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 ------- 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 ------- 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. November 2002 DRAFT - DO NOT QUOTE OR CITE ------- PREFACE This project work plan has been prepared as a managerial and management information tool for the U.S. Environmental Protection Agency's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. November 2002 ii DRAFT - DO NOT QUOTE OR CITE ------- TABLE OF CONTENTS.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 November 2002 iii DRAFT - DO NOT QUOTE OR CITE ------- 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. ------- 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). November 2002 2 DRAFT - DO NOT QUOTE OR CITE ------- 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. November 2002 3 DRAFT - DO NOT QUOTE OR CITE ------- 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) November 2002 4 DRAFT - DO NOT QUOTE OR CITE ------- 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. November 2002 5 DRAFT - DO NOT QUOTE OR CITE ------- 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 November 2002 6 DRAFT - DO NOT QUOTE OR CITE ------- 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 November 2002 7 DRAFT - DO NOT QUOTE OR CITE ------- 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 November 2002 8 DRAFT - DO NOT QUOTE OR CITE ------- 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. November 2002 9 DRAFT - DO NOT QUOTE OR CITE ------- 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. November 2002 10 DRAFT - DO NOT QUOTE OR CITE ------- 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? November 2002 11 DRAFT - DO NOT QUOTE OR CITE ------- 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? November 2002 12 DRAFT - DO NOT QUOTE OR CITE ------- 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? November 2002 13 DRAFT - DO NOT QUOTE OR CITE ------- 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) November 2002 14 DRAFT - DO NOT QUOTE OR CITE ------- 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? November 2002 15 DRAFT - DO NOT QUOTE OR CITE ------- 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 November 2002 16 DRAFT - DO NOT QUOTE OR CITE ------- Figure 1. Summary of Criteria Document Preparation Process to o o to Preparation and Internal Review of NCEA Air Quality Criteria Documents Phase I: Document Planning and Initiation Initiation of Literature Search and Article Procurement ProceduresNotice 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 PreparationDefinition of Document Contents Briefing of EPA Science Advisory Board (SAB/CAS AC) on Document Plan and ContentsRevise Plan as Advised Phase II: Preparation of Working Draft Accumulation and Analysis of Pertinent Literature Writing of Rough Drafts of Document SectionsMainly Summarizing Relevant Published Studies Preliminary Meeting of Authors to Expand Initial DraftsInitiate 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 H I o o z o H lO 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 ------- 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 November 2002 18 DRAFT - DO NOT QUOTE OR CITE ------- 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 November 2002 19 DRAFT - DO NOT QUOTE OR CITE ------- 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. November 2002 20 DRAFT - DO NOT QUOTE OR CITE ------- 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. November 2002 21 DRAFT - DO NOT QUOTE OR CITE ------- 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 November 2002 A-l DRAFT - DO NOT QUOTE OR CITE ------- 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 B-l DRAFT - DO NOT QUOTE OR CITE ------- 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 November 2002 B-2 DRAFT - DO NOT QUOTE OR CITE ------- 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 B-3 DRAFT - DO NOT QUOTE OR CITE ------- 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 B-4 DRAFT - DO NOT QUOTE OR CITE ------- 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 November 2002 B-5 DRAFT - DO NOT QUOTE OR CITE ------- 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 B-6 DRAFT - DO NOT QUOTE OR CITE ------- 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 B-7 DRAFT - DO NOT QUOTE OR CITE ------- 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 B-8 DRAFT - DO NOT QUOTE OR CITE ------- 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 C-l DRAFT - DO NOT QUOTE OR CITE ------- 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 C-2 DRAFT - DO NOT QUOTE OR CITE ------- 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 C-3 DRAFT - DO NOT QUOTE OR CITE ------- 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 C-4 DRAFT - DO NOT QUOTE OR CITE ------- 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 C-5 DRAFT - DO NOT QUOTE OR CITE ------- 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 C-6 DRAFT - DO NOT QUOTE OR CITE ------- 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 November 2002 D-l DRAFT - DO NOT QUOTE OR CITE ------- 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 November 2002 D-2 DRAFT - DO NOT QUOTE OR CITE ------- 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 November 2002 D-3 DRAFT - DO NOT QUOTE OR CITE ------- PROPOSED CONTENTS (cont'd) Page 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 November 2002 D-4 DRAFT - DO NOT QUOTE OR CITE ------- PROPOSED CONTENTS (cont'd) Page 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 November 2002 D-5 DRAFT - DO NOT QUOTE OR CITE ------- PROPOSED CONTENTS (cont'd) Page 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 November 2002 D-6 DRAFT - DO NOT QUOTE OR CITE ------- 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 November 2002 E-l DRAFT - DO NOT QUOTE OR CITE ------- 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 November 2002 E-2 DRAFT - DO NOT QUOTE OR CITE ------- 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 POSTAGE & FEES PAID EPA PERMIT No. G-35 iJ'nisad States . Environ rr:entei 'Protection Agency If you do not wish to receive these reports CHECK HERE ~; detach copy or copy, and return to the address in the upper left-hand comer. Office of Research and Development National Center for Environmental Assessment Research Triangle Park, NC 27711 Official Business Penalty for Private Use $300 NCEA-R-1068 November 2002 ------- |