[Federal Register Volume 61, Number 241 (Friday, December 13, 1996)] [Proposed Rules] [Pages 65716-65750] From the Federal Register Online via the Government Publishing Office [www.gpo.gov] [FR Doc No: 96-30903] [[Page 65715]] _______________________________________________________________________ Part III Environmental Protection Agency _______________________________________________________________________ 40 CFR Part 50 National Ambient Air Quality Standards for Ozone; Proposed Rule Federal Register / Vol. 61, No. 241 / Friday, December 13, 1996 / Proposed Rules [[Page 65716]] ENVIRONMENTAL PROTECTION AGENCY 40 CFR Part 50 [AD-FRL-5659-4] RIN 2060-AE57 National Ambient Air Quality Standards for Ozone: Proposed Decision AGENCY: Environmental Protection Agency (EPA). ACTION: Proposed rule. ----------------------------------------------------------------------- SUMMARY: In accordance with sections 108 and 109 of the Clean Air Act (Act), EPA has reviewed the air quality criteria and national ambient air quality standards (NAAQS) for ozone (O
3) and particulate matter (PM). Based on these reviews, the EPA proposes to change the standards for both classes of pollutants. This document describes EPA's proposed changes with respect to the NAAQS for O 3. The EPA's proposed actions with respect to PM are being proposed elsewhere in today's Federal Register. Nonetheless, EPA has concluded that the effects and control of each are in many instances linked and will be affected by the other. For this reason, EPA intends to review and, as appropriate, modify both standards on a similar schedule, with promulgation of revised O 3 standards in June of 1997, concurrent with promulgation of revised standards for PM. Doing so will permit States, localities and industry to address the control of these and related pollutants on a more consistent basis. Ozone and related pollutants have long been recognized, in both clinical and epidemiological research, to affect public health. The proposed revised standard would provide protection for children and other at-risk populations against a wide range of O 3-induced health effects, including decreased lung function (primarily in children active outdoors), increased respiratory symptoms (particularly in highly sensitive individuals), hospital admissions and emergency room visits for respiratory causes (among children and adults with pre- existing respiratory disease such as asthma), inflammation of the lung, and possible long-term damage to the lungs. With respect to O 3, EPA proposes to change the current primary standard (last modified in 1979) in several respects: 1. Since longer exposure periods are of greater concern at lower O 3 concentrations, attainment of the standard would no longer be based upon 1-hour averages, but instead on 8-hour averages. This improvement was unanimously recommended by EPA's Clean Air Scientific Advisory Committee (CASAC). 2. As a result of this change in averaging time, the level of the standard would be lowered from the present 0.12 parts per million (ppm). The EPA solicits comment on alternative levels of 0.09 ppm, which generally represents the continuation of the present level of protection, and 0.08 ppm, an increased level of protection. Based upon its review, EPA is proposing the 0.08 ppm standard to provide increased protection for children and asthmatics. The EPA also solicits comment on retaining the current primary standard and on an alternative 8-hour standard at a level of 0.07 ppm. 3. In addition, EPA proposes to change the test for attainment (i.e., the form) of the new standard. Currently, the test of attainment is whether a site exceeds the 1-hour standard on an average of no more than once per year, averaged over three years. Given the natural variation in hourly O 3 levels, this ``one expected exceedance'' test can result in relatively unstable attainment/nonattainment designations. The CASAC recommended a change to a more stable form; consistent with this recommendation, EPA proposes a form based on a 3- year average of 8-hour O 3 concentrations. The EPA solicits comment on a range of such concentration-based forms. The EPA proposes to replace the current secondary standard with one of two alternative standards: one set identical to the proposed new primary standard or, alternatively, a new seasonal standard expressed as a sum of hourly O 3 concentrations greater than or equal to 0.06 ppm, cumulated over 12 hours per day during the consecutive 3-month period of maximum concentrations during the O 3 monitoring season, set at a level of 25 ppm-hour. Either of the proposed alternative secondary standards would provide increased protection against O 3- induced effects, such as agricultural crop loss, damage to forests and ecosystems, and visible foliar injury to sensitive species. DATES: Written comments on this proposed rule must be received by February 18, 1997. ADDRESSES: Submit comments (in duplicate if possible) on the proposed rule to: Office of Air and Radiation Docket and Information Center (6102) Attn: Docket No. A-95-58, Environmental Protection Agency, 401 M St., SW., Washington, DC 20460. Public Hearing: The EPA will announce in a separate Federal Register document the date, time, and address of the public hearing on this proposed rule. FOR FURTHER INFORMATION CONTACT: Dr. David McKee, MD-15, Air Quality Standards and Strategies Division, Office of Air Quality Planning and Standards, U.S. Environmental Protection Agency, Research Triangle Park, NC 27711, Telephone: (919) 541-5288. SUPPLEMENTARY INFORMATION: Docket Docket No. A-95-58 incorporates by reference Docket No. A-92-17, and the docket established for the air quality criteria document (Docket No. ECAO-CD-92-0786). The docket may be inspected between 8:00 a.m. and 5:30 p.m. on weekdays, and a reasonable fee may be charged for copying. Availability of Related Information Certain documents are available from the U.S. Department of Commerce, National Technical Information Service, 5285 Port Royal Road, Springfield, VA 22161. Available documents include: Air Quality Criteria for O 3 and Other Photochemical Oxidants (``Criteria Document'') (three volumes, EPA/600/P-93-004aF through EPA/600/P-93- 004cF, July 1996, NTIS # PB-96-185574, $169.50 paper copy, $58.00 microfiche); and the Review of the National Ambient Air Quality Standards for O 3: Assessment of Scientific and Technical Information (``Staff Paper'')(EPA-452/R-96-007, June 1996, NTIS #PB-96- 203435, $67.00 paper copy and $21.50 microfiche). (Add a $3.00 handling charge per order.) A limited number of copies of other documents generated in connection with this standard review, such as documents pertaining to human exposure and health risk assessments, and vegetation exposure, risk, and benefits analyses can be obtained from: U.S. Environmental Protection Agency Library (MD-35), Research Triangle Park, NC 27711, telephone (919) 541-2777. These and other related documents are also available for inspection and copying in the EPA docket identified above. The Staff Paper and human exposure and health risk assessment support documents are now available on the Agency's Office of Air Quality Planning and Standards (OAQPS) Technology Transfer Network (TTN) Bulletin Board System (BBS) in the Clean Air Act Amendments area, under Title I, Policy/Guidance Documents. To access the bulletin board, a modem and communications software are necessary. [[Page 65717]] To dial up, set your communications software to 8 data bits, no parity and one stop bit. Dial (919) 541-5742 and follow the on-screen instructions to register for access. After registering, proceed to choice `` Gateway to TTN Technical Areas'', then choose `` CAAA BBS''. From the main menu, choose ``<1> Title I: Attain/Maint of NAAQS'', then `` Policy Guidance Documents''. To access these documents through the World Wide Web, click on ``TTN BBSWeb'', then proceed to the Gateway to TTN Technical areas, as above. If assistance is needed in accessing the system, call the help desk at (919) 541-5384 in Research Triangle Park, NC. Implementation Activities When the proposed revisions to the primary and secondary standards are implemented by the States, utility, automobile, petroleum, and chemical industries are likely to be affected, as well as other manufacturing concerns that emit volatile organic compounds or nitrogen oxides. The extent of such effects will depend on implementation policies and control strategies adopted by States to assure attainment and maintenance of the proposed standards. The EPA is developing appropriate policies and control strategies to assist States in the implementation of the proposed revisions to both the primary and secondary O
3 NAAQS. The resulting implementation strategies will then be published for public comment in the future. Table of Contents The following topics are discussed in today's preamble: I. Background A. Legislative Requirements B. Related Control Requirements C. Review of Air Quality Criteria and Standards for O 3 II. Rationale for Proposed Decision on the Primary Standard A. Health Effects Information 1. Effects of Short-term and Prolonged O 3 Exposures 2. Potential Effects of Long-term O 3 Exposures 3. Adversity of Effects for Individuals B. Human Exposure and Risk Assessments C. Conclusions on the Elements of the Primary Standard 1. Averaging Time 2. Level 3. Form D. Proposed Decision on the Primary Standard III. Communication of Public Health Information IV. Rationale for Proposed Decision on the Secondary Standard A. Effects on Vegetation B. Biologically Relevant Exposure Indices C. Vegetation Exposure and Risk Analyses D. Conclusions on the Elements of the Secondary Standard 1. Averaging Time 2. Form 3. Level E. Proposed Decision on the Secondary Standard V. Revisions to Appendix H--Interpretation of the NAAQS for Ozone A. Data Completeness B. Data Handling and Rounding Conventions VI. Technical Changes to Appendices D and E VII. Implementation Program VIII. Regulatory and Environmental Impact Analyses References I. Background A. Legislative Requirements Two sections of the Act govern the establishment, review, and revision of NAAQS. Section 108 (42 U.S.C. 7408) directs the Administrator to identify pollutants which ``may reasonably be anticipated to endanger public health and welfare'' and to issue air quality criteria for them. These air quality criteria are to ``accurately reflect the latest scientific knowledge useful in indicating the kind and extent of all identifiable effects on public health or welfare which may be expected from the presence of [a] pollutant in the ambient air * * *.'' Section 109 (42 U.S.C. 7409) directs the Administrator to propose and promulgate ``primary'' and ``secondary'' NAAQS for pollutants identified under section 108. Section 109(b)(1) defines a primary standard as one ``the attainment and maintenance of which, in the judgment of the Administrator, based on the criteria and allowing an adequate margin of safety, [are] requisite to protect the public health.'' The margin of safety requirement was intended to address uncertainties associated with inconclusive scientific and technical information available at the time of standard setting, as well as to provide a reasonable degree of protection against hazards that research has not yet identified. Both kinds of uncertainties are components of the risk associated with pollution at levels below those at which human health effects can be said to occur with reasonable scientific certainty. Thus, by selecting primary standards that provide an adequate margin of safety, the Administrator is seeking not only to prevent pollution levels that have been demonstrated to be harmful but also to prevent lower pollutant levels that she finds may pose an unacceptable risk of harm, even if the risk is not precisely identified as to nature or degree. The Act does not require the Administrator to establish a primary NAAQS at a zero-risk level but rather at a level that reduces risk sufficiently so as to protect public health with an adequate margin of safety. A secondary standard, as defined in section 109(b)(2), must ``specify a level of air quality the attainment and maintenance of which, in the judgment of the Administrator, based on [the] criteria, [are] requisite to protect the public welfare from any known or anticipated adverse effects associated with the presence of [the] pollutant in the ambient air.'' Welfare effects as defined in section 302(h) (42 U.S.C. 7602(h)) include, but are not limited to, ``effects on soils, water, crops, vegetation, manmade materials, animals, wildlife, weather, visibility and climate, damage to and deterioration of property, and hazards to transportation, as well as effects on economic values and on personal comfort and well-being.'' Section 109(d)(1) of the Act requires periodic review and, if appropriate, revision of existing air quality criteria and NAAQS. Section 109(d)(2) requires appointment of an independent scientific review committee to review criteria and standards and recommend new standards or revisions of existing criteria and standards, as appropriate. The committee established under section 109(d)(2) is known as the Clean Air Scientific Advisory Committee (CASAC), a standing committee of EPA's Science Advisory Board. B. Related Control Requirements States are primarily responsible for ensuring attainment and maintenance of ambient air quality standards once EPA has established them. Under section 110 of the Act (42 U.S.C. 7410) and related provisions, States are to submit, for EPA approval, State implementation plans (SIP's) that provide for the attainment and maintenance of such standards through control programs directed to sources of the pollutants involved. The States, in conjunction with EPA, also administer the prevention of significant deterioration program (42 U.S.C. 7470-7479) for these pollutants. In addition, Federal programs provide for nationwide reductions in emissions of these and other air pollutants through the Federal Motor Vehicle Control Program under title II of the Act (42 U.S.C. 7521-7574), which involves controls for automobile, truck, bus, motorcycle, and aircraft emissions; the new source performance standards under section 111 (42 U.S.C. 7411); and the national emission standards for hazardous air pollutants under section 112 (42 U.S.C. 7412). [[Page 65718]] C. Review of Air Quality Criteria and Standards for O 3 The last review of O 3 air quality criteria and standards was completed in March 1993 with notice of a final decision not to revise the existing primary and secondary standards (58 FR 13008). The existing primary and secondary standards are each set at a level of 0.12 ppm, with a 1-hour averaging time and a 1-expected-exceedance form, such that the standards are attained when the expected number of days per calendar year with maximum hourly average concentrations above 0.12 ppm is equal to or less than 1, averaged over 3 years (as determined by 40 CFR Part 50, Appendix H).1 --------------------------------------------------------------------------- \1\ A more complete history of the O 3 NAAQS is presented in section II.B of the Office of Air Quality Planning and Standards Staff Paper, Review of National Ambient Air Quality Standards for O 3: Assessment of Scientific and Technical Information (U.S. EPA, 1996b). --------------------------------------------------------------------------- The EPA initiated this current review in August 1992 with the development of a revised Air Quality Criteria Document for O 3 and Other Photochemical Oxidants (henceforth the ``Criteria Document''). Several workshops were held by EPA's National Center for Environmental Assessment (NCEA) to discuss health and welfare effects information during the summer and fall of 1993. An external review draft of the Criteria Document made available to the public and to the CASAC in the spring of 1994 was reviewed at a public CASAC meeting held on July 30- 31, 1994. Based on comments made at the meeting, NCEA staff prepared a second external review draft, which was reviewed at a public CASAC meeting on March 20-21, 1995. At the same meeting, the CASAC also reviewed draft portions of a staff paper prepared by the Office of Air Quality Planning and Standards (OAQPS), Review of National Ambient Air Quality Standards for Ozone: Assessment of Scientific and Technical Information (henceforth, the ``Staff Paper''), focusing on health effects and the primary NAAQS. Taking into account CASAC and public comments, staff revised both documents and made new drafts available for public and CASAC review during the summer of 1995. The OAQPS staff also prepared and made available draft portions of the Staff Paper focusing on welfare effects and the secondary standard. A public CASAC meeting was held on September 19-20, 1995, at which time CASAC came to closure in its review of the draft Criteria Document and the primary standard sections of the draft Staff Paper. In a November 28, 1995 letter from the CASAC chair to the Administrator, CASAC advised that the final draft Criteria Document ``provides an adequate review of the available scientific data and relevant studies of O 3 and related photochemical oxidants'' (Wolff, 1995a). Further, in a November 30, 1995 letter, CASAC advised the Administrator that the primary standard portion of the draft Staff Paper ``provides an adequate scientific basis for making regulatory decisions concerning a primary O 3 standard'' (Wolff, 1995b). The final Criteria Document (U.S. EPA, 1996a) reflects CASAC and public comments received at and subsequent to the September 1995 CASAC meeting. Based on comments on the Staff Paper from the September 1995 CASAC meeting, revisions were made to the secondary standard sections of the Staff Paper, which were reviewed at a public CASAC meeting held on March 21, 1996. At that meeting and in a subsequent letter to the Administrator, CASAC concluded that the secondary standard sections of the draft Staff Paper ``provide an appropriate scientific basis for making regulatory decisions concerning a secondary O 3 standard'' (Wolff, 1996). The focus of this current review of the air quality criteria and standards for O 3 and related photochemical oxidants is on public health and welfare effects associated with exposure to ambient levels of tropospheric O 3. Tropospheric O 3 is chemically identical to stratospheric O 3, which is produced miles above the earth's surface and provides a protective shield from excess ultraviolet radiation. In contrast, tropospheric O 3 at sufficient concentrations has been associated with harmful effects due to its oxidative properties and its presence in the air that people and plants take up during respiratory processes. Ozone is not emitted directly from mobile or stationary sources but, like other photochemical oxidants, commonly exists in the ambient air as an atmospheric transformation product. Ozone formation is the result of chemical reactions of volatile organic compounds (VOC), nitrogen oxides (NO X), and oxygen in the presence of sunlight and generally at elevated temperatures. A detailed discussion of atmospheric formation, ambient concentrations, and health and welfare effects associated with exposure to O 3 can be found in the final Criteria Document (U.S. EPA, 1996a) and in the final Staff Paper (U.S. EPA, 1996b). This review of the scientific criteria for O 3 has occurred simultaneously with the review of the criteria for particulate matter (PM). These criteria reviews, as well as related implementation strategy activities to date, have brought out important linkages between PM and O 3. A number of community epidemiological studies have found similar health effects to be associated with exposure to PM and O 3, including, for example, aggravation of respiratory disease (e.g., asthma), increased respiratory symptoms, and increased hospital admissions and emergency room visits for respiratory causes. Laboratory studies have suggested potential interactions between O 3 and various constituents of PM. Other key similarities relating to exposure patterns and implementation strategies exist between PM, specifically fine particles, and O 3. These similarities include: (1) Atmospheric residence times of several days, leading to large urban and regional-scale transport of the pollutants; (2) similar gaseous precursors, including NO X and VOC, which contribute to the formation of both O 3 and fine particles in the atmosphere; (3) similar combustion-related source categories, such as coal and oil- fired power generation and industrial boilers and mobile sources, which emit particles directly as well as gaseous precursors of particles (e.g., sulfur oxides (SO X), NO X, VOC) and O 3 (e.g., NO X, VOC); and (4) similar atmospheric chemistry driven by the same chemical reactions and intermediate chemical species that form both high fine particle and O 3 levels. High fine particle levels are also associated with significant impairment of visibility on a regional scale. These similarities provide opportunities for optimizing technical analysis tools (i.e., monitoring networks, emission inventories, air quality models) and integrated emission reduction strategies to yield important co-benefits across various air quality management programs. These co-benefits could result in a net reduction of the regulatory burden on some source category sectors that would otherwise be impacted by separate O 3, PM, and visibility protection control strategies. In recognition of the multiple linkages and similarities in effects and the potential benefits of integrating the Agency's approaches to providing for appropriate protection of public health and welfare from exposure to PM and O 3, EPA is conducting the reviews of the NAAQS for both pollutants on the same schedule. Accordingly, today's Federal Register contains a separate notice announcing proposed revisions to the PM NAAQS. Linking the PM and O 3 review schedules provides an important [[Page 65719]] opportunity for more effective and efficient air quality management-- both in terms of communicating a more complete description of the health and welfare effects associated with the major components of urban and regional air pollution, and by helping the States and local areas to plan jointly to address both PM and O 3 air pollution at the same time with one process, and to work jointly with industry to address common sources of air pollution. The EPA believes this integrated approach will lead to more effective and efficient protection of public health and the environment. II. Rationale for Proposed Decision on the Primary Standard This notice presents the Administrator's proposed decision to replace the existing 1-hour O 3 primary NAAQS with a new 8-hour standard, based on a thorough review, in the Criteria Document, of the latest scientific information on human health effects associated with exposure to ambient levels of O 3, including evaluation of key studies published through 1995. This decision also takes into account and is consistent with: (1) Staff assessments of the most policy- relevant information in the Criteria Document and staff analyses of human exposure and risk, presented in the Staff Paper, upon which staff recommendations for a new O 3 primary standard are based; (2) CASAC advice and recommendations, as reflected in discussion of drafts of the Criteria Document and Staff Paper at public meetings, in separate written comments, and in CASAC's letters to the Administrator; and (3) public comments received during the development of these documents, either in connection with CASAC meetings or separately. The rationale for the proposed revisions of the O 3 primary NAAQS includes consideration of: (1) Health effects information to inform judgments as to the likelihood that exposures to ambient O 3 result in adverse health effects for exposed individuals; (2) insights gained from human exposure and risk assessments to provide a broader perspective for judgments about protecting public health from the risks associated with O 3 exposure; (3) specific conclusions with regard to the elements of a standard (i.e., averaging time, level, and form) that, taken together, would be appropriate to protect public health with an adequate margin of safety; and (4) alternative views of the significance of the effects and factors to be considered in policy judgments about the appropriate level of the standard. A. Health Effects Information The following summary of human health effects associated with exposure to ambient levels of O 3 is based on integrative information from human clinical, epidemiological, and animal toxicological studies, as presented in the Criteria Document and Staff Paper. Based on this information, an array of health effects has been attributed to short-term (1 to 3 hours), prolonged (6 to 8 hours), and long-term (months to years) exposures to O 3. Acute health effects 2 induced by short-term exposures to O 3, generally while individuals were engaged in heavy exertion, include transient pulmonary function responses, transient respiratory symptoms, and effects on exercise performance. The current O 3 primary NAAQS is generally based on these acute effects associated with heavy exercise and short- term exposures. Other health effects associated with short-term or prolonged O 3 exposures include increased airway responsiveness, susceptibility to respiratory infection, increased hospital admissions and emergency room visits, and transient pulmonary inflammation. --------------------------------------------------------------------------- \2\ ``Acute health'' effects of O 3 are defined as those effects induced by short-term and prolonged exposures to O 3. Examples of these effects are functional, symptomatic, biochemical, and physiologic changes. --------------------------------------------------------------------------- Since the last review of the air quality criteria for O 3 was completed, available information has increased substantially on effects associated with prolonged and long-term exposures. Based on this new information, similar acute health effects have been observed following prolonged exposures at concentrations of O 3 as low as 0.08 ppm and at moderate levels of exertion.\2\ Although chronic effects 3 such as structural damage to pulmonary tissue and carcinogenicity have been investigated in a substantial number of laboratory animal studies, these effects have not been adequately established in human studies to draw any conclusions at this time. --------------------------------------------------------------------------- \3\ ``Chronic health'' effects of O 3 are defined as those effects induced by long-term exposures to O 3. Examples of these effects are structural damage to lung tissue and accelerated decline in baseline lung function. --------------------------------------------------------------------------- This array of effects is briefly summarized below for short-term and prolonged O 3 exposures, and for long-term O 3 exposures. Further, judgments are presented with respect to when these physiological effects become so significant that they should be regarded as adverse to the health of individuals experiencing the effects. 1. Effects of Short-term and Prolonged O 3 Exposures a. Pulmonary Function Responses Transient reductions in pulmonary function have been observed in healthy individuals and those with impaired respiratory symptoms (e.g., asthmatic individuals) as a result of both short-term and prolonged exposures to O 3. The strongest and most quantifiable exposure- response information on such pulmonary function responses to O 3 has come from controlled human exposure studies. The evidence from such studies clearly shows that reductions in lung function are enhanced by increased levels of activity involving exertion, typically reported as ``exercise'' in clinical studies, and by increased O 3 concentrations. Pulmonary function decrements generally tend to return to baseline levels shortly after short-term exposure, and effects are typically attenuated upon repeated short-term exposures over several days. As discussed in section V.C.1 of the Staff Paper, numerous experimental studies of exercising adults have demonstrated decrements in lung function both for exposures of 1-3 hours at 0.12 ppm O 3 and for exposures of 6.6 hours at 0.08 ppm O 3. These studies provide conclusive evidence that O 3 levels commonly monitored in the ambient air induce lung function decrements in exercising adults. The extent of lung function decrements varies considerably among individuals. Further, numerous summer camp studies provide an extensive and reliable database on lung function responses to ambient O 3 and other pollutants in children and adolescents living in the Northeastern U.S., southern California, and Southern Canada. Lung function changes reported at ambient O 3 concentrations in these studies are comparable to those reported in children and adults exposed under controlled experimental conditions, although direct comparisons are difficult to make because of differences in experimental design and analytical approach. b. Respiratory Symptoms and Effects on Exercise Performance As discussed in section V.C.2 of the Staff Paper, various transient human respiratory symptoms, including cough, throat irritation, chest pain on deep inspiration, nausea, and shortness of breath, have been induced by O 3 exposures of both healthy individuals and those with impaired respiratory systems. Increasing O 3 exposure durations and levels have been shown to elicit increasingly more severe [[Page 65720]] symptoms that persist for longer periods in increasingly larger numbers of individuals. Symptomatic and pulmonary function responses follow a similar time course during an acute exposure and the subsequent recovery, as well as over the course of several days during repeated exposures. As with pulmonary function responses, the severity of symptomatic responses varies considerably among subjects. For some outdoor workers or active people who are highly responsive to ambient O 3, respiratory symptoms may cause reduced productivity or may curb the ability or desire to engage in normal activities. Furthermore, O 3-induced interference with exercise performance, either by reducing maximal sustainable levels of activity or reducing the duration of activity that can be tolerated at a particular work level, is likely related to such symptomatic responses. c. Increased Airway Responsiveness Increased airway responsiveness is an indication that the airways are predisposed to bronchoconstriction which can be induced by a wide variety of external stimuli (e.g., pollens, dust, cold air, sulfur dioxide (SO 2), etc.). A high level of bronchial responsiveness is characteristic of asthma. Ozone exposure causes increased responsiveness of the pulmonary airways to subsequent challenge with bronchoconstrictor drugs such as histamine or methacholine. Changes in airway responsiveness tend to resolve somewhat more slowly than pulmonary function changes, typically disappearing after 24 hours, and appear to be less likely to attenuate with repeated exposure. As a result of increased airway responsiveness induced by O 3 exposure, human airways may be more susceptible to a variety of stimuli, including antigens, chemicals, and particles. For example, as cited in section V.C.3 of the Staff Paper, healthy subjects after being exposed to O 3 concentrations as low as 0.20 ppm for 1 hour and 0.08 ppm for 6.6 hours have experienced small increases in nonspecific bronchial responsiveness, which usually resolve within 24 hours. Asthmatic subjects typically have increased airway responsiveness at baseline. Whereas the differences in baseline nonspecific bronchial responsiveness between healthy individuals and sensitive asthmatics may be as much as 100-fold, changes induced by O 3 exposure are usually only 2- to 4-fold. With regard to O 3-induced increases in airway responsiveness (e.g., to specific inhaled antigens, cold air, and SO 2) ongoing studies will need to be completed and evaluated before conclusions can be drawn. Because enhanced response to antigens in asthmatics could lead to increased morbidity (i.e., medical treatment, emergency room visits, hospital admissions) or to more persistent alterations in airway responsiveness, these health endpoints raise concern for public health, particularly for individuals with impaired respiratory systems. d. Increased Susceptibility to Respiratory Infection When functioning normally, the human respiratory tract, like that of other mammals, has numerous closely integrated defense mechanisms that provide protection from the adverse effects of a wide variety of inhaled particles and microbes. To the extent that these defense mechanisms can be broken down or impaired by the inhalation of O 3, as discussed in section V.C.4 of the Staff Paper, O 3 exposures can result in increased susceptibility to respiratory infection and related respiratory dysfunction. Evidence of such effects has come primarily from a very large number of laboratory animal studies with generally consistent results. One of the few studies of moderately exercising human subjects exposed to 0.08 ppm O 3 for 6.6 hours reported decrements in alveolar macrophage function, the first line of defense against inhaled microorganisms and particles in the lower airways and air sacs. No single experimental human study or group of animal studies conclusively demonstrates that human susceptibility to respiratory infection is increased by exposure to O 3. However, taken as a whole, the data suggest that acute O 3 exposures can impair the host defense capability of both humans and animals, possibly by depressing alveolar macrophage function and perhaps also by decreasing mucociliary clearance of inhaled particles and microorganisms. This suggests that humans exposed to O 3 may be predisposed to bacterial infections in the lower respiratory tract. The seriousness of such infections may depend on how quickly bacteria develop virulence factors and how rapidly mechanisms are mobilized to compensate for depressed alveolar macrophage function. e. Hospital Admissions and Emergency Room Visits Increased summertime hospital admissions and emergency room visits for respiratory causes have been associated with ambient exposures to O 3 and other environmental factors. As cited in section V.C.5 of the Staff Paper, numerous studies conducted in various locations in the Eastern United States (U.S.) and Canada consistently have shown a relationship between ambient O 3 levels and increased incidence of emergency room visits and hospital admissions for respiratory causes, even after controlling for modifying factors, as well as when considering only concentrations <0.12 ppm=""> 3. Such associations between elevated ambient O 3 during summer months and increased hospital admissions have a plausible biological basis in the human and animal evidence of functional, symptomatic, and physiologic effects discussed above and in the increased susceptibility to respiratory infections observed in laboratory animals. Individuals with preexisting respiratory disease (e.g., asthma, chronic obstructive pulmonary disease) may generally be at increased risk of such effects, and some individuals with respiratory disease may have an inherently greater sensitivity to O 3. On the other hand, individuals with more severe respiratory disease are less likely to engage in the level of exertion associated with provoking responses to O 3 exposures in healthy humans. On balance, it is reasonable to conclude that evidence of O 3-induced increased airway resistance, nonspecific bronchial responsiveness, susceptibility to respiratory infection, increased airway permeability, airway inflammation, and incidence of asthma attacks suggests that ambient O 3 exposure could be a cause of increased hospital admissions, particularly for asthmatics. f. Pulmonary Inflammation Respiratory inflammation can be considered to be a host response to injury and indicators of inflammation as evidence that respiratory cell damage has occurred. Inflammation induced by exposure of humans to O 3 may have several potential outcomes: (1) Inflammation induced by a single exposure (or even several exposures over the course of a season) could resolve entirely; (2) repeated acute inflammation could develop into a chronic inflammatory state; (3) continued inflammation could alter the structure and function of other pulmonary tissue, leading to disease processes such as fibrosis; (4) inflammation could interfere with the body's host defense response to particles and inhaled microorganisms, particularly in potentially vulnerable populations such as children and older individuals; and (5) inflammation could amplify the lung's response to other agents such as allergens or toxins. For humans, only the first of these potential [[Page 65721]] outcomes has been demonstrated in the laboratory. However, this is expected because regulations concerning human experimental studies require that long-term damage be avoided. Hence, study protocols only involved brief exposures. Exposures of laboratory animals to O 3 for periods 8 hours have been shown to result in cell damage, inflammation, and increased leakage of proteins from blood into the air spaces of the respiratory tract. In general, higher O 3 concentrations are required to elicit a response equivalent to that of humans. This may partly result from study design differences, in which humans were exposed while exercising, whereas most animal studies were done at rest, resulting in differences in effective ventilation rates. Laboratory animals studies done at night, during the animals' active period, or in which ventilation rates were increased with coexposure to carbon dioxide (CO 2) tend to support this view. The extent and course of inflammation and its constitutive elements has been evaluated by using bronchoalveolar lavage (BAL) to sample cells and fluid from the lung and lower airways of humans exposed to O 3. Several such studies cited in section V.C.7 of the Staff Paper have shown that exercising humans exposed (1 to 4 hours) to 0.2 to 0.6 ppm O 3 had O 3-induced markers of inflammation and cell damage. The lowest concentration of prolonged O 3 exposure tested in humans, 0.08 ppm for 6.6 hours with moderate exercise, also induced small but statistically significant increases in these endpoints. Thus, it is reasonable to conclude that repeated acute inflammatory response and cellular damage discussed above is potentially a matter of public health concern; however, it is also recognized that most, if not all, of these effects begin to resolve in most individuals within 24 hours if the exposure to O 3 is not repeated. Of possibly greater public health concern is the potential for chronic respiratory damage which could be the result of repeated O 3 exposures occurring over a season or a lifetime. Evidence for these chronic effects is discussed below. 2. Potential Effects of Long-term O 3 Exposures Epidemiologic studies that have investigated potential associations between long-term O 3 exposures and chronic respiratory effects in humans thus far have provided only suggestive evidence of such a relationship. Most studies investigating this association have been cross-sectional in design and have been compromised by incomplete control of confounding variables and inadequate exposure information. Other studies have attempted to follow variably exposed groups prospectively. As cited in Section V.C.8 of the Staff Paper, studies conducted in southern California and Canada have compared lung function changes over several years between populations living in communities with high and low ambient O 3 levels. The findings suggest small, but consistent, decrements in lung function among inhabitants of the more highly polluted communities; however, associations between O 3 and other copollutants and problems with study population loss have reduced the level of confidence in these conclusions. In a large number of animal toxicology studies, ``lesions'' 4 in the centriacinar regions of the lung (i.e., the portion of the lung where the region that conducts air and the region that exchanges gas are joined) are well established as one of the hallmarks of O 3 toxicity. Studies have been conducted using rats, mice, and primates. In one study in which rats were exposed to an urban pattern of O 3 exposure, changes indicative of cell and tissue damage were reported, although post-exposure damage was mainly reversible. A similar study of identically exposed groups of rats found: (1) Increases in expiratory resistance suggesting central airway narrowing after 78 weeks of exposure, (2) reduced tidal volumes at all evaluation times during the exposure, and (3) generally reduced breathing frequency, although no single evaluation time was statistically significant. Another related study with a similar protocol reported reduced lung volume, which is consistent with a ``stiffer'' lung (i.e., restrictive lung disease). A recent multicenter chronic study illustrates some of the complex interrelationships among the structural, functional, and biochemical effects. The three types of health endpoints mentioned above were evaluated in a collaborative project using rats exposed for 20 months. Lung biochemistry and structure were affected at 0.5 ppm and 1.00 ppm O 3, but not at 0.12 ppm O 3, although no effects on pulmonary function were observed at any exposure level. --------------------------------------------------------------------------- \4\ Differing views have been expressed by CASAC panel members regarding the use of the term ``lesion'' to describe the O 3- induced morphological (i.e., structural) abnormalities observed in toxicological studies. Section V.C.8 of the Staff Paper describes and discusses these degenerative changes in more detail. --------------------------------------------------------------------------- In summary, the collective data on long-term exposure to O 3 garnered in studies of laboratory animals and human populations have many ambiguities. It is clear from toxicology data that the distribution of O 3 ``lesions'' is roughly similar across species (including monkeys, rats, mice) with responses that are concentration dependent (and perhaps time or exposure-pattern dependent). Under certain conditions, some of these structural changes may become irreversible. It is unclear, however, whether ambient exposure scenarios encountered by humans result in similar ``lesions'' or whether there are resultant functional or impaired health outcomes in humans chronically exposed to O 3. The epidemiologic lung function studies generally parallel those of the animal studies, but these studies lack good information on individual O 3 exposure history and are frequently confounded by personal or copollutant variables. Thus, the Administrator recognizes that there is a lack of a clear understanding of the significance of repeated, long-term inflammatory responses, and that there is a need for continued research in this important area. Nevertheless, the currently available information provides at least a biologically plausible basis for considering the possibility that repeated inflammation associated with exposure to O 3 over a lifetime may result in sufficient damage to respiratory tissue such that individuals later in life may experience a reduced quality of life, although such relationships remain highly uncertain. Studies of laboratory animals exposed to O 3 have been relatively inconclusive with regard to genotoxicity and carcinogenicity, particularly at lower O 3 concentrations. Only long-term exposure of laboratory animals to a high concentration of O 3 (1.0 ppm) has been shown to evoke a limited degree of carcinogenic activity in one strain of female mice, whereas rats were unaffected. Furthermore, there was no concentration response relationship established, perhaps due to the limited scope of the studies, and there is inadequate information from other research to provide mechanistic support for the finding in mice. (For further discussion, see section V.C.9 in the Staff Paper.) Several epidemiologic studies cited in Section V.C.6 of the Staff Paper have attempted to find associations between daily mortality and O 3 concentrations in various cities around the U.S. Although an association between ambient O 3 exposure in areas with very high O 3 levels and daily mortality has been suggested by these studies, the data are limited. 3. Adversity of Effects for Individuals Some population groups have been identified as being sensitive to effects [[Page 65722]] associated with exposures to ambient O 3 levels, such that individuals within these groups are at increased risk of experiencing the above effects. Such groups at increased risk include active children and outdoor workers who regularly engage in outdoor activities that involve heavy levels of exertion during short-term periods of elevated ambient O 3 levels or moderate levels of exertion during prolonged periods of elevated ambient O 3 levels. Exertion increases the amount of O 3 entering the airways and can cause O 3 to penetrate to peripheral regions of the lung where lung tissue is more likely to be damaged. Secondly, individuals characterized as having preexisting respiratory disease (e.g., asthma or chronic obstructive lung disease), while not necessarily more responsive than healthy individuals in terms of the magnitude of pulmonary function decrements or symptomatic responses, may be at increased risk. That is, the impact of O 3-induced responses on already-compromised respiratory systems may more noticeably impair an individual's ability to engage in normal activity or may be more likely to result in increased self-medication or medical treatment. It is recognized that limitations on using such individuals in experimental studies have prevented a more complete assessment of the full range of potential responses to O 3 or their health significance in such individuals. Finally, some individuals are unusually responsive to O 3 relative to other individuals with similar levels of activity or with a similar health status and may experience much greater functional and symptomatic effects from exposure to O 3 than the average individual response. The mechanisms and characteristics responsible for increased sensitivity to O 3 exposure have not been defined; thus, it is not clear whether these ``hyperresponders'' constitute a population subgroup with a specific risk factor or simply represent the upper end of the O 3 response distributions within the general and at-risk populations. In making judgments as to when the effects discussed above become significant enough that they should be regarded as adverse to the health of individuals in these sensitive populations, the Administrator has looked to guidelines published by the American Thoracic Society (ATS) and the advice of CASAC. While recognizing that perceptions of ``medical significance'' and ``normal activity'' may differ among physicians, lung physiologists, and experimental subjects, the ATS (1985) defined adverse respiratory health effects as ``medically significant physiologic or pathologic changes generally evidenced by one or more of the following: (1) Interference with the normal activity of the affected person or persons, (2) episodic respiratory illness, (3) incapacitating illness, (4) permanent respiratory injury, and/or (5) progressive respiratory dysfunction.'' Human health effects for which clear, causal relationships with exposure to O 3 have been demonstrated (e.g., functional and symptomatic responses) fall into the first category listed in the ATS definition. Human health effects for which statistically significant associations have been reported in epidemiology studies fall into the second and third categories. These more serious effects include respiratory illness that may require medication (e.g., asthma), but not necessarily hospitalization, as well as emergency room visits and hospital admissions for acute occurrences of respiratory morbidity. Human health effects for which associations have been suggested but not conclusively demonstrated fall primarily into the last two categories. Evidence of these most serious health endpoints for O 3 comes from studies of effects in laboratory animals, which can be extrapolated to humans only with a significant degree of uncertainty, and from human epidemiological studies. Application of these guidelines, in particular to the least serious category of effects related to ambient O 3 exposures, involves judgments about which medical experts on the CASAC panel and public commenters have expressed a diversity of views. To help frame such judgments, the EPA staff defined gradations of individual functional responses (e.g., decrements in forced expiratory volume (FEV 1), increased airway responsiveness) and symptomatic responses (e.g., cough, chest pain, wheeze), together with judgments as to the potential impact on individuals experiencing varying degrees of severity of these responses. These gradations and impacts, summarized below, are discussed in the Criteria Document (Chapter 9) and Staff Paper (section V.F, Table V-4a, 4b, 4c for individuals with impaired respiratory systems and Table V-5a, 5b, 5c for healthy individuals) and incorporate significant input from the CASAC panel of medical experts. The CASAC panel expressed a consensus view that these ``criteria for the determination of an adverse physiological response was reasonable'' (Wolff, 1995b). For individuals with impaired respiratory systems, small functional responses (e.g., FEV 1 decrements of 3% to 10%, increased nonspecific bronchial responsiveness <100%, lasting="" less="" than="" 4="" hours)="" and/or="" mild="" symptomatic="" responses="" (e.g.,="" cough="" with="" deep="" breath,="" discomfort="" just="" noticeable="" on="" exercise="" or="" deep="" breath,="" lasting="" less="" than="" 4="" hours)="" would="" likely="" interfere="" with="" normal="" activity="" (and,="" therefore,="" be="" considered="" adverse="" under="" the="" ats="" guidelines)="" for="" relatively="" few="" such="" individuals="" and="" would="" likely="" result="" in="" the="" use="" of="" normal="" medication="" as="" needed.="" moderate="" functional="" responses="" (e.g.,=""> 1 decrements 10% but <20%, increased="" nonspecific="" bronchial="" responsiveness=""> 300%, lasting up to 24 hours) and/ or moderate symptomatic responses (frequent spontaneous cough, marked discomfort on exercise or deep breath, wheeze accompanied by shortness of breath, lasting up to 24 hours) would likely interfere with normal activity for many such individuals and would likely result in additional or more frequent use of medication. Large functional responses (e.g., FEV 1 decrements 20%, increased nonspecific bronchial responsiveness >300%, lasting longer than 24 hours) and/or severe symptomatic responses (e.g., persistent uncontrollable cough, severe discomfort on exercise or deep breath, persistent wheeze accompanied by shortness of breath, lasting longer than 24 hours) would likely interfere with normal activity for most such individuals and would likely increase the likelihood of seeking medical treatment or visiting an emergency room. For active healthy individuals, it is judged that moderate levels of functional responses (e.g., FEV 1 decrements >10% but <20% lasting="" up="" to="" 24="" hours)="" and/or="" moderate="" symptomatic="" responses="" (e.g.,="" frequent="" spontaneous="" cough,="" marked="" discomfort="" on="" exercise="" or="" deep="" breath,="" lasting="" up="" to="" 24="" hours)="" would="" likely="" interfere="" with="" normal="" activity="" (and,="" therefore,="" be="" considered="" adverse="" under="" the="" ats="" guidelines)="" for="" relatively="" few="" sensitive="" individuals="" in="" the="" at-risk="" populations="" of="" concern="" (active="" children="" and="" outdoor="" workers).="" further,="" it="" is="" judged="" that="" large="" functional="" responses="" (e.g.,=""> 1 decrements >20% lasting longer than 24 hours) and/or severe symptomatic responses (e.g., persistent uncontrollable cough, severe discomfort on exercise or deep breath, lasting longer than 24 hours) would likely interfere with normal activity for many sensitive individuals. In judging the extent to which such impacts represent effects that should be regarded as adverse to the health status of individuals, an additional factor that [[Page 65723]] the Administrator has considered is whether such effects are experienced repeatedly by an individual during the course of a year or only on a single occasion. While some experts would judge single occurrences of moderate responses to be a ``nuisance,'' especially for healthy individuals, a more general consensus view of the adversity of such moderate responses emerges as the frequency of occurrence increases. Thus, the Administrator agrees with the judgments presented in the Staff Paper that repeated occurrences of moderate responses, even in otherwise healthy individuals, may be considered to be adverse since they could well set the stage for more serious illness. B. Human Exposure and Risk Assessments To put judgments about health effects that are adverse for individuals into a broader public health context, the Administrator has taken into account the results of human exposure and risk assessments. This broader context includes consideration, to the extent possible, of the size of particular population groups at risk for various effects, the likelihood that exposures of concern will occur for individuals in such groups under varying air quality scenarios, and the kind and degree of uncertainties inherent in assessing the risks involved. Such considerations provide a basis for judgments about the various levels of risk and the adequacy of public health protection afforded by the current NAAQS and alternative standards. 1. Exposure Analyses The EPA conducted exposure analyses to estimate O 3 exposures for the general population and two at-risk populations, ``outdoor children'' and ``outdoor workers,'' living in nine representative U.S. urban areas. The areas include a significant fraction of the U.S. urban population, 41.7 million people, the largest areas with major O 3 nonattainment problems, and areas that are in attainment with the current NAAQS. Exposure estimates were developed for a recent year, as well as for modeled air quality that simulated conditions associated with attainment of the current NAAQS and various alternative standards. The exposure analyses provide estimates of the size of at-risk populations exposed to various concentrations under different regulatory scenarios, as presented in section V.G of the Staff Paper and summarized below. These estimates are an important input to the risk assessment summarized in the next section. The probabilistic NAAQS exposure model for O 3 (pNEM/O 3) used in these analyses builds on earlier deterministic versions of NEM by modeling random processes within the exposure simulation. The pNEM/ O 3 model takes into account the most significant factors contributing to total human O 3 exposure, including the temporal and spatial distribution of people and O 3 concentrations throughout an urban area, the variation of O 3 levels within each microenvironment, and the effects of exertion (which is represented by ventilation rate) on O 3 uptake in exposed individuals. A more detailed description of pNEM/O 3 and its application is presented in section V.G of the Staff Paper and associated technical support documents (Johnson et al., 1994; Johnson et al., 1996 a,b; McCurdy, 1994a). The regulatory scenarios examined in the exposure analyses include 1-hour O 3 standards of 0.12 ppm (the current NAAQS) and 0.10 ppm, and 8-hour standards of 0.07, 0.08, and 0.09 ppm, the range of alternative 8-hour standards recommended in the Staff Paper and supported by CASAC as the appropriate range for consideration in this review. These analyses used 1- and 5-expected-exceedance forms of the standards and are based on use of a single year of data. These estimates were also used to roughly bound exposure estimates for other concentration-based forms of the standard under consideration (e.g., the second- and fifth-highest daily maximum 8-hour average O 3 concentration, averaged over a 3-year period) by using air quality analyses that compare alternative forms of the standard, as presented in Section IV and Appendix A of the Staff Paper. The estimated exposures reflect what would be expected in a typical or average year in an area just attaining a given standard over a 3-year compliance period. Additional air quality and exposure analyses were done to estimate the exposures that would be expected in the worst year of a 3- year compliance period. The exposure estimates were done in terms of both ``people exposed'' (i.e., the number of people who experience a given level of air pollution, or higher, at least one time during the time period of analysis) and ``occurrences of exposure'' (i.e., the number of times a given level of pollution is experienced by the population of interest). Individual exposures were estimated in terms of dose, where dose is defined as the product of O 3 concentration and ventilation rate over a defined period. Distributions of exposure estimates over the entire range of actual or simulated ambient O 3 concentrations were developed as important input to the risk analysis, although results also were developed in terms of the frequency of exposures to ambient O 3 concentrations above the lowest O 3 concentrations at which health effects have been clearly associated with exposure to O 3 in controlled human exposure studies (i.e., 0.12 ppm, 1-hour average, and 0.08 ppm, 8-hour average, respectively). Key observations important in comparing estimated exposures associated with attainment of the current NAAQS and alternative standards under consideration include: (1) Children who are active outdoors (representing approximately 7% of the population in the study areas) appear to be the at-risk population group examined with the highest percentage and number of individuals exposed to O 3 concentrations at and above which there is evidence of health effects, particularly for 8-hour average exposures at moderate exertion to O 3 concentrations 0.08 ppm. (2) On both an absolute number and a percentage basis, exposure estimates are higher for the 8-hour average effects level of 0.08 ppm at moderate exertion than for the 1-hour average effects level of 0.12 ppm at heavy exertion. (3) Estimated exposures above these effects cutpoints, even on a percentage basis, vary significantly across the urban areas examined in this analysis. However, general patterns of exposure can be seen in comparing the current NAAQS and alternative standards, particularly in looking at the seven current nonattainment areas examined. For example, for estimates of the mean percent of outdoor children exposed to 8-hour average O 3 concentrations 0.08 ppm while at moderate exertion, the following patterns are seen: the range of estimates associated with the current 1-hour NAAQS is approximately 1-21%, dropping to approximately <3% for="" a="" 0.10="" ppm="" 1-hour="" standard.="" for="" alternative="" 8-hour="" standards="" (of="" the="" same="" 1-expected-exceedance="" form="" as="" the="" current="" naaqs),="" the="" estimated="" ranges="" of="" mean="" percentages="" of="" outdoor="" children="" exposed="" are="" approximately="" 3-7%="" for="" a="" 0.09="" ppm="" standard,="" 0-1.3%="" for="" a="" 0.08="" ppm="" standard,="" and="" from="" essentially="" 0="" in="" most="" areas="" to=""><0.1% for="" a="" 0.07="" ppm="" standard.="" (4)="" in="" general,="" there="" are="" relatively="" small="" differences="" in="" comparing="" the="" distributions="" of="" 8-hour="" exposure="" estimates="" for="" outdoor="" children="" associated="" with="" 1-="" and="" 5-expected="" exceedance="" forms="" of="" any="" given="" alternative="" standard,="" although="" at="" particular="" cutpoints="" on="" the="" distribution,="" [[page="" 65724]]="" differences="" between="" these="" two="" forms="" can="" appear="" to="" be="" significant="" in="" some="" areas.="" (5)="" based="" on="" comparisons="" of="" air="" quality="" distributions,="" estimated="" exposures="" are="" generally="" comparable="" for="" 8-hour="" standards="" with="" 5-="" expected-exceedance="" and="" fifth="" highest="" daily="" maximum="" concentration="" forms.="" in="" either="" case,="" exposure="" estimates="" for="" the="" worst="" year="" of="" a="" 3-="" year="" compliance="" period="" would="" be="" higher="" than="" for="" the="" average="" or="" typical="" year,="" with="" the="" magnitude="" of="" the="" difference="" varying="" across="" areas.="" for="" example,="" for="" an="" 8-hour,="" 0.08="" ppm="" standard="" of="" either="" form,="" about="" 95%="" of="" current="" nonattainment="" areas="" would="" have="" 10="" or="" fewer="" exceedances="" of="" the="" 0.08="" ppm="" level="" in="" the="" worst="" year,="" compared="" to="" an="" average="" of="" less="" than="" 5="" exceedances="" in="" the="" typical="" year.="" exposures="" estimated="" for="" a="" year="" in="" which="" there="" were="" 10="" exceedances="" of="" the="" 0.08="" ppm="" level="" would="" be="" roughly="" comparable="" to="" the="" exposures="" estimated="" to="" occur="" upon="" attainment="" in="" a="" typical="" year="" of="" a="" 0.09="" ppm,="" 8-hour="" standard,="" with="" 1-="" to="" 5-expected-="" exceedance="" forms.="" in="" taking="" these="" observations="" into="" account,="" the="" administrator="" and="" casac="" recognize="" the="" uncertainties="" and="" limitations="" associated="" with="" such="" analyses,="" including="" the="" considerable,="" but="" unquantifiable,="" degree="" of="" uncertainty="" associated="" with="" a="" number="" of="" important="" inputs="" to="" the="" exposure="" model.="" a="" key="" uncertainty="" in="" model="" inputs="" results="" from="" the="" availability="" of="" only="" a="" limited="" human="" activity="" database,="" with="" regard="" to="" both="" the="" number="" of="" subjects="" who="" contributed="" daily="" activity="" diary="" data="" and="" the="" short="" time="" periods="" over="" which="" subjects="" recorded="" their="" daily="" activity="" patterns.="" these="" limitations="" may="" not="" adequately="" account="" for="" day-to-day="" repetition="" of="" activities="" common="" to="" children,="" such="" that="" the="" number="" of="" people="" who="" experience="" multiple="" occurrences="" of="" high="" exposure="" levels="" may="" be="" underestimated.="" small="" sample="" size="" also="" limits="" the="" extent="" to="" which="" ventilation="" rates="" associated="" with="" various="" activities="" may="" be="" representative="" of="" the="" population="" group="" to="" which="" they="" are="" applied="" in="" the="" model.="" in="" addition,="" the="" air="" quality="" adjustment="" procedure="" used="" to="" simulate="" air="" quality="" distributions="" associated="" with="" attaining="" alternative="" standards,="" while="" based="" on="" statistical="" analyses="" of="" empirical="" data,="" incorporates="" significant="" uncertainty,="" especially="" when="" applied="" to="" areas="" requiring="" very="" large="" reductions="" in="" air="" quality="" to="" attain="" the="" alternative="" standards="" examined="" or="" to="" areas="" that="" are="" now="" in="" attainment="" with="" the="" current="" naaqs.="" a="" more="" complete="" discussion="" of="" these="" uncertainties="" and="" limitations="" is="" presented="" in="" the="" staff="" paper="" and="" the="" technical="" support="" documents="" (johnson="" et="" al.,="" 1996a,b).="" 2.="" risk="" assessment="" the="" epa="" conducted="" an="" assessment="" of="" health="" risks="" for="" several="" categories="" of="" respiratory="" effects="" associated="" with="" attainment="" of="" alternative="" 1-="" and="" 8-hour=""> 3 NAAQS and under a recent year of air quality (``as is'' air quality). The O 3 health risk assessment considers the same alternative air quality scenarios and the same nine urban areas that were examined in the human exposure analyses described above. The objective of the risk assessment was to estimate the magnitude of risks to population groups believed by EPA and CASAC to be at greatest risk either due to increased exposures (i.e., outdoor children and outdoor workers) or increased susceptibility (e.g., asthmatics) while characterizing, as explicitly as possible, the range and implications of uncertainties in the existing scientific database. While the risk estimates are subject to uncertainties as discussed below and should not be viewed as demonstrated health impacts, EPA believes they do represent reasonable estimates as to the possible extent of risk for these effects given the available information. Although it does not cover all health effects caused by O 3, the risk assessment was intended as a tool, together with other information presented in the Staff Paper and in the revised Criteria Document, to aid the Administrator in judging which alternative O 3 NAAQS would reduce risks sufficiently to protect public health with an adequate margin of safety. The health risk assessment builds upon the earlier O 3 NAAQS health risk assessment work developed during the previous review of the standard. The health risk model takes into account (1) concentration- response or exposure-response relationships used to characterize various respiratory effects of O 3 exposure, (2) distributions of O 3 1-hour and 8-hour daily maximum concentrations upon attainment of alternative NAAQS obtained from the pNEM/O 3 analyses described above, and (3) distributions of population exposure, in terms of both the number of individuals in the general population, outdoor workers, and outdoor children exposed and the number of occurrences of exposure, upon attainment of alternative O 3 NAAQS, obtained from the O 3 exposure analyses. A more detailed description of the risk assessment methodology and its application is presented in Section V.H of the Staff Paper and associated technical support document (Whitfield et al., 1996). a. Adverse Lung Function and Respiratory Symptom Responses Risk estimates have been developed for several of the respiratory effects observed in controlled human exposure studies to be associated with O 3 exposure. These include lung function decrements (measured as changes in FEV 1) and moderate or severe pain on deep inspiration (PDI). Each of the effects is associated with a particular averaging time and, for most of the acute (1- to 8-hour) responses, effects also are estimated separately for specific ventilation ranges [measured as equivalent ventilation rate (EVR)] that correspond to the EVR ranges observed in the health studies used to derive exposure- response relationships. An effect, or endpoint, can be defined in terms of a measure of biological response and the amount of change in that measure thought to be of concern. For lung function decrements, estimates are provided for the lower end, midpoint, and upper end of the range of response that might be considered an adverse health effect (i.e., 10, 15, or 20% FEV 1 decrements) as discussed in II.A.3 above. For acute symptomatic effects, estimates are provided for responses that EPA considers to be of most concern (e.g., moderate and severe PDI). Due to limitations in the available data, the risk assessment provides estimates only for each individual health endpoint rather than various combinations of functional and symptomatic responses. The acute exposure-response relationships developed were based on the clinical studies and were applied to ``outdoor children,'' ``outdoor workers,'' and the general population. While these specific clinical studies only included adults aged 18-35, findings from other clinical studies and summer camp field studies in at least six different locations in the northeast United States, Canada, and Southern California indicate changes in lung function in healthy children similar to those observed in healthy adults exposed to O 3 under controlled chamber conditions. While different risk measures are provided by the O 3 health risk assessment, EPA has focused on ``headcount risk'' estimates. Headcount risk provides estimates of both the number of people affected and the number of incidences of a given health effect, considering individuals' personal exposures as they go about their daily activities (e.g., from indoors to outdoors, moving from place to place, and engaging in activities at different exertion levels). [[Page 65725]] A major input to the headcount risk model is the series of population exposure distributions for the alternative NAAQS analyzed. Using available exposure estimates, risk estimates were calculated for the nine urban areas examined in the exposure analysis. For 8-hour exposures under moderate exertion, outdoor children represent the population group experiencing the greatest exposure, and, therefore, this population also has the highest risk estimates in terms of the percent of the population estimated to respond. Therefore, this summary of results focuses on the risk estimates for outdoor children. Whitfield et al. (1996) presents results of the headcount risk estimates for each of the nine urban areas for outdoor children and outdoor workers. Table 1 presents a summary of risk estimates for 8-hour and 1-hour health endpoints for outdoor children upon attainment of alternative 8- hour, 1- and 5-expected exceedance standards and the current 0.12 ppm, 1-hour standard. The risk estimates in Table 1 are for effects associated with exposure under moderate exertion. These risk estimates represent an aggregate estimate for the nine urban areas examined; an aggregate estimate is presented since there is significant variability in this risk measure across the areas. The uncertainty in these risk estimates associated with sample size considerations is characterized by the 90 percentile credible intervals shown. Table 1.--Percent of Outdoor Children Estimated to Experience Various Health Effects 1 or More Times per Year Associated With 8- and 1-Hour Ozone Exposures Upon Attaining Alternative Standards* ---------------------------------------------------------------------------------------------------------------- Alternative standards Pulmonary function Pulmonary function Moderate or severe ----------------------------------------------------- decrements, FEV 1 decrements, FEV 1 pain on deep 15% 20% inspiration Level Averaging time and form associated with 8- associated with 8- associated with 1- hour exposures hour exposures hour exposures ---------------------------------------------------------------------------------------------------------------- 0.07 ppm................ 8-hour, 1 expected 3.0 0.4 (0.1-1.8) 0.3 (0.01-1.9) exceedance. **(1.0-6.6) 0.08 ppm................ 8-hour, 1 expected 5.1 (2.2-9.6) 1.4 (0.5-3.7) 0.6 (0.05-2.7) exceedance. 8-hour, 5 expected 6.7 (3.3-11.9) 2.3 (0.8-5.3) 0.8 (0.1-3.2) exceedances. 0.09 ppm................ 8-hour, 1 expected 7.7 (3.3-13.3) 2.7 (1.0-6.1) 0.9 (0.1-3.5) exceedance. 8-hour, 5 expected 9.5 (5.1-15.9) 3.8 (1.5-7.9) 1.3 (0.2-4.2) exceedances. 0.12 ppm................ 1-hour, 1 expected 8.3 (8.2-14.2) 3.0 (1.1-6.6) 1.0 (0.1-3.6) exceedance. ---------------------------------------------------------------------------------------------------------------- * Estimates represent aggregate results for 9 urban areas examined. The total number of outdoor children residing in the 9 urban areas was 3.1 million. ** 90% credible interval. Key observations important in comparing estimated health risks associated with attainment of the current NAAQS and alternative standards under consideration include: (1) On both an absolute number and a percentage basis, risk estimates are higher for effects associated with 8-hour exposures under moderate exertion than for effects associated with 1-hour exposures under heavy exertion. (2) Reflecting a continuum of risk, there is a decreasing trend in the median estimates of the population estimated to experience the lung function and symptomatic responses as one moves along the range of alternative 8-hour average, 1-expected exceedance standards under consideration. For example, based on the aggregate risk estimates summarized in Table 1, the median percent of outdoor children estimated to experience FEV 1 decrements greater than 15% is reduced from about 7.7% for a 0.09 ppm, 8-hour standard to about 5.1% for a 0.08 ppm, 8-hour standard. Attaining a 0.07 ppm, 8-hour standard results in a further reduction to about 3.0% of outdoor children estimated to experience this effect. (3) In general, the differences in risk estimates for outdoor children associated with 1- and 5-expected exceedance standards set at the same standard level are relatively modest within the continuum of risk. For example, the risk estimates for lung function decrements 15% associated with a 5-expected exceedance standard set at 0.08 ppm fall between the risk estimates for the 0.08 and 0.09 ppm, 1- expected exceedance, 8-hour standards. Similarly, the risk estimates for a 5-expected exceedance standard set at 0.09 ppm fall between the risk estimates for the 0.09 and 0.10 ppm, 1-expected exceedance, 8-hour standards. The risk estimates for the current 0.12 ppm, 1-hour standard fall between the risk estimates for the 0.09 ppm, 1- and 5-expected exceedance standards. (4) Multiple occurrences of lung function decrements 15% and 20% associated with 8-hour exposures under moderate exertion are estimated to occur for outdoor children upon attainment of any of the alternative 1- or 8-hour standards analyzed. The average seasonal numbers of occurrences per responder across the urban areas included in the analysis range from four to about nine for lung function decrements 15% and from two to about five for lung function decrements >20%, such that some individuals will experience more frequent occurrences of effects during the O 3 season, whereas others will experience fewer occurrences than the average in any given area. (5) Based on comparisons of air quality distributions, risk estimates are generally comparable between 8-hour standards with 5- expected exceedances or fifth-highest daily maximum concentration forms. As noted in the previous discussion of the exposure estimates, for either form the worst year of a 3-year compliance period would be higher than for the average or typical year. For example, about 95% of current nonattainment areas meeting either form of an 8-hour, 0.08 ppm standard would have 10 or fewer exceedances in the worst year, compared to an average of less than five exceedances in a typical year. Risk estimates for a year in which there were 10 exceedances of 0.08 ppm, 8- hour average vary from urban area to urban area but fall between the risk estimates for a 5-expected exceedance standard of 0.08 ppm and a 5-expected exceedance standard set at 0.09 ppm. The EPA believes, and CASAC concurred, that the models selected to estimate exposure and risk are appropriate and that the methods used to conduct the health risk assessment represent the state of the art. Nevertheless, the Administrator and CASAC recognize that there are many uncertainties inherent in such analyses. The resulting ranges of quantitative risk [[Page 65726]] estimates do not reflect all of the uncertainties associated with the numerous assumptions inherent in such analyses (Wolff, 1995b). Some of the most important caveats and limitations concerning the health risk assessment for lung function and respiratory symptom endpoints include: (1) The uncertainties and limitations associated with the exposure analyses discussed above, (2) the extrapolation of exposure-response functions below the lowest-observed-effects levels to an estimated background level of 0.04 ppm, and (3) the inability to account for some factors which are known to affect the exposure-response relationships (e.g., assigning children the same symptomatic response rates as observed for adults and not adjusting response rates to reflect the increase and attenuation of responses that have been observed in studies of lung function and symptoms upon repeated exposures). A more complete discussion of assumptions and uncertainties is contained in the Staff Paper and in the technical support document (Whitfield et al., 1996). b. Excess Respiratory-Related Hospital Admissions As discussed earlier in this notice, several epidemiology studies, mainly conducted in the northeastern portion of the U.S. and southeastern Canada, have reported excess daily respiratory-related hospital admissions associated with elevated O 3 levels during the O 3 season. To gain insight into the possible impact of just attaining alternative 1- and 8-hour O 3 standards, EPA has developed a risk model for this endpoint. The model is based on the regression coefficient (and the corresponding standard error) developed by Thurston et al. (1992) for New York City and estimated daily maximum hourly average O 3 levels over an entire season at various monitors in New York City upon attainment of alternative standards (as developed for the pNEM/O 3 analysis). The regression coefficient (11.7 admissions/ppm O 3/106 people) and its standard error (4.7 admissions/ppm O 3/106 people) were used to define a probabilistic concentration-response relationship. The model is described in more detail in Whitfield et al. (1996). One-hour daily maximum O 3 concentrations for one O 3 season under various alternative air quality standards were used to estimate the number of excess respiratory-related admissions of asthmatics (i.e., those attributable to O 3 concentrations higher than background). The O 3 concentration-response relationship developed by Thurston et al. (1992) was based on air quality data from the Queens monitor. Therefore, the risk estimates based on the Queens County monitor most closely represent the air quality index used in the original study and are summarized below. In each analysis, the air quality was adjusted to just attaining a particular standard at the monitor with the highest O 3 levels for the New York area, and the O 3 levels were adjusted at the other monitors using the procedures described in Johnson et al. (1996a). Based on Table V-20 in the Staff Paper, the hospital admissions model results in a median estimate of excess respiratory-related admissions for asthmatic individuals attributable to O 3 exposure of approximately 390 (with a 90% credible interval of approximately 130-640) per year for the New York City area based on ``as is'' air quality using 1991 data. Just attaining the current 0.12 ppm, 1-hour standard is estimated to reduce excess hospital admissions to about 210 (with a 90% credible interval of 70-340), which is approximately a 50% decrease in O 3-induced admissions due to concentrations in excess of the estimated 0.04 ppm estimated background level. Upon attaining the 0.08 ppm, 8-hour, 1 expected exceedance standard, for example, the median estimate for excess respiratory-related hospital admissions attributable to O 3 exposure is further reduced to approximately 115 (with a 90% credible interval of approximately of 40-190). This represents a 70% decrease in O 3-induced hospital admissions from the ``as is'' scenario and about a 45% decrease from the current 1-hour standard. It should be recognized that the O 3-induced excess hospital admissions represent a relatively small fraction of the overall respiratory-related hospital admissions for asthmatics over the seven month O 3 season. Based on an estimated 15,000 admissions per year during the O 3 season, the reduction in hospital admissions for asthmatics for any respiratory-related reason in going from ``as is'' air quality to attaining a 0.08 ppm, 8-hour, 1-expected exceedance standard is about 2%. Similarly, the reduction from attaining the current 1-hour standard to attaining a 0.08 ppm, 8-hour, 1-expected exceedance standard represents about a 0.6% decrease in total respiratory admissions for asthmatics due to all causes. Key observations important in comparing hospital admission risk estimates associated with attainment of the current NAAQS and alternative standards under consideration include: (1) Risk estimates for excess hospital admissions for asthmatics attributable to O 3 exposures in excess of an estimated background level of 0.04 ppm are projected to be significantly reduced (about 45%) under a 0.08 ppm, 8-hour, 1-expected exceedance standard compared to the current 1-hour NAAQS. (2) The excess hospital admissions risk estimates associated with 1- and 5-expected exceedance standards set at 0.08 ppm are very similar. (3) When viewed from the perspective of respiratory-related admissions for asthmatics due to all causes, the excess hospital admissions attributable to O 3 exposures in excess of an estimated background concentration of 0.04 ppm constitute a relatively small portion of total admissions. For example, comparing the risk estimates associated with the current 1-hour NAAQS and a 0.08 ppm, 8-hour, 1- expected exceedance standard results in only about a 0.6% reduction in respiratory hospital admissions for asthmatics due to all causes. In taking these observations into account, the Administrator recognizes the uncertainties and limitations associated with the hospital admission risk assessment. These include: (1) The inability at this time to quantitatively extrapolate the risk estimates for the New York City area to other urban areas, (2) uncertainty associated with the underlying epidemiological study that served as the basis for developing the concentration-response relationship used in the analysis, and (3) uncertainties associated with the air quality adjustment procedure used to simulate attainment of alternative standards for the New York City area. A more complete discussion of these uncertainties and limitations is presented in the Staff Paper and technical support document (Whitfield et al., 1996). c. Conclusions on the Elements of the Primary Standard In selecting a primary standard for O 3, the Administrator must specify: (1) Averaging time, (2) O 3 concentration (i.e., level), and (3) form (i.e., the air quality statistic to be used as a basis for determining compliance with the standard).5 All three of these elements are necessary to define a standard. Based on the assessment of relevant scientific and technical information in the Criteria Document, section VI of the Staff Paper outlines a number of key factors to be considered in specifying each of these elements, as well as recommendations to focus consideration on a discrete range of options for each [[Page 65727]] element. The factors reflect an integration of information on acute and chronic health effects associated with exposure to ambient O 3; expert judgments on the adversity of such effects for individuals; and policy judgments, informed by air quality analyses and quantitative risk assessment when possible, as to the point at which risks would be reduced sufficiently to achieve protection of public health with an adequate margin of safety. --------------------------------------------------------------------------- \5\ This review focused only on a standard for O 3, as the most appropriate surrogate for photochemical oxidants. --------------------------------------------------------------------------- This approach to selecting a proposed primary standard was endorsed by members of CASAC (Wolff, 1995b), particularly through their advice to the Administrator that ``EPA's risk assessments must play a central role in identifying an appropriate level'' and their recognition that the selection of a specific concentration and form ``is a policy judgment.'' Further, it was the consensus view of CASAC that the ranges of levels (0.07 to 0.09 ppm) and forms (1 to 5 exceedances) recommended in the Staff Paper were appropriate. Thus, the Administrator has focused her consideration on the recommended options and key factors outlined in the Staff Paper. The considerations that were most influential in the Administrator's selection of each specific element of the proposed standard are outlined below. 1. Averaging Time The Administrator concurs with the unanimous recommendation of CASAC (Wolff, 1995b) ``that the present 1-hr standard be eliminated and replaced with an 8-hr standard,'' and that more research is needed to resolve uncertainties about potential chronic effects before appropriate consideration can be given to establishing a long-term (e.g., seasonal or annual) standard. These judgments are supported by the following key observations and conclusions: (1) The 1-hour averaging time specified in the current NAAQS was originally selected primarily on the basis of health effects associated with short-term (i.e., 1- to 3-hour) exposures, with qualitative consideration given to preliminary information on potential associations with longer exposure periods. (2) Substantial new health effects information available for consideration in this review demonstrates associations between a wide range of health effects and prolonged (i.e., 6- to 8-hours) exposures below the level of the current 1-hour NAAQS. (3) Results from the quantitative risk analyses show that attaining a standard with a 1-hour averaging time reduces the risk of experiencing health effects associated with both 1-hour and 8-hour exposures. Likewise, attaining an 8-hour standard reduces the risk of experiencing health effects associated with both 8-hour and 1-hour exposures. Thus, reductions in risks from both short-term and prolonged exposures can be achieved through a primary standard with an averaging time of either 1 or 8 hours. As a result, establishment of both 1-hour and 8-hour standards would not be necessary to reduce risks associated with the full range of observed acute health effects. (4) The 8-hour averaging time is more directly associated with health effects of concern at lower O 3 concentrations than is the 1-hour averaging time. It was thus the consensus of CASAC ``that an 8- hr standard was more appropriate for a human health-based standard than a 1-hr standard.'' (Wolff, 1995b) (5) While there is a large animal toxicology database providing clear evidence of associations between long-term (e.g., from several months to years) exposures and lung tissue damage, with additional evidence of reduced lung elasticity and accelerated loss of lung function, there is not corresponding evidence for humans. Moreover, the state of the science has not progressed sufficiently to permit quantitative extrapolation of the animal-study findings to humans. Thus, the Administrator concludes that consideration of a separate long-term O 3 standard is not appropriate at this time. As discussed below, however, the Administrator has considered the possibility of long-term effects in selecting the level of the standard, which will provide protection against such effects to the extent they may occur in humans, by lowering overall air quality distributions and, thus, reducing cumulative long-term exposures. 2. Level The Administrator's consideration of an appropriate level for an 8- hour standard to protect public health with an adequate margin of safety necessarily reflects a recognition, as emphasized by CASAC, that it is likely that ``O 3 may elicit a continuum of biological responses down to background concentrations'' (Wolff, 1995b). Thus, in the absence of any discernible threshold, it is not possible to select a level below which absolutely no effects are likely to occur. Nor does it seem possible, in the Administrator's judgment, to identify a level at which it can be concluded with confidence that no ``adverse'' effects are likely to occur. In such a case, as CASAC has advised, the traditional paradigm for standard-setting cannot be applied in the usual way, and assessments of risk ``must play a central role in identifying an appropriate level'' (Wolff, 1995b). Thus, the Administrator's task becomes one of attempting to select a standard level that will reduce risks sufficiently to protect public health with an adequate margin of safety, since a zero-risk standard is neither possible nor required by the Act. Consequently, as CASAC recognized, ``the selection of a specific level * * * is a policy judgment'' (Wolff, 1995b). The Administrator's policy judgment on the level of the proposed standard is framed by the above considerations and informed by the following key observations and conclusions: (1) During the last review of the O 3 criteria and standards, the CASAC concluded that the existing 1-hour standard set at 0.12 ppm O 3 provided ``little, if any, margin of safety,'' and the upper end of the range of consideration for a 1-hour standard should be 0.12 ppm (McClellan, 1989). In addition, several members of the CASAC panel recommended that consideration should be given to a lower 1-hour level of 0.10 ppm to offer some protection against effects for which there was preliminary information at that time of associations with 8-hour exposures to O