[Federal Register Volume 61, Number 241 (Friday, December 13, 1996)] [Proposed Rules] [Pages 65638-65713] From the Federal Register Online via the Government Publishing Office [www.gpo.gov] [FR Doc No: 96-30897] [[Page 65637]] _______________________________________________________________________ Part II Environmental Protection Agency _______________________________________________________________________ 40 CFR Part 50 National Ambient Air Quality Standards for Particulate Matter; Proposed Rule Federal Register / Vol. 61, No. 241 / Friday, December 13, 1996 / Proposed Rules [[Page 65638]] ENVIRONMENTAL PROTECTION AGENCY 40 CFR Part 50 [AD-FRL-5659-5] RIN 2060-AE66 National Ambient Air Quality Standards for Particulate Matter: 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 particulate matter (PM) and for ozone (O
3). Based on these reviews, EPA proposes to change the standards for both classes of pollutants. This document describes EPA's proposed changes with respect to the NAAQS for PM. The EPA's proposed actions with respect to O 3 are being proposed elsewhere in today's Federal Register. With respect to PM, EPA proposes to revise the current primary PM 10 standards by adding two new primary PM 2.5 standards set at 15 g/m\3\, annual mean, and 50 g/m\3\, 24-hour average, to provide increased protection against a wide range of PM- related health effects, including premature mortality and increased hospital admissions and emergency room visits (primarily in the elderly and individuals with cardiopulmonary disease); increased respiratory symptoms and disease (in children and individuals with cardiopulmonary disease such as asthma); decreased lung function (particularly in children and individuals with asthma); and alterations in lung tissue and structure and in respiratory tract defense mechanisms. The proposed annual PM 2.5 standard would be based on the 3-year average of the annual arithmetic mean PM 2.5 concentrations, spatially averaged across an area. The proposed 24-hour PM 2.5 standard would be based on the 3-year average of the 98th percentile of 24-hour PM 2.5 concentrations at each monitor within an area. The EPA also solicits comment on two alternative approaches for selecting the levels of PM 2.5 standards. The EPA proposes to revise the current 24-hour primary PM 10 standard of 150 g/m\3\ by replacing the 1- expected-exceedance form with a 98th percentile form, averaged over 3 years at each monitor within an area, and solicits comment on an alternative proposal to revoke the 24-hour PM 10 standard. The EPA also proposes to retain the current annual primary PM 10 standard of 50 g/m\3\. Further, EPA proposes new data handling conventions for calculating 98th percentile values and spatial averages (Appendix K), proposes to revise the reference method for monitoring PM as PM 10 (Appendix J), and proposes a new reference method for monitoring PM as PM 2.5 (Appendix L). The EPA proposes to revise the current secondary standards by making them identical to the suite of proposed primary standards. In the Administrator's judgment, these standards, in conjunction with the establishment of a regional haze program under section 169A of the Act, would provide appropriate protection against PM-related public welfare effects including soiling, material damage, and visibility impairment. DATES: Written comments on this proposed rule must be received by February 18, 1997. ADDRESSES: Submit comments in duplicate if possible on the proposed action to: Office of Air and Radiation Docket and Information Center (6102), Attention: Docket No. A-95-54, U.S. Environmental Protection Agency, 401 M St., SW., Washington, DC 20460. Public hearings: 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: Ms. Patricia Koman, MD-15, Air Quality Strategies and Standards Division, Office of Air Quality Planning and Standards, U.S. Environmental Protection Agency, Research Triangle Park, North Carolina 27711, telephone: (919) 541-5170. SUPPLEMENTARY INFORMATION: Docket Docket No. A-95-54 incorporates by reference the docket established for the air quality criteria document (Docket No. ECAO-CD-92-0671). The docket may be inspected at the above address 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, Virginia 22161. Available documents include: Air Quality Criteria for Particulate Matter (Criteria Document) (three volumes, EPA/600/P-95-001aF thru EPA/600/P-95-001cF, April 1996, NTIS # PB-96- 168224, $234.00 paper copy); and Review of the National Ambient Air Quality Standards for Particulate Matter: Policy Assessment of Scientific and Technical Information (Staff Paper) (EPA-452/R-96-013, July 1996, NTIS # PB-97-115406, $47.00 paper copy and $19.50 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 technical support documents pertaining to air quality, monitoring, and health risk assessment, 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 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. 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 revisions to the primary and secondary PM standards are implemented by the States, the utility, petroleum, mining, iron and steel, automobile, and chemical industries are likely to be affected, as well as other manufacturing concerns that emit PM or precursors to PM. The extent of such effects will depend on implementation policies and control strategies adopted by the States to assure attainment and maintenance of revised standards. The EPA is developing appropriate policies and control strategies to assist States in the implementation of the proposed revisions to the PM NAAQS. The resulting implementation strategies [[Page 65639]] will be proposed 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 PM II. Rationale for Proposed Decisions on Primary Standards A. Health Effects Information 1. Nature of the Effects 2. Sensitive Subpopulations 3. Evaluation of Health Effects Evidence 4. Particulate Matter Fractions of Concern B. Quantitative Risk Assessment 1. Overview 2. Key Observations C. Need for Revision of the Current Primary PM Standards D. Indicators of PM 1. Indicators for the Fine Fraction of PM
10 2. Indicators for the Coarse Fraction of PM 10 E. Averaging Time of PM 2.5 Standards 1. Short-term PM 2.5 Standard 2. Long-term PM 2.5 Standard 3. Combined Effect of Annual and 24-Hour Standards F. Form of PM 2.5 Standards 1. Annual Standard 2. 24-Hour Standard G. Levels for the Annual and 24-Hour PM 2.5 Standards H. Conclusions Regarding the Current PM 10 Standards 1. Averaging Time and Form 2. Levels for Alternative Averaging Times I. Proposed Decisions on Primary Standards III. Rationale for Proposed Decision on the Secondary Standards A. Visibility Impairment B. Materials Damage and Soiling Effects C. Proposed Decision on Secondary Standards IV. Revisions to Appendix K--Interpretation of the PM NAAQS A. PM 2.5 Computations and Data Handling Conventions B. PM 10 Computations and Data Handling Conventions V. Reference Methods for the Determination of Particulate Matter as PM 10 and PM 2.5 in the Atmosphere A. Revisions to Appendix J--Reference Method for PM 10 B. Appendix L--New Reference Method for PM 2.5 VI. Implementation Program VII. 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). C. Review of Air Quality Criteria and Standards for PM Particulate matter is the generic term for a broad class of chemically and physically diverse substances that exist as discrete particles (liquid droplets or solids) over a wide range of sizes. Particles originate from a variety of anthropogenic stationary and mobile sources as well as from natural sources. Particles may be emitted directly or formed in the atmosphere by transformations of gaseous emissions such as sulfur oxides (SO X), nitrogen oxides (NO X), and volatile organic compounds (VOC). The chemical and physical properties of PM vary greatly with time, region, meteorology, and source category, thus complicating the assessment of health and welfare effects. The last review of PM air quality criteria and standards was completed in [[Page 65640]] July 1987 with notice of a final decision to revise the existing standards (52 FR 24854, July 1, 1987). In that decision, EPA changed the indicator for particles from total suspended particles (TSP) to PM 10.1 Identical primary and secondary PM 10 standards were set for two averaging times: (1) 50 g/m3, expected annual arithmetic mean, averaged over 3 years, and (2) 150 g/ m3, 24-hour average, with no more than one expected exceedance per year.2 --------------------------------------------------------------------------- \1\ PM 10 refers to particles with an aerodynamic diameter less than or equal to a nominal 10 micrometers. \2\A more complete history of the PM NAAQS is presented in section II.B of the OAQPS Staff Paper, Review of National Ambient Air Quality Standards for Particulate Matter: Assessment of Scientific and Technical Information (U.S. EPA, 1996b). --------------------------------------------------------------------------- The EPA formally initiated the current review of the air quality criteria for PM in April 1994 by announcing its intention to develop a revised Air Quality Criteria Document for Particulate Matter (henceforth, the ``Criteria Document''). Thereafter, the EPA presented its plans for review of the criteria and standards for PM under a highly accelerated, court-ordered schedule 3 at a public meeting of the CASAC in December 1994. Several workshops were held by EPA's National Center for Environmental Assessment (NCEA) to discuss important new health effects information in November 1994 and January 1995. External review drafts of the Criteria Document were made available for public comment and were reviewed by CASAC at public meetings held in August and December 1995 and February 1996. The CASAC came to closure in its review of the Criteria Document, advising the Administrator in a March 15, 1996 closure letter (Wolff, 1996a) that ``although our understanding of the health effects of PM is far from complete, a revised Criteria Document which incorporates the Panel's latest comments will provide an adequate review of the available scientific data and relevant studies of PM.'' CASAC and public comments from these meetings and from subsequent written comments and the closure letter were incorporated as appropriate in the final Criteria Document (U.S. EPA, 1996a). --------------------------------------------------------------------------- \3\ A court order entered in American Lung Association v. Browner, CIV-93-643-TUC-ACM (D. Ariz., October 6, 1994), as subsequently modified, requires publication of proposed and final decisions on the review of the PM NAAQS by November 29, 1996 and June 28, 1997, respectively. --------------------------------------------------------------------------- External review drafts of a staff paper prepared by the Office of Air Quality Planning and Standards (OAQPS), Review of the National Ambient Air Quality Standards for Particulate Matter: Assessment of Scientific and Technical Information (henceforth, the ``Staff Paper'') were made available for public comment and were reviewed by CASAC at public meetings in December 1995 and May 1996.4 The CASAC came to closure in its review of the Staff Paper, advising the Administrator in a June 13, 1996 closure letter (Wolff, 1996b) that ``the Staff Paper, when revised, will provide an adequate summary of our present understanding of the scientific basis for making regulatory decisions concerning PM standards.'' CASAC and public comments from these meetings, subsequent written comments, and the CASAC closure letter were incorporated as appropriate in the final Staff Paper (U.S. EPA, 1996b). --------------------------------------------------------------------------- \4\ The Staff Paper evaluates policy implications of the key studies and scientific information in the Criteria Document, identifies critical elements that EPA staff believes should be considered, and presents staff conclusions and recommendations of suggested options for the Administrator's consideration. --------------------------------------------------------------------------- The principal focus of this current review of the air quality criteria and standards for PM is on recent epidemiological evidence reporting associations between ambient concentrations of PM and a range of serious health effects. Particular attention has been given to several size-specific classes of particles, including PM 10 and the principal fractions of PM 10, referred to as the fine (PM 2.5) 5 and coarse (PM 10-2.5) 6 fractions. As discussed in the Criteria Document, fine and coarse fraction particles can be differentiated by their sources and formation processes and their chemical and physical properties, including behavior in the atmosphere. Detailed discussions of atmospheric formation, ambient concentrations, and health and welfare effects of PM, as well as quantitative estimates of human health risks associated with exposure to PM, can be found in the Criteria Document and Staff Paper. --------------------------------------------------------------------------- \5\ PM 2.5 refers to particles with an aerodynamic diameter less than or equal to a nominal 2.5 micrometers. \6\ PM 10-2.5 refers to those particles with an aerodynamic diameter less than or equal to a nominal 10 micrometers but greater than 2.5 micrometers. --------------------------------------------------------------------------- This review of the scientific criteria for PM has occurred simultaneously with the review of the criteria for ozone (O 3). These criteria reviews as well as related implementation strategy activities to date have brought out important linkages between O 3 and PM. A number of community epidemiological studies have found similar health effects to be associated with exposure to O 3 and PM, 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 found potential interactions between O 3 and various constituents of PM. Other key similarities relating to exposure patterns and implementation strategies exist between O 3 and PM, specifically fine particles. 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., 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 O 3 and fine particle 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 O 3 and PM, EPA plans to complete the review of the NAAQS for both pollutants on the same schedule. Accordingly, today's Federal Register contains a separate notice announcing proposed revisions to the O 3 NAAQS. Linking the O 3 and PM review schedules provides an important opportunity to materially improve the nation's air quality management programs--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 [[Page 65641]] work together 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 Decisions on Primary Standards This notice presents the Administrator's proposed decisions to establish new annual and 24-hour PM 2.5 primary standards and to revise the form of the current 24-hour PM 10 primary NAAQS, based on a thorough review, in the Criteria Document, of the latest scientific information on known and potential human health effects associated with exposure to PM at levels typically found in the ambient air. These decisions also take into account and are consistent with: (1) Staff Paper assessments of the most policy-relevant information in the Criteria Document, upon which staff recommendations for new and revised primary standards are based; (2) CASAC advice and recommendations, as reflected in discussions of drafts of the Criteria Document and Staff Paper at public meetings, in separate written comments, and in the CASAC's closure letters to the Administrator; and (3) public comments received during the development of these documents, either in connection with CASAC meetings or separately. As discussed more fully below, the rationale for the proposed revisions of the PM primary NAAQS includes consideration of: (1) Health effects information, and alternative views on the appropriate interpretation and use of the information, as the basis for judgments about the risks to public health presented by population exposures to ambient PM; (2) insights gained from a quantitative risk assessment conducted to provide a broader perspective for judgments about protecting public health from the risks associated with PM exposures; and (3) specific conclusions regarding the need for revisions to the current standards and the elements of PM standards (i.e., indicator, averaging time, form, and level) that, taken together, would be appropriate to protect public health with an adequate margin of safety. As with virtually any policy-relevant scientific research, there is uncertainty in the characterization of health effects attributable to exposure to ambient PM. As discussed below, however, there is now a greatly expanded body of health effects information as compared with that available during the last review of the PM standards. Moreover, the recent evidence on PM-related health effects has undergone an unusually high degree of scrutiny and reanalysis over the past several years, beginning with a series of workshops held early in the review process to discuss important new information. A number of opportunities were provided for public comment on successive drafts of the Criteria Document and Staff Paper, as well as for intensive peer review of these documents by CASAC at several public meetings attended by many knowledgeable individuals and representatives of interested organizations. In addition, there have been a number of important scientific conferences, symposia, and colloquia on PM issues, sponsored by the EPA and others, in the U.S. and abroad, during this period. While significant uncertainties exist, the review of the health effects information has been thorough and deliberate. In the judgment of the Administrator, this intensive evaluation of the scientific evidence has provided an adequate basis for regulatory decision making at this time, as well as for the comprehensive research plan recently developed by EPA, and reviewed by CASAC and others, for improving our future understanding of the relationships between ambient PM exposures and health effects. A. Health Effects Information This section outlines key information contained in the Criteria Document (Chapters 10-13) and the Staff Paper (Chapter V) on known and potential health effects associated with airborne PM, alone and in combination with other pollutants that are routinely present in the ambient air. The information highlighted here summarizes: (1) The nature of the effects that have been reported to be associated with ambient PM; (2) sensitive subpopulations that appear to be at greater risk to such effects; (3) an integrated evaluation of the health effects evidence; and (4) the PM fractions of greatest concern to health. Since the last review of the PM criteria and standards, the most significant new evidence on the health effects of PM is the greatly expanded body of community epidemiological studies. The Criteria Document stated that these recent studies provide ``evidence that serious health effects (mortality, exacerbation of chronic disease, increased hospital admissions, etc.) are associated with exposures to ambient levels of PM found in contemporary U.S. urban airsheds even at concentrations below current U.S. PM standards'' (U.S. EPA, 1996a, p. 13-1). Although a variety of responses to constituents of ambient PM have been hypothesized to contribute to the reported health effects, the relevant toxicological and controlled human studies published to date have not identified an accepted mechanism(s) that would explain how such relatively low concentrations of ambient PM might cause the health effects reported in the epidemiological literature. The discussion below notes the key issues raised in assessing community epidemiological studies, including alternative interpretations of the evidence, both for individual studies and for the evidence as a whole. 1. Nature of the Effects As discussed in the Criteria Document and Staff Paper, the key health effects categories associated with PM include: (1) Premature mortality; (2) aggravation of respiratory and cardiovascular disease (as indicated by increased hospital admissions and emergency room visits, school absences, work loss days, and restricted activity days); (3) changes in lung function and increased respiratory symptoms; (4) changes to lung tissues and structure; and (5) altered respiratory defense mechanisms. Most of these effects have been consistently associated with ambient PM concentrations, which have been used as a measure of population exposure, in a number of community epidemiological studies. Additional information and insights on these effects are provided by studies of animal toxicology and controlled human exposures to various constituents of PM conducted at higher-than- ambient concentrations. Although, as noted above, mechanisms by which particles cause effects have not been elucidated, there is general agreement that the cardio-respiratory system is the major target of PM effects. a. Mortality i. Short-Term Exposure Studies As discussed in the Staff Paper, the most notable evidence on the health effects of community air pollution containing high concentrations of PM has come from the dramatic pollution episodes of Belgium's industrial Meuse Valley, Donora, Pennsylvania, and London, England. Based on analyses of a series of episodes in London, there was general acceptance in the last Criteria Document (U.S. EPA, 1982a) and in critical reviews of PM-associated health effects that London air pollution at high concentrations (at or above 500- [[Page 65642]] 1000 g/m 3 of PM 7 and sulfur dioxide (SO 2)) was causally related to increased mortality. Further analyses of daily mortality over 14 London winters suggested that particles were more likely to be responsible for the associations of health effects with air pollution than SO 2, and that the association continued to the lower concentrations of PM measured in London (150 g/m3, measured as BS). --------------------------------------------------------------------------- \7\ Measured as British Smoke (BS), which gauges the darkness of PM collected on a filter and is most sensitive to combustion generated carbon particles. When calibrated to a mass measurement, as in the historical London studies, BS is an indicator of fine mode particles. --------------------------------------------------------------------------- From 1987 to present, numerous epidemiological studies using improved statistical techniques and expanded particle monitoring data have reported statistically significant 8 positive associations between increased daily or several-day average concentrations of PM [as measured by a variety of indices, including TSP, PM 10, PM 2.5, sulfate, and BS] and premature mortality in communities across the U.S. as well as in Europe and South America. Of 38 analyses and reanalyses of these studies (referred to as daily mortality studies) published between 1988 and 1996, most found statistically significant associations between increases in short-term ambient PM concentrations and total non-accidental mortality (U.S. EPA, 1996a, Table 12-2). --------------------------------------------------------------------------- \8\ Statistically significant results are reported at a 95% confidence level. --------------------------------------------------------------------------- More specifically, the effects estimates for PM 10 reported in these studies fall within a range of approximately 2 to 8 percent increase in the relative risk 9 of mortality for a 50 g/ m3 increase in 24-hour average PM 10 concentrations. The consistency in these results is notable, particularly since these studies examined PM-mortality relationships in 18 different locations varying significantly in climate, human activity patterns, aerosol composition, and amounts of co-occurring gaseous pollutants [e.g., SO 2 and ozone(O3)], using a variety of statistical techniques. A rough estimate of the incremental relative risk attributed to PM concentrations seen in the worst London episode also falls within this range (U.S. EPA, 1996b, p. V-13). It is also important to note that the magnitude of the relative risks, while significant from a public health perspective because the potentially exposed population is large, are small compared to those usually found in epidemiological studies of occupational and other risk factors. --------------------------------------------------------------------------- \9\ Many of the recent epidemiological studies report effects estimates in terms of a percentage increase in the risk of mortality in the study population (as compared to the baseline rate in the population as a whole) associated with a specific increase in ambient PM concentrations measured by one or more outdoor monitors. These effects estimates generally are based on a statistical model of the entire study period, which typically spanned multiple years or seasons. --------------------------------------------------------------------------- Some of these daily mortality studies examined PM-mortality associations for both total non-accidental mortality and cause-specific mortality. In general, such studies have reported higher relative risks for respiratory and cardiovascular causes of death than for total mortality, as well as higher risks for mortality in the elderly (>65 years of age) than for mortality in the general population. ii. Long-Term Exposure Studies By the time of the previous review of the PM criteria in 1987, numerous epidemiological studies of a cross-sectional design had reported statistically significant associations linking higher long- term (single or multi-year) concentrations of various indices of PM with higher mortality rates across numerous U.S. communities. However, the usefulness of such studies for quantitative purposes was at that time limited by the lack of supporting evidence available from daily mortality studies or the toxicological literature, and by unaddressed confounders and methodological problems inherent in these cross- sectional studies. More recently, epidemiological studies of a prospective-cohort design have been conducted, including in particular the Six City study (Dockery et al., 1993) and the American Cancer Society (ACS) study (Pope et al., 1995), that lend support to the earlier cross-sectional studies of mortality. These two recent studies reflect significant methodological advances over the earlier studies, including the use of subject-specific information, and provide evidence for an association between long-term PM concentrations and mortality. At least some fraction of mortality was reported to reflect cumulative PM impacts in addition to those associated with short-term concentrations (U.S. EPA, 1996a, p. 13-34). The Six City study, which followed more than 8,000 adults for 14 years, found that long-term PM concentrations (PM 15/10, PM 2.5, and sulfate) in six U.S. cities were statistically significantly associated with increased rates of total mortality and cardiopulmonary mortality, even after adjustment for smoking, education level, and occupation. Specifically, this study reported increases in relative risk of 26% and 37% for total and cardiopulmonary-related mortality, respectively, between the cities with the highest and lowest PM concentrations. The ACS study was designed to follow up on the findings from the Six City study, using a much larger number of individuals (more than half a million adults followed for seven years) and cities. The ACS investigators reported that, after adjustment for other risk factors, multi-year concentrations of PM 2.5 (for 47 U.S. cities) and sulfate (for 151 cities) were found to be statistically significantly associated with both total and cardiopulmonary mortality. The ACS study reported increases in relative risk of 17% and 31% for total and cardiopulmonary mortality, respectively. Some reviewers have raised concerns regarding the adequacy of the adjustment for confounders in these prospective-cohort studies, maintaining that other uncontrolled factors may be responsible for the observed mortality rates (Lipfert and Wyzga, 1995; Moolgavkar and Luebeck, 1996; Moolgavkar, 1994). The Criteria Document indicates, however, that it is unlikely that these studies overlooked plausible confounders, although the addition of factors not taken into account might well alter the magnitude of the association (U.S. EPA, 1996a, p. 12-180). In particular, the Criteria Document cautions that the magnitude of relative risks associated with PM concentrations reported in these studies may be overestimated because some of the effects may be due to historical PM concentrations that were significantly higher than the ones used to estimate population exposures in these studies. The Criteria Document concludes that the Six City and ACS studies, taken together with the earlier cross-sectional studies, suggest that: 1) there may be increases in mortality in disease categories that are consistent with long-term exposure to PM, and 2) at least some fraction of these deaths reflects cumulative PM impacts greater than those reported in the daily mortality studies (U.S. EPA, 1996a, p. 13-34). iii. Degree of Lifespan Shortening The degree of lifespan shortening associated with PM exposure in these studies is viewed by many as an important consideration in evaluating mortality effects in a public health context. The epidemiological findings of associations between short- and long-term ambient PM concentrations and premature mortality provide some insight into this issue. The mortality effects estimates associated with long- term PM concentrations in the prospective-cohort studies are [[Page 65643]] considerably larger (Six City study) to somewhat larger (ACS study) than those from the daily mortality studies, suggesting that a substantial portion of the deaths associated with long-term PM exposure may be independent of the deaths associated with short-term exposure (U.S. EPA, 1996a, p. 13-44). The Criteria Document suggests that the extent of lifespan shortening implied by the long-term exposure studies could be on the order of years (U.S. EPA, 1996a, p. 13-45). As discussed in the Staff Paper, attempts to quantitatively evaluate the extent of lifespan shortening in the daily mortality studies to date provide no more than suggestive results, with the investigators recognizing that more research is needed in this area (U.S. EPA, 1996b, p. V-19-20). The limited analyses available suggest that at least some portion of the daily mortality associated with PM may occur in individuals who would have died within days in the absence of PM exposure (U.S. EPA, 1996b, p. V-19-20). Researchers in this area also note that it is possible that the reported deaths might be substantially premature if a person becomes seriously ill but would have otherwise recovered without the extra stress of PM exposure (U.S. EPA, 1996b, p. V-19-20). Quantification of the degree of lifespan shortening inherent in the long- and short-term exposure mortality studies is difficult and requires assumptions about life expectancies given other risk factors besides PM exposure, including the ages at which PM-attributable deaths occur and the general levels of medical care available to sensitive subpopulations in an area. Because of these uncertainties, it is not possible to develop with confidence quantitative estimates of the extent of life-shortening accompanying the increased mortality rates that have been associated with exposures to PM (U.S. EPA, 1996a, p. 13- 45). b. Aggravation of Respiratory and Cardiovascular Disease Given the statistically significant positive associations between ambient PM concentrations and mortality outlined above, it is reasonable to expect that community epidemiological studies should also find increased PM-morbidity associations. As noted in the Criteria Document, this is indeed the case. Twelve of the 13 epidemiological studies of hospital admissions in North America (U.S. EPA, 1996a, Table 13-3) report statistically significant positive associations between short-term concentrations of PM and hospital admissions for respiratory-related and cardiac diseases. More specifically, these studies report increases from 6 to 25 percent in the relative risk of hospital admissions for respiratory disease, pneumonia, and chronic obstructive pulmonary disease (COPD), for a 50 g/m3 increase in 24-hour average PM 10 concentrations. A smaller, but statistically significant, increase in relative risk of 2 percent was reported in one study of hospital admissions for ischemic heart disease.10 --------------------------------------------------------------------------- \10\ Ischemic heart disease is a general term for heart diseases in which there is an insufficient blood supply to the heart muscle. --------------------------------------------------------------------------- Indirect measures of morbidity, including school absences, restricted activity days, and work loss days have also been used as indicators of acute respiratory conditions in community studies of PM. For example, the statistically significant association reported between short-term PM concentrations and school absences is consistent with an effect from PM exposure, because respiratory conditions are the most frequent cause of school absences (U.S. EPA, 1996a, Chapter 12). Recent studies have also reported statistically significant associations between short-term PM concentrations and both (1) respiratory-related restricted activity days and (2) work loss days (U.S. EPA, 1996b, p. V- 22). c. Altered Lung Function and Increased Respiratory Symptoms Community epidemiological studies of ambient PM concentrations and laboratory studies of human and animal exposures to high concentrations of PM components show that PM exposure can be associated with altered lung function and increased respiratory symptoms. A number of epidemiological studies in the U.S. (U.S. EPA, 1996a, Tables 13-3 and 13-4) show associations between short-term PM concentrations and increased upper and lower respiratory symptoms and cough, as well as decreases in pulmonary function [e.g., forced expiratory capacity for one second (FEV 1) and peak expiratory flow rate (PEFR)]. Taken together, these studies suggest that sensitive individuals, such as children (especially those with asthma or pre-existing respiratory symptoms), may have increased or aggravated symptoms associated with PM exposure, with or without reduced lung function. Results from respiratory symptom studies of long-term PM concentrations (U.S. EPA, 1996a, Table 13-5) are consistent with and supportive of the associations reported for short-term PM concentrations. Studies conducted in multiple U.S. communities in recent years have reported that increased symptoms of respiratory ailments in children, including bronchitis, are associated with increasing annual PM concentrations across the communities (U.S. EPA, 1996a, p. 12-372). Recent evidence for an association between long-term exposure to PM and decreased lung function in children and adults is suggestive, but more limited (U.S. EPA, 1996a, p. 12-202). The increased risk for respiratory symptoms and related respiratory morbidity reported in the epidemiological studies is important not only because of the immediate and near-term symptoms produced, but also because of the longer-term potential for increases in the development of chronic lung disease. Specifically, recurrent childhood respiratory illness has been suggested to be a risk factor for later susceptibility to lung damage (U.S. EPA, 1996b, p. V-27). d. Alteration of Lung Tissue and Structure Community epidemiological studies have generally not been used to evaluate the extent to which exposure to PM directly alters lung tissues and cellular components, although some autopsy studies have found limited qualitative evidence of such effects from community air pollution (U.S. EPA, 1996b, p. V-27). Evidence of morphological (i.e., structural) damage from PM exposure has come primarily from animal and occupational studies of high concentrations of acid aerosols and other PM components, including coarse particle dusts. While morphological alterations have been extensively studied for exposures to acid aerosols, such studies have been conducted at concentrations well above current ambient levels. Long-term exposure of animals to somewhat lower concentrations of acid mixtures have been shown to induce morphological changes, which may be relevant to clinical small airway disease. Recent work in animals using lower concentrations, approaching ambient levels, of ammonium sulfate and nitrate suggest morphometric changes that could lead to a decrease in compliance or a ``stiffening'' of the lung (U.S. EPA, 1996b, p. V-27-29). Occupational exposure to crystalline silica, which is a component of coarse dust, has been associated with a specific form of pulmonary inflammation and fibrosis (silicosis) (U.S. EPA, 1996a, p. 11-127). Based on analyses of the silica content of resuspended crustal material collected from several U.S. cities as part of the last review, staff concluded that [[Page 65644]] the risk of silicosis at levels permitted by the current annual PM 10 NAAQS was low. The 1982 Staff Paper (U.S. EPA, 1982b) summarized qualitative evidence for morphometric changes associated with long-term exposure to crustal dusts, as suggested by autopsy studies of humans and animals exposed to various crustal dusts near or slightly above current ambient levels in the Southwest; however, no inferences regarding quantitative exposures of concern can be drawn from these studies. e. Changes in Respiratory Defense Mechanisms Responses to air pollutants often depend upon their interaction with respiratory tract defense mechanisms that can detoxify or physically remove inhaled material (e.g., antigenic stimulation of the immune system and mucocilliary clearance). Either depression or over- activation of such defense systems may be involved in the development of lung diseases (U.S. EPA, 1996a, p. 11-55). Acid aerosols (H 2SO 4) have been shown to alter mucocilliary clearance in healthy human subjects at levels as low as 100 g/m3; such effects are also reported in animals (U.S. EPA, 1996a, pp. 11-60-61). Persistent impairment of clearance may lead to the inception or progression of acute or chronic respiratory disease, and may be a plausible link between acid aerosol exposure and respiratory disease. Alveolar macrophages play a role in resistance to bacterial infection, the induction and expression of immune reactions, and the production of a number of biologically active chemicals that are involved in respiratory defense mechanisms (U.S. EPA, 1996a, pp. 11-56- 66). Various exposures to PM constituents (e.g., acid aerosols, sulfates, and road dust) at concentrations that range from near to well above ambient levels have been shown to affect such macrophage functions in experimental animals (U.S. EPA, 1996b, pp. V-29-31). 2. Sensitive Subpopulations The recent epidemiological information summarized in the Criteria Document provides evidence that several subpopulations are apparently more sensitive (i.e., more susceptible than the general population) to the effects of community air pollution containing PM. As discussed above, the observed effects in these subpopulations range from the decreases in pulmonary function reported in children to increased mortality reported in the elderly and in individuals with cardiopulmonary disease. Such subpopulations may experience effects at lower levels of PM than the general population, and the severity of effects may be greater. Based on a qualitative assessment of the epidemiological evidence of effects associated with PM for subpopulations that appear to be at greatest risk with respect to particular health endpoints (U.S. EPA, 1996a, Tables 13-6, 13-7), the Staff Paper draws the following conclusions with respect to sensitive subpopulations (U.S. EPA, 1996b, pp. V-31-36): (1) Individuals with respiratory disease (e.g., COPD, acute bronchitis) and cardiovascular disease (e.g., ischemic heart disease) are at greater risk of premature mortality and hospitalization due to exposure to ambient PM. (2) Individuals with infectious respiratory disease (e.g., pneumonia) are at greater risk of premature mortality and morbidity (e.g., hospitalization, aggravation of respiratory symptoms) due to exposure to ambient PM. Also, exposure to PM may increase individuals susceptibility to respiratory infections. (3) Elderly individuals are also at greater risk of premature mortality and hospitalization for cardiopulmonary causes due to exposure to ambient PM. (4) Children are at greater risk of increased respiratory symptoms and decreased lung function due to exposure to ambient PM. (5) Asthmatic children and adults are at risk of exacerbation of symptoms associated with asthma, and increased need for medical attention, due to exposure to PM. 3. Evaluation of Health Effects Evidence As discussed above, a range of serious health effects in sensitive subpopulations has been associated with ambient PM concentrations in a large number of community epidemiological studies. Questions as to whether the reported associations represent causal relationships can be addressed by consideration of the adequacy and strength of the individual studies; the consistency of the associations, as evidenced by repeated observations by different investigators, in different places, circumstances, and time; the coherence of the associations (i.e., the logical or systematic interrelationships between different types of health effects); and the biological plausibility of the reported associations. Because of limitations in the available evidence from controlled laboratory studies of PM components, it is generally recognized that an understanding of biological mechanisms that could explain the reported associations has not yet emerged. Thus, the following discussion focuses on the epidemiological evidence as a basis for assessing the weight of evidence for inferences about the causality of the relationships between health effects and exposures to ambient PM concentrations. In particular, issues associated with interpreting individual study results are presented, followed by a discussion of the consistency and coherence of the health effects evidence as a whole. a. Interpretation of Individual Study Results While it is widely accepted that serious effects are causally related to the high concentrations of air pollution observed in the historical episodes, there is less consensus as to the most appropriate interpretation of the more recent studies finding associations of such effects with ambient PM concentrations below the levels of the current NAAQS (e.g., Schwartz, 1994b; Dockery et al., 1995; Moolgolvkar et al., 1995b; Moolgolvkar and Luebeck, 1996; Li and Roth, 1995; Samet et al., 1996; Wyzga and Lipfert, 1995b): In this regard, several viewpoints currently exist on how best to interpret the epidemiology data: one sees PM exposure indicators as surrogate measures of complex ambient air pollution mixtures and reported PM-related effects represent those of the overall mixture; another holds that reported PM-related effects are attributable to PM components (per se) of the air pollution mixture and reflect independent PM effects; or PM can be viewed both as a surrogate indicator as well as a specific cause of health effects. In any case, reduction of PM exposure would lead to reductions in the frequency and severity of the PM-associated health effects. (U.S. EPA, 1996a, p. 13-31) Such alternative interpretations as to the causality underlying the reported PM-effects associations result from a number of specific issues that have been raised regarding the adequacy and strength of individual studies. Of particular concern is the possibility that independent risk factors, related to both ambient PM concentrations and the reported effects, could potentially confound or modify the apparent PM-effects associations. Possible independent risk factors include weather-related variables and other pollutants present in the ambient air (e.g., SO 2, CO, O 3, NO 2), which have been addressed to varying degrees in most of the epidemiological studies. Other concerns are related to the influence of the choice of statistical models used by investigators and to the uncertainties introduced by the imprecision in measurements of ambient air pollutants, as well as the use of such measurements as surrogates for population exposures.11 The Criteria [[Page 65645]] Document and Staff Paper evaluated the studies with respect to each of these issues, as summarized below: --------------------------------------------------------------------------- \11\ In subsequent discussions, the term ``exposure misclassification'' is used to refer to combined uncertainties introduced by the related issues of errors in measurement of pollution and in the use of outdoor measurements to index population exposures. --------------------------------------------------------------------------- (1) Many recent studies, including a reanalysis by the Health Effects Institute (HEI) (Samet et al., 1996), have considered the influence of weather on the results reported in studies of short-term exposures, because fluctuations in weather are associated with both changes in PM and other pollutant levels and the reported health effects. The Criteria Document concludes that the PM effects estimates are relatively insensitive to the different methods of weather adjustment used in these studies, that the role of weather-related variables has been addressed adequately, and that it is highly unlikely that weather can explain a substantially greater portion of the health effects attributed to PM than has already been accounted for in the models (U.S. EPA, 1996a, p. 13-54). (2) A number of recent reanalyses of daily mortality studies have examined the influence of other pollutants that commonly occur in the ambient air together with PM. Most attention has been focused on Philadelphia, where extensive data are available on TSP, NO 2, O 3, CO, and SO 2. In fact, reanalyses of the Philadelphia data have led HEI investigators to conclude that a single pollutant cannot be readily identified as the best predictor of air pollution-related mortality in Philadelphia based on analyses of Philadelphia data alone (Samet et al., 1996). Based on such single-city analyses, some have argued that estimated PM effects may be overstated or potentially non- existent due to confounding by other pollutants that might actually be responsible for the effects. While it is reasonable to expect that other pollutants may play a role in modifying the magnitude of the estimated effects of PM on mortality, either through pollutant interactions or independent effects, the extent of any such co- pollutant modification is less clear. The Criteria Document notes that some mortality and morbidity studies have found little change in the PM relative risk estimates after inclusion of other co-pollutants in the model, and, in analyses where the PM relative risk estimates were reduced, the PM effects estimates typically remained statistically significant. Accordingly, the Criteria Document concludes that the PM- effects associations are valid and, in a number of studies, not seriously confounded by co-pollutants (U.S. EPA, 1996a, p. 13-57). (3) Many investigators have examined how the choice of statistical models or the ways in which they were specified may have influenced reported PM-effects associations. In reviewing this issue, the Criteria Document finds that, while model specification is important and can influence PM-effects estimates, appropriate modeling strategies have been adopted by most investigators (U.S. EPA, 1996a, section 13.4.2.2). The Criteria Document concludes that, ``the largely consistent specific results, indicative of significant positive associations of ambient PM exposures and human mortality/morbidity effects, are not model specific, nor are they artifactually derived due to misspecification of any specific model. The robustness of the results of different modeling strategies and approaches increases our confidence in their validity'' (U.S. EPA, 1996a, p. 13-54). (4) A difficulty noted by many reviewers in interpreting the epidemiological studies, particularly for quantitative purposes, is the uncertainty and possible bias introduced by the use of outdoor monitors to estimate a population-level index of exposure. Even in studies where outdoor PM levels near population centers are well represented by monitors, the extent to which fluctuations in outdoor concentrations are found to affect indoor concentrations and personal exposure to PM of outdoor origin remains an issue of importance. This issue is particularly salient since some of the sensitive subpopulations in the daily mortality and hospital admissions studies can be expected to spend more time indoors than the general population. Some commentors have expressed concerns regarding the lack of correlation shown in some studies that made cross-sectional comparisons of outdoor PM with indoor or personal exposures to PM (which includes PM from the indoor and personal environment). The Criteria Document found, however, that on a longitudinal basis (e.g., day-to-day), personal exposure to PM 10 can be well correlated with outdoor measurements, and that the effects reported in the short-term epidemiological studies are not due to indoor-generated particles (U.S. EPA, 1996a, p. 1-10). Specifically, the Criteria Document concluded that ``the measurements of daily variations of ambient PM concentrations, as used in the time-series epidemiological studies of Chapter 12, have a plausible linkage to the daily variations of human exposures to PM from ambient sources, for the populations represented by the ambient monitoring stations'' (U.S. EPA, 1996a, p. 1-10). The strength of the correspondence between outdoor concentrations and personal exposure levels on a day-to-day basis serves to reduce, but not eliminate, the potential error introduced by using outside monitors as a surrogate for personal exposure. Some commentors have suggested the net effect of misclassifying total exposure to PM might bias reported relationships between outdoor PM and mortality (or morbidity) effects towards a linear, non-threshold relationship, when in fact a threshold model of response may be more appropriate. While such a threshold has not been demonstrated in studies to date, the potential influence of exposure misclassification serves to increase the uncertainty in the reported concentration-response relationships, particularly for the lower range of concentrations. (5) A closely related issue, namely errors in the measurement of the concentrations of air pollutants, can also introduce uncertainty and bias in effects estimates reported in epidemiological studies of PM and co-pollutants. While questions about the magnitude of measurement error and its effect on the PM-health effects associations have not been resolved, some aspects of this issue have been examined in two recent studies (Schwartz and Morris, 1995; Schwartz et al., 1996). These results suggest that the influence of measurement error for individual variables is to bias the PM-effects estimates downward (i.e., to underestimate effects). These analyses, however, do not assess the potential effect of exposure misclassification on effects estimates for different components of PM, or for other co-pollutants. In such multiple pollutant analyses, measurement error or, more generally, exposure misclassification can theoretically bias effects estimates of PM or co-pollutants in either direction, introducing further uncertainties in the estimated concentration-response relationships for all pollutants (U.S. EPA, 1996b, pp. V-39-43). A comprehensive, formal treatment of the potential influences of exposure misclassification is, therefore, an important research need. As noted below, however, the available evidence on the consistency of the PM effects relationships in multiple urban locations with widely varying indoor/outdoor conditions and a variety of monitoring approaches makes it less likely that the observed findings are an artifact of errors in measurement of pollution or of exposure. [[Page 65646]] b. Consistency and Coherence of the Health Effects Evidence As discussed above, the individual epidemiological studies indicate that health effects are likely associated with PM, even after taking into account issues regarding the adequacy and strength of these studies. However, because individual studies are inherently limited as a basis for addressing questions of causality, the consistency and coherence of the evidence across the studies have also been considered in the Criteria Document (U.S. EPA, 1996a, section 13.4.2.5) and Staff Paper (U.S. EPA, 1996b, pp. V-54-58), as summarized below. Of the more than 80 community epidemiological studies that evaluated associations between short-term concentrations of various PM indicators and mortality and morbidity endpoints (U.S. EPA, 1996a, Tables 12-2, 12-8 to 13), more than 60 such studies reported positive, statistically significant associations. These studies have been conducted by a number of different investigators, in a number of geographic locations throughout the world (with different climates and co-pollutants), using a variety of statistical techniques, and with varying temporal relationships. Despite these differences, the finding of statistically significant associations is relatively consistent across the studies (U.S. EPA, 1996a, Table 12-2). More specifically, in looking across those studies that evaluated associations between short-term PM 10 concentrations and mortality and morbidity endpoints, various aspects of consistency and coherence can be observed. These observations are discussed below in reference to Figure 1 (adapted from Figure V-2 in the Staff Paper). Figure 1 displays the estimated relative risk for a 50 g/m\3\ increase in measured 24-hour PM 10 levels, derived from studies that the Criteria Document concluded permit quantitative comparisons across various cause-specific mortality and morbidity endpoints (i.e., respiratory hospital admissions, COPD or ischemic heart disease hospital admissions, and cough and lower and upper respiratory symptoms) (U.S. EPA, 1996b, Tables V-4, V-6; U.S. EPA, 1996a, Section 12.3.2.2). Figure 1 illustrates that the effects estimates for each health endpoint are relatively consistent across the studies. Some variation would be expected, however, due to the differences among the study areas in the concentrations and relative composition of PM and other air pollutants, and in the demographic and socioeconomic characteristics of the study populations, including the distributions of sensitive subpopulations, as well as a result of random error. Thus, the Criteria Document concludes that the relatively small ranges of variability in the effects estimates observed in these studies are consistent with expectations based on assuming causal relationships between mortality and morbidity effects and PM exposure (U.S. EPA, 1996a, Section 13.4.1.1). BILLING CODE 6560-50-P [[Page 65647]] [GRAPHIC] [TIFF OMITTED] TP13DE96.001 BILLING CODE 6560-50-C [[Page 65648]] As noted above, it is reasonable to expect that co-pollutants present in the study areas might modify the apparent effects of PM by atmospheric interactions (e.g., through dissolution/adsorption or aerosol formation reactions) or by independent and/or interactive effects on sensitive subpopulations (e.g., respiratory function changes from exposures to O 3 or SO 2). Moreover, the possibility of exposure misclassification for primary gaseous pollutants (e.g., CO, SO 2) could diminish their apparent significance relative to PM. If such PM effects modification was occurring to an appreciable degree, the associations with PM would be expected to be consistently high in areas with high co-pollutant concentrations, and consistently low in areas with low co-pollutant concentrations. On the contrary, in an examination of reported PM 10-mortality associations as a function of the varying levels of co-pollutants in study areas, consistent effects estimates were observed across wide ranges of co-pollutant concentrations (U.S. EPA, 1996b, Figures V-3a, V-3b). While it is possible that different pollutants may serve to confound or otherwise influence particles in different areas, it seems unlikely that this would lead to such similar associations and consistent relative risk estimates as have been reported for PM in a large number of studies. In addition to the consistency observed in the PM associations for each health endpoint, these studies also exhibit coherence in the kinds of health effects that have been associated with PM exposure. For example, the association of PM with mortality is mainly linked to respiratory and cardiovascular causes, which is coherent with the observed PM associations with respiratory- and cardiovascular-related hospital admissions. Coherence is also observed across studies of both short- and long- term exposures to PM. For example, the existence of statistically significant PM-mortality associations from long-term as well as short- term exposures reinforces the likelihood that PM is a causal factor for premature mortality relative to that which might be reasonably inferred from either type of study alone. Furthermore, the fact that mortality has been associated with both short- and long-term exposures is important with respect to the credibility of ambient PM as a cause of mortality involving significant life-years lost. If there was no evidence of excess mortality from studies of long-term exposures, it might be inferred based on the short-term studies that reported daily mortality was due solely to lifespan shortening of only days or weeks in individuals already near death. This qualitative coherence is further supported by the quantitative coherence across several health endpoints. For example, if the relationships were causal, PM-related hospitalization would be expected to occur substantially more frequently than PM-related mortality (even though many deaths attributed to air pollution probably do not occur in hospitals). The Criteria Document notes that is indeed the case (U.S. EPA, 1996a, p. 13-64 and Table 13-8). Based on the relative risk estimates from the short-term exposure studies, expected increases in respiratory- and cardiovascular-related hospital admission rates associated with PM are substantially larger than the expected increases in mortality rates for the same causes. The coherence in the epidemiological evidence is strengthened by those studies in which different health effects are associated with ambient PM concentrations in the same study population. Specifically, studies of Detroit, Birmingham, Philadelphia, and Utah Valley all find that ambient PM concentrations in each of these cities are associated with increases in a variety of respiratory- and cardiovascular-related health effects in the elderly and adult subpopulations in these cities (U.S. EPA, 1996a, p. 13-66). As summarized above, there is evidence that PM exposure is associated with increased risk for health effects ranging in severity from asymptomatic pulmonary function decrements, to respiratory and cardiopulmonary illness requiring hospitalization, to excess mortality from respiratory and cardiovascular causes (U.S. EPA, 1996a, p. 13-67). The consistency and coherence of the epidemiological evidence greatly adds to the strength and plausibility of the reported associations. The Criteria Document concludes that the overall coherence of the health effects evidence suggests (a likely causal role of ambient PM in contributing to the reported effects) (U.S. EPA, 1996a, p. 13-1). 4. Particulate Matter Fractions of Concern The previous criteria and standards review included an integrated examination of available literature on the potential mechanisms, consequences, and observed responses to particle deposition in the major regions of the respiratory tract (U.S. EPA, 1982b). The review concluded with general agreement that particles that deposit in the thoracic region (tracheobronchial and alveolar regions) (i.e., particles smaller than 10 m diameter), were of greatest concern for public health. Thus, the PM NAAQS were revised as a result of the last review from TSP to PM 10 standards. Particle dosimetry and mechanistic considerations developed in the current review continue to support the view that, for particles that typically occur in the ambient air, those that are capable of penetrating to the thoracic regions of the respiratory tract are of greatest concern to health (U.S. EPA, 1996b, Section V). Section V.F of the Staff Paper summarizes the evidence regarding the health effects associated with the fine (PM 2.5) and coarse (PM 10-2.5) fractions of PM 10. Both fine and coarse fraction particles can deposit in the thoracic regions of the respiratory tract. However, based on atmospheric chemistry, exposure, and mechanistic considerations, the Criteria Document concludes it would be most appropriate to ``consider fine and coarse mode particles as separate subclasses of pollutants'' (U.S. EPA, 1996a, p. 13-94), and to measure them separately as a basis for planning effective control strategies. Given the significant physical and chemical differences between the two subclasses of PM 10 (U.S. EPA, 1996b, pp. V-69-78), it is reasonable to expect that differences may exist between fine and coarse fraction particles in both the nature of potential effects and the relative concentrations required to produce such effects. The Criteria Document highlights a number of specific components of PM that could be of concern to health, including components typically within the fine fraction (e.g., acid aerosols including sulfates, certain transition metals, diesel particles, and ultrafine particles), and other components typically within the coarse fraction (e.g., silica, resuspended dust, and bioaerosols). While components of both fractions can produce health effects, in general the fine fraction appears to contain more of the reactive substances potentially linked to the kinds of effects observed in the epidemiological studies. The fine fraction also contains by far the largest number of particles and a much larger aggregate surface area than the coarse fraction. The greater surface area of the fine fraction increases the potential for surface absorption of other potentially toxic components of PM (e.g., metals, acids, organic materials), and dissolution or absorption of pollutant [[Page 65649]] gases and their subsequent deposition in the thoracic region. The Staff Paper presents the available quantitative and qualitative information on the effects of fine particles and its constituents (U.S. EPA, 1996b, pp. V-60-63). Because of the number of pertinent studies published since the last review, far more quantitative epidemiological data exist today for relating fine particles to mortality, morbidity, and lung function changes in sensitive subpopulations, in terms of both short- and long-term ambient concentrations, than was the case for PM 10 at the conclusion of the last review.\12\ Like the more numerous PM 10 studies, the fine particle studies (e.g., studies using PM 2.5, sulfates) generally find statistically significant positive associations between fine particle concentrations and mortality and morbidity endpoints, with more than 20 studies conducted in a number of geographic locations throughout the world, including the U.S., Canada, and Europe. More specifically, daily mortality effects estimates reported for PM 2.5 fall within the range of approximately 3 to 6 percent increases in relative risk for a 25 g/m\3\ increase in 24-hour average PM 2.5 concentrations, for those cities with statistically significant positive associations (U.S. EPA, 1996b, Table V-12). This collection of studies shows qualitative coherence in the types of health effects associated with fine particle exposure including mortality, morbidity, symptoms, and changes in lung function (U.S. EPA, 1996b, Tables V-11 to V-13). --------------------------------------------------------------------------- \12\ The 1986 Staff Paper cited PM studies conducted in essentially 3 locations as a basis for the 24-hour standard, and 4 studies involving a total of 10 cities as a basis for the annual standard; none measured PM 10 directly (EPA, 1986b). --------------------------------------------------------------------------- By contrast, the current review finds much less direct epidemiological or toxicological evidence regarding the potential effects of coarse fraction particles at typical ambient concentrations. As discussed in the Staff Paper, community epidemiological studies directly comparing the effects of fine and coarse fraction particles provide evidence that reported PM associations with mortality and decreased lung function in children are more likely associated with fine fraction particles (U.S. EPA, 1996b, pp. V-63-67). On the other hand, both past and current reviews of occupational and toxicological literature have found ample qualitative reasons for concern about higher-than-ambient concentrations of coarse fraction particles. At such elevated levels, coarse fraction particles are linked to short- term effects such as aggravation of asthma and increased upper respiratory illness, which are consistent with enhanced deposition of coarse fraction particles in the tracheobronchial region (U.S. EPA, 1996a, p. 13-51). Children may be particularly sensitive to such an effect, since they typically spend more time in outdoor activities, such that they may encounter higher exposures and doses of coarse fraction particles than other potentially sensitive populations. In addition, long-term deposition of insoluble coarse fraction particles in the alveolar region may have the potential for enhanced toxicity, in part because clearance from this region of the lung is significantly slower than from the tracheobronchial region. Limited qualitative support for this concern is found in autopsy studies of animals and humans exposed to various ambient crustal dusts at or slightly above ambient levels typical in the Southwest. Unlike the case for fine particles, the clearest community epidemiological evidence regarding coarse fraction particles finds such effects only in areas with numerous marked exceedances of the current PM 10 standard (U.S. EPA, 1996a, p. 13-51). In this regard, it appears that the weight of the available evidence allowing direct comparisons between the two size fractions of PM 10 suggests that ambient coarse fraction particles are either less potent or a poorer surrogate for community effects of air pollution than are fine fraction particles. B. Quantitative Risk Assessment The Staff Paper presents the results of a quantitative assessment of health risks for two example cities, including risk estimates for several categories of health effects associated with: (1) existing PM air quality levels, (2) projected PM air quality levels that would occur upon attainment of the current PM 10 standards, and (3) projected PM air quality levels that would occur upon attainment of alternative PM 2.5 standards. As an integral part of this assessment, qualitative and, where possible, quantitative characterizations of the uncertainties in the resulting risk estimates have been developed, as well as information on baseline incidence rates for the health effects considered. The risk assessment is intended as an aid to the Administrator in judging which alternative PM NAAQS would reduce risks sufficiently to protect public health with an adequate margin of safety, recognizing that such standards will not be risk- free. As discussed in Section A above, the Criteria Document concludes that the overall consistency and coherence of the epidemiological evidence suggests a likely causal role of ambient PM in contributing to adverse health effects. An alternative interpretation is that PM may be serving as an index for the complex mixture of pollutants in urban air. The manner in which the PM epidemiological evidence is used in this risk assessment is consistent with either of these alternative interpretations of the evidence. Despite the consistency and coherence of the epidemiological evidence reporting health effects associated with PM, EPA cautions that quantitative risk estimates derived from these studies include significant uncertainty, and thus, should not be viewed as demonstrated health impacts. EPA believes, however, that they do represent reasonable estimates as to the possible extent of risk for these effects given the available information. 1. Overview The following discussion briefly summarizes the scope of the risk assessment and key components of the risk model. A more detailed discussion of the risk assessment methodology and results is presented in the Staff Paper and technical support documents (Abt Associates, 1996a, b). The risk assessment focused on selected health effects endpoints discussed above for which adequate quantitative information is available (U.S. EPA, 1996a, Table VI-2), including increased daily mortality, increased hospital admissions for respiratory and cardiopulmonary causes, and increased respiratory symptoms in children. All concentration-response relationships used in the assessment were based on findings from human epidemiological studies, and consequently rely on fixed-site, population-oriented, ambient monitors as a surrogate for actual PM exposures. Risk estimates were developed for the urban centers of two example cities, one eastern (Philadelphia County) and one western (Southeast Los Angeles County), for which sufficient PM 10 and PM 2.5 air quality data were available. Risk estimates were calculated only for ambient PM levels in excess of estimated annual average background levels. 13 This approach of estimating [[Page 65650]] risks in excess of background was judged to be more relevant to policy decisions regarding ambient air quality standards than risk estimates that include effects potentially attributable to uncontrollable background PM concentrations. For these analyses, an estimate of the annual average background level was used, rather than a maximum 24-hour value, since estimated risks were aggregated for each day throughout the year. Risks have been estimated for a recent year of PM air quality data in each of the two example cities. Risk estimates were calculated for Los Angeles County with PM levels adjusted downward to just attain the current PM 10 standards. Finally, risk estimates were also calculated for both example cities where PM levels were further adjusted to just attain various alternative PM 2.5 standards. --------------------------------------------------------------------------- \13\ As discussed in Chapter IV of the Staff Paper, annual average background levels of PM 2.5 are estimated to range from approximately 1-4 g/m\3\ in western areas and 2-5 g/m\3\ in eastern areas, with the maximum 24-hour levels estimated to reach as high as about 15-20 g/m\3\ over the course of a year. Background PM is defined in the Staff Paper as the distribution of PM concentrations that would be observed in the U.S. in the absence of anthropogenic emissions of PM and precursor emissions of VOC, NO x, and SO x in North America. --------------------------------------------------------------------------- As discussed in Chapter 13 of the Criteria Document, the interpretation of specific concentration-response relationships is the most problematic issue in conducting risk assessments for PM-associated health effects at this time, due to (1) the absence of clear evidence regarding mechanisms of action for the various health effects of interest; (2) uncertainties about the shape of the concentration- response relationships; and (3) concern about whether the use of ambient PM 2.5 and ambient PM 10 fixed-site monitoring data adequately reflects the relevant population exposures to PM that are responsible for the reported health effects. The reported study results used in this assessment are based on linear concentration-response models extending only down to the lowest PM concentrations observed within each study. \14\ Thus, concentration-response relationships were not extrapolated below the range of the PM concentration air quality data reported in any given study. Alternatively, the data do not rule out the possibility of an underlying non-linear, threshold concentration-response relationship. Although these alternative interpretations of study results could significantly affect estimated risks, only very limited information is available to aid in resolving this issue (U.S. EPA, 1996a, section 13.6.5). Thus, the approach taken in the PM risk assessment is to address alternative concentration- response models through sensitivity and integrated uncertainty analyses to develop ranges of estimated risks, rather than characterizing any particular set of risk estimates as representing the ``best'' estimates. --------------------------------------------------------------------------- \14\ See Table VI-2 in the Staff Paper (U.S. EPA, 1996b) for information about the reported PM mean and range of concentration levels observed in the various epidemiological studies used in the risk assessment. --------------------------------------------------------------------------- Risk estimates for PM-associated health effects in excess of background PM levels (i.e., excess risk) were initially developed based on a set of ``base case'' assumptions. These base case assumptions reflect the use of: (1) Mid-point estimates from the ranges of estimated annual average background concentrations for the eastern and western regions of the U.S. to represent typical background levels; (2) essentially linear concentration-response relationships down to the lowest PM level observed in each study; and (3) annual distributions of 24-hour PM 10 and PM 2.5 concentrations that were obtained by taking a recent year of PM air quality data in each example city and adjusting all PM concentrations exceeding the estimated background concentration level by the same percentage to simulate attainment of alternative standards (referred to as a ``proportional rollback'' approach). While there are many different methods of adjusting PM air quality distributions to reflect future attainment of alternative standards, analysis of historical data (Abt, 1996b) support the use of such a proportional method for adjusting air quality values. For comparison with alternative standards, it is desirable to estimate health risks associated with PM air quality that do not include the effect of concentrations in excess of those allowed by the current PM 10 standards. Since the air quality in one of the two cities examined, Los Angeles, exceeded the current PM 10 standards, both PM 10 and PM 2.5 concentrations were proportionally rolled back (preserving the PM 2.5/PM 10 ratio) to air quality concentrations that just attain the current PM 10 standards. While this necessarily introduces additional uncertainty into the risk estimates, it is required in order to compare risks associated with attaining the current PM 10 standards with risks associated with attainment of alternative PM 2.5 standards. Sensitivity analyses have been conducted to examine the impact on the risk estimates of these and other assumptions, by varying each assumption independently. For example, the impact of using alternative estimates for background concentrations was examined by replacing the mid-point estimate with the lower and the upper end of the range of estimated annual average background levels. In addition, integrated uncertainty analyses have been conducted specifically for the excess mortality associated with PM exposures to examine the range of risk estimates when several key assumptions and uncertainties are considered simultaneously, rather than one at a time. The key issues examined in the integrated uncertainty analyses include: (1) Variability in the underlying concentration-response relationship resulting from combining the results of PM 2.5 mortality studies in six cities to estimate the relative risks in the two example cities; (2) consideration of alternative potential threshold concentrations; (3) inclusion of the range of estimates for PM background levels; and (4) use of alternative PM air quality adjustment procedures to simulate attainment of alternative standards based on analysis of historical data. 2. Key Observations The discussion below highlights the key observations and insights from the risk assessment, together with important caveats and limitations. (1) Fairly wide ranges of estimates of the incidence of PM- related mortality and morbidity effects were calculated for the two locations analyzed when the effects of key uncertainties and alternative assumptions were considered. This point is illustrated below for mortality estimates using base case and alternative assumptions, as well as for morbidity estimates using base case assumptions alone.15 For example, the incidence of mortality associated with short-term PM 2.5 exposures upon attainment of the current PM 10 standards was estimated to range from approximately 400 to 1,000 deaths per year in Los Angeles County (with a population of 3.6 million) under base case assumptions, and from approximately 100 to 1,000 deaths using alternative assumptions considered in the integrated uncertainty analysis.16 For Philadelphia County (with a population of 1.6 million), a city with better air quality than Los Angeles and already well below the current PM 10 [[Page 65651]] standards, estimated mortality associated with short-term PM 2.5 exposures ranged from approximately 200 to 500 deaths per year under base case assumptions, and from approximately 20 to 500 deaths per year under alternative assumptions considered in the integrated uncertainty analyses.17 --------------------------------------------------------------------------- \15\ In the examples presented here the ranges of estimated incidences are based on the 90 percent credible intervals from the risk analyses. The 90 percent credible interval represents the range from the 5th percentile to the 95th percentile of the estimated risk distribution, and provides a reasonable characterization of the range of estimated values that results from the various uncertainties that could be incorporated quantitatively in the risk analyses. \16\ Incidence estimates of roughly 400 to 1,000 excess deaths per year represent roughly 2 to 4 percent of the total mortality incidence in Los Angeles County. \17\ Incidence estimates of 200 to 500 excess deaths per year associated with PM exposures represent roughly 1 to 2.5 percent of total mortality in Philadelphia County. --------------------------------------------------------------------------- Morbidity effects associated with exposures to PM 2.5 are estimated using base case assumptions to range from approximately 250 to 1,600 respiratory-related hospital admissions per year and from 23,000 to 58,000 cases of respiratory symptoms in children per year for Los Angeles.18 For Philadelphia County, morbidity effects associated with exposures to PM 2.5 are estimated using base case assumptions to range from about 70 to 450 respiratory-related hospital admissions and from 6,000 to 15,000 cases of respiratory symptoms per year.19 --------------------------------------------------------------------------- \18\ Incidence estimates of 250 to 1,600 respiratory-related hospital admissions associated with PM exposures represent roughly 1.5 to 10 percent of total respiratory-related hospital admissions in Los Angeles County. Incidence estimates of 23,000 to 58,000 cases of respiratory symptoms represent roughly 15 to 40 percent of total respiratory symptom cases in Los Angeles County. \19\ Incidence estimates of 70 to 450 cardiopulmonary-related hospital admissions associated with PM exposures represent roughly 0.5 to 3.5 percent of total respiratory-related hospital admissions in Philadelphia County. Incidence estimates of 6,000 to 15,000 cases of respiratory symptoms associated with PM exposures represent roughly 10 to 30 percent of total respiratory symptom cases in Philadelphia County. --------------------------------------------------------------------------- (2) Risk estimates associated with attainment of alternative PM 2.5 standards described in the Staff Paper show highly variable reductions in PM-associated risk which are a function of the particular city and the levels of the standards. Risk estimates for PM-associated mortality and morbidity health effects have been estimated for alternative annual PM 2.5 standards 20 of 15 and 20 g/m3, alone and in combination with alternative daily standards 21 ranging from 25 to 65 g/ m3. For two cases considering only annual PM 2.5 standards, the mean estimates (using base case assumptions) of excess mortality and morbidity associated with short-term PM 2.5 exposures in Los Angeles County were reduced by roughly 45-50% for attainment of an annual PM 2.5 standard level of 15 g/m3, and by roughly 20-25% for attainment of an annual standard level of 20 g/m3.22 These estimates of risk reduction are incremental to the risk reductions associated with attainment of the current PM 10 standards as explained above. Similarly, for an area already in attainment with the current PM 10 standards (Philadelphia County), mean estimates of excess morbidity and mortality associated with short-term exposures to PM 2.5 were not affected by an annual standard of 20 g/m3 but were reduced by about 15-20% upon attainment of an annual PM 2.5 standard of 15 g/m3.23 --------------------------------------------------------------------------- \20\ The annual standards analyzed were simulated by adjusting the annual average concentration at the population-oriented monitor in the study area with the highest measured values to the standard level under consideration. \21\ The alternative daily standards analyzed were the 1- expected-exceedance form of the standard. \22\ In Los Angeles County, a 45-50% reduction in excess mortality and morbidity associated with short-term PM 2.5 exposures represents decreases of roughly 320 excess deaths, 540 cardiopulmonary-related hospital admissions, and 22,000 cases of respiratory symptoms; a 20-25% reduction represents decreases of roughly 150 excess deaths, 250 cardiopulmonary-related hospital admissions, and 11,000 cases of respiratory symptoms. \23\ In Philadelphia County, a 15-20% reduction in excess mortality and morbidity associated with short-term PM 2.5 exposures represents decreases of roughly 60 excess deaths, 70 cardiopulmonary-related hospital admissions, and 2,000 cases of respiratory symptoms. --------------------------------------------------------------------------- As noted above, risk estimates for PM-associated mortality and morbidity health effects also have been estimated for alternative 24- hour PM 2.5 standards ranging from 25 to 65 g/m3 (in combination with an annual standard of 20 g/m3). These combinations of standards result in cases for which the 24-hour standard was generally controlling the degree of risk reduction. Mean estimates of excess mortality and morbidity associated with short-term PM 2.5 exposures in Los Angeles County were reduced by roughly 85% for a daily standard of 25 g/m3, and by roughly 40-50% for a daily standard of 65 g/m3, beyond the risks associated with attainment of the current PM 10 standards when base case assumptions were used.24 Similarly, for Philadelphia County, the mean estimates of excess mortality and morbidity were reduced by roughly 70-75% for a daily standard of 25 g/m3, and about 10% for a daily standard of 65 g/m3.25 --------------------------------------------------------------------------- \24\ In Los Angeles County, an 85% reduction in excess mortality and morbidity associated with short-term PM 2.5 exposures represents decreases of roughly 590 excess deaths, 1000 cardiopulmonary-related hospital admissions, and 37,000 cases of respiratory symptoms; a 40-50% reduction represents decreases of roughly 280 excess deaths, 480 cardiopulmonary-related hospital admissions, and 20,000 cases of respiratory symptoms. \25\ In Philadelphia County, a 70-75% reduction in excess mortality and morbidity associated with short-term PM 2.5 exposures represents decreases of roughly 260 excess deaths, 320 cardiopulmonary-related hospital admissions, and 8,000 cases of respiratory symptoms; a 10% reduction represents decreases of roughly 40 excess deaths, 50 cardiopulmonary-related hospital admissions, and 1,000 cases of respiratory symptoms. (3) Based on the results from the sensitivity analyses of key uncertainties and the integrated uncertainty analyses, the single most important factor influencing the uncertainty associated with the risk estimates is whether or not a threshold concentration exists below which PM-associated health risks are not likely to --------------------------------------------------------------------------- occur. Alternative assumed threshold concentrations considered in these analyses result in as much as a 3- to 4-fold difference in estimated risk associated with PM exposures in Los Angeles County (U.S. EPA, 1996b, Figure VI-8; Abt Associates, 1996b, Exhibits 7.19 and 7.20) depending on the likelihood imputed to various PM 2.5 threshold concentrations. In an area with PM concentrations well below the current PM standards (e.g., Philadelphia County), differences in risk associated with a recent year of PM air quality may be even greater for alternative threshold assumptions, since these locations would be expected to have a greater proportion of PM concentrations below assumed threshold concentrations. (4) Based on results from the sensitivity analyses of key uncertainties and/or the integrated uncertainty analyses, quantitative consideration of the following uncertainties is estimated to have a much more modest impact on the risk estimates: (a) Inclusion of individual co-pollutant species when estimating PM effect sizes (based on reported estimates of effects modification); (b) the choice of approach to adjusting the slope of the concentration-response relationship when analyzing alternative possible threshold concentrations; (c) the value chosen to represent average background PM concentrations; and (d) the choice of air quality adjustment approaches for simulating attainment of alternative PM standards. (5) Additional sources of uncertainty associated with risk analyses of alternative PM 2.5 standard scenarios which could not be addressed quantitatively include: (a) Uncertainty in the pattern of air quality concentration reductions that would be observed across the distribution of 24-hour PM 2.5 concentrations in areas attaining the standards, and (b) uncertainty concerning the degree to which PM concentration-response relationships may reflect contributions from other pollutants, or the particular contribution of certain constituents of PM 2.5, and whether such constituents would be reduced in similar proportion as the reduction in PM 2.5. To the extent concentrations of other combustion source co- pollutants are reduced more or less than PM 2.5 concentrations in attaining alternative PM 2.5 standards, estimates of health effects reduced by such standards would be expected to be related to the degree to which these co-pollutants in fact play a role in producing or modifying PM-associated effects. Similarly, if specific constituents of PM 2.5 mass have differing potencies in [[Page 65652]] producing effects relative to other PM 2.5 constituents, estimates of risk reduced would be expected to vary if these constituent concentrations are reduced to different degrees by control strategies designed to attain alternative PM 2.5 standards. (6) The peak 24-hour PM 2.5 concentrations appear to contribute a relatively small amount to the total health risk posed by the entire air quality distribution as compared to the risks associated with the low to mid-range concentrations. Standards with a 24-hour averaging time are traditionally based on the highest 24-hour values observed in a year, concentrations for which the risk on an individual day is highest. However, examining a typical distribution of ambient 24-hour PM 2.5 concentrations over the course of a year in conjunction with PM 2.5 concentration-response relationships, as illustrated in Figures 2a, 2b, and 2c, the peak PM 2.5 concentrations contribute much less to the total health risk over a year than the low- to mid-range PM 2.5 concentrations. More specifically, Figures 2a, 2b, and 2c illustrate some of the characteristics of the integration of air quality distributions and concentration-response relationships as used to predict total risk from ambient particle exposures across a year. These figures show the relative contribution of different portions of a typical urban ambient PM 2.5 concentration distribution to mortality risk from short-term exposures. As shown in Figures 2b and 2c, low- to mid-range concentrations (e.g., 10-50 g/m3) account for the largest amount of estimated mortality risk on an annualized basis. The portion of the air quality distribution that contributes significantly to total health risk over the course of a year is, of course, smaller if effects thresholds are assumed or if much higher levels of estimated background PM 2.5 concentrations are used (Figure 2c). However, even with this assumption, most of the aggregate risk associated with short-term exposures likely results from the large number of days during which the 24-hour average concentrations are in the low- to mid-range, below peak 24-hour concentrations. Even though higher 24-hour concentrations, including peaks above 70 g/ m3, clearly contribute more mortality per day than low- to mid- range concentrations, the much larger number of days within the low- to mid-ranges results in this interval being associated with the largest proportion of the total risk. BILLING CODE 6560-50-P [GRAPHIC] [TIFF OMITTED] TP13DE96.048 Figure 2a. Illustrative Air Quality Distribution of 24-Hour PM 2.5 Concentrations--This figure shows an example of a frequency distribution of the number of days exceeding various 24- hour average PM 2.5 concentrations over a year. [GRAPHIC] [TIFF OMITTED] TP13DE96.049 Figure 2b. Estimated Mortality Risks Using A Non-Threshold Concentration-Response Relationship--This figure illustrates the proportion of estimated mortality incidence, using a non-threshold concentration-response relationship, associated with each concentration range shown above in Figure 2a. [[Page 65653]] [GRAPHIC] [TIFF OMITTED] TP13DE96.050 BILLING CODE 6560-50-C Figure 2c. Estimated Mortality Risks Using An Illustrative Threshold Concentration-Response Relationship--This figure illustrates the proportion of estimated mortality incidence, using an example threshold concentration of 18 g/m3 PM 2.5, associated with each concentration range shown above in Figure 2a. An annual PM 2.5 standard would almost certainly require areas whose air quality concentrations are above those necessary for attainment to reduce PM