Draft O 3 NPR

- January 5, 2010 Deliberative, Do Not Quote or Cite 6560 - 50 - P 1 ENVIRONMENTAL PROTECTION AGENCY 2 3 40 CFR Part 50 4 5 [EPA - HQ - OAR- 2005 - 0172; FRL - ] 6 7 RIN 2060 - this # has not been assigned yet 8 9 National Ambient Air Quality Standards for Ozone 10 11 12 AGENCY: Environmental Protection Agency (EPA). 13 ACTION: Proposed r ule

. 14 SUMMARY: Based on its reconsideration of the primary and secondary

national 15 ambient air quality

standards (NAAQS) for ozone (O 3 ) set in March 2008, EPA proposes 16 to set different primary and secondary

standards than those set in 200 8 to provide 17 requisite protection of public health and welfare, respectivel y. With regard to the 18 primary

standard for O 3 , EPA proposes that the level of the 8

- hour primary standard, 19 which was set at 0.075 ppm in the 2008 final rule, should instead be set at a lower level 20 within the range of 0.060 to 0.070 parts per million (ppm), to provide increased 21 protection for children and other “at risk” populations against an array of O 3 - related 22 adverse health effects that range from decreased lung function and increased respiratory 23 sy mptoms to serious indicators of respiratory morbidity

including emergency

department 24 visits and hospital admissions for respiratory causes, and possibly

cardiovascular

- related 25 morbidity

as well as total non

- accidental and cardiopulmonary mortality . With regard to 26 the secondary

standard for O 3 , EPA proposes that the secondary O 3 standard, which was 27 set identical to the revised primary standard in the 2008 final rule, should instead be a 28
new cumulative, seasonal standard expressed as an annual index of the sum of weighted 29Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 2 hourly concentrations, cumulated over 12 hours per day (8:00 am to 8:00 pm) during the 1 consecutive 3

- month period within the O 3 season with the maximum index value, set at a 2 level within the range of 7 to 15 ppm

- hours, t o provide increased protection against O 3 - 3 related adverse impacts on vegetation and forested ecos ys tems. 4 DATES: Written comments on this proposed rule must be received b y [insert date 60 5 days after date of publication in the Federal Register]
. 6 Public Hearings : Three public hearings are scheduled for this proposed rule. 7 Two of the public hearings will be held on February 2, 2010 in Arlington, Virginia and 8 Houston, Texas. The third public hearing will be held on February 4, 2010 in 9 Sacramento, California. 10 ADDRESSES: Submit your comments, identified by Docket ID No. EPA

- HQ
- OAR
11 2005
- 0172, by

one of the following methods: 12

 www.regulations.gov : Follow the on

- line instructions for submitting comments. 13

 Email: a - and

- r - Docket@epa.gov

. 14

 Fax: 202
- 566
- 9744
. 15

 Mail: Docket No. EPA

- HQ
- OAR
- 2005
- 0172, Environmental Protection Agency , 16 Mail code 6102T, 1200 Pennsylvania Ave., NW, Washington, DC 20460. Please 17 include a total of two c opies. 18

 Hand Delivery : Docket No. EPA

- HQ
- OAR
- 2005
- 0172, Environmental 19 Protection Agency , EPA West, Room 3334, 1301 Constitution Ave., NW, 20 Washington, DC. Such deliveries are onl y accepted during the Docket’s normal 21 hours of operation, and special arrang ements should be made for deliveries of 22 boxed information. 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 3 Public Hearings : Three public hearings are scheduled for this proposed rule. 1 Two of the public hearings will be held on February 2, 2010 in Arlington, Virginia and 2 Houston, Texas. The third publ ic hearing will be held on February 4, 2010 in 3 Sacramento, California. The hearings will be held at the following locations: 4 Arlington, Virginia

– February 2, 2010 5 6 Hyatt Regency

Cry stal City

@ Reagan National Airport 7 Washington Room (located on the Ballroom Level) 8 2799 Jefferson Davis Highway 9 Arlington, Virginia 22202 10 Telephone: 703

- 418
- 1234 11 12 Houston, Texas

– February 2, 2010 13 14 Hilton Houston Hobby Airport 15 Moody

Ballroom (located on the ground floor) 16 8181 Airport Boulevard 17 Houston, Texas 77061 18 Telephone: 713
- 645
- 3000 19 20 Sacramento, California

– February 4, 2010 21 22 Four Points by

Sheraton Sacramento International Airport 23 Natomas Ballroom 24 4900 Duckhorn Drive 25 Sacramento, California 95834 26 Telephone: 916

- 263
- 9000 27 See the SUPPLEMENTARY INFORMATION under “Public H earings” for 28 further information. 29 Instructions: Direct your comments to Docket ID No. EPA

- HQ
- OAR
- 2005
- 30 0172. The EPA’s policy is that all comments received will be included in the public 31 docket without change and may be made available online at www.regulations.gov , 32 including any personal information provided, unless the comment includes information 33 claimed to be Confidential Business Information (CBI) or other information whose 34Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 4 disclosure is restricted b y statute . Do not submit information that you consider to be CBI 1 or otherwise protected through www.regulations.gov or email. The www.regulations.gov 2 website is an “anonym ous access” s ys tem, which means EPA will not know your identity 3 or contact information unless you provide it in the body of your comment. If you send an 4 email comment directl y t o EPA without going through www.regulations.gov , your email 5 address will be automatically captured and included as part of the comment that is placed 6 in the public docket and made available on the Internet. If you submit an electronic 7 comment, EPA recommends that you include your name and oth er contact information in 8 the body

of your comment and with any disk or CD

- ROM you submit. If EPA cannot 9 read your comment due to technical difficulties and cannot contact you for clarification, 10 EPA may

not be able to consider your comment. Electronic fi les should avoid the use of 11 special characters, any form of encry ption, and be free of any

defects or viruses. 12 Docket: All documents in the docket are listed in the www.regulations.gov index. 13 Although listed in the index, some information is not publicly available, e.g., CBI or 14 other information whose disclosure is restricted b y statute. Certain other material, such 15 as cop yri ghted material, will be publicly available only

in hard copy . Publicly

available 16 doc ket materials are available either electronically in www.regulations.gov or in hard 17 copy

at the Air and Radiation Docket and Information Center, EPA/DC, EPA West, 18 Room 3334, 1301 Constitution Ave., NW, Washington , DC. The Public Reading Room 19 is open from 8:30 a.m. to 4:30 p.m., Monday through Friday , excluding legal holiday s. 20 The telephone number for the Public Reading Room is (202) 566

- 1744 and the telephone 21 number for the Air and Radiation Docket and Informati on Center is (202) 566

- 1742. 22Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 5 FOR FURTHER INFORMATION CONTACT: Ms. Susan Lyon Stone, Health and 1 Environmental Impacts Division, Office of Air Quality Planning and Standards, U.S. 2 Environmental Protection Agency , Mail code C504

- 06, Research Triangle Park , NC 3 27711; telephone: 919

- 541
- 1146 ; fax: 919

- 541
- 0237; email: stone.susan@epa.gov

. 4 SUPPLEMENTARY INFORMATION: 5 General Information 6 What Should I Consider as I Prepare My Comments for EPA? 7 1. Submitting CBI. Do not submit this information to EPA through 8 www.regulations.gov or email. Clearl y mark the part or all of the information that you 9 claim to be CBI. For CBI information in a disk or CD ROM that you mail to EPA, mark 10 the outside of the disk or CD ROM as CBI and then identify electronically

within the disk 11 or CD ROM the specific information that is claimed as CBI. In addition to one complete 12 version of the comment that includes information claimed as CBI, a cop y o f the comment 13 that does not contain the information claimed as CBI must be submitted for inclusion in 14 the public docket. Information so marked will not be disclosed except in accordance with 15 procedures set forth in 40 CFR part 2. 16 2. Tips for Preparing Y our Comments. When submitting comments, remember 17 to: 18

 Id entify

the rulemaking by

docket number and other identifying information 19 (subject heading, Federal Register date and page number). 20

 Follow directions

– The Agency may ask you to respond to specific que stions or 21 organize comments by referencing a Code of Federal Regulations (CFR) part or 22 section number. 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 6  Explain why

you agree or disagree, suggest alternatives, and substitute language 1 for your requested changes. 2

 Describe any assumptions and provide any tec hnical information and/or data that 3 yo u used. 4

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

 Explain your views as clearl y as possible, avoiding the use of profanity or 6 personal threats. 7

 Make sure to submit your comments b y the comment period deadline identified. 8 Availability of Related Information 9 A number of documents relevant to this rulemaking are available on EPA web 10 sites. The Air Quality Criteria for Ozone and Related Photochemical Oxidants ( 2006 11 Criteria Document) (two volumes, EPA/ and EPA/, date) is available on EPA ’ s National 12 Center for Environmental Assessment web site. To obtain this document, go to 13 http://www.epa.gov/ncea , and click on Ozone in the Quick Finder section

. This will open 14 a page with a link to the March 2006 Air Quality Criteria Document. The 2007 Staff 15 Paper, human exposure and health risk assessments, vegetation exposure and impact 16 assessment, and other related technical documents are available on EPA ’ s Office of Air 17 Quality

Planning and Standards (OAQPS) Technology Transfer Network (TTN) web site. 18 The updated final 2007 Staff Paper is available at: 19 http://epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_sp.html and the exposure and risk 20 assessments and other related technical documents are available at 21 http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_td.html . The Response to 22 Significant Comments Document is available at: 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 7 http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_rc.html . These and other related 1 documents are also avail able for inspection and copying in the EPA docket identified 2 above. 3 Public Hearings 4 The public hearings on February 2, 2010 and February

4, 2010 will provide 5 interested parties the opportunity to present data, views, or arguments concerning the 6 proposed r

ule. The EPA may

ask clarifying questions during the oral presentations, but 7 will not respond to the presentations at that time. Written statements and supporting 8 information submitted during the comment period will be considered with the same 9 weight as any oral comments and supporting information presented at the public hearing. 10 Written comments must be received b y the last day of the comment period, as specified 11 in this proposed rulemaking. 12 The public hearings will begin at 9:30 a.m. and continue unti l 7:30 p.m. (local 13 time) or later, if necessary , depending on the number of speakers wishing to participate. 14 The EPA will make every effort to accommodate all speakers that arrive and register 15 before 7:30 p.m. A lunch break is scheduled from 12:30 p.m. until 2:00 p.m. 16 If you would like to present oral testimony at the hearings, please notify Ms. 17 Tricia Crabtree (C504

- 02), U.S. EPA, Research Triangle Park, NC 27711. The preferred 18 method for registering is by e - mail ( crabtree.tricia@epa.gov). Ms. Crabtree may be 19 reached b y telephone at (919) 541

- 5688. She will arrange a general time slot for you to 20 speak. The EPA will make every effort to follow the schedule as closel y as possible on 21 the day

of the hearing

. 22Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 8 Oral testimony

will be limited to five (5) minutes for each commenter to address 1 the proposal. We will not be providing equipment for commenters to show overhead 2 slides or make computerized slide presentations unless we receive special requests in 3 advance. Commenters should notify Ms. Crabtree if they

will need specific audiovisual 4 (AV) equipment. Commenters should also notify Ms. Crabtree if they need specific 5 translation services for non

- English speaking commenters. The EPA encourages 6 commenters to provide written versions of their oral testimonies either electronically on 7 computer disk, CD

- ROM, or in paper cop y. 8 The hearing schedules, including lists of speakers, will be posted on EPA’s web 9 site for the proposal at http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_fr.html 10 prior to the hearing. Verbatim transcripts of the hearings and written statements will be 11 included in the rulemaking docket. 12 Children’s Environmental Health 13 Consideration of children’s environmental health play s a central role in the 14 reconsideration of the 2008 final decision on the O 3 NAAQS and EPA’s decision to 15 propose to set the 8

- hour primary O 3 standard at a level within the range of 0.060 to 16 0. 070 ppm. Technical information that pertains to children, including the evaluation of 17 scientific evidence, policy considerations, and exposure and risk assessments, is 18 discussed in all of the documents listed above in the section on the availability of re lated 19 information. These documents include: the Air Quality Criteria for Ozone and Other 20 Related Photochemical Oxidants; the 2007 Staff Paper; exposure and risk assessments 21 and other related documents; and the Response to Significant Comments. All of the se 22 documents are available on the Web, as described above, and are in the public docket for 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 9 this rulemaking. The public is invited to submit comments or identify peer - reviewed 1 studies and data that assess effects of early life exposure to O 3 . 2 Table of Con tents 3 The following topics are discussed in this preamble: 4 I. Background 5 A. Legislative Requirements 6 B. Related Control Requirements 7 C. Review of Air Quality Criteria and Standards for O 3 8 D. Reconsideration of the 2008 O 3 NAAQS Final Rule 9 1. Decisio n to Initiate a Rulemaking to Reconsider 10 2. Ongoing Litigation 11 12 II. Rationale for Proposed Decision on the Level of the Primary Standard 13 A. Health Effects Information 14 1. Overview of Mechanisms 15 2. Nature of Effects 16 3. Interpretation and Integratio n of Health Evidence 17 4. O 3 - Related Impacts on Public Health 18 B. Human Exposure and Health Risk Assessments 19 1. Exposure Analy ses 20 2. Quantitative Health Risk Assessment 21 C. Reconsideration of the Level of the Primary Standard 22 1. Evidence and Exposure/Risk

- B ased Considerations 23 2
. CASAC Views Prior to 2008 Decision 24 3
. Basis for 2008 Decision on the Primary Standard 25 4
. CASAC Advice Following 2008 Decision 26 5
. Administrator’s Proposed Conclusions 27 D. Proposed Decision on the Level of the Primary Standard 28 29 III. Communication of Public Health Information 30 31 IV
. Rationale for Proposed Decision on the Secondary Standard 32 A. Vegetation Effects Information 33 1. Mechanisms 34 2. Nature of Effects 35 3. Adversity of Effects 36 B. Biologically Relevant Exposure Indices 37 C. Veg etation Exposure and Impact Assessment 38 1. Exposure Characterization 39 2. Assessment of Risks to Vegetation 40 D. Reconsideration of Secondary Standard 41Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 10 1. Considerations Regarding 2007 Proposed Cumulative Seasonal 1 Standard 2 2. Considerations Regarding 2007 Proposed 8
- Hour Standard 3 3
. Basis for 2008 Decision on the Secondary Standard 4 4
. CASAC Views Following 2008 Decision 5 5
. Administrator’s Proposed Conclusions 6 E. Proposed Decision on the Secondary O 3 Standard 7 8 V. Revision of Appendix P

-- Interpretation of the NAAQS for O 3 and Proposed 9 Revisions to the Exceptional Events Rule 10 A. Background 11 B. Interpretation of the Secondary O 3 Standard 12 C. Clarifications Related to the Primary Standard 13 D. Revisions to Exceptions from Standard Data Completeness Requirements 14 for th e Primary Standard 15 E. Elimination of the Requirement for 90 Percent Completeness of Dail y 16 Data across Three Years 17 F. Administrator Discretion to Use Incomplete Data 18 G. Truncation versus Rounding 19 H. Data Selection 20 I. Exceptional Events Information Submissio n Schedule 21 22 VI
. Ambient Monitoring Related to Proposed O 3 Standards 23 A. Background 24 B. Urban Monitoring Requirements 25 C. Non
- Urban Monitoring Requirements 26 D. Revisions to the L ength of the Required O 3 Monitoring Season 27 28 VII. Implementation of Proposed O 3 Standards 29 A. Designations 30 B. State Implementation Plans 31 C. Trans
- boundary Emissions 32 33 VI I I. Statutory

and Executive Order Reviews 34 A. Executive Order 12866: Regulatory Planning and Review 35 B. Paperwork Reduction Act 36 C. Regulatory Flexibility

Act 37 D. Unfunded Mandates Refo rm Act 38 E. Executive Order 13132: Federalism 39 F. Executive Order 13175: Consultation and Coordination with Indian Tribal 40 Governments 41 G. Executive Order 13045: Protection of Chil dren from Environmental 42 Health and Safety Risks 43 H. Executive Order 13211: Actions that Significantly Affect Energy

Suppl y, 44 Distribution or Use 45 I. National Technology Transfer and Advancement Act 46Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 11 J. Executive Order 12898: Federal Actions to Address Environmental Justice 1 in Minority Populations and L ow - In come Populations 2 3 References 4 5 I. Background 6 Th e proposed decision s presented in this notice are based on a reconsideration of 7 the 2008 O 3 NAAQS final rule (73 FR 16436, March 27, 2008), which revised the level 8 of the 8

- hour primary O 3 standard to 0.075 ppm and revised the secondary O 3 s tandard by 9 making it identical to the revised primary standard. This reconsideration is based on the 10 scientific and technical information and analy ses on which the March 2008 O 3 NAAQS 11 rulemaking was based . Therefore, much of the information included in this notice is 12 drawn directly

from information included in the 2007 proposed rule (72 FR 37818 , July 13 11, 2007 ) and the 2008 final rule (73 FR 16436). 14 A. Legislative Requirements 15 Two sections of the Clean Air Act (CAA) govern the establishment and revision 16
o f the NAAQS. Section 108 (42 U.S.C. 7408) directs the Administrator to identify and 17 list “ air pollutants ” that in h er “ judgment, cause or contribute to air pollution which may 18 reasonabl y be anticipated to endanger public health or welfare ” and satisfy two other 19 criteria, including “ whose presence . . . in the ambient air results from numerous or 20 diverse mobile or stationary sources ” and to issue air quality criteria for those that are 21 listed. Air quality

criteria are intended to “ accurately reflect the latest scientific 22 knowledge useful in indicating the kind and extent of all identifiable effects on public 23 health or welfare which may be expected from the presence of [a] pollutant in the 24 ambient air . . . . ” 25Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 12 Section 109 (42 U.S.C. 7409) directs the Adminis trator to propose and 1 promulgate “primary” and “ secondary” NAAQS for pollutants for which air quality 2 criteria are issued. Section 109(b)(1) defines a primary standard as one “ the attainment 3 and maintenance of which in the judgment of the Administrator, b ased on such criteria 4 and allowing an adequate margin of safety , are requisite to protect the public health. ” 1 A 5 secondary

standard, as defined in section 109(b)(2), must “ specify a level of air quality 6 the attainment and maintenance of which, in the judgment of the Administrator, based on 7 such criteria, is requisite to protect the public welfare from any known or anticipated 8 adverse effects associated with the presence of such air pollutant in the ambient air. ” 2 9 The requirement that primary standards inc lude an adequate margin of safety was 10 intended to address uncertainties associated with inconclusive scientific and technical 11 information available at the time of standard setting. It was also intended to provide a 12 reasonable degree of protection against hazards that research has not yet identified. Lead 13 Industries Association v. EPA , 647 F.2d 1130, 1154 (D.C. Cir 1980), cert. denied, 449 14 U.S. 1042 (1980); American Petroleum Institute v. Costle , 665 F.2d 1176, 1186 (D.C. 15 Cir. 1981), cert. denied, 455 U.S. 1034 (1982). Both kinds of uncertainties are 16 components of the risk associated with pollution at levels below those at which human 17

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, 91 st 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 transportatio n, as well as effects on economic values and on personal comfort and well

- being. ”Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 13 health effects can be said to occur with reasonable scientific certainty . Thus, in selecting 1 primary

standards that includ e an adequate margin of safety, the Administrator is seeking 2 not only

to prevent pollution levels that have been demonstrated to be harmful but also to 3 prevent lower pollutant levels that may pose an unacceptable risk of harm, even if the risk 4 is not preci sely

identified as to nature or degree. The CAA does not require the 5 Administrator to establish a primary NAAQS at a zero
- risk level or at background 6 concentration levels, see Lead Industries Association v. EPA , 647 F.2d at 1156 n. 51, but 7 rather at a lev el that reduces risk sufficiently so as to protect public health with an 8 adequate margin of safety

. 9 In addressing the requirement for an adequate margin of safety, EPA considers 10 such factors as the nature and severity of the health effects involved, the si ze of the 11 population(s) at risk, and the kind and degree of the uncertainties that must be addressed. 12 The selection of any particular approach to providing an adequate margin of safety is a 13 policy

choice left specifically

to the Administrator ’ s judgment. Lead Industries 14 Association v. EPA , 647 F.2d at 1161

- 62; Whitman v. American Trucking Associations , 15 531 U.S. 457, 495 (2001). 16 In setting standards that are “requisite” to protect public health and welfare, as 17 provided in section 109(b), EPA’s task is to e stablish standards that are neither more nor 18 less stringent than necessary for these purposes. Whitman v. America Trucking 19 Associations , 531 U.S. 457, 473. In establishing “requisite” primary and secondary 20 standards, EPA may not consider the costs of imp lementing the standards. Id. at 471. 21 Section 109(d)(1) of the CAA requires that “not later than December 31, 1980, 22 and at 5

- ye ar intervals thereafter, the Administrator shall complete a thorough review of 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 14 the criteria published under section 108 and th e national ambient air quality standards . . . 1 and shall make such revisions in such criteria and standards and promulgate such new 2 standards as may

be appropriate . . . . ” Section 109(d)(2) requires that an independent 3 scientific review committee “ shall complete a review of the criteria . . . and the national 4 primary

and secondary

ambient air quality

standards . . . and shall recommend to the 5 Administrator any

new . . . standards and revisions of existing criteria and standards as 6 may be appropriate . .

. . ” This independent review function is performed by the Clean 7 Air Scientific Advisory Committee (CASAC) of EPA ’ s Science Advisory Board. 8 B. Related Control Requirements 9 States have primary responsibility

for ensuring attainment and maintenance of 10 ambient air quality

standards once EPA has established them. Under section 110 of the 11 Act (42 U.S.C. 7410) and related provisions, States are to submit, for EPA approval, 12 State implementation plans (SIPs) that provide for the attainment and maintenance of 13 such standards through control programs directed to emission sources. 14 The majority of man

- made nitrogen oxides (NO x) and volatile organic compounds 15 (VOC ) emissions that contribute to O 3 formation in the United States come from three 16 ty pes of sources: mobile sources, industrial processes (which include consumer and 17 commercial products), and the electric power industry

. 3 Mobile sources and the electric 18 power industry

were responsible for 78 percent of annual NO x emissions in 2004. That 19 same year, 99 percent o f man

- made VOC emissions came from industrial processes 20 (including solvents) and mobile sources. Emissions from natural sources, such as trees, 21

3 See EPA report, Evaluating Ozone Control Programs in the Eastern United States: Focus on the NOx Budget Trading Program, 2004

.Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 15 may also comprise a significant portion of total VOC emissions in certain regions of the 1 country , especially

during the O 3 season, which are considered natural background 2 emissions. 3 The E PA has developed new emissions standards for many types of stationary 4 sources and for nearl y every class of mobile sources in the last decade to reduce O 3 by 5 decreasing emissions o f NO x and VOC. These programs complement State and local 6 efforts to improve O 3 air quality and meet the 0.084 ppm 8

- hour national standards. 7 Under title II of the CAA, 42 U.S.C. 7521

- 7574), EPA has established new emissions 8 standards for nearl y every typ e of automobile, truck, bus, motorcycle, earth mover, and 9 aircraft engine, and for the fuels used to power these engines. EPA also established new 10 standards for the smaller engines used in small watercraft, lawn and garden equipment. 11 In March 2008, EPA p romulgated new standards for locomotive and marine diesel 12 engines and in August 2009, proposed to control emissions from ocean

- going vessels. 13 Benefits from engine standards increase modestl y each ye ar as older, more

14 polluting vehicles and engines are rep laced with newer, cleaner models. In time, these 15 programs will yield substantial emission reductions. Benefits from fuel programs 16 generall y begin as soon as a new fuel is available. 17 The reduction of VOC emissions from industrial processes has been achiev ed 18 either directly

or indirectly

through implementation of control technology standards, 19 including maximum achievable control technology , reasonabl y available control 20 technology , and best available control technology standards; or are anticipated due to 21 proposed or upcoming proposals based on generally available control technology or best 22 available controls under provisions related to consumer and commercial products. These 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 16 standards have resulted in VOC emission reductions of almost a million tons per year 1 accumulated starting in 1997 from a variety of sources including combustion sources, 2 coating categories, and chemical manufacturing. EPA has also finalized emission 3 standards and fuel requirements for new stationary engines. In the area of consumer and 4 commercial products, EPA has finalized new national VOC emission standards for 5 aerosol coatings and is working toward amending existing rules to establish new 6 nationwide VOC content limits for household and institutional consumer products and 7 architectural and industrial maintenance coatings. The aerosol coatings rule took effect 8 in July

2009; the compliance date for both the amended consumer product rule and 9 architectural coatings rule is anticipated to be January 2011. These actions are expected 10 to yi eld significant new VOC reductions

– about 200,000 tons per year. Additionally, in 11 ozone nonattainment areas, we anticipate reductions of an additional 25,000 tons per year 12 as States adopt rules this year implementing control techniques recommendations is sued 13 in 2008 for 4 additional categories of consumer and commercial products, typically 14 surface coatings and adhesives used in industrial manufacturing operations. These 15 emission reductions primarily result from solvent controls and ty picall y occur where and 16 when the solvent is used, such as during manufacturing processes. 17 The power industry is one of the largest emitters of NO x in the United States. 18 Power industry

emission sources include large electric generating units (EGU) and some 19 large industrial boilers and turbines . The EPA’s landmark Clean Air Interstate Rule 20 (CAIR), issued on March 10, 2005, was designed to permanentl y cap power industry 21 emissions of NO x in the eastern United States. The first phase of the cap was to begin in 22 2009, and a low er second phase cap was to begin in 2015. The EPA had projected that 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 17 by 2015, the CAIR and other programs w ould reduce NO x emissions during the O 3 season 1 by about 50 percent and annual NO x emissions by about 60 percent from 2003 levels in 2 the Eastern U.S. However, o n July 11, 2008 and December 23, 2008, the U.S. Court of 3 Appeals for the D.C. Circuit issued decisions on petitions for review of the CAIR. In its 4 July 11 opinion, the court found CAIR unlawful and decided to vacate CAIR and its 5 associated Fed eral implementation plans ( FIPs ) in their entirety. On December 23, the 6 court granted EPA’s petition for rehearing to the extent that it remanded without vacatur 7 for EPA to conduct further proceedings consistent with the Court’s prior opinion. Under 8 this decision, CAIR will remain in place onl y until replaced b y EPA with a rule that is 9 consistent with the Court’s July 11 opinion. The EPA recognizes the need in our CAIR 10 replacement effort to address the reconsidered ozone standard, and we are currentl y 11
as sessing our options for the best way to accomplish this. It should also be noted that 12
new electric generating units ( EGUs ) are also subject to NO x limits under New Source 13 Performance Standards (NSPS) under CAA section 111, as well as either nonattainment 14 new source review or prevention of significant deterioration requirements. 15 With respect to agricultural sources, the U.S. Department of Agriculture (USDA) 16 has approved conservation sy stems and activities that reduce agricultural emissions of 17 NO x and VOC. Current practices that may reduce emissions of NO x and VOC include 18 engine replacement programs, diesel retrofit programs, manipulation of pesticide 19 applications including timing of applications, and animal feeding operations waste 20 management techniques. The EPA recognizes that USDA has been working with the 21 agricultural community to develop conservation sy stems and activities to control 22 emissions of O 3 precursors. 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 18 These conservation activities are voluntaril y adopted through the use of incentives 1 provide d to the agricultural producer. In cases where the States need these measures to 2 attain the standard, the measures could be adopted. The EPA will continue to work with 3 USDA on these activities with efforts to identify and/or improve the control efficienc ies, 4 prioritize the adoption of these conservation sy stems and activities, and ensure that 5 appropriate criteria are used for identifying the most effective application of conservation 6 sy stems and activities. 7 The EPA will work together with USDA and with S tates to identify appropriate 8 measures to meet the primary and secondary

standards, including site

- specific 9 conservation s ys tems and activities. Based on prior experience identifying conservation 10 measures and practices to meet the PM NAAQS requirements, the EPA will use a similar 11 process to identify

measures that could meet the O 3 requirements. The EPA anticipates 12 that certain USDA

- approved conservation sy stems and activities that reduce agricultural 13 emissions of NO x and VOC may be able to satisfy

the requirements for applicable 14 sources to implement reasonably available control measures for purposes of attaining the 15 primary

and secondary

O 3 NAAQS. 16 C. Review of Air Quality Criteria and Standards for O 3 17 In 1971, EPA first established primary and secondary

NAAQS for photochemical 18 oxidants (36 FR 8186). Both primary and secondary

standards were set at a level of 0.08 19 parts per million (ppm), 1

- hr average, total photochemical oxidants, not to be exceeded 20 more than one hr per ye ar. In 1977, EPA announced the first periodic review of the air 21 quality

criteria in accordance with section 109(d)(1) of the Act. The EPA published a 22 final decision in 1979 (44 FR 8202). Both primary and secondary standard levels w ere 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 19 revised from 0.08 to 0.12 ppm. The indicator was revised from photochemical oxidants 1 to O 3 , and the form of the standards w as revised from a deterministic to a statistical form, 2 which defined attainment of the standards as occurring when the expected number of 3 day s per calendar year with maximum hourly average concentration greater than 0.12 4 ppm is equal to or less than one. In 1983, EPA announced that the second periodic 5 review of the primary and secondary

standards for O 3 had been initiated. Following 6 review and publication of air quality criteria and a supplement, EPA published a 7 proposed decision (57 FR 35542) in August 1992 that announced EPA’s intention to 8 proceed as rapidl y as possible with the next review of the air quality criteria and 9 standards for O 3 in light of emerging evidence of health eff ects related to 6

- to 8
- hr O 3 10 exposures. In March 1993, EPA concluded the review by deciding that revisions to the 11 standards were not warranted at that time (58 FR 13008). 12 In August 1992 (57 FR 35542), EPA announced plans to initiate the third periodic 13
review of the air quality criteria and O 3 NAAQS
. O n the basis of the scientific evidence 14 contained in the 1996 CD (U.S. EPA 1996a) and the 1996 Staff Paper (U.S. EPA, 15 1996b), and related technical support documents, linking exposures to ambient O 3 to 16 adver se health and welfare effects at levels allowed by the then existing standards , EPA 17 proposed to revise the primary and secondary

O 3 standards in December 1996 (61 FR 18 65716). The EPA proposed to replac e the then existing 1

- h our primary and secondary 19 standards with 8

- h our average O 3 standards set at a level of 0.08 ppm ( equivalent to 20 0.084 ppm using standard rounding conventions )

. The EPA also proposed, in the 21 alternative, to establish a new distinct secondary standard using a biologically based 22 cumulative seasonal form . The EPA completed the review in July 1997 (62 FR 38856 ) 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 20 by setting the primary

standard at a level of 0.08 ppm, based on the annual fourth

- highest 1 daily maximum 8

- hr average concentration, averaged over three ye ars, and setting the 2 secondary standard identical to the revised primary standard. 3 The EPA initiated the most recent periodic review of the air quality criteria and 4 standards for O 3 in September 2000 with a call for information (65 FR 57810 ; Sept ember 5 26, 2000 ) for the development of a revised Air Quality Criteria Document for O 3 and 6 Other Photochemical Oxidants (henceforth the " 2006 Criteria Document"). A project 7 work plan (EPA, 2002) for the preparation of the Criteria Document was released in 8 November 2002 for CASAC and public rev iew. The EPA held a series of workshops in 9 mid

- 2003 on several draft chapters of the Criteria Document to obtain broad input from 10 the relevant scientific communities. These workshops helped to inform the preparation 11 of the first draft Criteria Document ( EPA, 2005a), which was released for CASAC and 12 public review on January 31, 2005; a CASAC meeting was held on May 4
- 5, 2005 to 13 review the first draft Criteria Document. A second draft Criteria Document (EPA, 14 2005b) was released for CASAC and public review on August 31, 2005, and was 15 discussed along with a first draft Staff Paper (EPA, 2005c) at a CASAC meeting held on 16 December 6

- 8, 2005. In a February 16, 2006 letter to the Administrator, CASAC 17 provided comments on the second draft Criteria Document (Henderson, 2006a), and the 18 final 2006 Criteria Document (EPA, 2006a) was released on March 21, 2006. In a June 19 8, 2006 letter to the Administrator (Henderson, 2006b) , CASAC provided additional 20 advice to the Agency concerning chapter 8 of the final 2006 Criteri a Document 21 (Integrative S ynthesis) to help inform the second draft Staff Paper. 22Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 21 A second draft Staff Paper (EPA, 2006b) was released on July 17, 2006 and 1 reviewed b y CASAC on August 24
- 25, 2006. In an October 24, 2006 letter to the 2 Administrator, CASAC provided advice and recommendations to the Agency concerning 3 the second draft Staff Paper (Henderson, 2006c). A final 2007 Staff Paper (EPA, 2007 a) 4 was released on January 31, 2007. In a March 26, 2007 letter (Henderson, 2007), 5 CASAC offered additional advice to the Administrator with regard to recommendations 6 and revisions to the primary and secondary

O 3 NAAQS. 7 The schedule for completion of the 2008 rulemaking was governed by a consent 8 decree resolving a lawsuit filed in March 2003 b y a group of plaintiffs representing 9 national environmental and public health organizations, alleging that EPA had failed to 10 complete the review within the period provided b y statute. 4 The modified consent decree 11 that governed the 2008 rulemaking , entered b y the court on December 16, 2004, provided 12 that EPA sign for publication notices of proposed and final rulemaking concerning its 13 review of the O 3 NAAQS no later than March 28, 2007 and December 19, 2007, 14 respectivel y. Th at consent decree was further modified in October 2006 to change these 15 proposed and final rulemaking dates to no later than May 30, 2007 and February

20, 16 2008, respectivel y. These dates for signing the publication notices of proposed and final 17 rulemaking were further extended to no later than June 20, 20 07 and March 12, 2008, 18 respectivel y. The proposed decision was signed on June 20, 2007 and published in the 19 Federal Register on July 11, 2007 (72 FR 37818)

. 20 Public hearings on the proposed decision were held on Thursday , August 30, 2007 21 in Philadelphia, PA and Los Angeles, CA . On Wednesday , September 5, 2007 , hearings 22

4 American Lung Association v. W hitman (No. 1:03CV00778, D.D.C. 2003).Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 22 were held in Atlanta, GA, Chicago, IL, and Houston, TX . A large number of comments 1 were received from various commenters on the 2007 proposed revisions to the O 3 2 NAAQS. A comprehensive summary of all significant comments, along with EPA’s 3 responses (henceforth “Response to Comments”), can be found in the docket for the 2008 4 rulemaking, which is also the docket for this reconsideration rulemaking

. 5 The EPA’s final decision on the O 3 NAAAQS w as published in the Federal 6 Register on March 27, 2008 (73 FR 16436)

. In th e 2008 rulemaking , EPA revised the 7 level of the 8

- hour primary standard for O 3 to 0.075 parts per million (ppm), expressed to 8 three decimal places. With regard to the secondary standard for O 3 , EPA revised the 8

- 9 hour standard b y making it identical to the revised primary standard. The EPA also made 10 conforming changes to the Air Quality Index (AQI) for O 3 , setting an AQI value of 100 11 equal to 0.075 ppm, 8

- hour average, and making p roportional changes to the AQI values 12 of 50, 150 and 200. 13 D. Reconsideration of the 2008 O 3 NAAQS Final Rule 14 Consistent with a directive of the new Administration regarding the review of new 15 and pending regulations (Emanuel memorandum, 74 FR 4435 ; January 26, 2009), the 16 Administrator reviewed a number of actions that were taken in the last year by the 17 previous Administration. The 2008 final rule was included in this review in recognition 18 of the central role that the NAAQS play in enabling EPA to fulfill its mission to protect 19 the nation’s public health and welfare. In her review, the Administrator was mindful of 20 the need for judgments concerning the NAAQS to be based on a strong scientific 21 foundation which is developed through a transparent and credible NAAQS review 22Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 23 process, consistent with the core values highlighted in President Obama’s memorandum 1 on scientific integrity (March 9, 2009). 2 1. Decision to Initiate a Rulemaking to Reconsider 3 In her review of the 2008 final rule, several aspects of the final rule related to the 4 primary

and secondary

standards stood out to the Administrator. As an initial matter, the 5 Administrator noted that the 2008 final rule concluded that the 1997 primary and 6 secondary

O 3 standards were not adequate to protect public health and public welfare, 7 and that revisions were necessary to provide increased protection. With respect to 8 revision of the primary standard, the Administrator noted that the revised level 9 established in the 2008 final rule was above the range that had been unanimously 10 recommended b y CASAC. 5 She also noted that EPA received comments from a large 11 number of commenters from the medical and public health communities, including 12 EPA’s Children’s Health Protection Advisory Committee, all of which endorsed levels 13
w ithin CASAC’s recommended range. 14 With respect to revision of the secondary O 3 standard, the Administrator noted 15 that the 2008 final rule differed substantially from CASAC’s recommendations that EPA 16 adopt a new secondary O 3 standard based on a cumulative, s easonal measure of exposure

. 17 The 2008 final rule revised the secondary standard to be identical to the revised primary 18 standard, which is based on an 8
- hour dail y maximum measure of exposure. She also 19 noted that EPA received comments from a number of commenters representing 20

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 O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 24 environmental interests, all of which endorsed CASAC;s recommendation for a new 1 cumulative, seasonal secondary standard. 6 2 Subsequent to issuance of the 2008 final rule, in April 2008, CASAC took the 3 unusual step of sending EPA a lett er expressing strong, unanimous disagreement with 4 EPA’s decisions on both the primary and secondary

standards (Henderson, 2008). The 5 CASAC explained that it did not endorse the revised primary O 3 standard as being 6 sufficiently

protective of public health because it failed to satisfy the explicit stipulation 7 of the Act to provide an adequate margin of safety . The CASAC also expressed the view 8 that failing to revise the secondary standard to a cumulative, seasonal form was not 9 supported by

the available sci ence. In addition to CASAC’s letter, the Administrator 10 noted a recent adverse ruling issued by the U.S. Court of Appeals for the District of 11 Columbia Circuit on another NAAQS decision. In February 2009, the DC Circuit 12 remanded the Agency's decisions on the primary annual and secondary

standards for fine 13 particles (PM 2.5 ). In so doing, the Court found that EPA had not adequatel y explained the 14 basis for its decisions, including why CASAC’s recommendations for a more health

15 protective primary

annual standard and for secondary standards different from the 16 primary

standards were not accepted. American Farm Bureau v. EPA , 559 F.3d. 512 17 (D.C. Cir. 2009). 18 Based on her review of the information described above, the Administrator is 19 initiating a rulemaking to re consider parts of the 2008 final rule. Specifically , the 20 Administrator is reconsidering the level of the primary standard to ensure that it is 21

6 The Administrator also noted the exchange that had occurred between EPA and the O ffice 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 O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 25 sufficiently

protective of public health, as discussed in section II below, and is 1 reconsidering all aspect s of the secondary standard to ensure that it appropriately reflects 2 the available science and is sufficiently protective of public welfare , as discussed in 3 section IV below . Based on her review, the Administrator has serious cause for concern 4 regarding whether the revisions to the primary and secondary

O 3 standards adopted in the 5 2008 final rule satisfy the requirements of the CAA , in light of the body of scientific 6 evidence before the Agency . In addition, the importance of the O 3 NAAQS to public 7 health and w elfare weigh heavily in favor of reconsidering parts of the 2008 final rule as 8 soon as possible, based on the scientific and technical information upon which the 2008 9 final rule was based

. 10 Also, EPA conducted a provisional assessment of “new” scientific papers ( EPA, 11 2009) of scientific literature evaluating health and ecological effects of O 3 exposure 12 published since the close of the 2006 Criteria Document upon which the 2008 O 3 13 NAAQS were based. The Administrator notes that the provisional assessment of “new” 14 science found that such studies did not materially change the conclusions in the 2006 15 Criteria Document. This provisional assessment is supportive of the Administrator’s 16 decision to reconsider parts of the 2008 final rule at this time, based on the scientific and 17 technical information available for the 2008 final rule, as compared to foregoing such 18 reconsideration and taking appropriate action in the future as part of the next periodic 19 review of the air quality criteria and NAAQS, which will include such scientific and 20 technical information

. 21 The reconsideration of parts of the 2008 final rule discussed in this notice is based 22 on the scientific and technical record from the 2008 rulemaking, including public 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 26 comments and CASAC advice and recommendation s. The information that was assessed 1 during the 2008 rulemaking includes information in the 2006 Criteria Document (EPA, 2 2006 a), the 2007 Policy Assessment of Scientific and Technical Information, referred to 3 as the 2007 Staff Paper (EPA, 2007 b ), and related technical support documents including 4 the 2007 REAs (U.S. EPA, 2007 c ; Abt Associates, 2007a,b). Scientific and technical 5 information developed since the 2006 C riteria Document will be considered in the next 6 periodic review, instead of this reconsideration rulemaking, allowing the new information 7 to receive careful and comprehensive review b y CASAC and the public before it is used 8 as a basis in a rulemaking that determines whether to revise the NAAQS. 9 2. Ongoing Litigation 10 In May

2008, f ollowing publi cation of the 2008 final rule, numerous groups , 11 including state, public health, environmental, and industry petitioners, challenged EPA's 12 decisions in federal court. The challenges were consolidated as State of Mississippi, et al. 13 v. EPA (No. 08

- 1200, D.C . Cir. 2008). On March 10, 2009, EPA filed an unopposed 14 motion requesting that the Court vacate the briefing schedule and hold the consolidated 15 cases in abeyance. The Agency stated its desire to allow time for appropriate officials 16 from the new Administration to review the O 3 standards to determine whether they 17 should be maintained, modified or otherwise reconsidered. The EPA further requested 18 that it be directed to notify the Court and all the parties of any actions it has taken or 19 intends to take, if any , within 180 day s of the Court vacating the briefing schedule. On 20 March 19, 2009, the Court granted EPA's motion. Pursuant to the Court's order, on 21 September 16, 2009 EPA notified the Court and the parties of its decision to initiate a 22 rulemaking to re consider the primary and secondary

O 3 standards set in March 2008 to 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 27 ensure they satisfy

the requirements of the CAA 7 In its notice to the Court, EPA stated 1 that this notice of proposed rulemaking would be signed b y December 21, 2009, and that 2 the final r

ule will be signed by

August 31, 2010. 3 4 II. Rationale for Proposed Decision on the Level of the Primary Standard 5 As an initial matter, the Administrator note s that the 2008 final rule concluded 6 that the 1997 primary O 3 standard was “not sufficient and thu s not requisit e to protect 7 public health with an adequate margin of safety , and that revision is needed to provide 8 increased public health protection ” (73 FR 16472). Th e Administrator is not 9 reconsidering this aspect of the 2008 decision , which is based o n the reasons discussed in 10 section II.B of the 2008 final rule ( 73 FR 16443
- 16472). The Administrator also notes 11 that the 2008 final rule concluded that it was appropriate to retain the O 3 indicator, the 8

- 12 hour averaging time , and form of the primary O 3 s tandard (specified as the annual fourth

13 highest dail y maximum 8

- hour concentration, averaged over 3 ye ars) , while concluding 14 that revision of the standard level was appropriate

. 8 Th e Administrator is not 15 reconsidering these aspect s of the 2008 decision , which are based on the reasons 16 discussed in sections II.C.1

- 3 of the 2008 final rule , which address the indicator, 17

7 The EPA also separatel y announced that it will move quickly to implement any new stan dards that might res ult from this reconsideration. To reduce the workload for states during the interim period of reconsideration, the A gency 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 O 3 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 dail y maximum 8

- hour concentration, averaged over 3 years, were adopted in the 1997 final rule and retained in the 2008 rulemaking.Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 28 averaging time, and form, respectivel y, of the primary O 3 standard (73 FR 16472

- 16475). 1 For these reasons, the Administrator is not reopening the 2008 decision with regard to the 2 need to revise the 1997 primary O 3 standard nor with regard to the indicator, averaging 3 time, and form of the 2008 primary O 3 standard. Thus, the information that follows in 4 this section specificall y focuses on a reco nsideration of level of the primary O 3 standard. 5 This section presents the rationale for the Administrator’s proposed decision that 6 the O 3 primary

standard , which was set at a level of 0.075 ppm in the 2008 final rule , 7 should instead be set at a lo wer leve l within the range from 0.060 to 0.070 ppm. As 8 discussed more full y below, th e rationale for the proposed range of standard levels is 9 based on a thorough review of the latest scientific information on human health effects 10 associated with the presence of O 3 in the ambient air presented in the 2006 Criteria 11 Document . This rationale also takes into account: (1) staff assessments of the most 12 policy

- relevant information in the 2006 Criteria Document and staff anal ys es of air 13 quality , human exposure, and health risks, presented in the 2007 Staff Paper, upon which 14 staff recommendations for revisions to the primary O 3 standard in the 2008 rulemaking 15
were based; (2) CASAC advice and recommendations, as reflected in discussions of 16 drafts of the 2006 Criteria Document and 2007 Staff Paper at public meetings, in separate 17 written comments, and in CASAC’s letters to the Administrator both before and after the 18 2008 rulemaking ; and (3) public comments received during the development of these 19 documents, either in connectio n with CASAC meetings or separatel y , and on the 2007 20 proposed rule

. 21 In developing this rationale, the Administrator recognizes that the CAA requires 22 her to reach a public health policy judgment as to what standard would be requisite to 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 29 protect public health with an adequate margin of safety, based on scientific evidence and 1 technical assessments that have inherent uncertainties and limitations. This judgment 2 requires making reasoned decisions as to what weight to place on various types of 3 evidence and asse ssments , and on the related uncertainties and limitations

. Thus, in 4 selecting standard levels to propose , and subsequently in selecting a final level, the 5 Administrator is seeking not only to prevent O 3 levels that have been demonstrated to be 6 harmful but also to prevent lower O 3 levels that may pose an unacceptable risk of harm, 7 even if the risk is not precisely identified as to nature or degree. 8 In this proposed rule , EPA has drawn upon an integrative s ynthesis of the entire 9 body of evidence, published through early 2006, on human health effects associated with 10 the presence of O 3 in the ambient air. As discussed below in section II.A, this body of 11 evidence addresses a broad range of health endpoints associated with exposure to ambient 12 levels of O 3 (EPA, 2006a, chapter 8), and includes over one hundred epidemiologic 13 studies conducted in the U.S., Canada, and many countries around the world. 9 In 14
re considering this evidence, EPA focuses on those health endpoints that have been 15 demo nstrated to be caused by exposure to O 3 , or for which the 2006 Criteria Document 16 judges associations with O 3 to be causal, likely causal, or for which the evidence is highly 17 suggestive that O 3 contributes to the reported effects. This rationale also draws upon the 18 results of quantitative exposure and risk assessments, discussed below in section II.B. 19 Section II.C focuses on the considerations upon which the Administrator’s proposed 20

9 Inits assessment of the epidemiological evidence judged to be most relevant to making decisions on the level of the O 3 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 O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 30 con c lusions on the level of the primary standard are based

. Policy

- relevant evidence

1 based and exposure/risk

- based considerations are discussed, and the rationale for the 2 2008 final rulemaking on the primary standard and CASAC advice, given both prior to 3 the development of the 2007 propos ed rule and following the 2008 final rul e , are 4 summarized . Finally , the Administrator’s proposed conclusions on the level of the 5 primary

standard are presented. Section II.D summarizes the proposed decision on the 6 level of the primary O 3 standard and the solicitation of public comments

. 7 Judgments made in the 2006 Criteria Document and 2007 Staff Paper about the 8 extent to which relationships between various health endpoints and short

- term exposures 9 to ambient O 3 are likely causal have been informed by several factors. As discussed 10 below in section II.A, these factors include the nature of the evidence (i.e., controlled 11 human exposure, epidemiological, and/or toxicological studies) and the weight of 12 evidence, which takes into account such considerations as biological plausibility, 13 coherence of ev idence, strength of association, and consistency of evidence. 14 In assessing the health effects data base for O 3 , it is clear that human studies 15 provide the most directl y applicable information for determining causality because they 16 are not limited by

the un certainties of dosimetry differences and species sensitivity 17 differences, which would need to be addressed in extrapolating animal toxicology data to 18 human health effects. Controlled human exposure studies provide data with the highest 19 level of confidence since they provide human health effects data under closely monitored 20 conditions and can provide exposure

- response relationships. Epidemiological data 21 provide evidence of associations between ambient O 3 levels and more serious acute and 22 chronic health eff

ects (e.g., hospital admissions and mortality) that cannot be assessed in 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 31 controlled human exposure studies. For these studies the degree of uncertainty 1 introduced b y potentially confounding variables (e.g., other pollutants, temperature) and 2 other factor s affects the level of confidence that the health effects being investigated are 3 attributable to O 3 exposures, alone and in combination with other copollutants. 4 In using a weight of evidence approach to inform judgments about the degree of 5 confidence that various health effects are likel y to be caused b y exposure to O 3 , 6 confidence increases as the number of studies consistently reporting a particular health 7 endpoint grows and as other factors, such as biological plausibility and strength, 8 consistency , and coherence of evidence, increase. Conclusions regarding biological 9 plausibility, consistency , and coherence of evidence of O 3 - related health effects are 10 drawn from the integration of epidemiological studies with mechanistic information from 11 controlled hum an exposure studies and animal toxicological studies. As discussed below, 12 this ty

pe of mechanistic linkage has been firml y established for several respiratory 13 endpoints (e.g., lung function decrements, lung inflammation) but remains far more 14 equivocal for cardiovascular endpoints (e.g., cardiovascular

- related hospital admissions). 15 For epidemiological studies, strength of association refers to the magnitude of the 16 association and its statistical strength, which includes assessment of both effects estimate 17 size and precision. In general, when associations yield large relative risk estimates, it is 18 less likely

that the association could be completely accounted for by

a potential 19 confounder or some other bias. Consistency refers to the persistent finding of an 20 association between exposure and outcome in multiple studies of adequate power in 21 different persons, places, circumstances and times. For example, the magnitude of effect 22Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 32 estimates is relatively

consistent across recent studies showing association betw een short

1 term, but not long

- term, O 3 exposure and mortality. 2 Based on the information discussed below in sections II.A.1

– II.A.3, judgments 3 concerning the extent to which relationships between various health endpoints and 4 ambient O 3 exposures are likely causal are summarized below in section II.A.3.c. These 5 judgments reflect the nature of the evidence and the overall weight of the evidence, and 6 are taken into consideration in the quantitative exposure and risk assessments, discussed 7 below in s ection II. B. 8 To put judgments about health effects that have been demonstrated to be caused 9 by exposure to O 3 , or for which the 2006 Criteria Document judges associations with O 3 10 to be causal, likel y causal, or for which the evidence is highl y suggestive that O 3 11
co ntributes to the reported effects into a broader public health context, EPA has drawn 12 upon the results of the quantitative exposure and risk assessments. These assessments 13 provide estimates of the likelihood that individuals in particular population group s that 14 are at risk for various O 3 - related phy siological health effects would experience 15 “exposures of concern” and specific health endpoints under varying air quality scenarios 16 ( i.e. , just meeting various standards 10 ), as well as characterizations of the kind and degree 17 of uncertainties inherent in such estimates. 18 In th e 2008 final rulemaking and in this reconsideration, the term “exposures of 19 concern” is defined as personal exposures while at moderate or greater exertion to 8

- hour 20

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 O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 33 average ambient O 3 levels at and above specific benchmark levels which represent 1 exposure levels at which O 3 - related health effects are known or can reasonably be 2 inferred to occur in some individuals, as discussed below in section II.B.1. 11 The EPA 3 emphasizes that although the an al ys is of “exposures of concern” was conducted using 4 three discrete benchmark levels (i.e., 0.080, 0.070, and 0.060 ppm), the concept is more 5 appropriatel y viewed as a continuum with greater confidence and less uncertainty about 6 the existence of health eff ects at the upper end and less confidence and greater 7 uncertainty as one considers increasingly lower O 3 exposure levels. The EPA recognizes 8 that there is no sharp breakpoint within the continuum ranging from at and above 0.080 9 ppm down to 0.060 ppm. In considering the concept of exposures of concern, it is 10 important to balance concerns about the potential for health effects and their severity with 11 the increasing uncertainty associated with our understanding of the likelihood of such 12 effects at lower O 3 l evels. 13 Within the context of this continuum, e stimates of exposures of concern at 14 discrete benchmark levels provide some perspective on the public health impacts of O 3 - 15 related health effects that have been demonstrated in controlled human exposure and 16 t oxicological studies but cannot be evaluated in quantitative risk assessments, such as 17 lung inflammation, increased airway responsiveness, and changes in host defenses. They 18

11 Exposures of concern were also considered in the 1997 review of the O 3 NAAQS, and were judged by EPA to be an important indicator of the public health impacts of those O 3 - related effects for which information wa s too li mited 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 O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 34 also help in understanding the extent to which such impacts have the potential to be 1 reduced b y m eeting various standards. These O 3 - related phy siological effects are 2 plausibly

linked to the increased morbidity seen in epidemiological studies (e.g., as 3 indicated b y increased medication use in asthmatics , school absences in all children , and 4 emergency

department visits and hospital admissions in people with lung disease ). 5 Estimates of the number of people likel y to experience exposures of concern cannot be 6 directly

translated into quantitative estimates of the number of people likely to experience 7 specific health effects, since sufficient information to draw such comparisons is not 8 available

-- if such information were available, these health outcomes would have been 9 included in the quantitative risk assessment. Due to individual variab ility in 10 responsiveness, onl y a subset of individuals who have exposures at and above a specific 11 benchmark level can be expected to experience such adverse health effects, and 12 susceptible subpopulations such as those with asthma are expected to be affected more b y 13 such exposures than healthy individuals. The amount of weight to place on the estimates 14 of exposures of concern at any of these benchmark levels depends in part on the weight 15 of the scientific evidence concerning health effects associated with O 3 exposures at and 16 above that benchmark level. It also depends on judgments about the importance from a 17 public health perspective of the health effects that are known or can reasonably be 18 inferred to occur as a result of exposures at and above the benchmar k level. Such public 19 health policy

judgments are embodied in the NAAQS standard setting criteria (i.e., 20 standards that, in the judgment of the Administrator, are requisite to protect public health 21 with an adequate margin of safety)

. 22Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 35 As discussed below in section II.B

. 2 , the quantitative health risk assessment 1 conducted as part of th e 2008 final rulemaking includes estimates of risks of lung 2 function decrements in asthmatic and all school age children, respiratory sy mptoms in 3 asthmatic children, respiratory- related hospital admissions, and non

- accidental and 4 cardiorespiratory

- related mortality associated with recent ambient O 3 levels, as well as 5 risk reductions and remaining risks associated with just meeting the then current 0.084 6 ppm standard and various alternative O 3 standards in a number of example urban areas. 7 There are two parts to this risk assessment: one part is based on combining information 8 from controlled human exposure studies with modeled population exposure, and the other 9 part is based on c ombining information from community epidemiological studies with 10 either monitored or adjusted ambient concentrations levels. This assessment provide s 11 estimates of the potential magnitude of O 3 - related health effects, as well as a 12 characterization of the uncertainties and variability inherent in such estimates . This 13 assessment also provide s insights into the distribution of risks and patterns of risk 14 reductions associated with meeting alternative O 3 standards. 15 As discussed below, a substantial amount of n ew research conducted since the 16 1997 review of the O 3 NAAQS was available to in form the 2008 final rulemaking , with 17 important new information coming from epidemiologic studies as well as from controlled 18 human exposure, toxicological, and dosimetric studies . The research studies newl y 19 available in the 2008 final rulemaking that were evaluated in the 2006 Criteria Document 20 and the exposure and risk assessments presented in the 2007 Staff Paper have undergone 21 intensive scrutiny

through multiple layers of peer review and many opportunities for 22 public review and comment. While important uncertainties remain in the qualitative and 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 36 quantitative characterizations of health effects attributable to exposure to ambient O 3 , and 1 while different interpretations of these uncertainties can result in different public health 2 policy

judgments, the review of this information has been extensive and deliberate. In 3 the judgment of the Administrator, this intensive evaluation of the scientific evidence 4 provides an adequate basis for this reconsideration of the 2008 final rulemaking

. 5 A. Health Effects Information 6 This section outlines key information contained in the 2006 Criteria Document 7 (chapters 4

- 8) and in the 2007 Staff Paper (chapter 3) on known or potential effects on 8 publ ic health which may be expected from the presence of O 3 in ambient air. The 9 information highlighted here summarizes: (1) new information available on potential 10 mechanisms for health effects associated with exposure to O 3 ; (2) the nature of effects 11 that h ave been associated directly with exposure to O 3 and indirectly with the presence of 12 O 3 in ambient air; (3) an integrative interpretation of the evidence, focusing on the 13 biological plausibility and coherence of the evidence; and (4) considerations in 14 characterizing the public health impact of O 3 , including the identification of “at risk” 15 populations. 16 The decision in the 1997 review focused primarily on evidence from short

- term 17 (e.g., 1 to 3 hours) and prolonged ( 6 to 8 hours) controlled

- exposure studies reporting 18 lung function decrements, respiratory s ymptoms, and respiratory inflammation in 19 humans, as well as epidemiology studies reporting excess hospital admissions and 20 emergency

department (ED) visits for respiratory causes. The 2006 C riteria D ocument 21 prepared for th e 2008 rulemaking emphasize d the large number of epidemiological 22 studies published since the last review with these and additional health endpoints, 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 37 including the effects of acute (short

- term and prolonged) and chronic exposures to O 3 on 1 lun g function decrements and enhanced respiratory sy mptoms in asthmatic individuals, 2 school absences , and premature mortality . It also emphasize d important new information 3 from toxicology , dosimetry , and controlled human exposure studies. Highlights of the 4 evidence include: 5 (1) Two new controlled human

- exposure studies are now available that examine 6 respiratory

effects associated with prolonged O 3 exposures at levels below 0.080 ppm, 7 which was the lowest exposure level that had been examined in the 1997 review. 8 (2) Numerous controlled human

- exposure studies have examined indicators of 9 O 3 - induced inflammatory response in both the upper respiratory tract (URT) and lower 10 respiratory

tract (LRT), and increased airway responsiveness to allergens in subjects wi th 11 allergic asthma and allergic rhinitis exposed to O 3 , while other studies have examined 12 changes in host defense capability following O 3 exposure of healthy young adults. 13 (3) Animal toxicology studies provide new information regarding mechanisms of 14 acti on, increased susceptibility to respiratory

infection, and the biological plausibility of 15 acute effects and chronic, irreversible respiratory damage. 16 (4) Numerous acute exposure epidemiological studies published during the past 17 decade offer added evidenc e of ambient O 3 - related lung function decrements and 18 respiratory

s ymptoms in phy sicall y active healthy subjects and greater responses in 19 asthmatic subjects, as well as evidence on new health endpoints, such as the relationships 20 between ambient O 3 concentrations and asthma medication use and school absenteeism, 21 and between ambient O 3 and cardiac

- related phys iological endpoints. 22Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 38 (5) Several additional studies have been published over the last decade examining 1 the temporal associations between O 3 exposures and emergency department visits for 2 asthma and other respiratory diseases and respiratory

- related hospital admissions. 3 (6) A large number of newly available epidemiological studies have examined 4 the effects of acute exposure to PM and O 3 on mortality , not abl y including large multicity 5 studies that provide much more robust and credible information than was available in the 6 1997 review, as well as recent meta

- anal ys es that have evaluated potential sources of 7 heterogeneity

in O 3 - mortality

associations. 8 1. Overview of Mechanisms 9 Evidence on possible mechanisms by which exposure to O 3 may result in acute 10 and chronic health effects is discussed in chapters 5 and 6 of the 2006 Criteria 11 Document. 12 Evidence from dosimetry , toxicological, and human exposure studie s has 12 contributed to an understanding of the mechanisms that help to explain the biological 13 plausibility

and coherence of evidence for O 3 - induced respiratory health effects reported 14 in epidemiological studies. More detailed information about the phy siolog ical 15 mechanisms related to the respiratory effects of short

- and long

- term exposure to O 3 can 16 be found in section II.A.3.b.i and II.A.3.b.iii, respectivel y. In the past, however, little 17 information was available to help explain potential biological mechanisms which linked 18 O 3 exposure to premature mortality or cardiovascular effects. As discussed more fully in 19 section II.A.3.b.ii below, since the 1997 review an emerging body of animal toxicology 20

12 While most of the available evidence addresses mechanisms for O 3 , O 3 clearly serves as an indicator for the total photochemical oxidant mixture found in the ambient air. Some effects may

be caused b y one or more components in the overall pollutant mix, either separatel y or in combination with O 3 . However, O 3 clearl y dominates these other oxidants with their concentrations only being a few percent of the O 3 concentration.Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 39 and controlled human exposure evidence is beginning to sugges t mechanisms that may 1 mediate acute O 3 cardiovascular effects. While much is known about mechanisms that 2 play a role in O 3 - related respiratory effects, additional research is needed to more clearl y 3 understand the role that O 3 may have in contributing to c ardiovascular effects. 4 With regard to the mechanisms related to short

- term respiratory effects, scientific 5 evidence discussed in the 2006 Criteria Document (section 5.2) indicates that reactions of 6 O 3 with lipids and antioxidants in the epithelial lining fluid and the epithelial cell 7 membranes of the lung can be the initial step in mediating deleterious health effects of 8 O 3 . This initial step activates a cascade of events that lead to oxidative stress, injury , 9 inflammation, airway epithelial damage and in creased alveolar permeability to vascular 10 fluids. Inflammation can be accompanied b y increased airway responsiveness, which is 11 an increased bronchoconstrictive response to airway irritants and allergens. Continued 12 respiratory

inflammation also can alter the ability of the body to respond to infectious 13 agents, allergens and toxins. Acute inflammatory responses to O 3 in some healthy people 14 are well documented, and precursors to lung injury are observed within 3 hours after 15 exposure in humans. Repeated respiratory inflammation can lead to a chronic 16 inflammatory

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

diseases such as fibrosis and emphys ema (EPA, 2006a , section 8.6.2). The 18 severity of s ymptoms and magnitude of response to acute exposures depend on inhaled 19 dose, as well as on individual susceptibility to O 3 , as discussed below. At the same O 3 20 dose, individuals who are more susceptible to O 3 will have a larger response than those 21 who are less susceptible; among individuals with similar susceptibility, those who receive 22 a larger dose will have a larger response to O 3 . 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 40 The inhaled dose is the product of O 3 concentration (C), minute ventilation or 1 ventilation rate, and duration of exposure (T), or (C × ventilation rate × T). A large body 2 of data regarding the interdependent effect of these components of inhaled dose on 3 pulmonary

responses was assessed in the 1986 and 1996 O 3 Criteria Documents. In an 4 attempt to describe O 3 dose

- response characteristics, acute respo nses were modeled as a 5 function of total inhaled O 3 dose, which was generally found to be a better predictor of 6 response than O 3 concentration, ventilation rate, or duration of exposure, alone, or as a 7 combination of any two of these factors (EPA 2006a, se ction 6.2). Predicted O 3 - induced 8 decrements in lung function have been shown to be a function of exposure concentration, 9 duration and exercise level for healthy , young adults (McDonnell et al., 1997). A meta
10 anal ys is of 21 studies (Mudway and Kelly , 2004 ) showed that markers of inflammation 11 and increased cellular permeability in healthy

subjects are associated with total O 3 dose. 12 The 2006 C riteria D ocument summarizes information on potentially susceptible 13 and vulnerable groups in section 8.7. As describ ed there, the term susceptibility refers to 14 innate (e.g., genetic or developmental) or acquired (e.g., personal risk factors, age) 15 factors that make individuals more likely to experience effects with exposure to 16 pollutants. A number of population groups and lifestages have been identified as 17 potentially

susceptible to health effects as a result of O 3 exposure, including people with 18 existing lung diseases, including asthma , children and older adults, and people who have 19 larger than normal lung function resp onses that may be due to genetic susceptibility

. In 20 addition, some population groups and lifestages have been identified as having increased 21 vulnerability to O 3 - related effects due to increased likelihood of exposure while at 22 elevated ventilation rates, including healthy children and adults who are active outdoors, 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 41 for example, o utdoor workers , and joggers

. Taken together, the susceptible and 1 vulnerable groups are more commonly referred to as "at

- risk" groups 13 , as discussed 2 more fully

below in section II. A.4.b. 3 Based on a substantial body of new evidence from animal, controlled human 4 exposure and epidemiological studies , the 2006 Criteria Document concludes that people 5 with asthma and other preexisting pulmonary disease s are likely

to be among those at 6 in creased risk from O 3 exposure. Altered physiological, morphological and biochemical 7 states ty

pical of respiratory

diseases like asthma, COPD and chronic bronchitis may 8 render people sensitive to additional oxidative burden induced b y O 3 exposure (EPA 9 2006 a, section 8.7). Children and adults with asthma are the group that has been studied 10 most extensively . Evidence from controlled human exposure studies indicates that 11 asthmatics may

exhibit larger lung function decrements in response to O 3 exposure than 12 h ealthy

controls. As discussed more full y in section II.A.4.b.ii b elow, as thmatics present 13 a differential response profile for cellular, molecular, and biochemical parameters ( EPA, 14 2006a, section 8.7.1 ) that are altered in response to acute O 3 exposure. They can have 15 larger inflammatory responses, as manifested b y l arger increases in markers of 16 inflammation such as white bloods cells (e.g., PMNs) or inflammatory cy tokines. 17 Asthmatics, and people with allergic rhinitis, are more likely to mount an allergic

- ty

pe 18 response upon exposure to O 3 , as manifested b y increases in white blood cells associated 19

13 Inprevious Staff Papers and Federal Register notices announcing proposed and fin al decisions on the O 3 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 ty pes of population groups.Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 42 with allergy

(i.e., eosinophils) and related molecules, which increase inflammation in the 1 airway s. The increased inflammatory and allergic responses also may b e associated with 2 the larger late

- phase responses that asthmatics can experience, which can include 3 increased bronchoconstrictor responses to irritant substances or allergens and additional 4 inflammation. Inaddition to the experimental evidence of lung function decrements, 5 respiratory

s ymptoms, and other respiratory effects in asthmatic populations, two large 6 U.S. epidemiological studies as well as several smaller U.S. and international studies, 7 have reported fairl y robust associations between ambient O 3 c oncentrations and measures 8 of lung function and daily sy mptoms (e.g., chest tightness, wheeze, shortness of breath) 9 in children with moderate to severe asthma and between O 3 and increased asthma 10 medication use (EPA, 2007a, chapter 6). Thes e responses in a sthmatics and others with 11 lung disease provide biological plausibility for the more serious respiratory morbidity 12 effects observed in epidemiological studies , such as emergency department visits and 13 hospital admissions

. 14 Children with and without asthma were found to be particularly susceptible to O 3 15 effects on lung function and generall y have greater lung function responses than older 16 people. The American Academy of Pediatrics (2004) notes that children and infants are 17 among the population groups most sus ceptible to many air pollutants, including O 3 . This 18 is in part because their lungs are still developing. For example, eighty percent of alveoli 19 are formed after birth, and changes in lung development continue through adolescence 20 (Dietert et al., 2000). Moreover, children have high minute ventilation rates and 21 relativel y high levels of physical activity which also increases their O 3 dose (Plunkett et 22 al., 1992). Thus, children are at

- risk due to both their susceptibility and vulnerability

. 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 43 Looking more broadl y at age - related differences in susceptibility, several 1 mortality

studies have investigated age

- related differences in O 3 effects (EPA, 2006a, 2 section 7.6.7.2), primarily in the older adult population. Among the studies that observed 3 positive associ ations between O 3 and mortality, a comparison of all age or younger age 4 (

 65 years of age) O 3 - mortality effect estimates to that of the elderly population (>65 5 ye ars) indicates that, in general, the elderl y population is more susceptible to O 3 mortality 6 effects. There is supporting evidence of age

- related differences in susceptibility to O 3 7 lung function effects. The 2006 Criteria Document (section 7.6.7.2) concludes that the 8 elderl y population (>65 years of age) appear to be at greater risk of O 3 - related mortality 9 and hospitalizations compared to all age s or younger populations, and children (<18 ye ars 10 of age) experience other potentially adverse respiratory

health outcomes with increased 11 O 3 exposure. 12 Controlled human exposure studies have also indicated a high degree of 13 interindividual variability in some of the pulmonary phy siological parameters, such as 14 lung function decrements. The variable effects in individuals have been found to be 15 reproducible, in other words, a person who has a large lung function response after 16 exposure to O 3 will likely have about the same response if exposed again to the same 17 dose of O 3 (EPA 2006a, section 6 .1)

. In controlled human exposure studies, group mean 18 responses are not representative of this segment of the population that has much larger 19 than average responses to O 3 . Recent studies, discussed in section II.A.4.b.iv below, 20 reported a role for genetic poly morphism (i.e., the occurrence together in the same 21 population of more than one allele or genetic marker at the same locus with the least 22 frequent allele or marker occurring more frequently than can be accounted for by 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 44 mutation alone) in observed differences in antioxidant enzy mes and genes involved in 1 inflammation to modulate pulmonary function and inflammatory responses to O 3 2 exposure. These observations suggest a potential role for these markers in the innate 3 susceptibility

to O 3 , however, the validity of these markers and their relevance in the 4 context of prediction to population studies needs additional experimentation. 5 C ontrolled human exposure studies that provide information about mechanisms of 6 the initial response to O 3 (e.g., lung function decrements, inflammation, and injury to the 7 lung) also inform the selection of appropriate lag times to analyze in epidemiological 8 studies through elucidation of the time course of these responses (EPA 2006a, section 9 8.4.3). Based on the results of these studies, it would be reasonable to expect that lung 10 function decrements could be detected epidemiologically within lags of 0 (same day) or 1 11 to 2 day s following O 3 exposure, given the rapid onset of lung function changes and their 12 persistence for 24 to 48 hours among more responsive human subjects in controlled 13 human exposure studies. Other responses take longer to develop and can persist for 14 longer periods of time. For example, although asthmatic individuals may begin to 15 experience s ymptoms soon after O 3 exposure, it may take any where from 1 to 3 day s 16 after exposure for these subjects to seek medical attention as a result of increased airway 17 responsiveness or inflammatio n that may persist for 2 to 3 days. This may be reflected 18 by epidemiologic observations of significantly increased risk for asthma

- related 19 emergency

department visits or hospital admissions with 1

- to 3
- day lags, or, perhaps, 20 enhanced distributed lag risk s (combined across 3 day s) for such morbidity indicators. 21 Analogousl y, one might project increased mortality within 0

- to 3
- day lags as a possible 22 consequence of O 3 - induced increases in clotting agents arising from the cascade of 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 45 events, starting with cel l injury described above, occurring within 12 to 24 hours of O 3 1 exposure. The time course for many of these initial responses to O 3 is highly variable

. 2 Moreover these observations pertain only to the initial response to O 3 . Consequent 3 responses can foll ow. For example, Jörres et al., (1996) found that in subjects with 4 asthma and allergic rhinitis, a maximum percent fall in FEV 1 of 27.9% and 7.8%, 5 respectivel y, occurred 3 days after O 3 exposure when they were challenged with of the 6 highest common dose of allergen. 7 2. Nature of Effects 8 The 2006 Criteria Document provides new evidence that notabl y enhances our 9 understanding of short

- term and prolonged exposure effects, including effects on lung 10 function, sy

mptoms, and inflammatory effects reported in controlled exposure studies. 11 These studies support and extend the findings of the previous Criteria Document. There 12 is also a significant body of new epidemiological evidence of associations between short

13 term and prolonged exposure to O 3 and effects such a s premature mortality , hospital 14 admissions and emergency department visits for respiratory (e.g., asthma) causes. Key 15 epidemiological and controlled human exposure studies are summarized below and 16 discussed in chapter 3 of the 2007 Staff Paper, which is b ased on scientific evidence 17 critically

reviewed in chapters 5, 6, and 7 of the 2006 Criteria Document, as well as the 18 Criteria Document’s integration of scientific evidence contained in chapter 8. 14 19 Conclusions drawn about O 3 - related health effects are b ased upon the full body of 20

14 Health effects discussions are also drawn from the more detailed information and tables presented in the Criteria Document’s annexes.Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 46 evidence from controlled human exposure, epidemiological and toxicological data 1 contained in the 2006 Criteria Document. 2
a. Morbidity 3 This section summarizes scientific information on the effects of inhalation of O 3 , 4 including public health effects of short

- term, prolonged, and long

- term exposures on 5 respiratory

morbidity and cardiovascular s ys tem effects, as discussed in chapters 6, 7 and 6 8 of the 2006 Criteria Document and chapter 3 of the 2007 Staff Paper. This section also 7 summarizes the uncertainty about the potential indirect effects on public health associated 8 with changes due to increases in UV

- B radiation exposure, such as UV

- B radiation

9 related skin cancers, that may be associated with reductions in ambient levels of ground

10 level O 3 , as discussed in chapter 10 of the 2006 Criteria Document and chapter 3 of the 11 2007 Staff Paper. 12 i. Effects on the Respiratory Sy stem from Short

- term and Prolonged O 3 Exposures 13 Controlled human exposure studies have shown that O 3 induces a variety of health 14 effects, including: lung function decrements, respiratory sy mptoms, increased airway 15 responsiveness, respiratory inflammation and permeability , increased susceptibility to 16 respiratory

infection, and acute morphological effects. Epidemi ology studies have 17 reported associations between O 3 exposures (i.e., 1

- hour, 8

- hour and 24

- hour) and a wide 18 range of respiratory

- related health effects including: pulmonary function decrements; 19 respiratory

s ymptoms; increased asthma medication use; increa sed school absences; 20 increased emergency department visits and hospital admissions. 21 (a ) Pulmonary Function Decrements, Respiratory Symptoms, and Asthma Medication 22 Use 23 24 (i) Results from Controlled Human Exposure Studies 25Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 47 1 A large number of studies published prior to 1996 that investigated short

- term O 3 2 exposure health effects on the respiratory s ys tem from short

- term O 3 exposures were 3 reviewed in the 1986 and 1996 Criteria Documents (EPA, 1986, 1996 a). In the 1997 4 review, 0.50 ppm was the lowest O 3 concentr ation at which statistically significant 5 reductions in forced vital capacity (FVC) and forced expiratory volume in 1 second 6 (FEV 1 ) were reported in sedentary subjects. During exercise, spirometric (lung function) 7 and sy

mptomatic responses were observed at much lower O 3 exposures. When minute 8 ventilation was considerably increased b y continuous exercise (CE) during O 3 exposures 9 lasting 2 hour or less at > 0.12 ppm, healthy subjects generally

experienced decreases in 10 FEV 1 , FVC, and other measures of lung function; increases in specific airway resistance 11 (sRaw), breathing frequency , and airway responsiveness; and s ymptoms such as cough, 12 pain on deep inspiration, shortness of breath, throat irritation, and wheezing. When 13 exposures were increased to 4

- to 8
- ho urs in duration, statistically significant lung 14 function and s ymptom responses were reported at O 3 concentrations as low as 0.08 ppm 15 and at lower minute ventilation (i.e., moderate rather than high level exercise) than the 16 shorter duration studies. 17 The mo st important observations drawn from studies reviewed in the 1996 18 Criteria Document were that: (1) young healthy adults exposed to O 3 concentrations > 19 0.080 ppm develop significant, reversible, transient decrements in pulmonary function if 20 minute ventilation or duration of exposure is increased sufficiently ; (2) children 21 experience similar lung function responses but report lesser s ymptoms from O 3 exposure 22 relative to young adults; (3) O 3 - induced lung function responses are decreased in the 23 elderl y relativ e to young adults; (4) there is a large degree of intersubject variability in 24Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 48 phy siological and s ymptomatic responses to O 3 but responses tend to be reproducible 1 within a given individual over a period of several months; (5) subjects exposed 2 repeatedly

to O 3 for several day s show an attenuation of response upon successive 3 exposures, but this attenuation is lost after about a week without exposure; and (6) acute 4 O 3 exposure initiates an inflammatory response which may

persist for at least 18 to 24 5 hours post exposure. 6 The development of these respiratory effects is time

- dependent during both 7 exposure and recovery periods, with great overlap for development and disappearance of 8 the effects. In healthy human subjects exposed to ty pical ambient O 3 levels near 0.120 9 ppm, lung function responses largel y resolve within 4 to 6 hours postexposure, but 10 cellular effects persist for about 24 hours. In these healthy subjects, small residual lung 11 function effects are almost completely gone within 24 hours, while in hy pe rresponsive 12 subjects, recovery

can take as much as 48 hour to return to baseline. The majority of 13 these responses are attenuated after repeated consecutive exposures, but such attenuation 14 to O 3 is lost one week postexposure. 15 Since 1996, there have been a number of studies published investigating lung 16 function and s ymptomatic responses that generally support the observations previously 17 drawn. Recent studies for acute exposures of 1 to 2 hours and 6 to 8 hours in duration are 18 compiled in the 2007 Staff Pap er (Appendix 3C). As summarized in more detail in the 19 2007 Staff Paper (section 3.3.1.1), among the more important of the recent studies that 20 examined changes in FEV 1 in large numbers of subjects over a range of 1

- 2 hours at 21 exposure levels of 0.080 to 0. 40 ppm were studies by McDonnell et al. (1997) and 22Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 49 Ultman et al. (2004). These studies observed considerable intersubject variability in 1 FEV 1 decrements, which was consistent with findings in the 1996 Criteria Document. 2 For prolonged exposures (4 to 8 ho urs) in the range of 0.080 to 0.160 ppm O 3 3 using moderate intermittent exercise and typicall y using square

- wave exposure patterns 4 (i.e., a constant exposure level during time of exposure), several pre

- and post

- 1996 5 studies (Folinsbee et al., 1988,1994; Ho rstman et al., 1990; Adams, 2002, 2003a, 2006) 6 have reported statistically significant lung function responses and increased sy mptoms in 7 healthy

adults with increasing duration of exposure, O 3 concentration, and minute 8 ventilation. Studies that employed triangular exposure patterns (i.e., integrated exposures 9 that begin at a low level, rise to a peak, and return to a low level during the exposure) 10 (Hazucha et al., 1992; Adams 2003a, 2006) suggest that the triangular exposure pattern 11 can potentiall y lead to greater FEV 1 decrements and respiratory s ymptoms than square

12 wave exposures (when the overall O 3 doses are equal). These results suggest that peak 13 exposures, reflective of the pattern of ambient O 3 concentrations in some locations, are 14 important in terms of O 3 health effects. 15 McDonnell (1996) used data from a series of studies to investigate the frequency 16 distributions of FEV 1 decrements following 6.6 hour exposures and found statistically 17 significant, but relativel y small, group mean decreases in averag e FEV 1 responses 18 (between 5 and 10 percent) at 0.080 ppm O 3 . 15 Notably , about 26 percent of the 60 19 exposed subjects had lung function decrements > 10 percent, including about 8 percent of 20

15 Th is 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 O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 50 the subjects that experienced large decrements (>20 percent) (EPA, 2 007b, Figure 3

- 1A). 1 These results (which were not corrected for exercise in filtered air responses) demonstrate 2 that while average responses may be relatively

small at the 0.080 ppm exposure level, 3 some individuals experience more severe effects that may be clinicall y significant

. 4 Similar results at the 0.080 ppm exposure level ( for 6.6 h ours during intermittent 5 exercise ) were seen in more recent studies of 30 healthy young adults by

Adams (2002, 6 2006). 16 In Adams (2006) , relativel y small but statistical ly significant lung function 7 decrements and respiratory s ymptom responses were found (for both square

- wave and 8 triangular exposure patterns), with 17 percent of the subjects (5 of 30) experiencing > 10 9 percent FEV 1 decrements (comparing pre

- and post

- expos ures) when the results were not 10 corrected for the effects of exercise alone in filtered air (EPA, 2007b, Figure 3

- 1B) and 11 with 23 percent of subjects (7 of 30) experiencing such effects when the results were 12 corrected (EPA, 2007b, p. 3

- 6). 17 13 These studies by Adams (2002, 2006) were notable in that they were the only 14 controlled exposure human studies available at the time of the 2008 rulemaking that 15 examined respiratory effects associated with prolonged O 3 exposures at levels below 16 0.080 ppm, which was the l owest exposure level that had been examined in the 1997 17 review. The Adams (2006) study investigated a range of exposure levels (0.000, 0.040, 18 0.060, and 0.080 ppm O 3 ) using square

- wave and triangular exposure patterns. The study 19

16 Th ese studies, conducted at a facility at the University

of California, in Davis, CA, reported O 3 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 O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 51 was designed to examine h our- by

- hour changes in pulmonary function (FEV 1 ) and 1 respiratory

s ymptom responses (total subjective s ymptoms (TSS) and pain on deep 2 inspiration (PDI)) between the se various exposure protocols at six different time points 3 within the exposure periods to inv estigate the effects of different patterns of exposure. At 4 the 0.060 ppm exposure level, the author reported no statistically significant differences 5 for FEV 1 decrements nor for most respiratory s ymptoms responses. Statistically 6 significant responses wer e reported only for TSS for the triangular exposure pattern 7 toward the end of the exposure period, with the PDI responses being noted as following a 8 closely

similar pattern (Adams, 2006, p. 131

- 132). EPA’s reanaly sis of the data from the 9 Adams (2006) study addressed the more fundamental question of whether there were 10 statistically

significant differences in responses before and after the 6.6 hour exposure 11 period (Brown, 2007), and used a standard statistical method appropriate for a simple 12 before

- and

- after comparison. The statistical method used by EPA had been used 13 previously

by other researchers to address this same question. EPA’s reanaly sis of the 14 data from the Adams (2006) study , comparing FEV 1 responses pre - and post

- exposure at 15 the 0.060 ppm exposure level, found small group mean differences from responses to 16 filtered air that were statistically significant (Brown, 2007). 18 17 Further examination of the post

- exposure FEV 1 data and mean data at other time 18 points and concentrations also suggest a patter n of response at 0.06 ppm that is consistent 19
18 Dr. Adams submitted comments on EPA ’s reanalysis in which he concluded that the FEV 1 response in healthy young adults at the 0.06 0 ppm exposure level in his study (Adams, 2006a) does not demonstrate a significant mean effect by ordinarily acceptable statistical analys is , but is rather in somewhat of a gray area, both in terms of a biologicall y 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 C omments (EPA, 2008, pp. 26

- 28).Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 52 with a dose

- response relationship rather than random variability

. For example, the 1 response at 5.6 hours was similar to that of the post

- exposure 6.6 hour response and 2 appeared to also differ from the FA respon se. At the 0.08 ppm level, the subject s in this 3 study did not appear to be more responsive to O 3 than subjects in previous studies , as the 4 observed response was similar to that of previous studies (Adams, 2003 a,b ; Horstman et 5 al., 1990; McDonnell et al., 1991 )

. Although of much smaller magnitude, the temporal 6 pattern of the 0.06 ppm response was generally consistent with the temporal patterns of 7 response to higher concentrations of O 3 in this and other studies. The se findings are not 8 unexpected because the previously observed group mean FEV 1 responses to 0.08 ppm 9 were in the range of 6

- 9% suggesting that exposure to lower concentrations of O 3 would 10 result in smaller, but real group mean FEV 1 decrements , i.e., the responses to 0.060 ppm 11 O 3 are consistent w ith the presence of a smooth exposure

- response curve with responses 12 that do not end abruptly below 0.080 ppm

. 13 Moreover, the Adams studies (2002, 2006) also report a small percentage of 14 subjects experiencing moderate lung function decrements (> 10 percent) at the 0.060 ppm 15 exposure level. Based on study data (Adams, 2006) provided by the author, 7 percent of 16 the subjects (2 of 30 subjects) experienced notable FEV 1 decrements (  10 percent) with 17 the square wave exposure pattern at the 0.060 ppm exposure lev el (comparing pre

- and 18 post - exposures) when the results were corrected for the effects of exercise alone in 19 filtered air (EPA, 2007 b , p. 3
- 6). Furthermore, in a prior publication (Adams, 2002), the 20 author stated that, “some sensitive subjects experience notable effects at 0.06 ppm,” 21 based on the observation that 20% of subjects exposed to 0.06 ppm O 3 (in a face mask 22 exposure study) had greater than a 10% decrement in FEV 1 even though the group mean 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 53 response was not statistically different from the filtered air response. The effects 1 described b y Adams (2002), along with the reanaly sis of the Adams (2006) data as 2 described above, demonstrate considerable inter

- individual variability in responses of 3 healthy

adults at the 0.060 ppmlevel with some individuals e xperiencing greater than 4 10% decrements in FEV 1 . The observation of statistically significant small group mean 5 lung function decrements in healthy adults at 0.060 ppm O 3 lowers the lowest

- observed

6 effects level found in controlled human exposure studies f or lung function decrements 7 and respiratory

s ymptoms
. 8 Of potentially greater concern is the magnitude of the lung function decrements in 9 the small group of healthy subjects who had the largest responses (i.e., FEV 1 decrements 10
> 10%). This is a concern b ecause for active healthy people, moderate levels of 11 functional responses (e.g., FEV 1 decrements of > 10% but < 20%) and/or moderate 12 sy mptomatic responses would likely interfere with normal activity for relatively

few 13 responsive individuals. However, for people with lung disease, even moderate functional 14 or sy

mptomatic responses would likely interfere with normal activity for many 15 individuals, and would likely result in more frequent use of medication (see section II.A.4 16 below)

. 17 (ii) Results of Epidemi ological and Field Studies 18 A relativel y large number of field studies investigating the effects of ambient O 3 19 concentrations, in combination with other air pollutants, on lung function decrements and 20 respiratory

s ymptoms ha s been published over the last d ecade that support the m ajor 21 findings of the 1996 Criteria Document that lung function changes, as measured b y 22 decrements in FEV 1 or peak expiratory flow (PEF), and respiratory s ymptoms in healthy 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 54 adults and asthmatic children are closel y correlated to amb ient O 3 concentrations. Pre

1 1996 field studies focused primarily on children attending summer camps and found O 3 - 2 related impacts on measures of lung function, but not respiratory s ymptoms, in healthy 3 children. The newer studies have expanded to evaluate O 3 - related effects on outdoor 4 workers, athletes, the elderly , hikers, school children, and asthmatics. Collectivel y, these 5 studies confirm and extend clinical observations that prolonged (i.e., 6

- 8 hour) exposure 6 periods, combined with elevated levels of exertion or exercise, increase the dose of O 3 to 7 the lungs at a given ambient exposure level and result in larger lung function effects . The 8 results of one large study of hikers (Korrick et al., 1998), which report ed outcome 9 measures stratified b y several factors (e.g., gender, age, smoking status, presence of 10 asthma) within a population capable of more than normal exertion , provide useful insight

. 11 In this study, lung function was measured before and after hiking, and individual O 3 12 exposure s were estimate d by averaging hourly O 3 concentration s from ambient monitors 13 located at the base and summit. The mean 8

- h our average O 3 concentration was 0.040 14 ppm (8

- hour average concentration range of 0.021 ppm to 0.074 ppm O 3 ) . Decreased 15 lung function was associated with O 3 exposure, with the greatest effect estimates reported 16 for the subgroup that reported having asthma or wheezing, and for those who hiked for 17 longer periods of time. 18 Asthma panel studies conducted both in the U.S. and in other countries have 19 report ed that decrements in PEF are associated with routine O 3 exposures among 20 asthmatic and healthy people. One large U.S. multicity study, the National Cooperative 21 Inner City

Asthma Study or NCI CAS, (Mortimer et al., 2002) examined O 3 - related 22 changes in PEF in 846 asthmatic children from 8 urban areas and reported that the 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 55 incidence of > 10 percent decrements in morning PEF are associated with increases in 8

- 1 hour average O 3 for a 5

- day cumulative lag, suggesting that O 3 exposure may be 2 associated with clinical ly significant changes in PEF in asthmatic children; however, no 3 associations were reported with evening PEF. The mean 8

- hour average O 3 was 0.048 4 ppm across the 8 cities. Excluding days when 8

- hour average O 3 was greater than 0.080 5 ppm (less than 5 perc ent of day s), the associations with morning PEF remained 6 statistically

significant. Mortimer et al. (2002) discussed potential biological mechanisms 7 for delayed effects on pulmonary function in asthma, which included increased 8 nonspecific airway

responsiv eness secondary to airway inflammation due to O 3 exposure. 9 Two other panel studies (Romieu et al., 1996, 1997) carried out simultaneously in 10 northern and southwestern Mexico City with mildly

asthmatic school children reported 11 statistically

significant O 3 - related reductions in PEF, with variations in effect depending 12 on lag time and time of day . Mean 1
- hour maximum O 3 concentrations in these locations 13 ranged from 0.190 ppm in northern Mexico City to 0.196 ppm in southwestern Mexico 14 City . While several stu dies report statisticall y significant associations between O 3 15 exposure and reduced PEF in asthmatics, other studies did not, possibly due to low levels 16 of O 3 exposure. EPA concludes that these studies collectively indicate that O 3 may

be 17 associated with s hort

- term declines in lung function in asthmatic individuals and that the 18 Mortimer et al. (2002) study showed statistically

significant effects at concentrations in 19 the range below 0.080 ppm O 3 . 20 Most of the panel studies which have investigated associatio ns between O 3 21 exposure and respiratory sy mptoms or increased use of asthma medication are focused on 22 asthmatic children. Two large U.S. studies (Mortimer et al., 2002; Gent et al., 2003) have 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 56 reported associations between ambient O 3 concentrations and dai ly sy mptoms/asthma 1 medication use, even after adjustment for copollutants. Results were more mixed, 2 meaning that a greater proportion of studies were not both positive and statistically 3 significant, across smaller U.S. and international studies that focus ed on these health 4 endpoints. 5 The NCI CAS reported morning s ymptoms in 846 asthmatic children from 8 U.S. 6 urban areas to be most strongl y associated with a cumulative 1

- to 4
- day lag of O 3 7 concentrations (Mortimer et al., 2002). The NCICAS used standard p rotocols that 8 included instructing caretakers of the subjects to record s ymptoms ( including cough, 9 chest tightness, and wheeze ) in the daily diary by observing or asking the child. While 10 these associations were not statistically significant in several cities, when the individual 11 data are pooled from all eight cities, statisticall y significant effects were observed for the 12 incidence of s ymptoms. The authors also reported that the odds ratios remained 13 essentially

the same and statistically significant for the incidence of morning s ymptoms 14 when day s with 8

- hour O 3 concentrations above 0.080 ppm were excluded. These days 15 represented less than 5 percent of day s in the study

. 16 Gent and colleagues (2003) followed 271 asthmatic children under age 12 and 17 living in southern New England for 6 months (April through September) using a daily 18 sy mptom diary

. They

found that m ean 1
- h our max O 3 and 8

- h our max O 3 concentrations 19
were 0.0586 ppm and 0.0513 ppm , respectivel y. The data were anal yz ed for two 20 separate groups of subjects, those who used maintenance asthma medications during the 21 follow

- up period and those who did not. The need for regular medication was considered 22 to be a prox y for more severe asthma. Not taking any medication on a regular basis and 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 57 not needing to use a bronchodilator would suggest the presence of very mild asthma. 1 Statistically

significant e ffects of 1

- day lag O 3 were observed on a variety of respiratory 2 sy mptoms only

in the medication user group. Both daily 1
- h our max and 8

- h our max O 3 3
concentrations were similarly related to s ymptoms such as chest tightness and shortness 4 of breath. Effects of O 3 , but not PM 2.5 , remained significant and even increased in 5 magnitude in two

- pollutant models. Some of the associations were noted at 1

- h our max 6 O 3 levels below 0.060 ppm . In contrast, no effects were observed among asthmatics not 7 using maintenance medication. In terms of person

- day s of follow

- up, this is one of the 8 larger studies currentl y available that address symptom outcomes in relation to O 3 and 9 provides supportive evidence for effects of O 3 independent of PM 2.5 . Study limitations 10 include the post

- hoc nature of the population stratification by medication use

. Also, the 11 study

did not account for all of the important meteorological factors that might influence 12 these results, such as relative humidity or dew point. 13 The multicity study by Mortimer et al. (2002), which examined an asthmatic 14 population representative of the United States, and several single

- city studies indicate a 15 robust associati on of O 3 concentrations with respiratory s ymptoms and increased 16 medication use in asthmatics. While there are a number of well

- conducted, albeit 17 relativel y smaller, U.S. studies which showed onl y limited or a lack of evidence for 18 sy mptom increases associated with O 3 exposure, these studies had less statistical power 19 and/or were conducted in areas with relativel y low 1
- hour maximum average O 3 levels, in 20 the range of 0.03 to 0.09 ppm. The 2006 Criteria Document concludes that the asthma 21 panel studies, as a group, and the NCICAS in particular, indicate a positive association 22 between ambient concentrations and respiratory s ymptoms and increased medication use 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 58 in asthmatics. The evidence has continued to expand since 1996 and now is considered 1 to be much stronger than in the 1997 review of the O 3 primary standard. 2 School absenteeism is another potential surrogate for the health implications of O 3 3 exposure in children. The association between school absenteeism and ambient O 3 4 concentrations was assessed in two relativel y large field studies. The first study , Chen et 5 al. (2000) , examined total daily school absenteeism in about 28,000 elementary school 6 students in Nevada over a 2

- year period (after adjusting for PM 10 and CO concentrations) 7 and found that ambient O 3 concentrations with a distributed lag of 14 day s were 8 statistically

significantly associated with an increased rate of school absences

. The 9 second study , Gilliland et al. (2001) , studied O 3 - related absences among about 2,000 4 th 10 grade students in 12 s outhern California communities and found statistically significant 11 associations between 8

- h our average O 3 concentrations (with a distributed lag out to 30 12 day s) and all absence categories, and particularl y for respiratory causes. Neither PM 10 13 nor NO 2 were associated with any respiratory

or nonrespiratory

illness

- related absences 14 in single pollutant models. The 2006 Criteria Document concludes that these studies of 15 school absences suggest that ambient O 3 concentrations, accumulated over two to four 16 weeks, may

be associated with school absenteeism, and particularl y illness

- related 17 absences, but further replication is needed before firm conclusions can be reached 18 regarding the effect of O 3 on school absences

. In addition, more research is needed to 19 help shed light on the implications of variation in the duration of the lag structures (i.e., 1 20 day , 5 day s, 14 day s, and 30 day s) found both across studies and within data sets by 21 health endpoint and exposure metric. 22 (b ) Increased Airway Responsiveness 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 59 As discuss ed in more detail in the 2006 Criteria Document (section 6.8) and the 1 2007 Staff Paper (section 3.3.1.1.2), increased airway responsiveness, also known as 2 airway

hy perresponsiveness (AHR) or bronchial hy perreactivity , refers to a condition in 3 which the propensity for the airways to bronchoconstrict due to a variety of stimuli (e.g., 4 exposure to cold air, allergens, or exercise) becomes augmented. This condition is 5 ty picall y quantified b y m easuring the decrement in pulmonary function after inhalation 6 exposure to specific (e.g., antigen, allergen) or nonspecific (e.g., methacholine, 7 histamine) bronchoconstrictor stimuli. Exposure to O 3 causes an increase in airway 8 responsiveness as indicated by a reduction in the concentration of stimuli required to 9 produce a given reduction in FEV 1 or increase in airway obstruction. Increased airway 10 responsiveness is an important consequence of exposure to O 3 because its presence 11 means that the airway s are predisposed to narrowing on exposure to various stimuli, such 12 as spe cific allergens, cold air or SO 2 . Statistically significant and clinicall y relevant 13 decreases in pulmonary function have been observed in earl y phase allergen response in 14 subjects with allergic rhinitis after consecutive (4

- day) 3

- hour exposures to 0.125 ppm O 3 15 (Holz et al., 2002). Similar increased airway responsiveness in asthmatics to house dust 16 mite antigen 16 to 18 hours after exposure to a single dose of O 3 (0.160 ppm for 7.6 17 hours) was observed. These observations, based on O 3 exposures to levels much higher 18 than the 0.084 ppm standard level suggest that O 3 exposure may be a clinically

important 19 factor that can exacerbate the response to ambient bronchoconstrictor substances in 20 individuals with preexisting allergic asthma or rhinitis. Further, O 3 may have an 21 immediate impact on the lung function of asthmatics as well as contribute to effects that 22 persist for longer periods. 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 60 Kreit et al. (1989) found that O 3 can induce increased airway responsiveness in 1 asthmatic subjects to O 3 , who ty pically hav e increased airway

responsiveness at baseline. 2 A subsequent study

( Jörres et al., 1996) suggested an increase in specific (i.e., allergen

3 induced) airway

reactivity

in subjects with allergic asthma, and to a lesser extent in 4 subjects with allergic rhiniti s after short

- term exposure to higher O 3 levels; other studies 5 reported similar results. According to one study (Folinsbee and Hazucha, 2000), changes 6 in airway

responsiveness after O 3 exposure resolve more slowl y than changes in FEV 1 or 7 respiratory

s ympt oms. Other studies of repeated exposure to O 3 suggest that changes in 8 airway

responsiveness tend to be somewhat less affected by attenuation with consecutive 9 exposures than changes in FEV 1 (EPA, 2006a, section 6.8). 10 The 2006 Criteria Document (section 6. 8) concludes that O 3 exposure is linked 11 with increased airway responsiveness. Both human and animal studies indicate that 12 increased airway

responsiveness is not mechanistically associated with inflammation, and 13 does not appear to be strongl y associated wi th initial decrements in lung function or 14 increases in sy

mptoms. As a result of increased airway responsiveness induced b y O 3 15 exposure, human airway s may be more susceptible to a variety of stimuli, including 16 antigens, chemicals, and particles. Because a sthmatic subjects ty pically have increased 17 airway

respon siveness at baseline, enhanced bronchial response to antigens in asthmatics 18 raises potential public health concerns as they could lead to increased mo rbidity (e.g., 19 medication usage , school absences, emergency room visits, hospital admissions) or to 20 more persistent alterations in airway responsiveness (EPA 2006a, p. 8

- 21). As such, 21 increased airway

responsiveness after O 3 exposure represents a plausible link between O 3 22 exposure and increased hospital admissions. 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 61 (c) Respiratory Inflammation and Increased Permeability 1 Based on evidence from the 1997 review, acute inflammatory responses in the 2 lung have been observed subsequent to 6.6 h our O 3 exposures to the lowest tested level

-- 3 0.08 0 ppm -- in healthy adults engaged in moderately high exercise (section 6.9 of the 4 2006 Criteria Document and section 3.3.1.3 of the 2007 Staff Paper). Some of these prior 5 studies suggest that inflammatory responses may

be detected in some individuals 6 following O 3 exposures in the absence of O 3 - induced pulmonary decrements in those 7 subjects. These studies also demonstrate that s hort

- term exposures to O 3 also can cause 8 increased permeability in the lungs of human s and experimental animals

. Inflammatory 9 responses and epith elial permeability have been seen to be independent of spirometric 10 responses. Not onl y are the newer lung inflammation and increased cellular permeability 11 findings discussed in the 2006 Criteria Document (section 8.4.2) consistent with the 1997 12 review, but they

provide better characterization of the phy siological mechanisms by 13 which O 3 causes these effects. 14 Lung inflammation and increased permeability , which are distinct events 15 controlled by

different mechanisms, are two commonly observed effects of O 3 exposure 16 observed in all of the species studied. Increased cellular permeability is a d isruption of 17 the lung barrier that leads to leakage of serum proteins, influx of poly morphonuclear 18 leukocy

tes (neutrophils or PMNs), release of bioactive mediators, and movement of 19 compounds from the airspaces into the blood. 20Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 62 A number of controlled human exposure studies have analyzed bronchoalveolar 1 lavage (BAL) and nasal lavage (NL) 19 fluids and cells for markers of inflammation and 2 lung damage (EPA, 2006a, Annex AX6 ). Increased lung inflammation is demonstrated 3 by the presence o f neutrophils found in BAL fluid in the lungs, which has long been 4 accepted as a hallmark of inflammation. It is apparent, however, that inflammation 5 within airway

tissues may

persist beyond the point that inflammatory cells are found in 6 the BAL fluid. Soluble mediators of inflammation, such as cy tokines and arachidonic 7 acid metabolites have been measured in the BAL fluid of humans exposed to O 3 . In 8 addition to their role in inflammation, m any of these compounds have 9 bronchoconstrictive properties and may be involved in increased airway responsiveness 10 following O 3 exposure . An in vitro study of epithelial cells from nonatopic and atopic 11 asthmatics exposed to 0.01 0 to 0.10 0 ppm O 3 showed significantl y increased 12 permeability

compared to cells from normal persons. This indicates a potentially inherent 13 susceptibility

of cells from asthmatic individuals for O 3 - induced permeability

. 14 In the 1996 C riteria D ocument , assessment of controlled human exposure studies 15 indicated that a single, acute (1 to 4 h our s ) O 3 exposure ( > 0.08 0 to 0.1 00 ppm) of 16 subjects engaged in moderate to heavy exercise could induce a number of cellular and 17 biochemical changes suggestive of pulmonary inflammation and lung perm eability (EPA, 18 2006a , p. 8
- 22). These changes persisted for at least 18 h ours. Markers from BAL fluid 19 following both 2

- hour and 4

- hour O 3 exposure s repeated up to 5 day s indicate that there 20

19 Graham and Koren (1990) compared inflammatory mediators present in NL and BAL fluids of humans exposed to 0.4 ppm O 3 for 2 hours and found similar increases in PMNs in both fluids, suggesting a qualitative correlation betw een inflammatory changes in the lower airway s (BAL) and upper respiratory tract (NL).Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 63 is ongoing cellular damage irrespective of attenuation of some c ellular inflammatory 1 responses of the airway s, pulmonary function, and sy

mptom scores (EPA, 2006a, p. 8

- 2 22). Acute airway

inflammation was shown in Devlin et al. (1990) to occur among adults 3 exposed to 0.08 0 ppm O 3 for 6.6 h our s with exercise

. McBride et al. (1994) reported 4 that asthmatic subjects were more sensitive than non

- asthmatics to upper airway 5 inflammation for O 3 exposures that did n ot affect pulmonary function (EPA, 2006a , p. 6
- 6 33). However, the public health significance of these changes is n ot entirely clear. 7 The studies reporting inflammatory responses and markers of lung injury have 8 clearl y demonstrated that there is significant variation in response of subjects exposed, 9 especiall y to 6.6 hour s O 3 exposures at 0.08 0 and 0.100 ppm. To provide some 10 perspective on the public health impact for these effects, the 2007 Staff Paper (section 11 3.3.1.1.3) note s that one study (Devlin et al., 1991) showed that roughl y 10 to 50 percent 12 of the 18 young healthy adult subjects experienced notable increa ses (i.e., > 2 fold 13 increase) in most of the inflammatory and cellular injury

indicators anal yz ed, associated 14 with 6.6

- hour exposures at 0.08 0 ppm. Similar, although in some cases higher, fractions 15 of the population of 10 healthy adults tested saw > 2 fol d increases associated with 6.6

- 16 hour exposures to 0.10 0 ppm. The authors of this study expressed the view that 17 “susceptible subpopulations such as the very young, elderl y, and people with pulmonary 18 impairment or disease may be even more affected” (Devlin et al., 1991). 19 Since 1996, a substantial number of human exposure studies have been published 20 which have provided important new information on lung inflammation and epithelial 21 permeability . Mudway and Kelly

(2004) examined O 3 - induced inflammatory respo nses 22 and epithelial permeability with a meta

- analy sis of 21 controlled human exposure studies 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 64 and showed that an influx in neutrophils and protein in healthy subjects is associated with 1 total O 3 dose (product of O 3 concentration, exposure duration, and minute ventilation) 2 (EPA, 2006a , p. 6
- 34). Results of the anal ys is suggest that the time course for 3 inflammatory

responses (including recruitment of neutrophils and other soluble 4 mediators) is not clearl y established, but there is evidence that attenuation profiles for 5 many

of these parameters are different (EPA, 2006a , p. 8
- 22). 6 The 2006 C riteria D ocument (chapter 8) concludes that interaction of O 3 with 7 lipid constituents of epithelial lining fluid (ELF) and cell membranes and the induction of 8 oxidative s tress is implicated in injury and inflammation. Alterations in the expression of 9 cy tokines, chemokines, and adhesion molecules, indicative of an ongoing oxidative stress 10 response, as well as injury repair and regeneration processes, have been reported in 11 animal toxicology

and human in vitro studies evaluating biochemical mediators 12 implicated in injury and inflammation. While antioxidants in ELF confer some 13 protection, O 3 reactivity is not eliminated at environmentally relevant exposures (2006 14 Criteria Document, p. 8
- 24) . Further, antioxidant reactivity with O 3 is both species

15 specific and dose

- dependent. 16 (d ) Increased Susceptibility to Respiratory Infection 17 As discussed in more detail in the 2006 C riteria D ocument (sections 5.2.2, 6.9.6, 18 and 8.4.2), short - term exposures to O 3 have been shown to impair phy siological defense 19 capabilities in experimental animals by depressing alveolar macrophage (AM) functions 20 and by

altering the mucociliary

clearance of inhaled particles and microbes resulting in 21 increased susceptibility to respiratory

infection. Short

- term O 3 exposures also interfere 22 with the clearance process by accelerating clearance for low doses and slowing clearance 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 65 for high doses. Animal toxicological studies have reported that acute O 3 exposures 1
su ppress alveolar phagocytosis and immune system functions. Impairment of host 2 defenses and subsequent increased susceptibility to bacterial lung infection in laboratory 3 animals has been induced by short

- term exposures to O 3 levels as low as 0.08 0 ppm. 4 A single controlled human exposure study reviewed in the 1996 Criteria 5 Document (p. 8
- 26) reported that exposure to 0.08 0 to 0.10 0 ppm O 3 for 6.6 h ours (with 6 moderate exercise) induced decrements in the ability of AMs to phagocy

tose 7 microorganisms . Integrating the recent animal study results with human exposure 8
evidence available in the 1996 Criteria Document, the 2006 Criteria Document concludes 9 that available evidence indicates that short

- term O 3 exposures have the potential to impair 10 host defenses in hum ans , primarily by interfering with AM function. Any impairment in 11 AM function may

lead to decreased clearance of microorganisms or nonviable particles. 12 Compromised AM functions in asthmatics may increase their susceptibility to other O 3 13 effects, the effe cts of particles, and respiratory infections (EPA, 2006a, p. 8

- 26). 14 (e) Morphological Effects 15 The 1996 Criteria Document found that short

- term O 3 exposures cause similar 16 alterations in lung morphology in all laboratory

animal species studied, including 17 pri mates. As discussed in the 2007 Staff Paper (section 3.3.1.1.5), cells in the 18 centriacinar region (CAR) of the lung (the segment between the last conducting airway 19 and the gas exchange region) have been recognized as a primary target of O 3 - induced 20 damage (epithelial cell necrosis and remodeling of respiratory bronchioles), possibly 21 because epithelium in this region receives the greatest dose of O 3 delivered to the lower 22 respiratory

tract. Following chronic O 3 exposure, structural changes have been observe d 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 66 in the CAR, the region typically affected in most chronic airway diseases of the human 1 lung (EPA, 2006a, p. 8

- 24). 2 Ciliated cells in the nasal cavity and airway s, as well as Ty pe I cells in the gas

3 exchange region, are also identified as targets. While short

- term O 3 exposures can cause 4 epithelial cell profileration and fibrolitic changes in the CAR, these changes appear to be 5 transient with recovery occurring after exposure, depending on species and O 3 dose. The 6 potential impacts of repeated short

- term and chronic morphological effects of O 3 7 exposure are discussed below in the section on effects from long

- term exposures. Long
8 term or prolonged exposure has been found to cause chronic lesions similar to early 9 lesions found in individuals with respiratory bronchiolitis, which have the potential to 10 progress to fibrotic lung disease (2006 Criteria Document, p. 8

- 25). 11 Recent studies continue to show that short

- term and sub

- chronic exposures to O 3 12 cause similar alterations in lung structure in a variety of exp erimental animal species. 13 For example, a series of new studies that used infant rhesus monkey s and simulated 14 seasonal ambient exposure (0.5 ppm 8 hours/day for 5 day s, every

14 day s for 11 15 episodes) reported remodeling in the distal airways; abnormalities in tracheal basement 16 membrane; eosinophil accumulation in conducting airways; and decrements in airway 17 innervation (2006 Criteria Document, p. 8

- 25). Based on evidence from animal 18 toxicological studies, short

- term and sub

- chronic exposures to O 3 can caus e 19 morphological changes in the respiratory s ys tems, particularl y in the CAR, of a number 20 of laboratory

animal species (EPA, 2006a, section 5.2.4). 21 (f ) Emergency Department Visits/Hospital Admissions for Respiratory Causes 22Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 67 In creased summertime emergency d epartment visits and hospital admissions for 1 respiratory

causes have been associated with ambient exposures to O 3 . As discussed in 2 section 3.3.1.1.6 of the 2007 Staff Paper, numerous studies conducted in various 3 location s in the U.S. and Canada consistently have shown a relationship between ambient 4 O 3 levels and incre ased incidence of emergency department visits and hospital 5 admissions for respiratory causes, even after controlling fo r modifying factors, such as 6 weather and copollutants. Such associations between elevated ambient O 3 during 7 summer months and increased hospital admissions have a plausible biological basis in the 8 human and animal evidence of functional, sy mptomatic, and physiologic effects 9 discussed above and in the increased susceptibility t o respiratory

infections observed in 10 laboratory

animals. 11 In the 1997 review of the O 3 NAAQS, the C riteria Document evaluated 12 emergency

department visits and hospital admissions as possible outcomes following 13 exposure to O 3 (EPA, 2006a , section 7.3). Th e evidence was l imited for emergency 14 department visits, but results of several studies generall y indicated that short

- term 15 exposures to O 3 were associated with respiratory emergency

department visits. The 16 strongest and most consistent evidence, at both lo wer levels (i.e., below 0.120 ppm 1
- 17 hour max O 3 ) and at higher levels ( above 0.12 0 ppm 1
- h our max O 3 ) , was found in the 18 group of studies which investigated summertime 20 daily hospital admissions for 19 respiratory

causes in different eastern North American cities. These studies consistently 20 demonstrat ed that ambient O 3 levels were associated with increased hospital admissions 21

20 Discussion of the reasons for focusing on warm season studies is found in the section 2.A.3.a below.Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 68 and accounted for about one to three excess respiratory hospital admissions per million 1 persons with each 0. 100 pp m increase in 1

- h our m ax O 3 , after adjustment for possible 2 confounding effects of temperature and cop ollutants. Overall, the 1996 Criteria 3 Document concluded that there was strong evidence that ambient O 3 exposures can cause 4 significant exacerbations of preexisting respiratory disease in the general public. Excess 5 respiratory

- related hospital admissions associated with O 3 exposures for the New York 6 City area (based on Thurston et al., 1992) were included in the quantitative risk 7 assessment in the 1997 review and are included in the current assessment along with 8 estimates for respiratory

- related hospital admissions in Cleveland, Detroit, and Los 9 Angeles ba sed on more recent studies (2007 Staff Paper, chapter 5). S ignificant 10 uncertainties and the difficulty of obtaining reliable baseline incidence numbers resulted 11 in emergency

department visits not being used in the quantitative risk assessment in 12 either the 1997 or the 2008 O 3 NAAQS review. 13 In the past decade, a number of studies have examined the temporal pattern 14 associations between O 3 exposures and emergency department v isits for respiratory 15 causes (EPA, 2006a , section 7.3.2). These studies are summarized in the 2006 C riteria 16 D ocument ( c hapter 7 Annex) and some are shown in Figure 1 ( in section II.A.3)

. 17 Respiratory

causes f or emergency

department visits include asthma, bronchitis, 18 emphy sema, pneumonia, and other upper and lower respiratory infections, such as 19 influenza, but asthma visits ty pically dominate the daily

incidence counts. Most studies 20 report positive association s with O 3 . Among studies with adequate controls for seasonal 21 patterns, many reported at least one significant positive association involving O 3 . 22Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 69 In reviewing evidence for associations between emergency department visits for 1 asthma and short

- term O 3 expo sures , the 2006 Criteria Document (Figure 7

- 8, p. 7
- 6 8) 2 notes that in general, O 3 effect estimates from summer only anal ys es tended to be 3 positive and larger compared to results from cool season or all ye ar anal ys es . Several of 4 the studies reported signif icant associations between O 3 concentrations and emergency 5 department visits for respiratory causes , in particular asthma . However, inconsistencies 6 were observed which were at least partially attributable to differences in model 7 specifications and anal ys i s approach among various studies. For example, ambient O 3 8 concentrations, length of the study period, and statistical methods used to control 9 confounding b y seasonal patterns and copollutants appear to affect the observed O 3 ef fect 10 on emergency

department visits. 11 Hospital admissions studies focus specificall y on unscheduled admissions because 12
unscheduled hospital admissions occur in response to unanticipated disease exacerbations 13 and are more likel y than scheduled admissions to be affected b y variatio ns in 14 environmental factors, such as dail y O 3 levels

. Results of a fairl y large number of these 15 studies published during the past decade are summarized in 2006 C riteria D ocument 16 (chapter 7 Annex), and results of U.S. and Canadian studies are shown in Figure 1 below 17 ( in section II.A.3 ) . As a group, these hospital admissions studies tend to be larger 18 geographically

and temporally

than the emergency

department visit studies and provide 19 results that are generally more consistent. The strongest associations o f respiratory 20 hospital admissions with O 3 concentrations were observed using short lag periods, in 21 particular for a 0

- day lag (same day

exposure) and a 1

- day

lag (previous day exposure). 22 Most studies in the United States and Canada indicated positive, s tatistically significant 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 70 associations between ambient O 3 concentrations and respiratory hospital admissions in 1 the warm season. However, not all studies found a statistically significant relationship 2 with O 3 , possibly

because of very

low ambient O 3 levels . Anal ys es for confounding 3 using multipollutant regression models suggest that copollutants generally do not 4 confound the association between O 3 and respiratory hospitalizations. Ozone effect 5 estimates were robust to PM adjustment in all

- year and warm

- sea son onl y data. 6 Overall, the 2006 Criteria Document concludes that positive and robust 7 associations were found between ambient O 3 concentrations and various respiratory 8 disease hospitalization outcomes, when focusing particularl y on results of warm

- seaso n 9 anal ys es. Recent studies also generally indicate a positive association between O 3 10 concentrations and emergency department visits for a sthma during the warm season 11 (EPA, 2006a , p. 7
- 175). These positive and robust associations are supported by the 12 controlled human exposure , animal toxicologic al , and epidemiologic al evidence for lung 13 function decrements, increased respiratory s ymptoms, airway

inflammation, and 14 increased airway

resp onsiveness. Taken t ogether, the overall evidence supports a causal 15 relatio nship between acute ambient O 3 exposures and increased respiratory morbidity 16
outcomes resulting in increased emergency department visits and hospitalizatio ns during 17 the warm season (EPA, 2006a , p. 8
- 77). 18 ii. Effects on the Respiratory Sy stem of Long

- term O 3 Exposures 19 The 1996 Criteria Document concluded that there was insufficient evidence from 20 the limited number of studies to determine whether long

- term O 3 exposures resulted in 21 chronic health effects at ambient levels observed in the U.S. However, the ag gregate 22 evidence suggested that O 3 exposure, along with other environmental factors, could be 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 71 responsible for health effects in exposed populations. Animal toxicological studies 1 carried out in the 1980’s and 1990’s demonstrated that long

- term exposures can result in 2 a variety of morphological effects, including permanent changes in the small airway s of 3 the lungs, including remodeling of the distal airways and CAR and deposition of 4 collagen, possibly

representing fibrotic changes. These changes result from the damage 5 and repair processes that occur with repeated exposure. Fibrotic changes were also found 6 to persist after months of exposure providing a potential pathophy siologic basis for 7 changes in airway

function observed in children in some recent epidemiological studies. 8 It appears that variable seasonal ambient patterns of exposure may be of greater concern 9 than continuous daily exposures. 10 Several studies published since 1996 have investigated lung function changes 11 over seasonal time periods (EPA, 20 06a, section 7.5.3). The 2006 Criteria Document (p. 12 7
- 114) summarizes these studies which collectively indicate that seasonal O 3 exposure is 13 associated with smaller growth

- related increases in lung function in children than they 14 would have experienced liv ing in areas with lower O 3 levels. There is some limited 15 evidence that seasonal O 3 also may affect lung function growth in young adults, although 16 the uncertainty about the role of copollutants makes it difficult to attribute the effects to 17 O 3 alone. 18 Lung capacity grows during childhood and adolescence as body size increases, 19 reaches a maximum during the twenties, and then begins to decline steadil y and 20 progressivel y with age. Long

- term exposure to air pollution has long been thought to 21 contribute to slow er growth in lung capacity, diminished maximally attained capacity, 22 and/or more rapid decline in lung capacity with age (EPA, 2006a, section 7.5.4). 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 72 Toxicological findings evaluated in the 1996 Criteria Document demonstrated that 1 repeated dail y exposure o f rats to an episodic profile of O 3 caused small, but significant, 2 decrements in growth

- related lung function that were consistent with earl y indicators of 3 focal fibrogenesis in the proximal alveolar region, without overt fibrosis. Because O 3 at 4 sufficient concentrations is a strong respiratory irritant and has been shown to cause 5 inflammation and restructuring of the respiratory airway s, it is plausible that long

- term 6 O 3 exposures might have a negative impact on baseline lung function, particularl y during 7 childhood when these exposures might be associated with long

- term risks. 8 Several epidemiological studies published since 1996 have examined the 9 relationship between lung function development and long

- term O 3 exposure. The most 10 extensive and robust study of respiratory effects in relation to long

- term air pollution 11 exposures among children in the U.S. is the Children’s Health Study carried out in 12 12 communities of southern California starting in 1993. One anal ys is (Peters et al., 1999a) 13 examined the relationship between long

- term O 3 exposures and self

- reports of respiratory 14 sy mptoms and asthma in a cross sectional anal ys is and found a limited relationship 15 between outcomes of current asthma, bronchitis, cough and wheeze and a 0.040 ppm 16 increase in 1

- hour m ax O 3 (EPA, 2006a, p. 7

- 115). Another anal ys is (Peters et al., 17 1999b) examined the relationship between lung function at baseline and levels of air 18 pollution in the community . They reported evidence that annual mean O 3 levels were 19 associated with decreas es in FVC, FEV 1 , PEF and forced expiratory flow (FEF 25
- 75 ) (the 20 latter two being statistically significant) among females but not males. In a separate 21 anal ys is (Gauderman et al., 2000) of 4 th , 7 th , and 10 th grade students, a longitudinal 22 anal ys is of lung function development over four years found no association with O 3 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 73 exposure. The Children’s Health Study enrolled a second cohort of more than 1500 1 fourth graders in 1996 (Gauderman et al., 2002). While the strongest associations with 2 negative lung functi on growth were observed with acid vapors in this cohort, children 3 from communities with higher 4

- ye ar average O 3 levels also experienced smaller 4 increases in various lung function parameters. The strongest relationship with O 3 was 5 with PEF. Specificall y, children from the least

- polluted community had a small but 6 statistically

significant increase in PEF as compared to those from the most

- polluted 7 communities. Intwo - pollutant models, only 8
- hour average O 3 and NO 2 were significant 8 joint predictors of FEV 1 and maximal midexpiratory flow (MMEF). Although results 9 from the second cohort of children are supportive of a weak association, the definitive 8

- 10 ye ar follow

- up anal ys is of the first cohort (Gauderman et al., 2004a) provides little 11 evidence that long

- ter m exposure to ambient O 3 at current levels is associated with 12 significant deficits in the growth rate of lung function in children. Avol et al. (2001) 13 examined children who had moved away from participating communities in southern 14 California to other stat es with improved air quality. They found that a negative, but not 15 statistically

significant, association was observed between O 3 and lung function 16 parameters. Collectively, the results of these reports from the children’s health cohorts 17 provide little ev idence to support an impact of long

- term O 3 exposures on lung function 18 development. 19 Evidence for a significant relationship between long

- term O 3 exposures and 20 decrements in maximally attained lung function was reported in a nationwide study of 21 first year Yale students (Kinney et al., 1998; Galizia and Kinney , 1999) (EPA, 2006a, p. 22 7
- 120). Males had much larger effect estimates than females, which might reflect higher 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 74 outdoor activity

levels and correspondingl y higher O 3 exposures during childhood. A 1 simi lar study

of college freshmen at University of California at Berkeley also reported 2 significant effects of long

- term O 3 exposures on lung function (Künzli et al., 1997; Tager 3 et al., 1998). In a comparison of students whose city of origin was either Los Angeles or 4 San Francisco, long

- term O 3 exposures were associated with significant changes in mid

5 and end

- expiratory

flow measures, which could be considered early indicators for 6 pathologic changes that might progress to COPD. 7 There have been a few studi es that investigated associations between long

- term 8 O 3 exposures and the onset of new cases of asthma (EPA, 2006a, section 7.5.6). The 9 Adventist Health and Smog (AHSMOG) study cohort of about 4,000 was drawn from 10 nonsmoking, non

- Hispanic white adult Seventh Day Adventists living in California 11 (Greer et al., 1993; McDonnell et al., 1999). During the ten

- year follow

- up in 1987, a 12 statistically

significant increased relative risk of asthma development was observed in 13 males, compared to a nonsignificant relative risk in females (Greer et al., 1993). In the 14 15
- ye ar follow

- up in 1992, it was reported that for males, there was a statistically 15 significant increased relative risk of developing asthma associated with 8

- hour average 16 O 3 exposures, but there was no ev idence of an association in females. Consistency of 17 results in the two studies with different follow

- up times provides supportive evidence of 18 the potential for an association between long

- term O 3 exposure and asthma incidence in 19 adult males; however, representativeness of this cohort to the general U.S. population 20 may

be limited (EPA, 2006a, p. 7

- 125). 21 In a similar study (McConnell et al., 2002) of incident asthma among children 22 (ages 9 to 16 at enrollment), annual surveys of 3,535 children initially with out asthma 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 75 were used to identify

new - onset asthma cases as part of the Children’s Health Study . Six 1 high

- O 3 and six low

- O 3 communities were identified where the children resided. There 2 were 265 children who reported new

- onset asthma during the follow

- up period. 3 Although asthma risk was no higher for all residents of the six high

- O 3 communities 4 versus the six low

- O 3 communities, asthma risk was 3.3 times greater for children who 5 played three or more sports as compared with children who played no sports wi thin the 6 high

- O 3 communities. This association was absent in the communities with lower O 3 7 concentrations. No other pollutants were found to be associated with new

- onset asthma 8 (EPA, 2006a, p. 7

- 125). Playing sports may result in extended outdoor activi ty and 9 exposure occurring during periods when O 3 levels are higher. It should be noted, 10 however, that the results of the Children’s Health Study were based on a small number of 11
new - onset asthma cases among children who played three or more sports. Future 12 replication of these findings in other cohorts would help determine whether a causal 13 interpretation is appropriate. 14 In animal toxicology studies, the progression of morphological effects reported 15 during and after a chronic exposure in the range of 0.50 to 1.00 ppm O 3 (well above 16 current ambient levels) is complex, with inflammation peaking over the first few days of 17 exposure, then dropping, then plateauing, and finally , largely disappearing (EPA, 2006a, 18 section 5.2.4.4). By contrast, fibrotic changes in the tissue increase very slowly over 19 months of exposure, and, after exposure ceases, the changes sometimes persist or 20 increase. Epithelial hy perplasia peaks soon after the inflammatory response but is 21 usually

maintained in both the nose and lungs with continuous exposure; it also does not 22 return to pre - exposure levels after the end of exposure. Patterns of exposure in this same 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 76 concentration range determine effects, with 18 months of daily exposure, causing less 1 morphologic damage than exposures on altern ating months. This is important as 2 environmental O 3 exposure is ty pically seasonal. Long

- term studies by Plopper and 3 colleagues (Evans et al., 2003; Schelegle et al., 2003; Chen et al., 2003; Plopper and 4 Fanucchi, 2000) investigated infant rhesus monkey s exposed to simulated, seasonal O 3 5 and demonstrated: 1) remodeling in the distal airway s, 2) abnormalities in tracheal 6 basement membrane; 3) eosinophil accumulation in conducting airways; and 4) 7 decrements in airway innervation (EPA, 2006a, p. 5

- 45). Thes e findings provide 8 additional information regarding possible injury

- repair processes occurring with long

9 term O 3 exposures suggesting that these processes are onl y partially reversible and may 10 progress following cessation of O 3 exposure. Further, these processes may lead to 11 nonreversible structural damage to lung tissue; however, there is still too much 12 uncertainty to characterize the significance of these findings to human exposure profiles 13 and effect levels (EPA, 2006a, p. 8

- 25). 14 In summary , in the past decade, important new longitudinal studies have 15 examined the effect of chronic O 3 exposure on respiratory health outcomes. Limited 16 evidence from recent long

- term morbidity studies have suggested in some cases that 17 chronic exposure to O 3 may be associated with seasonal declines in lung function or 18 reduced lung function development, increases in inflammation, and development of 19 asthma in children and adults. Seasonal decrements or smaller increases in lung function 20 measures have been reported in several st udies; however, the extent to which these 21 changes are transient remains uncertain. While there is supportive evidence from animal 22 studies involving effects from chronic exposures, large uncertainties still remain as to 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 77 whether current ambient levels and exposure patterns might cause these same effects in 1 human populations. The 2006 Criteria Document concludes that epidemiological studies 2 of new asthma development and longer

- term lung function declines remain inconclusive 3 at present (EPA, 2006a, p. 7

- 134). 4 iii. Effects on the Cardiovascular Sy stem of O 3 Exposure 5 At the time of the 1997 review, the possibility of O 3 - induced cardiovascular 6 effects was largel y unrecognized. Since then, a very limited body of evidence from 7 animal, controlled human exposure , and epidemiologic studies has emerged that provides 8 evidence for some potential plausible mechanisms for how O 3 exposures might exert 9 cardiovascular s ys tem effects, however further research is needed to substantiate these 10 potential mechanisms. Possible mechanisms may involve O 3 - induced secretions of 11 vasoconstrictive substances and/or effects on neuronal reflexes that may result in 12 increased arterial blood pressure and/or altered electrophy siologic control of heart rate or 13 rhy thm. Some animal toxicology studies have shown O 3 - induced decreases in heart rate, 14 mean arterial pressure, and core temperature. One controlled human exposure study that 15 evaluated effects of O 3 exposure on cardiovascular health outcomes found no significant 16 O 3 - induced differences in ECG or blood pressure in healthy or hyp ertensive subjects but 17 did observe a significant O 3 - induced increase the alveolar

- to - arterial PO 2 gradient and 18 heart rate in both groups resulting in an overall increase in myocardial work and 19 impairment in pulmonary gas exchange (Gong et al., 1998). In another controlled human 20 exposure study , inhalation of a mixture of PM 2.5 and O 3 by healthy subjects increased 21 brachial artery

vasoconstriction and reactivity (Brook et al., 2002). 22Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 78 The evidence from a few animal studies also includes potential direct effects such 1
as O 3 - induced release from lung epithelial cells of platelet activating factor (PAF) that 2 may contribute to blood clot formation that would have the potential to increase the risk 3 of serious cardiovascular outcomes (e.g., heart attack, stroke, mortality). Also, 4 interactions of O 3 with surfactant components in epithelial lining fluid of the lung may 5 result in production of oxy sterols and reactive oxygen species that may exhibit PAF

- like 6 activity

contributing t o clotting and also may exert cy totoxic effects on lung and heart 7 muscle cells. 8 Epidemiologic al panel and field studies that examined associations between O 3 9 and various cardiac phys iologic endpoints have yielded limited evidence suggestive of a 10 potenti al association between acute O 3 exposure and altered heart rate variability (HRV), 11 ventricular arrhythmias, and incidence of heart attacks (myocardial infarction or MI). A 12 number of epidemiological studies have also reported associations between short

- ter m 13 exposures and hospitalization for cardiovascular diseases. As shown in Figure 7

- 13 of 14 the 2006 Criteria Document, many of the studies reported negative or inconsistent 15 associations . Some other studies, especiall y those that examined the relationship wh en 16 O 3 exposures were higher, have found robust positive associations between O 3 and 17 cardiovascular hospital admissions ( EPA, 2006a , p. 7
- 82). For example, one study 18 reported a positive association between O 3 and cardiovascular hospital admissions in 19 Toronto, Canada in a summer

- only anal ys is (Burnett et al., 1997b). The results were 20 robust to adjustment for various PM indices, whereas the PM effects diminished when 21 adjust ed for gaseous pollutants. Other studies stratified their anal ys is by temperature 22Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 79 ( i. e., by warms days versus cool days ) . Several analy ses using warm season day s 1 consistently

produced positive associations. 2 The epidemiologic evidence for cardiovascular morbidity is much weaker than for 3 respiratory

morbidity, with only

one of several U.S. and Canadian studies showing 4 statistically

significant positive associations of cardiovascular hospitalizations with 5
warm - season O 3 concentrations. Most of the available European and Australian studies, 6 all of which conducted all

- ye ar O 3 analy ses, did not find an association between short

7 term O 3 concentrations and cardiovascular hospitalizations. Overall, the currentl y 8 available evidence is inconclusive regarding an association between cardiovascular 9 hospital admissions and ambient O 3 exposure (EPA, 2006 a, p. 7
- 83). 10 In summary , b ased on the evidence from animal toxicology , controlled human 11 exposure, and epidemiological studies, from the 2006 Criteria Document (p. 8

- 77) 12 concludes that this generally limited body

of evidence is suggestive that O 3 can direc tly 13 and/or indirectl y contribute to cardiovascular

- related morbidity , but that much needs to 14 be done to more full y integrate links between ambient O 3 exposures and adverse 15 cardiovascular outcomes. 16 b. Mortality 17 i. Mortality

and Short

- term O 3 Exposure 18 The 1 996 Criteria Document concluded that an association between daily 19 mortality and O 3 concentration for areas with high O 3 levels (e.g., Los Angeles) was 20 suggested. However, due to a very limited number of studies available at that time, there 21 was insufficient evidence to conclude that the observed association was likely caus al

. 22Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 80 The 2006 Criteria Document include d results from numerous epidemiological 1 anal ys es of the relationship between O 3 and mortality

. Additional single city analyses 2 have also been con ducted since 1996, however, the most pivotal studies in EPA’s (and 3 CASAC’s) finding of increased support for the relationship between premature mortality 4 and O 3 is in part related to differences in study design

– limiting anal ys es to warm 5 seasons, better c ontrol for copollutants, particularly PM, and use of multicity designs 6 (both time series and meta

- anal ytic designs). Key findings are available from multicity 7 time

- series studies that report associations between O 3 and mortality . These studies 8 include an al ys es using data from 90 U.S. cities in the National Mortality, Morbidity and 9 Air Pollution (NMMAPS) study (Dominici et al., 2003) and from 95 U.S. communities in 10 an extension to the NMMAPS analy ses (Bell et al., 2004). 11 The original 90

- city NMMAPS anal ys is, with data from 1987 to 1994, was 12 primarily

focused on investigating effects of PM 10 on mortality . A significant association 13 was reported between mortality and 24

- h our average O 3 concentrations in anal ys es using 14 all available data as well as in the warm season only analy ses (Dominici et al., 2003). 15 The estimate using all available data was about half that for the summer

- only data at a lag 16 of 1

- day . The extended NMMAPS analy sis included data from 95 U.S. cities and 17 included an additional 6 years of data, from 1987

- 2000 (Bell et al., 2004) . S ignificant 18 associations were reported between O 3 and mortality in anal ys es using all available data

. 19 The effect estimate for increased mortality was approximately 0.5 percent per 0.020 ppm 20 change in 24
- h our averag e O 3 measured on the same day , and approximately 1.04 percent 21 per 0.020 ppm change in 24
- h our average O 3 in a 7

- day distributed lag model (EPA, 22 2006a , p. 7
- 88). In anal yses using onl y data from the warm season, the results were not 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 81 significantl y different from the full

- ye ar results. The authors also report that O 3 - mortality 1 associations were robust to adjustment for PM (EPA, 2006a , p. 7
- 100). Using a subset of 2 the NMMAPS data set, Huang et al. (2005) focused on associations between 3 cardiopulmonary

mortal ity and O 3 exposure (24

- h our av era g e ) during the summer season 4 only . The authors report an approximate 1.47 percent increase per 0.0 20 pp m change in 5 O 3 concentration measured on the same day and an approximate 2.52 percent increase per 6 0.0 20 pp m change in O 3 concentration usin g a 7
- day distributed lag model . These 7 findings suggest that the effect of O 3 on mortality is immediate but also persists for 8 several days. 9 As discussed below in section II.A.3.a, confounding by weather, especially 10 temperature, is complicated by the fact that higher temperatures are associated with the 11 increased photochemical activities that are important for O 3 formation. Using a case

12 crossover study design, Schwartz (2005) assessed associations between daily maximum 13 concentratio ns and mortality, matching case and control periods by temperature, and 14 using data onl y from the warm season. The reported effect estimate of approximately 15 0.92 percent change in mortality per 0.0 40 pp m O 3 (1

- h our maximum) was similar to 16 time

- series analy sis results with adjustment for temperature ( approximately 0.76 percent 17 per 0.0 40 pp m O 3 ), suggesting that associations between O 3 and mortality were robust to 18 the different adjustment methods for temperature. 19 An initial publication from APHEA, a European multicity study , reported 20 statistically

significant associations between daily maximum O 3 concentrations and 21 mortality in four cities in a full year anal ys is (Toulomi et al., 1997). An extended 22 anal ys is was done using data from 23 cities throughout Europ e (Gry paris et al., 2004). In 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 82 this report, a positive but not statistically significant association was found between 1 mortality

and 1

- h our daily

maximum O 3 in a full year anal ys is . Gry paris et al. (2004) 2 noted that there was a considerable seasonal difference in the O 3 effect on mortality ; thus, 3 the small effect for the all

- ye ar data might be attributable to inadequate adjustment for 4 confounding b y seasonality. Focusing on anal ys es using summer measurements, the 5 authors report statistically significant a ssociations with total mortality, cardiovascular 6 mortality and respirato ry mortality (EPA, 2006a , p. 7
- 93, 7
- 99). 7 Numerous single

- city analyses have also reported associations between mortality 8 and short

- term O 3 exposure, especiall y for those anal ys es using warm season data. As 9 shown in Figure 7

- 21 of the 2006 C riteria D ocument , the results of recent publications 10 show a pattern of positive, often statistically significant associations between short

- term 11 O 3 exposure and m ortality during the warm season. In considering results from year 12 round anal ys es, there remains a pattern of positive results but the findings are less 13 consistent. In most single

- city anal ys es, effect estimates were not substantially changed 14 with adjustment for PM (EPA, 2006a, Figure 7

- 22 ). 15 In addition, several meta

- anal ys es have been conducted on the relationship 16 between O 3 and mortality . As described in section 7.4.4 of the 2006 C riteria D ocument , 17 these anal ys es reported fairly consistent and positive combined effect estimates rangin g 18 from approximately 1.5 to 2.5 percent increase in mortality for a standardized change in 19 O 3 (EPA, 2006a , Figure 7

- 20). Three recent meta

- anal ys es evaluated potential sources of 20 heterogeneity

in O 3 - mortality

associations (Bell et al., 2005; Ito et al., 2 005; L ev y et al., 21 2005). The 2006 C riteria D ocument (p. 7

- 96) observes common findings across all three 22 anal ys es, in that all reported that effect estimates were larger in warm season anal ys es, 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 83 reanal ys is of results using default convergence criteria in g eneralized additive models 1 (GAM) did not change the effect estimates, and there was no strong evidence of 2 confounding b y PM. Bell et al. (2005) and Ito et al. (2005) both provided suggestive 3 evidence of publication bias, but O 3 - mortality associations remained after accounting for 4 that potential bias. The 2006 C riteria D ocument concludes that the “positive O 3 effects 5 estimates, along with the sensitivity anal ys es in these three meta

- anal ys es, provide 6 evidence of a robust association between ambient O 3 and mortality” (EPA, 2006a, p. 7

- 7 97). 8 Most of the single

- pollutant model estimates from single

- city studies range from 9 0.5 to 5 percent excess deaths per standardized increments. Corresponding summary 10 estimates in large U.S. multicity studies ranged between 0.5 to 1 percent with some 11 studies noting heterogenei ty across cities and studies (EPA, 2006a , p. 7
- 110). 12 Finally , from those studies that included assessment of associations with specific 13 causes of death, it appears that effect estimates for association s with cardiovascular 14 mortality

are larger than those for total mortality

. The meta

- anal ys is by Bell et al. (2005) 15 observed a slightly

larger effect estimate for cardiovascular mortality compared to 16 mortality

from all causes. The effect estimate for resp iratory mortality was 17 approximately

one - half that of cardiovascular mortality in the meta

- anal ys is. However, 18 other studies have observed larger effect estimates for respiratory mortality compared to 19 cardiovascular mortality. The apparent inconsistency re garding the effect size of O 3 - 20 related respiratory

mortality may be due to reduced statistical power in this subcategory 21 of mortality

(EPA, 2006a , p. 7
- 108). 22Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 84 In summary , many single

- and multi city studies observed positive associations of 1 ambient O 3 concentrations with total nonaccidental and cardiopulmonary mortality . The 2 2006 C riteria D ocument finds that the results from U.S. multicity time

- series studies 3 provide the strongest evidence to date for O 3 effects on acute mortality. Recent meta
4 anal ys es also indicate positive risk estimates that are unlikel y to be confounded by PM; 5 however, future work is needed to better understand the influence of model specifications 6 on the risk coefficient (EPA, 2006a , p. 7
- 175). A meta
- anal ys is that examined specific 7
ca uses of mortality

found that the cardiovascular mortality risk estimates were higher 8 than those for total mortality . For cardiovascular mortality , the 2006 C riteria D ocument 9 (Figure 7

- 25, p. 7
- 106) suggests that effect estimates are consistently positive and more 10 likely

to be larger and statistically significant in warm season anal ys es. The findings 11 regarding the effect size for respiratory mortality have been less consistent, possibly 12 because of lower statistical power in this subcategory of mortality

. The 2006 Criteria 13 Document (p. 8

- 78) concludes that these findings are highl y suggestive that short

- term O 3 14 exposure directly

or indirectly

contribute to non

- accidental and cardiopulmonary

- related 15 mortality , but additional research is needed to more fully establish underl yi ng 16 mechanisms by

which such effects occur. 21 17

21 Incommenting on the Criteria Document, the CASAC Ozone Panel rai sed questions about the implications of these time

- series results in a poli cy 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 onl y 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 highl y 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 andDraft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 85 ii. Mortality

and Long

- term O 3 Exposure 1 Little evidence was available in the 1997 review on the potential for associations 2 between mortality and long

- term exposure to O 3 . In the Harvard Six Ci ty prospective 3 cohort anal ys is, the authors report that mortality was not associated with long

- term 4 exposure to O 3 (Dockery et al., 1993). The authors note that the range of O 3 5 concentrations across the six cities was small, which may have limited the pow er of the 6 study

to detect associations between mortality and O 3 levels (EPA, 2006a , p. 7
- 127). 7 As discussed in section 7.5.8 of the 2006 Criteria Document , in this review there 8 are results available from three prospective cohort studies: the American C ancer Society 9 (ACS) study (Pope et al., 2002) , the Adventist Health and Smog (AHSMOG) study 10 (Beeson et al., 1998; Abbey et al., 1999) , and the U.S. Veterans Cohort study (Lipfert et 11 al., 2000, 2003) . In addition, a major reanal ys is report includes evaluation of data from 12 the Harvard Six City cohort study

(Krewski et al., 2000). 22 This reanal ys is also includes 13 additional evaluation of data from the initial ACS cohort study report that had only 14 reported results of associations between mortality and long

- ter m exposure to fine 15 particles and sulfates (Pope et al., 1995 ). This reanaly sis was discussed in the 2007 Staff 16 Paper (section 3.3.2.2) but not in the 2006 Criteria Document. 17 In this reanal ys is of data from the previous Harvard Six City prospective cohort 18 study , the investigators replicated and validated the findings of the original studies, and 19 cardiorespiratory

mortality for inclusion in the quantitative ri sk assessment to be appropriate.” (Henderson, 2006b)

22 This reanal ys is 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).Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 86 the report included additional quantitative results beyond those available in the original 1 report (Krewski et al., 2000). In the reanal ys is of data from the Harvard Six Cities study, 2 the effect estimate for the association between long

- term O 3 concentrations and mortality 3 was negative and nearl y statistically significant (relative risk = 0.87, 95 percent CI : 0.76, 4 1.00). 5 The ACS study is based on health data from a large prospective cohort of 6 approximately

500,000 adults and air quality data from about 150 U.S. cities. The initial 7 report (Pope et al., 1995) focused on associations with fine particles and sulfates, for 8 which significant associations had been report ed in the earlier Harvard Six Cities study 9 (Dockery

et al., 1993). As part of the major reanalysis of these data, results for 10 associations with other air pollutants were also reported, and the authors report that no 11 significant associations were found between O 3 and all

- cause mortality

. However, a 12 significant association was reported for cardiopulmonary mortality in the warm season 13 (Krewski et al., 2000)

. The ACS II study (Pope et al., 2002) reported results of 14 associations with an extended data base; th e mortality records for the cohort had been 15 updated to include 16 ye ars of follow

- up (compared with 8 years in the first report) and 16 more recent air quality data were included in the anal ys es. Similar to the earlier 17 reanal ys is, a marginall y significant as sociation was observed between long

- term exposure 18 to O 3 and cardiopulmonary mortality in the warm season. No other associations with 19 mortality

were observed in both the full

- ye ar and warm season anal ys es. 20 The Adventist Health and Smog (AHSMOG) cohort in cludes about 6,000 adults 21 living in California. In two studies from this cohort, a significant association has been 22 reported between long

- term O 3 exposure and increased risk of lung cancer mortality 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 87 among males only

(Beeson et al., 1998; Abbey et al., 199 9). No significant associations 1 were reported between long

- term O 3 exposure and mortality from all causes or 2 cardiopulmonary

causes. Due to the small numbers of lung cancer deaths (12 for males, 3 18 for females) and the precision of the effect estimate (i .e., the wi de confidence 4 intervals), the 2006 Criteria Document (p. 7
- 130) discussed concerns about the 5 plausibility

of the reported association with lung cancer. 6 The U.S. Veterans Coh ort study (Lipfert et al., 2000 , 2003) of approximately 7 50,000 middle

- aged males diagnosed with hy pertension, reported some positive 8 associations between mortality and peak O 3 exposures (95 th percentile level for several 9 ye ars of data). The study included numerous analy ses using subsets of exposure and 10 mortality

follow

- up periods which spanned the years 1960 to 1996. In the results of 11 anal ys es using deaths and O 3 exposure estimates concurrently across the study

period, 12 there were positive, statistically significant associations between peak O 3 and mortality 13 (EPA, 2006a , p. 7
- 129). 14 Overall, the 2006 Criteria Document (p. 7

- 130) concludes that consistent 15 associations have not been reported between long

- term O 3 exposure and all

- cause, 16 cardiopulmon ary or lung cancer mortality

. 17
c. Role of Ground

- level O 3 in Solar Radiation

- related Human Health Effects 18 Be yond the direct health effects attributable to inhalation exposure to O 3 in the 19 ambient air discussed above, the 2006 Criteria Document also assesses potential indirect 20 effec ts related to the presence of O 3 in the ambient air by considering the role of ground

21 level O 3 in mediating human health effects that may be directly

attributable to exposure 22 to solar ultraviolet radiation (UV

- B). The 2006 Criteria Document (chapter 10) f ocuses 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 88 this assessment on three key factors, including those factors that govern (1) UV

- B 1 radiation flux at the earth’s surface, (2) human exposure to UV

- B radiation, and (3) 2 human health effects due to UV

- B radiation. In so doing, the 2006 Criteria Docum ent 3 provides a thorough analysis of the current understanding of the relationship between 4 reducing ground

- level O 3 concentrations and the potential impact these reductions might 5 have on increasing UV

- B surface fluxes and indirectly contributing to UV

- B rel ated 6 health effects. 7 There are many factors that influence UV

- B radiation penetration to the earth’s 8 surface, including latitude, altitude, cloud cover, surface albedo, PM concentration and 9 composition, and gas phase pollution. Of these, only latitude and altitude can be defined 10 with small uncertainty in any effort to assess the changes in UV

- B flux that may be 11 attributable to any changes in tropospheric O 3 as a result of any revision to the O 3 12 NAAQS. Such an assessment of UV

- B related health effects woul d also need to take into 13 account human habits, such as outdoor activities (including age

- and occupation

- related 14 exposure patterns), dress and skin care to adequately estimate UV

- B exposure levels. 15 However, little is known about the impact of these factors on individual exposure to UV

16 B. 17 Moreover, detailed information does not exist regarding other factors that are 18 relevant to assessing changes in disease incidence, including: ty pe (e.g., peak or 19 cumulative) and time period (e.g., childhood, lifetime, current) of exposures related to 20 various adverse health outcomes (e.g., damage to the skin, including skin cancer; damage 21 to the eye, such as cataracts; and immune sy stem suppression); wavelength dependency 22 of biological responses; and interindividual variabil ity in UV

- B resistance to such health 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 89 outcomes. Beyond these well recognized adverse health effects associated with various 1 wavelengths of UV radiation, the 2006 Criteria Document (section 10.2.3.6) also 2 discusses protective effects of UV

- B radiation. Re cent reports indicate the necessity of 3 UV
- B in producing vitamin D . V itamin D deficiency can cause metabolic bone disease 4 among children and adults, and may also increase the risk of many common chronic 5 diseases (e.g., typ e I diabetes and rheumatoid arthritis) as well as the risk of various ty pes 6 of cancers. Thus, the 2006 Criteria Document concludes that any assessment that 7 attempts to quantify

the consequences of increased UV

- B exposure on humans due to 8 reduced ground

- level O 3 must include consideration of both negative and positive effects. 9 H owever, as with other impacts of UV

- B on human health, this beneficial effect of UV

- B 10 radiation has not been studied in sufficient detail to allow for a credible health benefits or 11 risk assessment. In conclusion, the effect of changes in surface

- level O 3 concentrations 12 on UV
- B
- induced health outcomes cannot yet be critically assessed within reasonable 13 uncertainty ( 2006 Criteria Document, p. 10

- 36). 14 The Agency last considered indirect effects of O 3 in the ambient air in its 2003 15 final response to a remand of the Agency ’s 1997 decision to revise the O 3 NAAQS. In so 16 doing, based on the available information in the 1997 review, EPA determined that the 17 information linking (a) changes in patterns of ground

- level O 3 concentrations likely to 18 occur as a result of programs implemented to attain the 1997 O 3 NAAQS to (b) changes 19 in relevant exposures to UV

- B radiation of concern to public health was too uncertain at 20 that time to warrant any relaxation in the level of public health protection previously 21 determined to be requisite to protect against the demonstrated direct adverse respiratory 22 effects of exposure to O 3 in the ambient air (68 FR 614). At that time, the more recent 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 90 information on protective effects of UV

- B radiation was not available, such that only 1 adverse UV

- B
- related effects could be considered. Taking into consideration the more 2 recent information available for the 2008 review, the 2006 Criteria Document and 2007 3 Staff Paper conclude that the effect of changes in ground

- level O 3 concentrations, likely 4 to occur as a result of revising the O 3 NAAQS , on UV
- B
- induced health outcomes, 5 including whether these changes would ultimately result in increased or decreased 6 incidence of UV

- B
- related diseases, cannot yet be cri tically assessed. 7 3. Interpretation and Integration of Health Evidence 8 As discussed below, in assessing the health evidence, the 2006 Criteria Document 9 integrates findings from experimental (e.g., toxicological, dosimetric and controlled 10 human exposure) and epidemiological studies, to make judgments about the extent to 11 which causal inferences can be made about observed associations between health 12 endpoints and exposure to O 3 . In evaluating the evidence from epidemiological studies, 13 the EPA focuses on we ll

- recognized criteria, including: the strength of reported 14 associations, including the magnitude and precision of reported effect estimates and their 15 statistical significance; the robustness of reported associations, or stability in the effect 16 estimates after considering factors such as alternative models and model specification, 17 potential confounding b y co - pollutants, and issues related to the consequences of 18 exposure measurement error; potential aggregation bias in pooling data; and the 19 consistency of the effects associations as observed by looking across results of multiple

20 and single

- city studies conducted b y different investigators in different places and times. 21 Consideration is also given to evaluating concentration

- response relationships observed 22 in epidemiological studies to inform judgments about the potential for threshold levels for 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 91 O 3 - related effects. Integrating more broadl y across epidemiological and experimental 1 evidence, the 2006 Criteria Document also focuses on the coherence and plausi bility of 2 observed O 3 - related health effects to reach judgments about the extent to which causal 3 inferences can be made about observed associations between health endpoints and 4 exposure to O 3 in the ambient air. 5
a. Assessment of Evidence from Epidemiological Studies 6 Key

e lements of the evaluation of epidemiological studies are briefl y summarized 7 below. 8 (1) The strength of associations most directly refers to the magnitude of the 9 reported relative risk estimates. Taking a broader view, the 2006 C riteri a D ocument 10 draws upon the criteria summarized in a recent report from the U.S. Surgeon General, 11 which define strength of an association as “the magnitude of the association and its 12 statistical strength” which includes assessment of both effect estimate siz e and precision, 13 which is related to the statistical power of the study (CDC, 2004). In general, when 14 associations are strong in terms of yi elding large relative risk estimates, it is less likely 15 that the association could be completel y accounted for b y a potential confounder or some 16 other source of bias , whereas w ith associations that yield small relative risk estimates it is 17 especiall y important to consider potential confounding and other factors in assessing 18 causality

. Effect estimates between O 3 and s ome of the health outcomes are generally 19 small in size and could thus be characterized as weak. For example, effect estimates for 20 associations with mortality generall y range from 0.5 to 5 percent increases per 0.0 40 pp m 21 increase in 1

- h our max imum O 3 or equivalent, whereas associations for hospitalization 22 range up to 50 percent increases per standardized O 3 increment. However, the 2006 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 92 C riteria D ocument notes that there are large multicity studies that find small associations 1 between short

- term O 3 exposure and mortality or morbidity and have done so with great 2 precision due to the statistical power of the studies (p. 8
- 40). That is, the power of the 3 studies allows the authors to reliably distinguish even weak relationships from the null 4 hy pothesis with statistical confidence. 5 (2) In evaluating the robustness of associations, the 2006 Criteria Document 6 (sections 7.1.3 and 8.4.4.3) and 2007 Staff Paper (section 3.4.2) have primarily 7 considered the impact of exposure error, potential confounding b y copollutants, and 8 alternative models and model specifications. 9 In time

- series and panel studies, the temporal (e.g., daily or hourly) changes in 10 ambient O 3 concentrations measured at centrally

- located ambient monitoring stations are 11 generall y used to represent a c ommunity ’s exposure to ambient O 3 . In prospective cohort 12
or cross - sectional studies, air quality data averaged over a period of months to years are 13 used as indicators of a community ’s long

- term exposure to ambient O 3 and other 14 pollutants. In both ty pes o f anal ys es, exposure error is an important consideration, as 15 actual exposures to individuals in the population will vary across the community

. 16 Ozone concentrations measured at central ambient monitoring sites may explain, 17 at least partiall y, the variance in individual exposures to ambient O 3 ; however, this 18 relationship is influenced by various factors related to building ventilation practices and 19 personal behaviors. Further, the pattern of exposure misclassification error and the 20 influence of confounders may differ across the outcomes of interest as well as in 21 susceptible populations. As discussed in the 2006 C riteria D ocument (s ection 3.9 ) , only a 22 limited number of studies have examined the relationship between ambient O 3 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 93 concentrations and personal expo sures to ambient O 3 . One of the strongest predictors of 1 the relationship between ambient concentrations and personal exposures appears to be 2 time spent outdoors. The strongest relationships were observed in outdoor workers 3 (Brauer and Brook, 1995, 1997; O’Neill et al., 2004 ). Statistically significant 4 correlations between ambient concentrations and personal exposures were also observed 5 for children, who likely spend more time outdoors in the warm season (Linn et al., 1996; 6 Xu et al., 2005) . There is som e concern about the extent to which ambient concentrations 7 are representative of personal O 3 exposures of another particularly susceptible group of 8 individuals, the debilitated elderl y, since those who suffer from chronic cardiovascular or 9 respiratory

conditions may

tend to protect themselves more than healthy individuals from 10 environmental threats by reducing their exposure to both O 3 and its confounders, such as 11 high temperature and PM. Studies by Sarnat et al. (2001, 2005) that included this 12 susceptible group reported mixed results for associations between ambient O 3 13 concentrations and personal exposures to O 3 . Collectively , these studies observed that 14 the daily

averaged personal O 3 exposures tend to be well correlated with ambient O 3 15 concentrations despite the substantial variability that existed among the personal 16 measurements. These studies provide supportive evidence that ambient O 3 17 concentrations from central monitors may serve as valid surrogate measures for mean 18 personal exposures experienced b y the population, which is of most relevance for time

19 series studies. A better understanding of the relationship between ambient concentrations 20 and personal exposures, as well as of the other factors that affect relationship will 21 improve the interpretation of concentration

- population health response associations 22 observed. 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 94 The 2006 C riteria D ocument (section 7.1.3.1) also discusses the potential 1 influence of exposure error on epidemiologic study results . Zeger et al. (2000) outlined 2 the components to exposure measurement error , finding that ambient exposure can be 3 assumed to be the product of the ambient concentration and an attenuation factor (i.e., 4 building filter) and that p anel studies and time

- series studies that use ambient 5 concentrations instead o f personal exposure measurements will estimate a health risk that 6 is attenuated b y that factor. Navidi et al. (1999) used data from a children’s cohort study 7 to compare effect estimates from a simulated “true” exposure level to results of anal ys es 8 from O 3 exposures determined by several methods , finding that O 3 exposures based on 9 the use of ambient monitoring data overestimate the individual’s O 3 exposure and thus 10 generall y result in O 3 effect estimates that are biased downward (EPA, 2006a , p. 7
- 8). 11 Simil arly, in a reanal ys is of a study by Burnett et al. (1994) on the acute respiratory 12 effects of ambient air pollution, Zidek et al. (1998) reported that accounting for 13 measurement error , as well as making a few additional changes to the analysis, resulted in 14 qualitatively

similar conclusions, but the effects estimates were cons iderably larger in 15 magnitude (EPA, 2006a , p. 7
- 8). A simulation study by Sheppard et al. (2005) also 16 considered attenuation of the risk based on personal behavior, their microenvironment, 17 and the qualities of the pollutant in time

- series studies. Of particular interest is their 18 finding that risk estimates were not further attenuated in time

- series studies even when 19 the correlations between personal exposures and ambient concentrations were weak. In 20 addition to overestimation of exposure and the resulting underestimation of effects, the 21 use of ambient O 3 concentrations may obscure the presence of thresholds in 22 epid emiologic studies (EPA, 2006a, p. 7

- 9). 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 95 As discussed in the 2006 C riteri a D ocument (s ection 3.9 ) , using ambient 1 concentrations to determine exposure generally overestimates true personal O 3 exposures 2 by approximately

2
- to 4
- fold in available studies, resulting in attenuated risk estimates. 3 The implication is that the effects being estimated occur at fairl y low exposures and the 4 potency

of O 3 is greater than these effects estimates indicate. As very few studies 5 evaluating O 3 health effects with personal O 3 exposure measurements exist in the 6 literature, effect estimates determined from ambient O 3 concentrations must be evaluated 7 and used with caution to assess the health risks of O 3 . Inthe absence of available data on 8 personal O 3 exposure, the use of routinel y monitored ambient O 3 concentrations as a 9 surrogate for personal exposures is not generally expected to change the principal 10 conclusions from O 3 epidemiologic studies. Therefore, population health risk estimates 11 derived using ambient O 3 levels from currentl y available observational studies, with 12 appropriate caveats about personal exposure considerations, remain useful. The 2006 13 C riteria D ocument recommends caution in the quantitative use of effect estimates 14 calculated using ambient O 3 concentrations as they may lead to underestimation of the 15 potency

of O 3 . However, the 2007 S taff Paper observes that the use of these risk 16 estimates for comparing relative risk reductions between alternative ambient O 3 standards 17 considered in the risk assessment (discussed below in section II.B.2) is less likel y to 18 suffer from this concern. 19 Confounding occurs when a health effect that is caused by one risk factor is 20 attributed to another variable that is correlated with the causal risk factor; 21 epidemiological anal ys es attempt to adjust or control for potential confounders. 22 Copollutants (e. g., PM, CO, SO 2 and NO 2 ) can meet the criteria for potential confounding 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 96 in O 3 - health associations if they are potential risk factors for the health effect under study 1 and are correlated with O 3 . Effect modifiers include variables that may influence the 2 h ealth response to the pollutant exposure (e.g., co

- pollutants, individual susceptibility , 3 smoking or age). Both are important considerations for evaluating effects in a mixture of 4 pollutants, but for confounding, the emphasis is on controlling or adjusting for potential 5 confounders in estimating the effects of one pollutant, while the emphasis for effect 6 modification is on identifyingand assessing the effects for different modifiers. 7 The 2006 C riteria D ocument (p. 7
- 148 ) observes that O 3 is generally not highl y 8 correlated with other criteria pollutants (e.g., PM 10 , CO, SO 2 and NO 2 ), but may be more 9 highl y correlated with secondary fine particles, especiall y during the summer months , 10 and that the degree of correlation between O 3 and other pollutants may vary across 11 seasons. For example, positive associations are observed between O 3 and pollutants such 12 as fine particles during the warmer months, but negative correlations may be obser ved 13 during the cooler months (EPA, 2006a , p. 7
- 17). Thus, the 2006 C riteria D ocument 14 (section 7.6.4) pay s particular attention to the results of season

- specific analy ses and 15 studies that assess effects of PM in potential confounding of O 3 - health relationships. The 16 2006 C riteria D ocument also discussed the limitations of commonly used multipollutant 17 models that include the difficulty in interpreting results where the copollutants are highly 18 colinear, or where correlations between pollutants chang e b y season (EPA, 2006a , p. 7
- 19 150). This is particularl y the situation where O 3 and a copollutant, such as sulfates, are 20 formed under the same atmospheric condition; in such cases multipollutant models would 21 produce unstable and possibly misleading results (EPA, 2006a , p. 7
- 152). 22Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 97 For mortality, the results from numerous multicity and sing le

- city studies indicate 1 that O 3 - mortality

associations do not appear to be substantially changed in multipollutant 2 models including PM 10 or PM 2.5 (EPA, 2006a , p. 7
- 101 ; Figure 7

- 22 ). Focusing on 3 results of warm season analy ses, effect estimates for O 3 - mo rtality associations are fairl y 4 robust to adjustment for PM in multipollutant models (EPA, 2006a , p. 7
- 102 ; Figure 7

- 5 23 ). The 2006 C riteria D ocument concludes that in the few multipollutant anal ys es 6 conducted for these endpoints, copollutants generally do not confound the relationship 7 between O 3 and respiratory hospitalization (EPA, 2006a , p. 7
- 79 to 7
- 80 ; Figure 7

- 12 ). 8 Multipollutant models were not used as commonly in studies of relationships between 9 respiratory

s ymptoms or lung function with O 3 , but th e 2006 C riteria D ocument reports 10 that results of available analy ses indicate that such associations generally were robust to 11 adjustment for PM 2.5 (p. 7
- 154). For example, in a large multicity study of asthmatic 12 children (Mortimer et al., 2002), the O 3 eff ect was attenuated, but there was still a 13 positive association ; in Gent et al. (2003), effects of O 3 , but not PM 2.5 , remained 14 statistically

significant and even increased in magni tude in two

- pollutant models (EPA, 15 2006a , p. 7
- 53). C onsidering this body of studies, the 2006 Criteria Document (p. 7

- 154) 16 concludes: “Multipollultant regression anal ys es indicated that O 3 risk estimates, in 17 general, were not sensitive to the inclusion of copollutants, including PM 2.5 and sulfate. 18 These results suggest that the effects of O 3 on respiratory health outcomes appear to be 19 robust and independent of the e ffects of other copollutants .” 20 The 2006 C riteria D ocument (p. 7

- 14) observes that another challenge of time

21 series epidemiological analysis is assessing the relation ship between O 3 and health 22 outcomes while avoiding bias due to confounding by other time

- varying factors, 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 98 particularl y seasonal trends and weather variables . These variables are of particular 1 interest because O 3 concentrations have a well

- characterized se asonal pattern and are also 2 highl y correlated with changes in temperature , such that it can be difficult to distinguish 3 whether effects are associated with O 3 or with seasonal or weather variables in statistical 4 anal ys es. 5 The 2006 Criteria Document (s ecti on 7.1.3.4 ) discusses statistical modeling 6 approaches that have been used to adjust for time

- varying factors, highlighting a series of 7 anal ys es that were done in a Health Effects Institute

- funded reanaly sis of numerous time

8 series studies. While the focus of these reanal ys es was on associations with PM, a 9 number of investigators also examined the sensitivity of O 3 coefficients to the extent of 10 adjustment for temporal trends and weather factors. In addition, several recent studies, 11 including U.S. multicity studies (Bell et al., 2005; Huang et al., 2005; Schwartz et al., 12 2005) and a meta

- analy sis study (Ito et al., 2005), evaluated the effect of model 13 specification on O 3 - mortality associations. As discussed in the 2006 C riteria D ocument 14 (section 7.6.3.1), these studies generally report that associations reported with O 3 are not 15 substantially

changed with alternative modeling strategies for adjusting for temporal 16 trends and meteorologic effects. In the meta

- analy sis by Ito et al. (2005), a separate 17 multicity anal ys is was presented that found that alternative adjustments for weather 18 resulted in up to 2

- fold difference in the O 3 effect estimate. S ignificant confounding can 19 occur when strong seasonal cycles are present, suggesting that season

- specific results are 20 more generall y robust than year

- round results in such cases. A number of 21 epidemiological studies have conducted season

- specific anal ys es, and have generall y 22Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 99 reported stronger and more precise effect estimates for O 3 associations in the warm 1 season than in anal ys es conducted in the cool seasons or over the full year . 2 (3) Consistency refers to the persistent finding of an association between 3 exposure and outcome in multiple studies of adequate power in different persons, places, 4 circumstances and times (CDC, 2004). In considering results from multicity studies and 5 single

- city

studies in different areas, the 2006 C riteria D ocument (p. 8
- 41 ) observes 6 general consistency

in effects of short

- term O 3 exposure on mortality , respiratory 7 hospitalization and o th er respiratory health outcomes . The variations in effects that are 8 observed may

be attributable to differences in relative personal exposure to O 3 , as well as 9 varying concentrations and composition of copollutants present in different regions. 10 Thus, the 2006 C riteria D ocument (p.8
- 41 ) concludes that “consideration of consistency 11 or heterogeneity of effects is appropriatel y understood as an evaluation of the similarity 12 or general concordance of results, rather than an expectation of finding quantitative 13
re sult s with a very

narrow range.” 14 (4) The 2007 Staff Paper recognizes that it is likely that there are biological 15 thresholds for different health effects in individuals or groups of individuals with similar 16 innate characteristics and health status. For O 3 exposure, individual thresholds would 17 presumabl y vary substantially from person to person due to individual differences in 18 genetic susceptibility , pre - existing disease conditions and possibly individual risk factors 19 such as diet or exercise levels (and c ould even vary from one time to another for a given 20 person). Thus, it would be difficult to detect a distinct threshold at the population level 21 below which no individual would experience a given effect, especiall y if some members 22Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 100 of a population are unusu ally sensitive even down to very low concentrations ( EPA, 1 2004, p. 9
- 43
- 9
- 44). 2 Some studies have tested associations between O 3 and health outcomes after 3 removal of day s with higher O 3 levels from the data set; such anal ys es do not necessaril y 4 indicate the presence or absence of a threshold, but provide some information on whether 5 the relationship is found using onl y lower

- concentration data. For example, using data 6 from 95 U.S. cities, Bell et al. (2004) found that the effect estimate for an associatio n 7 between short

- term O 3 exposure and mortality was little changed when days exceeding 8 0.0 60 pp m (24

- h our average) were excluded in the anal ys is. Using data from 8 U.S. 9 cities, Mortimer and colleagues (2002) also reported that associations between O 3 and 10 b oth lung function and respiratory s ymptoms remained statistically significant and of the 11 same or greater magnitude in effect size when concentrations greater than 0.0 80 ppm (8

- 12 hour average) were excluded (EPA, 2006a , p. 7
- 46). Several single

- city studies also 13 report similar findings of associations that remain or are increased in magnitude and 14 statistical significance when data at the upper end of the concentration range are removed 15 (EPA, 2006a, section 7.6.5)

. 16 Other time

- series epidemiological studies h ave used statistical modeling 17 approaches to evaluate whether thresholds exist in associations between short

- term O 3 18 exposure and mortality . As discussed in section 7.6.5 of the 2006 C riteria D ocument , one 19 European multicity study included evaluation of th e shape of the concentration

- response 20 curve, and observed no deviation from a linear function across the range of O 3 21 measurements from the study (Gry paris et al., 2004; EPA, 2006a p. 7
- 154). Several 22Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 101 single

- city

studies also observed a monotonic increase in associations between O 3 and 1 morbidity

that suggest that no population threshold exists (EPA, 2006a , p. 7
- 159). 2 On the other hand, a study in Korea used several different modeling approaches 3 and reported that a threshold model provided the best fit for the data. The results 4 suggested a potential threshold level of about 0.0 45 pp m (1

- h our maximum 5 concentration; < 0.0 35 pp m , 8
- h our average ) for an association between mortality and 6 short

- term O 3 exposure during the summer months (Kim et al., 2004; EPA, 2006 a , p. 8
- 7 43). The authors reported larger effect estimates for the association for data above the 8 potential threshold level, suggesting that an O 3 - mortality association might be 9 underestimated in the non

- threshold model. A threshold anal ys is recently repo rted b y 10 Bell et al. (2006) for 98 U.S. communities, including the same 95 communities in Bell et 11 al. (2004), indicated that if a population threshold existed for mortality , it would likely 12 fall below a 24

- h our average O 3 concentration of 0.0 15 pp m (< 0.0 25 pp m , 8
- h our 13 average ). In addition, Burnett and colleagues (1997 a,b ) plotted the relationships between 14 air pollutant concentrations and both respiratory and cardiovascular hospitalization, and it 15 appears in these results that the associations with O 3 are found in the concentration range 16 above about 0.0 30 ppm (1

- h our maximum; < 0.025 ppm, 8

- hour average). Vedal and 17 colleagues (2003) reported a significant association between O 3 and mortality in British 18 Columbia where O 3 concentrations were quite low (mean 1
- hour maximum concentration 19 of 0.0 273 pp m). The authors did not specificall y t est for threshold levels, but the fact that 20 the association was found in an area with such low O 3 concentrations suggests that any 21 potential threshold level would be quite low in this data set. 22Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 102 In summary , the 2006 C riteria D ocument finds that, taken together, the available 1 evidence from controlled human exposure and epidemiological studies suggests that no 2 clear conclusion can now be reached with regard to possible threshold l evels for O 3 - 3 related effe cts (EPA, 2006a , p. 8
- 44). Thus, the available epidemiological evidence 4 neither supports nor refutes the existence of thresholds at the population level for effects 5 such as increased hospital admissions and premature mortality

. There are limitations in 6 epidemiological studies that make discerning thresholds in populations difficult, 7 including low data density in the lower concentration ranges, the possible influence of 8 exposure measurement error, and interindividual differences in susceptibility to O 3 - 9 related effects in populations. There is the possibility that thresholds for individuals may 10 exist in reported associations at fairl y low levels within the range of air quality observed 11 in the studies but not be detectable as population thresholds in epidemiological anal ys es. 12 b. Biological Plausibility and Coherence of Evidence 13 The body

of epidemiological studies discussed in the 2007 Staff Paper 14 emphasizes the role of O 3 in association with a variety of adverse respiratory and 15 cardiovascular effects. While recognizing a variety of plausible mechanisms, there exists 16 a general consensus suggesting that O 3 , could either directly or through initiation, 17 interfere with basic cellular oxidation processes responsible for inflammation, reduced 18 antioxidant capacity , atherosclerosis and other effects. Reasoning that O 3 influences 19 cellular chemistry

through basic oxidative properties (as opposed to a unique chemical 20 interaction), other reactive oxidizing species (ROS) in the atmosphere acting either 21 independentl y or in combination with O 3 may also contribute to a number of adverse 22 respiratory

and cardiovascular health effects. Consequently , the role of O 3 should be 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 103 considered more broadl y as O 3 behaves as a generator of numerous oxidative spec ies in 1 the atmosphere. 2 In considering the biological plausibility of reported O 3 - related effects, the 2007 3 Staff Paper (section 3.4.6) considers this broader question of health effects of pollutant 4 mixtures containing O 3 . The potential for O 3 - related enh ancements of PM formation, 5 particle uptake, and exacerbation of PM

- induced cardiovascular effects underscores the 6 importance of considering contributions of O 3 interactions with other often co

- occurring 7 air pollutants to health effects due to O 3 - containing pollutant mixes. The 2007 Staff 8 Paper summarizes some examples of important pollutant mixture effects from studies that 9 evaluate interactions of O 3 with other co

- occurring pollutants, as discussed in chapters 4, 10 5, and 6 of the 2006 Criteria Document. 11 A ll of the ty pes of interactive effects of O 3 with other co

- occurring gaseous and 12 nongaseous viable and nonviable PM components of ambient air mixes noted above 13 argue that O 3 acts not only alone but that O 3 also is a surrogate indicator for air pollution 14 mi xes which may

enhance the risk of adverse effects due to O 3 acting in combination 15 with other pollutants. Viewed from this perspective, those epidemiologic findings of 16 morbidity

and mortality

associations, with ambient O 3 concentrations extending to quite 17 low levels in many

cases, become more understandable and plausible. 18 Th e 2006 C riteria D ocument integrates epidemiological studies with mechanistic 19 information from controlled human exposure studies and animal toxicological studies to 20 draw conclusions regarding the coherence of evidence and biological plausibility of O 3 - 21 related health effects to reach judgments about the causal nature of observed associations. 22 As summarized below, coherence and biological plausibility is discussed for each of the 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 104 following ty

pes of O 3 - related effects: short

- term effects on the respiratory sy stem, effects 1 on the cardiovascular s ys tem, effects related to long

- term O 3 exposure, and short

- term 2 mortality

- related health endpoints. 3 i. Coherence and Plausibility of Short

- term Effe cts on the Respiratory Sy stem 4 Acute respiratory morbidity

effects that have been associated with short

- term 5 exposure to O 3 include such health endpoints as decrements in lung function, increased 6 respiratory

s ymptoms, increased airway responsiveness, airway inflammation, increased 7 permeability

related to epithelial injury , immune sy stem effects, emergency department 8 visits for respiratory diseases, and hospitalization due to respiratory illness

. 9 Recent epidemiological studies have supported evidence availa ble in the previous 10 O 3 NAAQS review on associations between ambient O 3 exposure and decline in lung 11 function for children. The 2006 C riteria D ocument (p. 8

- 34) concludes that exposure to 12 ambient O 3 has a significant effect on lung function and is associated with increased 13 respiratory

s ymptoms and medication us e, particularly in asthmatics. Short

- term 14 exposure to O 3 has also been associated with more severe morbidity endpoints, such as 15 emergency

department visits and hospital admissions for respiratory cas es, including 16 specific respiratory illness (e.g., asthma) (EPA, 2006a , sections 7.3.2 and 7.3.3). In 17 addition, a few epidemiological studies have reported positive associations between 18 short

- term O 3 exposure and respiratory mortality, though the associatio ns are not 19 general ly

statisticall y significant (EPA, 2006a , p. 7
- 108). 20 Considering the evidence from epidemiological studies, the results described 21 above provide evidence for coherence in O 3 - related effects on the respiratory sy stem. 22 Effect estimates fro m U.S. and Canadian studies are shown in Figure 1 , where it can be 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 105 seen that mostly

positive associations have been reported with respiratory effects ranging 1 from respiratory

s ymptoms, such as cough or wheeze, to hospitalization for various 2 respiratory

dis eases, and there is suggestive evidence for associations with respiratory 3 mortality . Many of the reported associations are statistically significant , particularl y in 4 the warm season

. In Figure 1, the central effect estimate is indicated by a square for e ach 5 result, with the vertical bar representing the 95 percent confidence interval around the 6 estimate. In the discussions that follow, an individual study result is considered to be 7 statistically

significant if the 95 percent confidence interval does not include zero. 23 8 Positive effect estimates indicate increases in the health outcome with O 3 exposure. In 9 considering these results as a whole, it is important to consider not only whether 10 statistical significance at the 95 percent confidence level is repor ted in individual studies 11 but also the general pattern of results, focusing in particular on studies with greater 12 statistical power that report relativel y more precise results. 13

23 Results for studies of respiratory s ymptoms 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.Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 106 1

2Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 107 Considering also evidence from toxicological, co ntrolled human exposure , and 1 field studies, the 2006 C riteria D ocument (section 8.6) discusses biological plausibility 2 and coherence of evidence for acute O 3 - induced respiratory health effects. Inhalation of 3 O 3 for several hours while subjects are phys ically active can elicit both acute adverse 4 p athophy siological changes and subjectiv e respiratory tract s ymptoms (EPA, 2006a , 5 section 8.4.2). Acute pulmonary responses observed in healthy humans exposed to O 3 at 6 ambient concentrations include: decreased inspiratory capacity; mild 7 bronchoconstriction; rapid, shallow breathing during exercise; subjective sy mptoms of 8 tracheobronchial airway irritation, including cough and pain on deep inspiration; 9 decreases in measures of lung function; and increased airway res istance. The severity of 10 sy mptoms and magnitude of response depends on inhaled dose, individual O 3 sensitivity, 11 and the degree of attenuation or enhancement of response resulting from previous O 3 12 exposures. Lung function studies of several animal species acutel y exposed to relatively 13 low O 3 levels from a toxicological perspective ( i.e., 0.25 to 0.4 ppm) show responses 14 similar to those observed in humans, including increased breathing frequency , decreased 15 tidal volume, increased resistance, and decreased F VC. Alterations in breathing pattern 16 return to normal within hours of exposure, and attenuation in functional responses 17 following repeated O 3 exposures is similar to those observed in humans. 18 Phy siological and biochemical alterations investigated in cont rolled human 19 exposure and animal toxicology studies tend to support certain hy potheses of underl ying 20 pathological mechanisms which lead to the development of respiratory

- related effects 21 reported in epidemiology studies (e.g., increased hospitalization and medication use). 22 Some of these are: (a) decrements in lung function, (b) bronchoconstriction, (c) 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 108 increased airway

responsiveness, (d) airway inflammation, (e) epithelial injury , (f) 1 immune sy stem activation, (g) host defense impairment, and (h) sensitiv ity of individuals, 2 which depends on at least a person’s age, disease status , genetic susceptibility , and the 3 degree of attenuation present due to prior exposures. The time sequence, magnitude, and 4 overlap of these complex events, both in ter ms of develop ment and recovery , illustrate 5 the inherent difficulty of interpreting the biological plausibility of O 3 - induced 6
cardiopulmonary

health effects (EPA, 2006a , p. 8
- 48). 7 The interaction of O 3 with airway epithelial cell membranes and ELF to form 8 lipid ozonati on products and ROS is supported by numerous human, animal and in vitro 9 studies. Ozonation products and ROS initiate a cascade of events that lead to oxidative 10 stress, injury , inflammation, airway epithelial damage and increased epithelial damage 11 and increased alveolar permeability to vascular fluids. Repeated respiratory 12 inflammation can lead to a chronic inflammatory state with altered lung structure and 13 lung function and may lead to chronic respiratory diseases su ch as fibrosis and 14 emphy sema (EPA, 2006 a , section 8.6.2). Continued respiratory inflammation also can 15 alter the ability

to respond to infectious agents, allergens and toxins. Acute inflammatory 16 responses to O 3 are well documented, and lung injury appears within 3 h our s after 17 exposure in human s . 18 Taken together, the 2006 C riteria D ocument concludes that the evidence from 19 experimental human and animal toxicology studies indicates that acute O 3 exposure is 20 causall y associated with respiratory s ys tem effects . These effect s includ e O 3 - induced 21 pulm onary

function decrements ; respiratory s ymptoms ; lung inflammation and increased 22 lung permeability ; airway hy perresponsiveness ; increased uptake of nonviable and viable 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 109 particles ; and consequent increased susceptibility to PM
- related toxic effects and 1 resp iratory

infections (EPA, 2006a, p. 8

- 48). 2 ii. Coherence and Plausibility of Effects on the Cardiovascular S ys tem 3 There is very limited experimental evidence of animals and humans that has 4 evaluated possible mechanisms or phy siological pathway s by which acute O 3 exposures 5 may induce cardiovascular s ys tem effects. Ozone induces lung injury , inflammation, and 6 impaired mucociliary clearance, with a host of associated biochemical changes all leading 7 to increased lung epithelial permeability. As noted above in section II.A.2.a, the 8 generation of lipid ozonation products and ROS in lung tissues can influence pulmonary 9 hemody

namics, and ultimately

the cardiovascular sy stem. Other potential mechanisms 10 by which O 3 exposure may

be associated with cardiovascular disease outcomes have been 11 described. Laboratory animals exposed to relatively high O 3 concentrations (≥ 0.5 ppm) 12 demonstrate tissue edema in the heart and lungs. Ozone

- induced changes in heart rate, 13 edema of heart tissue, and increased tissue and serum levels of ANF found with 8

- h our 14 0.5 ppm O 3 exposure in animal toxicology studies (Vesel y et al., 1994a,b,c) also raise the 15 possibility

of potential cardiovascular effects of acute ambient O 3 exposures. 16 Animal toxicology studies have found both transient and persistent ventilatory 17 responses with and without progressive decreases in heart rat e (Arito et al., 1997). 18 Observations of O 3 - induced vasoconstriction in a controlled human exposure study by 19 Brook et al. (2002) suggests another possible mechanism for O 3 - related exacerbations of 20 preexisting cardiovascular disease. One controlled human s tudy (Gong et al., 1998) 21 evaluated potential cardiovascular health effects of O 3 exposure. The overall results did 22 not indicate acute cardiovascular effects of O 3 in either the hypertensive or control 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 110 subjects. The authors observed an increase in rate

- pressure product and heart rate, a 1 decrement for FEV 1 , and a >10 mm Hg increase in the alveolar/arterial pressure 2 difference for O 2 following O 3 exposure. Foster et al. (1993) demonstrated that even in 3 relativel y young healthy adults, O 3 exposure can cause ventilation to shift away from the 4 well

- perfused basal lung. This effect of O 3 on ventilation distribution may persist beyond 5 24
- h our s post - exposure (Foster et al., 1997). These findings suggest that O 3 may exert 6 cardiovascular effects indirectly by impairing alveolar

- arterial O 2 transfer and potentially 7 reducing O 2 supply

to the myocardium. Ozone exposure may increase myo cardial work 8 and impair pulmonary gas exchange to a degree that could perhaps be clinically 9 important in persons with significant preex isting cardiovascular impairment. 10 As noted above in section II.A.2.a, a limited number of new epidemiological 11 studies have reported associations between short

- term O 3 exposure and effects on the 12 cardiovascular s ys tem. Among these studies, three were population

- based and involved 13 relativel y large cohorts ; two of these studies evaluated associations between O 3 and HRV 14 and the other study evaluated the association between O 3 levels and the relative risk of 15 MIor heart attack . Such studies may offer more in formative results based on their large 16 subject

- pool and design. Results from these three studies were suggestive of an 17 association between O 3 exposure and the cardiovascular endpoints studied. In other 18 recent studies on the incidence of heart attacks and some more subtle cardiovascular 19 health endpoints, such as changes in HRV or cardiac arrhythmia, some but not all studies 20 reported associations with short

- term exposure to O 3 (EPA, 2006a, section 7.2.7.1). 21 From these studies, the 2006 Criteria Document co ncludes that the “current evidence is 22Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 111 rather limited but suggestive of a potential effect on HRV, ventricular ar rhythmias, and 1 MIincidence” (EPA, 2006a , p. 7
- 65). 2 An increasing number of studies have evaluated the association between O 3 3 exposure and cardiovascular hospital admissions. As discussed in section 7.3.4 of the 4 2006 C riteria D ocument , many reported negative or inconsistent associations, whereas 5 other studies, especially those that examined the relationship when O 3 exposures were 6 higher, have fo und positive and robust associations between O 3 and cardiovascular 7 hospital admissions. The 2006 C riteria D ocument (p. 7

- 83) finds that the overall 8 evidence from these studies remains inconclusive regarding the effect of O 3 on 9
cardiovascular hospitalizati ons . The 2006 C riteria D ocument notes that the suggestive 10 positive epidemiologic findings of O 3 exposure on cardiac autonomic control, including 11 effects on HRV, ventricular arrhythmias and heart attacks , and reported associations 12 between O 3 exposure and c ardiovascular hospitalizations generall y in the warm season 13 gain credibility

and scientific support from the results of experimental animal toxicology 14 and controlled human exposure studies, which are indicative of plausible pathway s by 15 which O 3 may exert c ardiovascular effects (EPA, 2006a , s ection 8.6.1). 16 iii. Coherence and Plausibility of Effects Related to Long

- Term O 3 Exposure 17 Controlled human exposure studies cannot evaluate effects of long

- term 18 exposures to O 3 ; there is some evidence available from to xicological studies. While early 19 animal toxicology

studies of long

- term O 3 exposures were conducted using continuous 20 exposures, more recent studies have focused on exposures which mimic diurnal and 21 seasonal patterns and more realistic O 3 exposure levels ( EPA, 2006a , p. 8
- 50). Studies of 22 monkey s that compared these two exposure scenarios found increased airway pathology 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 112 only with the latter design. Persistent and irreversible effects reported in chronic animal 1 toxicology

studies suggest that additional co mplementary human data are neede d from 2 epidemiologic studies (EPA, 2006a , p. 8
- 50). 3 There is limited evidence from human studies for long

- term O 3 - induced effects on 4 lung function. As discussed in section 8.6.2 of the 2006 C riteria D ocument , previous 5 epid emiological studies have provided onl y inconclusive evidence for either mortality or 6 morbidity

effects of long

- term O 3 exposure. The 2006 C riteria D ocument (p. 8

- 50) 7 observes that the inconsistency in findings may

be due to a lack of precise exposure 8 info rmation, the possibility of selection bias, and the difficulty of controlling for 9 confounders . Several new longitudinal epidemiology studies have evaluated associations 10 between long

- term O 3 exposures and morbidity and mortality

and suggest that these long

11 term exposures may be related to changes in lung function in children; however, little 12 evidence is available to support a relationship between chronic O 3 exposure and mortal ity 13 or lung cancer incidence (EPA, 2006a , p. 8
- 50). 14 The 2006 C riteria D ocument (p . 8
- 51) concludes that evidence from animal 15 toxicology

studies strongly

suggests that chronic O 3 exposure is capable of damaging the 16 distal airway s and proximal alveoli, resulting in lung tissue remodeling leading to 17 apparent irreversible changes. Such structural changes and compromised lung function 18 caused b y persistent inflammation may exacerbate the progression and development of 19 chronic lung disease. Together with the limited evidence available from epidemiological 20 studies, these findings offer some insight into potential biological mechanisms for 21 suggested associations between long

- term or seasonal exposures to O 3 and reduced lung 22Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 113 function development in children which have been obser ved in epidemiologic studies 1 (EPA, 2006a , p. 8
- 51). 2 iv. Coherence an d Plausibility of Short

- Term Mortality

- Related Health Endpoints 3 An extensive epidemiological literature on air pollution related mortality risk 4 estimates from the U.S., Canada, and Europe is discussed in the 2006 Criteria Document 5 (sections 7.4 and 8.6.3) . These single

- and multicity mortality studies coupled with 6 results from meta - anal ys es generally indicate associations between acute O 3 exposure and 7 elevated risk for all

- cause mortality , even after adjustment for the influence of season and 8 PM exposure . Several single

- city studies that specificall y evaluated the relationship 9 between O 3 exposure and cardiopulmonary mortality also reported results suggestive of a 10 positive association (EPA, 2006a , p. 8
- 51). These mortality studies suggest a pattern of 11 eff ects for causality that have biologicall y plausible explanations, but our knowledge 12 regarding potential underlying mechanisms is very limited at this time and requires 13 further research. Most of the phy siological and biochemical parameters investigated in 14 human and animal studies suggest that O 3 - induced biochemical effects are relatively 15 transient and attenuate over time. The 2006 C riteria D ocument (p. 8

- 52) hy pothesizes a 16 generic pathway

of O 3 - induced lung damage, potentially involving oxidative lung 17 dama ge with subsequent inflammation and/or decline in lung function leading to 18 respiratory

distress in some sensitive population groups (e.g., asthmatics), or other 19 plausible pathway s noted below that may lead to O 3 - related contributions to 20 cardiovascular effe cts that ultimately increase risk of mortality

. 21 The third National Health and Nutrition Examination Survey f ollow

- up data 22 anal ys is indicates that about 20 percent of the adult population has reduced FEV 1 values, 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 114 suggesting impaired lung function in a significant portion of the population. Most of 1 these individuals have COPD, asthma or fibrotic lung disease (Manino et al., 2003), 2 which are associated with persistent low

- grade inflammation. Furthermore, patients with 3 COPD are at increased risk for cardiov ascular disease. Also, lung disease with 4 underlying inflammation may be linked to low

- grade systemic inflammation associated 5 with atherosclerosis, independent of cigarette smoking (EPA, 2006a , p. 8
- 52). Lung 6 function decrements in persons with cardiopulm onary disease have been associated with 7 inflammatory

markers, such as C

- reactive protein (CRP) in the blood. At a population 8 level it has been found that individuals with the lowest FEV 1 values have the highest 9 levels of CRP, and those with the highest FEV 1 values have the lowest CRP levels 10 (Manino et al., 2003; Sin and Man, 2003). This complex series of phy siological and 11 biochemical reactions following O 3 exposure may tilt the biological homeostasis 12 mechanisms which could lead to adverse health effects in people with compromised 13 cardiopulmonary

s ys tems. 14 S everal other typ es of newly available data also support reasonable hy potheses 15 that may

help to explain the findings of O 3 - related increases in cardiovascular mortality 16 observed in some epidemiological studies. These include the direct effect of O 3 on 17 increasing PAF in lung tissue that can then enter the general circulation and possibly 18 contribute to increased risk of blood clot formation and the consequent increased risk of 19 heart attacks , cerebrovascular events (stroke), or associated cardiovascular

- related 20 mortality . Ozone reactions with cholesterol in lung surfactant to form epoxides and 21 oxysterols that are cy totoxic to lung and heart muscles and that contribute to 22 atherosclerotic plaque formation in arterial walls represent another potential pathway

. 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 115 Stimulation of airway

irritant receptors may

lead to increases in tissue and serum levels 1 of ANF, changes in heart rate, and edema of heart tissue. A few new field and panel 2 studies of human adults have reported associations between ambient O 3 concentrations 3 and changes in cardiac autonomic control (e.g., HRV, ventricular arrhythmias, and MI). 4 These represent plausible pathway s that may lead to O 3 - related contributions to 5 cardiovascular effects that ultimately increase the risk of mortality

. 6 In addition, O 3 - induced increases in lung permeability allow more ready

entry for 7 inhaled PM into the blood stream, and thus O 3 exposure may increase the risk of PM

8 related cardiovascular effects. Furthermore, in creased ambient O 3 levels contribute to 9 ultrafine PM formation in the ambient air and indoor environments. Thus, the 10 contributions of elevated ambient O 3 concentrations to ultrafine PM formation and 11 human exposure, along with the enhanced uptake of inhale d fine particles, consequentl y 12 may

contribute to exacerbation of PM

- induced cardiovascular effects in addition to those 13 more directl y induced b y O 3 (EPA, 2006a , p. 8
- 53). 14
c. Summary 15 Judgments concerning the extent to which relationships between various he alth 16 endpoints and ambient O 3 exposures are likely to be causal are informed by the 17 conclusions and discussion in the 2006 Criteria Document as discussed above and 18 summarized in section 3.7.5 of the 2007 Staff Paper. These judgments reflect the nature 19 of the evidence and the overall weight of the evidence, and are taken into consideration in 20 the quantitative risk assessment discussed below in section II.B.2. 21 For example, there is a very high level of confidence that O 3 induces lung 22 function decrements in healthy adults and children due in part to the dozens of controlled 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 116 human exposure and epidemiological studies consistently showing such effects. The 1 2006 Criteria Document (p. 8

- 74) states that these studies provide clear evidence of 2 causality

for associ ations between short

- term O 3 exposures and statistically significant 3 declines in lung function in children, asthmatics and adults who exercise outdoors. An 4 increase in respiratory symptoms (e.g., cough, shortness of breath) has been observed in 5 controlled human exposure studies of short

- term O 3 exposures, and significant 6 associations between ambient O 3 exposures and a wide variety of respiratory s ymptoms 7 have been reported in epidemiology studies (EPA, 2006a, p. 8

- 75). Population time

8 series studies showing robust associations between O 3 exposures and respiratory hospital 9 admissions and emergency department visits are strongl y supported b y controlled human 10 exposure, animal toxicological, and epidemiological evidence for O 3 - related lung 11 function decrements, respiratory s ymptoms, airway

inflammation, and airway 12 hy perreactivity . The 2006 Criteria Document (p. 8

- 77) concludes that, taken together, the 13 overall evidence supports the inference of a causal relationship between acute ambient O 3 14 exposures and increa sed respiratory morbidity outcomes resulting in increased 15 emergency

department visits and hospitalizations during the warm season. Further, 16 recent epidemiologic evidence has been characterized in the 2006 Criteria Document (p. 17 8
- 78) as highl y suggestive that O 3 directly or indirectly

contributes to non

- accidental and 18 cardiopulmonary

- related mortality

. 19 4. O 3 - Related Impacts on Public Health 20 The following discussion draws from chapters 6 and 7 and section 8.7 of the 2006 21 Criteria Document and section 3.6 of the 2007 Staff Paper to characterize factors which 22 modify

responsiveness to O 3, populations potentially at risk for O 3 - related health effects, 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 117 the adversity of O 3 - related effects, and the size of the at

- risk populations in the U.S.. 1 These considerations are all important elements in characterizing the potential public 2 health impacts associated with exposure to ambient O 3. 3
a. Factors That Modify Responsiveness to Ozone 4 There are numerous factors that can modify individual responsiveness to O 3 . 5 These include: influence of phy sical activity; age; gender and hormonal influences; 6 racial, ethnic and socioeconomic status (SES) factors; environmental factors; and 7 oxidant

- antioxidant balance. These factors are discussed in more detail in section 6.5 of 8 the 2006 Criteria Document. 9 It is well established that phy sical activity increases an individual’s minute 10 ventilation and will thus increase the dose of O 3 inhaled (EPA, 2006a, section 6.5.4). 11 In creased phys ical activity results in deeper penetration of O 3 into more distal regions of 12 the lungs, which are more sensitive to acute O 3 response and injury . This will result in 13 greater lung function decrements for acute exposures of individuals during increased 14 phy sical activity . Research has shown that respiratory effects are observed at lower O 3 15 concentrations if the level of exertion is increased and/or duration of exposure and 16 exertion are extended. Predicted O 3 - induced decrements in lung function have been 17 shown to be a function of exposure concentration, duration and exercise level for healthy , 18 yo ung adults (McDonnell et al., 1997). 19 Most of the studies investigating the influence of age have used lung function 20 decrements and s ymptoms as measures of response. For healthy adults, lung function and 21 sy mptom respo nses to O 3 decline as age increases. The rate of decline in O 3 22 responsiveness appears greater in those 18 to 35 years old compared to those 35 to 55 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 118 ye ars old, while there is very little change after age 55. In one study (Seal et al., 1996) 1 anal yz ing a l arge data set, a 5.4% decrement in FEV 1 on average was estimated for 20 2 ye ar old individuals exposed to 0.12 ppm O 3 for 2.3 hours, whereas similar exposure of 3 35 year old individuals resulted in a 2.6% decrement on average. While healthy children 4 tend not to report respiratory s ymptoms when exposed to low levels of O 3 , for subjects 18 5 to 36 years old s ymptom responses induced by O 3 are observed but tend to decrease with 6 increasing age within this range (McDonnell et al., 1999). 7 Limited evidence of gender differences in response to O 3 exposure has suggested 8 that females may

be predisposed to a greater susceptibility to O 3 . L ower plasma and NL 9 fluid levels of the most prevalent antioxidant, uric acid, in females relative to males may 10 be a contributing facto r. Consequently , reduced removal of O 3 in the upper airway s may 11 promote deeper penetration. However, most of the evidence on gender differences 12 appears to be equivocal, with one study (Hazucha et al., 2003) suggesting that 13 phy siological responses of youn g healthy males and females may be comparable (EPA, 14 2006a, section 6.5.2). 15 A few studies have suggested that ethnic minorities might be more responsive to 16 O 3 than Caucasian population groups (EPA, 2006a, section 6.5.3). This may be more the 17 result of a l ack of adequate health care and socioeconomic status (SES) than any 18 differences in sensitivity to O 3 . The limited data available, which have investigated the 19 influence of race, ethnic or other related factors on responsiveness to O 3, prevent drawing 20 any c lear conclusions at this time. 21 Few human studies have examined the potential influence of environmental 22 factors such as the sensitivity of individuals who voluntarily smoke tobacco (i.e., 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 119 smokers) and the effect of high temperatures on O 3 responsiveness. New controlled 1 human exposure studies have confirmed that smokers are less responsive to O 3 than 2 nonsmokers; however, time course of development and recovery of these effects, as well 3 as reproducibility , was not different from nonsmokers (EPA, 2006a, section 6.5.5). 4 In fluence of ambient temperature on pulmonary effects induced by O 3 has been studied 5 very little, but additive effects of heat and O 3 exposure have been reported. 6 Antioxidants, which scavenge free radicals and limit lipid peroxidation in the 7 ELF, are the first line of defense against oxidative stress. Ozone exposure leads to 8 absorption of O 3 in the ELF with subsequent depletion of antioxidant in the nasal ELF, 9 but concentration and antioxidant enzy me activity

in ELF or plasma do not appear re lated 10 to O 3 responsiveness (EPA 2006a, section 6.5.6). Controlled studies of dietary 11 antioxidant supplements have shown some protective effects on lung function decrements 12 but not on sy

mptoms and airway

inflammatory

responses. Dietary

antioxidant 13 supplem ents have provided some protection to asthmatics by attenuating post

- exposure 14 airway

hy perresponsiveness. Animal studies have also supported the protective effects of 15 ELF antioxidants. 16 b. At

-Risk Subgroups for O 3 -Related Effects 17 Several characteristics m ay increase the extent to which a population group shows 18 increased susceptibility or vulnerability . Information on potentially susceptible and 19 vulnerable groups is summarized in section 8.7 of the 2006 Criteria Document

. As 20 described there, the term susc eptibility refers to innate (e.g., genetic or developmental) or 21 acquired (e.g., personal risk factors, age) factors that make individuals more likely to 22 experience effects with exposure to pollutants. A number of population groups have been 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 120 identified as potentially

susceptible to health effects as a result of O 3 exposure, including 1 people with existing lung diseases, including asthma , children and older adults, and 2 people who have larger than normal lung function responses that may be due to genetic 3
susceptibility

. In addition, some population groups have been identified as having 4 increased vulnerability to O 3 - related effects due to increased likelihood of exposure while 5 at elevated ventilation rates, including healthy children and adults who are active 6
o utdoors, for example, o utdoor workers , and joggers

. Taken together, the susceptible and 7 vulnerable groups make up "at

- risk" groups. 24 8 i. Active People 9 A large group of individuals at risk from O 3 exposure consists of outdoor workers 10 and children, adolescents, and adults who engage in outdoor activities involving exertion 11 or exercise during summer daylight hours when ambient O 3 concentrations tend to be 12 higher. This conclusion is based on a large number of controlled

- human exposure studies 13 and several epidemiologic field/panel studies which have been conducted with healthy 14 children and adults and those with preexisting respiratory diseases (EPA 2006a, sections 15 6.2, 6.3, 7.2, and 8.4.4). The controlled human exposure studies show a clear O 3 16 exposure - respon se relationship with increasing spirometric and s ymptomatic response as 17 exercise level increases. Furthermore, O 3 - induced response increases as time of exposure 18 increases. Studies of outdoor workers and others who participate in outdoor activities 19 indicat e that extended exposures to O 3 at elevated exertion levels can produce marked 20

24 Inth e Staff Paper and documents from previous O 3 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.Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 121 effects on lung function, as discussed above in section IIA.2 (Brauer et al., 1996; Höppe 1 et al., 1995; Korrick et al., 1998; McConnell et al., 2002). 2 These field studies with subjects at elevated exertion levels support the extensive 3 evidence derived from controlled human exposure studies. The majority of controlled 4 human exposure studies has examined the effects of O 3 exposure in subjects performing 5 continuous or intermittent exercise for variable periods of time and has reported 6
s ignificant O 3 - induced respiratory responses. The epidemiologic studies discussed above 7 also indicate that prolonged exposure periods, combined with elevated levels of exertion 8 or exercise, may

magni fy O 3 effects on lung function. Thus, outdoor workers and others 9 who participate in higher exertion activities outdoors during the time of day when high 10 peak O 3 concentrations occur appear to be particularly vulnerable to O 3 effects on 11 respiratory

health. Although these studies show a wide variability of response and 12 sensitivity

among subjects and the factors contributing to this variability continue to be 13 incompletely

understood, the effect of increased exertion is consistent. It should be noted 14 that th is wide variability of response and sensitivity among subjects may

be in part due to 15 the wide range of other highl y reactive photochemical oxidants coexisting with O 3 in the 16 ambient air. 17 ii. People with Lung Disease 18 People with preexisting pulmonary disea se are among those at increased risk from 19 O 3 exposure. Altered physiological, morphological, and biochemical states ty pical of 20 respiratory

diseases like asthma, COPD, and chronic bronchitis may render people 21 sensitive to additional oxidative burden induce d by O 3 exposure. At the time of the 1997 22 review, it was concluded that these groups were at greater risk because the impact of O 3 - 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 122 induced responses on already- compromised respiratory s ys tems would noticeabl y impair 1 an individual's ability to engage in no rmal activity or would be more likel y to result in 2 increased self

- medication or medical treatment. At that time there was little evidence that 3 people with pre

- existing disease were more responsive than healthy individuals in terms 4 of the magnitude of lung function decrements or sy mptomatic responses. The new results 5 from controlled exposure and epidemiologic studies continue to indicate that individuals 6 with preexisting pulmonary disease are a sensitive population for O 3 - related health 7 effects. 8 Several c ontrolled human exposure studies reviewed in the 1996 Criteria 9 Document on atopic and asthmatic subjects have suggested but not clearl y demonstrated 10 enhanced responsiveness to acute O 3 exposure compared to healthy subjects. The 11 majority

of the newer studi es reviewed in Chapter 6 of the 2006 Criteria Document 12 indicate that asthmatics are more sensitive than normal subjects in manifesting O 3 - 13 induced lung function decrements. In one key study (Horstman et al., 1995), the FEV 1 14 decrement observed in the asthmatics was significantly larger than in the healthy subjects 15 (19% versus 10%, respectively). There was also a notable tendency for a greater group 16 mean O 3 - induced decrease in FEF 25
- 75 in asthmatics relative to the healthy subjects (24% 17 versus 15%, respectiv el y). A significant positive correlation in asthmatics was also 18 reported between the magnitude of O 3 - induced spirometric responses and baseline lung 19 function, i.e., responses increased with severity of disease. 20 Asthmatics present a differential response profile for cellular, molecular, and 21 biochemical parameters (2006 Criteria Document, Figure 8

- 1) that are altered in response 22 to acute O 3 exposure. Ozone
- induced increases in neutrophils, IL

- 8 and protein were 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 123 found to be significantly

higher in the BAL f

luid from asthmatics compared to healthy 1 subjects, suggesting mechanisms for the increased sensitivity of asthmatics (Basha et al., 2 1994; McBride et al., 1994; Scannell et al., 1996; Hiltermann et al., 1999; Holz et al., 3 1999; Bosson et al., 2003). Neutrophils, or PMNs, are the white blood cells most 4 associated with inflammation. IL

- 8 is an inflammatory cy tokine with a number of 5 biological effects, primarily on neutrophils. The major role of this cy tokine is to attract 6 and activate neutrophils. Protein in the airway s is leaked from the circulatory s ys tem, 7 and is a marker for increased cellular permeability. 8 Bronchial constriction following provocation with O 3 and/or allergens presents a 9 two - phase response. The earl y response is mediated by release of histamine and 10 leukotrienes that leads to contraction of smooth muscle cells in the bronchi, narrowing 11 the lumen and decreasing the airflow. In people with allergic airway disease, including 12 people with rhinitis and asthma, these mediators also cause accumulation of eosinophils 13 in the airway s (Bascom et al., 1990; Jorres et al., 1996; Peden et al., 1995 and 1997; 14 Frampton et al., 1997 ; Michelson et al., 1999; Hiltermann et al., 1999; Holz et al., 2002; 15 Vagaggini et al., 2002). In asthma, the eosinophil, which increases inflammation and 16 allergic responses, is the cell most frequentl y associated with exacerbations of the 17 disease. A study b y Bosson et al. (2003) evaluated the difference in O 3 - induced 18 bronchial epithelial cy tokine expression between healthy and asthmatic subjects. After 19 O 3 exposure the epithelial expression of IL

- 5 and GM

- CSF increased significantly in 20 asthmatics, compared to healthy subjects. Asthma is associated with Th2

- related airway 21 response (allergic response), and IL

- 5 is an important Th2

- related cy tokine. The O 3 - 22 induced increase in IL

- 5, and also in GM

- CSF, which affects the growth, activation and 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 124 survival of eosinophils, may indicate an effect on the Th2

- related airway response and on 1 airway

eosinophils. The authors reported that the O 3 - induced Th2

- related cy tokine 2 responses that were found within the asthmatic group may indicate a worsening of their 3 asthmatic airway

inflammation and thus suggest a plausible link to epidemiological data 4 indicating O 3 - associated increases in bronchial reactivity and hospital admissions. 5 The accumulation of eosinophils in the airways of asthmatics is followed by 6 production of mucus and a late

- phase bronchial constriction and reduced airflow. In a 7 study

of 16 intermittent asthmatics, Hiltermann et al. (1999) found that there was a 8 significant inverse correlation between the O 3 - induced change in the percentage of 9 eosinophils in induced sputum and the change in PC 20 , the concentration of methacholine 10 causing a 20% decrease in FEV 1 . Characteristic O 3 - induced inflammatory airway 11 neutrophilia at one time was considered a leading mechanism of airway 12 hy perresponsiveness. However, Hiltermann et al. (1999) determined that the O 3 - induced 13 change in percentage neutrophils in sputum was not significantl y related to the change in 14 PC 20 . These results are consistent with the results of Zhang et al. (1995), which found 15 neutrophilia in a murine model to be only coincidentally

associated with airway 16 hy perresponsiveness, i.e., there was no cause and effect relationship . (2006 Criteria 17 Document, AX 6
- 26). Hiltermann et al. (1999) concluded that the results point to the role 18 of eosinophils in O 3 - induced airway hy perresponsiveness. Increases in O 3 - induced 19 nonspecific airway

responsiveness incidence and duration could hav e important clinical 20 implications for asthmatics. 21 Two studies (Jörres et al., 1996; Holz et al., 2002) observed increased airway 22 responsiveness to O 3 exposure with bronchial allergen challenge in subjects with 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 125 preexisting allergic airway disease. Jörre s et al. (1996) found that O 3 causes an increased 1 response to bronchial allergen challenge in subjects with allergic rhinitis and mild allergic 2 asthma. The subjects were exposed to 0.25 ppm O 3 for 3 hours with IE. Airway 3 responsiveness to methacholine was determined 1 hour before and after exposure; 4 responsiveness to allergen was determined 3 hours after exposure. Statistically 5 significant decreases in FEV 1 occurred in subjects with allergic rhinitis (13.8%) and 6 allergic asthma (10.6%), and in healthy controls (7.3%). Methacholine responsiveness 7 was statistically

increased in asthmatics, but not in subjects with allergic rhinitis or 8 healthy

controls. Airway responsiveness to an individual’s historical allergen (either 9 grass and birch pollen, house dust m ite, or animal dander) was significantly increased 10 after O 3 exposure when compared to FA exposure. In subjects with asthma and allergic 11 rhinitis, a maximum percent fall in FEV 1 of 27.9% and 7.8%, respectivel y, occurred 3 12 day s after O 3 exposure when they w ere challenged with of the highest common dose of 13 allergen. The authors concluded that subjects with asthma or allergic rhinitis, without 14 asthma, could be at risk if a high O 3 exposure is followed by a high dose of allergen. 15 Holz et al. (2002) reported an earl y phase lung function response in subjects with rhinitis 16 after a consecutive 4

- day exposure to 0.125 ppm O 3 that resulted in a clinically relevant 17 (>20%) decrease in FEV 1 . Ozone
- induced exacerbation of airway responsiveness 18 persists longer and attenuates more slowl y than O 3 - induced lung function decrements and 19 respiratory

s ymptom responses and can have important clinical implications for 20 asthmatics. 21 A small number of in vitro studies corroborate the differences in the responses of 22 asthmatic and healthy subject generally

found in controlled human exposure studies. In 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 126 vitro studies (Schierhorn et al., 1999) of nasal mucosal biopsies from atopic and 1 nonatopic subjects exposed to 0.1 ppm O 3 found significant differences in release of IL

- 4, 2 IL
- 6, IL
- 8, and TNF

- α. Another study by Schierhorn et al. (2002) found significant 3 differences in the O 3 - induced release of the neuropeptides neurokinin A and substance P 4 for allergic patients in comparison to nonallergic controls, suggesting increased activation 5 of sensory

nerves by

O 3 in the allergic tissues. Another study by Bay ram et al. (2002) 6 using in vitro culture of bronchial epithelial cells recovered from atopic and nonatopic 7 asthmatics also found significant increases in epithelial permeability in response to O 3 8 exposure. 9 The new data on airway responsiveness, inflammation, and various molecular 10 markers of inflammation and bronchoconstriction indicate that people with asthma and 11 allergic rhinitis (with or without asthma) comprise susceptible groups for O 3 - induced 12 adverse effects. This body of evidence indicates that controlled human exposure and 13 epidemiological panel studies of lung function decrements and respiratory sy mptoms that 14 evaluate onl y healthy, non

- asthmatic subjects likely underestimate the ef fects of O 3 15 exposure on asthmatics and other susceptible populations. The effects of O 3 on lung 16 function, inflammation, and increased airway responsiveness demonstrated in subjects 17 with asthma and other allergic airway diseases, provide plausible mechanis ms underlying 18 the more serious respiratory morbidity effects, such as emergency department visits and 19 hospital admissions, and respiratory mortality effects. 20 A number of epidemiological studies have been conducted using asthmatic study 21 populations. The ma jority of epidemiological panel studies that evaluated respiratory 22 sy mptoms and medication use related to O 3 exposures focused on children. These studies 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 127 suggest that O 3 exposure is associated with increased respiratory s ymptoms and 1 medication use in chil dren with asthma. Other reported effects include respiratory 2 sy mptoms, lung function decrements, and emergency department visits, as discussed in 3 the 2006 Criteria Document (section 7.6.7.1). Strong evidence from a large multicity 4 study

(Mortimer et al., 2002), along with support from several single

- city s tudies indicate 5 that O 3 exposure is associated with increased respiratory s ymptoms and medication use in 6 children with asthma. With regard to ambient O 3 levels and increased hospital 7 admissions and emergency department visits for asthma and other respiratory causes, 8 strong and consistent evidence establishes a correlation between O 3 exposure and 9 increased exacerbations of preexisting respiratory disease for 1

- hour maximum O 3 10 concentrations <0.12 ppm. As discussed above and in the 2006 Criteria Document, 11 section 7.3, several hospital admission and emergency department visit studies in the 12 U.S., Canada, and Europe have reported positive associations between increase in O 3 and 13 increased risk of emergency department visits and hospital admissions for asthma other 14 respiratory

diseases, especially

during the warm season. 15 In summary , based on a substantial new body of evidence from animal, controlled 16 human exposure and epidemiological studies the 2006 Criteria D ocument (section x.x) 17 concludes that people with asthma and other preexisting pulmonary diseases are among 18 those at increased risk from O 3 exposure. Evidence from controlled human exposure 19 studies indicates that asthmatics may exhibit larger lung function decrements and can 20 have larger inflammatory responses in response to O 3 exposure than healthy controls. 21 Asthmatics present a different response profile for cellular, molecular, and biochemical 22 parameters that are altered in response to acute O 3 exposure. Asthmatics, and people 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 128 with allergic rhinitis, are more likely to mount an allergic

- ty

pe response upon exposure to 1 O 3 , as manifested b y increases in white blood cells associated with allergy and related 2 molecules, which increase inflammation in the airways . The increased inflammatory and 3 allergic responses also may be associated with the larger late

- phase responses that 4 asthmatics can experience, which can include increased bronchoconstrictor responses to 5 irritant substances or allergens and additional inflammation. Epidemiological studies 6 have reported fairl y robust associations between ambient O 3 concentrations and measures 7 of lung function and daily respiratory sy mptoms (e.g., chest tightness, wheeze, shortness 8 of breath) in children with moderate to severe asthma and between O 3 and increased 9 asthma medication use. These more serious responses in asthmatics and others with lung 10 disease provide biological plausibility for the respiratory

morbidity

effects observed in 11 epidemiological studies, such as em ergency department visits and hospital admissions. 12 The body

of evidence from controlled human exposure and epidemiological studies, 13 which includes asthmatic as well as non

- asthmatic subjects, indicates that controlled 14 human exposure studies of lung functi on decrements and respiratory s ymptoms that 15 evaluate onl y healthy, non

- asthmatic subjects likely underestimate the effects of O 3 16 exposure on asthmatics and other susceptible populations. 17 Newl y available reports from controlled human exposure studies (se e chapter 6 in 18 the 2006 Criteria Document) utilized subjects with preexisting cardiopulmonary diseases 19 such as COPD, asthma, allergic rhinitis, and hy pertension. The data generated from these 20 studies that evaluated changes in spirometry did not find clear differences between 21 filtered air and O 3 exposure in COPD subjects. However, the new data on airway 22 responsiveness, inflammation, and various molecular markers of inflammation and 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 129 bronchoconstriction indicate that people with atopic asthma and allergic rhinitis comprise 1 susceptible groups for O 3 - induced adverse health effects. 2 Although controlled human exposure studies have not found evidence of larger 3 spirometric responses to O 3 in people with COPD relative to healthy subjects, this may be 4 due to the fact that most people with COPD are older adults who would not be expected 5 to be as responsive based on their age. However, in section 8.7.1, the 2006 Criteria 6 Document notes that new epidemiological evidence indicates that people with COPD 7 may be more likel y to experience other effects, including emergency room visits, hospital 8 admissions, or premature mortality . For example, results from an analy sis of five 9 European cities indicated strong and consistent O 3 effects on unscheduled respiratory 10 hospital adm issions, including COPD (Anderson et al., 1997). Also, an analy sis of a 9

- 11 ye ar data set for the whole population of the Netherlands provided risk estimates for more 12 specific causes of mortality , including COPD (Hoek et al., 2000, 2001; reanaly sis Hoek, 13 20 03); a positive, but nonsignificant, excess risk of COPD

- related mortality was found to 14 be associated with short

- term O 3 concentrations. Moreover, a s indicated by Gong et al. 15 (1998), the effects of O 3 exposure on alveolar

- arterial ox ygen gradients may be more 16 pronounced in patients with preexisting obstructive lung diseases. Relative to healthy 17 elderl y subjects, COPD patients have reduced gas exchange and low SaO 2 . Any 18 inflammatory

or edematous responses due to O 3 delivered to the well

- ventilated regions 19 of the lung in COPD subjects could further inhibit gas exchange and reduce oxygen 20 saturation. In addition, O 3 - induced vasoconstriction could also acutel y induce pulmonary 21 hy pertension. Inducing pulmonary vasoconstriction and hy

pertension in these patients 22 would perhaps worsen their condition, especially if their right ventricular function was 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 130 already compromised (EPA, 2006a, section 6.10). These controlled human exposure and 1 epidemiological studies indicate that people with pre

- existing lung diseases other than 2 asthma are also at greater risk from O 3 exposure than people without lung disease. 3 iii. Children and Older Adults 4 Supporting evidence exists for heterogeneity in the effects of O 3 by age. As 5 discussed in section 6.5.1 of the 2006 Criteria Document, children, adolescents, and 6 yo ung adults (<18 y

rs of age) appear, on average, to have nearly equivalent spirometric 7 responses to O 3 , but have greater responses than middle

- aged and older adults when 8 exposed to comparable O 3 doses. Sy mptomatic responses to O 3 exposure, however, do 9 not appear to occur in healthy children, but are observed in asthmatic children, 10 particularl y those who use maintenance medications. For adults (>17 yr s of age) 11 sy mptoms graduall y decrease with increasing age. In contrast to young adults, the 12 diminished sy

mptomatic responses in children and the diminished sy mptomatic and 13 spirometric responses in older adults increases the likelihood that these groups continue 14 outdoor activities leading to greater O 3 exposure and dose. 15 As desc ribed in the section 7.6.7.2 of the 2006 Criteria Document, many 16 epidemiological field studies focused on the effect of O 3 on the respiratory health of 17 school children. In general, children experienced decrements in lung function 18 parameters, including PEF , FEV 1 , and FVC. Increases in respiratory s ymptoms and 19 asthma medication use were also observed in asthmatic children. In one German study, 20 children with and without asthma were found to be particularly susceptible to O 3 effects 21 on lung function. Approx imately 20 percent of the children, both with and without 22Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 131 asthma, experienced a greater than 10 percent change in FEV 1 , compared to only 5 1 percent of the elderly population and athletes (Höppe et al., 2003)

. 2 The American Academy of P ediatrics (2004) notes that children and infants are 3 among the population groups most susceptible to many air pollutants, including O 3 . This 4 is in part because their lungs are still developing. For example, eighty percent of alveoli 5 are formed after birth, and changes in lung development continue through adolescence 6 (Dietert et al., 2000). Children are also likely to spend more time outdoors than adults, 7 which results in increased exposure to air pollutants (Wiley et al., 1991a,b). Moreover, 8 children have high minute ventilation rates and high levels of phy sical activity which also 9 increases their dose (Plunkett et al., 1992). 10 Several mortality studies have investigated age

- related differences in O 3 effects 11 (EPA, 2006a, section 7.6 .7.2). Older adults are also often classified as being particularl y 12 susceptible to air pollution. The 2006 Criteria Document (p. 8

- 60) concludes that the 13 basis for increased O 3 sensitivity among the elderly is not known, but one hy pothesis is 14 that it may be related to changes in the respiratory tract lining fluid antioxidant defense 15 network (Kelly

et al., 2003). Older adults have lower baseline lung function than 16 yo unger people, and are also more likely to have preexisting lung and heart disease. 17 In crea sed susceptibility of older adults to O 3 health effects is most clearl y i ndicated in the 18 newer mortality

studies. Among the studies that observed positive associations between 19 O 3 and mortality , a comparison of all age or younger age (  65 years of age) O 3 - mortality 20 effect estimates to that of the elderl y population (>65 years) indicates that, in general, the 21 elderl y population is more susceptible to O 3 mortality effects. The meta

- analy sis by Bell 22 et al. (2005) found a larger mortality effect estimate for the elderl y than for all ages. In 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 132 the large U.S. 95 communities study (Bell et al., 2004), mortality effect estimates were 1 slightly

higher for those aged 65 to 74 years, compared to individuals less than 65 years 2 and 75 years or greater. The absolute effect of O 3 on premature mortality may be 3 substantially

greater in the elderl y population because of higher rates of preexisting 4 respiratory

and cardiac diseases. The 2006 Criteria Document (p. 7

- 177) concludes that 5 the elderl y population (>65 years of age) appear to be at greater risk of O 3 - related 6 mortality

and hospitalizations compared to all ages or younger populations. 7 The 2006 Criteria Document notes that, collectively , there is supportin g evidence 8 of age

- related differences in susceptibility to O 3 lung function effects. The elderl y 9 population (>65 years of age) appear to be at increased risk of O 3 - related mortality and 10 hospitalizations, and children (<18 ye ars of age) experience other po tentially adverse 11 respiratory

health outcomes with increased O 3 exposure (EPA, 2006a, section 7.6.7.2). 12 iv. People with Increased Responsiveness to Ozone 13 New animal toxicology studies using various strains of mice and rats have 14 identified O 3 - sensitive and resistant strains and illustrated the importance of genetic 15 background in determining O 3 susceptibility (EPA, 2006a, section 8.7.4)

. C ontrolled 16 human exposure studies have also indicated a high degree of variability in some of the 17 pulmonary

phy siologic al parameters. The variable effects in individuals have been found 18 to be reproducible, in other words, a person who has a large lung function response after 19 exposure to O 3 will likely have about the same response if exposed again to the same 20 dose of O 3 . Incontrolled human exposure studies, group mean responses are not 21 representative of this segment of the population that has much larger than average 22 responses to O 3 . Recent studies of asthmatics by David et al. (2003) and Romieu et al. 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 133 (2004) reported a role for genetic pol ym orphism in observed differences in antioxidant 1 enzy mes and genes involved in inflammation to modulate lung function and 2 inflammatory

responses to O 3 exposure. 25 3 Biochemical and molecular parameters extensively evaluated in these exp eriments 4 were used to identify specific loci on chromosomes and, in some cases, to relate the 5 differential expression of specific genes to biochemical and phys iological differences 6 observed among these species. Utilizing O 3 - sensitive and O 3 - resistant spec ies, it has 7 been possible to identify the involvement of increased airway reactivity and inflammation 8 processes in O 3 susceptibility

. However, most of these studies were carried out using 9 relativel y high doses of O 3 , making the relevance of these studies questionable in human 10 health effects assessment. The genes and genetic loci identified in these studies may 11 serve as useful biomarkers in the future

. 12
v. Other Population Groups 13 There is limited, new evidence supporting associations between short

- term O 3 14 exposures and a range of effects on the cardiovascular sy stem. Some but not all, 15 epidemiological studies have reported associations between short

- term O 3 exposures and 16 the incidence of heart attacks and more subtle cardiovascular health endpoints, such as 17 changes in HRV and cardiac arrhy thmia. Others have reported associations with 18 hospitalization or emergency department visits for cardiovascular diseases, although the 19

25 Similar to animal toxicology studies refe rred above, a pol ym orphism in a specific proinflammatory cy tokine gene has been implicated in O 3 - 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 O 3 , however, the validity of these markers and their relevance in the context of prediction to population studies requires additional research

.Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 134 results across the studies are not consistent. Studies also report associations betw een 1 short

- term O 3 exposure and mortality from cardiovascular or cardiopulmonary causes. 2 The 2006 Criteria Document (p. 7

- 65) concludes that current cardiovascular effects 3 evidence from some field studies is rather limited but supportive of a potential eff ect of 4 short

- term O 3 exposure and HRV, cardiac arrhythmia, and heart attack incidence. In the 5 2006 Criteria Document’s evaluation of studies of hospital admissions for cardiovascular 6 disease (EPA 2006a, section 7.3.4), it is concluded that evidence from this growing group 7 of studies is generall y inconclusive regarding an association with O 3 in studies conducted 8 during the warm season (EPA 2006a, p. 7

- 83). This body of evidence suggests that 9 people with heart disease may be at increased risk from short

- ter m exposures to O 3; 10 however, more evidence is needed to conclude that people with heart disease are a 11 susceptible population. 12 Other groups that might have enhanced sensitivity to O 3 , but for which there is 13 currentl y very little evidence, include groups bas ed on race, gender and SES, and those 14 with nutritional deficiencies, which presents factors which modify responsiveness to O 3 . 15
c. Adversity of Effects 16 In the 2008 rulemaking, in making judgments as to when various O 3 - related 17 effects become regarded as adverse to the health of individuals, EPA looked to guidelines 18 published by

the American Thoracic Society (ATS) and the advice of CASAC. While 19 recognizing that perceptions of “medical significance” and “normal activity” may differ 20Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 135 among phys icians, lung phy siologists and experimental subjects, the ATS (1985) 26 1 defined adverse respiratory health effects as “medically significant physiologic changes 2 generall y evidenced b y one or more of the following: (1) interference with the normal 3 activity

of the affected pe rson or persons, (2) episodic respiratory illness, (3) 4 incapacitating illness, (4) permanent respiratory injury , and/or (5) progressive respiratory 5 dy sfunction.” During the 1997 review, it was concluded that there was evidence of 6 causal associations from controlled human exposure studies for effects in the first of 7 these five ATS

- defined categories, evidence of statistically significant associations from 8 epidemiological studies for effects in the second and third categories, and evidence from 9 animal toxico logy

studies, which could be extrapolated to humans only with a significant 10 degree of uncertainty, for the last two categories. 11 For ethical reasons, clear causal evidence from controlled human exposure studies 12 still covers only

effects in the first catego ry . However, for this review there are results 13 from epidemiological studies, upon which to base judgments about adversity, for effects 14 in all of the categories. Statistically significant and robust associations have been 15 reported in epidemiology studies falling into the second and third categories. These more 16 serious effects include respiratory events (e.g., triggering asthma attacks) that may 17 require medication (e.g., asthma), but not necessarily hospitalization, as well as 18 respiratory

hospital admissio ns and emergency department visits for respiratory causes. 19

26 In2000, 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 fundamentall y 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.Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 136 Less conclusive, but still positive associations have been reported for school absences 1 and cardiovascular hospital admissions. Human health effects for which associations 2 have been suggested through evidence from epidemiological and animal toxicology 3 studies, but have not been conclusively demonstrated still fall primarily into the last two 4 categories. In the 1997 review of the O 3 standard, evidence for these more serious effects 5 came from studi es of effects in laboratory animals. Evidence from animal studies 6 evaluated in the 2006 Criteria Document strongl y suggests that O 3 is capable of 7 damaging the distal airway s and proximal alveoli, resulting in lung tissue remodeling 8 leading to apparently irreversible changes. Recent advancements of dosimetry modeling 9 also provide a better basis for extrapolation from animals to humans. Information from 10 epidemiological studies provides supporting, but limited evidence of irreversible 11 respiratory

effects in humans than was available in the prior review. Moreover, the 12 findings from single

- city and multicity

time

- series epidemiology studies and meta

13 anal ys es of these epidemiological studies are highly suggestive of an association between 14 short

- term O 3 exposure and mortality particularl y in the warm season. 15 While O 3 has been associated with effects that are clearl y adverse, application of 16 these guidelines, in particular to the least serious category of effects related to ambient O 3 17 exposures, involves judgments about which medical experts on the CASAC panel and 18 public commenters have expressed diverse views in the past. To help frame such 19 judgments, EPA staff have defined specific ranges of functional responses (e.g., 20 decrements in FEV 1 and airway responsiven ess) and sy

mptomatic responses (e.g., cough, 21 chest pain, wheeze), together with judgments as to the potential impact on individuals 22 experiencing varying degrees of severity of these responses, that have been used in 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 137 previous NAAQS reviews. These ranges of pulmonary responses and their associated 1 potential impacts are summarized in Tables 3

- 2 and 3

- 3 of the 2007 Staff Paper. 2 For active healthy people, moderate levels of functional responses (e.g., FEV 1 3 decrements of > 10 percent but < 20 percent , lasting u p to 24 hours) and/or moderate 4 sy mptomatic responses (e.g., frequent spontaneous cough, marked discomfort on exercise 5 or deep breath, lasting up to 24 hours) would likely interfere with normal activity for 6 relativel y few responsive individuals. On the oth er hand, EPA staff determined that large 7 functional responses (e.g., FEV 1 decrements > 20 percent , lasting longer than 24 hours) 8 and/or severe s ymptomatic responses (e.g., persistent uncontrollable cough, severe 9 discomfort on exercise or deep breath, lasting longer than 24 hours) would likely interfere 10 with normal activities for many responsive individuals. EPA staff determined that these 11 would be considered adverse under ATS guidelines. In the context of standard setting, 12 CASAC indicated that a focus on the mid to upper end of the range of moderate levels of 13 functional responses (e.g., FEV 1 decrements  15 percent but < 20 percent) is appropriate 14 for estimating potentiall y adverse lung function decrements in active healthy people. 15 However, for people with lung disease, even moderate functional (e.g., FEV 1 decrements 16
> 10 percent but < 20 percent , lasting up to 24 hours) or s ymptomatic responses (e.g., 17 frequent spontaneous cough, marked discomfort on exercise or with deep breath, wheeze 18 accompanied b y shortness of breath, lasting up to 24 hours) would likely interfere with 19 normal activity

for many individuals, and would likely result in more frequent use of 20 medication. For people with lung disease, large functional responses (e.g., FEV 1 21 decrements > 20 per cent, lasting longer than 24 hours) and/or severe s ymptomatic 22 responses (e.g., persistent uncontrollable cough, severe discomfort on exercise or deep 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 138 breath, persistent wheeze accompanied b y shortness of breath, lasting longer than 24 1 hours) would likely

interfere with normal activity for most individuals and would 2 increase the likelihood that these individuals would seek medical treatment. In the 3 context of standard setting, the CASAC indicated (Henderson, 2006c) that a focus on the 4 lower end of the range of moderate levels of functional responses (e.g., FEV 1 decrements 5  10 percent) is most appropriate for estimating potentially adverse lung function 6 decrements in people with lung disease. 7 In judging the extent to which these impacts represent effects th at should be 8 regarded as adverse to the health status of individuals, an additional factor that has been 9 considered in previous NAAQS reviews is whether such effects are experienced 10 repeatedly

during the course of a year or onl y on a single occasion. Whil e some experts 11 would judge single occurrences of moderate responses to be a “nuisance,” especially for 12 healthy

individuals, a more general consensus view of the adversity of such moderate 13 responses emerges as the frequency of occurrence increases. 14 The new guidance builds upon and expands the 1985 definition of adversity in 15 several way s. There is an increased focus on quality of life measures as indicators of 16 adversity. There is also a more specific consideration of population risk. Exposure to air 17 pollution that increases the risk of an adverse effect to the entire population is adverse, 18 even though it may not increase the risk of any individual to an unacceptable level. For 19 example, a population of asthmatics could have a distribution of lung function such that 20 no individual has a level associated with significant impairment. Exposure to air 21 pollution could shift the distribution to lower levels that still do not bring any individual 22 to a level that is associated with clinically r elevant effects. However, this would be 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 139 considered to be adverse because individuals within the population would have 1 diminished reserve function, and therefore would be at increased risk if affected b y 2 another agent. 3 Of the various effects of O 3 expos ure that have been studied, many would meet 4 the ATS definition of adversity . Such effects include, for example, any detectible level 5 of permanent lung function loss attributable to air pollution, including both reductions in 6 lung growth or acceleration of the age

- related decline of lung function; exacerbations of 7 disease in individuals with chronic cardiopulmonary diseases; reversible loss of lung 8 function in combination with the presence of s ymptoms; as well as more serious effects 9 such as those requiring medical care including hospitalization and, obviously , mortality. 10 d. Size of At

-Risk Populations 11 Although O 3 - related health risk estimates may appear to be small, their 12 significance from an overall public health perspective is determined by the large numbers 13 of individuals in the population groups potentially at - risk for O 3 - related health effects 14 discussed above

. For example, a population of concern includes people with respiratory 15 disease, which includes approximately 11 percent of U.S. adults and 13 percent of 16 children who hav e been diagnosed with asthma and 6 percent of adults with chronic 17 obstructive pulmonary disease (chronic bronchitis and/or emphy sema) in 2002 and 2003 18 (Table 8

- 4 in the 2006 Criteria Document, section 8.7.5.2). More broadly , i ndiv iduals 19 with preexisting cardiopulmonary disease may constitute an additional population of 20
concern , with potentially tens of millions of people included in each disease category

. In 21 addition, populations based on age group also comprise substantial segments of the 22 population that may be potentially

at risk for O 3 - related health impacts. Based on U.S. 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 140 census data from 2003, about 26 percent of the U.S. population are under 18 years of age 1 and 12 percent are 65 ye ars of age or older. Hence, large proportio ns of the U.S. 2 population are included in life stages that are most likely to have increased susceptibility 3 to the health effects of O 3 and or those with the highest ambient O 3 exposure s . 4 The 2006 Criteria Document (section 8.7.5.2) notes that the health statistics data 5 illustrate what is known as the “p yr amid” of effects. At the top of the py ramid, there are 6 approximately

2.5 millions deaths from all causes per year in the U.S. population, with 7 about 100,000 deaths from chronic lower respiratory diseases . For respiratory health 8 diseases, there are nearl y 4 million hospital discharges per ye ar , 14 million emergency 9 department visits, 112 million ambulatory care visits, and an estimated 700 million 10 restricted activity

day s per year due to respiratory condi tions from all causes per ye ar . 11 Applying small risk estimates for the O 3 - related contribution to such health effects with 12 relativel y large baseline levels of health outcomes can result in quite large public health 13 impacts related to ambient O 3 exposure. Thus, even a small percentage reduction in O 3 14 health impacts on cardiopulmonary diseases would reflect a large number of avoided 15
cases. In considering this information together with the concentration

- response 16 relationship s that have been observed between exposure to O 3 and various health 17 endpoints, the 2006 Criteria Document (section 8.7.5.2) concludes that e xposure to 18 ambient O 3 likely

has a significant impact on public health in the U.S. 19 B. Human Exposure and Health Risk Assessments 20 To put judgments about health effects that are adverse for individuals into a 21 broader public health context, EPA has developed and applied models to estimate human 22 exposures and health risks. This broader context includes consideration of the size of 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 141 particular population groups at risk for various effects, the likelihood that exposures of 1 concern will occur for individuals in such groups under varying air quality scenarios, 2 estimates of the number of people likel y to experience O 3 - related effects, the variability 3 in estimate d exposures and risks, and the kind and degree of uncertainties inherent in 4 assessing the exposures and risks involved. 5 As discussed below there are a number of important uncertainties that affect the 6 exposure and health risk estimates. It is also impo rtant to note that there have been 7 significant improvements in both the exposure and health risk model. CASAC expressed 8 the view that the exposure anal ys is represents a state

- of

- the

- art modeling approach and 9 that the health risk assessment was “well done, balanced and reasonabl y communicated 10 (Henderson, 2006c). While recognizing and considering the kind and degree of 11 uncertainties in both the exposure and health risk estimates, the 2007 Staff Paper (pp. 6
- 12 20 to 6
- 21) judged that the quality of the estimat es is such that they are suitable to be 13 used as an input to the Administrator’s decisions on the O 3 primary standard. 14 In modeling exposures and health risks associated with just meeting the current 15 and alternative O 3 standards, EPA has simulated air quali ty to represent conditions just 16 meeting these standards based on O 3 air quality patterns in several recent years and on 17 how the shape of the O 3 air quality distribution have changed over time based on 18 historical trends in monitored O 3 air quality data. As described in the 2007 Staff Paper 19 ( EPA, 2007b, section 4.5.8) and discussed below, recent O 3 air quality distributions have 20 been statistically

adjusted to simulate just meeting the current and selected alternative 21 standards. These simulations do not refl ect any consideration of specific control 22 programs or strategies designed to achieve the reductions in emissions required to meet 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 142 the specified standards. Further, these simulations do not represent predictions of when, 1 whether, or how areas might meet th e specified standards. 27 2 As noted in section I.C above, around the time of the release of the final 2007 3 Staff Paper in January 2007, EPA discovered a small error in the exposure model that 4 when corrected resulted in slight increases in the simulated exp osures. Since the 5 exposure estimates are an input to the lung function portion of the health risk assessment, 6 this correction also resulted in slight increases in the lung function risk estimates as well. 7 The exposure and risk estimates discussed in this notice reflect the corrected estimates, 8 and thus are slightly different than the exposure and risk estimates cited in the January 9 31, 2007 Staff Paper. 28 10 1. Exposure Analy ses 11
a. Overview 12 As part of the 2008 rulemaking, the EPA conducted exposure anal ys es using a 13 simulation model to estimate O 3 exposures for the general population, school age 14 children (ages 5

- 18), and school age children with asthma living in 12 U.S. metropolitan 15 areas representing different regions of the country where the then current 8

- h our O 3 16 standard is not met. The emphasis on children reflects the finding of the 1997 O 3 17 NAAQS review that children are an important at

- risk group. The 12 modeled areas 18 combined represent a significant fraction of the U.S. urban population, 89 million pe ople, 19

27 Modeling that projects whether and how areas might attain alternative standards in a future ye ar is presented in the Regulatory Impact Anal ys is 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 list ed in the Availability of Related Information section of this notice.Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 143 including 18 million school age children of whom approximately 2.6 million have 1 asthma. The selection of urban areas to include in the exposure anal ys is took into 2 consideration the location of O 3 epidemiological studies, the availability of ambient O 3 3 data, and the desire to represent a range of geographic areas, population demographics, 4 and O 3 climatology . These selection criteria are discussed further in chapter 5 of the 5 2007 Staff Paper (EPA, 2007b) . The geographic extent of each modeled area co nsists of 6 the census tracts in the combined statistical area (CSA) as defined b y OMB (OMB, 7 2005). 29 8 Exposure estimates were developed using a probabilistic exposure model that is 9 designed to explicitly model the numerous sources of variability that affec t people’s 10 exposures. As discussed below, the model estimates population exposures by simulating 11 human activity

patterns, air conditioning prevalence, air exchange rates, and other 12 factors. The modeled exposure estimates were developed for three recent years of 13 ambient O 3 concentrations (2002, 2003, and 2004), as well as for O 3 concentrations 14 adjusted to simulate conditions associated with just meeting the then current NAAQS and 15 various alternative 8

- hour standards based on the three year period 2002

- 2004
. 30 This 16 exposure assessment is more fully described and presented in the 2007 Staff Paper and in 17 a technical support document, Ozone Population Exposure Analysis for Selected Urban 18
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

- Ely

ria, OH; Detroit

- Warren
- Flint, MI ; Houston
- Bayt own - Huntsville, TX; L os Angeles

- Long Beach

- Riverside, CA; New York

- Newark

- Bridgeport, NY

-NJ
CT
- PA; Philadelphia

- Camden

- Vineland, PA

-NJ
- DE
- MD; Sacramento
-- Arden

- Arcade

-- Truckee, CA

-NV; St. Louis

- St. Charles

- Farmington , MO
- IL; Washington

- Baltimore

-N. Virginia, DC

- MD
- VA
- WV

30 All 12 of the CSAs modeled did not meet the 0.084 ppm O 3 NAAQS for the three ye ar period examined.Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 144 Areas (EPA, 2007c ; hereafter Exposure Analy sis TSD). The scope and methodology for 1 this exposure assessment were developed over the last few ye ars with considerable input 2 from the CASAC Ozone Panel and the public. 31 3 The goals of the O 3 exposure assessment were: (1) to provide estimates of the size 4 of at

- risk populations exposed to various levels associated with recent O 3 concentrations, 5 and with just meeting the current O 3 NAAQS and alternative O 3 standards, in specific 6 urban areas; (2) to provide distributions of exposure estimates over the entire range of 7 ambient O 3 concentrations as an important input to the lung function risk assessment 8 summarized below in section II.B.2; (3) to develop a better understanding of the 9 influence of various inputs and assumptions on the exposure estimates; and (4) to gain 10 insight into the distrib ution of exposures and patterns of exposure reductions associated 11 with meeting alternative O 3 standards. 12 The EPA recognizes that there are many sources of variability and uncertainty 13 inherent in the inputs to this assessment and that there is uncertainty in the resulting O 3 14 exposure estimates. With respect to variability , the exposure modeling approach 15 accounts for variability in ambient O 3 levels, demographic characteristics, phy siological 16 attributes, activity

patterns, and factors affecting microenvironmental (e.g., indoor) 17 concentrations. In EPA’s judgment, the most important uncertainties affecting the 18

31 The general approach used in the human exposure assessment was described in the draft He alth Asse ssment 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 O 3 Panel on May

5, 2005. In October 2005, OAQPS released the first draft of the Staff Paper containing a chapter discussing the exposure anal ys es and first draft of the Exposure Analy ses 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 Anal ys es TSD for CASAC review and public comment which was held by the CASAC O 3 Panel on August 24

- 25, 2006.Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 145 exposure estimates are related to the modeling of human activity patterns over an O 3 1 season, the modeling of variations in ambient concentrations near roadways, and the 2 modeling of air exchange rates that affect the amount of O 3 that penetrates indoors. 3 Another important uncertainty that affects the estimation of how many exposures are 4 associated with moderate or greater exertion is the characterizati on of energy expenditure 5 for children engaged in various activities. As discussed in more detail in the 2007 Staff 6 Paper ( EPA, 2007b, section 4.3.4.7), the uncertainty in energy expenditure values carries 7 over to the uncertainty of the modeled breathing rates, which are important since they are 8 used to classify

exposures occurring at moderate or greater exertion which are the 9 relevant exposures since O 3 - related effects observe d in controlled human exposure 10 studies only

are observed when individuals are eng aged in some form of exercise. The 11 uncertainties in the exposure model inputs and the estimated exposures have been 12 assessed using quantitative uncertainty and sensitivity

anal ys es. Details are discussed in 13 the 2007 Staff Paper (section 4.6) and in a te chnical memorandum describing the 14 exposure modeling uncertainty analy sis (Langstaff, 2007). 15 b. Scope and Key Components 16 Population exposures to O 3 are primaril y driven by ambient outdoor 17 concentrations, which vary by time of day , location, and peoples’ ac tivities. Outdoor O 3 18 concentration estimates used in the exposure assessment are provided b y m easurements 19 and statistical adjustments to the measured concentrations. The current exposure anal ys is 20 allows comparisons of population exposures to O 3 within each urban area, associated 21 with current O 3 levels and with O 3 levels just meeting several potential alternative air 22 quality

standards or scenarios. Human exposure, regardless of the pollutant, depends on 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 146 where individuals are located and what they are doing. Inhalation exposure models are 1 useful in realisticall y estimating personal exposures to O 3 based on activity

- specific 2 breathing rates, particularly when recognizing that large scale population exposure 3 measurement studies have not been conducted that a re representative of the overall 4 population or at risk subpopulations. 5 The model EPA used to simulate O 3 population exposure is the Air Pollutants 6 Exposure Model (APEX), the human inhalation exposure model within the Total Risk 7 Integrated Methodology (TRIM) framework (EPA, 2006c,d). APEX is conceptuall y 8 based on the probabilistic NAAQS exposure model for O 3 (pNEM/O 3 ) used in the last O 3 9 NAAQS review. Since that time the model has been restructured, improved, and 10 expanded to reflect conceptual advances in the science of exposure modeling and newer 11 input data available for the model. Key improvements to algorithms include replacement 12 of the cohort approach with a probabilistic sampling approach focused on individuals, 13 accounting for fatigue and ox ygen debt after exercise in the calculation of breathing rates, 14 and a new approach for construction of longitudinal activity patterns for simulated 15 persons. Major improvements to data input to the model include updated air exchange 16 rates, more recent census and co mmuting data, and a greatl y expanded daily time

17 activities database. 18 APEX is a probabilistic model designed to explicitly model the numerous sources 19 of variability

that affect people’s exposures. APEX simulates the movement of 20 individuals through time and space and estimates their exposures to O 3 in indoor, 21 outdoor, and in

- vehicle microenvironments. The exposure model takes into account the 22 most significant factors contributing to total human O 3 exposure, including the temporal 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 147 and spatial distribution of people and O 3 concentrations throughout an urban area, the 1 variation of O 3 levels within each microenvironment, and the effects of exertion on 2 breathing rate in exposed individuals. A more detailed description of APEX and its 3 application is presented in chapter 4 of the 2007 Staff Paper and associated technical 4 documents (EPA, 2006b,c,d). 5 Several methods have been used to evaluate the APEX model and to characterize 6 the uncertainty of the model estimates. These include conducting model evaluation, 7
sens itivity

anal ys es, and a detailed uncertainty analysis for one urban area. These are 8 discussed fully

in the 2007 Staff Paper (section 4.6) and in Langstaff (2007). The 9 uncertainty of model structure was judged to be of lesser importance than the 10 uncertainties of the model inputs and parameters. Model structure refers to the 11 algorithms in APEX designed to simulate the processes that result in people’s exposures, 12 for example, the way that APEX models exposures to individuals when they are near 13 roads. The uncertainties in the model input data (e.g., measurement error, ambient 14 concentrations, air exchange rates, and activity pattern data) have been assessed 15 individually, and their impact on the uncertainty in the modeled exposure estimates was 16 assessed in a unified quantitative analy sis with results expressed in the form of estimated 17 confidence ranges around the estimated measures of exposure. This uncertainty anal ys is 18 was conducted for one urban area (Boston) using the observed 2002 O 3 concentrations 19 and 200 2 concentrations adjusted to simulate just meeting the current standard, with the 20 expectation that the results would be similar for other cities and ye ars. One significant 21 source of uncertainty , due to limitations in the database used to model peoples’ daily 22 activities, was not included in the unified anal ys is, and was assessed through separate 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 148 sensitivity

anal ys es. This analy sis indicates that the uncertainty of the exposure results is 1 relativel y small. For example, 95 percent uncertainty intervals were calculated for the 2 APEX estimates of the percent of children or asthmatic children with exposures above 3 0.060, 0.070, or 0.080 ppm under moderate exertion, for two air quality scenarios 4 (current 2002 and 2002 adjusted to simulate just meeting the current standard) in Boston 5 ( Langstaff, 2007 , Tables 26 and 27 ). The 95 percent uncertainty intervals for this set of 6 12 exposure estimates indicate the possibility of underpredictions of the exposure 7 estimates ranging from 3 to 25 percent of the modeled estimate s, and overpredictions 8 ranging from 4 to 11 percent of the estimates. For example, APEX estimates the percent 9 of asthmatic children with exposures above 0.070 ppm under moderate exertion to be 24 10 percent, for Boston 2002 O 3 concentrations adjusted to simulate just meeting the current 11 standard. The 95 percent uncertainty interval for this estimate is 23 − 30 percent, or
- 4 to 12 +25 percent of the estimate. These uncertainty intervals do not include the uncertainty 13 engendered b y limitations of the activity d atabase, which is in the range of one to ten 14 percent. 15 The exposure periods modeled here are the O 3 seasons in 2002, 2003, and 2004. 16 The O 3 season in each area includes the period of the year where elevated O 3 levels tend 17 to be observed and for which routine hourl y O 3 monitoring data are available. Ty pically 18 this period spans from March or April through September or October, or in some areas, 19 spanning the entire ye ar. Three ye ars were modeled to reflect the substantial year - to - year 20 variability

that occurs in O 3 levels and related meteorological conditions, and because the 21 standard is specified in terms of a three

- ye ar period. The year- to - ye ar variability 22 observed in O 3 levels is due to a combination of different weather patterns and the 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 149 variation in emiss ions of O 3 precursors. Nationally , 2002 was a relativel y high ye ar with 1 respect to the 4 th highest daily maximum 8

- hour O 3 levels observed in urban areas across 2 the U.S. (EPA, 2007 b , Figure 2

- 16), with the mean of the distribution of O 3 levels for the 3 urb an monitors being in the upper third among the years 1990 through 2006. In contrast, 4 on a national basis, 2004 is the lowest year on record through 2006 for this same air 5 quality

statistic, and 8

- hour daily maximum O 3 levels observed in most, but not all of the 6 12 urban areas included in the exposure and risk analy ses were relatively low compared 7 to other recent years. The 4 th highest daily maximum 8

- hour O 3 levels observed in 2003 8 in the 12 urban areas and nationally generall y were between those observed in 2002 and 9 2004. 10 Regulatory

scenarios examined in the 2008 rulemaking include the then current 11 0.08 ppm, average of the 4th daily maximum 8

- hour averages over a three year period 12 standard; standards with the same form but with alternative levels of 0.080 , 0.074, 0.070, 13 and 0.064 ppm; standards specified as the average of the 3rd highest dail y maximum 8

- 14 hour averages over a three year period with alternative levels of 0.084 and 0.074 ppm; 15 and a standard specified as the average of the 5th highest dail y max imum 8

- hour averages 16 over a three ye ar period with a level of 0.074 ppm. 32 The then current standard used a 17 rounding convention that allows areas to have an average of the 4th dail y m aximum 8

- 18 hour averages as high as 0.084 ppm and still meet the standard. All alternative standards 19

32 The 8

- hour O 3 standard established in 1997 was 0.08 ppm, but the rounding convention specified that the average of the 4 th daily maximum 8

- hour average concentr ations over a three

- ye ar period must be at 0.084 ppm or lower to be in attainment of this standard. When EPA staff selected alternative standards to anal yz e, 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 O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 150 anal yz ed were intended to reflect improved precision in the measurement of ambient 1 concentrations (in ppm) , where the precision would extend to three instead of two 2 decimal places. 3 The then current standard and all alternative standards were modeled using a 4 quadratic rollback approach to adjust the hourly concentrations observed in 2002

- 2004 to 5 yi eld a design value 33 corresponding to the standard being anal yz ed. The quadratic 6 rollback technique reduces higher concentrations more than lower concentrations near 7 ambient background levels. 34 This procedure was considered in a sensitivity anal ys is in 8 the 1997 review of the O 3 standard and has been shown to be more realistic than a linear, 9 proportional rollback method, where all of th e ambient concentrations are reduced b y the 10 same factor. 11

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 O 3 NAAQS, the 3

- year average of the annual 4 th

- highest dail y maximum 8

- h our average concentrations, based on the monitor within (or downwind of) an urban area yielding the highest 3

- ye ar 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 O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 1 51 c. Exposure Estimates and Key Observations 1 The exposure assessment, which provides estimates of the number of people 2 exposed to different levels of ambient O 3 while at specified exertion levels, 35 serve two 3 purposes. First, the entire range of modeled personal exposures to ambient O 3 is an 4 essential input to the portion of the health risk assessment based on exposure

- response 5 functions from controlled human exposure studies, discussed in the next sec tion. Second, 6 estimates of personal exposures to ambient O 3 concentrations at and above specific 7 benchmark levels provide some perspective on the public health impacts of health effects 8 that cannot currentl y be evaluate d in quantitative risk assessments that may occur at 9 current air quality

levels, and the extent to which such impacts might be reduced by 10 meeting the current and alternative standards. This is especially true when there are 11 exposure levels at which it is known or can reasonably be inferred that specific O 3 - related 12 health effects are occurring. In this notice, exposures at and above these benchmark 13 concentrations are refer red to as “exposures of concern.” 14 It is important to note that although the anal ys is of “exposures of concern” was 15 condu cted using three discrete benchmark levels (i.e., 0.080, 0.070, and 0.060 ppm), the 16 concept is more appropriately viewed as a continuum with greater confidence and less 17

35 As discussed above in Section II.A, O 3 health responses observed in controlled human exposure s tudies 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 b y an equivalent ventilation rate (EVR), ventilation normalized by body surface area (BSA, in m2 ), which is calculated as VE/BSA, where VE is the ventilation rate (liters/minute). Moderate and greater exertion levels were defined as EVR > 13 liters/min

- m2 (Whitfield et al., 1996) to c orrespond to the exertion levels measured in most subjects studied in the controlled human exposure studies that reported health effects associated with 6.6 hour O 3 exposures.Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 152 uncertainty about the existence of health effects at the upper end and less confidence and 1 greater uncertainty

as one considers increasingl y l ower O 3 exposure levels. The EPA 2 recognizes that there is no sharp breakpoint within the continuum ranging from at and 3 above 0.080 ppm down to 0.060 ppm. In considering the concept of exposures of 4
co ncern, it is important to balance concerns about the potential for health effects and their 5 severity with the increasing uncertainty associated with our understanding of the 6 likelihood of such effects at lower O 3 levels. 7 Within the context of this continuum, estimates of exposures of concern at 8 discrete benchmark levels provide some perspective on the public health impacts of O 3 - 9 related health effects that have been demonstrated in controlled human exposure and 10 toxicological studies but cannot be evaluated in quantitative risk assessments, such as 11 lung inflammation, increased airway responsiveness, and changes in host defenses. They 12 also help in understanding the extent to which such impacts have the potential to be 13 reduced b y m eeting the current and alt ernative standards. In the selection of specific 14 benchmark concentrations for this anal ys is, staff first considered the exposure level of 15 0.080 ppm, at which there is a substantial amount of controlled human exposure evidence 16 demonstrating a range of O 3 - related health effects including lung inflammation and 17 airway

responsiveness in healthy individuals. Thus, as in the 1997 review, this level was 18 selected as a benchmark level for this assessment of exposures of concern. Evidence 19 newly

available in this re view is the basis for identifying additional, lower benchmark 20 levels of 0.070 and 0.060 ppm for this assessment. 21 More specificall y, as discussed above in section II.A.2, evidence available from 22 controlled human exposure and epidemiological studies indicat es that people with asthma 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 153 have larger and more serious effects than healthy i ndividuals, including lung function, 1 respiratory

s ymptoms, increased airway responsiveness, and pulmonary inflammation, 2 which has been shown to be a more sensitive marker than lung function responses. 3 Further, a substantial new body of evidence from epidemiological studies shows 4 associations with serious respiratory morbidity and cardiopulmonary mortality effects at 5 O 3 levels that extend below 0.080 ppm. Additional, but very lim ited new evidence from 6 controlled human exposure studies shows lung function decrements and respiratory 7 sy mptoms in healthy

subjects at an O 3 exposure level of 0.060 ppm. The selected 8 benchmark level of 0.070 ppm reflects the new information that asthmati cs have larger 9 and more serious effects than healthy people and therefore controlled human exposure 10 studies done with healthy subjects may underestimate effects in this group, as well as the 11 substantial body

of epidemiological evidence of associations with O 3 levels below 0.080 12 ppm. The selected benchmark level of 0.060 ppm additionally reflects the very

limited 13 new evidence from controlled human exposure studies that show lung function 14 decrements and respiratory s ymptoms in some healthy subjects at the 0. 060 ppm 15 exposure level, recognizing that asthmatics are likely to have more serious responses and 16 that lung function is not likely to be as sensitive a marker for O 3 effects as is lung 17 inflammation. 18 The estimates of exposures of concern were reported in t erms of both “people 19 exposed” (the number and percent of people who experience a given level of O 3 20 concentrations, or higher, at least one time during the O 3 season in a given year) and 21 “occurrences of exposure” (the number of times a given level of pollution is experienced 22 by the population of interest, expressed in terms of person

- day s of occurrences). 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 154 Estimating exposures of concern is important because it provides some indication of the 1 potential public health impacts of a range of O 3 - related health outcomes, such as lung 2 inflammation, increased airway responsiveness, and changes in host defenses. These 3 particular health effects have been demonstrated in controlled human exposure studies of 4 healthy

individuals to occur at levels as low as 0.080 ppm O 3 , but have not been 5 evaluated at lower levels in controlled human exposure studies. The EPA did not include 6 these effects in the quantitative risk assessment due to a lack of adequate information on 7 the exposure

- response relationships. 8 The 1997 O 3 NAAQS review estimated exposures associated with 1

- hour heav y 9 exertion, 1

- hour moderate exertion, and 8

- hour moderate exertion for children, outdoor 10 workers, and the general population. The EPA’s analy sis in the 1997 Staff Paper showed 11 that exposure estimates ba sed on the 8

- hour moderate exertion scenario for children 12 yi elded the largest number of children experiencing exposures at or above exposures of 13
concern. Consequently , EPA chose to focus on the 8

- hour moderate and greater exertion 14 exposures in all and asthmatic school age children in the current exposure assessment. 15 While outdoor workers and other adults who engage in moderate or greater exertion for 16 prolonged durations while outdoors during the day in areas experiencing elevated O 3 17 concentrations also are at risk for experiencing exposures associated with O 3 - related 18 health effects, EPA did not focus on quantitative estimates for these populations due to 19 the lack of information about the number of individuals who regularly work or exercise 20 outdoors. Thus, the exposure estimates presented here and in the 2007 Staff Paper are 21 most useful for making relative comparisons across alternative air quality scenarios and 22Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 155 do not represent the total exposures in all children or other groups within the general 1 populatio n associated with the air quality scenarios. 2 P opulation exposures to O 3 were estimated in 12 urban areas for 2002, 2003, and 3 2004 air quality , and also using O 3 concentrations adjusted to just meet the then current 4 and several alternative standards. The estimates of 8

- hour exposures of concern at and 5 above benchmark levels of 0.080, 0.070, and 0.060 ppm aggregated across all 12 areas 6 are shown in Table 1 for air quality scenarios just meeting the current and four alternative 7 8
- hour average standards

. 36 Ta ble 1 provides estimates of the number and percent of 8 school age children and asthmatic school age children exposed, with daily 8
- hour 9 maximum exposures at or above each O 3 benchmark level of exposures of concern, while 10 at intermittent moderate or greater exertion and based on O 3 concentrations observed in 11 2002 and 2004. Table 1 summarizes estimates for 2002 and 2004 because these years 12 reflect years that bracket relativel y higher and lower O 3 levels, with year 2003 generall y 13 containing O 3 levels in between when considering the 12 urban areas modeled. This 14 table also reports the percent change in the number of persons exposed when a given 15 alternative standard is compared with the then current standard. 16 Key

observations important in comparing exposure esti mates associated with just 17 meeting the current NAAQS and alternative standards under consideration include: 18 (1) As shown in Table 6

- 1 of the 2007 Staff Paper, the patterns of exposure in 19 terms of percentages of the population exceeding a given exposure l evel are very similar 20 for the general population and for asthmatic and all school age (5

- 18) children, although 21

36 The full range of quantitative exposure estimates associated with just meetin g the 0.084 ppm and alternative O 3 standards are presented in c hapter 4 and Appendix 4A of the 2007 Staff Paper.Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 156 children are about twice as likely to be exposed, based on the percent of the population 1 exposed, at any

given level. 2 (2) As shown in Table 1 below, the number and percentage of asthmatic and all 3 school

- age children aggregated across the 12 urban areas estimated to experience one or 4 more exposures of concern decline from simulations of just meeting the then current 5 0.084 ppm standard to simulati ons of alternative 8

- hour standards b y varying amounts 6 depending on the benchmark level, the population subgroup considered, and the year 7 chosen. For example, the estimated percentage of school age children experiencing one 8 or more exposures ≥ 0.070 ppm, while engaged in moderate or greater exertion, during an 9 O 3 season is about 18 percent of this population when the 0.084 ppm standard is met 10 using the 2002 simulation; this is reduced to about 12, 4, 1, and 0.2 percent of children 11 upon meeting alternative s tandards of 0.080, 0.074, 0.070, and 0.064 ppm, respectivel y 12 (all specified in terms of the 4 th highest daily maximum 8

- hour average), using the 2002 13 simulation. 14 15Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 157 Table 1. Number and Percent of All and Asthmatic School Age Children in 12 1 Urban Areas Estim ated to Experience 8 - Hour Ozone Exposures Above 0.080, 0.070, 2 and 0.060 ppm While at Moderate or Greater Exertion, One or More Times Per 3 Season , and the Number of Occurrences Associated with Just Meeting Alternative 4 8 - Hour Standards Based on Adjusting 20 02 and 2004 Air Quality Data 1,2 5 Benchmark Levels of Exposures of Concern (ppm) 8
- Hour Air

Quality Standards 3 (ppm) All Children, ages 5

- 18

Aggregate for 12 urban areas Asthmatic Children, ages 5

- 18 Aggregate for 12 urban areas Number of Children Expose d (% 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%) 52 0,000 (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%] 0.07 4 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 Moderat e or greater exertion is defined as having an 8

- hour average equivalent ventilation rate > 13 l

- mi n/m2

. 6 2 Estimates are the aggregate results based on 12 combined statistical areas (Atlanta, Boston, Chicago, Cleveland, 7 Detroit, Houston, Los Angeles, New Yo rk, Philadelphia, Sacramento, St. Louis, and Washington, D.C.). Estimates 8 are for the ozone season which is all year in Houston, Los Angeles and Sacramento and March or April to 9 September or October for the remaining urban areas. 10 3 All standards summarize d here have the same form as the 8

- hour standard established in 1997 which is specified 11 as the 3

- year average of the annual 4 th highest daily maximum 8

- hour average concentrations must be at or below 12 the concentration level specified. As described in the 2007 Staff Paper ( EPA, 2007b, section 4.5.8), recent O 3 air 13 quality distributions have been statistically adjusted to simulate just meeting the 0.084 ppm standard and selected 14Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 158 alternative standards. These simulations do not represent predictions of when, whether, or how areas might meet 1 the specified standards. 2 3Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 159 (3) Substantial year- to - year variability in exposure estimates is observed over the 1 three

- ye ar modeling period. For example, the estimated number of school age children 2 experiencing one or more exposures  0.070 ppm during an O 3 season when a 0.084 ppm 3 standard is met in the 12 urban areas included in the anal ys is is 3.3, 1.0, or 0.3 million for 4 the 2002, 2003, and 2004 simulations, respectively. 5 (4) There is substantial variability observed ac ross the 12 urban areas in the 6 percent of the population subgroups estimated to experience exposures of concern. For 7 example, when 2002 O 3 concentrations are simulated to just meet a 0.084 ppm standard, 8 the aggregate 12 urban area estimate is 18 percent o f all school age children are estimated 9 to experience O 3 exposures  0.070 ppm (Table 1 below), while the range of exposure 10 estimates in the 12 urban areas considered separately for all children range from 1 to 38 11 percent (EPA, 2007 b , p. 4
- 48 , Exhibit 2 ). There was also variability in exposure 12 estimates among the modeled areas when using the 2004 air quality simulation for the 13 same scenario; however it was reduced and ranged from 0 to 7 percent in the 12 urban 14 areas (EPA, 2007 b , p. 4
- 60 , Exhibit 8 ). 15 (5) O f particular note, as discussed above in section II.A of this notice, high inter

16 individual variability in responsiveness means that only a subset of individuals in these 17 groups who are exposed at and above a given benchmark level would actually be 18 expecte d to experience such adverse health effects. 19 (6) In considering these observations, it is important to take into account the 20 variability , uncertainties, and limitations associated with this assessment, including the 21 degree of uncertainty associated with a number of model inputs and uncertainty in the 22 model itself, as discussed above. 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 160 2. Quantitative Health Risk Assessment 1 This section discusses the approach used to develop quantitative health risk 2 estimates associated with exposures to O 3 building upon a more limited risk assessment 3 that was conducted during the last review. 37 As part of the 1997 review, EPA conducted 4 a health risk assessment that produced risk estimates for the number and percent of 5 children and outdoor workers experiencing lung function and respiratory symptoms 6 associated with O 3 exposures for 9 urban areas. 38 The risk assessment for the 1997 7 review also included risk estimates for excess respiratory

- related hospital admissions 8 related to O 3 concentrations for New York City . In the last review, the risk estimates 9 played a significant role in both the staff recommendations and in the proposed and final 10 decisions to revise the O 3 standards. The health risk assessment conducted for the current 11 review builds upon the methodology and lessons learned from the prior review. 12
a. Overview 13 The updated health risk assessment conducted as part of the 2008 rulemaking 14 includes estimates of (1) risks of lung function decrements in all and asthmatic school age 15 children, respiratory s ymptoms in asthmatic c hildren, respiratory

- related hospital 16 admissions, and non

- accidental and cardiorespiratory

- related mortality associated with 17 recent ambient O 3 levels; (2) risk reductions and remaining risks associated with just 18 meeting the then current 0.084 ppm 8

- hour O 3 NAAQS; and (3) risk reductions and 19
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 anal ys es conducted during the last review were: Chicago, Denver, Houston, L os Angeles, Miami, New York City, Philadelphia, St. Louis, and Washington, D.C.Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 161 remaining risks associated with just meeting various alternative 8

- hour O 3 NAAQS in a 1 number of example urban areas. This risk assessment is more fully described and 2 presented in chapter 5 of the 2007 Staff Paper and in a technical support document 3 (TSD), Ozone Health Risk Assessment for Selected Urban Areas (Abt Associates, 2007a , 4 hereafter referred to as “Risk Assessment TSD”). The scope and methodology for this 5 risk assessment were developed over the last few years with considerable input from the 6 CASAC O 3 Panel and the public. 39 The information contained in these documents 7 included specific criteria for the selection of health endpoints, studies, and locations to 8 include in the assessment. In a peer review letter sent by CASAC to the Administrator 9 documenting its advice in October 2006 (Henderson, 2006c), the CASAC O 3 Panel 10 concluded that the risk assessment was “well done, balanced, and reasonably 11 communicated” and that the selection of health endpoints for inclusio n in the quantitative 12 risk assessment was appropriate. 13 The goals of the risk assessment are: (1) to provide estimates of the potential 14 magnitude of several morbidity effects and mortality

associated with current O 3 levels, 15 and with meeting the then current 0.084 ppm standard and alternative 8

- hour O 3 16 standards in specific urban areas; (2) to develop a better understanding of the influence of 17 various inputs and assumptions on the risk estimates; and (3) to gain insights into the 18

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 O 3 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 O 3 Panel on Augu st 24
- 25, 2006.Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 162 distribution of risks and patterns of risk reductions associated with meeting alternative O 3 1 standards. The health risk assessment is intended to be dependent on and reflect the 2 overall weight and nature of the health effects evidence discussed above in section II.A 3 and in more detail in the 2006 Criteria Document and 2007 Staff Paper. While not 4 independent of the overall evaluation of the health effects evidence, the quantitative 5 health risk assessment provides additional insights regarding the relative public health 6 implications associated with just meeting a 0.084 ppm standard and several alternative 8

- 7 hour standards. 8 The risk assessment covers a variety of health effects for which there is adequate 9 information to develop quantitative risk estimates. However, as noted b y C ASAC 10 (Henderson, 2007) and in the 2007 Staff Paper, there are a number of health endpoints 11 (e.g., increased lung inflammation, increased airway responsiveness, impaired host 12 defenses, increased medication usage for asthmatics, increased emergency department 13 vi sits for respiratory causes, and increased school absences) for which there currently is 14 insufficient information to develop quantitative risk estimates, but which are important to 15 consider in assessing the overall public health impacts associated with exp osures to O 3 . 16 These additional health endpoints are discussed above in section II.A.2 and are also taken 17 into account in considering the level of exposures of concern in populations particularl y 18 at risk, discussed above in this notice. 19 There are two part s to the health risk assessment: one based on combining 20 information from controlled human exposure studies with modeled population exposure 21 and the other based on combining information from community epidemiological studies 22 with either monitored or adjust ed ambient concentrations levels. Both parts of the risk 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 163 assessment were implemented within a new probabilistic version of TRIM.Risk, the 1 component of EPA’s Total Risk Integrated Methodology (TRIM) model framework that 2 estimates human health risks. 3 The E PA recognizes that there are many sources of uncertainty and variability in 4 the inputs to this assessment and that there is significant variability and uncertainty

in the 5 resulting O 3 risk estimates. As discussed in chapters 2, 5, and 6 of the 2007 Staff Paper, 6 there is significant ye ar- to - ye ar and city- to - city variability

related to the air quality

data 7 that affects both the controlled human exposure studies

- based and epidemiological 8 studies

- based parts of the risk assessment. There are also uncertaintie s associated with 9 the air quality

adjustment procedure used to simulate just meeting various alternative 10 standards. In the prior review, different statistical approaches using alternative functional 11 forms (i.e., quadratic, proportional, Weibull) were used to reflect how O 3 air quality 12 concentrations have historically changed. Based on sensitivity anal ys es conducted in the 13 prior review, the choice of alternative air quality adjustment procedures had only a 14 modest impact on the risk estimates (EPA, 2007 b , p . 6
- 20). With respect to uncertainties 15 about estimated background concentrations, as discussed below and in the 2007 Staff 16 Paper ( section 5.4.3), alternative assumptions about background levels have a variable 17 impact depending on the location, standard, and health endpoint anal yz ed. 18 With respect to the lung function part of the health risk assessment, key 19 uncertainties include uncertainties in the exposure estimates, discussed above, and 20 uncertainties associated with the shape of the exposure

- response r elationship, especiall y 21 at levels below 0.08 ppm, 8

- hour average, where only very limited data are available 22 down to 0.04 ppm and there is an absence of data below 0.04 ppm (EPA, 2007 b , pp.6
- 20 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 164 to 6
- 21). Concerning the part of the risk assessment based on effects reported in 1 epidemiological studies, important uncertainties include uncertainties (1) surrounding 2 estimates of the O 3 coefficients for concentration

- response relationships used in the 3 assessment, (2) involving the shape of the concentration

- respo nse relationship and 4 whether or not a population threshold or non

- linear relationship exists within the range of 5 concentrations examined in the studies, (3) related to the extent to which concentration

6 response relationships derived from studies in a given location and time when O 3 levels 7 were higher or behavior and /or housing conditions were different provide accurate 8 representations of the relationships for the same locations with lower air quality 9 distributions and/or different behavior and/or housing c onditions, and (4) concerning the 10 possible role of co

- pollutants which also may have varied between the time of the studies 11 and the current assessment period. An important additional uncertainty for the mortality 12 risk estimates is the extent to which the associations reported between O3 and non

13 accidental and cardiorespiratory mortality actuall y reflect causal relationships. 14 As discussed below, some of these uncertainties have been addressed 15 quantitatively

in the form of estimated confidence ranges around central risk estimates; 16 others are addressed through separate sensitivity analy ses (e.g., the influence of 17 alternative estimates for policy

- relevant background levels) or are characterized 18 qualitatively . For both parts of the health risk assessment, statistical uncertainty due to 19 sampling error has been characterized and is expressed in terms of 95 percent credible 20 intervals. The EPA recognizes that these credible intervals do not reflect all of the 21 uncertainties noted above. 22 b. Scope and Key Component s 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 165 The health risk assessment is based on the information evaluated in the 2006 1 Criteria Document. The risk assessment includes several categories of health effects and 2 estimates risks associated with just meeting a 0.084 ppm standard and alternative 8

- ho ur 3 O 3 NAAQS and with several individual recent years of air quality (i.e., 2002, 2003, and 4 2004). The risk assessment considers the same alternative air quality scenarios that were 5 examined in the human exposure analyses described above. Risk estimates w ere 6 developed for up to 12 urban areas selected to illustrate the public health impacts 7 associated with these air quality scenarios. 40 As discussed above in section II.B.1, the 8 selection of urban areas was largel y determined by identifying areas in the U.S . which 9 represented a range of geographic areas, population demographics, and climatology ; with 10 an emphasis on areas that did not meet the then current 0.084 ppm 8

- hour O 3 NAAQS 11 and which included the largest areas with O 3 nonattainment problems. The sele ction 12 criteria also included whether or not there were acceptable epidemiological studies 13 available that reported concentration

- response relationships for the health endpoints 14 selected for inclusion in the assessment. 15 The short

- term exposure related health endpoints selected for inclusion in the 16 quantitative risk assessment include those for which the 2006 Criteria Document or the 17 2007 Staff Paper concluded that the evidence as a whole supports the general conclusion 18 that O 3 , acting alone and/or in combination with other components in the ambient air 19

40 The 12 urban areas are the same urban areas evaluated in the exposure analy sis 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 O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 166 pollution mix, is either clearl y causal or is judged to be likely causal. Some health effects 1 met this criterion of likely causality , but were not included in the risk assessment for 2 other reasons, such as ins ufficient exposure

- response data or lack of baseline incidence 3 data. 4 As discussed in the section above describing the exposure analy sis, in order to 5 estimate the health risks associated with just meeting various alternative 8

- hour O 3 6 NAAQS, it is necessary t o estimate the distribution of hourly O 3 concentrations that 7 would occur under any gi ven standard. Since compliance is based on a 3

- year average, 8 the amount of control has been applied to each ye ar of data (i.e., 2002 to 2004) to 9 estimate risks for a s ingle O 3 season or single warm O 3 season, depending on the health 10 effect, based on a simulation that adjusted each of these individual years so that the three 11 ye ar period would just meet the specified standard. 12 Consistent with the risk assessment approa ch used in the last review, the risk 13 estimates developed for both recent air quality levels and just meeting the then current 14 0.084 ppm standard and selected alternative 8

- hour standards represent risks associated 15 with O 3 levels attributable to anthropogenic sources and activities (i.e., risk associated 16 with concentrations above “policy

- relevant background”). Policy

- relevant background 17 O 3 concentrations used in the O 3 risk assessment were defined in chapter 2 of the 2007 18 Staff Paper (pp. 2
- 48

– 2
- 55) as th e O 3 concentrations that would be observed in the U.S. 19 in the absence of anthropogenic emissions of precursors (e.g., VOC, NO x , and CO) in the 20 U.S., Canada, and Mexico. The results of a global tropospheric O 3 model (GEOS

21 CHEM) have been used to estimate m onthly background daily

diurnal profiles for each of 22 the 12 urban areas for each month of the O 3 season using meteorology for the year 2001. 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 167 Based on the results of the GEOS

- CHEM model, the Criteria Document indicates that 1 background O 3 concentrations are generall y predicted to be in the range of 0.015 to 0.035 2 ppm in the afternoon, and they are generally

lower under conditions conducive to man

3 made O 3 episodes. 41 4 This approach of estimating risks in excess of background is judged to be more 5 relevant to policy

decisions regarding ambient air quality standards than risk estimates 6 that include effects potentially attributable to uncontrollable background O 3 7 concentrations. Sensitivity analy ses examining the impact of alternative estimates for 8 background on lung function and mortality risk estimates have been developed and are 9 included in the 2007 Staff Paper and Risk Assessment TSD and key observations are 10 discussed below. Further, CASAC noted the difficulties and complexities associated 11 with available app roaches to estimating policy

- relevant background concentrations 12 (Henderson, 2007). 13 In the first part of the risk assessment, lung function decrement, as measured by 14 FEV 1 , is the only

health response that is based on data from controlled human exposure 15 studies. As discussed above, there is clear evidence of a causal relationship between lung 16 function decrements and O 3 exposures for school age children engaged in moderate 17 exertion based on numerous controlled human exposure and summer camp field studies 18
co nducted b y various investigators. Risk estimates have been developed for O 3 - related 19 lung function decrements (measured as changes in FEV 1 ) for all school age children 20

41 EPA notes that the estimated level of policy

- relevant backgro und O 3 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 O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 168 (ages 5 to 18) and a subset of this group, asthmatic school age children (ages 5 to 18), 1 whose average exertion over an 8

- hour period was moderate or greater. The exposure 2 period and exertion level were chosen to generall y match the exposure period and 3 exertion level used in the controlled human exposure studies that were the basis for the 4
e xposure - response relationships. A combined data set including individual level data 5 from the Folinsbee et al. (1988), Horstman et al. (1990), and McDonnell et al. (1991) 6 studies, used in the previous risk assessment, and more recent data from Adams (2002, 7 2003 a , 2006) have been used to estimate probabilistic exposure

- response relationships for 8 8
- hour exposures under different definitions of lung function response (i.e., ≥10, 15, and 9 20 percent decrements in FEV 1 ). As discussed in the 2007 Staff Paper (p.5
- 27), while 10 these specific controlled human exposure studies only included healthy

adults aged 18

- 11 35, findings from other controlled human exposure studies and summer camp field 12 studies involving school age children in at least six different locations in the northeastern 13 United States, Canada, and Southern California indicated changes in lung function in 14 healthy

children similar to those observed in healthy adults exposed to O 3 under 15 controlled chamber conditions. 16 Consistent with advice from CASAC (Henderson, 2006c), EPA has considered 17 both linear and logistic functional forms in estimating the probabilistic exposure

- response 18 relationships for lung function responses. A Bayesian Markov Chain Monte Carlo 19 approach, described in more detail in the Risk Asse ssment TSD, has been used that 20 incorporates both model uncertainty and uncertainty due to sample size in the combined 21 data set that served as the basis for the assessment. The EPA has chosen a model 22 reflecting a 90 percent weighting on a logistic form and a 10 percent weighting on a 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 169 linear form as the base case for the risk assessment. The basis for this choice is that the 1 logistic form provides a very good fit to the combined data set, but a linear model cannot 2 be entirel y ruled out since there are onl y very limited data (i.e., 30 subjects) at the two 3 lowest exposure levels (i.e., 0.040 and 0.060 ppm). The EPA has conducted a sensitivity 4 anal ys is which examines the impact on the lung function risk estimates of two alternative 5 choices, an 80 percent logis tic/20 percent linear split and a 50 percent logistic/50 percent 6 linear split. 7 As noted above, risk estimates have been developed for three measures of lung 8 function response (i.e., ≥10, 15, and 20 percent decrements in FEV 1 ). However, the 2007 9 Staff Pap er and risk estimates summarized below focus on FEV 1 decrements ≥15 percent 10 for all school age children and ≥10 percent for asthmatic school age children, consistent 11 with the advice from CASAC (Henderson, 2006c) that these levels of response represent 12 indi cators of adverse health effects in these populations. The Risk Assessment TSD and 13 2007 Staff Paper present the broader range of risk estimates including all three measures 14 of lung function response. 15 Developing risk estimates for lung function decrement s involved combining 16 probabilistic exposure

- response relationships based on the combined data set from 17 several controlled human exposure studies with population exposure distributions for all 18 and asthmatic school age children associated with recent air quality and air quality 19 simulated to just meet the then current 0.084 ppm standard and alternative 8

- hour O 3 20 NAAQS based on the results from the exposure analy sis described in the previous 21 section. The risk estimates have been developed for 12 large urban areas for the O 3 22Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 170 season. 42 These 12 urban areas include approximately 18.3 million school age children, 1 of which 2.6 million are asthmatic school age children. 43 2 In addition to uncertainties arising from sample size considerations, which are 3 quantitatively

c haracterized and presented as 95 percentile credible intervals, there are 4 additional uncertainties and caveats associated with the lung function risk estimates. 5 These include uncertainties about the shape of the exposure

- response relationship, 6 particularl y at levels below 0.080 ppm, and about policy

- relevant background levels, for 7 which sensitivity

anal ys es have been conducted. Additional important caveats and 8 uncertainties concerning the lung function portion of the health risk assessment include: 9 (1) the uncertainties and limitations associated with the exposure estimates discussed 10 above and (2) the inability to account for some factors which are known to affect the 11 exposure - response relationships (e.g., assigning healthy and asthmatic children the same 12 responses as observed in healthy adult subjects and not adjusting response rates to reflect 13 the increase and attenuation of responses that have been observed in studies of lung 14 function responses upon repeated exposures). A more complete discussion of 15
a ssumptions and uncertainties is contained in chapter 5 of the 2007 Staff Paper and in the 16 Risk Assessment TSD

. 17 The second part of the risk assessment is based on health effects observed in 18 epidemiological studies. Based on a review of the evidence evaluated in the 2006 19

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 O 3 season is defined as a period running from March o r April to September or October. In 3 of the urban areas (Houston, L os Angeles, and Sacramento), the O 3 season is defined as the entire year.Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 171 Criteria Document and 2007 Staff Paper, as well as the criteria discussed in chapter 5 of 1 the 2007 Staff Paper, the following categories of health endpoints associated with short

2 term exposures to ambient O 3 concentrations were included in the risk assessment: 3 respiratory

s ymptoms in moderate to severe asthmatic children, hospital admissions for 4 respiratory

causes, and non

- accidental and cardiorespiratory mortality. As discussed 5 above, there is strong evidence of a causal relationship for the respiratory morbidity 6 endpoints included in the risk assessment. With respect to nonaccidental and 7 cardiorespiratory

mortality , the 2006 Criteria Document concludes that there is strong 8 evidence which is highl y suggestive of a causal relationship between nonaccidental and 9 cardiorespiratory

- related mortality and O 3 exposures during the warm O 3 season. As 10 discussed in the 2007 Staff Paper (chapter 5), EPA also recognizes that for some of the 11 effects observed in epidemiological studies, such as increase d respiratory

- related hospital 12 admissions and nonaccidental and cardiorespiratory mortality, O 3 may

be serving as an 13 indicator for reactive oxidant species in the overall photochemical oxidant mix and that 14 these other constituents may be responsible in who le or part for the observed effects. 15 Risk estimates for each health endpoint category were onl y developed for areas 16 that were the same or close to the location where at least one concentration

- response 17 function for the health endpoint had been estimated. 44 Thus, for respiratory sy mptoms in 18 moderate to severe asthmatic children onl y the Boston urban area was included and four 19 urban areas were included for respiratory

- related hospital admissions. Nonaccidental 20

44 The geographic boundaries for the urban areas included in this portion of the risk assessment were generall y 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 O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 172 mortality risk estimates were developed for 12 urban areas and 8 urban areas were 1 included for cardiorespiratory mortality

. 2 The concentration

- response relationships used in the assessment are based on 3 findings from human epidemiological studies that have relied on fixed

- site ambient 4 monitors as a surrogate for actual ambient O 3 exposures. In order to estimate the 5 incidence of a particular health effect associated with recent air quality in a specific 6 county

or set of counties attributable to ambient O 3 exposures in excess of background, as 7 well as the change in incidence corresponding to a given change in O 3 levels resulting 8 from just meeting various 8

- hour O 3 standards, three elements are required for this part of 9 the risk assessment. These elements are: (1) air quality information (including recent air 10 quality

data for O 3 from ambient monitors for the selected location, estimates of 11 background O 3 concentrations appropriate for that location, and a method for adjusting 12 the recent data to reflect patterns of air quality estimated to occur when the area just 13 meets a given O 3 standard); (2) relative risk

- based concentration

- response functions that 14 provide an estimate of the relationship between the health endpoints of interest and 15 ambient O 3 concentration; and (3) annual or seasonal baseline health eff ects incidence 16 rates and population data, which are needed to provide an estimate of the seasonal 17 baseline incidence of health effects in an area before any changes in O 3 air quality

. 18 A key

component in the portion of the risk assessment based on epidemio logical 19 studies is the set of concentration

- response functions which provide estimates of the 20 relationships between each health endpoint of interest and changes in ambient O 3 21 concentrations. Studies often report more than one estimated concentration

- respo nse 22 function for the same location and health endpoint. Sometimes models include different 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 173 sets of co

- pollutants and/or different lag periods between the ambient concentrations and 1 reported health responses. For some health endpoints, there are studies that estimated 2 multicity and single

- city O 3 concentration

- response functions. While the Risk 3 Assessment TSD and chapter 5 of the 2007 Staff Paper present a more comprehensive set 4 of risk estimates, EPA has focused on estimates based on multicity studies wh ere 5 available. As discussed in chapter 5 of the 2007 Staff Paper, the advantages of rel yi ng 6
more heavil y on concentration

- response functions based on multicity studies include: (1) 7 more precise effect estimates due to larger data sets, reducing the uncertainty around the 8 estimated coefficient; (2) greater consistency in data handling and model specification 9 that can eliminate city- to - city variation due to study

design; and (3) less likelihood of 10 publication bias or exclusion of reporting of negative or non significant findings. Where 11 studies reported different effect estimates for varying lag periods, consistent with the 12 2006 Criteria Document, single day lag periods of 0 to 1 day s were used for associations 13 with respiratory

hospital admissions and mortality. For mortality associated with 14 exposure to O 3 which may result over a several day period after exposure, distributed lag 15 models, which take into account the contribution to mortality effects over several days, 16 were used where available 17 One of the most important elements affecting uncertainties in the 18 epidemiological

- based portion of the risk assessment is the concentration

- response 19 relationships used in the assessment. The uncertainty resulting from the statistical 20 uncertainty associated with the estim ate of the O 3 coefficient in the concentration

21 response function was characterized either b y confidence intervals or b y Bayesian 22 credible intervals around the corresponding point estimates of risk. Confidence and 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 174 credible intervals express the range within which the true risk is likely to fall if the only 1 uncertainty surrounding the O 3 coefficient involved sampling error. Other uncertainties, 2 such as differences in study location, time period (i.e., the years in which the study was 3 conducted), and model uncertainties are not represented by the confidence or credible 4 intervals presented, but were addressed b y presenting estimates for different urban areas, 5 by including risk estimates based on studies using different time periods and models, 6 where available, and/or are discussed throughout section 5.3 of the 2007 Staff Paper. 7 Because O 3 effects observed in the epidemiological studies have been more clearly and 8 consistently

shown for warm season anal ys es, all anal ys es for this portion of the risk 9 assessment w ere carried out for the same time period, April through September. 10 The 2006 Criteria Document (p. 8

- 44) finds that no definitive conclusion can be 11 reached with regard to the existence of population thresholds in epidemiologic al studies

. 12 The EPA recogni zes, however, the possibility that thresholds for individuals may exist 13 for reported associations at fairl y low levels within the range of air quality observed in 14 the studies, but not be detectable as population thresholds in epidemiological anal ys es. 15 Bas ed on the 2006 Criteria Document’s conclusions, EPA judged and CASAC concurred, 16 that there is insufficient evidence to support use of potential population threshold levels 17 in the quantitative risk assessment. However, EPA recognizes that there is increasing 18 uncertainty about the concentration

- response relationship at lower concentrations which 19 is not captured b y the characterization of the statistical uncertainty due to sampling error. 20 Therefore, the risk estimates for respiratory s ymptoms in moderate to severe asthmatic 21 children, respiratory

- related hospital admissions, and premature mortality associated with 22Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 175 exposure to O 3 must be considered in light of uncertainties about whether or not these O 3 - 1 related effects occur in these populations at very low O 3 concentrations. 2 With respect to variability within this portion of the risk assessment, there is 3 variability

among concentration

- response functions describing the relation between O 3 4 and both respiratory

- related hospital admissions and nonaccidental and c ardiorespiratory 5 mortality

across urban areas. This variability is likely due to differences in population 6 (e.g., age distribution), population activities that affect exposure to O 3 (e.g., use of air 7 conditioning), levels and composition of co

- pollutants, baseline incidence rates, and/or 8 other factors that vary across urban areas. The risk assessment incorporates some of the 9 variability

in key inputs to the anal ys is by

using location

- specific inputs (e.g., location

10 specific concentration

- response function s, baseline incidence rates, and air quality data). 11 Although spatial variability in these key

inputs across all U.S. locations has not been fully 12 characterized, variability across the selected locations is imbedded in the analy sis by 13 using, to the extent possible, inputs specific to each urban area. 14
c. Risk Estimates and Key Observations 15 The 2007 Staff Paper (chapter 5) and Risk Assessment TSD present risk estimates 16 associated with just meeting the then current 0.084 ppm standard and several alternative 17 8
- hour standards, as well as three recent years of air quality as represented by

2002, 2003, 18 and 2004 monitoring data. As discussed in the exposure anal ys is section above, there is 19 considerable city

- to - city and year - to - ye ar variability in the O 3 levels during this period, 20 which results in significant variability in both portions of the health risk assessment. 21 In the 1997 risk assessment, risks for lung function decrements associated with 1

- 22 hour heav y exertion, 1

- hour moderate exertion, and 8

- hour moderat e exertion exposures 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 176 were estimated. Since the 8

- hour moderate exertion exposure scenario for children 1 clearl y resulted in the greatest health risks in terms of lung function decrements, EPA 2 chose to include onl y the 8

- hour moderate exertion exposures in the risk assessment for 3 this health endpoint. Thus, the risk estimates presented here and in the 2007 Staff Paper 4 are most useful for making relative comparisons across alternative air quality scenarios 5 and do not represent the total risks for lung functi on decrements in children or other 6 groups within the general population associated with any of the air quality

scenarios. 7 Thus, some outdoor workers and adults engaged in moderate exertion over multi

- hour 8 periods (e.g., 6

- 8 hour exposures) also would be e xpected to experience similar lung 9 function decrements. However, the percentage of each of these other subpopulations 10 expected to experience these effects is expected to be smaller than all school age children 11 who tend to spend more hours outdoors while active based on the exposure anal ys es 12 conducted during the prior review. 13 Table 2 presents a summary of the risk estimates for lung function decrements for 14 the 0.084 ppm standard set in 1997 and several alternative 8

- hour standard levels with the 15 same for

m. The estimates are for the aggregate number 16 17Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 177 Table 2. Number and Percent of All and Asthmatic School Age Children in Several 1 Urban Areas Estimated to Experience Moderate or Greater Lung Function 2 Responses One or More Times Per Season Associated with 8 - Hour Ozone Exposures 3 Associated with Just Meeting Alternative 8 - Hour Standards Based on Adjusting 4 2002 and 2004 Air Quality Data 1,2 5

6 1 Associ ated with exposures while engaged in moderate or greater exertion, which is defined as having an 8

- 7 hour average equivalent ventilation rate > 13 l

- mi n/m2

. 8 2 Estimates are the aggregate central tendency results based on either 12 urban areas (Atlanta, Boston , 9 Chicago, Cleveland, Detroit, Houston, Los Angeles, New York, Philadelphia, Sacramento, St. Louis, and 10 Washington, D.C.) or 5 urban areas (Atlanta, Chicago, Houston, Los Angeles, New York). Estimates are 11 for the O 3 season which is all year in Houston, Lo s Angeles and Sacramento and March or April to 12 September or October for the remaining urban areas. 13 3 All standards summarized here have the same form as the 8

- hour standard set in 1997, which is specified 14 as the 3

- year average of the annual 4 th highest dail y maximum 8

- hour average concentrations. As described 15 in the 2007 Staff Paper (section 4.5.8), recent O 3 air quality distributions have been statistically adjusted to 16 simulate just meeting the 0.084 ppm standard set in 1997 and selected alternative standards. These 17 simulations do not represent predictions of when, whether, or how areas might meet the specified standards 18 4NA (not available) indicates that EPA did not develop risk estimates for these scenarios for the asthmatic 19 school age children populatio n. 20 21 22 8
- Hour Air Quality Standards 3 All Children, ages 5

- 18

FEV 1 > 15 percent Aggregate for 12 urban areas Number of Children Affected (% of

all) [% reduction from 0.084 ppm

standard] Asthmatic Children, ages 5

- 18 FEV 1 > 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 % reduc tion] 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 O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 178 and percent of all school age children across 12 urban areas and the aggregate number 1 and percent of asthmatic school age children across 5 urban areas 45 who are estimated to 2 have at least 1 moderate or greater lung function response (defined as FEV 1 > 15 percent 3 in all children and > 10 percent in asthmatic children) associated with 8

- hour exposures 4 to O 3 while engaged in moderate or greater exertion on average over the 8

- hour period. 5 The lung function risk estimates summarized in Table 2 illustrate the year- to - ye ar 6 variability

in both remaining risk associated with a relativel y high ye ar (i.e., based on 7 adjusting 2002 O 3 air quality data) and relativel y l ow year (based on adjusting 2004 O 3 8 air quality

data) as well as the year- to - year variability in the risk reduction estimated to 9 occur associated with various alternative standards relative to just meeting the then 10 current 0.084 ppm standard. For example, it is estimated that about 610,000 school age 11 children (3.2 percent of school age children) would experience 1 or more moderate lung 12 function decrements for the 12 urban areas associated with O 3 levels just meeting a 0.084 13 ppm standard based on 2002 air quality data compared to 230,000 (1.2 percent of 14 children) associated with just meeting a 0.084 ppm standard based on 2004 air quality 15 data. 16 As discussed in the 2007 Staff Paper, a child may experience multiple 17 occurrences of a lung function response during the O 3 season. For example, upon 18 meeting a 0.084 ppm 8

- hour standard, the median estimates are that about 610,000 19 children would experience a moderate or greater lung function response 1 or more times 20

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, Chicag o, Houston, L os Angeles, and New York City

.Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 179 for the aggregate of the 12 urban areas over a single O 3 season (based on the 2002 1 simulation), and that there would be almost 3.2 million total occur rences. Thus, on 2 average it is estimated that there would be about 5 occurrences per O 3 season per 3 responding child for air quality just meeting a 0.084 ppm 8

- hour standard across the 12 4 urban areas. While the estimated number of occurrences per O 3 seaso n is lower when 5 based on the 2004 simulation than for the 2002 simulation, the estimated number of 6 occurrences per responding child is similar. The EPA recognizes that some children in 7 the population might have only 1 or 2 occurrences while others may have 6 or more 8 occurrences per O 3 season. Risk estimates based on adjusting 2003 air quality to 9 simulate just meeting the a 0.084 ppm standard and alternative 8

- hour standards are 10 intermediate to the estimates presented in Table 2 above in this notice and are presented 11 in the 2007 Staff Paper (chapter 5) and Risk Assessment TSD. 12 For just meeting a 0.084 ppm 8

- hour standard, Table 5

- 8 in the 2007 Staff Paper 13 shows that median estimates across the 12 urban areas for all school age children 14 experiencing 1 or more moderate lung function decrements ranges from 0.9 to 5.4 percent 15 based on the 2002 simulation and from 0.8 to 2.2 percent based on the 2004 simulation. 16 Risk estimates for each urban area included in the assessment, for each of the three ye ars 17 anal yz ed, and for additional alternative standards are presented in chapter 5 of the 2007 18 Staff Paper and in the Risk Assessment TSD. 19 For just meeting a 0.084 ppm 8

- hour standard, the median estimates across the 5 20 urban areas for asthmatic school age children ran ge from 3.4 to 10.9 percent based on the 21 2002 simulation and from 3.2 to 6.9 percent based on the 2004 simulation. 22Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 180 Key observations important in comparing estimated lung function risks associated 1 with just meeting the 0.084 ppm NAAQS and alternative standards under consideration 2 include: 3 (1) As discussed above, there is significant ye ar to year variability in the range of 4 median estimates of the number of school age children (ages 5

- 18) estimated to 5 experience at least one FEV 1 decrement  15 percent due to 8
- hour O 3 exposures across 6 the 12 urban areas anal yz ed, and similarly across the 5 urban areas anal yz ed for asthmatic 7 school age children (ages 5

- 18) estimated to experience at least one FEV 1 decrement > 10 8 percent, when various 8

- hour standards are ju st met. 9 (2) For asthmatic school age children, the median estimates of occurrences of 10 FEV 1 decrements > 10% range from 52,000 to nearly 510,000 responses associated with 11 just meeting a 0.084 ppm standard (based on the 2002 simulation) and range from 61,00 0 12 to about 240,000 occurrences (based on the 2004 simulation). These risk estimates 13 would be reduced to a range of 14,000 to about 275,000 occurrences (2002 simulation) 14 and to about 18,000 to nearly 125,000 occurrences (2004 simulation) upon just meeting 15 the most stringent alternative 8

- hour standard (0.064 ppm, 4 th highest). The average 16 number of occurrences per asthmatic child in an O 3 season ranged from about 6 to 11 17 associated with just meeting a 0.084 ppm standard (2002 simulation). The average 18 numb er of occurrences per asthmatic child ranged from 4 to 12 upon meeting the most 19 stringent alternative examined (0.064 ppm, 4th

- highest) based on the 2002 simulation. 20 The number of occurrences per asthmatic child is similar for the scenarios based on the 21 2 004 simulation. 22Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 181 As discussed above, several epidemiological studies have reported increased 1 respiratory

morbidity outcomes (e.g., respiratory symptoms in moderate to severe 2 asthmatic children, respiratory

- related hospital admissions) and increased nonacci dental 3 and cardiorespiratory mortality associated with exposure to ambient O 3 concentrations. 4 The results and key

observations from this portion of the risk assessment are presented 5 below: 6 (1) Estimates for increased respiratory s ymptoms (i.e., chest tightness, shortness 7 of breath, and wheeze) in moderate/severe asthmatic children (ages 0

- 12) were developed 8 for the Boston urban area only . The median estimated number of days involving chest 9 tightness (using the concentration

- response relationship with only O 3 in the model) is 10 about 6,100 (based on the 2002 simulation) and about 4,500 (based on the 2004 11 simulation) upon meeting a 0.084 ppm 8

- hour standard and this is reduced to about 4,600 12 day s (2002 simulation) and 3,100 day s (2004 simulation) upon meeting the most 13 stringent alternative examined (0.064 ppm, 4th

- highest dail y maximum 8

- hour average). 14 This corresponds to 11 percent (2002 simulation) and 8 percent (2004 simulation) of total 15 incidence of chest tightness upon meeting a 0.084 ppm 8

- hour standard and to about 8 16 percent (2002 simulation) and 5.5 percent (2004 simulation) of total incidence of chest 17 tightness upon meeting a 0.064 ppm, 4th

- highest daily maximum 8

- hour average 18 standard. Similar patterns of effects and reductions in effects are obs erved for each of the 19 respiratory

s ymptoms examined. 20 (2) The 2007 Staf f Paper and Risk Assessment TSD present unscheduled hospital 21 admission risk estimates for respiratory illness and asthma in New York City associated 22 with short

- term exposures to O 3 c oncentrations in excess of background levels from April 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 182 through September for several recent ye ars (2002, 2003, and 2004) and upon just meeting 1 a 0.084 ppm standard and alternative 8

- hour standards based on simulating O 3 levels 2 using 2002

- 2004 O 3 air quali ty data. For total respiratory illness, EPA estimates about 3 6.4 cases per 100,000 relevant population (2002 simulation) and about 4.6 cases per 4 100,000 relevant population (2004 simulation), which represents 1.5 percent (2002 5 simulation) and 1.0 percent ( 2004 simulation) of total incidence or about 510 cases (2002 6 simulation) and about 370 cases (2004 simulation) upon just meeting a 0.084 ppm 8

- hour 7 standard. For asthma

- related hospital admissions, which are a subset of total respiratory 8 illness admission s, the estimates are about 5.5 cases per 100,000 relevant population 9 (2002 simulation) and about 3.9 cases per 100,000 relevant population (2004 simulation), 10 which represents about 3.3 percent (2002 simulation) and 2.4 percent (2004 simulation) 11 of total in cidence or about 440 cases (2002) and about 310 cases (2004) for this same air 12 quality

scenario. 13 For increasingl y more stringent alternative 8

- hour standards, there is a gradual 14 reduction in respiratory illness cases per 100,000 relevant population from 6.4 cases per 15 100,000 upon just meeting a 0.084 ppm 8

- hour standard to 4.6 cases per 100,000 under 16 the most stringent 8

- hour standard (i.e., 0.064 ppm, average 4th

- highest daily maximum) 17 anal yz ed based on the 2002 simulation. Similarly , based on the 2004 simulation there is 18 a gradual reduction from 4.6 cases per 100,000 relevant population upon just meeting a 19 0.084 ppm 8
- hour standard to 3.0 cases per 100,000 under a 0.064 ppm, average 4 th

– 20 highest dail y maximum standard. 21 Additional respiratory

- related h ospital admission estimates for three other 22 locations are provided in the Risk Assessment TSD. The EPA notes that the 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 183 concentration

- response functions for each of these locations examined different outcomes 1 in different age groups (e.g., > age 30 in Los Angeles, >age 64 in Cleveland and Detroit, 2 vs. all ages in New York City), making comparison of the risk estimates across the areas 3 very difficult. 4 (3) Based on the median estimates for incidence for nonaccidental mortality 5 (based on the Bell et al. (2004 ) 95 cities concentration

- response function), meeting the 6 most stringent standard (0.064 ppm) is estimated to reduce mortality by 40 percent of 7 what it would be associated with just meeting a 0.084 ppm standard (based on the 2002 8 simulation). The patterns for cardiorespiratory mortality are similar. The aggregate O 3 - 9 related cardiorespiratory mortality upon just meeting the most stringent standard shown is 10 estimated to be about 42 percent of what it would be upon just meeting a 0.084 ppm 11 standard, using simulated O 3 concentrations that just meet a 0.084 ppm standard and 12 alternative 8

- hour standards based on the 2002 simulation. Using the 2004 simulation, 13 the corresponding reductions show a similar pattern but are somewhat greater. 14 (4) Much of the contrib ution to the risk estimates for non

- accidental and 15 cardiorespiratory

mortality upon just meeting a 0.084 ppm 8

- hour standard is associated 16 with 24

- hour O 3 concentrations between background and 0.040 ppm. Based on 17 examining relationships between 24

- hour co ncentrations averaged across the monitors 18 within an urban area and 8

- hour dail y maximum concentrations, 8

- hour daily maximum 19 levels at the highest monitor in an urban area associated with these averaged 24

- hour 20 levels are generally about twice as high as the 24

- hour levels. Thus, most O 3 - related 21 nonaccidental mortality is estimated to occur when O 3 concentrations are between 22Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 184 background and when the highest monitor in the urban area is at or below 0.080 ppm, 8

- 1 hour average concentration. 2 The discussion bel ow highlights additional observations and insights from the O 3 3 risk assessment, together with important uncertainties and limitations. 4 (1) As discussed in the 2007 Staff Paper (section 5.4.5) , EPA has greater 5 confidence in relative comparisons in risk es timates between alternative standards than in 6 the absolute magnitude of risk estimates associated with any particular standard. 7 (2) Significant year- to - year variability in O 3 concentrations combined with the 8 use of a 3

- ye ar design value to determine th e amount of air quality adjustment to be 9 applied to each ye ar analyzed, results in significant year- to - ye ar variability in the annual 10 health risk estimates upon just meeting various 8

- hour standards. 11 (3) There is noticeable city

- to - city variability in es timated O 3 - related incidence of 12 morbidity

and mortality

across the 12 urban areas anal yz ed for both recent years of air 13 quality

and for air quality adjusted to simulate just meeting a 0.084 ppm standard and 14 selected potential alternative standards. This v ariability is likel y due to differences in air 15 quality

distributions, differences in exposure related to many factors including varying 16 activity

patterns and air exchange rates, differences in baseline incidence rates, and 17 differences in susceptible populations and age distributions across the 12 urban areas. 18 (4) With respect to the uncertainties about estimated policy

- relevant background 19 concentrations, as discussed in the 2007 Staff Paper (section 5.4.3), alternative 20 assumptions about background levels had a variable impact depending on the health 21 effect considered and the location and standard analyzed in terms of the absolute 22 magnitude and relative changes in the risk estimates. There was relativel y little impact 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 185 on either absolute magnitude or relative changes in lung function risk estimates due to 1 alternative assumptions about background levels. With respect to O 3 - related non

2 accidental mortality , while notable differences (i.e., greater than 50 percent) 46 were 3 observed for nonaccidental mortality in some areas, particularl y for more stringent 4 standards, the overall pattern of estimated reductions, expressed in terms of percentage 5 reduction relative to the 0.084 ppm standard, was significantl y less impacted. 6 C. Reconsideration of the Level of the Prim ary Standa rd 7 1. Evidence and Exposure/Risk

- Based Considerations 8 The approach used in the 2007 Staff Paper as a basis for staff recommendations 9 on standard levels builds upon and broadens the general approach used by EPA in the 10 1997 review. This approach reflects the more extensive and stronger body of evidence 11 available for the 2008 rulemaking on a broader range of health effects associated with 12 exposure to O 3 , including : (1) additional respiratory

- related endpoints ; (2) new 13 information about the mechanis ms underl ying respiratory morbidity

effects supporting a 14 judgment that the link between O 3 exposure and these effects is causal; (3) newly 15 identified cardiovascular

- related health endpoints from animal toxicology and controlled 16 human exposures studies that are highl y suggestive that O 3 can directly or indirectly 17 contribute to cardiovascular morbidity , and (4) new U.S. multicity time series studies, 18 single city studies, and several meta

- anal ys es of these studies that provide relatively 19 strong evidence for as sociations between short

- term O 3 exposures and all

- cause 20

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 O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 186 (nonaccidental) mortality, at levels below the current primary standard : as well as (5) a 1 substantial body

of new evidence of increased susceptibility in people with asthma and 2 other lung diseases

. In evaluating evidence

- based and exposure/risk

- based 3 considerations, the 2007 Staff Paper considered : (1) the ranges of levels of alternative 4 standards that are supported by the evidence, and the uncertainties and limitations in that 5 evidence and (2) the extent to which specific levels of alternative standards reduce the 6 estimated exposures of concern and risks attributable to O 3 and other photochemical 7 oxidants, and the uncertainties associated with the estimated exposure and risk 8 reductions

. 9
a. Evidence

- based Considerations 10 In taking into account evidence

- based considerations, the 2007 Staff Paper 11 evaluated available evidence from controlled human exposure studies and 12 epidemiological studies, as well as the uncertainties and limitations in that evidence. In 13 particular, it focused on the extent to which controlled human exposure studies provide 14 evidence of lowest

- observed

- effects levels and the extent to which epidemiological 15 studies provide evidence of associations that extend down to the lower levels of O 3 16 concentrations observed in the studies or some indication of potential effect thresholds in 17 terms of 8

- hour average O 3 concentrations. 18 The most certain evidence of adverse health effects from exposure to O 3 comes 19 from the controlled human exposure studi es , as discussed above in section II.A.2 , and the 20 large bulk of this evidence derives from studies of exposures at levels of 0.080 ppm and 21 above. At those levels, there is consistent evidence of lung function decrements and 22Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 187 respiratory

s ymptoms in healthy young adults, as well as evidence of inflammation and 1 other medicall y significant airway responses. 2 Two studies by Adams (2002, 2006) , newl y available for consideration in the 3 2008 rulemaking, are the only available controlled human exposure studies that examine 4 respiratory

effects associated with prolonged O 3 exposures at levels below 0.080 ppm, 5 which was the lowest exposure level that had been examined in the 199 7 review. As 6 discussed above in section II.A.2.a.i.(a)(i), the Adams (2006) study investig ated a range 7 of exposure levels, including 0.060 and 0.080 ppm O 3 , and analyzed hour

- by

- hour 8 changes in responses, including lung function (measured in term of decrements in FEV 1 ) 9 and respiratory

s ymptom s, to investigate the effects of different patterns o f exposure. At 10 the 0.060 ppm exposure level, the author reported no statistically significant differences 11 for lung function decrements; statistically significant responses were reported for total 12 subjective respiratory symptoms toward the end of the expos ure period for one exposure 13 pattern
. The EPA’s reanaly sis (Brown, 2007) of the data from the Adams (2006) study 14 addressed the more fundamental question of whether there were statistically significant 15 changes in lung function from a 6.6
- hour exposure to 0. 060 ppm O3 versus filtered air 16 and used a standard statistical method appropriate for a simple paired comparison. This 17 reanal ys is found small group mean lung function decrements in healthy adults at the 18 0.060 ppm exposure level to be statistically signifi cantly

different from responses 19 associated with filtered air exposure. 20 Moreover , the Adams’ studies also report a small percentage of subjects (7 to 20 21 percent) experienc ed lung function decrement s ( > 10 percent) at the 0.060 ppm exposure 22 level. This is a concern because, f or active healthy

people, moderate levels of functional 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 188 responses (e.g., FEV 1 decrements of > 10% but < 20%) and/or moderate respiratory 1 sy mptom responses would likely interfere with normal activity for relatively

few 2 responsive individu als. However, for people with lung disease, even moderate functional 3 or sy mptomatic responses would likely interfere with normal activity for many 4 individuals, and would likely result in more frequent use of medication. In the context of 5 standard setting , the CASAC indicated (Henderson, 2006c) that a focus on the lower end 6 of the range of moderate levels of functional responses (e.g., FEV 1 decrements  10%) is 7 most appropriate for estimating potentially adverse lung function decrements in people 8 with lung disease. Therefore, the results of the Adams studies which indicate that a small 9 percentage of healthy, non - asthmatic subjects are likely to experience FEV 1 decrements  10 10% when exposed to 0.060 ppm O 3 have implications for setting a standard that prote cts 11 public health, including the health of sensitive populations such as asthmatics, with an 12 adequate margin of safety

. 13 In considering the se most recent controlled human exposure studies , the 2007 14 Staff Paper concluded that these studies provide evidence of a lowest

- observed

- effects 15 level of 0.060 ppm for potentially adverse lung function decrements and respiratory 16 sy mptoms in some healthy

adults while at prolonged moderate exertion. It further 17 conclude d that since people with asthma, particularly children, have been found to be 18 more sensitive and to experience larger decrements in lung function in response to O 3 19 exposures than would healthy adults, the 0.060 ppm exposure level also can be 20 interpreted as representing a level likel y to cause adverse lung function decrements and 21 respiratory

s ymptoms in children with asthma and more generall y in people with 22 respiratory

disease. 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 189 In considering controlled human exposure studies of pulmonary inflammation, 1 airway

responsiveness, and impaired host defense capabilities, discussed above in section 2 II.A.2.a.i, the 2007 Staff Paper note d that these studies provide evidence of a lowest

3 observed

- effects level for such effects in healthy adults at prolonged moderate exertion of 4 0.08 0 ppm , the lowest level tested

. Moreover there is no evidence that the 0.080 ppm 5 level is a threshold for these effects. Studies reporting inflammatory responses and 6 markers of lung injury have clearly

demonstrated that there is significant variation in 7 response of subjects exposed, even to O 3 exposures at 0.080 ppm. One study showed 8 notable interindividual variability in young healthy adult subjects in most of the 9 inflammatory

and cellular injury

indicators anal yz ed at 0.080 ppm. This inter

- individual 10 variability suggests that some portion of the population would likely experience such 11 effects at exposure levels extending well below 0.080 ppm. 12 As discussed above , these phy siological effects have been linked to aggravation 13 of asthma and increased susceptibility to respiratory

infection, potentially

leading to 14 increased medication use, increased school and work absences, increased visits to 15 doctors’ offices and emergency departments, and increased hospital admissions. Further, 16 pulmonary

inflammation is related to increased cellular permeability in the lung, which 17 may

be a mechanism by

which O 3 exposure can lead to cardiovascular s ys tem effects, 18 and to potential chronic effects such as chronic bronchitis or long

- term damage to the 19 lungs that can lead to reduced quality of life. These are all indicators of adverse O 3 - 20 related morbidity effects, which are consistent with and lend plausibility to the adverse 21 morbidity

effects and mortality

effects observed in epidemiological studies. 22Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 190 S ignificant associations between ambient O 3 exposures and a wide variety of 1 respiratory sy

mptoms and other morbidity outcomes (e.g., asthma medication use, school 2 absences, emergency department visits, and hospital admissions) have been reported in 3 epidemiolog ical studies , as discussed above in section II.A.2.a.i

. Overal l, the 2006 4 Criteria Document concludes that positive and robust associations were found between 5 ambient O 3 concentrations and various respiratory disease hospitalization outcomes, 6 when focusing particularly on results of warm

- season anal ys es. Recent studies also 7 generall y indicate a positive association between O 3 concentrations and emergency 8 department visits for a sthma during the warm season. These positive and robust 9 associations are supported by the controlled human exposure , animal toxicologic al , an d 10 epidemiologic al evidence for lung function decrements, increased respiratory s ymptoms, 11 airway

inflammation, and increased airway resp onsiveness. Taken t ogether, the overall 12 evidence supports a causal relationship between acute ambient O 3 exposures and 13 increased respiratory morbidity

outcomes resulting in increased emergency department 14 visits and hospitalizatio ns during the warm season (EPA, 2006a, p. 8

- 77). 15 Moreover , many single

- and multicity epidemiological studies observed positive 16 associations of amb ient O 3 concentrations with total nonaccidental and cardiopulmonary 17 mortality

. As discussed above in section II.A.2.b.i, the 2006 C riteria D ocument finds that 18 the results from U.S. multicity time

- series studies provide the strongest evidence to date 19 for O 3 effects on acute mortality . Recent meta
- analy ses also indicate positive risk 20 estimates that are unlikely to be confounded b y P M; however, future work is needed to 21 better understand the influence of model specifications on the magnitude of risk. The 22 2006 C riteria D ocument concludes that the “positive O 3 effects estimates, along with the 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 191 sensitivity

anal ys es in these three meta

- anal ys es, provide evidence of a robust association 1 between ambient O 3 and mortality” (EPA, 2006a, p. 7

- 97). In summary , the 2006 2 Criteria Document (p. 8

- 78) concludes that these findings are highl y suggestive that 3 short

- term O 3 exposure directly or indirectl y contribute to non

- accidental and 4 cardiopulmonary

- related mortality , but additional research is needed to more fully 5 establis h underlying mechanisms by which such effects occur. 6 The 2007 Staff Paper considered the epidemiological studies to evaluate evidence 7 related to potential effects thresholds at the population level for morbidity and mortality 8 effects. As discussed above in section II.A.3.a (and more fully in the 2007 Staff Paper in 9 chapter 3 and the 2006 Criteria Document in chapter 7), a number of time

- series studies 10 have used statistical modeling approaches to evaluate potential thresholds at the 11 population level

. A few such studies reported some suggestive evidence of possible 12 thresholds for morbidity and mortality

outcomes in terms of 24

- hour, 8

- hour, and 1

- hour 13 averaging times. These results, taken together, provide some indication of possible 8

- 14 hour average threshol d levels from below about 0.025 to 0.035 ppm (within the range of 15 background concentrations) up to approximately 0.050 ppm. Other studies, however, 16 observe linear concentration

- response functions suggesting no effect threshold. The 2007 17 Staff Paper (p.6

- 60) concluded that the statistically significant associations between 18 ambient O 3 concentrations and lung function decrements, respiratory s ymptoms, 19 indicators of respiratory morbidity

including increase emergency department visits and 20 hospital admissions, and possibly mortality reported in a large number of studies likely 21 extend down to ambient O 3 concentrations that are well below the level of the then 22 current standard (0.084 ppm). These associations also extend well below the level of the 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 192 standard set in 2008 (0.075 ppm) in that the highest level at which there is any indication 1 of a threshold is approximately 0.050 ppm. Toward the lower end of the range of O 3 2 concentrations observed in such studies, ranging down to background levels (i.e., 0.035 3 to 0.01 5 ppm), however, the 2007 Staff Paper stated that there is increasing uncertainty as 4 to whether the observed associations remain plausibly related to exposures to ambient O 3 , 5 rather than to the broader mix of air pollutants present in the ambient atmosphere. 6 The 2007 Staff Paper also considered studies that did subset analy ses, which 7 included only

days with ambient O 3 concentrations below the level of the then current 8 standard, or below even lower O 3 concentrations, and continue to report statistically 9 significant associations. Notably , as discussed above, Bell et al. (2006) conducted a 10 subset anal ys is that continued to show statistically significant mortality associations even 11 when only

day s with a maximum 8

- hour average O 3 concentration below a value of 12
a pproximately

0.061 ppm were included. 47 Also of note is the large multicity NCICAS 13 (Mortimer et al., 2002) that reported statisticall y significant associations between ambient 14 O 3 concentrations and lung function decrements even when day s with 8

- hour averag e O 3 15 levels greater than 0.080 ppm were excluded (which consisted of less than 5 percent of 16 the days in the eight urban areas in the study). 17 Further, as discussed above in section II.A.3.a, there are limitations in 18 epidemiological studies that make discerning thresholds in populations difficult, 19 including low data density in the lower concentration ranges, the possible influence of 20 exposure measurement error, and interindividual differences in susceptibility to O 3 - 21

47 Bell et al. (2006) referred to this level as being approxim ately equivalent to 120 μg/m 3 , daily

8
- hour maximum, the World Health Organization guideline and European Commission target value for O 3 .Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 193 related effects in populations. There is the possibility that thresholds for individuals may 1 exist in reported associations at fairl y low levels within the range of air quality observed 2 in the studies but not be detectable as population thresholds in epidemiological anal ys es. 3 Based on the above co nsiderations, the 2007 Staff Paper recognize d that the 4 available evidence neither supports nor refutes the existence of effect thresholds at the 5 population level for morbidity and mortality

effects , and that if a population threshold 6 level does exist, it w ould likely be well below the level of the then current standard and 7 possibly

within the range of background levels . Taken together, these considerations also 8 support the conclusion that if a population threshold level does exist, it would likely be 9 well below the level of the 0.075 ppm, 8

- hour average, standard set in 2008. 10 In looking more broadl y at evidence from animal toxicological, controlled human 11 exposure, and epidemiological studies , the 2006 Criteria Document f oun d substantial 12 evidence, newl y avai lable in the 2008 rulemaking, that people with asthma and other 13 preexisting pulmonary disease s are among those at increased risk from O 3 exposure. 14 Altered phys iological, morphological , and biochemical states ty pical of respiratory 15 diseases like asthma, CO PD , and chronic bronchitis may render people sensitive to 16 additional oxidative burden induced b y O 3 exposure (EPA , 2006a, section 8.7). Children 17 and adults with asthma are the group s that have been studied most extensively . Evidence 18 from controlled human exposure studies indicates that asthmatics may exhibit larger lung 19 function decrements in response to O 3 exposure than healthy controls. As discussed more 20 fully

in section II.A.4 above, as thmatics present a different response profile for cellular, 21 molecular, and biochemical parameters ( EPA, 2006a, Figure 8

- 1) that are altered in 22 response to acute O 3 exposure. They can have larger inflammatory responses, as 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 194 manifested b y larger increases in markers of inflammation such as white bloods cells 1 (e.g., PMNs) o r inflammatory cy tokines. Asthmatics, and people with allergic rhinitis, 2 are more likely

to have an allergic

- ty

pe response upon exposure to O 3 , as manifested b y 3 increases in white blood cells associated with allergy (i.e., eosinophils) and related 4 molecul es, which increase inflammation in the airways. The increased inflammatory and 5 allergic responses also may be associated with the larger late

- phase responses that 6 asthmatics can experience, which can include increased bronchoconstrictor responses to 7 irrit ant substances or allergens and additional inflammation. 8 In addition to the experimental evidence of lung function decrements, respiratory 9 sy mptoms, and other respiratory effects in asthmatic populations, two large U.S. 10 epidemiological studies as well as several smaller U.S. and international studies, have 11 reported fairl y robust associations between ambient O 3 concentrations and measures of 12 lung function and daily respiratory

s ymptoms (e.g., chest tightness, wheeze, shortness of 13 breath) in children with m oderate to severe asthma and between O 3 and increased asthma 14 medication use (EPA, 2007a, chapter 6). These more serious responses in asthmatics and 15 others with lung disease provide biological plausibility for the respiratory

morbidity 16 effects observed in epidemiological studies , such as emergency department visits and 17 hospital admissions

. 18 The body

of evidence from controlled human exposure and epidemiological 19 studies, which includes asthmatic as well as non

- asthmatic subjects, indicates that 20 controlled hum an exposure studies of lung function decrements and respiratory 21 sy mptoms that evaluate only healthy , non - asthmatic subjects likely underestimate the 22 effects of O 3 exposure on asthmatics and other susceptible populations. Therefore, 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 195 relative to the healthy , non - asthmatic subjects used in most controlled human exposure 1 studies, including the Adams (2002, 2006) studies, a greater proportion of people with 2 asthma may

be affected, and those who are affected may have as large or larger lung 3 function and s ymptomatic responses at ambient exposures to 0.060 ppm O 3 . This 4 indicates that the lowest

- observed

- effects levels demonstrated in controlled human 5 exposure studies that use only healthy subjects may

not reflect the lowest levels at which 6 people with asthma or other lung diseases may respond. 7 Being mindful of the uncertainties and limitations inherent in interpreting the 8 available evidence, the 2007 Staff Paper state d the view that the range of alternative O 3 9 standards for consideration should take into account information on lowest

- observed

10 effects levels in controlled human exposure studies as well as indications of possible 11 effects thresholds reported in some epidemiological studies and questions of biological 12 plausibility

in attributing associations observed down to background levels to O 3 13 exposures alone. Based on the evidence and these considerations, it concluded that the 14 upper end of the range of consideration should be somewhat below 0.080 ppm, the 15 lowest

- observed

- effects level for effects such as pulmonary inflammation, increased 16 airway

responsiveness and impaired host

- defense capabilities in healthy adults while at 17 prolonged moderate exertion. The 2007 Staff Paper also conclude d that the lower end o f 18 the range of alternative O 3 standards appropriate for consideration should be the lowest

19 observed

- effects level for potentially adverse lung function decrements and respiratory 20 sy mptoms in some healthy adults, 0.060 ppm. 21 b. Exposure and Risk

- based Considerations 22Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 196 In addition to the evidence

- based considerations informing staff recommendations 1 on alternative levels, as discussed above in section II.B, the 2007 Staff Paper also 2 evaluated quantitative exposures and health risks estimated to occur upon meeting the 3 then current 0.084 ppm standard and alternative standards. 48 Inso doing, it presented the 4 important uncertainties and limitations associated with these exposure and risk 5 assessments (discussed above in section II.B and more fully in chapters 4 and 5 of the 6 2007 Staff Paper). 7 The 2007 Staff Paper (and the CASAC) also recognized that the exposure and risk 8 anal ys es could not provide a full picture of the O 3 exposures and O 3 - related health risks 9 posed nationally

. The EPA did not have sufficient information to evaluate all relevant at

10 risk groups (e.g., outdoor workers) or all O 3 - related health outcomes (e.g., increased 11 medication use, school absences, and emergency department visits that are part of the 12 broader p yr amid of effects discussed above in section II.A.4.d), and the scope of the 2007 13 Staff Paper anal ys es was generall y limited to estimating exposures and risks in 12 urban 14 areas across the U.S., and to only five or just one area for some health effects included in 15 the risk assessment. Thus, national

- scale public health impacts of ambient O 3 expo sures 16 are clearl y much larger than the quantitative estimates of O 3 - related incidences of adverse 17 health effects and the numbers of children likel y t o experience exposures of concern 18 associated with meeting the 0.084 ppm standard or alternative standards. On the other 19

48 As described in the 2007 Staff Paper (section 4.5.8) and discussed above in section II.B, recent O 3 air quality distributions have been statisticall y 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 ye ar is presented in the Regulatory Impact Analy sis being prepared in connection with this rulemaking.Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 197 hand, inter

- individual variability in responsiveness means that only a subset of 1 individuals in each group estimated to experience exposures exceeding a given 2 benchmark exposure of concern level would actually be expected to experience such 3
adverse health effects. 4 The 2007 Staff Paper focused on alternative standards with the same form as the 5 then current 0.084 ppm O 3 standard (i.e. the 0.074/4, 0.070/4 and 0.064/4 scenarios). 49 6 Having concluded in the 2007 Staff Paper that it was appropriat e to consider a range of 7 standard levels from somewhat below 0.080 ppm down to as low as 0.060 ppm, the 2007 8 Staff Paper looked to results of the anal ys es of exposure and risk for the 0.074/4 scenario 9 to represent the public health impacts of selecting a s tandard in the upper part of the 10 range, the results of analyses of the 0.070/4 scenario to represent the impacts in the 11 middle part of the range, and the results of the analy ses of the 0.064/4 scenario to 12 represent the lower part of the range. 13 As discusse d in section II.B.1 of this notice, the exposure estimates presented in 14 the 2007 Staff Paper are for the number and percent of all children and asthmatic children 15 exposed, and the number of person

- day s (occurrences) of exposures, with daily 8
- hour 16 maximum exposures at or above several benchmark levels while at intermittent moderate 17 or greater exertion. Exposures above selected benchmark levels provide some 18 perspective on the public health impacts of health effects that cannot currently be 19 evaluated in quantitative risk assessments but that may occur at existing air quality levels, 20

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 av erage. For example, the 8

- hour standard established in 1997 is identified as “ 0.084/4.”Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 198 and the extent to which such impacts might be reduced b y meeting alternative standard 1 levels. As described in section II.B.1.c above, the 2007 Staff Paper refers to exposures at 2 and above these benchmark levels as “exposures of concern.” The 2007 Staff Paper 3 notes that exposures of concern, and the health outcomes they represent, likely

occur 4 across a range of O 3 exposure levels, such that there is no one exposure level that 5 addresses all public health concerns. As noted above in section II.B., EPA also has 6 acknowledged that the concept is more appropriately viewed as a continuum with greater 7 confidence and less uncertainty about the existence of health effects at the upper end and 8 less confidence and greater uncertainty as one considers increasingl y lower O 3 exposure 9 levels. 10 Consistent with advice from CASAC, the 2007 Staff Paper estimates exposures 11 of concern not only at 0.080 ppm O 3 , a level at which there are clearl y demons trated 12 effects, but also at 0.070 and 0.060 ppm O 3 levels where there is some evidence that 13 health effects are likel y to occur in some individuals. The 2007 Staff Paper recognizes 14 that there will be varying degrees of concern about exposures at each of th ese levels, 15 based in part on the population groups experiencing them. Given that there is clear 16 evidence of inflammation, increased airway responsiveness, and changes in host defenses 17 in healthy

people exposed to 0.080 ppm and reason to infer that such ef fects will continue 18 at lower exposure levels, but with increasing uncertainty about the extent to which such 19 effects occur at lower O 3 concentrations, the 2007 Staff Paper and discussion below, 20 focus on exposures of concern at or above benchmark levels of 0.070 and 0.060 ppm O 3 21 for purposes of evaluating alternative standards. The focus on these two benchmark 22 levels reflects the following evidence

- based considerations, discussed above in section 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 199 II.C.1, that raise concerns about adverse health effects like ly occurring at levels below 1 0.080 ppm: (1) that there is limited , but important, new evidence from controlled human 2 exposure studies showing lung function decrements and respiratory s ymptoms in some 3 healthy

subjects at 0.060 ppm; (2) that asthmatics are likel y to have more serious 4 responses than healthy individuals; (3) that lung function is not likely to be as sensitive a 5 marker for O 3 effects as lung inflammation; and (4) that there is epidemiological 6 evidence which reports associations with O 3 levels that extend well below 0.080 ppm. 7 Table 3 below summarizes the exposure estimates for all children and asthmatic 8 children for the 0.060 and 0.070 ppm health effect benchmark levels associated with O 3 9 levels adjusted to just meet 0.074/4, 0.070/4, and 0 .064/4 alternative 8

- hour standards 10 based on a generally poorer year of air quality (2002) and based on a generally better year 11 of air quality (2004). This table includes exposure estimates reflecting the aggregate 12 estimate for the 12 urban areas as well as the range across these same 12 areas. As 13 shown in Table 3 below, the percent of population exposed over the selected benchmark 14 levels is very

similar for all and asthmatic school age children. Thus, the following 15 discussion focuses primarily on the exposure estimates for asthmatic children, 16 recognizing that the pattern of exposure estimates is similar for all children when 17 expressed in terms of percentage of the population. 18 As noted in section II.B.2 and shown in Tables 1 and 3 of this notice, substantial 19 ye ar- to - ye ar variability is observed, ranging to over an order of magnitude at the higher 20 alternative standard levels, in estimates of the number of children and the number of 21 occurrences of exposures of concern at both the 0.060 and 0.070 ppm benchmark levels. 22 As shown in Table 3, and discussed more full y below, aggregate estimates of exposures 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 200 of concern for the 12 urban areas included in the assessment are considerably larger for 1 the benchmark level of ≥ 0.060 ppm O 3 , compared to the 0.070 ppm benchmark, while 2 the pattern of ye ar - to - year variability is fairl y similar. 3 As shown in Table 3, aggregate estimates of exposures of concern for a 0.060 4 ppm benchmark level vary considerabl y among the three alternative standards included in 5 this table, particularl y for the 2002 simulations (a year with generall y poorer air quality in 6 most, but not all areas). For air quality just meeting a 0.074/4 standard approximately 7 27% of asthmatic children, based on the 2002 simulation, and approximately 2% of 8 asthm atic children based on the 2004 simulation (a year with better air quality in most but 9 not all areas), are estimated to experience one or more exposures of concern at the 10 benchmark level of ≥ 0.060 ppm O 3 . Considering a 0.070/4 standard using the same 11 ben chmark level (0.060 ppm), about 18% of asthmatic children are estimated to 12 experience one or more exposures of concern, in a year with poorer air quality (2002), 13 and only

about 1% in a year with better air quality (2004). For the most stringent 14 standard e xamined (a 0.064/4 standard), about 6% of asthmatic children are estimated to 15 experience one or more exposures of concern in the simulation based on the ye ar with 16 poorer air quality

(2002), and exposures of concern at the 0.060 ppm benchmark level are 17
essentially

eliminated based on a year with better air quality (2004). 18 Table 3 also provides aggregate exposure estimates for the 12 urban areas where a 19 benchmark level o f ≥ 0.070 ppm is used. Based on the year with poorer air quality 20 (2002), the estimate of the percent of asthmatic children exposed one or more times is 21 about 5% when a 0.074/4 standard is just met; based on a ye ar with better air quality 22 (2004) , exposures of concern are essentially eliminated. For this same benchmark (0.070 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 201 ppm), when a 0.070 /4 standard is just met, estimates range from about 2% of asthmatic 1 children exposed one or more times over this benchmark based on a ye ar with poorer air 2 quality

(2002), and exposures of concern are essentially eliminated based on a year with 3 better air quality

(2004). At the 0.070 ppm benchmark, just meeting a 0.064/4 standard 4 essentially

eliminates exposures of concern regardless of the year that is used as the basis 5 for the analy sis. 6 The 2007 Staff Paper also notes that there is substantial city

- to - ci ty variability

in 7 these estimates, and notes that it is appropriate to consider not just the aggregate 8 estimates across all cities, but also to consider the public health impacts in cities that 9 receive relatively

less protection from the alternative standards. As shown in Table 3, in 10 considering the benchmark level of > 0.060 ppm, while the aggregate percentage of 11 asthmatic children estimated to experience one or more exposures of concern across all 12 12 cities for a 0.074/4 standard is about 27% based on th e year with poorer air quality 13 (2002), it ranges up to approximately 51% for asthmatic children in the city with the least 14 degree of protection from that alternative standard. Similarly, for air quality just meeting 15 a 0.070/4 standard, the aggregate percentage of asthmatic children estimated to 16 experience one or more exposures of concern across all 12 cities is 18% based on the year 17 with poorer air quality , but it ranges up to about 41% in the city with the least degree of 18 protection associated with just m eeting that alternative standard. For just meeting a 19 0.064/4 standard, the aggregate estimate of asthmatic children experiencing exposures of 20 concern for the 0.060 ppm benchmark is about 6% based on the ye ar with poorer air 21 quality

and ranges up to 16% in the city with the least degree of protection. 22Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 202 This pattern of city- to - city variability

also occurs at the benchmark level of ≥ 1 0.070 ppm associated with air quality just meeting these same three alternative standards 2 ( i.e., 0.074/4, 0.070/4, and 0.064/4) . While the aggregate percentage of asthmatic 3 children estimated to experience such exposures of concern across all 12 cities is about 4 5% based on the ye ar with poorer air quality for just meeting the 0.074/4 standard, it 5 ranges up to 14% in the city with the least degree of protection associated with that 6 alternative standard. For just meeting a 0.070/4 standard the aggregate estimate is 2% of 7 asthmatic children experiencing exposures of concern for the 0.070 ppm benchmark 8 based on the ye ar with poorer air quality and ranges up to 6% in the city with the least 9 degree of protection. The aggregate estimate for exposures of concern is further reduced 10 to 0.2% of asthmatic children for this same benchmark level for air quality just meeting a 11 0.064/4 standard based on the year with poorer air quality and ranges up to 1% in the city 12 with the least degree of protection. 13 In addition to observing the fraction of the population estimated to experience 14 exposures of concern associated with just meeting alternative standards, EPA also took 15 into consideration in the 2007 Staff Paper the percent reduction in exposures of concern 16 and health risks associated with alternative standards relative to just meeting the then 17 current 0.084/4 standards. For the current decision it is also informative to consider the 18 incremental reductions in exposures of concern associated with more stringent alternative 19 standards relative to the 0.075 ppm standard. As shown in Table 1 above , at the > 0.060 20 ppm benchmark level based on a year with poorer air quality , the reduction in exposures 21 of concern for asthmatic children in going from the 0.074/4 standard (which 22 approximates the 0.075 ppm standard adopted in 2008) down to a 0.064/4 standard is 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 203 observed to be very

similar to the reduction esti mated to occur in going from then current 1 0.084/4 standard down to a 0.074/4 standard. More specifically , the estimates for 2 asthmatic children are reduced from 47% (about 1.2 million children) associated with 3 meeting a 0.084/4 standard down to 27% (about 700,000 children) for just meeting a 4 0.074/4 standard and the estimates are reduced further to about 6% (about 150,000 5 children) associated with just meeting a 0.064/4 standard in the 12 urban areas included 6 in the assessment. In a year with better air qu ality (2004), exposures estimated to exceed 7 the 0.060 ppm benchmark in asthmatic children one or more times in a ye ar are reduced 8 from 11% associated with just meeting a 0.084/4 standard down to about 2% for a 9 0.074/4 standard and are essentially eliminate d when a 0.064/4 standard is just met. 10 Turning to consideration of the risk assessment estimates, Table 2 above 11 summarizes the risk estimates for moderate lung function decrements in both all school 12 age children and asthmatic school age children associ ated with just meeting several 13 alternative standards based on simulations involving a ye ar with relativel y poorer air 14 quality

(2002) and a ye ar with relatively better air quality

(2004). As shown in Table 2, 15 for the 2002 simulation the reduction in the number of asthmatic children estimated to 16 experience one or more moderate lung function decrements going from a 0.074/4 17 standard down to a 0.064/4 standard is roughly equivalent to the additional health 18 protection afforded associated with just meeting a 0.07 4/4 standard relative to then 19 current 0.084/4 standard. More specificall y, for just 5 urban areas, it is estimated that 20 nearl y 8% of asthmatic children (130,000 children) would experience one or more 21 occurrences of moderate lung function decrements per ye ar at a 0.084/4 standard and this 22 would be reduced to about 5% (90,000 children) at a 0.074/4 standard and further 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 204 reduced down to about 3% (50,000 children) at a 0.064/4 standard. Based on the 2002 1 simulations, the percent reduction associated with just meeting a 0.064/4 standard relative 2 to then current 0.084/4 standard is about 62% which is about twice the reduction in risk 3 compared to the estimated 31% reduction associated with just meeting a 0.074/4 4 standard. As shown in Table 2 above , similar patter ns were observed in reductions in 5 lung function risk for all school age children in 12 urban areas associated with these 6 alternative standards. 7 Figures 6

- 5 and 6

- 6 in the 2007 Staff Paper (EPA , 2007 b ) show the percent 8 reduction in non

- accidental mortality risk estimates associated with just meeting the same 9 alternative standards discussed above relative to just meeting the then current 0.084/4 10 standard for 12 urban areas, based on adjusting 2002 and 2004 air quality data. These 11 figures also provide perspec tive on the extent to which the risks in these years (i.e., 2002 12 and 2004) are greater than those estimated to occur upon meeting the then current 0.084/4 13 standard (in terms of a negative percent reduction relative to a 0.084/4 standard). Based 14 on the 200 2 simulations (EPA, 2007 b, Figure 6

- 5 ), the estimated reduction in non

15 accidental mortality is about 30 to 70% across the 12 urban areas for just meeting a 16 0.064/4 standard relative to the then current 0.084/4 standard. This reduction is roughl y 17 twice the 15 to 30% estimated reduction across the 12 urban areas associated with just 18 meeting a 0.074/4 standard relative to a 0.084/4 standard. While the estimated incidence 19 is lower based on the 2004 simulations (EPA, 2007 b, Figure 6

- 6 ), the pattern of risk 20 red uctions among alternative standards is roughly similar to that observed for the 2002 21 simulations. 22Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 205 In addition to the risk estimates for lung function decrements in all school age 1 children and non

- accidental mortality that were estimated for 12 urban area s and lung 2 function decrements in asthmatic children for 5 urban areas, a similar pattern of 3 incremental reductions in health risks was shown for two health outcomes where risks 4 were estimated in one city only for each of these outcomes. These included re ductions in 5 respiratory

s ymptoms in asthmatic children (EPA, 2007 b; Boston, Table 6

- 9 ) and 6 respiratory

- related hospital admissions (EPA, 2007a ; New York City , Table 6

- 10 ) 7 associated with just meeting alternative 8

- hour standards set at 0.074 ppm, 0.070 ppm , 8 and 0.064 ppm relative to just meeting the then current 0.084 ppm standard. Using the 9 2002 simulation, a standard set at 0.074/4 is estimated to reduce the incidence of 10 sy mptom day s in children with moderate to severe asthma in the Boston area by about 15 11 percent relative to a 0.084/4 standard. With this reduction, it is estimated that about 1 12 respiratory

s ymptom day in 8 during the O 3 season would be attributable to O 3 exposure. 13 A standard set at 0.064/4 is estimated, based on the 2002 simulation, to reduce the 14 incidence of s ymptom day s in children with moderate to severe asthma in the Boston area 15 by about a 25 to 30 percent reduction relative to a 0.084 ppm standard, which is roughl y 16 twice the reduction compared to that provided b y a 0.074/4 standard. But even with this 17 reduction, it is estimated that 1 respiratory s ymptom day

in 10 during the O 3 season is 18 attributable to O 3 exposure 19 As shown in Table 6

- 10 (EPA, 2007 b ) estimated incidence of respiratory

- related 20 hospital admissions in one urban area (N ew York City) was reduced b y 14 to 17 percent 21 by a standard set at 0.074/4 relative to then current 0.084/4 standard, in the year with 22 relativel y high and relatively low O 3 air quality levels, respectivel y. Similar to the 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 206 pattern observed for the other he alth outcomes discussed above, the reduction in 1 incidence of respiratory

- related hospital admissions for a 0.064/4 standard relative to a 2 0.084/4 standard is about twice that associated with a 0.074/4 standard relative to a 3 0.084/4 standard. 4 Table 3. Numb er and Percent of All and Asthmatic School Age Children in 12 5 Urban Areas Estimated to Experience 8 - Hour Ozone Exposures Above 0.060 and 6 0.070 ppm While at Moderate or Greater Exertion, One or More Times Per Season 7 Associated with Just Meeting Alternative 8 - Hour Standards Based on Adjusting 8 2002 and 2004 Air Quality Data 1,2 9 Benchmark Levels of Exposures of Concern (ppm) 8
- Hour Air

Quality Standards 3 (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 o r greater exertion is defined as having an 8

- hour average equivalent ventilation rate > 13 l

- mi n/m2

. 10 2 Estimates are the aggregate results based on 12 combined statistical areas (Atlanta, Boston, Chicago, Cleveland, 11 Detroit, Houston, Los Angeles, New York, Philadelphia, Sacramento, St. Louis, and Washington, D.C.). Estimates 12 are for the ozone 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. 14 3 All standards summarized h ere have the same form as the 8

- hour standard established in 1997 which is 15 specified as the 3

- year average of the annual 4 th highest daily maximum 8

- hour average concentrations 16 must be at or below the concentration level specified. As described in the 200 7 Staff Paper ( EPA, 2007b, 17 section 4.5.8), recent O 3 air quality distributions have been statistically adjusted to simulate just meeting 18 the 0.084 ppm standard and selected alternative standards. These simulations do not represent predictions 19 of when, whe ther, or how areas might meet the specified standards 20 21 22 23 24Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 207 2
. CASAC Views Prior to 2008 Decision 1 In comments on the second draft Staff Paper, CASAC stated in its letter to the 2 Administrator, “ the CASAC unanimously recommends that the current primary ozon e 3 NAAQS be revised and that the level that should be considered for the revised standard 4 be from 0.060 to 0.070 ppm ” (Henderson, 2006c, p. 5 ) . This recommendation followed 5 from its more general recommendation that the 0.084 ppm standard needed to be 6 subst antially

reduced to be protective of human health, particularl y in at

- risk 7 subpopulations. 8 The CASAC Panel noted that beneficial reductions in some adverse health effects 9 were estimated to occur upon meeting the lowest standard level (0.064 ppm) considered 10 in the risk assessment (Henderson, 2006c, p. 4). The lower end of this range reflects 11 CASAC’s views that “[ w ]hile data exist that adverse health effects may occur at levels 12 lower than 0.060 ppm, these data are less certain and achievable gains in prot ecting 13 human health can be accomplished through lowering the ozone NAAQS to a level 14 between 0.060 and 0.070 ppm.” (id.). 15 In a subsequent letter sent specificall y to offer advice to aid the Administrator and 16 Agency

staff in developing the O 3 proposal, the CASAC reiterated that the Panel 17 members “ were unanimous in recommending that the level of the current primary ozone 18 standard should be lowered from 0.08 ppm to no greater than 0.070 ppm ” (Henderson, 19 2007, p. 2). Further, the CASAC Panel expressed the v iew that the 2006 Criteria 20 Document and 2007 Staff Paper, together with the information in its earlier letter, provide 21 “overwhelming scientific evidence for this recommendation,” and emphasized the Clean 22Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 208 Air Act requirement that the primary standard must b e set to protect the public health 1 with an adequate margin of safety (id.). 2 3
. Basis for 2008 Decision on the Primary Standard 3 This section presents the rationale for the 2008 final decision on the primary O 3 4 standard as presented in the 2008 final rule ( 73 FR 16475). The EPA’s conclusions on 5 the level of the standard began b y noting that, having carefully considered the public 6 comments on the appropriate level of the O 3 standard, EPA concluded that the 7 fundamental scientific conclusions on the effects of O 3 reached in the 2006 Criteria 8 Document and 2007 Staff Paper remained valid. In considering the level at which the 9 primary

O 3 standard should be set, EPA placed primary consideration on the body of 10 scientific evidence available in the 2008 final rulemaking on the health effects associated 11 with O 3 exposure, while viewing the results of exposure and risk assessment s as 12 providing information in support of the decision. In considering the available scientific 13 evidence, EPA concluded that a focus on the prop osed range of 0.070 to 0.075 ppm was 14 appropriate in light of the large body of controlled human exposure and epidemiological 15 and other scientific evidence. The notice stated that this body of evidence did not support 16 retaining the then current 0.084 ppm 8

- hour O 3 standard, as suggested b y some 17 commenters, nor did it support setting a level just below 0.080 ppm, because, based on 18 the entire body of evidence, such a level would not provide a significant increase in 19 protection compared to the 0.084 ppm standard. Further, such a level would not be 20 appreciably

below the level in controlled human exposure studies at which adverse 21 effects have been demonstrated (i.e., 0.080 ppm). The notice also stated that the body of 22 evidence did not support setting a level of 0.060 ppm or below, as suggested by other 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 209 commenters. In evaluating the information from the exposure assessment and the risk 1 assessment, EPA judged that this information did not provide a clear enough basis for 2 choosing a specific level within the range of 0.075 to 0.070 ppm. 3 In making a final judgment about the level of the primary O 3 standard, EPA noted 4 that the level of 0.075 ppm is above the range recommended by the CASAC (i.e., 0.070 5 to 0.060 ppm). The notice stated that in placing great weight o n the views of CASAC, 6 careful consideration had been given to CASAC’s stated views and the scientific basis 7 and policy

views for the range it recommended. In so doing, EPA full y agreed that the 8 scientific evidence supports the conclusion that the current standard wa s not adequate and 9 must be revised. 10 With respect to CASAC’s recommended range of standard levels, EPA observed 11 that the basis for CASAC’s recommendation appeared to be a mixture of scientific and 12 policy

considerations. While in general agreement with CASAC’s views concerning the 13 interpretation of the scientific evidence, EPA noted that there was no bright line clearl y 14 directing the choice of level, and the choice of what was appropriate was clearl y a public 15 health policy

judgment entrusted to the EPA Administrator. This judgment must include 16 consideration of the strengths and limitations of the evidence and the appropriate 17 inferences to be drawn from the evidence and the exposure and risk assessments. In 18 reviewing the basis for the CASAC Panel ’s recommendation for the range of the O 3 19 standard, EPA observed that it reached a different policy judgment than the CASAC 20 Panel based on apparently placing different weight in two areas: the role of the evidence 21 from the Adams studies and the relative we ight placed on the results from the exposure 22 and risk assessments. While EPA found the evidence reporting effects at the 0.060 ppm 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 210 level from the Adams studies to be too limited to support a primary focus at this level, 1 EPA observed that the CASAC Panel a ppeared to place greater weight on this evidence, 2 as indicated b y its recommendation of a range down to 0.060 ppm. It was noted that 3 while the CASAC Panel supported a level of 0.060 ppm, they also supported a level 4 above 0.060, which indicated that they did not believe that the results of Adams studies 5 meant that the level of the standard had to be set at 0.060 ppm. The EPA also observed 6 that the CASAC Panel appeared to place greater weight on the results of the risk 7 assessment as a basis for its recommen ded range. In referring to the risk assessment 8 results for lung function, respiratory s ymptoms, hospital admissions and mortality , the 9 CASAC Panel concluded that: “beneficial effects in terms of reduction of adverse health 10 effects were calculated to occur at the lowest concentration considered (i.e., 0.064 ppm)” 11 (Henderson, 2006c, p.4). However, EPA more heavily weighed the implications of the 12 uncertainties associated with the Agency ’s quantitative human exposure and health risk 13 assessments. Given these uncertainties, EPA did not agree that these assessment results 14 appropriatel y served as a primary basis for concluding that levels at or below 0.070 ppm 15 were required for the 8

- hour O 3 standard. 16 The notice stated that after carefull y taking the above comm ents and 17 considerations into account, and fully considering the scientific and policy views of the 18 CASAC, EPA decided to revise the level of the primary 8
- hour O 3 standard to 0.075 19 ppm. The EPA judged, based on the available evidence, that a standard set at this level 20 would be requisite to protect public health with an adequate margin of safety , including 21 the health of sensitive subpopulations, from serious health effects including respiratory 22 morbidity, that w ere judged to be causally associated with short - term and prolonged 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 211 exposures to O 3 , and premature mortality. The EPA also judged that a standard set at this 1 level provides a significant increase in protection compared to the 0.084 ppm standard, 2 and is appreciabl y below 0.080 ppm, the level in control led human exposure studies at 3 which adverse effects have been demonstrated. At a level of 0.075 ppm, exposures at and 4 above the benchmark of 0.080 ppm are essentially eliminated, and exposures at and 5 above the benchmark of 0.070 are substantiall y reduced or eliminated for the vast 6 majority

of people in at

- risk groups. A standard set at a level lower than 0.075 would 7 only result in significant further public health protection if, in fact, there is a continuum 8 of health risks in areas with 8

- hour average O 3 concentrations that are well below the 9 concentrations observed in the key controlled human exposure studies and if the reported 10 associations observed in epidemiological studies are, in fact, causall y related to O 3 at 11 those lower levels. Based on the avai lable evidence, EPA was not prepared to make 12 these assumptions . Taking into account the uncertainties that remained in interpreting the 13 evidence from available controlled human exposure and epidemiological studies at very 14 low levels, EPA noted that the likelihood of obtaining benefits to public health decreased 15 with a standard set below 0.075 ppm O 3 , while the likelihood of requiring reductions in 16 ambient concentrations that go beyond those that are needed to protect public health 17 increased. The EPA judge d that the appropriate balance to be drawn, based on the entire 18 body

of evidence and information available in the 2008 final rulemaking, was to set the 19 8
- hour primary

standard at 0.075 ppm. The EPA expressed the belief that a standard set 20 at 0.075 ppm would be sufficient to protect public health with an adequate margin of 21 safety, and did not believe that a lower standard was needed to provide this degree of 22 protection. The EPA further asserted that this judgment appropriatel y considered the 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 212 requirement fo r a standard that was neither more nor less stringent than necessary for this 1 purpose and recognized that the CAA does not require that primary standards be set at a 2
zero - risk level, but rather at a level that reduces risk sufficiently so as to protect pub lic 3 health with an adequate margin of safety

. 4 4
. CASAC Advice Following 2008 Decision 5 Following the 2008 decision on the O 3 standard, serious questions were raised as 6 to whether the standard met the requirements of the CAA. In April 2008, the members of 7 the CASAC Ozone Review Panel sent a letter to EPA stating “In our most

- recent letters 8 to you on this subject

- dated October 2006 and March 2007

- the CASAC unanimously 9 recommended selection of an 8

- hour average Ozone NAAQS within the range of 0.060 to 10 0. 070 parts per million for the primary (human health

- based) Ozone NAAQS” 11 (Henderson, 2008)

. The letter continued: “The CASAC now wishes to convey , by means 12 of this letter, its additional, unsolicited advice with regard to the primary and secondary 13 Ozone NAAQS. In doing so, the participating members of the CASAC Ozone Review 14 Panel are unanimous in strongly urging you or your successor as EPA Administrator to 15 ensure that these recommendations be considered during the next review cycle for the 16 Ozone NAAQS tha t will begin next year” (id.)

. Moreover, the CASAC Panel noted that 17 “numerous medical organizations and public health groups have also expressed their 18 support of these CASAC recommendations.” (id.) The letter further stated the following 19 strong, unanimou s view: 20 [the CASAC did] “ not endorse the new primary ozone standard as being 21 sufficient protective of public health. The CASAC

— as the Agency ’s 22 statutorily

- established science advisory committee for advising you on the 23 national ambient air quality standards

— unanimously recommended 24Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 213 decreasing the primary

standard to within the range of 0.060

–0.070 ppm. 1 It is the Committee’s consensus scientific opinion that your decision to set 2 the primary

ozone standard above this range fails to satisfy the explicit 3 stipulations of the Clean Air Act that you ensure an adequate margin of 4 safety for all individuals, including sensitive populations” (Henderson, 5 2008). 6 5
. Administrator’s Proposed Conclusions 7 For the reasons discussed below, the Administrator proposes to set a new level for 8 the 8
- hour primary

O 3 within the range from 0.0 6 0 to 0.0 7 0 ppm
. 50 Inreaching this 9 proposed decision, the Administrator has considered: the evidence

- based considerations 10 from the 2006 Criteria Document and the 2007 Staff Paper; the result s of the exposure 11 and risk assessments discussed above and in the 2007 Staff Paper; CASAC advice and 12 recommendations provided in CASAC’s letters to the Administrator both during and 13 following the 2008 rulemaking ; EPA staff recommendations; and public comments 14 received in conjunction with review of drafts of these documents and on the 2007 15 proposed rule. In considering what level of an 8
- hour O 3 standard is requisite to protect 16 public health with an adequate margin of safety, the Administrator is mindful th at this 17 choice requires judgments based on an interpretation of the evidence and other 18 information that neither overstates nor understates the strength and limitations of the 19 evidence and information. 20 The Administrator notes that the most certain evidence of adverse health effects 21 from exposure to O 3 comes from the controlled human exposure studies, and that the 22
50 As discussed above at the beginning of section II, the Administrator has focused her reconsideration of the primary O 3 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 O 3 standard to provide increased public health protection nor with regard to the indicator, averaging period, and form of the 2008 standard.Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 214 large bulk of this evidence derives from studies of exposures at levels of 0.080 ppm and 1 above. At those levels, there is consistent evidence of lung function decrements and 2 respiratory

s ymptoms in healthy

young adults, as well as evidence of O 3 - induced 3 pulmonary

inflammation, airway

responsiveness, impaired host defense capabilities , and 4 other medicall y significant airway responses. Moreover , there is no evidence that the 5 0.080 ppm exposure level is a threshold for any of these types of respiratory effects. 6 Rather, there is now controlled human exposure evidence , including studies of lung 7 function decrements and respiratory s ymptoms at the 0.060 ppm exposure level, that 8 strengthens our previous understanding that this array of respiratory

responses are likel y 9 to occur in some healthy adults at such lower levels

. 10 In particular, the Administrator notes two studies by Adams (2002, 2006) , newly 11 availab le in the 2008 rulemaking, that examine d lung function and respiratory sy mptom 12 effects associated with prolonged O 3 exposures at levels below 0.080 ppm, as well as 13 EPA’s reanaly sis of the data from the Adams (2006) study at a 0.060 ppm exposure level. 14 As discussed above, while the author’s anal ys is focused on hour

- by

- hour comparisons of 15 effects, for the purpose of exploring responses associated with different patterns of 16 exposure, EPA’s reanalysis focused on addressing the more fundamental question of 17 whether the pre - to post - exposure change in lung function differed between a 6.6
- hour 18 exposure to 0.060 ppm O 3 versus a 6.6 hour exposure to clean filtered air

. The 19 Administrator notes that this reanal ys is found small, but statistically significant group 20
mean differences in lung function decrements in healthy adults at the 0.060 ppm exposure 21 level, which is now the lowest

- observed

- effects level for these effects. Moreover, these 22 studies also report a small percentage of subjects (7 to 20 percent) experienc ed moderate 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 215 lung function decrement s ( > 10 percent) at the 0.060 ppm exposure level. While for 1 active healthy

people, moderate levels of functional responses (e.g., FEV 1 decrements of 2
> 10% but < 20%) and/or moderate respiratory s ymptom responses would likel y interfere 3 with normal activity for relatively

few responsive individuals , the Administrator notes 4 that for people with lung disease, even moderate functional or sy mptomatic responses 5 would likely

interfere with normal activity for many individuals, and w ould likely result 6 in more frequent use of medication. Further, she notes that CASAC indicated that a 7 focus on the lower end of the range of moderate levels of functional responses (e.g., 8 FEV 1 decrements  10%) is most appropriate for estimating potential ly adverse lung 9 function decrements in people with lung disease (Henderson, 2006c). 10 The Administrator also notes that many public commenters on the 2007 proposed 11 rule raised a number of questions about the weight that should be placed on the Adams 12 studie s and EPA’s reanaly sis of data from the Adams (2006) study . Some commenters 13 expressed the view that the results of the se studies and EPA’s reanal ys is provided support 14 for setting a standard level below the proposed range , while others raised questions abo ut 15 EPA ’s reanaly sis and generall y expressed the view that the study results were not robust 16 enough to reach conclusions about respiratory effects at the 0.060 ppm exposure level. 51 17 Based on all the above considerations, the Administrator concludes that the 18 Adams studies provide limited but important evidence which adds to the overall bo dy of 19 evidence that inform s her proposed decision on the range of levels within which a 20 standard could be set that would be requisite to protect public health with an adequate 21

51 The EPA respon d e d to these comments in the 2008 final rule ( 73 FR 16454
- 5 ).Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 216 margin of safety , including the health of at

- risk populations such as people with lung 1 disease. 2 In considering controlled human exposure studies reporting O 3 - induced 3 pulmonary

inflammation, airway

responsiveness, and impaired host defense capabili ties 4 at exposure levels down to 0.080 ppm, the lowest level at which these effects have been 5 tested , the Administrator notes that these physiological effects have been linked to 6 aggravation of asthma and increased susceptibility to respiratory infection, p otentially 7 leading to increased medication use, increased school and work absences, increased visits 8 to doctors’ offices and emergency departments, and increased hospital admissions, 9 especiall y in people with lung disease. These phy siological effects are all indicators of 10 potential adverse O 3 - related morbidity effects, which are consistent with and lend 11 plausibility

to the associations observed between O 3 and adverse morbidity effects and 12 mortality

effects in epidemiological studies. 13 With regard to epidemi ological studies, the Administrator observes that 14 statistically significant associations between ambient O 3 levels and a wide array of 15 respiratory

s ymptoms and other morbidity outcomes including school absences, 16 emergency

department visits, and hospital admissions have been reported in a large 17 number of studies. More specificall y, positive and robust associations were found 18 between ambient O 3 concentrations and respiratory hospital admissions and emergency 19 department visits , when focusing particularl y on the results of warm season anal ys es. 20 Taken together, the overall body of evidence from controlled human exposure, 21 toxicological, and epidemiological studies supports the inference of a causal relationship 22 between acute ambient O 3 exposures and increased re spiratory morbidity outcomes 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 217 resulting in increased emergency department visits and hospitalizations during the warm 1 season. Further, the Administrator notes that recent epidemiological evidence is highly 2 suggestive that O 3 directly or indirectl y contributes to non - accidental and 3 cardiopulmonary

- related mortality

. 4 The Administrator also considered the epidemiological evidence with regard to 5 considering potential effects thresholds at the population level for morbidity and 6 mortality

effects. As discussed a

bove, while some studies provide some indication of 7 possible 8

- hour average threshold levels from below about 0.025 to 0.035 ppm (within 8 the range of background concentrations) up to approximately 0.050 ppm, other studies 9 observe linear concentration

- respo nse functions suggesting that there may be no effects 10 thresholds at the population level above background concentrations. In addition, other 11 studies conducted subset anal ys es that included only day s with ambient O 3 concentrations 12 below the level of the th en current standard, or below even lower O 3 concentrations, 13 including a level as low as 0.061 ppm, and continue to report statistically significant 14 associations. The Administrator notes that the relationships between ambient O 3 15 concentrations and lung fun ction decrements, respiratory sy mptoms, indicators of 16 respiratory

morbidity including increased respiratory

- related emergency department visits 17 and hospital admissions, and possibly mortality reported in a large number of studies 18 likely

extend down to ambi ent O 3 concentrations well below the level of the standard set 19 in 2008 (0.075 ppm), in that the highest level at which there is any indication of a 20 threshold is approximately 0.050 ppm. The Administrator notes as well that toward the 21 lower end of the rang e of O 3 concentrations observed in such studies, ranging down to 22 background levels (i.e., 0.035 to 0.015 ppm), there is increasing uncertainty as to whether 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 218 the observed associations remain plausibly related to exposures to ambient O 3 , rather than 1 to the b roader mix of air pollutants present in the ambient atmosphere. She also notes 2 that there are limitations in epidemiological studies that make discerning population 3 thresholds difficult, as discussed above, such that there is the possibility that threshol ds 4 for individuals may

exist in reported associations at fairly low levels within the range of 5 air quality

observed in the studies but not be detectable as population thresholds in 6 epidemiological anal ys es. 7 In looking more broadl y at evidence from animal t oxicological, controlled human 8 exposure, and epidemiological studies, the Administrator finds substantial evidence, 9 newly

available for consideration in the 2008 rulemaking, that people with asthma and 10 other preexisting pulmonary diseases are among those at increased risk from O 3 11 exposure. As discussed above, altered phy siological, morphological , and biochemical 12 states ty

pical of respiratory

diseases like asthma, COPD , and chronic bronchitis may 13 render people sensitive to additional oxidative burden induce d by O 3 exposure. Children 14 and adults with asthma are the group that has been studied most extensively . Evidence 15 from controlled human exposure studies indicates that asthmatics and people with 16 allergic rhinitis may exhibit larger lung function decrement s in response to O 3 exposure 17 than healthy subjects and that they can have larger inflammatory responses. The 18 Administrator also notes that two large U.S. epidemiological studies , as well as several 19 smaller U.S. and international studies, have reported fairl y robust associations between 20 ambient O 3 concentrations and measures of lung function and daily s ymptoms (e.g., chest 21 tightness, wheeze, shortness of breath) in children with moderate to severe asthma and 22 between O 3 and increased asthma medication use. These more serious responses in 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 219 asthmatics and others with lung disease provide biological plausibility for the respiratory 1 morbidity

effects observed in epidemiological studies, such as respiratory

- related 2 emergency

department visits and hospital admissio ns. 3 The Administrator also observes that a substantial body of evidence from 4 controlled human exposure and epidemiological studies indicates that relative to the 5 healthy , non - asthmatic subjects used in most controlled human exposure studies, a 6 greater prop ortion of people with asthma may be affected, and those who are affected 7 may have as large or larger lung function and s ymptomatic responses to O 3 exposures. 8 Thus, the Administrator concludes that controlled human exposure studies of lung 9 function decrements and respiratory s ymptoms that evaluate onl y healthy, non

- asthmatic 10 subjects likely

underestimate the effects of O 3 exposure on asthmatics and other 11 susceptible populations. 12 In addition to the evidence

- based considerations discussed above , the 13 Administrator also considered quantitative exposures and health risks estimated to occur 14 associated with air quality simulated to just meet various standard level s to help inform 15 judgments about a range of standard levels for consideration that could provide an 16 app ropriate degree of public health protection. In so doing, she is mindful of the 17 important uncertainties and limitations that are associated with the exposure and risk 18 assessments, as discussed in more detail in the 2007 Staff Paper, and above in sections 19 II.B and II.C. 1.b . Beyond these uncertainties, the Administrator also recognized 20 important limitations related to the exposure and risk analy ses. For example, EPA did 21 not have sufficient information to evaluate all relevant at - risk groups (e.g., outdoor 22 workers) or all O 3 - related health outcomes (e.g., increased medication use, school 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 220 absences, emergency

department visits), and the scope of the anal ys es was generall y 1 limited to estimating exposures and risks in 12 urban areas across the U.S., and to only 2 five or just one area for some health effects . Thus, it is clear that national

- scale public 3 health impacts of ambient O 3 exposures are much larger than the quantitative estimates of 4 O 3 - related incidences of adverse health effects and the numbers of children likely to 5 experience exposures of concern associated with meeting the then current standard or 6 alternative standards. Taking these limitations into account, the CASAC advised EPA 7 not to rely

solel y on the results of the exposure and risk assessments in considering 8 alternative standards, but also to place significant weight on the body of evidence of O 3 - 9 related health effects in drawing conclusions about an appropriate range of levels for 10 consideration. The Administrator agrees with this advice

. 11 Turning first to the results of the exposure assessment, the Administrator focused 12 on the extent to which alternative standard levels , approximately at and below the 0.0 75 13 ppm O 3 standard set in the 2008 final rule , are estimated to reduce exposures over the 14 0. 060 and 0.070 ppm health effects benchmark levels, for all and asthmatic school age 15 children in the 12 urban areas included in the assessment. 52 The Administrator also took 16 note that the lowest standard level included in the exposure and health risk assess ments 17 was 0.064 ppm and that additional reductions in exposures over the selected health 18 benchmark levels would be anticipated for just meeting a 0.060 ppm standard. 19 As an initial matter, the Administrator recognized that the concept of “exposures 20 of conc ern” is more appropriately viewed as a continuum , with greater confidence and 21

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 O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 221 less uncertainty about the existence of health effects at the upper end and less confidence 1 and greater uncertainty as one considers increasingl y lower O 3 exposure levels. In 2
co nsidering the concept of exposures of concern, the Administrator also noted that it is 3 important to balance concerns about the potential for health effects and their severity with 4 the increasing uncertainty associated with our understanding of the likeliho od of such 5 effects at lower O 3 levels. Within the context of this continuum, estimates of exposures 6 of concern at discrete benchmark levels provide some perspective on the public health 7 impacts of O 3 - related phy siological effects that have been demonstrated in controlled 8 human exposure and toxicological studies but cannot be evaluated in quantitative risk 9 assessments, such as lung inflammation, increased airway responsiveness, and changes in 10 host defenses. They also help in understanding the extent to whi ch such impacts have the 11 potential to be reduced by meeting alternative standards. As discussed in II.C.1.a above, 12 these O 3 - related phys iological effects are plausibly linked to the increased morbidity seen 13 in epidemiological studies (e.g., as indicated b y increased medication use in asthmatics, 14 school absences in all children, and emergency department visits and hospital admissions 15 in people with lung disease). 16 Estimates of the number of people likel y to experience exposures of concern 17 cannot be directl y translated into quantitative estimates of the number of people likely to 18 experience specific health effects, since sufficient information to draw such comparisons 19 is not available

-- if such information were available, these health outcomes would have 20 be en included in the quantitative risk assessment. Due to individual variability in 21 responsiveness, onl y a subset of individuals who have exposures at and above a specific 22 benchmark level are expected to experience such adverse health effects, and susceptib le 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 222 population groups such as those with asthma are expected to be affected more by such 1 exposures than healthy individuals. 2 For the reasons discussed in section II.C.1.b above, the Administrator has 3 concluded that it is appropriate to focus on both the 0.0 60 and 0.070 ppm health effect 4 benchmarks for her decision on the primary standard . In summary , the focus on these 5 two benchmark levels reflects the following evidence

- based considerations, discussed 6 above in section II.C.1.a, that raise concerns about adverse health effects likely occurring 7 at levels below 0.080 ppm: (1) that there is limited, but important, new evidence from 8 controlled human exposure studies showing lung function decrements and respiratory 9 sy mptoms in some healthy

subjects at 0.060 ppm; (2) that asthmatics are likely to have 10 more serious responses than healthy individuals; (3) that lung function is not likely to be 11 as sensitive a marker for O 3 effects as lung inflammation; and (4) that there is 12 epidemiological evidence which reports ass ociations between ambient O 3 concentrations 13 and respiratory

s ymptoms, ED visits, hospital admissions, and premature mortality in 14 areas with O 3 levels that extend well below 0.080 ppm. 15 Based on the exposure and risk considerations discussed in detail in the 2007 16 Staff Paper and presented in sections II.B and II.C.1.b above , the Administrator notes the 17 following important observations from these assessments: 1) there is a similar pattern for 18 all children and asthmatic school age children in terms of exposures of concern over 19 selected benchmark levels when estimates are expressed in terms of percentage of the 20 population ; 2) the aggregate estimates of exposures of concern reflecting estimates for the 21 12 urban areas included in the assessment are considerabl y larger for the benchmark level 22 of 0.060 ppm compared to the 0.070 ppm benchmark ; 3) there is notable year- to - ye ar 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 223 variability

in exposure and risk estimates with higher exposure and risk estimates 1 occurring in simulations involving a ye ar with generall y po orer air quality in most areas 2 (2002) compared to a ye ar with generally better air quality

(2004); and 4) there is 3 significant city

- to - city variability

in exposure and risk estimates, with some cities 4 receiving considerabl y less protection associated with air quality just meeting the same 5 standard

. As discussed above, the Administrator believes that it is appropriate to 6 consider not just the aggregate estimates across all cities, but also to consider the public 7 health impacts in cities that receive relativ ely less protection from alternative standards 8 under consideration. Similarly , the Administrator believes that year- to - ye ar variability 9 should also be considered in making judgments about which standards will protect public 10 health with an adequate margin of safety

. 11 In addition, significant reductions in exposures of concern and risk have been 12 estimated to occur across standard levels anal yz ed. The magnitudes of exposure and risk 13 reductions estimated to occur in going from a 0.074 ppm standard to a 0.064 ppm 14 standard are as large as those estimated to occur in going from the then current 0.084 15 ppm standard to a 0.074 ppm standard. Consequently , the reduction in risk that can be 16 achieved b y going from a standard of 0.074 ppm to a standard of 0.064 ppm is 17
c omparable to the risk reduction that can be achieved by moving from the 1997 O 3 18 standard, effectively a 0.084 ppm standard, to a standard very close to the 2008 standard 19 of 0.075 ppm. 20 The Administrator also observes that estimates of exposures of concern associated 21 with air quality

just meeting the alternative standards below 0.080 ppm (i.e., 0.074, 22 0.070, and 0.064 ppm , the levels included in the assessment) are notably lower than 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 224 estimates for alternative standards set at and above 0.080 ppm. As shown in Table 6

- 8 in 1 the 2007 Staff Paper, just meeting a 0.080 ppm standard is associated with an aggregate 2 estimate of exposures of concern of about 13% of asthmatic children at the 0.070 ppm 3 benchmark level, ranging up to 31% in the city with the least degree of protection in a 4 ye ar with generall y poorer air quality, and an aggregate estimate of exposures of concern 5 of about 40% of asthmatic children, ranging up to 63% in the city with the least degree of 6 protection at the 0.060 ppm benchmark level. Based on the exposure estimates presented 7 in Table 3 in this notice, she observes that standards included in the assessment below 8 0.080 ppm (i.e., 0.074, 0.070, and 0.064 ppm), are estimated to have substantially lower 9 estimates of exposures of concern at the 0.070 ppm benchmark level. Similarly , she 10 notes that exposures of concern at the 0.060 ppm benchmark associated with alternative 11 standards below 0.080 ppm are appreciably lower than exposures associated with 12 standards at or above 0.080 ppm, especiall y for stan dards set at 0.064 and 0.070 ppm. 13 As noted previousl y, the Administrator also recognize s that the risk estimates for 14 health outcomes included in the risk assessment are limited and that the overall health 15 effects evidence is indicative of a much broader array of O 3 - related health effects that are 16 part of a “p yramid of effects” that include various indicators of morbidity that could not 17 be included in the risk assessment (e.g., school absences, increased medication use, 18 doctor’s visits, and emergency department visits) , some of which have a greater impact 19 on at - risk groups. Consideration of such unquantified risks for this array of health 20 effects, taken together with the estimates of exposures of concern and the quantified 21 health risks discussed above , supp orts the Administrator’s evidence

- based conclusion that 22 revising the standard level to a level well below 0.080 ppm will provide important 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 225 increased public health protection, especially for at

- risk groups such as people with 1 asthma or other lung disease, a s well as children and older adults, particularly those 2 active outdoors, and outdoor workers 3 Based on the evidence

- and exposure/risk

- based considerations discussed above, 4 the Administrator concludes that it is appropriate to set the level of the primary O 3 5 standard to a level well below 0.080 ppm, a level at which the evidence provides a high 6 degree of certainty about the adverse effects of O 3 exposure in healthy people, to provide 7 an adequate margin of safety for at

- risk groups. In selecting a proposed range of levels, 8 the Administrator believes it is appropriate to consider the following information: (1) the 9 strong body of evidence from controlled human exposure studies evaluating healthy 10 people at exposure levels of 0.080 ppm and above that demonstrat e d lung function 11 decrements, respiratory sy mptoms, pulmonary

inflammation, and other medically 12 significant airway

responses, as well as limited but important evidence of lung function 13 decrements and respiratory s ymptoms in healthy

people down to O 3 exposure levels of 14 0.060 ppm; (2) the substantial body of evidence from controlled human exposure and 15 epidemiological studies indicating that people with asthma are likel y to experience larger 16 and more serious effects than healthy people; (3) the body of epidemiol ogical evidence 17 indicating associations are observed for a wide range of serious health effects, including 18 respiratory

- related emergency department visits and hospital admissions and premature 19 mortality , across distributions of ambient O 3 concentrations th at extend below the current 20 standard level of 0.075 ppm, as well as questions of biological plausibility in attributing 21 the observed effects to O 3 alone at the lower end of the concentration ranges extending 22 down to background levels; and (4) the estimates of exposures of concern and risks for a 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 226 range of health effects that indicate that important improvements in public health are very 1 likely

associated with O 3 levels just meeting alternative standards , especially for 2 standards set at 0.070 and 0.064 ppm (the lowest levels included in the assessment) , 3 relative to standards set at and above 0.080 ppm

. 4 The Administrator next considered what standard level well below 0.080 ppm 5 would be requisite to protect public health, including the health of at

- risk groups, with an 6 adequate margin of safety that is sufficient but not more than necessary to achieve that 7 result. The assessment of a standard level calls for consideration of both the degree of 8 risk to public health at alternative levels of the standard as well as the certainty that such 9 risk will occur at any specific level

. Based on the information available in the 2008 10 rulemaking, there is no evidence

- based bright line that indicates a single appropriate 11 level . Instead there is a combination of scientific ev idence and other information that 12 needs to be considered as a whole in making this public health policy judgment, and 13 selecting a standard level from a range of potentially reasonable values. 14 As an initial matter, the Administrator considered whether the s tandard level of 15 0.075 ppm set in the 2008 final rule is sufficientl y below 0.080 ppm to be requisite to 16 protect public health with an adequate margin of safety. In considering this standard 17 level, the Administrator looked to the rationale for selecting t his level presented in the 18 2008 final rule, as summarized above in section II.C.3. In that rationale, EPA observed 19 that a level of 0.075 ppm is above the range of 0.060 to 0.070 ppm recommended b y 20 CASAC, and that the CASAC Panel appeared to place greater weight on the evidence 21 from the Adams studies and on the results of the exposure and risk assessments, whereas 22 EPA placed greater weight on the limitations and uncertainties associated with that 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 227 evidence and the quantitative exposure and risk assessments. Additionally , EPA’s 1 rationale did not discuss and thus placed no weight on exposures of concern relative to 2 the 0.060 ppm benchmark . Further, EPA concluded that “[a] standard set at a lower level 3 than 0.075 ppm would only result in significant further public health protection if, in fact, 4 there is a continuum of health risks in areas with 8

- hour average O 3 con centrations that 5 are well below the concentrations observed in the key controlled human exposure studies 6 and if the reported associations observed in epidemiological studies are, in fact, causall y 7 related to O 3 at those lower levels. Based on the availabl e evidence, [EPA] is not 8 prepared to make these assumptions” (73 FR 16483). 9 In reconsidering the entire body of evidence available in the 2008 rulemaking, 10 including the Agency ’s own assessment of the epidemiological evidence in the 2006 11 Criteria Document, and placing significant weight on the views of CASAC, the 12 Administrator now conclud es that important and significant risks to public health are 13 likely

to occur at a standard level of 0.075 ppm . She judges that a standard level of 0.075 14 ppm is not sufficient to provide protection with an adequate margin of safety

. In support 15 of this conclusion, the Administrator finds that setting a stand ard that would protect 16 public health, including the health of at

- risk populations, with an adequate margin of 17 safety should reasonabl y depend upon giving some weight to the results of the Adams 18 studies and EPA's reanalysis of the Adams's data, and to how ef fectivel y alternative 19 standard levels would serve to limit exposures of concern relative to the 0.060 ppm 20 benchmark level as well as to the 0.070 ppm benchmark level. The Administrator notes 21 that EPA’s risk assessment estimates comparable risk reductions in going from a 0.074 22 ppm standard to a 0.064 ppm standard as were estimated in going from the then current 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 228 0.084 ppm standard down to a 0.074 ppm standard for an array of health effects analyzed

. 1 These estimates include reductions in risk for lung functi on decrements in all and 2 asthmatic school age children, respiratory s ymptoms in asthmatic children, respiratory

3 related hospital admissions, and non

- accidental mortality

. 4 Further, based on the exposure assessment estimates discussed above, the 5 Administrator notes that for air quality just meeting a 0.074 ppm standard, approximately 6 27% of asthmatic school age children and 25% of all school age children are estimated to 7 experience one or more exposures of concern over the 0.060 ppm benchmark level based 8
on simulations for a year with generall y poorer air quality; this estimate increases to 9 about 50% of asthmatic and all children in the city with the least degree of protection. 10 The Administrator judges that these estimates are large and strongl y suggest significant 11 public health impacts would likely remain in many

areas with air quality

just meeting a 12 0.075 ppm O 3 standard. 13 In light of these estimates and the available evidence, the Administrator agrees 14 with CASAC’s conclusion that important public health protections can be achieved b y a 15 standard set below 0.075 ppm, within the range of 0.060 to 0.070 ppm. Inaddition, based 16 on both the evidence

- and exposure/risk

- based considerations summarized above, the 17 Administrator concludes that a standard set as high as 0.075 w ould not be considered 18 requisite to protect public health with an adequate margin of safety, and that 19 consideration of lower levels is warranted. In considering such lower levels, the 20 Administrator recognizes that the CAA requires her to reach a public health policy 21 judgment as to what standard would be requisite to protect public health with an adequate 22 margin of safety , based on scientific evidence and technical assessments that have 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 229 inherent uncertainties and limitations. This judgment requires making reasoned decisions 1 as to what weight to place on various types of evidence and assessments and on the 2 related uncertainties and limitations. 3 In selecting a level below 0.075 ppm that would serve as an appropriate upper end 4 for a range of levels to propose, the Administrator has considered a more cautious 5 approach to interpreting the available evidence and exposure/risk

- based information

– 6 that is, an approach that places significant weight on uncertainties and limitations in the 7 information so as to avoid potentially overestimating public health risks and protection 8 likely

to be associated with just meeting a particular standard level. In so doing, she 9 notes that the most certain evidence of adverse health effects from exposure to O 3 comes 10 from the controlled human exposure studies, and that the large bulk of this evidence 11 derives from studies of exposures at levels of 0.080 ppm and above. At those levels, 12 there is consistent evidence of lung function decrements and respiratory s ymptoms in 13 healthy young adults, as well as evidence of inflammation and other medically significant 14 airway

responses. Further , she takes note of the limited but important evidence from 15 controlled human exposure studies indicating that lung function decrements and 16 sy mptom s can occur in healthy peopl e at levels as low as 0.060 ppm, while also 17 recognizing the limitations in that evidence, as discussed above in sections II.A.1 and 18 II.C.1.a. She also notes that some people with asthma are likel y to experience larger and 19
more serious effects than the healthy subjects evaluated in the controlled exposure 20 studies , while recognizing that there is uncertainty about the magnitude of such 21 differences. In considering the available epidemiological studies , she recognizes that 22 they pro vide evidence of serious respiratory morbidity

effects, including respiratory

- 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 230 related emergency

department visits and hospital admissions, and non

- accidental 1 mortality at levels well below 0.080 ppm, while also recognizing that there is increasing 2 uncertainty associated with the likelihood that such effects occur at decreasing O 3 levels 3 down to background levels . Considering the exposure/risk information, as shown in 4 Table 3, the Administrator observes that a standard set at 0.070 ppm would likely 5 substantially

limit exposures of concern relative to the 0.070 ppm benchmark level, while 6 affording far less protection against exposures of concern relative to the 0.060 ppm 7 benchmark level. To the extent that more weight is placed on protection relative to the 8 higher benchmark level, and more weight is placed on the uncertainties associated with 9 the epidemiological evidence, a standard set at 0.070 ppm might be considered to be 10 adequatel y protective. Taken together, this type of cautious approach to interpretin g the 11 evidence and the exposure/risk information serve s as the basis for the Administrator ’s 12 conclu sion that the upper end of the proposed range should be set at 0.070 ppm O 3 . 13 In selecting a level that would serve as an appropriate lower end for a range of 14 levels to propose, the Administrator has considered a more precautionary approach to 15 interpreting the available evidence and exposure/risk

- based information

– that is, an 16 approach that places less weight on uncertainties and limitations in the information so as 17 to avoid potentially underestimating public health improvements likely to be associated 18 with just meeting a particular standard level. In so doing, the Administrator notes the 19 limited, but important evidence of a lowest

- observed

- effects level at 0. 060 ppm O 3 from 20 controlled human exposure studies reporting lung function decrements and respiratory 21 sy mptoms in healthy

subjects . Notably , these studies also report that a small percentage 22 of subjects (7 to 20 percent) experienc ed moderate lung function decrement s ( > 10 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 231 percent) at the 0.060 ppm exposure leve l, recognizing that f or people with lung disease, 1 such moderate functional or sy mptomatic responses would likely interfere with normal 2 activity

for many individuals, and would likely result in more frequent use of medication

. 3 In addition, a substantial body of evidence indicat es that people with asthma are likel y to 4 experience larger and more serious effects than healthy people and therefore controlled 5 human exposure studies done with healthy subjects likely underestimate effects in this at 6 risk population. 7 Moreover, epidemiological studies provide evidence of serious respiratory 8 morbidity

effects, including respiratory

- related emergency department visits and hospital 9 admissions, and non

- accidental m ortality at O 3 levels that may plausibl y extend down to 10 at least 0.060 ppm even when considering the uncertainties inherent in such studies

. The 11 Administrator notes that the controlled human exposure studies conducted at 0.060 ppm 12 provide some biological plausibility for associations between respiratory morbidity

and 13 mortality

effects found in epidemiological studies and O 3 exposures down to 0.060 ppm. 14 Considering the exposure information, as shown in Table 3, the Administrator observes 15 that a standard set at 0.064 ppm would likely essentially

eliminate exposures of concern 16 relative to the 0.070 ppm benchmark level, while appreciably limiting exposures of 17 concern relative to the 0.060 ppm benchmark level to approximately 6 percent of 18 asthmatic children in the aggregate across 12 cities and up to 16 percent in the city that 19 would receive the least protection. While not addressed in the exposure assessment done 20 as part of the 2008 rulemaking, a standard set at 0.060 ppm would be expected to provide 21 somewhat greater protection from such exposures, which is important to the extent that 22 more weight is placed on providing protection relative to the lower benchmark level. 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 232 Taken together, the Administrator concludes that this precautionary approach to 1 interpreting the evidence and the exposure/risk information supports a level of 0.060 ppm 2 as the lower end of the proposed range. 3 The Administrator has also concluded that the lower end of the proposed range 4 should not extend below 0.060 ppm O 3 . Inreaching this co nclusion, she gives significant 5 weight to the recommendation of the CASAC panel that 0.060 ppm should be the lower 6 end of the range for consideration (Henderson, 2006c). In the Administrator's view, the 7 evidence from controlled human exposure studies at the 0.060 ppm exposure level, the 8 lowest level tested, is not robust enough to support consideration of a lower level. While 9 some epidemiological studies provide evidence of serious respiratory morbidity

effects 10 and non

- accidental mortality with no evidenc e of a threshold, the Administrator notes 11 that other studies provide evidence of a potential threshold somewhat below 0.060 ppm. 12 Moreover, there are limitations in epidemiological studies that make discerning 13 population thresholds difficult, including few er observations in the range of lower 14 concentrations, concerns related to exposure measurement error, the possible role of 15 copollutants and effects modifiers, and interindividual differences in susceptibility to O 3 - 16 related effects. In the Administrator’s judgment, these limitations in epidemiological 17 studies , including the limitations in judging the causality of observed associations at 18 lower O 3 levels, and the lack of robust controlled human exposure data at 0.060 ppm 19 make it difficult to interpret this evidence as a basis for a standard level set below 0.060 20 ppm. Thus, in selecting 0.060 ppm as the lower end of the range for the proposed level 21 of the O 3 standard, the Administrator has taken into account information on the lowest

22 observed

- effects levels in controlled human exposure studies, indications of possible 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 233 thresholds reported in some epidemiological studies, the increasing uncertainty in the 1 epidemiological evidence at even lower levels, as well as evidence about increased 2 susceptibility

of people with asthma and also other lung diseases. In so doing, she 3 concludes that a primary O 3 standard set below 0.060 ppm would be more than is 4 necessary to protect public health with an adequate margin of safety for at

- risk groups. 5 In reaching her proposed d ecision, the Administrator has also considered the 6 public comments that were received on the 2007 proposed rule (72 FR 37818). The 7 Administrator notes that there were sharpl y divergent views expressed by two general 8 sets of commenters with regard to consi dering the health effects evidence, results of 9 exposure and risk assessments, and the advice of the CASAC panel. On one hand, 10 medical groups, health effects researchers, public health organizations, environmental 11 grou

ps , and some s tate , tribal and local air pollution control agencies strongly supported a 12 standard set within the range recommended b y the CASAC. These commenters generally 13 placed significant weight on the more recent evidence from controlled human exposure 14 studies, down to the 0.060 ppm expos ure level, as well as on the epidemiological studies 15 and the results of the exposure and risk assessment conducted for the 2008 rulemaking. 16 Many

of these commenters took a more precautionary view and supported a standard set 17 at 0.060 ppm O 3 , the lower end of the CASAC recommended range. The Administrator 18 notes that these views are generall y consistent with her proposed conclusions. On the 19 other hand, another group of commenters primarily representing industry associations 20 and businesses and some s tate environmental agencies , primaril y expressed the view that 21 the more recent evidence from controlled human exposure, the epidemiological studies, 22 and the results of exposure and human health risk assessments were so uncertain that they 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 234 did not provide a basis for making any changes to the then current 0.084 ppm O 3 standard 1 set in 1997. This group of commenters generally argu ed that the health effects evidence 2 newly

available in the 2008 rulemaking, the results of the exposure and health risk 3 assessments, and the advice of the CASAC were flawed . For the reasons discussed 4 above, the Administrator does not agree with the later group of commenters that 5 essentially

no weight should be placed on any of the new evidence or assessments that 6 were available for consideration in the 2008 rulemaking. 7 Based on consideration of the entire body of evidence and information available 8 in the 2008 rulemaking, including exposure and risk estimates , as well as the 9 recommendations of CASAC, the Administrator proposes to set the lev el of the primary 10 8
- hour O 3 standard to a level within the range of 0.060 to 0.070 ppm
. A standard level 11 within this range would reduce the risk of a variety of health effects associated with 12 exposure to O 3 , including the respiratory s ymptoms and lung fun ction effects 13 demonstrated in the controlled human exposure studies, and th e respiratory

- related 14 emergency

department visits, hospital admissions and mortality effects observed in the 15 epidemiological studies. All of these effects are indicative of a much broader array of 16 O 3 - related health endpoints, such as school absences and increased medication use, that 17 are plausibl y linked to these observed effects. Depending o n the weight placed on the 18 evidence and information available in the 2008 rulemaking, as we ll as the uncertainties 19 and limitations in the evidence and information, a standard could be set within this range 20 at a level that would be requisite to protect public health with an adequate margin of 21 safety. 22Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 235 In reaching this proposed decision, as discus sed above, the Admini strator has 1 focused on the nature of the increased public health protection that would be afforded b y 2 a standard set within the proposed range of levels relative to the protection afforded b y 3 the standard set in 2008. Having considere d the public comments received on the 2007 4 proposed rule in reaching this proposed decision that reconsiders the 2008 final rule , the 5 Administrator is interested in again receiving public comment on the benefits to public 6 health associated with a standard set at specific level s within the proposed range relative 7 to the benefits associated with the standard set in 2008. 8 D. Proposed Decision on the Level of the Primary Standard 9 For the reasons discussed above, and taking into account information and 10
assessm ents presented in the 2006 Criteria Document and 2007 Staff Paper, the advice 11 and recommendations of CASAC, and public comments received during the 2008 12 rulemaking, the Administrator proposes to set a new level for the 8

- hour primary O 3 13 standard. Specific ally , the Administrator proposes to set the level of the 8
- hour primary 14 O 3 standard to within a range of 0

. 060 to 0.070 ppm. The proposed 8

- hour primary 15 standard would be met at an ambient air monitoring site when the 3

- ye ar average of the 16 annual forth

- hi ghest daily maximum 8

- hour average O 3 concentration is less than or 17 equal to the level of the standard that is promulgated. Thus, the Administrator proposes 18 to set a standard with a level within this range

. S he solicits comment on th is range and 19 on the a

ppropriate weight to place on the various ty pes of available evidence, the 20 exposure and risk assessment results, and the uncertainties and limitations related to this 21 information , as well as on the benefits to public health associated with a standard set 22
w ithin this range relative to the benefits associated with the standard set in 2008

. 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 236 1 III. Communication of Public Health Information 2 In formation on the public health implications of ambient concentrations of criteria 3 pollutants is currently made available primarily through EPA's Air Quality Index (AQI) 4 program. The current Air Quality Index has been in use since its inception in 1999 (64 5 FR 42530). It provides accurate, timely , and easily understandable information about 6 daily levels of pollution (40 CFR 58.50). The AQI establishes a nationall y uniform 7 sy stem of indexing pollution levels for O 3 , carbon monoxide, nitrogen dioxide, 8 particulate matter and sulfur dioxide. The AQI converts pollutant concentrations in a 9 community's air to a number on a scale from 0 to 500. Reported AQI values enable the 10 public to know whether air pollution levels in a particular location are characterized as 11 good (0

- 50), moderate (51

- 100), unhealthy for sensitive groups (101

- 150), unhealthy 12 (151

- 200), very

unhealthy

( 201
- 300), or hazardous (300

- 500). The AQI index value 13 of 100 ty

pically corresponds to the level of the short

- term NAAQS for each pollutant. 14 An AQI value greater than 100 means that a pollutant is in one of the unhealthy 15 categories (i.e., unhealthy fo r sensitive groups, unhealthy , very unhealthy , or hazardous) 16 on a given day ; whereas an AQI value at or below 100 means that a pollutant 17 concentration is in one of the satisfactory categories (i.e., moderate or good). Decisions 18 about the pollutant concentrations at which to set the various AQI breakpoints, that 19 delineate the various AQI categories, draw directly from the underl ying health 20 information that supports the NAAQS review. 21 In the 2008 rulemaking, the AQI for O 3 was revised by setting an AQI value of 22 100 equal to 0.075 ppm, 8

- hour average, the level of the revised primary O 3 standard. 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 237 The other AQI breakpoints were also revised as follows: An AQIvalue of 50 is set at 1 0.059 ppm; an AQI value of 150 was set at 0.095 ppm; and an AQI value of 200 wa s set 2 at 0.115 ppm. All these levels are averaged over 8 hours. These levels were developed 3 by making proportional adjustments to the other AQI breakpoints (i.e., AQI values of 50, 4 150 and 200). 5 The Agency

recognizes the importance of revising the AQI in a timel y manner to 6 be consistent with any revisions to the NAAQS. Therefore, having proposed to set a new 7 level for the 2008 primary 8
- hour O 3 standard in th is action, EPA also proposes to 8 finalize conforming changes to the AQI in connection with the A gency's final decision on 9 the level of the primary O 3 standard. These conforming changes would include setting 10 the 100 level of the AQI at the same level as th at set for th e primary O 3 standard resulting 11 from this rulemaking , and also making proportional adjustments to AQIbreakpoints at 12 the lower end of the range (i.e., AQI values of 50, 150 and 200). EPA does not propose 13 to change breakpoints at the higher end of the range (from 300 to 500), which would 14 apply

to state contingency

plans or the Significant Harm Level (40 CFR 51.16), because 15 the information from this reconsideration of the 2008 final rule does not inform decisions 16 about breakpoints at those higher levels. 17 With re spect to reporting requirements (40 CFR Part 58, §58.50), EPA proposes 18 to require that the AQI be reported in all metropolitan and micropolitan statistical a reas 19 where O 3 monitoring is required , as discussed below in section VI . The Agency solicits 20 comments on our proposed approach to AQI reporting requirements. We are also 21 revising 40 CFR Part 58, §58.50 (c) to require the reporting requirements to be based on 22 the latest available census figures, rather than the most recent decennial U.S. census. 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 238 This change is consistent with our current practice of using the latest population fi gures 1 to make monitoring requirements more responsive to changes in population. 2 3 IV. Rationale for Proposed Decision on the Secondary Standard 4 As an initial matter, the Administrator notes that the 2008 final rule concluded 5 that (1) the protection afforded b y the 1997 secondary O 3 standard was “not sufficient 6 and that the standard needs to be revised to provide additional protection from known and 7 anticipated adverse effects on sensitive natural vegetation and sensitive ecosystems, and 8 that such a revised standard could also be expected to provide additional protection to 9 sensitive ornamental vegetation” and (2) “that there is not adequate information to 10 establish a separate secondary standard based on other effects of O 3 on public welfare” 11 (73 FR 16497). The Administrator is not reconsidering these aspects of the 2008 12 decision, which are based on the reasons discussed in section IV.B of the 2008 final rule 13 (73 FR 16489

- 16497). The Administrator also notes that the 2008 final rule concluded 14 that it was appropriate to retain the O 3 indicator for the secondary O 3 standard

. The 15 Administrator is not reconsidering th is aspect of the 2008 decision , which was based on 16 the reasons discussed in sections IV.B and IV.C of the 2008 final rule (73 FR 16489

- 17 16497). F or these reasons, the Administrator is not reopening the 2008 decision with 18 regard to the need to revise the 1997 secondary O 3 standard to provide additional 19 protection from known and anticipated adverse effects on sensitive natural vegetation and 20 sensitiv e ecos ys tems, nor with regard to the appropriate indicator for the secondary 21 standard. Thus, the information that follows in this section specifically focuses on a 22 reconsideration of the 8

- hour secondary O 3 standard set in the 2008 final rule for the 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 239 purp ose of determining whether and, if so, how to revise the form, averaging time, and 1 level of the standard to provide appropriate protection from known and anticipated 2 adverse effects on sensitive natural vegetation and sensitive ecos ys tems. 3 This section presents the rationale for the Administrator’s proposed decision that 4 the secondary O 3 standard, which was set identical to the revised primary standard in the 5 2008 final rule, should instead be a new cumulative, seasonal standard . This standard is 6 expresse d in terms of a concentration

- weighted form commonly called W126, which uses 7
a sigmoidal weighting function to assign a weight to each hourl y O 3 concentration within 8 the 12 hour daylight period (8:00 am to 8:00 pm). This daily ozone index is defined as 9 f ollows: 10 

#  

  pm i

am i i c C w W daily i 8
8 126 , where C i = hourly O 3 at hour i, and C c e w 126 4403 1 1

   . 11
The daily

index values are then summed over each month within the O 3 season, and the 12 annual highest consecutive three month sum is determined. The proposed standard 13 consists of the three

- ye ar average of this highest three

- month statistic, set at a level 14 within the range of 7 to 15 ppm
- hours. 15 As discussed more full y below, th e rationale for this proposed new standard is 16 based on a thorough review , in the 200 6 Criteria Document, of the latest scientific 17 information on vegetation , ecological and other public welfare effects associated with the 18 presence of O 3 in the ambient air. This rationale also takes into account and is consistent 19 with : (1) staff assessments of the most policy

- relevant information in the 2006 Criteria 20 Document and staff analy ses of air quality, vegetation effects evidence, exposure , and 21 risk s, presented in the 2007 Staff Paper, upon which staff recommendations for revisions 22 to the secondary O 3 standard are based; (2) CASAC advice and recommendations as 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 240 reflected in discussion s of drafts of the 2006 Criteria Document and 2007 Staff Paper at 1 public meetings, in separate written comments, and in CASAC's letters to the 2 Administrator , both before and after the 2008 rulemaking, and (3) public comments 3 received during development of these documents , either in conjunction with CASAC 4 meetings or separatel y ; and on the 2007 proposed rule, and (4) consideration of the 5 degree of protection to vegetation potentially afforded by

the 2008 8

- hour standard. 6 In developing this rationale, the Administrator has again focused on direct O 3 7 effects on vegetation, specificall y drawing upon an integrative s ynthesis of the entire 8 body of evidence (EPA, 2006a, chapter 9 ), published through early 2006, on the broad 9 array of vegetation effects associated with the presence of O 3 in the ambient air. In 10 addition, because O 3 can also indirectly affect other ecos ys tem component s such as soils, 11 water, and wildlife, and their a ssociated ecos ys tem goods and services, through its effects 12 on vegetation, a qualitative discussion of these other indirect impacts is also included, 13 though these effects were not quantifiable at th e time of the 2008 rulemaking

. As 14 discussed below in section IV.A, the peer

- reviewed literature includes studies conducted 15 in the U.S., Canada, Europe, and many other countries around the world. 53 In 16 reconsidering this evidence, a s was concluded in the 2008 rulemaking , and based on the 17 body

of scientific literat

ure assessed in the 2006 Criteria Document, the Administrator 18 continues to believes that it is reasonable to conclude that a secondary standard protecting 19 the public welfare from known or anticipated adverse effects to trees and native 20

53 Inits assessment of the evidence judged to be most relevant to m aking decisions on the level of the O 3 secondary standard, however, EPA has placed greater weight on U.S. studies, due to the often species

- , site

- and climate

- specific nature of O 3 - related vegetation response.Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 241 vegetation would als o afford increased protection from adverse effects to other 1 environmental components relevant to the public welfare, including ecos ys t em services 2 and function. Section IV.B focuses on considerations related to biologically relevant 3 exposure indices. This rationale also draws upon the results of quantitative exposure and 4 risk assessments, discussed below in section IV.C. Section IV.D focuses on the 5 considerations upon which the Administrator’s proposed conclusions are based. 6 Considerations regarding a cumulative seasonal standard as well as an 8

- hour standard 7 are discussed, and the rationale for the 2008 decision on the secondary standard and 8 CASAC advice, given both prior to the development of the 2007 proposed rule and 9 following the 2008 final rule, are summarized. Finally , the Administrator’s proposed 10 conclusions on the secondary standard are presented. Section IV.E summarizes the 11 proposed decision on the secondary O 3 standard and the solicitation of public comments. 12 As with virtually any policy

- relevant vegetation effects research, there is 13 uncertainty in the characterization of vegetation effects attributable to exposure to 14 ambient O 3 . As discussed below, however, research conducted since the 1997 review 15 provides important information coming from f ield

- based exposure studies, including free 16 air, gradient, and biomonitoring surveys, in addition to the more traditional open top 17 chamber (OTC) studies. Moreover, the newl y available studies evaluated in the 2006 18 Criteria Document have undergone intensive scrutiny through multiple layers of peer 19 review and many opportunities for public review and comment. While important 20 uncertainties remain, the review of the vegetation effects information has been extensive 21 and deliberate. In the judgment of the Admini strator, the intensive evaluation of the 22Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 242 scientific evidence that has occurred provides an adequate basis for this reconsideration 1 of the 2008 rulemaking. 2 A. Vegetation Effects Information 3 This section outlines key information contained in the 2006 Crit eria Document 4 (chapter 9) and in the 2007 Staff Paper (chapter 7) on known or anticipated effects on 5 public welfare associated with the presence of O 3 in ambient air. The information 6 highlighted here summarizes: (1) new information available in the 2008 r ulemaking on 7 potential mechanisms for vegetation effects associated with exposure to O 3 ; (2) the nature 8 of effects on vegetation that have been associated with exposure to O 3 and consequent 9 potential impacts on ecosy stems; and (3) considerations in charact erizing what constitutes 10 an adverse welfare impact of O 3 . 11 Exposures to O 3 have been associated quantitatively and qualitatively with a wide 12 range of vegetation effects. The decision in the 1997 review to set a more protective 13 secondary

standard primarily reflected consideration of the quantitative information on 14 vegetation effects available at that time, particularly growth impairment (e.g., biomass 15 loss) in sensitive forest tree species during the seedling growth stage and yi eld loss in 16 important commerc ial crops. This information, derived mainl y using the open top 17 chamber ( OTC ) exposure method, found cumulative, seasonal O 3 exposures were most 18 strongl y associated with observed vegetation response. The 2006 Criteria Document 19 dis cusses a number of additi onal studies that support and strengthen key conclusions 20 regarding O 3 effects on vegetation and ecos ys tems found in the previous Criteria 21 Document (EPA, 1996a, 2006a), including further clarification of the underlying 22 mechanistic and phys iological processe s at the sub

- cellular, cellular , and whole sy stem 23 levels within the plant. More importantly , however, in the context of this review, new 24Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 243 quantitative information is now available across a broader array of vegetation effects 1 (e.g., growth impairment during seedlings, saplings and mature tree growth stages, visible 2 foliar injury , and yield loss in annual crops) and across a more diverse set of exposure 3 methods, including chamber, free air, gradient, model, and field

- based observation. The 4
non - chambered, fie ld

- based study results begin to address one of the key data gaps cited 5 by EPA in the 1997 review. 6 The following discussion of the policy

- relevant science regarding vegetation 7 effects associated with cumulative, seasonal exposures to ambient levels of O 3 integrates 8 information from the 2006 Criteria Document (chapter 9) and the 2007 Staff Paper 9 (chapter 7). 10 1. Mechanisms 11 S cientific understanding regarding O 3 impacts at the genetic, phys iological, and 12 mechanistic levels helps to explain the biological p lausibility and coherence of the 13 evidence for O 3 - induced vegetation effects and informs the interpretation of predictions 14 of risk associated with vegetation response at ambient O 3 exposure levels. In most cases, 15 the mechanisms of response are similar regardless of the degree of sensitivity of the 16 species. The evidence assessed in the 200 6 Criteria Document (EPA, 2006a) regarding 17 the O 3 - induced changes in phy siology continues to support the information discussed in 18 the 1997 review (EPA, 1996a, 2006a)

. In addition, during the last decade understanding 19 of the cellular processes within plants has been further clarified and enhanced. This 20 section reviews the key scientific conclusions identified in 1996 Criteria Document 21 (EPA, 1996a), and incorporates recent information from the Criteria Document (EPA, 22 2006a). This section describes: (1) plant uptake of O 3 , (2) O 3 - induced cellular to 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 244 sy stemic response, (3) plant compensation and detoxification mechanisms, (4) O 3 - 1 induced changes to plant metabolism, and (5) pl ant response to chronic O 3 exposures. 2
a. Plant Uptake of Ozone 3 To cause injury , O 3 must first enter the plant through openings in the leaves called 4 stomata. Leaves exist in a three dimensional environment called the plant canopy, where 5 each leaf has a unique orientation and receives a different exposure to ambient air, 6 microclimatological conditions, and sunlight. Inaddition, a plant may be located within a 7 stand of other plants which further modifies ambient air exchange with individual leaves. 8 Not all O 3 entering a plant canop y is absorbed into the leaf stomata, but may be adsorbed 9 to other surfaces e.g., leaf cuticles, stems, and soil (termed non

- stomatal deposition) or 10 scavenged b y reactions with intra

- canop y biogenic VOCs and naturally occurring N Ox 11 emissions from soils. Because O 3 does not ty pically penetrate the leaf’s cuticle, it must 12 reach the stomatal openings in the leaf for absorption to occur. The movement of O 3 and 13 other gases such as CO 2 into and out of leaves is controlled by stomatal guard cells that 14 regulate the size of the stomatal aperture s . These guard cells respond to a variety of 15 internal species

- specific factors as well as external site specific environmental factors 16 such as light, temperature, humidity , CO 2 concentration, soil fertility , water status, and in 17
some cases , the presence of air pollutants, including O 3 . These modifying factors 18 produce stomatal cond uctances that vary

between leaves of the same plant, individuals 19 and genotypes within a species a s well as diurnally an d seasonall y. 20 b. Cellular to Systemic Response 21 Once inside the leaf , O 3 can react with a variety of biochemical compounds that 22 are exposed to the air spaces within the leaf or it can be dissolved into the water lining the 23 cell wall of the air spaces

. Once in the aqueous phase, O 3 can be rapidly altered to form 24Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 245 oxidative products that can diffuse more readily into and through the cell and react with 1 many

biochemical compounds. E arl y step s in a series of O 3 - induced events that can lead 2 to leaf injury

se ems to involve alteration in cell membrane function, including membrane 3 transport properties (EPA, 2006a) and/or reactions with organic molecules that in certain 4 circumstances result in the generation of signaling compounds

. The generation of such 5 signaling compounds can lead to a cascade of events. One such signaling molecule is 6 hydrogen peroxide (H 2 O 2 ). The presence of higher

- than

- normal levels of H 2 O 2 within the 7 leaf is a potential trigger for a set of metabolic reactions that include those typical of the 8 well documented “wounding” response or pathogen defense pathway generated b y 9 cutting of the leaf or b y pathogen/insect attack. Ethylene is another compound produced 10 when plants are subjected to biotic or abiotic stressors. Increased ethylene productio n by 11 plants exposed to O 3 stress was identified as a consistent marker for O 3 exposure in 12 studies conducted decades ago (Tingey et al., 1976). 13
c. Compensation and Detoxification 14 Ozone injury will not occur if (1) the rate and amount of O 3 uptake is smal l 15 enough for the plant to detoxify or metabolize O 3 or its metabolites or (2) the plant is able 16 to repair or compensate for the O 3 impacts (Tingey and Taylor, 1982; U.S. EPA, 1996a). 17 With regard to the first, a few studies have documented direct stomatal closure or 18 restriction in the presence of O 3 in some species , which limits O 3 uptake and potential 19 subsequent injury

. This response may be initiated ranging from within minutes to hours 20 or day s of exposure (Moldau et al., 1990; Dann and Pell, 1989; Weber et al., 1993). 21 However, exclusion of O 3 simultaneously restricts the uptake of CO 2 , which also limits 22 photosy

nthesis and growth. Inaddition, antioxidants present in plants can effectivel y 23 protect tissue against damage from low levels of oxidants by diss ipating excess oxidizing 24Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 246 power. Since 1996, the role of detoxification in providing a level of resistance to O 3 has 1 been further investigated. A number of antioxidants have been found in plants. 2 H owever, the pattern of changes in the amounts of these antioxidants varies greatl y 3 among different species and conditions. Most recent reports indicate that ascorbate 4 within the cell wall provides the first significant opportunity for detoxification to occur. 5 In spite of the new research, however, it is still not clear as to what extent detoxification 6 protects against O 3 injury. Specificall y, data are needed on potential rates of antioxidant 7 production, sub

- cellular location(s) of antioxidants, and whether generation of these 8 antioxidants in response to O 3 - ind uced stress potentially

diverts resources and energy 9 away

from other vital uses

. Thus, the 2006 Criteria Document concludes that scientific 10 understanding of the detoxification mechanisms is not yet complete and requires further 11 investigation (EPA, 2006a). 12 Regarding the second, o nce O 3 injury has occurred in leaf tissue, some plants are 13 able to repair or compensate for the impacts. In general, plants have a variety of 14 compensatory

mechanisms for low levels of stress including reallocation of resources, 15 ch anges in root/shoot ratio, production of new tissue, and/or biochemical shifts, such as 16 increased photosy

nthetic capacity

in new foliage and changes in respiration rates, 17 indicating possible repair or replacement of damaged membranes or enzy mes. Since 18 the se mechanisms are genetically determined, not all plants have the same complement of 19 compensatory

mechanisms or degree of tolerance, and these may vary over the life of the 20 plant as no t all stages of a plant’s development are equall y sensitive to O 3 . At h igher 21 levels or over longer periods of O 3 stress, some of these compensatory mechanisms, such 22 as a reallocation of resources away from storage in the roots in favor of leaves or shoots, 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 247 could occur at a cost to the overall health of the plant

. However, it is not yet clear to 1 what degree or how the use of plant resources for repair or compensatory processes 2 affects the overall carbohydrate budget or subsequent plant response to O 3 or other 3 stresses (EPA, 1996a, EPA, 2006a). 4 d. Changes to Plant Metabolism 5 Ozone inhibits photosy nthesis, the process by

which plants produce energy rich 6 compounds (e.g., carbohydrates) in the leaves. This impairment can result from direct 7 impact to chloroplast function and/or O 3 - induced stomatal closure resulting in reduced 8 up take of CO 2 . A large body of literature published since 1996 has further elucidated the 9 mechanism of effect of O 3 within the chloroplast. Pell et al. (1997) showed that O 3 10 exposure results in a loss of the central carbox yl ating enz ym e that play s an important role 11 in the production of carbohydrates. Due to its central importance, any decrease in this 12 enzy

me may have severe consequences for the plant’s productivity

. Several recent 13 studies have found that O 3 has a greater effect as leaves age, with the gre atest impact of 14 O 3 occurring on the oldest leaves (Fiscus et al., 1997; Reid and Fiscus, 1998; Noormets et 15 al., 2001; Morgan et al., 2004). The loss of this key enzy me as a function of increasing 16 O 3 exposure is also linked to an earl y senescence or a spee ding up of normal 17 development leading to senescence. If total plant photosy nthesis is sufficiently

reduced, 18 the plant will respond by reallocating the remaining carbohydrate at the level of the 19 whole organism (EPA, 1996a, 2006a). This reallocation of car bohydrate away

from the 20 roots into above ground vegetative components can have serious implications for 21 perennial species , as discussed below

. 22
e. Plant Response to Chronic Ozone Exposures 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 248 Though many changes that occur with O 3 exposure can be observed wi thin hours, 1 or perhaps day s, of the exposure, including those connect ed with wounding , other effects 2 take longer to occur and tend to become most obvious after chronic seasonal exposures to 3 low O 3 concentrations. These lower chronic exposures have been linked to senescence or 4 some other phys iological response very closel y linked to senescence. In perennial plant 5 species, a reduction in carbohydrate storage in one year may result in the limitation of 6 growth the following ye ar (Andersen et al., 1997). Such “carry
- over” effects have been 7 documented in the growth of tree seedlings (Hogsett et al., 1989; Sasek et al., 1991; 8 Temple et al., 1993; EPA, 1996a) and in roots (Andersen et al., 1991; EPA, 1996a). 9 Though it is not fully understood how chronic seasonal O 3 exposure affects long

- term 10 growth and resistance to other biotic and abiotic insults in long

- lived trees, accumulation 11 of these carry

- over effects over time could affect survival and reproduction. 12 2. Nature of Effects 13 Ozone injury at the cellular lev el can accumulate sufficientl y to induce effects at 14 the level of a whole leaf or plant. The se larger scale effects can include: reduced 15 carbohydrate production and /or reallocation; reduced growth and/or reproduction; visible 16 foliar injury

and /or premature senescence; and reduced plant vigor. Much of what is now 17 known about these O 3 - related effects, as summarized below, is based on research that 18 was available in th e 1997 review. Studies available in the 2008 rulemaking continue to 19 support and expand this knowledge (EPA, 2006a). 20
a. Carbohydrate Production and Allocation 21 When total plant photosy nthesis is sufficiently

reduced, the plant will respond by 22 reallocating the remaining carbohydrate at the level of the whole organism. Many studies 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 249 have demonstrated that root growth is more sensitive to O 3 exposure than stem or leaf 1 growth (EPA, 2006a). When fewer carbohydrates are present in the roots, less energy is 2 available for root

- related functions such as acquisition of water and nutrients. In 3 addition, by

inhibiting photosy

nthesis and the amount of carbohydrates available for 4 transfer to the roots , O 3 can disrupt the association between soil fungi and host plants. 5 Fungi in the soil form a sy mbiotic relationship with many terrestrial plants. For host 6 pl ants, these fungi improve the uptake of nutrients, protect the roots against pathogens, 7 produce plant growth hormones, and may transport carbohydrates from one plant to 8 another (EPA, 1996a). These below ground effects have recentl y been documented in the 9 field (Grulke et al., 1998 ; Grulke and Balduman, 1999 ). Data from a long

- studied 10 pollution gradient in the San Bernardino Mountains of southern California suggest that 11 O 3 substantially

reduces ro ot growth in natural stands of P onderosa pine ( Pinus 12 ponderosa ). Root growth in mature tre es was decreased at least 87 percent in a high

13 pollution site as compared to a low

- pollution site (Grulke et al., 1998), and a similar 14 pattern was found in a separate study with whole

- tree harvest along this gradient (Grulke 15 and Balduman, 1999). Though effects on other ecosy stem components were not 16 examined, a reduction of root growth of this magnitude c ould have signifi cant 17 implications for the below

- ground communities at those sites. Because effects on leaf 18 and needle carb ohydrate content under O 3 stress can range from a reduction (Barnes et 19 al., 1990; Miller et al., 1989), to no effect (Alscher et al., 1989), to an increase (Luethy20 Krause and Landolt, 1990), studies that examine only above

- ground vegetative 21 components may miss important O 3 - induced changes below ground. These below

- 22Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 250 ground changes could signal a shift in nutrient cycling with significance at the ecos ys tem 1 level (Young and Sanzone, 2002). 2 b. Growth Effects on Trees 3 Studies comparing the O 3 - related growth r esponse of different vegetation types 4 (coniferous and deciduous) and growth stages (e.g., seedling and mature) have 5 established that on average, individual coniferous trees are less sensitive than deciduous 6 trees , and deciduous trees are generall y less sen sitive to O 3 than most annual plants, with 7 the exception of a few fast growing deciduous tree species (e.g., quaking aspen, b lack 8 cherry , and cottonwood) , which are highl y sensitive an d, in some cases, as much or more 9 sensitive to O 3 than sensitive annual plants. In addition, studies have shown that the 10 relationship between O 3 sensitivity in seedling and mature growth stages of trees can vary 11 widely , with seedling growth being more sensitive to O 3 exposures in some species, 12 while in others, the mature growth stage is the more O 3 sensitive. In general, mature 13 deciduous trees are li kel y to be more sensitive to O 3 than deciduous seedlings, and 14 mature evergreen trees are likely to be less sensitive to O 3 than their seedling 15 counterparts
. Based on these result s, stomatal conductance, O 3 uptake, and O 3 effects 16 cannot be assumed to be equivalent in seedlings and mature trees. 17 In the 1997 review (EPA, 1996b), anal ys es of the effects of O 3 on trees were 18 limited to 11 tree species for which concentration

- response (C

- R) functions for the 19 seedling growth stage had been developed from OTC studies conducted b y the National 20 Health and Environmental Effects Research Lab, Western Ecology Division (NHEERL

21 WED). A number of replicate studies were conducted on these species, leading to a total 22 of 49 experimental cases. The 2007 Staff Paper present ed a graph of the composite 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 251 regression equation that combines the results of the C

- R functions developed for each of 1 the 49 cases. The NHEERL

- WED study predicted relative biomass lo ss at various 2 expo sure levels in terms of a 12

- hour W126. For example , 50 percent of the tree seedling 3 cases would be protected from greater than 10 percent biomass loss at a 3

- month, 12

- hour 4 W126 of approximately 2 4 ppm - h our, while 75 percent of cases wo uld be protected from 5 10 percent biomass loss at a 3
- month, 12

- hour W126 level of approximately 1 6 ppm 6 h our. 7 Since the 1997 review, only a few studies have developed C

- R functions for 8 additional tree seedling species (EPA, 2006a). One such study is of particular importance 9 because it documented growth effects in the field of a similar magnitude as those 10 previously seen in OTC studies but without the use of chambers or other fumigation 11 methods (Gregg et al., 2003) . This study placed eastern cottonwood ( Pop ulus deltoides ) 12 saplings at sites along a continuum of ambient O 3 exposures that graduall y increased 13 from urban to rural areas in the New York City area (Gregg et al., 2003). Eastern 14 cottonwood is a fast growing O 3 sensitive tree species that is important ecologicall y along 15 streams and commercially for p ulpwood, furniture manufacturing, and as a possible new 16 source for energy

biomass (Burns and Hankola, 1990). Gregg et al. (2003) found that the 17
co ttonwood saplings grown in urban New York City grew faster than saplings grown in 18 downwind rural areas . Because these saplings were grown in pots with carefully 19 controlled soil nutrient and moisture levels, the authors were able to control for most of 20 the differences between sites. After carefully considering the se and other factors, the 21 authors concluded the primary explanation for the difference in growth was the gradient 22 of cumulative O 3 exposure s that increased as one moved downwind from urban to less 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 252 urban and more rural sites. Itwas determined that the low er O 3 exposure within the city 1 center was due to NO x titration reactions which removed O 3 from the ambient air

. The 2 authors were able to reproduce the growth responses observed in the field in a companion 3 OTC experiment, confirm ing O 3 as the stressor indu cing the growth loss response (Gregg 4 et al., 2003). 5 Another recent set of studies employed a modified Free Air CO 2 Enrichment 6 (FACE) methodology to expose vegetation to elevated O 3 without the use of chambers. 7 This exposure method was originally develop ed to expose vegetation to elevated levels of 8 CO 2 , but was later modified to include O 3 exposure in Illinois (SoyFACE) and Wisconsin 9 (AspenFACE) for so yb ean and deciduous trees, respectively (Dickson et al., 2000; 10 Morgan et al., 2004). The FACE method rel eases gas (e.g., CO 2 , O 3 ) from a series of 11 orifices placed along the length of the vertical pipes surrounding a circular field plot and 12 uses the prevailing wind to distribute it . This exposure method has many characteristics 13 that differ from those associat ed with the OTC. Most significantl y, this exposure method 14 more closel y replicate s conditions in the field than do OTCs. This is because, except for 15 O 3 levels which are varied across co

- located plots, plants are exposed to the same 16 ambient growing conditi ons that occur naturally in the field (e.g., location

- specific 17 pollutant mixtures; climate conditions such as light, temperature and precipitation; insect 18 pests, pathogens). By using one of several co

- located plots as a control (e.g., receives no 19 addition al O 3 ), and by exposing the other rings to differing levels of elevated O 3 , the 20 growth response signal that is due solely to the change in O 3 exposure can be clearly 21 determined. Furthermore , the FACE s ys tem can expand vertically with the growth of 22Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 253 trees, allowing for exposure experiments to span numerous years , an especially useful 1 capability

in forest research

. 2 On the other hand, the FACE methodology also has the undesirable characteristic 3 of potentially

creating hotspots near O 3 gas release orifices or gradients of exposure in the 4 outer ring of trees within the plots, such that averaging results across the entire ring 5 potentially

overestimates the response. In recognition of this possibility, researchers at 6 the AspenFACE experiment al site only measured trees in the center core of each ring, 7 (e.g., at least 5

- 6 meters away from the emission sites of O 3 ) (Dickson et al 2000, 8 Karnosky et al. 2005) . By taking this precaution, i t is unlikely that their measurements 9 were influenced b y any potential hotspots or gradients of exposure within the FACE 10 rings. Taking all of the above into account, r esults from th e Wisconsin FACE site on 11 quaking a spen appear to demonstrate that the detrimental effects of O 3 exposure seen on 12 tree growth and s ymptom expressio n in OTC s can be observed in the field using this 13 exposure method (Karnosky et al., 1999; 2005). 14 The 2007 Staff Paper thus concluded that the combined evidence from the 15 AspenFACE and Gregg et al. (2 003) field studies provide compelling and important 16 support for the appropriateness of continued use of the C
- R functions derived using OTC 17 from the NHEERL

- WED studies to estimate risk to these tree seedlings under ambient 18 field exposure conditions. These studies make a significant contribution to the coherence 19 of the weight of evidence available in this review and provide additional evidence that 20 O 3 - induced effects observed in chambers also occur in the field

. 21 Trees and other perennials, in addition to cumulating the effects of O 3 exposures 22 over the annual growing s eason, can also cumulate effects across multiple years. It has 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 254 been reported that effects can “carry over” from one year to another (EPA, 2006a). 1 Growth affected b y a reduction in carbohydrate storage in one ye ar may result in the 2 limitation of growth in the following ye ar (Andersen, et al., 1997 ) . Carry
- over effects 3 have been documented in the growth of some tree seedling s (Hogsett et al. 1989; Simini 4 et al., 1992; Temple et al., 1993) and in roots (Andersen et al., 1991; EPA, 1996a). On 5 the basis of p ast and recent OTC and field study data, ambient O 3 exposures that occur 6 during the growing season in the United States are sufficient to potentially affect the 7 annual growth of a number of sensitive seedling tree species. However, because most 8 studies do not take into account the possibility of carry over effects on growth in 9 subsequent years, the true implication of these annual biomass losses may be missed. It 10 is likely

that under ambient exposure conditions, some sensitive trees and perennial 11 plants c ould experience compounded impacts that result from multiple ye ar exposures. 12
c. Visible Foliar Injury 13 Cellular injury to leaves due to exposure to O 3 can and often does become visible

. 14 Acute injury

usuall y appears within 24 hours after exposure to O 3 an d, depending on 15 species, can occur under a range of exposures and durations from 0.04 0 ppm for a period 16 of 4 hours to 0.41 0 ppm for 0.5 hours for crops and 0.06 0 ppm for 4 hours to 0.51 0 ppm 17 for 1 hour for trees and shrubs (Jacobson, 1977). Chronic injury may be mild to severe. In 18 some cases, cell death or premature leaf senescence may occur. The significance of O 3 19 injury

at the leaf and whole plant levels depends on how much of the total leaf area of the 20 plant has been affected, as well as the plant’s age , size, developmental stage, and degree 21 of functional redundancy among the existing leaf area. As a result, it is not presentl y 22Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 255 possible to determine, with consistency across species and environments, what degree of 1 injury

at the leaf level has significan ce to the vigor of the whole plant. 2 The presence of visible symptoms due to O 3 exposures can, however, b y itself, 3 represent an adverse impact to the public welfare. Specificall y, it can reduce the market 4 value of certain leafy crops (such as spinach, lettuce), impact the aesthetic value of 5 ornamentals (such as petunia, geranium, and poinsettia) in urban landscapes, and affect 6 the aesthetic value of scenic vistas in protected natural areas such as national parks and 7 wilderness areas. Many businesses rel y on healthy looking vegetation for their 8 livelihoods (e.g., horticulturalists, landscapers, Christmas tree growers, farmers of leafy 9 crops) and a variety

of ornamental species have been listed as sensitive to O 3 (Abt 10 Associates Inc , 199 5 ). Though not quantified, there is likely some level of economic 11 impact to businesses and homeowners from O 3 - related injury on sensitive ornamental 12 species due to the cost associated with more frequent replacement and/or increased 13 maintenance (fertilizer or pesticide applic ation). In addition, because O 3 not only results 14 in discoloration of leaves but can lead to more rapid senescence (early shedding of 15 leaves) there potentiall y could be some lost tourist dollars at sites where fall foliage is 16 less available or attractive. 17 The use of sensitive plants as biological indicators to detect phy totoxic levels of 18 O 3 is a longstanding and effective methodology (Chappelka and Samuelson, 1998; 19 Manning and Krupa, 1992). Each bioindicator exhibits ty pical O 3 injury

sy mptoms when 20 exposed under appropriate conditions. These s ymptoms are considered diagnostic as they 21 have been verified in exposure

- response studies under experimental conditions

. Inrecent 22 ye ars, field survey s of visible foliar injury s ymptoms have b ecome more common, with 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 256 greater attention to the standardization of methods and the use of reliable indicator 1 species (Campbell et al., 2000; Smith et al., 2003). Specificall y, the Unites States Forest 2 Service (USFS) through the Forest Health Monitoring Program (FHM) (1990

- 2001) and 3 currentl y the Forest Inventory and Anal ys is (FIA) Program collects data regarding the 4 incidence and severity of visible foliar injury

on a variety of O 3 sensitive plant species 5 throughout the U.S. (Coulston et al. 2003, 2004; Smith et al. 2003). 6 Since the conclusion of the 199 7 review, the FIA monitoring program network 7 and database has continued to expand. This network continues to document foliar injury 8 sy mptoms in the field under ambient exposure conditions. Recent surve y results show 9 that O 3 - induced foliar injury incidence is widespread across the country . The visible 10 foliar injury

indicator has been identified as a means to track O 3 exposure stress trends in 11 the nation’s natural plant communities as highlighted in EPA’ s most recent Report on the 12 Environment (EPA, 2003a; http://www.epa.gov/indicators/roe). 13 Previous Criteria Documents have noted the difficulty in relating visible foliar 14 injury

s ymptoms to other vegetation effects such as individual tree growth, stand growth, 15
or ecos ys tem characteristics (EPA, 1996a) and this difficulty remains to the present day 16 (EPA, 2006a)

. It is important to note that direct links between O 3 induced visible foliar 17 injury

s ymptoms and other adver se effects are not alway s found. There fore, visible foliar 18 injury

cannot serve as a reliable surrogate measure for other O 3 - related vegetation effects 19 because other effects (e.g., biomass loss) have been reported with and wi thout visible 20 injury . In some cases, visible foliar sy mptoms have been correlated with decreased 21 vegetative growth (Karnosky et al., 1996; Peterson et al., 1987; Somers et al., 1998) and 22 with impaired reproductive function (Black et al., 2000; Chappelka, 2002). Therefore, 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 257 the lack of visible injury

should not be construed to indicate a lack of phyt otoxic 1 concentrations of O 3 nor absence of other non

- visible O 3 effects. 2 d. Reduced Plant Vigor 3 Though O 3 levels over most of the U.S. are not high enough to kill vegetation 4 directly , current levels have been shown to reduce the ability of many s ensitive species 5 and genotypes within species to adapt to or withstand other environmental stresses. 6 These O 3 effects may include increased susceptibility to freezing temperatures, increased 7 vulnerability

to pest infestations and/or root disease, and compromised ability to compete 8 for available resource s. As an example of the latter, when species with differing O 3 - 9 sensitivities occur together, O 3 - sensitive species may experience a greater reduction in 10 growth than more O 3 - tolerant species , which then can better compete for available 11
resources . The result of such above effects can produce a loss in plant vigor in O 3 - 12 sensitive species that over time may lead to premature plant death. 13
e. Ecosystems 14 Ecosy stems are comprised of complex assemblages of organisms and the phy sical 15 environment with which they interact. Each level of organization within an ecos ys tem 16 has functional and structural characteristics. At the ecos ys tem level, functional 17 characteristics include, but are not limited to, energy flow; nutrient, hydrologic, and 18 biogeochemical cycling; and maintenance of food chains. The sum of the functions 19 carried out by

ecos ys tem components provides many benefits to humankind, as in the 20 case of forest ecos ys tems (Smith, 1992). Some of these benefits , also termed “ecos ys tem 21 goods and services”, include food, fiber production, aesthetics, genetic diversity , 22 maintenance of water quality , air quality , and climate, and energy exchange. A 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 258 conceptual framework for discussing the effects of stressor s, including air pollutants such 1 as O 3 , on ecosy stems was developed by the EPA Science Advisory Board (Young and 2 Sanzone, 2002). Inthis report, the authors identify six essential ecological attributes 3 (EEAs) of ecos ys tems including landscape condition, b iotic condition, chemical/phy sical 4 condition, ecological processes, hydrology/geomorphology, and natural disturbance 5 regime

. Each EEA is depicted as one of six triangles that together build a hexagon. On 6 the outside of each triangle is a list of stressor s that can act on the EEA. Tropospheric O 3 7 is listed as a stressor of both biotic condition and the chemical/physical condition of 8
ecos ys tems. As each EEA is linked to all the other s, it is clearl y envisioned in this 9 framework that O 3 could either directly or indirectly

impact all of the EEAs associated 10 with an ecos ys tem that is being stressed b y O 3 . 11 Vegetation often play s an influential role in defining the structure and function of 12
an ecos ys tem, as evidenced by the use of dominant vegetation forms to classify many 13 ty pes of natural ecos ys tems, e.g., tundra, wetland, deciduous forest, and conifer forest. 14 Plants simultaneously inhabit both above

- and below

- ground environments, integrating 15 and influencing key ecosy stem cycles of energy , water, and nutrient s. When a sufficient 16 number of individual plants within a community have been affected, O 3 - related effects 17
can be propagated up to ecos ys tem - level effects. Thus, through its impact on vegetation, 18 O 3 can be an important ecosy stem s tressor
. 19 i. Potential Ozone Alteration of Ecos ys tem Structure and Function 20 The 2006 Criteria Document outlines seven case studies where O 3 effects on 21
ecos ys tems have either been documented or are suspected. The oldest and clearest 22 example involves the San Bernardino Mountain forest ecos ys tem in California. This 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 259 sy stem experienced chronic high O 3 exposures over a period of 50 or more years. The 1 O 3 - sensitive and co

- dominant species of ponderosa and Jeffrey pine demonstrated severe 2 levels of foliar injury , premature senescence, and needle fall that decreased the 3 photosy

nthetic capacity of stressed pines and reduced the production of carbohydrates 4 resulting in a decrease in radial growth and in the height of stressed trees. It was also 5 observed that ponderosa and Jeffrey pines w ith slight to severe crown injury lost basal 6 area in relation to competing species that are more tolerant to O 3 . Due to a loss of vigor, 7 the se trees eventuall y succumbed to the bark beetle, leading to elevated levels of tree 8 death. Increased mortality of susceptible trees shifted the community composition 9 towards white fir and incense cedar, effectivel y reversing the development of the normal 10 fire climax mixture dominated by ponderosa and Jeffrey

pines, and leading to increased 11 fire susceptibility . At th e same time, numerous other organisms and processes were also 12 affected either directl y or indirectly, including successional patterns of fungal microflora 13 and their relationship to the decomposer community . Nutrient availability was influenced 14 by the heav y litter and thick needle layer under stands with the most severe needle injury 15 and defoliation. In this example, O 3 appeared to be a predisposing factor that led to 16 increased drought stress, windthrow, root diseases, and insect infestation (Takemoto et 17
al., 2001). Thus, through its effects on tree water balance, cold hardiness, tolerance to 18 wind, and susceptibility to insect and disease pests, O 3 potentially impacted the 19
ecos ys tem - related EEA of natural disturbance regime (e.g., fire, erosion). Although the 20 role of O 3 was extremel y difficult to separate from other con founding factors, such as 21 high nitrogen deposition, there is evidence that this shift in species composition has 22 altered the structure and dy namics of associated food webs (Pronos et al ., 19 99) and 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 260 carbon (C) and nitrogen (N) cycling (Arbaugh et al., 2003). Ongoing and new research in 1 this important ecosy stem is needed to reveal the extent to which ecosy stem services have 2 been affected and to what extent strong causal linkages between historic and/or current 3 ambient O 3 exposures and observed ecos ys tem - level effects can be made. 4 Ozone has also been reported to be a selective pressure among sensitive tree 5 species (e.g., eastern white pine) in the east. The nature of community dy namics in 6
eas tern forests is different, however, than in the west, consisting of a wider diversity of 7 species and uneven aged stands, and the O 3 levels are less severe. Therefore, lower level 8 chronic O 3 stress in the east is more likely to produce subtle long

- term forest responses 9 such as shifts in species composition, rather than wide

- spread community degradation. 10 Some of the best

- documented studies of population and community response to 11 O 3 effects are the long

- term studies of common plantain ( Plantago major) in n ative plant 12 communities in the United Kingdom (Davison and Reiling, 1995; Lyons et al., 1997; 13 Reiling and Davison, 1992c). Elevated O 3 significantly decreased the growth of sensitive 14 populations of common plantain (Pearson et al., 1996; Reiling and Daviso n, 1992a, b; 15 Whitfield et al., 1997) and reduced its fitness as determined b y decreased reproductive 16 success (Pearson et al., 1996; Reiling and Davison, 1992a). While spatial comparisons of 17 population responses to O 3 are complicated b y other environmental factors, rapid changes 18 in O 3 resistance were imposed by ambient levels and variations in O 3 exposure (Davison 19 and Reiling, 1995). Specifically , in this case study, it appeared that O 3 - sensitive 20 individuals are being removed by O 3 stress and the genetic v ariation represented in the 21 population could be declining. If genetic diversity and variation is lost in ecosystems, 22 there may

be increased vulnerability of the sy stem to other biotic and abiotic stressors, 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 261 and ultimately

a change in the EEAs and associat ed services provided b y those 1
ecos ys tems. 2 Recent free

- air exposure experiments have also provided new insight into how O 3 3 may be altering ecos ys tem structure and function (Karnosky et al., 2005). For example, a 4 field O 3 exposure experiment at the AspenFA CE site in Wisconsin (described in section 5 IV .A.2.b. above) was designed to examine the effects of both elevated CO 2 and O 3 on 6 mixed stands of aspen ( Populus tremuloides ), birch ( Betula papyrifera ), and sugar maple 7 ( Acer saccharum ) that are characteristic of Great Lakes aspen

- dominated forests 8 (Karnosky et al., 2003; Karnosky et al., 1999). They

found evidence that the effects on 9 above

- and below

- ground growth and phy siological processes have cascaded through the 10
ecos ys tem, even affecting microbial communities (Larson et al., 2002; Phillips et al., 11 2002). This study

also confirmed earlier observations of O 3 - induced changes in trophic 12 interactions involving keystone tree species, as well as important insect pests and their 13 natural enemies (Awmack et al., 2 004; Holton et al., 2003; Percy et al., 2002). 14 Collectively these examples suggest that O 3 is an important stressor in natural 15
ecos ys tems, but it is difficult to quantify the contribution of O 3 due to the combination of 16 other stresses present in ecosy stems. In most cases, because onl y a few components in 17 each of these ecos ys tems have been examined and characterized for O 3 effects, the full 18 extent of ecosy stem changes in these example ecosy stems is not fully understood. 19 Clearly , there is a need for highl y integrated ecosystem studies that specifically 20 investigate the effect of O 3 on ecosy stem structure and function in order to fully 21 determine the extent to which O 3 is altering ecos ys tem services. Continued research, 22Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 262 employing new approaches, will be nece ssary to fully understand the extent to which O 3 1 is affecting ecos ys tem services. 2 ii. Effects on Ecos ys tem Services and Carbon Sequestration 3 Since it has been established that O 3 affects photosy nthesis and growth of plants, 4 O 3 is most likely

affecting th e productivity of forest ecosy stems. Therefore, it is 5 desirable to link effects on growth and productivity to essential ecos ys tem services. 6 However, it is very

difficult to quantify

ecos ys tem - level productivity losses because of 7 the amount of complexity in scaling from the leaf

- level or individual plant to the 8
ecos ys tem level, and because not all organisms in an ecos ys tem are equally affected b y 9 O 3 . 10 Terrestrial ecos ys tems are important in the Earth's carbon (C) balance and could 11 help offset emissions of CO 2 by humans if anthropogenic C is sequestered in vegetation 12 and soils. The annual increase in atmospheric CO 2 is less than the total inputs from fossil 13 fuel burning and land use changes (Prentice et al., 2001) , and much of this discrepancy is 14 thought to be attributable to CO 2 uptake by plant photosy

nthesis (Tans & White, 1998). 15 Temperate forests of the northern hemisphere have been estimated to be a net sink of 16 about 0.6 to 0.7 petagrams (Pg) C per year (Goodale et al. 2002). Ozone interferes with 17 phot osy

nthesis, causes some plants to senesce leaves prematurely , and in some cases, 18 reduces allocation to stem and root tissue. Thus, O 3 decreases the potential for C 19 sequestration. For the purposes of this discussion, C sequestration is defined as the net 20 exchange of carbon b y the terrestrial biosphere. However, long

- term storage in the soil 21 organic matter is considered to be the most stable form of C storage in ecosy stems. 22Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 263 In a study including all ecosy stem types, Felzer et al. (2004), estimated that U.S

. 1 net primary

production (net flux of C into an ecosy stem) was decreased by 2.6
- 6.8 2 percent due to O 3 pollution in the late 1980's to early 1990's. Ozone not only

reduces C 3 sequestration in existing forests, it can also affect reforestation projects (Beedlow et al. 4 2004). This effect, in turn, has been found to ultimately inhibit C sequestration in forest 5 soils which act as long

- term C storage (Lo ya et al., 2003; Beedlow et al. 2004). The 6 interaction of rising O 3 pollution and rising CO 2 concentrations in the coming decades 7 complicates predictions of future sequestration potential. Models generally predict that, 8 in the future, C sequestration will increase with increasing CO 2 , but often do not account 9 for the decrease in productivity due to the local eff

ects of current or potentially increasing 10 levels of tropospheric O 3 . In the presence of high O 3 levels, the stimulatory effect of 11 rising CO 2 concentrations on forest productivity has been estimated to be reduced by 12 more that 20 percent (Tingey et al., 200 1; Ollinger et al. 2002; Karnosky et al., 2003). 13 In summary , it would be anticipated that meeting lower O 3 standards would 14 increase the amount of CO 2 uptake by many ecos ystems in the U.S. However, the 15 amount of this improvement would be heavil y dependent on the species composition of 16 those ecos ys tems. Many ecos ys tems in the U.S. do have O 3 sensitive plants. For, 17 example forest ecos ys tems with dominant species such as aspen or ponderosa pine would 18 be expected to increase CO 2 uptake more with lower O 3 th an forests with more O 3 19 tolerant species. 20 A recent critique of the secondary NAAQS review process published in the report 21 by the National Academy

of Sciences on Air Quality Management in the United States 22 (NRC, 2004) stated that “EPA’s current practice fo r setting secondary standards for most 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 264 criteria pollutants does not appear to be sufficiently protective of sensitive crops and 1
ecos ys tems...” This report made several specific recommendations for improving the 2 secondary

NAAQS process and concluded that “ There is growing evidence that tighter 3 standards to protect sensitive ecos ys tems in the United States are needed....” An effort 4 has been recently initiated within the Agency to identify

indicators of ecological 5 condition whose responses can be clearl y linked to changes in air quality that are 6 attributable to Agency environmental programs

. Using a single indicator to represent the 7 complex linkages and dynamic cycles that define ecos ys tem condition will always have 8 limitation s. With respect to O 3 - related i mpacts on ecos ys tem condition, only two 9 candidate indicators , foliar injury (as described above ) and radial growth in trees, have 10 been suggested

. Thus, while at the present time, most O 3 - related effects on ecos ys tems 11 must be inferred from observed or predicted O 3 - related effects on individual plants , 12 additional research at the ecos ys tem level could identify new indicators and/or establish 13 stronger causal linkages between O 3 - induced plant effects and ecos ys tem condition. 14 f

. Yield Reductions in Crops 15 Ozo ne can interfere with carbon gain (photosy nthesis) and allocation of carbon 16 with or without the presence of visible foliar injury. As a result of decreased 17 carbohydrate availability , fewer carbohydrates are available for plant growth, 18 reproduction, and/or yi eld. Recent studies have further confirmed and demonstrated O 3 19 effects on different stages of plant reproduction, including pollen germination, pollen 20 tube growth, fertilization, and abortion of reproductive structures, as reviewed by Black 21 et al. (200 0). For seed

- bearing plants, these reproductive effects will culminate in 22 reduced seed production or yield. 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 265 As described in the 1997 review and again in the 2006 Criteria Document and 1 2007 Staff Paper, the National Crop L oss Assessment Network (NCLAN) studies 2 undertaken in the earl y to mid

- 1980's provide the largest, most uniform database on the 3 effects of O 3 on agricultural crop yi elds. The NCLAN protocol was designed to produce 4 crop exposure - response data representative of the areas in the U.S. where the crops were 5 ty picall y grown. In total, 15 species (e.g., corn, soybean, winter wheat, tobacco, 6 sorghum, cotton, barley , peanuts, dry beans, potato, lettuce, turnip, and hay [alfalfa, 7 clover, and fescue]), accounting for greater than 85 percent of U.S. agricultural acreage 8 planted at that time, were studied. Of these 15 species, 13 species including 38 different 9 cultivars were combined in 54 cases representing unique combinations of cultivars, sites, 10 water regimes, and exposure conditions. Crops were grown under typical farm 11 conditions and exposed in open

- top chambers to ambient O 3 , sub

- ambient O 3 , and above 12 ambient O 3 . Robust C

- R functions were developed for each of these crop species. These 13 results showed that 50 percent of the studied cases would be protected from greater than 14 10 percent yi eld loss at a W126 level of 21 ppm

- hour, while a W126 of 13 ppm

- hour 15 would provide protection for 75 percent of the cases studied from greater than 10 percent 16 yi eld loss . 17 Recent studies continue to find yield loss levels in crop species studied previously 18 under NCLAN that reflect the earlier findings. In other words, there has been no 19 evidence that crops are becoming more tolerant of O 3 (EPA, 2006a). For cotton, some 20 newer varieties have been found to have hi gher yi eld loss due to O 3 compared to older 21 varieties (Olszy

k et al., 1993, Grantz and McCool, 1992). In a meta

- anal ys is of 53 22 studies, Morgan et al. (2003) found consistent deleterious effects of O 3 exposures on 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 266 soy bean from studies published between 197 3 and 2001. Further, early results from the 1 field

- based exposure experiment SoyFACE in Illinois indicate a lack of any apparent 2 difference in the O 3 tolerance of old and recent cultivars of soy bean in a study

of 22 3 soy bean varieties (Long et al., 2002). Thus, the 2007 Staff Paper conclude d that the 4 recent scientific literature continues to support the conclusions of the 1996 Criteria 5 Document that ambient O 3 concentrations are reducing the yi eld of major crops in the 6 U.S. 7 In addition to the effects described on annual crop species, several studies 8 published since the 1997 review have focused on perennial forage crops (EPA, 2006a). 9 These recent results confirm that O 3 is also impacting yi elds and quality of multiple

- year 10 forage crops at sufficient magnitude to have nutritional and possibly economic 11 implications to their use as ruminant animal feed at O 3 exposures that occur in some 12 ye ars over large areas of the U.S. 13 3. Adversity

of Effects 14 The 2007 Staff Paper recognize d that the statute requires that a secondary 15 standard be protective against “adverse” O 3 effects , not all identifiable O 3 - induced 16 effects. In considering what constitutes a vegetation effect that is adverse to the public 17 welfare, the 2007 Staff Paper recognizes that O 3 can cause a variety of vegetation effects, 18 beginning at the level of the individual cell and accumulating up to the level of whole 19 leaves, plants, plant populations, communities and whole ecos ys tems, not all of which 20 have been classified in past reviews as “adverse” to public welfare. 21 Previous reviews have classified O 3 vegetation effects as either “injury” or 22 “damage” to help in determining adversity . Specifically , “injury” is defined as 23 encompassing all plant reactions, including reversible changes or changes in plant 24Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 267 met abolism (e.g., altered photosy nthetic rate), altered plant quality , or reduced growth, 1 that does not impair the intended use or value of the plant (Guderian, 1977). In contrast, 2 “damage” has been defined to include those injury effects that reach sufficient magnitude 3 as to also reduce or impair the intended use or value of the plant. Examples of effects 4 that are classified as damage include reductions in aesthetic values (e.g., foliar injury in 5 ornamental species) as well as losses in terms of weight, number, or size of the plant part 6 that is harvested (reduced yield or biomass production). Yield loss also may include 7 changes in crop quality , i.e., phy sical appearance, chemical composition, or the ability to 8 withstand storage, while biomass loss includes slower growth in species harvested for 9 timber or other fiber uses. While this construct has proved useful in the past, it appears to 10 be most useful in the context of evaluating effects on single plants or species grown in 11 monocultures such as agricultural crops or managed forests. It is less clear how it might 12 apply

to potential effects on natural forests or entire ecos ys tems when O 3 - induced species 13 level impacts lead to shifts in species composition and/or associated ecos ys tem services 14 such as nutrient c ycling or hydrologic cycles, where the intended use or value of the 15 sy stem has not been specifically identified. 16 A more recent construct for assessing risks to forests described in Hogsett et al. 17 (1997) suggests that “adverse effects could be classified into one or more of the following 18 categories: (1) economic production, (2) ecological structure, (3) genetic resources, and 19 (4) cultural values.” This approach expands the context for evaluating the adversity of 20 O 3 - related effects beyond the species level. Another recent publication, A Framework for 21 Assessing and Reporting on Ecological Condition: an SAB report (Young and Sanzone, 22 2002), provides additional support for expanding the consideration of adversity beyond 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 268 the species level by

making explicit th e linkages between stress

- related effects (e.g., O 3 1 exposure) at the species level and at higher levels within an ecos ys tem hierarchy. Taking 2 this recent literature into account, the 2007 Staff Paper concludes that a d etermination of 3 what constitutes an “adverse” welfare effect in the context of the secondary NAAQS 4 review can appropriatel y occur within this broader paradigm

. 5 B. Biologically Relevant Exposure Indices 6 The 2006 Criteria Document concluded that O 3 exposure indices that cumulate 7 differentiall y weighted hourly concentrations are the best candidates for relating exposure 8 to plant growth responses. This conclusion follows from the extensive evaluation of the 9 relevant studies in the 1996 Criteria Document (EPA, 1996a) and the recent evaluation of 10 studies that have been published since that time. The following selections , taken from the 11 1996 Criteria Document (EPA, 1996a , section 5.5 ), further elucidate the depth and 12 strength of these conclusions. Specificall y, with respect to the importance of t aking into 13 account exposure duration, the 1996 Criteria Document stated, “when O 3 effects are the 14 primary

cause of variation in plant response, plants from replicate studies of varying 15 duration showed greater reductions in yield or growth when exposed for the longer 16 duratio n ” and “ the mean exposure index of unspecified duration could not account for the 17 ye ar- to - ye ar variation in response” (EPA, 1996a, pg. 5

- 96). Further, “b ecause the mean 18 exposure index treats all concentrations equall y and does not specif icall y include an 19 exposure duration component, the use of a mean exposure index for characterizing plant 20 exposures appears inappropriate for relating exposure with vegetation effects” (EPA, 21 1996a, pg. 5
- 88). Regarding the relative importance of higher con centrations than lower 22 in determining plant response, the 1996 Criteria Document concluded that “the ultimate 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 269 impact of long

- term exposures to O 3 on crops and seedling biomass response depends on 1 the integration of repeated peak concentrations during the growth of the plant” (EPA, 2 1996a, pg. 5
- 104). Further, “at this time, exposure indices that weight the hourly O 3 3 concentrations differentially appear to be the best candidates for relating exposure with 4 predicted plant response” (EPA, 1996a, pgs. 5

- 136). 5 At the conclusion of the 1997 review, the biological basis for a cumulative, 6 seasonal form was not in dispute. There was general agreement between EPA and 7 CASAC, based on their review of the air quality criteria, that a cumulative, seasonal form 8
was more biologicall y based than the then current 1

- hour and newly proposed 8

- hour 9 average form. However, in selecting a specific form appropriate for a secondary 10 standard , there was less agreement. An evaluation of the performance of several 11 cumulative season al forms in predicting plant response data taken from OTC experiments 12 had found that all performed about equall y well and was unable to distinguish between 13 them (EPA, 1996a) . In selecting between two of these cumulative forms, the SUM06 54 14 and W126, in the absence of biological evidence to distinguish between them, EPA based 15 its decision on both science and policy considerations. Specificall y, these were: (1) all 16 cumulative, peak

- weighted exposure indices considered, including W126 and SUM06, 17 were about equ all y good as exposure measures to predict exposure

- response relationships 18 reported in the NCLAN crop studies; and (2) the SUM06 form would not be influenced 19 by PRB O 3 concentrations (defined at the time as 0.03 to 0.05 ppm) under many typical 20 air quality

distributions. On the basis of these considerations, EPA chose the SUM06 as 21

54 The SUM06 index is defined as the sum of al l hourly O 3 concentrations greater or equal to 0.06 ppm over a specified time.Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 270 the most appropriate cumulative, seasonal form to consider when proposing an alternative 1 secondary

standard form ( 61 FR 65716 ). 2 Though the scientific justification for a cumulative, seasonal form was generally 3 accepted in the 1997 review, an anal ys is undertaken by EPA at that time had shown that 4 there was considerable overlap between areas that would be expected not to meet the 5 range of alternative 8

- hour standards being considere d for the primary NAAQS and those 6 expected not to meet the range of values (expressed in terms of the seasonal SUM06 7 index) of concern for vegetation. This result suggested that improvements in national air 8 quality

expected to result from attaining an 8

- h our primary standard within the 9 recommended range of levels would also be expected to significantl y reduce levels of 10 concern for vegetation in those same areas. Thus, in the 1996 proposed rule, EPA 11 proposed two alternatives for consideration: one alternative was to make the secondary 12 standard equal in every way to the proposed 8

- hour, 0.08 ppm primary standard; and the 13 second was to establish a cumulative, seasonal secondary standard in terms of a SUM06 14 form as also appropriate to protect public welfare f rom known or anticipated adverse 15 effects given the available scientific knowledge and that such a seasonal standard “...is 16 more biologically

relevant...” (61 FR 65716). 17 In the 1997 final rule, EPA decided to make the secondary standard identical to 18 the primary

standard. The EPA acknowledged, however, that “it remained uncertain as to 19 the extent to which air quality improvements designed to reduce 8

- hr average O 3 20 concentrations averaged over a 3

- ye ar period would reduce O 3 exposures measured b y a 21 seasonal SUM 06 index.” (62 FR 38876) In other words, it was uncertain as to whether 22 the 8

- hour average form would, in practice, provide sufficient protection for vegetation 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 271 from the cumulative, seasonal and concentration

- weighted exposures described in the 1 scientific literature as of concern. 2 On the basis of that history , th e 2007 Staff Paper (chapter 7) revisited the issue of 3 whether the SUM06 was still the most appropriate choice of cumulative, seasonal form 4 for a secondary

standard to protect the public welfare from known and anticipated 5 adverse vegetation effects in light of the new information available in this review. 6 Specificall y, the 2007 Staff Paper considered: (1) the continued lack of evidence within 7 the vegetation effects literature of a biological thresh old for vegetation exposures of 8 concern; and (2) new estimates of PRB that were lower than in the 1997 review. The 9 W126 form, also evaluated in the 1997 review, was again selected for comparison with 10 the SUM06 form. Regarding the first consideration, the 2007 Staff Paper noted that the 11 W126 form, by

its incorporation of a continuous sigmoidal weighting scheme, does not 12 create an artificiall y imposed concentration threshold , yet also giv es proportionally more 13 weight to the higher and ty picall y more biologi cally potent concentrations, as supported 14 by the scientific evidence. Second, the index value is not significantl y influenced b y O 3 15 concentrations within the range of estimated PRB, as the weights assigned by the 16 sigmoidal weighting scheme to concentratio ns in this range are near zero . Thus, it would 17 also provide a more appropriate target for air quality management programs designed to 18 reduce emissions from anthropogenic sources contributing to O 3 formation. On the basis 19 of these considerations, the 2007 Staff Paper concluded that the W126 form was the most 20 biologicall y- relevant cumulative, seasonal form appropriate to consider in the context of 21 the 2008 rulemaking. 22 C. Vegetation Exposure and Impact Assessment 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 272 The vegetation exposure and impact assessment conducted for the 2008 1 rulemaking and described in the 2007 Staff paper, consisted of exposure, risk and 2 benefits anal ys es and improve d and built upon similar anal ys es performed in the 1997 3 review (EPA 1996b). The vegetation exposure assessment was perf ormed using 4 interpolation and included information from ambient monitoring networks and results 5 from air quality modeling. The vegetation risk assessment included both tree and crop 6 anal ys es. The tree risk analy sis includes three distinct lines of eviden ce: (1) observations 7 of visible foliar injury in the field linked to monitored O 3 air quality for the years 2001

– 8 2004; (2) estimates of seedling growth loss under then current and alternative O 3 9 exposure conditions; and (3) simulated mature tree growth reductions using the TREGRO 10 model to simulate the effect of meeting alternative air quality standards on the predicted 11 annual growth of a single western species (ponderosa pine) and two eastern species (red 12 maple and tulip poplar). The crop anal ys is includes estimates of the risks to crop yi elds 13 from then current and alternative O 3 exposure conditions and the associated change in 14 economic benefits expected to accrue in the agriculture sector upon meeting the levels of 15 various alternative standards. Each element of the assessment is described below, 16 including discussions of known sources and ranges of uncertainties associated with the 17 elements of this assessment. 18 1. Exposure C haracterization 19 Though numerous effects of O 3 on vegetation have been documented as discussed 20 above, it is important in considering risk to examine O 3 air quality patterns in the U.S. 21 relative to the location of O 3 sensitive species that have a known concentration

- response 22Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 273 in order to predict whether adverse effects are occurring at current levels of air quality , 1 and whether they

are likely to occur under alternative standard forms and levels. 2 The most important information about exposure to vegetation comes from the O 3 3 monitoring data that are available from two national networks: (1) Air Quality Sy stem 4 (AQS; http://www.epa.gov/ttn/airs/airsaqs ) and (2) Clean Air Status and Trends Network 5 (CASTNET; http://www.epa.gov/castnet/). The AQS monitoring network currentl y has 6 over 1100 active O 3 monitors which are generally sited near population centers. 7 However, this network also includes approximately 36 monitors located in national parks. 8 CASTNET is the nation's primary source for data on dry

acidic deposition and rural, 9 ground

- level O 3 . It consists of over 80 sites across the eastern and western U.S. and is 10 cooperativel y operated and funded with the National Park Service. In the 1997 O 3 11 NAAQS final rule, it was acknowledged that because the national air quality surveillance 12 network for O 3 was designed principall y to monitor O 3 exposure in populated areas, there 13 was limited measured data available to characterize O 3 air quality in rural and remote 14 sites. Since the 1997 review, there has b een a small increase in the number of CASTNET 15 sites (from approximately 52 sites in 1992 to 84 sites in 2004), however these monitors 16 are not used for attainment designations. 17 National p arks represent areas of nationall y recognized ecological and public 18 welfare significance, which have been afforded a high level of protection by Congress
. 19 Two recent reports presented some discussion of O 3 trends in a subset of national parks: 20 The Ozone Report: Measuring Progress Through 2003 (EPA, 2004), and 2005 Annual 21 Performance and Progress Report: Air Quality in National Parks (NPS, 2005). 22 Unfortunatel y, much of this information is presented only in terms of the current 8

- hr 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 274 average form. The 2007 Staff Paper anal yz ed available air quality data in terms of the 1
cumulative 12

- hour W126 form from 2001 to 2005 for a subset of national parks and 2 other significant natural areas representing 4 general regions of the U.S. Many of these 3 national parks and natural areas have monitored O 3 levels above concentrations that have 4 been shown to decrease plant growth and above the 12

- hour W126 levels analyzed in this 5 review. For example, the Great Smokey Mountain, Rocky

Mountain, Grand Canyon, 6 Yosemite and Sequoia National Parks all had more than one ye ar within the 2001

- 2005 7 period with a 12

- hour W126 above 21 ppm

- hour. This level of exposure has been 8 associated with approximately no more than 10 percent biomass loss in 50 percent of the 9 49 tree seedling cases studied in the NHEERL

- WED experiments (Lee and Hogsett, 10 1996). Black cherry ( Prunus serotina ), an important O 3 - sensitive tree species in the 11 eastern U.S., occurs in the Great Smoky Mountain National Park and is estimated to have 12 O 3 - related seedling biomass loss of approximately 40 percent when exposed to a 3 13 month, 12

- hour W126 O 3 level greater than 21 ppm

- hour. Ponderosa pine ( Pinus 14 ponderosa ) which occurs in the Grand Canyon, Yosemite and Sequoia National Parks has 15 been reported to have approximately 10 percent biomass losses at 3 month, 12 hour 16 W126 O 3 levels as low as 17 ppm
- hour (Lee and Hogsett, 1996). Impacts on seedlings 17 may

potentiall y affect long

- term tree growth and survival, ultimately affecting the 18 competitiveness of O 3 - sensitive tree species and genoty pes within forest stands. 19 In order to characterize exposures to vegetation at the national scale, however, the 20 2007 Staff Paper concluded that it could not rely solely on limited site

- specific 21 monitoring data, and that it was necessary to select an interpolation method that could be 22 used to characterize O 3 air qu ality over broad geographic areas. The 2007 Staff Paper 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 275 therefore investigated the appropriateness of using the O 3 outputs from the EPA/NOAA 1 Community

Multi

- scale Air Quality

(CMAQ) 55 model sy stem 2 (http://www.epa.gov/asmdnerl/CMAQ , By un and Ching, 1999; Arnold et al. 2003, Eder 3 and Yu, 2005) to improve spatial interpolations based solel y on existing monitoring 4 networks. Due to the significant resources required to run CMAQ, model outputs were 5 only available for a limited number of years. For the 2008 rulemaking, the most recent 6 outputs available at the time from CMAQ version 4.5 were for the ye ar 2001
. 7 Based on the significant difference in monitor network density between the 8 eastern and western U.S., the 2007 Staff Paper concluded that it was appropriate to use 9 separate interpolation techniques in these two regions. Only AQS and CASTNET 10 monitoring data were used for the eastern interpolation , since it was determined that 11 enhancing the interpolation with C MAQ data did not add much information to the eastern 12 U.S. interpolation. Inthe western U.S., however, where rural monitoring i s more sparse, 13 O 3 values generated b y the CMAQ mode l were used to develop scaling factors to 14 augment the interpolation

. 15 In ord er to characterize uncertainties associated with the interpolation method, 16 monitored O 3 concentrations were s ys tematically compared to interpolated O 3 17 concentrations in areas where monitors were located . In general, the interpolation 18

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/O 3 , particul ate matter, and nutrient deposition) holistically . The CMAQ model can generate estimates of hourl y O 3 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 O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 276 method used in the current review performed well in many areas in the U.S., although it 1 under

- predicted higher 12

- hour W126 exposures in rural areas. Due to the important 2 influence of higher exposures in determining risks to plants, this feature of the 3 interpolated surface could result in an under

- estimation of risks to vegetation in some 4 areas. Taking these uncertainties into account, and given the absence of more complete 5 rural monitoring data, this approach was used in developing national vegetation exposure 6 and risk asses sments that estimate relative changes in risk for the various alternative 7 standards anal yz ed. 8 To evaluate changing vegetation exposures and risks under selected air quality 9 scenarios, the 2007 Staff Paper utilized 2001 base year O 3 air quality distributio ns that 10 had been adjusted with a rollback method (Horst and Duff, 1995; Rizzo, 2005 , 2006) to 11 reflect meeting the then current and alternative secondary standard options. This 12 technique combines both linear and quadratic elements to reduce higher O 3 13
concentrations more than lower ones. In this regard, the rollback method attempts to 14 account for reductions in emissions without greatly affecting lower concentrations. The 15 following O 3 air quality s cenarios were anal yz ed: (1) 4th

- highest daily maximum 8

- hour 16 average: 0.08 4 ppm (the effective level of the then current standard) and 0.070 ppm 17 levels; (2) 3

- month, 12

- hour. SUM06: 25 ppm

- hour (proposed in the 199 7 review) and 15 18 ppm - hour levels; and (3) 3

- month, 12

- hour W126: 21 ppm
- h our and 13 ppm

- hour levels. 19 The two 8

- hour average levels were chosen as possible alternatives of the then 20 current form for comparison with the cumulative, seasonal alternative forms. The 21 SUM06 scenarios were very similar to the W126 scenarios. Since the W126 was judged 22 to be the m ore biologically

- relevant cumulative, seasonal form, onl y the results for the 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 277 W126 scenarios are summarized below. For the W126 form, the two levels were selected 1 on the basis of the associated levels of tree seedling biomass loss and crop yield loss 2 prot ection identified in the NHEERL

- WED and NCLAN studies, respectively

. 3 Specificall y, the upper level of W126 (21 ppm

- hour) was associated with a level of tree 4 and crop protection of approximately no more than 10 percent growth or yi eld loss in 50 5 percent of cases studied. Alternativel y, the lower level of W126 (13 ppm

- hour) was 6 associated with a level of tree seedling and crop protection of approximately no more 7 than 10 percent growth or yield loss in 75 percent of studied cases. 8 The following discussion highlights key observations drawn from comparing 9 predicted changes in interpolated air quality under each alternative standard form and 10 level scenario for the base year, 2001: 11 (1) Under the base ye ar (2001) “as is” air quality , a large portion of California had 12 12
- hr W126 O 3 levels above 31 ppm

- hour, which has been associated with approximately 13 no more than 14 percent biomass loss in 50 percent of tree seedling cases studies. 14 Broader multi

- state regions in the east (NC, TN, KY, IN, OH, PA, NJ, NY, DE, MD, 15 VA) and west (CA, NV, AZ, OK, TX) are predicted to have levels of air quality above 16 the W126 level of 21 ppm

- hour, which is approximately equal to the secondary

standard 17 proposed in 1996 and is associated with approximately no more than 10 percent biomass 18 loss in 50 percent of tree seedling cases studied. Much of the east and Arizona and 19 California have 12

- hour W126 O 3 level s above 13 ppm

- hour , which has been associated 20 with approximately no more than 10 percent biomass loss in 7 5 percent of tree seedling 21
cases studied. The results of the exposure assessment indicate that current air quality 22 levels could result in significant impacts to vegetation in some areas. 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 278 (2) When 2001 air quality wa s rolled back to meet the then current 8
- hour , 0.084 1 ppm secondary standard, the overall 3

- month 12

- hour W126 O 3 levels were somewhat 2 improved, but not substantially . Under this scenario, there were still many areas in 3 California with 12

- hour W126 O 3 levels above 31 ppm

- hour. A broad multi

- state region 4 in the east (NC , TN, KY, IN, OH, PA, MD) and west (CA, NV, AZ, OK, TX) were still 5 predicted to have O 3 levels above the W126 level of 21 ppm

- hour. 6 (3) Exposures generated for just meeting a 0.070 ppm, 4th

- highest maximum 8

- 7 hour average alternative standard showed substa ntially improved O 3 air quality

when 8 compared to just meeting the then current 8
- hour standard. Most areas were predicted to 9 have O 3 levels below the W126 level of 21 ppm

- h our, although some areas in the east 10 (KY, TN, MI, AR, MO, IL) and west (CA, NV, AZ, UT, NM, CO, OK, TX) were still 11 predicted to have O 3 levels above the W126 level of 13 ppm

- hour. 12 These results suggest that meeting a 0.070 ppm, 8

- hour secondary standard would 13 provide substantially improved protection in some areas for vegetation from se asonal O 3 14 exposures of concern. The 2007 Staff Paper recognizes, however, that some areas 15 meeting a 0.070 ppm 8

- hour standard could continue to have elevated seasonal 16 exposures, including forested park lands and other natural areas, and Class I areas which 17 are federally

mandated to preserve certain air quality related values. This is especiall y 18 important in the high elevation forests in the Western U.S. where there are few O 3 19 monitors. This is because the air quality patterns in remote areas can result in relatively 20 low 8

- hour averages while still experiencing relatively high cumulative exposures. 21 To further characterize O 3 air quality in terms of various secondary standard 22 forms , an anal ys is was performed in the 2007 Staff Paper to evaluate the extent t o which 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 2 79 county- level O 3 air quality measured in terms of various levels of the current 8

- hour 1 average form overlapped with that measured in terms of various levels of the 12

- hour 2 W126 cumulative, seasonal form. The 2007 Staff Paper presented this analy sis using 3 2002
- 2004 56 county- level O 3 air quality data from AQS sites and the subset of 4 CASTNET sites having the highest O 3 levels for the counties in which they are located

. 5 S ince the current 8

- hour average secondary form is a 3

- year average , the analy sis initially 6 compared the 3

- ye ar averages of both the 8

- hour and W126 form s. In addition, 7 recogni zing that some vegetation effects (e.g. crop yield loss and foliar injury) are driven 8 solely

by annual O 3 exposures and are ty picall y evaluated with respect to exp osures 9 within th e annual growing season, the 2007 Staff Paper also presented a comparison of 10 the current 3
- year average 8
- hour form to the annual W126 form for the individual years, 11 2002 and 2004. 12 Results of the 3

- ye ar average comparison s showed that of the counties with air 13 quality

meeting the 3
- ye ar average form of a 0.08 4 ppm, 8
- hour average standard, 7 14 counties showed 3

- ye ar average W126 values above the 21 ppm
- hour level. At the lower 15 W126 level of 13 ppm

- hour, 135 counties with air quality meeting the 3

- year average 16 form of a 0.084 ppm, 8

- hour average standard, would be above this W126 level

. In 17 addition, when the 3

- ye ar average of an 8

- hour form was compared to annual W126 18 values , further variability in the degree of overlap between the 8

- hour form and W126 19 form became apparent. For example, the relatively high 2002 O 3 air quality ye ar showed 20 a greater degree of overlap between those areas that would meet the levels analyzed for 21

56 This analy sis was updated using 2003

- 2005 air quality as it became available, finding similar results.Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 280 the current 8

- hour and alternative levels of the W126 form than did th e relatively low O 3 1 2004 air quality

year. This lack of a consistent degree of overlap between the two forms 2 in different air quality years demonstrates that annual vegetation would be expected to 3 receive widel y differing degrees of protection from cumulative seasonal exposures in 4 some areas from ye ar to year, even when the 3

- ye ar average of the 8

- hour form was 5 consistently

met. 6 It is clear that thi s anal ys is is limited by the lack of monitoring in rural areas 7 where important vegetation and ecos ys tems are located , especiall y at higher elevation 8 sites. This is b ecause O 3 air quality distributions at high elevation sites often do not 9 reflect the ty

pical urban and near

- urban pattern of low morning and evening O 3 10 concentrations with a high mid

- day peak , but in stead maintain relativel y flat patterns with 11 many

concentrations in the mid

- range (e.g., 0.05

- 0.09 ppm) for extended periods. These 12 conditions can lead to relatively low daily maximum 8

- hour averages concurrentl y with 13 high cumulative values so that there is potential ly less overlap between an 8
- hour average 14 and a cumulative, seasonal form at these sites. The 2007 Staff Paper conclude d that it i s 15 reasonable to anticipate that additional unmonitored rural high elevation areas important 16 for vegetation may

no t be adequatel y protected even with a lower level of the 8

- hour 17 form. 18 The 2006 Criteria Document discusses policy relevant background (PRB) levels 19 for high elevation sites and makes the following observations: (1) PRB concentrations of 20 0.04 to 0.05 ppm oc cur occasionall y at high

- elevation sites (e.g., >1.5 km) in the spring 21 due to the free

- tropospheric influence, including some limited contribution from 22 hemispheric pollution (O 3 produced from anthropogenic emissions outside North 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 281 America); and (2) while stratospheric intrusions might occasionally elevate O 3 at high

1 altitude sites, these events are rare at surface sites

. Therefore, the 2007 Staff Paper 2 conclude d that springtime PRB levels in the range identified above and rare stratospheric 3 intrusions of O 3 are unlikely to be a major influence on 3

- month cumulative seasonal 4 W126 values. 5 It further remains uncertain as to the extent to which air quality improvements 6 designed to reduce 8

- hour O 3 average concentrations would reduce O 3 exposures 7 measured b y a se asonal, cumulative W126 index. The 2007 Staff Paper indicated this to 8 be an important consideration because: (1) the biological database stresses the 9 importance of cumulative, seasonal exposures in determining plant response; (2) plants 10 have not been spe cifically tested for the importance of dail y maximum 8

- hour O 3 11 concentrations in relation to plant response; and (3) the effects of attainment of a 8

- hour 12 standard in upwind urban areas on rural air quality distributions cannot be characterized 13 with confid ence due to the lack of monitoring data in rural and remote areas. These 14 factors are important considerations in determining whether the current 8

- hour form can 15 appropriatel y provide requisite protection for vegetation. 16 2. Assessment of Risk s to Vegetati on 17 The 2007 Staff Paper presents res ults from quantitative and qualitative risk 18 assessments of O 3 risks to vegetation (EPA, 2007). In the 1997 review, crop yield and 19 seedling biomass loss OTC data provided the basis for staff anal ys es, conclusions, and 20
recommendations (EPA, 1996b). Since then, several additional lines of evidence have 21 progressed sufficientl y to provide staff with a more complete and coherent picture of the 22 scope of O 3 - related vegetation risks, especiall y those faced b y seedling, sapling and 23 mature tree species growing in field settings, and indirectly , forested ecos ys tems. 24Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 282 Specificall y, research published after the 1997 review reflects an increased emphasis on 1 field

- based exposure methods (e.g., free air exposure and ambient gradient), i mproved 2 field survey

biomonitoring techniques, and mechanistic tree process models. Findings 3 from each of these research areas are discussed separatel y below. In conducting these 4 assessments, the Staff Paper anal ys es relied on both measured and modeled air quality 5 information. For some effects, like visible foliar injury and modeled mature tree growth 6 response, onl y monitored air quality information was used. For other effects categories 7 (e.g., crop yi eld and tree seedling growth), staff relied on inter polated O 3 exposures. 8
a. Visible foliar injury 9 As discussed above (section IV.A.2.c), sy stematic injury surveys have 10 document ed visible foliar injury s ymptoms diagnostic of phy totoxic O 3 exposures on 11 sensitive bioindicator plants. These survey s have produced more expansive evidence 12 than that available at the time of the 1997 review that visible foliar injury is occurring in 13 many

areas of the U.S. under current ambient conditions. The 2007 Staff Paper presents 14 an assessment combining recent U.S. Forest Service Forest Inventory and Analy sis (FIA) 15 biomonitoring site data with the county level air quality

data for those counties 16 containing the FIA biomonitoring sites. This assessment showed that incidence of visible 17 foliar injury

ranged from 21 to 39 percent during the four

- ye ar period (2001

- 2004) across 18 all counties with air quality levels at or below that of a 0.08 4 ppm, 8
- hour standard. Of 19 the counties that met an 8

- hour level of 0.07 0 ppm in those years, 11 to 30 percent still 20 had incidence of visible foliar injury . The magnitude of these percentages suggests that 21 phy totoxic exposures sufficient to induce visible foliar injury would still occur in many 22 areas after meeting the level of a 0.084 ppm secondary standard or alternative 0.07 0 ppm 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 283 8
- hour standard. Additionally , the data show ed that visible foliar injury occurrence wa s 1 geographically

widespread and occurring on a variety of plant species in forested and 2 other natural s ys tems. Linking visible foliar injury to other plant effects is still 3 problematic. However, its presence indicates that other O 3 – related vegetation effects 4 could also be present. 5 b. Seedling and mature tree biomass loss 6 In the 1997 review, anal yses of the effects of O 3 on trees were limited to 11 tree 7 species for which C

- R fun ctions for the seedling growth stage had been developed from 8 OTC studies conducted by the NHEERL

- WED. Important tree species such as quaking 9 aspen, ponderosa pine, black cherry , and tulip poplar were found to be sensitive to 10 cumulative seasonal O 3 exposures. Work done since the 1997 review at the AspenFACE 11 site in Wisconsin on quaking aspen (Karnosky et al., 2005) and a gradient study 12 performed in the New York City area (Gregg et al. 2003) has confirmed the detrimental 13 effects of O 3 exposure on tree growth in field studies without chambers and beyond the 14 seedling stage (King et al 2005). These field studies are discussed above in section IV.A. 15 To update the seedling biomass loss risk analy sis, C

- R functions for biomass loss 16 for available seedling tree sp ecies taken from the 2006 C riteria D ocument and 17 information on tree growing regions derived from the U.S. Department of Agriculture's 18 Atlas of United States Trees were combined with projections of O 3 air quality based on 19 2001 interpolated exposures, to pro duce estimated biomass loss for each of the seedling 20 tree species individually . Maps of these biomass loss projections are presented in the 21 2007 Staff Paper. For example, quaking aspen had a wide range of O 3 exposure s across 22 its growing range and therefo re, showed significant variability in percentages of projected 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 284 seedling biomass loss across its range. Quaking aspen seedling biomass loss was 1 projected to be greater than 4 percent over much of its geographic range, though it can 2 reach above 10 percent in areas of Ohio, Penns yl vania, New York, New Jersey and 3 California. Biomass loss for black cherry was projected to be greater than 20 percent in 4 approximately

half its range. Greater than 30 percent biomass loss for black cherry was 5 projected in North Carolina, Tennessee, Indiana, Ohio, Pennsylvania, Arizona, Michigan, 6 New York, New Jersey , Maryland and Delaware. For ponderosa pine, an important tree 7 species in the western U.S., biomass loss was projected to be above 10 percent in much 8 of its range in California. Biomass loss still occurred in many tree species when O 3 air 9 quality

was adjusted to meet the then current 8
- hour standard of 0.084 ppm . For instance, 10 black cherry , ponderosa pine, eastern white pine, and aspen had estimated median 11 seedling bio mass losses over portions of their growing range as high as 24, 11, 6, and 6 12 percent , respectively , when O 3 air quality was rolled back to just meet a 0.084 ppm , 8
- 13 hour standard. The 2007 Staff Paper noted that these results are for tree seedlin gs and 14 that mature trees of the same species may have more or less of a response to O 3 exposure. 15 Due to the potential for compounding effects over multiple years, experts at a c onsensus 16
w orkshop on O 3 vegetation effects and secondary standards, hereinafte r referred to as the 17 1996 Consensus Workshop, reported in a subsequent 1997 Workshop Report, that a 18 biomass loss greater than 2 percent annuall y can be significant (Heck and Cowling, 19 1997). . Decreased seedling root growth and survivability could affect overall stand health 20 and composition in the long term. 21 In addition to the estimation of O 3 effe cts on seedling growth, recent work 22 available in the 2008 rulemaking has enhanced our understanding of risks beyond the 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 285 seedling stage. In order to better characterize the potential O 3 effects on mature tree 1 growth, a tree growth model (TREGRO) was used as a tool to evaluate the effect of 2 changing O 3 air quality under just meet scenarios for selected alternative O 3 standards on 3 the growth of mature trees. TREGRO is a process - based, individual tree growth 4 simulation model (Weinstein et al, 1991) . This model has been used to evaluate the 5 effects of a variety of O 3 exposure scenarios on several species of trees by incorporating 6 concurrent climate data in different regions of the U.S. to account for O 3 and 7 climate/meteorology interactions (Tingey

et al., 2001; Weinstein et al., 1991; Retzlaff et 8 al., 2000; L aurence et al., 1993; L aurence et al., 2001; Weinstein et al., 2005). The 9 model provides an analy tical framework that accounts for the nonlinear relationship 10 between O 3 exposure and response. The interactions between O 3 exposure, precipitation 11 and temperature are integrated as they affect vegetation, thus providing an internal 12 consistency

for comparing effects in trees under different exposure scenarios and climatic 13 conditions. An earlier assessment of the effectiveness of national ambient air quality 14 standards in place since the earl y 1970s took advantage of 40 ye ars of air quality and 15 climate data for the Crestlin e site in the San Bernardino Mountains of California to 16 simulate ponderosa pine growth over time with the improving air quality using TREGRO 17 (Tingey

et al., 2004). 18 The TREGRO model was used to assess growth of Ponderosa pine in the San 19 Bernardino Mountain s of California (Crestline) and the growth of yellow poplar and red 20 maple in the Appalachian mountains of Virginia and North Carolina, Shenandoah 21 National Park (Big Meadows) and Linville Gorge Wilderness Area (Cranberry), 22 respectivel y. Total tree growth a ssociated with ‘as is’ air quality , and air quality adjusted 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 286 to just meet alternative O 3 standards was assessed. Ponderosa pine is one of the most 1 widely

distributed pines in western North America, a major source of timber, important 2 as wildlife habitat, and valued for aesthetics (Burns and Honkala, 1990). Red maple is 3 one of the most abundant species in the eastern U.S. and is important for its brilliant fall 4 foliage and highl y desirable wildlife browse food (Burns and Honkala, 1990). Yellow 5 poplar is an abundant species in the southern Appalachian forest. It is 10 percent of the 6 cove hardwood stands in southern Appalachians which are widely viewed as some of the 7 country ’s most treasured forests because the protected, rich, moist set of conditions 8 permi t trees to grow the largest in the eastern U.S. The wood has high commercial value 9 because of its versatility and as a substitute for increasingl y scarce softwoods in furniture 10 and framing construction. Yellow poplar is also valued as a honey tree, a source of 11 wildlife food, and a shade tree for large areas (Burns and Honkala, 1990). 12 The 2007 Staff Paper analy ses found that just meeting a 0.084 ppm standard 13 would likely

continue to allow O 3 - related reductions in annual net biomass gain in these 14 species. This is based on model outputs that estimate that as O 3 levels are reduced below 15 those of a 0.084 ppm standard, significant improvements in growth would occur. For 16 instance, estimated growth in red maple increased by 4 and 3 percent at Big Meadows 17 and C ranberry

sites, respectivel y, when air quality was rolled back to just met a W126 18 value of 13 ppm

- hour. Yellow poplar was projected to have a growth increase between 19 0.6 and 8 percent under the same scenario at the two eastern sites. 20 Though there is unce rtainty associated with the above anal ys es, this information 21 should be given careful consideration in light of several other pieces of evidence. 22 Specificall y, new evidence from experimental studies that go beyond the seedling growth 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 287 stage continues to sho w decreased growth under elevated O 3 (King et al. 2005). Some 1 mature trees such as red oak have shown an even greater sensitivity of photosy

nthesis to 2 O 3 than seedlings of the same species (Hanson et al., 1994). As indicated above, smaller 3 growth loss in crements may be significant for perennial species. The potential for 4 cumulative “carry

over” effects as well as compounding also must be considered. The 5 accumulation of such “carry

- over” effects over time may affect long

- term survival and 6 reproduction of individuals and ultimately the abundance of sensitive tree species in 7 forest stands. 8
c. Crops 9 As discussed in the 2007 Staff Paper, risk of O 3 exposure and associated 10 monetized benefits were estimated for commodity crops, fruits and vegetables. Similar to 11 the tree seedling anal ys is, this analy sis combined C

- R information on crops, crop 12 growing regions and interpolated exposures during each crop growing season. NCLAN 13 crop functions were used for commodity crops. According to USDA National 14 Agricultural Statistical Survey (NASS) data, the 9 commodity crop species (e.g., cotton, 15 field corn, grain sorghum, peanut, so ybean, winter wheat, lettuce, kidney bean, potato) 16 included in the 2007 Staff Paper anal ys is accounted for 69 percent of 2004 principal crop 17
ac reage planted in the U.S. in 2004. 57 The C

- R functions for six fruit and vegetable 18 species (tomatoes

- processing, grapes, onions, rice, cantaloupes, Valencia oranges) were 19

57 Principal crops as defined by the USDA include corn, sorghum, oats, barley , winter wheat, rye, Durum wheat, other spring wheat, rice, so yb eans, p eanuts, 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/pcp

bba/acrg0605.pdf

).Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 288 identified from the California fruit and vegetable anal ys is from the 1997 review (Abt 1 Associates Inc, 1995). The 2007 Staff Paper noted that fruit and vegetable studies were 2 not part of the NCLAN program and C

- R functions were available onl y in terms of 3 seasonal 7

- hour or 12

- hour mean index. This index form is considered less effective in 4 predicting plant response for a given change in air quality than the cumulative form used 5 with other crops. Therefore, the fruit and vegetable C

- R functions were considered more 6 uncertain than those for commodity crops. 7 Analy ses in the 2007 Staff Paper showed that some of the most important 8 commodity

crops such as soy

bean, winter wheat and cotton had some projected losses 9 under the 2001 base year air quality. So ybean yi eld losses were projected to be 2

- 4 10 percent in parts of Pennsylvania, New Jersey , Maryl and and Texas. Winter wheat was 11 projected to have yi eld losses of 2

- 6 percent in parts of California. Additionally , cotton 12 was projected to have yi eld losses of above 6 percent in parts of California, Texas and 13 North Carolina in 2001. The risk assessm ent estimated that just meeting the then current 14 0.084 ppm, 8
- hour standard would still allow O 3 – related yi eld loss to occur in some 15 commodity

crop species and fruit and vegetable species currentl y grown in the U.S. For 16 example, based on median C

- R functi on response, in counties with the highest O 3 levels, 17 potatoes and cotton had estimated yield losses of 9

- 15 percent and 5

- 10 percent , 18 respectivel y, when O 3 air quality just met the level of a 0.084 ppm, 8
- hour standard. 19 Estimated yield improved in these c ounties when the alternative W126 standard levels 20 were met. The very important soy

bean crop had generall y small yi eld losses throughout 21 the country

under just meeting the then current standard (0

- 4 percent). 22Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 289 The 2007 Staff Paper also presented estimate s of monetized benefits for crops 1 associated with a 0.084 ppm, 8
- hour and alternative standards. The Agriculture 2 Simulation Model (AGSIM) (Taylor, 1994; Taylor, 1993) was used to calculate annual 3 average changes in total undiscounted economic surplus for commodity crops and fruits 4 and vegetables when the then current and alternative standard levels were met. Meeting 5 the various alternative standards did show some significant benefits beyond a 0.084 ppm, 6 8
- hour standard. However, the 2007 Staff Paper reco gnized that the AGSIM economic 7 benefits estimates also incorporate several sources of uncertainty , including: (1) 8 estimates of economic benefits derived from use of the more uncertain C

- R relationships 9 for fruits and vegetables; (2) uncertain assumptions about the treatment and effect of 10 government farm pay ment programs ; and (3) uncertain assumptions about near

- term 11 changes in the agriculture sector due to the increased use of crops as biofuels. Although 12 the AGSIM model results provided a relative compari son of agricultural benefits between 13 alternative standards, the se uncertainties limited the utility of the absolute numbers. 14 D. Reconsideration of Secondary Standard 15 As discussed above at the beginning of section IV, this reconsideration of the 16 secondary O 3 standard set in the 2008 rulemaking focuses on reconsidering certain 17 elements of the standard, the form, averaging times, and level. The general approach for 18 setting a secondary O 3 standard used in the 2008 rulemaking, and in the previous 1997 19 rulemaking , was to consider two basic policy options: setting a distinct secondary 20 standard with a biologically relevant form and averaging times, or setting a secondary 21 standard identical to the primary standard. In the 2007 proposed rule, both such options 22 were evaluated, commented on by CASAC and the public, and proposed, as discussed 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 290 below in sections IV.D.1 and IV.D.2, respectively . In the 2008 final rule, EPA decided to 1 set the secondary

standard identical to the revised 8

- hour primary standard, as discussed 2 below in section IV.D.3. Section IV.D.4 summarizes comments received from CASAC 3 following the 2008 decision. The Administrator’s proposed conclusions based on this 4 reconsideration are presented in section IV.D.5. 5 1. Considerations Regarding th e 2007 Proposed Cumulative Seasonal Standard 6
a. Form 7 The 2006 Criteria Document and 2007 Staff Paper conclude d that the recent 8 vegetation effects literature evaluated in the 2008 rulemaking strengthen ed and 9 reaffirm ed conclusions made in the 1997 revi ew that the use of a cumulative exposure 10 index that differentially weights ambient concentrations is best able to relate ambient 11 exposures to vegetation response at this time (EPA, 2006a, b ; see also discussion in IV.B 12 above ). The 199 7 review focused in parti cular on two of these cumulative forms, the 13 SUM06 and W126. In th e 2008 rulemaking, the 2007 Staff Paper again evaluated the se 14 two form s in light of two key pieces of then recent information: estimates of PRB that 15
were lower than in the 1997 review, and c ontinued lack of evidence within the vegetation 16 effects literature of a biological threshold for vegetation exposures of concern. On the 17 basis of those policy and science

- related considerations, the 2007 Staff Paper concluded 18 that the W126 form was more a ppropriate in the context of the 2008 r ulemaking

. 19 Specificall y, the W126 form , by its incorporation of a sigmoidal weighting scheme, does 20 not create an artificially imposed concentration threshold, gives proportionally more 21 weight to the higher and ty pically more biologically

potent concentrations, and is not 22 significantl y influenced by O 3 concentrations within the range of estimated PRB. The 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 291 Staff Paper further concluded that “it is not appropriate to continue to use an 8

- hour 1 averaging time for the secon dary standard” and that “the 8

- hour average form should be 2 replaced with a cumulative, seasonal, concentration weighted form” (EPA, 2007b; pg.8

- 3 25). 4 The CASAC , b ased on its assessment of the same vegetation effects science, 5 agreed with the 2006 Criteria Do cument and 2007 Staff Paper and unanimously 6 concluded that it is not appropriate to try to protect vegetation from the known or 7 anticipated adverse effects of ambient O 3 by continuing to promulgate identical primary 8 and secondary

standards for O 3 . Moreover, the members of the CASAC and a substantial 9 majority

of the CASAC O 3 Panel agreed with 2007 Staff Paper conclusions and 10 encouraged EPA to establish an alternative cumulative secondary standard for O 3 and 11 related photochemical oxidants that is distinctly different in averaging time, form and 12 level from the current or potentially revised 8

- hour primary

standard. The CASAC also 13 stated that “the recommended metric for the secondary ozone standard is the 14 (sigmoidall y- weighted) W126 index” (Henderson, 2007). 15 The EPA agre ed with the conclusions drawn in the 2006 Criteria Document, 2007 16 Staff Paper and b y CASAC that the scientific evidence available in the 2008 rulemaking 17 continue d to demonstrate the cumulative nature of O 3 - induced plant effects and the need 18 to give greater weight to higher concentrations. Thus, EPA concluded that a cumulative 19 exposure index that differentially weights O 3 concentrations represents a reasonable 20 policy

choice for a seasonal secondary standard to protect against the effects of O 3 o n 21 vegetation

. The EPA f urther agree d with both the 2007 Staff Paper and CASAC th at the 22 most appropriate cumulative , concentration

- weighted form to consider in the 2008 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 292 r ulemaking wa s the sigmoidally weighted W126 form , due to EPA’s recognition that 1 there is no evidence in the literature for an exposure threshold that would be appropriate 2 across all O 3 - sensitive vegetation and that this form is unlikely to be significantly 3 influenced b y O 3 air quality within the range of PRB levels identified in this rulemaking. 4 Thus, in 2007 EPA proposed as one option to replace the then current 0.084 ppm, 8

- hour 5 average secondary

standard with a standard defined in terms of the cumulative, seasonal 6 W126 form. The EPA also proposed the option of making the secondary identical to the 7 proposed revised primary standard. 8 b. Averaging Times 58 9 The 2007 Staff Paper, in addition to form, also considered what exposure periods 10 or durations are most relevant for vegetation, which, unlike people, is exposed to ambient 11 air continuousl y throughout its lifespan. For annual species, this lifespan encompasses a 12 period of onl y one ye ar or less; while for perennials, lifespans can range from a few ye ars 13 to decades or centuries. However, because O 3 levels are not continuousl y elevated and 14 p lants are not equally sensitive to O 3 over the course of a day, season or lifetime, it 15 becomes necessary to identify

periods of exposure that have the most relevance for plant 16 response. The 2007 Staff Paper discussed e xposure periods relevant for vegetati on in 17 terms of a seasonal window and a diurnal window, and it also discussed defining the 18 standard in terms of an annual index value versus a 3
- year average of annual index 19 values

. The numbered paragraphs below present the 2007 Staff Paper discussions on 20

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 O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 293 these exposure periods, and the annual versus 3

- ye ar average index value, followed by a 1 discussion of CASAC views and EPA proposed conclusions. 2 (1) In considering an appropriate seasonal window, the 2007 Staff Paper 3 recognize d that, in general, many annual crops are grown for periods of a few months 4 before being harvested. In contrast, other annual and perennial species may be 5 photosy

ntheticall y active longer, and for some species and locations, throughout the 6 entire year. In general, the period of maximum phy siological activity and thus, maximum 7 potential O 3 uptake for annual crops, herbaceous species, and deciduous trees and shrubs 8 coincides with some or all of the intra

- annual period defined as the O 3 season, which 9 varies on a state

- by

- state basis. Th is is because the high temperature and high light 10 conditions that promote the formation of tropospheric O 3 also promote physiological 11 activity

in vegetation. 12 The 2007 Staff Paper note d that the selection of any single seasonal exposure 13 period for a national standard would represent a compromise, given the significant 14 variability

in growth patterns and lengths of growing seasons among the wide range of 15 vegetation species occurring within the U.S. that may experience adverse effects 16 associated with O 3 e xposures. However, the 2007 Staff Paper further conclude d that the 17 consecutive 3

- month period within the O 3 season with the highest W126 index value 18 (e.g., maximum 3 month period) would, in most cases, likely coincide with the period of 19 greatest plant sensitivi ty on an annual basis. Therefore, the 2007 Staff Paper again 20 conclude d , as it did in the 199 7 review , that the annual maximum consecutive 3

- month 21 period is a reasonable seasonal time period, when combined with a cumulative, 22 concentration weighted form, fo r protection of sensitive vegetation. 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 294 (2) In considering an appropriate diurnal window, the Staff Paper recognize d that 1 over the course of the 24

- hour diurnal period, plant stomatal conductance varies in 2 response to changes in light level, soil moisture and other environmentall y and 3 geneticall y controlled factors. In general, stomata are most open during daylight hours in 4 order to allow sufficient CO 2 uptake for use in carbohydrate production through the light

5 driven process of photosynthesis. At most l ocations, O 3 concentrations are also highest 6 during the day

time, and thus, most likely to coincide with maximum stomatal uptake. It 7 is also known however, that in some species, stomata may remain open sufficiently at 8 night to allow for some nocturnal uptake to occur. In addition, at some rural, high 9 elevation sites, the O 3 concentrations remain relatively flat over the course of the day , 10 often at levels above estimated PRB. At these sites, nighttime W126 values can be of 11 similar magnitude as daytime valu es, though the significance of these exposures is much 12 less certain. This is because O 3 uptake during daylight hours is known to impair the 13 light

- driven process of photosy nthesis, which can then lead to impacts on carbohydrate 14 production, plant growth, reproduction (yield) and root function. It is less clear at this 15 time to what extent and by what mechanisms O 3 uptake at night adversel y impacts plant 16 function. In addition, many species have not been shown to take up O 3 at night and/or do 17 not occur in are as with elevated nighttime O 3 concentrations. 18 In reviewing the information on this topic that became available after the 1997 19 review, the 2007 Staff Paper considered the information compiled in a summary report by 20 Musselman and Minnick (2000)

. This work report ed that some species take up O 3 at 21 night, but that the degree of nocturnal stomatal conductance varies widely between 22 species and its relevance to overall O 3 - induced vegetation effects remain unclear. In 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 295 considering this inform ation, the 2007 Staff Paper concluded that for the vast majority of 1 studied species, day

time exposures represent the majority of diurnal plant O 3 uptake and 2 are responsible for inducing the plant response of most significance to the health and 3 productivity

of the plant (e.g., reduced carbohydrate production). Until additional 4 information is available about the extent to which co

- occurrence of sensitive species and 5 elevated nocturnal O 3 exposures exists, and what levels of nighttime uptake are adverse 6 to affected species, the 2 007 Staff Paper concluded that this information continues to be 7 preliminary , and does not provide a basis for reaching a different conclusion regarding 8 the diurnal window at this time. The 2007 Staff Paper further noted that additional 9 research is needed to address the degree to which a 12
- hour diurnal window may be 10 under

- protective in areas where elevated nighttime levels of O 3 co - occur with sensitive 11 species with a high degree of nocturnal stomatal conductance. Thus, as in the 1997 12 review, the 2007 Staf f Paper again conclude d that based on the available science, the 13 day time 12

- hour window (8 :00 a . m . to 8 :00 p . m . ) is the most appropriate period over 14 which to cumulate diurnal O 3 exposures, specifically those most relevant to plant growth 15 and yield response s. 16 (3) In considering whether the standard should be defined in terms of an annual 17 index value or a 3
- ye ar averag e of annual index values , the 2007 Staff Paper recognized 18 that though most cumulative seasonal exposure levels of concern for vegetation have 19 been expressed in terms of the annual timeframe, it may be appropriate to consider a 3

- 20 ye ar averag e for purposes of standard stability . However, the 2007 Staff Paper note d that 21 for certain welfare effects of concern (e.g., foliar injury , yield loss for annual crops, 22 growth effects on other annual vegetation and potentially tree seedlings), an annual time 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 296 frame may

be a more appropriate period in which to assess what level would provide the 1 requisite degree of protection, while for other welfare effects (e. g., mature tree biomass 2 loss), a 3

- year averag e may also be appropriate. Thus, the 2007 Staff Paper conclude d 3 that it is appropriate to consider both an annual and a 3

- year averag e . Further, the 2007 4 Staff Paper conclude d that should a 3

- year average of the 12

- hour W126 form be 5 selected, a lower standard level should be considered to reduce the potential of adverse 6 impacts to annual species from a single high O 3 ye ar that could still occur while attaining 7 a standard on average over 3 years. 8 The CASAC, i n considering what seasonal , diurnal , and annual or multiyear time 9 periods are most appropriate when combined with a cumulative, seasonal form to protect 10 vegetation from exposures of concern , agreed that the 2007 Staff Paper conclusion 11 regarding the 3
- month seasonal period and 12
- hour daylight window was appropriate, 12 with the distinction that both of these time periods likely represents the minimum time 13 periods of importance. In particular, one O 3 P anel member commented that for some 14 species, additional O 3 exposures of importance were occurring outside the 3

- month 15 seasonal and 12

- hour diurnal windows. Further, the CASAC concluded that multi

- year 16 averaging to promote a “stable” secondary standard is less appropriate for a cumulative, 17 seasonal secondary stan dard than for a primary standard based on daily maximum 8

- hour 18 concentrations . The CASAC further concluded that if multi

- ye ar averaging is emplo yed 19 to afford greater stability of the secondary

standard, the level of the standard should be 20 revised downward to assure that the desired degree of protection is not exceeded in 21 individual years. 22Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 297 The EPA , in determining which seasonal and diurnal time periods are most 1 appropriate to propose , took into account the 2007 Staff Paper and CASAC views. In 2 being careful to consider what is needed to provide the requisite degree of protection, no 3 more and no less, in 2007 EPA propose d that the 3

- month seasonal period and 12

- hour 4 daylight period are appropriate. Based on the 2007 Staff Paper conclusions discussed 5 above, E PA was mindful that there is the potential for under

- protection with a 12

- hour 6 diurnal window in areas with sufficiently elevated nighttime levels of O 3 where sensitive 7 species with a high degree of nocturnal stomatal conductance occur. On the other hand, 8 EPA also recognized that a longer diurnal window (e.g., 24

- hour) has the possibility of 9
over- protecting vegetation in areas where nighttime O 3 levels remain relatively high but 10 where no species having significant nocturnal uptake exist. Inweighing these 11 considerations, EPA agree d with the 2007 Staff Paper conclusion that until additional 12 information is available about the extent to which this co

- occurrence of sensitive species 13 and elevated nocturnal O 3 exposures exists, and what levels of nighttime uptake are 14 adverse to affected species, this information does not provide a basis for reaching a 15 different conclusion at this time. The EPA also considered to what extent the 3

- month 16 period within the O 3 season was appropriate, recognizing that many species of vegetation 17 have longer growing seasons. The EPA further propose d that the maximum 3

- month 18 period is sufficient and appropriate to characterize O 3 exposure levels associated with 19 known levels of plant response. Therefore, EPA propose d that the most appropriate 20 exposure periods for a cumulative, seasonal form is the day time 12

- hour window (8:00 21 a.m. to 8:00 p.m.) during the consecutive 3

- month period within the O 3 monitoring 22 season with the maximum W126 index value. 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 298 The EPA also propose d an annual rather than a multi

- year cumulative, seasonal 1 standard. In proposing this option , EPA also believe d that it was appropriate to consider 2 the benefits to the public welfare that would accrue from establishing a 3

- year average 3 secondary

standard, and solicit ed comment on this alternative. In so doing, EPA also 4 agree d with 2007 Staff Paper and CASAC conclusions that should a 3

- ye ar standard be 5 finalized, the level of the standard should be set so as to provide the requisite degree of 6 protection for those vegetation effects judged to be adverse to the public welfare within a 7 single annual period. 8
c. Level 9 The 2007 Staff Paper, in identifying a range of levels for a 3

- month, 12

- hour 10 W126 annual form appropriate to protect the public welfare from adverse impacts to 11 vegetation from O 3 exposures, consider ed what information from the array of vegetation 12 effects evidence and exposure and risk assessment results was most useful. Regarding 13 the vegetation effects evidence , the 2007 Staff Paper f ound stronger support than what 14 was available at the time of the 1997 review for an increased level of protection for trees 15 and ecos ys tems. Specifically , this expanded body of support includes: (1) additional 16 field based data from free air, gradient and biomonitoring survey s demons trating adverse 17 levels of O 3 - induced above and/or below

- ground growth reductions on trees at the 18 seedling, sapling and mature growth stages and incidence of visible foliar injury 19 occurring at biomonitoring sites in the field at ambient levels of exposure; (2) qualitative 20 support from free air (e.g., AspenFACE) and gradient studies on a limited number of tree 21 species for the continued appropriateness of using OTC

- derived C

- R functions to predict 22 tree seedling response in the field; (3) studies that continue to document below

- ground 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 299 effects on root growth and “carry

- over” effects occurring in subsequent years from O 3 1 exposures; and (4) increased recognition and understanding of the structure and function 2 of ecos ys tems and the complex linkages through which O 3 , and other stressors, acting at 3 the organism and species level can influence higher levels within the ecosystem hierarchy 4 and disrupt essential ecological attributes critical to the maintenance of ecosystem goods 5 and services important to the public welfare. 6 Based on the above observations and on the vegetation effects and the results of 7 the exposure and impact assessment summarized above, the 2007 Staff Paper conclude d 8 that just meeting the then current standard would still allow adverse levels of tree 9
se edling biomass loss in sensitive commerciall y and ecologicall y important tree species 10 in many

regions of the country . Seedling risk assessment results showed that some tree 11 seedling species are extremely sensitive (e.g., cottonwood, black cherry and aspen), with 12 annual biomass losses occurring in the field of the same or greater magnitude that that of 13 annual crops. Such information from the tree seedling risk assessment suggests that O 3 14 levels would need to be substantially reduced to protect sensitive tree seedlings like black 15 cherry

from growth and foliar injury effects. 16 In addition to the currently quantifiable risks to trees from ambient exposures, the 17 2007 Staff Paper also considered the more subtle impacts of O 3 acting in synergy with 18 other natural and man

- made stressors to adversel y affect individual plants, populations 19 and whole s ys tems. By disrupting the photosy

nthetic process, decreasing carbon storage 20 in the roots, increasing early senescence of leaves and affecting water use efficiency in 21 tre es, O 3 exposures could potentially disrupt or change the nutrient and water flow of an 22 entire s ys tem. Weakened trees can become more susceptible to other environmental 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 300 stresses such as pest and pathogen outbreaks or harsh weather conditions. Though it is 1 not possible to quantify all the ecological and societal benefits associated with varying 2 levels of alternative secondary standards, the 2007 Staff Paper conclude d that this 3 information should be weighed in considering the extent to which a secondary stan dard 4 should be set so as to provide potential protection against effects that are anticipated to 5
occur. 6 In addition, th e 2007 Staff Paper also recognized that in the 1997 review, EPA 7 took into account the results of a 1996 C onsensus W orkshop

. At this w orkshop, a group 8 of independent scientists expressed their judgments on what standard form(s) and level(s) 9 would provide vegetation with adequate protection from O 3 - related adverse effects. 10 Consensus was reached with respect to selecting appropriate range s of levels in terms of a 11 cumulative, seasonal 3
- month, 12

- hr SUM06 standard for a number of vegetation effects 12 endpoints. These ranges are identified below, with the estimated approximate equivalent 13 W126 standard values shown in parentheses. For growth effects to tree seedlings in 14 natural forest stands, a consensus was reached that a SUM06 range of 10 to 15 (W126 15 range of 7 to 13) ppm

- hour would be protective. For growth effects to tree seedlings and 16 saplings in plantations, the consensus SUM06 range wa s 12 to 16 (W126 range of 9 to 17 14) ppm

- hour. For visible foliar injury to natural ecos ys tems, the consensus SUM06 18 range was 8 to 12 (W126 range of 5 to 9) ppm

- hour. 19 Taking these consensus statements into account, EPA stated in the 1997 final rule 20 (62 FR 3 8856) that “ the report lends important support to the view that the current 21 secondary

standard is not adequatel y protective of vegetation ...[and]... foreshadows the 22Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 301 direction of future scientific research in this area, the results of which could be important 1 in future reviews of the O 3 secondary standard” (62 FR 38856). 2 Given the importance EPA put on the consensus report in the 1997 review, the 3 2007 Staff Paper considered to what extent research published after 1997 provided 4 empirical support for the ranges of levels identified by the experts as protective of 5 different types of O 3 - induced effects. With regard to O 3 - induced biomass loss in 6 sensitive tree seedlings/saplings growing in natural forest stands, the information 7 discussed in the 2007 Staff Paper, including the evidence from free air and gradient 8 studies, provides additional direct support for the conclusion that the 1996 Consensus 9 Workshop approximate W126 range of 7

- 13 ppm
- hour was an appropriate range to 10 consider in selecting a protective level. With regard to visible foliar injury , the available 11 evidence, including the 2007 Staff Paper anal ys is of incidence in counties with FIA 12 monitoring sites and air quality data, showed significant levels of county

- level visible 13 foliar injury

incidence at the W126 level of 13 ppm

- hour. However, because this analy sis 14 did not address risks of this effect at lower levels of O 3 air quality , and because there is a 15 significant uncertainty in predicting the degree of visible foliar injury s ymptoms expected 16 for lower levels of O 3 air quality , the evidence provides less certain but qualitative 17 directional support for the 1996 Consensus Workshop range of 5 to 9 ppm - hour to protect 18 against this effect

. With regard to O 3 - induced effects on plantation trees, there is far l ess 19 direct information available. Though some forest plantation trees are O 3 - sensitive, the 20 monoculture nature of these stands makes uncertain the degree to which competition for 21 resources might play a role and to what degree the variety of management practices 22 applied would be expected to mitigate the O 3 - induced effects. Thus, it is difficult to 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 302 distinguish a protective range of levels for plantation trees from a range of levels that 1 would be protective of O 3 - sensitive tree seedlings and saplings in natural forest stands. 2 Therefore, on the basis of the strength of the evidence available, the 2007 Staff Paper 3 concluded that it was appropriate to consider a range for a 3

- month, 12

- hour, W126 4 standard that include d the 1996 consensus recommendations for gro wth effects in tree 5 seedlings in natural forest stands (i.e., 7

- 13 ppm
- hour in terms of a W126 form)

. 6 In considering the available information on O 3 - related effects on crops in the 2008 7 rulemaking, the 2007 Staff Paper observed the following regarding the strength of the 8 underlying crop science: (1) nothing in the recent literature points to a change in the 9 relationship between O 3 exposure and crop response across the range of species and/or 10 cultivars of commodity crops currently

grown in the U.S. that co uld be construed to make 11 less appropriate the use of commodity crop C
- R functions developed in the NCLAN 12 program; (2) new field

- based studies (e.g., SoyFACE) provide qualitative support in a 13 few limited cases for the appropriateness of using OTC

- derived C

- R functions to predict 14 crop response in the field; and (3) refinements in the exposure, risk and benefits 15 assessments in this review reduce some of the uncertainties present in the 199 7 review

. 16 On the basis of these observations, the 2007 Staff Paper conc lude d that nothing in the 17 newly

assessed information call ed into question the strength of the underl yi ng science 18 upon which EPA based its proposed decision in the 1997 review to select a level of a 19 cumulative, seasonal form associated with protecting 50 pe rcent of crop cases from no 20 more than 10 percent yi eld loss as providing the requisite degree of protection for 21 commodity

crops. 22Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 303 The 2007 Staff Paper then considered whether any additional information is 1 available to inform judgments as to the adversity of various O 3 - induced levels of crop 2 yi eld loss to the public welfare. As noted above, the 2007 Staff Paper observe d that 3 agricultural s ys tems are heavily managed, and that in addition to stress from O 3 , the 4 annual productivity of agricultural sy stems is vulnerable to disruption from many other 5 stressors (e.g., weather, insects, disease), whose impact in any given ye ar can greatly 6 outweigh the direct reduction in annual productivity resulting from elevated O 3 7 exposures. On the other hand, O 3 can also more subtly impact crop and forage nutritive 8 quality

and indirectly

exacerbate the severity

of the impact from other stressors. Though 9 these latter effects currently cannot be quantified, they should be considered in judging to 10 what extent a level of protecti on selected to protect commodity crops should be 11 precautionary

. 12 Based on the above considerations, the 2007 Staff Paper conclude d that the level 13 of protection (no more than 10% yi eld or biomass loss in 50% of studied cases) judged 14 requisite in the 1997 rev iew to protect the public welfare from adverse levels of O 3 - 15 induced reductions in crop yields and tree seedling biomass loss , as provided by a W126 16 level of 21 ppm

- hour, remains appropriate for consideration as an upper bound of a range 17 of appropriate lev els. 18 Thus, the 2007 Staff Paper conclude d , based on all the above considerations, that 19 an appropriate range of 3

- month, 12

- hour W126 levels wa s 7 to 21 ppm
- hour, 20 recognizing that the level selected is largely a policy judgment as to the requisite level of 21 protection needed. In determining the requisite level of protection for crops and trees, 22 and indirectl y, ecos ys tems, the 2007 Staff Paper recognize d that it is appropriate to weigh 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 304 the importance of the predicted risks of these effects in the overall cont ext of public 1 welfare protection, along with a determination as to the appropriate weight to place on 2 the associated uncertainties and limitations of this information. 3 The CASAC, in its final letter to the Administrator (Henderson, 2007), agreed 4 with the 2007 Staff Paper recommendations that the lower bound of the range within 5 which a seasonal W126 welfare

- based (secondary) O 3 standard should be considered is 6 approximately

7 ppm
- hour; however, it did not agree with s taff’s recommendation that 7 the upper bo und of the range for consideration should be as high as 21 ppm

- hour . Rather, 8 CASAC recommended that the upper bound of the range considered should be no higher 9 than 15 ppm

- hour, which is just above the upper ends of the ranges identified in the 1996 10 Consensus Workshop as being protective of tree seedlings and saplings grown in natural 11 forest stands and in plantations. The lower end of this range (7 ppm

- hour) is the same as 12 the lower end of the range identified in the 199 6 Consensus Workshop as protective of 13 tree seedlings in natural forest stands from growth effects

. 14 In the 2007 proposed rule, taking 2007 Staff Paper and CASAC views into 15 account, EPA propose d a range of level s for a cumulative, seasonal secondary standard as 16 expressed in terms of the maxi mum 3 month, 12

- hour W126 form, in the range of 7 to 21 17 ppm - hour. This range encompasses the range of levels recommended b y C ASAC, and 18 also includes a higher level as recommended for consideration in the 2007 Staff Paper. 19 Given the uncertainty in determining the risk attributable to various levels of exposure to 20 O 3 , EPA believe d, as a public welfare policy judgment , that this wa s a reasonable range 21 to propose. 22 2. Considerations Regarding the 2007 Proposed 8

- Hour Standard 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 305 In the 1997 review, the 1996 Staff Paper included an anal ys is to compare the 1 degree of overlap between areas that would be expected not to meet the range of 2 alternative 8

- hour standards being considered for the primary NAAQS and those 3 expected not to meet the range of values (expressed in terms of the seasonal SUM06 4 index) of concern for vegetation. This result suggested that improvements in national air 5 quality

expected to result from attaining an 8

- hour primary standard within the 6 recommended range of levels would also be expected to red uce levels of concern for 7 vegetation in those same areas. In the 1997 final rule, the decision was made, on the 8 basis of both science and policy considerations, to make the secondary identical to the 9 primary

standard. Itacknowledged, however, that uncertainties remained “as to the 10 extent to which air quality improvements designed to reduce 8

- hour average O 3 11 concentrations averaged over a 3

- ye ar period would reduce O 3 exposures measured b y a 12 seasonal SUM06 index” (62 FR 38876). 13 On the basis of that histo ry , the 2007 Staff Paper analyzed the degree of overlap 14 expected between alternative 8

- hour and cumulative seasonal secondary standards (as 15 discussed above in section IV.C.1) using then recent air quality . Based on the results, the 16 2007 Staff Paper conclude d that the degree to which the then current 8
- hour standard 17 form and level would overlap with areas of concern for vegetation expressed in terms of 18 the 12

- hour W126 standard is inconsistent from year to year and would depend greatl y on 19 the level of the 1 2
- hour W126 and 8

- hour standards selected and the distribution of 20 hourly

O 3 concentrations within the annual and/or 3

- ye ar average period. 21 Thus, though the 2007 Staff Paper recognize d again that meeting the current or 22 alternative levels of the 8

- hour ave rage standard could result in air quality improvements 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 306 that would potentially

benefit vegetation in some areas, it urge d caution be used in 1 evaluating the likely vegetation impacts associated with a given level of air quality 2 expressed in terms of the 8

- ho ur average form in the absence of parallel W126 3 information. This caution wa s due to the concern that th e anal ys is in the 2007 Staff 4 Paper may

not be an accurate reflection of the true situation in non

- monitored, rural 5 counties due to the lack of more complete monitor coverage in many rural areas. Further, 6 of the counties that did not show overlap between the two standard forms, most were 7 located in rural/remote high elevation areas which have O 3 air quality patterns that are 8 ty picall y different from thos e associated with urban and near urban sites at lower 9 elevations . Because the majority of such areas are currently not monitored, it is believed 10 there are likel y to be additional areas that have similar air quality distributions that would 11 lead to the sam e disconnect between forms. Thus, the 2007 Staff Paper conclude d that it 12 remain ed problematic to determine the appropriate level of protection for vegetation 13 using an 8

- hour average form. 14 The CASAC recognized that an important difference between the effec ts of acute 15 exposures to O 3 on human health and the effects of O 3 exposures on welfare is that 16 vegetation effects are more dependent on the cumulative exposure to, and uptake of, O 3 17 over the course of the entire growing season (Henderson, 2006c). The CASA C O 3 Panel 18 members were unanimous in concluding the protection of natural terrestrial ecos ys tems 19 and managed agricultural crops requires a secondary O 3 standard that is substantially 20 different from the primary O 3 standard in averaging time, level, and form (Henderson, 21 2007). 22Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 307 In considering the appropriateness of proposing a revised secondary standard that 1 would be identical to the proposed primary standard, EPA took into account the approach 2 used by

the Agency

in the 1997 review, the conclusions of the 200 7 Staff Paper, CASAC 3 advice, and the views of public commenters. The EPA first considered the 2007 Staff 4 Paper anal ys is of the projected degree of overlap between counties with air quality 5 expected to meet various alternative levels of an 8

- hour standard and alternative levels of 6 a W126 standard based on monitored air quality data. This anal ys is showed significant 7 overlap within the proposed range of the primary 8
- hour form and selected levels of the 8 W126 standard form being considered, with the degree of overlap between these two 9 forms depending greatl y on the levels selected and the distribution of hourly O 3 10 concentrations within the annual and/or 3

- ye ar average period. On this basis, EPA 11 concluded that a secondary standard set identical to the proposed primary standard would 12 provide a significant degree of additional protection for vegetation as compared to that 13 provided b y the current secondary standard. The EPA also recognize d that lack of rural 14 monitoring data made uncertain the degree to which the proposed 8

- hour or W126 15 alternative s would be protective, and that there would be the potential for not providing 16 the appropriate degree of protection for vegetation in areas with air quality distributions 17 that result in a high cumulative, seasonal exposure but do not result in high 8

- hour 18 average exposures. While this potential for under

- protection using an 8

- hour standard 19
wa s clear, the number and size of areas at issue and the degree of risk wa s hard to 20 determine. On the other hand, EPA also considered at that time that there was a potential 21 risk of over

- protection with a cumulative, seasonal standard given the inherent 22 uncertainties associated with moving to a new form for the secondary standard , in 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 308 particular those associated with predicting exposure and risk patterns based on a limited 1 rural monitoring network

. 2 The EPA also considered the views and recommendations of CASAC, and agree d 3 that a cumulative, seasonal standard is the most biologicall y relevant way to relate 4 exposure to plant growth respon se. However, as reflected in the public comment s , EPA 5 also recognize d that there remain ed significant uncertainties in determining or 6 quantifying the degree of risk attributable to varying levels of O 3 exposure, the degree of 7 protection that any specific cumulative, seasonal standard would produce, and the 8 associated potential for error in determining the standard that will provide a requisite 9 degree of protection

-- i.e. , sufficient but not more than what is necessary . Given this 10 uncertainty, EPA also be lieve d it wa s appropriate to consider the degree of protection that 11 would be afforded b y a secondary standard that wa s identical to the then proposed 12 primary

standard. Based on its consideration of the full range of views as described 13 above, and in the 20 07 proposed rule, EPA propose d as a second option to revise the 14 secondary

standard to be identical in every way to the then proposed primary standard. 15 3. Basis for 2008 Decision on the Secondary Standard 16 In the 2008 final rule, EPA noted that deciding on the appropriate secondary 17 standard involved making a choice between two possible alternatives, each with their 18 strengths and weaknesses. The 2008 final rule reported that within the Administration at 19 that time there had been a robust discussion of the same strengths and weaknesses 20 associated with each option that were identified earlier . The process b y which EPA 21 reached its final conclusion is described in the final rule (73 FR 16497)

. The rationale for 22 the 2008 decision presented in the final rule (73 FR 16499

– 16500) is described below. 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 309 In considering the appropriateness of establishing a new standard defined in terms 1 of a cumulative, seasonal form, or revising the then current secondary standard by 2 making it identical to the revised 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. In giving consideration to the approach 5 taken in the 1997 review, EPA first considered the 2007 Staff Paper anal ys is of the 6 projected degree of overlap between counties with air quality expected to meet the 7 revised 8

- hour primary standard, set at a level of 0.075 ppm, and alternative levels of a 8 W126 standard based on currentl y monitored air qu ality data. This anal ys is showed 9 significant overlap between the revised 8

- hour primary standard and selected levels of the 10 W126 standard form being considered, with the degree of overlap between these 11 alternative standards depending greatl y on the W126 level selected and the distribution of 12 hourly

O 3 concentrations within the annual and/or 3

- ye ar average period. 59 On this basis, 13 as an initial matter, EPA concluded that a secondary standard set identical to the 14 proposed primary

standard would provide a sign ificant degree of additional protection for 15 vegetation as compared to that provided by the then current 0.084 ppm secondary 16 standard. In further considering the significant uncertainties that remain in the available 17 body

of evidence of O 3 - related vegetati on effects and in the exposure and risk analy ses 18 conducted for the 2008 rulemaking, and the difficulty in determining at what point 19 various ty

pes of vegetation effects become adverse for sensitive vegetation and 20
ecos ys tems, EPA focused its consideration on a level for an alternative W126 standard at 21

59 Prior to publication of the 2008 final rule, EPA did further anal ys is of the degree of overlap to extend the 2007 Staff Paper analy ses, and that analy sis was available in the docket.Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 310 the upper end of the proposed range (i.e., 21 ppm

- hour). The 2007 Staff Paper anal ys is 1 showed that at that W126 standard level, there would be essentially no counties with air 2 quality

that would be expected both to exceed such an alternative W126 standard and to 3 meet the revised 8

- hour primary standard

– that is, based on this anal ys is of currentl y 4 monitored counties, a W126 standard would be unlikely to provide additional protection 5 in any monitored areas beyond that likely to be provided by

the revised primary

standard. 6 The EPA also recognized that the general lack of rural monitoring data made 7 uncertain the degree to which the revised 8

- hour standard or an alternative W126 8 standard would be protective in those areas , and that there would be the potential for not 9 providing the appropriate degree of protection for vegetation in areas with air quality 10 distributions that result in a high cumulative, seasonal exposure but do not result in high 11 8
- hour average exposure s. While this potential for under

- protection using an 8

- hour 12 standard was clear, the number and size of areas at issue and the degree of risk was hard 13 to determine. However, EPA concluded at that time that an 8

- hour standard would also 14 tend to avoid the po tential for providing more protection than is necessary , a risk that 15 EPA concluded would arise from moving to a new form for the secondary standard 16 despite significant uncertainty in determining the degree of risk for any exposure level 17 and the appropriate level of protection, as well as uncertainty in predicting exposure and 18 risk patterns. 19 The EPA also considered the views and recommendations of CASAC, and agreed 20 that a cumulative, seasonal standard was the most biologicall y relevant way to relate 21 exposure to plant growth response. However, as reflected in some public comments, 22 EPA also judged that there remained significant uncertainties in determining or 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 311 quantifying the degree of risk attributable to varying levels of O 3 exposure, the degree of 1 protectio n that any specific cumulative, seasonal standard would produce, and the 2 associated potential for error in determining the standard that will provide a requisite 3 degree of protection

— i.e., sufficient but not more than what is necessary . Given these 4 signi ficant uncertainties, EPA concluded at that time that establishing a new secondary 5 standard with a cumulative, seasonal form would result in uncertain benefits beyond 6 those afforded b y the revised primary standard and therefore may be more than necessary 7 t o provide the requisite degree of protection. 8 Based on its consideration of the views discussed above, EPA judged in the 2008 9 rulemaking that the appropriate balance to be drawn was to revise the secondary standard 10 to be identical in every way to the revis ed primary standard. The EPA believed that such 11 a standard would be sufficient to protect public welfare from known or anticipated 12 adverse effects, and did not believe that an alternative cumulative, seasonal standard was 13 needed to provide this degree of protection. The EPA believed that this judgment 14 appropriatel y considered the requirement for a standard that is neither more nor less 15 stringent than necessary for this purpose. 16 For the reasons discussed above, and taking into account information and 17
assess ments presented in the 2006 Criteria Document and 2007 Staff Paper, the advice 18 and recommendations of the CASAC Panel, and the public comments to date, EPA 19 decided to revise the existing 8

- hour secondary standard. Specifically , EPA revised the 20 then current 8
- hour average 0.084 ppm secondary standard by

making it identical to the 21 revised 8
- hour primary standard set at a level of 0.075 ppm. 22 4. CASAC Views Following 2008 Decision 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 312 Following the 2008 decision on the O 3 standards, serious questions were raised as 1 to whether the standards met the requirements of the CAA. In April 2008, the members 2 of the CASAC Ozone Review Panel sent a letter to EPA stating “ In our most
- recent 3 letters to you on this subject

- dated October 2006 and March 2007

- ... the Committee 4 recommended an alternative secondary standard of cumulative form that is substantially 5 different from the primary Ozone NAAQS in averaging time, level and form

— 6 specifically, the W126 index within the range of 7 to 15 ppm

- hour, accumulated over at 7 least the 12 “daylight” hours and the three maximum ozone months of the summer 8 growing season” (Henderson, 2008). The letter continued: “The CASAC now wishes to 9 convey , by

means of this letter, its additional, unsolicited advice with regard to the 10 primary

and se condary

Ozone NAAQS. In doing so, the participating members of the 11 CASAC Ozone Review Panel are unanimous in strongly urging you or your successor as 12 EPA Administrator to ensure that these recommendations be considered during the next 13 review cycle for the Ozone NAAQS that will begin next year” (id.). The letter further 14 stated the following views: 15 The CASAC was ... greatly disappointed that you failed to change the 16 form of the secondary standard to make it different from the primary 17 standard. As stated in the preamble to the Final Rule, even in the previous 18 1996 ozone review, “there was general agreement between the EPA staff, 19 CASAC, and the Administrator, ... that a cumulative, seasonal form was 20 more biologically relevant than the previous 1

- hour and new 8

- hour 21 average forms (61 FR 65716)” for the secondary standard. Therefore, in 22 both the previous review and in this review, the Agency staff and its 23 advisors agreed that a change in the form of the secondary standard was 24 scientifically well

- justified. 25 26Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 313 : : : : ; 1 2 Unfortunatel y, this scientifically

- sound app roach of using a cumulative 3 exposure index for welfare effects was not adopted, and the default 4 position of using the primary standard for the secondary standard was 5 once again instituted. Keeping the same form for the secondary Ozone 6 NAAQS as for the prim ary standard is not supported by current scientific 7 knowledge indicating that different indicator variables are needed to 8 protect vegetation compared to public health. The CASAC was further 9 disappointed that a secondary standard of the W126 form was not 10 co nsidered from within the Committee’s previously

- recommended range 11 of 7 to 15 ppm

- hour. The CASAC sincerely hopes that, in the next round of 12 Ozone NAAQS review, the Agency will be able to support and establish a 13 reasonable and scientifically

- defensible cumu lative form for the secondary 14 standard. (Henderson, 2008) 15 16 5. Administrator’s Proposed Conclusions 17 For the reasons discussed below, the Administrator proposes to set a cumulative 18 seasonal standard expressed as an annual index of the sum of weighted hourl y 19 concentrations (i.e., the W126 form) , cumulated over 12 hours per day (8:00 am to 8:00 20 pm) d

uring the consecutive 3
- month period within the O 3 season with the maximum 21 index value , set at a level within the range of 7 to 15 ppm
- hour. This proposed decisi on 22 takes into account the information and assessments presented in the 2006 Criteria 23 Document and the 2007 Staff Paper and related technical support documents, the advice 24 and recommendations of CASAC both during and following the 2008 rulemaking, and 25 publi c comments received in conjunction with review of drafts of these documents and 26 on the 2007 proposed rule. 27Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 314 a. Form 1 As discussed above in section IV.B, the 2006 Criteria Document and 2007 Staff 2 Paper concluded that the recent vegetation effects literature evaluated in th e 2008 3
r ulemaking strengthens and reaffirms conclusions made in the 1997 revi ew that the use of 4 a cumulative exposure index that differentially weights ambient concentrations is best 5 able to relate ambient exposures to vegetation response. Th e 1997 review focused in 6 particular on two of these cumulative forms, the SUM06 and W126 (EPA, 1996) . Given 7 that the data available at that time were unable to distinguish between these forms, the 8 EPA , based on the policy consideration of not including O 3 concentrations considered to 9 be within the PRB , estimated at that time to be between 0.03 and 0.05 ppm , concluded 10 that the SUM06 form would be the more appropriate choice for a cumulative, exposure 11 index for a secondary standard

. 12 In the 2008 rulemaking , the 2007 Staff Paper evaluated the continued 13 appropriateness of the SUM06 form in light of new estimates of PRB that were lower 14 than in the 1997 review, and the continued lack of evidence within the vegetation effects 15 literature of a biological threshold for vegetation exposures of concern. On the basis of 16 th e se policy

and science

- related considerations, the 2007 Staff Paper conclude d that the 17 W126 form wa s the mo re appropriate cumulative, concentration

- weighted form

. 18 Specificall y, the W126, by its incor poration of a sigmoidal weighting scheme, does not 19 create an artificiall y imposed concentration threshold, gives proportionally more weight 20 to the higher and typically more biologically potent concentrations, and is not 21 significantl y influenced by O 3 concentrations within the range of estimated PRB. 22Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 315 As discussed above, the CASAC , b ased on its assessment of the same vegetation 1 effects science, agreed with the 2006 Criteria Document and 2007 Staff Paper and 2 unanimously

concluded that protection of vegetatio n from the known or anticipated 3 adverse effects of ambient O 3 “requires a secondary standard that is substantially 4 different from the primary standard in averaging time, level, and form,” i.e. not identical 5 to the primary

standard for O 3 (Henderson, 2007)

. Moreover, the members of CASAC 6 and a substantial majority of the other CASAC Panel members agreed with 2007 Staff 7 Paper conclusions and encouraged EPA to establish an alternative cumulative secondary 8 standard for O 3 and related photochemical oxidants that is distinctly different in 9 averaging time, form and level from the then current or potentially revised 8

- hour 10 primary

standard (Henderson, 2006c). The CASAC Panel also stated that “the 11 recommended metric for the secondary ozone standard is the (sigmoidally weighted) 12 W126 index” (Henderson, 2007). 13 In reconsidering the 2008 final rule, the Administrator agree s with the conclusions 14 drawn in the 2006 Criteria Document, 2007 Staff Paper and b y CASAC that the scientific 15 evidence available in the 2008 r ulemaking continue s to demonstrate the cumulative 16 nature of O 3 - induced plant effects and the need to give greater weight to higher 17 concentrations. Thus, the Administrator concludes that a cumulative exposure index that 18 differentiall y weights O 3 concentrations rep resent s a reasonable policy choice for a 19 secondary

standard to protect against the effects of O 3 on vegetation The Administrator 20 further agree s with both the 2007 Staff Paper and CASAC th at the most appropriate 21 cumulative , concentration

- weighted form to consider i s the sigmoidall y weighted W126 22 form 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 316 The Administrator notes that in the 2007 proposed rule, EPA proposed a second 1 option of revis ing the then current 8

- hour average secondary standard by

making it 2 identical to the proposed 8

- hour primary standard . The 2007 Staff Paper analyzed the 3 degree of overlap expected between alternative 8

- hour and cumulative seasonal 4 secondary

standards using recent air quality monitoring data. Based on the results, the 5 2007 Staff Paper conclude d that the degree to which the current 8

- hour standard form and 6 level would overlap with areas of concern for vegetation expressed in terms of the 12

- 7 hour W126 standard is inconsistent from year to year and would depend greatly on the 8 level of the 12

- hour W126 and 8

- hour standards selected and the distribution of hourly O 3 9 concentrations within the annual and/or 3

- ye ar average period. The 2007 Staff Paper also 10 recognize d that meeting the then current or alternative levels of the 8

- hour average 11 standard could result in air quality i mprovements that would potentially benefit 12
ve getation in some areas, but urged caution be used in evaluating the likely vegetation 13 impacts associated with a given level of air quality expressed in terms of the 8

- hour 14 average form in the absence of parallel W126 information. This caution was due to the 15 concern that th e anal ys is in the 2007 Staff Paper may not be an accurate reflection of the 16 true situation in non

- monitored, rural counties due to the lack of more complete monitor 17 coverage in many rural areas . Further, of the counties that did not show overlap between 18 the two standard forms, most were located in rural/remote high elevation areas which 19 have O 3 air quality patterns that are typicall y different from those associated with urban 20 and near urban sit es at lower elevations . Because the majority of such areas are currentl y 21 not monitored, there are likely to be additional areas that have similar air quality 22 distributions that would lead to the same disconnect between forms. Thus, the 2007 Staff 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 317 Paper c onclude d that it remains problematic to determine the appropriate level of 1 protection for vegetation using an 8

- hour average form

. 2 The Administrator also notes that CASAC recognized that an important difference 3 between the effects of acute exposures to O 3 on human health and the effects of O 3 4 exposures on welfare is that vegetation effects are more dependent on the cumulative 5 exposure to, and uptake of, O 3 over the course of the entire growing season (Henderson, 6 2006c). The CASAC O 3 Panel members were unanimous in concluding the protection of 7 natural terrestrial ecos ys tems and managed agricultural crops requires a secondary O 3 8 standard that is substantially different from the primary O 3 standard in form, averaging 9 time, and level (Henderson, 2007). 10 In reach ing her proposed decision in this reconsideration of the 2008 final rule, 11 the Administrator has considered the comments received on the 2007 proposed rule 12 regarding revising the secondary standard either to reflect a new, cumulative form or b y 13 remaining eq

ual to a revised primary

standard. The commenters generally fell into two 14 groups. 15 One group of commenters , including environmental organizations, strongl y 16 supported the proposed option of moving to a cumulative, seasonal standard, generall y 17 based on the r easoning explained in the 2007 proposal

. Commenters in this group also 18 expressed serious concerns with the other proposed option of setting a secondary O 3 19 standard in terms of the same form and averaging time (i.e., daily maximum 8

- hour 20 average O 3 concentrati on) as the primary standard. These commenters expressed the 21 view that such a standard would fail to protect public welfare because the maximum daily 22 8
- hour average O 3 concentration failed to adequately characterize harmful O 3 exposures 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 318 to vegetation. This view was generall y based on the observation that there is no 1 consistent relationship in areas across the U.S. between 8

- hour peak O 3 concentrations 2 and the longer

- term cumulative exposures aggregated over a growing season that are 3 biologicall y relevant in characterizing O 3 - related effects on sensitive vegetation. Thus, as 4 EPA noted in the 2007 proposed rule, there is a lack of a rational connection between the 5 level of an 8

- hour standard and the requisite degree of protection required for a secondary 6 O 3 NAAQS. 7 Another group of commenters , including industry organizations, agreed that a 8 cumulative form of the standard may better match the underl ying data , but expressed the 9 view that remaining uncertainties associated with the vegetation effects evidenc e and/or 10 EPA’s exposure, risk and benefits assessments were so great that the available 11 information did not provide an adequate basis to adopt a standard with a level based on a 12 cumulative, seasonal form. These commenters asserted that because of the subs tantial 13 uncertainties remaining at the time of the 2008 rulemaking, the benefits of changing to a 14 W126 form were too uncertain to warrant revising the form of the standard at that time. 15 The Administrator notes that in both the 1997 and the 2008 decisions, EPA 16 recognized that the risk to vegetation from O 3 exposures comes from cumulative 17 exposures over a season or seasons. The CASAC has fully endorsed this view based on 18 the available scientific evidence and assessments, and there is no significant disagreement 19 on this issue by

commenters. Thus, it is clear that the purpose of the secondary O 3 20 NAAQS should be to provide an appropriate degree of protection against cumulative, 21 seasonal exposures to O 3 that are known or anticipated to harm sensitive vegetation or 22
ecos ys tems. In reconsidering the 2008 final rule, the Administrator recognizes that the 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 319 issue before the Agency

is what form of the standard is most appropriate to perform that 1 function. 2 Within this framework, the Administrator recognizes that it is c lear that a 3 cumulative, seasonal form has a distinct advantage in protecting against cumulative, 4 seasonal exposures. Such a form is specifically designed to measure directly the kind of 5 O 3 exposures that can cause harm to vegetation. In contrast, an 8

- ho ur standard does not 6 measure cumulative, seasonal exposures directl y, and can onl y indirectl y afford some 7 degree of protection against such exposures. To the extent that clear relationships exist 8 between 8

- hour dail y peak O 3 concentrations and cumulative, seasonal exposures, the 8

- 9 hour form and averaging time would have the potential to be effective as an indirect 10 surrogate. However, as discussed in the 2007 proposed rule and the 2008 final rule, the 11 evidence shows that there are known types of O 3 air quality patterns that can lead to high 12 levels of cumulative, seasonal O 3 exposures without the occurrence of high daily 8
- hour 13 peak O 3 concentrations. An 8
- hour form and averaging time is an indirect way to 14
measure biologicall y relevant exposure pattern s , is poorly correlated with such exposure 15 patterns, and therefore is less likely to identify

and protect against the kind of cumulative, 16 seasonal exposure patterns that have been determined to be harmful. 17 P ast arguments or reasons for not moving to a cumulative, seasonal form, with 18 appropriate exposure periods, have not been based on disagreement over the biological 19 relevance of the cumulative, seasonal form, or the recognized disadvantages of an 8

- hour 20 standard in measuring and identifying a specified cumulative, seasonal exposure pattern. 21 The reasons for not moving to such a form have been based on concerns over whether 22 EPA has an adequate basis to identify the nature and magnitude of cumulative, seasonal 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 320 exp osure patterns that the standard should be designed to protect against, given the 1 various uncertainties in the evidence and the lack of rural O 3 monitoring data. This most 2 directly

translates into a concern over whether EPA has an adequate basis to determ ine an 3 appropriate level for a cumulative, seasonal secondary standard. 4 The Administrator has also considered issues associated with selection of the 5 W126 cumulative form, as reflected in the following assertions made by some 6 comment er s on the 2007 propose d rule: (1) the W126 form lacks a biological basis, since 7 it is merely

a mathematical expression of exposure that has been fit to specific responses 8 in OTC studies, such that its relevance for real world biological responses is unclear; (2) 9 a flux

- based m odel would be a better choice than a cumulative metric because it is an 10 improvement over the many limitations and simplifications associated with the 11 cumulative form; however, there is insufficient data to apply such a model at present; (3) 12 the European experience with cumulative O 3 metrics has been disappointing and now 13 Europeans are working on their second level approach, which will be flux

- based; and (4) 14 a second index that reflects the accumulation of peaks at or above 0.10 ppm (called 15 N100) should be added to a W126 index to achieve appropriate protection

. 16 With regard to whether the W126 index lacks a biological basis, the 17 Administrator finds no basis for reaching such a conclusion. As discussed above in 18 section IV.B, the vegetation effects science is clear that exposures of concern to plants 19 are not based on one discrete 8

- hour period but on the repeated occurrence of elevated O 3 20 levels throughout the plant’s growing season. The cumulative nature of the W126 is 21 supported by

the basic biological under standing that plants in the U.S. are generall y most 22 biologicall y active during the warm season and are exposed to ambient O 3 throughout 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 321 this biologically

active period. In addition, it has been shown in the scientific literature 1 that all else being equal, plants respond more to higher O 3 concentrations, with no 2 evidence of an exposure threshold for vegetation effects. The W126 sigmoidal weighting 3 function reflects both of these understandings, b y not including a threshold below which 4 concentrations are no t included, and by differentially

weighting concentrations to give 5 greater weight to higher concentrations and less weight to lower ones. 6 With regard to whether a flux

- based model would be a better choice, the 2007 7 Staff Paper acknowledged that flux model s may produce a more accurate calculation of 8 dose to a specific plant species in a specific area. However, dose

- response relationships 9 have not been developed for these flux calculations for plants growing in the U.S. 10 Further, flux calculations require l arge amounts of data for the phys iology of each plant 11 species and the local conditions for the growing range of each plant species. These 12 exercises may

be useful for limited small

- scale risk assessments, but do not provide an 13 appropriate basis for a natio nal standard at this time. 14 With regard to dissatisfaction with the performance of a particular cumulative 15 index in use in Europe, 60 and growing interest in development of flux

- based models, the 16 2007 Staff Paper (Appendix 7A) noted that “because of a lack of flux

- response data, a 17 cumulative, cutoff concentration based (e.g., AOT40) exposure index will remain in use 18 in Europe for the near future for most crops and for forests and semi

- natural herbaceous 19 vegetation (Ashmore et al., 2004a).” Further, like the S UM06 index, the AOT40 index 20

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) b y subtracting 40 ppb from the value of each hourly concentration above t hat threshold and then cumulating each hourl y difference over a specified window.Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 322 incorporates a threshold below which concentrations are not considered. Though the 1 AOT40 threshold is lower than the threshold value in SUM06, the 2007 Staff Paper 2 concluded that the vegetation effects information does not prov ide evidence of an effects 3 threshold that applies to all species. Thus, the Administrator concludes neither of these 4 forms is as biologicall y relevant as the W126 form. 5 With regard to consideration of coupling a W126 form with a separate N100 6 index, there was very little research on the N100 index or a coupled approach to be 7 evaluated in the 2008 rulemaking. The CASAC, after reviewing all the information in 8 the 2006 Criteria Document and the 2007 Staff Paper, did not recommend an additional 9 N100 index for consideration. Therefore, there is no basis at this time to judge the extent 10 to which such a coupled W126

-N100 form would be a better choice than the proposed 11 W126 form. Further, the W126 form incorporates a weighting scheme that places greater 12 weight o n increasing concentrations and gives every concentration of 0.10 ppm and 13 above an equal weight of 1, which is the highest weight in this sigmoidal weighting 14 function. 15 In summary , having considered the scientific information and assessment results 16 availa

ble in the 2008 rulemaking as discussed above in this proposal notice, as well as the 17 recommendations of the staff and CASAC, and having taken into consideration issues 18 raised in public comments received as part of the 2008 rulemaking , and recognizing the 19 determinations made below in section IV.D.5.c on level, the Administrator concludes that 20 it is appropriate to set the secondary standard using a cumulative, seasonal form. The 21 Administrator also concludes that the W126 form is best suited to reflect the b iological 22 impacts of O 3 exposure on vegetation, and that there is adequate certainty in the 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 323 information available in the 2008 rulemaking to support such a change in form. Thus, the 1 Administrator proposes to set the secondary standard using a cumulative, s easonal W126 2 form. 3 b. Averaging Times 61 4 5 The Administrator, in addition to reconsidering what form of a secondary 6 standard is most appropriate for protecting vegetation, is also reconsidering what 7 exposure periods (e.g., seasonal window, diurnal window), and what standard index, in 8 terms of an annual index value versus a 3
- ye ar average of annual index values, are most 9 appropriate when used in conjunction with the W126 cumulative seasonal form. Based 10 on the information set forth in the 2007 Staff Paper, as well as CASAC views, as 11 discussed above in section IV.D.1.b, the Administrator has reached conclusions regarding 12 exposure periods, and the annual versus 3

- ye ar average index, that have the most 13 biological relevance for plant response, as discussed below. 14 In considering an appropriate seasonal window , the Administrator notes that the 15 2007 Staff Paper concluded that the consecutive 3

- month period within the O 3 season 16 with the highest W126 index value (e.g., maximum 3

- month period) was a reasonable 17 seasonal ti me period to consider. The Administrator further notes that the 2007 Staff 18 Paper acknowledged that the selection of any single seasonal exposure period for a 19 national standard would necessarily represent a compromise, given the significant 20 variability

in growth patterns and lengths of growing seasons among the wide range of 21

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 speci fied period of time are cumulated, not averaged.Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 324 sensitive vegetation species occurring within the U.S. However, the Administrator also 1 considered the Staff Paper conclusion that the period of maximum potential plant uptake 2 of O 3 wo uld also likely coincide with the period of highest O 3 occurring within the intra

3 annual period defined as the O 3 season , since the high temperature and light conditions 4 conducive to O 3 formation are also conducive for plant activity . The Administrator al so 5 observes that the CASAC panel was supportive of the Staff Paper views, while 6 recognizing that 3 months likely represented the minimum timeframe appropriate to 7 consider. Therefore, the Administrator conclude s, on these bases, that the consecutive 3

- 8 month period within the O 3 season with the highest W126 index value (e.g., maximum 3

- 9 month period) remains an appropriate seasonal window to propose for the protection of 10 sensitive vegetation. 11 With regard to consideration of an appropriate diurnal window, the Administrator 12 has taken into account the 2007 Staff Paper conclusion that for the vast majority of 13 studied species, day time exposures represent the majority of diurnal plant O 3 uptake and 14 are responsible for inducing the plant response of most significance to the health and 15 productivity

of the plant (e.g., reduced carbohydrate production). The Administrator is 16 also aware, based on discussions in the 2007 Staff Paper that there are some number of 17 species that show non

- negligible amounts of O 3 uptake at night due to incomplete 18 stomatal closure. In reaching her conclusion that the 2007 Staff Paper recommendation 19 of a 12
- hour day

time window (8 :00 a . m . to 8 :00 p . m . ) remains the most appropriate 20 period over which to cumulate diurnal O 3 exposures, specificall y those most relevant to 21 plant growth and yi eld responses , the Administrator places weight on the fact that the 22 CASAC comments were also supportive of this diurnal window, recognizing again that it 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 325 likely represents a minimum period over which plants can be vulnerable to O 3 uptake

. 1 Therefore, the Administrator is again proposing the 12

- hour day time window (8:00 a.m. 2 to 8:00 p.m.) as an appropriate diurnal window to protect against O 3 - induced plant 3 effects. 4 Lastl y, in considering whether an annual or a 3
- ye ar averag e index is more 5 appropriate, the Administrator notes that in addition to the available scientific evidence 6 regarding plant effects that can be brought to bear, there are also other public welfare 7 considerations that may be appropriate to consider. In taking this view, the Administrator 8 notes that the 2007 Staff Paper recognized that though most cumulative seasonal 9 exposure levels of concern for vegetation have been expressed in terms of the annual 10 timeframe, it may

be appropriate to consider a 3

- year averag e for purposes of standard 11 stability

. The Administrator has considered that while the 2007 Staff Paper notes that for 12 certain welfare effects of concern (e.g., foliar injury , yield loss for annual crops, growth 13 effects on other annual vegetation and potentiall y tree seedlings), an annual time frame 14 may

be a more appropriate period in which to assess what level would provide the 15 requisite degree of protection, for other welfare effects (e.g., mature tree biomass loss), it 16 also points out that a 3
- ye ar averag e may also be appropriate. The Administrator further 17 observes that in concluding that it was appropriate to consider both an annual and a 3

- 18 ye ar average , the 2007 Staff Paper also conclude d that should a 3

- ye ar average of the 3
- 19 month, 12
- hour W12 6 form be selected, a potentially lower level should be considered to 20 reduce the potential of adverse impacts to annual species from a single high O 3 year that 21 could still occur while attaining a standard on average over 3

- ye ars. The Administrator 22 also t ook note that the CASAC Panel, in addressing this issue of annual versus 3

- ye ar 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 326 average concluded that multi

- year averaging to promote a “stable” secondary standard is 1 less appropriate for a cumulative, seasonal secondary standard than for a primary 2 standard based on maximum 8

- hour concentrations , and further concluded that if multi

3 ye ar averaging is employed to increase the stability of the secondary

standard, the level 4 of the standard should be revised downward to assure that the desired degree of 5 protection is not exceeded in individual years. The Administrator, in considering the 6 merits of both the annual and 3

- year average, and taking into account both the 2007 Staff 7 Paper and CASAC views, concludes that it is important to place more weight on the 8 publ ic welfare benefit in having a stable standard, and that appropriate protection for 9 vegetation can be achieved using a 3

- ye ar average form. The Administrator is thus 10 proposing a 3

- ye ar average. However, given the uncertain nature of the evidence and 11 potential concerns with using a 3

- ye ar average form, the Administrator is proposing to 12 take comment on the appropriateness of the specific seasonal and diurnal exposure 13 periods proposed, as well as the use of a 3

- ye ar average, and, as discussed below, the 14 impact that selection of these proposed seasonal and diurnal exposure periods would 15 have, in conjunction with a 3

- year average form, on the appropriateness of the proposed 16 range of levels. 17
c . Level 18 i. Considerations Regarding 2007 Proposed Range of Levels 19 The 2007 Staff Paper, in identifying a range of levels for a 3

- month, 12

- hour 20 (day

time) W126 standard appropriate for the Administrator to consider in protecting the 21 public welfare from known or anticipated adverse effects to vegetation from O 3 22 exposures, con sidered what information from the array of vegetation effects evidence and 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 327 exposure and risk assessment results was most useful. With respect to the vegetation 1 effects evidence, the 2007 Staff Paper found stronger support than what was available at 2 the ti me of the 1997 review for an increased level of protection for trees and forested 3
ecos ys tems. Specifically, th e expanded body of evidence included: (1) additional field 4 based data from free air, gradient and biomonitoring survey s demonstrating adverse 5 lev els of O 3 - induced growth reductions on trees at the seedling, sapling and mature 6 growth stages and incidence of visible foliar injury occurring at biomonitoring sites in the 7 field at ambient levels of exposure; (2) qualitative support from free air (e.g., 8 AspenFACE) and gradient studies on a limited number of tree species for the continued 9 appropriateness of using OTC

- derived C

- R functions to predict tree seedling response in 10 the field; (3) studies that continue d to document below

- ground effects on root gro wth and 11 “carry
- over” effects occurring in subsequent years from O 3 exposures; and (4) increased 12 recognition and understanding of the structure and function of ecos ys tems and the 13 complex linkages through which O 3 , and other stressors, acting at the organism and 14 species level can influence higher levels within the ecos ys tem hierarchy and disrupt 15 essential ecological attributes critical to the maintenance of ecos ys tem goods and services 16 important to the public welfare. 17 Based on the above sources of vegetation effects information and the results of 18 the exposure and risk assessment s summarized above, the 2007 Staff Paper concluded 19 that just meeting the then current 0.084 ppm, 8
- hour average standard would continue to 20 allow adverse levels of O 3 - induced effects to occur in sensitive commercially and 21 ecologicall y important tree species in many regions of the country . The 2007 Staff Paper 22 further concluded that air quality levels would need to be substantially reduced to protect 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 328 sensitive tree seedlings , such as black cherry , aspen, and cottonwood, from these growth 1 and foliar injury

effects. 2 In addition to the currently quantifiable risks to trees from ambient exposures, the 3 2007 Staff Paper also considere d the more subtle impacts of O 3 acting in synergy with 4 other natural and man

- made stressors to adversel y affect individual plants, populations 5 and whole s ys tems. By disrupting the photosy

nthetic process, decreasing carbon storage 6 in the roots, increasing early senescence of leaves and affecting water use efficiency in 7 trees, O 3 exposures could potentially disrupt or change the nutrient and water flow of an 8 entire s ys tem. Weakened trees can become more susceptible to other environmental 9 stresses such as pest and pathogen outbreaks or harsh weather conditions. Though it is 10 not possible to quantify all the ecological and societal benefits associated with varying 11 levels of alternative secondary standards, the 2007 Staff Paper conclude d that this 12 information should be weighed in considering the extent to which a seconda ry standard 13 should be set so as to provide potential protection against effects that are anticipated to 14
occur. 15 The 2007 Staff Paper also recognized that in the 1997 review, EPA took into 16 account the results of a 1996 C onsensus W orkshop

. At this workshop, a group of 17 independent scientists expressed their judgments on what standard form(s) and level(s) 18 would provide vegetation with adequate protection from O 3 - related adverse effects. 19 Consensus was reached on protective ranges of levels in terms of a cumulative, seasonal 20 3
- month, 12

- hr SUM06 standard for a number of vegetation effects endpoints. These 21 ranges are identified below, with the estimated approximate equivalent W126 standard 22 level s shown in parentheses. For growth effects to tree seedlings in nat ural forest stands, 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 329 a consensus was reached that a SUM06 range of 10 to 15 (W126 range of 7 to 13) ppm

1 hour would be protective. For growth effects to tree seedlings and saplings in 2 plantations, the consensus SUM06 range was 12 to 16 (W126 range of 9 to 1 4) ppm

3 hour. For visible foliar injury to natural ecos ys tems, the consensus SUM06 range was 8 4 to 12 (W126 range of 5 to 9) ppm

- hour. 5 The 2007 Staff Paper then considered to what extent recent research provided 6 empirical support for the ranges of levels identified by the experts as protective of 7 different types of O 3 - induced effects. As discussed above in section IV.D.1.c, the 2007 8 Staff Paper concluded on the basis of the available evidence that it was appropriate to 9 consider a range for a 3

- month, 12

- h our, W126 standard level that included the 1996 10 C onsensus Workshop recommendations regarding a range of levels protective against O 3 - 11 induced growth effects in tree seedlings in natural forest stands (i.e., 7

- 13 ppm
- hour in 12 terms of a W126 form)

. 13 In consid ering the newly available information on O 3 - related effects on crops in 14 this review, the 2007 Staff Paper observe d the following regarding the strength of the 15 underlying crop science: (1) nothing in the recent literature points to a change in the 16 relation ship between O 3 exposure and crop response across the range of species and/or 17 cultivars of commodity crops currently

grown in the U.S. that could be construed to make 18 less appropriate the use of commodity crop C
- R functions developed in the NCLAN 19 program; (2) new field

- based studies (e.g., SoyFACE) provide qualitative support in a 20 few limited cases for the appropriateness of using OTC

- derived C

- R functions to predict 21 crop response in the field; and (3) refinements in the exposure, risk and benefits 22
assessments in this review reduce some of the uncertainties present in 1996. On the basis 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 330 of these observations, the 2007 Staff Paper conclude d that nothing in the newly assessed 1 information calls into question the strength of the underlying science upon which EP A 2 based its proposed decision in the last review to select a level of a cumulative, seasonal 3 form associated with protecting 50 percent of crop cases from no more than 10 percent 4 yi eld loss as providing the requisite degree of protection for commodity crop s. 5 The 2007 Staff Paper then considered whether any additional information wa s 6 available to inform judgments as to the adversity of various O 3 - induced levels of crop 7 yi eld loss to the public welfare. As noted above, the 2007 Staff Paper observed that 8 agricultural s ys tems are heavily managed, and that in addition to stress from O 3 , the 9 annual productivity

of agricultural sy stems is vulnerable to disruption from many other 10 stressors (e.g., weather, insects, disease), whose impact in any given ye ar can greatly 11 outweigh the direct reduction in annual productivity resulting from elevated O 3 12 exposures. On the other hand, O 3 can also more subtly impact crop and forage nutritive 13 quality

and indirectly

exacerbate the severity

of the impact from other stressors. Since 14 these latter effects could n ot be quantified at that time , they could only be considered 15 qualitatively

in reaching judgments about an appropriate degree of protection for 16 commodity

crops from O 3 –

related effects. 17 Based on the above considerations, the 2007 Staff Paper concluded that the level 18 of protection judged requisite in the 1997 review to protect the public welfare from 19 adverse levels of O 3 –induced reductions in crop yields and tree seedling biomass loss , as 20 approximately provided by a W126 level of 21 ppm

- hour, remained appropriate for 21 consideration as an upper bound of a range of appropriate levels. The 2007 Staff Paper 22 also recognized that a standard set at this level would not protect the most sensitive 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 331 species or individuals within a species from all potential effects related to O 3 exposures 1 and further, that this level derives from the extensive and quantitative historic and recent 2 crop effects database, as well as current staff exposure and risk anal ys es (EPA, 2007, pg. 3 8
- 22). 4 In identif

ying a lower bound for the range of alternative standard levels 5 appropriate for consideration, staff conclude d that several lines of evidence point ed to the 6 need for greater protection for tree seedlings, mature trees, and associated forested 7
ecos ys tems. S taff believed that tree growth wa s an important endpoint to consider 8 because it is related to other aspects of societal welfare such as sustainable production of 9 timber and related goods, recreation, and carbon (CO 2 ) sequestration. Impacts on tree 10 growth can also affect ecosy stems through shifts in species composition and the loss of 11 genetic diversity due to the loss of O 3 sensitive individuals or species. In selecting an 12 appropriate level of protection for trees, staff considered the results of the 1996 13 C onsensus W orkshop which identified the SUM06 range of 10 to 15 (W126 of 7 to 13) 14 ppm - h our for growth effects to tree seedlings in natural forest stands. 15 Because staff believed that O 3 - related effects on forest tree species are important 16 public welfare e ffect s of concern , it therefore concluded, based on the above, that it wa s 17 appropriate to include 7 ppm
- hour as the lower bound of the recommended range, the 18 lower end of the approximate range recommended by CASAC (Henderson, 2006c) and 19 identified by

the 1 996 Consensus Workshop participants as protective of forest trees

. At 20 this lower end of the range, staff anticipated, b ased on its analy ses of risks of tree 21 seedling biomass loss and mature tree growth reductions and on the basis of the scientific 22 effects literature, that adverse effects of O 3 on forested ecos ys tems would be substantially 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 332 reduced

. Further, staff anticipated that the lower end of this range would provide 1 increased protection from the more subtle impacts of O 3 acting in s ynergy with other 2
n atural and man

- made stressors to adversely affect individual plants, populations and 3 whole sy stems. Staff also noted that b y disrupting the photosy nthetic process, decreasing 4 carbon storage in the roots, increasing earl y senescence of leaves and affecting water use 5 efficiency

in trees, O 3 exposure could potentiall y disrupt or change the nutrient and water 6 flow of an entire sy stem. Such w eakened trees can become more susceptible to other 7 environmental stresses such as pest and pathogen outbreaks or harsh we ather conditions. 8 While recognizing that it is not possible to quantify all the ecological and societal 9 benefits associated with varying levels of alternative secondary standards, staff believ e d 10 that this information should be weighed in considering the extent to which a secondary 11 standard should be precautionary in nature in protecting against effects that have not yet 12 been adequatel y studied and evaluated. 13 Thus, the 2007 Staff Paper concluded, based on all the above considerations, that 14 an appropriate range of levels, for an annual standard using a 3
- month, 12

- hour W126 15 form, for the Administrator to consider was 7 to 21 ppm
- hour, recognizing that the level 16 selected is largely

a policy judgment as to the requisite level of protection needed. In 17 determining the requisite level of protection for crops and trees, the 2007 Staff Paper 18 recognized that it wa s appropriate to weigh the importance of the predicted risks of these 19 effects in the overall context of public welfare protection, along with a determinatio n as 20 to the appropriate weight to place on the associated uncertainties and limitations of this 21 information. 22 ii

. CASAC and Public Comments Prior to 2008 Decision 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 333 In considering the evidence described in both the 2006 Criteria Document and 1 2006 draft Staf

f Paper, CASAC, in its October 24, 2006 letter to the Administrator, 2 expressed its view regarding the appropriate form and range of levels for the 3 Administrator to consider. The CASAC preferred a seasonal 3

- month W126 standard in 4 a range that is the appro ximate equivalent of the SUM06 at 10 to 20 ppm
- h our . 5 Following the 2007 proposal, EPA received additional CASAC and public comments 6 regarding an appropriate range of levels of a W126 form for the Administrator to 7 consider in finalizing a revised secondary NAAQS for O 3 . The CASAC, in its final letter 8 to the Administrator (Henderson, 2007), agreed with the 2007 Staff Paper 9 recommendations that the lower bound of the range within which a seasonal W126 10 secondary

O 3 standard should be considered is approximate ly 7 ppm
- hour; however, it 11 did not agree with s taff’s recommendation that the upper bound of the range should be as 12 high as 21 ppm

- hour. Rather, as discussed above in section IV.D.1.c, the CASAC Panel 13 recommended that the upper bound of the range considered should be no higher than a 14 W126 of 15 ppm
- hour for an annual standard

. 15 The comments received from the public fell into two groups. One group of 16 commenters supported the CASAC recommended range of 7

- 15 ppm
- hour for a W126 17 standard. Many of these sam e commenters further emphasized the lower end of the 18 proposed range as necessary to provide adequate protection for sensitive species. These 19 commenters based their recommendation primarily on four sources of information: (1) 20 field

- based evidence of foli ar injury occurring on sensitive species at air quality levels 21 well below that of the current standard; (2) the 1996 Consensus Workshop 22 recommendations for protective levels in terms of cumulative exposures for different 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 334 vegetation ty

pes; (3) CASAC advice and recommendations; and (4) studies published 1 after the close of the 2006 Criteria Document that potentially strengthen the link between 2 species level impacts and ecos ys tem response. 3 The other group of commenters did not support revising the current se condary 4 standard. These commenters primaril y focused on uncertainties regarding the sources of 5 information relied upon by the first group of commenters as support for a level within the 6 range of levels recommended by CASAC. These uncertainties included: (1) potential 7 confounders, such as soil moisture, on visible foliar injury and the lack of a clear 8 relationship between visible foliar injury s ymptoms and other vegetation effects; (2) lack 9 of documentation of the basis for the recommendations from the 1 996 Consensus 10 Workshop in selecting a range of levels, indicating that these recommendations should be 11 used with great caution; (3) failure of CASAC and EPA to take into account the monitor 12 height measurement gradient when making their recommendations conc erning the level 13 of the secondary

standard; and (4) inability to quantitatively

estimate ecosy stem effects 14 of O 3 or to extrapolate meaningfully from effects on individual plants to ecosy stem 15 effects due to inadequate data. 16 iii

. Conclusions on Level 17 The Administrator is proposing to set a cumulative, seasonal standard expressed 18 in terms of the maximum 3

- month, 12

- hour W126 form, in the range of 7 to 15 ppm

19 hour

. In reaching this proposed decision about an appropriate range of levels for the 20 secondary

stand ard , the Administrator has considered the following : the evidence 21 described in the 2006 Criteria Document and the 2007 Staff Paper; the results of the 22 vegetation exposure and risk assessments discussed above and in the 2007 Staff Paper, 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 335 giving weight to the assessments as judged appropriate; the CASAC Panel’s advice and 1 recommendations in the CASAC’s letters to the Administrator; EPA staff 2 recommendations; and public comments received during the development of these 3 documents, either in connection with CAS AC meetings or separatel y. In considering 4 what range of level s of a cumulative 3

- month standard to propose, the Administrator 5 note s that that this choice requires judgment as to what standard will protect the public 6 welfare from any known or anticipated adverse effects. This choice must be based on an 7 interpretation of the evidence and other information , such as the expos ure and risk 8 assessments, that neither overstates nor understates the strength and limitations of the 9 evidence and information nor the a ppropriate inferences to be drawn. In taking all of the 10 above into consideration, the Administrator also notes that there is no bright line clearl y 11 directing the choice of level for any of the effects of concern, and the choice of what is 12 appropriate is c learl y a public welfare policy judgment entrusted to the Administrator. 13 In particular, the Administrator has given careful consideration to the following: 14 1) the nature and degree of effects of O 3 to the public welfare, including what constitutes 15 an adverse effect; 2) the strengths and limitations of the evidence that is available 16 regarding known or anticipated adverse effects from cumulative, seasonal exposures, and 17 its usefulness in informing selection of a proposed range; and 3) CASAC’s views 18 regarding the strength of the evidence and its adequacy to inform a range of levels. Each 19 of these topics is discussed in turn below. 20 In determining the nature and degree of effects of O 3 on the public welfare, the 21 Administrator recognizes that the significance to the public welfare of O 3 - induced effects 22 on sensitive v egetation growing within the U.S. can vary , depending on the nature of the 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 336 effect, the intended use of the sensitive plants or ecosy stems, and the ty pes of 1 environments in which the sensitive vegetation and ecos ys tems are located. Any given 2 O 3 - related eff

ect on vegetation and ecos ys tems (e.g., biomass loss, foliar injury), 3 therefore, may

be judged to have a different degree of impact on the public depending, 4 for example, on whether that effect occurs in a Class I area, a city park, or commercial 5 cropland. In her judgment, it is appropriate that this variation in the significance of O 3 - 6 related vegetation effects should be taken into consideration in judging the level of 7 ambient O 3 that is requisite to protect the public welfare from any known or anticipated 8 adverse effects

. In this regard, the Administrator agrees with the definition of adversity 9 as described above in section IV.A.3 and in the 2008 rulemaking. As a result, the 10 Administrator concludes that of those known and anticipated O 3 - related vegetation and 11
ecos ys tem effects identified and discussed in this reconsideration, the highest priority and 12 significance should be given to those that occur on sensitive species that are known to or 13 are likel y to occur in federall y protected areas such as Class I areas 62 or on lands set aside 14 by States, Tribes and public interest groups to provide similar benefits to the public 15 welfare, for residents on those lands, as well as visitors to those areas. 16 Likewise, the Administrator also notes that the same known or anticipated O 3 - 17 induced effects, occurring in other areas may call for less protection. For example, the 18 maintenance of adequate agricultural crop yi elds is extremely important to the public 19

62 For example, the level of protection granted b y Congress under the Wilderness Act of 1964 for designated “wilderness areas” requires that these areas “ shall be administered for the use and enjo ym ent 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 W ilderness Act, 1964).Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 337 welfare and is currentl y achieved through the application of intensive management 1 practices, including in some cases, genetic engineering. These management practices, in 2 conjunction with market forces and government programs, assure an appropriate balance 3 is reached between costs of production and market availability

. Thus, while research on 4 agricultural crop species remains useful in illuminating mechanisms of action and 5 phy siological processes, information from this sector on O 3 - induced effects is considered 6 less useful in informing judgments on what level(s) would b e sufficient but not more than 7 necessary

to protect the public welfare. With respect to commercial production of 8 commodities, the Administrator notes that judgments about the extent to which O 3 - related 9 effects on commercially managed vegetation are advers e from a public welfare 10 perspective are particularly difficult to reach, given that what is known about the 11 relationship between O 3 exposures and agricultural crop yi eld response derives largel y 12 from data generated almost 20 years ago. The Administrator recognizes that there is 13 substantial uncertainty atthis time as to whether these data remain relevant to the 14 majority

of species and cultivars of crops being grown in the field today . In addition, the 15 extensive management of such vegetation may to some de gree mitigate potential O 3 - 16 related effects. The management practices used on these lands are highl y variable and 17 are designed to achieve optimal yields, taking into consideration various environmental 18 conditions. Thus, the Administrator concludes there i s no need for such additional 19 protection for agricultural crops through the NAAQS. 20 The Administrator also recognizes that O 3 - related effects on sensitive vegetation 21 can occur in other areas that have not been afforded special Federal protections, ranging 22 f rom effects on vegetation growing in residential or commercial settings, such as 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 338 ornamentals used in urban/suburban landscaping, to vegetation grown in land use 1 categories that are heavily managed for commercial production of commodities such as 2 timber. F or vegetation used for residential or commercial ornamental purposes, such as 3 urban/suburban landscaping, the Administrator believes that there is not adequate 4 information at this time to establish a secondary standard based specificall y on 5 impairment of urban/suburban landscaping and other uses of ornamental vegetation, but 6 notes that a secondary standard revised to provide protection for sensitive natural 7 vegetation and ecos ys tems would likely also provide some degree of protection for such 8 ornamental veg etation. 9 Based on the above, the Administrator finds that the ty pes of information most 10 useful in informing the selection of an appropriate range of protective levels is 11 appropriatel y focused on information regarding exposures and responses of sensitive 12 trees and other native species known or anticipated to occur in protected areas such as 13 Class Iareas or on lands set aside by States, Tribes and public interest groups to provide 14 similar benefits to the public welfare, for residents on those lands, as well as visitors to 15 those areas. 16 With regard to the available evidence, the Administrator finds the coherence and 17 strength of the weight of evidence from the large body of available literature compelling. 18 This evidence addresses a broad array of O 3 - induced e ffects on a variety of tree species 19 across a range of growth stages (i.e., seedlings, saplings and mature trees) using diverse 20 field

- based (e.g. free air, gradient and ambient) and OTC exposure methods. It 21 demonstrates that significant numbers of forest tree species are potentially experiencing 22Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 339 O 3 - induced stress under levels of ambient air quality , both at and below the level of the 1 1997 standard

. 2 In particular, the Administrator notes the evidence from recent field

- based studies 3 and a gradient study of e astern cottonwood saplings (Gregg et al., 2003). She observes 4 that this study found that cottonwood saplings grown in urban New York City grew faster 5 than saplings grown in downwind rural areas where cumulative O 3 exposures were 6 higher , and the difference in biomass production between the urban site with the lowest 7 cumulative exposure and the rural site with the highest cumulative exposure i s 8 dramatic ( Figure 7

- 17 in the 200 7 Staff Paper)

. The Administrator further notes that 9 cottonwood is one of the mos t sensitive tree species studied to date and it is also 10 important both from an ecological and pub l ic welfare perspective , as discussed above in 11 section IV.A.2.b and in the 2007 Staff Paper

. 12 The Administrator also notes the evidence related to the O 3 - induce d effect of 13 visible foliar injury . The Administrator observes that the visible foliar injury database 14 created from the ambient field

- based monitoring network managed by the Unites States 15 Forest Service (USFS) Forest Inventory and Analy sis (FIA) Program ha s continued to 16 expand s ince the conclusion of the 199 7 review . In utilizing this dataset, EPA staff 17 collaborated with FIA staff to compare the incidence of visible foliar injury at different 18 levels of air quality b y county throughout the U.S. in counties with FIA monitoring sites. 19 In considering the results of this analy sis, depicted in Table 7

- 4 of the 2007 Staff Paper, 20 the Administrator notes that for the 2001

- 2004 period , the percent of counties with 21 documented foliar injury at a level approximately e quivalent to the W126 of 21 ppm

22 h our, was 26 to 49 percent, while at the lower level approximately equivalent to a W126 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 340 of 13 ppm

- h our , incidence values ranged from 12 t o 35 percent
. The Administrator 1 believes it likely

that some sensitive species occurri ng in speciall y protected areas would 2 also exhibit visible foliar injury s ymptoms to a similar degree at these exposure levels

. 3 She further notes that while direct links between O 3 induced visible foliar injury 4 sy mptoms and other adverse effects (e.g., bi omass loss) are not always found, visible 5 foliar injury

in itself is considered by the National Park Service (NPS) to affect adversel y 6 air quality

related values (AQRV) in Class I areas

. 7 The Administrator places significant weight on the judgments of CASAC

. In so 8 doing, the Administrator has carefull y considered its stated views and the basis for the 9 range of levels the CASAC O 3 Panel recommended

. In its 2007 letter to the 10 Administrator, the CASAC O 3 Panel agreed with EPA s taff recommendations that the 11 lo wer bound of the range within which a seasonal W126 O 3 standard should be 12 considered is approximately 7 ppm
- hour. H owever, “ it does not agree with Staff’s 13 recommendations that the upper bound of the range should be as high as 21 ppm

- hour. 14 Rather, the Pane l recommends that the upper bound of the range considered should be no 15 higher than 15 ppm

- hour, which the Panel estimates is approximately equivalent to a 16 seasonal 12

- hour SUM06 level of 20 ppm

- hour” (Henderson, 2007). The Administrator 17 notes that CASAC views concerning an appropriate range of levels for the Administrator 18 to consider were presented after CASAC had considered the entire body of evidence 19 presented in both the 2006 Criteria Document and 2007 Staff Paper, and are generall y 20 consistent with the 1996 Consensus Workshop recommendations. 21 In considering the issues raised b y commenters on the 2007 proposed rule, the 22 Administrator noted that many public commenters supported the range of levels 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 341 recommended b y CASAC. The Administrator also considered the views expressed by 1 the NPS as to what range of levels it identified as useful in helping it achieve its mandate 2 to protect AQRVs in national parks and wilderness areas and to provide a level of 3 protection for its resources in keeping with the Congressio nal mandate set forth in The 4 Wilderness Act of 1964. In so doing, the Administrator notes that the NPS supported the 5 range recommended b y CASAC, while emphasizing that the lower end of the range was 6 more appropriate. The NPS notes that though some visibl e foliar injury would still be 7 expected to occur above the lower end of the CASAC recommended range (i.e. 7 ppm

8 hour), the potential for growth impacts at that level would be very low. It further notes 9 that most of these parks contain aspen, black cherry , or ponderosa pine, all sensitive 10 species predicted to have significant growth effects at current W126 levels. 11 The Administrator also considered those comments that highlighted sources of 12 uncertainty in the evidence and risk assessments (summarized above in section 13 IV .D.5.c.ii) to inform her judgments on how much weight to place on these associated 14 uncertainties, as discussed below. 15 With regard to the issue of possible confounders of foliar injury information, the 16 Administrator recognizes that visible foliar injury , like other O 3 - induced plant effects, is 17 moderated b y environmental factors other than O 3 exposure. However, the Administrator 18 also notes that the O 3 - related visible foliar injury effect persisted across a four year period 19 (2001

- 2004), despite ye ar- to - year variability in meteorology and other environmental 20 factors (see Table 7

- 4 in the 2007 Staff Paper). She also notes that approximately 26 to 21 49 percent of counties had visible foliar injury incidence at the approximate W126 level 22 of 21 ppm

- hour , while at a W126 level of 13 ppm

- hour, this range of percentages 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 342 dropped to approximately 12 to 23 percent. In an area such as a national park, where 1 visitors come in part for the aesthetic quality of the landscape, the Administrator 2 recognizes that visible foliar injury incidence is an important welfare effect which should 3 be considered in determining an appropriately protective standard level. 4 With regard to the issues of what weight to place on the recommendations from 5 the 1996 Consensus Workshop in selecting a range of levels, as the 1997 Workshop 6 Report did not clearl y document the basis for its recommendations, the Administrator 7 recognizes that the absence of such documentation does call for care in placing weight on 8 such recommendations. However, the Administrator notes that the workshop participants 9 were asked to review both the 1996 O 3 Criteria Document and Staff Paper, representing 10 the most up to date compilation of the state of the science available at that time, in order 11 to ensure that their expert judgments made were also informed by the latest science. She 12 also notes that another group of experts, the CASAC O 3 Panel, reached a similar 13 consensus based upon an expanded body of scientific evidence. In addition, the 2007 14 Staff Paper evaluated the same recommendations in the context of subsequent empirical 15 evidence, and reached similar views, with the exception of the upper end of the 16 recommended range, which in the 2007 Staff Paper was based on effects on commercial 17 crops that had been considered in the 1997 review. While it would alway s be more 18 useful to have documentation of the reasoning and basis for an expert’s advice, in this 19 case the Administrator judges that the 1996 Consensus Workshop recommendations 20 should be given substantial weight. 21 With regard to other issues raised b y some commenters related to uncertainties in 22 the technical evidence and anal ys es, the Administrator notes that such issues had been 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 343 addressed in the 2007 Staff Paper that reflected CASAC’s advice on such issues. For 1
e xample, while the Administrator recognizes that uncertainty remains as to what level of 2 annual tree seedling biomass loss when compounded over multiple years should be 3 judged adverse to the public welfare, she believes that the potential for such anticipat ed 4 effects should be considered in judging to what degree a standard should be 5 precautionary

. 6 In considering all of the issues discussed above, the Administrator has decided to 7 propose a range of 7

- 15 ppm
- hour. In selecting as an upper bound a level of 1 5 ppm
8 hour, the Administrator notes that this level was specificall y supported b y the CASAC O 3 9 Panel and is just above the range identified in the 1996 Consensus Workshop report as 10 needed to provide adequate protection for trees growing in natural areas. In addition, the 11 NPS, along with many public commenters, were in support of the CASAC range, 12 including the upper bound of 15 ppm

- hour, and indicated that lower values within this 13 range would be more protective for sensitive trees in protected areas from b iomass loss 14 and visible foliar injury sy mptoms. 15 While the upper end of this range is lower than the upper end of 21 ppm

- hour 16 recommended in the 2007 Staff Paper, this upper level of 21 ppm

- hour was originall y put 17 forward in the 1997 review in terms of a SUM06 of 25 ppm

- hour (W126 of 21 ppm

- hour) 18 and was justified on the basis that it was predicted to allow up to 10% biomass loss 19 annually

in 50% of studied commercial crops and tree seedling species. Recognizing the 20 significant uncertainties that are assoc iated with evaluating effects on commercial crops 21 from a public welfare perspective, the Administrator now concludes that commercial crop 22 data are no longer useful for setting the upper level of the range for proposal. 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 344 With regard to her selection of a proposed range, the Administrator has 1 considered that the direction from Congress to provide a high degree of protection in 2 Class Iareas creates a clearer target for gauging what ty pes and magnitudes of effects 3 would be known or anticipated to affect the intended use of these and other similarly 4 protected areas, that would thus be considered adverse to the public welfare. Such 5 similar areas include lands set aside by States, Tribes and public interest groups to 6 provide similar benefits to the public welfare , for residents on those lands, as well as 7 visitors to those areas, The Administrator also believes that in order to preserve 8 wilderness areas in an unimpaired state for future generations, she must consider a level 9 that affords substantial protection fro m known adverse O 3 - related effects of biomass loss 10 and foliar injury

on sensitive tree species, as well as a level that takes into account 11 potential “anticipated” adverse O 3 - related effects , including effects that result in 12 continued impairment in the year following O 3 exposure (i.e., carry

- over effects) , below 13 ground impacts , ecos ys tem level impacts, and reduced CO 2 sequestration 14 While the Administrator acknowledges that growth effects and visible foliar 15 injury

can still occur in sensitive species at leve ls below the upper bound of the proposed 16 range, the Administrator also recognizes that some significant uncertainties remain 17 regarding the risk of these effects, as discussed above. For example, the Administrator 18 concludes that remaining uncertainties mak e it difficult to judge the point at which visible 19 foliar injury

becomes adverse to the public welfare in various ty pes of specially

protected 20 areas. Uncertainties associated with monitoring ambient exposures must be considered in 21 evaluating the strength of predictions regarding the degree of tree seedling growth 22 impairment estimated to occur at varying ambient exposures. These uncertainties add to 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 345 the challenge of judging which exposure levels are expected be associated with levels of 1 tree seedling growth effects considered adverse to public welfare The Administrator 2 believes that it is important to consider these uncertainties, and the weight to place on 3 such uncertainties, in selecting a range of standard levels to propose. Establishing 15 4 ppm - hour a s the upper end of the proposed range reflects her judgment regarding the 5 appropriate weight to place on these uncertainties in determining the degree of protection 6 that is warranted for known and anticipated adverse effects. 7 With regard to her selection o f a lower bound for the proposed range, the 8 Administrator believes that if weight is placed on taking a more precautionary approach, 9 recognizing that the real world impacts on trees and ecos ys tems could, in some cases, be 10 greater than predicted, then the l ower end of the range of 7 ppm

- hour could be warranted. 11 There is clear evidence that higher cumulative exposures can occur in rural areas 12 downwind of urban areas and potentially in Class I areas. Unmonitored high elevation 13 sites would also likely have higher cumulative exposures than lower elevation sites that 14 are currentl y monitored. All of these considerations lead the Administrator to propose 7 15 ppm - hour as the low end of the proposed range. 16 As discussed above in section IV.D.5.a, the main opposition to changing to a 17 secondary

standard with a cumulative, seasonal form has been the view that EPA does 18 not have an adequate basis to identify the kinds and ty

pes of cumulative, seasonal 19 exposure patterns that the standard should be designed to protect against, given the 20 various uncertainties in the evidence, and whether EPA has an adequate basis to 21 determine an appropriate level for a cumulative, seasonal secondary standard. While 22 EPA agreed with this position in the 1997 review , the Administrator believes that the 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 346 evidence before her appropriately supports a secondary

standard that is distinctly 1 different in form and averaging time from the 8

- hour primary standard , and that such a 2 standard is necessary to provide sufficient protection from cumulative, seasonal 3 exposures to O 3 . 4 While a different conclusion on this issue was reached in the 1997 review, the 5 current conclusion that an exposure index that is cumulative and seasonal in nature, and 6 therefore that setting a standard based on such a form is necessary and appropriate , is 7 based on information newly available in the 2008 rulemaking , which strengthens the 8 information available in the 1997 review and reduces remaining uncertainties

. 9 Such newly

available information includes quanti tative information for a broader 10 array

of vegetation effects (extending to sapling and mature tree growth stages ) obtained 11 using a more diverse set of field

- based research study designs and improved anal ytical 12 methods for assessing O 3 - related exposures and risks as discussed above in sections 13 IV .A
- C
. 14

. These new ly available studies also provide important support to the quantitative 15 estimates of impaired tree growth based on earlier studies available in the 1997 review 16 and address one of the key data gaps cited in the 1997 review. Additional qualitative 17 information is also available regarding improved understanding of linkages between 18 stress - related effects of O 3 exposures at the species level and those at higher levels within 19
ecos ys tems. Finall y, this information includes the us e of new anal ytical methods , 20 including a new multi

- pollutant, multi

- scale air quality model used to characterize 21 exposures of O 3 - sensitive tree and crop species further address uncertainties in the 22Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 347 assessments done in the 1997 review. In total, this newly available information increase s 1 the Administrator’s confidence in important aspects of this rulemaking 2 The decision in 2008 to set the secondary O 3 standard identical to the 8

- hour 3 primary

standard largel y mirrored the decision in 1997, but failed to account for this 4 significant increase in the body of knowledge available to support the 2008 rulemaking. 5 This body

of knowledge, while continuing to reflect significant uncertainties, provides an 6 appropriate basis for determining a level of a cumulative, seas onal standard that, in the 7 judgment of the Administrator, provides sufficient but not more than necessary protection 8 from cumulative, seasonal exposures to O 3 . This is clearl y so when compared to a 9 standard that uses an indirect form that is not biologically relevant, an 8

- hour average 10 standard aimed at peak daily exposures. This judgment is full y consistent with the advice 11 provided b y CASAC. 12 After carefully taking the above considerations into account, and giving 13 significant weight to the views of CA SAC, the Administrator has decided to propose a 14 range of level s of 7

- 15 ppm
- hour for a cumulative, seasonal secondary O 3 standard 15 expressed as an index of the annual sum of weighted hourly concentrations (i.e., the 16 W126 form), cumulated over 12 hours per day during the consecutive 3

- month period 17 within the O 3 season with the maximum index value, averaged over three years . In the 18 Administrator's judgment, based on the information available in the 2008 rulemaking , a 19 standard could be set within this range th at would be requisite to protect public welfare 20 from known or anticipated adverse effects to O 3 - sensitive vegetation and ecosy stems. In 21 the Administrator’s judgment, a standard set at a level below the lower end of the range is 22 not now supported by the we ight of evidence and would not give sufficient weight to the 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 348 important uncertainties and limitations inherent in the available scientific evidence and in 1 the quantitative assessments conducted for the 2008 rulemaking. A standard set at a level 2 above the u

pper end of the range is also not now supported by the weight of evidence and 3 would not give sufficient weight to the credible inferences that the Agency has drawn 4 from the scientific evidence nor to the quantitative assessments conducted for the 2008 5 rulemaking. The Administrator judges that the appropriate balance to be drawn, based on 6 the entire body of evidence and information available in the 2008 rulemaking, is a range 7 between 7 and 15 ppm

- hour. On balance, the Administrator believes that a standard 8 could be set within this range that would be sufficient but not more than necessary to 9 protect public welfare from known or anticipated adverse effects due to O 3 . 10 In reaching this proposed decision, as discussed above, the Admini strator has 11 focused on the nature of the benefits associated with setting a distinct secondary standard 12 with a cumulative , seasonal form relative to a standard with a peak dail y 8
- hour average 13 form , as well as on assessments that quantify the degree of protection likely to be 14 afforded by

such standards

. Inso doing, the Administrator has acknowledge d limitations 15 in quantifying the expected benefits asso ci ated with the proposed cumulative seasonal 16 standard relative to the secondary standard set in 2008. Having considered the public 17 comments received on the 2007 proposed rule in reaching this proposed decision, the 18 Administrator is interested in again receiving public comment on the benefits to public 19 welfare associated with the proposed cumulative seasonal standard set at specific l evels 20 within the proposed range relative to the standard set in 2008. 21 22 E

. Proposed Decision on the Secondary O 3 Standard 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 349 For the reasons discussed above, and taking into account information and 1 assessments presented in the 2006 Criteria Document and 2007 Staff Paper, the advice 2 and recommendations of CASAC, and the public comments received in conjunction with 3 the 2008 rulemaking , the Administrator has decided to propose to set a new cumulative, 4 seasonal secondary

O 3 standard with a form expressed as an ind ex of the annual sum of 5 weighted hourl y concentrations (i.e., the W126 form), cumulated over 12 hours per day 6 (8:00 am to 8:00 pm) during the consecutive 3

- month period within the O 3 season with 7 the maximum index value, averaged over three ye ars, set within a range of 7 to 15 ppm 8 hour. The Administrator solicits comment on the weight that is appropriately placed on 9 the various ty

pes of evidence and anal ys es upon which this proposed standard is based, 10 and on the appropriate weight to be placed on the uncertainties in this information, as 11 well as on the benefits to public welfare associated with the proposed standard relative to 12 the benefits associated with the standard set in 2008

. 13 Data handling conventio ns for the proposed new secondary O 3 standard are 14 specified in the proposed addition of a new section to 40 CFR 50 Appendix P, as 15 discussed in section V below. Is sues related to monitoring requirements for the proposed 16 new secondary

O 3 standard are discus sed below in section VI. 17 18 V. Interpretation of the NAAQS for O 3 and Proposed Revisions to the 19 Exceptional Events Rule 20 Appendix P to 40 CFR part 50 , Interpretation of the Primary and Secondary 21 National Ambient Air Quality Standards for Ozone , address es dat a completeness 22 requirements, data reporting, handling, and rounding conventions, and example 23 calculations

. The current Appendix P explain s the computations necessary for 24Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 350 determining when the current identical primary and secondary

standards are met. The 1 EP A is proposing to revise Appendix P to reflect the proposed revisions to the primary 2 and secondary O 3 NAAQS discussed above and to make other changes described below

. 3 As discussed below, the proposed revisions to Appendix P include the 4 following: the addition of data interpretation procedures applicable to the proposed 5 cumulative, seasonal secondary NAAQS (see section V.B); clarification of certain 6 language in the current provisions applicable to the primary NAAQS to reduce potential 7 confusion (section V .C); revisions to the provisions regarding the use of incomplete data 8 sets for purposes of the primary NAAQS and the data completeness requirements across 9 three ye ars (sections V.D and V.E); the addition of a provision providing the 10 Administrator discretio n to use incomplete data as if it were complete, for the purpose of 11 the primary

NAAQS (section V.F); a change from truncation to rounding of multi

- hour 12 and multi

- ye ar average O 3 concentrations for the purposes of the primary standard 13 (section V.G); and the addition of provisions addressing data to be used in making 14 comparisons to the NAAQS (section V.H). The proposed revisions also include changes 15 in organization for greater clarity and consistency with other data interpretation 16 appendices to 40 CFR part 5 0, which are not further described in this preamble. 17 The EPA is also proposing changes to the O 3 - specific deadlines, in 40 CFR 50.14, 18 by which s tates must flag ambient air data that they believe have been affected by 19 exceptional events and submit initial descriptions of those events, and the deadlines by 20 which s tates must submit detailed justifications to support the exclusion of that data from 21 EPA determinations of attainment or nonattainment with the NAAQS. The O 3 - specific 22Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 351 deadlines in the current 40 CF R 50.14 would not be appropriate given the anticipated 1 schedule for the designations of areas under the proposed revised O 3 NAAQS. 2 A. Background 3 The purpose of a data interpretation appendix in general is to provide the practical 4 details on how to make a comparison between multi

- day and possibly

multi

- monitor 5 ambient air concentration data and the level of the NAAQS, so that determinations of 6 compliance and violation are as objective as possible. Data interpretation guidelines also 7 provide criteria for determining whether there are sufficient data to make a NAAQS level 8 comparison at all. Appendix P was promulgated in March 2008 along with the most 9 recent revisions to the primary and secondary

O 3 NAAQS. It is very

similar to Appendix 10 I, Interpretation of the 8

- Hour Primary and Secondary

National Ambient Air Quality 11 Standards for Ozone , which was adopted in 1997 when the O 3 NAAQS were first revised 12 to have an 8

- hour averaging period rather than the earlier 1

- hour averaging period, along 13 with other changes in form and level. The onl y substantive difference between Appendix 14 I and the current version of Appendix P is that Appendix P contains truncation 15 procedures consistent with the additional decimal digit used to express the level of the 16 2008 NAAQS in parts per million (0.075 ppm) compared to the 1997 NAAQS (0.08 17 ppm). In July

2007, EPA had also proposed to include in Appendix P data interpretation 18 procedures for the proposed cumulative, seasonal secondary O 3 NAAQS, but these 19 procedures were not finalized given that the final secondary NAAQS was identical in all 20 respects to the final primary NAAQS. 21 An exceptional event is defined in 40 CFR 50.1 as an event that affects air 22 quality , is not reasonably controllable or preventable, is an event caused b y human 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 352 ac tivity that is unlikely

to recur at a particular location or a natural event, and is 1 determined b y the Administrator in accordance with 40 CFR 50.14 to be an exceptional 2 event. Air quality data that are determined to have been affected by an exceptional event 3 under the procedural steps and substantive criteria specified in section 50.14 may be 4 excluded from consideration when EPA makes a determination that an area is meeting or 5 violating the associated NAAQS. The key procedural deadlin es in section 50.14 are that 6
a s tate must notify

EPA that data have been affected by an event, i.e., “flag” the data in 7 the Air Quality

S ys tems (AQS) database, and provide an initial description of the event 8 by July 1 of the ye ar after the data are collected, and that the State must submit the full 9 justification for exclusion within 3 years after the quarter in which the data were 10 collected. However, if a regulatory decision based on the data, for example a designation 11 action, is anticipated, the schedule is shortened and all information must be submitted to 12 EPA no later than a ye ar before the decision is to be made. This generic schedule 13 presents problems when a NAAQS has been recently revised, as discussed in section V.I 14 below

. On May

15, 2009, EPA finalized a set of O 3 - sp ecific deadlines that corrected 15 these problems at the time with respect to the 2008 NAAQS revisions (74 FR 23307). 16 However, because of the anticipated effect of the current reconsideration on the schedule 17 for O 3 designations, the schedule problems will re surface unless the deadlines are 18 adjusted again. 19 B. Interpretation of the Secondary O 3 Standard 20 The EPA is proposing data interpretation procedures for the proposed secondary 21 O 3 NAAQS , which is defined in terms of a specific cumulative, seasonal fo rm, 22
commonly

referred to as the W126 form, as described above in section IV . The proposed 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 353 new section 4 of Appendix P on data interpretation for the secondary standard contains 1 the following main features. 2 The “design value” for the secondary standard, the statistic for a monitoring site 3 which would be compared to the level of the secondary standard to determine if the site 4 meets the standard, would be the average of the annual maximum values of the three

5 month index value from three calendar ye ars. 6 The new s ection would provide clear directions and examples for the calculation 7 of the daily

index value, the monthly cumulative index value, the annual maximum index 8 value for a year, and the design value itself. 9 Only

the data from the required O 3 monitoring seas on would be examined to 10 determine the annual maximum index value; any additional period of monitoring 11 undertaken voluntarily by a state would not be considered. The EPA believes that 12 because of the recentl y proposed extension of the required monitoring se asons in many 13 states (74 FR 34525, July 16, 2009), as discussed below in section VI, such a period of 14 voluntary

monitoring would be unlikely to have such high index values as to affect the 15 annual maximum index value. Moreover, the proposed required monito ring season may 16 encompass the most active growing season in many areas. The EPA invites comment on 17 whether instead the entire actual O 3 monitoring period should be considered, to eliminate 18 any possibility

that the highest cumulative index value that can b e determined with 19 available data might be missed. 20 For each month in a three

- month period, O 3 data would have to be available for at 21 least 75 percent of daylight hours (defined for this purpose as 8:00 a.m.

– 7:59 p.m. L ST ). 22 If data are available for at l east 75 percent but fewer than 100 percent of these daylight 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 354 hours in a month, the cumulative index value calculated from the available daylight hours 1 in the month would be increased to compensate for the missing hours, based on an 2 assumption that the miss ing hours would have the same distribution of O 3 concentrations 3 as the available hours. A substitution test is also proposed, b y which months in which 4 fewer than 75 percent of daylight hours have O 3 concentration data might also be useable 5 for calculating a valid cumulative index value. Such months would be used if the 6 available O 3 concentrations are so high that even substituting low concentration values 7 for enough missing data to meet the 75 percent requirement would result in a design 8 value greater than the level of the standard . The low value that would be substituted 9 would be the lowest 1

- hour O 3 concentration observed at the monitoring site during 10 daylight hours during the required O 3 monitoring season, in that calendar ye ar , or one 11 half the method detection limit (MDL) of the ozone instrument, whichever is higher. 63 12 The EPA notes that while this proposed approach to identifying the substitution 13 value for the secondary standard is technically

appropriate, it would necessitate data 14 processing effort s during implementation that might be avoidable via some other 15 approach that is also technically reasonable. We therefore invite comment on such 16 alternative approaches, and we may adopt another approach in the final rule. For 17 example, for simplicity the substituted 1

- hour O 3 concentration value could instead 18

63 Because onl y 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 O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 355 simply alway s be zero or one

- half the MDL of the O 3 instrument, noting that because of 1 the sigmoidal weighting factor the exact magnitude of the low substitution value may 2 ty picall y make very little difference to the annual index value. Also, using the previous 3 calendar year as the source of the substitution value instead of the current calendar year 4 would have the advantage of allowing all parties to know earl y in each ye ar what the 5 substitution valu e will be. 6 The EPA is proposing that all decimal digits be retained in intermediate steps of 7 the calculation of the cumulative index, with the result rounded to have no decimal digits 8 when expressed in ppm

- hours before comparison the level of the secondary NAAQS. 9 EPA expects that the three months over which the cumulative weighted index 10 value is highest will generally occur in the middle of each ye ar. Therefore, the proposed 11 new section 4 of Appendix P presumes this, and does not address a situation in which the 12 three months of maximum cumulative index spans two calendar years, for example 13 December to February . The EPA invites comment on whether a provision addressing 14 such a remote possibility is needed and what its terms should be. For example, the 15 pro cess of checking each three month period in a calendar year to determine which gives 16 the highest index value could include the combinations of December/January /February 17 and November/December/January within one calendar year. 18 C. Clarifications Related to th e Primary Standard 19 The EPA is proposing two clarifying changes to Appendix P to make 20 unambiguous two aspects of data interpretation for the primary 8
- hour standard. The first 21 change clarifies that the standard data completeness requirement that valid dai ly 22 maximum 8

- hour values exist for 75 percent of all days refers to days within the required 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 356 O 3 monitoring season only. The current wording of Appendix P is somewhat open to a 1 reading that the requirement applies to all day s in the actual monitoring record for the site 2 in question, which could be longer than the required season if a state voluntarily monitors 3 on additional day s, or shorter than the required season if a monitor has started or ceased 4 operation sometime during the required season. The O 3 dat a completeness requirement is 5 intended to avoid a determination that an area has met the NAAQS when in fact more 6 than a reasonable number of day s with high O 3 potential were not successfully monitored. 7 This purpose can be served if the data within the req uired O 3 monitoring season only are 8 reasonabl y complete, because as mentioned above EPA has proposed to revise the 9 required O 3 seasons so that they encompass all day s with potential for an exceedance of 10 even the lowest proposed level for the primary standard. Unsuccessful monitoring 11 outside the required season should not be an obstacle to a finding of attainment. 12 However, if an O 3 monitor has missed more than 25 percent of the required O 3 13 monitoring season, for example because it started or stopped operation mid

- season, this 14 should prevent a finding of attainment based on a three

- ye ar period that includes that 15
season. The proposed clarifying language reflects EPA’s actual intention and our past 16 practice in applying Appendix P for regulatory purposes , and Appendix Ias well. 64 17 The second proposed clarifying change would make it clear that when 18 determining the fourth

- highest dail y maximum 8

- hour O 3 concentration for a year, all 19

64 At present, EPA’s Air Quality Sy stem (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 onl y over the required ozone monitoring season.Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 357 day s with monitoring data are to be considered, not just day s within the required O 3 1 monitoring season. This proposed clarifying language also reflects EPA’s actual 2 intention and our past practice in appl yi ng Appendix P, and Appendix Ias well. While 3 EPA believes it to be quite unlikely that an exceedance will occur outside the proposed 4 revised required O 3 monitoring seasons and have a high enough concentration to affect 5 the selection of the fourth

- highest concentration for the year, when and if such an 6 occurrence does happen, the data should not be ignored. 7 D. Revision to Exceptions from Standard Data Completeness Requirements for the 8 Primary Standard 9 The EPA is proposing to revise portions of Appendix P that describe certain 10 exceptions to the standard data completeness requirements, under which a monitoring site 11 can in some cases be determined to be meeting or violating the primary NAAQS despite 12 not meeting the standard data completeness requirements. These changes would make 13 Appendix P more logical in certain types of cases with incomplete data. While the 14 particular types of cas es whose outcome would be different with these changes have been 15 rare historically , there may be more such affected cases in the future in conjunction with 16 a primary

O 3 standard revised to a level within the range of levels proposed in this action. 17 The st andard data completeness requirements in Appendix P for the primary O 3 18 NAAQS appl y a 75 percent requirement at each of three stages of data completeness 19 testing. As discussed below, for each stage, there is an existing exception to the 75 20 percent requirem ent. 21 In the first stage, an 8

- hour period can be considered to have a valid 8

- hour 22 average O 3 concentration only if at least 75 percent of the hours, i.e., 6 or more hours, 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 358 have a valid hourly

O 3 value. The provided exception is that if there are 5 or fewer hours 1 but if substituting a very low value (specificall y, one - half the MDL of the O 3 instrument) 2 for all the missing hours results in a hy pothetical 8

- hour average that is above the level of 3 the primary

standard, the 8

- hour period is considered valid and is assigned the 4 hy pothetical level resulting from the data substitution. 65 For example, if the O 3 5 concentration was 0.125 ppm for 5 hours, substituting a typical MDL/2 value of 0.0025 6 ppm for three missing hours would result in an 8

- hour average of 0.07 9 ppm, which is an 7 exceedance of the current primary standard, so the valid 8

- hour average for the period 8 would be taken to be 0.079 ppm. I f this value is higher than one or more of the highest 9 four dail y maximum 8

- hour concentrations otherwise calculated for the ye ar, considering 10 it to be valid affects the value identified as the fourth

- highest for the ye ar and thus also 11 affects the final design value. The logical problem with this approach is that it is possible 12 for a hypothetical 8

- hour average with su ch substitution to be below the level of the 13 NAAQS, thus not meeting the current condition for the exception, but for it to still make 14 a critical difference in making the three

- year design value be above the level of the 15 NAAQS, because a three

- ye ar design value can include (and be sensitive to the exact 16 value of) an annual fourth

- highest daily maximum that is not above the level of the 17 NAAQS. This could be the case if the hypothetical 8

- hour average with substitution is 18 the maximum concentration 8

- hour period for its day , and the day is one of the highest 19 four O 3 days of the year. Whether it actually is the case would further depend on the 20

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 O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 359 value of the 8

- hour average itself, the values of the next highest daily maximum 8

- hour 1 average concentration in the year, and the values of the annual fourth

- highest daily 2 maximum 8

- hour concentration from the other two years. If the substituted 8

- hour 3 average would make a critical difference, it should be treated as valid and used in the 4 calculation of the three

- year d esign value, even if it is not itself above the level of the 5 standard. Another problem is that one

- half of the MDL , which ty picall y is about 0.0025 6 ppm, is very

likel y to be considerabl y lower than the actual O 3 concentrations that were 7 not successfull y m easured. Thus, while the one

- half

- MDL
- substituted value is prevented 8 from being an overestimate of the actual 8

- hour average concentration, it is an 9 unreasonabl y low estimate of that concentration which may have the effect of allowing a 10 site with actual O 3 levels above the standard to be found to meet the standard. The 11 condition in the exception requiring a one

- half

- MDL
- substituted “8

- hour” average to be 12 above the level of the NAAQS is therefore inappropriate. 13 In the second stage of data completeness tes ting, 75 percent of the 24 possible 8

- 14 hour time blocks, which is 18 or more, must have valid 8

- hour average concentrations 15 values. The intent of this requirement is to make sure that most of the day was actuall y 16 monitored, such that the highest concentration 8

- hour period was likel y to be captured in 17 the data. When this is not the case, the day is not considered in selecting the annual 18 fourth

- highest dail y maximum 8

- hour concentration and no credit for the day’s 19 monitoring is given towards the third stage of data interpretation (see below). The 20 provided exception in the current Appendix P is that a day is considered valid if at least 21 one 8
- hour period has an average concentration above the level of the standard. 22 However, as in the first stage, it is poss ible for an 8

- hour period with an average 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 360 concentration at or below the level of the NAAQS to play a critical role in whether the 1 three

- ye ar design value meets the standard. Invalidating the day could have the effect of 2 causing a lower value to be selecte d as the annual fourth

- highest dail y maximum 8

- hour 3 concentration, leading to a three

- year design value that does not exceed the NAAQS 4 while it would have exceeded if the day and the 8

- hour average value had been treated as 5 valid. The condition in the exc eption requiring at least one 8

- hour average during the day 6 to be above the level of the NAAQS is therefore inappropriate. 7 In the third stage of data completeness testing, a completeness criterion is applied 8 for the number of day s in the required O 3 seaso n that have a valid maximum 8

- hour 9 average, i.e., day s that have met the completeness conditions in the first two stages or 10 have met the condition for an exception. Specifically , for each of the three years being 11 used in the design value calculation, the number of valid day s within the required O 3 12 monitoring season (with no credit for extra days outside the season) must be at least 75 13 percent of the day s in the required O 3 season, and the number of valid day s across all 14 three ye ars must be 90 percent of th e day s in the three seasons. 66 The provided exception 15 to the 75/90 percent requirement is that data from a year with less than 75 percent of 16 seasonal day s can nevertheless be used if during the year at least one day ’s maximum 8

- 17 hour average O 3 concentratio n was above the level of the standard and if the three

- ye ar 18

66 EPA also is proposing eliminate this 90 percent requirement, see section V.E. The point made in this paragraph applies with o r without the 90 percent requirement in place.Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 361 design value is also above the standard. 67 The problem with this exception, similar to the 1 problems with the exceptions in the first and second stages of data completeness testing, 2 is that a daily maximum 8

- hour concentration that is at or below the level of the NAAQS 3 can nevertheless make a critical difference in making the three

- ye ar design value be 4 above the level of the NAAQS. When it does, an incorrect final result will be reached if 5 the year of data is not granted an exception to the 75/90 percent requirement. 6 Specificall y, there would be no valid three

- year design value and no conclusion would be 7 reached as to attainment or nonattainment, despite it being clear that the actual situation 8 is nonattainment, in the sense that successful collection of additional hours and days of 9 monitoring data could not possibly have resulted in a passing three

- year design value. 10 Moreover, since the three

- ye ar design value is the average of the fourth

- highest daily 11 maximum 8

- hour concentration from each year, there is no logical connection between 12 the design value and the existence of a single daily maximum concentration greater than 13 the level of the standard, which is the current condition for the exception fo r this stage of 14 testing for data incompleteness. 15 EPA proposes to remedy this situation by replacing the three separate statements 16 of the exceptions to the three standard completeness requirements with a new data 17 substitution step that addresses the root c ause of the data incompleteness situation: 18 missing hourly

concentrations which make it doubtful whether actual maximum daily 8
- 19 hour concentrations were measured on a reasonably large percentage of the days during 20

67 EPA notes that in the current versions of Appendix Iand P, it is not explicit that this provided exception also applies in the case of three ye ars which each have 75 percent or more of day s 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 O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 362 the required O 3 monitoring season of each ye ar. In the event that onl y 1, 2, 3, 4, or 5 1 hourly

averages are available for an 8

- hour period , a partiall y substituted 8
- hour average 2 would be computed by substituting for all the hours without hourly averages a low hourl y 3 average value selected as fol lows, and then us ing 8 as the divisor. 68 For days within the 4 required O 3 monitoring season, the substitution value would be the lowest hourly average 5 O 3 concentration observed for that hour of the day (local standard time) on any day 6 during the required O 3 monitoring season of that year , or one - half the MDL, whichever is 7 higher . Using this value makes it highl y unlikely that the resulting partiall y substituted 8

- 8 hour average concentration is higher than the actual concentration. Therefore, using the 9 parti ally

substituted 8

- hour average in the design value calculation procedure is highl y 10 unlikely

to result in an incorrect finding that a site does not meet the standard, but it may 11 lead to a correct finding that a site does not meet the standard in some cases in which 12 there would be no finding possible or an incorrect finding under the current version of 13 Appendix P. However, the use of the higher of the lowest observed same - hour 14 concentration or one - half the MDLcould be problematic if a robust set of hourly 15 measurements is not available for the ye ar, for example if a monitor began operation late 16 in an ozone season. In such a case, the lowest observed same - hour concentration might 17 not be low enough to eliminate all possibility that the value used for substitution is higher 18 than the missing concentration value. To reduce this likelihood to essentially zero, we 19 are proposing that if the number of same - hour concentration values available for the 20 required O 3 monitoring season for the ye ar is less than 50 percent of the number of day s 21

68 Appendix P now provides that in the event that only 6 or 7 hourl y 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 O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 363 during the required O 3 monitoring season, one

- half the MDL of the O 3 instrument would 1 be used in the substitution instead of the lowest observed concentration. We invite 2 comment on whether another percentage should be used for this purpose instead of 50 3 percent
. 4 The EPA notes that while this proposed approach to identifying the substitution 5 value for the primary standard is technically

appropriate, it would necessitate new data 6 processing efforts during implementation that might be avoidable via some other 7 approach that is also technically reasonable. There may

also be approaches which are 8 more technically

appropriate. We therefore invite comment on such alternative 9 approaches, and we may adopt another approach in the final rule. Examples of simpler 10 approaches would be to identify in the final rule a fixed substitution value other than one

11 half the MDL, to accept as valid 8

- hour periods with only five measured hourly 12 concentrations, to interpret between two hourly concentrations to obtain a substitute for a 13 single missing hourl y concentration, or to use the previous calendar ye ar as the source of 14 the substitution value instead of the current calendar year (thereb y allowing all parties to 15 know earl y in each ye ar what the substitution value will be). Examples of more complex 16 approaches that might be more technically appropriate include selecting a low percentile 17 of the available same

- hour concentration data rather than the lowest value to be the 18 substitution value, or selecting the low est same - hour value from the same calendar 19 quarter or month (of the current ye ar or the most recent year) rather than from the entire 20 required ozone monitoring season. We also invite comment on whether the proposed 21 approach to substitution should be used at all and if not what other approach should be 22 used to address the potential problem just described. 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 364 We propose that for simplicity and to further reduce any risk of a false finding 1 that a site does not meet the standard, for days outside the required O 3 monitoring season, 2 the substitution value would alway s be one - half the MDL of the O 3 instrument . We 3 similarly

invite comment on this aspect. 4 There would be no condition that a partially substituted 8

- hour average exceed the 5 level of the standard for i t be used in calculating the design value, unlike is now the case. 6 An 8
- hour period with no available hourl y averages at all would not have a valid 8

- hour 7 average , as is now the case

. 8 In addition, to complete the solution to the problems described above, we are 9 proposing that a design value that is greater than the level of the primary standard would 10 be valid provided that in each ye ar there were at least four day s with at least one valid 8

- 11 hour concentration. 69 One or more of these 8

- hour average concentrations could be the 12 partially

substituted 8

- hour average concentration resulting from the above described 13 substitution procedure. In such a case, there is essentially no possibility

that more 14 complete monitoring data would have shown the site to be meeting the NAAQS. It is 15 appropriate to include all 8

- hour averages including those involving substitution when 16 testing for an exceedance of the standard, because those averages are extremely unlike to 17 be overestimates of actual concentrations. 18

69 The requirement that there be at least four days with at least one hourl y measurement is actual ly

redundant and is state d only for ease of understanding, since there would be no annual fourth

- highest dail y 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 O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 365 Finally , a des ign value equal to or less than the level of the standard would be 1 valid only

if at least 75 percent of the days in the required O 3 monitoring season of each 2 ye ar have dail y maximum 8

- hour concentrations that are based on at least 18 periods with 3 at least 6 hourl y concentrations. This ensures that a site will be found to meet the 4 standard onl y when a reasonably high percentage of the day s in the required O 3 5 monitoring season have reasonabl y complete hourly data. In this situation, it would be 6 inappropriat e to count the 8

- hour periods with five or fewer actual hourl y measurement 7 values towards the 75 percent requirement when testing for whether a site meets the 8 standard, because those 8
- hour averages will be based on substitution of low values and 9 therefore will be underestimates of actual concentrations. The only way to be reasonabl y 10 certain that no 8

- hour period had a high enough concentration so as to contribute to a 11 design value over the level of the standard is to have at least 18 periods in which 12 subs titution for missing O 3 values was not needed. This provision has the same effect as 13 several elements of the current Appendix P considered together, and thus is not a 14 substantive change. 15 E. Elimination of the Requirement for 90 Percent Completeness of Dai ly Data 16 across Three Years 17 As stat ed above in section VI.D, Appendix P currently requires that in order for a 18 design value equal to or less than the standard to be valid, at least 75 percent of days in 19 each of three ye ars must have a valid daily maximum 8

- hour average concentration value, 20 i.e., that many

day s must have at least 18 8

- hour periods with at least 6 reported hourl y 21 concentrations each. Appendix P also requires that the average of the percentages from 22 three consecutive ye ars be at least 90 perc ent. The EPA is proposing to eliminate this 90 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 366 percent requirement for the average of three ye ars and to retain onl y the requirement that 1 each individual ye ar have a percentage of at least 75 percent. 2 The 90 percent requirement was incorporated into Appendix I(the data 3 interpretation appendix for the 0.08 ppm O 3 NAAQS) in 1997 with an explanation that 4 EPA had observed that 90 percent of O 3 monitoring sites routinel y achieved 90 percent 5 data capture. The EPA now notes, however, that while the majority of monitoring sites 6 do achieve 90 percent or better data capture in any given ye ar, there are exceptions every 7 ye ar. The 90 percent requirement applied to the average percentage over three years is 8 quite unforgiving if there has been one ye ar with relativel y low data completeness. For 9 example, if one year just met the 75 percent requirement, the remaining two years would 10 have to achieve a 97.5 percent data capture rate in order for the three years to meet the 90 11 percent requirement. This would allow only 4 missed hours of measurements per week, 12 which would be challenging. The consequences for states could be important, under the 13 current requirement. One possible result could be that an area actually in nonattainment 14 with the NAAQS might have to be designated unclassifiable, although the substitution 15 procedure proposed for cases of incomplete data, as described above in section VI .D, 16 provides a path to an appropriate nonattainment finding in at least some cases. Another 17 possible result is that a nonattainm ent area which had actuall y come into attainment could 18 be unable to receive an attainment determination until three more ye ars of sufficientl y 19 complete data are collected. This might, for example, result in an area which has 20 achieved needed emissions reductions by its attainment deadline nevertheless being 21 bumped up to a higher classification. 22Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 367 The 90 percent requirement over three ye ars has the potential to treat two areas 1 disparatel y, for no obvious logical reason. Consider two areas with identical air quality. 2 Suppose the first area has annual completeness percentages of 75, 95, and 95 percent 3 (averaging to 85 percent and thus failing the 90 percent requirement) and the second area 4 has annual completeness percentages of 75, 98, and 98 percent (averagin g to 90 percent). 5 Suppose that the three

- ye ar design values in both areas are below the level of the 6 NAAQS. Practically speaking, the most important uncertainty about whether each area 7 actuall y meets the NAAQS is the low data capture rate in the first ye ar. There is no 8 obvious logic why the fact that the second area achieves marginall y better data capture in 9 the second and third ye ar should permit it to receive an attainment finding despite this 10 uncertainty, while the first area may not. 11 The EPA also no tes that for the other gaseous criteria pollutants

– sulfur dioxide, 12 carbon monoxide and nitrogen dioxide

– the completeness requirement is for 75 percent 13 completeness of hourl y measurements in an individual year. 70 14 For these reasons, EPA proposes to eliminate the 90 percent requirement across 15 three ye ars of data but to retain the 75 percent requirement for individual ye ars. The EPA 16 notes that as a practical matter, the current 90 percent requirement in effect requires a 17 minimum data capture rate somewhat above 75 percent in each year, because if data 18 capture in any one ye ar were as low as 75 percent the required data capture in the other 19 ye ars would be very hard to achieve. The minimum annual data capture rate is 20

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 ye ars.Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 368 effectivel y somewhere in the range of 80 p ercent (implying a requirement to achieve 95 1 percent data capture in the two remaining ye ars in order to meet the 90 percent 2 requirement across three years) and 85 percent (implying a requirement to achieve 92.5 3 percent data capture in the two remaining ye ars). The EPA invites comment on whether 4 instead of retaining the 75 percent completeness requirement in each individual year, the 5 requirement should be 80 percent or 85 percent. 6 F

. Administrator Discretion to Use Incomplete Data 7 The EPA is proposing that the Administrator have general discretion to use 8 incomplete data to calculate design values that would be treated as valid for comparison 9 to the NAAQS despite the incompleteness, either at the request of a state or at her own 10 initiative

. Similar provisi ons exi st already for the PM 2.5 and lead NAAQS, and EPA has 11 recentl y proposed such provisions to accompany the proposed 1

- hour NO 2 and SO 2 12 primary

NAAQS. The Administrator would consider monitoring site closures/moves, 13 monitoring diligence, and nearb y con centrations in determining whether to use such data. 14 G. Truncation versus Rounding 15 Almost all State agencies now report hourl y O 3 concentrations in parts per 16 million to three decimal places, since the ty pical incremental sensitivity of currentl y used 17 O 3 monitors is 0.001 ppm. Inthe current Appendix P approach, in calculating 8

- hour 18 average O 3 concentrations from such hourl y data any calculated digits past the third 19 decimal place are truncated rather than retained or rounded back to three decimal places

. 20 Also, in calculating 3

- ye ar averages of the fourth

- highest dail y maximum 8

- hour average 21 concentrations, Appendix P currently requires the result to be reported to the third 22 decimal place with digits to the right of the third decimal place truncated. In this regard, 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 369 Appendix P follows the precedent of Appendix I , except that Appendix P is based on a 1 NAAQS level specified to three decimal places (0.075 ppm) while Appendix Iaddressed 2 the case of a NAAQS level specified to onl y two decimal places (0.08 ppm). In the 3 rulemaking that concluded in 2008 by establishing the 0.075 ppm level, EPA noted that 4 the 2007 Staff Paper demonstrated that taking into account th e precision and bias in 1

- 5 hour O 3 measurements , the 8

- hour design value had an uncertainty of appr oximately 6 0.001 ppm. Thus, EPA considered any value less than 0.001 ppm to be highly un certain 7 and, therefore, proposed and adopted truncation to the third decimal place for reporting 1

- 8 hour O 3 concentrations and for both the individual 8

- hour averages us ed to determine the 9 annual fourth max imum and the 3

- ye ar average of the fourth maxima. 10 The effect of this repeated truncation is that there is a consistent downward bias in 11 the calculation of the three

- year design value. The size of this bias can be nota ble. For 12 example, seven hours with O 3 concentrations of 0.076 ppm plus one hour of 0.075 ppm 13 results in an 8

- hour average of 0.075 ppm after truncation, nearl y a full 0.001 ppm below 14 the actual 8

- hour average of 0.075875 ppm. Seven hours with O 3 concentr ations of 0.077 15 ppm plus one hour of 0.076 ppm results in an 8

- hour average of 0.076 ppm after 16 truncation. One ye ar with the first pattern plus two years with the second pattern would 17 give a three

- ye ar design value of 0.075 ppm, meeting the NAAQS, even th ough 23 of the 18 24 individual 1

- hour concentrations involved in the calculation of the design value were 19 above 0.075 ppm. 20 The EPA has decided to reconsider this aspect of O 3 data interpretation. 21 Specificall y, we are proposing that (1) 1

- hour concentration s continue to be reported to 22 only

three decimal places, the same as is now specified in Appendix P, i.e., that the 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 370 current practice of truncation of the 1

- hour data to the nearest 0.001 ppm be retained; (2) 1 all digits resulting from the calculation of 8

- ho ur averages be retained; and (3) the three

2 ye ar average of annual fourth

- highest daily maximum 8

- hour concentrations be rounded 3 to three decimal places before comparison to the NAAQS. The EPA continues to believe 4 that given the uncertainty in individual 1

- hour O 3 concentration measurements it is 5 appropriate to truncate those measurements at three decimal places (many O 3 instruments 6 are programmed to onl y report three digits anyw ay). However, the calculations of 8

- hour 7 averages and three

- ye ar averages are mathematical steps, not a measurement process 8 subject to uncertainties, and EPA perceives no logic in having a consistent downward 9 bias by

truncating the results of these mathematical steps. The EPA notes that the O 3 10 NAAQS is the only NAAQS for which multi

- hour, multi

- day , or multi

- ye ar averages of 11 concentrations are truncated rather than rounded. The proposed change will make this 12 aspect of O 3 data interpretation consistent with data interpretation procedures for the 13 other criteria pollutants. 14 H Data Se lection 15 The current version of Appendix P does not explicitly address the issue of what 16 ambient monitoring data for O 3 can and must be compared to the O 3 NAAQS. The EPA 17 proposes to add to Appendix P language addressing this issue. This language is simil ar to 18 provisions recentl y proposed to be included in new data interpretation appendices for 19 nitrogen dioxide and sulfur dioxide. The new section of Appendix P would clarify that 20 all quality

assured data collected with approved monitoring methods and known to EPA 21 shall be compared to the NAAQS, even if not submitted to EPA’s Air Quality Sy stem. 22 The section also addresses the question of what O 3 data should be used when two or more 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 371 O 3 monitors have been operating and have reported data for the same period at one 1 monitoring site. 2 I

. Exceptional Events Information Submission Schedule 3 States are responsible for identifying air quality data that they

believe warrant 4 special consideration, including data affected b y exceptional events. States identify such 5 data b y flagging (making a notation in a designated field in the electronic data record) 6 specific values in the Air Quality S ys tem (AQS) database. States must flag the data and 7 submit a justification that the data are affected b y exceptional events if they wish EPA to 8 consider excluding the data in determining whether or not an area is attaining the new O 3 9 NAAQS. 10 All states that include areas that could exceed the O 3 NAAQS and could therefore 11 be designated as nonattainment for the O 3 NAAQS have the potential to be affected by 12 this rulemaking. Therefore, this action applies to all states; to local air quality agencies to 13 which a state has delegated relevant responsibilities for air quality management including 14 air quality

monitoring and data anal ys is; and to Tribal air quality agencies where 15 appropriate. The Exceptional Events Rule preamble describes in greater detail to whom 16 the r

ule applies ( 72 FR 13562
- 13563 March 22, 2007). 17 The CAA Section 319(b)(2) authorizes EPA to promulgate regulations that 18 govern the review and handling of air quality monitoring data influenced by exceptional 19 events. Under this authority , EPA promulgated the Exceptional Events Rule (Treatment 20 of Data Influenced by Exceptional Events (72 FR 13560, March 22, 2007) which sets a 21 schedule for states to flag monitored data affected by exceptional events in AQS and for 22 them to submit documentation to demonstrate that the flagged data values were caused by 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 372 an exceptional event. Under this schedule, a state must initially notify EPA that data 1 have been affected b y an exceptional event b y July 1 of the year after the data are 2 collected; this is accomplished by flagging the data in AQS. The state must also include 3 an initial description of the event when flagging the data. In addition, the s tate is required 4 to submit a full demonstration to justify exclusion of such data within three years after 5 the quarter in which the data were collected, or if a regulatory decision based on the data 6 (such as a designation action) is anticipated, the demons tration must be submitted to EPA 7 no later than one ye ar before the decision is to be made. 8 The rule also authorizes EPA to revise data flagging and documentation schedules 9 for data used in the initial designation of areas under a new NAAQS. Th e generic 10 schedule, while appropriate for the period after initial designations have been made under 11 a NAAQS, may

need adjustment when a new NAAQS is promulgated because until the 12 level and form of the NAAQS have been promulgated , a state would not have complete 13 kn owledge of the criteria for excluding data. In these cases , the generic schedule may 14 preclude states from submitting timely flags and associated documentation for otherwise 15 approvable exceptional events. This could, if not modified, result in some areas receiving 16 a nonattainment designation when the NAAQS violations were legitimately due to 17 exceptional events. 18 As a result of the Administrator’s decision to reconsider the 2008 O 3 NAAQS, 19 EPA is proposing to revise the exceptional events flagging and docum entation schedule 20 to correspond to the designations schedule s that EPA is considering for the proposed 21 revisions to the primary and secondary O 3 NAAQS. The designation schedules under 22 consideration are discussed in greater detail below in section VII.A an d summarized 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 373 here. The CAA requires EPA to promulgate the initial designations for all areas no later 1 than 2 years from the promulgation of a new NAAQS. Such period may be extended for 2 up to one year if EPA has insufficient information. (See CAA sectio n 107(d).) For a 3 new primary O 3 standard, EPA intends to issue designations on an accelerated schedule. 4 For a new seasonal secondary O 3 standard, EPA is considering two alternative schedules 5 for initial area designations

. 6 Primary

Standard : If

, as a result of the reconsideration, EPA promulgates a new 7 primary O 3 standard on August 31, 2010, EPA is proposing that state Governors would 8 need to submit their initial designation recommendations to EPA by January 7 , 201 1
. 9 EPA would promulgate the final desi gnations in July 2011 to allow sufficient time for the 10 designations to be published and effective by August 31, 2011. EPA expects to base the 11 final designations for the primary O3 standard on three consecutive ye ars of certified air 12 quality

monitoring dat a from the years 2007
- 2009 or 2008
- 2010, if available. EPA is 13 proposing that for exceptional event claims made for data ye ars 2007
- 2009, states must 14 flag and provide an initial description and detailed documentation by November 1, 2010. 15 For data collecte d during data year 2010, EPA is proposing that exceptional event data 16 that states want EPA to exclude from consideration in the designations process must be 17 flagged with an initial description and fully documented by March 1, 2011 or 60 day s 18 after the end of the quarter when the event occurred, whichever date is first. To meet this 19 proposed 60

- day

deadline, a state would also have to submit the O 3 concentration data to 20 AQS sooner than the normal deadline for such submission , which is 90 days after the end 21 of the calendar quarter. EPA believes this is a reasonable expectation given that most 22 states currently

submit O 3 data earlier than the 90

- day deadline. 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 374 Secondary

Standard : If

, as a result of the reconsideration, EPA promulgates a 1
new seasonal secondary O 3 standard by August 31, 2010, EPA is taking comment on two 2 alternative designations schedules. Under the first alternative, EPA would designate 3 areas for the secondary standard on the same accelerated schedule discussed above for 4 the primary

standard. Under the second alternative, EPA would designate areas for the 5 secondary

standard on the maximum 2

- year schedule provided under the CAA. 6 Accelerated Schedule : Under the accelerated schedule for a seasonal secondary O 3 7 NAAQS , EPA is proposing that for e xceptional event claims made for data years 2007
- 8 2009, states must flag and provide an initial description and detailed documentation by 9 November 1, 2010. For data collected during data year 2010, EPA is proposing that 10 exceptional event data that states w ant EPA to exclude from consideration in the 11 designations process must be flagged with an initial description and full y documented b y 12 March 1, 2011 or 60 days after the end of the quarter when the event occurred, whichever 13 date is first. 14 2

-

year Schedule : Under the 2
- ye ar schedule, states would have 1 ye ar, or by 15 August 2011, to submit their designations recommendations and EPA would finalize 16 designations under the new secondary standard by

August 2012. EPA expects to base 17 final designations for a new se asonal secondary standard on the most recent three years of 18 certified air quality monitoring data, which would ty picall y be from the years 2009
- 2011 19 in this case. Exceptional event data claims used from years 2008
- 20 10 must be flagged 20 with an initial desc ription included in AQS and submitted with complete documentation 21 supporting such claims by July 1, 201 1 . Exceptional event data claims from data year 22 2011 must be flagged with an initial description and submitted with complete 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 375 documentation supporting such claims 6 0 day s after the end of the calendar quarter when 1 the event occurred or March 1, 201 2 , whichever occurs first. 2 Therefore, using the authority provided in CAA section 319(b)(2) and in the 3 Exceptional Events Rule at 40 CFR 50.14 (c)(2)(vi), EP A is proposing to modify the 4 schedule for data flagging and submission of demonstrations for exceptional events data 5 considered for initial designations under the proposed reconsidered O 3 p rimary and 6
s econdary

NAAQS, as follows: 7 8 Table 1. Schedule for Exc eptional Event Flagging and 9 Documentation Submission for Data to be Used in 10 Designations Decisions for New NAAQS 11 12 NAAQS

Pollutant/ Standard/(Level )/ Promulgation Date Air Quality

Data Collected for Calendar Year Event Flagging

& Initial Description Deadlin e Detailed

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

2010 60 Day s after the end

of the calendar quarter in which the event occurred or March 1, 2011, whichever date occurs firstb 60 Day s 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

- ye ar Schedule

- to be Promulgated b y August 31, 2010 2008 July 1, 2011 b July 1, 2011 a

2009
- 2010 July 1, 2011 b July 1, 2011 bDraft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 376 2011 60 Day s after the end

of the calendar quarter in which the event occurred or March 1, 2012, whichever occurs firstb 60 Day s 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, 2010 b November 1, 2010 b

2010 60 Day s after the end

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

of the calendar quarter in which the event occurred or March 1, 2011, whichever date occurs firstbDraft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 377
a These dates are unchanged from those published in the origin al rulemaking.
b In dicates 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 VI. Am bient Monitoring Related to Proposed O 3 Standards 3 Presently , States (including the District of Columbia, Puerto Rico, and the Virgin 4 Islands, and including local agencies when so delegated by the State) are required to 5 operate minimum numbers of EPA

- approved O 3 monitors based on the population of 6 each of their Metropolitan Statistical Areas (MSA) and the most recently measured O 3 7 levels in each area. Each State (or in some cases portions of a State) also has a required 8 O 3 monitoring season based on historical experience on when O 3 levels are high enough 9 to be of regulatory

or public health concern. These requirements are contained in 40 CFR 10 part 58 Appendix D , Network Design Criteria for Ambient Air Quality Monitoring. See 11Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 378 section 4.1, especially

Tables D

–2 and D

–3. These requirements were last revised on 1 October 17, 2006 as part of a comprehensive review of ambient monitoring requirements 2 for all criteria po llutants (71 FR 61236). 3 A. Background 4 In the 2007 proposed rule for the O 3 NAAQS (72 FR 37818), EPA did not 5 propose specific changes to monitoring requirements to support the proposed NAAQS 6 revisions, but instead solicited comment on several key matters that were expected to be 7 important issues affecting the potential redesign of monitoring networks if revisions to 8 the NAAQS were finalized. These matters included O 3 monitoring requirements in urban 9 areas, the potential need for monitoring to support multiple objectives important to 10 characterization in non

- urban areas including the support of the secondary O 3 NAAQS, 11 and the length of the required O 3 monitoring seasons. Comments on these monitoring 12 issues were received during the ensuing public comment period, and these comments 13 were summarized in the 2008 final rule for the O 3 NAAQS (73 FR 16501). As noted in 14 that action, EPA stated its intention to propose, in a separate rulemaking, the specific 15 changes to O 3 monitoring requirements that were deemed nece ssary to support the 16 revised 2008 O 3 NAAQS which set the level of the primary 8
- hour O 3 standard to 0.075 17 ppm and set the secondary standard identical in all respects to the primary standard . EPA 18 published these proposed changes to O 3 monitoring requirements in a proposal dated July 19 16, 2009, Ambient Ozone Monitoring Regulations: Revisions to Network Design 20 Requirements (74 FR 34525). The EPA currentl y plans to finalize these changes in a 21 final O 3 monitoring rule in 2010, either before or in conjunction w ith the final rule on the 22 O 3 NAAQS. 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 379 In the following sections, the specific provisions of the 2009 O 3 monitoring 1 proposal are briefl y reviewed, and then discussed in the context of the proposed revisions 2 of the 2008 O 3 NAAQS that have been discussed earli er in this notice. 3 B. Urban Monitoring Requirements 4 As noted earlier, current O 3 monitoring requirements for urban areas are based on 5 two factors: MSA population and the most recent 3

- ye ar design value concentrations 6 within each MSA. There are higher min imum monitoring requirements for areas that 7 have most recent design values greater than or equal to 85 percent of the NAAQS (i.e., 8 design value concentrations that are greater than or equal to 85 percent of the level of the 9 NAAQS), and lower requirements f or areas that have design values less than 85 percent 10 of the NAAQS. These minimum monitoring requirements for O 3 were revised during the 11 2006 monitoring rulemaking to ensure that additional monitors would be required in 12 areas with higher design values and to also ensure that these requirements would remain 13 applicable through future NAAQS reviews and potential revisions of the standards. 14 Accordingl y, these requirements do not need to be updated with the revisions of the O 3 15 NAAQS proposed in this action sin ce the 85 percent threshold will be applied to the 16 standard levels that are finalized for the primary and secondary

standards. 71 For example, 17 given the range of levels of the primary standard being proposed, the level of the 85 18

71 The requirements specified in Table D

- 2 of Appendix D to part 58, as noted in the third footnote of T able D

- 2, are applicable to the levels of the O 3 NAAQS as defined in 40 CFR part 50. Accordingl y, the 85 percent threshold for requiring higher minimum monitoring requirements within MSAs would apply to the proposed levels for the cumulative, seasonal sec ondary standard as well as to the proposed levels of the 8

- hour primary standard.Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 380 percent threshold that requires greater minimum monitoring requirements ranges from 1 0.051 ppm (85 percent of 0.060 ppm) to 0.060 ppm (85 percent of 0.070 ppm). 2 EPA did propose one change to urban monitoring requirements in the 2009 O 3 3 monitoring proposal. Specificall y, EPA proposed to modif y the minimum O 3 monitoring 4 requirements to require one monitor to be placed in MSAs of populations ranging from 5 50,000 to less than 350,000 in situations where there is no current monitor and no history 6 of O 3 monitoring within the previous 5 ye ar s indicating a design value of less than 85 7 percent of the revised NAAQS. 72 Since this proposed change to minimum requirements 8 is also subject to the 85 percent threshold, EPA believes that the proposed change 9 remains appropriate to support the revisions t o the primary and secondary O 3 NAAQS 10 proposed in this action. 11 C. Non

- Urban Monitoring Requirements 12 In the 2007 proposed rule for the O 3 NAAQS, EPA solicited comment on the 13 status of monitoring requirements for non

- urban areas, specificall y whether non

- urb an 14 areas with sensitive vegetation that are onl y currently sparsely monitored for O 3 could 15 experience undetected violations of the secondary NAAQS as a result of transport from 16 urban areas with high precursor emissions and/or O 3 concentrations or from form ation of 17 additional O 3 from precursors emitted from sources outside urban areas. 18 Comments that were received in response to the 2009 O 3 NAAQS monitoring 19 proposal noted the voluntary nature of most non - urban O 3 monitoring and the resulting 20 relative lack of non - urban O 3 monitors in some areas. These commenters stated that EPA 21 should consider adding monitoring requirements to support the secondary NAAQS by 22

72 These MSAs are not currently required to monitor for O 3 .Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 381 requiring O 3 monitors in locations that contain O 3 - sensitive plants or ecos ys tems. These 1 commenters al so noted that the placement of current O 3 monitors may not be appropriate 2 for evaluating issues such as vegetation exposure since many of these monitors were 3 likely

loc ated to meet other objectives. 4 Based on these comments as well as analy ses of O 3 concentrations from 5 discretionary

non - urban monitors located across the U.S, EPA included new proposed 6
non - urban O 3 monitoring requirements in the 2009 O 3 monitoring proposal. These 7 proposed requirements are intended to satisfy several important objectives including : (1) 8 better characterization of O 3 concentrations to which O 3 - sensitive vegetation and 9
ecos ys tems are exposed in rural/remote areas to ensure that potential secondary NAAQS 10 violations are measured ; (2) assessment of O 3 concentrations in smaller communities 11 located outside of the larger urban MSAs covered by urban monitoring requirements; and 12 (3) the assessment of the location and severity of maximum O 3 concentrations that occur 13 in non

- urban areas and may be attributable to upwind urban sources. For reasons noted 14 below, EPA believes that these proposed O 3 monitoring requirements are sufficient to 15 support the revisions to the O 3 NAAQS proposed in this action. 16 With regard to the first objective, we note uncertainties will remain about the O 3 17 concentrati ons to which sensitive natural vegetation and ecos ys tems are exposed until 18 additional monitors are sited in National Parks, State and/or tribal areas, wilderness areas, 19 and other similar locations with sensitive ecosy stems that are set aside to provide sim ilar 20 public welfare benefits. These monitors would support evaluation of the secondary 21 NAAQS with a more robust data set than is now available. As noted in the 2009 O 3 22 monitoring proposal, EPA proposed that States operate at least one monitor to be located 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 382 in areas such as some Federal, State, Tribal, or private lands, including wilderness areas 1 that have O 3 - sensitive natural vegetation and/or ecosystems. If EPA finalizes a 2 cumulative, seasonal secondary standard at the lower end of the proposed range, then it is 3 plausible that additional O 3 monitors, above the number required b y the monitoring 4 proposal, may

be needed in such areas to provide adequate coverage of locations likely to 5 experience violations of the revised secondary NAAQS. These additional m onitors could 6 be established through discretionary State initiatives to supplement minimum monitoring 7 requirements, negotiated agreements between States and EPA Regional Administrators, 8 or through a future rulemaking that addresses potential increased O 3 m onitoring 9 requirements to specifically address the need for additional monitoring to ensure 10 detection of secondary standard violations. 11 With regard to the second objective of characterizing elevated ambient O 3 levels 12 to which people are exposed in smaller communities located outside of the larger urban 13 MSAs , the likelihood of measuring concentrations that approach or exceed the levels of 14 the NAAQS due to the transport of O 3 from upwind areas and/or the formation of O 3 due 15 to precursor emissions from industrial sources outside of urban areas is clearly increased 16 due to the revised NAAQS proposed in this action. Given that the anal ys es described in 17 the 2009 O 3 monitoring proposal demonstrated that 50 percent of existing monitors 18 located in such Micropolitan S tatistical Areas 73 exceeded the current NAAQS and nearl y 19 all monitors recorded design values greater than or equal to 85 percent of the current 20 NAAQS, the potential for violations in such areas can onl y be increased with the 21

73 Defined as areas having at least one urban cluster of at least 10,000 but less than a population of 50,000.Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 383 NAAQS revisions proposed in this action. As noted for the first non

- urban monitoring 1 objective, it is plausible that additional O 3 monitors, above the number required by the 2 2009 monitoring proposal may be needed in Micropolitan Statistical Areas to provide 3 adequate coverage of location s likely to experience violations of the proposed lower 4 primary

NAAQS levels. These additional monitors could be established through 5 discretionary

State initiatives to supplement minimum monitoring requirements, 6 negotiated requirements between States and EPA Regional Administrators, or through a 7 future rulemaking that addresses potential increased O 3 monitoring requirements to 8 specificall y address the need for additional monitoring to ensure detection of primary 9 standard violations in smaller communities. 10 The third proposed non

- urban monitoring objective, requiring O 3 monitors to be 11 located in the area of expected maximum O 3 concentration outside of any MSA, 12 potentially

including the far downwind transport zones of currentl y well

- monitored urban 13 areas, is not directly related to the level of the O 3 NAAQS. It is instead intended to 14 ensure that all parts of a State meet the NAAQS and that all necessary emission control 15 strategies have been included in State Implementation Plans. Accordingl y, this proposed 16
m onitoring objective remains applicable independent of revisions to the O 3 NAAQS 17 proposed in this action. 18 D. Revisions to the Length of the Required O3 Monitoring Seasons 19 Ozone monitoring is only required during the seasons of the year that are 20 conducive t o O 3 formation. These seasons vary in length as the conditions that determine 21 the likely

O 3 formation (i.e., seasonall y- dependent factors such as ambient temperature, 22 strength of solar insolation, and length of day) differ by location. In some locations, 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 384 conditions conducive to O 3 formation are limited to a few summer months of the year 1 while in other locations these conditions occur ye ar- round. As a result, the length of 2 currentl y required O 3 monitoring seasons can vary from a length of 4 months in colder 3 climates to a length of 12 months in warmer climates. 4 The 2009 O 3 monitoring proposal also addressed the issue of whether in some 5 areas the required O 3 monitoring season should be made longer. The proposal also 6 addressed the status of any currentl y effe ctive Regional Administrator

- granted waiver 7 approvals to O 3 monitoring seasons, and the impact of proposed changes to monitoring 8 requirements on such waiver approvals. 9 The EPA performed several anal ys es in support of proposed changes to the 10 required O 3 mo nitoring seasons. The first anal ys is determined the number of observed 11 exceedances of the 0.075 ppm level of the current 8

- hour NAAQS in the months falling 12 outside the currentl y required local O 3 monitoring season using monitors in areas that 13 collected O 3 data ye ar- round in 2004

–2006. The second analy sis examined observed 14 occurrences of dail y maximum 8

- hour O 3 averages of at least 0.060 ppm. This threshold 15 was chosen because it represented 80 percent of the current 0.075 ppm NAAQS level and 16 provides an in dicator of ambient conditions that may be conducive to the formation of O 3 17 concentrations that approach or exceed the NAAQS. While proposals for revising each 18 State’s required monitoring season were based on observed data in and surrounding each 19 State, st atistically

predicted exceedances were also used to validate conclusions for each 20 State. 21 The aforementioned analy ses provided several results. The anal ys is of observed 22 exceedances of the 0.075 ppm level of the current O 3 NAAQS indicated occurrences in 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 385 e ight States during months outside of the current required monitoring season. The eight 1 States were Maine, Massachusetts, New Hampshire, New Jersey , New York, South 2 Carolina, Vermont, and Wyoming. With the exception of Wyoming, these exceedances 3 occurred in a very

limited manner and timeframe, just before the beginning of these 4 States’ required O 3 monitoring season (beginning in these States on April 1). The 5 frequency

of observed occurrences of maximum 8

- hour average O 3 levels of at least 6 0.060 ppm was quit e high across the country in months outside of the current required 7 monitoring season. A total of 32 States experienced such occurrences; 22 States had such 8 levels only

before the required monitoring season; 9 States had such levels both before 9 and after the required monitoring season; and 1 State had such levels only after the 10 required monitoring season. In a number of cases, the frequency of such ambient 11 concentrations was high, with some States experiencing between 31 to 46 out

- of

- season 12 day s during 200 4 to 2006 at a high percentage of all operating year - round O 3 monitors. 13 Based on these analy ses, EPA proposed a lengthening of the O 3 monitoring 14 season requirements in many areas. The 2009 proposed changes were based not only on 15 the goal of monitoring out - of

- season O 3 NAAQS violations but also on the goal of 16 ensuring monitoring when ambient O 3 levels reach 80 percent of the NAAQS so that 17 persons unusually

sensitive to O 3 would be alerted to potential NAAQS exceedances. 18 The EPA believes that the factors u sed to support the 2009 proposed changes to 19 O 3 monitoring seasons are appropriate to support the revisions of the O 3 NAAQS 20 proposed in this action. With regard to the primary standard, we note that the lower end 21 of the range being proposed is an 8

- hour level of 0.060 ppm, which is identical to the 22 ambient O 3 level that was utilized in one of the analyses discussed above. Although that 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 386 level was chosen to provide an indicator of ambient levels that were below but 1 approaching the level of the NAAQS and henc e to serve as an alert to potential 2 exceedances, we note that EPA’s traditional practice had been to base the length of 3 required O 3 monitoring seasons on the likelihood of measuring exceedances of the level 4 of the NAAQS. Therefore, if EPA finalizes the le vel of the primary standard at the lower 5 end of the proposed range, the O 3 monitoring seasons that have been proposed as part of 6 the 2009 O 3 monitoring proposal would provide sufficient monitoring coverage to ensure 7 the goal of measuring potential violatio ns of the primary standard. 8 One O 3 monitoring season issue that was not considered in the 2009 O 3 9 monitoring proposal was the question of whether analy ses of ambient data based on 8

- 10 hour average statistics would also indicate whether the resulting propose d monitoring 11 seasons would capture the cumulative maximum consecutive 3

- month O 3 levels 12 necessary

to compute design values based on the secondary NAAQS proposed in this 13 action, which is defined in terms of a W126 cumulative peak

- weighted index, as 14 discusse d above in section IV
. If areas experienced high cumulative index values during 15 months outside of the required O 3 monitoring seasons (based on 8

- hour statistics), then 16 further revisions to the required monitoring seasons might be necessary to ensure 17 monit oring during all months important to the calculation of design values for the revised 18 form proposed for the secondary NAAQS. A related issue is whether such high 19 cumulative O 3 values also occurred during time periods that are biologically relevant for 20 O 3 - sensitive vegetation. 21 The EPA is not proposing additional revisions to O 3 monitoring seasons at this 22 time. Additional analyses of the distribution of elevated cumulative W126 index values 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 387 will be conducted, and the biologically relevant seasonal issue wi ll be further reviewed. 1 Based on the results of these anal ys es, EPA may consider proposing further revisions to 2 the O 3 monitoring season as related to the secondary O 3 NAAQS
. 3 4 VI I . Implementation of Proposed O 3 Standards 5 A. Designations 6 After EPA establ ishes or revises a NAAQS, the CAA directs EPA and the states 7 to take steps to ensure that the new or revised NAAQS are met. The first step is to 8 identify

areas of the country

that do not meet the new or revised NAAQS. This step is 9 known as the initial area designations. 10 The CAA provides that, "By such date as the Administrator may reasonably 11 require, but not later than 1 year after promulgation of a new or revised national ambient 12 air quality

standard f

or any pollutant under section 109, the Governor o f each state shall * 13 * * submit to the Administrator a list of all areas (or portions thereof) in the state" that 14 designates those areas as nonattainment, attainment, or unclassifiable. The CAA 15 specifies that, "The Administrator may not require the Govern or to submit the required 16 list sooner than 120 day s after promulgating a new or revised national ambient air quality 17 standard." The CAA defines an area as nonattainment if it is violating the NAAQS or if 18 it is contributing to a violation in a nearb y area. (See CAA section 107(d)(1).) 19 The CAA further provides, "Upon promulgation or revision of a national ambient 20 air quality

standard , the Administrator shall promulgate the designations of all areas (or 21 portions thereof) * * * as expeditiously as practicabl e, but in no case later than 2 years 22 from the date of promulgation of the new or revised national ambient air quality standard

. 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 388 Such period may

be extended for up to one ye ar in the event the Administrator has 1 insufficient information to promulgate the de signations. ” EPA is required to notify states 2 of any intended modifications to their recommendations that EPA may deem necessary 3 no later than 120 day s prior to promulgating designations . States then have an 4 opportunity

to demonstrate why

any such propos ed modification is inappropriate. 5 Whether or not a state provides a recommendation, EPA must promulgate the designation 6 that the Agency

deems appropriate. (See CAA section 107(d)(1)(B).) 7 On September 16, 2009, when the Administrator announced her decis ion to 8 reconsider the 2008 O 3 NAAQS, she also indicated that the Agency would work with 9 states to accelerate implementation of the standards adopted after reconsideration , 10 including the initial area designations process. Acceleration of designations for the 11 primary

standard would help limit any delay s in health protections associated with the 12 reconsideration of the standards. If a secondary standard different from the primary 13 standard is adopted, this would be the first time different primary and secondary 14 standards would be in place for the O 3 standards. While welfare protection is also 15 important, for the reasons provided below, we are providing alternative schedules for 16 designating areas for the secondary standard. 17 If, as a result of the reconsideratio n, EPA determines that the record supports a 18 primary

standard different from that promulgate d in 2008 and promulgates such different 19 primary O 3 NAAQS in 2010, EPA intends to promulgate final designations on an 20 accelerated schedule to allow the designations to be effective in 1 year. In order to meet 21 such a schedule, EPA is proposing that the deadline for states to submit their designations 22 recommendations for the revised 2010 primary standard be 12 9 days after promulgation 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 389 of that primary standard. EPA re cognizes that the proposed deadline would be an 1 ambitious schedule. Therefore, EPA intends to provide technical information and 2 guidance for states as early as possible to facilitate the development of their 3 recommendations. Many of the areas that would be violating the proposed primary ozone 4 standard are also violating the 2008 ozone standards. State Governors have provided 5 recommendations on these areas pursuant to the 2008 standards and recommendations 6 may not need much further evaluation. 7 Based on this proposed schedule, if EPA promulgates a new primary standard on 8 August 31, 2010, state Governors would need to submit their initial designation 9 recommendations to EPA by January 7 , 2011 . If the Administrator intends to modify any 10 state recommendation, EPA would notify the Governor no later than March 2011, 120 11 day s prior to promulgating the final designations. States would then have an opportunity 12 to comment on EPA's intended designations before EPA promulgates the final 13 designations. EPA would promulgate the final designations in July 2011 to allow 14 sufficient time for the designations to be published and effective b y August 31, 2011. 15 EPA expects to base the final designations for the primary O 3 standard on three 16 consecutive ye ars of certified air qu ality monitoring data from the ye ars 2007
- 2009 or 17 from 2008

- 2010, if available. 18 If

, as a result of the reconsideration, EPA promulgates a distinct secondary 19 standard that differs from that promulgated in 2008 and also differs from the 2010 20 primary

stan dard, as proposed above, EPA is proposing two alternative deadlines for 21 states to submit their designations recommendations. Under the first alternative, EPA 22 would designate areas for the secondary standard on the same accelerated schedule 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 390 discussed abov e for the primary standard. In order to meet that schedule, EPA is 1 proposing that states submit their recommendations for the revised 2010 secondary 2 standard 12 9 day s after promulgation of that secondary standard. Accordingl y, if EPA 3 promulgates the new secondary standard on August 31, 2010, state Governors would 4 need to submit their initial designation recommendations to EPA by January 7 , 201 1
. 5 Weighing in favor of designating areas for the secondary standard at the same 6 time as designations for the primary standard is that planning for both standards would 7 occur on the same schedule. Our examination of current air quality data from the existing 8 monitoring network indicates that for levels of the primary and secondary

standards 9 proposed in this action, it is likely that the vast majority

of areas violating the secondary 10 standard would overlap with areas violating the primary standard. In this case, 11 implementing requirements for the primary and secondary

standards on different 12 schedules could present re source challenges to state and local agencies b y requiring 13 duplication of effort and hindering consideration of all factors when deciding which 14 control strategies to adopt for each standard. For example, if designations for the 15 secondary

standard were del ayed b y a certain period (e.g., a ye ar) beyond the 16 designations for the primary standard, then EPA would likely delay submission of 17 attainment SIPs for the secondary standard for a similar period beyond the proposed date 18 for submission of the attainment SIPs for the primary standard . In this case, the initial 19 transportation conformity determination for the secondary standard would be required 20 later than the initial determination for the primary standard by

the difference in time 21 between the effective dates of the two designations

. 22Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 391 Under the second alternative, EPA would designate areas for the secondary 1 standard on the maximum 2

- ye ar schedule provided under the CAA. To meet that 2

- ye ar 2 schedule, EPA is proposing that states submit their recommendations f or the revised 3 secondary

standard no later than 1 year after promulgation of the 2010 secondary 4 standard

. Accordingl y, i f EPA promulgates a secondary standard on August 31, 2010, 5 that differs from the primary standard, as proposed, under the alternative 2

- ye ar 6 designations schedule, state Governors would need to submit their initial designation 7 recommendations to EPA by August 31, 2011 . If the Administrator intends to modify 8 any state recommendation, EPA would notify the Governor no later than May 201 2, 1 20 9 day s prior to the 2

- ye ar deadline for promulgating the final designations. States would 10 then have an opportunity to comment on EPA's intended designations before EPA 11 promulgates the final designations. EPA would promulgate the final designations for the 12 secondary

standard by

August 31, 201 2
. EPA expects to base the final designations in 13 August 2012 for a different secondary standard on the most recent three consecutive 14 ye ars of certified air quality monitoring data, which would be from the ye ars 2009
- 2011. 15 In the past, EPA has alway s set the secondary O 3 standard to be identical to the 16 primary O 3 standard and the standards have embodied relativel y short

- term average 17 concentrations (e.g., 1

- hour or 8

- hour) . In this action, EPA is proposing a cumulative, 18 seasonal secondary standard that differs from the proposed primary standard . EPA has 19 not previously

set a seasonal secondary standard for O 3 . Therefore, EPA and states do 20 not have experience in implementing this ty pe of secondary O 3 standard or in 21 determining what area boundaries would be appropriate. As we further explore 22 implementation considerations for the secondary standard, we may

encounter 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 392 unanticipated issues that may require additional time to address. Thus, EPA is 1 considering whether an accelerated schedule for a seasonal secondary standard would 2 provide adequate time for resolving issues that we cannot now anticipate. If EPA 3 designates areas for the secondary standard on a 2

- ye ar schedule, we note that we expect 4 that accelerated implementation of the health

- based primary standard wo uld also result in 5 accelerated welfare benefits. EPA requests comment on factors affecting the efficient 6 and effective implementation of a secondary standard that differs from the primary 7 standard in the cont ext of establishing designations schedules. 8 EPA notes , as discussed in greater detail above in section VI, that it has proposed 9 a monitoring rule that would increase the density of monitoring in National Parks and 10 other non

- urban and lesser populated areas (July 16, 2009; 74 FR 34525). The proposed 11 requirements are intended to satisfy several important objectives, including better 12 characterization of O 3 exposures to O 3 - sensitive vegetation and ecos ys tems in 13 rural/remote areas to ensure that potential secondary NAAQS violations are measured. 14 As proposed, the new monitors would not be deployed until 2012 or 2013. Therefore, 15 data from these monitors would not be available for use within the statutory timeframe 16 for EPA to complete designations for a 2010 seco ndary standard regardless of which 17 schedule EPA follows. 18 While CAA section 107 specificall y addresses states, EPA intends to follow the 19 same process for tribes to the extent practicable, pursuant to section 301(d) of the CAA 20 regarding tribal authority, and the Trib al Authority Rule (63 FR 7254; February 12, 21 1998). 22Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 393 In a separate notice e lsewhere in today ’s Federal Register , EPA is announcing 1 that it is using its authority under the CAA to extend by 1 year the deadline for 2 promulgating initial area designations for the O 3 NAAQS that were promulgated in 3 March 2008. The new deadline is March 12, 2011. Th at notice explains the basis for the 4 deadline extension. As mentioned above, on September 16, 2009, EPA notified the Court 5 of its decision to initiate a rulemaking to reconsider the primary and secondary O 3 6 NAAQS set in March 2008 to ensure they satisfy the requirements of the CAA. In its 7 notice to the Court, EPA stated that the final rule would be signed b y August 31, 2010. 8 Extending the deadline f or promulgating designations for the 2008 O 3 NAAQS until 9 March 12, 2011 will allow EPA to complete the reconsideration rulemaking for the 2008 10 O 3 NAAQS before determining whether it is necessary to finalize designations for th ose 11 NAAQS or, instead, whether it is necessary to begin the designation process for different 12 NAAQS promulgated pursuant to the reconsideration

. 13 B. State Implementation Plans 14 The CAA section 110 provides the general requirements for SIPs. Within 3 years 15 after the promulgation of new or revised NAAQS (or such shorter period as the 16 Administrator may

prescribe) each State must adopt and submit “infrastructure” SIPs to 17 EPA to address the requirements of section 110(a)(1). Thus, States should submit these 18 SIPs no later than August 21, 201 3, three ye ars after promulgation of the reconsidered 19 ozone standard in 2010. These “infrastructure SIPs” provide assurances of State 20 resources and authorities, and establish the basic State programs, to implement, maintain, 21 and enforce new or revised standards. 22Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 394 In addition to the infrastructure SIPs, which appl y to all States, CAA title I , part D 1 outlines the State requirements for achieving clean air in designated nonattainment areas. 2 These requirements include timelines for when designated nonattainm ent areas must 3 attain the standards, deadlines for developing SIPs that demonstrate how the State will 4 ensure attainment of the standards, and specific emissions control requirements . EPA 5 plans to address how these requirements, such as attainment demonstrations and 6 attainment dates, reasonable further progress , new source review, conformity , and other 7 implementation requirements, apply to the O 3 NAAQS promulgated pursuant to the 8 reconsideration in a subsequent rulemaking. Also in that rulemaking EPA will establish 9 deadlines for submission of nonattainment area SIPs but anticipates that the deadlines 10 will be no later than the end of December 2013, or 28 months after final designations. 11 C

. Trans
- boundary E missions 12 Cross border O 3 contributions from within North America (Canada and Mexico) 13 entering the U.S. are generall y thought to be small. Section 179B of the Clean Air Act 14 allows designated nonattainment areas to petition EPA to consider whether such a 15 locality

might have met a clean air standard “but for” cross border contributions. To 16 date, few areas have petitioned EPA under this authority . The impact of foreign 17 emissions on domestic air quality in the United States is a challenging and complex 18 problem to assess. EPA is engaged in a number of activities to improve our 19 understanding of international transport. As work progresses on these activities, EPA 20 will be able to better address the uncertainties associated with trans

- boundary flows of air 21 pollution and their impacts. 22 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 395 VI I I . Statutory and Executive Order Reviews 1 A . Executive Order 12866: Regulatory Planning and Review 2 Under section 3(f)(1) of Executive Order (EO) 12866 (58 FR 51735, October 4, 3 1993), the O 3 NAAQS action is an “economicall y significant regulatory action” because 4 it is likely

to have an annual effect on the economy of $100 million or more. 5 Accordingl y, EPA submitted this action to the Office of Management and Budget (OMB) 6 for review under EO 12866 and any changes made in response to OMB recommendations 7 have been documented in the docket for this action. In addition, EPA prepared this 8 regulatory

impact anal ys is (RIA) of the potential costs and benefits associated with this 9 action. This anal ys is is contained in the Regulatory Impact Anal ys is for the Ozone 10 NAAQS Reconsideration, October, 2009 (henceforth, “RIA”). A cop y of the anal ys is is 11 available in the RIA docket (EPA

- HQ
- OAR
- 2007
- 0225) and the anal ys is is briefly 12 summarized here. The RIA estimates the costs and monetized human health and welfare 13 benefits of attaining five alternative O 3 NAAQS nationwide. Specificall y, the RIA 14 examines the alternatives of 0.079 ppm, 0.075 ppm, 0.070 ppm, 0.065 ppm, and 0.060 15 ppm. The RIA contains illustrative anal ys es that consider a limited number of emissions 16 control scenarios that States and Regi onal Planning Organizations might implement to 17 achieve these alternative O 3 NAAQS. However, the Clean Air Act (CAA) and judicial 18 decisions make clear that the economic and technical feasibility of attaining ambient 19 standards are not to be considered in setting or revising NAAQS, although such factors 20 may

be considered in the development of State plans to implement the standards. 21 Accordingl y, although an RIA has been prepared, the results of the RIA have not been 22 considered in issuing this proposed rule. 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 396 B

. Paperwork Reduction Act 1 This action does not impose an information collection burden under the 2 provisions of the Paperwork Reduction Act, 44 U.S.C. 3501 et seq. There are no 3 information collection requirements directl y associated with the establishment of a 4 NAAQS under section 109 of the CAA. 5 Burden means the total time, effort, or financial resources expended b y persons to 6 generate, maintain, retain, or disclose or provide information to or for a Federal agency. 7 This includes the time needed to review instructions; develop, acquire, install, and utilize 8 technology

and sy stems for the purposes of collecting, validating, and verifying 9 information, processing and maintaining information, and disclosing and providing 10 information; adjust the existing way s to compl y with any previously

applicable 11 instructions and requirements; train personnel to be able to respond to a collection of 12 information; search data sources; complete and review the collection of information; and 13 transmit or otherwise disclose the infor mation. 14 An agency

may not conduct or sponsor, and a person is not required to respond to 15 a collection of information unless it displays a currently valid OMB control number. The 16 OMB control numbers for EPA's regulations in 40 CFR are listed in 40 CFR part 9. 17 C. Regulatory Flexibility Act 18 The Regulatory Flexibility

Act (RFA) generall y requires an agency to prepare a 19 regulatory

flexibility

analy sis of any

rule subject to notice and comment rulemaking 20 requirements under the Administrative Procedure Act or any other statute unless the 21 agency

certifies that the rule will not have a significant economic impact on a substantial 22Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 397 number of small entities. Small entities include small businesses, small organizations, 1 and small governmental jurisdictions. 2 For pur

poses of assessing the impacts of today ’s proposed rule on small entities, 3 small entity

is defined as: (1) a small business that is a small industrial entity as defined 4 by the Small Business Administration’s (SBA) regulations at 13 CFR 121.201; (2) a 5
small governmental jurisdiction that is a government of a city, county, town, school 6 district or special district with a population of less than 50,000; and (3) a small 7 organization that is any not - for

- profit enterprise which is independently owned and 8 operat ed and is not dominant in its field. 9 After considering the economic impacts of today's proposed rule on small entities, 10 I certify

that this action will not have a significant economic impact on a substantial 11 number of small entities. This proposed rule will not impose any requirements on small 12 entities. Rather, this rule establishes national standards for allowable concentrations of 13 O 3 in ambient air as required by section 109 of the CAA. See also American Trucking 14 Associations v. EPA . 175 F. 3d at 1044

- 45 (NAAQS do not have significant impacts 15 upon small entities because NAAQS themselves impose no regulations upon small 16 entities). We continue to be interested in the potential impacts of the proposed rule on 17 small entities and welcome comments on issues related to such impacts 18 D. Unfunded Mandates Reform Act 19 Title II of the Unfunded Mandates Reform Act of 1995 (UMRA), Public Law 20 104
- 4, establishes requirements for Federal agencies to assess the effects of their 21 regulatory

actions on State, local, and Tribal governments and the private sector. Under 22 section 202 of the UMRA, EPA generally must prepare a written statement, including a 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 398 cost - benefit anal ys is, for proposed and final rules with “Federal mandates” that may 1 result in expenditures to State, local , and Tribal governments, in the aggregate, or to the 2 private sector, of $100 million or more in any 1 year. Before promulgating an EPA rule 3 for which a written statement is needed, section 205 of the UMRA generally requires 4 EPA to identify

and consider a reasonable number of regulatory alternatives and to adopt 5 the least costly , most cost - effective or least burdensome alternative that achieves the 6 objectives of the rule. The provisions of section 205 do not apply when they

are 7 inconsistent with applicable law. Moreover, section 205 allows EPA to adopt an 8 alternative other than the least costly , most cost - effective or least burdensome alternative 9 if the Administrator publishes with the final rule an explanation why that alternative was 10 not adopted. Before EPA establishes any regulatory requirements that may significantl y 11 or uniquely

affect small governments, including Tribal governments, it must have 12 developed under section 203 of the UMRA a small government agency plan. The plan 13 must provide for notifying potentiall y affected small governments, enabling officials of 14 affected small governments to have meaningful and timely input in the development of 15 EPA regulatory

proposals with significant Federal intergovernmental mandates, and 16 informing, educating, and advising small governments on compliance with the regulatory 17 requirements. 18 Today ’s proposed rule contains no Federal mandates (under the regulatory 19 provisions of Title II of the UMRA) for State, local, or Tribal governments or the private 20 sector. The proposed rule imposes no new expenditure or enforceable duty on any State, 21 local or Tribal governments or the private sector, and EPA has determined that this 22 proposed rule contains no regulatory requirements that might significantly or uniquely 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 399 affect small governments. Furthermore, as indicated previousl y, in setting a NAAQS 1 EPA cannot consider the economic or technological feasibility of attaining ambient air 2 quality

standards, although such factors may be considered to a degree in the 3 development of State plans to implement the standards. See also American Trucking 4 Associations v. EPA , 175 F. 3d at 1043 (noting that because EPA is precluded from 5 considering costs of implementation in establishing NAAQS, preparation of a Regulatory 6 Impact Anal ys is pursuant to the Unfunded Mandates Reform Act would not furnish any 7 information which the court could consider in reviewing the NAAQS). Accordingl y, 8 EPA has determined that the provisions of sections 202, 203, and 205 of the UMRA do 9 not apply

to this proposed deci sion. The EPA acknowledges, however, that any 10 corresponding revisions to associated SIP requirements and air quality surveillance 11 requirements, 40 CFR part 51 and 40 CFR part 58, respectivel y, might result in such 12 effects. Accordingly , EPA will address, as appropriate, unfunded mandates if and when 13 it proposes any revisions to 40 CFR parts 51 or 58. 14 E. Executive Order 13132: Federalism 15 Executive Order 13132, entitled “Federalism” (64 FR 43255, August 10, 1999), 16 requires EPA to develop an accountable proc ess to ensure “meaningful and timely input 17 by State and local officials in the development of regulatory policies that have federalism 18 implications.” “Policies that have federalism implications” is defined in the Executive 19 Order to include regulations that have “substantial direct effects on the States, on the 20 relationship between the national government and the States, or on the distribution of 21 power and responsibilities among the various levels of government.” 22Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 400 This proposed rule does not have federali sm implications. It will not have 1 substantial direct effects on the States, on the relationship between the national 2 government and the States, or on the distribution of power and responsibilities among the 3 various levels of government, as specified in Ex ecutive Order 13132. The rule does not 4 alter the relationship between the Federal government and the States regarding the 5 establishment and implementation of air quality improvement programs as codified in the 6 CAA. Under section 109 of the CAA, EPA is mandated to establish NAAQS; however, 7 CAA section 116 preserves the rights of States to establish more stringent requirements if 8 deemed necessary

by a State. Furthermore, this proposed rule does not impact CAA 9 section 107 which establishes that the States h ave primary responsibility

for 10 implementation of the NAAQS. Finall y, as noted in section E (above) on UMRA, this 11 rule does not impose significant costs on State, local, or Tribal governments or the private 12 sector. Thus, Executive Order 13132 does not app ly to this rule. 13 However, as also noted in section E (above) on UMRA, EPA recognizes that 14 States will have a substantial interest in this rule and any corresponding revisions to 15 associated SIP requirements and air quality surveillance requirements, 40 CFR part 51 16 and 40 CFR part 58, respectivel y. Therefore, in the spirit of Executive Order 13132, and 17 consistent with EPA policy to promote communications between EPA and State and local 18 governments, EPA specifically solicits comment on this proposed rule fro m State and 19 local officials. 20 F. Executive Order 13175: Consultation and Coordination with Indian Tribal 21 Governments 22 23 Executive Order 13175, entitled “Consultation and Coordination with Indian 24 Tribal Governments” (65 FR 67249, November 9, 2000), requires E PA to develop an 25Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 401 accountable process to ensure “meaningful and timely input by tribal officials in the 1 development of regulatory policies that have tribal implications.” This rule concerns the 2 establishment of O 3 NAAQS. The Tribal Authority Rule gives Tribes the opportunity to 3 develop and implement CAA programs such as the O 3 NAAQS, but it leaves to the 4 discretion of the Tribe whether to develop these programs and which programs, or 5 appropriate elements of a program, they will adopt. 6 This proposed rule does not have Tribal implications, as specified in Executive 7 Order 13175. Itdoes not have a substantial direct effect on one or more Indian Tribes, 8 since Tribes are not obligated to adopt or implement any NAAQS. Thus, Executive 9 Order 13175 does not app ly to this rule. 10 Although Executive Order 13175 does not appl y t o this rule, EPA contacted tribal 11 environmental professionals during the development of the March 2008 rule. The EPA 12 staff participated in the regularl y scheduled Tribal Air call sponsored b y the National 13 Tribal Air Association during the spring of 2007 as the proposal was under development. 14 EPA specificall y solicits additional comment on this proposed rule from Tribal officials. 15 G. Executive Order 13045: Protection of Children from Environm ental Health & 16 Safety Risks 17 18 Executive Order 13045, “Protection of Children from Environmental Health Risks 19 and Safety Risks” (62 FR 19885, April 23, 1997) applies to any rule that: (1) is 20 determined to be “economically significant” as defined under Executive Order 12866, 21 and (2) concerns an environmental health or safety risk that EPA has reason to believe 22 may

have a disproportionate effect on children. If the regulatory action meets both 23 criteria, the Agency must evaluate the environmental health or sa fety effects of the 24Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 402 planned rule on children, and explain why the planned regulation is preferable to other 1 potentially

effective and reasonabl y feasible alternatives considered b y the Agency

. 2 This proposed rule is subject to Executive Order 13045 because it is an 3 economicall y significant regulatory action as defined by Executive Order 12866, and we 4 believe that the environmental health risk addressed by this action may

have a 5 disproportionate effect on children. The proposed rule will establish uniform n ational 6 ambient air quality

standards for O 3 ; these standards are designed to protect public health 7 with an adequate margin of safety, as required b y CAA section 109. However, the 8 protection offered b y these standards may be especially important for children because 9 children, especiall y children with asthma, along with other sensitive population 10 subgroups such as all people with lung disease and people active outdoors, are potentiall y 11 susceptible to health effects resulting from O 3 exposure. Because children are considered 12 a potentially

susceptible population, we have carefully evaluated the environmental 13 health effects of exposure to O 3 pollution among children. Discussions of the results of 14 the evaluation of the scientific evidence, policy consideration s, and the exposure and risk 15 assessments pertaining to children are contained in sections II. B and II.C of this 16 preamble. A listing of the documents that contain the evaluation of scientific evidence, 17 policy

considerations, and exposure and risk assessments that pertain to children is found 18 in the section on Children’s Environmental Health in the Supplementary Information 19 section of this preamble, and a cop y of all documents have been placed in the public 20 docket for this action. The public is invited to s ubmit comments or identify peer21 reviewed studies and data that assess effects of early life exposure to O 3 . 22 H. Executive Order 13211: Actions that Significantly Affect Energy Supply, 23 Distribution or Use 24Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 403 1 This proposed rule is not a “significant energy action” as defined in Executive 2 Order 13211, “Actions Concerning Regulations That Significantl y Affect Energy Supply, 3 Distribution, or Use” (66 FR 28355 (May 22, 2001)) because in the Agency ’s judgment it 4 is not likely

to have a significant adverse effect on the supply , distribution, or use of 5 energy . The purpose of this rule is to establish revised NAAQS for O 3 . The rule does not 6 prescribe specific pollution control strategies b y which these ambient standards will be 7 met. Such strategies will be developed by States on a case
- by

- case basis, and EPA 8 cannot predict whether the control options selected by States will include regulations on 9 energy

suppliers, distributors, or users. Thus, EPA concludes that this rule is not likely to 10 have any adverse energy effe cts and does not constitute a significant energy action as 11 defined in Executive Order 13211. 12 I. National Technology Transfer and Advancement Act 13 Section 12(d) of the National Technology Transfer and Advancement Act of 1995 14 (NTTAA), Public Law No. 104

- 113, §12(d) (15 U.S.C. 272 note) directs EPA to use 15 voluntary

consensus standards in its regulatory activities unless to do so would be 16 inconsistent with applicable law or otherwise impractical. Voluntary consensus standards 17 are technical standards (e.g., mat erials specifications, test methods, sampling procedures, 18 and business practices) that are developed or adopted by voluntary

consensus standards 19 bodies. The NTTAA directs EPA to provide Congress, through OMB, explanations 20 when the Agency

decides not to us e available and applicable voluntary consensus 21 standards. 22 This proposed rulemaking does not involve technical standards. Therefore, EPA is 23 not considering the use of any voluntary consensus standards. 24Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 404 J. Executive Order 12898: Federal Actions to Address E nvironmental Justice in 1 Minority Populations and Low

-Income Populations 2 3 Executive Order 12898 (59 FR 7629 (Feb. 16, 1994)) establishes federal 4 executive policy

on environmental justice. Its main provision directs federal agencies, to 5 the greatest extent practicable and permitted b y law, to make environmental justice part 6 of their mission by

identifying and addressing, as appropriate, disproportionately high 7 and adverse human health or environmental effects of their programs, policies, and 8 activities on m inority populations and low

- income populations in the United States. 9 EPA has determined that this proposed rule will not have disproportionatel y high 10 and adverse human health or environmental effects on minority or low

- income 11 populations because it increases the level of environmental protection for all affected 12 populations without having any disproportionately high and adverse human health or 13 environmental effects on any population, including any minority or low

- income 14 population. The proposed rule wil l establish uniform national standards for O 3 air 15 pollution. 16 17 List of Subjects in 40 CFR Part 50 18 Environmental protection, Air pollution control, Carbon monoxide, Lead, Nitrogen 19 dioxide, Ozone, Particulate matter, Sulfur oxides. 20 21 22 23

_________________ 24 Date d: 25 26

_____________________________ 27 Lisa P. Jackson, Administrator 28 29Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 405 1 References 2 Abbey , D. E.; Nishino, N.; McDonnell, W. F.; Burchette, R. J.; Knutsen, S. F.; Beeson, 3 W. L .; Yang, J. X. (1999) L ong - term inhalable particles and other air pollutants 4 related to mortality in nonsmokers. Am. J. Respir. Crit. Care Med. 159: 373

- 382. 5 6 Abt Associates Inc. (1995) Ozone NAAQS benefits analy sis: California crops. Report to 7 U.S. EPA, July 1995
. EPA Docket No. A

- 95
- 58 Item I I
- I
- 3 8 9 Abt Associates Inc. (2007a) Ozone Health Risk Assessment for Selected Urban Areas. 10 Prepared for Office of Air Quality Planning and Standards, U.S. Environmental 11 Protection Agency , Research Triangle Park, NC. July 2007; EPA report no. EPA
12 452/R

- 07
- 009. Available online at: 13 http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_td.html

. 14 15 Abt Associates Inc. (2007b) Technical Report on Ozone Exposure, Risk, and Impacts 16 Asses sments for Vegetation: Final Report. Prepared for Office of Air Quality 17 Planning and Standards, U.S. Environmental Protection Agency , Research Triangle 18 Park, NC. January 2007; EPA report no. EPA
- 452/R

- 07
- 002. Available online at: 19 http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_td.html

. 20 21 Adams, W. C. (2002) Comparison of chamber and face

- mask 6.6

- hour exposures to 22 ozone on pulmonary function and sy

mptoms responses. Inhalation Toxicol. 14: 23 745
- 764. 24 25 Adams, W. C. (2003a) Comparison of chamber and face mask 6.6

- hour exposure to 0.08 26 ppm ozone via square

- wave and triangular profiles on pulmonary responses. 27 Inhalation Toxicol. 15: 265

- 281. 28 29 Adams, W. C. (2003b) Relation of pulm onary responses induced b y 6.6 hour exposures 30 to 0.08 ppm ozone and 2

- hour exposures to 0.30 ppm via chamber and face

- mask 31 inhalation. Inhalation Toxicol. 15: 745

- 759. 32 33 Adams, W. C. (2006) Comparison of chamber 6.6 hour exposures to 0.04

- 0.08 ppm 34 ozone v ia square

- wave and triangular profiles on pulmonary responses. Inhalation 35 Toxicol. 18: 127

- 136. 36 37 Adams, W.C. (2007) C omment on EPA memorandum: The effects of ozone on lung 38 function at 0.06 ppm in healthy adults. October 9. EPA

- HQ
- OAR
- 2005
- 0172
- 39 4783. 40 41 American Academy of Pediatrics, Committee on Environmental Health. (2004) Ambient 42 air pollution: health hazards to children. Pediatrics 114: 1699

- 1707. 43 44Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 406 American Thoracic Society . (1985) Guidelines as to what constitutes an adverse 1 respiratory

health effect, with special reference to epidemiologic studies of air 2 pollution. Am. Rev. Respir. Dis. 131: 666

- 668. 3 4 American Thoracic Society (2000) What constitutes an adverse effect of air pollution? 5 Am. J. Respir. Crit. Care Med. 161: pp. 665

- 673. 6 7 Andersen, C. P .; Hogsett, W. E.; Wessling, R.; Plocher, M. (1991) Ozone decreases 8 spring root growth and root carbohydrate content in ponderosa pine the ye ar 9 following exposure. Can. J. For. Res. 21: 1288

- 1291. 10 11 Anderson, H. R.; Spix, C.; Medina, S.; Schouten, J. P.; Ca stellsague, J.; Rossi, G.; 12 Zmirou, D.; Touloumi, G.; Wojty niak, B.; Ponka, A.; Bacharova, L.; Schwartz, J.; 13 Katsouyanni, K. (1997) Air pollution and daily admissions for chronic obstructive 14 pulmonary

disease in 6 European cities: results from the APHEA pro ject. Eur. 15 Respir. J. 10: 1064

- 1071. 16 17 Arbaugh, M.; By

tnerowicz, A.; Grulke, N.; Fenn, M.; Poth, M.; Temple, P.; Miller, P. 18 (2003) Photochemical smog effects in mixed conifer forests along a natural 19 gradient of ozone and nitrogen deposition in the San Berna rdino Mountains. 20 Environ. Int . 29: 401
- 406. 21 22 Arnold J.R.; R. L . Dennis; G. S. Tonnesen, (2003) Diagnostic evaluation of numerical air 23 quality

models with specialized ambient observations: testing the Community 24 Multiscale Air Quality modeling s ys tem (CMAQ) at selected SOS 95 ground sites, 25 Atmos. Environ. 37: 1185

- 1198. 26 27 Ashmore, M.; Emberson, L .; Karlsson, P. E.; Pleijel, H. (2004) New directions: a new 28 generation of ozone critical levels for the protection of vegetation in Europe 29 (correspondence). Atmos. Environ. 38: 2213

- 2214. 30 31 Arito, H.; Takahashi, M.; Iwasaki, T.; Uchiyama, I. (1997) Age

- related changes in 32 ventilatory

and heart rate responses to acute ozone exposure in the conscious rat. 33 Ind. Health 35: 78

- 86. 34 35 Avol, E. L .; Gauderman , W. J.; Tan, S. M.; L ondon, S. J.; Peters, J. M. (2001) 36 Respiratory effects of relocating to areas of differing air pollution levels. Am. J. 37 Respir. Crit. Care Med. 164: 2067

- 2072. 38 39 Awmack, C. S.; Harrington, R.; Lindroth, R. L . (2004) Aphid individual performance 40 may

not predict population responses to elevated CO2 or O 3 . Global Change Biol. 41 10: 1414
- 1423. 42 43 Barnes, J. D.; Eamus, D.; Brown, K. A. (1990) The influence of ozone, acid mist and 44 soilnutrient status on Norway spruce [Picea abies (L.) Karst.]: II . photosy nthesis, 45Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 4 07 dark respiration and soluble carbohydrates of trees during late autumn. New 1 Phy

tol. 115: 149

- 156. 2 3 Bascom, R.; Naclerio, R. M.; Fitzgerald, T. K.; Kagey

- Sobotka, A.; Proud, D. (1990) 4 Effect of ozone inhalation on the response to nasal challenge with antigen of 5 allergic subjects. Am. Rev. Respir. Dis. 142: 594

- 601. 6 7 Basha, M. A.; Gross, K. B.; Gwizdala, C. J.; Haidar, A. H.; Popovich, J., Jr. (1994) 8 Bronchoalveolar lavage neutrophilia in asthmatic and healthy volunteers after 9 controlled exp osure to ozone and filtered purified air. Chest 106: 1757

- 1765. 10 11 Beedlow P.A., Tingey D.T., Phillips D.L ., Hogsett W.E. & Olszy k D.M. (2004) Rising 12 atmospheric CO2 and carbon sequestration in forests. Frontiers in Ecology and 13 the Environment 2, 315

–322. 14 15 B eeson, W. L.; Abbey , D. E.; Knutsen, S. F. (1998) L ong - term concentrations of ambient 16 air pollutants and incident lung cancer in California adults: results from the 17 AHSMOG study . Environ. Health Perspect. 106: 813

- 823. 18 19 Bell, M. L.; McDermott, A.; Zeger, S . L.; Samet, J. M.; Dominici, F. (2004) Ozone and 20 short

- term mortality in 95 US urban communities, 1987

- 2000. JAMA J. Am. Med. 21 Assoc. 292: 2372
- 2378. 22 23 Bell, M. L.; Dominici, F.; Samet, J. M. (2005) A meta

- anal ys is of time

- series studies of 24 ozone and mortality with comparison to the national morbidity , mortality , and air 25 pollution study . Epidemiology 16: 436
- 445. 26 27 Bell, M. L.; Peng, R. D.; Dominici, F. (2006) The exposure

- response curve for ozone and 28 risk of mortality and the adequacy

of current ozone regul ations. Environ. Health 29 Perspect.: doi:10.1289/ehp.8816. Available online at: http://dx.doi.org/ [23 30 January , 2006]. 31 32 Bosson, J.; Stenfors, N.; Bucht, A.; Helleday , R.; Pourazar, J.; Holgate, S. T.; Kelly , F. J.; 33 Sandström, T.; Wilson, S.; Frew, A. J.; Blomberg, A. (2003) Ozone

- induced 34 bronchial epithelial cy tokine expression differs between healthy and asthmatic 35 subjects. Clin. Exp. Allergy 33: 777
- 782. 36 37 Brauer, M.; Blair, J.; Vedal, S. (1995) Effect of ambient ozone exposure on lung function 38 in farm w orkers. Am. J. Respir. Crit. Care Med. 154: 981

- 987. 39 40 Brauer, M.; Blair, J.; Vedal, S. (1996) Effect of ambient ozone exposure on lung function 41 in farm workers. Am. J. Respir. Crit. Care Med. 154: 981

- 987. 42 43 Brauer, M.; Brook, J. R. (1997) Ozone personal exposures and health effects for selected 44 groups residing in the Fraser Valley . In: Stey n, D. G.; Bottenheim, J. W., eds. The 45Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 408 Lower Fraser Valley

Oxidants/Pacific '93 Field Study . Atmos. Environ. 31: 2113

- 1 2121. 2 3 Black, V. J.; Black, C. R.; Roberts, J. A.; St ewart, C. A. (2000) Impact of ozone on the 4 reproductive development of plants. New Phy tol. 147: 421

- 447. 5 6 Brook, R. D.; Brook, J. R.; Urch, B.; Vincent, R.; Rajagopalan, S.; Silverman, F. (2002) 7 Inhalation of fine particulate air pollution and ozone causes acute arterial 8 vasoconstriction in healthy adults. Circulation 105: 1534

- 1536. 9 10 Brown, J. S. The effects of ozone on lung function at 0.06 ppm in healthy adults. June 11 14, 2007. Memo to the Ozone NAAQS Review Docket. EPA

- HQ
- OAR
- 20 05
- 12 0172
- 0175. Available online at: 13 http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_td.html

. 14 15 Burnett, R. T.; Dales, R. E.; Raizenne, M. E.; Krewski, D.; Summers, P. W.; Ro berts, G. 16 R.; Raad

- Young, M.; Dann, T.; Brook, J. (1994) Effects of low ambient levels of 17 ozone and sulfates on the frequency of respiratory

admissions to Ontario 18 hospitals. Environ. Res. 65: 172

- 194. 19 20 Burnett, R. T.; Brook, J. R.; Yung, W. T.; Dales, R. E .; Krewski, D. (1997a) Association 21 between ozone and hospitalization for respiratory diseases in 16 Canadian cities. 22 Environ. Res. 72: 24

- 31. 23 24 Burnett, R. T.; Cakmak, S.; Brook, J. R.; Krewski, D. (1997b) The role of particulate size 25 and chemistry in the a ssociation between summertime ambient air pollution and 26 hospitalization for cardiorespiratory diseases. Environ. Health Perspect. 105: 614

- 27 620. 28 29 Burns, R. M., Honkala, B. H., tech. coords. (1990) Silvics of North America: 1. Conifers; 30 2. Hardwoods. Agriculture Handbook 654. U.S. Department of Agriculture, Forest 31 Service, Washington, DC. vol.2, p. 877
. 32 33 By un, D.W., Ching, J.K.S. (Eds.), 1999. Science Algorithms of the EPA Models

- 3 34 Community

Multiscale Air Quality

Model (CMAQ) Modeling S ys tem. EPA/600/R

35 99/03 0, U.S. Environmental Protection Agency , Office of Research and 36 Development, Washington, DC 20460. 37 38 Campbell, S.; Temple, P.; Pronos, J.; Rochefort, R.; Andersen, C. (2000) Monitoring for 39 ozone injury in west coast (Oregon, Washington, California) forests in 1998. 40 Portland, OR: U.S. Department of Agriculture, Forest Service, Pacific Northwest 41 Research Station; general technical report no. PNW

- GTR
- 495. Available: 42 http://www.fs.fed.us/pnw/gtrs.htm [11 April, 2003]. 43 44 Centers for Disease Control and Prevention. (2004) The health consequences of smoking: 45 a report of the Surgeon General. Atlanta, GA: U.S. Department of Health and 46Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 409 Human Services, National Center for Chronic Disease Prevention and Health 1 Promotion, Office on Smoking and Health. Available: 2 http://www .cdc.gov/tobacco/sgr/sgr_2004/chapters.htm (18 August, 2004). 3 4 Chappelka, A. H. (2002) Reproductive development of blackberry (Rubus cuneifolius) as 5 influenced b y ozone. New Phytol. 155: 249

- 255. 6 7 Chappelka, A. H.; Samuelson, L . J. (1998) Ambient ozone eff ects on forest trees of the 8 eastern United States: a review. New Phy tol. 139: 91

- 108. 9 10 Chen, L .; Jennison, B. L.; Yang, W.; Omaye, S. T. (2000) Elementary school 11 absenteeism and air pollution. Inhalation Toxicol. 12: 997

- 101
. 12 13 Chen, C.
- Y.; Bonham, A. C.; Plopper, C. G.; Joad, J. P. (2003) Plasticity in respiratory 14 motor control: selected contribution: neuroplasticity in nucleus tractus solitarius 15 neurons following episodic ozone exposure in infant primates. J. Appl. Phy siol. 16 94: 819
- 8 27. 17 18 Clean Air Scientific Advisory Committee (CASAC) (2006) Transcript of Public Meeting 19 Held in Research Triangle Park, N.C. on August 24, 2006. 20 21 Cox, W. M.; Camalier, L. (2006) The effect of measurement error on 8

- hour ozone 22 design concentrations. Memo to the Ozone NAAQS Review Docket. EPA

- HQ
23 OAR
- 2005
- 0172
- 0026. Available online at: 24 http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_td.html

. 25 26 Coulston, J. W., Smith , G. C. and Smith, W. D. (2003) “Regional assessment of ozone 27 sensitive tree species using bioindicator plants.” Environmental Monitoring and 28 Assessment 83: 113

– 127. 29 30 Coulston, J. W., K. H. Ri itters and G. C. Smith (2004) A Preliminary Assessment of the 31 Montréal P rocess Indicators of Air Pollution for the United States. Environmental 32 Monitoring and Assessment 95: 57

–74. 33 34 Dann, M. S.; Pell, E. J. (1989) Decline of activity and quantity of ribulose 35 bisphosphatecarbox yl ase/oxygenase and net photosy nthesis in ozone

- tre ated 36 potato foliage. PlantPhy siol. 91: 427
- 432. 37 38 David, G. L.; Romieu, I .; Sienra

- Monge, J. J.; Collins, W. J.; Ramirez

- Aguilar, M.; Del 39 Rio

-Navarro, B. E.;Reyes - Ruiz, N. I .; Morris, R. W.; Marzec, J. M.; L ondon, S. J. 40 (2003) Nicotinamide adenine dinucleotide (phosphate) reduced:quinone 41 oxidoreductase and glutathione s

- transferase m1 poly morphism and childhood 42 asthma. Am. J. Respir. Crit. Care Med. 168: 1199

- 1204. 43 44 Davison, A. W.; Reiling, K. (1995) A rapid change in ozone resistance of Plantago major 45 after summers with high ozone concentrations. New Phy tol . 131: 337
- 344. 46Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 410 1 Devlin, R. B.; McDonnell, W. F.; Koren, H. S.; Becker, S. (1990) Prolonged exposure of 2 humans to 0.10 and 0.08 ppm ozone results in inflammation in the lung. Presented 3 at: 83rd annual meeting of the Air & Waste Management Association; June; 4 Pittsburgh, PA. Pittsburgh, PA: Air & Waste Management Association; paper no. 5 90
- 150.2. 6 7 Devlin, R. B.; McDonnell, W. F.; Mann, R.; Becker, S.; House, D. E.; Schreinemachers, 8 D.; Koren, H. S. (1991) Expo sure of humans to ambient levels of ozone for 6.6 9 hrs causes cellular and biochemical changes in the lung. Am. J. Respir. Cell Mol. 10 Biol. 4: 72

- 81. 11 12 Dickson, R. E., Lewin K. F., Isebrands J. G., Coleman M. D., Heilman W. E., 13 Riemenschneider D. E., Sober J. , Host G. E., Zak D. F., Hendrey G. R., Pregitzer 14 K. S. and Karnosky D. F. (2000) Forest atmosphere carbon transfer storage

- II 15 (FACTS II)

– The aspen free

- air CO 2 and O 3 enrichment (FACE) project in an 16 overview. USDA Forest Service North Central Research Station. General Tech. 17 Rep. NC
- 214. 68pp. 18 19 Dietert, R. R.; Etzel, R. A.; Chen, D.; Halonen, M.; Holladay , S. D.; Jarabek, A. M.; 20 Landreth, K.; Peden, D. B.; Pinkerton, K.; Smialowicz, R. J.; Zoetis, T. (2000) 21 Workshop to identify critical window of expos ure for children's health: immune and 22 respiratory

s ys tems work group summary . Environ. Health Perspect. Suppl. 108(3): 23 483
- 490. 24 25 Dockery , D. W.; Pope, C. A., III; Xu, X.; Spengler, J. D.; Ware, J. H.; Fay , M. E.; Ferris, 26 B. G., Jr.; Speizer, F. E. (1993) An association between air pollution and mortality 27 in six U.S. cities. N. Engl. J. Med. 329: 1753

- 1759. 28 29 Dominici, F.; McDermott, A.; Daniels, M.; Zeger, S. L .; Samet, J. M. (2003) Mortality 30 among residents of 90 cities. In: Revised anal ys es of time

- series studies of air 31 pollution and health. Special report. Boston, MA: Health Effects Institute; pp. 9

- 32 24. Available: http://www.healtheffects.org/Pubs/TimeSeries.pdf [12 May , 33 2004]. 34 Duff, M., Horst, R. L., Johnson, T. R. (1998) “Quadratic Rollback: A Technique to 35 Model Ambient Concentrations Due to Undefined Emission Controls.” Presented 36 at the Air and Waste Management Annual Meeting. San Diego, California. June 37 14
- 18, 1998. 38 39 Eder, B. and S. Yu, 2006: A performance evaluation of the 2004 release of Models

- 3 40 CMAQ, Atmos. Environ. 40: 4811
- 4824. Special issue on Model Evaluation: 41 Evaluation of Urban and Regional Eulerian Air Quality Models. 42 43 Environmental Protection Agency (1986) Air quality criteria for ozone and other 44 photochemical oxidants. Research Triang le Park, NC: Office of Health and 45 Environmental Assessment, Environmental Criteria and Assessment Office; 46Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 411 report nos. EPA
- 600/8

- 84
- 020aF
- eF. 5v. Available from: NTIS, Springfield, VA; 1 PB87
- 142949. 2 3 Environmental Protection Agency (1996a) Air quality

criteria for ozone and related 4 photochemical oxidants. Research Triangle Park, NC: Office of Research and 5 Development; EPA report no. EPA/600/AP

- 93/004aF

- cF. 3v. Available from: 6 NTI S, Springfield, VA; PB96

- 185582, PB96
- 185590, and PB96

- 185608. Available 7 onlin e at: http://cfpub.epa.gov/ncea/cfm/recordisplay .cfm?deid=2831

. 8 9 Environmental Protection Agency (1996b) Review of National Ambient Air Quality 10 Standards for Ozone: Assessment of Sci entific and Technical Information. OAQPS 11 Staff Paper (Final) Research Triangle Park, NC: Office of Air Quality Planning and 12 Standards; EPA report no. EPA/452/R

- 96
- 007. Available online at: 13 http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_pr_sp.html

. 14 15 Environmental Protection Agency (2002) Project Work Plan for Revised Air Quality 16 Criteria for Ozone and Related Photochemical Oxidants. Research Triangle Park, 17 NC: National Center for Environmental Assessment; EPA report no. NCEA

- R
18 1068. 19 20 Environmental Protection Agency (2004) The Ozone Report: Measuring Progress 21 through 2003. EPA/454/K

- 04
- 001. Office of Air Quality Planning and 22 Standards, Research Triangle Park, NC. 23 24 Environmental Protection Agency (2005a) Air Quality

Criteria for Ozone and Related 25 Photochemical Oxidants (First External Review Draft). Washington, DC: National 26 Center for Environmental Assessment; EPA report no. EPA/600/R

- 05/004aA

- cA. 27 Available online at: http://cfpub.epa.gov/ncea/cfm/recordisplay .cfm?deid=114523

. 28 29 Environmental Protection Agency (2005b) Air Quality

Criteria for Ozone and Related 30 Photochemical Oxidants (Second External Review Draft) Washington, DC: 31 National Center for Environmental Assessment; EPA report no. EPA/600/R

32 05/004aB

- cB. Available online at: 33 http://cfpub.epa.gov/ncea/cfm/recordisplay .cfm?deid=137307
. 34 35 Environmental Protection Agency (2005c) Review of the national ambient air quality 36 standards for ozone: assessment of scientific and technical information. OAQPS 37 staff paper (First Draft). Research Triangle Park, NC: Office of Air Quality 38 Planning and Standards; EPA report no. EPA

- 452/D

- 05
- 002. Available online at: 39 http://epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_sp.html

. 40 41 Environmental Protection Agency (2005d) Health Asse ssment Plan for Review of the National Ambient Air Quality Standards for O zone. Office of Air Quality Planning and Standards, Research Triangle Park, NC. April 2005 . Available electronically on the internet at: http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_pd.html

. 42Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 412 Environmental Protection Agency (2006a) Air Quality

Criteria for Ozone and Related 1 Photochemical Oxidants. (Final) Washington, DC: National Center for 2 Environm ental Assessment; EPA report no. EPA/600/R

- 05/004aB

- cB. Available 3 online at: http://cfpub.epa.gov/ncea/cfm/recordisplay .cfm?deid=149923

. 4 5 Environmental Protection Agency (2006b) Review of the national ambient air quality 6 standards for ozone: assessment of scientific and technical information. OAQPS 7 staff paper. (Second Draft). Research Triangle Park, NC: Office of Air Quality 8 Planning and Standards; EPA report no. EPA

- 452/D

- 05
- 002. Available online at: 9 http://epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_sp.html

. 10 11 Environmental Protection Agency (2007a) Review of the national ambient air quality 12 standards for ozo ne: assessment of scientific and technical information. OAQPS 13 staff paper. (Final) January 2007. Research Triangle Park, NC: Office of Air 14 Quality

Planning and Standards; EPA report no. EPA

- 452/R

- 07
- 003. Available 15 online at: http://epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_sp.html

. 16 17 Environmental Protection Agency (2007b) Review of the national ambient air quality 18 standards for ozone: assessment of scientific and technical information. OAQPS 19 staff paper. (Updated Final) July 2007. Research Triangle Park, NC: Office of Air 20 Quality

Planning and Standards; EPA report no. EPA

- 452/R

- 07
- 007. Available 21 online at: http://epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_sp.html

. 22 23 Environmental Protection Agency (2007c) Ozone Population Exposure Analy sis for 24 Selected Urban Areas. (Updated Final) July 2007. Research Triangle Park, NC: 25 Office of Air Quality Planning and Stand ards; EPA report no. EPA

- 452/R

- 07
- 010. 26 Available online at: 27 http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_td.html

. 28 29 Environmental Protection Agency (2008) Responses to Significant Comments on the 30 2007 Proposed Rule on the National Ambient Air Quality Standards for Ozone 31 (July

11, 2007; 72 FR 37818). March 2008. Research Triangle Park, NC; Office of 32 Air Quality

Planning and Standards. Available online at: 33 http://www.epa.g ov/ttn/naaqs/standards/ozone/s_o3_cr_rc.html

. 34 35 Enviro nmental Protection Agency (2009) Provisional Assessment of Recent Studies on 36 Health and Ecological Effects of Ozone Exposure. September 2009. Research 37 Triangle Park : National Center for Environmental Assessment; EPA report no. 38 EPA/ 600/R

- 09/101

. 39 40 Evans, M. J.; Fanucchi, M. V.; Baker, G. L.; Van Winkle, L . S.; Pantle, L. M.; Nishio, S. 41 J.; Schelegle, E. S.; Gershwhin, L . J.; Miller, L . A.; Hyde, D. M.; Sannes, P. L .; 42 Plopper, C. G. (2003) Aty pical development of the tracheal basement membrane 43 zone of infant rhesus monkey s exposed to ozone and allergen. Am. J. Phy siol. 44 285: L 931
- L939. 45 46Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 413 Felzer, B.; Kickligher, D.; Melillo, J.; Wang, C.; Zhuang, Q.; Prinn, R. (2004) Effects of 1 ozone on net primary production and carbon sequestration in the conterminous 2 United States using a biogeochemistry model. Tellus B 56 (3), 230

- 248. 3 4 Fiore, A. M.; Jacob, D. J.; Bey , I.; Yantosca, R. M.; Field, B. D.; Fusco, A. C.; 5 Wilkinson, J. G. (2002) Background ozone over the United States in summer: 6 origin, trend, and contribution to pollution episodes. J. Geophy s. Res. (Atmos.) 7 107(D15): 10.1029/2001JD000982. 8 9 Fiore, A. M.; Jacob, D. J.; Liu, H.; Yantosca, R. M.; Fairlie, T. D.; Fusco, A. C.; Li, Q. 10 (2003) Variability in surface ozone background over the United States: 11 implications for Air Quality Policy . J. of Geophy sical Research, 108(D24)19

- 1
- 19
- 12 12. 13 14 Fiscus, E. L.; Reid, C. D.; Miller, J. E.; Heagle, A. S. (1997) Elevated CO 2 reduces O 3 15 flux and O 3 - ind uced yield losses in soy

beans: possible implications for elevated 16 CO 2 stu dies. J. Exp. Bot. 48: 307

- 313. 17 18 Folinsbee, L. J.; McDonnell, W. F.; Horstman, D. H. (1988) Pulmonary function and 19 sy

mptom responses after 6.6

- h our exposure to 0.12 ppm ozone with mod erate 20 exercise. JAPCA 38: 28

- 35. 21 22 Folinsbee, L. J.; Horstman, D. H.; Kehrl, H. R.; Harder, S.; Abdul

- Salaam, S.; Ives, P. J. 23 (1994) Respiratory responses to repeated prolonged exposure to 0.12 ppm ozone. 24 Am. J. Respir. Crit. Care Med. 149: 98

- 105. 25 26 Folinsb ee, L. J.; Hazucha, M. J. (2000) Time course of response to ozone exposure in 27 healthy

adult females. Inhalation Toxicol. 12: 151

- 167. 28 29 Foster, W. M.; Silver, J. A.; Groth, M. L . (1993) Exposure to ozone alters regional 30 function and particle dosimetry in th e human lung. J. Appl. Physiol. 75: 31 1938
- 1945. 32 33 Foster, W. M.; Weinmann, G. G.; Menkes, E.; Macri, K. (1997) Acute exposure of 34 humans to ozone impairs small airway function. Ann. Occup. Hyg. 41(suppl. 1): 35 659
- 666. 36 Frampton, M. W.; Morrow, P. E.; Torres, A. ; Cox, C.; Voter, K. Z.; Utell, M. J.; Gib b, F. 37 R.; Speers, D. M. (1997) Ozone responsiveness in smokers and nonsmokers. Am. 38 J. Respir. Crit. Care Med. 155: 116
- 121. 39 40 Galizia, A.; Kinney , P. L. (1999) Long

- term residence in areas of high ozone: 41 association s with respiratory health in a nationwide sample of nonsmoking young 42 adults. Environ. Health Perspect. 107: 675

- 679. 43 44 Gauderman, W. J.; McConnell, R.; Gilliland, F.; London, S.; Thomas, D.; Avol, E.; Vora, 45 H.; Berhane, K.; Rappaport, E. B.; Lurmann, F.; Margolis, H. G.; Peters, J. (2000) 46Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 414 Association between air pollution and lung function growth in southern California 1 children. Am. J. Respir. Crit. Care Med. 162: 1383

- 1390. 2 3 Gauderman, W. J.; Gilliland, G. F.; Vora, H.; Avol, E.; Stram, D.; McConnell, R.; 4 Thomas, D.; Lurmann, F.; Margolis, H. G.; Rappaport, E. B.; Berhane, K.; Peters, 5 J. M. (2002) Association between air pollution and lung function growth in 6 southern California children: results from a second cohort. Am. J. Respir. Crit. 7 Care Med. 166: 76

- 84
. 8 9 Gauderman, W. J.; Avol, E.; Gilliland, F.; Vora, H.; Thomas, D.; Berhane, K.; 10 McConnell, R.; Kuenzli, N.; Lurmann, F.; Rappaport, E.; Margolis, H.; Bates, D.; 11 Peters, J. (2004a) The effect of air pollution on lung development from 10 to 18 12 ye ars of age. N. Engl. J. Med. 351: 1057

- 1067. 13 14 Gauderman, W. J.; Avol, E.; Gilliland, F. (2004b) Air pollution and lung function [reply 15 letter]. N. Engl. J. Med. 351: 2653. 16 17 Gent, J. F.; Triche, E. W.; Holford, T. R.; Belanger, K.; Bracken, M. B.; Beckett, W. S.; 18 Lead erer, B. P. (2003) Association of low

- level ozone and fine particles with 19 respiratory

s ymptoms in children with asthma. JAMA J. Am. Med. Assoc. 290: 20 1859
- 1867. 21 22 Gilliland, F. D.; Berhane, K.; Rappaport, E. B.; Thomas, D. C.; Avol, E.; Gauderman, W. 23 J.; L o ndon, S. J.; Margolis, H. G.; McConnell, R.; Islam, K. T.; Peters, J. M. 24 (2001) The effects of ambient air pollution on school absenteeism due to 25 respiratory

illnesses. Epidemiology

12: 43
- 54. 26 27 Goldstein, A. H.; Millet, D. B.; McKay , M.; Jaegle, L .; Horow itz, L .; Cooper, O. ; 28 Hudman, R.; Jacob, D; Oltmans, S; Clarke, A. (2004) Impact of Asian emissions on 29 observations at Trinidad Head, California, during ITCT 2K2. J. of Geophys ical 30 Research, 109(D23S17), doi: 10.1029/2003JD004406. 31 32 Gong, H., Jr.; Wong, R.; Sarma, R. J.; Linn, W. S.; Sullivan, E. D.; Shamoo, D. A.; 33 Ander son, K. R.; Prasad, S. B. (1998 ) Cardiovascular effects of ozone exposure in 34 human volunteers. Am. J. Respir. Crit. Care Med. 158: 538
- 546. 35 36 Goodale, C. L., Apps, M. J., Birdsey , R. A., Field, C. B., Heath, L. S., Houghton, R. A., 37 Jenkins, J. C., Kohlmaier, G. H., Kurz, W., Liu, S., Nabuurs, G.

- J., Nilsson, S. 38 and Shvidenko, A. Z. (2002) Forest carbon sinks in the northern hemisphere. 39 Ecol. Appl. 12, 891

– 899. 40 41 Grantz, D.A., McCool, P.H. (1992) Effect of ozone on Pima and Acala cottons in the San 42 Joaquin Valley . In: Herber, D.J., Richter, D.A. (Eds.), Proceedings 1992 Beltwide 43 Cotton Conferences, vol 3.National Cotton Council of America, Memphis, TN, 44 pp. 1082

– 1084. 45 46Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 415 Greer, J. R.; Abbey , D. E.; Burchette, R. J. (1993) Asthma related to occupational and 1 ambient air pollutants in nonsmokers. J. Occup. Med. 35: 909

- 915. 2 3 Gregg, J. W.; Jones, C. G.; Dawson, T. E. (2003) Urbanization effects on tree growth in 4 the vicinity

of New York City

. Nature 424: 1 83
- 187. 5 6 Grulke, N. E.; Andersen, C. P.; Fenn, M. E.; Miller, P. R. (1998) Ozone exposure and 7 nitrogen deposition lowers root biomass of ponderosa pine in the San Bernardino 8 Mountains, California. Environ. Pollut. 103: 63

- 73. 9 10 Grulke, N. E.; Balduman, L . ( 1999) Deciduous conifers: high N deposition and O 3 11 exposure effects on growth and biomass allocation in ponderosa pine. Water Air 12 Soil Pollut. 116: 235

- 248. 13 14 Gry paris, A.; Forsberg, B.; Katsouyanni, K.; Analitis, A.; Touloumi, G.; Schwartz, J.; 15 Samoli, E.; Medina, S.; Anderson, H. R.; Niciu, E. M.; Wichmann, H.

- E.; Kriz, 16 B.; Kosnik, M.; Skorkovsky , J.; Vonk, J. M.; Dörtbudak, Z. (2004) Acute effects 17 of ozone on mortality from the "air pollution and health: a European approach" 18 project. Am. J. Respir. Crit. Care Med. 170: 1080

- 1087. 19 20 Guderian, R. (1977) Discussion of the suitability of plant responses as a basis for air 21 pollution control measures. In: Billings, W. D.; Golley , F.; Lange, O. L.; Olson, J. 22 S., eds. Air pollution: phytotoxicity of acidic gases and its significance in air 23 pollution control. Berlin, Federal Republic of Germany : Springer Verlag; pp. 75

- 24 97. 25 26 Hanson, P., Samuelson, L., Wullschleger, S., Tabberer, T.; Edwards, G. (1994) “Seasonal 27 patterns of light

- saturated photosy nthesis and leaf con ductance for mature and 28 seedling Quercus rubra L. foliage: differential sensitivity to ozone exposure.” Tree 29 Phy siology

14:1351
- 1366. 30 31 Hazucha, M. J.; Folinsbee, L . J.; Seal, E., Jr. (1992) Effects of steady

- state and variable 32 ozone concentration profiles on pulmonary function. Am. Rev. Respir. Dis. 146: 33 1487
- 1493. 34 35 Hazucha, M. J.; Folinsbee, L . J.; Bromberg, P. A. (2003) Distribution and reproducibility 36 of spirometric response to ozone by gender and age. J. Appl. Phy siol. 95: 1917

- 37 1925. 38 39 Heck, W. W.; Cowl ing, E. B. (1997) The need for a long term cumulative secondary 40 ozone standard

- an ecological perspective. EM (January): 23

- 33
. 41 42 Henderson, R. (2006a) Letter from CASAC Chairman Rogene Henderson to EPA 43 Administrator Stephen Johnson. February 16, 2006, EPA
- CASAC
- 06
- 003. 44 45Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 416 Henderson, R. (2006b) Letter from CASAC Chairman Rogene Henderson to EPA 1 Administrator Stephen Johnson. June 5, 2006, EPA

- CASAC
- 06
- 007. 2 3 Henderson, R. (2006c) Letter from CASAC Chairman Rogene Henderson to EPA 4 Administrator Stephen Johnson. October 24, 2006, EPA

- CASAC
- 07
- 001. 5 6 Henderson, R. (2007) Letter from CASAC Chairman Rogene Henderson to EPA 7 Administrator Stephen Johnson. March 26, 2007, EPA

- CASAC
- 07
- 002. 8 9 Henderson , R. (2008 ) Letter from CASAC Chairman Rogene Henderson to EPA 10 Administrator Stephen Johnson. April 7, 2008, EPA

- CASAC
- 08
- 009
. 11 12 Hill, A.B. (1965) The environment and disease: association or causation? Proc. R. Soc. 13 Med. 58: 295

- 300. 14 15 Hiltermann, J. T. N.; L apperre, T. S.; Van Bree, L.; Steerenberg, P. A.; Brahim, J. J.; 16 Sont, J. K.; Sterk, P. J.; Hiemstra, P. S.; Stolk, J. (1999) Ozone

- induced 17 inflammation assessed in sputum and bronchial lavage fluid from asthmatics: a 18 new noninvasive tool in epidemiologic studies on air pollution and asthma. Free 19 Radical Biol. Med. 27: 1 448
- 1454. 20 21 Hoek, G. (2003) Dail y mortality and air pollution in The Netherlands. In: Revised 22 anal ys es of time

- series studies of air pollution and health. Special report. Boston, 23 MA: Health Effects Institute; pp. 133

- 142. Available: 24 http://www.healtheffects .org/Pubs/TimeSeries.pdf [12 May , 2004]. 25 26 Hoek, G.; Brunekreef, B.; Verhoeff, A.; Van Wijnen, J.; Fischer, P. (2000) Daily 27 mortality

and air pollution in the Netherlands. J. Air Waste Manage. Assoc. 50: 28 1380
- 1389. 29 30 Hoek, G.; Brunekreef, B.; Fischer, P.; Van Wijnen, J. (2001) The association between air 31 pollution and heart failure, arrhythmia, embolism, thrombosis, and other 32 cardiovascular causes of death in a time series study . Epidemiology 12: 355
- 357. 33 34 Hogsett, W. E.; Tingey , D. T.; Hendricks, C.; Rossi, D. (1989) Sensitivity of western 35 conifers to SO2 and seasonal interaction of acid fog and ozone. In: Olson, R. K.; 36 Lefohn, A. S., eds. Effects of air pollution on western forests [an A&WMA 37 sy

mposium; June; Anaheim, CA]. Air Pollution Control Association; p p. 469
- 491 38 (APCA transactions series: no. 16). 39 40 Holton, M. K.; Lindroth, R. L .; Nordheim, E. V. (2003) Foliar quality influences tree

41 herbivore

- parisitoid interactions: effects of elevated CO2, O 3 , and plant genoty pe. 42 Oecologia 137: 233

- 244. 43 44Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 417 Holz, O.; Müc ke, M.; Paasch, K.; Böhme, S.; Timm, P.; Richter, K.; Magnussen, H.; 1 Jörres, R. A. (2002) Repeated ozone exposures enhance bronchial allergen 2 responses in subjects with rhinitis or asthma. Clin. Exp. Allergy . 32: 681
- 689. 3 4 Höppe, P.; Praml, G.; Rabe, G.; Lindner, J.; Fruhmann, G.; Kessel, R. (1995 ) 5 Environmental ozone field study on pulmonary

and subjective responses of 6 assumed risk groups. Environ. Res. 71: 109

- 121. 7 8 Horst, R.; Duff, M. (1995). Concentration data transformation and the quadratic rollback 9 m ethodology

(Round 2, Revised). Unpublished memorandum to R. Rodríguez, U.S. 10 EPA, June 8. 11 12 Horstman, D. H.; Folinsbee, L. J.; Ives, P. J.; Abdul

- Salaam, S.; McDonnell, W. F. 13 (1990) Ozone concentration and pulmonary response relationships for 6.6

- hr 14 exposure s with five hours of moderate exercise to 0.08, 0.10, and 0.12 ppm. Am. 15 Rev. Respir. Dis. 142: 1158

- 1163. 16 17 Horstman, D. H.; Ball, B. A.; Brown, J.; Gerrity, T.; Folinsbee, L. J. (1995) Comparison 18 of pulmonary responses of asthmatic and nonasthmatic subject s performing light 19 exercise while exposed to a low level of ozone. Toxicol. Ind. Health 11: 369

- 385. 20 21 Huang, Y.; Dominici, F.; Bell, M. L. (2005) Bayesian hierarchical distributed lag models 22 for summer ozone exposure and cardio

- respiratory mortality. Environmetrics 16: 23 547
- 562. 24 25 Is ebrands, J. G.; Dickson, R. E.; Rebbeck, J.; Karnosky , D. F. (2000) Interacting effects 26 of multiple stresses on growth and phy siological processes in northern forest trees. 27 In: Mickler, R. A.; Birsdey , R. A.; Hom, J., eds. Respons es of northern U.S. forests 28 to environmental change. New York, NY: Springer

- Verlag; pp. 149

- 180. 29 (Ecological studies: v. 139). 30 31 Is ebrands, J. G.; McDonald, E. P.; Kruger, E.; Hendrey , G.; Percy , K.; Pregitzer, K.; 32 Sober, J.; Karnosky , D. F. (2001) Growth responses of Populus tremuloides clones 33 to interacting carbon dioxide and tropospheric ozone. Environ. Pollut. 115: 359

- 34 371. 35 36 Ito, K.; De Leon, S. F.; Lippmann, M. (2005) Associations between ozone and daily 37 mortality , anal ys is and meta

- analy sis. Epidemiol ogy 16: 446
- 457. 38 39 Jacobson, J. S. (1977) The effects of photochemical oxidants on vegetation. In: Ozon und 40 Begleitsubstanzen im photochemischen Smog: das Kolloquium [Ozone and 41 related substances in photochemical smog: the colloquium]; September 1976; 42 Dusse ldorf, Federal Republic of Germany. Dusseldorf, Federal Republic of 43 Germany: VDI
- Verlag GmbH; pp. 163

- 173. (VDI

- Berichte nr. 270). 44 45Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 418 Johnson, T. (1997) “Sensitivity of Exposure Estimates to Air Quality Adjustment 1 Procedure,” Letter to Harvey Richmond, Offic e of Air Quality Planning and 2 Standards, U.S. Environmental Protection Agency, Research Triangle Park, North 3 Carolina. 4 5 Jörres, R.; Nowak, D.; Magnussen, H.; Speckin, P.; Koschy k, S. (1996) The effect of 6 ozone exposure on allergen responsiveness in subject s with asthma or rhinitis. 7 Am. J. Respir. Crit. Care Med. 153: 56

- 64. 8 9 Karnosky, D. F., Z.E.Gagnon, R.E. Dickson, M.D. Coleman, E.H. Lee, J.G. I sebrands, 10 (1996) “Changes in growth, leaf abscission, biomass associated with seasonal 11 tropospheric ozone expos ures of Populus tremuloides clones and seedlings.” Can. 12 J. For. Res. 26: 23
- 37. 13 14 Karnosky, D.F., B. Mankovska, K. Percy, R.E. Dickson, G.K. Podila, J. Sober, A. 15 Noormets, G. Hendrey , M.D. Coleman, M. Kubiske, K.S. Pregi tzer, and J.G. 16 Is ebrands (1999) “Eff ects of tropospheric O 3 on trembling aspen and interaction 17 with CO 2 : Results from an O 3 - gradient and a FACE experiment.” J. Water, Air 18 and Soil Pollut. 116: 311

- 322. 19 20 Karnosky, D. F.; Zak, D. R.; Pregitzer, K. S.; Awmack, C. S.; Bockheim, J. G.; Dickson, 21 R . E.; Hendrey , G. R.; Host, G. E.; King, J. S.; Kopper, B. J.; Kruger, E. L.; 22 Kubiske, M. E.; Lindroth, R. L .; Mattson, W. J.; McDonald, E. P. (2003) 23 Tropospheric O 3 moderates responses of temperate hardwood forests to elevated 24 CO2: A sy

nthesis of molecular to ecos ys tem results from the Aspen FACE 25 project. Funct. Ecol. 17: 289

- 304. 26 27 Karnosky, D.F., Pregitzer, K.S., Zak, D.R., Kubiske, M.E., Hendrey , G.R., Weinstein, D., 28 Nosal, M. & Percy , K.E. (2005) Scaling ozone responses of forest trees to the 29 ecos ys tem level in a changing climate. Plant Cell Environ.28, 965

–981. 30 31 Kelly , F. J.; Dunster, C.; Mudway , I. (2003) Air pollution and the elderly : 32 oxidant/antioxidant issues worth consideration. Eur. Respir. J. Suppl. 40: 70S
- 75S. 33 34 Kim, S.

- Y.; L ee, J.
- T.; Hong, Y.
- C.; Ahn, K.

- J.; Kim, H. (2004) Determining the 35 threshold effect of ozone on daily mortality: an analy sis of ozone and mortality in 36 Seoul, Korea, 1995

- 1999. Environ. Res. 94: 113

- 119. 37 38 King, J.S., M. E. Kubiske, K. S. Pregitzer, G. R. Hendrey , E. P. McDonal d, C. P. 39 Giardina, V. S. Quinn, D. F. Karnosky . (2005) Tropospheric O 3 compromises net 40 primary

production in young stands of trembling aspen, paper birch and sugar 41 maple in response to elevated atmospheric CO 2 . New Phy tologist. 168:623

– 636. 42 43 Kinney , P. L. ; Aggarwal, M.; Nikiforov, S. V.; Nadas, A. (1998) Methods dev elopment 44 for epidemiologic investigations of the health effects of prolonged ozone exposure. 45 Part III: an approach to retrospective estimation of lifetime ozone exposure using a 46Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 419 questionnaire an d ambient monitoring data (U.S. sites). Cambridge, MA: Health 1 Effects Institute; research report no. 81; pp. 79

- 108. 2 3 Korrick, S. A.; Neas, L. M.; Dockery , D. W.; Gold, D. R.; Allen, G. A.; Hill, L . B.; 4 Kimball, K. D.; Rosner, B. A.; Speizer, F. E. (1998) Effects of ozone and other 5 pollutants on the pulmonary function of adult hikers. Environ. Health Perspect. 6 106: 93
- 99. 7 8 Koutrakis, P.; Suh, H.H.; Sarnat, J. A.; Brown, K. W.; Coull, B.A; Schwartz, J. (2005) 9 Characterization of particulate and gas exposure s of sensitive subpopulations living 10 in Baltimore and Boston. HEI Research Report 131. 11 12 Kreit, J. W.; Gross, K. B.; Moore, T. B.; Lorenzen, T. J.; D'Arcy , J.; Eschenbacher, W. L. 13 (1989) Ozone

- induced changes in pulmonary function and bronchial responsiven ess 14 in asthmatics . J. Appl. Phy siol. 66: 217

- 222. 15 16 Krewski, D.; Burnett, R. T.; Goldberg, M. S.; Hoover, K.; Siemiatycki, J,; Jerrett, M.; 17 Abrahamowicz, M.; White, W. H. (2000) Reanaly sis of the Harvard Six Cities 18 Study

and the American Cancer Society Study of particulate air pollution and 19 mortality . A special report of the Institute’s particle epidemiology reanal ys is 20 project. Cambridge, MA: Health Effects Institute. 21 22 Künzli, N.; Lurmann, F.; Segal, M.; Ngo, L.; Balmes, J.; Tager, I. B. (1997) Associati on 23 between lifetime ambient ozone exposure and pulmonary function in college 24 freshmen

— results of a pilot study . Environ. Res. 72: 8

- 23. 25 26 Langstaff, J. (2007) Analysis of Uncertainty in Ozone Population Exposure Modeling. 27 January

31, 2007. Memo to the Ozon e NAAQS Review Docket. EPA

- HQ
- OAR
28 2005
- 0172
- 0174. Available online at: 29 http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_td.html

. 30 31 Larson, J. L .; Zak, D. R.; Sinsabaugh, R. L. (2002) Extracellular enzy me activity

beneath 32 temperate trees growing under elevated carbon dioxide and ozone. Soil Sci. Soc. 33 Am. J. 66: 1848
- 1856. 34 35 Laurence, J.A.,Kohut, R.J., Amundson, R.G., (1993). Use of TREGRO to simulate the 36 effects of ozone on the growth of red spruce seedlings. Forest Science. 39: 453

- 37 464. 38 39 Laurence, J. A.; Retzlaff, W. A.; Kern, J. S.; L ee, E. H.; Hogsett, W. E.; Weinstein, D. A. 40 (2001) Predicting the regional impact of ozone and precipitation on the growth of 41 loblolly

pine and yellow poplar using linked TREGRO and ZELG models. For. 42 Ecol. Manage. 146: 247

- 263. 43 44 Lee, E. H.; Hogsett, W. E. (1996) Methodology for calculating inputs for ozone 45 secondary

standard benefits analy sis: part II. Report prepared for Office of Air 46Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 420 Quality P lanning and Standards, Air Quality Strategies and Standards Division, 1 U.S. Environmental Protection Agency , Research Triangle Park, N.C., March. 2 EPA Docket No. A

- 95
- 58 Item II
- I
- 265. 3 4 Lefohn, A.S.; Runeckles, V.C.; Krupa, S.V.; Shadwick, D.S. (1989) Impo rtant 5 considerations for establishing a secondary ozone standard to protect vegetation. 6 JAPCA 39, pp. 1039
- 1045. 7 8 Lev y, J. I.; Chemery nski, S. M.; Sarnat, J. A. (2005) Ozone exposure and mortality , an 9 empiric Bayes metaregression analy sis. Epidemiology 16 : 458
- 468. 10 11 Linn, W. S.; Shamoo, D. A.; Anderson, K. R.; Peng, R.

- C.; Avol, E. L.; Hackney , J. D.; 12 Gong, H., Jr. (1996) Short

- term air pollution exposures and responses in Los 13 Angeles area schoolchildren. J. Exposure Anal. Environ. Epidemiol. 6: 449

- 472. 14 15 Lipfert, F. W.; Perry , H. M., Jr.; Miller, J. P.; Baty , J. D.; Wy zg a, R. E.; Carmody , S. E. 16 (2000) The Washington University

- EPRIveterans' cohort mortality study : 17 preliminary

results. In: Grant, L. D., ed. PM2000: particulate matter and health. 18 Inhalation Toxicol. 12(suppl. 4): 41

- 73. 19 20 Lipfert, F. W.; Perry , H. M., Jr.; Miller, J. P.; Baty , J. D.; Wy zg a, R. E.; Carmody , S. E. 21 (2003) Air pollution, blood pressure, and their long

- term associations with 22 mortality . Inhalation Toxicol. 15: 493

- 512. 23 24 Long, S., N elson, R.L., Ainsworth, L ., Hollis, K., Mies, T., Morgan, P., Naidu, S., Ort, 25 D.R., Webster, R., Zhu, X. Adapting So ybean To Current And Future Change In 26 Atmospheric Composition. Do We Need More Than Field Sel ection Under 27 Current Conditions. Cellular and M olecular Biology of Soy bean Biennial 28 Conference. (2002) p . 401. 29 http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=1 30 42752 31 32 Lo ya W.M., Pregitzer K.S., Karberg N.J., King J.S. & Giardina C.P. (2003) Reduction of 33 soil carbon formation b y tropospheric ozone under elevated carbon dioxide. 34 Nature 425, 705

–707. 35 36 Luethy- Krause, B.; Landolt, W. (1990) Effects of ozone on starch accumulation in 37 No rway

spruce (Picea abies). Trees 4: 107

- 110. 38 39 Lyo ns, T. M.; Barnes, J. D.; Davison, A. W. (1997) Relationships between ozone 40 resistance and climate in European populations of Plantago major. New Phy tol. 41 136: 503
- 510. 42 43 Manning, W. J.; Krupa, S. V. (1992) Experimental methodology for studying the effects 44 of ozone on crops and trees. In: Lefohn, A. S., ed. Surface level ozone exposures 45 and their effects on vegetation. Chelsea, MI: Lewis Publishers, Inc.; pp. 93
- 156. 46Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 421 1 Mannino, D. M.; Ford, E. S.; Redd, S. C. (2 003) Obstructive and restrictive lung disease 2 and markers of inflammation: data from the Third National Health and Nutrition 3 Examination. Am. J. Med. 114: 758

- 762. 4 5 Marty , M. (2007a) Letter from CHPAC Chair to the Administrator. March 23. EPA

- HQ
6 OAR
- 2005
- 0172
- 0105. 7 8 Marty , M. (2007b) Letter from CHPAC Chair to the Administrator. September 4. EPA

9 HQ
- OAR
- 2005
- 0172
- 2031. 10 11 McBride, D. E.; Koenig, J. Q.; Luchtel, D. L.; Williams, P. V.; Henderson, W. R., Jr. 12 (1994) Inflammatory effects of ozone in the upper airway s of subjects with asthma. 13 Am. J. Respir. Crit. Care Med. 149: 1192

- 1197. 14 15 McCluney , L. (2007) Ozone 1

- Hour to 8
- Hour Ratios for the 2002

- 2004 Design Value 16 Period. January 18, 2007. Memo to the Ozone NAAQS Review Docket. EPA

- HQ
17 OAR
- 0172
- 0073. 18 19 McConnel l, R.; Berhane, K.; Gilliland, F.; L ondon, S. J.; I slam, T.; Gauderman, W. J.; 20 Avol, E.; Margolis, H. G.; Peters, J. M. (2002) Asthma in exercising children 21 exposed to ozone: a cohort study . Lancet 359: 386
- 391. 22 23 McDonnell, W. F.; Kehrl, H.R.; Abdul

- Sal aam, S.; Ives, P.J.; Folinsbee, L.J.; Devlin, 24 R.B.; O’Neil, J.J.; Horstman, D. H. (1991) Respiratory response of humans exposed 25 to low levels of ozone for 6.6 hours. Arch. Environ. Health 46: 145

- 150. 26 27 McDonnell, W. F. (1996) Individual variability in human lung function responses to 28 ozone exposure. Environ. Toxicol. Pharmacol. 2: 171

- 175. 29 30 McDonnell, W. F.; Stewart, P. W.; Andreoni, S.; Seal, E., Jr.; Kehrl, H. R.; Horstman, D. 31 H.; Folinsbee, L. J.; Smith, M. V. (1997) Prediction of ozone

- induced FEV1 32 ch anges: effects of concentration, duration, and ventilation. Am. J. Respir. Crit. 33 Care Med. 156: 715

- 722. 34 35 McDonnell, W. F.; Abbey , D. E.; Nishino, N.; Lebowitz, M. D. (1999) L ong - term 36 ambient ozone concentration and the incidence of asthma in nonsmoking ad ults: 37 the ahsmog study. Environ. Res. 80: 110

- 121. 38 39 McLaughlin, S.B., Nosal, M., Wullschleger, S.D., Sun, G. (2007a) Interactive effects of 40 ozone and climate on tree growth and water use in a southern Appalachian forest in 41 the USA. New Phyt ologist 174:1 09
- 124 42 43 McLaughlin, S.B., Wullschleger, S.D., Sun, G. and Nosal, M. (2007b) Interactive effects 44 of ozone and climate on water use, soil moisture content and streamflow in a 45 southern Appalachian forest in the USA. New Phytologist 174: 125

- 136
. 46Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 422 1 Michelson, P. H.; Dailey , L .; Devlin, R. B.; Peden, D. B. (1999) Ozone effects on the 2 immediate

- phase response to allergen in the nasal airway s of allergic asthmatic 3 subjects. Otolary ngol. Head Neck Surg. 120: 225

- 232. 4 5 Miller, P. R.; McBride, J. R.; Schilling, S. L .; Gomez, A. P. (1989) Trend of ozone 6 damage to conifer forests between 1974 and 1988 in the San Bernardino Mountains 7 of southern California. In: Olson, R. K.; L efohn, A. S., eds. Effects of air pollution 8 on western forests [an A&WMA sy mposium; June; Anahe im, CA]. Air and Waste 9 Management Association; pp. 309

- 323. (APCA transactions series, no. 16). 10 11 Moldau, H.; Söber, J.; Söber, A. (1990) Differential sensitivity of stomata and mesophyll 12 tosudden exposure of bean shoots to ozone. Photosy nthetica 24: 446

- 45 8. 13 14 Morgan, P. B.; Ainsworth, E. A.; L ong, S. P. (2003) How does elevated ozone impact 15 soy

bean? A meta

- anal ys is of photosy nthesis, growth and yield. Plant Cell 16 Environ. 26: 1317

- 1328. 17 18 Morgan, P.B., Bernacchi, C.J. , Ort, D.R., L ong, S.P. (2004) An in vivo analy sis of the 19 effect of season

- long open

- air elevation of ozone to anticipated 2050 levels on 20 photosy

nthesis in soy

bean. Plant Physiology

135: 2348
- 2357. 21 22 Mortimer, K. M.; Neas, L. M.; Dockery , D. W.; Redline, S.; Tager, I. B. (2002) The 23 effect of air pollution on inner

- city children with asthm a. Eur. Respir. J. 19: 699

- 24 705. 25 26 Mudway , I. S.; Kelly , F. J. (2004) An investigation of inhaled ozone dose and the 27 magnitude of airway inflammation in healthy

adults. Am. J. Respir. Crit. Care 28 Med. 169: 1089

- 1095
. 29 30 Musselman, R.C.; Lefohn, A.S.; Massman, W.J.; Heath, R.L. (2006) A critical review 31 and anal ys is of the use of exposure

- and flux

- based ozone indices for predicting 32 vegetation effects. Atmos. Environ.. 40:1869

- 1888. 33 34 National Association of Clean Air Ag encies (NACAA) (2007) Letter and Comments Sent 35 to Docket No. OAR

- 2005
- 0172 re: Proposed Rule

– National Ambient Air Quality 36 Standards for Ozone. Docket No. OAR

- 2005
- 0172
- 4274. October 9, 2007. 37 38 NPS (2005) 2005 Annual Performance & Progress Report: Air Qu ality in National 39 Parks. National Park Service. 40 http://www2.nature.nps.gov/air/Pubs/pdf/gpra/Gpra2005_Report_03202006_Fin 41 al.pdf 42 43 National Park Service (NPS) Letter and Comments Sent to Docket No. OAR

- 2005
- 0172 44 re: Proposed Rule

– National Ambient Air Qual ity Standards for Ozone. Docket 45 No. OAR
- 2005
- 0172
- 4934. September 27, 2007 46Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 423 1 Navidi, W.; Thomas, D.; Langholz, B.; Stram, D. (1999) Statistical methods for 2 epidemiologic studies of the health effects of air pollution. Cambridge, MA: 3 Health Effects Institute; research report no. 86. 4 5 Noormets, A.; Sober, A.; Pell, E. J.; Dickson, R. E.; Posila, G. K.; Sober, J.; I sebrands, J. 6 G.; Karnosky, D. F. (2001) Stomatal and non

- stomatal limitation to 7 photosy

nthesis in two trembling aspen (Populus tremuloides Michx) clones 8 exposed to elevated CO2 and/or O 3 . Plant Cell Environ. 24: 327

- 336. 9 10 Ollinger, S. V., Aber, J. D., Reich, P. B. and Freuder, R. J. (2002) Interactive effects 11 of nitrogen deposition, tropospheric ozone, elevated CO2 and land use history 12 on the carbon dy namics of northern hardwood forests. Glob. Change Biol. 8(6), 13 545

– 562. 14 15 Olszy

k, D., By tnerowlez, A., Kats, G., Reagan, C., Hake, S., Kerby , T., Millhouse, 16 D., Roberts, B., Anderson, C., L ee, H. (1993) Cotton yield losses and ambient 17 ozone concentrations in California’s San Joaquin Valley . Journal of 18 Environmental Quality 22, 602

– 611. 19 20 OMB (2005). Update of Statistical Area Definitions and Guidance on Their Uses. 21 U.S. Office of Management and Budget, Bulletin No. 05

- 02. February 22, 2005. 22 23 O'Neill, M. S.; L oomis, D.; Borja

- Aburto, V. H. (2004) Ozone, area social conditions, 24 and mortality in Mexico City . Environ. Res. 94: 234

- 242. 25 26 Pearson, S.; Davison, A. W.; Reiling, K.; Ashenden, T.; Ollerenshaw, J. H. (1996) 27 The effects of different ozone exposures on three contrasting populations of 28 Plantago major . New Phy tol. 132: 493

- 502. 29 30 Peden, D. B.; Setzer, R. W., Jr.; Devlin, R. B. (1995) Ozone exposure has both a 31 priming effect on allergen

- induced responses and an intrinsic inflammatory 32 ac tion in the nasal airways of perenniall y allergic asthmatics. Am. J. Respir. 33 Crit. Care Med. 151: 1336

- 1345. 34 35 Peden, D. B.; B oehlecke, B.; Horstman, D.; Devlin, R. (1997) Prolonged acute 36 exposure to 0.16 ppm ozone induces eosinophilic airway inflammation in 37 asthmatic subjects with allergies. J. Allergy Clin. Immunol. 100: 802

- 808. 38 39 Pell, E. J.; Schlagnhaufer, C. D.; Arteca, R. N. (1997) Ozone

- induced oxidative stress: 40 mechanisms of action and reaction. Phys iol. Plant. 100: 264

- 273. 41 42 Percy , K. E.; Awmack, C. S.; Lindroth, R. L .; Kubiske, M. E.; Kopper, B. J.; I sebrands, J. 43 G.; Pregitzer, K. S.; Hendry , G. R.; Dickson, R. E.; Zak, D. R.; Oksanen, E.; 44 Sober, J.; Harrington, R.; Karnosky, D. F. (2002) Altered performance of forest 45Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 424 pests under atmospheres enriche d with CO2 and O 3 . Nature (London) 420: 403

- 1 407
. 2 3 Percy , K. E.; Nosal, M.; Heilman, W.; Dann, T; Sober, J.; L egge, A. H.; Karnosky , D. F. 4 (2007) New exposure

- based metric approach for evaluating O3 risk to North 5 American aspen forests. Environmental Pollution 147:3 554

- 566. 6 7 Peters, J. M.; Avol, E.; Navidi, W.; L ondon, S. J.; Gauderman, W. J.; Lurmann, F.; Linn, 8 W. S.; Margolis, H.; Rappaport, E.; Gong, H., Jr.; Thomas, D. C. (1999a) A study 9 of twelve southern California communities with differing levels and types of air 10 pollution. I . Prevalence of respiratory morbidity . Am. J. Respir. Crit. Care Med. 11 159: 760
- 767. 12 13 Peters, J. M.; Avol, E.; Gauderman, W. J.; Linn, W. S.; Navidi, W.; L ondon, S. J.; 14 Margolis, H.; Rappaport, E.; Vora, H.; Gong, H., Jr.; Thomas, D. C. (1999b) A 15 study

of twelve southern California communities with differing levels and ty pes 16 of air pollution. II. Effects on pulmonary function. Am. J. Respir. Crit. Care Med. 17 159: 768
- 775. 18 19 Peterson, D. L.; Arbaugh, M. J.; Wakefield, V. A.; Miller, P . R. (1987) Evidence of 20 growth reduction in ozone

- injured Jeffrey pine (Pinus jeffreyi Grev and Balf) in 21 Sequoia and Kings Canyon National Parks. JAPCA 37: 906

- 912. 22 23 Phillips, R. L .; Zak, D. R.; Holmes, W. E.; White, D. C. (2002) Microbial community 24 compos ition and function beneath temperate trees exposed to elevated 25 atmospheric carbon dioxide and ozone. Oecologia 131: 236

- 244. 26 27 Plopper, C. G.; Fanucchi, M. V. (2000) Do urban environmental pollutants exacerbate 28 childhood lung diseases? Environ. Health Perspect. 108: A252

- A25 3. 29 30 Plunkett, L . M.; Turnbull, D.; Rodricks, J. V. (1992) Differences between adults and 31 children affecting exposure assessment. In: Guzelian, P. S.; Henry , D. J.; Olin, S. 32 S., eds. Similarities and differences between children and adults: implications for 33 risk assessment. Washington, DC: ILSI Press, pp. 79

- 96. 34 35 Pope, C. A., III; Thun, M. J.; Namboodiri, M. M.; Dockery , D. W.; Evans, J. S.; Speizer, 36 F. E.; Heath, C. W., Jr. (1995) Particulate air pollution as a predictor of mortality 37 in a prospective study of U.S. adults. Am. J. Respir. Crit. Care Med. 151: 669

- 38 674. 39 40 Pope, C. A., III; Burnett, R. T.; Thun, M. J.; Calle, E. E.; Krewski, D.; Ito, K.; Thurston, 41 G. D. (2002) Lung cancer, cardiopulmonary mortality , and long

- term exposure to 42 fine particulate air pollution. JAMA J. Am. Med. Assoc. 287: 1132

- 1141. 43 44 Prentice IC, Farquhar GD, Fasham MJR, et al. (2001) The Carbon C ycle and 45 Atmospheric Carbon Dioxide. In Climate Change 2001: The Scientific Ba sis. 46Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 425 Contribution of Working Group I to the Third Assessment Report of the 1 Intergovernmental Panel on Climate Change. (ed J. T. Houghton YD, D. J. 2 Griggs, M. Noguer, P. J. van der Linder, X. Dai, K. Maskell, and C. A. 3 Johnson), pp. 241

- 280. Cambridge Univ ersity Press, Cambridge, United 4 Kingdom and New York, NY, USA. 5 6 Pronos, J.; Merrill, L .; Dahlsten, D. (1999) Insects and pathogens in a pollution

- stressed 7 forest. In: Miller, P. R.; McBride, J. R., eds. Oxidant air pollution impacts in the 8 montane forests of southern California. Springer, pp. 317

- 337. 9 10 Reid, C. D.; Fiscus, E. L . (1998) Effects of elevated [CO2] and/or ozone on limitations 11 to CO2 assimilation in soy bean (Gl ycine max). J. Exp. Bot. 49: 885

- 895. 12 13 Reiling, K.; Davison, A. W. (1992a) Effects of a short ozone exposure given at 14 different stages in the development of Plantago major L. New Phyt ol. 121: 643

- 15 647. 16 17 Reiling, K.; Davison, A. W. (1992b) The response of native, herbaceous species to 18 ozone: growth and fluorescence screening. New Phy tol. 120 : 29
- 37. 19 20 Retzlaff, W. A.; Arthur, M. A.; Grulke, N. E.; Weinstein, D. A.; Gollands, B. (2000) Use 21 of a single

- tree simulation model to predict effects of ozone and drought on 22 growth of a white fir tree. Tree Phys iol. 20: 195

- 202. 23 24 Rizzo, M (2005). Evaluation of a quadratic approach for adjusting distributions of hourly 25 ozone concentrations to meet air quality standards. November 7, 2005. Available 26 online at: http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_td.html. 27 28 Rizzo, M. (2006). A distributional comparison between different rollback methodologies 29 applied to ambient ozone concentrations. August 23, 2006. Available online at: 30 http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_td.html

. 31 32 Romieu, I .; Meneses, F.; Ruiz, S.; Sienra, J. J.; Huerta, J.; White, M. C.; Etzel, R. A. 33 (1996) Effects of air pollution on the respiratory health of asthmatic children 34 living in Mexico City . Am. J. Respir. Crit. Care Med. 154: 300
- 307. 35 36 Romieu, I .; Meneses, F.; Ruiz, S.; Huerta, J.; Sienra, J. J.; White, M.; Etzel, R.; 37 Hernandez, M. (1997) Effects of intermittent ozone exposure on peak expiratory 38 flow and respiratory s ymptoms among asthmatic children in Mexico City . Arch. 39 Environ. Health 52: 368

- 376. 40 41 Romieu, I .; Sienra

- Monge, J. J.; Ramírez
- Aguilar, M.; Moreno

- Macias, H.; Reyes - Ruiz, 42 N. I.; Estela del Rio

-Navarro, B.; Hernández

- Avila, M.; L ondon, S. J. (2004) 43 Genetic pol ym orphism of GSTM1 and antioxidant supplementation influence lung 44 f

unction in relation to ozone exposure in asthmatic children in Mexico City . Thorax 45 59: 8
- 10. 46Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 426 1 Sarnat, J. A.; Schwartz, J.; Catalano, P. J.; Suh, H. H. (2001) Gaseous pollutants in 2 particulate matter epidemiology : confounders or surrogates? Environ. Health 3 Perspect. 109: 1053
- 1061. 4 5 Sarnat, J. A.; Brown, K. W.; Schwartz, J.; Coull, B. A.; Koutrakis, P. (2005) Ambient gas 6 concentrations and personal particulate matter exposures: implications for studying 7 the health effects of particles. Epidemiology 16: 385
- 3 95. 8 9 Sarnat, J. A.; Coull, B. A.; Schwartz, J; Gold, D. R.; Suh, H. H. (2006) Factors affecting 10 the association between ambient concentrations and personal exposure to particles 11 and gases. Environ. Health Perspect. 114(5):649

- 654. 12 13 Sasek, T. W.; Richardso n, C. J.; Fendick, E. A.; Bevington, S. R.; Kress, L. W. (1991) 14 Carryover effects of acid rain and ozone on the physiology of multiple flushes of 15 loblolly

pine seedlings. For. Sci. 37: 1078

- 1098. 16 17 Scannell, C.; Chen, L .; Aris, R. M.; Tager, I.; Christian, D.; Ferrando, R.; Welch, B.; 18 Kelly , T.; Balmes, J. R. (1996) Greater ozone

- induced inflammatory responses in 19 subjects with asthma. Am. J. Respir. Crit. Care Med. 154: 24
- 29. 20 21 Schwartz, J. (2005) How sensitive is the association between ozone and daily deat hs to 22 control for temperature? Am. J. Respir. Crit. Care Med. 171: 627

- 631. 23 24 Schildcrout, J. S.; Sheppard, L.; Lumley , T.; Slaughter, J. C.; Koenig, J. Q.; Shapiro, G. 25 G. (2006) Ambient air pollution and asthma exacerbations in children: an eight 26 city

analysis. Am. J. Epidemiol. 164(5):505

- 517. 27 28 Schierhorn, K.; Hanf, G.; Fischer, A.; Umland, B.; Olze, H.; Kunkel, G. (2002) Ozone

29 induced release of neuropeptides from human nasal mucosa cells. Int. Arch. 30 Allergy

Immunol. 129: 145

- 151. 31 32 Sheppard, L.; Slaughter, J. C.; Schildcrout, J.; Liu, L

. - J. S.; Lumley , T. (2005) Exposure 33 and measurement contributions to estimates of acute air pollution effects. J. 34 Exposure Anal. Environ. Epidemiol. 15: 366

- 376. 35 36 Simini, M.; Skelly, J. M.; Davis, D. D.; Savage, J. E.; Comrie, A. C. (1992) Sensitivity of 37 four hardwood species to ambient ozone in north central Penns ylvania. Can. J. 38 For. Res. 22: 1789
- 1799. 39 40 Sin, D. D.; Man, S. F. P. (2003) Why are patients with chronic obstructive pulmonary 41 disease at increased risk of cardiovascular diseases? Circulation 107: 1514

- 1519. 42 43 Sitch, S.; Cox, P. M.; Collins, W. J.; Huntingford, C. (2007) Indirect radiative forcing of 44 climate change through ozone effects on the land

- carbon sink. Nature (London, 45 U.K.) 448: 791

- 794. 46Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 427 1 Smith, W. H. (1992) Air pollution effects on ecosystem processes. In: Barker, J. R.; 2 Tingey , D. T., eds. Air pollution effects on biodiversity . Van Nostrand Reinhold; 3 pp. 234
- 260. 4 5 Smith, G., Coulston J., Jepsen, J. and Prichard, T. (2003) “A national ozone 6 biomonitoring program: Results from field surveys of ozone sensitive plants in 7 northeastern forest (1994

–2000)” Environmental Monitoring and Assessment 87(3): 8 271 −291. 9 10 Somers, G. L .; Chappelka, A. H.; Rosseau, P.; Renfro, J. R. (1998) Empirical evidence of 11 growth de cline related to visible ozone injury . For. Ecol. Manage. 104: 129

- 137. 12 13 Tager, I. B.; Künzli, N.; Lurmann, F.; Ngo, L.; Segal, M.; Balmes, J. (1998) Methods 14 development for epidemiologic investigations of the health effects of prolonged 15 ozone exposure. Part II : an approach to retrospective estimation of lifetime ozone 16 exposure using a questionnaire and ambient monitoring data (California sites). 17 Cambridge, MA: Health Effects Institute; research report no. 81; pp. 27

- 78. 18 19 Takemoto, B. K.; By tnerowicz, A.; F enn, M. E. (2001) Current and future effects of 20 ozone and atmospheric nitrogen deposition on California's mixed conifer forests. 21 For. Ecol. Manage . 144: 159
- 173. 22 23 Tans P
. P
. , White J

. W
. C
. (1998) In balance, with a little help from the plants. Science, 24 281, 183
- 184. 25 26 Taylor, C.R. “AGSIM: Model Description and Documentation.” Agricultural Sector 27 Models for the United States. C.R. Taylor, K.H. Reichelderfer, and S.R. Johnson, 28 eds. Ames IA: Iowa State University Press, (1993). 29 30 Taylor R. (1994) “Deterministic versus stochastic evaluation of the aggregate economic 31 effects of price support programs” Agricultural Systems 44: 461

- 473. 32 33 Temple, P. J.; Riechers, G. H.; Miller, P. R.; Lennox, R. W. (1993) Growth responses of 34 ponderosa pine to longterm exposure to ozone, wet and dry acidic deposition, and 35 drought. Can. J. For. Res. 23: 59

- 66. 36 37 Thurston, G.D.; Ito, K.; Kinney , P.L.; Lippmann, M. (1992) A multi

- ye ar study of air 38 pollution and respiratory hospital admissions in three New York State 39 metropolitan areas: resul ts for 1988 and 1989 summers. J. Exposure Anal. 40 Environ. Epidemiol. 2:429

- 450. 41 42 Tingey , D. T.; Standley , C.; Field, R. W. (1976) Stress ethylene evolution: a measure of 43 ozone effects on plants. Atmos. Environ. 10: 969

- 974. 44 45Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 428 Tingey , D. T.; Taylor, G. E., Jr. (1982) Variation in plant response to ozone: a conceptual 1 model of phy siological events. In: Unsworth, M. H.; Ormrod, D. P., eds. Effects 2 of gaseous air pollution in agriculture and horticulture. London, United Kingdom: 3 Butterworth Scientific; pp. 113

- 1 38. 4 5 Tingey , D. T.; Laurence, J. A.; Weber, J. A.; Greene, J.; Hogsett, W. E.; Brown, S.; L ee, 6 E. H. (2001) Elevated CO2 and temperature alter the response of Pinus ponderosa 7 to ozone: A simulation analy sis. Ecol. Appl .11: 1412
- 1424. 8 9 Tingey , D. T.; Hogsett, W. E.; Lee, E. H.; Laurence, J. A. (2004) Stricter ozone ambient 10 air quality

standard has beneficial effect on Ponderosa pine in California. Environ. 11 Manage . 34: 397
- 405
. 12 13 Touloumi, G.; Katsouyanni, K.; Zmirou, D.; Schwartz, J.; Spix, C.; Ponce de Leon, A.; 14 Tobias, A.; Quennel, P.; Rabczenko, D.; Bacharova, L .; Bisanti, L.; Vonk, J. M.; 15 Ponka, A. (1997) Short

- term effects of ambient oxidant exposure on mortality : a 16 combined anal ys is within the APHEA project. Am. J. Epidemiol. 146: 177
- 185. 17 18 U.S. Department of Agriculture, 2006. The PLANTS Database (http://plants.usda.gov, 19 December 2006). National Plant Data Center, Baton Rouge, LA. 20 21 Ultman, J. S.; Ben

- Jebria, A.; Arnold, S. F. (2004) Uptake distribution of ozone in human 22 lungs: intersubject variability in phy siologic response. Boston, MA: Health 23 Effects Institute. 24 25 Vagaggini, B.; Taccola, M.; Clanchetti, S.; Carnevali, S.; Bartoli, M. L .; Bacci, E.; Dente, 26 F. L.; Di Franco, A.; Giannini, D.; Paggiaro, P. L. (2002) Ozone exposure 27 increases eosinophilic airway response induced b y previous allergen challenge. 28 Am. J. Respir. Crit. Care Med. 166: 1073

- 1077. 29 30 Vedal, S.; Brauer, M.; White, R.; Petkau, J. (2003) Air pollution and daily mortality in a 31 city

with low levels of pollution. Environ. Health Perspect. 111: 45

- 51. 32 33 Vesel y, D. L.; Giordano, A. T.; Raska

- Emery , P.; Montgomery , M. R. (1994a) Ozone 34 increases amino

- and carboxy

- terminal atrial natriuretic factor prohormone 35 peptides in lung, heart, and circulation. J. Biochem. Toxicol. 9: 107
- 112. 36 37 Vesel y, D. L.; Giordano, A. T.; Raska

- Emery , P.; Montgomery , M. R. (1994b) Increase 38 in atrial natriuretic factor in the lungs, heart, and circulatory s ys tem owing to 39 ozone. Chest 105: 1551

- 1554. 40 41 Vesel y, D. L.; Giordano, A. T.; Raska

- Emery , P.; Montgomery , M. R. (1994c) Ozone 42 increases atrial natriuretic peptides in heart, lung and circulation of aged vs. adult 43 animals. Gerontology (Basel) 40: 227

- 236. 44 45Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 429 Weber, J. A.; Clark , C. S.; Hogsett, W. E. (1993) Analy sis of the relationship(s) among 1 O 3 upt ake, conductance, and photosy nthesis in needles of Pinus ponderosa. Tree 2 Phy siol. 13: 157

- 172. 3 4 Weinstein, D.A., Beloin, R.M., R.D. Yanai (1991) “Modeling changes in red spruce 5 carbon balance and allocation in response to interacting ozone and nutrient 6 stress.” Tree Phy siology 9: 127
- 146. 7 8 Weinstein, D.A., J.A. Laurence, W.A. Retzlaff, J.S. Kern, E.H. Lee, W.E. Hogsett, J. 9 Weber (2005) Predicting the effects of tropospheric ozone on regional 10 productivity of ponderosa pine and white fir. Forest Ecology and M anagement 11 205: 73
- 89. 12 13 Whitfield, R.; Biller, W.; Jusko, M.; and Keisler, J. (1996) A Probabilistic Assessment 14 of Health Risks Associated with Short

- and Long

- Term Exposure to Tropospheric 15 Ozone. Argonne National Laboratory , Argonne, IL. 16 17 Whit field, R. (1997) A Probabilistic Assessment of Health Risks Associated with Short

18 term Exposure to Tropospheric Ozone: A Supplement. Argonne National 19 Laboratory , Argonne, IL. 20 21 Whitfield, C. P.; Davison, A. W.; Ashenden, T. W. (1997) Artifici al selection and 22 heritability

of ozone resistance in two populations of Plantago major. New Phy tol. 23 137: 645
- 655. 24 25 Whitfield, R.G.; Richmond, H.M.; and Johnson, T.R. (1998) “Overview of Ozone Human 26 Exposure and Health Risk Analy ses Used in the U.S. EPA’s Review of the Ozone 27 Air Quality

Standard,” pp.483

- 516 in: T. Schneider, ed. Air Pollution in the 21 st 28 Century : Priority Issues and Policy Elsevier; Amsterdam. 29 30 Wolff, G.T. (1995) Letter from Chairman of Clean Air Scientific Advisory Committee to 31 the EPA Adm inistrator, dated November 30, 1995. EPA

- SAB
- CASAC
- LTR
- 96
- 32 002. 33 34 Wolff, G.T. (1996) Letter from Chairman of Clean Air Scientific Advisory Committee to 35 the EPA Administrator, dated April 4, 1996. EPA

- SAB
- CASAC
- LTR
- 96
- 006. 36 37 Xu, X.; Ding, H.; Wang, X. (1995) A cute effects of total suspended particles and sulfur 38 dioxides on preterm delivery : a community

- based cohort study . Arch. Environ. 39 Health 50: 407

- 415. 40 41 Young , T. F.; Sanzone, S., eds. (2002) A framework for assessing and reporting on 42 ecological condition: an SAB report. Washington, DC: U.S. Environmental 43 Protection Agency , Science Advisory Board; report no. EPA

- SAB
- EPEC
- 02
- 009. 44 Available online at: 45Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 430 http://yosemite.epa.gov/sab/sabproduct.nsf/C3F89E598D843B58852570CA007571 1 7E/$File/epec02009a.pdf

. 2 3 Zeger, S. L.; Thomas, D.; Dominici, F.; Samet, J. M.; Schwartz, J.; Dockery , D.; Cohen, 4 A. (2000) Exposure measurement error in time

- series studies of air pollution: 5 concepts and consequences. Environ. Health Perspect. 108: 419

- 426. 6 7 Zhang, L.
- Y.; Levitt, R. C.; Kleeberger, S. R. (1995) Differential susceptibility to ozone 8 induced airway s hy perreactivity

in inbred strains of mice. Exp. Lung Res. 21: 9 503
- 518
. 10 11 Zidek, J. V.; White, R.; Le, N. D.; Sun, W.; Burnett, R. T. (1998) Imputing unmeasured 12 explanatory

variables in environmental epidemiology with application to health 13 impact anal ys is of air pollution. Environ. Ecol. Stat. 5: 99

- 115. 14 15Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 431 For the reasons set forth in the preamble, part 50 of Chapter 1 of Title 40 of the code of 1 Federal regulations is proposed to be amended as follows: 2 3 PART 50 -- NATIONAL PRIMARY AND SECONDARY AMBIENT AIR 4 QUALITY STANDARDS 5 6 1. The authority citation for part 50 continues to read as follows: 7 8 Authority: 42 U.S.C. 7401 et seq. 9 10 2. Section 50.15 i s revis ed to read as follows: 11 12 ' 50.15 National primary and secondary ambient air quality standards for ozone. 13 (a) The level of the national 8

- hour primary ambient air qual ity

standard for O 3 is (0.060

- 14 0.070) parts per million (ppm), daily maximum 8

- hour average, measured by a reference 15 method based on Appendix D to this part and designated in accordance with part 53 of 16 this chapter or an equivalent method designated in acco rdance with part 53 of this 17 chapter

. 18 (b) The 8

- hour primary O 3 ambient air quality

standard is met at an ambient air quality 19 monitoring site when the average of the annual fourth

- highest daily maximum 8

- hour 20 average O 3 concentration is less than or equal t o (0.060

- 0.070) ppm, as determined in 21 accordance with appendix P to this part. 22 (c) The level of the national secondary ambient air quality

standard for O 3 is a cumulative 23 index value of (7

- 15) ppm

- hours, measured b y a reference method based on Appendix D 24 t o this part and designated in accordance with part 53 of this chapter or an equivalent 25 method designated in accordance with part 53 of this chapter

. 26 (d) The secondary

O 3 ambient air quality

standard is a seasonal standard expressed as a 27 sum of weighted hourl y concentrations, cumulated over the12 hour daylight period from 28 8:00 a.m. to 8:00 p.m. local standard time, during the consecutive 3

- month period within 29Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 432 the O 3 monitoring season with the maximum index value. The secondary O 3 standard is 1 met at an ambient air quality monitoring site when the annual maximum consecutive 3

- 2 month cumulative index value (W126) is less than or equal to (7

- 15) ppm

- hours, as 3 determined in accordance with appendix P to this part. 4 5 3. Appendix P is revis ed to read as follows: 6 Appe ndix P to Part 50 -- Interpretation of the Primary and Secondary National 7 Am bient Air Quality Standards for Ozone . 8 1. General 9 (a) This appendix explains the data handling conventions and computations necessary for 10 determining whether the 8

- hour primary an d secondary

national ambient air quality 11 standards for ozone specified in §50. 15 are met at an ambient ozone air quality 12 monitoring site. Ozone is measured in the ambient air by a reference method based on 13 Appendix D of this part, as applicable, and designated in accordance with part 53 of this 14 chapter, or b y an equivalent method designated in accordance with part 53 of this chapter. 15 Data reporting, data handling, and computation procedures to be used in making 16 comparisons between reported ozone concentrations and the level s of the ozone standard s 17 are specified in the following sections. 18 (b) Whether to exclude, retain, or make adjustments to the data affected b y exceptional 19 events, including stratospheric ozone intrusion and other natural events , is determ ined b y 20 the requirements under § 50.1, § 50.14 and § 51.930. 21 (c) The terms used in this appendix are defined as follows: 22Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 433 8

- hour average is the rolling average of eight hourly ozone concentrations as 1 explained in section 3 of this appendix. 2 Annual fourth

- h ighest daily maximum refers to the fourth

- highest value measured 3 at a monitoring site during a particular year. 4 Annual Cumulative W 126 Index is the maximum sum over three consecutive 5 calendar months of the monthly W126 index in a year, as explained in section 4 of this 6 appendix. 7 Daily maximum 8

- hour average concentration refers to the maximum calculated 8 8
- hour average for a particular day as explained in section 3 of this appendix. 9 Daily W

126 Index is the sum of the sigmoidally weighted hourly ozone 10
concentrations during the 12

- hour daylight period, 8:00 a.m. to 7:59 p.m. local standard 11 time (L ST). 12 Design values are the metrics (i.e., statistics) that are compared to the primary 13 and secondary NAAQS levels to determine compliance, calculated as shown in sec tions 3 14 and 4 of this appendix. 15 Monthly W126 Index is the sum of the dail y W126 index over one calendar month 16 during the required ozone monitoring season , adjusted for incomplete data if appropriate, 17 as explained in section 4 of this appendix. 18 Required oz one monitoring season refers to the span of time within a calendar 19 ye ar when individual States are required to measure ambient ozone concentrations as 20 listed in part 58 Appendix D to this chapter. 21 Year refers to calendar year. 22 2. Requirements for Data Used for Comparisons w ith the Ozone NAAQS 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 434 (a) All valid FRM/FEM ozone data submitted to EPA's Air Quality S ys tem (AQS), or 1 otherwise available to EPA, meeting the requirements of part 58 of this chapter including 2 appendices A, C, and E shall be used in design value calculations. 3 (b) When two or more ozone monitors are operated at a site, the state may in advance 4 designate o ne of them as the primary monitor. If the state has not made this designation, 5 the Administrator will make the designation, either in advance or retrospectively . Design 6 values will be developed using onl y the data from the primary monitor, if this results in a 7 valid design value. If data from the primary monitor do not allow the development of a 8 valid design value, data solely from the other monitor(s) will be used in turn to develop a 9 valid design value, if this results in a valid design value. If there are three or more 10 monitors, the order for such comparison of the other monitors will be determined by the 11 Administrator. The Administrator may combine data from different monitors in different 12 ye ars for the purpose of developing a valid primary or secondary standard design value, if 13 a valid design value cannot be developed solel y with the data from a single monitor. 14 However, data from two or mo re monitors in the same year at the same site will not be 15 combined in an attempt to meet data completeness requirements, except if one monitor 16 has phy sically

replaced another instrument permanently , in which case the two 17 instruments will be considered to b e the same monitor, or if the state has switched the 18 designation of the primary monitor from one instrument to another during the year. 19 (c) Hourly

average concentrations shall be reported in parts per million (ppm) to the third 20 decimal place, with additio nal digits to the right of the third decimal place truncated. The 21 start of each hour shall be identified in local standard time (L ST). 22 3. Comparison to the Primary Standard for Ozone 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 435 (a) Computing 8

- hour averages 1 Running 8

- hour averages shall be computed from the hourly ozone concentration data for 2 each hour of the ye ar and shall be stored in the first, or start, hour of the 8

- hour period. 3 In the event that onl y 6 or 7 hourly averages are available, the valid 8

- hour average shall 4 be computed on the basis of the hours available, using 6 or 7 as the divisor. In the event 5 that only

1, 2, 3, 4, or 5 hourly

averages are available, the 8

- hour average shall be 6 computed on the basis of substituting for all the hours without hourly averages a low 7 hourly

average value selected as follows, us ing 8 as the divisor. For day s within the 8 required ozone monitoring season, the substitution value shall be the lowest hourly 9 average ozone concentration observed during the same hour (local standard time) of any 10 day in the required ozone monitoring season of that year , or one - half of the method 11 detection limit of the ozone instrument, whichever is higher. H owever, if the number of 12
same - hour concentration values available for the required ozone monitoring season for 13 the year, fro m which the lowest observed hourl y concentration would be identified for 14 purposes of this substitution, is less than 50% of the number of day s during the required 15 ozone monitoring season, one

- half the method detection limit of the ozone instrument 16 shall be used in the substitution. For days outside the required ozone monitoring season, 17 the substitution value shall be one - half the method detection limit of the ozone 18 instrument

. An 8
- hour period with no available hourly averages does not have a valid 8

- 19 hour average. The computed 8

- hour average ozone concentrations are not rounded or 20 truncated. 21 (b) Daily maximum 8

- hour average concentrations 22Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 436 There are 24 8

- hour periods in each calendar day . Some of these may not have valid 8

- 1 hour averages, under section 3(a). The daily maximum 8

- hour concentration for a given 2 calendar day

is the highest of the valid 8

- hour average concentrations computed for that 3 day . This process is repeated, yielding a dail y maximum 8

- hour average ozone 4 concentration for each day with ambient ozone monitoring data, including days outside 5 the required ozone monitoring season if data are available. The dail y maximum 8

- hour 6 concentrations from two consecutive day s may have some hourl y concentrations in 7 common. Generally , overlapping dail y maximum 8
- hour averages are not likely , except 8 in those non

- urban monitoring locations with less pronounced diurnal variation in hourly 9 concentrations. Inthese cases, the maximum 8

- hour average concentration from each day 10 is used, even if the two averages have some hours in common. 11 (c) Primary Standard Design Value 12 The primary

standard design value is the annual fourth

- highest daily maximum 8

- hour 13 ozone concentration considering all day s with monitoring data including any day s outside 14 the required ozone monitoring season, expressed in parts per million, averaged over three 15 ye ars. The 3

- ye ar average shall be computed using the three most recent, consecutive 16 ye ars of monitoring data that can yield a valid design value. For a design value to be valid 17 for comparison to the standard, the monitoring data set on which it is based must meet the 18 data completeness requirements described in section 3(d). The computed 3

- ye ar average 19 of the annual fourth

- highest daily maximum 8

- hour average ozone concentrations shall 20 be round ed to three decimal places. Values equal to or greater than 0.xxx5 ppm shall 21 round up. 22 (d ) Data Completeness Requirements for a Valid Design Value 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 437 (i) A design value greater than the standard is valid if in each of the three years there are 1 at least four day s with a daily maximum 8

- hour average concentration. Under sections 2 3(a) and 3(b), there will be a dail y maximum 8

- hour average concentration on any day 3 with at least one hourl y concentration. One or more of these four days may be outside the 4 required ozone monitoring season. 5 (ii) A design value less than or equal to the standard is valid if for at least 75% of the 6 day s in the required ozone monitoring season in each of the three years there are at least 7 18 8
- hour averages in the day that are based on at least 6 measured hourl y average 8 concentrations. 9 (iii) When computing whether the minimum data completeness requirement in section 10 3(d)(ii) has been met for the purpose of showing that a design value equal to or less than 11 the standard is valid, meteorolo gi cal or ambient data may be sufficient to demonstrate 12 that ozone levels on day s with missing data would not have affected the design value . At 13 the request of the state, the Regional Administrator may consider demonstrations that 14 meteorological conditions on one or more days in the required ozone monitoring season 15 which do not have at least 18 8

- hour averages in the day that are based on at least 6 16 measured hourly

average concentrations could not have caused a daily maximum 8

- hour 17 concentration high enough to have been one of the four highest daily maximum 8

- hour 18 concentrations for the ye ar. At the request of the state, day s so demonstrated may be 19 counted towards the 75% requirement for the purpose of validating the design value, 20 subject to the approval of the Regional Administrator. 21 (vi) Years that do not meet the completeness criteria stated in 3(d)(ii) may nevertheless 22 be used to calculate a design value that will be deemed valid with the approval of, or at 23Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 438 the initiative of, the Administrator, who may consider factors such as monitoring site 1 closures/moves, monitoring diligence, the consistency and levels of the valid 2 concentration measurements that are available, and nearb y concentrations in determining 3 whether to use such data. 4 (e) Comparison with the Primary Ozone Standard 5 ( i ) The primary ozone ambient air quality standard is met at an ambient air quality 6 monitoring site when the design value is less than or equal to [0.075] ppm. 7 ( ii) Comparison with the primary ozone standard is demonstrated b y ex amples 1 and 2 as 8 follows: 9 Example 1. Ambient monitoring site attaining the primary ozone standard. 10 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% 0.09250 0 0.090 375 0.08512 5 0.0783 75 0.078 125 2007 96% 0.0847 50 0.0835 00 0.075 375 0.0718 75 0.070 625 2008 98% 0.0808 75 0.0797 50 0. 077 625 0.0755 00 0.060 375 Average 0.07525 0 Rounded 0.075 11 As shown in E xample 1, this monitoring site meets the primary ozone standard because 12 the 3

- ye ar average of the annual fourth

- highest daily maximum 8

- hour average ozone 13 concentrations (i. e., 0.07 5256 ppm , rounded to 0.075 ppm) is less than or equal to [0.075] 14 ppm. The data completeness requirement is also met because no single ye ar has less than 15 75% data completeness. In Example 1, the individual 8

- hour averages and the 3

- year 16Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 439 average are shown with six decimal digits. In actual calculations, all digits supported by 1 the calculator or calculation software must be retained

. 2 3 Example 2. Ambient monitoring site failing to meet the primary ozone standard. 4 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% 0.10512 5 0 .103 500 0.101125 0.0786 25 0.0723 75 2007 74% 0.1042 50 0.103 625 0.09 3000 0.0802 50 0.0695 00 2008 98% 0.103 125 0.101 875 0.1017 50 0.075 375 0.0746 25 Average 0.078 083 Rounded 0.078 5 As shown in Example 2, the data ca pture in 2007 is less than 75%. The primary ozone 6 standard is not met for this monitoring site because the 3

- ye ar average of the fourth

7 highest dail y maximum 8

- hour average ozone concentrations (i.e., 0.078083 ppm, 8 rounded to 0.078 ppm) is greater than [0.075] ppm and is therefore valid despite this 9 incompleteness. In Example 2, the individual 8

- hour averages and the 3

- ye ar average are 10 shown with six decimal digits. In actual calculations, all digits supported by the 11 calculator or calculation software must be retained

. 12 4. Secondary Ambient Air Quality Standard for Ozone 13 (a) Computing the daily W1 26 index value. 14 The secondary ozone ambient air quality standard is a seasonal standard expressed as a 15 sum of weighted hourl y concentrations, cumulated over the 12 hour daylight period fro m 16 8:00 a.m. to 8:00 p.m. local standard time, during the consecutive 3

- month period within 17 the ozone monitoring season with the maximum index value. The first step in 18Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 440 determining whether the standard is met at a monitoring site is to comput e the daily 1 W126 index value for each day by appl ying the sigmoidal weighting function in Equation 2 1 to each reported measurement of hourl y average concentration

. 3 Equation 1 4 

#  

  pm i

am i i c C w W daily i 8
8 126 5
where C i = hourly O 3 at hour i, and C c e w 126 4403 1 1

   . 6 The computed value of the sigmoidall y weighted hourly concentration is not rounded or 7 truncated

. The dail y W126 index is formed by summing the twelve computed hourly 8 values, retaining all decimal places. An illustration of computing a daily W126 index 9 value is below : 10 11 Example 3. D aily W126 index value calculation for an ambient ozone monitoring site. 12 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 0.069667Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 441 6:00 p.m. 0.065 0.029260 7:00 p.m. 0.056 0.011676 Sum=Daily W126 index value 0.625406 ppm - ho urs 1 In Example 3 , the individual weighted concentrations and their sum are shown with six 2 decimal digits. In actual calculations, all digits supported by the calculator or calculation 3 software must be retained

. There are no data completeness requirements for the daily 4 index . If fewer than 12 hourly values are available, only the available hours are weighted 5 and summed. However, there are data completeness requirements for the monthly W126 6 index values and a required adjustment for incomplete data, as des cribe in the next 7 section. 8 (b) Computing the Monthly W 126 Index 9 As described in section 4(a), the daily index value is computed at each monitoring site for 10 each calendar day

in each month during the required ozone monitoring season with no 11 rounding or truncation. The monthly W126 index is the sum of the daily index values 12
over one calendar month

. At an individual monitoring site, a monthl y W126 index is 13 valid if hourly

average ozone concentrations are available for at least 75% of the possible 14 daylight h ours in the month. For months with more than 75% but less than 100% data 15 completeness, the monthly W126 value shall be adjusted for incomplete data by 16 multiplying the unadjusted monthly W126 index value b y the ratio of the number of 17 possible reporting hours to the number of hours with reported ambient hourly 18 concentrations using Equation 2 in this appendix: 19 20 Equation 2 21Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 442 

## 12)/v * (n (D.I.) = M.I. n
1

= j 

## *       

#  1 where, 2 M.I
. = the adjusted monthly W126 index , 3 D.I. = daily W126 index (i.e., the daily sum of the sigmoidally w eighted 4 daylight hourly concentrations ) , 5
n = the number of day s in the calendar month, 6
v = the number of daylight reporting hours (8:00 a.m.
– 7:59 p.m. 7 LST) in the month with reported valid hourl y ozone concentrations. 8 9 The resulting adjusted value of the monthly W126 index shall not be rounded or 10 truncated. 11 (b) Secondary Standard Design Value 12 The secondary standard design value is the 3
- ye ar average of the annual 13 maximum consecutive 3
- month sum of adjusted monthly W126 index value s expressed 14 in ppm

- hours . Specifically , the annual W126 index value is computed on a calendar 15 ye ar basis using the three highest, consecutive adjusted monthly W126 index values. 16 The 3

- ye ar average shall be computed using the most recent, consecutive three calendar 17 ye ars of monitoring data meeting the data completeness requirements described in section 18 4(c). The computed 3

- ye ar average of the annual maximum consecutive 3

- month sum of 19 adjusted monthly

W126 index values in ppm

- hours shall be rounded to a whole number 20 with deci mal values equal to or greater than 0.500 rounding up. 21 (c) Data Completeness Requirement 22Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 443 (i) The annual W126 index is valid for purposes of calculating a 3

- year design value if 1 each full calendar month in the required ozone monitoring season has at least 75% data 2 completeness for daylight hours. 3 (ii) If one or more months during the ozone monitoring seasons of three successive ye ars 4 has less than 75% data completeness, the three ye ars shall nevertheless be used in the 5 computation of a valid design value f or the site if substituting the lowest hourly ozone 6 concentration observed during daylight hours in the required ozone monitoring season of 7 each ye ar , or one - half of the method detection limit of the ozone instrument, whichever is 8 higher, for enough of the missing hourly concentrations within each incomplete month to 9 make the month 75% complete, and then adjusting for the remaining missing data using 10 Equation 2, above results in a design value greater than the level of the standard

. 11 (d ) Comparisons with the Secondary Ozone Standard 12 (i) The secondary ambient ozone air quality standard is met at an ambient air quality 13 monitoring site when the design value is less than or equal to [15] ppm - hours. 14 ( ii) Comparison with the secondary ozone standard is demonstrat ed by example 4 as 15 follows: 16 17 Example 4

. Ambient Monitoring Site Failing to Meet the Secondary Ozone Standard 18 April May June July August September October Overall

2006 Adjusted monthly W126 index 4.442 9.124 12.983 16.153 13.555 4.364 1.302 3
- M onth sum na na 26.549 38.260 42.691 34.072 19.221 2006 Maximum 42.691 42.691 2007Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 444 Adjusted monthly W126 index 3.114 7.214 8.214 8.111 7.455 7.331 5.115 3
- Month sum na na 18.542 23.539 23.780 22.897 19.901 2007 Maximum 23.780 23. 780 2008 Adjusted monthly W126 index 4.574 5.978 6.786 8.214 5.579 4.331 2.115 3
- Month sum na na 17.338 20.978 20.579 18.124 12.025 2008 Maximum 20.978 20.978 3
- Year average W126 index 29.149666 Rounded 29 1 As shown in example 4, the secondary ozone standard is not met for this monitoring site 2 because the 3

- ye ar average of the annual W126 index value for this site is greater than 3 [15] ppm - ho urs : 4 3
- ye ar average W126 index = (42.69 1 + 23.78 0 + 20.97 8 )/3 = 29.1 49666 , which ro unds to 5 29 ppm
- hours

. 6 In Example 4, the adjusted monthly W126 index values and the 3
- month sums of the 7 adjusted monthly W126 index values are shown with three decimal digits. In actual 8 calculations, all digits supported b y the calculator or calculation so ftware must be 9 retained. 10Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 445 1 4. Section 50.14 is amended by adding entries for "Primary and Secondary Ozone 2 Standards” to the end of the table in paragraph (c)(2)(vi) to read as follows: 3 § 50.14 Treatment of air quality monitoring data influenced by exception al 4 events. 5
* * * * * 6
7 (c) *** 8
9 (2) *** 10
11 (vi) *** 12 13 Table 1. Schedule for Exceptional Event Flagging and 14 Documentation Submission for Data to be Used in 15 Designations Decisions for New NAAQS 16 17 NAAQS

Pollutant/ Standard/(Level )/ Promulgation Date Air Quality

D ata Collected for Calendar Year Event Flagging

& Initial Description Deadline Detailed

Documentation Submission Deadline

******* Primary Ozone/ 8
- Hr 2007
- 2009 November 1, 2010 b November 1, 2010 bDraft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 446 Standard (Level TBD) Promulgated by August 31, 2010 201 0 60 Days after the end of the calendar quarter in which the event occurred or March 1, 2011, whichever date occurs first b 60 Days after

the end of the calendar quarter in which the event occurred or March 1, 2011, whichever date occurs first b Secondary O zone/ (Level TBD)Alternative 2

- ye ar Schedule

- to be Promulgated b y August 31, 2010 2008 July 1, 2011 b July 1, 2011 a

2009
- 2010 July 1, 2011 b July 1, 2011 b 2011 60 Days after

the end of the calendar quarter in which the event occurre d or March 1, 2012 , whichever occurs first b 60 Days after

the end of the calendar quarter in which t he event occurred or March 1, 2012 , whichever occurs first b Secondary Ozone / (Level TBD)
- Alternative Accelerated Schedule
- to be Promulgated by August 31, 2010 2007
- 2009 Nove mber 1, 2010 b November 1, 2010 b

2010 60 Days after

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

the end of the calendar quarter in which the event occurred or March 1, 2011, whic hever date occurs first bDraft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 447 a These dates are unchanged from those published in the original rulemaking.
b In dicates 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 est ablish 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. Section 58.50 (c) is revised and (d) is added to read as follow s: 5 § 58.50 Index reporting. 6 (c) The population of a m etropolitan statistical area for purposes of index reporting is the 7 latest available U.S. census population. 8 (d) For O 3 , reporting is required in metropolitan and micropolitan statistical areas 9 wherever monitoring is required under Appendix D to Part 58

— SLAMS M inimum O 3 10 M onitoring Requirements. 11 12 6. Appendix G of Part 58 (3) is revised to read as follows: 13Draft O 3 NPR

– January 5, 20 10 Deliberative, Do Not Quote or Cite 448 Appendix G to Part 58

—Uniform Air Quality Index (AQI) and Daily Reporting 1 3. Must I Report the AQI? 2 You must report the AQI daily if yours is a metropolitan statistical area (MSA) with a 3 population over 350,000. For O 3 , reporting is required in metropolitan and micropolitan 4 statistical areas wherever monitoring is required under Appendix D to Part 58

— SLAMS 5 M inimum O 3 M onitoring Requirements. 6