Draft O3 NPR - January 5, 2010 Deliberative, Do Not Quote or Cite

1 6560-50-P

2 ENVIRONMENTAL PROTECTION AGENCY

3

4 40 CFR Part 50

5

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

7

8 RIN 2060- this # has not been assigned yet

9 

10 National Ambient Air Quality Standards for Ozone

11

12

13 AGENCY: Environmental Protection Agency (EPA).

14 ACTION: Proposed rule.

15 SUMMARY: Based on its reconsideration of the primary and secondary national 

16 ambient air quality standards (NAAQS) for ozone (O3) set in March 2008, EPA proposes 

17 to set different primary and secondary standards than those set in 2008 to provide 

18 requisite protection of public health and welfare, respectively. With regard to the 

19 primary standard for O3, EPA proposes that the level of the 8-hour primary standard, 

20 which was set at 0.075 ppm in the 2008 final rule, should instead be set at a lower level 

21 within the range of 0.060 to 0.070 parts per million (ppm), to provide increased 

22 protection for children and other “at risk” populations against an array of O3-related 

23 adverse health effects that range from decreased lung function and increased respiratory

24 symptoms to serious indicators of respiratory morbidity including emergency department 

25 visits and hospital admissions for respiratory causes, and possibly cardiovascular-related 

26 morbidity as well as total non-accidental and cardiopulmonary mortality. With regard to 

27 the secondary standard for O3, EPA proposes that the secondary O3 standard, which was 

28 set identical to the revised primary standard in the 2008 final rule, should instead be a 

29 new cumulative, seasonal standard expressed as an annual index of the sum of weighted 
Draft O3 NPR –January 5, 2010 2 Deliberative, Do Not Quote or Cite

1 hourly concentrations, cumulated over 12 hours per day (8:00 am to 8:00 pm) during the 

2 consecutive 3-month period within the O3 season with the maximum index value, set at a 

3 level within the range of 7 to 15 ppm-hours, to provide increased protection against O3-

4 related adverse impacts on vegetation and forested ecosystems.

5 DATES: Written comments on this proposed rule must be received by [insert date 60

6 days after date of publication in the Federal Register].

7 Public Hearings: Three public hearings are scheduled for this proposed rule. 

8 Two of the public hearings will be held on February 2, 2010 in Arlington, Virginia and 

9 Houston, Texas. The third public hearing will be held on February 4, 2010 in 

10 Sacramento, California.

11 ADDRESSES: Submit your comments, identified by Docket ID No. EPA-HQ-OAR12 2005-0172, by one of the following methods:

13  www.regulations.gov: Follow the on-line instructions for submitting comments.

14  Email: a-and-r-Docket@epa.gov.

15  Fax: 202-566-9744.

16  Mail: Docket No. EPA-HQ-OAR-2005-0172, Environmental Protection Agency, 

17 Mail code 6102T, 1200 Pennsylvania Ave., NW, Washington, DC 20460. Please 

18 include a total of two copies. 

19  Hand Delivery: Docket No. EPA-HQ-OAR-2005-0172, Environmental 

20 Protection Agency, EPA West, Room 3334, 1301 Constitution Ave., NW, 

21 Washington, DC. Such deliveries are only accepted during the Docket’s normal 

22 hours of operation, and special arrangements should be made for deliveries of 

23 boxed information.
Draft O3 NPR –January 5, 2010 3 Deliberative, Do Not Quote or Cite

1 Public Hearings: Three public hearings are scheduled for this proposed rule. 

2 Two of the public hearings will be held on February 2, 2010 in Arlington, Virginia and 

3 Houston, Texas. The third public hearing will be held on February 4, 2010 in 

4 Sacramento, California. The hearings will be held at the following locations:

5 Arlington, Virginia – February 2, 2010

6

7 Hyatt Regency Crystal City @ Reagan National Airport

8 Washington Room (located on the Ballroom Level)

9 2799 Jefferson Davis Highway

10 Arlington, Virginia 22202

11 Telephone: 703-418-1234

12

13 Houston, Texas – February 2, 2010

14

15 Hilton Houston Hobby Airport

16 Moody Ballroom (located on the ground floor)

17 8181 Airport Boulevard

18 Houston, Texas 77061

19 Telephone: 713-645-3000

20

21 Sacramento, California – February 4, 2010

22

23 Four Points by Sheraton Sacramento International Airport

24 Natomas Ballroom

25 4900 Duckhorn Drive

26 Sacramento, California 95834

27 Telephone: 916-263-9000

28 See the SUPPLEMENTARY INFORMATION under “Public Hearings” for 

29 further information.

30 Instructions: Direct your comments to Docket ID No. EPA-HQ-OAR-2005-

31 0172. The EPA’s policy is that all comments received will be included in the public 

32 docket without change and may be made available online at www.regulations.gov, 

33 including any personal information provided, unless the comment includes information 

34 claimed to be Confidential Business Information (CBI) or other information whose 
Draft O3 NPR –January 5, 2010 4 Deliberative, Do Not Quote or Cite

1 disclosure is restricted by statute. Do not submit information that you consider to be CBI 

2 or otherwise protected through www.regulations.gov or email. The www.regulations.gov

3 website is an “anonymous access” system, which means EPA will not know your identity

4 or contact information unless you provide it in the body of your comment. If you send an 

5 email comment directly to EPA without going through www.regulations.gov, your email 

6 address will be automatically captured and included as part of the comment that is placed 

7 in the public docket and made available on the Internet. If you submit an electronic 

8 comment, EPA recommends that you include your name and other contact information in 

9 the body of your comment and with any disk or CD-ROM you submit. If EPA cannot 

10 read your comment due to technical difficulties and cannot contact you for clarification, 

11 EPA may not be able to consider your comment. Electronic files should avoid the use of 

12 special characters, any form of encryption, and be free of any defects or viruses. 

13 Docket: All documents in the docket are listed in the www.regulations.gov index. 

14 Although listed in the index, some information is not publicly available, e.g., CBI or 

15 other information whose disclosure is restricted by statute. Certain other material, such 

16 as copyrighted material, will be publicly available only in hard copy. Publicly available 

17 docket materials are available either electronically in www.regulations.gov or in hard 

18 copy at the Air and Radiation Docket and Information Center, EPA/DC, EPA West, 

19 Room 3334, 1301 Constitution Ave., NW, Washington, DC. The Public Reading Room 

20 is open from 8:30 a.m. to 4:30 p.m., Monday through Friday, excluding legal holidays. 

21 The telephone number for the Public Reading Room is (202) 566-1744 and the telephone 

22 number for the Air and Radiation Docket and Information Center is (202) 566-1742. 
Draft O3 NPR –January 5, 2010 5 Deliberative, Do Not Quote or Cite

1 FOR FURTHER INFORMATION CONTACT: Ms. Susan Lyon Stone, Health and 

2 Environmental Impacts Division, Office of Air Quality Planning and Standards, U.S. 

3 Environmental Protection Agency, Mail code C504-06, Research Triangle Park, NC 

4 27711; telephone: 919-541-1146; fax: 919-541-0237; email: stone.susan@epa.gov.

5 SUPPLEMENTARY INFORMATION:

6 General Information

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

8 1. Submitting CBI. Do not submit this information to EPA through 

9 www.regulations.gov or email. Clearly mark the part or all of the information that you 

10 claim to be CBI. For CBI information in a disk or CD ROM that you mail to EPA, mark 

11 the outside of the disk or CD ROM as CBI and then identify electronically within the disk 

12 or CD ROM the specific information that is claimed as CBI. In addition to one complete 

13 version of the comment that includes information claimed as CBI, a copy of the comment 

14 that does not contain the information claimed as CBI must be submitted for inclusion in 

15 the public docket. Information so marked will not be disclosed except in accordance with 

16 procedures set forth in 40 CFR part 2.

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

18 to:

19  Identify the rulemaking by docket number and other identifying information 

20 (subject heading, Federal Register date and page number).

21  Follow directions – The Agency may ask you to respond to specific questions or 

22 organize comments by referencing a Code of Federal Regulations (CFR) part or 

23 section number.
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1  Explain why you agree or disagree, suggest alternatives, and substitute language 

2 for your requested changes.

3  Describe any assumptions and provide any technical information and/or data that 

4 you used.

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

6  Explain your views as clearly as possible, avoiding the use of profanity or 

7 personal threats.

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

9 Availability of Related Information

10 A number of documents relevant to this rulemaking are available on EPA web 

11 sites. The Air Quality Criteria for Ozone and Related Photochemical Oxidants (2006 

12 Criteria Document) (two volumes, EPA/ and EPA/, date) is available on EPA’s National 

13 Center for Environmental Assessment web site. To obtain this document, go to 

14 http://www.epa.gov/ncea, and click on Ozone in the Quick Finder section. This will open 

15 a page with a link to the March 2006 Air Quality Criteria Document. The 2007 Staff 

16 Paper, human exposure and health risk assessments, vegetation exposure and impact 

17 assessment, and other related technical documents are available on EPA’s Office of Air 

18 Quality Planning and Standards (OAQPS) Technology Transfer Network (TTN) web site. 

19 The updated final 2007 Staff Paper is available at: 

20 http://epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_sp.html and the exposure and risk 

21 assessments and other related technical documents are available at 

22 http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_td.html. The Response to 

23 Significant Comments Document is available at: 
Draft O3 NPR –January 5, 2010 7 Deliberative, Do Not Quote or Cite

1 http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_rc.html. These and other related 

2 documents are also available for inspection and copying in the EPA docket identified 

3 above.

4 Public Hearings

5 The public hearings on February 2, 2010 and February 4, 2010 will provide 

6 interested parties the opportunity to present data, views, or arguments concerning the 

7 proposed rule. The EPA may ask clarifying questions during the oral presentations, but 

8 will not respond to the presentations at that time. Written statements and supporting 

9 information submitted during the comment period will be considered with the same 

10 weight as any oral comments and supporting information presented at the public hearing. 

11 Written comments must be received by the last day of the comment period, as specified 

12 in this proposed rulemaking.

13 The public hearings will begin at 9:30 a.m. and continue until 7:30 p.m. (local 

14 time) or later, if necessary, depending on the number of speakers wishing to participate. 

15 The EPA will make every effort to accommodate all speakers that arrive and register 

16 before 7:30 p.m. A lunch break is scheduled from 12:30 p.m. until 2:00 p.m.

17 If you would like to present oral testimony at the hearings, please notify Ms. 

18 Tricia Crabtree (C504-02), U.S. EPA, Research Triangle Park, NC 27711. The preferred 

19 method for registering is by e-mail (crabtree.tricia@epa.gov). Ms. Crabtree may be 

20 reached by telephone at (919) 541-5688. She will arrange a general time slot for you to 

21 speak. The EPA will make every effort to follow the schedule as closely as possible on 

22 the day of the hearing.
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1 Oral testimony will be limited to five (5) minutes for each commenter to address 

2 the proposal. We will not be providing equipment for commenters to show overhead 

3 slides or make computerized slide presentations unless we receive special requests in 

4 advance. Commenters should notify Ms. Crabtree if they will need specific audiovisual 

5 (AV) equipment. Commenters should also notify Ms. Crabtree if they need specific 

6 translation services for non-English speaking commenters. The EPA encourages 

7 commenters to provide written versions of their oral testimonies either electronically on 

8 computer disk, CD-ROM, or in paper copy.

9 The hearing schedules, including lists of speakers, will be posted on EPA’s web 

10 site for the proposal at http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_fr.html

11 prior to the hearing. Verbatim transcripts of the hearings and written statements will be 

12 included in the rulemaking docket.

13 Children’s Environmental Health 

14 Consideration of children’s environmental health plays a central role in the 

15 reconsideration of the 2008 final decision on the O3 NAAQS and EPA’s decision to 

16 propose to set the 8-hour primary O3 standard at a level within the range of 0.060 to 

17 0.070 ppm. Technical information that pertains to children, including the evaluation of 

18 scientific evidence, policy considerations, and exposure and risk assessments, is 

19 discussed in all of the documents listed above in the section on the availability of related 

20 information. These documents include: the Air Quality Criteria for Ozone and Other 

21 Related Photochemical Oxidants; the 2007 Staff Paper; exposure and risk assessments 

22 and other related documents; and the Response to Significant Comments. All of these 

23 documents are available on the Web, as described above, and are in the public docket for 
Draft O3 NPR –January 5, 2010 9 Deliberative, Do Not Quote or Cite

1 this rulemaking. The public is invited to submit comments or identify peer-reviewed 

2 studies and data that assess effects of early life exposure to O3.

3 Table of Contents

4 The following topics are discussed in this preamble:

5 I. Background

6 A. Legislative Requirements 

7 B. Related Control Requirements

8 C. Review of Air Quality Criteria and Standards for O3

9 D. Reconsideration of the 2008 O3 NAAQS Final Rule

10 1. Decision to Initiate a Rulemaking to Reconsider

11 2. Ongoing Litigation

12

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

14 A. Health Effects Information

15 1. Overview of Mechanisms

16 2. Nature of Effects

17 3. Interpretation and Integration of Health Evidence

18 4. O3-Related Impacts on Public Health

19 B. Human Exposure and Health Risk Assessments

20 1. Exposure Analyses

21 2. Quantitative Health Risk Assessment

22 C. Reconsideration of the Level of the Primary Standard

23 1. Evidence and Exposure/Risk-Based Considerations

24 2. CASAC Views Prior to 2008 Decision

25 3. Basis for 2008 Decision on the Primary Standard

26 4. CASAC Advice Following 2008 Decision

27 5. Administrator’s Proposed Conclusions

28 D. Proposed Decision on the Level of the Primary Standard

29

30 III. Communication of Public Health Information

31

32 IV. Rationale for Proposed Decision on the Secondary Standard

33 A. Vegetation Effects Information

34 1. Mechanisms

35 2. Nature of Effects

36 3. Adversity of Effects

37 B. Biologically Relevant Exposure Indices

38 C. Vegetation Exposure and Impact Assessment

39 1. Exposure Characterization

40 2. Assessment of Risks to Vegetation

41 D. Reconsideration of Secondary Standard
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1 1. Considerations Regarding 2007 Proposed Cumulative Seasonal 

2 Standard

3 2. Considerations Regarding 2007 Proposed 8-Hour Standard

4 3. Basis for 2008 Decision on the Secondary Standard

5 4. CASAC Views Following 2008 Decision

6 5. Administrator’s Proposed Conclusions

7 E. Proposed Decision on the Secondary O3 Standard

8

9 V. Revision of Appendix P -- Interpretation of the NAAQS for O3 and Proposed 

10 Revisions to the Exceptional Events Rule

11 A. Background

12 B. Interpretation of the Secondary O3 Standard

13 C. Clarifications Related to the Primary Standard

14 D. Revisions to Exceptions from Standard Data Completeness Requirements 

15 for the Primary Standard

16 E. Elimination of the Requirement for 90 Percent Completeness of Daily 

17 Data across Three Years

18 F. Administrator Discretion to Use Incomplete Data

19 G. Truncation versus Rounding

20 H. Data Selection

21 I. Exceptional Events Information Submission Schedule

22

23 VI. Ambient Monitoring Related to Proposed O3 Standards

24 A. Background

25 B. Urban Monitoring Requirements

26 C. Non-Urban Monitoring Requirements

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

28

29 VII. Implementation of Proposed O3 Standards

30 A. Designations

31 B. State Implementation Plans

32 C. Trans-boundary Emissions

33

34 VIII. Statutory and Executive Order Reviews

35 A. Executive Order 12866: Regulatory Planning and Review

36 B. Paperwork Reduction Act

37 C. Regulatory Flexibility Act

38 D. Unfunded Mandates Reform Act

39 E. Executive Order 13132: Federalism

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

41 Governments

42 G. Executive Order 13045: Protection of Children from Environmental 

43 Health and Safety Risks

44 H. Executive Order 13211: Actions that Significantly Affect Energy Supply, 

45 Distribution or Use

46 I. National Technology Transfer and Advancement Act
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1 J. Executive Order 12898: Federal Actions to Address Environmental Justice 

2 in Minority Populations and Low-Income Populations

3

4 References

5

6 I. Background

7 The proposed decisions presented in this notice are based on a reconsideration of 

8 the 2008 O3 NAAQS final rule (73 FR 16436, March 27, 2008), which revised the level 

9 of the 8-hour primary O3 standard to 0.075 ppm and revised the secondary O3 standard by

10 making it identical to the revised primary standard. This reconsideration is based on the 

11 scientific and technical information and analyses on which the March 2008 O3 NAAQS

12 rulemaking was based. Therefore, much of the information included in this notice is 

13 drawn directly from information included in the 2007 proposed rule (72 FR 37818, July

14 11, 2007) and the 2008 final rule (73 FR 16436).

15 A. Legislative Requirements

16 Two sections of the Clean Air Act (CAA) govern the establishment and revision 

17 of the NAAQS. Section 108 (42 U.S.C. 7408) directs the Administrator to identify and 

18 list “air pollutants” that in her “judgment, cause or contribute to air pollution which may

19 reasonably be anticipated to endanger public health or welfare” and satisfy two other 

20 criteria, including “whose presence . . . in the ambient air results from numerous or 

21 diverse mobile or stationary sources” and to issue air quality criteria for those that are 

22 listed. Air quality criteria are intended to “accurately reflect the latest scientific 

23 knowledge useful in indicating the kind and extent of all identifiable effects on public 

24 health or welfare which may be expected from the presence of [a] pollutant in the 

25 ambient air . . . .”
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1 Section 109 (42 U.S.C. 7409) directs the Administrator to propose and 

2 promulgate “primary” and “secondary” NAAQS for pollutants for which air quality

3 criteria are issued. Section 109(b)(1) defines a primary standard as one “the attainment 

4 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

5 A 

6 secondary standard, as defined in section 109(b)(2), must “specify a level of air quality 

7 the attainment and maintenance of which, in the judgment of the Administrator, based on 

8 such criteria, is requisite to protect the public welfare from any known or anticipated 

adverse effects associated with the presence of such air pollutant in the ambient air.”

2

9

10 The requirement that primary standards include an adequate margin of safety was 

11 intended to address uncertainties associated with inconclusive scientific and technical 

12 information available at the time of standard setting. It was also intended to provide a 

13 reasonable degree of protection against hazards that research has not yet identified. Lead 

14 Industries Association v. EPA, 647 F.2d 1130, 1154 (D.C. Cir 1980), cert. denied, 449 

15 U.S. 1042 (1980); American Petroleum Institute v. Costle, 665 F.2d 1176, 1186 (D.C. 

16 Cir. 1981), cert. denied, 455 U.S. 1034 (1982). Both kinds of uncertainties are 

17 components of the risk associated with pollution at levels below those at which human 

 

1

The legislative history of section 109 indicates that a primary standard is to be 

set at “the maximum permissible ambient air level . . . which will protect the health of 

any [sensitive] group of the population,” and that for this purpose “reference should be 

made to a representative sample of persons comprising the sensitive group rather than to 

a single person in such a group” [S. Rep. No. 91-1196, 91st Cong., 2d Sess. 10 (1970)].

2 Welfare effects as defined in section 302(h) (42 U.S.C. 7602(h)) include, but are 

not limited to, “effects on soils, water, crops, vegetation, man-made materials, animals, 

wildlife, weather, visibility, and climate, damage to and deterioration of property, and 

hazards to transportation, as well as effects on economic values and on personal comfort 

and well-being.”
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1 health effects can be said to occur with reasonable scientific certainty. Thus, in selecting 

2 primary standards that include an adequate margin of safety, the Administrator is seeking 

3 not only to prevent pollution levels that have been demonstrated to be harmful but also to 

4 prevent lower pollutant levels that may pose an unacceptable risk of harm, even if the risk 

5 is not precisely identified as to nature or degree. The CAA does not require the 

6 Administrator to establish a primary NAAQS at a zero-risk level or at background 

7 concentration levels, see Lead Industries Association v. EPA, 647 F.2d at 1156 n. 51, but 

8 rather at a level that reduces risk sufficiently so as to protect public health with an 

9 adequate margin of safety.

10 In addressing the requirement for an adequate margin of safety, EPA considers 

11 such factors as the nature and severity of the health effects involved, the size of the 

12 population(s) at risk, and the kind and degree of the uncertainties that must be addressed. 

13 The selection of any particular approach to providing an adequate margin of safety is a 

14 policy choice left specifically to the Administrator’s judgment. Lead Industries

15 Association v. EPA, 647 F.2d at 1161-62; Whitman v. American Trucking Associations, 

16 531 U.S. 457, 495 (2001).

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

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

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

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

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

22 Section 109(d)(1) of the CAA requires that “not later than December 31, 1980, 

23 and at 5-year intervals thereafter, the Administrator shall complete a thorough review of 
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1 the criteria published under section 108 and the national ambient air quality standards . . . 

2 and shall make such revisions in such criteria and standards and promulgate such new 

3 standards as may be appropriate . . . .” Section 109(d)(2) requires that an independent 

4 scientific review committee “shall complete a review of the criteria . . . and the national 

5 primary and secondary ambient air quality standards . . . and shall recommend to the 

6 Administrator any new . . . standards and revisions of existing criteria and standards as 

7 may be appropriate . . . .” This independent review function is performed by the Clean 

8 Air Scientific Advisory Committee (CASAC) of EPA’s Science Advisory Board.

9 B. Related Control Requirements

10 States have primary responsibility for ensuring attainment and maintenance of 

11 ambient air quality standards once EPA has established them. Under section 110 of the 

12 Act (42 U.S.C. 7410) and related provisions, States are to submit, for EPA approval, 

13 State implementation plans (SIPs) that provide for the attainment and maintenance of 

14 such standards through control programs directed to emission sources. 

15 The majority of man-made nitrogen oxides (NOx) and volatile organic compounds 

16 (VOC) emissions that contribute to O3 formation in the United States come from three 

17 types of sources: mobile sources, industrial processes (which include consumer and 

commercial products), and the electric power industry.

3

18 Mobile sources and the electric 

19 power industry were responsible for 78 percent of annual NOx emissions in 2004. That 

20 same year, 99 percent of man-made VOC emissions came from industrial processes 

21 (including solvents) and mobile sources. Emissions from natural sources, such as trees, 

 

3

 See EPA report, Evaluating Ozone Control Programs in the Eastern United 

States: Focus on the NOx Budget Trading Program, 2004.
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1 may also comprise a significant portion of total VOC emissions in certain regions of the 

2 country, especially during the O3 season, which are considered natural background 

3 emissions.

4 The EPA has developed new emissions standards for many types of stationary 

5 sources and for nearly every class of mobile sources in the last decade to reduce O3 by

6 decreasing emissions of NOx and VOC. These programs complement State and local 

7 efforts to improve O3 air quality and meet the 0.084 ppm 8-hour national standards. 

8 Under title II of the CAA, 42 U.S.C. 7521-7574), EPA has established new emissions 

9 standards for nearly every type of automobile, truck, bus, motorcycle, earth mover, and 

10 aircraft engine, and for the fuels used to power these engines. EPA also established new 

11 standards for the smaller engines used in small watercraft, lawn and garden equipment. 

12 In March 2008, EPA promulgated new standards for locomotive and marine diesel 

13 engines and in August 2009, proposed to control emissions from ocean-going vessels. 

14 Benefits from engine standards increase modestly each year as older, more15 polluting vehicles and engines are replaced with newer, cleaner models. In time, these 

16 programs will yield substantial emission reductions. Benefits from fuel programs 

17 generally begin as soon as a new fuel is available.

18 The reduction of VOC emissions from industrial processes has been achieved 

19 either directly or indirectly through implementation of control technology standards, 

20 including maximum achievable control technology, reasonably available control 

21 technology, and best available control technology standards; or are anticipated due to 

22 proposed or upcoming proposals based on generally available control technology or best 

23 available controls under provisions related to consumer and commercial products. These 
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1 standards have resulted in VOC emission reductions of almost a million tons per year 

2 accumulated starting in 1997 from a variety of sources including combustion sources, 

3 coating categories, and chemical manufacturing. EPA has also finalized emission 

4 standards and fuel requirements for new stationary engines. In the area of consumer and 

5 commercial products, EPA has finalized new national VOC emission standards for 

6 aerosol coatings and is working toward amending existing rules to establish new 

7 nationwide VOC content limits for household and institutional consumer products and 

8 architectural and industrial maintenance coatings. The aerosol coatings rule took effect 

9 in July 2009; the compliance date for both the amended consumer product rule and 

10 architectural coatings rule is anticipated to be January 2011. These actions are expected 

11 to yield significant new VOC reductions – about 200,000 tons per year. Additionally, in 

12 ozone nonattainment areas, we anticipate reductions of an additional 25,000 tons per year 

13 as States adopt rules this year implementing control techniques recommendations issued 

14 in 2008 for 4 additional categories of consumer and commercial products, typically

15 surface coatings and adhesives used in industrial manufacturing operations. These 

16 emission reductions primarily result from solvent controls and typically occur where and 

17 when the solvent is used, such as during manufacturing processes. 

18 The power industry is one of the largest emitters of NOx in the United States. 

19 Power industry emission sources include large electric generating units (EGU) and some 

20 large industrial boilers and turbines. The EPA’s landmark Clean Air Interstate Rule 

21 (CAIR), issued on March 10, 2005, was designed to permanently cap power industry

22 emissions of NOx in the eastern United States. The first phase of the cap was to begin in 

23 2009, and a lower second phase cap was to begin in 2015. The EPA had projected that 
Draft O3 NPR –January 5, 2010 17 Deliberative, Do Not Quote or Cite

1 by 2015, the CAIR and other programs would reduce NOx emissions during the O3 season 

2 by about 50 percent and annual NOx emissions by about 60 percent from 2003 levels in 

3 the Eastern U.S. However, on July 11, 2008 and December 23, 2008, the U.S. Court of 

4 Appeals for the D.C. Circuit issued decisions on petitions for review of the CAIR. In its 

5 July 11 opinion, the court found CAIR unlawful and decided to vacate CAIR and its 

6 associated Federal implementation plans (FIPs) in their entirety. On December 23, the 

7 court granted EPA’s petition for rehearing to the extent that it remanded without vacatur 

8 for EPA to conduct further proceedings consistent with the Court’s prior opinion. Under 

9 this decision, CAIR will remain in place only until replaced by EPA with a rule that is 

10 consistent with the Court’s July 11 opinion. The EPA recognizes the need in our CAIR 

11 replacement effort to address the reconsidered ozone standard, and we are currently 

12 assessing our options for the best way to accomplish this. It should also be noted that 

13 new electric generating units (EGUs) are also subject to NOx limits under New Source

14 Performance Standards (NSPS) under CAA section 111, as well as either nonattainment

15 new source review or prevention of significant deterioration requirements.

16 With respect to agricultural sources, the U.S. Department of Agriculture (USDA) 

17 has approved conservation systems and activities that reduce agricultural emissions of 

18 NOx and VOC. Current practices that may reduce emissions of NOx and VOC include 

19 engine replacement programs, diesel retrofit programs, manipulation of pesticide 

20 applications including timing of applications, and animal feeding operations waste 

21 management techniques. The EPA recognizes that USDA has been working with the 

22 agricultural community to develop conservation systems and activities to control 

23 emissions of O3 precursors.
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1 These conservation activities are voluntarily adopted through the use of incentives 

2 provided to the agricultural producer. In cases where the States need these measures to 

3 attain the standard, the measures could be adopted. The EPA will continue to work with 

4 USDA on these activities with efforts to identify and/or improve the control efficiencies, 

5 prioritize the adoption of these conservation systems and activities, and ensure that 

6 appropriate criteria are used for identifying the most effective application of conservation 

7 systems and activities. 

8 The EPA will work together with USDA and with States to identify appropriate 

9 measures to meet the primary and secondary standards, including site-specific 

10 conservation systems and activities. Based on prior experience identifying conservation 

11 measures and practices to meet the PM NAAQS requirements, the EPA will use a similar 

12 process to identify measures that could meet the O3 requirements. The EPA anticipates

13 that certain USDA-approved conservation systems and activities that reduce agricultural 

14 emissions of NOx and VOC may be able to satisfy the requirements for applicable 

15 sources to implement reasonably available control measures for purposes of attaining the 

16 primary and secondary O3 NAAQS.

17 C. Review of Air Quality Criteria and Standards for O3

18 In 1971, EPA first established primary and secondary NAAQS for photochemical 

19 oxidants (36 FR 8186). Both primary and secondary standards were set at a level of 0.08 

20 parts per million (ppm), 1-hr average, total photochemical oxidants, not to be exceeded 

21 more than one hr per year. In 1977, EPA announced the first periodic review of the air 

22 quality criteria in accordance with section 109(d)(1) of the Act. The EPA published a 

23 final decision in 1979 (44 FR 8202). Both primary and secondary standard levels were
Draft O3 NPR –January 5, 2010 19 Deliberative, Do Not Quote or Cite

1 revised from 0.08 to 0.12 ppm. The indicator was revised from photochemical oxidants 

2 to O3, and the form of the standards was revised from a deterministic to a statistical form, 

3 which defined attainment of the standards as occurring when the expected number of 

4 days per calendar year with maximum hourly average concentration greater than 0.12 

5 ppm is equal to or less than one. In 1983, EPA announced that the second periodic 

6 review of the primary and secondary standards for O3 had been initiated. Following 

7 review and publication of air quality criteria and a supplement, EPA published a 

8 proposed decision (57 FR 35542) in August 1992 that announced EPA’s intention to 

9 proceed as rapidly as possible with the next review of the air quality criteria and 

10 standards for O3 in light of emerging evidence of health effects related to 6- to 8-hr O3

11 exposures. In March 1993, EPA concluded the review by deciding that revisions to the 

12 standards were not warranted at that time (58 FR 13008).

13 In August 1992 (57 FR 35542), EPA announced plans to initiate the third periodic 

14 review of the air quality criteria and O3 NAAQS. On the basis of the scientific evidence

15 contained in the 1996 CD (U.S. EPA 1996a) and the 1996 Staff Paper (U.S. EPA, 

16 1996b), and related technical support documents, linking exposures to ambient O3 to 

17 adverse health and welfare effects at levels allowed by the then existing standards, EPA 

18 proposed to revise the primary and secondary O3 standards in December 1996 (61 FR 

19 65716). The EPA proposed to replace the then existing 1-hour primary and secondary

20 standards with 8-hour average O3 standards set at a level of 0.08 ppm (equivalent to 

21 0.084 ppm using standard rounding conventions). The EPA also proposed, in the 

22 alternative, to establish a new distinct secondary standard using a biologically based 

23 cumulative seasonal form. The EPA completed the review in July 1997 (62 FR 38856)
Draft O3 NPR –January 5, 2010 20 Deliberative, Do Not Quote or Cite

1 by setting the primary standard at a level of 0.08 ppm, based on the annual fourth-highest 

2 daily maximum 8-hr average concentration, averaged over three years, and setting the 

3 secondary standard identical to the revised primary standard.

4 The EPA initiated the most recent periodic review of the air quality criteria and 

5 standards for O3 in September 2000 with a call for information (65 FR 57810; September

6 26, 2000) for the development of a revised Air Quality Criteria Document for O3 and 

7 Other Photochemical Oxidants (henceforth the "2006 Criteria Document"). A project 

8 work plan (EPA, 2002) for the preparation of the Criteria Document was released in 

9 November 2002 for CASAC and public review. The EPA held a series of workshops in 

10 mid-2003 on several draft chapters of the Criteria Document to obtain broad input from 

11 the relevant scientific communities. These workshops helped to inform the preparation 

12 of the first draft Criteria Document (EPA, 2005a), which was released for CASAC and 

13 public review on January 31, 2005; a CASAC meeting was held on May 4-5, 2005 to 

14 review the first draft Criteria Document. A second draft Criteria Document (EPA, 

15 2005b) was released for CASAC and public review on August 31, 2005, and was 

16 discussed along with a first draft Staff Paper (EPA, 2005c) at a CASAC meeting held on 

17 December 6-8, 2005. In a February 16, 2006 letter to the Administrator, CASAC 

18 provided comments on the second draft Criteria Document (Henderson, 2006a), and the 

19 final 2006 Criteria Document (EPA, 2006a) was released on March 21, 2006. In a June 

20 8, 2006 letter to the Administrator (Henderson, 2006b), CASAC provided additional 

21 advice to the Agency concerning chapter 8 of the final 2006 Criteria Document 

22 (Integrative Synthesis) to help inform the second draft Staff Paper. 
Draft O3 NPR –January 5, 2010 21 Deliberative, Do Not Quote or Cite

1 A second draft Staff Paper (EPA, 2006b) was released on July 17, 2006 and 

2 reviewed by CASAC on August 24-25, 2006. In an October 24, 2006 letter to the 

3 Administrator, CASAC provided advice and recommendations to the Agency concerning 

4 the second draft Staff Paper (Henderson, 2006c). A final 2007 Staff Paper (EPA, 2007a) 

5 was released on January 31, 2007. In a March 26, 2007 letter (Henderson, 2007), 

6 CASAC offered additional advice to the Administrator with regard to recommendations 

7 and revisions to the primary and secondary O3 NAAQS. 

8 The schedule for completion of the 2008 rulemaking was governed by a consent 

9 decree resolving a lawsuit filed in March 2003 by a group of plaintiffs representing 

10 national environmental and public health organizations, alleging that EPA had failed to 

complete the review within the period provided by statute.411 The modified consent decree 

12 that governed the 2008 rulemaking, entered by the court on December 16, 2004, provided 

13 that EPA sign for publication notices of proposed and final rulemaking concerning its 

14 review of the O3 NAAQS no later than March 28, 2007 and December 19, 2007, 

15 respectively. That consent decree was further modified in October 2006 to change these 

16 proposed and final rulemaking dates to no later than May 30, 2007 and February 20, 

17 2008, respectively. These dates for signing the publication notices of proposed and final 

18 rulemaking were further extended to no later than June 20, 2007 and March 12, 2008, 

19 respectively. The proposed decision was signed on June 20, 2007 and published in the 

20 Federal Register on July 11, 2007 (72 FR 37818).

21 Public hearings on the proposed decision were held on Thursday, August 30, 2007

22 in Philadelphia, PA and Los Angeles, CA. On Wednesday, September 5, 2007, hearings 

 

4

American Lung Association v. Whitman (No. 1:03CV00778, D.D.C. 2003).
Draft O3 NPR –January 5, 2010 22 Deliberative, Do Not Quote or Cite

1 were held in Atlanta, GA, Chicago, IL, and Houston, TX. A large number of comments 

2 were received from various commenters on the 2007 proposed revisions to the O3

3 NAAQS. A comprehensive summary of all significant comments, along with EPA’s 

4 responses (henceforth “Response to Comments”), can be found in the docket for the 2008

5 rulemaking, which is also the docket for this reconsideration rulemaking.

6 The EPA’s final decision on the O3 NAAAQS was published in the Federal 

7 Register on March 27, 2008 (73 FR 16436). In the 2008 rulemaking, EPA revised the 

8 level of the 8-hour primary standard for O3 to 0.075 parts per million (ppm), expressed to 

9 three decimal places. With regard to the secondary standard for O3, EPA revised the 8-

10 hour standard by making it identical to the revised primary standard. The EPA also made 

11 conforming changes to the Air Quality Index (AQI) for O3, setting an AQI value of 100 

12 equal to 0.075 ppm, 8-hour average, and making proportional changes to the AQI values 

13 of 50, 150 and 200. 

14 D. Reconsideration of the 2008 O3 NAAQS Final Rule

15 Consistent with a directive of the new Administration regarding the review of new 

16 and pending regulations (Emanuel memorandum, 74 FR 4435; January 26, 2009), the 

17 Administrator reviewed a number of actions that were taken in the last year by the 

18 previous Administration. The 2008 final rule was included in this review in recognition 

19 of the central role that the NAAQS play in enabling EPA to fulfill its mission to protect 

20 the nation’s public health and welfare. In her review, the Administrator was mindful of 

21 the need for judgments concerning the NAAQS to be based on a strong scientific 

22 foundation which is developed through a transparent and credible NAAQS review 
Draft O3 NPR –January 5, 2010 23 Deliberative, Do Not Quote or Cite

1 process, consistent with the core values highlighted in President Obama’s memorandum 

2 on scientific integrity (March 9, 2009).

3 1. Decision to Initiate a Rulemaking to Reconsider

4 In her review of the 2008 final rule, several aspects of the final rule related to the 

5 primary and secondary standards stood out to the Administrator. As an initial matter, the 

6 Administrator noted that the 2008 final rule concluded that the 1997 primary and 

7 secondary O3 standards were not adequate to protect public health and public welfare, 

8 and that revisions were necessary to provide increased protection. With respect to 

9 revision of the primary standard, the Administrator noted that the revised level 

10 established in the 2008 final rule was above the range that had been unanimously

recommended by CASAC.511 She also noted that EPA received comments from a large 

12 number of commenters from the medical and public health communities, including 

13 EPA’s Children’s Health Protection Advisory Committee, all of which endorsed levels 

14 within CASAC’s recommended range.

15 With respect to revision of the secondary O3 standard, the Administrator noted 

16 that the 2008 final rule differed substantially from CASAC’s recommendations that EPA 

17 adopt a new secondary O3 standard based on a cumulative, seasonal measure of exposure. 

18 The 2008 final rule revised the secondary standard to be identical to the revised primary

19 standard, which is based on an 8-hour daily maximum measure of exposure. She also 

20 noted that EPA received comments from a number of commenters representing 

 

5

The level of the 8-hour primary ozone standard was set at 0.075 ppm, while 

CASAC unanimously recommended a range between 0.060 and 0.070 ppm. 
Draft O3 NPR –January 5, 2010 24 Deliberative, Do Not Quote or Cite

1 environmental interests, all of which endorsed CASAC;s recommendation for a new 

cumulative, seasonal secondary standard.62 

3 Subsequent to issuance of the 2008 final rule, in April 2008, CASAC took the 

4 unusual step of sending EPA a letter expressing strong, unanimous disagreement with 

5 EPA’s decisions on both the primary and secondary standards (Henderson, 2008). The 

6 CASAC explained that it did not endorse the revised primary O3 standard as being 

7 sufficiently protective of public health because it failed to satisfy the explicit stipulation 

8 of the Act to provide an adequate margin of safety. The CASAC also expressed the view 

9 that failing to revise the secondary standard to a cumulative, seasonal form was not 

10 supported by the available science. In addition to CASAC’s letter, the Administrator 

11 noted a recent adverse ruling issued by the U.S. Court of Appeals for the District of 

12 Columbia Circuit on another NAAQS decision. In February 2009, the DC Circuit 

13 remanded the Agency's decisions on the primary annual and secondary standards for fine 

14 particles (PM2.5). In so doing, the Court found that EPA had not adequately explained the 

15 basis for its decisions, including why CASAC’s recommendations for a more health16 protective primary annual standard and for secondary standards different from the 

17 primary standards were not accepted. American Farm Bureau v. EPA, 559 F.3d. 512 

18 (D.C. Cir. 2009). 

19 Based on her review of the information described above, the Administrator is 

20 initiating a rulemaking to reconsider parts of the 2008 final rule. Specifically, the 

21 Administrator is reconsidering the level of the primary standard to ensure that it is 

 

6

The Administrator also noted the exchange that had occurred between EPA and 

the Office of Management and Budget (OMB) with regard to the final decision on the 

secondary standard, as discussed in the 2008 final rule (73 FR 16497).
Draft O3 NPR –January 5, 2010 25 Deliberative, Do Not Quote or Cite

1 sufficiently protective of public health, as discussed in section II below, and is 

2 reconsidering all aspects of the secondary standard to ensure that it appropriately reflects 

3 the available science and is sufficiently protective of public welfare, as discussed in 

4 section IV below. Based on her review, the Administrator has serious cause for concern 

5 regarding whether the revisions to the primary and secondary O3 standards adopted in the 

6 2008 final rule satisfy the requirements of the CAA, in light of the body of scientific 

7 evidence before the Agency. In addition, the importance of the O3 NAAQS to public 

8 health and welfare weigh heavily in favor of reconsidering parts of the 2008 final rule as 

9 soon as possible, based on the scientific and technical information upon which the 2008 

10 final rule was based. 

11 Also, EPA conducted a provisional assessment of “new” scientific papers (EPA, 

12 2009) of scientific literature evaluating health and ecological effects of O3 exposure 

13 published since the close of the 2006 Criteria Document upon which the 2008 O3

14 NAAQS were based. The Administrator notes that the provisional assessment of “new” 

15 science found that such studies did not materially change the conclusions in the 2006 

16 Criteria Document. This provisional assessment is supportive of the Administrator’s 

17 decision to reconsider parts of the 2008 final rule at this time, based on the scientific and 

18 technical information available for the 2008 final rule, as compared to foregoing such 

19 reconsideration and taking appropriate action in the future as part of the next periodic 

20 review of the air quality criteria and NAAQS, which will include such scientific and 

21 technical information.

22 The reconsideration of parts of the 2008 final rule discussed in this notice is based

23 on the scientific and technical record from the 2008 rulemaking, including public 
Draft O3 NPR –January 5, 2010 26 Deliberative, Do Not Quote or Cite

1 comments and CASAC advice and recommendations. The information that was assessed 

2 during the 2008 rulemaking includes information in the 2006 Criteria Document (EPA, 

3 2006a), the 2007 Policy Assessment of Scientific and Technical Information, referred to 

4 as the 2007 Staff Paper (EPA, 2007b), and related technical support documents including 

5 the 2007 REAs (U.S. EPA, 2007c; Abt Associates, 2007a,b). Scientific and technical 

6 information developed since the 2006 Criteria Document will be considered in the next 

7 periodic review, instead of this reconsideration rulemaking, allowing the new information 

8 to receive careful and comprehensive review by CASAC and the public before it is used 

9 as a basis in a rulemaking that determines whether to revise the NAAQS. 

10 2. Ongoing Litigation

11 In May 2008, following publication of the 2008 final rule, numerous groups, 

12 including state, public health, environmental, and industry petitioners, challenged EPA's 

13 decisions in federal court. The challenges were consolidated as State of Mississippi, et al. 

14 v. EPA (No. 08-1200, D.C. Cir. 2008). On March 10, 2009, EPA filed an unopposed 

15 motion requesting that the Court vacate the briefing schedule and hold the consolidated 

16 cases in abeyance. The Agency stated its desire to allow time for appropriate officials 

17 from the new Administration to review the O3 standards to determine whether they

18 should be maintained, modified or otherwise reconsidered. The EPA further requested 

19 that it be directed to notify the Court and all the parties of any actions it has taken or 

20 intends to take, if any, within 180 days of the Court vacating the briefing schedule. On 

21 March 19, 2009, the Court granted EPA's motion. Pursuant to the Court's order, on 

22 September 16, 2009 EPA notified the Court and the parties of its decision to initiate a 

23 rulemaking to reconsider the primary and secondary O3 standards set in March 2008 to 
Draft O3 NPR –January 5, 2010 27 Deliberative, Do Not Quote or Cite

ensure they satisfy the requirements of the CAA71 In its notice to the Court, EPA stated 

2 that this notice of proposed rulemaking would be signed by December 21, 2009, and that 

3 the final rule will be signed by August 31, 2010.

4

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

6 As an initial matter, the Administrator notes that the 2008 final rule concluded 

7 that the 1997 primary O3 standard was “not sufficient and thus not requisite to protect 

8 public health with an adequate margin of safety, and that revision is needed to provide 

9 increased public health protection” (73 FR 16472). The Administrator is not 

10 reconsidering this aspect of the 2008 decision, which is based on the reasons discussed in 

11 section II.B of the 2008 final rule (73 FR 16443-16472). The Administrator also notes

12 that the 2008 final rule concluded that it was appropriate to retain the O3 indicator, the 8-

13 hour averaging time, and form of the primary O3 standard (specified as the annual fourth14 highest daily maximum 8-hour concentration, averaged over 3 years), while concluding 

that revision of the standard level was appropriate.

8

15 The Administrator is not 

16 reconsidering these aspects of the 2008 decision, which are based on the reasons 

17 discussed in sections II.C.1-3 of the 2008 final rule, which address the indicator, 

 

7

The EPA also separately announced that it will move quickly to implement any

new standards that might result from this reconsideration. To reduce the workload for 

states during the interim period of reconsideration, the Agency intends to propose to defer

compliance with the CAA requirement to designate areas as attainment or nonattainment. 

EPA will work with states, local governments and tribes to ensure that air quality is 

protected during that time.

8

The use of O3 as the indicator for photochemical oxidants was adopted in the 

1979 final rule and retained in subsequent rulemaking. An 8-hour averaging time and a 

form based on the annual fourth-highest daily maximum 8-hour concentration, averaged 

over 3 years, were adopted in the 1997 final rule and retained in the 2008 rulemaking. 
Draft O3 NPR –January 5, 2010 28 Deliberative, Do Not Quote or Cite

1 averaging time, and form, respectively, of the primary O3 standard (73 FR 16472-16475). 

2 For these reasons, the Administrator is not reopening the 2008 decision with regard to the 

3 need to revise the 1997 primary O3 standard nor with regard to the indicator, averaging 

4 time, and form of the 2008 primary O3 standard. Thus, the information that follows in 

5 this section specifically focuses on a reconsideration of level of the primary O3 standard.

6 This section presents the rationale for the Administrator’s proposed decision that

7 the O3 primary standard, which was set at a level of 0.075 ppm in the 2008 final rule, 

8 should instead be set at a lower level within the range from 0.060 to 0.070 ppm. As 

9 discussed more fully below, the rationale for the proposed range of standard levels is 

10 based on a thorough review of the latest scientific information on human health effects 

11 associated with the presence of O3 in the ambient air presented in the 2006 Criteria 

12 Document. This rationale also takes into account: (1) staff assessments of the most 

13 policy-relevant information in the 2006 Criteria Document and staff analyses of air 

14 quality, human exposure, and health risks, presented in the 2007 Staff Paper, upon which 

15 staff recommendations for revisions to the primary O3 standard in the 2008 rulemaking

16 were based; (2) CASAC advice and recommendations, as reflected in discussions of 

17 drafts of the 2006 Criteria Document and 2007 Staff Paper at public meetings, in separate 

18 written comments, and in CASAC’s letters to the Administrator both before and after the 

19 2008 rulemaking; and (3) public comments received during the development of these 

20 documents, either in connection with CASAC meetings or separately, and on the 2007 

21 proposed rule.

22 In developing this rationale, the Administrator recognizes that the CAA requires 

23 her to reach a public health policy judgment as to what standard would be requisite to 
Draft O3 NPR –January 5, 2010 29 Deliberative, Do Not Quote or Cite

1 protect public health with an adequate margin of safety, based on scientific evidence and 

2 technical assessments that have inherent uncertainties and limitations. This judgment 

3 requires making reasoned decisions as to what weight to place on various types of 

4 evidence and assessments, and on the related uncertainties and limitations. Thus, in 

5 selecting standard levels to propose, and subsequently in selecting a final level, the 

6 Administrator is seeking not only to prevent O3 levels that have been demonstrated to be 

7 harmful but also to prevent lower O3 levels that may pose an unacceptable risk of harm, 

8 even if the risk is not precisely identified as to nature or degree.

9 In this proposed rule, EPA has drawn upon an integrative synthesis of the entire 

10 body of evidence, published through early 2006, on human health effects associated with 

11 the presence of O3 in the ambient air. As discussed below in section II.A, this body of 

12 evidence addresses a broad range of health endpoints associated with exposure to ambient 

13 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.914 In

15 reconsidering this evidence, EPA focuses on those health endpoints that have been 

16 demonstrated to be caused by exposure to O3, or for which the 2006 Criteria Document 

17 judges associations with O3 to be causal, likely causal, or for which the evidence is highly

18 suggestive that O3 contributes to the reported effects. This rationale also draws upon the 

19 results of quantitative exposure and risk assessments, discussed below in section II.B. 

20 Section II.C focuses on the considerations upon which the Administrator’s proposed 

 

9

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.
Draft O3 NPR –January 5, 2010 30 Deliberative, Do Not Quote or Cite

1 conclusions on the level of the primary standard are based. Policy-relevant evidence2 based and exposure/risk-based considerations are discussed, and the rationale for the 

3 2008 final rulemaking on the primary standard and CASAC advice, given both prior to 

4 the development of the 2007 proposed rule and following the 2008 final rule, are 

5 summarized. Finally, the Administrator’s proposed conclusions on the level of the 

6 primary standard are presented. Section II.D summarizes the proposed decision on the 

7 level of the primary O3 standard and the solicitation of public comments.

8 Judgments made in the 2006 Criteria Document and 2007 Staff Paper about the 

9 extent to which relationships between various health endpoints and short-term exposures 

10 to ambient O3 are likely causal have been informed by several factors. As discussed 

11 below in section II.A, these factors include the nature of the evidence (i.e., controlled 

12 human exposure, epidemiological, and/or toxicological studies) and the weight of 

13 evidence, which takes into account such considerations as biological plausibility, 

14 coherence of evidence, strength of association, and consistency of evidence.

15 In assessing the health effects data base for O3, it is clear that human studies 

16 provide the most directly applicable information for determining causality because they

17 are not limited by the uncertainties of dosimetry differences and species sensitivity

18 differences, which would need to be addressed in extrapolating animal toxicology data to 

19 human health effects. Controlled human exposure studies provide data with the highest 

20 level of confidence since they provide human health effects data under closely monitored 

21 conditions and can provide exposure-response relationships. Epidemiological data 

22 provide evidence of associations between ambient O3 levels and more serious acute and 

23 chronic health effects (e.g., hospital admissions and mortality) that cannot be assessed in 
Draft O3 NPR –January 5, 2010 31 Deliberative, Do Not Quote or Cite

1 controlled human exposure studies. For these studies the degree of uncertainty

2 introduced by potentially confounding variables (e.g., other pollutants, temperature) and 

3 other factors affects the level of confidence that the health effects being investigated are 

4 attributable to O3 exposures, alone and in combination with other copollutants. 

5 In using a weight of evidence approach to inform judgments about the degree of 

6 confidence that various health effects are likely to be caused by exposure to O3, 

7 confidence increases as the number of studies consistently reporting a particular health 

8 endpoint grows and as other factors, such as biological plausibility and strength, 

9 consistency, and coherence of evidence, increase. Conclusions regarding biological 

10 plausibility, consistency, and coherence of evidence of O3-related health effects are 

11 drawn from the integration of epidemiological studies with mechanistic information from 

12 controlled human exposure studies and animal toxicological studies. As discussed below, 

13 this type of mechanistic linkage has been firmly established for several respiratory 

14 endpoints (e.g., lung function decrements, lung inflammation) but remains far more 

15 equivocal for cardiovascular endpoints (e.g., cardiovascular-related hospital admissions). 

16 For epidemiological studies, strength of association refers to the magnitude of the 

17 association and its statistical strength, which includes assessment of both effects estimate 

18 size and precision. In general, when associations yield large relative risk estimates, it is 

19 less likely that the association could be completely accounted for by a potential 

20 confounder or some other bias. Consistency refers to the persistent finding of an 

21 association between exposure and outcome in multiple studies of adequate power in 

22 different persons, places, circumstances and times. For example, the magnitude of effect 
Draft O3 NPR –January 5, 2010 32 Deliberative, Do Not Quote or Cite

1 estimates is relatively consistent across recent studies showing association between short2 term, but not long-term, O3 exposure and mortality.

3 Based on the information discussed below in sections II.A.1 – II.A.3, judgments 

4 concerning the extent to which relationships between various health endpoints and 

5 ambient O3 exposures are likely causal are summarized below in section II.A.3.c. These 

6 judgments reflect the nature of the evidence and the overall weight of the evidence, and 

7 are taken into consideration in the quantitative exposure and risk assessments, discussed 

8 below in section II.B.

9 To put judgments about health effects that have been demonstrated to be caused 

10 by exposure to O3, or for which the 2006 Criteria Document judges associations with O3

11 to be causal, likely causal, or for which the evidence is highly suggestive that O3

12 contributes to the reported effects into a broader public health context, EPA has drawn 

13 upon the results of the quantitative exposure and risk assessments. These assessments 

14 provide estimates of the likelihood that individuals in particular population groups that 

15 are at risk for various O3-related physiological health effects would experience 

16 “exposures of concern” and specific health endpoints under varying air quality scenarios 

(i.e., just meeting various standards10 17 ), as well as characterizations of the kind and degree 

18 of uncertainties inherent in such estimates.

19 In the 2008 final rulemaking and in this reconsideration, the term “exposures of 

20 concern” is defined as personal exposures while at moderate or greater exertion to 8-hour 

 

10 The exposure assessment done as part of the 2008 final rulemaking considered 

several air quality scenarios, including just meeting what was then the current standard 

set at a level of 0.084 ppm, as well as just meeting alternative standards at levels of 

0.080, 0.074, 0.070, and 0.064 ppm.
Draft O3 NPR –January 5, 2010 33 Deliberative, Do Not Quote or Cite

1 average ambient O3 levels at and above specific benchmark levels which represent 

2 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.1.11 3 The EPA 

4 emphasizes that although the analysis of “exposures of concern” was conducted using 

5 three discrete benchmark levels (i.e., 0.080, 0.070, and 0.060 ppm), the concept is more 

6 appropriately viewed as a continuum with greater confidence and less uncertainty about 

7 the existence of health effects at the upper end and less confidence and greater 

8 uncertainty as one considers increasingly lower O3 exposure levels. The EPA recognizes 

9 that there is no sharp breakpoint within the continuum ranging from at and above 0.080 

10 ppm down to 0.060 ppm. In considering the concept of exposures of concern, it is 

11 important to balance concerns about the potential for health effects and their severity with 

12 the increasing uncertainty associated with our understanding of the likelihood of such 

13 effects at lower O3 levels. 

14 Within the context of this continuum, estimates of exposures of concern at 

15 discrete benchmark levels provide some perspective on the public health impacts of O3-

16 related health effects that have been demonstrated in controlled human exposure and 

17 toxicological studies but cannot be evaluated in quantitative risk assessments, such as 

18 lung inflammation, increased airway responsiveness, and changes in host defenses. They

 

11 Exposures of concern were also considered in the 1997 review of the O3

NAAQS, and were judged by EPA to be an important indicator of the public health 

impacts of those O3-related effects for which information was too limited to develop 

quantitative estimates of risk but which had been observed in humans at and above the 

benchmark level of 0.08 ppm for 6- to 8-hour exposures . . . including increased

nonspecific bronchial responsiveness (for example, aggravation of asthma), decreased 

pulmonary defense mechanisms (suggestive of increased susceptibility to respiratory

infection), and indicators of pulmonary inflammation (related to potential aggravation of 

chronic bronchitis or long-term damage to the lungs). (62 FR 38868)
Draft O3 NPR –January 5, 2010 34 Deliberative, Do Not Quote or Cite

1 also help in understanding the extent to which such impacts have the potential to be

2 reduced by meeting various standards. These O3-related physiological effects are 

3 plausibly linked to the increased morbidity seen in epidemiological studies (e.g., as 

4 indicated by increased medication use in asthmatics, school absences in all children, and 

5 emergency department visits and hospital admissions in people with lung disease). 

6 Estimates of the number of people likely to experience exposures of concern cannot be 

7 directly translated into quantitative estimates of the number of people likely to experience 

8 specific health effects, since sufficient information to draw such comparisons is not 

9 available -- if such information were available, these health outcomes would have been 

10 included in the quantitative risk assessment. Due to individual variability in 

11 responsiveness, only a subset of individuals who have exposures at and above a specific 

12 benchmark level can be expected to experience such adverse health effects, and

13 susceptible subpopulations such as those with asthma are expected to be affected more by 

14 such exposures than healthy individuals. The amount of weight to place on the estimates 

15 of exposures of concern at any of these benchmark levels depends in part on the weight 

16 of the scientific evidence concerning health effects associated with O3 exposures at and 

17 above that benchmark level. It also depends on judgments about the importance from a 

18 public health perspective of the health effects that are known or can reasonably be 

19 inferred to occur as a result of exposures at and above the benchmark level. Such public 

20 health policy judgments are embodied in the NAAQS standard setting criteria (i.e., 

21 standards that, in the judgment of the Administrator, are requisite to protect public health 

22 with an adequate margin of safety).
Draft O3 NPR –January 5, 2010 35 Deliberative, Do Not Quote or Cite

1 As discussed below in section II.B.2, the quantitative health risk assessment 

2 conducted as part of the 2008 final rulemaking includes estimates of risks of lung 

3 function decrements in asthmatic and all school age children, respiratory symptoms in 

4 asthmatic children, respiratory-related hospital admissions, and non-accidental and 

5 cardiorespiratory-related mortality associated with recent ambient O3 levels, as well as 

6 risk reductions and remaining risks associated with just meeting the then current 0.084 

7 ppm standard and various alternative O3 standards in a number of example urban areas. 

8 There are two parts to this risk assessment: one part is based on combining information 

9 from controlled human exposure studies with modeled population exposure, and the other 

10 part is based on combining information from community epidemiological studies with 

11 either monitored or adjusted ambient concentrations levels. This assessment provides

12 estimates of the potential magnitude of O3-related health effects, as well as a 

13 characterization of the uncertainties and variability inherent in such estimates. This 

14 assessment also provides insights into the distribution of risks and patterns of risk 

15 reductions associated with meeting alternative O3 standards.

16 As discussed below, a substantial amount of new research conducted since the 

17 1997 review of the O3 NAAQS was available to inform the 2008 final rulemaking, with 

18 important new information coming from epidemiologic studies as well as from controlled 

19 human exposure, toxicological, and dosimetric studies. The research studies newly 

20 available in the 2008 final rulemaking that were evaluated in the 2006 Criteria Document 

21 and the exposure and risk assessments presented in the 2007 Staff Paper have undergone 

22 intensive scrutiny through multiple layers of peer review and many opportunities for 

23 public review and comment. While important uncertainties remain in the qualitative and 
Draft O3 NPR –January 5, 2010 36 Deliberative, Do Not Quote or Cite

1 quantitative characterizations of health effects attributable to exposure to ambient O3, and 

2 while different interpretations of these uncertainties can result in different public health 

3 policy judgments, the review of this information has been extensive and deliberate. In 

4 the judgment of the Administrator, this intensive evaluation of the scientific evidence 

5 provides an adequate basis for this reconsideration of the 2008 final rulemaking.

6 A. Health Effects Information

7 This section outlines key information contained in the 2006 Criteria Document 

8 (chapters 4-8) and in the 2007 Staff Paper (chapter 3) on known or potential effects on 

9 public health which may be expected from the presence of O3 in ambient air. The 

10 information highlighted here summarizes: (1) new information available on potential 

11 mechanisms for health effects associated with exposure to O3; (2) the nature of effects 

12 that have been associated directly with exposure to O3 and indirectly with the presence of 

13 O3 in ambient air; (3) an integrative interpretation of the evidence, focusing on the 

14 biological plausibility and coherence of the evidence; and (4) considerations in 

15 characterizing the public health impact of O3, including the identification of “at risk” 

16 populations.

17 The decision in the 1997 review focused primarily on evidence from short-term 

18 (e.g., 1 to 3 hours) and prolonged ( 6 to 8 hours) controlled-exposure studies reporting 

19 lung function decrements, respiratory symptoms, and respiratory inflammation in 

20 humans, as well as epidemiology studies reporting excess hospital admissions and 

21 emergency department (ED) visits for respiratory causes. The 2006 Criteria Document

22 prepared for the 2008 rulemaking emphasized the large number of epidemiological 

23 studies published since the last review with these and additional health endpoints, 
Draft O3 NPR –January 5, 2010 37 Deliberative, Do Not Quote or Cite

1 including the effects of acute (short-term and prolonged) and chronic exposures to O3 on 

2 lung function decrements and enhanced respiratory symptoms in asthmatic individuals, 

3 school absences, and premature mortality. It also emphasized important new information 

4 from toxicology, dosimetry, and controlled human exposure studies. Highlights of the 

5 evidence include:

6 (1) Two new controlled human-exposure studies are now available that examine 

7 respiratory effects associated with prolonged O3 exposures at levels below 0.080 ppm, 

8 which was the lowest exposure level that had been examined in the 1997 review.

9 (2) Numerous controlled human-exposure studies have examined indicators of 

10 O3-induced inflammatory response in both the upper respiratory tract (URT) and lower 

11 respiratory tract (LRT), and increased airway responsiveness to allergens in subjects with 

12 allergic asthma and allergic rhinitis exposed to O3, while other studies have examined 

13 changes in host defense capability following O3 exposure of healthy young adults.

14 (3) Animal toxicology studies provide new information regarding mechanisms of 

15 action, increased susceptibility to respiratory infection, and the biological plausibility of 

16 acute effects and chronic, irreversible respiratory damage.

17 (4) Numerous acute exposure epidemiological studies published during the past 

18 decade offer added evidence of ambient O3-related lung function decrements and 

19 respiratory symptoms in physically active healthy subjects and greater responses in 

20 asthmatic subjects, as well as evidence on new health endpoints, such as the relationships 

21 between ambient O3 concentrations and asthma medication use and school absenteeism, 

22 and between ambient O3 and cardiac-related physiological endpoints.
Draft O3 NPR –January 5, 2010 38 Deliberative, Do Not Quote or Cite

1 (5) Several additional studies have been published over the last decade examining 

2 the temporal associations between O3 exposures and emergency department visits for 

3 asthma and other respiratory diseases and respiratory-related hospital admissions.

4 (6) A large number of newly available epidemiological studies have examined 

5 the effects of acute exposure to PM and O3 on mortality, notably including large multicity 

6 studies that provide much more robust and credible information than was available in the 

7 1997 review, as well as recent meta-analyses that have evaluated potential sources of 

8 heterogeneity in O3-mortality associations.

9 1. Overview of Mechanisms

10 Evidence on possible mechanisms by which exposure to O3 may result in acute 

11 and chronic health effects is discussed in chapters 5 and 6 of the 2006 Criteria 

Document.12 12 Evidence from dosimetry, toxicological, and human exposure studies has 

13 contributed to an understanding of the mechanisms that help to explain the biological 

14 plausibility and coherence of evidence for O3-induced respiratory health effects reported 

15 in epidemiological studies. More detailed information about the physiological 

16 mechanisms related to the respiratory effects of short- and long-term exposure to O3 can 

17 be found in section II.A.3.b.i and II.A.3.b.iii, respectively. In the past, however, little 

18 information was available to help explain potential biological mechanisms which linked 

19 O3 exposure to premature mortality or cardiovascular effects. As discussed more fully in 

20 section II.A.3.b.ii below, since the 1997 review an emerging body of animal toxicology 

 

12 While most of the available evidence addresses mechanisms for O3, O3 clearly

serves as an indicator for the total photochemical oxidant mixture found in the ambient 

air. Some effects may be caused by one or more components in the overall pollutant mix, 

either separately or in combination with O3. However, O3 clearly dominates these other 

oxidants with their concentrations only being a few percent of the O3 concentration.
Draft O3 NPR –January 5, 2010 39 Deliberative, Do Not Quote or Cite

1 and controlled human exposure evidence is beginning to suggest mechanisms that may

2 mediate acute O3 cardiovascular effects. While much is known about mechanisms that 

3 play a role in O3-related respiratory effects, additional research is needed to more clearly 

4 understand the role that O3 may have in contributing to cardiovascular effects.

5 With regard to the mechanisms related to short-term respiratory effects, scientific 

6 evidence discussed in the 2006 Criteria Document (section 5.2) indicates that reactions of 

7 O3 with lipids and antioxidants in the epithelial lining fluid and the epithelial cell 

8 membranes of the lung can be the initial step in mediating deleterious health effects of 

9 O3. This initial step activates a cascade of events that lead to oxidative stress, injury, 

10 inflammation, airway epithelial damage and increased alveolar permeability to vascular 

11 fluids. Inflammation can be accompanied by increased airway responsiveness, which is 

12 an increased bronchoconstrictive response to airway irritants and allergens. Continued 

13 respiratory inflammation also can alter the ability of the body to respond to infectious 

14 agents, allergens and toxins. Acute inflammatory responses to O3 in some healthy people 

15 are well documented, and precursors to lung injury are observed within 3 hours after 

16 exposure in humans. Repeated respiratory inflammation can lead to a chronic 

17 inflammatory state with altered lung structure and lung function and may lead to chronic 

18 respiratory diseases such as fibrosis and emphysema (EPA, 2006a, section 8.6.2). The 

19 severity of symptoms and magnitude of response to acute exposures depend on inhaled 

20 dose, as well as on individual susceptibility to O3, as discussed below. At the same O3

21 dose, individuals who are more susceptible to O3 will have a larger response than those 

22 who are less susceptible; among individuals with similar susceptibility, those who receive 

23 a larger dose will have a larger response to O3.
Draft O3 NPR –January 5, 2010 40 Deliberative, Do Not Quote or Cite

1 The inhaled dose is the product of O3 concentration (C), minute ventilation or 

2 ventilation rate, and duration of exposure (T), or (C × ventilation rate × T). A large body 

3 of data regarding the interdependent effect of these components of inhaled dose on 

4 pulmonary responses was assessed in the 1986 and 1996 O3 Criteria Documents. In an 

5 attempt to describe O3 dose-response characteristics, acute responses were modeled as a 

6 function of total inhaled O3 dose, which was generally found to be a better predictor of 

7 response than O3 concentration, ventilation rate, or duration of exposure, alone, or as a 

8 combination of any two of these factors (EPA 2006a, section 6.2). Predicted O3-induced 

9 decrements in lung function have been shown to be a function of exposure concentration, 

10 duration and exercise level for healthy, young adults (McDonnell et al., 1997). A meta11 analysis of 21 studies (Mudway and Kelly, 2004) showed that markers of inflammation 

12 and increased cellular permeability in healthy subjects are associated with total O3 dose.

13 The 2006 Criteria Document summarizes information on potentially susceptible 

14 and vulnerable groups in section 8.7. As described there, the term susceptibility refers to 

15 innate (e.g., genetic or developmental) or acquired (e.g., personal risk factors, age) 

16 factors that make individuals more likely to experience effects with exposure to 

17 pollutants. A number of population groups and lifestages have been identified as 

18 potentially susceptible to health effects as a result of O3 exposure, including people with 

19 existing lung diseases, including asthma, children and older adults, and people who have 

20 larger than normal lung function responses that may be due to genetic susceptibility. In 

21 addition, some population groups and lifestages have been identified as having increased 

22 vulnerability to O3-related effects due to increased likelihood of exposure while at 

23 elevated ventilation rates, including healthy children and adults who are active outdoors, 
Draft O3 NPR –January 5, 2010 41 Deliberative, Do Not Quote or Cite

1 for example, outdoor workers, and joggers. Taken together, the susceptible and 

vulnerable groups are more commonly referred to as "at-risk" groups13 2 , as discussed 

3 more fully below in section II.A.4.b.

4 Based on a substantial body of new evidence from animal, controlled human 

5 exposure and epidemiological studies, the 2006 Criteria Document concludes that people 

6 with asthma and other preexisting pulmonary diseases are likely to be among those at 

7 increased risk from O3 exposure. Altered physiological, morphological and biochemical 

8 states typical of respiratory diseases like asthma, COPD and chronic bronchitis may

9 render people sensitive to additional oxidative burden induced by O3 exposure (EPA 

10 2006a, section 8.7). Children and adults with asthma are the group that has been studied 

11 most extensively. Evidence from controlled human exposure studies indicates that 

12 asthmatics may exhibit larger lung function decrements in response to O3 exposure than 

13 healthy controls. As discussed more fully in section II.A.4.b.ii below, asthmatics present 

14 a differential response profile for cellular, molecular, and biochemical parameters (EPA, 

15 2006a, section 8.7.1) that are altered in response to acute O3 exposure. They can have 

16 larger inflammatory responses, as manifested by larger increases in markers of 

17 inflammation such as white bloods cells (e.g., PMNs) or inflammatory cytokines. 

18 Asthmatics, and people with allergic rhinitis, are more likely to mount an allergic-type 

19 response upon exposure to O3, as manifested by increases in white blood cells associated 

 

13 In previous Staff Papers and Federal Register notices announcing proposed and 

final decisions on the O3 and other NAAQS, EPA has used the phrase “sensitive 

population groups” to include both population groups that are at increased risk because 

they are more intrinsically susceptible and population groups that are more vulnerable 

due to an increased potential for exposure. In this notice, we use the phrase, “at risk” 

populations to include both types of population groups.
Draft O3 NPR –January 5, 2010 42 Deliberative, Do Not Quote or Cite

1 with allergy (i.e., eosinophils) and related molecules, which increase inflammation in the 

2 airways. The increased inflammatory and allergic responses also may be associated with 

3 the larger late-phase responses that asthmatics can experience, which can include 

4 increased bronchoconstrictor responses to irritant substances or allergens and additional 

5 inflammation. In addition to the experimental evidence of lung function decrements, 

6 respiratory symptoms, and other respiratory effects in asthmatic populations, two large 

7 U.S. epidemiological studies as well as several smaller U.S. and international studies, 

8 have reported fairly robust associations between ambient O3 concentrations and measures 

9 of lung function and daily symptoms (e.g., chest tightness, wheeze, shortness of breath) 

10 in children with moderate to severe asthma and between O3 and increased asthma 

11 medication use (EPA, 2007a, chapter 6). These responses in asthmatics and others with 

12 lung disease provide biological plausibility for the more serious respiratory morbidity

13 effects observed in epidemiological studies, such as emergency department visits and 

14 hospital admissions.

15 Children with and without asthma were found to be particularly susceptible to O3

16 effects on lung function and generally have greater lung function responses than older 

17 people. The American Academy of Pediatrics (2004) notes that children and infants are 

18 among the population groups most susceptible to many air pollutants, including O3. This 

19 is in part because their lungs are still developing. For example, eighty percent of alveoli 

20 are formed after birth, and changes in lung development continue through adolescence 

21 (Dietert et al., 2000). Moreover, children have high minute ventilation rates and 

22 relatively high levels of physical activity which also increases their O3 dose (Plunkett et 

23 al., 1992). Thus, children are at-risk due to both their susceptibility and vulnerability.
Draft O3 NPR –January 5, 2010 43 Deliberative, Do Not Quote or Cite

1 Looking more broadly at age-related differences in susceptibility, several 

2 mortality studies have investigated age-related differences in O3 effects (EPA, 2006a, 

3 section 7.6.7.2), primarily in the older adult population. Among the studies that observed 

4 positive associations between O3 and mortality, a comparison of all age or younger age 

5 (65 years of age) O3-mortality effect estimates to that of the elderly population (>65 

6 years) indicates that, in general, the elderly population is more susceptible to O3 mortality

7 effects. There is supporting evidence of age-related differences in susceptibility to O3

8 lung function effects. The 2006 Criteria Document (section 7.6.7.2) concludes that the 

9 elderly population (>65 years of age) appear to be at greater risk of O3-related mortality

10 and hospitalizations compared to all ages or younger populations, and children (<18 years 

11 of age) experience other potentially adverse respiratory health outcomes with increased 

12 O3 exposure. 

13 Controlled human exposure studies have also indicated a high degree of 

14 interindividual variability in some of the pulmonary physiological parameters, such as 

15 lung function decrements. The variable effects in individuals have been found to be 

16 reproducible, in other words, a person who has a large lung function response after 

17 exposure to O3 will likely have about the same response if exposed again to the same 

18 dose of O3 (EPA 2006a, section 6.1). In controlled human exposure studies, group mean 

19 responses are not representative of this segment of the population that has much larger 

20 than average responses to O3. Recent studies, discussed in section II.A.4.b.iv below, 

21 reported a role for genetic polymorphism (i.e., the occurrence together in the same 

22 population of more than one allele or genetic marker at the same locus with the least 

23 frequent allele or marker occurring more frequently than can be accounted for by
Draft O3 NPR –January 5, 2010 44 Deliberative, Do Not Quote or Cite

1 mutation alone) in observed differences in antioxidant enzymes and genes involved in 

2 inflammation to modulate pulmonary function and inflammatory responses to O3 

3 exposure. These observations suggest a potential role for these markers in the innate 

4 susceptibility to O3, however, the validity of these markers and their relevance in the 

5 context of prediction to population studies needs additional experimentation.

6 Controlled human exposure studies that provide information about mechanisms of 

7 the initial response to O3 (e.g., lung function decrements, inflammation, and injury to the 

8 lung) also inform the selection of appropriate lag times to analyze in epidemiological 

9 studies through elucidation of the time course of these responses (EPA 2006a, section 

10 8.4.3). Based on the results of these studies, it would be reasonable to expect that lung 

11 function decrements could be detected epidemiologically within lags of 0 (same day) or 1 

12 to 2 days following O3 exposure, given the rapid onset of lung function changes and their 

13 persistence for 24 to 48 hours among more responsive human subjects in controlled 

14 human exposure studies. Other responses take longer to develop and can persist for 

15 longer periods of time. For example, although asthmatic individuals may begin to 

16 experience symptoms soon after O3 exposure, it may take anywhere from 1 to 3 days 

17 after exposure for these subjects to seek medical attention as a result of increased airway

18 responsiveness or inflammation that may persist for 2 to 3 days. This may be reflected 

19 by epidemiologic observations of significantly increased risk for asthma-related 

20 emergency department visits or hospital admissions with 1- to 3-day lags, or, perhaps, 

21 enhanced distributed lag risks (combined across 3 days) for such morbidity indicators. 

22 Analogously, one might project increased mortality within 0- to 3-day lags as a possible 

23 consequence of O3-induced increases in clotting agents arising from the cascade of 
Draft O3 NPR –January 5, 2010 45 Deliberative, Do Not Quote or Cite

1 events, starting with cell injury described above, occurring within 12 to 24 hours of O3

2 exposure. The time course for many of these initial responses to O3 is highly variable. 

3 Moreover these observations pertain only to the initial response to O3. Consequent 

4 responses can follow. For example, Jörres et al., (1996) found that in subjects with 

5 asthma and allergic rhinitis, a maximum percent fall in FEV1 of 27.9% and 7.8%, 

6 respectively, occurred 3 days after O3 exposure when they were challenged with of the 

7 highest common dose of allergen. 

8 2. Nature of Effects

9 The 2006 Criteria Document provides new evidence that notably enhances our 

10 understanding of short-term and prolonged exposure effects, including effects on lung 

11 function, symptoms, and inflammatory effects reported in controlled exposure studies. 

12 These studies support and extend the findings of the previous Criteria Document. There 

13 is also a significant body of new epidemiological evidence of associations between short14 term and prolonged exposure to O3 and effects such as premature mortality, hospital 

15 admissions and emergency department visits for respiratory (e.g., asthma) causes. Key

16 epidemiological and controlled human exposure studies are summarized below and 

17 discussed in chapter 3 of the 2007 Staff Paper, which is based on scientific evidence 

18 critically reviewed in chapters 5, 6, and 7 of the 2006 Criteria Document, as well as the 

Criteria Document’s integration of scientific evidence contained in chapter 8.14 19 

20 Conclusions drawn about O3-related health effects are based upon the full body of 

 

14 Health effects discussions are also drawn from the more detailed information 

and tables presented in the Criteria Document’s annexes.
Draft O3 NPR –January 5, 2010 46 Deliberative, Do Not Quote or Cite

1 evidence from controlled human exposure, epidemiological and toxicological data 

2 contained in the 2006 Criteria Document. 

3 a. Morbidity

4 This section summarizes scientific information on the effects of inhalation of O3, 

5 including public health effects of short-term, prolonged, and long-term exposures on 

6 respiratory morbidity and cardiovascular system effects, as discussed in chapters 6, 7 and 

7 8 of the 2006 Criteria Document and chapter 3 of the 2007 Staff Paper. This section also

8 summarizes the uncertainty about the potential indirect effects on public health associated 

9 with changes due to increases in UV-B radiation exposure, such as UV-B radiation10 related skin cancers, that may be associated with reductions in ambient levels of ground11 level O3, as discussed in chapter 10 of the 2006 Criteria Document and chapter 3 of the 

12 2007 Staff Paper.

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

14 Controlled human exposure studies have shown that O3 induces a variety of health 

15 effects, including: lung function decrements, respiratory symptoms, increased airway

16 responsiveness, respiratory inflammation and permeability, increased susceptibility to 

17 respiratory infection, and acute morphological effects. Epidemiology studies have 

18 reported associations between O3 exposures (i.e., 1-hour, 8-hour and 24-hour) and a wide 

19 range of respiratory-related health effects including: pulmonary function decrements; 

20 respiratory symptoms; increased asthma medication use; increased school absences; 

21 increased emergency department visits and hospital admissions.

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

23 Use

24

25 (i) Results from Controlled Human Exposure Studies
Draft O3 NPR –January 5, 2010 47 Deliberative, Do Not Quote or Cite

1

2 A large number of studies published prior to 1996 that investigated short-term O3

3 exposure health effects on the respiratory system from short-term O3 exposures were 

4 reviewed in the 1986 and 1996 Criteria Documents (EPA, 1986, 1996a). In the 1997 

5 review, 0.50 ppm was the lowest O3 concentration at which statistically significant 

6 reductions in forced vital capacity (FVC) and forced expiratory volume in 1 second 

7 (FEV1) were reported in sedentary subjects. During exercise, spirometric (lung function) 

8 and symptomatic responses were observed at much lower O3 exposures. When minute 

9 ventilation was considerably increased by continuous exercise (CE) during O3 exposures 

10 lasting 2 hour or less at > 0.12 ppm, healthy subjects generally experienced decreases in 

11 FEV1, FVC, and other measures of lung function; increases in specific airway resistance 

12 (sRaw), breathing frequency, and airway responsiveness; and symptoms such as cough, 

13 pain on deep inspiration, shortness of breath, throat irritation, and wheezing. When 

14 exposures were increased to 4- to 8-hours in duration, statistically significant lung 

15 function and symptom responses were reported at O3 concentrations as low as 0.08 ppm 

16 and at lower minute ventilation (i.e., moderate rather than high level exercise) than the 

17 shorter duration studies.

18 The most important observations drawn from studies reviewed in the 1996 

19 Criteria Document were that: (1) young healthy adults exposed to O3 concentrations >

20 0.080 ppm develop significant, reversible, transient decrements in pulmonary function if

21 minute ventilation or duration of exposure is increased sufficiently; (2) children 

22 experience similar lung function responses but report lesser symptoms from O3 exposure 

23 relative to young adults; (3) O3-induced lung function responses are decreased in the 

24 elderly relative to young adults; (4) there is a large degree of intersubject variability in 
Draft O3 NPR –January 5, 2010 48 Deliberative, Do Not Quote or Cite

1 physiological and symptomatic responses to O3 but responses tend to be reproducible 

2 within a given individual over a period of several months; (5) subjects exposed 

3 repeatedly to O3 for several days show an attenuation of response upon successive 

4 exposures, but this attenuation is lost after about a week without exposure; and (6) acute 

5 O3 exposure initiates an inflammatory response which may persist for at least 18 to 24 

6 hours post exposure.

7 The development of these respiratory effects is time-dependent during both 

8 exposure and recovery periods, with great overlap for development and disappearance of 

9 the effects. In healthy human subjects exposed to typical ambient O3 levels near 0.120 

10 ppm, lung function responses largely resolve within 4 to 6 hours postexposure, but 

11 cellular effects persist for about 24 hours. In these healthy subjects, small residual lung 

12 function effects are almost completely gone within 24 hours, while in hyperresponsive 

13 subjects, recovery can take as much as 48 hour to return to baseline. The majority of 

14 these responses are attenuated after repeated consecutive exposures, but such attenuation 

15 to O3 is lost one week postexposure. 

16 Since 1996, there have been a number of studies published investigating lung 

17 function and symptomatic responses that generally support the observations previously

18 drawn. Recent studies for acute exposures of 1 to 2 hours and 6 to 8 hours in duration are 

19 compiled in the 2007 Staff Paper (Appendix 3C). As summarized in more detail in the 

20 2007 Staff Paper (section 3.3.1.1), among the more important of the recent studies that 

21 examined changes in FEV1 in large numbers of subjects over a range of 1-2 hours at 

22 exposure levels of 0.080 to 0.40 ppm were studies by McDonnell et al. (1997) and 
Draft O3 NPR –January 5, 2010 49 Deliberative, Do Not Quote or Cite

1 Ultman et al. (2004). These studies observed considerable intersubject variability in 

2 FEV1 decrements, which was consistent with findings in the 1996 Criteria Document.

3 For prolonged exposures (4 to 8 hours) in the range of 0.080 to 0.160 ppm O3

4 using moderate intermittent exercise and typically using square-wave exposure patterns 

5 (i.e., a constant exposure level during time of exposure), several pre- and post-1996 

6 studies (Folinsbee et al., 1988,1994; Horstman et al., 1990; Adams, 2002, 2003a, 2006) 

7 have reported statistically significant lung function responses and increased symptoms in 

8 healthy adults with increasing duration of exposure, O3 concentration, and minute 

9 ventilation. Studies that employed triangular exposure patterns (i.e., integrated exposures 

10 that begin at a low level, rise to a peak, and return to a low level during the exposure) 

11 (Hazucha et al., 1992; Adams 2003a, 2006) suggest that the triangular exposure pattern 

12 can potentially lead to greater FEV1 decrements and respiratory symptoms than square13 wave exposures (when the overall O3 doses are equal). These results suggest that peak 

14 exposures, reflective of the pattern of ambient O3 concentrations in some locations, are 

15 important in terms of O3 health effects.

16 McDonnell (1996) used data from a series of studies to investigate the frequency

17 distributions of FEV1 decrements following 6.6 hour exposures and found statistically

18 significant, but relatively small, group mean decreases in average FEV1 responses 

(between 5 and 10 percent) at 0.080 ppm O3.

15 19 Notably, about 26 percent of the 60 

20 exposed subjects had lung function decrements > 10 percent, including about 8 percent of 

 

15 This study and other studies (Folinsbee et al., 1988; Horstman et al, 1990; and 

McDonnell et al., 1991), conducted in EPA’s human studies research facility in Chapel 

Hill, NC, measured ozone concentrations to within +/- 5 percent or +/- 0.004 ppm at the 

0.080 ppm exposure level.
Draft O3 NPR –January 5, 2010 50 Deliberative, Do Not Quote or Cite

1 the subjects that experienced large decrements (>20 percent) (EPA, 2007b, Figure 3-1A). 

2 These results (which were not corrected for exercise in filtered air responses) demonstrate 

3 that while average responses may be relatively small at the 0.080 ppm exposure level, 

4 some individuals experience more severe effects that may be clinically significant. 

5 Similar results at the 0.080 ppm exposure level (for 6.6 hours during intermittent

6 exercise) were seen in more recent studies of 30 healthy young adults by Adams (2002, 

2006).16 7 In Adams (2006), relatively small but statistically significant lung function 

8 decrements and respiratory symptom responses were found (for both square-wave and 

9 triangular exposure patterns), with 17 percent of the subjects (5 of 30) experiencing > 10 

10 percent FEV1 decrements (comparing pre- and post-exposures) when the results were not 

11 corrected for the effects of exercise alone in filtered air (EPA, 2007b, Figure 3-1B) and 

12 with 23 percent of subjects (7 of 30) experiencing such effects when the results were 

corrected (EPA, 2007b, p. 3-6).17 13

14 These studies by Adams (2002, 2006) were notable in that they were the only

15 controlled exposure human studies available at the time of the 2008 rulemaking that 

16 examined respiratory effects associated with prolonged O3 exposures at levels below 

17 0.080 ppm, which was the lowest exposure level that had been examined in the 1997 

18 review. The Adams (2006) study investigated a range of exposure levels (0.000, 0.040, 

19 0.060, and 0.080 ppm O3) using square-wave and triangular exposure patterns. The study

 

16 These studies, conducted at a facility at the University of California, in Davis, 

CA, reported O3 concentrations to be accurate within +/- 0.003 ppm over the range of 

concentrations included in these studies.

17 These distributional results presented in the Criteria Document and Staff Paper 

for the Adams (2006) study are based on data for squate-wave exposures to 0.080 ppm 

that were not included in the publication but were obtained from the author.
Draft O3 NPR –January 5, 2010 51 Deliberative, Do Not Quote or Cite

1 was designed to examine hour-by-hour changes in pulmonary function (FEV1) and 

2 respiratory symptom responses (total subjective symptoms (TSS) and pain on deep 

3 inspiration (PDI)) between these various exposure protocols at six different time points 

4 within the exposure periods to investigate the effects of different patterns of exposure. At 

5 the 0.060 ppm exposure level, the author reported no statistically significant differences 

6 for FEV1 decrements nor for most respiratory symptoms responses. Statistically

7 significant responses were reported only for TSS for the triangular exposure pattern 

8 toward the end of the exposure period, with the PDI responses being noted as following a 

9 closely similar pattern (Adams, 2006, p. 131-132). EPA’s reanalysis of the data from the 

10 Adams (2006) study addressed the more fundamental question of whether there were 

11 statistically significant differences in responses before and after the 6.6 hour exposure 

12 period (Brown, 2007), and used a standard statistical method appropriate for a simple 

13 before-and-after comparison. The statistical method used by EPA had been used 

14 previously by other researchers to address this same question. EPA’s reanalysis of the 

15 data from the Adams (2006) study, comparing FEV1 responses pre- and post-exposure at 

16 the 0.060 ppm exposure level, found small group mean differences from responses to 

filtered air that were statistically significant (Brown, 2007).18 17

18 Further examination of the post-exposure FEV1 data and mean data at other time

19 points and concentrations also suggest a pattern of response at 0.06 ppm that is consistent 

 

18 Dr. Adams submitted comments on EPA’s reanalysis in which he concluded 

that the FEV1 response in healthy young adults at the 0.060 ppm exposure level in his 

study (Adams, 2006a) does not demonstrate a significant mean effect by ordinarily

acceptable statistical analysis, but is rather in somewhat of a gray area, both in terms of a 

biologically meaningful response and a statistically significant response (Adams, 2007). 

The EPA responded to these comments in the 2008 final rule (73 FR 16455) and in the 

Response to Comments (EPA, 2008, pp. 26-28).
Draft O3 NPR –January 5, 2010 52 Deliberative, Do Not Quote or Cite

1 with a dose-response relationship rather than random variability. For example, the

2 response at 5.6 hours was similar to that of the post-exposure 6.6 hour response and 

3 appeared to also differ from the FA response. At the 0.08 ppm level, the subjects in this 

4 study did not appear to be more responsive to O3 than subjects in previous studies, as the 

5 observed response was similar to that of previous studies (Adams, 2003a,b; Horstman et 

6 al., 1990; McDonnell et al., 1991). Although of much smaller magnitude, the temporal 

7 pattern of the 0.06 ppm response was generally consistent with the temporal patterns of 

8 response to higher concentrations of O3 in this and other studies. These findings are not 

9 unexpected because the previously observed group mean FEV1 responses to 0.08 ppm 

10 were in the range of 6-9% suggesting that exposure to lower concentrations of O3 would 

11 result in smaller, but real group mean FEV1 decrements, i.e., the responses to 0.060 ppm 

12 O3 are consistent with the presence of a smooth exposure-response curve with responses 

13 that do not end abruptly below 0.080 ppm.

14 Moreover, the Adams studies (2002, 2006) also report a small percentage of 

15 subjects experiencing moderate lung function decrements (> 10 percent) at the 0.060 ppm 

16 exposure level. Based on study data (Adams, 2006) provided by the author, 7 percent of 

17 the subjects (2 of 30 subjects) experienced notable FEV1 decrements ( 10 percent) with 

18 the square wave exposure pattern at the 0.060 ppm exposure level (comparing pre- and 

19 post-exposures) when the results were corrected for the effects of exercise alone in 

20 filtered air (EPA, 2007b, p. 3-6). Furthermore, in a prior publication (Adams, 2002), the 

21 author stated that, “some sensitive subjects experience notable effects at 0.06 ppm,” 

22 based on the observation that 20% of subjects exposed to 0.06 ppm O3 (in a face mask 

23 exposure study) had greater than a 10% decrement in FEV1 even though the group mean 
Draft O3 NPR –January 5, 2010 53 Deliberative, Do Not Quote or Cite

1 response was not statistically different from the filtered air response. The effects 

2 described by Adams (2002), along with the reanalysis of the Adams (2006) data as 

3 described above, demonstrate considerable inter-individual variability in responses of 

4 healthy adults at the 0.060 ppmlevel with some individuals experiencing greater than 

5 10% decrements in FEV1. The observation of statistically significant small group mean 

6 lung function decrements in healthy adults at 0.060 ppm O3 lowers the lowest-observed7 effects level found in controlled human exposure studies for lung function decrements 

8 and respiratory symptoms. 

9 Of potentially greater concern is the magnitude of the lung function decrements in 

10 the small group of healthy subjects who had the largest responses (i.e., FEV1 decrements 

11 > 10%). This is a concern because for active healthy people, moderate levels of 

12 functional responses (e.g., FEV1 decrements of > 10% but < 20%) and/or moderate 

13 symptomatic responses would likely interfere with normal activity for relatively few 

14 responsive individuals. However, for people with lung disease, even moderate functional 

15 or symptomatic responses would likely interfere with normal activity for many

16 individuals, and would likely result in more frequent use of medication (see section II.A.4 

17 below). 

18 (ii) Results of Epidemiological and Field Studies

19 A relatively large number of field studies investigating the effects of ambient O3 

20 concentrations, in combination with other air pollutants, on lung function decrements and 

21 respiratory symptoms has been published over the last decade that support the major 

22 findings of the 1996 Criteria Document that lung function changes, as measured by 

23 decrements in FEV1 or peak expiratory flow (PEF), and respiratory symptoms in healthy
Draft O3 NPR –January 5, 2010 54 Deliberative, Do Not Quote or Cite

1 adults and asthmatic children are closely correlated to ambient O3 concentrations. Pre2 1996 field studies focused primarily on children attending summer camps and found O3-

3 related impacts on measures of lung function, but not respiratory symptoms, in healthy

4 children. The newer studies have expanded to evaluate O3-related effects on outdoor 

5 workers, athletes, the elderly, hikers, school children, and asthmatics. Collectively, these 

6 studies confirm and extend clinical observations that prolonged (i.e., 6-8 hour) exposure 

7 periods, combined with elevated levels of exertion or exercise, increase the dose of O3 to 

8 the lungs at a given ambient exposure level and result in larger lung function effects. The 

9 results of one large study of hikers (Korrick et al., 1998), which reported outcome 

10 measures stratified by several factors (e.g., gender, age, smoking status, presence of 

11 asthma) within a population capable of more than normal exertion, provide useful insight. 

12 In this study, lung function was measured before and after hiking, and individual O3

13 exposures were estimated by averaging hourly O3 concentrations from ambient monitors 

14 located at the base and summit. The mean 8-hour average O3 concentration was 0.040 

15 ppm (8-hour average concentration range of 0.021 ppm to 0.074 ppm O3). Decreased 

16 lung function was associated with O3 exposure, with the greatest effect estimates reported 

17 for the subgroup that reported having asthma or wheezing, and for those who hiked for 

18 longer periods of time.

19 Asthma panel studies conducted both in the U.S. and in other countries have 

20 reported that decrements in PEF are associated with routine O3 exposures among 

21 asthmatic and healthy people. One large U.S. multicity study, the National Cooperative 

22 Inner City Asthma Study or NCICAS, (Mortimer et al., 2002) examined O3-related 

23 changes in PEF in 846 asthmatic children from 8 urban areas and reported that the 
Draft O3 NPR –January 5, 2010 55 Deliberative, Do Not Quote or Cite

1 incidence of > 10 percent decrements in morning PEF are associated with increases in 8-

2 hour average O3 for a 5-day cumulative lag, suggesting that O3 exposure may be 

3 associated with clinically significant changes in PEF in asthmatic children; however, no 

4 associations were reported with evening PEF. The mean 8-hour average O3 was 0.048 

5 ppm across the 8 cities. Excluding days when 8-hour average O3 was greater than 0.080 

6 ppm (less than 5 percent of days), the associations with morning PEF remained 

7 statistically significant. Mortimer et al. (2002) discussed potential biological mechanisms 

8 for delayed effects on pulmonary function in asthma, which included increased 

9 nonspecific airway responsiveness secondary to airway inflammation due to O3 exposure. 

10 Two other panel studies (Romieu et al., 1996, 1997) carried out simultaneously in 

11 northern and southwestern Mexico City with mildly asthmatic school children reported 

12 statistically significant O3-related reductions in PEF, with variations in effect depending 

13 on lag time and time of day. Mean 1-hour maximum O3 concentrations in these locations 

14 ranged from 0.190 ppm in northern Mexico City to 0.196 ppm in southwestern Mexico 

15 City. While several studies report statistically significant associations between O3

16 exposure and reduced PEF in asthmatics, other studies did not, possibly due to low levels 

17 of O3 exposure. EPA concludes that these studies collectively indicate that O3 may be 

18 associated with short-term declines in lung function in asthmatic individuals and that the 

19 Mortimer et al. (2002) study showed statistically significant effects at concentrations in 

20 the range below 0.080 ppm O3.

21 Most of the panel studies which have investigated associations between O3

22 exposure and respiratory symptoms or increased use of asthma medication are focused on 

23 asthmatic children. Two large U.S. studies (Mortimer et al., 2002; Gent et al., 2003) have 
Draft O3 NPR –January 5, 2010 56 Deliberative, Do Not Quote or Cite

1 reported associations between ambient O3 concentrations and daily symptoms/asthma 

2 medication use, even after adjustment for copollutants. Results were more mixed, 

3 meaning that a greater proportion of studies were not both positive and statistically

4 significant, across smaller U.S. and international studies that focused on these health 

5 endpoints.

6 The NCICAS reported morning symptoms in 846 asthmatic children from 8 U.S. 

7 urban areas to be most strongly associated with a cumulative 1- to 4-day lag of O3

8 concentrations (Mortimer et al., 2002). The NCICAS used standard protocols that 

9 included instructing caretakers of the subjects to record symptoms (including cough, 

10 chest tightness, and wheeze) in the daily diary by observing or asking the child. While 

11 these associations were not statistically significant in several cities, when the individual 

12 data are pooled from all eight cities, statistically significant effects were observed for the 

13 incidence of symptoms. The authors also reported that the odds ratios remained 

14 essentially the same and statistically significant for the incidence of morning symptoms 

15 when days with 8-hour O3 concentrations above 0.080 ppm were excluded. These days 

16 represented less than 5 percent of days in the study.

17 Gent and colleagues (2003) followed 271 asthmatic children under age 12 and 

18 living in southern New England for 6 months (April through September) using a daily

19 symptom diary. They found that mean 1-hour max O3 and 8-hour max O3 concentrations 

20 were 0.0586 ppm and 0.0513 ppm , respectively. The data were analyzed for two 

21 separate groups of subjects, those who used maintenance asthma medications during the 

22 follow-up period and those who did not. The need for regular medication was considered 

23 to be a proxy for more severe asthma. Not taking any medication on a regular basis and 
Draft O3 NPR –January 5, 2010 57 Deliberative, Do Not Quote or Cite

1 not needing to use a bronchodilator would suggest the presence of very mild asthma. 

2 Statistically significant effects of 1-day lag O3 were observed on a variety of respiratory

3 symptoms only in the medication user group. Both daily 1-hour max and 8-hour max O3 

4 concentrations were similarly related to symptoms such as chest tightness and shortness 

5 of breath. Effects of O3, but not PM2.5, remained significant and even increased in 

6 magnitude in two-pollutant models. Some of the associations were noted at 1-hour max 

7 O3 levels below 0.060 ppm. In contrast, no effects were observed among asthmatics not 

8 using maintenance medication. In terms of person-days of follow-up, this is one of the 

9 larger studies currently available that address symptom outcomes in relation to O3 and 

10 provides supportive evidence for effects of O3 independent of PM2.5. Study limitations 

11 include the post-hoc nature of the population stratification by medication use. Also, the 

12 study did not account for all of the important meteorological factors that might influence 

13 these results, such as relative humidity or dew point. 

14 The multicity study by Mortimer et al. (2002), which examined an asthmatic 

15 population representative of the United States, and several single-city studies indicate a 

16 robust association of O3 concentrations with respiratory symptoms and increased 

17 medication use in asthmatics. While there are a number of well-conducted, albeit 

18 relatively smaller, U.S. studies which showed only limited or a lack of evidence for 

19 symptom increases associated with O3 exposure, these studies had less statistical power 

20 and/or were conducted in areas with relatively low 1-hour maximum average O3 levels, in 

21 the range of 0.03 to 0.09 ppm. The 2006 Criteria Document concludes that the asthma 

22 panel studies, as a group, and the NCICAS in particular, indicate a positive association 

23 between ambient concentrations and respiratory symptoms and increased medication use 
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1 in asthmatics. The evidence has continued to expand since 1996 and now is considered 

2 to be much stronger than in the 1997 review of the O3 primary standard.

3 School absenteeism is another potential surrogate for the health implications of O3 

4 exposure in children. The association between school absenteeism and ambient O3

5 concentrations was assessed in two relatively large field studies. The first study, Chen et 

6 al. (2000), examined total daily school absenteeism in about 28,000 elementary school 

7 students in Nevada over a 2-year period (after adjusting for PM10 and CO concentrations) 

8 and found that ambient O3 concentrations with a distributed lag of 14 days were 

9 statistically significantly associated with an increased rate of school absences. The 

second study, Gilliland et al. (2001), studied O3-related absences among about 2,000 4

th 10

11 grade students in 12 southern California communities and found statistically significant 

12 associations between 8-hour average O3 concentrations (with a distributed lag out to 30 

13 days) and all absence categories, and particularly for respiratory causes. Neither PM10

14 nor NO2 were associated with any respiratory or nonrespiratory illness-related absences 

15 in single pollutant models. The 2006 Criteria Document concludes that these studies of 

16 school absences suggest that ambient O3 concentrations, accumulated over two to four 

17 weeks, may be associated with school absenteeism, and particularly illness-related 

18 absences, but further replication is needed before firm conclusions can be reached 

19 regarding the effect of O3 on school absences. In addition, more research is needed to 

20 help shed light on the implications of variation in the duration of the lag structures (i.e., 1 

21 day, 5 days, 14 days, and 30 days) found both across studies and within data sets by

22 health endpoint and exposure metric.

23 (b) Increased Airway Responsiveness
Draft O3 NPR –January 5, 2010 59 Deliberative, Do Not Quote or Cite

1 As discussed in more detail in the 2006 Criteria Document (section 6.8) and the 

2 2007 Staff Paper (section 3.3.1.1.2), increased airway responsiveness, also known as 

3 airway hyperresponsiveness (AHR) or bronchial hyperreactivity, refers to a condition in 

4 which the propensity for the airways to bronchoconstrict due to a variety of stimuli (e.g., 

5 exposure to cold air, allergens, or exercise) becomes augmented. This condition is 

6 typically quantified by measuring the decrement in pulmonary function after inhalation 

7 exposure to specific (e.g., antigen, allergen) or nonspecific (e.g., methacholine, 

8 histamine) bronchoconstrictor stimuli. Exposure to O3 causes an increase in airway

9 responsiveness as indicated by a reduction in the concentration of stimuli required to 

10 produce a given reduction in FEV1 or increase in airway obstruction. Increased airway

11 responsiveness is an important consequence of exposure to O3 because its presence 

12 means that the airways are predisposed to narrowing on exposure to various stimuli, such 

13 as specific allergens, cold air or SO2. Statistically significant and clinically relevant 

14 decreases in pulmonary function have been observed in early phase allergen response in 

15 subjects with allergic rhinitis after consecutive (4-day) 3-hour exposures to 0.125 ppm O3

16 (Holz et al., 2002). Similar increased airway responsiveness in asthmatics to house dust 

17 mite antigen 16 to 18 hours after exposure to a single dose of O3 (0.160 ppm for 7.6 

18 hours) was observed. These observations, based on O3 exposures to levels much higher 

19 than the 0.084 ppm standard level suggest that O3 exposure may be a clinically important 

20 factor that can exacerbate the response to ambient bronchoconstrictor substances in 

21 individuals with preexisting allergic asthma or rhinitis. Further, O3 may have an 

22 immediate impact on the lung function of asthmatics as well as contribute to effects that 

23 persist for longer periods. 
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1 Kreit et al. (1989) found that O3 can induce increased airway responsiveness in 

2 asthmatic subjects to O3, who typically have increased airway responsiveness at baseline. 

3 A subsequent study (Jörres et al., 1996) suggested an increase in specific (i.e., allergen4 induced) airway reactivity in subjects with allergic asthma, and to a lesser extent in 

5 subjects with allergic rhinitis after short-term exposure to higher O3 levels; other studies 

6 reported similar results. According to one study (Folinsbee and Hazucha, 2000), changes 

7 in airway responsiveness after O3 exposure resolve more slowly than changes in FEV1 or 

8 respiratory symptoms. Other studies of repeated exposure to O3 suggest that changes in 

9 airway responsiveness tend to be somewhat less affected by attenuation with consecutive 

10 exposures than changes in FEV1 (EPA, 2006a, section 6.8).

11 The 2006 Criteria Document (section 6.8) concludes that O3 exposure is linked 

12 with increased airway responsiveness. Both human and animal studies indicate that 

13 increased airway responsiveness is not mechanistically associated with inflammation, and 

14 does not appear to be strongly associated with initial decrements in lung function or 

15 increases in symptoms. As a result of increased airway responsiveness induced by O3

16 exposure, human airways may be more susceptible to a variety of stimuli, including 

17 antigens, chemicals, and particles. Because asthmatic subjects typically have increased 

18 airway responsiveness at baseline, enhanced bronchial response to antigens in asthmatics 

19 raises potential public health concerns as they could lead to increased morbidity (e.g., 

20 medication usage, school absences, emergency room visits, hospital admissions) or to 

21 more persistent alterations in airway responsiveness (EPA 2006a, p. 8-21). As such, 

22 increased airway responsiveness after O3 exposure represents a plausible link between O3

23 exposure and increased hospital admissions. 
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1 (c) Respiratory Inflammation and Increased Permeability

2 Based on evidence from the 1997 review, acute inflammatory responses in the 

3 lung have been observed subsequent to 6.6 hour O3 exposures to the lowest tested level --

4 0.080 ppm -- in healthy adults engaged in moderately high exercise (section 6.9 of the 

5 2006 Criteria Document and section 3.3.1.3 of the 2007 Staff Paper). Some of these prior 

6 studies suggest that inflammatory responses may be detected in some individuals 

7 following O3 exposures in the absence of O3-induced pulmonary decrements in those 

8 subjects. These studies also demonstrate that short-term exposures to O3 also can cause 

9 increased permeability in the lungs of humans and experimental animals. Inflammatory

10 responses and epithelial permeability have been seen to be independent of spirometric 

11 responses. Not only are the newer lung inflammation and increased cellular permeability

12 findings discussed in the 2006 Criteria Document (section 8.4.2) consistent with the 1997

13 review, but they provide better characterization of the physiological mechanisms by

14 which O3 causes these effects. 

15 Lung inflammation and increased permeability, which are distinct events 

16 controlled by different mechanisms, are two commonly observed effects of O3 exposure 

17 observed in all of the species studied. Increased cellular permeability is a disruption of 

18 the lung barrier that leads to leakage of serum proteins, influx of polymorphonuclear 

19 leukocytes (neutrophils or PMNs), release of bioactive mediators, and movement of 

20 compounds from the airspaces into the blood. 
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1 A number of controlled human exposure studies have analyzed bronchoalveolar 

lavage (BAL) and nasal lavage (NL)19 2 fluids and cells for markers of inflammation and 

3 lung damage (EPA, 2006a, Annex AX6). Increased lung inflammation is demonstrated 

4 by the presence of neutrophils found in BAL fluid in the lungs, which has long been 

5 accepted as a hallmark of inflammation. It is apparent, however, that inflammation 

6 within airway tissues may persist beyond the point that inflammatory cells are found in 

7 the BAL fluid. Soluble mediators of inflammation, such as cytokines and arachidonic 

8 acid metabolites have been measured in the BAL fluid of humans exposed to O3. In 

9 addition to their role in inflammation, many of these compounds have 

10 bronchoconstrictive properties and may be involved in increased airway responsiveness 

11 following O3 exposure. An in vitro study of epithelial cells from nonatopic and atopic 

12 asthmatics exposed to 0.010 to 0.100 ppm O3 showed significantly increased 

13 permeability compared to cells from normal persons. This indicates a potentially inherent 

14 susceptibility of cells from asthmatic individuals for O3-induced permeability. 

15 In the 1996 Criteria Document, assessment of controlled human exposure studies 

16 indicated that a single, acute (1 to 4 hours) O3 exposure (> 0.080 to 0.100 ppm) of 

17 subjects engaged in moderate to heavy exercise could induce a number of cellular and 

18 biochemical changes suggestive of pulmonary inflammation and lung permeability (EPA, 

19 2006a, p. 8-22). These changes persisted for at least 18 hours. Markers from BAL fluid 

20 following both 2-hour and 4-hour O3 exposures repeated up to 5 days indicate that there 

 

19 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).
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1 is ongoing cellular damage irrespective of attenuation of some cellular inflammatory

2 responses of the airways, pulmonary function, and symptom scores (EPA, 2006a, p. 8-

3 22). Acute airway inflammation was shown in Devlin et al. (1990) to occur among adults 

4 exposed to 0.080 ppm O3 for 6.6 hours with exercise. McBride et al. (1994) reported 

5 that asthmatic subjects were more sensitive than non-asthmatics to upper airway

6 inflammation for O3 exposures that did not affect pulmonary function (EPA, 2006a, p. 6-

7 33). However, the public health significance of these changes is not entirely clear. 

8 The studies reporting inflammatory responses and markers of lung injury have 

9 clearly demonstrated that there is significant variation in response of subjects exposed, 

10 especially to 6.6 hours O3 exposures at 0.080 and 0.100 ppm. To provide some 

11 perspective on the public health impact for these effects, the 2007 Staff Paper (section 

12 3.3.1.1.3) notes that one study (Devlin et al., 1991) showed that roughly 10 to 50 percent

13 of the 18 young healthy adult subjects experienced notable increases (i.e., > 2 fold 

14 increase) in most of the inflammatory and cellular injury indicators analyzed, associated 

15 with 6.6-hour exposures at 0.080 ppm. Similar, although in some cases higher, fractions 

16 of the population of 10 healthy adults tested saw > 2 fold increases associated with 6.6-

17 hour exposures to 0.100 ppm. The authors of this study expressed the view that 

18 “susceptible subpopulations such as the very young, elderly, and people with pulmonary 

19 impairment or disease may be even more affected” (Devlin et al., 1991). 

20 Since 1996, a substantial number of human exposure studies have been published 

21 which have provided important new information on lung inflammation and epithelial 

22 permeability. Mudway and Kelly (2004) examined O3-induced inflammatory responses 

23 and epithelial permeability with a meta-analysis of 21 controlled human exposure studies 
Draft O3 NPR –January 5, 2010 64 Deliberative, Do Not Quote or Cite

1 and showed that an influx in neutrophils and protein in healthy subjects is associated with 

2 total O3 dose (product of O3 concentration, exposure duration, and minute ventilation) 

3 (EPA, 2006a, p. 6-34). Results of the analysis suggest that the time course for 

4 inflammatory responses (including recruitment of neutrophils and other soluble 

5 mediators) is not clearly established, but there is evidence that attenuation profiles for 

6 many of these parameters are different (EPA, 2006a, p. 8-22).

7 The 2006 Criteria Document (chapter 8) concludes that interaction of O3 with 

8 lipid constituents of epithelial lining fluid (ELF) and cell membranes and the induction of 

9 oxidative stress is implicated in injury and inflammation. Alterations in the expression of 

10 cytokines, chemokines, and adhesion molecules, indicative of an ongoing oxidative stress 

11 response, as well as injury repair and regeneration processes, have been reported in 

12 animal toxicology and human in vitro studies evaluating biochemical mediators 

13 implicated in injury and inflammation. While antioxidants in ELF confer some 

14 protection, O3 reactivity is not eliminated at environmentally relevant exposures (2006 

15 Criteria Document, p. 8-24). Further, antioxidant reactivity with O3 is both species16 specific and dose-dependent.

17 (d) Increased Susceptibility to Respiratory Infection

18 As discussed in more detail in the 2006 Criteria Document (sections 5.2.2, 6.9.6, 

19 and 8.4.2), short-term exposures to O3 have been shown to impair physiological defense 

20 capabilities in experimental animals by depressing alveolar macrophage (AM) functions 

21 and by altering the mucociliary clearance of inhaled particles and microbes resulting in 

22 increased susceptibility to respiratory infection. Short-term O3 exposures also interfere 

23 with the clearance process by accelerating clearance for low doses and slowing clearance 
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1 for high doses. Animal toxicological studies have reported that acute O3 exposures 

2 suppress alveolar phagocytosis and immune system functions. Impairment of host 

3 defenses and subsequent increased susceptibility to bacterial lung infection in laboratory

4 animals has been induced by short-term exposures to O3 levels as low as 0.080 ppm. 

5 A single controlled human exposure study reviewed in the 1996 Criteria 

6 Document (p. 8-26) reported that exposure to 0.080 to 0.100 ppm O3 for 6.6 hours (with 

7 moderate exercise) induced decrements in the ability of AMs to phagocytose 

8 microorganisms. Integrating the recent animal study results with human exposure 

9 evidence available in the 1996 Criteria Document, the 2006 Criteria Document concludes 

10 that available evidence indicates that short-term O3 exposures have the potential to impair 

11 host defenses in humans, primarily by interfering with AM function. Any impairment in 

12 AM function may lead to decreased clearance of microorganisms or nonviable particles. 

13 Compromised AM functions in asthmatics may increase their susceptibility to other O3

14 effects, the effects of particles, and respiratory infections (EPA, 2006a, p. 8-26).

15 (e) Morphological Effects

16 The 1996 Criteria Document found that short-term O3 exposures cause similar

17 alterations in lung morphology in all laboratory animal species studied, including 

18 primates. As discussed in the 2007 Staff Paper (section 3.3.1.1.5), cells in the 

19 centriacinar region (CAR) of the lung (the segment between the last conducting airway

20 and the gas exchange region) have been recognized as a primary target of O3-induced 

21 damage (epithelial cell necrosis and remodeling of respiratory bronchioles), possibly

22 because epithelium in this region receives the greatest dose of O3 delivered to the lower 

23 respiratory tract. Following chronic O3 exposure, structural changes have been observed 
Draft O3 NPR –January 5, 2010 66 Deliberative, Do Not Quote or Cite

1 in the CAR, the region typically affected in most chronic airway diseases of the human 

2 lung (EPA, 2006a, p. 8-24).

3 Ciliated cells in the nasal cavity and airways, as well as Type I cells in the gas4 exchange region, are also identified as targets. While short-term O3 exposures can cause 

5 epithelial cell profileration and fibrolitic changes in the CAR, these changes appear to be 

6 transient with recovery occurring after exposure, depending on species and O3 dose. The 

7 potential impacts of repeated short-term and chronic morphological effects of O3

8 exposure are discussed below in the section on effects from long-term exposures. Long9 term or prolonged exposure has been found to cause chronic lesions similar to early

10 lesions found in individuals with respiratory bronchiolitis, which have the potential to 

11 progress to fibrotic lung disease (2006 Criteria Document, p. 8-25).

12 Recent studies continue to show that short-term and sub-chronic exposures to O3

13 cause similar alterations in lung structure in a variety of experimental animal species. 

14 For example, a series of new studies that used infant rhesus monkeys and simulated 

15 seasonal ambient exposure (0.5 ppm 8 hours/day for 5 days, every 14 days for 11 

16 episodes) reported remodeling in the distal airways; abnormalities in tracheal basement 

17 membrane; eosinophil accumulation in conducting airways; and decrements in airway

18 innervation (2006 Criteria Document, p. 8-25). Based on evidence from animal 

19 toxicological studies, short-term and sub-chronic exposures to O3 can cause 

20 morphological changes in the respiratory systems, particularly in the CAR, of a number 

21 of laboratory animal species (EPA, 2006a, section 5.2.4).

22 (f) Emergency Department Visits/Hospital Admissions for Respiratory Causes
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1 Increased summertime emergency department visits and hospital admissions for

2 respiratory causes have been associated with ambient exposures to O3. As discussed in 

3 section 3.3.1.1.6 of the 2007 Staff Paper, numerous studies conducted in various 

4 locations in the U.S. and Canada consistently have shown a relationship between ambient 

5 O3 levels and increased incidence of emergency department visits and hospital 

6 admissions for respiratory causes, even after controlling for modifying factors, such as 

7 weather and copollutants. Such associations between elevated ambient O3 during 

8 summer months and increased hospital admissions have a plausible biological basis in the 

9 human and animal evidence of functional, symptomatic, and physiologic effects 

10 discussed above and in the increased susceptibility to respiratory infections observed in 

11 laboratory animals. 

12 In the 1997 review of the O3 NAAQS, the Criteria Document evaluated 

13 emergency department visits and hospital admissions as possible outcomes following 

14 exposure to O3 (EPA, 2006a, section 7.3). The evidence was limited for emergency

15 department visits, but results of several studies generally indicated that short-term 

16 exposures to O3 were associated with respiratory emergency department visits. The 

17 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) 18 , was found in the 

group of studies which investigated summertime20 19 daily hospital admissions for 

20 respiratory causes in different eastern North American cities. These studies consistently

21 demonstrated that ambient O3 levels were associated with increased hospital admissions 

 

20 Discussion of the reasons for focusing on warm season studies is found in the 

section 2.A.3.a below.
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1 and accounted for about one to three excess respiratory hospital admissions per million 

2 persons with each 0.100 ppm increase in 1-hour max O3, after adjustment for possible 

3 confounding effects of temperature and copollutants. Overall, the 1996 Criteria 

4 Document concluded that there was strong evidence that ambient O3 exposures can cause 

5 significant exacerbations of preexisting respiratory disease in the general public. Excess 

6 respiratory-related hospital admissions associated with O3 exposures for the New York 

7 City area (based on Thurston et al., 1992) were included in the quantitative risk 

8 assessment in the 1997 review and are included in the current assessment along with 

9 estimates for respiratory-related hospital admissions in Cleveland, Detroit, and Los 

10 Angeles based on more recent studies (2007 Staff Paper, chapter 5). Significant 

11 uncertainties and the difficulty of obtaining reliable baseline incidence numbers resulted 

12 in emergency department visits not being used in the quantitative risk assessment in 

13 either the 1997 or the 2008 O3 NAAQS review.

14 In the past decade, a number of studies have examined the temporal pattern 

15 associations between O3 exposures and emergency department visits for respiratory

16 causes (EPA, 2006a, section 7.3.2). These studies are summarized in the 2006 Criteria 

17 Document (chapter 7 Annex) and some are shown in Figure 1 (in section II.A.3). 

18 Respiratory causes for emergency department visits include asthma, bronchitis, 

19 emphysema, pneumonia, and other upper and lower respiratory infections, such as 

20 influenza, but asthma visits typically dominate the daily incidence counts. Most studies 

21 report positive associations with O3. Among studies with adequate controls for seasonal 

22 patterns, many reported at least one significant positive association involving O3.
Draft O3 NPR –January 5, 2010 69 Deliberative, Do Not Quote or Cite

1 In reviewing evidence for associations between emergency department visits for 

2 asthma and short-term O3 exposures, the 2006 Criteria Document (Figure 7-8, p. 7-68) 

3 notes that in general, O3 effect estimates from summer only analyses tended to be 

4 positive and larger compared to results from cool season or all year analyses. Several of 

5 the studies reported significant associations between O3 concentrations and emergency

6 department visits for respiratory causes, in particular asthma. However, inconsistencies 

7 were observed which were at least partially attributable to differences in model 

8 specifications and analysis approach among various studies. For example, ambient O3

9 concentrations, length of the study period, and statistical methods used to control 

10 confounding by seasonal patterns and copollutants appear to affect the observed O3 effect 

11 on emergency department visits. 

12 Hospital admissions studies focus specifically on unscheduled admissions because 

13 unscheduled hospital admissions occur in response to unanticipated disease exacerbations 

14 and are more likely than scheduled admissions to be affected by variations in 

15 environmental factors, such as daily O3 levels. Results of a fairly large number of these 

16 studies published during the past decade are summarized in 2006 Criteria Document

17 (chapter 7 Annex), and results of U.S. and Canadian studies are shown in Figure 1 below 

18 (in section II.A.3). As a group, these hospital admissions studies tend to be larger 

19 geographically and temporally than the emergency department visit studies and provide 

20 results that are generally more consistent. The strongest associations of respiratory

21 hospital admissions with O3 concentrations were observed using short lag periods, in 

22 particular for a 0-day lag (same day exposure) and a 1-day lag (previous day exposure). 

23 Most studies in the United States and Canada indicated positive, statistically significant 
Draft O3 NPR –January 5, 2010 70 Deliberative, Do Not Quote or Cite

1 associations between ambient O3 concentrations and respiratory hospital admissions in 

2 the warm season. However, not all studies found a statistically significant relationship 

3 with O3, possibly because of very low ambient O3 levels. Analyses for confounding 

4 using multipollutant regression models suggest that copollutants generally do not 

5 confound the association between O3 and respiratory hospitalizations. Ozone effect 

6 estimates were robust to PM adjustment in all-year and warm-season only data. 

7 Overall, the 2006 Criteria Document concludes that positive and robust 

8 associations were found between ambient O3 concentrations and various respiratory

9 disease hospitalization outcomes, when focusing particularly on results of warm-season 

10 analyses. Recent studies also generally indicate a positive association between O3

11 concentrations and emergency department visits for asthma during the warm season 

12 (EPA, 2006a, p. 7-175). These positive and robust associations are supported by the 

13 controlled human exposure, animal toxicological, and epidemiological evidence for lung 

14 function decrements, increased respiratory symptoms, airway inflammation, and 

15 increased airway responsiveness. Taken together, the overall evidence supports a causal 

16 relationship between acute ambient O3 exposures and increased respiratory morbidity

17 outcomes resulting in increased emergency department visits and hospitalizations during 

18 the warm season (EPA, 2006a, p. 8-77).

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

20 The 1996 Criteria Document concluded that there was insufficient evidence from 

21 the limited number of studies to determine whether long-term O3 exposures resulted in 

22 chronic health effects at ambient levels observed in the U.S. However, the aggregate 

23 evidence suggested that O3 exposure, along with other environmental factors, could be 
Draft O3 NPR –January 5, 2010 71 Deliberative, Do Not Quote or Cite

1 responsible for health effects in exposed populations. Animal toxicological studies 

2 carried out in the 1980’s and 1990’s demonstrated that long-term exposures can result in 

3 a variety of morphological effects, including permanent changes in the small airways of 

4 the lungs, including remodeling of the distal airways and CAR and deposition of 

5 collagen, possibly representing fibrotic changes. These changes result from the damage 

6 and repair processes that occur with repeated exposure. Fibrotic changes were also found 

7 to persist after months of exposure providing a potential pathophysiologic basis for 

8 changes in airway function observed in children in some recent epidemiological studies. 

9 It appears that variable seasonal ambient patterns of exposure may be of greater concern 

10 than continuous daily exposures. 

11 Several studies published since 1996 have investigated lung function changes 

12 over seasonal time periods (EPA, 2006a, section 7.5.3). The 2006 Criteria Document (p. 

13 7-114) summarizes these studies which collectively indicate that seasonal O3 exposure is 

14 associated with smaller growth-related increases in lung function in children than they

15 would have experienced living in areas with lower O3 levels. There is some limited 

16 evidence that seasonal O3 also may affect lung function growth in young adults, although 

17 the uncertainty about the role of copollutants makes it difficult to attribute the effects to 

18 O3 alone.

19 Lung capacity grows during childhood and adolescence as body size increases, 

20 reaches a maximum during the twenties, and then begins to decline steadily and 

21 progressively with age. Long-term exposure to air pollution has long been thought to 

22 contribute to slower growth in lung capacity, diminished maximally attained capacity, 

23 and/or more rapid decline in lung capacity with age (EPA, 2006a, section 7.5.4). 
Draft O3 NPR –January 5, 2010 72 Deliberative, Do Not Quote or Cite

1 Toxicological findings evaluated in the 1996 Criteria Document demonstrated that 

2 repeated daily exposure of rats to an episodic profile of O3 caused small, but significant, 

3 decrements in growth-related lung function that were consistent with early indicators of 

4 focal fibrogenesis in the proximal alveolar region, without overt fibrosis. Because O3 at 

5 sufficient concentrations is a strong respiratory irritant and has been shown to cause 

6 inflammation and restructuring of the respiratory airways, it is plausible that long-term 

7 O3 exposures might have a negative impact on baseline lung function, particularly during

8 childhood when these exposures might be associated with long-term risks.

9 Several epidemiological studies published since 1996 have examined the 

10 relationship between lung function development and long-term O3 exposure. The most 

11 extensive and robust study of respiratory effects in relation to long-term air pollution 

12 exposures among children in the U.S. is the Children’s Health Study carried out in 12 

13 communities of southern California starting in 1993. One analysis (Peters et al., 1999a) 

14 examined the relationship between long-term O3 exposures and self-reports of respiratory

15 symptoms and asthma in a cross sectional analysis and found a limited relationship 

16 between outcomes of current asthma, bronchitis, cough and wheeze and a 0.040 ppm 

17 increase in 1-hour max O3 (EPA, 2006a, p. 7-115). Another analysis (Peters et al., 

18 1999b) examined the relationship between lung function at baseline and levels of air 

19 pollution in the community. They reported evidence that annual mean O3 levels were 

20 associated with decreases in FVC, FEV1, PEF and forced expiratory flow (FEF25-75) (the 

21 latter two being statistically significant) among females but not males. In a separate 

analysis (Gauderman et al., 2000) of 4th, 7th, and 10th 22 grade students, a longitudinal 

23 analysis of lung function development over four years found no association with O3
Draft O3 NPR –January 5, 2010 73 Deliberative, Do Not Quote or Cite

1 exposure. The Children’s Health Study enrolled a second cohort of more than 1500 

2 fourth graders in 1996 (Gauderman et al., 2002). While the strongest associations with 

3 negative lung function growth were observed with acid vapors in this cohort, children 

4 from communities with higher 4-year average O3 levels also experienced smaller 

5 increases in various lung function parameters. The strongest relationship with O3 was 

6 with PEF. Specifically, children from the least-polluted community had a small but 

7 statistically significant increase in PEF as compared to those from the most-polluted 

8 communities. In two-pollutant models, only 8-hour average O3 and NO2 were significant 

9 joint predictors of FEV1 and maximal midexpiratory flow (MMEF). Although results 

10 from the second cohort of children are supportive of a weak association, the definitive 8-

11 year follow-up analysis of the first cohort (Gauderman et al., 2004a) provides little 

12 evidence that long-term exposure to ambient O3 at current levels is associated with 

13 significant deficits in the growth rate of lung function in children. Avol et al. (2001) 

14 examined children who had moved away from participating communities in southern 

15 California to other states with improved air quality. They found that a negative, but not 

16 statistically significant, association was observed between O3 and lung function 

17 parameters. Collectively, the results of these reports from the children’s health cohorts 

18 provide little evidence to support an impact of long-term O3 exposures on lung function 

19 development.

20 Evidence for a significant relationship between long-term O3 exposures and 

21 decrements in maximally attained lung function was reported in a nationwide study of 

22 first year Yale students (Kinney et al., 1998; Galizia and Kinney, 1999) (EPA, 2006a, p. 

23 7-120). Males had much larger effect estimates than females, which might reflect higher 
Draft O3 NPR –January 5, 2010 74 Deliberative, Do Not Quote or Cite

1 outdoor activity levels and correspondingly higher O3 exposures during childhood. A 

2 similar study of college freshmen at University of California at Berkeley also reported 

3 significant effects of long-term O3 exposures on lung function (Künzli et al., 1997; Tager 

4 et al., 1998). In a comparison of students whose city of origin was either Los Angeles or 

5 San Francisco, long-term O3 exposures were associated with significant changes in mid6 and end-expiratory flow measures, which could be considered early indicators for 

7 pathologic changes that might progress to COPD. 

8 There have been a few studies that investigated associations between long-term 

9 O3 exposures and the onset of new cases of asthma (EPA, 2006a, section 7.5.6). The 

10 Adventist Health and Smog (AHSMOG) study cohort of about 4,000 was drawn from 

11 nonsmoking, non-Hispanic white adult Seventh Day Adventists living in California 

12 (Greer et al., 1993; McDonnell et al., 1999). During the ten-year follow-up in 1987, a 

13 statistically significant increased relative risk of asthma development was observed in 

14 males, compared to a nonsignificant relative risk in females (Greer et al., 1993). In the 

15 15-year follow-up in 1992, it was reported that for males, there was a statistically

16 significant increased relative risk of developing asthma associated with 8-hour average

17 O3 exposures, but there was no evidence of an association in females. Consistency of 

18 results in the two studies with different follow-up times provides supportive evidence of 

19 the potential for an association between long-term O3 exposure and asthma incidence in 

20 adult males; however, representativeness of this cohort to the general U.S. population 

21 may be limited (EPA, 2006a, p. 7-125).

22 In a similar study (McConnell et al., 2002) of incident asthma among children 

23 (ages 9 to 16 at enrollment), annual surveys of 3,535 children initially without asthma 
Draft O3 NPR –January 5, 2010 75 Deliberative, Do Not Quote or Cite

1 were used to identify new-onset asthma cases as part of the Children’s Health Study. Six 

2 high-O3 and six low-O3 communities were identified where the children resided. There 

3 were 265 children who reported new-onset asthma during the follow-up period. 

4 Although asthma risk was no higher for all residents of the six high-O3 communities 

5 versus the six low-O3 communities, asthma risk was 3.3 times greater for children who 

6 played three or more sports as compared with children who played no sports within the 

7 high-O3 communities. This association was absent in the communities with lower O3 

8 concentrations. No other pollutants were found to be associated with new-onset asthma 

9 (EPA, 2006a, p. 7-125). Playing sports may result in extended outdoor activity and 

10 exposure occurring during periods when O3 levels are higher. It should be noted, 

11 however, that the results of the Children’s Health Study were based on a small number of 

12 new-onset asthma cases among children who played three or more sports. Future

13 replication of these findings in other cohorts would help determine whether a causal 

14 interpretation is appropriate.

15 In animal toxicology studies, the progression of morphological effects reported 

16 during and after a chronic exposure in the range of 0.50 to 1.00 ppm O3 (well above 

17 current ambient levels)is complex, with inflammation peaking over the first few days of 

18 exposure, then dropping, then plateauing, and finally, largely disappearing (EPA, 2006a, 

19 section 5.2.4.4). By contrast, fibrotic changes in the tissue increase very slowly over 

20 months of exposure, and, after exposure ceases, the changes sometimes persist or 

21 increase. Epithelial hyperplasia peaks soon after the inflammatory response but is 

22 usually maintained in both the nose and lungs with continuous exposure; it also does not 

23 return to pre-exposure levels after the end of exposure. Patterns of exposure in this same 
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1 concentration range determine effects, with 18 months of daily exposure, causing less 

2 morphologic damage than exposures on alternating months. This is important as 

3 environmental O3 exposure is typically seasonal. Long-term studies by Plopper and 

4 colleagues (Evans et al., 2003; Schelegle et al., 2003; Chen et al., 2003; Plopper and 

5 Fanucchi, 2000) investigated infant rhesus monkeys exposed to simulated, seasonal O3

6 and demonstrated: 1) remodeling in the distal airways, 2) abnormalities in tracheal 

7 basement membrane; 3) eosinophil accumulation in conducting airways; and 4) 

8 decrements in airway innervation (EPA, 2006a, p. 5-45). These findings provide 

9 additional information regarding possible injury-repair processes occurring with long10 term O3 exposures suggesting that these processes are only partially reversible and may 

11 progress following cessation of O3 exposure. Further, these processes may lead to 

12 nonreversible structural damage to lung tissue; however, there is still too much 

13 uncertainty to characterize the significance of these findings to human exposure profiles 

14 and effect levels (EPA, 2006a, p. 8-25).

15 In summary, in the past decade, important new longitudinal studies have 

16 examined the effect of chronic O3 exposure on respiratory health outcomes. Limited 

17 evidence from recent long-term morbidity studies have suggested in some cases that 

18 chronic exposure to O3 may be associated with seasonal declines in lung function or 

19 reduced lung function development, increases in inflammation, and development of 

20 asthma in children and adults. Seasonal decrements or smaller increases in lung function 

21 measures have been reported in several studies; however, the extent to which these 

22 changes are transient remains uncertain. While there is supportive evidence from animal 

23 studies involving effects from chronic exposures, large uncertainties still remain as to 
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1 whether current ambient levels and exposure patterns might cause these same effects in 

2 human populations. The 2006 Criteria Document concludes that epidemiological studies 

3 of new asthma development and longer-term lung function declines remain inconclusive 

4 at present (EPA, 2006a, p. 7-134). 

5 iii. Effects on the Cardiovascular System of O3 Exposure

6 At the time of the 1997 review, the possibility of O3-induced cardiovascular 

7 effects was largely unrecognized. Since then, a very limited body of evidence from 

8 animal, controlled human exposure, and epidemiologic studies has emerged that provides 

9 evidence for some potential plausible mechanisms for how O3 exposures might exert 

10 cardiovascular system effects, however further research is needed to substantiate these 

11 potential mechanisms. Possible mechanisms may involve O3-induced secretions of 

12 vasoconstrictive substances and/or effects on neuronal reflexes that may result in 

13 increased arterial blood pressure and/or altered electrophysiologic control of heart rate or 

14 rhythm. Some animal toxicology studies have shown O3-induced decreases in heart rate, 

15 mean arterial pressure, and core temperature. One controlled human exposure study that 

16 evaluated effects of O3 exposure on cardiovascular health outcomes found no significant 

17 O3-induced differences in ECG or blood pressure in healthy or hypertensive subjects but 

18 did observe a significant O3-induced increase the alveolar-to-arterial PO2 gradient and 

19 heart rate in both groups resulting in an overall increase in myocardial work and 

20 impairment in pulmonary gas exchange (Gong et al., 1998). In another controlled human 

21 exposure study, inhalation of a mixture of PM2.5 and O3 by healthy subjects increased 

22 brachial artery vasoconstriction and reactivity (Brook et al., 2002).
Draft O3 NPR –January 5, 2010 78 Deliberative, Do Not Quote or Cite

1 The evidence from a few animal studies also includes potential direct effects such 

2 as O3-induced release from lung epithelial cells of platelet activating factor (PAF) that 

3 may contribute to blood clot formation that would have the potential to increase the risk 

4 of serious cardiovascular outcomes (e.g., heart attack, stroke, mortality). Also, 

5 interactions of O3 with surfactant components in epithelial lining fluid of the lung may

6 result in production of oxysterols and reactive oxygen species that may exhibit PAF-like 

7 activity contributing to clotting and also may exert cytotoxic effects on lung and heart 

8 muscle cells. 

9 Epidemiological panel and field studies that examined associations between O3

10 and various cardiac physiologic endpoints have yielded limited evidence suggestive of a 

11 potential association between acute O3 exposure and altered heart rate variability (HRV), 

12 ventricular arrhythmias, and incidence of heart attacks (myocardial infarction or MI). A 

13 number of epidemiological studies have also reported associations between short-term 

14 exposures and hospitalization for cardiovascular diseases. As shown in Figure 7-13 of 

15 the 2006 Criteria Document, many of the studies reported negative or inconsistent 

16 associations. Some other studies, especially those that examined the relationship when 

17 O3 exposures were higher, have found robust positive associations between O3 and 

18 cardiovascular hospital admissions (EPA, 2006a, p. 7-82). For example, one study

19 reported a positive association between O3 and cardiovascular hospital admissions in 

20 Toronto, Canada in a summer-only analysis (Burnett et al., 1997b). The results were 

21 robust to adjustment for various PM indices, whereas the PM effects diminished when 

22 adjusted for gaseous pollutants. Other studies stratified their analysis by temperature 
Draft O3 NPR –January 5, 2010 79 Deliberative, Do Not Quote or Cite

1 (i.e., by warms days versus cool days). Several analyses using warm season days 

2 consistently produced positive associations. 

3 The epidemiologic evidence for cardiovascular morbidity is much weaker than for 

4 respiratory morbidity, with only one of several U.S. and Canadian studies showing 

5 statistically significant positive associations of cardiovascular hospitalizations with 

6 warm-season O3 concentrations. Most of the available European and Australian studies, 

7 all of which conducted all-year O3 analyses, did not find an association between short8 term O3 concentrations and cardiovascular hospitalizations. Overall, the currently 

9 available evidence is inconclusive regarding an association between cardiovascular 

10 hospital admissions and ambient O3 exposure (EPA, 2006a, p. 7-83).

11 In summary, based on the evidence from animal toxicology, controlled human 

12 exposure, and epidemiological studies, from the 2006 Criteria Document (p. 8-77) 

13 concludes that this generally limited body of evidence is suggestive that O3 can directly

14 and/or indirectly contribute to cardiovascular-related morbidity, but that much needs to 

15 be done to more fully integrate links between ambient O3 exposures and adverse 

16 cardiovascular outcomes.

17 b. Mortality

18 i. Mortality and Short-term O3 Exposure

19 The 1996 Criteria Document concluded that an association between daily

20 mortality and O3 concentration for areas with high O3 levels (e.g., Los Angeles) was 

21 suggested. However, due to a very limited number of studies available at that time, there 

22 was insufficient evidence to conclude that the observed association was likely causal. 
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1 The 2006 Criteria Document included results from numerous epidemiological 

2 analyses of the relationship between O3 and mortality. Additional single city analyses 

3 have also been conducted since 1996, however, the most pivotal studies in EPA’s (and 

4 CASAC’s) finding of increased support for the relationship between premature mortality

5 and O3 is in part related to differences in study design – limiting analyses to warm 

6 seasons, better control for copollutants, particularly PM, and use of multicity designs 

7 (both time series and meta-analytic designs). Key findings are available from multicity

8 time-series studies that report associations between O3 and mortality. These studies 

9 include analyses using data from 90 U.S. cities in the National Mortality, Morbidity and 

10 Air Pollution (NMMAPS) study (Dominici et al., 2003) and from 95 U.S. communities in 

11 an extension to the NMMAPS analyses (Bell et al., 2004). 

12 The original 90-city NMMAPS analysis, with data from 1987 to 1994, was 

13 primarily focused on investigating effects of PM10 on mortality. A significant association 

14 was reported between mortality and 24-hour average O3 concentrations in analyses using 

15 all available data as well as in the warm season only analyses (Dominici et al., 2003). 

16 The estimate using all available data was about half that for the summer-only data at a lag 

17 of 1-day. The extended NMMAPS analysis included data from 95 U.S. cities and 

18 included an additional 6 years of data, from 1987-2000 (Bell et al., 2004). Significant 

19 associations were reported between O3 and mortality in analyses using all available data. 

20 The effect estimate for increased mortality was approximately 0.5 percent per 0.020 ppm 

21 change in 24-hour average O3 measured on the same day, and approximately 1.04 percent

22 per 0.020 ppm change in 24-hour average O3 in a 7-day distributed lag model (EPA, 

23 2006a, p. 7-88). In analyses using only data from the warm season, the results were not 
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1 significantly different from the full-year results. The authors also report that O3-mortality

2 associations were robust to adjustment for PM (EPA, 2006a, p. 7-100). Using a subset of 

3 the NMMAPS data set, Huang et al. (2005) focused on associations between 

4 cardiopulmonary mortality and O3 exposure (24-hour average) during the summer season 

5 only. The authors report an approximate 1.47 percent increase per 0.020 ppm change in 

6 O3 concentration measured on the same day and an approximate 2.52 percent increase per 

7 0.020 ppm change in O3 concentration using a 7-day distributed lag model. These 

8 findings suggest that the effect of O3 on mortality is immediate but also persists for 

9 several days. 

10 As discussed below in section II.A.3.a, confounding by weather, especially 

11 temperature, is complicated by the fact that higher temperatures are associated with the 

12 increased photochemical activities that are important for O3 formation. Using a case13 crossover study design, Schwartz (2005) assessed associations between daily maximum 

14 concentrations and mortality, matching case and control periods by temperature, and 

15 using data only from the warm season. The reported effect estimate of approximately

16 0.92 percent change in mortality per 0.040 ppm O3 (1-hour maximum) was similar to 

17 time-series analysis results with adjustment for temperature (approximately 0.76 percent

18 per 0.040 ppm O3), suggesting that associations between O3 and mortality were robust to 

19 the different adjustment methods for temperature.

20 An initial publication from APHEA, a European multicity study, reported 

21 statistically significant associations between daily maximum O3 concentrations and 

22 mortality in four cities in a full year analysis (Toulomi et al., 1997). An extended 

23 analysis was done using data from 23 cities throughout Europe (Gryparis et al., 2004). In 
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1 this report, a positive but not statistically significant association was found between 

2 mortality and 1-hour daily maximum O3 in a full year analysis. Gryparis et al. (2004) 

3 noted that there was a considerable seasonal difference in the O3 effect on mortality; thus, 

4 the small effect for the all-year data might be attributable to inadequate adjustment for 

5 confounding by seasonality. Focusing on analyses using summer measurements, the 

6 authors report statistically significant associations with total mortality, cardiovascular 

7 mortality and respiratory mortality (EPA, 2006a, p. 7-93, 7-99).

8 Numerous single-city analyses have also reported associations between mortality 

9 and short-term O3 exposure, especially for those analyses using warm season data. As 

10 shown in Figure 7-21 of the 2006 Criteria Document, the results of recent publications 

11 show a pattern of positive, often statistically significant associations between short-term 

12 O3 exposure and mortality during the warm season. In considering results from year13 round analyses, there remains a pattern of positive results but the findings are less 

14 consistent. In most single-city analyses, effect estimates were not substantially changed 

15 with adjustment for PM (EPA, 2006a, Figure 7-22). 

16 In addition, several meta-analyses have been conducted on the relationship 

17 between O3 and mortality. As described in section 7.4.4 of the 2006 Criteria Document, 

18 these analyses reported fairly consistent and positive combined effect estimates ranging 

19 from approximately 1.5 to 2.5 percent increase in mortality for a standardized change in 

20 O3 (EPA, 2006a, Figure 7-20). Three recent meta-analyses evaluated potential sources of 

21 heterogeneity in O3-mortality associations (Bell et al., 2005; Ito et al., 2005; Levy et al., 

22 2005). The 2006 Criteria Document (p. 7-96) observes common findings across all three 

23 analyses, in that all reported that effect estimates were larger in warm season analyses, 
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1 reanalysis of results using default convergence criteria in generalized additive models 

2 (GAM) did not change the effect estimates, and there was no strong evidence of 

3 confounding by PM. Bell et al. (2005) and Ito et al. (2005) both provided suggestive 

4 evidence of publication bias, but O3-mortality associations remained after accounting for 

5 that potential bias. The 2006 Criteria Document concludes that the “positive O3 effects 

6 estimates, along with the sensitivity analyses in these three meta-analyses, provide 

7 evidence of a robust association between ambient O3 and mortality” (EPA, 2006a, p. 7-

8 97). 

9 Most of the single-pollutant model estimates from single-city studies range from 

10 0.5 to 5 percent excess deaths per standardized increments. Corresponding summary

11 estimates in large U.S. multicity studies ranged between 0.5 to 1 percent with some 

12 studies noting heterogeneity across cities and studies (EPA, 2006a, p. 7-110).

13 Finally, from those studies that included assessment of associations with specific 

14 causes of death, it appears that effect estimates for associations with cardiovascular 

15 mortality are larger than those for total mortality. The meta-analysis by Bell et al. (2005) 

16 observed a slightly larger effect estimate for cardiovascular mortality compared to 

17 mortality from all causes. The effect estimate for respiratory mortality was 

18 approximately one-half that of cardiovascular mortality in the meta-analysis. However, 

19 other studies have observed larger effect estimates for respiratory mortality compared to 

20 cardiovascular mortality. The apparent inconsistency regarding the effect size of O3-

21 related respiratory mortality may be due to reduced statistical power in this subcategory

22 of mortality (EPA, 2006a, p. 7-108).
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1 In summary, many single- and multicity studies observed positive associations of 

2 ambient O3 concentrations with total nonaccidental and cardiopulmonary mortality. The 

3 2006 Criteria Document finds that the results from U.S. multicity time-series studies 

4 provide the strongest evidence to date for O3 effects on acute mortality. Recent meta5 analyses also indicate positive risk estimates that are unlikely to be confounded by PM; 

6 however, future work is needed to better understand the influence of model specifications 

7 on the risk coefficient (EPA, 2006a, p. 7-175). A meta-analysis that examined specific 

8 causes of mortality found that the cardiovascular mortality risk estimates were higher 

9 than those for total mortality. For cardiovascular mortality, the 2006 Criteria Document

10 (Figure 7-25, p. 7-106) suggests that effect estimates are consistently positive and more 

11 likely to be larger and statistically significant in warm season analyses. The findings 

12 regarding the effect size for respiratory mortality have been less consistent, possibly

13 because of lower statistical power in this subcategory of mortality. The 2006 Criteria 

14 Document (p. 8-78) concludes that these findings are highly suggestive that short-term O3 

15 exposure directly or indirectly contribute to non-accidental and cardiopulmonary-related 

16 mortality, but additional research is needed to more fully establish underlying 

mechanisms by which such effects occur.21 17

 

21 In commenting on the Criteria Document, the CASAC Ozone Panel raised 

questions about the implications of these time-series results in a policy context, 

emphasizing that “...while the time-series study design is a powerful tool to detect very 

small effects that could not be detected using other designs, it is also a blunt tool” 

(Henderson, 2006b). They note that “. . .not only is the interpretation of these 

associations complicated by the fact that the day-to-day variation in concentrations of 

these pollutants is, to a varying degree, determined by meteorology, the pollutants are 

often part of a large and highly correlated mix of pollutants, only a very few of which are 

measured” (Henderson, 2006b). Even with these uncertainties, the CASAC Ozone Panel, 

in its review of the Staff Paper, found “...premature total non-accidental and 
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1 ii. Mortality and Long-term O3 Exposure

2 Little evidence was available in the 1997 review on the potential for associations 

3 between mortality and long-term exposure to O3. In the Harvard Six City prospective 

4 cohort analysis, the authors report that mortality was not associated with long-term 

5 exposure to O3 (Dockery et al., 1993). The authors note that the range of O3

6 concentrations across the six cities was small, which may have limited the power of the 

7 study to detect associations between mortality and O3 levels (EPA, 2006a, p. 7-127). 

8 As discussed in section 7.5.8 of the 2006 Criteria Document, in this review there 

9 are results available from three prospective cohort studies: the American Cancer Society 

10 (ACS) study (Pope et al., 2002), the Adventist Health and Smog (AHSMOG) study

11 (Beeson et al., 1998; Abbey et al., 1999), and the U.S. Veterans Cohort study (Lipfert et 

12 al., 2000, 2003). In addition, a major reanalysis report includes evaluation of data from 

the Harvard Six City cohort study (Krewski et al., 2000). 22 13 This reanalysis also includes 

14 additional evaluation of data from the initial ACS cohort study report that had only

15 reported results of associations between mortality and long-term exposure to fine 

16 particles and sulfates (Pope et al., 1995). This reanalysis was discussed in the 2007 Staff 

17 Paper (section 3.3.2.2) but not in the 2006 Criteria Document.

18 In this reanalysis of data from the previous Harvard Six City prospective cohort

19 study, the investigators replicated and validated the findings of the original studies, and 

 

cardiorespiratory mortality for inclusion in the quantitative risk assessment to be 

appropriate.” (Henderson, 2006b)

22 This reanalysis report and the original prospective cohort study findings are 

discussed in more detail in section 8.2.3 of the Air Quality Criteria for Particulate Matter

(EPA, 2004).
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1 the report included additional quantitative results beyond those available in the original 

2 report (Krewski et al., 2000). In the reanalysis of data from the Harvard Six Cities study, 

3 the effect estimate for the association between long-term O3 concentrations and mortality

4 was negative and nearly statistically significant (relative risk = 0.87, 95 percent CI: 0.76, 

5 1.00).

6 The ACS study is based on health data from a large prospective cohort of 

7 approximately 500,000 adults and air quality data from about 150 U.S. cities. The initial 

8 report (Pope et al., 1995) focused on associations with fine particles and sulfates, for 

9 which significant associations had been reported in the earlier Harvard Six Cities study

10 (Dockery et al., 1993). As part of the major reanalysis of these data, results for 

11 associations with other air pollutants were also reported, and the authors report that no 

12 significant associations were found between O3 and all-cause mortality. However, a

13 significant association was reported for cardiopulmonary mortality in the warm season 

14 (Krewski et al., 2000). The ACS II study (Pope et al., 2002) reported results of 

15 associations with an extended data base; the mortality records for the cohort had been 

16 updated to include 16 years of follow-up (compared with 8 years in the first report) and 

17 more recent air quality data were included in the analyses. Similar to the earlier 

18 reanalysis, a marginally significant association was observed between long-term exposure 

19 to O3 and cardiopulmonary mortality in the warm season. No other associations with 

20 mortality were observed in both the full-year and warm season analyses. 

21 The Adventist Health and Smog (AHSMOG) cohort includes about 6,000 adults 

22 living in California. In two studies from this cohort, a significant association has been 

23 reported between long-term O3 exposure and increased risk of lung cancer mortality
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1 among males only (Beeson et al., 1998; Abbey et al., 1999). No significant associations 

2 were reported between long-term O3 exposure and mortality from all causes or 

3 cardiopulmonary causes. Due to the small numbers of lung cancer deaths (12 for males, 

4 18 for females) and the precision of the effect estimate (i.e., the wide confidence 

5 intervals), the 2006 Criteria Document (p. 7-130) discussed concerns about the 

6 plausibility of the reported association with lung cancer. 

7 The U.S. Veterans Cohort study (Lipfert et al., 2000, 2003) of approximately

8 50,000 middle-aged males diagnosed with hypertension, reported some positive 

associations between mortality and peak O3 exposures (95th 9 percentile level for several 

10 years of data). The study included numerous analyses using subsets of exposure and 

11 mortality follow-up periods which spanned the years 1960 to 1996. In the results of 

12 analyses using deaths and O3 exposure estimates concurrently across the study period, 

13 there were positive, statistically significant associations between peak O3 and mortality

14 (EPA, 2006a, p. 7-129).

15 Overall, the 2006 Criteria Document (p. 7-130) concludes that consistent 

16 associations have not been reported between long-term O3 exposure and all-cause, 

17 cardiopulmonary or lung cancer mortality.

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

19 Beyond the direct health effects attributable to inhalation exposure to O3 in the 

20 ambient air discussed above, the 2006 Criteria Document also assesses potential indirect

21 effects related to the presence of O3 in the ambient air by considering the role of ground22 level O3 in mediating human health effects that may be directly attributable to exposure 

23 to solar ultraviolet radiation (UV-B). The 2006 Criteria Document (chapter 10) focuses 
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1 this assessment on three key factors, including those factors that govern (1) UV-B 

2 radiation flux at the earth’s surface, (2) human exposure to UV-B radiation, and (3) 

3 human health effects due to UV-B radiation. In so doing, the 2006 Criteria Document 

4 provides a thorough analysis of the current understanding of the relationship between 

5 reducing ground-level O3 concentrations and the potential impact these reductions might 

6 have on increasing UV-B surface fluxes and indirectly contributing to UV-B related 

7 health effects.

8 There are many factors that influence UV-B radiation penetration to the earth’s 

9 surface, including latitude, altitude, cloud cover, surface albedo, PM concentration and 

10 composition, and gas phase pollution. Of these, only latitude and altitude can be defined 

11 with small uncertainty in any effort to assess the changes in UV-B flux that may be 

12 attributable to any changes in tropospheric O3 as a result of any revision to the O3

13 NAAQS. Such an assessment of UV-B related health effects would also need to take into 

14 account human habits, such as outdoor activities (including age- and occupation-related 

15 exposure patterns), dress and skin care to adequately estimate UV-B exposure levels. 

16 However, little is known about the impact of these factors on individual exposure to UV17 B.

18 Moreover, detailed information does not exist regarding other factors that are 

19 relevant to assessing changes in disease incidence, including: type (e.g., peak or 

20 cumulative) and time period (e.g., childhood, lifetime, current) of exposures related to 

21 various adverse health outcomes (e.g., damage to the skin, including skin cancer; damage 

22 to the eye, such as cataracts; and immune system suppression); wavelength dependency

23 of biological responses; and interindividual variability in UV-B resistance to such health 
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1 outcomes. Beyond these well recognized adverse health effects associated with various 

2 wavelengths of UV radiation, the 2006 Criteria Document (section 10.2.3.6) also 

3 discusses protective effects of UV-B radiation. Recent reports indicate the necessity of 

4 UV-B in producing vitamin D. Vitamin D deficiency can cause metabolic bone disease 

5 among children and adults, and may also increase the risk of many common chronic 

6 diseases (e.g., type I diabetes and rheumatoid arthritis) as well as the risk of various types 

7 of cancers. Thus, the 2006 Criteria Document concludes that any assessment that 

8 attempts to quantify the consequences of increased UV-B exposure on humans due to 

9 reduced ground-level O3 must include consideration of both negative and positive effects. 

10 However, as with other impacts of UV-B on human health, this beneficial effect of UV-B 

11 radiation has not been studied in sufficient detail to allow for a credible health benefits or 

12 risk assessment. In conclusion, the effect of changes in surface-level O3 concentrations 

13 on UV-B-induced health outcomes cannot yet be critically assessed within reasonable 

14 uncertainty (2006 Criteria Document, p. 10-36).

15 The Agency last considered indirect effects of O3 in the ambient air in its 2003 

16 final response to a remand of the Agency’s 1997 decision to revise the O3 NAAQS. In so 

17 doing, based on the available information in the 1997 review, EPA determined that the 

18 information linking (a) changes in patterns of ground-level O3 concentrations likely to 

19 occur as a result of programs implemented to attain the 1997 O3 NAAQS to (b) changes 

20 in relevant exposures to UV-B radiation of concern to public health was too uncertain at 

21 that time to warrant any relaxation in the level of public health protection previously

22 determined to be requisite to protect against the demonstrated direct adverse respiratory

23 effects of exposure to O3 in the ambient air (68 FR 614). At that time, the more recent 
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1 information on protective effects of UV-B radiation was not available, such that only

2 adverse UV-B-related effects could be considered. Taking into consideration the more 

3 recent information available for the 2008 review, the 2006 Criteria Document and 2007 

4 Staff Paper conclude that the effect of changes in ground-level O3 concentrations, likely

5 to occur as a result of revising the O3 NAAQS, on UV-B-induced health outcomes, 

6 including whether these changes would ultimately result in increased or decreased 

7 incidence of UV-B-related diseases, cannot yet be critically assessed. 

8 3. Interpretation and Integration of Health Evidence

9 As discussed below, in assessing the health evidence, the 2006 Criteria Document 

10 integrates findings from experimental (e.g., toxicological, dosimetric and controlled 

11 human exposure) and epidemiological studies, to make judgments about the extent to 

12 which causal inferences can be made about observed associations between health 

13 endpoints and exposure to O3. In evaluating the evidence from epidemiological studies, 

14 the EPA focuses on well-recognized criteria, including: the strength of reported 

15 associations, including the magnitude and precision of reported effect estimates and their 

16 statistical significance; the robustness of reported associations, or stability in the effect 

17 estimates after considering factors such as alternative models and model specification, 

18 potential confounding by co-pollutants, and issues related to the consequences of 

19 exposure measurement error; potential aggregation bias in pooling data; and the 

20 consistency of the effects associations as observed by looking across results of multiple21 and single-city studies conducted by different investigators in different places and times. 

22 Consideration is also given to evaluating concentration-response relationships observed

23 in epidemiological studies to inform judgments about the potential for threshold levels for 
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1 O3-related effects. Integrating more broadly across epidemiological and experimental 

2 evidence, the 2006 Criteria Document also focuses on the coherence and plausibility of 

3 observed O3-related health effects to reach judgments about the extent to which causal 

4 inferences can be made about observed associations between health endpoints and 

5 exposure to O3 in the ambient air. 

6 a. Assessment of Evidence from Epidemiological Studies

7 Key elements of the evaluation of epidemiological studies are briefly summarized 

8 below.

9 (1) The strength of associations most directly refers to the magnitude of the 

10 reported relative risk estimates. Taking a broader view, the 2006 Criteria Document

11 draws upon the criteria summarized in a recent report from the U.S. Surgeon General, 

12 which define strength of an association as “the magnitude of the association and its 

13 statistical strength” which includes assessment of both effect estimate size and precision, 

14 which is related to the statistical power of the study (CDC, 2004). In general, when 

15 associations are strong in terms of yielding large relative risk estimates, it is less likely

16 that the association could be completely accounted for by a potential confounder or some 

17 other source of bias, whereas with associations that yield small relative risk estimates it is 

18 especially important to consider potential confounding and other factors in assessing 

19 causality. Effect estimates between O3 and some of the health outcomes are generally

20 small in size and could thus be characterized as weak. For example, effect estimates for 

21 associations with mortality generally range from 0.5 to 5 percent increases per 0.040 ppm

22 increase in 1-hour maximum O3 or equivalent, whereas associations for hospitalization 

23 range up to 50 percent increases per standardized O3 increment. However, the 2006
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1 Criteria Document notes that there are large multicity studies that find small associations 

2 between short-term O3 exposure and mortality or morbidity and have done so with great 

3 precision due to the statistical power of the studies (p. 8-40). That is, the power of the 

4 studies allows the authors to reliably distinguish even weak relationships from the null 

5 hypothesis with statistical confidence.

6 (2) In evaluating the robustness of associations, the 2006 Criteria Document 

7 (sections 7.1.3 and 8.4.4.3) and 2007 Staff Paper (section 3.4.2) have primarily

8 considered the impact of exposure error, potential confounding by copollutants, and 

9 alternative models and model specifications.

10 In time-series and panel studies, the temporal (e.g., daily or hourly) changes in 

11 ambient O3 concentrations measured at centrally-located ambient monitoring stations are 

12 generally used to represent a community’s exposure to ambient O3. In prospective cohort 

13 or cross-sectional studies, air quality data averaged over a period of months to years are 

14 used as indicators of a community’s long-term exposure to ambient O3 and other 

15 pollutants. In both types of analyses, exposure error is an important consideration, as 

16 actual exposures to individuals in the population will vary across the community.

17 Ozone concentrations measured at central ambient monitoring sites may explain, 

18 at least partially, the variance in individual exposures to ambient O3; however, this 

19 relationship is influenced by various factors related to building ventilation practices and 

20 personal behaviors. Further, the pattern of exposure misclassification error and the 

21 influence of confounders may differ across the outcomes of interest as well as in 

22 susceptible populations. As discussed in the 2006 Criteria Document (section 3.9), only a 

23 limited number of studies have examined the relationship between ambient O3
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1 concentrations and personal exposures to ambient O3. One of the strongest predictors of 

2 the relationship between ambient concentrations and personal exposures appears to be 

3 time spent outdoors. The strongest relationships were observed in outdoor workers 

4 (Brauer and Brook, 1995, 1997; O’Neill et al., 2004). Statistically significant 

5 correlations between ambient concentrations and personal exposures were also observed 

6 for children, who likely spend more time outdoors in the warm season (Linn et al., 1996; 

7 Xu et al., 2005). There is some concern about the extent to which ambient concentrations 

8 are representative of personal O3 exposures of another particularly susceptible group of 

9 individuals, the debilitated elderly, since those who suffer from chronic cardiovascular or 

10 respiratory conditions may tend to protect themselves more than healthy individuals from 

11 environmental threats by reducing their exposure to both O3 and its confounders, such as 

12 high temperature and PM. Studies by Sarnat et al. (2001, 2005) that included this 

13 susceptible group reported mixed results for associations between ambient O3

14 concentrations and personal exposures to O3. Collectively, these studies observed that 

15 the daily averaged personal O3 exposures tend to be well correlated with ambient O3

16 concentrations despite the substantial variability that existed among the personal 

17 measurements. These studies provide supportive evidence that ambient O3

18 concentrations from central monitors may serve as valid surrogate measures for mean 

19 personal exposures experienced by the population, which is of most relevance for time20 series studies. A better understanding of the relationship between ambient concentrations 

21 and personal exposures, as well as of the other factors that affect relationship will 

22 improve the interpretation of concentration-population health response associations 

23 observed. 
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1 The 2006 Criteria Document (section 7.1.3.1) also discusses the potential 

2 influence of exposure error on epidemiologic study results. Zeger et al. (2000) outlined 

3 the components to exposure measurement error, finding that ambient exposure can be 

4 assumed to be the product of the ambient concentration and an attenuation factor (i.e., 

5 building filter) and that panel studies and time-series studies that use ambient 

6 concentrations instead of personal exposure measurements will estimate a health risk that 

7 is attenuated by that factor. Navidi et al. (1999) used data from a children’s cohort study 

8 to compare effect estimates from a simulated “true” exposure level to results of analyses 

9 from O3 exposures determined by several methods, finding that O3 exposures based on 

10 the use of ambient monitoring data overestimate the individual’s O3 exposure and thus 

11 generally result in O3 effect estimates that are biased downward (EPA, 2006a, p. 7-8). 

12 Similarly, in a reanalysis of a study by Burnett et al. (1994) on the acute respiratory

13 effects of ambient air pollution, Zidek et al. (1998) reported that accounting for 

14 measurement error, as well as making a few additional changes to the analysis, resulted in

15 qualitatively similar conclusions, but the effects estimates were considerably larger in 

16 magnitude (EPA, 2006a, p. 7-8). A simulation study by Sheppard et al. (2005) also 

17 considered attenuation of the risk based on personal behavior, their microenvironment, 

18 and the qualities of the pollutant in time-series studies. Of particular interest is their 

19 finding that risk estimates were not further attenuated in time-series studies even when 

20 the correlations between personal exposures and ambient concentrations were weak. In 

21 addition to overestimation of exposure and the resulting underestimation of effects, the 

22 use of ambient O3 concentrations may obscure the presence of thresholds in 

23 epidemiologic studies (EPA, 2006a, p. 7-9).
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1 As discussed in the 2006 Criteria Document (section 3.9), using ambient 

2 concentrations to determine exposure generally overestimates true personal O3 exposures 

3 by approximately 2- to 4-fold in available studies, resulting in attenuated risk estimates. 

4 The implication is that the effects being estimated occur at fairly low exposures and the 

5 potency of O3 is greater than these effects estimates indicate. As very few studies 

6 evaluating O3 health effects with personal O3 exposure measurements exist in the 

7 literature, effect estimates determined from ambient O3 concentrations must be evaluated 

8 and used with caution to assess the health risks of O3. In the absence of available data on 

9 personal O3 exposure, the use of routinely monitored ambient O3 concentrations as a 

10 surrogate for personal exposures is not generally expected to change the principal 

11 conclusions from O3 epidemiologic studies. Therefore, population health risk estimates 

12 derived using ambient O3 levels from currently available observational studies, with 

13 appropriate caveats about personal exposure considerations, remain useful. The 2006

14 Criteria Document recommends caution in the quantitative use of effect estimates 

15 calculated using ambient O3 concentrations as they may lead to underestimation of the 

16 potency of O3. However, the 2007 Staff Paper observes that the use of these risk 

17 estimates for comparing relative risk reductions between alternative ambient O3 standards 

18 considered in the risk assessment (discussed below in section II.B.2) is less likely to 

19 suffer from this concern.

20 Confounding occurs when a health effect that is caused by one risk factor is 

21 attributed to another variable that is correlated with the causal risk factor; 

22 epidemiological analyses attempt to adjust or control for potential confounders. 

23 Copollutants (e.g., PM, CO, SO2 and NO2) can meet the criteria for potential confounding 
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1 in O3-health associations if they are potential risk factors for the health effect under study

2 and are correlated with O3. Effect modifiers include variables that may influence the 

3 health response to the pollutant exposure (e.g., co-pollutants, individual susceptibility, 

4 smoking or age). Both are important considerations for evaluating effects in a mixture of 

5 pollutants, but for confounding, the emphasis is on controlling or adjusting for potential 

6 confounders in estimating the effects of one pollutant, while the emphasis for effect 

7 modification is on identifying and assessing the effects for different modifiers.

8 The 2006 Criteria Document (p. 7-148) observes that O3 is generally not highly 

9 correlated with other criteria pollutants (e.g., PM10, CO, SO2 and NO2), but may be more 

10 highly correlated with secondary fine particles, especially during the summer months, 

11 and that the degree of correlation between O3 and other pollutants may vary across 

12 seasons. For example, positive associations are observed between O3 and pollutants such 

13 as fine particles during the warmer months, but negative correlations may be observed 

14 during the cooler months (EPA, 2006a, p. 7-17). Thus, the 2006 Criteria Document

15 (section 7.6.4) pays particular attention to the results of season-specific analyses and 

16 studies that assess effects of PM in potential confounding of O3-health relationships. The

17 2006 Criteria Document also discussed the limitations of commonly used multipollutant 

18 models that include the difficulty in interpreting results where the copollutants are highly

19 colinear, or where correlations between pollutants change by season (EPA, 2006a, p. 7-

20 150). This is particularly the situation where O3 and a copollutant, such as sulfates, are 

21 formed under the same atmospheric condition; in such cases multipollutant models would 

22 produce unstable and possibly misleading results (EPA, 2006a, p. 7-152).
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1 For mortality, the results from numerous multicity and single-city studies indicate 

2 that O3-mortality associations do not appear to be substantially changed in multipollutant 

3 models including PM10 or PM2.5 (EPA, 2006a, p. 7-101; Figure 7-22). Focusing on 

4 results of warm season analyses, effect estimates for O3-mortality associations are fairly 

5 robust to adjustment for PM in multipollutant models (EPA, 2006a, p. 7-102; Figure 7-

6 23). The 2006 Criteria Document concludes that in the few multipollutant analyses 

7 conducted for these endpoints, copollutants generally do not confound the relationship 

8 between O3 and respiratory hospitalization (EPA, 2006a, p. 7-79 to 7-80; Figure 7-12). 

9 Multipollutant models were not used as commonly in studies of relationships between 

10 respiratory symptoms or lung function with O3, but the 2006 Criteria Document reports 

11 that results of available analyses indicate that such associations generally were robust to 

12 adjustment for PM2.5 (p. 7-154). For example, in a large multicity study of asthmatic 

13 children (Mortimer et al., 2002), the O3 effect was attenuated, but there was still a 

14 positive association; in Gent et al. (2003), effects of O3, but not PM2.5, remained 

15 statistically significant and even increased in magnitude in two-pollutant models (EPA, 

16 2006a, p. 7-53). Considering this body of studies, the 2006 Criteria Document (p. 7-154) 

17 concludes: “Multipollultant regression analyses indicated that O3 risk estimates, in 

18 general, were not sensitive to the inclusion of copollutants, including PM2.5 and sulfate.

19 These results suggest that the effects of O3 on respiratory health outcomes appear to be 

20 robust and independent of the effects of other copollutants.”

21 The 2006 Criteria Document (p. 7-14) observes that another challenge of time22 series epidemiological analysis is assessing the relationship between O3 and health 

23 outcomes while avoiding bias due to confounding by other time-varying factors, 
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1 particularly seasonal trends and weather variables. These variables are of particular 

2 interest because O3 concentrations have a well-characterized seasonal pattern and are also 

3 highly correlated with changes in temperature, such that it can be difficult to distinguish 

4 whether effects are associated with O3 or with seasonal or weather variables in statistical 

5 analyses.

6 The 2006 Criteria Document (section 7.1.3.4) discusses statistical modeling 

7 approaches that have been used to adjust for time-varying factors, highlighting a series of 

8 analyses that were done in a Health Effects Institute-funded reanalysis of numerous time9 series studies. While the focus of these reanalyses was on associations with PM, a 

10 number of investigators also examined the sensitivity of O3 coefficients to the extent of 

11 adjustment for temporal trends and weather factors. In addition, several recent studies, 

12 including U.S. multicity studies (Bell et al., 2005; Huang et al., 2005; Schwartz et al., 

13 2005) and a meta-analysis study (Ito et al., 2005), evaluated the effect of model 

14 specification on O3-mortality associations. As discussed in the 2006 Criteria Document

15 (section 7.6.3.1), these studies generally report that associations reported with O3 are not 

16 substantially changed with alternative modeling strategies for adjusting for temporal 

17 trends and meteorologic effects. In the meta-analysis by Ito et al. (2005), a separate 

18 multicity analysis was presented that found that alternative adjustments for weather 

19 resulted in up to 2-fold difference in the O3 effect estimate. Significant confounding can 

20 occur when strong seasonal cycles are present, suggesting that season-specific results are 

21 more generally robust than year-round results in such cases. A number of 

22 epidemiological studies have conducted season-specific analyses, and have generally 
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1 reported stronger and more precise effect estimates for O3 associations in the warm 

2 season than in analyses conducted in the cool seasons or over the full year.

3 (3) Consistency refers to the persistent finding of an association between 

4 exposure and outcome in multiple studies of adequate power in different persons, places, 

5 circumstances and times (CDC, 2004). In considering results from multicity studies and 

6 single-city studies in different areas, the 2006 Criteria Document (p. 8-41) observes 

7 general consistency in effects of short-term O3 exposure on mortality, respiratory

8 hospitalization and other respiratory health outcomes. The variations in effects that are 

9 observed may be attributable to differences in relative personal exposure to O3, as well as 

10 varying concentrations and composition of copollutants present in different regions. 

11 Thus, the 2006 Criteria Document (p.8-41) concludes that “consideration of consistency

12 or heterogeneity of effects is appropriately understood as an evaluation of the similarity 

13 or general concordance of results, rather than an expectation of finding quantitative 

14 results with a very narrow range.”

15 (4) The 2007 Staff Paper recognizes that it is likely that there are biological 

16 thresholds for different health effects in individuals or groups of individuals with similar 

17 innate characteristics and health status. For O3 exposure, individual thresholds would 

18 presumably vary substantially from person to person due to individual differences in 

19 genetic susceptibility, pre-existing disease conditions and possibly individual risk factors 

20 such as diet or exercise levels (and could even vary from one time to another for a given 

21 person). Thus, it would be difficult to detect a distinct threshold at the population level 

22 below which no individual would experience a given effect, especially if some members 
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1 of a population are unusually sensitive even down to very low concentrations (EPA, 

2 2004, p. 9-43 - 9-44).

3 Some studies have tested associations between O3 and health outcomes after 

4 removal of days with higher O3 levels from the data set; such analyses do not necessarily 

5 indicate the presence or absence of a threshold, but provide some information on whether 

6 the relationship is found using only lower-concentration data. For example, using data 

7 from 95 U.S. cities, Bell et al. (2004) found that the effect estimate for an association 

8 between short-term O3 exposure and mortality was little changed when days exceeding 

9 0.060 ppm (24-hour average) were excluded in the analysis. Using data from 8 U.S. 

10 cities, Mortimer and colleagues (2002) also reported that associations between O3 and 

11 both lung function and respiratory symptoms remained statistically significant and of the 

12 same or greater magnitude in effect size when concentrations greater than 0.080 ppm (8-

13 hour average) were excluded (EPA, 2006a, p. 7-46). Several single-city studies also 

14 report similar findings of associations that remain or are increased in magnitude and 

15 statistical significance when data at the upper end of the concentration range are removed

16 (EPA, 2006a, section 7.6.5).

17 Other time-series epidemiological studies have used statistical modeling 

18 approaches to evaluate whether thresholds exist in associations between short-term O3

19 exposure and mortality. As discussed in section 7.6.5 of the 2006 Criteria Document, one 

20 European multicity study included evaluation of the shape of the concentration-response 

21 curve, and observed no deviation from a linear function across the range of O3

22 measurements from the study (Gryparis et al., 2004; EPA, 2006a p. 7-154). Several 
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1 single-city studies also observed a monotonic increase in associations between O3 and 

2 morbidity that suggest that no population threshold exists (EPA, 2006a, p. 7-159).

3 On the other hand, a study in Korea used several different modeling approaches 

4 and reported that a threshold model provided the best fit for the data. The results 

5 suggested a potential threshold level of about 0.045 ppm (1-hour maximum 

6 concentration; < 0.035 ppm, 8-hour average) for an association between mortality and 

7 short-term O3 exposure during the summer months (Kim et al., 2004; EPA, 2006a, p. 8-

8 43). The authors reported larger effect estimates for the association for data above the 

9 potential threshold level, suggesting that an O3-mortality association might be 

10 underestimated in the non-threshold model. A threshold analysis recently reported by 

11 Bell et al. (2006) for 98 U.S. communities, including the same 95 communities in Bell et 

12 al. (2004), indicated that if a population threshold existed for mortality, it would likely

13 fall below a 24-hour average O3 concentration of 0.015 ppm (< 0.025 ppm, 8-hour 

14 average). In addition, Burnett and colleagues (1997a,b) plotted the relationships between 

15 air pollutant concentrations and both respiratory and cardiovascular hospitalization, and it 

16 appears in these results that the associations with O3 are found in the concentration range 

17 above about 0.030 ppm (1-hour maximum; < 0.025 ppm, 8-hour average). Vedal and 

18 colleagues (2003) reported a significant association between O3 and mortality in British 

19 Columbia where O3 concentrations were quite low (mean 1-hour maximum concentration 

20 of 0.0273 ppm). The authors did not specifically test for threshold levels, but the fact that 

21 the association was found in an area with such low O3 concentrations suggests that any 

22 potential threshold level would be quite low in this data set.
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1 In summary, the 2006 Criteria Document finds that, taken together, the available 

2 evidence from controlled human exposure and epidemiological studies suggests that no 

3 clear conclusion can now be reached with regard to possible threshold levels for O3-

4 related effects (EPA, 2006a, p. 8-44). Thus, the available epidemiological evidence 

5 neither supports nor refutes the existence of thresholds at the population level for effects 

6 such as increased hospital admissions and premature mortality. There are limitations in 

7 epidemiological studies that make discerning thresholds in populations difficult, 

8 including low data density in the lower concentration ranges, the possible influence of 

9 exposure measurement error, and interindividual differences in susceptibility to O3-

10 related effects in populations. There is the possibility that thresholds for individuals may

11 exist in reported associations at fairly low levels within the range of air quality observed 

12 in the studies but not be detectable as population thresholds in epidemiological analyses.

13 b. Biological Plausibility and Coherence of Evidence

14 The body of epidemiological studies discussed in the 2007 Staff Paper 

15 emphasizes the role of O3 in association with a variety of adverse respiratory and 

16 cardiovascular effects. While recognizing a variety of plausible mechanisms, there exists 

17 a general consensus suggesting that O3, could either directly or through initiation, 

18 interfere with basic cellular oxidation processes responsible for inflammation, reduced 

19 antioxidant capacity, atherosclerosis and other effects. Reasoning that O3 influences 

20 cellular chemistry through basic oxidative properties (as opposed to a unique chemical 

21 interaction), other reactive oxidizing species (ROS) in the atmosphere acting either 

22 independently or in combination with O3 may also contribute to a number of adverse 

23 respiratory and cardiovascular health effects. Consequently, the role of O3 should be 
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1 considered more broadly as O3 behaves as a generator of numerous oxidative species in 

2 the atmosphere.

3 In considering the biological plausibility of reported O3-related effects, the 2007 

4 Staff Paper (section 3.4.6) considers this broader question of health effects of pollutant 

5 mixtures containing O3. The potential for O3-related enhancements of PM formation, 

6 particle uptake, and exacerbation of PM-induced cardiovascular effects underscores the 

7 importance of considering contributions of O3 interactions with other often co-occurring 

8 air pollutants to health effects due to O3-containing pollutant mixes. The 2007 Staff 

9 Paper summarizes some examples of important pollutant mixture effects from studies that 

10 evaluate interactions of O3 with other co-occurring pollutants, as discussed in chapters 4, 

11 5, and 6 of the 2006 Criteria Document.

12 All of the types of interactive effects of O3 with other co-occurring gaseous and 

13 nongaseous viable and nonviable PM components of ambient air mixes noted above 

14 argue that O3 acts not only alone but that O3 also is a surrogate indicator for air pollution 

15 mixes which may enhance the risk of adverse effects due to O3 acting in combination 

16 with other pollutants. Viewed from this perspective, those epidemiologic findings of 

17 morbidity and mortality associations, with ambient O3 concentrations extending to quite 

18 low levels in many cases, become more understandable and plausible.

19 The 2006 Criteria Document integrates epidemiological studies with mechanistic 

20 information from controlled human exposure studies and animal toxicological studies to 

21 draw conclusions regarding the coherence of evidence and biological plausibility of O3-

22 related health effects to reach judgments about the causal nature of observed associations. 

23 As summarized below, coherence and biological plausibility is discussed for each of the 
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1 following types of O3-related effects: short-term effects on the respiratory system, effects 

2 on the cardiovascular system, effects related to long-term O3 exposure, and short-term 

3 mortality-related health endpoints.

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

5 Acute respiratory morbidity effects that have been associated with short-term 

6 exposure to O3 include such health endpoints as decrements in lung function, increased 

7 respiratory symptoms, increased airway responsiveness, airway inflammation, increased 

8 permeability related to epithelial injury, immune system effects, emergency department

9 visits for respiratory diseases, and hospitalization due to respiratory illness.

10 Recent epidemiological studies have supported evidence available in the previous 

11 O3 NAAQS review on associations between ambient O3 exposure and decline in lung 

12 function for children. The 2006 Criteria Document (p. 8-34) concludes that exposure to 

13 ambient O3 has a significant effect on lung function and is associated with increased 

14 respiratory symptoms and medication use, particularly in asthmatics. Short-term 

15 exposure to O3 has also been associated with more severe morbidity endpoints, such as 

16 emergency department visits and hospital admissions for respiratory cases, including 

17 specific respiratory illness (e.g., asthma) (EPA, 2006a, sections 7.3.2 and 7.3.3). In 

18 addition, a few epidemiological studies have reported positive associations between 

19 short-term O3 exposure and respiratory mortality, though the associations are not 

20 generally statistically significant (EPA, 2006a, p. 7-108).

21 Considering the evidence from epidemiological studies, the results described 

22 above provide evidence for coherence in O3-related effects on the respiratory system. 

23 Effect estimates from U.S. and Canadian studies are shown in Figure 1, where it can be 
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1 seen that mostly positive associations have been reported with respiratory effects ranging 

2 from respiratory symptoms, such as cough or wheeze, to hospitalization for various 

3 respiratory diseases, and there is suggestive evidence for associations with respiratory

4 mortality. Many of the reported associations are statistically significant, particularly in 

5 the warm season. In Figure 1, the central effect estimate is indicated by a square for each 

6 result, with the vertical bar representing the 95 percent confidence interval around the 

7 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.23 8 

9 Positive effect estimates indicate increases in the health outcome with O3 exposure. In 

10 considering these results as a whole, it is important to consider not only whether 

11 statistical significance at the 95 percent confidence level is reported in individual studies 

12 but also the general pattern of results, focusing in particular on studies with greater 

13 statistical power that report relatively more precise results.

 

23 Results for studies of respiratory symptoms are presented as odds ratios; an 

odds ratio of 1.0 is equivalent to no effect, and thus is presented as equivalent to the zero 

effect estimate line.
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1

2
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1 Considering also evidence from toxicological, controlled human exposure, and 

2 field studies, the 2006 Criteria Document (section 8.6) discusses biological plausibility

3 and coherence of evidence for acute O3-induced respiratory health effects. Inhalation of 

4 O3 for several hours while subjects are physically active can elicit both acute adverse

5 pathophysiological changes and subjective respiratory tract symptoms (EPA, 2006a, 

6 section 8.4.2). Acute pulmonary responses observed in healthy humans exposed to O3 at 

7 ambient concentrations include: decreased inspiratory capacity; mild 

8 bronchoconstriction; rapid, shallow breathing during exercise; subjective symptoms of 

9 tracheobronchial airway irritation, including cough and pain on deep inspiration; 

10 decreases in measures of lung function; and increased airway resistance. The severity of 

11 symptoms and magnitude of response depends on inhaled dose, individual O3 sensitivity, 

12 and the degree of attenuation or enhancement of response resulting from previous O3

13 exposures. Lung function studies of several animal species acutely exposed to relatively 

14 low O3 levels from a toxicological perspective (i.e., 0.25 to 0.4 ppm) show responses 

15 similar to those observed in humans, including increased breathing frequency, decreased 

16 tidal volume, increased resistance, and decreased FVC. Alterations in breathing pattern 

17 return to normal within hours of exposure, and attenuation in functional responses 

18 following repeated O3 exposures is similar to those observed in humans.

19 Physiological and biochemical alterations investigated in controlled human 

20 exposure and animal toxicology studies tend to support certain hypotheses of underlying 

21 pathological mechanisms which lead to the development of respiratory-related effects 

22 reported in epidemiology studies (e.g., increased hospitalization and medication use). 

23 Some of these are: (a) decrements in lung function, (b) bronchoconstriction, (c) 
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1 increased airway responsiveness, (d) airway inflammation, (e) epithelial injury, (f) 

2 immune system activation, (g) host defense impairment, and (h) sensitivity of individuals, 

3 which depends on at least a person’s age, disease status, genetic susceptibility, and the 

4 degree of attenuation present due to prior exposures. The time sequence, magnitude, and 

5 overlap of these complex events, both in terms of development and recovery, illustrate 

6 the inherent difficulty of interpreting the biological plausibility of O3-induced 

7 cardiopulmonary health effects (EPA, 2006a, p. 8-48).

8 The interaction of O3 with airway epithelial cell membranes and ELF to form 

9 lipid ozonation products and ROS is supported by numerous human, animal and in vitro 

10 studies. Ozonation products and ROS initiate a cascade of events that lead to oxidative 

11 stress, injury, inflammation, airway epithelial damage and increased epithelial damage 

12 and increased alveolar permeability to vascular fluids. Repeated respiratory 

13 inflammation can lead to a chronic inflammatory state with altered lung structure and 

14 lung function and may lead to chronic respiratory diseases such as fibrosis and 

15 emphysema (EPA, 2006a, section 8.6.2). Continued respiratory inflammation also can 

16 alter the ability to respond to infectious agents, allergens and toxins. Acute inflammatory

17 responses to O3 are well documented, and lung injury appears within 3 hours after 

18 exposure in humans.

19 Taken together, the 2006 Criteria Document concludes that the evidence from 

20 experimental human and animal toxicology studies indicates that acute O3 exposure is 

21 causally associated with respiratory system effects. These effects include O3-induced 

22 pulmonary function decrements; respiratory symptoms; lung inflammation and increased 

23 lung permeability; airway hyperresponsiveness; increased uptake of nonviable and viable 
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1 particles; and consequent increased susceptibility to PM-related toxic effects and 

2 respiratory infections (EPA, 2006a, p. 8-48). 

3 ii. Coherence and Plausibility of Effects on the Cardiovascular System 

4 There is very limited experimental evidence of animals and humans that has 

5 evaluated possible mechanisms or physiological pathways by which acute O3 exposures 

6 may induce cardiovascular system effects. Ozone induces lung injury, inflammation, and 

7 impaired mucociliary clearance, with a host of associated biochemical changes all leading 

8 to increased lung epithelial permeability. As noted above in section II.A.2.a, the

9 generation of lipid ozonation products and ROS in lung tissues can influence pulmonary

10 hemodynamics, and ultimately the cardiovascular system. Other potential mechanisms 

11 by which O3 exposure may be associated with cardiovascular disease outcomes have been 

12 described. Laboratory animals exposed to relatively high O3 concentrations (≥ 0.5 ppm) 

13 demonstrate tissue edema in the heart and lungs. Ozone-induced changes in heart rate, 

14 edema of heart tissue, and increased tissue and serum levels of ANF found with 8-hour

15 0.5 ppm O3 exposure in animal toxicology studies (Vesely et al., 1994a,b,c) also raise the 

16 possibility of potential cardiovascular effects of acute ambient O3 exposures.

17 Animal toxicology studies have found both transient and persistent ventilatory

18 responses with and without progressive decreases in heart rate (Arito et al., 1997). 

19 Observations of O3-induced vasoconstriction in a controlled human exposure study by

20 Brook et al. (2002) suggests another possible mechanism for O3-related exacerbations of 

21 preexisting cardiovascular disease. One controlled human study (Gong et al., 1998) 

22 evaluated potential cardiovascular health effects of O3 exposure. The overall results did 

23 not indicate acute cardiovascular effects of O3 in either the hypertensive or control 
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1 subjects. The authors observed an increase in rate-pressure product and heart rate, a 

2 decrement for FEV1, and a >10 mm Hg increase in the alveolar/arterial pressure 

3 difference for O2 following O3 exposure. Foster et al. (1993) demonstrated that even in 

4 relatively young healthy adults, O3 exposure can cause ventilation to shift away from the 

5 well-perfused basal lung. This effect of O3 on ventilation distribution may persist beyond 

6 24-hours post-exposure (Foster et al., 1997). These findings suggest that O3 may exert 

7 cardiovascular effects indirectly by impairing alveolar-arterial O2 transfer and potentially

8 reducing O2 supply to the myocardium. Ozone exposure may increase myocardial work 

9 and impair pulmonary gas exchange to a degree that could perhaps be clinically

10 important in persons with significant preexisting cardiovascular impairment. 

11 As noted above in section II.A.2.a, a limited number of new epidemiological 

12 studies have reported associations between short-term O3 exposure and effects on the 

13 cardiovascular system. Among these studies, three were population-based and involved 

14 relatively large cohorts; two of these studies evaluated associations between O3 and HRV 

15 and the other study evaluated the association between O3 levels and the relative risk of 

16 MI or heart attack. Such studies may offer more informative results based on their large 

17 subject-pool and design. Results from these three studies were suggestive of an 

18 association between O3 exposure and the cardiovascular endpoints studied. In other 

19 recent studies on the incidence of heart attacks and some more subtle cardiovascular 

20 health endpoints, such as changes in HRV or cardiac arrhythmia, some but not all studies 

21 reported associations with short-term exposure to O3 (EPA, 2006a, section 7.2.7.1). 

22 From these studies, the 2006 Criteria Document concludes that the “current evidence is 
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1 rather limited but suggestive of a potential effect on HRV, ventricular arrhythmias, and 

2 MI incidence” (EPA, 2006a, p. 7-65).

3 An increasing number of studies have evaluated the association between O3

4 exposure and cardiovascular hospital admissions. As discussed in section 7.3.4 of the

5 2006 Criteria Document, many reported negative or inconsistent associations, whereas 

6 other studies, especially those that examined the relationship when O3 exposures were 

7 higher, have found positive and robust associations between O3 and cardiovascular 

8 hospital admissions. The 2006 Criteria Document (p. 7-83) finds that the overall 

9 evidence from these studies remains inconclusive regarding the effect of O3 on 

10 cardiovascular hospitalizations. The 2006 Criteria Document notes that the suggestive 

11 positive epidemiologic findings of O3 exposure on cardiac autonomic control, including 

12 effects on HRV, ventricular arrhythmias and heart attacks, and reported associations 

13 between O3 exposure and cardiovascular hospitalizations generally in the warm season 

14 gain credibility and scientific support from the results of experimental animal toxicology

15 and controlled human exposure studies, which are indicative of plausible pathways by

16 which O3 may exert cardiovascular effects (EPA, 2006a, section 8.6.1).

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

18 Controlled human exposure studies cannot evaluate effects of long-term 

19 exposures to O3; there is some evidence available from toxicological studies. While early

20 animal toxicology studies of long-term O3 exposures were conducted using continuous 

21 exposures, more recent studies have focused on exposures which mimic diurnal and 

22 seasonal patterns and more realistic O3 exposure levels (EPA, 2006a, p. 8-50). Studies of 

23 monkeys that compared these two exposure scenarios found increased airway pathology
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1 only with the latter design. Persistent and irreversible effects reported in chronic animal 

2 toxicology studies suggest that additional complementary human data are needed from 

3 epidemiologic studies (EPA, 2006a, p. 8-50).

4 There is limited evidence from human studies for long-term O3-induced effects on 

5 lung function. As discussed in section 8.6.2 of the 2006 Criteria Document, previous 

6 epidemiological studies have provided only inconclusive evidence for either mortality or 

7 morbidity effects of long-term O3 exposure. The 2006 Criteria Document (p. 8-50) 

8 observes that the inconsistency in findings may be due to a lack of precise exposure 

9 information, the possibility of selection bias, and the difficulty of controlling for 

10 confounders. Several new longitudinal epidemiology studies have evaluated associations 

11 between long-term O3 exposures and morbidity and mortality and suggest that these long12 term exposures may be related to changes in lung function in children; however, little 

13 evidence is available to support a relationship between chronic O3 exposure and mortality

14 or lung cancer incidence (EPA, 2006a, p. 8-50).

15 The 2006 Criteria Document (p. 8-51) concludes that evidence from animal 

16 toxicology studies strongly suggests that chronic O3 exposure is capable of damaging the 

17 distal airways and proximal alveoli, resulting in lung tissue remodeling leading to 

18 apparent irreversible changes. Such structural changes and compromised lung function 

19 caused by persistent inflammation may exacerbate the progression and development of 

20 chronic lung disease. Together with the limited evidence available from epidemiological 

21 studies, these findings offer some insight into potential biological mechanisms for 

22 suggested associations between long-term or seasonal exposures to O3 and reduced lung 
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1 function development in children which have been observed in epidemiologic studies 

2 (EPA, 2006a, p. 8-51).

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

4 An extensive epidemiological literature on air pollution related mortality risk 

5 estimates from the U.S., Canada, and Europe is discussed in the 2006 Criteria Document

6 (sections 7.4 and 8.6.3). These single- and multicity mortality studies coupled with

7 results from meta-analyses generally indicate associations between acute O3 exposure and 

8 elevated risk for all-cause mortality, even after adjustment for the influence of season and 

9 PM exposure. Several single-city studies that specifically evaluated the relationship 

10 between O3 exposure and cardiopulmonary mortality also reported results suggestive of a 

11 positive association (EPA, 2006a, p. 8-51). These mortality studies suggest a pattern of 

12 effects for causality that have biologically plausible explanations, but our knowledge 

13 regarding potential underlying mechanisms is very limited at this time and requires 

14 further research. Most of the physiological and biochemical parameters investigated in 

15 human and animal studies suggest that O3-induced biochemical effects are relatively

16 transient and attenuate over time. The 2006 Criteria Document (p. 8-52) hypothesizes a 

17 generic pathway of O3-induced lung damage, potentially involving oxidative lung 

18 damage with subsequent inflammation and/or decline in lung function leading to 

19 respiratory distress in some sensitive population groups (e.g., asthmatics), or other 

20 plausible pathways noted below that may lead to O3-related contributions to 

21 cardiovascular effects that ultimately increase risk of mortality. 

22 The third National Health and Nutrition Examination Survey follow-up data 

23 analysis indicates that about 20 percent of the adult population has reduced FEV1 values, 
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1 suggesting impaired lung function in a significant portion of the population. Most of 

2 these individuals have COPD, asthma or fibrotic lung disease (Manino et al., 2003), 

3 which are associated with persistent low-grade inflammation. Furthermore, patients with 

4 COPD are at increased risk for cardiovascular disease. Also, lung disease with 

5 underlying inflammation may be linked to low-grade systemic inflammation associated 

6 with atherosclerosis, independent of cigarette smoking (EPA, 2006a, p. 8-52). Lung 

7 function decrements in persons with cardiopulmonary disease have been associated with 

8 inflammatory markers, such as C-reactive protein (CRP) in the blood. At a population 

9 level it has been found that individuals with the lowest FEV1 values have the highest 

10 levels of CRP, and those with the highest FEV1 values have the lowest CRP levels 

11 (Manino et al., 2003; Sin and Man, 2003). This complex series of physiological and 

12 biochemical reactions following O3 exposure may tilt the biological homeostasis 

13 mechanisms which could lead to adverse health effects in people with compromised 

14 cardiopulmonary systems. 

15 Several other types of newly available data also support reasonable hypotheses 

16 that may help to explain the findings of O3-related increases in cardiovascular mortality

17 observed in some epidemiological studies. These include the direct effect of O3 on 

18 increasing PAF in lung tissue that can then enter the general circulation and possibly

19 contribute to increased risk of blood clot formation and the consequent increased risk of 

20 heart attacks, cerebrovascular events (stroke), or associated cardiovascular-related 

21 mortality. Ozone reactions with cholesterol in lung surfactant to form epoxides and 

22 oxysterols that are cytotoxic to lung and heart muscles and that contribute to 

23 atherosclerotic plaque formation in arterial walls represent another potential pathway. 
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1 Stimulation of airway irritant receptors may lead to increases in tissue and serum levels 

2 of ANF, changes in heart rate, and edema of heart tissue. A few new field and panel 

3 studies of human adults have reported associations between ambient O3 concentrations 

4 and changes in cardiac autonomic control (e.g., HRV, ventricular arrhythmias, and MI). 

5 These represent plausible pathways that may lead to O3-related contributions to 

6 cardiovascular effects that ultimately increase the risk of mortality.

7 In addition, O3-induced increases in lung permeability allow more ready entry for 

8 inhaled PM into the blood stream, and thus O3 exposure may increase the risk of PM9 related cardiovascular effects. Furthermore, increased ambient O3 levels contribute to 

10 ultrafine PM formation in the ambient air and indoor environments. Thus, the 

11 contributions of elevated ambient O3 concentrations to ultrafine PM formation and 

12 human exposure, along with the enhanced uptake of inhaled fine particles, consequently 

13 may contribute to exacerbation of PM-induced cardiovascular effects in addition to those 

14 more directly induced by O3 (EPA, 2006a, p. 8-53).

15 c. Summary

16 Judgments concerning the extent to which relationships between various health 

17 endpoints and ambient O3 exposures are likely to be causal are informed by the 

18 conclusions and discussion in the 2006 Criteria Document as discussed above and 

19 summarized in section 3.7.5 of the 2007 Staff Paper. These judgments reflect the nature 

20 of the evidence and the overall weight of the evidence, and are taken into consideration in 

21 the quantitative risk assessment discussed below in section II.B.2.

22 For example, there is a very high level of confidence that O3 induces lung 

23 function decrements in healthy adults and children due in part to the dozens of controlled 
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1 human exposure and epidemiological studies consistently showing such effects. The 

2 2006 Criteria Document (p. 8-74) states that these studies provide clear evidence of 

3 causality for associations between short-term O3 exposures and statistically significant 

4 declines in lung function in children, asthmatics and adults who exercise outdoors. An 

5 increase in respiratory symptoms (e.g., cough, shortness of breath) has been observed in 

6 controlled human exposure studies of short-term O3 exposures, and significant 

7 associations between ambient O3 exposures and a wide variety of respiratory symptoms 

8 have been reported in epidemiology studies (EPA, 2006a, p. 8-75). Population time9 series studies showing robust associations between O3 exposures and respiratory hospital 

10 admissions and emergency department visits are strongly supported by controlled human 

11 exposure, animal toxicological, and epidemiological evidence for O3-related lung 

12 function decrements, respiratory symptoms, airway inflammation, and airway

13 hyperreactivity. The 2006 Criteria Document (p. 8-77) concludes that, taken together, the 

14 overall evidence supports the inference of a causal relationship between acute ambient O3

15 exposures and increased respiratory morbidity outcomes resulting in increased 

16 emergency department visits and hospitalizations during the warm season. Further, 

17 recent epidemiologic evidence has been characterized in the 2006 Criteria Document (p. 

18 8-78) as highly suggestive that O3 directly or indirectly contributes to non-accidental and 

19 cardiopulmonary-related mortality.

20 4. O3-Related Impacts on Public Health

21 The following discussion draws from chapters 6 and 7 and section 8.7 of the 2006 

22 Criteria Document and section 3.6 of the 2007 Staff Paper to characterize factors which 

23 modify responsiveness to O3, populations potentially at risk for O3-related health effects, 
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1 the adversity of O3-related effects, and the size of the at-risk populations in the U.S.. 

2 These considerations are all important elements in characterizing the potential public 

3 health impacts associated with exposure to ambient O3.

4 a. Factors That Modify Responsiveness to Ozone

5 There are numerous factors that can modify individual responsiveness to O3. 

6 These include: influence of physical activity; age; gender and hormonal influences; 

7 racial, ethnic and socioeconomic status (SES) factors; environmental factors; and 

8 oxidant-antioxidant balance. These factors are discussed in more detail in section 6.5 of 

9 the 2006 Criteria Document. 

10 It is well established that physical activity increases an individual’s minute 

11 ventilation and will thus increase the dose of O3 inhaled (EPA, 2006a, section 6.5.4). 

12 Increased physical activity results in deeper penetration of O3 into more distal regions of 

13 the lungs, which are more sensitive to acute O3 response and injury. This will result in 

14 greater lung function decrements for acute exposures of individuals during increased 

15 physical activity. Research has shown that respiratory effects are observed at lower O3 

16 concentrations if the level of exertion is increased and/or duration of exposure and 

17 exertion are extended. Predicted O3-induced decrements in lung function have been 

18 shown to be a function of exposure concentration, duration and exercise level for healthy, 

19 young adults (McDonnell et al., 1997).

20 Most of the studies investigating the influence of age have used lung function 

21 decrements and symptoms as measures of response. For healthy adults, lung function and 

22 symptom responses to O3 decline as age increases. The rate of decline in O3

23 responsiveness appears greater in those 18 to 35 years old compared to those 35 to 55 
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1 years old, while there is very little change after age 55. In one study (Seal et al., 1996) 

2 analyzing a large data set, a 5.4% decrement in FEV1 on average was estimated for 20 

3 year old individuals exposed to 0.12 ppm O3 for 2.3 hours, whereas similar exposure of 

4 35 year old individuals resulted in a 2.6% decrement on average. While healthy children 

5 tend not to report respiratory symptoms when exposed to low levels of O3, for subjects 18 

6 to 36 years old symptom responses induced by O3 are observed but tend to decrease with 

7 increasing age within this range (McDonnell et al., 1999).

8 Limited evidence of gender differences in response to O3 exposure has suggested 

9 that females may be predisposed to a greater susceptibility to O3. Lower plasma and NL 

10 fluid levels of the most prevalent antioxidant, uric acid, in females relative to males may 

11 be a contributing factor. Consequently, reduced removal of O3 in the upper airways may

12 promote deeper penetration. However, most of the evidence on gender differences 

13 appears to be equivocal, with one study (Hazucha et al., 2003) suggesting that 

14 physiological responses of young healthy males and females may be comparable (EPA, 

15 2006a, section 6.5.2).

16 A few studies have suggested that ethnic minorities might be more responsive to

17 O3 than Caucasian population groups (EPA, 2006a, section 6.5.3). This may be more the 

18 result of a lack of adequate health care and socioeconomic status (SES) than any

19 differences in sensitivity to O3. The limited data available, which have investigated the 

20 influence of race, ethnic or other related factors on responsiveness to O3, prevent drawing 

21 any clear conclusions at this time.

22 Few human studies have examined the potential influence of environmental 

23 factors such as the sensitivity of individuals who voluntarily smoke tobacco (i.e., 
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1 smokers) and the effect of high temperatures on O3 responsiveness. New controlled 

2 human exposure studies have confirmed that smokers are less responsive to O3 than 

3 nonsmokers; however, time course of development and recovery of these effects, as well 

4 as reproducibility, was not different from nonsmokers (EPA, 2006a, section 6.5.5). 

5 Influence of ambient temperature on pulmonary effects induced by O3 has been studied 

6 very little, but additive effects of heat and O3 exposure have been reported.

7 Antioxidants, which scavenge free radicals and limit lipid peroxidation in the 

8 ELF, are the first line of defense against oxidative stress. Ozone exposure leads to 

9 absorption of O3 in the ELF with subsequent depletion of antioxidant in the nasal ELF, 

10 but concentration and antioxidant enzyme activity in ELF or plasma do not appear related 

11 to O3 responsiveness (EPA 2006a, section 6.5.6). Controlled studies of dietary

12 antioxidant supplements have shown some protective effects on lung function decrements 

13 but not on symptoms and airway inflammatory responses. Dietary antioxidant 

14 supplements have provided some protection to asthmatics by attenuating post-exposure 

15 airway hyperresponsiveness. Animal studies have also supported the protective effects of 

16 ELF antioxidants.

17 b. At-Risk Subgroups for O3-Related Effects

18 Several characteristics may increase the extent to which a population group shows 

19 increased susceptibility or vulnerability. Information on potentially susceptible and

20 vulnerable groups is summarized in section 8.7 of the 2006 Criteria Document. As 

21 described there, the term susceptibility refers to innate (e.g., genetic or developmental) or 

22 acquired (e.g., personal risk factors, age) factors that make individuals more likely to 

23 experience effects with exposure to pollutants. A number of population groups have been 
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1 identified as potentially susceptible to health effects as a result of O3 exposure, including 

2 people with existing lung diseases, including asthma, children and older adults, and

3 people who have larger than normal lung function responses that may be due to genetic 

4 susceptibility. In addition, some population groups have been identified as having 

5 increased vulnerability to O3-related effects due to increased likelihood of exposure while 

6 at elevated ventilation rates, including healthy children and adults who are active 

7 outdoors, for example, outdoor workers, and joggers. Taken together, the susceptible and 

vulnerable groups make up "at-risk" groups.24 8

9 i. Active People

10 A large group of individuals at risk from O3 exposure consists of outdoor workers 

11 and children, adolescents, and adults who engage in outdoor activities involving exertion 

12 or exercise during summer daylight hours when ambient O3 concentrations tend to be 

13 higher. This conclusion is based on a large number of controlled-human exposure studies 

14 and several epidemiologic field/panel studies which have been conducted with healthy

15 children and adults and those with preexisting respiratory diseases (EPA 2006a, sections 

16 6.2, 6.3, 7.2, and 8.4.4). The controlled human exposure studies show a clear O3 

17 exposure-response relationship with increasing spirometric and symptomatic response as 

18 exercise level increases. Furthermore, O3-induced response increases as time of exposure 

19 increases. Studies of outdoor workers and others who participate in outdoor activities 

20 indicate that extended exposures to O3 at elevated exertion levels can produce marked 

 

24 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.
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1 effects on lung function, as discussed above in section IIA.2 (Brauer et al., 1996; Höppe 

2 et al., 1995; Korrick et al., 1998; McConnell et al., 2002).

3 These field studies with subjects at elevated exertion levels support the extensive 

4 evidence derived from controlled human exposure studies. The majority of controlled 

5 human exposure studies has examined the effects of O3 exposure in subjects performing 

6 continuous or intermittent exercise for variable periods of time and has reported 

7 significant O3-induced respiratory responses. The epidemiologic studies discussed above 

8 also indicate that prolonged exposure periods, combined with elevated levels of exertion 

9 or exercise, may magnify O3 effects on lung function. Thus, outdoor workers and others 

10 who participate in higher exertion activities outdoors during the time of day when high 

11 peak O3 concentrations occur appear to be particularly vulnerable to O3 effects on 

12 respiratory health. Although these studies show a wide variability of response and 

13 sensitivity among subjects and the factors contributing to this variability continue to be 

14 incompletely understood, the effect of increased exertion is consistent. It should be noted 

15 that this wide variability of response and sensitivity among subjects may be in part due to 

16 the wide range of other highly reactive photochemical oxidants coexisting with O3 in the 

17 ambient air.

18 ii. People with Lung Disease

19 People with preexisting pulmonary disease are among those at increased risk from 

20 O3 exposure. Altered physiological, morphological, and biochemical states typical of 

21 respiratory diseases like asthma, COPD, and chronic bronchitis may render people 

22 sensitive to additional oxidative burden induced by O3 exposure. At the time of the 1997 

23 review, it was concluded that these groups were at greater risk because the impact of O3-
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1 induced responses on already-compromised respiratory systems would noticeably impair 

2 an individual's ability to engage in normal activity or would be more likely to result in 

3 increased self-medication or medical treatment. At that time there was little evidence that 

4 people with pre-existing disease were more responsive than healthy individuals in terms 

5 of the magnitude of lung function decrements or symptomatic responses. The new results 

6 from controlled exposure and epidemiologic studies continue to indicate that individuals 

7 with preexisting pulmonary disease are a sensitive population for O3-related health 

8 effects.

9 Several controlled human exposure studies reviewed in the 1996 Criteria 

10 Document on atopic and asthmatic subjects have suggested but not clearly demonstrated 

11 enhanced responsiveness to acute O3 exposure compared to healthy subjects. The 

12 majority of the newer studies reviewed in Chapter 6 of the 2006 Criteria Document 

13 indicate that asthmatics are more sensitive than normal subjects in manifesting O3-

14 induced lung function decrements. In one key study (Horstman et al., 1995), the FEV1

15 decrement observed in the asthmatics was significantly larger than in the healthy subjects 

16 (19% versus 10%, respectively). There was also a notable tendency for a greater group 

17 mean O3-induced decrease in FEF25-75 in asthmatics relative to the healthy subjects (24% 

18 versus 15%, respectively). A significant positive correlation in asthmatics was also 

19 reported between the magnitude of O3-induced spirometric responses and baseline lung 

20 function, i.e., responses increased with severity of disease.

21 Asthmatics present a differential response profile for cellular, molecular, and 

22 biochemical parameters (2006 Criteria Document, Figure 8-1) that are altered in response 

23 to acute O3 exposure. Ozone-induced increases in neutrophils, IL-8 and protein were 
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1 found to be significantly higher in the BAL fluid from asthmatics compared to healthy

2 subjects, suggesting mechanisms for the increased sensitivity of asthmatics (Basha et al., 

3 1994; McBride et al., 1994; Scannell et al., 1996; Hiltermann et al., 1999; Holz et al., 

4 1999; Bosson et al., 2003). Neutrophils, or PMNs, are the white blood cells most 

5 associated with inflammation. IL-8 is an inflammatory cytokine with a number of 

6 biological effects, primarily on neutrophils. The major role of this cytokine is to attract 

7 and activate neutrophils. Protein in the airways is leaked from the circulatory system, 

8 and is a marker for increased cellular permeability. 

9 Bronchial constriction following provocation with O3 and/or allergens presents a 

10 two-phase response. The early response is mediated by release of histamine and 

11 leukotrienes that leads to contraction of smooth muscle cells in the bronchi, narrowing 

12 the lumen and decreasing the airflow. In people with allergic airway disease, including 

13 people with rhinitis and asthma, these mediators also cause accumulation of eosinophils 

14 in the airways (Bascom et al., 1990; Jorres et al., 1996; Peden et al., 1995 and 1997; 

15 Frampton et al., 1997; Michelson et al., 1999; Hiltermann et al., 1999; Holz et al., 2002; 

16 Vagaggini et al., 2002). In asthma, the eosinophil, which increases inflammation and 

17 allergic responses, is the cell most frequently associated with exacerbations of the 

18 disease. A study by Bosson et al. (2003) evaluated the difference in O3-induced 

19 bronchial epithelial cytokine expression between healthy and asthmatic subjects. After 

20 O3 exposure the epithelial expression of IL-5 and GM-CSF increased significantly in 

21 asthmatics, compared to healthy subjects. Asthma is associated with Th2-related airway

22 response (allergic response), and IL-5 is an important Th2-related cytokine. The O3-

23 induced increase in IL-5, and also in GM-CSF, which affects the growth, activation and 
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1 survival of eosinophils, may indicate an effect on the Th2-related airway response and on 

2 airway eosinophils. The authors reported that the O3-induced Th2-related cytokine 

3 responses that were found within the asthmatic group may indicate a worsening of their 

4 asthmatic airway inflammation and thus suggest a plausible link to epidemiological data 

5 indicating O3-associated increases in bronchial reactivity and hospital admissions. 

6 The accumulation of eosinophils in the airways of asthmatics is followed by 

7 production of mucus and a late-phase bronchial constriction and reduced airflow. In a 

8 study of 16 intermittent asthmatics, Hiltermann et al. (1999) found that there was a 

9 significant inverse correlation between the O3-induced change in the percentage of 

10 eosinophils in induced sputum and the change in PC20, the concentration of methacholine 

11 causing a 20% decrease in FEV1. Characteristic O3-induced inflammatory airway

12 neutrophilia at one time was considered a leading mechanism of airway

13 hyperresponsiveness. However, Hiltermann et al. (1999) determined that the O3-induced 

14 change in percentage neutrophils in sputum was not significantly related to the change in 

15 PC20. These results are consistent with the results of Zhang et al. (1995), which found 

16 neutrophilia in a murine model to be only coincidentally associated with airway

17 hyperresponsiveness, i.e., there was no cause and effect relationship. (2006 Criteria 

18 Document, AX 6-26). Hiltermann et al. (1999) concluded that the results point to the role 

19 of eosinophils in O3-induced airway hyperresponsiveness. Increases in O3-induced 

20 nonspecific airway responsiveness incidence and duration could have important clinical 

21 implications for asthmatics. 

22 Two studies (Jörres et al., 1996; Holz et al., 2002) observed increased airway

23 responsiveness to O3 exposure with bronchial allergen challenge in subjects with 
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1 preexisting allergic airway disease. Jörres et al. (1996) found that O3 causes an increased 

2 response to bronchial allergen challenge in subjects with allergic rhinitis and mild allergic 

3 asthma. The subjects were exposed to 0.25 ppm O3 for 3 hours with IE. Airway

4 responsiveness to methacholine was determined 1 hour before and after exposure; 

5 responsiveness to allergen was determined 3 hours after exposure. Statistically

6 significant decreases in FEV1 occurred in subjects with allergic rhinitis (13.8%) and 

7 allergic asthma (10.6%), and in healthy controls (7.3%). Methacholine responsiveness 

8 was statistically increased in asthmatics, but not in subjects with allergic rhinitis or 

9 healthy controls. Airway responsiveness to an individual’s historical allergen (either 

10 grass and birch pollen, house dust mite, or animal dander) was significantly increased 

11 after O3 exposure when compared to FA exposure. In subjects with asthma and allergic 

12 rhinitis, a maximum percent fall in FEV1 of 27.9% and 7.8%, respectively, occurred 3 

13 days after O3 exposure when they were challenged with of the highest common dose of 

14 allergen. The authors concluded that subjects with asthma or allergic rhinitis, without 

15 asthma, could be at risk if a high O3 exposure is followed by a high dose of allergen. 

16 Holz et al. (2002) reported an early phase lung function response in subjects with rhinitis 

17 after a consecutive 4-day exposure to 0.125 ppm O3 that resulted in a clinically relevant 

18 (>20%) decrease in FEV1. Ozone-induced exacerbation of airway responsiveness 

19 persists longer and attenuates more slowly than O3-induced lung function decrements and 

20 respiratory symptom responses and can have important clinical implications for 

21 asthmatics.

22 A small number of in vitro studies corroborate the differences in the responses of 

23 asthmatic and healthy subject generally found in controlled human exposure studies. In 
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1 vitro studies (Schierhorn et al., 1999) of nasal mucosal biopsies from atopic and 

2 nonatopic subjects exposed to 0.1 ppm O3 found significant differences in release of IL-4, 

3 IL-6, IL-8, and TNF-α. Another study by Schierhorn et al. (2002) found significant 

4 differences in the O3-induced release of the neuropeptides neurokinin A and substance P 

5 for allergic patients in comparison to nonallergic controls, suggesting increased activation 

6 of sensory nerves by O3 in the allergic tissues. Another study by Bayram et al. (2002) 

7 using in vitro culture of bronchial epithelial cells recovered from atopic and nonatopic 

8 asthmatics also found significant increases in epithelial permeability in response to O3

9 exposure. 

10 The new data on airway responsiveness, inflammation, and various molecular 

11 markers of inflammation and bronchoconstriction indicate that people with asthma and 

12 allergic rhinitis (with or without asthma) comprise susceptible groups for O3-induced 

13 adverse effects. This body of evidence indicates that controlled human exposure and 

14 epidemiological panel studies of lung function decrements and respiratory symptoms that 

15 evaluate only healthy, non-asthmatic subjects likely underestimate the effects of O3

16 exposure on asthmatics and other susceptible populations. The effects of O3 on lung 

17 function, inflammation, and increased airway responsiveness demonstrated in subjects 

18 with asthma and other allergic airway diseases, provide plausible mechanisms underlying 

19 the more serious respiratory morbidity effects, such as emergency department visits and 

20 hospital admissions, and respiratory mortality effects.

21 A number of epidemiological studies have been conducted using asthmatic study

22 populations. The majority of epidemiological panel studies that evaluated respiratory

23 symptoms and medication use related to O3 exposures focused on children. These studies 
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1 suggest that O3 exposure is associated with increased respiratory symptoms and 

2 medication use in children with asthma. Other reported effects include respiratory

3 symptoms, lung function decrements, and emergency department visits, as discussed in 

4 the 2006 Criteria Document (section 7.6.7.1). Strong evidence from a large multicity

5 study (Mortimer et al., 2002), along with support from several single-city studies indicate 

6 that O3 exposure is associated with increased respiratory symptoms and medication use in 

7 children with asthma. With regard to ambient O3 levels and increased hospital 

8 admissions and emergency department visits for asthma and other respiratory causes, 

9 strong and consistent evidence establishes a correlation between O3 exposure and 

10 increased exacerbations of preexisting respiratory disease for 1-hour maximum O3

11 concentrations <0.12 ppm. As discussed above and in the 2006 Criteria Document, 

12 section 7.3, several hospital admission and emergency department visit studies in the 

13 U.S., Canada, and Europe have reported positive associations between increase in O3 and 

14 increased risk of emergency department visits and hospital admissions for asthma other 

15 respiratory diseases, especially during the warm season.

16 In summary, based on a substantial new body of evidence from animal, controlled 

17 human exposure and epidemiological studies the 2006 Criteria Document (section x.x)

18 concludes that people with asthma and other preexisting pulmonary diseases are among 

19 those at increased risk from O3 exposure. Evidence from controlled human exposure 

20 studies indicates that asthmatics may exhibit larger lung function decrements and can 

21 have larger inflammatory responses in response to O3 exposure than healthy controls. 

22 Asthmatics present a different response profile for cellular, molecular, and biochemical 

23 parameters that are altered in response to acute O3 exposure. Asthmatics, and people 
Draft O3 NPR –January 5, 2010 128 Deliberative, Do Not Quote or Cite

1 with allergic rhinitis, are more likely to mount an allergic-type response upon exposure to 

2 O3, as manifested by increases in white blood cells associated with allergy and related 

3 molecules, which increase inflammation in the airways. The increased inflammatory and 

4 allergic responses also may be associated with the larger late-phase responses that 

5 asthmatics can experience, which can include increased bronchoconstrictor responses to 

6 irritant substances or allergens and additional inflammation. Epidemiological studies 

7 have reported fairly robust associations between ambient O3 concentrations and measures 

8 of lung function and daily respiratory symptoms (e.g., chest tightness, wheeze, shortness 

9 of breath) in children with moderate to severe asthma and between O3 and increased 

10 asthma medication use. These more serious responses in asthmatics and others with lung 

11 disease provide biological plausibility for the respiratory morbidity effects observed in 

12 epidemiological studies, such as emergency department visits and hospital admissions. 

13 The body of evidence from controlled human exposure and epidemiological studies, 

14 which includes asthmatic as well as non-asthmatic subjects, indicates that controlled 

15 human exposure studies of lung function decrements and respiratory symptoms that 

16 evaluate only healthy, non-asthmatic subjects likely underestimate the effects of O3

17 exposure on asthmatics and other susceptible populations. 

18 Newly available reports from controlled human exposure studies (see chapter 6 in 

19 the 2006 Criteria Document) utilized subjects with preexisting cardiopulmonary diseases 

20 such as COPD, asthma, allergic rhinitis, and hypertension. The data generated from these 

21 studies that evaluated changes in spirometry did not find clear differences between 

22 filtered air and O3 exposure in COPD subjects. However, the new data on airway

23 responsiveness, inflammation, and various molecular markers of inflammation and 
Draft O3 NPR –January 5, 2010 129 Deliberative, Do Not Quote or Cite

1 bronchoconstriction indicate that people with atopic asthma and allergic rhinitis comprise 

2 susceptible groups for O3-induced adverse health effects. 

3 Although controlled human exposure studies have not found evidence of larger 

4 spirometric responses to O3 in people with COPD relative to healthy subjects, this may be 

5 due to the fact that most people with COPD are older adults who would not be expected 

6 to be as responsive based on their age. However, in section 8.7.1, the 2006 Criteria 

7 Document notes that new epidemiological evidence indicates that people with COPD 

8 may be more likely to experience other effects, including emergency room visits, hospital 

9 admissions, or premature mortality. For example, results from an analysis of five 

10 European cities indicated strong and consistent O3 effects on unscheduled respiratory

11 hospital admissions, including COPD (Anderson et al., 1997). Also, an analysis of a 9-

12 year data set for the whole population of the Netherlands provided risk estimates for more 

13 specific causes of mortality, including COPD (Hoek et al., 2000, 2001; reanalysis Hoek, 

14 2003); a positive, but nonsignificant, excess risk of COPD-related mortality was found to 

15 be associated with short-term O3 concentrations. Moreover, as indicated by Gong et al. 

16 (1998), the effects of O3 exposure on alveolar-arterial oxygen gradients may be more 

17 pronounced in patients with preexisting obstructive lung diseases. Relative to healthy

18 elderly subjects, COPD patients have reduced gas exchange and low SaO2. Any

19 inflammatory or edematous responses due to O3 delivered to the well-ventilated regions

20 of the lung in COPD subjects could further inhibit gas exchange and reduce oxygen 

21 saturation. In addition, O3-induced vasoconstriction could also acutely induce pulmonary

22 hypertension. Inducing pulmonary vasoconstriction and hypertension in these patients 

23 would perhaps worsen their condition, especially if their right ventricular function was 
Draft O3 NPR –January 5, 2010 130 Deliberative, Do Not Quote or Cite

1 already compromised (EPA, 2006a, section 6.10). These controlled human exposure and 

2 epidemiological studies indicate that people with pre-existing lung diseases other than 

3 asthma are also at greater risk from O3 exposure than people without lung disease.

4 iii. Children and Older Adults

5 Supporting evidence exists for heterogeneity in the effects of O3 by age. As 

6 discussed in section 6.5.1 of the 2006 Criteria Document, children, adolescents, and 

7 young adults (<18 yrs of age) appear, on average, to have nearly equivalent spirometric 

8 responses to O3, but have greater responses than middle-aged and older adults when 

9 exposed to comparable O3 doses. Symptomatic responses to O3 exposure, however, do 

10 not appear to occur in healthy children, but are observed in asthmatic children, 

11 particularly those who use maintenance medications. For adults (>17 yrs of age) 

12 symptoms gradually decrease with increasing age. In contrast to young adults, the 

13 diminished symptomatic responses in children and the diminished symptomatic and 

14 spirometric responses in older adults increases the likelihood that these groups continue 

15 outdoor activities leading to greater O3 exposure and dose.

16 As described in the section 7.6.7.2 of the 2006 Criteria Document, many

17 epidemiological field studies focused on the effect of O3 on the respiratory health of 

18 school children. In general, children experienced decrements in lung function 

19 parameters, including PEF, FEV1, and FVC. Increases in respiratory symptoms and 

20 asthma medication use were also observed in asthmatic children. In one German study, 

21 children with and without asthma were found to be particularly susceptible to O3 effects 

22 on lung function. Approximately 20 percent of the children, both with and without 
Draft O3 NPR –January 5, 2010 131 Deliberative, Do Not Quote or Cite

1 asthma, experienced a greater than 10 percent change in FEV1, compared to only 5

2 percent of the elderly population and athletes (Höppe et al., 2003).

3 The American Academy of Pediatrics (2004) notes that children and infants are 

4 among the population groups most susceptible to many air pollutants, including O3. This 

5 is in part because their lungs are still developing. For example, eighty percent of alveoli 

6 are formed after birth, and changes in lung development continue through adolescence 

7 (Dietert et al., 2000). Children are also likely to spend more time outdoors than adults, 

8 which results in increased exposure to air pollutants (Wiley et al., 1991a,b). Moreover, 

9 children have high minute ventilation rates and high levels of physical activity which also 

10 increases their dose (Plunkett et al., 1992).

11 Several mortality studies have investigated age-related differences in O3 effects 

12 (EPA, 2006a, section 7.6.7.2). Older adults are also often classified as being particularly 

13 susceptible to air pollution. The 2006 Criteria Document (p. 8-60) concludes that the 

14 basis for increased O3 sensitivity among the elderly is not known, but one hypothesis is 

15 that it may be related to changes in the respiratory tract lining fluid antioxidant defense 

16 network (Kelly et al., 2003). Older adults have lower baseline lung function than 

17 younger people, and are also more likely to have preexisting lung and heart disease. 

18 Increased susceptibility of older adults to O3 health effects is most clearly indicated in the 

19 newer mortality studies. Among the studies that observed positive associations between 

20 O3 and mortality, a comparison of all age or younger age (65 years of age) O3-mortality

21 effect estimates to that of the elderly population (>65 years) indicates that, in general, the 

22 elderly population is more susceptible to O3 mortality effects. The meta-analysis by Bell 

23 et al. (2005) found a larger mortality effect estimate for the elderly than for all ages. In 
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1 the large U.S. 95 communities study (Bell et al., 2004), mortality effect estimates were 

2 slightly higher for those aged 65 to 74 years, compared to individuals less than 65 years 

3 and 75 years or greater. The absolute effect of O3 on premature mortality may be 

4 substantially greater in the elderly population because of higher rates of preexisting 

5 respiratory and cardiac diseases. The 2006 Criteria Document (p. 7-177) concludes that

6 the elderly population (>65 years of age) appear to be at greater risk of O3-related 

7 mortality and hospitalizations compared to all ages or younger populations.

8 The 2006 Criteria Document notes that, collectively, there is supporting evidence 

9 of age-related differences in susceptibility to O3 lung function effects. The elderly 

10 population (>65 years of age) appear to be at increased risk of O3-related mortality and 

11 hospitalizations, and children (<18 years of age) experience other potentially adverse 

12 respiratory health outcomes with increased O3 exposure (EPA, 2006a, section 7.6.7.2). 

13 iv. People with Increased Responsiveness to Ozone

14 New animal toxicology studies using various strains of mice and rats have 

15 identified O3-sensitive and resistant strains and illustrated the importance of genetic 

16 background in determining O3 susceptibility (EPA, 2006a, section 8.7.4). Controlled 

17 human exposure studies have also indicated a high degree of variability in some of the 

18 pulmonary physiological parameters. The variable effects in individuals have been found 

19 to be reproducible, in other words, a person who has a large lung function response after 

20 exposure to O3 will likely have about the same response if exposed again to the same 

21 dose of O3. In controlled human exposure studies, group mean responses are not 

22 representative of this segment of the population that has much larger than average 

23 responses to O3. Recent studies of asthmatics by David et al. (2003) and Romieu et al. 
Draft O3 NPR –January 5, 2010 133 Deliberative, Do Not Quote or Cite

1 (2004) reported a role for genetic polymorphism in observed differences in antioxidant 

2 enzymes and genes involved in inflammation to modulate lung function and 

inflammatory responses to O3 exposure.25 3

4 Biochemical and molecular parameters extensively evaluated in these experiments 

5 were used to identify specific loci on chromosomes and, in some cases, to relate the 

6 differential expression of specific genes to biochemical and physiological differences 

7 observed among these species. Utilizing O3-sensitive and O3-resistant species, it has 

8 been possible to identify the involvement of increased airway reactivity and inflammation 

9 processes in O3 susceptibility. However, most of these studies were carried out using 

10 relatively high doses of O3, making the relevance of these studies questionable in human 

11 health effects assessment. The genes and genetic loci identified in these studies may

12 serve as useful biomarkers in the future.

13 v. Other Population Groups

14 There is limited, new evidence supporting associations between short-term O3

15 exposures and a range of effects on the cardiovascular system. Some but not all, 

16 epidemiological studies have reported associations between short-term O3 exposures and 

17 the incidence of heart attacks and more subtle cardiovascular health endpoints, such as 

18 changes in HRV and cardiac arrhythmia. Others have reported associations with 

19 hospitalization or emergency department visits for cardiovascular diseases, although the 

 

25 Similar to animal toxicology studies referred above, a polymorphism in a 

specific proinflammatory cytokine gene has been implicated in O3-induced lung function 

changes in healthy, mild asthmatics and individuals with rhinitis. These observations 

suggest a potential role for these markers in the innate susceptibility to O3, however, the 

validity of these markers and their relevance in the context of prediction to population 

studies requires additional research.
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1 results across the studies are not consistent. Studies also report associations between 

2 short-term O3 exposure and mortality from cardiovascular or cardiopulmonary causes. 

3 The 2006 Criteria Document (p. 7-65) concludes that current cardiovascular effects 

4 evidence from some field studies is rather limited but supportive of a potential effect of 

5 short-term O3 exposure and HRV, cardiac arrhythmia, and heart attack incidence. In the 

6 2006 Criteria Document’s evaluation of studies of hospital admissions for cardiovascular 

7 disease (EPA 2006a, section 7.3.4), it is concluded that evidence from this growing group 

8 of studies is generally inconclusive regarding an association with O3 in studies conducted 

9 during the warm season (EPA 2006a, p. 7-83). This body of evidence suggests that 

10 people with heart disease may be at increased risk from short-term exposures to O3;

11 however, more evidence is needed to conclude that people with heart disease are a 

12 susceptible population.

13 Other groups that might have enhanced sensitivity to O3, but for which there is 

14 currently very little evidence, include groups based on race, gender and SES, and those 

15 with nutritional deficiencies, which presents factors which modify responsiveness to O3.

16 c. Adversity of Effects

17 In the 2008 rulemaking, in making judgments as to when various O3-related 

18 effects become regarded as adverse to the health of individuals, EPA looked to guidelines 

19 published by the American Thoracic Society (ATS) and the advice of CASAC. While 

20 recognizing that perceptions of “medical significance” and “normal activity” may differ 
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among physicians, lung physiologists and experimental subjects, the ATS (1985)26 1

2 defined adverse respiratory health effects as “medically significant physiologic changes 

3 generally evidenced by one or more of the following: (1) interference with the normal 

4 activity of the affected person or persons, (2) episodic respiratory illness, (3) 

5 incapacitating illness, (4) permanent respiratory injury, and/or (5) progressive respiratory

6 dysfunction.” During the 1997 review, it was concluded that there was evidence of 

7 causal associations from controlled human exposure studies for effects in the first of 

8 these five ATS-defined categories, evidence of statistically significant associations from 

9 epidemiological studies for effects in the second and third categories, and evidence from 

10 animal toxicology studies, which could be extrapolated to humans only with a significant 

11 degree of uncertainty, for the last two categories.

12 For ethical reasons, clear causal evidence from controlled human exposure studies 

13 still covers only effects in the first category. However, for this review there are results 

14 from epidemiological studies, upon which to base judgments about adversity, for effects 

15 in all of the categories. Statistically significant and robust associations have been 

16 reported in epidemiology studies falling into the second and third categories. These more 

17 serious effects include respiratory events (e.g., triggering asthma attacks) that may

18 require medication (e.g., asthma), but not necessarily hospitalization, as well as 

19 respiratory hospital admissions and emergency department visits for respiratory causes. 

 

26 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.
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1 Less conclusive, but still positive associations have been reported for school absences 

2 and cardiovascular hospital admissions. Human health effects for which associations 

3 have been suggested through evidence from epidemiological and animal toxicology

4 studies, but have not been conclusively demonstrated still fall primarily into the last two 

5 categories. In the 1997 review of the O3 standard, evidence for these more serious effects 

6 came from studies of effects in laboratory animals. Evidence from animal studies 

7 evaluated in the 2006 Criteria Document strongly suggests that O3 is capable of 

8 damaging the distal airways and proximal alveoli, resulting in lung tissue remodeling 

9 leading to apparently irreversible changes. Recent advancements of dosimetry modeling 

10 also provide a better basis for extrapolation from animals to humans. Information from 

11 epidemiological studies provides supporting, but limited evidence of irreversible 

12 respiratory effects in humans than was available in the prior review. Moreover, the 

13 findings from single-city and multicity time-series epidemiology studies and meta14 analyses of these epidemiological studies are highly suggestive of an association between 

15 short-term O3 exposure and mortality particularly in the warm season. 

16 While O3 has been associated with effects that are clearly adverse, application of 

17 these guidelines, in particular to the least serious category of effects related to ambient O3

18 exposures, involves judgments about which medical experts on the CASAC panel and 

19 public commenters have expressed diverse views in the past. To help frame such 

20 judgments, EPA staff have defined specific ranges of functional responses (e.g., 

21 decrements in FEV1 and airway responsiveness) and symptomatic responses (e.g., cough, 

22 chest pain, wheeze), together with judgments as to the potential impact on individuals 

23 experiencing varying degrees of severity of these responses, that have been used in 
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1 previous NAAQS reviews. These ranges of pulmonary responses and their associated 

2 potential impacts are summarized in Tables 3-2 and 3-3 of the 2007 Staff Paper.

3 For active healthy people, moderate levels of functional responses (e.g., FEV1

4 decrements of > 10 percent but < 20 percent, lasting up to 24 hours) and/or moderate 

5 symptomatic responses (e.g., frequent spontaneous cough, marked discomfort on exercise 

6 or deep breath, lasting up to 24 hours) would likely interfere with normal activity for 

7 relatively few responsive individuals. On the other hand, EPA staff determined that large 

8 functional responses (e.g., FEV1 decrements > 20 percent, lasting longer than 24 hours) 

9 and/or severe symptomatic responses (e.g., persistent uncontrollable cough, severe 

10 discomfort on exercise or deep breath, lasting longer than 24 hours) would likely interfere 

11 with normal activities for many responsive individuals. EPA staff determined that these 

12 would be considered adverse under ATS guidelines. In the context of standard setting, 

13 CASAC indicated that a focus on the mid to upper end of the range of moderate levels of 

14 functional responses (e.g., FEV1 decrements  15 percent but < 20 percent) is appropriate 

15 for estimating potentially adverse lung function decrements in active healthy people. 

16 However, for people with lung disease, even moderate functional (e.g., FEV1 decrements 

17 > 10 percent but < 20 percent, lasting up to 24 hours) or symptomatic responses (e.g., 

18 frequent spontaneous cough, marked discomfort on exercise or with deep breath, wheeze 

19 accompanied by shortness of breath, lasting up to 24 hours) would likely interfere with 

20 normal activity for many individuals, and would likely result in more frequent use of 

21 medication. For people with lung disease, large functional responses (e.g., FEV1

22 decrements > 20 percent, lasting longer than 24 hours) and/or severe symptomatic 

23 responses (e.g., persistent uncontrollable cough, severe discomfort on exercise or deep 
Draft O3 NPR –January 5, 2010 138 Deliberative, Do Not Quote or Cite

1 breath, persistent wheeze accompanied by shortness of breath, lasting longer than 24 

2 hours) would likely interfere with normal activity for most individuals and would 

3 increase the likelihood that these individuals would seek medical treatment. In the 

4 context of standard setting, the CASAC indicated (Henderson, 2006c) that a focus on the 

5 lower end of the range of moderate levels of functional responses (e.g., FEV1 decrements 

6  10 percent) is most appropriate for estimating potentially adverse lung function 

7 decrements in people with lung disease.

8 In judging the extent to which these impacts represent effects that should be 

9 regarded as adverse to the health status of individuals, an additional factor that has been 

10 considered in previous NAAQS reviews is whether such effects are experienced 

11 repeatedly during the course of a year or only on a single occasion. While some experts 

12 would judge single occurrences of moderate responses to be a “nuisance,” especially for 

13 healthy individuals, a more general consensus view of the adversity of such moderate 

14 responses emerges as the frequency of occurrence increases.

15 The new guidance builds upon and expands the 1985 definition of adversity in 

16 several ways. There is an increased focus on quality of life measures as indicators of 

17 adversity. There is also a more specific consideration of population risk. Exposure to air 

18 pollution that increases the risk of an adverse effect to the entire population is adverse, 

19 even though it may not increase the risk of any individual to an unacceptable level. For 

20 example, a population of asthmatics could have a distribution of lung function such that 

21 no individual has a level associated with significant impairment. Exposure to air 

22 pollution could shift the distribution to lower levels that still do not bring any individual 

23 to a level that is associated with clinically relevant effects. However, this would be 
Draft O3 NPR –January 5, 2010 139 Deliberative, Do Not Quote or Cite

1 considered to be adverse because individuals within the population would have 

2 diminished reserve function, and therefore would be at increased risk if affected by 

3 another agent. 

4 Of the various effects of O3 exposure that have been studied, many would meet 

5 the ATS definition of adversity. Such effects include, for example, any detectible level 

6 of permanent lung function loss attributable to air pollution, including both reductions in 

7 lung growth or acceleration of the age-related decline of lung function; exacerbations of 

8 disease in individuals with chronic cardiopulmonary diseases; reversible loss of lung 

9 function in combination with the presence of symptoms; as well as more serious effects 

10 such as those requiring medical care including hospitalization and, obviously, mortality.

11 d. Size of At-Risk Populations

12 Although O3-related health risk estimates may appear to be small, their 

13 significance from an overall public health perspective is determined by the large numbers 

14 of individuals in the population groups potentially at-risk for O3-related health effects 

15 discussed above. For example, a population of concern includes people with respiratory

16 disease, which includes approximately 11 percent of U.S. adults and 13 percent of 

17 children who have been diagnosed with asthma and 6 percent of adults with chronic 

18 obstructive pulmonary disease (chronic bronchitis and/or emphysema) in 2002 and 2003

19 (Table 8-4 in the 2006 Criteria Document, section 8.7.5.2). More broadly, individuals 

20 with preexisting cardiopulmonary disease may constitute an additional population of 

21 concern, with potentially tens of millions of people included in each disease category. In 

22 addition, populations based on age group also comprise substantial segments of the 

23 population that may be potentially at risk for O3-related health impacts. Based on U.S. 
Draft O3 NPR –January 5, 2010 140 Deliberative, Do Not Quote or Cite

1 census data from 2003, about 26 percent of the U.S. population are under 18 years of age 

2 and 12 percent are 65 years of age or older. Hence, large proportions of the U.S. 

3 population are included in life stages that are most likely to have increased susceptibility

4 to the health effects of O3 and or those with the highest ambient O3 exposures.

5 The 2006 Criteria Document (section 8.7.5.2) notes that the health statistics data 

6 illustrate what is known as the “pyramid” of effects. At the top of the pyramid, there are 

7 approximately 2.5 millions deaths from all causes per year in the U.S. population, with 

8 about 100,000 deaths from chronic lower respiratory diseases. For respiratory health 

9 diseases, there are nearly 4 million hospital discharges per year, 14 million emergency

10 department visits, 112 million ambulatory care visits, and an estimated 700 million 

11 restricted activity days per year due to respiratory conditions from all causes per year. 

12 Applying small risk estimates for the O3-related contribution to such health effects with 

13 relatively large baseline levels of health outcomes can result in quite large public health 

14 impacts related to ambient O3 exposure. Thus, even a small percentage reduction in O3

15 health impacts on cardiopulmonary diseases would reflect a large number of avoided 

16 cases. In considering this information together with the concentration-response 

17 relationships that have been observed between exposure to O3 and various health 

18 endpoints, the 2006 Criteria Document (section 8.7.5.2) concludes that exposure to 

19 ambient O3 likely has a significant impact on public health in the U.S.

20 B. Human Exposure and Health Risk Assessments

21 To put judgments about health effects that are adverse for individuals into a 

22 broader public health context, EPA has developed and applied models to estimate human 

23 exposures and health risks. This broader context includes consideration of the size of 
Draft O3 NPR –January 5, 2010 141 Deliberative, Do Not Quote or Cite

1 particular population groups at risk for various effects, the likelihood that exposures of 

2 concern will occur for individuals in such groups under varying air quality scenarios, 

3 estimates of the number of people likely to experience O3-related effects, the variability

4 in estimated exposures and risks, and the kind and degree of uncertainties inherent in 

5 assessing the exposures and risks involved. 

6 As discussed below there are a number of important uncertainties that affect the 

7 exposure and health risk estimates. It is also important to note that there have been 

8 significant improvements in both the exposure and health risk model. CASAC expressed 

9 the view that the exposure analysis represents a state-of-the-art modeling approach and 

10 that the health risk assessment was “well done, balanced and reasonably communicated 

11 (Henderson, 2006c). While recognizing and considering the kind and degree of 

12 uncertainties in both the exposure and health risk estimates, the 2007 Staff Paper (pp. 6-

13 20 to 6-21) judged that the quality of the estimates is such that they are suitable to be 

14 used as an input to the Administrator’s decisions on the O3 primary standard.

15 In modeling exposures and health risks associated with just meeting the current 

16 and alternative O3 standards, EPA has simulated air quality to represent conditions just 

17 meeting these standards based on O3 air quality patterns in several recent years and on 

18 how the shape of the O3 air quality distribution have changed over time based on 

19 historical trends in monitored O3 air quality data. As described in the 2007 Staff Paper 

20 (EPA, 2007b, section 4.5.8) and discussed below, recent O3 air quality distributions have 

21 been statistically adjusted to simulate just meeting the current and selected alternative 

22 standards. These simulations do not reflect any consideration of specific control 

23 programs or strategies designed to achieve the reductions in emissions required to meet 
Draft O3 NPR –January 5, 2010 142 Deliberative, Do Not Quote or Cite

1 the specified standards. Further, these simulations do not represent predictions of when, 

whether, or how areas might meet the specified standards.27 2 

3 As noted in section I.C above, around the time of the release of the final 2007 

4 Staff Paper in January 2007, EPA discovered a small error in the exposure model that 

5 when corrected resulted in slight increases in the simulated exposures. Since the 

6 exposure estimates are an input to the lung function portion of the health risk assessment, 

7 this correction also resulted in slight increases in the lung function risk estimates as well. 

8 The exposure and risk estimates discussed in this notice reflect the corrected estimates, 

9 and thus are slightly different than the exposure and risk estimates cited in the January

31, 2007 Staff Paper.28 10

11 1. Exposure Analyses

12 a. Overview

13 As part of the 2008 rulemaking, the EPA conducted exposure analyses using a 

14 simulation model to estimate O3 exposures for the general population, school age 

15 children (ages 5-18), and school age children with asthma living in 12 U.S. metropolitan 

16 areas representing different regions of the country where the then current 8-hour O3

17 standard is not met. The emphasis on children reflects the finding of the 1997 O3

18 NAAQS review that children are an important at-risk group. The 12 modeled areas 

19 combined represent a significant fraction of the U.S. urban population, 89 million people, 

 

27 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.

28 EPA made available corrected versions of the final 2007 Staff Paper, and 

human exposure and health risk assessment technical support documents in July 2007 on 

the EPA web site listed in the Availability of Related Information section of this notice.
Draft O3 NPR –January 5, 2010 143 Deliberative, Do Not Quote or Cite

1 including 18 million school age children of whom approximately 2.6 million have 

2 asthma. The selection of urban areas to include in the exposure analysis took into 

3 consideration the location of O3 epidemiological studies, the availability of ambient O3

4 data, and the desire to represent a range of geographic areas, population demographics, 

5 and O3 climatology. These selection criteria are discussed further in chapter 5 of the 

6 2007 Staff Paper (EPA, 2007b). The geographic extent of each modeled area consists of 

7 the census tracts in the combined statistical area (CSA) as defined by OMB (OMB, 

2005).29 8 

9 Exposure estimates were developed using a probabilistic exposure model that is 

10 designed to explicitly model the numerous sources of variability that affect people’s 

11 exposures. As discussed below, the model estimates population exposures by simulating 

12 human activity patterns, air conditioning prevalence, air exchange rates, and other 

13 factors. The modeled exposure estimates were developed for three recent years of 

14 ambient O3 concentrations (2002, 2003, and 2004), as well as for O3 concentrations 

15 adjusted to simulate conditions associated with just meeting the then current NAAQS and 

various alternative 8-hour standards based on the three year period 2002-2004.

30 16 This 

17 exposure assessment is more fully described and presented in the 2007 Staff Paper and in 

18 a technical support document, Ozone Population Exposure Analysis for Selected Urban 

 

29 The 12 CSAs modeled are: Atlanta-Sandy Springs-Gainesville, GA-AL; 

Boston-Worcester-Manchester, MA-NH; Chicago-Naperville-Michigan City, IL-IN-WI; 

Cleveland-Akron-Elyria, OH; Detroit-Warren-Flint, MI; Houston-Baytown-Huntsville, 

TX; Los Angeles-Long Beach-Riverside, CA; New York-Newark-Bridgeport, NY-NJCT-PA; Philadelphia-Camden-Vineland, PA-NJ-DE-MD; Sacramento--Arden-Arcade--

Truckee, CA-NV; St. Louis-St. Charles-Farmington, MO-IL; Washington-Baltimore-N. 

Virginia, DC-MD-VA-WV

30 All 12 of the CSAs modeled did not meet the 0.084 ppm O3 NAAQS for the 

three year period examined.
Draft O3 NPR –January 5, 2010 144 Deliberative, Do Not Quote or Cite

1 Areas (EPA, 2007c; hereafter Exposure Analysis TSD). The scope and methodology for 

2 this exposure assessment were developed over the last few years with considerable input 

from the CASAC Ozone Panel and the public.31 3

4 The goals of the O3 exposure assessment were: (1) to provide estimates of the size 

5 of at-risk populations exposed to various levels associated with recent O3 concentrations, 

6 and with just meeting the current O3 NAAQS and alternative O3 standards, in specific 

7 urban areas; (2) to provide distributions of exposure estimates over the entire range of 

8 ambient O3 concentrations as an important input to the lung function risk assessment 

9 summarized below in section II.B.2; (3) to develop a better understanding of the 

10 influence of various inputs and assumptions on the exposure estimates; and (4) to gain 

11 insight into the distribution of exposures and patterns of exposure reductions associated 

12 with meeting alternative O3 standards. 

13 The EPA recognizes that there are many sources of variability and uncertainty

14 inherent in the inputs to this assessment and that there is uncertainty in the resulting O3

15 exposure estimates. With respect to variability, the exposure modeling approach 

16 accounts for variability in ambient O3 levels, demographic characteristics, physiological 

17 attributes, activity patterns, and factors affecting microenvironmental (e.g., indoor) 

18 concentrations. In EPA’s judgment, the most important uncertainties affecting the 

 

31 The general approach used in the human exposure assessment was described in 

the draft Health Assessment Plan (EPA, 2005d) that was released to the CASAC and 

general public in April 2005 and was the subject of a consultation with the CASAC O3

Panel on May 5, 2005. In October 2005, OAQPS released the first draft of the Staff 

Paper containing a chapter discussing the exposure analyses and first draft of the 

Exposure Analyses TSD for CASAC consultation and public review on December 8, 

2005. In July 2006, OAQPS released the second draft of the Staff Paper and second draft 

of the Exposure Analyses TSD for CASAC review and public comment which was held 

by the CASAC O3 Panel on August 24-25, 2006. 
Draft O3 NPR –January 5, 2010 145 Deliberative, Do Not Quote or Cite

1 exposure estimates are related to the modeling of human activity patterns over an O3

2 season, the modeling of variations in ambient concentrations near roadways, and the 

3 modeling of air exchange rates that affect the amount of O3 that penetrates indoors. 

4 Another important uncertainty that affects the estimation of how many exposures are 

5 associated with moderate or greater exertion is the characterization of energy expenditure 

6 for children engaged in various activities. As discussed in more detail in the 2007 Staff 

7 Paper (EPA, 2007b, section 4.3.4.7), the uncertainty in energy expenditure values carries 

8 over to the uncertainty of the modeled breathing rates, which are important since they are 

9 used to classify exposures occurring at moderate or greater exertion which are the 

10 relevant exposures since O3-related effects observed in controlled human exposure 

11 studies only are observed when individuals are engaged in some form of exercise. The 

12 uncertainties in the exposure model inputs and the estimated exposures have been 

13 assessed using quantitative uncertainty and sensitivity analyses. Details are discussed in 

14 the 2007 Staff Paper (section 4.6) and in a technical memorandum describing the 

15 exposure modeling uncertainty analysis (Langstaff, 2007).

16 b. Scope and Key Components

17 Population exposures to O3 are primarily driven by ambient outdoor 

18 concentrations, which vary by time of day, location, and peoples’ activities. Outdoor O3

19 concentration estimates used in the exposure assessment are provided by measurements 

20 and statistical adjustments to the measured concentrations. The current exposure analysis 

21 allows comparisons of population exposures to O3 within each urban area, associated 

22 with current O3 levels and with O3 levels just meeting several potential alternative air 

23 quality standards or scenarios. Human exposure, regardless of the pollutant, depends on 
Draft O3 NPR –January 5, 2010 146 Deliberative, Do Not Quote or Cite

1 where individuals are located and what they are doing. Inhalation exposure models are 

2 useful in realistically estimating personal exposures to O3 based on activity-specific 

3 breathing rates, particularly when recognizing that large scale population exposure 

4 measurement studies have not been conducted that are representative of the overall 

5 population or at risk subpopulations.

6 The model EPA used to simulate O3 population exposure is the Air Pollutants 

7 Exposure Model (APEX), the human inhalation exposure model within the Total Risk 

8 Integrated Methodology (TRIM) framework (EPA, 2006c,d). APEX is conceptually 

9 based on the probabilistic NAAQS exposure model for O3 (pNEM/O3) used in the last O3

10 NAAQS review. Since that time the model has been restructured, improved, and 

11 expanded to reflect conceptual advances in the science of exposure modeling and newer 

12 input data available for the model. Key improvements to algorithms include replacement 

13 of the cohort approach with a probabilistic sampling approach focused on individuals, 

14 accounting for fatigue and oxygen debt after exercise in the calculation of breathing rates, 

15 and a new approach for construction of longitudinal activity patterns for simulated 

16 persons. Major improvements to data input to the model include updated air exchange 

17 rates, more recent census and commuting data, and a greatly expanded daily time18 activities database. 

19 APEX is a probabilistic model designed to explicitly model the numerous sources 

20 of variability that affect people’s exposures. APEX simulates the movement of 

21 individuals through time and space and estimates their exposures to O3 in indoor, 

22 outdoor, and in-vehicle microenvironments. The exposure model takes into account the 

23 most significant factors contributing to total human O3 exposure, including the temporal 
Draft O3 NPR –January 5, 2010 147 Deliberative, Do Not Quote or Cite

1 and spatial distribution of people and O3 concentrations throughout an urban area, the 

2 variation of O3 levels within each microenvironment, and the effects of exertion on 

3 breathing rate in exposed individuals. A more detailed description of APEX and its 

4 application is presented in chapter 4 of the 2007 Staff Paper and associated technical 

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

6 Several methods have been used to evaluate the APEX model and to characterize 

7 the uncertainty of the model estimates. These include conducting model evaluation, 

8 sensitivity analyses, and a detailed uncertainty analysis for one urban area. These are 

9 discussed fully in the 2007 Staff Paper (section 4.6) and in Langstaff (2007). The 

10 uncertainty of model structure was judged to be of lesser importance than the 

11 uncertainties of the model inputs and parameters. Model structure refers to the 

12 algorithms in APEX designed to simulate the processes that result in people’s exposures, 

13 for example, the way that APEX models exposures to individuals when they are near 

14 roads. The uncertainties in the model input data (e.g., measurement error, ambient 

15 concentrations, air exchange rates, and activity pattern data) have been assessed 

16 individually, and their impact on the uncertainty in the modeled exposure estimates was 

17 assessed in a unified quantitative analysis with results expressed in the form of estimated 

18 confidence ranges around the estimated measures of exposure. This uncertainty analysis 

19 was conducted for one urban area (Boston) using the observed 2002 O3 concentrations 

20 and 2002 concentrations adjusted to simulate just meeting the current standard, with the 

21 expectation that the results would be similar for other cities and years. One significant 

22 source of uncertainty, due to limitations in the database used to model peoples’ daily

23 activities, was not included in the unified analysis, and was assessed through separate 
Draft O3 NPR –January 5, 2010 148 Deliberative, Do Not Quote or Cite

1 sensitivity analyses. This analysis indicates that the uncertainty of the exposure results is 

2 relatively small. For example, 95 percent uncertainty intervals were calculated for the 

3 APEX estimates of the percent of children or asthmatic children with exposures above 

4 0.060, 0.070, or 0.080 ppm under moderate exertion, for two air quality scenarios 

5 (current 2002 and 2002 adjusted to simulate just meeting the current standard) in Boston 

6 (Langstaff, 2007, Tables 26 and 27). The 95 percent uncertainty intervals for this set of 

7 12 exposure estimates indicate the possibility of underpredictions of the exposure 

8 estimates ranging from 3 to 25 percent of the modeled estimates, and overpredictions 

9 ranging from 4 to 11 percent of the estimates. For example, APEX estimates the percent 

10 of asthmatic children with exposures above 0.070 ppm under moderate exertion to be 24 

11 percent, for Boston 2002 O3 concentrations adjusted to simulate just meeting the current 

12 standard. The 95 percent uncertainty interval for this estimate is 23 − 30 percent, or -4 to 

13 +25 percent of the estimate. These uncertainty intervals do not include the uncertainty 

14 engendered by limitations of the activity database, which is in the range of one to ten 

15 percent.

16 The exposure periods modeled here are the O3 seasons in 2002, 2003, and 2004. 

17 The O3 season in each area includes the period of the year where elevated O3 levels tend 

18 to be observed and for which routine hourly O3 monitoring data are available. Typically

19 this period spans from March or April through September or October, or in some areas, 

20 spanning the entire year. Three years were modeled to reflect the substantial year-to-year 

21 variability that occurs in O3 levels and related meteorological conditions, and because the 

22 standard is specified in terms of a three-year period. The year-to-year variability

23 observed in O3 levels is due to a combination of different weather patterns and the 
Draft O3 NPR –January 5, 2010 149 Deliberative, Do Not Quote or Cite

1 variation in emissions of O3 precursors. Nationally, 2002 was a relatively high year with 

respect to the 4th 2 highest daily maximum 8-hour O3 levels observed in urban areas across 

3 the U.S. (EPA, 2007b, Figure 2-16), with the mean of the distribution of O3 levels for the 

4 urban monitors being in the upper third among the years 1990 through 2006. In contrast, 

5 on a national basis, 2004 is the lowest year on record through 2006 for this same air 

6 quality statistic, and 8-hour daily maximum O3 levels observed in most, but not all of the 

7 12 urban areas included in the exposure and risk analyses were relatively low compared 

to other recent years. The 4th 8 highest daily maximum 8-hour O3 levels observed in 2003 

9 in the 12 urban areas and nationally generally were between those observed in 2002 and 

10 2004.

11 Regulatory scenarios examined in the 2008 rulemaking include the then current 

12 0.08 ppm, average of the 4th daily maximum 8-hour averages over a three year period 

13 standard; standards with the same form but with alternative levels of 0.080, 0.074, 0.070, 

14 and 0.064 ppm; standards specified as the average of the 3rd highest daily maximum 8-

15 hour averages over a three year period with alternative levels of 0.084 and 0.074 ppm; 

16 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.32 17 The then current standard used a 

18 rounding convention that allows areas to have an average of the 4th daily maximum 8-

19 hour averages as high as 0.084 ppm and still meet the standard. All alternative standards 

 

32 The 8-hour O3 standard established in 1997 was 0.08 ppm, but the rounding 

convention specified that the average of the 4th daily maximum 8-hour average 

concentrations over a three-year period must be at 0.084 ppm or lower to be in attainment 

of this standard. When EPA staff selected alternative standards to analyze, it was 

presumed that the same type of rounding convention would be used, and thus alternative 

standards of 0.084, 0.074, 0.064 ppm were chosen. 
Draft O3 NPR –January 5, 2010 150 Deliberative, Do Not Quote or Cite

1 analyzed were intended to reflect improved precision in the measurement of ambient 

2 concentrations (in ppm), where the precision would extend to three instead of two 

3 decimal places. 

4 The then current standard and all alternative standards were modeled using a 

5 quadratic rollback approach to adjust the hourly concentrations observed in 2002-2004 to 

yield a design value33 6 corresponding to the standard being analyzed. The quadratic 

7 rollback technique reduces higher concentrations more than lower concentrations near 

ambient background levels.34 8 This procedure was considered in a sensitivity analysis in 

9 the 1997 review of the O3 standard and has been shown to be more realistic than a linear, 

10 proportional rollback method, where all of the ambient concentrations are reduced by the 

11 same factor.

 

33 A design value is a statistic that describes the air quality status of a given area 

relative to the level of the NAAQS. Design values are often based on multiple years of 

data, consistent with specification of the NAAQS in Part 50 of the CFR. For the 8-hour

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

concentrations, based on the monitor within (or downwind of) an urban area yielding the 

highest 3-year average, is the design value.

34 The quadratic rollback approach and evaluation of this approach are described 

by Johnson (1997), Duff et al. (1998) and Rizzo (2005, 2006).
Draft O3 NPR –January 5, 2010 151 Deliberative, Do Not Quote or Cite

1 c. Exposure Estimates and Key Observations

2 The exposure assessment, which provides estimates of the number of people 

exposed to different levels of ambient O3 while at specified exertion levels,35 3 serve two 

4 purposes. First, the entire range of modeled personal exposures to ambient O3 is an 

5 essential input to the portion of the health risk assessment based on exposure-response 

6 functions from controlled human exposure studies, discussed in the next section. Second, 

7 estimates of personal exposures to ambient O3 concentrations at and above specific 

8 benchmark levels provide some perspective on the public health impacts of health effects 

9 that cannot currently be evaluated in quantitative risk assessments that may occur at 

10 current air quality levels, and the extent to which such impacts might be reduced by

11 meeting the current and alternative standards. This is especially true when there are 

12 exposure levels at which it is known or can reasonably be inferred that specific O3-related 

13 health effects are occurring. In this notice, exposures at and above these benchmark 

14 concentrations are referred to as “exposures of concern.”

15 It is important to note that although the analysis of “exposures of concern” was 

16 conducted using three discrete benchmark levels (i.e., 0.080, 0.070, and 0.060 ppm), the 

17 concept is more appropriately viewed as a continuum with greater confidence and less 

 

35 As discussed above in Section II.A, O3 health responses observed in controlled 

human exposure studies are associated with exposures while engaged in moderate or 

greater exertion and, therefore, these are the exposure measures of interest. The level of 

exertion of individuals engaged in particular activities is measured by an equivalent 

ventilation rate (EVR), ventilation normalized by body surface area (BSA, in m2), which 

is calculated as VE/BSA, where VE is the ventilation rate (liters/minute). Moderate and 

greater exertion levels were defined as EVR > 13 liters/min-m

2

(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.
Draft O3 NPR –January 5, 2010 152 Deliberative, Do Not Quote or Cite

1 uncertainty about the existence of health effects at the upper end and less confidence and 

2 greater uncertainty as one considers increasingly lower O3 exposure levels. The EPA 

3 recognizes that there is no sharp breakpoint within the continuum ranging from at and 

4 above 0.080 ppm down to 0.060 ppm. In considering the concept of exposures of 

5 concern, it is important to balance concerns about the potential for health effects and their 

6 severity with the increasing uncertainty associated with our understanding of the 

7 likelihood of such effects at lower O3 levels. 

8 Within the context of this continuum, estimates of exposures of concern at 

9 discrete benchmark levels provide some perspective on the public health impacts of O3-

10 related health effects that have been demonstrated in controlled human exposure and 

11 toxicological studies but cannot be evaluated in quantitative risk assessments, such as 

12 lung inflammation, increased airway responsiveness, and changes in host defenses. They

13 also help in understanding the extent to which such impacts have the potential to be 

14 reduced by meeting the current and alternative standards. In the selection of specific 

15 benchmark concentrations for this analysis, staff first considered the exposure level of 

16 0.080 ppm, at which there is a substantial amount of controlled human exposure evidence 

17 demonstrating a range of O3-related health effects including lung inflammation and 

18 airway responsiveness in healthy individuals. Thus, as in the 1997 review, this level was 

19 selected as a benchmark level for this assessment of exposures of concern. Evidence 

20 newly available in this review is the basis for identifying additional, lower benchmark 

21 levels of 0.070 and 0.060 ppm for this assessment.

22 More specifically, as discussed above in section II.A.2, evidence available from 

23 controlled human exposure and epidemiological studies indicates that people with asthma 
Draft O3 NPR –January 5, 2010 153 Deliberative, Do Not Quote or Cite

1 have larger and more serious effects than healthy individuals, including lung function, 

2 respiratory symptoms, increased airway responsiveness, and pulmonary inflammation, 

3 which has been shown to be a more sensitive marker than lung function responses. 

4 Further, a substantial new body of evidence from epidemiological studies shows 

5 associations with serious respiratory morbidity and cardiopulmonary mortality effects at 

6 O3 levels that extend below 0.080 ppm. Additional, but very limited new evidence from 

7 controlled human exposure studies shows lung function decrements and respiratory

8 symptoms in healthy subjects at an O3 exposure level of 0.060 ppm. The selected 

9 benchmark level of 0.070 ppm reflects the new information that asthmatics have larger 

10 and more serious effects than healthy people and therefore controlled human exposure 

11 studies done with healthy subjects may underestimate effects in this group, as well as the 

12 substantial body of epidemiological evidence of associations with O3 levels below 0.080 

13 ppm. The selected benchmark level of 0.060 ppm additionally reflects the very limited 

14 new evidence from controlled human exposure studies that show lung function 

15 decrements and respiratory symptoms in some healthy subjects at the 0.060 ppm 

16 exposure level, recognizing that asthmatics are likely to have more serious responses and 

17 that lung function is not likely to be as sensitive a marker for O3 effects as is lung 

18 inflammation.

19 The estimates of exposures of concern were reported in terms of both “people 

20 exposed” (the number and percent of people who experience a given level of O3

21 concentrations, or higher, at least one time during the O3 season in a given year) and 

22 “occurrences of exposure” (the number of times a given level of pollution is experienced 

23 by the population of interest, expressed in terms of person-days of occurrences). 
Draft O3 NPR –January 5, 2010 154 Deliberative, Do Not Quote or Cite

1 Estimating exposures of concern is important because it provides some indication of the 

2 potential public health impacts of a range of O3-related health outcomes, such as lung 

3 inflammation, increased airway responsiveness, and changes in host defenses. These 

4 particular health effects have been demonstrated in controlled human exposure studies of 

5 healthy individuals to occur at levels as low as 0.080 ppm O3, but have not been 

6 evaluated at lower levels in controlled human exposure studies. The EPA did not include 

7 these effects in the quantitative risk assessment due to a lack of adequate information on 

8 the exposure-response relationships.

9 The 1997 O3 NAAQS review estimated exposures associated with 1-hour heavy 

10 exertion, 1-hour moderate exertion, and 8-hour moderate exertion for children, outdoor 

11 workers, and the general population. The EPA’s analysis in the 1997 Staff Paper showed 

12 that exposure estimates based on the 8-hour moderate exertion scenario for children 

13 yielded the largest number of children experiencing exposures at or above exposures of 

14 concern. Consequently, EPA chose to focus on the 8-hour moderate and greater exertion 

15 exposures in all and asthmatic school age children in the current exposure assessment. 

16 While outdoor workers and other adults who engage in moderate or greater exertion for 

17 prolonged durations while outdoors during the day in areas experiencing elevated O3

18 concentrations also are at risk for experiencing exposures associated with O3-related 

19 health effects, EPA did not focus on quantitative estimates for these populations due to 

20 the lack of information about the number of individuals who regularly work or exercise 

21 outdoors. Thus, the exposure estimates presented here and in the 2007 Staff Paper are 

22 most useful for making relative comparisons across alternative air quality scenarios and 
Draft O3 NPR –January 5, 2010 155 Deliberative, Do Not Quote or Cite

1 do not represent the total exposures in all children or other groups within the general 

2 population associated with the air quality scenarios.

3 Population exposures to O3 were estimated in 12 urban areas for 2002, 2003, and 

4 2004 air quality, and also using O3 concentrations adjusted to just meet the then current 

5 and several alternative standards. The estimates of 8-hour exposures of concern at and 

6 above benchmark levels of 0.080, 0.070, and 0.060 ppm aggregated across all 12 areas 

7 are shown in Table 1 for air quality scenarios just meeting the current and four alternative 

8-hour average standards.

36 8 Table 1 provides estimates of the number and percent of 

9 school age children and asthmatic school age children exposed, with daily 8-hour 

10 maximum exposures at or above each O3 benchmark level of exposures of concern, while 

11 at intermittent moderate or greater exertion and based on O3 concentrations observed in 

12 2002 and 2004. Table 1 summarizes estimates for 2002 and 2004 because these years 

13 reflect years that bracket relatively higher and lower O3 levels, with year 2003 generally 

14 containing O3 levels in between when considering the 12 urban areas modeled. This 

15 table also reports the percent change in the number of persons exposed when a given 

16 alternative standard is compared with the then current standard.

17 Key observations important in comparing exposure estimates associated with just 

18 meeting the current NAAQS and alternative standards under consideration include:

19 (1) As shown in Table 6-1 of the 2007 Staff Paper, the patterns of exposure in 

20 terms of percentages of the population exceeding a given exposure level are very similar 

21 for the general population and for asthmatic and all school age (5-18) children, although 

 

36 The full range of quantitative exposure estimates associated with just meeting 

the 0.084 ppm and alternative O3 standards are presented in chapter 4 and Appendix 4A 

of the 2007 Staff Paper.
Draft O3 NPR –January 5, 2010 156 Deliberative, Do Not Quote or Cite

1 children are about twice as likely to be exposed, based on the percent of the population 

2 exposed, at any given level.

3 (2) As shown in Table 1 below, the number and percentage of asthmatic and all 

4 school-age children aggregated across the 12 urban areas estimated to experience one or 

5 more exposures of concern decline from simulations of just meeting the then current 

6 0.084 ppm standard to simulations of alternative 8-hour standards by varying amounts 

7 depending on the benchmark level, the population subgroup considered, and the year 

8 chosen. For example, the estimated percentage of school age children experiencing one 

9 or more exposures ≥ 0.070 ppm, while engaged in moderate or greater exertion, during an 

10 O3 season is about 18 percent of this population when the 0.084 ppm standard is met 

11 using the 2002 simulation; this is reduced to about 12, 4, 1, and 0.2 percent of children 

12 upon meeting alternative standards of 0.080, 0.074, 0.070, and 0.064 ppm, respectively 

(all specified in terms of the 4th 13 highest daily maximum 8-hour average), using the 2002 

14 simulation. 

15
Draft O3 NPR –January 5, 2010 157 Deliberative, Do Not Quote or Cite

1 Table 1. Number and Percent of All and Asthmatic School Age Children in 12 

2 Urban Areas Estimated to Experience 8-Hour Ozone Exposures Above 0.080, 0.070, 

3 and 0.060 ppm While at Moderate or Greater Exertion, One or More Times Per 

4 Season, and the Number of Occurrences Associated with Just Meeting Alternative 

8-Hour Standards Based on Adjusting 2002 and 2004 Air Quality Data1,2 5

Benchmark 

Levels of 

Exposures

of Concern

(ppm)

8-Hour Air 

Quality 

Standards3

(ppm)

All Children, ages 5-18 

Aggregate for 12 urban areas

Asthmatic Children, ages 5-18

Aggregate for 12 urban areas

Number of Children Exposed (% of all) 

[% reduction from 0.084 ppm standard]

Number of Children Exposed (% of group)

[% reduction from 0.084 ppm standard]

2002 2004 2002 2004

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

0.080 290,000 (2%)

[70%]

10,000 (0%)

[67%]

50,000 (2%)

[54%]

0 (0%)

0.074 60,000 (0%)

[91%]

0 (0%)

[100%]

10,000 (0%)

[91%]

0 (0%)

0.070 10,000 (0%)

[98%]

0 (0%)

[100%]

0 (0%)

[100%]

0 (0%)

0.064 0 (0%)

[100%]

0 (0%)

[100%]

0 (0%)

[100%]

0 (0%)

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

0.080 2,160,000 (12%)

[35%]

100,000 (1%)

[62%]

330,000 (13%)

[36%]

10,000 (0%)

[75%]

0.074 770,000 (4%)

[77%]

20,000 (0%)

[92%]

120,000 (5%)

[77% ]

0 (0%)

[100%]

0.070 270,000 (1%)

[92%]

0 (0%)

[100%]

50,000 (2%)

[90%]

0 (0%)

[100%]

0.064 30,000 (0.2%)

[99%]

0 (0%)

[100%]

10,000 (0.2%)

[98% ]

0 (0%)

[100%]

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

0.080 6,730,000 (37%

[16%]

1,050,000 (6%)

[42%]

1,020,000 (40%)

[16%]

150,000 (6%)

[44%]

0.074 4,550,000 (25%)

[43%]

350,000 (2%)

[80%]

700,000 (27%)

[42%]

50,000 (2%)

[81%]

0.070 3,000,000 (16%)

[62%]

110,000 (1%)

[94%]

460,000 (18%)

[62%]

10,000 (1%)

[96%]

0.064 950,000 (5%)

[88%]

10,000 (0%)

[99%]

150,000 (6%)

[88%]

0 (0%)

[100%]

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

6 .

2 7 Estimates are the aggregate results based on 12 combined statistical areas (Atlanta, Boston, Chicago, Cleveland, 

8 Detroit, Houston, Los Angeles, New York, Philadelphia, Sacramento, St. Louis, and Washington, D.C.). Estimates 

9 are for the ozone season which is all year in Houston, Los Angeles and Sacramento and March or April to 

10 September or October for the remaining urban areas.

3 11 All standards summarized here have the same form as the 8-hour standard established in 1997 which is specified 

as the 3-year average of the annual 4th 12 highest daily maximum 8-hour average concentrations must be at or below

13 the concentration level specified. As described in the 2007 Staff Paper (EPA, 2007b, section 4.5.8), recent O3 air 

14 quality distributions have been statistically adjusted to simulate just meeting the 0.084 ppm standard and selected 
Draft O3 NPR –January 5, 2010 158 Deliberative, Do Not Quote or Cite

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

2 the specified standards.

3
Draft O3 NPR –January 5, 2010 159 Deliberative, Do Not Quote or Cite

1 (3) Substantial year-to-year variability in exposure estimates is observed over the 

2 three-year modeling period. For example, the estimated number of school age children 

3 experiencing one or more exposures  0.070 ppm during an O3 season when a 0.084 ppm 

4 standard is met in the 12 urban areas included in the analysis is 3.3, 1.0, or 0.3 million for 

5 the 2002, 2003, and 2004 simulations, respectively.

6 (4) There is substantial variability observed across the 12 urban areas in the 

7 percent of the population subgroups estimated to experience exposures of concern. For 

8 example, when 2002 O3 concentrations are simulated to just meet a 0.084 ppm standard, 

9 the aggregate 12 urban area estimate is 18 percent of all school age children are estimated 

10 to experience O3 exposures  0.070 ppm (Table 1 below), while the range of exposure 

11 estimates in the 12 urban areas considered separately for all children range from 1 to 38 

12 percent (EPA, 2007b, p. 4-48, Exhibit 2). There was also variability in exposure 

13 estimates among the modeled areas when using the 2004 air quality simulation for the 

14 same scenario; however it was reduced and ranged from 0 to 7 percent in the 12 urban 

15 areas (EPA, 2007b, p. 4-60, Exhibit 8).

16 (5) Of particular note, as discussed above in section II.A of this notice, high inter17 individual variability in responsiveness means that only a subset of individuals in these 

18 groups who are exposed at and above a given benchmark level would actually be 

19 expected to experience such adverse health effects.

20 (6) In considering these observations, it is important to take into account the 

21 variability, uncertainties, and limitations associated with this assessment, including the 

22 degree of uncertainty associated with a number of model inputs and uncertainty in the 

23 model itself, as discussed above.
Draft O3 NPR –January 5, 2010 160 Deliberative, Do Not Quote or Cite

1 2. Quantitative Health Risk Assessment

2 This section discusses the approach used to develop quantitative health risk 

3 estimates associated with exposures to O3 building upon a more limited risk assessment 

that was conducted during the last review.37 4 As part of the 1997 review, EPA conducted 

5 a health risk assessment that produced risk estimates for the number and percent of 

6 children and outdoor workers experiencing lung function and respiratory symptoms 

associated with O3 exposures for 9 urban areas.38 7 The risk assessment for the 1997 

8 review also included risk estimates for excess respiratory-related hospital admissions 

9 related to O3 concentrations for New York City. In the last review, the risk estimates 

10 played a significant role in both the staff recommendations and in the proposed and final 

11 decisions to revise the O3 standards. The health risk assessment conducted for the current 

12 review builds upon the methodology and lessons learned from the prior review. 

13 a. Overview

14 The updated health risk assessment conducted as part of the 2008 rulemaking 

15 includes estimates of (1) risks of lung function decrements in all and asthmatic school age 

16 children, respiratory symptoms in asthmatic children, respiratory-related hospital 

17 admissions, and non-accidental and cardiorespiratory-related mortality associated with 

18 recent ambient O3 levels; (2) risk reductions and remaining risks associated with just 

19 meeting the then current 0.084 ppm 8-hour O3 NAAQS; and (3) risk reductions and 

 

37 The methodology, scope, and results from the risk assessment conducted in the 

last review are described in Chapter 6 of the 1996 Staff Paper (EPA, 1996) and in several 

technical reports (Whitfield et al., 1996; Whitfield, 1997) and publication (Whitfield et 

al., 1998). 

38 The 9 urban study areas included in the exposure and risk analyses conducted 

during the last review were: Chicago, Denver, Houston, Los Angeles, Miami, New York 

City, Philadelphia, St. Louis, and Washington, D.C.
Draft O3 NPR –January 5, 2010 161 Deliberative, Do Not Quote or Cite

1 remaining risks associated with just meeting various alternative 8-hour O3 NAAQS in a 

2 number of example urban areas. This risk assessment is more fully described and 

3 presented in chapter 5 of the 2007 Staff Paper and in a technical support document 

4 (TSD), Ozone Health Risk Assessment for Selected Urban Areas (Abt Associates, 2007a, 

5 hereafter referred to as “Risk Assessment TSD”). The scope and methodology for this 

6 risk assessment were developed over the last few years with considerable input from the 

CASAC O3 Panel and the public.39 7 The information contained in these documents 

8 included specific criteria for the selection of health endpoints, studies, and locations to 

9 include in the assessment. In a peer review letter sent by CASAC to the Administrator 

10 documenting its advice in October 2006 (Henderson, 2006c), the CASAC O3 Panel 

11 concluded that the risk assessment was “well done, balanced, and reasonably 

12 communicated” and that the selection of health endpoints for inclusion in the quantitative 

13 risk assessment was appropriate. 

14 The goals of the risk assessment are: (1) to provide estimates of the potential 

15 magnitude of several morbidity effects and mortality associated with current O3 levels, 

16 and with meeting the then current 0.084 ppm standard and alternative 8-hour O3

17 standards in specific urban areas; (2) to develop a better understanding of the influence of 

18 various inputs and assumptions on the risk estimates; and (3) to gain insights into the 

 

39 The general approach used in the health risk assessment was described in the 

draft Health Assessment Plan (EPA, 2005d) that was released to the CASAC and general 

public in April 2005 and was the subject of a consultation with the CASAC O3 Panel on 

May 5, 2005. In October 2005, OAQPS released the first draft of the Staff Paper 

containing a chapter discussing the risk assessment and first draft of the Risk Assessment 

TSD for CASAC consultation and public review on December 8, 2005. In July 2006, 

OAQPS released the second draft of the Staff Paper and second draft of the Risk 

Assessment TSD for CASAC review and public comment which was held by the 

CASAC O3 Panel on August 24-25, 2006. 
Draft O3 NPR –January 5, 2010 162 Deliberative, Do Not Quote or Cite

1 distribution of risks and patterns of risk reductions associated with meeting alternative O3

2 standards. The health risk assessment is intended to be dependent on and reflect the 

3 overall weight and nature of the health effects evidence discussed above in section II.A 

4 and in more detail in the 2006 Criteria Document and 2007 Staff Paper. While not 

5 independent of the overall evaluation of the health effects evidence, the quantitative 

6 health risk assessment provides additional insights regarding the relative public health 

7 implications associated with just meeting a 0.084 ppm standard and several alternative 8-

8 hour standards.

9 The risk assessment covers a variety of health effects for which there is adequate 

10 information to develop quantitative risk estimates. However, as noted by CASAC

11 (Henderson, 2007) and in the 2007 Staff Paper, there are a number of health endpoints 

12 (e.g., increased lung inflammation, increased airway responsiveness, impaired host 

13 defenses, increased medication usage for asthmatics, increased emergency department 

14 visits for respiratory causes, and increased school absences) for which there currently is 

15 insufficient information to develop quantitative risk estimates, but which are important to 

16 consider in assessing the overall public health impacts associated with exposures to O3. 

17 These additional health endpoints are discussed above in section II.A.2 and are also taken 

18 into account in considering the level of exposures of concern in populations particularly 

19 at risk, discussed above in this notice.

20 There are two parts to the health risk assessment: one based on combining 

21 information from controlled human exposure studies with modeled population exposure 

22 and the other based on combining information from community epidemiological studies 

23 with either monitored or adjusted ambient concentrations levels. Both parts of the risk 
Draft O3 NPR –January 5, 2010 163 Deliberative, Do Not Quote or Cite

1 assessment were implemented within a new probabilistic version of TRIM.Risk, the 

2 component of EPA’s Total Risk Integrated Methodology (TRIM) model framework that 

3 estimates human health risks.

4 The EPA recognizes that there are many sources of uncertainty and variability in 

5 the inputs to this assessment and that there is significant variability and uncertainty in the 

6 resulting O3 risk estimates. As discussed in chapters 2, 5, and 6 of the 2007 Staff Paper, 

7 there is significant year-to-year and city-to-city variability related to the air quality data 

8 that affects both the controlled human exposure studies-based and epidemiological 

9 studies-based parts of the risk assessment. There are also uncertainties associated with 

10 the air quality adjustment procedure used to simulate just meeting various alternative 

11 standards. In the prior review, different statistical approaches using alternative functional 

12 forms (i.e., quadratic, proportional, Weibull) were used to reflect how O3 air quality

13 concentrations have historically changed. Based on sensitivity analyses conducted in the 

14 prior review, the choice of alternative air quality adjustment procedures had only a 

15 modest impact on the risk estimates (EPA, 2007b, p. 6-20). With respect to uncertainties 

16 about estimated background concentrations, as discussed below and in the 2007 Staff 

17 Paper (section 5.4.3), alternative assumptions about background levels have a variable 

18 impact depending on the location, standard, and health endpoint analyzed. 

19 With respect to the lung function part of the health risk assessment, key

20 uncertainties include uncertainties in the exposure estimates, discussed above, and 

21 uncertainties associated with the shape of the exposure-response relationship, especially 

22 at levels below 0.08 ppm, 8-hour average, where only very limited data are available 

23 down to 0.04 ppm and there is an absence of data below 0.04 ppm (EPA, 2007b, pp.6-20 
Draft O3 NPR –January 5, 2010 164 Deliberative, Do Not Quote or Cite

1 to 6-21). Concerning the part of the risk assessment based on effects reported in 

2 epidemiological studies, important uncertainties include uncertainties (1) surrounding 

3 estimates of the O3 coefficients for concentration-response relationships used in the 

4 assessment, (2) involving the shape of the concentration-response relationship and 

5 whether or not a population threshold or non-linear relationship exists within the range of 

6 concentrations examined in the studies, (3) related to the extent to which concentration7 response relationships derived from studies in a given location and time when O3 levels 

8 were higher or behavior and /or housing conditions were different provide accurate 

9 representations of the relationships for the same locations with lower air quality

10 distributions and/or different behavior and/or housing conditions, and (4) concerning the 

11 possible role of co-pollutants which also may have varied between the time of the studies 

12 and the current assessment period. An important additional uncertainty for the mortality 

13 risk estimates is the extent to which the associations reported between O3 and non14 accidental and cardiorespiratory mortality actually reflect causal relationships.

15 As discussed below, some of these uncertainties have been addressed 

16 quantitatively in the form of estimated confidence ranges around central risk estimates; 

17 others are addressed through separate sensitivity analyses (e.g., the influence of 

18 alternative estimates for policy-relevant background levels) or are characterized 

19 qualitatively. For both parts of the health risk assessment, statistical uncertainty due to 

20 sampling error has been characterized and is expressed in terms of 95 percent credible 

21 intervals. The EPA recognizes that these credible intervals do not reflect all of the 

22 uncertainties noted above. 

23 b. Scope and Key Components
Draft O3 NPR –January 5, 2010 165 Deliberative, Do Not Quote or Cite

1 The health risk assessment is based on the information evaluated in the 2006 

2 Criteria Document. The risk assessment includes several categories of health effects and 

3 estimates risks associated with just meeting a 0.084 ppm standard and alternative 8-hour 

4 O3 NAAQS and with several individual recent years of air quality (i.e., 2002, 2003, and 

5 2004). The risk assessment considers the same alternative air quality scenarios that were 

6 examined in the human exposure analyses described above. Risk estimates were 

7 developed for up to 12 urban areas selected to illustrate the public health impacts 

associated with these air quality scenarios.40 8 As discussed above in section II.B.1, the 

9 selection of urban areas was largely determined by identifying areas in the U.S. which 

10 represented a range of geographic areas, population demographics, and climatology; with 

11 an emphasis on areas that did not meet the then current 0.084 ppm 8-hour O3 NAAQS 

12 and which included the largest areas with O3 nonattainment problems. The selection 

13 criteria also included whether or not there were acceptable epidemiological studies 

14 available that reported concentration-response relationships for the health endpoints 

15 selected for inclusion in the assessment.

16 The short-term exposure related health endpoints selected for inclusion in the 

17 quantitative risk assessment include those for which the 2006 Criteria Document or the 

18 2007 Staff Paper concluded that the evidence as a whole supports the general conclusion 

19 that O3, acting alone and/or in combination with other components in the ambient air 

 

40 The 12 urban areas are the same urban areas evaluated in the exposure analysis 

discussed in the prior section. However, for most of the health endpoints based on 

findings from epidemiological studies, the geographic areas and populations examined in 

the health risk assessment were limited to those counties included in the original 

epidemiological studies that served as the basis for the concentration-response 

relationships.
Draft O3 NPR –January 5, 2010 166 Deliberative, Do Not Quote or Cite

1 pollution mix, is either clearly causal or is judged to be likely causal. Some health effects 

2 met this criterion of likely causality, but were not included in the risk assessment for 

3 other reasons, such as insufficient exposure-response data or lack of baseline incidence 

4 data.

5 As discussed in the section above describing the exposure analysis, in order to 

6 estimate the health risks associated with just meeting various alternative 8-hour O3

7 NAAQS, it is necessary to estimate the distribution of hourly O3 concentrations that 

8 would occur under any given standard. Since compliance is based on a 3-year average, 

9 the amount of control has been applied to each year of data (i.e., 2002 to 2004) to 

10 estimate risks for a single O3 season or single warm O3 season, depending on the health 

11 effect, based on a simulation that adjusted each of these individual years so that the three 

12 year period would just meet the specified standard. 

13 Consistent with the risk assessment approach used in the last review, the risk 

14 estimates developed for both recent air quality levels and just meeting the then current 

15 0.084 ppm standard and selected alternative 8-hour standards represent risks associated 

16 with O3 levels attributable to anthropogenic sources and activities (i.e., risk associated 

17 with concentrations above “policy-relevant background”). Policy-relevant background 

18 O3 concentrations used in the O3 risk assessment were defined in chapter 2 of the 2007 

19 Staff Paper (pp. 2-48 – 2-55) as the O3 concentrations that would be observed in the U.S. 

20 in the absence of anthropogenic emissions of precursors (e.g., VOC, NOx, and CO) in the 

21 U.S., Canada, and Mexico. The results of a global tropospheric O3 model (GEOS22 CHEM) have been used to estimate monthly background daily diurnal profiles for each of 

23 the 12 urban areas for each month of the O3 season using meteorology for the year 2001. 
Draft O3 NPR –January 5, 2010 167 Deliberative, Do Not Quote or Cite

1 Based on the results of the GEOS-CHEM model, the Criteria Document indicates that 

2 background O3 concentrations are generally predicted to be in the range of 0.015 to 0.035 

3 ppm in the afternoon, and they are generally lower under conditions conducive to manmade O3 episodes.41 4 

5 This approach of estimating risks in excess of background is judged to be more 

6 relevant to policy decisions regarding ambient air quality standards than risk estimates 

7 that include effects potentially attributable to uncontrollable background O3

8 concentrations. Sensitivity analyses examining the impact of alternative estimates for 

9 background on lung function and mortality risk estimates have been developed and are 

10 included in the 2007 Staff Paper and Risk Assessment TSD and key observations are 

11 discussed below. Further, CASAC noted the difficulties and complexities associated 

12 with available approaches to estimating policy-relevant background concentrations 

13 (Henderson, 2007). 

14 In the first part of the risk assessment, lung function decrement, as measured by

15 FEV1, is the only health response that is based on data from controlled human exposure 

16 studies. As discussed above, there is clear evidence of a causal relationship between lung 

17 function decrements and O3 exposures for school age children engaged in moderate 

18 exertion based on numerous controlled human exposure and summer camp field studies 

19 conducted by various investigators. Risk estimates have been developed for O3-related 

20 lung function decrements (measured as changes in FEV1) for all school age children 

 

41 EPA notes that the estimated level of policy-relevant background O3 used in the 

prior risk assessment was a single concentration of 0.04 ppm, which was the midpoint of 

the range of levels for policy-relevant background that was provided in the 1996 Criteria 

Document. 
Draft O3 NPR –January 5, 2010 168 Deliberative, Do Not Quote or Cite

1 (ages 5 to 18) and a subset of this group, asthmatic school age children (ages 5 to 18),

2 whose average exertion over an 8-hour period was moderate or greater. The exposure 

3 period and exertion level were chosen to generally match the exposure period and 

4 exertion level used in the controlled human exposure studies that were the basis for the 

5 exposure-response relationships. A combined data set including individual level data 

6 from the Folinsbee et al. (1988), Horstman et al. (1990), and McDonnell et al. (1991) 

7 studies, used in the previous risk assessment, and more recent data from Adams (2002,

8 2003a, 2006) have been used to estimate probabilistic exposure-response relationships for 

9 8-hour exposures under different definitions of lung function response (i.e., ≥10, 15, and 

10 20 percent decrements in FEV1). As discussed in the 2007 Staff Paper (p.5-27), while 

11 these specific controlled human exposure studies only included healthy adults aged 18-

12 35, findings from other controlled human exposure studies and summer camp field 

13 studies involving school age children in at least six different locations in the northeastern 

14 United States, Canada, and Southern California indicated changes in lung function in 

15 healthy children similar to those observed in healthy adults exposed to O3 under 

16 controlled chamber conditions. 

17 Consistent with advice from CASAC (Henderson, 2006c), EPA has considered 

18 both linear and logistic functional forms in estimating the probabilistic exposure-response 

19 relationships for lung function responses. A Bayesian Markov Chain Monte Carlo 

20 approach, described in more detail in the Risk Assessment TSD, has been used that 

21 incorporates both model uncertainty and uncertainty due to sample size in the combined 

22 data set that served as the basis for the assessment. The EPA has chosen a model 

23 reflecting a 90 percent weighting on a logistic form and a 10 percent weighting on a 
Draft O3 NPR –January 5, 2010 169 Deliberative, Do Not Quote or Cite

1 linear form as the base case for the risk assessment. The basis for this choice is that the 

2 logistic form provides a very good fit to the combined data set, but a linear model cannot 

3 be entirely ruled out since there are only very limited data (i.e., 30 subjects) at the two 

4 lowest exposure levels (i.e., 0.040 and 0.060 ppm). The EPA has conducted a sensitivity

5 analysis which examines the impact on the lung function risk estimates of two alternative 

6 choices, an 80 percent logistic/20 percent linear split and a 50 percent logistic/50 percent 

7 linear split.

8 As noted above, risk estimates have been developed for three measures of lung 

9 function response (i.e., ≥10, 15, and 20 percent decrements in FEV1). However, the 2007 

10 Staff Paper and risk estimates summarized below focus on FEV1 decrements ≥15 percent

11 for all school age children and ≥10 percent for asthmatic school age children, consistent 

12 with the advice from CASAC (Henderson, 2006c) that these levels of response represent 

13 indicators of adverse health effects in these populations. The Risk Assessment TSD and 

14 2007 Staff Paper present the broader range of risk estimates including all three measures 

15 of lung function response. 

16 Developing risk estimates for lung function decrements involved combining 

17 probabilistic exposure-response relationships based on the combined data set from 

18 several controlled human exposure studies with population exposure distributions for all 

19 and asthmatic school age children associated with recent air quality and air quality

20 simulated to just meet the then current 0.084 ppm standard and alternative 8-hour O3

21 NAAQS based on the results from the exposure analysis described in the previous 

22 section. The risk estimates have been developed for 12 large urban areas for the O3
Draft O3 NPR –January 5, 2010 170 Deliberative, Do Not Quote or Cite

season.42 1 These 12 urban areas include approximately 18.3 million school age children, 

of which 2.6 million are asthmatic school age children.43 2

3 In addition to uncertainties arising from sample size considerations, which are 

4 quantitatively characterized and presented as 95 percentile credible intervals, there are 

5 additional uncertainties and caveats associated with the lung function risk estimates. 

6 These include uncertainties about the shape of the exposure-response relationship, 

7 particularly at levels below 0.080 ppm, and about policy-relevant background levels, for 

8 which sensitivity analyses have been conducted. Additional important caveats and 

9 uncertainties concerning the lung function portion of the health risk assessment include: 

10 (1) the uncertainties and limitations associated with the exposure estimates discussed 

11 above and (2) the inability to account for some factors which are known to affect the 

12 exposure-response relationships (e.g., assigning healthy and asthmatic children the same

13 responses as observed in healthy adult subjects and not adjusting response rates to reflect 

14 the increase and attenuation of responses that have been observed in studies of lung 

15 function responses upon repeated exposures). A more complete discussion of 

16 assumptions and uncertainties is contained in chapter 5 of the 2007 Staff Paper and in the 

17 Risk Assessment TSD.

18 The second part of the risk assessment is based on health effects observed in 

19 epidemiological studies. Based on a review of the evidence evaluated in the 2006 

 

42 As discussed above in section II.B.1, the urban areas were defined using the 

consolidated statistical areas definition and the total population residing in the 12 urban 

areas was approximately 88.5 million people.

43 For 9 of the 12 urban areas, the O3 season is defined as a period running from 

March or April to September or October. In 3 of the urban areas (Houston, Los Angeles, 

and Sacramento), the O3 season is defined as the entire year.
Draft O3 NPR –January 5, 2010 171 Deliberative, Do Not Quote or Cite

1 Criteria Document and 2007 Staff Paper, as well as the criteria discussed in chapter 5 of 

2 the 2007 Staff Paper, the following categories of health endpoints associated with short3 term exposures to ambient O3 concentrations were included in the risk assessment: 

4 respiratory symptoms in moderate to severe asthmatic children, hospital admissions for 

5 respiratory causes, and non-accidental and cardiorespiratory mortality. As discussed 

6 above, there is strong evidence of a causal relationship for the respiratory morbidity

7 endpoints included in the risk assessment. With respect to nonaccidental and 

8 cardiorespiratory mortality, the 2006 Criteria Document concludes that there is strong 

9 evidence which is highly suggestive of a causal relationship between nonaccidental and 

10 cardiorespiratory-related mortality and O3 exposures during the warm O3 season. As 

11 discussed in the 2007 Staff Paper (chapter 5), EPA also recognizes that for some of the 

12 effects observed in epidemiological studies, such as increased respiratory-related hospital 

13 admissions and nonaccidental and cardiorespiratory mortality, O3 may be serving as an 

14 indicator for reactive oxidant species in the overall photochemical oxidant mix and that 

15 these other constituents may be responsible in whole or part for the observed effects.

16 Risk estimates for each health endpoint category were only developed for areas 

17 that were the same or close to the location where at least one concentration-response 

function for the health endpoint had been estimated.44 18 Thus, for respiratory symptoms in 

19 moderate to severe asthmatic children only the Boston urban area was included and four 

20 urban areas were included for respiratory-related hospital admissions. Nonaccidental 

 

44 The geographic boundaries for the urban areas included in this portion of the 

risk assessment were generally matched to the geographic boundaries used in the 

epidemiological studies that served as the basis for the concentration-response functions. 

In most cases, the urban areas were defined as either a single county or a few counties for 

this portion of the risk assessment.
Draft O3 NPR –January 5, 2010 172 Deliberative, Do Not Quote or Cite

1 mortality risk estimates were developed for 12 urban areas and 8 urban areas were 

2 included for cardiorespiratory mortality. 

3 The concentration-response relationships used in the assessment are based on 

4 findings from human epidemiological studies that have relied on fixed-site ambient 

5 monitors as a surrogate for actual ambient O3 exposures. In order to estimate the 

6 incidence of a particular health effect associated with recent air quality in a specific 

7 county or set of counties attributable to ambient O3 exposures in excess of background, as 

8 well as the change in incidence corresponding to a given change in O3 levels resulting 

9 from just meeting various 8-hour O3 standards, three elements are required for this part of 

10 the risk assessment. These elements are: (1) air quality information (including recent air 

11 quality data for O3 from ambient monitors for the selected location, estimates of 

12 background O3 concentrations appropriate for that location, and a method for adjusting 

13 the recent data to reflect patterns of air quality estimated to occur when the area just 

14 meets a given O3 standard); (2) relative risk-based concentration-response functions that 

15 provide an estimate of the relationship between the health endpoints of interest and 

16 ambient O3 concentration; and (3) annual or seasonal baseline health effects incidence 

17 rates and population data, which are needed to provide an estimate of the seasonal 

18 baseline incidence of health effects in an area before any changes in O3 air quality.

19 A key component in the portion of the risk assessment based on epidemiological 

20 studies is the set of concentration-response functions which provide estimates of the 

21 relationships between each health endpoint of interest and changes in ambient O3

22 concentrations. Studies often report more than one estimated concentration-response 

23 function for the same location and health endpoint. Sometimes models include different 
Draft O3 NPR –January 5, 2010 173 Deliberative, Do Not Quote or Cite

1 sets of co-pollutants and/or different lag periods between the ambient concentrations and 

2 reported health responses. For some health endpoints, there are studies that estimated 

3 multicity and single-city O3 concentration-response functions. While the Risk 

4 Assessment TSD and chapter 5 of the 2007 Staff Paper present a more comprehensive set 

5 of risk estimates, EPA has focused on estimates based on multicity studies where 

6 available. As discussed in chapter 5 of the 2007 Staff Paper, the advantages of relying 

7 more heavily on concentration-response functions based on multicity studies include: (1) 

8 more precise effect estimates due to larger data sets, reducing the uncertainty around the 

9 estimated coefficient; (2) greater consistency in data handling and model specification 

10 that can eliminate city-to-city variation due to study design; and (3) less likelihood of 

11 publication bias or exclusion of reporting of negative or nonsignificant findings. Where 

12 studies reported different effect estimates for varying lag periods, consistent with the 

13 2006 Criteria Document, single day lag periods of 0 to 1 days were used for associations 

14 with respiratory hospital admissions and mortality. For mortality associated with 

15 exposure to O3 which may result over a several day period after exposure, distributed lag 

16 models, which take into account the contribution to mortality effects over several days, 

17 were used where available

18 One of the most important elements affecting uncertainties in the 

19 epidemiological-based portion of the risk assessment is the concentration-response 

20 relationships used in the assessment. The uncertainty resulting from the statistical 

21 uncertainty associated with the estimate of the O3 coefficient in the concentration22 response function was characterized either by confidence intervals or by Bayesian 

23 credible intervals around the corresponding point estimates of risk. Confidence and 
Draft O3 NPR –January 5, 2010 174 Deliberative, Do Not Quote or Cite

1 credible intervals express the range within which the true risk is likely to fall if the only

2 uncertainty surrounding the O3 coefficient involved sampling error. Other uncertainties, 

3 such as differences in study location, time period (i.e., the years in which the study was 

4 conducted), and model uncertainties are not represented by the confidence or credible 

5 intervals presented, but were addressed by presenting estimates for different urban areas, 

6 by including risk estimates based on studies using different time periods and models, 

7 where available, and/or are discussed throughout section 5.3 of the 2007 Staff Paper. 

8 Because O3 effects observed in the epidemiological studies have been more clearly and 

9 consistently shown for warm season analyses, all analyses for this portion of the risk 

10 assessment were carried out for the same time period, April through September. 

11 The 2006 Criteria Document (p. 8-44) finds that no definitive conclusion can be 

12 reached with regard to the existence of population thresholds in epidemiological studies. 

13 The EPA recognizes, however, the possibility that thresholds for individuals may exist 

14 for reported associations at fairly low levels within the range of air quality observed in 

15 the studies, but not be detectable as population thresholds in epidemiological analyses. 

16 Based on the 2006 Criteria Document’s conclusions, EPA judged and CASAC concurred, 

17 that there is insufficient evidence to support use of potential population threshold levels 

18 in the quantitative risk assessment. However, EPA recognizes that there is increasing 

19 uncertainty about the concentration-response relationship at lower concentrations which 

20 is not captured by the characterization of the statistical uncertainty due to sampling error. 

21 Therefore, the risk estimates for respiratory symptoms in moderate to severe asthmatic 

22 children, respiratory-related hospital admissions, and premature mortality associated with 
Draft O3 NPR –January 5, 2010 175 Deliberative, Do Not Quote or Cite

1 exposure to O3 must be considered in light of uncertainties about whether or not these O3-

2 related effects occur in these populations at very low O3 concentrations.

3 With respect to variability within this portion of the risk assessment, there is 

4 variability among concentration-response functions describing the relation between O3

5 and both respiratory-related hospital admissions and nonaccidental and cardiorespiratory

6 mortality across urban areas. This variability is likely due to differences in population 

7 (e.g., age distribution), population activities that affect exposure to O3 (e.g., use of air 

8 conditioning), levels and composition of co-pollutants, baseline incidence rates, and/or 

9 other factors that vary across urban areas. The risk assessment incorporates some of the 

10 variability in key inputs to the analysis by using location-specific inputs (e.g., location11 specific concentration-response functions, baseline incidence rates, and air quality data). 

12 Although spatial variability in these key inputs across all U.S. locations has not been fully

13 characterized, variability across the selected locations is imbedded in the analysis by

14 using, to the extent possible, inputs specific to each urban area.

15 c. Risk Estimates and Key Observations

16 The 2007 Staff Paper (chapter 5) and Risk Assessment TSD present risk estimates 

17 associated with just meeting the then current 0.084 ppm standard and several alternative 

18 8-hour standards, as well as three recent years of air quality as represented by 2002, 2003, 

19 and 2004 monitoring data. As discussed in the exposure analysis section above, there is 

20 considerable city-to-city and year-to-year variability in the O3 levels during this period, 

21 which results in significant variability in both portions of the health risk assessment. 

22 In the 1997 risk assessment, risks for lung function decrements associated with 1-

23 hour heavy exertion, 1-hour moderate exertion, and 8-hour moderate exertion exposures 
Draft O3 NPR –January 5, 2010 176 Deliberative, Do Not Quote or Cite

1 were estimated. Since the 8-hour moderate exertion exposure scenario for children 

2 clearly resulted in the greatest health risks in terms of lung function decrements, EPA 

3 chose to include only the 8-hour moderate exertion exposures in the risk assessment for 

4 this health endpoint. Thus, the risk estimates presented here and in the 2007 Staff Paper 

5 are most useful for making relative comparisons across alternative air quality scenarios 

6 and do not represent the total risks for lung function decrements in children or other 

7 groups within the general population associated with any of the air quality scenarios. 

8 Thus, some outdoor workers and adults engaged in moderate exertion over multi-hour 

9 periods (e.g., 6-8 hour exposures) also would be expected to experience similar lung 

10 function decrements. However, the percentage of each of these other subpopulations 

11 expected to experience these effects is expected to be smaller than all school age children 

12 who tend to spend more hours outdoors while active based on the exposure analyses 

13 conducted during the prior review. 

14 Table 2 presents a summary of the risk estimates for lung function decrements for 

15 the 0.084 ppm standard set in 1997 and several alternative 8-hour standard levels with the 

16 same form. The estimates are for the aggregate number 

17
Draft O3 NPR –January 5, 2010 177 Deliberative, Do Not Quote or Cite

1 Table 2. Number and Percent of All and Asthmatic School Age Children in Several 

2 Urban Areas Estimated to Experience Moderate or Greater Lung Function 

3 Responses One or More Times Per Season Associated with 8-Hour Ozone Exposures 

4 Associated with Just Meeting Alternative 8-Hour Standards Based on Adjusting 

2002 and 2004 Air Quality Data1,2 5

6

1

7 Associated with exposures while engaged in moderate or greater exertion, which is defined as having an 8-

hour average equivalent ventilation rate > 13 l-min/m28 .

2

9 Estimates are the aggregate central tendency results based on either 12 urban areas (Atlanta, Boston, 

10 Chicago, Cleveland, Detroit, Houston, Los Angeles, New York, Philadelphia, Sacramento, St. Louis, and 

11 Washington, D.C.) or 5 urban areas (Atlanta, Chicago, Houston, Los Angeles, New York). Estimates are 

12 for the O3 season which is all year in Houston, Los Angeles and Sacramento and March or April to 

13 September or October for the remaining urban areas.

3

14 All standards summarized here have the same form as the 8-hour standard set in 1997, which is specified 

as the 3-year average of the annual 4th 15 highest daily maximum 8-hour average concentrations. As described 

16 in the 2007 Staff Paper (section 4.5.8), recent O3 air quality distributions have been statistically adjusted to 

17 simulate just meeting the 0.084 ppm standard set in 1997 and selected alternative standards. These 

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

4

19 NA (not available) indicates that EPA did not develop risk estimates for these scenarios for the asthmatic 

20 school age children population.

21

22

8-Hour Air 

Quality

Standards3

All Children, ages 5-18

FEV1 > 15 percent

Aggregate for 12 urban areas

Number of Children Affected (% of 

all)

[% reduction from 0.084 ppm 

standard]

Asthmatic Children, ages 5-18

FEV1 > 10 percent

Aggregate for 5 urban areas 

Number of Children Affected (% of 

group)

[% reduction from 0.084 ppm standard]

2002 2004 2002 2004]

0.084 ppm

(Standard 

set in 

1997)

610,000 (3.3%) 230,000 (1.2%) 130,000 (7.8%) 70,000 (4.2%)

0.080 ppm 490,000 (2.7%)

[20% reduction]

180,000 (1.0%)

[22% reduction]

NA4 NA

0.074 ppm 340,000 (1.9%)

[44% reduction]

130,000 (0.7%)

[43% reduction]

90,000 (5.0%)

[31 % reduction]

40,000 (2.7%)

[43% reduction]

0.070 ppm 260,000 (1.5%)

[57% reduction]

100,000 (0.5%)

[57% reduction]

NA NA

0.064 ppm 180,000 (1.0%)

[70% reduction]

70,000 (0.4%)

[70% reduction]

50,000 (3.0%)

[62% reduction]

20,000 (1.5%)

[71% reduction]
Draft O3 NPR –January 5, 2010 178 Deliberative, Do Not Quote or Cite

1 and percent of all school age children across 12 urban areas and the aggregate number 

and percent of asthmatic school age children across 5 urban areas45 2 who are estimated to 

3 have at least 1 moderate or greater lung function response (defined as FEV1 > 15 percent

4 in all children and > 10 percent in asthmatic children) associated with 8-hour exposures 

5 to O3 while engaged in moderate or greater exertion on average over the 8-hour period. 

6 The lung function risk estimates summarized in Table 2 illustrate the year-to-year 

7 variability in both remaining risk associated with a relatively high year (i.e., based on 

8 adjusting 2002 O3 air quality data) and relatively low year (based on adjusting 2004 O3

9 air quality data) as well as the year-to-year variability in the risk reduction estimated to 

10 occur associated with various alternative standards relative to just meeting the then 

11 current 0.084 ppm standard. For example, it is estimated that about 610,000 school age 

12 children (3.2 percent of school age children) would experience 1 or more moderate lung 

13 function decrements for the 12 urban areas associated with O3 levels just meeting a 0.084 

14 ppm standard based on 2002 air quality data compared to 230,000 (1.2 percent of 

15 children) associated with just meeting a 0.084 ppm standard based on 2004 air quality

16 data.

17 As discussed in the 2007 Staff Paper, a child may experience multiple 

18 occurrences of a lung function response during the O3 season. For example, upon 

19 meeting a 0.084 ppm 8-hour standard, the median estimates are that about 610,000 

20 children would experience a moderate or greater lung function response 1 or more times 

 

45 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.
Draft O3 NPR –January 5, 2010 179 Deliberative, Do Not Quote or Cite

1 for the aggregate of the 12 urban areas over a single O3 season (based on the 2002 

2 simulation), and that there would be almost 3.2 million total occurrences. Thus, on 

3 average it is estimated that there would be about 5 occurrences per O3 season per 

4 responding child for air quality just meeting a 0.084 ppm 8-hour standard across the 12 

5 urban areas. While the estimated number of occurrences per O3 season is lower when 

6 based on the 2004 simulation than for the 2002 simulation, the estimated number of 

7 occurrences per responding child is similar. The EPA recognizes that some children in 

8 the population might have only 1 or 2 occurrences while others may have 6 or more 

9 occurrences per O3 season. Risk estimates based on adjusting 2003 air quality to 

10 simulate just meeting the a 0.084 ppm standard and alternative 8-hour standards are 

11 intermediate to the estimates presented in Table 2 above in this notice and are presented 

12 in the 2007 Staff Paper (chapter 5) and Risk Assessment TSD.

13 For just meeting a 0.084 ppm 8-hour standard, Table 5-8 in the 2007 Staff Paper 

14 shows that median estimates across the 12 urban areas for all school age children 

15 experiencing 1 or more moderate lung function decrements ranges from 0.9 to 5.4 percent

16 based on the 2002 simulation and from 0.8 to 2.2 percent based on the 2004 simulation. 

17 Risk estimates for each urban area included in the assessment, for each of the three years 

18 analyzed, and for additional alternative standards are presented in chapter 5 of the 2007 

19 Staff Paper and in the Risk Assessment TSD. 

20 For just meeting a 0.084 ppm 8-hour standard, the median estimates across the 5 

21 urban areas for asthmatic school age children range from 3.4 to 10.9 percent based on the 

22 2002 simulation and from 3.2 to 6.9 percent based on the 2004 simulation.
Draft O3 NPR –January 5, 2010 180 Deliberative, Do Not Quote or Cite

1 Key observations important in comparing estimated lung function risks associated 

2 with just meeting the 0.084 ppm NAAQS and alternative standards under consideration 

3 include:

4 (1) As discussed above, there is significant year to year variability in the range of 

5 median estimates of the number of school age children (ages 5-18) estimated to 

6 experience at least one FEV1 decrement  15 percent due to 8-hour O3 exposures across 

7 the 12 urban areas analyzed, and similarly across the 5 urban areas analyzed for asthmatic 

8 school age children (ages 5-18) estimated to experience at least one FEV1 decrement > 10 

9 percent, when various 8-hour standards are just met.

10 (2) For asthmatic school age children, the median estimates of occurrences of 

11 FEV1 decrements >10% range from 52,000 to nearly 510,000 responses associated with 

12 just meeting a 0.084 ppm standard (based on the 2002 simulation) and range from 61,000 

13 to about 240,000 occurrences (based on the 2004 simulation). These risk estimates 

14 would be reduced to a range of 14,000 to about 275,000 occurrences (2002 simulation) 

15 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 16 highest). The average 

17 number of occurrences per asthmatic child in an O3 season ranged from about 6 to 11 

18 associated with just meeting a 0.084 ppm standard (2002 simulation). The average 

19 number of occurrences per asthmatic child ranged from 4 to 12 upon meeting the most 

20 stringent alternative examined (0.064 ppm, 4th-highest) based on the 2002 simulation. 

21 The number of occurrences per asthmatic child is similar for the scenarios based on the 

22 2004 simulation.
Draft O3 NPR –January 5, 2010 181 Deliberative, Do Not Quote or Cite

1 As discussed above, several epidemiological studies have reported increased 

2 respiratory morbidity outcomes (e.g., respiratory symptoms in moderate to severe 

3 asthmatic children, respiratory-related hospital admissions) and increased nonaccidental 

4 and cardiorespiratory mortality associated with exposure to ambient O3 concentrations. 

5 The results and key observations from this portion of the risk assessment are presented 

6 below: 

7 (1) Estimates for increased respiratory symptoms (i.e., chest tightness, shortness 

8 of breath, and wheeze) in moderate/severe asthmatic children (ages 0-12) were developed 

9 for the Boston urban area only. The median estimated number of days involving chest 

10 tightness (using the concentration-response relationship with only O3 in the model) is 

11 about 6,100 (based on the 2002 simulation) and about 4,500 (based on the 2004 

12 simulation) upon meeting a 0.084 ppm 8-hour standard and this is reduced to about 4,600 

13 days (2002 simulation) and 3,100 days (2004 simulation) upon meeting the most 

14 stringent alternative examined (0.064 ppm, 4th-highest daily maximum 8-hour average). 

15 This corresponds to 11 percent (2002 simulation) and 8 percent (2004 simulation) of total 

16 incidence of chest tightness upon meeting a 0.084 ppm 8-hour standard and to about 8 

17 percent (2002 simulation) and 5.5 percent (2004 simulation) of total incidence of chest 

18 tightness upon meeting a 0.064 ppm, 4th-highest daily maximum 8-hour average 

19 standard. Similar patterns of effects and reductions in effects are observed for each of the 

20 respiratory symptoms examined. 

21 (2) The 2007 Staff Paper and Risk Assessment TSD present unscheduled hospital 

22 admission risk estimates for respiratory illness and asthma in New York City associated 

23 with short-term exposures to O3 concentrations in excess of background levels from April 
Draft O3 NPR –January 5, 2010 182 Deliberative, Do Not Quote or Cite

1 through September for several recent years (2002, 2003, and 2004) and upon just meeting 

2 a 0.084 ppm standard and alternative 8-hour standards based on simulating O3 levels 

3 using 2002-2004 O3 air quality data. For total respiratory illness, EPA estimates about 

4 6.4 cases per 100,000 relevant population (2002 simulation) and about 4.6 cases per 

5 100,000 relevant population (2004 simulation), which represents 1.5 percent (2002 

6 simulation) and 1.0 percent (2004 simulation) of total incidence or about 510 cases (2002 

7 simulation) and about 370 cases (2004 simulation) upon just meeting a 0.084 ppm 8-hour 

8 standard. For asthma-related hospital admissions, which are a subset of total respiratory

9 illness admissions, the estimates are about 5.5 cases per 100,000 relevant population 

10 (2002 simulation) and about 3.9 cases per 100,000 relevant population (2004 simulation), 

11 which represents about 3.3 percent (2002 simulation) and 2.4 percent (2004 simulation)

12 of total incidence or about 440 cases (2002) and about 310 cases (2004) for this same air 

13 quality scenario. 

14 For increasingly more stringent alternative 8-hour standards, there is a gradual 

15 reduction in respiratory illness cases per 100,000 relevant population from 6.4 cases per 

16 100,000 upon just meeting a 0.084 ppm 8-hour standard to 4.6 cases per 100,000 under 

17 the most stringent 8-hour standard (i.e., 0.064 ppm, average 4th-highest daily maximum) 

18 analyzed based on the 2002 simulation. Similarly, based on the 2004 simulation there is 

19 a gradual reduction from 4.6 cases per 100,000 relevant population upon just meeting a 

0.084 ppm 8-hour standard to 3.0 cases per 100,000 under a 0.064 ppm, average 4th 20 –

21 highest daily maximum standard.

22 Additional respiratory-related hospital admission estimates for three other 

23 locations are provided in the Risk Assessment TSD. The EPA notes that the 
Draft O3 NPR –January 5, 2010 183 Deliberative, Do Not Quote or Cite

1 concentration-response functions for each of these locations examined different outcomes 

2 in different age groups (e.g., > age 30 in Los Angeles, >age 64 in Cleveland and Detroit, 

3 vs. all ages in New York City), making comparison of the risk estimates across the areas 

4 very difficult.

5 (3) Based on the median estimates for incidence for nonaccidental mortality 

6 (based on the Bell et al. (2004) 95 cities concentration-response function), meeting the 

7 most stringent standard (0.064 ppm) is estimated to reduce mortality by 40 percent of 

8 what it would be associated with just meeting a 0.084 ppm standard (based on the 2002 

9 simulation). The patterns for cardiorespiratory mortality are similar. The aggregate O3-

10 related cardiorespiratory mortality upon just meeting the most stringent standard shown is 

11 estimated to be about 42 percent of what it would be upon just meeting a 0.084 ppm 

12 standard, using simulated O3 concentrations that just meet a 0.084 ppm standard and 

13 alternative 8-hour standards based on the 2002 simulation. Using the 2004 simulation, 

14 the corresponding reductions show a similar pattern but are somewhat greater.

15 (4) Much of the contribution to the risk estimates for non-accidental and 

16 cardiorespiratory mortality upon just meeting a 0.084 ppm 8-hour standard is associated 

17 with 24-hour O3 concentrations between background and 0.040 ppm. Based on 

18 examining relationships between 24-hour concentrations averaged across the monitors 

19 within an urban area and 8-hour daily maximum concentrations, 8-hour daily maximum 

20 levels at the highest monitor in an urban area associated with these averaged 24-hour 

21 levels are generally about twice as high as the 24-hour levels. Thus, most O3-related 

22 nonaccidental mortality is estimated to occur when O3 concentrations are between 
Draft O3 NPR –January 5, 2010 184 Deliberative, Do Not Quote or Cite

1 background and when the highest monitor in the urban area is at or below 0.080 ppm, 8-

2 hour average concentration.

3 The discussion below highlights additional observations and insights from the O3

4 risk assessment, together with important uncertainties and limitations.

5 (1) As discussed in the 2007 Staff Paper (section 5.4.5), EPA has greater 

6 confidence in relative comparisons in risk estimates between alternative standards than in 

7 the absolute magnitude of risk estimates associated with any particular standard. 

8 (2) Significant year-to-year variability in O3 concentrations combined with the 

9 use of a 3-year design value to determine the amount of air quality adjustment to be 

10 applied to each year analyzed, results in significant year-to-year variability in the annual 

11 health risk estimates upon just meeting various 8-hour standards.

12 (3) There is noticeable city-to-city variability in estimated O3-related incidence of 

13 morbidity and mortality across the 12 urban areas analyzed for both recent years of air 

14 quality and for air quality adjusted to simulate just meeting a 0.084 ppm standard and 

15 selected potential alternative standards. This variability is likely due to differences in air 

16 quality distributions, differences in exposure related to many factors including varying 

17 activity patterns and air exchange rates, differences in baseline incidence rates, and 

18 differences in susceptible populations and age distributions across the 12 urban areas.

19 (4) With respect to the uncertainties about estimated policy-relevant background 

20 concentrations, as discussed in the 2007 Staff Paper (section 5.4.3), alternative 

21 assumptions about background levels had a variable impact depending on the health 

22 effect considered and the location and standard analyzed in terms of the absolute 

23 magnitude and relative changes in the risk estimates. There was relatively little impact 
Draft O3 NPR –January 5, 2010 185 Deliberative, Do Not Quote or Cite

1 on either absolute magnitude or relative changes in lung function risk estimates due to 

2 alternative assumptions about background levels. With respect to O3-related nonaccidental mortality, while notable differences (i.e., greater than 50 percent)46 3 were 

4 observed for nonaccidental mortality in some areas, particularly for more stringent 

5 standards, the overall pattern of estimated reductions, expressed in terms of percentage 

6 reduction relative to the 0.084 ppm standard, was significantly less impacted.

7 C. Reconsideration of the Level of the Primary Standard

8 1. Evidence and Exposure/Risk-Based Considerations

9 The approach used in the 2007 Staff Paper as a basis for staff recommendations 

10 on standard levels builds upon and broadens the general approach used by EPA in the 

11 1997 review. This approach reflects the more extensive and stronger body of evidence 

12 available for the 2008 rulemaking on a broader range of health effects associated with 

13 exposure to O3, including: (1) additional respiratory-related endpoints; (2) new 

14 information about the mechanisms underlying respiratory morbidity effects supporting a 

15 judgment that the link between O3 exposure and these effects is causal; (3) newly

16 identified cardiovascular-related health endpoints from animal toxicology and controlled 

17 human exposures studies that are highly suggestive that O3 can directly or indirectly

18 contribute to cardiovascular morbidity, and (4) new U.S. multicity time series studies, 

19 single city studies, and several meta-analyses of these studies that provide relatively

20 strong evidence for associations between short-term O3 exposures and all-cause 

 

46 For example, assuming lower background levels resulted in increased estimates 

of non-accidental mortality incidence per 100,000 that were often 50 to 100 percent 

greater than the base case estimates; assuming higher background levels resulted in 

decreased estimates of non-accidental mortality incidence per 100,000 that were less than 

the base case estimates by 50 percent or more in many of the areas. 
Draft O3 NPR –January 5, 2010 186 Deliberative, Do Not Quote or Cite

1 (nonaccidental) mortality, at levels below the current primary standard: as well as (5) a 

2 substantial body of new evidence of increased susceptibility in people with asthma and 

3 other lung diseases. In evaluating evidence-based and exposure/risk-based 

4 considerations, the 2007 Staff Paper considered: (1) the ranges of levels of alternative 

5 standards that are supported by the evidence, and the uncertainties and limitations in that 

6 evidence and (2) the extent to which specific levels of alternative standards reduce the 

7 estimated exposures of concern and risks attributable to O3 and other photochemical 

8 oxidants, and the uncertainties associated with the estimated exposure and risk 

9 reductions.

10 a. Evidence-based Considerations

11 In taking into account evidence-based considerations, the 2007 Staff Paper 

12 evaluated available evidence from controlled human exposure studies and 

13 epidemiological studies, as well as the uncertainties and limitations in that evidence. In 

14 particular, it focused on the extent to which controlled human exposure studies provide 

15 evidence of lowest-observed-effects levels and the extent to which epidemiological 

16 studies provide evidence of associations that extend down to the lower levels of O3

17 concentrations observed in the studies or some indication of potential effect thresholds in 

18 terms of 8-hour average O3 concentrations.

19 The most certain evidence of adverse health effects from exposure to O3 comes 

20 from the controlled human exposure studies, as discussed above in section II.A.2, and the 

21 large bulk of this evidence derives from studies of exposures at levels of 0.080 ppm and 

22 above. At those levels, there is consistent evidence of lung function decrements and 
Draft O3 NPR –January 5, 2010 187 Deliberative, Do Not Quote or Cite

1 respiratory symptoms in healthy young adults, as well as evidence of inflammation and 

2 other medically significant airway responses. 

3 Two studies by Adams (2002, 2006), newly available for consideration in the 

4 2008 rulemaking, are the only available controlled human exposure studies that examine 

5 respiratory effects associated with prolonged O3 exposures at levels below 0.080 ppm, 

6 which was the lowest exposure level that had been examined in the 1997 review. As 

7 discussed above in section II.A.2.a.i.(a)(i), the Adams (2006) study investigated a range 

8 of exposure levels, including 0.060 and 0.080 ppm O3, and analyzed hour-by-hour 

9 changes in responses, including lung function (measured in term of decrements in FEV1) 

10 and respiratory symptoms, to investigate the effects of different patterns of exposure. At 

11 the 0.060 ppm exposure level, the author reported no statistically significant differences 

12 for lung function decrements; statistically significant responses were reported for total 

13 subjective respiratory symptoms toward the end of the exposure period for one exposure 

14 pattern. The EPA’s reanalysis (Brown, 2007) of the data from the Adams (2006) study

15 addressed the more fundamental question of whether there were statistically significant 

16 changes in lung function from a 6.6-hour exposure to 0.060 ppm O3 versus filtered air 

17 and used a standard statistical method appropriate for a simple paired comparison. This 

18 reanalysis found small group mean lung function decrements in healthy adults at the 

19 0.060 ppm exposure level to be statistically significantly different from responses 

20 associated with filtered air exposure.

21 Moreover, the Adams’ studies also report a small percentage of subjects (7 to 20 

22 percent) experienced lung function decrements (> 10 percent) at the 0.060 ppm exposure 

23 level. This is a concern because, for active healthy people, moderate levels of functional 
Draft O3 NPR –January 5, 2010 188 Deliberative, Do Not Quote or Cite

1 responses (e.g., FEV1 decrements of > 10% but < 20%) and/or moderate respiratory

2 symptom responses would likely interfere with normal activity for relatively few 

3 responsive individuals. However, for people with lung disease, even moderate functional 

4 or symptomatic responses would likely interfere with normal activity for many

5 individuals, and would likely result in more frequent use of medication. In the context of 

6 standard setting, the CASAC indicated (Henderson, 2006c) that a focus on the lower end 

7 of the range of moderate levels of functional responses (e.g., FEV1 decrements  10%) is 

8 most appropriate for estimating potentially adverse lung function decrements in people 

9 with lung disease. Therefore, the results of the Adams studies which indicate that a small 

10 percentage of healthy, non-asthmatic subjects are likely to experience FEV1 decrements 

11 10% when exposed to 0.060 ppm O3 have implications for setting a standard that protects 

12 public health, including the health of sensitive populations such as asthmatics, with an 

13 adequate margin of safety. 

14 In considering these most recent controlled human exposure studies, the 2007 

15 Staff Paper concluded that these studies provide evidence of a lowest-observed-effects 

16 level of 0.060 ppm for potentially adverse lung function decrements and respiratory

17 symptoms in some healthy adults while at prolonged moderate exertion. It further 

18 concluded that since people with asthma, particularly children, have been found to be 

19 more sensitive and to experience larger decrements in lung function in response to O3

20 exposures than would healthy adults, the 0.060 ppm exposure level also can be 

21 interpreted as representing a level likely to cause adverse lung function decrements and 

22 respiratory symptoms in children with asthma and more generally in people with 

23 respiratory disease.
Draft O3 NPR –January 5, 2010 189 Deliberative, Do Not Quote or Cite

1 In considering controlled human exposure studies of pulmonary inflammation, 

2 airway responsiveness, and impaired host defense capabilities, discussed above in section 

3 II.A.2.a.i, the 2007 Staff Paper noted that these studies provide evidence of a lowest4 observed-effects level for such effects in healthy adults at prolonged moderate exertion of 

5 0.080 ppm, the lowest level tested. Moreover there is no evidence that the 0.080 ppm 

6 level is a threshold for these effects. Studies reporting inflammatory responses and 

7 markers of lung injury have clearly demonstrated that there is significant variation in 

8 response of subjects exposed, even to O3 exposures at 0.080 ppm. One study showed 

9 notable interindividual variability in young healthy adult subjects in most of the 

10 inflammatory and cellular injury indicators analyzed at 0.080 ppm. This inter-individual 

11 variability suggests that some portion of the population would likely experience such 

12 effects at exposure levels extending well below 0.080 ppm. 

13 As discussed above, these physiological effects have been linked to aggravation 

14 of asthma and increased susceptibility to respiratory infection, potentially leading to 

15 increased medication use, increased school and work absences, increased visits to 

16 doctors’ offices and emergency departments, and increased hospital admissions. Further, 

17 pulmonary inflammation is related to increased cellular permeability in the lung, which 

18 may be a mechanism by which O3 exposure can lead to cardiovascular system effects, 

19 and to potential chronic effects such as chronic bronchitis or long-term damage to the 

20 lungs that can lead to reduced quality of life. These are all indicators of adverse O3-

21 related morbidity effects, which are consistent with and lend plausibility to the adverse 

22 morbidity effects and mortality effects observed in epidemiological studies.
Draft O3 NPR –January 5, 2010 190 Deliberative, Do Not Quote or Cite

1 Significant associations between ambient O3 exposures and a wide variety of 

2 respiratory symptoms and other morbidity outcomes (e.g., asthma medication use, school 

3 absences, emergency department visits, and hospital admissions) have been reported in 

4 epidemiological studies, as discussed above in section II.A.2.a.i. Overall, the 2006 

5 Criteria Document concludes that positive and robust associations were found between 

6 ambient O3 concentrations and various respiratory disease hospitalization outcomes, 

7 when focusing particularly on results of warm-season analyses. Recent studies also 

8 generally indicate a positive association between O3 concentrations and emergency

9 department visits for asthma during the warm season. These positive and robust 

10 associations are supported by the controlled human exposure, animal toxicological, and 

11 epidemiological evidence for lung function decrements, increased respiratory symptoms, 

12 airway inflammation, and increased airway responsiveness. Taken together, the overall 

13 evidence supports a causal relationship between acute ambient O3 exposures and 

14 increased respiratory morbidity outcomes resulting in increased emergency department

15 visits and hospitalizations during the warm season (EPA, 2006a, p. 8-77).

16 Moreover, many single- and multicity epidemiological studies observed positive 

17 associations of ambient O3 concentrations with total nonaccidental and cardiopulmonary

18 mortality. As discussed above in section II.A.2.b.i, the 2006 Criteria Document finds that 

19 the results from U.S. multicity time-series studies provide the strongest evidence to date 

20 for O3 effects on acute mortality. Recent meta-analyses also indicate positive risk 

21 estimates that are unlikely to be confounded by PM; however, future work is needed to 

22 better understand the influence of model specifications on the magnitude of risk. The

23 2006 Criteria Document concludes that the “positive O3 effects estimates, along with the 
Draft O3 NPR –January 5, 2010 191 Deliberative, Do Not Quote or Cite

1 sensitivity analyses in these three meta-analyses, provide evidence of a robust association 

2 between ambient O3 and mortality” (EPA, 2006a, p. 7-97). In summary, the 2006

3 Criteria Document (p. 8-78) concludes that these findings are highly suggestive that 

4 short-term O3 exposure directly or indirectly contribute to non-accidental and 

5 cardiopulmonary-related mortality, but additional research is needed to more fully

6 establish underlying mechanisms by which such effects occur.

7 The 2007 Staff Paper considered the epidemiological studies to evaluate evidence 

8 related to potential effects thresholds at the population level for morbidity and mortality

9 effects. As discussed above in section II.A.3.a (and more fully in the 2007 Staff Paper in 

10 chapter 3 and the 2006 Criteria Document in chapter 7), a number of time-series studies 

11 have used statistical modeling approaches to evaluate potential thresholds at the 

12 population level. A few such studies reported some suggestive evidence of possible 

13 thresholds for morbidity and mortality outcomes in terms of 24-hour, 8-hour, and 1-hour 

14 averaging times. These results, taken together, provide some indication of possible 8-

15 hour average threshold levels from below about 0.025 to 0.035 ppm (within the range of 

16 background concentrations) up to approximately 0.050 ppm. Other studies, however, 

17 observe linear concentration-response functions suggesting no effect threshold. The 2007 

18 Staff Paper (p.6-60) concluded that the statistically significant associations between 

19 ambient O3 concentrations and lung function decrements, respiratory symptoms, 

20 indicators of respiratory morbidity including increase emergency department visits and 

21 hospital admissions, and possibly mortality reported in a large number of studies likely

22 extend down to ambient O3 concentrations that are well below the level of the then 

23 current standard (0.084 ppm). These associations also extend well below the level of the 
Draft O3 NPR –January 5, 2010 192 Deliberative, Do Not Quote or Cite

1 standard set in 2008 (0.075 ppm) in that the highest level at which there is any indication 

2 of a threshold is approximately 0.050 ppm. Toward the lower end of the range of O3

3 concentrations observed in such studies, ranging down to background levels (i.e., 0.035 

4 to 0.015 ppm), however, the 2007 Staff Paper stated that there is increasing uncertainty as 

5 to whether the observed associations remain plausibly related to exposures to ambient O3, 

6 rather than to the broader mix of air pollutants present in the ambient atmosphere.

7 The 2007 Staff Paper also considered studies that did subset analyses, which 

8 included only days with ambient O3 concentrations below the level of the then current 

9 standard, or below even lower O3 concentrations, and continue to report statistically

10 significant associations. Notably, as discussed above, Bell et al. (2006) conducted a 

11 subset analysis that continued to show statistically significant mortality associations even 

12 when only days with a maximum 8-hour average O3 concentration below a value of 

approximately 0.061 ppm were included.47 13 Also of note is the large multicity NCICAS 

14 (Mortimer et al., 2002) that reported statistically significant associations between ambient 

15 O3 concentrations and lung function decrements even when days with 8-hour average O3

16 levels greater than 0.080 ppm were excluded (which consisted of less than 5 percent of 

17 the days in the eight urban areas in the study).

18 Further, as discussed above in section II.A.3.a, there are limitations in 

19 epidemiological studies that make discerning thresholds in populations difficult, 

20 including low data density in the lower concentration ranges, the possible influence of 

21 exposure measurement error, and interindividual differences in susceptibility to O3-

 

47 Bell et al. (2006) referred to this level as being approximately equivalent to 120 

μg/m3, daily 8-hour maximum, the World Health Organization guideline and European 

Commission target value for O3.
Draft O3 NPR –January 5, 2010 193 Deliberative, Do Not Quote or Cite

1 related effects in populations. There is the possibility that thresholds for individuals may

2 exist in reported associations at fairly low levels within the range of air quality observed 

3 in the studies but not be detectable as population thresholds in epidemiological analyses.

4 Based on the above considerations, the 2007 Staff Paper recognized that the 

5 available evidence neither supports nor refutes the existence of effect thresholds at the 

6 population level for morbidity and mortality effects, and that if a population threshold 

7 level does exist, it would likely be well below the level of the then current standard and 

8 possibly within the range of background levels. Taken together, these considerations also 

9 support the conclusion that if a population threshold level does exist, it would likely be 

10 well below the level of the 0.075 ppm, 8-hour average, standard set in 2008.

11 In looking more broadly at evidence from animal toxicological, controlled human 

12 exposure, and epidemiological studies, the 2006 Criteria Document found substantial 

13 evidence, newly available in the 2008 rulemaking, that people with asthma and other 

14 preexisting pulmonary diseases are among those at increased risk from O3 exposure. 

15 Altered physiological, morphological, and biochemical states typical of respiratory

16 diseases like asthma, COPD, and chronic bronchitis may render people sensitive to 

17 additional oxidative burden induced by O3 exposure (EPA, 2006a, section 8.7). Children 

18 and adults with asthma are the groups that have been studied most extensively. Evidence 

19 from controlled human exposure studies indicates that asthmatics may exhibit larger lung 

20 function decrements in response to O3 exposure than healthy controls. As discussed more 

21 fully in section II.A.4 above, asthmatics present a different response profile for cellular, 

22 molecular, and biochemical parameters (EPA, 2006a, Figure 8-1) that are altered in 

23 response to acute O3 exposure. They can have larger inflammatory responses, as 
Draft O3 NPR –January 5, 2010 194 Deliberative, Do Not Quote or Cite

1 manifested by larger increases in markers of inflammation such as white bloods cells 

2 (e.g., PMNs) or inflammatory cytokines. Asthmatics, and people with allergic rhinitis, 

3 are more likely to have an allergic-type response upon exposure to O3, as manifested by 

4 increases in white blood cells associated with allergy (i.e., eosinophils) and related 

5 molecules, which increase inflammation in the airways. The increased inflammatory and 

6 allergic responses also may be associated with the larger late-phase responses that 

7 asthmatics can experience, which can include increased bronchoconstrictor responses to 

8 irritant substances or allergens and additional inflammation. 

9 In addition to the experimental evidence of lung function decrements, respiratory

10 symptoms, and other respiratory effects in asthmatic populations, two large U.S. 

11 epidemiological studies as well as several smaller U.S. and international studies, have 

12 reported fairly robust associations between ambient O3 concentrations and measures of 

13 lung function and daily respiratory symptoms (e.g., chest tightness, wheeze, shortness of 

14 breath) in children with moderate to severe asthma and between O3 and increased asthma 

15 medication use (EPA, 2007a, chapter 6). These more serious responses in asthmatics and 

16 others with lung disease provide biological plausibility for the respiratory morbidity

17 effects observed in epidemiological studies, such as emergency department visits and 

18 hospital admissions.

19 The body of evidence from controlled human exposure and epidemiological 

20 studies, which includes asthmatic as well as non-asthmatic subjects, indicates that 

21 controlled human exposure studies of lung function decrements and respiratory

22 symptoms that evaluate only healthy, non-asthmatic subjects likely underestimate the 

23 effects of O3 exposure on asthmatics and other susceptible populations. Therefore, 
Draft O3 NPR –January 5, 2010 195 Deliberative, Do Not Quote or Cite

1 relative to the healthy, non-asthmatic subjects used in most controlled human exposure 

2 studies, including the Adams (2002, 2006) studies, a greater proportion of people with 

3 asthma may be affected, and those who are affected may have as large or larger lung 

4 function and symptomatic responses at ambient exposures to 0.060 ppm O3. This 

5 indicates that the lowest-observed-effects levels demonstrated in controlled human 

6 exposure studies that use only healthy subjects may not reflect the lowest levels at which 

7 people with asthma or other lung diseases may respond. 

8 Being mindful of the uncertainties and limitations inherent in interpreting the 

9 available evidence, the 2007 Staff Paper stated the view that the range of alternative O3

10 standards for consideration should take into account information on lowest-observed11 effects levels in controlled human exposure studies as well as indications of possible 

12 effects thresholds reported in some epidemiological studies and questions of biological 

13 plausibility in attributing associations observed down to background levels to O3

14 exposures alone. Based on the evidence and these considerations, it concluded that the 

15 upper end of the range of consideration should be somewhat below 0.080 ppm, the 

16 lowest-observed-effects level for effects such as pulmonary inflammation, increased 

17 airway responsiveness and impaired host-defense capabilities in healthy adults while at 

18 prolonged moderate exertion. The 2007 Staff Paper also concluded that the lower end of

19 the range of alternative O3 standards appropriate for consideration should be the lowest20 observed-effects level for potentially adverse lung function decrements and respiratory

21 symptoms in some healthy adults, 0.060 ppm. 

22 b. Exposure and Risk-based Considerations
Draft O3 NPR –January 5, 2010 196 Deliberative, Do Not Quote or Cite

1 In addition to the evidence-based considerations informing staff recommendations 

2 on alternative levels, as discussed above in section II.B, the 2007 Staff Paper also 

3 evaluated quantitative exposures and health risks estimated to occur upon meeting the 

then current 0.084 ppm standard and alternative standards.48 4 In so doing, it presented the 

5 important uncertainties and limitations associated with these exposure and risk 

6 assessments (discussed above in section II.B and more fully in chapters 4 and 5 of the 

7 2007 Staff Paper). 

8 The 2007 Staff Paper (and the CASAC) also recognized that the exposure and risk 

9 analyses could not provide a full picture of the O3 exposures and O3-related health risks 

10 posed nationally. The EPA did not have sufficient information to evaluate all relevant at11 risk groups (e.g., outdoor workers) or all O3-related health outcomes (e.g., increased 

12 medication use, school absences, and emergency department visits that are part of the 

13 broader pyramid of effects discussed above in section II.A.4.d), and the scope of the 2007 

14 Staff Paper analyses was generally limited to estimating exposures and risks in 12 urban 

15 areas across the U.S., and to only five or just one area for some health effects included in 

16 the risk assessment. Thus, national-scale public health impacts of ambient O3 exposures 

17 are clearly much larger than the quantitative estimates of O3-related incidences of adverse 

18 health effects and the numbers of children likely to experience exposures of concern 

19 associated with meeting the 0.084 ppm standard or alternative standards. On the other 

 

48 As described in the 2007 Staff Paper (section 4.5.8) and discussed above in 

section II.B, recent O3 air quality distributions have been statistically adjusted to simulate 

just meeting the then current 0.084 ppm standard and selected alternative standards. 

These simulations do not represent predictions of when, whether, or how areas might 

meet the specified standards. Modeling that projects whether and how areas might attain 

alternative standards in a future year is presented in the Regulatory Impact Analysis 

being prepared in connection with this rulemaking.
Draft O3 NPR –January 5, 2010 197 Deliberative, Do Not Quote or Cite

1 hand, inter-individual variability in responsiveness means that only a subset of 

2 individuals in each group estimated to experience exposures exceeding a given 

3 benchmark exposure of concern level would actually be expected to experience such 

4 adverse health effects. 

5 The 2007 Staff Paper focused on alternative standards with the same form as the 

then current 0.084 ppm O3 standard (i.e. the 0.074/4, 0.070/4 and 0.064/4 scenarios).49 6 

7 Having concluded in the 2007 Staff Paper that it was appropriate to consider a range of 

8 standard levels from somewhat below 0.080 ppm down to as low as 0.060 ppm, the 2007 

9 Staff Paper looked to results of the analyses of exposure and risk for the 0.074/4 scenario 

10 to represent the public health impacts of selecting a standard in the upper part of the 

11 range, the results of analyses of the 0.070/4 scenario to represent the impacts in the 

12 middle part of the range, and the results of the analyses of the 0.064/4 scenario to 

13 represent the lower part of the range.

14 As discussed in section II.B.1 of this notice, the exposure estimates presented in 

15 the 2007 Staff Paper are for the number and percent of all children and asthmatic children 

16 exposed, and the number of person-days (occurrences) of exposures, with daily 8-hour 

17 maximum exposures at or above several benchmark levels while at intermittent moderate 

18 or greater exertion. Exposures above selected benchmark levels provide some 

19 perspective on the public health impacts of health effects that cannot currently be 

20 evaluated in quantitative risk assessments but that may occur at existing air quality levels, 

 

49 The abbreviated notation used to identify the then current 0.084 ppm standard

and alternative standards in this section and in the risk assessment section of the Staff 

Paper is in terms of ppm and the nth highest daily maximum 8-hour average. For 

example, the 8-hour standard established in 1997 is identified as “0.084/4.”
Draft O3 NPR –January 5, 2010 198 Deliberative, Do Not Quote or Cite

1 and the extent to which such impacts might be reduced by meeting alternative standard 

2 levels. As described in section II.B.1.c above, the 2007 Staff Paper refers to exposures at 

3 and above these benchmark levels as “exposures of concern.” The 2007 Staff Paper 

4 notes that exposures of concern, and the health outcomes they represent, likely occur 

5 across a range of O3 exposure levels, such that there is no one exposure level that 

6 addresses all public health concerns. As noted above in section II.B., EPA also has

7 acknowledged that the concept is more appropriately viewed as a continuum with greater 

8 confidence and less uncertainty about the existence of health effects at the upper end and 

9 less confidence and greater uncertainty as one considers increasingly lower O3 exposure 

10 levels. 

11 Consistent with advice from CASAC, the 2007 Staff Paper estimates exposures 

12 of concern not only at 0.080 ppm O3, a level at which there are clearly demonstrated 

13 effects, but also at 0.070 and 0.060 ppm O3 levels where there is some evidence that 

14 health effects are likely to occur in some individuals. The 2007 Staff Paper recognizes 

15 that there will be varying degrees of concern about exposures at each of these levels, 

16 based in part on the population groups experiencing them. Given that there is clear 

17 evidence of inflammation, increased airway responsiveness, and changes in host defenses 

18 in healthy people exposed to 0.080 ppm and reason to infer that such effects will continue 

19 at lower exposure levels, but with increasing uncertainty about the extent to which such 

20 effects occur at lower O3 concentrations, the 2007 Staff Paper and discussion below, 

21 focus on exposures of concern at or above benchmark levels of 0.070 and 0.060 ppm O3

22 for purposes of evaluating alternative standards. The focus on these two benchmark 

23 levels reflects the following evidence-based considerations, discussed above in section 
Draft O3 NPR –January 5, 2010 199 Deliberative, Do Not Quote or Cite

1 II.C.1, that raise concerns about adverse health effects likely occurring at levels below 

2 0.080 ppm: (1) that there is limited , but important, new evidence from controlled human 

3 exposure studies showing lung function decrements and respiratory symptoms in some 

4 healthy subjects at 0.060 ppm; (2) that asthmatics are likely to have more serious 

5 responses than healthy individuals; (3) that lung function is not likely to be as sensitive a 

6 marker for O3 effects as lung inflammation; and (4) that there is epidemiological 

7 evidence which reports associations with O3 levels that extend well below 0.080 ppm. 

8 Table 3 below summarizes the exposure estimates for all children and asthmatic 

9 children for the 0.060 and 0.070 ppm health effect benchmark levels associated with O3

10 levels adjusted to just meet 0.074/4, 0.070/4, and 0.064/4 alternative 8-hour standards 

11 based on a generally poorer year of air quality (2002) and based on a generally better year 

12 of air quality (2004). This table includes exposure estimates reflecting the aggregate 

13 estimate for the 12 urban areas as well as the range across these same 12 areas. As 

14 shown in Table 3 below, the percent of population exposed over the selected benchmark 

15 levels is very similar for all and asthmatic school age children. Thus, the following 

16 discussion focuses primarily on the exposure estimates for asthmatic children, 

17 recognizing that the pattern of exposure estimates is similar for all children when 

18 expressed in terms of percentage of the population.

19 As noted in section II.B.2 and shown in Tables 1 and 3 of this notice, substantial 

20 year-to-year variability is observed, ranging to over an order of magnitude at the higher 

21 alternative standard levels, in estimates of the number of children and the number of 

22 occurrences of exposures of concern at both the 0.060 and 0.070 ppm benchmark levels. 

23 As shown in Table 3, and discussed more fully below, aggregate estimates of exposures 
Draft O3 NPR –January 5, 2010 200 Deliberative, Do Not Quote or Cite

1 of concern for the 12 urban areas included in the assessment are considerably larger for 

2 the benchmark level of ≥ 0.060 ppm O3, compared to the 0.070 ppm benchmark, while 

3 the pattern of year-to-year variability is fairly similar. 

4 As shown in Table 3, aggregate estimates of exposures of concern for a 0.060 

5 ppm benchmark level vary considerably among the three alternative standards included in 

6 this table, particularly for the 2002 simulations (a year with generally poorer air quality in 

7 most, but not all areas). For air quality just meeting a 0.074/4 standard approximately

8 27% of asthmatic children, based on the 2002 simulation, and approximately 2% of 

9 asthmatic children based on the 2004 simulation (a year with better air quality in most but 

10 not all areas), are estimated to experience one or more exposures of concern at the 

11 benchmark level of ≥ 0.060 ppm O3. Considering a 0.070/4 standard using the same 

12 benchmark level (0.060 ppm), about 18% of asthmatic children are estimated to 

13 experience one or more exposures of concern, in a year with poorer air quality (2002), 

14 and only about 1% in a year with better air quality (2004). For the most stringent 

15 standard examined (a 0.064/4 standard), about 6% of asthmatic children are estimated to 

16 experience one or more exposures of concern in the simulation based on the year with 

17 poorer air quality (2002), and exposures of concern at the 0.060 ppm benchmark level are 

18 essentially eliminated based on a year with better air quality (2004).

19 Table 3 also provides aggregate exposure estimates for the 12 urban areas where a 

20 benchmark level of ≥ 0.070 ppm is used. Based on the year with poorer air quality

21 (2002), the estimate of the percent of asthmatic children exposed one or more times is 

22 about 5% when a 0.074/4 standard is just met; based on a year with better air quality

23 (2004), exposures of concern are essentially eliminated. For this same benchmark (0.070 
Draft O3 NPR –January 5, 2010 201 Deliberative, Do Not Quote or Cite

1 ppm), when a 0.070/4 standard is just met, estimates range from about 2% of asthmatic 

2 children exposed one or more times over this benchmark based on a year with poorer air 

3 quality (2002), and exposures of concern are essentially eliminated based on a year with 

4 better air quality (2004). At the 0.070 ppm benchmark, just meeting a 0.064/4 standard 

5 essentially eliminates exposures of concern regardless of the year that is used as the basis 

6 for the analysis.

7 The 2007 Staff Paper also notes that there is substantial city-to-city variability in 

8 these estimates, and notes that it is appropriate to consider not just the aggregate 

9 estimates across all cities, but also to consider the public health impacts in cities that 

10 receive relatively less protection from the alternative standards. As shown in Table 3, in 

11 considering the benchmark level of > 0.060 ppm, while the aggregate percentage of 

12 asthmatic children estimated to experience one or more exposures of concern across all 

13 12 cities for a 0.074/4 standard is about 27% based on the year with poorer air quality

14 (2002), it ranges up to approximately 51% for asthmatic children in the city with the least 

15 degree of protection from that alternative standard. Similarly, for air quality just meeting 

16 a 0.070/4 standard, the aggregate percentage of asthmatic children estimated to 

17 experience one or more exposures of concern across all 12 cities is 18% based on the year 

18 with poorer air quality, but it ranges up to about 41% in the city with the least degree of 

19 protection associated with just meeting that alternative standard. For just meeting a 

20 0.064/4 standard, the aggregate estimate of asthmatic children experiencing exposures of 

21 concern for the 0.060 ppm benchmark is about 6% based on the year with poorer air 

22 quality and ranges up to 16% in the city with the least degree of protection. 
Draft O3 NPR –January 5, 2010 202 Deliberative, Do Not Quote or Cite

1 This pattern of city-to-city variability also occurs at the benchmark level of ≥ 

2 0.070 ppm associated with air quality just meeting these same three alternative standards 

3 (i.e., 0.074/4, 0.070/4, and 0.064/4). While the aggregate percentage of asthmatic 

4 children estimated to experience such exposures of concern across all 12 cities is about 

5 5% based on the year with poorer air quality for just meeting the 0.074/4 standard, it 

6 ranges up to 14% in the city with the least degree of protection associated with that 

7 alternative standard. For just meeting a 0.070/4 standard the aggregate estimate is 2% of 

8 asthmatic children experiencing exposures of concern for the 0.070 ppm benchmark 

9 based on the year with poorer air quality and ranges up to 6% in the city with the least 

10 degree of protection. The aggregate estimate for exposures of concern is further reduced 

11 to 0.2% of asthmatic children for this same benchmark level for air quality just meeting a 

12 0.064/4 standard based on the year with poorer air quality and ranges up to 1% in the city

13 with the least degree of protection. 

14 In addition to observing the fraction of the population estimated to experience 

15 exposures of concern associated with just meeting alternative standards, EPA also took 

16 into consideration in the 2007 Staff Paper the percent reduction in exposures of concern 

17 and health risks associated with alternative standards relative to just meeting the then 

18 current 0.084/4 standards. For the current decision it is also informative to consider the 

19 incremental reductions in exposures of concern associated with more stringent alternative 

20 standards relative to the 0.075 ppm standard. As shown in Table 1 above, at the > 0.060 

21 ppm benchmark level based on a year with poorer air quality, the reduction in exposures 

22 of concern for asthmatic children in going from the 0.074/4 standard (which 

23 approximates the 0.075 ppm standard adopted in 2008) down to a 0.064/4 standard is 
Draft O3 NPR –January 5, 2010 203 Deliberative, Do Not Quote or Cite

1 observed to be very similar to the reduction estimated to occur in going from then current 

2 0.084/4 standard down to a 0.074/4 standard. More specifically, the estimates for 

3 asthmatic children are reduced from 47% (about 1.2 million children) associated with 

4 meeting a 0.084/4 standard down to 27% (about 700,000 children) for just meeting a 

5 0.074/4 standard and the estimates are reduced further to about 6% (about 150,000 

6 children) associated with just meeting a 0.064/4 standard in the 12 urban areas included 

7 in the assessment. In a year with better air quality (2004), exposures estimated to exceed 

8 the 0.060 ppm benchmark in asthmatic children one or more times in a year are reduced 

9 from 11% associated with just meeting a 0.084/4 standard down to about 2% for a 

10 0.074/4 standard and are essentially eliminated when a 0.064/4 standard is just met. 

11 Turning to consideration of the risk assessment estimates, Table 2 above 

12 summarizes the risk estimates for moderate lung function decrements in both all school 

13 age children and asthmatic school age children associated with just meeting several 

14 alternative standards based on simulations involving a year with relatively poorer air 

15 quality (2002) and a year with relatively better air quality (2004). As shown in Table 2, 

16 for the 2002 simulation the reduction in the number of asthmatic children estimated to 

17 experience one or more moderate lung function decrements going from a 0.074/4 

18 standard down to a 0.064/4 standard is roughly equivalent to the additional health 

19 protection afforded associated with just meeting a 0.074/4 standard relative to then 

20 current 0.084/4 standard. More specifically, for just 5 urban areas, it is estimated that 

21 nearly 8% of asthmatic children (130,000 children) would experience one or more 

22 occurrences of moderate lung function decrements per year at a 0.084/4 standard and this 

23 would be reduced to about 5% (90,000 children) at a 0.074/4 standard and further 
Draft O3 NPR –January 5, 2010 204 Deliberative, Do Not Quote or Cite

1 reduced down to about 3% (50,000 children) at a 0.064/4 standard. Based on the 2002 

2 simulations, the percent reduction associated with just meeting a 0.064/4 standard relative 

3 to then current 0.084/4 standard is about 62% which is about twice the reduction in risk 

4 compared to the estimated 31% reduction associated with just meeting a 0.074/4 

5 standard. As shown in Table 2 above, similar patterns were observed in reductions in 

6 lung function risk for all school age children in 12 urban areas associated with these 

7 alternative standards.

8 Figures 6-5 and 6-6 in the 2007 Staff Paper (EPA, 2007b) show the percent 

9 reduction in non-accidental mortality risk estimates associated with just meeting the same 

10 alternative standards discussed above relative to just meeting the then current 0.084/4 

11 standard for 12 urban areas, based on adjusting 2002 and 2004 air quality data. These 

12 figures also provide perspective on the extent to which the risks in these years (i.e., 2002 

13 and 2004) are greater than those estimated to occur upon meeting the then current 0.084/4 

14 standard (in terms of a negative percent reduction relative to a 0.084/4 standard). Based 

15 on the 2002 simulations (EPA, 2007b, Figure 6-5), the estimated reduction in non16 accidental mortality is about 30 to 70% across the 12 urban areas for just meeting a 

17 0.064/4 standard relative to the then current 0.084/4 standard. This reduction is roughly 

18 twice the 15 to 30% estimated reduction across the 12 urban areas associated with just 

19 meeting a 0.074/4 standard relative to a 0.084/4 standard. While the estimated incidence 

20 is lower based on the 2004 simulations (EPA, 2007b, Figure 6-6), the pattern of risk 

21 reductions among alternative standards is roughly similar to that observed for the 2002 

22 simulations. 
Draft O3 NPR –January 5, 2010 205 Deliberative, Do Not Quote or Cite

1 In addition to the risk estimates for lung function decrements in all school age 

2 children and non-accidental mortality that were estimated for 12 urban areas and lung 

3 function decrements in asthmatic children for 5 urban areas, a similar pattern of 

4 incremental reductions in health risks was shown for two health outcomes where risks 

5 were estimated in one city only for each of these outcomes. These included reductions in 

6 respiratory symptoms in asthmatic children (EPA, 2007b; Boston, Table 6-9) and 

7 respiratory-related hospital admissions (EPA, 2007a; New York City, Table 6-10) 

8 associated with just meeting alternative 8-hour standards set at 0.074 ppm, 0.070 ppm, 

9 and 0.064 ppm relative to just meeting the then current 0.084 ppm standard. Using the 

10 2002 simulation, a standard set at 0.074/4 is estimated to reduce the incidence of 

11 symptom days in children with moderate to severe asthma in the Boston area by about 15 

12 percent relative to a 0.084/4 standard. With this reduction, it is estimated that about 1 

13 respiratory symptom day in 8 during the O3 season would be attributable to O3 exposure. 

14 A standard set at 0.064/4 is estimated, based on the 2002 simulation, to reduce the 

15 incidence of symptom days in children with moderate to severe asthma in the Boston area 

16 by about a 25 to 30 percent reduction relative to a 0.084 ppm standard, which is roughly 

17 twice the reduction compared to that provided by a 0.074/4 standard. But even with this 

18 reduction, it is estimated that 1 respiratory symptom day in 10 during the O3 season is 

19 attributable to O3 exposure

20 As shown in Table 6-10 (EPA, 2007b) estimated incidence of respiratory-related 

21 hospital admissions in one urban area (New York City) was reduced by 14 to 17 percent

22 by a standard set at 0.074/4 relative to then current 0.084/4 standard, in the year with 

23 relatively high and relatively low O3 air quality levels, respectively. Similar to the 
Draft O3 NPR –January 5, 2010 206 Deliberative, Do Not Quote or Cite

1 pattern observed for the other health outcomes discussed above, the reduction in 

2 incidence of respiratory-related hospital admissions for a 0.064/4 standard relative to a 

3 0.084/4 standard is about twice that associated with a 0.074/4 standard relative to a 

4 0.084/4 standard.

5 Table 3. Number and Percent of All and Asthmatic School Age Children in 12 

6 Urban Areas Estimated to Experience 8-Hour Ozone Exposures Above 0.060 and 

7 0.070 ppm While at Moderate or Greater Exertion, One or More Times Per Season 

8 Associated with Just Meeting Alternative 8-Hour Standards Based on Adjusting 

2002 and 2004 Air Quality Data1,2 9

Benchmark 

Levels of 

Exposures

of Concern

(ppm)

8-Hour Air 

Quality 

Standards3

(ppm)

All Children, ages 5-18 

Aggregate for 12 urban areas

Asthmatic Children, ages 5-18

Aggregate for 12 urban areas

Number of Children Exposed (% of all children) 

[Range across 12 cities, % of all children]

Number of Children Exposed (% of group)

[Range across 12 cities, % of group ]

2002 2004 2002 2004

0.070

0.074 770,000 (4%)

[0 – 13%]

20,000 (0%)

[0 - 1%]

120,000 (5%)

[0 - 14% ]

0 (0%)

[0 - 1%]

0.070 270,000 (1%)

[0 - 5%]

0 (0%)

[0%]

50,000 (2%)

[0 - 6%]

0 (0%)

[0%]

0.064 30,000 (0.2%)

[0 - 1%]

0 (0%)

[0%]

10,000 (0.2%)

[0 - 1% ]

0 (0%)

[0%]

0.060

0.074 4,550,000 (25%)

[1 - 48%]

350,000 (2%)

[0 - 9%]

700,000 (27%)

[1 -51%]

50,000 (2%)

[0 - 9%]

0.070 3,000,000 (16%)

[1 - 36%]

110,000 (1%)

[0 - 4%]

460,000 (18%)

[0 - 41%]

10,000 (1%)

[0 - 3%]

0.064 950,000 (5%)

[0 - 17%]

10,000 (0%)

[0 - 1%]

150,000 (6%)

[0 - 16%]

0 (0%)

[0 - 1%]

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

10 .

2 11 Estimates are the aggregate results based on 12 combined statistical areas (Atlanta, Boston, Chicago, Cleveland, 

12 Detroit, Houston, Los Angeles, New York, Philadelphia, Sacramento, St. Louis, and Washington, D.C.). Estimates 

13 are for the ozone season which is all year in Houston, Los Angeles and Sacramento and March or April to 

14 September or October for the remaining urban areas.

3 15 All standards summarized here have the same form as the 8-hour standard established in 1997 which is 

specified as the 3-year average of the annual 4th 16 highest daily maximum 8-hour average concentrations 

17 must be at or below the concentration level specified. As described in the 2007 Staff Paper (EPA, 2007b, 

18 section 4.5.8), recent O3 air quality distributions have been statistically adjusted to simulate just meeting 

19 the 0.084 ppm standard and selected alternative standards. These simulations do not represent predictions 

20 of when, whether, or how areas might meet the specified standards

21

22

23

24
Draft O3 NPR –January 5, 2010 207 Deliberative, Do Not Quote or Cite

1 2. CASAC Views Prior to 2008 Decision 

2 In comments on the second draft Staff Paper, CASAC stated in its letter to the 

3 Administrator, “the CASAC unanimously recommends that the current primary ozone 

4 NAAQS be revised and that the level that should be considered for the revised standard 

5 be from 0.060 to 0.070 ppm” (Henderson, 2006c, p. 5). This recommendation followed 

6 from its more general recommendation that the 0.084 ppm standard needed to be 

7 substantially reduced to be protective of human health, particularly in at-risk 

8 subpopulations. 

9 The CASAC Panel noted that beneficial reductions in some adverse health effects 

10 were estimated to occur upon meeting the lowest standard level (0.064 ppm) considered 

11 in the risk assessment (Henderson, 2006c, p. 4). The lower end of this range reflects 

12 CASAC’s views that “[w]hile data exist that adverse health effects may occur at levels 

13 lower than 0.060 ppm, these data are less certain and achievable gains in protecting 

14 human health can be accomplished through lowering the ozone NAAQS to a level 

15 between 0.060 and 0.070 ppm.” (id.). 

16 In a subsequent letter sent specifically to offer advice to aid the Administrator and 

17 Agency staff in developing the O3 proposal, the CASAC reiterated that the Panel 

18 members “were unanimous in recommending that the level of the current primary ozone 

19 standard should be lowered from 0.08 ppm to no greater than 0.070 ppm” (Henderson, 

20 2007, p. 2). Further, the CASAC Panel expressed the view that the 2006 Criteria 

21 Document and 2007 Staff Paper, together with the information in its earlier letter, provide 

22 “overwhelming scientific evidence for this recommendation,” and emphasized the Clean 
Draft O3 NPR –January 5, 2010 208 Deliberative, Do Not Quote or Cite

1 Air Act requirement that the primary standard must be set to protect the public health 

2 with an adequate margin of safety (id.).

3 3. Basis for 2008 Decision on the Primary Standard

4 This section presents the rationale for the 2008 final decision on the primary O3

5 standard as presented in the 2008 final rule (73 FR 16475). The EPA’s conclusions on 

6 the level of the standard began by noting that, having carefully considered the public 

7 comments on the appropriate level of the O3 standard, EPA concluded that the 

8 fundamental scientific conclusions on the effects of O3 reached in the 2006 Criteria 

9 Document and 2007 Staff Paper remained valid. In considering the level at which the 

10 primary O3 standard should be set, EPA placed primary consideration on the body of 

11 scientific evidence available in the 2008 final rulemaking on the health effects associated 

12 with O3 exposure, while viewing the results of exposure and risk assessments as 

13 providing information in support of the decision. In considering the available scientific 

14 evidence, EPA concluded that a focus on the proposed range of 0.070 to 0.075 ppm was 

15 appropriate in light of the large body of controlled human exposure and epidemiological 

16 and other scientific evidence. The notice stated that this body of evidence did not support 

17 retaining the then current 0.084 ppm 8-hour O3 standard, as suggested by some 

18 commenters, nor did it support setting a level just below 0.080 ppm, because, based on 

19 the entire body of evidence, such a level would not provide a significant increase in 

20 protection compared to the 0.084 ppm standard. Further, such a level would not be 

21 appreciably below the level in controlled human exposure studies at which adverse 

22 effects have been demonstrated (i.e., 0.080 ppm). The notice also stated that the body of 

23 evidence did not support setting a level of 0.060 ppm or below, as suggested by other 
Draft O3 NPR –January 5, 2010 209 Deliberative, Do Not Quote or Cite

1 commenters. In evaluating the information from the exposure assessment and the risk 

2 assessment, EPA judged that this information did not provide a clear enough basis for 

3 choosing a specific level within the range of 0.075 to 0.070 ppm. 

4 In making a final judgment about the level of the primary O3 standard, EPA noted 

5 that the level of 0.075 ppm is above the range recommended by the CASAC (i.e., 0.070 

6 to 0.060 ppm). The notice stated that in placing great weight on the views of CASAC, 

7 careful consideration had been given to CASAC’s stated views and the scientific basis 

8 and policy views for the range it recommended. In so doing, EPA fully agreed that the 

9 scientific evidence supports the conclusion that the current standard was not adequate and 

10 must be revised.

11 With respect to CASAC’s recommended range of standard levels, EPA observed 

12 that the basis for CASAC’s recommendation appeared to be a mixture of scientific and 

13 policy considerations. While in general agreement with CASAC’s views concerning the 

14 interpretation of the scientific evidence, EPA noted that there was no bright line clearly 

15 directing the choice of level, and the choice of what was appropriate was clearly a public 

16 health policy judgment entrusted to the EPA Administrator. This judgment must include 

17 consideration of the strengths and limitations of the evidence and the appropriate 

18 inferences to be drawn from the evidence and the exposure and risk assessments. In 

19 reviewing the basis for the CASAC Panel’s recommendation for the range of the O3

20 standard, EPA observed that it reached a different policy judgment than the CASAC 

21 Panel based on apparently placing different weight in two areas: the role of the evidence 

22 from the Adams studies and the relative weight placed on the results from the exposure 

23 and risk assessments. While EPA found the evidence reporting effects at the 0.060 ppm 
Draft O3 NPR –January 5, 2010 210 Deliberative, Do Not Quote or Cite

1 level from the Adams studies to be too limited to support a primary focus at this level, 

2 EPA observed that the CASAC Panel appeared to place greater weight on this evidence, 

3 as indicated by its recommendation of a range down to 0.060 ppm. It was noted that 

4 while the CASAC Panel supported a level of 0.060 ppm, they also supported a level 

5 above 0.060, which indicated that they did not believe that the results of Adams studies 

6 meant that the level of the standard had to be set at 0.060 ppm. The EPA also observed 

7 that the CASAC Panel appeared to place greater weight on the results of the risk 

8 assessment as a basis for its recommended range. In referring to the risk assessment 

9 results for lung function, respiratory symptoms, hospital admissions and mortality, the 

10 CASAC Panel concluded that: “beneficial effects in terms of reduction of adverse health 

11 effects were calculated to occur at the lowest concentration considered (i.e., 0.064 ppm)” 

12 (Henderson, 2006c, p.4). However, EPA more heavily weighed the implications of the 

13 uncertainties associated with the Agency’s quantitative human exposure and health risk 

14 assessments. Given these uncertainties, EPA did not agree that these assessment results 

15 appropriately served as a primary basis for concluding that levels at or below 0.070 ppm 

16 were required for the 8-hour O3 standard.

17 The notice stated that after carefully taking the above comments and 

18 considerations into account, and fully considering the scientific and policy views of the 

19 CASAC, EPA decided to revise the level of the primary 8-hour O3 standard to 0.075 

20 ppm. The EPA judged, based on the available evidence, that a standard set at this level 

21 would be requisite to protect public health with an adequate margin of safety, including 

22 the health of sensitive subpopulations, from serious health effects including respiratory

23 morbidity, that were judged to be causally associated with short-term and prolonged 
Draft O3 NPR –January 5, 2010 211 Deliberative, Do Not Quote or Cite

1 exposures to O3, and premature mortality. The EPA also judged that a standard set at this 

2 level provides a significant increase in protection compared to the 0.084 ppm standard, 

3 and is appreciably below 0.080 ppm, the level in controlled human exposure studies at 

4 which adverse effects have been demonstrated. At a level of 0.075 ppm, exposures at and 

5 above the benchmark of 0.080 ppm are essentially eliminated, and exposures at and 

6 above the benchmark of 0.070 are substantially reduced or eliminated for the vast 

7 majority of people in at-risk groups. A standard set at a level lower than 0.075 would 

8 only result in significant further public health protection if, in fact, there is a continuum 

9 of health risks in areas with 8-hour average O3 concentrations that are well below the 

10 concentrations observed in the key controlled human exposure studies and if the reported 

11 associations observed in epidemiological studies are, in fact, causally related to O3 at 

12 those lower levels. Based on the available evidence, EPA was not prepared to make 

13 these assumptions. Taking into account the uncertainties that remained in interpreting the 

14 evidence from available controlled human exposure and epidemiological studies at very

15 low levels, EPA noted that the likelihood of obtaining benefits to public health decreased 

16 with a standard set below 0.075 ppm O3, while the likelihood of requiring reductions in 

17 ambient concentrations that go beyond those that are needed to protect public health 

18 increased. The EPA judged that the appropriate balance to be drawn, based on the entire 

19 body of evidence and information available in the 2008 final rulemaking, was to set the 

20 8-hour primary standard at 0.075 ppm. The EPA expressed the belief that a standard set 

21 at 0.075 ppm would be sufficient to protect public health with an adequate margin of 

22 safety, and did not believe that a lower standard was needed to provide this degree of 

23 protection. The EPA further asserted that this judgment appropriately considered the 
Draft O3 NPR –January 5, 2010 212 Deliberative, Do Not Quote or Cite

1 requirement for a standard that was neither more nor less stringent than necessary for this 

2 purpose and recognized that the CAA does not require that primary standards be set at a 

3 zero-risk level, but rather at a level that reduces risk sufficiently so as to protect public 

4 health with an adequate margin of safety.

5 4. CASAC Advice Following 2008 Decision

6 Following the 2008 decision on the O3 standard, serious questions were raised as 

7 to whether the standard met the requirements of the CAA. In April 2008, the members of

8 the CASAC Ozone Review Panel sent a letter to EPA stating “In our most-recent letters 

9 to you on this subject - dated October 2006 and March 2007 - the CASAC unanimously

10 recommended selection of an 8-hour average Ozone NAAQS within the range of 0.060 to 

11 0.070 parts per million for the primary (human health-based) Ozone NAAQS” 

12 (Henderson, 2008). The letter continued: “The CASAC now wishes to convey, by means 

13 of this letter, its additional, unsolicited advice with regard to the primary and secondary

14 Ozone NAAQS. In doing so, the participating members of the CASAC Ozone Review 

15 Panel are unanimous in strongly urging you or your successor as EPA Administrator to 

16 ensure that these recommendations be considered during the next review cycle for the 

17 Ozone NAAQS that will begin next year” (id.). Moreover, the CASAC Panel noted that 

18 “numerous medical organizations and public health groups have also expressed their 

19 support of these CASAC recommendations.” (id.) The letter further stated the following 

20 strong, unanimous view:

21 [the CASAC did] “not endorse the new primary ozone standard as being 

22 sufficient protective of public health. The CASAC — as the Agency’s 

23 statutorily-established science advisory committee for advising you on the 

24 national ambient air quality standards — unanimously recommended 
Draft O3 NPR –January 5, 2010 213 Deliberative, Do Not Quote or Cite

1 decreasing the primary standard to within the range of 0.060–0.070 ppm. 

2 It is the Committee’s consensus scientific opinion that your decision to set 

3 the primary ozone standard above this range fails to satisfy the explicit 

4 stipulations of the Clean Air Act that you ensure an adequate margin of 

5 safety for all individuals, including sensitive populations” (Henderson, 

6 2008).

7 5. Administrator’s Proposed Conclusions

8 For the reasons discussed below, the Administrator proposes to set a new level for 

the 8-hour primary O3 within the range from 0.060 to 0.070 ppm.

50 9 In reaching this

10 proposed decision, the Administrator has considered: the evidence-based considerations 

11 from the 2006 Criteria Document and the 2007 Staff Paper; the results of the exposure 

12 and risk assessments discussed above and in the 2007 Staff Paper; CASAC advice and 

13 recommendations provided in CASAC’s letters to the Administrator both during and 

14 following the 2008 rulemaking; EPA staff recommendations; and public comments 

15 received in conjunction with review of drafts of these documents and on the 2007 

16 proposed rule. In considering what level of an 8-hour O3 standard is requisite to protect 

17 public health with an adequate margin of safety, the Administrator is mindful that this 

18 choice requires judgments based on an interpretation of the evidence and other 

19 information that neither overstates nor understates the strength and limitations of the 

20 evidence and information.

21 The Administrator notes that the most certain evidence of adverse health effects 

22 from exposure to O3 comes from the controlled human exposure studies, and that the 

 

50 As discussed above at the beginning of section II, the Administrator has 

focused her reconsideration of the primary O3 standard set in the 2008 final rule on the 

level of the standard, having decided not to reopen the 2008 final rule with regard to the 

need to revise the 1997 primary O3 standard to provide increased public health protection 

nor with regard to the indicator, averaging period, and form of the 2008 standard.
Draft O3 NPR –January 5, 2010 214 Deliberative, Do Not Quote or Cite

1 large bulk of this evidence derives from studies of exposures at levels of 0.080 ppm and 

2 above. At those levels, there is consistent evidence of lung function decrements and 

3 respiratory symptoms in healthy young adults, as well as evidence of O3-induced 

4 pulmonary inflammation, airway responsiveness, impaired host defense capabilities, and 

5 other medically significant airway responses. Moreover, there is no evidence that the 

6 0.080 ppm exposure level is a threshold for any of these types of respiratory effects. 

7 Rather, there is now controlled human exposure evidence, including studies of lung 

8 function decrements and respiratory symptoms at the 0.060 ppm exposure level, that 

9 strengthens our previous understanding that this array of respiratory responses are likely 

10 to occur in some healthy adults at such lower levels.

11 In particular, the Administrator notes two studies by Adams (2002, 2006), newly

12 available in the 2008 rulemaking, that examined lung function and respiratory symptom

13 effects associated with prolonged O3 exposures at levels below 0.080 ppm, as well as 

14 EPA’s reanalysis of the data from the Adams (2006) study at a 0.060 ppm exposure level. 

15 As discussed above, while the author’s analysis focused on hour-by-hour comparisons of 

16 effects, for the purpose of exploring responses associated with different patterns of 

17 exposure, EPA’s reanalysis focused on addressing the more fundamental question of 

18 whether the pre- to post-exposure change in lung function differed between a 6.6-hour 

19 exposure to 0.060 ppm O3 versus a 6.6 hour exposure to clean filtered air. The 

20 Administrator notes that this reanalysis found small, but statistically significant group 

21 mean differences in lung function decrements in healthy adults at the 0.060 ppm exposure 

22 level, which is now the lowest-observed-effects level for these effects. Moreover, these 

23 studies also report a small percentage of subjects (7 to 20 percent) experienced moderate 
Draft O3 NPR –January 5, 2010 215 Deliberative, Do Not Quote or Cite

1 lung function decrements (> 10 percent) at the 0.060 ppm exposure level. While for 

2 active healthy people, moderate levels of functional responses (e.g., FEV1 decrements of 

3 > 10% but < 20%) and/or moderate respiratory symptom responses would likely interfere 

4 with normal activity for relatively few responsive individuals, the Administrator notes 

5 that for people with lung disease, even moderate functional or symptomatic responses 

6 would likely interfere with normal activity for many individuals, and would likely result 

7 in more frequent use of medication. Further, she notes that CASAC indicated that a 

8 focus on the lower end of the range of moderate levels of functional responses (e.g., 

9 FEV1 decrements  10%) is most appropriate for estimating potentially adverse lung 

10 function decrements in people with lung disease (Henderson, 2006c). 

11 The Administrator also notes that many public commenters on the 2007 proposed 

12 rule raised a number of questions about the weight that should be placed on the Adams 

13 studies and EPA’s reanalysis of data from the Adams (2006) study. Some commenters 

14 expressed the view that the results of these studies and EPA’s reanalysis provided support 

15 for setting a standard level below the proposed range, while others raised questions about 

16 EPA’s reanalysis and generally expressed the view that the study results were not robust 

enough to reach conclusions about respiratory effects at the 0.060 ppm exposure level.51 17

18 Based on all the above considerations, the Administrator concludes that the 

19 Adams studies provide limited but important evidence which adds to the overall body of 

20 evidence that informs her proposed decision on the range of levels within which a 

21 standard could be set that would be requisite to protect public health with an adequate 

 

51 The EPA responded to these comments in the 2008 final rule (73 FR 16454-5).
Draft O3 NPR –January 5, 2010 216 Deliberative, Do Not Quote or Cite

1 margin of safety, including the health of at-risk populations such as people with lung 

2 disease.

3 In considering controlled human exposure studies reporting O3-induced 

4 pulmonary inflammation, airway responsiveness, and impaired host defense capabilities

5 at exposure levels down to 0.080 ppm, the lowest level at which these effects have been 

6 tested, the Administrator notes that these physiological effects have been linked to 

7 aggravation of asthma and increased susceptibility to respiratory infection, potentially

8 leading to increased medication use, increased school and work absences, increased visits 

9 to doctors’ offices and emergency departments, and increased hospital admissions, 

10 especially in people with lung disease. These physiological effects are all indicators of 

11 potential adverse O3-related morbidity effects, which are consistent with and lend 

12 plausibility to the associations observed between O3 and adverse morbidity effects and 

13 mortality effects in epidemiological studies.

14 With regard to epidemiological studies, the Administrator observes that 

15 statistically significant associations between ambient O3 levels and a wide array of 

16 respiratory symptoms and other morbidity outcomes including school absences, 

17 emergency department visits, and hospital admissions have been reported in a large 

18 number of studies. More specifically, positive and robust associations were found 

19 between ambient O3 concentrations and respiratory hospital admissions and emergency

20 department visits, when focusing particularly on the results of warm season analyses. 

21 Taken together, the overall body of evidence from controlled human exposure, 

22 toxicological, and epidemiological studies supports the inference of a causal relationship 

23 between acute ambient O3 exposures and increased respiratory morbidity outcomes 
Draft O3 NPR –January 5, 2010 217 Deliberative, Do Not Quote or Cite

1 resulting in increased emergency department visits and hospitalizations during the warm 

2 season. Further, the Administrator notes that recent epidemiological evidence is highly

3 suggestive that O3 directly or indirectly contributes to non-accidental and 

4 cardiopulmonary-related mortality.

5 The Administrator also considered the epidemiological evidence with regard to 

6 considering potential effects thresholds at the population level for morbidity and 

7 mortality effects. As discussed above, while some studies provide some indication of 

8 possible 8-hour average threshold levels from below about 0.025 to 0.035 ppm (within 

9 the range of background concentrations) up to approximately 0.050 ppm, other studies 

10 observe linear concentration-response functions suggesting that there may be no effects 

11 thresholds at the population level above background concentrations. In addition, other 

12 studies conducted subset analyses that included only days with ambient O3 concentrations 

13 below the level of the then current standard, or below even lower O3 concentrations, 

14 including a level as low as 0.061 ppm, and continue to report statistically significant 

15 associations. The Administrator notes that the relationships between ambient O3

16 concentrations and lung function decrements, respiratory symptoms, indicators of 

17 respiratory morbidity including increased respiratory-related emergency department visits 

18 and hospital admissions, and possibly mortality reported in a large number of studies 

19 likely extend down to ambient O3 concentrations well below the level of the standard set 

20 in 2008 (0.075 ppm), in that the highest level at which there is any indication of a 

21 threshold is approximately 0.050 ppm. The Administrator notes as well that toward the 

22 lower end of the range of O3 concentrations observed in such studies, ranging down to 

23 background levels (i.e., 0.035 to 0.015 ppm), there is increasing uncertainty as to whether 
Draft O3 NPR –January 5, 2010 218 Deliberative, Do Not Quote or Cite

1 the observed associations remain plausibly related to exposures to ambient O3, rather than 

2 to the broader mix of air pollutants present in the ambient atmosphere. She also notes 

3 that there are limitations in epidemiological studies that make discerning population 

4 thresholds difficult, as discussed above, such that there is the possibility that thresholds 

5 for individuals may exist in reported associations at fairly low levels within the range of 

6 air quality observed in the studies but not be detectable as population thresholds in 

7 epidemiological analyses.

8 In looking more broadly at evidence from animal toxicological, controlled human 

9 exposure, and epidemiological studies, the Administrator finds substantial evidence, 

10 newly available for consideration in the 2008 rulemaking, that people with asthma and 

11 other preexisting pulmonary diseases are among those at increased risk from O3

12 exposure. As discussed above, altered physiological, morphological, and biochemical 

13 states typical of respiratory diseases like asthma, COPD, and chronic bronchitis may

14 render people sensitive to additional oxidative burden induced by O3 exposure. Children 

15 and adults with asthma are the group that has been studied most extensively. Evidence 

16 from controlled human exposure studies indicates that asthmatics and people with 

17 allergic rhinitis may exhibit larger lung function decrements in response to O3 exposure 

18 than healthy subjects and that they can have larger inflammatory responses. The 

19 Administrator also notes that two large U.S. epidemiological studies, as well as several 

20 smaller U.S. and international studies, have reported fairly robust associations between 

21 ambient O3 concentrations and measures of lung function and daily symptoms (e.g., chest 

22 tightness, wheeze, shortness of breath) in children with moderate to severe asthma and 

23 between O3 and increased asthma medication use. These more serious responses in 
Draft O3 NPR –January 5, 2010 219 Deliberative, Do Not Quote or Cite

1 asthmatics and others with lung disease provide biological plausibility for the respiratory

2 morbidity effects observed in epidemiological studies, such as respiratory-related 

3 emergency department visits and hospital admissions.

4 The Administrator also observes that a substantial body of evidence from 

5 controlled human exposure and epidemiological studies indicates that relative to the 

6 healthy, non-asthmatic subjects used in most controlled human exposure studies, a 

7 greater proportion of people with asthma may be affected, and those who are affected 

8 may have as large or larger lung function and symptomatic responses to O3 exposures. 

9 Thus, the Administrator concludes that controlled human exposure studies of lung 

10 function decrements and respiratory symptoms that evaluate only healthy, non-asthmatic 

11 subjects likely underestimate the effects of O3 exposure on asthmatics and other 

12 susceptible populations.

13 In addition to the evidence-based considerations discussed above, the 

14 Administrator also considered quantitative exposures and health risks estimated to occur 

15 associated with air quality simulated to just meet various standard levels to help inform 

16 judgments about a range of standard levels for consideration that could provide an 

17 appropriate degree of public health protection. In so doing, she is mindful of the 

18 important uncertainties and limitations that are associated with the exposure and risk 

19 assessments, as discussed in more detail in the 2007 Staff Paper, and above in sections 

20 II.B and II.C.1.b. Beyond these uncertainties, the Administrator also recognized 

21 important limitations related to the exposure and risk analyses. For example, EPA did 

22 not have sufficient information to evaluate all relevant at-risk groups (e.g., outdoor 

23 workers) or all O3-related health outcomes (e.g., increased medication use, school 
Draft O3 NPR –January 5, 2010 220 Deliberative, Do Not Quote or Cite

1 absences, emergency department visits), and the scope of the analyses was generally 

2 limited to estimating exposures and risks in 12 urban areas across the U.S., and to only

3 five or just one area for some health effects. Thus, it is clear that national-scale public 

4 health impacts of ambient O3 exposures are much larger than the quantitative estimates of 

5 O3-related incidences of adverse health effects and the numbers of children likely to 

6 experience exposures of concern associated with meeting the then current standard or 

7 alternative standards. Taking these limitations into account, the CASAC advised EPA 

8 not to rely solely on the results of the exposure and risk assessments in considering 

9 alternative standards, but also to place significant weight on the body of evidence of O3-

10 related health effects in drawing conclusions about an appropriate range of levels for 

11 consideration. The Administrator agrees with this advice. 

12 Turning first to the results of the exposure assessment, the Administrator focused 

13 on the extent to which alternative standard levels, approximately at and below the 0.075

14 ppm O3 standard set in the 2008 final rule, are estimated to reduce exposures over the 

15 0.060 and 0.070 ppm health effects benchmark levels, for all and asthmatic school age 

children in the 12 urban areas included in the assessment.52 16 The Administrator also took 

17 note that the lowest standard level included in the exposure and health risk assessments 

18 was 0.064 ppm and that additional reductions in exposures over the selected health 

19 benchmark levels would be anticipated for just meeting a 0.060 ppm standard. 

20 As an initial matter, the Administrator recognized that the concept of “exposures 

21 of concern” is more appropriately viewed as a continuum, with greater confidence and 

 

52 As noted in section II.C.1.b.above, the Administrator focused on alternative 

standards with different levels but the same form and averaging time as the primary

standard set in 2008.
Draft O3 NPR –January 5, 2010 221 Deliberative, Do Not Quote or Cite

1 less uncertainty about the existence of health effects at the upper end and less confidence 

2 and greater uncertainty as one considers increasingly lower O3 exposure levels. In 

3 considering the concept of exposures of concern, the Administrator also noted that it is 

4 important to balance concerns about the potential for health effects and their severity with 

5 the increasing uncertainty associated with our understanding of the likelihood of such 

6 effects at lower O3 levels. Within the context of this continuum, estimates of exposures 

7 of concern at discrete benchmark levels provide some perspective on the public health 

8 impacts of O3-related physiological effects that have been demonstrated in controlled 

9 human exposure and toxicological studies but cannot be evaluated in quantitative risk 

10 assessments, such as lung inflammation, increased airway responsiveness, and changes in 

11 host defenses. They also help in understanding the extent to which such impacts have the 

12 potential to be reduced by meeting alternative standards. As discussed in II.C.1.a above, 

13 these O3-related physiological effects are plausibly linked to the increased morbidity seen 

14 in epidemiological studies (e.g., as indicated by increased medication use in asthmatics, 

15 school absences in all children, and emergency department visits and hospital admissions 

16 in people with lung disease). 

17 Estimates of the number of people likely to experience exposures of concern 

18 cannot be directly translated into quantitative estimates of the number of people likely to 

19 experience specific health effects, since sufficient information to draw such comparisons 

20 is not available -- if such information were available, these health outcomes would have 

21 been included in the quantitative risk assessment. Due to individual variability in 

22 responsiveness, only a subset of individuals who have exposures at and above a specific 

23 benchmark level are expected to experience such adverse health effects, and susceptible 
Draft O3 NPR –January 5, 2010 222 Deliberative, Do Not Quote or Cite

1 population groups such as those with asthma are expected to be affected more by such 

2 exposures than healthy individuals.

3 For the reasons discussed in section II.C.1.b above, the Administrator has 

4 concluded that it is appropriate to focus on both the 0.060 and 0.070 ppm health effect 

5 benchmarks for her decision on the primary standard. In summary, the focus on these 

6 two benchmark levels reflects the following evidence-based considerations, discussed 

7 above in section II.C.1.a, that raise concerns about adverse health effects likely occurring 

8 at levels below 0.080 ppm: (1) that there is limited, but important, new evidence from 

9 controlled human exposure studies showing lung function decrements and respiratory

10 symptoms in some healthy subjects at 0.060 ppm; (2) that asthmatics are likely to have 

11 more serious responses than healthy individuals; (3) that lung function is not likely to be 

12 as sensitive a marker for O3 effects as lung inflammation; and (4) that there is 

13 epidemiological evidence which reports associations between ambient O3 concentrations 

14 and respiratory symptoms, ED visits, hospital admissions, and premature mortality in

15 areas with O3 levels that extend well below 0.080 ppm. 

16 Based on the exposure and risk considerations discussed in detail in the 2007 

17 Staff Paper and presented in sections II.B and II.C.1.b above, the Administrator notes the 

18 following important observations from these assessments: 1) there is a similar pattern for

19 all children and asthmatic school age children in terms of exposures of concern over 

20 selected benchmark levels when estimates are expressed in terms of percentage of the 

21 population; 2) the aggregate estimates of exposures of concern reflecting estimates for the 

22 12 urban areas included in the assessment are considerably larger for the benchmark level 

23 of 0.060 ppm compared to the 0.070 ppm benchmark; 3) there is notable year-to-year 
Draft O3 NPR –January 5, 2010 223 Deliberative, Do Not Quote or Cite

1 variability in exposure and risk estimates with higher exposure and risk estimates 

2 occurring in simulations involving a year with generally poorer air quality in most areas 

3 (2002) compared to a year with generally better air quality (2004); and 4) there is 

4 significant city-to-city variability in exposure and risk estimates, with some cities 

5 receiving considerably less protection associated with air quality just meeting the same 

6 standard. As discussed above, the Administrator believes that it is appropriate to 

7 consider not just the aggregate estimates across all cities, but also to consider the public 

8 health impacts in cities that receive relatively less protection from alternative standards 

9 under consideration. Similarly, the Administrator believes that year-to-year variability

10 should also be considered in making judgments about which standards will protect public 

11 health with an adequate margin of safety.

12 In addition, significant reductions in exposures of concern and risk have been 

13 estimated to occur across standard levels analyzed. The magnitudes of exposure and risk 

14 reductions estimated to occur in going from a 0.074 ppm standard to a 0.064 ppm 

15 standard are as large as those estimated to occur in going from the then current 0.084 

16 ppm standard to a 0.074 ppm standard. Consequently, the reduction in risk that can be 

17 achieved by going from a standard of 0.074 ppm to a standard of 0.064 ppm is

18 comparable to the risk reduction that can be achieved by moving from the 1997 O3

19 standard, effectively a 0.084 ppm standard, to a standard very close to the 2008 standard 

20 of 0.075 ppm. 

21 The Administrator also observes that estimates of exposures of concern associated 

22 with air quality just meeting the alternative standards below 0.080 ppm (i.e., 0.074, 

23 0.070, and 0.064 ppm, the levels included in the assessment) are notably lower than 
Draft O3 NPR –January 5, 2010 224 Deliberative, Do Not Quote or Cite

1 estimates for alternative standards set at and above 0.080 ppm. As shown in Table 6-8 in 

2 the 2007 Staff Paper, just meeting a 0.080 ppm standard is associated with an aggregate 

3 estimate of exposures of concern of about 13% of asthmatic children at the 0.070 ppm 

4 benchmark level, ranging up to 31% in the city with the least degree of protection in a 

5 year with generally poorer air quality, and an aggregate estimate of exposures of concern 

6 of about 40% of asthmatic children, ranging up to 63% in the city with the least degree of 

7 protection at the 0.060 ppm benchmark level. Based on the exposure estimates presented 

8 in Table 3 in this notice, she observes that standards included in the assessment below 

9 0.080 ppm (i.e., 0.074, 0.070, and 0.064 ppm), are estimated to have substantially lower 

10 estimates of exposures of concern at the 0.070 ppm benchmark level. Similarly, she 

11 notes that exposures of concern at the 0.060 ppm benchmark associated with alternative 

12 standards below 0.080 ppm are appreciably lower than exposures associated with 

13 standards at or above 0.080 ppm, especially for standards set at 0.064 and 0.070 ppm. 

14 As noted previously, the Administrator also recognizes that the risk estimates for 

15 health outcomes included in the risk assessment are limited and that the overall health 

16 effects evidence is indicative of a much broader array of O3-related health effects that are 

17 part of a “pyramid of effects” that include various indicators of morbidity that could not 

18 be included in the risk assessment (e.g., school absences, increased medication use, 

19 doctor’s visits, and emergency department visits), some of which have a greater impact 

20 on at-risk groups. Consideration of such unquantified risks for this array of health 

21 effects, taken together with the estimates of exposures of concern and the quantified 

22 health risks discussed above, supports the Administrator’s evidence-based conclusion that 

23 revising the standard level to a level well below 0.080 ppm will provide important 
Draft O3 NPR –January 5, 2010 225 Deliberative, Do Not Quote or Cite

1 increased public health protection, especially for at-risk groups such as people with 

2 asthma or other lung disease, as well as children and older adults, particularly those 

3 active outdoors, and outdoor workers

4 Based on the evidence- and exposure/risk-based considerations discussed above, 

5 the Administrator concludes that it is appropriate to set the level of the primary O3

6 standard to a level well below 0.080 ppm, a level at which the evidence provides a high 

7 degree of certainty about the adverse effects of O3 exposure in healthy people, to provide 

8 an adequate margin of safety for at-risk groups. In selecting a proposed range of levels, 

9 the Administrator believes it is appropriate to consider the following information: (1) the 

10 strong body of evidence from controlled human exposure studies evaluating healthy

11 people at exposure levels of 0.080 ppm and above that demonstrated lung function 

12 decrements, respiratory symptoms, pulmonary inflammation, and other medically

13 significant airway responses, as well as limited but important evidence of lung function 

14 decrements and respiratory symptoms in healthy people down to O3 exposure levels of 

15 0.060 ppm; (2) the substantial body of evidence from controlled human exposure and 

16 epidemiological studies indicating that people with asthma are likely to experience larger 

17 and more serious effects than healthy people; (3) the body of epidemiological evidence 

18 indicating associations are observed for a wide range of serious health effects, including 

19 respiratory-related emergency department visits and hospital admissions and premature 

20 mortality, across distributions of ambient O3 concentrations that extend below the current 

21 standard level of 0.075 ppm, as well as questions of biological plausibility in attributing 

22 the observed effects to O3 alone at the lower end of the concentration ranges extending 

23 down to background levels; and (4) the estimates of exposures of concern and risks for a 
Draft O3 NPR –January 5, 2010 226 Deliberative, Do Not Quote or Cite

1 range of health effects that indicate that important improvements in public health are very

2 likely associated with O3 levels just meeting alternative standards, especially for 

3 standards set at 0.070 and 0.064 ppm (the lowest levels included in the assessment), 

4 relative to standards set at and above 0.080 ppm. 

5 The Administrator next considered what standard level well below 0.080 ppm 

6 would be requisite to protect public health, including the health of at-risk groups, with an 

7 adequate margin of safety that is sufficient but not more than necessary to achieve that 

8 result. The assessment of a standard level calls for consideration of both the degree of 

9 risk to public health at alternative levels of the standard as well as the certainty that such 

10 risk will occur at any specific level. Based on the information available in the 2008 

11 rulemaking, there is no evidence-based bright line that indicates a single appropriate 

12 level. Instead there is a combination of scientific evidence and other information that 

13 needs to be considered as a whole in making this public health policy judgment, and 

14 selecting a standard level from a range of potentially reasonable values.

15 As an initial matter, the Administrator considered whether the standard level of 

16 0.075 ppm set in the 2008 final rule is sufficiently below 0.080 ppm to be requisite to 

17 protect public health with an adequate margin of safety. In considering this standard 

18 level, the Administrator looked to the rationale for selecting this level presented in the 

19 2008 final rule, as summarized above in section II.C.3. In that rationale, EPA observed 

20 that a level of 0.075 ppm is above the range of 0.060 to 0.070 ppm recommended by 

21 CASAC, and that the CASAC Panel appeared to place greater weight on the evidence 

22 from the Adams studies and on the results of the exposure and risk assessments, whereas 

23 EPA placed greater weight on the limitations and uncertainties associated with that 
Draft O3 NPR –January 5, 2010 227 Deliberative, Do Not Quote or Cite

1 evidence and the quantitative exposure and risk assessments. Additionally, EPA’s 

2 rationale did not discuss and thus placed no weight on exposures of concern relative to 

3 the 0.060 ppm benchmark. Further, EPA concluded that “[a] standard set at a lower level 

4 than 0.075 ppm would only result in significant further public health protection if, in fact, 

5 there is a continuum of health risks in areas with 8-hour average O3 concentrations that 

6 are well below the concentrations observed in the key controlled human exposure studies 

7 and if the reported associations observed in epidemiological studies are, in fact, causally 

8 related to O3 at those lower levels. Based on the available evidence, [EPA] is not 

9 prepared to make these assumptions” (73 FR 16483). 

10 In reconsidering the entire body of evidence available in the 2008 rulemaking, 

11 including the Agency’s own assessment of the epidemiological evidence in the 2006 

12 Criteria Document, and placing significant weight on the views of CASAC, the 

13 Administrator now concludes that important and significant risks to public health are 

14 likely to occur at a standard level of 0.075 ppm. She judges that a standard level of 0.075 

15 ppm is not sufficient to provide protection with an adequate margin of safety. In support 

16 of this conclusion, the Administrator finds that setting a standard that would protect 

17 public health, including the health of at-risk populations, with an adequate margin of 

18 safety should reasonably depend upon giving some weight to the results of the Adams 

19 studies and EPA's reanalysis of the Adams's data, and to how effectively alternative 

20 standard levels would serve to limit exposures of concern relative to the 0.060 ppm 

21 benchmark level as well as to the 0.070 ppm benchmark level. The Administrator notes 

22 that EPA’s risk assessment estimates comparable risk reductions in going from a 0.074 

23 ppm standard to a 0.064 ppm standard as were estimated in going from the then current 
Draft O3 NPR –January 5, 2010 228 Deliberative, Do Not Quote or Cite

1 0.084 ppm standard down to a 0.074 ppm standard for an array of health effects analyzed. 

2 These estimates include reductions in risk for lung function decrements in all and 

3 asthmatic school age children, respiratory symptoms in asthmatic children, respiratory4 related hospital admissions, and non-accidental mortality. 

5 Further, based on the exposure assessment estimates discussed above, the 

6 Administrator notes that for air quality just meeting a 0.074 ppm standard, approximately 

7 27% of asthmatic school age children and 25% of all school age children are estimated to 

8 experience one or more exposures of concern over the 0.060 ppm benchmark level based 

9 on simulations for a year with generally poorer air quality; this estimate increases to 

10 about 50% of asthmatic and all children in the city with the least degree of protection. 

11 The Administrator judges that these estimates are large and strongly suggest significant 

12 public health impacts would likely remain in many areas with air quality just meeting a 

13 0.075 ppm O3 standard.

14 In light of these estimates and the available evidence, the Administrator agrees 

15 with CASAC’s conclusion that important public health protections can be achieved by a 

16 standard set below 0.075 ppm, within the range of 0.060 to 0.070 ppm. In addition, based 

17 on both the evidence- and exposure/risk-based considerations summarized above, the 

18 Administrator concludes that a standard set as high as 0.075 would not be considered 

19 requisite to protect public health with an adequate margin of safety, and that 

20 consideration of lower levels is warranted. In considering such lower levels, the 

21 Administrator recognizes that the CAA requires her to reach a public health policy

22 judgment as to what standard would be requisite to protect public health with an adequate 

23 margin of safety, based on scientific evidence and technical assessments that have 
Draft O3 NPR –January 5, 2010 229 Deliberative, Do Not Quote or Cite

1 inherent uncertainties and limitations. This judgment requires making reasoned decisions 

2 as to what weight to place on various types of evidence and assessments and on the 

3 related uncertainties and limitations.

4 In selecting a level below 0.075 ppm that would serve as an appropriate upper end 

5 for a range of levels to propose, the Administrator has considered a more cautious 

6 approach to interpreting the available evidence and exposure/risk-based information –

7 that is, an approach that places significant weight on uncertainties and limitations in the 

8 information so as to avoid potentially overestimating public health risks and protection

9 likely to be associated with just meeting a particular standard level. In so doing, she 

10 notes that the most certain evidence of adverse health effects from exposure to O3 comes 

11 from the controlled human exposure studies, and that the large bulk of this evidence 

12 derives from studies of exposures at levels of 0.080 ppm and above. At those levels, 

13 there is consistent evidence of lung function decrements and respiratory symptoms in 

14 healthy young adults, as well as evidence of inflammation and other medically significant 

15 airway responses. Further, she takes note of the limited but important evidence from 

16 controlled human exposure studies indicating that lung function decrements and 

17 symptoms can occur in healthy people at levels as low as 0.060 ppm, while also 

18 recognizing the limitations in that evidence, as discussed above in sections II.A.1 and 

19 II.C.1.a. She also notes that some people with asthma are likely to experience larger and 

20 more serious effects than the healthy subjects evaluated in the controlled exposure 

21 studies, while recognizing that there is uncertainty about the magnitude of such 

22 differences. In considering the available epidemiological studies, she recognizes that 

23 they provide evidence of serious respiratory morbidity effects, including respiratory-
Draft O3 NPR –January 5, 2010 230 Deliberative, Do Not Quote or Cite

1 related emergency department visits and hospital admissions, and non-accidental 

2 mortality at levels well below 0.080 ppm, while also recognizing that there is increasing 

3 uncertainty associated with the likelihood that such effects occur at decreasing O3 levels

4 down to background levels. Considering the exposure/risk information, as shown in 

5 Table 3, the Administrator observes that a standard set at 0.070 ppm would likely

6 substantially limit exposures of concern relative to the 0.070 ppm benchmark level, while 

7 affording far less protection against exposures of concern relative to the 0.060 ppm 

8 benchmark level. To the extent that more weight is placed on protection relative to the 

9 higher benchmark level, and more weight is placed on the uncertainties associated with 

10 the epidemiological evidence, a standard set at 0.070 ppm might be considered to be 

11 adequately protective. Taken together, this type of cautious approach to interpreting the 

12 evidence and the exposure/risk information serves as the basis for the Administrator’s

13 conclusion that the upper end of the proposed range should be set at 0.070 ppm O3.

14 In selecting a level that would serve as an appropriate lower end for a range of

15 levels to propose, the Administrator has considered a more precautionary approach to 

16 interpreting the available evidence and exposure/risk-based information – that is, an 

17 approach that places less weight on uncertainties and limitations in the information so as 

18 to avoid potentially underestimating public health improvements likely to be associated 

19 with just meeting a particular standard level. In so doing, the Administrator notes the

20 limited, but important evidence of a lowest-observed-effects level at 0.060 ppm O3 from 

21 controlled human exposure studies reporting lung function decrements and respiratory

22 symptoms in healthy subjects. Notably, these studies also report that a small percentage 

23 of subjects (7 to 20 percent) experienced moderate lung function decrements (> 10 
Draft O3 NPR –January 5, 2010 231 Deliberative, Do Not Quote or Cite

1 percent) at the 0.060 ppm exposure level, recognizing that for people with lung disease, 

2 such moderate functional or symptomatic responses would likely interfere with normal 

3 activity for many individuals, and would likely result in more frequent use of medication. 

4 In addition, a substantial body of evidence indicates that people with asthma are likely to 

5 experience larger and more serious effects than healthy people and therefore controlled 

6 human exposure studies done with healthy subjects likely underestimate effects in this at7 risk population. 

8 Moreover, epidemiological studies provide evidence of serious respiratory

9 morbidity effects, including respiratory-related emergency department visits and hospital 

10 admissions, and non-accidental mortality at O3 levels that may plausibly extend down to

11 at least 0.060 ppm even when considering the uncertainties inherent in such studies. The 

12 Administrator notes that the controlled human exposure studies conducted at 0.060 ppm 

13 provide some biological plausibility for associations between respiratory morbidity and 

14 mortality effects found in epidemiological studies and O3 exposures down to 0.060 ppm. 

15 Considering the exposure information, as shown in Table 3, the Administrator observes 

16 that a standard set at 0.064 ppm would likely essentially eliminate exposures of concern 

17 relative to the 0.070 ppm benchmark level, while appreciably limiting exposures of 

18 concern relative to the 0.060 ppm benchmark level to approximately 6 percent of 

19 asthmatic children in the aggregate across 12 cities and up to 16 percent in the city that 

20 would receive the least protection. While not addressed in the exposure assessment done 

21 as part of the 2008 rulemaking, a standard set at 0.060 ppm would be expected to provide 

22 somewhat greater protection from such exposures, which is important to the extent that 

23 more weight is placed on providing protection relative to the lower benchmark level. 
Draft O3 NPR –January 5, 2010 232 Deliberative, Do Not Quote or Cite

1 Taken together, the Administrator concludes that this precautionary approach to 

2 interpreting the evidence and the exposure/risk information supports a level of 0.060 ppm 

3 as the lower end of the proposed range. 

4 The Administrator has also concluded that the lower end of the proposed range 

5 should not extend below 0.060 ppm O3. In reaching this conclusion, she gives significant 

6 weight to the recommendation of the CASAC panel that 0.060 ppm should be the lower 

7 end of the range for consideration (Henderson, 2006c). In the Administrator's view, the 

8 evidence from controlled human exposure studies at the 0.060 ppm exposure level, the 

9 lowest level tested, is not robust enough to support consideration of a lower level. While 

10 some epidemiological studies provide evidence of serious respiratory morbidity effects 

11 and non-accidental mortality with no evidence of a threshold, the Administrator notes 

12 that other studies provide evidence of a potential threshold somewhat below 0.060 ppm. 

13 Moreover, there are limitations in epidemiological studies that make discerning 

14 population thresholds difficult, including fewer observations in the range of lower 

15 concentrations, concerns related to exposure measurement error, the possible role of 

16 copollutants and effects modifiers, and interindividual differences in susceptibility to O3-

17 related effects. In the Administrator’s judgment, these limitations in epidemiological 

18 studies, including the limitations in judging the causality of observed associations at 

19 lower O3 levels, and the lack of robust controlled human exposure data at 0.060 ppm

20 make it difficult to interpret this evidence as a basis for a standard level set below 0.060 

21 ppm. Thus, in selecting 0.060 ppm as the lower end of the range for the proposed level 

22 of the O3 standard, the Administrator has taken into account information on the lowest23 observed-effects levels in controlled human exposure studies, indications of possible 
Draft O3 NPR –January 5, 2010 233 Deliberative, Do Not Quote or Cite

1 thresholds reported in some epidemiological studies, the increasing uncertainty in the 

2 epidemiological evidence at even lower levels, as well as evidence about increased 

3 susceptibility of people with asthma and also other lung diseases. In so doing, she 

4 concludes that a primary O3 standard set below 0.060 ppm would be more than is 

5 necessary to protect public health with an adequate margin of safety for at-risk groups. 

6 In reaching her proposed decision, the Administrator has also considered the 

7 public comments that were received on the 2007 proposed rule (72 FR 37818). The 

8 Administrator notes that there were sharply divergent views expressed by two general 

9 sets of commenters with regard to considering the health effects evidence, results of 

10 exposure and risk assessments, and the advice of the CASAC panel. On one hand, 

11 medical groups, health effects researchers, public health organizations, environmental 

12 groups, and some state, tribal and local air pollution control agencies strongly supported a 

13 standard set within the range recommended by the CASAC. These commenters generally 

14 placed significant weight on the more recent evidence from controlled human exposure 

15 studies, down to the 0.060 ppm exposure level, as well as on the epidemiological studies 

16 and the results of the exposure and risk assessment conducted for the 2008 rulemaking. 

17 Many of these commenters took a more precautionary view and supported a standard set 

18 at 0.060 ppm O3, the lower end of the CASAC recommended range. The Administrator 

19 notes that these views are generally consistent with her proposed conclusions. On the 

20 other hand, another group of commenters primarily representing industry associations 

21 and businesses and some state environmental agencies, primarily expressed the view that 

22 the more recent evidence from controlled human exposure, the epidemiological studies, 

23 and the results of exposure and human health risk assessments were so uncertain that they
Draft O3 NPR –January 5, 2010 234 Deliberative, Do Not Quote or Cite

1 did not provide a basis for making any changes to the then current 0.084 ppm O3 standard 

2 set in 1997. This group of commenters generally argued that the health effects evidence 

3 newly available in the 2008 rulemaking, the results of the exposure and health risk 

4 assessments, and the advice of the CASAC were flawed. For the reasons discussed 

5 above, the Administrator does not agree with the later group of commenters that 

6 essentially no weight should be placed on any of the new evidence or assessments that 

7 were available for consideration in the 2008 rulemaking.

8 Based on consideration of the entire body of evidence and information available

9 in the 2008 rulemaking, including exposure and risk estimates, as well as the

10 recommendations of CASAC, the Administrator proposes to set the level of the primary

11 8-hour O3 standard to a level within the range of 0.060 to 0.070 ppm. A standard level 

12 within this range would reduce the risk of a variety of health effects associated with

13 exposure to O3, including the respiratory symptoms and lung function effects 

14 demonstrated in the controlled human exposure studies, and the respiratory-related

15 emergency department visits, hospital admissions and mortality effects observed in the 

16 epidemiological studies. All of these effects are indicative of a much broader array of

17 O3-related health endpoints, such as school absences and increased medication use, that 

18 are plausibly linked to these observed effects. Depending on the weight placed on the 

19 evidence and information available in the 2008 rulemaking, as well as the uncertainties 

20 and limitations in the evidence and information, a standard could be set within this range 

21 at a level that would be requisite to protect public health with an adequate margin of 

22 safety.
Draft O3 NPR –January 5, 2010 235 Deliberative, Do Not Quote or Cite

1 In reaching this proposed decision, as discussed above, the Administrator has 

2 focused on the nature of the increased public health protection that would be afforded by 

3 a standard set within the proposed range of levels relative to the protection afforded by 

4 the standard set in 2008. Having considered the public comments received on the 2007 

5 proposed rule in reaching this proposed decision that reconsiders the 2008 final rule, the 

6 Administrator is interested in again receiving public comment on the benefits to public 

7 health associated with a standard set at specific levels within the proposed range relative 

8 to the benefits associated with the standard set in 2008.

9 D. Proposed Decision on the Level of the Primary Standard

10 For the reasons discussed above, and taking into account information and 

11 assessments presented in the 2006 Criteria Document and 2007 Staff Paper, the advice 

12 and recommendations of CASAC, and public comments received during the 2008 

13 rulemaking, the Administrator proposes to set a new level for the 8-hour primary O3

14 standard. Specifically, the Administrator proposes to set the level of the 8-hour primary

15 O3 standard to within a range of 0.060 to 0.070 ppm. The proposed 8-hour primary

16 standard would be met at an ambient air monitoring site when the 3-year average of the 

17 annual forth-highest daily maximum 8-hour average O3 concentration is less than or 

18 equal to the level of the standard that is promulgated. Thus, the Administrator proposes 

19 to set a standard with a level within this range. She solicits comment on this range and 

20 on the appropriate weight to place on the various types of available evidence, the 

21 exposure and risk assessment results, and the uncertainties and limitations related to this 

22 information, as well as on the benefits to public health associated with a standard set 

23 within this range relative to the benefits associated with the standard set in 2008.
Draft O3 NPR –January 5, 2010 236 Deliberative, Do Not Quote or Cite

1

2 III. Communication of Public Health Information

3 Information on the public health implications of ambient concentrations of criteria 

4 pollutants is currently made available primarily through EPA's Air Quality Index (AQI) 

5 program. The current Air Quality Index has been in use since its inception in 1999 (64 

6 FR 42530). It provides accurate, timely, and easily understandable information about 

7 daily levels of pollution (40 CFR 58.50). The AQI establishes a nationally uniform 

8 system of indexing pollution levels for O3, carbon monoxide, nitrogen dioxide, 

9 particulate matter and sulfur dioxide. The AQI converts pollutant concentrations in a 

10 community's air to a number on a scale from 0 to 500. Reported AQI values enable the 

11 public to know whether air pollution levels in a particular location are characterized as 

12 good (0 - 50), moderate (51 - 100), unhealthy for sensitive groups (101 - 150), unhealthy

13 (151 - 200), very unhealthy (201 - 300), or hazardous (300 - 500). The AQI index value 

14 of 100 typically corresponds to the level of the short-term NAAQS for each pollutant. 

15 An AQI value greater than 100 means that a pollutant is in one of the unhealthy

16 categories (i.e., unhealthy for sensitive groups, unhealthy, very unhealthy, or hazardous) 

17 on a given day; whereas an AQI value at or below 100 means that a pollutant 

18 concentration is in one of the satisfactory categories (i.e., moderate or good). Decisions 

19 about the pollutant concentrations at which to set the various AQI breakpoints, that 

20 delineate the various AQI categories, draw directly from the underlying health 

21 information that supports the NAAQS review.

22 In the 2008 rulemaking, the AQI for O3 was revised by setting an AQI value of 

23 100 equal to 0.075 ppm, 8-hour average, the level of the revised primary O3 standard. 
Draft O3 NPR –January 5, 2010 237 Deliberative, Do Not Quote or Cite

1 The other AQI breakpoints were also revised as follows: An AQI value of 50 is set at 

2 0.059 ppm; an AQI value of 150 was set at 0.095 ppm; and an AQI value of 200 was set 

3 at 0.115 ppm. All these levels are averaged over 8 hours. These levels were developed 

4 by making proportional adjustments to the other AQI breakpoints (i.e., AQI values of 50, 

5 150 and 200). 

6 The Agency recognizes the importance of revising the AQI in a timely manner to 

7 be consistent with any revisions to the NAAQS. Therefore, having proposed to set a new 

8 level for the 2008 primary 8-hour O3 standard in this action, EPA also proposes to 

9 finalize conforming changes to the AQI in connection with the Agency's final decision on 

10 the level of the primary O3 standard. These conforming changes would include setting 

11 the 100 level of the AQI at the same level as that set for the primary O3 standard resulting 

12 from this rulemaking, and also making proportional adjustments to AQI breakpoints at 

13 the lower end of the range (i.e., AQI values of 50, 150 and 200). EPA does not propose 

14 to change breakpoints at the higher end of the range (from 300 to 500), which would 

15 apply to state contingency plans or the Significant Harm Level (40 CFR 51.16), because 

16 the information from this reconsideration of the 2008 final rule does not inform decisions 

17 about breakpoints at those higher levels.

18 With respect to reporting requirements (40 CFR Part 58, §58.50), EPA proposes 

19 to require that the AQI be reported in all metropolitan and micropolitan statistical areas 

20 where O3 monitoring is required, as discussed below in section VI. The Agency solicits 

21 comments on our proposed approach to AQI reporting requirements. We are also 

22 revising 40 CFR Part 58, §58.50 (c) to require the reporting requirements to be based on 

23 the latest available census figures, rather than the most recent decennial U.S. census. 
Draft O3 NPR –January 5, 2010 238 Deliberative, Do Not Quote or Cite

1 This change is consistent with our current practice of using the latest population figures 

2 to make monitoring requirements more responsive to changes in population.

3

4 IV. Rationale for Proposed Decision on the Secondary Standard

5 As an initial matter, the Administrator notes that the 2008 final rule concluded 

6 that (1) the protection afforded by the 1997 secondary O3 standard was “not sufficient 

7 and that the standard needs to be revised to provide additional protection from known and 

8 anticipated adverse effects on sensitive natural vegetation and sensitive ecosystems, and 

9 that such a revised standard could also be expected to provide additional protection to 

10 sensitive ornamental vegetation” and (2) “that there is not adequate information to 

11 establish a separate secondary standard based on other effects of O3 on public welfare” 

12 (73 FR 16497). The Administrator is not reconsidering these aspects of the 2008 

13 decision, which are based on the reasons discussed in section IV.B of the 2008 final rule 

14 (73 FR 16489-16497). The Administrator also notes that the 2008 final rule concluded 

15 that it was appropriate to retain the O3 indicator for the secondary O3 standard. The 

16 Administrator is not reconsidering this aspect of the 2008 decision, which was based on 

17 the reasons discussed in sections IV.B and IV.C of the 2008 final rule (73 FR 16489-

18 16497). For these reasons, the Administrator is not reopening the 2008 decision with 

19 regard to the need to revise the 1997 secondary O3 standard to provide additional 

20 protection from known and anticipated adverse effects on sensitive natural vegetation and 

21 sensitive ecosystems, nor with regard to the appropriate indicator for the secondary

22 standard. Thus, the information that follows in this section specifically focuses on a 

23 reconsideration of the 8-hour secondary O3 standard set in the 2008 final rule for the 
Draft O3 NPR –January 5, 2010 239 Deliberative, Do Not Quote or Cite

1 purpose of determining whether and, if so, how to revise the form, averaging time, and 

2 level of the standard to provide appropriate protection from known and anticipated 

3 adverse effects on sensitive natural vegetation and sensitive ecosystems.

4 This section presents the rationale for the Administrator’s proposed decision that 

5 the secondary O3 standard, which was set identical to the revised primary standard in the 

6 2008 final rule, should instead be a new cumulative, seasonal standard. This standard is

7 expressed in terms of a concentration-weighted form commonly called W126, which uses

8 a sigmoidal weighting function to assign a weight to each hourly O3 concentration within 

9 the 12 hour daylight period (8:00 am to 8:00 pm). This daily ozone index is defined as 

10 follows:

 







i pm

i am

daily W wc Ci

i

8

8

126 , where Ci = hourly O3 at hour i, and c C

e

w 126 1 4403

1





11  .

12 The daily index values are then summed over each month within the O3 season, and the 

13 annual highest consecutive three month sum is determined. The proposed standard 

14 consists of the three-year average of this highest three-month statistic, set at a level 

15 within the range of 7 to 15 ppm-hours.

16 As discussed more fully below, the rationale for this proposed new standard is 

17 based on a thorough review, in the 2006 Criteria Document, of the latest scientific 

18 information on vegetation, ecological and other public welfare effects associated with the 

19 presence of O3 in the ambient air. This rationale also takes into account and is consistent 

20 with: (1) staff assessments of the most policy-relevant information in the 2006 Criteria 

21 Document and staff analyses of air quality, vegetation effects evidence, exposure, and 

22 risks, presented in the 2007 Staff Paper, upon which staff recommendations for revisions 

23 to the secondary O3 standard are based; (2) CASAC advice and recommendations as 
Draft O3 NPR –January 5, 2010 240 Deliberative, Do Not Quote or Cite

1 reflected in discussions of drafts of the 2006 Criteria Document and 2007 Staff Paper at 

2 public meetings, in separate written comments, and in CASAC's letters to the 

3 Administrator, both before and after the 2008 rulemaking, and (3) public comments 

4 received during development of these documents, either in conjunction with CASAC 

5 meetings or separately; and on the 2007 proposed rule, and (4) consideration of the 

6 degree of protection to vegetation potentially afforded by the 2008 8-hour standard.

7 In developing this rationale, the Administrator has again focused on direct O3

8 effects on vegetation, specifically drawing upon an integrative synthesis of the entire 

9 body of evidence (EPA, 2006a, chapter 9), published through early 2006, on the broad 

10 array of vegetation effects associated with the presence of O3 in the ambient air. In 

11 addition, because O3 can also indirectly affect other ecosystem components such as soils, 

12 water, and wildlife, and their associated ecosystem goods and services, through its effects 

13 on vegetation, a qualitative discussion of these other indirect impacts is also included, 

14 though these effects were not quantifiable at the time of the 2008 rulemaking. As 

15 discussed below in section IV.A, the peer-reviewed literature includes studies conducted 

in the U.S., Canada, Europe, and many other countries around the world.53 16 In

17 reconsidering this evidence, as was concluded in the 2008 rulemaking, and based on the 

18 body of scientific literature assessed in the 2006 Criteria Document, the Administrator

19 continues to believes that it is reasonable to conclude that a secondary standard protecting 

20 the public welfare from known or anticipated adverse effects to trees and native 

 

53 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.
Draft O3 NPR –January 5, 2010 241 Deliberative, Do Not Quote or Cite

1 vegetation would also afford increased protection from adverse effects to other 

2 environmental components relevant to the public welfare, including ecosystem services 

3 and function. Section IV.B focuses on considerations related to biologically relevant 

4 exposure indices. This rationale also draws upon the results of quantitative exposure and 

5 risk assessments, discussed below in section IV.C. Section IV.D focuses on the 

6 considerations upon which the Administrator’s proposed conclusions are based. 

7 Considerations regarding a cumulative seasonal standard as well as an 8-hour standard 

8 are discussed, and the rationale for the 2008 decision on the secondary standard and 

9 CASAC advice, given both prior to the development of the 2007 proposed rule and 

10 following the 2008 final rule, are summarized. Finally, the Administrator’s proposed 

11 conclusions on the secondary standard are presented. Section IV.E summarizes the 

12 proposed decision on the secondary O3 standard and the solicitation of public comments.

13 As with virtually any policy-relevant vegetation effects research, there is 

14 uncertainty in the characterization of vegetation effects attributable to exposure to 

15 ambient O3. As discussed below, however, research conducted since the 1997 review 

16 provides important information coming from field-based exposure studies, including free 

17 air, gradient, and biomonitoring surveys, in addition to the more traditional open top 

18 chamber (OTC) studies. Moreover, the newly available studies evaluated in the 2006 

19 Criteria Document have undergone intensive scrutiny through multiple layers of peer 

20 review and many opportunities for public review and comment. While important 

21 uncertainties remain, the review of the vegetation effects information has been extensive 

22 and deliberate. In the judgment of the Administrator, the intensive evaluation of the 
Draft O3 NPR –January 5, 2010 242 Deliberative, Do Not Quote or Cite

1 scientific evidence that has occurred provides an adequate basis for this reconsideration 

2 of the 2008 rulemaking.

3 A. Vegetation Effects Information 

4 This section outlines key information contained in the 2006 Criteria Document 

5 (chapter 9) and in the 2007 Staff Paper (chapter 7) on known or anticipated effects on 

6 public welfare associated with the presence of O3 in ambient air. The information 

7 highlighted here summarizes: (1) new information available in the 2008 rulemaking on 

8 potential mechanisms for vegetation effects associated with exposure to O3; (2) the nature 

9 of effects on vegetation that have been associated with exposure to O3 and consequent 

10 potential impacts on ecosystems; and (3) considerations in characterizing what constitutes 

11 an adverse welfare impact of O3.

12 Exposures to O3 have been associated quantitatively and qualitatively with a wide 

13 range of vegetation effects. The decision in the 1997 review to set a more protective 

14 secondary standard primarily reflected consideration of the quantitative information on 

15 vegetation effects available at that time, particularly growth impairment (e.g., biomass 

16 loss) in sensitive forest tree species during the seedling growth stage and yield loss in 

17 important commercial crops. This information, derived mainly using the open top 

18 chamber (OTC) exposure method, found cumulative, seasonal O3 exposures were most 

19 strongly associated with observed vegetation response. The 2006 Criteria Document 

20 discusses a number of additional studies that support and strengthen key conclusions 

21 regarding O3 effects on vegetation and ecosystems found in the previous Criteria 

22 Document (EPA, 1996a, 2006a), including further clarification of the underlying 

23 mechanistic and physiological processes at the sub-cellular, cellular, and whole system 

24 levels within the plant. More importantly, however, in the context of this review, new 
Draft O3 NPR –January 5, 2010 243 Deliberative, Do Not Quote or Cite

1 quantitative information is now available across a broader array of vegetation effects 

2 (e.g., growth impairment during seedlings, saplings and mature tree growth stages, visible 

3 foliar injury, and yield loss in annual crops) and across a more diverse set of exposure 

4 methods, including chamber, free air, gradient, model, and field-based observation. The 

5 non-chambered, field-based study results begin to address one of the key data gaps cited 

6 by EPA in the 1997 review. 

7 The following discussion of the policy-relevant science regarding vegetation 

8 effects associated with cumulative, seasonal exposures to ambient levels of O3 integrates 

9 information from the 2006 Criteria Document (chapter 9) and the 2007 Staff Paper 

10 (chapter 7). 

11 1. Mechanisms 

12 Scientific understanding regarding O3 impacts at the genetic, physiological, and 

13 mechanistic levels helps to explain the biological plausibility and coherence of the 

14 evidence for O3-induced vegetation effects and informs the interpretation of predictions 

15 of risk associated with vegetation response at ambient O3 exposure levels. In most cases, 

16 the mechanisms of response are similar regardless of the degree of sensitivity of the 

17 species. The evidence assessed in the 2006 Criteria Document (EPA, 2006a) regarding 

18 the O3-induced changes in physiology continues to support the information discussed in 

19 the 1997 review (EPA, 1996a, 2006a). In addition, during the last decade understanding 

20 of the cellular processes within plants has been further clarified and enhanced. This 

21 section reviews the key scientific conclusions identified in 1996 Criteria Document 

22 (EPA, 1996a), and incorporates recent information from the Criteria Document (EPA, 

23 2006a). This section describes: (1) plant uptake of O3, (2) O3-induced cellular to 
Draft O3 NPR –January 5, 2010 244 Deliberative, Do Not Quote or Cite

1 systemic response, (3) plant compensation and detoxification mechanisms, (4) O3-

2 induced changes to plant metabolism, and (5) plant response to chronic O3 exposures.

3 a. Plant Uptake of Ozone 

4 To cause injury, O3 must first enter the plant through openings in the leaves called 

5 stomata. Leaves exist in a three dimensional environment called the plant canopy, where 

6 each leaf has a unique orientation and receives a different exposure to ambient air, 

7 microclimatological conditions, and sunlight. In addition, a plant may be located within a 

8 stand of other plants which further modifies ambient air exchange with individual leaves. 

9 Not all O3 entering a plant canopy is absorbed into the leaf stomata, but may be adsorbed 

10 to other surfaces e.g., leaf cuticles, stems, and soil (termed non-stomatal deposition) or 

11 scavenged by reactions with intra-canopy biogenic VOCs and naturally occurring NOx 

12 emissions from soils. Because O3 does not typically penetrate the leaf’s cuticle, it must 

13 reach the stomatal openings in the leaf for absorption to occur. The movement of O3 and 

14 other gases such as CO2 into and out of leaves is controlled by stomatal guard cells that 

15 regulate the size of the stomatal apertures. These guard cells respond to a variety of 

16 internal species-specific factors as well as external site specific environmental factors 

17 such as light, temperature, humidity, CO2 concentration, soil fertility, water status, and in 

18 some cases, the presence of air pollutants, including O3. These modifying factors 

19 produce stomatal conductances that vary between leaves of the same plant, individuals 

20 and genotypes within a species as well as diurnally and seasonally. 

21 b. Cellular to Systemic Response 

22 Once inside the leaf, O3 can react with a variety of biochemical compounds that 

23 are exposed to the air spaces within the leaf or it can be dissolved into the water lining the 

24 cell wall of the air spaces. Once in the aqueous phase, O3 can be rapidly altered to form 
Draft O3 NPR –January 5, 2010 245 Deliberative, Do Not Quote or Cite

1 oxidative products that can diffuse more readily into and through the cell and react with 

2 many biochemical compounds. Early steps in a series of O3-induced events that can lead 

3 to leaf injury seems to involve alteration in cell membrane function, including membrane 

4 transport properties (EPA, 2006a) and/or reactions with organic molecules that in certain 

5 circumstances result in the generation of signaling compounds. The generation of such 

6 signaling compounds can lead to a cascade of events. One such signaling molecule is 

7 hydrogen peroxide (H2O2). The presence of higher-than-normal levels of H2O2 within the 

8 leaf is a potential trigger for a set of metabolic reactions that include those typical of the 

9 well documented “wounding” response or pathogen defense pathway generated by 

10 cutting of the leaf or by pathogen/insect attack. Ethylene is another compound produced 

11 when plants are subjected to biotic or abiotic stressors. Increased ethylene production by

12 plants exposed to O3 stress was identified as a consistent marker for O3 exposure in 

13 studies conducted decades ago (Tingey et al., 1976). 

14 c. Compensation and Detoxification 

15 Ozone injury will not occur if (1) the rate and amount of O3 uptake is small 

16 enough for the plant to detoxify or metabolize O3 or its metabolites or (2) the plant is able 

17 to repair or compensate for the O3 impacts (Tingey and Taylor, 1982; U.S. EPA, 1996a). 

18 With regard to the first, a few studies have documented direct stomatal closure or 

19 restriction in the presence of O3 in some species, which limits O3 uptake and potential 

20 subsequent injury. This response may be initiated ranging from within minutes to hours 

21 or days of exposure (Moldau et al., 1990; Dann and Pell, 1989; Weber et al., 1993). 

22 However, exclusion of O3 simultaneously restricts the uptake of CO2, which also limits 

23 photosynthesis and growth. In addition, antioxidants present in plants can effectively 

24 protect tissue against damage from low levels of oxidants by dissipating excess oxidizing 
Draft O3 NPR –January 5, 2010 246 Deliberative, Do Not Quote or Cite

1 power. Since 1996, the role of detoxification in providing a level of resistance to O3 has 

2 been further investigated. A number of antioxidants have been found in plants.

3 However, the pattern of changes in the amounts of these antioxidants varies greatly 

4 among different species and conditions. Most recent reports indicate that ascorbate 

5 within the cell wall provides the first significant opportunity for detoxification to occur. 

6 In spite of the new research, however, it is still not clear as to what extent detoxification 

7 protects against O3 injury. Specifically, data are needed on potential rates of antioxidant 

8 production, sub-cellular location(s) of antioxidants, and whether generation of these 

9 antioxidants in response to O3-induced stress potentially diverts resources and energy

10 away from other vital uses. Thus, the 2006 Criteria Document concludes that scientific 

11 understanding of the detoxification mechanisms is not yet complete and requires further 

12 investigation (EPA, 2006a).

13 Regarding the second, once O3 injury has occurred in leaf tissue, some plants are 

14 able to repair or compensate for the impacts. In general, plants have a variety of 

15 compensatory mechanisms for low levels of stress including reallocation of resources, 

16 changes in root/shoot ratio, production of new tissue, and/or biochemical shifts, such as 

17 increased photosynthetic capacity in new foliage and changes in respiration rates, 

18 indicating possible repair or replacement of damaged membranes or enzymes. Since 

19 these mechanisms are genetically determined, not all plants have the same complement of 

20 compensatory mechanisms or degree of tolerance, and these may vary over the life of the 

21 plant as not all stages of a plant’s development are equally sensitive to O3. At higher 

22 levels or over longer periods of O3 stress, some of these compensatory mechanisms, such 

23 as a reallocation of resources away from storage in the roots in favor of leaves or shoots, 
Draft O3 NPR –January 5, 2010 247 Deliberative, Do Not Quote or Cite

1 could occur at a cost to the overall health of the plant. However, it is not yet clear to 

2 what degree or how the use of plant resources for repair or compensatory processes 

3 affects the overall carbohydrate budget or subsequent plant response to O3 or other 

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

5 d. Changes to Plant Metabolism 

6 Ozone inhibits photosynthesis, the process by which plants produce energy rich 

7 compounds (e.g., carbohydrates) in the leaves. This impairment can result from direct 

8 impact to chloroplast function and/or O3-induced stomatal closure resulting in reduced 

9 uptake of CO2. A large body of literature published since 1996 has further elucidated the 

10 mechanism of effect of O3 within the chloroplast. Pell et al. (1997) showed that O3

11 exposure results in a loss of the central carboxylating enzyme that plays an important role 

12 in the production of carbohydrates. Due to its central importance, any decrease in this 

13 enzyme may have severe consequences for the plant’s productivity. Several recent 

14 studies have found that O3 has a greater effect as leaves age, with the greatest impact of 

15 O3 occurring on the oldest leaves (Fiscus et al., 1997; Reid and Fiscus, 1998; Noormets et 

16 al., 2001; Morgan et al., 2004). The loss of this key enzyme as a function of increasing 

17 O3 exposure is also linked to an early senescence or a speeding up of normal 

18 development leading to senescence. If total plant photosynthesis is sufficiently reduced, 

19 the plant will respond by reallocating the remaining carbohydrate at the level of the 

20 whole organism (EPA, 1996a, 2006a). This reallocation of carbohydrate away from the 

21 roots into above ground vegetative components can have serious implications for 

22 perennial species, as discussed below.

23 e. Plant Response to Chronic Ozone Exposures 
Draft O3 NPR –January 5, 2010 248 Deliberative, Do Not Quote or Cite

1 Though many changes that occur with O3 exposure can be observed within hours, 

2 or perhaps days, of the exposure, including those connected with wounding, other effects 

3 take longer to occur and tend to become most obvious after chronic seasonal exposures to 

4 low O3 concentrations. These lower chronic exposures have been linked to senescence or 

5 some other physiological response very closely linked to senescence. In perennial plant 

6 species, a reduction in carbohydrate storage in one year may result in the limitation of 

7 growth the following year (Andersen et al., 1997). Such “carry-over” effects have been 

8 documented in the growth of tree seedlings (Hogsett et al., 1989; Sasek et al., 1991; 

9 Temple et al., 1993; EPA, 1996a) and in roots (Andersen et al., 1991; EPA, 1996a). 

10 Though it is not fully understood how chronic seasonal O3 exposure affects long-term 

11 growth and resistance to other biotic and abiotic insults in long-lived trees, accumulation 

12 of these carry-over effects over time could affect survival and reproduction. 

13 2. Nature of Effects

14 Ozone injury at the cellular level can accumulate sufficiently to induce effects at

15 the level of a whole leaf or plant. These larger scale effects can include: reduced 

16 carbohydrate production and/or reallocation; reduced growth and/or reproduction; visible 

17 foliar injury and/or premature senescence; and reduced plant vigor. Much of what is now 

18 known about these O3-related effects, as summarized below, is based on research that 

19 was available in the 1997 review. Studies available in the 2008 rulemaking continue to 

20 support and expand this knowledge (EPA, 2006a). 

21 a. Carbohydrate Production and Allocation 

22 When total plant photosynthesis is sufficiently reduced, the plant will respond by

23 reallocating the remaining carbohydrate at the level of the whole organism. Many studies 
Draft O3 NPR –January 5, 2010 249 Deliberative, Do Not Quote or Cite

1 have demonstrated that root growth is more sensitive to O3 exposure than stem or leaf 

2 growth (EPA, 2006a). When fewer carbohydrates are present in the roots, less energy is

3 available for root-related functions such as acquisition of water and nutrients. In 

4 addition, by inhibiting photosynthesis and the amount of carbohydrates available for 

5 transfer to the roots, O3 can disrupt the association between soil fungi and host plants. 

6 Fungi in the soil form a symbiotic relationship with many terrestrial plants. For host 

7 plants, these fungi improve the uptake of nutrients, protect the roots against pathogens, 

8 produce plant growth hormones, and may transport carbohydrates from one plant to 

9 another (EPA, 1996a). These below ground effects have recently been documented in the 

10 field (Grulke et al., 1998; Grulke and Balduman, 1999). Data from a long-studied 

11 pollution gradient in the San Bernardino Mountains of southern California suggest that 

12 O3 substantially reduces root growth in natural stands of Ponderosa pine (Pinus 

13 ponderosa). Root growth in mature trees was decreased at least 87 percent in a high14 pollution site as compared to a low-pollution site (Grulke et al., 1998), and a similar 

15 pattern was found in a separate study with whole-tree harvest along this gradient (Grulke

16 and Balduman, 1999). Though effects on other ecosystem components were not 

17 examined, a reduction of root growth of this magnitude could have significant 

18 implications for the below-ground communities at those sites. Because effects on leaf 

19 and needle carbohydrate content under O3 stress can range from a reduction (Barnes et 

20 al., 1990; Miller et al., 1989), to no effect (Alscher et al., 1989), to an increase (Luethy21 Krause and Landolt, 1990), studies that examine only above-ground vegetative 

22 components may miss important O3-induced changes below ground. These below-
Draft O3 NPR –January 5, 2010 250 Deliberative, Do Not Quote or Cite

1 ground changes could signal a shift in nutrient cycling with significance at the ecosystem 

2 level (Young and Sanzone, 2002). 

3 b. Growth Effects on Trees

4 Studies comparing the O3-related growth response of different vegetation types 

5 (coniferous and deciduous) and growth stages (e.g., seedling and mature) have 

6 established that on average, individual coniferous trees are less sensitive than deciduous 

7 trees, and deciduous trees are generally less sensitive to O3 than most annual plants, with 

8 the exception of a few fast growing deciduous tree species (e.g., quaking aspen, black 

9 cherry, and cottonwood), which are highly sensitive and, in some cases, as much or more 

10 sensitive to O3 than sensitive annual plants. In addition, studies have shown that the 

11 relationship between O3 sensitivity in seedling and mature growth stages of trees can vary

12 widely, with seedling growth being more sensitive to O3 exposures in some species, 

13 while in others, the mature growth stage is the more O3 sensitive. In general, mature 

14 deciduous trees are likely to be more sensitive to O3 than deciduous seedlings, and

15 mature evergreen trees are likely to be less sensitive to O3 than their seedling

16 counterparts. Based on these results, stomatal conductance, O3 uptake, and O3 effects 

17 cannot be assumed to be equivalent in seedlings and mature trees.

18 In the 1997 review (EPA, 1996b), analyses of the effects of O3 on trees were 

19 limited to 11 tree species for which concentration-response (C-R) functions for the 

20 seedling growth stage had been developed from OTC studies conducted by the National 

21 Health and Environmental Effects Research Lab, Western Ecology Division (NHEERL22 WED). A number of replicate studies were conducted on these species, leading to a total 

23 of 49 experimental cases. The 2007 Staff Paper presented a graph of the composite 
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1 regression equation that combines the results of the C-R functions developed for each of 

2 the 49 cases. The NHEERL-WED study predicted relative biomass loss at various 

3 exposure levels in terms of a 12-hour W126. For example, 50 percent of the tree seedling 

4 cases would be protected from greater than 10 percent biomass loss at a 3-month, 12-hour

5 W126 of approximately 24 ppm-hour, while 75 percent of cases would be protected from 

6 10 percent biomass loss at a 3-month, 12-hour W126 level of approximately 16 ppm7 hour.

8 Since the 1997 review, only a few studies have developed C-R functions for 

9 additional tree seedling species (EPA, 2006a). One such study is of particular importance 

10 because it documented growth effects in the field of a similar magnitude as those

11 previously seen in OTC studies but without the use of chambers or other fumigation

12 methods (Gregg et al., 2003). This study placed eastern cottonwood (Populus deltoides) 

13 saplings at sites along a continuum of ambient O3 exposures that gradually increased 

14 from urban to rural areas in the New York City area (Gregg et al., 2003). Eastern 

15 cottonwood is a fast growing O3 sensitive tree species that is important ecologically along 

16 streams and commercially for pulpwood, furniture manufacturing, and as a possible new 

17 source for energy biomass (Burns and Hankola, 1990). Gregg et al. (2003) found that the 

18 cottonwood saplings grown in urban New York City grew faster than saplings grown in 

19 downwind rural areas. Because these saplings were grown in pots with carefully

20 controlled soil nutrient and moisture levels, the authors were able to control for most of 

21 the differences between sites. After carefully considering these and other factors, the

22 authors concluded the primary explanation for the difference in growth was the gradient 

23 of cumulative O3 exposures that increased as one moved downwind from urban to less 
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1 urban and more rural sites. It was determined that the lower O3 exposure within the city

2 center was due to NOx titration reactions which removed O3 from the ambient air. The 

3 authors were able to reproduce the growth responses observed in the field in a companion 

4 OTC experiment, confirming O3 as the stressor inducing the growth loss response (Gregg 

5 et al., 2003). 

6 Another recent set of studies employed a modified Free Air CO2 Enrichment 

7 (FACE) methodology to expose vegetation to elevated O3 without the use of chambers. 

8 This exposure method was originally developed to expose vegetation to elevated levels of 

9 CO2, but was later modified to include O3 exposure in Illinois (SoyFACE) and Wisconsin 

10 (AspenFACE) for soybean and deciduous trees, respectively (Dickson et al., 2000; 

11 Morgan et al., 2004). The FACE method releases gas (e.g., CO2, O3) from a series of 

12 orifices placed along the length of the vertical pipes surrounding a circular field plot and 

13 uses the prevailing wind to distribute it. This exposure method has many characteristics 

14 that differ from those associated with the OTC. Most significantly, this exposure method 

15 more closely replicates conditions in the field than do OTCs. This is because, except for 

16 O3 levels which are varied across co-located plots, plants are exposed to the same 

17 ambient growing conditions that occur naturally in the field (e.g., location-specific 

18 pollutant mixtures; climate conditions such as light, temperature and precipitation; insect 

19 pests, pathogens). By using one of several co-located plots as a control (e.g., receives no 

20 additional O3), and by exposing the other rings to differing levels of elevated O3, the 

21 growth response signal that is due solely to the change in O3 exposure can be clearly

22 determined. Furthermore, the FACE system can expand vertically with the growth of 
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1 trees, allowing for exposure experiments to span numerous years, an especially useful 

2 capability in forest research. 

3 On the other hand, the FACE methodology also has the undesirable characteristic 

4 of potentially creating hotspots near O3 gas release orifices or gradients of exposure in the 

5 outer ring of trees within the plots, such that averaging results across the entire ring 

6 potentially overestimates the response. In recognition of this possibility, researchers at 

7 the AspenFACE experimental site only measured trees in the center core of each ring, 

8 (e.g., at least 5-6 meters away from the emission sites of O3) (Dickson et al 2000, 

9 Karnosky et al. 2005). By taking this precaution, it is unlikely that their measurements 

10 were influenced by any potential hotspots or gradients of exposure within the FACE 

11 rings. Taking all of the above into account, results from the Wisconsin FACE site on 

12 quaking aspen appear to demonstrate that the detrimental effects of O3 exposure seen on 

13 tree growth and symptom expression in OTCs can be observed in the field using this 

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

15 The 2007 Staff Paper thus concluded that the combined evidence from the 

16 AspenFACE and Gregg et al. (2003) field studies provide compelling and important 

17 support for the appropriateness of continued use of the C-R functions derived using OTC 

18 from the NHEERL-WED studies to estimate risk to these tree seedlings under ambient 

19 field exposure conditions. These studies make a significant contribution to the coherence 

20 of the weight of evidence available in this review and provide additional evidence that 

21 O3-induced effects observed in chambers also occur in the field. 

22 Trees and other perennials, in addition to cumulating the effects of O3 exposures 

23 over the annual growing season, can also cumulate effects across multiple years. It has 
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1 been reported that effects can “carry over” from one year to another (EPA, 2006a). 

2 Growth affected by a reduction in carbohydrate storage in one year may result in the 

3 limitation of growth in the following year (Andersen, et al., 1997). Carry-over effects 

4 have been documented in the growth of some tree seedlings (Hogsett et al. 1989; Simini 

5 et al., 1992; Temple et al., 1993) and in roots (Andersen et al., 1991; EPA, 1996a). On 

6 the basis of past and recent OTC and field study data, ambient O3 exposures that occur 

7 during the growing season in the United States are sufficient to potentially affect the 

8 annual growth of a number of sensitive seedling tree species. However, because most 

9 studies do not take into account the possibility of carry over effects on growth in 

10 subsequent years, the true implication of these annual biomass losses may be missed. It 

11 is likely that under ambient exposure conditions, some sensitive trees and perennial 

12 plants could experience compounded impacts that result from multiple year exposures.

13 c. Visible Foliar Injury 

14 Cellular injury to leaves due to exposure to O3 can and often does become visible. 

15 Acute injury usually appears within 24 hours after exposure to O3 and, depending on 

16 species, can occur under a range of exposures and durations from 0.040 ppm for a period 

17 of 4 hours to 0.410 ppm for 0.5 hours for crops and 0.060 ppm for 4 hours to 0.510 ppm 

18 for 1 hour for trees and shrubs (Jacobson, 1977). Chronic injury may be mild to severe. In 

19 some cases, cell death or premature leaf senescence may occur. The significance of O3

20 injury at the leaf and whole plant levels depends on how much of the total leaf area of the 

21 plant has been affected, as well as the plant’s age, size, developmental stage, and degree 

22 of functional redundancy among the existing leaf area. As a result, it is not presently 
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1 possible to determine, with consistency across species and environments, what degree of 

2 injury at the leaf level has significance to the vigor of the whole plant. 

3 The presence of visible symptoms due to O3 exposures can, however, by itself, 

4 represent an adverse impact to the public welfare. Specifically, it can reduce the market 

5 value of certain leafy crops (such as spinach, lettuce), impact the aesthetic value of 

6 ornamentals (such as petunia, geranium, and poinsettia) in urban landscapes, and affect 

7 the aesthetic value of scenic vistas in protected natural areas such as national parks and 

8 wilderness areas. Many businesses rely on healthy looking vegetation for their 

9 livelihoods (e.g., horticulturalists, landscapers, Christmas tree growers, farmers of leafy

10 crops) and a variety of ornamental species have been listed as sensitive to O3 (Abt

11 Associates Inc, 1995). Though not quantified, there is likely some level of economic 

12 impact to businesses and homeowners from O3-related injury on sensitive ornamental 

13 species due to the cost associated with more frequent replacement and/or increased 

14 maintenance (fertilizer or pesticide application). In addition, because O3 not only results 

15 in discoloration of leaves but can lead to more rapid senescence (early shedding of 

16 leaves) there potentially could be some lost tourist dollars at sites where fall foliage is 

17 less available or attractive. 

18 The use of sensitive plants as biological indicators to detect phytotoxic levels of 

19 O3 is a longstanding and effective methodology (Chappelka and Samuelson, 1998; 

20 Manning and Krupa, 1992). Each bioindicator exhibits typical O3 injury symptoms when 

21 exposed under appropriate conditions. These symptoms are considered diagnostic as they

22 have been verified in exposure-response studies under experimental conditions. In recent 

23 years, field surveys of visible foliar injury symptoms have become more common, with 
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1 greater attention to the standardization of methods and the use of reliable indicator 

2 species (Campbell et al., 2000; Smith et al., 2003). Specifically, the Unites States Forest 

3 Service (USFS) through the Forest Health Monitoring Program (FHM) (1990 - 2001) and 

4 currently the Forest Inventory and Analysis (FIA) Program collects data regarding the 

5 incidence and severity of visible foliar injury on a variety of O3 sensitive plant species 

6 throughout the U.S. (Coulston et al. 2003, 2004; Smith et al. 2003). 

7 Since the conclusion of the 1997 review, the FIA monitoring program network 

8 and database has continued to expand. This network continues to document foliar injury

9 symptoms in the field under ambient exposure conditions. Recent survey results show 

10 that O3-induced foliar injury incidence is widespread across the country. The visible 

11 foliar injury indicator has been identified as a means to track O3 exposure stress trends in 

12 the nation’s natural plant communities as highlighted in EPA’s most recent Report on the 

13 Environment (EPA, 2003a; http://www.epa.gov/indicators/roe). 

14 Previous Criteria Documents have noted the difficulty in relating visible foliar 

15 injury symptoms to other vegetation effects such as individual tree growth, stand growth, 

16 or ecosystem characteristics (EPA, 1996a) and this difficulty remains to the present day

17 (EPA, 2006a). It is important to note that direct links between O3 induced visible foliar 

18 injury symptoms and other adverse effects are not always found. Therefore, visible foliar 

19 injury cannot serve as a reliable surrogate measure for other O3-related vegetation effects 

20 because other effects (e.g., biomass loss) have been reported with and without visible 

21 injury. In some cases, visible foliar symptoms have been correlated with decreased 

22 vegetative growth (Karnosky et al., 1996; Peterson et al., 1987; Somers et al., 1998) and 

23 with impaired reproductive function (Black et al., 2000; Chappelka, 2002). Therefore, 
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1 the lack of visible injury should not be construed to indicate a lack of phytotoxic 

2 concentrations of O3 nor absence of other non-visible O3 effects.

3 d. Reduced Plant Vigor 

4 Though O3 levels over most of the U.S. are not high enough to kill vegetation 

5 directly, current levels have been shown to reduce the ability of many sensitive species 

6 and genotypes within species to adapt to or withstand other environmental stresses. 

7 These O3 effects may include increased susceptibility to freezing temperatures, increased 

8 vulnerability to pest infestations and/or root disease, and compromised ability to compete 

9 for available resources. As an example of the latter, when species with differing O3-

10 sensitivities occur together, O3-sensitive species may experience a greater reduction in 

11 growth than more O3-tolerant species, which then can better compete for available 

12 resources. The result of such above effects can produce a loss in plant vigor in O3-

13 sensitive species that over time may lead to premature plant death.

14 e. Ecosystems 

15 Ecosystems are comprised of complex assemblages of organisms and the physical 

16 environment with which they interact. Each level of organization within an ecosystem 

17 has functional and structural characteristics. At the ecosystem level, functional 

18 characteristics include, but are not limited to, energy flow; nutrient, hydrologic, and 

19 biogeochemical cycling; and maintenance of food chains. The sum of the functions 

20 carried out by ecosystem components provides many benefits to humankind, as in the 

21 case of forest ecosystems (Smith, 1992). Some of these benefits, also termed “ecosystem 

22 goods and services”, include food, fiber production, aesthetics, genetic diversity, 

23 maintenance of water quality, air quality, and climate, and energy exchange. A 
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1 conceptual framework for discussing the effects of stressors, including air pollutants such 

2 as O3, on ecosystems was developed by the EPA Science Advisory Board (Young and 

3 Sanzone, 2002). In this report, the authors identify six essential ecological attributes 

4 (EEAs) of ecosystems including landscape condition, biotic condition, chemical/physical 

5 condition, ecological processes, hydrology/geomorphology, and natural disturbance 

6 regime. Each EEA is depicted as one of six triangles that together build a hexagon. On 

7 the outside of each triangle is a list of stressors that can act on the EEA. Tropospheric O3

8 is listed as a stressor of both biotic condition and the chemical/physical condition of 

9 ecosystems. As each EEA is linked to all the others, it is clearly envisioned in this 

10 framework that O3 could either directly or indirectly impact all of the EEAs associated 

11 with an ecosystem that is being stressed by O3. 

12 Vegetation often plays an influential role in defining the structure and function of 

13 an ecosystem, as evidenced by the use of dominant vegetation forms to classify many 

14 types of natural ecosystems, e.g., tundra, wetland, deciduous forest, and conifer forest. 

15 Plants simultaneously inhabit both above-and below-ground environments, integrating 

16 and influencing key ecosystem cycles of energy, water, and nutrients. When a sufficient 

17 number of individual plants within a community have been affected, O3-related effects 

18 can be propagated up to ecosystem-level effects. Thus, through its impact on vegetation, 

19 O3 can be an important ecosystem stressor. 

20 i. Potential Ozone Alteration of Ecosystem Structure and Function

21 The 2006 Criteria Document outlines seven case studies where O3 effects on 

22 ecosystems have either been documented or are suspected. The oldest and clearest 

23 example involves the San Bernardino Mountain forest ecosystem in California. This 
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1 system experienced chronic high O3 exposures over a period of 50 or more years. The 

2 O3-sensitive and co-dominant species of ponderosa and Jeffrey pine demonstrated severe 

3 levels of foliar injury, premature senescence, and needle fall that decreased the 

4 photosynthetic capacity of stressed pines and reduced the production of carbohydrates 

5 resulting in a decrease in radial growth and in the height of stressed trees. It was also 

6 observed that ponderosa and Jeffrey pines with slight to severe crown injury lost basal 

7 area in relation to competing species that are more tolerant to O3. Due to a loss of vigor, 

8 these trees eventually succumbed to the bark beetle, leading to elevated levels of tree 

9 death. Increased mortality of susceptible trees shifted the community composition 

10 towards white fir and incense cedar, effectively reversing the development of the normal 

11 fire climax mixture dominated by ponderosa and Jeffrey pines, and leading to increased 

12 fire susceptibility. At the same time, numerous other organisms and processes were also 

13 affected either directly or indirectly, including successional patterns of fungal microflora 

14 and their relationship to the decomposer community. Nutrient availability was influenced 

15 by the heavy litter and thick needle layer under stands with the most severe needle injury

16 and defoliation. In this example, O3 appeared to be a predisposing factor that led to 

17 increased drought stress, windthrow, root diseases, and insect infestation (Takemoto et 

18 al., 2001). Thus, through its effects on tree water balance, cold hardiness, tolerance to 

19 wind, and susceptibility to insect and disease pests, O3 potentially impacted the 

20 ecosystem-related EEA of natural disturbance regime (e.g., fire, erosion). Although the 

21 role of O3 was extremely difficult to separate from other confounding factors, such as 

22 high nitrogen deposition, there is evidence that this shift in species composition has 

23 altered the structure and dynamics of associated food webs (Pronos et al., 1999) and 
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1 carbon (C) and nitrogen (N) cycling (Arbaugh et al., 2003). Ongoing and new research in 

2 this important ecosystem is needed to reveal the extent to which ecosystem services have 

3 been affected and to what extent strong causal linkages between historic and/or current 

4 ambient O3 exposures and observed ecosystem-level effects can be made. 

5 Ozone has also been reported to be a selective pressure among sensitive tree 

6 species (e.g., eastern white pine) in the east. The nature of community dynamics in 

7 eastern forests is different, however, than in the west, consisting of a wider diversity of 

8 species and uneven aged stands, and the O3 levels are less severe. Therefore, lower level 

9 chronic O3 stress in the east is more likely to produce subtle long-term forest responses 

10 such as shifts in species composition, rather than wide-spread community degradation. 

11 Some of the best-documented studies of population and community response to 

12 O3 effects are the long-term studies of common plantain (Plantago major) in native plant 

13 communities in the United Kingdom (Davison and Reiling, 1995; Lyons et al., 1997; 

14 Reiling and Davison, 1992c). Elevated O3 significantly decreased the growth of sensitive 

15 populations of common plantain (Pearson et al., 1996; Reiling and Davison, 1992a, b; 

16 Whitfield et al., 1997) and reduced its fitness as determined by decreased reproductive 

17 success (Pearson et al., 1996; Reiling and Davison, 1992a). While spatial comparisons of 

18 population responses to O3 are complicated by other environmental factors, rapid changes 

19 in O3 resistance were imposed by ambient levels and variations in O3 exposure (Davison 

20 and Reiling, 1995). Specifically, in this case study, it appeared that O3-sensitive 

21 individuals are being removed by O3 stress and the genetic variation represented in the 

22 population could be declining. If genetic diversity and variation is lost in ecosystems, 

23 there may be increased vulnerability of the system to other biotic and abiotic stressors, 
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1 and ultimately a change in the EEAs and associated services provided by those 

2 ecosystems.

3 Recent free-air exposure experiments have also provided new insight into how O3

4 may be altering ecosystem structure and function (Karnosky et al., 2005). For example, a 

5 field O3 exposure experiment at the AspenFACE site in Wisconsin (described in section 

6 IV.A.2.b. above) was designed to examine the effects of both elevated CO2 and O3 on 

7 mixed stands of aspen (Populus tremuloides), birch (Betula papyrifera), and sugar maple 

8 (Acer saccharum) that are characteristic of Great Lakes aspen-dominated forests 

9 (Karnosky et al., 2003; Karnosky et al., 1999). They found evidence that the effects on 

10 above- and below-ground growth and physiological processes have cascaded through the 

11 ecosystem, even affecting microbial communities (Larson et al., 2002; Phillips et al., 

12 2002). This study also confirmed earlier observations of O3-induced changes in trophic 

13 interactions involving keystone tree species, as well as important insect pests and their 

14 natural enemies (Awmack et al., 2004; Holton et al., 2003; Percy et al., 2002). 

15 Collectively these examples suggest that O3 is an important stressor in natural 

16 ecosystems, but it is difficult to quantify the contribution of O3 due to the combination of 

17 other stresses present in ecosystems. In most cases, because only a few components in 

18 each of these ecosystems have been examined and characterized for O3 effects, the full 

19 extent of ecosystem changes in these example ecosystems is not fully understood. 

20 Clearly, there is a need for highly integrated ecosystem studies that specifically 

21 investigate the effect of O3 on ecosystem structure and function in order to fully

22 determine the extent to which O3 is altering ecosystem services. Continued research, 
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1 employing new approaches, will be necessary to fully understand the extent to which O3

2 is affecting ecosystem services.

3 ii. Effects on Ecosystem Services and Carbon Sequestration 

4 Since it has been established that O3 affects photosynthesis and growth of plants, 

5 O3 is most likely affecting the productivity of forest ecosystems. Therefore, it is 

6 desirable to link effects on growth and productivity to essential ecosystem services. 

7 However, it is very difficult to quantify ecosystem-level productivity losses because of 

8 the amount of complexity in scaling from the leaf-level or individual plant to the 

9 ecosystem level, and because not all organisms in an ecosystem are equally affected by 

10 O3.

11 Terrestrial ecosystems are important in the Earth's carbon (C) balance and could 

12 help offset emissions of CO2 by humans if anthropogenic C is sequestered in vegetation 

13 and soils. The annual increase in atmospheric CO2 is less than the total inputs from fossil 

14 fuel burning and land use changes (Prentice et al., 2001), and much of this discrepancy is

15 thought to be attributable to CO2 uptake by plant photosynthesis (Tans & White, 1998). 

16 Temperate forests of the northern hemisphere have been estimated to be a net sink of

17 about 0.6 to 0.7 petagrams (Pg) C per year (Goodale et al. 2002). Ozone interferes with 

18 photosynthesis, causes some plants to senesce leaves prematurely, and in some cases, 

19 reduces allocation to stem and root tissue. Thus, O3 decreases the potential for C 

20 sequestration. For the purposes of this discussion, C sequestration is defined as the net 

21 exchange of carbon by the terrestrial biosphere. However, long-term storage in the soil 

22 organic matter is considered to be the most stable form of C storage in ecosystems.
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1 In a study including all ecosystem types, Felzer et al. (2004), estimated that U.S. 

2 net primary production (net flux of C into an ecosystem) was decreased by 2.6-6.8

3 percent due to O3 pollution in the late 1980's to early 1990's. Ozone not only reduces C 

4 sequestration in existing forests, it can also affect reforestation projects (Beedlow et al. 

5 2004). This effect, in turn, has been found to ultimately inhibit C sequestration in forest 

6 soils which act as long-term C storage (Loya et al., 2003; Beedlow et al. 2004). The 

7 interaction of rising O3 pollution and rising CO2 concentrations in the coming decades 

8 complicates predictions of future sequestration potential. Models generally predict that, 

9 in the future, C sequestration will increase with increasing CO2, but often do not account 

10 for the decrease in productivity due to the local effects of current or potentially increasing 

11 levels of tropospheric O3. In the presence of high O3 levels, the stimulatory effect of 

12 rising CO2 concentrations on forest productivity has been estimated to be reduced by

13 more that 20 percent (Tingey et al., 2001; Ollinger et al. 2002; Karnosky et al., 2003). 

14 In summary, it would be anticipated that meeting lower O3 standards would 

15 increase the amount of CO2 uptake by many ecosystems in the U.S. However, the 

16 amount of this improvement would be heavily dependent on the species composition of 

17 those ecosystems. Many ecosystems in the U.S. do have O3 sensitive plants. For, 

18 example forest ecosystems with dominant species such as aspen or ponderosa pine would 

19 be expected to increase CO2 uptake more with lower O3 than forests with more O3

20 tolerant species.

21 A recent critique of the secondary NAAQS review process published in the report 

22 by the National Academy of Sciences on Air Quality Management in the United States 

23 (NRC, 2004) stated that “EPA’s current practice for setting secondary standards for most 
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1 criteria pollutants does not appear to be sufficiently protective of sensitive crops and 

2 ecosystems...” This report made several specific recommendations for improving the 

3 secondary NAAQS process and concluded that “There is growing evidence that tighter 

4 standards to protect sensitive ecosystems in the United States are needed....” An effort 

5 has been recently initiated within the Agency to identify indicators of ecological 

6 condition whose responses can be clearly linked to changes in air quality that are 

7 attributable to Agency environmental programs. Using a single indicator to represent the 

8 complex linkages and dynamic cycles that define ecosystem condition will always have 

9 limitations. With respect to O3-related impacts on ecosystem condition, only two 

10 candidate indicators, foliar injury (as described above) and radial growth in trees, have 

11 been suggested. Thus, while at the present time, most O3-related effects on ecosystems 

12 must be inferred from observed or predicted O3-related effects on individual plants, 

13 additional research at the ecosystem level could identify new indicators and/or establish 

14 stronger causal linkages between O3-induced plant effects and ecosystem condition. 

15 f. Yield Reductions in Crops

16 Ozone can interfere with carbon gain (photosynthesis) and allocation of carbon 

17 with or without the presence of visible foliar injury. As a result of decreased 

18 carbohydrate availability, fewer carbohydrates are available for plant growth, 

19 reproduction, and/or yield. Recent studies have further confirmed and demonstrated O3

20 effects on different stages of plant reproduction, including pollen germination, pollen 

21 tube growth, fertilization, and abortion of reproductive structures, as reviewed by Black 

22 et al. (2000). For seed-bearing plants, these reproductive effects will culminate in 

23 reduced seed production or yield. 
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1 As described in the 1997 review and again in the 2006 Criteria Document and 

2 2007 Staff Paper, the National Crop Loss Assessment Network (NCLAN) studies 

3 undertaken in the early to mid-1980's provide the largest, most uniform database on the 

4 effects of O3 on agricultural crop yields. The NCLAN protocol was designed to produce 

5 crop exposure-response data representative of the areas in the U.S. where the crops were 

6 typically grown. In total, 15 species (e.g., corn, soybean, winter wheat, tobacco, 

7 sorghum, cotton, barley, peanuts, dry beans, potato, lettuce, turnip, and hay [alfalfa, 

8 clover, and fescue]), accounting for greater than 85 percent of U.S. agricultural acreage 

9 planted at that time, were studied. Of these 15 species, 13 species including 38 different 

10 cultivars were combined in 54 cases representing unique combinations of cultivars, sites, 

11 water regimes, and exposure conditions. Crops were grown under typical farm 

12 conditions and exposed in open-top chambers to ambient O3, sub-ambient O3, and above 

13 ambient O3. Robust C-R functions were developed for each of these crop species. These 

14 results showed that 50 percent of the studied cases would be protected from greater than 

15 10 percent yield loss at a W126 level of 21 ppm-hour, while a W126 of 13 ppm-hour 

16 would provide protection for 75 percent of the cases studied from greater than 10 percent

17 yield loss. 

18 Recent studies continue to find yield loss levels in crop species studied previously

19 under NCLAN that reflect the earlier findings. In other words, there has been no 

20 evidence that crops are becoming more tolerant of O3 (EPA, 2006a). For cotton, some 

21 newer varieties have been found to have higher yield loss due to O3 compared to older 

22 varieties (Olszyk et al., 1993, Grantz and McCool, 1992). In a meta-analysis of 53 

23 studies, Morgan et al. (2003) found consistent deleterious effects of O3 exposures on 
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1 soybean from studies published between 1973 and 2001. Further, early results from the 

2 field-based exposure experiment SoyFACE in Illinois indicate a lack of any apparent 

3 difference in the O3 tolerance of old and recent cultivars of soybean in a study of 22 

4 soybean varieties (Long et al., 2002). Thus, the 2007 Staff Paper concluded that the 

5 recent scientific literature continues to support the conclusions of the 1996 Criteria 

6 Document that ambient O3 concentrations are reducing the yield of major crops in the 

7 U.S.

8 In addition to the effects described on annual crop species, several studies 

9 published since the 1997 review have focused on perennial forage crops (EPA, 2006a). 

10 These recent results confirm that O3 is also impacting yields and quality of multiple-year 

11 forage crops at sufficient magnitude to have nutritional and possibly economic 

12 implications to their use as ruminant animal feed at O3 exposures that occur in some 

13 years over large areas of the U.S. 

14 3. Adversity of Effects

15 The 2007 Staff Paper recognized that the statute requires that a secondary

16 standard be protective against “adverse” O3 effects, not all identifiable O3-induced 

17 effects. In considering what constitutes a vegetation effect that is adverse to the public 

18 welfare, the 2007 Staff Paper recognizes that O3 can cause a variety of vegetation effects, 

19 beginning at the level of the individual cell and accumulating up to the level of whole 

20 leaves, plants, plant populations, communities and whole ecosystems, not all of which 

21 have been classified in past reviews as “adverse” to public welfare. 

22 Previous reviews have classified O3 vegetation effects as either “injury” or 

23 “damage” to help in determining adversity. Specifically, “injury” is defined as 

24 encompassing all plant reactions, including reversible changes or changes in plant 
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1 metabolism (e.g., altered photosynthetic rate), altered plant quality, or reduced growth, 

2 that does not impair the intended use or value of the plant (Guderian, 1977). In contrast, 

3 “damage” has been defined to include those injury effects that reach sufficient magnitude 

4 as to also reduce or impair the intended use or value of the plant. Examples of effects 

5 that are classified as damage include reductions in aesthetic values (e.g., foliar injury in 

6 ornamental species) as well as losses in terms of weight, number, or size of the plant part 

7 that is harvested (reduced yield or biomass production). Yield loss also may include 

8 changes in crop quality, i.e., physical appearance, chemical composition, or the ability to 

9 withstand storage, while biomass loss includes slower growth in species harvested for 

10 timber or other fiber uses. While this construct has proved useful in the past, it appears to 

11 be most useful in the context of evaluating effects on single plants or species grown in 

12 monocultures such as agricultural crops or managed forests. It is less clear how it might 

13 apply to potential effects on natural forests or entire ecosystems when O3-induced species 

14 level impacts lead to shifts in species composition and/or associated ecosystem services 

15 such as nutrient cycling or hydrologic cycles, where the intended use or value of the 

16 system has not been specifically identified.

17 A more recent construct for assessing risks to forests described in Hogsett et al. 

18 (1997) suggests that “adverse effects could be classified into one or more of the following 

19 categories: (1) economic production, (2) ecological structure, (3) genetic resources, and 

20 (4) cultural values.” This approach expands the context for evaluating the adversity of 

21 O3-related effects beyond the species level. Another recent publication, A Framework for 

22 Assessing and Reporting on Ecological Condition: an SAB report (Young and Sanzone, 

23 2002), provides additional support for expanding the consideration of adversity beyond 
Draft O3 NPR –January 5, 2010 268 Deliberative, Do Not Quote or Cite

1 the species level by making explicit the linkages between stress- related effects (e.g., O3

2 exposure) at the species level and at higher levels within an ecosystem hierarchy. Taking 

3 this recent literature into account, the 2007 Staff Paper concludes that a determination of 

4 what constitutes an “adverse” welfare effect in the context of the secondary NAAQS 

5 review can appropriately occur within this broader paradigm.

6 B. Biologically Relevant Exposure Indices

7 The 2006 Criteria Document concluded that O3 exposure indices that cumulate 

8 differentially weighted hourly concentrations are the best candidates for relating exposure 

9 to plant growth responses. This conclusion follows from the extensive evaluation of the 

10 relevant studies in the 1996 Criteria Document (EPA, 1996a) and the recent evaluation of

11 studies that have been published since that time. The following selections, taken from the 

12 1996 Criteria Document (EPA, 1996a, section 5.5), further elucidate the depth and 

13 strength of these conclusions. Specifically, with respect to the importance of taking into 

14 account exposure duration, the 1996 Criteria Document stated, “when O3 effects are the 

15 primary cause of variation in plant response, plants from replicate studies of varying 

16 duration showed greater reductions in yield or growth when exposed for the longer 

17 duration” and “the mean exposure index of unspecified duration could not account for the 

18 year-to-year variation in response” (EPA, 1996a, pg. 5-96). Further, “because the mean 

19 exposure index treats all concentrations equally and does not specifically include an 

20 exposure duration component, the use of a mean exposure index for characterizing plant 

21 exposures appears inappropriate for relating exposure with vegetation effects” (EPA, 

22 1996a, pg. 5-88). Regarding the relative importance of higher concentrations than lower 

23 in determining plant response, the 1996 Criteria Document concluded that “the ultimate 
Draft O3 NPR –January 5, 2010 269 Deliberative, Do Not Quote or Cite

1 impact of long-term exposures to O3 on crops and seedling biomass response depends on 

2 the integration of repeated peak concentrations during the growth of the plant” (EPA, 

3 1996a, pg. 5-104). Further, “at this time, exposure indices that weight the hourly O3

4 concentrations differentially appear to be the best candidates for relating exposure with 

5 predicted plant response” (EPA, 1996a, pgs. 5-136). 

6 At the conclusion of the 1997 review, the biological basis for a cumulative, 

7 seasonal form was not in dispute. There was general agreement between EPA and

8 CASAC, based on their review of the air quality criteria, that a cumulative, seasonal form 

9 was more biologically based than the then current 1-hour and newly proposed 8-hour 

10 average form. However, in selecting a specific form appropriate for a secondary

11 standard, there was less agreement. An evaluation of the performance of several 

12 cumulative seasonal forms in predicting plant response data taken from OTC experiments 

13 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 SUM0654 14

15 and W126, in the absence of biological evidence to distinguish between them, EPA based 

16 its decision on both science and policy considerations. Specifically, these were: (1) all 

17 cumulative, peak-weighted exposure indices considered, including W126 and SUM06, 

18 were about equally good as exposure measures to predict exposure-response relationships 

19 reported in the NCLAN crop studies; and (2) the SUM06 form would not be influenced 

20 by PRB O3 concentrations (defined at the time as 0.03 to 0.05 ppm) under many typical 

21 air quality distributions. On the basis of these considerations, EPA chose the SUM06 as 

 

54 The SUM06 index is defined as the sum of all hourly O3 concentrations greater 

or equal to 0.06 ppm over a specified time.
Draft O3 NPR –January 5, 2010 270 Deliberative, Do Not Quote or Cite

1 the most appropriate cumulative, seasonal form to consider when proposing an alternative 

2 secondary standard form (61 FR 65716). 

3 Though the scientific justification for a cumulative, seasonal form was generally

4 accepted in the 1997 review, an analysis undertaken by EPA at that time had shown that 

5 there was considerable overlap between areas that would be expected not to meet the 

6 range of alternative 8-hour standards being considered for the primary NAAQS and those 

7 expected not to meet the range of values (expressed in terms of the seasonal SUM06 

8 index) of concern for vegetation. This result suggested that improvements in national air 

9 quality expected to result from attaining an 8-hour primary standard within the 

10 recommended range of levels would also be expected to significantly reduce levels of 

11 concern for vegetation in those same areas. Thus, in the 1996 proposed rule, EPA

12 proposed two alternatives for consideration: one alternative was to make the secondary

13 standard equal in every way to the proposed 8-hour, 0.08 ppm primary standard; and the 

14 second was to establish a cumulative, seasonal secondary standard in terms of a SUM06 

15 form as also appropriate to protect public welfare from known or anticipated adverse 

16 effects given the available scientific knowledge and that such a seasonal standard “...is 

17 more biologically relevant...” (61 FR 65716). 

18 In the 1997 final rule, EPA decided to make the secondary standard identical to 

19 the primary standard. The EPA acknowledged, however, that “it remained uncertain as to 

20 the extent to which air quality improvements designed to reduce 8-hr average O3

21 concentrations averaged over a 3-year period would reduce O3 exposures measured by a 

22 seasonal SUM06 index.” (62 FR 38876) In other words, it was uncertain as to whether 

23 the 8-hour average form would, in practice, provide sufficient protection for vegetation 
Draft O3 NPR –January 5, 2010 271 Deliberative, Do Not Quote or Cite

1 from the cumulative, seasonal and concentration-weighted exposures described in the 

2 scientific literature as of concern.

3 On the basis of that history, the 2007 Staff Paper (chapter 7) revisited the issue of 

4 whether the SUM06 was still the most appropriate choice of cumulative, seasonal form 

5 for a secondary standard to protect the public welfare from known and anticipated 

6 adverse vegetation effects in light of the new information available in this review. 

7 Specifically, the 2007 Staff Paper considered: (1) the continued lack of evidence within 

8 the vegetation effects literature of a biological threshold for vegetation exposures of 

9 concern; and (2) new estimates of PRB that were lower than in the 1997 review. The 

10 W126 form, also evaluated in the 1997 review, was again selected for comparison with 

11 the SUM06 form. Regarding the first consideration, the 2007 Staff Paper noted that the 

12 W126 form, by its incorporation of a continuous sigmoidal weighting scheme, does not 

13 create an artificially imposed concentration threshold, yet also gives proportionally more 

14 weight to the higher and typically more biologically potent concentrations, as supported

15 by the scientific evidence. Second, the index value is not significantly influenced by O3

16 concentrations within the range of estimated PRB, as the weights assigned by the 

17 sigmoidal weighting scheme to concentrations in this range are near zero. Thus, it would 

18 also provide a more appropriate target for air quality management programs designed to 

19 reduce emissions from anthropogenic sources contributing to O3 formation. On the basis 

20 of these considerations, the 2007 Staff Paper concluded that the W126 form was the most 

21 biologically-relevant cumulative, seasonal form appropriate to consider in the context of 

22 the 2008 rulemaking.

23 C. Vegetation Exposure and Impact Assessment
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1 The vegetation exposure and impact assessment conducted for the 2008

2 rulemaking and described in the 2007 Staff paper, consisted of exposure, risk and 

3 benefits analyses and improved and built upon similar analyses performed in the 1997

4 review (EPA 1996b). The vegetation exposure assessment was performed using 

5 interpolation and included information from ambient monitoring networks and results 

6 from air quality modeling. The vegetation risk assessment included both tree and crop 

7 analyses. The tree risk analysis includes three distinct lines of evidence: (1) observations 

8 of visible foliar injury in the field linked to monitored O3 air quality for the years 2001 –

9 2004; (2) estimates of seedling growth loss under then current and alternative O3

10 exposure conditions; and (3) simulated mature tree growth reductions using the TREGRO 

11 model to simulate the effect of meeting alternative air quality standards on the predicted 

12 annual growth of a single western species (ponderosa pine) and two eastern species (red 

13 maple and tulip poplar). The crop analysis includes estimates of the risks to crop yields 

14 from then current and alternative O3 exposure conditions and the associated change in 

15 economic benefits expected to accrue in the agriculture sector upon meeting the levels of 

16 various alternative standards. Each element of the assessment is described below, 

17 including discussions of known sources and ranges of uncertainties associated with the 

18 elements of this assessment.

19 1. Exposure Characterization

20 Though numerous effects of O3 on vegetation have been documented as discussed 

21 above, it is important in considering risk to examine O3 air quality patterns in the U.S. 

22 relative to the location of O3 sensitive species that have a known concentration-response 
Draft O3 NPR –January 5, 2010 273 Deliberative, Do Not Quote or Cite

1 in order to predict whether adverse effects are occurring at current levels of air quality, 

2 and whether they are likely to occur under alternative standard forms and levels. 

3 The most important information about exposure to vegetation comes from the O3

4 monitoring data that are available from two national networks: (1) Air Quality System 

5 (AQS; http://www.epa.gov/ttn/airs/airsaqs) and (2) Clean Air Status and Trends Network 

6 (CASTNET; http://www.epa.gov/castnet/). The AQS monitoring network currently has 

7 over 1100 active O3 monitors which are generally sited near population centers. 

8 However, this network also includes approximately 36 monitors located in national parks. 

9 CASTNET is the nation's primary source for data on dry acidic deposition and rural, 

10 ground-level O3. It consists of over 80 sites across the eastern and western U.S. and is 

11 cooperatively operated and funded with the National Park Service. In the 1997 O3

12 NAAQS final rule, it was acknowledged that because the national air quality surveillance 

13 network for O3 was designed principally to monitor O3 exposure in populated areas, there 

14 was limited measured data available to characterize O3 air quality in rural and remote 

15 sites. Since the 1997 review, there has been a small increase in the number of CASTNET 

16 sites (from approximately 52 sites in 1992 to 84 sites in 2004), however these monitors 

17 are not used for attainment designations. 

18 National parks represent areas of nationally recognized ecological and public

19 welfare significance, which have been afforded a high level of protection by Congress. 

20 Two recent reports presented some discussion of O3 trends in a subset of national parks: 

21 The Ozone Report: Measuring Progress Through 2003 (EPA, 2004), and 2005 Annual 

22 Performance and Progress Report: Air Quality in National Parks (NPS, 2005). 

23 Unfortunately, much of this information is presented only in terms of the current 8-hr 
Draft O3 NPR –January 5, 2010 274 Deliberative, Do Not Quote or Cite

1 average form. The 2007 Staff Paper analyzed available air quality data in terms of the 

2 cumulative 12-hour W126 form from 2001 to 2005 for a subset of national parks and 

3 other significant natural areas representing 4 general regions of the U.S. Many of these 

4 national parks and natural areas have monitored O3 levels above concentrations that have 

5 been shown to decrease plant growth and above the 12-hour W126 levels analyzed in this 

6 review. For example, the Great Smokey Mountain, Rocky Mountain, Grand Canyon, 

7 Yosemite and Sequoia National Parks all had more than one year within the 2001-2005 

8 period with a 12-hour W126 above 21 ppm-hour. This level of exposure has been 

9 associated with approximately no more than 10 percent biomass loss in 50 percent of the 

10 49 tree seedling cases studied in the NHEERL-WED experiments (Lee and Hogsett, 

11 1996). Black cherry (Prunus serotina), an important O3-sensitive tree species in the 

12 eastern U.S., occurs in the Great Smoky Mountain National Park and is estimated to have

13 O3-related seedling biomass loss of approximately 40 percent when exposed to a 3 

14 month, 12-hour W126 O3 level greater than 21 ppm-hour. Ponderosa pine (Pinus 

15 ponderosa) which occurs in the Grand Canyon, Yosemite and Sequoia National Parks has 

16 been reported to have approximately 10 percent biomass losses at 3 month, 12 hour 

17 W126 O3 levels as low as 17 ppm-hour (Lee and Hogsett, 1996). Impacts on seedlings 

18 may potentially affect long-term tree growth and survival, ultimately affecting the 

19 competitiveness of O3-sensitive tree species and genotypes within forest stands.

20 In order to characterize exposures to vegetation at the national scale, however, the 

21 2007 Staff Paper concluded that it could not rely solely on limited site-specific 

22 monitoring data, and that it was necessary to select an interpolation method that could be 

23 used to characterize O3 air quality over broad geographic areas. The 2007 Staff Paper 
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1 therefore investigated the appropriateness of using the O3 outputs from the EPA/NOAA 

Community Multi-scale Air Quality (CMAQ)55 2 model system 

3 (http://www.epa.gov/asmdnerl/CMAQ, Byun and Ching, 1999; Arnold et al. 2003, Eder 

4 and Yu, 2005) to improve spatial interpolations based solely on existing monitoring 

5 networks. Due to the significant resources required to run CMAQ, model outputs were 

6 only available for a limited number of years. For the 2008 rulemaking, the most recent

7 outputs available at the time from CMAQ version 4.5 were for the year 2001.

8 Based on the significant difference in monitor network density between the 

9 eastern and western U.S., the 2007 Staff Paper concluded that it was appropriate to use 

10 separate interpolation techniques in these two regions. Only AQS and CASTNET 

11 monitoring data were used for the eastern interpolation, since it was determined that 

12 enhancing the interpolation with CMAQ data did not add much information to the eastern 

13 U.S. interpolation. In the western U.S., however, where rural monitoring is more sparse, 

14 O3 values generated by the CMAQ model were used to develop scaling factors to 

15 augment the interpolation. 

16 In order to characterize uncertainties associated with the interpolation method, 

17 monitored O3 concentrations were systematically compared to interpolated O3

18 concentrations in areas where monitors were located. In general, the interpolation 

 

55 The CMAQ model is a multi-pollutant, multiscale air quality model that 

contains state-of-the-science techniques for simulating atmospheric and land processes 

that affect the transport, transformation, and deposition of atmospheric pollutants and/or 

their precursors on both regional and urban scales. It is designed as a science-based 

modeling tool for handling many major pollutants (including photochemical oxidants/O3, 

particulate matter, and nutrient deposition) holistically. The CMAQ model can generate

estimates of hourly O3 concentrations for the contiguous U.S., making it possible to 

express model outputs in terms of a variety of exposure indices (e.g., W126, 8-hour 

average).
Draft O3 NPR –January 5, 2010 276 Deliberative, Do Not Quote or Cite

1 method used in the current review performed well in many areas in the U.S., although it 

2 under-predicted higher 12-hour W126 exposures in rural areas. Due to the important 

3 influence of higher exposures in determining risks to plants, this feature of the 

4 interpolated surface could result in an under-estimation of risks to vegetation in some 

5 areas. Taking these uncertainties into account, and given the absence of more complete 

6 rural monitoring data, this approach was used in developing national vegetation exposure 

7 and risk assessments that estimate relative changes in risk for the various alternative 

8 standards analyzed.

9 To evaluate changing vegetation exposures and risks under selected air quality

10 scenarios, the 2007 Staff Paper utilized 2001 base year O3 air quality distributions that 

11 had been adjusted with a rollback method (Horst and Duff, 1995; Rizzo, 2005, 2006) to 

12 reflect meeting the then current and alternative secondary standard options. This 

13 technique combines both linear and quadratic elements to reduce higher O3

14 concentrations more than lower ones. In this regard, the rollback method attempts to 

15 account for reductions in emissions without greatly affecting lower concentrations. The 

16 following O3 air quality scenarios were analyzed: (1) 4th-highest daily maximum 8-hour

17 average: 0.084 ppm (the effective level of the then current standard) and 0.070 ppm 

18 levels; (2) 3-month, 12-hour. SUM06: 25 ppm-hour (proposed in the 1997 review) and 15 

19 ppm-hour levels; and (3) 3-month, 12-hour W126: 21 ppm-hour and 13 ppm-hour levels.

20 The two 8-hour average levels were chosen as possible alternatives of the then 

21 current form for comparison with the cumulative, seasonal alternative forms. The 

22 SUM06 scenarios were very similar to the W126 scenarios. Since the W126 was judged 

23 to be the more biologically-relevant cumulative, seasonal form, only the results for the 
Draft O3 NPR –January 5, 2010 277 Deliberative, Do Not Quote or Cite

1 W126 scenarios are summarized below. For the W126 form, the two levels were selected 

2 on the basis of the associated levels of tree seedling biomass loss and crop yield loss 

3 protection identified in the NHEERL-WED and NCLAN studies, respectively. 

4 Specifically, the upper level of W126 (21 ppm-hour) was associated with a level of tree 

5 and crop protection of approximately no more than 10 percent growth or yield loss in 50

6 percent of cases studied. Alternatively, the lower level of W126 (13 ppm-hour) was 

7 associated with a level of tree seedling and crop protection of approximately no more 

8 than 10 percent growth or yield loss in 75 percent of studied cases. 

9 The following discussion highlights key observations drawn from comparing 

10 predicted changes in interpolated air quality under each alternative standard form and 

11 level scenario for the base year, 2001:

12 (1) Under the base year (2001) “as is” air quality, a large portion of California had 

13 12-hr W126 O3 levels above 31 ppm-hour, which has been associated with approximately

14 no more than 14 percent biomass loss in 50 percent of tree seedling cases studies. 

15 Broader multi-state regions in the east (NC, TN, KY, IN, OH, PA, NJ, NY, DE, MD,

16 VA) and west (CA, NV, AZ, OK, TX) are predicted to have levels of air quality above 

17 the W126 level of 21 ppm-hour, which is approximately equal to the secondary standard 

18 proposed in 1996 and is associated with approximately no more than 10 percent biomass

19 loss in 50 percent of tree seedling cases studied. Much of the east and Arizona and 

20 California have 12-hour W126 O3 levels above 13 ppm-hour, which has been associated 

21 with approximately no more than 10 percent biomass loss in 75 percent of tree seedling

22 cases studied. The results of the exposure assessment indicate that current air quality

23 levels could result in significant impacts to vegetation in some areas.
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1 (2) When 2001 air quality was rolled back to meet the then current 8-hour, 0.084 

2 ppm secondary standard, the overall 3-month 12-hour W126 O3 levels were somewhat 

3 improved, but not substantially. Under this scenario, there were still many areas in 

4 California with 12-hour W126 O3 levels above 31 ppm-hour. A broad multi-state region 

5 in the east (NC, TN, KY, IN, OH, PA, MD) and west (CA, NV, AZ, OK, TX) were still 

6 predicted to have O3 levels above the W126 level of 21 ppm-hour.

7 (3) Exposures generated for just meeting a 0.070 ppm, 4th-highest maximum 8-

8 hour average alternative standard showed substantially improved O3 air quality when 

9 compared to just meeting the then current 8-hour standard. Most areas were predicted to 

10 have O3 levels below the W126 level of 21 ppm-hour, although some areas in the east 

11 (KY, TN, MI, AR, MO, IL) and west (CA, NV, AZ, UT, NM, CO, OK, TX) were still 

12 predicted to have O3 levels above the W126 level of 13 ppm-hour.

13 These results suggest that meeting a 0.070 ppm, 8-hour secondary standard would 

14 provide substantially improved protection in some areas for vegetation from seasonal O3

15 exposures of concern. The 2007 Staff Paper recognizes, however, that some areas 

16 meeting a 0.070 ppm 8-hour standard could continue to have elevated seasonal 

17 exposures, including forested park lands and other natural areas, and Class I areas which 

18 are federally mandated to preserve certain air quality related values. This is especially 

19 important in the high elevation forests in the Western U.S. where there are few O3

20 monitors. This is because the air quality patterns in remote areas can result in relatively

21 low 8-hour averages while still experiencing relatively high cumulative exposures.

22 To further characterize O3 air quality in terms of various secondary standard 

23 forms, an analysis was performed in the 2007 Staff Paper to evaluate the extent to which 
Draft O3 NPR –January 5, 2010 279 Deliberative, Do Not Quote or Cite

1 county-level O3 air quality measured in terms of various levels of the current 8-hour 

2 average form overlapped with that measured in terms of various levels of the 12-hour 

3 W126 cumulative, seasonal form. The 2007 Staff Paper presented this analysis using 

2002-200456 4 county-level O3 air quality data from AQS sites and the subset of 

5 CASTNET sites having the highest O3 levels for the counties in which they are located. 

6 Since the current 8-hour average secondary form is a 3-year average, the analysis initially

7 compared the 3-year averages of both the 8-hour and W126 forms. In addition,

8 recognizing that some vegetation effects (e.g. crop yield loss and foliar injury) are driven 

9 solely by annual O3 exposures and are typically evaluated with respect to exposures 

10 within the annual growing season, the 2007 Staff Paper also presented a comparison of 

11 the current 3-year average 8-hour form to the annual W126 form for the individual years,

12 2002 and 2004.

13 Results of the 3-year average comparisons showed that of the counties with air 

14 quality meeting the 3-year average form of a 0.084 ppm, 8-hour average standard, 7 

15 counties showed 3-year average W126 values above the 21 ppm-hour level. At the lower 

16 W126 level of 13 ppm-hour, 135 counties with air quality meeting the 3-year average 

17 form of a 0.084 ppm, 8-hour average standard, would be above this W126 level. In 

18 addition, when the 3-year average of an 8-hour form was compared to annual W126 

19 values, further variability in the degree of overlap between the 8-hour form and W126 

20 form became apparent. For example, the relatively high 2002 O3 air quality year showed 

21 a greater degree of overlap between those areas that would meet the levels analyzed for 

 

56 This analysis was updated using 2003-2005 air quality as it became available, 

finding similar results.
Draft O3 NPR –January 5, 2010 280 Deliberative, Do Not Quote or Cite

1 the current 8-hour and alternative levels of the W126 form than did the relatively low O3

2 2004 air quality year. This lack of a consistent degree of overlap between the two forms 

3 in different air quality years demonstrates that annual vegetation would be expected to 

4 receive widely differing degrees of protection from cumulative seasonal exposures in 

5 some areas from year to year, even when the 3-year average of the 8-hour form was 

6 consistently met.

7 It is clear that this analysis is limited by the lack of monitoring in rural areas 

8 where important vegetation and ecosystems are located, especially at higher elevation 

9 sites. This is because O3 air quality distributions at high elevation sites often do not 

10 reflect the typical urban and near-urban pattern of low morning and evening O3

11 concentrations with a high mid-day peak, but instead maintain relatively flat patterns with 

12 many concentrations in the mid-range (e.g., 0.05-0.09 ppm) for extended periods. These 

13 conditions can lead to relatively low daily maximum 8-hour averages concurrently with 

14 high cumulative values so that there is potentially less overlap between an 8-hour average 

15 and a cumulative, seasonal form at these sites. The 2007 Staff Paper concluded that it is 

16 reasonable to anticipate that additional unmonitored rural high elevation areas important 

17 for vegetation may not be adequately protected even with a lower level of the 8-hour 

18 form.

19 The 2006 Criteria Document discusses policy relevant background (PRB) levels 

20 for high elevation sites and makes the following observations: (1) PRB concentrations of 

21 0.04 to 0.05 ppm occur occasionally at high-elevation sites (e.g., >1.5 km) in the spring 

22 due to the free-tropospheric influence, including some limited contribution from 

23 hemispheric pollution (O3 produced from anthropogenic emissions outside North 
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1 America); and (2) while stratospheric intrusions might occasionally elevate O3 at high2 altitude sites, these events are rare at surface sites. Therefore, the 2007 Staff Paper 

3 concluded that springtime PRB levels in the range identified above and rare stratospheric 

4 intrusions of O3 are unlikely to be a major influence on 3-month cumulative seasonal 

5 W126 values.

6 It further remains uncertain as to the extent to which air quality improvements 

7 designed to reduce 8-hour O3 average concentrations would reduce O3 exposures 

8 measured by a seasonal, cumulative W126 index. The 2007 Staff Paper indicated this to 

9 be an important consideration because: (1) the biological database stresses the 

10 importance of cumulative, seasonal exposures in determining plant response; (2) plants 

11 have not been specifically tested for the importance of daily maximum 8-hour O3

12 concentrations in relation to plant response; and (3) the effects of attainment of a 8-hour 

13 standard in upwind urban areas on rural air quality distributions cannot be characterized 

14 with confidence due to the lack of monitoring data in rural and remote areas. These 

15 factors are important considerations in determining whether the current 8-hour form can 

16 appropriately provide requisite protection for vegetation.

17 2. Assessment of Risks to Vegetation

18 The 2007 Staff Paper presents results from quantitative and qualitative risk 

19 assessments of O3 risks to vegetation (EPA, 2007). In the 1997 review, crop yield and 

20 seedling biomass loss OTC data provided the basis for staff analyses, conclusions, and 

21 recommendations (EPA, 1996b). Since then, several additional lines of evidence have 

22 progressed sufficiently to provide staff with a more complete and coherent picture of the 

23 scope of O3-related vegetation risks, especially those faced by seedling, sapling and 

24 mature tree species growing in field settings, and indirectly, forested ecosystems. 
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1 Specifically, research published after the 1997 review reflects an increased emphasis on 

2 field-based exposure methods (e.g., free air exposure and ambient gradient), improved 

3 field survey biomonitoring techniques, and mechanistic tree process models. Findings 

4 from each of these research areas are discussed separately below. In conducting these 

5 assessments, the Staff Paper analyses relied on both measured and modeled air quality

6 information. For some effects, like visible foliar injury and modeled mature tree growth 

7 response, only monitored air quality information was used. For other effects categories 

8 (e.g., crop yield and tree seedling growth), staff relied on interpolated O3 exposures. 

9 a. Visible foliar injury

10 As discussed above (section IV.A.2.c), systematic injury surveys have 

11 documented visible foliar injury symptoms diagnostic of phytotoxic O3 exposures on 

12 sensitive bioindicator plants. These surveys have produced more expansive evidence 

13 than that available at the time of the 1997 review that visible foliar injury is occurring in 

14 many areas of the U.S. under current ambient conditions. The 2007 Staff Paper presents 

15 an assessment combining recent U.S. Forest Service Forest Inventory and Analysis (FIA) 

16 biomonitoring site data with the county level air quality data for those counties 

17 containing the FIA biomonitoring sites. This assessment showed that incidence of visible 

18 foliar injury ranged from 21 to 39 percent during the four-year period (2001-2004) across 

19 all counties with air quality levels at or below that of a 0.084 ppm, 8-hour standard. Of 

20 the counties that met an 8-hour level of 0.070 ppm in those years, 11 to 30 percent still 

21 had incidence of visible foliar injury. The magnitude of these percentages suggests that 

22 phytotoxic exposures sufficient to induce visible foliar injury would still occur in many

23 areas after meeting the level of a 0.084 ppm secondary standard or alternative 0.070 ppm 
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1 8-hour standard. Additionally, the data showed that visible foliar injury occurrence was 

2 geographically widespread and occurring on a variety of plant species in forested and 

3 other natural systems. Linking visible foliar injury to other plant effects is still 

4 problematic. However, its presence indicates that other O3–related vegetation effects 

5 could also be present. 

6 b. Seedling and mature tree biomass loss

7 In the 1997 review, analyses of the effects of O3 on trees were limited to 11 tree 

8 species for which C-R functions for the seedling growth stage had been developed from 

9 OTC studies conducted by the NHEERL-WED. Important tree species such as quaking 

10 aspen, ponderosa pine, black cherry, and tulip poplar were found to be sensitive to 

11 cumulative seasonal O3 exposures. Work done since the 1997 review at the AspenFACE 

12 site in Wisconsin on quaking aspen (Karnosky et al., 2005) and a gradient study

13 performed in the New York City area (Gregg et al. 2003) has confirmed the detrimental 

14 effects of O3 exposure on tree growth in field studies without chambers and beyond the 

15 seedling stage (King et al 2005). These field studies are discussed above in section IV.A.

16 To update the seedling biomass loss risk analysis, C-R functions for biomass loss 

17 for available seedling tree species taken from the 2006 Criteria Document and 

18 information on tree growing regions derived from the U.S. Department of Agriculture's 

19 Atlas of United States Trees were combined with projections of O3 air quality based on 

20 2001 interpolated exposures, to produce estimated biomass loss for each of the seedling 

21 tree species individually. Maps of these biomass loss projections are presented in the

22 2007 Staff Paper. For example, quaking aspen had a wide range of O3 exposures across 

23 its growing range and therefore, showed significant variability in percentages of projected 
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1 seedling biomass loss across its range. Quaking aspen seedling biomass loss was 

2 projected to be greater than 4 percent over much of its geographic range, though it can 

3 reach above 10 percent in areas of Ohio, Pennsylvania, New York, New Jersey and 

4 California. Biomass loss for black cherry was projected to be greater than 20 percent in 

5 approximately half its range. Greater than 30 percent biomass loss for black cherry was 

6 projected in North Carolina, Tennessee, Indiana, Ohio, Pennsylvania, Arizona, Michigan, 

7 New York, New Jersey, Maryland and Delaware. For ponderosa pine, an important tree 

8 species in the western U.S., biomass loss was projected to be above 10 percent in much 

9 of its range in California. Biomass loss still occurred in many tree species when O3 air 

10 quality was adjusted to meet the then current 8-hour standard of 0.084 ppm. For instance, 

11 black cherry, ponderosa pine, eastern white pine, and aspen had estimated median 

12 seedling biomass losses over portions of their growing range as high as 24, 11, 6, and 6

13 percent, respectively, when O3 air quality was rolled back to just meet a 0.084 ppm, 8-

14 hour standard. The 2007 Staff Paper noted that these results are for tree seedlings and 

15 that mature trees of the same species may have more or less of a response to O3 exposure. 

16 Due to the potential for compounding effects over multiple years, experts at a consensus 

17 workshop on O3 vegetation effects and secondary standards, hereinafter referred to as the 

18 1996 Consensus Workshop, reported in a subsequent 1997 Workshop Report, that a 

19 biomass loss greater than 2 percent annually can be significant (Heck and Cowling, 

20 1997).. Decreased seedling root growth and survivability could affect overall stand health 

21 and composition in the long term.

22 In addition to the estimation of O3 effects on seedling growth, recent work

23 available in the 2008 rulemaking has enhanced our understanding of risks beyond the 
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1 seedling stage. In order to better characterize the potential O3 effects on mature tree 

2 growth, a tree growth model (TREGRO) was used as a tool to evaluate the effect of 

3 changing O3 air quality under just meet scenarios for selected alternative O3 standards on 

4 the growth of mature trees. TREGRO is a process-based, individual tree growth 

5 simulation model (Weinstein et al, 1991). This model has been used to evaluate the 

6 effects of a variety of O3 exposure scenarios on several species of trees by incorporating

7 concurrent climate data in different regions of the U.S. to account for O3 and 

8 climate/meteorology interactions (Tingey et al., 2001; Weinstein et al., 1991; Retzlaff et 

9 al., 2000; Laurence et al., 1993; Laurence et al., 2001; Weinstein et al., 2005). The 

10 model provides an analytical framework that accounts for the nonlinear relationship 

11 between O3 exposure and response. The interactions between O3 exposure, precipitation 

12 and temperature are integrated as they affect vegetation, thus providing an internal 

13 consistency for comparing effects in trees under different exposure scenarios and climatic 

14 conditions. An earlier assessment of the effectiveness of national ambient air quality

15 standards in place since the early 1970s took advantage of 40 years of air quality and 

16 climate data for the Crestline site in the San Bernardino Mountains of California to 

17 simulate ponderosa pine growth over time with the improving air quality using TREGRO 

18 (Tingey et al., 2004).

19 The TREGRO model was used to assess growth of Ponderosa pine in the San 

20 Bernardino Mountains of California (Crestline) and the growth of yellow poplar and red 

21 maple in the Appalachian mountains of Virginia and North Carolina, Shenandoah 

22 National Park (Big Meadows) and Linville Gorge Wilderness Area (Cranberry), 

23 respectively. Total tree growth associated with ‘as is’ air quality, and air quality adjusted 
Draft O3 NPR –January 5, 2010 286 Deliberative, Do Not Quote or Cite

1 to just meet alternative O3 standards was assessed. Ponderosa pine is one of the most 

2 widely distributed pines in western North America, a major source of timber, important 

3 as wildlife habitat, and valued for aesthetics (Burns and Honkala, 1990). Red maple is 

4 one of the most abundant species in the eastern U.S. and is important for its brilliant fall 

5 foliage and highly desirable wildlife browse food (Burns and Honkala, 1990). Yellow 

6 poplar is an abundant species in the southern Appalachian forest. It is 10 percent of the 

7 cove hardwood stands in southern Appalachians which are widely viewed as some of the 

8 country’s most treasured forests because the protected, rich, moist set of conditions 

9 permit trees to grow the largest in the eastern U.S. The wood has high commercial value 

10 because of its versatility and as a substitute for increasingly scarce softwoods in furniture 

11 and framing construction. Yellow poplar is also valued as a honey tree, a source of 

12 wildlife food, and a shade tree for large areas (Burns and Honkala, 1990). 

13 The 2007 Staff Paper analyses found that just meeting a 0.084 ppm standard 

14 would likely continue to allow O3-related reductions in annual net biomass gain in these 

15 species. This is based on model outputs that estimate that as O3 levels are reduced below 

16 those of a 0.084 ppm standard, significant improvements in growth would occur. For 

17 instance, estimated growth in red maple increased by 4 and 3 percent at Big Meadows 

18 and Cranberry sites, respectively, when air quality was rolled back to just met a W126 

19 value of 13 ppm-hour. Yellow poplar was projected to have a growth increase between 

20 0.6 and 8 percent under the same scenario at the two eastern sites.

21 Though there is uncertainty associated with the above analyses, this information 

22 should be given careful consideration in light of several other pieces of evidence. 

23 Specifically, new evidence from experimental studies that go beyond the seedling growth 
Draft O3 NPR –January 5, 2010 287 Deliberative, Do Not Quote or Cite

1 stage continues to show decreased growth under elevated O3 (King et al. 2005). Some 

2 mature trees such as red oak have shown an even greater sensitivity of photosynthesis to 

3 O3 than seedlings of the same species (Hanson et al., 1994). As indicated above, smaller 

4 growth loss increments may be significant for perennial species. The potential for 

5 cumulative “carry over” effects as well as compounding also must be considered. The 

6 accumulation of such “carry-over” effects over time may affect long-term survival and 

7 reproduction of individuals and ultimately the abundance of sensitive tree species in 

8 forest stands.

9 c. Crops

10 As discussed in the 2007 Staff Paper, risk of O3 exposure and associated 

11 monetized benefits were estimated for commodity crops, fruits and vegetables. Similar to 

12 the tree seedling analysis, this analysis combined C-R information on crops, crop 

13 growing regions and interpolated exposures during each crop growing season. NCLAN 

14 crop functions were used for commodity crops. According to USDA National 

15 Agricultural Statistical Survey (NASS) data, the 9 commodity crop species (e.g., cotton, 

16 field corn, grain sorghum, peanut, soybean, winter wheat, lettuce, kidney bean, potato) 

17 included in the 2007 Staff Paper analysis accounted for 69 percent of 2004 principal crop 

acreage planted in the U.S. in 2004.57 18 The C-R functions for six fruit and vegetable 

19 species (tomatoes-processing, grapes, onions, rice, cantaloupes, Valencia oranges) were 

 

57 Principal crops as defined by the USDA include corn, sorghum, oats, barley, 

winter wheat, rye, Durum wheat, other spring wheat, rice, soybeans, peanuts, sunflower, 

cotton, dry edible beans, potatoes, sugar beets, canola, proso millet, hay, tobacco, and 

sugarcane. Acreage data for the principal crops were taken from the USDA NASS 2005 

Acreage Report (http://usda.mannlib.cornell.edu/reports/nassr/field/pcpbba/acrg0605.pdf). 
Draft O3 NPR –January 5, 2010 288 Deliberative, Do Not Quote or Cite

1 identified from the California fruit and vegetable analysis from the 1997 review (Abt

2 Associates Inc, 1995). The 2007 Staff Paper noted that fruit and vegetable studies were 

3 not part of the NCLAN program and C-R functions were available only in terms of 

4 seasonal 7-hour or 12-hour mean index. This index form is considered less effective in 

5 predicting plant response for a given change in air quality than the cumulative form used 

6 with other crops. Therefore, the fruit and vegetable C-R functions were considered more 

7 uncertain than those for commodity crops.

8 Analyses in the 2007 Staff Paper showed that some of the most important 

9 commodity crops such as soybean, winter wheat and cotton had some projected losses 

10 under the 2001 base year air quality. Soybean yield losses were projected to be 2-4

11 percent in parts of Pennsylvania, New Jersey, Maryland and Texas. Winter wheat was 

12 projected to have yield losses of 2-6 percent in parts of California. Additionally, cotton 

13 was projected to have yield losses of above 6 percent in parts of California, Texas and 

14 North Carolina in 2001. The risk assessment estimated that just meeting the then current 

15 0.084 ppm, 8-hour standard would still allow O3–related yield loss to occur in some 

16 commodity crop species and fruit and vegetable species currently grown in the U.S. For 

17 example, based on median C-R function response, in counties with the highest O3 levels, 

18 potatoes and cotton had estimated yield losses of 9-15 percent and 5-10 percent, 

19 respectively, when O3 air quality just met the level of a 0.084 ppm, 8-hour standard. 

20 Estimated yield improved in these counties when the alternative W126 standard levels 

21 were met. The very important soybean crop had generally small yield losses throughout 

22 the country under just meeting the then current standard (0-4 percent). 
Draft O3 NPR –January 5, 2010 289 Deliberative, Do Not Quote or Cite

1 The 2007 Staff Paper also presented estimates of monetized benefits for crops 

2 associated with a 0.084 ppm, 8-hour and alternative standards. The Agriculture 

3 Simulation Model (AGSIM) (Taylor, 1994; Taylor, 1993) was used to calculate annual 

4 average changes in total undiscounted economic surplus for commodity crops and fruits 

5 and vegetables when the then current and alternative standard levels were met. Meeting 

6 the various alternative standards did show some significant benefits beyond a 0.084 ppm, 

7 8-hour standard. However, the 2007 Staff Paper recognized that the AGSIM economic 

8 benefits estimates also incorporate several sources of uncertainty, including: (1)

9 estimates of economic benefits derived from use of the more uncertain C-R relationships

10 for fruits and vegetables; (2) uncertain assumptions about the treatment and effect of 

11 government farm payment programs; and (3) uncertain assumptions about near-term 

12 changes in the agriculture sector due to the increased use of crops as biofuels. Although 

13 the AGSIM model results provided a relative comparison of agricultural benefits between 

14 alternative standards, these uncertainties limited the utility of the absolute numbers.

15 D. Reconsideration of Secondary Standard

16 As discussed above at the beginning of section IV, this reconsideration of the 

17 secondary O3 standard set in the 2008 rulemaking focuses on reconsidering certain 

18 elements of the standard, the form, averaging times, and level. The general approach for 

19 setting a secondary O3 standard used in the 2008 rulemaking, and in the previous 1997 

20 rulemaking, was to consider two basic policy options: setting a distinct secondary

21 standard with a biologically relevant form and averaging times, or setting a secondary

22 standard identical to the primary standard. In the 2007 proposed rule, both such options 

23 were evaluated, commented on by CASAC and the public, and proposed, as discussed 
Draft O3 NPR –January 5, 2010 290 Deliberative, Do Not Quote or Cite

1 below in sections IV.D.1 and IV.D.2, respectively. In the 2008 final rule, EPA decided to 

2 set the secondary standard identical to the revised 8-hour primary standard, as discussed 

3 below in section IV.D.3. Section IV.D.4 summarizes comments received from CASAC 

4 following the 2008 decision. The Administrator’s proposed conclusions based on this 

5 reconsideration are presented in section IV.D.5.

6 1. Considerations Regarding the 2007 Proposed Cumulative Seasonal Standard 

7 a. Form

8 The 2006 Criteria Document and 2007 Staff Paper concluded that the recent 

9 vegetation effects literature evaluated in the 2008 rulemaking strengthened and 

10 reaffirmed conclusions made in the 1997 review that the use of a cumulative exposure 

11 index that differentially weights ambient concentrations is best able to relate ambient 

12 exposures to vegetation response at this time (EPA, 2006a, b; see also discussion in IV.B 

13 above). The 1997 review focused in particular on two of these cumulative forms, the 

14 SUM06 and W126. In the 2008 rulemaking, the 2007 Staff Paper again evaluated these

15 two forms in light of two key pieces of then recent information: estimates of PRB that 

16 were lower than in the 1997 review, and continued lack of evidence within the vegetation 

17 effects literature of a biological threshold for vegetation exposures of concern. On the 

18 basis of those policy and science-related considerations, the 2007 Staff Paper concluded 

19 that the W126 form was more appropriate in the context of the 2008 rulemaking. 

20 Specifically, the W126 form, by its incorporation of a sigmoidal weighting scheme, does 

21 not create an artificially imposed concentration threshold, gives proportionally more 

22 weight to the higher and typically more biologically potent concentrations, and is not 

23 significantly influenced by O3 concentrations within the range of estimated PRB. The 
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1 Staff Paper further concluded that “it is not appropriate to continue to use an 8-hour 

2 averaging time for the secondary standard” and that “the 8-hour average form should be 

3 replaced with a cumulative, seasonal, concentration weighted form” (EPA, 2007b; pg.8-

4 25).

5 The CASAC, based on its assessment of the same vegetation effects science, 

6 agreed with the 2006 Criteria Document and 2007 Staff Paper and unanimously

7 concluded that it is not appropriate to try to protect vegetation from the known or 

8 anticipated adverse effects of ambient O3 by continuing to promulgate identical primary

9 and secondary standards for O3. Moreover, the members of the CASAC and a substantial 

10 majority of the CASAC O3 Panel agreed with 2007 Staff Paper conclusions and 

11 encouraged EPA to establish an alternative cumulative secondary standard for O3 and 

12 related photochemical oxidants that is distinctly different in averaging time, form and 

13 level from the current or potentially revised 8-hour primary standard. The CASAC also 

14 stated that “the recommended metric for the secondary ozone standard is the 

15 (sigmoidally-weighted) W126 index” (Henderson, 2007). 

16 The EPA agreed with the conclusions drawn in the 2006 Criteria Document, 2007 

17 Staff Paper and by CASAC that the scientific evidence available in the 2008 rulemaking

18 continued to demonstrate the cumulative nature of O3-induced plant effects and the need 

19 to give greater weight to higher concentrations. Thus, EPA concluded that a cumulative 

20 exposure index that differentially weights O3 concentrations represents a reasonable 

21 policy choice for a seasonal secondary standard to protect against the effects of O3 on 

22 vegetation. The EPA further agreed with both the 2007 Staff Paper and CASAC that the 

23 most appropriate cumulative, concentration-weighted form to consider in the 2008
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1 rulemaking was the sigmoidally weighted W126 form, due to EPA’s recognition that 

2 there is no evidence in the literature for an exposure threshold that would be appropriate 

3 across all O3-sensitive vegetation and that this form is unlikely to be significantly

4 influenced by O3 air quality within the range of PRB levels identified in this rulemaking. 

5 Thus, in 2007 EPA proposed as one option to replace the then current 0.084 ppm, 8-hour 

6 average secondary standard with a standard defined in terms of the cumulative, seasonal 

7 W126 form. The EPA also proposed the option of making the secondary identical to the 

8 proposed revised primary standard.

b. Averaging Times58 9

10 The 2007 Staff Paper, in addition to form, also considered what exposure periods 

11 or durations are most relevant for vegetation, which, unlike people, is exposed to ambient 

12 air continuously throughout its lifespan. For annual species, this lifespan encompasses a 

13 period of only one year or less; while for perennials, lifespans can range from a few years 

14 to decades or centuries. However, because O3 levels are not continuously elevated and 

15 plants are not equally sensitive to O3 over the course of a day, season or lifetime, it 

16 becomes necessary to identify periods of exposure that have the most relevance for plant 

17 response. The 2007 Staff Paper discussed exposure periods relevant for vegetation in 

18 terms of a seasonal window and a diurnal window, and it also discussed defining the 

19 standard in terms of an annual index value versus a 3-year average of annual index 

20 values. The numbered paragraphs below present the 2007 Staff Paper discussions on 

 

58 While the term “averaging time” is used, for the cumulative, seasonal standard 

the seasonal and diurnal time periods at issue are those over which exposures during a 

specified period of time are cumulated, not averaged.
Draft O3 NPR –January 5, 2010 293 Deliberative, Do Not Quote or Cite

1 these exposure periods, and the annual versus 3-year average index value, followed by a 

2 discussion of CASAC views and EPA proposed conclusions.

3 (1) In considering an appropriate seasonal window, the 2007 Staff Paper 

4 recognized that, in general, many annual crops are grown for periods of a few months 

5 before being harvested. In contrast, other annual and perennial species may be 

6 photosynthetically active longer, and for some species and locations, throughout the 

7 entire year. In general, the period of maximum physiological activity and thus, maximum 

8 potential O3 uptake for annual crops, herbaceous species, and deciduous trees and shrubs 

9 coincides with some or all of the intra-annual period defined as the O3 season, which 

10 varies on a state-by-state basis. This is because the high temperature and high light 

11 conditions that promote the formation of tropospheric O3 also promote physiological 

12 activity in vegetation.

13 The 2007 Staff Paper noted that the selection of any single seasonal exposure 

14 period for a national standard would represent a compromise, given the significant 

15 variability in growth patterns and lengths of growing seasons among the wide range of

16 vegetation species occurring within the U.S. that may experience adverse effects 

17 associated with O3 exposures. However, the 2007 Staff Paper further concluded that the 

18 consecutive 3-month period within the O3 season with the highest W126 index value 

19 (e.g., maximum 3 month period) would, in most cases, likely coincide with the period of 

20 greatest plant sensitivity on an annual basis. Therefore, the 2007 Staff Paper again 

21 concluded, as it did in the 1997 review, that the annual maximum consecutive 3-month 

22 period is a reasonable seasonal time period, when combined with a cumulative, 

23 concentration weighted form, for protection of sensitive vegetation.
Draft O3 NPR –January 5, 2010 294 Deliberative, Do Not Quote or Cite

1 (2) In considering an appropriate diurnal window, the Staff Paper recognized that 

2 over the course of the 24-hour diurnal period, plant stomatal conductance varies in 

3 response to changes in light level, soil moisture and other environmentally and 

4 genetically controlled factors. In general, stomata are most open during daylight hours in 

5 order to allow sufficient CO2 uptake for use in carbohydrate production through the light6 driven process of photosynthesis. At most locations, O3 concentrations are also highest 

7 during the daytime, and thus, most likely to coincide with maximum stomatal uptake. It 

8 is also known however, that in some species, stomata may remain open sufficiently at 

9 night to allow for some nocturnal uptake to occur. In addition, at some rural, high 

10 elevation sites, the O3 concentrations remain relatively flat over the course of the day, 

11 often at levels above estimated PRB. At these sites, nighttime W126 values can be of 

12 similar magnitude as daytime values, though the significance of these exposures is much 

13 less certain. This is because O3 uptake during daylight hours is known to impair the 

14 light-driven process of photosynthesis, which can then lead to impacts on carbohydrate 

15 production, plant growth, reproduction (yield) and root function. It is less clear at this 

16 time to what extent and by what mechanisms O3 uptake at night adversely impacts plant 

17 function. In addition, many species have not been shown to take up O3 at night and/or do 

18 not occur in areas with elevated nighttime O3 concentrations. 

19 In reviewing the information on this topic that became available after the 1997 

20 review, the 2007 Staff Paper considered the information compiled in a summary report by

21 Musselman and Minnick (2000). This work reported that some species take up O3 at 

22 night, but that the degree of nocturnal stomatal conductance varies widely between 

23 species and its relevance to overall O3-induced vegetation effects remain unclear. In 
Draft O3 NPR –January 5, 2010 295 Deliberative, Do Not Quote or Cite

1 considering this information, the 2007 Staff Paper concluded that for the vast majority of 

2 studied species, daytime exposures represent the majority of diurnal plant O3 uptake and 

3 are responsible for inducing the plant response of most significance to the health and 

4 productivity of the plant (e.g., reduced carbohydrate production). Until additional 

5 information is available about the extent to which co-occurrence of sensitive species and 

6 elevated nocturnal O3 exposures exists, and what levels of nighttime uptake are adverse 

7 to affected species, the 2007 Staff Paper concluded that this information continues to be 

8 preliminary, and does not provide a basis for reaching a different conclusion regarding 

9 the diurnal window at this time. The 2007 Staff Paper further noted that additional 

10 research is needed to address the degree to which a 12-hour diurnal window may be 

11 under-protective in areas where elevated nighttime levels of O3 co-occur with sensitive 

12 species with a high degree of nocturnal stomatal conductance. Thus, as in the 1997

13 review, the 2007 Staff Paper again concluded that based on the available science, the 

14 daytime 12-hour window (8:00 a.m. to 8:00 p.m.) is the most appropriate period over 

15 which to cumulate diurnal O3 exposures, specifically those most relevant to plant growth 

16 and yield responses.

17 (3) In considering whether the standard should be defined in terms of an annual

18 index value or a 3-year average of annual index values, the 2007 Staff Paper recognized 

19 that though most cumulative seasonal exposure levels of concern for vegetation have 

20 been expressed in terms of the annual timeframe, it may be appropriate to consider a 3-

21 year average for purposes of standard stability. However, the 2007 Staff Paper noted that 

22 for certain welfare effects of concern (e.g., foliar injury, yield loss for annual crops, 

23 growth effects on other annual vegetation and potentially tree seedlings), an annual time 
Draft O3 NPR –January 5, 2010 296 Deliberative, Do Not Quote or Cite

1 frame may be a more appropriate period in which to assess what level would provide the 

2 requisite degree of protection, while for other welfare effects (e.g., mature tree biomass 

3 loss), a 3-year average may also be appropriate. Thus, the 2007 Staff Paper concluded

4 that it is appropriate to consider both an annual and a 3-year average. Further, the 2007 

5 Staff Paper concluded that should a 3-year average of the 12-hour W126 form be 

6 selected, a lower standard level should be considered to reduce the potential of adverse 

7 impacts to annual species from a single high O3 year that could still occur while attaining 

8 a standard on average over 3 years. 

9 The CASAC, in considering what seasonal, diurnal, and annual or multiyear time 

10 periods are most appropriate when combined with a cumulative, seasonal form to protect 

11 vegetation from exposures of concern, agreed that the 2007 Staff Paper conclusion 

12 regarding the 3-month seasonal period and 12-hour daylight window was appropriate, 

13 with the distinction that both of these time periods likely represents the minimum time 

14 periods of importance. In particular, one O3 Panel member commented that for some 

15 species, additional O3 exposures of importance were occurring outside the 3-month 

16 seasonal and 12-hour diurnal windows. Further, the CASAC concluded that multi-year 

17 averaging to promote a “stable” secondary standard is less appropriate for a cumulative, 

18 seasonal secondary standard than for a primary standard based on daily maximum 8-hour 

19 concentrations. The CASAC further concluded that if multi-year averaging is employed 

20 to afford greater stability of the secondary standard, the level of the standard should be 

21 revised downward to assure that the desired degree of protection is not exceeded in 

22 individual years.
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1 The EPA, in determining which seasonal and diurnal time periods are most 

2 appropriate to propose, took into account the 2007 Staff Paper and CASAC views. In 

3 being careful to consider what is needed to provide the requisite degree of protection, no 

4 more and no less, in 2007 EPA proposed that the 3-month seasonal period and 12-hour 

5 daylight period are appropriate. Based on the 2007 Staff Paper conclusions discussed 

6 above, EPA was mindful that there is the potential for under-protection with a 12-hour 

7 diurnal window in areas with sufficiently elevated nighttime levels of O3 where sensitive 

8 species with a high degree of nocturnal stomatal conductance occur. On the other hand,

9 EPA also recognized that a longer diurnal window (e.g., 24-hour) has the possibility of 

10 over-protecting vegetation in areas where nighttime O3 levels remain relatively high but 

11 where no species having significant nocturnal uptake exist. In weighing these

12 considerations, EPA agreed with the 2007 Staff Paper conclusion that until additional 

13 information is available about the extent to which this co-occurrence of sensitive species 

14 and elevated nocturnal O3 exposures exists, and what levels of nighttime uptake are 

15 adverse to affected species, this information does not provide a basis for reaching a 

16 different conclusion at this time. The EPA also considered to what extent the 3-month 

17 period within the O3 season was appropriate, recognizing that many species of vegetation 

18 have longer growing seasons. The EPA further proposed that the maximum 3-month 

19 period is sufficient and appropriate to characterize O3 exposure levels associated with 

20 known levels of plant response. Therefore, EPA proposed that the most appropriate 

21 exposure periods for a cumulative, seasonal form is the daytime 12-hour window (8:00 

22 a.m. to 8:00 p.m.) during the consecutive 3-month period within the O3 monitoring 

23 season with the maximum W126 index value.
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1 The EPA also proposed an annual rather than a multi-year cumulative, seasonal 

2 standard. In proposing this option, EPA also believed that it was appropriate to consider 

3 the benefits to the public welfare that would accrue from establishing a 3-year average 

4 secondary standard, and solicited comment on this alternative. In so doing, EPA also 

5 agreed with 2007 Staff Paper and CASAC conclusions that should a 3-year standard be 

6 finalized, the level of the standard should be set so as to provide the requisite degree of 

7 protection for those vegetation effects judged to be adverse to the public welfare within a 

8 single annual period. 

9 c. Level

10 The 2007 Staff Paper, in identifying a range of levels for a 3-month, 12-hour 

11 W126 annual form appropriate to protect the public welfare from adverse impacts to 

12 vegetation from O3 exposures, considered what information from the array of vegetation 

13 effects evidence and exposure and risk assessment results was most useful. Regarding 

14 the vegetation effects evidence, the 2007 Staff Paper found stronger support than what 

15 was available at the time of the 1997 review for an increased level of protection for trees 

16 and ecosystems. Specifically, this expanded body of support includes: (1) additional 

17 field based data from free air, gradient and biomonitoring surveys demonstrating adverse 

18 levels of O3-induced above and/or below-ground growth reductions on trees at the 

19 seedling, sapling and mature growth stages and incidence of visible foliar injury

20 occurring at biomonitoring sites in the field at ambient levels of exposure; (2) qualitative 

21 support from free air (e.g., AspenFACE) and gradient studies on a limited number of tree 

22 species for the continued appropriateness of using OTC-derived C-R functions to predict 

23 tree seedling response in the field; (3) studies that continue to document below-ground 
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1 effects on root growth and “carry-over” effects occurring in subsequent years from O3

2 exposures; and (4) increased recognition and understanding of the structure and function 

3 of ecosystems and the complex linkages through which O3, and other stressors, acting at 

4 the organism and species level can influence higher levels within the ecosystem hierarchy 

5 and disrupt essential ecological attributes critical to the maintenance of ecosystem goods 

6 and services important to the public welfare. 

7 Based on the above observations and on the vegetation effects and the results of 

8 the exposure and impact assessment summarized above, the 2007 Staff Paper concluded

9 that just meeting the then current standard would still allow adverse levels of tree 

10 seedling biomass loss in sensitive commercially and ecologically important tree species 

11 in many regions of the country. Seedling risk assessment results showed that some tree 

12 seedling species are extremely sensitive (e.g., cottonwood, black cherry and aspen), with 

13 annual biomass losses occurring in the field of the same or greater magnitude that that of 

14 annual crops. Such information from the tree seedling risk assessment suggests that O3

15 levels would need to be substantially reduced to protect sensitive tree seedlings like black 

16 cherry from growth and foliar injury effects. 

17 In addition to the currently quantifiable risks to trees from ambient exposures, the 

18 2007 Staff Paper also considered the more subtle impacts of O3 acting in synergy with 

19 other natural and man-made stressors to adversely affect individual plants, populations 

20 and whole systems. By disrupting the photosynthetic process, decreasing carbon storage 

21 in the roots, increasing early senescence of leaves and affecting water use efficiency in 

22 trees, O3 exposures could potentially disrupt or change the nutrient and water flow of an 

23 entire system. Weakened trees can become more susceptible to other environmental 
Draft O3 NPR –January 5, 2010 300 Deliberative, Do Not Quote or Cite

1 stresses such as pest and pathogen outbreaks or harsh weather conditions. Though it is

2 not possible to quantify all the ecological and societal benefits associated with varying 

3 levels of alternative secondary standards, the 2007 Staff Paper concluded that this 

4 information should be weighed in considering the extent to which a secondary standard 

5 should be set so as to provide potential protection against effects that are anticipated to 

6 occur. 

7 In addition, the 2007 Staff Paper also recognized that in the 1997 review, EPA 

8 took into account the results of a 1996 Consensus Workshop. At this workshop, a group 

9 of independent scientists expressed their judgments on what standard form(s) and level(s) 

10 would provide vegetation with adequate protection from O3-related adverse effects. 

11 Consensus was reached with respect to selecting appropriate ranges of levels in terms of a 

12 cumulative, seasonal 3-month, 12-hr SUM06 standard for a number of vegetation effects 

13 endpoints. These ranges are identified below, with the estimated approximate equivalent 

14 W126 standard values shown in parentheses. For growth effects to tree seedlings in 

15 natural forest stands, a consensus was reached that a SUM06 range of 10 to 15 (W126 

16 range of 7 to 13) ppm-hour would be protective. For growth effects to tree seedlings and 

17 saplings in plantations, the consensus SUM06 range was 12 to 16 (W126 range of 9 to 

18 14) ppm-hour. For visible foliar injury to natural ecosystems, the consensus SUM06 

19 range was 8 to 12 (W126 range of 5 to 9) ppm-hour.

20 Taking these consensus statements into account, EPA stated in the 1997 final rule 

21 (62 FR 38856) that “the report lends important support to the view that the current 

22 secondary standard is not adequately protective of vegetation...[and]... foreshadows the 
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1 direction of future scientific research in this area, the results of which could be important 

2 in future reviews of the O3 secondary standard” (62 FR 38856). 

3 Given the importance EPA put on the consensus report in the 1997 review, the 

4 2007 Staff Paper considered to what extent research published after 1997 provided 

5 empirical support for the ranges of levels identified by the experts as protective of 

6 different types of O3-induced effects. With regard to O3-induced biomass loss in 

7 sensitive tree seedlings/saplings growing in natural forest stands, the information 

8 discussed in the 2007 Staff Paper, including the evidence from free air and gradient 

9 studies, provides additional direct support for the conclusion that the 1996 Consensus 

10 Workshop approximate W126 range of 7-13 ppm-hour was an appropriate range to 

11 consider in selecting a protective level. With regard to visible foliar injury, the available 

12 evidence, including the 2007 Staff Paper analysis of incidence in counties with FIA 

13 monitoring sites and air quality data, showed significant levels of county-level visible 

14 foliar injury incidence at the W126 level of 13 ppm-hour. However, because this analysis 

15 did not address risks of this effect at lower levels of O3 air quality, and because there is a 

16 significant uncertainty in predicting the degree of visible foliar injury symptoms expected 

17 for lower levels of O3 air quality, the evidence provides less certain but qualitative 

18 directional support for the 1996 Consensus Workshop range of 5 to 9 ppm-hour to protect 

19 against this effect. With regard to O3-induced effects on plantation trees, there is far less 

20 direct information available. Though some forest plantation trees are O3-sensitive, the 

21 monoculture nature of these stands makes uncertain the degree to which competition for 

22 resources might play a role and to what degree the variety of management practices 

23 applied would be expected to mitigate the O3-induced effects. Thus, it is difficult to 
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1 distinguish a protective range of levels for plantation trees from a range of levels that 

2 would be protective of O3-sensitive tree seedlings and saplings in natural forest stands. 

3 Therefore, on the basis of the strength of the evidence available, the 2007 Staff Paper 

4 concluded that it was appropriate to consider a range for a 3-month, 12-hour, W126 

5 standard that included the 1996 consensus recommendations for growth effects in tree 

6 seedlings in natural forest stands (i.e., 7-13 ppm-hour in terms of a W126 form).

7 In considering the available information on O3-related effects on crops in the 2008

8 rulemaking, the 2007 Staff Paper observed the following regarding the strength of the 

9 underlying crop science: (1) nothing in the recent literature points to a change in the 

10 relationship between O3 exposure and crop response across the range of species and/or 

11 cultivars of commodity crops currently grown in the U.S. that could be construed to make 

12 less appropriate the use of commodity crop C-R functions developed in the NCLAN 

13 program; (2) new field-based studies (e.g., SoyFACE) provide qualitative support in a 

14 few limited cases for the appropriateness of using OTC-derived C-R functions to predict 

15 crop response in the field; and (3) refinements in the exposure, risk and benefits 

16 assessments in this review reduce some of the uncertainties present in the 1997 review. 

17 On the basis of these observations, the 2007 Staff Paper concluded that nothing in the 

18 newly assessed information called into question the strength of the underlying science 

19 upon which EPA based its proposed decision in the 1997 review to select a level of a 

20 cumulative, seasonal form associated with protecting 50 percent of crop cases from no 

21 more than 10 percent yield loss as providing the requisite degree of protection for 

22 commodity crops. 
Draft O3 NPR –January 5, 2010 303 Deliberative, Do Not Quote or Cite

1 The 2007 Staff Paper then considered whether any additional information is 

2 available to inform judgments as to the adversity of various O3-induced levels of crop 

3 yield loss to the public welfare. As noted above, the 2007 Staff Paper observed that 

4 agricultural systems are heavily managed, and that in addition to stress from O3, the 

5 annual productivity of agricultural systems is vulnerable to disruption from many other 

6 stressors (e.g., weather, insects, disease), whose impact in any given year can greatly

7 outweigh the direct reduction in annual productivity resulting from elevated O3

8 exposures. On the other hand, O3 can also more subtly impact crop and forage nutritive 

9 quality and indirectly exacerbate the severity of the impact from other stressors. Though 

10 these latter effects currently cannot be quantified, they should be considered in judging to 

11 what extent a level of protection selected to protect commodity crops should be 

12 precautionary.

13 Based on the above considerations, the 2007 Staff Paper concluded that the level 

14 of protection (no more than 10% yield or biomass loss in 50% of studied cases) judged 

15 requisite in the 1997 review to protect the public welfare from adverse levels of O3-

16 induced reductions in crop yields and tree seedling biomass loss, as provided by a W126 

17 level of 21 ppm-hour, remains appropriate for consideration as an upper bound of a range 

18 of appropriate levels.

19 Thus, the 2007 Staff Paper concluded, based on all the above considerations, that 

20 an appropriate range of 3-month, 12-hour W126 levels was 7 to 21 ppm-hour, 

21 recognizing that the level selected is largely a policy judgment as to the requisite level of 

22 protection needed. In determining the requisite level of protection for crops and trees,

23 and indirectly, ecosystems, the 2007 Staff Paper recognized that it is appropriate to weigh 
Draft O3 NPR –January 5, 2010 304 Deliberative, Do Not Quote or Cite

1 the importance of the predicted risks of these effects in the overall context of public 

2 welfare protection, along with a determination as to the appropriate weight to place on 

3 the associated uncertainties and limitations of this information. 

4 The CASAC, in its final letter to the Administrator (Henderson, 2007), agreed 

5 with the 2007 Staff Paper recommendations that the lower bound of the range within 

6 which a seasonal W126 welfare-based (secondary) O3 standard should be considered is 

7 approximately 7 ppm-hour; however, it did not agree with staff’s recommendation that 

8 the upper bound of the range for consideration should be as high as 21 ppm-hour. Rather, 

9 CASAC recommended that the upper bound of the range considered should be no higher 

10 than 15 ppm-hour, which is just above the upper ends of the ranges identified in the 1996 

11 Consensus Workshop as being protective of tree seedlings and saplings grown in natural 

12 forest stands and in plantations. The lower end of this range (7 ppm-hour) is the same as 

13 the lower end of the range identified in the 1996 Consensus Workshop as protective of 

14 tree seedlings in natural forest stands from growth effects.

15 In the 2007 proposed rule, taking 2007 Staff Paper and CASAC views into 

16 account, EPA proposed a range of levels for a cumulative, seasonal secondary standard as 

17 expressed in terms of the maximum 3 month, 12-hour W126 form, in the range of 7 to 21 

18 ppm-hour. This range encompasses the range of levels recommended by CASAC, and 

19 also includes a higher level as recommended for consideration in the 2007 Staff Paper. 

20 Given the uncertainty in determining the risk attributable to various levels of exposure to 

21 O3, EPA believed, as a public welfare policy judgment, that this was a reasonable range 

22 to propose.

23 2. Considerations Regarding the 2007 Proposed 8-Hour Standard
Draft O3 NPR –January 5, 2010 305 Deliberative, Do Not Quote or Cite

1 In the 1997 review, the 1996 Staff Paper included an analysis to compare the 

2 degree of overlap between areas that would be expected not to meet the range of 

3 alternative 8-hour standards being considered for the primary NAAQS and those 

4 expected not to meet the range of values (expressed in terms of the seasonal SUM06 

5 index) of concern for vegetation. This result suggested that improvements in national air 

6 quality expected to result from attaining an 8-hour primary standard within the 

7 recommended range of levels would also be expected to reduce levels of concern for 

8 vegetation in those same areas. In the 1997 final rule, the decision was made, on the 

9 basis of both science and policy considerations, to make the secondary identical to the 

10 primary standard. It acknowledged, however, that uncertainties remained “as to the 

11 extent to which air quality improvements designed to reduce 8-hour average O3

12 concentrations averaged over a 3-year period would reduce O3 exposures measured by a 

13 seasonal SUM06 index” (62 FR 38876). 

14 On the basis of that history, the 2007 Staff Paper analyzed the degree of overlap 

15 expected between alternative 8-hour and cumulative seasonal secondary standards (as 

16 discussed above in section IV.C.1) using then recent air quality. Based on the results, the 

17 2007 Staff Paper concluded that the degree to which the then current 8-hour standard 

18 form and level would overlap with areas of concern for vegetation expressed in terms of 

19 the 12-hour W126 standard is inconsistent from year to year and would depend greatly on 

20 the level of the 12-hour W126 and 8-hour standards selected and the distribution of 

21 hourly O3 concentrations within the annual and/or 3-year average period. 

22 Thus, though the 2007 Staff Paper recognized again that meeting the current or 

23 alternative levels of the 8-hour average standard could result in air quality improvements 
Draft O3 NPR –January 5, 2010 306 Deliberative, Do Not Quote or Cite

1 that would potentially benefit vegetation in some areas, it urged caution be used in 

2 evaluating the likely vegetation impacts associated with a given level of air quality

3 expressed in terms of the 8-hour average form in the absence of parallel W126 

4 information. This caution was due to the concern that the analysis in the 2007 Staff 

5 Paper may not be an accurate reflection of the true situation in non-monitored, rural 

6 counties due to the lack of more complete monitor coverage in many rural areas. Further, 

7 of the counties that did not show overlap between the two standard forms, most were 

8 located in rural/remote high elevation areas which have O3 air quality patterns that are 

9 typically different from those associated with urban and near urban sites at lower 

10 elevations. Because the majority of such areas are currently not monitored, it is believed 

11 there are likely to be additional areas that have similar air quality distributions that would 

12 lead to the same disconnect between forms. Thus, the 2007 Staff Paper concluded that it 

13 remained problematic to determine the appropriate level of protection for vegetation 

14 using an 8-hour average form.

15 The CASAC recognized that an important difference between the effects of acute 

16 exposures to O3 on human health and the effects of O3 exposures on welfare is that 

17 vegetation effects are more dependent on the cumulative exposure to, and uptake of, O3

18 over the course of the entire growing season (Henderson, 2006c). The CASAC O3 Panel 

19 members were unanimous in concluding the protection of natural terrestrial ecosystems 

20 and managed agricultural crops requires a secondary O3 standard that is substantially

21 different from the primary O3 standard in averaging time, level, and form (Henderson, 

22 2007).
Draft O3 NPR –January 5, 2010 307 Deliberative, Do Not Quote or Cite

1 In considering the appropriateness of proposing a revised secondary standard that 

2 would be identical to the proposed primary standard, EPA took into account the approach 

3 used by the Agency in the 1997 review, the conclusions of the 2007 Staff Paper, CASAC 

4 advice, and the views of public commenters. The EPA first considered the 2007 Staff 

5 Paper analysis of the projected degree of overlap between counties with air quality

6 expected to meet various alternative levels of an 8-hour standard and alternative levels of 

7 a W126 standard based on monitored air quality data. This analysis showed significant 

8 overlap within the proposed range of the primary 8-hour form and selected levels of the 

9 W126 standard form being considered, with the degree of overlap between these two 

10 forms depending greatly on the levels selected and the distribution of hourly O3

11 concentrations within the annual and/or 3-year average period. On this basis, EPA

12 concluded that a secondary standard set identical to the proposed primary standard would 

13 provide a significant degree of additional protection for vegetation as compared to that 

14 provided by the current secondary standard. The EPA also recognized that lack of rural 

15 monitoring data made uncertain the degree to which the proposed 8-hour or W126 

16 alternatives would be protective, and that there would be the potential for not providing 

17 the appropriate degree of protection for vegetation in areas with air quality distributions 

18 that result in a high cumulative, seasonal exposure but do not result in high 8-hour 

19 average exposures. While this potential for under-protection using an 8-hour standard 

20 was clear, the number and size of areas at issue and the degree of risk was hard to 

21 determine. On the other hand, EPA also considered at that time that there was a potential 

22 risk of over-protection with a cumulative, seasonal standard given the inherent 

23 uncertainties associated with moving to a new form for the secondary standard, in 
Draft O3 NPR –January 5, 2010 308 Deliberative, Do Not Quote or Cite

1 particular those associated with predicting exposure and risk patterns based on a limited 

2 rural monitoring network. 

3 The EPA also considered the views and recommendations of CASAC, and agreed

4 that a cumulative, seasonal standard is the most biologically relevant way to relate 

5 exposure to plant growth response. However, as reflected in the public comments, EPA

6 also recognized that there remained significant uncertainties in determining or 

7 quantifying the degree of risk attributable to varying levels of O3 exposure, the degree of 

8 protection that any specific cumulative, seasonal standard would produce, and the 

9 associated potential for error in determining the standard that will provide a requisite 

10 degree of protection -- i.e., sufficient but not more than what is necessary. Given this 

11 uncertainty, EPA also believed it was appropriate to consider the degree of protection that 

12 would be afforded by a secondary standard that was identical to the then proposed 

13 primary standard. Based on its consideration of the full range of views as described 

14 above, and in the 2007 proposed rule, EPA proposed as a second option to revise the 

15 secondary standard to be identical in every way to the then proposed primary standard.

16 3. Basis for 2008 Decision on the Secondary Standard

17 In the 2008 final rule, EPA noted that deciding on the appropriate secondary 

18 standard involved making a choice between two possible alternatives, each with their 

19 strengths and weaknesses. The 2008 final rule reported that within the Administration at 

20 that time there had been a robust discussion of the same strengths and weaknesses 

21 associated with each option that were identified earlier. The process by which EPA 

22 reached its final conclusion is described in the final rule (73 FR 16497). The rationale for 

23 the 2008 decision presented in the final rule (73 FR 16499 – 16500) is described below. 
Draft O3 NPR –January 5, 2010 309 Deliberative, Do Not Quote or Cite

1 In considering the appropriateness of establishing a new standard defined in terms 

2 of a cumulative, seasonal form, or revising the then current secondary standard by

3 making it identical to the revised primary standard, EPA took into account the approach 

4 used by the Agency in the 1997 review, the conclusions of the 2007 Staff Paper, CASAC 

5 advice, and the views of public commenters. In giving consideration to the approach 

6 taken in the 1997 review, EPA first considered the 2007 Staff Paper analysis of the 

7 projected degree of overlap between counties with air quality expected to meet the 

8 revised 8-hour primary standard, set at a level of 0.075 ppm, and alternative levels of a 

9 W126 standard based on currently monitored air quality data. This analysis showed 

10 significant overlap between the revised 8-hour primary standard and selected levels of the 

11 W126 standard form being considered, with the degree of overlap between these 

12 alternative standards depending greatly on the W126 level selected and the distribution of 

hourly O3 concentrations within the annual and/or 3-year average period.59 13 On this basis, 

14 as an initial matter, EPA concluded that a secondary standard set identical to the 

15 proposed primary standard would provide a significant degree of additional protection for 

16 vegetation as compared to that provided by the then current 0.084 ppm secondary

17 standard. In further considering the significant uncertainties that remain in the available 

18 body of evidence of O3-related vegetation effects and in the exposure and risk analyses 

19 conducted for the 2008 rulemaking, and the difficulty in determining at what point 

20 various types of vegetation effects become adverse for sensitive vegetation and 

21 ecosystems, EPA focused its consideration on a level for an alternative W126 standard at 

 

59 Prior to publication of the 2008 final rule, EPA did further analysis of the 

degree of overlap to extend the 2007 Staff Paper analyses, and that analysis was available 

in the docket.
Draft O3 NPR –January 5, 2010 310 Deliberative, Do Not Quote or Cite

1 the upper end of the proposed range (i.e., 21 ppm-hour). The 2007 Staff Paper analysis 

2 showed that at that W126 standard level, there would be essentially no counties with air 

3 quality that would be expected both to exceed such an alternative W126 standard and to 

4 meet the revised 8-hour primary standard – that is, based on this analysis of currently 

5 monitored counties, a W126 standard would be unlikely to provide additional protection 

6 in any monitored areas beyond that likely to be provided by the revised primary standard.

7 The EPA also recognized that the general lack of rural monitoring data made 

8 uncertain the degree to which the revised 8-hour standard or an alternative W126 

9 standard would be protective in those areas, and that there would be the potential for not 

10 providing the appropriate degree of protection for vegetation in areas with air quality

11 distributions that result in a high cumulative, seasonal exposure but do not result in high 

12 8-hour average exposures. While this potential for under-protection using an 8-hour 

13 standard was clear, the number and size of areas at issue and the degree of risk was hard 

14 to determine. However, EPA concluded at that time that an 8-hour standard would also 

15 tend to avoid the potential for providing more protection than is necessary, a risk that 

16 EPA concluded would arise from moving to a new form for the secondary standard 

17 despite significant uncertainty in determining the degree of risk for any exposure level 

18 and the appropriate level of protection, as well as uncertainty in predicting exposure and 

19 risk patterns.

20 The EPA also considered the views and recommendations of CASAC, and agreed 

21 that a cumulative, seasonal standard was the most biologically relevant way to relate 

22 exposure to plant growth response. However, as reflected in some public comments, 

23 EPA also judged that there remained significant uncertainties in determining or 
Draft O3 NPR –January 5, 2010 311 Deliberative, Do Not Quote or Cite

1 quantifying the degree of risk attributable to varying levels of O3 exposure, the degree of 

2 protection that any specific cumulative, seasonal standard would produce, and the 

3 associated potential for error in determining the standard that will provide a requisite 

4 degree of protection — i.e., sufficient but not more than what is necessary. Given these 

5 significant uncertainties, EPA concluded at that time that establishing a new secondary

6 standard with a cumulative, seasonal form would result in uncertain benefits beyond 

7 those afforded by the revised primary standard and therefore may be more than necessary

8 to provide the requisite degree of protection.

9 Based on its consideration of the views discussed above, EPA judged in the 2008 

10 rulemaking that the appropriate balance to be drawn was to revise the secondary standard 

11 to be identical in every way to the revised primary standard. The EPA believed that such 

12 a standard would be sufficient to protect public welfare from known or anticipated 

13 adverse effects, and did not believe that an alternative cumulative, seasonal standard was 

14 needed to provide this degree of protection. The EPA believed that this judgment 

15 appropriately considered the requirement for a standard that is neither more nor less 

16 stringent than necessary for this purpose.

17 For the reasons discussed above, and taking into account information and 

18 assessments presented in the 2006 Criteria Document and 2007 Staff Paper, the advice 

19 and recommendations of the CASAC Panel, and the public comments to date, EPA 

20 decided to revise the existing 8-hour secondary standard. Specifically, EPA revised the 

21 then current 8-hour average 0.084 ppm secondary standard by making it identical to the 

22 revised 8-hour primary standard set at a level of 0.075 ppm.

23 4. CASAC Views Following 2008 Decision 
Draft O3 NPR –January 5, 2010 312 Deliberative, Do Not Quote or Cite

1 Following the 2008 decision on the O3 standards, serious questions were raised as 

2 to whether the standards met the requirements of the CAA. In April 2008, the members 

3 of the CASAC Ozone Review Panel sent a letter to EPA stating “In our most-recent 

4 letters to you on this subject - dated October 2006 and March 2007 - ... the Committee 

5 recommended an alternative secondary standard of cumulative form that is substantially 

6 different from the primary Ozone NAAQS in averaging time, level and form —

7 specifically, the W126 index within the range of 7 to 15 ppm-hour, accumulated over at 

8 least the 12 “daylight” hours and the three maximum ozone months of the summer 

9 growing season” (Henderson, 2008). The letter continued: “The CASAC now wishes to 

10 convey, by means of this letter, its additional, unsolicited advice with regard to the 

11 primary and secondary Ozone NAAQS. In doing so, the participating members of the 

12 CASAC Ozone Review Panel are unanimous in strongly urging you or your successor as 

13 EPA Administrator to ensure that these recommendations be considered during the next 

14 review cycle for the Ozone NAAQS that will begin next year” (id.). The letter further 

15 stated the following views:

16 The CASAC was ... greatly disappointed that you failed to change the 

17 form of the secondary standard to make it different from the primary

18 standard. As stated in the preamble to the Final Rule, even in the previous 

19 1996 ozone review, “there was general agreement between the EPA staff, 

20 CASAC, and the Administrator, ... that a cumulative, seasonal form was 

21 more biologically relevant than the previous 1-hour and new 8-hour

22 average forms (61 FR 65716)” for the secondary standard. Therefore, in 

23 both the previous review and in this review, the Agency staff and its 

24 advisors agreed that a change in the form of the secondary standard was 

25 scientifically well-justified.

26
Draft O3 NPR –January 5, 2010 313 Deliberative, Do Not Quote or Cite

1 : : : : ;

2

3 Unfortunately, this scientifically-sound approach of using a cumulative 

4 exposure index for welfare effects was not adopted, and the default 

5 position of using the primary standard for the secondary standard was 

6 once again instituted. Keeping the same form for the secondary Ozone 

7 NAAQS as for the primary standard is not supported by current scientific 

8 knowledge indicating that different indicator variables are needed to 

9 protect vegetation compared to public health. The CASAC was further 

10 disappointed that a secondary standard of the W126 form was not 

11 considered from within the Committee’s previously-recommended range 

12 of 7 to 15 ppm-hour. The CASAC sincerely hopes that, in the next round of 

13 Ozone NAAQS review, the Agency will be able to support and establish a 

14 reasonable and scientifically-defensible cumulative form for the secondary 

15 standard. (Henderson, 2008)

16

17 5. Administrator’s Proposed Conclusions

18 For the reasons discussed below, the Administrator proposes to set a cumulative 

19 seasonal standard expressed as an annual index of the sum of weighted hourly 

20 concentrations (i.e., the W126 form), cumulated over 12 hours per day (8:00 am to 8:00 

21 pm) during the consecutive 3-month period within the O3 season with the maximum 

22 index value, set at a level within the range of 7 to 15 ppm-hour. This proposed decision 

23 takes into account the information and assessments presented in the 2006 Criteria 

24 Document and the 2007 Staff Paper and related technical support documents, the advice 

25 and recommendations of CASAC both during and following the 2008 rulemaking, and 

26 public comments received in conjunction with review of drafts of these documents and 

27 on the 2007 proposed rule.
Draft O3 NPR –January 5, 2010 314 Deliberative, Do Not Quote or Cite

1 a. Form

2 As discussed above in section IV.B, the 2006 Criteria Document and 2007 Staff 

3 Paper concluded that the recent vegetation effects literature evaluated in the 2008

4 rulemaking strengthens and reaffirms conclusions made in the 1997 review that the use of 

5 a cumulative exposure index that differentially weights ambient concentrations is best 

6 able to relate ambient exposures to vegetation response. The 1997 review focused in 

7 particular on two of these cumulative forms, the SUM06 and W126 (EPA, 1996). Given 

8 that the data available at that time were unable to distinguish between these forms, the 

9 EPA, based on the policy consideration of not including O3 concentrations considered to 

10 be within the PRB, estimated at that time to be between 0.03 and 0.05 ppm, concluded 

11 that the SUM06 form would be the more appropriate choice for a cumulative, exposure 

12 index for a secondary standard. 

13 In the 2008 rulemaking, the 2007 Staff Paper evaluated the continued 

14 appropriateness of the SUM06 form in light of new estimates of PRB that were lower 

15 than in the 1997 review, and the continued lack of evidence within the vegetation effects 

16 literature of a biological threshold for vegetation exposures of concern. On the basis of 

17 these policy and science-related considerations, the 2007 Staff Paper concluded that the 

18 W126 form was the more appropriate cumulative, concentration-weighted form. 

19 Specifically, the W126, by its incorporation of a sigmoidal weighting scheme, does not 

20 create an artificially imposed concentration threshold, gives proportionally more weight 

21 to the higher and typically more biologically potent concentrations, and is not 

22 significantly influenced by O3 concentrations within the range of estimated PRB. 
Draft O3 NPR –January 5, 2010 315 Deliberative, Do Not Quote or Cite

1 As discussed above, the CASAC, based on its assessment of the same vegetation 

2 effects science, agreed with the 2006 Criteria Document and 2007 Staff Paper and 

3 unanimously concluded that protection of vegetation from the known or anticipated 

4 adverse effects of ambient O3 “requires a secondary standard that is substantially

5 different from the primary standard in averaging time, level, and form,” i.e. not identical 

6 to the primary standard for O3 (Henderson, 2007). Moreover, the members of CASAC 

7 and a substantial majority of the other CASAC Panel members agreed with 2007 Staff 

8 Paper conclusions and encouraged EPA to establish an alternative cumulative secondary

9 standard for O3 and related photochemical oxidants that is distinctly different in 

10 averaging time, form and level from the then current or potentially revised 8-hour 

11 primary standard (Henderson, 2006c). The CASAC Panel also stated that “the 

12 recommended metric for the secondary ozone standard is the (sigmoidally weighted) 

13 W126 index” (Henderson, 2007).

14 In reconsidering the 2008 final rule, the Administrator agrees with the conclusions 

15 drawn in the 2006 Criteria Document, 2007 Staff Paper and by CASAC that the scientific 

16 evidence available in the 2008 rulemaking continues to demonstrate the cumulative 

17 nature of O3-induced plant effects and the need to give greater weight to higher 

18 concentrations. Thus, the Administrator concludes that a cumulative exposure index that 

19 differentially weights O3 concentrations represents a reasonable policy choice for a 

20 secondary standard to protect against the effects of O3 on vegetation The Administrator 

21 further agrees with both the 2007 Staff Paper and CASAC that the most appropriate 

22 cumulative, concentration-weighted form to consider is the sigmoidally weighted W126 

23 form
Draft O3 NPR –January 5, 2010 316 Deliberative, Do Not Quote or Cite

1 The Administrator notes that in the 2007 proposed rule, EPA proposed a second 

2 option of revising the then current 8-hour average secondary standard by making it 

3 identical to the proposed 8-hour primary standard. The 2007 Staff Paper analyzed the 

4 degree of overlap expected between alternative 8-hour and cumulative seasonal 

5 secondary standards using recent air quality monitoring data. Based on the results, the 

6 2007 Staff Paper concluded that the degree to which the current 8-hour standard form and 

7 level would overlap with areas of concern for vegetation expressed in terms of the 12-

8 hour W126 standard is inconsistent from year to year and would depend greatly on the 

9 level of the 12-hour W126 and 8-hour standards selected and the distribution of hourly O3

10 concentrations within the annual and/or 3-year average period. The 2007 Staff Paper also

11 recognized that meeting the then current or alternative levels of the 8-hour average 

12 standard could result in air quality improvements that would potentially benefit 

13 vegetation in some areas, but urged caution be used in evaluating the likely vegetation 

14 impacts associated with a given level of air quality expressed in terms of the 8-hour 

15 average form in the absence of parallel W126 information. This caution was due to the 

16 concern that the analysis in the 2007 Staff Paper may not be an accurate reflection of the 

17 true situation in non-monitored, rural counties due to the lack of more complete monitor 

18 coverage in many rural areas. Further, of the counties that did not show overlap between 

19 the two standard forms, most were located in rural/remote high elevation areas which 

20 have O3 air quality patterns that are typically different from those associated with urban 

21 and near urban sites at lower elevations. Because the majority of such areas are currently 

22 not monitored, there are likely to be additional areas that have similar air quality

23 distributions that would lead to the same disconnect between forms. Thus, the 2007 Staff 
Draft O3 NPR –January 5, 2010 317 Deliberative, Do Not Quote or Cite

1 Paper concluded that it remains problematic to determine the appropriate level of 

2 protection for vegetation using an 8-hour average form.

3 The Administrator also notes that CASAC recognized that an important difference 

4 between the effects of acute exposures to O3 on human health and the effects of O3

5 exposures on welfare is that vegetation effects are more dependent on the cumulative 

6 exposure to, and uptake of, O3 over the course of the entire growing season (Henderson, 

7 2006c). The CASAC O3 Panel members were unanimous in concluding the protection of 

8 natural terrestrial ecosystems and managed agricultural crops requires a secondary O3

9 standard that is substantially different from the primary O3 standard in form, averaging 

10 time, and level (Henderson, 2007).

11 In reaching her proposed decision in this reconsideration of the 2008 final rule, 

12 the Administrator has considered the comments received on the 2007 proposed rule 

13 regarding revising the secondary standard either to reflect a new, cumulative form or by 

14 remaining equal to a revised primary standard. The commenters generally fell into two 

15 groups.

16 One group of commenters, including environmental organizations, strongly 

17 supported the proposed option of moving to a cumulative, seasonal standard, generally 

18 based on the reasoning explained in the 2007 proposal. Commenters in this group also 

19 expressed serious concerns with the other proposed option of setting a secondary O3

20 standard in terms of the same form and averaging time (i.e., daily maximum 8-hour 

21 average O3 concentration) as the primary standard. These commenters expressed the 

22 view that such a standard would fail to protect public welfare because the maximum daily

23 8-hour average O3 concentration failed to adequately characterize harmful O3 exposures 
Draft O3 NPR –January 5, 2010 318 Deliberative, Do Not Quote or Cite

1 to vegetation. This view was generally based on the observation that there is no 

2 consistent relationship in areas across the U.S. between 8-hour peak O3 concentrations 

3 and the longer-term cumulative exposures aggregated over a growing season that are 

4 biologically relevant in characterizing O3-related effects on sensitive vegetation. Thus, as 

5 EPA noted in the 2007 proposed rule, there is a lack of a rational connection between the 

6 level of an 8-hour standard and the requisite degree of protection required for a secondary

7 O3 NAAQS.

8 Another group of commenters, including industry organizations, agreed that a 

9 cumulative form of the standard may better match the underlying data, but expressed the 

10 view that remaining uncertainties associated with the vegetation effects evidence and/or 

11 EPA’s exposure, risk and benefits assessments were so great that the available 

12 information did not provide an adequate basis to adopt a standard with a level based on a 

13 cumulative, seasonal form. These commenters asserted that because of the substantial 

14 uncertainties remaining at the time of the 2008 rulemaking, the benefits of changing to a 

15 W126 form were too uncertain to warrant revising the form of the standard at that time.

16 The Administrator notes that in both the 1997 and the 2008 decisions, EPA 

17 recognized that the risk to vegetation from O3 exposures comes from cumulative 

18 exposures over a season or seasons. The CASAC has fully endorsed this view based on 

19 the available scientific evidence and assessments, and there is no significant disagreement 

20 on this issue by commenters. Thus, it is clear that the purpose of the secondary O3

21 NAAQS should be to provide an appropriate degree of protection against cumulative, 

22 seasonal exposures to O3 that are known or anticipated to harm sensitive vegetation or 

23 ecosystems. In reconsidering the 2008 final rule, the Administrator recognizes that the 
Draft O3 NPR –January 5, 2010 319 Deliberative, Do Not Quote or Cite

1 issue before the Agency is what form of the standard is most appropriate to perform that 

2 function.

3 Within this framework, the Administrator recognizes that it is clear that a 

4 cumulative, seasonal form has a distinct advantage in protecting against cumulative, 

5 seasonal exposures. Such a form is specifically designed to measure directly the kind of 

6 O3 exposures that can cause harm to vegetation. In contrast, an 8-hour standard does not 

7 measure cumulative, seasonal exposures directly, and can only indirectly afford some 

8 degree of protection against such exposures. To the extent that clear relationships exist 

9 between 8-hour daily peak O3 concentrations and cumulative, seasonal exposures, the 8-

10 hour form and averaging time would have the potential to be effective as an indirect 

11 surrogate. However, as discussed in the 2007 proposed rule and the 2008 final rule, the 

12 evidence shows that there are known types of O3 air quality patterns that can lead to high 

13 levels of cumulative, seasonal O3 exposures without the occurrence of high daily 8-hour 

14 peak O3 concentrations. An 8-hour form and averaging time is an indirect way to 

15 measure biologically relevant exposure patterns, is poorly correlated with such exposure 

16 patterns, and therefore is less likely to identify and protect against the kind of cumulative, 

17 seasonal exposure patterns that have been determined to be harmful. 

18 Past arguments or reasons for not moving to a cumulative, seasonal form, with 

19 appropriate exposure periods, have not been based on disagreement over the biological 

20 relevance of the cumulative, seasonal form, or the recognized disadvantages of an 8-hour 

21 standard in measuring and identifying a specified cumulative, seasonal exposure pattern. 

22 The reasons for not moving to such a form have been based on concerns over whether 

23 EPA has an adequate basis to identify the nature and magnitude of cumulative, seasonal 
Draft O3 NPR –January 5, 2010 320 Deliberative, Do Not Quote or Cite

1 exposure patterns that the standard should be designed to protect against, given the 

2 various uncertainties in the evidence and the lack of rural O3 monitoring data. This most 

3 directly translates into a concern over whether EPA has an adequate basis to determine an 

4 appropriate level for a cumulative, seasonal secondary standard.

5 The Administrator has also considered issues associated with selection of the 

6 W126 cumulative form, as reflected in the following assertions made by some

7 commenters on the 2007 proposed rule: (1) the W126 form lacks a biological basis, since 

8 it is merely a mathematical expression of exposure that has been fit to specific responses 

9 in OTC studies, such that its relevance for real world biological responses is unclear; (2) 

10 a flux-based model would be a better choice than a cumulative metric because it is an 

11 improvement over the many limitations and simplifications associated with the 

12 cumulative form; however, there is insufficient data to apply such a model at present; (3) 

13 the European experience with cumulative O3 metrics has been disappointing and now 

14 Europeans are working on their second level approach, which will be flux-based; and (4) 

15 a second index that reflects the accumulation of peaks at or above 0.10 ppm (called 

16 N100) should be added to a W126 index to achieve appropriate protection.

17 With regard to whether the W126 index lacks a biological basis, the 

18 Administrator finds no basis for reaching such a conclusion. As discussed above in 

19 section IV.B, the vegetation effects science is clear that exposures of concern to plants 

20 are not based on one discrete 8-hour period but on the repeated occurrence of elevated O3

21 levels throughout the plant’s growing season. The cumulative nature of the W126 is 

22 supported by the basic biological understanding that plants in the U.S. are generally most 

23 biologically active during the warm season and are exposed to ambient O3 throughout 
Draft O3 NPR –January 5, 2010 321 Deliberative, Do Not Quote or Cite

1 this biologically active period. In addition, it has been shown in the scientific literature 

2 that all else being equal, plants respond more to higher O3 concentrations, with no 

3 evidence of an exposure threshold for vegetation effects. The W126 sigmoidal weighting 

4 function reflects both of these understandings, by not including a threshold below which 

5 concentrations are not included, and by differentially weighting concentrations to give 

6 greater weight to higher concentrations and less weight to lower ones. 

7 With regard to whether a flux-based model would be a better choice, the 2007 

8 Staff Paper acknowledged that flux models may produce a more accurate calculation of 

9 dose to a specific plant species in a specific area. However, dose-response relationships 

10 have not been developed for these flux calculations for plants growing in the U.S. 

11 Further, flux calculations require large amounts of data for the physiology of each plant 

12 species and the local conditions for the growing range of each plant species. These 

13 exercises may be useful for limited small-scale risk assessments, but do not provide an 

14 appropriate basis for a national standard at this time.

15 With regard to dissatisfaction with the performance of a particular cumulative 

index in use in Europe,60 16 and growing interest in development of flux-based models, the 

17 2007 Staff Paper (Appendix 7A) noted that “because of a lack of flux-response data, a 

18 cumulative, cutoff concentration based (e.g., AOT40) exposure index will remain in use 

19 in Europe for the near future for most crops and for forests and semi-natural herbaceous 

20 vegetation (Ashmore et al., 2004a).” Further, like the SUM06 index, the AOT40 index 

 

60 The AOT40 index used in Europe is a cumulative index that incorporates a 

threshold at 0.04 ppm (40 ppb). This index is calculated as the area over the threshold 

(AOT) by subtracting 40 ppb from the value of each hourly concentration above that 

threshold and then cumulating each hourly difference over a specified window.
Draft O3 NPR –January 5, 2010 322 Deliberative, Do Not Quote or Cite

1 incorporates a threshold below which concentrations are not considered. Though the 

2 AOT40 threshold is lower than the threshold value in SUM06, the 2007 Staff Paper 

3 concluded that the vegetation effects information does not provide evidence of an effects 

4 threshold that applies to all species. Thus, the Administrator concludes neither of these 

5 forms is as biologically relevant as the W126 form.

6 With regard to consideration of coupling a W126 form with a separate N100 

7 index, there was very little research on the N100 index or a coupled approach to be 

8 evaluated in the 2008 rulemaking. The CASAC, after reviewing all the information in 

9 the 2006 Criteria Document and the 2007 Staff Paper, did not recommend an additional 

10 N100 index for consideration. Therefore, there is no basis at this time to judge the extent 

11 to which such a coupled W126-N100 form would be a better choice than the proposed 

12 W126 form. Further, the W126 form incorporates a weighting scheme that places greater 

13 weight on increasing concentrations and gives every concentration of 0.10 ppm and 

14 above an equal weight of 1, which is the highest weight in this sigmoidal weighting 

15 function. 

16 In summary, having considered the scientific information and assessment results 

17 available in the 2008 rulemaking as discussed above in this proposal notice, as well as the 

18 recommendations of the staff and CASAC, and having taken into consideration issues 

19 raised in public comments received as part of the 2008 rulemaking, and recognizing the 

20 determinations made below in section IV.D.5.c on level, the Administrator concludes that 

21 it is appropriate to set the secondary standard using a cumulative, seasonal form. The 

22 Administrator also concludes that the W126 form is best suited to reflect the biological 

23 impacts of O3 exposure on vegetation, and that there is adequate certainty in the 
Draft O3 NPR –January 5, 2010 323 Deliberative, Do Not Quote or Cite

1 information available in the 2008 rulemaking to support such a change in form. Thus, the 

2 Administrator proposes to set the secondary standard using a cumulative, seasonal W126 

3 form.

b. Averaging Times61 4

5

6 The Administrator, in addition to reconsidering what form of a secondary

7 standard is most appropriate for protecting vegetation, is also reconsidering what 

8 exposure periods (e.g., seasonal window, diurnal window), and what standard index, in 

9 terms of an annual index value versus a 3-year average of annual index values, are most 

10 appropriate when used in conjunction with the W126 cumulative seasonal form. Based 

11 on the information set forth in the 2007 Staff Paper, as well as CASAC views, as 

12 discussed above in section IV.D.1.b, the Administrator has reached conclusions regarding 

13 exposure periods, and the annual versus 3-year average index, that have the most 

14 biological relevance for plant response, as discussed below.

15 In considering an appropriate seasonal window, the Administrator notes that the 

16 2007 Staff Paper concluded that the consecutive 3-month period within the O3 season 

17 with the highest W126 index value (e.g., maximum 3-month period) was a reasonable 

18 seasonal time period to consider. The Administrator further notes that the 2007 Staff 

19 Paper acknowledged that the selection of any single seasonal exposure period for a 

20 national standard would necessarily represent a compromise, given the significant 

21 variability in growth patterns and lengths of growing seasons among the wide range of 

 

61 While the term “averaging time” is used, for the cumulative, seasonal standard 

the seasonal and diurnal time periods at issue are those over which exposures during a 

specified period of time are cumulated, not averaged.
Draft O3 NPR –January 5, 2010 324 Deliberative, Do Not Quote or Cite

1 sensitive vegetation species occurring within the U.S. However, the Administrator also 

2 considered the Staff Paper conclusion that the period of maximum potential plant uptake 

3 of O3 would also likely coincide with the period of highest O3 occurring within the intra4 annual period defined as the O3 season, since the high temperature and light conditions 

5 conducive to O3 formation are also conducive for plant activity. The Administrator also 

6 observes that the CASAC panel was supportive of the Staff Paper views, while 

7 recognizing that 3 months likely represented the minimum timeframe appropriate to 

8 consider. Therefore, the Administrator concludes, on these bases, that the consecutive 3-

9 month period within the O3 season with the highest W126 index value (e.g., maximum 3-

10 month period) remains an appropriate seasonal window to propose for the protection of 

11 sensitive vegetation.

12 With regard to consideration of an appropriate diurnal window, the Administrator 

13 has taken into account the 2007 Staff Paper conclusion that for the vast majority of 

14 studied species, daytime exposures represent the majority of diurnal plant O3 uptake and 

15 are responsible for inducing the plant response of most significance to the health and 

16 productivity of the plant (e.g., reduced carbohydrate production). The Administrator is 

17 also aware, based on discussions in the 2007 Staff Paper that there are some number of 

18 species that show non-negligible amounts of O3 uptake at night due to incomplete 

19 stomatal closure. In reaching her conclusion that the 2007 Staff Paper recommendation 

20 of a 12-hour daytime window (8:00 a.m. to 8:00 p.m.) remains the most appropriate 

21 period over which to cumulate diurnal O3 exposures, specifically those most relevant to 

22 plant growth and yield responses, the Administrator places weight on the fact that the 

23 CASAC comments were also supportive of this diurnal window, recognizing again that it 
Draft O3 NPR –January 5, 2010 325 Deliberative, Do Not Quote or Cite

1 likely represents a minimum period over which plants can be vulnerable to O3 uptake. 

2 Therefore, the Administrator is again proposing the 12-hour daytime window (8:00 a.m. 

3 to 8:00 p.m.) as an appropriate diurnal window to protect against O3-induced plant 

4 effects.

5 Lastly, in considering whether an annual or a 3-year average index is more 

6 appropriate, the Administrator notes that in addition to the available scientific evidence 

7 regarding plant effects that can be brought to bear, there are also other public welfare 

8 considerations that may be appropriate to consider. In taking this view, the Administrator 

9 notes that the 2007 Staff Paper recognized that though most cumulative seasonal 

10 exposure levels of concern for vegetation have been expressed in terms of the annual 

11 timeframe, it may be appropriate to consider a 3-year average for purposes of standard 

12 stability. The Administrator has considered that while the 2007 Staff Paper notes that for 

13 certain welfare effects of concern (e.g., foliar injury, yield loss for annual crops, growth 

14 effects on other annual vegetation and potentially tree seedlings), an annual time frame 

15 may be a more appropriate period in which to assess what level would provide the 

16 requisite degree of protection, for other welfare effects (e.g., mature tree biomass loss), it 

17 also points out that a 3-year average may also be appropriate. The Administrator further 

18 observes that in concluding that it was appropriate to consider both an annual and a 3-

19 year average, the 2007 Staff Paper also concluded that should a 3-year average of the 3-

20 month, 12-hour W126 form be selected, a potentially lower level should be considered to 

21 reduce the potential of adverse impacts to annual species from a single high O3 year that 

22 could still occur while attaining a standard on average over 3-years. The Administrator 

23 also took note that the CASAC Panel, in addressing this issue of annual versus 3-year 
Draft O3 NPR –January 5, 2010 326 Deliberative, Do Not Quote or Cite

1 average concluded that multi-year averaging to promote a “stable” secondary standard is 

2 less appropriate for a cumulative, seasonal secondary standard than for a primary

3 standard based on maximum 8-hour concentrations, and further concluded that if multi4 year averaging is employed to increase the stability of the secondary standard, the level 

5 of the standard should be revised downward to assure that the desired degree of 

6 protection is not exceeded in individual years. The Administrator, in considering the 

7 merits of both the annual and 3-year average, and taking into account both the 2007 Staff 

8 Paper and CASAC views, concludes that it is important to place more weight on the 

9 public welfare benefit in having a stable standard, and that appropriate protection for 

10 vegetation can be achieved using a 3-year average form. The Administrator is thus 

11 proposing a 3-year average. However, given the uncertain nature of the evidence and 

12 potential concerns with using a 3-year average form, the Administrator is proposing to 

13 take comment on the appropriateness of the specific seasonal and diurnal exposure 

14 periods proposed, as well as the use of a 3-year average, and, as discussed below, the 

15 impact that selection of these proposed seasonal and diurnal exposure periods would 

16 have, in conjunction with a 3-year average form, on the appropriateness of the proposed 

17 range of levels. 

18 c. Level

19 i. Considerations Regarding 2007 Proposed Range of Levels

20 The 2007 Staff Paper, in identifying a range of levels for a 3-month, 12-hour 

21 (daytime) W126 standard appropriate for the Administrator to consider in protecting the 

22 public welfare from known or anticipated adverse effects to vegetation from O3

23 exposures, considered what information from the array of vegetation effects evidence and 
Draft O3 NPR –January 5, 2010 327 Deliberative, Do Not Quote or Cite

1 exposure and risk assessment results was most useful. With respect to the vegetation 

2 effects evidence, the 2007 Staff Paper found stronger support than what was available at 

3 the time of the 1997 review for an increased level of protection for trees and forested 

4 ecosystems. Specifically, the expanded body of evidence included: (1) additional field 

5 based data from free air, gradient and biomonitoring surveys demonstrating adverse 

6 levels of O3-induced growth reductions on trees at the seedling, sapling and mature 

7 growth stages and incidence of visible foliar injury occurring at biomonitoring sites in the 

8 field at ambient levels of exposure; (2) qualitative support from free air (e.g., 

9 AspenFACE) and gradient studies on a limited number of tree species for the continued 

10 appropriateness of using OTC-derived C-R functions to predict tree seedling response in 

11 the field; (3) studies that continued to document below-ground effects on root growth and 

12 “carry-over” effects occurring in subsequent years from O3 exposures; and (4) increased 

13 recognition and understanding of the structure and function of ecosystems and the 

14 complex linkages through which O3, and other stressors, acting at the organism and 

15 species level can influence higher levels within the ecosystem hierarchy and disrupt 

16 essential ecological attributes critical to the maintenance of ecosystem goods and services 

17 important to the public welfare. 

18 Based on the above sources of vegetation effects information and the results of 

19 the exposure and risk assessments summarized above, the 2007 Staff Paper concluded 

20 that just meeting the then current 0.084 ppm, 8-hour average standard would continue to

21 allow adverse levels of O3-induced effects to occur in sensitive commercially and 

22 ecologically important tree species in many regions of the country. The 2007 Staff Paper 

23 further concluded that air quality levels would need to be substantially reduced to protect 
Draft O3 NPR –January 5, 2010 328 Deliberative, Do Not Quote or Cite

1 sensitive tree seedlings, such as black cherry, aspen, and cottonwood, from these growth 

2 and foliar injury effects.

3 In addition to the currently quantifiable risks to trees from ambient exposures, the 

4 2007 Staff Paper also considered the more subtle impacts of O3 acting in synergy with 

5 other natural and man-made stressors to adversely affect individual plants, populations 

6 and whole systems. By disrupting the photosynthetic process, decreasing carbon storage 

7 in the roots, increasing early senescence of leaves and affecting water use efficiency in 

8 trees, O3 exposures could potentially disrupt or change the nutrient and water flow of an 

9 entire system. Weakened trees can become more susceptible to other environmental 

10 stresses such as pest and pathogen outbreaks or harsh weather conditions. Though it is 

11 not possible to quantify all the ecological and societal benefits associated with varying 

12 levels of alternative secondary standards, the 2007 Staff Paper concluded that this 

13 information should be weighed in considering the extent to which a secondary standard 

14 should be set so as to provide potential protection against effects that are anticipated to 

15 occur.

16 The 2007 Staff Paper also recognized that in the 1997 review, EPA took into 

17 account the results of a 1996 Consensus Workshop. At this workshop, a group of 

18 independent scientists expressed their judgments on what standard form(s) and level(s) 

19 would provide vegetation with adequate protection from O3-related adverse effects. 

20 Consensus was reached on protective ranges of levels in terms of a cumulative, seasonal 

21 3-month, 12-hr SUM06 standard for a number of vegetation effects endpoints. These 

22 ranges are identified below, with the estimated approximate equivalent W126 standard 

23 levels shown in parentheses. For growth effects to tree seedlings in natural forest stands, 
Draft O3 NPR –January 5, 2010 329 Deliberative, Do Not Quote or Cite

1 a consensus was reached that a SUM06 range of 10 to 15 (W126 range of 7 to 13) ppm2 hour would be protective. For growth effects to tree seedlings and saplings in 

3 plantations, the consensus SUM06 range was 12 to 16 (W126 range of 9 to 14) ppm4 hour. For visible foliar injury to natural ecosystems, the consensus SUM06 range was 8 

5 to 12 (W126 range of 5 to 9) ppm-hour. 

6 The 2007 Staff Paper then considered to what extent recent research provided 

7 empirical support for the ranges of levels identified by the experts as protective of 

8 different types of O3-induced effects. As discussed above in section IV.D.1.c, the 2007 

9 Staff Paper concluded on the basis of the available evidence that it was appropriate to 

10 consider a range for a 3-month, 12-hour, W126 standard level that included the 1996 

11 Consensus Workshop recommendations regarding a range of levels protective against O3-

12 induced growth effects in tree seedlings in natural forest stands (i.e., 7-13 ppm-hour in 

13 terms of a W126 form).

14 In considering the newly available information on O3-related effects on crops in 

15 this review, the 2007 Staff Paper observed the following regarding the strength of the 

16 underlying crop science: (1) nothing in the recent literature points to a change in the 

17 relationship between O3 exposure and crop response across the range of species and/or 

18 cultivars of commodity crops currently grown in the U.S. that could be construed to make 

19 less appropriate the use of commodity crop C-R functions developed in the NCLAN 

20 program; (2) new field-based studies (e.g., SoyFACE) provide qualitative support in a 

21 few limited cases for the appropriateness of using OTC-derived C-R functions to predict 

22 crop response in the field; and (3) refinements in the exposure, risk and benefits 

23 assessments in this review reduce some of the uncertainties present in 1996. On the basis 
Draft O3 NPR –January 5, 2010 330 Deliberative, Do Not Quote or Cite

1 of these observations, the 2007 Staff Paper concluded that nothing in the newly assessed 

2 information calls into question the strength of the underlying science upon which EPA

3 based its proposed decision in the last review to select a level of a cumulative, seasonal 

4 form associated with protecting 50 percent of crop cases from no more than 10 percent 

5 yield loss as providing the requisite degree of protection for commodity crops. 

6 The 2007 Staff Paper then considered whether any additional information was 

7 available to inform judgments as to the adversity of various O3-induced levels of crop 

8 yield loss to the public welfare. As noted above, the 2007 Staff Paper observed that 

9 agricultural systems are heavily managed, and that in addition to stress from O3, the 

10 annual productivity of agricultural systems is vulnerable to disruption from many other 

11 stressors (e.g., weather, insects, disease), whose impact in any given year can greatly

12 outweigh the direct reduction in annual productivity resulting from elevated O3

13 exposures. On the other hand, O3 can also more subtly impact crop and forage nutritive 

14 quality and indirectly exacerbate the severity of the impact from other stressors. Since 

15 these latter effects could not be quantified at that time, they could only be considered 

16 qualitatively in reaching judgments about an appropriate degree of protection for 

17 commodity crops from O3–related effects.

18 Based on the above considerations, the 2007 Staff Paper concluded that the level 

19 of protection judged requisite in the 1997 review to protect the public welfare from 

20 adverse levels of O3–induced reductions in crop yields and tree seedling biomass loss, as 

21 approximately provided by a W126 level of 21 ppm-hour, remained appropriate for 

22 consideration as an upper bound of a range of appropriate levels. The 2007 Staff Paper 

23 also recognized that a standard set at this level would not protect the most sensitive 
Draft O3 NPR –January 5, 2010 331 Deliberative, Do Not Quote or Cite

1 species or individuals within a species from all potential effects related to O3 exposures 

2 and further, that this level derives from the extensive and quantitative historic and recent 

3 crop effects database, as well as current staff exposure and risk analyses (EPA, 2007, pg. 

4 8-22). 

5 In identifying a lower bound for the range of alternative standard levels 

6 appropriate for consideration, staff concluded that several lines of evidence pointed to the 

7 need for greater protection for tree seedlings, mature trees, and associated forested 

8 ecosystems. Staff believed that tree growth was an important endpoint to consider 

9 because it is related to other aspects of societal welfare such as sustainable production of 

10 timber and related goods, recreation, and carbon (CO2) sequestration. Impacts on tree 

11 growth can also affect ecosystems through shifts in species composition and the loss of 

12 genetic diversity due to the loss of O3 sensitive individuals or species. In selecting an 

13 appropriate level of protection for trees, staff considered the results of the 1996

14 Consensus Workshop which identified the SUM06 range of 10 to 15 (W126 of 7 to 13) 

15 ppm-hour for growth effects to tree seedlings in natural forest stands. 

16 Because staff believed that O3-related effects on forest tree species are important 

17 public welfare effects of concern, it therefore concluded, based on the above, that it was 

18 appropriate to include 7 ppm-hour as the lower bound of the recommended range, the 

19 lower end of the approximate range recommended by CASAC (Henderson, 2006c) and 

20 identified by the 1996 Consensus Workshop participants as protective of forest trees. At 

21 this lower end of the range, staff anticipated, based on its analyses of risks of tree 

22 seedling biomass loss and mature tree growth reductions and on the basis of the scientific 

23 effects literature, that adverse effects of O3 on forested ecosystems would be substantially
Draft O3 NPR –January 5, 2010 332 Deliberative, Do Not Quote or Cite

1 reduced. Further, staff anticipated that the lower end of this range would provide 

2 increased protection from the more subtle impacts of O3 acting in synergy with other 

3 natural and man-made stressors to adversely affect individual plants, populations and 

4 whole systems. Staff also noted that by disrupting the photosynthetic process, decreasing 

5 carbon storage in the roots, increasing early senescence of leaves and affecting water use 

6 efficiency in trees, O3 exposure could potentially disrupt or change the nutrient and water 

7 flow of an entire system. Such weakened trees can become more susceptible to other 

8 environmental stresses such as pest and pathogen outbreaks or harsh weather conditions. 

9 While recognizing that it is not possible to quantify all the ecological and societal 

10 benefits associated with varying levels of alternative secondary standards, staff believed

11 that this information should be weighed in considering the extent to which a secondary

12 standard should be precautionary in nature in protecting against effects that have not yet 

13 been adequately studied and evaluated.

14 Thus, the 2007 Staff Paper concluded, based on all the above considerations, that 

15 an appropriate range of levels, for an annual standard using a 3-month, 12-hour W126 

16 form, for the Administrator to consider was 7 to 21 ppm-hour, recognizing that the level 

17 selected is largely a policy judgment as to the requisite level of protection needed. In 

18 determining the requisite level of protection for crops and trees, the 2007 Staff Paper 

19 recognized that it was appropriate to weigh the importance of the predicted risks of these 

20 effects in the overall context of public welfare protection, along with a determination as 

21 to the appropriate weight to place on the associated uncertainties and limitations of this 

22 information. 

23 ii. CASAC and Public Comments Prior to 2008 Decision
Draft O3 NPR –January 5, 2010 333 Deliberative, Do Not Quote or Cite

1 In considering the evidence described in both the 2006 Criteria Document and 

2 2006 draft Staff Paper, CASAC, in its October 24, 2006 letter to the Administrator, 

3 expressed its view regarding the appropriate form and range of levels for the 

4 Administrator to consider. The CASAC preferred a seasonal 3-month W126 standard in 

5 a range that is the approximate equivalent of the SUM06 at 10 to 20 ppm-hour. 

6 Following the 2007 proposal, EPA received additional CASAC and public comments 

7 regarding an appropriate range of levels of a W126 form for the Administrator to 

8 consider in finalizing a revised secondary NAAQS for O3. The CASAC, in its final letter 

9 to the Administrator (Henderson, 2007), agreed with the 2007 Staff Paper 

10 recommendations that the lower bound of the range within which a seasonal W126 

11 secondary O3 standard should be considered is approximately 7 ppm-hour; however, it 

12 did not agree with staff’s recommendation that the upper bound of the range should be as 

13 high as 21 ppm-hour. Rather, as discussed above in section IV.D.1.c, the CASAC Panel 

14 recommended that the upper bound of the range considered should be no higher than a 

15 W126 of 15 ppm-hour for an annual standard. 

16 The comments received from the public fell into two groups. One group of 

17 commenters supported the CASAC recommended range of 7- 15 ppm-hour for a W126 

18 standard. Many of these same commenters further emphasized the lower end of the 

19 proposed range as necessary to provide adequate protection for sensitive species. These 

20 commenters based their recommendation primarily on four sources of information: (1) 

21 field-based evidence of foliar injury occurring on sensitive species at air quality levels 

22 well below that of the current standard; (2) the 1996 Consensus Workshop 

23 recommendations for protective levels in terms of cumulative exposures for different 
Draft O3 NPR –January 5, 2010 334 Deliberative, Do Not Quote or Cite

1 vegetation types; (3) CASAC advice and recommendations; and (4) studies published 

2 after the close of the 2006 Criteria Document that potentially strengthen the link between 

3 species level impacts and ecosystem response. 

4 The other group of commenters did not support revising the current secondary

5 standard. These commenters primarily focused on uncertainties regarding the sources of 

6 information relied upon by the first group of commenters as support for a level within the 

7 range of levels recommended by CASAC. These uncertainties included: (1) potential 

8 confounders, such as soil moisture, on visible foliar injury and the lack of a clear 

9 relationship between visible foliar injury symptoms and other vegetation effects; (2) lack 

10 of documentation of the basis for the recommendations from the 1996 Consensus 

11 Workshop in selecting a range of levels, indicating that these recommendations should be 

12 used with great caution; (3) failure of CASAC and EPA to take into account the monitor 

13 height measurement gradient when making their recommendations concerning the level 

14 of the secondary standard; and (4) inability to quantitatively estimate ecosystem effects 

15 of O3 or to extrapolate meaningfully from effects on individual plants to ecosystem 

16 effects due to inadequate data.

17 iii. Conclusions on Level

18 The Administrator is proposing to set a cumulative, seasonal standard expressed 

19 in terms of the maximum 3-month, 12-hour W126 form, in the range of 7 to 15 ppm20 hour. In reaching this proposed decision about an appropriate range of levels for the 

21 secondary standard, the Administrator has considered the following: the evidence

22 described in the 2006 Criteria Document and the 2007 Staff Paper; the results of the 

23 vegetation exposure and risk assessments discussed above and in the 2007 Staff Paper, 
Draft O3 NPR –January 5, 2010 335 Deliberative, Do Not Quote or Cite

1 giving weight to the assessments as judged appropriate; the CASAC Panel’s advice and 

2 recommendations in the CASAC’s letters to the Administrator; EPA staff 

3 recommendations; and public comments received during the development of these 

4 documents, either in connection with CASAC meetings or separately. In considering 

5 what range of levels of a cumulative 3-month standard to propose, the Administrator 

6 notes that that this choice requires judgment as to what standard will protect the public 

7 welfare from any known or anticipated adverse effects. This choice must be based on an 

8 interpretation of the evidence and other information, such as the exposure and risk 

9 assessments, that neither overstates nor understates the strength and limitations of the 

10 evidence and information nor the appropriate inferences to be drawn. In taking all of the 

11 above into consideration, the Administrator also notes that there is no bright line clearly 

12 directing the choice of level for any of the effects of concern, and the choice of what is 

13 appropriate is clearly a public welfare policy judgment entrusted to the Administrator.

14 In particular, the Administrator has given careful consideration to the following: 

15 1) the nature and degree of effects of O3 to the public welfare, including what constitutes 

16 an adverse effect; 2) the strengths and limitations of the evidence that is available 

17 regarding known or anticipated adverse effects from cumulative, seasonal exposures, and 

18 its usefulness in informing selection of a proposed range; and 3) CASAC’s views 

19 regarding the strength of the evidence and its adequacy to inform a range of levels. Each 

20 of these topics is discussed in turn below.

21 In determining the nature and degree of effects of O3 on the public welfare, the 

22 Administrator recognizes that the significance to the public welfare of O3-induced effects 

23 on sensitive vegetation growing within the U.S. can vary, depending on the nature of the 
Draft O3 NPR –January 5, 2010 336 Deliberative, Do Not Quote or Cite

1 effect, the intended use of the sensitive plants or ecosystems, and the types of 

2 environments in which the sensitive vegetation and ecosystems are located. Any given 

3 O3-related effect on vegetation and ecosystems (e.g., biomass loss, foliar injury), 

4 therefore, may be judged to have a different degree of impact on the public depending, 

5 for example, on whether that effect occurs in a Class I area, a city park, or commercial 

6 cropland. In her judgment, it is appropriate that this variation in the significance of O3-

7 related vegetation effects should be taken into consideration in judging the level of 

8 ambient O3 that is requisite to protect the public welfare from any known or anticipated

9 adverse effects. In this regard, the Administrator agrees with the definition of adversity 

10 as described above in section IV.A.3 and in the 2008 rulemaking. As a result, the 

11 Administrator concludes that of those known and anticipated O3-related vegetation and 

12 ecosystem effects identified and discussed in this reconsideration, the highest priority and 

13 significance should be given to those that occur on sensitive species that are known to or 

are likely to occur in federally protected areas such as Class I areas62 14 or on lands set aside 

15 by States, Tribes and public interest groups to provide similar benefits to the public 

16 welfare, for residents on those lands, as well as visitors to those areas. 

17 Likewise, the Administrator also notes that the same known or anticipated O3-

18 induced effects, occurring in other areas may call for less protection. For example, the 

19 maintenance of adequate agricultural crop yields is extremely important to the public 

 

62 For example, the level of protection granted by Congress under the Wilderness 

Act of 1964 for designated “wilderness areas” requires that these areas “shall be 

administered for the use and enjoyment of the American people in such manner as will 

leave them unimpaired for future use as wilderness, and so as to provide for the 

protection of these areas, the preservation of their wilderness character” (The Wilderness 

Act, 1964). 
Draft O3 NPR –January 5, 2010 337 Deliberative, Do Not Quote or Cite

1 welfare and is currently achieved through the application of intensive management 

2 practices, including in some cases, genetic engineering. These management practices, in 

3 conjunction with market forces and government programs, assure an appropriate balance 

4 is reached between costs of production and market availability. Thus, while research on 

5 agricultural crop species remains useful in illuminating mechanisms of action and 

6 physiological processes, information from this sector on O3-induced effects is considered 

7 less useful in informing judgments on what level(s) would be sufficient but not more than 

8 necessary to protect the public welfare. With respect to commercial production of 

9 commodities, the Administrator notes that judgments about the extent to which O3-related 

10 effects on commercially managed vegetation are adverse from a public welfare 

11 perspective are particularly difficult to reach, given that what is known about the 

12 relationship between O3 exposures and agricultural crop yield response derives largely 

13 from data generated almost 20 years ago. The Administrator recognizes that there is 

14 substantial uncertainty at this time as to whether these data remain relevant to the 

15 majority of species and cultivars of crops being grown in the field today. In addition, the 

16 extensive management of such vegetation may to some degree mitigate potential O3-

17 related effects. The management practices used on these lands are highly variable and 

18 are designed to achieve optimal yields, taking into consideration various environmental 

19 conditions. Thus, the Administrator concludes there is no need for such additional 

20 protection for agricultural crops through the NAAQS.

21 The Administrator also recognizes that O3-related effects on sensitive vegetation 

22 can occur in other areas that have not been afforded special Federal protections, ranging 

23 from effects on vegetation growing in residential or commercial settings, such as 
Draft O3 NPR –January 5, 2010 338 Deliberative, Do Not Quote or Cite

1 ornamentals used in urban/suburban landscaping, to vegetation grown in land use 

2 categories that are heavily managed for commercial production of commodities such as 

3 timber. For vegetation used for residential or commercial ornamental purposes, such as 

4 urban/suburban landscaping, the Administrator believes that there is not adequate 

5 information at this time to establish a secondary standard based specifically on 

6 impairment of urban/suburban landscaping and other uses of ornamental vegetation, but 

7 notes that a secondary standard revised to provide protection for sensitive natural 

8 vegetation and ecosystems would likely also provide some degree of protection for such 

9 ornamental vegetation.

10 Based on the above, the Administrator finds that the types of information most 

11 useful in informing the selection of an appropriate range of protective levels is 

12 appropriately focused on information regarding exposures and responses of sensitive 

13 trees and other native species known or anticipated to occur in protected areas such as 

14 Class I areas or on lands set aside by States, Tribes and public interest groups to provide 

15 similar benefits to the public welfare, for residents on those lands, as well as visitors to 

16 those areas. 

17 With regard to the available evidence, the Administrator finds the coherence and 

18 strength of the weight of evidence from the large body of available literature compelling. 

19 This evidence addresses a broad array of O3-induced effects on a variety of tree species 

20 across a range of growth stages (i.e., seedlings, saplings and mature trees) using diverse 

21 field-based (e.g. free air, gradient and ambient) and OTC exposure methods. It 

22 demonstrates that significant numbers of forest tree species are potentially experiencing 
Draft O3 NPR –January 5, 2010 339 Deliberative, Do Not Quote or Cite

1 O3-induced stress under levels of ambient air quality, both at and below the level of the 

2 1997 standard. 

3 In particular, the Administrator notes the evidence from recent field-based studies 

4 and a gradient study of eastern cottonwood saplings (Gregg et al., 2003). She observes 

5 that this study found that cottonwood saplings grown in urban New York City grew faster 

6 than saplings grown in downwind rural areas where cumulative O3 exposures were 

7 higher, and the difference in biomass production between the urban site with the lowest 

8 cumulative exposure and the rural site with the highest cumulative exposure is 

9 dramatic (Figure 7-17 in the 2007 Staff Paper). The Administrator further notes that 

10 cottonwood is one of the most sensitive tree species studied to date and it is also 

11 important both from an ecological and public welfare perspective, as discussed above in 

12 section IV.A.2.b and in the 2007 Staff Paper.

13 The Administrator also notes the evidence related to the O3-induced effect of 

14 visible foliar injury. The Administrator observes that the visible foliar injury database 

15 created from the ambient field-based monitoring network managed by the Unites States 

16 Forest Service (USFS) Forest Inventory and Analysis (FIA) Program has continued to 

17 expand since the conclusion of the 1997 review. In utilizing this dataset, EPA staff

18 collaborated with FIA staff to compare the incidence of visible foliar injury at different 

19 levels of air quality by county throughout the U.S. in counties with FIA monitoring sites. 

20 In considering the results of this analysis, depicted in Table 7-4 of the 2007 Staff Paper, 

21 the Administrator notes that for the 2001-2004 period, the percent of counties with 

22 documented foliar injury at a level approximately equivalent to the W126 of 21 ppm23 hour, was 26 to 49 percent, while at the lower level approximately equivalent to a W126 
Draft O3 NPR –January 5, 2010 340 Deliberative, Do Not Quote or Cite

1 of 13 ppm-hour, incidence values ranged from 12 to 35 percent. The Administrator 

2 believes it likely that some sensitive species occurring in specially protected areas would

3 also exhibit visible foliar injury symptoms to a similar degree at these exposure levels. 

4 She further notes that while direct links between O3 induced visible foliar injury

5 symptoms and other adverse effects (e.g., biomass loss) are not always found, visible 

6 foliar injury in itself is considered by the National Park Service (NPS) to affect adversely

7 air quality related values (AQRV) in Class I areas.

8 The Administrator places significant weight on the judgments of CASAC. In so 

9 doing, the Administrator has carefully considered its stated views and the basis for the 

10 range of levels the CASAC O3 Panel recommended. In its 2007 letter to the 

11 Administrator, the CASAC O3 Panel agreed with EPA staff recommendations that the 

12 lower bound of the range within which a seasonal W126 O3 standard should be 

13 considered is approximately 7 ppm-hour. However, “it does not agree with Staff’s 

14 recommendations that the upper bound of the range should be as high as 21 ppm-hour. 

15 Rather, the Panel recommends that the upper bound of the range considered should be no 

16 higher than 15 ppm-hour, which the Panel estimates is approximately equivalent to a 

17 seasonal 12-hour SUM06 level of 20 ppm-hour” (Henderson, 2007). The Administrator 

18 notes that CASAC views concerning an appropriate range of levels for the Administrator 

19 to consider were presented after CASAC had considered the entire body of evidence 

20 presented in both the 2006 Criteria Document and 2007 Staff Paper, and are generally 

21 consistent with the 1996 Consensus Workshop recommendations.

22 In considering the issues raised by commenters on the 2007 proposed rule, the 

23 Administrator noted that many public commenters supported the range of levels 
Draft O3 NPR –January 5, 2010 341 Deliberative, Do Not Quote or Cite

1 recommended by CASAC. The Administrator also considered the views expressed by

2 the NPS as to what range of levels it identified as useful in helping it achieve its mandate 

3 to protect AQRVs in national parks and wilderness areas and to provide a level of 

4 protection for its resources in keeping with the Congressional mandate set forth in The 

5 Wilderness Act of 1964. In so doing, the Administrator notes that the NPS supported the 

6 range recommended by CASAC, while emphasizing that the lower end of the range was 

7 more appropriate. The NPS notes that though some visible foliar injury would still be 

8 expected to occur above the lower end of the CASAC recommended range (i.e. 7 ppm9 hour), the potential for growth impacts at that level would be very low. It further notes 

10 that most of these parks contain aspen, black cherry, or ponderosa pine, all sensitive 

11 species predicted to have significant growth effects at current W126 levels.

12 The Administrator also considered those comments that highlighted sources of 

13 uncertainty in the evidence and risk assessments (summarized above in section 

14 IV.D.5.c.ii) to inform her judgments on how much weight to place on these associated 

15 uncertainties, as discussed below.

16 With regard to the issue of possible confounders of foliar injury information, the 

17 Administrator recognizes that visible foliar injury, like other O3-induced plant effects, is 

18 moderated by environmental factors other than O3 exposure. However, the Administrator 

19 also notes that the O3-related visible foliar injury effect persisted across a four year period 

20 (2001-2004), despite year-to-year variability in meteorology and other environmental 

21 factors (see Table 7-4 in the 2007 Staff Paper). She also notes that approximately 26 to 

22 49 percent of counties had visible foliar injury incidence at the approximate W126 level 

23 of 21 ppm-hour, while at a W126 level of 13 ppm-hour, this range of percentages 
Draft O3 NPR –January 5, 2010 342 Deliberative, Do Not Quote or Cite

1 dropped to approximately 12 to 23 percent. In an area such as a national park, where 

2 visitors come in part for the aesthetic quality of the landscape, the Administrator 

3 recognizes that visible foliar injury incidence is an important welfare effect which should 

4 be considered in determining an appropriately protective standard level. 

5 With regard to the issues of what weight to place on the recommendations from 

6 the 1996 Consensus Workshop in selecting a range of levels, as the 1997 Workshop 

7 Report did not clearly document the basis for its recommendations, the Administrator 

8 recognizes that the absence of such documentation does call for care in placing weight on 

9 such recommendations. However, the Administrator notes that the workshop participants 

10 were asked to review both the 1996 O3 Criteria Document and Staff Paper, representing 

11 the most up to date compilation of the state of the science available at that time, in order 

12 to ensure that their expert judgments made were also informed by the latest science. She 

13 also notes that another group of experts, the CASAC O3 Panel, reached a similar 

14 consensus based upon an expanded body of scientific evidence. In addition, the 2007 

15 Staff Paper evaluated the same recommendations in the context of subsequent empirical 

16 evidence, and reached similar views, with the exception of the upper end of the 

17 recommended range, which in the 2007 Staff Paper was based on effects on commercial 

18 crops that had been considered in the 1997 review. While it would always be more 

19 useful to have documentation of the reasoning and basis for an expert’s advice, in this 

20 case the Administrator judges that the 1996 Consensus Workshop recommendations 

21 should be given substantial weight.

22 With regard to other issues raised by some commenters related to uncertainties in 

23 the technical evidence and analyses, the Administrator notes that such issues had been 
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1 addressed in the 2007 Staff Paper that reflected CASAC’s advice on such issues. For 

2 example, while the Administrator recognizes that uncertainty remains as to what level of 

3 annual tree seedling biomass loss when compounded over multiple years should be 

4 judged adverse to the public welfare, she believes that the potential for such anticipated 

5 effects should be considered in judging to what degree a standard should be 

6 precautionary.

7 In considering all of the issues discussed above, the Administrator has decided to 

8 propose a range of 7-15 ppm-hour. In selecting as an upper bound a level of 15 ppm9 hour, the Administrator notes that this level was specifically supported by the CASAC O3

10 Panel and is just above the range identified in the 1996 Consensus Workshop report as 

11 needed to provide adequate protection for trees growing in natural areas. In addition, the 

12 NPS, along with many public commenters, were in support of the CASAC range, 

13 including the upper bound of 15 ppm-hour, and indicated that lower values within this 

14 range would be more protective for sensitive trees in protected areas from biomass loss 

15 and visible foliar injury symptoms. 

16 While the upper end of this range is lower than the upper end of 21 ppm-hour 

17 recommended in the 2007 Staff Paper, this upper level of 21 ppm-hour was originally put 

18 forward in the 1997 review in terms of a SUM06 of 25 ppm-hour (W126 of 21 ppm-hour) 

19 and was justified on the basis that it was predicted to allow up to 10% biomass loss 

20 annually in 50% of studied commercial crops and tree seedling species. Recognizing the 

21 significant uncertainties that are associated with evaluating effects on commercial crops 

22 from a public welfare perspective, the Administrator now concludes that commercial crop 

23 data are no longer useful for setting the upper level of the range for proposal.
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1 With regard to her selection of a proposed range, the Administrator has 

2 considered that the direction from Congress to provide a high degree of protection in 

3 Class I areas creates a clearer target for gauging what types and magnitudes of effects 

4 would be known or anticipated to affect the intended use of these and other similarly

5 protected areas, that would thus be considered adverse to the public welfare. Such 

6 similar areas include lands set aside by States, Tribes and public interest groups to 

7 provide similar benefits to the public welfare, for residents on those lands, as well as 

8 visitors to those areas, The Administrator also believes that in order to preserve 

9 wilderness areas in an unimpaired state for future generations, she must consider a level 

10 that affords substantial protection from known adverse O3-related effects of biomass loss 

11 and foliar injury on sensitive tree species, as well as a level that takes into account 

12 potential “anticipated” adverse O3-related effects, including effects that result in 

13 continued impairment in the year following O3 exposure (i.e., carry-over effects), below 

14 ground impacts, ecosystem level impacts, and reduced CO2 sequestration

15 While the Administrator acknowledges that growth effects and visible foliar 

16 injury can still occur in sensitive species at levels below the upper bound of the proposed 

17 range, the Administrator also recognizes that some significant uncertainties remain 

18 regarding the risk of these effects, as discussed above. For example, the Administrator 

19 concludes that remaining uncertainties make it difficult to judge the point at which visible 

20 foliar injury becomes adverse to the public welfare in various types of specially protected 

21 areas. Uncertainties associated with monitoring ambient exposures must be considered in 

22 evaluating the strength of predictions regarding the degree of tree seedling growth 

23 impairment estimated to occur at varying ambient exposures. These uncertainties add to 
Draft O3 NPR –January 5, 2010 345 Deliberative, Do Not Quote or Cite

1 the challenge of judging which exposure levels are expected be associated with levels of 

2 tree seedling growth effects considered adverse to public welfare The Administrator 

3 believes that it is important to consider these uncertainties, and the weight to place on 

4 such uncertainties, in selecting a range of standard levels to propose. Establishing 15 

5 ppm-hour as the upper end of the proposed range reflects her judgment regarding the 

6 appropriate weight to place on these uncertainties in determining the degree of protection 

7 that is warranted for known and anticipated adverse effects.

8 With regard to her selection of a lower bound for the proposed range, the 

9 Administrator believes that if weight is placed on taking a more precautionary approach, 

10 recognizing that the real world impacts on trees and ecosystems could, in some cases, be 

11 greater than predicted, then the lower end of the range of 7 ppm-hour could be warranted. 

12 There is clear evidence that higher cumulative exposures can occur in rural areas 

13 downwind of urban areas and potentially in Class I areas. Unmonitored high elevation 

14 sites would also likely have higher cumulative exposures than lower elevation sites that 

15 are currently monitored. All of these considerations lead the Administrator to propose 7 

16 ppm-hour as the low end of the proposed range.

17 As discussed above in section IV.D.5.a, the main opposition to changing to a 

18 secondary standard with a cumulative, seasonal form has been the view that EPA does 

19 not have an adequate basis to identify the kinds and types of cumulative, seasonal 

20 exposure patterns that the standard should be designed to protect against, given the 

21 various uncertainties in the evidence, and whether EPA has an adequate basis to 

22 determine an appropriate level for a cumulative, seasonal secondary standard. While 

23 EPA agreed with this position in the 1997 review, the Administrator believes that the 
Draft O3 NPR –January 5, 2010 346 Deliberative, Do Not Quote or Cite

1 evidence before her appropriately supports a secondary standard that is distinctly

2 different in form and averaging time from the 8-hour primary standard, and that such a 

3 standard is necessary to provide sufficient protection from cumulative, seasonal

4 exposures to O3. 

5 While a different conclusion on this issue was reached in the 1997 review, the 

6 current conclusion that an exposure index that is cumulative and seasonal in nature, and 

7 therefore that setting a standard based on such a form is necessary and appropriate, is 

8 based on information newly available in the 2008 rulemaking, which strengthens the 

9 information available in the 1997 review and reduces remaining uncertainties. 

10 Such newly available information includes quantitative information for a broader 

11 array of vegetation effects (extending to sapling and mature tree growth stages) obtained 

12 using a more diverse set of field-based research study designs and improved analytical 

13 methods for assessing O3-related exposures and risks as discussed above in sections 

14 IV.A-C. 

15 . These newly available studies also provide important support to the quantitative 

16 estimates of impaired tree growth based on earlier studies available in the 1997 review 

17 and address one of the key data gaps cited in the 1997 review. Additional qualitative 

18 information is also available regarding improved understanding of linkages between 

19 stress-related effects of O3 exposures at the species level and those at higher levels within 

20 ecosystems. Finally, this information includes the use of new analytical methods, 

21 including a new multi-pollutant, multi-scale air quality model used to characterize 

22 exposures of O3-sensitive tree and crop species further address uncertainties in the 
Draft O3 NPR –January 5, 2010 347 Deliberative, Do Not Quote or Cite

1 assessments done in the 1997 review. In total, this newly available information increases

2 the Administrator’s confidence in important aspects of this rulemaking

3 The decision in 2008 to set the secondary O3 standard identical to the 8-hour 

4 primary standard largely mirrored the decision in 1997, but failed to account for this 

5 significant increase in the body of knowledge available to support the 2008 rulemaking. 

6 This body of knowledge, while continuing to reflect significant uncertainties, provides an 

7 appropriate basis for determining a level of a cumulative, seasonal standard that, in the 

8 judgment of the Administrator, provides sufficient but not more than necessary protection 

9 from cumulative, seasonal exposures to O3. This is clearly so when compared to a 

10 standard that uses an indirect form that is not biologically relevant, an 8-hour average 

11 standard aimed at peak daily exposures. This judgment is fully consistent with the advice 

12 provided by CASAC. 

13 After carefully taking the above considerations into account, and giving 

14 significant weight to the views of CASAC, the Administrator has decided to propose a 

15 range of levels of 7-15 ppm-hour for a cumulative, seasonal secondary O3 standard 

16 expressed as an index of the annual sum of weighted hourly concentrations (i.e., the 

17 W126 form), cumulated over 12 hours per day during the consecutive 3-month period 

18 within the O3 season with the maximum index value, averaged over three years. In the 

19 Administrator's judgment, based on the information available in the 2008 rulemaking, a 

20 standard could be set within this range that would be requisite to protect public welfare 

21 from known or anticipated adverse effects to O3-sensitive vegetation and ecosystems. In 

22 the Administrator’s judgment, a standard set at a level below the lower end of the range is 

23 not now supported by the weight of evidence and would not give sufficient weight to the 
Draft O3 NPR –January 5, 2010 348 Deliberative, Do Not Quote or Cite

1 important uncertainties and limitations inherent in the available scientific evidence and in 

2 the quantitative assessments conducted for the 2008 rulemaking. A standard set at a level 

3 above the upper end of the range is also not now supported by the weight of evidence and 

4 would not give sufficient weight to the credible inferences that the Agency has drawn 

5 from the scientific evidence nor to the quantitative assessments conducted for the 2008 

6 rulemaking. The Administrator judges that the appropriate balance to be drawn, based on 

7 the entire body of evidence and information available in the 2008 rulemaking, is a range 

8 between 7 and 15 ppm-hour. On balance, the Administrator believes that a standard

9 could be set within this range that would be sufficient but not more than necessary to 

10 protect public welfare from known or anticipated adverse effects due to O3.

11 In reaching this proposed decision, as discussed above, the Administrator has 

12 focused on the nature of the benefits associated with setting a distinct secondary standard 

13 with a cumulative, seasonal form relative to a standard with a peak daily 8-hour average 

14 form, as well as on assessments that quantify the degree of protection likely to be 

15 afforded by such standards. In so doing, the Administrator has acknowledged limitations 

16 in quantifying the expected benefits associated with the proposed cumulative seasonal 

17 standard relative to the secondary standard set in 2008. Having considered the public

18 comments received on the 2007 proposed rule in reaching this proposed decision, the 

19 Administrator is interested in again receiving public comment on the benefits to public 

20 welfare associated with the proposed cumulative seasonal standard set at specific levels 

21 within the proposed range relative to the standard set in 2008.

22

23 E. Proposed Decision on the Secondary O3 Standard
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1 For the reasons discussed above, and taking into account information and 

2 assessments presented in the 2006 Criteria Document and 2007 Staff Paper, the advice 

3 and recommendations of CASAC, and the public comments received in conjunction with 

4 the 2008 rulemaking, the Administrator has decided to propose to set a new cumulative, 

5 seasonal secondary O3 standard with a form expressed as an index of the annual sum of 

6 weighted hourly concentrations (i.e., the W126 form), cumulated over 12 hours per day 

7 (8:00 am to 8:00 pm) during the consecutive 3-month period within the O3 season with 

8 the maximum index value, averaged over three years, set within a range of 7 to 15 ppm9 hour. The Administrator solicits comment on the weight that is appropriately placed on 

10 the various types of evidence and analyses upon which this proposed standard is based, 

11 and on the appropriate weight to be placed on the uncertainties in this information, as 

12 well as on the benefits to public welfare associated with the proposed standard relative to 

13 the benefits associated with the standard set in 2008.

14 Data handling conventions for the proposed new secondary O3 standard are 

15 specified in the proposed addition of a new section to 40 CFR 50 Appendix P, as 

16 discussed in section V below. Issues related to monitoring requirements for the proposed 

17 new secondary O3 standard are discussed below in section VI.

18

19 V. Interpretation of the NAAQS for O3 and Proposed Revisions to the 

20 Exceptional Events Rule

21 Appendix P to 40 CFR part 50, Interpretation of the Primary and Secondary

22 National Ambient Air Quality Standards for Ozone, addresses data completeness 

23 requirements, data reporting, handling, and rounding conventions, and example 

24 calculations. The current Appendix P explains the computations necessary for 
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1 determining when the current identical primary and secondary standards are met. The 

2 EPA is proposing to revise Appendix P to reflect the proposed revisions to the primary

3 and secondary O3 NAAQS discussed above and to make other changes described below.

4 As discussed below, the proposed revisions to Appendix P include the 

5 following: the addition of data interpretation procedures applicable to the proposed 

6 cumulative, seasonal secondary NAAQS (see section V.B); clarification of certain 

7 language in the current provisions applicable to the primary NAAQS to reduce potential 

8 confusion (section V.C); revisions to the provisions regarding the use of incomplete data 

9 sets for purposes of the primary NAAQS and the data completeness requirements across 

10 three years (sections V.D and V.E); the addition of a provision providing the 

11 Administrator discretion to use incomplete data as if it were complete, for the purpose of 

12 the primary NAAQS (section V.F); a change from truncation to rounding of multi-hour 

13 and multi-year average O3 concentrations for the purposes of the primary standard 

14 (section V.G); and the addition of provisions addressing data to be used in making 

15 comparisons to the NAAQS (section V.H). The proposed revisions also include changes 

16 in organization for greater clarity and consistency with other data interpretation 

17 appendices to 40 CFR part 50, which are not further described in this preamble.

18 The EPA is also proposing changes to the O3-specific deadlines, in 40 CFR 50.14, 

19 by which states must flag ambient air data that they believe have been affected by

20 exceptional events and submit initial descriptions of those events, and the deadlines by

21 which states must submit detailed justifications to support the exclusion of that data from 

22 EPA determinations of attainment or nonattainment with the NAAQS. The O3-specific
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1 deadlines in the current 40 CFR 50.14 would not be appropriate given the anticipated 

2 schedule for the designations of areas under the proposed revised O3 NAAQS.

3 A. Background

4 The purpose of a data interpretation appendix in general is to provide the practical 

5 details on how to make a comparison between multi-day and possibly multi-monitor 

6 ambient air concentration data and the level of the NAAQS, so that determinations of 

7 compliance and violation are as objective as possible. Data interpretation guidelines also 

8 provide criteria for determining whether there are sufficient data to make a NAAQS level 

9 comparison at all. Appendix P was promulgated in March 2008 along with the most 

10 recent revisions to the primary and secondary O3 NAAQS. It is very similar to Appendix 

11 I, Interpretation of the 8-Hour Primary and Secondary National Ambient Air Quality

12 Standards for Ozone, which was adopted in 1997 when the O3 NAAQS were first revised 

13 to have an 8-hour averaging period rather than the earlier 1-hour averaging period, along 

14 with other changes in form and level. The only substantive difference between Appendix 

15 I and the current version of Appendix P is that Appendix P contains truncation 

16 procedures consistent with the additional decimal digit used to express the level of the 

17 2008 NAAQS in parts per million (0.075 ppm) compared to the 1997 NAAQS (0.08 

18 ppm). In July 2007, EPA had also proposed to include in Appendix P data interpretation 

19 procedures for the proposed cumulative, seasonal secondary O3 NAAQS, but these 

20 procedures were not finalized given that the final secondary NAAQS was identical in all 

21 respects to the final primary NAAQS.

22 An exceptional event is defined in 40 CFR 50.1 as an event that affects air 

23 quality, is not reasonably controllable or preventable, is an event caused by human 
Draft O3 NPR –January 5, 2010 352 Deliberative, Do Not Quote or Cite

1 activity that is unlikely to recur at a particular location or a natural event, and is 

2 determined by the Administrator in accordance with 40 CFR 50.14 to be an exceptional 

3 event. Air quality data that are determined to have been affected by an exceptional event 

4 under the procedural steps and substantive criteria specified in section 50.14 may be 

5 excluded from consideration when EPA makes a determination that an area is meeting or 

6 violating the associated NAAQS. The key procedural deadlines in section 50.14 are that 

7 a state must notify EPA that data have been affected by an event, i.e., “flag” the data in 

8 the Air Quality Systems (AQS) database, and provide an initial description of the event 

9 by July 1 of the year after the data are collected, and that the State must submit the full 

10 justification for exclusion within 3 years after the quarter in which the data were 

11 collected. However, if a regulatory decision based on the data, for example a designation 

12 action, is anticipated, the schedule is shortened and all information must be submitted to 

13 EPA no later than a year before the decision is to be made. This generic schedule 

14 presents problems when a NAAQS has been recently revised, as discussed in section V.I 

15 below. On May 15, 2009, EPA finalized a set of O3-specific deadlines that corrected 

16 these problems at the time with respect to the 2008 NAAQS revisions (74 FR 23307). 

17 However, because of the anticipated effect of the current reconsideration on the schedule 

18 for O3 designations, the schedule problems will resurface unless the deadlines are 

19 adjusted again.

20 B. Interpretation of the Secondary O3 Standard

21 The EPA is proposing data interpretation procedures for the proposed secondary

22 O3 NAAQS, which is defined in terms of a specific cumulative, seasonal form, 

23 commonly referred to as the W126 form, as described above in section IV. The proposed 
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1 new section 4 of Appendix P on data interpretation for the secondary standard contains 

2 the following main features. 

3 The “design value” for the secondary standard, the statistic for a monitoring site 

4 which would be compared to the level of the secondary standard to determine if the site 

5 meets the standard, would be the average of the annual maximum values of the three6 month index value from three calendar years. 

7 The new section would provide clear directions and examples for the calculation 

8 of the daily index value, the monthly cumulative index value, the annual maximum index 

9 value for a year, and the design value itself.

10 Only the data from the required O3 monitoring season would be examined to 

11 determine the annual maximum index value; any additional period of monitoring 

12 undertaken voluntarily by a state would not be considered. The EPA believes that 

13 because of the recently proposed extension of the required monitoring seasons in many

14 states (74 FR 34525, July 16, 2009), as discussed below in section VI, such a period of 

15 voluntary monitoring would be unlikely to have such high index values as to affect the 

16 annual maximum index value. Moreover, the proposed required monitoring season may

17 encompass the most active growing season in many areas. The EPA invites comment on 

18 whether instead the entire actual O3 monitoring period should be considered, to eliminate 

19 any possibility that the highest cumulative index value that can be determined with 

20 available data might be missed.

21 For each month in a three-month period, O3 data would have to be available for at 

22 least 75 percent of daylight hours (defined for this purpose as 8:00 a.m. – 7:59 p.m. LST). 

23 If data are available for at least 75 percent but fewer than 100 percent of these daylight 
Draft O3 NPR –January 5, 2010 354 Deliberative, Do Not Quote or Cite

1 hours in a month, the cumulative index value calculated from the available daylight hours 

2 in the month would be increased to compensate for the missing hours, based on an 

3 assumption that the missing hours would have the same distribution of O3 concentrations 

4 as the available hours. A substitution test is also proposed, by which months in which 

5 fewer than 75 percent of daylight hours have O3 concentration data might also be useable 

6 for calculating a valid cumulative index value. Such months would be used if the 

7 available O3 concentrations are so high that even substituting low concentration values

8 for enough missing data to meet the 75 percent requirement would result in a design 

9 value greater than the level of the standard. The low value that would be substituted 

10 would be the lowest 1-hour O3 concentration observed at the monitoring site during 

11 daylight hours during the required O3 monitoring season, in that calendar year, or onehalf the method detection limit (MDL) of the ozone instrument, whichever is higher. 63 12

13 The EPA notes that while this proposed approach to identifying the substitution 

14 value for the secondary standard is technically appropriate, it would necessitate data 

15 processing efforts during implementation that might be avoidable via some other 

16 approach that is also technically reasonable. We therefore invite comment on such 

17 alternative approaches, and we may adopt another approach in the final rule. For 

18 example, for simplicity the substituted 1-hour O3 concentration value could instead 

 

63 Because only enough missing 1-hour ozone values would be substituted as 

needed to meet the 75 percent completeness requirement, to avoid unreasonable 

underestimation of the true W126 index, tying the the selection of the substitution value 

to the hour of the missing value, as is proposed for data substitution for the purpose of the 

primary standard (see section V.D), would introduce considerable complexity by

requiring an algorithm for determining which specific missing values would be 

substituted. Therfore, EPA is proposing this simpler substitution approach for the 

secondary standard.
Draft O3 NPR –January 5, 2010 355 Deliberative, Do Not Quote or Cite

1 simply always be zero or one-half the MDL of the O3 instrument, noting that because of 

2 the sigmoidal weighting factor the exact magnitude of the low substitution value may

3 typically make very little difference to the annual index value. Also, using the previous 

4 calendar year as the source of the substitution value instead of the current calendar year 

5 would have the advantage of allowing all parties to know early in each year what the 

6 substitution value will be.

7 The EPA is proposing that all decimal digits be retained in intermediate steps of 

8 the calculation of the cumulative index, with the result rounded to have no decimal digits 

9 when expressed in ppm-hours before comparison the level of the secondary NAAQS.

10 EPA expects that the three months over which the cumulative weighted index 

11 value is highest will generally occur in the middle of each year. Therefore, the proposed 

12 new section 4 of Appendix P presumes this, and does not address a situation in which the 

13 three months of maximum cumulative index spans two calendar years, for example 

14 December to February. The EPA invites comment on whether a provision addressing 

15 such a remote possibility is needed and what its terms should be. For example, the 

16 process of checking each three month period in a calendar year to determine which gives 

17 the highest index value could include the combinations of December/January/February

18 and November/December/January within one calendar year.

19 C. Clarifications Related to the Primary Standard

20 The EPA is proposing two clarifying changes to Appendix P to make 

21 unambiguous two aspects of data interpretation for the primary 8-hour standard. The first 

22 change clarifies that the standard data completeness requirement that valid daily

23 maximum 8-hour values exist for 75 percent of all days refers to days within the required 
Draft O3 NPR –January 5, 2010 356 Deliberative, Do Not Quote or Cite

1 O3 monitoring season only. The current wording of Appendix P is somewhat open to a 

2 reading that the requirement applies to all days in the actual monitoring record for the site 

3 in question, which could be longer than the required season if a state voluntarily monitors 

4 on additional days, or shorter than the required season if a monitor has started or ceased 

5 operation sometime during the required season. The O3 data completeness requirement is 

6 intended to avoid a determination that an area has met the NAAQS when in fact more 

7 than a reasonable number of days with high O3 potential were not successfully monitored. 

8 This purpose can be served if the data within the required O3 monitoring season only are 

9 reasonably complete, because as mentioned above EPA has proposed to revise the 

10 required O3 seasons so that they encompass all days with potential for an exceedance of 

11 even the lowest proposed level for the primary standard. Unsuccessful monitoring 

12 outside the required season should not be an obstacle to a finding of attainment. 

13 However, if an O3 monitor has missed more than 25 percent of the required O3

14 monitoring season, for example because it started or stopped operation mid-season, this 

15 should prevent a finding of attainment based on a three-year period that includes that 

16 season. The proposed clarifying language reflects EPA’s actual intention and our past 

practice in applying Appendix P for regulatory purposes, and Appendix I as well. 64 17

18 The second proposed clarifying change would make it clear that when 

19 determining the fourth-highest daily maximum 8-hour O3 concentration for a year, all 

 

64 At present, EPA’s Air Quality System (AQS) for storing and reporting air 

quality data provides a completeness report that is based on yet a third approach, in which 

the period for reporting data completeness is the required monitoring season plus any

extension needed to encompass any exceedances that may have occurred outside the 

required season. However, EPA’s practice for regulatory purposes has been to consider 

completeness only over the required ozone monitoring season.
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1 days with monitoring data are to be considered, not just days within the required O3

2 monitoring season. This proposed clarifying language also reflects EPA’s actual 

3 intention and our past practice in applying Appendix P, and Appendix I as well. While 

4 EPA believes it to be quite unlikely that an exceedance will occur outside the proposed 

5 revised required O3 monitoring seasons and have a high enough concentration to affect 

6 the selection of the fourth-highest concentration for the year, when and if such an 

7 occurrence does happen, the data should not be ignored.

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

9 Primary Standard

10 The EPA is proposing to revise portions of Appendix P that describe certain 

11 exceptions to the standard data completeness requirements, under which a monitoring site 

12 can in some cases be determined to be meeting or violating the primary NAAQS despite 

13 not meeting the standard data completeness requirements. These changes would make 

14 Appendix P more logical in certain types of cases with incomplete data. While the 

15 particular types of cases whose outcome would be different with these changes have been 

16 rare historically, there may be more such affected cases in the future in conjunction with 

17 a primary O3 standard revised to a level within the range of levels proposed in this action.

18 The standard data completeness requirements in Appendix P for the primary O3

19 NAAQS apply a 75 percent requirement at each of three stages of data completeness 

20 testing. As discussed below, for each stage, there is an existing exception to the 75 

21 percent requirement.

22 In the first stage, an 8-hour period can be considered to have a valid 8-hour 

23 average O3 concentration only if at least 75 percent of the hours, i.e., 6 or more hours, 
Draft O3 NPR –January 5, 2010 358 Deliberative, Do Not Quote or Cite

1 have a valid hourly O3 value. The provided exception is that if there are 5 or fewer hours 

2 but if substituting a very low value (specifically, one-half the MDL of the O3 instrument) 

3 for all the missing hours results in a hypothetical 8-hour average that is above the level of 

4 the primary standard, the 8-hour period is considered valid and is assigned the 

hypothetical level resulting from the data substitution.65 5 For example, if the O3

6 concentration was 0.125 ppm for 5 hours, substituting a typical MDL/2 value of 0.0025 

7 ppm for three missing hours would result in an 8-hour average of 0.079 ppm, which is an 

8 exceedance of the current primary standard, so the valid 8-hour average for the period 

9 would be taken to be 0.079 ppm. If this value is higher than one or more of the highest 

10 four daily maximum 8-hour concentrations otherwise calculated for the year, considering 

11 it to be valid affects the value identified as the fourth-highest for the year and thus also 

12 affects the final design value. The logical problem with this approach is that it is possible 

13 for a hypothetical 8-hour average with such substitution to be below the level of the 

14 NAAQS, thus not meeting the current condition for the exception, but for it to still make 

15 a critical difference in making the three-year design value be above the level of the 

16 NAAQS, because a three-year design value can include (and be sensitive to the exact 

17 value of) an annual fourth-highest daily maximum that is not above the level of the 

18 NAAQS. This could be the case if the hypothetical 8-hour average with substitution is 

19 the maximum concentration 8-hour period for its day, and the day is one of the highest 

20 four O3 days of the year. Whether it actually is the case would further depend on the 

 

65 Actually, it is an interpretation of the text of Appendix P, section 2.1, that the 

average resulting from the data substitution is to be taken as the “8-hour” average, rather 

than the average of the available 5 or fewer hours of data, which would be higher. The 

text is not entirely clear on this point.
Draft O3 NPR –January 5, 2010 359 Deliberative, Do Not Quote or Cite

1 value of the 8-hour average itself, the values of the next highest daily maximum 8-hour 

2 average concentration in the year, and the values of the annual fourth-highest daily

3 maximum 8-hour concentration from the other two years. If the substituted 8-hour 

4 average would make a critical difference, it should be treated as valid and used in the 

5 calculation of the three-year design value, even if it is not itself above the level of the 

6 standard. Another problem is that one-half of the MDL, which typically is about 0.0025 

7 ppm, is very likely to be considerably lower than the actual O3 concentrations that were 

8 not successfully measured. Thus, while the one-half-MDL-substituted value is prevented 

9 from being an overestimate of the actual 8-hour average concentration, it is an 

10 unreasonably low estimate of that concentration which may have the effect of allowing a 

11 site with actual O3 levels above the standard to be found to meet the standard. The 

12 condition in the exception requiring a one-half-MDL-substituted “8-hour” average to be 

13 above the level of the NAAQS is therefore inappropriate.

14 In the second stage of data completeness testing, 75 percent of the 24 possible 8-

15 hour time blocks, which is 18 or more, must have valid 8-hour average concentrations 

16 values. The intent of this requirement is to make sure that most of the day was actually 

17 monitored, such that the highest concentration 8-hour period was likely to be captured in 

18 the data. When this is not the case, the day is not considered in selecting the annual 

19 fourth-highest daily maximum 8-hour concentration and no credit for the day’s 

20 monitoring is given towards the third stage of data interpretation (see below). The 

21 provided exception in the current Appendix P is that a day is considered valid if at least 

22 one 8-hour period has an average concentration above the level of the standard. 

23 However, as in the first stage, it is possible for an 8-hour period with an average 
Draft O3 NPR –January 5, 2010 360 Deliberative, Do Not Quote or Cite

1 concentration at or below the level of the NAAQS to play a critical role in whether the 

2 three-year design value meets the standard. Invalidating the day could have the effect of 

3 causing a lower value to be selected as the annual fourth-highest daily maximum 8-hour 

4 concentration, leading to a three-year design value that does not exceed the NAAQS 

5 while it would have exceeded if the day and the 8-hour average value had been treated as 

6 valid. The condition in the exception requiring at least one 8-hour average during the day

7 to be above the level of the NAAQS is therefore inappropriate.

8 In the third stage of data completeness testing, a completeness criterion is applied 

9 for the number of days in the required O3 season that have a valid maximum 8-hour 

10 average, i.e., days that have met the completeness conditions in the first two stages or 

11 have met the condition for an exception. Specifically, for each of the three years being 

12 used in the design value calculation, the number of valid days within the required O3

13 monitoring season (with no credit for extra days outside the season) must be at least 75 

14 percent of the days in the required O3 season, and the number of valid days across all 

three years must be 90 percent of the days in the three seasons.66 15 The provided exception 

16 to the 75/90 percent requirement is that data from a year with less than 75 percent of 

17 seasonal days can nevertheless be used if during the year at least one day’s maximum 8-

18 hour average O3 concentration was above the level of the standard and if the three-year 

 

66 EPA also is proposing eliminate this 90 percent requirement, see section V.E. 

The point made in this paragraph applies with or without the 90 percent requirement in 

place.
Draft O3 NPR –January 5, 2010 361 Deliberative, Do Not Quote or Cite

design value is also above the standard.67 1 The problem with this exception, similar to the 

2 problems with the exceptions in the first and second stages of data completeness testing, 

3 is that a daily maximum 8-hour concentration that is at or below the level of the NAAQS 

4 can nevertheless make a critical difference in making the three-year design value be 

5 above the level of the NAAQS. When it does, an incorrect final result will be reached if 

6 the year of data is not granted an exception to the 75/90 percent requirement. 

7 Specifically, there would be no valid three-year design value and no conclusion would be 

8 reached as to attainment or nonattainment, despite it being clear that the actual situation 

9 is nonattainment, in the sense that successful collection of additional hours and days of 

10 monitoring data could not possibly have resulted in a passing three-year design value. 

11 Moreover, since the three-year design value is the average of the fourth-highest daily

12 maximum 8-hour concentration from each year, there is no logical connection between 

13 the design value and the existence of a single daily maximum concentration greater than 

14 the level of the standard, which is the current condition for the exception for this stage of 

15 testing for data incompleteness.

16 EPA proposes to remedy this situation by replacing the three separate statements 

17 of the exceptions to the three standard completeness requirements with a new data 

18 substitution step that addresses the root cause of the data incompleteness situation: 

19 missing hourly concentrations which make it doubtful whether actual maximum daily 8-

20 hour concentrations were measured on a reasonably large percentage of the days during 

 

67 EPA notes that in the current versions of Appendix I and P, it is not explicit that 

this provided exception also applies in the case of three years which each have 75 percent 

or more of days with valid data but less than 90 percent across three years. Because EPA 

is proposing to remove the 90 percent requirement (see section V.E) this ambiguity does 

not need correction.
Draft O3 NPR –January 5, 2010 362 Deliberative, Do Not Quote or Cite

1 the required O3 monitoring season of each year. In the event that only 1, 2, 3, 4, or 5 

2 hourly averages are available for an 8-hour period, a partially substituted 8-hour average 

3 would be computed by substituting for all the hours without hourly averages a low hourly 

average value selected as follows, and then using 8 as the divisor.68 4 For days within the 

5 required O3 monitoring season, the substitution value would be the lowest hourly average 

6 O3 concentration observed for that hour of the day (local standard time) on any day

7 during the required O3 monitoring season of that year, or one-half the MDL, whichever is 

8 higher. Using this value makes it highly unlikely that the resulting partially substituted 8-

9 hour average concentration is higher than the actual concentration. Therefore, using the 

10 partially substituted 8-hour average in the design value calculation procedure is highly 

11 unlikely to result in an incorrect finding that a site does not meet the standard, but it may

12 lead to a correct finding that a site does not meet the standard in some cases in which 

13 there would be no finding possible or an incorrect finding under the current version of 

14 Appendix P. However, the use of the higher of the lowest observed same-hour

15 concentration or one-half the MDL could be problematic if a robust set of hourly

16 measurements is not available for the year, for example if a monitor began operation late 

17 in an ozone season. In such a case, the lowest observed same-hour concentration might 

18 not be low enough to eliminate all possibility that the value used for substitution is higher 

19 than the missing concentration value. To reduce this likelihood to essentially zero, we 

20 are proposing that if the number of same-hour concentration values available for the 

21 required O3 monitoring season for the year is less than 50 percent of the number of days

 

68 Appendix P now provides that in the event that only 6 or 7 hourly averages are 

available, the valid 8-hour average shall be computed on the basis of the hours available, 

using 6 or 7 as the divisor. We are not proposing to change this provision.
Draft O3 NPR –January 5, 2010 363 Deliberative, Do Not Quote or Cite

1 during the required O3 monitoring season, one-half the MDL of the O3 instrument would

2 be used in the substitution instead of the lowest observed concentration. We invite 

3 comment on whether another percentage should be used for this purpose instead of 50 

4 percent. 

5 The EPA notes that while this proposed approach to identifying the substitution 

6 value for the primary standard is technically appropriate, it would necessitate new data 

7 processing efforts during implementation that might be avoidable via some other 

8 approach that is also technically reasonable. There may also be approaches which are 

9 more technically appropriate. We therefore invite comment on such alternative 

10 approaches, and we may adopt another approach in the final rule. Examples of simpler 

11 approaches would be to identify in the final rule a fixed substitution value other than one12 half the MDL, to accept as valid 8-hour periods with only five measured hourly

13 concentrations, to interpret between two hourly concentrations to obtain a substitute for a 

14 single missing hourly concentration, or to use the previous calendar year as the source of 

15 the substitution value instead of the current calendar year (thereby allowing all parties to 

16 know early in each year what the substitution value will be). Examples of more complex 

17 approaches that might be more technically appropriate include selecting a low percentile 

18 of the available same-hour concentration data rather than the lowest value to be the 

19 substitution value, or selecting the lowest same-hour value from the same calendar 

20 quarter or month (of the current year or the most recent year) rather than from the entire 

21 required ozone monitoring season. We also invite comment on whether the proposed 

22 approach to substitution should be used at all and if not what other approach should be 

23 used to address the potential problem just described.
Draft O3 NPR –January 5, 2010 364 Deliberative, Do Not Quote or Cite

1 We propose that for simplicity and to further reduce any risk of a false finding 

2 that a site does not meet the standard, for days outside the required O3 monitoring season, 

3 the substitution value would always be one-half the MDL of the O3 instrument. We 

4 similarly invite comment on this aspect.

5 There would be no condition that a partially substituted 8-hour average exceed the 

6 level of the standard for it be used in calculating the design value, unlike is now the case. 

7 An 8-hour period with no available hourly averages at all would not have a valid 8-hour 

8 average, as is now the case.

9 In addition, to complete the solution to the problems described above, we are 

10 proposing that a design value that is greater than the level of the primary standard would 

11 be valid provided that in each year there were at least four days with at least one valid 8-

hour concentration.69 12 One or more of these 8-hour average concentrations could be the 

13 partially substituted 8-hour average concentration resulting from the above described 

14 substitution procedure. In such a case, there is essentially no possibility that more 

15 complete monitoring data would have shown the site to be meeting the NAAQS. It is 

16 appropriate to include all 8-hour averages including those involving substitution when 

17 testing for an exceedance of the standard, because those averages are extremely unlike to 

18 be overestimates of actual concentrations.

 

69 The requirement that there be at least four days with at least one hourly 

measurement is actually redundant and is stated only for ease of understanding, since 

there would be no annual fourth-highest daily maximum 8-hour concentration unless 

there are at least four days with monitoring data, and a single hourly data point is 

necessary and sufficient (with the proposed substitution step) to generate a daily

maximum 8-hour concentration.
Draft O3 NPR –January 5, 2010 365 Deliberative, Do Not Quote or Cite

1 Finally, a design value equal to or less than the level of the standard would be 

2 valid only if at least 75 percent of the days in the required O3 monitoring season of each 

3 year have daily maximum 8-hour concentrations that are based on at least 18 periods with 

4 at least 6 hourly concentrations. This ensures that a site will be found to meet the 

5 standard only when a reasonably high percentage of the days in the required O3

6 monitoring season have reasonably complete hourly data. In this situation, it would be 

7 inappropriate to count the 8-hour periods with five or fewer actual hourly measurement 

8 values towards the 75 percent requirement when testing for whether a site meets the 

9 standard, because those 8-hour averages will be based on substitution of low values and 

10 therefore will be underestimates of actual concentrations. The only way to be reasonably 

11 certain that no 8-hour period had a high enough concentration so as to contribute to a 

12 design value over the level of the standard is to have at least 18 periods in which 

13 substitution for missing O3 values was not needed. This provision has the same effect as 

14 several elements of the current Appendix P considered together, and thus is not a 

15 substantive change.

16 E. Elimination of the Requirement for 90 Percent Completeness of Daily Data 

17 across Three Years

18 As stated above in section VI.D, Appendix P currently requires that in order for a 

19 design value equal to or less than the standard to be valid, at least 75 percent of days in 

20 each of three years must have a valid daily maximum 8-hour average concentration value, 

21 i.e., that many days must have at least 18 8-hour periods with at least 6 reported hourly 

22 concentrations each. Appendix P also requires that the average of the percentages from 

23 three consecutive years be at least 90 percent. The EPA is proposing to eliminate this 90 
Draft O3 NPR –January 5, 2010 366 Deliberative, Do Not Quote or Cite

1 percent requirement for the average of three years and to retain only the requirement that 

2 each individual year have a percentage of at least 75 percent.

3 The 90 percent requirement was incorporated into Appendix I (the data 

4 interpretation appendix for the 0.08 ppm O3 NAAQS) in 1997 with an explanation that 

5 EPA had observed that 90 percent of O3 monitoring sites routinely achieved 90 percent 

6 data capture. The EPA now notes, however, that while the majority of monitoring sites 

7 do achieve 90 percent or better data capture in any given year, there are exceptions every

8 year. The 90 percent requirement applied to the average percentage over three years is 

9 quite unforgiving if there has been one year with relatively low data completeness. For 

10 example, if one year just met the 75 percent requirement, the remaining two years would 

11 have to achieve a 97.5 percent data capture rate in order for the three years to meet the 90 

12 percent requirement. This would allow only 4 missed hours of measurements per week, 

13 which would be challenging. The consequences for states could be important, under the 

14 current requirement. One possible result could be that an area actually in nonattainment 

15 with the NAAQS might have to be designated unclassifiable, although the substitution 

16 procedure proposed for cases of incomplete data, as described above in section VI.D, 

17 provides a path to an appropriate nonattainment finding in at least some cases. Another 

18 possible result is that a nonattainment area which had actually come into attainment could 

19 be unable to receive an attainment determination until three more years of sufficiently 

20 complete data are collected. This might, for example, result in an area which has 

21 achieved needed emissions reductions by its attainment deadline nevertheless being 

22 bumped up to a higher classification.
Draft O3 NPR –January 5, 2010 367 Deliberative, Do Not Quote or Cite

1 The 90 percent requirement over three years has the potential to treat two areas 

2 disparately, for no obvious logical reason. Consider two areas with identical air quality. 

3 Suppose the first area has annual completeness percentages of 75, 95, and 95 percent 

4 (averaging to 85 percent and thus failing the 90 percent requirement) and the second area 

5 has annual completeness percentages of 75, 98, and 98 percent (averaging to 90 percent). 

6 Suppose that the three-year design values in both areas are below the level of the 

7 NAAQS. Practically speaking, the most important uncertainty about whether each area 

8 actually meets the NAAQS is the low data capture rate in the first year. There is no 

9 obvious logic why the fact that the second area achieves marginally better data capture in 

10 the second and third year should permit it to receive an attainment finding despite this 

11 uncertainty, while the first area may not.

12 The EPA also notes that for the other gaseous criteria pollutants – sulfur dioxide, 

13 carbon monoxide and nitrogen dioxide – the completeness requirement is for 75 percent 

completeness of hourly measurements in an individual year.70 14

15 For these reasons, EPA proposes to eliminate the 90 percent requirement across 

16 three years of data but to retain the 75 percent requirement for individual years. The EPA 

17 notes that as a practical matter, the current 90 percent requirement in effect requires a 

18 minimum data capture rate somewhat above 75 percent in each year, because if data 

19 capture in any one year were as low as 75 percent the required data capture in the other 

20 years would be very hard to achieve. The minimum annual data capture rate is 

 

70 EPA has recently proposed to amend the completeness requirements for sulfur 

dioxide and nitrogen dioxide to add quarterly 75 percent completeness requirements in 

connection with proposals to establish 1-hour primary NAAQS for these pollutants, still 

with no requirement for 90 percent completeness across three years.
Draft O3 NPR –January 5, 2010 368 Deliberative, Do Not Quote or Cite

1 effectively somewhere in the range of 80 percent (implying a requirement to achieve 95 

2 percent data capture in the two remaining years in order to meet the 90 percent 

3 requirement across three years) and 85 percent (implying a requirement to achieve 92.5 

4 percent data capture in the two remaining years). The EPA invites comment on whether 

5 instead of retaining the 75 percent completeness requirement in each individual year, the 

6 requirement should be 80 percent or 85 percent.

7 F. Administrator Discretion to Use Incomplete Data

8 The EPA is proposing that the Administrator have general discretion to use 

9 incomplete data to calculate design values that would be treated as valid for comparison 

10 to the NAAQS despite the incompleteness, either at the request of a state or at her own 

11 initiative. Similar provisions exist already for the PM2.5 and lead NAAQS, and EPA has 

12 recently proposed such provisions to accompany the proposed 1-hour NO2 and SO2

13 primary NAAQS. The Administrator would consider monitoring site closures/moves, 

14 monitoring diligence, and nearby concentrations in determining whether to use such data.

15 G. Truncation versus Rounding 

16 Almost all State agencies now report hourly O3 concentrations in parts per 

17 million to three decimal places, since the typical incremental sensitivity of currently used 

18 O3 monitors is 0.001 ppm. In the current Appendix P approach, in calculating 8-hour

19 average O3 concentrations from such hourly data any calculated digits past the third 

20 decimal place are truncated rather than retained or rounded back to three decimal places. 

21 Also, in calculating 3-year averages of the fourth-highest daily maximum 8-hour average 

22 concentrations, Appendix P currently requires the result to be reported to the third 

23 decimal place with digits to the right of the third decimal place truncated. In this regard, 
Draft O3 NPR –January 5, 2010 369 Deliberative, Do Not Quote or Cite

1 Appendix P follows the precedent of Appendix I, except that Appendix P is based on a 

2 NAAQS level specified to three decimal places (0.075 ppm) while Appendix I addressed 

3 the case of a NAAQS level specified to only two decimal places (0.08 ppm). In the 

4 rulemaking that concluded in 2008 by establishing the 0.075 ppm level, EPA noted that 

5 the 2007 Staff Paper demonstrated that taking into account the precision and bias in 1-

6 hour O3 measurements, the 8-hour design value had an uncertainty of approximately

7 0.001 ppm. Thus, EPA considered any value less than 0.001 ppm to be highly uncertain 

8 and, therefore, proposed and adopted truncation to the third decimal place for reporting 1-

9 hour O3 concentrations and for both the individual 8-hour averages used to determine the 

10 annual fourth maximum and the 3-year average of the fourth maxima.

11 The effect of this repeated truncation is that there is a consistent downward bias in 

12 the calculation of the three-year design value. The size of this bias can be notable. For 

13 example, seven hours with O3 concentrations of 0.076 ppm plus one hour of 0.075 ppm 

14 results in an 8-hour average of 0.075 ppm after truncation, nearly a full 0.001 ppm below 

15 the actual 8-hour average of 0.075875 ppm. Seven hours with O3 concentrations of 0.077 

16 ppm plus one hour of 0.076 ppm results in an 8-hour average of 0.076 ppm after 

17 truncation. One year with the first pattern plus two years with the second pattern would 

18 give a three-year design value of 0.075 ppm, meeting the NAAQS, even though 23 of the 

19 24 individual 1-hour concentrations involved in the calculation of the design value were 

20 above 0.075 ppm.

21 The EPA has decided to reconsider this aspect of O3 data interpretation. 

22 Specifically, we are proposing that (1) 1-hour concentrations continue to be reported to 

23 only three decimal places, the same as is now specified in Appendix P, i.e., that the 
Draft O3 NPR –January 5, 2010 370 Deliberative, Do Not Quote or Cite

1 current practice of truncation of the 1-hour data to the nearest 0.001 ppm be retained; (2) 

2 all digits resulting from the calculation of 8-hour averages be retained; and (3) the three3 year average of annual fourth-highest daily maximum 8-hour concentrations be rounded 

4 to three decimal places before comparison to the NAAQS. The EPA continues to believe 

5 that given the uncertainty in individual 1-hour O3 concentration measurements it is 

6 appropriate to truncate those measurements at three decimal places (many O3 instruments 

7 are programmed to only report three digits anyway). However, the calculations of 8-hour 

8 averages and three-year averages are mathematical steps, not a measurement process 

9 subject to uncertainties, and EPA perceives no logic in having a consistent downward 

10 bias by truncating the results of these mathematical steps. The EPA notes that the O3

11 NAAQS is the only NAAQS for which multi-hour, multi-day, or multi-year averages of 

12 concentrations are truncated rather than rounded. The proposed change will make this 

13 aspect of O3 data interpretation consistent with data interpretation procedures for the 

14 other criteria pollutants.

15 H Data Selection

16 The current version of Appendix P does not explicitly address the issue of what 

17 ambient monitoring data for O3 can and must be compared to the O3 NAAQS. The EPA 

18 proposes to add to Appendix P language addressing this issue. This language is similar to 

19 provisions recently proposed to be included in new data interpretation appendices for 

20 nitrogen dioxide and sulfur dioxide. The new section of Appendix P would clarify that 

21 all quality assured data collected with approved monitoring methods and known to EPA 

22 shall be compared to the NAAQS, even if not submitted to EPA’s Air Quality System. 

23 The section also addresses the question of what O3 data should be used when two or more 
Draft O3 NPR –January 5, 2010 371 Deliberative, Do Not Quote or Cite

1 O3 monitors have been operating and have reported data for the same period at one 

2 monitoring site. 

3 I. Exceptional Events Information Submission Schedule

4 States are responsible for identifying air quality data that they believe warrant 

5 special consideration, including data affected by exceptional events. States identify such 

6 data by flagging (making a notation in a designated field in the electronic data record) 

7 specific values in the Air Quality System (AQS) database. States must flag the data and 

8 submit a justification that the data are affected by exceptional events if they wish EPA to 

9 consider excluding the data in determining whether or not an area is attaining the new O3

10 NAAQS.

11 All states that include areas that could exceed the O3 NAAQS and could therefore 

12 be designated as nonattainment for the O3 NAAQS have the potential to be affected by

13 this rulemaking. Therefore, this action applies to all states; to local air quality agencies to 

14 which a state has delegated relevant responsibilities for air quality management including 

15 air quality monitoring and data analysis; and to Tribal air quality agencies where 

16 appropriate. The Exceptional Events Rule preamble describes in greater detail to whom 

17 the rule applies (72 FR 13562-13563 March 22, 2007).

18 The CAA Section 319(b)(2) authorizes EPA to promulgate regulations that 

19 govern the review and handling of air quality monitoring data influenced by exceptional 

20 events. Under this authority, EPA promulgated the Exceptional Events Rule (Treatment 

21 of Data Influenced by Exceptional Events (72 FR 13560, March 22, 2007) which sets a 

22 schedule for states to flag monitored data affected by exceptional events in AQS and for 

23 them to submit documentation to demonstrate that the flagged data values were caused by
Draft O3 NPR –January 5, 2010 372 Deliberative, Do Not Quote or Cite

1 an exceptional event. Under this schedule, a state must initially notify EPA that data 

2 have been affected by an exceptional event by July 1 of the year after the data are 

3 collected; this is accomplished by flagging the data in AQS. The state must also include 

4 an initial description of the event when flagging the data. In addition, the state is required 

5 to submit a full demonstration to justify exclusion of such data within three years after 

6 the quarter in which the data were collected, or if a regulatory decision based on the data 

7 (such as a designation action) is anticipated, the demonstration must be submitted to EPA 

8 no later than one year before the decision is to be made. 

9 The rule also authorizes EPA to revise data flagging and documentation schedules 

10 for data used in the initial designation of areas under a new NAAQS. The generic

11 schedule, while appropriate for the period after initial designations have been made under 

12 a NAAQS, may need adjustment when a new NAAQS is promulgated because until the 

13 level and form of the NAAQS have been promulgated, a state would not have complete 

14 knowledge of the criteria for excluding data. In these cases, the generic schedule may

15 preclude states from submitting timely flags and associated documentation for otherwise 

16 approvable exceptional events. This could, if not modified, result in some areas receiving 

17 a nonattainment designation when the NAAQS violations were legitimately due to 

18 exceptional events.

19 As a result of the Administrator’s decision to reconsider the 2008 O3 NAAQS, 

20 EPA is proposing to revise the exceptional events flagging and documentation schedule 

21 to correspond to the designations schedules that EPA is considering for the proposed 

22 revisions to the primary and secondary O3 NAAQS. The designation schedules under 

23 consideration are discussed in greater detail below in section VII.A and summarized 
Draft O3 NPR –January 5, 2010 373 Deliberative, Do Not Quote or Cite

1 here. The CAA requires EPA to promulgate the initial designations for all areas no later 

2 than 2 years from the promulgation of a new NAAQS. Such period may be extended for 

3 up to one year if EPA has insufficient information. (See CAA section 107(d).) For a 

4 new primary O3 standard, EPA intends to issue designations on an accelerated schedule. 

5 For a new seasonal secondary O3 standard, EPA is considering two alternative schedules 

6 for initial area designations.

7 Primary Standard: If, as a result of the reconsideration, EPA promulgates a new

8 primary O3 standard on August 31, 2010, EPA is proposing that state Governors would 

9 need to submit their initial designation recommendations to EPA by January 7, 2011. 

10 EPA would promulgate the final designations in July 2011 to allow sufficient time for the 

11 designations to be published and effective by August 31, 2011. EPA expects to base the 

12 final designations for the primary O3 standard on three consecutive years of certified air 

13 quality monitoring data from the years 2007-2009 or 2008-2010, if available. EPA is 

14 proposing that for exceptional event claims made for data years 2007-2009, states must 

15 flag and provide an initial description and detailed documentation by November 1, 2010. 

16 For data collected during data year 2010, EPA is proposing that exceptional event data 

17 that states want EPA to exclude from consideration in the designations process must be 

18 flagged with an initial description and fully documented by March 1, 2011 or 60 days 

19 after the end of the quarter when the event occurred, whichever date is first. To meet this 

20 proposed 60-day deadline, a state would also have to submit the O3 concentration data to 

21 AQS sooner than the normal deadline for such submission, which is 90 days after the end 

22 of the calendar quarter. EPA believes this is a reasonable expectation given that most 

23 states currently submit O3 data earlier than the 90-day deadline.
Draft O3 NPR –January 5, 2010 374 Deliberative, Do Not Quote or Cite

1 Secondary Standard: If, as a result of the reconsideration, EPA promulgates a 

2 new seasonal secondary O3 standard by August 31, 2010, EPA is taking comment on two

3 alternative designations schedules. Under the first alternative, EPA would designate 

4 areas for the secondary standard on the same accelerated schedule discussed above for 

5 the primary standard. Under the second alternative, EPA would designate areas for the 

6 secondary standard on the maximum 2-year schedule provided under the CAA. 

7 Accelerated Schedule: Under the accelerated schedule for a seasonal secondary O3

8 NAAQS, EPA is proposing that for exceptional event claims made for data years 2007-

9 2009, states must flag and provide an initial description and detailed documentation by

10 November 1, 2010. For data collected during data year 2010, EPA is proposing that 

11 exceptional event data that states want EPA to exclude from consideration in the 

12 designations process must be flagged with an initial description and fully documented by 

13 March 1, 2011 or 60 days after the end of the quarter when the event occurred, whichever 

14 date is first.

15 2-year Schedule: Under the 2-year schedule, states would have 1 year, or by

16 August 2011, to submit their designations recommendations and EPA would finalize 

17 designations under the new secondary standard by August 2012. EPA expects to base 

18 final designations for a new seasonal secondary standard on the most recent three years of 

19 certified air quality monitoring data, which would typically be from the years 2009-2011 

20 in this case. Exceptional event data claims used from years 2008-2010 must be flagged 

21 with an initial description included in AQS and submitted with complete documentation 

22 supporting such claims by July 1, 2011. Exceptional event data claims from data year 

23 2011 must be flagged with an initial description and submitted with complete 
Draft O3 NPR –January 5, 2010 375 Deliberative, Do Not Quote or Cite

1 documentation supporting such claims 60 days after the end of the calendar quarter when 

2 the event occurred or March 1, 2012, whichever occurs first. 

3 Therefore, using the authority provided in CAA section 319(b)(2) and in the 

4 Exceptional Events Rule at 40 CFR 50.14 (c)(2)(vi), EPA is proposing to modify the 

5 schedule for data flagging and submission of demonstrations for exceptional events data 

6 considered for initial designations under the proposed reconsidered O3 primary and 

7 secondary NAAQS, as follows:

8

9 Table 1. Schedule for Exceptional Event Flagging and 

10 Documentation Submission for Data to be Used in 

11 Designations Decisions for New NAAQS

12

NAAQS 

Pollutant/

Standard/(Level

)/

Promulgation 

Date

Air Quality 

Data Collected 

for Calendar 

Year

Event Flagging 

& Initial 

Description 

Deadline

Detailed 

Documentation 

Submission 

Deadline

Primary Ozone/8-Hr

Standard (Level 

TBD)

Promulgated by

August 31, 2010

2007-2009 November 1, 2010b November 1, 

2010b

2010 60 Days after the end 

of the calendar quarter 

in which the event 

occurred or March 1, 

2011, whichever date 

occurs firstb

60 Days after the end 

of the calendar quarter 

in which the event 

occurred or March 1, 

2011, whichever date 

occurs firstb

Secondary Ozone/ 

(Level 

TBD)Alternative 2-

year Schedule- to be 

Promulgated by 

August 31, 2010 

2008 July 1, 2011bJuly 1, 2011a

2009-2010 July 1, 2011bJuly 1, 2011b
Draft O3 NPR –January 5, 2010 376 Deliberative, Do Not Quote or Cite

2011 60 Days after the end 

of the calendar quarter 

in which the event 

occurred or March 1, 

2012, whichever 

occurs firstb

60 Days after the end 

of the calendar quarter 

in which the event

occurred or March 1, 

2012, whichever 

occurs firstb

Secondary 

Ozone/ (Level 

TBD)-

Alternative 

Accelerated 

Schedule -to be 

Promulgated by 

August 31, 2010

2007-2009 November 1, 2010b November 1, 2010b

2010 60 Days after the end 

of the calendar quarter 

in which the event 

occurred or March 1, 

2011, whichever date 

occurs firstb

60 Days after the end 

of the calendar quarter 

in which the event 

occurred or March 1, 

2011, whichever date 

occurs firstb
Draft O3 NPR –January 5, 2010 377 Deliberative, Do Not Quote or Cite

a These dates are 

unchanged from 

those published in 

the original 

rulemaking.

b Indicates change 

from general 

schedule in 40 

CFR 50.14.

Note: EPA notes that 

the table of revised 

deadlines only applies 

to data EPA will use to 

establish the final 

initial designations for 

new NAAQS. The 

general schedule 

applies for all other 

purposes, most 

notably, for data used 

by EPA for 

redesignations to 

attainment.

1

2

3 VI. Ambient Monitoring Related to Proposed O3 Standards

4 Presently, States (including the District of Columbia, Puerto Rico, and the Virgin 

5 Islands, and including local agencies when so delegated by the State) are required to 

6 operate minimum numbers of EPA-approved O3 monitors based on the population of 

7 each of their Metropolitan Statistical Areas (MSA) and the most recently measured O3

8 levels in each area. Each State (or in some cases portions of a State) also has a required 

9 O3 monitoring season based on historical experience on when O3 levels are high enough 

10 to be of regulatory or public health concern. These requirements are contained in 40 CFR 

11 part 58 Appendix D, Network Design Criteria for Ambient Air Quality Monitoring. See 
Draft O3 NPR –January 5, 2010 378 Deliberative, Do Not Quote or Cite

1 section 4.1, especially Tables D–2 and D–3. These requirements were last revised on 

2 October 17, 2006 as part of a comprehensive review of ambient monitoring requirements 

3 for all criteria pollutants (71 FR 61236).

4 A. Background

5 In the 2007 proposed rule for the O3 NAAQS (72 FR 37818), EPA did not 

6 propose specific changes to monitoring requirements to support the proposed NAAQS 

7 revisions, but instead solicited comment on several key matters that were expected to be 

8 important issues affecting the potential redesign of monitoring networks if revisions to 

9 the NAAQS were finalized. These matters included O3 monitoring requirements in urban 

10 areas, the potential need for monitoring to support multiple objectives important to 

11 characterization in non-urban areas including the support of the secondary O3 NAAQS, 

12 and the length of the required O3 monitoring seasons. Comments on these monitoring 

13 issues were received during the ensuing public comment period, and these comments 

14 were summarized in the 2008 final rule for the O3 NAAQS (73 FR 16501). As noted in 

15 that action, EPA stated its intention to propose, in a separate rulemaking, the specific 

16 changes to O3 monitoring requirements that were deemed necessary to support the 

17 revised 2008 O3 NAAQS which set the level of the primary 8-hour O3 standard to 0.075 

18 ppm and set the secondary standard identical in all respects to the primary standard. EPA 

19 published these proposed changes to O3 monitoring requirements in a proposal dated July

20 16, 2009, Ambient Ozone Monitoring Regulations: Revisions to Network Design 

21 Requirements (74 FR 34525). The EPA currently plans to finalize these changes in a 

22 final O3 monitoring rule in 2010, either before or in conjunction with the final rule on the 

23 O3 NAAQS.
Draft O3 NPR –January 5, 2010 379 Deliberative, Do Not Quote or Cite

1 In the following sections, the specific provisions of the 2009 O3 monitoring 

2 proposal are briefly reviewed, and then discussed in the context of the proposed revisions 

3 of the 2008 O3 NAAQS that have been discussed earlier in this notice.

4 B. Urban Monitoring Requirements

5 As noted earlier, current O3 monitoring requirements for urban areas are based on 

6 two factors: MSA population and the most recent 3-year design value concentrations 

7 within each MSA. There are higher minimum monitoring requirements for areas that 

8 have most recent design values greater than or equal to 85 percent of the NAAQS (i.e., 

9 design value concentrations that are greater than or equal to 85 percent of the level of the 

10 NAAQS), and lower requirements for areas that have design values less than 85 percent 

11 of the NAAQS. These minimum monitoring requirements for O3 were revised during the 

12 2006 monitoring rulemaking to ensure that additional monitors would be required in 

13 areas with higher design values and to also ensure that these requirements would remain 

14 applicable through future NAAQS reviews and potential revisions of the standards. 

15 Accordingly, these requirements do not need to be updated with the revisions of the O3

16 NAAQS proposed in this action since the 85 percent threshold will be applied to the 

standard levels that are finalized for the primary and secondary standards.71 17 For example, 

18 given the range of levels of the primary standard being proposed, the level of the 85 

 

71 The requirements specified in Table D-2 of Appendix D to part 58, as noted in 

the third footnote of Table D-2, are applicable to the levels of the O3 NAAQS as defined 

in 40 CFR part 50. Accordingly, the 85 percent threshold for requiring higher minimum 

monitoring requirements within MSAs would apply to the proposed levels for the 

cumulative, seasonal secondary standard as well as to the proposed levels of the 8-hour 

primary standard.
Draft O3 NPR –January 5, 2010 380 Deliberative, Do Not Quote or Cite

1 percent threshold that requires greater minimum monitoring requirements ranges from 

2 0.051 ppm (85 percent of 0.060 ppm) to 0.060 ppm (85 percent of 0.070 ppm).

3 EPA did propose one change to urban monitoring requirements in the 2009 O3

4 monitoring proposal. Specifically, EPA proposed to modify the minimum O3 monitoring 

5 requirements to require one monitor to be placed in MSAs of populations ranging from 

6 50,000 to less than 350,000 in situations where there is no current monitor and no history

7 of O3 monitoring within the previous 5 years indicating a design value of less than 85

percent of the revised NAAQS.72 8 Since this proposed change to minimum requirements 

9 is also subject to the 85 percent threshold, EPA believes that the proposed change 

10 remains appropriate to support the revisions to the primary and secondary O3 NAAQS 

11 proposed in this action.

12 C. Non-Urban Monitoring Requirements

13 In the 2007 proposed rule for the O3 NAAQS, EPA solicited comment on the 

14 status of monitoring requirements for non-urban areas, specifically whether non-urban 

15 areas with sensitive vegetation that are only currently sparsely monitored for O3 could 

16 experience undetected violations of the secondary NAAQS as a result of transport from 

17 urban areas with high precursor emissions and/or O3 concentrations or from formation of 

18 additional O3 from precursors emitted from sources outside urban areas.

19 Comments that were received in response to the 2009 O3 NAAQS monitoring 

20 proposal noted the voluntary nature of most non-urban O3 monitoring and the resulting 

21 relative lack of non-urban O3 monitors in some areas. These commenters stated that EPA 

22 should consider adding monitoring requirements to support the secondary NAAQS by

 

72 These MSAs are not currently required to monitor for O3.
Draft O3 NPR –January 5, 2010 381 Deliberative, Do Not Quote or Cite

1 requiring O3 monitors in locations that contain O3-sensitive plants or ecosystems. These 

2 commenters also noted that the placement of current O3 monitors may not be appropriate 

3 for evaluating issues such as vegetation exposure since many of these monitors were 

4 likely located to meet other objectives.

5 Based on these comments as well as analyses of O3 concentrations from 

6 discretionary non-urban monitors located across the U.S, EPA included new proposed 

7 non-urban O3 monitoring requirements in the 2009 O3 monitoring proposal. These 

8 proposed requirements are intended to satisfy several important objectives including: (1) 

9 better characterization of O3 concentrations to which O3-sensitive vegetation and 

10 ecosystems are exposed in rural/remote areas to ensure that potential secondary NAAQS 

11 violations are measured; (2) assessment of O3 concentrations in smaller communities 

12 located outside of the larger urban MSAs covered by urban monitoring requirements; and 

13 (3) the assessment of the location and severity of maximum O3 concentrations that occur 

14 in non-urban areas and may be attributable to upwind urban sources. For reasons noted 

15 below, EPA believes that these proposed O3 monitoring requirements are sufficient to 

16 support the revisions to the O3 NAAQS proposed in this action.

17 With regard to the first objective, we note uncertainties will remain about the O3 

18 concentrations to which sensitive natural vegetation and ecosystems are exposed until 

19 additional monitors are sited in National Parks, State and/or tribal areas, wilderness areas, 

20 and other similar locations with sensitive ecosystems that are set aside to provide similar 

21 public welfare benefits. These monitors would support evaluation of the secondary 

22 NAAQS with a more robust data set than is now available. As noted in the 2009 O3

23 monitoring proposal, EPA proposed that States operate at least one monitor to be located 
Draft O3 NPR –January 5, 2010 382 Deliberative, Do Not Quote or Cite

1 in areas such as some Federal, State, Tribal, or private lands, including wilderness areas 

2 that have O3-sensitive natural vegetation and/or ecosystems. If EPA finalizes a 

3 cumulative, seasonal secondary standard at the lower end of the proposed range, then it is 

4 plausible that additional O3 monitors, above the number required by the monitoring 

5 proposal, may be needed in such areas to provide adequate coverage of locations likely to 

6 experience violations of the revised secondary NAAQS. These additional monitors could 

7 be established through discretionary State initiatives to supplement minimum monitoring 

8 requirements, negotiated agreements between States and EPA Regional Administrators, 

9 or through a future rulemaking that addresses potential increased O3 monitoring 

10 requirements to specifically address the need for additional monitoring to ensure 

11 detection of secondary standard violations.

12 With regard to the second objective of characterizing elevated ambient O3 levels

13 to which people are exposed in smaller communities located outside of the larger urban 

14 MSAs, the likelihood of measuring concentrations that approach or exceed the levels of 

15 the NAAQS due to the transport of O3 from upwind areas and/or the formation of O3 due 

16 to precursor emissions from industrial sources outside of urban areas is clearly increased 

17 due to the revised NAAQS proposed in this action. Given that the analyses described in 

18 the 2009 O3 monitoring proposal demonstrated that 50 percent of existing monitors 

located in such Micropolitan Statistical Areas73 19 exceeded the current NAAQS and nearly 

20 all monitors recorded design values greater than or equal to 85 percent of the current 

21 NAAQS, the potential for violations in such areas can only be increased with the 

 

73 Defined as areas having at least one urban cluster of at least 10,000 but less 

than a population of 50,000.
Draft O3 NPR –January 5, 2010 383 Deliberative, Do Not Quote or Cite

1 NAAQS revisions proposed in this action. As noted for the first non-urban monitoring 

2 objective, it is plausible that additional O3 monitors, above the number required by the 

3 2009 monitoring proposal may be needed in Micropolitan Statistical Areas to provide 

4 adequate coverage of locations likely to experience violations of the proposed lower 

5 primary NAAQS levels. These additional monitors could be established through 

6 discretionary State initiatives to supplement minimum monitoring requirements, 

7 negotiated requirements between States and EPA Regional Administrators, or through a 

8 future rulemaking that addresses potential increased O3 monitoring requirements to 

9 specifically address the need for additional monitoring to ensure detection of primary 

10 standard violations in smaller communities.

11 The third proposed non-urban monitoring objective, requiring O3 monitors to be 

12 located in the area of expected maximum O3 concentration outside of any MSA, 

13 potentially including the far downwind transport zones of currently well-monitored urban 

14 areas, is not directly related to the level of the O3 NAAQS. It is instead intended to 

15 ensure that all parts of a State meet the NAAQS and that all necessary emission control 

16 strategies have been included in State Implementation Plans. Accordingly, this proposed 

17 monitoring objective remains applicable independent of revisions to the O3 NAAQS 

18 proposed in this action.

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

20 Ozone monitoring is only required during the seasons of the year that are 

21 conducive to O3 formation. These seasons vary in length as the conditions that determine 

22 the likely O3 formation (i.e., seasonally-dependent factors such as ambient temperature, 

23 strength of solar insolation, and length of day) differ by location. In some locations, 
Draft O3 NPR –January 5, 2010 384 Deliberative, Do Not Quote or Cite

1 conditions conducive to O3 formation are limited to a few summer months of the year 

2 while in other locations these conditions occur year-round. As a result, the length of 

3 currently required O3 monitoring seasons can vary from a length of 4 months in colder

4 climates to a length of 12 months in warmer climates. 

5 The 2009 O3 monitoring proposal also addressed the issue of whether in some 

6 areas the required O3 monitoring season should be made longer. The proposal also 

7 addressed the status of any currently effective Regional Administrator-granted waiver 

8 approvals to O3 monitoring seasons, and the impact of proposed changes to monitoring 

9 requirements on such waiver approvals.

10 The EPA performed several analyses in support of proposed changes to the 

11 required O3 monitoring seasons. The first analysis determined the number of observed 

12 exceedances of the 0.075 ppm level of the current 8-hour NAAQS in the months falling 

13 outside the currently required local O3 monitoring season using monitors in areas that 

14 collected O3 data year-round in 2004–2006. The second analysis examined observed 

15 occurrences of daily maximum 8-hour O3 averages of at least 0.060 ppm. This threshold 

16 was chosen because it represented 80 percent of the current 0.075 ppm NAAQS level and 

17 provides an indicator of ambient conditions that may be conducive to the formation of O3

18 concentrations that approach or exceed the NAAQS. While proposals for revising each 

19 State’s required monitoring season were based on observed data in and surrounding each 

20 State, statistically predicted exceedances were also used to validate conclusions for each 

21 State. 

22 The aforementioned analyses provided several results. The analysis of observed 

23 exceedances of the 0.075 ppm level of the current O3 NAAQS indicated occurrences in 
Draft O3 NPR –January 5, 2010 385 Deliberative, Do Not Quote or Cite

1 eight States during months outside of the current required monitoring season. The eight 

2 States were Maine, Massachusetts, New Hampshire, New Jersey, New York, South 

3 Carolina, Vermont, and Wyoming. With the exception of Wyoming, these exceedances 

4 occurred in a very limited manner and timeframe, just before the beginning of these 

5 States’ required O3 monitoring season (beginning in these States on April 1). The 

6 frequency of observed occurrences of maximum 8-hour average O3 levels of at least 

7 0.060 ppm was quite high across the country in months outside of the current required 

8 monitoring season. A total of 32 States experienced such occurrences; 22 States had such 

9 levels only before the required monitoring season; 9 States had such levels both before 

10 and after the required monitoring season; and 1 State had such levels only after the 

11 required monitoring season. In a number of cases, the frequency of such ambient 

12 concentrations was high, with some States experiencing between 31 to 46 out-of-season 

13 days during 2004 to 2006 at a high percentage of all operating year-round O3 monitors.

14 Based on these analyses, EPA proposed a lengthening of the O3 monitoring 

15 season requirements in many areas. The 2009 proposed changes were based not only on 

16 the goal of monitoring out-of-season O3 NAAQS violations but also on the goal of 

17 ensuring monitoring when ambient O3 levels reach 80 percent of the NAAQS so that 

18 persons unusually sensitive to O3 would be alerted to potential NAAQS exceedances.

19 The EPA believes that the factors used to support the 2009 proposed changes to 

20 O3 monitoring seasons are appropriate to support the revisions of the O3 NAAQS 

21 proposed in this action. With regard to the primary standard, we note that the lower end 

22 of the range being proposed is an 8-hour level of 0.060 ppm, which is identical to the 

23 ambient O3 level that was utilized in one of the analyses discussed above. Although that 
Draft O3 NPR –January 5, 2010 386 Deliberative, Do Not Quote or Cite

1 level was chosen to provide an indicator of ambient levels that were below but 

2 approaching the level of the NAAQS and hence to serve as an alert to potential 

3 exceedances, we note that EPA’s traditional practice had been to base the length of 

4 required O3 monitoring seasons on the likelihood of measuring exceedances of the level 

5 of the NAAQS. Therefore, if EPA finalizes the level of the primary standard at the lower 

6 end of the proposed range, the O3 monitoring seasons that have been proposed as part of 

7 the 2009 O3 monitoring proposal would provide sufficient monitoring coverage to ensure 

8 the goal of measuring potential violations of the primary standard.

9 One O3 monitoring season issue that was not considered in the 2009 O3

10 monitoring proposal was the question of whether analyses of ambient data based on 8-

11 hour average statistics would also indicate whether the resulting proposed monitoring 

12 seasons would capture the cumulative maximum consecutive 3-month O3 levels 

13 necessary to compute design values based on the secondary NAAQS proposed in this 

14 action, which is defined in terms of a W126 cumulative peak-weighted index, as 

15 discussed above in section IV. If areas experienced high cumulative index values during 

16 months outside of the required O3 monitoring seasons (based on 8-hour statistics), then 

17 further revisions to the required monitoring seasons might be necessary to ensure 

18 monitoring during all months important to the calculation of design values for the revised 

19 form proposed for the secondary NAAQS. A related issue is whether such high 

20 cumulative O3 values also occurred during time periods that are biologically relevant for 

21 O3-sensitive vegetation.

22 The EPA is not proposing additional revisions to O3 monitoring seasons at this 

23 time. Additional analyses of the distribution of elevated cumulative W126 index values 
Draft O3 NPR –January 5, 2010 387 Deliberative, Do Not Quote or Cite

1 will be conducted, and the biologically relevant seasonal issue will be further reviewed. 

2 Based on the results of these analyses, EPA may consider proposing further revisions to 

3 the O3 monitoring season as related to the secondary O3 NAAQS.

4

5 VII. Implementation of Proposed O3 Standards

6 A. Designations

7 After EPA establishes or revises a NAAQS, the CAA directs EPA and the states 

8 to take steps to ensure that the new or revised NAAQS are met. The first step is to 

9 identify areas of the country that do not meet the new or revised NAAQS. This step is 

10 known as the initial area designations. 

11 The CAA provides that, "By such date as the Administrator may reasonably

12 require, but not later than 1 year after promulgation of a new or revised national ambient 

13 air quality standard for any pollutant under section 109, the Governor of each state shall * 

14 * * submit to the Administrator a list of all areas (or portions thereof) in the state" that 

15 designates those areas as nonattainment, attainment, or unclassifiable. The CAA 

16 specifies that, "The Administrator may not require the Governor to submit the required 

17 list sooner than 120 days after promulgating a new or revised national ambient air quality

18 standard." The CAA defines an area as nonattainment if it is violating the NAAQS or if 

19 it is contributing to a violation in a nearby area. (See CAA section 107(d)(1).)

20 The CAA further provides, "Upon promulgation or revision of a national ambient 

21 air quality standard, the Administrator shall promulgate the designations of all areas (or 

22 portions thereof) * * * as expeditiously as practicable, but in no case later than 2 years 

23 from the date of promulgation of the new or revised national ambient air quality standard. 
Draft O3 NPR –January 5, 2010 388 Deliberative, Do Not Quote or Cite

1 Such period may be extended for up to one year in the event the Administrator has 

2 insufficient information to promulgate the designations.” EPA is required to notify states 

3 of any intended modifications to their recommendations that EPA may deem necessary

4 no later than 120 days prior to promulgating designations. States then have an 

5 opportunity to demonstrate why any such proposed modification is inappropriate. 

6 Whether or not a state provides a recommendation, EPA must promulgate the designation 

7 that the Agency deems appropriate. (See CAA section 107(d)(1)(B).)

8 On September 16, 2009, when the Administrator announced her decision to 

9 reconsider the 2008 O3 NAAQS, she also indicated that the Agency would work with 

10 states to accelerate implementation of the standards adopted after reconsideration, 

11 including the initial area designations process. Acceleration of designations for the 

12 primary standard would help limit any delays in health protections associated with the 

13 reconsideration of the standards. If a secondary standard different from the primary

14 standard is adopted, this would be the first time different primary and secondary 

15 standards would be in place for the O3 standards. While welfare protection is also 

16 important, for the reasons provided below, we are providing alternative schedules for 

17 designating areas for the secondary standard.

18 If, as a result of the reconsideration, EPA determines that the record supports a 

19 primary standard different from that promulgated in 2008 and promulgates such different 

20 primary O3 NAAQS in 2010, EPA intends to promulgate final designations on an 

21 accelerated schedule to allow the designations to be effective in 1 year. In order to meet 

22 such a schedule, EPA is proposing that the deadline for states to submit their designations 

23 recommendations for the revised 2010 primary standard be 129 days after promulgation 
Draft O3 NPR –January 5, 2010 389 Deliberative, Do Not Quote or Cite

1 of that primary standard. EPA recognizes that the proposed deadline would be an 

2 ambitious schedule. Therefore, EPA intends to provide technical information and 

3 guidance for states as early as possible to facilitate the development of their 

4 recommendations. Many of the areas that would be violating the proposed primary ozone 

5 standard are also violating the 2008 ozone standards. State Governors have provided 

6 recommendations on these areas pursuant to the 2008 standards and recommendations 

7 may not need much further evaluation.

8 Based on this proposed schedule, if EPA promulgates a new primary standard on 

9 August 31, 2010, state Governors would need to submit their initial designation 

10 recommendations to EPA by January 7, 2011. If the Administrator intends to modify any 

11 state recommendation, EPA would notify the Governor no later than March 2011, 120 

12 days prior to promulgating the final designations. States would then have an opportunity

13 to comment on EPA's intended designations before EPA promulgates the final 

14 designations. EPA would promulgate the final designations in July 2011 to allow 

15 sufficient time for the designations to be published and effective by August 31, 2011. 

16 EPA expects to base the final designations for the primary O3 standard on three 

17 consecutive years of certified air quality monitoring data from the years 2007-2009 or 

18 from 2008-2010, if available. 

19 If, as a result of the reconsideration, EPA promulgates a distinct secondary

20 standard that differs from that promulgated in 2008 and also differs from the 2010 

21 primary standard, as proposed above, EPA is proposing two alternative deadlines for 

22 states to submit their designations recommendations. Under the first alternative, EPA 

23 would designate areas for the secondary standard on the same accelerated schedule 
Draft O3 NPR –January 5, 2010 390 Deliberative, Do Not Quote or Cite

1 discussed above for the primary standard. In order to meet that schedule, EPA is 

2 proposing that states submit their recommendations for the revised 2010 secondary

3 standard 129 days after promulgation of that secondary standard. Accordingly, if EPA 

4 promulgates the new secondary standard on August 31, 2010, state Governors would 

5 need to submit their initial designation recommendations to EPA by January 7, 2011.

6 Weighing in favor of designating areas for the secondary standard at the same 

7 time as designations for the primary standard is that planning for both standards would 

8 occur on the same schedule. Our examination of current air quality data from the existing 

9 monitoring network indicates that for levels of the primary and secondary standards 

10 proposed in this action, it is likely that the vast majority of areas violating the secondary

11 standard would overlap with areas violating the primary standard. In this case, 

12 implementing requirements for the primary and secondary standards on different 

13 schedules could present resource challenges to state and local agencies by requiring 

14 duplication of effort and hindering consideration of all factors when deciding which 

15 control strategies to adopt for each standard. For example, if designations for the 

16 secondary standard were delayed by a certain period (e.g., a year) beyond the 

17 designations for the primary standard, then EPA would likely delay submission of 

18 attainment SIPs for the secondary standard for a similar period beyond the proposed date 

19 for submission of the attainment SIPs for the primary standard. In this case, the initial

20 transportation conformity determination for the secondary standard would be required 

21 later than the initial determination for the primary standard by the difference in time 

22 between the effective dates of the two designations. 
Draft O3 NPR –January 5, 2010 391 Deliberative, Do Not Quote or Cite

1 Under the second alternative, EPA would designate areas for the secondary

2 standard on the maximum 2-year schedule provided under the CAA. To meet that 2-year 

3 schedule, EPA is proposing that states submit their recommendations for the revised 

4 secondary standard no later than 1 year after promulgation of the 2010 secondary

5 standard. Accordingly, if EPA promulgates a secondary standard on August 31, 2010,

6 that differs from the primary standard, as proposed, under the alternative 2-year 

7 designations schedule, state Governors would need to submit their initial designation 

8 recommendations to EPA by August 31, 2011. If the Administrator intends to modify

9 any state recommendation, EPA would notify the Governor no later than May 2012, 120 

10 days prior to the 2-year deadline for promulgating the final designations. States would 

11 then have an opportunity to comment on EPA's intended designations before EPA 

12 promulgates the final designations. EPA would promulgate the final designations for the 

13 secondary standard by August 31, 2012. EPA expects to base the final designations in 

14 August 2012 for a different secondary standard on the most recent three consecutive 

15 years of certified air quality monitoring data, which would be from the years 2009-2011. 

16 In the past, EPA has always set the secondary O3 standard to be identical to the 

17 primary O3 standard and the standards have embodied relatively short-term average 

18 concentrations (e.g., 1-hour or 8-hour). In this action, EPA is proposing a cumulative, 

19 seasonal secondary standard that differs from the proposed primary standard. EPA has 

20 not previously set a seasonal secondary standard for O3. Therefore, EPA and states do 

21 not have experience in implementing this type of secondary O3 standard or in 

22 determining what area boundaries would be appropriate. As we further explore 

23 implementation considerations for the secondary standard, we may encounter 
Draft O3 NPR –January 5, 2010 392 Deliberative, Do Not Quote or Cite

1 unanticipated issues that may require additional time to address. Thus, EPA is 

2 considering whether an accelerated schedule for a seasonal secondary standard would 

3 provide adequate time for resolving issues that we cannot now anticipate. If EPA 

4 designates areas for the secondary standard on a 2-year schedule, we note that we expect 

5 that accelerated implementation of the health-based primary standard would also result in 

6 accelerated welfare benefits. EPA requests comment on factors affecting the efficient 

7 and effective implementation of a secondary standard that differs from the primary

8 standard in the context of establishing designations schedules.

9 EPA notes, as discussed in greater detail above in section VI, that it has proposed 

10 a monitoring rule that would increase the density of monitoring in National Parks and 

11 other non-urban and lesser populated areas (July 16, 2009; 74 FR 34525). The proposed 

12 requirements are intended to satisfy several important objectives, including better 

13 characterization of O3 exposures to O3-sensitive vegetation and ecosystems in 

14 rural/remote areas to ensure that potential secondary NAAQS violations are measured. 

15 As proposed, the new monitors would not be deployed until 2012 or 2013. Therefore, 

16 data from these monitors would not be available for use within the statutory timeframe 

17 for EPA to complete designations for a 2010 secondary standard regardless of which 

18 schedule EPA follows. 

19 While CAA section 107 specifically addresses states, EPA intends to follow the 

20 same process for tribes to the extent practicable, pursuant to section 301(d) of the CAA 

21 regarding tribal authority, and the Tribal Authority Rule (63 FR 7254; February 12, 

22 1998). 
Draft O3 NPR –January 5, 2010 393 Deliberative, Do Not Quote or Cite

1 In a separate notice elsewhere in today’s Federal Register, EPA is announcing

2 that it is using its authority under the CAA to extend by 1 year the deadline for 

3 promulgating initial area designations for the O3 NAAQS that were promulgated in 

4 March 2008. The new deadline is March 12, 2011. That notice explains the basis for the 

5 deadline extension. As mentioned above, on September 16, 2009, EPA notified the Court 

6 of its decision to initiate a rulemaking to reconsider the primary and secondary O3

7 NAAQS set in March 2008 to ensure they satisfy the requirements of the CAA. In its 

8 notice to the Court, EPA stated that the final rule would be signed by August 31, 2010. 

9 Extending the deadline for promulgating designations for the 2008 O3 NAAQS until 

10 March 12, 2011 will allow EPA to complete the reconsideration rulemaking for the 2008 

11 O3 NAAQS before determining whether it is necessary to finalize designations for those

12 NAAQS or, instead, whether it is necessary to begin the designation process for different 

13 NAAQS promulgated pursuant to the reconsideration.

14 B. State Implementation Plans 

15 The CAA section 110 provides the general requirements for SIPs. Within 3 years 

16 after the promulgation of new or revised NAAQS (or such shorter period as the 

17 Administrator may prescribe) each State must adopt and submit “infrastructure” SIPs to 

18 EPA to address the requirements of section 110(a)(1). Thus, States should submit these 

19 SIPs no later than August 21, 2013, three years after promulgation of the reconsidered 

20 ozone standard in 2010. These “infrastructure SIPs” provide assurances of State 

21 resources and authorities, and establish the basic State programs, to implement, maintain, 

22 and enforce new or revised standards. 
Draft O3 NPR –January 5, 2010 394 Deliberative, Do Not Quote or Cite

1 In addition to the infrastructure SIPs, which apply to all States, CAA title I, part D 

2 outlines the State requirements for achieving clean air in designated nonattainment areas. 

3 These requirements include timelines for when designated nonattainment areas must 

4 attain the standards, deadlines for developing SIPs that demonstrate how the State will 

5 ensure attainment of the standards, and specific emissions control requirements. EPA

6 plans to address how these requirements, such as attainment demonstrations and 

7 attainment dates, reasonable further progress, new source review, conformity, and other 

8 implementation requirements, apply to the O3 NAAQS promulgated pursuant to the 

9 reconsideration in a subsequent rulemaking. Also in that rulemaking EPA will establish 

10 deadlines for submission of nonattainment area SIPs but anticipates that the deadlines 

11 will be no later than the end of December 2013, or 28 months after final designations.

12 C. Trans-boundary Emissions

13 Cross border O3 contributions from within North America (Canada and Mexico) 

14 entering the U.S. are generally thought to be small. Section 179B of the Clean Air Act 

15 allows designated nonattainment areas to petition EPA to consider whether such a 

16 locality might have met a clean air standard “but for” cross border contributions. To 

17 date, few areas have petitioned EPA under this authority. The impact of foreign 

18 emissions on domestic air quality in the United States is a challenging and complex 

19 problem to assess. EPA is engaged in a number of activities to improve our 

20 understanding of international transport. As work progresses on these activities, EPA 

21 will be able to better address the uncertainties associated with trans-boundary flows of air 

22 pollution and their impacts.

23
Draft O3 NPR –January 5, 2010 395 Deliberative, Do Not Quote or Cite

1 VIII. Statutory and Executive Order Reviews

2 A. Executive Order 12866: Regulatory Planning and Review 

3 Under section 3(f)(1) of Executive Order (EO) 12866 (58 FR 51735, October 4, 

4 1993), the O3 NAAQS action is an “economically significant regulatory action” because 

5 it is likely to have an annual effect on the economy of $100 million or more. 

6 Accordingly, EPA submitted this action to the Office of Management and Budget (OMB) 

7 for review under EO 12866 and any changes made in response to OMB recommendations 

8 have been documented in the docket for this action. In addition, EPA prepared this 

9 regulatory impact analysis (RIA) of the potential costs and benefits associated with this 

10 action. This analysis is contained in the Regulatory Impact Analysis for the Ozone 

11 NAAQS Reconsideration, October, 2009 (henceforth, “RIA”). A copy of the analysis is 

12 available in the RIA docket (EPA-HQ-OAR-2007-0225) and the analysis is briefly

13 summarized here. The RIA estimates the costs and monetized human health and welfare 

14 benefits of attaining five alternative O3 NAAQS nationwide. Specifically, the RIA 

15 examines the alternatives of 0.079 ppm, 0.075 ppm, 0.070 ppm, 0.065 ppm, and 0.060 

16 ppm. The RIA contains illustrative analyses that consider a limited number of emissions 

17 control scenarios that States and Regional Planning Organizations might implement to 

18 achieve these alternative O3 NAAQS. However, the Clean Air Act (CAA) and judicial 

19 decisions make clear that the economic and technical feasibility of attaining ambient 

20 standards are not to be considered in setting or revising NAAQS, although such factors 

21 may be considered in the development of State plans to implement the standards. 

22 Accordingly, although an RIA has been prepared, the results of the RIA have not been 

23 considered in issuing this proposed rule.
Draft O3 NPR –January 5, 2010 396 Deliberative, Do Not Quote or Cite

1 B. Paperwork Reduction Act

2 This action does not impose an information collection burden under the 

3 provisions of the Paperwork Reduction Act, 44 U.S.C. 3501 et seq. There are no 

4 information collection requirements directly associated with the establishment of a 

5 NAAQS under section 109 of the CAA.

6 Burden means the total time, effort, or financial resources expended by persons to 

7 generate, maintain, retain, or disclose or provide information to or for a Federal agency. 

8 This includes the time needed to review instructions; develop, acquire, install, and utilize 

9 technology and systems for the purposes of collecting, validating, and verifying

10 information, processing and maintaining information, and disclosing and providing 

11 information; adjust the existing ways to comply with any previously applicable 

12 instructions and requirements; train personnel to be able to respond to a collection of 

13 information; search data sources; complete and review the collection of information; and 

14 transmit or otherwise disclose the information. 

15 An agency may not conduct or sponsor, and a person is not required to respond to 

16 a collection of information unless it displays a currently valid OMB control number. The 

17 OMB control numbers for EPA's regulations in 40 CFR are listed in 40 CFR part 9.

18 C. Regulatory Flexibility Act

19 The Regulatory Flexibility Act (RFA) generally requires an agency to prepare a 

20 regulatory flexibility analysis of any rule subject to notice and comment rulemaking 

21 requirements under the Administrative Procedure Act or any other statute unless the 

22 agency certifies that the rule will not have a significant economic impact on a substantial 
Draft O3 NPR –January 5, 2010 397 Deliberative, Do Not Quote or Cite

1 number of small entities. Small entities include small businesses, small organizations, 

2 and small governmental jurisdictions.

3 For purposes of assessing the impacts of today’s proposed rule on small entities, 

4 small entity is defined as: (1) a small business that is a small industrial entity as defined 

5 by the Small Business Administration’s (SBA) regulations at 13 CFR 121.201; (2) a 

6 small governmental jurisdiction that is a government of a city, county, town, school 

7 district or special district with a population of less than 50,000; and (3) a small 

8 organization that is any not-for-profit enterprise which is independently owned and 

9 operated and is not dominant in its field.

10 After considering the economic impacts of today's proposed rule on small entities, 

11 I certify that this action will not have a significant economic impact on a substantial 

12 number of small entities. This proposed rule will not impose any requirements on small 

13 entities. Rather, this rule establishes national standards for allowable concentrations of 

14 O3 in ambient air as required by section 109 of the CAA. See also American Trucking 

15 Associations v. EPA. 175 F. 3d at 1044-45 (NAAQS do not have significant impacts 

16 upon small entities because NAAQS themselves impose no regulations upon small 

17 entities). We continue to be interested in the potential impacts of the proposed rule on 

18 small entities and welcome comments on issues related to such impacts

19 D. Unfunded Mandates Reform Act

20 Title II of the Unfunded Mandates Reform Act of 1995 (UMRA), Public Law 

21 104-4, establishes requirements for Federal agencies to assess the effects of their 

22 regulatory actions on State, local, and Tribal governments and the private sector. Under 

23 section 202 of the UMRA, EPA generally must prepare a written statement, including a 
Draft O3 NPR –January 5, 2010 398 Deliberative, Do Not Quote or Cite

1 cost-benefit analysis, for proposed and final rules with “Federal mandates” that may

2 result in expenditures to State, local, and Tribal governments, in the aggregate, or to the 

3 private sector, of $100 million or more in any 1 year. Before promulgating an EPA rule 

4 for which a written statement is needed, section 205 of the UMRA generally requires 

5 EPA to identify and consider a reasonable number of regulatory alternatives and to adopt 

6 the least costly, most cost-effective or least burdensome alternative that achieves the 

7 objectives of the rule. The provisions of section 205 do not apply when they are 

8 inconsistent with applicable law. Moreover, section 205 allows EPA to adopt an 

9 alternative other than the least costly, most cost-effective or least burdensome alternative 

10 if the Administrator publishes with the final rule an explanation why that alternative was 

11 not adopted. Before EPA establishes any regulatory requirements that may significantly 

12 or uniquely affect small governments, including Tribal governments, it must have 

13 developed under section 203 of the UMRA a small government agency plan. The plan 

14 must provide for notifying potentially affected small governments, enabling officials of 

15 affected small governments to have meaningful and timely input in the development of 

16 EPA regulatory proposals with significant Federal intergovernmental mandates, and 

17 informing, educating, and advising small governments on compliance with the regulatory

18 requirements. 

19 Today’s proposed rule contains no Federal mandates (under the regulatory

20 provisions of Title II of the UMRA) for State, local, or Tribal governments or the private 

21 sector. The proposed rule imposes no new expenditure or enforceable duty on any State, 

22 local or Tribal governments or the private sector, and EPA has determined that this 

23 proposed rule contains no regulatory requirements that might significantly or uniquely
Draft O3 NPR –January 5, 2010 399 Deliberative, Do Not Quote or Cite

1 affect small governments. Furthermore, as indicated previously, in setting a NAAQS 

2 EPA cannot consider the economic or technological feasibility of attaining ambient air 

3 quality standards, although such factors may be considered to a degree in the 

4 development of State plans to implement the standards. See also American Trucking 

5 Associations v. EPA, 175 F. 3d at 1043 (noting that because EPA is precluded from 

6 considering costs of implementation in establishing NAAQS, preparation of a Regulatory

7 Impact Analysis pursuant to the Unfunded Mandates Reform Act would not furnish any 

8 information which the court could consider in reviewing the NAAQS). Accordingly, 

9 EPA has determined that the provisions of sections 202, 203, and 205 of the UMRA do 

10 not apply to this proposed decision. The EPA acknowledges, however, that any

11 corresponding revisions to associated SIP requirements and air quality surveillance 

12 requirements, 40 CFR part 51 and 40 CFR part 58, respectively, might result in such 

13 effects. Accordingly, EPA will address, as appropriate, unfunded mandates if and when 

14 it proposes any revisions to 40 CFR parts 51 or 58.

15 E. Executive Order 13132: Federalism

16 Executive Order 13132, entitled “Federalism” (64 FR 43255, August 10, 1999), 

17 requires EPA to develop an accountable process to ensure “meaningful and timely input 

18 by State and local officials in the development of regulatory policies that have federalism 

19 implications.” “Policies that have federalism implications” is defined in the Executive 

20 Order to include regulations that have “substantial direct effects on the States, on the 

21 relationship between the national government and the States, or on the distribution of 

22 power and responsibilities among the various levels of government.” 
Draft O3 NPR –January 5, 2010 400 Deliberative, Do Not Quote or Cite

1 This proposed rule does not have federalism implications. It will not have 

2 substantial direct effects on the States, on the relationship between the national 

3 government and the States, or on the distribution of power and responsibilities among the 

4 various levels of government, as specified in Executive Order 13132. The rule does not 

5 alter the relationship between the Federal government and the States regarding the 

6 establishment and implementation of air quality improvement programs as codified in the 

7 CAA. Under section 109 of the CAA, EPA is mandated to establish NAAQS; however, 

8 CAA section 116 preserves the rights of States to establish more stringent requirements if 

9 deemed necessary by a State. Furthermore, this proposed rule does not impact CAA 

10 section 107 which establishes that the States have primary responsibility for 

11 implementation of the NAAQS. Finally, as noted in section E (above) on UMRA, this 

12 rule does not impose significant costs on State, local, or Tribal governments or the private 

13 sector. Thus, Executive Order 13132 does not apply to this rule.

14 However, as also noted in section E (above) on UMRA, EPA recognizes that 

15 States will have a substantial interest in this rule and any corresponding revisions to 

16 associated SIP requirements and air quality surveillance requirements, 40 CFR part 51 

17 and 40 CFR part 58, respectively. Therefore, in the spirit of Executive Order 13132, and 

18 consistent with EPA policy to promote communications between EPA and State and local 

19 governments, EPA specifically solicits comment on this proposed rule from State and 

20 local officials.

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

22 Governments

23

24 Executive Order 13175, entitled “Consultation and Coordination with Indian 

25 Tribal Governments” (65 FR 67249, November 9, 2000), requires EPA to develop an 
Draft O3 NPR –January 5, 2010 401 Deliberative, Do Not Quote or Cite

1 accountable process to ensure “meaningful and timely input by tribal officials in the 

2 development of regulatory policies that have tribal implications.” This rule concerns the 

3 establishment of O3 NAAQS. The Tribal Authority Rule gives Tribes the opportunity to 

4 develop and implement CAA programs such as the O3 NAAQS, but it leaves to the 

5 discretion of the Tribe whether to develop these programs and which programs, or 

6 appropriate elements of a program, they will adopt. 

7 This proposed rule does not have Tribal implications, as specified in Executive 

8 Order 13175. It does not have a substantial direct effect on one or more Indian Tribes, 

9 since Tribes are not obligated to adopt or implement any NAAQS. Thus, Executive 

10 Order 13175 does not apply to this rule.

11 Although Executive Order 13175 does not apply to this rule, EPA contacted tribal 

12 environmental professionals during the development of the March 2008 rule. The EPA 

13 staff participated in the regularly scheduled Tribal Air call sponsored by the National 

14 Tribal Air Association during the spring of 2007 as the proposal was under development. 

15 EPA specifically solicits additional comment on this proposed rule from Tribal officials.

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

17 Safety Risks

18

19 Executive Order 13045, “Protection of Children from Environmental Health Risks 

20 and Safety Risks” (62 FR 19885, April 23, 1997) applies to any rule that: (1) is 

21 determined to be “economically significant” as defined under Executive Order 12866, 

22 and (2) concerns an environmental health or safety risk that EPA has reason to believe 

23 may have a disproportionate effect on children. If the regulatory action meets both 

24 criteria, the Agency must evaluate the environmental health or safety effects of the 
Draft O3 NPR –January 5, 2010 402 Deliberative, Do Not Quote or Cite

1 planned rule on children, and explain why the planned regulation is preferable to other 

2 potentially effective and reasonably feasible alternatives considered by the Agency.

3 This proposed rule is subject to Executive Order 13045 because it is an 

4 economically significant regulatory action as defined by Executive Order 12866, and we 

5 believe that the environmental health risk addressed by this action may have a 

6 disproportionate effect on children. The proposed rule will establish uniform national 

7 ambient air quality standards for O3; these standards are designed to protect public health 

8 with an adequate margin of safety, as required by CAA section 109. However, the 

9 protection offered by these standards may be especially important for children because 

10 children, especially children with asthma, along with other sensitive population 

11 subgroups such as all people with lung disease and people active outdoors, are potentially 

12 susceptible to health effects resulting from O3 exposure. Because children are considered 

13 a potentially susceptible population, we have carefully evaluated the environmental 

14 health effects of exposure to O3 pollution among children. Discussions of the results of 

15 the evaluation of the scientific evidence, policy considerations, and the exposure and risk 

16 assessments pertaining to children are contained in sections II.B and II.C of this 

17 preamble. A listing of the documents that contain the evaluation of scientific evidence, 

18 policy considerations, and exposure and risk assessments that pertain to children is found 

19 in the section on Children’s Environmental Health in the Supplementary Information 

20 section of this preamble, and a copy of all documents have been placed in the public 

21 docket for this action. The public is invited to submit comments or identify peer22 reviewed studies and data that assess effects of early life exposure to O3. 

23 H. Executive Order 13211: Actions that Significantly Affect Energy Supply, 

24 Distribution or Use
Draft O3 NPR –January 5, 2010 403 Deliberative, Do Not Quote or Cite

1

2 This proposed rule is not a “significant energy action” as defined in Executive 

3 Order 13211, “Actions Concerning Regulations That Significantly Affect Energy Supply, 

4 Distribution, or Use” (66 FR 28355 (May 22, 2001)) because in the Agency’s judgment it 

5 is not likely to have a significant adverse effect on the supply, distribution, or use of 

6 energy. The purpose of this rule is to establish revised NAAQS for O3. The rule does not 

7 prescribe specific pollution control strategies by which these ambient standards will be 

8 met. Such strategies will be developed by States on a case-by-case basis, and EPA 

9 cannot predict whether the control options selected by States will include regulations on 

10 energy suppliers, distributors, or users. Thus, EPA concludes that this rule is not likely to 

11 have any adverse energy effects and does not constitute a significant energy action as 

12 defined in Executive Order 13211.

13 I. National Technology Transfer and Advancement Act

14 Section 12(d) of the National Technology Transfer and Advancement Act of 1995 

15 (NTTAA), Public Law No. 104-113, §12(d) (15 U.S.C. 272 note) directs EPA to use 

16 voluntary consensus standards in its regulatory activities unless to do so would be 

17 inconsistent with applicable law or otherwise impractical. Voluntary consensus standards 

18 are technical standards (e.g., materials specifications, test methods, sampling procedures, 

19 and business practices) that are developed or adopted by voluntary consensus standards 

20 bodies. The NTTAA directs EPA to provide Congress, through OMB, explanations 

21 when the Agency decides not to use available and applicable voluntary consensus 

22 standards.

23 This proposed rulemaking does not involve technical standards. Therefore, EPA is 

24 not considering the use of any voluntary consensus standards.
Draft O3 NPR –January 5, 2010 404 Deliberative, Do Not Quote or Cite

1 J. Executive Order 12898: Federal Actions to Address Environmental Justice in 

2 Minority Populations and Low-Income Populations

3

4 Executive Order 12898 (59 FR 7629 (Feb. 16, 1994)) establishes federal 

5 executive policy on environmental justice. Its main provision directs federal agencies, to 

6 the greatest extent practicable and permitted by law, to make environmental justice part 

7 of their mission by identifying and addressing, as appropriate, disproportionately high 

8 and adverse human health or environmental effects of their programs, policies, and 

9 activities on minority populations and low-income populations in the United States. 

10 EPA has determined that this proposed rule will not have disproportionately high 

11 and adverse human health or environmental effects on minority or low-income 

12 populations because it increases the level of environmental protection for all affected 

13 populations without having any disproportionately high and adverse human health or 

14 environmental effects on any population, including any minority or low-income 

15 population. The proposed rule will establish uniform national standards for O3 air 

16 pollution.

17

18 List of Subjects in 40 CFR Part 50

19 Environmental protection, Air pollution control, Carbon monoxide, Lead, Nitrogen 

20 dioxide, Ozone, Particulate matter, Sulfur oxides.

21

22

23

24 _________________

25 Dated:

26

27 _____________________________

28 Lisa P. Jackson, Administrator

29
Draft O3 NPR –January 5, 2010 405 Deliberative, Do Not Quote or Cite

1

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Draft O3 NPR –January 5, 2010 431 Deliberative, Do Not Quote or Cite

1 For the reasons set forth in the preamble, part 50 of Chapter 1 of Title 40 of the code of 

2 Federal regulations is proposed to be amended as follows:

3

4 PART 50--NATIONAL PRIMARY AND SECONDARY AMBIENT AIR 

5 QUALITY STANDARDS

6

7 1. The authority citation for part 50 continues to read as follows:

8

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

10

11 2. Section 50.15 is revised to read as follows:

12

13 ' 50.15 National primary and secondary ambient air quality standards for ozone.

14 (a) The level of the national 8-hour primary ambient air quality standard for O3 is (0.060-

15 0.070) parts per million (ppm), daily maximum 8-hour average, measured by a reference 

16 method based on Appendix D to this part and designated in accordance with part 53 of 

17 this chapter or an equivalent method designated in accordance with part 53 of this 

18 chapter.

19 (b) The 8-hour primary O3 ambient air quality standard is met at an ambient air quality

20 monitoring site when the average of the annual fourth-highest daily maximum 8-hour 

21 average O3 concentration is less than or equal to (0.060-0.070) ppm, as determined in 

22 accordance with appendix P to this part.

23 (c) The level of the national secondary ambient air quality standard for O3 is a cumulative 

24 index value of (7-15) ppm-hours, measured by a reference method based on Appendix D 

25 to this part and designated in accordance with part 53 of this chapter or an equivalent 

26 method designated in accordance with part 53 of this chapter.

27 (d) The secondary O3 ambient air quality standard is a seasonal standard expressed as a 

28 sum of weighted hourly concentrations, cumulated over the12 hour daylight period from 

29 8:00 a.m. to 8:00 p.m. local standard time, during the consecutive 3-month period within 
Draft O3 NPR –January 5, 2010 432 Deliberative, Do Not Quote or Cite

1 the O3 monitoring season with the maximum index value. The secondary O3 standard is 

2 met at an ambient air quality monitoring site when the annual maximum consecutive 3-

3 month cumulative index value (W126) is less than or equal to (7-15) ppm-hours, as 

4 determined in accordance with appendix P to this part.

5

6 3. Appendix P is revised to read as follows:

7 Appendix P to Part 50 -- Interpretation of the Primary and Secondary National 

8 Ambient Air Quality Standards for Ozone.

9 1. General

10 (a) This appendix explains the data handling conventions and computations necessary for 

11 determining whether the 8-hour primary and secondary national ambient air quality

12 standards for ozone specified in §50.15 are met at an ambient ozone air quality

13 monitoring site. Ozone is measured in the ambient air by a reference method based on 

14 Appendix D of this part, as applicable, and designated in accordance with part 53 of this 

15 chapter, or by an equivalent method designated in accordance with part 53 of this chapter.

16 Data reporting, data handling, and computation procedures to be used in making 

17 comparisons between reported ozone concentrations and the levels of the ozone standards

18 are specified in the following sections. 

19 (b)Whether to exclude, retain, or make adjustments to the data affected by exceptional 

20 events, including stratospheric ozone intrusion and other natural events, is determined by 

21 the requirements under §50.1, §50.14 and §51.930.

22 (c) The terms used in this appendix are defined as follows: 
Draft O3 NPR –January 5, 2010 433 Deliberative, Do Not Quote or Cite

1 8-hour average is the rolling average of eight hourly ozone concentrations as 

2 explained in section 3 of this appendix.

3 Annual fourth-highest daily maximum refers to the fourth-highest value measured 

4 at a monitoring site during a particular year.

5 Annual Cumulative W126 Index is the maximum sum over three consecutive 

6 calendar months of the monthly W126 index in a year, as explained in section 4 of this 

7 appendix.

8 Daily maximum 8-hour average concentration refers to the maximum calculated 

9 8-hour average for a particular day as explained in section 3 of this appendix.

10 Daily W126 Index is the sum of the sigmoidally weighted hourly ozone 

11 concentrations during the 12-hour daylight period, 8:00 a.m. to 7:59 p.m. local standard 

12 time (LST).

13 Design values are the metrics (i.e., statistics) that are compared to the primary 

14 and secondary NAAQS levels to determine compliance, calculated as shown in sections 3 

15 and 4 of this appendix.

16 Monthly W126 Index is the sum of the daily W126 index over one calendar month 

17 during the required ozone monitoring season, adjusted for incomplete data if appropriate,

18 as explained in section 4 of this appendix.

19 Required ozone monitoring season refers to the span of time within a calendar 

20 year when individual States are required to measure ambient ozone concentrations as 

21 listed in part 58 Appendix D to this chapter.

22 Year refers to calendar year.

23 2. Requirements for Data Used for Comparisons with the Ozone NAAQS
Draft O3 NPR –January 5, 2010 434 Deliberative, Do Not Quote or Cite

1 (a) All valid FRM/FEM ozone data submitted to EPA's Air Quality System (AQS), or 

2 otherwise available to EPA, meeting the requirements of part 58 of this chapter including 

3 appendices A, C, and E shall be used in design value calculations.

4 (b) When two or more ozone monitors are operated at a site, the state may in advance 

5 designate one of them as the primary monitor. If the state has not made this designation, 

6 the Administrator will make the designation, either in advance or retrospectively. Design 

7 values will be developed using only the data from the primary monitor, if this results in a 

8 valid design value. If data from the primary monitor do not allow the development of a 

9 valid design value, data solely from the other monitor(s) will be used in turn to develop a 

10 valid design value, if this results in a valid design value. If there are three or more 

11 monitors, the order for such comparison of the other monitors will be determined by the 

12 Administrator. The Administrator may combine data from different monitors in different 

13 years for the purpose of developing a valid primary or secondary standard design value, if 

14 a valid design value cannot be developed solely with the data from a single monitor. 

15 However, data from two or more monitors in the same year at the same site will not be 

16 combined in an attempt to meet data completeness requirements, except if one monitor 

17 has physically replaced another instrument permanently, in which case the two 

18 instruments will be considered to be the same monitor, or if the state has switched the 

19 designation of the primary monitor from one instrument to another during the year. 

20 (c) Hourly average concentrations shall be reported in parts per million (ppm) to the third 

21 decimal place, with additional digits to the right of the third decimal place truncated. The 

22 start of each hour shall be identified in local standard time (LST).

23 3. Comparison to the Primary Standard for Ozone
Draft O3 NPR –January 5, 2010 435 Deliberative, Do Not Quote or Cite

1 (a) Computing 8-hour averages

2 Running 8-hour averages shall be computed from the hourly ozone concentration data for 

3 each hour of the year and shall be stored in the first, or start, hour of the 8-hour period. 

4 In the event that only 6 or 7 hourly averages are available, the valid 8-hour average shall 

5 be computed on the basis of the hours available, using 6 or 7 as the divisor. In the event 

6 that only 1, 2, 3, 4, or 5 hourly averages are available, the 8-hour average shall be 

7 computed on the basis of substituting for all the hours without hourly averages a low 

8 hourly average value selected as follows, using 8 as the divisor. For days within the 

9 required ozone monitoring season, the substitution value shall be the lowest hourly

10 average ozone concentration observed during the same hour (local standard time) of any

11 day in the required ozone monitoring season of that year, or one-half of the method 

12 detection limit of the ozone instrument, whichever is higher. However, if the number of 

13 same-hour concentration values available for the required ozone monitoring season for 

14 the year, from which the lowest observed hourly concentration would be identified for 

15 purposes of this substitution, is less than 50% of the number of days during the required 

16 ozone monitoring season, one-half the method detection limit of the ozone instrument 

17 shall be used in the substitution. For days outside the required ozone monitoring season, 

18 the substitution value shall be one-half the method detection limit of the ozone 

19 instrument. An 8-hour period with no available hourly averages does not have a valid 8-

20 hour average. The computed 8-hour average ozone concentrations are not rounded or 

21 truncated.

22 (b) Daily maximum 8-hour average concentrations
Draft O3 NPR –January 5, 2010 436 Deliberative, Do Not Quote or Cite

1 There are 24 8-hour periods in each calendar day. Some of these may not have valid 8-

2 hour averages, under section 3(a). The daily maximum 8-hour concentration for a given 

3 calendar day is the highest of the valid 8-hour average concentrations computed for that 

4 day. This process is repeated, yielding a daily maximum 8-hour average ozone 

5 concentration for each day with ambient ozone monitoring data, including days outside 

6 the required ozone monitoring season if data are available. The daily maximum 8-hour 

7 concentrations from two consecutive days may have some hourly concentrations in 

8 common. Generally, overlapping daily maximum 8-hour averages are not likely, except 

9 in those non-urban monitoring locations with less pronounced diurnal variation in hourly

10 concentrations. In these cases, the maximum 8-hour average concentration from each day

11 is used, even if the two averages have some hours in common.

12 (c) Primary Standard Design Value

13 The primary standard design value is the annual fourth-highest daily maximum 8-hour 

14 ozone concentration considering all days with monitoring data including any days outside 

15 the required ozone monitoring season, expressed in parts per million, averaged over three 

16 years. The 3-year average shall be computed using the three most recent, consecutive 

17 years of monitoring data that can yield a valid design value. For a design value to be valid 

18 for comparison to the standard, the monitoring data set on which it is based must meet the 

19 data completeness requirements described in section 3(d). The computed 3-year average 

20 of the annual fourth-highest daily maximum 8-hour average ozone concentrations shall 

21 be rounded to three decimal places. Values equal to or greater than 0.xxx5 ppm shall 

22 round up.

23 (d) Data Completeness Requirements for a Valid Design Value
Draft O3 NPR –January 5, 2010 437 Deliberative, Do Not Quote or Cite

1 (i) A design value greater than the standard is valid if in each of the three years there are 

2 at least four days with a daily maximum 8-hour average concentration. Under sections 

3 3(a) and 3(b), there will be a daily maximum 8-hour average concentration on any day

4 with at least one hourly concentration. One or more of these four days may be outside the 

5 required ozone monitoring season.

6 (ii) A design value less than or equal to the standard is valid if for at least 75% of the 

7 days in the required ozone monitoring season in each of the three years there are at least 

8 18 8-hour averages in the day that are based on at least 6 measured hourly average 

9 concentrations. 

10 (iii) When computing whether the minimum data completeness requirement in section 

11 3(d)(ii) has been met for the purpose of showing that a design value equal to or less than 

12 the standard is valid, meteorological or ambient data may be sufficient to demonstrate 

13 that ozone levels on days with missing data would not have affected the design value. At 

14 the request of the state, the Regional Administrator may consider demonstrations that 

15 meteorological conditions on one or more days in the required ozone monitoring season 

16 which do not have at least 18 8-hour averages in the day that are based on at least 6 

17 measured hourly average concentrations could not have caused a daily maximum 8-hour 

18 concentration high enough to have been one of the four highest daily maximum 8-hour 

19 concentrations for the year. At the request of the state, days so demonstrated may be 

20 counted towards the 75% requirement for the purpose of validating the design value, 

21 subject to the approval of the Regional Administrator.

22 (vi) Years that do not meet the completeness criteria stated in 3(d)(ii) may nevertheless 

23 be used to calculate a design value that will be deemed valid with the approval of, or at 
Draft O3 NPR –January 5, 2010 438 Deliberative, Do Not Quote or Cite

1 the initiative of, the Administrator, who may consider factors such as monitoring site 

2 closures/moves, monitoring diligence, the consistency and levels of the valid 

3 concentration measurements that are available, and nearby concentrations in determining 

4 whether to use such data. 

5 (e) Comparison with the Primary Ozone Standard

6 (i) The primary ozone ambient air quality standard is met at an ambient air quality

7 monitoring site when the design value is less than or equal to [0.075] ppm.

8 (ii) Comparison with the primary ozone standard is demonstrated by examples 1 and 2 as 

9 follows:

10 Example 1. Ambient monitoring site attaining the primary ozone standard. 

Year Percent

Valid Days 

(Within the 

Required 

Monitoring 

Season)

1st

Highest 

Daily Max 8-

hour Conc.

(ppm)

2nd Highest

Daily Max

8-hour Conc.

(ppm)

3rd Highest

Daily Max

8-hour Conc.

(ppm)

4th Highest

Daily Max

8-hour Conc.

(ppm)

5th Highest

Daily Max

8-hour Conc.

(ppm)

2006 80% 0.092500 0.090375 0.085125 0.078375 0.078125

2007 96% 0.084750 0.083500 0.075375 0.071875 0.070625

2008 98% 0.080875 0.079750 0.077625 0.075500 0.060375

Average 0.075250

Rounded 0.075

11

12 As shown in Example 1, this monitoring site meets the primary ozone standard because 

13 the 3-year average of the annual fourth-highest daily maximum 8-hour average ozone

14 concentrations (i.e., 0.075256 ppm, rounded to 0.075 ppm) is less than or equal to [0.075] 

15 ppm. The data completeness requirement is also met because no single year has less than 

16 75% data completeness. In Example 1, the individual 8-hour averages and the 3-year 
Draft O3 NPR –January 5, 2010 439 Deliberative, Do Not Quote or Cite

1 average are shown with six decimal digits. In actual calculations, all digits supported by

2 the calculator or calculation software must be retained. 

3

4 Example 2. Ambient monitoring site failing to meet the primary ozone standard.

Year Percent

Valid Days

(Within the

Required 

Monitoring 

Season)

1st

Highest 

Daily Max 8-

hour Conc.

(ppm)

2nd Highest

Daily Max

8-hour Conc.

(ppm)

3rd Highest

Daily Max

8-hour Conc.

(ppm)

4th Highest

Daily Max

8-hour Conc.

(ppm)

5th Highest

Daily Max

8-hour Conc.

(ppm)

2006 96% 0.105125 0.103500 0.101125 0.078625 0.072375

2007 74% 0.104250 0.103625 0.093000 0.080250 0.069500

2008 98% 0.103125 0.101875 0.101750 0.075375 0.074625

Average 0.078083

Rounded 0.078

5 

6 As shown in Example 2, the data capture in 2007 is less than 75%. The primary ozone

7 standard is not met for this monitoring site because the 3-year average of the fourth8 highest daily maximum 8-hour average ozone concentrations (i.e., 0.078083 ppm, 

9 rounded to 0.078 ppm) is greater than [0.075] ppm and is therefore valid despite this 

10 incompleteness. In Example 2, the individual 8-hour averages and the 3-year average are 

11 shown with six decimal digits. In actual calculations, all digits supported by the 

12 calculator or calculation software must be retained.

13 4. Secondary Ambient Air Quality Standard for Ozone

14 (a) Computing the daily W126 index value. 

15 The secondary ozone ambient air quality standard is a seasonal standard expressed as a 

16 sum of weighted hourly concentrations, cumulated over the 12 hour daylight period from 

17 8:00 a.m. to 8:00 p.m. local standard time, during the consecutive 3-month period within 

18 the ozone monitoring season with the maximum index value. The first step in 
Draft O3 NPR –January 5, 2010 440 Deliberative, Do Not Quote or Cite

1 determining whether the standard is met at a monitoring site is to compute the daily

2 W126 index value for each day by applying the sigmoidal weighting function in Equation 

3 1 to each reported measurement of hourly average concentration.

4 Equation 1









i pm

i am

daily W wc Ci

i

8

8

5 126

where Ci = hourly O3 at hour i, and c C

e

w 126 1 4403

1





6  .

7 The computed value of the sigmoidally weighted hourly concentration is not rounded or 

8 truncated. The daily W126 index is formed by summing the twelve computed hourly 

9 values, retaining all decimal places. An illustration of computing a daily W126 index 

10 value is below: 

11

12 Example 3. Daily W126 index value calculation for an ambient ozone monitoring site.

Start of hour Concentration (ppm) Weighted Concentration (ppm)

8:00 a.m. 0.045 0.002781

9:00 a.m. 0.060 0.018218

10:00 a.m. 0.075 0.055701

11:00 a.m. 0.080 0.067537

12:00 p.m. 0.079 0.065327

1:00 p.m. 0.082 0.071715

2:00 p.m. 0.085 0.077394

3:00 p.m. 0.088 0.082448

4:00 p.m. 0.083 0.073683

5:00 p.m. 0.081 0.069667
Draft O3 NPR –January 5, 2010 441 Deliberative, Do Not Quote or Cite

6:00 p.m. 0.065 0.029260

7:00 p.m. 0.056 0.011676

Sum=Daily W126 index value 0.625406 ppm-hours

1

2 In Example 3, the individual weighted concentrations and their sum are shown with six 

3 decimal digits. In actual calculations, all digits supported by the calculator or calculation 

4 software must be retained. There are no data completeness requirements for the daily

5 index. If fewer than 12 hourly values are available, only the available hours are weighted 

6 and summed. However, there are data completeness requirements for the monthly W126 

7 index values and a required adjustment for incomplete data, as describe in the next 

8 section. 

9 (b) Computing the Monthly W126 Index

10 As described in section 4(a), the daily index value is computed at each monitoring site for 

11 each calendar day in each month during the required ozone monitoring season with no 

12 rounding or truncation. The monthly W126 index is the sum of the daily index values 

13 over one calendar month. At an individual monitoring site, a monthly W126 index is 

14 valid if hourly average ozone concentrations are available for at least 75% of the possible 

15 daylight hours in the month. For months with more than 75% but less than 100% data 

16 completeness, the monthly W126 value shall be adjusted for incomplete data by

17 multiplying the unadjusted monthly W126 index value by the ratio of the number of 

18 possible reporting hours to the number of hours with reported ambient hourly

19 concentrations using Equation 2 in this appendix:

20

21 Equation 2
Draft O3 NPR –January 5, 2010 442 Deliberative, Do Not Quote or Cite

M.I.= (D.I.) (n* 12)/v

n

j=1

 *











1 

2 where,

3 M.I. = the adjusted monthly W126 index, 

4 D.I. = daily W126 index (i.e., the daily sum of the sigmoidally weighted 

5 daylight hourly concentrations),

6 n = the number of days in the calendar month,

7 v = the number of daylight reporting hours (8:00 a.m. – 7:59 p.m.

8 LST) in the month with reported valid hourly ozone concentrations.

9

10 The resulting adjusted value of the monthly W126 index shall not be rounded or 

11 truncated.

12 (b) Secondary Standard Design Value

13 The secondary standard design value is the 3-year average of the annual 

14 maximum consecutive 3-month sum of adjusted monthly W126 index values expressed 

15 in ppm-hours. Specifically, the annual W126 index value is computed on a calendar 

16 year basis using the three highest, consecutive adjusted monthly W126 index values. 

17 The 3-year average shall be computed using the most recent, consecutive three calendar 

18 years of monitoring data meeting the data completeness requirements described in section 

19 4(c). The computed 3-year average of the annual maximum consecutive 3-month sum of 

20 adjusted monthly W126 index values in ppm-hours shall be rounded to a whole number

21 with decimal values equal to or greater than 0.500 rounding up. 

22 (c) Data Completeness Requirement
Draft O3 NPR –January 5, 2010 443 Deliberative, Do Not Quote or Cite

1 (i) The annual W126 index is valid for purposes of calculating a 3-year design value if 

2 each full calendar month in the required ozone monitoring season has at least 75% data 

3 completeness for daylight hours. 

4 (ii) If one or more months during the ozone monitoring seasons of three successive years 

5 has less than 75% data completeness, the three years shall nevertheless be used in the 

6 computation of a valid design value for the site if substituting the lowest hourly ozone 

7 concentration observed during daylight hours in the required ozone monitoring season of 

8 each year, or one-half of the method detection limit of the ozone instrument, whichever is 

9 higher, for enough of the missing hourly concentrations within each incomplete month to 

10 make the month 75% complete, and then adjusting for the remaining missing data using 

11 Equation 2, above results in a design value greater than the level of the standard. 

12 (d) Comparisons with the Secondary Ozone Standard

13 (i) The secondary ambient ozone air quality standard is met at an ambient air quality

14 monitoring site when the design value is less than or equal to [15] ppm-hours.

15 (ii) Comparison with the secondary ozone standard is demonstrated by example 4 as 

16 follows:

17

18 Example 4. Ambient Monitoring Site Failing to Meet the Secondary Ozone Standard

April May June July August September October Overa

2006

Adjusted monthly 

W126 index

4.442 9.124 12.983 16.153 13.555 4.364 1.302

3-Month sum na na 26.549 38.260 42.691 34.072 19.221

2006 Maximum 42.691 42.69

2007
Draft O3 NPR –January 5, 2010 444 Deliberative, Do Not Quote or Cite

Adjusted monthly 

W126 index

3.114 7.214 8.214 8.111 7.455 7.331 5.115

3-Month sum na na 18.542 23.539 23.780 22.897 19.901

2007 Maximum 23.780 23.78

2008

Adjusted monthly 

W126 index

4.574 5.978 6.786 8.214 5.579 4.331 2.115

3-Month sum na na 17.338 20.978 20.579 18.124 12.025

2008 Maximum 20.978 20.97

3-Year average 

W126 index

29.149

Rounded 29

1

2 As shown in example 4, the secondary ozone standard is not met for this monitoring site 

3 because the 3-year average of the annual W126 index value for this site is greater than 

4 [15] ppm-hours:

5 3-year average W126 index = (42.691+ 23.780+ 20.978)/3 = 29.149666, which rounds to 

6 29 ppm-hours.

7 In Example 4, the adjusted monthly W126 index values and the 3-month sums of the

8 adjusted monthly W126 index values are shown with three decimal digits. In actual 

9 calculations, all digits supported by the calculator or calculation software must be 

10 retained.
Draft O3 NPR –January 5, 2010 445 Deliberative, Do Not Quote or Cite

1

2 4. Section 50.14 is amended by adding entries for "Primary and Secondary Ozone 

3 Standards” to the end of the table in paragraph (c)(2)(vi) to read as follows:

4 § 50.14 Treatment of air quality monitoring data influenced by exceptional 

5 events.

6 * * * * *

7

8 (c) ***

9

10 (2) ***

11

12 (vi) ***

13

14 Table 1. Schedule for Exceptional Event Flagging and 

15 Documentation Submission for Data to be Used in 

16 Designations Decisions for New NAAQS

17

NAAQS 

Pollutant/

Standard/(Level

)/

Promulgation 

Date

Air Quality 

Data Collected 

for Calendar 

Year

Event Flagging 

& Initial 

Description 

Deadline

Detailed 

Documentation 

Submission 

Deadline

*******

Primary 

Ozone/8-Hr 

2007-2009 November 1, 

2010b

November 1, 

2010b
Draft O3 NPR –January 5, 2010 446 Deliberative, Do Not Quote or Cite

Standard (Level 

TBD) 

Promulgated by 

August 31, 2010

2010 60 Days after 

the end of the 

calendar 

quarter in 

which the event 

occurred or 

March 1, 2011, 

whichever date 

occurs firstb

60 Days after 

the end of the 

calendar 

quarter in 

which the event 

occurred or 

March 1, 2011, 

whichever date 

occurs firstb

Secondary Ozone/ 

(Level 

TBD)Alternative 2-

year Schedule- to be 

Promulgated by 

August 31, 2010 

2008 July 1, 2011bJuly 1, 2011a

2009-2010 July 1, 2011b

July 1, 2011b

2011 60 Days after 

the end of the 

calendar 

quarter in 

which the event 

occurred or 

March 1, 2012, 

whichever 

occurs firstb

60 Days after 

the end of the 

calendar 

quarter in 

which the event 

occurred or 

March 1, 2012, 

whichever 

occurs firstb

Secondary 

Ozone/ (Level 

TBD)-

Alternative 

Accelerated 

Schedule -to be 

Promulgated by 

August 31, 2010

2007-2009 November 1, 

2010b

November 1, 

2010b

2010 60 Days after 

the end of the 

calendar 

quarter in 

which the event 

occurred or 

March 1, 2011, 

whichever date 

occurs firstb

60 Days after 

the end of the 

calendar 

quarter in 

which the event 

occurred or 

March 1, 2011, 

whichever date 

occurs firstb
Draft O3 NPR –January 5, 2010 447 Deliberative, Do Not Quote or Cite

a These dates are 

unchanged from 

those published in 

the original 

rulemaking.

b Indicates change 

from general 

schedule in 40 

CFR 50.14.

Note: EPA notes that 

the table of revised 

deadlines only applies 

to data EPA will use to 

establish the final 

initial designations for 

new NAAQS. The 

general schedule 

applies for all other 

purposes, most 

notably, for data used 

by EPA for 

redesignations to 

attainment.

1

2

3 *****

4

5 5. Section 58.50 (c) is revised and (d) is added to read as follows:

6 § 58.50 Index reporting.

7 (c) The population of a metropolitan statistical area for purposes of index reporting is the 

8 latest available U.S. census population.

9 (d) For O3, reporting is required in metropolitan and micropolitan statistical areas 

10 wherever monitoring is required under Appendix D to Part 58—SLAMS Minimum O3

11 Monitoring Requirements.

12

13 6. Appendix G of Part 58 (3) is revised to read as follows:
Draft O3 NPR –January 5, 2010 448 Deliberative, Do Not Quote or Cite

1 Appendix G to Part 58—Uniform Air Quality Index (AQI) and Daily Reporting

2 3. Must I Report the AQI?

3 You must report the AQI daily if yours is a metropolitan statistical area (MSA) with a

4 population over 350,000. For O3, reporting is required in metropolitan and micropolitan 

5 statistical areas wherever monitoring is required under Appendix D to Part 58—SLAMS 

6 Minimum O3 Monitoring Requirements.