NCEA-R-1068
November 2002
CASAC Review Draft
Project Work Plan for Revised Air Quality
Criteria For Ozone and Related
Photochemical Oxidants
National Center for Environment Assessment
Office of Research and Development
U. S. Environmental Protection Agency
Research Triangle Park, NC 27711

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United States
Environmental
Protection Agency
Project Work Plan for
Revised Air Quality Criteria
for Ozone and Related
Photochemical Oxidants
This document is a preliminary draft.
It has not been formally released by EPA
and should not at this stage be construed
to represent Agency policy. It is being
circulated for comment on its technical
accuracy and policy implications.
Notice

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DISCLAIMER	
This document is an external draft for review purposes only and does not constitute U.S.
Environmental Protection Agency policy. Mention of trade names or commercial products does not
constitute endorsement or recommendation for use.
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PREFACE
This project work plan has been prepared as a managerial and management information tool for the
U.S. Environmental Protection Agency's National Center for Environmental Assessment Division in
Research Triangle Park, NC. It will be modified and amended from time to time, as necessary, to reflect
actual project requirements and progress. As a result, any proposed schedules and outlines, or any lists of
technical coordinator assignments, authors, or reviewers are subject to change.
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TABLE OF CONTENTS.
I.	INTRODUCTION	 1
A.	LEGISLATIVE BACKGROUND 	 1
B.	REGULATORY BACKGROUND	 2
II.	SCIENTIFIC BACKGROUND AND KEY ISSUES 	 6
A.	HEALTH EFFECTS OF EXPOSURE TO OZONE	 6
B.	ECOLOGICAL EFFECTS OF EXPOSURE TO OZONE	 8
C.	SUMMARY OF MAJOR ISSUES TO BE ADDRESSED IN THE
PREPARATION OF AIR QUALITY CRITERIA FOR OZONE AND
RELATED PHOTOCHEMICAL OXIDANTS 	 10
C.l Specific Issues on Ozone Photochemistry	 10
C.2 Specific Issues on Environmental Ozone Concentrations	 10
C.3 Specific Environmental Effects Issues Related to Ozone	 10
C.4 Specific Health Effects Issues Related to Ozone 	 13
ID. ORGANIZATIONAL STRUCTURE AND PLANNING 		16
A.	ORGANIZATION AND CONTENT		16
B.	METHODS AND PROCEDURES FOR DOCUMENT PREPARATION 		16
C.	PERSONNEL 		18
D.	APPROACH		18
E.	PUBLIC AND SCIENTIFIC PEER REVIEW		19
1.	Review and Revision of the Peer-Review Workshop Draft		19
2.	Public Review of the External Review Draft		19
3.	Review by the Clean Air Scientific Advisory Committee		19
REFERENCES	 21
APPENDKA 	 A-l
APPENDIX B 	 B-l
APPENDIX C 		 C-l
APPENDIX D 	 D-l
APPENDIX E 	 E-l
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I. INTRODUCTION
A. LEGISLATIVE BACKGROUND
Two sections of the Clean Air Act (CAA) govern the establishment, review, and revision of
National Ambient Air Quality Standards (NAAQS). Section 108 (42 U.S.C. 7408) directs the
Administrator of the U.S. Environmental Protection Agency (EPA) to identify ubiquitous pollutants that
may be reasonably anticipated to endanger public health or welfare and to issue air quality criteria for
them. These air quality criteria are to reflect the latest scientific information useful in indicating the kind
and extent of all identifiable effects on public health or welfare that may be expected from the presence
of the pollutant in ambient air.
Section 109(a) of the CAA (42 U.S.C. 7409) directs the Administrator of EPA to propose and
promulgate primary and secondary NAAQS for pollutants identified under Section 108. Section
109(b)(1) defines a primary standard as one that, in the judgment of the Administrator, if attained and
maintained is requisite to protect the public health (see inset) based on the criteria and allowing for an
adequate margin of safety. The secondary standard, as defined in Section 109(b)(2), must specify a level
of air quality that, in the judgment of the Administrator, if attained and maintained, is requisite to protect
the public welfare (see inset) from any known or anticipated adverse effects associated with the presence
of the pollutant in ambient air, based on the criteria.
PUBLIC HEALTH EFFECTS
¦	i .Effects qjx tfoe .health of the gepeial
population, dr identifiable groups Within the .
.1 population, who are exposed to pollutants in
ambient air:
¦	'Effects on mortality
¦] Effects on morbidity
* Effects another health conditions inesllldiii^ :
indicators of:
•	pre-morbid processes, .
.. '..risk factors, and ' 	
•	disease

PUBLIC WELFARE EFFECTS
. ¦
Efforts onpersonalcoinfcirf and well-being
a
Effects on economic values
¦
Deterioration of property
¦
Hazards to transportation
M
Effetts on the environment, including:

• animals
• • ¦* vegetation

~ climate ..
:• * visibility

• • crops	
.. ~ water

.» materials
• Weather

~ soils	
• ¦ • wildlife


Source; U;S. Code (1999)
Section 109(d) of the CAA (42 U.S.C. 7409) requires periodic review and, if appropriate, revision of
existing criteria and standards. If, in the Administrator's judgment, the Agency's review and revision of
criteria make appropriate the proposal of new or revised standards, such standards are to be revised and
promulgated in accordance with Section 109(b). Alternatively, the Administrator may find that revision
of the standards is inappropriate and conclude the review by leaving the existing standards unchanged.

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B. REGULATORY BACKGROUND1
On April 30,1971, the EPA promulgated primary and secondary NAAQS for photochemical
oxidants under Section 109 of the CAA (36 FR 8186). These were set at an hourly average of 0.08 ppm
total photochemical oxidants not to be exceeded more than 1 h per year. On April 20, 1977, the EPA
announced (42 FR 20493) the first review and updating of the 1970 Air Quality Criteria Document
(AQCD) for Photochemical Oxidants in accordance with Section 109(d) of the CAA. In preparing the
AQCD, the EPA made two external review drafts of the document available for public comment, and
these drafts were peer reviewed by the Subcommittee on Scientific Criteria for Photochemical Oxidants
of EPA's Science Advisory Board (SAB). A final revised AQCD for ozone (03) and other photochemical
oxidants was published on June 22, 1978.
Based on the 1978 revised AQCD and taking into account the advice and recommendations of the
Subcommittee, and the comments received from the public, the EPA announced (44 FR 8202) a final
decision to revise the NAAQS for photochemical oxidants on February 8,1979. The final rulemaking
revised the primary standard from 0.08 ppm to 0.12 ppm, set the secondary standard to be the same as
the primary standard, changed the chemical designation of the standards from photochemical oxidants to
03, and revised the definition of the point at which the standard is attained to "when the expected number
of days per calendar year with maximum hourly average concentrations above 0.12 ppm is equal to or
less than one" (see Table 1).
Table 1. National Ambient Air Quality Standards (NAAQS) for Ozone
Date of Promulgation
Primary and Secondary NAAQS
Averaging Time
February 8,1979
0.12 ppm" (235 ^g/m3)
1 hb
July 18, 1997
0.08 ppm" (157 /ig/m3)
8 hc
*1 ppm = 1962 //g/m\ 1 jug/m3 = 5.097 x 10"4 ppm @ 25 °C, 760 mm Hg.
bThe standard is attained when the expected number of days per calendar year with a maximum hourly average concentration
above
235 ^g/m3 (0.12 ppm) is equal to or less than one.
cBased on the 3-year average of the annual fourth-highest daily maximum 8-h average concentration measured at each monitor
within an area.
Source: Federal Register (1979, 1997)
On March 17, 1982, in response to requirements of Section 109(d) of the CAA, the EPA
announced (47 FR 11561) that it planned to revise the existing 1978 AQCD for 03 and other
photochemical oxidants, and on August 22,1983, it announced (48 FR 38009) that review of the primary
and secondary NAAQS for 03 had been initiated. Two public peer-review workshops on draft chapters
of the revised AQCD were held on December 15-17,1982, and on November 16-18, 1983. The EPA
'This text is excerpted and adapted from the "Proposed Decision on the National Ambient Air Quality Standards for Ozone,"
Preamble (40 CFR Part 50; Federal Register 57: 35542-35557, 1992) and updated from the "National Ambient Air Quality
Standards for Ozone; Final Rule" (40 CFR 50; Federal Register 62: 38856-38896, 1997).
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considered comments made at both workshops in preparing the first external review draft that was made
available (49 FR 29845) on July 24,1984, for public review.
On February 13,1985 (50 FR 6049), and on April 2,1986 (51 FR 11339), the EPA announced two
public meetings of the Clean Air Scientific Advisory Committee (CASAC) of EPA's SAB to be held on
March 4-6,1985, and on April 21-22, 1986, respectively. At these meetings, the CASAC reviewed
external drafts of the revised AQCD for 03 and other photochemical oxidants. After completion of this
review, the CASAC forwarded to the Administrator of EPA a closure letter, dated October 22,1986, that
stated the document "represents a scientifically balanced and defensible summary of the extensive
scientific literature." The EPA released the final draft document in August 1986.
The first draft of the Staff Paper "Review of the National Ambient Air Quality Standards for
Ozone: Assessment of Scientific and Technical Information" was reviewed by CASAC at a public
meeting on April 21-22,1986. At that meeting, the CASAC recommended that prior to closure new
information on prolonged exposure effects of 03 be considered in a second draft of the Staff Paper. The
CASAC reviewed this second draft and also a presentation of new and emerging information on the
health and welfare effects of 03 at a public review meeting held on December 14-15,1987. The CASAC
concluded that sufficient new information existed to recommend incorporation of relevant new data into
a supplement to the 1986 AQCD (03 Supplement) and in a third draft of the Staff Paper.
A draft 03 Supplement, "Summary of Selected New Information on Effects of Ozone on Health
and Vegetation: Draft Supplement to Air Quality Criteria for Ozone and Other Photochemical
Oxidants," and the revised Staff Paper were made available to CASAC and to the public in November
1988. The 03 Supplement reviewed and evaluated selected literature concerning exposure- and
concentration-response relationships observed for health effects in humans and experimental animals and
for vegetation effects that appeared as peer-reviewed journal publications or as proceedings papers from
1986 through early 1989. On December 14-15,1988, CASAC held a public meeting to review these
documents. The CASAC sent the Administrator a closure letter, dated May 1, 1989, that stated the draft
03 Supplement, the 1986 AQCD, and the draft Staff Paper "provide an adequate scientific basis for the
EPA to retain or revise the primary and secondary standards of ozone." The CASAC concluded that it
would be some time before enough new information on the health effects of multihour and chronic
exposure to 03 would be published in scientific journals to receive full peer review and, thus, be suitable
for inclusion in a criteria document. The CASAC further concluded that such information could be
considered in the next review of the 03 NAAQS. A final version of the 03 Supplement has been
published (U.S. Environmental Protection Agency, 1992).
On October 22, 1991, the American Lung Association and other plaintiffs filed suit to compel the
Agency to complete the review of the criteria and standards for 03 in accordance with the CAA. The
U.S. District Court for the Eastern District of New York subsequently issued an order requiring the EPA
to announce its proposed decision on whether to revise the standards for 03 by August 1, 1992, and to
announce its final decision by March 1, 1993.
The proposed decision on 03 appearing in the Federal Register on August 10, 1992 (57 FR 35542),
indicated that revision of the existing 1-h NAAQS was not appropriate at this time. A public hearing on
this decision took place on September 1, 1992, at the EPA Education Center in Washington, DC, and
public comments were received through October 9,1992. The final decision not to revise the 1-h
NAAQS was published in the Federal Register on March 9,1993 (58 FR 13008). This decision,
however, did not take into consideration a number of recent studies on the health and welfare effects of
03 that were published since the last literature review in early 1989.
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The Agency initiated consideration of such studies as part of the next congressionally-mandated
periodic review of criteria and NAAQS for Ozone. The new studies were assessed in revised workshop
draft 03 AQCD chapters that were peer reviewed in July and September 1993, followed by public release
of the First External Review Draft in February 1994 and CASAC review on July 20-21, 1994. A new
(revised) 03 AQCD was released and reviewed by CASAC on March 21-25,1995, with final CASAC
review on September 19-20, 1995. Closure was recognized in a November 28, 1995 letter to the EPA
Administrator. The final AQCD for 03 was published in July 1996.
The first draft of the Staff Paper, "Review of the National Ambient Air Quality Standards for
Ozone: Assessment of Scientific and Technical Information," also was reviewed by CASAC at the March
21-22, 1995 public meeting. Subsequent drafts of the Staff Paper were reviewed by CASAC at public
meetings held on September 19-20,1995 and March 21,1996. Closure on the primary and secondary
standard portions of the draft Staff Paper was recognized in letters to the EPA Administrator dated
November 30,1995 and April 4,1996, respectively. The final Staff Paper for 03 was published in June
1996.
On December 13,1996 EPA published its proposed decision to revise the 03 NAAQS (61 FR
65716). EPA provided extensive opportunities for public comment on the proposed decision, including
several public hearings and two national satellite telecasts. EPA's final decisipn to promulgate a new 8-h
03 NAAQS (see Table 1) was published on July 18,1997 (62 FR 38856).
Following promulgation, numerous petitions2 for review of the standards were filed in the U.S.
Court of Appeals for the District of Columbia Circuit (D.C. Circuit). On May 14, 1999 the Court
remanded die 03 NAAQS to EPA3, finding that section 109 of the CAA, as interpreted by EPA, effected
an unconstitutional delegation of legislative authority. In addition, the Court directed that, in responding
to the remand, EPA should consider the potential beneficial health effects of 03 pollution in shielding the
public from the effects of solar ultraviolet (UV) radiation. On January 27, 2000, EPA petitioned the U.S.
Supreme Court for certiorari on the constitutional issue (and two other issues), but did not request review
of the D.C. Circuit ruling regarding the potential beneficial health effects of 03. On February 27, 2001
the U.S. Supreme Court unanimously reversed the judgment of the D.C. Circuit on the constitutional
issue4, holding that section 109 of the CAA does not delegate legislative power to the EPA in
contravention of the Constitution, and remanded the case to the D.C. Circuit to consider challenges to the
03 NAAQS that had not been addressed by that Court's earlier decisions. On March 26, 2002, the D C.
Circuit issued its final decision5, finding the 1997 03 NAAQS to be "neither arbitrary nor capricious,"
and denied the remaining petitions for review.
On November 14, 2001 EPA proposed to respond to the Court's remand to consider the potential
beneficial health effects of 03 pollution in shielding the public from the effects of solar UV radiation by
leaving the 1997 8-h NAAQS unchanged. EPA anticipates publishing its final response to this remand in
Fall 2002.
The EPA's National Center for Environmental Assessment Division in Research Triangle Park, NC
(NCEA-RTP) is proceeding with the next periodic review of the air quality criteria for 03. Under the
\American Trucking Associations v. EPA, No. 97-1441
'American Trucking Associations v. EPA, 175 F.3d 1027 (D.C. Cir., 1999)
*Whitman v. American Trucking Associations, 531 U.S. 457 (2001)
American Trucking Associations v. EPA, 283 F.3d 355, (D.C. Cir. 2002)
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processes established in Sections 108 and 109 of the CAA, the EPA began by announcing the
commencement of the review in the Federal Register with a call for information (see Appendix A). After
carefully assessing and evaluating the pertinent new studies, the EPA will then prepare a preliminary
draft of a revised criteria document and subject it sequentially to review at expert peer-review
workshops, by the public, and by the CASAC. Once the CASAC has reviewed the first external review
draft of the revised criteria document, thus providing a preliminary basis for review of the existing
standards, the EPA's Office of Air Quality Planning and Standards (OAQPS) staff will prepare a draft
Staff Paper assessing the most significant information contained in the draft criteria document and
develop recommendations on whether to retain or revise, if appropriate, the NAAQS for 03. Subsequent
reviews by the public and by CASAC will occur, as necessary. A proposed schedule and project status
for the overall criteria document preparation process can be found in Table 2.
Table 2. Proposed Schedule for Revised Ozone Air Quality Criteria
Document Development6
Maior Milestones
Tareet Dates
1.
Literature Search
Ongoing
2.
Initiate Draft Project Work Plan
August 2000
3.
Initiate Procurement Requests for Phase I Document Preparation
August 2000
4.
Federal Register Call for Information
September 26, 2000
5.
Initiate Procurement Requests for Phase II Document Preparation
March-August 2001
6.
Release of Draft Project Plan for Public Comment
December 2001
7.
End of Public Comment Period
March 2002
8.
Release of Draft Project Plan for CASAC Review
December 2002
9.
CASAC/SAB Public Meeting to Review Project Work Plan
January 2003
10.
First (Internal) Rough Draft of Document Chapters
January 2003
11.
Workshop Draft of Criteria Document Chapters
February 2003
12.
Peer-Review Workshop(s)
March/April 2003
13.
First External Review Draft (ERD1)
June 2003
14.
Public Comment Period (90 days)
July-Sept 2003
15.
CASAC/SAB Public Review Meeting (First External Review Draft)
Oct/Nov 2003
16.
Send Proposed Final Draft to CASAC
March 2004
17.
Public Comment Period
March-May 2004
18.
CASAC/SAB Public Review Meeting (Closure)
June 2004
19.
Final Draft Document
August 2004
'Proposed schedule will be modified from time to time, as necessary, to reflect actual project requirements and progress.
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II. SCIENTIFIC BACKGROUND AND KEY ISSUES
The following sections on health (Section A) and ecological (Section B) effects associated with 03
exposures of human populations and biological components of natural and managed ecosystems
summarize information presented in the 1996 AQCD (U.S. Environmental Protection Agency, 1996).
A third section (Section C) identifies major issues to be addressed in the preparation of a revised 03
AQCD, including not only new issues related to the health and environmental effects of 03 exposure, but
also issues associated with 03 photochemistry; issues on environmental 03 concentrations attributable to
anthropogenic and background sources; and issues related to the health and environmental effects
associated with changes in solar UV radiation and global warming, as mediated by changes in
tropospheric 03.
A. HEALTH EFFECTS OF EXPOSURE TO OZONE
Ozone is a respiratory tract irritant that reacts primarily with the lungs (see Table 3). Large
variability is common between individuals in their responsiveness to the acute pulmonary-function
effects of ozone. About 5 to 20% of individuals tested in clinical trials experienced pulmonary function
decrements or respiratory symptoms at 03 levels lower than those affecting many others. Thus, data from
controlled human studies indicate that acute, reversible decrements in lung function and increased
respiratory symptoms, such as cough and shortness of breath, occur in some individuals exposed for 1 to
3 hours to 03 concentrations as low as 0.12 to 0.16 ppm while performing heavy exercise (e.g., running).
These effects may decrease exercise performance in certain individuals, particularly at the higher 03
concentrations within this range. With more prolonged exposure (up to 7 hours), similar health effects
are found at even lower 03 concentrations ranging from 0.08 to 0.12 ppm in individuals performing
moderate exercise (e.g., brisk walking). Children and adolescents (si8 years old) respond to 03
exposure in a similar manner as young adults, except for less reporting of respiratory symptoms, while
older adults (^50 years old) may, in fact, have smaller changes in lung function and symptoms. Low
ambient 03 exposure also has been linked with the exacerbation of symptoms in individuals with
respiratory disease (e.g., asthma), leading to increased hospital admissions and increased visits to
emergency departments during warm weather. It is not clear what effects other pollutants, other
environmental factors (e.g., temperature and relative humidity), and allergens may have in conjunction
with 03 exposure.
In humans, 7-hr 03 exposures also have been associated with inflammation of the lungs which may
be involved in the progression from acute to chronic health effects. Human epidemiology studies, as well
as studies involving laboratory animals, suggest there may be persistent pulmonary-impairment effects
associated with chronic 03 exposure. Thus, many health professionals are concerned that repeated
exposure to 03 over a lifetime may compromise normal lung function, possibly increase development of
lung fibrosis, and may even accelerate lung function decline associated with the aging of the lung.
Research is needed to assess if such effects are actually occurring in naturally exposed populations,
as well as to determine the temporal exposure patterns that may be associated with particular chronic
effects.
Controlled exposure studies conducted with humans have demonstrated that, with repeated daily
exposure to 03, there is an increase from the first to the second day in the magnitude of pulmonary
function changes (e.g., constriction of airways leading to reduction of air flow into the lungs). However,
with continued daily exposures these effects become much smaller in size from the third or fourth day
onwards. This attenuation phenomenon was previously termed "adaptation" or "habituation" and was
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Table 3. Summary of Pulmonary Effects from Exposure to Ozone
Health Effect(s)"	At-Risk Population6,0
Decrements in lung function (reduced ability to	Moderate and heavily exercising children
take a deep breath) and increased respiratory	and adults
symptoms (cough, shortness of breath, pain upon
deep inspiration) with 1 to 3 hour (i0.12 ppm)
or 7 hour (2:0.08 ppm) exposures; increased
inflammatory indicators with 2 horn (2:0.4 ppm)
or 7 hour (sO.08 ppm) exposures
Reduced maximal exercise performance with
high ambient exposure (^ 0.18 ppm)
Exacerbation of respiratory symptoms with low
ambient 03 exposure, increased ambient
temperature, and other environmental factors,
resulting in increased hospital admissions and
emergency department visits for respiratory
causes during warm weather.
Increased susceptibility to bacterial respiratory
infections based on experimental animal studies
Changes in lung structure, function, and
biochemistry indicative of airway irritation and
inflammation following long-term exposures of
experimental animals; possible development of
chronic lung disease	
"EPA has an existing significant harm level of 0.6 ppm 03 for an averaging time of 1 hr. Exposure under these
conditions would be expected to create life-threatening or permanently disabling health effects in significant
portions of the population engaged in light exercise.
"Exercising individuals in the general population, especially where outdoor activity results in markedly
increased minute ventilation, may be particularly responsive to ozone exposure.
"Ethical concerns have limited the research in persons with preexisting respiratory disease such that low Oa
concentrations and light exercise levels were utilized or "mild" cases were evaluated; however, functional or
symptomatic effects of the same magnitude in individuals with reduced lung function may have greater clinical
significance than for healthy adults wjthout preexisting disease states.
interpreted by some to represent a beneficial biological coping mechanism to repeated ozone exposure.
New evidence, however, has clarified that this attenuation is neither permanent nor likely to be
beneficial. That is, persons showing the attenuation upon first exposure to 03 over multiple days show
the same magnitude of their original response upon reexposure to 03 after a week or so without 03
exposure. Also, persons living in high background 03 areas show similar responses upon initial exposure
to higher peak 03 levels. Lastly, the attenuation of acute response, when it occurs during later days of
Heavily exercising children and adults
Individuals with asthma
Unknown
Unknown
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multi-day 03 pollution episodes, allows more air flow into the lungs. This exposure increases the delivery
of more 03 to lung tissue and increases the risk of more serious chronic exposure effects of the types
noted above. This is supported by animal studies that found less attenuation of responses such as
inflammation, even though pulmonary function changes were attenuated upon repeated 03 exposure.
A number of factors will determine the response of a given individual to 03 exposure. Certainly,
03 concentrations measured by fixed-site urban monitors will be a factor. But 03 concentrations can vary
over time and place within a specific urban area. In addition, frequent periods of ambient exposure,
particularly at high 03 concentrations, also may affect responsiveness to 03 during other sequential
periods of exposure. Individual exposure, therefore, will vary depending on where the individual lives
and works and how long the person is exposed to 03 at their respective locations. Since pulmonary
function will affect the amount of 03 inhaled, it is also important to know the type and level of activity
performed under these exposure conditions to better understand the consequences.
Even if exposure history is well defined, some individuals may be more 03 sensitive because of
their medical history. In individuals with pre-existing pulmonary disorders, such as asthma or chronic
obstructive pulmonary disease (COPD), decreases in pulmonary function produced by exposure to ozone,
while similar to those experienced by healthy individuals, represent a further decline in lung volumes and
flows that are already diminished. It is possible that such declines may further impair the ability of these
individuals to perform normal activities.
Studies of children show that their pulmonary function response to acute 03 exposure is similar to
that of adults. However, children, whose lungs are still developing, may be more likely to experience
high 03 doses insofar as they exercise outdoors more than the typical adult. Preliminary laboratory
animal studies have indicated some age-dependent lung responses to 03. However, additional research is
needed in this area. Thus, special attention should be given to evaluation of 03 levels in areas and at
times when children are at school or play.
B. ECOLOGICAL EFFECTS OF EXPOSURE TO OZONE
Ozone is the gaseous pollutant most injurious to the many different biological components that
make up all natural and managed ecosystems (U.S. Environmental Protection Agency, 1986, 1996).
Ozone, more than any other air pollutant, is known to impair the growth of agricultural crops and native
vegetation in ecosystems throughout the United States. Exposure of vegetation to 03 inhibits
photosynthesis, alters carbon allocation, and interferes with mycorrhizal formation in tree roots.
Disruption of these important physiological processes can suppress the growth of trees, shrubs, and
herbaceous vegetation by decreasing their capacity to form the carbon compounds needed for growth and
maintenance and their ability to absorb water and mineral nutrients from soil. In addition, loss of vigor
increases susceptibility of trees and crops to insects and pathogens, and reduces their capacity to
reproduce.
Only 03 that enters the plant through openings in the leaves (termed stomata) can impair plant
processes. Ozone injury will not be detected if (1) the rate of 03 uptake is small enough for the plant to
detoxify or metabolize 03 or its reaction products, or (2) the plant is able to repair or compensate for the
03 effects. Also, an effect will occur only if sufficient 03 reaches the sensitive sites within a leaf cell.
The uptake and movement of 03 to sensitive cellular sites are subject to various biochemical and
physiological controls. The magnitude of 03-induced effects will depend upon the physical environment
of the plant, including both macro- and micro-climatic factors; the chemical environment of the plant,
including other gaseous pollutants; and biological factors, including genetic potential, developmental age
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of the plant, and interaction with plant disease-causing organisms. Cellular injury may manifest itself in
a number of ways, including visible foliar injury; premature senescence; reduced growth or yield, or
both; reduced plant vigor; and sometimes death. The alterations in the biochemical and physiological
processes mentioned above may occur with or without visible injury to the plant.
Through the process of photosynthesis, green plants use the sun's radiant energy to combine
carbon dioxide from the atmosphere with water taken up through the roots to form sugars (chemical
energy). These sugars are made for use by plants, but all other organisms that are directly or indirectly
dependent upon green plants for food also utilize this stored chemical energy.
The sugars (carbon compounds) formed during photosynthesis are moved about the plant to buds,
stems, leaves, and roots to be used during growth, maintenance, and reproduction. Ozone-induced
inhibition of photosynthesis decreases the amount of sugars that plants can produce and, therefore, alter
the allocation and translocation of the sugars from the leaves and shoots to the roots. In addition, when
03 injuiy occurs, plants use the sugars and other stored compounds to repair injured tissues, rendering
them unavailable for growth, maintenance, and reproduction.
Sugars translocated from the leaves to the roots are of particular importance in forming
mycorrhizae, a symbiotic relationship between the roots of most plants and the mycelia of soil fungi.
Mycorrhizae play an important role in the root uptake of mineral nutrients, especially nitrogen, and water
from the soil. Many studies have shown that plants cannot compete with other plants for nutrients and
water, and in many cases, lose vigor and die when prevented from forming mycorrhizae or when the
mycorrhizal relationship is disrupted. Plants unable to absorb water and mineral nutrients from the soil
are more susceptible to drought, insect infestation, and attack by pathogens. Mycorrhizae have also been
shown to protect trees from root diseases.
Not all plants are sensitive to 03. Sensitive plant species, however, are found throughout the
United States. A wide range in sensitivity exists both within and among plant species. For example,
though most plant species differ in 03 sensitivity, different cultivars of crop plants within the same
species also may differ in sensitivity.
Fumigation studies (in the laboratory or field, on crops or trees) suggest that plants will exhibit a
response to 03 concentrations above 0.06 ppm within hours of exposure. Concern arises from the fact
that 03 is a regional pollutant. Concentrations across most of eastern North America exceed 0.06 ppm
during most of the growing season.
Reductions in growth and reproduction (yield) of agricultural crop plants due to 03 exposure occur
during their life span, which is usually only one growing season. Trees and shrubs, on the other hand,
live for many years. They must cope with the cumulative effects of both short- and long-term stresses.
The needles of sensitive trees, such as eastern white pine, may develop visible symptoms within days of
exposure to high 03 concentrations. Repeated episodic 03 exposures above 0.08 ppm lasting from hours
to several days have been shown to have the greatest impact on growth and reproduction of both crops
and trees. In most cases, tree responses are more subtle because growth responses take time. Decreased
growth and dieback in trees may not become noticeable for years and are usually the result of cumulative
responses to continuing 03 exposures, as well as interaction with other stresses, over a period of many
years. Studies in the San Bernardino Mountains of California, on the Cumberland Plateau of East
Tennessee, and in the Appalachian Mountains of Virginia, indicate that reductions in growth,
determinable from growth rings, began as early as 20 years before the studies began. When
measurements were available, all growth reductions could be associated with 1-h 03 concentrations
exceeding 0.08 ppm.
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In conplusion, 03 has been shown to be the gaseous criteria air pollutant most injurious to plants.
It is a regional pollutant. During the growing season, plant exposure to phytotoxic concentrations occurs
throughout the United States east of the Mississippi River and near urban areas of the western United
States. The effects of 03 on plant growth, especially crop plants, are well documented. The biochemical
and physiological processes in plants that are altered by the entrance of 03 through the leaves are
generally recognized, even though the exact manner in which 03 alters them is not yet fully understood.
G SUMMARY OF MAJOR ISSUES TO BE ADDRESSED IN THE PREPARATION
OF AIR QUALITY CRITERIA FOR OZONE AND RELATED
PHOTOCHEMICAL OXIDANTS
A number of issues continue to be identified by authors and reviewers of the previous Air Quality
Criteria Document (AQCD) on ozone (03) and other photochemical oxidants (U.S. Environmental
Protection Agency, 1996). Many of these issues were enumerated following public discussions on draft
versions of the AQCD or the Staff Paper or in comments received from the Clean Air Scientific Advisory
Committee of the EPA's Science Advisory Board. They are listed below, by subject category, as a series
of questions that need to be addressed in the next revision of the 03 criteria document.
C.1 Specific Issues on Ozone Photochemistry
•	What is the current level of understanding of atmospheric chemistry involving 03?
•	What is the effect of particulate matter on the photochemical production and destruction of ozone?
•	How important to background concentrations is the intrusion of ozone from the stratosphere into the
troposphere?
•	How important is the downward transport of ozone and its precursors from layers of elevated
concentrations of these species in the mid-troposphere? What is the origin of these layers?
•	What is the effect of ozone produced in polluted boundary layers of the United States on the
photochemistry of the background atmosphere?
C.2 Specific Issues on Environmental Ozone Concentrations
•	What fraction of observed regional ozone concentrations can be attributed to other sources such as
anthropogenic emissions outside North America?
•	What are the spatial concentration patterns of oxidants other than ozone, for example, PAN and how do
these differ from ozone?
•	How well do the statistics of ozone concentrations obtained using one averaging period relate to those
obtained using different averaging periods?
C.3 Specific Environmental Effects Issues Related to Ozone
The previous review (U.S. Environmental Protection Agency, 1996) indicated that remaining
uncertainties in available data for a number of environmental effects categories increased the difficulties
associated with developing qualitative or quantifiable risks to various components of agronomic,
forested, and natural ecosystems. The following issues address these uncertainties in the data and
identify new scientific information that would help select an appropriate secondary standard that is
protective of crops, natural vegetation, and ecosystem components and processes.
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The common theme at a recent international air pollution conference held in Research Triangle
Park, North Carolina was the need for more complete information on air pollutant interactions. The era
of single pollutant - single species ecological risk assessment may be drawing to a close. The need to
better understand how ozone influences ecosystems in a complex and changing global climate has come
to the forefront in recent years. Due to financial and logistical constraints of conducting large-scale
studies, multistressor-multispecies ecological risk assessments will require new and innovative
approaches that may rely more on modeling pollutant exposure and ecosystem response.
The four major categories where additional environmental effects information is needed are shown
below, with research and monitoring assessment questions put forth for elucidative purposes. Questions
are grouped by subcategories within each of the four major categories.
1.	Exposure Dynamics: monitoring to determine ambient ozone concentrations encountered in urban,
rural farm/forest areas, exposure patterns (episodes), concentrations vs flux, relationship between
chamber and field exposure data, plant uptake;
a.	Modeling
•	What is the state of the science in modeling ozone concentration gradients across plant canopies,
plant communities, or multiple ecological resource landscapes?
•	How precise and accurate are these models?
•	How well can these models be extrapolated temporally and spatially within or across different
forest types, crops, ecophysiographic regions, the urban-rural interface, etc.?
•	Can passive samplers be useful to "fill in the gaps" in model-derived ozone concentrations at
remote areas where continuous ozone monitoring is not routinely performed?
b.	Exposure Regimes
•	How do episodic exposures (predisposition) alter plant or animal response to chronic, cumulative
ozone exposures?
•	How do we translate fumigation chamber results, that are typically conducted on tree seedlings or
crops, to whole trees, forest stands, ecosystems, watersheds, airsheds, or ecophysiographic
regions?
2.	Plant/Animal Response and Mode of Action: biological, chemical and physical, especially cellular
biochemical physiological mechanisms; individual plant sensitivity/ genetic composition; site/habitat
influences; pest, disease, and abiotic stress interactions;
a. Plants
•	Is there new information regarding ozone's mode of action once it enters a plant?
•	Are there genetic markers that can be identified using state-of-the-art molecular biological
methodologies that differentiate ozone tolerant and intolerant cultivars and species?
•	What is known about ozone's effects on floral ecosystem components in combination with other
air pollutants?
•	How does ozone, both singly and in combination with other air pollutants, influence plant-
pathogen and plant-pest interactions?
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b. Wildlife
•	Are the exposure effects of ozone on mammalian wildlife similar to human exposure responses?
•	Has ozone altered the nutritional content of forage for domestic animals or wildlife populations?
•	What is known about ozone's effects on faunal ecosystem components in combination with other
air pollutants?
3.	Ecosystems: increase understanding of the exposure/response relationships of sensitive individual
plant species and forest trees to ozone, under ambient conditions, characterize the impact of exposure
on interspecific competition on both above- and below-ground interactions and on ecosystem
products and services.
a.	Biodiversity
•	Does tropospheric ozone influence the biodiversity of ecological systems?
•	Moreover, if ozone has already brought about a change in biodiversity, can such a change alter the
production of biogenic precursors that, in turn, influence natural ozone formation?
b.	Terrestrial-Aquatic Interface
•	Have terrestrial ecosystem effects of ozone exposure affected aquatic ecosystems?
•	Has ozone altered the nutrient cycling in forested catchments that may manifest themselves as
changes in water chemistry at the stream and watershed levels?
4.	Solar UV Radiation Transmission and Global Climate Change
•	What is the role of ozone in the planetary boundary layer in attenuating solar UV-B radiation?
•	How is this role affected by the presence of other scattering and absorbing pollutants, for example
fine particles in the planetary boundary layer?
•	What is known about environmental effects of changes in solar UV radiation transmission
mediated by changes in tropospheric ozone concentrations?
•	What is the contribution of ozone generated in polluted boundary layers to radiative forcing and
hence to climate change?
•	What is known about environmental effects of global climate changes mediated by changes in
tropospheric ozone concentrations?
5.	Assessment: assessment of economic impacts on products (crops, forests, etc.) and ecosystem
services, benefits derived from control of ozone exposures. Removal of as many of the uncertainties
.cited above as possible will benefit and assist EPA in developing a secondary NAAQS for ozone that
will protect vegetation and other ecosystem components and processes.
a. Economics
•	Have new and innovative methods evolved for monetizing ecosystem services and non-
consumptive use products (e.g., aesthetics, recreation, plant nutritional quality for wildlife)?
•	Have the economic impacts of ozone on consumptive-use ecosystem products (e.g., crop yields,
timber) been reassessed and revised since the last criteria document?
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b. Scaling Up
• What recent advances, if any, now allow for localized or spatiotemporalty disparate data sets to be
aggregated for regional ecological effects assessments?
C.4 Specific Health Effects Issues Related to Ozone
1.	The concentration, duration, and nature of real-world, human exposure to ozone and other
potentially harmful environmental exposures.
•	What is the cunrent status of population-based information on total human ozone exposure and
spatial and temporal patterns of exposures of sensitive population groups?
•	What is the current level of understanding of human exposure to other potentially harmful air
pollutants that co-exist with ozone in the ambient air?
•	What is the current level of understanding about changes in human exposure to solar ultraviolet
radiation mediated by changes in tropospheric ozone concentrations?
•	How do human activity patterns and variable sun-seeking or sun-avoidance behaviors affect long-
term ultraviolet radiation exposures of sensitive population groups?
2.	Determination of factors influencing ozone dosimetry and the magnitude of ozone response
•	What are the inherent interspecies differences in sensitivity to ozone and ozone dosimetry in
different regions of the respiratory tract?
•	What ozone reaction products can be found in the respiratory tract cells, tissues, or fluids as
biomarkers of short- or long-term ozone exposure?
3.	Effects of repeated short-term, prolonged, or long-term ozone exposure on potential histopathologic,
pathophysiologic and clinical sequelae of respiratory disease (e.g., increased decline in lung
function, increased asthma incidence, elevated daily mortality, and increased frequency of
hospitalization and emergency room visits)
•	Does repeated, short-term or prolonged exposure to ozone cause permanent loss of lung function
or acceleration of lung function loss rate in adults?
•	Does repeated, short-term or prolonged exposure to ozone cause retardation of lung function
growth rate in children?
•	Does long-term ozone exposure promote development of asthma or chronic lung disease?
•	Does long-term ozone exposure promote shortening of human life span via promotion of such
diseases?
4.	Health risks of continuous versus intermittent daily exposure to ozone
•	What annual and seasonal patterns of long-term ozone exposure are most instrumental in
promoting potentially harmful health effects?
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5.	Identification of groups potentially at-risk from ozone exposure as well as the host and
environmental factors responsible for differential susceptibility to ozone
•	What is the nature of health effects in persons with pre-existing disease who are exposed to
ozone? What are the quantitative relationships between ambient ozone exposures and the
frequencies of these effects?
•	Will repeated, elevated short-term exposure to ozone affect disease outcome?
•	Is susceptibility to the effects of short-term ozone exposure associated with long-term ozone
susceptibility?
•	What host and environmental factors (e.g., demographic, socioeconomic, and genetic) are
•	associated with susceptibility to short- and long-term exposure to ozone?
6.	Studies on the attenuation ("adaptation") of ozone effects with repeated exposures
•	Does "adaptation" to repeated, short-term ozone exposure actually increase the long-term dose of
ozone, and thereby increase disease risk in persons who "adapt"?
7.	Role of inflammation in response to ozone
•	What is the nature and time-course of lung inflammation in healthy persons and persons with
pre-existing lung disease like asthma?
•	What is the significance of the inflammatory response to ozone inferred from bronchoalveolar
lavage?
8.	Biological mechanisms of action of ozone
•	What are the mechanisms and time-courses of ozone-induced cellular and tissue injury, repair, and
remodeling?
•	What are the effects of age, gender, and pre-existing disease on cellular and tissue responses to
ozone-induced injury?
9.	Quantitative laboratory animal-to-man extrapolation of effects (also see #2 above)
•	What are the interspecies differences in basic mechanisms of lung injury and repair, irrespective
of environmental pollution effects on these processes?
•	Which ozone-induced health effects are sufficiently characterized to be quantitatively compared
across species?
10.	Interaction of ozone with other air pollutants
•	What is the nature of health effects in persons exposed to multi-pollutant mixtures that contain
ozone in comparison to exposure to ozone alone?
•	What is the nature of health effects in persons exposed to multi-pollutant mixtures with and
without ozone?
11.	Influence of ozone on host defenses against infectious and neoplastic disease
12.	Tests evaluating small airway function in humans (e.g., small-airway resistance, gas-exchange
surface and oxygen diffusion capacity, and ventilation-perfusion mismatches)
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13.	Influence of ozone exposure on inhaled particle dosimetry
14.	The responses of bronchial and alveolar epithelium to ozone in humans
15.	Genotoxic, carcinogenic, and co-carcinogenic effects of ozone
16.	Extra pulmonary effects of ozone
•	What are the indirect effects of ozone in non-pulmonary tissues originating from inhalation
exposure?
•	What are the direct exposure effects of ozone on surface organs and tissues (e.g., effects on the
skin, hair, and mucous membranes of the eye)?
17.	Effects of changes in exposure to ultraviolet (U V) B radiation mediated by changes in tropospheric
ozone concentrations.
•	What is the general nature of health effects associated with UV-B radiation exposures?
•	What is known about susceptible population groups and the effects of short- and long-term
exposure patterns?
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III. Organizational structure and Planning
A. ORGANIZATION AND CONTENT
The updated AQCD for 03 and related photochemical oxidants will critically evaluate and assess
scientific information on the health and welfare effects associated with exposure to the concentrations of
these pollutants in ambient air. The document is not intended to be an exhaustive literature review.
Rather, the cited references should reflect the current state of knowledge on the most relevant issues
pertinent to the NAAQS for 03, now set at 0.12 ppm for 1 h and 0.08 ppm for 8 h. Although emphasis is
placed on the presentation of health and welfare effects data, other scientific data will be presented and
evaluated in order to provide a better understanding of the nature, sources, distribution, measurement,
and concentrations of 03 and related photochemical oxidants in ambient air, as well as the measurement
of population exposure to these pollutants.
The focus of the selected scientific information in the text will come from more recent literature
published since completion of the previous 03 AQCD (U.S. Environmental Protection Agency, 1996).
Emphasis will be placed on studies conducted at or near 03 concentrations found in ambient air. Other
studies may be included if they contain unique data, such as the documentation of a previously
unreported effect or of a mechanism for an observed effect; or if they were multiple-concentration studies
designed to provide exposure-response relationships. Generally, this is not an issue for human clinical or
epidemiology studies. However, for animal toxicology studies, typically only those studies conducted at
less than 1 ppm 03 will be considered. Key information from studies assessed in the previous 03 AQCD
and whose data impacted the derivation of the current NAAQS will briefly be summarized in the text,
along with specific citations to the previous document. Prior studies will also be discussed if they are
(1) open to reinterpretation in light of newer data, or (2) potentially useful in deriving revised standards
for 03. Generally, only published information that has undergone scientific peer review will be included
in the criteria document. Newer studies not published in the open literature but meeting high standards
of scientific reporting may also be included.
The proposed structure of the document will begin with an Executive Summary and Conclusions.
Chapter 1 will provide a brief introduction and present information on the legislative background and
purpose of the document, as well as an overview of the organization of the document. Chapter 2 will
provide information on the physics and chemistry of 03 and related photochemical oxidants in the
atmosphere; and Chapter 3 will cover environmental concentrations, patterns, and exposure estimates.
Chapter 4 will deal with ecological and other environmental effects of 03 and related photochemical
oxidants. Chapters 5, 6, and 7 will discuss animal toxicological studies, human health effects from
controlled-exposure studies, and epidemiologic studies of ambient air exposure to humans, respectively.
The final chapter (Chapter 8) will be an integrative and interpretive evaluation of health and
environmental risks.
B. METHODS AND PROCEDURES FOR DOCUMENT PREPARATION
The procedures for developing the revised criteria document for 03 and related photochemical
oxidants will be essentially the same as those used for recent criteria documents (Figure 1). Briefly, the
respective responsibilities are as follows. The Director of NCEA-RTP appoints a project manager and
team whose responsibility is developing the project work plan for preparation of the 03 criteria
document. NCEA-RTP's Director also invites input from individuals in other EPA program and policy
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Figure 1. Summary of Criteria Document Preparation Process
to
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to
Preparation and Internal Review of NCEA Air Quality Criteria Documents
Phase I: Document Planning and Initiation
•	Initiation of Literature Search and Article Procurement Procedures—Notice in Federal
Register
•	Assignment of Project Manager and Other NCEA-RTP Staff Members to Document
Preparation Team
•	Recruitment of Internal EPA Task Force and Outside Contributing Consultants
•	Development of Work Plan and Timetable for Document Preparation—Definition
of Document Contents
•	Briefing of EPA Science Advisory Board (SAB/CAS AC) on Document Plan and
Contents—Revise Plan as Advised
Phase II: Preparation of Working Draft
•	Accumulation and Analysis of Pertinent Literature
•	Writing of Rough Drafts of Document Sections—Mainly Summarizing Relevant
Published Studies
•	Preliminary Meeting of Authors to Expand Initial Drafts—Initiate Critical
Assessment of Studies
•	Typing and Circulation of Working Draft to Internal Task Force and Outside Reviewing
Consultants
External Peer Review of NCEA Air Quality Criteria Documents
Phase IV: Public Review of External Draft
•	Publication of Federal Register Notice Announcing Availability of External
Review Draft of Document
•	Circulation of External Draft to Other Government Agencies, EPA's SAB,
CASAC, and the General Public
•	In-Depth Cataloging, Review, and Analysis of Public Comments and Preparation
of Proposed Revisions
•	Presentation and Review of External Draft and Revisions at Public CASAC
Meeting
Phase V: Post CASAC Meeting Document Revision
•	Debriefing of NCEA-RTP Staff) Other EPA Personnel, and Consultants Regarding
CASAC Recommendations
•	Assignment of Specific Revision Responsibilities to NCEA-RTP Staff Members and
Contributing Consultants
•	Execution of Revision Assignments and Consultation with Individual CASAC
Members as Needed
•	Typing, Editing, and Reproduction of Revised Draft and Resubmittal of Document
to CASAC
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o
o
z
o
H
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c
o
a
3
o
3
Phase III: Review and Revision of Working Draft
•	Convening of NCEA-RTP Team, Document Authors, EPA Internal Task Force, and
Reviewing Consultants at Revision Workshop Open to Public
•	Follow-Up Meetings of NCEA-RTP Staff) Reviewers, and Authors as Necessary to
Resolve Revision Issues
•	Post-Workshop Revision of Document Working Draft
•	Critical Reading and Editing of Draft by NCEA-RTP Staff
•	Typing, Graphics, and Printing of External Review Draft
Phase VI: Final CASAC Closure and Publication
•	Recirculation of External Review Draft for Public Comment CASAC Meeting
•	Presentation and Review of External Draft and Revisions at Public CASAC
Meeting
•	Submittal of Written CASAC Committee Closure Letter on Document to EPA
Administrator
•	Typing, Editing, and Printing to Preprint Draft Publication of Document at Time
of NAAQS Proposal

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offices listed on the EPA Work Group (see Appendix B). The resulting project plan will be discussed
with CAS AC and then revised, as appropriate. A literature search has been ongoing to collect references
on the health effects of 03. Additional literature searches will be initiated on other respective areas to be
covered in the criteria document; and NCEA-RTP has developed a reference information base to access
the references and provide quality assurance and quality control functions. Specific chapter or section
authors are selected on the basis of their expertise in the subject areas and their familiarity with the
relevant literature. Both EPA and non-EPA scientific experts will be involved in this effort. The main
focus of the revised criteria document will be an evaluation and interpretation of data that deal with 03
air quality effects on health and welfare as chosen by these scientific experts. A workshop convened to
review the draft criteria document chapters will focus on the selection of pertinent studies included in the
chapters, the potential need for additional information to be added to the chapters, and the quality of the
summarization and interpretation of the literature. The respective authors of the draft chapters will revise
them on the basis of the workshop recommendations. If needed, the revised chapters will be recirculated
to workshop participants for further review. After resolution of outstanding issues and comments,
NCEA-RTP will release the document as the first external review draft for public comment and CASAC
review. Any necessary revisions will be made on the basis of the public comments and CASAC
recommendations before the final version of the criteria document is released.
C. PERSONNEL
Mr. James A. Raub will serve as the NCEA-RTP project manager and will also provide overall
technical guidance for the health effects chapters. Other proposed NCEA-RTP project team members
providing overall technical guidance for individual chapters are as follows: Dr. Joseph Pinto for the
chapter on chemistry and physics; Ms. Beverly Comfort, Dr. Joseph Pinto, and Mr. William Ewald for
the chapter on environmental concentrations, patterns, and potential exposures; Dr. J.H.B. Garner and Dr.
Timothy Lewis for the chapter on environmental effects; Mr. James A. Raub for the chapters on
toxicological effects and controlled human exposure studies; and Dr. Robert Chapman for review and
evaluation of epidemiological studies. Additional technical assistance on health effects and air quality
will be obtained directly from EPA scientists in the National Exposure Research Laboratory, National
Health and Environmental Effects Research Laboratory, and the Office of Air Quality Planning and
Standards. If not available ftom within EPA, scientific expertise will be obtained from outside EPA
utilizing small purchase requests for professional services. Members of NCEA-RTP's project team and
other EPA and non-EPA personnel expected to contribute to the document are listed in Appendix C.
D. APPROACH
Discussions will be held with the authors at the initial stages of document development to acquaint
them with detailed guidelines and specifications. Subsequent workshops may be conducted to facilitate
continuity within and between chapters. The authors will be provided copies of the previous criteria
document (U.S. Environmental Protection Agency, 1996). New sections for the updated document
should summarize the information presented in the previous documents, including reference to the "key"
studies noted above. Once this background information is presented, the remainder of the sections
should be updated with a discussion of the newer literature. In some cases where no new information is
available, the summary from the previous criteria document will suffice.
A list of references published since completion of the 1996 criteria document will be made
available to the authors. The references will be selected from information data base searches conducted
by EPA. Hard copies of any of these references will be supplied upon request. Additional references
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may need to be added to the list (e.g., missed or recently published papers or "in press" publications).
Authors must furnish a copy of each reference cited in the text that was not listed on the bibliographies of
new references or was not cited in the previous criteria document or the addendum to that document.
As an aid in selecting pertinent new literature, the authors will also be provided with the summary
of issues that need to be addressed in the preparation of the revised air quality criteria document for 03.
These issues were identified by authors and reviewers of the previous documents and continue to be
enumerated following public discussions, workshops, or in comments received by EPA. The list of
issues may not be complete, however, and the author should feel free to discuss any other issues that have
not been identified.
A good approach to evaluation of selected literature is to separate studies into three groups. The
first group (relevant) includes those studies directly relevant to the issues identified in the previous
section. The second, or may be relevant group, includes research that possibly should be mentioned.
The final group (not relevant) is a repository for studies that obviously are not relevant to assessing
health and welfare effects for standard-setting activities. The first and second groups can be further
subdivided into most relevant, less relevant, and least relevant references. The most relevant material
should be discussed first in the section. Less relevant material should receive a lower priority. Least
relevant results may be mentioned only briefly, put into a table, or left out of the document. The most
important studies identified by this evaluative approach should be fully described. Readability should be
emphasized. Documents are read not only by the author's peers but also by people with different interests
and levels of expertise. These people initiate important legal, economic, and societal actions. The
proposed chapter and section outline for the 03 criteria document appears in Appendix D.
E. PUBLIC AND SCIENTIFIC PEER REVIEW
1.	Review and Revision of the Peer-Review Workshop Draft
When the main chapters (other than the Executive Summary) of the working draft document have
been completed by the authors, a series of workshops will be convened by the NCEA-RTP Project Team.
The workshops will include the document authors, EPA Work Group participants, and external
peer-reviewers chosen on the basis of scientific expertise within specific areas covered. The workshops
will be open to the public, as announced in a Federal Register Notice.
2.	Public Review of the External Review Draft
After the workshop peer review process is completed, the authors, contributing reviewers, and
NCEA-RTP Project Team will resolve comments, as necessary, to revise the draft chapters in preparation
for an External Review Draft (ERD) document. After clearance by the U.S. EPA, the document will be
released to the public through a Federal Register Notice. Electronic and printed copies of the ERD will
be made available for review during a specified time period of usually 60 to 90 days. Written comments
are solicited during this time.
3.	Review by the Clean Air Scientific Advisory Committee
At the time the External Review Draft is released to the public, the document is to be sent to the
Clean Air Scientific Advisory Committee (CASAC) of EPA's Science Advisory Board established under
the Federal Advisory Committee Act (see Appendix E). The CASAC members and selected consultants
will review the draft document and discuss their comments in a public meeting announced in the Federal
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Register. At the meeting the NCEA-RTP Project Team plans to present a summary of key issues raised
by public comments received on the document and be prepared to discuss proposed revisions, if
indicated. At the end of the meeting, the CASAC will present their summary comments and
recommendations for disposition of the document. Several options are possible at that time. Comments
on the document may be serious enough to warrant another complete revision cycle and release of a
second ERD; or specific chapters of the document may need major revision before reconsideration of the
document; or only minor revisions of the document would be required. When satisfied that the document
provides an appropriate scientific basis for review and possible revision of the 03 NAAQS, the CASAC
will submit a written letter of closure to the EPA Administrator. The final document is subsequently
printed and announced in the Federal Register.
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References
Federal Register. (1979) National primary and secondary ambient air quality standards: revisions to
the National Ambient Air Quality Standards for photochemical oxidants. F. R. (February 8)
44: 8202-8237.
Federal Register (1992) Proposed Decision on the National Ambient Air Quality Standards for Ozone,
Preamble. 40 CFR Part 50; Federal Register 57: 35542-35557.
Federal Register (1997) National Ambient Air Quality Standards for Ozone; Final Rule. 40 CFR 50;
Federal Register 62: 38856-38896
U.S. Code (1999) Clean Air Act, title Ill-general, Section 302, definitions (h) effects on welfare.
U.S.C. 42: § 7602.
U.S. Environmental Protection Agency. (1986) Air quality criteria for ozone and other photochemical
oxidants. Research Triangle Park, NC: Office of Health and Environmental Assessment,
Environmental Criteria and Assessment Office; EPA report nos. EPA-600/8-84-020aF-eF.
Available from NTIS, Springfield, VA; PB87-142949.
U.S. Environmental Protection Agency. (1992) Summary of selected new information on effects of ozone
on health and vegetation: supplement to 1986 air quality criteria for ozone and other photochemical
oxidants. Research Triangle Park, NC: Office of Health and Environmental Assessment,
Environmental Criteria and Assessment Office; EPA report no. EPA/600/8-88/105F. Available
from NTIS, Springfield, VA; PB92-235670.
U.S. Environmental Protection Agency. (1996) Air quality criteria for ozone and related photochemical
oxidants. Research Triangle Park, NC: Office of Research and Development; report nos.
EPA/600/AP-93/004aF-cF. 3v. Available from: NTIS, Springfield, VA; PB96-185582,
PB96-185590, and PB96-185608. Available online at: www.epa.gov/ncea/ozone.htm.
U.S. Environmental Protection Agency. (2000) Science policy council peer review handbook. 2nd ed.
Washington, DC: Science Policy Council; report; no. EPA-100-B-00-001.
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APPENDIX A
ENVIRONMENTAL PROTECTION AGENCY
[FRL-6877-1]
Air Quality Criteria for Ozone and Related Photochemical Oxidants
AGENCY
Environmental Protection Agency.
ACTION
Notice; call for information.
SUMMARY
The National Center for Environmental Assessment, Office of Research and Development, of the
U.S. Environmental Protection Agency (EPA) is undertaking to update and revise, where appropriate, the
Air Quality Criteria for Ozone and Related Photochemical Oxidants (EPA-600/P-93-004aF-cF)
published in July 1996.
Since completion of the 1996 ozone criteria document, the EPA has continued to collect scientific
information on the effects of ground-level ozone on health and vegetation. A summary and evaluation of
this and other selected literature that may be particularly relevant to a review of the National Ambient
Air Quality Standards for ozone will be presented in the forthcoming revised criteria document.
As part of this continuing review, interested parties are invited to assist the EPA in developing and
refining the scientific information base for updating the air quality criteria for ozone. While EPA has
continued to follow the literature and gather appropriate studies since early 1996, the Agency is
interested in additional new information, particularly concerning the effects expected from the presence
of ground-level ozone in the ambient air on: human's and laboratory animals; vegetation, both in
agroecosystems (crops) and in natural ecosystems; nonbiological materials; and global climate. EPA also
seeks recent information in other areas of ozone research such as its chemistry and physics, sources and
emissions, analytical methodology, transport and transformation in the environment, and ambient
concentrations. To be considered for inclusion in the revised criteria document, submitted information
should be published, accepted for publication, or have been presented at a public scientific meeting.
DATES
All communications and information must be submitted by December 1, 2000, and addressed to the
Project Manager for Ozone and Related Photochemical Oxidants, National Center for Environmental
Assessment (MD-52), U.S. Environmental Protection Agency, Research Triangle Park, NC 27711.
Dated: September 15, 2000.
William H. Farland,
Director, National Center for Environmental Assessment.
[FR Doc. 00-24676 Filed 9-26-00; 8:45 am]
BILLING CODE 6560-50-U
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APPENDIX B
EPA WORK GROUP FOR AIR QUALITY CRITERIA FOR OZONE
AND RELATED PHOTOCHEMICAL OXIDANTS
Dr. Christian Andersen	Ecosystems
National Health and Environmental Effects Research Laboratory
U.S. Environmental Protection Agency
200 S.W. 35th Street
Corvallis, OR 97333
(541) 7544791 tel
Mr. Allen C. Basala	Economic assessment
Office of Air Quality Planning and Standards (C-339-01)
U.S. Environmental Protection Agency
Research Triangle Park, N.C. 27711
(919) 541-5622
Dr. Robert S. Chapman	Epidemiology
National Center for Environmental Assessment (B-243-01)
U.S. Environmental Protection Agency
Research Triangle Park, NC 27711
(919) 541-2229 tel
(919) 541-1818 fax
Ms. Beverly M. Comfort	Indoor air quality
National Center for Environmental Assessment (B-243-01)
U.S. Environmental Protection Agency
Research Triangle Park, NC 27711
(919) 5414165 tel
(919) 541-1818 fax
Dr. Daniel L. Costa	Toxicology
National Health and Environmental
Effects Research Laboratory (B-305-02)
U.S. Environmental Protection Agency
Research Triangle Park, NC 27711
(919) 541-2532 tel
(919) 541-0026fax
Dr. Robin L. Dennis	Atmospheric modeling
National Exposure Research Laboratory (E-243-01)
U.S. Environmental Protection Agency
Research Triangle Park, NC 27711
(919) 541-2870 tel
November 2002
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EPA WORK GROUP
(confd)
Dr. Robert B. Devlin
National Health and Environmental
Inflammation;
Lung cell biology
Effects Research Laboratory (MD-58)
U.S. Environmental Protection Agency
Research Triangle Park, NC 27711
(919) 966-6256 tel
(919) 966-6271 fax
Mr. William G. Ewald	Environmental
National Center for Environmental Assessment (B-243-01)	Concentration
U.S. Environmental Protection Agency
Research Triangle Park, NC 27711
(919) 541-4164
Mr. Robert Fegley	Oversight
Office of Science Policy (8104R)
U.S. Environmental Protection Agency
1200 Pennsylvania Ave., NW
Washington, DC 20460
(202) 564-6786 tel
Dr. J.H.B. Garner	Crops/Ornamentals;
National Center for Environmental Assessment (B-243-01)	Trees; Ecosystems
U.S. Environmental Protection Agency
Research Triangle Park, NC 27711
(919) 5414153 tel
Dr. Ian Gilmour	Immunotoxicology
National Health and Environmental
Effects Research Laboratory (MD-92)
U.S. Environmental Protection Agency
Research Triangle Park, NC 27711
(919) 541-0015 tel
Dr. Lester D. Grant	Oversight
National Center for Environmental Assessment (B-243-01)
U.S. Environmental Protection Agency
Research Triangle Park, NC 27711
(919) 541-4173 tel
Dr. Gary E. Hatch	Surfactant; Antioxidants;
National Health and Environmental	Toxicology
Effects Research Laboratory (MD-82)
U.S. Environmental Protection Agency
Research Triangle Park, NC 27711
(919) 541-2658 tel
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EPA WORK GROUP
(confd)
Mr. James B. Hemby
Office of Air Quality Planning and Standards (C-304-01)
U.S. Environmental Protection Agency
Research Triangle Park, NC 27711
(919) 541-5459 tel
Concentrations
Dr. William E. Hogsett
National Health and Environmental
Exposure;
Plant pathology
Effects Research Laboratory
U.S. Environmental Protection Agency
200 S.W. 35th Street
Corvallis, OR 97333
(541) 7544632 tel
(541) 7544799fax
Dr. Howard R. Kehrl	Asthma; Allergy
National Health and Environmental
Effects Research Laboratory (MD-58B)
U.S. Environmental Protection Agency
Research Triangle Park, NC 27711
(919) 966-6208 tel
Dr. Hillel S. Koren	Asthma; Immunology
National Health and Environmental
Effects Research Laboratory (MD-58)
U.S. Environmental Protection Agency
Research Triangle Park, NC 27711
(919) 966-6200 tel
Dr. Dennis Kotchmar	Epidemiology;
National Center for Environmental Assessment (B-243-01)	Panel studies
U.S. Environmental Protection Agency
Research Triangle Park, NC 27711
(919) 5414158 tel
(919) 541-1818 fax
Dr. E. Henry Lee
National Health and Environmental Effects Research Laboratory
U.S. Environmental Protection Agency
200 S. W. 35th Street
Corvallis, OR 97333
Exposure Statistics
November 2002
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EPA WORK GROUP
(confd)
Dr. Charles W. Lewis
National Exposure Research Laboratory (E-205-03)
U.S. Environmental Protection Agency
Research Triangle Park, NC 27711
(919) 541-3154 tel
Dr. Timothy E. Lewis
National Center for Environmental Assessment (B-243-01)
U.S. Environmental Protection Agency
Research Triangle Park, NC 27711
(919) 541- 0673 tel
(919) 541-1818 fax
Dr. Deborah J. Luecken
National Exposure Research Laboratory (E-205-02)
U.S. Environmental Protection Agency
Research Triangle Park, NC 27711
(919) 541-0244 tel
Dr. Michael C. Madden
National Health and Environmental
Effects Research Laboratory (MD-58B)
U.S. Environmental Protection Agency
Research Triangle Park, NC 27711
(919) 966-6257 tel
Dr. Deborah Mangis
National Exposure Research Laboratory (D-305-01)
U.S. Environmental Protection Agency
Research Triangle Park, NC 27711
(919) 541-3086 tel
Dr. Allan Marcus
National Center for Environmental Assessment (B-243-01)
U.S. Environmental Protection Agency
Research Triangle Park, NC 27711
(919) 541-0636 tel
(919) 541-1818 fax
Dr. Karen M. Martin
Office of Air Quality Planning and Standards (C-539-01)
U.S. Environmental Protection Agency
Research Triangle Park, NC 27711
(919) 541-5274 tel
Source apportionment
Terrestrial and aquatic
ecosystem effects
Atmospheric chemistry
Mechanisms; Antioxidants;
Multipollutant interactions
Ecosystems; Exposure
Epidemiology; Statistics
Consultation
November 2002
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EPA WORK GROUP
(cont'd)
Dr. William A. McClenny
National Exposure Research Laboratory (D-205-03)
U.S. Environmental Protection Agency
Research Triangle Park, NC 27711
(919) 541-3158 tel
Methods
Mr. Thomas R. McCurdy
National Exposure Research Laboratory (E-205-02)
U.S. Environmental Protection Agency
Research Triangle Park, NC 27711
(919) 541-0782 tel
Exposure;
Activity patterns
Dr. William F. McDonnell
National Health and Environmental
Effects Research Laboratory (MD-58B)
U.S. Environmental Protection Agency
Research Triangle Park, NC 27711
(919) 966-6220 tel
(919) 966-6212 fax
Epidemiology;
Controlled Human
exposure
Dr. David J. McKee
Human health
Office of Air Quality Planning and Standards (C-539-01)
U.S. Environmental Protection Agency
Research Triangle Park, NC 27711
(919) 541-5288 tel
(919) 541-0237fax
Mr. David C. Misenheimer	Emissions
Office of Air Quality Planning and Standards (D-205-01)
U.S. Environmental Protection Agency
Research Triangle Park, NC 27711
(919) 541-5473 tel
Dr. Lucas Neas	Epidemiology;
National Health and Environmental	Children's health
Effects Research Laboratory (MD-58)
U.S. Environmental Protection Agency
Research Triangle Park, NC 27711
(919) 966-9961 tel
Ms. Sharon V. Nizich	Air quality; Trends
Office of Air Quality Planning and Standards (C-339-02)
U.S. Environmental Protection Agency
Research Triangle Park, NC 27711
(919) 541-2825 tel
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EPA WORK GROUP
(confd)
Dr. David Olszyk	Crops & Ornamentals
National Health and Environmental
Effects Research Laboratory
U.S. Environmental Protection Agency
200 S.W. 35th Street
Corvallis, OR 97333
Dr. John H. Overton
National Health and Environmental
Effects Research Laboratory (MD-82)
U.S. Environmental Protection Agency
Research Triangle Park, NC 27711
(919) 541-5715 tel
(919) 541-5394fax
Dr. Joseph P. Pinto
National Center for Environmental Assessment (B-243-01)
U.S. Environmental Protection Agency
Research Triangle Park, NC 27711
(919) 541-2183 tel
(919) 541-1818 fax
Mr. Norman C. Possiel
Office of Air Quality Planning and Standards (D-243-01)
U.S. Environmental Protection Agency
Research Triangle Park, NC 27711
(919) 541-5692 tel
Mr. James A. Raub	Toxicology
National Center for Environmental Assessment (B-243-01)
U.S. Environmental Protection Agency
Research Triangle Park, NC 27711
(919) 541-4157 tel
(919) 541-1818 fax
Mr. Harvey M. Richmond	Exposure modeling
Office of Air Quality Planning and Standards (C-539-01)
U.S. Environmental Protection Agency
Research Triangle Park, NC 27711
(919) 541-5271 tel
(919) 541-0824fax
Deposition modeling;
Dosimetry
Air Chemistry;
Global effects
Atmospheric modeling
November 2002
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EPA WORK GROUP
(cont'd)
Mr. William E. Russo	Consultation
National Health and Environmental
Effects Research Laboratory (B-305-02)
U.S. Environmental Protection Agency
Research Triangle Park, NC 27711
(919) 541-7869 tel
Ms. Victoria A. Sandiford	Ecosystems
Office of Air Quality Planning and Standards (C-539-01)
U.S. Environmental Protection Agency
Research Triangle Park, NC 27711
(919) 541-2629 tel
Mr. Kenneth L. Schere	Atmospheric modeling
National Exposure Research Laboratory (E-243-03)
U.S. Environmental Protection Agency
Research Triangle Park, NC 27711
(919) 541-3795 tel
(919) 541-1379fax
Dr. Elston Seal	Controlled human
National Health and Environmental	exposure;
Effects Research Laboratory (MD-58A)	Sensitive subjects
U.S. Environmental Protection Agency
Research Triangle Park, NC 27711
(919) 966-6217 tel
Dr. MaryJane Selgrade	Immunotoxicology;
National Health and Environmental	T-cell pathways
Effects Research Laboratory (MD-82)
U.S. Environmental Protection Agency
Research Triangle Park, NC 27711
(919) 541-1821 tel
Dr. Jack H. Shreffler	Global; UV
National Exposure Research Laboratory (E-205-02)
U.S. Environmental Protection Agency
Research Triangle Park, NC 27711
(919) 541-2194 tel
November 2002
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EPA WORK GROUP
(cont'd)
Dr. Joseph H. Somers
Office of Mobile Sources
U.S. Environmental Protection Agency
2565 Plymouth Road
Ann Arbor, MI 48105
(313) 668-4321 tel
Precursor emissions
Dr. Sharon K. Taylor	Terrestrial ecosystem
National Center for Environmental assessment (B-105-07)	effects; wildlife
U.S. Environmental Protection Agency
Research Triangle Park, NC 27711
(919) 541-4930 tel
Dr. William P. Watkinson	Cardiac dysrhythmias/
National Health and Environmental	arrhythmias
Effects Research Laboratory (MD-82)
U.S. Environmental Protection Agency
Research Triangle Park, NC 27711
(919) 5414018 tel
November 2002
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APPENDIX C
NCEA-RTP PROJECT TEAM AND OTHER TECHNICAL CONSULTANTS
NCEA-RTP Project Team
Scientific Staff
Mr. James A. Raub — Health Scientist, National Center for Environmental Assessment (B-243-01),
U.S. Environmental Protection Agency, Research Triangle Park, NC 27711
Dr. Robert S. Chapman — Medical Officer, National Center for Environmental Assessment
(B-243-01), U.S. Environmental Protection Agency, Research Triangle Park, NC 27711
Ms. Beverly M. Comfort — Health Scientist, National Center for Environmental Assessment
(B-243-01), U.S. Environmental Protection Agency, Research Triangle Park, NC 27711
Dr. Robert W. Elias — Health Scientist, National Center for Environmental Assessment (B-243-01),
U.S. Environmental Protection Agency, Research Triangle Park, NC 27711
Mr. William G. Ewald — Health Scientist, National Center for Environmental Assessment (B-243-01),
U.S. Environmental Protection Agency, Research Triangle Park, NC 27711
Dr. J.H.B. Garner — Ecologist, National Center for Environmental Assessment (B-243-01), U.S.
Environmental Protection Agency, Research Triangle Park, NC 27711
Dr. Timothy E. Lewis — Ecologist, National Center for Environmental Assessment (B-243-01),
U.S. Environmental Protection Agency, Research Triangle Park, NC 27711
Dr. Allan Marcus — Statistician, National Center for Environmental Assessment (B-243-01),
U.S. Environmental Protection Agency, Research Triangle Park, NC 27711
Dr. Joseph P. Pinto — Physical Scientist, National Center for Environmental Assessment (B-243-01),
U.S. Environmental Protection Agency, Research Triangle Park, NC 27711
Technical Support Staff
Ms. Nancy Broom — Computer Specialist, National Center for Environmental Assessment (B-243-01),
U.S. Environmental Protection Agency, Research Triangle Park, NC 27711
Mr. Douglas B. Fennell — Technical Information Specialist, National Center for Environmental
Assessment (B-243-01), U.S. Environmental Protection Agency, Research Triangle Park, NC 27711
Ms. Emily R. Lee — Management Analyst, National Center for Environmental Assessment (B-243-01),
U.S. Environmental Protection Agency, Research Triangle Park,
November 2002
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NCEA-RTP PROJECT TEAM AND OTHER
TECHNICAL CONSULTANTS
(confd)
Technical Support Staff (cont'd)
Ms. Diane H. Ray — Program Specialist, National Center for Environmental Assessment (B-243-01),
U.S. Environmental Protection Agency, Research Triangle Park, NC 27711
Ms. Donna Wicker — Management Analyst, National Center for Environmental Assessment (B-243-
01), U.S. Environmental Protection Agency, Research Triangle Park, NC 27711
Other EPA Contributors
Dr. Christian Andersen — National Health and Environmental Effects Research Laboratory, U.S.
Environmental Protection Agency, 200 SW 35th Street, Corvallis, OR 97333
Dr. Daniel L. Costa — National Health and Environmental Effects Research Laboratoiy (B-305-02),
U.S. Environmental Protection Agency, Research Triangle Park, NC 27711
Dr. Robert B. Devlin — National Health and Environmental Effects Research Laboratory (MD-58),
U.S. Environmental Protection Agency, Research Triangle Park, NC 27711
Dr. Bruce W. Gay — National Exposure Research Laboratory (E-205-05), U.S. Environmental
Protection Agency, Research Triangle Park, NC 27711
Dr. Ian Gilmour — National Health and Environmental Effects Research Laboratory (MD-92),
U.S. Environmental Protection Agency, Research Triangle Park, NC 27711
Dr. Gary E. Hatch — National Health and Environmental Effects Research Laboratory (MD-82),
U.S. Environmental Protection Agency, Research Triangle Park, NC 27711
Dr. William E. Hogsett — National Health and Environmental Effects Research Laboratory, U.S.
Environmental Protection Agency, 200 SW 35th Street, Corvallis, OR 97333
Dr. Hillel S. Koren — National Health and Environmental Effects Research Laboratory (MD-58C), U.S.
Environmental Protection Agency, Research Triangle Park, NC 27711
Dr. John Laurence — National Health and Environmental Effects Research Laboratory, U.S.
Environmental Protection Agency, 200 SW 35th Street, Corvallis, OR 97333
Dr. E. Henry Lee — National Health and Environmental Effects Research Laboratory, U.S.
Environmental Protection Agency, 200 SW 35th Street, Corvallis, OR 97333
Dr. Charles W. Lewis — National Exposure Research Laboratory (E-205-03), U.S. Environmental
Protection Agency, Research Triangle Park, NC 27711
Dr. Michael C. Madden — National Health and Environmental Effects Research Laboratory (MD-58B),
U.S. Environmental Protection Agency, Research Triangle Park, NC 27711
November 2002
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NCEA-RTP PROJECT TEAM AND OTHER
TECHNICAL CONSULTANTS
(confd)
Other EPA Contributors (cont'd)
Dr. William F. McDonnell — National Health and Environmental Effects Research Laboratory
(MD-58B), U.S. Environmental Protection Agency, Research Triangle Park, NC 27711
Dr. Lucas Neas — National Health and Environmental Effects Research Laboratory (MD-82),
U.S. Environmental Protection Agency, Research Triangle Park, NC 27711
Dr. David Olszyk — National Health and Environmental Effects Research Laboratory,
U.S. Environmental Protection Agency, 200 SW 35th Street, Corvallis, OR 97333
Dr. John H. Overton — National Health and Environmental Effects Research Laboratory (MD-82),
U.S. Environmental Protection Agency, Research Triangle Park, NC 27711
Dr. MaryJane K. Selgrade — National Health and Environmental Effects Research Laboratory
(MD-82), U.S. Environmental Protection Agency, Research Triangle Park, NC 27711
Non-EPA Consultants (Potential Sources7)
Dr. William C. Adams — Exercise Biology Program, University of California, Davis, CA 95616
Dr. Richard M. Adams — Department of Agriculture and Resource Economics, Oregon State
University, Corvallis, OR 97331
Dr. Robert M. Aris — Lung Biology Center, San Francisco General Hospital, Bldg. 1, Rm. 150,
1001 Potrero Ave., San Francisco, CA 94110
Dr. Roger Atkinson — Department of Soil and Environmental Sciences, University of California, 900
Watkins Avenue, Riverside, CA 92521
Dr. John R. Balmes — Center for Occupational and Environmental Heath, San Francisco General
Hospital, 1001 Potrero Avenue, Bldg. 30, 5th Floor, San Francisco, CA 94110
Dr. David J.P. Bassett — Department of Occupational and Environmental Health, College of Pharmacy
and Allied Health Professions, Shapero Hall, Wayne State University, Detroit, MI 48202
Dr. Deepak K. Bhalla — Department of Community and Environmental Medicine, University of
California, Irvine, CA 92717
'The list of non-EPA scientists is proposed on the basis of published, peer-reviewed scientific publications on topic areas that are
likely to be included in the revised criteria document or on the basis of previous involvement as an author, contributor, or
reviewer of the 1996 criteria document. Contractual agreements for professional services would be the likely mechanism for
obtaining their participation in workshops and their contributions to the revised air quality document for 03.
November 2002
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NCEA-RTP PROJECT TEAM AND OTHER
TECHNICAL CONSULTANTS
(cont'd)
Non-EPA Consultants (cont'd)
Dr. Richard T. Burnett — Health & Welfare Canada, Tunney's Pasture, Ottawa, Ontario K1A OL2
CANADA.
Dr. Russell R. Dickerson — Department of Meteorology, The University of Maryland, College Park,
MD 20742
Dr. Deborah M. Drechsler — Research Division, California Air Resources Board, Sacramento, CA
95812
Dr. Henry Gong, Jr. — Department of Medicine, Rancho Los Amigos National Rehabilitation Center,
Downey, CA 90242
Dr. Beverly A. Hale — Department of Horticultural Science, University of Guelph, Guelph,
Ontario, NIG 2W1, Canada
Dr. Milan J. Hazucha — Department of Medicine, Center for Environmental Medicine, Asthma, and
Lung Biology, The University of North Carolina, Chapel Hill,-NC 27599
Dr. Robert L. Heath — Department of Botany and Plant Sciences, University of California, Riverside,
CA 92507
Mr. Michael W. Holdren — Battelle, 505 King Avenue, Columbus, OH 43201
Dr. Kazuhiko Ito — Department of Environmental Medicine, New York University School of Medicine,
Tuxedo, NY 10987
Dr. George J. Jakab — Department of Environmental Health Sciences, The Johns Hopkins University,
School of Hygiene and Public Health, 615 N. Wolfe Street, Baltimore, MD 21209
Dr. David F. Karnosky — School of Forestry and Wood Products, Michigan Technological University,
Houghton, MI 49931
Dr. Thomas J. Kelly — Battelle, 505 King Avenue, Columbus, OH 43201
Dr. Patrick L. Kinney — Division of Environmental Health Sciences, Mailman School of Public Health
at Columbia University, New York, NY 10032
Dr. Tadeusz Kleindienst — ManTech Environmental Technology, Inc., Suite 200, Park Forty Plaza
Durham, NC 27713
Dr. Joseph R. Landolph — Department of Microbiology, USC Comprehensive Cancer Center, USC
School of Medicine, Norris Cancer Hospital and Research Institute, 1441 Eastlake Avenue, Los
Angeles, CA 90033
November 2002
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NCEA-RTP PROJECT TEAM AND OTHER
TECHNICAL CONSULTANTS
(cont'd)
Non-EPA Consultants (cont'd)
Dr. Allen S. Lefohn — A.S.L. & Associates, 111 Last Chance Gulch, Suite 4A, Helena, MT 59601
Dr. Paul Miller — Pacific Southwest Forest and Range Experiment Station, USDA-Forest Service Fire
Lab, 4955 Canyon Crest Dr., Riverside, CA 92507
Mr. Doug Murray — TRC Environmental Corporation, 5 Waterside Crossing, Windsor, CT 06095
Dr. Robert Musselman — USDA Forest Service, Rocky Mountain Experiment Station, 240 West
Prospect Road, Fort Collins, CO 80526
Dr. Charles G. Plopper — Department of Anatomy, Physiology, and Cell Biology, School of Veterinary
Medicine, University of California, Davis, CA 95616
Dr. Victor Runeckles — Department of Plant Science, University of British Columbia, Vancouver,
British Columbia, V6T 1Z4, Canada
Dr. Perry J. Samson — Department of Atmospheric, Oceanic, and Space Sciences, University of
Michigan, 2455 Hay ward Street, Ann Arbor, MI 48109
Dr. Edward S. Schelegle — Department of Anatomy, Physiology, and Cell Biology, School of
Veterinary Medicine, University of California, Davis, CA 95616
Dr. Richard B. Schlesinger — Institute of Environmental Medicine, New York University Medical
Center, Long Meadow Road, Tuxedo, NY 10987
Dr. John H. Seinfeld — Division of Engineering and Applied Science, California Institute of
Technology, 391 South Holliston Avenue, Pasadena, CA 91125
Dr. Ira B. Tager — VA Medical Center, 1 IE, 4150 Clement Street, San Francisco, CA 90059
Dr. Patrick J. Temple — Consultant, Riverside, CA 92506
Dr. George D. Thurston — Institute of Environmental Medicine, New York University Medical Center,
Long Meadow Road, Tuxedo, NY 10987
Dr. Walter S. Tyler — Department of Anatomy, School of Veterinary Medicine, University of
California, Davis, CA 95616
Dr. Clifford Weisel — Environmental Occupational and Health Science Institute, 170 Feelingwysen
Road, Piscataway, NJ 08854
Dr. Halvor (Hal) Westberg — Department of Civil and Environmental Engineering, Washington State
University, Pullman, WA 99164
November 2002
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NCEA-RTP PROJECT TEAM AND OTHER
TECHNICAL CONSULTANTS
(cont'd)
Non-EPA Consultants (cont'd)
Dr. Robert Willis — ManTech Environmental Technology, Inc., Suite 200, Park Forty Plaza, Durham,
NC 27713
Dr. Peter Woodbury — USDA Forest Service, Northeastern Research Station, Durham, NH 03824
November 2002
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APPENDIX D
PROPOSED CONTENTS AIR QUALITY CRITERIA FOR OZONE
AND RELATED PHOTOCHEMICAL OXIDANTS
Page
LIST OF TABLES	
LIST OF FIGURES	
AUTHORS, CONTRIBUTORS, AND REVIEWERS 	
EXECUTIVE SUMMARY AND CONCLUSIONS	
1.	INTRODUCTION	
2.	CHEMISTRY, AND PHYSICS OF OZONE AND RELATED
PHOTOCHEMICAL OXIDANTS	
2.1	INTRODUCTION	
2.2	TROPOSHERIC OZONE CHEMISTRY	
2.2.1	Atmospheric Structure	
2.2.2	Overview of Ozone Chemistry 	
2.2.3	Initiation of the Oxidation of Volatile Organic Compounds	
2.2.4	Chemistry of Nitrogen Oxides in the Troposphere	
2.2.5	The Methane Oxidation Cycle	
2.2.6	Chemistry of Ozone Formation in the Polluted Troposphere	
2.3	PHYSICAL AND CHEMICAL PROCESSES INFLUENCING THE
ABUNDANCE OF OZONE	
2.3.1	Atmospheric Transport 	
2.3.1.1	Tropospheric Transport	
2.3.1.2	Stratospheric-Tropospheric Ozone Exchange	
2.3.2	The Relation of Ozone to Solar Ultraviolet Radiation And Temperature	
2.3.2.1	Solar Ultraviolet Radiation	
2.3.2.2	Temperature 	
2.3.3	The Relation of Ozone to its Precursors and Other Oxidants	
2.3.3.1	Relation Between Ozone and Nitrogen Oxides 	
2.3.3.2	Relation Between Ozone and Volatile Organic Compounds 	
2.4	METHODS USED TO CALCULATE RELATIONS BETWEEN OZONE,
ITS PRECURSORS, AND OTHER OXIDANTS 	
2.4.1	Chemistry-Transport Models	
2.4.2	Emissions of Ozone Precursors	
2.4.3	Receptor Modeling of Ozone Precursors	
2.5	Analytical Methods for Measuring Oxidants and Their Precursors	
2.6	SUMMARY AND CONCLUSIONS 	
REFERENCES 	
3.	ENVIRONMENTAL CONCENTRATIONS, PATTERNS, AND EXPOSURE
ESTIMATES	 	
3.1	INTRODUCTION	
3.2	SURFACE OZONE CONCENTRATIONS	
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PROPOSED CONTENTS
(cont'd)
Page
3.2.1	Background Concentrations	
3.2.2	Urban Area Concentrations	
3.2.3	Nonurban Area Concentrations	
3.3	DIURNAL PATTERNS IN OZONE CONCENTRATIONS	
3.4	SEASONAL PATTERNS IN OZONE CONCENTRATIONS 	
3.5	SPATIAL VARIATIONS IN OZONE CONCENTRATIONS	
3.5.1	Urban-Nonurban Concentration Gradients	
3.5.2	Vertical and Altitudinal Gradients and Geographic Variations 	
3.5.3	Other Spatial Variations in Ambient Ozone Concentrations	
3.6	HISTORICAL TRENDS IN OZONE CONCENTRATIONS 	
3.7	CONCENTRATIONS AND PATTERNS OF RELATED PHOTOCHEMICAL
OXIDANTS	
3.7.1	Concentrations	
3.7.2	Temporal Patterns 	
3.8	RELATIONSHIP BETWEEN SURFACE CONCENTRATIONS OF OZONE
AND OTHER POLLUTANTS	
3.8.1	Co-occurrence of Ozone with Nitrogen Oxides 	
3.8.2	Co-occurrence of Ozone with Sulfur Oxides	•	
3.8.3	Co-occurrence of Ozone with Particulate Matter 	
3.9	INDOOR OZONE CONCENTRATIONS
3.10	TOTAL EXPOSURE ASSESSMENTS FOR OZONE 	
3.10.1	Human Population Exposure	
3.10.2	Natural and Agroecosystem Exposure	
3.11	SUMMARY 	
REFERENCES 	
4. ENVIRONMENTAL EFFECTS OF OZONE AND RELATED
PHOTOCHEMICAL OXIDANTS	
4.1	INTRODUCTION	
4.2	METHODOLOGIES USED IN VEGETATION RESEARCH 	
4.2.1	Fumigation Systems	
4.2.2	Experimental Design and Data Analysis	
4.2.3	Mechanistic Process Models	
4.2.4	Summary
4.3	SPECIES RESPONSE/MODE OF ACTION	
4.3.1	Introduction	
4.3.2	Ozone Uptake	
4.3.3	Resistance Mechanisms	
4.3.4	Physiological Effects of Ozone	
4.3.5	Role of Age and Size Influencing Response to Ozone 	
4.3.6	Summary 	
4.4	FACTORS THAT MODIFY PLANT RESPONSE TO OZONE . 		
4.4.1	Modification of Functional Growth Responses	
4.4.2	Genetics	
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PROPOSED CONTENTS
(cont'd)
Page
4.4.3	Environmental Biological Factors	
4.4.4	Physical Environmental Factors 	
4.4.5	Nutritional Factors	
4.4.6	Interactions with Other Pollutants	
4.4.7	Interactions with Agricultural Chemicals 	
4.4.8	Factors Associated with Global Climate Change 	
4.4.9	Summary 	
4.5	EXPOSURE/RESPONSE OF PLANT SPECIES	
4.5.1	Introduction	
4.5.2	Summary of Conclusions from the Previous Criteria Document 	
4.5.3	Recent Studies (post-1995) of Effects of Ozone on Short-Lived (Annual
and Biennial) Species 	
4.5.4	Recent Studies (post-1995) of Effects on Ozone on Long-Lived
(Perennial) Species 	
4.5.5	Summary 	
4.6	EFFECTS OF OZONE ON NATURAL ECOSYSTEMS 	
4.6.1	Introduction	
4.6.2	Ecosystem Response to Stress	
4.6.3	Effects of Ozone Exposure on Natural Ecosystems 	
4.6.4	Ecosystem Response to Stress	
4.6.5	Summary 	
4.7	ECONOMIC EFFECTS OF OZONE ON AGRICULTURE, FORESTRY,
AND ECOSYSTEMS	
4.7.1	The Measurement of Economic Information (Benefits and Costs)	
4.7.2	Current Understanding of Economic Effects of Air Pollutants on Agriculture
and Other Vegetation	
4.7.3	Agriculture	
4.7.4	Forests (Tree Species) and Natural Ecosystems 	
4.7.5	Recent (post-1993) Studies of the Effects on Agriculture, Forests,
and Ecosystems 	
4.7.6	Current Limitations on Natural Science and Economic Information 	
4.7.7	Summary 	
4.8	EFFECTS OF OZONE ON NONBIOLOGICAL MATERIALS
4.9	EFFECTS OF OZONE ON SOLAR ULTRAVIOLET RADIATION
TRANSMISSION AND GLOBAL CLIMATE CHANGE PROCESSES	
4.10	SUMMARY AND CONCLUSIONS 	
REFERENCES
5. TOXICOLOGICAL EFFECTS OF OZONE AND RELATED PHOTOCHEMICAL
OXIDANTS		
5.1	INTRODUCTION	
5.2	DOSIMETRY OF OZONE IN THE RESPIRATORY TRACT	
5.2.1	Experimental Ozone Dosimetry Data 	
5.2.2	Dosimetry Modeling 	
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5.2.3	Species Sensitivity	
5.2.4	Animal-to-Human Extrapolation	
5.3	RESPIRATORY TRACT EFFECTS OF OZONE	
5.3.1	Inflammation and Lung Permeability Changes	
5.3.2	Lung Host Defenses	
5.3.3	Morphological Effects	
5.3.4	Effects on Pulmonary Function	
5.3.5	Biochemical Effects	
5.3.6	Mutagenic and Carcinogenic Potential for Ozone	
5.4	SYSTEMIC EFFECTS OF OZONE	
5.4.1	Neurobehavioral Effects 	
5.4.2	Neuroendocrine Effects	
5.4.3	Cardiovascular Effects	
5.4.4	Reproductive and Developmental Effects	
5.4.5	Effects on the Liver and Spleen	
5.4.6	Effects on Cutaneous and Ocular Tissues	
5.5	INTERACTIONS OF OZONE WITH OTHER CO-OCCURRING POLLUTANTS 	
5.5.1	Ozone and Sulfur Oxides	
5.5.2	Ozone and Nitrogen-Containing Pollutants	
5.5.3	Ozone and Complex Mixtures Including Particulate Matter	
5.6	EFFECTS OF RELATED PHOTOCHEMICAL OXIDANTS	
5.7	SUMMARY AND CONCLUSIONS 	
REFERENCES 	
6. CONTROLLED HUMAN EXPOSURE STUDIES OF OZONE AND RELATED
PHOTOCHEMICAL OXIDANTS	
6.1	INTRODUCTION	
6.2	PULMONARY FUNCTION EFFECTS OF ONE- TO THREE-HOUR
OZONE EXPOSURES	
6.2.1	Healthy Subjects 	
6.2.2	The Ozone Concentration-Response Relationship 	
6.2.3	Mechanisms of Acute Pulmonary Function Responses	
6.2.4	Subjects with Preexisting Disease	
6.2.5	Influence of Gender, Age, Ethnic, and Environmental Factors	
6.2.6	Repeated Exposures to Ozone	
6.3	PULMONARY FUNCTION EFFECTS OF PROLONGED
(MULTIHOUR) OZONE EXPOSURES 	
6.4	EFFECTS ON EXERCISE PERFORMANCE 	
6.5	INCREASED AIRWAY RESPONSIVENESS 	
6.6	INFLAMMATION AND HOST DEFENSE 	
6.6.1	Introduction	
6.6.2	Inflammation Assessed by Bronchoalveolar Lavage	
6.6.3	Time Course of Inflammatory Response	
6.6.4	Effect of Anti-Inflammatory Agents on Ozone-Induced Inflammation	
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6.6.5	Use of Nasal Lavage to Assess Ozone-Induced Inflammation in the
Upper Respiratory Tract 	
6.6.6	Changes in Host Defense Capability Following Ozone Exposure 	
6.7	HUMAN DOSIMETRY OF OZONE 	
6.7.1	Regional Ozone Uptake in the Lung	
6.7.2	Extrapulmonary Effects	
6.8	OZONE MIXED WITH OTHER POLLUTANTS 	
6.8.1	Ozone and Sulfur Oxides	
6.8.2	Ozone and Nitrogen-Containing Pollutants	
6.8.3	Ozone and Other Pollutants Including Particulate Matter	
6.8.4	Summary 	
6.9	SYMPTOMS AND PULMONARY FUNCTION IN CONTROLLED
STUDIES OF AMBIENT AIR EXPOSURES
6.9.1	Field Studies 	
6.9.2	High-Altitude Studies 	
6.10	SUMMARY AND CONCLUSIONS 	
6.10.1	Effects on Pulmonary Function	
6.10.2	Symptom Responses to Ozone	
6.10.3	Effects on Exercise Performance	
6.10.4	Effects on Airway Responsiveness	
6.10.5	Inflammation and Host Defense Effects 	
6.10.6	Factors Modifying Responsiveness to Ozone	
6.10.7	Effects of Ozone Mixed with Other Pollutants	
REFERENCES 	
7. EPIDEMIOLOGIC STUDIES OF AMBIENT OZONE EXPOSURE	
7.1	INTRODUCTION	
7.2	EFFECTS OF SHORT-TERM AMBIENT EXPOSURE
7.2.1	Individual-Level Repeated-Measures Studies	
7.2.1.1	Issues in the interpretation of individual-level studies	
7.2.1.2	Camp studies of lung function in children 	
7.2.1.3	Lung function in exercising population groups 	
7.2.1.4	Panel studies of lung function	
7.2.1.5	Panel studies of symptom frequency and performance	
7.2.1.6	Panel studies of aggravation of preexisting respiratory disease	
7.2.2	Aggregate Population (Ecological) Time Series Studies	
7.2.2.1	Emergency room visits and hospital admissions	
7.2.2.2	Recent respiratory hospital admissions studies from the air
pollution and health, a European approach (APHEA) project	
7.2.2.3	Daily mortality 	
7.2.2.4	Studies of oral antioxidant supplementation and lung function	
7.2.3	Summary 	
7.3	EFFECTS OF LONG-TERM AMBIENT OZONE EXPOSURE	
7.3.1 Histopathologic and Immunologic Effects 	
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7.3.2	Pulmonary Function, Respiratory Symptoms, Chronic Respiratory
Disease, and Respiratory Cancer	
7.3.3	Other Chronic Disease Morbidity and Mortality Studies 	
7.3.4	Summary 	
7.4 SUMMARY AND CONCLUSIONS 	
REFERENCES 	
8. EVALUATION OF HUMAN HEALTH RISKS AND EFFECTS ON THE
ENVIRONMENT	 	
8.1	INTRODUCTION	
8.2	SOURCES AND EXPOSURE	
8.3	EVALUATION OF EFFECTS ON ECOSYSTEMS	
8.4	EVALUATION OF HEALTH RISKS FROM SHORT-TERM OR REPEATED
OZONE EXPOSURE 	
8.4.1	Health Effects in the General Human Population	
8.4.2	Health Effects in Susceptible Population Groups	
8.5	HEALTH RISKS FROM LONG-TERM OZONE EXPOSURE 	
8.5.1	Effects Associated With Exposures in Human Populations 	
8.5.2	Extrapolation of Effects Observed in Laboratory Animals to
Human Populations 	
8.6	HEALTH AND ENVIRONMENTAL RISKS FROM EXPOSURE TO OTHER
PHOTOCHEMICAL OXIDANTS AND POLLUTANT MIXTURES 	
8.7	HEALTH AND ENVIRONMENTAL RISKS FROM EXPOSURE TO
ULTRAVIOLET-B RADIATION MEDIATED BY CHANGES IN
TROPOSPHERIC OZONE CONCENTRATIONS 	
8.8	CONCLUSIONS	
REFERENCES 	
APPENDIX: GLOSSARY OF TERMS AND SYMBOLS	
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APPENDIX E
SCIENCE ADVISORY BOARD CLEAN AIR SCIENTIFIC
ADVISORY COMMITTEE MEMBERS
Fiscal Year 2001
The Clean Air Scientific Advisoiy Committee (CASAC) has a statutorily mandated responsibility
to review and offer scientific and technical advice to the Administrator on the air quality criteria and
regulatory documents that form the basis for the national ambient air quality standards (NAAQS), which
are currently lead, particulate matter (PM), ozone and other photochemical oxidants (03), carbon
monoxide (CO), nitrogen oxides (NO*) and sulfur oxides (SO*).
CHAIR
Dr. Philip Hopke
Robert A. Plane Professor
Department of Chemical Engineering
Clarkson University
Potsdam, NY 13699
PAST CHAIR
Dr. Joe Mauderly
Vice President and Senior Scientist
Lovelace Respiratory Research Institute
Albuquerque, NM 87185
MEMBERS
Dr. Frederick Miller
Director of Respiratory Toxicology Research
Chemical Industry Institute of Toxicology
Research Triangle Park, NC 27709
Mr. Richard Poirot
Environmental Analyst
Department of Environmental Conservation
Vermont Agency of Natural Resources
Waterbury, VT 05671
Dr. Frank Speizer
Edward Kass Professor of Medicine
Channing Laboratory
Harvard Medical School
Boston, MA 02115
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SCIENCE ADVISORY BOARD
(cont'd)
Dr. George Taylor
Professor, Honors Program
George Mason University
Fairfax, VA 22030
Dr. Sverre Vedal
Professor of Medicine
Respiratory Division
Vancouver General Hospital
Vancouver, BC Canada V57 3J5
Dr. Barbara Zielinska
Research Professor
Atmospheric Sciences Division
Desert Research Institute
Reno, NV 89512
SCIENCE ADVISORY BOARD STAFF
Mr. Fred A. Butterfield, HI
Designated Federal Officer
Clean Air Scientific Advisory Committee
Science Advisory Board (1400A)
US Environmental Protection Agency
Washington, DC 20460
Ms. Zisa Lubarov-Walton
Management Assistant
Science Advisory Board (1400A)
US Environmental Protection Agency
Washington, DC 20460
updated: August 8, 2002
www.epa.gov/sab/casmem02.htm
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Please make all necessary changes in the below label,
detach copy or copy, and return to the address in the upper
left-hand corner.
PRESORTED STANDARD
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If you do not wish to receive these reports CHECK HERE ~;
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NCEA-R-1068
November 2002

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