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<EMAIL_ADDRESS><EMAIL_ADDRESS>.

Fax:<PHONE_NUMBER>.

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:<PHONE_NUMBER>

Houston, Texas – February 2, 2010

Hilton Houston Hobby Airport

Moody Ballroom (located on the ground floor)

8181 Airport Boulevard

Houston, Texas  77061

Telephone:<PHONE_NUMBER>

Sacramento, California – February 4, 2010

Four Points by Sheraton Sacramento International Airport

Natomas Ballroom

4900 Duckhorn Drive

Sacramento, California  95834

Telephone:<PHONE_NUMBER>

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<PHONE_NUMBER> and the telephone number for the Air and
Radiation Docket and Information Center is<PHONE_NUMBER>.

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:<PHONE_NUMBER>; fax:
919-541-0237; email:    HYPERLINK<EMAIL_ADDRESS><EMAIL_ADDRESS>.

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<EMAIL_ADDRESS><EMAIL_ADDRESS>).
Ms. Crabtree may be reached by telephone at<PHONE_NUMBER>.  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 <IP_ADDRESS>) 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 <IP_ADDRESS>), 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 <IP_ADDRESS>.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 <IP_ADDRESS> 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 <IP_ADDRESS>.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 <IP_ADDRESS>.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 <IP_ADDRESS>.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