mediating
human health effects that may be directly attributable to exposure to
solar ultraviolet radiation (UV-B).  The 2006 Criteria Document (chapter
10) focuses this assessment on three key factors, including those
factors that govern (1) UV-B radiation flux at the earth’s surface,
(2) human exposure to UV-B radiation, and (3) human health effects due
to UV-B radiation.  In so doing, the 2006 Criteria Document provides a
thorough analysis of the current understanding of the relationship
between reducing ground-level O3 concentrations and the potential impact
these reductions might have on increasing UV-B surface fluxes and
indirectly contributing to UV-B related health effects.

There are many factors that influence UV-B radiation penetration to the
earth’s surface, including latitude, altitude, cloud cover, surface
albedo, PM concentration and composition, and gas phase pollution.  Of
these, only latitude and altitude can be defined with small uncertainty
in any effort to assess the changes in UV-B flux that may be
attributable to any changes in tropospheric O3 as a result of any
revision to the O3 NAAQS.  Such an assessment of UV-B related health
effects would also need to take into account human habits, such as
outdoor activities (including age- and occupation-related exposure
patterns), dress and skin care to adequately estimate UV-B exposure
levels.  However, little is known about the impact of these factors on
individual exposure to UV-B.

Moreover, detailed information does not exist regarding other factors
that are relevant to assessing changes in disease incidence, including:
type (e.g., peak or cumulative) and time period (e.g., childhood,
lifetime, current) of exposures related to various adverse health
outcomes (e.g., damage to the skin, including skin cancer; damage to the
eye, such as cataracts; and immune system suppression); wavelength
dependency of biological responses; and interindividual variability in
UV-B resistance to such health outcomes.  Beyond these well recognized
adverse health effects associated with various wavelengths of UV
radiation, the 2006 Criteria Document (section 10.2.3.6) also discusses
protective effects of UV-B radiation.  Recent reports indicate the
necessity of UV-B in producing vitamin D.  Vitamin D deficiency can
cause metabolic bone disease among children and adults, and may also
increase the risk of many common chronic diseases (e.g., type I diabetes
and rheumatoid arthritis) as well as the risk of various types of
cancers.  Thus, the 2006 Criteria Document concludes that any assessment
that attempts to quantify the consequences of increased UV-B exposure on
humans due to reduced ground-level O3 must include consideration of both
negative and positive effects.  However, as with other impacts of UV-B
on human health, this beneficial effect of UV-B radiation has not been
studied in sufficient detail to allow for a credible health benefits or
risk assessment.  In conclusion, the effect of changes in surface-level
O3 concentrations on UV-B-induced health outcomes cannot yet be
critically assessed within reasonable uncertainty (2006 Criteria
Document, p. 10-36).

The Agency last considered indirect effects of O3 in the ambient air in
its 2003 final response to a remand of the Agency’s 1997 decision to
revise the O3 NAAQS.  In so doing, based on the available information in
the 1997 review, EPA determined that the information linking (a) changes
in patterns of ground-level O3 concentrations likely to occur as a
result of programs implemented to attain the 1997 O3 NAAQS to (b)
changes in relevant exposures to UV-B radiation of concern to public
health was too uncertain at that time to warrant any relaxation in the
level of public health protection previously determined to be requisite
to protect against the demonstrated direct adverse respiratory effects
of exposure to O3 in the ambient air (68 FR 614).  At that time, the
more recent information on protective effects of UV-B radiation was not
available, such that only adverse UV-B-related effects could be
considered.  Taking into consideration the more recent information
available for the 2008 review, the 2006 Criteria Document and 2007 Staff
Paper conclude that the effect of changes in ground-level O3
concentrations, likely to occur as a result of revising the O3 NAAQS, on
UV-B-induced health outcomes, including whether these changes would
ultimately result in increased or decreased incidence of UV-B-related
diseases, cannot yet be critically assessed.  

3.	Interpretation and Integration of Health Evidence

	As discussed below, in assessing the health evidence, the 2006 Criteria
Document integrates findings from experimental (e.g., toxicological,
dosimetric and controlled human exposure) and epidemiological studies,
to make judgments about the extent to which causal inferences can be
made about observed associations between health endpoints and exposure
to O3.  In evaluating the evidence from epidemiological studies, the EPA
focuses on well-recognized criteria, including:  the strength of
reported associations, including the magnitude and precision of reported
effect estimates and their statistical significance; the robustness of
reported associations, or stability in the effect estimates  after
considering factors such as alternative models and model specification,
potential confounding by co-pollutants, and issues related to the
consequences of exposure measurement error; potential aggregation bias
in pooling data; and the consistency of the effects associations as
observed by looking across results of multiple- and single-city studies
conducted by different investigators in different places and times. 
Consideration is also given to evaluating concentration-response
relationships observed in epidemiological studies to inform judgments
about the potential for threshold levels for O3-related effects. 
Integrating more broadly across epidemiological and experimental
evidence, the 2006 Criteria Document also focuses on the coherence and
plausibility of observed O3-related health effects to reach judgments
about the extent to which causal inferences can be made about observed
associations between health endpoints and exposure to O3 in the ambient
air.  

a.	Assessment of Evidence from Epidemiological Studies

	Key elements of the evaluation of epidemiological studies are briefly
summarized below.

	(1)  The strength of associations most directly refers to the magnitude
of the reported relative risk estimates.  Taking a broader view, the
2006 Criteria Document draws upon the criteria summarized in a recent
report from the U.S. Surgeon General, which define strength of an
association as “the magnitude of the association and its statistical
strength” which includes assessment of both effect estimate size and
precision, which is related to the statistical power of the study (CDC,
2004).  In general, when associations are strong in terms of yielding
large relative risk estimates, it is less likely that the association
could be completely accounted for by a potential confounder or some
other source of bias, whereas with associations that yield small
relative risk estimates it is especially important to consider potential
confounding and other factors in assessing causality.  Effect estimates
between O3 and some of the health outcomes are generally small in size
and could thus be characterized as weak.  For example, effect estimates
for associations with mortality generally range from 0.5 to 5 percent
increases per 0.040 ppm increase in 1-hour maximum O3 or equivalent,
whereas associations for hospitalization range up to 50 percent
increases per standardized O3 increment.  However, the 2006 Criteria
Document notes that there are large multicity studies that find small
associations between short-term O3 exposure and mortality or morbidity
and have done so with great precision due to the statistical power of
the studies (p. 8-40).  That is, the power of the studies allows the
authors to reliably distinguish even weak relationships from the null
hypothesis with statistical confidence.

	(2)  In evaluating the robustness of associations, the 2006 Criteria
Document (sections 7.1.3 and 8.4.4.3) and 2007 Staff Paper (section
3.4.2) have primarily considered the impact of exposure error, potential
confounding by copollutants, and alternative models and model
specifications.

	In time-series and panel studies, the temporal (e.g., daily or hourly)
changes in ambient O3 concentrations measured at centrally-located
ambient monitoring stations are generally used to represent a
community’s exposure to ambient O3.  In prospective cohort or
cross-sectional studies, air quality data averaged over a period of
months to years are used as indicators of a community’s long-term
exposure to ambient O3 and other pollutants.  In both types of analyses,
exposure error is an important consideration, as actual exposures to
individuals in the population will vary across the community.

	Ozone concentrations measured at central ambient monitoring sites may
explain, at least partially, the variance in individual exposures to
ambient O3; however, this relationship is influenced by various factors
related to building ventilation practices and personal behaviors. 
Further, the pattern of exposure misclassification error and the
influence of confounders may differ across the outcomes of interest as
well as in susceptible populations.  As discussed in the 2006 Criteria
Document (section 3.9), only a limited number of studies have examined
the relationship between ambient O3 concentrations and personal
exposures to ambient O3.  One of the strongest predictors of the
relationship between ambient concentrations and personal exposures
appears to be time spent outdoors.  The strongest relationships were
observed in outdoor workers (Brauer and Brook, 1995, 1997; O’Neill et
al., 2004).  Statistically significant correlations between ambient
concentrations and personal exposures were also observed for children,
who likely spend more time outdoors in the warm season (Linn et al.,
1996; Xu et al., 2005).  There is some concern about the extent to which
ambient concentrations are representative of personal O3 exposures of
another particularly susceptible group of individuals, the debilitated
elderly, since those who suffer from chronic cardiovascular or
respiratory conditions may tend to protect themselves more than healthy
individuals from environmental threats by reducing their exposure to
both O3 and its confounders, such as high temperature and PM.  Studies
by Sarnat et al. (2001, 2005) that included this susceptible group
reported mixed results for associations between ambient O3
concentrations and personal exposures to O3.  Collectively, these
studies observed that the daily averaged personal O3 exposures tend to
be well correlated with ambient O3 concentrations despite the
substantial variability that existed among the personal measurements. 
These studies provide supportive evidence that ambient O3 concentrations
from central monitors may serve as valid surrogate measures for mean
personal exposures experienced by the population, which is of most
relevance for time-series studies.  A better understanding of the
relationship between ambient concentrations and personal exposures, as
well as of the other factors that affect relationship will improve the
interpretation of concentration-population health response associations
observed.    

	The 2006 Criteria Document (section 7.1.3.1) also discusses the
potential influence of exposure error on epidemiologic study results. 
Zeger et al. (2000) outlined the components to exposure measurement
error, finding that ambient exposure can be assumed to be the product of
the ambient concentration and an attenuation factor (i.e., building
filter) and that panel studies and time-series studies that use ambient
concentrations instead of personal exposure measurements will estimate a
health risk that is attenuated by that factor.  Navidi et al. (1999)
used data from a children’s cohort study to compare effect estimates
from a simulated “true” exposure level to results of analyses from
O3 exposures determined by several methods, finding that O3 exposures
based on the use of ambient monitoring data overestimate the
individual’s O3 exposure and thus generally result in O3 effect
estimates that are biased downward (EPA, 2006a, p. 7-8).  Similarly, in
a reanalysis of a study by Burnett et al. (1994) on the acute
respiratory effects of ambient air pollution, Zidek et al. (1998)
reported that accounting for measurement error, as well as making a few
additional changes to the analysis, resulted in qualitatively similar
conclusions, but the effects estimates were considerably larger in
magnitude (EPA, 2006a, p. 7-8).  A simulation study by Sheppard et al.
(2005) also considered attenuation of the risk based on personal
behavior, their microenvironment, and the qualities of the pollutant in
time-series studies.  Of particular interest is their finding that risk
estimates were not further attenuated in time-series studies even when
the correlations between personal exposures and ambient concentrations
were weak.  In addition to overestimation of exposure and the resulting
underestimation of effects, the use of ambient O3 concentrations may
obscure the presence of thresholds in epidemiologic studies (EPA, 2006a,
p. 7-9).

	As discussed in the 2006 Criteria Document (section 3.9), using ambient
concentrations to determine exposure generally overestimates true
personal O3 exposures by approximately 2- to 4-fold in available
studies, resulting in attenuated risk estimates.  The implication is
that the effects being estimated occur at fairly low exposures and the
potency of O3 is greater than these effects estimates indicate.  As very
few studies evaluating O3 health effects with personal O3 exposure
measurements exist in the literature, effect estimates determined from
ambient O3 concentrations must be evaluated and used with caution to
assess the health risks of O3.  In the absence of available data on
personal O3 exposure, the use of routinely monitored ambient O3
concentrations as a surrogate for personal exposures is not generally
expected to change the principal conclusions from O3 epidemiologic
studies.  Therefore, population health risk estimates derived using
ambient O3 levels from currently available observational studies, with
appropriate caveats about personal exposure considerations, remain
useful.  The 2006 Criteria Document recommends caution in the
quantitative use of effect estimates calculated using ambient O3
concentrations as they may lead to underestimation of the potency of O3.
 However, the 2007 Staff Paper observes that the use of these risk
estimates for comparing relative risk reductions between alternative
ambient O3 standards considered in the risk assessment (discussed below
in section II.B.2) is less likely to suffer from this concern.

	Confounding occurs when a health effect that is caused by one risk
factor is attributed to another variable that is correlated with the
causal risk factor; epidemiological analyses attempt to adjust or
control for potential confounders.  Copollutants (e.g., PM, CO, SO2 and
NO2) can meet the criteria for potential confounding in O3-health
associations if they are potential risk factors for the health effect
under study and are correlated with O3.  Effect modifiers include
variables that may influence the health response to the pollutant
exposure (e.g., co-pollutants, individual susceptibility, smoking or
age).  Both are important considerations for evaluating effects in a
mixture of pollutants, but for confounding, the emphasis is on
controlling or adjusting for potential confounders in estimating the
effects of one pollutant, while the emphasis for effect modification is
on identifying and assessing the effects for different modifiers.

The 2006 Criteria Document (p. 7-148) observes that O3 is generally not
highly correlated with other criteria pollutants (e.g., PM10, CO, SO2
and NO2), but may be more highly correlated with secondary fine
particles, especially during the summer months, and that the degree of
correlation between O3 and other pollutants may vary across seasons. 
For example, positive associations are observed between O3 and
pollutants such as fine particles during the warmer months, but negative
correlations may be observed during the cooler months (EPA, 2006a, p.
7-17).  Thus, the 2006 Criteria Document (section 7.6.4) pays particular
attention to the results of season-specific analyses and studies that
assess effects of PM in potential confounding of O3-health
relationships.  The 2006 Criteria Document also discussed the
limitations of commonly used multipollutant models that include the
difficulty in interpreting results where the copollutants are highly
colinear, or where correlations between pollutants change by season
(EPA, 2006a, p. 7-150).  This is particularly the situation where O3 and
a copollutant, such as sulfates, are formed under the same atmospheric
condition; in such cases multipollutant models would produce unstable
and possibly misleading results (EPA, 2006a, p. 7-152).

	For mortality, the results from numerous multicity and single-city
studies indicate that O3-mortality associations do not appear to be
substantially changed in multipollutant models including PM10 or PM2.5
(EPA, 2006a, p. 7-101; Figure 7-22).  Focusing on results of warm season
analyses, effect estimates for O3-mortality associations are fairly
robust to adjustment for PM in multipollutant models (EPA, 2006a, p.
7-102; Figure 7-23).  The 2006 Criteria Document concludes that in the
few multipollutant analyses conducted for these endpoints, copollutants
generally do not confound the relationship between O3 and respiratory
hospitalization (EPA, 2006a, p. 7-79 to 7-80; Figure 7-12). 
Multipollutant models were not used as commonly in studies of
relationships between respiratory symptoms or lung function with O3, but
the 2006 Criteria Document reports that results of available analyses
indicate that such associations generally were robust to adjustment for
PM2.5 (p. 7-154).  For example, in a large multicity study of asthmatic
children (Mortimer et al., 2002), the O3 effect was attenuated, but
there was still a positive association; in Gent et al. (2003), effects
of O3, but not PM2.5, remained statistically significant and even
increased in magnitude in two-pollutant models (EPA, 2006a, p. 7-53). 
Considering this body of studies, the 2006 Criteria Document (p. 7-154)
concludes:  “Multipollultant regression analyses indicated that O3
risk estimates, in general, were not sensitive to the inclusion of
copollutants, including PM2.5 and sulfate.  These results suggest that
the effects of O3 on respiratory health outcomes appear to be robust and
independent of the effects of other copollutants.”

	The 2006 Criteria Document (p. 7-14) observes that another challenge of
time-series epidemiological analysis is assessing the relationship
between O3 and health outcomes while avoiding bias due to confounding by
other time-varying factors, particularly seasonal trends and weather
variables.  These variables are of particular interest because O3
concentrations have a well-characterized seasonal pattern and are also
highly correlated with changes in temperature, such that it can be
difficult to distinguish whether effects are associated with O3 or with
seasonal or weather variables in statistical analyses.

	The 2006 Criteria Document (section 7.1.3.4) discusses statistical
modeling approaches that have been used to adjust for time-varying
factors, highlighting a series of analyses that were done in a Health
Effects Institute-funded reanalysis of numerous time-series studies. 
While the focus of these reanalyses was on associations with PM, a
number of investigators also examined the sensitivity of O3 coefficients
to the extent of adjustment for temporal trends and weather factors.  In
addition, several recent studies, including U.S. multicity studies (Bell
et al., 2005; Huang et al., 2005; Schwartz et al., 2005) and a
meta-analysis study (Ito et al., 2005), evaluated the effect of model
specification on O3-mortality associations.  As discussed in the 2006
Criteria Document (section 7.6.3.1), these studies generally report that
associations reported with O3 are not substantially changed with
alternative modeling strategies for adjusting for temporal trends and
meteorologic effects.  In the meta-analysis by Ito et al. (2005), a
separate multicity analysis was presented that found that alternative
adjustments for weather resulted in up to 2-fold difference in the O3
effect estimate.  Significant confounding can occur when strong seasonal
cycles are present, suggesting that season-specific results are more
generally robust than year-round results in such cases.  A number of
epidemiological studies have conducted season-specific analyses, and
have generally reported stronger and more precise effect estimates for
O3 associations in the warm season than in analyses conducted in the
cool seasons or over the full year.

	(3)  Consistency refers to the persistent finding of an association
between exposure and outcome in multiple studies of adequate power in
different persons, places, circumstances and times (CDC, 2004).  In
considering results from multicity studies and single-city studies in
different areas, the 2006 Criteria Document (p. 8-41) observes general
consistency in effects of short-term O3 exposure on mortality,
respiratory hospitalization and other respiratory health outcomes.  The
variations in effects that are observed may be attributable to
differences in relative personal exposure to O3, as well as varying
concentrations and composition of copollutants present in different
regions.  Thus, the 2006 Criteria Document (p.8-41) concludes that
“consideration of consistency or heterogeneity of effects is
appropriately understood as an evaluation of the similarity or general
concordance of results, rather than an expectation of finding
quantitative results with a very narrow range.”

	(4)  The 2007 Staff Paper recognizes that it is likely that there are
biological thresholds for different health effects in individuals or
groups of individuals with similar innate characteristics and health
status.  For O3 exposure, individual thresholds would presumably vary
substantially from person to person due to individual differences in
genetic susceptibility, pre-existing disease conditions and possibly
individual risk factors such as diet or exercise levels (and could even
vary from one time to another for a given person).  Thus, it would be
difficult to detect a distinct threshold at the population level below
which no individual would experience a given effect, especially if some
members of a population are unusually sensitive even down to very low
concentrations (EPA, 2004, p. 9-43 - 9-44).

	Some studies have tested associations between O3 and health outcomes
after removal of days with higher O3 levels from the data set; such
analyses do not necessarily indicate the presence or absence of a
threshold, but provide some information on whether the relationship is
found using only lower-concentration data.  For example, using data from
95 U.S. cities, Bell et al. (2004) found that the effect estimate for an
association between short-term O3 exposure and mortality was little
changed when days exceeding 0.060 ppm (24-hour average) were excluded in
the analysis.  Using data from 8 U.S. cities, Mortimer and colleagues
(2002) also reported that associations between O3 and both lung function
and respiratory symptoms remained statistically significant and of the
same or greater magnitude in effect size when concentrations greater
than 0.080 ppm (8-hour average) were excluded (EPA, 2006a, p. 7-46). 
Several single-city studies also report similar findings of associations
that remain or are increased in magnitude and statistical significance
when data at the upper end of the concentration range are removed (EPA,
2006a, section 7.6.5).	

	Other time-series epidemiological studies have used statistical
modeling approaches to evaluate whether thresholds exist in associations
between short-term O3 exposure and mortality.  As discussed in section
7.6.5 of the 2006 Criteria Document, one European multicity study
included evaluation of the shape of the concentration-response curve,
and observed no deviation from a linear function across the range of O3
measurements from the study (Gryparis et al., 2004; EPA, 2006a p.
7-154).  Several single-city studies also observed a monotonic increase
in associations between O3 and morbidity that suggest that no population
threshold exists (EPA, 2006a, p. 7-159).

	On the other hand, a study in Korea used several different modeling
approaches and reported that a threshold model provided the best fit for
the data.  The results suggested a potential threshold level of about
0.045 ppm (1-hour maximum concentration; < 0.035 ppm, 8-hour average)
for an association between mortality and short-term O3 exposure during
the summer months (Kim et al., 2004; EPA, 2006a, p. 8-43).  The authors
reported larger effect estimates for the association for data above the
potential threshold level, suggesting that an O3-mortality association
might be underestimated in the non-threshold model.  A threshold
analysis recently reported by Bell et al. (2006) for 98 U.S.
communities, including the same 95 communities in Bell et al. (2004),
indicated that if a population threshold existed for mortality, it would
likely fall below a 24-hour average O3 concentration of 0.015 ppm (<
0.025 ppm, 8-hour average).  In addition, Burnett and colleagues
(1997a,b) plotted the relationships between air pollutant concentrations
and both respiratory and cardiovascular hospitalization, and it appears
in these results that the associations with O3 are found in the
concentration range above about 0.030 ppm (1-hour maximum; < 0.025 ppm,
8-hour average).  Vedal and colleagues (2003) reported a significant
association between O3 and mortality in British Columbia where O3
concentrations were quite low (mean 1-hour maximum concentration of
0.0273 ppm).  The authors did not specifically test for threshold
levels, but the fact that the association was found in an area with such
low O3 concentrations suggests that any potential threshold level would
be quite low in this data set.

	In summary, the 2006 Criteria Document finds that, taken together, the
available evidence from controlled human exposure and epidemiological
studies suggests that no clear conclusion can now be reached with regard
to possible threshold levels for O3-related effects (EPA, 2006a, p.
8-44).  Thus, the available epidemiological evidence neither supports
nor refutes the existence of thresholds at the population level for
effects such as increased hospital admissions and premature mortality. 
There are limitations in epidemiological studies that make discerning
thresholds in populations difficult, including low data density in the
lower concentration ranges, the possible influence of exposure
measurement error, and interindividual differences in susceptibility to
O3-related effects in populations.  There is the possibility that
thresholds for individuals may exist in reported associations at fairly
low levels within the range of air quality observed in the studies but
not be detectable as population thresholds in epidemiological analyses.

b.	 Biological Plausibility and Coherence of Evidence

	The body of epidemiological studies discussed in the 2007 Staff Paper
emphasizes the role of O3 in association with a variety of adverse
respiratory and cardiovascular effects.  While recognizing a variety of
plausible mechanisms, there exists a general consensus suggesting that
O3, could either directly or through initiation, interfere with basic
cellular oxidation processes responsible for inflammation, reduced
antioxidant capacity, atherosclerosis and other effects.  Reasoning that
O3 influences cellular chemistry through basic oxidative properties (as
opposed to a unique chemical interaction), other reactive oxidizing
species (ROS) in the atmosphere acting either independently or in
combination with O3 may also contribute to a number of adverse
respiratory and cardiovascular health effects.  Consequently, the role
of O3 should be considered more broadly as O3 behaves as a generator of
numerous oxidative species in the atmosphere.

	In considering the biological plausibility of reported O3-related
effects, the 2007 Staff Paper (section 3.4.6) considers this broader
question of health effects of pollutant mixtures containing O3.  The
potential for O3-related enhancements of PM formation, particle uptake,
and exacerbation of PM-induced cardiovascular effects underscores the
importance of considering contributions of O3 interactions with other
often co-occurring air pollutants to health effects due to O3-containing
pollutant mixes.  The 2007 Staff Paper summarizes some examples of
important pollutant mixture effects from studies that evaluate
interactions of O3 with other co-occurring pollutants, as discussed in
chapters 4, 5, and 6 of the 2006 Criteria Document.

	All of the types of interactive effects of O3 with other co-occurring
gaseous and nongaseous viable and nonviable PM components of ambient air
mixes noted above argue that O3 acts not only alone but that O3 also is
a surrogate indicator for air pollution mixes which may enhance the risk
of adverse effects due to O3 acting in combination with other
pollutants.  Viewed from this perspective, those epidemiologic findings
of morbidity and mortality associations, with ambient O3 concentrations
extending to quite low levels in many cases, become more understandable
and plausible.

	The 2006 Criteria Document integrates epidemiological studies with
mechanistic information from controlled human exposure studies and
animal toxicological studies to draw conclusions regarding the coherence
of evidence and biological plausibility of O3-related health effects to
reach judgments about the causal nature of observed associations.  As
summarized below, coherence and biological plausibility is discussed for
each of the following types of O3-related effects:  short-term effects
on the respiratory system, effects on the cardiovascular system, effects
related to long-term O3 exposure, and short-term mortality-related
health endpoints.

i.	Coherence and Plausibility of Short-term Effects on the Respiratory
System

	Acute respiratory morbidity effects that have been associated with
short-term exposure to O3 include such health endpoints as decrements in
lung function, increased respiratory symptoms, increased airway
responsiveness, airway inflammation, increased permeability related to
epithelial injury, immune system effects, emergency department visits
for respiratory diseases, and hospitalization due to respiratory
illness.

	Recent epidemiological studies have supported evidence available in the
previous O3 NAAQS review on associations between ambient O3 exposure and
decline in lung function for children.  The 2006 Criteria Document (p.
8-34) concludes that exposure to ambient O3 has a significant effect on
lung function and is associated with increased respiratory symptoms and
medication use, particularly in asthmatics.  Short-term exposure to O3
has also been associated with more severe morbidity endpoints, such as
emergency department visits and hospital admissions for respiratory
cases, including specific respiratory illness (e.g., asthma) (EPA,
2006a, sections 7.3.2 and 7.3.3). In addition, a few epidemiological
studies have reported positive associations between short-term O3
exposure and respiratory mortality, though the associations are not
generally statistically significant (EPA, 2006a, p. 7-108).

	Considering the evidence from epidemiological studies, the results
described above provide evidence for coherence in O3-related effects on
the respiratory system.  Effect estimates from U.S. and Canadian studies
are shown in Figure 1, where it can be seen that mostly positive
associations have been reported with respiratory effects ranging from
respiratory symptoms, such as cough or wheeze, to hospitalization for
various respiratory diseases, and there is suggestive evidence for
associations with respiratory mortality.  Many of the reported
associations are statistically significant, particularly in the warm
season.  In Figure 1, the central effect estimate is indicated by a
square for each result, with the vertical bar representing the 95
percent confidence interval around the estimate.  In the discussions
that follow, an individual study result is considered to be
statistically significant if the 95 percent confidence interval does not
include zero.  Positive effect estimates indicate increases in the
health outcome with O3 exposure.  In considering these results as a
whole, it is important to consider not only whether statistical
significance at the 95 percent confidence level is reported in
individual studies but also the general pattern of results, focusing in
particular on studies with greater statistical power that report
relatively more precise results.

 

	Considering also evidence from toxicological, controlled human
exposure, and field studies, the 2006 Criteria Document (section 8.6)
discusses biological plausibility and coherence of evidence for acute
O3-induced respiratory health effects.  Inhalation of O3 for several
hours while subjects are physically active can elicit both acute adverse
pathophysiological changes and subjective respiratory tract symptoms
(EPA, 2006a, section 8.4.2).  Acute pulmonary responses observed in
healthy humans exposed to O3 at ambient concentrations include: 
decreased inspiratory capacity; mild bronchoconstriction; rapid, shallow
breathing during exercise; subjective symptoms of tracheobronchial
airway irritation, including cough and pain on deep inspiration;
decreases in measures of lung function; and increased airway resistance.
 The severity of symptoms and magnitude of response depends on inhaled
dose, individual O3 sensitivity, and the degree of attenuation or
enhancement of response resulting from previous O3 exposures.  Lung
function studies of several animal species acutely exposed to relatively
low O3 levels from a toxicological perspective (i.e., 0.25 to 0.4 ppm)
show responses similar to those observed in humans, including increased
breathing frequency, decreased tidal volume, increased resistance, and
decreased FVC.  Alterations in breathing pattern return to normal within
hours of exposure, and attenuation in functional responses following
repeated O3 exposures is similar to those observed in humans.

	Physiological and biochemical alterations investigated in controlled
human exposure and animal toxicology studies tend to support certain
hypotheses of underlying pathological mechanisms which lead to the
development of respiratory-related effects reported in epidemiology
studies (e.g., increased hospitalization and medication use).  Some of
these are:  (a) decrements in lung function, (b) bronchoconstriction,
(c) increased airway responsiveness, (d) airway inflammation, (e)
epithelial injury, (f) immune system activation, (g) host defense
impairment, and (h) sensitivity of individuals, which depends on at
least a person’s age, disease status, genetic susceptibility, and the
degree of attenuation present due to prior exposures.  The time
sequence, magnitude, and overlap of these complex events, both in terms
of development and recovery, illustrate the inherent difficulty of
interpreting the biological plausibility of O3-induced cardiopulmonary
health effects (EPA, 2006a, p. 8-48).

	The interaction of O3 with airway epithelial cell membranes and ELF to
form lipid ozonation products and ROS is supported by numerous human,
animal and in vitro studies.  Ozonation products and ROS initiate a
cascade of events that lead to oxidative stress, injury, inflammation,
airway epithelial damage and increased epithelial damage and increased
alveolar permeability to vascular fluids.  Repeated respiratory
inflammation can lead to a chronic inflammatory state with altered lung
structure and lung function and may lead to chronic respiratory diseases
such as fibrosis and emphysema (EPA, 2006a, section 8.6.2).  Continued
respiratory inflammation also can alter the ability to respond to
infectious agents, allergens and toxins.  Acute inflammatory responses
to O3 are well documented, and lung injury appears within 3 hours after
exposure in humans.

	Taken together, the 2006 Criteria Document concludes that the evidence
from experimental human and animal toxicology studies indicates that
acute O3 exposure is causally associated with respiratory system
effects.  These effects include O3-induced pulmonary function
decrements; respiratory symptoms; lung inflammation and increased lung
permeability; airway hyperresponsiveness; increased uptake of nonviable
and viable particles; and consequent increased susceptibility to
PM-related toxic effects and respiratory infections (EPA, 2006a, p.
8-48).  

ii.	Coherence and Plausibility of Effects on the Cardiovascular System 

 concentrations (≥ 0.5 ppm) demonstrate tissue edema in the heart and
lungs.  Ozone-induced changes in heart rate, edema of heart tissue, and
increased tissue and serum levels of ANF found with 8-hour 0.5 ppm O3
exposure in animal toxicology studies (Vesely et al., 1994a,b,c) also
raise the possibility of potential cardiovascular effects of acute
ambient O3 exposures.

	Animal toxicology studies have found both transient and persistent
ventilatory responses with and without progressive decreases in heart
rate (Arito et al., 1997).  Observations of O3-induced vasoconstriction
in a controlled human exposure study by Brook et al. (2002) suggests
another possible mechanism for O3-related exacerbations of preexisting
cardiovascular disease.  One controlled human study (Gong et al., 1998)
evaluated potential cardiovascular health effects of O3 exposure.  The
overall results did not indicate acute cardiovascular effects of O3 in
either the hypertensive or control subjects.  The authors observed an
increase in rate-pressure product and heart rate, a decrement for FEV1,
and a >10 mm Hg increase in the alveolar/arterial pressure difference
for O2 following O3 exposure.  Foster et al. (1993) demonstrated that
even in relatively young healthy adults, O3 exposure can cause
ventilation to shift away from the well-perfused basal lung.  This
effect of O3 on ventilation distribution may persist beyond 24-hours
post-exposure (Foster et al., 1997).  These findings suggest that O3 may
exert cardiovascular effects indirectly by impairing alveolar-arterial
O2 transfer and potentially reducing O2 supply to the myocardium. Ozone
exposure may increase myocardial work and impair pulmonary gas exchange
to a degree that could perhaps be clinically important in persons with
significant preexisting cardiovascular impairment. 

	As noted above in section II.A.2.a, a limited number of new
epidemiological studies have reported associations between short-term O3
exposure and effects on the cardiovascular system.  Among these studies,
three were population-based and involved relatively large cohorts; two
of these studies evaluated associations between O3 and HRV and the other
study evaluated the association between O3 levels and the relative risk
of MI or heart attack.  Such studies may offer more informative results
based on their large subject-pool and design.  Results from these three
studies were suggestive of an association between O3 exposure and the
cardiovascular endpoints studied.  In other recent studies on the
incidence of heart attacks and some more subtle cardiovascular health
endpoints, such as changes in HRV or cardiac arrhythmia, some but not
all studies reported associations with short-term exposure to O3 (EPA,
2006a, section 7.2.7.1).  From these studies, the 2006 Criteria Document
concludes that the “current evidence is rather limited but suggestive
of a potential effect on HRV, ventricular arrhythmias, and MI
incidence” (EPA, 2006a, p. 7-65).

	An increasing number of studies have evaluated the association between
O3 exposure and cardiovascular hospital admissions.  As discussed in
section 7.3.4 of the 2006 Criteria Document, many reported negative or
inconsistent associations, whereas other studies, especially those that
examined the relationship when O3 exposures were higher, have found
positive and robust associations between O3 and cardiovascular hospital
admissions.  The 2006 Criteria Document (p. 7-83) finds that the overall
evidence from these studies remains inconclusive regarding the effect of
O3 on cardiovascular hospitalizations.  The 2006 Criteria Document notes
that the suggestive positive epidemiologic findings of O3 exposure on
cardiac autonomic control, including effects on HRV, ventricular
arrhythmias and heart attacks, and reported associations between O3
exposure and cardiovascular hospitalizations generally in the warm
season gain credibility and scientific support from the results of
experimental animal toxicology and controlled human exposure studies,
which are indicative of plausible pathways by which O3 may exert
cardiovascular effects (EPA, 2006a, section 8.6.1).

iii.	Coherence and Plausibility of Effects Related to Long-Term O3
Exposure

	Controlled human exposure studies cannot evaluate effects of long-term
exposures to O3; there is some evidence available from toxicological
studies.  While early animal toxicology studies of long-term O3
exposures were conducted using continuous exposures, more recent studies
have focused on exposures which mimic diurnal and seasonal patterns and
more realistic O3 exposure levels (EPA, 2006a, p. 8-50).  Studies of
monkeys that compared these two exposure scenarios found increased
airway pathology only with the latter design.  Persistent and
irreversible effects reported in chronic animal toxicology studies
suggest that additional complementary human data are needed from
epidemiologic studies (EPA, 2006a, p. 8-50).

	There is limited evidence from human studies for long-term O3-induced
effects on lung function.  As discussed in section 8.6.2 of the 2006
Criteria Document, previous epidemiological studies have provided only
inconclusive evidence for either mortality or morbidity effects of
long-term O3 exposure.  The 2006 Criteria Document (p. 8-50) observes
that the inconsistency in findings may be due to a lack of precise
exposure information, the possibility of selection bias, and the
difficulty of controlling for confounders.  Several new longitudinal
epidemiology studies have evaluated associations between long-term O3
exposures and morbidity and mortality and suggest that these long-term
exposures may be related to changes in lung function in children;
however, little evidence is available to support a relationship between
chronic O3 exposure and mortality or lung cancer incidence (EPA, 2006a,
p. 8-50).

	The 2006 Criteria Document (p. 8-51) concludes that evidence from
animal toxicology studies strongly suggests that chronic O3 exposure is
capable of damaging the distal airways and proximal alveoli, resulting
in lung tissue remodeling leading to apparent irreversible changes. 
Such structural changes and compromised lung function caused by
persistent inflammation may exacerbate the progression and development
of chronic lung disease.  Together with the limited evidence available
from epidemiological studies, these findings offer some insight into
potential biological mechanisms for suggested associations between
long-term or seasonal exposures to O3 and reduced lung function
development in children which have been observed in epidemiologic
studies (EPA, 2006a, p. 8-51).

iv.	Coherence and Plausibility of Short-Term Mortality-Related Health
Endpoints

	An extensive epidemiological literature on air pollution related
mortality risk estimates from the U.S., Canada, and Europe is discussed
in the 2006 Criteria Document (sections 7.4 and 8.6.3).  These single-
and multicity mortality studies coupled with results from meta-analyses
generally indicate associations between acute O3 exposure and elevated
risk for all-cause mortality, even after adjustment for the influence of
season and PM exposure.  Several single-city studies that specifically
evaluated the relationship between O3 exposure and cardiopulmonary
mortality also reported results suggestive of a positive association
(EPA, 2006a, p. 8-51).  These mortality studies suggest a pattern of
effects for causality that have biologically plausible explanations, but
our knowledge regarding potential underlying mechanisms is very limited
at this time and requires further research.  Most of the physiological
and biochemical parameters investigated in human and animal studies
suggest that O3-induced biochemical effects are relatively transient and
attenuate over time.  The 2006 Criteria Document (p. 8-52) hypothesizes
a generic pathway of O3-induced lung damage, potentially involving
oxidative lung damage with subsequent inflammation and/or decline in
lung function leading to respiratory distress in some sensitive
population groups (e.g., asthmatics), or other plausible pathways noted
below that may lead to O3-related contributions to cardiovascular
effects that ultimately increase risk of mortality. 

	The third National Health and Nutrition Examination Survey follow-up
data analysis indicates that about 20 percent of the adult population
has reduced FEV1 values, suggesting impaired lung function in a
significant portion of the population.  Most of these individuals have
COPD, asthma or fibrotic lung disease (Manino et al., 2003), which are
associated with persistent low-grade inflammation.  Furthermore,
patients with COPD are at increased risk for cardiovascular disease. 
Also, lung disease with underlying inflammation may be linked to
low-grade systemic inflammation associated with atherosclerosis,
independent of cigarette smoking (EPA, 2006a, p. 8-52).  Lung function
decrements in persons with cardiopulmonary disease have been associated
with inflammatory markers, such as C-reactive protein (CRP) in the
blood.  At a population level it has been found that individuals with
the lowest FEV1 values have the highest levels of CRP, and those with
the highest FEV1 values have the lowest CRP levels (Manino et al., 2003;
Sin and Man, 2003).  This complex series of physiological and
biochemical reactions following O3 exposure may tilt the biological
homeostasis mechanisms which could lead to adverse health effects in
people with compromised cardiopulmonary systems.   

	Several other types of newly available data also support reasonable
hypotheses that may help to explain the findings of O3-related increases
in cardiovascular mortality observed in some epidemiological studies. 
These include the direct effect of O3 on increasing PAF in lung tissue
that can then enter the general circulation and possibly contribute to
increased risk of blood clot formation and the consequent increased risk
of heart attacks, cerebrovascular events (stroke), or associated
cardiovascular-related mortality.  Ozone reactions with cholesterol in
lung surfactant to form epoxides and oxysterols that are cytotoxic to
lung and heart muscles and that contribute to atherosclerotic plaque
formation in arterial walls represent another potential pathway. 
Stimulation of airway irritant receptors may lead to increases in tissue
and serum levels of ANF, changes in heart rate, and edema of heart
tissue.  A few new field and panel studies of human adults have reported
associations between ambient O3 concentrations and changes in cardiac
autonomic control (e.g., HRV, ventricular arrhythmias, and MI).  These
represent plausible pathways that may lead to O3-related contributions
to cardiovascular effects that ultimately increase the risk of
mortality.

	In addition, O3-induced increases in lung permeability allow more ready
entry for inhaled PM into the blood stream, and thus O3 exposure may
increase the risk of PM-related cardiovascular effects.  Furthermore,
increased ambient O3 levels contribute to ultrafine PM formation in the
ambient air and indoor environments.  Thus, the contributions of
elevated ambient O3 concentrations to ultrafine PM formation and human
exposure, along with the enhanced uptake of inhaled fine particles,
consequently may contribute to exacerbation of PM-induced cardiovascular
effects in addition to those more directly induced by O3 (EPA, 2006a, p.
8-53).

c.	Summary

	Judgments concerning the extent to which relationships between various
health endpoints and ambient O3 exposures are likely to be causal are
informed by the conclusions and discussion in the 2006 Criteria Document
as discussed above and summarized in section 3.7.5 of the 2007 Staff
Paper.  These judgments reflect the nature of the evidence and the
overall weight of the evidence, and are taken into consideration in the
quantitative risk assessment discussed below in section II.B.2.

	For example, there is a very high level of confidence that O3 induces
lung function decrements in healthy adults and children due in part to
the dozens of controlled human exposure and epidemiological studies
consistently showing such effects.  The 2006 Criteria Document (p. 8-74)
states that these studies provide clear evidence of causality for
associations between short-term O3 exposures and statistically
significant declines in lung function in children, asthmatics and adults
who exercise outdoors.  An increase in respiratory symptoms (e.g.,
cough, shortness of breath) has been observed in controlled human
exposure studies of short-term O3 exposures, and significant
associations between ambient O3 exposures and a wide variety of
respiratory symptoms have been reported in epidemiology studies (EPA,
2006a, p. 8-75).  Population time-series studies showing robust
associations between O3 exposures and respiratory hospital admissions
and emergency department visits are strongly supported by controlled
human exposure, animal toxicological, and epidemiological evidence for
O3-related lung function decrements, respiratory symptoms, airway
inflammation, and airway hyperreactivity.  The 2006 Criteria Document
(p. 8-77) concludes that, taken together, the overall evidence supports
the inference of a causal relationship between acute ambient O3
exposures and increased respiratory morbidity outcomes resulting in
increased emergency department visits and hospitalizations during the
warm season.  Further, recent epidemiologic evidence has been
characterized in the 2006 Criteria Document (p. 8-78) as highly
suggestive that O3 directly or indirectly contributes to non-accidental
and cardiopulmonary-related mortality.

4.	O3-Related Impacts on Public Health

	The following discussion draws from chapters 6 and 7 and section 8.7 of
the 2006 Criteria Document and section 3.6 of the 2007 Staff Paper to
characterize factors which modify responsiveness to O3, populations
potentially at risk for O3-related health effects, the adversity of
O3-related effects, and the size of the at-risk populations in the U.S..
 These considerations are all important elements in characterizing the
potential public health impacts associated with exposure to ambient O3.

a.	Factors That Modify Responsiveness to Ozone

	There are numerous factors that can modify individual responsiveness to
O3.  These include:  influence of physical activity; age; gender and
hormonal influences; racial, ethnic and socioeconomic status (SES)
factors; environmental factors; and oxidant-antioxidant balance.  These
factors are discussed in more detail in section 6.5 of the 2006 Criteria
Document.  

	It is well established that physical activity increases an
individual’s minute ventilation and will thus increase the dose of O3
inhaled (EPA, 2006a, section 6.5.4).  Increased physical activity
results in deeper penetration of O3 into more distal regions of the
lungs, which are more sensitive to acute O3 response and injury.  This
will result in greater lung function decrements for acute exposures of
individuals during increased physical activity.  Research has shown that
respiratory effects are observed at lower O3 concentrations if the level
of exertion is increased and/or duration of exposure and exertion are
extended.  Predicted O3-induced decrements in lung function have been
shown to be a function of exposure concentration, duration and exercise
level for healthy, young adults (McDonnell et al., 1997).

	Most of the studies investigating the influence of age have used lung
function decrements and symptoms as measures of response. For healthy
adults, lung function and symptom responses to O3 decline as age
increases.  The rate of decline in O3 responsiveness appears greater in
those 18 to 35 years old compared to those 35 to 55 years old, while
there is very little change after age 55.  In one study (Seal et al.,
1996) analyzing a large data set, a 5.4% decrement in FEV1 on average
was estimated for 20 year old individuals exposed to 0.12 ppm O3 for 2.3
hours, whereas similar exposure of 35 year old individuals resulted in a
2.6% decrement on average.  While healthy children tend not to report
respiratory symptoms when exposed to low levels of O3, for subjects 18
to 36 years old symptom responses induced by O3 are observed but tend to
decrease with increasing age within this range (McDonnell et al., 1999).

	Limited evidence of gender differences in response to O3 exposure has
suggested that females may be predisposed to a greater susceptibility to
O3.  Lower plasma and NL fluid levels of the most prevalent antioxidant,
uric acid, in females relative to males may be a contributing factor. 
Consequently, reduced removal of O3 in the upper airways may promote
deeper penetration.  However, most of the evidence on gender differences
appears to be equivocal, with one study (Hazucha et al., 2003)
suggesting that physiological responses of young healthy males and
females may be comparable (EPA, 2006a, section 6.5.2).

	A few studies have suggested that ethnic minorities might be more
responsive to O3 than Caucasian population groups (EPA, 2006a, section
6.5.3).  This may be more the result of a lack of adequate health care
and socioeconomic status (SES) than any differences in sensitivity to
O3.  The limited data available, which have investigated the influence
of race, ethnic or other related factors on responsiveness to O3,
prevent drawing any clear conclusions at this time.

	Few human studies have examined the potential influence of
environmental factors such as the sensitivity of individuals who
voluntarily smoke tobacco (i.e., smokers) and the effect of high
temperatures on O3 responsiveness.  New controlled human exposure
studies have confirmed that smokers are less responsive to O3 than
nonsmokers; however, time course of development and recovery of these
effects, as well as reproducibility, was not different from nonsmokers
(EPA, 2006a, section 6.5.5).  Influence of ambient temperature on
pulmonary effects induced by O3 has been studied very little, but
additive effects of heat and O3 exposure have been reported.

	Antioxidants, which scavenge free radicals and limit lipid peroxidation
in the ELF, are the first line of defense against oxidative stress. 
Ozone exposure leads to absorption of O3 in the ELF with subsequent
depletion of antioxidant in the nasal ELF, but concentration and
antioxidant enzyme activity in ELF or plasma do not appear related to O3
responsiveness (EPA 2006a, section 6.5.6).  Controlled studies of
dietary antioxidant supplements have shown some protective effects on
lung function decrements but not on symptoms and airway inflammatory
responses.  Dietary antioxidant supplements have provided some
protection to asthmatics by attenuating post-exposure airway
hyperresponsiveness.  Animal studies have also supported the protective
effects of ELF antioxidants.

b.	At-Risk Subgroups for O3-Related Effects

	Several characteristics may increase the extent to which a population
group shows increased susceptibility or vulnerability.  Information on
potentially susceptible and vulnerable groups is summarized in section
8.7 of the 2006 Criteria Document.  As described there, the term
susceptibility refers to innate (e.g., genetic or developmental) or
acquired (e.g., personal risk factors, age) factors that make
individuals more likely to experience effects with exposure to
pollutants.  A number of population groups have been identified as
potentially susceptible to health effects as a result of O3 exposure,
including people with existing lung diseases, including asthma, children
and older adults, and people who have larger than normal lung function
responses that may be due to genetic susceptibility.  In addition, some
population groups have been identified as having increased vulnerability
to O3-related effects due to increased likelihood of exposure while at
elevated ventilation rates, including healthy children and adults who
are active outdoors, for example, outdoor workers, and joggers.  Taken
together, the susceptible and vulnerable groups make up "at-risk"
groups.

i.	Active People

	A large group of individuals at risk from O3 exposure consists of
outdoor workers and children, adolescents, and adults who engage in
outdoor activities involving exertion or exercise during summer daylight
hours when ambient O3 concentrations tend to be higher.  This conclusion
is based on a large number of controlled-human exposure studies and
several epidemiologic field/panel studies which have been conducted with
healthy children and adults and those with preexisting respiratory
diseases (EPA 2006a, sections 6.2, 6.3, 7.2, and 8.4.4).   The
controlled human exposure studies show a clear O3 exposure-response
relationship with increasing spirometric and symptomatic response as
exercise level increases. Furthermore, O3-induced response increases as
time of exposure increases.  Studies of outdoor workers and others who
participate in outdoor activities indicate that extended exposures to O3
at elevated exertion levels can produce marked effects on lung function,
as discussed above in section IIA.2 (Brauer et al., 1996; Höppe et al.,
1995; Korrick et al., 1998; McConnell et al., 2002).

	These field studies with subjects at elevated exertion levels support
the extensive evidence derived from controlled human exposure studies. 
The majority of controlled human exposure studies has examined the
effects of O3 exposure in subjects performing continuous or intermittent
exercise for variable periods of time and has reported significant
O3-induced respiratory responses.  The epidemiologic studies discussed
above also indicate that prolonged exposure periods, combined with
elevated levels of exertion or exercise, may magnify O3 effects on lung
function.  Thus, outdoor workers and others who participate in higher
exertion activities outdoors during the time of day when high peak O3
concentrations occur appear to be particularly vulnerable to O3 effects
on respiratory health.  Although these studies show a wide variability
of response and sensitivity among subjects and the factors contributing
to this variability continue to be incompletely understood, the effect
of increased exertion is consistent.  It should be noted that this wide
variability of response and sensitivity among subjects may be in part
due to the wide range of other highly reactive photochemical oxidants
coexisting with O3 in the ambient air.

ii.	People with Lung Disease

	People with preexisting pulmonary disease are among those at increased
risk from O3 exposure.  Altered physiological, morphological, and
biochemical states typical of respiratory diseases like asthma, COPD,
and chronic bronchitis may render people sensitive to additional
oxidative burden induced by O3 exposure.  At the time of the 1997
review, it was concluded that these groups were at greater risk because
the impact of O3-induced responses on already-compromised respiratory
systems would noticeably impair an individual's ability to engage in
normal activity or would be more likely to result in increased
self-medication or medical treatment.  At that time there was little
evidence that people with pre-existing disease were more responsive than
healthy individuals in terms of the magnitude of lung function
decrements or symptomatic responses.  The new results from controlled
exposure and epidemiologic studies continue to indicate that individuals
with preexisting pulmonary disease are a sensitive population for
O3-related health effects.

	Several controlled human exposure studies reviewed in the 1996 Criteria
Document on atopic and asthmatic subjects have suggested but not clearly
demonstrated enhanced responsiveness to acute O3 exposure compared to
healthy subjects.  The majority of the newer studies reviewed in Chapter
6 of the 2006 Criteria Document indicate that asthmatics are more
sensitive than normal subjects in manifesting O3-induced lung function
decrements.  In one key study (Horstman et al., 1995), the FEV1
decrement observed in the asthmatics was significantly larger than in
the healthy subjects (19% versus 10%, respectively).  There was also a
notable tendency for a greater group mean O3-induced decrease in
FEF25-75 in asthmatics relative to the healthy subjects (24% versus 15%,
respectively).  A significant positive correlation in asthmatics was
also reported between the magnitude of O3-induced spirometric responses
and baseline lung function, i.e., responses increased with severity of
disease.

	Asthmatics present a differential response profile for cellular,
molecular, and biochemical parameters (2006 Criteria Document, Figure
8-1) that are altered in response to acute O3 exposure.  Ozone-induced
increases in neutrophils, IL-8 and protein were found to be
significantly higher in the BAL fluid from asthmatics compared to
healthy subjects, suggesting mechanisms for the increased sensitivity of
asthmatics (Basha et al., 1994; McBride et al., 1994; Scannell et al.,
1996; Hiltermann et al., 1999; Holz et al., 1999; Bosson et al., 2003). 
Neutrophils, or PMNs, are the white blood cells most associated with
inflammation.  IL-8 is an inflammatory cytokine with a number of
biological effects, primarily on neutrophils.  The major role of this
cytokine is to attract and activate neutrophils.  Protein in the airways
is leaked from the circulatory system, and is a marker for increased
cellular permeability.  

	Bronchial constriction following provocation with O3 and/or allergens
presents a two-phase response.  The early response is mediated by
release of histamine and leukotrienes that leads to contraction of
smooth muscle cells in the bronchi, narrowing the lumen and decreasing
the airflow.  In people with allergic airway disease, including people
with rhinitis and asthma, these mediators also cause accumulation of
eosinophils in the airways (Bascom et al., 1990; Jorres et al., 1996;
Peden et al., 1995 and 1997; Frampton et al., 1997; Michelson et al.,
1999; Hiltermann et al., 1999; Holz et al., 2002; Vagaggini et al.,
2002).  In asthma, the eosinophil, which increases inflammation and
allergic responses, is the cell most frequently associated with
exacerbations of the disease.  A study by Bosson et al. (2003) evaluated
the difference in O3-induced bronchial epithelial cytokine expression
between healthy and asthmatic subjects.  After O3 exposure the
epithelial expression of IL-5 and GM-CSF increased significantly in
asthmatics, compared to healthy subjects.  Asthma is associated with
Th2-related airway response (allergic response), and IL-5 is an
important Th2-related cytokine.  The O3-induced increase in IL-5, and
also in GM-CSF, which affects the growth, activation and survival of
eosinophils, may indicate an effect on the Th2-related airway response
and on airway eosinophils.  The authors reported that the O3-induced
Th2-related cytokine responses that were found within the asthmatic
group may indicate a worsening of their asthmatic airway inflammation
and thus suggest a plausible link to epidemiological data indicating
O3-associated increases in bronchial reactivity and hospital admissions.
 

	The accumulation of eosinophils in the airways of asthmatics is
followed by production of mucus and a late-phase bronchial constriction
and reduced airflow.  In a study of 16 intermittent asthmatics,
Hiltermann et al. (1999) found that there was a significant inverse
correlation between the O3-induced change in the percentage of
eosinophils in induced sputum and the change in PC20, the concentration
of methacholine causing a 20% decrease in FEV1.  Characteristic
O3-induced inflammatory airway neutrophilia at one time was considered a
leading mechanism of airway hyperresponsiveness.  However, Hiltermann et
al. (1999) determined that the O3-induced change in percentage
neutrophils in sputum was not significantly related to the change in
PC20.  These results are consistent with the results of Zhang et al.
(1995), which found neutrophilia in a murine model to be only
coincidentally associated with airway hyperresponsiveness, i.e., there
was no cause and effect relationship. (2006 Criteria Document, AX 6-26).
 Hiltermann et al. (1999) concluded that the results point to the role
of eosinophils in O3-induced airway hyperresponsiveness.  Increases in
O3-induced nonspecific airway responsiveness incidence and duration
could have important clinical implications for asthmatics.  

	Two studies (Jörres et al., 1996; Holz et al., 2002) observed
increased airway responsiveness to O3 exposure with bronchial allergen
challenge in subjects with preexisting allergic airway disease.  Jörres
et al. (1996) found that O3 causes an increased response to bronchial
allergen challenge in subjects with allergic rhinitis and mild allergic
asthma.  The subjects were exposed to 0.25 ppm O3 for 3 hours with IE.
Airway responsiveness to methacholine was determined 1 hour before and
after exposure; responsiveness to allergen was determined 3 hours after
exposure.  Statistically significant decreases in FEV1 occurred in
subjects with allergic rhinitis (13.8%) and allergic asthma (10.6%), and
in healthy controls (7.3%).  Methacholine responsiveness was
statistically increased in asthmatics, but not in subjects with allergic
rhinitis or healthy controls.  Airway responsiveness to an
individual’s historical allergen (either grass and birch pollen, house
dust mite, or animal dander) was significantly increased after O3
exposure when compared to FA exposure.  In subjects with asthma and
allergic rhinitis, a maximum percent fall in FEV1 of 27.9% and 7.8%,
respectively, occurred 3 days after O3 exposure when they were
challenged with of the highest common dose of allergen.  The authors
concluded that subjects with asthma or allergic rhinitis, without
asthma, could be at risk if a high O3 exposure is followed by a high
dose of allergen.  

Holz et al. (2002) reported an early phase lung function response in
subjects with rhinitis after a consecutive 4-day exposure to 0.125 ppm
O3 that resulted in a clinically relevant (>20%) decrease in FEV1. 
Ozone-induced exacerbation of airway responsiveness persists longer and
attenuates more slowly than O3-induced lung function decrements and
respiratory symptom responses and can have important clinical
implications for asthmatics.

and TNF-α.  Another study by Schierhorn et al. (2002) found significant
differences in the O3-induced release of the neuropeptides neurokinin A
and substance P for allergic patients in comparison to nonallergic
controls, suggesting increased activation of sensory nerves by O3 in the
allergic tissues.  Another study by Bayram et al. (2002) using in vitro
culture of bronchial epithelial cells recovered from atopic and
nonatopic asthmatics also found significant increases in epithelial
permeability in response to O3 exposure.  

	The new data on airway responsiveness, inflammation, and various
molecular markers of inflammation and bronchoconstriction indicate that
people with asthma and allergic rhinitis (with or without asthma)
comprise susceptible groups for O3-induced adverse effects.  This body
of evidence indicates that controlled human exposure and epidemiological
panel studies of lung function decrements and respiratory symptoms that
evaluate only healthy, non-asthmatic subjects likely underestimate the
effects of O3 exposure on asthmatics and other susceptible populations. 
The effects of O3 on lung function, inflammation, and increased airway
responsiveness demonstrated in subjects with asthma and other allergic
airway diseases, provide plausible mechanisms underlying the more
serious respiratory morbidity effects, such as emergency department
visits and hospital admissions, and respiratory mortality effects.

A number of epidemiological studies have been conducted using asthmatic
study populations.  The majority of epidemiological panel studies that
evaluated respiratory symptoms and medication use related to O3
exposures focused on children.  These studies suggest that O3 exposure
is associated with increased respiratory symptoms and medication use in
children with asthma.  Other reported effects include respiratory
symptoms, lung function decrements, and emergency department visits, as
discussed in the 2006 Criteria Document (section 7.6.7.1).  Strong
evidence from a large multicity study (Mortimer et al., 2002), along
with support from several single-city studies indicate that O3 exposure
is associated with increased respiratory symptoms and medication use in
children with asthma.  With regard to ambient O3 levels and increased
hospital admissions and emergency department visits for asthma and other
respiratory causes, strong and consistent evidence establishes a
correlation between O3 exposure and increased exacerbations of
preexisting respiratory disease for 1-hour maximum O3 concentrations
<0.12 ppm.  As discussed above and in the 2006 Criteria Document,
section 7.3, several hospital admission and emergency department visit
studies in the U.S., Canada, and Europe have reported positive
associations between increase in O3 and increased risk of emergency
department visits and hospital admissions for asthma other respiratory
diseases, especially during the warm season.

In summary, based on a substantial new body of evidence from animal,
controlled human exposure and epidemiological studies the 2006 Criteria
Document (section x.x) concludes that people with asthma and other
preexisting pulmonary diseases are among those at increased risk from O3
exposure.  Evidence from controlled human exposure studies indicates
that asthmatics may exhibit larger lung function decrements and can have
larger inflammatory responses in response to O3 exposure than healthy
controls.  Asthmatics present a different response profile for cellular,
molecular, and biochemical parameters that are altered in response to
acute O3 exposure.  Asthmatics, and people with allergic rhinitis, are
more likely to mount an allergic-type response upon exposure to O3, as
manifested by increases in white blood cells associated with allergy and
related molecules, which increase inflammation in the airways.  The
increased inflammatory and allergic responses also may be associated
with the larger late-phase responses that asthmatics can experience,
which can include increased bronchoconstrictor responses to irritant
substances or allergens and additional inflammation.  Epidemiological
studies have reported fairly robust associations between ambient O3
concentrations and measures of lung function and daily respiratory
symptoms (e.g., chest tightness, wheeze, shortness of breath) in
children with moderate to severe asthma and between O3 and increased
asthma medication use.  These more serious responses in asthmatics and
others with lung disease provide biological plausibility for the
respiratory morbidity effects observed in epidemiological studies, such
as emergency department visits and hospital admissions.  The body of
evidence from controlled human exposure and epidemiological studies,
which includes asthmatic as well as non-asthmatic subjects, indicates
that controlled human exposure studies of lung function decrements and
respiratory symptoms that evaluate only healthy, non-asthmatic subjects
likely underestimate the effects of O3 exposure on asthmatics and other
susceptible populations.  

	Newly available reports from controlled human exposure studies (see
chapter 6 in the 2006 Criteria Document) utilized subjects with
preexisting cardiopulmonary diseases such as COPD, asthma, allergic
rhinitis, and hypertension.  The data generated from these studies that
evaluated changes in spirometry did not find clear differences between
filtered air and O3 exposure in COPD subjects.  However, the new data on
airway responsiveness, inflammation, and various molecular markers of
inflammation and bronchoconstriction indicate that people with atopic
asthma and allergic rhinitis comprise susceptible groups for O3-induced
adverse health effects.  

Although controlled human exposure studies have not found evidence of
larger spirometric responses to O3 in people with COPD relative to
healthy subjects, this may be due to the fact that most people with COPD
are older adults who would not be expected to be as responsive based on
their age.  However, in section 8.7.1, the  2006 Criteria Document notes
that new epidemiological evidence indicates that people with COPD may be
more likely to experience other effects, including emergency room
visits, hospital admissions, or premature mortality.  For example,
results from an analysis of five European cities indicated strong and
consistent O3 effects on unscheduled respiratory hospital admissions,
including COPD (Anderson et al., 1997).  Also, an analysis of a 9-year
data set for the whole population of the Netherlands provided risk
estimates for more specific causes of mortality, including COPD (Hoek et
al., 2000, 2001; reanalysis Hoek, 2003); a positive, but nonsignificant,
excess risk of COPD-related mortality was found to be associated with
short-term O3 concentrations.  Moreover, as indicated by Gong et al.
(1998), the effects of O3 exposure on alveolar-arterial oxygen gradients
may be more pronounced in patients with preexisting obstructive lung
diseases.  Relative to healthy elderly subjects, COPD patients have
reduced gas exchange and low SaO2.  Any inflammatory or edematous
responses due to O3 delivered to the well-ventilated regions of the lung
in COPD subjects could further inhibit gas exchange and reduce oxygen
saturation.  In addition, O3-induced vasoconstriction could also acutely
induce pulmonary hypertension.  Inducing pulmonary vasoconstriction and
hypertension in these patients would perhaps worsen their condition,
especially if their right ventricular function was already compromised
(EPA, 2006a, section 6.10).  These controlled human exposure and
epidemiological studies indicate that people with pre-existing lung
diseases other than asthma are also at greater risk from O3 exposure
than people without lung disease.

iii.	Children and Older Adults

	Supporting evidence exists for heterogeneity in the effects of O3 by
age.  As discussed in section 6.5.1 of the 2006 Criteria Document,
children, adolescents, and young adults (<18 yrs of age) appear, on
average, to have nearly equivalent spirometric responses to O3, but have
greater responses than middle-aged and older adults when exposed to
comparable O3 doses.  Symptomatic responses to O3 exposure, however, do
not appear to occur in healthy children, but are observed in asthmatic
children, particularly those who use maintenance medications.  For
adults (>17 yrs of age) symptoms gradually decrease with increasing age.
 In contrast to young adults, the diminished symptomatic responses in
children and the diminished symptomatic and spirometric responses in
older adults increases the likelihood that these groups continue outdoor
activities leading to greater O3 exposure and dose.

	As described in the section 7.6.7.2 of the 2006 Criteria Document, many
epidemiological field studies focused on the effect of O3 on the
respiratory health of school children.  In general, children experienced
decrements in lung function parameters, including PEF, FEV1, and FVC. 
Increases in respiratory symptoms and asthma medication use were also
observed in asthmatic children.  In one German study, children with and
without asthma were found to be particularly susceptible to O3 effects
on lung function.  Approximately 20 percent of the children, both with
and without asthma, experienced a greater than 10 percent change in
FEV1, compared to only 5 percent of the elderly population and athletes 
 SEQ CHAPTER \h \r 1 (Höppe et al., 2003).

	The American Academy of Pediatrics (2004) notes that children and
infants are among the population groups most susceptible to many air
pollutants, including O3.  This is in part because their lungs are still
developing.  For example, eighty percent of alveoli are formed after
birth, and changes in lung development continue through adolescence
(Dietert et al., 2000).  Children are also likely to spend more time
outdoors than adults, which results in increased exposure to air
pollutants (Wiley et al., 1991a,b).  Moreover, children have high minute
ventilation rates and high levels of physical activity which also
increases their dose (Plunkett et al., 1992).

65 years of age) O3-mortality effect estimates to that of the elderly
population (>65 years) indicates that, in general, the elderly
population is more susceptible to O3 mortality effects.    SEQ CHAPTER
\h \r 1 The meta-analysis by Bell et al. (2005) found a larger mortality
effect estimate for the elderly than for all ages.  In the large U.S. 95
communities study (Bell et al., 2004), mortality effect estimates were
slightly higher for those aged 65 to 74 years, compared to individuals
less than 65 years and 75 years or greater.  The absolute effect of O3
on premature mortality may be substantially greater in the elderly
population because of higher rates of preexisting respiratory and
cardiac diseases.  The 2006 Criteria Document (p. 7-177) concludes that
the elderly population (>65 years of age) appear to be at greater risk
of O3-related mortality and hospitalizations compared to all ages or
younger populations.

	  SEQ CHAPTER \h \r 1 The 2006 Criteria Document notes that,
collectively, there is supporting evidence of age-related differences in
susceptibility to O3 lung function effects.  The elderly population (>65
years of age) appear to be at increased risk of O3-related mortality and
hospitalizations, and children (<18 years of age) experience other
potentially adverse respiratory health outcomes with increased O3
exposure (EPA, 2006a, section 7.6.7.2).  

iv.	People with Increased Responsiveness to Ozone

	New animal toxicology studies using various strains of mice and rats
have identified O3-sensitive and resistant strains and illustrated the
importance of genetic background in determining O3 susceptibility (EPA,
2006a, section 8.7.4).  Controlled human exposure studies have also
indicated a high degree of variability in some of the pulmonary
physiological parameters.  The variable effects in individuals have been
found to be reproducible, in other words, a person who has a large lung
function response after exposure to O3 will likely have about the same
response if exposed again to the same dose of O3.  In controlled human
exposure studies, group mean responses are not representative of this
segment of the population that has much larger than average responses to
O3.  Recent studies of asthmatics by David et al. (2003) and Romieu et
al. (2004) reported a role for genetic polymorphism in observed
differences in antioxidant enzymes and genes involved in inflammation to
modulate lung function and inflammatory responses to O3 exposure.  

	Biochemical and molecular parameters extensively evaluated in these
experiments were used to identify specific loci on chromosomes and, in
some cases, to relate the differential expression of specific genes to
biochemical and physiological differences observed among these species. 
Utilizing O3-sensitive and O3-resistant species, it has been possible to
identify the involvement of increased airway reactivity and inflammation
processes in O3 susceptibility.  However, most of these studies were
carried out using relatively high doses of O3, making the relevance of
these studies questionable in human health effects assessment.  The
genes and genetic loci identified in these studies may serve as useful
biomarkers in the future.  

v.	Other Population Groups

	There is limited, new evidence supporting associations between
short-term O3 exposures and a range of effects on the cardiovascular
system.  Some but not all, epidemiological studies have reported
associations between short-term O3 exposures and the incidence of heart
attacks and more subtle cardiovascular health endpoints, such as changes
in HRV and cardiac arrhythmia.  Others have reported associations with
hospitalization or emergency department visits for cardiovascular
diseases, although the results across the studies are not consistent. 
Studies also report associations between short-term O3 exposure and
mortality from cardiovascular or cardiopulmonary causes.  The 2006
Criteria Document (p. 7-65) concludes that current cardiovascular
effects evidence from some field studies is rather limited but
supportive of a potential effect of short-term O3 exposure and HRV,
cardiac arrhythmia, and heart attack incidence.  In the 2006 Criteria
Document’s evaluation of studies of hospital admissions for
cardiovascular disease (EPA 2006a, section 7.3.4), it is concluded that
evidence from this growing group of studies is generally inconclusive
regarding an association with O3 in studies conducted during the warm
season (EPA 2006a, p. 7-83).  This body of evidence suggests that people
with heart disease may be at increased risk from short-term exposures to
O3; however, more evidence is needed to conclude that people with heart
disease are a susceptible population.

	Other groups that might have enhanced sensitivity to O3, but for which
there is currently very little evidence, include groups based on race,
gender and SES, and those with nutritional deficiencies, which presents
factors which modify responsiveness to O3.

c. 	Adversity of Effects

	In the 2008 rulemaking, in making judgments as to when various
O3-related effects become regarded as adverse to the health of
individuals, EPA looked to guidelines published by the American Thoracic
Society (ATS) and the advice of CASAC.  While recognizing that
perceptions of “medical significance” and “normal activity” may
differ among physicians, lung physiologists and experimental subjects,
the ATS (1985) defined adverse respiratory health effects as
“medically significant physiologic changes generally evidenced by one
or more of the following: (1) interference with the normal activity of
the affected person or persons, (2) episodic respiratory illness, (3)
incapacitating illness, (4) permanent respiratory injury, and/or (5)
progressive respiratory dysfunction.”  During the 1997 review, it was
concluded that there was evidence of causal associations from controlled
human exposure studies for effects in the first of these five
ATS-defined categories, evidence of statistically significant
associations from epidemiological studies for effects in the second and
third categories, and evidence from animal toxicology studies, which
could be extrapolated to humans only with a significant degree of
uncertainty, for the last two categories.

	For ethical reasons, clear causal evidence from controlled human
exposure studies still covers only effects in the first category. 
However, for this review there are results from epidemiological studies,
upon which to base judgments about adversity, for effects in all of the
categories.  Statistically significant and robust associations have been
reported in epidemiology studies falling into the second and third
categories.  These more serious effects include respiratory events
(e.g., triggering asthma attacks) that may require medication (e.g.,
asthma), but not necessarily hospitalization, as well as respiratory
hospital admissions and emergency department visits for respiratory
causes.  Less conclusive, but still positive associations have been
reported for school absences and cardiovascular hospital admissions. 
Human health effects for which associations have been suggested through
evidence from epidemiological and animal toxicology studies, but have
not been conclusively demonstrated still fall primarily into the last
two categories.  In the 1997 review of the O3 standard, evidence for
these more serious effects came from studies of effects in laboratory
animals.  Evidence from animal studies evaluated in the 2006 Criteria
Document strongly suggests that O3 is capable of damaging the distal
airways and proximal alveoli, resulting in lung tissue remodeling
leading to apparently irreversible changes.  Recent advancements of
dosimetry modeling also provide a better basis for extrapolation from
animals to humans.  Information from epidemiological studies provides
supporting, but limited evidence of irreversible respiratory effects in
humans than was available in the prior review.  Moreover, the findings
from single-city and multicity time-series epidemiology studies and
meta-analyses of these epidemiological studies are highly suggestive of
an association between short-term O3 exposure and mortality particularly
in the warm season. 

	While O3 has been associated with effects that are clearly adverse,
application of these guidelines, in particular to the least serious
category of effects related to ambient O3 exposures, involves judgments
about which medical experts on the CASAC panel and public commenters
have expressed diverse views in the past.  To help frame such judgments,
EPA staff have defined specific ranges of functional responses (e.g.,
decrements in FEV1 and airway responsiveness) and symptomatic responses
(e.g., cough, chest pain, wheeze), together with judgments as to the
potential impact on individuals experiencing varying degrees of severity
of these responses, that have been used in previous NAAQS reviews. 
These ranges of pulmonary responses and their associated potential
impacts are summarized in Tables 3-2 and 3-3 of the 2007 Staff Paper.

	For active healthy people, moderate levels of functional responses
(e.g., FEV1 decrements of > 10 percent but < 20 percent, lasting up to
24 hours) and/or moderate symptomatic responses (e.g., frequent
spontaneous cough, marked discomfort on exercise or deep breath, lasting
up to 24 hours) would likely interfere with normal activity for
relatively few responsive individuals.  On the other hand, EPA staff
determined that large functional responses (e.g., FEV1 decrements > 20
percent, lasting longer than 24 hours) and/or severe symptomatic
responses (e.g., persistent uncontrollable cough, severe discomfort on
exercise or deep breath, lasting longer than 24 hours) would likely
interfere with normal activities for many responsive individuals.  EPA
staff determined that these would be considered adverse under ATS
guidelines.  In the context of standard setting, CASAC indicated that a
focus on the mid to upper end of the range of moderate levels of
functional responses (e.g., FEV1 decrements ( 15 percent but < 20
percent) is appropriate for estimating potentially adverse lung function
decrements in active healthy people.  However, for people with lung
disease, even moderate functional (e.g., FEV1 decrements > 10 percent
but < 20 percent, lasting up to 24 hours) or symptomatic responses
(e.g., frequent spontaneous cough, marked discomfort on exercise or with
deep breath, wheeze accompanied by shortness of breath, lasting up to 24
hours) would likely interfere with normal activity for many individuals,
and would likely result in more frequent use of medication.  For people
with lung disease, large functional responses (e.g., FEV1 decrements >
20 percent, lasting longer than 24 hours) and/or severe symptomatic
responses (e.g., persistent uncontrollable cough, severe discomfort on
exercise or deep breath, persistent wheeze accompanied by shortness of
breath, lasting longer than 24 hours) would likely interfere with normal
activity for most individuals and would increase the likelihood that
these individuals would seek medical treatment.  In the context of
standard setting, the CASAC indicated (Henderson, 2006c) that a focus on
the lower end of the range of moderate levels of functional responses
(e.g., FEV1 decrements ( 10 percent) is most appropriate for estimating
potentially adverse lung function decrements in people with lung
disease.

	In judging the extent to which these impacts represent effects that
should be regarded as adverse to the health status of individuals, an
additional factor that has been considered in previous NAAQS reviews is
whether such effects are experienced repeatedly during the course of a
year or only on a single occasion.  While some experts would judge
single occurrences of moderate responses to be a “nuisance,”
especially for healthy individuals, a more general consensus view of the
adversity of such moderate responses emerges as the frequency of
occurrence increases.

	  SEQ CHAPTER \h \r 1 The new guidance builds upon and expands the 1985
definition of adversity in several ways.  There is an increased focus on
quality of life measures as indicators of adversity.  There is also a
more specific consideration of population risk.  Exposure to air
pollution that increases the risk of an adverse effect to the entire
population is adverse, even though it may not increase the risk of any
individual to an unacceptable level.  For example, a population of
asthmatics could have a distribution of lung function such that no
individual has a level associated with significant impairment.  Exposure
to air pollution could shift the distribution to lower levels that still
do not bring any individual to a level that is associated with
clinically relevant effects.  However, this would be considered to be
adverse because individuals within the population would have diminished
reserve function, and therefore would be at increased risk if affected
by another agent.  

	Of the various effects of O3 exposure that have been studied, many
would meet the ATS definition of adversity.  Such effects include, for
example, any detectible level of permanent lung function loss
attributable to air pollution, including both reductions in lung growth
or acceleration of the age-related decline of lung function;
exacerbations of disease in individuals with chronic cardiopulmonary
diseases; reversible loss of lung function in combination with the
presence of symptoms; as well as more serious effects such as those
requiring medical care including hospitalization and, obviously,
mortality.

d.	Size of At-Risk Populations

	Although O3-related health risk estimates may appear to be small, their
significance from an overall public health perspective is determined by
the large numbers of individuals in the population groups potentially
at-risk for O3-related health effects discussed above.  For example, a
population of concern includes people with respiratory disease, which
includes approximately 11 percent of U.S. adults and 13 percent of
children who have been diagnosed with asthma and 6 percent of adults
with chronic obstructive pulmonary disease (chronic bronchitis and/or
emphysema) in 2002 and 2003 (Table 8-4 in the 2006 Criteria Document,
section 8.7.5.2).  More broadly, individuals with preexisting
cardiopulmonary disease may constitute an additional population of
concern, with potentially tens of millions of people included in each
disease category.  In addition, populations based on age group also
comprise substantial segments of the population that may be potentially
at risk for O3-related health impacts. Based on U.S. census data from
2003, about 26 percent of the U.S. population are under 18 years of age
and 12 percent  are 65 years of age or older.  Hence, large proportions
of the U.S. population are included in life stages that are most likely
to have increased susceptibility to the health effects of O3 and or
those with the highest ambient O3 exposures.

	The 2006 Criteria Document (section 8.7.5.2) notes that the health
statistics data illustrate what is known as the “pyramid” of
effects.  At the top of the pyramid, there are approximately 2.5
millions deaths from all causes per year in the U.S. population, with
about 100,000 deaths from chronic lower respiratory diseases.  For
respiratory health diseases, there are nearly 4 million hospital
discharges per year, 14 million emergency department visits, 112 million
ambulatory care visits, and an estimated 700 million restricted activity
days per year due to respiratory conditions from all causes per year. 
Applying small risk estimates for the O3-related contribution to such
health effects with relatively large baseline levels of health outcomes
can result in quite large public health impacts related to ambient O3
exposure.  Thus, even a small percentage reduction in O3 health impacts
on cardiopulmonary diseases would reflect a large number of avoided
cases.  In considering this information together with the
concentration-response relationships that have been observed between
exposure to O3 and various health endpoints, the 2006 Criteria Document
(section 8.7.5.2) concludes that exposure to ambient O3 likely has a
significant impact on public health in the U.S.

B.	Human Exposure and Health Risk Assessments

	To put judgments about health effects that are adverse for individuals
into a broader public health context, EPA has developed and applied
models to estimate human exposures and health risks.  This broader
context includes consideration of the size of particular population
groups at risk for various effects, the likelihood that exposures of
concern will occur for individuals in such groups under varying air
quality scenarios, estimates of the number of people likely to
experience O3-related effects, the variability in estimated exposures
and risks, and the kind and degree of uncertainties inherent in
assessing the exposures and risks involved.  

	As discussed below there are a number of important uncertainties that
affect the exposure and health risk estimates.  It is also important to
note that there have been significant improvements in both the exposure
and health risk model.  CASAC expressed the view that the exposure
analysis represents a state-of-the-art modeling approach and that the
health risk assessment was “well done, balanced and reasonably
communicated (Henderson, 2006c).  While recognizing and considering the
kind and degree of uncertainties in both the exposure and health risk
estimates, the 2007 Staff Paper (pp. 6-20 to 6-21) judged that the
quality of the estimates is such that they are suitable to be used as an
input to the Administrator’s decisions on the O3 primary standard.

	In modeling exposures and health risks associated with just meeting the
current and alternative O3 standards, EPA has simulated air quality to
represent conditions just meeting these standards based on O3 air
quality patterns in several recent years and on how the shape of the O3
air quality distribution have changed over time based on historical
trends in monitored O3 air quality data.  As described in the 2007 Staff
Paper (EPA, 2007b, section 4.5.8) and discussed below, recent O3 air
quality distributions have been statistically adjusted to simulate just
meeting the current and selected alternative standards.  These
simulations do not reflect any consideration of specific control
programs or strategies designed to achieve the reductions in emissions
required to meet the specified standards.  Further, these simulations do
not represent predictions of when, whether, or how areas might meet the
specified standards.  

	As noted in section I.C above, around the time of the release of the
final 2007 Staff Paper in January 2007, EPA discovered a small error in
the exposure model that when corrected resulted in slight increases in
the simulated exposures.  Since the exposure estimates are an input to
the lung function portion of the health risk assessment, this correction
also resulted in slight increases in the lung function risk estimates as
well.  The exposure and risk estimates discussed in this notice reflect
the corrected estimates, and thus are slightly different than the
exposure and risk estimates cited in the January 31, 2007 Staff Paper.

1.	Exposure Analyses

a.	Overview

	As part of the 2008 rulemaking, the EPA conducted exposure analyses
using a simulation model to estimate O3 exposures for the general
population, school age children (ages 5-18), and school age children
with asthma living in 12 U.S. metropolitan areas representing different
regions of the country where the then current 8-hour O3 standard is not
met.  The emphasis on children reflects the finding of the 1997 O3 NAAQS
review that children are an important at-risk group.  The 12 modeled
areas combined represent a significant fraction of the U.S. urban
population, 89 million people, including 18 million school age children
of whom approximately 2.6 million have asthma.  The selection of urban
areas to include in the exposure analysis took into consideration the
location of O3 epidemiological studies, the availability of ambient O3
data, and the desire to represent a range of geographic areas,
population demographics, and O3 climatology.  These selection criteria
are discussed further in chapter 5 of the 2007 Staff Paper (EPA, 2007b).
 The geographic extent of each modeled area consists of the census
tracts in the combined statistical area (CSA) as defined by OMB (OMB,
2005).  

	Exposure estimates were developed using a probabilistic exposure model
that is designed to explicitly model the numerous sources of variability
that affect people’s exposures.  As discussed below, the model
estimates population exposures by simulating human activity patterns,
air conditioning prevalence, air exchange rates, and other factors.  The
modeled exposure estimates were developed for three recent years of
ambient O3 concentrations (2002, 2003, and 2004), as well as for O3
concentrations adjusted to simulate conditions associated with just
meeting the then current NAAQS and various alternative 8-hour standards
based on the three year period 2002-2004.  This exposure assessment is
more fully described and presented in the 2007 Staff Paper and in a
technical support document, Ozone Population Exposure Analysis for
Selected Urban Areas (EPA, 2007c; hereafter Exposure Analysis TSD).  The
scope and methodology for this exposure assessment were developed over
the last few years with considerable input from the CASAC Ozone Panel
and the public.

	The goals of the O3 exposure assessment were: (1) to provide estimates
of the size of at-risk populations exposed to various levels associated
with recent O3 concentrations, and with just meeting the current O3
NAAQS and alternative O3 standards, in specific urban areas; (2) to
provide distributions of exposure estimates over the entire range of
ambient O3 concentrations as an important input to the lung function
risk assessment summarized below in section II.B.2; (3) to develop a
better understanding of the influence of various inputs and assumptions
on the exposure estimates; and (4) to gain insight into the distribution
of exposures and patterns of exposure reductions associated with meeting
alternative O3 standards.  

	The EPA recognizes that there are many sources of variability and
uncertainty inherent in the inputs to this assessment and that there is
uncertainty in the resulting O3 exposure estimates.  With respect to
variability, the exposure modeling approach accounts for variability in
ambient O3 levels, demographic characteristics, physiological
attributes, activity patterns, and factors affecting microenvironmental
(e.g., indoor) concentrations.  In EPA’s judgment, the most important
uncertainties affecting the exposure estimates are related to the
modeling of human activity patterns over an O3 season, the modeling of
variations in ambient concentrations near roadways, and the modeling of
air exchange rates that affect the amount of O3 that penetrates indoors.
 Another important uncertainty that affects the estimation of how many
exposures are associated with moderate or greater exertion is the
characterization of energy expenditure for children engaged in various
activities.  As discussed in more detail in the 2007 Staff Paper (EPA,
2007b, section 4.3.4.7), the uncertainty in energy expenditure values
carries over to the uncertainty of the modeled breathing rates, which
are important since they are used to classify exposures occurring at
moderate or greater exertion which are the relevant exposures since
O3-related effects observed in controlled human exposure studies only
are observed when individuals are engaged in some form of exercise.  
The uncertainties in the exposure model inputs and the estimated
exposures have been assessed using quantitative uncertainty and
sensitivity analyses.  Details are discussed in the 2007 Staff Paper
(section 4.6) and in a technical memorandum describing the exposure
modeling uncertainty analysis (Langstaff, 2007).

b.	Scope and Key Components

	Population exposures to O3 are primarily driven by ambient outdoor
concentrations, which vary by time of day, location, and peoples’
activities.  Outdoor O3 concentration estimates used in the exposure
assessment are provided by measurements and statistical adjustments to
the measured concentrations.  The current exposure analysis allows
comparisons of population exposures to O3 within each urban area,
associated with current O3 levels and with O3 levels just meeting
several potential alternative air quality standards or scenarios.  Human
exposure, regardless of the pollutant, depends on where individuals are
located and what they are doing.  Inhalation exposure models are useful
in realistically estimating personal exposures to O3 based on
activity-specific breathing rates, particularly when recognizing that
large scale population exposure measurement studies have not been
conducted that are representative of the overall population or at risk
subpopulations.

	The model EPA used to simulate O3 population exposure is the Air
Pollutants Exposure Model (APEX), the human inhalation exposure model
within the Total Risk Integrated Methodology (TRIM) framework (EPA,
2006c,d).  APEX is conceptually based on the probabilistic NAAQS
exposure model for O3 (pNEM/O3) used in the last O3 NAAQS review.  Since
that time the model has been restructured, improved, and expanded to
reflect conceptual advances in the science of exposure modeling and
newer input data available for the model.  Key improvements to
algorithms include replacement of the cohort approach with a
probabilistic sampling approach focused on individuals, accounting for
fatigue and oxygen debt after exercise in the calculation of breathing
rates, and a new approach for construction of longitudinal activity
patterns for simulated persons.  Major improvements to data input to the
model include updated air exchange rates, more recent census and
commuting data, and a greatly expanded daily time-activities database.  

	APEX is a probabilistic model designed to explicitly model the numerous
sources of variability that affect people’s exposures.  APEX simulates
the movement of individuals through time and space and estimates their
exposures to O3 in indoor, outdoor, and in-vehicle microenvironments. 
The exposure model takes into account the most significant factors
contributing to total human O3 exposure, including the temporal and
spatial distribution of people and O3 concentrations throughout an urban
area, the variation of O3 levels within each microenvironment, and the
effects of exertion on breathing rate in exposed individuals.  A more
detailed description of APEX and its application is presented in chapter
4 of the 2007 Staff Paper and associated technical documents (EPA,
2006b,c,d).

Several methods have been used to evaluate the APEX model and to
characterize the uncertainty of the model estimates.  These include
conducting model evaluation, sensitivity analyses, and a detailed
uncertainty analysis for one urban area.  These are discussed fully in
the 2007 Staff Paper (section 4.6) and in Langstaff (2007).  The
uncertainty of model structure was judged to be of lesser importance
than the uncertainties of the model inputs and parameters.  Model
structure refers to the algorithms in APEX designed to simulate the
processes that result in people’s exposures, for example, the way that
APEX models exposures to individuals when they are near roads.  The
uncertainties in the model input data (e.g., measurement error, ambient
concentrations, air exchange rates, and activity pattern data) have been
assessed individually, and their impact on the uncertainty in the
modeled exposure estimates was assessed in a unified quantitative
analysis with results expressed in the form of estimated confidence
ranges around the estimated measures of exposure.  This uncertainty
analysis was conducted for one urban area (Boston) using the observed
2002 O3 concentrations and 2002 concentrations adjusted to simulate just
meeting the current standard, with the expectation that the results
would be similar for other cities and years.  One significant source of
uncertainty, due to limitations in the database used to model peoples’
daily activities, was not included in the unified analysis, and was
assessed through separate sensitivity analyses.  This analysis indicates
that the uncertainty of the exposure results is relatively small.  For
example, 95 percent uncertainty intervals were calculated for the APEX
estimates of the percent of children or asthmatic children with
exposures above 0.060, 0.070, or 0.080 ppm under moderate exertion, for
two air quality scenarios (current 2002 and 2002 adjusted to simulate
just meeting the current standard) in Boston (Langstaff, 2007, Tables 26
and 27).  The 95 percent uncertainty intervals for this set of 12
exposure estimates indicate the possibility of underpredictions of the
exposure estimates ranging from 3 to 25 percent of the modeled
estimates, and overpredictions ranging from 4 to 11 percent of the
estimates.  For example, APEX estimates the percent of asthmatic
children with exposures above 0.070 ppm under moderate exertion to be 24
percent, for Boston 2002 O3 concentrations adjusted to simulate just
meeting the current standard.  The 95 percent uncertainty interval for
this estimate is 23 − 30 percent, or -4 to +25 percent of the
estimate.  These uncertainty intervals do not include the uncertainty
engendered by limitations of the activity database, which is in the
range of one to ten percent.

The exposure periods modeled here are the O3 seasons in 2002, 2003, and
2004.  The O3 season in each area includes the period of the year where
elevated O3 levels tend to be observed and for which routine hourly O3
monitoring data are available.  Typically this period spans from March
or April through September or October, or in some areas, spanning the
entire year.  Three years were modeled to reflect the substantial
year-to-year variability that occurs in O3 levels and related
meteorological conditions, and because the standard is specified in
terms of a three-year period.  The year-to-year variability observed in
O3 levels is due to a combination of different weather patterns and the
variation in emissions of O3 precursors.  Nationally, 2002 was a
relatively high year with respect to the 4th highest daily maximum
8-hour O3 levels observed in urban areas across the U.S. (EPA, 2007b,
Figure 2-16), with the mean of the distribution of O3 levels for the
urban monitors being in the upper third among the years 1990 through
2006.  In contrast, on a national basis, 2004 is the lowest year on
record through 2006 for this same air quality statistic, and 8-hour
daily maximum O3 levels observed in most, but not all of the 12 urban
areas included in the exposure and risk analyses were relatively low
compared to other recent years.  The 4th highest daily maximum 8-hour O3
levels observed in 2003 in the 12 urban areas and nationally generally
were between those observed in 2002 and 2004.

Regulatory scenarios examined in the 2008 rulemaking include the then
current 0.08 ppm, average of the 4th daily maximum 8-hour averages over
a three year period standard; standards with the same form but with
alternative levels of 0.080, 0.074, 0.070, and 0.064 ppm; standards
specified as the average of the 3rd highest daily maximum 8-hour
averages over a three year period with alternative levels of 0.084 and
0.074 ppm; and a standard specified as the average of the 5th highest
daily maximum 8-hour averages over a three year period with a level of
0.074 ppm.  The then current standard used a rounding convention that
allows areas to have an average of the 4th daily maximum 8-hour averages
as high as 0.084 ppm and still meet the standard.  All alternative
standards analyzed were intended to reflect improved precision in the
measurement of ambient concentrations (in ppm), where the precision
would extend to three instead of two decimal places.  

	The then current standard and all alternative standards were modeled
using a quadratic rollback approach to adjust the hourly concentrations
observed in 2002-2004 to yield a design value corresponding to the
standard being analyzed.  The quadratic rollback technique reduces
higher concentrations more than lower concentrations near ambient
background levels.  This procedure was considered in a sensitivity
analysis in the 1997 review of the O3 standard and has been shown to be
more realistic than a linear, proportional rollback method, where all of
the ambient concentrations are reduced by the same factor.

c.	Exposure Estimates and Key Observations

	The exposure assessment, which provides estimates of the number of
people exposed to different levels of ambient O3 while at specified
exertion levels, serve two purposes.  First, the entire range of modeled
personal exposures to ambient O3 is an essential input to the portion of
the health risk assessment based on exposure-response functions from
controlled human exposure studies, discussed in the next section. 
Second, estimates of personal exposures to ambient O3 concentrations at
and above specific benchmark levels provide some perspective on the
public health impacts of health effects that cannot currently be
evaluated in quantitative risk assessments that may occur at current air
quality levels, and the extent to which such impacts might be reduced by
meeting the current and alternative standards.  This is especially true
when there are exposure levels at which it is known or can reasonably be
inferred that specific O3-related health effects are occurring.  In this
notice, exposures at and above these benchmark concentrations are
referred to as “exposures of concern.”

	It is important to note that although the analysis of “exposures of
concern” was conducted using three discrete benchmark levels (i.e.,
0.080, 0.070, and 0.060 ppm), the concept is more appropriately viewed
as a continuum with greater confidence and less uncertainty about the
existence of health effects at the upper end and less confidence and
greater uncertainty as one considers increasingly lower O3 exposure
levels.  The EPA recognizes that there is no sharp breakpoint within the
continuum ranging from at and above 0.080 ppm down to 0.060 ppm.  In
considering the concept of exposures of concern, it is important to
balance concerns about the potential for health effects and their
severity with the increasing uncertainty associated with our
understanding of the likelihood of such effects at lower O3 levels.  

	Within the context of this continuum, estimates of exposures of concern
at discrete benchmark levels provide some perspective on the public
health impacts of O3-related health effects that have been demonstrated
in controlled human exposure and toxicological studies but cannot be
evaluated in quantitative risk assessments, such as lung inflammation,
increased airway responsiveness, and changes in host defenses.  They
also help in understanding the extent to which such impacts have the
potential to be reduced by meeting the current and alternative
standards.  In the selection of specific benchmark concentrations for
this analysis, staff first considered the exposure level of 0.080 ppm,
at which there is a substantial amount of controlled human exposure
evidence demonstrating a range of O3-related health effects including
lung inflammation and airway responsiveness in healthy individuals. 
Thus, as in the 1997 review, this level was selected as a benchmark
level for this assessment of exposures of concern.  Evidence newly
available in this review is the basis for identifying additional, lower
benchmark levels of 0.070 and 0.060 ppm for this assessment.

	More specifically, as discussed above in section II.A.2, evidence
available from controlled human exposure and epidemiological studies
indicates that people with asthma have larger and more serious effects
than healthy individuals, including lung function, respiratory symptoms,
increased airway responsiveness, and pulmonary inflammation, which has
been shown to be a more sensitive marker than lung function responses. 
Further, a substantial new body of evidence from epidemiological studies
shows associations with serious respiratory morbidity and
cardiopulmonary mortality effects at O3 levels that extend below 0.080
ppm.  Additional, but very limited new evidence from controlled human
exposure studies shows lung function decrements and respiratory symptoms
in healthy subjects at an O3 exposure level of 0.060 ppm.  The selected
benchmark level of 0.070 ppm reflects the new information that
asthmatics have larger and more serious effects than healthy people and
therefore controlled human exposure studies done with healthy subjects
may underestimate effects in this group, as well as the substantial body
of epidemiological evidence of associations with O3 levels below 0.080
ppm.  The selected benchmark level of 0.060 ppm additionally reflects
the very limited new evidence from controlled human exposure studies
that show lung function decrements and respiratory symptoms in some
healthy subjects at the 0.060 ppm exposure level, recognizing that
asthmatics are likely to have more serious responses and that lung
function is not likely to be as sensitive a marker for O3 effects as is
lung inflammation.

	The estimates of exposures of concern were reported in terms of both
“people exposed” (the number and percent of people who experience a
given level of O3 concentrations, or higher, at least one time during
the O3 season in a given year) and “occurrences of exposure” (the
number of times a given level of pollution is experienced by the
population of interest, expressed in terms of person-days of
occurrences).  Estimating exposures of concern is important because it
provides some indication of the potential public health impacts of a
range of O3-related health outcomes, such as lung inflammation,
increased airway responsiveness, and changes in host defenses.  These
particular health effects have been demonstrated in controlled human
exposure studies of healthy individuals to occur at levels as low as
0.080 ppm O3, but have not been evaluated at lower levels in controlled
human exposure studies.  The EPA did not include these effects in the
quantitative risk assessment due to a lack of adequate information on
the exposure-response relationships.

	The 1997 O3 NAAQS review estimated exposures associated with 1-hour
heavy exertion, 1-hour moderate exertion, and 8-hour moderate exertion
for children, outdoor workers, and the general population.  The EPA’s
analysis in the 1997 Staff Paper showed that exposure estimates based on
the 8-hour moderate exertion scenario for children yielded the largest
number of children experiencing exposures at or above exposures of
concern.  Consequently, EPA chose to focus on the 8-hour moderate and
greater exertion exposures in all and asthmatic school age children in
the current exposure assessment. While outdoor workers and other adults
who engage in moderate or greater exertion for prolonged durations while
outdoors during the day in areas experiencing elevated O3 concentrations
also are at risk for experiencing exposures associated with O3-related
health effects, EPA did not focus on quantitative estimates for these
populations due to the lack of information about the number of
individuals who regularly work or exercise outdoors.  Thus, the exposure
estimates presented here and in the 2007 Staff Paper are most useful for
making relative comparisons across alternative air quality scenarios and
do not represent the total exposures in all children or other groups
within the general population associated with the air quality scenarios.

	Population exposures to O3 were estimated in 12 urban areas for 2002,
2003, and 2004 air quality, and also using O3 concentrations adjusted to
just meet the then current and several alternative standards.  The
estimates of 8-hour exposures of concern at and above benchmark levels
of 0.080, 0.070, and 0.060 ppm aggregated across all 12 areas are shown
in Table 1 for air quality scenarios just meeting the current and four
alternative 8-hour average standards.  Table 1 provides estimates of the
number and percent of school age children and asthmatic school age
children exposed, with daily 8-hour maximum exposures at or above each
O3 benchmark level of exposures of concern, while at intermittent
moderate or greater exertion and based on O3 concentrations observed in
2002 and 2004.  Table 1 summarizes estimates for 2002 and 2004 because
these years reflect years that bracket relatively higher and lower O3
levels, with year 2003 generally containing O3 levels in between when
considering the 12 urban areas modeled.  This table also reports the
percent change in the number of persons exposed when a given alternative
standard is compared with the then current standard.

	Key observations important in comparing exposure estimates associated
with just meeting the current NAAQS and alternative standards under
consideration include:

	(1)  As shown in Table 6-1 of the 2007 Staff Paper, the patterns of
exposure in terms of percentages of the population exceeding a given
exposure level are very similar for the general population and for
asthmatic and all school age (5-18) children, although children are
about twice as likely to be exposed, based on the percent of the
population exposed, at any given level.

	(2)  As shown in Table 1 below, the number and percentage of asthmatic
and all school-age children aggregated across the 12 urban areas
estimated to experience one or more exposures of concern decline from
simulations of just meeting the then current 0.084 ppm standard to
simulations of alternative 8-hour standards by varying amounts depending
on the benchmark level, the population subgroup considered, and the year
chosen.  For example, the estimated percentage of school age children
experiencing one or more exposures ≥ 0.070 ppm, while engaged in
moderate or greater exertion, during an O3 season is about 18 percent of
this population when the 0.084 ppm standard is met using the 2002
simulation; this is reduced to about 12, 4, 1, and 0.2 percent of
children upon meeting alternative standards of 0.080, 0.074, 0.070, and
0.064 ppm, respectively (all specified in terms of the 4th highest daily
maximum 8-hour average), using the 2002 simulation. 

Table 1.  Number and Percent of All and Asthmatic School Age Children
in 12 Urban Areas Estimated to Experience 8-Hour Ozone Exposures Above
0.080, 0.070, and 0.060 ppm While at Moderate or Greater Exertion, One
or More Times Per Season, and the Number of Occurrences Associated with
Just Meeting Alternative 8-Hour Standards Based on Adjusting 2002 and
2004 Air Quality Data1,2

Benchmark Levels of Exposures

of Concern

(ppm)	8-Hour Air Quality Standards3

(ppm)	All Children, ages 5-18 

Aggregate for 12 urban areas	Asthmatic Children, ages 5-18

Aggregate for 12 urban areas

Number of Children Exposed (% of all) 

[% reduction from 0.084 ppm standard]	Number of Children Exposed (% of
group)

[% reduction from 0.084 ppm standard]

2002	2004	2002	2004

0.080	0.084	700,000 (4%)	30,000 (0%)	110,000 (4%)	0 (0%)

	0.080	290,000 (2%)

[70%]	10,000 (0%)

[67%]	50,000 (2%)

[54%]	0 (0%)

	0.074	60,000 (0%)

[91%]	0 (0%)

[100%]	10,000 (0%)

[91%]	0 (0%)

	0.070	10,000 (0%)

[98%]	0 (0%)

[100%]	0 (0%)

[100%]	0 (0%)

	0.064	0 (0%)

[100%]	0 (0%)

[100%]	0 (0%)

[100%]	0 (0%)

0.070	0.084	3,340,000 (18%)	260,000 (1%)	520,000 (20%)	40,000 (1%)

	0.080	2,160,000 (12%)

[35%]	100,000 (1%)

[62%]	330,000 (13%)

[36%]	10,000 (0%)

[75%]

	0.074	770,000 (4%)

[77%]	20,000 (0%)

[92%]	120,000 (5%)

[77% ]	0 (0%)

[100%]

	0.070	270,000 (1%)

[92%]	0 (0%)

[100%]	50,000 (2%)

[90%]	0 (0%)

[100%]

	0.064	30,000 (0.2%)

[99%]	0 (0%)

[100%]	10,000 (0.2%)

[98% ]	0 (0%)

[100%]

0.060	0.084	7,970,000 (44%)	1,800,000 (10%)	1,210,000 (47%)	270,000
(11%)

	0.080	6,730,000 (37%

[16%]	1,050,000 (6%)

[42%]	1,020,000 (40%)

[16%]	150,000 (6%)

[44%]

	0.074	4,550,000 (25%)

[43%]	350,000 (2%)

[80%]	700,000 (27%)

[42%]	50,000 (2%)

[81%]

	0.070	3,000,000 (16%)

[62%]	110,000 (1%)

[94%]	460,000 (18%)

[62%]	10,000 (1%)

[96%]

	0.064	950,000 (5%)

[88%]	10,000 (0%)

[99%]	150,000 (6%)

[88%]	0 (0%)

[100%]

1 Moderate or greater exertion is defined as having an 8-hour average
equivalent ventilation rate > 13 l-min/m2.

2 Estimates are the aggregate results based on 12 combined statistical
areas (Atlanta, Boston, Chicago, Cleveland, Detroit, Houston, Los
Angeles, New York, Philadelphia, Sacramento, St. Louis, and Washington,
D.C.).  Estimates are for the ozone season which is all year in Houston,
Los Angeles and Sacramento and March or April to September or October
for the remaining urban areas.

3 All standards summarized here have the same form as the 8-hour
standard established in 1997 which is specified as the 3-year average of
the annual 4th highest daily maximum 8-hour average concentrations must
be at or below the concentration level specified.  As described in the
2007 Staff Paper (EPA, 2007b, section 4.5.8), recent O3 air quality
distributions have been statistically adjusted to simulate just meeting
the 0.084 ppm standard and selected alternative standards.  These
simulations do not represent predictions of when, whether, or how areas
might meet the specified standards.

	(3)  Substantial year-to-year variability in exposure estimates is
observed over the three-year modeling period.  For example, the
estimated number of school age children experiencing one or more
exposures ( 0.070 ppm during an O3 season when a 0.084 ppm standard is
met in the 12 urban areas included in the analysis is 3.3, 1.0, or 0.3
million for the 2002, 2003, and 2004 simulations, respectively.

	(4)  There is substantial variability observed across the 12 urban
areas in the percent of the population subgroups estimated to experience
exposures of concern.  For example, when 2002 O3 concentrations are
simulated to just meet a 0.084 ppm standard, the aggregate 12 urban area
estimate is 18 percent of all school age children are estimated to
experience O3 exposures ( 0.070 ppm (Table 1 below), while the range of
exposure estimates in the 12 urban areas considered separately for all
children range from 1 to 38 percent (EPA, 2007b, p. 4-48, Exhibit 2). 
There was also variability in exposure estimates among the modeled areas
when using the 2004 air quality simulation for the same scenario;
however it was reduced and ranged from 0 to 7 percent in the 12 urban
areas (EPA, 2007b, p. 4-60, Exhibit 8).

	(5) Of particular note, as discussed above in section II.A of this
notice, high inter-individual variability in responsiveness means that
only a subset of individuals in these groups who are exposed at and
above a given benchmark level would actually be expected to experience
such adverse health effects.

 	(6)  In considering these observations, it is important to take into
account the variability, uncertainties, and limitations associated with
this assessment, including the degree of uncertainty associated with a
number of model inputs and uncertainty in the model itself, as discussed
above.

2.	Quantitative Health Risk Assessment

This section discusses the approach used to develop quantitative health
risk estimates associated with exposures to O3 building upon a more
limited risk assessment that was conducted during the last review.  As
part of the 1997 review, EPA conducted a health risk assessment that
produced risk estimates for the number and percent of children and
outdoor workers experiencing lung function and respiratory symptoms
associated with O3 exposures for 9 urban areas.  The risk assessment for
the 1997 review also included risk estimates for excess
respiratory-related hospital admissions related to O3 concentrations for
New York City.  In the last review, the risk estimates played a
significant role in both the staff recommendations and in the proposed
and final decisions to revise the O3 standards.  The health risk
assessment conducted for the current review builds upon the methodology
and lessons learned from the prior review.  

Overview

The updated health risk assessment conducted as part of the 2008
rulemaking includes estimates of (1) risks of lung function decrements
in all and asthmatic school age children, respiratory symptoms in
asthmatic children, respiratory-related hospital admissions, and
non-accidental and cardiorespiratory-related mortality associated with
recent ambient O3 levels; (2) risk reductions and remaining risks
associated with just meeting the then current 0.084 ppm 8-hour O3 NAAQS;
and (3) risk reductions and remaining risks associated with just meeting
various alternative 8-hour O3 NAAQS in a number of example urban areas. 
This risk assessment is more fully described and presented in chapter 5
of the 2007 Staff Paper and in a technical support document (TSD), Ozone
Health Risk Assessment for Selected Urban Areas (Abt Associates, 2007a,
hereafter referred to as “Risk Assessment TSD”).  The scope and
methodology for this risk assessment were developed over the last few
years with considerable input from the CASAC O3 Panel and the public. 
The information contained in these documents included specific criteria
for the selection of health endpoints, studies, and locations to include
in the assessment.  In a peer review letter sent by CASAC to the
Administrator documenting its advice in October 2006 (Henderson, 2006c),
the CASAC O3 Panel concluded that the risk assessment was “well done,
balanced, and reasonably communicated” and that the selection of
health endpoints for inclusion in the quantitative risk assessment was
appropriate.  

	The goals of the risk assessment are: (1) to provide estimates of the
potential magnitude of several morbidity effects and mortality
associated with current O3 levels, and with meeting the then current
0.084 ppm standard and alternative 8-hour O3 standards in specific urban
areas; (2) to develop a better understanding of the influence of various
inputs and assumptions on the risk estimates; and (3) to gain insights
into the distribution of risks and patterns of risk reductions
associated with meeting alternative O3 standards.  The health risk
assessment is intended to be dependent on and reflect the overall weight
and nature of the health effects evidence discussed above in section
II.A and in more detail in the 2006 Criteria Document and 2007 Staff
Paper.  While not independent of the overall evaluation of the health
effects evidence, the quantitative health risk assessment provides
additional insights regarding the relative public health implications
associated with just meeting a 0.084 ppm standard and several
alternative 8-hour standards.

	The risk assessment covers a variety of health effects for which there
is adequate information to develop quantitative risk estimates. 
However, as noted by CASAC (Henderson, 2007) and in the 2007 Staff
Paper, there are a number of health endpoints (e.g., increased lung
inflammation, increased airway responsiveness, impaired host defenses,
increased medication usage for asthmatics, increased emergency
department visits for respiratory causes, and increased school absences)
for which there currently is insufficient information to develop
quantitative risk estimates, but which are important to consider in
assessing the overall public health impacts associated with exposures to
O3.  These additional health endpoints are discussed above in section
II.A.2 and are also taken into account in considering the level of
exposures of concern in populations particularly at risk, discussed
above in this notice.

	There are two parts to the health risk assessment:  one based on
combining information from controlled human exposure studies with
modeled population exposure and the other based on combining information
from community epidemiological studies with either monitored or adjusted
ambient concentrations levels.  Both parts of the risk assessment were
implemented within a new probabilistic version of TRIM.Risk, the
component of EPA’s Total Risk Integrated Methodology (TRIM) model
framework that estimates human health risks.

	The EPA recognizes that there are many sources of uncertainty and
variability in the inputs to this assessment and that there is
significant variability and uncertainty in the resulting O3 risk
estimates.  As discussed in chapters 2, 5, and 6 of the 2007 Staff
Paper, there is significant year-to-year and city-to-city variability
related to the air quality data that affects both the controlled human
exposure studies-based and epidemiological studies-based parts of the
risk assessment.  There are also uncertainties associated with the air
quality adjustment procedure used to simulate just meeting various
alternative standards.  In the prior review, different statistical
approaches using alternative functional forms (i.e., quadratic,
proportional, Weibull) were used to reflect how O3 air quality
concentrations have historically changed.  Based on sensitivity analyses
conducted in the prior review, the choice of alternative air quality
adjustment procedures had only a modest impact on the risk estimates
(EPA, 2007b, p. 6-20).  With respect to uncertainties about estimated
background concentrations, as discussed below and in the 2007 Staff
Paper (section 5.4.3), alternative assumptions about background levels
have a variable impact depending on the location, standard, and health
endpoint analyzed.  

	With respect to the lung function part of the health risk assessment,
key uncertainties include uncertainties in the exposure estimates,
discussed above, and uncertainties associated with the shape of the
exposure-response relationship, especially at levels below 0.08 ppm,
8-hour average, where only very limited data are available down to 0.04
ppm and there is an absence of data below 0.04 ppm (EPA, 2007b, pp.6-20
to 6-21).  Concerning the part of the risk assessment based on effects
reported in epidemiological studies, important uncertainties include
uncertainties (1) surrounding estimates of the O3 coefficients for
concentration-response relationships used in the assessment, (2)
involving the shape of the concentration-response relationship and
whether or not a population threshold or non-linear relationship exists
within the range of concentrations examined in the studies, (3) related
to the extent to which concentration-response relationships derived from
studies in a given location and time when O3 levels were higher or
behavior and /or housing conditions were different provide accurate
representations of the relationships for the same locations with lower
air quality distributions and/or different behavior and/or housing
conditions, and (4) concerning the possible role of co-pollutants which
also may have varied between the time of the studies and the current
assessment period.  An important additional uncertainty for the
mortality risk estimates is the extent to which the associations
reported between O3 and non-accidental and cardiorespiratory mortality
actually reflect causal relationships.

	As discussed below, some of these uncertainties have been addressed
quantitatively in the form of estimated confidence ranges around central
risk estimates; others are addressed through separate sensitivity
analyses (e.g., the influence of alternative estimates for
policy-relevant background levels) or are characterized qualitatively. 
For both parts of the health risk assessment, statistical uncertainty
due to sampling error has been characterized and is expressed in terms
of 95 percent credible intervals.  The EPA recognizes that these
credible intervals do not reflect all of the uncertainties noted above. 

b.	Scope and Key Components

	The health risk assessment is based on the information evaluated in the
2006 Criteria Document.  The risk assessment includes several categories
of health effects and estimates risks associated with just meeting a
0.084 ppm standard and alternative 8-hour O3 NAAQS and with several
individual recent years of air quality (i.e., 2002, 2003, and 2004). 
The risk assessment considers the same alternative air quality scenarios
that were examined in the human exposure analyses described above.  Risk
estimates were developed for up to 12 urban areas selected to illustrate
the public health impacts associated with these air quality scenarios. 
As discussed above in section II.B.1, the selection of urban areas was
largely determined by identifying areas in the U.S. which represented a
range of geographic areas, population demographics, and climatology;
with an emphasis on areas that did not meet the then current 0.084 ppm
8-hour O3 NAAQS and which included the largest areas with O3
nonattainment problems.  The selection criteria also included whether or
not there were acceptable epidemiological studies available that
reported concentration-response relationships for the health endpoints
selected for inclusion in the assessment.

	The short-term exposure related health endpoints selected for inclusion
in the quantitative risk assessment include those for which the 2006
Criteria Document or the 2007 Staff Paper concluded that the evidence as
a whole supports the general conclusion that O3, acting alone and/or in
combination with other components in the ambient air pollution mix, is
either clearly causal or is judged to be likely causal.  Some health
effects met this criterion of likely causality, but were not included in
the risk assessment for other reasons, such as insufficient
exposure-response data or lack of baseline incidence data.

	As discussed in the section above describing the exposure analysis, in
order to estimate the health risks associated with just meeting various
alternative 8-hour O3 NAAQS, it is necessary to estimate the
distribution of hourly O3 concentrations that would occur under any
given standard.  Since compliance is based on a 3-year average, the
amount of control has been applied to each year of data (i.e., 2002 to
2004) to estimate risks for a single O3 season or single warm O3 season,
depending on the health effect, based on a simulation that adjusted each
of these individual years so that the three year period would just meet
the specified standard.  

	Consistent with the risk assessment approach used in the last review,
the risk estimates developed for both recent air quality levels and just
meeting the then current 0.084 ppm standard and selected alternative
8-hour standards represent risks associated with O3 levels attributable
to anthropogenic sources and activities (i.e., risk associated with
concentrations above “policy-relevant background”).  Policy-relevant
background O3 concentrations used in the O3 risk assessment were defined
in chapter 2 of the 2007 Staff Paper (pp. 2-48 – 2-55) as the O3
concentrations that would be observed in the U.S. in the absence of
anthropogenic emissions of precursors (e.g., VOC, NOx, and CO) in the
U.S., Canada, and Mexico.  The results of a global tropospheric O3 model
(GEOS-CHEM) have been used to estimate monthly background daily diurnal
profiles for each of the 12 urban areas for each month of the O3 season
using meteorology for the year 2001.  Based on the results of the
GEOS-CHEM model, the Criteria Document indicates that background O3
concentrations are generally predicted to be in the range of 0.015 to
0.035 ppm in the afternoon, and they are generally lower under
conditions conducive to man-made O3 episodes.  

	This approach of estimating risks in excess of background is judged to
be more relevant to policy decisions regarding ambient air quality
standards than risk estimates that include effects potentially
attributable to uncontrollable background O3 concentrations. 
Sensitivity analyses examining the impact of alternative estimates for
background on lung function and mortality risk estimates have been
developed and are included in the 2007 Staff Paper and Risk Assessment
TSD and key observations are discussed below.  Further, CASAC noted the
difficulties and complexities associated with available approaches to
estimating policy-relevant background concentrations (Henderson, 2007). 

In the first part of the risk assessment, lung function decrement, as
measured by FEV1, is the only health response that is based on data from
controlled human exposure studies.  As discussed above, there is clear
evidence of a causal relationship between lung function decrements and
O3 exposures for school age children engaged in moderate exertion based
on numerous controlled human exposure and summer camp field studies
conducted by various investigators.  Risk estimates have been developed
for O3-related lung function decrements (measured as changes in FEV1)
for all school age children (ages 5 to 18) and a subset of this group,
asthmatic school age children (ages 5 to 18), whose average exertion
over an 8-hour period was moderate or greater.  The exposure period and
exertion level were chosen to generally match the exposure period and
exertion level used in the controlled human exposure studies that were
the basis for the exposure-response relationships.  A combined data set
including individual level data from the Folinsbee et al. (1988),
Horstman et al. (1990), and McDonnell et al. (1991) studies, used in the
previous risk assessment, and more recent data from Adams (2002, 2003a,
2006) have been used to estimate probabilistic exposure-response
relationships for 8-hour exposures under different definitions of lung
function response (i.e., ≥10, 15, and 20 percent decrements in FEV1). 
As discussed in the 2007 Staff Paper (p.5-27), while these specific
controlled human exposure studies only included healthy adults aged
18-35, findings from other controlled human exposure studies and summer
camp field studies involving school age children in at least six
different locations in the northeastern United States, Canada, and
Southern California indicated changes in lung function in healthy
children similar to those observed in healthy adults exposed to O3 under
controlled chamber conditions.  

	Consistent with advice from CASAC (Henderson, 2006c), EPA has
considered both linear and logistic functional forms in estimating the
probabilistic exposure-response relationships for lung function
responses.  A Bayesian Markov Chain Monte Carlo approach, described in
more detail in the Risk Assessment TSD, has been used that incorporates
both model uncertainty and uncertainty due to sample size in the
combined data set that served as the basis for the assessment.  The EPA
has chosen a model reflecting a 90 percent weighting on a logistic form
and a 10 percent weighting on a linear form as the base case for the
risk assessment.  The basis for this choice is that the logistic form
provides a very good fit to the combined data set, but a linear model
cannot be entirely ruled out since there are only very limited data
(i.e., 30 subjects) at the two lowest exposure levels (i.e., 0.040 and
0.060 ppm).  The EPA has conducted a sensitivity analysis which examines
the impact on the lung function risk estimates of two alternative
choices, an 80 percent logistic/20 percent linear split and a 50 percent
logistic/50 percent linear split.

	As noted above, risk estimates have been developed for three measures
of lung function response (i.e., ≥10, 15, and 20 percent decrements in
FEV1).  However, the 2007 Staff Paper and risk estimates summarized
below focus on FEV1 decrements ≥15 percent for all school age children
and ≥10 percent for asthmatic school age children, consistent with the
advice from CASAC (Henderson, 2006c) that these levels of response
represent indicators of adverse health effects in these populations. 
The Risk Assessment TSD and 2007 Staff Paper present the broader range
of risk estimates including all three measures of lung function
response. 

	Developing risk estimates for lung function decrements involved
combining probabilistic exposure-response relationships based on the
combined data set from several controlled human exposure studies with
population exposure distributions for all and asthmatic school age
children associated with recent air quality and air quality simulated to
just meet the then current 0.084 ppm standard and alternative 8-hour O3
NAAQS based on the results from the exposure analysis described in the
previous section.  The risk estimates have been developed for 12 large
urban areas for the O3 season.  These 12 urban areas include
approximately 18.3 million school age children, of which 2.6 million are
asthmatic school age children.

	In addition to uncertainties arising from sample size considerations,
which are quantitatively characterized and presented as 95 percentile
credible intervals, there are additional uncertainties and caveats
associated with the lung function risk estimates.  These include
uncertainties about the shape of the exposure-response relationship,
particularly at levels below 0.080 ppm, and about policy-relevant
background levels, for which sensitivity analyses have been conducted. 
Additional important caveats and uncertainties concerning the lung
function portion of the health risk assessment include:  (1) the
uncertainties and limitations associated with the exposure estimates
discussed above and (2) the inability to account for some factors which
are known to affect the exposure-response relationships (e.g., assigning
healthy and asthmatic children the same responses as observed in 
healthy adult subjects and not adjusting response rates to reflect the
increase and attenuation of responses that have been observed in studies
of lung function responses upon repeated exposures).  A more complete
discussion of assumptions and uncertainties is contained in chapter 5 of
the 2007 Staff Paper and in the Risk Assessment TSD.	

	The second part of the risk assessment is based on health effects
observed in epidemiological studies.  Based on a review of the evidence
evaluated in the 2006 Criteria Document and 2007 Staff Paper, as well as
the criteria discussed in chapter 5 of the 2007 Staff Paper, the
following categories of health endpoints associated with short-term
exposures to ambient O3 concentrations were included in the risk
assessment:  respiratory symptoms in moderate to severe asthmatic
children, hospital admissions for respiratory causes, and non-accidental
and cardiorespiratory mortality.  As discussed above, there is strong
evidence of a causal relationship for the respiratory morbidity
endpoints included in the risk assessment.  With respect to
nonaccidental and cardiorespiratory mortality, the 2006 Criteria
Document concludes that there is strong evidence which is highly
suggestive of a causal relationship between nonaccidental and
cardiorespiratory-related mortality and O3 exposures during the warm O3
season.  As discussed in the 2007 Staff Paper (chapter 5), EPA also
recognizes that for some of the effects observed in epidemiological
studies, such as increased respiratory-related hospital admissions and
nonaccidental and cardiorespiratory mortality, O3 may be serving as an
indicator for reactive oxidant species in the overall photochemical
oxidant mix and that these other constituents may be responsible in
whole or part for the observed effects.

	Risk estimates for each health endpoint category were only developed
for areas that were the same or close to the location where at least one
concentration-response function for the health endpoint had been
estimated.  Thus, for respiratory symptoms in moderate to severe
asthmatic children only the Boston urban area was included and four
urban areas were included for respiratory-related hospital admissions. 
Nonaccidental mortality risk estimates were developed for 12 urban areas
and 8 urban areas were included for cardiorespiratory mortality.  

	The concentration-response relationships used in the assessment are
based on findings from human epidemiological studies that have relied on
fixed-site ambient monitors as a surrogate for actual ambient O3
exposures.  In order to estimate the incidence of a particular health
effect associated with recent air quality in a specific county or set of
counties attributable to ambient O3 exposures in excess of background,
as well as the change in incidence corresponding to a given change in O3
levels resulting from just meeting various 8-hour O3 standards, three
elements are required for this part of the risk assessment.  These
elements are:  (1) air quality information (including recent air quality
data for O3 from ambient monitors for the selected location, estimates
of background O3 concentrations appropriate for that location, and a
method for adjusting the recent data to reflect patterns of air quality
estimated to occur when the area just meets a given O3 standard); (2)
relative risk-based concentration-response functions that provide an
estimate of the relationship between the health endpoints of interest
and ambient O3 concentration; and (3) annual or seasonal baseline health
effects incidence rates and population data, which are needed to provide
an estimate of the seasonal baseline incidence of health effects in an
area before any changes in O3 air quality.

	A key component in the portion of the risk assessment based on
epidemiological studies is the set of concentration-response functions
which provide estimates of the relationships between each health
endpoint of interest and changes in ambient O3 concentrations.  Studies
often report more than one estimated concentration-response function for
the same location and health endpoint.  Sometimes models include
different sets of co-pollutants and/or different lag periods between the
ambient concentrations and reported health responses.  For some health
endpoints, there are studies that estimated multicity and single-city O3
concentration-response functions.  While the Risk Assessment TSD and
chapter 5 of the 2007 Staff Paper present a more comprehensive set of
risk estimates, EPA has focused on estimates based on multicity studies
where available.  As discussed in chapter 5 of the 2007 Staff Paper, the
advantages of relying more heavily on concentration-response functions
based on multicity studies include: (1) more precise effect estimates
due to larger data sets, reducing the uncertainty around the estimated
coefficient; (2) greater consistency in data handling and model
specification that can eliminate city-to-city variation due to study
design; and (3) less likelihood of publication bias or exclusion of
reporting of negative or nonsignificant findings.  Where studies
reported different effect estimates for varying lag periods, consistent
with the 2006 Criteria Document, single day lag periods of 0 to 1 days
were used for associations with respiratory hospital admissions and
mortality.  For mortality associated with exposure to O3 which may
result over a several day period after exposure, distributed lag models,
which take into account the contribution to mortality effects over
several days, were used where available

	One of the most important elements affecting uncertainties in the
epidemiological-based portion of the risk assessment is the
concentration-response relationships used in the assessment.  The
uncertainty resulting from the statistical uncertainty associated with
the estimate of the O3 coefficient in the concentration-response
function was characterized either by confidence intervals or by Bayesian
credible intervals around the corresponding point estimates of risk. 
Confidence and credible intervals express the range within which the
true risk is likely to fall if the only uncertainty surrounding the O3
coefficient involved sampling error.  Other uncertainties, such as
differences in study location, time period (i.e., the years in which the
study was conducted), and model uncertainties are not represented by the
confidence or credible intervals presented, but were addressed by
presenting estimates for different urban areas, by including risk
estimates based on studies using different time periods and models,
where available, and/or are discussed throughout section 5.3 of the 2007
Staff Paper.  Because O3 effects observed in the epidemiological studies
have been more clearly and consistently shown for warm season analyses,
all analyses for this portion of the risk assessment were carried out
for the same time period, April through September.  

	The 2006 Criteria Document (p. 8-44) finds that no definitive
conclusion can be reached with regard to the existence of population
thresholds in epidemiological studies.  The EPA recognizes, however, the
possibility that thresholds for individuals may exist for reported
associations at fairly low levels within the range of air quality
observed in the studies, but not be detectable as population thresholds
in epidemiological analyses.  Based on the 2006 Criteria Document’s
conclusions, EPA judged and CASAC concurred, that there is insufficient
evidence to support use of potential population threshold levels in the
quantitative risk assessment.  However, EPA recognizes that there is
increasing uncertainty about the concentration-response relationship at
lower concentrations which is not captured by the characterization of
the statistical uncertainty due to sampling error.  Therefore, the risk
estimates for respiratory symptoms in moderate to severe asthmatic
children, respiratory-related hospital admissions, and premature
mortality associated with exposure to O3 must be considered in light of
uncertainties about whether or not these O3-related effects occur in
these populations at very low O3 concentrations.

	With respect to variability within this portion of the risk assessment,
there is variability among concentration-response functions describing
the relation between O3 and both respiratory-related hospital admissions
and nonaccidental and cardiorespiratory mortality across urban areas. 
This variability is likely due to differences in population (e.g., age
distribution), population activities that affect exposure to O3 (e.g.,
use of air conditioning), levels and composition of co-pollutants,
baseline incidence rates, and/or other factors that vary across urban
areas.  The risk assessment incorporates some of the variability in key
inputs to the analysis by using location-specific inputs (e.g.,
location-specific concentration-response functions, baseline incidence
rates, and air quality data).  Although spatial variability in these key
inputs across all U.S. locations has not been fully characterized,
variability across the selected locations is imbedded in the analysis by
using, to the extent possible, inputs specific to each urban area.

c.	Risk Estimates and Key Observations

	The 2007 Staff Paper (chapter 5) and Risk Assessment TSD present risk
estimates associated with just meeting the then current 0.084 ppm
standard and several alternative 8-hour standards, as well as three
recent years of air quality as represented by 2002, 2003, and 2004
monitoring data.  As discussed in the exposure analysis section above,
there is considerable city-to-city and year-to-year variability in the
O3 levels during this period, which results in significant variability
in both portions of the health risk assessment.  

	In the 1997 risk assessment, risks for lung function decrements
associated with 1-hour heavy exertion, 1-hour moderate exertion, and
8-hour moderate exertion exposures were estimated.  Since the 8-hour
moderate exertion exposure scenario for children clearly resulted in the
greatest health risks in terms of lung function decrements, EPA chose to
include only the 8-hour moderate exertion exposures in the risk
assessment for this health endpoint.  Thus, the risk estimates presented
here and in the 2007 Staff Paper are most useful for making relative
comparisons across alternative air quality scenarios and do not
represent the total risks for lung function decrements in children or
other groups within the general population associated with any of the
air quality scenarios.  Thus, some outdoor workers and adults engaged in
moderate exertion over multi-hour periods (e.g., 6-8 hour exposures)
also would be expected to experience similar lung function decrements. 
However, the percentage of each of these other subpopulations expected
to experience these effects is expected to be smaller than all school
age children who tend to spend more hours outdoors while active based on
the exposure analyses conducted during the prior review.  

	Table 2 presents a summary of the risk estimates for lung function
decrements for the 0.084 ppm standard set in 1997 and several
alternative 8-hour standard levels with the same form.  The estimates
are for the aggregate number 

Table 2.  Number and Percent of All and Asthmatic School Age Children
in Several Urban Areas Estimated to Experience Moderate or Greater Lung
Function Responses One or More Times Per Season Associated with 8-Hour
Ozone Exposures  Associated with Just Meeting Alternative 8-Hour
Standards Based on Adjusting 2002 and 2004 Air Quality Data1,2

8-Hour Air Quality Standards3	All Children, ages 5-18

FEV1  > 15 percent 

Aggregate for 12 urban areas

Number of Children Affected (% of all)

[% reduction from 0.084 ppm standard]	Asthmatic Children, ages 5-18

FEV1  > 10 percent

Aggregate for 5 urban areas 

Number of Children Affected (% of group)

[% reduction from 0.084 ppm standard]

	2002	2004	2002	2004]

0.084 ppm

(Standard set in 1997)	610,000 (3.3%)

	230,000 (1.2%)	130,000 (7.8%)

	70,000 (4.2%)

0.080 ppm	490,000 (2.7%)

[20% reduction]	180,000 (1.0%)

[22% reduction]	NA4	NA

0.074 ppm	340,000 (1.9%)

[44% reduction]	130,000 (0.7%)

[43% reduction]	90,000 (5.0%)

[31 % reduction]	40,000 (2.7%)

[43% reduction]

0.070 ppm	260,000 (1.5%)

[57% reduction]	100,000 (0.5%)

[57% reduction]	NA	NA

0.064 ppm	180,000 (1.0%)

[70% reduction]	70,000 (0.4%)

[70% reduction]	50,000 (3.0%)

[62% reduction]	20,000 (1.5%)

[71% reduction]

1Associated with exposures while engaged in moderate or greater
exertion, which is defined as having an 8-hour average equivalent
ventilation rate > 13 l-min/m2.

2Estimates are the aggregate central tendency results based on either 12
urban areas (Atlanta, Boston, Chicago, Cleveland, Detroit, Houston, Los
Angeles, New York, Philadelphia, Sacramento, St. Louis, and Washington,
D.C.) or 5 urban areas (Atlanta, Chicago, Houston, Los Angeles, New
York).  Estimates are for the O3 season which is all year in Houston,
Los Angeles and Sacramento and March or April to September or October
for the remaining urban areas.

3All standards summarized here have the same form as the 8-hour standard
set in 1997, which is specified as the 3-year average of the annual 4th
highest daily maximum 8-hour average concentrations.  As described in
the 2007 Staff Paper (section 4.5.8), recent O3 air quality
distributions have been statistically adjusted to simulate just meeting
the 0.084 ppm standard set in 1997 and selected alternative standards. 
These simulations do not represent predictions of when, whether, or how
areas might meet the specified standards

4NA (not available) indicates that EPA did not develop risk estimates
for these scenarios for the asthmatic school age children population.

and percent of all school age children across 12 urban areas and the
aggregate number and percent of asthmatic school age children across 5
urban areas who are estimated to have at least 1 moderate or greater
lung function response (defined as FEV1 > 15 percent in all children and
> 10 percent in asthmatic children) associated with 8-hour exposures to
O3 while engaged in moderate or greater exertion on average over the
8-hour period.  The lung function risk estimates summarized in Table 2
illustrate the year-to-year variability in both remaining risk
associated with a relatively high year (i.e., based on adjusting 2002 O3
air quality data) and relatively low year (based on adjusting 2004 O3
air quality data) as well as the year-to-year variability in the risk
reduction estimated to occur associated with various alternative
standards relative to just meeting the then current 0.084 ppm standard. 
For example, it is estimated that about 610,000 school age children (3.2
percent of school age children) would experience 1 or more moderate lung
function decrements for the 12 urban areas associated with O3 levels
just meeting a 0.084 ppm standard based on 2002 air quality data
compared to 230,000 (1.2 percent of children) associated with just
meeting a 0.084 ppm standard based on 2004 air quality data.

	As discussed in the 2007 Staff Paper, a child may experience multiple
occurrences of a lung function response during the O3 season.  For
example, upon meeting a 0.084 ppm 8-hour standard, the median estimates
are that about 610,000 children would experience a moderate or greater
lung function response 1 or more times for the aggregate of the 12 urban
areas over a single O3 season (based on the 2002 simulation), and that
there would be almost 3.2 million total occurrences.  Thus, on average
it is estimated that there would be about 5 occurrences per O3 season
per responding child for air quality just meeting a 0.084 ppm 8-hour
standard across the 12 urban areas.  While the estimated number of
occurrences per O3 season is lower when based on the 2004 simulation
than for the 2002 simulation, the estimated number of occurrences per
responding child is similar. The EPA recognizes that some children in
the population might have only 1 or 2 occurrences while others may have
6 or more occurrences per O3 season.  Risk estimates based on adjusting
2003 air quality to simulate just meeting the a 0.084 ppm standard and
alternative 8-hour standards are intermediate to the estimates presented
in Table 2 above in this notice and are presented in the 2007 Staff
Paper (chapter 5) and Risk Assessment TSD.

	For just meeting a 0.084 ppm 8-hour standard, Table 5-8 in the 2007
Staff Paper shows that median estimates across the 12 urban areas for
all school age children experiencing 1 or more moderate lung function
decrements ranges from 0.9 to 5.4 percent based on the 2002 simulation
and from 0.8 to 2.2 percent based on the 2004 simulation.  Risk
estimates for each urban area included in the assessment, for each of
the three years analyzed, and for additional alternative standards are
presented in chapter 5 of the 2007 Staff Paper and in the Risk
Assessment TSD.  

	For just meeting a 0.084 ppm 8-hour standard, the median estimates
across the 5 urban areas for asthmatic school age children range from
3.4 to 10.9 percent based on the 2002 simulation and from 3.2 to 6.9
percent based on the 2004 simulation.

	Key observations important in comparing estimated lung function risks
associated with just meeting the 0.084 ppm NAAQS and alternative
standards under consideration include:

	(1)  As discussed above, there is significant year to year variability
in the range of median estimates of the number of school age children
(ages 5-18) estimated to experience at least one FEV1 decrement ( 15
percent due to 8-hour O3 exposures across the 12 urban areas analyzed,
and similarly across the 5 urban areas analyzed for asthmatic school age
children (ages 5-18) estimated to experience at least one FEV1 decrement
> 10 percent, when various 8-hour standards are just met.

	(2)  For asthmatic school age children, the median estimates of
occurrences of FEV1 decrements >10% range from 52,000 to nearly 510,000
responses associated with just meeting a 0.084 ppm standard (based on
the 2002 simulation) and range from 61,000 to about 240,000 occurrences
(based on the 2004 simulation).  These risk estimates would be reduced
to a range of 14,000 to about 275,000 occurrences (2002 simulation) and
to about 18,000 to nearly 125,000 occurrences (2004 simulation) upon
just meeting the most stringent alternative 8-hour standard (0.064 ppm,
4th highest).  The average number of occurrences per asthmatic child in
an O3 season ranged from about 6 to 11 associated with just meeting a
0.084 ppm standard (2002 simulation).  The average number of occurrences
per asthmatic child ranged from 4 to 12 upon meeting the most stringent
alternative examined (0.064 ppm, 4th-highest) based on the 2002
simulation.  The number of occurrences per asthmatic child is similar
for the scenarios based on the 2004 simulation.

	As discussed above, several epidemiological studies have reported
increased respiratory morbidity outcomes (e.g., respiratory symptoms in
moderate to severe asthmatic children, respiratory-related hospital
admissions) and increased nonaccidental and cardiorespiratory mortality
associated with exposure to ambient O3 concentrations.  The results and
key observations from this portion of the risk assessment are presented
below:  

	(1)  Estimates for increased respiratory symptoms (i.e., chest
tightness, shortness of breath, and wheeze) in moderate/severe asthmatic
children (ages 0-12) were developed for the Boston urban area only.  The
median estimated number of days involving chest tightness (using the
concentration-response relationship with only O3 in the model) is about
6,100 (based on the 2002 simulation) and about 4,500 (based on the 2004
simulation) upon meeting a 0.084 ppm 8-hour standard and this is reduced
to about 4,600 days (2002 simulation) and 3,100 days (2004 simulation)
upon meeting the most stringent alternative examined (0.064 ppm,
4th-highest daily maximum 8-hour average).  This corresponds to 11
percent (2002 simulation) and 8 percent (2004 simulation) of total
incidence of chest tightness upon meeting a 0.084 ppm 8-hour standard
and to about 8 percent (2002 simulation) and 5.5 percent (2004
simulation) of total incidence of chest tightness upon meeting a 0.064
ppm, 4th-highest daily maximum 8-hour average standard.  Similar
patterns of effects and reductions in effects are observed for each of
the respiratory symptoms examined.  

	(2)  The 2007 Staff Paper and Risk Assessment TSD present unscheduled
hospital admission risk estimates for respiratory illness and asthma in
New York City associated with short-term exposures to O3 concentrations
in excess of background levels from April through September for several
recent years (2002, 2003, and 2004) and upon just meeting a 0.084 ppm
standard and alternative 8-hour standards based on simulating O3 levels
using 2002-2004 O3 air quality data.  For total respiratory illness, EPA
estimates about 6.4 cases per 100,000 relevant population (2002
simulation) and about 4.6 cases per 100,000 relevant population (2004
simulation), which represents 1.5 percent (2002 simulation) and 1.0
percent (2004 simulation) of total incidence or about 510 cases (2002
simulation) and about 370 cases (2004 simulation) upon just meeting a
0.084 ppm 8-hour standard.  For asthma-related hospital admissions,
which are a subset of total respiratory illness admissions, the
estimates are about 5.5 cases per 100,000 relevant population (2002
simulation) and about 3.9 cases per 100,000 relevant population (2004
simulation), which represents about 3.3 percent (2002 simulation) and
2.4 percent (2004 simulation) of total incidence or about 440 cases
(2002) and about 310 cases (2004) for this same air quality scenario.  

	For increasingly more stringent alternative 8-hour standards, there is
a gradual reduction in respiratory illness cases per 100,000 relevant
population from 6.4 cases per 100,000 upon just meeting a 0.084 ppm
8-hour standard to 4.6 cases per 100,000 under the most stringent 8-hour
standard (i.e., 0.064 ppm, average 4th-highest daily maximum) analyzed
based on the 2002 simulation.  Similarly, based on the 2004 simulation
there is a gradual reduction from 4.6 cases per 100,000 relevant
population upon just meeting a 0.084 ppm 8-hour standard to 3.0 cases
per 100,000 under a 0.064 ppm, average 4th –highest daily maximum
standard.

	Additional respiratory-related hospital admission estimates for three
other locations are provided in the Risk Assessment TSD.  The EPA notes
that the concentration-response functions for each of these locations
examined different outcomes in different age groups (e.g., > age 30 in
Los Angeles, >age 64 in Cleveland and Detroit, vs. all ages in New York
City), making comparison of the risk estimates across the areas very
difficult.

	(3)  Based on the median estimates for incidence for nonaccidental
mortality (based on the Bell et al. (2004) 95 cities
concentration-response function), meeting the most stringent standard
(0.064 ppm) is estimated to reduce mortality by 40 percent of what it
would be associated with just meeting a 0.084 ppm standard (based on the
2002 simulation).  The patterns for cardiorespiratory mortality are
similar.  The aggregate O3-related cardiorespiratory mortality upon just
meeting the most stringent standard shown is estimated to be about 42
percent of what it would be upon just meeting a 0.084 ppm standard,
using simulated O3 concentrations that just meet a 0.084 ppm standard
and alternative 8-hour standards based on the 2002 simulation.  Using
the 2004 simulation, the corresponding reductions show a similar pattern
but are somewhat greater.

	(4)  Much of the contribution to the risk estimates for non-accidental
and cardiorespiratory mortality upon just meeting a 0.084 ppm 8-hour
standard is associated with 24-hour O3 concentrations between background
and 0.040 ppm.  Based on examining relationships between 24-hour
concentrations averaged across the monitors within an urban area and
8-hour daily maximum concentrations, 8-hour daily maximum levels at the
highest monitor in an urban area associated with these averaged 24-hour
levels are generally about twice as high as the 24-hour levels.  Thus,
most O3-related nonaccidental mortality is estimated to occur when O3
concentrations are between background and when the highest monitor in
the urban area is at or below 0.080 ppm, 8-hour average concentration.

	The discussion below highlights additional observations and insights
from the O3 risk assessment, together with important uncertainties and
limitations.

	(1)  As discussed in the 2007 Staff Paper (section 5.4.5), EPA has
greater confidence in relative comparisons in risk estimates between
alternative standards than in the absolute magnitude of risk estimates
associated with any particular standard.  

	(2)  Significant year-to-year variability in O3 concentrations combined
with the use of a 3-year design value to determine the amount of air
quality adjustment to be applied to each year analyzed, results in
significant year-to-year variability in the annual health risk estimates
upon just meeting various 8-hour standards.

	(3)  There is noticeable city-to-city variability in estimated
O3-related incidence of morbidity and mortality across the 12 urban
areas analyzed for both recent years of air quality and for air quality
adjusted to simulate just meeting a 0.084 ppm standard and selected
potential alternative standards.  This variability is likely due to
differences in air quality distributions, differences in exposure
related to many factors including varying activity patterns and air
exchange rates, differences in baseline incidence rates, and differences
in susceptible populations and age distributions across the 12 urban
areas.

	(4)  With respect to the uncertainties about estimated policy-relevant
background concentrations, as discussed in the 2007 Staff Paper (section
5.4.3), alternative assumptions about background levels had a variable
impact depending on the health effect considered and the location and
standard analyzed in terms of the absolute magnitude and relative
changes in the risk estimates.  There was relatively little impact on
either absolute magnitude or relative changes in lung function risk
estimates due to alternative assumptions about background levels.  With
respect to O3-related non-accidental mortality, while notable
differences (i.e., greater than 50 percent) were observed for
nonaccidental mortality in some areas, particularly for more stringent
standards, the overall pattern of estimated reductions, expressed in
terms of percentage reduction relative to the 0.084 ppm standard, was
significantly less impacted.

C.	Reconsideration of the Level of the Primary Standard

1.	Evidence and Exposure/Risk-Based Considerations

The approach used in the 2007 Staff Paper as a basis for staff
recommendations on standard levels builds upon and broadens the general
approach used by EPA in the 1997 review.  This approach reflects the
more extensive and stronger body of evidence available for the 2008
rulemaking on a broader range of health effects associated with exposure
to O3, including:  (1) additional respiratory-related endpoints; (2) new
information about the mechanisms underlying respiratory morbidity
effects supporting a judgment that the link between O3 exposure and
these effects is causal; (3) newly identified cardiovascular-related
health endpoints from animal toxicology and controlled human exposures
studies that are highly suggestive that O3 can directly or indirectly
contribute to cardiovascular morbidity, and (4) new U.S. multicity time
series studies, single city studies, and several meta-analyses of these
studies that provide relatively strong evidence for associations between
short-term O3 exposures and all-cause (nonaccidental) mortality, at
levels below the current primary standard: as well as (5) a substantial
body of new evidence of increased susceptibility in people with asthma
and other lung diseases.  In evaluating evidence-based and
exposure/risk-based considerations, the 2007 Staff Paper considered: 
(1) the ranges of levels of alternative standards that are supported by
the evidence, and the uncertainties and limitations in that evidence and
(2) the extent to which specific levels of alternative standards reduce
the estimated exposures of concern and risks attributable to O3 and
other photochemical oxidants, and the uncertainties associated with the
estimated exposure and risk reductions.

a.	Evidence-based Considerations

In taking into account evidence-based considerations, the 2007 Staff
Paper evaluated available evidence from controlled human exposure
studies and epidemiological studies, as well as the uncertainties and
limitations in that evidence.  In particular, it focused on the extent
to which controlled human exposure studies provide evidence of
lowest-observed-effects levels and the extent to which epidemiological
studies provide evidence of associations that extend down to the lower
levels of O3 concentrations observed in the studies or some indication
of potential effect thresholds in terms of 8-hour average O3
concentrations.

The most certain evidence of adverse health effects from exposure to O3
comes from the controlled human exposure studies, as discussed above in
section II.A.2, and the large bulk of this evidence derives from studies
of exposures at levels of 0.080 ppm and above.  At those levels, there
is consistent evidence of lung function decrements and respiratory
symptoms in healthy young adults, as well as evidence of inflammation
and other medically significant airway responses. 

	Two studies by Adams (2002, 2006), newly available for consideration in
the 2008 rulemaking, are the only available controlled human exposure
studies that examine respiratory effects associated with prolonged O3
exposures at levels below 0.080 ppm, which was the lowest exposure level
that had been examined in the 1997 review.  As discussed above in
section II.A.2.a.i.(a)(i), the Adams (2006) study investigated a range
of exposure levels, including 0.060 and 0.080 ppm O3, and analyzed
hour-by-hour changes in responses, including lung function (measured in
term of decrements in FEV1) and respiratory symptoms, to investigate the
effects of different patterns of exposure.  At the 0.060 ppm exposure
level, the author reported no statistically significant differences for
lung function decrements; statistically significant responses were
reported for total subjective respiratory symptoms toward the end of the
exposure period for one exposure pattern.  The EPA’s reanalysis
(Brown, 2007) of the data from the Adams (2006) study addressed the more
fundamental question of whether there were statistically significant
changes in lung function from a 6.6-hour exposure to 0.060 ppm O3 versus
filtered air and used a standard statistical method appropriate for a
simple paired comparison.  This reanalysis found small group mean lung
function decrements in healthy adults at the 0.060 ppm exposure level to
be statistically significantly different from responses associated with
filtered air exposure.

Moreover, the Adams’ studies also report a small percentage of
subjects (7 to 20 percent) experienced lung function decrements (> 10
percent) at the 0.060 ppm exposure level.  This is a concern because,
for active healthy people, moderate levels of functional responses
(e.g., FEV1 decrements of > 10% but < 20%) and/or moderate respiratory
symptom responses would likely interfere with normal activity for
relatively few responsive individuals.  However, for people with lung
disease, even moderate functional or symptomatic responses would likely
interfere with normal activity for many individuals, and would likely
result in more frequent use of medication.  In the context of standard
setting, the CASAC indicated (Henderson, 2006c) that a focus on the
lower end of the range of moderate levels of functional responses (e.g.,
FEV1 decrements ( 10%) is most appropriate for estimating potentially
adverse lung function decrements in people with lung disease. 
Therefore, the results of the Adams studies which indicate that a small
percentage of healthy, non-asthmatic subjects are likely to experience
FEV1 decrements ( 10% when exposed to 0.060 ppm O3 have implications for
setting a standard that protects public health, including the health of
sensitive populations such as asthmatics, with an adequate margin of
safety. 

In considering these most recent controlled human exposure studies, the
2007 Staff Paper concluded that these studies provide evidence of a
lowest-observed-effects level of 0.060 ppm for potentially adverse lung
function decrements and respiratory symptoms in some healthy adults
while at prolonged moderate exertion.  It further concluded that since
people with asthma, particularly children, have been found to be more
sensitive and to experience larger decrements in lung function in
response to O3 exposures than would healthy adults, the 0.060 ppm
exposure level also can be interpreted as representing a level likely to
cause adverse lung function decrements and respiratory symptoms in
children with asthma and more generally in people with respiratory
disease.

In considering controlled human exposure studies of pulmonary
inflammation, airway responsiveness, and impaired host defense
capabilities, discussed above in section II.A.2.a.i, the 2007 Staff
Paper noted that these studies provide evidence of a
lowest-observed-effects level for such effects in healthy adults at
prolonged moderate exertion of 0.080 ppm, the lowest level tested. 
Moreover there is no evidence that the 0.080 ppm level is a threshold
for these effects.  Studies reporting inflammatory responses and markers
of lung injury have clearly demonstrated that there is significant
variation in response of subjects exposed, even to O3 exposures at 0.080
ppm.  One study showed notable interindividual variability in young
healthy adult subjects in most of the inflammatory and cellular injury
indicators analyzed at 0.080 ppm.  This inter-individual variability
suggests that some portion of the population would likely experience
such effects at exposure levels extending well below 0.080 ppm. 

As discussed above, these physiological effects have been linked to
aggravation of asthma and increased susceptibility to respiratory
infection, potentially leading to increased medication use, increased
school and work absences, increased visits to doctors’ offices and
emergency departments, and increased hospital admissions.  Further,
pulmonary inflammation is related to increased cellular permeability in
the lung, which may be a mechanism by which O3 exposure can lead to
cardiovascular system effects, and to potential chronic effects such as
chronic bronchitis or long-term damage to the lungs that can lead to
reduced quality of life.  These are all indicators of adverse O3-related
morbidity effects, which are consistent with and lend plausibility to
the adverse morbidity effects and mortality effects observed in
epidemiological studies.

Significant associations between ambient O3 exposures and a wide variety
of respiratory symptoms and other morbidity outcomes (e.g., asthma
medication use, school absences, emergency department visits, and
hospital admissions) have been reported in epidemiological studies, as
discussed above in section II.A.2.a.i.  Overall, the 2006 Criteria
Document concludes that positive and robust associations were found
between ambient O3 concentrations and various respiratory disease
hospitalization outcomes, when focusing particularly on results of
warm-season analyses.  Recent studies also generally indicate a positive
association between O3 concentrations and emergency department visits
for asthma during the warm season.  These positive and robust
associations are supported by the controlled human exposure, animal
toxicological, and epidemiological evidence for lung function
decrements, increased respiratory symptoms, airway inflammation, and
increased airway responsiveness.  Taken together, the overall evidence
supports a causal relationship between acute ambient O3 exposures and
increased respiratory morbidity outcomes resulting in increased
emergency department visits and hospitalizations during the warm season
(EPA, 2006a, p. 8-77).

Moreover, many single- and multicity epidemiological studies observed
positive associations of ambient O3 concentrations with total
nonaccidental and cardiopulmonary mortality.  As discussed above in
section II.A.2.b.i, the 2006 Criteria Document finds that the results
from U.S. multicity time-series studies provide the strongest evidence
to date for O3 effects on acute mortality.  Recent meta-analyses also
indicate positive risk estimates that are unlikely to be confounded by
PM; however, future work is needed to better understand the influence of
model specifications on the magnitude of risk. The 2006 Criteria
Document concludes that the “positive O3 effects estimates, along with
the sensitivity analyses in these three meta-analyses, provide evidence
of a robust association between ambient O3 and mortality” (EPA, 2006a,
p. 7-97).   In summary, the 2006 Criteria Document (p. 8-78) concludes
that these findings are highly suggestive that short-term O3 exposure
directly or indirectly contribute to non-accidental and
cardiopulmonary-related mortality, but additional research is needed to
more fully establish underlying mechanisms by which such effects occur.

The 2007 Staff Paper considered the epidemiological studies to evaluate
evidence related to potential effects thresholds at the population level
for morbidity and mortality effects.  As discussed above in section
II.A.3.a (and more fully in the 2007 Staff Paper in chapter 3 and the
2006 Criteria Document in chapter 7), a number of time-series studies
have used statistical modeling approaches to evaluate potential
thresholds at the population level.  A few such studies reported some
suggestive evidence of possible thresholds for morbidity and mortality
outcomes in terms of 24-hour, 8-hour, and 1-hour averaging times.  These
results, taken together, provide some indication of possible 8-hour
average threshold levels from below about 0.025 to 0.035 ppm (within the
range of background concentrations) up to approximately 0.050 ppm. 
Other studies, however, observe linear concentration-response functions
suggesting no effect threshold.  The 2007 Staff Paper (p.6-60) concluded
that the statistically significant associations between ambient O3
concentrations and lung function decrements, respiratory symptoms,
indicators of respiratory morbidity including increase emergency
department visits and hospital admissions, and possibly mortality
reported in a large number of studies likely extend down to ambient O3
concentrations that are well below the level of the then current
standard (0.084 ppm).  These associations also extend well below the
level of the standard set in 2008 (0.075 ppm) in that the highest level
at which there is any indication of a threshold is approximately 0.050
ppm.  Toward the lower end of the range of O3 concentrations observed in
such studies, ranging down to background levels (i.e., 0.035 to 0.015
ppm), however, the 2007 Staff Paper stated that there is increasing
uncertainty as to whether the observed associations remain plausibly
related to exposures to ambient O3, rather than to the broader mix of
air pollutants present in the ambient atmosphere.

The 2007 Staff Paper also considered studies that did subset analyses,
which included only days with ambient O3 concentrations below the level
of the then current standard, or below even lower O3 concentrations, and
continue to report statistically significant associations.  Notably, as
discussed above, Bell et al. (2006) conducted a subset analysis that
continued to show statistically significant mortality associations even
when only days with a maximum 8-hour average O3 concentration below a
value of approximately 0.061 ppm were included.  Also of note is the
large multicity NCICAS (Mortimer et al., 2002) that reported
statistically significant associations between ambient O3 concentrations
and lung function decrements even when days with 8-hour average O3
levels greater than 0.080 ppm were excluded (which consisted of less
than 5 percent of the days in the eight urban areas in the study).

Further, as discussed above in section II.A.3.a, there are limitations
in epidemiological studies that make discerning thresholds in
populations difficult, including low data density in the lower
concentration ranges, the possible influence of exposure measurement
error, and interindividual differences in susceptibility to O3-related
effects in populations.  There is the possibility that thresholds for
individuals may exist in reported associations at fairly low levels
within the range of air quality observed in the studies but not be
detectable as population thresholds in epidemiological analyses.

Based on the above considerations, the 2007 Staff Paper recognized that
the available evidence neither supports nor refutes the existence of
effect thresholds at the population level for morbidity and mortality
effects, and that if a population threshold level does exist, it would
likely be well below the level of the then current standard and possibly
within the range of background levels.  Taken together, these
considerations also support the conclusion that if a population
threshold level does exist, it would likely be well below the level of
the 0.075 ppm, 8-hour average, standard set in 2008.

In looking more broadly at evidence from animal toxicological,
controlled human exposure, and epidemiological studies, the 2006
Criteria Document found substantial evidence, newly available in the
2008 rulemaking, that people with asthma and other preexisting pulmonary
diseases are among those at increased risk from O3 exposure.  Altered
physiological, morphological, and biochemical states typical of
respiratory diseases like asthma, COPD, and chronic bronchitis may
render people sensitive to additional oxidative burden induced by O3
exposure (EPA, 2006a, section 8.7).  Children and adults with asthma are
the groups that have been studied most extensively.  Evidence from
controlled human exposure studies indicates that asthmatics may exhibit
larger lung function decrements in response to O3 exposure than healthy
controls.  As discussed more fully in section II.A.4 above, asthmatics
present a different response profile for cellular, molecular, and
biochemical parameters (EPA, 2006a, Figure 8-1) that are altered in
response to acute O3 exposure.  They can have larger inflammatory
responses, as manifested by larger increases in markers of inflammation
such as white bloods cells (e.g., PMNs) or inflammatory cytokines. 
Asthmatics, and people with allergic rhinitis, are more likely to have
an allergic-type response upon exposure to O3, as manifested by
increases in white blood cells associated with allergy (i.e.,
eosinophils) and related molecules, which increase inflammation in the
airways.  The increased inflammatory and allergic responses also may be
associated with the larger late-phase responses that asthmatics can
experience, which can include increased bronchoconstrictor responses to
irritant substances or allergens and additional inflammation.  

In addition to the experimental evidence of lung function decrements,
respiratory symptoms, and other respiratory effects in asthmatic
populations, two large U.S. epidemiological studies as well as several
smaller U.S. and international studies, have reported fairly robust
associations between ambient O3 concentrations and measures of lung
function and daily respiratory symptoms (e.g., chest tightness, wheeze,
shortness of breath) in children with moderate to severe asthma and
between O3 and increased asthma medication use (EPA, 2007a, chapter 6). 
These more serious responses in asthmatics and others with lung disease
provide biological plausibility for the respiratory morbidity effects
observed in epidemiological studies, such as emergency department visits
and hospital admissions.

The body of evidence from controlled human exposure and epidemiological
studies, which includes asthmatic as well as non-asthmatic subjects,
indicates that controlled human exposure studies of lung function
decrements and respiratory symptoms that evaluate only healthy,
non-asthmatic subjects likely underestimate the effects of O3 exposure
on asthmatics and other susceptible populations.  Therefore, relative to
the healthy, non-asthmatic subjects used in most controlled human
exposure studies, including the Adams (2002, 2006) studies, a greater
proportion of people with asthma may be affected, and those who are
affected may have as large or larger lung function and symptomatic
responses at ambient exposures to 0.060 ppm O3.  This indicates that the
lowest-observed-effects levels demonstrated in controlled human exposure
studies that use only healthy subjects may not reflect the lowest levels
at which people with asthma or other lung diseases may respond. 

Being mindful of the uncertainties and limitations inherent in
interpreting the available evidence, the 2007 Staff Paper stated the
view that the range of alternative O3 standards for consideration should
take into account information on lowest-observed-effects levels in
controlled human exposure studies as well as indications of possible
effects thresholds reported in some epidemiological studies and
questions of biological plausibility in attributing associations
observed down to background levels to O3 exposures alone.  Based on the
evidence and these considerations, it concluded that the upper end of
the range of consideration should be somewhat below 0.080 ppm, the
lowest-observed-effects level for effects such as pulmonary
inflammation, increased airway responsiveness and impaired host-defense
capabilities in healthy adults while at prolonged moderate exertion. 
The 2007 Staff Paper also concluded that the lower end of the range of
alternative O3 standards appropriate for consideration should be the
lowest-observed-effects level for potentially adverse lung function
decrements and respiratory symptoms in some healthy adults, 0.060 ppm. 

b. 	Exposure and Risk-based Considerations

	In addition to the evidence-based considerations informing staff
recommendations on alternative levels, as discussed above in section
II.B, the 2007 Staff Paper also evaluated quantitative exposures and
health risks estimated to occur upon meeting the then current 0.084 ppm
standard and alternative standards.  In so doing, it presented the
important uncertainties and limitations associated with these exposure
and risk assessments (discussed above in section II.B and more fully in
chapters 4 and 5 of the 2007 Staff Paper).  

	The 2007 Staff Paper (and the CASAC) also recognized that the exposure
and risk analyses could not provide a full picture of the O3 exposures
and O3-related health risks posed nationally.  The EPA did not have
sufficient information to evaluate all relevant at-risk groups (e.g.,
outdoor workers) or all O3-related health outcomes (e.g., increased
medication use, school absences, and emergency department visits that
are part of the broader pyramid of effects discussed above in section
II.A.4.d), and the scope of the 2007 Staff Paper analyses was generally
limited to estimating exposures and risks in 12 urban areas across the
U.S., and to only five or just one area for some health effects included
in the  risk assessment.  Thus, national-scale public health impacts of
ambient O3 exposures are clearly much larger than the quantitative
estimates of O3-related incidences of adverse health effects and the
numbers of children likely to experience exposures of concern associated
with meeting the 0.084 ppm standard or alternative standards.  On the
other hand, inter-individual variability in responsiveness means that
only a subset of individuals in each group estimated to experience
exposures exceeding a given benchmark exposure of concern level would
actually be expected to experience such adverse health effects. 

	The 2007 Staff Paper focused on alternative standards with the same
form as the then current 0.084 ppm O3 standard (i.e. the 0.074/4,
0.070/4 and 0.064/4 scenarios).  Having concluded in the 2007 Staff
Paper that it was appropriate to consider a range of standard levels
from somewhat below 0.080 ppm down to as low as 0.060 ppm, the 2007
Staff Paper looked to results of the analyses of exposure and risk for
the 0.074/4 scenario to represent the public health impacts of selecting
a standard in the upper part of the range, the results of analyses of
the 0.070/4 scenario to represent the impacts in the middle part of the
range, and the results of the analyses of the 0.064/4 scenario to
represent the lower part of the range.

	As discussed in section II.B.1 of this notice, the exposure estimates
presented in the 2007 Staff Paper are for the number and percent of all
children and asthmatic children exposed, and the number of person-days
(occurrences) of exposures, with daily 8-hour maximum exposures at or
above several benchmark levels while at intermittent moderate or greater
exertion.  Exposures above selected benchmark levels provide some
perspective on the public health impacts of health effects that cannot
currently be evaluated in quantitative risk assessments but that may
occur at existing air quality levels, and the extent to which such
impacts might be reduced by meeting alternative standard levels.  As
described in section II.B.1.c above, the 2007 Staff Paper refers to
exposures at and above these benchmark levels as “exposures of
concern.”  The 2007 Staff Paper notes that exposures of concern, and
the health outcomes they represent, likely occur across a range of O3
exposure levels, such that there is no one exposure level that addresses
all public health concerns.  As noted above in section II.B., EPA also
has acknowledged that the concept is more appropriately viewed as a
continuum with greater confidence and less uncertainty about the
existence of health effects at the upper end and less confidence and
greater uncertainty as one considers increasingly lower O3 exposure
levels.  

 Consistent with advice from CASAC, the 2007 Staff Paper estimates
exposures of concern not only at 0.080 ppm O3, a level at which there
are clearly demonstrated effects, but also at 0.070 and 0.060 ppm O3
levels where there is some evidence that health effects are likely to
occur in some individuals.  The 2007 Staff Paper recognizes that there
will be varying degrees of concern about exposures at each of these
levels, based in part on the population groups experiencing them.  Given
that there is clear evidence of inflammation, increased airway
responsiveness, and changes in host defenses in healthy people exposed
to 0.080 ppm and reason to infer that such effects will continue at
lower exposure levels, but with increasing uncertainty about the extent
to which such effects occur at lower O3 concentrations, the 2007 Staff
Paper and discussion below, focus on exposures of concern at or above
benchmark levels of 0.070 and 0.060 ppm O3 for purposes of evaluating
alternative standards.  The focus on these two benchmark levels reflects
the following evidence-based considerations, discussed above in section
II.C.1, that raise concerns about adverse health effects likely
occurring at levels below 0.080 ppm:  (1) that there is limited , but
important, new evidence from controlled human exposure studies showing
lung function decrements and respiratory symptoms in some healthy
subjects at 0.060 ppm; (2)  that asthmatics are likely to have more
serious responses than healthy individuals; (3) that lung function is
not likely to be as sensitive a marker for O3 effects as lung
inflammation; and (4) that there is epidemiological evidence which
reports associations with O3 levels that extend well below 0.080 ppm.  

 Table 3 below summarizes the exposure estimates for all children and
asthmatic children for the 0.060 and 0.070 ppm health effect benchmark
levels associated with O3 levels adjusted to just meet 0.074/4, 0.070/4,
and 0.064/4 alternative 8-hour standards based on a generally poorer
year of air quality (2002) and based on a generally better year of air
quality (2004).  This table includes exposure estimates reflecting the
aggregate estimate for the 12 urban areas as well as the range across
these same 12 areas.  As shown in Table 3 below, the percent of
population exposed over the selected benchmark levels is very similar
for all and asthmatic school age children.  Thus, the following
discussion focuses primarily on the exposure estimates for asthmatic
children, recognizing that the pattern of exposure estimates is similar
for all children when expressed in terms of percentage of the
population.

As noted in section II.B.2 and shown in Tables 1 and 3 of this notice,
substantial year-to-year variability is observed, ranging to over an
order of magnitude at the higher alternative standard levels, in
estimates of the number of children and the number of occurrences of
exposures of concern at both  the 0.060 and 0.070 ppm benchmark levels. 
As shown in Table 3, and discussed more fully below, aggregate estimates
of exposures of concern for the 12 urban areas included in the
assessment are considerably larger for the benchmark level of ≥ 0.060
ppm O3, compared to the 0.070 ppm benchmark, while the pattern of
year-to-year variability is fairly similar.  

   As shown in Table 3, aggregate estimates of exposures of concern for
a 0.060 ppm benchmark level vary considerably among the three
alternative standards included in this table, particularly for the 2002
simulations (a year with generally poorer air quality in most, but not
all areas).  For air quality just meeting a 0.074/4 standard
approximately 27% of asthmatic children, based on the 2002 simulation,
and approximately 2% of asthmatic children based on the 2004 simulation
(a year with better air quality in most but not all areas), are
estimated to experience one or more exposures of concern at the
benchmark level of ≥ 0.060 ppm O3.  Considering a 0.070/4 standard
using the same benchmark level (0.060 ppm), about 18% of asthmatic
children are estimated to experience one or more exposures of concern,
in a year with poorer air quality (2002), and only about 1% in a year
with better air quality (2004).  For the most stringent standard
examined (a 0.064/4 standard), about 6% of asthmatic children are
estimated to experience one or more exposures of concern in the
simulation based on the year with poorer air quality (2002), and
exposures of concern at the 0.060 ppm benchmark level are essentially
eliminated based on a year with better air quality (2004).

Table 3 also provides aggregate exposure estimates for the 12 urban
areas where a benchmark level of ≥ 0.070 ppm is used.  Based on the
year with poorer air quality (2002), the estimate of the percent of
asthmatic children exposed one or more times is about 5% when a 0.074/4
standard is just met; based on a year with better air quality (2004),
exposures of concern are essentially eliminated.  For this same
benchmark (0.070 ppm), when a 0.070/4 standard is just met, estimates
range from about 2% of asthmatic children exposed one or more times over
this benchmark based on a year with poorer air quality (2002), and
exposures of concern are essentially eliminated based on a year with
better air quality (2004).  At the 0.070 ppm benchmark, just meeting a
0.064/4 standard essentially eliminates exposures of concern regardless
of the year that is used as the basis for the analysis.

	The 2007 Staff Paper also notes that there is substantial city-to-city
variability in these estimates, and notes that it is appropriate to
consider not just the aggregate estimates across all cities, but also to
consider the public health impacts in cities that receive relatively
less protection from the alternative standards.  As shown in Table 3, in
considering the benchmark level of > 0.060 ppm, while the aggregate
percentage of asthmatic children estimated to experience one or more
exposures of concern across all 12 cities for a 0.074/4 standard is
about 27% based on the year with poorer air quality (2002), it ranges up
to approximately 51% for asthmatic children in the city with the least
degree of protection from that alternative standard.  Similarly, for air
quality just meeting a 0.070/4 standard, the aggregate percentage of
asthmatic children estimated to experience one or more exposures of
concern across all 12 cities is 18% based on the year with poorer air
quality, but it ranges up to about 41% in the city with the least degree
of protection associated with just meeting that alternative standard. 
For just meeting a 0.064/4 standard, the aggregate estimate of asthmatic
children experiencing exposures of concern for the 0.060 ppm benchmark
is about 6% based on the year with poorer air quality and ranges up to
16% in the city with the least degree of protection. 

This pattern of city-to-city variability also occurs at the benchmark
level of ≥ 0.070 ppm associated with air quality just meeting these
same three alternative standards (i.e., 0.074/4, 0.070/4, and 0.064/4). 
While the aggregate percentage of asthmatic children estimated to
experience such exposures of concern across all 12 cities is about 5%
based on the year with poorer air quality for just meeting the 0.074/4
standard, it ranges up to 14% in the city with the least degree of
protection associated with that alternative standard.  For just meeting
a 0.070/4 standard the aggregate estimate is 2% of asthmatic children
experiencing exposures of concern for the 0.070 ppm benchmark based on
the year with poorer air quality and ranges up to 6% in the city with
the least degree of protection.  The aggregate estimate for exposures of
concern is further reduced to 0.2% of asthmatic children for this same
benchmark level for air quality just meeting a 0.064/4 standard based on
the year with poorer air quality and ranges up to 1% in the city with
the least degree of protection. 

In addition to observing the fraction of the population estimated to
experience exposures of concern associated with just meeting alternative
standards, EPA also took into consideration in the 2007 Staff Paper the
percent reduction in exposures of concern and health risks associated
with alternative standards relative to just meeting the then current
0.084/4 standards.  For the current decision it is also informative to
consider the incremental reductions in exposures of concern associated
with more stringent alternative standards relative to the 0.075 ppm
standard.  As shown in Table 1 above, at the > 0.060 ppm benchmark level
based on a year with poorer air quality, the reduction in exposures of
concern for asthmatic children in going from the 0.074/4 standard (which
approximates the 0.075 ppm standard adopted in 2008) down to a 0.064/4
standard is observed to be very similar to the reduction estimated to
occur in going from then current 0.084/4 standard down to a 0.074/4
standard.  More specifically, the estimates for asthmatic children are
reduced from 47% (about 1.2 million children) associated with meeting a
0.084/4 standard down to 27% (about 700,000 children) for just meeting a
0.074/4 standard and the estimates are reduced further to about 6%
(about 150,000 children) associated with just meeting a 0.064/4 standard
in the 12 urban areas included in the assessment.  In a year with better
air quality (2004), exposures estimated to exceed the 0.060 ppm
benchmark in asthmatic children one or more times in a year are reduced
from 11% associated with just meeting a 0.084/4 standard down to about
2% for a 0.074/4 standard and are essentially eliminated when a 0.064/4
standard is just met.    

Turning to consideration of the risk assessment estimates, Table 2 above
summarizes the risk estimates for moderate lung function decrements in
both all school age children and asthmatic school age children
associated with just meeting several alternative standards based on
simulations involving a year with relatively poorer air quality (2002)
and a year with relatively better air quality (2004).  As shown in Table
2, for the 2002 simulation the reduction in the number of asthmatic
children estimated to experience one or more moderate lung function
decrements going from a 0.074/4 standard down to a 0.064/4 standard is
roughly equivalent to the additional health protection afforded
associated with just meeting a 0.074/4 standard relative to then current
0.084/4 standard.  More specifically, for just 5 urban areas, it is
estimated that nearly 8% of asthmatic children (130,000 children) would
experience one or more occurrences of moderate lung function decrements
per year at a 0.084/4 standard and this would be reduced to about 5%
(90,000 children) at a 0.074/4 standard and further reduced down to
about 3% (50,000 children) at a 0.064/4 standard.  Based on the 2002
simulations, the percent reduction associated with just meeting a
0.064/4 standard relative to then current 0.084/4 standard is about 62%
which is about twice the reduction in risk compared to the estimated 31%
reduction associated with just meeting a 0.074/4 standard.  As shown in
Table 2 above, similar patterns were observed in reductions in lung
function risk for all school age children in 12 urban areas associated
with these alternative standards.

Figures 6-5 and 6-6 in the 2007 Staff Paper (EPA, 2007b) show the
percent reduction in non-accidental mortality risk estimates associated
with just meeting the same alternative standards discussed above
relative to just meeting the then current 0.084/4 standard for 12 urban
areas, based on adjusting 2002 and 2004 air quality data.  These figures
also provide perspective on the extent to which the risks in these years
(i.e., 2002 and 2004) are greater than those estimated to occur upon
meeting the then current 0.084/4 standard (in terms of a negative
percent reduction relative to a 0.084/4 standard).  Based on the 2002
simulations (EPA, 2007b, Figure 6-5), the estimated reduction in
non-accidental mortality is about 30 to 70% across the 12 urban areas
for just meeting a 0.064/4 standard relative to the then current 0.084/4
standard.  This reduction is roughly twice the 15 to 30% estimated
reduction across the 12 urban areas associated with just meeting a
0.074/4 standard relative to a 0.084/4 standard.  While the estimated
incidence is lower based on the 2004 simulations (EPA, 2007b, Figure
6-6), the pattern of risk reductions among alternative standards is
roughly similar to that observed for the 2002 simulations.  

In addition to the risk estimates for lung function decrements in all
school age children and non-accidental mortality that were estimated for
12 urban areas and lung function decrements in asthmatic children for 5
urban areas, a similar pattern of incremental reductions in health risks
was shown for two health outcomes where risks were estimated in one city
only for each of these outcomes.  These included reductions in
respiratory symptoms in asthmatic children (EPA, 2007b; Boston, Table
6-9) and respiratory-related hospital admissions (EPA, 2007a; New York
City, Table 6-10) associated with just meeting alternative 8-hour
standards set at 0.074 ppm, 0.070 ppm, and 0.064 ppm relative to just
meeting the then current 0.084 ppm standard.  Using the 2002 simulation,
a standard set at 0.074/4 is estimated to reduce the incidence of
symptom days in children with moderate to severe asthma in the Boston
area by about 15 percent relative to a 0.084/4 standard.  With this
reduction, it is estimated that about 1 respiratory symptom day in 8
during the O3 season would be attributable to O3 exposure.  A standard
set at 0.064/4 is estimated, based on the 2002 simulation, to reduce the
incidence of symptom days in children with moderate to severe asthma in
the Boston area by about a 25 to 30 percent reduction relative to a
0.084 ppm standard, which is roughly twice the reduction compared to
that provided by a 0.074/4 standard.  But even with this reduction, it
is estimated that 1 respiratory symptom day in 10 during the O3 season
is attributable to O3 exposure

As shown in Table 6-10 (EPA, 2007b) estimated incidence of
respiratory-related hospital admissions in one urban area (New York
City) was reduced by 14 to 17 percent by a standard set at 0.074/4
relative to then current 0.084/4 standard, in the year with relatively
high and relatively low O3 air quality levels, respectively.  Similar to
the pattern observed for the other health outcomes discussed above, the
reduction in incidence of respiratory-related hospital admissions for a
0.064/4 standard relative to a 0.084/4 standard is about twice that
associated with a 0.074/4 standard relative to a 0.084/4 standard.

Table 3.  Number and Percent of All and Asthmatic School Age Children in
12 Urban Areas Estimated to Experience 8-Hour Ozone Exposures Above
0.060 and 0.070 ppm While at Moderate or Greater Exertion, One or More
Times Per Season  Associated with Just Meeting Alternative 8-Hour
Standards Based on Adjusting 2002 and 2004 Air Quality Data1,2

Benchmark Levels of Exposures

of Concern

(ppm)	8-Hour Air Quality Standards3

(ppm)	All Children, ages 5-18 

Aggregate for 12 urban areas	Asthmatic Children, ages 5-18

Aggregate for 12 urban areas

Number of Children Exposed (% of all children) 

[Range across 12 cities, % of all children]	Number of Children Exposed
(% of group)

[Range across 12 cities, % of group ]

2002	2004	2002	2004

0.070	0.074	770,000 (4%)

[0 – 13%]	20,000 (0%)

[0 - 1%]	120,000 (5%)

[0 - 14% ]	0 (0%)

[0 - 1%]

	0.070	270,000 (1%)

[0 - 5%]	0 (0%)

[0%]	50,000 (2%)

[0 - 6%]	0 (0%)

[0%]

	0.064	30,000 (0.2%)

[0 - 1%]	0 (0%)

[0%]	10,000 (0.2%)

[0 - 1% ]	0 (0%)

[0%]

0.060	0.074	4,550,000 (25%)

[1 - 48%]	350,000 (2%)

[0 - 9%]	700,000 (27%)

[1 -51%]	50,000 (2%)

[0 - 9%]

	0.070	3,000,000 (16%)

[1 - 36%]	110,000 (1%)

[0 - 4%]	460,000 (18%)

[0 - 41%]	10,000 (1%)

[0 - 3%]

	0.064	950,000 (5%)

[0 - 17%]	10,000 (0%)

[0 - 1%]	150,000 (6%)

[0 - 16%]	0 (0%)

[0 - 1%]

1 Moderate or greater exertion is defined as having an 8-hour average
equivalent ventilation rate > 13 l-min/m2.

2 Estimates are the aggregate results based on 12 combined statistical
areas (Atlanta, Boston, Chicago, Cleveland, Detroit, Houston, Los
Angeles, New York, Philadelphia, Sacramento, St. Louis, and Washington,
D.C.).  Estimates are for the ozone season which is all year in Houston,
Los Angeles and Sacramento and March or April to September or October
for the remaining urban areas.

3 All standards summarized here have the same form as the 8-hour
standard established in 1997 which is specified as the 3-year average of
the annual 4th highest daily maximum 8-hour average concentrations must
be at or below the concentration level specified.  As described in the
2007 Staff Paper (EPA, 2007b, section 4.5.8), recent O3 air quality
distributions have been statistically adjusted to simulate just meeting
the 0.084 ppm standard and selected alternative standards.  These
simulations do not represent predictions of when, whether, or how areas
might meet the specified standards

2.	CASAC Views Prior to 2008 Decision 	

	In comments on the second draft Staff Paper, CASAC stated in its letter
to the Administrator, “the CASAC unanimously recommends that the
current primary ozone NAAQS be revised and that the level that should be
considered for the revised standard be from 0.060 to 0.070 ppm”
(Henderson, 2006c, p. 5).  This recommendation followed from its more
general recommendation that the 0.084 ppm standard needed to be
substantially reduced to be protective of human health, particularly in
at-risk subpopulations.  

	The CASAC Panel noted that beneficial reductions in some adverse health
effects were estimated to occur upon meeting the lowest standard level
(0.064 ppm) considered in the risk assessment (Henderson, 2006c, p. 4). 
The lower end of this range reflects CASAC’s views that “[w]hile
data exist that adverse health effects may occur at levels lower than
0.060 ppm, these data are less certain and achievable gains in
protecting human health can be accomplished through lowering the ozone
NAAQS to a level between 0.060 and 0.070 ppm.”  (id.).  

	In a subsequent letter sent specifically to offer advice to aid the
Administrator and Agency staff in developing the O3 proposal, the CASAC
reiterated that the Panel members “were unanimous in recommending that
the level of the current primary ozone standard should be lowered from
0.08 ppm to no greater than 0.070 ppm” (Henderson, 2007, p. 2). 
Further, the CASAC Panel expressed the view that the 2006 Criteria
Document and 2007 Staff Paper, together with the information in its
earlier letter, provide “overwhelming scientific evidence for this
recommendation,” and emphasized the Clean Air Act requirement that the
primary standard must be set to protect the public health with an
adequate margin of safety (id.).

3.	Basis for 2008 Decision on the Primary Standard

	This section presents the rationale for the 2008 final decision on the
primary O3 standard as presented in the 2008 final rule (73 FR 16475). 
The EPA’s conclusions on the level of the standard began by noting
that, having carefully considered the public comments on the appropriate
level of the O3 standard, EPA concluded that the fundamental scientific
conclusions on the effects of O3 reached in the 2006 Criteria Document
and 2007 Staff Paper remained valid.  In considering the level at which
the primary O3 standard should be set, EPA placed primary consideration
on the body of scientific evidence available in the 2008 final
rulemaking on the health effects associated with O3 exposure, while
viewing the results of exposure and risk assessments as providing
information in support of the decision.  In considering the available
scientific evidence, EPA concluded that a focus on the proposed range of
0.070 to 0.075 ppm was appropriate in light of the large body of
controlled human exposure and epidemiological and other scientific
evidence.  The notice stated that this body of evidence did not support
retaining the then current 0.084 ppm 8-hour O3 standard, as suggested by
some commenters, nor did it support setting a level just below 0.080
ppm, because, based on the entire body of evidence, such a level would
not provide a significant increase in protection compared to the 0.084
ppm standard.  Further, such a level would not be appreciably below the
level in controlled human exposure studies at which adverse effects have
been demonstrated (i.e., 0.080 ppm).  The notice also stated that the
body of evidence did not support setting a level of 0.060 ppm or below,
as suggested by other commenters.  In evaluating the information from
the exposure assessment and the risk assessment, EPA judged that this
information did not provide a clear enough basis for choosing a specific
level within the range of 0.075 to 0.070 ppm.  

In making a final judgment about the level of the primary O3 standard,
EPA noted that the level of 0.075 ppm is above the range recommended by
the CASAC (i.e., 0.070 to 0.060 ppm).  The notice stated that in placing
great weight on the views of CASAC, careful consideration had been given
to CASAC’s stated views and the scientific basis and policy views for
the range it recommended.  In so doing, EPA fully agreed that the
scientific evidence supports the conclusion that the current standard
was not adequate and must be revised.

	With respect to CASAC’s recommended range of standard levels, EPA
observed that the basis for CASAC’s recommendation appeared to be a
mixture of scientific and policy considerations.  While in general
agreement with CASAC’s views concerning the interpretation of the
scientific evidence, EPA noted that there was no bright line clearly
directing the choice of level, and the choice of what was appropriate
was clearly a public health policy judgment entrusted to the EPA
Administrator.  This judgment must include consideration of the
strengths and limitations of the evidence and the appropriate inferences
to be drawn from the evidence and the exposure and risk assessments.  In
reviewing the basis for the CASAC Panel’s recommendation for the range
of the O3 standard, EPA observed that it reached a different policy
judgment than the CASAC Panel based on apparently placing different
weight in two areas: the role of the evidence from the Adams studies and
the relative weight placed on the results from the exposure and risk
assessments. 	While EPA found the evidence reporting effects at the
0.060 ppm level from the Adams studies to be too limited to support a
primary focus at this level, EPA observed that the CASAC Panel appeared
to place greater weight on this evidence, as indicated by its
recommendation of a range down to 0.060 ppm.  It was noted that while
the CASAC Panel supported a level of 0.060 ppm, they also supported a
level above 0.060, which indicated that they did not believe that the
results of Adams studies meant that the level of the standard had to be
set at 0.060 ppm.  The EPA also observed that the CASAC Panel appeared
to place greater weight on the results of the risk assessment as a basis
for its recommended range.  In referring to the risk assessment results
for lung function, respiratory symptoms, hospital admissions and
mortality, the CASAC Panel concluded that:  “beneficial effects in
terms of reduction of adverse health effects were calculated to occur at
the lowest concentration considered (i.e., 0.064 ppm)” (Henderson,
2006c, p.4).  However, EPA more heavily weighed the implications of the
uncertainties associated with the Agency’s quantitative human exposure
and health risk assessments.  Given these uncertainties, EPA did not
agree that these assessment results appropriately served as a primary
basis for concluding that levels at or below 0.070 ppm were required for
the 8-hour O3 standard.

	The notice stated that after carefully taking the above comments and
considerations into account, and fully considering the scientific and
policy views of the CASAC, EPA decided to revise the level of the
primary 8-hour O3 standard to 0.075 ppm.  The EPA judged, based on the
available evidence, that a standard set at this level would be requisite
to protect public health with an adequate margin of safety, including
the health of sensitive subpopulations, from serious health effects
including respiratory morbidity, that were judged to be causally
associated with short-term and prolonged exposures to O3, and premature
mortality.  The EPA also judged that a standard set at this level
provides a significant increase in protection compared to the 0.084 ppm
standard, and is appreciably below 0.080 ppm, the level in controlled
human exposure studies at which adverse effects have been demonstrated. 
At a level of 0.075 ppm, exposures at and above the benchmark of 0.080
ppm are essentially eliminated, and exposures at and above the benchmark
of 0.070 are substantially reduced or eliminated for the vast majority
of people in at-risk groups.  A standard set at a level lower than 0.075
would only result in significant further public health protection if, in
fact, there is a continuum of health risks in areas with 8-hour average
O3 concentrations that are well below the concentrations observed in the
key controlled human exposure studies and if the reported associations
observed in epidemiological studies are, in fact, causally related to O3
at those lower levels.  Based on the available evidence, EPA was not
prepared to make these assumptions.  Taking into account the
uncertainties that remained in interpreting the evidence from available
controlled human exposure and epidemiological studies at very low
levels, EPA noted that the likelihood of obtaining benefits to public
health decreased with a standard set below 0.075 ppm O3, while the
likelihood of requiring reductions in ambient concentrations that go
beyond those that are needed to protect public health increased.  The
EPA judged that the appropriate balance to be drawn, based on the entire
body of evidence and information available in the 2008 final rulemaking,
was to set the 8-hour primary standard at 0.075 ppm.  The EPA expressed
the belief that a standard set at 0.075 ppm would be sufficient to
protect public health with an adequate margin of safety, and did not
believe that a lower standard was needed to provide this degree of
protection.  The EPA further asserted that this judgment appropriately
considered the requirement for a standard that was neither more nor less
stringent than necessary for this purpose and recognized that the CAA
does not require that primary standards be set at a zero-risk level, but
rather at a level that reduces risk sufficiently so as to protect public
health with an adequate margin of safety.

4. 	CASAC Advice Following 2008 Decision

	Following the 2008 decision on the O3 standard, serious questions were
raised as to whether the standard met the requirements of the CAA.  In
April 2008, the members of the CASAC Ozone Review Panel sent a letter to
EPA stating “In our most-recent letters to you on this subject - dated
October 2006 and March 2007 - the CASAC unanimously recommended
selection of an 8-hour average Ozone NAAQS within the range of 0.060 to
0.070 parts per million for the primary (human health-based) Ozone
NAAQS” (Henderson, 2008).  The letter continued: “The CASAC now
wishes to convey, by means of this letter, its additional, unsolicited
advice with regard to the primary and secondary Ozone NAAQS.  In doing
so, the participating members of the CASAC Ozone Review Panel are
unanimous in strongly urging you or your successor as EPA Administrator
to ensure that these recommendations be considered during the next
review cycle for the Ozone NAAQS that will begin next year” (id.). 
Moreover, the CASAC Panel noted that “numerous medical organizations
and public health groups have also expressed their support of these
CASAC recommendations.” (id.)  The letter further stated the following
strong, unanimous view:

[the CASAC did] “not endorse the new primary ozone standard as being
sufficient protective of public health.  The CASAC — as the Agency’s
statutorily-established science advisory committee for advising you on
the national ambient air quality standards — unanimously recommended
decreasing the primary standard to within the range of 0.060–0.070
ppm. It is the Committee’s consensus scientific opinion that your
decision to set the primary ozone standard above this range fails to
satisfy the explicit stipulations of the Clean Air Act that you ensure
an adequate margin of safety for all individuals, including sensitive
populations” (Henderson, 2008).

 5.	Administrator’s Proposed Conclusions

For the reasons discussed below, the Administrator proposes to set a new
level for the 8-hour primary O3 within the range from 0.060 to 0.070
ppm.  In reaching this proposed decision, the Administrator has
considered:  the evidence-based considerations from the 2006 Criteria
Document and the 2007 Staff Paper; the results of the exposure and risk
assessments discussed above and in the 2007 Staff Paper; CASAC advice
and recommendations provided in CASAC’s letters to the Administrator
both during and following the 2008 rulemaking; EPA staff
recommendations; and public comments received in conjunction with review
of drafts of these documents and on the 2007 proposed rule.  In
considering what level of an 8-hour O3 standard is requisite to protect
public health with an adequate margin of safety, the Administrator is
mindful that this choice requires judgments based on an interpretation
of the evidence and other information that neither overstates nor
understates the strength and limitations of the evidence and
information.

The Administrator notes that the most certain evidence of adverse health
effects from exposure to O3 comes from the controlled human exposure
studies, and that the large bulk of this evidence derives from studies
of exposures at levels of 0.080 ppm and above.  At those levels, there
is consistent evidence of lung function decrements and respiratory
symptoms in healthy young adults, as well as evidence of O3-induced
pulmonary inflammation, airway responsiveness, impaired host defense
capabilities, and other medically significant airway responses. 
Moreover, there is no evidence that the 0.080 ppm exposure level is a
threshold for any of these types of respiratory effects.  Rather, there
is now controlled human exposure evidence, including studies of lung
function decrements and respiratory symptoms at the 0.060 ppm exposure
level, that strengthens our previous understanding that this array of
respiratory responses are likely to occur in some healthy adults at such
lower levels.

In particular, the Administrator notes two studies by Adams (2002,
2006), newly available in the 2008 rulemaking, that examined lung
function and respiratory symptom effects associated with prolonged O3
exposures at levels below 0.080 ppm, as well as EPA’s reanalysis of
the data from the Adams (2006) study at a 0.060 ppm exposure level.  As
discussed above, while the author’s analysis focused on hour-by-hour
comparisons of effects, for the purpose of exploring responses
associated with different patterns of exposure, EPA’s reanalysis
focused on addressing the more fundamental question of whether the pre-
to post-exposure change in lung function differed between a 6.6-hour
exposure to 0.060 ppm O3 versus a 6.6 hour exposure to clean filtered
air.  The Administrator notes that this reanalysis found small, but
statistically significant group mean differences in lung function
decrements in healthy adults at the 0.060 ppm exposure level, which is
now the lowest-observed-effects level for these effects.  Moreover,
these studies also report a small percentage of subjects (7 to 20
percent) experienced moderate lung function decrements (> 10 percent) at
the 0.060 ppm exposure level.  While for active healthy people, moderate
levels of functional responses (e.g., FEV1 decrements of > 10% but <
20%) and/or moderate respiratory symptom responses would likely
interfere with normal activity for relatively few responsive
individuals, the Administrator notes that for people with lung disease,
even moderate functional or symptomatic responses would likely interfere
with normal activity for many individuals, and would likely result in
more frequent use of medication.  Further, she notes that CASAC
indicated that a focus on the lower end of the range of moderate levels
of functional responses (e.g., FEV1 decrements ( 10%) is most
appropriate for estimating potentially adverse lung function decrements
in people with lung disease (Henderson, 2006c).  

The Administrator also notes that many public commenters on the 2007
proposed rule raised a number of questions about the weight that should
be placed on the Adams studies and EPA’s reanalysis of data from the
Adams (2006) study.  Some commenters expressed the view that the results
of these studies and EPA’s reanalysis provided support for setting a
standard level below the proposed range, while others raised questions
about EPA’s reanalysis and generally expressed the view that the study
results were not robust enough to reach conclusions about respiratory
effects at the 0.060 ppm exposure level.

Based on all the abovethese considerations, the Administrator concludes
that the Adams studies provide limited but important evidence which adds
to the overall body of evidence that to informs her proposed decision on
the range of levels within which a standard could be set that would be
requisite to protect public health with an adequate margin of safety,
including the health of at-risk populations such as people with lung
disease.

In considering controlled human exposure studies reporting O3-induced
pulmonary inflammation, airway responsiveness, and impaired host defense
capabilities at exposure levels down to 0.080 ppm, the lowest level at
which these effects have been tested, the Administrator notes that these
physiological effects have been linked to aggravation of asthma and
increased susceptibility to respiratory infection, potentially leading
to increased medication use, increased school and work absences,
increased visits to doctors’ offices and emergency departments, and
increased hospital admissions, especially in people with lung disease. 
These physiological effects are all indicators of potential adverse
O3-related morbidity effects, which are consistent with and lend
plausibility to the associations observed between O3 and adverse
morbidity effects and mortality effects in epidemiological studies.

With regard to epidemiological studies, the Administrator observes that
statistically significant associations between ambient O3 levels and a
wide array of respiratory symptoms and other morbidity outcomes
including school absences, emergency department visits, and hospital
admissions have been reported in a large number of studies.  More
specifically, positive and robust associations were found between
ambient O3 concentrations and respiratory hospital admissions and
emergency department visits, when focusing particularly on the results
of warm season analyses.  Taken together, the overall body of evidence
from controlled human exposure, toxicological, and epidemiological
studies supports the inference of a causal relationship between acute
ambient O3 exposures and increased respiratory morbidity outcomes
resulting in increased emergency department visits and hospitalizations
during the warm season.  Further, the Administrator notes that recent
epidemiological evidence is highly suggestive that O3 directly or
indirectly contributes to non-accidental and cardiopulmonary-related
mortality.

The Administrator also considered the epidemiological evidence with
regard to considering potential effects thresholds at the population
level for morbidity and mortality effects.  As discussed above, while
some studies provide some indication of possible 8-hour average
threshold levels from below about 0.025 to 0.035 ppm (within the range
of background concentrations) up to approximately 0.050 ppm, other
studies observe linear concentration-response functions suggesting that
there may be no effects thresholds at the population level above
background concentrations.  In addition, other studies conducted subset
analyses that included only days with ambient O3 concentrations below
the level of the then current standard, or below even lower O3
concentrations, including a level as low as 0.061 ppm, and continue to
report statistically significant associations.  The Administrator notes
that the relationships between ambient O3 concentrations and lung
function decrements, respiratory symptoms, indicators of respiratory
morbidity including increased respiratory-related emergency department
visits and hospital admissions, and possibly mortality reported in a
large number of studies likely extend down to ambient O3 concentrations
well below the level of the standard set in 2008 (0.075 ppm), in that
the highest level at which there is any indication of a threshold is
approximately 0.050 ppm.  The Administrator notes as well that toward
the lower end of the range of O3 concentrations observed in such
studies, ranging down to background levels (i.e., 0.035 to 0.015 ppm),
there is increasing uncertainty as to whether the observed associations
remain plausibly related to exposures to ambient O3, rather than to the
broader mix of air pollutants present in the ambient atmosphere.  She
also notes that there are limitations in epidemiological studies that
make discerning population thresholds difficult, as discussed above,
such that there is the possibility that thresholds for individuals may
exist in reported associations at fairly low levels within the range of
air quality observed in the studies but not be detectable as population
thresholds in epidemiological analyses.

In looking more broadly at evidence from animal toxicological,
controlled human exposure, and epidemiological studies, the
Administrator finds substantial evidence, newly available for
consideration in the 2008 rulemaking, that people with asthma and other
preexisting pulmonary diseases are among those at increased risk from O3
exposure.  As discussed above, altered physiological, morphological, and
biochemical states typical of respiratory diseases like asthma, COPD,
and chronic bronchitis may render people sensitive to additional
oxidative burden induced by O3 exposure.  Children and adults with
asthma are the group that has been studied most extensively.  Evidence
from controlled human exposure studies indicates that asthmatics and
people with allergic rhinitis may exhibit larger lung function
decrements in response to O3 exposure than healthy subjects and that
they can have larger inflammatory responses.  The Administrator also
notes that two large U.S. epidemiological studies, as well as several
smaller U.S. and international studies, have reported fairly robust
associations between ambient O3 concentrations and measures of lung
function and daily symptoms (e.g., chest tightness, wheeze, shortness of
breath) in children with moderate to severe asthma and between O3 and
increased asthma medication use.  These more serious responses in
asthmatics and others with lung disease provide biological plausibility
for the respiratory morbidity effects observed in epidemiological
studies, such as respiratory-related emergency department visits and
hospital admissions.

The Administrator also observes that a substantial body of evidence from
controlled human exposure and epidemiological studies indicates that
relative to the healthy, non-asthmatic subjects used in most controlled
human exposure studies, a greater proportion of people with asthma may
be affected, and those who are affected may have as large or larger lung
function and symptomatic responses to O3 exposures.  Thus, the
Administrator concludes that controlled human exposure studies of lung
function decrements and respiratory symptoms that evaluate only healthy,
non-asthmatic subjects likely underestimate the effects of O3 exposure
on asthmatics and other susceptible populations.

In addition to the evidence-based considerations discussed above, the
Administrator also considered quantitative exposures and health risks
estimated to occur associated with air quality simulated to just meet
various standard levels to help inform judgments about a range of
standard levels for consideration that could provide an appropriate
degree of public health protection.  In so doing, she is mindful of the
important uncertainties and limitations that are associated with the
exposure and risk assessments, as discussed in more detail in the 2007
Staff Paper, and above in sections II.B and II.C.1.b.  Beyond these
uncertainties, the Administrator also recognized important limitations
related to the exposure and risk analyses.  For example, EPA did not
have sufficient information to evaluate all relevant at-risk groups
(e.g., outdoor workers) or all O3-related health outcomes (e.g.,
increased medication use, school absences, emergency department visits),
and the scope of the analyses was generally limited to estimating
exposures and risks in 12 urban areas across the U.S., and to only five
or just one area for some health effects.  Thus, it is clear that
national-scale public health impacts of ambient O3 exposures are much
larger than the quantitative estimates of O3-related incidences of
adverse health effects and the numbers of children likely to experience
exposures of concern associated with meeting the then current standard
or alternative standards.  Taking these limitations into account, the
CASAC advised EPA not to rely solely on the results of the exposure and
risk assessments in considering alternative standards, but also to place
significant weight on the body of evidence of O3-related health effects
in drawing conclusions about an appropriate range of levels for
consideration.  The Administrator agrees with this advice.  

Turning first to the results of the exposure assessment, the
Administrator focused on the extent to which alternative standard
levels, approximately at and below the 0.075 ppm O3 standard set in the
2008 final rule, are estimated to reduce exposures over the 0.060 and
0.070 ppm health effects benchmark levels, for all and asthmatic school
age children in the 12 urban areas included in the assessment.  The
Administrator also took note that the lowest standard level included in
the exposure and health risk assessments was 0.064 ppm and that
additional reductions in exposures over the selected health benchmark
levels would be anticipated for just meeting a 0.060 ppm standard. 

As an initial matter, the Administrator recognized that the concept of
“exposures of concern” is more appropriately viewed as a continuum,
with greater confidence and less uncertainty about the existence of
health effects at the upper end and less confidence and greater
uncertainty as one considers increasingly lower O3 exposure levels.  In
considering the concept of exposures of concern, the Administrator also
noted that it is important to balance concerns about the potential for
health effects and their severity with the increasing uncertainty
associated with our understanding of the likelihood of such effects at
lower O3 levels.  Within the context of this continuum, estimates of
exposures of concern at discrete benchmark levels provide some
perspective on the public health impacts of O3-related physiological
effects that have been demonstrated in controlled human exposure and
toxicological studies but cannot be evaluated in quantitative risk
assessments, such as lung inflammation, increased airway responsiveness,
and changes in host defenses.  They also help in understanding the
extent to which such impacts have the potential to be reduced by meeting
alternative standards.  As discussed in II.C.1.a above, these O3-related
physiological effects are plausibly linked to the increased morbidity
seen in epidemiological studies (e.g., as indicated by increased
medication use in asthmatics, school absences in all children, and
emergency department visits and hospital admissions in people with lung
disease).  

Estimates of the number of people likely to experience exposures of
concern cannot be directly translated into quantitative estimates of the
number of people likely to experience specific health effects, since
sufficient information to draw such comparisons is not available -- if
such information were available, these health outcomes would have been
included in the quantitative risk assessment.  Due to individual
variability in responsiveness, only a subset of individuals who have
exposures at and above a specific benchmark level are expected to
experience such adverse health effects, and susceptible population
groups such as those with asthma are expected to be affected more by
such exposures than healthy individuals.

For the reasons discussed in section II.C.1.b above, the Administrator
has concluded that it is appropriate to focus on both the 0.060 and
0.070 ppm health effect benchmarks for her decision on the primary
standard.  In summary, the focus on these two benchmark levels reflects
the following evidence-based considerations, discussed above in section
II.C.1.a, that raise concerns about adverse health effects likely
occurring at levels below 0.080 ppm:  (1) that there is limited, but
important, new evidence from controlled human exposure studies showing
lung function decrements and respiratory symptoms in some healthy
subjects at 0.060 ppm; (2)  that asthmatics are likely to have more
serious responses than healthy individuals; (3) that lung function is
not likely to be as sensitive a marker for O3 effects as lung
inflammation; and (4) that there is epidemiological evidence which
reports associations between ambient O3 concentrations and respiratory
symptoms, ED visits, hospital admissions, and premature mortality in
areas with O3 levels that extend well below 0.080 ppm.  

Based on the exposure and risk considerations discussed in detail in the
2007 Staff Paper and presented in sections II.B and II.C.1.b above, the
Administrator notes the following important observations from these
assessments:  1) there is a similar pattern for all children and
asthmatic school age children in terms of exposures of concern over
selected benchmark levels when estimates are expressed in terms of
percentage of the population; 2) the aggregate estimates of exposures of
concern reflecting estimates for the 12 urban areas included in the
assessment are considerably larger for the benchmark level of 0.060 ppm
compared to the 0.070 ppm benchmark; 3) there is notable year-to-year
variability in exposure and risk estimates with higher exposure and risk
estimates occurring in simulations involving a year with generally
poorer air quality in most areas (2002) compared to a year with
generally better air quality (2004); and 4) there is significant
city-to-city variability in exposure and risk estimates, with some
cities receiving considerably less protection associated with air
quality just meeting the same standard.  As discussed above, the
Administrator believes that it is appropriate to consider not just the
aggregate estimates across all cities, but also to consider the public
health impacts in cities that receive relatively less protection from
alternative standards under consideration.  Similarly, the Administrator
believes that year-to-year variability should also be considered in
making judgments about which standards will protect public health with
an adequate margin of safety.

In addition, significant reductions in exposures of concern and risk
have been estimated to occur across standard levels analyzed.  The
magnitudes of exposure and risk reductions estimated to occur in going
from a 0.074 ppm standard to a 0.064 ppm standard are as large as those
estimated to occur in going from the then current 0.084 ppm standard to
a 0.074 ppm standard.  Consequently, the reduction in risk that can be
achieved by going from a standard of 0.074 ppm to a standard of 0.064
ppm is  comparable to the risk reduction that can be achieved by moving
from the 1997 O3 standard, effectively a 0.084 ppm standard, to a
standard very close to the 2008 standard of 0.075 ppm. 

The Administrator also observes that estimates of exposures of concern
associated with air quality just meeting the alternative standards below
0.080 ppm (i.e., 0.074, 0.070, and 0.064 ppm, the levels included in the
assessment) are notably lower than estimates for alternative standards
set at and above 0.080 ppm.  As shown in Table 6-8 in the 2007 Staff
Paper, just meeting a 0.080 ppm standard is associated with an aggregate
estimate of exposures of concern of about 13% of asthmatic children at
the 0.070 ppm benchmark level, ranging up to 31% in the city with the
least degree of protection in a year with generally poorer air quality,
and an aggregate estimate of exposures of concern of about 40% of
asthmatic children, ranging up to 63% in the city with the least degree
of protection at the 0.060 ppm benchmark level.  Based on the exposure
estimates presented in Table 3 in this notice, she observes that
standards included in the assessment below 0.080 ppm (i.e., 0.074,
0.070, and 0.064 ppm), are estimated to have substantially lower
estimates of exposures of concern at the 0.070 ppm benchmark level. 
Similarly, she notes that exposures of concern at the 0.060 ppm
benchmark associated with alternative standards below 0.080 ppm are
appreciably lower than exposures associated with standards at or above
0.080 ppm, especially for standards set at 0.064 and 0.070 ppm. 

As noted previously, the Administrator also recognizes that the risk
estimates for health outcomes included in the risk assessment are
limited and that the overall health effects evidence is indicative of a
much broader array of O3-related health effects that are part of a
“pyramid of effects” that include various indicators of morbidity
that could not be included in the risk assessment (e.g., school
absences, increased medication use, doctor’s visits, and emergency
department visits), some of which have a greater impact on at-risk
groups.  Consideration of such unquantified risks for this array of
health effects, taken together with the estimates of exposures of
concern and the quantified health risks discussed above, supports the
Administrator’s evidence-based conclusion that revising the standard
level to a level well below 0.080 ppm will provide important increased
public health protection, especially for at-risk groups such as people
with asthma or other lung disease, as well as children and older adults,
particularly those active outdoors, and outdoor workers

Based on the evidence- and exposure/risk-based considerations discussed
above, the Administrator concludes that it is appropriate to set the
level of the primary O3 standard to a level well below 0.080 ppm, a
level at which the evidence provides a high degree of certainty about
the adverse effects of O3 exposure in healthy people, to provide an
adequate margin of safety for at-risk groups.  In selecting a proposed
range of levels, the Administrator believes it is appropriate to
consider the following information:  (1) the strong body of evidence
from controlled human exposure studies evaluating healthy people at
exposure levels of 0.080 ppm and above that demonstrated lung function
decrements, respiratory symptoms, pulmonary inflammation, and other
medically significant airway responses, as well as limited but important
evidence of lung function decrements and respiratory symptoms in healthy
people down to O3 exposure levels of 0.060 ppm; (2) the substantial body
of evidence from controlled human exposure and epidemiological studies
indicating that people with asthma are likely to experience larger and
more serious effects than healthy people; (3) the body of
epidemiological evidence indicating associations are observed for a wide
range of serious health effects, including respiratory-related emergency
department visits and hospital admissions and premature mortality,
across distributions of ambient O3 concentrations that extend below the
current standard level of 0.075 ppm, as well as questions of biological
plausibility in attributing the observed effects to O3 alone at the
lower end of the concentration ranges extending down to background
levels; and (4) the estimates of exposures of concern and risks for a
range of health effects that indicate that important improvements in
public health are very likely associated with O3 levels just meeting
alternative standards, especially for standards set at 0.070 and 0.064
ppm (the lowest levels included in the assessment), relative to
standards set at and above 0.080 ppm. 

The Administrator next considered what standard level well below 0.080
ppm would be requisite to protect public health, including the health of
at-risk groups, with an adequate margin of safety that is sufficient but
not more than necessary to achieve that result.  The assessment of a
standard level calls for consideration of both the degree of risk to
public health at alternative levels of the standard as well as the
certainty that such risk will occur at any specific level.  Based on the
information available in the 2008 rulemaking, there is no evidence-based
bright line that indicates a single appropriate level.  Instead there is
a combination of scientific evidence and other information that needs to
be considered as a whole in making this public health policy judgment,
and selecting a standard level from a range of potentially reasonable
values.

As an initial matter, the Administrator considered whether the standard
level of 0.075 ppm set in the 2008 final rule is sufficiently below
0.080 ppm to be requisite to protect public health with an adequate
margin of safety.  In considering this standard level, the Administrator
looked to the rationale for selecting this level presented in the 2008
final rule, as summarized above in section II.C.3.  In that rationale,
EPA observed that a level of 0.075 ppm is above the range of 0.060 to
0.070 ppm recommended by CASAC, and that the CASAC Panel appeared to
place greater weight on the evidence from the Adams studies and on the
results of the exposure and risk assessments, whereas EPA placed greater
weight on the limitations and uncertainties associated with that
evidence and the quantitative exposure and risk assessments. 
Additionally, EPA’s rationale did not discuss and thus
placedapparently gave no weight at all toon exposures of concern
relative to the 0.060 ppm benchmark which reflected the
lowest-observed-effects level for lung function effects observed in
healthy adults in the Adams studies.  Further, EPA concluded that “[a]
standard set at a lower level than 0.075 ppm would only result in
significant further public health protection if, in fact, there is a
continuum of health risks in areas with 8-hour average O3 concentrations
that are well below the concentrations observed in the key controlled
human exposure studies and if the reported associations observed in
epidemiological studies are, in fact, causally related to O3 at those
lower levels.  Based on the available evidence, [EPA] is not prepared to
make these assumptions” (73 FR 16483).  	

In reconsidering the entire body of evidence available in the 2008
rulemaking, including the Agency’s own assessment of the
epidemiological evidence in the 2006 Criteria Document, and placing
significant weight on the views of CASAC, the Administrator now finds a
compelling basis for concludesing that important and significant risks
to public health are likely to occur at a standard level of 0.075 ppm
based on the controlled human exposure, toxicological, and
epidemiological evidence.  She judges that a standard level of 0.075 ppm
is not sufficient to provide protection with an adequate margin of
safety.  In support of this conclusion, the Administrator finds that
setting a standard that would protect public health, including the
health of at-risk populations, with an adequate margin of safety should
reasonably depend upon giving some weight to the results of the Adams
studies and EPA's reanalysis of the Adams's data, and to how effectively
alternative standard levels would serve to limit exposures of concern
relative to the 0.060 ppm benchmark level as well as to the 0.070 ppm
benchmark level.  The Administrator notes that EPA’s risk assessment
estimates comparable risk reductions in going from a 0.074 ppm standard
to a 0.064 ppm standard as were estimated in going from the then current
0.084 ppm standard down to a 0.074 ppm standard for an array of health
effects analyzed.  These estimates include reductions in risk for lung
function decrements in all and asthmatic school age children,
respiratory symptoms in asthmatic children, respiratory-related hospital
admissions, and non-accidental mortality.  

Further, based on the exposure assessment estimates discussed above, the
Administrator notes that for air quality just meeting a 0.074 ppm
standard, approximately 27% of asthmatic school age children and 25% of
all school age children are estimated to experience one or more
exposures of concern over the 0.060 ppm benchmark level based on
simulations for a year with generally poorer air quality; this estimate
increases to about 50% of asthmatic and all children in the city with
the least degree of protection.  The Administrator judges that these
estimates are large and strongly suggest significant public health
impacts would likely remain in many areas with air quality just meeting
a 0.075 ppm O3 standard.

In light of these estimates and the available evidence, the
Administrator agrees with CASAC’s conclusion that important public
health protections can be achieved by a standard set below 0.075 ppm,
within the range of 0.060 to 0.070 ppm.  In addition, based on both the
evidence- and exposure/risk-based considerations summarized above, the
Administrator concludes that a standard set as high as 0.075 would not
be considered requisite to protect public health with an adequate margin
of safety, and that consideration of lower levels is warranted.  In
considering such lower levels, the Administrator recognizes that the CAA
requires her to reach a public health policy judgment as to what
standard would be requisite to protect public health with an adequate
margin of safety, based on scientific evidence and technical assessments
that have inherent uncertainties and limitations.  This judgment
requires making reasoned decisions as to what weight to place on various
types of evidence and assessments and on the related uncertainties and
limitations.

In selecting a level below 0.075 ppm that would serve as an appropriate
upper end for a range of levels to propose, the Administrator has
considered a more cautious approach to interpreting the available
evidence and exposure/risk-based information – that is, an approach
that places significant weight on uncertainties and limitations in the
information so as to avoid potentially overestimating public health
risks and protection likely to be associated with just meeting a
particular standard level.   In so doing, she notes that the most
certain evidence of adverse health effects from exposure to O3 comes
from the controlled human exposure studies, and that the large bulk of
this evidence derives from studies of exposures at levels of 0.080 ppm
and above.  At those levels, there is consistent evidence of lung
function decrements and respiratory symptoms in healthy young adults, as
well as evidence of inflammation and other medically significant airway
responses.  Further, she takes note of the limited but important
evidence from controlled human exposure studies indicating that lung
function decrements and symptoms can occur in healthy people at levels
as low as 0.060 ppm, while also recognizing the limitations in that
evidence, as discussed above in sections II.A.1 and II.C.1.a.  She also
notes that some people with asthma are likely to experience larger and
more serious effects than the healthy subjects evaluated in the
controlled exposure studies, while recognizing that there is uncertainty
about the magnitude of such differences.  In considering the available
epidemiological studies, she recognizes that they provide evidence of
serious respiratory morbidity effects, including respiratory-related
emergency department visits and hospital admissions, and non-accidental
mortality at levels well below 0.080 ppm, while also recognizing that
there is increasing uncertainty associated with the likelihood that such
effects occur at decreasing O3 levels down to background levels. 
Considering the exposure/risk information, as shown in Table 3, the
Administrator observes that a standard set at 0.070 ppm would likely
substantially limit exposures of concern relative to the 0.070 ppm
benchmark level, while affording far less protection against exposures
of concern relative to the 0.060 ppm benchmark level.  To the extent
that more weight is placed on protection relative to the higher
benchmark level, and more weight is placed on the uncertainties
associated with the epidemiological evidence, a standard set at 0.070
ppm might be considered to be adequately protective.  Taken together,
this type of cautious approach to interpreting the evidence and the
exposure/risk information serves as the basis for the Administrator’s
conclusion that the upper end of the proposed range should be set at
0.070 ppm O3.

In selecting a level that would serve as an appropriate lower end for a
range of levels to propose, the Administrator has considered a more
precautionary approach to interpreting the available evidence and
exposure/risk-based information – that is, an approach that places
less weight on uncertainties and limitations in the information so as to
avoid potentially underestimating public health improvements likely to
be associated with just meeting a particular standard level.  In so
doing, the Administrator notes the limited, but important evidence of a
lowest-observed-effects level at 0.060 ppm O3 from controlled human
exposure studies reporting lung function decrements and respiratory
symptoms in healthy subjects.  Notably, these studies also report that a
small percentage of subjects (7 to 20 percent) experienced moderate lung
function decrements (> 10 percent) at the 0.060 ppm exposure level,
recognizing that for people with lung disease, such moderate functional
or symptomatic responses would likely interfere with normal activity for
many individuals, and would likely result in more frequent use of
medication.  In addition, a substantial body of evidence indicates that
people with asthma are likely to experience larger and more serious
effects than healthy people and therefore controlled human exposure
studies done with healthy subjects likely underestimate effects in this
at-risk population.  

Moreover, epidemiological studies provide evidence of serious
respiratory morbidity effects, including respiratory-related emergency
department visits and hospital admissions, and non-accidental mortality
at O3 levels that may plausibly extend down to at least 0.060 ppm even
when considering the uncertainties inherent in such studies.  The
Administrator notes that the controlled human exposure studies conducted
at 0.060 ppm provide some biological plausibility for associations
between respiratory morbidity and mortality effects found in
epidemiological studies and O3 exposures down to 0.060 ppm.  Considering
the exposure information, as shown in Table 3, the Administrator
observes that a standard set at 0.064 ppm would likely essentially
eliminate exposures of concern relative to the 0.070 ppm benchmark
level, while appreciably limiting exposures of concern relative to the
0.060 ppm benchmark level to approximately 6 percent of asthmatic
children in the aggregate across 12 cities and up to 16 percent in the
city that would receive the least protection.  While not addressed in
the exposure assessment done as part of the 2008 rulemaking, a standard
set at 0.060 ppm would be expected to provide somewhat greater
protection from such exposures, which is important to the extent that
more weight is placed on providing protection relative to the lower
benchmark level.  Taken together, the Administrator concludes that this
precautionary approach to interpreting the evidence and the
exposure/risk information supports a level of 0.060 ppm as the lower end
of the proposed range.  

The Administrator has also concluded that the lower end of the proposed
range should not extend below 0.060 ppm O3.  In reaching this
conclusion, she gives significant weight to the recommendation of the
CASAC panel that 0.060 ppm should be the lower end of the range for
consideration (Henderson, 2006c).  In the Administrator's view, the
evidence from controlled human exposure studies at the 0.060 ppm
exposure level, the lowest level tested, is not robust enough to support
consideration of a lower level.  While some epidemiological studies
provide evidence of serious respiratory morbidity effects and
non-accidental mortality with no evidence of a threshold, the
Administrator notes that other studies provide evidence of a potential
threshold somewhat below 0.060 ppm.  Moreover, there are limitations in
epidemiological studies that make discerning population thresholds
difficult, including fewer observations in the range of lower
concentrations, concerns related to exposure measurement error, the
possible role of copollutants and effects modifiers, and interindividual
differences in susceptibility to O3-related effects.  In the
Administrator’s judgment, these limitations in epidemiological
studies, including the limitations in judging the causality of observed
associations at lower O3 levels, and the lack of robust controlled human
exposure data at 0.060 ppm make it difficult to interpret this evidence
as a basis for a standard level set below 0.060 ppm.  Thus, in selecting
0.060 ppm as the lower end of the range for the proposed level of the O3
standard, the Administrator has taken into account information on the
lowest-observed-effects levels in controlled human exposure studies,
indications of possible thresholds reported in some epidemiological
studies, the increasing uncertainty in the epidemiological evidence at
even lower levels, as well as evidence about increased susceptibility of
people with asthma and also other lung diseases.  In so doing, she
concludes that a primary O3 standard set below 0.060 ppm would be more
than is necessary to protect public health with an adequate margin of
safety for at-risk groups.  

In reaching her proposed decision, the Administrator has also considered
the public comments that were received on the 2007 proposed rule (72 FR
37818).  The Administrator notes that there were sharply divergent views
expressed by two general sets of commenters with regard to considering
the health effects evidence, results of exposure and risk assessments,
and the advice of the CASAC panel.  On one hand, medical groups, health
effects researchers, public health organizations, environmental groups,
and some state, tribal and local air pollution control agencies strongly
supported a standard set within the range recommended by the CASAC. 
These commenters generally placed significant weight on the more recent
evidence from controlled human exposure studies, down to the 0.060 ppm
exposure level, as well as on the epidemiological studies and the
results of the exposure and risk assessment conducted for the 2008
rulemaking.  Many of these commenters took a more precautionary view and
supported a standard set at 0.060 ppm O3, the lower end of the CASAC
recommended range.  The Administrator notes that these views are
generally consistent with her proposed conclusions.  On the other hand,
another group of commenters primarily representing industry associations
and businesses and some state environmental agencies, primarily
expressed the view that the more recent evidence from controlled human
exposure, the epidemiological studies, and the results of exposure and
human health risk assessments were so uncertain that they did not
provide a basis for making any changes to the then current 0.084 ppm O3
standard set in 1997.  This group of commenters generally argued that
the health effects evidence newly available in the 2008 rulemaking, the
results of the exposure and health risk assessments, and the advice of
the CASAC were flawed.  For the reasons discussed above, the
Administrator does not agree with the later group of commenters that
essentially no weight should be placed on any of the new evidence or
assessments that were available for consideration in the 2008
rulemaking. 

Based on consideration of the entire body of evidence and information
available in the 2008 rulemaking, including exposure and risk estimates,
as well as the recommendations of CASAC, the Administrator proposes to
set the level of the primary 8-hour O3 standard to a level within the
range of 0.060 to 0.070 ppm.  A standard level within this range would
reduce the risk of a variety of health effects associated with exposure
to O3, including the respiratory symptoms and lung function effects
demonstrated in the controlled human exposure studies, and the
respiratory-related emergency department visits, hospital admissions and
mortality effects observed in the epidemiological studies.  All of these
effects are indicative of a much broader array of O3-related health
endpoints, such as school absences and increased medication use, that
are plausibly linked to these observed effects.  Depending on the weight
placed on the evidence and information available in the 2008 rulemaking,
as well as the uncertainties and limitations in the evidence and
information, a standard could be set within this range  at a level that
would be requisite to protect public health with an adequate margin of
safety.

In reaching this proposed decision, as discussed above, the
Administrator has focused on the nature of the increased public health
protection that would be afforded by a standard set within the proposed
range of levels relative to the protection afforded by the standard set
in 2008.  Having considered the public comments received on the 2007
proposed rule in reaching this proposed decision that reconsiders the
2008 final rule, the Administrator is interested in again receiving
public comment on the benefits to public health associated with a
standard set at specific levels within the proposed range relative to
the benefits associated with the standard set in 2008.  

D.	Proposed Decision on the Level of the Primary Standard

For the reasons discussed above, and taking into account information and
assessments presented in the 2006 Criteria Document and 2007 Staff
Paper, the advice and recommendations of CASAC, and public comments
received during the 2008 rulemaking, the Administrator proposes to set a
new level for the 8-hour primary O3 standard.  Specifically, the
Administrator proposes to set the level of the 8-hour primary O3
standard to within a range of 0.060 to 0.070 ppm.  The proposed 8-hour
primary standard would be met at an ambient air monitoring site when the
3-year average of the annual forth-highest daily maximum 8-hour average
O3 concentration is less than or equal to the level of the standard that
is promulgated.  Thus, the Administrator proposes to set a standard with
a level within this range.  She solicits comment on this range and on
the appropriate weight to place on the various types of available
evidence, the exposure and risk assessment results, and the
uncertainties and limitations related to this information, as well as on
the benefits to public health associated with a standard set within this
range relative to the benefits associated with the standard set in 2008.

III.	Communication of Public Health Information

	Information on the public health implications of ambient concentrations
of criteria pollutants is currently made available primarily through
EPA's Air Quality Index (AQI) program.  The current Air Quality Index
has been in use since its inception in 1999 (64 FR 42530).  It provides
accurate, timely, and easily understandable information about daily
levels of pollution (40 CFR 58.50).  The AQI establishes a nationally
uniform system of indexing pollution levels for O3, carbon monoxide,
nitrogen dioxide, particulate matter and sulfur dioxide.  The AQI
converts pollutant concentrations in a community's air to a number on a
scale from 0 to 500.  Reported AQI values enable the public to know
whether air pollution levels in a particular location are characterized
as good (0 - 50), moderate (51 - 100), unhealthy for sensitive groups
(101 - 150), unhealthy (151 - 200), very unhealthy (201 - 300), or
hazardous (300 - 500).  The AQI index value of 100 typically corresponds
to the level of the short-term NAAQS for each pollutant.  An AQI value
greater than 100 means that a pollutant is in one of the unhealthy
categories (i.e., unhealthy for sensitive groups, unhealthy, very
unhealthy, or hazardous) on a given day; whereas an AQI value at or
below 100 means that a pollutant concentration is in one of the
satisfactory categories (i.e., moderate or good).  Decisions about the
pollutant concentrations at which to set the various AQI breakpoints,
that delineate the various AQI categories, draw directly from the
underlying health information that supports the NAAQS review.

	In the 2008 rulemaking, the AQI for O3 was revised by setting an AQI
value of 100 equal to 0.075 ppm, 8-hour average, the level of the
revised primary O3 standard.  The other AQI breakpoints were also
revised as follows:  An AQI value of 50 is set at 0.059 ppm; an AQI
value of 150 was set at 0.095 ppm; and an AQI value of 200 was set at
0.115 ppm.  All these levels are averaged over 8 hours.  These levels
were developed by making proportional adjustments to the other AQI
breakpoints (i.e., AQI values of 50, 150 and 200).  

The Agency recognizes the importance of revising the AQI in a timely
manner to be consistent with any revisions to the NAAQS.  Therefore,
having proposed to set a new level for the 2008 primary 8-hour O3
standard in this action, EPA also proposes to finalize conforming
changes to the AQI in connection with the Agency's final decision on the
level of the primary O3 standard.  These conforming changes would
include setting the 100 level of the AQI at the same level as that set
for the primary O3 standard resulting from this rulemaking, and also
making proportional adjustments to AQI breakpoints at the lower end of
the range (i.e., AQI values of 50, 150 and 200).  EPA does not propose
to change breakpoints at the higher end of the range (from 300 to 500),
which would apply to state contingency plans or the Significant Harm
Level (40 CFR 51.16), because the information from this reconsideration
of the 2008 final rule does not inform decisions about breakpoints at
those higher levels.

With respect to reporting requirements (40 CFR Part 58, §58.50), EPA
proposes to require that the AQI be reported in all metropolitan and
micropolitan statistical areas where O3 monitoring is required, as
discussed below in section VI.  The Agency solicits comments on our
proposed approach to AQI reporting requirements.  We are also revising
40 CFR Part 58, §58.50 (c) to require the reporting requirements to be
based on the latest available census figures, rather than the most
recent decennial U.S. census.  This change is consistent with our
current practice of using the latest population figures to make
monitoring requirements more responsive to changes in population.

IV. 	Rationale for Proposed Decision on the Secondary Standard

	As an initial matter, the Administrator notes that the 2008 final rule
concluded that (1) the protection afforded by the 1997 secondary O3
standard was “not sufficient and that the standard needs to be revised
to provide additional protection from known and anticipated adverse
effects on sensitive natural vegetation and sensitive ecosystems, and
that such a revised standard could also be expected to provide
additional protection to sensitive ornamental vegetation” and (2)
“that there is not adequate information to establish a separate
secondary standard based on other effects of O3 on public welfare” (73
FR 16497).  The Administrator is not reconsidering these aspects of the
2008 decision, which are based on the reasons discussed in section IV.B
of the 2008 final rule (73 FR 16489-16497).  The Administrator also
notes that the 2008 final rule concluded that it was appropriate to
retain the O3 indicator for the secondary O3 standard.   The
Administrator is not reconsidering this aspect of the 2008 decision,
which was based on the reasons discussed in sections IV.B and IV.C of
the 2008 final rule (73 FR 16489-16497).  For these reasons, the
Administrator is not reopening the 2008 decision with regard to the need
to revise the 1997 secondary O3 standard to provide additional
protection from known and anticipated adverse effects on sensitive
natural vegetation and sensitive ecosystems, nor with regard to the
appropriate indicator for the secondary standard.  Thus, the information
that follows in this section specifically focuses on a reconsideration
of the 8-hour secondary O3 standard set in the 2008 final rule for the
purpose of determining whether and, if so, how to revise the form,
averaging time, and level of the standard to provide appropriate
protection from known and anticipated adverse effects on sensitive
natural vegetation and sensitive ecosystems.

	This section presents the rationale for the Administrator’s proposed
decision that the secondary O3 standard, which was set identical to the
revised primary standard in the 2008 final rule, should instead be a new
cumulative, seasonal standard.  This standard is expressed in terms of a
concentration-weighted form commonly called W126, which uses a sigmoidal
weighting function to assign a weight to each hourly O3 concentration
within the 12 hour daylight period (8:00 am to 8:00 pm).   This daily
ozone index is defined as follows:

 .

 The daily index values are then summed over each month within the O3
season, and the annual highest consecutive three month sum is
determined.  The proposed standard consists of the three-year average of
this highest three-month statistic, set at a level within the range of 7
to 15 ppm-hours.

	As discussed more fully below, the rationale for this proposed new
standard is based on a thorough review, in the 2006 Criteria Document,
of the latest scientific information on vegetation, ecological and other
public welfare effects associated with the presence of O3 in the ambient
air.  This rationale also takes into account and is consistent with: 
(1) staff assessments of the most policy-relevant information in the
2006 Criteria Document and staff analyses of air quality, vegetation
effects evidence, exposure, and risks, presented in the 2007 Staff
Paper, upon which staff recommendations for revisions to the secondary
O3 standard are based; (2) CASAC advice and recommendations as reflected
in discussions of drafts of the 2006 Criteria Document and 2007 Staff
Paper at public meetings, in separate written comments, and in CASAC's
letters to the Administrator, both before and after the 2008 rulemaking,
and (3) public comments received during development of these documents,
either in conjunction with CASAC meetings or separately; and on the 2007
proposed rule, and (4) consideration of the degree of protection to
vegetation potentially afforded by the 2008 8-hour standard.

	In developing this rationale, the Administrator has again focused on
direct O3 effects on vegetation, specifically drawing upon an
integrative synthesis of the entire body of evidence (EPA, 2006a,
chapter 9), published through early 2006, on the broad array of
vegetation effects associated with the presence of O3 in the ambient
air.  In addition, because O3 can also indirectly affect other ecosystem
components such as soils, water, and wildlife, and their associated
ecosystem goods and services, through its effects on vegetation, a
qualitative discussion of these other indirect impacts is also included,
though these effects were not quantifiable at the time of the 2008
rulemaking.  As discussed below in section IV.A, the peer-reviewed
literature includes studies conducted in the U.S., Canada, Europe, and
many other countries around the world.  In reconsidering this evidence,
as was concluded in the 2008 rulemaking, and based on the body of
scientific literature assessed in the 2006 Criteria Document, the
Administrator continues to believes that it is reasonable to conclude
that a secondary standard protecting the public welfare from known or
anticipated adverse effects to trees and native vegetation would also
afford increased protection from adverse effects to other environmental
components relevant to the public welfare, including ecosystem services
and function.  Section IV.B focuses on considerations related to
biologically relevant exposure indices.  This rationale also draws upon
the results of quantitative exposure and risk assessments, discussed
below in section IV.C.  Section IV.D focuses on the considerations upon
which the Administrator’s proposed conclusions are based. 
Considerations regarding a cumulative seasonal standard as well as an
8-hour standard are discussed, and the rationale for the 2008 decision
on the secondary standard and CASAC advice, given both prior to the
development of the 2007 proposed rule and following the 2008 final rule,
are summarized.  Finally, the Administrator’s proposed conclusions on
the secondary standard are presented.  Section IV.E summarizes the
proposed decision on the secondary O3 standard and the solicitation of
public comments.

	As with virtually any policy-relevant vegetation effects research,
there is uncertainty in the characterization of vegetation effects
attributable to exposure to ambient O3.  As discussed below, however,
research conducted since the 1997 review provides important information
coming from field-based exposure studies, including free air, gradient,
and biomonitoring surveys, in addition to the more traditional open top
chamber (OTC) studies. Moreover, the newly available studies evaluated
in the 2006 Criteria Document have undergone intensive scrutiny through
multiple layers of peer review and many opportunities for public review
and comment.  While important uncertainties remain, the review of the
vegetation effects information has been extensive and deliberate.  In
the judgment of the Administrator, the intensive evaluation of the
scientific evidence that has occurred provides an adequate basis for
this reconsideration of the 2008 rulemaking.

A.	Vegetation Effects Information  

	This section outlines key information contained in the 2006 Criteria
Document (chapter 9) and in the 2007 Staff Paper (chapter 7) on known or
anticipated effects on public welfare associated with the presence of O3
in ambient air.  The information highlighted here summarizes: (1) new
information available in the 2008 rulemaking on potential mechanisms for
vegetation effects associated with exposure to O3; (2) the nature of
effects on vegetation that have been associated with exposure to O3 and
consequent potential impacts on ecosystems; and (3) considerations in
characterizing what constitutes an adverse welfare impact of O3.

	Exposures to O3 have been associated quantitatively and qualitatively
with a wide range of vegetation effects.  The decision in the 1997
review to set a more protective secondary standard primarily reflected
consideration of the quantitative information on vegetation effects
available at that time, particularly growth impairment (e.g., biomass
loss) in sensitive forest tree species during the seedling growth stage
and yield loss in important commercial crops.  This information, derived
mainly using the open top chamber (OTC) exposure method, found
cumulative, seasonal O3 exposures were most strongly associated with
observed vegetation response.  The 2006 Criteria Document discusses a
number of additional studies that support and strengthen key conclusions
regarding O3 effects on vegetation and ecosystems found in the previous
Criteria Document (EPA, 1996a, 2006a), including further clarification
of the underlying mechanistic and physiological processes at the
sub-cellular, cellular, and whole system levels within the plant.  More
importantly, however, in the context of this review, new quantitative
information is now available across a broader array of vegetation
effects (e.g., growth impairment during seedlings, saplings and mature
tree growth stages, visible foliar injury, and yield loss in annual
crops) and across a more diverse set of exposure methods, including
chamber, free air, gradient, model, and field-based observation.  The
non-chambered, field-based study results begin to address one of the key
data gaps cited by EPA in the 1997 review.  

	The following discussion of the policy-relevant science regarding
vegetation effects associated with cumulative, seasonal exposures to
ambient levels of O3 integrates information from the 2006 Criteria
Document (chapter 9) and the 2007 Staff Paper (chapter 7).  

1.	Mechanisms 

Scientific understanding regarding O3 impacts at the genetic,
physiological, and mechanistic levels helps to explain the biological
plausibility and coherence of the evidence for O3-induced vegetation
effects and informs the interpretation of predictions of risk associated
with vegetation response at ambient O3 exposure levels.  In most cases,
the mechanisms of response are similar regardless of the degree of
sensitivity of the species.  The evidence assessed in the 2006 Criteria
Document (EPA, 2006a) regarding the O3-induced changes in physiology
continues to support the information discussed in the 1997 review (EPA,
1996a, 2006a).  In addition, during the last decade understanding of the
cellular processes within plants has been further clarified and
enhanced.  This section reviews the key scientific conclusions
identified in 1996 Criteria Document (EPA, 1996a), and incorporates
recent information from the Criteria Document (EPA, 2006a).  This
section describes: (1) plant uptake of O3, (2) O3-induced cellular to
systemic response, (3) plant compensation and detoxification mechanisms,
(4) O3-induced changes to plant metabolism, and (5) plant response to
chronic O3 exposures.

a.	Plant Uptake of Ozone  

To cause injury, O3 must first enter the plant through openings in the
leaves called stomata.  Leaves exist in a three dimensional environment
called the plant canopy, where each leaf has a unique orientation and
receives a different exposure to ambient air, microclimatological
conditions, and sunlight.  In addition, a plant may be located within a
stand of other plants which further modifies ambient air exchange with
individual leaves.  Not all O3 entering a plant canopy is absorbed into
the leaf stomata, but may be adsorbed to other surfaces e.g., leaf
cuticles, stems, and soil (termed non-stomatal deposition) or scavenged
by reactions with intra-canopy biogenic VOCs and naturally occurring NOx
emissions from soils.  Because O3 does not typically penetrate the
leaf’s cuticle, it must reach the stomatal openings in the leaf for
absorption to occur.  The movement of O3 and other gases such as CO2
into and out of leaves is controlled by stomatal guard cells that
regulate the size of the stomatal apertures.  These guard cells respond
to a variety of internal species-specific factors as well as external
site specific environmental factors such as light, temperature,
humidity, CO2 concentration, soil fertility, water status, and in some
cases, the presence of air pollutants, including O3.  These modifying
factors produce stomatal conductances that vary between leaves of the
same plant, individuals and genotypes within a species as well as
diurnally and seasonally.  

b.	Cellular to Systemic Response  

Once inside the leaf, O3 can react with a variety of biochemical
compounds that are exposed to the air spaces within the leaf or it can
be dissolved into the water lining the cell wall of the air spaces. 
Once in the aqueous phase, O3 can be rapidly altered to form oxidative
products that can diffuse more readily into and through the cell and
react with many biochemical compounds.  Early steps in a series of
O3-induced events that can lead to leaf injury seems to involve
alteration in cell membrane function, including membrane transport
properties (EPA, 2006a) and/or reactions with organic molecules that in
certain circumstances result in the generation of signaling compounds. 
The generation of such signaling compounds can lead to a cascade of
events.  One such signaling molecule is hydrogen peroxide (H2O2). The
presence of higher-than-normal levels of H2O2 within the leaf is a
potential trigger for a set of metabolic reactions that include those
typical of the well documented “wounding” response or pathogen
defense pathway generated by cutting of the leaf or by pathogen/insect
attack.  Ethylene is another compound produced when plants are subjected
to biotic or abiotic stressors. Increased ethylene production by plants
exposed to O3 stress was identified as a consistent marker for O3
exposure in studies conducted decades ago (Tingey et al., 1976). 

c.	Compensation and Detoxification  

Ozone injury will not occur if (1) the rate and amount of O3 uptake is
small enough for the plant to detoxify or metabolize O3 or its
metabolites or (2) the plant is able to repair or compensate for the O3
impacts (Tingey and Taylor, 1982; U.S. EPA, 1996a).  With regard to the
first, a few studies have documented direct stomatal closure or
restriction in the presence of O3 in some species, which limits O3
uptake and potential subsequent injury.  This response may be initiated
ranging from within minutes to hours or days of exposure (Moldau et al.,
1990; Dann and Pell, 1989; Weber et al., 1993).  However, exclusion of
O3 simultaneously restricts the uptake of CO2, which also limits
photosynthesis and growth.  In addition, antioxidants present in plants
can effectively protect tissue against damage from low levels of
oxidants by dissipating excess oxidizing power.  Since 1996, the role of
detoxification in providing a level of resistance to O3 has been further
investigated.  A number of antioxidants have been found in plants. 
However, the pattern of changes in the amounts of these antioxidants
varies greatly among different species and conditions.  Most recent
reports indicate that ascorbate within the cell wall provides the first
significant opportunity for detoxification to occur.  In spite of the
new research, however, it is still not clear as to what extent
detoxification protects against O3 injury.  Specifically, data are
needed on potential rates of antioxidant production, sub-cellular
location(s) of antioxidants, and whether generation of these
antioxidants in response to O3-induced stress potentially diverts
resources and energy away from other vital uses.  Thus, the 2006
Criteria Document concludes that scientific understanding of the
detoxification mechanisms is not yet complete and requires further
investigation (EPA, 2006a). 

Regarding the second, once O3 injury has occurred in leaf tissue, some
plants are able to repair or compensate for the impacts.  In general,
plants have a variety of compensatory mechanisms for low levels of
stress including reallocation of resources, changes in root/shoot ratio,
production of new tissue, and/or biochemical shifts, such as increased
photosynthetic capacity in new foliage and changes in respiration rates,
indicating possible repair or replacement of damaged membranes or
enzymes.  Since these mechanisms are genetically determined, not all
plants have the same complement of compensatory mechanisms or degree of
tolerance, and these may vary over the life of the plant as not all
stages of a plant’s development are equally sensitive to O3.  At
higher levels or over longer periods of O3 stress, some of these
compensatory mechanisms, such as a reallocation of resources away from
storage in the roots in favor of leaves or shoots, could occur at a cost
to the overall health of the plant.  However, it is not yet clear to
what degree or how the use of plant resources for repair or compensatory
processes affects the overall carbohydrate budget or subsequent plant
response to O3 or other stresses (EPA, 1996a, EPA, 2006a).

d.	 Changes to Plant Metabolism  

Ozone inhibits photosynthesis, the process by which plants produce
energy rich compounds (e.g., carbohydrates) in the leaves.  This
impairment can result from direct impact to chloroplast function and/or
O3-induced stomatal closure resulting in reduced uptake of CO2.  A large
body of literature published since 1996 has further elucidated the
mechanism of effect of O3 within the chloroplast.  Pell et al. (1997)
showed that O3 exposure results in a loss of the central carboxylating
enzyme that plays an important role in the production of carbohydrates. 
Due to its central importance, any decrease in this enzyme may have
severe consequences for the plant’s productivity.  Several recent
studies have found that O3 has a greater effect as leaves age, with the
greatest impact of O3 occurring on the oldest leaves (Fiscus et al.,
1997; Reid and Fiscus, 1998; Noormets et al., 2001; Morgan et al.,
2004).  The loss of this key enzyme as a function of increasing O3
exposure is also linked to an early senescence or a speeding up of
normal development leading to senescence.  If total plant photosynthesis
is sufficiently reduced, the plant will respond by reallocating the
remaining carbohydrate at the level of the whole organism (EPA, 1996a,
2006a).  This reallocation of carbohydrate away from the roots into
above ground vegetative components can have serious implications for
perennial species, as discussed below.

e.	Plant Response to Chronic Ozone Exposures  

Though many changes that occur with O3 exposure can be observed within
hours, or perhaps days, of the exposure, including those connected with
wounding, other effects take longer to occur and tend to become most
obvious after chronic seasonal exposures to low O3 concentrations. 
These lower chronic exposures have been linked to senescence or some
other physiological response very closely linked to senescence.  In
perennial plant species, a reduction in carbohydrate storage in one year
may result in the limitation of growth the following year (Andersen et
al., 1997).  Such “carry-over” effects have been documented in the
growth of tree seedlings (Hogsett et al., 1989; Sasek et al., 1991;
Temple et al., 1993; EPA, 1996a) and in roots (Andersen et al., 1991;
EPA, 1996a).  Though it is not fully understood how chronic seasonal O3
exposure affects long-term growth and resistance to other biotic and
abiotic insults in long-lived trees, accumulation of these carry-over
effects over time could affect survival and reproduction.  

2.	Nature of Effects

Ozone injury at the cellular level can accumulate sufficiently to induce
effects at the level of a whole leaf or plant.  These larger scale
effects can include: reduced carbohydrate production and/or
reallocation; reduced growth and/or reproduction; visible foliar injury
and/or premature senescence; and reduced plant vigor.  Much of what is
now known about these O3-related effects, as summarized below, is based
on research that was available in the 1997 review.  Studies available in
the 2008 rulemaking continue to support and expand this knowledge (EPA,
2006a). 

a.	 Carbohydrate Production and Allocation  

	When total plant photosynthesis is sufficiently reduced, the plant will
respond by reallocating the remaining carbohydrate at the level of the
whole organism.  Many studies have demonstrated that root growth is more
sensitive to O3 exposure than stem or leaf growth (EPA, 2006a). When
fewer carbohydrates are present in the roots, less energy is available
for root-related functions such as acquisition of water and nutrients. 
In addition, by inhibiting photosynthesis and the amount of
carbohydrates available for transfer to the roots, O3 can disrupt the
association between soil fungi and host plants.  Fungi in the soil form
a symbiotic relationship with many terrestrial plants.  For host plants,
these fungi improve the uptake of nutrients, protect the roots against
pathogens, produce plant growth hormones, and may transport
carbohydrates from one plant to another (EPA, 1996a).  These below
ground effects have recently been documented in the field (Grulke et
al., 1998; Grulke and Balduman, 1999).  Data from a long-studied
pollution gradient in the San Bernardino Mountains of southern
California suggest that O3 substantially reduces root growth in natural
stands of Ponderosa pine (Pinus ponderosa).  Root growth in mature trees
was decreased at least 87 percent in a high-pollution site as compared
to a low-pollution site (Grulke et al., 1998), and a similar pattern was
found in a separate study with whole-tree harvest along this gradient
(Grulke and Balduman, 1999).  Though effects on other ecosystem
components were not examined, a reduction of root growth of this
magnitude could have significant implications for the below-ground
communities at those sites.  Because effects on leaf and needle
carbohydrate content under O3 stress can range from a reduction (Barnes
et al., 1990; Miller et al., 1989), to no effect (Alscher et al., 1989),
to an increase (Luethy-Krause and Landolt, 1990), studies that examine
only above-ground vegetative components may miss important O3-induced
changes below ground.  These below-ground changes could signal a shift
in nutrient cycling with significance at the ecosystem level (Young and
Sanzone, 2002).  

b.	Growth Effects on Trees

	Studies comparing the O3-related growth response of different
vegetation types (coniferous and deciduous) and growth stages (e.g.,
seedling and mature) have established that on average, individual
coniferous trees are less sensitive than deciduous trees, and deciduous
trees are generally less sensitive to O3 than most annual plants, with
the exception of a few fast growing deciduous tree species (e.g.,
quaking aspen, black cherry, and cottonwood), which are highly sensitive
and, in some cases, as much or more sensitive to O3 than sensitive
annual plants.  In addition, studies have shown that the relationship
between O3 sensitivity in seedling and mature growth stages of trees can
vary widely, with seedling growth being more sensitive to O3 exposures
in some species, while in others, the mature growth stage is the more O3
sensitive.  In general, mature deciduous trees are likely to be more
sensitive to O3 than deciduous seedlings, and mature evergreen trees are
likely to be less sensitive to O3 than their seedling counterparts. 
Based on these results, stomatal conductance, O3 uptake, and O3 effects
cannot be assumed to be equivalent in seedlings and mature trees.

In the 1997 review (EPA, 1996b), analyses of the effects of O3 on trees
were limited to 11 tree species for which concentration-response (C-R)
functions for the seedling growth stage had been developed from OTC
studies conducted by the National Health and Environmental Effects
Research Lab, Western Ecology Division (NHEERL-WED).  A number of
replicate studies were conducted on these species, leading to a total of
49 experimental cases.  The 2007 Staff Paper presented a graph of the
composite regression equation that combines the results of the C-R
functions developed for each of the 49 cases.  The NHEERL-WED study
predicted relative biomass loss at various exposure levels in terms of a
12-hour W126.  For example, 50 percent of the tree seedling cases would
be protected from greater than 10 percent biomass loss at a 3-month,
12-hour W126 of approximately 24 ppm-hour, while 75 percent of cases
would be protected from 10 percent biomass loss at a 3-month, 12-hour
W126 level of approximately 16 ppm-hour.

Since the 1997 review, only a few studies have developed C-R functions
for additional tree seedling species (EPA, 2006a).  One such study is of
particular importance because it documented growth effects in the field
of a similar magnitude as those previously seen in OTC studies but
without the use of chambers or other fumigation methods (Gregg et al.,
2003).  This study placed eastern cottonwood (Populus deltoides)
saplings at sites along a continuum of ambient O3 exposures that
gradually increased from urban to rural areas in the New York City area
(Gregg et al., 2003).  Eastern cottonwood is a fast growing O3 sensitive
tree species that is important ecologically along streams and
commercially for pulpwood, furniture manufacturing, and as a possible
new source for energy biomass (Burns and Hankola, 1990).  Gregg et al.
(2003) found that the cottonwood saplings grown in urban New York City
grew faster than saplings grown in downwind rural areas.  Because these
saplings were grown in pots with carefully controlled soil nutrient and
moisture levels, the authors were able to control for most of the
differences between sites. After carefully considering these and other
factors, the authors concluded the primary explanation for the
difference in growth was the gradient of cumulative O3 exposures that
increased as one moved downwind from urban to less urban and more rural
sites.  It was determined that the lower O3 exposure within the city
center was due to NOx titration reactions which removed O3 from the
ambient air.  The authors were able to reproduce the growth responses
observed in the field in a companion OTC experiment, confirming O3 as
the stressor inducing the growth loss response (Gregg et al., 2003).  

Another recent set of studies employed a modified Free Air CO2
Enrichment (FACE) methodology to expose vegetation to elevated O3
without the use of chambers.  This exposure method was originally
developed to expose vegetation to elevated levels of CO2, but was later
modified to include O3 exposure in Illinois (SoyFACE) and Wisconsin
(AspenFACE) for soybean and deciduous trees, respectively (Dickson et
al., 2000; Morgan et al., 2004).  The FACE method releases gas (e.g.,
CO2, O3) from a series of orifices placed along the length of the
vertical pipes surrounding a circular field plot and uses the prevailing
wind to distribute it. This exposure method has many characteristics
that differ from those associated with the OTC.  Most significantly,
this exposure method more closely replicates conditions in the field
than do OTCs.  This is because, except for O3 levels which are varied
across co-located plots, plants are exposed to the same ambient growing
conditions that occur naturally in the field (e.g., location-specific
pollutant mixtures; climate conditions such as light, temperature and
precipitation; insect pests, pathogens).  By using one of several
co-located plots as a control (e.g., receives no additional O3), and by
exposing the other rings to differing levels of elevated O3, the growth
response signal that is due solely to the change in O3 exposure can be
clearly determined.  Furthermore, the FACE system can expand vertically
with the growth of trees, allowing for exposure experiments to span
numerous years, an especially useful capability in forest research.  

On the other hand, the FACE methodology also has the undesirable
characteristic of potentially creating hotspots near O3 gas release
orifices or gradients of exposure in the outer ring of trees within the
plots, such that averaging results across the entire ring potentially
overestimates the response.  In recognition of this possibility,
researchers at the AspenFACE experimental site only measured trees in
the center core of each ring, (e.g., at least 5-6 meters away from the
emission sites of O3) (Dickson et al 2000, Karnosky et al. 2005).  By
taking this precaution, it is unlikely that their measurements were
influenced by any potential hotspots or gradients of exposure within the
FACE rings.  Taking all of the above into account, results from the
Wisconsin FACE site on quaking aspen appear to demonstrate that the
detrimental effects of O3 exposure seen on tree growth and symptom
expression in OTCs can be observed in the field using this exposure
method (Karnosky et al., 1999; 2005).  

The 2007 Staff Paper thus concluded that the combined evidence from the
AspenFACE and Gregg et al. (2003) field studies provide compelling and
important support for the appropriateness of continued use of the C-R
functions derived using OTC from the NHEERL-WED studies to estimate risk
to these tree seedlings under ambient field exposure conditions.  These
studies make a significant contribution to the coherence of the weight
of evidence available in this review and provide additional evidence
that O3-induced effects observed in chambers also occur in the field.  

Trees and other perennials, in addition to cumulating the effects of O3
exposures over the annual growing season, can also cumulate effects
across multiple years.  It has been reported that effects can “carry
over” from one year to another (EPA, 2006a).  Growth affected by a
reduction in carbohydrate storage in one year may result in the
limitation of growth in the following year (Andersen, et al., 1997). 
Carry-over effects have been documented in the growth of some tree
seedlings (Hogsett et al. 1989; Simini et al., 1992; Temple et al.,
1993) and in roots (Andersen et al., 1991; EPA, 1996a).  On the basis of
past and recent OTC and field study data, ambient O3 exposures that
occur during the growing season in the United States are sufficient to
potentially affect the annual growth of a number of sensitive seedling
tree species.  However, because most studies do not take into account
the possibility of carry over effects on growth in subsequent years, the
true implication of these annual biomass losses may be missed.  It is
likely that under ambient exposure conditions, some sensitive trees and
perennial plants could experience compounded impacts that result from
multiple year exposures.

c.	Visible Foliar Injury  

Cellular injury to leaves due to exposure to O3 can and often does
become visible.  Acute injury usually appears within 24 hours after
exposure to O3 and, depending on species, can occur under a range of
exposures and durations from 0.040 ppm for a period of 4 hours to 0.410
ppm for 0.5 hours for crops and 0.060 ppm for 4 hours to 0.510 ppm for 1
hour for trees and shrubs (Jacobson, 1977). Chronic injury may be mild
to severe. In some cases, cell death or premature leaf senescence may
occur.  The significance of O3 injury at the leaf and whole plant levels
depends on how much of the total leaf area of the plant has been
affected, as well as the plant’s age, size, developmental stage, and
degree of functional redundancy among the existing leaf area.  As a
result, it is not presently possible to determine, with consistency
across species and environments, what degree of injury at the leaf level
has significance to the vigor of the whole plant.  

The presence of visible symptoms due to O3 exposures can, however, by
itself, represent an adverse impact to the public welfare. 
Specifically, it can reduce the market value of certain leafy crops
(such as spinach, lettuce), impact the aesthetic value of ornamentals
(such as petunia, geranium, and poinsettia) in urban landscapes, and
affect the aesthetic value of scenic vistas in protected natural areas
such as national parks and wilderness areas.  Many businesses rely on
healthy looking vegetation for their livelihoods (e.g.,
horticulturalists, landscapers, Christmas tree growers, farmers of leafy
crops) and a variety of ornamental species have been listed as sensitive
to O3 (Abt Associates Inc, 1995).  Though not quantified, there is
likely some level of economic impact to businesses and homeowners from
O3-related injury on sensitive ornamental species due to the cost
associated with more frequent replacement and/or increased maintenance
(fertilizer or pesticide application).  In addition, because O3 not only
results in discoloration of leaves but can lead to more rapid senescence
(early shedding of leaves) there potentially could be some lost tourist
dollars at sites where fall foliage is less available or attractive.  

T  SEQ CHAPTER \h \r 1 he use of sensitive plants as biological
indicators to detect phytotoxic levels of O3 is a longstanding and
effective methodology (Chappelka and Samuelson, 1998; Manning and Krupa,
1992).  Each bioindicator exhibits typical O3 injury symptoms when
exposed under appropriate conditions.  These symptoms are considered
diagnostic as they have been verified in exposure-response studies under
experimental conditions.  In recent years, field surveys of visible
foliar injury symptoms have become more common, with greater attention
to the standardization of methods and the use of reliable indicator
species (Campbell et al., 2000; Smith et al., 2003). Specifically, the
Unites States Forest Service (USFS) through the Forest Health Monitoring
Program (FHM) (1990 - 2001) and currently the Forest Inventory and
Analysis (FIA) Program collects data regarding the incidence and
severity of visible foliar injury on a variety of O3 sensitive plant
species throughout the U.S. (Coulston et al. 2003, 2004; Smith et al.
2003). 

	Since the conclusion of the 1997 review, the FIA monitoring program
network and database has continued to expand.  This network continues to
document foliar injury symptoms in the field under ambient exposure
conditions.  Recent survey results show that O3-induced foliar injury
incidence is widespread across the country.  The visible foliar injury
indicator has been identified as a means to track O3 exposure stress
trends in the nation’s natural plant communities as highlighted in
EPA’s most recent Report on the Environment (EPA, 2003a;
http://www.epa.gov/indicators/roe).  

Previous Criteria Documents have noted the difficulty in relating
visible foliar injury symptoms to other vegetation effects such as
individual tree growth, stand growth, or ecosystem characteristics (EPA,
1996a) and this difficulty remains to the present day (EPA, 2006a).  It
is important to note that direct links between O3 induced visible foliar
injury symptoms and other adverse effects are not always found. 
Therefore, visible foliar injury cannot serve as a reliable surrogate
measure for other O3-related vegetation effects because other effects
(e.g., biomass loss) have been reported with and without visible injury.
 In some cases, visible foliar symptoms have been correlated with
decreased vegetative growth (Karnosky et al., 1996; Peterson et al.,
1987; Somers et al., 1998) and with impaired reproductive function
(Black et al., 2000; Chappelka, 2002).  Therefore, the lack of visible
injury should not be construed to indicate a lack of phytotoxic
concentrations of O3 nor absence of other non-visible O3 effects.

d.	Reduced Plant Vigor  

Though O3 levels over most of the U.S. are not high enough to kill
vegetation directly, current levels have been shown to reduce the
ability of many sensitive species and genotypes within species to adapt
to or withstand other environmental stresses.  These O3 effects may
include increased susceptibility to freezing temperatures, increased
vulnerability to pest infestations and/or root disease, and compromised
ability to compete for available resources.  As an example of the
latter, when species with differing O3-sensitivities occur together,
O3-sensitive species may experience a greater reduction in growth than
more O3-tolerant species, which then can better compete for available
resources.  The result of such above effects can produce a loss in plant
vigor in O3-sensitive species that over time may lead to premature plant
death.

Ecosystems  

Ecosystems are comprised of complex assemblages of organisms and the
physical environment with which they interact.  Each level of
organization within an ecosystem has functional and structural
characteristics.  At the ecosystem level, functional characteristics
include, but are not limited to, energy flow; nutrient, hydrologic, and
biogeochemical cycling; and maintenance of food chains.  The sum of the
functions carried out by ecosystem components provides many benefits to
humankind, as in the case of forest ecosystems (Smith, 1992).  Some of
these benefits, also termed “ecosystem goods and services”, include
food, fiber production, aesthetics, genetic diversity, maintenance of
water quality, air quality, and climate, and energy exchange.  A
conceptual framework for discussing the effects of stressors, including
air pollutants such as O3, on ecosystems was developed by the EPA
Science Advisory Board (Young and Sanzone, 2002).  In this report, the
authors identify six essential ecological attributes (EEAs) of
ecosystems including landscape condition, biotic condition,
chemical/physical condition, ecological processes,
hydrology/geomorphology, and natural disturbance regime.  Each EEA is
depicted as one of six triangles that together build a hexagon.  On the
outside of each triangle is a list of stressors that can act on the EEA.
 Tropospheric O3 is listed as a stressor of both biotic condition and
the chemical/physical condition of ecosystems.  As each EEA is linked to
all the others, it is clearly envisioned in this framework that O3 could
either directly or indirectly impact all of the EEAs associated with an
ecosystem that is being stressed by O3.  

Vegetation often plays an influential role in defining the structure and
function of an ecosystem, as evidenced by the use of dominant vegetation
forms to classify many types of natural ecosystems, e.g., tundra,
wetland, deciduous forest, and conifer forest.  Plants simultaneously
inhabit both above-and below-ground environments, integrating and
influencing key ecosystem cycles of energy, water, and nutrients.  When
a sufficient number of individual plants within a community have been
affected, O3-related effects can be propagated up to ecosystem-level
effects.  Thus, through its impact on vegetation, O3 can be an important
ecosystem stressor.  

i.	Potential Ozone Alteration of Ecosystem Structure and Function

	The 2006 Criteria Document outlines seven case studies where O3 effects
on ecosystems have either been documented or are suspected.  The oldest
and clearest example involves the San Bernardino Mountain forest
ecosystem in California.  This system experienced chronic high O3
exposures over a period of 50 or more years.  The O3-sensitive and
co-dominant species of ponderosa and Jeffrey pine demonstrated severe
levels of foliar injury, premature senescence, and needle fall that
decreased the photosynthetic capacity of stressed pines and reduced the
production of carbohydrates resulting in a decrease in radial growth and
in the height of stressed trees.  It was also observed that ponderosa
and Jeffrey pines with slight to severe crown injury lost basal area in
relation to competing species that are more tolerant to O3.  Due to a
loss of vigor, these trees eventually succumbed to the bark beetle,
leading to elevated levels of tree death.  Increased mortality of
susceptible trees shifted the community composition towards white fir
and incense cedar, effectively reversing the development of the normal
fire climax mixture dominated by ponderosa and Jeffrey pines, and
leading to increased fire susceptibility.  At the same time, numerous
other organisms and processes were also affected either directly or
indirectly, including successional patterns of fungal microflora and
their relationship to the decomposer community.  Nutrient availability
was influenced by the heavy litter and thick needle layer under stands
with the most severe needle injury and defoliation.  In this example, O3
appeared to be a predisposing factor that led to increased drought
stress, windthrow, root diseases, and insect infestation (Takemoto et
al., 2001).  Thus, through its effects on tree water balance, cold
hardiness, tolerance to wind, and susceptibility to insect and disease
pests, O3 potentially impacted the ecosystem-related EEA of natural
disturbance regime (e.g., fire, erosion).  Although the role of O3 was
extremely difficult to separate from other confounding factors, such as
high nitrogen deposition, there is evidence that this shift in species
composition has altered the structure and dynamics of associated food
webs (Pronos et al., 1999) and carbon (C) and nitrogen (N) cycling
(Arbaugh et al., 2003).  Ongoing and new research in this important
ecosystem is needed to reveal the extent to which ecosystem services
have been affected and to what extent strong causal linkages between
historic and/or current ambient O3 exposures and observed
ecosystem-level effects can be made. 

	Ozone has also been reported to be a selective pressure among sensitive
tree species (e.g., eastern white pine) in the east.  The nature of
community dynamics in eastern forests is different, however, than in the
west, consisting of a wider diversity of species and uneven aged stands,
and the O3 levels are less severe.  Therefore, lower level chronic O3
stress in the east is more likely to produce subtle long-term forest
responses such as shifts in species composition, rather than wide-spread
community degradation.  

	Some of the best-documented studies of population and community
response to O3 effects are the long-term studies of common plantain
(Plantago major) in native plant communities in the United Kingdom
(Davison and Reiling, 1995; Lyons et al., 1997; Reiling and Davison,
1992c).  Elevated O3 significantly decreased the growth of sensitive
populations of common plantain (Pearson et al., 1996; Reiling and
Davison, 1992a, b; Whitfield et al., 1997) and reduced its fitness as
determined by decreased reproductive success (Pearson et al., 1996;
Reiling and Davison, 1992a).  While spatial comparisons of population
responses to O3 are complicated by other environmental factors, rapid
changes in O3 resistance were imposed by ambient levels and variations
in O3 exposure (Davison and Reiling, 1995).  Specifically, in this case
study, it appeared that O3-sensitive individuals are being removed by O3
stress and the genetic variation represented in the population could be
declining.  If genetic diversity and variation is lost in ecosystems,
there may be increased vulnerability of the system to other biotic and
abiotic stressors, and ultimately a change in the EEAs and associated
services provided by those ecosystems.

	Recent free-air exposure experiments have also provided new insight
into how O3 may be altering ecosystem structure and function (Karnosky
et al., 2005).  For example, a field O3 exposure experiment at the
AspenFACE site in Wisconsin (described in section IV.A.2.b. above) was
designed to examine the effects of both elevated CO2 and O3  on mixed
stands of aspen (Populus tremuloides), birch (Betula papyrifera), and
sugar maple (Acer saccharum) that are characteristic of Great Lakes
aspen-dominated forests (Karnosky et al., 2003; Karnosky et al., 1999). 
They found evidence that the effects on above- and below-ground growth
and physiological processes have cascaded through the ecosystem, even
affecting microbial communities (Larson et al., 2002; Phillips et al.,
2002).  This study also confirmed earlier observations of O3-induced
changes in trophic interactions involving keystone tree species, as well
as important insect pests and their natural enemies (Awmack et al.,
2004; Holton et al., 2003; Percy et al., 2002). 

	Collectively these examples suggest that O3 is an important stressor in
natural ecosystems, but it is difficult to quantify the contribution of
O3 due to the combination of other stresses present in ecosystems.  In
most cases, because only a few components in each of these ecosystems
have been examined and characterized for O3 effects, the full extent of
ecosystem changes in these example ecosystems is not fully understood. 
Clearly, there is a need for highly integrated ecosystem studies that
specifically investigate the effect of O3 on ecosystem structure and
function in order to fully determine the extent to which O3 is altering
ecosystem services.  Continued research, employing new approaches, will
be necessary to fully understand the extent to which O3 is affecting
ecosystem services.

ii.	Effects on Ecosystem Services and Carbon Sequestration  

Since it has been established that O3 affects photosynthesis and growth
of plants, O3 is most likely affecting the productivity of forest
ecosystems.  Therefore, it is desirable to link effects on growth and
productivity to essential ecosystem services.  However, it is very
difficult to quantify ecosystem-level productivity losses because of the
amount of complexity in scaling from the leaf-level or individual plant
to the ecosystem level, and because not all organisms in an ecosystem
are equally affected by O3.

	Terrestrial ecosystems are important in the Earth's carbon (C) balance
and could help offset emissions of CO2 by humans if anthropogenic C is
sequestered in vegetation and soils.  The annual increase in atmospheric
CO2 is less than the total inputs from fossil fuel burning and land use
changes (Prentice et al., 2001), and much of this discrepancy is thought
to be attributable to CO2 uptake by plant photosynthesis (Tans & White,
1998).  Temperate forests of the northern hemisphere have been estimated
to be a net sink of about 0.6 to 0.7 petagrams (Pg) C per year (Goodale
et al. 2002).  Ozone interferes with photosynthesis, causes some plants
to senesce leaves prematurely, and in some cases, reduces allocation to
stem and root tissue.  Thus, O3 decreases the potential for C
sequestration.  For the purposes of this discussion, C sequestration is
defined as the net exchange of carbon by the terrestrial biosphere. 
However, long-term storage in the soil organic matter is considered to
be the most stable form of C storage in ecosystems.

	In a study including all ecosystem types, Felzer et al. (2004),
estimated that U.S. net primary production (net flux of C into an
ecosystem) was decreased by 2.6-6.8 percent due to O3 pollution in the
late 1980's to early 1990's.  Ozone not only reduces C sequestration in
existing forests, it can also affect reforestation projects (Beedlow et
al. 2004).  This effect, in turn, has been found to ultimately inhibit C
sequestration in forest soils which act as long-term C storage (Loya et
al., 2003; Beedlow et al. 2004).  The interaction of rising O3 pollution
and rising CO2 concentrations in the coming decades complicates
predictions of future sequestration potential.  Models generally predict
that, in the future, C sequestration will increase with increasing CO2,
but often do not account for the decrease in productivity due to the
local effects of current or potentially increasing levels of
tropospheric O3.  In the presence of high O3 levels, the stimulatory
effect of rising CO2 concentrations on forest productivity has been
estimated to be reduced by more that 20 percent (Tingey et al., 2001;
Ollinger et al. 2002; Karnosky et al., 2003). 

	In summary, it would be anticipated that meeting lower O3 standards
would increase the amount of CO2 uptake by many ecosystems in the U.S. 
However, the amount of this improvement would be heavily dependent on
the species composition of those ecosystems.  Many ecosystems in the
U.S. do have O3 sensitive plants.  For, example forest ecosystems with
dominant species such as aspen or ponderosa pine would be expected to
increase CO2 uptake more with lower O3 than forests with more O3
tolerant species.

	A recent critique of the secondary NAAQS review process published in
the report by the National Academy of Sciences on Air Quality Management
in the United States (NRC, 2004) stated that “EPA’s current practice
for setting secondary standards for most criteria pollutants does not
appear to be sufficiently protective of sensitive crops and
ecosystems...”  This report made several specific recommendations for
improving the secondary NAAQS process and concluded that “There is
growing evidence that tighter standards to protect sensitive ecosystems
in the United States are needed....”  An effort has been recently
initiated within the Agency to identify indicators of ecological
condition whose responses can be clearly linked to changes in air
quality that are attributable to Agency environmental programs.  Using a
single indicator to represent the complex linkages and dynamic cycles
that define ecosystem condition will always have limitations.  With
respect to O3-related impacts on ecosystem condition, only two candidate
indicators, foliar injury (as described above) and radial growth in
trees, have been suggested.  Thus, while at the present time, most
O3-related effects on ecosystems must be inferred from observed or
predicted O3-related effects on individual plants, additional research
at the ecosystem level could identify new indicators and/or establish
stronger causal linkages between O3-induced plant effects and ecosystem
condition.  

f.	Yield Reductions in Crops 

	Ozone can interfere with carbon gain (photosynthesis) and allocation of
carbon with or without the presence of visible foliar injury.  As a
result of decreased carbohydrate availability, fewer carbohydrates are
available for plant growth, reproduction, and/or yield.  Recent studies
have further confirmed and demonstrated O3 effects on different stages
of plant reproduction, including pollen germination, pollen tube growth,
fertilization, and abortion of reproductive structures, as reviewed by
Black et al. (2000).  For seed-bearing plants, these reproductive
effects will culminate in reduced seed production or yield.  

	As described in the 1997 review and again in the 2006 Criteria Document
and 2007 Staff Paper, the National Crop Loss Assessment Network (NCLAN)
studies undertaken in the early to mid-1980's provide the largest, most
uniform database on the effects of O3 on agricultural crop yields.  The
NCLAN protocol was designed to produce crop exposure-response data
representative of the areas in the U.S. where the crops were typically
grown.  In total, 15 species (e.g., corn, soybean, winter wheat,
tobacco, sorghum, cotton, barley, peanuts, dry beans, potato, lettuce,
turnip, and hay [alfalfa, clover, and fescue]), accounting for greater
than 85 percent of U.S. agricultural acreage planted at that time, were
studied.  Of these 15 species, 13 species including 38 different
cultivars were combined in 54 cases representing unique combinations of
cultivars, sites, water regimes, and exposure conditions.  Crops were
grown under typical farm conditions and exposed in open-top chambers to
ambient O3, sub-ambient O3, and above ambient O3.  Robust C-R functions
were developed for each of these crop species.  These results showed
that 50 percent of the studied cases would be protected from greater
than 10 percent yield loss at a W126 level of 21 ppm-hour, while a W126
of 13 ppm-hour would provide protection for 75 percent of the cases
studied from greater than 10 percent yield loss.  

	Recent studies continue to find yield loss levels in crop species
studied previously under NCLAN that reflect the earlier findings.  In
other words, there has been no evidence that crops are becoming more
tolerant of O3 (EPA, 2006a).  For cotton, some newer varieties have been
found to have higher yield loss due to O3 compared to older varieties
(Olszyk et al., 1993, Grantz and McCool, 1992).  In a meta-analysis of
53 studies, Morgan et al. (2003) found consistent deleterious effects of
O3 exposures on soybean from studies published between 1973 and 2001. 
Further, early results from the field-based exposure experiment SoyFACE
in Illinois indicate a lack of any apparent difference in the O3
tolerance of old and recent cultivars of soybean in a study of 22
soybean varieties (Long et al., 2002).  Thus, the 2007 Staff Paper
concluded that the recent scientific literature continues to support the
conclusions of the 1996 Criteria Document that ambient O3 concentrations
are reducing the yield of major crops in the U.S.

	In addition to the effects described on annual crop species, several
studies published since the 1997 review have focused on perennial forage
crops (EPA, 2006a).  These recent results confirm that O3 is also
impacting yields and quality of multiple-year forage crops at sufficient
magnitude to have nutritional and possibly economic implications to
their use as ruminant animal feed at O3 exposures that occur in some
years over large areas of the U.S.  

3.	Adversity of Effects

The 2007 Staff Paper recognized that the statute requires that a
secondary standard be protective against “adverse” O3 effects, not
all identifiable O3-induced effects.  In considering what constitutes a
vegetation effect that is adverse to the public welfare, the 2007 Staff
Paper recognizes that O3 can cause a variety of vegetation effects,
beginning at the level of the individual cell and accumulating up to the
level of whole leaves, plants, plant populations, communities and whole
ecosystems, not all of which have been classified in past reviews as
“adverse” to public welfare.  

Previous reviews have classified O3 vegetation effects as either
“injury” or “damage” to help in determining adversity. 
Specifically, “injury” is defined as encompassing all plant
reactions, including reversible changes or changes in plant metabolism
(e.g., altered photosynthetic rate), altered plant quality, or reduced
growth, that does not impair the intended use or value of the plant
(Guderian, 1977).  In contrast, “damage” has been defined to include
those injury effects that reach sufficient magnitude as to also reduce
or impair the intended use or value of the plant.  Examples of effects
that are classified as damage include reductions in aesthetic values
(e.g., foliar injury in ornamental species) as well as losses in terms
of weight, number, or size of the plant part that is harvested (reduced
yield or biomass production).  Yield loss also may include changes in
crop quality, i.e., physical appearance, chemical composition, or the
ability to withstand storage, while biomass loss includes slower growth
in species harvested for timber or other fiber uses.  While this
construct has proved useful in the past, it appears to be most useful in
the context of evaluating effects on single plants or species grown in
monocultures such as agricultural crops or managed forests.  It is less
clear how it might apply to potential effects on natural forests or
entire ecosystems when O3-induced species level impacts lead to shifts
in species composition and/or associated ecosystem services such as
nutrient cycling or hydrologic cycles, where the intended use or value
of the system has not been specifically identified.

	A more recent construct for assessing risks to forests described in
Hogsett et al. (1997) suggests that “adverse effects could be
classified into one or more of the following categories: (1) economic
production, (2) ecological structure, (3) genetic resources, and (4)
cultural values.”  This approach expands the context for evaluating
the adversity of O3-related effects beyond the species level.  Another
recent publication, A Framework for Assessing and Reporting on
Ecological Condition: an SAB report (Young and Sanzone, 2002), provides
additional support for  expanding the consideration of adversity beyond
the species level by making explicit the linkages between stress-
related effects (e.g., O3 exposure) at the species level and at higher
levels within an ecosystem hierarchy.  Taking this recent literature
into account, the 2007 Staff Paper concludes that a determination of
what constitutes an “adverse” welfare effect in the context of the
secondary NAAQS review can appropriately occur within this broader
paradigm.

B.	Biologically Relevant Exposure Indices

	The 2006 Criteria Document concluded that O3 exposure indices that
cumulate differentially weighted hourly concentrations are the best
candidates for relating exposure to plant growth responses.  This
conclusion follows from the extensive evaluation of the relevant studies
in the 1996 Criteria Document (EPA, 1996a) and the recent evaluation of
studies that have been published since that time.  The following
selections, taken from the 1996 Criteria Document (EPA, 1996a, section
5.5), further elucidate the depth and strength of these conclusions. 
Specifically, with respect to the importance of taking into account
exposure duration, the 1996 Criteria Document stated, “when O3 effects
are the primary cause of variation in plant response, plants from
replicate studies of varying duration showed greater reductions in yield
or growth when exposed for the longer duration” and “the mean
exposure index of unspecified duration could not account for the
year-to-year variation in response” (EPA, 1996a, pg. 5-96).  Further,
“because the mean exposure index treats all concentrations equally and
does not specifically include an exposure duration component, the use of
a mean exposure index for characterizing plant exposures appears
inappropriate for relating exposure with vegetation effects” (EPA,
1996a, pg. 5-88).  Regarding the relative importance of higher
concentrations than lower in determining plant response, the 1996
Criteria Document concluded that “the ultimate impact of long-term
exposures to O3 on crops and seedling biomass response depends on the
integration of repeated peak concentrations during the growth of the
plant” (EPA, 1996a, pg. 5-104).  Further, “at this time, exposure
indices that weight the hourly O3 concentrations differentially appear
to be the best candidates for relating exposure with predicted plant
response” (EPA, 1996a, pgs. 5-136).  

	At the conclusion of the 1997 review, the biological basis for a
cumulative, seasonal form was not in dispute.  There was general
agreement between EPA and CASAC, based on their review of the air
quality criteria, that a cumulative, seasonal form was more biologically
based than the then current 1-hour and newly proposed 8-hour average
form.  However, in selecting a specific form appropriate for a secondary
standard, there was less agreement.  An evaluation of the performance of
several  cumulative seasonal forms in predicting plant response data
taken from OTC experiments had found that all performed about equally
well and was unable to distinguish between them (EPA, 1996a).  In
selecting between two of these cumulative forms, the SUM06 and W126, in
the absence of biological evidence to distinguish between them, EPA
based its decision on both science and policy considerations. 
Specifically, these were: (1) all cumulative, peak-weighted exposure
indices considered, including W126 and SUM06, were about equally good as
exposure measures to predict exposure-response relationships reported in
the NCLAN crop studies; and (2) the SUM06 form would not be influenced
by PRB O3 concentrations (defined at the time as 0.03 to 0.05 ppm) under
many typical air quality distributions.  On the basis of these
considerations, EPA chose the SUM06 as the most appropriate cumulative,
seasonal form to consider when proposing an alternative secondary
standard form (61 FR 65716). 

	Though the scientific justification for a cumulative, seasonal form was
generally accepted in the 1997 review, an analysis undertaken by EPA at
that time had shown that there was considerable overlap between areas
that would be expected not to meet the range of alternative 8-hour
standards being considered for the primary NAAQS and those expected not
to meet the range of values (expressed in terms of the seasonal SUM06
index) of concern for vegetation.  This result suggested that
improvements in national air quality expected to result from attaining
an 8-hour primary standard within the recommended range of levels would
also be expected to significantly reduce levels of concern for
vegetation in those same areas.  Thus, in the 1996 proposed rule, EPA
proposed two alternatives for consideration:  one alternative was to
make the secondary standard equal in every way to the proposed 8-hour,
0.08 ppm primary standard; and the second was to establish a cumulative,
seasonal secondary standard in terms of a SUM06 form as also appropriate
to protect public welfare from known or anticipated adverse effects
given the available scientific knowledge and that such a seasonal
standard “…is more biologically relevant…” (61 FR 65716).  

In the 1997 final rule, EPA decided to make the secondary standard
identical to the primary standard.  The EPA acknowledged, however, that
“it remained uncertain as to the extent to which air quality
improvements designed to reduce 8-hr average O3 concentrations averaged
over a 3-year period would reduce O3 exposures measured by a seasonal
SUM06 index.” (62 FR 38876)  In other words, it was uncertain as to
whether the 8-hour average form would, in practice, provide sufficient
protection for vegetation from the cumulative, seasonal and
concentration-weighted exposures described in the scientific literature
as of concern.

	On the basis of that history, the 2007 Staff Paper (chapter 7)
revisited the issue of whether the SUM06 was still the most appropriate
choice of cumulative, seasonal form for a secondary standard to protect
the public welfare from known and anticipated adverse vegetation effects
in light of the new information available in this review.  Specifically,
the 2007 Staff Paper considered: (1) the continued lack of evidence
within the vegetation effects literature of a biological threshold for
vegetation exposures of concern; and (2) new estimates of PRB that were
lower than in the 1997 review.  The W126 form, also evaluated in the
1997 review, was again selected for comparison with the SUM06 form. 
Regarding the first consideration, the 2007 Staff Paper noted that the
W126 form, by its incorporation of a continuous sigmoidal weighting
scheme, does not create an artificially imposed concentration threshold,
yet also gives proportionally more weight to the higher and typically
more biologically potent concentrations, as supported by the scientific
evidence.  Second, the index value is not significantly influenced by O3
concentrations within the range of estimated PRB, as the weights
assigned by the sigmoidal weighting scheme to concentrations in this
range are near zero.  Thus, it would also provide a more appropriate
target for air quality management programs designed to reduce emissions
from anthropogenic sources contributing to O3 formation.  On the basis
of these considerations, the 2007 Staff Paper concluded that the W126
form was the most biologically-relevant cumulative, seasonal form
appropriate to consider in the context of the 2008 rulemaking.

C.	Vegetation Exposure and Impact Assessment

	The vegetation exposure and impact assessment conducted for the 2008
rulemaking and described in the 2007 Staff paper, consisted of exposure,
risk and benefits analyses and improved and built upon similar analyses
performed in the 1997 review (EPA 1996b).  The vegetation exposure
assessment was performed using interpolation and included information
from ambient monitoring networks and results from air quality modeling. 
The vegetation risk assessment included both tree and crop analyses. 
The tree risk analysis includes three distinct lines of evidence:  (1)
observations of visible foliar injury in the field linked to monitored
O3 air quality for the years 2001 – 2004;  (2) estimates of seedling
growth loss under then current and alternative O3 exposure conditions;
and (3) simulated mature tree growth reductions using the TREGRO model
to simulate the effect of meeting alternative air quality standards on
the predicted annual growth of a single western species (ponderosa pine)
and two eastern species (red maple and tulip poplar).  The crop analysis
includes estimates of the risks to crop yields from then current and
alternative O3 exposure conditions and the associated change in economic
benefits expected to accrue in the agriculture sector upon meeting the
levels of various alternative standards.  Each element of the assessment
is described below, including discussions of known sources and ranges of
uncertainties associated with the elements of this assessment.

1.	Exposure Characterization

	Though numerous effects of O3 on vegetation have been documented as
discussed above, it is important in considering risk to examine O3 air
quality patterns in the U.S. relative to the location of O3 sensitive
species that have a known concentration-response in order to predict
whether adverse effects are occurring at current levels of air quality,
and whether they are likely to occur under alternative standard forms
and levels.  

	The most important information about exposure to vegetation comes from
the O3 monitoring data that are available from two national networks:
(1) Air Quality System (AQS;   HYPERLINK
"http://www.epa.gov/ttn/airs/airsaqs" 
http://www.epa.gov/ttn/airs/airsaqs ) and (2) Clean Air Status and
Trends Network (CASTNET;   HYPERLINK "http://www.epa.gov/castnet/" 
http://www.epa.gov/castnet/ ).  The AQS monitoring network currently has
over 1100 active O3 monitors which are generally sited near population
centers.  However, this network also includes approximately 36 monitors
located in national parks.  CASTNET is the nation's primary source for
data on dry acidic deposition and rural, ground-level O3.  It consists
of over 80 sites across the eastern and western U.S. and is
cooperatively operated and funded with the National Park Service.  In
the 1997 O3 NAAQS final rule, it was acknowledged that because the
national air quality surveillance network for O3 was designed
principally to monitor O3 exposure in populated areas, there was limited
measured data available to characterize O3 air quality in rural and
remote sites.  Since the 1997 review, there has been a small increase in
the number of CASTNET sites (from approximately 52 sites in 1992 to 84
sites in 2004), however these monitors are not used for attainment
designations.  

	National parks represent areas of nationally recognized ecological and
public welfare significance, which have been afforded a high level of
protection by Congress.  Two recent reports presented some discussion of
O3 trends in a subset of national parks:  The Ozone Report: Measuring
Progress Through 2003 (EPA, 2004), and 2005 Annual Performance and
Progress Report: Air Quality in National Parks (NPS, 2005). 
Unfortunately, much of this information is presented only in terms of
the current 8-hr average form.  The 2007 Staff Paper analyzed available
air quality data in terms of the cumulative 12-hour W126 form from 2001
to 2005 for a subset of national parks and other significant natural
areas representing 4 general regions of the U.S.  Many of these national
parks and natural areas have monitored O3 levels above concentrations
that have been shown to decrease plant growth and above the 12-hour W126
levels analyzed in this review.  For example, the Great Smokey Mountain,
Rocky Mountain, Grand Canyon, Yosemite and Sequoia National Parks all
had more than one year within the 2001-2005 period with a 12-hour W126
above 21 ppm-hour.  This level of exposure has been associated with
approximately no more than 10 percent biomass loss in 50 percent of the
49 tree seedling cases studied in the NHEERL-WED experiments (Lee and
Hogsett, 1996).  Black cherry (Prunus serotina), an important
O3-sensitive tree species in the eastern U.S., occurs in the Great Smoky
Mountain National Park and is estimated to have O3-related seedling
biomass loss of approximately 40 percent when exposed to a 3 month,
12-hour W126 O3 level greater than 21 ppm-hour.  Ponderosa pine (Pinus
ponderosa) which occurs in the Grand Canyon, Yosemite and Sequoia
National Parks has been reported to have approximately 10 percent
biomass losses at 3 month, 12 hour W126 O3 levels as low as 17 ppm-hour
(Lee and Hogsett, 1996).  Impacts on seedlings may potentially affect
long-term tree growth and survival, ultimately affecting the
competitiveness of O3-sensitive tree species and genotypes within forest
stands.

In order to characterize exposures to vegetation at the national scale,
however, the 2007 Staff Paper concluded that it could not rely solely on
limited site-specific monitoring data, and that it was necessary to
select an interpolation method that could be used to characterize O3 air
quality over broad geographic areas.  The 2007 Staff Paper therefore
investigated the appropriateness of using the O3 outputs from the
EPA/NOAA Community Multi-scale Air Quality (CMAQ) model system ( 
HYPERLINK "http://www.epa.gov/asmdnerl/CMAQ" 
http://www.epa.gov/asmdnerl/CMAQ , Byun and Ching, 1999; Arnold et al.
2003, Eder and Yu, 2005) to improve spatial interpolations based solely
on existing monitoring networks.  Due to the significant resources
required to run CMAQ, model outputs were only available for a limited
number of years.  For the 2008 rulemaking, the most recent outputs
available at the time from CMAQ version 4.5 were for the year 2001.

	Based on the significant difference in monitor network density between
the eastern and western U.S., the 2007 Staff Paper concluded that it was
appropriate to use separate interpolation techniques in these two
regions.  Only AQS and CASTNET monitoring data were used for the eastern
interpolation, since it was determined that enhancing the interpolation
with CMAQ data did not add much information to the eastern U.S.
interpolation.  In the western U.S., however, where rural monitoring is
more sparse, O3 values generated by the CMAQ model were used to develop
scaling factors to augment the interpolation.  

In order to characterize uncertainties associated with the interpolation
method, monitored O3 concentrations were systematically compared to
interpolated O3 concentrations in areas where monitors were located.  In
general, the interpolation method used in the current review performed
well in many areas in the U.S., although it under-predicted higher
12-hour W126 exposures in rural areas.  Due to the important influence
of higher exposures in determining risks to plants, this feature of the
interpolated surface could result in an under-estimation of risks to
vegetation in some areas.  Taking these uncertainties into account, and
given the absence of more complete rural monitoring data, this approach
was used in developing national vegetation exposure and risk assessments
that estimate relative changes in risk for the various alternative
standards analyzed.

	To evaluate changing vegetation exposures and risks under selected air
quality scenarios, the 2007 Staff Paper utilized 2001 base year O3 air
quality distributions that had been adjusted with a rollback method
(Horst and Duff, 1995; Rizzo, 2005, 2006) to reflect meeting the then
current and alternative secondary standard options.  This technique
combines both linear and quadratic elements to reduce higher O3
concentrations more than lower ones.  In this regard, the rollback
method attempts to account for reductions in emissions without greatly
affecting lower concentrations.  The following O3 air quality scenarios
were analyzed: (1) 4th-highest daily maximum 8-hour average: 0.084 ppm
(the effective level of the then current standard) and 0.070 ppm levels;
(2) 3-month, 12-hour. SUM06: 25 ppm-hour (proposed in the 1997 review)
and 15 ppm-hour levels; and (3) 3-month, 12-hour W126: 21 ppm-hour and
13 ppm-hour levels.

	The two 8-hour average levels were chosen as possible alternatives of
the then current form for comparison with the cumulative, seasonal
alternative forms.  The SUM06 scenarios were very similar to the W126
scenarios.  Since the W126 was judged to be the more
biologically-relevant cumulative, seasonal form, only the results for
the W126 scenarios are summarized below.  For the W126 form, the two
levels were selected on the basis of the associated levels of tree
seedling biomass loss and crop yield loss protection identified in the
NHEERL-WED and NCLAN studies, respectively.  Specifically, the upper
level of W126 (21 ppm-hour) was associated with a level of tree and crop
protection of approximately no more than 10 percent growth or yield loss
in 50 percent of cases studied.  Alternatively, the lower level of W126
(13 ppm-hour) was associated with a level of tree seedling and crop
protection of approximately no more than 10 percent growth or yield loss
in 75 percent of studied cases.  

	The following discussion highlights key observations drawn from
comparing predicted changes in interpolated air quality under each
alternative standard form and level scenario for the base year, 2001:

(1) Under the base year (2001) “as is” air quality, a large portion
of California had 12-hr W126 O3 levels above 31 ppm-hour, which has been
associated with approximately no more than 14 percent biomass loss in 50
percent of tree seedling cases studies.  Broader multi-state regions in
the east (NC, TN, KY, IN, OH, PA, NJ, NY, DE, MD, VA) and west (CA, NV,
AZ, OK, TX) are predicted to have levels of air quality above the W126
level of 21 ppm-hour, which is approximately equal to the secondary
standard proposed in 1996 and is associated with approximately no more
than 10 percent biomass loss in 50 percent of tree seedling cases
studied.  Much of the east and Arizona and California have 12-hour W126
O3 levels above 13 ppm-hour, which has been associated with
approximately no more than 10 percent biomass loss in 75 percent of tree
seedling cases studied.  The results of the exposure assessment indicate
that current air quality levels could result in significant impacts to
vegetation in some areas.

	(2) When 2001 air quality was rolled back to meet the then current
8-hour, 0.084 ppm secondary standard, the overall 3-month 12-hour W126
O3 levels were somewhat improved, but not substantially.  Under this
scenario, there were still many areas in California with 12-hour W126 O3
levels above 31 ppm-hour.  A broad multi-state region in the east (NC,
TN, KY, IN, OH, PA, MD) and west (CA, NV, AZ, OK, TX) were still
predicted to have O3 levels above the W126 level of 21 ppm-hour.

	(3) Exposures generated for just meeting a 0.070 ppm, 4th-highest
maximum 8-hour average alternative standard showed substantially
improved O3 air quality when compared to just meeting the then current
8-hour standard.  Most areas were predicted to have O3 levels below the
W126 level of 21 ppm-hour, although some areas in the east (KY, TN, MI,
AR, MO, IL) and west (CA, NV, AZ, UT, NM, CO, OK, TX) were still
predicted to have O3 levels above the W126 level of 13 ppm-hour.

	These results suggest that meeting a 0.070 ppm, 8-hour secondary
standard would provide substantially improved protection in some areas
for vegetation from seasonal O3 exposures of concern.  The 2007 Staff
Paper recognizes, however, that some areas meeting a 0.070 ppm 8-hour
standard could continue to have elevated seasonal exposures, including
forested park lands and other natural areas, and Class I areas which are
federally mandated to preserve certain air quality related values.  This
is especially important in the high elevation forests in the Western
U.S. where there are few O3 monitors.  This is because the air quality
patterns in remote areas can result in relatively low 8-hour averages
while still experiencing relatively high cumulative exposures.

	To further characterize O3 air quality in terms of various secondary
standard forms, an analysis was performed in the 2007 Staff Paper to
evaluate the extent to which county-level O3 air quality measured in
terms of various levels of the current 8-hour average form overlapped
with that measured in terms of various levels of the 12-hour W126
cumulative, seasonal form.  The 2007 Staff Paper presented this analysis
using 2002-2004 county-level O3 air quality data from AQS sites and the
subset of CASTNET sites having the highest O3 levels for the counties in
which they are located.  Since the current 8-hour average secondary form
is a 3-year average, the analysis initially compared the 3-year averages
of both the 8-hour and W126 forms.  In addition, recognizing that some
vegetation effects (e.g. crop yield loss and foliar injury) are driven
solely by annual O3 exposures and are typically evaluated with respect
to exposures within the annual growing season, the 2007 Staff Paper also
presented a comparison of the current 3-year average 8-hour form to the
annual W126 form for the individual years, 2002 and 2004.

	Results of the 3-year average comparisons showed that of the counties
with air quality meeting the 3-year average form of a 0.084 ppm, 8-hour
average standard, 7 counties showed 3-year average W126 values above the
21 ppm-hour level.  At the lower W126 level of 13 ppm-hour, 135 counties
with air quality meeting the 3-year average form of a 0.084 ppm, 8-hour
average standard, would be above this W126 level.  In addition, when the
3-year average of an 8-hour form was compared to annual W126 values,
further variability in the degree of overlap between the 8-hour form and
W126 form became apparent.  For example, the relatively high 2002 O3 air
quality year showed a greater degree of overlap between those areas that
would meet the levels analyzed for the current 8-hour and alternative
levels of the W126 form than did the relatively low O3 2004 air quality
year.  This lack of a consistent degree of overlap between the two forms
in different air quality years demonstrates that annual vegetation would
be expected to receive widely differing degrees of protection from
cumulative seasonal exposures in some areas from year to year, even when
the 3-year average of the 8-hour form was consistently met.

It is clear that this analysis is limited by the lack of monitoring in
rural areas where important vegetation and ecosystems are located,
especially at higher elevation sites.  This is because O3 air quality
distributions at high elevation sites often do not reflect the typical
urban and near-urban pattern of low morning and evening O3
concentrations with a high mid-day peak, but instead maintain relatively
flat patterns with many concentrations in the mid-range (e.g., 0.05-0.09
ppm) for extended periods.  These conditions can lead to relatively low
daily maximum 8-hour averages concurrently with high cumulative values
so that there is potentially less overlap between an 8-hour average and
a cumulative, seasonal form at these sites.  The 2007 Staff Paper
concluded that it is reasonable to anticipate that additional
unmonitored rural high elevation areas important for vegetation may not
be adequately protected even with a lower level of the 8-hour form.

The 2006 Criteria Document discusses policy relevant background (PRB)
levels for high elevation sites and makes the following observations: 
(1) PRB concentrations of 0.04 to 0.05 ppm occur occasionally at
high-elevation sites (e.g., >1.5 km) in the spring due to the
free-tropospheric influence, including some limited contribution from
hemispheric pollution (O3 produced from anthropogenic emissions outside
North America); and (2) while stratospheric intrusions might
occasionally elevate O3 at high-altitude sites, these events are rare at
surface sites.  Therefore, the 2007 Staff Paper concluded that
springtime PRB levels in the range identified above and rare
stratospheric intrusions of O3 are unlikely to be a major influence on
3-month cumulative seasonal W126 values.

It further remains uncertain as to the extent to which air quality
improvements designed to reduce 8-hour O3 average concentrations would
reduce O3 exposures measured by a seasonal, cumulative W126 index.  The
2007 Staff Paper indicated this to be an important consideration
because:  (1) the biological database stresses the importance of
cumulative, seasonal exposures in determining plant response; (2) plants
have not been specifically tested for the importance of daily maximum
8-hour O3 concentrations in relation to plant response; and (3) the
effects of attainment of a 8-hour standard in upwind urban areas on
rural air quality distributions cannot be characterized with confidence
due to the lack of monitoring data in rural and remote areas.  These
factors are important considerations in determining whether the current
8-hour form can appropriately provide requisite protection for
vegetation.

2. 	Assessment of Risks to Vegetation

	The 2007 Staff Paper presents results from quantitative and qualitative
risk assessments of O3 risks to vegetation (EPA, 2007).  In the 1997
review, crop yield and seedling biomass loss OTC data provided the basis
for staff analyses, conclusions, and recommendations (EPA, 1996b). 
Since then, several additional lines of evidence have progressed
sufficiently to provide staff with a more complete and coherent picture
of the scope of O3-related vegetation risks, especially those faced by
seedling, sapling and mature tree species growing in field settings, and
indirectly, forested ecosystems.  Specifically, research published after
the 1997 review reflects an increased emphasis on field-based exposure
methods (e.g., free air exposure and ambient gradient), improved field
survey biomonitoring techniques, and mechanistic tree process models. 
Findings from each of these research areas are discussed separately
below.  In conducting these assessments, the Staff Paper analyses relied
on both measured and modeled air quality information.  For some effects,
like visible foliar injury and modeled mature tree growth response, only
monitored air quality information was used.  For other effects
categories (e.g., crop yield and tree seedling growth), staff relied on
interpolated O3 exposures.  

a.	Visible foliar injury

	As discussed above (section IV.A.2.c), systematic injury surveys have
documented visible foliar injury symptoms diagnostic of phytotoxic O3
exposures on sensitive bioindicator plants.  These surveys have produced
more expansive evidence than that available at the time of the 1997
review that visible foliar injury is occurring in many areas of the U.S.
under current ambient conditions.  The 2007 Staff Paper presents an
assessment combining recent U.S. Forest Service Forest Inventory and
Analysis (FIA) biomonitoring site data with the county level air quality
data for those counties containing the FIA biomonitoring sites.  This
assessment showed that incidence of visible foliar injury ranged from 21
to 39 percent during the four-year period (2001-2004) across all
counties with air quality levels at or below that of a 0.084 ppm, 8-hour
standard.  Of the counties that met an 8-hour level of 0.070 ppm in
those years, 11 to 30 percent still had incidence of visible foliar
injury.  The magnitude of these percentages suggests that phytotoxic
exposures sufficient to induce visible foliar injury would still occur
in many areas after meeting the level of a 0.084 ppm secondary standard
or alternative 0.070 ppm 8-hour standard.  Additionally, the data showed
that visible foliar injury occurrence was geographically widespread and
occurring on a variety of plant species in forested and other natural
systems.  Linking visible foliar injury to other plant effects is still
problematic.  However, its presence indicates that other O3–related
vegetation effects could also be present.  

b.	Seedling and mature tree biomass loss

	In the 1997 review, analyses of the effects of O3 on trees were limited
to 11 tree species for which C-R functions for the seedling growth stage
had been developed from OTC studies conducted by the NHEERL-WED. 
Important tree species such as quaking aspen, ponderosa pine, black
cherry, and tulip poplar were found to be sensitive to cumulative
seasonal O3 exposures.  Work done since the 1997 review at the AspenFACE
site in Wisconsin on quaking aspen (Karnosky et al., 2005) and a
gradient study performed in the New York City area (Gregg et al. 2003)
has confirmed the detrimental effects of O3 exposure on tree growth in
field studies without chambers and beyond the seedling stage (King et al
2005).  These field studies are discussed above in section IV.A.

	To update the seedling biomass loss risk analysis, C-R functions for
biomass loss for available seedling tree species taken from the 2006
Criteria Document and information on tree growing regions derived from
the U.S. Department of Agriculture's Atlas of United States Trees were
combined with projections of O3 air quality based on 2001 interpolated
exposures, to produce estimated biomass loss for each of the seedling
tree species individually.  Maps of these biomass loss projections are
presented in the 2007 Staff Paper.  For example, quaking aspen had a
wide range of O3 exposures across its growing range and therefore,
showed significant variability in percentages of projected seedling
biomass loss across its range.  Quaking aspen seedling biomass loss was
projected to be greater than 4 percent over much of its geographic
range, though it can reach above 10 percent in areas of Ohio,
Pennsylvania, New York, New Jersey and California.  Biomass loss for
black cherry was projected to be greater than 20 percent in
approximately half its range.  Greater than 30 percent biomass loss for
black cherry was projected in North Carolina, Tennessee, Indiana, Ohio,
Pennsylvania, Arizona, Michigan, New York, New Jersey, Maryland and
Delaware.  For ponderosa pine, an important tree species in the western
U.S., biomass loss was projected to be above 10 percent in much of its
range in California.  Biomass loss still occurred in many tree species
when O3 air quality was adjusted to meet the then current 8-hour
standard of 0.084 ppm.  For instance, black cherry, ponderosa pine,
eastern white pine, and aspen had estimated median seedling biomass
losses over portions of their growing range as high as 24, 11, 6, and 6
percent, respectively, when O3 air quality was rolled back to just meet
thea current0.084 ppm, 8-hour standard.  The 2007 Staff Paper noted that
these results are for tree seedlings and that mature trees of the same
species may have more or less of a response to O3 exposure.  Due to the
potential for compounding effects over multiple years, experts at a
consensus workshop on O3 vegetation effects and secondary standards,
hereinafter referred to as the 1996 Consensus Workshop, reported in a
subsequent 1997 Workshop Report, that a biomass loss greater than 2
percent annually can be significant (Heck and Cowling, 1997).. Decreased
seedling root growth and survivability could affect overall stand health
and composition in the long term.

In addition to the estimation of O3 effects on seedling growth, recent
work available in the 2008 rulemaking has enhanced our understanding of
risks beyond the seedling stage.  In order to better characterize the
potential O3 effects on mature tree growth, a tree growth model (TREGRO)
was used as a tool to evaluate the effect of changing O3 air quality
under just meet scenarios for selected alternative O3 standards on the
growth of mature trees.  TREGRO is a process-based, individual tree
growth simulation model (Weinstein et al, 1991).  This model has been
used to evaluate the effects of a variety of O3 exposure scenarios on
several species of trees by incorporating concurrent climate data in
different regions of the U.S. to account for O3 and climate/meteorology
interactions (Tingey et al., 2001; Weinstein et al., 1991; Retzlaff et
al., 2000; Laurence et al., 1993; Laurence et al., 2001; Weinstein et
al., 2005).  The model provides an analytical framework that accounts
for the nonlinear relationship between O3 exposure and response.  The
interactions between O3 exposure, precipitation and temperature are
integrated as they affect vegetation, thus providing an internal
consistency for comparing effects in trees under different exposure
scenarios and climatic conditions.  An earlier assessment of the
effectiveness of national ambient air quality standards in place since
the early 1970s took advantage of 40 years of air quality and climate
data for the Crestline site in the San Bernardino Mountains of
California to simulate ponderosa pine growth over time with the
improving air quality using TREGRO (Tingey et al., 2004).

	The TREGRO model was used to assess growth of Ponderosa pine in the San
Bernardino Mountains of California (Crestline) and the growth of yellow
poplar and red maple in the Appalachian mountains of Virginia and North
Carolina, Shenandoah National Park (Big Meadows) and Linville Gorge
Wilderness Area (Cranberry), respectively.  Total tree growth associated
with ‘as is’ air quality, and air quality adjusted to just meet
alternative O3 standards was assessed.  Ponderosa pine is one of the
most widely distributed pines in western North America, a major source
of timber, important as wildlife habitat, and valued for aesthetics
(Burns and Honkala, 1990).  Red maple is one of the most abundant
species in the eastern U.S. and is important for its brilliant fall
foliage and highly desirable wildlife browse food (Burns and Honkala,
1990).  Yellow poplar is an abundant species in the southern Appalachian
forest.  It is 10 percent of the cove hardwood stands in southern
Appalachians which are widely viewed as some of the country’s most
treasured forests because the protected, rich, moist set of conditions
permit trees to grow the largest in the eastern U.S.  The wood has high
commercial value because of its versatility and as a substitute for
increasingly scarce softwoods in furniture and framing construction.
Yellow poplar is also valued as a honey tree, a source of wildlife food,
and a shade tree for large areas (Burns and Honkala, 1990).  

	The 2007 Staff Paper analyses found that just meeting a 0.084 ppm
standard would likely continue to allow O3-related reductions in annual
net biomass gain in these species.  This is based on model outputs that
estimate that as O3 levels are reduced below those of a 0.084 ppm
standard, significant improvements in growth would occur.  For instance,
estimated growth in red maple increased by 4 and 3 percent at Big
Meadows and Cranberry sites, respectively, when air quality was rolled
back to just met a W126 value of 13 ppm-hour.  Yellow poplar was
projected to have a growth increase between 0.6 and 8 percent under the
same scenario at the two eastern sites.

	Though there is uncertainty associated with the above analyses, this
information should be given careful consideration in light of several
other pieces of evidence.  Specifically, new evidence from experimental
studies that go beyond the seedling growth stage continues to show
decreased growth under elevated O3 (King et al. 2005).  Some mature
trees such as red oak have shown an even greater sensitivity of
photosynthesis to O3 than seedlings of the same species (Hanson et al.,
1994).  As indicated above, smaller growth loss increments may be
significant for perennial species.  The potential for cumulative
“carry over” effects as well as compounding also must be considered.
 The accumulation of such “carry-over” effects over time may affect
long-term survival and reproduction of individuals and ultimately the
abundance of sensitive tree species in forest stands.

c.	 Crops

	As discussed in the 2007 Staff Paper, risk of O3 exposure and
associated monetized benefits were estimated for commodity crops, fruits
and vegetables.  Similar to the tree seedling analysis, this analysis
combined C-R information on crops, crop growing regions and interpolated
exposures during each crop growing season.  NCLAN crop functions were
used for commodity crops.  According to USDA National Agricultural
Statistical Survey (NASS) data, the 9 commodity crop species (e.g.,
cotton, field corn, grain sorghum, peanut, soybean, winter wheat,
lettuce, kidney bean, potato) included in the 2007 Staff Paper analysis
accounted for 69 percent of 2004 principal crop acreage planted in the
U.S. in 2004.  The C-R functions for six fruit and vegetable species
(tomatoes-processing, grapes, onions, rice, cantaloupes, Valencia
oranges) were identified from the California fruit and vegetable
analysis from the 1997 review (Abt Associates Inc, 1995).  The 2007
Staff Paper noted that fruit and vegetable studies were not part of the
NCLAN program and C-R functions were available only in terms of seasonal
7-hour or 12-hour mean index.  This index form is considered less
effective in predicting plant response for a given change in air quality
than the cumulative form used with other crops.  Therefore, the fruit
and vegetable C-R functions were considered more uncertain than those
for commodity crops.

Analyses in the 2007 Staff Paper showed that some of the most important
commodity crops such as soybean, winter wheat and cotton had some
projected losses under the 2001 base year air quality.  Soybean yield
losses were projected to be 2-4 percent in parts of Pennsylvania, New
Jersey, Maryland and Texas.  Winter wheat was projected to have yield
losses of 2-6 percent in parts of California.  Additionally, cotton was
projected to have yield losses of above 6 percent in parts of
California, Texas and North Carolina in 2001.  The risk assessment
estimated that just meeting the then current 0.084 ppm, 8-hour standard
would still allow O3–related yield loss to occur in some commodity
crop species and fruit and vegetable species currently grown in the U.S.
 For example, based on median C-R function response, in counties with
the highest O3 levels, potatoes and cotton had estimated yield losses of
9-15 percent and 5-10 percent, respectively, when O3 air quality just
met the level of a 0.084 ppm, 8-hour standard.  Estimated yield improved
in these counties when the alternative W126 standard levels were met. 
The very important soybean crop had generally small yield losses
throughout the country under just meeting the then current standard (0-4
percent).  

	The 2007 Staff Paper also presented estimates of monetized benefits for
crops associated with a 0.084 ppm, 8-hour and alternative standards. 
The Agriculture Simulation Model (AGSIM) (Taylor, 1994; Taylor, 1993)
was used to calculate annual average changes in total undiscounted
economic surplus for commodity crops and fruits and vegetables when the
then current and alternative standard levels were met.  Meeting the
various alternative standards did show some significant benefits beyond
a 0.084 ppm, 8-hour standard.  However, the 2007 Staff Paper recognized
that the AGSIM economic benefits estimates also incorporate several
sources of uncertainty, including:  (1) estimates of economic benefits
derived from use of the more uncertain C-R relationships for fruits and
vegetables; (2) uncertain assumptions about the treatment and effect of
government farm payment programs; and (3) uncertain assumptions about
near-term changes in the agriculture sector due to the increased use of
crops as biofuels.  Although the AGSIM model results provided a relative
comparison of agricultural benefits between alternative standards, these
uncertainties limited the utility of the absolute numbers.

D.	Reconsideration of Secondary Standard

	As discussed above at the beginning of section IV, this reconsideration
of the secondary O3 standard set in the 2008 rulemaking focuses on
reconsidering certain elements of the standard, the form, averaging
times, and level.  The general approach for setting a secondary O3
standard used in the 2008 rulemaking, and in the previous 1997
rulemaking in 1997, was to consider two basic policy options:  setting a
distinct secondary standard with a biologically relevant form and
averaging times, or setting a secondary standard identical to the
primary standard.  In the 2007 proposed rule, both such options were
evaluated, commented on by CASAC and the public, and proposed, as
discussed below in sections IV.D.1 and IV.D.2, respectively.  In the
2008 final rule, EPA decided to set the secondary standard identical to
the revised 8-hour primary standard, as discussed below in section
IV.D.3.  Section IV.D.4 summarizes comments received from CASAC
following the 2008 decision.  The Administrator’s proposed conclusions
based on this reconsideration are presented in section IV.D.5.

1.	Considerations Regarding the 2007 Proposed Cumulative Seasonal
Standard 

a.	Form

The 2006 Criteria Document and 2007 Staff Paper concluded that the
recent vegetation effects literature evaluated in the 2008 rulemaking
strengthened and reaffirmed conclusions made in the 1997 review that the
use of a cumulative exposure index that differentially weights ambient
concentrations is best able to relate ambient exposures to vegetation
response at this time (EPA, 2006a, b; see also discussion in IV.B
above).  The 1997 review focused in particular on two of these
cumulative forms, the SUM06 and W126.  In the 2008 rulemaking, the 2007
Staff Paper again evaluated these two forms in light of two key pieces
of then recent information: estimates of PRB that were lower than in the
1997 review, and continued lack of evidence within the vegetation
effects literature of a biological threshold for vegetation exposures of
concern.  On the basis of those policy and science-related
considerations, the 2007 Staff Paper concluded that the W126 form was
more appropriate in the context of the 2008 rulemaking.  Specifically,
the W126 form, by its incorporation of a sigmoidal weighting scheme,
does not create an artificially imposed concentration threshold, gives
proportionally more weight to the higher and typically more biologically
potent concentrations, and is not significantly influenced by O3
concentrations within the range of estimated PRB. The Staff Paper
further concluded that “it is not appropriate to continue to use an
8-hour averaging time for the secondary standard” and that “the
8-hour average form should be replaced with a cumulative, seasonal,
concentration weighted form” (EPA, 2007b; pg.8-25).

The CASAC, based on its assessment of the same vegetation effects
science, agreed with the 2006 Criteria Document and 2007 Staff Paper and
unanimously concluded that it is not appropriate to try to protect
vegetation from the known or anticipated adverse effects of ambient O3
by continuing to promulgate identical primary and secondary standards
for O3.  Moreover, the members of the CASAC and a substantial majority
of the CASAC O3 Panel agreed with 2007 Staff Paper conclusions and
encouraged EPA to establish an alternative cumulative secondary standard
for O3 and related photochemical oxidants that is distinctly different
in averaging time, form and level from the current or potentially
revised 8-hour primary standard.  The CASAC also stated that “the
recommended metric for the secondary ozone standard is the
(sigmoidally-weighted) W126 index” (Henderson, 2007). 

The EPA agreed with the conclusions drawn in the 2006 Criteria Document,
2007 Staff Paper and by CASAC that the scientific evidence available in
the 2008 rulemaking continued to demonstrate the cumulative nature of
O3-induced plant effects and the need to give greater weight to higher
concentrations.  Thus, EPA concluded that a cumulative exposure index
that differentially weights O3 concentrations represents a reasonable
policy choice for a seasonal secondary standard to protect against the
effects of O3 on vegetation.  The EPA further agreed with both the 2007
Staff Paper and CASAC that the most appropriate cumulative,
concentration-weighted form to consider in the 2008 rulemaking was the
sigmoidally weighted W126 form, due to EPA’s recognition that there is
no evidence in the literature for an exposure threshold that would be
appropriate across all O3-sensitive vegetation and that this form is
unlikely to be significantly influenced by O3 air quality within the
range of PRB levels identified in this rulemaking.  Thus, in 2007 EPA
proposed as one option to replace the then current 0.084 ppm, 8-hour
average secondary standard with a standard defined in terms of the
cumulative, seasonal W126 form.  The EPA also proposed the option of
making the secondary identical to the proposed revised primary standard.

b.	Averaging Times 

	The 2007 Staff Paper, in addition to form, also considered what
exposure periods or durations are most relevant for vegetation, which,
unlike people, is exposed to ambient air continuously throughout its
lifespan.  For annual species, this lifespan encompasses a period of
only one year or less; while for perennials, lifespans can range from a
few years to decades or centuries.  However, because O3 levels are not
continuously elevated and plants are not equally sensitive to O3 over
the course of a day, season or lifetime, it becomes necessary to
identify periods of exposure that have the most relevance for plant
response.  The 2007 Staff Paper discussed exposure periods relevant for
vegetation in terms of a seasonal window and a diurnal window, and it
also discussed defining the standard in terms of an annual index value
versus a 3-year average of annual index values.  The numbered paragraphs
below present the 2007 Staff Paper discussions on these exposure
periods, and the annual versus 3-year average index value, followed by a
discussion of CASAC views and EPA proposed conclusions.

(1)  In considering an appropriate seasonal window, the 2007 Staff Paper
recognized that, in general, many annual crops are grown for periods of
a few months before being harvested.  In contrast, other annual and
perennial species may be photosynthetically active longer, and for some
species and locations, throughout the entire year.  In general, the
period of maximum physiological activity and thus, maximum potential O3
uptake for annual crops, herbaceous species, and deciduous trees and
shrubs coincides with some or all of the intra-annual period defined as
the O3 season, which varies on a state-by-state basis.  This is because
the high temperature and high light conditions that promote the
formation of tropospheric O3 also promote physiological activity in
vegetation.

The 2007 Staff Paper noted that the selection of any single seasonal
exposure period for a national standard would represent a compromise,
given the significant variability in growth patterns and lengths of
growing seasons among the wide range of vegetation species occurring
within the U.S. that may experience adverse effects associated with O3
exposures.  However, the 2007 Staff Paper further concluded that the
consecutive 3-month period within the O3 season with the highest W126
index value (e.g., maximum 3 month period) would, in most cases, likely
coincide with the period of greatest plant sensitivity on an annual
basis.  Therefore, the 2007 Staff Paper again concluded, as it did in
the 1997 review, that the annual maximum consecutive 3-month period is a
reasonable seasonal time period, when combined with a cumulative,
concentration weighted form, for protection of sensitive vegetation.

	(2)  In considering an appropriate diurnal window, the Staff Paper
recognized that over the course of the 24-hour diurnal period, plant
stomatal conductance varies in response to changes in light level, soil
moisture and other environmentally and genetically controlled factors. 
In general, stomata are most open during daylight hours in order to
allow sufficient CO2 uptake for use in carbohydrate production through
the light-driven process of photosynthesis.  At most locations, O3
concentrations are also highest during the daytime, and thus, most
likely to coincide with maximum stomatal uptake.  It is also known
however, that in some species, stomata may remain open sufficiently at
night to allow for some nocturnal uptake to occur.  In addition, at some
rural, high elevation sites, the O3 concentrations remain relatively
flat over the course of the day, often at levels above estimated PRB. 
At these sites, nighttime W126 values can be of similar magnitude as
daytime values, though the significance of these exposures is much less
certain.  This is because O3 uptake during daylight hours is known to
impair the light-driven process of photosynthesis, which can then lead
to impacts on carbohydrate production, plant growth, reproduction
(yield) and root function.  It is less clear at this time to what extent
and by what mechanisms O3 uptake at night adversely impacts plant
function.  In addition, many species have not been shown to take up O3
at night and/or do not occur in areas with elevated nighttime O3
concentrations.  

In reviewing the information on this topic that became available after
the 1997 review, the 2007 Staff Paper considered the information
compiled in a summary report by Musselman and Minnick (2000).  This work
reported that some species take up O3 at night, but that the degree of
nocturnal stomatal conductance varies widely between species and its
relevance to overall O3-induced vegetation effects remain unclear.  In
considering this information, the 2007 Staff Paper concluded that for
the vast majority of studied species, daytime exposures represent the
majority of diurnal plant O3 uptake and are responsible for inducing the
plant response of most significance to the health and productivity of
the plant (e.g., reduced carbohydrate production).  Until additional
information is available about the extent to which co-occurrence of
sensitive species and elevated nocturnal O3 exposures exists, and what
levels of nighttime uptake are adverse to affected species, the 2007
Staff Paper concluded that this information continues to be preliminary,
and does not provide a basis for reaching a different conclusion
regarding the diurnal window at this time.  The 2007 Staff Paper further
noted that additional research is needed to address the degree to which
a 12-hour diurnal window may be under-protective in areas where elevated
nighttime levels of O3 co-occur with sensitive species with a high
degree of nocturnal stomatal conductance.  Thus, as in the 1997 review,
the 2007 Staff Paper again concluded that based on the available
science, the daytime 12-hour window (8:00 a.m. to 8:00 p.m.) is the most
appropriate period over which to cumulate diurnal O3 exposures,
specifically those most relevant to plant growth and yield responses.

(3)  In considering whether the standard should be defined in terms of
an annual index value or a 3-year average of annual index values, the
2007 Staff Paper recognized that though most cumulative seasonal
exposure levels of concern for vegetation have been expressed in terms
of the annual timeframe, it may be appropriate to consider a 3-year
average for purposes of standard stability.  However, the 2007 Staff
Paper noted that for certain welfare effects of concern (e.g., foliar
injury, yield loss for annual crops, growth effects on other annual
vegetation and potentially tree seedlings), an annual time frame may be
a more appropriate period in which to assess what level would provide
the requisite degree of protection, while for other welfare effects
(e.g., mature tree biomass loss), a 3-year average may also be
appropriate.  Thus, the 2007 Staff Paper concluded that it is
appropriate to consider both an annual and a 3-year average.  Further,
the 2007 Staff Paper concluded that should a 3-year average of the
12-hour W126 form be selected, a lower standard level should be
considered to reduce the potential of adverse impacts to annual species
from a single high O3 year that could still occur while attaining a
standard on average over 3 years.  

The CASAC, in considering what seasonal, diurnal, and annual or
multiyear time periods are most appropriate when combined with a
cumulative, seasonal form to protect vegetation from exposures of
concern, agreed that the 2007 Staff Paper conclusion regarding the
3-month seasonal period and 12-hour daylight window was appropriate,
with the distinction that both of these time periods likely represents
the minimum time periods of importance.  In particular, one O3 Panel
member commented that for some species, additional O3 exposures of
importance were occurring outside the 3-month seasonal and 12-hour
diurnal windows.  Further, the CASAC concluded that multi-year averaging
to promote a “stable” secondary standard is less appropriate for a
cumulative, seasonal secondary standard than for a primary standard
based on daily maximum 8-hour concentrations.  The CASAC further
concluded that if multi-year averaging is employed to afford greater
stability of the secondary standard, the level of the standard should be
revised downward to assure that the desired degree of protection is not
exceeded in individual years.

The EPA, in determining which seasonal and diurnal time periods are most
appropriate to propose, took into account the 2007 Staff Paper and CASAC
views.  In being careful to consider what is needed to provide the
requisite degree of protection, no more and no less, in 2007 EPA
proposed that the 3-month seasonal period and 12-hour daylight period
are appropriate.  Based on the 2007 Staff Paper conclusions discussed
above, EPA was mindful that there is the potential for under-protection
with a 12-hour diurnal window in areas with sufficiently elevated
nighttime levels of O3 where sensitive species with a high degree of
nocturnal stomatal conductance occur.  On the other hand, EPA also
recognized that a longer diurnal window (e.g., 24-hour) has the
possibility of over-protecting vegetation in areas where nighttime O3
levels remain relatively high but where no species having significant
nocturnal uptake exist.  In weighing these considerations, EPA agreed
with the 2007 Staff Paper conclusion that until additional information
is available about the extent to which this co-occurrence of sensitive
species and elevated nocturnal O3 exposures exists, and what levels of
nighttime uptake are adverse to affected species, this information does
not provide a basis for reaching a different conclusion at this time. 
The EPA also considered to what extent the 3-month period within the O3
season was appropriate, recognizing that many species of vegetation have
longer growing seasons.  The EPA further proposed that the maximum
3-month period is sufficient and appropriate to characterize O3 exposure
levels associated with known levels of plant response.  Therefore, EPA
proposed that the most appropriate exposure periods for a cumulative,
seasonal form is the daytime 12-hour window (8:00 a.m. to 8:00 p.m.)
during the consecutive 3-month period within the O3 monitoring season
with the maximum W126 index value.

The EPA also proposed an annual rather than a multi-year cumulative,
seasonal standard.  In proposing this option, EPA also believed that it
was appropriate to consider the benefits to the public welfare that
would accrue from establishing a 3-year average secondary standard, and
solicited comment on this alternative.  In so doing,  EPA also agreed
with 2007 Staff Paper and CASAC conclusions that should a 3-year
standard be finalized, the level of the standard should be set so as to
provide the requisite degree of  protection for those vegetation effects
judged to be adverse to the public welfare within a single annual
period.  

c.	Level 

The 2007 Staff Paper, in identifying a range of levels for a 3-month,
12-hour W126 annual form appropriate to protect the public welfare from
adverse impacts to vegetation from O3 exposures, considered what
information from the array of vegetation effects evidence and exposure
and risk assessment results was most useful.  Regarding the vegetation
effects evidence, the 2007 Staff Paper found stronger support than what
was available at the time of the 1997 review for an increased level of
protection for trees and ecosystems.  Specifically, this expanded body
of support includes:  (1) additional field based data from free air,
gradient and biomonitoring surveys demonstrating adverse levels of
O3-induced above and/or below-ground growth reductions on trees at the
seedling, sapling and mature growth stages and incidence of visible
foliar injury occurring at biomonitoring sites in the field at ambient
levels of exposure; (2) qualitative support from free air (e.g.,
AspenFACE) and gradient studies on a limited number of tree species for
the continued appropriateness of using OTC-derived C-R functions to
predict tree seedling response in the field; (3) studies that continue
to document below-ground effects on root growth and “carry-over”
effects occurring in subsequent years from O3 exposures; and (4)
increased recognition and understanding of the structure and function of
ecosystems and the complex linkages through which O3, and other
stressors, acting at the organism and species level can influence higher
levels within the ecosystem hierarchy and disrupt essential ecological
attributes critical to the maintenance of ecosystem goods and services
important to the public welfare. 

Based on the above observations and on the vegetation effects and the
results of the exposure and impact assessment summarized above, the 2007
Staff Paper concluded that just meeting the then current standard would
still allow adverse levels of tree seedling biomass loss in sensitive
commercially and ecologically important tree species in many regions of
the country.  Seedling risk assessment results showed that some tree
seedling species are extremely sensitive (e.g., cottonwood, black cherry
and aspen), with annual biomass losses occurring in the field of the
same or greater magnitude that that of annual crops.  Such information
from the tree seedling risk assessment suggests that O3 levels would
need to be substantially reduced to protect sensitive tree seedlings
like black cherry from growth and foliar injury effects.  

In addition to the currently quantifiable risks to trees from ambient
exposures, the 2007 Staff Paper also considered the more subtle impacts
of O3 acting in synergy with other natural and man-made stressors to
adversely affect individual plants, populations and whole systems.  By
disrupting the photosynthetic process, decreasing carbon storage in the
roots, increasing early senescence of leaves and affecting water use
efficiency in trees, O3 exposures could potentially disrupt or change
the nutrient and water flow of an entire system.  Weakened trees can
become more susceptible to other environmental stresses such as pest and
pathogen outbreaks or harsh weather conditions.  Though it is not
possible to quantify all the ecological and societal benefits associated
with varying levels of alternative secondary standards, the 2007 Staff
Paper concluded that this information should be weighed in considering
the extent to which a secondary standard should be set so as to provide
potential protection against effects that are anticipated to occur.  

	In addition, the 2007 Staff Paper also recognized that in the 1997
review, EPA took into account the results of a 1996 Consensus Workshop. 
At this workshop, a group of independent scientists expressed their
judgments on what standard form(s) and level(s) would provide vegetation
with adequate protection from O3-related adverse effects.  Consensus was
reached with respect to selecting appropriate ranges of levels in terms
of a cumulative, seasonal 3-month, 12-hr SUM06 standard for a number of
vegetation effects endpoints.  These ranges are identified below, with
the estimated approximate equivalent W126 standard values shown in
parentheses.  For growth effects to tree seedlings in natural forest
stands, a consensus was reached that a SUM06 range of 10 to 15 (W126
range of 7 to 13) ppm-hour would be protective.  For growth effects to
tree seedlings and saplings in plantations, the consensus SUM06 range
was 12 to 16 (W126 range of 9 to 14) ppm-hour.  For visible foliar
injury to natural ecosystems, the consensus SUM06 range was 8 to 12
(W126 range of 5 to 9) ppm-hour.

Taking these consensus statements into account, EPA stated in the 1997
final rule (62 FR 38856) that “the report lends important support to
the view that the current secondary standard is not adequately
protective of vegetation…[and]… foreshadows the direction of future
scientific research in this area, the results of which could be
important in future reviews of the O3 secondary standard” (62 FR
38856).  

Given the importance EPA put on the consensus report in the 1997 review,
the 2007 Staff Paper considered to what extent research published after
1997 provided empirical support for the ranges of levels identified by
the experts as protective of different types of O3-induced effects.  
With regard to O3-induced biomass loss in sensitive tree
seedlings/saplings growing in natural forest stands, the information
discussed in the 2007 Staff Paper, including the evidence from free air
and gradient studies, provides additional direct support for the
conclusion that the 1996 Consensus Workshop approximate W126 range of
7-13 ppm-hour was an appropriate range to consider in selecting a
protective level.  With regard to visible foliar injury, the available
evidence, including the 2007 Staff Paper analysis of incidence in
counties with FIA monitoring sites and air quality data, showed
significant levels of county-level visible foliar injury incidence at
the W126 level of 13 ppm-hour.  However, because this analysis did not
address risks of this effect at lower levels of O3 air quality, and
because there is a significant uncertainty in predicting the degree of
visible foliar injury symptoms expected for lower levels of O3 air
quality, the evidence provides less certain but qualitative directional
support for the 1996 Consensus Workshop range of 5 to 9 ppm-hour to
protect against this effect.  With regard to O3-induced effects on
plantation trees, there is far less direct information available. 
Though some forest plantation trees are O3-sensitive, the monoculture
nature of these stands makes uncertain the degree to which competition
for resources might play a role and to what degree the variety of
management practices applied would be expected to mitigate the
O3-induced effects.  Thus, it is difficult to distinguish a protective
range of levels for plantation trees from a range of levels that would
be protective of O3-sensitive tree seedlings and saplings in natural
forest stands.  Therefore, on the basis of the strength of the evidence
available, the 2007 Staff Paper concluded that it was appropriate to
consider a range for a 3-month, 12-hour, W126 standard that included the
1996 consensus recommendations for growth effects in tree seedlings in
natural forest stands (i.e., 7-13 ppm-hour in terms of a W126 form).

	In considering the available information on O3-related effects on crops
in the 2008 rulemaking, the 2007 Staff Paper observed the following
regarding the strength of the underlying crop science:  (1) nothing in
the recent literature points to a change in the relationship between O3
exposure and crop response across the range of species and/or cultivars
of commodity crops currently grown in the U.S. that could be construed
to make less appropriate the use of commodity crop C-R functions
developed in the NCLAN program; (2) new field-based studies (e.g.,
SoyFACE) provide qualitative support in a few limited cases for the
appropriateness of using OTC-derived C-R functions to predict crop
response in the field; and (3) refinements in the exposure, risk and
benefits assessments in this review reduce some of the uncertainties
present in the 1997 review.  On the basis of these observations, the
2007 Staff Paper concluded that nothing in the newly assessed
information called into question the strength of the underlying science
upon which EPA based its proposed decision in the 1997 review to select
a level of a cumulative, seasonal form associated with protecting 50
percent of crop cases from no more than 10 percent yield loss as
providing the requisite degree of protection for commodity crops.  

The 2007 Staff Paper then considered whether any additional information
is available to inform judgments as to the adversity of various
O3-induced levels of crop yield loss to the public welfare.  As noted
above, the 2007 Staff Paper observed that agricultural systems are
heavily managed, and that in addition to stress from O3, the annual
productivity of agricultural systems is vulnerable to disruption from
many other stressors (e.g., weather, insects, disease), whose impact in
any given year can greatly outweigh the direct reduction in annual
productivity resulting from elevated O3 exposures.  On the other hand,
O3 can also more subtly impact crop and forage nutritive quality and
indirectly exacerbate the severity of the impact from other stressors. 
Though these latter effects currently cannot be quantified, they should
be considered in judging to what extent a level of protection selected
to protect commodity crops should be precautionary.

Based on the above considerations, the 2007 Staff Paper concluded that
the level of protection (no more than 10% yield or biomass loss in 50%
of studied cases) judged requisite in the 1997 review to protect the
public welfare from adverse levels of O3–-induced reductions in crop
yields and tree seedling biomass loss, as provided by a W126 level of 21
ppm-hour, remains appropriate for consideration as an upper bound of a
range of appropriate levels.

Thus, the 2007 Staff Paper concluded, based on all the above
considerations, that an appropriate range of 3-month, 12-hour W126
levels was 7 to 21 ppm-hour, recognizing that the level selected is
largely a policy judgment as to the requisite level of protection
needed.  In determining the requisite level of protection for crops and
trees, and indirectly, ecosystems, the 2007 Staff Paper recognized that
it is appropriate to weigh the importance of the predicted risks of
these effects in the overall context of public welfare protection, along
with a determination as to the appropriate weight to place on the
associated uncertainties and limitations of this information.  

The CASAC, in its final letter to the Administrator (Henderson, 2007),
agreed with the 2007 Staff Paper recommendations that the lower bound of
the range within which a seasonal W126 welfare-based (secondary) O3
standard should be considered is approximately 7 ppm-hour; however, it
did not agree with staff’s recommendation that the upper bound of the
range for consideration should be as high as 21 ppm-hour.  Rather, CASAC
recommended that the upper bound of the range considered should be no
higher than 15 ppm-hour, which is just above the upper ends of the
ranges identified in the 1996 Consensus Workshop as being protective of
tree seedlings and saplings grown in natural forest stands and in
plantations.  The lower end of this range (7 ppm-hour) is the same as
the lower end of the range identified in the 1996 Consensus Workshop as
protective of tree seedlings in natural forest stands from growth
effects. 

In the 2007 proposed rule, taking 2007 Staff Paper and CASAC views into
account, EPA proposed a range of levels for a cumulative, seasonal
secondary standard as expressed in terms of the maximum 3 month, 12-hour
W126 form, in the range of 7 to 21 ppm-hour.  This range encompasses the
range of levels recommended by CASAC, and also includes a higher level
as recommended for consideration in the 2007 Staff Paper.  Given the
uncertainty in determining the risk attributable to various levels of
exposure to O3, EPA believed, as a public welfare policy judgment, that
this was a reasonable range to propose.

2.	Considerations Regarding the 2007 Proposed 8-Hour Standard

In the 1997 review, the 1996 Staff Paper included an analysis to compare
the degree of overlap between areas that would be expected not to meet
the range of alternative 8-hour standards being considered for the
primary NAAQS and those expected not to meet the range of values
(expressed in terms of the seasonal SUM06 index) of concern for
vegetation.  This result suggested that improvements in national air
quality expected to result from attaining an 8-hour primary standard
within the recommended range of levels would also be expected to reduce
levels of concern for vegetation in those same areas.  In the 1997 final
rule, the decision was made, on the basis of both science and policy
considerations, to make the secondary identical to the primary standard.
 It acknowledged, however, that uncertainties remained “as to the
extent to which air quality improvements designed to reduce 8-hour
average O3 concentrations averaged over a 3-year period would reduce O3
exposures measured by a seasonal SUM06 index” (62 FR 38876). 

On the basis of that history, the 2007 Staff Paper analyzed the degree
of overlap expected between alternative 8-hour and cumulative seasonal
secondary standards (as discussed above in section IV.C.1) using then
recent air quality.  Based on the results, the 2007 Staff Paper
concluded that the degree to which the then current 8-hour standard form
and level would overlap with areas of concern for vegetation expressed
in terms of the 12-hour W126 standard is inconsistent from year to year
and would depend greatly on the level of the 12-hour W126 and 8-hour
standards selected and the distribution of hourly O3 concentrations
within the annual and/or 3-year average period.  

Thus, though the 2007 Staff Paper recognized again that meeting the
current or alternative levels of the 8-hour average standard could
result in air quality improvements that would potentially benefit
vegetation in some areas, it urged caution be used in evaluating the
likely vegetation impacts associated with a given level of air quality
expressed in terms of the 8-hour average form in the absence of parallel
W126 information.  This caution was due to the concern that the analysis
in the 2007 Staff Paper may not be an accurate reflection of the true
situation in non-monitored, rural counties due to the lack of more
complete monitor coverage in many rural areas.  Further, of the counties
that did not show overlap between the two standard forms, most were
located in rural/remote high elevation areas which have O3 air quality
patterns that are typically different from those associated with urban
and near urban sites at lower elevations.  Because the majority of such
areas are currently not monitored, it is believed there are likely to be
additional areas that have similar air quality distributions that would
lead to the same disconnect between forms.  Thus, the 2007 Staff Paper
concluded that it remained problematic to determine the appropriate
level of protection for vegetation using an 8-hour average form.

The CASAC recognized that an important difference between the effects of
acute exposures to O3 on human health and the effects of O3 exposures on
welfare is that vegetation effects are more dependent on the cumulative
exposure to, and uptake of, O3 over the course of the entire growing
season (Henderson, 2006c).  The CASAC O3 Panel members were unanimous in
concluding the protection of natural terrestrial ecosystems and managed
agricultural crops requires a secondary O3 standard that is
substantially different from the primary O3 standard in averaging time,
level, and form (Henderson, 2007).

	In considering the appropriateness of proposing a revised secondary
standard that would be identical to the proposed primary standard, EPA
took into account the approach used by the Agency in the 1997 review,
the conclusions of the 2007 Staff Paper, CASAC advice, and the views of
public commenters.  The EPA first considered the 2007 Staff Paper
analysis of the projected degree of overlap between counties with air
quality expected to meet various alternative levels of an 8-hour
standard and alternative levels of a W126 standard based on monitored
air quality data.  This analysis showed significant overlap within the
proposed range of the primary 8-hour form and selected levels of the
W126 standard form being considered, with the degree of overlap between
these two forms depending greatly on the levels selected and the
distribution of hourly O3 concentrations within the annual and/or 3-year
average period.  On this basis, EPA concluded that a secondary standard
set identical to the proposed primary standard would provide a
significant degree of additional protection for vegetation as compared
to that provided by the current secondary standard.  The EPA also
recognized that lack of rural monitoring data made uncertain the degree
to which the proposed 8-hour or W126 alternatives would be protective,
and that there would be the potential for not providing the appropriate
degree of protection for vegetation in areas with air quality
distributions that result in a high cumulative, seasonal exposure but do
not result in high 8-hour average exposures.  While this potential for
under-protection using an 8-hour standard was clear, the number and size
of areas at issue and the degree of risk was hard to determine.  On the
other hand, EPA also considered at that time that there was a potential
risk of over-protection with a cumulative, seasonal standard given the
inherent uncertainties associated with moving to a new form for the
secondary standard, in particular those associated with predicting
exposure and risk patterns based on a limited rural monitoring network. 

The EPA also considered the views and recommendations of CASAC, and
agreed that a cumulative, seasonal standard is the most biologically
relevant way to relate exposure to plant growth response.  However, as
reflected in the public comments, EPA also recognized that there
remained significant uncertainties in determining or quantifying the
degree of risk attributable to varying levels of O3 exposure, the degree
of protection that any specific cumulative, seasonal standard would
produce, and the associated potential for error in determining the
standard that will provide a requisite degree of protection -- i.e.,
sufficient but not more than what is necessary.  Given this uncertainty,
EPA also believed it was appropriate to consider the degree of
protection that would be afforded by a secondary standard that was
identical to the then proposed primary standard.  Based on its
consideration of the full range of views as described above, and in the
2007 proposed rule, EPA proposed as a second option to revise the
secondary standard to be identical in every way to the then proposed
primary standard.

3.	Basis for 2008 Decision on the Secondary Standard

In the 2008 final rule, EPA noted that deciding on the appropriate
secondary standard involved making a choice between two possible
alternatives, each with their strengths and weaknesses.  The 2008 final
rule reported that within the Administration at that time there had been
a robust discussion of the same strengths and weaknesses associated with
each option that were identified earlier.  The process by which EPA
reached its final conclusion is described in the final rule (73 FR
16497).  The rationale for the 2008 decision presented in the final rule
(73 FR 16499 – 16500) is described below. 

In considering the appropriateness of establishing a new standard
defined in terms of a cumulative, seasonal form, or revising the then
current secondary standard by making it identical to the revised primary
standard, EPA took into account the approach used by the Agency in the
1997 review, the conclusions of the 2007 Staff Paper, CASAC advice, and
the views of public commenters.  In giving consideration to the approach
taken in the 1997 review, EPA first considered the 2007 Staff Paper
analysis of the projected degree of overlap between counties with air
quality expected to meet the revised 8-hour primary standard, set at a
level of 0.075 ppm, and alternative levels of a W126 standard based on
currently monitored air quality data. This analysis showed significant
overlap between the revised 8-hour primary standard and selected levels
of the W126 standard form being considered, with the degree of overlap
between these alternative standards depending greatly on the W126 level
selected and the distribution of hourly O3 concentrations within the
annual and/or 3-year average period.  On this basis, as an initial
matter, EPA concluded that a secondary standard set identical to the
proposed primary standard would provide a significant degree of
additional protection for vegetation as compared to that provided by the
then current 0.084 ppm secondary standard.  In further considering the
significant uncertainties that remain in the available body of evidence
of O3-related vegetation effects and in the exposure and risk analyses
conducted for the 2008 rulemaking, and the difficulty in determining at
what point various types of vegetation effects become adverse for
sensitive vegetation and ecosystems, EPA focused its consideration on a
level for an alternative W126 standard at the upper end of the proposed
range (i.e., 21 ppm-hour). The 2007 Staff Paper analysis showed that at
that W126 standard level, there would be essentially no counties with
air quality that would be expected both to exceed such an alternative
W126 standard and to meet the revised 8-hour primary standard – that
is, based on this analysis of currently monitored counties, a W126
standard would be unlikely to provide additional protection in any
monitored areas beyond that likely to be provided by the revised primary
standard.

The EPA also recognized that the general lack of rural monitoring data
made uncertain the degree to which the revised 8-hour standard or an
alternative W126 standard would be protective in those areas, and that
there would be the potential for not providing the appropriate degree of
protection for vegetation in areas with air quality distributions that
result in a high cumulative, seasonal exposure but do not result in high
8-hour average exposures. While this potential for under-protection
using an 8-hour standard was clear, the number and size of areas at
issue and the degree of risk was hard to determine. However, EPA
concluded at that time that an 8-hour standard would also tend to avoid
the potential for providing more protection than is necessary, a risk
that EPA concluded would arise from moving to a new form for the
secondary standard despite significant uncertainty in determining the
degree of risk for any exposure level and the appropriate level of
protection, as well as uncertainty in predicting exposure and risk
patterns.

The EPA also considered the views and recommendations of CASAC, and
agreed that a cumulative, seasonal standard was the most biologically
relevant way to relate exposure to plant growth response.  However, as
reflected in some public comments, EPA also judged that there remained
significant uncertainties in determining or quantifying the degree of
risk attributable to varying levels of O3 exposure, the degree of
protection that any specific cumulative, seasonal standard would
produce, and the associated potential for error in determining the
standard that will provide a requisite degree of protection — i.e.,
sufficient but not more than what is necessary. Given these significant
uncertainties, EPA concluded at that time that establishing a new
secondary standard with a cumulative, seasonal form would result in
uncertain benefits beyond those afforded by the revised primary standard
and therefore may be more than necessary to provide the requisite degree
of protection.

Based on its consideration of the views discussed above, EPA judged in
the 2008 rulemaking that the appropriate balance to be drawn was to
revise the secondary standard to be identical in every way to the
revised primary standard.  The EPA believed that such a standard would
be sufficient to protect public welfare from known or anticipated
adverse effects, and did not believe that an alternative cumulative,
seasonal standard was needed to provide this degree of protection. The
EPA believed that this judgment appropriately considered the requirement
for a standard that is neither more nor less stringent than necessary
for this purpose.

For the reasons discussed above, and taking into account information and
assessments presented in the 2006 Criteria Document and 2007 Staff
Paper, the advice and recommendations of the CASAC Panel, and the public
comments to date, EPA decided to revise the existing 8-hour secondary
standard.  Specifically, EPA revised the then current 8-hour average
0.084 ppm secondary standard by making it identical to the revised
8-hour primary standard set at a level of 0.075 ppm.

4.	CASAC Views Following 2008 Decision  

Following the 2008 decision on the O3 standards, serious questions were
raised as to whether the standards met the requirements of the CAA.  In
April 2008, the members of the CASAC Ozone Review Panel sent a letter to
EPA stating “In our most-recent letters to you on this subject - dated
October 2006 and March 2007 - … the Committee recommended an
alternative secondary standard of cumulative form that is substantially
different from the primary Ozone NAAQS in averaging time, level and form
— specifically, the W126 index within the range of 7 to 15 ppm-hour,
accumulated over at least the 12 “daylight” hours and the three
maximum ozone months of the summer growing season” (Henderson, 2008). 
The letter continued: “The CASAC now wishes to convey, by means of
this letter, its additional, unsolicited advice with regard to the
primary and secondary Ozone NAAQS. In doing so, the participating
members of the CASAC Ozone Review Panel are unanimous in strongly urging
you or your successor as EPA Administrator to ensure that these
recommendations be considered during the next review cycle for the Ozone
NAAQS that will begin next year” (id.).  The letter further stated the
following views:

The CASAC was … greatly disappointed that you failed to change the
form of the secondary standard to make it different from the primary
standard. As stated in the preamble to the Final Rule, even in the
previous 1996 ozone review, “there was general agreement between the
EPA staff, CASAC, and the Administrator, … that a cumulative, seasonal
form was more biologically relevant than the previous 1-hour and new
8-hour average forms (61 FR 65716)” for the secondary standard.
Therefore, in both the previous review and in this review, the Agency
staff and its advisors agreed that a change in the form of the secondary
standard was scientifically well-justified.

:   :  :  :  ;The CASAC was pleased to see that the EPA Deputy
Administrator clearly articulated a robust scientific defense of this
position when he responded to Ms. Susan Dudley of the Office of
Management and Budget (OMB) in a memorandum dated March 7, 2008 that,
“In light of the available information, EPA believes that
ozone-related effects on vegetation are clearly linked to cumulative,
seasonal exposures and are not appropriately characterized by the use of
a short-term (8-hour) daily measure of ozone exposure.” However, the
Committee was disappointed and surprised that written correspondence
from OMB to the Agency apparently thwarted the opportunity to take a
major step forward in setting a separate secondary ozone standard that
is different in form from the primary standard. The CASAC is
particularly dismayed at the suggestion that setting a secondary NAAQS
that is different from the primary NAAQS is somehow against the law —
which is not only at odds with a plain-language reading of the Clean Air
Act but is also contrary to the Agency’s previous actions in setting a
separate secondary standard for the initial NAAQS for both particulate
matter and sulfur oxides, the latter of which (i.e., for SO2) remains in
effect. 

Unfortunately, this scientifically-sound approach of using a cumulative
exposure index for welfare effects was not adopted, and the default
position of using the primary standard for the secondary standard was
once again instituted. Keeping the same form for the secondary Ozone
NAAQS as for the primary standard is not supported by current scientific
knowledge indicating that different indicator variables are needed to
protect vegetation compared to public health. The CASAC was further
disappointed that a secondary standard of the W126 form was not
considered from within the Committee’s previously-recommended range of
7 to 15 ppm-hour. The CASAC sincerely hopes that, in the next round of
Ozone NAAQS review, the Agency will be able to support and establish a
reasonable and scientifically-defensible cumulative form for the
secondary standard.  (Henderson, 2008)

5.	Administrator’s Proposed Conclusions

	For the reasons discussed below, the Administrator proposes to set a
cumulative seasonal standard expressed as an annual index of the sum of
weighted hourly concentrations (i.e., the W126 form), cumulated over 12
hours per day (8:00 am to 8:00 pm) during the consecutive 3-month period
within the O3 season with the maximum index value, set at a level within
the range of 7 to 15 ppm-hour.  This proposed decision takes into
account the information and assessments presented in the 2006 Criteria
Document and the 2007 Staff Paper and related technical support
documents, the advice and recommendations of CASAC both during and
following the 2008 rulemaking, and public comments received in
conjunction with review of drafts of these documents and on the 2007
proposed rule.

a.	Form

As discussed above in section IV.B, the 2006 Criteria Document and 2007
Staff Paper concluded that the recent vegetation effects literature
evaluated in the 2008 rulemaking strengthens and reaffirms conclusions
made in the 1997 review that the use of a cumulative exposure index that
differentially weights ambient concentrations is best able to relate
ambient exposures to vegetation response. The 1997 review focused in
particular on two of these cumulative forms, the SUM06 and W126 (EPA,
1996).  Given that the data available at that time were unable to
distinguish between these forms, the EPA, based on the policy
consideration of not including O3 concentrations considered to be within
the PRB, estimated at that time to be between 0.03 and 0.05 ppm,
concluded that the SUM06 form would be the more appropriate choice for a
cumulative, exposure index for a secondary standard.  

In the 2008 rulemaking, the 2007 Staff Paper evaluated the continued
appropriateness of the SUM06 form in light of new estimates of PRB that
were lower than in the 1997 review, and the continued lack of evidence
within the vegetation effects literature of a biological threshold for
vegetation exposures of concern.  On the basis of these policy and
science-related considerations, the 2007 Staff Paper concluded that the
W126 form was the more appropriate cumulative, concentration-weighted
form.  Specifically, the W126, by its incorporation of a sigmoidal
weighting scheme, does not create an artificially imposed concentration
threshold, gives proportionally more weight to the higher and typically
more biologically potent concentrations, and is not significantly
influenced by O3 concentrations within the range of estimated PRB.  

As discussed above, the CASAC, based on its assessment of the same
vegetation effects science, agreed with the 2006 Criteria Document and
2007 Staff Paper and unanimously concluded that protection of vegetation
from the known or anticipated adverse effects of ambient O3 “requires
a secondary standard that is substantially different from the primary
standard in averaging time, level, and form,” i.e. not identical to
the primary standard for O3 (Henderson, 2007).  Moreover, the members of
CASAC and a substantial majority of the other CASAC Panel members agreed
with 2007 Staff Paper conclusions and encouraged EPA to establish an
alternative cumulative secondary standard for O3 and related
photochemical oxidants that is distinctly different in averaging time,
form and level from the then current or potentially revised 8-hour
primary standard (Henderson, 2006c).  The CASAC Panel also stated that
“the recommended metric for the secondary ozone standard is the
(sigmoidally weighted) W126 index” (Henderson, 2007).

In reconsidering the 2008 final rule, the Administrator agrees with the
conclusions drawn in the 2006 Criteria Document, 2007 Staff Paper and by
CASAC that the scientific evidence available in the 2008 rulemaking
continues to demonstrate the cumulative nature of O3-induced plant
effects and the need to give greater weight to higher concentrations. 
Thus, the Administrator concludes that a cumulative exposure index that
differentially weights O3 concentrations represents a reasonable policy
choice for a secondary standard to protect against the effects of O3 on
vegetation   The Administrator further agrees with both the 2007 Staff
Paper and CASAC that the most appropriate cumulative,
concentration-weighted form to consider is the sigmoidally weighted W126
form

The Administrator notes that in the 2007 proposed rule, EPA proposed a
second option of revising the then current 8-hour average secondary
standard by making it identical to the proposed 8-hour primary standard.
 The 2007 Staff Paper analyzed the degree of overlap expected between
alternative 8-hour and cumulative seasonal secondary standards using
recent air quality monitoring data.  Based on the results, the 2007
Staff Paper concluded that the degree to which the current 8-hour
standard form and level would overlap with areas of concern for
vegetation expressed in terms of the 12-hour W126 standard is
inconsistent from year to year and would depend greatly on the level of
the 12-hour W126 and 8-hour standards selected and the distribution of
hourly O3 concentrations within the annual and/or 3-year average period.
 The 2007 Staff Paper also recognized that meeting the then current or
alternative levels of the 8-hour average standard could result in air
quality improvements that would potentially benefit vegetation in some
areas, but urged caution be used in evaluating the likely vegetation
impacts associated with a given level of air quality expressed in terms
of the 8-hour average form in the absence of parallel W126 information. 
This caution was due to the concern that the analysis in the 2007 Staff
Paper may not be an accurate reflection of the true situation in
non-monitored, rural counties due to the lack of more complete monitor
coverage in many rural areas.  Further, of the counties that did not
show overlap between the two standard forms, most were located in
rural/remote high elevation areas which have O3 air quality patterns
that are typically different from those associated with urban and near
urban sites at lower elevations.  Because the majority of such areas are
currently not monitored, there are likely to be additional areas that
have similar air quality distributions that would lead to the same
disconnect between forms.  Thus, the 2007 Staff Paper concluded that it
remains problematic to determine the appropriate level of protection for
vegetation using an 8-hour average form.

The Administrator also notes that CASAC recognized that an important
difference between the effects of acute exposures to O3 on human health
and the effects of O3 exposures on welfare is that vegetation effects
are more dependent on the cumulative exposure to, and uptake of, O3 over
the course of the entire growing season (Henderson, 2006c).  The CASAC
O3 Panel members were unanimous in concluding the protection of natural
terrestrial ecosystems and managed agricultural crops requires a
secondary O3 standard that is substantially different from the primary
O3 standard in form, averaging time, and level (Henderson, 2007).

In reaching her proposed decision in this reconsideration of the 2008
final rule, the Administrator has considered the comments received on
the 2007 proposed rule regarding revising the secondary standard either
to reflect a new, cumulative form or by remaining equal to a revised
primary standard.  The commenters generally fell into two groups.

One group of commenters, including environmental organizations, strongly
supported the proposed option of moving to a cumulative, seasonal
standard, generally based on the reasoning explained in the 2007
proposal.  Commenters in this group also expressed serious concerns with
the other proposed option of setting a secondary O3 standard in terms of
the same form and averaging time (i.e., daily maximum 8-hour average O3
concentration) as the primary standard.  These commenters expressed the
view that such a standard would fail to protect public welfare because
the maximum daily 8-hour average O3 concentration failed to adequately
characterize harmful O3 exposures to vegetation.  This view was
generally based on the observation that there is no consistent
relationship in areas across the U.S. between 8-hour peak O3
concentrations and the longer-term cumulative exposures aggregated over
a growing season that are biologically relevant in characterizing
O3-related effects on sensitive vegetation.  Thus, as EPA noted in the
2007 proposed rule, there is a lack of a rational connection between the
level of an 8-hour standard and the requisite degree of protection
required for a secondary O3 NAAQS.

Another group of commenters, including industry organizations, agreed
that a cumulative form of the standard may better match the underlying
data, but expressed the view that remaining uncertainties associated
with the vegetation effects evidence and/or EPA’s exposure, risk and
benefits assessments were so great that the available information did
not provide an adequate basis to adopt a standard with a level based on
a cumulative, seasonal form.  These commenters asserted that because of
the substantial uncertainties remaining at the time of the 2008
rulemaking, the benefits of changing to a W126 form were too uncertain
to warrant revising the form of the standard at that time.

The Administrator notes that in both the 1997 and the 2008 decisions,
EPA recognized that the risk to vegetation from O3 exposures comes from
cumulative exposures over a season or seasons.   The CASAC has fully
endorsed this view based on the available scientific evidence and
assessments, and there is no significant disagreement on this issue by
commenters.  Thus, it is clear that the purpose of the secondary O3
NAAQS should be to provide an appropriate degree of protection against
cumulative, seasonal exposures to O3 that are known or anticipated to
harm sensitive vegetation or ecosystems.  In reconsidering the 2008
final rule, the Administrator recognizes that the issue before the
Agency is what form of the standard is most appropriate to perform that
function.

Within this framework, the Administrator recognizes that it is clear
that a cumulative, seasonal form has a distinct advantage in protecting
against cumulative, seasonal exposures.  Such a form is specifically
designed to measure directly the kind of O3 exposures that can cause
harm to vegetation.  In contrast, an 8-hour standard does not measure
cumulative, seasonal exposures directly, and can only indirectly afford
some degree of protection against such exposures.  To the extent that
clear relationships exist between 8-hour daily peak O3 concentrations
and cumulative, seasonal exposures, the 8-hour form and averaging time
would have the potential to be effective as an indirect surrogate. 
However, as discussed in the 2007 proposed rule and the 2008 final rule,
the evidence shows that there are known types of O3 air quality patterns
that can lead to high levels of cumulative, seasonal O3 exposures
without the occurrence of high daily 8-hour peak O3 concentrations.  An
8-hour form and averaging time is an indirect way to measure the
biologically relevant exposure patterns, is poorly correlated with such
exposure patterns, and therefore provides less certainty that the
standard willis less likely to identify and protect against the kind of
cumulative, seasonal exposure patterns that have been determined to be
harmful. 

Past arguments or reasons for not moving to a cumulative, seasonal form,
with appropriate exposure periods, have not been based on disagreement
over the biological relevance of the cumulative, seasonal form, or the
recognized disadvantages of an 8-hour standard in measuring and
identifying a specified cumulative, seasonal exposure pattern.  The
reasons for not moving to such a form have been based on concerns over
whether EPA has an adequate basis to identify the nature and magnitude
of cumulative, seasonal exposure patterns that the standard should be
designed to protect against, given the various uncertainties in the
evidence and the lack of rural O3 monitoring data.  This most directly
translates into a concern over whether EPA has an adequate basis to
determine an appropriate level for a cumulative, seasonal secondary
standard.

The Administrator has also considered issues associated with selection
of the W126 cumulative form, as reflected in the following assertions
made by some commenters on the 2007 proposed rule:  (1) the W126 form
lacks a biological basis, since it is merely a mathematical expression
of exposure that has been fit to specific responses in OTC studies, such
that its relevance for real world biological responses is unclear; (2) a
flux-based model would be a better choice than a cumulative metric
because it is an improvement over the many limitations and
simplifications associated with the cumulative form; however, there is
insufficient data to apply such a model at present; (3) the European
experience with cumulative O3 metrics has been disappointing and now
Europeans are working on their second level approach, which will be
flux-based; and (4) a second index that reflects the accumulation of
peaks at or above 0.10 ppm (called N100)  should be added to a W126
index to achieve appropriate protection.

With regard to whether the W126 index lacks a biological basis, the
Administrator finds no basis for reaching such a conclusion.  As
discussed above in section IV.B, the vegetation effects science is clear
that exposures of concern to plants are not based on one discrete 8-hour
period but on the repeated occurrence of elevated O3 levels throughout
the plant’s growing season.  The cumulative nature of the W126 is
supported by the basic biological understanding that plants in the U.S.
are generally most biologically active during the warm season and are
exposed to ambient O3 throughout this biologically active period.  In
addition, it has been shown in the scientific literature that all else
being equal, plants respond more to higher O3 concentrations, with no
evidence of an exposure threshold for vegetation effects.  The W126
sigmoidal weighting function reflects both of these understandings, by
not including a threshold below which concentrations are not included,
and by differentially weighting concentrations to give greater weight to
higher concentrations and less weight to lower ones. 

With regard to whether a flux-based model would be a better choice, the
2007 Staff Paper acknowledged that flux models may produce a more
accurate calculation of dose to a specific plant species in a specific
area.  However, dose-response relationships have not been developed for
these flux calculations for plants growing in the U.S.  Further, flux
calculations require large amounts of data for the physiology of each
plant species and the local conditions for the growing range of each
plant species.  These exercises may be useful for limited small-scale
risk assessments, but do not provide an appropriate basis for a national
standard at this time.

With regard to dissatisfaction with the performance of a particular
cumulative index in use in Europe, and growing interest in development
of flux-based models, the 2007 Staff Paper (Appendix 7A) noted that
“because of a lack of flux-response data, a cumulative, cutoff
concentration based (e.g., AOT40) exposure index will remain in use in
Europe for the near future for most crops and for forests and
semi-natural herbaceous vegetation (Ashmore et al., 2004a).”  Further,
like the SUM06 index, the AOT40 index incorporates a threshold below
which concentrations are not considered.  Though the AOT40 threshold is
lower than the threshold value in SUM06, the 2007 Staff Paper concluded
that the vegetation effects information does not provide evidence of an
effects threshold that applies to all species.  Thus, the Administrator
concludes neither of these forms is as biologically relevant as the W126
form.

With regard to consideration of coupling a W126 form with a separate
N100 index, there was very little research on the N100 index or a
coupled approach to be evaluated in the 2008 rulemaking.  The CASAC,
after reviewing all the information in the 2006 Criteria Document and
the 2007 Staff Paper, did not recommend an additional N100 index for
consideration.  Therefore, there is no basis at this time to judge the
extent to which such a coupled W126-N100 form would be a better choice
than the proposed W126 form.  Further, the W126 form incorporates a
weighting scheme that places greater weight on increasing concentrations
and gives every concentration of 0.10 ppm and above an equal weight of
1, which is the highest weight in this sigmoidal weighting function. 

	In summary, having considered the scientific information and assessment
results available in the 2008 rulemaking as discussed above in this
proposal notice, as well as the recommendations of the staff and CASAC,
and having taken into consideration issues raised in public comments
received as part of the 2008 rulemaking, and recognizing the
determinations made below in section IV.D.5.c on level, the
Administrator concludes that it is appropriate to set the secondary
standard using a cumulative, seasonal form.  The Administrator also
concludes that the W126 form is best suited to reflect the biological
impacts of O3 exposure on vegetation, and that there is adequate
certainty in the information available in the 2008 rulemaking to support
such a change in form.  Thus, the Administrator proposes to set the
secondary standard using a cumulative, seasonal W126 form.

b.	Averaging Times

The Administrator, in addition to reconsidering what form of a secondary
standard is most appropriate for protecting vegetation, is also
reconsidering what exposure periods (e.g., seasonal window, diurnal
window), and what standard index, in terms of an annual index value
versus a 3-year average of annual index values, are most appropriate
when used in conjunction with the W126 cumulative seasonal form.   Based
on the information set forth in the 2007 Staff Paper, as well as CASAC
views, as discussed above in section IV.D.1.b, the Administrator has
reached conclusions regarding exposure periods, and the annual versus
3-year average index, that have the most biological relevance for plant
response, as discussed below.

In considering an appropriate seasonal window, the Administrator notes
that the 2007 Staff Paper concluded that the consecutive 3-month period
within the O3 season with the highest W126 index value (e.g., maximum
3-month period) was a reasonable seasonal time period to consider.  The
Administrator further notes that the 2007 Staff Paper acknowledged that
the selection of any single seasonal exposure period for a national
standard would necessarily represent a compromise, given the significant
variability in growth patterns and lengths of growing seasons among the
wide range of sensitive vegetation species occurring within the U.S.  
However, the Administrator also considered the Staff Paper conclusion
that the period of maximum potential plant uptake of O3 would also
likely coincide with the period of highest O3 occurring within the
intra-annual period defined as the O3 season, since the high temperature
and light conditions conducive to O3 formation are also conducive for
plant activity.  The Administrator also observes that the CASAC panel
was supportive of the Staff Paper views, while recognizing that 3 months
likely represented the minimum timeframe appropriate to consider. 
Therefore, the Administrator concludes, on these bases, that the
consecutive 3-month period within the O3 season with the highest W126
index value (e.g., maximum 3-month period) remains an appropriate
seasonal window to propose for the protection of sensitive vegetation.

With regard to consideration of an appropriate diurnal window, the
Administrator has taken into account the 2007 Staff Paper conclusion
that for the vast majority of studied species, daytime exposures
represent the majority of diurnal plant O3 uptake and are responsible
for inducing the plant response of most significance to the health and
productivity of the plant (e.g., reduced carbohydrate production).   The
Administrator is also aware, based on discussions in the 2007 Staff
Paper that there are some number of species that show non-negligible
amounts of O3 uptake at night due to incomplete stomatal closure.   In
reaching her conclusion that the 2007 Staff Paper recommendation of a
12-hour daytime window (8:00 a.m. to 8:00 p.m.) remains the most
appropriate period over which to cumulate diurnal O3 exposures,
specifically those most relevant to plant growth and yield responses,
the Administrator places weight on the fact that the CASAC comments were
also supportive of this diurnal window, recognizing again that it likely
represents a minimum period over which plants can be vulnerable to O3
uptake.  Therefore, the Administrator is again proposing the 12-hour
daytime window (8:00 a.m. to 8:00 p.m.) as an appropriate diurnal window
to protect against O3-induced plant effects.

Lastly, in considering whether an annual or a 3-year average index is
more appropriate, the Administrator notes that in addition to the
available scientific evidence regarding plant effects that can be
brought to bear, there are also other public welfare considerations that
may be appropriate to consider.  In taking this view, the Administrator
notes that the 2007 Staff Paper recognized that though most cumulative
seasonal exposure levels of concern for vegetation have been expressed
in terms of the annual timeframe, it may be appropriate to consider a
3-year average for purposes of standard stability.  The Administrator
has considered that while the 2007 Staff Paper notes that for certain
welfare effects of concern (e.g., foliar injury, yield loss for annual
crops, growth effects on other annual vegetation and potentially tree
seedlings), an annual time frame may be a more appropriate period in
which to assess what level would provide the requisite degree of
protection, for other welfare effects (e.g., mature tree biomass loss),
it also points out that a 3-year average may also be appropriate.  The
Administrator further observes that in concluding that it was
appropriate to consider both an annual and a 3-year average, the 2007
Staff Paper also concluded that should a 3-year average of the 3-month,
12-hour W126 form be selected, a potentially lower level should be
considered to reduce the potential of adverse impacts to annual species
from a single high O3 year that could still occur while attaining a
standard on average over 3-years.   The Administrator also took note
that the CASAC Panel, in addressing this issue of annual versus 3-year
average concluded that multi-year averaging to promote a “stable”
secondary standard is less appropriate for a cumulative, seasonal
secondary standard than for a primary standard based on maximum 8-hour
concentrations, and further concluded that if multi-year averaging is
employed to increase the stability of the secondary standard, the level
of the standard should be revised downward to assure that the desired
degree of protection is not exceeded in individual years.  The
Administrator, in considering the merits of both the annual and 3-year
average, and taking into account both the 2007 Staff Paper and CASAC
views, concludes that it is important to place more weight on the public
welfare benefit in having a stable standard, and that appropriate
protection for vegetation can be achieved using a 3-year average form. 
The Administrator is thus proposing a 3-year average.  However, given
the uncertain nature of the evidence and potential concerns with using a
3-year average form, the Administrator is proposing to take comment on
the appropriateness of the specific seasonal and diurnal exposure
periods proposed, as well as the use of a 3-year average, and, as
discussed below, the impact that selection of these proposed seasonal
and diurnal exposure periods would have, in conjunction with a 3-year
average form, on the appropriateness of the proposed range of levels. 

c.	Level

i.	Considerations Regarding 2007 Proposed Range of Levels

The 2007 Staff Paper, in identifying a range of levels for a 3-month,
12-hour (daytime) W126 standard appropriate for the Administrator to
consider in protecting the public welfare from known or anticipated
adverse effects to vegetation from O3 exposures, considered what
information from the array of vegetation effects evidence and exposure
and risk assessment results was most useful.  With respect to the
vegetation effects evidence, the 2007 Staff Paper found stronger support
than what was available at the time of the 1997 review for an increased
level of protection for trees and forested ecosystems.  Specifically,
the expanded body of evidence included: (1) additional field based data
from free air, gradient and biomonitoring surveys demonstrating adverse
levels of O3-induced growth reductions on trees at the seedling, sapling
and mature growth stages and incidence of visible foliar injury
occurring at biomonitoring sites in the field at ambient levels of
exposure; (2) qualitative support from free air (e.g., AspenFACE) and
gradient studies on a limited number of tree species for the continued
appropriateness of using OTC-derived C-R functions to predict tree
seedling response in the field; (3) studies that continued to document
below-ground effects on root growth and “carry-over” effects
occurring in subsequent years from O3 exposures; and (4) increased
recognition and understanding of the structure and function of
ecosystems and the complex linkages through which O3, and other
stressors, acting at the organism and species level can influence higher
levels within the ecosystem hierarchy and disrupt essential ecological
attributes critical to the maintenance of ecosystem goods and services
important to the public welfare. 

Based on the above sources of vegetation effects information and the
results of the exposure and risk assessments summarized above, the 2007
Staff Paper concluded that just meeting the then current 0.084 ppm,
8-hour average standard would continue to allow adverse levels of
O3-induced effects to occur in sensitive commercially and ecologically
important tree species in many regions of the country.  The 2007 Staff
Paper further concluded that air quality levels would need to be
substantially reduced to protect sensitive tree seedlings, such as black
cherry, aspen, and cottonwood, from these growth and foliar injury
effects.

In addition to the currently quantifiable risks to trees from ambient
exposures, the 2007 Staff Paper also considered the more subtle impacts
of O3 acting in synergy with other natural and man-made stressors to
adversely affect individual plants, populations and whole systems.  By
disrupting the photosynthetic process, decreasing carbon storage in the
roots, increasing early senescence of leaves and affecting water use
efficiency in trees, O3 exposures could potentially disrupt or change
the nutrient and water flow of an entire system.  Weakened trees can
become more susceptible to other environmental stresses such as pest and
pathogen outbreaks or harsh weather conditions.  Though it is not
possible to quantify all the ecological and societal benefits associated
with varying levels of alternative secondary standards, the 2007 Staff
Paper concluded that this information should be weighed in considering
the extent to which a secondary standard should be set so as to provide
potential protection against effects that are anticipated to occur.

	The 2007 Staff Paper also recognized that in the 1997 review, EPA took
into account the results of a 1996 Consensus Workshop.  At this
workshop, a group of independent scientists expressed their judgments on
what standard form(s) and level(s) would provide vegetation with
adequate protection from O3-related adverse effects.  Consensus was
reached on protective ranges of levels in terms of a cumulative,
seasonal 3-month, 12-hr SUM06 standard for a number of vegetation
effects endpoints.  These ranges are identified below, with the
estimated approximate equivalent W126 standard levels shown in
parentheses.  For growth effects to tree seedlings in natural forest
stands, a consensus was reached that a SUM06 range of 10 to 15 (W126
range of 7 to 13) ppm-hour would be protective.  For growth effects to
tree seedlings and saplings in plantations, the consensus SUM06 range
was 12 to 16 (W126 range of 9 to 14) ppm-hour.  For visible foliar
injury to natural ecosystems, the consensus SUM06 range was 8 to 12
(W126 range of 5 to 9) ppm-hour.  

The 2007 Staff Paper then considered to what extent recent research
provided empirical support for the ranges of levels identified by the
experts as protective of different types of O3-induced effects.  As
discussed above in section IV.D.1.c, the 2007 Staff Paper concluded on
the basis of the available evidence that it was appropriate to consider
a range for a 3-month, 12-hour, W126 standard level that included the
1996 Consensus Workshop recommendations regarding a range of levels
protective against O3-induced growth effects in tree seedlings in
natural forest stands (i.e., 7-13 ppm-hour in terms of a W126 form).

	In considering the newly available information on O3-related effects on
crops in this review, the 2007 Staff Paper observed the following
regarding the strength of the underlying crop science:  (1) nothing in
the recent literature points to a change in the relationship between O3
exposure and crop response across the range of species and/or cultivars
of commodity crops currently grown in the U.S. that could be construed
to make less appropriate the use of commodity crop C-R functions
developed in the NCLAN program; (2) new field-based studies (e.g.,
SoyFACE) provide qualitative support in a few limited cases for the
appropriateness of using OTC-derived C-R functions to predict crop
response in the field; and (3) refinements in the exposure, risk and
benefits assessments in this review reduce some of the uncertainties
present in 1996.  On the basis of these observations, the 2007 Staff
Paper concluded that nothing in the newly assessed information calls
into question the strength of the underlying science upon which EPA
based its proposed decision in the last review to select a level of a
cumulative, seasonal form associated with protecting 50 percent of crop
cases from no more than 10 percent yield loss as providing the requisite
degree of protection for commodity crops.  

The 2007 Staff Paper then considered whether any additional information
was available to inform judgments as to the adversity of various
O3-induced levels of crop yield loss to the public welfare.  As noted
above, the 2007 Staff Paper observed that agricultural systems are
heavily managed, and that in addition to stress from O3, the annual
productivity of agricultural systems is vulnerable to disruption from
many other stressors (e.g., weather, insects, disease), whose impact in
any given year can greatly outweigh the direct reduction in annual
productivity resulting from elevated O3 exposures.  On the other hand,
O3 can also more subtly impact crop and forage nutritive quality and
indirectly exacerbate the severity of the impact from other stressors. 
Since these latter effects could not be quantified at that time, they
could only be considered qualitatively in reaching judgments about an
appropriate degree of protection for commodity crops from O3–related
effects.

Based on the above considerations, the 2007 Staff Paper concluded that
the level of protection judged requisite in the 1997 review to protect
the public welfare from adverse levels of O3–induced reductions in
crop yields and tree seedling biomass loss, as approximately provided by
a W126 level of 21 ppm-hour, remained appropriate for consideration as
an upper bound of a range of appropriate levels.  The 2007 Staff Paper
also recognized that a standard set at this level would not protect the
most sensitive species or individuals within a species from all
potential effects related to O3 exposures and further, that this level
derives from the extensive and quantitative historic and recent crop
effects database, as well as current staff exposure and risk analyses
(EPA, 2007, pg. 8-22).   

In identifying a lower bound for the range of alternative standard
levels appropriate for consideration, staff concluded that several lines
of evidence pointed to the need for greater protection for tree
seedlings, mature trees, and associated forested ecosystems. Staff
believed that tree growth was an important endpoint to consider because
it is related to other aspects of societal welfare such as sustainable
production of timber and related goods, recreation, and carbon (CO2)
sequestration.  Impacts on tree growth can also affect ecosystems
through shifts in species composition and the loss of genetic diversity
due to the loss of O3 sensitive individuals or species.  In selecting an
appropriate level of protection for trees, staff considered the results
of the 1996 Consensus Workshop which identified the SUM06 range of 10 to
15 (W126 of 7 to 13) ppm-hour for growth effects to tree seedlings in
natural forest stands.  

Because staff believed that O3-related effects on forest tree species
are important public welfare effects of concern, it therefore concluded,
based on the above, that it was appropriate to include 7 ppm-hour as the
lower bound of the recommended range, the lower end of the approximate
range recommended by CASAC (Henderson, 2006c) and identified by the 1996
Consensus Workshop participants as protective of forest trees.  At this
lower end of the range, staff anticipated, based on its analyses of
risks of tree seedling biomass loss and mature tree growth reductions
and on the basis of the scientific effects literature, that adverse
effects of O3 on forested ecosystems would be substantially reduced. 
Further, staff anticipated that the lower end of this range would
provide increased protection from the more subtle impacts of O3 acting
in synergy with other natural and man-made stressors to adversely affect
individual plants, populations and whole systems. Staff also noted that
by disrupting the photosynthetic process, decreasing carbon storage in
the roots, increasing early senescence of leaves and affecting water use
efficiency in trees, O3 exposure could potentially disrupt or change the
nutrient and water flow of an entire system.  Such weakened trees can
become more susceptible to other environmental stresses such as pest and
pathogen outbreaks or harsh weather conditions. While recognizing that
it is not possible to quantify all the ecological and societal benefits
associated with varying levels of alternative secondary standards, staff
believed that this information should be weighed in considering the
extent to which a secondary standard should be precautionary in nature
in protecting against effects that have not yet been adequately studied
and evaluated. 

Thus, the 2007 Staff Paper concluded, based on all the above
considerations, that an appropriate range of levels, for an annual
standard using a 3-month, 12-hour W126 form, for the Administrator to
consider was 7 to 21 ppm-hour, recognizing that the level selected is
largely a policy judgment as to the requisite level of protection
needed.  In determining the requisite level of protection for crops and
trees, the 2007 Staff Paper recognized that it was appropriate to weigh
the importance of the predicted risks of these effects in the overall
context of public welfare protection, along with a determination as to
the appropriate weight to place on the associated uncertainties and
limitations of this information.  

ii.	CASAC and Public Comments Prior to 2008 Decision

In considering the evidence described in both the 2006 Criteria Document
and 2006 draft Staff Paper, CASAC, in its October 24, 2006 letter to the
Administrator, expressed its view regarding the appropriate form and
range of levels for the Administrator to consider.  The CASAC preferred
a seasonal 3-month W126 standard in a range that is the approximate
equivalent of the SUM06 at 10 to 20 ppm-hour.  Following the 2007
proposal, EPA received additional CASAC and public comments regarding an
appropriate range of levels of a W126 form for the Administrator to
consider in finalizing a revised secondary NAAQS for O3.  The CASAC, in
its final letter to the Administrator (Henderson, 2007), agreed with the
2007 Staff Paper recommendations that the lower bound of the range
within which a seasonal W126 secondary O3 standard should be considered
is approximately 7 ppm-hour; however, it did not agree with staff’s
recommendation that the upper bound of the range should be as high as 21
ppm-hour.  Rather, as discussed above in section IV.D.1.c, the CASAC
Panel recommended that the upper bound of the range considered should be
no higher than a W126 of 15 ppm-hour for an annual standard.  

The comments received from the public fell into two groups.  One group
of commenters supported the CASAC recommended range of 7- 15 ppm-hour
for a W126 standard.  Many of these same commenters further emphasized
the lower end of the proposed range as necessary to provide adequate
protection for sensitive species.  These commenters based their
recommendation primarily on four sources of information:  (1) 
field-based evidence of foliar injury occurring on sensitive species at
air quality levels well below that of the current standard; (2) the 1996
Consensus Workshop recommendations for protective levels in terms of
cumulative exposures for different vegetation types; (3) CASAC advice
and recommendations;  and (4) studies published after the close of the
2006 Criteria Document that potentially strengthen the link between
species level impacts and ecosystem response. 

	The other group of commenters did not support revising the current
secondary standard.  These commenters primarily focused on uncertainties
regarding the sources of information relied upon by the first group of
commenters as support for a level within the range of levels recommended
by CASAC.   These uncertainties included:  (1) potential confounders,
such as soil moisture, on visible foliar injury and the lack of a clear
relationship between visible foliar injury symptoms and other vegetation
effects; (2) lack of documentation of the basis for the recommendations
from the 1996 Consensus Workshop in selecting a range of levels,
indicating that these recommendations should be used with great caution;
(3) failure of CASAC and EPA to take into account the monitor height
measurement gradient when making their recommendations concerning the
level of the secondary standard; and  (4) inability to quantitatively
estimate ecosystem effects of O3 or to extrapolate meaningfully from
effects on individual plants to ecosystem effects due to inadequate
data.

iii.	Conclusions on Level

The Administrator is proposing to set a cumulative, seasonal standard
expressed in terms of the maximum 3-month, 12-hour W126 form, in the
range of 7 to 15 ppm-hour.  In reaching this proposed decision about an
appropriate range of levels for the secondary standard, the
Administrator has considered the following:  the evidence described in
the 2006 Criteria Document and the 2007 Staff Paper; the results of the
vegetation exposure and risk assessments discussed above and in the 2007
Staff Paper, giving weight to the assessments as judged appropriate; the
CASAC Panel’s advice and recommendations in the CASAC’s letters to
the Administrator; EPA staff recommendations; and public comments
received during the development of these documents, either in connection
with CASAC meetings or separately.  In considering what range of levels
of a cumulative 3-month standard to propose, the Administrator notes
that that this choice requires judgment as to what standard will protect
the public welfare from any known or anticipated adverse effects.  This
choice must be based on an interpretation of the evidence and other
information, such as the exposure and risk assessments, that neither
overstates nor understates the strength and limitations of the evidence
and information nor the appropriate inferences to be drawn.  In taking
all of the above into consideration, the Administrator also notes that
there is no bright line clearly directing the choice of level for any of
the effects of concern, and the choice of what is appropriate is clearly
a public welfare policy judgment entrusted to the Administrator.  This
judgment must include consideration of the strengths and limitations of
the evidence and the appropriate inferences to be drawn from the
evidence and the exposure and risk assessments. 

In particular, the Administrator has given careful consideration to the
following:  1) the nature and degree of effects of O3 to the public
welfare, including what constitutes an adverse effect; 2) the strengths
and limitations of the evidence that is available regarding known or
anticipated adverse effects from cumulative, seasonal exposures, and its
usefulness in informing selection of a proposed range; and 3) what are
CASAC’s views regarding the strength of the evidence and its adequacy
to inform a range of levels.  Each of these topics is discussed in turn
below.

In determining the nature and degree of effects of O3 on the public
welfare, the Administrator recognizes that the significance to the
public welfare of O3-induced effects on sensitive vegetation growing
within the U.S. can vary, depending on the nature of the effect, the
intended use of the sensitive plants or ecosystems, and the types of
environments in which the sensitive vegetation and ecosystems are
located.  Any given O3-related effect on vegetation and ecosystems
(e.g., biomass loss, foliar injury), therefore, may be judged to have a
different degree of impact on the public depending, for example, on
whether that effect occurs in a Class I area, a city park, or commercial
cropland.  In her judgment, it is appropriate that this variation in the
significance of O3-related vegetation effects should be taken into
consideration in judging the level of ambient O3 that is requisite to
protect the public welfare from any known or anticipated adverse
effects.   In this regard, the Administrator agrees with the definition
of adversity as described above in section IV.A.3 and in the 2008
rulemaking.   As a result, the Administrator concludes that of those
known and anticipated O3-related vegetation and ecosystem effects
identified and discussed in this reconsideration, the highest priority
and significance should be given to those that occur on sensitive
species that are known to or are likely to occur in federally protected
areas such as Class I areas or on lands set aside by States, Tribes and
public interest groups to provide similar benefits to the public
welfare, for residents on those lands, as well as visitors to those
areas.  

Likewise, the Administrator also notes that the same known or
anticipated O3-induced effects, occurring in other areas may call for
less protection.  For example, the maintenance of adequate agricultural
crop yields is extremely important to the public welfare and is
currently achieved through the application of intensive management
practices, including in some cases, genetic engineering.  These
management practices, in conjunction with market forces and government
programs, assure an appropriate balance is reached between costs of
production and market availability.  Thus, while research on
agricultural crop species remains useful in illuminating mechanisms of
action and physiological processes, information from this sector on
O3-induced effects is considered less useful in informing judgments on
what level(s) would be sufficient but not more than necessary to protect
the public welfare.  With respect to commercial production of
commodities, the Administrator notes that judgments about the extent to
which O3-related effects on commercially managed vegetation are adverse
from a public welfare perspective are particularly difficult to reach,
given that what is known about the relationship between O3 exposures and
agricultural crop yield response derives largely from data generated
almost 20 years ago.  The Administrator recognizes that there is
substantial uncertainty at this time as to whether these data remain
relevant to the majority of species and cultivars of crops being grown
in the field today.  In addition, the extensive management of such
vegetation may to some degree mitigate potential O3-related effects. 
The management practices used on these lands are highly variable and are
designed to achieve optimal yields, taking into consideration various
environmental conditions.  Thus, the Administrator concludes there is no
need for such additional protection for agricultural crops through the
NAAQS.

The Administrator also recognizes that O3-related effects on sensitive
vegetation can occur in other areas that have not been afforded special
Federal protections, ranging from effects on vegetation growing in
residential or commercial settings, such as ornamentals used in
urban/suburban landscaping, to vegetation grown in land use categories
that are heavily managed for commercial production of commodities such
as timber.  For vegetation used for residential or commercial ornamental
purposes, such as urban/suburban landscaping, the Administrator believes
that there is not adequate information at this time to establish a
secondary standard based specifically on impairment of urban/suburban
landscaping and other uses of ornamental vegetation, but notes that a
secondary standard revised to provide protection for sensitive natural
vegetation and ecosystems would likely also provide some degree of
protection for such ornamental vegetation.

Based on the above, the Administrator finds that the types of
information most useful in informing the selection of an appropriate
range of protective levels is appropriately focused on information
regarding exposures and responses of sensitive trees and other native
species known or anticipated to occur in protected areas such as Class I
areas or on lands set aside by States, Tribes and public interest groups
to provide similar benefits to the public welfare, for residents on
those lands, as well as visitors to those areas.  

With regard to the available evidence, the Administrator finds the
coherence and strength of the weight of evidence from the large body of
available literature compelling.  This evidence addresses a broad array
of O3-induced effects on a variety of tree species across a range of
growth stages (i.e., seedlings, saplings and mature trees) using diverse
field-based (e.g. free air, gradient and ambient) and OTC exposure
methods.  It demonstrates that significant numbers of forest tree
species are potentially experiencing O3-induced stress under levels of
ambient air quality, both at and below the level of the 1997 standard. 

In particular, the Administrator notes the evidence from recent
field-based studies and a gradient study of eastern cottonwood saplings
(Gregg et al., 2003).  She observes that this study found that
cottonwood saplings grown in urban New York City grew faster than
saplings grown in downwind rural areas where cumulative O3 exposures
were higher, and the difference in biomass production between the urban
site with the lowest cumulative exposure and the rural site with the
highest cumulative exposure is 

dramatic (Figure 7-17 in the 2007 Staff Paper).  The Administrator
further notes that cottonwood is one of the most sensitive tree species
studied to date and it is also important both from an ecological and
public welfare perspective, as discussed above in section IV.A.2.b and
in the 2007 Staff Paper.

The Administrator also notes the evidence related to the O3-induced
effect of visible foliar injury.  The Administrator observes that the
visible foliar injury database created from the ambient field-based
monitoring network managed by the Unites States Forest Service (USFS)
Forest Inventory and Analysis (FIA) Program has continued to expand
since the conclusion of the 1997 review.  In utilizing this dataset, EPA
staff collaborated with FIA staff to compare the incidence of visible
foliar injury at different levels of air quality by county throughout
the U.S. in counties with FIA monitoring sites.   In considering the
results of this analysis, depicted in Table 7-4 of the 2007 Staff Paper,
the Administrator notes that for the 2001-2004 period, the percent of
counties with documented foliar injury at a level approximately
equivalent to the W126 of 21 ppm-hour, was 26 to 49 percent, while at
the lower level approximately equivalent to a W126 of 13 ppm-hour,
incidence values ranged from 12 to 35 percent.  The Administrator
believes it likely that some sensitive species occurring in specially
protected areas would also exhibit visible foliar injury symptoms to a
similar degree at these exposure levels.  She further notes that while
direct links between O3 induced visible foliar injury symptoms and other
adverse effects (e.g., biomass loss) are not always found, visible
foliar injury in itself is considered by the National Park Service (NPS)
to affect adversely air quality related values (AQRV) in Class I areas.

The Administrator places significant weight on the judgments of CASAC. 
In so doing, the Administrator has carefully considered its stated views
and the basis for the range of levels the CASAC O3 Panel recommended. 
In its 2007 letter to the Administrator, the CASAC O3 Panel agreed with
EPA staff recommendations that the lower bound of the range within which
a seasonal W126 O3 standard should be considered is approximately 7
ppm-hour.  However, “it does not agree with Staff’s recommendations
that the upper bound of the range should be as high as 21 ppm-hour.
Rather, the Panel recommends that the upper bound of the range
considered should be no higher than 15 ppm-hour, which the Panel
estimates is approximately equivalent to a seasonal 12-hour SUM06 level
of 20 ppm-hour” (Henderson, 2007).   The Administrator notes that
CASAC views concerning an appropriate range of levels for the
Administrator to consider were presented after CASAC had considered the
entire body of evidence presented in both the 2006 Criteria Document and
2007 Staff Paper, and are generally consistent with the 1996 Consensus
Workshop recommendations.

In considering the issues raised by commenters on the 2007 proposed
rule, the Administrator noted that many public commenters supported the
range of levels recommended by CASAC.  The Administrator also considered
the views expressed by the NPS as to what range of levels it identified
as useful in helping it achieve its mandate to protect AQRVs in national
parks and wilderness areas and to provide a level of protection for its
resources in keeping with the Congressional mandate set forth in The
Wilderness Act of 1964.  In so doing, the Administrator notes that the
NPS supported the range recommended by CASAC, while emphasizing that the
lower end of the range was more appropriate.  The NPS notes that though
some visible foliar injury would still be expected to occur above the
lower end of the CASAC recommended range (i.e. 7 ppm-hour), the
potential for growth impacts at that level would be very low.  It
further notes that most of these parks contain aspen, black cherry, or
ponderosa pine, all sensitive species predicted to have significant
growth effects at current W126 levels.

The Administrator also considered those comments that highlighted
sources of uncertainty in the evidence and risk assessments (summarized
above in section IV.D.5.c.ii) to inform her judgments on how much weight
to place on these associated uncertainties, as discussed below.

With regard to the issue of possible confounders of foliar injury
information, the Administrator recognizes that visible foliar injury,
like other O3-induced plant effects, is moderated by environmental
factors other than O3 exposure.  However, the Administrator also notes
that the O3-related visible foliar injury effect persisted across a four
year period (2001-2004), despite year-to-year variability in meteorology
and other environmental factors (see Table 7-4 in the 2007 Staff Paper).
  She also notes that approximately 26 to 49 percent of counties had
visible foliar injury incidence at the approximate W126 level of 21
ppm-hour, while at a W126 level of 13 ppm-hour, this range of
percentages dropped to approximately 12 to 23 percent.  In an area such
as a national park, where visitors come in part for the aesthetic
quality of the landscape, the Administrator recognizes that visible
foliar injury incidence is an important welfare effect which should be
considered in determining an appropriately protective standard level.  

With regard to the issues of what weight to place on the recommendations
from the 1996 Consensus Workshop in selecting a range of levels, as the
1997 Workshop Report did not clearly document the basis for its
recommendations, the Administrator recognizes that the absence of such
documentation does call for care in placing weight on such
recommendations.  However, the Administrator notes that the workshop
participants were asked to review both the 1996 O3 Criteria Document and
Staff Paper, representing the most up to date compilation of the state
of the science available at that time, in order to ensure that their
expert judgments made were also informed by the latest science.  She
also notes that another group of experts, the CASAC O3 Panel, reached a
similar consensus based upon an expanded body of scientific evidence. 
In addition, the 2007 Staff Paper evaluated the same recommendations in
the context of subsequent empirical evidence, and reached similar views,
with the exception of the upper end of the recommended range, which in
the 2007 Staff Paper was based on effects on commercial crops that had
been considered in the 1997 review.  While it would always be more
useful to have documentation of the reasoning and basis for an
expert’s advice, in this case the Administrator judges that the 1996
Consensus Workshop recommendations should be given substantial weight.

With regard to other issues raised by some commenters related to
uncertainties in the technical evidence and analyses, the Administrator
notes that such issues had been addressed in the 2007 Staff Paper that
reflected CASAC’s advice on such issues.  For example, while the
Administrator recognizes that uncertainty remains as to what level of
annual tree seedling biomass loss when compounded over multiple years
should be judged adverse to the public welfare, she believes that the
potential for such anticipated effects should be considered in judging
to what degree a standard should be precautionary.

	In considering all of the issues discussed above, the Administrator has
decided to propose a range of 7-15 ppm-hour.  In selecting as an upper
bound a level of 15 ppm-hour, the Administrator notes that this level
was specifically supported by the CASAC O3 Panel and is just above the
range identified in the 1996 Consensus Workshop report as needed to
provide adequate protection for trees growing in natural areas.  In
addition, the NPS, along with many public commenters, were in support of
the CASAC range, including the upper bound of 15 ppm-hour, and 
indicated that lower values within this range would be more protective
for sensitive trees in protected areas from biomass loss and visible
foliar injury symptoms.  

While the upper end of this range is lower than the upper end of 21
ppm-hour recommended in the 2007 Staff Paper, this upper level of 21
ppm-hour was originally put forward in the 1997 review in terms of a
SUM06 of 25 ppm-hour (W126 of 21 ppm-hour) and was justified on the
basis that it was predicted to allow up to 10% biomass loss annually in
50% of studied commercial crops and tree seedling species.  Recognizing
the significant uncertainties that are associated with evaluating
effects on commercial crops from a public welfare perspective, the
Administrator now concludes that commercial crop data are no longer
useful for setting the upper level of the range for proposal.

	With regard to her selection of a proposed range, the Administrator has
considered that the direction from Congress to provide a high degree of
protection in Class I areas creates a clearer target for gauging what
types and magnitudes of effects would be known or anticipated to affect
the intended use of these and other similarly protected areas, that
would thus be considered adverse to the public welfare.  Such similar
areas include lands set aside by States, Tribes and public interest
groups to provide similar benefits to the public welfare, for residents
on those lands, as well as visitors to those areas,  The Administrator
also believes that in order to preserve wilderness areas in an
unimpaired state for future generations, she must consider a level that
affords substantial protection from known adverse O3-related effects of
biomass loss and foliar injury on sensitive tree species, as well as a
level that takes into account potential  “anticipated” adverse
O3-related effects, including effects that result in continued
impairment in the year following O3 exposure (i.e., carry-over effects),
below ground impacts, ecosystem level impacts, and reduced CO2
sequestration

While the Administrator acknowledges that growth effects and visible
foliar injury can still occur in sensitive species at levels below the
upper bound of the proposed range, the Administrator also recognizes
that some significant uncertainties remain regarding the risk of these
effects, as discussed above.  For example, the Administrator concludes
that remaining uncertainties make it difficult to judge the point at
which visible foliar injury becomes adverse to the public welfare in
various types of specially protected areas.  Uncertainties associated
with monitoring ambient exposures must be considered in evaluating the
strength of predictions regarding the degree of tree seedling growth
impairment estimated to occur at varying ambient exposures.  These
uncertainties add to the challenge of judging which exposure levels are
expected be associated with levels of tree seedling growth effects
considered adverse to public welfare   The Administrator believes that
it is important to consider these uncertainties, and the weight to place
on such uncertainties, in selecting a range of standard levels to
propose.  Establishing 15 ppm-hour as the upper end of the proposed
range reflects her judgment regarding the appropriate weight to place on
these uncertainties in determining the degree of protection that is
warranted for known and anticipated adverse effects.

With regard to her selection of a lower bound for the proposed range,
the Administrator believes that if weight is placed on taking a more
precautionary approach, recognizing that the real world impacts on trees
and ecosystems could, in some cases, be greater than predicted, then the
lower end of the range of 7 ppm-hour could be warranted. There is clear
evidence that higher cumulative exposures can occur in rural areas
downwind of urban areas and potentially in Class I areas.  Unmonitored
high elevation sites would also likely have higher cumulative exposures
than lower elevation sites that are currently monitored.  All of these
considerations lead the Administrator to propose 7 ppm-hour as the low
end of the proposed range.

As discussed above in section IV.D.5.a, the main opposition to changing
to a secondary standard with a cumulative, seasonal form has been the
view that EPA does not have an adequate basis to identify the kinds and
types of cumulative, seasonal exposure patterns that the standard should
be designed to protect against, given the various uncertainties in the
evidence, and whether EPA has an adequate basis to determine an
appropriate level for a cumulative, seasonal secondary standard.  While
EPA agreed with this position in the 1997 review, the Administrator
believes that the evidence before her appropriately supports a secondary
standard that is distinctly different in form and averaging time from
the 8-hour primary standard, and that such a standard is necessary to
provide sufficient protection from cumulative, seasonal exposures to O3.
 

While a different conclusion on this issue was reached in the 1997
review, the current conclusion that an exposure index that is cumulative
and seasonal in nature, and therefore that setting a standard based on
such a form is necessary and appropriate, is based on information newly
available in the 2008 rulemaking, which strengthens the information
available in the 1997 review and reduces remaining uncertainties.  

Such newly available information includes quantitative information for a
broader array of vegetation effects (extending to sapling and mature
tree growth stages) obtained using a more diverse set of field-based
research study designs and improved analytical methods for assessing
O3-related exposures and risks as discussed above in sections IV.A-C.  

.	These newly available studies also provide important support to the
quantitative estimates of impaired tree growth based on earlier studies
available in the 1997 review and address one of the key data gaps cited
in the 1997 review.  Additional qualitative information is also
available regarding improved understanding of linkages between
stress-related effects of O3 exposures at the species level and those at
higher levels within ecosystems.  Finally, this information includes the
use of new analytical methods, including a new multi-pollutant,
multi-scale air quality model used to characterize exposures of
O3-sensitive tree and crop species further address uncertainties in the
assessments done in the 1997 review.  In total, this newly available
information increases the Administrator’s confidence in important
aspects of this rulemaking

The decision in 2008 to set the secondary O3 standard identical to the
8-hour primary standard largely mirrored the decision in 1997, but
failed to account for this significant increase in the body of knowledge
available to support the 2008 rulemaking.  This body of knowledge, while
continuing to reflect significant uncertainties, provides an appropriate
basis for determining a level of a cumulative, seasonal standard that,
in the judgment of the Administrator, provides sufficient but not more
than necessary protection from cumulative, seasonal exposures to O3. 
This is clearly so when compared to a standard that uses an indirect
form that is not biologically relevant, an 8-hour average standard aimed
at peak daily exposures.  This judgment is fully consistent with the
advice provided by CASAC.    

After carefully taking the above considerations into account, and giving
significant weight to the views of CASAC, the Administrator has decided
to propose a range of levels of 7-15 ppm-hour for a cumulative, seasonal
secondary O3 standard expressed as an index of the annual sum of
weighted hourly concentrations (i.e., the W126 form), cumulated over 12
hours per day during the consecutive 3-month period within the O3 season
with the maximum index value, averaged over three years.  In the
Administrator's judgment, based on the information available in the 2008
rulemaking, a standard could be set within this range that would be
requisite to protect public welfare from known or anticipated adverse
effects to O3-sensitive vegetation and ecosystems.  In the
Administrator’s judgment, a standard set at a level below the lower
end of the range is not now supported by the weight of evidence and
would not give sufficient weight to the important uncertainties and
limitations inherent in the available scientific evidence and in the
quantitative assessments conducted for the 2008 rulemaking.  A standard
set at a level above the upper end of the range is also not now
supported by the weight of evidence and would not give sufficient weight
to the credible inferences that the Agency has drawn from the scientific
evidence nor to the quantitative assessments conducted for the 2008
rulemaking.  The Administrator judges that the appropriate balance to be
drawn, based on the entire body of evidence and information available in
the 2008 rulemaking, is a range between 7 and 15 ppm-hour.  On balance,
the Administrator believes that a standard could be set within this
range that would be sufficient but not more than necessary to protect
public welfare from known or anticipated adverse effects due to O3.

In reaching this proposed decision, as discussed above, the
Administrator has focused on the nature of the benefits associated with
setting a distinct secondary standard with a cumulative, seasonal form
relative to a standard with a peak daily 8-hour average form, as well as
on assessments that quantify the degree of protection likely to be
afforded by such standards.  In so doing, the Administrator has
acknowledged limitations in quantifying the expected benefits associated
with the proposed cumulative seasonal standard relative to the secondary
standard set in 2008.  Having considered the public comments received on
the 2007 proposed rule in reaching this proposed decision, the
Administrator is interested in again receiving public comment on the
benefits to public welfare associated with the proposed cumulative
seasonal standard set at specific levels within the proposed range
relative to the standard set in 2008. 

E.	Proposed Decision on the Secondary O3 Standard

For the reasons discussed above, and taking into account information and
assessments presented in the 2006 Criteria Document and 2007 Staff
Paper, the advice and recommendations of CASAC, and the public comments
received in conjunction with the 2008 rulemaking, the Administrator has
decided to propose to set a new cumulative, seasonal secondary O3
standard with a form expressed as an index of the annual sum of weighted
hourly concentrations (i.e., the W126 form), cumulated over 12 hours per
day (8:00 am to 8:00 pm) during the consecutive 3-month period within
the O3 season with the maximum index value, averaged over three years,
set within a range of 7 to 15 ppm-hour.  The Administrator solicits
comment on the weight that is appropriately placed on the various types
of evidence and analyses upon which this proposed standard is based, as
well asand on the appropriate weight to be placed on the uncertainties
in this information, to help inform selection of a final standardas well
as on the benefits to public welfare associated with the proposed
standard relative to the benefits associated with the standard set in
2008.

Data handling conventions for the proposed new secondary O3 standard are
specified in the proposed addition of a new section to 40 CFR 50
Appendix P, as discussed in section V below.  Issues related to
monitoring requirements for the proposed new secondary O3 standard are
discussed below in section VI.

V.	Interpretation of the NAAQS for O3 and Proposed Revisions to the
Exceptional Events Rule

	Appendix P to 40 CFR part 50, Interpretation of the Primary and
Secondary National Ambient Air Quality Standards for Ozone, addresses
data completeness requirements, data reporting, handling, and rounding
conventions, and example calculations. The current Appendix P explains
the computations necessary for determining when the current identical
primary and secondary standards are met. The EPA is proposing to revise
Appendix P to reflect the proposed revisions to the primary and
secondary O3 NAAQS discussed above and to make other changes described
below. 

	As discussed below, the proposed revisions to Appendix P include the
following:  the addition of data interpretation procedures applicable to
the proposed cumulative, seasonal secondary NAAQS (see section V.B);
clarification of certain language in the current provisions applicable
to the primary NAAQS to reduce potential confusion (section V.C);
revisions to the provisions regarding the use of incomplete data sets
for purposes of the primary NAAQS and the data completeness requirements
across three years (sections V.D and V.E); the addition of a provision
providing the Administrator discretion to use incomplete data as if it
were complete, for the purpose of the primary NAAQS (section V.F); a
change from truncation to rounding of multi-hour and multi-year average
O3 concentrations for the purposes of the primary standard (section
V.G); and the addition of provisions addressing data to be used in
making comparisons to the NAAQS (section V.H).  The proposed revisions
also include changes in organization for greater clarity and consistency
with other data interpretation appendices to 40 CFR part 50, which are
not further described in this preamble.

	The EPA is also proposing changes to the O3-specific deadlines, in 40
CFR 50.14, by which states must flag ambient air data that they believe
have been affected by exceptional events and submit initial descriptions
of those events, and the deadlines by which states must submit detailed
justifications to support the exclusion of that data from EPA
determinations of attainment or nonattainment with the NAAQS.  The
O3-specific deadlines in the current 40 CFR 50.14 would not be
appropriate given the anticipated schedule for the designations of areas
under the proposed revised O3 NAAQS.

A.	Background

	The purpose of a data interpretation appendix in general is to provide
the practical details on how to make a comparison between multi-day and
possibly multi-monitor ambient air concentration data and the level of
the NAAQS, so that determinations of compliance and violation are as
objective as possible.  Data interpretation guidelines also provide
criteria for determining whether there are sufficient data to make a
NAAQS level comparison at all.  Appendix P was promulgated in March 2008
along with the most recent revisions to the primary and secondary O3
NAAQS.  It is very similar to Appendix I, Interpretation of the 8-Hour
Primary and Secondary National Ambient Air Quality Standards for Ozone,
which was adopted in 1997 when the O3 NAAQS were first revised to have
an 8-hour averaging period rather than the earlier 1-hour averaging
period, along with other changes in form and level.  The only
substantive difference between Appendix I and the current version of
Appendix P is that Appendix P contains truncation procedures consistent
with the additional decimal digit used to express the level of the 2008
NAAQS in parts per million (0.075 ppm) compared to the 1997 NAAQS (0.08
ppm).  In July 2007, EPA had also proposed to include in Appendix P data
interpretation procedures for the proposed cumulative, seasonal
secondary O3 NAAQS, but these procedures were not finalized given that
the final secondary NAAQS was identical in all respects to the final
primary NAAQS.

	An exceptional event is defined in 40 CFR 50.1 as an event that affects
air quality, is not reasonably controllable or preventable, is an event
caused by human activity that is unlikely to recur at a particular
location or a natural event, and is determined by the Administrator in
accordance with 40 CFR 50.14 to be an exceptional event.  Air quality
data that are determined to have been affected by an exceptional event
under the procedural steps and substantive criteria specified in section
50.14 may be excluded from consideration when EPA makes a determination
that an area is meeting or violating the associated NAAQS.  The key
procedural deadlines in section 50.14 are that a state must notify EPA
that data have been affected by an event, i.e., “flag” the data in
the Air Quality Systems (AQS) database, and provide an initial
description of the event by July 1 of the year after the data are
collected, and that the State must submit the full justification for
exclusion within 3 years after the quarter in which the data were
collected.  However, if a regulatory decision based on the data, for
example a designation action, is anticipated, the schedule is shortened
and all information must be submitted to EPA no later than a year before
the decision is to be made.  This generic schedule presents problems
when a NAAQS has been recently revised, as discussed in section V.I
below.  On May 15, 2009, EPA finalized a set of O3-specific deadlines
that corrected these problems at the time with respect to the 2008 NAAQS
revisions (74 FR 23307).  However, because of the anticipated effect of
the current reconsideration on the schedule for O3 designations, the
schedule problems will resurface unless the deadlines are adjusted
again.

B.	Interpretation of the Secondary O3 Standard

	The EPA is proposing data interpretation procedures for the proposed
secondary O3 NAAQS, which is defined in terms of a specific cumulative,
seasonal form, commonly referred to as the W126 form, as described above
in section IV.  The proposed new section 4 of Appendix P on data
interpretation for the secondary standard contains the following main
features. 

	The “design value” for the secondary standard, the statistic for a
monitoring site which would be compared to the level of the secondary
standard to determine if the site meets the standard, would be the
average of the annual maximum values of the three-month index value from
three calendar years. 

	The new section would provide clear directions and examples for the
calculation of the daily index value, the monthly cumulative index
value, the annual maximum index value for a year, and the design value
itself.

	Only the data from the required O3 monitoring season would be examined
to determine the annual maximum index value; any additional period of
monitoring undertaken voluntarily by a state would not be considered. 
The EPA believes that because of the recently proposed extension of the
required monitoring seasons in many states (74 FR 34525, July 16, 2009),
as discussed below in section VI, such a period of voluntary monitoring
would be unlikely to have such high index values as to affect the annual
maximum index value.  Moreover, the proposed required monitoring season
may encompass the most active growing season in many areas.  The EPA
invites comment on whether instead the entire actual O3 monitoring
period should be considered, to eliminate any possibility that the
highest cumulative index value that can be determined with available
data might be missed.

	For each month in a three-month period, O3 data would have to be
available for at least 75 percent of daylight hours (defined for this
purpose as 8:00 a.m. – 7:59 p.m. LST).  If data are available for at
least 75 percent but fewer than 100 percent of these daylight hours in a
month, the cumulative index value calculated from the available daylight
hours in the month would be increased to compensate for the missing
hours, based on an assumption that the missing hours would have the same
distribution of O3 concentrations as the available hours.  A
substitution test is also proposed, by which months in which fewer than
75 percent of daylight hours have O3 concentration data might also be
useable for calculating a valid cumulative index value.  Such months
would be used if the available O3 concentrations are so high that even
substituting low concentration values for enough missing data to meet
the 75 percent requirement would result in a design value greater than
the level of the standard.  The low value that would be substituted
would be the lowest 1-hour O3 concentration observed at the monitoring
site during daylight hours during the required O3 monitoring season, in
that calendar year, or one-half the method detection limit (MDL) of the
ozone instrument, whichever is higher.  

	The EPA notes that while this proposed approach to identifying the
substitution value for the secondary standard is technically
appropriate, it would necessitate data processing efforts during
implementation that might be avoidable via some other approach that is
also technically reasonable.  We therefore invite comment on such
alternative approaches, and we may adopt another approach in the final
rule.  For example, for simplicity the substituted 1-hour O3
concentration value could instead simply always be zero or one-half the
MDL of the O3 instrument, noting that because of the sigmoidal weighting
factor the exact magnitude of the low substitution value may typically
make very little difference to the annual index value.  Also, using the
previous calendar year as the source of the substitution value instead
of the current calendar year would have the advantage of allowing all
parties to know early in each year what the substitution value will be.

	The EPA is proposing that all decimal digits be retained in
intermediate steps of the calculation of the cumulative index, with the
result rounded to have no decimal digits when expressed in ppm-hours
before comparison the level of the secondary NAAQS.

	EPA expects that the three months over which the cumulative weighted
index value is highest will generally occur in the middle of each year. 
Therefore, the proposed new section 4 of Appendix P presumes this, and
does not address a situation in which the three months of maximum
cumulative index spans two calendar years, for example December to
February.  The EPA invites comment on whether a provision addressing
such a remote possibility is needed and what its terms should be.  For
example, the process of checking each three month period in a calendar
year to determine which gives the highest index value could include the
combinations of December/January/February and November/December/January
within one calendar year.

C.	Clarifications Related to the Primary Standard

	The EPA is proposing two clarifying changes to Appendix P to make
unambiguous two aspects of data interpretation for the primary 8-hour
standard.  The first change clarifies that the standard data
completeness requirement that valid daily maximum 8-hour values exist
for 75 percent of all days refers to days within the required O3
monitoring season only.  The current wording of Appendix P is somewhat
open to a reading that the requirement applies to all days in the actual
monitoring record for the site in question, which could be longer than
the required season if a state voluntarily monitors on additional days,
or shorter than the required season if a monitor has started or ceased
operation sometime during the required season.  The O3 data completeness
requirement is intended to avoid a determination that an area has met
the NAAQS when in fact more than a reasonable number of days with high
O3 potential were not successfully monitored.  This purpose can be
served if the data within the required O3 monitoring season only are
reasonably complete, because as mentioned above EPA has proposed to
revise the required O3 seasons so that they encompass all days with
potential for an exceedance of even the lowest proposed level for the
primary standard.  Unsuccessful monitoring outside the required season
should not be an obstacle to a finding of attainment.  However, if an O3
monitor has missed more than 25 percent of the required O3 monitoring
season, for example because it started or stopped operation mid-season,
this should prevent a finding of attainment based on a three-year period
that includes that season.  The proposed clarifying language reflects
EPA’s actual intention and our past practice in applying Appendix P
for regulatory purposes, and Appendix I as well.  

	The second proposed clarifying change would make it clear that when
determining the fourth-highest daily maximum 8-hour O3 concentration for
a year, all days with monitoring data are to be considered, not just
days within the required O3 monitoring season.  This proposed clarifying
language also reflects EPA’s actual intention and our past practice in
applying Appendix P, and Appendix I as well.  While EPA believes it to
be quite unlikely that an exceedance will occur outside the proposed
revised required O3 monitoring seasons and have a high enough
concentration to affect the selection of the fourth-highest
concentration for the year, when and if such an occurrence does happen,
the data should not be ignored.

D.	Revision to Exceptions from Standard Data Completeness Requirements
for the Primary Standard

	The EPA is proposing to revise portions of Appendix P that describe
certain exceptions to the standard data completeness requirements, under
which a monitoring site can in some cases be determined to be meeting or
violating the primary NAAQS despite not meeting the standard data
completeness requirements.  These changes would make Appendix P more
logical in certain types of cases with incomplete data.  While the
particular types of cases whose outcome would be different with these
changes have been rare historically, there may be more such affected
cases in the future in conjunction with a primary O3 standard revised to
a level within the range of levels proposed in this action.

	The standard data completeness requirements in Appendix P for the
primary O3 NAAQS apply a 75 percent requirement at each of three stages
of data completeness testing.  As discussed below, for each stage, there
is an existing exception to the 75 percent requirement.

	In the first stage, an 8-hour period can be considered to have a valid
8-hour average O3 concentration only if at least 75 percent of the
hours, i.e., 6 or more hours, have a valid hourly O3 value.  The
provided exception is that if there are 5 or fewer hours but if
substituting a very low value (specifically, one-half the MDL of the O3
instrument) for all the missing hours results in a hypothetical 8-hour
average that is above the level of the primary standard, the 8-hour
period is considered valid and is assigned the hypothetical level
resulting from the data substitution.  For example, if the O3
concentration was 0.125 ppm for 5 hours, substituting a typical MDL/2
value of 0.0025 ppm for three missing hours would result in an 8-hour
average of 0.079 ppm, which is an exceedance of the current primary
standard, so the valid 8-hour average for the period would be taken to
be 0.079 ppm.  If this value is higher than one or more of the highest
four daily maximum 8-hour concentrations otherwise calculated for the
year, considering it to be valid affects the value identified as the
fourth-highest for the year and thus also affects the final design
value.  The logical problem with this approach is that it is possible
for a hypothetical 8-hour average with such substitution to be below the
level of the NAAQS, thus not meeting the current condition for the
exception, but for it to still make a critical difference in making the
three-year design value be above the level of the NAAQS, because a
three-year design value can include (and be sensitive to the exact value
of) an annual fourth-highest daily maximum that is not above the level
of the NAAQS.  This could be the case if the hypothetical 8-hour average
with substitution is the maximum concentration 8-hour period for its
day, and the day is one of the highest four O3 days of the year. 
Whether it actually is the case would further depend on the value of the
8-hour average itself, the values of the next highest daily maximum
8-hour average concentration in the year, and the values of the annual
fourth-highest daily maximum 8-hour concentration from the other two
years.  If the substituted 8-hour average would make a critical
difference, it should be treated as valid and used in the calculation of
the three-year design value, even if it is not itself above the level of
the standard.  Another problem is that one-half of the MDL, which
typically is about 0.0025 ppm, is very likely to be considerably lower
than the actual O3 concentrations that were not successfully measured. 
Thus, while the one-half-MDL-substituted value is prevented from being
an overestimate of the actual 8-hour average concentration, it is an
unreasonably low estimate of that concentration which may have the
effect of allowing a site with actual O3 levels above the standard to be
found to meet the standard.  The condition in the exception requiring a
one-half-MDL-substituted “8-hour” average to be above the level of
the NAAQS is therefore inappropriate.

	In the second stage of data completeness testing, 75 percent of the 24
possible 8-hour time blocks, which is 18 or more, must have valid 8-hour
average concentrations values.  The intent of this requirement is to
make sure that most of the day was actually monitored, such that the
highest concentration 8-hour period was likely to be captured in the
data.  When this is not the case, the day is not considered in selecting
the annual fourth-highest daily maximum 8-hour concentration and no
credit for the day’s monitoring is given towards the third stage of
data interpretation (see below).  The provided exception in the current
Appendix P is that a day is considered valid if at least one 8-hour
period has an average concentration above the level of the standard. 
However, as in the first stage, it is possible for an 8-hour period with
an average concentration at or below the level of the NAAQS to play a
critical role in whether the three-year design value meets the standard.
 Invalidating the day could have the effect of causing a lower value to
be selected as the annual fourth-highest daily maximum 8-hour
concentration, leading to a three-year design value that does not exceed
the NAAQS while it would have exceeded if the day and the 8-hour average
value had been treated as valid.  The condition in the exception
requiring at least one 8-hour average during the day to be above the
level of the NAAQS is therefore inappropriate.

	In the third stage of data completeness testing, a completeness
criterion is applied for the number of days in the required O3 season
that have a valid maximum 8-hour average, i.e., days that have met the
completeness conditions in the first two stages or have met the
condition for an exception.  Specifically, for each of the three years
being used in the design value calculation, the number of valid days
within the required O3 monitoring season (with no credit for extra days
outside the season) must be at least 75 percent of the days in the
required O3 season, and the number of valid days across all three years
must be 90 percent of the days in the three seasons.  The provided
exception to the 75/90 percent requirement is that data from a year with
less than 75 percent of seasonal days can nevertheless be used if during
the year at least one day’s maximum 8-hour average O3 concentration
was above the level of the standard and if the three-year design value
is also above the standard.  The problem with this exception, similar to
the problems with the exceptions in the first and second stages of data
completeness testing, is that a daily maximum 8-hour concentration that
is at or below the level of the NAAQS can nevertheless make a critical
difference in making the three-year design value be above the level of
the NAAQS.  When it does, an incorrect final result will be reached if
the year of data is not granted an exception to the 75/90 percent
requirement.  Specifically, there would be no valid three-year design
value and no conclusion would be reached as to attainment or
nonattainment, despite it being clear that the actual situation is
nonattainment, in the sense that successful collection of additional
hours and days of monitoring data could not possibly have resulted in a
passing three-year design value.  Moreover, since the three-year design
value is the average of the fourth-highest daily maximum 8-hour
concentration from each year, there is no logical connection between the
design value and the existence of a single daily maximum concentration
greater than the level of the standard, which is the current condition
for the exception for this stage of testing for data incompleteness.

	EPA proposes to remedy this situation by replacing the three separate
statements of the exceptions to the three standard completeness
requirements with a new data substitution step that addresses the root
cause of the data incompleteness situation:  missing hourly
concentrations which make it doubtful whether actual maximum daily
8-hour concentrations were measured on a reasonably large percentage of
the days during the required O3 monitoring season of each year.  In the
event that only 1, 2, 3, 4, or 5 hourly averages are available for an
8-hour period, a partially substituted 8-hour average would be computed
by substituting for all the hours without hourly averages a low hourly
average value selected as follows, and then using 8 as the divisor.  For
days within the required O3 monitoring season, the substitution value
would be the lowest hourly average O3 concentration observed for that
hour of the day (local standard time) on any day during the required O3
monitoring season of that year, or one-half the MDL, whichever is
higher.  Using this value makes it highly unlikely that the resulting
partially substituted 8-hour average concentration is higher than the
actual concentration.  Therefore, using the partially substituted 8-hour
average in the design value calculation procedure is highly unlikely to
result in an incorrect finding that a site does not meet the standard,
but it may lead to a correct finding that a site does not meet the
standard in some cases in which there would be no finding possible or an
incorrect finding under the current version of Appendix P.  However, the
use of the higher of the lowest observed same-hour concentration or
one-half the MDL could be problematic if a robust set of hourly
measurements is not available for the year, for example if a monitor
began operation late in an ozone season.  In such a case, the lowest
observed same-hour concentration might not be low enough to eliminate
all possibility that the value used for substitution is higher than the
missing concentration value.  To reduce this likelihood to essentially
zero, we are proposing that if the number of same-hour concentration
values available for the required O3 monitoring season for the year is
less than 50 percent of the number of days during the required O3
monitoring season, one-half the MDL of the O3 instrument would be used
in the substitution instead of the lowest observed concentration.  We
invite comment on whether another percentage should be used for this
purpose instead of 50 percent. 

	The EPA notes that while this proposed approach to identifying the
substitution value for the primary standard is technically appropriate,
it would necessitate new data processing efforts during implementation
that might be avoidable via some other approach that is also technically
reasonable.  There may also be approaches which are more technically
appropriate.  We therefore invite comment on such alternative
approaches, and we may adopt another approach in the final rule. 
Examples of simpler approaches would be to identify in the final rule a
fixed substitution value other than one-half the MDL, to accept as valid
8-hour periods with only five measured hourly concentrations, to
interpret between two hourly concentrations to obtain a substitute for a
single missing hourly concentration, or to use the previous calendar
year as the source of the substitution value instead of the current
calendar year (thereby allowing all parties to know early in each year
what the substitution value will be). Examples of more complex
approaches that might be more technically appropriate include selecting
a low percentile of the available same-hour concentration data rather
than the lowest value to be the substitution value, or selecting the
lowest same-hour value from the same calendar quarter or month (of the
current year or the most recent year) rather than from the entire
required ozone monitoring season.  We also invite comment on whether the
proposed approach to substitution should be used at all and if not what
other approach should be used to address the potential problem just
described.

	We propose that for simplicity and to further reduce any risk of a
false finding that a site does not meet the standard, for days outside
the required O3 monitoring season, the substitution value would always
be one-half the MDL of the O3 instrument.  We similarly invite comment
on this aspect.  

	There would be no condition that a partially substituted 8-hour average
exceed the level of the standard for it be used in calculating the
design value, unlike is now the case.  An 8-hour period with no
available hourly averages at all would not have a valid 8-hour average,
as is now the case.

	In addition, to complete the solution to the problems described above,
we are proposing that a design value that is greater than the level of
the primary standard would be valid provided that in each year there
were at least four days with at least one valid 8-hour concentration. 
One or more of these 8-hour average concentrations could be the
partially substituted 8-hour average concentration resulting from the
above described substitution procedure.  In such a case, there is
essentially no possibility that more complete monitoring data would have
shown the site to be meeting the NAAQS.  It is appropriate to include
all 8-hour averages including those involving substitution when testing
for an exceedance of the standard, because those averages are extremely
unlike to be overestimates of actual concentrations.

	Finally, a design value equal to or less than the level of the standard
would be valid only if at least 75 percent of the days in the required
O3 monitoring season of each year have daily maximum 8-hour
concentrations that are based on at least 18 periods with at least 6
hourly concentrations.  This ensures that a site will be found to meet
the standard only when a reasonably high percentage of the days in the
required O3 monitoring season have reasonably complete hourly data.  In
this situation, it would be inappropriate to count the 8-hour periods
with five or fewer actual hourly measurement values towards the 75
percent requirement when testing for whether a site meets the standard,
because those 8-hour averages will be based on substitution of low
values and therefore will be underestimates of actual concentrations. 
The only way to be reasonably certain that no 8-hour period had a high
enough concentration so as to contribute to a design value over the
level of the standard is to have at least 18 periods in which
substitution for missing O3 values was not needed.  This provision has
the same effect as several elements of the current Appendix P considered
together, and thus is not a substantive change.

E.	Elimination of the Requirement for 90 Percent Completeness of Daily
Data across Three Years

	As stated above in section VI.D, Appendix P currently requires that in
order for a design value equal to or less than the standard to be valid,
at least 75 percent of days in each of three years must have a valid
daily maximum 8-hour average concentration value, i.e., that many days
must have at least 18 8-hour periods with at least 6 reported hourly
concentrations each.  Appendix P also requires that the average of the
percentages from three consecutive years be at least 90 percent.  The
EPA is proposing to eliminate this 90 percent requirement for the
average of three years and to retain only the requirement that each
individual year have a percentage of at least 75 percent.

	The 90 percent requirement was incorporated into Appendix I (the data
interpretation appendix for the 0.08 ppm O3 NAAQS) in 1997 with an
explanation that EPA had observed that 90 percent of O3 monitoring sites
routinely achieved 90 percent data capture.  The EPA now notes, however,
that while the majority of monitoring sites do achieve 90 percent or
better data capture in any given year, there are exceptions every year. 
The 90 percent requirement applied to the average percentage over three
years is quite unforgiving if there has been one year with relatively
low data completeness.  For example, if one year just met the 75 percent
requirement, the remaining two years would have to achieve a 97.5
percent data capture rate in order for the three years to meet the 90
percent requirement.  This would allow only 4 missed hours of
measurements per week, which would be challenging.  The consequences for
states could be important, under the current requirement.  One possible
result could be that an area actually in nonattainment with the NAAQS
might have to be designated unclassifiable, although the substitution
procedure proposed for cases of incomplete data, as described above in
section VI.D, provides a path to an appropriate nonattainment finding in
at least some cases.  Another possible result is that a nonattainment
area which had actually come into attainment could be unable to receive
an attainment determination until three more years of sufficiently
complete data are collected.  This might, for example, result in an area
which has achieved needed emissions reductions by its attainment
deadline nevertheless being bumped up to a higher classification.

	The 90 percent requirement over three years has the potential to treat
two areas disparately, for no obvious logical reason.  Consider two
areas with identical air quality.  Suppose the first area has annual
completeness percentages of 75, 95, and 95 percent (averaging to 85
percent and thus failing the 90 percent requirement) and the second area
has annual completeness percentages of 75, 98, and 98 percent (averaging
to 90 percent).  Suppose that the three-year design values in both areas
are below the level of the NAAQS.  Practically speaking, the most
important uncertainty about whether each area actually meets the NAAQS
is the low data capture rate in the first year.  There is no obvious
logic why the fact that the second area achieves marginally better data
capture in the second and third year should permit it to receive an
attainment finding despite this uncertainty, while the first area may
not.

	The EPA also notes that for the other gaseous criteria pollutants –
sulfur dioxide, carbon monoxide and nitrogen dioxide – the
completeness requirement is for 75 percent completeness of hourly
measurements in an individual year.

	For these reasons, EPA proposes to eliminate the 90 percent requirement
across three years of data but to retain the 75 percent requirement for
individual years.  The EPA notes that as a practical matter, the current
90 percent requirement in effect requires a minimum data capture rate
somewhat above 75 percent in each year, because if data capture in any
one year were as low as 75 percent the required data capture in the
other years would be very hard to achieve.  The minimum annual data
capture rate is effectively somewhere in the range of 80 percent
(implying a requirement to achieve 95 percent data capture in the two
remaining years in order to meet the 90 percent requirement across three
years) and 85 percent (implying a requirement to achieve 92.5 percent
data capture in the two remaining years).  The EPA invites comment on
whether instead of retaining the 75 percent completeness requirement in
each individual year, the requirement should be 80 percent or 85
percent.

F.	Administrator Discretion to Use Incomplete Data

	The EPA is proposing that the Administrator have general discretion to
use incomplete data to calculate design values that would be treated as
valid for comparison to the NAAQS despite the incompleteness, either at
the request of a state or at her own initiative.  Similar provisions
exist already for the PM2.5 and lead NAAQS, and EPA has recently
proposed such provisions to accompany the proposed 1-hour NO2 and SO2
primary NAAQS.  The Administrator would consider monitoring site
closures/moves, monitoring diligence, and nearby concentrations in
determining whether to use such data.

G.	Truncation versus Rounding 

	 Almost all State agencies now report hourly O3 concentrations in parts
per million to three decimal places, since the typical incremental
sensitivity of currently used O3 monitors is 0.001 ppm.  In the current
Appendix P approach, in calculating 8-hour average O3 concentrations
from such hourly data any calculated digits past the third decimal place
are truncated rather than retained or rounded back to three decimal
places.  Also, in calculating 3-year averages of the fourth-highest
daily maximum 8-hour average concentrations, Appendix P currently
requires the result to be reported to the third decimal place with
digits to the right of the third decimal place truncated.  In this
regard, Appendix P follows the precedent of Appendix I, except that
Appendix P is based on a NAAQS level specified to three decimal places
(0.075 ppm) while Appendix I addressed the case of a NAAQS level
specified to only two decimal places (0.08 ppm).  In the rulemaking that
concluded in 2008 by establishing the 0.075 ppm level, EPA noted that
the 2007 Staff Paper demonstrated that taking into account the precision
and bias in 1-hour O3 measurements, the 8-hour design value had an
uncertainty of approximately 0.001 ppm.  Thus, EPA considered any value
less than 0.001 ppm to be highly uncertain and, therefore, proposed and
adopted truncation to the third decimal place for reporting 1-hour O3
concentrations and for both the individual 8-hour averages used to
determine the annual fourth maximum and the 3-year average of the fourth
maxima.

	The effect of this repeated truncation is that there is a consistent
downward bias in the calculation of the three-year design value.  The
size of this bias can be notable.  For example, seven hours with O3
concentrations of 0.076 ppm plus one hour of 0.075 ppm results in an
8-hour average of 0.075 ppm after truncation, nearly a full 0.001 ppm
below the actual 8-hour average of 0.075875 ppm.  Seven hours with O3
concentrations of 0.077 ppm plus one hour of 0.076 ppm results in an
8-hour average of 0.076 ppm after truncation.  One year with the first
pattern plus two years with the second pattern would give a three-year
design value of 0.075 ppm, meeting the NAAQS, even though 23 of the 24
individual 1-hour concentrations involved in the calculation of the
design value were above 0.075 ppm.

	The EPA has decided to reconsider this aspect of O3 data
interpretation.  Specifically, we are proposing that (1) 1-hour
concentrations continue to be reported to only three decimal places, the
same as is now specified in Appendix P, i.e., that the current practice
of truncation of the 1-hour data to the nearest 0.001 ppm be retained;
(2) all digits resulting from the calculation of 8-hour averages be
retained; and (3) the three-year average of annual fourth-highest daily
maximum 8-hour concentrations be rounded to three decimal places before
comparison to the NAAQS.  The EPA continues to believe that given the
uncertainty in individual 1-hour O3 concentration measurements it is
appropriate to truncate those measurements at three decimal places (many
O3 instruments are programmed to only report three digits anyway). 
However, the calculations of 8-hour averages and three-year averages are
mathematical steps, not a measurement process subject to uncertainties,
and EPA perceives no logic in having a consistent downward bias by
truncating the results of these mathematical steps.  The EPA notes that
the O3 NAAQS is the only NAAQS for which multi-hour, multi-day, or
multi-year averages of concentrations are truncated rather than rounded.
 The proposed change will make this aspect of O3 data interpretation
consistent with data interpretation procedures for the other criteria
pollutants.

H	 Data Selection

	The current version of Appendix P does not explicitly address the issue
of what ambient monitoring data for O3 can and must be compared to the
O3 NAAQS.  The EPA proposes to add to Appendix P language addressing
this issue.  This language is similar to provisions recently proposed to
be included in new data interpretation appendices for nitrogen dioxide
and sulfur dioxide.  The new section of Appendix P would clarify that
all quality assured data collected with approved monitoring methods and
known to EPA shall be compared to the NAAQS, even if not submitted to
EPA’s Air Quality System.  The section also addresses the question of
what O3 data should be used when two or more O3 monitors have been
operating and have reported data for the same period at one monitoring
site. 

I.  Exceptional Events Information Submission Schedule 

States are responsible for identifying air quality data that they
believe warrant special consideration, including data affected by
exceptional events.  States identify such data by flagging (making a
notation in a designated field in the electronic data record) specific
values in the Air Quality System (AQS) database.  States must flag the
data and submit a justification that the data are affected by
exceptional events if they wish EPA to consider excluding the data in
determining whether or not an area is attaining the new O3 NAAQS.

	All states that include areas that could exceed the O3 NAAQS and could
therefore be designated as nonattainment for the O3 NAAQS have the
potential to be affected by this rulemaking.  Therefore, this action
applies to all states; to local air quality agencies to which a state
has delegated relevant responsibilities for air quality management
including air quality monitoring and data analysis; and to Tribal air
quality agencies where appropriate.  The Exceptional Events Rule
preamble describes in greater detail to whom the rule applies (72 FR
13562-13563 March 22, 2007).

	The CAA Section 319(b)(2) authorizes EPA to promulgate regulations that
govern the review and handling of air quality monitoring data influenced
by exceptional events.  Under this authority, EPA promulgated the
Exceptional Events Rule (Treatment of Data Influenced by Exceptional
Events (72 FR 13560, March 22, 2007) which sets a schedule for states to
flag monitored data affected by exceptional events in AQS and for them
to submit documentation to demonstrate that the flagged data values were
caused by an exceptional event.  Under this schedule, a state must
initially notify EPA that data have been affected by an exceptional
event by July 1 of the year after the data are collected; this is
accomplished by flagging the data in AQS.  The state must also include
an initial description of the event when flagging the data.  In
addition, the state is required to submit a full demonstration to
justify exclusion of such data within three years after the quarter in
which the data were collected, or if a regulatory decision based on the
data (such as a designation action) is anticipated, the demonstration
must be submitted to EPA no later than one year before the decision is
to be made.  

	The rule also authorizes EPA to revise data flagging and documentation
schedules for data used in the initial designation of areas under a new
NAAQS.  The generic schedule, while appropriate for the period after
initial designations have been made under a NAAQS, may need adjustment
when a new NAAQS is promulgated because until the level and form of the
NAAQS have been promulgated, a state would not have complete knowledge
of the criteria for excluding data.  In these cases, the generic
schedule may preclude states from submitting timely flags and associated
documentation for otherwise approvable exceptional events.  This could,
if not modified, result in some areas receiving a nonattainment
designation when the NAAQS violations were legitimately due to
exceptional events.	

	As a result of the Administrator’s decision to reconsider the 2008 O3
NAAQS, EPA is proposing to revise the exceptional events flagging and
documentation schedule to correspond to the designations schedules that
EPA is considering for the proposed revisions to the primary and
secondary O3 NAAQS.  The designation schedules under consideration are
discussed in greater detail below in section VII.A and summarized  here.
 The CAA requires EPA to promulgate the initial designations for all
areas no later than 2 years from the promulgation of a new NAAQS.  Such
period may be extended for up to one year if EPA has insufficient
information.  (See CAA section 107(d).)    For a new primary O3
standard, EPA intends to issue designations on an accelerated schedule. 
For a new seasonal secondary O3 standard, EPA is considering two
alternative schedules for initial area designations. 

Primary Standard:  If, as a result of the reconsideration, EPA
promulgates a new primary O3 standard on August 31, 2010, EPA is
proposing that state Governors would need to submit their initial
designation recommendations to EPA by January 7, 2011.  EPA would
promulgate the final designations in July 2011 to allow sufficient time
for the designations to be published and effective by August 31, 2011. 
EPA expects to base the final designations for the primary O3 standard
on three consecutive years of certified air quality monitoring data from
the years 2007-2009 or 2008-2010, if available.  EPA is proposing that
for exceptional event claims made for data years 2007-2009, states must
flag and provide an initial description and detailed documentation by
November 1, 2010.  For data collected during data year 2010, EPA is
proposing that exceptional event data that states want EPA to exclude
from consideration in the designations process must be flagged with an
initial description and fully documented by March 1, 2011 or 60 days
after the end of the quarter when the event occurred, whichever date is
first.  To meet this proposed 60-day deadline, a state would also have
to submit the O3 concentration data to AQS sooner than the normal
deadline for such submission, which is 90 days after the end of the
calendar quarter.  EPA believes this is a reasonable expectation given
that most states currently submit O3 data earlier than the 90-day
deadline.

 Secondary Standard:  If, as a result of the reconsideration, EPA
promulgates a new seasonal secondary O3 standard by August 31, 2010, EPA
is taking comment on two alternative designations schedules.   Under the
first alternative, EPA would designate areas for the secondary standard
on the same accelerated schedule discussed above for the primary
standard.  Under the second alternative, EPA would designate areas for
the secondary standard on the maximum 2-year schedule provided under the
CAA. Accelerated Schedule:  Under the accelerated schedule for a
seasonal secondary O3 NAAQS, EPA is proposing that for exceptional event
claims made for data years 2007-2009, states must flag and provide an
initial description and detailed documentation by November 1, 2010.  For
data collected during data year 2010, EPA is proposing that exceptional
event data that states want EPA to exclude from consideration in the
designations process must be flagged with an initial description and
fully documented by March 1, 2011 or 60 days after the end of the
quarter when the event occurred, whichever date is first.

2-year  Schedule:  Under the 2-year schedule, states would have 1 year,
or by August 2011, to submit their designations recommendations and EPA
would finalize designations under the new secondary standard by August
2012.   EPA expects to base final designations for a new seasonal
secondary standard on the most recent three years of certified air
quality monitoring data, which would typically be from the years
2009-2011 in this case.  Exceptional event data claims used from years
2008-2010 must be flagged with an initial description included in AQS
and submitted with complete documentation supporting such claims by July
1, 2011.  Exceptional event data claims from data year 2011 must be
flagged with an initial description and submitted with complete
documentation supporting such claims 60 days after the end of the
calendar quarter when the event occurred or March 1, 2012, whichever
occurs first.   

	Therefore, using the authority provided in CAA section 319(b)(2) and in
the Exceptional Events Rule at 40 CFR 50.14 (c)(2)(vi), EPA is proposing
to modify the schedule for data flagging and submission of
demonstrations for exceptional events data considered for initial
designations under the proposed reconsidered O3 primary and secondary
NAAQS, as follows:

Table 1.  Schedule for Exceptional Event Flagging and Documentation
Submission for Data to be Used in Designations Decisions for New NAAQS

NAAQS Pollutant/

Standard/(Level)/

Promulgation Date	Air Quality Data Collected for Calendar Year	Event
Flagging & Initial Description Deadline	Detailed Documentation
Submission Deadline

Primary Ozone/8-Hr Standard (Level TBD) Promulgated by August 31, 2010
2007-2009	November 1, 2010b	November 1, 2010b

	2010	60 Days after the end of the calendar quarter in which the event
occurred or March 1, 2011, whichever date occurs firstb	60 Days after
the end of the calendar quarter in which the event occurred or March 1,
2011, whichever date occurs firstb

Secondary Ozone/ (Level TBD)Alternative 2-year Schedule- to be
Promulgated by August 31, 2010 	2008	July 1, 2011b	July 1, 2011a

	2009-2010	July 1, 2011b	July 1, 2011b

	2011	60 Days after the end of the calendar quarter in which the event
occurred or March 1, 2012, whichever occurs firstb	60 Days after the end
of the calendar quarter in which the event occurred or March 1, 2012,
whichever occurs firstb

Secondary Ozone/ (Level TBD)- Alternative Accelerated Schedule -to be
Promulgated by August 31, 2010	2007-2009	November 1, 2010b	November 1,
2010b

	2010	60 Days after the end of the calendar quarter in which the event
occurred or March 1, 2011, whichever date occurs firstb	60 Days after
the end of the calendar quarter in which the event occurred or March 1,
2011, whichever date occurs firstb

a These dates are unchanged from those published in the original
rulemaking.

b Indicates change from general schedule in 40 CFR 50.14.

Note:  EPA notes that the table of revised deadlines only applies to
data EPA will use to establish the final initial designations for new
NAAQS.  The general schedule applies for all other purposes, most
notably, for data used by EPA for redesignations to attainment.

	

VI.	Ambient Monitoring Related to Proposed O3 Standards

Presently, States (including the District of Columbia, Puerto Rico, and
the Virgin Islands, and including local agencies when so delegated by
the State) are required to operate minimum numbers of EPA-approved O3
monitors based on the population of each of their Metropolitan
Statistical Areas (MSA) and the most recently measured O3 levels in each
area. Each State (or in some cases portions of a State) also has a
required O3 monitoring season based on historical experience on when O3
levels are high enough to be of regulatory or public health concern. 
These requirements are contained in 40 CFR part 58 Appendix D, Network
Design Criteria for Ambient Air Quality Monitoring. See section 4.1,
especially Tables D–2 and D–3.  These requirements were last revised
on October 17, 2006 as part of a comprehensive review of ambient
monitoring requirements for all criteria pollutants (71 FR 61236).	

A.	Background

	In the 2007 proposed rule for the O3 NAAQS (72 FR 37818), EPA did not
propose specific changes to monitoring requirements to support the
proposed NAAQS revisions, but instead solicited comment on several key
matters that were expected to be important issues affecting the
potential redesign of monitoring networks if revisions to the NAAQS were
finalized.  These matters included O3 monitoring requirements in urban
areas, the potential need for monitoring to support multiple objectives
important to characterization in non-urban areas including the support
of the secondary O3 NAAQS, and the length of the required O3 monitoring
seasons.  Comments on these monitoring issues were received during the
ensuing public comment period, and these comments were summarized in the
2008 final rule for the O3 NAAQS (73 FR 16501).  As noted in that
action, EPA stated its intention to propose, in a separate rulemaking,
the specific changes to O3 monitoring requirements that were deemed
necessary to support the revised 2008 O3 NAAQS which set the level of
the primary 8-hour O3 standard to 0.075 ppm and set the secondary
standard identical in all respects to the primary standard.  EPA
published these proposed changes to O3 monitoring requirements in a
proposal dated July 16, 2009, Ambient Ozone Monitoring Regulations:
Revisions to Network Design Requirements (74 FR 34525).  The EPA
currently plans to finalize these changes in a final O3 monitoring rule
in 2010, either before or in conjunction with the final rule on the O3
NAAQS.

	In the following sections, the specific provisions of the 2009 O3
monitoring proposal are briefly reviewed, and then discussed in the
context of the proposed revisions of the 2008 O3 NAAQS that have been
discussed earlier in this notice.

B.	Urban Monitoring Requirements

As noted earlier, current O3 monitoring requirements for urban areas are
based on two factors:  MSA population and the most recent 3-year design
value concentrations within each MSA.  There are higher minimum
monitoring requirements for areas that have most recent design values
greater than or equal to 85 percent of the NAAQS (i.e., design value
concentrations that are greater than or equal to 85 percent of the level
of the NAAQS), and lower requirements for areas that have design values
less than 85 percent of the NAAQS.  These minimum monitoring
requirements for O3 were revised during the 2006 monitoring rulemaking
to ensure that additional monitors would be required in areas with
higher design values and to also ensure that these requirements would
remain applicable through future NAAQS reviews and potential revisions
of the standards.  Accordingly, these requirements do not need to be
updated with the revisions of the O3 NAAQS proposed in this action since
the 85 percent threshold will be applied to the standard levels that are
finalized for the primary and secondary standards.  For example, given
the range of levels of the primary standard being proposed, the level of
the 85 percent threshold that requires greater minimum monitoring
requirements ranges from 0.051 ppm (85 percent of 0.060 ppm) to 0.060
ppm (85 percent of 0.070 ppm).

	EPA did propose one change to urban monitoring requirements in the 2009
O3 monitoring proposal.  Specifically, EPA proposed to modify the
minimum O3 monitoring requirements to require one monitor to be placed
in MSAs of populations ranging from 50,000 to less than 350,000 in
situations where there is no current monitor and no history of O3
monitoring within the previous 5 years indicating a design value of less
than 85 percent of the revised NAAQS.  Since this proposed change to
minimum requirements is also subject to the 85 percent threshold, EPA
believes that the proposed change remains appropriate to support the
revisions to the primary and secondary O3 NAAQS proposed in this action.

C.	Non-Urban Monitoring Requirements

	In the 2007 proposed rule for the O3 NAAQS, EPA solicited comment on
the status of monitoring requirements for non-urban areas, specifically
whether non-urban areas with sensitive vegetation that are only
currently sparsely monitored for O3 could experience undetected
violations of the secondary NAAQS as a result of transport from urban
areas with high precursor emissions and/or O3 concentrations or from
formation of additional O3 from precursors emitted from sources outside
urban areas.

	Comments that were received in response to the 2009 O3 NAAQS monitoring
proposal noted the voluntary nature of most non-urban O3 monitoring and
the resulting relative lack of non-urban O3 monitors in some areas. 
These commenters stated that EPA should consider adding monitoring
requirements to support the secondary NAAQS by requiring O3 monitors in
locations that contain O3-sensitive plants or ecosystems.  These
commenters also noted that the placement of current O3 monitors may not
be appropriate for evaluating issues such as vegetation exposure since
many of these monitors were likely located to meet other objectives.

	Based on these comments as well as analyses of O3 concentrations from
discretionary non-urban monitors located across the U.S, EPA included
new proposed non-urban O3 monitoring requirements in the 2009 O3
monitoring proposal.  These proposed requirements are intended to
satisfy several important objectives including: (1) better
characterization of O3 concentrations to which O3-sensitive vegetation
and ecosystems are exposed in rural/remote areas to ensure that
potential secondary NAAQS violations are measured; (2) assessment of O3
concentrations in smaller communities located outside of the larger
urban MSAs covered by urban monitoring requirements; and (3) the
assessment of the location and severity of maximum O3 concentrations
that occur in non-urban areas and may be attributable to upwind urban
sources.  For reasons noted below, EPA believes that these proposed O3
monitoring requirements are sufficient to support the revisions to the
O3 NAAQS proposed in this action.

	With regard to the first objective, we note uncertainties will remain
about the O3 concentrations to which sensitive natural vegetation and
ecosystems are exposed until additional monitors are sited in National
Parks, State and/or tribal areas, wilderness areas, and other similar
locations with sensitive ecosystems that are set aside to provide
similar public welfare benefits.  These monitors would support
evaluation of the secondary NAAQS with a more robust data set than is
now available.  As noted in the 2009 O3 monitoring proposal, EPA
proposed that States operate at least one monitor to be located in areas
such as some Federal, State, Tribal, or private lands, including
wilderness areas that have O3-sensitive natural vegetation and/or
ecosystems.  If EPA finalizes a cumulative, seasonal secondary standard
at the lower end of the proposed range, then it is plausible that
additional O3 monitors, above the number required by the monitoring
proposal, may be needed in such areas to provide adequate coverage of
locations likely to experience violations of the revised secondary
NAAQS.  These additional monitors could be established through
discretionary State initiatives to supplement minimum monitoring
requirements, negotiated agreements between States and EPA Regional
Administrators, or through a future rulemaking that addresses potential
increased O3 monitoring requirements to specifically address the need
for additional monitoring to ensure detection of secondary standard
violations.

	With regard to the second objective of characterizing elevated ambient
O3 levels to which people are exposed in smaller communities located
outside of the larger urban MSAs, the likelihood of measuring
concentrations that approach or exceed the levels of the NAAQS due to
the transport of O3 from upwind areas and/or the formation of O3 due to
precursor emissions from industrial sources outside of urban areas is
clearly increased due to the revised NAAQS proposed in this action.
Given that the analyses described in the 2009 O3 monitoring proposal
demonstrated that 50 percent of existing monitors located in such
Micropolitan Statistical Areas exceeded the current NAAQS and nearly all
monitors recorded design values greater than or equal to 85 percent of
the current NAAQS, the potential for violations in such areas can only
be increased with the NAAQS revisions proposed in this action.  As noted
for the first non-urban monitoring objective, it is plausible that
additional O3 monitors, above the number required by the 2009 monitoring
proposal may be needed in Micropolitan Statistical Areas to provide
adequate coverage of locations likely to experience violations of the
proposed lower primary NAAQS levels.  These additional monitors could be
established through discretionary State initiatives to supplement
minimum monitoring requirements, negotiated requirements between States
and EPA Regional Administrators, or through a future rulemaking that
addresses potential increased O3 monitoring requirements to specifically
address the need for additional monitoring to ensure detection of
primary standard violations in smaller communities.

	The third proposed non-urban monitoring objective, requiring O3
monitors to be located in the area of expected maximum O3 concentration
outside of any MSA, potentially including the far downwind transport
zones of currently well-monitored urban areas, is not directly related
to the level of the O3 NAAQS.  It is instead intended to ensure that all
parts of a State meet the NAAQS and that all necessary emission control
strategies have been included in State Implementation Plans. 
Accordingly, this proposed monitoring objective remains applicable
independent of revisions to the O3 NAAQS proposed in this action.

D.	Revisions to the Length of the Required O3 Monitoring Seasons

	Ozone monitoring is only required during the seasons of the year that
are conducive to O3 formation. These seasons vary in length as the
conditions that determine the likely O3 formation (i.e.,
seasonally-dependent factors such as ambient temperature, strength of
solar insolation, and length of day) differ by location.  In some
locations, conditions conducive to O3 formation are limited to a few
summer months of the year while in other locations these conditions
occur year-round. As a result, the length of currently required O3
monitoring seasons can vary from a length of 4 months in colder climates
to a length of 12 months in warmer climates. 

The 2009 O3 monitoring proposal also addressed the issue of whether in
some areas the required O3 monitoring season should be made longer.  The
proposal also addressed the status of any currently effective Regional
Administrator-granted waiver approvals to O3 monitoring seasons, and the
impact of proposed changes to monitoring requirements on such waiver
approvals.

	The EPA performed several analyses in support of proposed changes to
the required O3 monitoring seasons.  The first analysis determined the
number of observed exceedances of the 0.075 ppm level of the current
8-hour NAAQS in the months falling outside the currently required local
O3 monitoring season using monitors in areas that collected O3 data
year-round in 2004–2006. The second analysis examined observed
occurrences of daily maximum 8-hour O3 averages of at least 0.060 ppm. 
This threshold was chosen because it represented 80 percent of the
current 0.075 ppm NAAQS level and provides an indicator of ambient
conditions that may be conducive to the formation of O3 concentrations
that approach or exceed the NAAQS.  While proposals for revising each
State’s required monitoring season were based on observed data in and
surrounding each State, statistically predicted exceedances were also
used to validate conclusions for each State. 

	The aforementioned analyses provided several results.  The analysis of
observed exceedances of the 0.075 ppm level of the current O3 NAAQS
indicated occurrences in eight States during months outside of the
current required monitoring season. The eight States were Maine,
Massachusetts, New Hampshire, New Jersey, New York, South Carolina,
Vermont, and Wyoming. With the exception of Wyoming, these exceedances
occurred in a very limited manner and timeframe, just before the
beginning of these States’ required O3 monitoring season (beginning in
these States on April 1).  The frequency of observed occurrences of
maximum 8-hour average O3 levels of at least 0.060 ppm was quite high
across the country in months outside of the current required monitoring
season.  A total of 32 States experienced such occurrences; 22 States
had such levels only before the required monitoring season; 9 States had
such levels both before and after the required monitoring season; and 1
State had such levels only after the required monitoring season. In a
number of cases, the frequency of such ambient concentrations was high,
with some States experiencing between 31 to 46 out-of-season days during
2004 to 2006 at a high percentage of all operating year-round O3
monitors.

	Based on these analyses, EPA proposed a lengthening of the O3
monitoring season requirements in many areas.  The 2009 proposed changes
were based not only on the goal of monitoring out-of-season O3 NAAQS
violations but also on the goal of ensuring monitoring when ambient O3
levels reach 80 percent of the NAAQS so that persons unusually sensitive
to O3 would be alerted to potential NAAQS exceedances.

	The EPA believes that the factors used to support the 2009 proposed
changes to O3 monitoring seasons are appropriate to support the
revisions of the O3 NAAQS proposed in this action.  With regard to the
primary standard, we note that the lower end of the range being proposed
is an 8-hour level of 0.060 ppm, which is identical to the ambient O3
level that was utilized in one of the analyses discussed above. 
Although that level was chosen to provide an indicator of ambient levels
that were below but approaching the level of the NAAQS and hence to
serve as an alert to potential exceedances, we note that EPA’s
traditional practice had been to base the length of required O3
monitoring seasons on the likelihood of measuring exceedances of the
level of the NAAQS.  Therefore, if EPA finalizes the level of the
primary standard at the lower end of the proposed range, the O3
monitoring seasons that have been proposed as part of the 2009 O3
monitoring proposal would provide sufficient monitoring coverage to
ensure the goal of measuring potential violations of the primary
standard.

	One O3 monitoring season issue that was not considered in the 2009 O3
monitoring proposal was the question of whether analyses of ambient data
based on 8-hour average statistics would also indicate whether the
resulting proposed monitoring seasons would capture the cumulative
maximum consecutive 3-month O3 levels necessary to compute design values
based on the secondary NAAQS proposed in this action, which is defined
in terms of a W126 cumulative peak-weighted index, as discussed above in
section IV.  If areas experienced high cumulative index values during
months outside of the required O3 monitoring seasons (based on 8-hour
statistics), then further revisions to the required monitoring seasons
might be necessary to ensure monitoring during all months important to
the calculation of design values for the revised form proposed for the
secondary NAAQS.  A related issue is whether such high cumulative O3
values also occurred during time periods that are biologically relevant
for O3-sensitive vegetation.

	The EPA is not proposing additional revisions to O3 monitoring seasons
at this time.  Additional analyses of the distribution of elevated
cumulative W126 index values will be conducted, and the biologically
relevant seasonal issue will be further reviewed.  Based on the results
of these analyses, EPA may consider proposing further revisions to the
O3 monitoring season as related to the secondary O3 NAAQS.

VII.	Implementation of Proposed O3 Standards

A.	Designations

 	After EPA establishes or revises a NAAQS, the CAA directs EPA and the
states to take steps to ensure that the new or revised NAAQS are met. 
The first step is to identify areas of the country that do not meet the
new or revised NAAQS.  This step is known as the initial area
designations.  

	The CAA provides that, "By such date as the Administrator may
reasonably require, but not later than 1 year after promulgation of a
new or revised national ambient air quality standard for any pollutant
under section 109, the Governor of each state shall * * * submit to the
Administrator a list of all areas (or portions thereof) in the state"
that designates those areas as nonattainment, attainment, or
unclassifiable.  The CAA specifies that, "The Administrator may not
require the Governor to submit the required list sooner than 120 days
after promulgating a new or revised national ambient air quality
standard."  The CAA defines an area as nonattainment if it is violating
the NAAQS or if it is contributing to a violation in a nearby area. 
(See CAA section 107(d)(1).)

	The CAA further provides, "Upon promulgation or revision of a national
ambient air quality standard, the Administrator shall promulgate the
designations of all areas (or portions thereof) * * * as expeditiously
as practicable, but in no case later than 2 years from the date of
promulgation of the new or revised national ambient air quality
standard.  Such period may be extended for up to one year in the event
the Administrator has insufficient information to promulgate the
designations.”  EPA is required to notify states of any intended
modifications to their recommendations that EPA may deem necessary no
later than 120 days prior to promulgating designations.  States then
have an opportunity to demonstrate why any such proposed modification is
inappropriate.   Whether or not a state provides a recommendation, EPA
must promulgate the designation that the Agency deems appropriate.  (See
CAA section 107(d)(1)(B).)

	On September 16, 2009, when the Administrator announced her decision to
reconsider the 2008 O3 NAAQS, she also indicated that the Agency would
work with states to accelerate implementation of the standards adopted
after reconsideration, including the initial area designations process. 
Acceleration of designations for the primary standard would help limit
any delays in health protections associated with the reconsideration of
the standards.  If a secondary standard different from the primary
standard is adopted, this would be the first time different primary and
secondary standards would be in place for the O3 standards.  While
welfare protection is also important, for the reasons provided below, we
are providing alternative schedules for designating areas for the
secondary standard.

	If, as a result of the reconsideration, EPA determines that the record
supports a primary standard different from that promulgated in 2008 and
promulgates such different primary O3 NAAQS in 2010, EPA intends to
promulgate final designations on an accelerated schedule to allow the
designations to be effective in 1 year.  In order to meet such a
schedule, EPA is proposing that the deadline for states to submit their
designations recommendations for the revised 2010 primary standard be
129 days after promulgation of that primary standard.  EPA recognizes
that the proposed deadline would be an ambitious schedule.  Therefore,
EPA intends to provide technical information and guidance for states as
early as possible to facilitate the development of their
recommendations.  Many of the areas that would be violating the proposed
primary ozone standard are also violating the 2008 ozone standards. 
State Governors have provided recommendations on these areas pursuant to
the 2008 standards and recommendations may not need much further
evaluation.

	Based on this proposed schedule, if EPA promulgates a new primary
standard on August 31, 2010, state Governors would need to submit their
initial designation recommendations to EPA by January 7, 2011.  If the
Administrator intends to modify any state recommendation, EPA would
notify the Governor no later than March 2011, 120 days prior to
promulgating the final designations.  States would then have an
opportunity to comment on EPA's intended designations before EPA
promulgates the final designations.  EPA would promulgate the final
designations in July 2011 to allow sufficient time for the designations
to be published and effective by August 31, 2011.  EPA expects to base
the final designations for the primary O3 standard on three consecutive
years of certified air quality monitoring data from the years 2007-2009
or from 2008-2010, if available.   

	If, as a result of the reconsideration, EPA promulgates a distinct
secondary standard that differs from that promulgated in 2008 and also
differs from the 2010 primary standard, as proposed above, EPA is
proposing two alternative deadlines for states to submit their
designations recommendations.   Under the first alternative, EPA would
designate areas for the secondary standard on the same accelerated
schedule discussed above for the primary standard.  In order to meet
that schedule, EPA is proposing that states submit their recommendations
for the revised 2010 secondary standard 129 days after promulgation of
that secondary standard.   Accordingly, if EPA promulgates the new
secondary standard on August 31, 2010, state Governors would need to
submit their initial designation recommendations to EPA by January 7,
2011.

	Weighing in favor of designating areas for the secondary standard at
the same time as designations for the primary standard is that planning
for both standards would occur on the same schedule.  Our examination of
current air quality data from the existing monitoring network indicates
that for levels of the primary and secondary standards proposed in this
action, it is likely that the vast majority of areas violating the
secondary standard would overlap with areas violating the primary
standard.  In this case, implementing requirements for the primary and
secondary standards on different schedules could present resource
challenges to state and local agencies by requiring duplication of
effort and hindering consideration of all factors when deciding which
control strategies to adopt for each standard.  For example, if
designations for the secondary standard were delayed by a certain period
(e.g., a year) beyond the designations for the primary standard, then
EPA would likely delay submission of attainment SIPs for the secondary
standard for a similar period beyond the proposed date for submission of
the attainment SIPs for the primary standard.  In this case, the initial
transportation conformity determination for the secondary standard would
be required later than the initial determination for the primary
standard by the difference in time between the effective dates of the
two designations.  

Under the second alternative, EPA would designate areas for the
secondary standard on the maximum 2-year schedule provided under the
CAA.  To meet that 2-year schedule, EPA is proposing that states submit
their recommendations for the revised secondary standard no later than 1
year after promulgation of the 2010 secondary standard.  Accordingly, if
EPA promulgates a secondary standard on August 31, 2010, that differs
from the primary standard, as proposed, under the alternative 2-year
designations schedule, state Governors would need to submit their
initial designation recommendations to EPA by August 31, 2011.  If the
Administrator intends to modify any state recommendation, EPA would
notify the Governor no later than May 2012, 120 days prior to the 2-year
deadline for promulgating the final designations.  States would then
have an opportunity to comment on EPA's intended designations before EPA
promulgates the final designations.  EPA would promulgate the final
designations for the secondary standard by August 31, 2012.  EPA expects
to base the final designations in August 2012 for a different secondary
standard on the most recent three consecutive years of certified air
quality monitoring data, which would be from the years 2009-2011.   

	In the past, EPA has always set the secondary O3 standard to be
identical to the primary O3 standard and the standards have embodied
relatively short-term average concentrations (e.g., 1-hour or 8-hour). 
In this action, EPA is proposing a cumulative, seasonal secondary
standard that differs from the proposed primary standard.  EPA has not
previously set a seasonal secondary standard for O3.  Therefore, EPA and
states do not have experience in implementing this type of secondary O3
standard or in determining what area boundaries would be appropriate. 
As we further explore implementation considerations for the secondary
standard, we may encounter unanticipated issues that may require
additional time to address.  Thus, EPA is considering whether an
accelerated schedule for a seasonal secondary standard would provide
adequate time for resolving issues that we cannot now anticipate.  If
EPA designates areas for the secondary standard on a 2-year schedule, we
note that we expect that accelerated implementation of the health-based
primary standard would also result in accelerated welfare benefits.  EPA
requests comment on factors affecting the efficient and effective
implementation of a secondary standard that differs from the primary
standard in the context of establishing designations schedules.

EPA notes, as discussed in greater detail above in section VI, that it
has proposed a monitoring rule that would increase the density of
monitoring in National Parks and other non-urban and lesser populated
areas (July 16, 2009; 74 FR 34525).  The proposed requirements are
intended to satisfy several important objectives, including better
characterization of O3 exposures to O3-sensitive vegetation and
ecosystems in rural/remote areas to ensure that potential secondary
NAAQS violations are measured.  As proposed, the new monitors would not
be deployed until 2012 or 2013.  Therefore, data from these monitors
would not be available for use within the statutory timeframe for EPA to
complete designations for a 2010 secondary standard regardless of which
schedule EPA follows.   

  	While CAA section 107 specifically addresses states, EPA intends to
follow the same process for tribes to the extent practicable, pursuant
to section 301(d) of the CAA regarding tribal authority, and the Tribal
Authority Rule (63 FR 7254;  February 12, 1998).  

	In a separate notice elsewhere in today’s Federal Register, EPA is
announcing that it is using its authority under the CAA to extend by 1
year the deadline for promulgating initial area designations for the O3
NAAQS that were promulgated in March 2008.  The new deadline is March
12, 2011.  That notice explains the basis for the deadline extension. 
As mentioned above, on September 16, 2009, EPA notified the Court of its
decision to initiate a rulemaking to reconsider the primary and
secondary O3 NAAQS set in March 2008 to ensure they satisfy the
requirements of the CAA.  In its notice to the Court, EPA stated that
the final rule would be signed by August 31, 2010.  Extending the
deadline for promulgating designations for the 2008 O3 NAAQS until March
12, 2011 will allow EPA to complete the reconsideration rulemaking for
the 2008 O3 NAAQS before determining whether it is necessary to finalize
designations for those NAAQS or, instead, whether it is necessary to
begin the designation process for different NAAQS promulgated pursuant
to the reconsideration.

B.	State Implementation Plans 

The CAA section 110 provides the general requirements for SIPs.  Within
3 years after the promulgation of new or revised NAAQS (or such shorter
period as the Administrator may prescribe) each State must adopt and
submit “infrastructure” SIPs to EPA to address the requirements of
section 110(a)(1).  Thus, States should submit these SIPs no later than
August 21, 2013, three years after promulgation of the reconsidered
ozone standard in 2010.  These “infrastructure SIPs” provide
assurances of State resources and authorities, and establish the basic
State programs, to implement, maintain, and enforce new or revised
standards.  

In addition to the infrastructure SIPs, which apply to all States, CAA
title I, part D outlines the State requirements for achieving clean air
in designated nonattainment areas.  These requirements include timelines
for when designated nonattainment areas must attain the standards,
deadlines for developing SIPs that demonstrate how the State will ensure
attainment of the standards, and specific emissions control
requirements.  EPA plans to address how these requirements, such as
attainment demonstrations and attainment dates, reasonable further
progress, new source review, conformity, and other implementation
requirements, apply to the O3 NAAQS promulgated pursuant to the
reconsideration in a subsequent rulemaking.  Also in that rulemaking EPA
will establish deadlines for submission of nonattainment area SIPs but
anticipates that the deadlines will be no later than the end of December
2013, or 28 months after final designations.

C.	Trans-boundary Emissions

	Cross border O3 contributions from within North America (Canada and
Mexico) entering the U.S. are generally thought to be small.  Section
179B of the Clean Air Act allows designated nonattainment areas to
petition EPA to consider whether such a locality might have met a clean
air standard “but for” cross border contributions.  To date, few
areas have petitioned EPA under this authority.  The impact of foreign
emissions on domestic air quality in the United States is a challenging
and complex problem to assess.  EPA is engaged in a number of activities
to improve our understanding of international transport.  As work
progresses on these activities, EPA will be able to better address the
uncertainties associated with trans-boundary flows of air pollution and
their impacts.

VIII.	Statutory and Executive Order Reviews

A.	Executive Order 12866: Regulatory Planning and Review  

	Under section 3(f)(1) of Executive Order (EO) 12866 (58 FR 51735,
October 4, 1993), the O3 NAAQS action is an “economically significant
regulatory action” because it is likely to have an annual effect on
the economy of $100 million or more.  Accordingly, EPA submitted this
action to the Office of Management and Budget (OMB) for review under EO
12866 and any changes made in response to OMB recommendations have been
documented in the docket for this action. In addition, EPA prepared this
regulatory impact analysis (RIA) of the potential costs and benefits
associated with this action. This analysis is contained in the
Regulatory Impact Analysis for the Ozone NAAQS Reconsideration, October,
2009 (henceforth, “RIA”). A copy of the analysis is available in the
RIA docket (EPA-HQ-OAR-2007-0225) and the analysis is briefly summarized
here. The RIA estimates the costs and monetized human health and welfare
benefits of attaining five alternative O3 NAAQS nationwide. 
Specifically, the RIA examines the alternatives of 0.079 ppm, 0.075 ppm,
0.070 ppm, 0.065 ppm, and 0.060 ppm. The RIA contains illustrative
analyses that consider a limited number of emissions control scenarios
that States and Regional Planning Organizations might implement to
achieve these alternative O3 NAAQS.  However, the Clean Air Act (CAA)
and judicial decisions make clear that the economic and technical
feasibility of attaining ambient standards are not to be considered in
setting or revising NAAQS, although such factors may be considered in
the development of State plans to implement the standards.  Accordingly,
although an RIA has been prepared, the results of the RIA have not been
considered in issuing this proposed rule.

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. There
are no information collection requirements directly associated with the
establishment of a NAAQS under section 109 of 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
in 40 CFR are listed in 40 CFR part 9.

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 businesses, small organizations,
and small governmental jurisdictions.

	For purposes of assessing the impacts of today’s proposed rule on
small entities, small entity is defined as:  (1) a small business that
is a small industrial entity as defined by the Small Business
Administration’s (SBA) regulations at 13 CFR 121.201;  (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 impacts of today's proposed rule on
small entities, I certify that this action will not have a significant
economic impact on a substantial number of small entities.  This
proposed rule will not impose any requirements on small entities. 
Rather, this rule establishes national standards for allowable
concentrations of O3 in ambient air as required by section 109 of the
CAA.  See also American Trucking Associations v. EPA. 175 F. 3d at
1044-45 (NAAQS do not have significant impacts upon small entities
because NAAQS themselves impose no regulations upon 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 104-4, 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 to 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 (under the
regulatory provisions of Title II of the UMRA) for State, local, or
Tribal governments or the private sector.  The proposed rule imposes no
new expenditure or enforceable duty on any State, local or Tribal
governments or the private sector, and EPA has determined that this
proposed rule contains no regulatory requirements that might
significantly or uniquely affect small governments.  Furthermore, as
indicated previously, in setting a NAAQS EPA cannot consider the
economic or technological feasibility of attaining ambient air quality
standards, although such factors may be considered to a degree in the
development of State plans to implement the standards.  See also
American Trucking Associations v. EPA, 175 F. 3d at 1043 (noting that
because EPA is precluded from considering costs of implementation in
establishing NAAQS, preparation of a Regulatory Impact Analysis pursuant
to the Unfunded Mandates Reform Act would not furnish any information
which the court could consider in reviewing the NAAQS).  Accordingly,
EPA has determined that the provisions of sections 202, 203, and 205 of
the UMRA do not apply to this proposed decision.  The EPA acknowledges,
however, that any corresponding revisions to associated SIP requirements
and air quality surveillance requirements, 40 CFR part 51 and 40 CFR
part 58, respectively, might result in such effects.  Accordingly, EPA
will address, as appropriate, unfunded mandates if and when it proposes
any revisions to 40 CFR parts 51 or 58.

E.	Executive Order 13132: Federalism

	Executive Order 13132, entitled “Federalism” (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.”  

	This proposed rule does not have federalism implications.  It will not
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, as
specified in Executive Order 13132.  The rule does not alter the
relationship between the Federal government and the States regarding the
establishment and implementation of air quality improvement programs as
codified in the CAA.  Under section 109 of the CAA, EPA is mandated to
establish NAAQS; however, CAA section 116 preserves the rights of States
to establish more stringent requirements if deemed necessary by a State.
 Furthermore, this proposed rule does not impact CAA section 107 which
establishes that the States have primary responsibility for
implementation of the NAAQS.  Finally, as noted in section E (above) on
UMRA, this rule does not impose significant costs on State, local, or
Tribal governments or the private sector.  Thus, Executive Order 13132
does not apply to this rule.

	However, as also noted in section E (above) on UMRA, EPA recognizes
that States will have a substantial interest in this rule and any
corresponding revisions to associated SIP requirements and air quality
surveillance requirements, 40 CFR part 51 and 40 CFR part 58,
respectively.  Therefore, in the spirit of Executive Order 13132, and
consistent with EPA policy to promote communications between EPA and
State and local governments, EPA specifically solicits comment on this
proposed rule from State and local officials.

F.	Executive Order 13175: Consultation and Coordination with Indian
Tribal Governments

	Executive Order 13175, entitled “Consultation and Coordination with
Indian Tribal Governments” (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.”  This rule concerns the establishment of O3
NAAQS.  The Tribal Authority Rule gives Tribes the opportunity to
develop and implement CAA programs such as the O3 NAAQS, but it leaves
to the discretion of the Tribe whether to develop these programs and
which programs, or appropriate elements of a program, they will adopt.  

	This proposed rule does not have Tribal implications, as specified in
Executive Order 13175.  It does not have a substantial direct effect on
one or more Indian Tribes, since Tribes are not obligated to adopt or
implement any NAAQS.  Thus, Executive Order 13175 does not apply to this
rule.

	Although Executive Order 13175 does not apply to this rule, EPA
contacted tribal environmental professionals during the development of
the March 2008 rule.  The EPA staff participated in the regularly
scheduled Tribal Air call sponsored by the National Tribal Air
Association during the spring of 2007 as the proposal was under
development.  EPA specifically solicits additional comment on this
proposed rule from Tribal officials.

G.	Executive Order 13045: Protection of Children from Environmental
Health & Safety Risks

	Executive Order 13045, “Protection of Children from Environmental
Health Risks and Safety Risks” (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.

	This proposed rule is subject to Executive Order 13045 because it is an
economically significant regulatory action as defined by Executive Order
12866, and we believe that the environmental health risk addressed by
this action may have a disproportionate effect on children.  The
proposed rule will establish uniform national ambient air quality
standards for O3; these standards are designed to protect public health
with an adequate margin of safety, as required by CAA section 109. 
However, the protection offered by these standards may be especially
important for children because children, especially children with
asthma, along with other sensitive population subgroups such as all
people with lung disease and people active outdoors, are potentially
susceptible to health effects resulting from O3 exposure.  Because
children are considered a potentially susceptible population, we have
carefully evaluated the environmental health effects of exposure to O3
pollution among children.  Discussions of the results of the evaluation
of the scientific evidence, policy considerations, and the exposure and
risk assessments pertaining to children are contained in sections II.B
and II.C of this preamble.  A listing of the documents that contain the
evaluation of scientific evidence, policy considerations, and exposure
and risk assessments that pertain to children is found in the section on
Children’s Environmental Health in the Supplementary Information
section of this preamble, and a copy of all documents have been placed
in the public docket for this action.  The public is invited to submit
comments or identify peer-reviewed studies and data that assess effects
of early life exposure to O3.  

Executive Order 13211: Actions that Significantly Affect Energy Supply,
Distribution or  Use

	This proposed rule is not a “significant energy action” as defined
in Executive Order 13211, “Actions Concerning Regulations That
Significantly Affect Energy Supply, Distribution, or Use” (66 FR 28355
(May 22, 2001)) because in the Agency’s judgment it is not likely to
have a significant adverse effect on the supply, distribution, or use of
energy.  The purpose of this rule is to establish revised NAAQS for O3. 
The rule does not prescribe specific pollution control strategies by
which these ambient standards will be met.  Such strategies will be
developed by States on a case-by-case basis, and EPA cannot predict
whether the control options selected by States will include regulations
on energy suppliers, distributors, or users.  Thus, EPA concludes that
this rule is not likely to have any adverse energy effects and does not
constitute a significant energy action as defined in Executive Order
13211.

I.	National Technology Transfer and Advancement Act

	Section 12(d) of the National Technology Transfer and Advancement Act
of 1995 (NTTAA), Public Law No. 104-113, §12(d) (15 U.S.C. 272 note)
directs EPA to use voluntary consensus standards in its regulatory
activities unless to do so would be inconsistent with applicable law or
otherwise impractical.  Voluntary consensus standards are technical
standards (e.g., materials specifications, test methods, sampling
procedures, and business practices) that are developed or adopted by
voluntary consensus standards bodies.  The NTTAA directs EPA to provide
Congress, through OMB, explanations when the Agency decides not to use
available and applicable voluntary consensus standards.

	This proposed rulemaking does not involve technical standards.
Therefore, EPA is not considering the use of any voluntary consensus
standards.

J.	Executive Order 12898: Federal Actions to Address Environmental
Justice in Minority Populations and Low-Income Populations

	Executive Order 12898 (59 FR 7629 (Feb. 16, 1994)) establishes federal
executive policy on environmental justice.  Its main provision directs
federal agencies, to the greatest extent practicable and permitted by
law, to make environmental justice part of their mission by identifying
and addressing, as appropriate, disproportionately high and adverse
human health or environmental effects of their programs, policies, and
activities on minority populations and low-income populations in the
United States.  

	EPA has determined that this proposed rule will not have
disproportionately high and adverse human health or environmental
effects on minority or low-income populations because it increases the
level of environmental protection for all affected populations without
having any disproportionately high and adverse human health or
environmental effects on any population, including any minority or
low-income population.  The proposed rule will establish uniform
national standards for O3 air pollution.

List of Subjects in 40 CFR Part 50

Environmental protection, Air pollution control, Carbon monoxide, Lead,
Nitrogen dioxide, Ozone, Particulate matter, Sulfur oxides.

_________________		

Dated:	

_____________________________

Lisa P. Jackson, Administrator



References

  SEQ CHAPTER \h \r 1 Abbey, D. E.; Nishino, N.; McDonnell, W. F.;
Burchette, R. J.; Knutsen, S. F.; Beeson, W.  L.; Yang, J. X. (1999)
Long-term inhalable particles and other air pollutants related to
mortality in nonsmokers. Am. J. Respir. Crit. Care Med. 159: 373-382.

  SEQ CHAPTER \h \r 1 Abt Associates Inc. (1995) Ozone NAAQS benefits
analysis: California crops.  Report to U.S. EPA, July 1995.  EPA Docket
No. A-95-58 Item II-I-3

Abt Associates Inc. (2007a) Ozone Health Risk Assessment for Selected
Urban Areas.  Prepared for Office of Air Quality Planning and Standards,
U.S. Environmental Protection Agency, Research Triangle Park, NC.  July
2007; EPA report no. EPA-452/R-07-009.  Available online at:   
HYPERLINK "http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_td.html"
 http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_td.html .

Abt Associates Inc. (2007b) Technical Report on Ozone Exposure, Risk,
and Impacts Assessments for Vegetation: Final Report.  Prepared for
Office of Air Quality Planning and Standards, U.S. Environmental
Protection Agency, Research Triangle Park, NC.  January 2007; EPA report
no. EPA-452/R-07-002.  Available online at:    HYPERLINK
"http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_td.html" 
http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_td.html . 

Adams, W. C. (2002) Comparison of chamber and face-mask 6.6-hour
exposures to ozone on pulmonary function and symptoms responses.
Inhalation Toxicol. 14: 745-764.

Adams, W. C. (2003a) Comparison of chamber and face mask 6.6-hour
exposure to 0.08 ppm ozone via square-wave and triangular profiles on
pulmonary responses. Inhalation Toxicol. 15: 265-281.

Adams, W. C. (2003b) Relation of pulmonary responses induced by 6.6 hour
exposures to 0.08 ppm ozone and 2-hour exposures to 0.30 ppm via chamber
and face-mask inhalation.  Inhalation Toxicol. 15: 745-759. 

Adams, W. C. (2006) Comparison of chamber 6.6 hour exposures to
0.04-0.08 ppm ozone via square-wave and triangular profiles on pulmonary
responses.  Inhalation Toxicol. 18: 127-136.

Adams, W.C. (2007) Comment on EPA memorandum: The effects of ozone on
lung function at 0.06 ppm in healthy adults. October 9. 
EPA-HQ-OAR-2005-0172-4783.

American Academy of Pediatrics, Committee on Environmental Health.
(2004) Ambient air pollution: health hazards to children. Pediatrics
114: 1699-1707.

American Thoracic Society. (1985) Guidelines as to what constitutes an
adverse respiratory health effect, with special reference to
epidemiologic studies of air pollution.  Am. Rev. Respir. Dis. 131: 
666-668.

American Thoracic Society (2000) What constitutes an adverse effect of
air pollution? Am. J. Respir. Crit. Care Med. 161:  pp. 665-673.

Andersen, C. P.; Hogsett, W. E.; Wessling, R.; Plocher, M. (1991) Ozone
decreases spring root growth and root carbohydrate content in ponderosa
pine the year following exposure. Can. J. For. Res. 21: 1288-1291.

Anderson, H. R.; Spix, C.; Medina, S.; Schouten, J. P.; Castellsague,
J.; Rossi, G.; Zmirou, D.; Touloumi, G.; Wojtyniak, B.; Ponka, A.;
Bacharova, L.; Schwartz, J.; Katsouyanni, K. (1997) Air pollution and
daily admissions for chronic obstructive pulmonary disease in 6 European
cities: results from the APHEA project. Eur. Respir. J. 10: 1064-1071.

Arbaugh, M.; Bytnerowicz, A.; Grulke, N.; Fenn, M.; Poth, M.; Temple,
P.; Miller, P. (2003) Photochemical smog effects in mixed conifer
forests along a natural gradient of ozone and nitrogen deposition in the
San Bernardino Mountains. Environ. Int. 29: 401-406.

Arnold J.R.; R. L. Dennis; G. S. Tonnesen, (2003) Diagnostic evaluation
of numerical air quality models with specialized ambient observations:
testing the Community Multiscale Air Quality modeling system (CMAQ) at
selected SOS 95 ground sites, Atmos. Environ. 37: 1185-1198.

Ashmore, M.; Emberson, L.; Karlsson, P. E.; Pleijel, H. (2004) New
directions: a new generation of ozone critical levels for the protection
of vegetation in Europe (correspondence). Atmos. Environ. 38: 2213-2214.

  SEQ CHAPTER \h \r 1 Arito, H.; Takahashi, M.; Iwasaki, T.; Uchiyama,
I. (1997) Age-related changes in ventilatory and heart rate responses to
acute ozone exposure in the conscious rat. Ind. Health 35: 78-86.

Avol, E. L.; Gauderman, W. J.; Tan, S. M.; London, S. J.; Peters, J. M.
(2001) Respiratory effects of relocating to areas of differing air
pollution levels. Am. J. Respir. Crit. Care Med. 164: 2067-2072.

Awmack, C. S.; Harrington, R.; Lindroth, R. L. (2004) Aphid individual
performance may not predict population responses to elevated CO2 or O3.
Global Change Biol. 10: 1414-1423.

Barnes, J. D.; Eamus, D.; Brown, K. A. (1990) The influence of ozone,
acid mist and soilnutrient status on Norway spruce [Picea abies (L.)
Karst.]: II. photosynthesis, dark respiration and soluble carbohydrates
of trees during late autumn. New Phytol. 115: 149-156.

Bascom, R.; Naclerio, R. M.; Fitzgerald, T. K.; Kagey-Sobotka, A.;
Proud, D. (1990) Effect of ozone inhalation on the response to nasal
challenge with antigen of allergic subjects. Am. Rev. Respir. Dis. 142:
594-601.

Basha, M. A.; Gross, K. B.; Gwizdala, C. J.; Haidar, A. H.; Popovich,
J., Jr. (1994) Bronchoalveolar lavage neutrophilia in asthmatic and
healthy volunteers after controlled exposure to ozone and filtered
purified air. Chest 106: 1757-1765.

Beedlow P.A., Tingey D.T., Phillips D.L., Hogsett W.E. & Olszyk D.M.
(2004) Rising atmospheric CO2 and carbon sequestration in forests.
Frontiers in Ecology and the Environment 2, 315–322.

Beeson, W. L.; Abbey, D. E.; Knutsen, S. F. (1998) Long-term
concentrations of ambient air pollutants and incident lung cancer in
California adults: results from the AHSMOG study. Environ. Health
Perspect. 106: 813-823.

Bell, M. L.; McDermott, A.; Zeger, S. L.; Samet, J. M.; Dominici, F.
(2004) Ozone and short-term mortality in 95 US urban communities,
1987-2000. JAMA J. Am. Med. Assoc. 292:  2372-2378.

Bell, M. L.; Dominici, F.; Samet, J. M. (2005) A meta-analysis of
time-series studies of ozone and mortality with comparison to the
national morbidity, mortality, and air pollution study. Epidemiology 16:
436-445.

Bell, M. L.; Peng, R. D.; Dominici, F. (2006) The exposure-response
curve for ozone and risk of mortality and the adequacy of current ozone
regulations.  Environ. Health Perspect.: doi:10.1289/ehp.8816. 
Available online at:  http://dx.doi.org/ [23 January, 2006].

Bosson, J.; Stenfors, N.; Bucht, A.; Helleday, R.; Pourazar, J.;
Holgate, S. T.; Kelly, F. J.; Sandström, T.; Wilson, S.; Frew, A. J.;
Blomberg, A. (2003) Ozone-induced bronchial epithelial cytokine
expression differs between healthy and asthmatic subjects. Clin. Exp.
Allergy 33:  777-782.

Brauer, M.; Blair, J.; Vedal, S. (1995) Effect of ambient ozone exposure
on lung function in farm workers. Am. J. Respir. Crit. Care Med. 154:
981-987.

Brauer, M.; Blair, J.; Vedal, S. (1996) Effect of ambient ozone exposure
on lung function in farm workers. Am. J. Respir. Crit. Care Med. 154:
981-987.

Brauer, M.; Brook, J. R. (1997) Ozone personal exposures and health
effects for selected groups residing in the Fraser Valley. In: Steyn, D.
G.; Bottenheim, J. W., eds. The Lower Fraser Valley Oxidants/Pacific '93
Field Study. Atmos. Environ. 31: 2113-2121.

Black, V. J.; Black, C. R.; Roberts, J. A.; Stewart, C. A. (2000) Impact
of ozone on the reproductive development of plants. New Phytol. 147:
421-447.

  SEQ CHAPTER \h \r 1 Brook, R. D.; Brook, J. R.; Urch, B.; Vincent, R.;
Rajagopalan, S.; Silverman, F. (2002) Inhalation of fine particulate air
pollution and ozone causes acute arterial vasoconstriction in healthy
adults. Circulation 105: 1534-1536.

Brown, J. S.  The effects of ozone on lung function at 0.06 ppm in
healthy adults.  June 14, 2007.  Memo to the Ozone NAAQS Review Docket. 
EPA-HQ-OAR-2005-0172-0175.  Available online at:    HYPERLINK
"http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_td.html" 
http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_td.html .

Burnett, R. T.; Dales, R. E.; Raizenne, M. E.; Krewski, D.; Summers, P.
W.; Roberts, G. R.; Raad-Young, M.; Dann, T.; Brook, J. (1994) Effects
of low ambient levels of ozone and sulfates on the frequency of
respiratory admissions to Ontario hospitals. Environ. Res. 65: 172-194.

Burnett, R. T.; Brook, J. R.; Yung, W. T.; Dales, R. E.; Krewski, D.
(1997a) Association between ozone and hospitalization for respiratory
diseases in 16 Canadian cities. Environ. Res. 72: 24-31.

Burnett, R. T.; Cakmak, S.; Brook, J. R.; Krewski, D. (1997b) The role
of particulate size and chemistry in the association between summertime
ambient air pollution and hospitalization for cardiorespiratory
diseases. Environ. Health Perspect. 105: 614-620.

Burns, R. M., Honkala, B. H., tech. coords. (1990) Silvics of North
America: 1. Conifers; 2. Hardwoods. Agriculture Handbook 654. U.S.
Department of Agriculture, Forest Service, Washington, DC. vol.2, p.
877.

Byun, D.W., Ching, J.K.S. (Eds.), 1999. Science Algorithms of the EPA
Models-3 Community Multiscale Air Quality Model (CMAQ) Modeling System.
EPA/600/R-99/030, U.S. Environmental Protection Agency, Office of
Research and Development, Washington, DC 20460.

Campbell, S.; Temple, P.; Pronos, J.; Rochefort, R.; Andersen, C. (2000)
Monitoring for ozone injury in west coast (Oregon, Washington,
California) forests in 1998. Portland, OR: U.S. Department of
Agriculture, Forest Service, Pacific Northwest Research Station; general
technical report no. PNW-GTR-495. Available:
http://www.fs.fed.us/pnw/gtrs.htm [11 April, 2003].

Centers for Disease Control and Prevention. (2004) The health
consequences of smoking: a report of the Surgeon General. Atlanta, GA:
U.S. Department of Health and Human Services, National Center for
Chronic Disease Prevention and Health Promotion, Office on Smoking and
Health. Available: http://www.cdc.gov/tobacco/sgr/sgr_2004/chapters.htm
(18 August, 2004).

Chappelka, A. H. (2002) Reproductive development of blackberry (Rubus
cuneifolius) as influenced by ozone. New Phytol. 155: 249-255.

Chappelka, A. H.; Samuelson, L. J. (1998) Ambient ozone effects on
forest trees of the eastern United States: a review. New Phytol. 139:
91-108.

Chen, L.; Jennison, B. L.; Yang, W.; Omaye, S. T. (2000) Elementary
school absenteeism and air pollution. Inhalation Toxicol. 12:  997-101.

  SEQ CHAPTER \h \r 1 Chen, C.-Y.; Bonham, A. C.; Plopper, C. G.; Joad,
J. P. (2003) Plasticity in respiratory motor control: selected
contribution: neuroplasticity in nucleus tractus solitarius neurons
following episodic ozone exposure in infant primates. J. Appl. Physiol.
94: 819-827.

Clean Air Scientific Advisory Committee (CASAC) (2006) Transcript of
Public Meeting Held in Research Triangle Park, N.C. on August 24, 2006.

Cox, W. M.; Camalier, L.  (2006) The effect of measurement error on
8-hour ozone design concentrations.  Memo to the Ozone NAAQS Review
Docket.  EPA-HQ-OAR-2005-0172-0026. Available online at:    HYPERLINK
"http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_td.html" 
http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_td.html .

Coulston, J. W., Smith, G. C. and Smith, W. D. (2003) “Regional
assessment of ozone sensitive tree species using bioindicator plants.”
Environmental Monitoring and Assessment 83: 113–127.

Coulston, J. W., K. H. Riitters and G. C. Smith (2004) A Preliminary
Assessment of the Montréal Process Indicators of Air Pollution for the
United States. Environmental Monitoring and Assessment 95: 57–74.

Dann, M. S.; Pell, E. J. (1989) Decline of activity and quantity of
ribulose bisphosphatecarboxylase/oxygenase and net photosynthesis in
ozone-treated potato foliage. PlantPhysiol. 91: 427-432.

David, G. L.; Romieu, I.; Sienra-Monge, J. J.; Collins, W. J.;
Ramirez-Aguilar, M.; Del Rio-Navarro, B. E.;Reyes-Ruiz, N. I.; Morris,
R. W.; Marzec, J. M.; London, S. J. (2003) Nicotinamide adenine
dinucleotide (phosphate) reduced:quinone oxidoreductase and glutathione
s-transferase m1 polymorphism and childhood asthma. Am. J. Respir. Crit.
Care Med. 168: 1199-1204.

Davison, A. W.; Reiling, K. (1995) A rapid change in ozone resistance of
Plantago major after summers with high ozone concentrations. New Phytol.
131: 337-344.

Devlin, R. B.; McDonnell, W. F.; Koren, H. S.; Becker, S. (1990)
Prolonged exposure of humans to 0.10 and 0.08 ppm ozone results in
inflammation in the lung. Presented at: 83rd annual meeting of the Air &
Waste Management Association; June; Pittsburgh, PA. Pittsburgh, PA: Air
& Waste Management Association; paper no. 90-150.2.

Devlin, R. B.; McDonnell, W. F.; Mann, R.; Becker, S.; House, D. E.;
Schreinemachers, D.; Koren, H. S. (1991) Exposure of humans to ambient
levels of ozone for 6.6 hrs causes cellular and biochemical changes in
the lung. Am. J. Respir. Cell Mol. Biol. 4: 72-81.

Dickson, R. E., Lewin K. F., Isebrands J. G., Coleman M. D., Heilman W.
E., Riemenschneider D. E., Sober J., Host G. E., Zak D. F., Hendrey G.
R., Pregitzer K. S. and Karnosky D. F. (2000)  Forest atmosphere carbon
transfer storage-II (FACTS II) – The aspen free-air CO2 and O3
enrichment (FACE) project in an overview. USDA Forest Service North
Central Research Station. General Tech. Rep. NC-214.  68pp. 

Dietert, R. R.; Etzel, R. A.; Chen, D.; Halonen, M.; Holladay, S. D.;
Jarabek, A. M.; Landreth, K.; Peden, D. B.; Pinkerton, K.; Smialowicz,
R. J.; Zoetis, T. (2000) Workshop to identify critical window of
exposure for children's health: immune and respiratory systems work
group summary. Environ. Health Perspect. Suppl. 108(3): 483-490.

Dockery, D. W.; Pope, C. A., III; Xu, X.; Spengler, J. D.; Ware, J. H.;
Fay, M. E.; Ferris, B. G., Jr.; Speizer, F. E. (1993) An association
between air pollution and mortality in six U.S. cities. N. Engl. J. Med.
329: 1753-1759.

Dominici, F.; McDermott, A.; Daniels, M.; Zeger, S. L.; Samet, J. M.
(2003) Mortality among residents of 90 cities. In:  Revised analyses of
time-series studies of air pollution and health. Special report. Boston,
MA:  Health Effects Institute; pp. 9-24. Available: 
http://www.healtheffects.org/Pubs/TimeSeries.pdf [12 May, 2004].

Duff, M., Horst, R. L., Johnson, T. R. (1998) “Quadratic Rollback: A
Technique to Model Ambient Concentrations Due to Undefined Emission
Controls.”  Presented at the Air and Waste Management Annual Meeting. 
San Diego, California.  June 14-18, 1998.

Eder, B. and S. Yu, 2006: A performance evaluation of the 2004 release
of Models-3 CMAQ, Atmos. Environ. 40: 4811-4824. Special issue on Model
Evaluation: Evaluation of Urban and Regional Eulerian Air Quality
Models.

Environmental Protection Agency (1986) Air quality criteria for ozone
and other photochemical oxidants. Research Triangle Park, NC: Office of
Health and Environmental Assessment, Environmental Criteria and
Assessment Office; report nos. EPA-600/8-84-020aF-eF. 5v. Available
from: NTIS, Springfield, VA; PB87-142949.

Environmental Protection Agency (1996a) Air quality criteria for ozone
and related photochemical oxidants. Research Triangle Park, NC:  Office
of Research and Development; EPA report no. EPA/600/AP-93/004aF-cF. 3v.
Available from:  NTIS, Springfield, VA; PB96-185582, PB96-185590, and
PB96-185608.  Available online at:   HYPERLINK
"http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=2831" 
http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=2831 .

Environmental Protection Agency (1996b) Review of National Ambient Air
Quality Standards for Ozone: Assessment of Scientific and Technical
Information. OAQPS Staff Paper (Final) Research Triangle Park, NC:
Office of Air Quality Planning and Standards; EPA report no.
EPA/452/R-96-007.  Available online at:    HYPERLINK
"http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_pr_sp.html" 
http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_pr_sp.html .

Environmental Protection Agency (2002) Project Work Plan for Revised Air
Quality Criteria for Ozone and Related Photochemical Oxidants. Research
Triangle Park, NC: National Center for Environmental Assessment; EPA
report no. NCEA-R-1068.

Environmental Protection Agency (2004) The Ozone Report: Measuring
Progress through 2003.  EPA/454/K-04-001.  Office of Air Quality
Planning and Standards, Research Triangle Park, NC.

Environmental Protection Agency (2005a) Air Quality Criteria for Ozone
and Related Photochemical Oxidants (First External Review Draft).
Washington, DC: National Center for Environmental Assessment; EPA report
no. EPA/600/R-05/004aA-cA. Available online at:   HYPERLINK
"http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=114523" 
http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=114523 .

Environmental Protection Agency (2005b) Air Quality Criteria for Ozone
and Related Photochemical Oxidants (Second External Review Draft)
Washington, DC: National Center for Environmental Assessment; EPA report
no. EPA/600/R-05/004aB-cB. Available online at:    HYPERLINK
"http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=137307" 
http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=137307 .

Environmental Protection Agency (2005c) Review of the national ambient
air quality standards for ozone: assessment of scientific and technical
information. OAQPS staff paper (First Draft). Research Triangle Park,
NC: Office of Air Quality Planning and Standards; EPA report no.
EPA-452/D-05-002. Available online at:   HYPERLINK
"http://epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_sp.html" 
http://epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_sp.html .

Environmental Protection Agency (2005d) Health Assessment Plan for
Review of the National Ambient Air Quality Standards for Ozone. Office
of Air Quality Planning and Standards, Research Triangle Park, NC. April
2005.  Available electronically on the internet at:   HYPERLINK
"http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_pd.html" 
http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_pd.html .

Environmental Protection Agency (2006a) Air Quality Criteria for Ozone
and Related Photochemical Oxidants. (Final) Washington, DC: National
Center for Environmental Assessment; EPA report no.
EPA/600/R-05/004aB-cB. Available online at:    HYPERLINK
"http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=149923" 
http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=149923 .

Environmental Protection Agency (2006b) Review of the national ambient
air quality standards for ozone: assessment of scientific and technical
information. OAQPS staff paper. (Second Draft). Research Triangle Park,
NC: Office of Air Quality Planning and Standards; EPA report no.
EPA-452/D-05-002. Available online at:    HYPERLINK
"http://epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_sp.html" 
http://epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_sp.html .

Environmental Protection Agency (2007a) Review of the national ambient
air quality standards for ozone: assessment of scientific and technical
information. OAQPS staff paper. (Final) January 2007.  Research Triangle
Park, NC: Office of Air Quality Planning and Standards; EPA report no.
EPA-452/R-07-003.  Available online at:    HYPERLINK
"http://epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_sp.html" 
http://epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_sp.html .

Environmental Protection Agency (2007b) Review of the national ambient
air quality standards for ozone: assessment of scientific and technical
information. OAQPS staff paper. (Updated Final) July 2007.  Research
Triangle Park, NC: Office of Air Quality Planning and Standards; EPA
report no. EPA-452/R-07-007.  Available online at:    HYPERLINK
"http://epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_sp.html" 
http://epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_sp.html .

Environmental Protection Agency (2007c) Ozone Population Exposure
Analysis for Selected Urban Areas. (Updated Final) July 2007.  Research
Triangle Park, NC: Office of Air Quality Planning and Standards; EPA
report no. EPA-452/R-07-010. Available online at:   HYPERLINK
"http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_td.html" 
http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_td.html .

Environmental Protection Agency (2008) Responses to Significant Comments
on the 2007 Proposed Rule on the National Ambient Air Quality Standards
for Ozone (July 11, 2007; 72 FR 37818).  March 2008. Research Triangle
Park, NC; Office of Air Quality Planning and Standards.  Available
online at:  http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_rc.html

.

Environmental Protection Agency (2009) Provisional Assessment of Recent
Studies on Health and Ecological Effects of Ozone Exposure.  September
2009.  Research Triangle Park: National Center for Environmental
Assessment; EPA report no. EPA/600/R-09/101. 

  SEQ CHAPTER \h \r 1 Evans, M. J.; Fanucchi, M. V.; Baker, G. L.; Van
Winkle, L. S.; Pantle, L. M.; Nishio, S. J.; Schelegle, E. S.;
Gershwhin, L. J.; Miller, L. A.; Hyde, D. M.; Sannes, P. L.; Plopper, C.
G. (2003) Atypical development of the tracheal basement membrane zone of
infant rhesus monkeys exposed to ozone and allergen. Am. J. Physiol.
285: L931-L939.

Felzer, B.; Kickligher, D.; Melillo, J.; Wang, C.; Zhuang, Q.; Prinn, R.
(2004) Effects of ozone on net primary production and carbon
sequestration in the conterminous United States using a biogeochemistry
model. Tellus B 56 (3), 230-248.

Fiore, A. M.; Jacob, D. J.; Bey, I.; Yantosca, R. M.; Field, B. D.;
Fusco, A. C.; Wilkinson, J. G. (2002)  Background ozone over the United
States in summer: origin, trend, and contribution to pollution episodes.
 J. Geophys. Res. (Atmos.) 107(D15): 10.1029/2001JD000982.

Fiore, A. M.; Jacob, D. J.; Liu, H.; Yantosca, R. M.; Fairlie, T. D.;
Fusco, A. C.; Li, Q. (2003)  Variability in surface ozone background
over the United States:  implications for Air Quality Policy.  J. of
Geophysical Research, 108(D24)19-1-19-12.

Fiscus, E. L.; Reid, C. D.; Miller, J. E.; Heagle, A. S. (1997) Elevated
CO2 reduces O3 flux and O3-induced yield losses in soybeans: possible
implications for elevated CO2 studies. J. Exp. Bot. 48: 307-313.

Folinsbee, L. J.; McDonnell, W. F.; Horstman, D. H. (1988) Pulmonary
function and symptom responses after 6.6-hour exposure to 0.12 ppm ozone
with moderate exercise. JAPCA 38: 28-35.

Folinsbee, L. J.; Horstman, D. H.; Kehrl, H. R.; Harder, S.;
Abdul-Salaam, S.; Ives, P. J. (1994) Respiratory responses to repeated
prolonged exposure to 0.12 ppm ozone. Am. J. Respir. Crit. Care Med.
149: 98-105.

Folinsbee, L. J.; Hazucha, M. J. (2000) Time course of response to ozone
exposure in healthy adult females. Inhalation Toxicol. 12: 151-167.

Foster, W. M.; Silver, J. A.; Groth, M. L. (1993) Exposure to ozone
alters regional function and particle dosimetry in the human lung. J.
Appl. Physiol. 75: 1938-1945.

Foster, W. M.; Weinmann, G. G.; Menkes, E.; Macri, K. (1997) Acute
exposure of humans to ozone impairs small airway function. Ann. Occup.
Hyg. 41(suppl. 1): 659-666.

Frampton, M. W.; Morrow, P. E.; Torres, A.; Cox, C.; Voter, K. Z.;
Utell, M. J.; Gibb, F. R.; Speers, D. M. (1997) Ozone responsiveness in
smokers and nonsmokers. Am. J. Respir. Crit. Care Med. 155: 116-121.

Galizia, A.; Kinney, P. L. (1999) Long-term residence in areas of high
ozone: associations with respiratory health in a nationwide sample of
nonsmoking young adults. Environ. Health Perspect. 107: 675-679.

Gauderman, W. J.; McConnell, R.; Gilliland, F.; London, S.; Thomas, D.;
Avol, E.; Vora, H.; Berhane, K.; Rappaport, E. B.; Lurmann, F.;
Margolis, H. G.; Peters, J. (2000) Association between air pollution and
lung function growth in southern California children. Am. J. Respir.
Crit. Care Med. 162: 1383-1390.

Gauderman, W. J.; Gilliland, G. F.; Vora, H.; Avol, E.; Stram, D.;
McConnell, R.; Thomas, D.; Lurmann, F.; Margolis, H. G.; Rappaport, E.
B.; Berhane, K.; Peters, J. M. (2002) Association between air pollution
and lung function growth in southern California children: results from a
second cohort. Am. J. Respir. Crit. Care Med. 166: 76-84.

Gauderman, W. J.; Avol, E.; Gilliland, F.; Vora, H.; Thomas, D.;
Berhane, K.; McConnell, R.; Kuenzli, N.; Lurmann, F.; Rappaport, E.;
Margolis, H.; Bates, D.; Peters, J. (2004a) The effect of air pollution
on lung development from 10 to 18 years of age. N. Engl. J. Med. 351:
1057-1067.

Gauderman, W. J.; Avol, E.; Gilliland, F. (2004b) Air pollution and lung
function [reply letter]. N. Engl. J. Med. 351: 2653.

Gent, J. F.; Triche, E. W.; Holford, T. R.; Belanger, K.; Bracken, M.
B.; Beckett, W. S.; Leaderer, B. P. (2003) Association of low-level
ozone and fine particles with respiratory symptoms in children with
asthma. JAMA J. Am. Med. Assoc. 290:  1859-1867.

Gilliland, F. D.; Berhane, K.; Rappaport, E. B.; Thomas, D. C.; Avol,
E.; Gauderman, W. J.; London, S. J.; Margolis, H. G.; McConnell, R.;
Islam, K. T.; Peters, J. M. (2001) The effects of ambient air pollution
on school absenteeism due to respiratory illnesses. Epidemiology 12: 
43-54.

Goldstein, A. H.; Millet, D. B.; McKay, M.; Jaegle, L.; Horowitz, L.;
Cooper, O.; Hudman, R.; Jacob, D; Oltmans, S; Clarke, A. (2004) Impact
of Asian emissions on observations at Trinidad Head, California, during
ITCT 2K2. J. of Geophysical Research, 109(D23S17), doi:
10.1029/2003JD004406.

Gong, H., Jr.; Wong, R.; Sarma, R. J.; Linn, W. S.; Sullivan, E. D.;
Shamoo, D. A.; Anderson, K. R.; Prasad, S. B. (1998) Cardiovascular
effects of ozone exposure in human volunteers. Am. J. Respir. Crit. Care
Med. 158: 538-546.

Goodale, C. L., Apps, M. J., Birdsey, R. A., Field, C. B., Heath, L. S.,
Houghton, R. A., Jenkins, J. C., Kohlmaier, G. H., Kurz, W., Liu, S.,
Nabuurs, G.-J., Nilsson, S. and Shvidenko, A. Z. (2002) Forest carbon
sinks in the northern hemisphere. Ecol. Appl. 12, 891–899.

Grantz, D.A., McCool, P.H. (1992) Effect of ozone on Pima and Acala
cottons in the San Joaquin Valley. In: Herber, D.J., Richter, D.A.
(Eds.), Proceedings 1992 Beltwide Cotton Conferences, vol 3.National
Cotton Council of America, Memphis, TN, pp. 1082–1084.

Greer, J. R.; Abbey, D. E.; Burchette, R. J. (1993) Asthma related to
occupational and ambient air pollutants in nonsmokers. J. Occup. Med.
35: 909-915.

Gregg, J. W.; Jones, C. G.; Dawson, T. E. (2003) Urbanization effects on
tree growth in the vicinity of New York City. Nature 424: 183-187.

Grulke, N. E.; Andersen, C. P.; Fenn, M. E.; Miller, P. R. (1998) Ozone
exposure and nitrogen deposition lowers root biomass of ponderosa pine
in the San Bernardino Mountains, California. Environ. Pollut. 103:
63-73.

Grulke, N. E.; Balduman, L. (1999) Deciduous conifers: high N deposition
and O3 exposure effects on growth and biomass allocation in ponderosa
pine. Water Air Soil Pollut. 116: 235-248.

Gryparis, A.; Forsberg, B.; Katsouyanni, K.; Analitis, A.; Touloumi, G.;
Schwartz, J.; Samoli, E.; Medina, S.; Anderson, H. R.; Niciu, E. M.;
Wichmann, H.-E.; Kriz, B.; Kosnik, M.; Skorkovsky, J.; Vonk, J. M.;
Dörtbudak, Z. (2004) Acute effects of ozone on mortality from the "air
pollution and health:  a European approach" project. Am. J. Respir.
Crit. Care Med. 170:  1080-1087.

Guderian, R. (1977) Discussion of the suitability of plant responses as
a basis for air pollution control measures. In: Billings, W. D.; Golley,
F.; Lange, O. L.; Olson, J. S., eds. Air pollution: phytotoxicity of
acidic gases and its significance in air pollution control. Berlin,
Federal Republic of Germany: Springer Verlag; pp. 75-97.

Hanson, P., Samuelson, L., Wullschleger, S., Tabberer, T.; Edwards, G.
(1994) “Seasonal patterns of light-saturated photosynthesis and leaf
conductance for mature and seedling Quercus rubra L. foliage:
differential sensitivity to ozone exposure.” Tree Physiology
14:1351-1366.

Hazucha, M. J.; Folinsbee, L. J.; Seal, E., Jr. (1992) Effects of
steady-state and variable ozone concentration profiles on pulmonary
function. Am. Rev. Respir. Dis. 146: 1487-1493.

Hazucha, M. J.; Folinsbee, L. J.; Bromberg, P. A. (2003) Distribution
and reproducibility of spirometric response to ozone by gender and age.
J. Appl. Physiol. 95:  1917-1925.

Heck, W. W.; Cowling, E. B. (1997) The need for a long term cumulative
secondary ozone standard - an ecological perspective. EM (January):
23-33.

Henderson, R. (2006a) Letter from CASAC Chairman Rogene Henderson to EPA
Administrator Stephen Johnson. February 16, 2006, EPA-CASAC-06-003.

Henderson, R. (2006b) Letter from CASAC Chairman Rogene Henderson to EPA
Administrator Stephen Johnson. June 5, 2006, EPA-CASAC-06-007.

Henderson, R. (2006c) Letter from CASAC Chairman Rogene Henderson to EPA
Administrator Stephen Johnson. October 24, 2006, EPA-CASAC-07-001.

Henderson, R. (2007) Letter from CASAC Chairman Rogene Henderson to EPA
Administrator Stephen Johnson. March 26, 2007, EPA-CASAC-07-002.

Henderson, R. (2008) Letter from CASAC Chairman Rogene Henderson to EPA
Administrator Stephen Johnson. April 7, 2008, EPA-CASAC-08-009.

Hill, A.B. (1965) The environment and disease:  association or
causation?  Proc. R. Soc. Med. 58: 295-300.

Hiltermann, J. T. N.; Lapperre, T. S.; Van Bree, L.; Steerenberg, P. A.;
Brahim, J. J.; Sont, J. K.; Sterk, P. J.; Hiemstra, P. S.; Stolk, J.
(1999) Ozone-induced inflammation assessed in sputum and bronchial
lavage fluid from asthmatics:  a new noninvasive tool in epidemiologic
studies on air pollution and asthma. Free Radical Biol. Med. 27: 
1448-1454.

Hoek, G. (2003) Daily mortality and air pollution in The Netherlands.
In: Revised analyses of time-series studies of air pollution and health.
Special report. Boston, MA: Health Effects Institute; pp. 133-142.
Available: http://www.healtheffects.org/Pubs/TimeSeries.pdf [12 May,
2004].

Hoek, G.; Brunekreef, B.; Verhoeff, A.; Van Wijnen, J.; Fischer, P.
(2000) Daily mortality and air pollution in the Netherlands. J. Air
Waste Manage. Assoc. 50: 1380-1389.

Hoek, G.; Brunekreef, B.; Fischer, P.; Van Wijnen, J. (2001) The
association between air pollution and heart failure, arrhythmia,
embolism, thrombosis, and other cardiovascular causes of death in a time
series study. Epidemiology 12: 355-357.

Hogsett, W. E.; Tingey, D. T.; Hendricks, C.; Rossi, D. (1989)
Sensitivity of western conifers to SO2 and seasonal interaction of acid
fog and ozone. In: Olson, R. K.; Lefohn, A. S., eds. Effects of air
pollution on western forests [an A&WMA symposium; June; Anaheim, CA].
Air Pollution Control Association; pp. 469-491 (APCA transactions
series: no. 16).

Holton, M. K.; Lindroth, R. L.; Nordheim, E. V. (2003) Foliar quality
influences tree-herbivore-parisitoid interactions: effects of elevated
CO2, O3, and plant genotype. Oecologia 137: 233-244.

Holz, O.; Mücke, M.; Paasch, K.; Böhme, S.; Timm, P.; Richter, K.;
Magnussen, H.; Jörres, R. A. (2002) Repeated ozone exposures enhance
bronchial allergen responses in subjects with rhinitis or asthma. Clin.
Exp. Allergy. 32: 681-689.

Höppe, P.; Praml, G.; Rabe, G.; Lindner, J.; Fruhmann, G.; Kessel, R.
(1995) Environmental ozone field study on pulmonary and subjective
responses of assumed risk groups. Environ. Res. 71: 109-121.

Horst, R.; Duff, M. (1995). Concentration data transformation and the
quadratic rollback methodology (Round 2, Revised). Unpublished
memorandum to R. Rodríguez, U.S. EPA, June 8.

Horstman, D. H.; Folinsbee, L. J.; Ives, P. J.; Abdul-Salaam, S.;
McDonnell, W. F. (1990) Ozone concentration and pulmonary response
relationships for 6.6-hr exposures with five hours of moderate exercise
to 0.08, 0.10, and 0.12 ppm. Am. Rev. Respir. Dis. 142: 1158-1163.

Horstman, D. H.; Ball, B. A.; Brown, J.; Gerrity, T.; Folinsbee, L. J.
(1995) Comparison of pulmonary responses of asthmatic and nonasthmatic
subjects performing light exercise while exposed to a low level of
ozone. Toxicol. Ind. Health 11: 369-385.

Huang, Y.; Dominici, F.; Bell, M. L. (2005) Bayesian hierarchical
distributed lag models for summer ozone exposure and cardio-respiratory
mortality. Environmetrics 16: 547-562.

Isebrands, J. G.; Dickson, R. E.; Rebbeck, J.; Karnosky, D. F. (2000)
Interacting effects of multiple stresses on growth and physiological
processes in northern forest trees. In: Mickler, R. A.; Birsdey, R. A.;
Hom, J., eds. Responses of northern U.S. forests to environmental
change. New York, NY: Springer-Verlag; pp. 149-180. (Ecological studies:
v. 139). 

Isebrands, J. G.; McDonald, E. P.; Kruger, E.; Hendrey, G.; Percy, K.;
Pregitzer, K.; Sober, J.; Karnosky, D. F. (2001) Growth responses of
Populus tremuloides clones to interacting carbon dioxide and
tropospheric ozone. Environ. Pollut. 115: 359-371.

Ito, K.; De Leon, S. F.; Lippmann, M. (2005) Associations between ozone
and daily mortality, analysis and meta-analysis. Epidemiology 16:
446-457.

Jacobson, J. S. (1977) The effects of photochemical oxidants on
vegetation. In: Ozon und Begleitsubstanzen im photochemischen Smog: das
Kolloquium [Ozone and related substances in photochemical smog: the
colloquium]; September 1976; Dusseldorf, Federal Republic of Germany.
Dusseldorf, Federal Republic of Germany: VDI-Verlag GmbH; pp. 163-173.
(VDI-Berichte nr. 270).

Johnson, T. (1997) “Sensitivity of Exposure Estimates to Air Quality
Adjustment Procedure,” Letter to Harvey Richmond, Office of Air
Quality Planning and Standards, U.S. Environmental Protection Agency,
Research Triangle Park, North Carolina.

Jörres, R.; Nowak, D.; Magnussen, H.; Speckin, P.; Koschyk, S. (1996)
The effect of ozone exposure on allergen responsiveness in subjects with
asthma or rhinitis. Am. J. Respir. Crit. Care Med. 153:  56-64.

Karnosky, D. F., Z.E.Gagnon, R.E. Dickson, M.D. Coleman, E.H. Lee, J.G.
Isebrands, (1996) “Changes in growth, leaf abscission, biomass
associated with seasonal tropospheric ozone exposures of Populus
tremuloides clones and seedlings.” Can. J. For. Res. 26: 23-37. 

Karnosky, D.F., B. Mankovska, K. Percy, R.E. Dickson, G.K. Podila, J.
Sober, A. Noormets, G. Hendrey, M.D. Coleman, M. Kubiske, K.S.
Pregitzer, and J.G. Isebrands (1999) “Effects of tropospheric O3 on
trembling aspen and interaction with CO2: Results from an O3-gradient
and a FACE experiment.” J. Water, Air and Soil Pollut. 116: 311-322.

Karnosky, D. F.; Zak, D. R.; Pregitzer, K. S.; Awmack, C. S.; Bockheim,
J. G.; Dickson, R. E.; Hendrey, G. R.; Host, G. E.; King, J. S.; Kopper,
B. J.; Kruger, E. L.; Kubiske, M. E.; Lindroth, R. L.; Mattson, W. J.;
McDonald, E. P. (2003) Tropospheric O3 moderates responses of temperate
hardwood forests to elevated CO2: A synthesis of molecular to ecosystem
results from the Aspen FACE project. Funct. Ecol. 17: 289-304.

Karnosky, D.F., Pregitzer, K.S., Zak, D.R., Kubiske, M.E., Hendrey,
G.R., Weinstein, D., Nosal, M. & Percy, K.E. (2005) Scaling ozone
responses of forest trees to the ecosystem level in a changing climate.
Plant Cell Environ.28, 965–981.

Kelly, F. J.; Dunster, C.; Mudway, I. (2003) Air pollution and the
elderly: oxidant/antioxidant issues worth consideration. Eur. Respir. J.
Suppl. 40: 70S-75S.

Kim, S.-Y.; Lee, J.-T.; Hong, Y.-C.; Ahn, K.-J.; Kim, H. (2004)
Determining the threshold effect of ozone on daily mortality: an
analysis of ozone and mortality in Seoul, Korea, 1995-1999. Environ.
Res. 94: 113-119.

King, J.S., M. E. Kubiske, K. S. Pregitzer, G. R. Hendrey, E. P.
McDonald, C. P. Giardina, V. S. Quinn, D. F. Karnosky. (2005)
Tropospheric O3 compromises net primary production in young stands of
trembling aspen, paper birch and sugar maple in response to elevated
atmospheric CO2.  New Phytologist. 168:623–636.

Kinney, P. L.; Aggarwal, M.; Nikiforov, S. V.; Nadas, A. (1998) Methods
development for epidemiologic investigations of the health effects of
prolonged ozone exposure. Part III: an approach to retrospective
estimation of lifetime ozone exposure using a questionnaire and ambient
monitoring data (U.S. sites). Cambridge, MA: Health Effects Institute;
research report no. 81; pp. 79-108.

Korrick, S. A.; Neas, L. M.; Dockery, D. W.; Gold, D. R.; Allen, G. A.;
Hill, L. B.; Kimball, K. D.; Rosner, B. A.; Speizer, F. E. (1998)
Effects of ozone and other pollutants on the pulmonary function of adult
hikers. Environ. Health Perspect. 106:  93-99.

Koutrakis, P.; Suh, H.H.; Sarnat, J. A.; Brown, K. W.; Coull, B.A;
Schwartz, J. (2005) Characterization of particulate and gas exposures of
sensitive subpopulations living in Baltimore and Boston.  HEI Research
Report 131.

Kreit, J. W.; Gross, K. B.; Moore, T. B.; Lorenzen, T. J.; D'Arcy, J.;
Eschenbacher, W. L. (1989) Ozone-induced changes in pulmonary function
and bronchial responsiveness in asthmatics. J. Appl. Physiol. 66:
217-222.

Krewski, D.; Burnett, R. T.; Goldberg, M. S.; Hoover, K.; Siemiatycki,
J,; Jerrett, M.; Abrahamowicz, M.; White, W. H.  (2000)  Reanalysis of
the Harvard Six Cities Study and the American Cancer Society Study of
particulate air pollution and mortality.  A special report of the
Institute’s particle epidemiology reanalysis project.  Cambridge, MA:
Health Effects Institute.

Künzli, N.; Lurmann, F.; Segal, M.; Ngo, L.; Balmes, J.; Tager, I. B.
(1997) Association between lifetime ambient ozone exposure and pulmonary
function in college freshmen—results of a pilot study. Environ. Res.
72: 8-23.

Langstaff, J. (2007) Analysis of Uncertainty in Ozone Population
Exposure Modeling. January 31, 2007.  Memo to the Ozone NAAQS Review
Docket.  EPA-HQ-OAR-2005-0172-0174.  Available online at:    HYPERLINK
"http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_td.html" 
http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_td.html .

Larson, J. L.; Zak, D. R.; Sinsabaugh, R. L. (2002) Extracellular enzyme
activity beneath temperate trees growing under elevated carbon dioxide
and ozone. Soil Sci. Soc. Am. J. 66: 1848-1856.

Laurence, J.A.,Kohut, R.J., Amundson, R.G.,  (1993). Use of TREGRO to
simulate the effects of ozone on the growth of red spruce seedlings.
Forest Science. 39: 453-464.

Laurence, J. A.; Retzlaff, W. A.; Kern, J. S.; Lee, E. H.; Hogsett, W.
E.; Weinstein, D. A. (2001) Predicting the regional impact of ozone and
precipitation on the growth of loblolly pine and yellow poplar using
linked TREGRO and ZELG models. For. Ecol. Manage. 146: 247-263. 

Lee, E. H.; Hogsett, W. E. (1996) Methodology for calculating inputs for
ozone secondary standard benefits analysis: part II. Report prepared for
Office of Air Quality Planning and Standards, Air Quality Strategies and
Standards Division, U.S. Environmental Protection Agency, Research
Triangle Park, N.C., March.  EPA Docket No. A-95-58 Item II-I-265.

Lefohn, A.S.; Runeckles, V.C.; Krupa, S.V.; Shadwick, D.S. (1989) 
Important considerations for establishing a secondary ozone standard to
protect vegetation.  JAPCA 39, pp. 1039-1045.

Levy, J. I.; Chemerynski, S. M.; Sarnat, J. A. (2005) Ozone exposure and
mortality, an empiric Bayes metaregression analysis. Epidemiology 16:
458-468.

Linn, W. S.; Shamoo, D. A.; Anderson, K. R.; Peng, R.-C.; Avol, E. L.;
Hackney, J. D.; Gong, H., Jr. (1996) Short-term air pollution exposures
and responses in Los Angeles area schoolchildren. J. Exposure Anal.
Environ. Epidemiol. 6: 449-472.

Lipfert, F. W.; Perry, H. M., Jr.; Miller, J. P.; Baty, J. D.; Wyzga, R.
E.; Carmody, S. E. (2000) The Washington University-EPRI veterans'
cohort mortality study: preliminary results. In: Grant, L. D., ed.
PM2000: particulate matter and health. Inhalation Toxicol. 12(suppl. 4):
41-73.

Lipfert, F. W.; Perry, H. M., Jr.; Miller, J. P.; Baty, J. D.; Wyzga, R.
E.; Carmody, S. E. (2003) Air pollution, blood pressure, and their
long-term associations with mortality. Inhalation Toxicol. 15: 493-512.

Long, S., Nelson, R.L., Ainsworth, L., Hollis, K., Mies, T., Morgan, P.,
Naidu, S., Ort, D.R., Webster, R., Zhu, X. Adapting Soybean To Current
And Future Change In Atmospheric Composition. Do We Need More Than Field
Selection Under Current Conditions. Cellular and Molecular Biology of
Soybean Biennial Conference. (2002) p. 401.    HYPERLINK
"http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_1
15=142752" 
http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_11
5=142752 

Loya W.M., Pregitzer K.S., Karberg N.J., King J.S. & Giardina C.P.
(2003) Reduction of soil carbon formation by tropospheric ozone under
elevated carbon dioxide. Nature 425, 705–707.

Luethy-Krause, B.; Landolt, W. (1990) Effects of ozone on starch
accumulation in Norway spruce (Picea abies). Trees 4: 107-110.

Lyons, T. M.; Barnes, J. D.; Davison, A. W. (1997) Relationships between
ozone resistance and climate in European populations of Plantago major.
New Phytol. 136: 503-510.

Manning, W. J.; Krupa, S. V. (1992) Experimental methodology for
studying the effects of ozone on crops and trees. In: Lefohn, A. S., ed.
Surface level ozone exposures and their effects on vegetation. Chelsea,
MI: Lewis Publishers, Inc.; pp. 93-156.

Mannino, D. M.; Ford, E. S.; Redd, S. C. (2003) Obstructive and
restrictive lung disease and markers of inflammation: data from the
Third National Health and Nutrition Examination. Am. J. Med. 114:
758-762.

Marty, M. (2007a) Letter from CHPAC Chair to the Administrator. March
23.  EPA-HQ-OAR-2005-0172-0105.  

Marty, M. (2007b) Letter from CHPAC Chair to the Administrator.
September 4.  EPA-HQ-OAR-2005-0172-2031.

McBride, D. E.; Koenig, J. Q.; Luchtel, D. L.; Williams, P. V.;
Henderson, W. R., Jr. (1994) Inflammatory effects of ozone in the upper
airways of subjects with asthma. Am. J. Respir. Crit. Care Med. 149:
1192-1197.

McCluney, L. (2007) Ozone 1-Hour to 8-Hour Ratios for the 2002-2004
Design Value Period. January 18, 2007. Memo to the Ozone NAAQS Review
Docket.  EPA-HQ-OAR-0172-0073.

McConnell, R.; Berhane, K.; Gilliland, F.; London, S. J.; Islam, T.;
Gauderman, W. J.; Avol, E.; Margolis, H. G.; Peters, J. M. (2002) Asthma
in exercising children exposed to ozone: a cohort study. Lancet 359:
386-391.

McDonnell, W. F.; Kehrl, H.R.; Abdul-Salaam, S.; Ives, P.J.; Folinsbee,
L.J.; Devlin, R.B.; O’Neil, J.J.; Horstman, D. H. (1991) Respiratory
response of humans exposed to low levels of ozone for 6.6 hours.  Arch.
Environ. Health 46:  145-150.

McDonnell, W. F. (1996) Individual variability in human lung function
responses to ozone exposure. Environ. Toxicol. Pharmacol. 2: 171-175.

McDonnell, W. F.; Stewart, P. W.; Andreoni, S.; Seal, E., Jr.; Kehrl, H.
R.; Horstman, D. H.; Folinsbee, L. J.; Smith, M. V. (1997) Prediction of
ozone-induced FEV1 changes: effects of concentration, duration, and
ventilation. Am. J. Respir. Crit. Care Med. 156: 715-722.

McDonnell, W. F.; Abbey, D. E.; Nishino, N.; Lebowitz, M. D. (1999)
Long-term ambient ozone concentration and the incidence of asthma in
nonsmoking adults: the ahsmog study. Environ. Res. 80: 110-121.

McLaughlin, S.B., Nosal, M., Wullschleger, S.D., Sun, G.  (2007a) 
Interactive effects of ozone and climate on tree growth and water use in
a southern Appalachian forest in the USA.  New Phytologist 174:109-124

McLaughlin, S.B., Wullschleger, S.D., Sun, G. and Nosal, M. (2007b) 
Interactive effects of ozone and climate on water use, soil moisture
content and streamflow in a southern Appalachian forest in the USA.  New
Phytologist 174: 125-136.

Michelson, P. H.; Dailey, L.; Devlin, R. B.; Peden, D. B. (1999) Ozone
effects on the immediate-phase response to allergen in the nasal airways
of allergic asthmatic subjects. Otolaryngol. Head Neck Surg. 120:
225-232.

Miller, P. R.; McBride, J. R.; Schilling, S. L.; Gomez, A. P. (1989)
Trend of ozone damage to conifer forests between 1974 and 1988 in the
San Bernardino Mountains of southern California. In: Olson, R. K.;
Lefohn, A. S., eds. Effects of air pollution on western forests [an
A&WMA symposium; June; Anaheim, CA]. Air and Waste Management
Association; pp. 309-323. (APCA transactions series, no. 16).

Moldau, H.; Söber, J.; Söber, A. (1990) Differential sensitivity of
stomata and mesophyll tosudden exposure of bean shoots to ozone.
Photosynthetica 24: 446-458.

Morgan, P. B.; Ainsworth, E. A.; Long, S. P. (2003) How does elevated
ozone impact soybean? A meta-analysis of photosynthesis, growth and
yield. Plant Cell Environ. 26: 1317-1328.

Morgan, P.B., Bernacchi, C.J., Ort, D.R., Long, S.P.  (2004) An in vivo
analysis of the effect of season-long open-air elevation of ozone to
anticipated 2050 levels on photosynthesis in soybean. Plant Physiology
135: 2348-2357. 

Mortimer, K. M.; Neas, L. M.; Dockery, D. W.; Redline, S.; Tager, I. B.
(2002) The effect of air pollution on inner-city children with asthma.
Eur. Respir. J. 19:  699-705.

Mudway, I. S.; Kelly, F. J. (2004) An investigation of inhaled ozone
dose and the magnitude of airway inflammation in healthy adults. Am. J.
Respir. Crit. Care Med. 169: 1089-1095.

Musselman, R.C.; Lefohn, A.S.; Massman, W.J.; Heath, R.L. (2006) A
critical review and analysis of the use of exposure- and flux-based
ozone indices for predicting vegetation effects.  Atmos. Environ..
40:1869-1888.

National Association of Clean Air Agencies (NACAA) (2007) Letter and
Comments Sent to Docket No. OAR-2005-0172 re: Proposed Rule – National
Ambient Air Quality Standards for Ozone.  Docket No. OAR-2005-0172-4274.
 October 9, 2007.

NPS (2005) 2005 Annual Performance & Progress Report: Air Quality in
National Parks. National Park Service.
http://www2.nature.nps.gov/air/Pubs/pdf/gpra/Gpra2005_Report_03202006_Fi
nal.pdf 

National Park Service (NPS) Letter and Comments Sent to Docket No.
OAR-2005-0172 re: Proposed Rule – National Ambient Air Quality
Standards for Ozone.  Docket No. OAR-2005-0172-4934.  September 27, 2007

Navidi, W.; Thomas, D.; Langholz, B.; Stram, D. (1999) Statistical
methods for epidemiologic studies of the health effects of air
pollution. Cambridge, MA: Health Effects Institute; research report no.
86.

Noormets, A.; Sober, A.; Pell, E. J.; Dickson, R. E.; Posila, G. K.;
Sober, J.; Isebrands, J. G.; Karnosky, D. F. (2001) Stomatal and
non-stomatal limitation to photosynthesis in two trembling aspen
(Populus tremuloides Michx) clones exposed to elevated CO2 and/or O3.
Plant Cell Environ. 24: 327-336.

Ollinger, S. V., Aber, J. D., Reich, P. B. and Freuder, R. J. (2002)
Interactive effects of nitrogen deposition, tropospheric ozone, elevated
CO2 and land use history on the carbon dynamics of northern hardwood
forests. Glob. Change Biol. 8(6), 545–562.

Olszyk, D., Bytnerowlez, A., Kats, G., Reagan, C., Hake, S., Kerby, T.,
Millhouse, D., Roberts, B., Anderson, C., Lee, H. (1993) Cotton yield
losses and ambient ozone concentrations in California’s San Joaquin
Valley. Journal of Environmental Quality 22, 602–611.

OMB (2005). Update of Statistical Area Definitions and Guidance on Their
Uses. U.S. Office of Management and Budget, Bulletin No. 05-02. February
22, 2005.

  SEQ CHAPTER \h \r 1 O'Neill, M. S.; Loomis, D.; Borja-Aburto, V. H.
(2004) Ozone, area social conditions, and mortality in Mexico City.
Environ. Res. 94: 234-242.

Pearson, S.; Davison, A. W.; Reiling, K.; Ashenden, T.; Ollerenshaw, J.
H. (1996) The effects of different ozone exposures on three contrasting
populations of Plantago major. New Phytol. 132: 493-502. 

Peden, D. B.; Setzer, R. W., Jr.; Devlin, R. B. (1995) Ozone exposure
has both a priming effect on allergen-induced responses and an intrinsic
inflammatory action in the nasal airways of perennially allergic
asthmatics. Am. J. Respir. Crit. Care Med. 151: 1336-1345.

Peden, D. B.; Boehlecke, B.; Horstman, D.; Devlin, R. (1997) Prolonged
acute exposure to 0.16 ppm ozone induces eosinophilic airway
inflammation in asthmatic subjects with allergies. J. Allergy Clin.
Immunol. 100: 802-808.

Pell, E. J.; Schlagnhaufer, C. D.; Arteca, R. N. (1997) Ozone-induced
oxidative stress: mechanisms of action and reaction. Physiol. Plant.
100: 264-273.

Percy, K. E.; Awmack, C. S.; Lindroth, R. L.; Kubiske, M. E.; Kopper, B.
J.; Isebrands, J. G.; Pregitzer, K. S.; Hendry, G. R.; Dickson, R. E.;
Zak, D. R.; Oksanen, E.; Sober, J.; Harrington, R.; Karnosky, D. F.
(2002) Altered performance of forest pests under atmospheres enriched
with CO2 and O3. Nature (London) 420: 403-407.

Percy, K. E.; Nosal, M.; Heilman, W.; Dann, T; Sober, J.; Legge, A. H.;
Karnosky, D. F. (2007) New exposure-based metric approach for evaluating
O3 risk to North American aspen forests. Environmental Pollution 147:3
554-566.

Peters, J. M.; Avol, E.; Navidi, W.; London, S. J.; Gauderman, W. J.;
Lurmann, F.; Linn, W. S.; Margolis, H.; Rappaport, E.; Gong, H., Jr.;
Thomas, D. C. (1999a) A study of twelve southern California communities
with differing levels and types of air pollution. I. Prevalence of
respiratory morbidity. Am. J. Respir. Crit. Care Med. 159: 760-767.

Peters, J. M.; Avol, E.; Gauderman, W. J.; Linn, W. S.; Navidi, W.;
London, S. J.; Margolis, H.; Rappaport, E.; Vora, H.; Gong, H., Jr.;
Thomas, D. C. (1999b) A study of twelve southern California communities
with differing levels and types of air pollution. II. Effects on
pulmonary function. Am. J. Respir. Crit. Care Med. 159: 768-775.

Peterson, D. L.; Arbaugh, M. J.; Wakefield, V. A.; Miller, P. R. (1987)
Evidence of growth reduction in ozone-injured Jeffrey pine (Pinus
jeffreyi Grev and Balf) in Sequoia and Kings Canyon National Parks.
JAPCA 37: 906-912.

Phillips, R. L.; Zak, D. R.; Holmes, W. E.; White, D. C. (2002)
Microbial community composition and function beneath temperate trees
exposed to elevated atmospheric carbon dioxide and ozone. Oecologia 131:
236-244.

  SEQ CHAPTER \h \r 1 Plopper, C. G.; Fanucchi, M. V. (2000) Do urban
environmental pollutants exacerbate childhood lung diseases? Environ.
Health Perspect. 108: A252-A253.

  SEQ CHAPTER \h \r 1 Plunkett, L. M.; Turnbull, D.; Rodricks, J. V.
(1992) Differences between adults and children affecting exposure
assessment. In: Guzelian, P. S.; Henry, D. J.; Olin, S. S., eds.
Similarities and differences between children and adults: implications
for risk assessment. Washington, DC: ILSI Press, pp. 79-96.

Pope, C. A., III; Thun, M. J.; Namboodiri, M. M.; Dockery, D. W.; Evans,
J. S.; Speizer, F. E.; Heath, C. W., Jr. (1995) Particulate air
pollution as a predictor of mortality in a prospective study of U.S.
adults. Am. J. Respir. Crit. Care Med. 151: 669-674.

Pope, C. A., III; Burnett, R. T.; Thun, M. J.; Calle, E. E.; Krewski,
D.; Ito, K.; Thurston, G. D. (2002) Lung cancer, cardiopulmonary
mortality, and long-term exposure to fine particulate air pollution.
JAMA J. Am. Med. Assoc. 287:  1132-1141.

Prentice IC, Farquhar GD, Fasham MJR, et al. (2001) The Carbon Cycle and
Atmospheric Carbon Dioxide. In Climate Change 2001: The Scientific
Basis.  Contribution of Working Group I to the Third Assessment Report
of the Intergovernmental Panel on Climate Change. (ed J. T. Houghton YD,
D. J. Griggs, M. Noguer, P. J. van der Linder, X. Dai, K. Maskell, and
C. A. Johnson), pp. 241-280. Cambridge University Press, Cambridge,
United Kingdom and New York, NY, USA.

Pronos, J.; Merrill, L.; Dahlsten, D. (1999) Insects and pathogens in a
pollution-stressed forest. In: Miller, P. R.; McBride, J. R., eds.
Oxidant air pollution impacts in the montane forests of southern
California. Springer, pp. 317-337.

Reid, C. D.; Fiscus, E. L. (1998) Effects of elevated [CO2] and/or ozone
on limitations to CO2 assimilation in soybean (Glycine max). J. Exp.
Bot. 49: 885-895.

Reiling, K.; Davison, A. W. (1992a) Effects of a short ozone exposure
given at different stages in the development of Plantago major L. New
Phytol. 121: 643-647. 

Reiling, K.; Davison, A. W. (1992b) The response of native, herbaceous
species to ozone: growth and fluorescence screening. New Phytol. 120:
29-37. 

Retzlaff, W. A.; Arthur, M. A.; Grulke, N. E.; Weinstein, D. A.;
Gollands, B. (2000) Use of a single-tree simulation model to predict
effects of ozone and drought on growth of a white fir tree. Tree
Physiol. 20: 195-202.

Rizzo, M (2005). Evaluation of a quadratic approach for adjusting
distributions of hourly ozone concentrations to meet air quality
standards. November 7, 2005.  Available online at: 
http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_td.html.

Rizzo, M. (2006). A distributional comparison between different rollback
methodologies applied to ambient ozone concentrations. August 23, 2006. 
Available online at:    HYPERLINK
"http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_td.html" 
http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_td.html .

Romieu, I.; Meneses, F.; Ruiz, S.; Sienra, J. J.; Huerta, J.; White, M.
C.; Etzel, R. A. (1996) Effects of air pollution on the respiratory
health of asthmatic children living in Mexico City. Am. J. Respir. Crit.
Care Med. 154: 300-307.

Romieu, I.; Meneses, F.; Ruiz, S.; Huerta, J.; Sienra, J. J.; White, M.;
Etzel, R.; Hernandez, M. (1997) Effects of intermittent ozone exposure
on peak expiratory flow and respiratory symptoms among asthmatic
children in Mexico City. Arch. Environ. Health 52: 368-376.

Romieu, I.; Sienra-Monge, J. J.; Ramírez-Aguilar, M.; Moreno-Macias,
H.; Reyes-Ruiz, N. I.; Estela del Rio-Navarro, B.; Hernández-Avila, M.;
London, S. J. (2004) Genetic polymorphism of GSTM1 and antioxidant
supplementation influence lung function in relation to ozone exposure in
asthmatic children in Mexico City. Thorax 59: 8-10.

Sarnat, J. A.; Schwartz, J.; Catalano, P. J.; Suh, H. H. (2001) Gaseous
pollutants in particulate matter epidemiology: confounders or
surrogates? Environ. Health Perspect. 109: 1053-1061.

Sarnat, J. A.; Brown, K. W.; Schwartz, J.; Coull, B. A.; Koutrakis, P.
(2005) Ambient gas concentrations and personal particulate matter
exposures: implications for studying the health effects of particles.
Epidemiology 16: 385-395.

Sarnat, J. A.; Coull, B. A.; Schwartz, J; Gold, D. R.; Suh, H. H. (2006)
Factors affecting the association between ambient concentrations and
personal exposure to particles and gases.  Environ. Health Perspect.
114(5):649-654.

Sasek, T. W.; Richardson, C. J.; Fendick, E. A.; Bevington, S. R.;
Kress, L. W. (1991) Carryover effects of acid rain and ozone on the
physiology of multiple flushes of loblolly pine seedlings. For. Sci. 37:
1078-1098.

Scannell, C.; Chen, L.; Aris, R. M.; Tager, I.; Christian, D.; Ferrando,
R.; Welch, B.; Kelly, T.; Balmes, J. R. (1996) Greater ozone-induced
inflammatory responses in subjects with asthma. Am. J. Respir. Crit.
Care Med. 154: 24-29.

Schwartz, J. (2005) How sensitive is the association between ozone and
daily deaths to control for temperature? Am. J. Respir. Crit. Care Med.
171: 627-631.

Schildcrout, J. S.; Sheppard, L.; Lumley, T.; Slaughter, J. C.; Koenig,
J. Q.; Shapiro, G. G.  (2006)  Ambient air pollution and asthma
exacerbations in children:  an eight city analysis.  Am. J. Epidemiol.
164(5):505-517.

Schierhorn, K.; Hanf, G.; Fischer, A.; Umland, B.; Olze, H.; Kunkel, G.
(2002) Ozone-induced release of neuropeptides from human nasal mucosa
cells. Int. Arch. Allergy Immunol. 129:  145-151.

Sheppard, L.; Slaughter, J. C.; Schildcrout, J.; Liu, L.-J. S.; Lumley,
T. (2005) Exposure and measurement contributions to estimates of acute
air pollution effects. J. Exposure Anal. Environ. Epidemiol. 15:
366-376.

Simini, M.; Skelly, J. M.; Davis, D. D.; Savage, J. E.; Comrie, A. C.
(1992) Sensitivity of four hardwood species to ambient ozone in north
central Pennsylvania. Can. J. For. Res. 22: 1789-1799.

Sin, D. D.; Man, S. F. P. (2003) Why are patients with chronic
obstructive pulmonary disease at increased risk of cardiovascular
diseases? Circulation 107: 1514-1519.

Sitch, S.; Cox, P. M.; Collins, W. J.; Huntingford, C. (2007) Indirect
radiative forcing of climate change through ozone effects on the
land-carbon sink. Nature (London, U.K.) 448: 791-794.

Smith, W. H. (1992) Air pollution effects on ecosystem processes. In:
Barker, J. R.; Tingey, D. T., eds. Air pollution effects on
biodiversity. Van Nostrand Reinhold; pp. 234-260.

Smith, G., Coulston J., Jepsen, J. and Prichard, T. (2003) “A national
ozone biomonitoring program: Results from field surveys of ozone
sensitive plants in northeastern forest (1994–2000)” Environmental
Monitoring and Assessment 87(3): 271−291.

Somers, G. L.; Chappelka, A. H.; Rosseau, P.; Renfro, J. R. (1998)
Empirical evidence of growth decline related to visible ozone injury.
For. Ecol. Manage. 104: 129-137.

Tager, I. B.; Künzli, N.; Lurmann, F.; Ngo, L.; Segal, M.; Balmes, J.
(1998) Methods development for epidemiologic investigations of the
health effects of prolonged ozone exposure. Part II: an approach to
retrospective estimation of lifetime ozone exposure using a
questionnaire and ambient monitoring data (California sites). Cambridge,
MA: Health Effects Institute; research report no. 81; pp. 27-78.

Takemoto, B. K.; Bytnerowicz, A.; Fenn, M. E. (2001) Current and future
effects of ozone and atmospheric nitrogen deposition on California's
mixed conifer forests. For. Ecol. Manage. 144: 159-173.

Tans P.P., White J.W.C. (1998) In balance, with a little help from the
plants. Science, 281, 183-184.

Taylor, C.R. “AGSIM: Model Description and Documentation.”
Agricultural Sector Models for the United States. C.R. Taylor, K.H.
Reichelderfer, and S.R. Johnson, eds. Ames IA: Iowa State University
Press, (1993).

Taylor R. (1994) “Deterministic versus stochastic evaluation of the
aggregate economic effects of price support programs” Agricultural
Systems 44: 461-473.

Temple, P. J.; Riechers, G. H.; Miller, P. R.; Lennox, R. W. (1993)
Growth responses of ponderosa pine to longterm exposure to ozone, wet
and dry acidic deposition, and drought. Can. J. For. Res. 23: 59-66.

Thurston, G.D.; Ito, K.; Kinney, P.L.; Lippmann, M. (1992) A multi-year
study of air pollution and respiratory hospital admissions in three New
York State metropolitan areas:  results for 1988 and 1989 summers.  J.
Exposure Anal. Environ. Epidemiol. 2:429-450.

Tingey, D. T.; Standley, C.; Field, R. W. (1976) Stress ethylene
evolution: a measure of ozone effects on plants. Atmos. Environ. 10:
969-974.

Tingey, D. T.; Taylor, G. E., Jr. (1982) Variation in plant response to
ozone: a conceptual model of physiological events. In: Unsworth, M. H.;
Ormrod, D. P., eds. Effects of gaseous air pollution in agriculture and
horticulture. London, United Kingdom: Butterworth Scientific; pp.
113-138.

Tingey, D. T.; Laurence, J. A.; Weber, J. A.; Greene, J.; Hogsett, W.
E.; Brown, S.; Lee, E. H. (2001) Elevated CO2 and temperature alter the
response of Pinus ponderosa to ozone: A simulation analysis. Ecol.
Appl.11: 1412-1424.

Tingey, D. T.; Hogsett, W. E.; Lee, E. H.; Laurence, J. A. (2004)
Stricter ozone ambient air quality standard has beneficial effect on
Ponderosa pine in California. Environ. Manage. 34: 397-405.

Touloumi, G.; Katsouyanni, K.; Zmirou, D.; Schwartz, J.; Spix, C.; Ponce
de Leon, A.; Tobias, A.; Quennel, P.; Rabczenko, D.; Bacharova, L.;
Bisanti, L.; Vonk, J. M.; Ponka, A. (1997) Short-term effects of ambient
oxidant exposure on mortality: a combined analysis within the APHEA
project. Am. J. Epidemiol. 146: 177-185.

U.S. Department of Agriculture, 2006.  The PLANTS Database
(http://plants.usda.gov, December 2006).  National Plant Data Center,
Baton Rouge, LA.

Ultman, J. S.; Ben-Jebria, A.; Arnold, S. F. (2004) Uptake distribution
of ozone in human lungs:  intersubject variability in physiologic
response. Boston, MA:  Health Effects Institute.

  SEQ CHAPTER \h \r 1 Vagaggini, B.; Taccola, M.; Clanchetti, S.;
Carnevali, S.; Bartoli, M. L.; Bacci, E.; Dente, F. L.; Di Franco, A.;
Giannini, D.; Paggiaro, P. L. (2002) Ozone exposure increases
eosinophilic airway response induced by previous allergen challenge. Am.
J. Respir. Crit. Care Med. 166: 1073-1077.

Vedal, S.; Brauer, M.; White, R.; Petkau, J. (2003) Air pollution and
daily mortality in a city with low levels of pollution. Environ. Health
Perspect. 111: 45-51.

Vesely, D. L.; Giordano, A. T.; Raska-Emery, P.; Montgomery, M. R.
(1994a) Ozone increases amino- and carboxy-terminal atrial natriuretic
factor prohormone peptides in lung, heart, and circulation. J. Biochem.
Toxicol. 9: 107-112.

Vesely, D. L.; Giordano, A. T.; Raska-Emery, P.; Montgomery, M. R.
(1994b) Increase in atrial natriuretic factor in the lungs, heart, and
circulatory system owing to ozone. Chest 105: 1551-1554.

Vesely, D. L.; Giordano, A. T.; Raska-Emery, P.; Montgomery, M. R.
(1994c) Ozone increases atrial natriuretic peptides in heart, lung and
circulation of aged vs. adult animals. Gerontology (Basel) 40: 227-236.

Weber, J. A.; Clark, C. S.; Hogsett, W. E. (1993) Analysis of the
relationship(s) among O3 uptake, conductance, and photosynthesis in
needles of Pinus ponderosa. Tree Physiol. 13: 157-172.

Weinstein, D.A., Beloin, R.M., R.D. Yanai (1991) “Modeling changes in
red spruce carbon balance and allocation in response to interacting
ozone and nutrient stress.” Tree Physiology 9: 127-146.

Weinstein, D.A., J.A. Laurence, W.A. Retzlaff, J.S. Kern, E.H. Lee, W.E.
Hogsett, J. Weber (2005) Predicting the effects of tropospheric ozone on
regional productivity of ponderosa pine and white fir. Forest Ecology
and Management 205: 73-89.

Whitfield, R.;  Biller, W.; Jusko, M.; and Keisler, J. (1996)  A
Probabilistic Assessment of Health Risks Associated with Short- and
Long-Term Exposure to Tropospheric Ozone.  Argonne National Laboratory,
Argonne, IL.

Whitfield, R. (1997)   SEQ CHAPTER \h \r 1 A Probabilistic Assessment of
Health Risks Associated with Short-term Exposure to Tropospheric Ozone: 
A Supplement.  Argonne National Laboratory, Argonne, IL. 

Whitfield, C. P.; Davison, A. W.; Ashenden, T. W. (1997) Artificial
selection and heritability of ozone resistance in two populations of
Plantago major. New Phytol. 137: 645-655.

Whitfield, R.G.; Richmond, H.M.; and Johnson, T.R. (1998) “Overview of
Ozone Human Exposure and Health Risk Analyses Used in the U.S. EPA’s
Review of the Ozone Air Quality Standard,” pp.483-516 in: T.
Schneider, ed. Air Pollution in the 21st Century: Priority Issues and
Policy Elsevier; Amsterdam.

Wolff, G.T. (1995) Letter from Chairman of Clean Air Scientific Advisory
Committee to the EPA Administrator, dated November 30, 1995.
EPA-SAB-CASAC-LTR-96-002.

Wolff, G.T. (1996) Letter from Chairman of Clean Air Scientific Advisory
Committee to the EPA Administrator, dated April 4, 1996.
EPA-SAB-CASAC-LTR-96-006.

Xu, X.; Ding, H.; Wang, X. (1995) Acute effects of total suspended
particles and sulfur dioxides on preterm delivery: a community-based
cohort study. Arch. Environ. Health 50: 407-415.

Young, T. F.; Sanzone, S., eds. (2002) A framework for assessing and
reporting on ecological condition: an SAB report. Washington, DC: U.S.
Environmental Protection Agency, Science Advisory Board; report no.
EPA-SAB-EPEC-02-009. Available online at:   HYPERLINK
"http://yosemite.epa.gov/sab/sabproduct.nsf/C3F89E598D843B58852570CA0075
717E/$File/epec02009a.pdf" 
http://yosemite.epa.gov/sab/sabproduct.nsf/C3F89E598D843B58852570CA00757
17E/$File/epec02009a.pdf .

Zeger, S. L.; Thomas, D.; Dominici, F.; Samet, J. M.; Schwartz, J.;
Dockery, D.; Cohen, A. (2000) Exposure measurement error in time-series
studies of air pollution: concepts and consequences. Environ. Health
Perspect. 108: 419-426.

Zhang, L.-Y.; Levitt, R. C.; Kleeberger, S. R. (1995) Differential
susceptibility to ozone-induced airways hyperreactivity in inbred
strains of mice. Exp. Lung Res. 21: 503-518.

Zidek, J. V.; White, R.; Le, N. D.; Sun, W.; Burnett, R. T. (1998)
Imputing unmeasured explanatory variables in environmental epidemiology
with application to health impact analysis of air pollution. Environ.
Ecol. Stat. 5: 99-115.

For the reasons set forth in the preamble, part 50 of Chapter 1 of
Title 40 of the code of Federal regulations is proposed to be amended as
follows:

PART 50--NATIONAL PRIMARY AND SECONDARY AMBIENT AIR QUALITY STANDARDS

1. The authority citation for part 50 continues to read as follows:

Authority:   42 U.S.C. 7401 et seq.   ADVANCE \d4 

2. Section 50.15 is revised to read as follows:

( 50.15 National primary and secondary ambient air quality standards for
ozone.

(a) The level of the national 8-hour primary ambient air quality
standard for O3 is (0.060-0.070) parts per million (ppm), daily maximum
8-hour average, measured by a reference method based on Appendix D to
this part and designated in accordance with part 53 of this chapter or
an equivalent method designated in accordance with part 53 of this
chapter.

(b) The 8-hour primary O3 ambient air quality standard is met at an
ambient air quality monitoring site when the average of the annual
fourth-highest daily maximum 8-hour average O3 concentration is less
than or equal to (0.060-0.070) ppm, as determined in accordance with
appendix P to this part.

(c) The level of the national secondary ambient air quality standard for
O3 is a cumulative index value of (7-15) ppm-hours, measured by a
reference method based on Appendix D to this part and designated in
accordance with part 53 of this chapter or an equivalent method
designated in accordance with part 53 of this chapter.

(d) The secondary O3 ambient air quality standard is a seasonal standard
expressed as a sum of weighted hourly concentrations, cumulated over
the12 hour daylight period from 8:00 a.m. to 8:00 p.m. local standard
time, during the consecutive 3-month period within the O3 monitoring
season with the maximum index value.  The secondary O3 standard is met
at an ambient air quality monitoring site when the annual maximum
consecutive 3-month cumulative index value (W126) is less than or equal
to (7-15) ppm-hours, as determined in accordance with appendix P to this
part.

3. Appendix P is revised to read as follows:

Appendix P to Part 50 -- Interpretation of the Primary and Secondary
National Ambient Air Quality Standards for Ozone.

1.  General

(a) This appendix explains the data handling conventions and
computations necessary for determining whether the 8-hour primary and
secondary national ambient air quality standards for ozone specified in
§50.15 are met at an ambient ozone air quality monitoring site.  Ozone
is measured in the ambient air by a reference method based on Appendix D
of this part, as applicable, and designated in accordance with part 53
of this chapter, or by an equivalent method designated in accordance
with part 53 of this chapter.  Data reporting, data handling, and
computation procedures to be used in making comparisons between reported
ozone concentrations and the levels of the ozone standards are specified
in the following sections. 

(b)Whether to exclude, retain, or make adjustments to the data affected
by exceptional events, including stratospheric ozone intrusion and other
natural events, is determined by the requirements under §50.1, §50.14
and §51.930.

(c) The terms used in this appendix are defined as follows: 	

	8-hour average is the rolling average of eight hourly ozone
concentrations as explained in section 3 of this appendix.

	Annual fourth-highest daily maximum refers to the fourth-highest value
measured at a monitoring site during a particular year.

Annual Cumulative W126 Index is the maximum sum over three consecutive
calendar months of the monthly W126 index in a year, as explained in
section 4 of this appendix.

	Daily maximum 8-hour average concentration refers to the maximum
calculated 8-hour average for a particular day as explained in section 3
of this appendix.

	Daily W126 Index is the sum of the sigmoidally weighted hourly ozone
concentrations during the 12-hour daylight period, 8:00 a.m. to 7:59
p.m. local standard time (LST).

Design values are the metrics (i.e., statistics) that are compared to
the primary and secondary NAAQS levels to determine compliance,
calculated as shown in sections 3 and 4 of this appendix.

Monthly W126 Index is the sum of the daily W126 index over one calendar
month during the required ozone monitoring season, adjusted for
incomplete data if appropriate, as explained in section 4 of this
appendix.

	Required ozone monitoring season refers to the span of time within a
calendar year when individual States are required to measure ambient
ozone concentrations as listed in part 58 Appendix D to this chapter.

	Year refers to calendar year.

2.	Requirements for Data Used for Comparisons with the Ozone NAAQS

(a) All valid FRM/FEM ozone data submitted to EPA's Air Quality System
(AQS), or otherwise available to EPA, meeting the requirements of part
58 of this chapter including appendices A, C, and E shall be used in
design value calculations.

(b) When two or more ozone monitors are operated at a site, the state
may in advance designate one of them as the primary monitor. If the
state has not made this designation, the Administrator will make the
designation, either in advance or retrospectively. Design values will be
developed using only the data from the primary monitor, if this results
in a valid design value. If data from the primary monitor do not allow
the development of a valid design value, data solely from the other
monitor(s) will be used in turn to develop a valid design value, if this
results in a valid design value. If there are three or more monitors,
the order for such comparison of the other monitors will be determined
by the Administrator. The Administrator may combine data from different
monitors in different years for the purpose of developing a valid
primary or secondary standard design value, if a valid design value
cannot be developed solely with the data from a single monitor. However,
data from two or more monitors in the same year at the same site will
not be combined in an attempt to meet data completeness requirements,
except if one monitor has physically replaced another instrument
permanently, in which case the two instruments will be considered to be
the same monitor, or if the state has switched the designation of the
primary monitor from one instrument to another during the year. 

(c) Hourly average concentrations shall be reported in parts per million
(ppm) to the third decimal place, with additional digits to the right of
the third decimal place truncated. The start of each hour shall be
identified in local standard time (LST).

3.	Comparison to the Primary Standard for Ozone

(a)  Computing 8-hour averages 

Running 8-hour averages shall be computed from the hourly ozone
concentration data for each hour of the year and shall be stored in the
first, or start, hour of the 8-hour period.  In the event that only 6 or
7 hourly averages are available, the valid 8-hour average shall be
computed on the basis of the hours available, using 6 or 7 as the
divisor. In the event that only 1, 2, 3, 4, or 5 hourly averages are
available, the 8-hour average shall be computed on the basis of
substituting for all the hours without hourly averages a low hourly
average value selected as follows, using 8 as the divisor. For days
within the required ozone monitoring season, the substitution value
shall be the lowest hourly average ozone concentration observed during
the same hour (local standard time) of any day in the required ozone
monitoring season of that year, or one-half of the method detection
limit of the ozone instrument, whichever is higher.  However, if the
number of same-hour concentration values available for the required
ozone monitoring season for the year, from which the lowest observed
hourly concentration would be identified for purposes of this
substitution, is less than 50% of the number of days during the required
ozone monitoring season, one-half the method detection limit of the
ozone instrument shall be used in the substitution. For days outside the
required ozone monitoring season, the substitution value shall be
one-half the method detection limit of the ozone instrument. An 8-hour
period with no available hourly averages does not have a valid 8-hour
average. The computed 8-hour average ozone concentrations are not
rounded or truncated.

(b) Daily maximum 8-hour average concentrations 

There are 24 8-hour periods in each calendar day. Some of these may not
have valid 8-hour averages, under section 3(a). The daily maximum 8-hour
concentration for a given calendar day is the highest of the valid
8-hour average concentrations computed for that day. This process is
repeated, yielding a daily maximum 8-hour average ozone concentration
for each day with ambient ozone monitoring data, including days outside
the required ozone monitoring season if data are available.  The daily
maximum 8-hour concentrations from two consecutive days may have some
hourly concentrations in common. Generally, overlapping daily maximum
8-hour averages are not likely, except in those non-urban monitoring
locations with less pronounced diurnal variation in hourly
concentrations. In these cases, the maximum 8-hour average concentration
from each day is used, even if the two averages have some hours in
common.

(c)  Primary Standard Design Value

The primary standard design value is the annual fourth-highest daily
maximum 8-hour ozone concentration considering all days with monitoring
data including any days outside the required ozone monitoring season,
expressed in parts per million, averaged over three years. The 3-year
average shall be computed using the three most recent, consecutive years
of monitoring data that can yield a valid design value. For a design
value to be valid for comparison to the standard, the monitoring data
set on which it is based must meet the data completeness requirements
described in section 3(d). The computed 3-year average of the annual
fourth-highest daily maximum 8-hour average ozone concentrations shall
be rounded to three decimal places.  Values equal to or greater than
0.xxx5 ppm shall round up.

(d)  Data Completeness Requirements for a Valid Design Value

(i) A design value greater than the standard is valid if in each of the
three years there are at least four days with a daily maximum 8-hour
average concentration. Under sections 3(a) and 3(b), there will be a
daily maximum 8-hour average concentration on any day with at least one
hourly concentration. One or more of these four days may be outside the
required ozone monitoring season.

(ii) A design value less than or equal to the standard is valid if for
at least 75% of the days in the required ozone monitoring season in each
of the three years there are at least 18 8-hour averages in the day that
are based on at least 6 measured hourly average concentrations. 

(iii) When computing whether the minimum data completeness requirement
in section 3(d)(ii) has been met for the purpose of showing that a
design value equal to or less than the standard is valid, meteorological
or ambient data may be sufficient to demonstrate that ozone levels on
days with missing data would not have affected the design value.  At the
request of the state, the Regional Administrator may consider
demonstrations that meteorological conditions on one or more days in the
required ozone monitoring season which do not have at least 18 8-hour
averages in the day that are based on at least 6 measured hourly average
concentrations could not have caused a daily maximum 8-hour
concentration high enough to have been one of the four highest daily
maximum 8-hour concentrations for the year.  At the request of the
state, days so demonstrated may be counted towards the 75% requirement
for the purpose of validating the design value, subject to the approval
of the Regional Administrator. 

(vi) Years that do not meet the completeness criteria stated in 3(d)(ii)
may nevertheless be used to calculate a design value that will be deemed
valid with the approval of, or at the initiative of, the Administrator,
who may consider factors such as monitoring site closures/moves,
monitoring diligence, the consistency and levels of the valid
concentration measurements that are available, and nearby concentrations
in determining whether to use such data.  

(e) Comparison with the Primary Ozone Standard

(i) The primary ozone ambient air quality standard is met at an ambient
air quality monitoring site when the design value is less than or equal
to [0.075] ppm.

 (ii) Comparison with the primary ozone standard is demonstrated by
examples 1 and 2 as follows:

Example 1.	Ambient monitoring site attaining the primary ozone standard.

Year	Percent

Valid Days (Within the Required Monitoring Season)

	1st

Highest 

Daily Max 8-hour Conc.

(ppm)	2nd Highest

Daily Max

8-hour Conc.

(ppm)	3rd Highest

Daily Max

8-hour Conc.

(ppm)	4th Highest

Daily Max

8-hour Conc.

(ppm)	5th Highest

Daily Max

8-hour Conc.

(ppm)

2006	80%	0.092500	0.090375	0.085125	0.078375	0.078125

2007	96%	0.084750	0.083500	0.075375	0.071875	0.070625

2008	98%	0.080875	0.079750	0.077625	0.075500	0.060375

Average

	0.075250

	Rounded

	0.075

	

As shown in Example 1, this monitoring site meets the primary ozone
standard because the 3-year average of the annual fourth-highest daily
maximum 8-hour average ozone concentrations (i.e., 0.075256 ppm, rounded
to 0.075 ppm) is less than or equal to [0.075] ppm.  The data
completeness requirement is also met because no single year has less
than 75% data completeness.  In Example 1, the individual 8-hour
averages and the 3-year average are shown with six decimal digits. In
actual calculations, all digits supported by the calculator or
calculation software must be retained.  

Example 2.  Ambient monitoring site failing to meet the primary ozone
standard.

Year	Percent

Valid Days

(Within the Required Monitoring Season)

	1st

Highest 

Daily Max 8-hour Conc.

(ppm)	2nd Highest

Daily Max

8-hour Conc.

(ppm)	3rd Highest

Daily Max

8-hour Conc.

(ppm)	4th Highest

Daily Max

8-hour Conc.

(ppm)	5th Highest

Daily Max

8-hour Conc.

(ppm)

2006	96%	0.105125	0.103500	0.101125	0.078625	0.072375

2007	74%	0.104250	0.103625	0.093000	0.080250	0.069500

2008	98%	0.103125	0.101875	0.101750	0.075375	0.074625

Average

	0.078083

	Rounded

	0.078

	       

As shown in Example 2, the data capture in 2007 is less than 75%. The
primary ozone standard is not met for this monitoring site because the
3-year average of the fourth-highest daily maximum 8-hour average ozone
concentrations (i.e., 0.078083 ppm, rounded to 0.078 ppm) is greater
than [0.075] ppm and is therefore valid despite this incompleteness. In
Example 2, the individual 8-hour averages and the 3-year average are
shown with six decimal digits. In actual calculations, all digits
supported by the calculator or calculation software must be retained.

4.	Secondary Ambient Air Quality Standard for Ozone

(a)	Computing the daily W126 index value.  

The secondary ozone ambient air quality standard is a seasonal standard
expressed as a sum of weighted hourly concentrations, cumulated over the
12 hour daylight period from 8:00 a.m. to 8:00 p.m. local standard time,
during the consecutive 3-month period within the ozone monitoring season
with the maximum index value. The first step in determining whether the
standard is met at a monitoring site is to compute the daily W126 index
value for each day by applying the sigmoidal weighting function in
Equation 1 to each reported measurement of hourly average concentration.

Equation 1

 

 .

The computed value of the sigmoidally weighted hourly concentration is
not rounded or truncated.  The daily W126 index is formed by summing the
twelve computed hourly values, retaining all decimal places.  An
illustration of computing a daily W126 index value is below: 

Example 3.	Daily W126 index value calculation for an ambient ozone
monitoring site.

Start of hour	Concentration (ppm)	Weighted Concentration (ppm)

8:00 a.m.	0.045	0.002781

9:00 a.m.	0.060	0.018218

10:00 a.m.	0.075	0.055701

11:00 a.m.	0.080	0.067537

12:00 p.m.	0.079	0.065327

1:00 p.m.	0.082	0.071715

2:00 p.m.	0.085	0.077394

3:00 p.m.	0.088	0.082448

4:00 p.m.	0.083	0.073683

5:00 p.m.	0.081	0.069667

6:00 p.m.	0.065	0.029260

7:00 p.m.	0.056	0.011676

Sum=Daily W126  index value 

0.625406 ppm-hours

In Example 3, the individual weighted concentrations and their sum are
shown with six decimal digits. In actual calculations, all digits
supported by the calculator or calculation software must be retained.
There are no data completeness requirements for the daily index.  If
fewer than 12 hourly values are available, only the available hours are
weighted and summed. However, there are data completeness requirements
for the monthly W126 index values and a required adjustment for
incomplete data, as describe in the next section. 

(b) Computing the Monthly W126 Index

As described in section 4(a), the daily index value is computed at each
monitoring site for each calendar day in each month during the required
ozone monitoring season with no rounding or truncation.  The monthly
W126 index is the sum of the daily index values over one calendar month.
 At an individual monitoring site, a monthly W126 index is valid if
hourly average ozone concentrations are available for at least 75% of
the possible daylight hours in the month.  For months with more than 75%
but less than 100% data completeness, the monthly W126 value shall be
adjusted for incomplete data by multiplying the unadjusted monthly W126
index value by the ratio of the number of possible reporting hours to
the number of hours with reported ambient hourly concentrations using
Equation 2 in this appendix:

Equation 2

 

where,

	M.I.	=	the adjusted monthly W126 index, 

	D.I.	=	daily W126 index (i.e., the daily sum of the sigmoidally
weighted daylight hourly concentrations),

	n	=	the number of days in the calendar month,

	v	=	the number of daylight reporting hours (8:00 a.m. – 7:59 p.m.
LST) in the month with reported valid hourly ozone concentrations.

The resulting adjusted value of the monthly W126 index shall not be
rounded or truncated.

(b)	Secondary Standard Design Value

	The secondary standard design value is the 3-year average of the annual
maximum consecutive 3-month sum of adjusted monthly W126 index values
expressed in ppm-hours.   Specifically, the annual W126 index value is
computed on a calendar year basis using the three highest, consecutive
adjusted monthly W126 index values.   The 3-year average shall be
computed using the most recent, consecutive three calendar years of
monitoring data meeting the data completeness requirements described in
section 4(c).  The computed 3-year average of the annual maximum
consecutive 3-month sum of adjusted monthly W126 index values in
ppm-hours shall be rounded to a whole number with decimal values equal
to or greater than 0.500 rounding up. 

(c) Data Completeness Requirement

(i) The annual W126 index is valid for purposes of calculating a 3-year
design value if each full calendar month in the required ozone
monitoring season has at least 75% data completeness for daylight hours.

(ii) If one or more months during the ozone monitoring seasons of three
successive years has less than 75% data completeness, the three years
shall nevertheless be used in the computation of a valid design value
for the site if substituting the lowest hourly ozone concentration
observed during daylight hours in the required ozone monitoring season
of each year, or one-half of the method detection limit of the ozone
instrument, whichever is higher, for enough of the missing hourly
concentrations within each incomplete month to make the month 75%
complete, and then adjusting for the remaining missing data using
Equation 2, above results in a design value greater than the level of
the standard. 

 (d)	Comparisons with the Secondary Ozone Standard

(i) The secondary ambient ozone air quality standard is met at an
ambient air quality monitoring site when the design value is less than
or equal to [15] ppm-hours.

(ii) Comparison with the secondary ozone standard is demonstrated by
example 4 as follows:

Example 4.	Ambient Monitoring Site Failing to Meet the Secondary Ozone
Standard

	April	May	June	July	August	September	October	Overall

2006

Adjusted monthly W126 index	4.442	9.124	12.983	16.153	13.555	4.364	1.302

	3-Month sum	na	na	26.549	38.260	42.691	34.072	19.221

	2006 Maximum

	42.691

	42.691

2007

Adjusted monthly W126 index	3.114	7.214	8.214	8.111	7.455	7.331	5.115

	3-Month sum	na	na	18.542	23.539	23.780	22.897	19.901

	2007 Maximum

	23.780

	23.780

2008

Adjusted monthly W126 index	4.574	5.978	6.786	8.214	5.579	4.331	2.115

	3-Month sum	na	na	17.338	20.978	20.579	18.124	12.025

	2008 Maximum

20.978

20.978

3-Year average W126 index

29.149666

Rounded

29

As shown in example 4, the secondary ozone standard is not met for this
monitoring site because the 3-year average of the annual W126 index
value for this site is greater than [15] ppm-hours:

3-year average W126 index = (42.691+ 23.780+ 20.978)/3 = 29.149666,
which rounds to 29 ppm-hours.

In Example 4, the adjusted monthly W126 index values and the 3-month
sums of the adjusted monthly W126 index values are shown with three
decimal digits.  In actual calculations, all digits supported by the
calculator or calculation software must be retained.

4. Section 50.14 is amended by adding entries for "Primary and Secondary
Ozone Standards” to the end of the table in paragraph (c)(2)(vi) to
read as follows:

§ 50.14 Treatment of air quality monitoring data influenced by
exceptional events.

* * * * *

(c) ***

(2) ***

(vi) ***

Table 1.  Schedule for Exceptional Event Flagging and Documentation
Submission for Data to be Used in Designations Decisions for New NAAQS

NAAQS Pollutant/

Standard/(Level)/

Promulgation Date	Air Quality Data Collected for Calendar Year	Event
Flagging & Initial Description Deadline	Detailed Documentation
Submission Deadline

*******

	Primary Ozone/8-Hr Standard (Level TBD) Promulgated by August 31, 2010
2007-2009	November 1, 2010b	November 1, 2010b

	2010	60 Days after the end of the calendar quarter in which the event
occurred or March 1, 2011, whichever date occurs firstb	60 Days after
the end of the calendar quarter in which the event occurred or March 1,
2011, whichever date occurs firstb

Secondary Ozone/ (Level TBD)Alternative 2-year Schedule- to be
Promulgated by August 31, 2010 	2008	July 1, 2011b	July 1, 2011a

	2009-2010	July 1, 2011b	July 1, 2011b

	2011	60 Days after the end of the calendar quarter in which the event
occurred or March 1, 2012, whichever occurs firstb	60 Days after the end
of the calendar quarter in which the event occurred or March 1, 2012,
whichever occurs firstb

Secondary Ozone/ (Level TBD)- Alternative Accelerated Schedule -to be
Promulgated by August 31, 2010	2007-2009	November 1, 2010b	November 1,
2010b

	2010	60 Days after the end of the calendar quarter in which the event
occurred or March 1, 2011, whichever date occurs firstb	60 Days after
the end of the calendar quarter in which the event occurred or March 1,
2011, whichever date occurs firstb

a These dates are unchanged from those published in the original
rulemaking.

b Indicates change from general schedule in 40 CFR 50.14.

Note:  EPA notes that the table of revised deadlines only applies to
data EPA will use to establish the final initial designations for new
NAAQS.  The general schedule applies for all other purposes, most
notably, for data used by EPA for redesignations to attainment.

	

 *****

5. Section 58.50 (c) is revised and (d) is added to read as follows:

§ 58.50  Index reporting.

 (c) The population of a metropolitan statistical area for purposes of
index reporting is the latest available U.S. census population.

(d) For O3, reporting is required in metropolitan and micropolitan
statistical areas wherever monitoring is required under Appendix D to
Part 58—SLAMS Minimum O3 Monitoring Requirements.

6.  Appendix G of Part 58 (3) is revised to read as follows:

Appendix G to Part 58—Uniform Air Quality Index (AQI) and Daily
Reporting 

3. Must I Report the AQI?

You must report the AQI daily if yours is a metropolitan statistical
area (MSA) with a population over 350,000.  For O3, reporting is
required in metropolitan and micropolitan statistical areas wherever
monitoring is required under Appendix D to Part 58—SLAMS Minimum O3
Monitoring Requirements.

 The legislative history of section 109 indicates that a primary
standard is to be set at “the maximum permissible ambient air level .
. . which will protect the health of any [sensitive] group of the
population,” and that for this purpose “reference should be made to
a representative sample of persons comprising the sensitive group rather
than to a single person in such a group” [S. Rep. No. 91-1196, 91st
Cong., 2d Sess. 10 (1970)].

 Welfare effects as defined in section 302(h) (42 U.S.C. 7602(h))
include, but are not limited to, “effects on soils, water, crops,
vegetation, man-made materials, animals, wildlife, weather, visibility,
and climate, damage to and deterioration of property, and hazards to
transportation, as well as effects on economic values and on personal
comfort and well-being.”

  See EPA report, Evaluating Ozone Control Programs in the Eastern
United States: Focus on the NOx Budget Trading Program, 2004.

 American Lung Association v. Whitman (No. 1:03CV00778, D.D.C. 2003).

 The level of the 8-hour primary ozone standard was set at 0.075 ppm,
while CASAC unanimously recommended a range between 0.060 and 0.070 ppm.
 

 The Administrator also noted the exchange that had occurred between EPA
and the Office of Management and Budget (OMB) with regard to the final
decision on the secondary standard, as discussed in the 2008 final rule
(73 FR 16497).

 The EPA also separately announced that it will move quickly to
implement any new standards that might result from this reconsideration.
 To reduce the workload for states during the interim period of
reconsideration, the Agency intends to propose to defer compliance with
the CAA requirement to designate areas as attainment or nonattainment. 
EPA will work with states, local governments and tribes to ensure that
air quality is protected during that time.

 The use of O3 as the indicator for photochemical oxidants was adopted
in the 1979 final rule and retained in subsequent rulemaking.  An 8-hour
averaging time and a form based on the annual fourth-highest daily
maximum 8-hour concentration, averaged over 3 years, were adopted in the
1997 final rule and retained in the 2008 rulemaking. 

 In its assessment of the epidemiological evidence judged to be most
relevant to making decisions on the level of the O3 primary standard,
EPA has placed greater weight on U.S. and Canadian epidemiologic
studies, since studies conducted in other countries may well reflect
different demographic and air pollution characteristics.

 The exposure assessment done as part of the 2008 final rulemaking
considered several air quality scenarios, including just meeting what
was then the current standard set at a level of 0.084 ppm, as well as
just meeting alternative standards at levels of 0.080, 0.074, 0.070, and
0.064 ppm.

 Exposures of concern were also considered in the 1997 review of the O3
NAAQS, and were judged by EPA to be an important indicator of the public
health impacts of those O3-related effects for which information was too
limited to develop quantitative estimates of risk but which had been
observed in humans at and above the benchmark level of 0.08 ppm for 6-
to 8-hour exposures . . . including increased nonspecific bronchial
responsiveness (for example, aggravation of asthma), decreased pulmonary
defense mechanisms (suggestive of increased susceptibility to
respiratory infection), and indicators of pulmonary inflammation
(related to potential aggravation of chronic bronchitis or long-term
damage to the lungs).  (62 FR 38868)

 While most of the available evidence addresses mechanisms for O3, O3
clearly serves as an indicator for the total photochemical oxidant
mixture found in the ambient air.  Some effects may be caused by one or
more components in the overall pollutant mix, either separately or in
combination with O3.  However, O3 clearly dominates these other oxidants
with their concentrations only being a few percent of the O3
concentration.

 In previous Staff Papers and Federal Register notices announcing
proposed and final decisions on the O3 and other NAAQS, EPA has used the
phrase “sensitive population groups” to include both population
groups that are at increased risk because they are more intrinsically
susceptible and population groups that are more vulnerable due to an
increased potential for exposure.  In this notice, we use the phrase,
“at risk” populations to include both types of population groups.

 Health effects discussions are also drawn from the more detailed
information and tables presented in the Criteria Document’s annexes.

 This study and other studies (Folinsbee et al., 1988; Horstman et al,
1990; and McDonnell et al., 1991), conducted in EPA’s human studies
research facility in Chapel Hill, NC, measured ozone concentrations to
within +/- 5 percent or +/- 0.004 ppm at the 0.080 ppm exposure level.

 These studies, conducted at a facility at the University of California,
in Davis, CA, reported O3 concentrations to be accurate within +/- 0.003
ppm over the range of concentrations included in these studies.

 These distributional results presented in the Criteria Document and
Staff Paper for the Adams (2006) study are based on data for squate-wave
exposures to 0.080 ppm that were not included in the publication but
were obtained from the author.

 Dr. Adams submitted comments on EPA’s reanalysis in which he
concluded that the FEV1 response in healthy young adults at the 0.060
ppm exposure level in his study (Adams, 2006a) does not demonstrate a
significant mean effect by ordinarily acceptable statistical analysis,
but is rather in somewhat of a gray area, both in terms of a
biologically meaningful response and a statistically significant
response (Adams, 2007).    The EPA responded to these comments in the
2008 final rule (73 FR 16455) and in the Response to Comments (EPA,
2008, pp. 26-28).

 Graham and Koren (1990) compared inflammatory mediators present in NL
and BAL fluids of humans exposed to 0.4 ppm O3 for 2 hours and found
similar increases in PMNs in both fluids, suggesting a qualitative
correlation between inflammatory changes in the lower airways (BAL) and
upper respiratory tract (NL).

 Discussion of the reasons for focusing on warm season studies is found
in the section 2.A.3.a below.

 In commenting on the Criteria Document, the CASAC Ozone Panel raised
questions about the implications of these time-series results in a
policy context, emphasizing that “…while the time-series study
design is a powerful tool to detect very small effects that could not be
detected using other designs, it is also a blunt tool” (Henderson,
2006b).  They note that “. . .not only is the interpretation of these
associations complicated by the fact that the day-to-day variation in
concentrations of these pollutants is, to a varying degree, determined
by meteorology, the pollutants are often part of a large and highly
correlated mix of pollutants, only a very few of which are measured”
(Henderson, 2006b).  Even with these uncertainties, the CASAC Ozone
Panel, in its review of the Staff Paper, found “…premature total
non-accidental and cardiorespiratory mortality for inclusion in the
quantitative risk assessment to be appropriate.” (Henderson, 2006b)

 This reanalysis report and the original prospective cohort study
findings are discussed in more detail in section 8.2.3 of the Air
Quality Criteria for Particulate Matter (EPA, 2004).

 Results for studies of respiratory symptoms are presented as odds
ratios; an odds ratio of 1.0 is equivalent to no effect, and thus is
presented as equivalent to the zero effect estimate line.

 In the Staff Paper and documents from previous O3 NAAQS reviews,
"at-risk" groups have also been called "sensitive" groups, to mean both
groups with greater inherent susceptibility and those more likely to be
exposed.

 Similar to animal toxicology studies referred above, a polymorphism in
a specific proinflammatory cytokine gene has been implicated in
O3-induced lung function changes in healthy, mild asthmatics and
individuals with rhinitis.  These observations suggest a potential role
for these markers in the innate susceptibility to O3, however, the
validity of these markers and their relevance in the context of
prediction to population studies requires additional research.

 In 2000, the American Thoracic Society (ATS) published an official
statement on “What Constitutes an Adverse Health Effect of Air
Pollution?” (ATS, 2000), which updated its earlier guidance (ATS,
1985). Overall, the new guidance does not fundamentally change the
approach previously taken to define adversity, nor does it suggest a
need at this time to change the structure or content of the tables
describing gradation of severity and adversity of effects described
below.

 Modeling that projects whether and how areas might attain alternative
standards in a future year is presented in the Regulatory Impact
Analysis being prepared in connection with this rulemaking.

 EPA made available corrected versions of the final 2007 Staff Paper,
and human exposure and health risk assessment technical support
documents in July 2007 on the EPA web site listed in the Availability of
Related Information section of this notice.

 The 12 CSAs modeled are:  Atlanta-Sandy Springs-Gainesville, GA-AL; 
Boston-Worcester-Manchester, MA-NH;  Chicago-Naperville-Michigan City,
IL-IN-WI;  Cleveland-Akron-Elyria, OH;  Detroit-Warren-Flint, MI; 
Houston-Baytown-Huntsville, TX;  Los Angeles-Long Beach-Riverside, CA; 
New York-Newark-Bridgeport, NY-NJ-CT-PA;  Philadelphia-Camden-Vineland,
PA-NJ-DE-MD;  Sacramento--Arden-Arcade--Truckee, CA-NV;  St. Louis-St.
Charles-Farmington, MO-IL;  Washington-Baltimore-N. Virginia,
DC-MD-VA-WV

 All 12 of the CSAs modeled did not meet the 0.084 ppm O3 NAAQS for the
three year period examined.

 The general approach used in the human exposure assessment was
described in the draft Health Assessment Plan (EPA, 2005d) that was
released to the CASAC and general public in April 2005 and was the
subject of a consultation with the CASAC O3 Panel on May 5, 2005.  In
October 2005, OAQPS released the first draft of the Staff Paper
containing a chapter discussing the exposure analyses and first draft of
the Exposure Analyses TSD for CASAC consultation and public review on
December 8, 2005.  In July 2006, OAQPS released the second draft of the
Staff Paper and second draft of the Exposure Analyses TSD for CASAC
review and public comment which was held by the CASAC O3 Panel on August
24-25, 2006.  

 The 8-hour O3 standard established in 1997 was 0.08 ppm, but the
rounding convention specified that the average of the 4th daily maximum
8-hour average concentrations over a three-year period must be at 0.084
ppm or lower to be in attainment of this standard.  When EPA staff
selected alternative standards to analyze, it was presumed that the same
type of rounding convention would be used, and thus alternative
standards of 0.084, 0.074, 0.064 ppm were chosen.   

 A design value is a statistic that describes the air quality status of
a given area relative to the level of the NAAQS.  Design values are
often based on multiple years of data, consistent with specification of
the NAAQS in Part 50 of the CFR.  For the 8-hour O3 NAAQS, the 3-year
average of the annual 4th-highest daily maximum 8-hour average
concentrations, based on the monitor within (or downwind of) an urban
area yielding the highest 3-year average, is the design value.

 The quadratic rollback approach and evaluation of this approach are
described by Johnson (1997), Duff et al. (1998) and Rizzo (2005, 2006).

 As discussed above in Section II.A, O3 health responses observed in
controlled human exposure studies are associated with exposures while
engaged in moderate or greater exertion and, therefore, these are the
exposure measures of interest.  The level of exertion of individuals
engaged in particular activities is measured by an equivalent
ventilation rate (EVR), ventilation normalized by body surface area
(BSA, in m2), which is calculated as VE/BSA, where VE is the ventilation
rate (liters/minute). Moderate and greater exertion levels were defined
as EVR > 13 liters/min-m2 (Whitfield et al., 1996) to correspond to the
exertion levels measured in most subjects studied in the controlled
human exposure studies that reported health effects associated with 6.6
hour O3 exposures.

	 The full range of quantitative exposure estimates associated with just
meeting the 0.084 ppm and alternative O3 standards are presented in
chapter 4 and Appendix 4A of the 2007 Staff Paper.

 The methodology, scope, and results from the risk assessment conducted
in the last review are described in Chapter 6 of the 1996 Staff Paper
(EPA, 1996) and in several technical reports (Whitfield et al., 1996;
Whitfield, 1997) and publication (Whitfield et al., 1998).  

 The 9 urban study areas included in the exposure and risk analyses
conducted during the last review were: Chicago, Denver, Houston, Los
Angeles, Miami, New York City, Philadelphia, St. Louis, and Washington,
D.C.

 The general approach used in the health risk assessment was described
in the draft Health Assessment Plan (EPA, 2005d) that was released to
the CASAC and general public in April 2005 and was the subject of a
consultation with the CASAC O3 Panel on May 5, 2005.  In October 2005,
OAQPS released the first draft of the Staff Paper containing a chapter
discussing the risk assessment and first draft of the Risk Assessment
TSD for CASAC consultation and public review on December 8, 2005.  In
July 2006, OAQPS released the second draft of the Staff Paper and second
draft of the Risk Assessment TSD for CASAC review and public comment
which was held by the CASAC O3 Panel on August 24-25, 2006.  

 The 12 urban areas are the same urban areas evaluated in the exposure
analysis discussed in the prior section.  However, for most of the
health endpoints based on findings from epidemiological studies, the
geographic areas and populations examined in the health risk assessment
were limited to those counties included in the original epidemiological
studies that served as the basis for the concentration-response
relationships.

 EPA notes that the estimated level of policy-relevant background O3
used in the prior risk assessment was a single concentration of 0.04
ppm, which was the midpoint of the range of levels for policy-relevant
background that was provided in the 1996 Criteria Document. 

 As discussed above in section II.B.1, the urban areas were defined
using the consolidated statistical areas definition and the total
population residing in the 12 urban areas was approximately 88.5 million
people.

 For 9 of the 12 urban areas, the O3 season is defined as a period
running from March or April to September or October.  In 3 of the urban
areas (Houston, Los Angeles, and Sacramento), the O3 season is defined
as the entire year.

 The geographic boundaries for the urban areas included in this portion
of the risk assessment were generally matched to the geographic
boundaries used in the epidemiological studies that served as the basis
for the concentration-response functions.  In most cases, the urban
areas were defined as either a single county or a few counties for this
portion of the risk assessment.

 Due to time constraints, lung function risk estimates for asthmatic
school age children were developed for only 5 of the 12 urban areas, and
the areas were selected to represent different geographic regions.  The
5 areas were: Atlanta, Chicago, Houston, Los Angeles, and New York City.

 For example, assuming lower background levels resulted in increased
estimates of non-accidental mortality incidence per 100,000 that were
often 50 to 100 percent greater than the base case estimates; assuming
higher background levels resulted in decreased estimates of
non-accidental mortality incidence per 100,000 that were less than the
base case estimates by 50 percent or more in many of the areas. 

 Bell et al. (2006) referred to this level as being approximately
equivalent to 120 µg/m3, daily 8-hour maximum, the World Health
Organization guideline and European Commission target value for O3.

 As described in the 2007 Staff Paper (section 4.5.8) and discussed
above in section II.B, recent O3 air quality distributions have been
statistically adjusted to simulate just meeting the then current 0.084
ppm standard and selected alternative standards.  These simulations do
not represent predictions of when, whether, or how areas might meet the
specified standards.  Modeling that projects whether and how areas might
attain alternative standards in a future year is presented in the
Regulatory Impact Analysis being prepared in connection with this
rulemaking.

 The abbreviated notation used to identify the then current 0.084 ppm
standard and alternative standards in this section and in the risk
assessment section of the Staff Paper is in terms of ppm and the nth
highest daily maximum 8-hour average.  For example, the 8-hour standard
established in 1997 is identified as “0.084/4.”

 As discussed above at the beginning of section II, the Administrator
has focused her reconsideration of the primary O3 standard set in the
2008 final rule on the level of the standard, having decided not to
reopen the 2008 final rule with regard to the need to revise the 1997
primary O3 standard to provide increased public health protection nor
with regard to the indicator, averaging period, and form of the 2008
standard.

 The EPA responded to these comments in the 2008 final rule (73 FR
16454-5).

 As noted in section II.C.1.b.above, the Administrator focused on
alternative standards with different levels but the same form and
averaging time as the primary standard set in 2008.

 In its assessment of the evidence judged to be most relevant to making
decisions on the level of the O3 secondary standard, however, EPA has
placed greater weight on U.S. studies, due to the often species-, site-
and climate-specific nature of O3-related vegetation response.

 The SUM06 index is defined as the sum of all hourly O3 concentrations
greater or equal to 0.06 ppm over a specified time.

 The CMAQ model is a multi-pollutant, multiscale air quality model that
contains state-of-the-science techniques for simulating atmospheric and
land processes that affect the transport, transformation, and deposition
of atmospheric pollutants and/or their precursors on both regional and
urban scales.  It is designed as a science-based modeling tool for
handling many major pollutants (including photochemical oxidants/O3,
particulate matter, and nutrient deposition) holistically.  The CMAQ
model can generate estimates of hourly O3 concentrations for the
contiguous U.S., making it possible to express model outputs in terms of
a variety of exposure indices (e.g., W126, 8-hour average).

 This analysis was updated using 2003-2005 air quality as it became
available, finding similar results.

	 Principal crops as defined by the USDA include corn, sorghum, oats,
barley, winter wheat, rye, Durum wheat, other spring wheat, rice,
soybeans, peanuts, sunflower, cotton, dry edible beans, potatoes, sugar
beets, canola, proso millet, hay, tobacco, and sugarcane.  Acreage data
for the principal crops were taken from the USDA NASS 2005 Acreage
Report (  HYPERLINK
"http://usda.mannlib.cornell.edu/reports/nassr/field/pcp-bba/acrg0605.pd
f" 
http://usda.mannlib.cornell.edu/reports/nassr/field/pcp-bba/acrg0605.pdf
). 

 While the term “averaging time” is used, for the cumulative,
seasonal standard the seasonal and diurnal time periods at issue are
those over which exposures during a specified period of time are
cumulated, not averaged.

 Prior to publication of the 2008 final rule, EPA did further analysis
of the degree of overlap to extend the 2007 Staff Paper analyses, and
that analysis was available in the docket.

 The AOT40 index used in Europe is a cumulative index that incorporates
a threshold at 0.04 ppm (40 ppb).  This index is calculated as the area
over the threshold (AOT) by subtracting 40 ppb from the value of each
hourly concentration above that threshold and then cumulating each
hourly difference over a specified window.

 While the term “averaging time” is used, for the cumulative,
seasonal standard the seasonal and diurnal time periods at issue are
those over which exposures during a specified period of time are
cumulated, not averaged.

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shall be administered for the use and enjoyment of the American people
in such manner as will leave them unimpaired for future use as
wilderness, and so as to provide for the protection of these areas, the
preservation of their wilderness character” (The Wilderness Act,
1964).  

 Because only enough missing 1-hour ozone values would be substituted as
needed to meet the 75 percent completeness requirement, to avoid
unreasonable underestimation of the true W126 index, tying the the
selection of the substitution value to the hour of the missing value, as
is proposed for data substitution for the purpose of the primary
standard (see section V.D), would introduce considerable complexity  by
requiring an algorithm for determining which specific missing values
would be substituted. Therfore, EPA is proposing this simpler
substitution approach for the secondary standard.

 At present, EPA’s Air Quality System (AQS) for storing and reporting
air quality data provides a completeness report that is based on yet a
third approach, in which the period for reporting data completeness is
the required monitoring season plus any extension needed to encompass
any exceedances that may have occurred outside the required season.
However, EPA’s practice for regulatory purposes has been to consider
completeness only over the required ozone monitoring season.

 Actually, it is an interpretation of the text of Appendix P, section
2.1, that the average resulting from the data substitution is to be
taken as the “8-hour” average, rather than the average of the
available 5 or fewer hours of data, which would be higher.  The text is
not entirely clear on this point.

 EPA also is proposing eliminate this 90 percent requirement, see
section V.E. The point made in this paragraph applies with or without
the 90 percent requirement in place.

 EPA notes that in the current versions of Appendix I and P, it is not
explicit that this provided exception also applies in the case of three
years which each have 75 percent or more of days with valid data but
less than 90 percent across three years. Because EPA is proposing to
remove the 90 percent requirement (see section V.E) this ambiguity does
not need correction.

 Appendix P now provides that in the event that only 6 or 7 hourly
averages are available, the valid 8-hour average shall be computed on
the basis of the hours available, using 6 or 7 as the divisor.  We are
not proposing to change this provision.

 The requirement that there be at least four days with at least one
hourly measurement is actually redundant and is stated only for ease of
understanding, since there would be no annual fourth-highest daily
maximum 8-hour concentration unless there are at least four days with
monitoring data, and a single hourly data point is necessary and
sufficient (with the proposed substitution step) to generate a daily
maximum 8-hour concentration.

 EPA has recently proposed to amend the completeness requirements for
sulfur dioxide and nitrogen dioxide to add quarterly 75 percent
completeness requirements in connection with proposals to establish
1-hour primary NAAQS for these pollutants, still with no requirement for
90 percent completeness across three years.

 The requirements specified in Table D-2 of Appendix D to part 58, as
noted in the third footnote of Table D-2, are applicable to the levels
of the O3 NAAQS as defined in 40 CFR part 50.  Accordingly, the 85
percent threshold for requiring higher minimum monitoring requirements
within MSAs would apply to the proposed levels for the cumulative,
seasonal secondary standard as well as to the proposed levels of the
8-hour primary standard.

 These MSAs are not currently required to monitor for O3.

 Defined as areas having at least one urban cluster of at least 10,000
but less than a population of 50,000.

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