Wednesday, 

July 11, 2007 

Part II 

Environmental 

Protection Agency 

40 CFR Part 50 

National Ambient Air Quality Standards 

for Ozone; Proposed Rule 


pwalker on PROD1PC71 with PROPOSALS2
37818 Federal Register / Vol. 72, No. 132 / Wednesday, July 11, 2007 / Proposed Rules 

ENVIRONMENTAL PROTECTION 

AGENCY 

40 CFR Part 50 

[EPA–HQ–OAR–2005–0172; FRL–8331–5] 

RIN 2060–AN24 

National Ambient Air Quality 

Standards for Ozone 

AGENCY: Environmental Protection 

Agency (EPA). 

ACTION: Proposed rule. 

SUMMARY: Based on its review of the air 

quality criteria for ozone (O3) and 

related photochemical oxidants and 

national ambient air quality standards 

(NAAQS) for O3, EPA proposes to make 

revisions to the primary and secondary 

NAAQS for O3 to provide requisite 

protection of public health and welfare, 

respectively, and to make corresponding 

revisions in data handling conventions 

for O3. 

With regard to the primary standard 

for O3, EPA proposes to revise the level 

of the 8-hour standard to a level within 

the range of 0.070 to 0.075 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 nonaccidental 

and cardiopulmonary mortality. The 

EPA also proposes to specify the level 

of the primary standard to the nearest 

thousandth ppm. The EPA solicits 

comment on alternative levels down to 

0.060 ppm and up to and including 

retaining the current 8-hour standard of 

0.08 ppm (effectively 0.084 ppm using 

current data rounding conventions). 

With regard to the secondary standard 

for O3, EPA proposes to revise the 

current 8-hour standard with one of two 

options to provide increased protection 

against O3-related adverse impacts on 

vegetation and forested ecosystems. One 

option is to replace the current standard 

with a cumulative, seasonal standard 

expressed as an index of the annual sum 

of weighted hourly concentrations, 

cumulated over 12 hours per day (8 a.m. 

to 8:00 p.m.) 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 21 ppm-hours. 

The other option is to make the 

secondary standard identical to the 

proposed primary 8-hour standard. The 

EPA solicits comment on specifying a 

cumulative, seasonal standard in terms 

of a 3-year average of the annual sums 

of weighted hourly concentrations; on 

the range of alternative 8-hour standard 

levels for which comment is being 

solicited for the primary standard, 

including retaining the current 

secondary standard, which is identical 

to the current primary standard; and on 

an alternative approach to setting a 

cumulative, seasonal secondary 

standard(s). 

DATES: Written comments on this 

proposed rule must be received by 

October 9, 2007. 

ADDRESSES: Submit your comments, 

identified by Docket ID No. EPA–HQ– 

OAR–2005–0172, by one of the 

following methods: 

• www.regulations.gov: Follow the 

on-line instructions for submitting 

comments. 

• E-mail: a-and-r-Docket@epa.gov. 

• Fax: 202–566–1741. 

• 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. 

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 

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 www.regulations.gov 

or e-mail. The www.regulations.gov Web 

site 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 e-mail 

comment directly to EPA without going 

through 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. For additional information 

about EPA’s public docket, visit the EPA 

Docket Center homepage at http:// 

www.epa.gov/epahome/dockets.htm. 

Docket: All documents in the docket 

are listed in the 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 

www.regulations.gov or in hard copy at 

the Air and Radiation Docket and 

Information Center, EPA/DC, EPA West, 

Room 3334, 1301 Constitution Ave., 

NW., Washington, DC. The Public 

Reading Room is open from 8:30 a.m. to 

4:30 p.m., Monday through Friday, 

excluding legal holidays. The telephone 

number for the Public Reading Room is 

(202) 566–1744 and the telephone 

number for the Air and Radiation 

Docket and Information Center is (202) 

566–1742. 

Public Hearings: The EPA intends to 

hold public hearings around the end of 

August to early September in several 

cities across the country, and will 

announce in a separate Federal Register 

notice the dates, times, and addresses of 

the public hearings on this proposed 

rule. 

FOR FURTHER INFORMATION CONTACT: Dr. 

David J. McKee, Health and 

Environmental Impacts Division, Office 

of Air Quality Planning and Standards, 

U.S. Environmental Protection Agency, 

Mail code C504–06, Research Triangle 

Park, NC 27711; telephone: 919–541– 

5288; fax: 919–541–0237; e-mail: 

mckee.dave@epa.gov. 

SUPPLEMENTARY INFORMATION: 

General Information 

What Should I Consider as I Prepare My 

Comments for EPA? 

1. Submitting CBI. Do not submit this 

information to EPA through 

www.regulations.gov or e-mail. 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 


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Federal Register / Vol. 72, No. 132 / Wednesday, July 11, 2007 / Proposed Rules 37819 

1The legislative history of section 109 indicates 

that a primary standard is to be set at ‘‘the 

maximum permissible ambient air level * * * 

which will protect the health of any [sensitive] 

group of the population,’’ and that for this purpose 

‘‘reference should be made to a representative 

sample of persons comprising the sensitive group 

rather than to a single person in such a group’’ [S. 

Rep. No. 91–1196, 91st Cong., 2d Sess. 10 (1970)]. 

2Welfare effects as defined in section 302(h) (42 

U.S.C. 7602(h)) include, but are not limited to, 

‘‘effects on soils, water, crops, vegetation, manContinued 

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. 

• If you estimate potential costs or 

burdens, explain how you arrived at 

your estimate in sufficient detail to 

allow for it to be reproduced. 

• 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 (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 http:// 

www.epa.gov/ncea, and click on 

‘‘Ozone.’’ The 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 Staff Paper is 

available at http://www.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 

http://www.epa.gov/ttn/naaqs/ 

standards/ozone/s_o3_cr_td.html. EPA 

will be making available corrected 

versions of the final Staff Paper and 

human exposure and health risk 

assessment technical support 

documents on these same EPA Web 

sites on or around July 16, 2007. These 

and other related documents are also 

available for inspection and copying in 

the EPA docket identified above. 

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

II. Rationale for Proposed Decision on the 

Primary Standard 

A. Health Effects Information 

1. Mechanisms 

2. Nature of Effects 

3. Interpretation and Integration of the 

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. Conclusions on the Adequacy of the 

Current Primary Standard 

1. Background 

2. Evidence- and Exposure/Risk-Based 

Considerations 

3. CASAC Views 

4. Administrator’s Proposed Conclusions 

Concerning Adequacy of Current 

Standard 

D. Conclusions on the Elements of the 

Primary Standard 

1. Indicator 

2. Averaging Time 

3. Form 

4. Level 

E. Proposed Decision on the Primary 

Standard 

III. Communication of Public Health 

Information 

IV. Rationale for Proposed Decision on the 

Secondary Standard 

A. Vegetation Effects Information 

1. Mechanisms Governing Plant Response 

to Ozone 

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. Conclusions on the Adequacy of the 

Current Standard 

1. Background 

2. Evidence- and Exposure/Risk-Based 

Considerations 

3. CASAC Views 

4. Administrator’s Proposed Conclusions 

Concerning Adequacy of Current 

Standard 

E. Conclusions on the Elements of the 

Secondary Standard 

1. Indicator 

2. Cumulative, Seasonal Standard 

3. 8-Hour Average Standard 

F. Proposed Decision on the Secondary 

Standard 

V. Creation of Appendix P—Interpretation of 

the NAAQS for Ozone 

A. Data Completeness 

B. Data Handling and Rounding O3

Conventions 

VI. Ambient Monitoring Related to Proposed 

Revised Standards 

VII. Statutory and Executive Order Reviews 

References 

I. Background 

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 his judgment, may reasonably be 

anticipated to endanger public health 

and welfare’’ and 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 identifiable effects on 

public health or welfare which may be 

expected from the presence of [a] 

pollutant in ambient air * * *.’’

Section 109 (42 U.S.C. 7409) directs 

the Administrator to propose and 

promulgate ‘‘primary’’ and ‘‘secondary’’

NAAQS for pollutants listed under 

section 108. 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.’’ 1 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 

[the] pollutant in the ambient air.’’ 2


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made materials, animals, wildlife, weather, 

visibility and climate, damage to and deterioration 

of property, and hazards to transportation, as well 

as effects on economic values and on personal 

comfort and well-being.’’

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 

(DC 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) (Breyer, J., concurring in part 

and concurring in judgment). 

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. American 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. As discussed by Justice Breyer in 

Whitman v. American Trucking 

Associations, however, ‘‘this 

interpretation of § 109 does not require 

the EPA to eliminate every health risk, 

however slight, at any economic cost, 

however great, to the point of ‘‘hurtling’’

industry over ‘‘the brink of ruin,’’ or 

even forcing ‘‘deindustrialization.’’ Id. 

at 494 (Breyer J., concurring in part and 

concurring in judgment) (citations 

omitted). Rather, as Justice Breyer 

explained: 

The statute, by its express terms, does not 

compel the elimination of all risk; and it 

grants the Administrator sufficient flexibility 

to avoid setting ambient air quality standards 

ruinous to industry. 

Section 109(b)(1) directs the Administrator 

to set standards that are ‘‘requisite to protect 

the public health’’ with ‘‘an adequate margin 

of safety.’’ But these words do not describe 

a world that is free of all risk—an impossible 

and undesirable objective. (citation omitted). 

Nor are the words ‘‘requisite’’ and ‘‘public 

health’’ to be understood independent of 

context. We consider football equipment 

‘‘safe’’ even if its use entails a level of risk 

that would make drinking water ‘‘unsafe’’ for 

consumption. And what counts as 

‘‘requisite’’ to protecting the public health 

will similarly vary with background 

circumstances, such as the public’s ordinary 

tolerance of the particular health risk in the 

particular context at issue. The Administrator 

can consider such background circumstances 

when ‘‘deciding what risks are acceptable in 

the world in which we live.’’ (citation 

omitted). 

The statute also permits the Administrator 

to take account of comparative health risks. 

That is to say, she may consider whether a 

proposed rule promotes safety overall. A rule 

likely to cause more harm to health than it 

prevents is not a rule that is ‘‘requisite to 

protect the public health.’’ For example, as 

the Court of Appeals held and the parties do 

not contest, the Administrator has the 

authority to determine to what extent 

possible health risks stemming from 

reductions in tropospheric ozone (which, it 

is claimed, helps prevent cataracts and skin 

cancer) should be taken into account in 

setting the ambient air quality standard for 

ozone. (citation omitted). 

The statute ultimately specifies that the 

standard set must be ‘‘requisite to protect the 

public health’’ ‘‘in the judgment of the 

Administrator,’’ § 109(b)(1), 84 Stat. 1680 

(emphasis added), a phrase that grants the 

Administrator considerable discretionary 

standard-setting authority. 

The statute’s words, then, authorize the 

Administrator to consider the severity of a 

pollutant’s potential adverse health effects, 

the number of those likely to be affected, the 

distribution of the adverse effects, and the 

uncertainties surrounding each estimate. 

(citation omitted). They permit the 

Administrator to take account of comparative 

health consequences. They allow her to take 

account of context when determining the 

acceptability of small risks to health. And 

they give her considerable discretion when 

she does so. 

This discretion would seem sufficient to 

avoid the extreme results that some of the 

industry parties fear. After all, the EPA, in 

setting standards that ‘‘protect the public 

health’’ with ‘‘an adequate margin of safety,’’

retains discretionary authority to avoid 

regulating risks that it reasonably concludes 

are trivial in context. Nor need regulation 

lead to deindustrialization. Preindustrial 

society was not a very healthy society; hence 

a standard demanding the return of the Stone 

Age would not prove ‘‘requisite to protect the 

public health.’’

Although I rely more heavily than does the 

Court upon legislative history and alternative 

sources of statutory flexibility, I reach the 

same ultimate conclusion. Section 109 does 

not delegate to the EPA authority to base the 

national ambient air quality standards, in 

whole or in part, upon the economic costs of 

compliance. 

Id. at 494–496. 

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 manmade NOX and 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 


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3See EPA report, Evaluating Ozone Control 

Programs in the Eastern United States: Focus on the 

NOX Budget Trading Program, 2004. 

power industry.3 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. 

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 current 

national standards. Under the Federal 

Motor Vehicle Control Program 

(FMVCP, see 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. Recently EPA proposed new 

standards for locomotive and marine 

diesel engines. 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. The EPA 

is currently working to finalize new 

federal rules, or amendments to existing 

rules, that will establish new 

nationwide VOC content limits for 

several categories of consumer and 

commercial products, including aerosol 

coatings, architectural and industrial 

maintenance coatings, and household 

and institutional commercial products. 

These rules will take effect in 2009, and 

will yield significant new reductions in 

nationwide VOC emissions—about 

200,000 tons per year. Additionally, in 

O3 nonattainment areas, we anticipate 

reductions of an additional 25,000 tons 

per year following completion of control 

technique recommendations for 3 

additional consumer and commercial 

product categories. 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 

and some large industrial boilers and 

turbines. The EPA’s landmark Clean Air 

Interstate Rule (CAIR), issued on March 

10, 2005, permanently caps power 

industry emissions of NOX in the 

eastern United States. The first phase of 

the cap begins in 2009, and a lower 

second phase cap begins in 2015. By 

2015, EPA projects that the CAIR and 

other programs in the Eastern U.S. will 

reduce power industry O3 season NOX

emissions in that region by about 50 

percent and annual NOX emissions by 

about 60 percent from 2003 levels. 

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 USDAapproved 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

Tropospheric (ground-level) O3 is 

formed from biogenic and 

anthropogenic precursor emissions. 

Naturally occurring O3 in the 

troposphere can result from biogenic 

organic precursors reacting with 

naturally occurring nitrogen oxides 

(NOX) and by stratospheric O3 intrusion 

into the troposphere. Anthropogenic 

precursors of O3, specifically NOX and 

volatile organic compounds (VOC), 

originate from a wide variety of 

stationary and mobile sources. Ambient 

O3 concentrations produced by these 

emissions are directly affected by 

temperature, solar radiation, wind speed 

and other meteorological factors. 

The last review of the O3 NAAQS was 

completed on July 18, 1997, based on 

the 1996 O3 CD (U.S. EPA, 1996a) and 

1996 O3 Staff Paper (U.S. EPA, 1996b). 

EPA revised the primary and secondary 

O3 standards on the basis of the then 

latest scientific evidence linking 

exposures to ambient O3 to adverse 

health and welfare effects at levels 

allowed by the 1-hour average standards 

(62 FR 38856). The O3 standards were 

revised by replacing the existing 

primary 1-hour average standard with 

an 8-hour average O3 standard set at a 

level of 0.08 ppm, which is equivalent 

to 0.084 ppm using the standard 

rounding conventions. The form of the 

primary standard was changed to the 

annual fourth-highest daily maximum 8- 

hour average concentration, averaged 

over three years. The secondary O3

standard was changed by making it 

identical in all respects to the revised 

primary standard. 

Following promulgation of the revised 

O3 NAAQS, petitions for review were 


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37822 Federal Register / Vol. 72, No. 132 / Wednesday, July 11, 2007 / Proposed Rules 

4On December 22, 2006, the D.C. Circuit vacated 

the April 30, 2004 implementation rule. South 

Coast Air Quality Management District v. EPA, 472 

F.3d 882. In March 2007, EPA requested the Court 

to reconsider its decision. 

5EPA plans to make available corrected versions 

of the final Staff Paper and the human exposure and 

health risk assessment technical support documents 

on or around July 16, 2007 on the EPA web site 

listed in the Availability of Related Information 

section of this notice. 

6American Lung Association v. Whitman (No. 

1:03CV00778, D.D.C. 2003). 

filed addressing a broad range of issues. 

In May 1999, in response to those 

challenges, the U.S. Court of Appeals for 

the District of Columbia Circuit held 

that EPA’s approach to establishing the 

level of the standards in 1997, both for 

the O3 and for the particulate matter 

(PM) NAAQS promulgated on the same 

day, effected ‘‘an unconstitutional 

delegation of legislative authority.’’

American Trucking Associations v. 

EPA, 175 F.3d 1027 (DC Cir., 1999). 

Although the D.C. Circuit stated that 

‘‘factors EPA uses in determining the 

degree of public health concern 

associated with different levels of O3

and PM are reasonable,’’ it remanded 

the rule to EPA, stating that when EPA 

considers these factors for potential 

non-threshold pollutants ‘‘what EPA 

lacks is any determinate criterion for 

drawing lines’’ to determine where the 

standards should be set. Id. at 1034. 

Consistent with EPA’s long-standing 

interpretation and DC Circuit precedent, 

the court also reaffirmed prior rulings 

holding that in setting the NAAQS, it is 

‘‘not permitted to consider the cost of 

implementing those standards.’’ Id. at 

1040–41. The DC Circuit further 

directed EPA to consider on remand the 

potential indirect beneficial health 

effects of O3 pollution in shielding the 

public from the effects of solar 

ultraviolet (UV) radiation, as well as the 

direct adverse health effects of O3

pollution. 

Both sides filed cross appeals on the 

constitutional and cost issues to the 

United States Supreme Court, and the 

Court granted certiorari. On February 

27, 2001, the U.S. Supreme Court issued 

a unanimous decision upholding the 

EPA’s position on both the 

constitutional and the cost issues. 

Whitman v. American Trucking 

Associations, 531 U.S. at 464, 475–76. 

On the constitutional issue, the Court 

held that the statutory requirement that 

NAAQS be ‘‘requisite’’ to protect public 

health with an adequate margin of safety 

sufficiently guided EPA’s discretion, 

affirming EPA’s approach of setting 

standards that are neither more nor less 

stringent than necessary. The Supreme 

Court remanded the case to the D.C. 

Circuit for resolution of any remaining 

issues that had not been addressed by 

that Court’s earlier decisions. Id. at 475–

76. On March 26, 2002, the D.C. Circuit 

Court rejected all remaining challenges 

to the NAAQS, holding under 

traditional standard of review that EPA 

‘‘engaged in reasoned decision-making’’

in setting the 1997 O3 NAAQS. 

Whitman v. American Trucking 

Associations, 283 F.3d 355 (DC Cir. 

2002). 

In response to the DC Circuit Court’s 

remand to consider the potential 

indirect beneficial health effects of O3 in 

shielding the public from the effects of 

solar (UV) radiation, on November 14, 

2001, EPA proposed to leave the 1997 

8-hour NAAQS unchanged (66 FR 

57267). After considering public 

comment on the proposed decision, 

EPA reaffirmed the 8-hour O3 NAAQS 

set in 1997 (68 FR 614). Finally, on 

April 30, 2004, EPA issued an 8-hour 

implementation rule that, among other 

things, provided that the 1-hour O3

NAAQS would no longer apply to areas 

one year after the effective date of the 

designation of those areas for the 8-hour 

NAAQS (69 FR 23966).4 For most areas, 

the date that the 1-hour NAAQS no 

longer applied was June 15, 2005. (See 

40 CFR 50.9 for details.) 

The EPA initiated this current review 

in September 2000 with a call for 

information (65 FR 57810) for the 

development of a revised Air Quality 

Criteria Document for O3 and Other 

Photochemical Oxidants (henceforth the 

‘‘Criteria Document’’). A project work 

plan (U.S. EPA, 2002) for the 

preparation of the Criteria Document 

was released in November 2002 for 

CASAC and public review. 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, the CASAC offered final 

comments on all chapters of the Criteria 

Document (Henderson, 2006a), and the 

final Criteria Document (EPA, 2006a) 

was released on March 21, 2006. In a 

June 8, 2006 letter (Henderson, 2006b) 

to the Administrator, the CASAC offered 

additional advice to the Agency 

concerning chapter 8 of the final 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 

and 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 Staff Paper (EPA, 2007) was 

released on January 31, 2007. Around 

the time of the release of the final Staff 

Paper in January 2007, EPA discovered 

a small error in the exposure model that 

when corrected resulted in slight 

increases in the human exposure 

estimates. Since the exposure estimates 

are an input to the lung function portion 

of the health risk assessment, this 

correction also resulted in slight 

increases in the lung function risk 

estimates as well. The exposure and risk 

estimates discussed in this notice reflect 

the corrected estimates, and thus are 

slightly different than the exposure and 

risk estimates cited in the January 31, 

2007 Staff Paper.5 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 this 

review is 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 current 

review within the period provided by 

statute.6 The modified consent decree 

that governs this review, entered by the 

court on December 16, 2004, provides 

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. This 

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. 

This action presents the 

Administrator’s proposed decisions on 

the review of the current primary and 

secondary O3 standards. Throughout 

this preamble a number of conclusions, 

findings, and determinations proposed 

by the Administrator are noted. While 


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7 In its assessment of the epidemiological 

evidence judged to be most relevant to making 

decisions on the level of the O3 primary standard, 

EPA has placed greater weight on U.S. and 

Canadian epidemiologic studies, since studies 

conducted in other countries may well reflect 

different demographic and air pollution 

characteristics. 

they identify the reasoning that supports 

this proposal, they are not intended to 

be final or conclusive in nature. The 

EPA invites general, specific, and/or 

technical comments on all issues 

involved with this proposal, including 

all such proposed judgments, 

conclusions, findings, and 

determinations. 

II. Rationale for Proposed Decision on 

the Primary Standard 

This section presents the rationale for 

the Administrator’s proposed decision 

to revise the existing 8-hour O3 primary 

standard by lowering the level of the 

standard to within a range from 0.070 to 

0.075 ppm, and to specify the standard 

to the nearest thousandth ppm (i.e., to 

the nearest parts per billion). As 

discussed more fully below, this 

rationale is based on a thorough review, 

in the Criteria Document, of the latest 

scientific information on human health 

effects associated with the presence of 

O3 in the ambient air. This rationale also 

takes into account and is consistent 

with: (1) Staff assessments of the most 

policy-relevant information in the 

Criteria Document and staff analyses of 

air quality, human exposure, and health 

risks, presented in the Staff Paper, upon 

which staff recommendations for 

revisions to the primary O3 standard are 

based; (2) CASAC advice and 

recommendations, as reflected in 

discussions of drafts of the Criteria 

Document and Staff Paper at public 

meetings, in separate written comments, 

and in CASAC’s letters to the 

Administrator; and (3) public comments 

received during the development of 

these documents, either in connection 

with CASAC meetings or separately. 

In developing this rationale, 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.7 In 

considering this evidence, EPA focuses 

on those health endpoints that have 

been demonstrated to be caused by 

exposure to O3, or for which the 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. Evidence- and exposure/risk-based 

considerations that form the basis for 

the Administrator’s proposed decisions 

on the adequacy of the current standard 

and on the elements of the range of 

proposed alternative standards are 

discussed below in sections II.C and 

II.D, respectively. 

Judgments made in the Criteria 

Document and 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 

effects data under closely monitored 

conditions and can provide exposureresponse 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 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 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 


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8Exposures of concern were also considered in 

the last review of the O3 NAAQS, and were judged 

by EPA to be an important indicator of the public 

health impacts of those O3-related effects for which 

information was too limited to develop quantitative 

estimates of risk but which had been observed in 

humans at and above the benchmark level of 0.08 

ppm for 6-to 8-hour exposures * * * including 

increased nonspecific bronchial responsiveness (for 

example, aggravation of asthma), decreased 

pulmonary defense mechanisms (suggestive of 

increased susceptibility to respiratory infection), 

and indicators of pulmonary inflammation (related 

to potential aggravation of chronic bronchitis or 

long-term damage to the lungs). (62 FR 38868) 

under varying air quality scenarios (e.g., 

just meeting the current or alternative 

standards), as well as characterizations 

of the kind and degree of uncertainties 

inherent in such estimates. 

In this review, 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.1.8 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. 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 human 

clinical and toxicological studies but 

cannot be evaluated in quantitative risk 

assessments, such as lung inflammation, 

increased airway responsiveness, and 

changes in host defenses. They also help 

in understanding the extent to which 

such impacts have the potential to be 

reduced by meeting the current and 

alternative standards. 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 this review 

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 current and various 

alternative O3 standards in a number of 

example urban areas. There were two 

parts to this risk assessment: one part 

was based on combining information 

from controlled human exposure studies 

with modeled population exposure, and 

the other part was based on combining 

information from community 

epidemiological studies with either 

monitored or adjusted ambient 

concentrations levels. This assessment 

not only provided 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 provided 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 has been 

conducted since the last review of the 

O3 NAAQS, with important new 

information coming from epidemiologic 

studies as well as from controlled 

human exposure, toxicological, and 

dosimetric studies. The newly available 

research studies evaluated in the 

Criteria Document and the exposure and 

risk assessments presented in the 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, 

the review of this information has been 

extensive and deliberate. In the 

judgment of the Administrator, this 

intensive evaluation of the scientific 

evidence has provided an adequate 

basis for regulatory decision making. 

This review also provides important 

input to EPA’s research plan for 

improving our future understanding of 

the effects of ambient O3 at lower levels, 

especially in at-risk population groups. 

A. Health Effects Information 

This section outlines key information 

contained in the Criteria Document 

(chapters 4–8) and in the 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’’

subpopulations. 

The decision in the last review 

focused primarily on evidence from 

short-term (e.g., 1 to 3 hours) and 

prolonged ( 6 to 8 hours) controlledexposure studies reporting lung 

function decrements, respiratory 

symptoms, and respiratory 

inflammation in humans, as well as 

epidemiology studies reporting excess 


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9While most of the available evidence addresses 

mechanisms for O3, O3 clearly serves as an indicator 

for the total photochemical oxidant mixture found 

in the ambient air. Some effects may be caused by 

one or more components in the overall pollutant 

mix, either separately or in combination with O3. 

hospital admissions and emergency 

department (ED) visits for respiratory 

causes. The Criteria Document prepared 

for this review emphasizes a 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 

emphasizes important new information 

from toxicology, dosimetry, and 

controlled human exposure studies. 

Highlights of the evidence include: 

(1) Two new controlled humanexposure 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 last review. 

(2) Numerous controlled humanexposure studies have examined 

indicators of O3-induced inflammatory 

response in both the upper respiratory 

tract (URT) and lower respiratory tract 

(LRT), while other studies have 

examined changes in host defense 

capability following O3 exposure of 

healthy young adults and increased 

airway responsiveness to allergens in 

subjects with allergic asthma and 

allergic rhinitis exposed to O3. 

(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 asthmatic subjects, as well 

as evidence on new health endpoints, 

such as the relationships between 

ambient O3 concentrations 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 respiratory 

diseases and on 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 last 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 

Criteria Document.9 Evidence from 

dosimetry, toxicology, 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 longterm 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 last review 

an emerging body of animal toxicology 

and human clinical 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 

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 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 can become apparent 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 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 x ventilation rate x 

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 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 have been identified as 

potentially susceptible to health effects 

as a result of O3 exposure, including 

people with existing lung diseases, 

including asthma, children and older 

adults, and people who have larger than 

normal lung function responses that 

may be due to genetic susceptibility. In 

addition, some population groups have 

been identified as having increased 


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10 In previous Staff Papers and Federal Register 

notices announcing proposed and final decisions on 

the O3 and other NAAQS, EPA has used the phrase 

‘‘sensitive population groups’’ to include both 

population groups that are at increased risk because 

they are more susceptible and population groups 

that are at increased risk due to increased 

vulnerability or exposure. In this notice, we use the 

phrase, ‘‘at risk’’ populations to include both types 

of population groups. 

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 ‘‘atrisk’’ groups 10, as discussed more fully 

below in section II.A.4.b. 

Based on new evidence from animal, 

human clinical and epidemiological 

studies the Criteria Document concludes 

that people with preexisting pulmonary 

disease 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 (CD, Figure 8–1) that are 

altered in response to acute O3

exposure. They can have larger 

inflammatory responses, as manifested 

by larger increases in markers of 

inflammation such as white bloods cells 

(e.g., PMNs) or inflammatory cytokines. 

Asthmatics, and people with allergic 

rhinitis, are more likely to 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. These more 

serious responses in asthmatics and 

others with lung disease provide 

biological plausibility for the respiratory 

morbidity effects observed in 

epidemiological studies. 

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. 

Looking more broadly at age-related 

differences in susceptibility, several 

mortality studies have investigated agerelated differences in O3 effects (EPA, 

2006a, section 7.6.7.2), primarily in the 

older adult population. Among the 

studies that observed positive 

associations between O3 and mortality, 

a comparison of all age or younger age 

(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. 

There is supporting evidence of agerelated differences in susceptibility to 

O3 lung function effects. The Criteria 

Document concludes that the elderly 

population (>65 years of age) appears 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 (EPA, 2006a, section 7.6.7.2). 

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, p. 6–2). In human clinical 

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.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. 

Clinical 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 clinical 

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, Jo ̈rres et al., 

(1996) found that in subjects with 


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11Health effects discussions are also drawn from 

the more detailed information and tables presented 

in the Criteria Document’s annexes. 

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 the highest common dose of 

allergen. 

2. Nature of Effects 

The 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 Staff Paper, which is 

based on scientific evidence critically 

reviewed in chapters 5, 6, and 7 of the 

Criteria Document, as well as the 

Criteria Document’s integration of 

scientific evidence contained in chapter 

8.11 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 

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 

Criteria Document and chapter 3 of the 

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 groundlevel O3, as discussed in chapter 10 of 

the Criteria Document and chapter 3 of 

the 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 shortterm O3 exposure health effects on the 

respiratory system from short-term O3

exposures were reviewed in the 1986 

and 1996 Criteria Documents (EPA, 

1986, 1996). In the last 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 post-exposure, 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 hours 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 Staff Paper (Appendix 3C). As 

summarized in more detail in the Staff 

Paper (section 3.3.1.1), among the more 

important of the recent studies that 

examined changes in FEV1 in large 

numbers of subjects over a range of 1–

2 hours at exposure levels of 0.080 to 

0.40 ppm were studies by McDonnell et 

al. (1997) and Ultman et al. (2004). 

These studies observed considerable 

intersubject variability in FEV1

decrements, which was consistent with 

findings in the 1996 Criteria Document. 

For prolonged exposures (4 to 8 

hours) in the range of 0.080 to 0.160 

ppm O3 using moderate intermittent 

exercise and typically using squareVerDate Aug<31>2005 18:26 Jul 10, 2007 Jkt 211001 PO 00000 Frm 00011 Fmt 4701 Sfmt 4702 E:\FR\FM\11JYP2.SGM 11JYP2

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12This study and other studies (Folinsbee et al., 

1988; Horstman et al., 1990; and McDonnell et al., 

1991), conducted in EPA’s clinical research facility 

in Chapel Hill, NC, measured ozone concentrations 

to within +/¥5 percent or +/¥0.004 ppm at the 

0.080 ppm exposure level. 13These studies, conducted at a facility at the 

University of California, in Davis, CA, reported O3

concentrations to be accurate within +/¥0.003 ppm 

over the range of concentrations included in these 

studies. 

14These distributional results presented in the 

Criteria Document and Staff Paper for the Adams 

studies are based on study data that were not 

included in the publication but were obtained from 

the author. 

15Brown, J.S. (2007). EPA Office of Research and 

Development memorandum to Ozone NAAQS 

Review Docket (OAR–2005–0172); Subject: The 

effects of ozone on lung function at 0.06 ppm in 

healthy adults, June 14, 2007. 

16Based 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, 

2007, p. 3–6). 

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 toxicology. 

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 O3.12 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, 2007, 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).13 In these 

studies, 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 postexposures) when the results were not 

corrected for the effects of exercise 

alone in filtered air (EPA, 2007, Figure 

3–1B) and with 23 percent of subjects (7 

of 30) experiencing such effects when 

the results were corrected (EPA, 2007, p. 

3–6).14

These studies by Adams (2002, 2006) 

are notable in that they are the only 

available controlled exposure human 

studies that examine respiratory effects 

associated with prolonged O3 exposures 

at levels below 0.080 ppm, which was 

the lowest exposure level that had been 

examined in the last 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 multiple 

comparisons of 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. 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, 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.15 Notably, these 

studies report a small percentage of 

subjects experiencing lung function 

decrement (≥ 10 percent) at the 0.060 

ppm exposure level.16

(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 have 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 persons. 

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 


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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 (SD 

80) in northern Mexico City to 0.196 

ppm (SD 78) 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 effect 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 (SD 19.0) and 0.0513 ppm 

(SD 15.5), respectively. The data were 

analyzed for two separate groups of 

subjects, those who used maintenance 

asthma medications during the followup 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 twopollutant 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 provides 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. Even so, the 

evidence has continued to expand since 

1996 and now is considered to be much 

stronger than in the previous review. 

The 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 previous 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. 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. 

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 illnessrelated absences in single pollutant 

models. The 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. 


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17 Graham and Koren (1990) compared 

inflammatory mediators present in NL and BAL 

fluids of humans exposed to 0.4 ppm O3 for 2 hours 

and found similar increases in PMNs in both fluids, 

suggesting a qualitative correlation between 

inflammatory changes in the lower airways (BAL) 

and upper respiratory tract (NL). 

(b) Increased Airway Responsiveness 

As discussed in more detail in the 

Criteria Document (section 6.8) and 

Staff Paper (section 3.3.1.1.2), increased 

airway responsiveness, also known as 

airway hyperresponsiveness (AHR) or 

bronchial hyperreactivity, refers to a 

condition in which the propensity for 

the airways to bronchoconstrict due to 

a variety of stimuli (e.g., exposure to 

cold air, allergens, or exercise) becomes 

augmented. This condition is typically 

quantified by measuring the decrement 

in pulmonary function after inhalation 

exposure to specific (e.g., antigen, 

allergen) or nonspecific (e.g., 

methacholine, histamine) 

bronchoconstrictor stimuli. Exposure to 

O3 causes an increase in airway 

responsiveness as indicated by a 

reduction in the concentration of 

stimuli required to produce a given 

reduction in FEV1 or 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 inhalation of 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 current 

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 (Jo ̈rres 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, p. 6–31). 

The 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 (Criteria Document, 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 previous 

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 Criteria 

Document and section 3.3.1.3 of the 

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 Criteria Document (pp. 8–21 to 8–

24) consistent with the previous 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)17 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 


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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 nonasthmatics 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 Staff Paper (section 3.3.1.1.3) notes 

that one study (Devlin et al., 1991) 

showed that roughly 10 to 50 percent of 

the 18 young healthy adult subjects 

experienced notable increases (i.e., ≥ 2 

fold increase) in most of the 

inflammatory and cellular injury 

indicators analyzed, associated with 6.6- 

hour exposures at 0.080 ppm. Similar, 

although in some cases higher, fractions 

of the population of 10 healthy adults 

tested saw > 2 fold increases associated 

with 6.6-hour exposures to 0.100 ppm. 

The authors of this study expressed the 

view that ‘‘susceptible subpopulations 

such as the very young, elderly, and 

people with pulmonary impairment or 

disease may be even more affected’’

(Devlin et al., 1991). 

Since 1996, a substantial number of 

human exposure studies have been 

published which have provided 

important new information on lung 

inflammation and epithelial 

permeability. Mudway and Kelly (2004) 

examined O3-induced inflammatory 

responses and epithelial permeability 

with a meta-analysis of 21 controlled 

human exposure studies and showed 

that an influx in neutrophils and protein 

in healthy subjects is associated with 

total O3 dose (product of O3

concentration, exposure duration, and 

minute ventilation) (EPA, 2006a, p. 6–

34). Results of the analysis suggest that 

the time course for inflammatory 

responses (including recruitment of 

neutrophils and other soluble 

mediators) is not clearly established, but 

there is evidence that attenuation 

profiles for many of these parameters 

are different (EPA, 2006a, p. 8–22). 

The 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 (Criteria Document, p. 8–24). 

Further, antioxidant reactivity with O3

is both species-specific and dosedependent. 

(d) Increased Susceptibility to 

Respiratory Infection 

As discussed in more detail in the 

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. Dysfunction 

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 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 (EPA, 

2006a, p. 8–26). Integrating the recent 

animal study results with human 

exposure evidence available in the 1996 

Criteria Document, the 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 

Staff Paper (section 3.3.1.1.5), cells in 

the centriacinar region (CAR) of the lung 

(the segment between the last 

conducting airway and the gas exchange 

region) have been recognized as a 

primary target of O3-induced damage 

(epithelial cell necrosis and remodeling 

of respiratory bronchioles), possibly 

because epithelium in this region 

receives the greatest dose of O3

delivered to the lower respiratory tract. 

Following chronic O3 exposure, 

structural changes have been observed 

in the CAR, the region typically affected 

in most chronic airway diseases of the 

human lung (EPA, 2006a, p. 8–24). 

Ciliated cells in the nasal cavity and 

airways, as well as Type I cells in the 

gas-exchange region, are also identified 

as targets. While short-term O3

exposures can cause epithelial cell 

proliferation and fibrolitic changes in 

the CAR, these changes appear to be 

transient with recovery time 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 of respiratory bronchiolitis, 

which have the potential to progress to 

fibrotic lung disease (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 

(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). 


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18 Discussion of the reasons for focusing on warm 

season studies is found in the section 2.A.3.a below. 

(f) Emergency Department Visits/ 

Hospital Admissions for Respiratory 

Causes 

Increased summertime emergency 

department visits and hospital 

admissions for respiratory causes have 

been associated with ambient exposures 

to O3. As discussed in section 3.3.1.1.6 

of the 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 last 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 

summertime18 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 respiratoryrelated 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 prior review and 

are included in the current assessment 

along with estimates for respiratoryrelated hospital admissions in 

Cleveland, Detroit, and Los Angeles 

based on more recent studies (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 last or the current 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 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. 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 Criteria Document 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 

(Figure 7–8, EPA, 2006a, p. 7–68). 

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. Thus, the 

Criteria Document has concluded that 

stratified analyses by season generally 

supported a positive association 

between O3 concentrations and 

emergency department visits for asthma 

in the warm season. 

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 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 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 human clinical, 

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). 


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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 Criteria Document (p. 

7–114) summarizes these studies 

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 and that there is some 

limited, as yet uncertain, evidence that 

seasonal O3 also may affect lung 

function 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 have longterm risks. 

Several epidemiological studies 

published since 1996 have examined 

the relationship between lung function 

development and long-term O3

exposure. The most extensive and 

robust study of respiratory effects in 

relation to long-term air pollution 

exposures among children in the U.S. is 

the Children’s Health Study carried out 

in 12 communities of southern 

California starting in 1993. One analysis 

(Peters et al., 1999a) examined the 

relationship between long-term O3

exposures and self-reports of respiratory 

symptoms and asthma in a cross 

sectional analysis and found a limited 

relationship between outcomes of 

current asthma, bronchitis, cough and 

wheeze and a 0.040 ppm increase in 1- 

hour max O3 (EPA, 2006a, p. 7–115). 

Another analysis (Peters et al., 1999b) 

examined the relationship between lung 

function at baseline and levels of air 

pollution in the community. They 

reported evidence that annual mean O3

levels were associated with decreases in 

FVC, FEV1, PEF and forced expiratory 

flow (FEF25–75) (the latter two being 

statistically significant) among females 

but not males. In a separate analysis 

(Gauderman et al., 2000) of 4th, 7th, and 

10th grade students, a longitudinal 

analysis of lung function development 

over four years found no association 

with O3 exposure. The Children’s 

Health Study enrolled a second cohort 

of more than 1500 fourth graders in 

1996 (Gauderman et al., 2002). While 

the strongest associations with negative 

lung function growth were observed 

with acid vapors in this cohort, children 

from communities with higher 4-year 

average O3 levels also experienced 

smaller increases in various lung 

function parameters. The strongest 

relationship with O3 was with PEF. 

Specifically, children from the leastpolluted community had a small but 

statistically significant increase in PEF 

as compared to those from the mostpolluted communities. In two-pollutant 

models, only 8-hour average O3 and NO2

were significant joint predictors of FEV1

and maximal midexpiratory flow 

(MMEF). Although results from the 

second cohort of children are supportive 

of a weak association, the definitive 8- 

year follow-up analysis of the first 

cohort (Gauderman et al., 2004a) 

provides little evidence that long-term 

exposure to ambient O3 at current levels 

is associated with significant deficits in 

the growth rate of lung function in 

children. Avol et al. (2001) examined 

children who had moved away from 

participating communities in southern 

California to other states with improved 

air quality. They found that a negative, 

but not statistically significant, 

association was observed between O3

and lung function parameters. 

Collectively, the results of these reports 

from the children’s health cohorts 

provide little evidence to support an 

impact of long-term O3 exposures on 

lung function development. 

Evidence for a significant relationship 

between long-term O3 exposures and 

decrements in maximally attained lung 

function was reported in a nationwide 

study of first year Yale students (Kinney 

et al., 1998; Galizia and Kinney, 1999) 

(EPA, 2006a, p. 7–120). Males had much 

larger effect estimates than females, 

which might reflect higher outdoor 

activity levels and correspondingly 

higher O3 exposures during childhood. 

A similar study of college freshmen at 

University of California at Berkeley also 

reported significant effects of long-term 

O3 exposures on lung function (Ku ̈nzli 

et al., 1997; Tager et al., 1998). In a 

comparison of students whose city of 

origin was either Los Angeles or San 

Francisco, long-term O3 exposures were 

associated with significant changes in 

mid- and end-expiratory flow measures, 

which could be considered early 

indicators for pathologic changes that 

might progress to COPD. 

There have been a few studies that 

investigated associations between longterm O3 exposures and the onset of new 

cases of asthma (EPA, 2006a, section 

7.5.6). The Adventist Health and Smog 

(AHSMOG) study cohort of about 4,000 

was drawn from nonsmoking, nonHispanic white adult Seventh Day 

Adventists living in California (Greer et 

al., 1993; McDonnell et al., 1999). 

During the ten-year follow-up in 1987, 

a statistically significant increased 

relative risk of asthma development was 

observed in males, compared to a 

nonsignificant relative risk in females 

(Greer et al., 1993). In the 15-year 

follow-up in 1992, it was reported that 

for males, there was a statistically 

significant increased relative risk of 

developing asthma associated with 8- 

hour average O3 exposures, but there 

was no evidence of an association in 

females. Consistency of results in the 

two studies with different follow-up 


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times provides supportive evidence of 

the potential for an association between 

long-term O3 exposure and asthma 

incidence in adult males; however, 

representativeness of this cohort to the 

general U.S. population may be limited 

(EPA, 2006a, p. 7–125). 

In a similar study (McConnell et al., 

2002) of incident asthma among 

children (ages 9 to 16 at enrollment), 

annual surveys of 3,535 children 

initially without asthma were used to 

identify new-onset asthma cases as part 

of the Children’s Health Study. Six 

high-O3 and six low-O3 communities 

were identified where the children 

resided. There were 265 children who 

reported new-onset asthma during the 

follow-up period. Although asthma risk 

was no higher for all residents of the six 

high-O3 communities versus the six 

low-O3 communities, asthma risk was 

3.3 times greater for children who 

played three or more sports as compared 

with children who played no sports 

within the high-O3 communities. This 

association was absent in the 

communities with lower O3

concentrations. No other pollutants 

were found to be associated with newonset asthma (EPA, 2006a, p. 7–125). 

Playing sports may result in extended 

outdoor activity and exposure occurring 

during periods when O3 levels are 

higher. It should be noted, however, that 

the results of the Children’s Health 

Study were based on a small number of 

new-onset asthma cases among children 

who played three or more sports. Future 

replication of these findings in other 

cohorts would help determine whether 

a causal interpretation is appropriate. 

In animal toxicology studies, the 

progression of morphological effects 

reported during and after a chronic 

exposure in the range of 0.50 to 1.00 

ppm O3 is complex, with inflammation 

peaking over the first few days of 

exposure, then dropping, then 

plateauing, and finally, largely 

disappearing (EPA, 2006a, section 

5.2.4.4). By contrast, fibrotic changes in 

the tissue increase very slowly over 

months of exposure, and, after exposure 

ceases, the changes sometimes persist or 

increase. Epithelial hyperplasia peaks 

soon after the inflammatory response 

but is usually maintained in both the 

nose and lungs with continuous 

exposure; it also does not return to preexposure levels after the end of 

exposure. Patterns of exposure in this 

same concentration range determine 

effects, with 18 months of daily 

exposure, causing less morphologic 

damage than exposures on alternating 

months. This is important as 

environmental O3 exposure is typically 

seasonal. Long-term studies by Plopper 

and colleagues (Evans et al., 2003; 

Schelegle et al., 2003; Chen et al., 2003; 

Plopper and Fanucchi, 2000) 

investigated infant rhesus monkeys 

exposed to simulated, seasonal O3 and 

demonstrated: (1) Remodeling in the 

distal airways, (2) abnormalities in 

tracheal basement membrane; (3) 

eosinophil accumulation in conducting 

airways; and (4) decrements in airway 

innervation (EPA, 2006a, p. 5–45). 

These findings provide additional 

information regarding possible injuryrepair processes occurring with longterm O3 exposures suggesting that these 

processes are only partially reversible 

and may progress following cessation of 

O3 exposure. Further, these processes 

may lead to nonreversible structural 

damage to lung tissue; however, there is 

still too much uncertainty to 

characterize the significance of these 

findings to human exposure profiles and 

effect levels (EPA, 2006a, p. 8–25). 

In summary, in the past decade, 

important new longitudinal studies 

have examined the effect of chronic O3

exposure on respiratory health 

outcomes. Limited evidence from recent 

long-term morbidity studies have 

suggested in some cases that chronic 

exposure to O3 may be associated with 

seasonal declines in lung function or 

reduced lung function development, 

increases in inflammation, and 

development of asthma in children and 

adults. Seasonal decrements or smaller 

increases in lung function measures 

have been reported in several studies; 

however, the extent to which these 

changes are transient remains uncertain. 

While there is supportive evidence from 

animal studies involving effects from 

chronic exposures, large uncertainties 

still remain as to whether current 

ambient levels and exposure patterns 

might cause these same effects in 

human populations. The Criteria 

Document concludes that 

epidemiological studies of new asthma 

development and longer-term lung 

function declines remain inconclusive 

at present (EPA, 2006a, p. 7–134). 

iii. Effects on the Cardiovascular System 

of O3 Exposure 

At the time of the 1997 review, the 

possibility of O3-induced cardiovascular 

effects was largely unrecognized. Since 

then, a very limited body of evidence 

from animal, controlled human 

exposure and epidemiologic studies has 

emerged that provides evidence for 

some potential plausible mechanisms 

for how O3 exposures might exert 

cardiovascular system effects, however 

much needs to be done to substantiate 

these potential mechanisms. Possible 

mechanisms may involve O3-induced 

secretions of vasoconstrictive 

substances and/or effects on neuronal 

reflexes that may result in increased 

arterial blood pressure and/or altered 

electrophysiologic control of heart rate 

or rhythm. Some animal toxicology 

studies have shown O3-induced 

decreases in heart rate, mean arterial 

pressure, and core temperature. One 

controlled human exposure study that 

evaluated effects of O3 exposure on 

cardiovascular health outcomes found 

no significant O3-induced differences in 

ECG or blood pressure in healthy or 

hypertensive subjects but did observe a 

significant O3-induced increase the 

alveolar-to-arterial PO2 gradient and 

heart rate in both groups resulting in an 

overall increase in myocardial work and 

impairment in pulmonary gas exchange 

(Gong et al., 1998). In another controlled 

human exposure study, inhalation of a 

mixture of PM2.5 and O3 by healthy 

subjects increased brachial artery 

vasoconstriction and reactivity (Brook et 

al., 2002). 

The evidence from a few animal 

studies also includes potential direct 

effects such as O3-induced release from 

lung epithelial cells of platelet 

activating factor (PAF) that may 

contribute to blood clot formation that 

would have the potential to increase the 

risk of serious cardiovascular outcomes 

(e.g., heart attack, stroke, mortality). 

Also, interactions of O3 with surfactant 

components in epithelial lining fluid of 

the lung may result in production of 

oxysterols and reactive oxygen species 

that may exhibit PAF-like activity 

contributing to clotting and also may 

exert cytotoxic effects on lung and heart 

muscle cells. 

Epidemiologic panel and field studies 

that examined associations between O3

and various cardiac physiologic 

endpoints have yielded limited 

evidence suggestive of a potential 

association between acute O3 exposure 

and altered heart rate variability, 

ventricular arrhythmias, and incidence 

of heart attacks. A number of 

epidemiological studies have also 

reported associations between shortterm exposures and hospitalization for 

cardiovascular diseases. As shown in 

Figure 7–13 of the Criteria Document, 

many of the studies reported negative or 

inconsistent associations. Some other 

studies, especially those that examined 

the relationship when O3 exposures 

were higher, have found robust positive 

associations between O3 and 

cardiovascular hospital admissions 

(EPA, 2006a, p. 7–82). For example, one 

study reported a positive association 

between O3 and cardiovascular hospital 

admissions in Toronto, Canada in a 

summer-only analysis (Burnett et al., 


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1997b). The results were robust to 

adjustment for various PM indices, 

whereas the PM effects diminished 

when adjusting for gaseous pollutants. 

Other studies stratified their analysis by 

temperature, i.e., by warm days versus 

cool days. Several analyses using warm 

season days consistently produced 

positive associations. 

The epidemiologic evidence for 

cardiovascular morbidity is much 

weaker than for respiratory morbidity, 

with only one of several U.S./Canadian 

studies showing statistically significant 

positive associations of cardiovascular 

hospitalizations with warm-season O3

concentrations. Most of the available 

European and Australian studies, all of 

which conducted all-year O3 analyses, 

did not find an association between 

short-term O3 concentrations and 

cardiovascular hospitalizations. Overall, 

the currently available evidence is 

inconclusive regarding an association 

between cardiovascular hospital 

admissions and ambient O3 exposure 

(EPA, 2006a, p. 7–83). 

In summary, based on the evidence 

from animal toxicology, human 

controlled exposure, and epidemiologic 

studies, from the Criteria Document 

concludes that this generally limited 

body of evidence is suggestive that O3

can directly and/or indirectly contribute 

to cardiovascular-related morbidity, but 

that much needs to be done to more 

fully integrate links between ambient O3

exposures and adverse cardiovascular 

outcomes (EPA, 2006a, p. 8–77). 

b. Mortality 

i. Mortality and Short-Term O3

Exposure 

The 1996 Criteria Document 

concluded that an association between 

daily mortality and O3 concentration for 

areas with high O3 levels (e.g., Los 

Angeles) was suggested. However, due 

to a very limited number of studies 

available at that time, there was 

insufficient evidence to conclude that 

the observed association was likely 

causal. 

The current Criteria Document 

includes results from numerous 

epidemiological analyses of the 

relationship between O3 and mortality. 

Additional single city analyses have 

also been conducted since 1996, 

however, the most pivotal studies in 

EPA’s (and CASAC’s) finding of 

increased support for the relationship 

between premature mortality and O3 is 

in part related to differences in study 

design—limiting analyses to warm 

seasons, better control for copollutants, 

particularly PM, and use of multicity 

designs (both time series and metaanalytic designs). Key findings are 

available from multi-city time-series 

studies that report associations between 

O3 and mortality. These studies include 

analyses using data from 90 U.S. cities 

in the National Mortality, Morbidity and 

Air Pollution (NMMAPS) study 

(Dominici et al., 2003) and from 95 U.S. 

communities in an extension to the 

NMMAPS analyses (Bell et al., 2004). 

The original 90-city NMMAPS 

analysis, with data from 1987 to 1994, 

was primarily focused on investigating 

effects of PM10 on mortality. A 

significant association was reported 

between mortality and 24-hour average 

O3 concentrations in analyses using all 

available data as well as in the warm 

season only analyses (Dominici et al., 

2003). The estimate using all available 

data was about half that for the summeronly data at a lag of 1-day. The extended 

NMMAPS analysis included data from 

95 U.S. cities and included an 

additional 6 years of data, from 1987–

2000 (Bell et al., 2004). Significant 

associations were reported between O3

and mortality in analyses using all 

available data. The effect estimate for 

increased mortality was approximately 

0.5 percent per 0.020 ppm change in 24- 

hour average O3 measured on the same 

day, and approximately 1.04 percent per 

0.020 ppm change in 24-hour average O3

in a 7-day distributed lag model (EPA, 

2006a, p. 7–88). In analyses using only 

data from the warm season, the results 

were not significantly different from the 

full-year results. The authors also report 

that O3-mortality associations were 

robust to adjustment for PM (EPA, 

2006a, p. 7–100). Using a subset of the 

NMMAPS data set, Huang et al. (2005) 

focused on associations between 

cardiopulmonary mortality and O3

exposure (24-hour average) during the 

summer season only. The authors report 

an approximate 1.47 percent increase 

per 0.020 ppm change in O3

concentration measured on the same 

day and an approximate 2.52 percent 

increase per 0.020 ppm change in O3

concentration using a 7-day distributed 

lag model. These findings suggest that 

the effect of O3 on mortality is 

immediate but also persists for several 

days. 

As discussed below in section 

II.A.3.a, confounding by weather, 

especially temperature, is complicated 

by the fact that higher temperatures are 

associated with the increased 

photochemical activities that are 

important for O3 formation. Using a 

case-crossover study design, Schwartz 

(2005) assessed associations between 

daily maximum concentrations and 

mortality, matching case and control 

periods by temperature, and using data 

only from the warm season. The 

reported effect estimate of 

approximately 0.92 percent change in 

mortality per 0.040 ppm O3 (1-hour 

maximum) was similar to time-series 

analysis results with adjustment for 

temperature (approximately 0.76 

percent per 0.040 ppm O3), suggesting 

that associations between O3 and 

mortality were robust to the different 

adjustment methods for temperature. 

An initial publication from APHEA, a 

European multi-city study, reported 

statistically significant associations 

between daily maximum O3

concentrations and mortality in four 

cities in a full year analysis (Toulomi et 

al., 1997). An extended analysis was 

done using data from 23 cities 

throughout Europe (Gryparis et al., 

2004). In this report, a positive but not 

statistically significant association was 

found between mortality and 1-hour 

daily maximum O3 in a full year 

analysis. Gryparis et al. (2004) noted 

that there was a considerable seasonal 

difference in the O3 effect on mortality; 

thus, the small effect for the all-year 

data might be attributable to inadequate 

adjustment for confounding by 

seasonality. Focusing on analyses using 

summer measurements, the authors 

report statistically significant 

associations with total mortality, 

cardiovascular mortality and with 

respiratory mortality (EPA, 2006a, p. 7–

93, 7–99). 

Numerous single-city analyses have 

also reported associations between 

mortality and short-term O3 exposure, 

especially for those analyses using 

warm season data. As shown in Figure 

7–21 of the Criteria Document, the 

results of recent publications show a 

pattern of positive, often statistically 

significant associations between shortterm O3 exposure and mortality during 

the warm season. In considering results 

from year-round analyses, there remains 

a pattern of positive results but the 

findings are less consistent. In most 

single-city analyses, effect estimates 

were not substantially changed with 

adjustment for PM (EPA, 2006a, Figure 

7–22). 

In addition, several meta-analyses 

have been conducted on the 

relationship between O3 and mortality. 

As described in section 7.4.4 of the 

Criteria Document, these analyses 

reported fairly consistent and positive 

combined effect estimates ranging from 

approximately 1.5 to 2.5 percent 

increase in mortality for a standardized 

change in O3 (EPA, 2006a, Figure 7–20). 

Three recent meta-analyses evaluated 

potential sources of heterogeneity in O3- 

mortality associations (Bell et al., 2005; 

Ito et al., 2005; Levy et al., 2005). The 


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19 In commenting on the Criteria Document, the 

CASAC Ozone Panel raised questions about the 

implications of these time-series results in a policy 

context, emphasizing that ‘‘* * * while the timeseries study design is a powerful tool to detect very 

small effects that could not be detected using other 

designs, it is also a blunt tool’’ (Henderson, 2006b). 

They note that ‘‘* * * not only is the interpretation 

of these associations complicated by the fact that 

the day-to-day variation in concentrations of these 

pollutants is, to a varying degree, determined by 

meteorology, the pollutants are often part of a large 

and highly correlated mix of pollutants, only a very 

few of which are measured’’ (Henderson, 2006b). 

Even with these uncertainties, the CASAC Ozone 

Panel, in its review of the Staff Paper, found ‘‘* * * 

premature total non-accidental and 

cardiorespiratory mortality for inclusion in the 

quantitative risk assessment to be appropriate.’’

(Henderson, 2006b). 

20This reanalysis report and the original 

prospective cohort study findings are discussed in 

more detail in section 8.2.3 of the Air Quality 

Criteria for Particulate Matter (EPA, 2004). 

Criteria Document (p. 7–96) observes 

common findings across all three 

analyses, in that all reported that effect 

estimates were larger in warm season 

analyses, reanalysis of results using 

default convergence criteria in 

generalized additive models (GAM) did 

not change the effect estimates, and 

there was no strong evidence of 

confounding by PM. Bell et al. (2005) 

and Ito et al. (2005) both provided 

suggestive evidence of publication bias, 

but O3-mortality associations remained 

after accounting for that potential bias. 

The Criteria Document concludes that 

the ‘‘positive O3 effects estimates, along 

with the sensitivity analyses in these 

three meta-analyses, provide evidence 

of a robust association between ambient 

O3 and mortality’’ (EPA, 2006a, p. 7–97). 

Most of the single-pollutant model 

estimates from single-city studies range 

from 0.5 to 5 percent excess deaths per 

standardized increments. Corresponding 

summary estimates in large U.S. multicity studies ranged between 0.5 to 1 

percent with some studies noting 

heterogeneity across cities and studies 

(EPA, 2006a, p. 7–110). 

Finally, from those studies that 

included assessment of associations 

with specific causes of death, it appears 

that effect estimates for associations 

with cardiovascular mortality are larger 

than those for total mortality. The metaanalysis by Bell et al. (2005) observed a 

slightly larger effect estimate for 

cardiovascular mortality compared to 

mortality from all causes. The effect 

estimate for respiratory mortality was 

approximately one-half that of 

cardiovascular mortality in the metaanalysis. However, other studies have 

observed larger effect estimates for 

respiratory mortality compared to 

cardiovascular mortality. The apparent 

inconsistency regarding the effect size of 

O3-related respiratory mortality may be 

due to reduced statistical power in this 

subcategory of mortality (EPA, 2006a, p. 

7–108). 

In summary, many single- and multicity studies observed positive 

associations of ambient O3

concentrations with total nonaccidental 

and cardiopulmonary mortality. The 

Criteria Document finds that the results 

from U.S. multi-city time-series studies 

provide the strongest evidence to date 

for O3 effects on acute mortality. Recent 

meta-analyses also indicate positive risk 

estimates that are unlikely to be 

confounded by PM; however, future 

work is needed to better understand the 

influence of model specifications on the 

risk coefficient (EPA, 2006a, p. 7–175). 

A meta-analysis that examined specific 

causes of mortality found that the 

cardiovascular mortality risk estimates 

were higher than those for total 

mortality. For cardiovascular mortality, 

the Criteria Document (Figure 7–25, p. 

7–106) suggests that effect estimates are 

consistently positive and more likely to 

be larger and statistically significant in 

warm season analyses. The findings 

regarding the effect size for respiratory 

mortality have been less consistent, 

possibly because of lower statistical 

power in this subcategory of mortality. 

The Criteria Document (p. 8–78) 

concludes that these findings are highly 

suggestive that short-term O3 exposure 

directly or indirectly contribute to nonaccidental and cardiopulmonary-related 

mortality, but additional research is 

needed to more fully establish 

underlying mechanisms by which such 

effects occur.19

ii. Mortality and Long-Term O3

Exposure 

Little evidence was available in the 

last review on the potential for 

associations between mortality and 

long-term exposure to O3. In the 

Harvard Six City prospective cohort 

analysis, the authors report that 

mortality was not associated with longterm exposure to O3 (Dockery et al., 

1993). The authors note that the range 

of O3 concentrations across the six cities 

was small, which may have limited the 

power of the study to detect associations 

between mortality and O3 levels (EPA, 

2006a, p. 7–127). 

As discussed in section 7.5.8 of the 

Criteria Document, in this review there 

are results available from three 

prospective cohort studies: the 

American Cancer Society (ACS) study 

(Pope et al., 2002), the Adventist Health 

and Smog (AHSMOG) study (Beeson et 

al., 1998; Abbey et al., 1999), and the 

U.S. Veterans Cohort study (Lipfert et 

al., 2000, 2003). In addition, a major 

reanalysis report includes evaluation of 

data from the Harvard Six City cohort 

study (Krewski et al., 2000).20 This 

reanalysis also includes additional 

evaluation of data from the initial ACS 

cohort study report that had only 

reported results of associations between 

mortality and long-term exposure to fine 

particles and sulfates (Pope et al., 1995). 

This reanalysis was discussed in the 

Staff Paper (section 3.3.2.2) but not in 

the Criteria Document. 

In this reanalysis of data from the 

previous Harvard Six City prospective 

cohort study, the investigators 

replicated and validated the findings of 

the original studies, and the report 

included additional quantitative results 

beyond those available in the original 

report (Krewski et al., 2000). In the 

reanalysis of data from the Harvard Six 

Cities study, the effect estimate for the 

association between long-term O3

concentrations and mortality was 

negative and nearly statistically 

significant (relative risk = 0.87, 95 

percent CI: 0.76, 1.00). 

The ACS study is based on health 

data from a large prospective cohort of 

approximately 500,000 adults and air 

quality data from about 150 U.S. cities. 

The initial report (Pope et al., 1995) 

focused on associations with fine 

particles and sulfates, for which 

significant associations had been 

reported in the earlier Harvard Six 

Cities study (Dockery et al., 1993). As 

part of the major reanalysis of these 

data, results for associations with other 

air pollutants were also reported, and 

the authors report that no significant 

associations were found between O3 and 

all-cause mortality. However, a 

significant association was reported for 

cardiopulmonary mortality in the warm 

season (Krewski et al., 2000). The ACS 

II study (Pope et al., 2002) reported 

results of associations with an extended 

data base; the mortality records for the 

cohort had been updated to include 16 

years of follow-up (compared with 8 

years in the first report) and more recent 

air quality data were included in the 

analyses. Similar to the earlier 

reanalysis, a marginally significant 

association was observed between longterm exposure to O3 and 

cardiopulmonary mortality in the warm 

season. No other associations with 

mortality were observed in both the fullyear and warm season analyses. 

The Adventist Health and Smog 

(AHSMOG) cohort includes about 6,000 

adults living in California. In two 

studies from this cohort, a significant 

association has been reported between 

long-term O3 exposure and increased 

risk of lung cancer mortality among 

males only (Beeson et al., 1998; Abbey 


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et al., 1999). No significant associations 

were reported between long-term O3

exposure and mortality from all causes 

or cardiopulmonary causes. Due to the 

small numbers of lung cancer deaths (12 

for males, 18 for females) and the 

precision of the effect estimate (i.e., the 

wide confidence intervals), the Criteria 

Document discussed concerns about the 

plausibility of the reported association 

with lung cancer (EPA, 2006a, p. 7–

130). 

The U.S. Veterans Cohort study 

(Lipfert et al., 2000, 2003) of 

approximately 50,000 middle-aged 

males diagnosed with hypertension, 

reported some positive associations 

between mortality and peak O3

exposures (95th percentile level for 

several years of data). The study 

included numerous analyses using 

subsets of exposure and mortality 

follow-up periods which spanned the 

years 1960 to 1996. In the results of 

analyses using deaths and O3 exposure 

estimates concurrently across the study 

period, there were positive, statistically 

significant associations between peak O3

and mortality (EPA, 2006a, p. 7–129). 

Overall, the Criteria Document 

concludes that consistent associations 

have not been reported between longterm O3 exposure and all-cause, 

cardiopulmonary or lung cancer 

mortality (EPA, 2006a, p. 7–130). 

c. Role of Ground-Level O3 in Solar 

Radiation-Related Human Health Effects 

Beyond the direct health effects 

attributable to inhalation exposure to O3

in the ambient air discussed above, the 

Criteria Document also assesses 

potential indirect effects related to the 

presence of O3 in the ambient air by 

considering the role of ground-level O3

in mediating human health effects that 

may be directly attributable to exposure 

to solar ultraviolet radiation (UV–B). 

The Criteria Document (chapter 10) 

focuses this assessment on three key 

factors, including those factors that 

govern (1) UV–B radiation flux at the 

earth’s surface, (2) human exposure to 

UV–B radiation, and (3) human health 

effects due to UV–B radiation. In so 

doing, the Criteria Document provides a 

thorough analysis of the current 

understanding of the relationship 

between reducing ground-level O3

concentrations and the potential impact 

these reductions might have on 

increasing UV–B surface fluxes and 

indirectly contributing to UV–B related 

health effects. 

There are many factors that influence 

UV–B radiation penetration to the 

earth’s surface, including latitude, 

altitude, cloud cover, surface albedo, 

PM concentration and composition, and 

gas phase pollution. Of these, only 

latitude and altitude can be defined 

with small uncertainty in any effort to 

assess the changes in UV–B flux that 

may be attributable to any changes in 

tropospheric O3 as a result of any 

revision to the O3 NAAQS. Such an 

assessment of UV–B related health 

effects would also need to take into 

account human habits, such as outdoor 

activities (including age- and 

occupation-related exposure patterns), 

dress and skin care to adequately 

estimate UV–B exposure levels. 

However, little is known about the 

impact of these factors on individual 

exposure to UV–B. 

Moreover, detailed information does 

not exist regarding other factors that are 

relevant to assessing changes in disease 

incidence, including: Type (e.g., peak or 

cumulative) and time period (e.g., 

childhood, lifetime, current) of 

exposures related to various adverse 

health outcomes (e.g., damage to the 

skin, including skin cancer; damage to 

the eye, such as cataracts; and immune 

system suppression); wavelength 

dependency of biological responses; and 

interindividual variability in UV–B 

resistance to such health outcomes. 

Beyond these well recognized adverse 

health effects associated with various 

wavelengths of UV radiation, the 

Criteria Document (section 10.2.3.6) also 

discusses protective effects of UV–B 

radiation. Recent reports indicate the 

necessity of UV–B in producing vitamin 

D, and that vitamin D deficiency can 

cause metabolic bone disease among 

children and adults, and may also 

increase the risk of many common 

chronic diseases (e.g., type I diabetes 

and rheumatoid arthritis) as well as the 

risk of various types of cancers. Thus, 

the Criteria Document concludes that 

any assessment that attempts to quantify 

the consequences of increased UV–B 

exposure on humans due to reduced 

ground-level O3 must include 

consideration of both negative and 

positive effects. However, as with other 

impacts of UV–B on human health, this 

beneficial effect of UV–B radiation has 

not been studied in sufficient detail to 

allow for a credible health benefits or 

risk assessment. In conclusion, the 

effect of changes in surface-level O3

concentrations on UV-induced health 

outcomes cannot yet be critically 

assessed within reasonable uncertainty 

(Criteria Document, p. 10–36). 

The Agency last considered indirect 

effects of O3 in the ambient air in its 

2003 final response to a remand of the 

Agency’s 1997 decision to revise the O3

NAAQS. In so doing, based on the 

available information in the last review, 

the Administrator determined that the 

information linking (a) Changes in 

patterns of ground-level O3

concentrations likely to occur as a result 

of programs implemented to attain the 

1997 O3 NAAQS to (b) changes in 

relevant exposures to UV–B radiation of 

concern to public health was too 

uncertain at that time to warrant any 

relaxation in the level of public health 

protection previously determined to be 

requisite to protect against the 

demonstrated direct adverse respiratory 

effects of exposure to O3 in the ambient 

air (68 FR 614). At that time, the more 

recent information on protective effects 

of UV–B radiation was not available, 

such that only adverse UV–B-related 

effects could be considered. Taking into 

consideration the more recent 

information available in this review, the 

Criteria Document and Staff Paper 

conclude that the effect of changes in 

ground-level O3 concentrations, likely to 

occur as a result of revising the O3

NAAQS, on UV-induced health 

outcomes, including whether these 

changes would ultimately result in 

increased or decreased incidence of 

UV–B-related diseases, cannot yet be 

critically assessed. EPA requests 

comment on available studies or data 

that would be relevant to conducting a 

critical assessment with reasonable 

certainty of UV-induced health 

outcomes and how evidence of UVinduced health outcomes might inform 

the Agency’s review of the primary O3

standard. 

3. Interpretation and Integration of 

Health Evidence 

As discussed below, in assessing the 

new health evidence, the Criteria 

Document integrates findings from 

experimental (e.g., toxicological, 

dosimetric and controlled human 

exposure) and epidemiological studies, 

to make judgments about the extent to 

which causal inferences can be made 

about observed associations between 

health endpoints and exposure to O3. In 

evaluating the evidence from 

epidemiological studies, the EPA 

focuses on well-recognized criteria, 

including: The strength of reported 

associations, including the magnitude 

and precision of reported effect 

estimates and their statistical 

significance; the robustness of reported 

associations, or stability in the effect 

estimates after considering factors such 

as alternative models and model 

specification, potential confounding by 

co-pollutants, and issues related to the 

consequences of exposure measurement 

error; potential aggregation bias in 

pooling data; and the consistency of the 

effects associations as observed by 

looking across results of multiple- and 


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single-city studies conducted by 

different investigators in different places 

and times. Consideration is also given to 

evaluating concentration-response 

relationships observed in 

epidemiological studies to inform 

judgments about the potential for 

threshold levels for O3-related effects. 

Integrating more broadly across 

epidemiological and experimental 

evidence, the Criteria Document also 

focuses on the coherence and 

plausibility of observed O3-related 

health effects to reach judgments about 

the extent to which causal inferences 

can be made about observed 

associations between health endpoints 

and exposure to O3 in the ambient air. 

a. Assessment of Evidence From 

Epidemiological Studies 

Key elements of the evaluation of 

epidemiological studies are briefly 

summarized below. 

(1) The strength of associations most 

directly refers to the magnitude of the 

reported relative risk estimates. Taking 

a broader view, the Criteria Document 

draws upon the criteria summarized in 

a recent report from the U.S. Surgeon 

General, which define strength of an 

association as ‘‘the magnitude of the 

association and its statistical strength’’

which includes assessment of both 

effect estimate size and precision, which 

is related to the statistical power of the 

study (CDC, 2004). In general, when 

associations are strong in terms of 

yielding large relative risk estimates, it 

is less likely that the association could 

be completely accounted for by a 

potential confounder or some other 

source of bias, whereas with 

associations that yield small relative 

risk estimates it is especially important 

to consider potential confounding and 

other factors in assessing causality. 

Effect estimates between O3 and some of 

the health outcomes are generally small 

in size and could thus be characterized 

as weak. For example, effect estimates 

for associations with mortality generally 

range from 0.5 to 5 percent increases per 

0.040 ppm increase in 1-hour maximum 

O3 or equivalent, whereas associations 

for hospitalization range up to 50 

percent increases per standardized O3

increment. However, the Criteria 

Document notes that there are large 

multicity studies that find small 

associations between short-term O3

exposure and mortality or morbidity 

and have done so with great precision 

due to the statistical power of the 

studies (EPA, 2006a, p. 8–40). That is, 

the power of the studies allows the 

authors to reliably distinguish even 

weak relationships from the null 

hypothesis with statistical confidence. 

(2) In evaluating the robustness of 

associations, the Criteria Document 

(sections 7.1.3 and 8.4.4.3) and Staff 

Paper (section 3.4.2) have primarily 

considered the impact of exposure error, 

potential confounding by copollutants, 

and alternative models and model 

specifications. 

In time-series and panel studies, the 

temporal (e.g., daily or hourly) changes 

in ambient O3 concentrations measured 

at centrally-located ambient monitoring 

stations are generally used to represent 

a community’s exposure to ambient O3. 

In prospective cohort or cross-sectional 

studies, air quality data averaged over a 

period of months to years are used as 

indicators of a community’s long-term 

exposure to ambient O3 and other 

pollutants. In both types of analyses, 

exposure error is an important 

consideration, as actual exposures to 

individuals in the population will vary 

across the community. 

Ozone concentrations measured at 

central ambient monitoring sites may 

explain, at least partially, the variance 

in individual exposures to ambient O3; 

however, this relationship is influenced 

by various factors related to building 

ventilation practices and personal 

behaviors. Further, the pattern of 

exposure misclassification error and the 

influence of confounders may differ 

across the outcomes of interest as well 

as in susceptible populations. As 

discussed in the Criteria Document 

(section 3.9), only a limited number of 

studies have examined the relationship 

between ambient O3 concentrations and 

personal exposures to ambient O3. One 

of the strongest predictors of the 

relationship between ambient 

concentrations and personal exposures 

appears to be time spent outdoors. The 

strongest relationships were observed in 

outdoor workers (Brauer and Brook, 

1995, 1997; O’Neill et al., 2004). 

Statistically significant correlations 

between ambient concentrations and 

personal exposures were also observed 

for children, who likely spend more 

time outdoors in the warm season (Linn 

et al., 1996; Xue et al., 2005). There is 

some concern about the extent to which 

ambient concentrations are 

representative of personal O3 exposures 

of another particularly susceptible 

group of individuals, the debilitated 

elderly, since those who suffer from 

chronic cardiovascular or respiratory 

conditions may tend to protect 

themselves more than healthy 

individuals from environmental threats 

by reducing their exposure to both O3

and its confounders, such as high 

temperature and PM. Studies by Sarnat 

et al. (2001, 2005) that included this 

susceptible group reported mixed 

results for associations between ambient 

O3 concentrations and personal 

exposures to O3. Collectively, these 

studies observed that the daily averaged 

personal O3 exposures tend to be well 

correlated with ambient O3

concentrations despite the substantial 

variability that existed among the 

personal measurements. These studies 

provide supportive evidence that 

ambient O3 concentrations from central 

monitors may serve as valid surrogate 

measures for mean personal exposures 

experienced by the population, which is 

of most relevance for time-series 

studies. A better understanding of the 

relationship between ambient 

concentrations and personal exposures, 

as well as of the other factors that affect 

relationship will improve the 

interpretation of concentrationpopulation health response associations 

observed. 

The Criteria Document (section 

7.1.3.1) also discusses the potential 

influence of exposure error on 

epidemiologic study results. Zeger et al. 

(2000) outlined the components to 

exposure measurement error, finding 

that ambient exposure can be assumed 

to be the product of the ambient 

concentration and an attenuation factor 

(i.e., building filter) and that panel 

studies and time-series studies that use 

ambient concentrations instead of 

personal exposure measurements will 

estimate a health risk that is attenuated 

by that factor. Navidi et al. (1999) used 

data from a children’s cohort study to 

compare effect estimates from a 

simulated ‘‘true’’ exposure level to 

results of analyses from O3 exposures 

determined by several methods, finding 

that O3 exposures based on the use of 

ambient monitoring data overestimate 

the individual’s O3 exposure and thus 

generally result in O3 effect estimates 

that are biased downward (EPA, 2006a, 

p. 7–8). Similarly, in a reanalysis of a 

study by Burnett et al. (1994) on the 

acute respiratory effects of ambient air 

pollution, Zidek et al. (1998) reported 

that accounting for measurement error, 

as well as making a few additional 

changes to the analysis, resulted in 

qualitatively similar conclusions, but 

the effects estimates were considerably 

larger in magnitude (EPA, 2006a, p. 7–

8). A simulation study by Sheppard et 

al. (2005) also considered attenuation of 

the risk based on personal behavior, 

their microenvironment, and the 

qualities of the pollutant in time-series 

studies. Of particular interest is their 

finding that risk estimates were not 

further attenuated in time-series studies 

even when the correlations between 

personal exposures and ambient 


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concentrations were weak. In addition 

to overestimation of exposure and the 

resulting underestimation of effects, the 

use of ambient O3 concentrations may 

obscure the presence of thresholds in 

epidemiologic studies (EPA, 2006a, p. 

7–9). 

As discussed in the Criteria Document 

(section 3.9), using ambient 

concentrations to determine exposure 

generally overestimates true personal O3

exposures by approximately 2- to 4-fold 

in available studies, resulting in 

attenuated risk estimates. The 

implication is that the effects being 

estimated occur at fairly low exposures 

and the potency of O3 is greater than 

these effects estimates indicate. As very 

few studies evaluating O3 health effects 

with personal O3 exposure 

measurements exist in the literature, 

effect estimates determined from 

ambient O3 concentrations must be 

evaluated and used with caution to 

assess the health risks of O3. In the 

absence of available data on personal O3

exposure, the use of routinely 

monitored ambient O3 concentrations as 

a surrogate for personal exposures is not 

generally expected to change the 

principal conclusions from O3

epidemiologic studies. Therefore, 

population health risk estimates derived 

using ambient O3 levels from currently 

available observational studies, with 

appropriate caveats about personal 

exposure considerations, remain useful. 

The Criteria Document recommends 

caution in the quantitative use of effect 

estimates calculated using ambient O3

concentrations as they may lead to 

underestimation of the potency of O3. 

However, the Staff Paper observes that 

the use of these risk estimates for 

comparing relative risk reductions 

between alternative ambient O3

standards considered in the risk 

assessment (discussed below in section 

II.B.2) is less likely to suffer from this 

concern. 

Confounding occurs when a health 

effect that is caused by one risk factor 

is attributed to another variable that is 

correlated with the causal risk factor; 

epidemiological analyses attempt to 

adjust or control for potential 

confounders. Copollutants (e.g., PM, 

CO, SO2 and NO2) can meet the criteria 

for potential confounding in O3-health 

associations if they are potential risk 

factors for the health effect under study 

and are correlated with O3. Effect 

modifiers include variables that may 

influence the health response to the 

pollutant exposure (e.g., co-pollutants, 

individual susceptibility, smoking or 

age). Both are important considerations 

for evaluating effects in a mixture of 

pollutants, but for confounding, the 

emphasis is on controlling or adjusting 

for potential confounders in estimating 

the effects of one pollutant, while the 

emphasis for effect modification is on 

identifying and assessing the effects for 

different modifiers. The Criteria 

Document (p. 7–148) observes that O3 is 

generally not highly correlated with 

other criteria pollutants (e.g., PM10, CO, 

SO2 and NO2), but may be more highly 

correlated with secondary fine particles, 

especially during the summer months, 

and that the degree of correlation 

between O3 and other pollutants may 

vary across seasons. For example, 

positive associations are observed 

between O3 and pollutants such as fine 

particles during the warmer months, but 

negative correlations may be observed 

during the cooler months (EPA, 2006a, 

p. 7–17). Thus, the Criteria Document 

(section 7.6.4) pays particular attention 

to the results of season-specific analyses 

and studies that assess effects of PM in 

potential confounding of O3-health 

relationships. The Criteria Document 

also discussed the limitations of 

commonly used multipollutant models 

that include the difficulty in 

interpreting results where the 

copollutants are highly colinear, or 

where correlations between pollutants 

change by season (EPA, 2006a, p. 7–

150). This is particularly the situation 

where O3 and a copollutant, such as 

sulfates, are formed under the same 

atmospheric condition; in such cases 

multipollutant models would produce 

unstable and possibly misleading results 

(EPA, 2006a, p. 7–152). 

For mortality, the results from 

numerous multi-city and single-city 

studies indicate that O3-mortality 

associations do not appear to be 

substantially changed in multipollutant 

models including PM10 or PM2.5 (EPA, 

2006a, p. 7–101; Figure 7–22). Focusing 

on results of warm season analyses, 

effect estimates for O3-mortality 

associations are fairly robust to 

adjustment for PM in multipollutant 

models (EPA, 2006a, p. 7–102; Figure 7–

23). The Criteria Document concludes 

that in the few multipollutant analyses 

conducted for these endpoints, 

copollutants generally do not confound 

the relationship between O3 and 

respiratory hospitalization (EPA, 2006a, 

p. 7–79 to 7–80; Figure 7–12). 

Multipollutant models were not used as 

commonly in studies of relationships 

between respiratory symptoms or lung 

function with O3, but the Criteria 

Document reports that results of 

available analyses indicate that such 

associations generally were robust to 

adjustment for PM2.5 (EPA, 2006a, p. 7–

154). For example, in a large multi-city 

study of asthmatic children (Mortimer et 

al., 2002), the O3 effect was attenuated, 

but there was still a positive association; 

in Gent et al. (2003), effects of O3, but 

not PM2.5, remained statistically 

significant and even increased in 

magnitude in two-pollutant models 

(EPA, 2006a, p. 7–53). Considering this 

body of studies, the Criteria Document 

concludes: ‘‘Multipollultant regression 

analyses indicated that O3 risk 

estimates, in general, were not sensitive 

to the inclusion of copollutants, 

including PM2.5 and sulfate. These 

results suggest that the effects of O3 on 

respiratory health outcomes appear to 

be robust and independent of the effects 

of other copollutants (EPA, 2006a, p. 7–

154).’’

The Criteria Document observes that 

another challenge of time-series 

epidemiological analysis is assessing the 

relationship between O3 and health 

outcomes while avoiding bias due to 

confounding by other time-varying 

factors, particularly seasonal trends and 

weather variables (EPA, 2006a, p. 7–14). 

These variables are of particular interest 

because O3 concentrations have a wellcharacterized seasonal pattern and are 

also highly correlated with changes in 

temperature, such that it can be difficult 

to distinguish whether effects are 

associated with O3 or with seasonal or 

weather variables in statistical analyses. 

The Criteria Document (section 

7.1.3.4) discusses statistical modeling 

approaches that have been used to 

adjust for time-varying factors, 

highlighting a series of analyses that 

were done in a Health Effects Institutefunded reanalysis of numerous timeseries studies. While the focus of these 

reanalyses was on associations with PM, 

a number of investigators also examined 

the sensitivity of O3 coefficients to the 

extent of adjustment for temporal trends 

and weather factors. In addition, several 

recent studies, including U.S. multi-city 

studies (Bell et al., 2005; Huang et al., 

2005; Schwartz et al., 2005) and a metaanalysis study (Ito et al., 2005), 

evaluated the effect of model 

specification on O3-mortality 

associations. As discussed in the 

Criteria Document (section 7.6.3.1), 

these studies generally report that 

associations reported with O3 are not 

substantially changed with alternative 

modeling strategies for adjusting for 

temporal trends and meteorologic 

effects. In the meta-analysis by Ito et al. 

(2005), a separate multi-city analysis 

was presented that found that 

alternative adjustments for weather 

resulted in up to 2-fold difference in the 

O3 effect estimate. Significant 

confounding can occur when strong 

seasonal cycles are present, suggesting 


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that season-specific results are more 

generally robust than year-round results 

in such cases. A number of 

epidemiological studies have conducted 

season-specific analyses, and have 

generally reported stronger and more 

precise effect estimates for O3

associations in the warm season than in 

analyses conducted in the cool seasons 

or over the full year. 

(3) Consistency refers to the persistent 

finding of an association between 

exposure and outcome in multiple 

studies of adequate power in different 

persons, places, circumstances and 

times (CDC, 2004). In considering 

results from multi-city studies and 

single-city studies in different areas, the 

Criteria Document (p. 8–41) observes 

general consistency in effects of shortterm O3 exposure on mortality, 

respiratory hospitalization and other 

respiratory health outcomes. The 

variations in effects that are observed 

may be attributable to differences in 

relative personal exposure to O3, as well 

as varying concentrations and 

composition of copollutants present in 

different regions. Thus, the Criteria 

Document (p. 8–41) concludes that 

‘‘consideration of consistency or 

heterogeneity of effects is appropriately 

understood as an evaluation of the 

similarity or general concordance of 

results, rather than an expectation of 

finding quantitative results with a very 

narrow range.’’

(4) The Staff Paper recognizes that it 

is likely that there are biological 

thresholds for different health effects in 

individuals or groups of individuals 

with similar innate characteristics and 

health status. For O3 exposure, 

individual thresholds would 

presumably vary substantially from 

person to person due to individual 

differences in genetic susceptibility, 

pre-existing disease conditions and 

possibly individual risk factors such as 

diet or exercise levels (and could even 

vary from one time to another for a 

given person). Thus, it would be 

difficult to detect a distinct threshold at 

the population level below which no 

individual would experience a given 

effect, especially if some members of a 

population are unusually sensitive even 

down to very low concentrations (EPA, 

2004, p. 9–43, 9–44). 

Some studies have tested associations 

between O3 and health outcomes after 

removal of days with higher O3 levels 

from the data set; such analyses do not 

necessarily indicate the presence or 

absence of a threshold, but provide 

some information on whether the 

relationship is found using only lowerconcentration data. For example, using 

data from 95 U.S. cities, Bell et al. 

(2004) found that the effect estimate for 

an association between short-term O3

exposure and mortality was little 

changed when days exceeding 0.060 

ppm (24-hour average) were excluded in 

the analysis. Bell et al. (2006) found no 

difference in estimated effect even when 

all days with 24-hour O3 concentrations 

<0.020 ppm were excluded (EPA, 2006a, 

p. 8–43). Using data from 8 U.S. cities, 

Mortimer and colleagues (2002) also 

reported that associations between O3

and both lung function and respiratory 

symptoms remained statistically 

significant and of the same or greater 

magnitude in effect size when 

concentrations greater than 0.080 ppm 

(8-hour average) were excluded (EPA, 

2006a, p. 7–46). Several single-city 

studies also report similar findings of 

associations that remain or are increased 

in magnitude and statistical significance 

when data at the upper end of the 

concentration range are removed (EPA, 

2006a, section 7.6.5). 

Other time-series epidemiological 

studies have used statistical modeling 

approaches to evaluate whether 

thresholds exist in associations between 

short-term O3 exposure and mortality. 

As discussed in section 7.6.5 of the 

Criteria Document, one European multicity study included evaluation of the 

shape of the concentration-response 

curve, and observed no deviation from 

a linear function across the range of O3

measurements from the study (Gryparis 

et al., 2004; EPA, 2006a, p. 7–154). 

Several single-city studies also observed 

a monotonic increase in associations 

between O3 and morbidity that suggest 

that no population threshold exists 

(EPA, 2006a, p. 7–159). 

On the other hand, a study in Korea 

used several different modeling 

approaches and reported that a 

threshold model provided the best fit for 

the data. The results suggested a 

potential threshold level of about 0.045 

ppm (1-hour maximum concentration; 

<0.035 ppm, 8-hour average) for an 

association between mortality and shortterm O3 exposure during the summer 

months (Kim et al., 2004; EPA, 2006a, 

p. 8–43). The authors reported larger 

effect estimates for the association for 

data above the potential threshold level, 

suggesting that an O3-mortality 

association might be underestimated in 

the non-threshold model. A threshold 

analysis recently reported by Bell et al. 

(2006) for 98 U.S. communities, 

including the same 95 communities in 

Bell et al. (2004), indicated that if a 

population threshold existed for 

mortality, it would likely fall below a 

24-hour average O3 concentration of 

0.015 ppm (<0.025 ppm, 8-hour 

average). In addition, Burnett and 

colleagues (1997a,b) plotted the 

relationships between air pollutant 

concentrations and both respiratory and 

cardiovascular hospitalization, and it 

appears in these results that the 

associations with O3 are found in the 

concentration range above about 0.030 

ppm (1-hour maximum; <0.025 ppm, 8- 

hour average). Vedal and colleagues 

(2003) reported a significant association 

between O3 and mortality in British 

Columbia where O3 concentrations were 

quite low (mean 1-hour maximum 

concentration of 0.0273 ppm). The 

authors did not specifically test for 

threshold levels, but the fact that the 

association was found in an area with 

such low O3 concentrations suggests 

that any potential threshold level would 

be quite low in this data set. 

In summary, the Criteria Document 

finds that, taken together, the available 

evidence from clinical and 

epidemiological studies suggests that no 

clear conclusion can now be reached 

with regard to possible threshold levels 

for O3-related effects (EPA, 2006a, p. 8–

44). Thus, the available epidemiological 

evidence neither supports nor refutes 

the existence of thresholds at the 

population level for effects such as 

increased hospital admissions and 

premature mortality. There are 

limitations in epidemiological studies 

that make discerning thresholds in 

populations difficult, including low 

data density in the lower concentration 

ranges, the possible influence of 

exposure measurement error, and 

interindividual differences in 

susceptibility to O3-related effects in 

populations. There is the possibility that 

thresholds for individuals may exist in 

reported associations at fairly low levels 

within the range of air quality observed 

in the studies but not be detectable as 

population thresholds in 

epidemiological analyses. 

b. Biological Plausibility and Coherence 

of Evidence 

The body of epidemiological studies 

discussed in the Staff Paper emphasizes 

the role of O3 in association with a 

variety of adverse respiratory and 

cardiovascular effects. While 

recognizing a variety of plausible 

mechanisms, there exists a general 

consensus suggesting that O3 could, 

either directly or through initiation, 

interfere with basic cellular oxidation 

processes responsible for inflammation, 

reduced antioxidant capacity, 

atherosclerosis and other effects. 

Reasoning that O3 influences cellular 

chemistry through basic oxidative 

properties (as opposed to a unique 

chemical interaction), other reactive 

oxidizing species (ROS) in the 


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21Results for studies of respiratory symptoms are 

presented as odds ratios; an odds ratio of 1.0 is 

equivalent to no effect, and thus is presented as 

equivalent to the zero effect estimate line. 

atmosphere acting either independently 

or in combination with O3 may also 

contribute to a number of adverse 

respiratory and cardiovascular health 

effects. Consequently, the role of O3

should be considered more broadly as 

O3 behaves as a generator of numerous 

oxidative species in the atmosphere. 

In considering the biological 

plausibility of reported O3-related 

effects, the Staff Paper (section 3.4.6) 

considers this broader question of 

health effects of pollutant mixtures 

containing O3. The potential for O3- 

related enhancements of PM formation, 

particle uptake, and exacerbation of PMinduced cardiovascular effects 

underscores the importance of 

considering contributions of O3

interactions with other often cooccurring air pollutants to health effects 

due to O3-containing pollutant mixes. 

The Staff Paper summarizes some 

examples of important pollutant 

mixture effects from studies that 

evaluate interactions of O3 with other 

co-occurring pollutants, as discussed in 

chapters 4, 5, and 6 of the Criteria 

Document. 

All of the types of interactive effects 

of O3 with other co-occurring gaseous 

and nongaseous viable and nonviable 

PM components of ambient air mixes 

noted above argue that O3 acts not only 

alone but that O3 also is a surrogate 

indicator for air pollution mixes which 

may enhance the risk of adverse effects 

due to O3 acting in combination with 

other pollutants. Viewed from this 

perspective, those epidemiologic 

findings of morbidity and mortality 

associations, with ambient O3

concentrations extending to quite low 

levels in many cases, become more 

understandable and plausible. 

The Criteria Document integrates 

epidemiological studies with 

mechanistic information from 

controlled human exposure studies and 

animal toxicological studies to draw 

conclusions regarding the coherence of 

evidence and biological plausibility of 

O3-related health effects to reach 

judgments about the causal nature of 

observed associations. As summarized 

below, coherence and biological 

plausibility are discussed for each of the 

following types of O3-related effects: 

short-term effects on the respiratory 

system, effects on the cardiovascular 

system, effects related to long-term O3

exposure, and short-term mortalityrelated health endpoints. 

i. Coherence and Plausibility of ShortTerm Effects on the Respiratory System 

Acute respiratory morbidity effects 

that have been associated with shortterm exposure to O3 include such health 

endpoints as decrements in lung 

function, increased airway 

responsiveness, airway inflammation, 

increased permeability related to 

epithelial injury, immune system 

effects, emergency department visits for 

respiratory diseases, and hospitalization 

due to respiratory illness. 

Recent epidemiological studies have 

supported evidence available in the 

previous O3 NAAQS review on 

associations between ambient O3

exposure and decline in lung function 

for children. The Criteria Document (p. 

8–34) concludes that exposure to 

ambient O3 has a significant effect on 

lung function and is associated with 

increased respiratory symptoms and 

medication use, particularly in 

asthmatics. Short-term exposure to O3

has also been associated with more 

severe morbidity endpoints, such as 

emergency department visits and 

hospital admissions for respiratory 

cases, including specific respiratory 

illness (e.g., asthma) (EPA, 2006a, 

sections 7.3.2 and 7.3.3). In addition, a 

few epidemiological studies have 

reported positive associations between 

short-term O3 exposure and respiratory 

mortality, though the associations are 

not generally statistically significant 

(EPA, 2006a, p. 7–108). 

Considering the evidence from 

epidemiological studies, the results 

described above provide evidence for 

coherence in O3-related effects on the 

respiratory system. Effect estimates from 

U.S. and Canadian studies are shown in 

Figure 1, where it can be seen that 

mostly positive associations have been 

reported with respiratory effects ranging 

from respiratory symptoms, such as 

cough or wheeze, to hospitalization for 

various respiratory diseases, and there is 

suggestive evidence for associations 

with respiratory mortality. Many of the 

reported associations are statistically 

significant, particularly in the warm 

season. In Figure 1, the central effect 

estimate is indicated by a square for 

each result, with the vertical bar 

representing the 95 percent confidence 

interval around the estimate. In the 

discussions that follow, an individual 

study result is considered to be 

statistically significant if the 95 percent 

confidence interval does not include 

zero.21 Positive effect estimates indicate 

increases in the health outcome with O3

exposure. In considering these results as 

a whole, it is important to consider not 

only whether statistical significance at 

the 95 percent confidence level is 

reported in individual studies but also 

the general pattern of results, focusing 

in particular on studies with greater 

statistical power that report relatively 

more precise results. 

BILLING CODE 6560–50–P 


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BILLING CODE 6560–50–C 

Considering also evidence from 

toxicological, chamber, and field 

studies, the Criteria Document (section 

8.6) discusses biological plausibility and 

coherence of evidence for acute O3- 

induced respiratory health effects. 

Inhalation of O3 for several hours while 

subjects are physically active can elicit 

both acute adverse pathophysiological 

changes and subjective respiratory tract 

symptoms (EPA, 2006a, section 8.4.2). 

Acute pulmonary responses observed in 

healthy humans exposed to O3 at 

ambient concentrations include: 

decreased inspiratory capacity; mild 

bronchoconstriction; rapid, shallow 

breathing during exercise; subjective 

symptoms of tracheobronchial airway 

irritation, including cough and pain on 

deep inspiration; decreases in measures 

of lung function; and increased airway 

resistance. The severity of symptoms 

and magnitude of response depends on 

inhaled dose, individual O3 sensitivity, 

and the degree of attenuation or 

enhancement of response resulting from 

previous O3 exposures. Lung function 

studies of several animal species acutely 

exposed to relatively low O3 levels (0.25 

to 0.4 ppm) show responses similar to 

those observed in humans, including 

increased breathing frequency, 

decreased tidal volume, increased 

resistance, and decreased FVC. 

Alterations in breathing pattern return 

to normal within hours of exposure, and 

attenuation in functional responses 


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following repeated O3 exposures is 

similar to those observed in humans. 

Physiological and biochemical 

alterations investigated in controlled 

human exposure and animal toxicology 

studies tend to support certain 

hypotheses of underlying pathological 

mechanisms which lead to the 

development of respiratory-related 

effects reported in epidemiology studies 

(e.g., increased hospitalization and 

medication use). Some of these are: (a) 

Decrements in lung function, (b) 

bronchoconstriction, (c) increased 

airway responsiveness, (d) airway 

inflammation, (e) epithelial injury, (f) 

immune system activation, (g) host 

defense impairment, and (h) sensitivity 

of individuals, which depends on at 

least a person’s age, disease status, 

genetic susceptibility, and the degree of 

attenuation present due to prior 

exposures. The time sequence, 

magnitude, and overlap of these 

complex events, both in terms of 

development and recovery, illustrate the 

inherent difficulty of interpreting the 

biological plausibility of O3-induced 

cardiopulmonary health effects (EPA, 

2006a, p. 8–48). 

The interaction of O3 with airway 

epithelial cell membranes and ELF to 

form lipid ozonation products and ROS 

is supported by numerous human, 

animal and in vitro studies. Ozonation 

products and ROS initiate a cascade of 

events that lead to oxidative stress, 

injury, inflammation, airway epithelial 

damage and increased epithelial damage 

and increased alveolar permeability to 

vascular fluids. Repeated respiratory 

inflammation can lead to a chronic 

inflammatory state with altered lung 

structure and lung function and may 

lead to chronic respiratory diseases such 

as fibrosis and emphysema (EPA, 2006a, 

section 8.6.2). Continued respiratory 

inflammation also can alter the ability to 

respond to infectious agents, allergens 

and toxins. Acute inflammatory 

responses to O3 are well documented, 

and lung injury can become apparent 

within 3 hours after exposure in 

humans. 

Taken together, the Criteria Document 

concludes that the evidence from 

experimental human and animal 

toxicology studies indicates that acute 

O3 exposure is causally associated with 

respiratory system effects, including O3- 

induced pulmonary function 

decrements, respiratory symptoms, lung 

inflammation, and increased lung 

permeability, airway 

hyperresponsiveness, increased uptake 

of nonviable and viable particles, and 

consequent increased susceptibility to 

PM-related toxic effects and respiratory 

infections (EPA, 2006a, p. 8–48). 

ii. Coherence and Plausibility of Effects 

on the Cardiovascular System 

There is very limited experimental 

evidence of animals and humans that 

has evaluated possible mechanisms or 

physiological pathways by which acute 

O3 exposures may induce 

cardiovascular system effects. Ozone 

induces lung injury, inflammation, and 

impaired mucociliary clearance, with a 

host of associated biochemical changes 

all leading to increased lung epithelial 

permeability. As noted above in section 

II.A.2.b, the generation of lipid 

ozonation products and ROS in lung 

tissues can influence pulmonary 

hemodynamics, and ultimately the 

cardiovascular system. Other potential 

mechanisms by which O3 exposure may 

be associated with cardiovascular 

disease outcomes have been described. 

Laboratory animals exposed to relatively 

high O3 concentrations (≥0.5 ppm) 

demonstrate tissue edema in the heart 

and lungs. Ozone-induced changes in 

heart rate, edema of heart tissue, and 

increased tissue and serum levels of 

ANF found with 8-hour 0.5 ppm O3

exposure in animal toxicology studies 

(Vesely et al., 1994a, b, c) also raise the 

possibility of potential cardiovascular 

effects of acute ambient O3 exposures. 

Animal toxicology studies have found 

both transient and persistent ventilatory 

responses with and without progressive 

decreases in heart rate (Arito et al., 

1997). Observations of O3-induced 

vasoconstriction in a controlled human 

exposure study by Brook et al. (2002) 

suggests another possible mechanism 

for O3-related exacerbations of 

preexisting cardiovascular disease. One 

controlled human study (Gong et al., 

1998) evaluated potential cardiovascular 

health effects of O3 exposure. The 

overall results did not indicate acute 

cardiovascular effects of O3 in either the 

hypertensive or control subjects. The 

authors observed an increase in ratepressure product and heart rate, a 

decrement for FEV1, and a >10 mm Hg 

increase in the alveolar/arterial pressure 

difference for O2 following O3 exposure. 

Foster et al. (1993) demonstrated that 

even in relatively young healthy adults, 

O3 exposure can cause ventilation to 

shift away from the well-perfused basal 

lung. This effect of O3 on ventilation 

distribution may persist beyond 24- 

hours post-exposure (Foster et al., 

1997). These findings suggest that O3

may exert cardiovascular effects 

indirectly by impairing alveolar-arterial 

O2 transfer and potentially reducing O2

supply to the myocardium. Ozone 

exposure may increase myocardial work 

and impair pulmonary gas exchange to 

a degree that could perhaps be clinically 

important in persons with significant 

preexisting cardiovascular impairment. 

As noted above in section II.A.2.b, a 

limited number of new epidemiological 

studies have reported associations 

between short-term O3 exposure and 

effects on the cardiovascular system. 

Among these studies, three were 

population-based and involved 

relatively large cohorts; two of these 

studies evaluated associations between 

O3 and heart rate variability (HRV) and 

the other study evaluated the 

association between O3 levels and the 

relative risk of myocardial infarction 

(MI). Such studies may offer more 

informative results based on their large 

subject-pool and design. Results from 

these three studies were suggestive of an 

association between O3 exposure and 

the cardiovascular endpoints studied. In 

other recent studies on the incidence of 

MI and some more subtle cardiovascular 

health endpoints, such as changes in 

HRV or cardiac arrhythmia, some but 

not all studies reported associations 

with short-term exposure to O3 (EPA, 

2006a, section 7.2.7.1). From these 

studies, the Criteria Document 

concludes that the ‘‘current evidence is 

rather limited but suggestive of a 

potential effect on HRV, ventricular 

arrhythmias, and MI incidence’’ (EPA, 

2006a, p. 7–65). 

An increasing number of studies have 

evaluated the association between O3

exposure and cardiovascular hospital 

admissions. As discussed in section 

7.3.4 of the Criteria Document, many 

reported negative or inconsistent 

associations, whereas other studies, 

especially those that examined the 

relationship when O3 exposures were 

higher, have found positive and robust 

associations between O3 and 

cardiovascular hospital admissions. The 

Criteria Document finds that the overall 

evidence from these studies remains 

inconclusive regarding the effect of O3

on cardiovascular hospitalizations (EPA, 

2006a, p. 7–83). 

The Criteria Document notes that the 

suggestive positive epidemiologic 

findings of O3 exposure on cardiac 

autonomic control, including effects on 

HRV, ventricular arrhythmias and MI, 

and reported associations between O3

exposure and cardiovascular 

hospitalizations generally in the warm 

season gain credibility and scientific 

support from the results of experimental 

animal toxicology and human clinical 

studies, which are indicative of 

plausible pathways by which O3 may 

exert cardiovascular effects (EPA, 2006a, 

section 8.6.1). 


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iii. Coherence and Plausibility of Effects 

Related to Long-Term O3 Exposure 

Human chamber studies can not 

evaluate effects of long-term exposures 

to O3; there is some evidence available 

from toxicological studies. While early 

animal toxicology studies of long-term 

O3 exposures were conducted using 

continuous exposures, more recent 

studies have focused on exposures 

which mimic diurnal and seasonal 

patterns and more realistic O3 exposure 

levels (EPA, 2006a, p. 8–50). Studies of 

monkeys that compared these two 

exposure scenarios found increased 

airway pathology only with the latter 

design. Persistent and irreversible 

effects reported in chronic animal 

toxicology studies suggest that 

additional complementary human data 

are needed from epidemiologic studies 

(EPA, 2006a, p. 8–50). 

There is limited evidence from human 

studies for long-term O3-induced effects 

on lung function. As discussed in 

section 8.6.2 of the Criteria Document, 

previous epidemiological studies have 

provided only inconclusive evidence for 

either mortality or morbidity effects of 

long-term O3 exposure. The Criteria 

Document observes that the 

inconsistency in findings may be due to 

a lack of precise exposure information, 

the possibility of selection bias, and the 

difficulty of controlling for confounders 

(EPA, 2006a, p. 8–50). Several new 

longitudinal epidemiology studies have 

evaluated associations between longterm O3 exposures and morbidity and 

mortality and suggest that these longterm exposures may be related to 

changes in lung function in children; 

however, little evidence is available to 

support a relationship between chronic 

O3 exposure and mortality or lung 

cancer incidence (EPA, 2006a, p. 8–50). 

The Criteria Document (p. 8–51) 

concludes that evidence from animal 

toxicology studies strongly suggests that 

chronic O3 exposure is capable of 

damaging the distal airways and 

proximal alveoli, resulting in lung tissue 

remodeling leading to apparent 

irreversible changes. Such structural 

changes and compromised pulmonary 

function caused by persistent 

inflammation may exacerbate the 

progression and development of chronic 

lung disease. Together with the limited 

evidence available from epidemiological 

studies, these findings offer some 

insight into potential biological 

mechanisms for suggested associations 

between long-term or seasonal 

exposures to O3 and reduced lung 

function development in children 

which have been observed in 

epidemiologic studies (EPA, 2006a, 

p. 8–51). 

iv. Coherence and Plausibility of ShortTerm Mortality-Related Health 

Endpoints 

An extensive epidemiological 

literature on air pollution related 

mortality risk estimates from the U.S., 

Canada, and Europe is discussed in the 

Criteria Document (sections 7.4 and 

8.6.3). These single- and multi-city 

mortality studies coupled with metaanalyses generally indicate associations 

between acute O3 exposure and elevated 

risk for all-cause mortality, even after 

adjustment for the influence of season 

and PM. Several single-city studies that 

specifically evaluated the relationship 

between O3 exposure and 

cardiopulmonary mortality also 

reported results suggestive of a positive 

association (EPA, 2006a, p. 8–51). These 

mortality studies suggest a pattern of 

effects for causality that have 

biologically plausible explanations, but 

our knowledge regarding potential 

underlying mechanisms is very limited 

at this time and requires further 

research. Most of the physiological and 

biochemical parameters investigated in 

human and animal studies suggest that 

O3-induced biochemical effects are 

relatively transient and attenuate over 

time. The Criteria Document (p. 8–52) 

hypothesizes a generic pathway of O3- 

induced lung damage, potentially 

involving oxidative lung damage with 

subsequent inflammation and/or decline 

in lung function leading to respiratory 

distress in some sensitive population 

groups (e.g., asthmatics), or other 

plausible pathways noted below that 

may lead to O3-related contributions to 

cardiovascular effects that ultimately 

increase risk of mortality. 

The third National Health and 

Nutrition Examination Follow-up data 

analysis indicates that about 20 percent 

of the adult population has reduced 

FEV1 values, suggesting impaired lung 

function in some portion of the 

population. Most of these individuals 

have COPD, asthma or fibrotic lung 

disease (Manino et al., 2003), which are 

associated with persistent low-grade 

inflammation. Furthermore, patients 

with COPD are at increased risk for 

cardiovascular disease. Also, lung 

disease with underlying inflammation 

may be linked to low-grade systemic 

inflammation associated with 

atherosclerosis, independent of cigarette 

smoking (EPA, 2006a, p. 8–52). Lung 

function decrements in persons with 

cardiopulmonary disease have been 

associated with inflammatory markers, 

such as C-reactive protein (CRP) in the 

blood. At a population level it has been 

found that individuals with the lowest 

FEV1 values have the highest levels of 

CRP, and those with the highest FEV1

values have the lowest CRP levels 

(Manino et al., 2003; Sin and Man, 

2003). This complex series of 

physiological and biochemical reactions 

following O3 exposure may tilt the 

biological homeostasis mechanisms 

which could lead to adverse health 

effects in people with compromised 

cardiopulmonary systems. 

Of much interest are several other 

types of newly available data that 

support reasonable hypotheses that may 

help to explain the findings of O3- 

related increases in cardiovascular 

mortality observed in some 

epidemiological studies. These include 

the direct effect of O3 on increasing PAF 

in lung tissue that can then enter the 

general circulation and possibly 

contribute to increased risk of blood clot 

formation and the consequent increased 

risk of MI, cerebrovascular events 

(stroke), or associated cardiovascularrelated mortality. Ozone reactions with 

cholesterol in lung surfactant to form 

epoxides and oxysterols that are 

cytotoxic to lung and heart muscles and 

that contribute to atherosclerotic plaque 

formation in arterial walls represent 

another potential pathway. Stimulation 

of airway irritant receptors may lead to 

increases in tissue and serum levels of 

ANF, changes in heart rate, and edema 

of heart tissue. A few new field and 

panel studies of human adults have 

reported associations between ambient 

O3 concentrations and changes in 

cardiac autonomic control (e.g., HRV, 

ventricular arrhythmias, and MI). These 

represent plausible pathways that may 

lead to O3-related contributions to 

cardiovascular effects that ultimately 

increase the risk of mortality. 

In addition, O3-induced increases in 

lung permeability allow more ready 

entry for inhaled PM into the blood 

stream, and O3 exposure may increase 

the risk of PM-related cardiovascular 

effects. Furthermore, increased ambient 

O3 levels contribute to ultrafine PM 

formation in the ambient air and indoor 

environments. Thus, the contributions 

of elevated ambient O3 concentrations to 

ultrafine PM formation and human 

exposure, along with the enhanced 

uptake of inhaled fine particles, 

consequently may contribute to 

exacerbation of PM-induced 

cardiovascular effects in addition to 

those more directly induced by O3 (EPA, 

2006a, p. 8–53). 

c. Summary 

Judgments concerning the extent to 

which relationships between various 

health endpoints and ambient O3


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exposures are likely causal are informed 

by the conclusions and discussion in 

the Criteria Document as discussed 

above and summarized in section 3.7.5 

of the Staff Paper. These judgments 

reflect the nature of the evidence and 

overall weight of the evidence, and are 

taken into consideration in the 

quantitative risk assessment discussed 

below in section II.B.2. 

For example, there is a very high level 

of confidence that O3 induces lung 

function decrements in healthy adults 

and children due in part to the dozens 

of controlled human exposure and 

epidemiological studies consistently 

showing such effects. The Criteria 

Document (p. 8–74) states that these 

studies provide clear evidence of 

causality for associations between shortterm O3 exposures and statistically 

significant declines in lung function in 

children, asthmatics and adults who 

exercise outdoors. An increase in 

respiratory symptoms (e.g., cough, 

shortness of breath) has been observed 

in controlled human exposure studies of 

short-term O3 exposures, and significant 

associations between ambient O3

exposures and a wide variety of 

symptoms have been reported in 

epidemiology studies (EPA, 2006a, p. 8–

75). Aggregate population time-series 

studies showing robust associations 

with respiratory hospital admissions 

and emergency department visits are 

strongly supported by human clinical, 

animal toxicologic, and epidemiologic 

evidence for O3-related lung function 

decrements, respiratory symptoms, 

airway inflammation, and airway 

hyperreactivity. The Criteria Document 

(p. 8–77) concludes that, taken together, 

the overall evidence supports the 

inference of a causal relationship 

between acute ambient O3 exposures 

and increased respiratory morbidity 

outcomes resulting in increased 

emergency department visits and 

hospitalizations during the warm 

season. Further, recent epidemiologic 

evidence has been characterized in the 

Criteria Document (p. 8–78) as highly 

suggestive that O3 directly or indirectly 

contributes to non-accidental and 

cardiopulmonary-related mortality. 

4. O3-Related Impacts on Public Health 

The following discussion draws from 

chapters 6 and 7 and section 8.7 of the 

Criteria Document and section 3.6 of the 

Staff Paper to characterize factors which 

modify responsiveness to O3, 

subpopulations potentially at risk for 

O3-related health effects, the adversity 

of O3-related effects, and the size of the 

at-risk subpopulations in the U.S. These 

considerations are all important 

elements in characterizing the potential 

public health impacts associated with 

exposure to ambient O3. 

a. Factors That Modify Responsiveness 

to Ozone 

There are numerous factors that can 

modify individual responsiveness to O3. 

These include: influence of physical 

activity; age; gender and hormonal 

influences; racial, ethnic and 

socioeconomic status (SES) factors; 

environmental factors; and oxidantantioxidant balance. These factors are 

discussed in more detail in section 6.5 

of the Criteria Document. 

It is well established that physical 

activity increases an individual’s 

minute ventilation and will thus 

increase the dose of O3 inhaled (EPA, 

2006a, section 6.5.4). Increased physical 

activity results in deeper penetration of 

O3 into more distal regions of the lungs, 

which are more sensitive to acute O3

response and injury. This will result in 

greater lung function decrements for 

acute exposures of individuals during 

increased physical activity. Research 

has shown that respiratory effects are 

observed at lower O3 concentrations if 

the level of exertion is increased and/or 

duration of exposure and exertion are 

extended. Predicted O3-induced 

decrements in lung function have been 

shown to be a function of exposure 

concentration, duration and exercise 

level for healthy, young adults 

(McDonnell et al., 1997). 

Most of the studies investigating the 

influence of age have used lung function 

decrements and symptoms as measures 

of response. For healthy adults, lung 

function and symptom responses to O3

decline as age increases. The rate of 

decline in O3 responsiveness appears 

greater in those 18 to 35 years old 

compared to those 35 to 55 years old, 

while there is very little change after age 

55. In one study (Seal et al., 1996) 

analyzing a large data set, a 5.4% 

decrement in FEV1 was estimated for 20 

year old individuals exposed to 0.12 

ppm O3, whereas similar exposure of 35 

year old individuals were estimated to 

have a 2.6% decrement. While healthy 

children tend not to report respiratory 

symptoms when exposed to low levels 

of O3, for subjects 18 to 36 years old 

symptom responses induced by O3 tend 

to decrease with increasing age 

(McDonnell et al., 1999). 

Limited evidence of gender 

differences in response to O3 exposure 

has suggested that females may be 

predisposed to a greater susceptibility to 

O3. Lower plasma and NL fluid levels of 

the most prevalent antioxidant, uric 

acid, in females relative to males may be 

a contributing factor. Consequently, 

reduced removal of O3 in the upper 

airways may promote deeper 

penetration. However, most of the 

evidence on gender differences appears 

to be equivocal, with one study 

(Hazucha et al., 2003) suggesting that 

physiological responses of young 

healthy males and females may be 

comparable (EPA, 2006a, section 6.5.2). 

A few studies have suggested that 

ethnic minorities might be more 

responsive to O3 than Caucasian 

population groups (EPA, 2006a, section 

6.5.3). This may be more the result of a 

lack of adequate health care and 

socioeconomic status (SES) than any 

differences in sensitivity to O3. The 

limited data available, which have 

investigated the influence of race, ethnic 

or other related factors on 

responsiveness to O3, prevent drawing 

any clear conclusions at this time. 

Few human studies have examined 

the potential influence of environmental 

factors such as the sensitivity of 

individuals who voluntarily smoke 

tobacco (i.e., smokers) and the effect of 

high temperatures. New controlled 

human exposure studies have confirmed 

that smokers are less responsive to O3

than nonsmokers; however, time course 

of development and recovery of these 

effects, as well as reproducibility, was 

not different from nonsmokers (EPA, 

2006a, section 6.5.5). Influence of 

ambient temperature on pulmonary 

effects induced by O3 has been studied 

very little, but additive effects of heat 

and O3 exposure have been reported. 

Antioxidants, which scavenge free 

radicals and limit lipid peroxidation in 

the ELF, are the first line of defense 

against oxidative stress. Ozone exposure 

leads to absorption of O3 in the ELF 

with subsequent depletion of 

antioxidant in the nasal ELF, but 

concentration and antioxidant enzyme 

activity in ELF or plasma do not appear 

related to O3 responsiveness (EPA 

2006a, section 6.5.6). Controlled studies 

of dietary antioxidant supplements have 

shown some protective effects on lung 

function decrements but not on 

symptoms and airway inflammatory 

responses. Dietary antioxidant 

supplements have provided some 

protection to asthmatics by attenuating 

post-exposure airway 

hyperresponsiveness. Animal studies 

have also supported the protective 

effects of ELF antioxidants. 

b. At-Risk Subgroups for O3-Related 

Effects 

Several characteristics may increase 

the extent to which a population group 

shows increased susceptibility or 

vulnerability. Information on potentially 

susceptible and vulnerable groups is 

summarized in section 8.7 of the 


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22 In the Staff Paper and documents from previous 

O3 NAAQS reviews, ‘‘at-risk’’ groups have also been 

called ‘‘sensitive’’ groups, to mean both groups with 

greater inherent susceptibility and those more likely 

to be exposed. 

Criteria Document. As described there, 

the term susceptibility refers to innate 

(e.g., genetic or developmental) or 

acquired (e.g., personal risk factors, age) 

factors that make individuals more 

likely to experience effects with 

exposure to pollutants. A number of 

population groups have been identified 

as potentially susceptible to health 

effects as a result of O3 exposure, 

including people with existing lung 

diseases, including asthma, children 

and older adults, and people who have 

larger than normal lung function 

responses that may be due to genetic 

susceptibility. In addition, some 

population groups have been identified 

as having increased vulnerability to O3- 

related effects due to increased 

likelihood of exposure while at elevated 

ventilation rates, including healthy 

children and adults who are active 

outdoors, for example, outdoor workers, 

and joggers. Taken together, the 

susceptible and vulnerable groups make 

up ‘‘at-risk’’ groups.22

i. Active People 

A large group of individuals at risk 

from O3 exposure consists of outdoor 

workers and children, adolescents, and 

adults who engage in outdoor activities 

involving exertion or exercise during 

summer daylight hours when ambient 

O3 concentrations tend to be higher. 

This conclusion is based on a large 

number of controlled-human exposure 

studies and several epidemiologic field/ 

panel studies which have been 

conducted with healthy children and 

adults and those with preexisting 

respiratory diseases (EPA 2006a, 

sections 6.2, 6.3, 7.2, and 8.4.4). The 

controlled human exposure studies 

show a clear O3 exposure-response 

relationship with increasing spirometric 

and symptomatic response as exercise 

level increases. Furthermore, O3- 

induced response increases as time of 

exposure increases. Studies of outdoor 

workers and others who participate in 

outdoor activities indicate that extended 

exposures to O3 at elevated exertion 

levels can produce marked effects on 

lung function, as discussed above in 

section IIA.2 (Brauer et al., 1996; Ho ̈ppe 

et al., 1995; Korrick et al., 1998; 

McConnell et al., 2002). 

These field studies with subjects at 

elevated exertion levels support the 

extensive evidence derived from 

controlled human exposure studies. The 

majority of human chamber studies 

have examined the effects of O3

exposure in subjects performing 

continuous or intermittent exercise for 

variable periods of time. Significant O3- 

induced respiratory responses have 

been observed in clinical studies of 

exercising individuals. The 

epidemiologic studies discussed above 

also indicate that prolonged exposure 

periods, combined with elevated levels 

of exertion or exercise, may magnify O3

effects on lung function. Thus, outdoor 

workers and others who participate in 

higher exertion activities outdoors 

during the time of day when high peak 

O3 concentrations occur appear to be 

particularly vulnerable to O3 effects on 

respiratory health. Although these 

studies show a wide variability of 

response and sensitivity among subjects 

and the factors contributing to this 

variability continue to be incompletely 

understood, the effect of increased 

exertion is consistent. It should be noted 

that this wide variability of response 

and sensitivity among subjects may be 

in part due to the wide range of other 

highly reactive photochemical oxidants 

coexisting with O3 in the ambient air. 

ii. People With Lung Disease 

People with preexisting pulmonary 

disease are 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. At the 

time of the last review, it was concluded 

that this group was at greater risk 

because the impact of O3-induced 

responses on already-compromised 

respiratory systems would noticeably 

impair an individual’s ability to engage 

in normal activity or would be more 

likely to result in increased selfmedication or medical treatment. At 

that time there was little evidence that 

people with pre-existing disease were 

more responsive than healthy 

individuals in terms of the magnitude of 

pulmonary function decrements or 

symptomatic responses. The new results 

from controlled exposure and 

epidemiologic studies continue to 

indicate that individuals with 

preexisting pulmonary disease are a 

sensitive subpopulation for O3 health 

effects. 

Several clinical studies reviewed in 

the 1996 Criteria Document on atopic 

and asthmatic subjects had suggested 

but not clearly demonstrated enhanced 

responsiveness to acute O3 exposure 

compared to healthy subjects. The 

majority of the newer studies reviewed 

in Chapter 6 of the Criteria Document 

indicate that asthmatics are as sensitive 

as, if not more sensitive than, normal 

subjects in manifesting O3-induced 

pulmonary function decrements. In one 

key study (Horstman et al., 1995), the 

FEV1 decrement observed in the 

asthmatics was significantly larger than 

in the healthy subjects (19% versus 

10%, respectively). There was also a 

notable tendency for a greater O3- 

induced decrease in FEF25–75 in 

asthmatics relative to the healthy 

subjects (24% versus 15%, 

respectively). A significant positive 

correlation in asthmatics was also 

reported between O3-induced 

spirometric responses and baseline lung 

function, i.e., responses increased with 

severity of disease. 

Asthmatics present a differential 

response profile for cellular, molecular, 

and biochemical parameters (Criteria 

Document, Figure 8–1) that are altered 

in response to acute O3 exposure. 

Ozone-induced increases in neutrophils, 

IL–8 and protein were found to be 

significantly higher in the BAL fluid 

from asthmatics compared to healthy 

subjects, suggesting mechanisms for the 

increased sensitivity of asthmatics 

(Basha et al., 1994; McBride et al., 1994; 

Scannell et al., 1996; Hiltermann et al., 

1999; Holz et al., 1999; Bosson et al., 

2003). Neutrophils, or PMNs, are the 

white blood cell most associated with 

inflammation. IL–8 is an inflammatory 

cytokine with a number of biological 

effects, primarily on neutrophils. The 

major role of this cytokine is to attract 

and activate neutrophils. Protein in the 

airways is leaked from the circulatory 

system, and is a marker for increased 

cellular permeability. 

Bronchial constriction following 

provocation with O3 and/or allergens 

presents a two-phase response. The 

early response is mediated by release of 

histamine and leukotrienes that leads to 

contraction of smooth muscle cells in 

the bronchi, narrowing the lumen and 

decreasing the airflow. In people with 

allergic airway disease, including 

people with rhinitis and asthma, these 

mediators also cause accumulation of 

eosinophils in the airways (Bascom et 

al., 1990; Jorres et al., 1996; Peden et al., 

1995 and 1997; Frampton et al., 1997a; 

Michelson et al., 1999; Hiltermann et 

al., 1999; Holz et al., 2002; Vagaggini et 

al., 2002). In asthma, the eosinophil, 

which increases inflammation and 

allergic responses, is the cell most 

frequently associated with exacerbations 

of the disease. A study by Bosson et al. 

(2003) evaluated the difference in O3- 

induced bronchial epithelial cytokine 

expression between healthy and 

asthmatic subjects. After O3 exposure 

the epithelial expression of IL–5 and 

GM-CSF increased significantly in 


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asthmatics, compared to healthy 

subjects. Asthma is associated with Th2- 

related airway response (allergic 

response), and IL–5 is an important 

Th2-related cytokine. The O3-induced 

increase in IL–5, and also in GM-CSF, 

which affects the growth, activation and 

survival of eosinophils, may indicate an 

effect on the Th2-related airway 

response and on airway eosinophils. 

The authors reported that the O3- 

induced Th2-related cytokine responses 

that were found within the asthmatic 

group may indicate a worsening of their 

asthmatic airway inflammation and thus 

suggest a plausible link to 

epidemiological data indicating O3- 

associated increases in bronchial 

reactivity and hospital admissions. 

The accumulation of eosinophils in 

the airways of asthmatics is followed by 

production of mucus and a late-phase 

bronchial constriction and reduced 

airflow. In a study of 16 intermittent 

asthmatics, Hiltermann et al. (1999) 

found that there was a significant 

inverse correlation between the O3- 

induced change in the percentage of 

eosinophils in induced sputum and the 

change in PC20, the concentration of 

methacholine causing a 20% decrease in 

FEV1. Characteristic O3-induced 

inflammatory airway neutrophilia at one 

time was considered a leading 

mechanism of airway 

hyperresponsiveness. However, 

Hiltermann et al. (1999) determined that 

the O3-induced change in percentage 

neutrophils in sputum was not 

significantly related to the change in 

PC20. These results are consistent with 

the results of Zhang et al. (1995), which 

found neutrophilia in a murine model to 

be only coincidentally associated with 

airway hyperresponsiveness, i.e., there 

was no cause and effect relationship. 

(Criteria Document, AX 6–26). 

Hiltermann et al. (1999) concluded that 

the results point to the role of 

eosinophils in O3-induced airway 

hyperresponsiveness. Increases in O3- 

induced nonspecific airway 

responsiveness incidence and duration 

could have important clinical 

implications for asthmatics. 

Two studies (Jo ̈rres et al., 1996; Holz 

et al., 2002) observed increased airway 

responsiveness to O3 exposure with 

bronchial allergen challenge in subjects 

with preexisting allergic airway disease. 

Jo ̈rres et al. (1996) found that O3 causes 

an increased response to bronchial 

allergen challenge in subjects with 

allergic rhinitis and mild allergic 

asthma. The subjects were exposed to 

0.25 ppm O3 for 3 hours with IE. Airway 

responsiveness to methacholine was 

determined 1 hour before and after 

exposure; responsiveness to allergen 

was determined 3 hours after exposure. 

Statistically significant decreases in 

FEV1 occurred in subjects with allergic 

rhinitis (13.8%) and allergic asthma 

(10.6%), and in healthy controls (7.3%). 

Methacholine responsiveness was 

statistically increased in asthmatics, but 

not in subjects with allergic rhinitis or 

healthy controls. Airway responsiveness 

to an individual’s historical allergen 

(either grass and birch pollen, house 

dust mite, or animal dander) was 

significantly increased after O3 exposure 

when compared to FA exposure. In 

subjects with asthma and allergic 

rhinitis, a maximum percent fall in 

FEV1 of 27.9% and 7.8%, respectively, 

occurred 3 days after O3 exposure when 

they were challenged with of the highest 

common dose of allergen. The authors 

concluded that subjects with asthma or 

allergic rhinitis, without asthma, could 

be at risk if a high O3 exposure is 

followed by a high dose of allergen. 

Holz et al. (2002) reported an early 

phase lung function response in subjects 

with rhinitis after a consecutive 4-day 

exposure to 0.125 ppm O3 that resulted 

in a clinically relevant (>20%) decrease 

in FEV1. Ozone-induced exacerbation of 

airway responsiveness persists longer 

and attenuates more slowly than O3- 

induced lung function decrements and 

respiratory symptom responses and can 

have important clinical implications for 

asthmatics. 

A small number of in vitro studies 

corroborate the differences in the 

responses of asthmatic and healthy 

subject generally found in controlled 

human exposure studies. In vitro 

studies (Schierhorn et al., 1999) of nasal 

mucosal biopsies from atopic and 

nonatopic subjects exposed to 0.1 ppm 

O3 found significant differences in 

release of IL–4, IL–6, IL–8, and TNF-a. 

Another study by Schierhorn et al. 

(2002) found significant differences in 

the O3-induced release of the 

neuropeptides neurokinin A and 

substance P for allergic patients in 

comparison to nonallergic controls, 

suggesting increased activation of 

sensory nerves by O3 in the allergic 

tissues. Another study by Bayram et al. 

(2002) using in vitro culture of 

bronchial epithelial cells recovered from 

atopic and nonatopic asthmatics also 

found significant increases in epithelial 

permeability in response to O3

exposure. 

The new data on airway 

responsiveness, inflammation, and 

various molecular markers of 

inflammation and bronchoconstriction 

indicate that people with asthma and 

allergic rhinitis (with or without 

asthma) comprise susceptible groups for 

O3-induced adverse effects. This body of 

evidence indicates that human clinical 

and epidemiological panel studies of 

lung function decrements and 

respiratory symptoms that evaluate only 

healthy, non-asthmatic subjects likely 

underestimate the effects of O3 exposure 

on asthmatics and other susceptible 

populations. The effects of O3 on lung 

function, inflammation, and increased 

airway responsiveness demonstrated in 

subjects with asthma and other allergic 

airway diseases, provide plausible 

mechanisms underlying the more 

serious respiratory morbidity effects, 

such as emergency department visits 

and hospital admissions, and 

respiratory mortality effects. 

A number of epidemiological studies 

have been conducted using asthmatic 

study populations. The majority of 

epidemiological panel studies that 

evaluated respiratory symptoms and 

medication use related to O3 exposures 

focused on children. These studies 

suggest that O3 exposure may be 

associated with increased respiratory 

symptoms and medication use in 

children with asthma. Other reported 

effects include respiratory symptoms, 

lung function decrements, and 

emergency department visits, as 

discussed in the Criteria Document 

(section 7.6.7.1). Strong evidence from a 

large multi-city study (Mortimer et al., 

2002), along with support from several 

single-city studies suggest that O3

exposure may be associated with 

increased respiratory symptoms and 

medication use in children with asthma. 

With regard to ambient O3 levels and 

increased hospital admissions and 

emergency department visits for asthma 

and other respiratory causes, strong and 

consistent evidence establishes a 

correlation between O3 exposure and 

increased exacerbations of preexisting 

respiratory disease for 1-hour maximum 

O3 concentrations <0.12 ppm. As 

discussed in the Criteria Document, 

section 7.3, several hospital admission 

and emergency department visit studies 

in the U.S., Canada, and Europe have 

reported positive associations between 

increase in O3 and increased risk of 

emergency department visits and 

hospital admissions for asthma and 

other respiratory diseases, especially 

during the warm season. Finally, from 

epidemiological studies that included 

assessment of associations with specific 

causes of death, some studies have 

observed larger effects estimates for 

respiratory mortality and others have 

observed larger effects estimates for 

cardiovascular mortality. The apparent 

inconsistency regarding the effect size of 

O3-related respiratory mortality may be 

due to reduced statistical power in this 


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subcategory of mortality (EPA, 2006a, p. 

7–108). 

Newly available reports from 

controlled human exposure studies (see 

chapter 6 in the Criteria Document) 

utilized subjects with preexisting 

cardiopulmonary diseases such as 

COPD, asthma, allergic rhinitis, and 

hypertension. The data generated from 

these studies that evaluated changes in 

spirometry did not find clear differences 

between filtered air and O3 exposure in 

COPD subjects. However, the new data 

on airway responsiveness, 

inflammation, and various molecular 

markers of inflammation and 

bronchoconstriction indicate that 

people with atopic asthma and allergic 

rhinitis comprise susceptible groups for 

O3-induced adverse health effects. 

Although controlled human exposure 

studies have not found evidence of 

larger spirometric changes in people 

with COPD relative to healthy subjects, 

this may be due to the fact that most 

people with COPD are older adults who 

would not be expected to have such 

changes based on their age. However, in 

section 8.7.1, the Criteria Document 

notes that new epidemiological 

evidence indicates that people with 

COPD may be more likely to experience 

other effects, including emergency room 

visits, hospital admissions, or premature 

mortality. For example, results from an 

analysis of five European cities 

indicated strong and consistent O3

effects on unscheduled respiratory 

hospital admissions, including COPD 

(Anderson et al., 1997). Also, an 

analysis of a 9-year data set for the 

whole population of the Netherlands 

provided risk estimates for more 

specific causes of mortality, including 

COPD (Hoek et al., 2000, 2001; 

reanalysis, Hoek, 2003); a positive, but 

nonsignificant, excess risk of COPDrelated mortality was found to be 

associated with short-term O3

concentrations. Moreover, as indicated 

by Gong et al. (1998), the effects of O3

exposure on alveolar-arterial oxygen 

gradients may be more pronounced in 

patients with preexisting obstructive 

lung diseases. Relative to healthy 

elderly subjects, COPD patients have 

reduced gas exchange and low SaO2. 

Any inflammatory or edematous 

responses due to O3 delivered to the 

well-ventilated regions of the COPD 

lung could further inhibit gas exchange 

and reduce oxygen saturation. In 

addition, O3-induced vasoconstriction 

could also acutely induce pulmonary 

hypertension. Inducing pulmonary 

vasoconstriction and hypertension in 

these patients would perhaps worsen 

their condition, especially if their right 

ventricular function was already 

compromised (EPA, 2006a, section 

6.10). 

iii. Children and Older Adults 

Supporting evidence exists for 

heterogeneity in the effects of O3 by age. 

As discussed in section 6.5.1 of the 

Criteria Document, children, 

adolescents, and young adults (<18 yrs 

of age) appear, on average, to have 

nearly equivalent spirometric responses 

to O3, but have greater responses than 

middle-aged and older adults when 

exposed to comparable O3 doses. 

Symptomatic responses to O3 exposure, 

however, do not appear to occur in 

healthy children, but are observed in 

asthmatic children, particularly those 

who use maintenance medications. For 

adults (>17 yrs of age) symptoms 

gradually decrease with increasing age. 

In contrast to young adults, the 

diminished symptomatic responses in 

children and the diminished 

symptomatic and spirometric responses 

in older adults increases the likelihood 

that these groups continue outdoor 

activities leading to greater O3 exposure 

and dose. 

As described in the section 7.6.7.2 of 

the Criteria Document, many 

epidemiological field studies focused on 

the effect of O3 on the respiratory health 

of school children. In general, children 

experienced decrements in pulmonary 

function parameters, including PEF, 

FEV1, and FVC. Increases in respiratory 

symptoms and asthma medication use 

were also observed in asthmatic 

children. In one German study, children 

with and without asthma were found to 

be particularly susceptible to O3 effects 

on lung function. Approximately 20% 

of the children, both with and without 

asthma, experienced a greater than 10% 

change in FEV1, compared to only 5% 

of the elderly population and athletes 

(Ho ̈ppe et al., 2003). 

The American Academy of Pediatrics 

(2004) notes that children and infants 

are among the population groups most 

susceptible to many air pollutants, 

including O3. This is in part because 

their lungs are still developing. For 

example, eighty percent of alveoli are 

formed after birth, and changes in lung 

development continue through 

adolescence (Dietert et al., 2000). 

Children are also likely to spend more 

time outdoors than adults, which results 

in increased exposure to air pollutants 

(Wiley et al., 1991a,b). Moreover, 

children have high minute ventilation 

rates and high levels of physical activity 

which also increases their dose 

(Plunkett et al., 1992). 

Several mortality studies have 

investigated age-related differences in 

O3 effects (EPA, 2006a, section 7.6.7.2). 

Older adults are also often classified as 

being particularly susceptible to air 

pollution. The basis for increased O3

sensitivity among the elderly is not 

known, but one hypothesis is that it 

may be related to changes in the 

respiratory tract lining fluid antioxidant 

defense network (Kelly et al., 2003). 

(EPA 2006a, p. 8–60) Older adults have 

lower baseline lung function than 

younger people, and are also more likely 

to have preexisting lung and heart 

disease. Increased susceptibility of older 

adults to O3 health effects is most 

clearly indicated in the newer mortality 

studies. Among the studies that 

observed positive associations between 

O3 and mortality, a comparison of all 

age or younger age (≤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. The meta-analysis by Bell et al. 

(2005) found a larger mortality effect 

estimate for the elderly than for all ages. 

In the large U.S. 95 communities study 

(Bell et al., 2004), mortality effect 

estimates were slightly higher for those 

aged 65 to 74 years, compared to 

individuals less than 65 years and 75 

years or greater. The absolute effect of 

O3 on premature mortality may be 

substantially greater in the elderly 

population because of higher rates of 

preexisting respiratory and cardiac 

diseases. The Criteria Document 

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 (EPA, 2006a, p. 7–

177). 

The Criteria Document notes that, 

collectively, there is supporting 

evidence of age-related differences in 

susceptibility to O3 lung function 

effects. The elderly population (>65 

years of age) appear to be at increased 

risk of O3-related mortality and 

hospitalizations, and children (<18 

years of age) experience other 

potentially adverse respiratory health 

outcomes with increased O3 exposure 

(EPA, 2006a, section 7.6.7.2). 

iv. People With Increased 

Responsiveness to Ozone 

New animal toxicology studies using 

various strains of mice and rats have 

identified O3-sensitive and resistant 

strains and illustrated the importance of 

genetic background in determining O3

susceptibility (EPA, 2006a, section 

8.7.4). Controlled human exposure 

studies have also indicated a high 

degree of variability in some of the 

pulmonary physiological parameters. 

The variable effects in individuals have 


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23Similar to animal toxicology studies referred 

above, a polymorphism in a specific 

proinflammatory cytokine gene has been implicated 

in O3-induced lung function changes in healthy, 

mild asthmatics and individuals with rhinitis. 

These observations suggest a potential role for these 

markers in the innate susceptibility to O3, however, 

the validity of these markers and their relevance in 

the context of prediction to population studies 

needs additional experimentation. 

24 In 2000, the American Thoracic Society (ATS) 

published an official statement on ‘‘What 

Constitutes an Adverse Health Effect of Air 

Pollution?’’ (ATS, 2000), which updated its earlier 

guidance (ATS, 1985). Overall, the new guidance 

does not fundamentally change the approach 

previously taken to define adversity, nor does it 

suggest a need at this time to change the structure 

or content of the tables describing gradation of 

severity and adversity of effects described below. 

been found to be reproducible, in other 

words, a person who has a large lung 

function response after exposure to O3

will likely have about the same response 

if exposed again to the same dose of O3. 

In human clinical studies, group mean 

responses are not representative of this 

segment of the population that has 

much larger than average responses to 

O3. Recent studies of asthmatics by 

David et al. (2003) and Romieu et al. 

(2004) reported a role for genetic 

polymorphism in observed differences 

in antioxidant enzymes and genes 

involved in inflammation to modulate 

pulmonary function and inflammatory 

responses to O3 exposure.23

Biochemical and molecular 

parameters extensively evaluated in 

these experiments were used to identify 

specific loci on chromosomes and, in 

some cases, to relate the differential 

expression of specific genes to 

biochemical and physiological 

differences observed among these 

species. Utilizing O3-sensitive and O3- 

resistant species, it has been possible to 

identify the involvement of increased 

airway reactivity and inflammation 

processes in O3 susceptibility. However, 

most of these studies were carried out 

using relatively high doses of O3, 

making the relevance of these studies 

questionable in human health effects 

assessment. The genes and genetic loci 

identified in these studies may serve as 

useful biomarkers and, ultimately, can 

likely be integrated with 

epidemiological studies. 

v. Other Population Groups 

There is limited, new evidence 

supporting associations between shortterm O3 exposures and a range of effects 

on the cardiovascular system. Some but 

not all, epidemiological studies have 

reported associations between shortterm O3 exposures and the incidence of 

MI and more subtle cardiovascular 

health endpoints, such as changes in 

HRV and cardiac arrhythmia. Others 

have reported associations with 

hospitalization or emergency 

department visits for cardiovascular 

diseases, although the results across the 

studies are not consistent. Studies also 

report associations between short-term 

O3 exposure and mortality from 

cardiovascular or cardiopulmonary 

causes. The Criteria Document 

concludes that current cardiovascular 

effects evidence from some field studies 

is rather limited but supportive of a 

potential effect of short-term O3

exposure and HRV, cardiac arrhythmia, 

and MI incidence (EPA, 2006a, p. 7–65). 

In the Criteria Document’s evaluation of 

studies of hospital admissions for 

cardiovascular disease (EPA 2006a, 

section 7.3.4), it is concluded that 

evidence from this growing group of 

studies is generally inconclusive 

regarding an association with O3 in 

studies conducted during the warm 

season (EPA 2006a, p. 7–83). This body 

of evidence suggests that people with 

heart disease may be at increased risk 

from short-term exposures to O3; 

however, more evidence is needed to 

conclude that people with heart disease 

are a susceptible population. 

Other groups that might have 

enhanced sensitivity to O3, but for 

which there is currently very little 

evidence, include groups based on race, 

gender and SES, and those with 

nutritional deficiencies, which presents 

factors which modify responsiveness to 

O3. 

c. Adversity of Effects 

In making judgments as to when 

various O3-related effects become 

regarded as adverse to the health of 

individuals, the Administrator has 

looked to guidelines published by the 

American Thoracic Society (ATS) and 

the advice of CASAC. While recognizing 

that perceptions of ‘‘medical 

significance’’ and ‘‘normal activity’’ may 

differ among physicians, lung 

physiologists and experimental subjects, 

the ATS (1985) 24 defined adverse 

respiratory health effects as ‘‘medically 

significant physiologic changes 

generally evidenced by one or more of 

the following: (1) Interference with the 

normal activity of the affected person or 

persons, (2) episodic respiratory illness, 

(3) incapacitating illness, (4) permanent 

respiratory injury, and/or (5) progressive 

respiratory dysfunction.’’ During the 

1997 review, it was concluded that there 

was evidence of causal associations 

from controlled human exposure studies 

for effects in the first of these five ATSdefined categories, evidence of 

statistically significant associations from 

epidemiological studies for effects in the 

second and third categories, and 

evidence from animal toxicology 

studies, which could be extrapolated to 

humans only with a significant degree 

of uncertainty, for the last two 

categories. 

For ethical reasons, clear causal 

evidence from controlled human 

exposure studies still covers only effects 

in the first category. However, for this 

review there are results from 

epidemiological studies, upon which to 

base judgments about adversity, for 

effects in all of the categories. 

Statistically significant and robust 

associations have been reported in 

epidemiology studies falling into the 

second and third categories. These more 

serious effects include respiratory 

events (e.g., triggering asthma attacks) 

that may require medication (e.g., 

asthma), but not necessarily 

hospitalization, as well as respiratory 

hospital admissions and emergency 

department visits for respiratory causes. 

Less conclusive, but still positive 

associations have been reported for 

school absences and cardiovascular 

hospital admissions. Human health 

effects for which associations have been 

suggested through evidence from 

epidemiological and animal toxicology 

studies, but have not been conclusively 

demonstrated still fall primarily into the 

last two categories. In the last review of 

the O3 standard, evidence for these more 

serious effects came from studies of 

effects in laboratory animals. Evidence 

from animal studies evaluated in this 

Criteria Document strongly suggests that 

O3 is capable of damaging the distal 

airways and proximal alveoli, resulting 

in lung tissue remodeling leading to 

apparently irreversible changes. Recent 

advancements of dosimetry modeling 

also provide a better basis for 

extrapolation from animals to humans. 

Information from epidemiological 

studies provides supporting, but limited 

evidence of irreversible respiratory 

effects in humans than was available in 

the prior review. Moreover, the findings 

from single-city and multi-city timeseries epidemiology studies and metaanalyses of these epidemiology studies 

are highly suggestive of an association 

between short-term O3 exposure and 

mortality particularly in the warm 

season. 

While O3 has been associated with 

effects that are clearly adverse, 

application of these guidelines, in 

particular to the least serious category of 

effects related to ambient O3 exposures, 

involves judgments about which 

medical experts on the CASAC panel 

and public commenters have expressed 

diverse views in the past. To help frame 

such judgments, EPA staff have defined 

specific ranges of functional responses 


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(e.g., decrements in FEV1 and airway 

responsiveness) and symptomatic 

responses (e.g., cough, chest pain, 

wheeze), together with judgments as to 

the potential impact on individuals 

experiencing varying degrees of severity 

of these responses, that have been used 

in previous NAAQS reviews. These 

ranges of pulmonary responses and their 

associated potential impacts are 

summarized in Tables 3–2 and 3–3 of 

the Staff Paper. 

For active healthy people, moderate 

levels of functional responses (e.g., FEV1

decrements of ≥10% but <20%, lasting 

up to 24 hours) and/or moderate 

symptomatic responses (e.g., frequent 

spontaneous cough, marked discomfort 

on exercise or deep breath, lasting up to 

24 hours) would likely interfere with 

normal activity for relatively few 

responsive individuals. On the other 

hand, EPA staff determined that large 

functional responses (e.g., FEV1

decrements ≥20%, lasting longer than 

24 hours) and/or severe symptomatic 

responses (e.g., persistent 

uncontrollable cough, severe discomfort 

on exercise or deep breath, lasting 

longer than 24 hours) would likely 

interfere with normal activities for many 

responsive individuals. EPA staff 

determined that these would be 

considered adverse under ATS 

guidelines. In the context of standard 

setting, CASAC indicated that a focus 

on the mid to upper end of the range of 

moderate levels of functional responses 

(e.g., FEV1 decrements ≥15% but <20%) 

is appropriate for estimating potentially 

adverse lung function decrements in 

active healthy people. However, for 

people with lung disease, even 

moderate functional (e.g., FEV1

decrements ≥10% but <20%, lasting up 

to 24 hours) or symptomatic responses 

(e.g., frequent spontaneous cough, 

marked discomfort on exercise or with 

deep breath, wheeze accompanied by 

shortness of breath, lasting up to 24 

hours) would likely interfere with 

normal activity for many individuals, 

and would likely result in more frequent 

use of medication. For people with lung 

disease, large functional responses (e.g., 

FEV1 decrements ≥20%, lasting longer 

than 24 hours) and/or severe 

symptomatic responses (e.g., persistent 

uncontrollable cough, severe discomfort 

on exercise or deep breath, persistent 

wheeze accompanied by shortness of 

breath, lasting longer than 24 hours) 

would likely interfere with normal 

activity for most individuals and would 

increase the likelihood that these 

individuals would seek medical 

treatment. In the context of standard 

setting, the CASAC indicated 

(Henderson, 2006c) that a focus on the 

lower end of the range of moderate 

levels of functional responses (e.g., FEV1

decrements ≥10%) is most appropriate 

for estimating potentially adverse lung 

function decrements in active healthy 

people. 

In judging the extent to which these 

impacts represent effects that should be 

regarded as adverse to the health status 

of individuals, an additional factor that 

has been considered in previous 

NAAQS reviews is whether such effects 

are experienced repeatedly during the 

course of a year or only on a single 

occasion. While some experts would 

judge single occurrences of moderate 

responses to be a ‘‘nuisance,’’ especially 

for healthy individuals, a more general 

consensus view of the adversity of such 

moderate responses emerges as the 

frequency of occurrence increases. 

The new guidance builds upon and 

expands the 1985 definition of adversity 

in several ways. There is an increased 

focus on quality of life measures as 

indicators of adversity. There is also a 

more specific consideration of 

population risk. Exposure to air 

pollution that increases the risk of an 

adverse effect to the entire population is 

adverse, even though it may not 

increase the risk of any individual to an 

unacceptable level. For example, a 

population of asthmatics could have a 

distribution of lung function such that 

no individual has a level associated 

with significant impairment. Exposure 

to air pollution could shift the 

distribution to lower levels that still do 

not bring any individual to a level that 

is associated with clinically relevant 

effects. However, this would be 

considered to be adverse because 

individuals within the population 

would have diminished reserve 

function, and therefore would be at 

increased risk if affected by another 

agent. 

Of the various effects of O3 exposure 

that have been studied, many would 

meet the ATS definition of adversity. 

Such effects include, for example, any 

detectible level of permanent lung 

function loss attributable to air 

pollution, including both reductions in 

lung growth or acceleration of the agerelated decline of lung function; 

exacerbations of disease in individuals 

with chronic cardiopulmonary diseases; 

reversible loss of lung function in 

combination with the presence of 

symptoms; as well as more serious 

effects such as those requiring medical 

care including hospitalization and, 

obviously, mortality. 

d. Size of At-Risk Subpopulations 

Although O3-related health risk 

estimates may appear to be small, their 

significance from an overall public 

health perspective is determined by the 

large numbers of individuals in the 

subpopulations potentially at-risk for 

O3-related health effects discussed 

above. For example, a population of 

concern includes people with 

respiratory disease, including 

approximately 11 percent of U.S. adults 

and 13 percent of children who have 

been diagnosed with asthma and 6 

percent of adults with chronic 

obstructive pulmonary disease (chronic 

bronchitis and/or emphysema) in 2002 

and 2003 (Table 8–4 in the Criteria 

Document, section 8.7.5.2). More 

broadly, individuals with preexisting 

cardiopulmonary disease may constitute 

an additional population of concern, 

with potentially tens of millions of 

people included in each disease 

category. In addition, subpopulations 

based on age group also comprise 

substantial segments of the population 

that may be potentially at risk for O3- 

related health impacts. Based on U.S. 

census data from 2003, about 26 percent 

of the U.S. population are under 18 

years of age and 12 percent are 65 years 

of age or older. Hence, large proportions 

of the U.S. population are included in 

age groups include those most likely to 

have increased susceptibility to the 

health effects of O3 and or those with 

the highest ambient O3 exposures. 

The Criteria Document (section 

8.7.5.2) notes that the health statistics 

data illustrate what is known as the 

‘‘pyramid’’ of effects. At the top of the 

pyramid, there are approximately 2.5 

millions deaths from all causes per year 

in the U.S. population, with about 

100,000 deaths from chronic lower 

respiratory diseases. For respiratory 

health diseases, there are nearly 4 

million hospital discharges per year, 14 

million emergency department visits, 

112 million ambulatory care visits, and 

an estimated 700 million restricted 

activity days per year due to respiratory 

conditions from all causes per year. 

Applying small risk estimates for the 

O3-related contribution to such health 

effects with relatively large baseline 

levels of health outcomes can result in 

quite large public health impacts related 

to ambient O3 exposure. Thus, even a 

small percentage reduction in O3 health 

impacts on cardiopulmonary diseases 

would reflect a large number of avoided 

cases. In considering this information 

together with the concentrationresponse relationships that have been 

observed between exposure to O3 and 

various health endpoints, the Criteria 


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25Modeling that projects whether and how areas 

might attain alternative standards in a future year 

is presented in the Regulatory Impact Analysis 

being prepared in connection with this rulemaking. 

26EPA plans to make available corrected versions 

of the final Staff Paper, and human exposure and 

health risk assessment technical support documents 

on or around July 16, 2007 on the EPA web site 

listed in the Availability of Related Information 

section of this notice. 

27The 12 CSAs modeled are: Atlanta-Sandy 

Springs-Gainesville, GA–AL; Boston-WorcesterManchester, MA–NH; Chicago-Naperville-Michigan 

City, IL–IN–WI; Cleveland-Akron-Elyria, OH; 

Detroit-Warren-Flint, MI; Houston-BaytownHuntsville, TX; Los Angeles-Long Beach-Riverside, 

CA; New York-Newark-Bridgeport, NY–NJ–CT–PA; 

Philadelphia-Camden-Vineland, PA–NJ–DE–MD; 

Sacramento-Arden-Arcade-Truckee, CA–NV; St. 

Louis-St. Charles-Farmington, MO–IL; WashingtonBaltimore-N. Virginia, DC–MD–VA–WV. 

28All 12 of the CSAs modeled did not meet the 

current O3 NAAQS for the three year period 

examined. 

29The general approach used in the current 

exposure assessment was described in the draft 

Health Assessment Plan (EPA, 2005a) that was 

released to the CASAC and general public in April 

2005 and was the subject of a consultation with the 

CASAC O3 Panel on May 5, 2005. In October 2005, 

OAQPS released the first draft of the Staff Paper 

containing a chapter discussing the exposure 

analyses and first draft of the Exposure Analyses 

TSD for CASAC consultation and public review on 

December 8, 2005. In July 2006, OAQPS released 

the second draft of the Staff Paper and second draft 

of the Exposure Analyses TSD for CASAC review 

and public comment which was held by the CASAC 

O3 Panel on August 24–25, 2006. 

Document (section 8.7.5.2) concludes 

that exposure to ambient O3 likely has 

a significant impact on public health in 

the U.S. 

B. Human Exposure and Health Risk 

Assessments 

To put judgments about health effects 

that are adverse for individuals into a 

broader public health context, EPA has 

developed and applied models to 

estimate human exposures and health 

risks. This broader context includes 

consideration of the size of particular 

population groups at risk for various 

effects, the likelihood that exposures of 

concern will occur for individuals in 

such groups under varying air quality 

scenarios, estimates of the number of 

people likely to experience O3-related 

effects, the variability in estimated 

exposures and risks, and the kind and 

degree of uncertainties inherent in 

assessing the exposures and risks 

involved. 

As discussed below there are a 

number of important uncertainties that 

affect the exposure and health risk 

estimates. It is also important to note 

that there have been significant 

improvements in both the exposure and 

health risk model. CASAC expressed the 

view that the exposure analysis 

represents a state-of-the-art modeling 

approach and that the health risk 

assessment was ‘‘well done, balanced 

and reasonably communicated’’

(Henderson, 2006c). While recognizing 

and considering the kind and degree of 

uncertainties in both the exposure and 

health risk estimates, the Staff Paper 

judged that the quality of the estimates 

is such that they are suitable to be used 

as an input to the Administrator’s 

decisions on the O3 primary standard 

(Staff Paper, p. 6–20—6–21). 

In modeling exposures and health 

risks associated with just meeting the 

current and alternative O3 standards, 

EPA has simulated air quality to 

represent conditions just meeting these 

standards based on O3 air quality 

patterns in several recent years and on 

how the shape of the O3 air quality 

distribution has changed over time 

based on historical trends in monitored 

O3 air quality data. As described in the 

Staff Paper (section 4.5.8) and discussed 

below, recent O3 air quality 

distributions have been statistically 

adjusted to simulate just meeting the 

current and selected alternative 

standards. These simulations do not 

reflect any consideration of specific 

control programs or strategies designed 

to achieve the reductions in emissions 

required to meet the specified 

standards. Further, these simulations do 

not represent predictions of when, 

whether, or how areas might meet the 

specified standards.25

As noted in section I.C above, around 

the time of the release of the final Staff 

Paper in January 2007, EPA discovered 

a small error in the exposure model that 

when corrected resulted in slight 

increases in the simulated exposures. 

Since the exposure estimates are an 

input to the lung function portion of the 

health risk assessment, this correction 

also resulted in slight increases in the 

lung function risk estimates as well. The 

exposure and risk estimates discussed 

in this notice reflect the corrected 

estimates, and thus are slightly different 

than the exposure and risk estimates 

cited in the January 31, 2007 Staff 

Paper.26

1. Exposure Analyses 

a. Overview 

The EPA conducted exposure 

analyses using a simulation model to 

estimate O3 exposures for the general 

population, school age children (ages 5–

18), and school age children with 

asthma living in 12 U.S. metropolitan 

areas representing different regions of 

the country where the current 8-hour O3

standard is not met. The emphasis on 

children reflects the finding of the last 

O3 NAAQS review that children are an 

important at-risk group. The 12 modeled 

areas combined represent a significant 

fraction of the U.S. urban population, 89 

million people, including 18 million 

school age children of whom 

approximately 2.6 million have asthma. 

The selection of urban areas to include 

in the exposure analysis took into 

consideration the location of O3

epidemiological studies, the availability 

of ambient O3 data, and the desire to 

represent a range of geographic areas, 

population demographics, and O3

climatology. These selection criteria are 

discussed further in chapter 5 of the 

Staff Paper. The geographic extent of 

each modeled area consists of the 

census tracts in the combined statistical 

area (CSA) as defined by OMB (OMB, 

2005).27

Exposure estimates were developed 

using a probabilistic exposure model 

that is designed to explicitly model the 

numerous sources of variability that 

affect people’s exposures. As discussed 

below, the model estimates population 

exposures by simulating human activity 

patterns, air conditioning prevalence, 

air exchange rates, and other factors. 

The modeled exposure estimates were 

developed for three recent years of 

ambient O3 concentrations (2002, 2003, 

and 2004), as well as for O3

concentrations adjusted to simulate 

conditions associated with just meeting 

the current NAAQS and various 

alternative 8-hour standards based on 

the three year period 2002–2004.28 This 

exposure assessment is more fully 

described and presented in the Staff 

Paper and in a technical support 

document, Ozone Population Exposure 

Analysis for Selected Urban Areas (US 

EPA, 2006b; hereafter Exposure 

Analysis TSD). The scope and 

methodology for this exposure 

assessment were developed over the last 

few years with considerable input from 

the CASAC Ozone Panel and the 

public.29

The goals of the O3 exposure 

assessment were: (1) To provide 

estimates of the size of at-risk 

populations exposed to various levels 

associated with recent O3

concentrations, and with just meeting 

the current O3 NAAQS and alternative 

O3 standards, in specific urban areas; (2) 

to provide distributions of exposure 

estimates over the entire range of 

ambient O3 concentrations as an 

important input to the lung function 

risk assessment summarized below in 

section II.B.2; (3) to develop a better 

understanding of the influence of 

various inputs and assumptions on the 

exposure estimates; and (4) to gain 

insight into the distribution of 

exposures and patterns of exposure 


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reductions associated with meeting 

alternative O3 standards. 

EPA recognizes that there are many 

sources of variability and uncertainty 

inherent in the inputs to this assessment 

and that there is uncertainty in the 

resulting O3 exposure estimates. With 

respect to variability, the exposure 

modeling approach accounts for 

variability in ambient O3 levels, 

demographic characteristics, 

physiological attributes, activity 

patterns, and factors affecting 

microenvironmental (e.g., indoor) 

concentrations. In EPA’s judgment, the 

most important uncertainties affecting 

the exposure estimates are related to the 

modeling of human activity patterns 

over an O3 season, the modeling of 

variations in ambient concentrations 

near roadways, and the modeling of air 

exchange rates that affect the amount of 

O3 that penetrates indoors. Another 

important uncertainty that affects the 

estimation of how many exposures are 

associated with moderate or greater 

exertion, is the characterization of 

energy expenditure for children engaged 

in various activities. As discussed in 

more detail in the Staff Paper (section 

4.3.4.7), the uncertainty in energy 

expenditure values carries over to the 

uncertainty of the modeled breathing 

rates, which are important since they 

are used to classify exposures occurring 

at moderate or greater exertion which 

are the relevant exposures since O3- 

related effects observed in clinical 

studies only are observed when 

individuals are engaged in some form of 

exercise. The uncertainties in the 

exposure model inputs and the 

estimated exposures have been assessed 

using quantitative uncertainty and 

sensitivity analyses. Details are 

discussed in the Staff Paper (section 4.6) 

and in a technical memorandum 

describing the exposure modeling 

uncertainty analysis (Langstaff, 2007). 

b. Scope and Key Components 

Population exposures to O3 are 

primarily driven by ambient outdoor 

concentrations, which vary by time of 

day, location, and peoples’ activities. 

Outdoor O3 concentration estimates 

used in the exposure assessment are 

provided by measurements and 

statistical adjustments to the measured 

concentrations. The current exposure 

analysis allows comparisons of 

population exposures to O3 within each 

urban area, associated with current O3

levels and with O3 levels just meeting 

several potential alternative air quality 

standards or scenarios. Human 

exposure, regardless of the pollutant, 

depends on where individuals are 

located and what they are doing. 

Inhalation exposure models are useful 

in realistically estimating personal 

exposures to O3 based on activityspecific breathing rates, particularly 

when recognizing that large scale 

population exposure measurement 

studies have not been conducted that 

are representative of the overall 

population or at-risk subpopulations. 

The model EPA used to simulate O3

population exposure is the Air 

Pollutants Exposure Model (APEX), the 

human inhalation exposure model 

within the Total Risk Integrated 

Methodology (TRIM) framework (EPA, 

2006c,d). APEX is conceptually based 

on the probabilistic NAAQS exposure 

model for O3 (pNEM/O3) used in the last 

O3 NAAQS review. Since that time, the 

model has been restructured, improved, 

and expanded to reflect conceptual 

advances in the science of exposure 

modeling and newer input data 

available for the model. Key 

improvements to algorithms include 

replacement of the cohort approach 

with a probabilistic sampling approach 

focused on individuals, accounting for 

fatigue and oxygen debt after exercise in 

the calculation of breathing rates, and a 

new approach for construction of 

longitudinal activity patterns for 

simulated persons. Major improvements 

to data input to the model include 

updated air exchange rates, more recent 

census and commuting data, and a 

greatly expanded daily time-activities 

database. 

APEX is a probabilistic model 

designed to explicitly model the 

numerous sources of variability that 

affect people’s exposures. APEX 

simulates the movement of individuals 

through time and space and estimates 

their exposures to O3 in indoor, outdoor, 

and in-vehicle microenvironments. The 

exposure model takes into account the 

most significant factors contributing to 

total human O3 exposure, including the 

temporal and spatial distribution of 

people and O3 concentrations 

throughout an urban area, the variation 

of O3 levels within each 

microenvironment, and the effects of 

exertion on breathing rate in exposed 

individuals. A more detailed 

description of APEX and its application 

is presented in chapter 4 of the Staff 

Paper and associated technical 

documents (EPA, 2006b, c, d). 

Several methods have been used to 

evaluate the APEX model and to 

characterize the uncertainty of the 

model estimates. These include 

conducting model evaluation, 

sensitivity analyses, and a detailed 

uncertainty analysis for one urban area. 

These are discussed fully in the Staff 

Paper (section 4.6) and in Langstaff 

(2007). The uncertainty of model 

structure was judged to be of lesser 

importance than the uncertainties of the 

model inputs and parameters. Model 

structure refers to the algorithms in 

APEX designed to simulate the 

processes that result in people’s 

exposures, for example, the way that 

APEX models exposures to individuals 

when they are near roads. The 

uncertainties in the model input data 

(e.g., measurement error, ambient 

concentrations, air exchange rates, and 

activity pattern data) have been assessed 

individually, and their impact on the 

uncertainty in the modeled exposure 

estimates was assessed in a unified 

quantitative analysis with results 

expressed in the form of estimated 

confidence ranges around the estimated 

measures of exposure. This uncertainty 

analysis was conducted for one urban 

area (Boston) using the observed 2002 

O3 concentrations and 2002 

concentrations adjusted to simulate just 

meeting the current standard, with the 

expectation that the results would be 

similar for other cities and years. One 

significant source of uncertainty, due to 

limitations in the database used to 

model peoples’ daily activities, was not 

included in the unified analysis, and 

was assessed through separate 

sensitivity analyses. This analysis 

indicates that the uncertainty of the 

exposure results is relatively small. For 

example, 95 percent uncertainty 

intervals were calculated for the APEX 

estimates of the percent of children or 

asthmatic children with exposures 

above 0.060, 0.070, or 0.080 ppm under 

moderate exertion, for two air quality 

scenarios (current 2002 and 2002 

adjusted to simulate just meeting the 

current standard) in Boston (Tables 26 

and 27 in Langstaff, 2007). The 95 

percent uncertainty intervals for this set 

of 12 exposure estimates indicate the 

possibility of underpredictions of the 

exposure estimates ranging from 3 to 25 

percent of the modeled estimates, and 

overpredictions ranging from 4 to 11 

percent of the estimates. For example, 

APEX estimates the percent of asthmatic 

children with exposures above 0.070 

ppm under moderate exertion to be 24 

percent, for Boston 2002 O3

concentrations adjusted to simulate just 

meeting the current standard. The 95 

percent uncertainty interval for this 

estimate is 23–30 percent, or ¥4 to +25 

percent of the estimate. These 

uncertainty intervals do not include the 

uncertainty engendered by limitations 

of the activity database, which is in the 

range of one to ten percent. 

The exposure periods modeled here 

are the O3 seasons in 2002, 2003, and 


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30The current O3 standard is 0.08 ppm, but the 

current rounding convention specifies that the 

average of the 4th daily maximum 8-hour average 

concentrations over a three-year period must be at 

0.084 ppm or lower to be in attainment of the 

standard. When EPA staff selected alternative 

standards to analyze, it was presumed that the same 

type of rounding convention would be used, and 

thus alternative standards of 0.084, 0.074, 0.064 

ppm were chosen. 

31A design value is a statistic that describes the 

air quality status of a given area relative to the level 

of the NAAQS. Design values are often based on 

multiple years of data, consistent with specification 

of the NAAQS in Part 50 of the CFR. For the current 

O3 NAAQS, the 3-year average of the annual 4thhighest daily maximum 8-hour average 

concentrations, based on the monitor within (or 

downwind of) an urban area yielding the highest 3- 

year average, is the design value. 

32The quadratic rollback approach and 

evaluation of this approach are described by 

Johnson (1997), Duff et al. (1998) and Rizzo (2005, 

2006). 

33As discussed above in Section II.A., O3 health 

responses observed in human clinical studies are 

associated with exposures while engaged in 

moderate or greater exertion and, therefore, these 

are the exposure measures of interest. The level of 

exertion of individuals engaged in particular 

activities is measured by an equivalent ventilation 

rate (EVR), ventilation normalized by body surface 

area (BSA, in m2), which is calculated as VE/BSA, 

where VE is the ventilation rate (liters/minute). 

Moderate and greater exertion levels were defined 

as EVR > 13 liters/min-m2 (Whitfield et al., 1996) 

to correspond to the exertion levels measured in 

most subjects studied in the controlled human 

exposure studies that reported health effects 

associated with 6.6 hour O3 exposures. 

2004. The O3 season in each area 

includes the period of the year where 

elevated O3 levels tend to be observed 

and for which routine hourly O3

monitoring data are available. Typically 

this period spans from March or April 

through September or October, or in 

some areas, spanning the entire year. 

Three years were modeled to reflect the 

substantial year-to-year variability that 

occurs in O3 levels and related 

meteorological conditions, and because 

the standard is specified in terms of a 

three-year period. The year-to-year 

variability observed in O3 levels is due 

to a combination of different weather 

patterns and the variation in emissions 

of O3 precursors. Nationally, 2002 was 

a relatively high year with respect to the 

4th highest daily maximum 8-hour O3

levels observed in urban areas across the 

U.S. (EPA, 2007, Figure 2–16), with the 

mean of the distribution of O3 levels for 

the urban monitors being in the upper 

third among the years 1990 through 

2006. In contrast, on a national basis, 

2004 is the lowest year on record 

through 2006 for this same air quality 

statistic, and 8-hour daily maximum O3

levels observed in most, but not all of 

the 12 urban areas included in the 

exposure and risk analyses were 

relatively low compared to other recent 

years. The 4th highest daily maximum 

8-hour O3 levels observed in 2003 in the 

12 urban areas and nationally generally 

were between those observed in 2002 

and 2004. 

Regulatory scenarios examined 

include the current 0.08 ppm, average of 

the 4th daily maximum 8-hour averages 

over a three year period standard; 

standards with the same form but with 

alternative levels of 0.080, 0.074, 0.070, 

and 0.064 ppm; standards specified as 

the average of the 3rd highest daily 

maximum 8-hour averages over a three 

year period with alternative levels of 

0.084 and 0.074 ppm; and a standard 

specified as the average of the 5th 

highest daily maximum 8-hour averages 

over a three year period with a level of 

0.074 ppm.30 The current standard uses 

a rounding convention that allows areas 

to have an average of the 4th daily 

maximum 8-hour averages as high as 

0.084 ppm and still meet the standard. 

All alternative standards analyzed were 

intended to reflect improved precision 

in the measurement of ambient 

concentrations, where the precision 

would extend to three instead of two 

decimal places (in ppm). 

The current standard and all 

alternative standards were modeled 

using a quadratic rollback approach to 

adjust the hourly concentrations 

observed in 2002–2004 to yield a design 

value 31 corresponding to the standard 

being analyzed. The quadratic rollback 

technique reduces higher concentrations 

more than lower concentrations near 

ambient background levels.32 This 

procedure was considered in a 

sensitivity analysis in the last review of 

the O3 standard and has been shown to 

be more realistic than a linear, 

proportional rollback method, where all 

of the ambient concentrations are 

reduced by the same factor. 

c. Exposure Estimates and Key 

Observations 

The exposure assessment, which 

provides estimates of the number of 

people exposed to different levels of 

ambient O3 while at specified exertion 

levels 33 serve two purposes. First, the 

entire range of modeled personal 

exposures to ambient O3 is an essential 

input to the portion of the health risk 

assessment based on exposure-response 

functions from controlled human 

exposure studies, discussed in the next 

section. Second, estimates of personal 

exposures to ambient O3 concentrations 

at and above specific benchmark levels 

provide some perspective on the public 

health impacts of health effects that we 

cannot currently evaluate in 

quantitative risk assessments that may 

occur at current air quality levels, and 

the extent to which such impacts might 

be reduced by meeting the current and 

alternative standards. This is especially 

true when there are exposure levels at 

which we know or can reasonably infer 

that specific O3-related health effects are 

occurring. We refer to exposures at and 

above these benchmark concentrations 

as ‘‘exposures of concern.’’

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. 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 human 

clinical and toxicological studies but 

cannot be evaluated in quantitative risk 

assessments, such as lung inflammation, 

increased airway responsiveness, and 

changes in host defenses. They also help 

in understanding the extent to which 

such impacts have the potential to be 

reduced by meeting the current and 

alternative standards. In the selection of 

specific benchmark concentrations for 

this analysis, we first considered the 

exposure level of 0.080 ppm, at which 

there is a substantial amount of clinical 

evidence demonstrating a range of O3- 

related health effects including lung 

inflammation and airway 

responsiveness in healthy individuals. 

Thus, as in the last review, this level 

was selected as a benchmark level for 

this assessment of exposures of concern. 

Evidence newly available in this review 

is the basis for identifying additional, 

lower benchmark levels of 0.070 and 

0.060 ppm for this assessment. 

More specifically, as discussed above 

in section II.A.2, evidence available 

from controlled human exposure and 

epidemiology studies indicates that 

people with asthma have larger and 

more serious effects than healthy 

individuals, including lung function, 

respiratory symptoms, increased airway 


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34The full range of quantitative exposure 

estimates associated with just meeting the current 

and alternative O3 standards are presented in 

chapter 4 and Appendix 4A of the Staff Paper. 

responsiveness, and pulmonary 

inflammation, which has been shown to 

be a more sensitive marker than lung 

function responses. Further, a 

substantial new body of evidence from 

epidemiology studies shows 

associations with serious respiratory 

morbidity and cardiopulmonary 

mortality effects at O3 levels that extend 

below 0.080 ppm. Additional, but very 

limited new evidence from controlled 

human exposure studies shows lung 

function decrements and respiratory 

symptoms in healthy subjects at an O3

exposure level of 0.060 ppm. The 

selected benchmark level of 0.070 ppm 

reflects the new information that 

asthmatics have larger and more serious 

effects than healthy people and 

therefore controlled human exposure 

studies done with healthy subjects may 

underestimate effects in this group, as 

well as the substantial body of 

epidemiological evidence of 

associations with O3 levels below 0.080 

ppm. The selected benchmark level of 

0.060 ppm additionally reflects the very 

limited new evidence from controlled 

human exposure studies that show lung 

function decrements and respiratory 

symptoms in some healthy subjects at 

the 0.060 ppm exposure level, 

recognizing that asthmatics are likely to 

have more serious responses and that 

lung function is not likely to be as 

sensitive a marker for O3 effects as is 

lung inflammation. 

The estimates of exposures of concern 

were reported in terms of both ‘‘people 

exposed’’ (the number and percent of 

people who experience a given level of 

O3 concentrations, or higher, at least one 

time during the O3 season in a given 

year) and ‘‘occurrences of exposure’’

(the number of times a given level of 

pollution is experienced by the 

population of interest, expressed in 

terms of person-days of occurrences). 

Estimating exposures of concern is 

important because it provides some 

indication of the potential public health 

impacts of a range of O3-related health 

outcomes, such as lung inflammation, 

increased airway responsiveness, and 

changes in host defenses. These 

particular health effects have been 

demonstrated in controlled human 

exposure studies of healthy individuals 

to occur at levels as low as 0.080 ppm 

O3, but have not been evaluated at lower 

levels in controlled human exposure 

studies. EPA has not included these 

effects in the quantitative risk 

assessment due to a lack of adequate 

information on the exposure-response 

relationships. 

The 1997 O3 NAAQS review 

estimated exposures associated with 1- 

hour heavy exertion, 1-hour moderate 

exertion, and 8-hour moderate exertion 

for children, outdoor workers, and the 

general population. EPA’s analysis in 

the 1997 Staff Paper showed that 

exposure estimates based on the 8-hour 

moderate exertion scenario for children 

yielded the largest number of children 

experiencing exposures at or above 

exposures of concern. Consequently, 

EPA has chosen to focus on the 8-hour 

moderate and greater exertion exposures 

in all and asthmatic school age children 

in the current exposure assessment. 

While outdoor workers and other adults 

who engage in moderate or greater 

exertion for prolonged durations while 

outdoors during the day in areas 

experiencing elevated O3 concentrations 

also are at risk for experiencing 

exposures associated with O3-related 

health effects, EPA did not focus on 

quantitative estimates for these 

populations due to the lack of 

information about the number of 

individuals who regularly work or 

exercise outdoors. Thus, the exposure 

estimates presented here and in the Staff 

Paper are most useful for making 

relative comparisons across alternative 

air quality scenarios and do not 

represent the total exposures in all 

children or other groups within the 

general population associated with the 

air quality scenarios. 

Population exposures to O3 were 

estimated in 12 urban areas for 2002, 

2003, and 2004 air quality, and also 

using O3 concentrations adjusted to just 

meet the current and several alternative 

standards. The estimates of 8-hour 

exposures of concern at and above 

benchmark levels of 0.080, 0.070, and 

0.060 ppm aggregated across all 12 areas 

are shown in Table 1 for air quality 

scenarios just meeting the current and 

four alternative 8-hour average 

standards.34 Table 1 provides estimates 

of the number and percent of school age 

children and asthmatic school age 

children exposed, with daily 8-hour 

maximum exposures at or above each O3

benchmark level of exposures of 

concern, while at intermittent moderate 

or greater exertion and based on O3

concentrations observed in 2002 and 

2004. Table 1 summarizes estimates for 

2002 and 2004, because these years 

reflect years that bracket relatively 

higher and lower O3 levels, with year 

2003 generally containing O3 levels in 

between when considering the 12 urban 

areas modeled. This table also reports 

the percent change in the number of 

persons exposed when a given 

alternative standard is compared with 

the current standard. 

Key observations important in 

comparing exposure estimates 

associated with just meeting the current 

NAAQS and alternative standards under 

consideration include: 

(1) As shown in Table 6–1 of the Staff 

Paper, the patterns of exposure in terms 

of percentages of the population 

exceeding a given exposure level are 

very similar for the general population 

and for asthmatic and all school age (5–

18) children, although children are 

about twice as likely to be exposed, 

based on the percent of the population 

exposed, at any given level. 

(2) As shown in Table 1 below, the 

number and percentage of asthmatic and 

all school-age children aggregated across 

the 12 urban areas estimated to 

experience 1 or more exposures of 

concern decline from simulations of just 

meeting the current standard to 

simulations of alternative 8-hour 

standards by varying amounts 

depending on the benchmark level, the 

population subgroup considered, and 

the year chosen. For example, the 

estimated percentage of school age 

children experiencing one or more 

exposures ≥ 0.070 ppm, while engaged 

in moderate or greater exertion, during 

an O3 season is about 18 percent of this 

population when the current standard is 

met using the 2002 simulation; this is 

reduced to about 12, 4, 1, and 0.2 

percent of children upon meeting 

alternative standards of 0.080, 0.074, 

0.070, and 0.064 ppm, respectively (all 

specified in terms of the 4th highest 

daily maximum 8-hour average), using 

the 2002 simulation. 


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35The methodology, scope, and results from the 

risk assessment conducted in the last review are 

described in Chapter 6 of the 1996 Staff Paper (EPA, 

1996) and in several technical reports (Whitfield et 

al., 1996; Whitfield, 1997) and publication 

(Whitfield et al., 1998). 

36The 9 urban study areas included in the 

exposure and risk analyses conducted during the 

last review were: Chicago, Denver, Houston, Los 

Angeles, Miami, New York City, Philadephia, St. 

Louis, and Washington, DC. 

TABLE 1.—NUMBER AND PERCENT OF ALL AND ASTHMATIC SCHOOL AGE CHILDREN IN 12 URBAN AREAS ESTIMATED TO

EXPERIENCE 8-HOUR OZONE EXPOSURES ABOVE 0.080, 0.070, AND 0.060 PPM WHILE AT MODERATE OR GREATER

EXERTION, ONE OR MORE TIMES PER SEASON AND THE NUMBER OF OCCURRENCES ASSOCIATED WITH JUST MEETING ALTERNATIVE 8-HOUR STANDARDS BASED ON ADJUSTING 2002 AND 2004 AIR QUALITY DATA1, 2

Benchmark 

levels of exposures of concern (ppm) 

8-Hour air 

quality standards3 (ppm) 

All children, ages 5–18 aggregate for 12 urban areas, 

number of children exposed (% of all) [%reduction 

from current standard] 

Asthmatic children, ages 5–18 Aggregate for 12 

urban areas, number of children exposed (% of 

group) [% reduction from current standard] 

2002 2004 2002 2004 

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

0.080 290,000 (2%) [70%] ........ 10,000 (0%) [67%] .......... 50,000 (2%) [54%] .......... 0 (0%) 

0.074 60,000 (0%) [91%] .......... 0 (0%) [100%] ................. 10,000 (0%) [91%] .......... 0 (0%) 

0.070 10,000 (0%) [98%] .......... 0 (0%) [100%] ................. 0 (0%) [100%] ................. 0 (0%) 

0.064 0 (0%) [100%] ................. 0 (0%) [100%] ................. 0 (0%) [100%] ................. 0 (0%) 

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

0.080 2,160,000 (12%) [35%] ... 100,000 (1%) [62%] ........ 330,000 (13%) [36%] ...... 10,000 (0%) [75%] 

0.074 770,000 (4%) [77%] ........ 20,000 (0%) [92%] .......... 120,000 (5%) [77%] ........ 0 (0%) [100%] 

0.070 270,000 (1%) [92%] ........ 0 (0%) [100%] ................. 50,000 (2%) [90%] .......... 0 (0%) [100%] 

0.064 30,000 (0.2%) [99%] ....... 0 (0%) [100%] ................. 10,000 (0.2%) [98% ] ...... 0 (0%) [100%] 

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

0.080 6,730,000 (37%) [16%] ... 1,050,000 (6%) [42%] ..... 1,020,000 (40%) [16%] ... 150,000 (6%) [44%] 

0.074 4,550,000 (25%) [43%] ... 350,000 (2%) [80%] ........ 700,000 (27%) [42%] ...... 50,000 (2%) [81%] 

0.070 3,000,000 (16%) [62%] ... 110,000 (1%) [94%] ........ 460,000 (18%) [62%] ...... 10,000 (1%) [96%] 

0.064 950,000 (5%) [88%] ........ 10,000 (0%) [99%] .......... 150,000 (6%) [88%] ........ 0 (0%) [100%] 

1 Moderate or greater exertion is defined as having an 8-hour average equivalent ventilation rate ≥ 13 l-min/m2. 2Estimates are the aggregate results based on 12 combined statistical areas (Atlanta, Boston, Chicago, Cleveland, Detroit, Houston, Los Angeles, New York, Philadelphia, Sacramento, St. Louis, and Washington, DC). Estimates are for the ozone season which is all year in Houston, 

Los Angeles and Sacramento and March or April to September or October for the remaining urban areas. 3All standards summarized here have the same form as the current 8-hour standard which is specified as the 3-year average of the annual 4th 

highest daily maximum 8-hour average concentrations must be at or below the concentration level specified. As described in the Staff Paper 

(section 4.5.8), recent O3 air quality distributions have been statistically adjusted to simulate just meeting the current and selected alternative 

standards. These simulations do not represent predictions of when, whether, or how areas might meet the specified standards. 

(3) Substantial year-to-year variability 

in exposure estimates is observed over 

the three-year modeling period. For 

example, the estimated number of 

school age children experiencing one or 

more exposures ≥0.070 ppm during an 

O3 season when the current standard is 

met in the 12 urban areas included in 

the analysis is 3.3, 1.0, or 0.3 million for 

the 2002, 2003, and 2004 simulations, 

respectively. 

(4) There is substantial variability 

observed across the 12 urban areas in 

the percent of the population subgroups 

estimated to experience exposures of 

concern. For example, when 2002 O3

concentrations are simulated to just 

meet the current standard, the aggregate 

12 urban area estimate is 18 percent of 

all school age children are estimated to 

experience O3 exposures (≥0.070 ppm 

(Table 1 below), while the range of 

exposure estimates in the 12 urban areas 

considered separately for all children 

range from 1 to 38 percent (EPA, 2007, 

Exhibit 2, p. 4–48). There was also 

variability in exposure estimates among 

the modeled areas when using the 2004 

air quality simulation for the same 

scenario; however it was reduced and 

ranged from 0 to 7 percent in the 12 

urban areas (EPA, 2007, Exhibit 8, p. 4–

60). 

(5) Of particular note, as discussed 

above in section II.A. of this notice, high 

inter-individual variability in 

responsiveness means that only a subset 

of individuals in these groups who are 

exposed at and above a given 

benchmark level would actually be 

expected to experience such adverse 

health effects. 

(6) In considering these observations, 

it is important to take into account the 

variability, uncertainties, and 

limitations associated with this 

assessment, including the degree of 

uncertainty associated with a number of 

model inputs and uncertainty in the 

model itself, as discussed above. 

2. Quantitative Health Risk Assessment 

This section discusses the approach 

used to develop quantitative health risk 

estimates associated with exposures to 

O3 building upon a more limited risk 

assessment that was conducted during 

the last review.35 As part of the last 

review, EPA conducted a health risk 

assessment that produced risk estimates 

for the number and percent of children 

and outdoor workers experiencing lung 

function and respiratory symptoms 

associated with O3 exposures for 9 

urban areas.36 The risk assessment for 

the last review also included risk 

estimates for excess respiratory-related 

hospital admissions related to O3

concentrations for New York City. In the 

last review, the risk estimates played a 

significant role in both the staff 

recommendations and in the proposed 

and final decisions to revise the O3

standards. The health risk assessment 

conducted for the current review builds 

upon the methodology and lessons 

learned from the prior review. 

a. Overview 

The updated health risk assessment 

conducted as part of this review 

includes estimates of (1) Risks of lung 

function decrements in all and 

asthmatic school age children, 

respiratory symptoms in asthmatic 

children, respiratory-related hospital 

admissions, and non-accidental and 

cardiorespiratory-related mortality 

associated with recent ambient O3

levels; (2) risk reductions and remaining 


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37The general approach used in the current risk 

assessment was described in the draft Health 

Assessment Plan (EPA, 2005a) that was released to 

the CASAC and general public in April 2005 and 

was the subject of a consultation with the CASAC 

O3 Panel on May 5, 2005. In October 2005, OAQPS 

released the first draft of the Staff Paper containing 

a chapter discussing the risk assessment and first 

draft of the Risk Assessment TSD for CASAC 

consultation and public review on December 8, 

2005. In July 2006, OAQPS released the second 

draft of the Staff Paper and second draft of the Risk 

Assessment TSD for CASAC review and public 

comment which was held by the CASAC O3 Panel 

on August 24–25, 2006. 

risks associated with just meeting the 

current 8-hour O3 NAAQS; and (3) risk 

reductions and remaining risks 

associated with just meeting various 

alternative 8-hour O3 NAAQS in a 

number of example urban areas. This 

risk assessment is more fully described 

and presented in the Staff Paper (EPA, 

2007, chapter 5) and in a technical 

support document (TSD), Ozone Health 

Risk Assessment for Selected Urban 

Areas (Abt Associates, 2006, hereafter 

referred to as ‘‘Risk Assessment TSD’’). 

The scope and methodology for this risk 

assessment were developed over the last 

few years with considerable input from 

the CASAC O3 Panel and the public.37

The information contained in these 

documents included specific criteria for 

the selection of health endpoints, 

studies, and locations to include in the 

assessment. In a peer review letter sent 

by CASAC to the Administrator 

documenting its advice in October 2006 

(Henderson, 2006c), the CASAC O3

Panel concluded that the risk 

assessment was ‘‘well done, balanced, 

and reasonably communicated’’ and that 

the selection of health endpoints for 

inclusion in the quantitative risk 

assessment was appropriate. 

The goals of the risk assessment are: 

(1) To provide estimates of the potential 

magnitude of several morbidity effects 

and mortality associated with current O3

levels, and with meeting the current and 

alternative 8-hour O3 standards in 

specific urban areas; (2) to develop a 

better understanding of the influence of 

various inputs and assumptions on the 

risk estimates; and (3) to gain insights 

into the distribution of risks and 

patterns of risk reductions associated 

with meeting alternative O3 standards. 

The health risk assessment is intended 

to be dependent on and reflect the 

overall weight and nature of the health 

effects evidence discussed above in 

section II.A and in more detail in the 

Criteria Document and Staff Paper. 

While not independent of the overall 

evaluation of the health effects 

evidence, the quantitative health risk 

assessment provides additional insights 

regarding the relative public health 

implications associated with just 

meeting the current and several 

alternative 8-hour standards. 

The risk assessment covers a variety 

of health effects for which there is 

adequate information to develop 

quantitative risk estimates. However, as 

noted by CASAC (Henderson, 2007) and 

in the Staff Paper, there are a number of 

health endpoints (e.g., increased lung 

inflammation, increased airway 

responsiveness, impaired host defenses, 

increased medication usage for 

asthmatics, increased emergency 

department visits for respiratory causes, 

and increased school absences) for 

which there currently is insufficient 

information to develop quantitative risk 

estimates, but which are important to 

consider in assessing the overall public 

health impacts associated with 

exposures to O3. These additional health 

endpoints are discussed above in 

section II.A.2 and are also taken into 

account in considering the level of 

exposures of concern in populations 

particularly at risk, discussed above in 

this notice. 

There are two parts to the health risk 

assessment: one based on combining 

information from controlled human 

exposure studies with modeled 

population exposure and the other 

based on combining information from 

community epidemiological studies 

with either monitored or adjusted 

ambient concentrations levels. Both 

parts of the risk assessment were 

implemented within a new probabilistic 

version of TRIM.Risk, the component of 

EPA’s Total Risk Integrated 

Methodology (TRIM) model framework 

that estimates human health risks. 

EPA recognizes that there are many 

sources of uncertainty and variability in 

the inputs to this assessment and that 

there is significant variability and 

uncertainty in the resulting O3 risk 

estimates. As discussed in chapters 2, 5, 

and 6 of the Staff Paper, there is 

significant year-to-year and city-to-city 

variability related to the air quality data 

that affects both the controlled human 

exposure studies-based and 

epidemiological studies-based parts of 

the risk assessment. There are also 

uncertainties associated with the air 

quality adjustment procedure used to 

simulate just meeting the current and 

selected alternative standards In the 

prior review, different statistical 

approaches using alternative functional 

forms (i.e., quadratic, proportional, 

Weibull) were used to reflect how O3 air 

quality concentrations have historically 

changed. Based on sensitivity analyses 

conducted in the prior review, the 

choice of alternative air quality 

adjustment procedures had only a 

modest impact on the risk estimates 

(EPA, 2007, p. 6–20). With respect to 

uncertainties about estimated 

background concentrations, as 

discussed below and in the Staff Paper 

(EPA 2007b, section 5.4.3), alternative 

assumptions about background levels 

have a variable impact depending on the 

location, standard, and health endpoint 

analyzed. 

With respect to the lung function part 

of the health risk assessment, key 

uncertainties include uncertainties in 

the exposure estimates, discussed 

above, and uncertainties associated with 

the shape of the exposure-response 

relationship, especially at levels below 

0.08 ppm, 8-hour average, where only 

very limited data are available down to 

0.04 ppm and there is an absence of data 

below 0.04 ppm (EPA, 2007, pp. 6–20—

6–21). Concerning the part of the risk 

assessment based on effects reported in 

epidemiological studies, important 

uncertainties include uncertainties (1) 

Surrounding estimates of the O3

coefficients for concentration-response 

relationships used in the assessment, (2) 

involving the shape of the 

concentration-response relationship and 

whether or not a population threshold 

or non-linear relationship exists within 

the range of concentrations examined in 

the studies, (3) related to the extent to 

which concentration-response 

relationships derived from studies in a 

given location and time when O3 levels 

were higher or behavior and /or housing 

conditions were different provide 

accurate representations of the 

relationships for the same locations 

with lower air quality distributions and/ 

or different behavior and/or housing 

conditions, and (4) concerning the 

possible role of co-pollutants which also 

may have varied between the time of the 

studies and the current assessment 

period. An important additional 

uncertainty for the mortality risk 

estimates is the extent to which the 

associations reported between O3 and 

non-accidental and cardiorespiratory 

mortality actually reflect causal 

relationships. 

As discussed below, some of these 

uncertainties have been addressed 

quantitatively in the form of estimated 

confidence ranges around central risk 

estimates; others are addressed through 

separate sensitivity analyses (e.g., the 

influence of alternative estimates for 

policy-relevant background levels) or 

are characterized qualitatively. For both 

parts of the health risk assessment, 

statistical uncertainty due to sampling 

error has been characterized and is 

expressed in terms of 95 percent 

credible intervals. EPA recognizes that 

these credible intervals do not reflect all 

of the uncertainties noted above. 


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38The 12 urban areas are the same urban areas 

evaluated in the exposure analysis discussed in the 

prior section. However, for most of the health 

endpoints based on findings from epidemiological 

studies, the geographic areas and populations 

examined in the health risk assessment were 

limited to those counties included in the original 

epidemiological studies that served as the basis for 

the concentration-response relationships. 

39EPA notes that the estimated level of policyrelevant background O3 used in the prior risk 

assessment was a single concentration of 0.04 ppm, 

which was the midpoint of the range of levels for 

policy-relevant background that was provided in 

the 1996 Criteria Document. 

40Recognizing the importance of this issue, EPA 

intends to conduct additional sensitivity analyses 

related to policy-relevant background and its 

implications for the risk assessment. 

b. Scope and Key Components 

The current health risk assessment is 

based on the information evaluated in 

the final Criteria Document. The risk 

assessment includes several categories 

of health effects and estimates risks 

associated with just meeting the current 

and alternative 8-hour O3 NAAQS and 

with several individual recent years of 

air quality (i.e., 2002, 2003, and 2004). 

The risk assessment considers the same 

alternative air quality scenarios that 

were examined in the human exposure 

analyses described above. Risk estimates 

were developed for up to 12 urban areas 

selected to illustrate the public health 

impacts associated with these air quality 

scenarios.38 As discussed above in 

section II.B.1, the selection of urban 

areas was largely determined by 

identifying areas in the U.S. which 

represented a range of geographic areas, 

population demographics, and 

climatology; with an emphasis on areas 

that do not meet the current 8-hour O3

NAAQS and which included the largest 

areas with O3 nonattainment problems. 

The selection criteria also included 

whether or not there were acceptable 

epidemiological studies available that 

reported concentration-response 

relationships for the health endpoints 

selected for inclusion in the assessment. 

The short-term exposure related 

health endpoints selected for inclusion 

in the quantitative risk assessment 

include those for which the final 

Criteria Document and or Staff Paper 

concluded that the evidence as a whole 

supports the general conclusion that O3, 

acting alone and/or in combination with 

other components in the ambient air 

pollution mix, is either clearly causal or 

is judged to be likely causal. Some 

health effects met this criterion of likely 

causality, but were not included in the 

risk assessment for other reasons, such 

as insufficient exposure-response data 

or lack of baseline incidence data. 

As discussed in the section above 

describing the exposure analysis, in 

order to estimate the health risks 

associated with just meeting the current 

and alternative 8-hour O3 NAAQS, it is 

necessary to estimate the distribution of 

hourly O3 concentrations that would 

occur under any given standard. Since 

compliance is based on a 3-year average, 

the amount of control has been applied 

to each year of data (i.e., 2002 to 2004) 

to estimate risks for a single O3 season 

or single warm O3 season, depending on 

the health effect, based on a simulation 

that adjusted each of these individual 

years so that the three year period 

would just meet the specified standard. 

Consistent with the risk assessment 

approach used in the last review, the 

risk estimates developed for both recent 

air quality levels and just meeting the 

current and selected alternative 8-hour 

standards represent risks associated 

with O3 levels attributable to 

anthropogenic sources and activities 

(i.e., risk associated with concentrations 

above ‘‘policy-relevant background’’). 

Policy-relevant background O3

concentrations used in the O3 risk 

assessment were defined in chapter 2 of 

the Staff Paper (EPA, 2007, pp. 2–48—

2–55) as the O3 concentrations that 

would be observed in the U.S. in the 

absence of anthropogenic emissions of 

precursors (e.g., VOC, NOX, and CO) in 

the U.S., Canada, and Mexico. The 

results of a global tropospheric O3

model (GEOS–CHEM) have been used to 

estimate monthly background daily 

diurnal profiles for each of the 12 urban 

areas for each month of the O3 season 

using meteorology for the year 2001. 

Based on the results of the GEOS–CHEM 

model, the Criteria Document indicates 

that background O3 concentrations are 

generally predicted to be in the range of 

0.015 to 0.035 ppm in the afternoon, 

and they are generally lower under 

conditions conducive to man-made O3

episodes.39

This approach of estimating risks in 

excess of background is judged to be 

more relevant to policy decisions 

regarding ambient air quality standards 

than risk estimates that include effects 

potentially attributable to 

uncontrollable background O3

concentrations. Sensitivity analyses 

examining the impact of alternative 

estimates for background on lung 

function and mortality risk estimates 

have been developed and are included 

in the Staff Paper and Risk Assessment 

TSD and key observations are discussed 

below. Further, CASAC noted the 

difficulties and complexities associated 

with available approaches to estimating 

policy-relevant background 

concentrations (Henderson, 2007). 

Recognizing these complexities, EPA 

requests comments on the new 

approach used in this review for 

estimating these levels as an input to the 

health risk assessment.40

In the first part of the current risk 

assessment, lung function decrement, as 

measured by FEV1, is the only health 

response that is based on data from 

controlled human exposure studies. As 

discussed above, there is clear evidence 

of a causal relationship between lung 

function decrements and O3 exposures 

for school age children engaged in 

moderate exertion based on numerous 

controlled human exposure and summer 

camp field studies conducted by various 

investigators. Risk estimates have been 

developed for O3-related lung function 

decrements (measured as changes in 

FEV1) for all school age children (ages 

5 to 18) and a subset of this group, 

asthmatic school age children (ages 5 to 

18), whose average exertion over an 8- 

hour period was moderate or greater. 

The exposure period and exertion level 

were chosen to generally match the 

exposure period and exertion level used 

in the controlled human exposure 

studies that were the basis for the 

exposure-response relationships. A 

combined data set including individual 

level data from the Folinsbee et al. 

(1988), Horstman et al. (1990), and 

McDonnell et al. (1991) studies, used in 

the previous risk assessment, and more 

recent data from Adams (2002, 2003, 

2006) have been used to estimate 

probabilistic exposure-response 

relationships for 8-hour exposures 

under different definitions of lung 

function response (i.e., ≥10, 15, and 20 

percent decrements in FEV1). As 

discussed in the Staff Paper (EPA, 2007, 

p. 5–27), while these specific controlled 

human exposure studies only included 

healthy adults aged 18–35, findings 

from other controlled human exposure 

studies and summer camp field studies 

involving school age children in at least 

six different locations in the 

northeastern United States, Canada, and 

Southern California indicated changes 

in lung function in healthy children 

similar to those observed in healthy 

adults exposed to O3 under controlled 

chamber conditions. 

Consistent with advice from CASAC 

(Henderson, 2006c), EPA has considered 

both linear and logistic functional forms 

in estimating the probabilistic exposureresponse relationships for lung function 

responses. A Bayesian Markov Chain 

Monte Carlo approach, described in 

more detail in the Risk Assessment TSD, 

has been used that incorporates both 

model uncertainty and uncertainty due 


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41As discussed above in section II.B.1, the urban 

areas were defined using the consolidated statistical 

areas definition and the total population residing in 

the 12 urban areas was approximately 88.5 million 

people. 

42For 9 of the 12 urban areas, the O3 season is 

defined as a period running from March or April 

to September or October. In 3 of the urban areas 

(Houston, Los Angeles, and Sacramento), the O3

season is defined as the entire year. 

43The geographic boundaries for the urban areas 

included in this portion of the risk assessment were 

generally matched to the geographic boundaries 

used in the epidemiological studies that served as 

the basis for the concentration-response functions. 

In most cases, the urban areas were defined as 

either a single county or a few counties for this 

portion of the risk assessment. 

to sample size in the combined data set 

that served as the basis for the 

assessment. EPA has chosen a model 

reflecting a 90 percent weighting on a 

logistic form and a 10 percent weighting 

on a linear form as the base case for the 

current risk assessment. The basis for 

this choice is that the logistic form 

provides a very good fit to the combined 

data set, but a linear model cannot be 

entirely ruled out since there are only 

very limited data (i.e., 30 subjects) at the 

two lowest exposure levels (i.e., 0.040 

and 0.060 ppm). EPA has conducted a 

sensitivity analysis which examines the 

impact on the lung function risk 

estimates of two alternative choices, an 

80 percent logistic/20 percent linear 

split and a 50 percent logistic/50 

percent linear split. 

As noted above, risk estimates have 

been developed for three measures of 

lung function response (i.e., ≥10, 15, and 

20 percent decrements in FEV1). 

However, the Staff Paper and risk 

estimates summarized below focus on 

FEV1 decrements ≥15 percent for all 

school age children and ≥10 percent for 

asthmatic school age children, 

consistent with the advice from CASAC 

(Henderson, 2006c) that these levels of 

response represent indicators of adverse 

health effects in these populations. The 

Risk Assessment TSD and Staff Paper 

present the broader range of risk 

estimates including all three measures 

of lung function response. 

Developing risk estimates for lung 

function decrements involved 

combining probabilistic exposureresponse relationships based on the 

combined data set from several 

controlled human exposure studies with 

population exposure distributions for all 

and asthmatic school age children 

associated with recent air quality and 

air quality simulated to just meet the 

current and alternative 8-hour O3

NAAQS based on the results from the 

exposure analysis described in the 

previous section. The risk estimates 

have been developed for 12 large urban 

areas for the O3 season.41 These 12 

urban areas include approximately 18.3 

million school age children, of which 

2.6 million are asthmatic school age 

children.42

In addition to uncertainties arising 

from sample size considerations, which 

are quantitatively characterized and 

presented as 95 percentile credible 

intervals, there are additional 

uncertainties and caveats associated 

with the lung function risk estimates. 

These include uncertainties about the 

shape of the exposure-response 

relationship, particularly at levels below 

0.080 ppm, and about policy-relevant 

background levels, for which sensitivity 

analyses have been conducted. 

Additional important caveats and 

uncertainties concerning the lung 

function portion of the health risk 

assessment include: (1) The 

uncertainties and limitations associated 

with the exposure estimates discussed 

above and (2) the inability to account for 

some factors which are known to affect 

the exposure-response relationships 

(e.g., assigning healthy and asthmatic 

children the same responses as observed 

in healthy adult subjects and not 

adjusting response rates to reflect the 

increase and attenuation of responses 

that have been observed in studies of 

lung function responses upon repeated 

exposures). A more complete discussion 

of assumptions and uncertainties is 

contained in chapter 5 of the Staff Paper 

and in the Risk Assessment TSD (Abt 

Associates, 2006). 

The second part of the risk assessment 

is based on health effects observed in 

epidemiological studies. Based on a 

review of the evidence evaluated in the 

Criteria Document and Staff Paper, as 

well as the criteria discussed in chapter 

5 of the Staff Paper, the following 

categories of health endpoints 

associated with short-term exposures to 

ambient O3 concentrations were 

included in the risk assessment: 

respiratory symptoms in moderate to 

severe asthmatic children, hospital 

admissions for respiratory causes, and 

non-accidental and cardiorespiratory 

mortality. As discussed above, there is 

strong evidence of a causal relationship 

for the respiratory morbidity endpoints 

included in the current risk assessment. 

With respect to nonaccidental and 

cardiorespiratory mortality, the Criteria 

Document concludes that there is strong 

evidence which is highly suggestive of 

a causal relationship between 

nonaccidental and cardiorespiratoryrelated mortality and O3 exposures 

during the warm O3 season. As 

discussed in the Staff Paper (chapter 5), 

EPA also recognizes that for some of the 

effects observed in epidemiological 

studies, such as increased respiratoryrelated hospital admissions and 

nonaccidental and cardiorespiratory 

mortality, O3 may be serving as an 

indicator for reactive oxidant species in 

the overall photochemical oxidant mix 

and that these other constituents may be 

responsible in whole or part for the 

observed effects. 

Risk estimates for each health 

endpoint category were only developed 

for areas that were the same or close to 

the location where at least one 

concentration-response function for the 

health endpoint had been estimated.43

Thus, for respiratory symptoms in 

moderate to severe asthmatic children 

only the Boston urban area was 

included and four urban areas were 

included for respiratory-related hospital 

admissions. Nonaccidental mortality 

risk estimates were developed for 12 

urban areas and 8 urban areas were 

included for cardiorespiratory mortality. 

The concentration-response 

relationships used in the assessment are 

based on findings from human 

epidemiological studies that have relied 

on fixed-site ambient monitors as a 

surrogate for actual ambient O3

exposures. In order to estimate the 

incidence of a particular health effect 

associated with recent air quality in a 

specific county or set of counties 

attributable to ambient O3 exposures in 

excess of background, as well as the 

change in incidence corresponding to a 

given change in O3 levels resulting from 

just meeting the current or alternative 8- 

hour O3 standards, three elements are 

required for this part of the risk 

assessment. These elements are: (1) Air 

quality information (including recent air 

quality data for O3 from ambient 

monitors for the selected location, 

estimates of background O3

concentrations appropriate for that 

location, and a method for adjusting the 

recent data to reflect patterns of air 

quality estimated to occur when the area 

just meets a given O3 standard); (2) 

relative risk-based concentrationresponse functions that provide an 

estimate of the relationship between the 

health endpoints of interest and ambient 

O3 concentration; and (3) annual or 

seasonal baseline health effects 

incidence rates and population data, 

which are needed to provide an estimate 

of the seasonal baseline incidence of 

health effects in an area before any 

changes in O3 air quality. 

A key component in the portion of the 

risk assessment based on 

epidemiological studies is the set of 

concentration-response functions which 

provide estimates of the relationships 


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between each health endpoint of 

interest and changes in ambient O3

concentrations. Studies often report 

more than one estimated concentrationresponse function for the same location 

and health endpoint. Sometimes models 

include different sets of co-pollutants 

and/or different lag periods between the 

ambient concentrations and reported 

health responses. For some health 

endpoints, there are studies that 

estimated multi-city and single-city O3

concentration-response functions. While 

the Risk Assessment TSD and chapter 5 

of the Staff Paper present a more 

comprehensive set of risk estimates, 

EPA has focused on estimates based on 

multi-city studies where available. The 

advantages of relying more heavily on 

concentration-response functions based 

on multi-city studies include: (1) More 

precise effect estimates due to larger 

data sets, reducing the uncertainty 

around the estimated coefficient; (2) 

greater consistency in data handling and 

model specification that can eliminate 

city-to-city variation due to study 

design; and (3) less likelihood of 

publication bias or exclusion of 

reporting of negative or nonsignificant 

findings. Where studies reported 

different effect estimates for varying lag 

periods, consistent with the Criteria 

Document, single day lag periods of 0 to 

1 days were used for associations with 

respiratory hospital admissions and 

mortality. For mortality associated with 

exposure to O3 which may result over a 

several day period after exposure, 

distributed lag models, which take into 

account the contribution to mortality 

effects over several days, were used 

where available. 

One of the most important elements 

affecting uncertainties in the 

epidemiological-based portion of the 

risk assessment is the concentrationresponse relationships used in the 

assessment. The uncertainty resulting 

from the statistical uncertainty 

associated with the estimate of the O3

coefficient in the concentrationresponse function was characterized 

either by confidence intervals or by 

Bayesian credible intervals around the 

corresponding point estimates of risk. 

Confidence and credible intervals 

express the range within which the true 

risk is likely to fall if the only 

uncertainty surrounding the O3

coefficient involved sampling error. 

Other uncertainties, such as differences 

in study location, time period (i.e., the 

years in which the study was 

conducted), and model uncertainties are 

not represented by the confidence or 

credible intervals presented, but were 

addressed by presenting estimates for 

different urban areas, by including risk 

estimates based on studies using 

different time periods and models, 

where available, and/or are discussed 

throughout section 5.3 of the Staff 

Paper. Because O3 effects observed in 

the epidemiological studies have been 

more clearly and consistently shown for 

warm season analyses, all analyses for 

this portion of the risk assessment were 

carried out for the same time period, 

April through September. 

The Criteria Document finds that no 

definitive conclusion can be reached 

with regard to the existence of 

population thresholds in 

epidemiological studies (Criteria 

Document, pp. 8–44). EPA recognizes, 

however, the possibility that thresholds 

for individuals may exist for reported 

associations at fairly low levels within 

the range of air quality observed in the 

studies, but not be detectable as 

population thresholds in 

epidemiological analyses. Based on the 

Criteria Document’s conclusions, EPA 

judged and CASAC concurred, that 

there is insufficient evidence to support 

use of potential population threshold 

levels in the quantitative risk 

assessment. However, EPA recognizes 

that there is increasing uncertainty 

about the concentration-response 

relationship at lower concentrations 

which is not captured by the 

characterization of the statistical 

uncertainty due to sampling error. 

Therefore, the risk estimates for 

respiratory symptoms in moderate to 

severe asthmatic children, respiratoryrelated hospital admissions, and 

premature mortality associated with 

exposure to O3 must be considered in 

light of uncertainties about whether or 

not these O3-related effects occur in 

these populations at very low O3

concentrations. 

With respect to variability within this 

portion of the risk assessment, there is 

variability among concentrationresponse functions describing the 

relation between O3 and both 

respiratory-related hospital admissions 

and nonaccidental and cardiorespiratory 

mortality across urban areas. This 

variability is likely due to differences in 

population (e.g., age distribution), 

population activities that affect 

exposure to O3 (e.g., use of air 

conditioning), levels and composition of 

co-pollutants, baseline incidence rates, 

and/or other factors that vary across 

urban areas. The current risk assessment 

incorporates some of the variability in 

key inputs to the analysis by using 

location-specific inputs (e.g., locationspecific concentration-response 

functions, baseline incidence rates, and 

air quality data). Although spatial 

variability in these key inputs across all 

U.S. locations has not been fully 

characterized, variability across the 

selected locations is imbedded in the 

analysis by using, to the extent possible, 

inputs specific to each urban area. 

c. Risk Estimates and Key Observations 

The Staff Paper (chapter 5) and Risk 

Assessment TSD present risk estimates 

associated with just meeting the current 

and several alternative 8-hour 

standards, as well as three recent years 

of air quality as represented by 2002, 

2003, and 2004 monitoring data. As 

discussed in the exposure analysis 

section above, there is considerable cityto-city and year-to-year variability in the 

O3 levels during this period, which 

results in significant variability in both 

portions of the health risk assessment. 

In the 1997 risk assessment, risks for 

lung function decrements associated 

with 1-hour heavy exertion, 1-hour 

moderate exertion, and 8-hour moderate 

exertion exposures were estimated. 

Since the 8-hour moderate exertion 

exposure scenario for children clearly 

resulted in the greatest health risks in 

terms of lung function decrements, EPA 

has chosen to include only the 8-hour 

moderate exertion exposures in the 

current risk assessment for this health 

endpoint. Thus, the risk estimates 

presented here and in the Staff Paper are 

most useful for making relative 

comparisons across alternative air 

quality scenarios and do not represent 

the total risks for lung function 

decrements in children or other groups 

within the general population 

associated with any of the air quality 

scenarios. Thus, some outdoor workers 

and adults engaged in moderate exertion 

over multi-hour periods (e.g., 6–8-hour 

exposures) also would be expected to 

experience similar lung function 

decrements. However, the percentage of 

each of these other subpopulations 

expected to experience these effects is 

expected to be smaller than all school 

age children who tend to spend more 

hours outdoors while active based on 

the exposure analyses conducted during 

the prior review. 

Table 2 presents a summary of the 

risk estimates for lung function 

decrements for the current standard and 

several alternative 8-hour standard 

levels with the same form as the current 

8-hour standard. The estimates are for 

the aggregate number and percent of all 

school age children across 12 urban 

areas and the aggregate number and 

percent of asthmatic school age children 


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44 Due to time constraints, lung function risk 

estimates for asthmatic school age children were 

developed for only 5 of the 12 urban areas, and the 

areas were selected to represent different 

geographic regions. The 5 areas were: Atlanta, 

Chicago, Houston, Los Angeles, and New York City. 

across 5 urban areas 44 who are 

estimated to have at least 1 moderate or 

greater lung function response (defined 

as FEV1 ≥15 percent in all children and 

≥10 percent in asthmatic children) 

associated with 8-hour exposures to O3

while engaged in moderate or greater 

exertion on average over the 8-hour 

period. The lung function risk estimates 

summarized in Table 2 illustrate the 

year-to-year variability in both 

remaining risk associated with a 

relatively high year (i.e., based on 

adjusting 2002 O3 air quality data) and 

relatively low year (based on adjusting 

2004 O3 air quality data) as well as the 

year-to-year variability in the risk 

reduction estimated to occur associated 

with various alternative standards 

relative to just meeting the current 

standard. For example, it is estimated 

that about 610,000 school age children 

(3.2 percent of school age children) 

would experience 1 or more moderate 

lung function decrements for the 12 

urban areas associated with O3 levels 

just meeting the current standard based 

on 2002 air quality data compared to 

230,000 (1.2 percent of children) 

associated with just meeting the current 

standard based on 2004 air quality data. 

TABLE 2.—NUMBER AND PERCENT OF ALL AND ASTHMATIC SCHOOL AGE CHILDREN IN SEVERAL URBAN AREAS ESTIMATED TO EXPERIENCE MODERATE OR GREATER LUNG FUNCTION RESPONSES 1 OR MORE TIMES PER SEASON ASSOCIATED WITH 8-HOUR OZONE EXPOSURES ASSOCIATED WITH JUST MEETING ALTERNATIVE 8-HOUR STANDARDS

BASED ON ADJUSTING 2002 AND 2004 AIR QUALITY DATA 1, 2

8-Hour air quality standards 3

All children, ages 5–18, FEV1 ≥15 percent, aggregate 

for 12 urban areas, number of children affected (% of 

all) [% reduction from current standard] 

Asthmatic children, ages 5–18, FEV1 ≥10 percent, aggregate for 5 urban areas, number of children affected 

(% of group) [% reduction from current standard] 

2002 2004 2002 2004] 

0.084 ppm (Current standard).610,000 (3.3%) ................. 230,000 (1.2%) ................. 130,000 (7.8%) ................. 70,000 (4.2%). 

0.080 ppm ......................... 490,000 (2.7%) [20% reduction].180,000 (1.0%) [22% reduction].NA4 ................................... NA. 

0.074 ppm ......................... 340,000 (1.9%) [44% reduction].130,000 (0.7%) [43% reduction].90,000 (5.0%) [31 % reduction].40,000 (2.7%) [43% reduction]. 

0.070 ppm ......................... 260,000 (1.5%) [57% reduction].100,000 (0.5%) [57% reduction].NA ..................................... NA. 

0.064 ppm ......................... 180,000 (1.0%) [70% reduction].70,000 (0.4%) [70% reduction].50,000 (3.0%) [62% reduction].20,000 (1.5%) [71% reduction]. 

1Associated with exposures while engaged in moderate or greater exertion which is defined as having an 8-hour average equivalent ventilation 

rate ≥13 l-min/m 2. 2Estimates are the aggregate central tendency results based on either 12 urban areas (Atlanta, Boston, Chicago, Cleveland, Detroit, Houston, 

Los Angeles, New York, Philadelphia, Sacramento, St. Louis, and Washington, DC) or 5 urban areas (Atlanta, Chicago, Houston, Los Angeles, 

New York). Estimates are for the O3 season which is all year in Houston, Los Angeles and Sacramento and March or April to September or October for the remaining urban areas. 3All standards summarized here have the same form as the current 8-hour standard which is specified as the 3-year average of the annual 4th 

highest daily maximum 8-hour average concentrations must be at or below the stated concentration level. As described in the Staff Paper (section 4.5.8), recent O3 air quality distributions have been statistically adjusted to simulate just meeting the current and selected alternative standards. These simulations do not represent predictions of when, whether, or how areas might meet the specified standards 4 NA (not available) indicates that EPA did not develop risk estimates for these scenarios for the asthmatic school age children population. 

As discussed in the Staff Paper, a 

child may experience multiple 

occurrences of a lung function response 

during the O3 season. For example, 

upon meeting the current 8-hour 

standard, the median estimates are that 

about 610,000 children would 

experience a moderate or greater lung 

function response 1 or more times for 

the aggregate of the 12 urban areas over 

a single O3 season (based on the 2002 

simulation), and that there would be 

almost 3.2 million total occurrences. 

Thus, on average it is estimated that 

there would be about 5 occurrences per 

O3 season per responding child for air 

quality just meeting the current 8-hour 

standard across the 12 urban areas. 

While the estimated number of 

occurrences per O3 season is lower 

when based on the 2004 simulation than 

for the 2002 simulation, the estimated 

number of occurrences per responding 

child is similar. EPA recognizes that 

some children in the population might 

have only 1 or 2 occurrences while 

others may have 6 or more occurrences 

per O3 season. Risk estimates based on 

adjusting 2003 air quality to simulate 

just meeting the current and alternative 

8-hour standards are intermediate to the 

estimates presented in Table 2 above in 

this notice and are presented in the Staff 

Paper (chapter 5) and Risk Assessment 

TSD. 

For just meeting the current 8-hour 

standard, Table 5–8 in the Staff Paper 

shows that median estimates across the 

12 urban areas for all school age 

children experiencing 1 or more 

moderate lung function decrements 

ranges from 0.9 to 5.4 percent based on 

the 2002 simulation and from 0.8 to 2.2 

percent based on the 2004 simulation. 

Risk estimates for each urban area 

included in the assessment, for each of 

the three years analyzed, and for 

additional alternative standards are 

presented in chapter 5 of the Staff Paper 

and in the Risk Assessment TSD. 

For just meeting the current 8-hour 

standard, the median estimates across 

the 5 urban areas for asthmatic school 

age children range from 3.4 to 10.9 

percent based on the 2002 simulation 

and from 3.2 to 6.9 percent based on the 

2004 simulation. 

Key observations important in 

comparing estimated lung function risks 

associated with attainment of the 

current NAAQS and alternative 

standards under consideration include: 

(1) As discussed above, there is 

significant year to year variability in the 

range of median estimates of the number 

of school age children (ages 5–18) 

estimated to experience at least one 

FEV1 decrement ≥15 percent due to 8- 

hour O3 exposures across the 12 urban 


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areas analyzed, and similarly across the 

5 urban areas analyzed for asthmatic 

school age children (ages 5–18) 

estimated to experience at least one 

FEV1 decrement ≥10 percent, when the 

current and alternative 8-hour standards 

are just met. 

(2) For asthmatic school age children, 

the median estimates of occurrences of 

FEV1 decrements ≥10% range from 

52,000 to nearly 510,000 responses 

associated with just meeting the current 

standard (based on the 2002 simulation) 

and range from 61,000 to about 240,000 

occurrences (based on the 2004 

simulation). These risk estimates would 

be reduced to a range of 14,000 to about 

275,000 occurrences (2002 simulation) 

and to about 18,000 to nearly 125,000 

occurrences (2004 simulation) upon just 

meeting the most stringent alternative 8- 

hour standard (0.064 ppm, 4th highest). 

The average number of occurrences per 

asthmatic child in an O3 season ranged 

from about 6 to 11 associated with just 

meeting the current standard (2002 

simulation). The average number of 

occurrences per asthmatic child ranged 

from 4 to 12 upon meeting the most 

stringent alternative examined (0.064 

ppm, 4th-highest) based on the 2002 

simulation. The number of occurrences 

per asthmatic child is similar for the 

scenarios based on the 2004 simulation. 

As discussed above, several 

epidemiological studies have reported 

increased respiratory morbidity 

outcomes (e.g., respiratory symptoms in 

moderate to severe asthmatic children, 

respiratory-related hospital admissions) 

and increased nonaccidental and 

cardiorespiratory mortality associated 

with exposure to ambient O3

concentrations. The results and key 

observations from this portion of the 

risk assessment are presented below: 

(1) Estimates for increased respiratory 

symptoms (i.e., chest tightness, 

shortness of breath, and wheeze) in 

moderate/severe asthmatic children 

(ages 0–12) were developed for the 

Boston urban area only. The median 

estimated number of days involving 

chest tightness (using the concentrationresponse relationship with only O3 in 

the model) is about 6,100 (based on the 

2002 simulation) and about 4,500 (based 

on the 2004 simulation) upon meeting 

the current 8-hour standard and this is 

reduced to about 4,600 days (2002 

simulation) and 3,100 days (2004 

simulation) upon meeting the most 

stringent alternative examined (0.064 

ppm, 4th-highest daily maximum 8- 

hour average). This corresponds to 11 

percent (2002 simulation) and 8 percent 

(2004 simulation) of total incidence of 

chest tightness upon meeting the 

current 8-hour standard and to about 8 

percent (2002 simulation) and 5.5 

percent (2004 simulation) of total 

incidence of chest tightness upon 

meeting a 0.064 ppm, 4th-highest daily 

maximum 8-hour average standard. 

Similar patterns of effects and 

reductions in effects are observed for 

each of the respiratory symptoms 

examined. 

(2) The Staff Paper and Risk 

Assessment TSD present unscheduled 

hospital admission risk estimates for 

respiratory illness and asthma in New 

York City associated with short-term 

exposures to O3 concentrations in 

excess of background levels from April 

through September for several recent 

years (2002, 2003, and 2004) and upon 

just meeting the current and alternative 

8-hour standards based on simulating 

O3 levels using 2002–2004 O3 air quality 

data. For total respiratory illness, EPA 

estimates about 6.4 cases per 100,000 

relevant population (2002 simulation) 

and about 4.6 cases per 100,000 relevant 

population (2004 simulation), which 

represents 1.5 percent (2002 simulation) 

and 1.0 percent (2004 simulation) of 

total incidence or about 510 cases (2002 

simulation) and about 370 cases (2004 

simulation) upon just meeting the 

current 8-hour standard. For asthmarelated hospital admissions, which are a 

subset of total respiratory illness 

admissions, the estimates are about 5.5 

cases per 100,000 relevant population 

(2002 simulation) and about 3.9 cases 

per 100,000 relevant population (2004 

simulation), which represents about 3.3 

percent (2002 simulation) and 2.4 

percent (2004 simulation) of total 

incidence or about 440 cases (2002) and 

about 310 cases (2004) for this same air 

quality scenario. 

For increasingly more stringent 

alternative 8-hour standards, there is a 

gradual reduction in respiratory illness 

cases per 100,000 relevant population 

from 6.4 cases per 100,000 upon just 

meeting the current 8-hour standard to 

4.6 cases per 100,000 under the most 

stringent 8-hour standard (i.e., 0.064 

ppm, average 4th-highest daily 

maximum) analyzed based on the 2002 

simulation. Similarly, based on the 2004 

simulation there is a gradual reduction 

from 4.6 cases per 100,000 relevant 

population upon just meeting the 

current 8-hour standard to 3.0 cases per 

100,000 under the 0.064 ppm, average 

4th-highest daily maximum standard. 

Additional respiratory-related 

hospital admission estimates for three 

other locations are provided in the Risk 

Assessment TSD. EPA notes that the 

concentration-response functions for 

each of these locations examined 

different outcomes in different age 

groups (e.g., > age 30 in Los Angeles, 

> age 64 in Cleveland and Detroit, vs. all 

ages in New York City), making 

comparison of the risk estimates across 

the areas very difficult. 

(3) Based on the median estimates for 

incidence for nonaccidental mortality 

(based on the Bell et al. (2004) 95 cities 

concentration-response function), 

meeting the most stringent standard 

(0.064 ppm) is estimated to reduce 

mortality by 40 percent of what it would 

be associated with just meeting the 

current standard (based on the 2002 

simulation). The patterns for 

cardiorespiratory mortality are similar. 

The aggregate O3-related 

cardiorespiratory mortality upon just 

meeting the most stringent standard 

shown is estimated to be about 42 

percent of what it would be upon just 

meeting the current standard, using 

simulated O3 concentrations that just 

meet the current and alternative 8-hour 

standards based on the 2002 simulation. 

Using the 2004 simulation, the 

corresponding reductions show a 

similar pattern but are somewhat 

greater. 

(4) Much of the contribution to the 

risk estimates for non-accidental and 

cardiorespiratory mortality upon just 

meeting the current 8-hour standard is 

associated with 24-hour O3

concentrations between background and 

0.040 ppm. Based on examining 

relationships between 24-hour 

concentrations averaged across the 

monitors within an urban area and 8- 

hour daily maximum concentrations, 8- 

hour daily maximum levels at the 

highest monitor in an urban area 

associated with these averaged 24-hour 

levels are generally about twice as high 

as the 24-hour levels. Thus, most O3- 

related nonaccidental mortality is 

estimated to occur when O3

concentrations are between background 

and when the highest monitor in the 

urban area is at or below 0.080 ppm, 8- 

hour average concentration. 

The discussion below highlights 

additional observations and insights 

from the O3 risk assessment, together 

with important uncertainties and 

limitations. 

(1) As discussed in the Staff Paper 

(section 5.4.5) EPA has greater 

confidence in relative comparisons in 

risk estimates between alternative 

standards than in the absolute 

magnitude of risk estimates associated 

with any particular standard. 

(2) Significant year-to-year variability 

in O3 concentrations combined with the 

use of a 3-year design value to 

determine the amount of air quality 

adjustment to be applied to each year 

analyzed, results in significant year-toyear variability in the annual health risk 


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45For example, assuming lower background 

levels resulted in increased estimates of nonaccidental mortality incidence per 100,000 that 

were often 50 to 100 percent greater than the base 

case estimates; assuming higher background levels 

resulted in decreased estimates of non-accidental 

mortality incidence per 100,000 that were less than 

the base case estimates by 50 percent or more in 

many of the areas. 

46 If the standard were to be specified to the 

nearest thousandth ppm, the current 0.08 ppm 8- 

hour standard would be equivalent to a standard set 

at 0.084 ppm, reflecting the data rounding 

conventions that are part of the definition of the 

current 8-hour standard. 

estimates upon just meeting the current 

and potential alternative 8-hour 

standards. 

(3) There is noticeable city-to-city 

variability in estimated O3-related 

incidence of morbidity and mortality 

across the 12 urban areas analyzed for 

both recent years of air quality and for 

air quality adjusted to simulate just 

meeting the current and selected 

potential alternative standards. This 

variability is likely due to differences in 

air quality distributions, differences in 

exposure related to many factors 

including varying activity patterns and 

air exchange rates, differences in 

baseline incidence rates, and differences 

in susceptible populations and age 

distributions across the 12 urban areas. 

(4) With respect to the uncertainties 

about estimated policy-relevant 

background concentrations, as 

discussed in the Staff Paper (section 

5.4.3), alternative assumptions about 

background levels had a variable impact 

depending on the health effect 

considered and the location and 

standard analyzed in terms of the 

absolute magnitude and relative changes 

in the risk estimates. There was 

relatively little impact on either 

absolute magnitude or relative changes 

in lung function risk estimates due to 

alternative assumptions about 

background levels. With respect to O3- 

related non-accidental mortality, while 

notable differences (i.e., greater than 50 

percent)45 were observed for 

nonaccidental mortality in some areas, 

particularly for more stringent 

standards, the overall pattern of 

estimated reductions, expressed in 

terms of percentage reduction relative to 

the current standard, was significantly 

less impacted. 

C. Conclusions on the Adequacy of the 

Current Primary Standard 

1. Background 

The initial issue to be addressed in 

the current review of the primary O3

standard is whether, in view of the 

advances in scientific knowledge and 

additional information, the existing 

standard should be revised. In 

evaluating whether it is appropriate to 

retain or revise the current standard, the 

Administrator builds upon the last 

review and reflects the broader body of 

evidence and information now 

available. The Administrator has taken 

into account both evidence-based and 

quantitative exposure- and risk-based 

considerations in developing 

conclusions on the adequacy of the 

current primary O3 standard. Evidencebased considerations include the 

assessment of evidence from controlled 

human exposure, animal toxicological, 

field, and epidemiological studies for a 

variety of health endpoints. For those 

endpoints based on epidemiological 

studies, greater weight has been placed 

on associations with health endpoints 

that are causal or likely causal based on 

an integrative synthesis of the entire 

body of evidence, including not only all 

available epidemiological evidence but 

also evidence from animal toxicological 

and controlled human exposure studies. 

Less weight has been placed on 

evidence of associations that were 

judged to be only suggestive of possible 

causal relationships. Consideration of 

quantitative exposure- and risk-based 

information draws from the results of 

the exposure and risk assessments 

described above. More specifically, 

estimates of the magnitude of O3-related 

exposures and risks associated with 

recent air quality levels, as well as the 

exposure and risk reductions likely to 

be associated with just meeting the 

current 8-hour primary O3 NAAQS, 

have been considered. 

In this review, a series of general 

questions frames the approach to 

reaching a decision on the adequacy of 

the current standard, such as the 

following: (1) To what extent does 

newly available information reinforce or 

call into question evidence of 

associations of O3 exposures with effects 

identified in the last review?; (2) to what 

extent has evidence of new effects and/ 

or at-risk populations become available 

since the last review?; (3) to what extent 

have important uncertainties identified 

in the last review been reduced and 

have new uncertainties emerged?; (4) to 

what extent does newly available 

information reinforce or call into 

question any of the basic elements of the 

current standards? 

The question of whether the available 

evidence supports consideration of a 

standard that is more protective than the 

current standard includes consideration 

of: (1) Whether there is evidence that 

associations, especially likely causal 

associations, extend to ambient O3

concentration levels that are as low as 

or lower than had previously been 

observed, and the important 

uncertainties associated with that 

evidence; (2) the extent to which 

exposures of concern and health risks 

are estimated to occur in areas upon 

meeting the current standard and the 

important uncertainties associated with 

the estimated exposures and risks; and 

(3) the extent to which the O3-related 

health effects indicated by the evidence 

and the exposure and risk assessments 

are considered important from a public 

health perspective, taking into account 

the nature and severity of the health 

effects, the size of the at-risk 

populations, and the kind and degree of 

the uncertainties associated with these 

considerations. 

The current primary O3 standard is an 

8-hour standard, which was set at a 

level of 0.08 ppm,46 with a form of the 

annual fourth-highest daily maximum 8- 

hour average concentration, averaged 

over three years. This standard was 

chosen to provide protection to the 

public, especially children and other atrisk populations, against a wide range of 

O3-induced health effects. As an 

introduction to this discussion of the 

adequacy of the current O3 standard, it 

is useful to summarize the key factors 

that formed the basis of the decision in 

the last review to revise the averaging 

time, level, and form of the then current 

1-hour standard. 

In the last review, the key factor in 

deciding to revise the averaging time of 

the primary standard was evidence from 

controlled human exposure studies of 

healthy young adult subjects exposed 

for 1 to 8 hours to O3. The best 

documented health endpoints in these 

studies were decrements in indices of 

lung function, such as forced expiratory 

volume in 1 second (FEV1), and 

respiratory symptoms, such as cough 

and chest pain on deep inspiration. For 

short-term exposures of 1 to 3 hours, 

group mean FEV1 decrements were 

statistically significant for O3

concentrations only at and above 0.12 

ppm, and only when subjects engaged 

in very heavy exertion. By contrast, 

evidence available in the prior review 

showed that prolonged exposures of 6 to 

8 hours produced statistically 

significant group mean FEV1

decrements at the lowest O3

concentrations evaluated in those 

studies, 0.080 ppm, even when 

experimental subjects were engaged in 

more realistic intermittent moderate 

exertion levels. The health significance 

of this newer evidence led to the 

conclusion in the 1997 final decision 

that the 8-hour averaging time is more 

directly associated with health effects of 

concern at lower O3 concentrations than 

is the 1-hour averaging time. 


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47 In the last review, ‘‘exposures of concern’’

referred to exposures at and above 0.08 ppm, 8-hour 

average, at which a range of health effects have been 

observed in controlled human studies, but for 

which data were too limited to allow for 

quantitative risk assessment. (62 FR 38860, July 18, 

1997). 

Based on the available evidence of O3- 

related health effects, the following 

factors were of particular importance in 

the last review in informing the 

selection of the level and form of a new 

8-hour standard: (1) Quantitative 

estimates of O3-related risks to active 

children, who were judged to be an atrisk subgroup of concern, in terms of 

transient and reversible respiratory 

effects judged to be adverse, including 

moderate to large decreases in lung 

function and moderate to severe pain on 

deep inspiration, and the uncertainty 

and variability in such estimates; (2) 

consideration of both the estimated 

percentages, total numbers of children, 

and number of times they were likely to 

experience such effects; (3) 

epidemiological evidence of 

associations between ambient O3 and 

increased respiratory hospital 

admissions, and quantitative estimates 

of percentages and total numbers of 

asthma-related admissions in one 

example urban area that were judged to 

be indicative of a pyramid of much 

larger effects, including respiratoryrelated hospital admissions, emergency 

department visits, doctor visits, and 

asthma attacks and related increased 

medication use; (4) quantitative 

estimates of the number of ‘‘exposures 

of concern47’’ (defined as exposures ≥ 

0.080 ppm for 6 to 8 hour) that active 

children are likely to experience, and 

the uncertainty and variability in such 

estimates; (5) the judgment that such 

exposures are an important indicator of 

public health impacts of O3-related 

effects for which information is too 

limited to develop quantitative risk 

estimates, including increased 

nonspecific bronchial responsiveness 

(e.g., related to aggravation of asthma), 

decreased pulmonary defense 

mechanisms (suggestive of increased 

susceptibility to respiratory infection), 

and indicators of pulmonary 

inflammation (related to potential 

aggravation of chronic bronchitis or 

long-term damage to the lungs); (6) the 

broader public health perspective of the 

number of people living in areas that 

would breathe cleaner air as a result of 

the revised standard; (7) consideration 

of the relative seriousness of various 

health effects and the relative degree of 

certainty in both the likelihood that 

people will experience various health 

effects and their medical significance; 

(8) the relationship of a standard level 

to estimated ‘‘background’’ levels 

associated with nonanthropogenic 

sources of O3; and (9) CASAC’s advice 

and recommendations. Additional 

factors considered in selecting the form 

of the standard included balancing the 

public health implications of the 

estimated number of times in an O3

season that the standard level might be 

exceeded in an area that is in attainment 

with the standard with the year-to-year 

stability of the air quality statistic, 

which can be particularly affected by 

years with unusual meteorology. A more 

stable air quality statistic serves to avoid 

disruptions to ongoing control programs 

that could result from moving into and 

out of attainment, thereby interrupting 

the public health protection afforded by 

such control programs. 

In reaching a final decision in the last 

review, the Administrator was mindful 

that O3 exhibits a continuum of effects, 

such that there is no discernible 

threshold above which public health 

protection requires that no exposures be 

allowed or below which all risks to 

public health can be avoided. The final 

decision reflected a recognition that 

important uncertainties remained, for 

example with regard to interpreting the 

role of other pollutants co-occurring 

with O3 in observed associations, 

understanding biological mechanisms of 

O3-related health effects, and estimating 

human exposures and quantitative risks 

to at-risk populations for these health 

effects. 

2. Evidence- and Exposure/Risk-Based 

Considerations in the Staff Paper 

The Staff Paper (section 6.3.1) 

considers the evidence presented in the 

Criteria Document as discussed above in 

section II.A as a basis for evaluating the 

adequacy of the current O3 standard, 

recognizing that important uncertainties 

remain. The extensive body of human 

clinical, toxicological, and 

epidemiological evidence serves as the 

basis for the judgments about O3-related 

health effects discussed above, 

including judgments about causal 

relationships with a range of respiratory 

morbidity effects, including lung 

function decrements, increased 

respiratory symptoms, airway 

inflammation, increased airway 

responsiveness, and respiratory-related 

hospitalizations and emergency 

department visits in the warm season, 

and about the evidence being highly 

suggestive that O3 directly or indirectly 

contributes to non-accidental and 

cardiopulmonary-related mortality. 

These judgments take into account 

important uncertainties that remain in 

interpreting this evidence. For example, 

with regard to the utility of time-series 

epidemiological studies to inform 

judgments about a NAAQS for an 

individual pollutant, such as O3, within 

a mix of highly correlated pollutants, 

such as the mix of oxidants produced in 

photochemical reactions in the 

atmosphere, the Staff Paper notes that 

there are limitations especially at 

ambient O3 concentrations below levels 

at which O3-related effects have been 

observed in controlled human exposure 

studies. The Staff Paper (section 3.4.5) 

also recognizes that the available 

epidemiological evidence neither 

supports nor refutes the existence of 

thresholds at the population level for 

effects such as increased hospital 

admissions and premature mortality. 

There are limitations in epidemiological 

studies that make discerning thresholds 

in populations difficult, including low 

data density in the lower concentration 

ranges, the possible influence of 

exposure measurement error, and 

variability in susceptibility to O3-related 

effects in populations. 

While noting these limitations in the 

interpretation of the findings from the 

epidemiological studies, the Staff Paper 

(section 3.4.5) concludes that if a 

population threshold level does exist, it 

would likely be well below the level of 

the current O3 standard and possibly 

within the range of background levels. 

As discussed above in section II.A.3.a, 

this conclusion is supported by several 

epidemiological studies that have 

explored the question of potential 

thresholds directly, either using a 

statistical curve-fitting approach to 

evaluate whether linear or non-linear 

models fit the data better using sub-sets 

of the data, where days over or under a 

specific cutpoint (e.g., 0.080 ppm or 

even lower O3 levels) were excluded 

and then evaluating the association for 

statistical significance. In addition to 

direct consideration of the 

epidemiological studies, findings from 

controlled human exposure studies 

discussed above in section II.A.2.a.i(a)(i) 

indicate that prolonged exposures 

produced statistically significant group 

mean FEV1 decrements and symptoms 

in healthy adult subjects at levels down 

to at least 0.060 ppm, with a small 

percentage of subjects experiencing 

notable effects (e.g., >10 percent FEV1

decrement, pain on deep inspiration). 

Controlled human exposure studies 

evaluated in the last review also found 

significant responses in indicators of 

lung inflammation and cell injury at 

0.080 ppm in healthy adult subjects. 

The effects in these controlled human 

exposure studies were observed in 

healthy young adult subjects, and it is 

likely that more serious responses, and 


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responses at lower levels, would occur 

in people with asthma and other 

respiratory diseases. These 

physiological effects have been linked to 

aggravation of asthma and increased 

susceptibility to respiratory infection, 

potentially leading to increased 

medication use, increased school and 

work absences, increased visits to 

doctors’ offices and emergency 

departments, and increased hospital 

admissions. The observations provide 

additional support for the conclusion in 

the Staff Paper that the associations 

observed in the epidemiological studies, 

particularly for respiratory-related 

effects and potentially for 

cardiovascular effects, extend down to 

O3 levels well below the current 

standard (i.e., 0.084 ppm) (EPA, 2007, p. 

6–7). 

As discussed above in section II.A 

and in the Staff Paper (section 3.7), the 

newly available information reinforces 

the judgments about the likelihood of 

causal relationships between O3

exposure and respiratory effects 

observed in the last review and 

broadens the evidence of O3-related 

associations to include additional 

respiratory-related endpoints, newly 

identified cardiovascular-related health 

endpoints, and mortality. Newly 

available evidence also has shown that 

people with asthma are likely to 

experience more serious effects than 

people who do not have asthma (section 

II.A.4.b.ii above). The Staff Paper also 

concludes that substantial progress has 

been made since the last review in 

advancing the understanding of 

potential mechanisms by which ambient 

O3, alone and in combination with other 

pollutants, is causally linked to a range 

of respiratory-related health endpoints, 

and may be causally linked to a range 

of cardiovascular-related health 

endpoints. Thus, the Staff Paper (section 

6.3.6) finds strong support in the 

evidence developed since the last 

review, for consideration of an O3

standard that is at least as protective as 

the current standard and finds no 

support for consideration of an O3

standard that is less protective than the 

current standard. This conclusion is 

consistent with the advice and 

recommendations of CASAC and with 

the views expressed by all interested 

parties who provided comments on 

drafts of the Staff Paper. While CASAC 

and some commenters supported 

revising the current standard to provide 

increased public health protection and 

other commenters supported retaining 

the current standard, no one who 

provided comments supported a 

standard that would be less protective 

than the current standard. 

a. Evidence-Based Considerations 

In looking more specifically at the 

controlled human exposure and 

epidemiological evidence (which is 

summarized in chapter 3 and Appendix 

3B of the Staff Paper), the Staff Paper 

first notes that controlled human 

exposure studies provide the clearest 

and most compelling evidence for an 

array of human health effects that are 

directly attributable to acute exposures 

to O3 per se. Evidence from such human 

studies, together with animal 

toxicological studies, help to provide 

biological plausibility for health effects 

observed in epidemiological studies. In 

considering the available evidence, the 

Staff Paper focuses on studies that 

examined health effects that have been 

demonstrated to be caused by exposure 

to O3, or for which the Criteria 

Document judges associations with O3

to be causal or likely causal, or for 

which the evidence is highly suggestive 

that O3 contributes to the reported 

effects. In considering the 

epidemiological evidence as a basis for 

reaching conclusions about the 

adequacy of the current standard, the 

Staff Paper focuses on studies reporting 

effects in the warm season, for which 

the effect estimates are more 

consistently positive and statistically 

significant than those from all-year 

studies. The Staff Paper (section 6.3.1.1) 

considers the extent to which such 

studies provide evidence of associations 

that extend down to ambient O3

concentrations below the level of the 

current standard, which would thereby 

call into question the adequacy of the 

current standard. In so doing, the Staff 

Paper notes, as discussed above, that if 

a population threshold level does exist 

for an effect observed in such studies, it 

would likely be at a level well below the 

level of the current standard. The Staff 

Paper (section 6.3.1.1) also attempts to 

characterize whether the area in which 

a study was conducted likely would or 

would not have met the current 

standard during the time of the study, 

although it recognizes that the 

confidence that would appropriately be 

placed on the associations observed in 

any given study, or on the extent to 

which the association would likely 

extend down to relatively low O3

concentrations, is not dependent on this 

distinction. Further, the Staff Paper 

considered studies that examined 

subsets of data that include only days 

with ambient O3 concentrations below 

the level of the current O3 standard, or 

below even lower O3 concentrations, 

and continue to report statistically 

significant associations. The Staff Paper 

(section 6.3.1.1) judges that such studies 

are directly relevant to considering the 

adequacy of the current standard, 

particularly in light of reported 

responses to O3 at levels below the 

current standard found in controlled 

human exposure studies. 

i. Lung Function, Respiratory 

Symptoms, and Other Respiratory 

Effects 

Health effects for which the Criteria 

Document continues to find clear 

evidence of causal associations with 

short-term O3 exposures include lung 

function decrements, respiratory 

symptoms, pulmonary inflammation, 

and increased airway responsiveness. In 

the last review, these O3-induced effects 

were demonstrated with statistical 

significance down to the lowest level 

tested in controlled human exposure 

studies at that time (i.e., 0.080 ppm). As 

discussed in chapter 3 of the Staff 

Paper, and in section II.A.2.a.i.(a)(i) 

above, two new studies are notable in 

that they are the only controlled human 

exposure studies that examined 

respiratory effects, including lung 

function decrements and respiratory 

symptoms, in healthy adults at lower 

exposure levels than had previously 

been examined. EPA’s reanalysis of the 

data from the most recent study shows 

small group mean decrements in lung 

function responses to be statistically 

significant at the 0.060 ppm exposure 

level, while the author’s analysis did 

not yield statistically significant lung 

function responses but did yield some 

statistically significant respiratory 

symptom responses toward the end of 

the exposure period. Notably, these 

studies report a small percentage of 

subjects experiencing lung function 

decrements (≥ 10 percent) at the 0.060 

ppm exposure level. These studies 

provide very limited evidence of O3- 

related lung function decrements and 

respiratory symptoms at this lower 

exposure level. 

The Staff Paper (section 3.3.1.1.1) 

notes that evidence from controlled 

human exposures studies indicates that 

people with moderate-to-severe asthma 

have somewhat larger decreases in lung 

function in response to O3 relative to 

healthy individuals and that lung 

function responses in people with 

asthma appear to be affected by baseline 

lung function (i.e., magnitude of 

responses increases with increasing 

disease severity). As discussed in the 

Criteria Document (p.8–80), this newer 

information expands our understanding 

of the physiological basis for increased 

sensitivity in people with asthma and 

other airway diseases, recognizing that 


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people with asthma present a different 

response profile for cellular, molecular, 

and biochemical responses than people 

who do not have asthma. New evidence 

indicates that some people with asthma 

have increased occurrence and duration 

of nonspecific airway responsiveness, 

which is an increased 

bronchoconstrictive response to airway 

irritants. Controlled human exposure 

studies also indicate that some people 

with allergic asthma and rhinitis have 

increased airway responsiveness to 

allergens following O3 exposure. 

Exposures to O3 exacerbated lung 

function decrements in people with preexisting allergic airway disease, with 

and without asthma. Ozone-induced 

exacerbation of airway responsiveness 

persists longer and attenuates more 

slowly than O3-induced lung function 

decrements and respiratory symptom 

responses and can have important 

clinical implications for asthmatics. 

The Staff Paper (p.6–10) also 

concludes that newly available human 

exposure studies suggest that some 

people with asthma also have increased 

inflammatory responses, relative to nonasthmatic subjects, and that this 

inflammation may take longer to 

resolve. The new data on airway 

responsiveness, inflammation, and 

various molecular markers of 

inflammation and bronchoconstriction 

indicate that people with asthma and 

allergic rhinitis (with or without 

asthma) comprise susceptible groups for 

O3-induced adverse effects. This body of 

evidence qualitatively informs the Staff 

Paper’s (pp.6–10 to 6–11) evaluation of 

the adequacy of the current O3 standard 

in that it indicates that human clinical 

and epidemiological panel studies of 

lung function decrements and 

respiratory symptoms that evaluate only 

healthy, non-asthmatic subjects likely 

underestimate the effects of O3 exposure 

on asthmatics and other susceptible 

populations. 

The Staff Paper (p.6–11) notes that in 

addition to the experimental evidence of 

lung function decrements, respiratory 

symptoms, and other respiratory effects 

in healthy and asthmatic populations 

discussed above, epidemiological 

studies have reported associations of 

lung function decrements and 

respiratory symptoms in several 

locations (Appendix 3B; also Figure 3–

4 for respiratory symptoms). As 

discussed in the Staff Paper (section 

3.3.1.1.1) and above, two large U.S. 

panel studies which together followed 

over 1000 asthmatic children on a daily 

basis (Mortimer et al., 2002, the 

National Cooperative Inner-City Asthma 

Study, or NCICAS; and Gent et al., 

2003), as well as several smaller U.S. 

and international studies, have reported 

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. Overall, the 

multi-city NCICAS (2002), Gent et al. 

(2003), and several other single-city 

studies indicate a robust positive 

association between ambient O3

concentrations and increased 

respiratory symptoms and increased 

medication use in asthmatics. 

In considering the large number of 

single-city epidemiological studies 

reporting lung function or respiratory 

symptoms in healthy or asthmatic 

populations (Staff Paper, Appendix 3B), 

the Staff Paper (p.6–11) notes that most 

such studies that reported positive and 

often statistically significant 

associations in the warm season were 

conducted in areas that likely would not 

have met the current standard. In 

considering the large multi-city NCICAS 

(Mortimer et al., 2002), the Staff Paper 

notes that the 98th percentile 8-hour 

daily maximum O3 concentrations at the 

monitor reporting the highest O3

concentrations in each of the study 

areas ranged from 0.084 ppm to >0.10 

ppm. However, the authors indicate that 

less than 5 percent of the days in the 

eight urban areas had 8-hour daily O3

concentrations exceeding 0.080 ppm. 

Moreover, the authors observed that 

when days with 8-hour average O3

levels greater than 0.080 ppm were 

excluded, similar effect estimates were 

seen compared to estimates which 

included all of the days. There are also 

a few other studies in which the 

relevant air quality statistics provide 

some indication that lung function and 

respiratory symptom effects may be 

occurring in areas that likely would 

have met the current standard (EPA, 

2007, p.6–12). 

ii. Respiratory Hospital Admissions and 

Emergency Department Visits 

At the time of the last review, many 

time-series studies indicated positive 

associations between ambient O3 and 

increased respiratory hospital 

admissions and emergency room visits, 

providing strong evidence for a 

relationship between O3 exposure and 

increased exacerbations of preexisting 

lung disease at O3 levels below the level 

of the then current 1-hour standard 

(EPA 2007, section 3.3.1.1.6). Analyses 

of data from studies conducted in the 

northeastern U.S. indicated that O3 air 

pollution was consistently and strongly 

associated with summertime respiratory 

hospital admissions. 

Since the last review, new 

epidemiological studies have evaluated 

the association between short-term 

exposures to O3 and unscheduled 

hospital admissions for respiratory 

causes. Large multi-city studies, as well 

as many studies from individual cities, 

have reported positive and often 

statistically significant O3 associations 

with total respiratory hospitalizations as 

well as asthma- and COPD-related 

hospitalizations, especially in studies 

analyzing the O3 effect during the 

summer or warm season. Analyses using 

multipollutant regression models 

generally indicate that copollutants do 

not confound the association between 

O3 and respiratory hospitalizations and 

that the O3 effect estimates were robust 

to PM adjustment in all-year and warmseason only data. The Criteria Document 

(p.8–77) concludes that the evidence 

supports a causal relationship between 

acute O3 exposures and increased 

respiratory-related hospitalizations 

during the warm season. 

In looking specifically at U.S. and 

Canadian respiratory hospitalization 

studies that reported positive and often 

statistically significant associations (and 

that either did not use GAM or were 

reanalyzed to address GAM-related 

problems), the Staff Paper (p.6–12) notes 

that many such studies were conducted 

in areas that likely would not have met 

the current O3 standard, with many 

providing only all-year effect estimates, 

and with some reporting a statistically 

significant association in the warm 

season. Of the studies that provide some 

indication that O3-related respiratory 

hospitalizations may be occurring in 

areas that likely would have met the 

current standard, the Staff Paper notes 

that some are all-year studies, whereas 

others reported statistically significant 

warm-season associations. 

Emergency department visits for 

respiratory causes have been the focus 

of a number of new studies that have 

examined visits related to asthma, 

COPD, bronchitis, pneumonia, and 

other upper and lower respiratory 

infections, such as influenza, with 

asthma visits typically dominating the 

daily incidence counts. Among studies 

with adequate controls for seasonal 

patterns, many reported at least one 

significant positive association 

involving O3. However, inconsistencies 

were observed which were at least 

partially attributable to differences in 

model specifications and analysis 

approach among various studies. 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. 

Almost all of the studies that reported 


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statistically significant effect estimates 

were conducted in areas that likely 

would not have met the current 

standard. The Criteria Document 

(section 7.3.2) concluded that analyses 

stratified by season generally supported 

a positive association between O3

concentrations and emergency 

department visits for asthma in the 

warm season. These studies provide 

evidence of effects in areas that likely 

would not have met the current 

standard and evidence of associations 

that likely extend down to relatively 

low ambient O3 concentrations. 

iii. Mortality 

The 1996 Criteria Document 

concluded that an association between 

daily mortality and O3 concentrations 

for areas with high O3 levels (e.g., Los 

Angeles) was suggested. However, due 

to a very limited number of studies 

available at that time, there was 

insufficient evidence to conclude that 

the observed association was likely 

causal, and thus the possibility that O3

exposure may be associated with 

mortality was not relied upon in the 

1997 decision on the O3 primary 

standard. 

Since the last review, as described 

above, the body of evidence with regard 

to O3-related health effects has been 

expanded by animal, human clinical, 

and epidemiological studies and now 

includes biologically plausible 

mechanisms by which O3 may affect the 

cardiovascular system. In addition, 

there is stronger information linking O3

to serious morbidity outcomes, such as 

hospitalization, that are associated with 

increased mortality. Thus, there is now 

a coherent body of evidence that 

describes a range of health outcomes 

from lung function decrements to 

hospitalization and premature mortality. 

Newly available large multi-city 

studies (Bell et al., 2004; Huang et 

al.,2005; and Schwartz 2005) designed 

specifically to examine the effect of O3

and other pollutants on mortality have 

provided much more robust and 

credible information. Together these 

studies have reported significant 

associations between O3 and mortality 

that were robust to adjustment for PM 

and different adjustment methods for 

temperature and suggest that the effect 

of O3 on mortality is immediate but also 

persists for several days. One recent 

multi-city study (Bell et al., 2006) 

examined the shape of the 

concentration-response function for the 

O3-mortality relationship in 98 U.S. 

urban communities for the period 1987 

to 2000 specifically to evaluate whether 

a ‘‘safe’’ threshold level exists. Results 

from various analytic methods all 

indicated that any threshold, if it exists, 

would likely occur at very low 

concentrations, far below the level of 

the current O3 NAAQS and nearing 

background levels. 

New data are also available from 

several single-city studies conducted 

world-wide, as well as from several 

meta-analyses that have combined 

information from multiple studies. 

Three recent meta-analyses evaluated 

potential sources of heterogeneity in O3- 

mortality associations. All three 

analyses reported common findings, 

including effect estimates that were 

statistically significant and larger in 

warm season analyses. Reanalysis of 

results using default GAM criteria did 

not change the effect estimates, and 

there was no strong evidence of 

confounding by PM. The Criteria 

Document (p.7–175) finds that the 

majority of these studies suggest that 

there is an elevated risk of total 

nonaccidental mortality associated with 

acute exposure to O3, especially in the 

summer or warm season when O3 levels 

are typically high, with somewhat larger 

effect estimate sizes for associations 

with cardiovascular mortality. 

Overall, the Criteria Document (p.8–

78) finds that the results from U.S. 

multi-city time-series studies, along 

with the meta-analyses, provide 

relatively strong evidence for 

associations between short-term O3

exposure and all-cause mortality even 

after adjustment for the influence of 

season and PM. The results of these 

analyses indicate that copollutants 

generally do not appear to substantially 

confound the association between O3

and mortality. In addition, several 

single-city studies observed positive 

associations of ambient O3

concentrations with total nonaccidental 

and cardiopulmonary mortality. 

Finally, from those studies that 

included assessment of associations 

with specific causes of death, it appears 

that effect estimates for associations 

with cardiovascular mortality are larger 

than those for total mortality; effect 

estimates for respiratory mortality are 

less consistent in size, possibly due to 

reduced statistical power in this 

subcategory of mortality. For 

cardiovascular mortality, the Criteria 

Document (p.7–106) suggests that effect 

estimates are consistently positive and 

more likely to be larger and statistically 

significant in warm season analyses. 

The Criteria Document (p.8–78) 

concludes that these findings are highly 

suggestive that short-term O3 exposure 

directly or indirectly contributes to 

nonaccidental and cardiopulmonaryrelated mortality, but additional 

research is needed to more fully 

establish underlying mechanisms by 

which such effects occur. 

b. Exposure- and Risk-Based 

Considerations 

As discussed above in section II.B, the 

Staff Paper also estimated quantitative 

exposures and health risks associated 

with recent air quality levels and with 

air quality that meets the current 

standard to help inform judgments 

about whether or not the current 

standard provides adequate protection 

of public health. In so doing, it 

presented the important uncertainties 

and limitations associated with the 

exposure and risk assessments 

(discussed above in section II.B and 

more fully in chapters 4 and 5 of the 

Staff Paper). 

The Staff Paper (and the CASAC) also 

recognized that the exposure and risk 

analyses could not provide a full picture 

of the O3 exposures and O3-related 

health risks posed nationally. The Staff 

Paper did not have sufficient 

information to evaluate all relevant atrisk groups (e.g., outdoor workers) or all 

O3-related health outcomes (e.g., 

increased medication use, school 

absences, and emergency department 

visits that are part of the broader 

pyramid of effects discussed above in 

section II.A.4.d), and the scope of the 

Staff Paper analyses was generally 

limited to estimating exposures and 

risks in 12 urban areas across the U.S., 

and to only five or just one area for 

some health effects included in the risk 

assessment. Thus, national-scale public 

health impacts of ambient O3 exposures 

are clearly much larger than the 

quantitative estimates of O3-related 

incidences of adverse health effects and 

the numbers of children likely to 

experience exposures of concern 

associated with recent air quality or air 

quality that just meets the current or 

alternative standards. On the other 

hand, inter-individual variability in 

responsiveness means that only a subset 

of individuals in each group estimated 

to experience exposures exceeding a 

given benchmark exposure of concern 

level would actually be expected to 

experience such adverse health effects. 

As described above in section II.B, the 

Staff Paper estimated exposures and 

risks for the three most recent years 

(2002–2004) for which data were 

available at the time of the analyses. 

Within this 3-year period, 2002 was a 

year with relatively higher O3 levels in 

most, but not all, areas and simulation 

of just meeting the current standard 

based on 2002 air quality data provides 

a generally more upper-end estimate of 

exposures and risks, while 2004 was a 

year with relatively lower O3 levels in 


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most, but not all, areas and simulation 

of just meeting the current standard 

using 2004 air quality data provides a 

generally more lower-end estimate of 

exposures and risks. 

i. Exposure Assessment Results 

As discussed above in section II.B.1, 

the Staff Paper estimates personal 

exposures to ambient O3 levels at and 

above specific benchmark levels to 

provide some perspective on the public 

health impacts of health effects that 

cannot currently be evaluated in 

quantitative risk assessments but that 

may occur at current air quality levels, 

and the extent to which such impacts 

might be reduced by meeting the current 

and alternative standards. As described 

in greater detail in section II.B.1.c 

above, the Staff Paper refers to 

exposures at and above these 

benchmark levels as ‘‘exposures of 

concern.’’ The Staff Paper notes that 

exposures of concern, and the health 

outcomes they represent, likely occur 

across a range of O3 exposure levels, 

such that there is no one exposure level 

that addresses all relevant public health 

concerns. Therefore, with the 

concurrence of the CASAC, the Staff 

Paper estimated exposures of concern 

not only at 0.080 ppm O3, a level at 

which there are demonstrated effects, 

but also at 0.070 and 0.060 ppm O3. The 

Staff Paper recognized that there will be 

varying degrees of concern about 

exposures at each of these levels, based 

in part on the population subgroups 

experiencing them. Given that there is 

clear evidence of inflammation, 

increased airway responsiveness, and 

changes in host defenses in healthy 

people exposed to 0.080 ppm O3 and 

reason to infer that such effects will 

continue at lower exposure levels, but 

with increasing uncertainty about the 

extent to which such effects occur at 

lower O3 concentrations, the Staff Paper, 

and the discussion below, focuses on 

exposures of concern at or above 

benchmark levels of 0.070 and 0.060 

ppm O3 for purposes of evaluating the 

adequacy of the current standard. 

The exposure estimates presented in 

the Staff Paper are for the number and 

percent of all school age children and 

asthmatic school age children exposed, 

and the number of person-days 

(occurrences) of exposures, with daily 8- 

hour maximum exposures at or above 

several benchmark levels while at 

intermittent moderate or greater 

exertion. As shown in the Table 1 in 

this notice, the percent of population 

exposed at any given level is very 

similar for all and asthmatic school age 

children. Substantial year-to-year 

variability in exposure estimates is 

observed, ranging to over an order of 

magnitude at the current standard level, 

in estimates of the number of children 

and, as shown in Table 6–1a and b of 

the Staff Paper, the number of 

occurrences of exposures of concern at 

both of these benchmark levels. The 

Staff Paper states that it is appropriate 

to consider not just the average 

estimates across all years, but also to 

consider public health impacts in year 

with relatively higher O3 levels. The 

Staff Paper also notes that there is 

substantial city-to-city variability in 

these estimates, and notes that it is 

appropriate to consider not just the 

aggregate estimates across all cities, but 

also to consider the public health 

impacts in cities that receive relatively 

less protection upon meeting the current 

standard. 

As discussed in the Staff Paper (EPA, 

2007b, see section 6.3.1.2), about 50 

percent of asthmatic or all school age 

children, representing nearly 1.3 million 

asthmatic children and about 8.5 

million school age children in the 12 

urban areas examined, are estimated to 

experience exposures of concern at or 

above the 0.070 ppm benchmark level 

(i.e., these individuals are estimated to 

experience 8-hour O3 exposures at or 

above 0.070 ppm while engaged in 

moderate or greater exertion 1 or more 

times during the O3 season) associated 

with 2002 O3 air quality levels. In 

contrast, about 17 percent of asthmatic 

and all school age children are 

estimated to experience exposures of 

concern at or above the 0.070 ppm 

benchmark level associated with 2004 

O3 air quality levels. Just meeting the 

current standard results in an aggregate 

estimate of about 20 percent of 

asthmatic or 18 percent or all school age 

children likely to experience exposures 

of concern at or above the 0.070 ppm 

benchmark level using the 2002 

simulation. The exposure estimates for 

this benchmark level range up to about 

40 percent of asthmatic or all school age 

children in the single city with the least 

degree of protection from this standard. 

Just meeting the current standard based 

on the 2004 simulation, results in an 

aggregate estimate of about 1 percent of 

asthmatic or all school age children 

experiencing exposures at the 0.07 ppm 

benchmark level. 

At the benchmark level of 0.060 ppm, 

about 70 percent of all or asthmatic 

school age children are estimated to 

experience exposures of concern at this 

benchmark level for the aggregate of the 

12 urban areas associated with 2002 O3

levels. Just meeting the current standard 

would result in an aggregate estimate of 

about 45 percent of asthmatic or all 

school age children likely to experience 

exposures of concern at or above the 

0.060 ppm benchmark level using the 

2002 simulation. The exposure 

estimates for this benchmark level range 

up to nearly 70 percent of all or 

asthmatic school age children in the 

single city with the least degree of 

protection associated with just meeting 

the current standard using the 2002 

simulation. The Staff Paper indicates an 

aggregate estimate of about 10 percent of 

asthmatic or all school age children 

would experience exposures at or above 

the 0.06 ppm benchmark level 

associated with just meeting the current 

standard using the 2004 simulation. 

ii. Risk Assessment Results 

As described in more detail in section 

II.B.2 above and in chapters 5 and 6 of 

the Staff Paper, risk estimates have been 

developed for several important health 

endpoints, including: (1) Lung function 

decrements (i.e., ≥15 percent and ≥20 

percent reductions in FEV1) in all 

school age children for 12 urban areas; 

(2) lung function decrements (i.e., ≥10 

percent and ≥20 percent reductions in 

FEV1) in asthmatic school age children 

for 5 urban areas (a subset of the 12 

urban areas); (3) respiratory symptoms 

(i.e., chest tightness, shortness of breath, 

wheeze) in moderate to severe asthmatic 

children for the Boston area; (4) 

respiratory-related hospital admissions 

for 3 urban areas; and (5) nonaccidental 

and cardiorespiratory mortality for 12 

urban areas for three recent years (2002 

to 2004) and for just meeting the current 

standard using a 2002 simulation and a 

2004 simulation. 

With regard to estimates of moderate 

lung function decrements, as shown in 

Tables 6–2 of the Staff Paper, meeting 

the current standard substantially 

reduces the estimated number of school 

age children experiencing one or more 

occurrences of FEV1 decrements ≥15 

percent for the 12 urban areas, going 

from about 1.3 million children (7 

percent of children) under 2002 air 

quality to about 610,000 (3 percent of 

children) based on the 2002 simulation, 

and from about 620,000 children (3 

percent of children) to about 230,000 (1 

percent of children) using the 2004 

simulation. In asthmatic children, the 

estimated number of children 

experiencing one or more occurrences of 

FEV1 decrements ≥10 percent for the 5 

urban areas goes from about 250,000 

children (16 percent of asthmatic 

children) under 2002 air quality to 

about 130,000 (8 percent of asthmatic 

children) using the 2002 simulation, 

and from about 160,000 (10 percent of 

asthmatic children) to about 70,000 (4 

percent of asthmatic children) using the 

2004 simulation. Thus, even when the 


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48 In defining at-risk groups this way we are 

including both groups with greater inherent 

sensitivity and those more likely to be exposed. 

current standard is met, about 4 to 8 

percent of asthmatic school age children 

are estimated to experience one or more 

occurrences of moderate lung function 

decrements, resulting in about 1 million 

occurrences (using the 2002 simulation) 

and nearly 700,000 occurrence (using 

the 2004 simulation) in just 5 urban 

areas. Moreover, the estimated number 

of occurrences of moderate or greater 

lung function decrements per child is 

on average approximately 6 to 7 in all 

children and 8 to 10 in asthmatic 

children in an O3 season, even when the 

current standard is met, depending on 

the year used to simulate meeting the 

current standard. In the 1997 review of 

the O3 standard a general consensus 

view of the adversity of such moderate 

responses emerged as the frequency of 

occurrences increases, with the 

judgment that repeated occurrences of 

moderate responses, even in otherwise 

healthy individuals, may be considered 

adverse since they may well set the 

stage for more serious illness. 

With regard to estimates of large lung 

function decrements, the Staff Paper 

notes that FEV1 decrements >20 percent 

would likely interfere with normal 

activities in many healthy individuals, 

therefore single occurrences would be 

considered to be adverse. In people with 

asthma, large lung function responses 

would likely interfere with normal 

activities for most individuals and 

would also increase the likelihood that 

these individuals would use additional 

medication or seek medical treatment. 

Not only would single occurrences be 

considered to be adverse to asthmatic 

individuals under the ATS definition, 

but they also would be cause for 

medical concern. While the current 

standard reduces the occurrences of 

large lung function decrements in all 

children and asthmatic children from 

about 60 to 70%, in a year with 

relatively higher O3 levels (2002), there 

are estimated to be about 500,000 

occurrences in all school children 

across the entire 12 urban areas, and 

about 40,000 occurrences in asthmatic 

children across just 5 urban areas. As 

noted above, it is clear that even when 

the current standard is met over a threeyear period, O3 levels in each year can 

vary considerably, as evidenced by 

relatively large differences between risk 

estimates based on 2002 to 2004 air 

quality. The Staff Paper expressed the 

view that it was appropriate to consider 

this yearly variation in O3 levels 

allowed by the current standard in 

judging the extent to which impacts on 

members of at-risk groups in a year with 

relatively higher O3 levels remains of 

concern from a public health 

perspective. 

With regard to other O3-related health 

effects, as shown in Tables 6–4 through 

6–6 of the Staff Paper, the estimated 

risks of respiratory symptom days in 

moderate to severe asthmatic children, 

respiratory-related hospital admissions, 

and non-accidental and 

cardiorespiratory mortality, 

respectively, are not reduced to as great 

an extent by meeting the current 

standard as are lung function 

decrements. For example, just meeting 

the current standard reduces the 

estimated average incidence of chest 

tightness in moderate to severe 

asthmatic children living in the Boston 

urban area by 11 to 15%, based on 2002 

and 2004 simulations, respectively, 

resulting in an estimated incidence of 

about 23,000 to 31,000 per 100,000 

children attributable to O3 exposure 

(Table 6–4). Just meeting the current 

standard is estimated to reduce the 

incidence of respiratory-related hospital 

admissions in the New York City urban 

area by about 16 to 18%, based on 2002 

and 2004 simulations, respectively, 

resulting in an estimated incidence per 

100,000 population of 4.6 to 6.4, 

respectively (Table 6–5). Across the 12 

urban areas, the estimates of nonaccidental mortality incidence per 

100,000 relevant population range from 

0.4 to 2.6 (for 2002) and 0.5 to 1.5 (for 

2004) (Table 6–6). Meeting the current 

standard results in a reduction of the 

estimated incidence per 100,000 

population to a range of 0.3 to 2.4 based 

on the 2002 simulation and a range of 

0.3 to 1.2 based on the 2004 simulation. 

Estimates for cardiorespiratory mortality 

show similar patterns. 

In considering the estimates of the 

proportion of population affected and 

the number of occurrences of the health 

effects that are included in the risk 

assessment, the Staff Paper notes that 

these limited estimates are indicative of 

a much broader array of O3-related 

health endpoints that are part of a 

‘‘pyramid of effects’’ that include 

various indicators of morbidity that 

could not be included in the risk 

assessment (e.g., school absences, 

increased medication use, emergency 

department visits) and which primarily 

affect members of at-risk groups. While 

the Staff Paper had sufficient 

information to estimate and consider the 

number of symptom days in children 

with moderate to severe asthma, it 

recognized that there are many other 

effects that may be associated with 

symptom days, such as increased 

medication use, school and work 

absences, or visits to doctors’ offices, for 

which there was not sufficient 

information to estimate risks but which 

are important to consider in assessing 

the adequacy of the current standard. 

The same is true for more serious, but 

less frequent effects. The Staff Paper 

estimated hospital admissions, but there 

was not sufficient information to 

estimate emergency department visits in 

a quantitative risk assessment. 

Consideration of such unquantified 

risks in the Staff Paper reinforces the 

Staff Paper conclusion that 

consideration should be given to 

revising the standard so as to provide 

increased public health protection, 

especially for at-risk groups such as 

people with asthma or other lung 

diseases, as well as children and older 

adults, particularly those active 

outdoors, and outdoor workers. 

c. Summary 

Based on the available information 

and taking into account the views of 

CASAC and public comments, the Staff 

Paper initially notes that all parties 

commenting on the NAAQS review 

agree that the standard should be at 

least as protective as the current 

standard, as no party suggested it 

should be revised to provide less 

protection. The Staff Paper concludes 

that the overall body of evidence clearly 

calls into question the adequacy of the 

current standard in protecting at-risk 

groups, notably including asthmatic 

children and other people with lung 

disease, as well as all children and older 

adults, especially those active outdoors, 

and outdoor workers,48 against an array 

of adverse health effects that range from 

decreased lung function to serious 

indicators of respiratory morbidity 

including emergency department visits 

and hospital admissions for respiratory 

causes, nonaccidental mortality, and 

possibly cardiovascular effects. The 

available information provides strong 

support for consideration of an O3

standard that would provide increased 

health protection for these at-risk 

groups. The Staff Paper also concludes 

that risks projected to remain upon 

meeting the current standard, based on 

the exposure and risk estimates 

discussed above and in more detail in 

the Staff Paper, are indicative of risks to 

at-risk groups that can be judged to be 

important from a public health 

perspective, which reinforces the Staff 

Paper conclusion that consideration 

should be given to revising the level of 

the standard so as to provide increased 


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public health protection (EPA, 2007, 

section 6.3.6). 

3. CASAC Views 

In its letter to the Administrator, the 

CASAC O3 Panel, with full endorsement 

of the chartered CASAC, unanimously 

concluded that there is ‘‘no scientific 

justification for retaining’’ the current 

primary O3 standard, and the current 

standard ‘‘needs to be substantially 

reduced to protect human health, 

particularly in sensitive 

subpopulations’’ (Henderson, 2006c, pp. 

1–2). In its rationale for this conclusion, 

the CASAC Panel concluded that ‘‘new 

evidence supports and build-upon key, 

health-related conclusions drawn in the 

1997 Ozone NAAQS review’’ (id., p. 3). 

The Panel points to studies discussed in 

chapter 3 and Appendix 3B of the Staff 

Paper in noting that several new singlecity studies and large multi-city studies 

have provided more evidence for 

adverse health effects at concentrations 

lower than the current standard, and 

that these epidemiological studies are 

backed-up by evidence from controlled 

human exposure studies. The Panel 

specifically noted evidence from the 

recent Adams (2006) study that reported 

statistically significant decrements in 

the lung function of healthy, moderately 

exercising adults at a 0.080 ppm 

exposure level, and importantly, also 

reported adverse lung function effects in 

some healthy individuals at 0.060 ppm. 

The Panel concluded that these results 

indicate that the current standard ‘‘is 

not sufficiently health-protective with 

an adequate margin of safety,’’ noting 

that that while similar studies in 

sensitive groups such as asthmatics 

have yet to be conducted, ‘‘people with 

asthma, and particularly children, have 

been found to be more sensitive and to 

experience larger decrements in lung 

function in response to O3 exposures 

than would healthy volunteers 

(Mortimer et al., 2002)’’ (Henderson, 

2006c, p. 4). 

The CASAC Panel also highlighted a 

number of O3-related adverse health 

effects, that are associated with 

exposure to ambient O3, below the level 

of the current standard, based on a 

broad range of epidemiological studies 

(Henderson, 2006c). These adverse 

health effects include increases in 

school absenteeism, respiratory hospital 

emergency department visits among 

asthmatics and patients with other 

respiratory diseases, hospitalizations for 

respiratory illnesses, symptoms 

associated with adverse health effects 

(including chest tightness and 

medication usage), and premature 

mortality (nonaccidental, 

cardiorespiratory deaths) reported at 

exposure levels well below the current 

standard. ‘‘The CASAC considers each 

of these findings to be an important 

indicator of adverse health effects’’

(Henderson, 2006c). 

The CASAC Panel expressed the view 

that more emphasis should be placed on 

the subjects in controlled human 

exposure studies with FEV1 decrements 

greater than 10 percent, which can be 

clinically significant, rather than on the 

relatively small average decrements. 

The Panel also emphasized significant 

O3-related inflammatory responses and 

markers of injury to the epithelial lining 

of the lung that are independent of 

spirometric responses. Further, the 

Panel expressed the view that the Staff 

Paper did not place enough emphasis on 

serious morbidity (e.g., hospital 

admissions) and mortality observed in 

epidemiology studies. On the basis of 

the large amount of recent data 

evaluating adverse health effects at 

levels at and below the current O3

standard, it was the unanimous opinion 

of the CASAC Panel that the current 

primary O3 standard is not adequate to 

protect human health, that the relevant 

scientific data do not support 

consideration of retaining the current 

standard, and that the current standard 

needs to be substantially reduced to be 

protective of human health, particularly 

in sensitive subpopulations (Henderson, 

2006c, pp. 4–5). 

Further, the CASAC letter noted that 

‘‘there is no longer significant scientific 

uncertainty regarding the CASAC’s 

conclusion that the current 8-hour 

primary NAAQS must be lowered’’

(Henderson, 2006c, p. 5). The Panel 

noted that a ‘‘large body of data clearly 

demonstrates adverse human health 

effects at the current level’’ of the 

standard, such that ‘‘[R]etaining this 

standard would continue to put large 

numbers of individuals at risk for 

respiratory effects and/or significant 

impact on quality of life including 

asthma exacerbations, emergency room 

visits, hospital admissions and 

mortality’’ (Henderson, 2006c). The 

Panel also noted that ‘‘scientific 

uncertainty does exist with regard to the 

lower level of O3 exposure that would 

be fully protective of human health,’’

concluding that ‘‘it is possible that there 

is no threshold for an O3-induced 

impact on human health and that some 

adverse events may occur at policyrelevant background’’ (Henderson, 

2006c, p.5). 

4. Administrator’s Proposed 

Conclusions Concerning Adequacy of 

Current Standard 

Based on the large body of evidence 

concerning the public health impacts of 

O3 pollution, including significant new 

evidence concerning effects at O3

concentrations below the level of the 

current standard, the Administrator 

proposes that the current standard does 

not protect public health with an 

adequate margin of safety and should be 

revised to provide additional public 

health protection. In considering 

whether the primary standard should be 

revised, the Administrator has carefully 

considered the conclusions contained in 

the Criteria Document, the rationale and 

recommendations contained in the Staff 

Paper, the advice and recommendations 

from the CASAC, and public comments 

to date. The Administrator notes that 

evidence of a range of respiratoryrelated morbidity effects seen in the last 

review has been considerably 

strengthened, both through toxicological 

and controlled human exposure studies 

as well as through many new panel and 

epidemiological studies. 

In addition, new evidence from 

controlled human exposure and 

epidemiological studies identifies 

people with asthma as an important 

susceptible population for which 

estimates of respiratory effects in the 

general population likely underestimate 

the magnitude or importance of these 

effects. New evidence about 

mechanisms of toxicity more completely 

explains the biological plausibility of 

O3-induced respiratory effects and is 

beginning to suggest mechanisms that 

may link O3 exposure to cardiovascular 

effects. Further, there is now relatively 

strong evidence for associations 

between O3 and total nonaccidental and 

cardiopulmonary mortality, even after 

adjustment for the influence of season 

and PM. Relative to the information that 

was available to inform the Agency’s 

1997 decision to set the current 

standard, the newly available evidence 

increases the Administrator’s 

confidence that respiratory morbidity 

effects such as lung function decrements 

and respiratory symptoms are causally 

related to O3 exposures, that indicators 

of respiratory morbidity such as 

emergency department visits and 

hospital admissions are causally related 

to O3 exposures, and that the evidence 

is highly suggestive that O3 exposures 

during the O3 season contribute to 

premature mortality. 

The Administrator judges that there is 

important new evidence demonstrating 

that exposures to O3 at levels below the 

level of the current standard are 

associated with a broad array of adverse 

health effects, especially in at-risk 

populations. These at-risk populations 

include people with asthma or other 

lung diseases who are likely to 

experience more serious effects from 


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49As discussed in section II.B.1.c above, 

‘‘exposures of concern’’ are estimates of 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 with varying degrees of certainty 

be inferred to occur in some individuals. Estimates 

of exposures of concern provide some perspective 

on the public health impacts of health effects that 

may occur in some individuals at recent air quality 

levels but cannot be evaluated in quantitative risk 

assessments, and the extent to which such impacts 

might be reduced by meeting the current and 

alternative standards. 

50As described in the Staff Paper (section 4.5.8) 

and discussed above, recent O3 air quality 

distributions have been statistically adjusted to 

simulate just meeting the current and selected 

alternative standards. These simulations do not 

represent predictions of when, whether, or how 

areas might meet the specified standards. 

exposure to O3. As discussed in section 

II.A.4 above, these groups also include 

children and older adults with 

increased susceptibility, as well as those 

who are likely to be vulnerable as a 

result of spending a lot of time outdoors 

engaged in physical activity, especially 

active children and outdoor workers. 

Examples of this important new 

evidence include demonstration of O3- 

induced lung function effects and 

respiratory symptoms in some healthy 

individuals down to the previously 

observed exposure level of 0.080 ppm, 

as well as very limited new evidence at 

exposure levels well below the level of 

the current standard. In addition, there 

is now epidemiological evidence of 

statistically significant O3-related 

associations with lung function and 

respiratory symptom effects, respiratoryrelated emergency department visits and 

hospital admissions, and increased 

mortality, in areas that likely would 

have met the current standard. There are 

also many epidemiological studies done 

in areas that likely would not have met 

the current standard but which 

nonetheless report statistically 

significant associations that generally 

extend down to ambient O3

concentrations that are below the level 

of the current standard. Further, there 

are a few studies that have examined 

subsets of data that include only days 

with ambient O3 concentrations below 

the level of the current standard, or 

below even much lower O3

concentrations, and continue to report 

statistically significant associations with 

respiratory morbidity outcomes and 

mortality. The Administrator recognizes 

that the evidence from controlled 

human exposure studies, together with 

animal toxicological studies, provides 

considerable support for the biological 

plausibility of the respiratory morbidity 

associations observed in the 

epidemiological studies and for 

concluding that the associations extend 

below the level of the current standard. 

Based on the strength of the currently 

available evidence of adverse health 

effects, and on the extent to which the 

evidence indicates that such effects 

result from exposures to ambient O3

concentrations below the level of the 

current standard, the Administrator 

judges that the current standard does 

not protect public health with an 

adequate margin of safety and that the 

standard should be revised to provide 

such protection, especially for at-risk 

groups, against a broad array of adverse 

health effects. 

In reaching this judgment, the 

Administrator has also considered the 

results of both the exposure and risk 

assessments conducted for this review, 

to provide some perspective on the 

extent to which at-risk groups would 

likely experience ‘‘exposures of 

concern’’ 49 and on the potential 

magnitude of the risk of experiencing 

various adverse health effects when 

recent air quality data (from 2002 to 

2004) are used to simulate meeting the 

current standard and alternative 

standards in a number of urban areas in 

the U.S.50 In considering the exposure 

assessment results, the Administrator is 

relying on analyses that define 

exposures of concern by three 

benchmark exposure levels: 0.080, 

0.070, and 0.060 ppm. Estimates of 

exposures of concern in at-risk groups at 

and above these benchmark levels, 

using O3 air quality data in 2002 and 

2004, provide some indication of the 

potential magnitude of the incidence of 

health outcomes that cannot currently 

be evaluated in a quantitative risk 

assessment, such as increased airway 

responsiveness, increased pulmonary 

inflammation, including increased 

cellular permeability, and decreased 

pulmonary defense mechanisms. These 

physiological effects have been 

demonstrated to occur in healthy people 

at O3 exposures as low as 0.080 ppm, 

the lowest level tested. They are 

associated with aggravation of asthma, 

increased medication use, increased 

school and work absences, increased 

susceptibility to respiratory infection, 

increased visits to doctors’ offices and 

emergency departments, increased 

admissions to hospitals, and possibly to 

cardiovascular system effects and 

chronic effects such as chronic 

bronchitis or long-term damage to the 

lungs that can lead to reduced quality of 

life. 

In considering these various 

benchmark levels for exposures of 

concern, the Administrator has focused 

primarily on estimated exposures at and 

above the 0.070 ppm benchmark level as 

an important surrogate measure for 

potentially more serious health effects 

in at-risk groups such as people with 

asthma. This judgment is based on the 

strong evidence of effects in healthy 

people at the 0.080 ppm exposure level 

and the new evidence that people with 

asthma are likely to experience larger 

and more serious effects than healthy 

people at the same level of exposure. In 

the Administrator’s view, this evidence 

does not support a focus on exposures 

at and above the benchmark level of 

0.080 ppm O3, as it would not 

adequately account for the increased 

risk of harm from exposure for members 

of at-risk groups, especially people with 

asthma. The Administrator also judges 

that the evidence of demonstrated 

effects is too limited to support a 

primary focus on exposures down to the 

lowest benchmark level considered of 

0.060 ppm. The Administrator 

particularly notes that although the 

analysis of ‘‘exposures of concern’’ was 

conducted to estimate exposures at and 

above three discrete benchmark levels 

(0.080, 0.070, and 0.060 ppm), the 

concept is appropriately viewed as a 

continuum. As discussed at the outset 

in section II.A above, the Administrator 

strives to balance concern 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 exposure levels. 

The Administrator observes that 

based on the aggregate exposure 

estimates for the 2002 simulation 

summarized above in Table 1 (section 

II.B.1) and in the Staff Paper (EPA, 

2007b, Table 6–7) for the 12 U.S. urban 

areas included in the exposure analysis, 

upon just meeting the current standard 

up to about 20 percent of asthmatic or 

all school age children are likely to 

experience one or more exposures of 

concern at and above the 0.070 ppm 

benchmark level; the 2004 simulation 

yielded an estimate of about 1 percent 

of such children. The Administrator 

notes from this comparison that there is 

substantial year-to-year variability, 

ranging up to an order of magnitude or 

more in estimates of the number of 

people and the number of occurrences 

of exposures of concern at and above 

this benchmark level. Moreover, within 

any given year, the exposure assessment 

indicates that there is substantial cityto-city variability in the estimates of the 

children exposed or the number of 

occurrences of exposure at and above 

this benchmark level. For example, cityspecific estimates of the percent of 

asthmatic or all school age children 

likely to experience exposures at and 

above the benchmark level of 0.070 ppm 


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ranges from about 1 percent up to about 

40 percent across the 12 urban areas 

upon just meeting the current standard 

based on the 2002 simulation; the 2004 

simulation yielded estimates that range 

from about 0 up to about 7 percent. The 

Administrator judges it is important to 

recognize the substantial year-to-year 

and city-to-city variability in 

considering these estimates. 

With regard to the results of the risk 

assessment, as discussed above, the 

Administrator recognizes that a 

simulation of just meeting the current 

standard in the cities included in the 

assessment indicate that the estimated 

risk is lower for all of the health 

endpoints evaluated. In considering the 

adequacy of the current standard, the 

Administrator has focused on the risks 

estimated to remain upon just meeting 

the current standard. Based on the 

aggregate risk estimates summarized 

above in Table 2 (section II.B.2 of this 

notice), the Administrator observes that 

upon just meeting the current standard 

based on the 2002 simulation, 

approximately 8 percent of asthmatic 

school age children across 5 urban areas 

(ranging up to about 11 percent in the 

city that receives relatively less 

protection) and approximately 3 percent 

of all school age children across 12 

urban areas (ranging up to over 5 

percent in the city that receives 

relatively less protection) would still be 

estimated to experience moderate or 

greater lung function decrements one or 

more times within an O3 season. The 

Administrator recognizes that, as with 

the estimates of exposures of concern, 

there is substantial year-to-year and 

city-to-city variability in these risk 

estimates. 

In addition to the percentage of 

asthmatic or all children estimated to 

experience 1 or more occurrences of an 

effect, the Administrator recognizes that 

some individuals are estimated to have 

multiple occurrences. For example, 

across all the cities in the assessment, 

approximately 6 to 7 occurrences of 

moderate or greater lung function 

decrements per child are estimated to 

occur in all children and approximately 

8 to 10 occurrences are estimated to 

occur in asthmatic children in an O3

season, even upon just meeting the 

current standard. In the last review, a 

general consensus view of the adversity 

of such responses emerged as the 

frequency of occurrences increases, with 

the judgment that repeated occurrences 

of moderate responses, even in 

otherwise healthy individuals, may be 

considered adverse since they may well 

set the stage for more serious illness. 

The Administrator continues to support 

this view. 

Large lung function decrements (i.e., 

≥20 percent FEV1 decrement) would 

likely interfere with normal activities in 

many healthy individuals, therefore 

single occurrences would be considered 

to be adverse. In people with asthma, 

large lung function responses (i.e., ≥ 20 

percent FEV1 decrement), would likely 

interfere with normal activities for most 

individuals and would also increase the 

likelihood that these individuals would 

use additional medication or seek 

medical treatment. Not only would 

single occurrences be considered to be 

adverse to asthmatic individuals under 

the ATS definition, but they also would 

be cause for medical concern for some 

individuals. Upon just meeting the 

current standard based on the 2002 

simulation, close to 1 percent of 

asthmatic and all school age children 

are estimated to experience one or more 

occurrences of large lung function 

decrements in the aggregate across 5 and 

12 urban areas, respectively, with close 

to 2 percent of both asthmatic and all 

school age children estimated to 

experience such effects in the city that 

receives relatively less protection from 

this standard. These estimates translate 

into approximately 500,000 occurrences 

of large lung function decrements in all 

children across 12 urban areas, and 

about 40,000 occurrences in asthmatic 

children across just 5 urban areas upon 

just meeting the current standard based 

on the 2002 simulation; the 2004 

simulation yielded estimates that 

translate into approximately 160,000 

and 10,000 such occurrences in all 

children and asthmatic children, 

respectively. 

Upon just meeting the current 

standard based on the 2002 simulation, 

the estimate of the O3-related risk of 

respiratory symptom days in moderate 

to severe asthmatic children in the 

Boston area is about 8,000 symptom 

days; the 2004 simulation yielded an 

estimate of about 6,000 such symptoms 

days. These estimates translate into as 

many as one symptom day in 6, and one 

symptom day in 8, respectively, that are 

attributable to O3 exposure during the 

O3 season of the total number of 

symptom days associated with all 

causes of respiratory symptoms in 

asthmatic children during those years. 

The estimated O3-related risk of 

respiratory-related hospital admissions 

upon just meeting the current standard 

based on the 2002 simulation is greater 

than 500 hospital admissions in the 

New York City area alone, or about 1.5 

percent of the total incidence of 

respiratory-related admissions 

associated with all causes; the 2004 

simulation yielded an estimate of 

approximately 400 such hospital 

admissions. For nonaccidental 

mortality, just meeting the current 

standard based on the 2002 simulation 

results in an estimated incidence of 

from 0.3 to 2.4 per 100,000 population; 

the 2004 simulation resulted in an 

estimated incidence of from 0.3 to 1.2 

per 100,000 population. Estimates for 

cardiorespiratory mortality show similar 

patterns. (Abt Associates, 2007, Table 4–

26). 

The Administrator recognizes that in 

considering the estimates of the 

proportion of population affected and 

the number of occurrences of those 

specific health effects that are included 

in the risk assessment, these limited 

estimates based on 2002 and 2004 

simulations are indicative of a much 

broader array of O3-related health 

endpoints that are part of a ‘‘pyramid of 

effects’’ (discussed above in section 

II.A.4.d) that include various indicators 

of morbidity that could not be included 

in the risk assessment (e.g., school 

absences, increased medication use, 

emergency department visits) and 

which primarily affect members of atrisk groups. Moreover, the 

Administrator notes that the CASAC 

Panel supported a qualitative 

consideration of the much broader array 

of O3-related health endpoints, and 

specifically referred to respiratory 

emergency department visits in 

asthmatics and people with other lung 

diseases, increased medication use, and 

increased respiratory symptoms 

reported at exposure levels well below 

the current standard. 

The Administrator believes the 

exposure and risk estimates discussed 

in the Staff Paper and summarized 

above are important from a public 

health perspective and are indicative of 

potential exposures and risks to at-risk 

groups. In reaching this proposed 

judgment, the Administrator considered 

the following factors: (1) The estimates 

of numbers of persons exposed at and 

above the 0.070 ppm benchmark level; 

(2) the risk estimates of the proportion 

of the population and number of 

occurrences of various health effects in 

areas upon just meeting the current 

standard; (3) the year-to-year and cityto-city variability in both the exposure 

and risk estimates; (4) the uncertainties 

in these estimates; and (5) recognition 

that there is a broader array of O3- 

related adverse health outcomes for 

which risk estimates could not be 

quantified (that are part of a broader 

‘‘pyramid of effects’’) and that the scope 

of the assessment was limited to just a 

sample of urban areas and to some but 

not all at-risk populations, leading to an 

incomplete estimation of public health 

impacts associated with O3 exposures 


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across the country. The Administrator 

also notes that it was the unanimous 

conclusion of the CASAC Panel that 

there is no scientific justification for 

retaining the current primary O3

standard, that the current standard is 

not sufficiently health-protective with 

an adequate margin of safety, and that 

the standard needs to be substantially 

reduced to protect human health, 

particularly in at-risk subpopulations. 

Based on all of these considerations, 

the Administrator proposes that the 

current O3 standard is not requisite to 

protect public health with an adequate 

margin of safety because it does not 

provide sufficient protection and that 

revision would result in increased 

public health protection, especially for 

members of at-risk groups. 

D. Conclusions on the Elements of the 

Primary Standard 

1. Indicator 

In the last review EPA focused on a 

standard for O3 as the most appropriate 

surrogate for ambient photochemical 

oxidants. In this review, while the 

complex atmospheric chemistry in 

which O3 plays a key role has been 

highlighted, no alternative to O3 has 

been advanced as being a more 

appropriate surrogate for ambient 

photochemical oxidants. 

The Staff Paper (section 2.2.2) notes 

that it is generally recognized that 

control of ambient O3 levels provides 

the best means of controlling 

photochemical oxidants. Among the 

photochemical oxidants, the acute 

exposure chamber, panel, and field 

epidemiological human health database 

provides specific evidence for O3 at 

levels commonly reported in the 

ambient air, in part because few other 

photochemical oxidants are routinely 

measured. However, recent 

investigations on copollutant 

interactions have used simulated urban 

photochemical oxidant mixes. These 

investigations suggest the need for 

similar studies to help in understanding 

the biological basis for effects observed 

in epidemiological studies that are 

associated with air pollutant mixtures, 

where O3 is used as the surrogate for the 

mix of photochemical oxidants. Meeting 

the O3 standard can be expected to 

provide some degree of protection 

against potential health effects that may 

be independently associated with other 

photochemical oxidants but which are 

not discernable from currently available 

studies indexed by O3 alone. Since the 

precursor emissions that lead to the 

formation of O3 generally also lead to 

the formation of other photochemical 

oxidants, measures leading to 

reductions in population exposures to 

O3 can generally be expected to lead to 

reductions in population exposures to 

other photochemical oxidants. 

The Staff Paper notes that while the 

new body of time-series epidemiological 

evidence cannot resolve questions about 

the relative contribution of other 

photochemical oxidant species to the 

range of morbidity and mortality effects 

associated with O3 in these types of 

studies, control of ambient O3 levels is 

generally understood to provide the best 

means of controlling photochemical 

oxidants in general, and thus of 

protecting against effects that may be 

associated with individual species and/ 

or the broader mix of photochemical 

oxidants, independent of effects 

specifically related to O3. 

In its letter to the Administrator, the 

CASAC O3 Panel noted that O3 is ‘‘the 

key indicator of the extent of oxidative 

chemistry and serves to integrate 

multiple pollutants.’’ CASAC also stated 

that ‘‘although O3 itself has direct effects 

on human health and ecosystems, it can 

also be considered as an indicator of the 

mixture of photochemical oxidants and 

of the oxidizing potency of the 

atmosphere’’ (Henderson, 2006c, p. 9). 

Based on the available information, 

and consistent with the views of EPA 

staff and the CASAC, the Administrator 

proposes to continue to use O3 as the 

indicator for a standard that is intended 

to address effects associated with 

exposure to O3, alone or in combination 

with related photochemical oxidants. In 

so doing, the Administrator recognizes 

that measures leading to reductions in 

population exposures to O3 will also 

reduce exposures to other 

photochemical oxidants. 

2. Averaging Time 

a. Short-Term and Prolonged (1 to 8 

Hours) 

The current 8-hour averaging time for 

the primary O3 NAAQS was set in 1997. 

At that time, the decision to revise the 

averaging time of the primary standard 

from 1 to 8 hours was supported by the 

following key observations and 

conclusions: 

(1) The 1-hour averaging time of the 

previous NAAQS was originally 

selected primarily on the basis of health 

effects associated with short-term (i.e., 

1- to 3-hour) exposures. 

(2) Substantial health effects 

information was available for the 1997 

review that demonstrated associations 

between a wide range of health effects 

(e.g., moderate to large lung function 

decrements, moderate to severe 

symptoms and pulmonary 

inflammation) and prolonged (i.e., 6- to 

8-hour) exposures below the level of the 

then current 1-hour NAAQS. 

(3) Results of the quantitative risk 

analyses showed that reductions in risks 

from both short-term and prolonged 

exposures could be achieved through a 

primary standard with an averaging 

period of either 1 or 8 hours. Thus 

establishing both a 1-hour and an 8-hour 

standard would not be necessary to 

reduce risks associated with the full 

range of observed health effects. 

(4) The 8-hour averaging time is more 

directly associated with health effects of 

concern at lower O3 concentrations than 

the 1-hour averaging time. It was thus 

the consensus of CASAC ‘‘that an 8- 

hour standard was more appropriate for 

a human health-based standard than a 1- 

hour standard.’’ (Wolff, 1995) 

(5) An 8-hour averaging results in a 

significantly more uniformly protective 

national standard than the then current 

1-hour standard. 

(6) An 8-hour averaging time 

effectively limits both 1- and 8-hour 

exposures of concern. 

In looking at the new information that 

is discussed in section 7.6.2 of the 

current Criteria Document, the Staff 

Paper noted that epidemiological 

studies have used various averaging 

periods for O3 concentrations, most 

commonly 1-hour, 8-hour and 24-hour 

averages. As described more specifically 

in sections 3.3 and 3.4 of the Staff 

Paper, in general the results presented 

from U.S. and Canadian studies show 

no consistent difference for various 

averaging times in different studies. 

Because the 8-hour averaging time 

continues to be more directly associated 

with health effects of concern from 

controlled human exposure studies at 

lower concentrations than do shorter 

averaging periods, the Staff Paper did 

not evaluate alternative averaging times 

in this review and did not conduct 

exposure or risk assessments for 

standards with averaging times other 

than 8 hours. 

The Staff Paper discusses an analysis 

of a recent three-year period of air 

quality data (2002 to 2004) which was 

conducted to determine whether the 

comparative 1- and 8-hour air quality 

patterns that were observed in the last 

review continue to be observed based on 

more recent air quality data. This 

updated air quality analysis (McCluney, 

2007) is very consistent with the 

analysis done in the last review in that 

it indicates that only two urban areas of 

the U.S. have such ‘‘peaky’’ air quality 

patterns such that the ratio of 1-hour to 

8-hour design values is greater than 1.5. 

This suggests that, based on recent air 

quality data, it is reasonable to again 

conclude that an 8-hour average 


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51The 1-expected-exceedance form essentially 

requires that the fourth-highest air quality value in 

3 years, based on adjustments for missing data, be 

less than or equal to the level of the standard for 

the standard to be met at an air quality monitoring 

site. 

standard at or below the current level 

would generally be expected to provide 

protection equal to or greater than the 

previous 1-hour standard of 0.12 ppm in 

almost all urban areas. Thus, the Staff 

Paper again concluded that setting a 

standard with an 8-hour averaging time 

can effectively limit both 1- and 8-hour 

exposures of concern and is appropriate 

to provide adequate and more uniform 

protection of public health from both 

short-term and prolonged exposures to 

O3 in the ambient air. 

In its letter to the Administrator, the 

CASAC O3 Panel supported the 

continued use of an 8-hour averaging 

time for the primary O3 standard 

(Henderson, 2006c, p. 2), as did many 

commenters. Some other commenters 

expressed the view that consideration 

should be given to setting or reinstating 

a 1-hour standard, in addition to 

maintaining the use of an 8-hour 

averaging time, to protect people in 

those parts of the country with 

relatively more ‘‘peaky’’ exposure 

profiles. These commenters point out 

that when controlled exposure studies 

using triangular exposure patterns (with 

relatively higher 1-hour peaks) have 

been compared to constant exposure 

patterns with the same aggregate O3

dose (in terms of concentration x time), 

‘‘peaky’’ exposure patterns are seen to 

lead to higher risks. The California Air 

Resources Board made particular note of 

this point, expressing the view that a 1- 

hour standard would more closely 

represent actual exposures, in that many 

people spend only 1 to 2 hours a day 

outdoors, and that it would be better 

matched to O3 concentration profiles 

along the coasts where O3 levels are 

typically high for shorter averaging 

periods than 8 hours. 

b. Long-term 

During the last review, there was a 

large animal toxicological database for 

consideration that provided clear 

evidence of associations between longterm (e.g., from several months to years) 

exposures and lung tissue damage, with 

additional evidence of reduced lung 

elasticity and accelerated loss of lung 

function. However, there was no 

corresponding evidence for humans, 

and the state of the science had not 

progressed sufficiently to allow 

quantitative extrapolation of the animal 

study findings to humans. For these 

reasons, consideration of a separate 

long-term primary O3 standard was not 

judged to be appropriate at that time, 

recognizing that the 8-hour standard 

would act to limit long-term exposures 

as well as short-term and prolonged 

exposures. 

Taking into consideration the 

currently available evidence on longterm O3 exposures, discussed above in 

section II.A.2.a.ii, the Staff Paper 

concludes that a health-based standard 

with a longer-term averaging time than 

8 hours is not warranted at this time. 

The Staff Paper notes that, while 

potentially more serious health effects 

have been identified as being associated 

with longer-term exposure studies of 

laboratory animals and in epidemiology 

studies, there remains substantial 

uncertainty regarding how these data 

could be used quantitatively to develop 

a basis for setting a long-term health 

standard. Because long-term air quality 

patterns would be improved in areas 

coming into attainment with an 8-hour 

standard, the potential risk of health 

effects associated with long-term 

exposures would be reduced in any area 

meeting an 8-hour standard. Thus, the 

Staff Paper did not recommend 

consideration of a long-term, healthbased standard at this time. 

In its final letter to the Administrator, 

the CASAC O3 Panel offered no views 

on the long-term exposure evidence, nor 

did it suggest that consideration of a 

primary O3 standard with a long-term 

averaging time was appropriate. In fact, 

the CASAC O3 Panel agreed with the 

choice of an 8-hour averaging time for 

the primary O3 NAAQS suggested by 

Agency staff (Henderson, 2007). 

Similarly, no commenters expressed 

support for considering such a longterm standard. 

c. Administrator’s Conclusions on 

Averaging Time 

In considering the information 

discussed above, CASAC views and 

public comments, the Administrator 

concludes that a standard with an 8- 

hour averaging time can effectively limit 

both 1- and 8-hour exposures of concern 

and that an 8-hour averaging time is 

appropriate to provide adequate and 

more uniform protection of public 

health from both short-term (1- to 3- 

hour) and prolonged (6- to 8-hour) 

exposures to O3 in the ambient air. This 

conclusion is based on the observations 

summarized above, particularly: (1) The 

fact that the 8-hour averaging time is 

more directly associated with health 

effects of concern at lower O3

concentrations than are averaging times 

of shorter duration and (2) results from 

quantitative risk analyses showing that 

attaining an 8-hour standard reduces the 

risk of experiencing health effects 

associated with both 8-hour and shorter 

duration exposures. Furthermore, the 

Administrator observes that the CASAC 

O3 Panel agreed with the choice of 

averaging time (Henderson, 2007). 

Therefore, the Administrator proposes 

to retain the 8-hour averaging time and 

is not proposing a separate 1-hour 

standard. The Administrator also 

concludes that a standard with a longterm averaging time is not warranted at 

this time. 

3. Form 

In 1997, the primary O3 NAAQS was 

changed from a ‘‘1-expectedexceedance’’ form per year over three 

years 51 to a concentration-based 

statistic, specifically the 3-year average 

of the annual fourth-highest daily 

maximum 8-hour concentrations. The 

principal advantage of the 

concentration-based form is that it is 

more directly related to the ambient O3

concentrations that are associated with 

the health effects. With a concentrationbased form, days on which higher O3

concentrations occur would weigh 

proportionally more than days with 

lower concentrations, since the actual 

concentrations are used in determining 

whether the standard is attained. That 

is, given that there is a continuum of 

effects associated with exposures to 

varying levels of O3, the extent to which 

public health is affected by exposure to 

ambient O3 is related to the actual 

magnitude of the O3 concentration, not 

just whether the concentration is above 

a specified level. 

During the 1997 review, consideration 

was given to a range of alternative 

forms, including the second-, third-, 

fourth- and fifth-highest daily maximum 

8-hour concentrations in an O3 season, 

recognizing that the public health risks 

associated with exposure to a pollutant 

without a clear, discernable threshold 

can be appropriately addressed through 

a standard that allows for multiple 

exceedances to provide increased 

stability, but that also significantly 

limits the number of days on which the 

level may be exceeded and the 

magnitude of such exceedances. 

Consideration was given to setting a 

standard with a form that would 

provide a margin of safety against 

possible, but uncertain chronic effects, 

and would also provide greater stability 

to ongoing control programs. The 

fourth-highest daily maximum was 

selected because it was decided that the 

differences in the degree of protection 

against potential chronic effects 

afforded by the alternatives within the 

range were not well enough understood 

to use any such differences as a basis for 


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52The Staff Paper notes that the 8-hour O3

standard adopted by the State of California in 2006 

is specified to the nearest thousandth part per 

million (at a level of 0.070 ppm) (http:// 

www.arb.ca.gov/research/aaqs/ozone-rs/ozoners.htm). 

choosing the most restrictive forms. On 

the other hand, the relatively large 

percentage of sites that would 

experience O3 peaks well above 0.080 

ppm and the number of days on which 

the level of the standard may be 

exceeded, even when attaining a fifthhighest 0.080 ppm concentration-based 

standard, argued against choosing that 

form. 

As an initial matter, the Staff Paper 

considered whether it is appropriate to 

continue to specify the level of the O3

standard to the nearest hundredth (two 

decimal places) ppm, or whether the 

precision with which ambient O3

concentrations are measured supports 

specifying the standard level to the 

thousandth ppm (i.e., to the part per 

billion (ppb)). The Staff Paper discusses 

an analysis conducted by EPA staff to 

determine the impact of ambient O3

measurement error on calculated 8-hour 

average O3 design value concentrations, 

which are compared to the level of the 

standard to determine whether the 

standard is attained (Cox and Camalier, 

2006). The results of this analysis 

suggest that instrument measurement 

error, or possible instrument bias, 

contribute very little to the uncertainty 

in design values. More specifically, 

measurement imprecision was 

determined to contribute less than 1 ppb 

to design value uncertainty, and a 

simulation study indicated that 

randomly occurring instrument bias 

could contribute approximately 1 ppb. 

EPA staff interpreted this analysis as 

being supportive of specifying the level 

of the standard to the nearest 

thousandth ppm. If the current standard 

were to be specified to this degree of 

precision, the current standard would 

effectively be at a level of 0.084 ppm, 

reflecting the data rounding conventions 

that are part of the definition of the 

current 0.080 ppm 8-hour standard. 

This information was provided to the 

CASAC O3 Panel and made available to 

the public. 

In evaluating alternative forms for the 

primary standard in conjunction with 

specific standard levels, the Staff Paper 

considered the adequacy of the public 

health protection provided by the 

combination of the level and form to be 

the foremost consideration. In addition, 

the Staff Paper recognized that it is 

important to have a form of the standard 

that is stable and insulated from the 

impacts of extreme meteorological 

events that are conducive to O3

formation. Such instability can have the 

effect of reducing public health 

protection, because frequent shifting in 

and out of attainment due to 

meteorological conditions can disrupt 

an area’s ongoing implementation plans 

and associated control programs. 

Providing more stability is one of the 

reasons that EPA moved to a 

concentration-based form in 1997. 

The Staff Paper considered two 

concentration-based forms of the 

standard: the nth-highest maximum 

concentration and a percentile-based 

form. A percentile-based statistic is 

useful for comparing datasets of varying 

length because it samples approximately 

the same place in the distribution of air 

quality values, whether the dataset is 

several months or several years long. 

However, a percentile-based form would 

allow more days with higher air quality 

values in locations with longer O3

seasons relative to places with shorter 

O3 seasons. An nth-highest maximum 

concentration form would more 

effectively ensure that people who live 

in areas with different length O3 seasons 

receive the same degree of public health 

protection. For this reason, the exposure 

and risk analyses were based on a form 

specified in terms of an nth-highest 

concentration, with n ranging from 3 

to 5. 

The results of some of these analyses 

are shown in the Staff Paper (Figures 6–

1 through 6–4) and specifically 

discussed in chapter 6. These figures 

illustrate the estimated percent change 

in risk estimates for the incidence of 

moderate or greater decrements in lung 

function (≥15 percent FEV1) in all 

school age children and moderate or 

greater lung function decrements (≥10 

percent FEV1) in asthmatic school age 

children, associated with going from 

meeting the current standard to meeting 

alternative standards with alternative 

forms based on the 2002 and 2004 

simulations. Figures 6–5 and 6–6 

illustrate the estimated percent of 

change in the estimated incidence of 

non-accidental mortality, associated 

with going from meeting the current 

standard to meeting alternative 

standards, based on the 2002 and 2004 

simulations. These results are generally 

representative of the patterns found in 

all of the analyses. The estimated 

reductions in risk associated with 

different forms of the standard, ranging 

from third- to fourth-highest daily 

maximum concentrations at 0.084 ppm, 

and from third- to fifth-highest daily 

maximum concentrations at 0.074 ppm, 

are generally less than the estimated 

reductions associated with the different 

levels that were analyzed. As seen in 

these figures, there is much city-to-city 

variability, particularly in the percent 

changes associated with going from a 

fourth-highest to third-highest form at 

the current level of 0.084 ppm, and with 

estimated reductions associated with 

the fifth-highest form at a 0.074 ppm 

level. In most cities, there are generally 

only small differences in the estimated 

reductions in risks associated with the 

third- to fifth-highest forms at a level of 

0.074 ppm simulated using 2002 and 

2004 O3 monitoring data. 

The Staff Paper noted that there is not 

a clear health-based threshold for 

selecting a particular nth-highest daily 

maximum form of the standard from 

among the ones analyzed. It also noted 

that the changes in the form considered 

in the analyses result in only small 

differences in the estimated reductions 

in risks in most cities, although in some 

cities larger differences are estimated. 

The Staff Paper concluded that a range 

of concentration-based forms from the 

third- to the fifth-highest daily 

maximum 8-hour average concentration 

is appropriate for consideration in 

setting the standard. Given that there is 

a continuum of effects associated with 

exposures to varying levels of O3, the 

extent to which public health is affected 

by exposure to ambient O3 is related to 

the actual magnitude of the O3

concentration, not just whether the 

concentration is above a specified level. 

The principal advantage of a 

concentration-based form is that it is 

more directly related to the ambient O3

concentrations that are associated with 

health effects. Robust, concentrationbased forms, in the range of the thirdto fifth-highest daily maximum 8-hour 

average concentration, including the 

current 4th-highest daily maximum 

form, minimize the inherent lack of 

year-to-year stability of exceedancebased forms and provide insulation 

from the impacts of extreme 

meteorological events. Such instability 

can have the effect of reducing public 

health protection by disrupting ongoing 

implementation plans and associated 

control programs. 

With regard to the precision of the 

standard, in their letter to the 

Administrator, the CASAC concluded 

that current monitoring technology 

‘‘allows accurate measurement of O3

concentrations with a precision of parts 

per billion’’ (Henderson, 2006c). The 

CASAC recommended that the 

specification of the level of the O3

standard should reflect this degree of 

precision (Henderson, 2006c). Some 

public comments supported specifying 

the standard in terms of parts per 

billion, or to three decimal places if 

specified in terms of parts per million.52

Other public commenters stated that the 


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basis for changing the current rounding 

procedures is not supported by a 

complete analysis of the O3 compliance 

monitoring procedures, including 

consideration of uncertainty related to 

humidity effects and interferences from 

aromatic compounds in the monitoring 

of O3 levels. 

With regard to the form of the 

standard, in their letter to the 

Administrator, CASAC recommended 

that ‘‘a range of concentration-based 

forms from the third-to the fifth-highest 

daily maximum 8-hour average 

concentration’’ be considered 

(Henderson, 2006c, p. 5). Some public 

commenters that expressed the view 

that the current primary O3 standard is 

not adequate also submitted comments 

that supported a more health-protective 

form of the standard than the current 

form (e.g., a second-or third-highest 

daily maximum form). Commenters who 

expressed the view that the current 

standard is adequate did not provide 

any views on alternative forms that 

would be appropriate for consideration 

should the Administrator consider 

revisions to the standard. 

The Administrator proposes that the 

level of the standard be specified to the 

nearest thousandth ppm, based on the 

staff’s analysis and conclusions 

discussed in the Staff Paper that current 

monitoring technology allows accurate 

measurement of O3 to support 

specifying the 8-hour standard to this 

degree of precision, and on CASAC’s 

recommendation with respect to this 

aspect of the standard. The 

Administrator invites comment on this 

proposal to specify the standard to the 

thousandth ppm. 

The Administrator recognizes that 

there is not a clear health-based 

threshold for selecting a particular nthhighest daily maximum form of the 

standard from among the ones analyzed 

in the Staff Paper, and that the current 

form of the standard provides a stable 

target for implementing programs to 

improve air quality. The Administrator 

also agrees that the adequacy of the 

public health protection provided by the 

combination of the level and form is a 

foremost consideration. Based on this, 

the Administrator proposes to retain the 

form of the current standard, 4th-highest 

daily maximum 8-hour average 

concentration, recognizing that the 

public health protection that would be 

provided by the standard is based on 

combining this form with the level 

discussed below. Mindful of the 

recommendation of the O3 CASAC 

Panel and the view expressed by 

commenters, the Administrator also 

invites comment on two alternative 

forms of the standard, the third- and the 

fifth-highest daily maximum 8-hour 

average concentrations. 

4. Level 

a. Evidence and Exposure/Risk Based 

Considerations in the Staff Paper 

The approach used in the Staff Paper 

as a basis for staff recommendations on 

standard levels builds upon and 

broadens the general approach used by 

EPA in the last review. This approach 

reflects the more extensive and stronger 

body of evidence now available on a 

broader range of health effects 

associated with exposure to O3, 

including: (1) Additional respiratoryrelated endpoints; (2) new information 

about the mechanisms underlying 

respiratory morbidity effects supporting 

a judgment that the link between O3

exposure and these effects is causal; (3) 

newly identified cardiovascular-related 

health endpoints from animal 

toxicology, and controlled human 

exposures studies that are highly 

suggestive that O3 can directly or 

indirectly contribute to cardiovascular 

morbidity, and (4) new U.S. multi-city 

time series studies, single city studies, 

and several meta-analyses of these 

studies that provide relatively strong 

evidence for associations between shortterm O3 exposures and all-cause 

(nonaccidental) mortality, at levels 

below the current primary standard: as 

well as (5) evidence of increased 

susceptibility in people with asthma 

and other lung diseases. In evaluating 

evidence-based and exposure/risk-based 

considerations, the Staff Paper 

considered: (1) The ranges of levels of 

alternative standards that are supported 

by the evidence, and the uncertainties 

and limitations in that evidence and (2) 

the extent to which specific levels of 

alternative standards reduce the 

estimated exposures of concern and 

risks attributable to O3 and other 

photochemical oxidants, and the 

uncertainties associated with the 

estimated exposure and risk reductions. 

In taking into account evidence-based 

considerations, the Staff Paper 

evaluated available evidence from 

controlled human exposure studies and 

epidemiological studies, as well as the 

uncertainties and limitations in that 

evidence. In particular, it focused on the 

extent to which controlled human 

exposure studies provide evidence of 

lowest-observed-effects levels and the 

extent to which epidemiological studies 

provide evidence of associations that 

extend down to the lower levels of O3

concentrations observed in the studies 

or some indication of potential effect 

thresholds in terms of 8-hour average O3

concentrations. 

In considering the available 

controlled human exposure studies, as 

discussed above in section 

II.A.2.a.i(a)(i), two new studies are 

notable in that they are the only 

controlled human exposure studies that 

examined respiratory effects, including 

lung function decrements and 

respiratory symptoms, in healthy adults 

at lower exposure levels than had 

previously been examined. EPA’s 

reanalysis of the data from the most 

recent study shows small group mean 

decrements in lung function responses 

to be statistically significant at the 0.060 

ppm exposure level, while the author’s 

analysis did not yield statistically 

significant lung function responses (but 

did yield some statistically significant 

respiratory symptom responses toward 

the end of the exposure period). 

Notably, these studies report a small 

percentage of subjects experiencing lung 

function decrements (> 10 percent) at 

the 0.060 ppm exposure level. These 

studies provide very limited evidence of 

O3-related lung function decrements 

and respiratory symptoms at this lower 

exposure level. 

In considering controlled human 

exposure studies of pulmonary 

inflammation, airway responsiveness, 

and impaired host defense capabilities, 

the Staff Paper notes that these studies 

provide evidence of a lowest-observedeffects level for such effects in healthy 

adults at prolonged moderate exertion of 

0.080 ppm. As discussed above, these 

physiological effects have been linked to 

aggravation of asthma and increased 

susceptibility to respiratory infection, 

potentially leading to increased 

medication use, increased school and 

work absences, increased visits to 

doctors’ offices and emergency 

departments, and increased hospital 

admissions. Further, pulmonary 

inflammation is related to increased 

cellular permeability in the lung, which 

may be a mechanism by which O3

exposure can lead to cardiovascular 

system effects, and to potential chronic 

effects such as chronic bronchitis or 

long-term damage to the lungs that can 

lead to reduced quality of life. These are 

all indicators of adverse O3-related 

morbidity effects, which are consistent 

with and lend plausibility to the adverse 

morbidity effects and mortality effects 

observed in epidemiological studies. 

In considering epidemiological 

studies, the Staff Paper first recognizes 

that the available evidence neither 

supports nor refutes the existence of 

effect thresholds at the population level 

for morbidity and mortality effects and 

that if a population threshold level does 

exist, it would likely be well below the 

level of the current O3 standard and 


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53Bell et al. (2006) referred to this level as being 

approximately equivalent to 120 μg/m3, daily 8- 

hour maximum, the World Health Organization 

guideline and European Commission target value 

for O3. 

54As described in the Staff Paper (section 4.5.8) 

and discussed above, recent O3 air quality 

distributions have been statistically adjusted to 

simulate just meeting the current and selected 

alternative standards. These simulations do not 

represent predictions of when, whether, or how 

areas might meet the specified standards. Modeling 

that projects whether and how areas might attain 

alternative standards in a future year is presented 

in the Regulatory Impact Analysis being prepared 

in connection with this rulemaking. 

55The abbreviated notation used to identify the 

current and alternative standards in this section and 

in the risk assessment section of the Staff Paper is 

in terms of ppm and the nth highest daily 

maximum 8-hour average. For example, the current 

standard is identified as ‘‘0.084/4.’’

possibly within the range of background 

levels. As discussed above (and more 

fully in the Staff Paper in chapter 3 and 

the Criteria Document in chapter 7), a 

number of studies reported some 

suggestive evidence of possible 

thresholds for morbidity and mortality 

outcomes in terms of 24-hour, 8-hour, 

and 1-hour averaging times. These 

results, taken together, provide some 

indication of possible 8-hour average 

threshold levels from below about 0.025 

to 0.035 ppm up to approximately 0.050 

ppm. Other studies, however, observe 

linear concentration-response functions 

suggesting no effect threshold. The Staff 

Paper concludes that the statistically 

significant associations between 

ambient O3 concentrations and lung 

function decrements, respiratory 

symptoms, indicators of respiratory 

morbidity including increased 

emergency department visits and 

hospitals admissions, and possibly 

mortality reported in a large number of 

studies likely extend down to ambient 

O3 concentrations that are well below 

the level of the current standard (EPA, 

2007, p. 6–60). Toward the lower end of 

the range of O3 concentrations observed 

in such studies, ranging down to 

background levels, however, the Staff 

paper states that there is increasing 

uncertainty as to whether the observed 

associations remain plausibly related to 

exposures to ambient O3, rather than to 

the broader mix of air pollutants present 

in the ambient atmosphere. 

The Staff Paper also considered 

studies that did subset analyses that 

include only days with ambient O3

concentrations below the level of the 

current standard, or below even lower 

O3 concentrations, and continue to 

report statistically significant 

associations. Notably, as discussed 

above, Bell et al. (2006) conducted a 

subset analysis that continued to show 

statistically significant associations even 

when only days with a maximum 8- 

hour average O3 concentration below a 

value of approximately 0.061 ppm were 

included.53 Also of note is the large 

multi-city NCICAS (Mortimer et al., 

2002) that reported statistically 

significant associations between 

ambient O3 concentrations and lung 

function decrements even when days 

with 8-hour average O3 levels greater 

than 0.080 ppm were excluded (which 

consisted of less than 5 percent of the 

days in the eight urban areas in the 

study). 

Being mindful of the uncertainties 

and limitations inherent in interpreting 

the available evidence, the Staff Paper 

states the view that the range of 

alternative O3 standards for 

consideration should take into account 

information on lowest-observed-effects 

levels in controlled human exposure 

studies as well as indications of possible 

effects thresholds reported in some 

epidemiological studies and questions 

of biological plausibility in attributing 

associations observed down to 

background levels to O3 exposures 

alone. Based on the evidence and these 

considerations, it concluded that the 

upper end of the range of consideration 

should be somewhat below 0.080 ppm, 

the lowest-observed-effects level for 

effects such as pulmonary 

inflammation, increased airway 

responsiveness and impaired hostdefense capabilities in healthy adults 

while at prolonged moderate exertion. 

The Staff Paper also concludes that the 

lower end to the range of alternative O3

standards appropriate for consideration 

should be the lowest-observed-effects 

level for potentially adverse lung 

function decrements and respiratory 

symptoms in some healthy adults, 0.060 

ppm. 

In addition to the evidence-based 

considerations informing staff 

recommendations on alternative levels, 

the Staff Paper also evaluated 

quantitative exposures and health risks 

estimated to occur upon meeting the 

current and alternative standards.54 In 

so doing, it presented the important 

uncertainties and limitations associated 

with these exposure and risk 

assessments. For example, the Staff 

Paper noted important uncertainties 

affecting the exposure estimates are 

related to modeling human activity 

patterns over an O3 season (especially 

repetitive exposures), modeling ambient 

concentrations near roadways and 

modeling building air exchange rates 

which impact estimates of indoor O3

concentrations. With regard to the risk 

assessment, important uncertainties 

include, for example, those related to 

exposure estimates for children engaged 

in moderate or greater exertion, as well 

as those related to estimation of 

concentration-response functions, 

specification of concentration-response 

models, the possible role of copollutants 

in interpreting reported associations 

with O3, and inferences of a likely 

causal relationship between O3

exposure and nonaccidental mortality 

(for risk estimates based on 

epidemiological studies). 

Beyond these uncertainties, the Staff 

Paper also recognized important 

limitations to the exposure and risk 

analyses. For example, the Staff Paper 

did not have sufficient information to 

evaluate all relevant at-risk groups (e.g., 

outdoor workers) or all O3-related health 

outcomes (e.g., increased medication 

use, school absences, emergency 

department visits), and the scope of the 

Staff Paper analyses was generally 

limited to estimating exposures and 

risks in 12 urban areas across the U.S., 

and to only five or just one area for 

some risk analyses. The Staff Paper 

notes that it is clear that national-scale 

public health impacts of ambient O3

exposures are much larger than the 

quantitative estimates of O3-related 

incidences of adverse health effects and 

the numbers of children likely to 

experience exposures of concern 

associated with meeting the current or 

alternative standards. On the other 

hand, due to individual variability in 

responsiveness, only a subset of 

individuals who are estimated to 

experience exposures of concern at and 

above a specific benchmark level can be 

expected to experience certain adverse 

health effects, although susceptible 

subpopulations such as those with 

asthma are expected to be affected more 

by such exposures than healthy 

individuals. In taking these limitations 

into account, the Staff Paper reflected 

CASAC’s advice not to rely solely on the 

results of the exposure and risk 

assessments in considering alternative 

standards, but also to place significant 

weight on the body of evidence of O3- 

related health effects in drawing 

conclusions about an appropriate range 

of levels for consideration. 

The Staff Paper focused on alternative 

standards with the same form as the 

current O3 standard (i.e. the 0.074/4, 

0.070/4 and 0.064/4 scenarios).55

Having concluded in the Staff Paper that 

it was appropriate to consider a range of 

standard levels from somewhat below 

0.080 ppm down to as low as 0.060 

ppm, the Staff Paper looked to results of 

the analyses of exposure and risk for the 

0.074/4 scenario to represent the public 

health impacts of selecting a standard in 


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the upper part of the range, the results 

of analyses of the 0.070/4 scenario to 

represent the impacts in the middle part 

of the range, and the results of the 

analyses of the 0.064/4 scenario to 

represent the lower part of the range. 

As discussed in section II.B.1 of this 

notice, the exposure estimates presented 

in the Staff Paper are for the number 

and percent of all children and 

asthmatic children exposed, and the 

number of person-days (occurrences) of 

exposures, with daily 8-hour maximum 

exposures at or above several 

benchmark levels while at intermittent 

moderate or greater exertion. For 

reasons discussed above in section 

II.C.2, the Staff Paper focused on 

exposures of concern at the 0.070 and 

0.060 ppm benchmark levels for the 

purpose of evaluating alternative 

standard levels. As shown in the Table 

1 in this notice, the percent of 

population exposed at any given level is 

very similar for all and asthmatic school 

age children. Substantial year-to-year 

variability in exposure estimates is 

observed, ranging to over an order of 

magnitude at the higher alternative 

standard levels, in estimates of the 

number of children and the number of 

occurrences of exposures of concern at 

both of these benchmark levels. The 

Staff Paper also notes that there is 

substantial city-to-city variability in 

these estimates, and notes that it is 

appropriate to consider not just the 

aggregate estimates across all cities, but 

also to consider the public health 

impacts in cities that receive relatively 

less protection from the alternative 

standards. 

As discussed in the Staff Paper, a 

standard set at the upper part of the 

range recommended by EPA staff (e.g., 

the 0.074/4 scenario) would result in an 

aggregate estimate of about 4 percent of 

all or asthmatic school age children 

likely to experience exposures of 

concern at the ≥0.070 ppm benchmark 

level based on the 2002 simulation, a 

year with relatively high O3 levels, 

while the estimates range up to 12 

percent of all or asthmatic school age 

children in the single city with the least 

degree of protection from this standard. 

Using the 2004 simulation, a year with 

relatively low O3 levels, exposures of 

concern at this level are essentially 

eliminated. At the benchmark level of 

≥0.060 ppm, in aggregate using the 2002 

simulation about 22 percent of all or 

asthmatic school age children are 

estimated to experience exposures of 

concern; this estimate ranges up to 

about 46 percent of all or asthmatic 

school age children in the single city 

with the least degree of protection from 

this standard. Using the 2004 

simulation, exposures of concern at this 

level are estimated to be substantially 

lower. A standard set at this level is 

estimated to reduce the number of all 

and asthmatic school age children 

estimated to experience one or more 

moderate lung function decrements by 

about 30 to 50 percent relative to the 

current standard, with city-to-city 

differences accounting for most of the 

variability in estimates. A standard set 

at this level is estimated to reduce nonaccidental mortality by about 10 to 40 

percent, with most of the variability 

occurring across the 12 city estimates. 

Using the 2002 simulation, a standard 

set at this level (the 0.074/4 scenario) is 

estimated to reduce the incidence of 

symptom days in children with 

moderate to severe asthma in the Boston 

area by about 1,000 days, a 15 percent 

reduction relative to the current 

standard. With this reduction, it is 

estimated that about 1 respiratory 

symptom day in 8 during the O3 season 

would be attributable to O3 exposure. 

Estimated incidence of respiratoryrelated hospital admissions was reduced 

by 14 to 17 percent by a standard set at 

this level relative to the current 

standard, in the year with relatively 

high and relatively low O3 air quality 

levels respectively. 

The Staff Paper notes that a standard 

set at the middle part of the staffrecommended range, as indicated by the 

estimates for the 0.070/4 scenario, 

would reduce the exposures of concern 

at the 0.070 ppm level substantially over 

the current standard, resulting in an 

aggregate estimate of about 1.5 to nearly 

2 percent of all or asthmatic school age 

children likely to experience exposures 

of concern even using the 2002 

simulation, and leaving approximately 5 

percent or less of children likely to 

experience exposures of concern in the 

city with the least degree of protection. 

Using the 2004 simulation, it essentially 

eliminates exposures of concern at this 

level. It reduces exposures of concern at 

the 0.060 ppm benchmark level less so, 

leaving larger percentages of all school 

age children unprotected using the 2002 

simulation (about 15 percent in 

aggregate) or in the city with the least 

protection from this standard (about 33 

percent). However, using the 2004 

simulation, it is estimated to reduce 

exposures of concern at this benchmark 

level to approximately 5 percent or less 

of children even in the city with the 

least degree of protection. It provides 

considerable additional protection for 

members of at-risk groups, over the 

current O3 standard, against respiratory 

morbidity effects such as lung function 

decrements, respiratory symptom days 

and hospital admissions, as well as nonaccidental mortality. 

A standard set at lower part of the 

staff-recommended range (e.g., the 

0.064/4 scenario), would result in an 

aggregate estimate of less than 0.5 

percent of all and asthmatic school age 

children likely to experience exposures 

of concern at the 0.070 ppm benchmark 

level using the 2002 simulation and 

only about 1 percent of all and 

asthmatic school age children in the city 

with the least degree of protection from 

this standard. At the benchmark level of 

0.060 ppm, in aggregate using the 2002 

simulation about 5 percent of all and 

asthmatic school age children are 

estimated to experience exposures of 

concern; this number ranges up to 15 

percent of all and asthmatic school age 

children in the city with the least degree 

of protection from this standard. A 

standard set at this level is estimated to 

reduce the number of all and asthmatic 

school age children estimated to 

experience one or more moderate lung 

function decrements by about 40 to 75 

percent over the current standard, and 

non-accidental mortality by about 25 to 

75 percent, with most of the variability 

occurring across the 12 city estimates. 

A standard set at the 0.064/4 scenario 

is estimated, based on the 2002 

simulation, to reduce the incidence of 

symptom days in children with 

moderate to severe asthma in the Boston 

area by about 1,900 days, about a 25 to 

30 percent reduction over the current 

standard. But even with this reduction, 

it is estimated that 1 respiratory 

symptom day in 10 during the O3 season 

is attributable to O3 exposure. Estimated 

incidence of respiratory-related hospital 

admissions would be reduced by 30 to 

35 percent over the current standard, a 

reduction of 125 to 150 hospital 

admissions in the New York City area 

alone, using the 2002 and 2004 

simulations, respectively. 

b. CASAC Views 

As stated in its letter to the 

Administrator, ‘‘the CASAC 

unanimously recommends that the 

current primary ozone NAAQS be 

revised and that the level that should be 

considered for the revised standard be 

from 0.060 to 0.070 ppm’’ (Henderson, 

2006c, p. 5). This recommendation 

follows from its more general 

recommendation, discussed above, that 

the current standard of 0.084 ppm needs 

to be substantially reduced to be 

protective of human health, particularly 

in at-risk subpopulations. The CASAC 

Panel noted that beneficial reductions in 

some adverse health effects were 

estimated to occur upon meeting the 

lowest standard level (0.064 ppm) 


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considered in the risk assessment 

(Henderson, 2006c, p. 4). The lower end 

of this range reflects CASAC’s views 

that ‘‘[W]hile data exist that adverse 

health effects may occur at levels lower 

than 0.060 ppm, these data are less 

certain and achievable gains in 

protecting human health can be 

accomplished through lowering the 

ozone NAAQS to a level between 0.060 

and 0.070 ppm.’’ (id.). In a subsequent 

letter to the Administrator, the CASAC 

reiterated that the Panel members ‘‘were 

unanimous in recommending that the 

level of the current primary ozone 

standard should be lowered from 0.08 

ppm to no greater than 0.070 ppm’’

(Henderson, 2007, p. 2). Further, the 

CASAC Panel expressed the view that 

the Criteria Document and Staff Paper, 

together with the information in its 

earlier letter, provide ‘‘overwhelming 

scientific evidence for this 

recommendation,’’ and emphasized the 

Clean Air Act requirement that the 

primary standard must be set to protect 

the public health with an adequate 

margin of safety (id.). 

c. Administrator’s Proposed 

Conclusions on Level 

For the reasons discussed below, and 

taking into account information and 

assessments presented in the Criteria 

Document and Staff Paper, the advice 

and recommendations of CASAC, and 

the public comments to date, the 

Administrator proposes to revise the 

existing 8-hour primary O3 standard. 

Specifically, the Administrator proposes 

to revise (1) The level of the primary O3

standard to within a range from 0.070 to 

0.075 ppm and (2) the degree of 

precision to which the level of the 

standard is specified to the thousandth 

ppm. 

However, in recognition of alternative 

views of the science, the exposure and 

risk assessments and the uncertainties 

inherent in these assessments, and the 

appropriate policy responses based on 

the currently available information, the 

Administrator also solicits comments on 

whether to proceed instead with: (1) 

Alternative levels of the 8-hour primary 

O3 standard, within ranges of below 

0.070 ppm down to 0.060 ppm and 

above 0.075 ppm up to and including 

retaining the current standard; (2) 

alternative forms of the standard, 

including the 3-year average of the 

annual third- and fifth-highest daily 

maximum 8-hour average O3

concentrations; and (3) retaining the 

degree of precision of the current 

standard (to the nearest hundredth 

ppm). Based on the comments received 

and the accompanying rationales, the 

Administrator may adopt other 

standards within the range of the 

alternative levels and forms identified 

above in lieu of the standards he is 

proposing today. 

The Administrator’s consideration of 

alternative levels of the primary O3

standard builds on his proposal, 

discussed above, that the overall body of 

evidence indicates that the current 8- 

hour O3 standard is not requisite to 

protect public health with an adequate 

margin of safety because it does not 

provide sufficient protection and that 

revision would result in increased 

public health protection, especially for 

members of at-risk groups, notably 

including asthmatic children and other 

people with lung disease, as well as all 

children and older adults, especially 

those active outdoors, and outdoor 

workers, against an array of adverse 

health effects. These effects range from 

health outcomes that could be 

quantified in the risk assessment, 

including decreased lung function, 

respiratory symptoms, serious 

indicators of respiratory morbidity such 

as hospital admissions for respiratory 

causes, and nonaccidental mortality, to 

health outcomes that could not be 

directly estimated, including pulmonary 

inflammation, increased medication 

use, emergency department visits, and 

possibly cardiovascular-related 

morbidity effects. In reaching a 

proposed decision about the level of the 

O3 primary standard, the Administrator 

has considered: the evidence-based 

considerations from the Criteria 

Document and the Staff Paper; the 

results of the exposure and risk 

assessments discussed above and in the 

Staff Paper, giving weight to the 

exposure and risk assessments as judged 

appropriate; CASAC advice and 

recommendations, as reflected in 

discussions of drafts of the Criteria 

Document and Staff Paper at public 

meetings, in separate written comments, 

and in CASAC’s letters to the 

Administrator; EPA staff 

recommendations; and public 

comments received during the 

development of these documents, either 

in connection with CASAC meetings or 

separately. In considering what 8-hour 

standard is requisite to protect public 

health with an adequate margin of 

safety, the Administrator is mindful that 

this choice requires judgment based on 

an interpretation of the evidence and 

other information that neither overstates 

nor understates the strength and 

limitations of the evidence and 

information nor the appropriate 

inferences to be drawn. 

The Administrator notes that the most 

certain evidence of adverse health 

effects from exposure to O3 comes from 

the clinical studies, and that the large 

bulk of this evidence derives from 

studies of exposures at levels of 0.080 

and above. At those levels, there is 

consistent evidence of lung function 

decrements and respiratory symptoms 

in healthy young adults, as well as 

evidence of inflammation and other 

medically significant airway responses. 

Moreover there is no evidence that the 

0.080 ppm level is a threshold for these 

effects. Although the Administrator 

takes note of the very limited new 

evidence of lung function decrements 

and respiratory symptoms in some 

healthy individuals at the 0.060 ppm 

exposure level, he judges this evidence 

too limited to support a primary focus 

at this level. The Administrator also 

notes that clinical studies, supported by 

epidemiological studies, provide 

important new evidence that people 

with asthma are likely to experience 

larger and more serious effects than 

healthy people from exposure to O3. 

There are also epidemiological studies 

that provide evidence of statistically 

significant associations between shortterm O3 exposures and more serious 

health effects such as emergency 

department visits and hospital 

admissions, and premature mortality, in 

areas that likely would have met the 

current standard. There are also many 

epidemiological studies done in areas 

that likely would not have met the 

current standard but which nonetheless 

report statistically significant 

associations that generally extend down 

to ambient O3 concentrations that are 

below the level of the current standard. 

Further, there are a few studies that 

have examined subsets of data that 

include only days with ambient O3

concentrations below the level of the 

current standard, or below even much 

lower O3 concentrations, and continue 

to report statistically significant 

associations with respiratory morbidity 

outcomes and mortality. In considering 

this evidence, the Administrator notes 

that the extent to which these studies 

provide evidence of causal relationships 

with exposures to O3 alone down to the 

lowest levels observed remains 

uncertain. To further inform the 

interpretation of this evidence, EPA 

seeks comment on the degree to which 

associations observed in 

epidemiological studies reflect causal 

relationships between important health 

endpoints and exposure to O3 alone at 

ambient O3 levels below the current 

standard. 

Therefore, the Administrator judges 

that revising the current standard to 

protect public health with an adequate 

margin of safety is warranted, and 


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would reduce risk to public health, 

based on: (1) The strong body of clinical 

evidence in healthy people at exposure 

levels of 0.080 and above of lung 

function decrements, respiratory 

symptoms, pulmonary inflammation, 

and other medically significant airway 

responses, as well as some indication of 

lung function decrements and 

respiratory symptoms at lower levels; 

(2) the substantial body of clinical and 

epidemiological evidence indicating 

that people with asthma are likely to 

experience larger and more serious 

effects than healthy people; and (3) the 

body of epidemiological evidence 

indicating associations are observed for 

a wide range of serious health effects, 

including respiratory emergency 

department visits and hospital 

admissions, and premature mortality, at 

and below 0.080 ppm. The 

Administrator also judges that the 

estimates of exposures of concern and 

risks remaining upon just meeting the 

current standard or a standard at the 

0.080 ppm level provide additional 

support for this view. For the same 

reasons, and the reasons discussed 

above in section II.C on the adequacy of 

the current standard, the Administrator 

judges that the standard should be set 

below 0.080 ppm, a level at which the 

evidence provides a high degree of 

certainty about the adverse effects of O3

exposure even in healthy people. 

The Administrator next considered 

what standard level below 0.080 ppm 

would be requisite to protect public 

health with an adequate margin of 

safety, that is sufficient but not more 

than necessary to achieve that result, 

recognizing that such a standard would 

result in increased public health 

protection. The assessment of a standard 

level calls for consideration of both the 

degree of additional protection that 

alternative levels of the standard might 

be expected to provide as well as the 

certainty that any specific level will in 

fact provide such protection. In the 

circumstances present in this review, 

there is no evidence-based bright line 

that indicates a single appropriate level; 

instead there is a combination of 

scientific evidence and other 

information that needs to be considered 

holistically in making this public health 

policy judgment, and selecting a 

standard level from a range of 

reasonable values. 

The Administrator notes that at 

exposure levels below 0.080 ppm there 

is only a very limited amount of 

evidence from clinical studies 

indicating effects in some healthy 

individuals at levels as low as 0.060 

ppm. The great majority of the evidence 

concerning effects below 0.080 ppm is 

from epidemiological studies. The 

epidemiological studies do not identify 

any bright-line threshold level for 

effects. At the same time, the 

epidemiological studies are not 

themselves direct evidence of a causal 

link between exposure to O3 and the 

occurrence of the effects. The 

Administrator considers these studies in 

the context of all the other available 

evidence in evaluating the degree of 

certainty that O3-related adverse health 

effects would occur at various ambient 

levels below 0.080 ppm, including the 

strong human clinical studies and the 

toxicological studies that demonstrate 

the biological plausibility and 

mechanisms for the effects of O3 on 

airway inflammation and increased 

airway responsiveness at exposure 

levels of 0.080 ppm and above. 

Based on consideration of the entire 

body of evidence and information 

available at this time, as well as the 

recommendations of CASAC, the 

Administrator proposes that a standard 

within the range of 0.070 to 0.075 ppm 

would be requisite to protect public 

health with an adequate margin of 

safety. A standard level within this 

range would reduce the risk of a variety 

of health effects associated with 

exposure to O3, including the 

respiratory symptoms and lung function 

effects demonstrated in the clinical 

studies, and the emergency department 

visits, hospital admissions and mortality 

effects indicated in the epidemiological 

studies. All of these effects are 

indicative of a much broader array of 

O3-related health endpoints, such as 

school absences and increased 

medication use, that are plausibly 

linked to these observed effects. 

The Administrator considered the 

degree of improvements in public health 

that potentially could be achieved by a 

standard of 0.070 to 0.075 ppm, giving 

weight to the exposure and risk 

assessments as he judged appropriate, as 

discussed below. In considering the 

results of the exposure assessment, as 

discussed above (section II.C.4), the 

Administrator has primarily focused on 

exposures at and above the 0.070 ppm 

benchmark level as an important 

surrogate measure for potentially more 

serious health effects for at-risk groups, 

including people with asthma. In so 

doing, the Administrator particularly 

notes that although the analysis of 

‘‘exposures of concern’’ was conducted 

to estimate exposures at and above three 

discrete benchmark levels, the concept 

is appropriately viewed as a continuum. 

As discussed above, the Administrator 

strives to balance concern 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 exposure levels. In focusing on this 

benchmark, the Administrator notes that 

upon just meeting a standard within the 

range of 0.070 to 0.075 ppm based on 

the 2002 simulation, the number of 

school age children likely to experience 

exposures at and above this benchmark 

level in aggregate (for the 12 cities in the 

assessment), is estimated to be 

approximately 2 to 4 percent of all and 

asthmatic children, and generally less 

than 10 percent of children even in 

cities that receive the least degree of 

protection from such a standard in a 

recent year with relatively high O3

levels. A standard within the 0.070 to 

0.075 ppm range would thus 

substantially reduce exposures of 

concern by about 90 to 80 percent, 

respectively, from those estimated to 

occur upon just meeting the current 

standard. While placing less weight on 

the results of the risk assessment, in 

light of the important uncertainties 

inherent in the assessment, the 

Administrator notes that the results 

indicate that a standard set within this 

range would likely reduce risks to atrisk groups from the O3-related health 

effects considered in the risk 

assessment, and by inference across the 

much broader array of O3-related health 

effects that can only be considered 

qualitatively, relative to the level of 

protection afforded by the current 

standard. This lends support to the 

proposed range. 

The Administrator judges that a 

standard set within the range of 0.070 to 

0.075 ppm would provide a degree of 

reduction in risk that is important from 

a public health perspective, and that a 

standard within this range would be 

requisite to protect public health, 

including the health of at-risk groups, 

with an adequate margin of safety. 

EPA’s evaluation of the body of 

scientific evidence and quantitative 

estimates of exposures and risks 

indicates that substantial reductions in 

public health risks would occur 

throughout this range. Because there is 

no bright line clearly directing the 

choice of level within this reasonable 

range, the choice of what is appropriate, 

considering the strengths and 

limitations of the evidence, and the 

appropriate inferences to be drawn from 

the evidence and the exposure and risk 

assessments, is a public health policy 

judgment. To further inform this 

judgment, EPA seeks comment on the 

extent to which the epidemiological and 

clinical evidence provides guidance as 

to the level of a standard that would be 

requisite to protect public health with 


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an adequate margin of safety, especially 

for at-risk groups. 

In considering the available 

information, the Administrator also 

judges that a standard level below 0.070 

ppm would not be appropriate. In 

reaching this judgment, the 

Administrator notes that there is only 

quite limited evidence from clinical 

studies at exposure levels below 0.080 

ppm O3. Moreover, the Administrator 

recognizes that in the body of 

epidemiological evidence, many studies 

report positive and statistically 

significant associations, while others 

report positive results that are not 

statistically significant, and a few do not 

report any positive O3-related 

associations. In addition, the 

Administrator judges that evidence of a 

causal relationship between adverse 

health outcomes and O3 exposures 

becomes increasingly uncertain at lower 

levels of exposure. 

The Administrator also has 

considered the results of the exposure 

assessments in reaching his judgment 

that a standard level below 0.070 ppm 

would not be appropriate. The 

Administrator notes that in considering 

the results from the exposure 

assessment, a standard set at the 0.070 

ppm level, with the same form as the 

current standard, is estimated to provide 

substantial reductions in exposures of 

concern (i.e., approximately 90 to 92 

percent reductions in the numbers of 

school age children and 94 percent 

reduction in the total number of 

occurrences) for both all and asthmatic 

school age children relative to just 

meeting the current standard based on 

a simulation of a recent year with 

relatively high O3 levels (2002). Thus, a 

0.070 ppm standard would be expected 

to provide protection from the 

exposures of concern that the 

Administrator has primarily focused on 

for over 98 percent of all and asthmatic 

school age children even in a year with 

relatively high O3 levels, increasing to 

over 99.9 percent of children in a year 

with relatively low O3 levels (2004). 

In considering the results of the 

health risk assessment, as discussed in 

section II.B above, the Administrator 

notes that there are important 

uncertainties and assumptions inherent 

in the risk assessment and that this 

assessment is most appropriately used 

to simulate trends and patterns that can 

be expected as well as providing 

informed but still imprecise estimates of 

the potential magnitude of risks. The 

Administrator particularly notes that as 

lower standard levels are modeled, 

including a standard set at a level below 

0.070 ppm, the risk assessment 

continues to assume a causal link 

between O3 exposures and the 

occurrence of the health effects 

examined, such that the assessment 

continues to indicate reductions in O3- 

related risks upon meeting a lower 

standard level. As discussed above, 

however, the Administrator recognizes 

that evidence of a causal relationship 

between adverse health effects and O3

exposures becomes increasingly 

uncertain at lower levels of exposure. 

Given all of the information available to 

him at this time, the Administrator 

judges that the increasing uncertainty of 

the existence and magnitude of 

additional public health protection that 

standards below 0.070 ppm might 

provide suggests that such lower 

standard levels would likely be below 

what is necessary to protect public 

health with an adequate margin of 

safety. 

In addition, the Administrator judges 

that a standard level higher than 0.075 

ppm would also not be appropriate. 

This judgment takes into consideration 

the information discussed above in 

section II.B, and is based on the strong 

body of clinical evidence in healthy 

people at exposure levels of 0.080 ppm 

and above, the substantial body of 

clinical and epidemiological evidence 

indicating that people with asthma are 

likely to experience larger and more 

serious effects than healthy people, the 

body of epidemiological evidence 

indicating that associations are observed 

for a wide range of more serious health 

effects at levels below 0.080 ppm, and 

the estimates of exposure and risk 

remaining upon just meeting a standard 

set at 0.080 ppm. The much greater 

certainty of the existence and magnitude 

of additional public health protection 

that such levels would forego provides 

the basis for judging that levels above 

0.075 ppm would be higher than what 

is requisite to protect public health, 

including the health of at-risk groups, 

with an adequate margin of safety. 

For the reasons discussed above, the 

Administrator proposes to revise the 

level of the primary O3 standard to 

within the range of 0.070 to 0.075 ppm. 

Having reached this decision based on 

the approach to interpreting the 

evidence described above, the 

Administrator recognizes that other 

approaches to selecting a standard level 

have been presented to the Agency. As 

described above, the CASAC has stated 

in two letters to the Administrator 

(Henderson, 2006c; Henderson, 2007) its 

unanimous recommendation that the 

current primary O3 NAAQS be revised 

to within the range from 0.060 to 0.070 

ppm. The CASAC Panel noted that 

while data exist that adverse health 

effects may occur at levels lower than 

0.060 ppm, these data are less certain 

and that achievable gains in protecting 

human health can be accomplished 

through lowering the O3 NAAQS to a 

level between 0.060 and 0.070 ppm. In 

addition to the views of CASAC 

described above, the Agency received 

the public comments described below. 

One group of commenters submitted 

comments that supported revising the 

level of the primary O3 standard from 

0.070 ppm down to or even below 0.060 

ppm, consistent with or below the range 

recommended by CASAC. In 

considering the available evidence as a 

basis for their views, these commenters 

generally noted that the controlled 

human exposure studies, showing 

statistically significant declines in lung 

function, and increases in respiratory 

symptoms, airway inflammation and 

airway responsiveness at a 0.080 ppm 

exposure level, were conducted with 

healthy adults, not members of at-risk 

groups including people with asthma 

and active children generally. Further, 

recognizing the substantial variability in 

response between subjects, some of 

these commenters felt that the number 

of subjects included in these studies 

was too small to ascertain the full range 

of responses, especially for at-risk 

groups. Such considerations in part 

were the basis for these commenters’

view that an O3 standard set at 0.080 

ppm is not protective of public health 

and has no margin of safety for at-risk 

groups. In addition, some of these 

commenters also noted that the World 

Health Organization’s guidelines for O3

air quality are in the range of 0.061 to 

0.051 ppm. 

In considering the results of the 

human exposure and health risk 

assessment, this group of commenters 

generally expressed the view that these 

assessments substantially underestimate 

the public health impacts of exposure to 

O3. For example, several commenters 

noted that the assessments are done for 

a limited number of cities, they do not 

address risks to important at-risk 

subpopulations (e.g., outdoor workers, 

active people who spend their summers 

outdoors, children up to 5 years of age), 

and they do not include many health 

effects that are important from a public 

health perspective (e.g., school 

absences, restricted activity days). 

Further, some of these commenters 

expressed the view that the primary O3

standard should be set to protect the 

most exposed and most vulnerable 

groups, and the fact that some children 

are frequently indoors, and thus at 

lower risk, should not weigh against 

setting a standard to protect those 

children who are active outdoors. To the 

extent the exposure and risk estimates 


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are considered, some of these 

commenters felt that primary 

consideration should be given to the 

estimates based on 2002 air quality, for 

which most areas had relatively higher 

O3 levels than in 2004, so as to ensure 

public health protection even in years 

with relatively worse O3 air quality 

levels. Some commenters also felt that 

the exposure analysis should focus on a 

benchmark concentration for exposures 

of concern at the 0.060 ppm level, the 

lower end of the range of alternative 

standards advocated by the CASAC 

Panel. 

In sharp contrast to the views 

discussed above, other public 

commenters supported retaining the 

current standard. In considering the 

available evidence as a basis for their 

views, these commenters challenged a 

number of aspects of the interpretation 

of the evidence presented in the Criteria 

Document. For example, some of these 

commenters asserted that EPA generally 

overestimates the magnitude and 

consistency of the results of short-term 

exposure epidemiological studies (e.g., 

for respiratory symptoms, school 

absences, hospital admissions, 

mortality), mistakenly links statistical 

significance and consistency with 

strength of associations, and 

underestimates the uncertainties in 

interpreting the results of such studies. 

Further, these commenters generally 

express the view that there is significant 

uncertainty related to the reliability of 

estimates from time-series studies, in 

that ambient monitors do not provide 

reliable estimates of personal exposures, 

such that the small reported morbidity 

and mortality risks are unlikely to be 

attributable to people’s exposures to O3. 

Rather, these commenters variously 

attribute the reported risks to the 

inability of time series studies to 

account for key model specification 

factors such as smoothing for timevarying parameters, meteorological 

factors, and removal of O3 by building 

ventilation systems, and confounding by 

co-pollutants. In particular, these 

commenters generally asserted that 

reported associations between shortterm O3 exposure and mortality are not 

causal, in that the reported relative risks 

are too small to provide a basis for 

inferring causality and the associations 

are most likely due to confounding, 

inappropriately specified statistical 

models, or publication bias. 

In considering the results of the 

human exposure and health risk 

assessment, this group of commenters 

generally expressed the view that these 

assessments are based on a number of 

studies that should not be used in 

quantitative risk assessment. For 

example, some commenters asserted 

that the results of time-series studies 

should not be used at all in quantitative 

risk assessments, that risk estimates 

from single city time-series studies 

should not be used since they are highly 

heterogeneous and influenced by 

publication bias, and that risk estimates 

from multi-city studies should not be 

used in estimating risk for individual 

cities. This group of commenters also 

generally expressed the view that the 

assessments generally overestimate the 

public health impacts of exposure to O3. 

Noting that the risk assessment used a 

nonlinear exposure-response function to 

estimate decreased lung function risks, 

some commenters expressed the view 

that a nonlinear approach should also 

be used to assess other acute morbidity 

effects and mortality. This view was in 

part based on judgments that it is not 

possible to determine if thresholds exist 

using time-series analyses and that the 

lack of association of O3 to mortality in 

the winter season is highly supportive 

of the likelihood of the existence of an 

effect threshold. With regard to the risk 

assessment based on controlled human 

exposure studies of lung function 

decrements, some commenters 

expressed the view that the assessment 

should not rely on what they 

characterized as ‘‘outlier’’ information 

to define exposure-response 

relationships, with reference to the data 

in the Adams (2006) study at the 0.060 

and 0.040 ppm exposure levels, but 

rather should focus on group central 

tendency response levels. Further, some 

commenters expressed the view that the 

air quality rollback algorithm used 

introduces significant uncertainty, 

especially when applied to areas 

requiring very large reductions in air 

quality to meet the alternative standards 

examined, and may result in 

overestimates in benefits from emission 

reductions. Some commenters noted 

that potential beneficial effects of O3 in 

shielding from UV–B radiation are not 

quantified in the assessment, and that 

the assessment should discuss the 

evidence for both adverse and beneficial 

effects with the same objectivity. 

Finally, some of these commenters 

asserted that since estimates of 

exposures of concern (which they 

defined as the benchmark concentration 

of 0.080 ppm) and lung function 

decrements are substantially below the 

estimates available when the current O3

standard was set in 1997, retaining the 

current standard is the most appropriate 

policy alternative. 

Some commenters also have raised 

concerns about potential uncertainties 

with regard to estimating policyrelevant background O3 levels 

including: (1) Stratospheric O3

contributions to the mid- and upper 

troposphere, which are relatively longlived (1 to 2 months), and are 

transported downward to the surface 

over time; (2) potential trends in 

stratospheric O3 levels due to changes in 

stratospheric circulation or to reduction 

of O3 depleting chemicals; (3) O3 levels 

due to lightning strikes in estimating 

policy-relevant background 

concentrations; and (4) potential 

uncertainty with regard to policyrelevant background O3 levels having to 

do with increases in O3 precursors 

elsewhere in the world. EPA asks for 

comments on these issues and on how 

they may relate to the estimation and 

consideration of policy-relevant 

background levels in setting the O3

standards. 

Several Governors, State Legislators, 

and other local officials have expressed 

concerns related to a more stringent 

standard. These officials recognize that 

State and local governments have 

important roles in developing and 

implementing policy that improve air 

quality while at the same time achieving 

economic and quality of life objectives. 

In addition, these officials note that 

States are just beginning to implement 

current air quality standards and raise 

concern with moving forward on 

revised standards without first realizing 

the results from the last revision. 

As a related concern, a number of 

areas—including some of the cities 

involved in the risk assessment—will 

have difficulty in complying with the 

current 8-hour standard within the next 

decade. As a result, the full public 

health gains in these areas from a more 

stringent 8-hour standard are unlikely to 

be realized for a number of years. In 

light of the fact that these public health 

gains may not fully materialize within 

the attainment date structure set forth in 

the Clean Air Act, some commenters 

question whether the Agency can or 

should consider these projected gains as 

a health based criterion for its 

decisionmaking. EPA requests comment 

on this view. 

The Administrator is mindful that the 

country has important goals related to 

the increased production and use of 

renewable energy, and that these new 

energy sources can have important 

public health, environmental and other 

benefits, such as national security 

benefits. In some contexts and 

situations, however, the use of 

renewable fuels may impact compliance 

with a lowered ozone NAAQS standard. 

For example, the Agency recently 

promulgated final regulations pursuant 

to section 211(o) of the Clean Air Act, 


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which was enacted as part of the Energy 

Policy Act of 2005. This provision 

requires the use of 7.5 billion gallons of 

renewable fuel by 2012, a level which 

will be greatly exceeded in practice. In 

the Regulatory Impact Analysis which 

accompanied the renewable fuel 

regulations, the Agency recognized the 

impact of this program on emissions 

related to ozone, toxics and greenhouse 

gases and otherwise reviewed the 

impacts on energy security. The 

Administrator requests comment on 

such factors and any relationship to this 

rulemaking, including the extent of 

EPA’s discretion under the Clean Air 

Act to take such factors into account 

(see section I.A). 

In general, these commenters’

concerns are consistent with the view 

that adopting a more stringent 8-hour 

standard now, without a better 

understanding of the health effects 

associated with O3 exposure at lower 

levels, would have an uncertain public 

health benefit. The Administrator 

recognizes that commenters have raised 

numerous concerns regarding various 

types of uncertainties in the available 

information, including for example 

uncertainties in (1) The assessment of 

exposures, (2) the estimation of 

concentration-response associations in 

the epidemiological studies, (3) the 

potential role of co-pollutants in 

interpreting the reported associations in 

epidemiological studies, and (4) the 

estimation of background 

concentrations. The Administrator has 

heard these concerns from Governors 

and other commenters and invites 

comment on whether it would be 

appropriate to retain the existing 

standard and delay considering 

modification of the 8-hour standard 

until the next NAAQS review, when a 

more complete body of information is 

expected to be available. 

Consistent with the goal of soliciting 

comment on a wide array of views, the 

Administrator also solicits comments on 

these alternative approaches and views, 

and on related standard levels, 

including levels down to 0.060 ppm and 

up to retaining the level of the current 

8-hour standard (i.e., effectively 0.084 

ppm with the current rounding 

convention). The Administrator 

recognizes that these sharply divergent 

views on the appropriate level of the 

standard are based on very different 

interpretations of the science itself, 

including its relative strengths and 

limitations, very different judgments as 

to how such scientific evidence should 

be used in making policy decisions on 

proposed standards, and very different 

public health policy judgments. 

E. Proposed Decision on the Primary 

Standard 

For the reasons discussed above, and 

taking into account information and 

assessments presented in the Criteria 

Document and Staff Paper, the advice 

and recommendations of CASAC, and 

the public comments to date, the 

Administrator proposes to revise the 

existing 8-hour primary O3 standard. 

Specifically, the Administrator proposes 

to revise: (1) The level of the primary O3

standard to within a range from 0.070 to 

0.075 ppm and (2) the degree of 

precision to which the level of the 

standard is specified to the thousandth 

ppm. The proposed 8-hour primary 

standard, with a level in the range of 

0.070 to 0.075 ppm, would be met at an 

ambient air monitoring site when the 3- 

year average of the annual forth-highest 

daily maximum 8-hour average O3

concentration is less than or equal to the 

level of the standard that is 

promulgated. Data handling 

conventions are specified in the 

proposed creation of Appendix P, as 

discussed in section V below. 

However, in recognition of alternative 

views of the science, the exposure and 

risk assessments and the uncertainties 

inherent in these assessments, and the 

appropriate policy responses based on 

the currently available information, the 

Administrator also solicits comments on 

whether to proceed instead with: (1) 

Alternative levels of the 8-hour primary 

O3 standard, within ranges of below 

0.070 ppm down to 0.060 ppm and 

above 0.075 ppm up to and including 

retaining the current standard; (2) 

alternative forms of the standard, 

including the 3-year average of the 

annual third- and fifth-highest daily 

maximum 8-hour average O3

concentrations; and (3) retaining the 

degree of precision of the current 

standard (to the nearest hundredth 

ppm). Based on the comments received 

and the accompanying rationales, the 

Administrator may adopt other 

standards within the range of the 

alternative levels and forms identified 

above in lieu of the standards he is 

proposing today. 

III. Communication of Public Health 

Information 

Information on the public health 

implications of ambient concentrations 

of criteria pollutants is currently made 

available primarily through EPA’s Air 

Quality Index (AQI) program. The 

current Air Quality Index has been in 

use since its inception in 1999 (64 FR 

42530). It provides accurate, timely, and 

easily understandable information about 

daily levels of pollution (40 CFR 58.50). 

The AQI establishes a nationally 

uniform system of indexing pollution 

levels for O3, carbon monoxide, nitrogen 

dioxide, particulate matter and sulfur 

dioxide. The AQI converts pollutant 

concentrations in a community’s air to 

a number on a scale from 0 to 500. 

Reported AQI values enable the public 

to know whether air pollution levels in 

a particular location are characterized as 

good (0–50), moderate (51–100), 

unhealthy for sensitive groups (101–

150), unhealthy (151–200), very 

unhealthy (201–300), or hazardous 

(300–500). The AQI index value of 100 

typically corresponds to the level of the 

short-term NAAQS for each pollutant. 

For the current O3 NAAQS, an 8-hour 

average concentration of 0.084 ppm 

corresponds to an AQI value of 100. An 

AQI value greater than 100 means that 

a pollutant is in one of the unhealthy 

categories (i.e., unhealthy for sensitive 

groups, unhealthy, very unhealthy, or 

hazardous) on a given day; an AQI value 

at or below 100 means that a pollutant 

concentration is in one of the 

satisfactory categories (i.e., moderate or 

good). Decisions about the pollutant 

concentrations at which to set the 

various AQI breakpoints, that delineate 

the various AQI categories, draw 

directly from the underlying health 

information that supports the NAAQS 

review. 

The Agency recognizes the 

importance of revising the AQI in a 

timely manner to be consistent with any 

revisions to the NAAQS. Therefore EPA 

proposes to finalize conforming changes 

to the AQI, in connection with the 

Agency’s final decision on the O3

NAAQS if revisions to the primary 

standard are promulgated. These 

conforming changes would include 

setting the 100 level of the AQI at the 

same level as the revised primary O3

NAAQS, and also making proportional 

adjustments to AQI breakpoints at the 

lower end of the range (i.e., AQI values 

of 50, 150 and 200). EPA does not 

propose to change breakpoints at the 

higher end of the range (from 300 to 

500), which would apply to state 

contingency plans or the Significant 

Harm Level (40 CFR 51.16), because the 

information from this review does not 

inform decisions about breakpoints at 

those higher levels. 

IV. Rationale for Proposed Decision on 

the Secondary Standard 

This section presents the rationale for 

the Administrator’s proposed decision 

to revise the existing 0.08 ppm, 8-hour 

O3 secondary NAAQS. The 

Administrator proposes to revise the 

current secondary standard by replacing 

it with one of two standard options. One 


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option is to adopt a new cumulative, 

seasonal concentration-weighted form, 

set at an annual level in the range of 7 

to 21 ppm-hours. This standard would 

be expressed as a sum of weighted 

hourly concentrations, cumulated over 

the 12-hour daylight period (8 a.m. to 8 

p.m.) during the consecutive 3-month 

period within the O3 monitoring season 

with the maximum index value. This 

concentration-weighted form is 

commonly called W126, and is defined 

as the sum of sigmoidally weighted 

hourly O3 concentrations over a 

specified period, where the daily 

sigmoidal weighting function is defined 

as: 

W w C hourly

e C i i 126 11 4403 == = +

, where C O at hour i, and w i3 Ci −

=

<

∑ 126

8

7

C

i AM

i PM

i

.

The other option is to revise the current 

secondary standard by making it 

identical to the proposed 8-hour 

primary standard, within the proposed 

range of 0.070 to 0.075 ppm. For this 

option, EPA also solicits comment on a 

wider range of 8-hour secondary 

standard levels, including down to 

0.060 ppm and up to and including 

retaining the current 8-hour secondary 

standard of 0.08 ppm. The 

Administrator has also considered and 

solicits comment on an alternative 

approach to setting a cumulative, 

seasonal standard(s). 

As discussed more fully below, the 

rationale for these proposed options is 

based on a thorough review of the latest 

scientific information on vegetation 

effects associated with exposure to 

ambient levels of O3, as assessed in the 

Criteria Document. This rationale also 

takes into account: (1) Staff assessments 

of the most policy-relevant information 

in the Criteria Document regarding the 

evidence of adverse effects of O3 to 

vegetation and ecosystems, information 

on biologically-relevant exposure 

metrics, and staff analyses of air quality, 

vegetation exposure and risks, presented 

in the Staff Paper and described in 

greater detail in the associated 

Technical Report on Ozone Exposure, 

Risk, and Impact Assessments for 

Vegetation (Abt, 2007), upon which staff 

recommendations for revisions to the 

secondary O3 standard are based; (2) 

CASAC advice and recommendations as 

reflected in discussion of drafts of the 

Criteria Document and Staff Paper at 

public meetings, in separate written 

comments, and in CASAC’s letters to 

the Administrator (Henderson, 2006a, b, 

c; 2007); (3) public comments received 

during development of these documents 

either in conjunction with CASAC 

meetings or separately; and (4) 

consideration of the degree of protection 

to vegetation potentially afforded by the 

proposed 8-hour primary standard. 

In developing this rationale, EPA has 

again focused on direct O3 effects on 

vegetation, specifically drawing upon an 

integrative synthesis of the entire body 

of evidence, published through early 

2006, on the broad array of vegetation 

effects associated with exposure to 

ambient levels of O3 (EPA, 2006a, 

chapter 9). In addition, because O3 can 

also indirectly affect other ecosystem 

components such as soils, water, and 

wildlife, and their associated ecosystem 

goods and services, through its effects 

on vegetation, a qualitative discussion 

of these other indirect impacts is also 

included, though these effects are not 

quantifiable at this time. As was 

concluded in the 1997 review, and 

based on the body of scientific literature 

assessed in the current Criteria 

Document, the Administrator believes 

that it is reasonable to conclude that a 

secondary standard protecting the 

public welfare from known or 

anticipated adverse effects to trees, 

native vegetation and crops would also 

afford increased protection from adverse 

effects to other environmental 

components relevant to the public 

welfare, including ecosystem services 

and function. The peer-reviewed 

literature includes studies conducted in 

the U.S., Canada, Europe, and many 

other countries around the world. In its 

assessment of the evidence judged to be 

most relevant to making decisions on 

the level of the O3 secondary standard, 

however, EPA has placed greater weight 

on U.S. studies, due to the often 

species-, site- and climate-specific 

nature of O3-related vegetation response. 

As with virtually any policy-relevant 

vegetation effects research, there is 

uncertainty in the characterization of 

vegetation effects attributable to 

exposure to ambient O3. As discussed 

below, however, research conducted 

since the last review provides important 

information coming from field-based 

exposure studies, including free air, 

gradient and biomonitoring surveys, in 

addition to the more traditional 

controlled open top chamber (OTC) 

studies. Moreover, the newly available 

studies evaluated in the Criteria 

Document have undergone intensive 

scrutiny through multiple layers of peer 

review and many opportunities for 

public review and comment. While 

important uncertainties remain, the 

review of the vegetation effects 

information has been extensive and 

deliberate. In the judgment of the 

Administrator, the intensive evaluation 

of the scientific evidence that has 

occurred in this review has provided an 

adequate basis for regulatory decisionmaking at this time. This review also 

provides important input to EPA’s 

research plan for improving our future 

understanding of the effects of ambient 

O3 at lower levels. 

A. Vegetation Effects Information 

This section outlines key information 

contained in the Criteria Document 

(chapter 9) and in the Staff Paper 

(chapter 7) on known or potential effects 

on public welfare 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 vegetation effects 

associated with exposure to O3; (2) the 

nature of effects on vegetation that have 

been associated with exposure to O3 and 

consequent potential impacts on 

ecosystems; and (3) considerations in 

characterizing what constitutes an 

adverse welfare impact of O3. 

Exposures to O3 have been associated 

quantitatively and qualitatively with a 

wide range of vegetation effects. The 

decision in the last review to set a more 

protective secondary standard primarily 

reflected consideration of the 

quantitative information on vegetation 

effects available at that time, 

particularly growth impairment (e.g., 

biomass loss) in sensitive forest tree 

species during the seedling growth stage 

and yield loss in important commercial 

crops. This information, derived mainly 

using the OTC exposure method, found 

cumulative, seasonal O3 exposures were 

most strongly associated with observed 

vegetation response. The Criteria 

Document prepared for this review 

discusses a number of additional studies 

that support and strengthen key 

conclusions regarding O3 effects on 

vegetation and ecosystems found in the 

previous Criteria Document (EPA, 

1996a, 2006a), including further 

clarification of the underlying 

mechanistic and physiological processes 

at the subcellular, cellular, and whole 


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system levels within the plant. More 

importantly, however, in the context of 

this review, new quantitative 

information is now available across a 

broader array of vegetation effects (e.g., 

growth impairment during seedlings, 

saplings and mature tree growth stages, 

visible foliar injury, and yield loss in 

annual crops) and across a more diverse 

set of exposure methods, including 

chamber, free air, gradient, model, and 

field-based observation. These nonchambered, field-based study results 

begin to address one of the key data 

gaps cited by the Administrator in the 

last review. 

The following discussion of the 

policy-relevant science regarding 

vegetation effects associated with 

cumulative, seasonal exposures to 

ambient levels of O3 integrates 

information from the Criteria Document 

(chapter 9) and the Staff Paper (chapter 

7). 

1. Mechanisms Governing Plant 

Response to Ozone 

The interpretation of predictions of 

risk associated with vegetation response 

at ambient O3 exposure levels can be 

informed by scientific understanding 

regarding O3 impacts at the genetic, 

physiological, and mechanistic levels. 

In most cases, the mechanisms of 

response are similar regardless of the 

degree of sensitivity of the species. The 

evidence assessed in the 2006 Criteria 

Document (EPA, 2006a) regarding the 

O3-induced changes in physiology 

continues to support the information 

discussed in the last review (EPA, 

1996a, 2006a). In addition, during the 

last decade understanding of the 

cellular processes within plants has 

been further clarified and enhanced. 

Therefore, this section reviews the key 

scientific conclusions identified in 1996 

Criteria Document (EPA, 1996a), and 

incorporates new information from the 

current Criteria Document (EPA, 2006a). 

This section describes: (1) Plant uptake 

of O3, (2) O3-induced cellular to 

systemic response, (3) plant 

compensation and detoxification 

mechanisms, (4) O3-induced changes to 

plant metabolism, and (5) plant 

response to chronic O3 exposures. 

a. Plant Uptake of Ozone 

To cause injury, O3 must first enter 

the plant through openings in the leaves 

called stomata. Leaves exist in a three 

dimensional environment called the 

plant canopy, where each leaf has a 

unique orientation and receives a 

different exposure to ambient air, 

microclimatological conditions, and 

sunlight. In addition, a plant may be 

located within a stand of other plants 

which further modifies ambient air 

exchange with individual leaves. Not all 

O3 entering a plant canopy is absorbed 

into the leaf stomata, but may be 

adsorbed to other surfaces e.g., leaf 

cuticles, stems, and soil (termed nonstomatal deposition) or scavenged by 

reactions with intra-canopy biogenic 

VOCs and naturally occurring NOX

emissions from soils. Because O3 does 

not penetrate the leaf’s cuticle, it must 

reach the stomatal openings in the leaf 

for absorption to occur. The movement 

of O3 and other gases such as CO2 into 

and out of leaves is controlled by 

stomatal guard cells that regulate the 

size of the stomatal apertures. These 

guard cells respond to a variety of 

internal species-specific factors as well 

as external site specific environmental 

factors such as light, temperature, 

humidity, CO2 concentration, soil 

fertility and water status, and in some 

cases the presence of air pollutants, 

including O3. These modifying factors 

produce stomatal conductance that vary 

between leaves of the same plant, 

individuals and genotypes within a 

species and diurnally and seasonally. 

b. Cellular to Systemic Response 

Once inside the leaf, O3 can react with 

a variety of biochemical compounds 

that are exposed to the air spaces within 

the leaf or it can be dissolved into the 

water lining the cell wall of the air 

spaces. Having entered the aqueous 

phase, O3 can be rapidly altered to form 

oxidative products that can diffuse more 

readily into and through the cell and 

react with many biochemical 

compounds. An early step in a series of 

O3-induced events that leads to leaf 

injury seems to involve alteration in cell 

membrane function, including 

membrane transport properties (EPA, 

2006a). One such signaling molecule is 

hydrogen peroxide (H2O2). The presence 

of higher-than-normal levels of H2O2

within the leaf is a potential trigger for 

a set of metabolic reactions that include 

those typical of the well documented 

‘‘wounding’’ response or pathogen 

defense pathway generated by cutting of 

the leaf or by pathogen/insect attack. 

Ethylene is another compound 

produced when plants are subjected to 

biotic or abiotic stressors. Increased 

ethylene production by plants exposed 

to O3 stress was identified as a 

consistent marker for O3 exposure in 

studies conducted decades ago (Tingey 

et al., 1976). 

c. Compensation and Detoxification 

Ozone injury will not occur if (1) the 

rate and amount of O3 uptake is small 

enough for the plant to detoxify or 

metabolize O3 or its metabolites or (2) 

the plant is able to repair or compensate 

for the O3 impacts (Tingey and Taylor, 

1982; U.S. EPA, 1996a). A few studies 

have documented direct stomatal 

closure or restriction in the presence of 

O3 in some species. This response may 

be initiated ranging from within 

minutes to hours or days of exposure 

(Moldau et al., 1990; Dann and Pell, 

1989; Weber et al., 1993). However, 

exclusion of O3 simultaneously restricts 

the uptake of CO2, which also limits 

photosynthesis and growth. In addition, 

antioxidants present in plants can 

effectively protect tissue against damage 

from low levels of oxidants by 

dissipating excess oxidizing power. 

Since 1996, the role of detoxification in 

providing a level of resistance to O3 has 

been further investigated. A number of 

antioxidants have been found in plants. 

However, the pattern of changes in the 

amounts of these antioxidants varies 

greatly among different species and 

conditions. Most recent reports indicate 

that ascorbate within the cell wall 

provides the first significant 

opportunity for detoxification to occur. 

In spite of the new research, however, 

it is still not clear as to what extent 

detoxification protects against O3 injury. 

Specifically, data are needed on 

potential rates of antioxidant 

production, subcellular location(s) of 

antioxidants, and whether generation of 

these antioxidants in response to O3- 

induced stress potentially diverts 

resources and energy away from other 

vital uses. Thus, the Criteria Document 

concludes that scientific understanding 

of the detoxification mechanisms is not 

yet complete and requires further 

investigation (EPA, 2006a). 

Once O3 injury has occurred in leaf 

tissue, some plants are able to repair or 

compensate for the impacts. In general, 

plants have a variety of compensatory 

mechanisms for low levels of stress 

including reallocation of resources, 

changes in root/shoot ratio, production 

of new tissue, and/or biochemical shifts, 

such as increased photosynthetic 

capacity in new foliage and changes in 

respiration rates, indicating possible 

repair or replacement of damaged 

membranes or enzymes. Since these 

mechanisms are genetically determined, 

not all plants have the same 

complement or degree of tolerance, nor 

are all stages of a plant’s development 

equally sensitive to O3. At higher levels 

or over longer periods of O3 stress, some 

of these compensatory mechanisms, 

such as a reallocation of resources away 

from storage in the roots in favor of 

leaves or shoots, could occur at a cost 

to the overall health of the plant. 

However, it is not yet clear to what 


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degree or how the use of plant resources 

for repair or compensatory processes 

affects the overall carbohydrate budget 

or subsequent plant response to O3 or 

other stresses (EPA, 1996a, EPA, 2006a). 

d. Changes to Plant Metabolism 

Ozone inhibits photosynthesis, the 

process by which plants produce energy 

rich compounds (e.g., carbohydrates) in 

the leaves. This impairment can result 

from direct impact to chloroplast 

function and/or O3-induced stomatal 

closure resulting in reduced uptake of 

CO2. A large body of literature 

published since 1996 has further 

elucidated the mechanism of the effect 

of O3 within the chloroplast. Pell et al. 

(1997) showed that O3 exposure results 

in a loss of the central carboxylating 

enzyme that plays an important role in 

the production of carbohydrates. Due to 

its central importance, any decrease in 

this enzyme may have severe 

consequences for the plant’s 

productivity. Several recent studies 

have found that O3 has a greater effect 

as leaves age, with the greatest impact 

of O3 occurring on the oldest leaves 

(Fiscus et al., 1997; Reid and Fiscus, 

1998; Noormets et al., 2001; Morgan et 

al., 2004). The loss of this key enzyme 

as a function of increasing O3 exposure 

is also linked to an early senescence or 

a speeding up of normal development 

leading to senescence. If total plant 

photosynthesis is sufficiently reduced, 

the plant will respond by reallocating 

the remaining carbohydrate at the level 

of the whole organism (EPA, 1996a, 

2006a). This reallocation of 

carbohydrate away from the roots into 

above ground vegetative components 

can have serious implications for 

perennial species. 

e. Plant Response to Chronic Ozone 

Exposures 

Though many changes that occur with 

O3 exposure can be observed within 

hours, or perhaps days, of the exposure, 

including those connected with 

wounding, other effects take longer to 

occur and tend to become most obvious 

after chronic exposures to low O3

concentrations. These chronic 

exposures have been linked to 

senescence or some other physiological 

response very closely linked to 

senescence. In perennial plant species, 

a reduction in carbohydrate storage in 

one year may result in the limitation of 

growth the following year (Andersen et 

al., 1997). Such ‘‘carry-over’’ effects 

have been documented in the growth of 

tree seedlings (Hogsett et al., 1989; 

Sasek et al., 1991; Temple et al., 1993; 

EPA, 1996a) and in roots (Andersen et 

al., 1991; EPA, 1996a). Though it is not 

fully understood how chronic O3 affects 

long-term growth and resistance to other 

biotic and abiotic insults in long-lived 

trees, accumulation of these carry-over 

effects over time could affect survival 

and reproduction. 

2. Nature of Effects 

Ozone injury at the cellular level, 

when it has accumulated sufficiently, 

will be propagated to the level of the 

whole leaf or plant. These larger scale 

effects can include: Reduced 

carbohydrate production and/or 

reallocation; reduced growth and/or 

reproduction; visible foliar injury and/ 

or premature senescence; and reduced 

plant vigor. Much of what is now 

known about these O3-related effects, as 

summarized below, is based on research 

that was available in the last review. 

Recent studies continue to support and 

expand this knowledge (EPA, 2006a). 

a. Carbohydrate Production and 

Allocation 

When total plant photosynthesis is 

sufficiently reduced, the plant will 

respond by reallocating the remaining 

carbohydrate at the level of the whole 

organism. Many studies have 

demonstrated that root growth is more 

sensitive to O3 exposure than stem or 

leaf growth (EPA, 2006a). When fewer 

carbohydrates are present in the roots, 

less energy will be available for rootrelated functions such as acquisition of 

water and nutrients. In addition, by 

inhibiting photosynthesis and the 

amount of carbohydrates available for 

transfer to the roots O3 can disrupt the 

association between soil fungi and host 

plants. Fungi in the soil form a 

symbiotic relationship with many 

terrestrial plants. For host plants, these 

fungi improve the uptake of nutrients, 

protect the roots against pathogens, 

produce plant growth hormones, and 

may transport carbohydrates from one 

plant to another (EPA, 1996a). These 

below-ground effects have recently been 

documented in the field (Grulke et al., 

1998; Grulke and Balduman, 1999). Data 

from a long-studied pollution gradient 

in the San Bernardino Mountains of 

southern California suggest that O3

substantially reduces root growth in 

natural stands of Ponderosa pine (Pinus 

ponderosa). Root growth in mature trees 

was decreased at least 87 percent in a 

high-pollution site as compared to a 

low-pollution site (Grulke et al., 1998), 

and a similar pattern was found in a 

separate study with whole-tree harvest 

along this gradient (Grulke and 

Balduman, 1999). Though effects on 

other ecosystem components were not 

examined, a reduction of root growth of 

this magnitude could have significant 

implications for the below-ground 

communities at those sites. Because 

effects on leaf and needle carbohydrate 

content under O3 stress can range from 

a reduction (Barnes et al., 1990; Miller 

et al., 1989), to no effect (Alscher et al., 

1989), to an increase (Luethy-Krause 

and Landolt, 1990), studies that 

examine only above-ground vegetative 

components may miss important O3- 

induced changes below ground. These 

below-ground changes could signal a 

shift in nutrient cycling with 

significance at the ecosystem level 

(Young and Sanzone, 2002). 

b. Growth Effects on Trees 

Studies comparing the O3-related 

growth response of different vegetation 

types (coniferous and deciduous) and 

growth stages (e.g., seedling and mature) 

have established that on average, 

individual coniferous trees are less 

sensitive than deciduous trees, and 

deciduous trees are generally less 

sensitive to O3 than most annual plants, 

with the exception of a few fast growing 

deciduous tree species (e.g., quaking 

aspen, black cherry, and cottonwood), 

which are highly sensitive and, in some 

cases, as much or more sensitive to O3

than sensitive annual plants. In 

addition, studies have shown that the 

relationship between O3 sensitivity in 

seedling and mature growth stages of 

trees can vary widely, with seedling 

growth being more sensitive to O3

exposures in some species, while in 

others, the mature growth stage is the 

more O3 sensitive. In general, mature 

deciduous trees are likely to be more 

sensitive to O3 than deciduous 

seedlings, and mature evergreen trees 

are likely to be less sensitive to O3 than 

their seedling counterparts. Based on 

these results, stomatal conductance, O3

uptake, and O3 effects cannot be 

assumed to be equivalent in seedlings 

and mature trees. 

In the last review (EPA, 1996b), 

analyses of the effects of O3 on trees 

were limited to 11 tree species for 

which concentration-response (C–R) 

functions for the seedling growth stage 

had been developed from OTC studies 

conducted by the National Health and 

Environmental Effects Research Lab, 

Western Ecology Division (NHEERL–

WED). A number of replicate studies 

were conducted on these species, 

leading to a total of 49 experimental 

cases. The Staff Paper presented a graph 

of the composite regression equation 

that combines the results of the C–R 

functions developed for each of the 49 

cases. The NHEERL–WED study 

predicted relative yield loss at various 

exposure levels in terms of a 12-hour 

W126. For example, 50 percent of the 


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56Only a few northern forest types in the U.S. 

have been well studied with respect to O3

exposures using the FACE method, though these 

systems are being used to expose numerous other 

ecosystem types to elevated levels of CO2. 

Additional FACE studies with O3 on other U.S. 

forest types would provide a better understanding 

of whether these results can be extrapolated to other 

forest types and mature forest stands. 

tree seedling cases would be protected 

from greater than 10 percent biomass 

loss at a 3-month, 12-hour W126 of 

approximately 24 ppm-hrs, while 75 

percent of cases would be protected 

from 10 percent biomass loss at a 3- 

month, 12-hour W126 level of 

approximately 16 ppm-hrs. 

Since the 1996 review, only a few 

studies have developed C–R functions 

for additional tree seedling species 

(EPA, 2006a). One such study is of 

particular importance in that it 

documented growth effects from O3

exposure in the field without the use of 

chambers or other fumigation methods 

that were as great as those seen in OTC 

studies (Gregg et al., 2003). This study 

placed Eastern cottonwood (Populus 

deltoides) saplings at sites along a 

continuum of ambient O3 exposures that 

gradually increased from urban to rural 

areas in the New York City area (Gregg 

et al., 2003). Eastern cottonwood was 

selected because it is fast growing, O3

sensitive and important ecologically, 

along stream banks, and commercially 

for pulpwood, furniture manufacturing, 

and as a possible new source for energy 

biomass (Burns and Hankola, 1990). 

Gregg et al. (2003) found that the 

cottonwood saplings grown in New 

York City grew faster than saplings 

grown in downwind rural areas. 

Because these saplings were grown in 

pots with carefully controlled soil 

nutrient and moisture levels, the 

authors were able to control for most of 

the differences between sites. After 

carefully considering these and other 

factors, the authors concluded the 

primary explanation for the difference 

in growth was the gradient of 

cumulative O3 exposures that increased 

as one moved downwind from urban to 

less urban and more rural sites. It was 

determined that the lower O3 exposure 

within the city center was due to NOX

titration reactions which removed O3

from the ambient air. The authors were 

able to reproduce the growth responses 

observed in the field in a companion 

OTC experiment, confirming O3 as the 

stressor inducing the growth loss 

response (Gregg et al., 2003). 

Another recent set of studies 

employed a modified Free Air CO2

Enrichment (FACE) methodology to 

expose vegetation to elevated O3

without the use of chambers. This 

exposure method was originally 

developed to expose vegetation to 

elevated levels of CO2, but has been 

modified to include O3 exposure in 

Illinois (SoyFACE) and Wisconsin 

(AspenFACE) for soybean and 

deciduous trees, respectively (Dickson 

et al., 2000; Morgan et al., 2004). The 

FACE method releases gas (e.g., CO2, O3) 

from a series of orifices placed along the 

length of the vertical pipes surrounding 

a circular field plot and uses the 

prevailing wind to distribute it. This 

exposure method has many 

characteristics that differ from those 

associated with the OTC. 

Most significantly, this exposure 

method more closely replicates 

conditions in the field than did OTCs. 

This is because, except for O3 levels 

which are varied across co-located plots, 

plants are exposed to the same ambient 

growing conditions that occur naturally 

in the field (e.g., location-specific 

pollutant mixtures; climate conditions 

such as light, temperature and 

precipitation; insect pests, pathogens). 

By using one of several co-located plots 

as a control (e.g., receives no additional 

O3), and by exposing the other rings to 

differing levels of elevated O3, the 

growth response signal that is due solely 

to the change in O3 exposure can be 

clearly determined. Furthermore, the 

FACE system can expand vertically with 

the growth of trees, allowing for 

exposure experiments to span numerous 

years, an especially useful capability in 

forest research. 

On the other hand, the FACE 

methodology also has the undesirable 

characteristic of potentially creating 

hotspots near O3 gas release orifices or 

gradients of exposure in the outer ring 

of trees within the plots, such that 

averaging results across the entire ring 

potentially overestimates the response. 

In recognition of this possibility, 

researchers at the AspenFACE 

experimental site only measured trees in 

the center core of each ring, (e.g., at least 

5–6 meters away from the emission sites 

of O3) (Dickson et al., 2000; Karnosky et 

al. 2005). By taking this precaution, it is 

unlikely that their measurements were 

influenced by any potential hotspots or 

gradients of exposure within the FACE 

rings. Taking all of the above into 

account, results from the Wisconsin 

FACE site on quaking aspen appear to 

demonstrate that the detrimental effects 

of O3 exposure seen on tree growth and 

symptom expression in OTCs can be 

observed in the field using this exposure 

method (Karnosky et al., 1999; 2005). 

The Staff Paper thus concluded that 

the combined evidence from the 

AspenFACE 56 and Gregg et al. (2003) 

field studies provide compelling and 

important support for the 

appropriateness of continued use of the 

C–R functions derived using OTC from 

the NHEERL–WED studies to estimate 

risk to these tree seedlings under 

ambient field exposure conditions. 

These studies make a significant 

contribution to the coherence in the 

weight of evidence available in this 

review and provide additional evidence 

that O3-induced effects observed in 

chambers also occur in the field. 

Trees and other perennials, in 

addition to cumulating the effects of O3

exposures over the annual growing 

season, can also cumulate effects across 

multiple years. It has been reported that 

effects can ‘‘carry over’’ from one year 

to another (EPA, 2006a). Growth 

affected by a reduction in carbohydrate 

storage in one year may result in the 

limitation of growth in the following 

year (Andersen, et al., 1997). Carry-over 

effects have been documented in the 

growth of some tree seedlings (Hogsett 

et al. 1989; Simini et al., 1992; Temple 

et al., 1993) and in roots (Andersen et 

al., 1991; EPA, 1996a). On the basis of 

past and recent OTC and field study 

data, ambient O3 exposures that occur 

during the growing season in the United 

States are sufficient to potentially affect 

the annual growth of a number of 

sensitive seedling tree species. 

However, because most studies do not 

take into account the possibility of carry 

over effects on growth in subsequent 

years, the true implication of these 

annual biomass losses may be missed. It 

is likely that under ambient exposure 

conditions, some sensitive trees and 

perennial plants could experience 

compounded impacts that result from 

multiple year exposures. 

c. Visible Foliar Injury 

Cellular injury can and often does 

become visible. Acute injury usually 

appears within 24 hours after exposure 

to O3 and, depending on species, can 

occur under a range of exposures and 

durations from 0.040 ppm for a period 

of 4 hours to 0.410 ppm for 0.5 hours 

for crops and 0.060 ppm for 4 hours to 

0.510 ppm for 1 hour for trees and 

shrubs (Jacobson, 1977). Chronic injury 

may be mild to severe. In some cases, 

cell death or premature leaf senescence 

may occur. The significance of O3 injury 

at the leaf and whole plant levels 

depends on how much of the total leaf 

area of the plant has been affected, as 

well as the plant’s age, size, 

developmental stage, and degree of 

functional redundancy among the 

existing leaf area. As a result, it is not 

presently possible to determine, with 

consistency across species and 

environments, what degree of injury at 


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the leaf level has significance to the 

vigor of the whole plant. 

The presence of visible symptoms due 

to O3 exposures can, however, by itself, 

represent an adverse impact to the 

public welfare. Specifically, it can 

reduce the market value of certain leafy 

crops (such as spinach, lettuce), impact 

the aesthetic value of ornamentals (such 

as petunia, geranium, and poinsettia) in 

urban landscapes, and affect the 

aesthetic value of scenic vistas in 

protected natural areas such as national 

parks and wilderness areas. Many 

businesses rely on healthy looking 

vegetation for their livelihoods (e.g., 

horticulturalists, landscapers, Christmas 

tree growers, farmers of leafy crops) and 

a variety of ornamental species have 

been listed as sensitive to O3 (Abt, 

1993). Though not quantified, there is 

likely some level of economic impact to 

businesses and homeowners from O3- 

related injury on sensitive ornamental 

species due to the cost associated with 

more frequent replacement and/or 

increased maintenance (fertilizer or 

pesticide application). In addition, 

because O3 not only results in 

discoloration of leaves but can lead to 

more rapid senescence (early shedding 

of leaves) there potentially could be 

some lost tourist dollars at sites where 

fall foliage is less available or attractive. 

The use of sensitive plants as 

biological indicators to detect 

phytotoxic levels of O3 is a longstanding 

and effective methodology (Chappelka 

and Samuelson, 1998; Manning and 

Krupa, 1992). Each bioindicator exhibits 

typical O3 injury symptoms when 

exposed under appropriate conditions. 

These symptoms are considered 

diagnostic as they have been verified in 

exposure-response studies under 

experimental conditions. In recent 

years, field surveys of visible foliar 

injury symptoms have become more 

common, with greater attention to the 

standardization of methods and the use 

of reliable indicator species (Campbell 

et al., 2000; Smith et al., 2003). 

Specifically, the United States Forest 

Service (USFS) through the Forest 

Health Monitoring Program (FHM) 

(1990–2001) and currently the Forest 

Inventory and Analysis (FIA) Program 

collects data regarding the incidence 

and severity of visible foliar injury on a 

variety of O3 sensitive plant species 

throughout the U.S. (Coulston et al. 

2003, 2004; Smith et al. 2003). 

Since the conclusion of the 1996 

NAAQS review, the FIA monitoring 

program network and database has 

continued to expand. This network 

continues to document foliar injury 

symptoms in the field under ambient 

exposure conditions. Recent survey 

results show that O3-induced foliar 

injury incidence is widespread across 

the country. The visible foliar injury 

indicator has been identified as a means 

to track O3 exposure stress trends in the 

nation’s natural plant communities as 

highlighted in EPA’s most recent Report 

on the Environment (EPA, 2003a; 

http://www.epa.gov/indicators/roe). 

Previous Criteria Documents have 

noted the difficulty in relating visible 

foliar injury symptoms to other 

vegetation effects such as individual 

tree growth, stand growth, or ecosystem 

characteristics (EPA, 1996a) and this 

difficulty remains to the present day 

(EPA, 2006a). It is important to note that 

direct links between O3 induced visible 

foliar injury symptoms and other 

adverse effects are not always found. 

Therefore, visible foliar injury cannot 

serve as a reliable surrogate measure for 

other O3-related vegetation effects 

because other effects (e.g., biomass loss) 

have been reported with and without 

visible injury. In a few cases, visible 

foliar symptoms have been correlated 

with decreased vegetative growth 

(Karnosky et al., 1996; Peterson et al., 

1987; Somers et al., 1998) and with 

impaired reproductive function (Black 

et al., 2000; Chappelka, 2002). 

Therefore, the lack of visible injury 

should not be construed to indicate a 

lack of phytotoxic concentrations of O3

nor absence of other non-visible O3

effects. 

d. Reduced Plant Vigor 

Though O3 levels over most of the 

U.S. are not high enough to kill 

vegetation directly, current levels have 

been shown to reduce the ability of 

many sensitive species and genotypes 

within species to adapt to or withstand 

other environmental stresses. These may 

include increased susceptibility to 

freezing temperatures, pest infestations 

and/or root disease, and compromised 

ability to compete for available 

resources. For example, when species 

with differing O3-sensitivities occur 

together, the resulting decrease in 

growth in O3-sensitive species may lead 

to an increase in growth of more O3- 

tolerant species, which are now able to 

better compete for available resources. 

The result of such above effects can 

produce a loss in plant vigor in O3- 

sensitive species that over time may 

lead to premature plant death. 

e. Ecosystems 

Ecosystems are comprised of complex 

assemblages of organisms and the 

physical environment with which they 

interact. Each level of organization 

within an ecosystem has functional and 

structural characteristics. At the 

ecosystem level, functional 

characteristics include, but are not 

limited to, energy flow; nutrient, 

hydrologic, and biogeochemical cycling; 

and maintenance of food chains. The 

sum of the functions carried out by 

ecosystem components provides many 

benefits to humankind, as in the case of 

forest ecosystems (Smith, 1992). Some 

of these benefits, also termed 

‘‘ecosystem goods and services’’, 

include food, fiber production, 

aesthetics, genetic diversity, 

maintenance of water quality, air 

quality, and climate, and energy 

exchange. A conceptual framework for 

discussing the effects of O3 on 

ecosystems was developed by the EPA 

Science Advisory Board (Young and 

Sanzone, 2002). In this report, the 

authors identify six essential ecological 

attributes (EEAs) include landscape 

condition, biotic condition, chemical/ 

physical condition, ecological 

processes, hydrology/geomorphology, 

and natural disturbance regime. Each 

EEA is depicted as one of six triangles 

that together build a hexagon. On the 

outside of each triangle is a list of 

stressors that can act on the EEA. 

Tropospheric O3 is listed as a stressor of 

both biotic condition and the chemical/ 

physical condition of ecosystems. As 

each EEA is linked to all the others, it 

is clearly envisioned in this framework 

that O3 could either directly or 

indirectly impact all of the EEAs 

associated with an ecosystem that is 

being stressed by O3. 

Vegetation often plays an influential 

role in defining the structure and 

function of an ecosystem, as evidenced 

by the use of dominant vegetation forms 

to classify many types of natural 

ecosystems, e.g., tundra, wetland, 

deciduous forest, and conifer forest. 

Plants simultaneously inhabit both 

above- and below-ground environments, 

integrating and influencing key 

ecosystem cycles of energy, water, and 

nutrients. When a sufficient number of 

individual plants within a community 

have been affected, O3-related effects 

can be propagated up to ecosystem-level 

effects. Thus, through its impact on 

vegetation, O3 can be an important 

ecosystem stressor. 

i. Potential Ozone Alteration of 

Ecosystem Structure and Function 

The Criteria Document (EPA, 2006a) 

outlines seven case studies where O3

effects on ecosystems have either been 

documented or are suspected. The 

oldest and clearest example involves the 

San Bernardino Mountain forest 

ecosystem in California. This system 

experienced chronic high O3 exposures 

over a period of 50 or more years. The 


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O3-sensitive and co-dominant species of 

ponderosa and Jeffrey pine 

demonstrated severe levels of foliar 

injury, premature senescence, and 

needle fall that decreased the 

photosynthetic capacity of stressed 

pines and reduced the production of 

carbohydrates resulting in a decrease in 

radial growth and in the height of 

stressed trees. It was also observed that 

ponderosa and Jeffrey pines with slight 

to severe crown injury lost basal area in 

relation to competing species that are 

more tolerant to O3. Due to a loss of 

vigor, these trees eventually succumbed 

to the bark beetle, leading to elevated 

levels of tree death. Increased mortality 

of susceptible trees shifted the 

community composition towards white 

fir and incense cedar, effectively 

reversing the development of the normal 

fire climax mixture dominated by 

ponderosa and Jeffrey pines, and 

leading to increased fire susceptibility. 

At the same time, numerous other 

organisms and processes were also 

affected either directly or indirectly, 

including successional patterns of 

fungal microflora and their relationship 

to the decomposer community. Nutrient 

availability was influenced by the heavy 

litter and thick needle layer under 

stands with the most severe needle 

injury and defoliation. The composition 

of lichens was significantly reduced. In 

this example, O3 appeared to be a 

predisposing factor that led to increased 

drought stress, windthrow, root 

diseases, and insect infestation 

(Takemoto et al., 2001). Thus, through 

its effects on tree water balance, cold 

hardiness, tolerance to wind, and 

susceptibility to insect and disease 

pests, O3 potentially impacted the 

ecosystem-related EEA of natural 

disturbance regime (e.g., fire, erosion). 

Although the role of O3 was extremely 

difficult to separate from other 

confounding factors, such as high 

nitrogen deposition, there is evidence 

that this shift in species composition 

has altered the structure and dynamics 

of associated food webs (Pronos et al., 

1999) and carbon (C) and nitrogen (N) 

cycling (Arbaugh et al., 2003). Ongoing 

and new research in this important 

ecosystem is needed to reveal the extent 

to which ecosystem services have been 

affected and to what extent strong 

causal linkages between historic and/or 

current ambient O3 exposures and 

observed ecosystem-level effects can be 

made. 

Ozone has also been reported to be a 

selective pressure among sensitive tree 

species (e.g., eastern white pine) in the 

east. The nature of community 

dynamics in eastern forests is different, 

however, than in the west, consisting of 

a wider diversity of species and uneven 

aged stands, and the O3 levels are less 

severe. Therefore, lower level chronic 

O3 stress in the east is more likely to 

produce subtle long-term forest 

responses such as shifts in species 

composition, rather than wide-spread 

community degradation. 

One of the best-documented studies of 

population and community response to 

O3 effects are the long-term studies of 

common plantain (Plantago major) in 

native plant communities in the United 

Kingdom (Davison and Reiling, 1995; 

Lyons et al., 1997; Reiling and Davison, 

1992c). Elevated O3 significantly 

decreased the growth of sensitive 

populations of common plantain 

(Pearson et al., 1996; Reiling and 

Davison, 1992a, b; Whitfield et al., 

1997) and reduced its fitness as 

determined by decreased reproductive 

success (Pearson et al., 1996; Reiling 

and Davison, 1992a). While spatial 

comparisons of population responses to 

O3 are complicated by other 

environmental factors, rapid changes in 

O3 resistance were imposed by ambient 

levels and variations in O3 exposure 

(Davison and Reiling, 1995). 

Specifically, in this case study, it 

appeared that O3-sensitive individuals 

are being removed by O3 stress and the 

genetic variation represented in the 

population could be declining. If genetic 

diversity and variation is lost in 

ecosystems, there may be increased 

vulnerability of the system to other 

biotic and abiotic stressors, and 

ultimately a change in the EEAs and 

associated services provided by those 

ecosystems. 

Recent free-air exposure experiments 

have also provided new insight into 

how O3 may be altering ecosystem 

structure and function (Karnosky et al., 

2005). For example, a field O3 exposure 

experiment at the AspenFACE site in 

Wisconsin (described in section 

IV.A.2.b. above) was designed to 

examine the effects of both elevated CO2

and O3 on mixed stands of aspen 

(Populus tremuloides), birch (Betula 

papyrifera), and sugar maple (Acer 

saccharum) that are characteristic of 

Great Lakes aspen-dominated forests 

(Karnosky et al., 2003; Karnosky et al., 

1999). They found evidence that the 

effects on above- and below-ground 

growth and physiological processes 

have cascaded through the ecosystem, 

even affecting microbial communities 

(Larson et al., 2002; Phillips et al., 

2002). This study also confirmed earlier 

observations of O3-induced changes in 

trophic interactions involving keystone 

tree species, as well as important insect 

pests and their natural enemies 

(Awmack et al., 2004; Holton et al., 

2003; Percy et al., 2002). 

Collectively these examples suggest 

that O3 is an important stressor in 

natural ecosystems, but it is difficult to 

quantify the contribution of O3 due to 

the combination of other stresses 

present in ecosystems. In most cases, 

because only a few components in each 

of these ecosystems have been examined 

and characterized for O3 effects, the full 

extent of ecosystem changes in these 

example ecosystems is not fully 

understood. Clearly, there is a need for 

highly integrated ecosystem studies that 

specifically investigate the effect of O3

on ecosystem structure and function in 

order to fully determine the extent to 

which O3 is altering ecosystem services. 

Continued research, employing new 

approaches, will be necessary to fully 

understand the extent to which O3 is 

affecting ecosystem services. 

ii. Effects on Ecosystem Services and 

Carbon Sequestration 

Since it has been established that O3

affects photosynthesis and growth of 

plants, O3 is most likely affecting the 

productivity of forest ecosystems. 

Therefore, it is desirable to link effects 

on growth and productivity to essential 

ecosystem services. However, it is very 

difficult to quantify ecosystem-level 

productivity losses because of the 

amount of complexity in scaling from 

the leaf-level or individual plant to the 

ecosystem level, and because not all 

organisms in an ecosystem are equally 

affected by O3. 

Terrestrial ecosystems are important 

in the Earth’s carbon (C) balance and 

could help offset emissions of CO2 by 

humans if anthropogenic C is 

sequestered in vegetation and soils. The 

annual increase in atmospheric CO2 is 

less than the total inputs from fossil fuel 

burning and land use changes (Prentice 

et al., 2001) and much of this 

discrepancy is thought to be attributable 

to CO2 uptake by plant photosynthesis 

(Tans & White, 1998). Temperate forests 

of the northern hemisphere have been 

estimated to be a net sink of C per year 

(Goodale et al. 2002). Ozone interferes 

with photosynthesis, causes some plants 

to senesce leaves prematurely and in 

some cases, reduces allocation to stem 

and root tissue. Thus, O3 decreases the 

potential for C sequestration. For the 

purposes of this discussion, C 

sequestration is defined as the net 

exchange of carbon by the terrestrial 

biosphere. However, long-term storage 

in the soil organic matter is considered 

to be the most stable form of C storage 

in ecosystems. 

In a study including all ecosystem 

types, Felzer et al. (2004), estimated that 


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57 Given the usefulness of generating robust C–R 

functions such as have been developed under 

NCLAN, it would be beneficial to employ a similar 

protocol to update and expand this research to 

include more recent and additional crop species 

and varieties, such as fruit and vegetable species, 

as well as recent O3 air quality. 

U.S. net primary production (net flux of 

C into an ecosystem) was decreased by 

2.6–6.8 percent due to O3 pollution in 

the late 1980’s to early 1990’s. Ozone 

not only reduces C sequestration in 

existing forests, it can also affect 

reforestation projects (Beedlow et al. 

2004). This effect, in turn, has been 

found to ultimately inhibit C 

sequestration in forest soils which act as 

long-term C storage (Loya et al., 2003; 

Beedlow et al. 2004). The interaction of 

rising O3 pollution and rising CO2

concentrations in the coming decades 

complicates predictions of future 

sequestration potential. Models 

generally predict that, in the future, C 

sequestration will increase with 

increasing CO2, but often do not account 

for the decrease in productivity due to 

the local effects of tropospheric O3. In 

the presence of high O3 levels, the 

stimulatory effect of rising CO2

concentrations on forest productivity 

has been estimated to be reduced by 

more that 20 percent (Tingey et al., 

2001; Ollinger et al. 2002; Karnosky et 

al., 2003). 

In summary, it would be anticipated 

that meeting lower O3 standards would 

increase the amount of CO2 uptake by 

many ecosystems in the U.S. However, 

the amount of this improvement would 

be heavily dependent on the species 

composition of those ecosystems. Many 

ecosystems in the U.S. do have O3

sensitive plants. For, example forest 

ecosystems with dominant species such 

as aspen or ponderosa pine would be 

expected to increase CO2 uptake more 

with lower O3 than forests with more O3

tolerant species. 

A recent critique of the secondary 

NAAQS review process published in the 

report by the National Academy of 

Sciences on Air Quality Management in 

the United States (NRC, 2004) stated 

that ‘‘EPA’s current practice for setting 

secondary standards for most criteria 

pollutants does not appear to be 

sufficiently protective of sensitive crops 

and ecosystems * * *.’’ This report 

made several specific recommendations 

for improving the secondary NAAQS 

process and concluded that ‘‘There is 

growing evidence that tighter standards 

to protect sensitive ecosystems in the 

United States are needed * * *.’’ An 

effort has been recently initiated within 

the Agency to identify indicators of 

ecological condition whose responses 

can be clearly linked to changes in air 

quality that are attributable to Agency 

environmental programs. Using a single 

indicator to represent the complex 

linkages and dynamic cycles that define 

ecosystem condition will always have 

limitations. With respect to O3-related 

impacts on ecosystem condition, only 

two candidate indicators, foliar injury 

(as described above) and radial growth 

in trees, have been suggested. Thus, 

while at the present time, most O3- 

related effects on ecosystems must be 

inferred from observed or predicted O3- 

related effects on individual plants, 

additional research at the ecosystem 

level could identify new indicators and/ 

or establish stronger causal linkages 

between O3-induced plant effects and 

ecosystem condition. 

f. Yield Reductions in Crops 

Ozone can interfere with carbon gain 

(photosynthesis) and allocation of 

carbon with or without the presence of 

visible foliar injury. As a result of 

decreased carbohydrate availability, 

fewer carbohydrates are available for 

plant growth, reproduction, and/or 

yield. Recent studies have further 

confirmed and demonstrated O3 effects 

on different stages of plant 

reproduction, including pollen 

germination, pollen tube growth, 

fertilization, and abortion of 

reproductive structures, as reviewed by 

Black et al. (2000). For seed-bearing 

plants, these reproductive effects will 

culminate in reduced seed production 

or yield. 

As described in the last review and 

again in the current Criteria Document 

and Staff Paper, the National Crop Loss 

Assessment Network (NCLAN) studies 

undertaken in the early to mid-1980’s 

provide the largest, most uniform 

database on the effects of O3 on 

agricultural crop yields. The NCLAN 

protocol was designed to produce crop 

exposure-response data representative 

of the areas in the U.S. where the crops 

were typically grown. In total, 15 

species (e.g., corn, soybean, winter 

wheat, tobacco, sorghum, cotton, barley, 

peanuts, dry beans, potato, lettuce, 

turnip, and hay [alfalfa, clover, and 

fescue]), accounting for greater than 85 

percent of U.S. agricultural acreage 

planted at that time, were studied. Of 

these 15 species, 13 species including 

38 different cultivars were combined in 

54 cases representing unique 

combinations of cultivars, sites, water 

regimes, and exposure conditions. Crops 

were grown under typical farm 

conditions and exposed in open-top 

chambers to ambient O3 and increased 

O3 above ambient (i.e., modified 

ambient). Robust C–R functions were 

developed for each of these crop 

species. These results showed that 50 

percent of the studied cases would be 

protected from greater than 10 percent 

yield loss at a W126 level of 21 ppmhour, while a W126 of 13 ppm-hour 

would provide protection for 75 percent 

of the cases studied from greater than 10 

percent yield loss. 

Recent studies continue to find yield 

loss levels in crop species studied 

previously under NCLAN that reflect 

the earlier findings57. In other words, 

there has been no evidence that crops 

are becoming more tolerant of O3 (EPA, 

2006a). For cotton, some newer varieties 

have been found to have higher yield 

loss due to O3 compared to older 

varieties (Olszyk et al., 1993, Grantz and 

McCool, 1992). In a meta-analysis of 53 

studies, Morgan et al. (2003) found 

consistent deleterious effects of O3

exposures on soybean from studies 

published between 1973 and 2001. 

Further, early results from the fieldbased exposure experiment SoyFACE in 

Illinois indicate a lack of any apparent 

difference in the O3 tolerance of old and 

recent cultivars of soybean in a study of 

22 soybean varieties (Long et al., 2002). 

Thus, the Staff Paper concluded that the 

recent scientific literature continues to 

support the conclusions of the 1996 

Criteria Document that ambient O3

concentrations are reducing the yield of 

major crops in the U.S. 

In addition to the effects described on 

annual crop species, several studies 

published since the last review have 

focused on perennial forage crops (EPA, 

2006a). These recent results confirm 

that O3 is also impacting yields and 

quality of multiple-year forage crops at 

sufficient magnitude to have nutritional 

and possibly economic implications to 

their use as ruminant animal feed at O3

exposures that occur in some years over 

large areas of the U.S. 

3. Adversity of Effects 

The Staff Paper recognized that the 

statute requires that a secondary 

standard be protective against ‘‘adverse’’

O3 effects, not all identifiable effects. In 

considering what constitutes a 

vegetation effect that is adverse to the 

public welfare, the Staff Paper 

recognizes that O3 can cause a variety of 

vegetation effects, beginning at the level 

of the individual cell and accumulating 

up to the level of whole leaves, plants, 

plant populations, communities and 

whole ecosystems, not all of which have 

been classified in past reviews as 

‘‘adverse’’ to public welfare. 

Previous reviews have classified O3

vegetation effects as either ‘‘injury’’ or 

‘‘damage’’ to help in determining 

adversity. Specifically, ‘‘injury’’ is 


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58SUM06: Sum of all hourly O3 concentrations 

greater or equal to 0.06 ppm over a specified time. 

defined as encompassing all plant 

reactions, including reversible changes 

or changes in plant metabolism (e.g., 

altered photosynthetic rate), altered 

plant quality, or reduced growth, that 

does not impair the intended use or 

value of the plant (Guderian, 1977). In 

contrast, ‘‘damage’’ has been defined to 

include those injury effects that reach 

sufficient magnitude as to also reduce or 

impair the intended use or value of the 

plant. Examples of effects that are 

classified as damage include reductions 

in aesthetic values (e.g., foliar injury in 

ornamental species) as well as losses in 

terms of weight, number, or size of the 

plant part that is harvested (reduced 

yield or biomass production). Yield loss 

also may include changes in crop 

quality, i.e., physical appearance, 

chemical composition, or the ability to 

withstand storage, while biomass loss 

includes slower growth in species 

harvested for timber or other fiber uses. 

While this construct has proved useful 

in the past, it appears to be most useful 

in the context of evaluating effects on 

single plants or species grown in 

monocultures such as agricultural crops 

or managed forests. It is less clear how 

it might apply to potential effects on 

natural forests or entire ecosystems 

when O3-induced species level impacts 

lead to shifts in species composition 

and/or associated ecosystem services 

such as nutrient cycling or hydrologic 

cycles, where the intended use or value 

of the system has not been specifically 

identified. 

A more recent construct for assessing 

risks to forests described in Hogsett et 

al. (1997) suggests that ‘‘adverse effects 

could be classified into one or more of 

the following categories: (1) Economic 

production, (2) ecological structure, (3) 

genetic resources, and (4) cultural 

values.’’ This approach expands the 

context for evaluating the adversity of 

O3-related effects beyond the species 

level. Another recent publication, A 

Framework for Assessing and Reporting 

on Ecological Condition: an SAB report 

(Young and Sanzone, 2002), provides 

additional support for expanding the 

consideration of adversity beyond the 

species level by making explicit the 

linkages between stress-related effects 

(e.g., O3 exposure) at the species level 

and at higher levels within an 

ecosystem hierarchy. Taking this recent 

literature into account, the Staff Paper 

concludes that a determination of what 

constitutes an ‘‘adverse’’ welfare effect 

in the context of the secondary NAAQS 

review can appropriately occur within 

this broader paradigm. 

B. Biologically Relevant Exposure 

Indices 

The Criteria Document concluded that 

O3 exposure indices that cumulate 

differentially weighted hourly 

concentrations are the best candidates 

for relating exposure to plant growth 

responses (EPA, 2006a). This conclusion 

follows from the extensive evaluation of 

the relevant studies in the 1996 Criteria 

Document (EPA, 1996a) and the recent 

evaluation of studies that have been 

published since that time (EPA, 2006a). 

The following selections, taken from 

section 5.5 the 1996 Criteria Document 

(EPA, 1996a), further elucidate the 

depth and strength of these conclusions. 

Specifically, with respect to the 

importance of taking into account 

exposure duration, the 1996 Criteria 

Document stated, ‘‘when O3 effects are 

the primary cause of variation in plant 

response, plants from replicate studies 

of varying duration showed greater 

reductions in yield or growth when 

exposed for the longer duration’’ and 

‘‘the mean exposure index of 

unspecified duration could not account 

for the year-to-year variation in 

response’’ (EPA, 1996a, pg. 5–96). 

Further, ‘‘because the mean exposure 

index treats all concentrations equally 

and does not specifically include an 

exposure duration component, the use 

of a mean exposure index for 

characterizing plant exposures appears 

inappropriate for relating exposure with 

vegetation effects’’ (EPA, 1996a, pg. 5–

88). Regarding the relative importance 

of higher concentrations than lower in 

determining plant response, the 1996 

Criteria Document concluded that ‘‘the 

ultimate impact of long-term exposures 

to O3 on crops and seedling biomass 

response depends on the integration of 

repeated peak concentrations during the 

growth of the plant’’ (EPA, 1996a, pg. 5–

104). Further, ‘‘at this time, exposure 

indices that weight the hourly O3

concentrations differentially appear to 

be the best candidates for relating 

exposure with predicted plant 

response’’ (EPA, 1996a, pgs. 5–136). 

At the conclusion of the last review, 

the biological basis for a cumulative, 

seasonal form was not in dispute. There 

was general agreement between the EPA 

staff, CASAC, and the Administrator, 

based on their review of the air quality 

criteria, that a cumulative, seasonal 

form was more biologically based than 

the then current 1-hour and newly 

proposed 8-hour average form. 

However, in selecting a specific form 

appropriate for a secondary standard, 

there was less agreement. An evaluation 

of the performance of several seasonal 

cumulative forms in predicting plant 

response data taken from OTC 

experiments had found that all 

performed about equally well and was 

unable to distinguish between them 

(EPA, 1996a). In selecting between two 

of these cumulative forms, the SUM06 58

and W126, in the absence of biological 

evidence to distinguish between them, 

the Administrator based her decision on 

both science and policy considerations. 

Specifically, these were: (1) All 

cumulative, peak-weighted exposure 

indices considered, including W126 and 

SUM06, were about equally good as 

exposure measures to predict exposureresponse relationships reported in the 

NCLAN crop studies; and (2) the 

SUM06 form would not be influenced 

by PRB O3 concentrations (defined at 

the time as 0.03 to 0.05 ppm) under 

many typical air quality distributions. 

On the basis of these considerations, the 

Administrator chose the SUM06 as the 

most appropriate cumulative, seasonal 

form to consider when proposing an 

alternative secondary standard form (61 

FR 65716). 

Though the scientific justification for 

a cumulative, seasonal form was 

generally accepted in the last review, an 

analysis undertaken by EPA at that time 

had shown that there was considerable 

overlap between areas that would be 

expected not to meet the range of 

alternative 8-hour standards being 

considered for the primary NAAQS and 

those expected not to meet the range of 

values (expressed in terms of the 

seasonal SUM06 index) of concern for 

vegetation. This result suggested that 

improvements in national air quality 

expected to result from attaining an 8- 

hour primary standard within the 

recommended range of levels would 

also be expected to significantly reduce 

levels of concern for vegetation in those 

same areas. Thus, in the notice of 

proposed rulemaking, the Administrator 

proposed two alternatives for 

consideration: one alternative was to 

make the secondary standard equal in 

every way to the proposed 8-hour, 0.08 

ppm primary standard; and the second 

was to establish a cumulative, seasonal 

secondary standard in terms of a SUM06 

form as also appropriate to protect 

public welfare from known or 

anticipated adverse effects given the 

available scientific knowledge and that 

such a seasonal standard ‘‘* * * is more 

biologically relevant * * *’’ (61 FR 

65716). 

In the 1997 final rule, the 

Administrator decided to make the 

secondary standard identical to the 

primary standard. She acknowledged, 


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however, that ‘‘it remained uncertain as 

to the extent to which air quality 

improvements designed to reduce 8-hr 

average O3 concentrations averaged over 

a 3-year period would reduce O3

exposures measured by a seasonal 

SUM06 index.’’ (62 FR 38876) In other 

words, it was uncertain as to whether 

the 8-hour average form would, in 

practice, provide sufficient protection 

for vegetation from the cumulative, 

seasonal and concentration-weighted 

exposures described in the scientific 

literature as of concern. 

On the basis of that history, chapter 

7 of the current Staff Paper revisited the 

issue of whether the SUM06 was still 

the most appropriate choice of 

cumulative, seasonal form for a 

secondary standard to protect the public 

welfare from known and anticipated 

adverse vegetation effects in light of the 

new information available in this 

review. Specifically, the Staff Paper 

considered: (1) The continued lack of 

evidence within the vegetation effects 

literature of a biological threshold for 

vegetation exposures of concern; and (2) 

new estimates of PRB that are lower 

than in the last review. The W126 form, 

also evaluated in the last review, was 

again selected for comparison with the 

SUM06 form. Regarding the first 

consideration, the Staff Paper noted that 

W126 form, by its incorporation of a 

continuous sigmoidal weighting 

scheme, does not create an artificially 

imposed concentration threshold, yet 

also gives proportionally more weight to 

the higher and typically more 

biologically potent concentrations, as 

supported by the scientific evidence. 

Second, the index value is not 

significantly influenced by O3

concentrations within the range of 

estimated PRB, as the weights assigned 

to concentrations in this range are very 

small. Thus, it would also provide a 

more appropriate target for air quality 

management programs designed to 

reduce emissions from anthropogenic 

sources contributing to O3 formation. 

On the basis of these considerations, the 

Staff Paper concludes that the W126 

form is the most biologically-relevant 

cumulative, seasonal form appropriate 

to consider in the context of the 

secondary standard review. 

C. Vegetation Exposure and Impact 

Assessment 

The vegetation exposure and impact 

assessment conducted for the current 

review and described in the Staff paper, 

consisted of exposure, risk and benefits 

analyses and improves and builds upon 

similar analyses performed in the last 

review (EPA 1996b). The vegetation 

exposure assessment was performed 

using interpolation and included 

information from ambient monitoring 

networks and results from air quality 

modeling. The vegetation risk 

assessment included both tree and crop 

analyses. The tree risk analysis includes 

three distinct lines of evidence: (1) 

Observations of visible foliar injury in 

the field linked to recent monitored O3

air quality for the years 2001–2004; (2) 

estimates of seedling growth loss under 

current and alternative O3 exposure 

conditions; and (3) simulated mature 

tree growth reductions using the 

TREGRO model to simulate the effect of 

meeting alternative air quality standards 

on the predicted annual growth of a 

single western species (ponderosa pine) 

and two eastern species (red maple and 

tulip poplar). The crop analysis 

includes estimates of the risks to crop 

yields from current and alternative O3

exposure conditions and the associated 

change in economic benefits expected to 

accrue in the agriculture sector upon 

meeting the levels of various alternative 

standards. Each element of the 

assessment is described below, 

including discussions of known sources 

and ranges of uncertainties associated 

with the elements of this assessment. 

1. Exposure Characterization 

Though numerous effects of O3 on 

vegetation have been documented as 

discussed above, it is important in 

considering risk to examine O3 air 

quality patterns in the U.S. relative to 

the location of O3 sensitive species that 

have a known concentration-response in 

order to predict whether adverse effects 

are occurring at current levels of air 

quality, and whether they are likely to 

occur under alternative standard forms 

and levels. 

The most important information about 

exposure to vegetation comes from the 

O3 monitoring data that are available 

from two national networks: (1) Air 

Quality System (AQS; http:// 

www.epa.gov/ttn/airs/airsaqs) and (2) 

Clean Air Status and Trends Network 

(CASTNET; http://www.epa.gov/ 

castnet/). The AQS monitoring network 

currently has over 1100 active O3

monitors which are generally sited near 

population centers. However, this 

network also includes approximately 36 

monitors located in national parks. 

CASTNET is the nation’s primary 

source for data on dry acidic deposition 

and rural, ground-level O3. It consists of 

over 80 sites across the eastern and 

western U.S. and is cooperatively 

operated and funded with the National 

Park Service. In the 1997 final O3 rule, 

it was acknowledged that because the 

national air quality surveillance 

network for O3 was designed principally 

to monitor O3 exposure in populated 

areas, there was limited measured data 

available to characterize O3 air quality 

in rural and remote sites. Since the last 

review, there has been a small increase 

in the number of CASTNET sites (from 

approximately 52 sites in 1992 to 84 

sites in 2004), however these monitors 

are not used for attainment 

designations. 

National parks represent areas of 

nationally recognized ecological and 

public welfare significance, which are 

afforded a higher level of protection. 

Two recent reports presented some 

discussion of O3 trends in a subset of 

national parks: The Ozone Report: 

Measuring Progress Through 2003 (EPA, 

2004), and 2005 Annual Performance 

and Progress Report: Air Quality in 

National Parks (NPS, 2005). 

Unfortunately, much of this information 

is presented only in terms of the current 

8-hr average form. The Staff Paper 

analyzed available air quality data in 

terms of the cumulative 12-hour W126 

form from 2001 to 2005 for a subset of 

national parks and other significant 

natural areas representing 4 general 

regions of the U.S. Many of these 

national parks and natural areas have 

monitored O3 levels above 

concentrations that have been shown to 

decrease plant growth and above the 12- 

hour W126 levels analyzed in this 

review. For example, the Great Smokey 

Mountain, Rocky Mountain, Grand 

Canyon, Yosemite and Sequoia National 

Parks all had more than one year within 

the 2001–2005 period with a 12-hour 

W126 above 21 ppm-hour. This level of 

exposure has been associated with 

approximately no more than 10 percent 

biomass loss in 50 percent of the 49 tree 

seedling cases studied in the NHEERL–

WED experiments (Lee and Hogsett, 

1996). Black cherry (Prunus serotina), 

an important O3-sensitive tree species in 

the eastern U.S., occurs in the Great 

Smoky Mountain National Park and is 

estimated to have O3-related seedling 

biomass loss of approximately 40 

percent when exposed to a 3-month, 12- 

hour W126 O3 level greater than 21 

ppm-hour. Ponderosa pine (Pinus 

ponderosa) which occurs in the Grand 

Canyon, Yosemite and Sequoia National 

Parks has been reported to have 

approximately 10 percent biomass 

losses at 3-month, 12-hour W126 O3

levels as low as 17 ppm-hour (Lee and 

Hogsett, 1996). Impacts on seedlings 

may potentially affect long-term tree 

growth and survival, ultimately 

affecting the competitiveness of O3- 

sensitive tree species and genotypes 

within forest stands. 

In order to characterize exposures to 

vegetation at the national scale, 


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59The CMAQ model is a multi-pollutant, 

multiscale air quality model that contains state-ofthe-science techniques for simulating all 

atmospheric and land processes that affect the 

transport, transformation, and deposition of 

atmospheric pollutants and/or their precursors on 

both regional and urban scales. It is designed as a 

science-based modeling tool for handling many 

major pollutants (including photochemical 

oxidants/O3, particulate matter, and nutrient 

deposition) holistically. The CMAQ model can 

generate estimates of hourly O3 concentrations for 

the contiguous U.S., making it possible to express 

model outputs in terms of a variety of exposure 

indices (e.g., W126, 8-hour average). 

however, the Staff Paper concluded that 

it could not rely solely on limited sitespecific monitoring data, and that it was 

necessary to select an interpolation 

method that could be used to 

characterize O3 air quality over broad 

geographic areas. The Staff Paper 

therefore investigated the 

appropriateness of using the O3 outputs 

from the EPA/NOAA Community Multiscale Air Quality (CMAQ) 59 model 

system (http://www.epa.gov/asmdnerl/ 

CMAQ, Byun and Ching, 1999; Arnold 

et al. 2003, Eder and Yu, 2005) to 

improve spatial interpolations based 

solely on existing monitoring networks. 

Due to the significant resources required 

to run CMAQ, model outputs were only 

available for a limited number of years. 

For this review, 2001 outputs from 

CMAQ version 4.5 were the most recent 

available. 

Based on the significant difference in 

monitor network density between the 

eastern and western U.S., the Staff Paper 

concluded that it was appropriate to use 

separate interpolation techniques in 

these two regions. AQS and CASTNET 

monitoring data were solely used for the 

eastern interpolation since it was 

determined that enhancing the 

interpolation with CMAQ data did not 

add much information to the eastern 

U.S. interpolation. In the western U.S., 

where rural monitoring is more sparse, 

O3 values generated by the CMAQ 

model were used to develop scaling 

factors to augment the interpolation. 

In order to characterize uncertainty in 

the interpolation method, monitored O3

concentrations were systematically 

compared to interpolated O3

concentrations in areas where monitors 

were located. In general, the 

interpolation method used in the 

current review performed well in many 

areas in the U.S., although it underpredicted higher 12-hour W126 

exposures in rural areas. Due to the 

important influence of higher exposures 

in determining risks to plants, this 

feature of the interpolated surface could 

result in an under-estimation of risks to 

vegetation in some areas. Taking these 

uncertainties into account, and given 

the absence of more complete rural 

monitoring data, this approach was used 

in developing national vegetation 

exposure and risk assessments that 

estimate relative changes in risk for the 

various alternative standards analyzed. 

To evaluate changing vegetation 

exposures and risks under selected air 

quality scenarios, the Staff Paper 

utilized adjusted 2001 base year O3 air 

quality distributions with a rollback 

method (Horst and Duff, 1995; Rizzo, 

2005 & 2006) to reflect meeting the 

current and alternative secondary 

standard options. This technique 

combines both linear and quadratic 

elements to reduce higher O3

concentrations more than lower ones. In 

this regard, the rollback method 

attempts to account for reductions in 

emissions without greatly affecting 

lower concentrations. The following O3

air quality scenarios were analyzed: (1) 

4th-highest daily maximum 8-hour 

average: 0.084 ppm (the effective level 

of the current standard) and 0.070 ppm 

levels; (2) 3-month, 12-hour. SUM06: 25 

ppm-hour (proposed in the 1996 review) 

and 15 ppm-hour levels; and (3) 3- 

month, 12-hour. W126: 21 ppm-hour 

and 13 ppm-hour levels. 

The two 8-hour average levels were 

chosen as possible alternatives of the 

current form for comparison with the 

cumulative, seasonal alternative forms. 

The SUM06 scenarios were very similar 

to the W126 scenarios. Since the W126 

was judged to be the more biologicallyrelevant cumulative, seasonal form, only 

the results for the W126 scenarios are 

summarized below. For the W126 form, 

the two levels were selected on the basis 

of the associated levels of tree seedling 

biomass loss and crop yield loss 

protection identified in the NHEERL–

WED and NCLAN studies, respectively. 

Specifically, the upper level of W126 

(21 ppm-hour) was associated with a 

level of tree and crop protection of 

approximately no more than 10 percent 

growth or yield loss in 50 percent of 

cases studied. Alternatively, the lower 

level of W126 (13 ppm-hour) was 

associated with a level of tree seedling 

and crop protection of approximately no 

more than 10 percent growth or yield 

loss in 75 percent of studied cases. 

The following discussion highlights 

key observations drawn from comparing 

predicted changes in interpolated air 

quality under each alternative standard 

form and level scenario for the base 

year, 2001: 

(1) Under the base year (2001) ‘‘as is’’

air quality, a large portion of California 

had 12-hr W126 O3 levels above 31 

ppm-hour, which has been associated 

with approximately no more than 14 

percent biomass loss in 50 percent of 

tree seedling cases studies. Broader 

multi-state regions in the east (NC, TN, 

KY, IN, OH, PA, NJ, NY, DE, MD, VA) 

and west (CA, NV, AZ, OK, TX) are 

predicted to have levels of air quality 

above the W126 level of 21 ppm-hour, 

which is approximately equal to the 

secondary standard proposed in 1996 

and is associated with approximately no 

more than 10 percent biomass loss in 50 

percent of tree seedling cases studied. 

Much of the east and Arizona and 

California have 12-hour W126 O3 levels 

above 13 ppm-hour which has been 

associated with approximately no more 

than 10 percent biomass loss in 75 

percent of tree seedling cases studied. 

The results of the exposure assessment 

indicate that current air quality levels 

could result in significant impacts to 

vegetation in some areas. 

(2) When 2001 air quality is rolled 

back to meet the current 8-hour 

secondary standard, the overall 3-month 

12-hour W126 O3 levels were somewhat 

improved, but not substantially. Under 

this scenario, there were still many 

areas in California with 12-hour W126 

O3 levels above 31 ppm-hour. A broad 

multi-state region in the east (NC, TN, 

KY, IN, OH, PA, MD) and west (CA, NV, 

AZ, OK, TX) were still predicted to have 

O3 levels above the W126 level of 21 

ppm-hour. 

(3) Exposures generated for just 

meeting a 0.070 ppm, 4th-highest 

maximum 8-hour average alternative 

standard showed substantially 

improved O3 air quality when compared 

to just meeting the current 0.08 ppm, 8- 

hour standard. Most areas were 

predicted to have O3 levels below the 

W126 level of 21 ppm-hr, although 

some areas in the east (KY, TN, MI, AR, 

MO, IL) and west (CA, NV, AZ, UT, NM, 

CO, OK, TX) were still predicted to have 

O3 levels above the W126 level of 13 

ppm-hour. 

These results suggest that meeting a 

proposed 0.070 ppm, 8-hour secondary 

standard would provide substantially 

improved protection in some areas for 

vegetation from seasonal O3 exposures 

of concern. The Staff Paper recognizes, 

however, that some areas meeting a 

0.070 ppm 8-hour standard could 

continue to have elevated seasonal 

exposures, including forested park lands 

and other natural areas, and Class I 

areas which are federally mandated to 

preserve certain air quality related 

values. This is especially important in 

the high elevation forests in the Western 

U.S. where there are few O3 monitors. 

This is because the air quality patterns 

in remote areas can result in relatively 

low 8-hour averages while still 

experiencing relatively high cumulative 

exposures. 


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60This analysis was updated using 2003–2005 air 

quality as it became available, finding similar 

results. 

To further characterize O3 air quality 

in terms of current and alternative 

secondary standard forms, an analysis 

was performed in the Staff Paper to 

evaluate the extent to which countylevel O3 air quality measured in terms 

of various levels of the current 8-hour 

average form overlapped with that 

measured in terms of various levels of 

the 12-hour W126 cumulative, seasonal 

form. The Staff Paper presented this 

analysis using recent (2002–2004) 60

county-level O3 air quality data from 

AQS sites and the subset of CASTNET 

sites having the highest O3 levels for the 

counties in which they are located. 

Since the current 8-hour average 

secondary form is a 3-year average, the 

analysis initially compared the 3-year 

averages of both the 8-hour and W126 

forms. In addition, recognizing that 

some vegetation effects (e.g. crop yield 

loss and foliar injury) are driven solely 

by annual O3 exposures and are 

typically evaluated with respect to 

exposures within the annual growing 

season, the Staff Paper also presented a 

comparison of the current 3-year 

average 8-hour form to the annual W126 

form for the individual years, 2002 and 

2004. 

Results of the 3-year average 

comparisons showed that of the 

counties with air quality meeting the 3- 

year average form of the 0.08 ppm, 8- 

hour average standard, 7 counties 

showed 3-year average W126 values 

above the 21 ppm-hour level. At the 

lower W126 level of 13 ppm-hours, 135 

counties with air quality meeting the 3- 

year average form of the 0.08 ppm, 8- 

hour average standard, would be above 

this W126 level. In addition, when the 

3-year average of the 8-hour form was 

compared to annual W126 values, 

further variability in the degree of 

overlap between the 8-hour form and 

W126 form became apparent. For 

example, the relatively high 2002 O3 air 

quality year showed a greater degree of 

overlap between those areas that would 

meet the levels analyzed for the current 

8-hour and alternative levels of the 

W126 form than did the relatively low 

O3 2004 air quality year. This lack of a 

consistent degree of overlap between the 

two forms in different air quality years 

demonstrates that annual vegetation 

would be expected to receive widely 

differing degrees of protection from 

cumulative seasonal exposures in some 

areas from year to year, even when the 

3-year average of the 8-hour form was 

consistently met. 

It is clear that this analysis is limited 

by the lack of monitoring in rural areas 

where important vegetation and 

ecosystems are located, especially at 

higher elevation sites. This is because 

O3 air quality distributions at high 

elevation sites often do not reflect the 

typical urban and near-urban pattern of 

low morning and evening O3

concentrations with a high mid-day 

peak, but instead maintain relatively flat 

patterns with many concentrations in 

the mid-range (e.g., 0.05–0.09 ppm) for 

extended periods. These conditions can 

lead to relatively low daily maximum 8- 

hour averages concurrently with high 

cumulative values so that there is 

potentially less overlap between an 8- 

hour average and a cumulative, seasonal 

form at these sites. The Staff Paper 

concludes that it is reasonable to 

anticipate that additional unmonitored 

rural high elevation areas important for 

vegetation may not be adequately 

protected even with a lower level of the 

8-hour form. 

The Criteria Document (EPA, 2006a), 

discusses policy relevant background 

(PRB) levels for high elevation sites and 

makes the following observations: (1) 

PRB concentrations of 0.04 to 0.05 ppm 

occur occasionally at high-elevation 

sites (e.g., >1.5 km) in the spring due to 

the free-tropospheric influence, 

including some limited contribution 

from hemispheric pollution (O3

produced from anthropogenic emissions 

outside North America); and (2) 

stratospheric intrusions might 

occasionally elevate O3 at high-altitude 

sites, however, these events are rare. 

Therefore, the Staff Paper concludes 

that springtime PRB levels in the range 

identified above and rare stratospheric 

intrusions of O3 are unlikely to 

influence 3 month cumulative seasonal 

W126 values significantly. 

It further remains uncertain as to the 

extent to which air quality 

improvements designed to reduce 8- 

hour O3 average concentrations would 

reduce O3 exposures measured by a 

seasonal, cumulative W126 index. The 

Staff Paper indicated this to be an 

important consideration because: (1) 

The biological database stresses the 

importance of cumulative, seasonal 

exposures in determining plant 

response; (2) plants have not been 

specifically tested for the importance of 

daily maximum 8-hour O3

concentrations in relation to plant 

response; and (3) the effects of 

attainment of an 8-hour standard in 

upwind urban areas on rural air quality 

distributions cannot be characterized 

with confidence due to the lack of 

monitoring data in rural and remote 

areas. These factors are important 

considerations in determining whether 

the current 8-hour form can 

appropriately provide requisite 

protection for vegetation. 

2. Assessment of Risk to Vegetation 

The Staff Paper presents results from 

quantitative and qualitative risk 

assessments of O3 risks to vegetation 

(EPA, 2007). In the last review, crop 

yield and seedling biomass loss OTC 

data provided the basis for staff 

analyses, conclusions, and 

recommendations (EPA, 1996b). Since 

then, several additional lines of 

evidence have progressed sufficiently to 

provide staff with a more complete and 

coherent picture of the scope of O3- 

related vegetation risks, especially those 

currently faced by seedling, sapling and 

mature tree species growing in field 

settings, and indirectly, forested 

ecosystems. Specifically, new research 

reflects an increased emphasis on fieldbased exposure methods (e.g., free air 

exposure and ambient gradient), 

improved field survey biomonitoring 

techniques, and mechanistic tree 

process models. Findings from each of 

these research areas are discussed 

separately below. In conducting these 

assessments, the Staff Paper analyses 

relied on both measured and modeled 

air quality information. For some 

effects, like visible foliar injury and 

modeled mature tree growth response, 

only monitored air quality information 

was used. For other effects categories 

(e.g., crop yield and tree seedling 

growth), staff relied on interpolated O3

exposures. 

a. Visible Foliar Injury 

As discussed earlier (Section A), 

recent systematic injury surveys 

continue to document visible foliar 

injury symptoms diagnostic of 

phytotoxic O3 exposures on sensitive 

bioindicator plants. These surveys 

produced more expansive evidence than 

that available at the time of the last 

review that visible foliar injury is 

occurring in many areas of the U.S. 

under current ambient conditions. The 

Staff Paper presents an assessment 

combining recent U.S. Forest Service 

Forest Inventory and Analysis (FIA) 

biomonitoring site data with the county 

level air quality data for those counties 

containing the FIA biomonitoring sites. 

This assessment showed that incidence 

of visible foliar injury ranged from 21 to 

39 percent during the four-year period 

(2001–2004) across all counties with air 

quality levels at or below that of the 

current 0.08 8-hour standard. Of the 

counties that met an 8-hour level of 0.07 

ppm in those years, 11 to 30 percent 

still had incidence of visible foliar 


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injury. The magnitude of these 

percentages suggests that phytotoxic 

exposures sufficient to induce visible 

foliar injury would still occur in many 

areas after meeting the level of the 

current secondary standard or 

alternative 0.07 ppm 8-hour standard. 

Additionally, the data show that visible 

foliar injury occurrence is 

geographically widespread and is 

occurring on a variety of plant species 

in forested and other natural systems. 

Linking visible foliar injury to other 

plant effects is still problematic. 

However, its presence indicates that 

other O3-related vegetation effects could 

also be present. 

b. Seedling and Mature Tree Biomass 

Loss 

In the last review (EPA, 1996b), 

analyses of the effects of O3 on trees 

were limited to 11 tree species for 

which C–R functions for the seedling 

growth stage had been developed from 

OTC studies conducted by the 

NHEERL–WED. Important tree species 

such as quaking aspen, ponderosa pine, 

black cherry, tulip poplar were found to 

be sensitive to cumulative seasonal O3

exposures. Work done since the 1996 

review at the AspenFACE site in 

Wisconsin on quaking aspen (Karnosky 

et al., 2005) and a gradient study 

performed in the New York City area 

(Gregg et al. 2003) has confirmed the 

detrimental effects of O3 exposure on 

tree growth in field studies without 

chambers and beyond the seedling stage 

(King et al., 2005). These field studies 

are discussed above in section IV.A. 

To update the seedling biomass loss 

analysis, C–R functions for biomass loss 

for available seedling tree species taken 

from the CD and information on tree 

growing regions derived from the U.S. 

Department of Agriculture’s Atlas of 

United States Trees were combined with 

projections of air quality based on 2001 

interpolated exposures, to produce 

estimated biomass loss for each of the 

seedling tree species individually. Maps 

of these biomass loss projections are 

presented in the Staff Paper. For 

example, quaking aspen had a wide 

range of O3 exposure across its growing 

range and therefore, showed significant 

variability in projected seedling biomass 

loss across its range. Quaking aspen 

seedling biomass loss was projected to 

be greater than 4 percent over much of 

its geographic range, though it can reach 

above 10 percent in areas of Ohio, 

Pennsylvania, New York, New Jersey 

and California. Biomass loss for black 

cherry was projected to be greater than 

20 percent in approximately half its 

range. Greater than 30 percent biomass 

loss for black cherry was projected in 

North Carolina, Tennessee, Indiana, 

Ohio, Pennsylvania, Arizona, Michigan, 

New York, New Jersey, Maryland and 

Delaware. For ponderosa pine, an 

important tree species in the western 

U.S., biomass loss was projected to be 

above 10 percent in much of its range 

in California. Biomass loss still occurred 

in many tree species when O3 air quality 

was adjusted to meet the current 8-hour 

standard. For instance, black cherry, 

ponderosa pine, eastern white pine, and 

aspen had estimated median seedling 

biomass losses over portions of their 

growing range as high as 24, 11, 6, and 

6 percent, respectively, when O3 air 

quality was rolled back to just meet the 

current 8-hour standard. The Staff Paper 

noted that these results are for tree 

seedlings and that mature trees of the 

same species may have more or less of 

a response to O3 exposure. Due to the 

potential for compounding effects over 

multiple years, a consensus workshop 

on O3 effects reported that a biomass 

loss greater than 2 percent annually can 

be significant (Heck and Cowling, 1997). 

Decreased seedling root growth and 

survivability could affect overall stand 

health and composition in the long 

term. 

In addition to the estimation of O3

effects on seedling growth, recent work 

has enhanced our understanding of risks 

beyond the seedling stage. In order to 

better characterize the potential O3

effects on mature tree growth, a tree 

growth model (TREGRO) was used as a 

tool to evaluate the effect of changing O3

air quality scenarios from just meeting 

alternative O3 standards on the growth 

of mature trees. TREGRO is a processbased, individual tree growth 

simulation model (Weinstein et al., 

1991) and has been used to evaluate the 

effects of a variety of O3 scenarios and 

linked with concurrent climate data to 

account for O3 and climate/meteorology 

interactions on several species of trees 

in different regions of the U.S. (Tingey 

et al., 2001; Weinstein et al., 1991; 

Retzlaff et al., 2000; Laurence et al., 

1993; Laurence et al., 2001; Weinstein et 

al., 2005). The model provides an 

analytical framework that accounts for 

the nonlinear relationship between O3

exposure and response. The interactions 

between O3 exposure, precipitation and 

temperature are integrated as they affect 

vegetation, thus providing an internal 

consistency for comparing effects in 

trees under different exposure scenarios 

and climatic conditions. An earlier 

assessment of the effectiveness of 

national ambient air quality standards 

in place since the early 1970s took 

advantage of 40 years of air quality and 

climate data for the Crestline site in the 

San Bernardino Mountains of California 

to simulate ponderosa pine growth over 

time with the improving air quality 

using TREGRO (Tingey et al., 2004). 

The TREGRO model was used to 

assess growth of Ponderosa pine in the 

San Bernardino Mountains of California 

(Crestline) and the growth of yellow 

poplar and red maple in the 

Appalachian mountains of Virginia and 

North Carolina, Shenandoah National 

Park (Big Meadows) and Linville Gorge 

Wilderness Area (Cranberry), 

respectively. Total tree growth 

associated with ’as is’ air quality, and 

air quality adjusted to just meet 

alternative O3 standards was assessed. 

Ponderosa pine is one of the most 

widely distributed pines in western 

North America, a major source of 

timber, important as wildlife habitat, 

and valued for aesthetics (Burns and 

Honkala, 1990). Red maple is one of the 

most abundant species in the eastern 

U.S. and is important for its brilliant fall 

foliage and highly desirable wildlife 

browse food (Burns and Honkala, 1990). 

Yellow poplar is an abundant species in 

the southern Appalachian forest. It is 10 

percent of the cove hardwood stands in 

southern Appalachians which are 

widely viewed as some of the country’s 

most treasured forests because the 

protected, rich, moist set of conditions 

permit trees to grow the largest in the 

eastern U.S. The wood has high 

commercial value because of its 

versatility and as a substitute for 

increasingly scarce softwoods in 

furniture and framing construction. 

Yellow poplar is also valued as a honey 

tree, a source of wildlife food, and a 

shade tree for large areas (Burns and 

Honkala, 1990). 

The Staff Paper analyses found that 

just meeting the current standard would 

likely continue to allow O3-related 

reductions in annual net biomass gain 

in these species. This is based on model 

outputs that estimate that as O3 levels 

are reduced below those of the current 

standard, significant improvements in 

growth would occur. For instance, 

estimated growth in red maple 

increased by 4 and 3 percent at Big 

Meadows and Cranberry sites, 

respectively, when air quality was 

rolled back to just met a W126 value of 

13 ppm-hour. Yellow poplar was 

projected to have a growth increase 

between 0.6 and 8 percent under the 

same scenario at the two eastern sites. 

Though there is uncertainty 

associated with the above analyses, this 

information should be given careful 

consideration in light of several other 

pieces of evidence. Specifically, new 

evidence from experimental studies that 

go beyond the seedling growth stage 


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61Principal crops as defined by the USDA 

include corn, sorghum, oats, barley, winter wheat, 

rye, Durum wheat, other spring wheat, rice, 

soybeans, peanuts, sunflower, cotton, dry edible 

beans, potatoes, sugar beets, canola, proso millet, 

hay, tobacco, and sugarcane. Acreage data for the 

principal crops were taken from the USDA NASS 

2005 Acreage Report (http:// 

usda.mannlib.cornell.edu/reports/nassr/field/pcpbba/acrg0605.pdf). 

continues to show decreased growth 

under elevated O3 (King et al., 2005). 

Some mature trees such as red oak have 

shown an even greater sensitivity of 

photosynthesis to O3 than seedlings of 

the same species (Hanson et al., 1994). 

As indicated above, smaller growth loss 

increments may be significant for 

perennial species. The potential for 

cumulative ‘‘carry over’’ effects as well 

as compounding must be considered. 

The accumulation of such ‘‘carry-over’’

effects over time may affect long-term 

survival and reproduction of 

individuals and ultimately the 

abundance of sensitive tree species in 

forest stands. 

c. Crops 

As discussed in the Staff Paper, risk 

of O3 exposure and associated 

monetized benefits were estimated for 

commodity crops, fruits and vegetables. 

Similar to the tree seedling analysis, this 

analysis combined C–R information on 

crops, crop growing regions and 

interpolated exposures during each crop 

growing season. NCLAN crop functions 

were used for commodity crops. 

According to USDA National 

Agricultural Statistical Survey (NASS) 

data, the 9 commodity crop species (e.g., 

cotton, field corn, grain sorghum, 

peanut, soybean, winter wheat, lettuce, 

kidney bean, potato) included in the 

Staff Paper analysis accounted for 69 

percent of 2004 principal crop acreage 

planted in the U.S. in 2004.61 The C–R 

functions for six fruit and vegetable 

species (tomatoes-processing, grapes, 

onions, rice, cantaloupes, Valencia 

oranges) were identified from the 

California fruit and vegetable analysis 

from the last review (Abt 1995). The 

Staff Paper noted that fruit and 

vegetable studies were not part of the 

NCLAN program and C–R functions 

were available only in terms of seasonal 

7-hour or 12-hour mean index. This 

index form is considered less effective 

in predicting plant response for a given 

change in air quality than the 

cumulative form used with other crops. 

Therefore, the fruit and vegetable C–R 

functions were considered more 

uncertain than those for commodity 

crops. 

Analyses in the Staff Paper showed 

that some of the most important 

commodity crops such as soybean, 

winter wheat and cotton had some 

projected losses under the 2001 base 

year air quality. Soybean yield losses 

were projected to be 2–4 percent in 

parts of Pennsylvania, New Jersey, 

Maryland and Texas. Winter wheat was 

projected to have yield losses of 2–6 

percent in parts of California. 

Additionally, cotton was projected to 

have yield losses of above 6 percent in 

parts of California, Texas and North 

Carolina in 2001. The risk assessment 

estimated that just meeting the current 

8-hour standard would still allow O3- 

related yield loss to occur in some 

commodity crop species and fruit and 

vegetable species currently grown in the 

U.S. For example, based on median C–

R function response, in counties with 

the highest O3 levels, potatoes and 

cotton had estimated yield losses of 9–

15 percent and 5–10 percent, 

respectively, when O3 air quality just 

met the level of the current standard. 

Estimated yield improved in these 

counties when the alternative W126 

standard levels were met. The very 

important soybean crop had generally 

small yield losses throughout the 

country under just meeting the current 

standard (0–4 percent). 

The Staff Paper also presented 

estimates of monetized benefits for 

crops associated with the current and 

alternative standards. The Agriculture 

Simulation Model (AGSIM) (Taylor, 

1994; Taylor, 1993) was used to 

calculate annual average changes in 

total undiscounted economic surplus for 

commodity crops and fruits and 

vegetables when current and alternative 

standard levels were met. Meeting the 

various alternative standards did show 

some significant benefits beyond the 

current 8-hour standard. However, the 

Staff Paper recognized the AGSIM 

modeled economic benefits had many 

uncertainties: For example, much of the 

economic benefits were from the fruits 

and vegetables which had uncertain C–

R relationships, there was uncertainty in 

assumptions about the treatment and 

effect of government farm payment 

programs, and there was also 

uncertainty about near-term changes in 

agriculture sector due to the increased 

use of crops as biofuels. Although the 

AGSIM model results provided a 

relative comparison of agricultural 

benefits between alternative standards, 

the uncertainties limited the utility of 

the absolute numbers. 

D. Conclusions on the Adequacy of the 

Current Standard 

1. Background 

The initial issue to be addressed in 

the current review of the secondary O3

standard is whether, in view of the 

advances in scientific knowledge 

reflected in the Criteria Document and 

additional information on exposure and 

risk discussed in the Staff Paper, the 

existing standard should be revised. The 

current secondary standard is a 3-year 

average of the annual 4th-highest 

maximum 8-hour average O3

concentration set at a level of 0.08 ppm. 

In evaluating whether it is appropriate 

to retain or revise the current secondary 

O3 standard, the Administrator adopts 

an approach in this review that builds 

upon the general approach used in the 

last review and reflects the broader body 

of evidence now available. 

In developing proposed conclusions 

on the adequacy of the current 

secondary O3 standard, the 

Administrator has considered a weightof-evidence approach that evaluated 

information across the variety of 

vegetation-related research areas 

described in the Criteria Document (e.g., 

seedling, sapling and mature forest tree 

species growth stages and commodity, 

fruit, vegetable and forage crop species), 

and included the assessments of air 

quality, exposures, and qualitative and 

quantitative risks associated with 

alternative air quality scenarios. 

Evidence-based considerations included 

assessment of vegetation effects 

evidence obtained from chamber, free 

air, gradient, model and field-based 

observation studies across an array of 

vegetation effects endpoints. Exposureand risk-based considerations were 

drawn from exposure and risk 

assessments that relied upon both 

monitored and interpolated O3

exposures as described in the Staff 

Paper. These assessments reflect the 

availability of new tools and assessment 

methods, as well as the larger and more 

diverse body of evidence available since 

the last review. Specifically, estimates 

of exposures and risks associated with 

recent O3 air quality levels, as well as 

estimates of the relative magnitude of 

exposure and risk reductions potentially 

associated with meeting the current 8- 

hour secondary O3 NAAQS and 

alternative standards, have also been 

considered, along with all known 

associated uncertainties. 

In this review, a series of general 

questions frames the approach to 

reaching a proposed decision on the 

adequacy of the current standard, 

beginning with: (1) To what extent does 

newly available information reinforce or 

call into question evidence of 

associations of O3 exposures with effects 

identified in the last review?; (2) to what 

extent does newly available information 

reinforce or call into question any of the 

basic elements of the current standard?; 


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and (3) to what extent have important 

uncertainties identified in the last 

review been reduced and have new 

uncertainties emerged? To the extent the 

available information suggests that 

revision of the current standard may be 

appropriate, the question of whether the 

available information supports 

consideration of a standard that is either 

more or less protective than the current 

standard is addressed, including: (1) 

Whether there is evidence that 

vegetation effects extend to ambient O3

concentration levels that are as low as 

or lower than had previously been 

observed, and what are the important 

uncertainties associated with that 

evidence?; (2) whether vegetation 

exposures and risks of concern 

estimated to occur in areas upon 

meeting the current standard are 

considered important from a public 

welfare perspective; and (3) what are the 

important uncertainties associated with 

the estimated risks? 

The current secondary standard was 

selected to provide protection to the 

public welfare against a range of O3- 

induced vegetation effects, particularly 

yield loss in agricultural crops and 

biomass loss in tree seedlings. As an 

introduction to the discussion in this 

section of the adequacy of the current 

O3 standard, it is useful to summarize 

the key factors that formed the basis of 

the decision in the last review to revise 

the averaging time, level and form of the 

then current 1-hour secondary standard. 

In the 1996 proposal notice (61 FR 

65716), the Administrator proposed to 

replace the then existing 1-hour O3

secondary NAAQS with one of two 

alternative new standards: a standard 

identical to the proposed and now 

current 0.08 ppm, 8-hour primary 

standard (described above), or 

alternatively, a new seasonal standard, 

SUM06, expressed as a sum of hourly 

concentrations greater than or equal to 

0.06 ppm, cumulated daily over a 12 

hour daylight window (8 am to 8 pm) 

during the maximum consecutive 3- 

month period (e.g., the consecutive 3 

month period with the highest SUM06 

index value) during the O3 monitoring 

season, set at a level of 25 ppm-hours. 

The latter form and level were selected 

to provide protection to vegetation on 

the basis of annual, rather than 3-year 

average, exposures. 

In the final rule for the O3 NAAQS 

published in July 1997 (62 FR 38877), 

the Administrator decided to replace the 

then current 1-hour, 0.12-ppm 

secondary NAAQS with a standard that 

was identical in every way to the new 

revised primary standard of an 0.08 

ppm annual 4th-highest maximum 8- 

hour average standard averaged over 3 

years. Her decision was based on: (1) 

Her judgment that the then existing 

secondary standard did not provide 

adequate protection for vegetation 

against the adverse welfare effects of O3; 

(2) CASAC advice ‘‘that a secondary 

NAAQS, more stringent than the present 

primary standard, was necessary to 

protect vegetation from O3’’ (Wolff, 

1996); (3) her judgment that the new 8- 

hour average standard would provide 

substantially improved protection for 

vegetation from O3-related adverse 

effects as compared to the level of 

protection provided by the then current 

1-hour, 0.12-ppm secondary standard; 

(4) recognition that significant 

uncertainties remained with respect to 

exposure dynamics, air quality 

relationships, and the exposure, risk, 

and monetized valuation analyses 

presented in the proposal, resulting in 

only rough estimates of the increased 

public welfare likely to be afforded by 

each of the proposed alternative 

standards; (5) her judgment that there 

was value in allowing more time to 

obtain additional information to better 

characterize O3-related vegetation 

effects under field conditions from 

additional research and to develop a 

more complete rural monitoring 

network and air quality database from 

which to evaluate the elements of an 

appropriate seasonal secondary 

standard; and (6) her judgment that 

there was value in allowing more time 

to evaluate more specifically the 

improvement in rural air quality and in 

O3-related vegetation effects resulting 

from measures designed to attain the 

new primary standard (62 FR 38877–

78). 

The Administrator further concluded 

(62 FR 38877–78) that continued 

research on the effects of O3 on 

vegetation under field conditions and 

on better characterizing the relationship 

between O3 exposure dynamics and 

plant response would be important in 

the next review because: (1) The 

available biological database highlighted 

the importance of cumulative, seasonal 

exposures as a primary determinant of 

plant responses; (2) the association 

between daily maximum 8-hour O3

concentrations and plant responses had 

not been specifically examined in field 

tests; (3) the impacts of attaining an 8- 

hour, 0.08 ppm primary standard in 

upwind urban areas on rural air quality 

distributions could not be characterized 

with confidence due to limited 

monitoring data and air quality 

modeling in rural and remote areas. 

2. Evidence- and Exposure/Risk-Based 

Considerations 

The new evidence available in this 

review as described in the Criteria 

Document continues to support and 

strengthen key policy-relevant 

conclusions drawn in the previous 

review (EPA, 2006a). Based on this new 

evidence, the current Criteria Document 

once more concludes that: (1) A plant’s 

response to O3 depends upon the 

cumulative nature of ambient exposure 

as well as the temporal dynamics of 

those concentrations; (2) current 

ambient concentrations in many areas of 

the country are sufficient to impair 

growth of numerous common and 

economically valuable plant and tree 

species; (3) the entrance of O3 into the 

leaf through the stomata is the critical 

step in O3 effects; (4) effects can occur 

with only a few hourly concentrations 

above 0.08 ppm; (5) other 

environmental biotic and abiotic factors 

are also influential to the overall impact 

of O3 on plants and trees; and (6) a high 

degree of uncertainty remains in our 

ability to assess the impact of O3 on 

ecosystem services. 

In light of the new evidence, as 

described in the Criteria Document, the 

Staff Paper evaluates the adequacy of 

the current standard based on 

assessments of both the most policyrelevant vegetation effects evidence and 

exposure and risk-based information, as 

summarized above in sections IV.A and 

IV.C, respectively. In evaluating the 

strength of this information, the Staff 

Paper takes into account the 

uncertainties and limitations in the 

scientific evidence and analyses as well 

as the views of CASAC. The Staff Paper 

concludes that progress has been made 

since the last review and generally finds 

support in the available effects- and 

exposure/risk-based information for 

consideration of an O3 standard that is 

more protective than the current 

standard. The Staff Paper further 

concludes that there is no support for 

consideration of an O3 standard that is 

less protective than the current 

standard. This general conclusion is 

consistent with the advice and 

recommendations of CASAC. 

a. Evidence-Based Considerations 

In the last review, crop yield and tree 

seedling biomass loss data obtained in 

OTC studies provided the basis for the 

Administrator’s judgment that the then 

current 1-hour, 0.12 ppm secondary 

standard was inadequate (EPA, 1996b). 

Since then, several additional lines of 

evidence have progressed sufficiently to 

provide a more complete and coherent 

picture of the scope of O3-related 


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vegetation risks, especially those 

currently faced by sensitive seedling, 

sapling and mature growth stage tree 

species growing in field settings, and 

their associated forested ecosystems. 

Specifically, new research reflects an 

increased emphasis on field-based 

exposure methods (e.g., free air, ambient 

gradient, and biomonitoring surveys). In 

reaching conclusions regarding the 

adequacy of the current standard, the 

Staff Paper has considered the 

combined information from all these 

areas together, along with associated 

uncertainties, in an integrated, weightof-evidence approach. 

Regarding the O3-induced effect of 

visible foliar injury, observations for the 

years 2001 to 2004 at USDA FIA 

biomonitoring sites showed widespread 

O3-induced leaf injury occurring in the 

field, including in forested ecosystems, 

under current ambient O3 conditions. 

For a few studied species, it has been 

shown that the presence of visible foliar 

injury is further linked to the presence 

of other vegetation effects (e.g., reduced 

plant growth and impaired below 

ground root development) (EPA, 2006), 

though for most species, this linkage has 

not been specifically studied or where 

studied, has not been found. 

Nevertheless, when visible foliar injury 

is present, the possibility that other O3- 

induced vegetation effects could also be 

present for some species should be 

considered. Likewise, the absence of 

visible foliar injury should not be 

construed to demonstrate the absence of 

other O3-induced vegetation effects. The 

Staff Paper concludes that it is not 

possible at this time to quantitatively 

assess the degree of visible foliar injury 

that should be judged adverse in all 

settings and across all species, and that 

other environmental factors can mitigate 

or exacerbate the degree of O3-induced 

visible foliar injury expressed at any 

given concentration of O3. However, the 

Staff Paper also concludes that the 

presence of visible foliar injury alone 

can be adverse to the public welfare, 

especially when it occurs in protected 

areas such as national parks and 

wilderness areas. Thus, on the basis of 

the available information on the 

widespread distribution of O3-sensitive 

species within the U.S. including in 

areas, such as national parks, which are 

afforded a higher degree of protection, 

the Staff Paper concludes that the 

current standard continues to allow 

levels of visible foliar injury in some 

locations that could reasonably be 

considered to be adverse from a public 

welfare perspective. Additional 

monitoring of both O3 air quality and 

foliar injury levels are needed in these 

areas of national significance to more 

fully characterize the spatial extent of 

this public welfare impact. 

With respect to O3-induced biomass 

loss in trees, the Staff Paper concludes 

that the significant new body of fieldbased research on trees strengthens the 

conclusions drawn on tree seedling 

biomass loss from earlier OTC work by 

documenting similar seedling responses 

in the field. For example, recent 

empirical studies conducted on quaking 

aspen at the AspenFACE site in 

Wisconsin have confirmed the 

detrimental effects of O3 exposure on 

tree growth in a field setting without 

chambers (Isebrands et al., 2000, 2001). 

In addition, results from an ambient 

gradient study (Gregg et al., 2003), 

which evaluated biomass loss in 

cottonwood along an urban-to-rural 

gradient at several locations, found that 

conditions in the field were sufficient to 

produce substantial biomass loss in 

cottonwood, with larger impacts 

observed in downwind rural areas due 

to the presence of higher O3

concentrations. These gradients from 

low urban to higher rural O3

concentrations occur when O3

precursors generated in urban areas are 

transported to downwind sites and are 

transformed into O3. In addition,O3

concentrations typically fall to near 0 

ppm at night in urban areas due to 

scavenging of O3 by NOX and other 

compounds. In contrast, rural areas, due 

to a lack of nighttime scavenging, tend 

to maintain elevated O3 concentrations 

for longer periods. On the basis of such 

key studies, the Staff Paper concludes 

that the expanded body of field-based 

evidence, in combination with the 

substantial corroborating evidence from 

OTC data, provides stronger evidence 

than that available in the last review 

that ambient levels of O3 are sufficient 

to produce visible foliar injury 

symptoms and biomass loss in sensitive 

vegetative species growing in natural 

environments. Further, the Staff Paper 

judges that the consistency in response 

in studied species/genotypes to O3

under a variety of exposure conditions 

and methodologies demonstrates that 

these sensitive genotypes and 

populations of plants are susceptible to 

adverse impacts from O3 exposures at 

levels known to occur in the ambient 

air. Due to the potential for 

compounded risks from repeated insults 

over multiple years in perennial species, 

the Staff Paper concludes that these 

sensitive subpopulations are not 

afforded adequate protection under the 

current secondary O3 standard. Despite 

the fact that only a relatively small 

portion of U.S. plant species have been 

studied with respect to O3 sensitivity, 

those species/genotypes shown to have 

O3 sensitivity span a broad range of 

vegetation types and public use 

categories, including direct-use 

categories like food production for 

human and domestic animal 

consumption; fiber, materials, and 

medicinal production; urban/private 

landscaping. Many of these species also 

contribute to the structure and 

functioning of natural ecosystems (e.g., 

the EEAs) and thus, to the goods and 

services those ecosystems provide 

(Young and Sanzone, 2002), including 

non-use categories such as relevance to 

public welfare based on their aesthetic, 

existence or wildlife habitat value. 

The Staff Paper therefore concludes 

that the current secondary standard is 

inadequate to protect the public welfare 

against the occurrence of known adverse 

levels of visible foliar injury and tree 

seedling biomass loss occurring in tree 

species (e.g., ponderosa pine, aspen, 

black cherry, cottonwood) that are 

sensitive and clearly important to the 

public welfare. 

b. Exposure- and Risk-Based 

Considerations 

The Staff Paper also presents the 

results of exposure and risk 

assessments. Due to multiple sources of 

uncertainty, both known and unknown, 

that continue to be associated with these 

analyses, the Staff Paper put less weight 

on this information in drawing 

conclusions on the adequacy of the 

current standard. However, the Staff 

Paper also recognizes that some progress 

has been made since the last review in 

better characterizing some of these 

associated uncertainties and, therefore 

concluded that the results of the 

exposure and risk assessments continue 

to provide information useful to 

informing judgments as to the relative 

changes in risks predicted to occur 

under exposure scenarios associated 

with the different standard alternatives 

considered. Importantly, with respect to 

two key uncertainties, the uncertainty 

associated with continued reliance on 

C–R functions developed from OTC 

exposure systems to predict plant 

response in the field and the potential 

for changes in tree seedling and crop 

sensitivities in the intervening period 

since the C–R functions were 

developed, the Staff Paper concluded 

that recent research has provided 

information useful in judging how much 

weight to put on these concerns. 

Specifically, new field-based studies, 

conducted on a limited number of tree 

seedling and crop species to date, 

demonstrate plant growth and visible 

foliar injury responses in the field that 


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are similar in nature and magnitude to 

those observed previously under OTC 

exposure conditions, lending qualitative 

support to the conclusion that OTC 

conditions do not fundamentally alter 

the nature of the O3-plant response. 

Second, nothing in the recent literature 

suggests that the O3 sensitivity of crop 

or tree species studied in the last review 

and for which C–R functions were 

developed has changed significantly in 

the intervening period. Indeed, in the 

few recent studies where this is 

examined, O3 sensitivities were found to 

be as great as or greater than those 

observed in the last review. 

i. Seedling and Mature Tree Biomass 

Loss 

Biomass loss in sensitive tree 

seedlings is predicted to occur under O3

exposures that meet the level of the 

current secondary standard. For 

instance, black cherry, ponderosa pine, 

eastern white pine, and aspen had 

estimated median seedling biomass 

losses as high as 24, 11, 6, and 6 

percent, respectively, over some 

portions of their growing ranges when 

air quality was rolled back to meet the 

current 8-hr standard with the 10 

percent downward adjustment for the 

potential O3 gradient between monitor 

height and short plant canopies applied. 

The Staff Paper notes that these results 

are for tree seedlings and that mature 

trees of the same species may have more 

or less of a response to O3 exposure. 

Decreased root growth associated with 

biomass loss has the potential to 

indirectly affect the vigor and 

survivability of tree seedlings. If such 

effects occur on a sufficient number of 

seedlings within a stand, overall stand 

health and composition can be affected 

in the long term. Thus, the Staff Paper 

concludes that these levels of estimated 

tree seedling growth reduction should 

be considered significant and 

potentially adverse, given that they are 

well above the 2 percent level of 

concern identified by the 1997 

consensus workshop (Heck and 

Cowling, 1997). 

Though there is significant 

uncertainty associated with this 

analysis, the Staff Paper recommends 

that this information should be given 

careful consideration in light of several 

other pieces of evidence. Specifically, 

limited evidence from experimental 

studies that go beyond the seedling 

growth stage continues to show 

decreased growth under elevated O3

levels (King et al., 2005). Some mature 

trees such as red oak have shown an 

even greater sensitivity of 

photosynthesis to O3 than seedlings of 

the same species (Hanson et al., 1994). 

The potential for effects to ‘‘carry over’’

to the following year or cumulate over 

multiple years, including the potential 

for compounding, must be considered. 

The accumulation of such ‘‘carry-over’’

effects over time may affect long-term 

survival and reproduction of individual 

trees and ultimately the abundance of 

sensitive tree species in forest stands. 

ii. Qualitative Ecosystem Risks 

In addition to the quantifiable risk 

categories discussed above, the Staff 

Paper presents qualitative discussions 

on a number of other public welfare 

effects categories. In so doing, the Staff 

Paper concludes that the quantified 

risks to vegetation estimated to be 

occurring under current air quality or 

upon meeting the current secondary 

standard likely represent only a portion 

of actual risks that may be occurring for 

a number of reasons. 

First, as mentioned above, out of the 

over 43,000 plant species catalogued as 

growing within the U.S. (USDA 

PLANTS database, USDA, NRCS, 2006), 

only a small percentage have been 

studied with respect to O3 sensitivity. 

Most of the studied species were 

selected because of their commercial 

importance or observed O3-induced 

visible foliar injury in the field. Given 

that O3 impacts to vegetation also 

include less obvious but often more 

significant impacts, such as reduced 

annual growth rates and below ground 

root loss, the paucity of information on 

other species means the number of O3- 

sensitive species that exists within U.S., 

could be greater than what is now 

known. Since no state in the lower 48 

states has less than seven known O3- 

sensitive plant species, with the 

majority of states having between 11 

and 30 (see Appendix 7J–2 in Staff 

Paper), protecting O3 sensitive 

vegetation is clearly important to the 

public welfare at the national scale. 

Second, the Staff Paper also takes into 

consideration the possibility that more 

subtle and hidden risks to ecosystems 

are potentially occurring in areas where 

vegetation is being significantly 

impacted. Given the importance of these 

qualitative and anticipated risks to 

important public welfare effects 

categories such as ecosystem impacts 

leading to potential losses or shifts in 

ecosystem goods and services (e.g., 

carbon sequestration, hydrology, and 

fire disturbance regimes), the Staff Paper 

concludes that any secondary standard 

set to protect against the known and 

quantifiable adverse effects to vegetation 

should also consider the anticipated, 

but currently unquantifiable, potential 

effects on natural ecosystems. 

iii. Crop Yield Loss 

Exposure and risk assessments in the 

Staff Paper estimated that meeting the 

current 8-hour standard would still 

allow O3-related yield loss to occur in 

several fruit and vegetable and 

commodity crop species currently 

grown in the U.S. These estimates of 

crop yield loss are substantially lower 

than those estimated in the last review 

as a result of several factors, including 

adjusted exposure levels to reflect the 

presence of a variable O3 gradient 

between monitor height and crop 

canopies, and use of a different 

econometric agricultural benefits model 

updated to reflect more recent 

agricultural policies (EPA, 2006b). 

Though these sources of uncertainty 

associated with the crop risk and 

benefits assessments were better 

documented in this review, the Staff 

Paper concludes that the presence of 

these uncertainties make the risk 

estimates suitable only as a basis for 

understanding potential trends in 

relative yield loss and economic 

benefits. The Staff Paper further 

recognizes that actual conditions in the 

field and management practices vary 

from farm to farm, that agricultural 

systems are heavily managed, and that 

adverse impacts from a variety of other 

factors (e.g., weather, insects, disease) 

can be orders of magnitude greater than 

that of yield impacts predicted for a 

given O3 exposure. Thus, the relevance 

of such estimated impacts on crop 

yields to the public welfare are 

considered highly uncertain and less 

useful as a basis for assessing the 

adequacy of the current standard. The 

Staff Paper notes, however, that in some 

experimental cases, exposure to O3 has 

made plants more sensitive or 

vulnerable to some of these other 

important stressors, including disease, 

insect pests, and harsh weather (EPA, 

2006a). The Staff Paper therefore 

concluded that this remains an 

important area of uncertainty and that 

additional research to better 

characterize the nature and significance 

of these interactions between O3 and 

other plant stressors would be useful. 

c. Summary 

In summary, the Staff Paper 

concludes that the current secondary O3

standard is inadequate. This conclusion 

is based on the extensive vegetation 

effects evidence, in particular the recent 

empirical field-based evidence on 

biomass loss in seedlings, saplings and 

mature trees, and foliar injury incidence 

that has become available in this review, 

which demonstrates the occurrence of 

adverse vegetation effects at ambient 


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62One CASAC Panel member reached different 

conclusions from those of the broader Panel 

regarding certain aspects of the vegetation effects 

information and the appropriate degree of emphasis 

that should be placed on the associated 

uncertainties. These concerns related to how the 

results of O3/vegetation exposure experiments 

carried out in OTC can be extrapolated to the 

ambient environment and how C–R functions 

developed in the 1980’s can be used today given 

that he did not expect that current crop species/ 

cultivars in use in 2002 would have the same O3

sensitivity as those studied in NCLAN (Henderson, 

2007, pg. C–18). 

levels of recent O3 air quality, as well as 

evidence and exposure- and risk-based 

analyses indicating that adverse effects 

would be predicted to occur under air 

quality scenarios that meet the current 

standard. 

3. CASAC Views 

In a letter to the Administrator 

(Henderson, 2006c), the CASAC O3

Panel, with full endorsement of the 

chartered CASAC, unanimously 

concluded that ‘‘despite limited recent 

research, it has become clear since the 

last review that adverse effects on a 

wide range of vegetation including 

visible foliar injury are to be expected 

and have been observed in areas that are 

below the level of the current 8-hour 

primary and secondary ozone 

standards.’’ Therefore, ‘‘based on the 

Ozone Panel’s review of Chapters 7 and 

8 [of the Staff Paper], the CASAC 

unanimously agrees that it is not 

appropriate to try to protect vegetation 

from the substantial, known or 

anticipated, direct and/or indirect, 

adverse effects of ambient O3 by 

continuing to promulgate identical 

primary and secondary standards for O3. 

Moreover, the members of the 

Committee and a substantial majority of 

the Ozone Panel agree with EPA staff 

conclusions and encourage the 

Administrator to establish an alternative 

cumulative secondary standard for O3

and related photochemical oxidants that 

is distinctly different in averaging time, 

form and level from the currently 

existing or potentially revised 8-hour 

primary standard’’ (Henderson, 

2006c).62

4. Administrator’s Proposed 

Conclusions Concerning Adequacy of 

Current Standard 

The Administrator recognizes that the 

secondary standard is to protect against 

‘‘adverse’’ O3 effects, discussed above in 

section IV.A.3. In considering what 

constitutes a vegetation effect that is 

also adverse to the public welfare, the 

Administrator took into account the 

Staff Paper conclusions regarding the 

nature and strength of the vegetation 

effects evidence, the exposure and risk 

assessment results, the degree to which 

the associated uncertainties should be 

considered in interpreting the results, 

and the views of CASAC and members 

of the public. On these bases, the 

Administrator proposes that the current 

secondary standard is inadequate to 

protect the public welfare from known 

and anticipated adverse O3-related 

effects on vegetation and ecosystems. 

Ozone levels that would be expected to 

remain after meeting the current 

secondary standard are sufficient to 

cause visible foliar injury, seedling and 

mature tree biomass loss, and crop yield 

reductions to degrees that could be 

considered adverse depending on the 

intended use of the plant and its 

significance to the public welfare, and 

the current secondary standard does not 

provide adequate protection from such 

effects. Other O3-induced effects 

described in the literature, including an 

impaired ability of many sensitive 

species and genotypes within species to 

adapt to or withstand other 

environmental stresses, such as freezing 

temperatures, pest infestations and/or 

disease, and to compete for available 

resources, would also be anticipated to 

occur. In the long run, the result of these 

impairments (e.g., loss in vigor) could 

lead to premature plant death in O3

sensitive species. Though effects on 

other ecosystem components have only 

been examined in isolated cases, effects 

such as those described above could 

have significant implications for plant 

community and associated species 

biodiversity and the structure and 

function of whole ecosystems. These 

considerations also support the 

proposed conclusion that the current 

secondary standard is not adequate and 

that revision is needed to provide 

additional public welfare protection. 

E. Conclusions on the Elements of the 

Secondary Standard 

Given his proposed conclusion that 

the current secondary standard is 

inadequate, the Administrator then 

considered what revisions to the 

standard are appropriate. In so doing, 

the Administrator has focused on 

revisions to the key standard elements 

of indicator, form, averaging time, and 

level. On the basis of the strength and 

coherence of the vegetation effects 

evidence suggesting that a biologicallybased standard for vegetation, at a 

minimum, should cumulate exposures 

and differentially-weight higher O3

concentrations, the Administrator 

judges that it is appropriate to consider 

revisions to the secondary standard that 

reflect this understanding. In addition, 

the Administrator also judges that the 

current 8-hour average form, though not 

based on the most biologically relevant 

and coherent vegetation effects 

literature, can also provide substantially 

improved protection to vegetation when 

set at an appropriate level. Therefore, 

the Administrator also considered 

whether revision to the level of the 

current 8-hour secondary standard 

might provide the requisite level of 

public welfare protection. In light of 

these considerations, as discussed 

below, the Administrator is proposing 

two options for revising the current 

secondary standard: one option is a 

cumulative seasonal standard (section 

IV.E.2) and the other option is an 8-hour 

average standard consistent with the 

revised 8-hour average standard 

proposed above for the primary 

standard (section IV.E.3). The 

Administrator has also considered an 

alternative approach to setting a 

cumulative, seasonal standard(s) as 

described below in section IV.E.2. 

1. Indicator 

In the last review, EPA focused on a 

standard for O3 as the most appropriate 

surrogate for ambient photochemical 

oxidants. In this review, while the 

complex atmospheric chemistry in 

which O3 plays a key role has been 

highlighted, no alternatives to O3 have 

been advanced as being a more 

appropriate surrogate for ambient 

photochemical oxidants. Thus, as is the 

case for the primary standard, 

(discussed above in section II.D.1.), the 

Administrator proposes to continue to 

use O3 as the indicator for a standard 

that is intended to address effects 

associated with exposure to O3, alone 

and in combination with related 

photochemical oxidants. In so doing, 

the Administrator recognizes that 

measures leading to reductions in 

vegetation exposures to O3 will also 

reduce exposures to other 

photochemical oxidants. 

2. Cumulative, Seasonal Standard 

The Administrator proposes to 

replace the current secondary standard 

with a new cumulative, seasonal 

standard expressed as an index of the 

annual sum of weighted hourly 

concentrations (using the W126 form), 

set at a level in the range of 7 to 21 ppmhours. The index would be cumulated 

over the 12-hour daylight period (8 a.m. 

to 8 p.m.) during the consecutive 3- 

month period within the O3 season with 

the maximum index value. In addition, 

as discussed below, the Administrator is 

considering an alternative approach to 

setting a cumulative, seasonal 

standard(s) that would afford differing 

degrees of protection for O3-related 

impacts on different types of vegetation 

with different intended uses. 


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63One CASAC Panel member expressed the view 

that the O3 exposure indices, SUM06 and W126, are 

simply mathematical expressions of exposure and, 

thus, cannot be said to have a biological basis 

(Henderson, 2007, pg. C–18). 64While the term ‘‘averaging time’’ is used, for 

the cumulative, seasonal standard the time period 

at issue is one over which exposures during a 

specified period of time are cumulated, not 

averaged. 

a. Form 

The current Criteria Document and 

Staff Paper concluded that the recent 

vegetation effects literature evaluated in 

this review strengthens and reaffirms 

conclusions made in the last review that 

the use of a cumulative exposure index 

that differentially-weights ambient 

concentrations is best able to relate 

ambient exposures to vegetation 

response at this time (EPA, 2006a, b; see 

also discussion in IV.B. above). The 

1996 review focused in particular on 

two of these cumulative forms, the 

SUM06 and W126. As described in the 

last review (EPA, 1996a, b) it was 

concluded that, based on statistical 

reanalysis of the NCLAN data, these 

different cumulative forms performed 

equally well in predicting crop yield 

loss response to O3 exposure. Given that 

the data available at that time were 

unable to distinguish between these 

forms, the Administrator, based on the 

policy consideration of not including O3

concentrations considered to be within 

the PRB, concluded that the SUM06 

form was the more appropriate choice 

for a secondary standard. 

In this review, the Staff Paper 

evaluated the continued 

appropriateness of the SUM06 form in 

light of two key pieces of information: 

new estimates of PRB that are lower 

than in the last review, and continued 

lack of evidence within the vegetation 

effects literature of a biological 

threshold for vegetation exposures of 

concern. On the basis of those policy 

and science-related considerations, the 

Staff Paper concluded that the W126 

form was more appropriate in the 

context of this review. Specifically, the 

W126, by its incorporation of a 

sigmoidal weighting scheme, does not 

create an artificially imposed 

concentration threshold, gives 

proportionally more weight to the 

higher and typically more biologically 

potent concentrations, and is not 

significantly influenced by O3

concentrations within the range of 

estimated PRB. 

The CASAC, based on its assessment 

of the same vegetation effects science, 

agreed with the Criteria Document and 

Staff Paper and unanimously concluded 

that it is not appropriate to try to protect 

vegetation from the known or 

anticipated adverse effects of ambient 

O3 by continuing to promulgate 

identical primary and secondary 

standards for O3. Moreover, the 

members of CASAC and a substantial 

majority of the CASAC O3 Panel agreed 

with Staff Paper conclusions and 

encouraged the Administrator to 

establish an alternative cumulative 

secondary standard for O3 and related 

photochemical oxidants that is 

distinctly different in averaging time, 

form, and level from the current or 

potentially revised 8-hour primary 

standard. The CASAC also stated that 

‘‘the recommended metric for the 

secondary ozone standard is the 

(sigmoidally-weighted) W126 index’’

(Henderson, 2007).63

The Administrator agrees with the 

conclusions drawn in the Criteria 

Document, Staff Paper and by CASAC 

that the scientific evidence available in 

the current review continues to 

demonstrate the cumulative nature of 

O3-induced plant effects and the need to 

give greater weight to higher 

concentrations. Thus, the Administrator 

concludes that a cumulative exposure 

index that differentially-weights O3

concentrations represents a reasonable 

policy choice for a seasonal secondary 

standard to protect against the effects of 

O3 on vegetation. The Administrator 

further agrees with both the Staff Paper 

and CASAC that the most appropriate 

cumulative, concentration-weighted 

form to consider in this review is the 

sigmoidally weighted W126 form, due 

to his recognition that there is no 

evidence in the literature for an 

exposure threshold that would be 

appropriate across all O3-sensitive 

vegetation and that this form is unlikely 

to be significantly influenced by O3 air 

quality within the range of PRB levels 

identified in this review. Thus, the 

Administrator proposes as one option to 

replace the current 8-hour average 

secondary standard form with the 

cumulative, seasonal W126 form. 

b. Averaging Times 64

The Staff Paper, in addition to form, 

also considers what ‘‘averaging’’ periods 

or exposure durations are most relevant 

for vegetation, which, unlike people, is 

exposed to ambient air continuously 

throughout its lifespan. For annual 

species, this lifespan encompasses a 

period of only one year or less; while for 

perennials, lifespans can range from a 

few years to decades or centuries. 

However, because O3 levels are not 

continuously elevated and plants are 

not equally sensitive to O3 over the 

course of a day, season or lifetime, it 

becomes necessary to identify periods of 

exposure that have the most relevance 

for plant response. Exposure periods are 

discussed below in terms of a seasonal 

window, a diurnal window, and an 

annual versus 3-year average standard. 

(1) In considering an appropriate 

seasonal window, the Staff Paper 

recognizes that, in general, many annual 

crops are grown for periods of a few 

months before being harvested. In 

contrast, other annual and perennial 

species may be photosynthetically 

active longer, and for some species and 

locations, throughout the entire year. In 

general, the period of maximum 

physiological activity and thus, 

maximum potential O3 uptake for 

annual crops, herbaceous species, and 

deciduous trees and shrubs coincides 

with some or all of the intra-annual 

period defined as the O3 season, which 

varies on a state-by-state basis. This is 

because the high temperature and high 

light conditions that promote the 

formation of tropospheric O3 also 

promote physiological activity in 

vegetation. 

The Staff Paper notes that the 

selection of any single seasonal 

exposure period for a national standard 

would represent a compromise, given 

the significant variability in growth 

patterns and lengths of growing seasons 

among the wide range of vegetation 

species occurring within the U.S. that 

may experience adverse effects 

associated with O3 exposures. However, 

the Staff Paper further concludes that 

the consecutive 3-month period within 

the O3 season with the highest W126 

index value (e.g., maximum 3 month 

period) would, in most cases, likely 

coincide with the period of greatest 

plant sensitivity on an annual basis. 

Therefore, the Staff Paper again 

concludes, as it did in 1996, that the 

annual maximum consecutive 3-month 

period is a reasonable seasonal time 

period, when combined with a 

cumulative, concentration weighted 

form, for protection of sensitive 

vegetation. 

(2) In considering an appropriate 

diurnal window, the Staff Paper 

recognizes that over the course of the 

24-hour diurnal period, plant stomatal 

conductance varies in response to 

changes in light level, soil moisture and 

other environmentally and genetically 

controlled factors. In general, stomata 

are most open during daylight hours in 

order to allow sufficient CO2 uptake for 

use in carbohydrate production through 

the light-driven process of 

photosynthesis. At most locations, O3

concentrations are also highest during 

the daytime, and thus, most likely to 

coincide with maximum stomatal 

uptake. It is also known however, that 

in some species, stomata may remain 


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open sufficiently at night to allow for 

some nocturnal uptake to occur. In 

addition, at some rural, high elevation 

sites, the O3 concentrations remain 

relatively flat over the course of the day, 

often at levels above estimated PRB. At 

these sites, nighttime W126 values can 

be of similar magnitude as daytime 

values, though the significance of these 

exposures is much less certain. This is 

because O3 uptake during daylight 

hours is known to impair the lightdriven process of photosynthesis, which 

can then lead to impacts on 

carbohydrate production, plant growth, 

reproduction (yield) and root function. 

It is less clear at this time to what extent 

and by what mechanisms O3 uptake at 

night adversely impacts plant function. 

In addition, many species do not take 

up O3 at night or occur in areas with 

elevated nighttime O3 concentrations. 

In light of a recent work on this topic 

conducted by Musselman and Minnick 

(2000), the Staff Paper again revisited 

the issue of what diurnal period is of 

most relevance in influencing O3- 

induced effects on vegetation. This work 

reports that some species take up O3 at 

night, but that the degree of nocturnal 

stomatal conductance varies widely 

between species and its relevance to 

overall O3-induced vegetation effects 

remain unclear. In considering this 

information, the Staff Paper concludes 

that for the vast majority of studied 

species, daytime exposures represent 

the majority of diurnal plant O3 uptake 

and are responsible for inducing the 

plant response of most significance to 

the health and productivity of the plant 

(e.g., reduced carbohydrate production). 

Until additional information is available 

about the extent to which co-occurrence 

of sensitive species and elevated 

nocturnal O3 exposures exists, and what 

levels of nighttime uptake are adverse to 

affected species, the Staff Paper 

concludes that this information 

continues to be preliminary, and does 

not provide a basis for reaching a 

different conclusion at this time. The 

Staff Paper further notes that additional 

research is needed to address the degree 

to which a 12-hour diurnal window may 

be under protective in areas where 

elevated nighttime levels of O3 co-occur 

with sensitive species with a high 

degree of nocturnal stomatal 

conductance. Thus, as in the last 

review, the Staff Paper again concludes 

that based on the available science, the 

daytime 12-hour window (8 a.m. to 8 

p.m.) is the most appropriate period 

over which to cumulate diurnal O3

exposures, specifically those most 

relevant to plant growth and yield 

responses. 

(3) In considering whether an annual 

or 3-year averaging period is more 

appropriate, the Staff Paper recognized 

that though most cumulative seasonal 

exposure levels of concern for 

vegetation have been expressed in terms 

of the annual timeframe, it may be 

appropriate to consider a 3-year 

averaging period for purposes of 

standard stability. However, the Staff 

Paper notes that for certain welfare 

effects of concern (e.g., foliar injury, 

yield loss for annual crops, growth 

effects on other annual vegetation and 

potentially tree seedlings), an annual 

time frame may be a more appropriate 

period in which to assess what level 

would provide the requisite degree of 

protection, while for other welfare 

effects (e.g., mature tree biomass loss), a 

3-year averaging period may also be 

appropriate. Thus, the Staff Paper 

concludes that it is appropriate to 

consider both an annual and a 3-year 

averaging period. Further, the Staff 

Paper concludes that should a 3-year 

average of the 12-hour W126 form be 

selected, a potentially lower level 

should be considered to reduce the 

potential of adverse impacts to annual 

species from a single high O3 year that 

could still occur while attaining a 

standard on average over 3-years. 

The CASAC, in considering what 

seasonal and diurnal time periods are 

most appropriate when combined with 

a cumulative, concentration-weighted 

form to protect vegetation from 

exposures of concern, agreed that the 

Staff Paper conclusion regarding the 3- 

month seasonal period and 12-hour 

daylight window was appropriate, with 

the distinction that both time 

designations likely represents the 

minimum time periods of importance. 

In particular, one O3 Panel member 

commented that for some species, 

additional O3 exposures of importance 

were occurring outside the 3-month 

seasonal and 12-hour diurnal windows. 

Further, the CASAC concluded that 

multi-year averaging to promote a 

‘‘stable’’ secondary standard is less 

appropriate for a cumulative, seasonal 

secondary standard than for a primary 

standard based on maximum 8-hour 

concentrations. CASAC further 

concluded that if multi-year averaging is 

employed to increase the stability of the 

secondary standard, the level of the 

standard should be revised downward 

to assure that the desired degree of 

protection is not exceeded in individual 

years. 

The Administrator, in determining 

which seasonal and diurnal time 

periods are most appropriate to propose, 

took into account Staff Paper and 

CASAC views. The Administrator, in 

being careful to consider what is needed 

to provide the requisite degree of 

protection, no more and no less, 

proposes that the 3-month seasonal 

period and 12-hour daylight period are 

appropriate. Based on the Staff Paper 

conclusions discussed above, the 

Administrator is mindful that there is 

the potential for under-protection with 

a 12-hour diurnal window in areas with 

sufficiently elevated nighttime levels of 

O3 where sensitive species with a high 

degree of nocturnal stomatal 

conductance occur. On the other hand, 

the Administrator also recognizes that a 

longer diurnal window (e.g., 24-hour) 

has the possibility of over-protecting 

vegetation in areas where nighttime O3

levels remain relatively high but where 

no species having significant nocturnal 

uptake exist. In weighing these 

considerations, the Administrator agrees 

with the Staff Paper conclusion that 

until additional information is available 

about the extent to which this cooccurrence of sensitive species and 

elevated nocturnal O3 exposures exists, 

and what levels of nighttime uptake are 

adverse to affected species, this 

information does not provide a basis for 

reaching a different conclusion at this 

time. The Administrator also considered 

to what extent the 3-month period 

within the O3 season was appropriate, 

recognizing that many species of 

vegetation have longer growing seasons. 

The Administrator further proposes that 

the maximum 3-month period is 

sufficient and appropriate to 

characterize O3 exposure levels 

associated with known levels of plant 

response. Therefore, the Administrator 

proposes that the most appropriate 

exposure periods for a cumulative, 

seasonal form is the daytime 12-hour 

window (8 a.m. to 8 p.m.) during the 

consecutive 3-month period within the 

O3 monitoring season with the 

maximum W126 index value. 

The Administrator also proposes an 

annual rather than a multi-year 

cumulative, seasonal standard. In 

proposing this alternative, the 

Administrator also believes that it is 

appropriate to consider the benefits to 

the public welfare that would accrue 

from establishing a 3-year average 

secondary standard, and solicits 

comment on this alternative. In so 

doing, the Administrator also agrees 

with Staff Paper and CASAC 

conclusions that should a 3-year 

standard be finalized, the level of the 

standard should be set so as to provide 

the requisite degree of protection for 

those vegetation effects judged to be 

adverse to the public welfare within a 

single annual period. 


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c. Level 

The Staff Paper, in identifying a range 

of levels for a 3-month, 12-hour W126 

annual form appropriate to protect the 

public welfare from adverse impacts to 

vegetation from O3 exposures, considers 

what information from the array of 

vegetation effects evidence and 

exposure and risk assessment results 

was most useful. In regards to the 

vegetation effects evidence, the Staff 

Paper finds stronger support than what 

was available at the time of the last 

review for an increased level of 

protection for trees and ecosystems. 

Specifically, this expanded body of 

support includes: (1) Additional field 

based data from free air, gradient and 

biomonitoring surveys demonstrating 

adverse levels of O3-induced above and/ 

or below-ground growth reductions on 

trees at the seedling, sapling and mature 

growth stages and incidence of visible 

foliar injury occurring at biomonitoring 

sites in the field at ambient levels of 

exposure; (2) qualitative support from 

free air (e.g., AspenFACE) and gradient 

studies on a limited number of tree 

species for the continued 

appropriateness of using OTC-derived 

C–R functions to predict tree seedling 

response in the field; (3) studies that 

continue to document below-ground 

effects on root growth and ‘‘carry-over’’

effects occurring in subsequent years 

from O3 exposures; and (4) increased 

recognition and understanding of the 

structure and function of ecosystems 

and the complex linkages through 

which O3, and other stressors, acting at 

the organism and species level can 

influence higher levels within the 

ecosystem hierarchy and disrupt 

essential ecological attributes critical to 

the maintenance of ecosystem goods 

and services important to the public 

welfare. 

Based on the above observations and 

on the vegetation effects and the results 

of the exposure and impact assessment 

summarized above, the Staff Paper 

concludes that just meeting the current 

standard would still allow adverse 

levels of tree seedling biomass loss in 

sensitive commercially and ecologically 

important tree species in many regions 

of the country. Seedling risk assessment 

results showed that some tree seedling 

species are extremely sensitive (e.g., 

cottonwood, black cherry and aspen), 

with annual biomass losses occurring in 

the field of the same or greater 

magnitude that that of annual crops. 

Such information from the tree seedling 

risk assessment suggests that air quality 

levels would need to be substantially 

reduced to protect sensitive tree 

seedlings like black cherry from growth 

and foliar injury effects. 

In addition to the currently 

quantifiable risks to trees from ambient 

exposures, the Staff Paper also considers 

the more subtle impacts of O3 acting in 

synergy with other natural and manmade stressors to adversely affect 

individual plants, populations and 

whole systems. By disrupting the 

photosynthetic process, decreasing 

carbon storage in the roots, increasing 

early senescence of leaves and affecting 

water use efficiency in trees, O3

exposures could potentially disrupt or 

change the nutrient and water flow of an 

entire system. Weakened trees can 

become more susceptible to other 

environmental stresses such as pest and 

pathogen outbreaks or harsh weather 

conditions. Though it is not possible to 

quantify all the ecological and societal 

benefits associated with varying levels 

of alternative secondary standards, the 

Staff Paper concludes that this 

information should be weighed in 

considering the extent to which a 

secondary standard should be set so as 

to provide potential protection against 

effects that are anticipated to occur. 

In addition, the Staff Paper also 

recognizes that in the last review, the 

Administrator took into account the 

results of a 1996 consensus-building 

workshop as described in a January 

1997 report (Heck and Cowling, 1997). 

At this workshop, a group of 

independent scientists expressed their 

judgments on what standard form(s) and 

level(s) would provide vegetation with 

adequate protection from O3-related 

adverse effects. Consensus was reached 

with respect to selecting appropriate 

ranges of levels in terms of a 

cumulative, seasonal 3-month, 12-hr 

SUM06 standard for a number of 

vegetation effects endpoints. These 

ranges are identified below, with the 

estimated approximate equivalent W126 

standard values shown in parentheses. 

For growth effects to tree seedlings in 

natural forest stands, a consensus was 

reached that a range of 10 to 15 (7 to 13) 

ppm-hours would be protective. For 

growth effects to tree seedlings and 

saplings in plantations, the consensus 

range was 12 to 16 (9 to 14) ppm-hours. 

For visible foliar injury to natural 

ecosystems, the consensus range was 8 

to 12 (5 to 9) ppm-hours (Heck and 

Cowling, 1997). 

Taking these consensus statements 

into account, the Administrator stated 

in the final rule (62 FR 38856) that ‘‘the 

report lends important support to the 

view that the current secondary 

standard is not adequately protective of 

vegetation * * * [and] * * * 

foreshadows the direction of future 

scientific research in this area, the 

results of which could be important in 

future reviews of the O3 secondary 

standard’’ (62 FR 38856). 

Given the importance the 

Administrator put on the consensus 

report in the last review, the Staff Paper 

considered to what extent new research 

provided empirical support for the 

ranges of levels identified by the experts 

as protective of different types of O3- 

induced effects. On the basis of new 

field-based tree seedling growth loss 

and foliar injury data, and including 

both the above quantitative and 

qualitative information regarding O3- 

induced effects on sensitive trees and 

forested ecosystems, the Staff Paper 

concludes that it is appropriate to 

consider a range for a 3-month, 12-hour, 

W126 standard that includes the 

consensus recommendations for growth 

effects in tree seedlings in natural forest 

stands. 

In considering the newly available 

information on O3-related effects on 

crops in this review, the Staff Paper 

observes the following regarding the 

strength of the underlying crop science: 

(1) Nothing in the recent literature 

points to a change in the relationship 

between O3 exposure and crop response 

across the range of species and/or 

cultivars of commodity crops currently 

grown in the U.S. that could be 

construed to make less appropriate the 

use of commodity crop C–R functions 

developed in the NCLAN program; (2) 

new field-based studies (e.g., SoyFACE) 

provide qualitative support in a few 

limited cases for the appropriateness of 

using OTC-derived C–R functions to 

predict crop response in the field; and 

(3) refinements in the exposure, risk and 

benefits assessments in this review 

reduce some of the uncertainties present 

in 1996. On the basis of these 

observations, the Staff Paper concludes 

that nothing in the newly assessed 

information calls into question the 

strength of the underlying science upon 

which the Administrator based her 

proposed decision in the last review to 

select a level of a cumulative, seasonal 

form associated with protecting 50 

percent of crop cases from no more than 

10 percent yield loss as providing the 

requisite degree of protection for 

commodity crops. 

The Staff Paper then considered 

whether any additional information is 

available to inform judgments as to the 

adversity of various O3-induced levels 

of crop yield loss to the public welfare. 

As noted above, the Staff Paper observes 

that agricultural systems are heavily 

managed, and that in addition to stress 

from O3, the annual productivity of 

agricultural systems is vulnerable to 


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65The Clean Air Act defines Class I areas as 

national parks over 6,000 acres, national wilderness 

areas and national memorial parks over 5,000 acres, 

and international parks. The National Park Service 

was created in 1916 by Congress through the 

National Park Service Organic Act in order to 

‘‘conserve the scenery and the natural and historic 

objects and the wild life therein and to provide for 

the enjoyment of the same in such manner and by 

such means as will leave them unimpaired for the 

enjoyment of future generations.’’

disruption from many other stressors 

(e.g., weather, insects, disease), whose 

impact in any given year can greatly 

outweigh the direct reduction in annual 

productivity resulting from elevated O3

exposures. On the other hand, O3 can 

also more subtly impact crop and forage 

nutritive quality and indirectly 

exacerbate the severity of the impact 

from other stressors. Though these latter 

effects currently cannot be quantified, 

they should be considered in judging to 

what extent a level of protection 

selected to protect commodity crops 

should be precautionary. 

Based on the above considerations, 

the Staff Paper concludes that the level 

of protection judged requisite in the last 

review to protect the public welfare 

from adverse levels of O3-induced 

reductions in crop yields, as provided 

by a W126 level of 21 ppm-hours, 

remains appropriate for consideration as 

an upper bound of a range of 

appropriate levels. 

Thus, the Staff Paper concludes, 

based on all the above considerations, 

that an appropriate range of 3-month, 

12-hour W126 levels is 7 to 21 ppmhours, recognizing that the level 

selected is largely a policy judgment as 

to the requisite level of protection 

needed. In determining the requisite 

level of protection for crops and trees, 

the Staff Paper recognizes that it is 

appropriate to weigh the importance of 

the predicted risks of these effects in the 

overall context of public welfare 

protection, along with a determination 

as to the appropriate weight to place on 

the associated uncertainties and 

limitations of this information. 

The CASAC, in its final letter to the 

Administrator (Henderson, 2007), 

agreed with the Staff Paper 

recommendations that the lower bound 

of the range within which a seasonal 

W126 welfare-based (secondary) O3

standard should be considered is 

approximately 7 ppm-hours; however, it 

did not agree with Staff’s 

recommendation that the upper bound 

of the range should be as high as 21 

ppm-hours. Rather, CASAC 

recommended that the upper bound of 

the range considered should be no 

higher than 15 ppm-hours, which the 

Panel estimates is approximately 

equivalent to a seasonal 12-hour SUM06 

level of 20 ppm-hours. The lower end of 

this range (7 ppm-hours) is the same as 

the lower end of the range identified in 

the 1997 Consensus Workshop as 

protective of tree seedlings in natural 

forest stands from growth effects (Heck 

and Cowling, 1997). 

The Administrator, taking Staff Paper 

and CASAC views into account, 

proposes a range of levels for a 

cumulative, seasonal secondary 

standard as expressed in terms of the 

maximum 3 month, 12-hour W126 form, 

in the range of 7 to 21 ppm-hours. This 

range encompasses the range of levels 

recommended by CASAC, and also 

includes a higher level as recommended 

in the Staff Paper. Given the uncertainty 

in determining the risk attributable to 

various levels of exposure to O3, the 

Administrator believes as a public 

welfare policy judgment that this is a 

reasonable range to propose. 

In taking into account the uncertainty 

associated with the above, the 

Administrator has also considered an 

alternative approach to establishing a 

secondary standard(s). This alternative 

approach would establish a cumulative, 

seasonal standard(s) that would afford 

differing degrees of protection for O3- 

related impacts on different types of 

vegetation with different intended uses. 

The Administrator recognizes that 

known O3-sensitive plant species 

growing within the U.S experience a 

variety of O3-induced effects, including 

visible foliar injury, biomass loss and 

yield loss, and that the public welfare 

significance of each of these effects can 

vary significantly, depending on the 

nature of the effect, the intended use of 

the plant, and/or the type of 

environment or location in which the 

plant grows. Any given O3-related effect 

on vegetation (e.g., biomass loss, or 

foliar injury) may be judged to have a 

different degree of impact on public 

welfare depending, for example, on 

whether that effect occurs in a Class I 

area, commercial cropland, or a city 

park. This variation in the significance 

of O3-related vegetation effects from a 

public welfare perspective across type 

of effect, intended plant use, and area 

grown means that the level of ambient 

O3 that is requisite to protect the public 

welfare may also vary. The level of 

ambient O3 that is requisite in a 

federally designated Class I area may be 

lower than the level that is requisite in 

a cropland area. EPA is therefore 

considering and soliciting comment on 

an alternative approach for the 

secondary O3 standard, with the aim of 

reasonably reflecting these variations. 

Specifically, the Administrator seeks 

comment on an alternative approach 

that would establish a suite of 

secondary standards. The suite of 

standards would contain different 

ambient levels, with each standard at a 

level that is requisite to protect public 

welfare for that variation in plant effect, 

use, and/or location. For example, a 

secondary standard intended to provide 

protection to natural systems valued for 

their aesthetic beauty and/or important 

ecological functions they might serve 

could be set at a lower, more protective 

level to provide the requisite degree of 

protection against a broad array of O3- 

related effects on important sensitive 

species in such areas. In contrast, while 

negative impacts on yield production in 

sensitive agricultural crops is also an 

important public welfare effect, O3- 

related reductions in yield may be 

considered less significant or adverse to 

the public welfare, depending on the 

degree of impact, since the intended use 

of such land is to produce optimum 

yields and croplands are already heavily 

managed to achieve that goal. Thus, a 

secondary standard set to provide the 

requisite degree of crop protection for 

such an area could be set at a higher 

level. 

The Administrator recognizes that 

variation in vegetation type and 

location, intended use, and impacts 

related to O3 exposure can be diverse, 

and believes that it is appropriate to 

consider whether it is appropriate and 

feasible to establish a suite of standards 

that accounts more broadly for such 

variation. EPA recognizes that this 

approach is unique with regard to 

secondary standards and will pose 

unique challenges, including how to 

classify areas according to intended use. 

Some geographic areas have already 

been identified for specific uses, such as 

Federal Class I areas,65 which are 

intended to conserve unimpaired 

natural ecosystems and their associated 

species for the enjoyment of future 

generations. Likewise, the USDA has 

classified cultivated areas in the U.S. 

into certain categories of intended use 

(such as cropland, rangeland, 

timberland) that could help inform the 

setting of a suite of standards. 

EPA is taking comment on all aspects 

of this alternative approach, including 

whether it is appropriate to set a suite 

of secondary standards that varies 

depending on use, location, and type of 

effect on vegetation. EPA invites 

comment on the appropriateness of this 

approach, from the scientific, legal, and 

policy perspectives, and on other factors 

that should be considered in 

determining the applicability of any one 

level within a suite of standards. 


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3. 8-Hour Average Standard 

The Administrator is also proposing 

to revise the current secondary standard 

by making it identical to the proposed 

8-hour primary standard, which is 

proposed to be within the range of 0.070 

to 0.075 ppm. For this option, EPA also 

solicits comment on a wider range of 8- 

hour standard levels, including levels 

down to 0.060 ppm and up to the 

current standard (i.e., effectively 0.084 

ppm with the current rounding 

convention). 

In the last review, the Staff Paper 

included an analysis to compare the 

degree of overlap between areas that 

would be expected not to meet the range 

of alternative 8-hour standards being 

considered for the primary NAAQS and 

those expected not to meet the range of 

values (expressed in terms of the 

seasonal SUM06 index) of concern for 

vegetation. This result suggested that 

improvements in national air quality 

expected to result from attaining an 8- 

hour primary standard within the 

recommended range of levels would 

also be expected to reduce levels of 

concern for vegetation in those same 

areas. In the 1997 final rule, the 

decision was made, on the basis of both 

science and policy considerations, to 

make the secondary identical to the 

primary standard. It acknowledged, 

however, that uncertainties remained 

‘‘as to the extent to which air quality 

improvements designed to reduce 8- 

hour average O3 concentrations 

averaged over a 3-year period would 

reduce O3 exposures measured by a 

seasonal SUM06 index’’ (62 FR 38876). 

On the basis of that history, the 

current Staff Paper analyzed the degree 

of overlap expected between alternative 

8-hour and cumulative seasonal 

secondary standards (as discussed above 

in section IV.C.1) using recent air 

quality. Based on the results, the Staff 

Paper concluded that the degree to 

which the current 8-hour standard form 

and level would overlap with areas of 

concern for vegetation expressed in 

terms of the 12-hour W126 standard is 

inconsistent from year to year and 

would depend greatly on the level of the 

12-hour W126 and 8-hour standards 

selected and the distribution of hourly 

O3 concentrations within the annual 

and/or 3-year average period. 

Thus, though the Staff Paper 

recognized again that meeting the 

current or alternative levels of the 8- 

hour average standard could result in air 

quality improvements that would 

potentially benefit vegetation in some 

areas, it urges caution be used in 

evaluating the likely vegetation impacts 

associated with a given level of air 

quality expressed in terms of the 8-hour 

average form in the absence of parallel 

W126 information. This caution is due 

to the concern that the analysis in the 

Staff Paper may not be an accurate 

reflection of the true situation in nonmonitored, rural counties due to the 

lack of more complete monitor coverage 

in many rural areas. Further, of the 

counties that did not show overlap 

between the two standard forms, most 

were located in rural/remote high 

elevation areas which have O3 air 

quality patterns that are typically 

different from those associated with 

urban and near urban sites at lower 

elevations. Because the majority of such 

areas are currently not monitored, it is 

believed there are likely to be additional 

areas that have similar air quality 

distributions that would lead to the 

same disconnect between forms. Thus, 

the Staff Paper concluded that it 

remains problematic to determine the 

appropriate level of protection for 

vegetation using an 8-hour average form. 

The CASAC recognized that an 

important difference between the effects 

of acute exposures to O3 on human 

health and the effects of O3 exposures 

on welfare is that vegetation effects are 

more dependent on the cumulative 

exposure to, and uptake of, O3 over the 

course of the entire growing season 

(Henderson, 2006c). The CASAC O3

Panel members were unanimous in 

concluding the protection of natural 

terrestrial ecosystems and managed 

agricultural crops requires a secondary 

O3 standard that is substantially 

different from the primary O3 standard 

in averaging time, level, and form 

(Henderson, 2007). 

A number of public commenters also 

presented views for the Administrator’s 

consideration regarding the adequacy of 

the current standard and whether or not 

revisions to that standard were 

warranted. These commenters did not 

support adopting an alternative, 

cumulative form for the secondary 

standard. These commenters stated that 

‘‘though directionally a cumulative form 

of the standard may better match the 

underlying data,’’ they believed further 

work is needed to determine whether a 

cumulative exposure index for the form 

of the secondary standard is necessary. 

These commenters identified a number 

of key concerns regarding the available 

evidence that, in their view, make it 

inappropriate to revise the secondary 

standard at this time. In particular they 

assert that (1) The key uncertainties, 

cited by the Administrator in the 1997 

review as reasons for deciding it was not 

appropriate to move forward with a 

seasonal secondary, have not been 

materially reduced in the current 

review; and (2) the exposure assessment 

is inaccurate and too uncertain due to 

the use of low estimates of PRB, an 

arbitrary rollback method that is 

uninformed by atmospheric chemistry 

from photochemical models, and the 

use of the CMAQ model in the west, 

whose biases and uncertainties are 

insufficiently characterized and 

evaluated. 

In considering the appropriateness of 

proposing a revised secondary standard 

that would be identical to the proposed 

primary standard, the Administrator 

took into account the approach used by 

the Agency in the last review, the 

conclusions of the Staff Paper, CASAC 

advice, and the views of public 

commenters. The Administrator first 

considered the Staff Paper analysis of 

the projected degree of overlap between 

counties with air quality expected to 

meet various alternative levels of an 8- 

hour standard and alternative levels of 

a W126 standard based on monitored air 

quality data. This analysis showed 

significant overlap within the proposed 

range of the primary 8-hour form and 

selected levels of the W126 standard 

form being considered, with the degree 

of overlap between these two forms 

depending greatly on the levels selected 

and the distribution of hourly O3

concentrations within the annual and/or 

3-year average period. On this basis, the 

Administrator recognizes that a 

secondary standard set identical to the 

proposed primary standard would 

provide a significant degree of 

additional protection for vegetation as 

compared to that provided by the 

current secondary standard. The 

Administrator also recognizes that lack 

of rural monitoring data makes 

uncertain the degree to which the 

proposed 8-hour or W126 alternatives 

would be protective, and that there 

would be the potential for not providing 

the appropriate degree of protection for 

vegetation in areas with air quality 

distributions that result in a high 

cumulative, seasonal exposure but do 

not result in high 8-hour average 

exposures. While this potential for 

under-protection is clear, the number 

and size of areas at issue and the degree 

of risk is hard to determine. However, 

such a standard would also tend to 

avoid the potential for providing more 

protection than is necessary, a risk that 

would arise from moving to a new form 

for the secondary standard despite 

significant uncertainty in determining 

the degree of risk for any exposure level 

and the appropriate level of protection, 

as well as uncertainty in predicting 

exposure and risk patterns. 

The Administrator also considered 

the views and recommendations of 


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CASAC, and agrees that a cumulative, 

seasonal standard is the most 

biologically relevant way to relate 

exposure to plant growth response. 

However, as reflected in the public 

comments, the Administrator also 

recognizes that there remain significant 

uncertainties in determining or 

quantifying the degree of risk 

attributable to varying levels of O3

exposure, the degree of protection that 

any specific cumulative, seasonal 

standard would produce, and the 

associated potential for error in 

determining the standard that will 

provide a requisite degree of 

protection—i.e. sufficient but not more 

than what is necessary. Given this 

uncertainty, the Administrator also 

believes it is appropriate to consider the 

degree of protection that would be 

afforded by a secondary standard that is 

identical to the proposed primary 

standard. Based on his consideration of 

the full range of views as described 

above, the Administrator proposes as a 

second option to revise the secondary 

standard to be identical in every way to 

the proposed primary standard. 

F. Proposed Decision on the Secondary 

Standard 

The Administrator proposes to 

replace the current secondary standard 

with one of two options. One option is 

a new cumulative, seasonal standard 

expressed as an index of the annual sum 

of weighted hourly concentrations 

(using the W126 form), set at a level in 

the range of 7 to 21 ppm-hours. The 

index would be cumulated over the 12- 

hour daylight period (8 a.m. to 8 p.m.) 

during the consecutive 3-month period 

within the O3 season with the maximum 

index value. The other option is to 

revise the current secondary standard by 

making it identical to the proposed 8- 

hour primary standard, which is 

proposed to be within the range of 0.070 

to 0.075 ppm. For this option, EPA also 

solicits comment on a wider range of 8- 

hour standard levels, including levels 

down to 0.060 ppm and up to the 

current standard (i.e., effectively 0.084 

ppm with the current rounding 

convention. The Administrator is also 

soliciting comment on an alternative 

approach for a setting cumulative, 

seasonal standard(s) that would afford 

differing degrees of protection for O3- 

related impacts on different types of 

vegetation with different intended uses. 

V. Creation of Appendix P— 

Interpretation of the NAAQS for Ozone 

The EPA is proposing to create 

Appendix P to 40 CFR part 50 to reflect 

the proposed revisions to the primary 

and secondary standards discussed 

above. This Appendix would explain 

the computations necessary for 

determining when the proposed primary 

and secondary standards are met. More 

specifically, Appendix P addresses data 

completeness requirements, data 

reporting, handling, and rounding 

conventions, and example calculations. 

Although EPA is proposing two 

alternative secondary standards, the 

proposed Appendix has been written to 

address a seasonal secondary standard 

expressed in the W126 form. If EPA 

adopts a secondary standard identical to 

the primary standard, Appendix P will 

be modified accordingly. The proposed 

Appendix also reflects the final rule 

promulgated on March 22, 2007 for the 

treatment of data influenced by 

exceptional events (72 FR 13560). 

Key elements of the proposed revisions 

to Appendix P are outlined below. 

A. Data Completeness 

The data completeness requirements 

in Appendix P proposed here for the 

proposed 8-hr primary standard 

secondary standards are the same as 

those in Appendix I to 40 CFR part 50 

required for the current standard. To 

satisfy the date completeness 

requirement, Appendix P would require 

90% data completeness, on average, for 

the 3-year period at a monitoring site, 

with no single year within the period 

having less than 75% data 

completeness. This data completeness 

requirement would have to be satisfied 

in order to determine that the 

standard(s) have been met at a 

monitoring site. A site could be found 

not to have met the standard(s) with less 

than complete data. EPA concluded in 

adopting these same data completeness 

requirements in Appendix I in 1997 that 

these proposed requirements are 

reasonable based on its earlier analysis 

of available air quality data that showed 

that 90% of all monitoring sites that are 

operated on a continuous basis 

routinely meet this objective. The EPA 

is seeking comment, however, on 

whether meteorological data would 

provide an objective basis for 

determining, on a day for which there 

is missing data, that the meteorological 

conditions were not conducive to high 

O3 concentrations, and therefore, that 

the day could be assumed to have an O3

concentration less than 0.070 to 0.075 

ppm. 

We are proposing separate data 

completeness requirements for the 

proposed seasonal secondary standard 

expressed in the W126 form. For such 

a standard, Appendix P would require 

a site to have 75% data completeness in 

a given month. Appendix P would also 

provide a mechanism for adjusting for 

missing data. Because this alternative is 

a seasonal cumulative index, 

representing a distribution of O3 values 

under a range of meteorological 

conditions, rather than a peak statistic, 

the EPA is proposing a missing data 

procedure that would require the 

monthly total index to be adjusted for 

incomplete data by multiplying the 

unadjusted W126 value by the ratio of 

the number of possible daylight hours 

(8:00 a.m. to 8:00 p.m.) to the number 

of hours with valid ambient hourly 

concentrations. This adjustment is 

analogous to calculating an estimated 

number of exceedances contained 

within part 50 Appendix I for the one 

hour O3 standard. 

B. Data Handling and Rounding 

Conventions 

Almost all State agencies now report 

hourly O3 concentrations to three 

decimal places, in ppm, since the 

typical incremental sensitivity of 

currently used O3 monitors is 0.001 

ppm. Consistent with the current 

approach for computing 8-hr averages, 

in calculating 8-hr average O3

concentrations from such hourly data, 

any calculated digits past the third 

decimal place would be truncated to 

preserve the number of significant digits 

in the reported data. In calculating 3- 

year averages of the fourth highest 

maximum 8-hr average concentrations, 

EPA is proposing to require the result to 

be reported to the third decimal place 

with digits to the right of the third 

decimal place truncated to preserve the 

number of significant digits in the 

reported data, as prescribed by the 

current standard. Analyses discussed in 

the Staff Paper demonstrated that taking 

into account the precision and bias in 1- 

hour O3 measurements, the 8-hour 

design value had an uncertainty of 

approximately 0.001 ppm. Thus, EPA 

considers any value less than 0.001 ppm 

to be highly uncertain and, therefore, 

proposes truncating both the individual 

8-hour averages used to determine the 

annual fourth maximum as well as the 

3-year average of the fourth maxima to 

the third decimal place. Nevertheless, 

EPA solicits comment on the 

appropriateness of rounding to the third 

decimal place as well as the policy 

reasons behind either truncating or 

rounding the 3-year average to the third 

decimal place (with 0.0005 and greater 

rounding up). EPA is also seeking 

comment on the scientific validity of 

truncating the three year average as 

opposed to rounding it as well as the 

policy reasons behind either truncating 

or rounding the average to the third 

decimal place. 


pwalker on PROD1PC71 with PROPOSALS2
37906 Federal Register / Vol. 72, No. 132 / Wednesday, July 11, 2007 / Proposed Rules 

66At present, not all ozone monitors at CASTNET 

sites are operated in full compliance with the 

quality assurance requirements of 40 CFR Part 58 

Appendix D, as they have not been primarily 

intended for regulatory use. The EPA is working 

towards such compliance in the near future and 

towards making CASTNET ozone data available 

through AQS. 

To determine whether the proposed 

standard is met, the calculated value of 

the fourth highest maximum 8-hour 

average concentrations, averaged over 

three years, would be compared to the 

level of the standard. As discussed in 

section II, the EPA is proposing to issue 

an 8-hr standard extending to three 

decimal places, based on the staff’s 

analysis and conclusions discussed in 

the Staff paper that expressing the 

proposed standard to the third decimal 

place is consistent with the precision 

requirements of the current O3

monitoring technology. Given that both 

the proposed standard and the 

calculated value of the 3-year average of 

the fourth highest maximum 8-hr O3

concentration are expressed to three 

decimal places, the two values can be 

compared directly. This is different than 

the approach for determining 

compliance with the current standard 

O3 standard. In comparing the 

calculated 3-year average (which is 

expressed to three decimal places) to the 

current standard O3 standard (which is 

expressed to only two decimal places), 

Appendix I requires the calculated 3- 

year average to be rounded to two 

decimal places. This additional step 

would not be necessary for the proposed 

standard given that the standard and the 

3-year average are each expressed to 

three decimal places. 

For the proposed seasonal secondary 

standard, the annual maximum 3-month 

W126 value computed on a calendar 

year basis using the three highest, 

consecutive monthly W126 values 

would be used as the summary statistic. 

The resulting value would then be 

compared to the level of the secondary 

O3 standard. The Agency is also 

interested in receiving comments 

regarding a 3-year average form 

summary statistic. 

VI. Ambient Monitoring Related to 

Proposed Revised O3 Standards 

The EPA is not proposing any specific 

changes to existing requirements for 

monitoring of O3 in the ambient air. 

However, we invite comment on a 

number of issues which naturally arise 

in connection with the proposed 

revision of the O3 NAAQS. The EPA 

may propose changes to some of the 

existing requirements at a later date. 

Current requirements regarding EPAapproved measurement methods for 

ambient O3 are stated in 40 CFR part 50 

Appendix D, Measurement Principle 

and Calibration Procedure for the 

Measurement of Ozone in the 

Atmosphere, and in 40 CFR part 53, 

Ambient Air Monitoring Reference and 

Equivalent Methods. The EPA does not 

intend to propose any changes to these 

requirements, because we believe these 

requirements would continue to be 

appropriate to support implementation 

of a revised O3 NAAQS. 

Presently, States (including the 

District of Columbia, Puerto Rico, and 

the Virgin Islands, and including local 

agencies when so delegated by the State) 

are required to operate minimum 

numbers of EPA-approved O3 monitors 

based on the population of each of their 

Metropolitan Statistical Areas (MSA) 

and the most recently measured O3

levels in each area. Each State (or in 

some cases portions of a State) also has 

a required O3 monitoring season based 

on historical experience on when O3

levels are high enough to be of 

regulatory or public health concern. 

These requirements are contained in 40 

CFR part 58 Appendix D, Network 

Design Criteria for Ambient Air Quality 

Monitoring. See section 4.1, especially 

Tables D–2 and D–3. These 

requirements were last revised on 

October 17, 2006 as part of a 

comprehensive review of ambient 

monitoring requirements for all criteria 

pollutants. (71 FR 61236) Certain 

deviations including minimum 

monitoring requirements and/or 

monitoring season requirements may be 

approved by the EPA Regional 

Administrator on a case-by-case basis. 

Required O3 monitoring seasons range 

from four to 12 months. The minimum 

number of monitors in an MSA ranges 

from zero (for an area with population 

under 350,000 and no recent history of 

an O3 design value greater than 85 

percent of the NAAQS) to four (for an 

area with population greater than 10 

million and an O3 design value greater 

than 85 percent of the NAAQS). Because 

these requirements apply at the MSA 

level, large urban areas consisting of 

multiple MSAs can require more than 

four monitors. For example, the New 

York-Newark-Bristol NY-NJ-CT-PA 

combined statistical area requires about 

14 monitors. In total, about 400 

monitors are required in MSAs, but 

about 1100 are actually operating in 

MSAs because most States operate more 

than the minimum required number of 

monitors. 

There are no EPA requirements for O3

monitoring in less populated areas 

outside of MSA boundaries (e.g., 

Metropolitan Statistical Areas) or in 

rural areas. However, there are about 

250 O3 monitors in counties that are not 

part of MSAs. Some required State 

monitors are placed downwind of the 

urban center of the MSA of interest in 

locations that are in some cases in a 

county outside the MSA itself; some 

States also operate a few rural monitors 

for research purposes. The EPA operates 

a network of about 56 O3 monitors as 

part of its Clean Air Status and Trends 

Network (CASTNET). The National Park 

Service (NPS) operates about 27 

monitors at other CASTNET sites. The 

NPS also has O3 monitoring stations in 

parks that are not part of the CASTNET 

dry deposition monitoring effort 

including multiple O3 stations in Great 

Smoky Mountains, Sequoia, Yosemite, 

and Joshua Tree National Parks. 

Required quality assurance 

procedures for O3 monitoring are given 

in 40 CFR Part 58 Appendix A, Quality 

Assurance Requirements for State and 

local air monitoring stations (SLAMS), 

special purpose monitors (SPM), and 

prevention of significant deterioration 

(PSD) Air Monitoring. The EPA does not 

intend to propose any changes to these 

quality assurance requirements, because 

we believe that the current 

measurement uncertainty goals and 

related procedures for assessing 

precision and bias as documented in 

paragraph 2.3.1.2 of Appendix A are 

appropriate to support the 

implementation of a revised O3 NAAQS. 

States are required to report O3 data 

quarterly to EPA’s Air Quality System 

(AQS), and most also voluntarily report 

their pre-validated O3 data on an hourly 

basis to EPA’s real time AirNow data 

system, where the data are used to 

forecast O3 concentrations and to 

provide public advisories. The National 

Park Service and many other 

organizations also report their O3 data to 

AQS and/or AirNow. The locations of 

currently operating O3 monitors which 

report data to EPA’s Air Quality System 

are available through the EPA AirData 

Web site http://www.epa.gov/air/data/ 

index.html. 

Data from O3 monitors at CASTNET 

stations are currently kept in a separate 

national data base.66

The EPA invites comments on O3

monitoring issues (other than O3

monitoring methods and quality 

assurance requirements), including the 

following: 

(1) Ozone monitoring network 

requirements in urban areas. Table D–2 

of 40 CFR Part 58 Appendix D is based 

on the percentage of the O3 NAAQS, 

with a break point at 85 percent of the 

NAAQS. Therefore, a revision of the 

NAAQS would automatically increase 

the required number of O3 monitors. For 

example, assuming a final NAAQS of 


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67EPA might instead treat one or more of these 

counties as having a design value based on a 

monitor in a nearby monitored county, in which 

case ozone monitoring might become required in 

certain currently unmonitored MSAs and the 

number of new required monitors would increase 

in the illustrative NAAQS example stated above. 

0.070 ppm for purposes of illustration 

only, about 70 MSAs with current O3

design values in the range of about 

0.060 ppm (about 85 percent of the 

current NAAQS) to 0.070 ppm (about 85 

percent of 0.070 ppm) would be 

affected, with most changing from no 

required monitors to one, or from one 

required monitor to two. Because most 

of these areas already are operating at 

least as many monitors as the possible 

new requirement, the number of 

monitors which would need to be 

initiated (or moved from a location of 

excess monitors) would be only about 

five monitors. About 100 MSAs with 

populations less than 350,000 presently 

are without any O3 monitors, and hence 

they do not have an O3 design value for 

use with Table D–2. If for the purpose 

of applying Table D–2, these areas are 

treated as if they have O3 concentrations 

below 85 percent of the revised NAAQS, 

then a NAAQS revision would not 

automatically result in a requirement for 

O3 monitoring in these MSAs.67 EPA 

invites comments on the 

appropriateness of the existing 

minimum monitoring requirements for 

purposes of implementing the proposed 

revised NAAQS, including the 

automatic changes to minimum 

monitoring requirements that would be 

triggered by a NAAQS revision. 

(2) Ozone monitoring seasons. As 

mentioned, the currently required O3

monitoring seasons range from four to 

12 months of the year. In some cases, O3

monitoring may start a couple of weeks 

before and may end a couple of weeks 

after the required season. With a lower 

O3 NAAQS, the issue arises of whether 

in some areas the required O3

monitoring season should be made 

longer. The EPA notes that under the 

existing regulations, the Regional 

Administrator may approve Staterequested deviations from the 

established O3 monitoring season but 

EPA may not increase the length of the 

season for an area at EPA’s own 

initiative other than by notice and 

comment rulemaking. 

(3) Monitoring to support 

implementation of a secondary O3

NAAQS. It is fair to say that the existing 

O3 monitoring requirements and current 

State monitoring practices are primarily 

oriented towards protecting against 

health effects in people, i.e., towards 

implementation of the primary NAAQS. 

This accounts for the focus on urban 

areas, which can combine large 

populations, large emissions of O3- 

forming precursors, and O3

concentrations of concern. The purpose 

of the secondary NAAQS is to protect 

against vegetation damage and other 

welfare effects, which can occur in both 

urban and rural areas. States have 

largely been given discretion on 

whether to add additional monitors 

aimed specifically at achieving the 

objectives of the previous and current 

secondary NAAQS. In urban areas, EPA 

in general believes that an O3

monitoring network (and monitoring 

season) appropriate to support 

implementation of the primary NAAQS 

will also be appropriate for 

implementing the secondary NAAQS. 

However, rural areas are presently only 

sparsely monitored for O3 so violations 

of the secondary NAAQS in areas with 

sensitive vegetation may occur 

undetected, as a result of transport from 

urban areas with high precursor 

emissions and/or O3 concentrations or 

from formation of additional O3 from 

precursors emitted from sources outside 

urban areas. It is conceivable that rural 

violations of a secondary NAAQS could 

occur in areas with sensitive vegetation 

even though urban monitoring networks 

are showing compliance with the 

primary NAAQS, whether the forms and 

levels of the two standards are the same 

or different. The EPA invites comment 

on the likelihood of this occurring 

under the possible combinations of 

primary and secondary standards 

proposed in this notice, and on whether, 

where, and how EPA should require 

monitoring in rural areas specifically 

aimed at implementation of the 

secondary NAAQS (and/or promote 

more voluntary monitoring or conduct 

monitoring itself in rural areas). 

VII. Statutory and Executive Order 

Reviews 

A. Executive Order 12866: Regulatory 

Planning and Review 

Under section 3(f)(1) of Executive 

Order (EO) 12866 (58 FR 51735, October 

4, 1993), the O3 NAAQS action is an 

‘‘economically significant regulatory 

action’’ because it is likely to have an 

annual effect on the economy of $100 

million or more. Accordingly, EPA 

prepared this regulatory impact analysis 

(RIA) of the potential costs and benefits 

associated with this action. The RIA 

estimates the costs and monetized 

human health and welfare benefits of 

attaining three alternative O3 NAAQS 

nationwide. Specifically, the RIA 

examines the alternatives of 0.075 ppm, 

0.070 ppm, and 0.065 ppm. The RIA 

contains illustrative analyses that 

consider a limited number of emissions 

control scenarios that States and 

Regional Planning Organizations might 

implement to achieve these alternative 

O3 NAAQS. However, the Clean Air Act 

(CAA) and judicial decisions make clear 

that the economic and technical 

feasibility of attaining ambient 

standards are not to be considered in 

setting or revising NAAQS, although 

such factors may be considered in the 

development of State plans to 

implement the standards. Accordingly, 

although an RIA has been prepared, the 

results of the RIA have not been 

considered in issuing this final rule. 

B. Paperwork Reduction Act 

This action does not impose an 

information collection burden under the 

provisions of the Paperwork Reduction 

Act, 44 U.S.C. 3501 et seq. There are no 

information collection requirements 

directly associated with the 

establishment of a NAAQS under 

section 109 of the CAA. 

Burden means the total time, effort, or 

financial resources expended by persons 

to generate, maintain, retain, or disclose 

or provide information to or for a 

Federal agency. This includes the time 

needed to review instructions; develop, 

acquire, install, and utilize technology 

and systems for the purposes of 

collecting, validating, and verifying 

information, processing and 

maintaining information, and disclosing 

and providing information; adjust the 

existing ways to comply with any 

previously applicable instructions and 

requirements; train personnel to be able 

to respond to a collection of 

information; search data sources; 

complete and review the collection of 

information; and transmit or otherwise 

disclose the information. 

An agency may not conduct or 

sponsor, and a person is not required to 

respond to a collection of information 

unless it displays a currently valid OMB 

control number. The OMB control 

numbers for EPA’s regulations in 40 

CFR are listed in 40 CFR part 9. 

C. Regulatory Flexibility Act 

The Regulatory Flexibility Act (RFA) 

generally requires an agency to prepare 

a regulatory flexibility analysis of any 

rule subject to notice and comment 

rulemaking requirements under the 

Administrative Procedure Act or any 

other statute unless the agency certifies 

that the rule will not have a significant 

economic impact on a substantial 

number of small entities. Small entities 

include small businesses, small 

organizations, and small governmental 

jurisdictions. 


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For purposes of assessing the impacts 

of today’s rule on small entities, small 

entity is defined as: (1) A small business 

that is a small industrial entity as 

defined by the Small Business 

Administration’s (SBA) regulations at 13 

CFR 121.201; (2) a small governmental 

jurisdiction that is a government of a 

city, county, town, school district or 

special district with a population of less 

than 50,000; and (3) a small 

organization that is any not-for-profit 

enterprise which is independently 

owned and operated and is not 

dominant in its field. 

After considering the economic 

impacts of today’s proposed rule on 

small entities, I certify that this action 

will not have a significant economic 

impact on a substantial number of small 

entities. This proposed rule will not 

impose any requirements on small 

entities. Rather, this rule establishes 

national standards for allowable 

concentrations of O3 in ambient air as 

required by section 109 of the CAA. See 

also American Trucking Associations v. 

EPA. 175 F. 3d at 1044–45 (NAAQS do 

not have significant impacts upon small 

entities because NAAQS themselves 

impose no regulations upon small 

entities). We continue to be interested in 

the potential impacts of the proposed 

rule on small entities and welcome 

comments on issues related to such 

impacts. 

D. Unfunded Mandates Reform Act 

Title II of the Unfunded Mandates 

Reform Act of 1995 (UMRA), Public 

Law 104–4, establishes requirements for 

Federal agencies to assess the effects of 

their regulatory actions on State, local, 

and Tribal governments and the private 

sector. Under section 202 of the UMRA, 

EPA generally must prepare a written 

statement, including a cost-benefit 

analysis, for proposed and final rules 

with ‘‘Federal mandates’’ that may 

result in expenditures to State, local, 

and Tribal governments, in the 

aggregate, or to the private sector, of 

$100 million or more in any 1 year. 

Before promulgating an EPA rule for 

which a written statement is needed, 

section 205 of the UMRA generally 

requires EPA to identify and consider a 

reasonable number of regulatory 

alternatives and to adopt the least 

costly, most cost-effective or least 

burdensome alternative that achieves 

the objectives of the rule. The 

provisions of section 205 do not apply 

when they are inconsistent with 

applicable law. Moreover, section 205 

allows EPA to adopt an alternative other 

than the least costly, most cost-effective 

or least burdensome alternative if the 

Administrator publishes with the final 

rule an explanation why that alternative 

was not adopted. Before EPA establishes 

any regulatory requirements that may 

significantly or uniquely affect small 

governments, including Tribal 

governments, it must have developed 

under section 203 of the UMRA a small 

government agency plan. The plan must 

provide for notifying potentially 

affected small governments, enabling 

officials of affected small governments 

to have meaningful and timely input in 

the development of EPA regulatory 

proposals with significant Federal 

intergovernmental mandates, and 

informing, educating, and advising 

small governments on compliance with 

the regulatory requirements. 

Today’s rule contains no Federal 

mandates (under the regulatory 

provisions of Title II of the UMRA) for 

State, local, or Tribal governments or 

the private sector. The rule imposes no 

new expenditure or enforceable duty on 

any State, local or Tribal governments or 

the private sector, and EPA has 

determined that this rule contains no 

regulatory requirements that might 

significantly or uniquely affect small 

governments. Furthermore, as indicated 

previously, in setting a NAAQS EPA 

cannot consider the economic or 

technological feasibility of attaining 

ambient air quality standards, although 

such factors may be considered to a 

degree in the development of State 

plans to implement the standards. See 

also American Trucking Associations v. 

EPA, 175 F. 3d at 1043 (noting that 

because EPA is precluded from 

considering costs of implementation in 

establishing NAAQS, preparation of a 

Regulatory Impact Analysis pursuant to 

the Unfunded Mandates Reform Act 

would not furnish any information 

which the court could consider in 

reviewing the NAAQS). Accordingly, 

EPA has determined that the provisions 

of sections 202, 203, and 205 of the 

UMRA do not apply to this proposed 

decision. The EPA acknowledges, 

however, that any corresponding 

revisions to associated SIP requirements 

and air quality surveillance 

requirements, 40 CFR part 51 and 40 

CFR part 58, respectively, might result 

in such effects. Accordingly, EPA will 

address, as appropriate, unfunded 

mandates if and when it proposes any 

revisions to 40 CFR parts 51 or 58. 

E. Executive Order 13132: Federalism 

Executive Order 13132, entitled 

‘‘Federalism’’ (64 FR 43255, August 10, 

1999), requires EPA to develop an 

accountable process to ensure 

‘‘meaningful and timely input by State 

and local officials in the development of 

regulatory policies that have federalism 

implications.’’ ‘‘Policies that have 

federalism implications’’ is defined in 

the Executive Order to include 

regulations that have ‘‘substantial direct 

effects on the States, on the relationship 

between the national government and 

the States, or on the distribution of 

power and responsibilities among the 

various levels of government.’’

This proposed rule does not have 

federalism implications. It will not have 

substantial direct effects on the States, 

on the relationship between the national 

government and the States, or on the 

distribution of power and 

responsibilities among the various 

levels of government, as specified in 

Executive Order 13132. The rule does 

not alter the relationship between the 

Federal government and the States 

regarding the establishment and 

implementation of air quality 

improvement programs as codified in 

the CAA. Under section 109 of the CAA, 

EPA is mandated to establish NAAQS; 

however, CAA section 116 preserves the 

rights of States to establish more 

stringent requirements if deemed 

necessary by a State. Furthermore, this 

rule does not impact CAA section 107 

which establishes that the States have 

primary responsibility for 

implementation of the NAAQS. Finally, 

as noted in section E (above) on UMRA, 

this rule does not impose significant 

costs on State, local, or Tribal 

governments or the private sector. Thus, 

Executive Order 13132 does not apply 

to this rule. 

However, as also noted in section E 

(above) on UMRA, EPA recognizes that 

States will have a substantial interest in 

this rule and any corresponding 

revisions to associated SIP requirements 

and air quality surveillance 

requirements, 40 CFR part 51 and 40 

CFR part 58, respectively. Therefore, in 

the spirit of Executive Order 13132, and 

consistent with EPA policy to promote 

communications between EPA and State 

and local governments, EPA specifically 

solicits comment on this proposed rule 

from State and local officials. 

F. Executive Order 13175: Consultation 

and Coordination With Indian Tribal 

Governments 

Executive Order 13175, entitled 

‘‘Consultation and Coordination with 

Indian Tribal Governments’’ (65 FR 

67249, November 9, 2000), requires EPA 

to develop an accountable process to 

ensure ‘‘meaningful and timely input by 

tribal officials in the development of 

regulatory policies that have tribal 

implications.’’ This rule concerns the 

establishment of O3 NAAQS. The Tribal 

Authority Rule gives Tribes the 

opportunity to develop and implement 


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CAA programs such as the O3 NAAQS, 

but it leaves to the discretion of the 

Tribe whether to develop these 

programs and which programs, or 

appropriate elements of a program, they 

will adopt. 

This proposed rule does not have 

Tribal implications, as specified in 

Executive Order 13175. It does not have 

a substantial direct effect on one or 

more Indian Tribes, since Tribes are not 

obligated to adopt or implement any 

NAAQS. Thus, Executive Order 13175 

does not apply to this rule. 

Although Executive Order 13175 does 

not apply to this rule, EPA contacted 

tribal environmental professionals 

during the development of this rule. The 

EPA staff participated in the regularly 

scheduled Tribal Air call sponsored by 

the National Tribal Air Association 

during the spring of 2007 as this 

proposal was under development. EPA 

specifically solicits additional comment 

on this proposed rule from Tribal 

officials. 

G. Executive Order 13045: Protection of 

Children From Environmental Health & 

Safety Risks 

Executive Order 13045, ‘‘Protection of 

Children from Environmental Health 

Risks and Safety Risks’’ (62 FR 19885, 

April 23, 1997) applies to any rule that: 

(1) Is determined to be ‘‘economically 

significant’’ as defined under Executive 

Order 12866, and (2) concerns an 

environmental health or safety risk that 

EPA has reason to believe may have a 

disproportionate effect on children. If 

the regulatory action meets both criteria, 

the Agency must evaluate the 

environmental health or safety effects of 

the planned rule on children, and 

explain why the planned regulation is 

preferable to other potentially effective 

and reasonably feasible alternatives 

considered by the Agency. 

This proposed rule is subject to 

Executive Order 13045 because it is an 

economically significant regulatory 

action as defined by Executive Order 

12866, and we believe that the 

environmental health risk addressed by 

this action may have a disproportionate 

effect on children. The proposed rule 

will establish uniform national ambient 

air quality standards for O3; these 

standards are designed to protect public 

health with an adequate margin of 

safety, as required by CAA section 109. 

However, the protection offered by these 

standards may be especially important 

for children because children, especially 

children with asthma, along with other 

sensitive population subgroups such as 

all people with lung disease and people 

active outdoors, are potentially 

susceptible to health effects resulting 

from O3 exposure. Because children are 

considered a potentially susceptible 

population, we have carefully evaluated 

the environmental health effects of 

exposure to O3 pollution among 

children. These effects and the size of 

the population affected are summarized 

in section 8.7 of the Criteria Document 

and section 3.6 of the Staff Paper, and 

the results of our evaluation of the 

effects of O3 pollution on children are 

discussed in sections II.A–C of this 

preamble. 

H. Executive Order 13211: Actions That 

Significantly Affect Energy Supply, 

Distribution or Use 

This proposed rule is not a 

‘‘significant energy action’’ as defined in 

Executive Order 13211, ‘‘Actions 

Concerning Regulations That 

Significantly Affect Energy Supply, 

Distribution, or Use’’ (66 FR 28355 (May 

22, 2001)) because in the Agency’s 

judgment it is not likely to have a 

significant adverse effect on the supply, 

distribution, or use of energy. The 

purpose of this rule is to establish 

revised NAAQS for O3. The rule does 

not prescribe specific pollution control 

strategies by which these ambient 

standards will be met. Such strategies 

will be developed by States on a caseby-case basis, and EPA cannot predict 

whether the control options selected by 

States will include regulations on 

energy suppliers, distributors, or users. 

Thus, EPA concludes that this rule is 

not likely to have any adverse energy 

effects and does not constitute a 

significant energy action as defined in 

Executive Order 13211. 

I. National Technology Transfer and 

Advancement Act 

Section 12(d) of the National 

Technology Transfer and Advancement 

Act of 1995 (NTTAA), Public Law No. 

104–113, § 12(d) (15 U.S.C. 272 note) 

directs EPA to use voluntary consensus 

standards in its regulatory activities 

unless to do so would be inconsistent 

with applicable law or otherwise 

impractical. Voluntary consensus 

standards are technical standards (e.g., 

materials specifications, test methods, 

sampling procedures, and business 

practices) that are developed or adopted 

by voluntary consensus standards 

bodies. The NTTAA directs EPA to 

provide Congress, through OMB, 

explanations when the Agency decides 

not to use available and applicable 

voluntary consensus standards. 

This proposed rulemaking does not 

involve technical standards. Therefore, 

EPA is not considering the use of any 

voluntary consensus standards. 

J. Executive Order 12898: Federal 

Actions To Address Environmental 

Justice in Minority Populations and 

Low-Income Populations 

Executive Order 12898 (59 FR 7629 

(Feb. 16, 1994)) establishes federal 

executive policy on environmental 

justice. Its main provision directs 

federal agencies, to the greatest extent 

practicable and permitted by law, to 

make environmental justice part of their 

mission by identifying and addressing, 

as appropriate, disproportionately high 

and adverse human health or 

environmental effects of their programs, 

policies, and activities on minority 

populations and low-income 

populations in the United States. 

EPA has determined that this 

proposed rule will not have 

disproportionately high and adverse 

human health or environmental effects 

on minority or low-income populations 

because it increases the level of 

environmental protection for all affected 

populations without having any 

disproportionately high and adverse 

human health or environmental effects 

on any population, including any 

minority or low-income population. The 

proposed rule will establish uniform 

national standards for O3 air pollution. 

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List of Subjects in 40 CFR Part 50 

Environmental protection, Air 

pollution control, Carbon monoxide, 

Lead, Nitrogen dioxide, Ozone, 

Particulate matter, Sulfur oxides. 

Dated: June 20, 2007. 

Stephen L. Johnson, 

Administrator. 

For the reasons stated in the 

preamble, title 40, chapter I of the code 

of Federal regulations is proposed to be 

amended as follows: 

PART 50—NATIONAL PRIMARY AND 

SECONDARY AMBIENT AIR QUALITY 

STANDARDS 

1. The authority citation for part 50 

continues to read as follows: 

Authority: 42 U.S.C. 7401 et seq. 

2. Section 50.15 is added to read as 

follows: 

§ 50.15 National primary and secondary 

ambient air quality standards for ozone. 

(a) The level of the national 8-hour 

primary ambient air quality standard for 

O3 is (0.070–0.075) parts per million 

(ppm), daily maximum 8-hour average, 

measured by a reference method based 

on Appendix D to this part and 

designated in accordance with part 53 of 

this chapter. 

(b) The 8-hour primary O3 ambient air 

quality standard is met at an ambient air 

quality monitoring site when the 

average of the annual fourth-highest 

daily maximum 8-hour average O3

concentration is less than or equal to 

(0.070–0.075) ppm, as determined in 

accordance with appendix P to this part. 

(c) The level of the national secondary 

ambient air quality standard for O3 is a 

cumulative index value of (7–21) ppmhours, measured by a reference method 

based on Appendix D to this part and 

designated in accordance with part 53 of 

this chapter. 

(d) The secondary O3 ambient air 

quality standard is a seasonal standard 

expressed as a sum of weighted hourly 

concentrations, cumulated over the 12 

hour daylight period from 8 a.m. to 8 

p.m. local standard time, during the 

consecutive 3-month period within the 

O3 monitoring season with the 

maximum index value. The secondary 

O3 standard is met at an ambient air 

quality monitoring site when the annual 

maximum consecutive 3-month 

cumulative index value (W126) is less 

than or equal to (7–21) ppm-hours, as 


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determined in accordance with 

appendix P to this part. 

3. Appendix P is added to read as 

follows: 

Appendix P to Part 50—Interpretation 

of the Primary and Secondary National 

Ambient Air Quality Standards for 

Ozone 

1. General 

(a) This appendix explains the data 

handling conventions and computations 

necessary for determining whether the 

national 8-hour primary and secondary 

ambient air quality standards for O3 specified 

in § 50.14 are met at an ambient O3 air 

quality monitoring site. Ozone is measured in 

the ambient air by a Federal reference 

method (FRM) based on appendix D of this 

part, as applicable, and designated in 

accordance with part 53 of this chapter, or by 

a Federal equivalent method (FEM) 

designated in accordance with part 53 of this 

chapter, or by an Approved Regional Method 

(ARM) designated in accordance with part 58 

of this chapter. Data reporting, data handling, 

and computation procedures to be used in 

making comparisons between reported O3

concentrations and the level of the O3

standard are specified in the following 

sections. Whether to exclude, retain, or make 

adjustments to the data affected by 

exceptional events, including stratospheric 

O3 intrusion and other natural events, is 

subject to the requirements under § 50.1, 

§ 50.14 and § 51.930. 

(b) The terms used in this appendix are 

defined as follows: 

8-hour average is the rolling average of 

hourly O3 concentrations as explained in 

section 2 of this appendix. 

Annual fourth highest daily maximum 

refers to the fourth highest value measured at 

a monitoring location during the O3 season 

for a particular year. 

Daily maximum 8-hour average 

concentration refers to the maximum 

calculated 8 hour average for a particular day 

as explained in section 2 of this appendix. 

Design values are the metrics (i.e., 

statistics) that are compared to the NAAQS 

levels to determine compliance, calculated as 

shown in sections 3 and 4 of this appendix. 

Ozone monitoring season refers to the span 

of time within a calendar year when 

individual States are required to measure 

ambient O3 concentrations as listed in part 58 

appendix D to this chapter. 

W126 is the weighted hourly O3

concentrations based on seasonal 

measurements as explained in section 4 of 

this appendix. 

Year refers to calendar year. 

2. Primary Ambient Air Quality Standard 

for Ozone 

2.1 Data Reporting and Handling 

Conventions 

Computing 8-hour averages. Hourly 

average concentrations shall be reported in 

parts per million (ppm) to the third decimal 

place, with additional digits to the right 

being truncated. Running 8-hour averages 

shall be computed from the hourly O3

concentration data for each hour of the year 

and the result shall be stored in the first, or 

start, hour of the 8-hour period. An 8-hour 

average shall be considered valid if at least 

75% of the hourly averages for the 8-hour 

period are available. In the event that only 6 

(or 7) hourly averages are available, the 8- 

hour average shall be computed on the basis 

of the hours available using 6 (or 7) as the 

divisor (8-hour periods with three or more 

missing hours shall not be ignored if, after 

substituting one-half the minimum detectable 

limit for the missing hourly concentrations, 

the 8-hour average concentration is greater 

than the level of the standard). The computed 

8-hour average O3 concentrations shall be 

reported to three decimal places (the 

insignificant digits to the right of the third 

decimal place are truncated, consistent with 

the data handling procedures for the reported 

data). 

Daily maximum 8-hour average 

concentrations. (a) There are 24 possible 

running 8-hour average O3 concentrations for 

each calendar day during the O3 monitoring 

season. The daily maximum 8-hour 

concentration for a given calendar day is the 

highest of the 24 possible 8-hour average 

concentrations computed for that day. This 

process is repeated, yielding a daily 

maximum 8-hour average O3 concentration 

for each calendar day with ambient O3

monitoring data. Because the 8-hour averages 

are recorded in the start hour, the daily 

maximum 8-hour concentrations from two 

consecutive days may have some hourly 

concentrations in common. Generally, 

overlapping daily maximum 8-hour averages 

are not likely, except in those non-urban 

monitoring locations with less pronounced 

diurnal variation in hourly concentrations. 

(b) An O3 monitoring day shall be counted 

as a valid day if valid 8-hour averages are 

available for at least 75% of possible hours 

in the day (i.e., at least 18 of the 24 averages). 

In the event that less than 75% of the 8-hour 

averages are available, a day shall also be 

counted as a valid day if the daily maximum 

8-hour average concentration for that day is 

greater than the level of the ambient 

standard. 

2.2 Primary Standard-Related Summary 

Statistic 

The standard-related summary statistic is 

the annual fourth-highest daily maximum 8- 

hour O3 concentration, expressed in parts per 

million, averaged over three years. The 3-year 

average shall be computed using the three 

most recent, consecutive calendar years of 

monitoring data meeting the data 

completeness requirements described in this 

appendix. The computed 3-year average of 

the annual fourth-highest daily maximum 8- 

hour average O3 concentrations shall be 

reported to three decimal places (the 

insignificant digits to the right of the third 

decimal place are truncated, consistent with 

the data handling procedures for the reported 

data). 

2.3 Comparisons With the Primary Ozone 

Standard 

(a) The primary O3 ambient air quality 

standard is met at an ambient air quality 

monitoring site when the 3-year average of 

the annual fourth-highest daily maximum 8- 

hour average O3 concentration is less than or 

equal to [0.070 to 0.075] ppm. 

(b) This comparison shall be based on three 

consecutive, complete calendar years of air 

quality monitoring data. This requirement is 

met for the three year period at a monitoring 

site if daily maximum 8-hour average 

concentrations are available for at least 90%, 

on average, of the days during the designated 

O3 monitoring season, with a minimum data 

completeness in any one year of at least 75% 

of the designated sampling days. When 

computing whether the minimum data 

completeness requirements have been met, 

meteorological or ambient data may be 

sufficient to demonstrate that meteorological 

conditions on missing days were not 

conducive to concentrations above the level 

of the standard. Missing days assumed less 

than the level of the standard are counted for 

the purpose of meeting the data completeness 

requirement, subject to the approval of the 

appropriate Regional Administrator. 

(c) Years with concentrations greater than 

the level of the standard shall not be ignored 

on the ground that they have less than 

complete data. Thus, in computing the 3-year 

average fourth maximum concentration, 

calendar years with less than 75% data 

completeness shall be included in the 

computation if the average annual fourth 

maximum 8-hour concentration is greater 

than the level of the standard. 

(d) Comparisons with the primary O3

standard is demonstrated by examples 1 and 

2 in paragraphs (d)(1) and (d)(2) respectively 

as follows: 

EXAMPLE 1.—AMBIENT MONITORING SITE ATTAINING THE PRIMARY O3 STANDARD

Year 

Percent valid 

days 

(percent) 

1st Highest 

daily max 

8-hour Conc. 

(ppm) 

2nd Highest 

daily max 

8-hour Conc. 

(ppm) 

3rd Highest 

daily max 

8-hour Conc. 

(ppm) 

4th Highest 

daily max 

8-hour Conc. 

(ppm) 

5th Highest 

daily max 

8-hour Conc. 

(ppm) 

2004 ......................................................... 100 0.092 0.090 0.085 0.079 0.078 

2005 ......................................................... 96 0.084 0.083 0.075 0.072 0.070 

2006 ......................................................... 98 0.080 0.079 0.073 0.061 0.060 


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37918 Federal Register / Vol. 72, No. 132 / Wednesday, July 11, 2007 / Proposed Rules 

EXAMPLE 1.—AMBIENT MONITORING SITE ATTAINING THE PRIMARY O3 STANDARD

Year 

Percent valid 

days 

(percent) 

1st Highest 

daily max 

8-hour Conc. 

(ppm) 

2nd Highest 

daily max 

8-hour Conc. 

(ppm) 

3rd Highest 

daily max 

8-hour Conc. 

(ppm) 

4th Highest 

daily max 

8-hour Conc. 

(ppm) 

5th Highest 

daily max 

8-hour Conc. 

(ppm) 

Average ............................................. 98 ........................ ........................ ........................ 0.070 ........................

(1) As shown in example 1, the primary 

standard is met at this monitoring site 

because the 3-year average of the annual 

fourth-highest daily maximum 8-hour 

average O3 concentrations (i.e., 0.0707 ppm, 

truncated to 0.070 ppm) is less than or equal 

to [0.070 to 0.75] ppm. The data 

completeness requirement is also met 

because the average percent of days with 

valid ambient monitoring data is greater than 

90%, and no single year has less than 75% 

data completeness. In Example 1, the 

individual 8-hour averages used to determine 

the annual fourth maximum are truncated to 

the third decimal place. 

EXAMPLE 2.—AMBIENT MONITORING SITE FAILING TO MEET THE PRIMARY O3 STANDARD

Year 

Percent valid 

days 

(percent) 

1st Highest 

daily max 

8-hour Conc. 

(ppm) 

2nd Highest 

daily max 

8-hour Conc. 

(ppm) 

3rd Highest 

daily max 

8-hour Conc. 

(ppm) 

4th Highest 

daily max 

8-hour Conc. 

(ppm) 

5th Highest 

daily max 

8-hour Conc. 

(ppm) 

2004 ......................................................... 96 0.105 0.103 0.103 0.102 0.102 

2005 ......................................................... 74 0.104 0.103 0.092 0.091 0.088 

2006 ......................................................... 98 0.103 0.101 0.101 0.095 0.094 

Average ............................................. 89 ........................ ........................ ........................ 0.096 ........................

As shown in example 2, the primary 

standard is not met at this monitoring site 

because the 3-year average of the fourthhighest daily maximum 8-hour average O3

concentrations (i.e., 0.0960 ppm, truncated to 

0.096 ppm) is greater than [0.070 to 0.075] 

ppm. Note that the O3 concentration data for 

2005 is used in these computations, even 

though the data capture is less than 75%, 

because the average fourth-highest daily 

maximum 8-hour average concentration is 

greater than [0.070 to 0.075] ppm. In Example 

2, the individual 8-hour averages used to 

determine the annual fourth maximum are 

truncated to the third decimal place. 

3. Design Values for Primary Ambient Air 

Quality Standards for Ozone 

The air quality design value at a 

monitoring site is defined as that 

concentration that when reduced to the level 

of the standard ensures that the site meets the 

standard. For a concentration-based standard, 

the air quality design value is simply the 

standard-related test statistic. Thus, for the 

primary standard, the 3-year average annual 

fourth-highest daily maximum 8-hour 

average O3 concentration is also the air 

quality design value for the site. 

4. Secondary Ambient Air Quality Standard 

for Ozone 

4.1 Data Reporting and Handling 

Conventions 

Computing the daily index value (D.I.). The 

secondary O3 standard is a seasonal standard 

expressed as the sum of weighted hourly 

concentrations, cumulated over the 12 hour 

daylight period, 8 a.m. to 8 p.m. local 

standard time (LST), during the maximum 

consecutive 3-month period within the O3

monitoring season. Hourly average 

concentrations for each hour from 8 a.m. to 

8 p.m. LST shall be reported in parts per 

million (ppm) to the third decimal place, 

with additional digits to the right being 

truncated. The first step in computing the 

daily index value, D.I., for the daylight hours 

is to apply a sigmoidal weighting function in 

the form of Equation 1 in this appendix: 

Equation 1

O

e 3 126 O

1

1 4403 3

∗ + ∗ ( )















 − ∗

to each measurement of hourly average 

concentration, where O3 is the average hourly 

O3 concentration expressed in ppm. The 

computed value of the sigmoidally weighted 

hourly concentration shall be expressed to 

three decimal places (the remaining digits to 

the right are truncated). An illustration of 

computing a daily index value is below: 

EXAMPLE 3.—DAILY INDEX VALUE CALCULATION FOR AN AMBIENT O3 MONITORING SITE

Start hour Concentration 

(ppm) 

Weighted 

concentration 

(ppm) 

8:00 AM ................................................................................................................................................................... 0.045 0.002 

9:00 AM ................................................................................................................................................................... 0.060 0.018 

10:00 AM ................................................................................................................................................................. 0.075 0.055 

11:00 AM ................................................................................................................................................................. 0.080 0.067 

12:00 PM ................................................................................................................................................................. 0.079 0.065 

1:00 PM ................................................................................................................................................................... 0.082 0.071 

2:00 PM ................................................................................................................................................................... 0.085 0.077 

3:00 PM ................................................................................................................................................................... 0.088 0.082 

4:00 PM ................................................................................................................................................................... 0.083 0.073 

5:00 PM ................................................................................................................................................................... 0.081 0.069 

6:00 PM ................................................................................................................................................................... 0.065 0.029 

7:00 PM ................................................................................................................................................................... 0.056 0.011 


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Daily index value (D.I.) = 0.002 + 0.018 + 

0.055 + 0.067 + 0.065 + 0.071 + 0.077 + 

0.082 + 0.073 + 0.069 + 0.029 + 0.011 = 

0.619 ppm-hours 

Computing the monthly cumulative index 

(W126). The daily index value is computed 

at each monitoring site for each calendar day 

in each month during the O3 monitoring. At 

an individual monitoring site, a month is 

counted as a valid O3 monitoring month if 

hourly average O3 concentrations are 

available for at least 75% of the possible 

index hours in the month. For months with 

less than 75% data completeness, the 

monthly cumulative index value shall be 

adjusted for incomplete sampling by 

multiplying the unadjusted W126 cumulative 

index value by the ratio of the number of 

possible daylight hours to the number of 

hours with valid ambient hourly 

concentrations using Equation 2 in this 

appendix: 

Equation 2

MI DI n v

j

n

. . ( . .) ( )/ = ∗∗ =

∑ 12 1

Where, 

M.I. = the monthly sum of the weighted 

daylight hours, 

D.I. = the daily sum of the weighted daylight 

hours, 

n = the number of days in the calendar 

month, 

v = the number of daylight hours (8:00 a.m.—

8:00 p.m. LST) with valid hourly O3

concentrations. 

4.2 Secondary Standard-related Summary 

Statistic 

The standard-related summary statistic is 

the annual maximum consecutive 3-month 

W126 value expressed in ppm-hours. 

Specifically, the annual W126 value is 

computed on a calendar year basis using the 

three highest, consecutive monthly W126 

values. 

4.3 Comparisons with the Secondary Ozone 

Standard 

The secondary ambient O3 air quality 

standard is met when the annual maximum 

W126 value based on a consecutive 3-month 

period at an O3 air quality monitoring site is 

less than or equal to [7 to 21] ppm-hours. The 

number of significant figures in the level of 

the standard dictates the rounding 

convention for comparing the computed 

W126 value with the level of the standard. 

The first decimal place of the computed 

W126 value is rounded, with values equal to 

or greater than of 0.5 rounding up. 

EXAMPLE 4.—CALCULATION OF THE MAXIMUM 3-MONTH W126 VALUE AT AN AMBIENT AIR QUALITY MONITORING SITE

FAILING TO MEET THE SECONDARY O3 STANDARD

April May June July August September October 

Monthly W126 ........................................... 4.442 9.124 12.983 16.153 13.555 4.364 1.302 

3-Month Total ............................................ na na 26.549 38.260 42.691 34.072 19.221 

As shown in example 4, the maximum 

consecutive 3-month W126 value for this site 

is 43 ppm-hours. Because 43 ppm-hours is 

greater than [7 to 21] ppm-hours, the 

secondary standard is not met at this ambient 

air quality monitoring site. 

[FR Doc. E7–12416 Filed 7–10–07; 8:45 am] 

BILLING CODE 6560–50–P 


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