# Policy Assessment for the Review of the Particulate Matter National Ambient Air Quality Standards

First External Review Draft

March 2010DISCLAIMER
This draft document has been prepared by staff from the Ambient Standards Group, Office of Air Quality Planning and Standards, U.S. Environmental Protection Agency. Any opinions, findings, conclusions , or recommendations are thos e of the authors and do not necessarily reflect the views of the EPA. This document is being circulated to obtain review and
comment from the Clean Air Scientific Advi sory Committee (CASAC) and the general public.
Comments on this draft document should be addressed to Beth Hassett-Sipple, U.S. Environmental Protection Agency, Office of Air Quality Planning and Standards, C504-06, Research Triangle Park, North Carolina 27711 (email: hassett-sipple.beth@epa.gov ).EPA 452/P-10-003
March 2010



# Policy Assessment for the Review of the Particulate Matter National Ambient Air Quality Standards First External Review Draft

U.S. Environmental Protection Agency
Office of Air and Radiation Office of Air Quality Planning and Standards Research Triangle Park, North Carolina 27711This page left intentionally blank.DRAFT DO NOT QUOTE OR CITE i MARCH 2010 

## TABLE OF CONTENTS

1 INTRODUCTION................................................................................................................ 1-1

1.1 PURPOSE.................................................................................................................. 1- 1

1.2 BACKGROUND ....................................................................................................... 1-2 1.2.1 Legislative Requirements.................................................................................1-2 1.2.2 Overview of the NAAQS Review Process ...................................................... 1-3 1.2.3 History of PM NAAQS Reviews..................................................................... 1-5 1.2.4 Litigation Related to the 2006 PM Standards................................................1-10 1.2.5 Current PM NAAQS Review......................................................................... 1-11

1.3 GENERAL APPROACH AND ORGANIZA TION OF THIS DOCUMENT........ 1-12

1.4 REFERENCES ........................................................................................................ 1-14

2 REVIEW OF THE PRIMARY STANDA RDS FOR FINE PARTICLES ..................... 2-1

2.1 APPROACH ..............................................................................................................2-2 2.1.1 Approaches Used in Previous Reviews ........................................................... 2-3 2.1.1.1 Review Completed in 1997............................................................. 2-3 2.1.1.2 Review Completed in 2006............................................................. 2-5 2.1.2 Remand of Primary Annual PM 2.5 Standard ....................................................2-8 2.1.3 Current Approach........................................................................................... 2-10
2.2 ADEQUACY OF CURRENT STANDARDS ........................................................ 2-14

2.2.1 Evidence-based Considerations ..................................................................... 2-15
2.2.2 Risk-based Considerations............................................................................. 2-43 2.2.3 Preliminary Staff Conclusions on Ad equacy of Current Standards...............2-55

2.3 CONSIDERATION OF ALTER NATIVE STANDARDS ..................................... 2-56

2.3.1 Indicator ......................................................................................................... 2-56 2.3.2 Averaging Times............................................................................................2-66
2.3.3 Forms ............................................................................................................. 2-71
2.3.3.1 Form of the Annual Standard........................................................2-71
2.3.3.2 Form of the 24-Hour Standard......................................................2-73
2.3.4 Alternative Levels to Address Hea lth Effects Related to Long-term PM 2.5 Exposures ........................................................................................................2-74 2.3.4.1 Evidence-based Considerations .................................................... 2-74
2.3.4.2 Risk-based Considerations............................................................ 2-81DRAFT DO NOT QUOTE OR CITE ii MARCH 2010 2.3.5 Alternative Levels to Address Hea lth Effects Related to Short-term PM 2.5 Exposures ........................................................................................................2-88 2.3.5.1 Evidence-based Considerations .................................................... 2-89
2.3.5.2 Risk-based Considerations to Inform Alternative Levels.............2-99 2.3.6 Preliminary Staff Conclusions on Alternat ive Levels to Address Health Effects Related to Long- and Short-term PM 2.5 Exposures ....................................... 2-104
2.4 PRELIMINARY STAFF CONCLUSIONS ON ALTERNATIVE FINE PARTICLE STANDARDS........................................................................................................ 2-108
2.5 KEY UNCERTAINTIES AND AREAS FO R FUTURE RESEARCH AND DATA COLLECTION ...................................................................................................... 2-110
2.6 REFERENCES ...................................................................................................... 2-111

3 REVIEW OF THE PRIMARY STAN DARD FOR THORACIC COARSE
PARTICLES...................................................................................................................... ...3-1

3.1 APPROACH ..............................................................................................................3-1 3.1.1 Approaches Used in Previous Reviews ........................................................... 3-2 3.1.1.1 Reviews Completed in 1987 and 1997 ................................................. 3-2 3.1.1.2 Review Completed in 2006................................................................... 3-3 3.1.2 Litigation of 2006 Final Rule for thoracic coarse particles .............................3-5 3.1.3 Approach in the Current Review ..................................................................... 3-7
3.2 ADEQUACY OF THE EXISTING PM 10 STANDARD .......................................... 3-8

3.2.1 Evidence of Effects Related to Ambi ent Thoracic Coarse Particles ...............3-9 3.2.2 Preliminary Staff Conclusions on Adequacy of Current PM 10 Standard.......3-22

3.3 CONSIDERATION OF POTENTIAL ALTERNATIVE STANDARDS .............. 3-25

3.3.1 Indicator......................................................................................................... 3-26
3.3.2 Consideration of Indicator in the Review Completed in 2006 ......................3-26
3.3.3 Evidence-Based Consideration of In dicator in the Current Review..............3-31 3.3.4 Averaging Time .............................................................................................3-34
3.3.5 Level and Form..............................................................................................3-35
3.3.6 Form............................................................................................................... 3-37
3.3.7 Level .............................................................................................................. 3-37

3.4 KEY UNCERTAINTIES AND AREAS FO R FUTURE RESEARCH AND DATA
COLLECTION .................................................................................................................... 3 -39

3.5 REFERENCES ........................................................................................................ 3-39

4 REVIEW OF THE SECONDARY STAN DARDS FOR VISIBILITY-RELATED
EFFECTS........................................................................................................................ ......4-1DRAFT DO NOT QUOTE OR CITE iii MARCH 2010 4.1 APPROACH ..............................................................................................................4-2 4.1.1 Approaches Used in Previous Reviews ........................................................... 4-2 4.1.2 Remand of Secondary PM 2.5 Standards ........................................................... 4-8 4.1.3 Current Approach ............................................................................................ 4-9
4.2 ADEQUACY OF CURRENT STANDARDS ........................................................ 4-10

4.2.1 Evidence-based Considerations ..................................................................... 4-10 4.2.2 Summary........................................................................................................ 4-28

4.3 CONSIDERATION OF ALTER NATIVE STANDARDS ..................................... 4-29

4.3.1 Nature of the Indicator...................................................................................4-30 4.3.2 Averaging and Applicable Times ..................................................................4-32
4.3.3 Alternative Levels/Forms ..............................................................................4-33
4.3.4 Performance of Alternative Standards........................................................... 4-35

4.4 PRELIMINARY STAFF CONCLU SIONS ON ALTERNATIVE
SECONDARY PM STANDARDS FOR VISIBILITY-RELATED
EFFECTS................................................................................................................. 4-42
4.5 REFERENCES ........................................................................................................ 4-45

APPENDIX 4A. INFORMATION REGARDING THE 1-HOUR PM2.5 MASS
INDICATOR ..................................................................................................................... .... A-1

5 REVIEW OF THE SECONDARY ST ANDARDS FOR OTHER WELFARE
EFFECTS....................................................................................................................... .......5-1

5.1 APPROACH ..............................................................................................................5-2 5.1.1 Approaches Used in Previous Reviews ........................................................... 5-2 5.1.2 Scope of Current NAAQS Reviews................................................................. 5-3 5.1.3 Current Approach ............................................................................................ 5-6

5.2 CLIMATE.................................................................................................................. 5- 6
5.2.1 Scope................................................................................................................ 5-7 5.2.2 Adequacy of the Current Standard...................................................................5-8 5.2.3 Preliminary Staff Conclusions.......................................................................5-11 5.2.4 Key Uncertainties and Areas for Future Research and Data Collection........5-12

5.3 ECOLOGICAL EFFECTS ...................................................................................... 5-13
5.3.1 Scope.............................................................................................................. 5-13 5.3.2 Adequacy of the Current Standard.................................................................5-16 5.3.3 Preliminary Staff Conclusions.......................................................................5-23DRAFT DO NOT QUOTE OR CITE iv MARCH 2010 5.3.4 Key Uncertainties and Areas for Future Research and Data Collection........5-24

5.4 MATERIALS........................................................................................................... 5-25
5.4.1 Scope.............................................................................................................. 5-25 5.4.2 Adequacy of the Current Standard.................................................................5-25 5.4.3 Preliminary Staff Conclusions.......................................................................5-27 5.4.4 Key Uncertainties and Areas for Future Research and Data Collection........5-28

5.5 REFERENCES ........................................................................................................ 5-28

### LIST OF TABLES 1

2 Table 1-1. Summary of Nationa l Ambient Air Quality Standards Promulgated for Particulate 3 Matter 1971-2006 ...................................................................................................... 1-6 4 Table 2-1. Summary of Caus ality Determinations for PM 2.5 .................................................... 2-16 5 Table 2-2. Estimated Incidence and Percent of Total Annual Incidence Associated with 6 Long-term PM 2.5 Exposure Based on Simulation of the Current Suite of Standards 7 (for IHD mortality based on 2007 PM 2.5 Concentrations) 1,2 ...................................2-46 8 Table 2-3. Estimated Incidence and Percent of Total Annual Incidence Associated with Short9 Term PM 2.5 Exposure Based on Simulation of the Current Suite of Standards (CV 10 mortality and hospital admissions based on 2007 PM 2.5 concentrations) 1,2 ............2-50 11 Table 2-4. Comparison of Air Quality Data for Selected Epidemiological Studies – 12 Long-term Mean Concentrations.............................................................................2-79 13 Table 2-5. Comparison of Air Quality Data for Se lected Epidemiological Studies– 98 Percentile 14 Values...................................................................................................................... 2-9 4 15 Table 3-1. Summary of Caus ality Determinations for PM 10-2.5 ................................................ 3-11 16 Table 3-2. PM 10 Concentrations in Cities wi th Statistically Significant PM 10-2.5 Effect 17 Estimates......................................................................................3-18 18 Table 4-1 Logit model estimated VAQ values corresponding to various percent acceptability 19 values for the four cities. .........................................................................................4-20 20 Table 4-2 Percentage of daily maximum hourly values of daylight PM light extinction 21 exceeding CPLs (excluding hours with relative humidity greater than 90 percent). 22 (adapted from Table 3-7 in UFVA)......................................................................... 4-25 23 Table 4-3 Percentage of daily maximum hourly values of daylight PM light extinction 24 exceeding CPLs when “just meeting” the current PM 2.5 NAAQS (15/35 μ g/m 3 ) 25 (excluding hours with relative humid ity greater than 90 percent). 26 (Adapted from Table 4-7 in UFVA)........................................................................ 4-28 27 Table 4.3 1. PM light extincti on design values for “just meeting” secondary NAAQS scenarios 28 based on measured PM light extinction (excluding hours with relative humidity 29 greater than 90 percent)........................................................................................... 4-38 30 Table 4.3-2 90th percentile maximum daily 1-ho ur PM light extinction design values (Mm-1) 31 after rollback to meet alternative standard of 60 μ g/m3, 40 μ g/m3, 30 μ g/m3,20 32
μ g/m3 and 10 μ g/m3 maximum daylight 1- hour PM mass concentration 33 for the 90th percentile.*...........................................................................................4-41 34 Table A-1. Percentage of days with daily maximum daylight 1-hour PM2.5 mass concentration 35 exceeding reference levels in 2005-2007 (e xcluding hour with relative humidity 36 greater than 90 percent)............................................................................................ A-3 37 Table A-2. Alternative NAAQS scenarios ba sed on daily maximum daylight 1-hour PM2.5 38 mass, averaged over three years (excluding hours with relative humidity greater than 39 90 percent)................................................................................................................ A-4 40 Table A-3. 2005-2007 design values for 1-hour PM2.5 mass (μg/m3 ).................................... A-7 41 Table A-4. Percentage reductio ns in non-PRB PM2.5 components required to meet NAAQS 42 scenarios based on 1-hour PM2.5 mass.................................................................... A-7 43Table A-5. Post-rollback design values fo r daily maximum 1-hour PM2.5 mass. Design 1 values are shown only for combinations of study area and scenario for which the 2 study area does not meet the scenario unde r current conditions, such that reductions 3 were made during the rollback modeling................................................................. A-9 4 Table A-6. Percentage of days across three years (two in the case of Phoenix and Houston) 5 with maximum 1-hour daylight PM light ex tinction above CPLs when “just meeting” 6 NAAQS scenarios based on 1-hour PM2.5 ma ss. Blue shading indicates no 7 reduction required from cu rrent conditions............................................................ A-16 8 Table 5-1. Scope of the current secondary PM NAAQS review and current NOx/SOx secondary 9 review. ....................................................................................................................... 5 -4 10 11 

### LIST OF FIGURES 12

13 Figure 2-1. Summary of Eff ect Estimates (per 10 μg/m 3 ) and Air Quality Distributions for 14 Long-term Exposure Studies ...................................................................................2-23 15 Figure 2-2. Distribution of study-specific area mean PM 2.5 concentrations. ............................ 2-75 16 Figure 2-3. Percent reduction in long-t erm exposure-related mortality risk ............................ 2-82 17 Figure 2-4 Summary of Eff ect Estimates (per 10 μg/m 3 ) – Short-term Exposure Studies........2-91 18 Figure 2-5. Distributi on of Study-specific 98 th Percentile Concentrations................................ 2-95 19 Figure 2-6. Percent Reduction in Short- term Exposure-related Mortality and 20 Morbidity Risk ......................................................................................................2-100 21 Figure 4-1 Summary of re sults of urban visibility studies in four cities , showing the identified 22 range of the 50% acceptan ce criteria ....................................................................4-19 23 Figure 4 2. Distribution of estimated maximum da ily daylight 1-hour PM light extinction across 24 the 2005-2007 period, by study area (excludi ng hours with relative humidity greater 25 than 90 percent). (Adapted from Figure 3-8 in UFVA)* ........................................4-24 26 Figure 4 3. Distribution of daylight 1-hour PM light extinction when rolled back to just meet 27 current PM fine NAAQS across the 2 005-2007 period, by study area (excluding 28 hours with relative humidity greater than 90 percent). ...........................................4-27 29 Figure 4.3-1 Scatter plots of PM light extinction versus PM 2.5 mass concentration of two cities 30 (from UFVA Appendix D, Figure D2)....................................................................4-32 31 Figure 4.3-2 Daily maximum dayli ght 1-hour light extinction af ter rollback to just meet a 32 scenario with daily maximum of 112 Mm -1 for the 90 th percentile excluding hours 33 with relative humidity greater than 90 percent........................................................4-37 34 Figure 4.3-3 Maximum daily day light 1-hour PM light extincti on under "just meet" conditions 35 for a NAAQS scenario based on 1-hour PM 2.5 mass of 30 μ g/m 3 , 90th percentile, 36 excluding relative humidity >90%. .........................................................................4-39 37 Figure A-1. 2005-2007 daily maximu m daylight 1-hour PM2.5 ma ss concentrations (μg/m3) 38 for the 15 study areas (excluding hours with relative humidity greater than 90 39 percent)..................................................................................................................... A- 2 40 Figure A-2. Distributions of maximum daily da ylight 1-hour PM light extinction under “just 41 meet” conditions for NAAQS scenarios based on 1-hour PM2.5 mass (excluding 42 hours >90% RH)..................................................................................................... A-11 43

### LIST OF ACRONYMS/ABBREVIATIONS 1

2 ACS American Cancer Society 3 AHR Airway Hyperesponsiveness 4 AHSMOG California Seventh Day Adventist Study 5 ANS Autonomic nervous system 6 AQCD Air Quality Criteria Document 7 AQS EPA’s Air Quality System 8
AR4 Fourth Assessment Report of the Intergovernmental Panel on Climate 9 Change 10 BC Black carbon 11 BenMAP Benefits Mapping Analysis Program 12 BP Blood pressure 13
C Carbon 14
Ca Calcium 15
CAA Clean Air Act 16
CAPs Concentrated Ambient Particles 17
CARB California Air Resources Board 18 CASAC Clean Air Scientific Advisory Committee 19
CBSA Consolidated Business Statistical Area 20
CBVD Cerebrovascular disease 21
CCN Cloud Condensation Nuclei 22 CCSP US Climate Change Science Program 23
Cd Cadmium 24 CHD Coronary Heart disease 25 CHF Congestive heart failure 26 CHS Childrens Health Study 27
CO Carbon Monoxide 28
COPD Chronic obstruc tive pulmonary disease 29 C-R Concentration-response relationship 30 CRP C-reactive protein 31 CSN Chemical Speciation Network 32 CTM Chemical transport models 33 Cu Copper 34CV Cardiovascular 1
CVD Cardiovascular disease 2
DE Diesel Exhaust 3
DEP Diesel Exhaust Particles 4
dv deciview 5 DVT Deep Vein Thrombosis 6
EC Elemental Carbon 7 ECG Electrocardiogram 8 ED Emergency department 9 EPA Environmental Protection Agency 10 FEM Federal Equivalent Method 11
FEV 1 Change in forced expiratory volume in one second 12
FRM Federal Reference Method 13
GAMs Generalized additive models 14
GEOS Global Scale Air Circulation Model 15
GHG Greenhouse Gas 16 GI Group Interviews 17
GLMs Generalized linear models 18
GSH Glutathione 19
GST Glutathione-S-transferase 20 HA Hospital admissions 21
HEI Health Effects Institute 22 Hg Mercury 23
HR Heart rate 24 HRV Heart rate variability 25
ICD International Classification of Disease 26 ICR Information Collection Request 27 IFG Investigative Focus Groups 28
IHD Ischemic heart disease 29 IMPROVE Interagency Monitoring of Protected Visual Environment 30 IPCC Intergovernmental Panel on Climate Change 31 IRP Integrated Review Plan 32 ISA Integrated Science Assessment 33
IT Intratracheal 34Km Kilometer 1 Lag Time between one event and another 2 Lag 0 Same day as the death, test, hos pital, ED, clinic, physician visit; 3 that occurs on the same day as the exposure to the pollutant(s) 4 Lag 0-x All the deaths test , hospital, ED, clinic, physic ian visit; that occurs 5 on the same day as the exposure to the pollutant(s) and the x days 6 following the day of exposure 7 MCAPS Medicare Air Pollution Study 8 MEA Millennium Ecosystem Assessment 9 MENTOR Modeling ENvironment for TOtal Risk 10 MI Myocardial infarction 11 Mm Megameter 12 MOA Mode(s) or mechanism(s) of action 13 MSA Metropolitan Statistical Area 14 N Nitrogen 15 NAAQS National Ambient Air Quality Standards 16
NCEA National Center for Environmental Assessment 17 NCore National Core Monitoring Network 18
Ni Nickel 19 NMMAPS National Morbidity, Mo rtality, and Air Pollution Study 20
NO Nitric Oxide 21
NO 2 Nitrogen dioxide 22
NO 3 - Nitrate 23 NOx Nitrogen oxides 24
NPS National Park Service 25
NRC National Research Council 26
NWS National Weather Service 27
O 3 Ozone 28 OAQPS Office of Air Qual ity Planning and Standards 29
OAR Office of Air and Radiation 30 OC Organic Carbon 31
OR Odds Ratio 32 ORD Office of Research and Development 33 OS Observational Study 34 PA Policy Assessment 35PA Pulmonary arterial 1 PAH Polyaromatic Hydrocarbon 2
Pb Lead 3 PEF Peak Expiratory Flow L/min 4
PM Particulate matter 5

PM 10 Particles with an upper 50% cut-point of 10± 0.5 μ m aerodynamic 6 diameter and a penetration curve as specified in the Code of 7 Federal Regulations. 8 PM 10-2.5 Particles with an upper 50% cut-point of 10 μ m aerodynamic 9 diameter and a lower 50% cut-point of 2.5 μ m aerodynamic 10 diameter. 11 12 PM 2.5 Particles with an upper 50% cut-point of 2.5 μ m aerodynamic 13 diameter and a penetration curve as specified in the Code of 14 Federal Regulations. 15 16 PM X The legal definition for PM X , as defined in the Code of Federal 17 Regulations, includes both a 50% cut-point and a penetration 18 curve. A 50% cut-point of X μ m diameter means that 50% of 19 particles with aerodynamic diameter of X are removed by the inlet 20 and 50% pass through the inlet a nd are collected on the filter. 21 Depending on the specific penetra tion curve specified, particles 22 larger than X μ m aerodynamic diameter are collected with an 23 efficiently than decreases rapidly for particles larger than X while 24 the collection efficiency for particles smaller than X increases 25 rapidly with decreasing size until 100 % efficiency is reached. 26 PRB Policy-Relevant Background 27 PSAS The French National Program on Air Pollution Health Effects 28
PT Prothrombin Time 29 PTT Partial Thomboplastin Time 30 QA Quality assurance 31 QT Time for depolarization and repolarization of the ventricles 32
RA Risk Assessment 33 REA Risk and Exposure Assessment 34 RF Radiative forcing 35 RH Relative humidity 36 RNS Reactive Nitrogen Species 37 ROS Reactive Oxygen Species 38
RR Relative risk 39SAB Science Advisory Board 1 SANDWICH Sulfate, Adjusted Nitrate, Derived Water, Inferred Carbonaceous 2 mass approach 3 SAP Synthesis and Assessment Product 4 SBP Systolic Blood Pressure 5 SD Standard deviation 6
SEARCH Southeastern Aerosol Re search and Characterization Study 7 SEDD State Emergency Department Databases 8
SES Socioeconomic Status 9
Si Silicon 10 SID State Inpatient Database 11 SMOKE Sparse Matrix Op erator Kernal Emissions 12
S Sulfur 13
SO 2 Sulfur Dioxide 14
SO 4 2- Sulfate 15
SO x Sulfur Oxides 16 SOPHIA Study of Particulates and Health in Atlanta 17 STP Standard Temperature and Pressure 18
TB Tracheobronchial 19 TSP Total suspended particulate 20 UFPs Ultrafine particles 21 UFVA Urban-Focused Visibility Assessment 22
V Vanadium 23 VAQ Visual Air Quality 24 VOC Volatile organic compounds 25 WACAP Western Airborne Contaminants Assessment Project 26
WHI Women’s Health Initiative 27
Zn Zinc 281 This page intentionally left blank. 2D raft Do Not Quote or Cite 1-1 March 2010 

### 1. INTRODUCTION 1

1.1 PURPOSE 2
The U.S. Environmental Protection Agency (EPA) is presently conducting a review of 3 the national ambient air quality standards (NAAQS ) for particulate matter (PM). The overall 4 plan and schedule for this review were presented in the Integrated Review Plan for the National 5 Ambient Air Quality Standards for Particulate Matter (IRP; US EPA, 2008a). The IRP 6 identified key policy-releva nt issues to be addressed in this re view as a series of questions that 7
frame our consideration of whether the current NAAQS for PM should be retained or revised. 8 This Policy Assessment (PA), prepared by st aff in the EPA’s Office of Air Quality 9 Planning and Standards (OAQPS), is intended to help “bridge th e gap” between the relevant 10 scientific information and assessments and the judgments required of the EPA Administrator in 11 determining whether, and if so, how, it is appropriate to revi se the NAAQS for PM. 1 This first 12 draft PA presents factors releva nt to EPA’s review of the prim ary (health-based) and secondary 13 (welfare-based) PM NAAQS. It focuses on both evidence- and risk-based information in 14 evaluating the adequacy of the current PM NAA QS and in identifying potential alternative 15
standards for consideration. In this first draf t PA, we consider the sc ientific and technical 16
information available in this review as assessed in the Integrated Scienc e Assessment for 17 Particulate Matter (Final Report) (ISA, US EPA, 2009a), the Quantitative Health Risk 18 Assessment for Particulate Matter – Second External Review Draft (US EPA, 2010a) and the 19 Particulate Matter Urban-Focused Visibility Assessment – Second External Review Draft (US 20 EPA, 2010b). In so doing, we focus on information that is most pertinent to evaluating the basic 21 elements of NAAQS: indicator 2 , averaging time, form, 3 and level. These elements, which 22 together serve to define each standard, must be considered collectively in evaluating the health 23 and welfare protection afforded by the PM standards. 24 We also recognize that part of the de finition of the NAAQS includes specifying 25 allowable monitoring methods by which the indicat or is to be measured as well as minimum 26 requirements for monitoring, such as monitor si ting criteria. Such monitoring issues were 27 identified in the IRP (US EPA, 2008a, chapter 7) a nd we plan to include a discussion of them in 28
the second draft PA. 29

1 Preparation of a PA by OAQPS staff reflects Administrator Jackson’s decision to modify the NAAQS review process that was presented in the IRP. See http://www.epa.gov/ttn/naaqs/review.html for more information on the current NAAQS review process.
2 The “indicator” of a standard define s the chemical species or mixture that is to be measured in determining whether an area attains the standard.
3 The “form” of a standard defines the ai r quality statistic that is to be compared to the level of the standard in determining whether an area attains the standard.D raft Do Not Quote or Cite 1-2 March 2010 Although this first draft PA should be of use to all parties interested in this PM NAAQS 1 review, it is written with an expectation that the reader has familiarity with the technical 2
discussions contained in the ISA (US EPA, 2009a) and in the draft quantitative risk and visibility 3 assessment documents (US EPA, 2010a,b). 4

1.2 BACKGROUND 5

1.2.1 Legislative Requirements 6
Two sections of the Clean Air Act (Act) gove rn the establishment and revision of the 7 NAAQS. Section 108 (42 U.S.C. se ction 7408) directs the Administ rator to identify and list air 8 pollutants that meet three specified criteria, in cluding air pollutants “emissions of which, in his 9 judgment, cause or contribute to air pollution wh ich may reasonably be anticipated to endanger 10 public health and welfare” and whose “presence . . . in the ambient air results from numerous or 11 diverse mobile or stationary sources” and to issue air quality criteria for th ose that are listed. Air 12 quality criteria are to “accurately reflect the late st scientific knowledge useful in indicating the 13 kind and extent of all identifiable effects on pub lic health or welfare which may be expected 14 from the presence of [a] pollutant in the ambient air . . .” 42 U.S.C. § 7408(b). 15 Section 109 (42 U.S.C. section 7409) dire cts the Administrator to propose and 16 promulgate “primary” and “secondary” NAAQS for po llutants for which air quality criteria are 17 issued. Section 109(b)(1) defines a primary standard as one “the attainment and maintenance of 18 which in the judgment of the Administrator, based on [air quality] criteria and allowing an 19 adequate margin of safety, are requi site to protect the public health.” 4 A secondary standard, as 20 defined in Section 109(b)(2), must “specify a leve l of air quality the attainment and maintenance 21 of which, in the judgment of the Administrator, base d on such [air quality] cr iteria, is requisite to 22 protect the public welfare from any known or anticipated advers e effects associated with the 23 presence of [the] pollutant in the ambient air.” 5 24 The requirement that primary standards incl ude an adequate margin of safety was 25
intended to address uncertainties associated with inconclusive scientific and technical 26
information available at the time of standard set ting. It was also intended to provide a reasonable 27 degree of protection against hazards th at research has not yet identified. Lead Industries 28

4 The legislative history of section 109 indicates that a primary standard is to be set at “the maximum permissible ambient air level . . . which will protect the health of an y [sensitive] group of the population,” and that for this purpose “reference should be made to a representative samp le of persons comprising the sensitive group rather than to a single person in such a group.” S. Rep. No. 91-1196, 91 st Cong., 2d Sess. 10 (1970).
5 Welfare effects as defined in section 302(h) (42 U.S.C. section 7602(h)) include, but are not limited to, “effects on soils, water, crops, vegetation, man-made materials, animals, wildlife, weather, visibility and climate, damage to and deterioration of property, and hazards to transportation, as well as effects on economic values and on personal comfort and well-being.”D raft Do Not Quote or Cite 1-3 March 2010 Association v. EPA, 647 F.2d 1130, 1154 (D.C. Cir 1980 ), cert. denied, 449 U.S. 1042 (1980); 1
American Petroleum Institute v. Costle , 665 F.2d 1176, 1186 (D.C. Cir. 1981), cert. denied, 455 2 U.S. 1034 (1982); American Farm Bureau Federation v. EPA, 559 F. 3d 512, 533 (D.C. Cir. 3 2009). Both kinds of uncertainties are components of the risk associated with pollution at levels 4
below those at which human health effects can be said to occur with reasonable scientific 5 certainty. Thus, in selecting primary standards th at include an adequate margin of safety, the 6 Administrator is seeking not only to prevent pollution levels that have been demonstrated to be 7 harmful but also to prevent lower pollutant leve ls that may pose an unacceptable risk of harm, 8 even if the risk is not precisely identified as to nature or degree. 9 In selecting a margin of safet y, EPA considers such factors as the nature and severity of 10 the health effects involved, the size of the susc eptible population(s) at risk, and the kind and 11 degree of the uncertainties that must be addresse d. The selection of any particular approach to 12 providing an adequate margin of safety is a policy choice left specifically to the Administrator’s 13 judgment. Lead Industries Association v. EPA , supra, 647 F.2d at 1161-62. 14 In setting standards that are “requisite” to protect public health a nd welfare, as provided 15 in section 109(b), EPA’s task is to establish standards that are neither more nor less stringent 16 than necessary for these purposes. In so doing, EPA may not consider th e costs of implementing 17 the standards. See generally Whitman v. American Trucking Associations , 531 U.S. 457, 471, 18 475-76 (2001). 19 Section 109(d) (1) of the Act requires that “not later than December 31, 1980, and at 5- 20 year intervals thereafter, the Administrator shall complete a thorough review of the criteria 21 published under section 108 and th e national ambient air quality st andards . . . and shall make 22
such revisions in such criteri a and standards and promulgate such new standards as may be 23 appropriate in accordance with section [108]... and subsection (b) . . .” 42 U.S.C. § 7409(d)(1). 24 Section 109(d)(2) requires that an independent sc ientific review committee “shall complete a 25
review of the criteria . . . and the national primary and secondary ambient air quality standards . . 26 . and shall recommend to the Administrator any new . . . standards and revisions of existing 27 criteria and standards as may be appropriate . . .” 42 U.S.C. § 7409(d)(2). Since the early 28 1980's, this independent review function has been performed by the Clean Air Scientific 29 Advisory Committee (CASAC). 30

1.2.2 Overview of the NAAQS Review Process 31
Since completion of the last PM NAAQS revi ew, the Agency has made a number of 32 changes to the process for reviewing the NAAQS. In making these changes, the Agency 33 consulted with CASAC and the public. This revi sed process contains four major components: 34 planning, science assessment, risk/exposure asse ssment, and policy assessment/rulemaking. 35D raft Do Not Quote or Cite 1-4 March 2010 The planning phase begins with a “kick-off” workshop to get input from external and 1 internal experts and the public regarding policy-rele vant issues from the last review and others 2 that have more recently emerged. The workshop di scussions help inform the preparation of an 3 IRP jointly by OAQPS and Office of Research and Development/National Center for 4 Environmental Assessment (ORD/NCEA) staff. A draft IRP is presente d for consultation with 5 CASAC and for public comment. A final IRP reflects consideration of CASAC and public 6 comments together with early guidance from Agen cy management. The IRP presents the policy7 relevant questions that will frame the review, th e review process and schedule, and descriptions 8 of the purpose, contents, and approach for developing each of the key documents. 9 The science assessment phase i nvolves the preparation of anISA by NCEA staff. The 10 ISA provides a concise evaluation and integration of the policy-relevant science, including key 11 science judgments that are important to inform the design and scope of the risk and exposure 12 assessments. The ISA and its supporting annexe s provide a comprehensive assessment of the 13
current scientific litera ture pertaining to known and anticipated effects on public health and 14 welfare associated with the pres ence of the pollutant in the ambi ent air, emphasizing information 15
that has become available since the last review . The process generally includes production of a 16 first and second draft ISA, which undergo CASAC and public review prior to completion of the 17
final ISA. 18 In the risk/exposure assessment phase, OAQPS staff draws upon information and 19 conclusions presented in the IS A to develop quantitative estimat es of the risks/exposures for 20
health and/or welfare effects asso ciated with current ambient levels of PM, with levels that just 21 meet the current standards, and with levels that just meet potential alternative standards. The 22 REAs present methods, key results, observations, and related uncertainties. These assessments 23 begin with preparation of a planning document th at discusses the scope and methods planned for 24 use in conducting the quantitative assessments. Scope and Methods Plans are generally prepared 25 in conjunction with the first draft ISA and pres ented for consultation with CASAC and for public 26 comment. Comments received on the Scope and Me thods Plans are considered by EPA staff in 27 conducting the analyses and prepar ing draft REAs. The process generally includes production of 28 first and second draft REAs, which undergo CASAC and public review pr ior to completion of 29
final REAs. 30 The review process ends with a policy assessment/rulemaking phase. Recent revisions to 31 process have reinstated the preparation of a Po licy Assessment (PA). The PA, like the previous 32 Staff Paper, integrates and interprets the in formation from the ISA and REAs to provide a 33 transparent staff analysis of the scientific basi s for alternative policy op tions for consideration by 34 the Administrator prior to the issuance of proposed and final ru les (Jackson, 2009). One or more 35 drafts of the PA undergo CASAC an d public review prior to completion of the final PA. The PA 36D raft Do Not Quote or Cite 1-5 March 2010 is intended to facilitate CASAC’s advice and recommendations to the Administrator on any new 1 standards or revisions to existing standards as may be appropriate, as provided for in the CAA. 2 Following issuance of the final PA, the Agency publishes a proposed rule, followed by a public 3 comment period. Taking into account comments received on the proposed rule, the Agency 4 issues a final rule to complete the rulemaking process. 5

1.2.3 History of PM NAAQS Reviews 6
The NAAQS for PM that have been promulga ted to date are summarized in Table 1-1 7 and briefly discussed below. Particulate matte r is the generic term for a broad class of 8 chemically and physically diverse substances that exist as discrete particles (liquid droplets or 9 solids) over a wide range of sizes, such that the indicator for a PM NAAQS has historically been 10 defined in terms of pa rticle size ranges. 11 The EPA first established NAAQS for PM in 1971 (36 FR 8186), based on the original 12 air quality criteria document (DHEW, 1969). Th e reference method specified for determining 13 attainment of the original standards was the high-volume sampler, which collects PM up to a 14 nominal size of 25 to 45 micrometers (μm) (referred to as total suspended pa rticles or TSP). The 15 primary standards (measured by th e indicator TSP) were 260 μg/m 3 , 24-hour average, not to be 16 exceeded more than once per year, and 75 μg/m 3 , annual geometric mean. The secondary 17 standard was 150 μg/m 3 , 24-hour average, not to be ex ceeded more than once per year. 18 In October 1979, EPA announced the first periodic review of the criter ia and NAAQS for PM, 19 and significant revisions to th e original standards were promulgated in 1987 (52 FR 24634, July 20 1, 1987). In that decision, EPA changed the indicator for PM from TSP to PM 10 , the latter 21 including particles with a median aerodynamic diameter 6 less than or equal to 10 μm, which 22 delineates thoracic particles (i.e ., that subset of inhalable pa rticles small enough to penetrate 23 beyond the larynx to the thoracic region of the re spiratory tract). The EPA also revised the 24 primary standards by: (1 ) replacing the 24-hour TSP st andard with a 24-hour PM 10 standard of 25 150 μg/m 3 with no more than one e xpected exceedance per year; and (2) replacing the annual 26
TSP standard with a PM 10 standard of 50 μg/m 3 , annual arithmetic mean. The secondary 27 standard was revised by replacing it with 24-hour and annual standard s identical in all respects to 28 the primary standards. The revi sions also included a new reference method for the measurement 29
of PM 10 in the ambient air and rules for determini ng attainment of the new standards. On 30

6 The more precise term is 50 percent cutpoint or 50 percent diameter (D 50 ). This is the aerodynamic particle diameter for which the efficiency of particle collection is 50 percent. Larger particles are not excluded altogether, but are collected with substantially d ecreasing efficiency and smaller particle s are collected with increasing (up to 100 percent) efficiency.D raft Do Not Quote or Cite 1-6 March 2010 Table 1-1. Summary of National Ambien t Air Quality Standards Promulgated for 1 Particulate Matter 1971-2006 7 2 3
Final Rule Indicator Ave. Time Level Form

24-hour 260 μg/m 3 (primary) 150 μg/m 3 (secondary) Not to be exceeded more than once
per year 1971 (36 FR 8186 April 30, 1971) TSP

Annual 75 μg/m 3 (primary) Annual average

24-hour 150 μg/m 3 Not to be exceeded more than once per year on average over a 3-year period 1987 (52 FR 24634; July 1, 1987) PM 10

Annual 50 μg/m 3 Annual arithmetic mean, averaged over 3 years
24-hour 65 μg/m 3 98 th percentile, averaged over 3 years PM 2.5 Annual 15 μg/m 3 Annual arithmetic mean, averaged over 3 years 8

24-hour 150 μg/m 3 Initially promulgated 99 th percentile, averaged over 3 years; when 1997 standards were vacated, the form of 1987 standards remained in place (not to be exceeded more than once per year on average over a 3-year period) 1997 (62 FR 38652 July 18, 1997) PM 10

Annual 50 μg/m 3 Annual arithmetic mean, averaged over 3 years
24-hour 35 μg/m 3 98 th percentile, averaged over 3 years PM 2.5 Annual 15 μg/m 3 Annual arithmetic mean, averaged over 3 years 9 2006 (71 FR 61144 October 17, 2006)

PM 10 24-hour 150 μg/m 3 Not to be exceeded more than once per year on average over a 3-year period
4

7 When not specified, primary and secondary standards are identical.
8 The level of the standard was to be compared to meas urements made at sites that represent “community-wide air quality” recording the highest level, or, if specific constraints were met, measurements from multiple communitywide air quality monitoring sites could be averaged (“spatial averaging”).
9 The constraints on the spatial averaging criteria were tig htened by further limiting the conditions under which some areas may average measurements from mu ltiple community-oriented monitors to determine compliance (see 71 FR 61165-61167).D raft Do Not Quote or Cite 1-7 March 2010 In April 1994, EPA announced its plans for the second periodic review of the criteria and 1 NAAQS for PM, and promulgated significant revisions to the NAAQS in 1997 (62 FR 38652, 2 judicial review, the revised standa rds were upheld in all respects. Natural Resources Defense 3 Council v. EPA, 902 F. 2d 962 (D.C. Cir. 1990), cert. denied, 498 U.S. 1082 (1991). July 18, 4 1997). Most significantly, EPA determined that although the PM NAAQS should continue to 5 focus on particles less than or equal to 10 μm in diameter, the fine and coarse fractions of PM 10 6 should be considered separately. New standards were added, using PM 2.5 , referring to particles 7 with a nominal median aerodynamic diameter less than or equal to 2.5 μm, as the indicator for 8 fine particles. The PM 10 standards were retained for the purpo se of regulating the coarse fraction 9
of PM 10 (referred to as thoracic coarse particles or coarse-fraction particles; generally including 10 particles with a nominal median aerodynamic diameter greater than 2.5 μm and less than or 11 equal to 10 μm, or PM 10-2.5 ). The EPA established two new PM 2.5 standards: an annual standard 12 of 15 μg/m 3 , based on the 3-year average of annual arithmetic mean PM 2.5 concentrations from 13 single or multiple monitors sited to repres ent community-wide air quality; and a 24-hour 14 standard of 65 μg/m 3 , based on the 3-year average of the 98th percentile of 24-hour PM 2.5 15 concentrations at each populati on-oriented monitor within an ar ea. Also, EPA established a new 16
reference method for the measurement of PM 2.5 in the ambient air and rules for determining 17
attainment of the new standards. To continue to address thoracic coarse particles, the annual 18

PM 10 standard was retained, while the form, but not the level, of the 24-hour PM 10 standard was 19
revised to be based on the 99 th percentile of 24-hour PM 10 concentrations at each monitor in an 20 area. The EPA revised the secondary standards by making them identical in all respects to the 21 primary standards. 22 Following promulgation of the revised PM NAAQS in 1997, petitions for review were 23 filed by a large number of partie s, addressing a broad range ofissues. In May 1998, a three24 judge panel of the U.S. Court of Appeals for the District of Colu mbia Circuit issu ed an initial 25 decision that upheld EPA’s decision to establish fine particle standards, holding that "the 26 growing empirical evidence dem onstrating a relationship between fine particle pollution and 27 adverse health effects amply justifies estab lishment of new fine particle standards." American 28 Trucking Associations v. EPA , 175 F. 3d 1027, 1055-56 (D.C. Cir. 1999) (rehearing granted in 29 part and denied in part, 195 F. 3d 4 (D.C. Cir. 1999), affirmed in part and reversed in part, 30 Whitman v. American Trucking Associations , 531 U.S. 457 (2001). The panel also found "ample 31 support" for EPA's decision to regulate coar se particle pollution, but vacated the 1997 PM 10 32 standards, concludi ng in part that PM 10 is a "poorly matched indica tor for coarse particulate 33 pollution" because it includes fine particles. Id . at 1053-55. Pursuant to the court’s decision, 34
EPA removed the vacated 1997 PM 10 standards from the Code of Federal Regulations (CFR) (69 35 FR 45592, July 30, 2004) and deleted the regulatory provision [at 40 CFR section 50.6(d)] that 36D raft Do Not Quote or Cite 1-8 March 2010 controlled the transition fr om the pre-existing 1987 PM 10 standards to the 1997 PM 10 standards. 1 The pre-existing 1987 PM 10 standards remained in place (65 FR 80776, December 22, 2000). 2 The Court also upheld EPA’s determination not to establish more stringe nt secondary standards 3 for fine particles to address eff ects on visibility (175 F. 3d at 1027). 4 More generally, the panel held (over a strong dissent) that EPA’s approach to 5 establishing the level of the standards in 1997, both for the PM and for the ozone (O 3 ) NAAQS 6 promulgated on the same day, effected “an unconstitutional delegation of legislative authority.” 7
Id . at 1034-40. Although the panel stated that “the factors EPA uses in determining the degree of 8 public health concern associated with different levels of ozone and PM are reasonable,” it 9 remanded the rule to EPA, stating that when EPA considers these factors for potential non10 threshold pollutants “what EPA lacks is any determinate criterion for drawing lines” to 11
determine where the standards should be set. Co nsistent with EPA’s l ong-standing interpretation 12 and D.C. Circuit precedent, the panel also reaffi rmed its prior holdings that in setting NAAQS 13 EPA is “not permitted to consider the co st of implementing those standards” Id . at 1040-41. 14 On EPA’s petition for rehearing, the panel adhered to its positi on on these points. 15 American Trucking Associations v. EPA , 195 F. 3d 4 (D.C. Cir. 1999). The full Court of 16 Appeals denied EPA’s request for rehearing en banc, with five judges dissenting. Id . at 13. Both 17 sides filed cross appeals on these issues to th e United States Supreme Court, which granted 18 certiorari. In February 2001, the Supreme C ourt issued a unanimous decision upholding EPA’s 19 position on both the constitutional and cost issues. Whitman v. American Trucking Associations
, 20 531 U.S. 457, 464, 475-76. On the constitutional issue, the Court held that the statutory 21 requirement that NAAQS be “requi site” to protect public health with an adequate margin of 22 safety sufficiently cabined EPA’s discretion, affi rming EPA’s approach of setting standards that 23 are neither more nor less stringent than necessa ry. The Supreme Court remanded the case to the 24 Court of Appeals for resolution of any remaining issues that had not b een addressed in that 25 court’s earlier rulings. Id . at 475-76. In March 2002, the Court of Appeals rejected all 26 remaining challenges to the standards, holding under the traditional standard of review that 27
EPA’s PM 2.5 standards were reasonably supported by the administrative record and were not 28 “arbitrary and capricious.” American Trucking Associations v. EPA, 283 F. 3d 355, 369-72 (D.C. 29 Cir. 2002). 30 In October 1997, EPA published its plans for the next periodic review of the air quality 31 criteria and NAAQS for PM (62 FR 55201, October 23, 1997), including the 1997 PM 2.5 32
standards and the 1987 PM 10 standards. After CASAC and pub lic review of several drafts, 33
NCEA finalized the Air Quality Criteria Document for Particulate Matter (henceforth, AQCD or 34 the "Criteria Document") in October 2004 (U.S. EPA, 2004) and OAQPS finalized an 35 assessment document, Particulate Matter Health Risk Asse ssment for Selected Urban Areas 36D raft Do Not Quote or Cite 1-9 March 2010 (Abt, 2005), and a “Staff Paper,” Review of the National Ambient Air Quality Standards for 1 Particulate Matter: Policy Assessment of Scientific and Tec hnical Information, in December 2 2005 (U.S. EPA, 2005). In conjunction with thei r review of the Staff Paper, CASAC provided 3
advice to the Adminstrator on revisions to the PM NAAQS (Henderson, 2005a). In particular, 4
most CASAC PM Panel members favored revising the level of the 24-hour PM 2.5 primary 5 standard in the range of 35 to 30 μg/m 3 with a 98 th percentile form, in c oncert with revising the 6
level of the annual PM 2.5 standard in the range of 14 to 13 μg/m 3 (Henderson, 2005a, p.7). For 7 thoracic coarse particles, the Panel ha d reservations in recommending a 24-hour PM 10-2.5 primary 8 standard, and agreed that there was a need for mo re research on the health effects of thoracic 9 coarse particles (Henderson, 2005b). With regard to secondary standards, most Panel members 10 strongly supported establishing a new, distinct secondary PM 2.5 standard to protect urban 11 visibility (Henderson, 2005a, p. 9). 12 On January 17, 2006, EPA proposed to revise the primary and secondary NAAQS for PM 13 (71 FR 2620) and solicited comment on a broad range of options. Proposed revisions included: 14 revising the level of the 24-hour PM 2.5 primary standard to 35 μg/m 3 ; revising the form, but not 15 the level, of the annual PM 2.5 primary standard by tightening th e constraints on the use of spatial 16 averaging; replacing the 24-hour PM 10 primary standard with a 24-hour standard defined in 17 terms of a new indicator, PM 10-2.5 10 set at a level of 70 μg/m 3 ; revoking the annual PM 10 primary 18 standard; and revising the secondary standards by making them iden tical in all respects to the 19 proposed suite of primary standards for fine and coarse particles. 11 Subsequent to the proposal, 20 CASAC provided additional advice to EPA in a letter to the Administrator requesting 21
reconsideration of CASAC’s recommendati ons for both the primary and secondary PM 2.5 22
standards as well as the standards for thor acic coarse particles (Henderson, 2006a). 23 On October 17, 2006, EPA promulgated revi sions to the PM NAAQS to provide 24 increased protection of public hea lth and welfare (71 FR 61144). W ith regard to the primary and 25 secondary standards for fine particles, EPA revised the level of the 24-hour PM 2.5 standard to 35 26 μg/m 3 , retained the level of the annual PM 2.5 standard at 15 μg/m 3 , and revised the form of the 27
annual PM 2.5 standard by adding further constraints on the optional use of spatial averaging. The 28 EPA revised the secondary standard s for fine particles by making them identical in all respects to 29 the primary standards. With regard to the prim ary and secondary standards for thoracic coarse 30

10 This proposed indicator was qualified so as to include any ambient mix of PM 10-2.5 dominated by particles generated by high-density traffic on paved roads, industrial sources, and construction sources, and to exclude any ambient mix of particles dominated by rural windblown dust and soils and agricultural and mining sources.
11 In recognition of an alternative view expressed by most members of the CASAC PM Panel, the Agency also solicited comments on a subdaily (4 to 8 hour averaging time) secondary PM 2.5 standard to address visibility impairment, within the range of 20 to 30 μg/m 3 and with a form within the range of the 92 nd to 98 th percentile (71 FR 2685).D raft Do Not Quote or Cite 1-10 March 2010 particles, EPA retained the le vel and form of the 24-hour PM 10 standard (such that the standard 1 remained at a level of 150 μg/m 3 with a one expected exceedan ce form), and revoked the annual 2

PM 10 standard. The EPA also established a new Federal Reference Method (FRM) for the 3
measurement of PM 10-2.5 in the ambient air (71 FR 61212-13). Although the standards for 4 thoracic coarse particles were not defined in terms of a PM 10-2.5 indicator, the new FRM for 5

PM 10-2.5 was established to provide a basis for ap proving Federal Equivale nt Methods (FEMs) 6 and to promote gathering scien tific data to support future reviews of the PM NAAQS. 7 Following issuance of the final rule, CASAC ar ticulated its concern that “EPA’s final 8 rule on the NAAQS for PM does not reflect several important as pects of the CASAC’s advice” 9 (Henderson et al, 2006b). With regard to the PM 2.5 annual primary standard, CASAC expressed 10 serious concerns regarding the decision to re tain the level of the standard at 15 μg/m 3 . With 11 regard to EPA’s final decisi on to retain the 24-hour PM 10 standard for thoracic coarse particles, 12 CASAC acknowledged concerns asso ciated with retaining this standard while recognizing the 13 need to have a standard in place to protect against effects associat ed with short-term exposures to 14 thoracic coarse particles. With regard to EPA’s final decision to revise the secondary PM 2.5 15
standards to be identical in all respects to the revised primary PM 2.5 standards, CASAC 16 expressed concerns that CASAC’s advice to establish a di stinct secondary standard for fine 17 particles to address visibility impairment was not followed. 18

1.2.4 Litigation Related to the 2006 PM Standards 19
Several parties filed petitions for review following promulgation of the revised PM 20 NAAQS in 2006. These petitions addressed the follo wing issues: (1) selec ting the level of the 21 primary annual PM 2.5 standard; (2) retaining PM 10 as the indicator of a standard for thoracic 22 coarse particles, re taining the level and form of the 24-hour PM 10 standard, and revoking the 23

PM 10 annual standard; and (3) setting the secondary PM 2.5 standards identical to the primary 24 standards. On February 24, 2009, the U.S. Court of Appeals for the District of Columbia Circuit 25 issued its opinion in the case American Farm Bureau Federation v. EPA , 559 F. 3d 512 (D.C. 26 Cir. 2009). The court remanded the primary annual PM 2.5 NAAQS to EPA because EPA failed 27 to adequately explain why the standard provide d the requisite protecti on from both short- and 28 long-term exposures to fine particles, in cluding protection for at-risk populations. American 29
Farm Bureau Federation v. EPA , 559 F. 3d 512, (D.C. Cir. 2009). With regard to the standards 30
for PM 10 , the court upheld EPA’s decisi ons to retain the 24-hour PM 10 standard to provide 31 protection from thoracic coar se particle exposures a nd to revoke the annual PM 10 . standard. 32
American Farm Bureau Federation at 533-38. With regard to the secondary PM 2.5 standards, the 33 court remanded the standards to EPA because the Agency failed to adequately explain why 34D raft Do Not Quote or Cite 1-11 March 2010 setting the secondary PM standards identical to the primary standard s provided the required 1 protection for public welfare, including pr otection from visibility impairment. 2
The decisions of the court with regard to these three issues are discussed in chapters 2, 3 3 and 4, respectively. The EPA is responding to the c ourt’s remands as part of the current review 4 of the PM NAAQS. 5

1.2.5 Current PM NAAQS Review 6

The EPA initiated the current revi ew of the air quality criteria for PM in June 2007 with a 7 general call for information (72 FR 35462, June 28, 2007). In July 2007, EPA held two “kick8 off” workshops on the primary and seconda ry PM NAAQS, respectively (72 FR 34003 and 9 34005, June 20, 2007). 12 These workshops provided an opportunity for the participants to 10 discuss the key policy-relevant issues ar ound which EPA would structure this PM NAAQS 11 review and the most meaningful new scienc e that would be available to inform our 12 understanding of these issues. 13 Based in part on the workshop discussions , EPA developed a draft IRP outlining the 14 schedule, process, and key policy-relevant questi ons that would guide the evaluation of the air 15 quality criteria for PM and the review of the primary and secondary PM NAAQS. On November 16 30, 2007, EPA held a consultation with CASAC 13 on the draft IRP (72 FR 63177, November 8, 17 2007), which included the opportunity for public comment. The final IRP (US EPA, 2008a) 18 incorporated comments from CASA C and the public on the draft plan as well as input from 19 senior Agency managers. 20 As part of the process of pr eparing the PM ISA, NCEA hoste d a peer review workshop in 21 June 2008 on preliminary drafts of key ISA chapters (73 FR 30391, May 27, 2008). The first 22 external review draft ISA (US EPA, 2008b) wa s reviewed by CASAC and the public at a 23 meeting held in April 2009 (74 FR 2688, Febr uary 19, 2009). Based on CASAC and public 24 comments, NCEA prepared a second draft ISA (US EPA, 2009b), which was reviewed by 25 CASAC and the public at a meeting held on October 5-6, 2009 (74 FR 46586, September 10, 26 2009). Based on CASAC and public comments, NCEA prepared the final ISA (US EPA, 27 2009a; 74 FR 66353, December 15, 2009). 28 In preparing the REA documents that build on the scientific evidence presented in the 29 ISA, OAQPS released two planning documents: Particulate Matter National Ambient Air 30

12 See workshop materials http://www.regulations.gov/s earch/Regs/home.html#home Docket ID numbers EPA-HQOAR-2007-0492-008; EPA-HQ-OAR-2007-0492-009; EPA-HQ-OAR-2007-0492-010; and EPA-HQ-OAR-2007- 0492-012.
13 The CASAC PM NAAQS Review Panel was consitituted to perform the statutorily required review of the criteria and standards for this review of the PM NAAQS. Fo r more information on the CASAC PM Panel, see http://yosemite.epa.gov/sab/sabpeople.nsf/WebCommi tteesSubcommittees/CASAC%20Particulate%20Matter%20R eview%20Panel.D raft Do Not Quote or Cite 1-12 March 2010 Quality Standards: Scope and Methods Plan for Health Risk and Exposure Assessment and 1
Particulate Matter National Am bient Air Quality Standards: Sc ope and Methods Plan for Urban 2 Visibility Impact Assessment (henceforth, Scope and Methods Plans, US EPA, 2009c,d). These 3 planning documents outlined the scope and approaches that staff planned to use in conducting 4 quantitative assessments as well as key issues that would be addressed as part of the assessments. 5 In designing and conducting the in itial health risk and visibility impact assessments, we 6 considered CASAC comments (Sam et 2009a,b) on the Scope and Me thods Plans made during an 7 April 2009 consultation (74 FR 1158 0, March 18, 2009) as well as public comments.. Two draft 8 assessment documents, Risk Assessment to Support the Review of the PM 2.5 Primary National 9 Ambient Air Quality Standards: External Review Draft - September 2009 (US EPA 2009e) and 10
Particulate Matter Urban-Focused Visibili ty Assessment - External Review Draft - September 11 2009 (US EPA, 2009f) were reviewed by CASAC and the public at a meeting held on October 5- 12 6, 2009. Based on CASAC (Samet 2009c,d) and pub lic comments, OAQPS staff revised these 13
draft documents and released second draft asse ssment documents (US EPA, 2010a,b) in January 14 and February 2010 (75 FR 4067, January 26, 2010) for CASAC and public review at an 15 upcoming meeting to be held on March 10-11, 2010. 16 A preliminary draft PA (US EPA, 2009g) was released in September 2009 for 17 informational purposes and to facilitate disc ussion with CASAC at the October 5-6, 2009 18 meeting on the overall structure, area s of focus, and level of detail to be included in the PA. This 19
first draft PA reflects consid eration of CASAC’s comments on the preliminary draft that 20 encouraged the development of a document focuse d on the key policy-relevant issues that draws 21 from and is not repetitive of in formation in the ISA and REAs. This first draft PA draws from 22 the information presented in the final ISA and the two second draft assessment documents. We 23 plan to present an overview of this documen t at the upcoming CASA C meeting on March 10-11, 24 2010, and CASAC and public review of this document will occur during an upcoming 25 teleconference to be held on April 8-9, 2010 (75 FR 8062, February 23, 2010). We will consider 26 CASAC and public comments on this first draft PA and on the two draft REAs in preparing a 27 second draft PA, which will be released for CASAC and public review. 28

1.3 GENERAL APPROACH AND ORGANI ZATION OF THIS DOCUMENT 29
This first draft PA includes staff’s prelim inary evaluation of the policy implications of 30 the scientific assessment of the evidence presented in the ISA and the results of quantitative 31 assessments based on that evidence presented in the second draft REAs. Taken together, this 32 information informs preliminary staff conclusion s and the identification of policy options for 33 consideration in addressing public health and welfare effects associated with exposure to ambient 34
PM. 35D raft Do Not Quote or Cite 1-13 March 2010 Since the last review, much new informati on is now available on PM air quality and 1
human health effects di rectly in terms of PM 2.5 and, to a much more limited degree, PM 10-2.5 and 2 ultrafine particles (UFPs). Since the purpose of this review is to evaluate the adequacy of the 3 current standards, which separately address fine and thoracic coar se particles, staff is focusing 4 this policy assessment and associated quantitativ e analyses primarily on the evidence related 5 directly to PM 2.5 and PM 10-2.5 . In so doing, we are considering PM 10 -related evidence primarily 6 to help inform our understanding of key issues and to help interpret and provide context for 7 understanding the public health and welfare impacts of ambient fine and coarse particles. We are 8 also considering the currently available evidence related to UFPs as well as PM 2.5 components to 9 aid in considering whether or not there is support to consider standards with a different size 10
fraction and/or distinct standard s focused on regulating specific PM 2.5 components or categories 11 of fine particle sources. 12 Following this introductory chapter, this doc ument is organized into two main parts: 13 review of the primary PM NAAQS (chapters 2 a nd 3) and review of the secondary PM NAAQS 14 (chapters 4 and 5). Chapters 2 and 3 present staff observations and preliminary conclusions 15 related to review of the primary standards for fine and thoracic coarse particles, respectively. 16 Each chapter begins with a discussion of policy assessment approaches and focuses on both 17 evidence-based and quantitative risk-based cons iderations. Preliminary staff conclusions are 18 presented with regard to the adequacy of the cu rrent primary standards an d potential alternative 19 primary standards for considerati on, in terms of indicators, averag ing times, forms, and levels. 20 Chapter 4 focuses on PM-related visibility impa irment, and presents staff observations and 21 preliminary conclusions with regard to the ad equacy of the current standards and potential 22 distinct secondary standards for consideration, in terms of altern ative indicators, averaging times, 23 forms, and levels. Chapter 5 focuses on other PM-related welfare effect s, including effects on 24 climate, ecological effects, and effects on ma terials, and presents staff observations and 25 preliminary conclusions with regard to the adequa cy of the current standards and the extent to 26 which information is available to support consideration of alte rnative standards. 27D raft Do Not Quote or Cite 1-14 March 2010 1.4 REFERENCES 1

Abt Associates (2005). Particulate Matter Health Risk Assessment for Selected Urban Areas. Final Report. 2 Bethesda, MD. Prepared for the Office of Air Qu ality Planning and Standards, U.S. Environmental 3 Protection Agency, Contract No. 68-D-03-002. EPA 452/R-05-007A. Available: 0 4

Henderson, R. (2005a). EPA’s Review of the Nationa l Ambient Air Quality Standards for Particulate Matter 5 (Second Draft PM Staff Paper, January 2005): A review by the Particulate Matter Review Panel of the EPA 6 Clean Air Scientific Advisory Committee. June 6, 2005. Available: http://www.epa.gov/sab/pdf/casac-05- 7 007.pdf

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Henderson, R. (2005b). Clean Air Scientific A dvisory Committee (CASAC) Re view of the EPA Staff 9 Recommendations Concerning a Potential Thoracic Coarse PM Standard in the Review of the National 10 Ambient Air Quality Standards for Particulate Matte r: Policy Assessment of Scientific and Technical 11 Information (Final PM OAQPS Staff Paper, EPA-452/R-05-005). September 15, 2005. Available: 12 http://www.epa.gov/sab/panels/casacpmpanel.html

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Henderson, R. (2006a). Letter from Dr. Rogene Henderso n, Chair, Clean Air Scientific Advisory Committee to the 14 Honorable Stephen L. Johnson, Administrator, US EPA. Clean Air Scientific Advisory Committee 15 Recommendations Concerning the Proposed National Ambient Air Quality Standards for Particulate 16 Matter. March 21, 2006. Available: h ttp://www.epa.gov/sab/pdf/ casac-ltr-06-002.pdf 17

Henderson, R.; Cowling, E.; Crapo, J.D..; Miller, F. J.; Poirot, R.L.; Speizer, F. ; Zielinska, B. (2006b). Letter from 18 Clean Air Scientific Advisory Committee to the Honorable Stephen L. Johnson, Administrator, US EPA. 19 Clean Air Scientific Advisory Committee Recommendati ons Concerning the Final National Ambient Air 20 Quality Standards for Particulate Matter. September 29, 2006. Available: 21 http://www.epa.gov/sab/pd f/casac-ltr-06-002.pdf 22

Jackson (2009). Memo from Administrator Lisa P. Jackson to Elizabeth Craig, Acting Assistant Administrator for 23 OAR and Lek Kadeli, Acting Assistant Administrator for ORD. Process for Reviewing the National 24 Ambient Air Quality Standards. May 21, 2009. Available: 25 http://www.epa.gov/ttn/naaqs/pdfs/N AAQSReviewProcessMemo52109.pdf

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Samet, J. (2009a). Letter from Clean Air Scientific Advisory Committee to the Honorable Lisa P. Jackson, 27 Administrator, US EPA. Consultation on EPA’ s Particulate Matter National Ambient Air Quality 28 Standards: Scope and Methods Plan for Health Risk and Exposure Assessment. May 21, 2009. Available: 29 http://yosemite.epa.gov/sab/sabproduct.nsf/723 FE644C5D758DF852575B D00763A32/$File/EPA30 CASAC-09-009-unsigned.pdf 31

Samet, J. (2009b). Letter from Clean Air Scientific Advisory Committee to the Honorable Lisa P. Jackson, 32 Administrator, US EPA. Consultation on EPA’ s Particulate Matter National Ambient Air Quality 33 Standards: Scope and Methods Plan for Urban Visib ility Impact Assessment. May 21, 2009. Available: 34 http://yosemite.epa.gov/sab/sabproduct.nsf/0F63D 7995F5850D5852575BD0077869C/$File/EPA-CASAC35 09-010-unsigned.pdf 36

Samet, J. (2009c). Letter from Clean Air Scientific Advisory Committee to the Honorable Lisa P. Jackson, 37 Administrator, US EPA. Review of the Risk Assessm ent to Support the Review of the Particulate Matter 38 (PM) Primary National Ambient Air Quality Standard s – External Review Draft (September 2009). 39 November 24, 2009. Available: 40 http://yosemite.epa.gov/sab/sabproduct.nsf/B C1ECC5D539EF72385257678006D5754/$File/EPA41 CASAC-10-003-unsigned.pdf 42

Samet, J. (2009d). Letter from Clean Air Scientific Advisory Committee to the Honorable Lisa P. Jackson, 43 Administrator, US EPA. Review of Particulate Matter Urban-Focused Visibility Assessment (External 44D raft Do Not Quote or Cite 1-15 March 2010 Review Draft, September 2009). November 24, 2009. Available: 1 http://yosemite.epa.gov/sab/sabproduct.nsf/15872217938041F685257678006A26E3/$File/EPA-CASAC2 10-002-unsigned.pdf 3

US Department of Health, Education and Welfare (DHEW) . (1969). Air Quality Criteria for Particulate Matter. 4 U.S. Government Printing Office, Washington DC, AP-49. 5

US EPA (2004). Air Quality Criteria for Particulate Matte r. National Center for Envi ronmental Assessment, Office 6 of Research and Development, U.S. Environmental Protection Agency, Research Triangle Park, NC 27711; 7 report no. EPA/600/P-99/002aF and EPA/600/P-99/002bF. October 2004. Available: 8 http://www.epa.gov/ttn/naaqs/standards/pm/s_pm_cr_cd.html 9

US EPA (2005). Review of the National Ambient Air Qua lity Standards for Particulate Matter: Policy Assessment 10 of Scientific and Technical Information, OAQPS Staff Paper. Research Triangle Park, NC 27711: Office 11 of Air Quality Planning and Standa rds; report no. EPA EPA-452/R-05-00 5a. December 2005. Available: 12 http://www.epa.gov/ttn/naaqs/standards/pm/s_pm_cr_sp.html 13

US EPA (2008a). Integrated Review Plan for the Nationa l Ambient Air Quality Standards for Particulate Matter. 14 National Center for Environmental Assessment and Office of Air Quality Planning and Standards, U.S. 15 Environmental Protection Agency, Research Triangle Park, NC. Report No. EPA 452/R-08-004. March 16 2008. Available at: http://www.epa.gov/ttn/naaqs/standards/pm/s_pm_2007_pd.html

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US EPA (2008b). Integrated Science Assessment for Par ticulate Matter: First External Review Draft. National 18 Center for Environmental Assessment-RTP Division, Office of Air Quality Planning and Standards, 19 Research Triangle Park, NC. EPA/600/R-08/1 39 and 139A. December 2008. Available: 20 http://www.epa.gov/ttn/naaqs/standards/pm/s_pm_2007_isa.html

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US EPA (2009a). Integrated Scien ce Assessment for Particulate Matter: Final Report. National Center for 22 Environmental Assessment-RTP Division, Office of Air Quality Planning and Standards, Research 23 Triangle Park, NC. EPA/600/R-08/139F. December 2009. Available: 24 http://www.epa.gov/ttn/naaqs/standards/pm/s_pm_2007_isa.html

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US EPA (2009b). Integrated Science Assessment for Par ticulate Matter: Second External Review Draft. National 26 Center for Environmental Assessment-RTP Division, Office of Air Quality Planning and Standards, 27 Research Triangle Park, NC. EPA/600/R-08/139B. July 2009. Available: 28 http://www.epa.gov/ttn/naaqs/standards/pm/s_pm_2007_isa.html

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US EPA (2009c). Particulate Matter National Ambient Air Qu ality Standards: Scope and Methods Plan for Health 30 Risk and Exposure Assessment. Office of Air Quality Planning and Standards, U.S. Environmental 31 Protection Agency, Research Triangle Park, NC. EPA-452/P-09-002. February 2009. Available: 32 http://www.epa.gov/ttn/naaqs/standards/pm/s_pm_2007_pd.html

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US EPA (2009d). Particulate Matter National Ambient Air Quality Standards: Scope and Methods Plan for Urban 34 Visibility Impact Assessment. Office of Air Qua lity Planning and Standards, U.S. Environmental 35 Protection Agency, Research Triangle Park, NC. EPA-452/P-09-001. February 2009. Available: 36 http://www.epa.gov/ttn/naaqs/standards/pm/s_pm_2007_pd.html

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US EPA (2009e). Risk Assessment to Support the Re view of the PM Primary National Ambient Air Quality 38 Standards - External Review Draft. Office of Air Qu ality Planning and Standards, U.S. Environmental 39 Protection Agency, Research Triangle Park, NC. EPA-452/P-09-006. September 2009. Available: 40 http://www.epa.gov/ttn/naaqs/standards/pm/s_pm_2007_risk.html

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US EPA (2009f). Particulate Matter Ur ban-Focused Visibility Assessment – Exte rnal Review Draft. Office of Air 42 Quality Planning and Standards, U.S. Environmenta l Protection Agency, Research Triangle Park, NC. 43D raft Do Not Quote or Cite 1-16 March 2010 EPA-452/P-09-005. September 2009. Available: 1 http://www.epa.gov/ttn/naaqs/standards/pm/s_pm_2007_risk.html

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US EPA (2009g). Policy Assessment for the Review of the Particulate Matter National Ambient Air Quality 3 Standards – Preliminary Draft. Office of Air Qu ality Planning and Standards, U.S. Environmental 4 Protection Agency, Research Triangle Park, NC. EPA-452/P-09-007. September 2009. Available: 5 http://www.epa.gov/ttn/naaqs/standards/pm/s_pm_2007_pa.html

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US EPA (2010a). Quantitative Risk Assessment for Partic ulate Matter – Second External Review Draft. Office of 7 Air Quality Planning and Standards, U.S. Environmental Protection Agency, Research Triangle Park, NC. 8 EPA-452/P-10-001. February 2010. Available: 9 http://www.epa.gov/ttn/naaqs/standards/pm/s_pm_2007_risk.html

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US EPA (2010b). Particulate Matter Urban-Focused Visib ility Assessment – Second External Review Draft. Office 11 of Air Quality Planning and Standards, U.S. Enviro nmental Protection Agency, Research Triangle Park, 12 NC. EPA-452/P-10-002. January 2010. Available: 13 http://www.epa.gov/ttn/naaqs/standards/pm/s_pm_2007_risk.html

. 14Draft Do Not Quote or Cite March 2010 2-1 

### 2 REVIEW OF THE PRIMARY STA NDARDS FOR FINE PARTICLES 1

This chapter presents preliminary staff conclu sions with regard to the adequacy of the 2 current suite of primary PM 2.5 standards and the alternative prim ary standards for fine particles 3 that are appropriate for consideration in this revi ew. Our assessment of these issues is framed by 4 a series of key policy-relevant questions, whic h expand upon those presente d in the Integrated 5 Review Plan (IRP) (US EPA, 2008a) at the outset of this review. The answ ers to these questions 6 will inform decisions on whether, and if so how, to revise the current suite of primary fine 7 particle standards. 8
Staff notes that final decisions regarding the primary standa rds must draw upon scientific 9 information and analyses about health effects and risks, as well as judgments about how to deal 10 with the range of uncertainties that are inhere nt in the scientific evidence and analyses. 11 Ultimately, the final decisions are largely public health policy judgments. Our approach to 12 informing these judgments, discussed more fully below, recognizes that the available health 13 effects evidence generally reflects a continuum cons isting of ambient levels at which scientists 14 generally agree that health eff ects are likely to occur through lower levels at which the likelihood 15 and magnitude of the response b ecome increasingly uncertain 16 Our current approach for reviewing the primar y standards for fine particles is presented 17 in section 2.1. Our preliminary conclusions re garding the adequacy of the current suite of 18 primary PM 2.5 standards are presented in section 2.2, focusing on both evidence-based and 19 quantitative risk-based considera tions. Section 2.3 presents our initial conclusions with respect 20 to alternative fine particle sta ndards, focusing on each of the basi c elements of the standards: 21 pollutant indicator (section 2.3.1), averaging time (s ection 2.3.2), form (secti on 2.3.3), and level. 22 We have evaluated separately th e protection that a suite of PM 2.5 standards with alternative levels 23 would likely provide against e ffects associated with long-te rm exposures (section 2.3.4) and 24 short-term exposures (section 2.3.5). These separate evaluations provide the basis for 25 preliminary integrated conclusions on alternativ e suites of standards th at would appropriately 26 protect against effects associated with both long - and short-term exposures to fine particles 27 (section 2.3.6) Section 2.4 summarizes all prel iminary staff conclusions on the primary fine 28 particle standards. The next draft of this chap ter will conclude with an initial overview of key 29 uncertainties and suggested future research ar eas and data collection efforts (section 2.5). 30

2.1 APPROACH 31 Staff’s approach for reviewing the current primary PM 2.5 standards builds upon and 32 broadens the approaches used in previous PM NAAQS reviews. Our current approach is based 33 on the updated scientific and technical inform ation presented in the Integrated Science 34Draft Do Not Quote or Cite March 2010 2-2 Assessment (ISA) and second draft quantitative ri sk assessment (RA). These assessments take 1 into consideration the currently available scientific information as well as enhanced tools and 2 methods for informing the current review. 3 The past and current approaches described below are all based most fundamentally on 4 using information from epidemiological studies to inform the selection of PM standards that, in 5 the Administrator’s judgment, protect public health with an adequate margin of safety. Such 6 information can be in the form of air quality di stributions over which health effect associations 7 have been observed, or in the form of concentr ation-response functions th at support quantitative 8 risk assessment. However, evidence- and ri sk-based approaches using information from 9 epidemiological studies to inform decisions on PM standards are complicated by the recognition 10 that no population threshold, below which it can be concluded with confidence that PM-related 11 effects do not occur, can be discerned from the av ailable evidence. As a result, any approach to 12 reaching decisions on what standards are appropria te necessarily requires judgments about how 13
to translate the information available from the epidemiological studies into a basis for 14 appropriate standards, which incl udes consideration of how to wei gh the uncertainties in reported 15
associations across the distributio ns of PM concentrations in the studies or in quantitative 16 estimates of risk. Such approaches are consistent with setting standards th at are neither more nor 17 less stringent than necessary, rec ognizing that a zero-risk standard is not required by the CAA. 18

2.1.1 Approaches Used in Previous Reviews 19 Staff has considered policy assessment approa ches used in past reviews to inform the 20 approach we are using in this review to reach preliminary conclusions regarding the adequacy of 21
the current standard and alternative standards that are appropriate to consider in this review. We 22 begin this section with a review of the approach used to set the orig inal fine particle standards in 23 1997 (section 2.1.1.1). The approach used to review and ultimately support revisions to these 24
standards in 2006 is discussed in section 2.1.1.2. L itigation related to the standards finalized in 25 2006, including the remand of the primary PM 2.5 annual standard are then discussed in section 26
2.1.1.3. 27

2.1.1.1 Review Completed in 1997 28

In setting the 1997 primary PM 2.5 annual and 24-hour standards, the Agency relied 29 primarily on an evidence-based approach that focused on epidemiological evidence, especially 30 from short-term exposure studies of fine particle s judged to be the strongest evidence at that 31 time. The EPA did not place much weight on qua ntitative risk estimates from the very limited 32 risk assessment conducted, but did conclude that the assessment results confirme d the general 33 conclusions drawn from the epidemiological evid ence that a serious public health problem was 34Draft Do Not Quote or Cite March 2010 2-3 associated with ambient PM levels allowed under the then current PM 10 standards (62 FR 1 38665/1, July 18, 1997). 2 The EPA considered the epidemiological ev idence and data on air quality relationships 3
to set an annual PM 2.5 standard that was intended to be the “generally controlling” standard; i.e., 4 the primary means of lowering both long- and short-term ambient co ncentrations of PM 2.5
. 1 In 5 conjunction with the annual standard , EPA also established a 24-hour PM 2.5 standard to provide 6 supplemental protection against da ys with high peak concentrati ons, localized “hotspots,” and 7 risks arising from seasonal emissions that mi ght not be well controlled by a national annual 8 standard. (62 FR 38669/3). Recogni zing that there are various ways to combine two standards to 9 achieve an appropriate degree of public health protection, such as an approach that only 10 considered short- and long-term exposure evidence, analyses, a nd standards independently, EPA 11
concluded that the selected a pproach based on a generally cont rolling annual standard was the 12 most effective and efficient approach. This conclusion was based in part on one of the key 13 observations from the quantitative risk assessment, that much if not most of the aggregate annual 14 risk associated with short-term exposures result s from the large number of days during which the 15 24-hour average concentrations are in the low- to mid-range, below the peak 24-hour 16 concentrations. As a result, loweri ng a wide range of ambient 24-hour PM 2.5 concentrations by 17 means of a generally controlling annual standa rd, as opposed to focusing on control of peak 24- 18 hour concentrations, was determined to be the mo st effective and efficient way to reduce total 19 population risk (62 FR 38670 to 38671). 20 In setting the level of the annual standard in 1997, EPA first determined a level for the 21 annual standard based on the short-term exposur e studies, and then considered whether the key 22 long-term exposure studies suggested the need for a lower level. While recognizing that health 23 effects may occur over the full ra nge of concentrations observed in the studies, EPA concluded 24 that the strongest evidence for short-term PM 2.5 -related effects occurs at concentrations near the 25 long-term (e.g., annual) average in the short-term exposure studies. Given the serious nature of 26 the potential effects, EPA selected a level for the annual standard at or below the long-term mean 27 concentrations in studies providing evidence of a ssociations with short- term exposures, placing 28 greatest weight on those short-term exposure studie s that reported clearly statistically significant 29 associations with mortality and morbidity effect s (62 FR 38676/1). Further consideration of the 30

1 In so doing, EPA noted that an annual standard would focus control programs on annual average PM 2.5concentrations, which would generally control the overall distribution of 24-hour exposure levels, as well as longterm exposure levels, and would also result in fewer and lower 24-hour peak concentrations. Alternatively, a 24- hour standard that focused controls on peak concentrations could also result in lower annual average concentrations. Thus, EPA recognized that either standard could provide some degree of protection from both short- and long-term exposures, with the other standard serving to address situ ations where the daily peaks and annual averages are not consistently correlated (62 FR 38669).Draft Do Not Quote or Cite March 2010 2-4 average PM 2.5 concentrations across the ci ties in the key long-term exposure studies of mortality 1 and respiratory effects in children did not pr ovide a basis for establishing a lower annual 2
standard level. Because the annual standard level selected was below the range of annual 3 concentrations most strongly associated with bo th short- and long-term exposure effects, and 4 because even small changes in annual means in th is concentration range could make significant 5
difference in overall risk reduction and total population exposures, EPA concluded that this 6 standard would provide an ade quate margin of safety agai nst effects observed in these 7 epidemiological studies (62 FR 68676/3). 8
The selection of the level of the annual standard was done in conjunction with having 9
first selected the form of the annual standard to be based on th e concentration measured at a 10 single monitor sited to represent community-wid e air quality, or a va lue resulting from an 11 average of measurements from multiple commun ity-wide air quality monitoring sites that met 12 specific criteria and constraints (“spatial averaging”). This decision emphasized consistency 13 with the types of air quality measurements that were used in the relevant epidemiological studies. 14 In reaching this decision, EPA recognized the im portance of ensuring that spatial averaging 15 would not result in inequities in th e level of protection provided by the PM 2.5 standards in some 16 areas. Because the annual standard, defined in terms of single or averaged community-wide air 17 quality monitoring sites, could not be expected to offer an adequate margin of safety against the 18 effects of all potential short-term exposures in areas with strong local or seasonal sources that 19 could not be directly evaluated in the epidemio logical studies, EPA set the level of the 24-hour 20 standard to supplement the control afforded by the annual standard based on air quality 21 relationships between annual and 24-hour concen trations. This appr oach was intended to 22 provide an adequate margin of safety against in frequent or isolated peak concentrations that 23
could occur in areas that attain the annual standard (62 FR 38677). 24

2.1.1.2 Review Completed in 2006 25

In 2006, EPA used a different evidence-based a pproach to assess the appropriateness of 26
the levels of the 24-hour and annual PM 2.5 standards. Based on an expanded body of 27 epidemiological evidence that was stronger and mo re robust, including both short- and long-term 28 exposure studies, the Administrator decided that using evidence of eff ects associated with 29 periods of exposure that were most closely matc hed to the averaging time of each standard was 30 the most appropriate public health policy approa ch for evaluating the scientific evidence to 31 inform selecting the level of each standard. T hus, the Administrator relied upon evidence from 32 the short-term exposure studies as the principa l basis for selecting th e level of the 24-hour PM 2.5 33 standard, with the 24-hour standard designed to protect against eff ects associated with short-term 34 exposures. The Administrator relied upon evid ence from long-term exposure studies as the 35Draft Do Not Quote or Cite March 2010 2-5 principal basis for selecti ng the level of the annual PM 2.5 standard, with th e annual standard 1 designed to protect agains t effects associated with long-term exposures. 2 With respect to quantitative ri sk-based considerations, the Administrator recognized that 3 the analyses conducted for this review were ba sed on “a more extensive body of data and [was] 4 more comprehensive in scope than the assessmen t conducted in the last review, but was mindful 5 that significant uncertainties c ontinue[d] to underlie the resulti ng risk estimates” (71 FR 61168/2, 6 October 17, 2006). 2 The Administrator determined that the estimates of risks likely to remain 7 upon attainment of the 1997 suite of PM 2.5 standards were indicative of risks that could be 8 reasonably judged important from a public health perspective, and, thus , supported revision of 9 the standards. However, the Administrator j udged that the quantitative risk assessment had 10 important limitations and did not provide an appropr iate basis for selecting either the level of the 11
24-hour or annual PM 2.5 standard (71 FR 61174/1-2). The Ad ministrator more heavily weighed 12 the implications of the uncertainties associated with the quantitative risk assessment than the 13 Clean Air Scientific Advisory Committee (CASAC ) apparently did in their comments on the 14 proposed rulemaking, where CASAC stated, “[w] hile the risk assessment is subject to 15 uncertainties, most of the PM Panel found EPA’s ri sk assessment to be of sufficient quality to 16 inform its recommendations...The risk analyses i ndicated that the uncertainties would increase 17 rapidly below an annual level of 13 μg/m 3 – and that was the basis for the PM Panel’s 18 recommendation of 13 μg/m 3 as the lower bound for the annual PM 2.5 standard level” 19 (Henderson, 2006a, p.3). 20 With regard to final decisions on the primary annual PM 2.5 standard, the Administrator 21 placed the greatest weight for determining the level of the annual sta ndard on the long-term 22
means of the concentrations associated with mo rtality effects in the tw o key long-term exposure 23 studies in the record, the American Cancer Soci ety (ACS) and Harvard Six Cities studies (71 FR 24 at 61172 to 61177). Important vali dation and reanalyses of the original ACS and Harvard Six 25 Cities studies provided “evidence of generally robust associations and provide[d] a basis for 26 greater confidence in the reported associations than in the last review, for example, in the extent 27 to which they have made progress in understand ing the importance of i ssues related to co28 pollutant confounding and the specif ication of statistical models.” Furthermore, the extended 29 ACS study provided “new evidence of morta lity related to lung cancer and further 30

2 Uncertainties identified in the quantitative risk assessment we re generally related to a lack of clear understanding of a number of important factors, including, for example, the shape of concentration-response functions, particularly when, as here, effect thresholds could neither be discerned nor determined not to exist; issues related to selection of appropriate statistical models for the analysis of the epidemiologic data; the role of potentially confounding and modifying factors in the concentration-response relationships; issues related to simulating how PM 2.5 air quality distributions would likely change in any given area upon attaining a particular standard, since strategies to reduce emissions were not yet defined; and whether there would be differential reductions in the many components within PM 2.5 and, if so, whether this would result in differential reductions in risk (71 FR 61168/2).Draft Do Not Quote or Cite March 2010 2-6 substantiate[d] the statistically significant asso ciations with cardiorespiratory-related mortality 1 observed in the original studies ” (71 FR 61172/1-2). The Admini strator also recognized the 2 availability of long-term exposure studies th at provided evidence of respiratory morbidity, 3 including changes in lung func tion measurements and decrease d growth in lung function as 4 reported in the 24-Cities st udy and the Southern California Children’s Health Study, 5 respectively. In retaining the leve l of the annual standard at 15 μg/m 3 , the Administrator selected 6 a level that was “appreciably be low” the long-term average concentrations reported in the key 7 long-term mortality studies and “basically at the same level” as the long-term average 8 concentrations in the key long-term respiratory morbidity studies. In the judgment of the 9 Administrator, the two long-term respiratory mo rbidity studies provided an uncertain basis for 10 setting the level of a national st andard, and therefore, did “not warrant setting a lower level for 11
the annual standard than the level warranted based on the key mortality studies” (71 FR 12 61176/3). 13 In considering the form of the primary annual PM 2.5 standard, the Admini strator retained 14
the form of the standard as an annual arithmetic mean, averaged over 3 years with modifications 15 that strengthen the standard by tightening the cr iteria for use of spatial averaging. Specifically, 16
the Administrator narrowed the ci rcumstances under which spatial averaging may be utilized. 17 Analyses conducted in the review completed in 2006, based on a much larger set of PM 2.5 air 18 quality data than was availabl e for the review completed in 1997, provided evidence concerning 19 the potential for disproportionate impacts on potentially vulnerable subpopulat ions. Specifically, 20 the results of the analyses suggested that “the highest concentrations in an area tend to be 21
measured at monitors located in areas wher e the surrounding population [was] more likely to 22 have lower education and income levels, and hi gher percentages of mi nority populations” (71 FR 23 61166/2, see also US EPA, 2005, section 5.3.6.1; Sc hmidt et al., 2005, Attachment A/Analysis 24 7). 3 25 In deciding to revise th e level of the 24-hour PM 2.5 standard from 65 μg/m 3 to 35 μg/m 3

, 26 the Administrator placed the greatest weight on the much expanded body of evidence from short27 term exposure studies, with a focus on U.S. and Canadian studies that had been reanalyzed, as 28 appropriate, to address st atistical modeling issues and that used relatively reliable air quality 29 data. A comprehensive evaluation considered and weighed a variety of evidence, including 30

3 As summarized in footnote 29 at 71 FR 61166/2, the 2004 AQCD noted that some epidemiologic studies, most notably the ACS study of associations between long-term PM 2.5 exposure and mortality, reported larger effect estimates in the cohort subgroup with lower education levels (US EPA, 2004, p 8-103). The 2004 AQCD also noted that lower education level may be a ma rker for lower socioeconomic status (S ES) that may be related to increased vulnerability to the effects of fine particle exposures, for ex ample, as a result of greater exposure from proximity to sources such as roadways and industry, as well as other fact ors such as poorer health st atus and access to health care (US EPA, 2004, section 9.2.4.5).Draft Do Not Quote or Cite March 2010 2-7 biological plausibility of asso ciations between various polluta nts and health outcomes, and 1 focused on the stability of the size of the effect estimates in time-series studies using both single2 and multi-pollutant models, rather than just looki ng at statistical significance in a large number 3 of alternative models to simplistically delineate between real and suspect associations (71 FR 4 61170/2). Emphasis was placed on those studies that provided evidence of statistically 5 significant associations in areas that would have met the then current annual and 24-hour PM 2.5 6 standards during the time of the study. The Administrator recogni zed that these studies provided 7
no evidence of clear effect thresholds or lowest-o bserved effect levels. Nonetheless, in focusing 8
on the 98 th percentile air quality values in these studies, the Admi nistrator sought to establish a 9 standard level that would require improvements in air quality generally in areas in which the 10 distribution of daily short-term exposure to PM 2.5 could reasonably be expected to be associated 11
with serious health effects. The Administrator recognized th at although future air quality 12 improvement strategies in any pa rticular area were not yet define d, most such strategies were 13 likely to move a broad distribution of PM 2.5 air quality values in an area lower, resulting in 14
reductions in risk associat ed with exposures to PM 2.5 levels across a wide ra nge of concentrations 15 and not just at the 98 th percentile concentra tions (71 FR 61168/3). 16

2.1.2 Remand of Primary Annual PM 2.5 Standard 17 As noted above in section1.2.4, several par ties filed petitions for review following 18 promulgation of the revised PM NAAQS in 2006. These petitions challenged several aspects of 19 the final rule including the selection of the level of the primary PM 2.5 annual standard. More 20 specifically, petitioners repr esenting environmental groups (American Lung Association, 21 Environmental Defense, and the National Parks C onservation Association) and several states and 22 state agencies argued that the decision to retain the level of the annual PM 2.5 standard at 15 23 μg/m 3 was “arbitrary, capricious, an abuse of di scretion, or otherwise not in accordance with 24 law.” 42 U.S.C. 7607(d)(9). The primary 24-hour PM 2.5 standard was not challenged by any of 25 the litigants and, thus, not considered in the court’s review and final decision. 26 On judicial review, the D.C. Ci rcuit remanded the primary annual PM 2.5 NAAQS to EPA 27 because the Agency failed to adequately explai n why the annual standard provided the requisite 28 protection from both short- and l ong-term exposures to fine pa rticles including protection for 29 susceptible populations. American Farm Bureau Federation v. EPA, 559 F. 3d 512 (D.C. Cir. 30 2009). With respect to human hea lth protection from short-term PM 2.5 exposures, the court 31 considered the different approaches used by EPA in the 1997 and 2006 PM NAAQS decisions as 32
summarized above. The court found that EPA fa iled to adequately explain why a 24-hour PM 2.5 33 standard by itself would provide the protection needed from shor t-term exposures and remanded 34
the annual PM 2.5 standard to EPA “for further considera tion of whether it is set at a level 35Draft Do Not Quote or Cite March 2010 2-8 requisite to protect the public health while provid ing an adequate margin of safety from the risk 1 of short-term exposures to PM 2.5 .” American Farm Bureau Fe deration, 559 F. 3d at 520-24. 2 With respect to protection from long-term expos ure to fine particles, the court found that 3 EPA failed to adequately explain how the current primary annual PM 2.5 standard provided an 4 adequate margin of safety for children and ot her susceptible populations. The court found that 5 EPA did not provide a reasonabl e explanation of w hy certain morbidity studies, including a 6 study of children in Southern California show ing lung damage associat ed with long-term PM 2.5 7 exposure (Gauderman et.al, 2000) and a multi-city study (24-Cities Study) evaluating decreased 8 lung function in children a ssociated with long-term PM 2.5 exposures (Raizenne et al., 1996), did 9 not call for a more stringent annual PM 2.5 standard. Id. at 522-23. Specifically, the court found 10
that: 11
12 EPA was unreasonably confident that, even though it relied so lely upon long-term 13 mortality studies, the revised standard would provide an adequate margin of safety with 14 respect to morbidity among children. Notably absent from the final rule, moreover, is 15 any indication of how the standard will adequate ly reduce risk to the elderly or to those 16 with certain heart or lung diseases despite (a) the EPA’s determination in its proposed 17 rule that those subpopulations ar e at greater risk from exposur e to fine particles and (b) 18 the evidence in the record supportin g that determination. Id. at 525. 19 20 Petitioners also objected to the EPA analysis of the long-term exposure studies arguing 21 that the EPA “unreasonably focused” upon the lo ng-term mean ambient concentrations of PM 2.5 22 in the ACS (17.7 μg/m 3 ) and the Harvard Six Cities Study (18 μg/m 3 ) and then set a level below 23
those concentrations for the annual PM 2.5 standard. Specifically, thes e petitioners claimed that 24 “this approach violates the re quirement of the Clean Air Act (CAA) that the NAAQS provide ‘an 25 adequate margin of safety’ which requires that EPA ‘err on the side of caution’” and argued that 26
the level of the annual standard should be revised lower because the most recent data from these 27
studies “showed adverse health effects in years when the mean ambient concentration of PM 2.5 28 was below 15 μg/m 3 .” Id. at 526. The court rejected th ese arguments stating: “The EPA, 29 mindful of its obligation to set a standard ‘not lower or highe r than is necessary...to protect 30 public health,’ Whitman, 531 U.S. at 475-76, reasonably decided to address long-term mean 31 concentrations in the ACS and Six Cities studies...We approved a similar approach to assuring 32 an adequate margin of safety in ATAIII and we do so again here.” Id. at 527. 33 Petitioners also challenged the Agency’s deci sion not to rely upon the quantitative risk 34 assessment in making final decisions on the level of the primary annual PM 2.5 standard. More 35 specifically, these petitioners ar gued that “[b]oth CASAC and EPA staff concluded that the 36 Agency’s risk assessment ... was of sufficient quality to deserve consideration in determining 37 the level of the annual standard necessary to prov ide an adequate margin of safety” and that, in 38Draft Do Not Quote or Cite March 2010 2-9 retaining the level of the annual standard at 15 μg/m 3 significant public health impacts remained 1 (State brief, pp. 22 to 23). The court rejected arguments that EPA was co mpelled to use a risk2 based approach to determine the level of the sta ndards, or otherwise compelled to use the risk 3 assessment quantitatively in the standard-setti ng process, concluding that EPA “reasonably 4 analyzed the risk assessment,” a nd deferred to the EPA’s assessment of “scientific data within its 5 technical expertise.” Id at 529-530. 6 In remanding the primary annual standard for reconsideration, the c ourt did not vacate the 7
annual standard. Id. at 530. 8

2.1.3 Current Approach 9 Staff’s approach in this review is founde d on a much expanded body of epidemiological 10 evidence, more extensive air quality data a nd analyses, and a more comprehensive risk 11
assessment relative to the information available in past reviews. As a result, our approach to 12 reaching conclusions about the adequacy of the current suite of PM 2.5 standards and potential 13
alternative standards that are a ppropriate for consideration is br oader and more integrative than 14 in past reviews. Our approach takes in to account both evidence-based and risk-based 15 considerations, and the uncertain ties related to both types of information, to inform the 16 preliminary conclusions presented in this first dr aft Policy Assessment (PA). In so doing, we are 17 seeking to provide as broad an array of options as is supportable by the available information, 18 recognizing that the selection of a specific approach to reaching final decisions on the primary 19

PM 2.5 standards will reflect the judgm ents of the Administrator as to what weight to place on the 20 various approaches and types of info rmation presented in the final PA. 21 As an initial matter, we believe it is most appropriate to consider the protection against 22

PM 2.5 -related mortality and morbidit y effects, associated with both long- and short-term 23 exposures, afforded by the annual and 24-hour standa rds taken together, rather than to consider 24 each standard separately. In so doing, we look at the types of evidence that can inform each 25 standard, then integrate the results of those cons iderations to reach preliminary conclusions about 26
the current and alternativ e suites of standards. This a pproach reflects the recognition that 27 changes in PM 2.5 air quality designed to meet an annual standard would likel y result not only in 28 lower annual average concentrations but also in fewer and lower peak 24-hour concentrations. 29 Conversely, we recognize that changes designed to meet a 24-hour standard would result not 30 only in fewer and lower peak 24-hour concentr ations but also in lower annual average 31 concentrations, especially to the extent that chan ges of a more regional, ra ther than local, nature 32
occur. The extent to which these two standard s are interrelated in any given area depends in 33 large part on the relative levels of the standa rds, the peak-to-mean ra tios that characterize air 34Draft Do Not Quote or Cite March 2010 2-10 quality patterns in an area, and whether changes in air quality designed to meet a given suite of 1 standards is of a more regiona l or more localized nature. 2 Our consideration of the protection afforded by the current and alternative suites of 3
standards focuses first on PM 2.5 -related health effects associated with long-term exposures, for 4 which quantitative estimates of risk s to public health are appreciably larger; we then also focus 5 on effects associated with short-term exposures . In both cases, we pl ace greatest weight on 6 associations that have been judged in the IS A to be causal and likely causal, while also 7 considering associations judged to be suggestive of a causal relati onship or that focus on specific 8 susceptible populations. We focus on studies conducted in the U.S. and Canada and place 9 relatively greater weight on statistically significant associations that yield relatively more precise 10 effect estimates and that are judged to be r obust to confounding by other ai r pollutants. In the 11 case of short-term exposure studies, we place gr eatest weight on large multi-city studies, while 12 also considering associations in single-city studies. 13 As part of our evidence-based approach, we first evaluate the evidence from long-term 14 exposure studies, as well as the uncertainties a nd limitations in that evidence, to assess the 15 degree to which the current and alternative suites of standards can be expected to protect against 16 effects related to long-term exposures. As in pa st reviews, we believe this evidence can most 17 directly help inform consideration of the protection afforded by an annual PM 2.5 standard. In 18 evaluating the long-term exposure evidence, we look at the aggregate long-term mean PM 2.5 19 concentration in each study, the range of long-term mean PM 2.5 concentrations across cities, and 20 the distribution of city-specific m eans in terms of the standard devi ation or interquartile range, to 21
the extent such data are available. In cons idering the adequacy of the current suite of PM 2.5 22 standards in protecting agains t long-term exposure-related e ffects, we consider whether 23 associations from long-term exposure studies ha ve been reported across areas in which the 24 aggregate long-term study mean c oncentrations are at or below the level of the current annual 25
standard. We conclude that su ch long-term exposure studies can reasonably be viewed as calling 26 into question the adequacy of the current annual standard. 27 In considering what alternative standards w ould be protective against effects observed in 28 such long-term exposure studies, we first note th e absence of any discer nable threshold within 29 the range of long-term mean con centrations reported in the long -term exposure studies. While 30 recognizing that health effects may occur over the full range of concentrations observed in the 31 studies, we believe that it is reasonable to conclude that the evidence of association is strongest 32 down to somewhat below the aggregate mean concentration, such as down to one standard 33
deviation below the mean or to the lower end of the interquartile range, which includes the range 34 in which the data in the study are most concentr ated. We also believe it is appropriate to 35 consider the long-term mean con centration at the point where th e confidence interval becomes 36Draft Do Not Quote or Cite March 2010 2-11 notably wider, suggestive of a concentration be low which the association becomes appreciably 1 more uncertain and the possibility that an e ffects threshold may exist becomes more likely. 2 Based on these considerations, we identify a range of a lternative annual standard levels that we 3 judge to be appropriate to cons ider for protecting against PM 2.5 -related long-term exposure 4
effects based on the evidence available in this review. 5
We next evaluate the evidence from short- term exposure studies, as well as the 6 uncertainties and limitations in that evidence, to assess the degree to which the current and 7
alternative suites of standards can be expected to protect agains t effects related to short-term 8 exposures. As in past reviews, it is staff’s view that this eviden ce can help inform consideration 9 of the protection afforded by bot h an annual and 24-hour standard. 4 In evaluating the short-term 10 exposure evidence, we look both at the aggregate long-term mean PM 2.5 concentrations in key 11
studies as well as the di stributions of 24-hour PM 2.5 concentrations, with a focus on the 98 th 12 percentile concentrations to match the form of th e current 24-hour standard, to the extent such 13
data are available. In evaluati ng the short-term exposure studies to help inform consideration of 14 the protection afforded by an annual PM 2.5 standard, we observe, based on quantitative risk 15 assessments conducted in past reviews, that much of the risk related to daily exposures, when 16 aggregated on an annual basis, results from th e large number of days during which the 24-hour 17 average concentrations are in the low- to mid-rang e of the entire distribution. Thus, to reduce the 18 aggregate short-term exposure-related risk, it is necessary to shift the bulk of the air quality 19 distribution to lower levels, not just to limit the concentrations on days when the PM 2.5 20 concentrations are relatively high. 21 While shifting the distribution can be accomp lished through control strategies aimed at 22 meeting either an annual or 24- hour standard, we have seen in quantitative risk assessments 23 conducted in this and past reviews that more c onsistent aggregated risk reductions across study 24 areas are likely to be accomplished through strate gies aimed at meeting an annual standard. 25 Thus, in considering the adequacy of the current suite of standards in pr otecting against effects 26 associated with short-term exposures, we consid er whether associations in short-term exposure 27 studies have been reported in areas in which th e aggregate long-term stud y mean concentrations 28
are at or below the level of the current annual standard, as well as by considering whether the 29
98 th percentile PM 2.5 concentrations in such studies are at or below the level of the current 24- 30
hour standard. We conclude that such short-te rm exposure studies can re asonably be viewed as 31 calling into question the adequacy of the current annual and/or 24-hour standards. 32

4 While this view is consistent with th at presented in the 2005 Staff Paper, in the review completed in 2006, as noted above, the Administrator chose to focus more narrowly and considered the short-term exposure evidence as a basis for the 24-hour standard alone.Draft Do Not Quote or Cite March 2010 2-12 In considering what alternative standards w ould be protective against effects observed in 1 such short-term exposure studies, we first note the absence of any discer nable threshold within 2 the distribution of 24-hour average concentrations in the short-term exposure studies. While 3 recognizing that health effects may occur over the full range of 24-hour concentrations observed 4 in the studies, as with the long-term exposure studie s, we believe that it is reasonable to conclude 5
that the evidence of asso ciation is strongest down to somewh at below the mean 24-hour average 6 concentration, such as down to one standard devi ation below the mean or to the lower end of the 7 interquartile range, where the data in the study are most concentr ated. We also believe it is 8 appropriate to consider whethe r, and if so, where in the distribution of 24-hour average 9
concentrations the confidence in terval becomes notably wider, suggestive of a concentration 10 below which the association becomes appreciably more uncertain and the possibility that an 11 effects threshold may exist becomes more likely. Based on these consider ations, we identify a 12 range of alternative annual sta ndard levels that we conclude are appropriate to consider for 13 protecting against PM 2.5 -related short-term exposure effects based on the evidence available in 14 this review. We also recognize that it is unlikely that an a nnual standard could effectively 15 protect against short-term exposur e-related effects in all areas acr oss the country, especially in 16 areas with relatively high peak-to-mean ratios in PM 2.5 concentrations or in areas that are 17 strongly affected by localized “hotspots” or by seasonal expos ures that may not be well 18 controlled by an annual standard. Thus, we also identify a range of alte rnative 24-hour standard 19 levels that we judge to be appropriate to consider for protecting against PM 2.5 -related short-term 20 exposure effects, in conjunction with a range of alternative annual sta ndards, based on the 21
evidence available in this review. 22
Based on the evidence-based considerations outlined above, we then develop integrated 23 preliminary conclusions with regard to alternat ive suites of standards, including both annual and 24 24-hour standards, that we believe are appropriate for considerati on in this review based on the 25 currently available evidence. In so doing, we discuss the roles that each standard might be 26 expected to play in the protection afford ed by alternative suites of standards. 27 Beyond these evidence-based considerations, we also consider the quantitative risk 28 estimates and the key observations presented in the second draft quantitative risk assessment 29 (RA). This assessment included an evaluation of 15 urban case study areas and estimated risk 30 associated with a number of health endpoints associated with long-te rm and short-term PM 2.5 31 exposures (US EPA, 2010a). As part of our ri sk-based considerations, we have considered 32 estimates of the magnitude of PM 2.5 -related risks associated with r ecent air quality levels and air 33 quality simulated to just meet the current and al ternative suites of sta ndards using alternative 34 simulation approaches. We have also characterized the risk re ductions, relative to the risks 35 remaining upon just meeting the current standards, a ssociated with just mee ting alternative suites 36Draft Do Not Quote or Cite March 2010 2-13 of standards. In so doing, we recognize the uncertainties inherent in such risk estimates, and 1 have taken such uncertainties into account by co nsidering the sensitivity of the “core” risk 2 estimates to alternative assumptions and met hods likely to have substantial impact on the 3 estimates. In addition, we have conducted additional analyses to characterize the 4 representativeness of the urban study areas within a broader national context. We have 5
considered this risk-based information to he lp inform our preliminary conclusions on the 6 adequacy of the current suite of standards, poten tial alternative suites of standards that are 7 appropriate for consideration in this review, and on the roles that th e annual and 24-hour 8 standards may play in affording protection against effects related to both long- and short-term 9

PM 2.5 exposures. 10 Our preliminary conclusions reflect our unde rstanding of both evidence-based and risk11 based considerations to inform two overarching questions related to: (1 ) the adequacy of the 12
current suite of PM 2.5 standards and (2) what potential altern ative standards, if any, should be 13 considered in this review to provide appropriate protection from the effect s associated with both 14 long- and short-term exposures to fine particles. In addressing these broad questions, we have 15 organized the discussions below around a series of more specific questions reflecting different 16 aspects of each overarching ques tion. When evaluating the health protection afforded by the 17 current or any alternative suites of standards considered, we ha ve taken into account the four 18 basic elements of the NAAQS (e.g., indicato r, averaging time, form, and level). 19 We believe that the approach outlined a bove, when presented in the final PA, will 20 provide a comprehensive basis to help inform the judgments required of the Administrator in 21 reaching decisions about the current and potential alternative primary PM 2.5 standards and in 22 responding to the remand of the 2006 annual PM 2.5 standard. 23

2.2 ADEQUACY OF CURRENT STANDARDS 24 In considering the adequacy of the current suite of PM 2.5 standards, staff addresses the 25 following overarching question: 26

Does the currently available scientific evidence and risk-based information, as reflected in 27 the ISA and RA, support or call into question the adequacy of the protection afforded by 28 the current suite of fine particle standards? 29 To inform the answer to this broad question, we have posed a series of more specific 30 questions to aid in considering the currently availa ble scientific evidence and the results of recent 31 quantitative risk analyses in a pol icy-relevant context, as discu ssed below. In considering the 32
scientific and technical informa tion, we reflect upon both the info rmation available in the last 33
review and information that is ne wly available since the last revi ew as assessed and presented in 34 the ISA and second draft RA (US EPA, 2009a; US EPA, 2010a). 35Draft Do Not Quote or Cite March 2010 2-14 2.2.1 Evidence-based Considerations 1 In reviewing the adequacy of the current suite of PM 2.5 standards, we have taken into 2
account evidence-based cons iderations primarily by assessing th e currently available evidence as 3 presented in the ISA. Our review of the adequ acy of the current standa rds begins by considering 4 causal inference, impacts on susceptible populati ons, and whether health effects have been 5 observed in areas where the air quality concentrat ions extend to levels lower than previously 6 reported. 7

 To what extent does the newly available sc ientific evidence a nd related uncertainties 8 strengthen or call into question evidence of as sociations between ambient fine particle 9 exposures and health effects? 10 In considering the strength of the associati ons between short- and long-term exposures to 11

PM 2.5 and health effects, we first recognize that, in the last review, EPA concluded that there was 12 “strong epidemiological evidence” for PM 2.5 linking short-term exposures with cardiovascular 13 and respiratory mortality and morbidity, and long -term exposures with ca rdiovascular and lung 14 cancer mortality and respiratory morbidity (U S EPA, 2004, p. 9-46; US EPA, 2005, p. 5-4). 15 Overall, the epidemiological evidence suppor ted “likely causal asso ciations” between PM 2.5 and 16 both mortality and morbidity from cardiovascul ar and respiratory diseases, based on “an 17 assessment of strength, robustness, and consis tency in results” (US EPA, 2004, p. 9-48). 18 In looking across the extensive new scientific evidence available in this review, our 19 overall understanding of health e ffects associated with fine par ticle exposures has been greatly 20 expanded. The currently available evidence is st ronger in comparison to evidence available in 21
the last review because of its breadth and the subs tantiation of previously observed health effects 22 (US EPA, 2009a, section 2.3.1). A number of larg e multi-city epidemiological studies have been 23 conducted throughout the U.S. including extended an alyses of studies that were important to 24 inform decisionmaking in the last review. Thes e studies have reported c onsistent increases in 25 morbidity and/or mortality related to ambient PM 2.5 concentrations, with the strongest evidence 26 reported for cardiovascular-related effects. In addition, the findings of new toxicological and 27 controlled human exposure studies provide stro nger support for a number of potential biologic 28 mechanisms or pathways for PM-related cardiova scular and respiratory effects (US EPA, 2009a, 29 chapter 5; Figures 5-4 and 5-5). In summary, th e ISA concludes, “[t]he new evidence ... greatly 30 expands upon the evidence availa ble in the 2004 PM AQCD particul arly in providing greater 31 understanding of the underlying mechanisms for PM 2.5 induced cardiovascular and respiratory 32 effects for both short- and long-term exposures” (US EPA, 2009a, p. 2-17). 33 As an initial matter, we note that since th e conclusion of the last PM NAAQS review, the 34 Agency has developed a more formal framework for reaching causal inferences from the body of 35 scientific evidence drawing upon the evaluati on and synthesis of evidence from across 36Draft Do Not Quote or Cite March 2010 2-15 epidemiological, controlled human exposure, and toxicological studies. This framework uses a 1 five-level hierarchy that classifies the overa ll weight of evidence and causality using the 2 following categorizations: causal relationship, likel y to be a causal relati onship, suggestive of a 3 causal relationship, inadequate to infer a causal relationship, a nd not likely to be a causal 4 relationship (US EPA, 2009a, Table 1-3). 5 In reaching causal inferences, EPA has c onsidered uncertainties that bear on our 6 understanding of the body of curre ntly available scientific ev idence (US EPA, 2009a, section 7 1.5). For example, in epidemiological studie s the potential for confounding bias remains an 8 important source of uncertainty in evaluating the health effects asso ciated with one pollutant that 9 is part of a larger, complex mixture of pollutants. Epidemiological studies attempt to disentangle 10 the effects of the air pollution mixture and identif y the health effects asso ciated with a specific 11 pollutant, such as PM 2.5 , using multivariate regression models to control for the potential 12 confounding effects by other polluta nts (e.g., gaseous co-pollutants 5 ) for which measurements 13 are available. However, there are several statistical issues influencing results generated using co14 pollutant models that lead to uncertainty in the quantitative interpretation of these results. In this 15 review, the uncertainties associ ated with the evaluation of th e body of scientific evidence for 16

PM 2.5 -associated health effects remain largely the sa me as in previous reviews (e.g., co-pollutant 17 confounding, exposure misclassification) and have been considered in reaching causality 18
determinations as discussed in the ISA. 19 Looking broadly to integrate epidemiological evidence with that from controlled human 20 exposure studies and toxicologic st udies and using this causal fr amework, the ISA concludes that 21 the collective evidence is largely consistent with past studies and substa ntially strengthens what 22
was known in the last review to reach the conclusion that a causal relationship exists between 23 both short- and long-term exposures to PM 2.5 and mortality and cardiovascular effects. 24 Furthermore, the ISA concludes that the collective evidence continues to support likely causal 25 associations between short- and long-term PM 2.5 exposures and respiratory effects. Additional 26
evidence is suggestive of a causal relationship between long-term PM 2.5 exposures and other 27 health effects, including developmental and reproductive effects (e.g., low birth weight) and 28 carcinogenic, mutagenic, and genotoxic (e.g., lu ng cancer mortality) effects. Table 2-1 29
summarizes the causal determinations for health outcomes associated with short- and long-term 30 exposures to PM 2.5 (US EPA, 2009a, sections 2.3.1 and 2.6). 31
32

5 A gaseous co-pollutant (e.g., O 3 , CO, SO 2 , NO 2 ) meets the criteria for potential confounding in PM 2.5 -related effects if: (1) it is a potential risk factor for the health effect under study; (2) it is correlated with PM 2.5 and (3) it does not act as an intermediate step in the pathway between PM 2.5 exposure and the health effect under study (US EPA, 2004, p. 8-10).Draft Do Not Quote or Cite March 2010 2-16 Table 2-1. Summary of Causality Determinations for PM 2.5 1
Exposure Duration Outcome Causality Determination Mortality Causal

Cardiovascular Effects Causal Respiratory Effects Li kely to be Causal Reproductive and Developmental Effects Suggestive Long-term

Cancer, Mutagenicity, Genotoxicity Effects Suggestive Mortality Causal

Cardiovascular Effects Causal Respiratory Effects Li kely to be Causal Short-term
Central Nervous System Effects Inadequate
Source: adapted from US EPA, 2009, Table 2-6. 2
Health Effects Associated with Long-term PM 2.5 Exposure 3
With regard to mortality associated with long-term PM 2.5 exposures, the ISA concludes 4 that newly available evidence significantly st rengthens the evidence linking long-term exposure 5
to PM 2.5 and mortality, while providing indicat ions that the magnitude of the PM 2.5 -mortality 6 association may be larger than previously estimated (US EPA, 2009a, sections 7.2.10, 7.2.11, 7 7.6.1; Figures 7-6 and 7-7). A number of large U. S. cohort studies have been published since the 8 last review. This evidence includes new analyses and insights from extended analyses of the 9 American Cancer Society (ACS) and Harvard Six Cities studies (US EPA, 2009a, pp 7-84 to 7- 10 85; Figure 7-6; Krewski et al., 2009 ; Pope et al., 2004; Jerrett et al ., 2005; Laden et al., 2006). In 11 addition, new long-term PM 2.5 exposure studies evaluating mo rtality impacts in additional 12
cohorts are now available. The Women’s Health Initiative has investigated the effects of PM 2.5 13
on cardiovascular-related mortal ity in post-menopausal women with no previous history of 14 cardiac disease (US EPA, 2009a, p. 7-87; Miller et al., 2007). Mortality impacts in older adults 15 using Medicare data have been reported by a number of investigator s (US EPA, 2009a, pp. 7-87 16 to 7-89; Eftim et al., 2008; Zeger et al ., 2007, 2008). We note that other long-term PM 2.5 17 exposure studies provide additional evidence of mortality associated with long-term PM 2.5 18 exposures as discussed more fully in section 7.6 of the ISA. Collectively, these long-term PM 2.5 19 exposure studies, along with the ev idence available in the last revi ew, provide us with consistent 20 and stronger evidence of associations between long-term exposure to PM 2.5 and mortality (U.S. 21 EPA, 2009a, sections 2.3.1 and 7.6). 22Draft Do Not Quote or Cite March 2010 2-17 When integrating the mortality evidence, EP A considered impacts on all-cause or non1 accidental mortality as well as cause-specific mortality (e.g., cardiovasc ular-related mortality, 2 respiratory-related mortality, lung cancer mortality) and reached the conclusion that there is a 3
causal association between mortality and long-term PM 2.5 exposure (US EPA, 2009a, pp. 2-12 4 and 7-96). The strongest evidence indicat es an association between long-term PM 2.5 exposures 5 and mortality due to cardiovascular disease, with additional evidence supporting an association 6
between PM 2.5 and mortality related to lung cancer (US EPA, 2009a, pp. 2-12, 7-81, and 7-95 to 7 7-96; Figure 7-7). We note that fewer long-term PM 2.5 exposure studies have evaluated the 8 respiratory component of cardiopulmonary morta lity, and the evidence to support an association 9 with long-term exposure to PM 2.5 and respiratory mortality is, therefore, much more limited (US 10 EPA 2009a, p. 2-12; Figure 7-7). The strength of associations for cause-specific mortality is 11 coherent with cardiovascular-related morbidity e ndpoints as discussed below. The most recent 12
evidence for cardiovascular-rela ted mortality in post-menopausal women indicates that the 13
evidence of association with long-term exposure to PM 2.5 in this population is “particularly 14 strong” (US EPA, 2009a, p. 7-96). 15 In addition, the strength of the causa l association between long-term PM 2.5 exposure and 16 mortality builds upon new studies providing evid ence of improvement in community health 17 following reduction in ambient fine particle concentrations. Pope et al. (2009) have documented 18 the population health benefits of reducing ambien t air pollution by correlati ng past reductions in 19
ambient PM 2.5 concentrations with increased life expect ancy. These investig ators report that 20 reductions in fine particle ambient concentr ations that occurred during the 1980s and 1990s 21 account for as much as 15 percent of the overall improvement in life expectancy in 51 U.S. 22 metropolitan areas also analyzed in the ACS study. The decrease in fine particle exposure was 23 reported to be associated with an estimated incr ease in mean life expectancy of approximately 5 24 to 9 months (US EPA, 2009a, p. 7-95; Pope et al., 2009). An extended an alysis of the Harvard 25 Six Cities study found that as cities cleaned up their air, locations with the largest reductions in 26

PM 2.5 saw the largest improvements in reduced mortality rates, while those with the smallest 27
decreases in PM 2.5 concentrations saw the smallest improvements in reduced mortality rates 28 (Laden et al., 2006). Reduced mortality risk ob served in this extended follow-up study was 29
related to deaths due to cardiova scular and respiratory-related di sease, but not from lung cancer 30 (US EPA, 2009a, p. 7-84). An additional exte nded follow-up to the Harvard Six Cities study 31 investigated the delay between changes in exposur e and changes in mortality. Schwartz et al. 32 (2008) reported that the effects of changes in PM 2.5 exposures were seen w ithin the 2 years prior 33 to death (US EPA, 2009a, p. 7-92; Figure 7-9). 34 With regard to cardiovascular eff ects associated with fine particle exposures, the ISA 35
includes consideration of both cardiovascular-rela ted mortality as well as morbidity effects and 36Draft Do Not Quote or Cite March 2010 2-18 concludes that a causal associa tion exists between long-term PM 2.5 exposure and cardiovascular 1 effects (US EPA, 2009a, pp. 2-12 and 7-19). Recent studies have provided new evidence linking 2 long-term exposure to PM 2.5 with cardiovascular outcomes that has “expanded upon the 3 continuum of effects ranging from the more s ubtle subclinical measur es to cardiopulmonary 4 mortality” (US EPA, 2009a, p. 2-17). Several new epidemiologic studies have examined the 5
association between cardiovasc ular effects and long-term PM 2.5 exposures in multi-city studies 6 conducted in the U.S. and Europe. The ISA concludes that the strongest evidence of 7
cardiovascular effects related to long-term exposure to PM 2.5 has been reported in recent studies 8 investigating cardiovascular-relate d mortality. This includes evid ence from a number of large, 9 multi-city U.S. long-term cohort studies includi ng extended follow-up analyses of the ACS and 10
Harvard Six Cities studies as well as the WHI as outlined above (US EPA, 2009a, sections 7.2.10 11 and 7.6.1; Krewski et al., 2009; Pope et al., 2004; Laden et al., 2006; Miller et al., 2007). Pope 12 et al. (2004) report a positive associat ion between mortality and long-term PM 2.5 exposure for a 13 number of specific cardiovascular diseases , including ischemic heart disease (IHD), 14 dysrhythmia, heart failure, and car diac arrest (US EPA, 2009a, p. 7- 84; Figure 7-7). Krewski et 15 al. (2009) provides further evidence and precisio n for IHD-related mortality associated with 16 long-term PM 2.5 exposure (US EPA, 2009a, p. 7-84, Figure 7-7). 17 Epidemiologic studies examining cardiovascul ar morbidity associated with long-term 18

PM 2.5 exposures were not available in the previous PM reviews. In the current review, studies 19
are now available that evaluate d a number of endpoints ranging from subtle indicators of 20
cardiovascular health to serious cl inical events associated with coronary heart disease (CHD) and 21 cerebrovascular disease (CVD) including myo cardial infarction (MI), coronary artery 22 revascularization (e.g., bypass graf t, angioplasty, stent, atherect omy), congestive heart failure 23 (CHF), and stroke. The most significant new evidence comes from the WHI study which 24 provides evidence of nonfatal cardiovascular even ts including both coronary and cerebrovascular 25 events in a cohort of post-menopausal women with no previous history of cardiac disease (Miller 26 et al., 2007; US EPA, 2009a, sections 7.2.9 and 7.6.1). 27 As noted in the ISA, there may be multiple mechanisms related to the observed 28
associations between PM 2.5 and cardiovascular effects, and th ese processes may be interlinked 29 (US EPA, 2009a, sections 5.2, 5.3, 5.5, 5.6, 5.7). For example, myocardial ischemia and MI may 30 occur as a result the proposed eff ects of PM on atherosclerosis, pla que instability, plaque rupture, 31 thrombosis, and/or altered vasore activity of coronary vessels. M yocardial ischemia and MI may 32 alter the conduction and depolarizat ion properties of the heart and le ad to arrhythmic events. In 33 addition, thrombosis may lead to st roke and/or thromboembolic dis ease. The ISA notes that “it 34
is not clear at this time whether PM initiates cardiovascular disease or whether it perturbs 35 existing disease” (US EPA, 2009a, p. 5-18). 36Draft Do Not Quote or Cite March 2010 2-19 Toxicological studies provide evidence that the cardiovascular morbidity effects observed 1 in epidemiological studies are biologically plausi ble and coherent with st udies of cardiovascular2 related mortality observed in long-term exposures as well as with studi es of cardiovascular3 related morbidity and mort ality associated with sh ort-term exposures to PM 2.5 as described below 4 (US EPA, 2009a, p 7-19). For example, it has been hypothesized that that exposure to PM 2.5 can 5 lead to myocardial ischemia through an effect on the autonomic nervous system or by altering 6 vasomotor function. Furthermore, PM-induced sy stemic inflammation and oxidative stress may 7
contribute to altered vasomotor function which has been demonstr ated as altered microvascular 8 reactivity, altered vessel tone, and re duced blood flow during ischemia. 6 Toxicological studies 9 demonstrating increased right ventricular pressu re and diminished cardiac contractility also 10 provide biological plausibility for the associations observed between PM 2.5 and CHF in 11 epidemiological studies (US EPA, 2009a, p. 2- 15). Additional eviden ce of cardiovascular12 related morbidity and mortality associated with long-term PM 2.5 exposures is discussed more 13 fully in section 7.2 of the ISA. Additional ev idence discussing potential mechanisms underlying 14 cardiovascular effects are discussed more fully in sections 5.2 through 5.6 of the ISA. 15 The ISA notes extended analyses of studies av ailable in the last review as well as new 16 epidemiologic studies conducted in the U.S. and abroad provide stronger evidence of respiratory17 related morbidity associated with long-term PM 2.5 exposure. As mentioned above, more limited 18 data are available for respiratory-related mortalit y effects. Considering morbidity and mortality 19 effect collectively, the ISA has concluded that there is continued suppor t for a likely causal 20 association between long-term PM 2.5 exposures and respiratory effect s. The strongest evidence 21 for respiratory-related effects available in this review is from studies that have evaluated 22 decrements in lung function growth, increased respiratory symptoms, and asthma development 23 (U.S. EPA, 2009a, sections 2.3.1.2, 7.3.1.1, and 7.3.2.1). 7 Specifically, extended analyses of the 24 Southern California Children’s Health Study (CHS ) provide evidence that clinically important 25 deficits in lung function 8 associated with long-term exposure to PM 2.5 persisted into early 26

6 The vasculature of all tissues is lined with endothelial cells that will naturally encounter any systemically absorbed toxin. The endothelium (1) maintains barrier integrity to ensure fluid compartmenta lization, (2) communicates dilatory and constrictive stimuli to vascular smooth muscle cells, and (3) recruits inflammatory cells to injured regions. Smooth muscle cells lie within the layer of endothelium and are crucial to the regulation of blood flow and pressure. In states of injury and disease, both cell types can exhibit dysfunction and even pathological responses. Endothelial dysfunction is a factor in many diseases and may contribute to the origin and/ or exacerbation of perfusion-limited diseases, such as MI or IHD, as we ll as hypertension. Endothelial dysfunction is also a characteristic feature of early and advanced atherosclerosis (US EPA, 2009a, p. 6-24).
7 Supporting evidence comes from studies “that observ ed associations between long-term exposure to PM 10 and an increase in respiratory symptoms and reducti ons in lung function grown in areas where PM 10 is dominated by PM 2.5 ” (US EPA, 2009a, p. 2-12). 8 Clinical significance was defined as a FEV 1 below 80% of the predicted value, a criterion commonly used in clinical settings to identify persons at increased risk for adverse respiratory conditions (US EPA, 2009a, p. 7-29-7- 30).Draft Do Not Quote or Cite March 2010 2-20 adulthood (U.S., EPA, 2009a, p. 7-27; Gauderman et al., 2004). Additional analyses of the CHS 1 cohort report an association between long-term PM 2.5 exposure and bronchitic symptoms (US 2 EPA, 2009a, p. 7-24; McConnell et al., 2003) and a strong modifying effect on the association 3 between lung function with asthma incidence (US EPA, 2009, 7-25; Islam et al., 2007). The 4 strength and robustness of the out comes observed in these more re cent reports from the Southern 5 California CHS, including evaluation of a broade r range of endpoints than previous CHS studies 6 with shorter follow-up periods, were larger in magnitude and more precise. Supporting these 7 results are new longitudinal cohort studies conduct ed by other researchers in varying locations 8 using different methods (U.S. EPA, 2009a, sect ion 7.3.9.1). New evidence from a U.S. cohort of 9 cystic fibrosis (CF) patien ts provides evidence of asso ciation between long-term PM 2.5 exposures 10 and exacerbations of respiratory symptoms resu lting in hospital admissions or use of home 11 intravenous antibiotics (US EPA, 2009a, p. 7-25; Goss et al., 2004). 12 Toxicological studies provide coherence and biological plausibility for the respiratory 13 effects observed in epidemiological studies (U S EPA, 2009a, p. 7-42). For example, pre- and 14 postnatal exposure to ambient levels of ur ban particles has been found to affect lung 15 development in an animal model (US EPA, 2009a , section 7.3.2.2; p. 7-43). This finding is 16 important because impaired lung development is one mechanism by which PM exposure may 17 decrease lung function growth in children (US EPA, 2009a, p. 2-12; section 7.3). Subchronic 18 and chronic toxicological studies of concentrated ambien t particles (CAPs) as well as evaluations 19 of specific sources of fine particles including, di esel exhaust (DE), roadway air, and woodsmoke 20 provide some evidence for altered pulmonary function, mild inflammation, oxidative responses, 21 immune suppression, and histopathol ogic changes. In addition, ex acerbated allergic responses 22 have been observed in animals exposed to DE and wood smoke (US EPA, 2009a, p. 2-12, 23 section 7.3). 24 With respect to respiratory-related mo rtality associated with long-term PM 2.5 exposure, 25
evidence is “limited and inconc lusive” (US EPA, 2009a, p. 7-41). The extended follow-up of the 26 Harvard Six Cities study reports a positive but non -statistically significan t association between 27 long-term PM 2.5 exposure and respiratory-related mortalit y (Laden et al., 2006). Pope et al. 28 (2004) found no association with long-term PM 2.5 exposure and respiratory-related mortality (US 29 EPA, 2009a, p. 7-84). There is emerging but lim ited evidence for an association between long30
term PM 2.5 exposure and respiratory mo rtality in post-neonatal infa nts where long-term exposure 31 was considered as approximately one month to one year (US EPA, 2009a, pp. 7-54 to 7-55). 32 Emerging evidence of short- and long-term exposure to PM 2.5 and respiratory morbidity effects 33 and infant mortality are coherent with the w eak respiratory mortality effects observed. 34 Beyond effects considered to have causal or likely causal associat ions with long-term 35

PM 2.5 exposure as discussed above, the ISA also not es health outcomes classified as having 36Draft Do Not Quote or Cite March 2010 2-21 evidence suggestive of a causal association with long-term PM 2.5 exposure. This includes two 1 broad categories of health outcomes: (1) repr oductive and developmental effects and (2) cancer, 2 mutagenicity, and genotoxicity effects (US EPA, 2009a, Table 2-6). With respect to 3 reproductive and developmental effects, the ISA notes, “[e]vidence is accumulating for PM 2.5 4 effects on low birth weight and in fant mortality, especially due to respiratory causes during the 5 post-neonatal period” (US EPA, 2009a, section 2 .3.1.2). New evidence available in this review 6 reports a significant associ ation between exposure to PM 2.5 during pregnancy and lower birth 7 weight, pre-term birth, and intrauterine growth restriction, respectivel y, and post-natal exposure 8
to PM 2.5 associated with an increased risk of infa nt mortality (US EPA, 2009a, section 7.4). The 9 ISA further notes that “[i]nfants and fetal deve lopment processes may be particularly vulnerable 10 to PM exposure, and although the physical mechanisms are not fully understood, several 11 hypotheses have been proposed involving direct e ffects on fetal health, al tered placenta function, 12
or indirect effects on the mother’s health ” (US EPA, 2009a, section 7.4.1). However, 13 toxicological studies provide some evidence which is coherent with an association between long14
term PM 2.5 exposure and adverse reproductive and devel opmental outcomes, but provide “little 15 mechanistic information or biological plausibi lity for an associati on between long-term PM 16 exposure and adverse birth outcomes (e.g., low birt h weight or infant mortality)” (US EPA, 17 2009a, p. 2-13). 18 With respect to cancer, mutagenic and genotoxic effects, “[m]ultiple epidemiologic 19
studies have shown a consistent positive associ ation between PM 2.5 and lung cancer mortality, 20 but studies have generally not reported associa tions between PM 2.5 and lung cancer incidence” 21 (US EPA, 2009a, sections 2.3.1.2 and 7.5; Table 7- 7; Figures 7-6 and 7-7). The extended 22 follow-up to the ACS study reported an association between long-term PM 2.5 exposure and lung 23 cancer mortality (US EPA, 2009a, p. 7-71; Krewski et al., 2009). The extended follow-up of the 24 Harvard Six Cities study also evaluated lung cance r mortality and reported a positive association 25 when considering the entire 25-year follow-up pe riod. However, estimated decreases in average 26

PM 2.5 concentrations between the first and second follow-up periods were not associated with 27 reduced lung cancer mortality (US EPA, 2009a, p. 7-71; Laden et al, 2006). Epidemiological 28 evidence is not currently available to evaluate ca ncer in organs or systems other than the lung 29 related to long-term exposure to PM 2.5 (US EPA, 2009a, p. 7-81). There is some evidence, 30 primarily from in vitro studies, providing biological pl ausibility for the PM-lung cancer 31 relationships observed in epidemiological studi es (US EPA, 2009a, p. 7-80). Toxicological 32 studies providing evidence of car cinogenicity, mutagenicity, a nd genotoxicity reported mixed 33
results as discussed in section 7.5 of the ISA. 34

Health Effects Associated with Short-term PM 2.5 Exposure 35Draft Do Not Quote or Cite March 2010 2-22 In considering effects associated with short-term PM 2.5 exposure, the body of currently 1 available scientific evidence has been expanded greatly by the publication of a number of new 2 multi-city time-series studies that have used unifo rm methodologies to investigate the effects of 3 short-term fine particle exposures on public health. This body of evidence provides a more 4 expansive data base and considers multiple locations representing varying regions and seasons 5 that provide evidence on the influence of climate and air pollution mixes on PM 2.5 -associated 6 health effects. These studies provide more precise estimates of the magnitude of effects 7
associated with short-term PM 2.5 exposure than most smaller-scale single-city studies that were 8 more commonly available in the last review (U.S. EPA 2009a, chapter 6). 9 With regard to mortality effects, looking br oadly across all of the available scientific 10 evidence, the ISA concludes that a causal association exists between short-term PM 2.5 exposure 11 and premature death. Extended and expanded analyses of multi-city studies available in the last 12 review as well as a large number of new U. S. multi-city and single-city short-term PM 2.5 13 exposure studies have found generally consistent positive associations between short-term PM 2.5 14 exposures and cardiovascular- and respiratory- related mortality as well as all-cause (non15 accidental) mortality (US EPA, 2009a, s ections 2.3.1.1, 6.2.11 and 6.5.2.2; Figures 6-26, 6-27, 16 and 6-28). These newly published U.S. multi-city short-term PM 2.5 exposure studies provide a 17 much larger body of evidence since the last revi ew. In an analysis of National Morbidity, 18 Mortality, and Air Pollution Study (NMMAPS) da ta, Dominici et al. (2007) reported 19 associations between fine particle exposures a nd all-cause and cardio-respiratory mortality (US 20 EPA, 2009a, p. 6-175, Figure 6-26). A Canadian mu lti-city study available in the last review 21 was expanded from 8 to 12 cities (Burnett and Go ldberg, 2003; Burnett et al., 2004). The results 22 of this expanded analysis were consistent with the earlier findings of a positive and statistically 23 significant association between short-term PM 2.5 exposure and mortalit y (US EPA, 2009a, p 6- 24 182, Figure 2-1). However, the influence of NO 2 and limited PM 2.5 data for several years during 25 the study period somewhat diminish these finding s and underscore the need for additional data 26 on the co-pollutants in relation to the PM 2.5 -mortality association. Zanobetti and Schwartz 27 (2009) reported positive (99%) a nd frequently statistically signif icant (55%) associations across 28
most of the 112 cities between short-term PM 2.5 exposure and total, cardiovascular-related, and 29 respiratory-related mortality (US EPA, 2009a , pp 6-176 to 6-179; Figures 6-23 and 6-24). 30 Collectively, these studies provide generally co nsistent and much stronger evidence than the 31
evidence available in the last review. 32 With respect to cardiovascular effects, th e ISA considers both cardiovascular-related 33 mortality as well as cardiovascular morbidity e ffects in reaching the conc lusion that there is a 34
causal association between short-term PM 2.5 exposure and cardiovascular effects. New multi35 city as well as single-city short-term PM 2.5 exposure studies conducted since the prior review 36Figure 2-1. Summary of Effect Estimates (per 10 μg/m3) and Air Quality Distributionsfor Long-term Exposure StudiesStudy OutcomeMean(SD)Mean– 1SDLower IQR Range EffectEstimate (95% CI)Zeger et al. (2008) All-Cause Mortality, Central U.S. 10.7* 9.8 9.8-12.2*Kim et al. (2004) Bronchitis (Children) 12.0 11-15***Zeger et al. (2008) All-Cause Mortality, Western U.S. 13.1* 10.4 10.4-18.5*Miller et al. (2007) CVD Morbidity or Mortality 13.5 (3.3) 10.2 11.6 3.4 – 28.3Eftim et al. (2008) All-Cause Mortality, ACS Sites 13.6 (2.8) 10.8 6.0-25.1Goss et al. (2004) All-Cause Mortality 13.7 (4.2) 9.5 11.8 11.8-15.9McConnell et al. (2003) Bronchitis (Children) 13.8 (7.7) 6.1 6-29Zeger et al. (2008) All-Cause Mortality, Eastern U.S. 14.0* 12.3 12.3-15.3*Krewski et al. (2009) All-Cause Mortality 14.0 (3.0) 11.0 11.8 5.8-22Eftim et al. (2008) All-Cause Mortality, Harv 6-Cities 14.1 (3.1) 11.0 9.6-19.1Lipfert et al. (2006) All-Cause Mortality 14.3 (3.0) 11.3 5.0 - ?Dockery et al. (1996) Bronchitis (Children) 14.5 (4.2) 10.3 5.8-20.7Woodruff et al. (2008) Infant Mortality (Respiratory) 14.9**** 12.0Laden et al. (2006) All-Cause Mortality 16.4 (5.6)* 10.8 10-22Woodruff et al. (2006) Infant Mortality (Respiratory) 19.2Enstrom (2005) All-Cause Mortality 23.4CHD Mortality, Females 29.0Chen et al. (2005)CHD Mortality, Males 29.0* Zeger et al. (2008) reported median with IQR; overall study reported median of 13.2 μg/m3( lower IQR - 11.1)**Estimated from data provided by study author***range of averages at 10 schools**** median for all cause mortality; median for survivors; = 14.8, lower end of IQR (11.7)Relative Risk / Odds RatioModified from Figure 2-2, US EPA, 2009a.Draft Do Not Quote or Cite March 2010 2-24 support a largely positive and freque ntly statistically significant relationship between short-term 1 exposure to PM 2.5 and cardiovascular-related disease, substantiating prior findings of a positive 2 relation between exposure to fine particles and cardiovascular morbidity. For example, short3 term exposure to PM 2.5 in association with cardiovascular and respiratory effects was evaluated 4 among a multi-city cohort of ol der adults participating in the Medicare Air Pollution Study 5 (MCAPS) (US EPA, 2009a, pp. 6-57 to 58; Domini ci et al, 2006a; Bell et al, 2008). Overall, 6
short-term PM 2.5 exposure studies available in the current review provi de consistent evidence of 7 a positive association between short-term PM 2.5 exposures and hospital admissions (HA) or 8 emergency department (ED) visits as well as premature mortality rela ted to cardiovascular 9 outcomes. The strongest evidence has been obs erved for cardiovascular morbidity effects 10 predominately associated with HA and ED visits reported for ischemic heart disease (IHD) and 11 congestive heart failure (CHF) and cardiovascul ar-related mortality (US EPA, 2009a, Figure 2-1, 12 p. 6-79, sections 6.2.10.3, 6.2.10.5, and 6.2.11; Bell et al ., 2008; Dominici et al., 2006a; Tolbert 13 et al., 2007; Zanobetti and Schw artz, 2009). Furthermore, thes e findings are supported by a 14 recent study of a multi-city cohort of women partic ipating in the Women’s Health Initiative that 15 reported a non-significantly associati on between short-term exposure to PM 2.5 and myocardial 16 ischemia (Zhang et al., 2009). 17 In focusing on respiratory effects, the ISA in tegrates evidence of respiratory-related 18 mortality with respiratory morbidity effects to re ach the conclusion that there is a likely causal 19
association between short-PM 2.5 exposure and respiratory effects. The strongest evidence from 20
short-term PM 2.5 exposure studies has been observed for respiratory-related ED visits and HAs 21 for chronic obstructive pulmonary disease (COPD) and respiratory infections (U.S. EPA, 2009a, 22 sections 2.3.1.1 and 6.3.8.3; Figures 2-1 and 6-13; Dominici et al., 2006a;). Evidence for PM 2.5 - 23 related respiratory effects has al so been observed in panel studie s, which indicate associations 24 with respiratory symptoms, pulmonary functi on, and pulmonary inflammation among asthmatic 25 children. Although not consistently observed, some controlled human exposure studies have 26 reported small decrements in various measur es of pulmonary function following controlled 27 exposures to PM 2.5 (US EPA, 20009a, p. 2-10). Furthermor e, the comparatively larger body of 28 toxicological evidence si nce the last review is coherent with short-term exposures to PM 2.5 and 29 respiratory effects (US EPA 2009a, section 6.3.10.1). 30
31 Summary 32 In considering the extent to which newly availa ble scientific evidence strengthens or calls 33 into question evidence of associations identified in the last review betwee n ambient fine particle 34 exposures and health effects, we recognize that much progress ha s been made in assessing some 35 key uncertainties related to our understanding of h ealth effects associated with short- and long- 36Draft Do Not Quote or Cite March 2010 2-25 term exposure to PM 2.5. As briefly discussed above as well as in the more complete discussion of 1 the evidence as assessed in the ISA, we note th at the newly available information combined with 2 information available in the last review pr ovides substantially str onger confidence in a causal 3
association between short- a nd long-term exposures to PM 2.5 and mortality and cardiovascular 4 effects. In addition, the newl y available evidence reinforc es and expands the evidence 5 supporting the likely causal nature of the associat ions between short- a nd long-term exposure to 6

PM 2.5 and respiratory effects. Causal inferences, as discussed in the ISA, are based not only on 7 the more expansive epidemiological evidence av ailable in this review but also reflects 8 consideration of important progress that has be en made to advance our understanding of a 9 number of potential biologic modes of actions or pathways for PM-related cardiovascular and 10 respiratory effects (US EPA 2009a, chapter 5). With respect to suggestive evidence for a 11 broader range of effects, the body of scientific evidence is somewhat expanded but is still limited 12 with respect to associat ions between long-term PM 2.5 exposures and developmental and 13 reproductive effects as well as cancer, mutagenic, and genotoxic effects. Thus, we reach the 14 preliminary conclusion that there is stronger a nd more consistent and coherent support for 15 associations between short- and long-term PM 2.5 exposure and a broader range of health 16 outcomes than was available in the last review, pr oviding the basis for fine particles at least as 17 protective as the current PM 2.5 standards. 18 Having reached this initial conclusion, we then consider how the new evidence informs 19 our understanding of susceptib le populations by asking the following question: 20

 To what extent does the newly available sc ientific evidence expand our understanding 21 of susceptible populations, including identi fication of new sus ceptible populations? 22 As an initial matter, interindividual varia tion in human responses to air pollutants 23 indicates that some population group s are at increased risk for the detrimental effects of ambient 24 exposure to PM. 9 To facilitate the iden tification of populations at gr eatest risk for PM-related 25 health effects, studies have eval uated factors that cont ribute to the susceptib ility or vulnerability 26
of an individual to PM. The definition for bot h of these terms has been found to vary across 27 studies, but in most instances suscep tibility refers to biological or intrinsic factors (e.g., lifestage, 28 gender) while vulnerability refers to non-biological or extrinsic factors (e.g., socioeconomic 29 status [SES]) (see US EPA, 2009a, Table 8-1). However, in many cases a factor identified that 30 increases an individual's risk for morbidity or mo rtality effects from expos ure to an air pollutant 31 (e.g., PM) cannot be easily categoriz ed as a susceptibility or vulnera bility factor. At times, the 32 terms susceptibility and vulnerability cannot be dis tinguished from one another. As it has been 33

9 Although studies have primarily used exposures to PM 10 or PM 2.5 , the available evidence suggests that the identified factors also increase risk from PM 10-2.5 (US EPA, 2009a, section 8.1.8).Draft Do Not Quote or Cite March 2010 2-26 defined in the ISA (US EPA, 2009a, p. 8-1), th e term “susceptible” encompasses both these 1 concepts. This document maintains that definition. 2 The 2004 AQCD noted that the existence of heart and lung disease was clearly linked 3 with increased susceptibility to effects fr om PM exposure, based on epidemiological and 4 toxicological studies along with dosimetric evidence. The epidemiological evidence for 5 increased susceptibility to PM in this populat ion was primarily derive d from studies of short6 term exposure. Long-term exposure studies sugges ted that PM may result in chronic respiratory 7 disease or decreased lung function growth, ther eby increasing susceptibility to short-term 8 changes in PM. It was also noted that studies available at that time supported considering older 9 adults and children, including possibly infants, as susceptible groups, recognizing that there is 10 likely overlap between age categories and the preexistence of cardiopulmonary diseases. 11 Emerging evidence indicated that people of lower (SES) or people who have particularly 12 elevated exposures, due to factors such as resi dential location, may be atgreater risk of PM13
related effects. The evidence av ailable at that time did not gene rally allow distinctions to be 14 drawn between the PM indicators, in terms of which groups might be more susceptible to PM 2.5 15
and/or PM 10-2.5
. 16 As discussed below, the ISA concludes th at the epidemiological, controlled human 17 exposure and toxicological studies continue to provide evidence of increased risk for various 18 populations, including people at certa in life stages, in this case ch ildren and older adults, people 19 with pre-existing cardiovascular and respiratory diseases (e.g., asthma), and people with lower 20 SES (US EPA, 2009a, section 2.4.1, chapter 8). This section expands on the discussion in the 21 ISA of susceptible populations in that it also cons iders supporting evidence for increased risk in 22 these populations from studies th at examined only one susceptible population. However it does 23 not contain information from the ISA for potenti ally susceptible populations for which there was 24
not sufficient evidence to it to dr aw conclusions about increased susceptibility (e.g., people with 25 diseases that involve chronic inflammation, such as diabetes, or with gene tic susceptibility). 26
Children and Older Adults 27 Childhood represents a life stage that has ge nerally been considered susceptible to 28 exposure to PM due to the following factors: children spend more time outdoors; children have 29 greater activity levels than adults; children have exposures resulting in higher doses per body 30 weight and lung surface area; and also because of the potential for irreversible effects on the 31 developing lung (US EPA, 2009a, section 8.1.1.2). Recent studies of long-term exposure to 32

PM 2.5 have greatly expanded the evidence for eff ects on lung development in children. The 33 extended follow-up for the Southern California CHS includes several ne w studies that report 34 positive associations between long-term exposure to PM 2.5 and respiratory morbidity, 35 particularly for such endpoints as lung functi on growth, respiratory symptoms (i.e., bronchitic 36Draft Do Not Quote or Cite March 2010 2-27 symptoms), and respiratory disease incidence (U S EPA, 2009a, section 7.3; Gauderman et al., 1 2004). New analyses have been conducted that include longer follow-up periods of the CHS 2 cohort through 18 years of ag e, provide evidence that effects from exposure to PM 2.5 persist into 3 early adulthood and are more robus t and larger in magnitude than reported for shorter follow-up 4 periods available in 2004. S upporting these results are new c ohort studies conducted by other 5
researchers in other locations with different methods that provide enhanced evidence for 6 respiratory effects related to long-term exposures to PM 10 that is dominated by PM 2.5 (US EPA, 7 2009a, section 7.3). New studies provide positive a ssociations from Mexico City, Sweden, and a 8 national cystic fibrosis cohort in the U.S. A natural experiment in Switzerland reported that 9 improving PM air quality may slow the annual ra te of decline in lung function in adulthood, 10 indicating benefits to public health. In addition, invest igators of the CHS suggest PM 2.5 may also 11
act as a modifier of the association between l ung function and asthma, inducing declines in lung 12
function and a concomitant increase in new onset asthma (Islam et al 2007). Thus, the ISA (US 13 EPA, 2009a, section 7.3.9.1) concludes that the da ta for respiratory morb idity in children are 14
consistent and coherent across several study designs, locations, and researchers. Preliminary 15 evidence from toxicological studies provides some coherence and biological plausibility for the 16 observed associations with lung function d ecrements (US EPA, 2009a, section 7.3.2.2). 17 With respect to short-term exposures to PM, the 2004 AQCD found that studies which 18 stratified results by age t ypically reported associations betwee n short-term exposures to PM and 19 respiratory-related health effects in children with asthma (US EPA, 2004, section 8.4.9). This 20 body of evidence has been strengthened by newly av ailable epidemiological studies that provide 21 evidence of reductions in lung function (FEV 1 ) and an increase in re spiratory symptoms and 22 medication use associated with PM exposur e among asthmatic children (US EPA, 2009a, 23 sections 6.3.1 and 6.3.2.1). These include two large, longitudinal studies in urban areas of the 24 US, as well as a number of smaller panel studies conducted in the U.S. (US EPA, 2009a, section 25 6.3.1). 26 No epidemiologic studies of pulmonary infl ammation were described in the 2004 AQCD. 27 Several new panel studies of children, using exhaled NO (eNO) as a biomarker of airway 28 inflammation, found generally positive associati ons between PM exposure and eNO levels in 29
asthmatic children who did not us e inhaled corticoste roids (US EPA, 2009a, section 6.3.3.1). 30 With respect to short-term increases in PM concentrations associated with respiratory31 related hospitalizations and ED visits, the ep idemiologic evidence presented in the 2004 AQCD 32 was consistent across studies (US EPA, 2004, section 8.3.2.5). Newly available evidence 33 provides further support for this relationship, with larger effect estimates observed among 34 children and older adults. However, effect estimates are clearly heterogeneous and sensitive to 35Draft Do Not Quote or Cite March 2010 2-28 choice of lag, with evidence of both regional and seasonal differen ces (US EPA, 2009a, sections 1 6.3.8 and 6.3.10). 2 Two recent toxicological studies, presented in the ISA (US EPA, 2009a, section 8.1.1.2), 3 provide biological plausibility for the increase in PM-related respiratory effects in children 4 observed in the epidemiological studies. These studies include effects on lung function, 5 pulmonary injury and evidence suggesting that th e developing lung is more susceptible to PM. 6 The ISA (US EPA, 2009a, p. 8-5) concludes that th e evidence from epidemiological studies that 7
have examined the health effects associated w ith all size fractions of PM and toxicological 8
studies that have examined i ndividual PM components provide support for the hypothesis that 9 children are at greater ri sk of respiratory effects from exposure to PM. 10 With respect to older adu lts, the 2004 AQCD (US EPA, 2004, section 9.2.4.2) concluded 11 that people aged 65+ years appear to be at somewhat higher risk for PM exacerbation of 12 cardiovascular-related disease effects and, perhap s, tend to experience hi gher PM-related total 13 (nonaccidental) mortality risk, as well. The high er prevalence of pre-ex isting cardiovascular and 14 respiratory diseases found in this age range co mpared to younger age groups increases risk, 15 primarily due to the gradual dec line in physiological processes as part of the aging process (US 16 EPA, 2009a, section 8.1.1.1). Therefore, some over lap exists between th is life stage and the 17 group of people with pre-existing diseases. 18 Newly available evidence for PM-related health effects in the older ad ult life stage spans 19 epidemiologic, controlled human exposure, and toxicological studies (US EPA, 2009a, section 20 8.1.1.1). One new large epidemiologic study (US EP A, 2009a, section 7.2.9; Miller et al., 2007) 21 of post-menopausal female residents of 36 U.S. metropolitan areas (age range = 50-79 yr) found 22
increases in PM 2.5 -related risk of MI, cor onary revascularization, 10 and their combination with 23 CHD-related death for participants free of C VD at baseline. While recent epidemiological 24
evidence for cardiovascular morbidit y effects in older adults in response to short-term exposure 25
to PM 2.5 and PM 10-2.5 is limited, when taken together with evidence from studies of PM 10 , 26 support is found for increased risk of cardiovascular morbidity in ol der adults. With regard to 27 respiratory morbidity, while some epidemiologic st udies have reported an in crease in respiratory 28 hospital admissions in individuals 65 years of ag e and older, consistent associations have not 29
been observed across all such studies. 30 With respect to mortality, recent epidemiologi c studies have also found that individuals 31 greater than 65 years old are at greater risk of all-cause (non-accident al) mortality upon short32 term exposure to both PM 2.5 and PM 10 , consistent with the findings of the 2004 AQCD. 33 Epidemiological studies that ex amined the association between mortality and long-term exposure 34

10 Coronary revascularization includes percutaneous coronary interventions, such as angioplasty.Draft Do Not Quote or Cite March 2010 2-29 to PM 2.5 and stratified the results by age (i.e., less th an 65 year of age compared to aged 65 and 1 older) reported results th at are consistent with the short-te rm exposure studies. However, in 2 sensitivity analyses studies have found evidence that risk declines with age starting at age 60 3
until there is no evidence of an asso ciation among people age 85 and older. 4 Controlled human exposure and dosimetry studies provide additional evidence for an 5
increase in cardiovascular a nd respiratory effects among older adults. Healthy older subjects 6 exposed to PM 2.5 concentrated ambient particles (CAPs) experienced significant decreases in 7 HRV (both in time and frequency) immediately following exposure, when compared to healthy 8 young subjects and to older adults with COPD (US EPA, 2009a, section 8.1.1.1). Dosimetry 9 studies have shown a depression of fine and coarse PM clearance in all regions of the respiratory 10 tract with increasing age beyond young adulthood. These results suggest that older adults are at 11 greater risk of PM-related respiratory health effects (US EPA, 2009a, section 8.1.1). 12 Animal toxicological studies have attempted to characteri ze the relationship between age 13
and PM-related health effects th rough the developmen t of models that mimic the physiologic 14 conditions associated with older people. For exam ple, arrhythmias have been observed in older, 15 but not younger, rats exposed to PM 2.5 CAPs. In addition, studies that used a mouse model of 16
terminal senescence observed various cardiovascu lar-related responses. Overall, these studies 17 provide biological plausibility for the increase in cardiovascular effects in older adults observed 18 in the controlled human exposure and epidemio logic studies (US EPA, 2009a, section 8.1.1). 19 In summary, the ISA concludes that evid ence from epidemiological, controlled human 20 exposure, and toxicological st udies provide coherence and bi ological plausibility for the 21 association between short-term exposure to PM a nd cardiovascular morbidity in older adults (US 22 EPA, 2009a, section 8.1.1.1). Add itional evidence from epidemiological studies that focus on 23 mortality and respiratory morbidity in response to short-term expos ure to PM also indicate that 24 older adults represent a susceptible life stage. 25 Pre-existing Cardiovascular or Respiratory Diseases 26 With regard to the risk from PM exposure to people with pre-existi ng cardiovascular or 27 respiratory diseases, the 2004 AQCD (US EPA, 2004, section 9.2.4.1) noted that a number of 28 time-series epidemiological studies reported increas ed risk in study subsets of individuals with 29 preexisting heart or lung diseases. Toxico logical studies using animal models of 30 cardiopulmonary disease provided ev idence suggestive of enhanced susceptibility to inhaled PM 31 in “compromised” hosts. Human dosimetry studies of subjects with COPD and asthma indicated 32 that airways disease leads to ve ry heterogeneous distributions of PM deposited within the lung. 33 These studies have shown up to 10-fold higher th an normal deposition at airway bifurcations, 34 thus creating “hot-spots” that ma y have biological implications. 35Draft Do Not Quote or Cite March 2010 2-30 The ISA notes that more recent epidemiol ogical and controlled human exposure studies 1 have directly examined the effect of PM on individuals with pre- existing diseases and 2 toxicological studies have employed disease m odels to identify whether exposure to PM 3 disproportionately effects certain populations (US EPA, 2009a, section 8.1.6). 4 The potential effect of underl ying cardiovascular diseases on PM-related health responses 5 has been examined using epidemiological studi es that stratify effect estimates by underlying 6 conditions or secondary diagnoses, and toxicological studies that us e animal models to mimic the 7 pathophysiological conditions associated with various cardiovascular diseases (e.g., MI, 8 ischemia, and atherosclerosis). A limited numb er of controlled human exposure studies have 9 also examined the potential rela tionship between cardiovascular di seases and exposure to PM in 10 individuals with underlying cardiova scular conditions, but these st udies have provided somewhat 11
inconsistent evidence for these associations. 12 One epidemiological study (US EPA, 2009a , section 7.2.9; Zanobetti and Schwartz, 13 2007) investigated associations between long-term exposure to PM 10 and the progression of 14 disease or reduced survival in a 21-city study of people discharged following an acute 15 myocardial infarction (MI). The study found si gnificant associations for mortality, CHF and 16 new hospitalization for MI. This is the first long-term study showing a significant association 17 between particle exposure and adverse post-MI ou tcomes in people who survived an MI. A few 18 toxicological studies examined potential effect modification of pre-ex isting cardiovascular 19 conditions on effects of long-term exposure to PM. In studies that focused on the cardiovascular 20 effects following subchronic exposure to PM in ApoE -/- mice, pathophysiological effects were 21 observed that included a decreasing trend in he art rate, physical activity, and temperature along 22 with responses in HRV; enhanced size of early atherosclerotic lesions wa s observed consistently 23
across studies. 24 The majority of the epidemiological literatur e that examined associations between short25 term exposure to PM and cardiovascular outcom es focuses on cardiovas cular-related hospital 26 admissions (HA) and emergency department (ED) visits. Hypertension is the pre-existing 27 condition that has been considered to the grea test extent when examining the association 28 between short-term exposure to PM and cardiovas cular-related HAs and ED visits. The results 29
of these studies have been mixed. There is also some new evidence from epidemiological 30
studies that individuals with pre-existing IHD are at greater risk from PM exposure, with 31 evidence from a toxicological st udy implicating impaired myocardial blood flow in the response. 32
Additional studies have examined the effects of PM on cardiac function in individuals with 33 dysrhythmia with mixed results. Limited a nd inconclusive evidence is available from 34 epidemiological studies that examined other pr e-existing cardiovascular conditions, such as CHF 35 and MI. Toxicological studies have provided some additional ev idence for the cardiovascular 36Draft Do Not Quote or Cite March 2010 2-31 health effects associated with exposure to PM in rodent models of underlying MI, but the 1
evidence is also inconclusive. Controlled human exposure studies that examined the effect of 2 pre-existing diseases on cardiovascular outcomes with exposure to PM are less consistent and 3 difficult to interpret in the context of the resu lts from the epidemiological and toxicological 4
studies. 5
A few new studies have also examined effect modification in mort ality associations. 6
These studies have found evidence of an increase in risk estimates for associations between PM 10 7 and mortality in individuals with underlying stroke, and effect m odification of the PM-mortality 8
association in indi viduals with CHF. 9 In summary, the newly available evidence from epidemiological and toxicological, and to 10 a lesser extent, controlled hu man exposure studies indicates increased susceptibility of 11 individuals with underlying cardiova scular diseases to PM exposure. Although the evidence for 12 some outcomes was inconsistent across epidemiologi cal and toxicological st udies, this could be 13 due to a variety of issues in cluding the PM size fraction used in the study, along with the study 14
location. 15 With regard to pre-existing respiratory illnesses, studies evaluated in the ISA have 16
examined the effect of these illnesses on mu ltiple health outcomes (e.g., mortality, asthma 17 symptoms) in response to exposure to ambient concentrations of PM (US EPA, 2009a, section 18 8.1.6.2). Epidemiological studies have examined th e effect of short-term exposure to PM on the 19 respiratory health of asthmatic individuals finding an increase in medication use and respiratory 20 symptoms (i.e., asthma symptoms, cough, shortne ss of breath, and chest tightness) with short21 term exposure to PM 2.5 , and morning symptoms and asthma attacks with short-term exposure to 22

PM 10 . Toxicological studies provide evidence that PM exposure results in allergic sensitization, 23 and that individuals with allerg ic airways conditions are at great er risk of allergic airways 24 responses upon exposure to PM 2.5 . Further, there is much more limited evidence which suggests 25 that non-allergic respiratory morbidities may also increase the susceptibility of an individual to 26 PM-related respiratory effects. 27 The results from the epidemiological and t oxicological studies th at focused on underlying 28 allergic airways disease are s upported by a series of controlled human exposure studies which 29 have shown that exposure to diesel exhaust part icles (DEPs) increases the allergic inflammatory 30 response in atopic individuals. However, other studies reporte d that healthy and asthmatic 31 subjects exposed to coarse, fine and ultrafin e CAPs, exhibited similar respiratory responses, 32 although these studies excluded moderate and severe asthmatics that would be expected to show 33 increased susceptibility to PM exposure. 34 With respect of pre-existing COPD, the resu lts of epidemiological studies have been 35
mixed. A few controlled huma n exposure studies examined th e effects of exposure to PM 2.5 36Draft Do Not Quote or Cite March 2010 2-32 CAPs on healthy and COPD subjects and found no signi ficant difference in re spiratory effects. 1 However, the results from dosimetric studies ha ve shown that COPD patients have increased 2 dose rates and impaired mucociliary clearan ce relative to age-matched healthy subjects, 3 suggesting that individuals with COPD are potentially at a great er risk of PM-related health 4 effects (US EPA, 2009a, section 3.2.1). 5 A few epidemiological studies examined the effect of underlying re spiratory illnesses on 6 the association between short- and long-term exposure to PM and mortality. Using different 7 pre-existing respiratory illnes ses, two studies found that short-term exposure to PM 10 increased 8 the risk of non-accidental mortality in individu als with a secondary diagnosis of pneumonia and 9 circulatory mortality in individuals with a secondary diagnosis of a respiratory il lnesses. Another 10 study observed an association be tween long-term exposure to PM 10 and mortality in individuals 11 that had previously been hosp italized for COPD. Together, th ese studies show the potential 12 effect of underlying respiratory illnesses on th e PM-mortality relationship (US EPA, 2009a, p. 8- 13 13). 14 In summary, with respect to the potential fo r increased risk from PM exposure to people 15 with respiratory disease, ove rall, the controlled human expos ure and toxicological studies 16 evaluated in the ISA provide biol ogical plausibility for the incr eased risk of health effects 17 observed in epidemiological studies among asthma tic individuals in response to PM exposure 18 (US EPA, 2009a, section 8.1.6.2). The evidence from studies that examined associations 19
between PM and health effects in indi viduals with COPD is inconsistent. 20
Socioeconomic Status 21 Socioeconomic status is a composite measure that usually consists of economic status, 22 measured by income; social status measured by education; and work status measured by 23 occupation. Based on data from the U.S. Cens us Bureau in 2006, from among commonly-used 24 indicators of SES, about 12% of individuals and 11% of families are below the poverty line (US 25 EPA, 2009a, section 8.1.7). Within the U.S. appr oximately 16% of the population does not have 26 a high school degree and only 27% have a bachel or’s degree or higher level of education (US 27 Census, 2009). Educational attainment generally coincides with an individual’s income level, 28 which is correlated to other surrogates of SES, such as residential environment. Additionally, 29
low SES individuals have been found to have a higher prevalence of pre-existing diseases; 30 limited access to medical treatment; and limited access to fresh foods leading to a reduced intake 31 of antioxidants, polyunsaturated fatty acids a nd vitamins, which can increase this population 32 group’s risk from PM. Low SES and surrogate s of SES such as educational attainment, 33
residential location and nutritional status have been shown in some studies to modify health 34 outcomes of PM exposure for a population. 35Draft Do Not Quote or Cite March 2010 2-33 The 2004 AQCD concluded there is effect m odification of long-term PM exposures1 mortality associations due to socioeconomic fact ors. In the ACS and Harvard Six Cities cohort 2 analyses on mortality risk with long-term exposure to PM 2.5 , there was clear evidence of greater 3 effects being reported in the cohort subgroups with lower ed ucation levels (US EPA 2004, 4 section 9.2.4.5). The ISA conclude s that this is further support ed by a reanalysis of the ACS 5 cohort (Krewski et al., 2009), which found mode rate evidence for increased lung cancer 6 mortality in individuals with a high school education or less in response to long-term exposure to 7

PM 2.5 (US EPA, 2009a, section 8.1.7). Another study examined whether long-term exposure to 8 traffic-related pollutants varied by SES at th e block group level. The authors found higher 9
concentrations of NO 2 associated with lower SES areas , which suggests that lower SES 10 individuals are disproportiona tely exposed to traffic-rela ted pollutants, including PM. 11 Among the studies of short-term PM exposure, the 2004 CD concluded that the evidence 12 was mixed regarding SES and PM-related health risks. New studies evaluated in the ISA 13
indicate that evidence of the infl uence of SES on health outcomes related to short-term exposures 14 is stronger (US EPA, 2009a, s ection 8.1.7). These include an increased risk in mortality 15 associated with short-term exposure to PM 2.5 and its components. Jerrett et al. (2004) examined 16 the modification of short-term mortality eff ects due to particulate air pollution exposure by 17 residential location in Hamilton, Canada. The aut hors found that the area of the city with the 18 highest SES characteristics (measured using the surrogate educational attainment) displayed no 19
evidence of effect modification wh ile the area with the lowest SE S characteristics had the largest 20 health effects. Another study noted an increased risk in mortality associated with short-term 21 exposure to PM 2.5 and its components for individuals with low SES, while additional analyses 22 stratified by education level have also observed c onsistent trends of increased mortality for PM 2.5 23
and PM 2.5 species for individuals with low edu cational attainment (US EPA 2009a, section 24 8.1.7). 25
Nutritional deficiencies have been associated with increased susceptibility to a variety of 26
infectious diseases and chronic health effect s. Low SES may decrease access to fresh food, 27 thereby nutritional deficiencies could increase su sceptibility to PM-related health effects. One 28 study that examined the association between exposure to PM 2.5 and HRV in individuals with 29 genetic polymorphisms associated with increased ri sk of CVD, found that when individuals with 30 these genetic polymorphisms increased their intake of B6, B12, or methionine, no PM 2.5 effect on 31
HRV was observed. 32
The ISA concludes that there is evidence that SES, measured using surrogates such as 33
educational attainment or re sidential location, modifies th e association between PM and 34 morbidity and mortality outcomes (US EPA, 20 09a, section 8.1.8). In addition, nutritional 35Draft Do Not Quote or Cite March 2010 2-34 status, another surrogate of SES, has been shown to have pr otective effects against PM exposure 1 in individuals that have a higher inta ke of some vitamins and nutrients. 2 Summary 3 In summary, we reach the preliminary conclusi on that there are several population groups 4 that are likely to be susceptible to PM-related e ffects. These groups include the life stages of 5 children and older adults, those w ith preexisting heart and lung diseas es, and those of lower SES. 6 We also preliminarily conclude that the availabl e evidence does not genera lly allow distinctions 7
to be drawn between the PM indicators, in terms of which groups might have greater 8 susceptibility to PM 2.5 and PM 10-2.5
. 9

 To what extent does the newly available scie ntific evidence report associations that 10 extend to air quality concentrations that are lower than had previously been observed 11 or that are observed in areas that would likely meet the current suite of PM 2.5 12 standards? 13 We now focus our attention on addressing the question of whether the available evidence 14 supports consideration of standards that are more protective than th e current suite of PM 2.5 15 standards. In addressing this question, we fi rst recognize that the ISA concludes there is no 16 evidence to support the existence of a discernabl e threshold below which effects would not occur 17 (US EPA, 2009a, section 2.4.3). We consider wh ether new evidence provides information for 18
health effects associated with ai r quality levels that are lower th an had previously been observed, 19 in particular to levels at or below the level of the current annual standard (15 μg/m 3 ) and/or to 20
levels at or below the level of th e current 24-hour standard (35 μg/m 3 ). As an initial matter, we 21
first focus on levels at which effects cl assified as having a causal or likely causal association 22
with PM 2.5 exposure have been observed. We consider effects classified as having suggestive 23
associations with PM 2.5 exposure in section 2.3 when considering the margin of safety provided 24 by alternative suites of st andards. We have evaluated the air quality data using the forms of the 25
current PM 2.5 standards. 11 26
Associations with Long-term PM 2.5 Exposure 27
With regard to mortality associated with long-term PM 2.5 exposure, in the last review, the 28 2004 AQCD placed greatest weight on the reanalyses and extensions of two prospective cohort 29 studies, the ACS and the Harvard Six Cities studi es, finding that these studies provided “strong 30 evidence” for associations with fine particle s and confirmed and stre ngthened the evidence 31 available in the review comple ted in 1997 (US EPA, 2004, p. 9-33; Krewski et al., 2000). In the 32

11 The current form of the annual PM 2.5 standard is the annual arithmetic mean , averaged over 3 years with limited conditions allowing spatial averaging. The current form of the 24-hour PM 2.5 standard is the 98 th percentile, averaged over 3 years.Draft Do Not Quote or Cite March 2010 2-35 current review, as stated above, staff notes that newly availabl e extended follow-up analyses of 1 the ACS and Harvard Six Cities studies provide consistent and stronger evidence of a causal 2 association with mortality at lower air quality distributions of PM 2.5
. 3 In considering studies of the ACS cohort, in the last review, the original and reanalysis 4 studies reported significant a ssociations between fine particles and mortality (US EPA, 2004, 5 8.2.3.2.1; Pope et al., 1995; Krewski et al., 2000). In addition, an extended analysis using the 6
ACS cohort also available in the last review doub led the original follow-up period to more than 7 16 years. This study continued to report statistically significant associations with long-term 8

PM 2.5 exposure with the incl usion of more recent PM 2.5 air quality data and triple the number of 9 deaths (US EPA, 2004, 8.2.3.2.2; Pope et al., 2002). As with the original ACS cohort study, no 10
evidence of a threshold was observe d in the relationships with to tal, cardiovascular-related, and 11 lung cancer mortality reported in this extended study. A recent extended analysis of the ACS 12
cohort available in this review lengthens the follow-up of this important study to 18 years (1982 13 to 2000) (US EPA, 2009a, pp. 7-84 to 7-85; Figure 7-6; Krewski et al., 2009). This extended 14 analysis has “confirmed with re markable consistency the association of mortality and exposure 15
to PM 2.5 reported in previous stud ies of the ACS data starting 15 years ago... and added 16 precision, especially for the evidence that ischemic heart disease is a cause of death particularly 17 affected by exposure” to PM 2.5 (HEI, 2009, p. 135). We note the decline in ambient PM 2.5 18 concentrations over 18 years, from an aggregat e long-term mean in 58 metropolitan statistical 19 areas (MSAs) of 21.2 (4.6) 12 μg/m 3 (ranging from approximately 9 to 34 μg/m 3 across cities) in 20 the original monitoring period (1979 to 1983) dec lining to air quality distributions reported for 21 the most recent years evaluated (1999-2000) fo r 116 MSAs with an aggregate long-term mean 22

PM 2.5 concentration of 14.0 (3.0) μg/m 3 (ranging from approximately 6 to 22 μg/m 3 across cities) 23 to an overall average acro ss all year of 17.1 (3.7) μg/m 3 (ranging from about 7.5 to 30 24 μg/m 3 )(US EPA, 2009a, Figure 7-6; Krew ski et al, 2009; Pope et. al, 2004). In addition, Eftim et 25 al., (2008) assessed the ACS sites using an ecological cr oss-sectional study design of a Medicare 26 cohort, incorporating more recen t air quality (2000-2002) with an aggregate long-term mean 27

PM 2.5 concentration of 13.6 (2.8) μg/m 3 (ranging from approximately 6 to 25 μg/m 3 ). This study 28 reported somewhat higher effect estimates than thos e reported by the original investigators. The 29 ISA concludes there may be several possible explan ations for this apparent increase, especially 30 that this is an older populati on or more likely because of the lack of personal confounder 31 information (e.g., past personal smoking information) that “led to an insufficient control for the 32
effects of these other variables’ effects on mo rtality, inflating the pollution effect estimates 33

12 Throughout this discussion concentrations reported are mean (standard deviation, SD) or median (interquartile range, IQR, 25 to 75%).Draft Do Not Quote or Cite March 2010 2-36 somewhat, similar to what has been found in the ACS analyses when only ecological-level 1
control variables were include d” (US EPA, 2009a, pp. 7-87 to 7- 88; Figures 7-6 and 7-7). 2 With respect to a the Harvard Six Cities study, Laden et al (2006) have extended 3 mortality follow-up for an addi tional eight years during a peri od of “reduced air pollution 4 concentrations” lengthening the follow-up period to 25 years. These investigators reported 5 statistically significant associations between long-term exposure to PM 2.5 and mortality for air 6 quality data for the original study period (1974 to 1989) as well as the extended follow-up period 7 (1990-1998). As noted in the ISA, this study prov ides evidence of a stat istically significant 8 reduction in mortality risk with decreasing long-term PM 2.5 concentrations (US EPA, 2009a, p. 9 7-84). Evidence from the original and reanalysis of the Harvard Six Cities study available in the 10 last review reported an a ggregate long-term mean PM 2.5 concentration of 18 μg/m 3 (ranging from 11 approximately 11 to 30 μg/m 3 across cities) (US EPA, 2004, p. x.x; Dockery et al., 1993; 12 Krewski et al., 2000). In the extended follo w-up period, an aggregate long-term mean PM 2.5 13 concentration of 14.8 (4.2) μg/m 3 (ranging from approximately 10 to 22 μg/m 3 across cities) with 14 an overall aggregate mean across bo th study periods of 16.4 (5.6) μg/m 3 (ranging from 15 approximately 11 to 25 μg/m 3 ) (US EPA, 2009a, Figure 7-6; La den et al., 2006; Laden, 2009). 16 This reduction was observed for total mortality as well as cardiovascular-related and respiratory17 related mortality but not deaths related to l ung cancer, “a disease with a longer latency period 18 and less reversibility” (Laden et al, 2006). The ISA notes that “a stat istically significant 19 reduction in mortality risk [was] re ported with reduced long-term PM 2.5 concentrations” (US 20 EPA, 2009a, p. 7-84). These findings suggest that the mortality effects of long-term air pollution 21 may be at least partially reversible over periods of a decade” (Laden et al ., 2006; Table 3). In an 22 additional analysis of the extended follo w-up of the Harvard Six Cities cohort study, 23 investigators reported the concentration-respons e relationship was linear and “clearly continuing 24
below the level” of the current annual standard (US EPA, 2009a, p. 7-92; Schwartz et al., 2008). 25 Eftim et al. (2008) also analyzed the Harvard Si x Cities study sites using a Medicare cohort with 26 more recent air quality data (2000-2002) and re ported consistent but somewhat higher effect 27 estimates with relation to the extended follow-up of this study conducted by Laden et al. (2006) 28 (US EPA, 2009a, pp. 77-87-7-88, Figures 7-6 and 7- 7). The aggregate long-term mean reported 29 in this study was 14.1(3.1) μg/m 3 (ranging from about 10 to 19 μg/m 3 ) (Eftim et al., 2008). 30 In addition to extended follow-up analyses of the ACS and Harvard Six Cities studies, 31
new evidence is available in this review from two new U.S. long-term cohort studies. The 32 Women’s Health Initiative (W HI) provides evidence of asso ciation between long-term PM 2.5 33 exposure and cardiovascular morbidity and mort ality effects. This study reported results 34
consistent with the ACS and Harvard Six Cities studies while identifying much larger relative 35 risk estimates per μg/m 3 . This study represents an impor tant new cohort of postmenopausal 36Draft Do Not Quote or Cite March 2010 2-37 women with no previous history of pre-existing cardiac disease, potentially a “h ealthier cohort 1 population” than that considered by the ACS a nd Harvard Six Cities studies (US EPA, 2009a, p. 2 7-87). The ISA notes, that the “PM 2.5 impacts may yield higher rela tive risk estimates in the 3 WHI population because the PM 2.5 risk is being compared to a much lower prevailing risk of 4 cardiovascular death in this select study popul ation” (US EPA, 2009a, p. 7-87). The overall 5

PM 2.5 concentration averaged across cities reported in this study was 13.5(3.3) μg/m 3 (ranging 6 from about 3.4 to 28 μg/m 3 ) (Miller et al., 2007). 7 A new retrospective cohort study, the Me dicare Cohort Air Pollution Study (MCAPS) 8 has evaluated long-term PM 2.5 exposure and mortality risk in ol der adults (65 years of age and 9 older) within 3 geographic regions . Zeger et al. (2007) reported that long-term exposure to PM 2.5 10 was significantly associated with an increase in mortality among Medi care participants, and 11 stronger associations were observed in eastern counties compared to a national estimate, and no 12 association was observed among West ern counties. However, effect estimates decreased by 50% 13 with adjustment for spatial confounding. In a subsequent retrospectiv e cohort study (MCAPS), 14 Zeger et al. (2008), reported that average 6-year exposure to PM 2.5 was significantly associated 15 with increased risk of mortality in the eastern and central regions. 13 In addition, the results 16 indicated that risk declined with increasing ag e, and similar to their earlier study, no association 17
was observed between PM 2.5 and mortality in the western region. Moreover, risk estimates were 18 similar to effect estimates reported in the ACS and Harvard Six Cities study, providing 19 coherence across prospective st udies for an association between long-term exposure to PM 2.5 and 20 mortality. This study reported as sociations between long-term PM 2.5 exposure and mortality for 21 the eastern and central regions th at were qualitatively similar to those reported in the ACS and 22 Harvard Six Cities studies. The long-term aggregate PM 2.5 median concentration reported 23 across all cities was 13.2 μg/m 3 (with an interquartile range from about 11 to 15 μg/m 3 ) (US 24 EPA, 2009a, p. 7-88; Zeger et al., 2008). 14 25 With respect to respiratory morbidity effects associated with long-term PM 2.5 exposure, 26 the 2004 AQCD concluded that new studies of a cohor t of children in Southern California had 27 built upon earlier limited evidence to provide evidence that long-term exposure to fine particles 28 was associated with development of chronic respiratory disease and reduced lung function 29 growth (US EPA, 2004, p. 9-33). The acros s-city mean of 2-week average PM 2.5 concentrations 30 reported in the initial Southern California Children’s Health Study was approximately 15.1 31

13 The Zeger et al. (2008) analysis included COPD as a pro xy for smoking status. The inve stigators reported the risk estimate for the eastern region declined and the central region increased using this adjustment. This result may possibly be related to bias introduced in using COPD as a proxy for smoking.
14 Zeger et al. (2008) assessed the relative risk of death associated with long-term PM 2.5 exposure for three U.S. regions. Median (IQR) PM 2.5 concentrations reported by region were: Eastern region - 14.0 μg/m 3 (12.3-15.3); Central region – 10.7 μg/m 3 (9.8-12.2); Western region – 13.1 μg/m 3 (10.4-18.5).Draft Do Not Quote or Cite March 2010 2-38 μg/m 3 (ranging from approximately 7 to 32 μg/m 3 ) (Peters et al., 1999). These results were found 1
to be consistent with results of cross-sectiona l analyses of the 24-City study by Dockery et al. 2 (1996) and Raizenne et al. (1996) which reported a long- term cross-city mean PM 2.5 3 concentration of 14.5(4.2) μg/m 3 (ranging from approximately 6 to 21 μg/m 3 ). Gauderman et al. 4 (2004) have now extended the analysis of the S outhern California Children’s Health Study to 8 5 years, following the children between the ages of 10 and 18, “a period of rapid lung 6 development” and reported that the “pollution-re lated deficits in the average growth in lung 7 function over the 8-year period resu lted in clinically important deficits in attained lung function 8 at the age of 18” (US EPA, 2009a, p. 7-27). The four year cross-city mean was 13.8 (7.7) μg/m 3 9 (ranging from approximately 6 to 29 μg/m 3 ) across the 12 study communities (McConnell et al., 10 2003). 11 In summary, newly available scientific evidence provides suppor t for associations 12 between long-term PM 2.5 exposure and mortality and morbidity effects that extend to air quality 13 levels that are lower than had previously been observed. These studies ev aluate a broader range 14
of health outcomes than were considered in th e last review and include extended follow-up for 15 prospective epidemiological studies that were impor tant in the last review as well as additional 16 evidence in important new cohorts. In looking across the body of scientific evidence and 17 focusing on the most recent years of air quality data considered in these studies, we observe 18 effects occurring below the le vel of the current annual PM 2.5 standard (US EPA, 2009a, chapter 19 7; Figures 2-2 and 7-7). 20

Associations with Short-term PM 2.5 Exposure 21

In the last review, in selecting the level of the 24-hour PM 2.5 standard, emphasis was 22 placed on short-term exposure studies and their 98 th percentile air qualit y values that provided 23
evidence of associated health effects in areas th at would have met the then current annual and 24
24-hour PM 2.5 standards during the time of the study. In focusing on the 98 th percentile value in 25 these studies the Administrator recognized that these studies did not prov ide evidence of clear 26
effect thresholds or lowest-obs erved levels. Therefore, the Ad ministrator sought to establish a 27 standard level that would require improvements in air quality generally in areas in which the 28 distribution of daily short-term exposure to PM 2.5 can reasonably be expect ed to be associated 29 with serious health outcomes (i .e., mortality, respiratory and card iovascular morbidity). In the 30 prior review, we noted an overall pattern of st atistically significant associations observed in 31 studies of short-term exposure to PM 2.5 across a wide range of 24- hour average 98th percentile 32 values in predominately single-city studies as well as a limited number of multi-city studies. A 33 predominance of studies with 98 th percentile values down to approximately 39 μg/m 3 (Burnett 34 and Goldberg, 2003) reported statistically signi ficant associations with mortality, hospital 35Draft Do Not Quote or Cite March 2010 2-39 admissions, and respiratory symptoms. Within the range of 24-hour average 98 th percentile 1

PM 2.5 concentrations of about 35 to 30 μg/m 3 , we did not observe a prep onderance of statistically 2 significant results. Furthermore, the lim ited number of studies in which the 98 th percentile values 3 were below this range did not provide a basis for reaching conclusions about associations at such 4 levels (71 FR 61168/3 – 61169/2, October 17, 2006). 5 As discussed in section 2.1.3, our current approach to reach ing preliminary conclusions 6 about the adequacy of the current suite of PM 2.5 standards is more integrative than the approach 7 used in the last review. In this review, in considering the adequacy of the current suite of 8 standards, in evaluating the currently available evidence from short-term PM 2.5 exposure studies, 9 we look both at the aggregate long-term mean PM 2.5 concentration in key studies as well as the 10
distributions of 24-hour PM 2.5 concentrations, with a focus on the 98 th percentile concentrations 11
to match the form of the current 24-hour standard , to the extent such da ta are available. 12 A number of new multi-city and single-city short-term PM 2.5 exposure studies and 13 additional analysis of a previous ly existing cohort study availabl e in this review examine the 14 association between short-term exposure to PM 2.5 and mortality and a broader range of 15 cardiovascular and respiratory mo rbidity endpoints. Multi-city st udies support a largely positive 16 and frequently statistically significant rela tionship between short-term exposure to PM 2.5 and 17 increased risk of mortality. In a multi-city time -series analysis of 112 U.S. cities, Zanobetti and 18 Schwartz (2009) reported that an overall 24-hour average 15 PM 2.5 level across all years of 34.3 19 (8.8) μg/m 3 (ranging from 17.9 to 80.3 μg/m 3 ) (US EPA, 2009a, Figure 6-24) from lag 0-1 days 20 were positively and significantly associated with all-cause, cardiovasc ular-related (e.g., 21 myocardial infarction, stroke), a nd respiratory-related mortality. Furthermore, city-specific 22 effect estimates included in Figure 6-24 of the ISA indicate the associat ion between short-term 23 exposure to PM 2.5 and total mortality and cardiovascula r mortality and respiratory mortality 24 endpoints is consistently positive for an overwhe lming majority (99%) of the 112 cities across a 25 wide range of air quality concentrations (U S EPA, 2009a, p. 6-178 to 179). In addition, the 26 authors report that for all-cause mortality city -specific effect estimates were statistically 27 significant for 55% of the 112 cities, with 24-hour PM 2.5 levels ranging from 18.4 to 64.9 μg/m 3

. 28
In the current review of evidence on mortalit y associated with short-term exposure to 29

PM 2.5 , we note that an expansion of the multi-city Canadian study from 8 (Burnett and Goldberg, 30 2003) to 12 Cities (Burnett et al 200 4) yielded results consistent with prior findings of a positive 31 and statistically significant association between an average 1-day lag 24-hour PM 2.5 exposure 32 across all years of 38.1 μg/m 3 (extending from 25 to 50 μg/m 3 ) and daily mortality (US EPA, 33 2009a, Figure 2-1). However, the influence of NO 2 and limited PM 2.5 data for several years 34

15 Concentrations reported for short-term studies are mean 98 th percentile (standard deviation, SD)Draft Do Not Quote or Cite March 2010 2-40 during the study period somewhat diminish thes e findings and underscore the need for more 1 frequent PM 2.5 measurements and additional data on co- pollutants to inform our understanding of 2
the PM 2.5 -mortality association. In gene ral, as can be seen in Fi gure 6-27 of the ISA, effect 3
estimates for associations between mo rtality and short-term exposure to PM 2.5 are positive and a 4 number are statistically signifi cant (ISA, US EPA, 2009a, p. 6-184). Larger effect estimates 5 were reported in some studies for associations with respiratory mortality in comparison to 6
cardiovascular and all-cause mo rtality, but these effect estim ate include larger confidence 7 intervals (i.e. less precision) si nce respiratory deaths comprise only a small proportion of total 8
deaths. 9 With regard to cardiovascular a nd respiratory morbidity effects, in the first analysis of the 10 MCAPS cohort conducted by Dominici et al ( 2006a) across 204 US c ounties, investigators 11 reported a statistically significant asso ciation between an average 24-hour PM 2.5 concentration 12 across all years of 34.8 μg/m 3 (extending from 10.4 to 85.6 μg/m 3 ) and hospitalizations for 13 cardiovascular and respiratory diseases. Furthermor e, a sub-analysis restricted to days with 24- 14 hour average concentrations of PM 2.5 at or below 35 μg/m 3 indicated that, in spite of a reduced 15 statistical power from a smaller number of study da ys, statistically significa nt associations were 16 still observed between short-term exposure to PM 2.5 and hospital admissions for cardiovascular 17 and respiratory diseases (Dominici, 2006b 16 )). These results along with the observation that 18 approximately 50% of PM 2.5 levels across the 204 counties ac ross all years were below the 24- 19 hour standard suggests that the ov erall health effects observed acr oss the U.S. are not primarily 20 driven by the higher end of the PM 2.5 air quality distribution (Cite Docket # for AQ provided by 21 authors). In an extended analysis of the MC APS study, Bell et al (2008) reported a positive and 22 statistically significant increase in cardiovascular hospitalizations associated with and average0- 23 day lag PM 2.5 concentration across all years of 34.2 (8.5) μg/m 3 (extending from 9.4 to 77.0 24 μg/m 3 ). In addition, significant increases in respir atory disease hospitaliza tions were associated 25
with mean PM 2.5 at lag 2. Furthermore, se veral single-city short-term PM 2.5 exposure studies 26 with average 98 th percentile PM 2.5 exposures below 35 μg/m 3 substantiate findings from the 27 aforementioned multi-city studies generally repo rting positive statistically significant and non28 significant associations for PM 2.5 exposures in relation to mortality, cardiovascular and 29 respiratory hospitalizations and ED visits (Figur e 2-4). Consequently, th ese short-term studies 30 provide evidence of PM 2.5 associated mortality and morbidity effects occurring at and below the 31
level of the current 24- hour standard. 32

16 This sub-analysis was not included in the original publication (Dominici et al., 2006a). Authors provided subanalysis results for the Administrator’s consideration as a letter to the docket following publication of the proposed rule in January 2006.Draft Do Not Quote or Cite March 2010 2-41 In considering long-term average ambi ent concentrations from short-term PM 2.5 exposure 1 studies, we recognize that in th e last review, several U.S. and Canadian studies provided 2
evidence of associations betw een short-term exposure to PM 2.5 and serious health effects in areas 3
with PM 2.5 levels at and above the le vel of the current annual PM 2.5 standard (15 μg/m 3 ). 4 Moreover, a few short-term PM 2.5 exposure studies (Figure 2-4) av ailable in that review provided 5 evidence of statistically signi ficant associations with PM 2.5 in relation to cardiovascular and 6 respiratory effects for areas in which long-term average PM 2.5 concentrations ranged between 12 7 and 14 μg/m 3 and 98 th percentile 24-hour concentrations ranged between 31 and 59 μg/m 3 (US 8 EPA, 2005, p. 5-7). 9 Similarly, in this review, many short-term PM 2.5 exposure studies, and in particular those 10 conducted across multiple cities, repo rt statistically significant eff ects with mean concentrations 11
below the level of the current annual standard. Dominici et al. (2006a) and Bell et al. (2008) 12 report 24-hour average PM 2.5 levels across all years of 13.4 (2.9) μg/m 3 (extending from 4.4 to 13 22.7 μg/m 3 ) and 12.9 (2.7) μg/m 3 (extending from 4.3 to 20.4 μg/m 3 ), respectively (US EPA, 14 2009a, Figure 2-1). Likewise, Zanobetti and Schw artz (2009) report city annual averages across 15 all years of 13.2 () μg/m 3 (extending from 6.6 μg/m 3 to 24.7 μg/m 3 ) (Figures 2-1 and 6-24, US 16 EPA, 2009a). In addition, Burnett et al. 2004, re ports city annual averag es across all years of 17 12.8 μg/m 3 (extending 8.1 to 16.7 μg/m 3 ) (Figure 2-1, ISA – US EPA, 2009a). Based on the 18 findings from these multi-city short-term PM 2.5 exposure studies, the IS A concludes that overall, 19 consistent positive associations have been reported for a range of mortality and cardiovascular 20 and respiratory morbidity effects for mean 24-hour PM 2.5 concentrations at and above 12.8 μg/m 3 21 (US EPA, section 2.3.1.1). 22 Taken together, these findings from single- and multi-city epidemiological studies of 23
short-term PM 2.5 exposure in relation to mortality and cardiovascular and respiratory morbidity 24 provide evidence of short-term PM 2.5 associated health effects occu rring at or below the current 25 levels of the 24-hour standard (Figure 2-1, US EPA, 2009a, p. 2-14). These findings are 26 bolstered by evidence of statistically significant PM 2.5 associated health effects occurring in 27 analyses restricted to days in which 24-hour average PM 2.5 levels were below 35 μg/m 3 28 (Dominici, 2006b). Multi-city sh ort-term studies conducted since th e prior review (Burnett et al. 29 2004; Dominici et al. 2006a; Be ll et al. 2008; Zanobetti and Sc hwartz, 2009) also provide 30 supportive evidence for short-term PM 2.5 exposure associated health e ffects occurring at levels at 31
and below the annual standard. 32 Summary 33 In evaluating the currently available scien tific evidence, we reach the preliminary 34 conclusion that the evidence from long and short-term PM 2.5 exposure studies, and in particular 35 those studies conducted across multiple U.S. cities cal ls into question whethe r the current suite of 36Draft Do Not Quote or Cite March 2010 2-42 PM 2.5 primary standards protects public health with an adequate ma rgin of safety from effects 1 associated with long- and short-term exposures to PM 2.5 . We also reach the preliminary 2 conclusion that this evidence prov ides strong support for considering fine particle standards that 3 would impart increased protection beyond that a fforded by the current annual and 24-hour PM 2.5 4 standards. More protective standards would re flect the substantially stronger and broader body 5 of evidence for mortality and cardiovascular and respiratory morbidity effects now available in 6
this review both at lower levels of air quality than had previously been observed and at levels 7 below the current annual (15 μg/m 3 ) and 24-hr (35 μg/m 3 ) PM 2.5 standards. 8

2.2.2 Risk-based Considerations 9 Looking beyond evidence-based considerations, staff also has considered the extent to 10
which health risks estimated to occur upon just meeting the current suite of PM 2.5 standards may 11 be judged to be important from a public health pe rspective, taking into ac count key uncertainties 12
associated with the estimated risks. 13 The quantitative risk assessment conducted in this review (US EPA, 2010a) builds upon 14 and expands upon the analyses conducted for th e previous review (US EPA, 2005, chapter 4; 15 Abt, 2005). As an initial matter, we recognize th at the previous quantitative risk assessment 16 incorporated alternative assumed cutpoints as surrogates for potent ial population thresholds. In 17 the current review, the ISA exam ined the available epidemiologic evidence to characterize the 18 shape of the concentration-res ponse (C-R) relationship and assess possible PM “thresholds” (i.e., 19
levels which PM 2.5 concentrations must exceed in order to elicit a health response). Overall, 20 based on limited evidence primarily focusing on cardiovascular-related hospital admissions and 21 emergency department visits associat ed with short-term exposures to PM 10 and mortality 22 associated with long-term exposure to PM 2.5 , using a variety of methods and models, the ISA 23 concludes the currently availabl e evidence supports the use of a no-threshold, log-linear model 24 (US EPA, 2009a, p. 2-25). Therefore, the quantit ative risk assessment conducted for this review 25 did not include assumed cutpoints as surroga tes for potential population thresholds. We 26 concluded that is was more appropriate to focus on alternative rollback strategies. 17 27 The assessment of uncertainty and variability completed for this analysis is more 28 comprehensive than had been done for previous ri sk assessments. This reflects, in part, the 29 development of methods by EPA staff to address pot entially important sour ces of variability and 30

17 While we have not included cutpoints in the risk a ssessment for the reasons cited, in the case of long-term exposure-related mortality, we have limited estimation of risk to ambient PM 2.5 levels above the lowest measured level (LML) of the epidemiological study from which the concentration-response function was obtained (Krewski et al., 2009; US EPA, 2010a, sec tion 3.2.3). In the case of short-term exposure-related mortality and morbidity, we modeled risk down to PRB. In both cases, this reflects consideration for the range of ambient PM 2.5 where we believe we have confidence in characterizing the nature of the CR function shape (and not an assumption that risk is negligible below these levels).Draft Do Not Quote or Cite March 2010 2-43 uncertainty. For example, to more fully explore po tential variability in the patterns of reductions 1
in ambient PM 2.5 that may occur upon just meeting the current and alternative standards, we 2 incorporated as part of the se nsitivity analysis, two additional rollback approaches (hybrid and 3 peak shaving) in addition to the proportional ro llback used in the core analysis. In addition, 4 recently published literature has allowed us to more rigorously examine the impact of uncertainty 5 related to specifying C-R functions for long-term exposure-related mortality through a series of 6 sensitivity analyses (i.e., Krew ski et al. (2009) provided extensiv e analysis of alternative model 7 specifications for mortality which could be readil y incorporated into our sensitivity analysis). 8 For this review, we have estimated risk for a set of health effects endpoints that reflected 9 consideration of the degree of support in the literature for a causal relationship between PM 2.5 10 exposure and the health effect of interest as assessed in the ISA, together with consideration of 11 the health significance of the endpoint. 18 Specifically, we have estimated risks for (a) all-cause, 12 IHD, cardiopulmonary and lung cancer mortality related to long-term PM 2.5 exposure, (b) non13 accidental, cardiovascular (CV) and respir atory mortality related to short-term PM 2.5 exposure, 14 and (c) cardiovascular-related and respiratory-related hospita l admissions (HA) and asthma15 related emergency department visits associated with short-term PM 2.5 exposure. While we have 16 modeled risk for a selection of long-term and short-term exposure-related endpoints, in the 17 discussion of risk estimates presented below, we focus on cardiovascular-rel ated endpoints, since 18 the causal association for these endpoints based on available literature is assessed in the ISA to 19 be the strongest of the endpoints considered. 20 In considering the health risks estimated in selected urban study ar eas to occur upon just 21 meeting the current suite of PM 2.5 standards, we focused on a core (primary) set of risk results 22 based on the application of modeling element c hoices (e.g., concentration-response functions, lag 23 periods) that have the greatest overall support in th e literature (hereafter referred to as the “core” 24 results). In addition, to gain insights into which sources of un certainty may have the greatest 25 impact on risk estimates when acting alone, or in combination with other sources of uncertainty, 26 as noted above, we conducted a series of single- element and multi-element sensitivity analyses to 27 generate a broader set of reasonable alternative risk estimates that allowed us to place the results 28 of the core analysis in context with regard to uncertainty. We also conducted additional analyses 29 to place the results of the urban study area anal ysis into a broader context for characterizing 30 potential national risks. While th e core risk estimates receive pr imary focus in the discussion of 31 risk estimates presented below, we do references the results of these additional supplemental 32

18 In addition, we considered whether sufficient information existed in the literature to develop C-R functions and whether we could obtain baseline incidence data necessary to generate risk estimates with a reasonable degree of confidence.Draft Do Not Quote or Cite March 2010 2-44 analyses in addressing overall confidence associat ed with the core risk estimates and in placing 1
the core risk estimates in a broader national-context. 2 An important factor to consider in interpreti ng risk results is that the magnitude of both 3 long- and short-term exposure-related ri sk depends primarily on annual-average PM 2.5 4 concentrations. Furthermore, reduc tions in both categories of risk, as we consider simulating just 5 meeting current and alternative su ites of standards, also depend primarily on changes in annual6 average PM 2.5 concentrations. 7 The role of annual-average ambient PM 2.5 concentrations in dr iving long-term exposure8 related risk is intuitive given that this risk category is modeled usi ng the annual-average air 9 quality metric. 19 The fact that short-term exposure-relate d risk is also driven by changes in long10 term average PM 2.5 concentrations is less intuitive, since changes in average daily PM 2.5 11 concentrations are used to estimate changes in risk for this category. 20 Analyses in previous PM 12 NAAQS risk assessments have shown that short- term exposure-related risks are not primarily 13 driven by the small number of days with PM 2.5 concentrations in the upper tail of the air quality 14 distribution, but rather by the large number of days with PM 2.5 concentrations at and around the 15 mean of the distribution. Consequently, cons ideration for changes in annual-average PM 2.5 16 concentrations will explain to a large extent changes in short-term exposure-related risk. 17 Therefore, in interpretin g patterns of long-term exposure-relate d risk, and the similar patterns we 18 observe in short-term exposure-related risk, we consider how simulating just meeting specific 19
suites of PM 2.5 standards impacts the annual-average PM 2.5 concentration for the study areas. 20 We have considered a series of questions to inform our understanding of the adequacy of 21 the current suite of fine partic le standards based on the insights obtained from the quantitative 22
risk assessment. The remainder of the di scussion is organized around these questions. 23

 What is the nature and magnitude of the long-term exposure-related risks remaining 24 upon just meeting the current suite of PM 2.5 standards? What level of confidence is 25 associated with these risk estimates? 26 Of the fifteen study areas included in the ri sk assessment, thirteen are simulated to 27 experience risk reductions upon meeting the current suite of standards. Of these thirteen study 28

19 As noted in section 3.2.1 of the second draft RA, esti mates of long-term exposure-related mortality are actually based on an average annual PM 2.5 level across monitors in a study area (i.e ., the composite monitor annual-average). Therefore, in considering changes in long-term exposure-related mortality, it is most appropriate to compare composite monitor estimates generated for a study area under each suite of standards. The maximum monitor annual-average for a study area (i.e., the annual de sign value) determines the percent reduction in PM 2.5 levels required to attain a particular standard. Both types of ai r quality estimates are provided in Tables F-49 and F-50 in Appendix F of the second draft RA and both are referenced in this discussion of core risk estimates, as appropriate.
20 Estimates of short-term exposure-related mortality and morbidity are based on composite monitor daily PM 2.5 . concentrations. However, similar to the case with long-ter m exposure-related mortality, it is the maximum monitor 98 th percentile 24-hour concentration (the 24-hour design va lue) that will determine the degree of reduction required to meet a given 24-hour standard.Draft Do Not Quote or Cite March 2010 2-45 areas, three areas (Atlanta, Birmingham and Houst on) have design values which resulted in the 1
current annual standard control ling. Therefore, in assessing the level of long-term exposure2 related mortality risk remaining upon just meeti ng the current annual standard, we focus on risk 3 estimates for these three study areas. Total incidence of PM 2.5 -related mortality ranges from 4 131-165 (Birmingham) to 344-434 (Houston) (Table 2- 2). The percent of total incidence of IHD 5 mortality attributable to PM 2.5 ranges from 10.7-13.6% (Houston) to 13.2-16.7% (Atlanta) (Table 6 2-2). Total incidence estimates for all-cause and cardiopulmonary mortality related to PM 2.5 7 exposure for these study areas are larg er than for IHD, while total PM 2.5 -attributable incidence 8 estimates for lung-cancer are lower. However, th e percent of total incide nce attributable to PM 2.5 9 exposure is larger for IHD than for the other mortality cate gories assessed. 10 The remaining ten study areas that would expe rience reductions in ri sk under the current 11 suite of standards (relative to ri sk under recent conditions) have de sign values which result in the 12
current 24-hour standard controlli ng. These study areas include: Baltimore, Detroit, Fresno, Los 13 Angeles, New York, Philadelphia, Pittsburgh, Salt Lake City, St. Louis, and Tacoma. Therefore, 14 we consider risk estimates for these study areas in assessing the degree of risk associated with 15 just meeting the current 24-hour st andard. Total incidence of PM 2.5 -related mortality ranges 16 from 15-19 (Salt Lake City) to 1,755-2,222 (New Yo rk City) (Table 2-2). The percent of total 17 incidence of IHD mortality attributable to PM 2.5 ranges from 2.9-3.7 (Salt Lake City) to 11.2- 18 14.2% (St. Louis) (Table 2-2). Total inciden ce estimates for all-cause and cardiopulmonary 19 mortality related to PM 2.5 exposure for these study areas are larger than for IHD, while total 20

PM 2.5 -attributable incidence estimates for lung-cancer are lower. However, the percent of total 21
incidence attributable to PM 2.5 exposure is larger for IHD than for the other mortality categories 22
assessed. 23
Estimates of risk under the current suite of st andards is significantly more variable for the 24 ten study areas where the 24-hour standard is cont rolling compared with the three study areas 25
where the current annual standard is controlling. This notable diffe rence in variability reflects the 26 fact that simulation of just meeting the current 24-hour standard (for t hose study areas where it is 27 controlling) produces varying impacts on annual-average PM 2.5 concentrations. By contrast, 28 simulation of just meeting the annual sta ndard results in similar annual-average PM 2.5 29 concentrations for those study areas where the annual standard is controlling. Because annual30 average PM 2.5 concentrations are one of the primary determinants of the level of long-term 31 exposure-related mortality risk, variation in this st atistic translates into gr eater variation in risk 32 remaining upon simulation of the current suite of standards for the ten st udy areas where the 24- 33 hour level is controlling. 34 A related point, which has bearing on the leve l of confidence associated with our risk 35 estimates, is the observation that several of th e study areas where the 24-hour standard was 36Draft Do Not Quote or Cite March 2010 2-46 Table 2-2. Estimated Incidence and Percent of Total Annual Incidence Associated with 1 Long-term PM 2.5 Exposure Based on Simulation of the Current Suite of Standards (for 2 IHD mortality based on 2007 PM 2.5 Concentrations) 1,2 3 4

5Draft Do Not Quote or Cite March 2010 2-47 controlling have annual-average PM 2.5 concentrations that are well below the level of the current 1 annual standard and in some instances, approa ching the lowest measured level (LML) of 5.8 2 μg/m 3 used as the lower bound for ri sk estimation. Although we are not able to quantify the 3 degree of increased uncertaint y, we do have reduced confiden ce in risk estimates involving 4 annual-average PM 2.5 concentrations that are substa ntially below the mean annual PM 2.5 5 concentrations reported by Krew ski et al. (2009) (14-21 μg/m 3 – see Table 1 in the study) and 6 approaching the LML of 5.8 μg/m 3 identified for that study. This reflects the fact that, while 7 available literature does not support a PM 2.5 -related threshold for health effects, we do have 8 increased uncertainty in characterizing the nature of the C-R function as we move away from the 9
central mass of observations in the epidemiological study from which the C-R functions was 10 obtained and towards the LML. Study areas with relatively low annual-average PM 2.5 11
concentrations less than the level of the current standard include: Tacoma (8.4 μg/m 3 ), Salt Lake 12 City (7.7 μg/m 3 ), and Fresno (9.9 μg/m 3 ) (note, that the current 24- hour standard is controlling 13 for all of these study areas – see US EPA, 2010a , Appendix F, Table F-49). Conversely, we note 14 that we would have greater confidence in applyi ng C-R functions in the risk assessment for those 15 study areas with annual-average PM 2.5 levels under the current suit e of standards near the range 16 of 14-21 μg/m 3 . Study areas in this category include: Atlanta, Birmingham and Houston (where 17 the annual standard is controlling) and Baltimore, Detroit, Philadelphia, St. Louis, New York 18 (where the 24-hour standard is controlling). 19 Consideration of variability in the spatial pattern of PM 2.5 reductions associated with 20
simulation of the current suite of standards suggests that this factor can impa ct risk estimates, 21 particularly in those instances where the 24-hour standard is controlling. For example, 22
consideration of a more locali zed pattern of reduction in PM 2.5 concentrations (as reflected in the 23 peak shaving rollback method), resulted in ri sk estimates for the 10 study areas where the 24- 24 hour standard is controlling that are from ~0 to 53% higher than those estimated assuming a 25 more regionalized pattern of PM 2.5 reductions (as reflected in the proportional rollback method 26 used in the core analysis). 27 Additional sensitivity analyses considering sour ces of uncertainty impacting the core risk 28 estimates focused on specification of the C-R function for long-term PM 2.5 exposure-related 29 mortality. This analysis suggest ed that most of the alternativ e model specifications supported by 30 available literature would produce risk estimates th at were higher (by up to a factor of 2 to 3) 31
than the core risk estimates. These fi ndings would apply both to estimates of PM 2.5 -attributable 32 IHD mortality incidence, as well as to estimates of the percent of total IHD mortality incidence 33
attributable to PM 2.5 exposure. 34 Taken together, the sensitivity analyses completed for this risk assessment, including 35 those considering variability in rollback methods as well as uncertainty in the form of C-R 36Draft Do Not Quote or Cite March 2010 2-48 functions, suggest that the set of alternative risk model specifications that we identified generally 1 produced risk estimates that are higher than the co re risk estimates. Furthermore, our decision to 2 model risk down to the LML (rather than to lower policy-relevant background (PRB) 3 concentrations) for long-term PM 2.5 exposure-related mortality, desp ite the lack of evidence for a 4 threshold, results in lower estimates of risk that would have resulted from modeling risk down to 5
PRB. These considerations increase our overall confidence that we did not over-state risks with 6 the core risk estimates. However, as noted a bove, there are different levels of confidence 7 associated with risk estimates reflecting the annual-average PM 2.5 concentrations associated 8 with the risk estimates (w ith lower confidence associat ed with annual-average PM 2.5 9 concentrations closer to the LML of 5.8 μg/m 3 ). 10

 What is the nature and magnitude of the short-term exposure-related risks remaining 11 upon just meeting the current suite of PM 2.5 standards? What level of confidence is 12 associated with these risk estimates? 13 As noted earlier, changes in annual-average PM 2.5 levels drive reduc tions in both long14 term and short-term exposure-related risk. Conse quently, patterns of risk reduction for long-term 15 exposure-related mortality associated with the su ite of annual standard le vels generally hold for 16 short-term exposure-related mortality and morbidity (although absolute levels of risk will differ). 17 As was done above for long-term exposure-related mortality, we have divided the discussion of 18 risk for short-term exposure-related mortality and morbidity, between (a ) the three study areas 19 where the current annual standard was driving and (b) the ten study areas where the 24-hour 20 standard was controlling. Again, this reflects the fact that these two groups of study areas had 21 different patterns of ri sk reduction under the curr ent suite of standards, reflecting differences in 22 the way the two standard levels effected annual-average PM 2.5 levels (i.e., fairly similar annual23 average PM 2.5 levels for study areas where the annual standard controls and more variable 24 annual-average PM 2.5 levels for study areas where th e 24-hour standard controls). 25 Total incidence of short-term exposure-re lated CV mortality attributable for PM 2.5 for the 26 three study areas where the curren t annual standard controls (Atla nta, Birmingham and Houston) 27 ranges from 32 (Atlanta) to 46 (Houston) (Table 2-3). The percent of total CV mortality 28
incidence attributable to PM 2.5 for this subset of study areas ra nges from 0.8% (Atlanta) to 0.9% 29 (Houston) (Table 2-3). Total incidence of CV hospital admissions (HA) attributable to PM 2.5 for 30 this group of study areas ranges from 16 (Birmi ngham) to 56 (Houston) (Table 2-3), while 31 percent of total incidence attributable to PM 2.5 ranges from 0.3% (Birmingham) to 0.4% 32 (Atlanta) (Table 2-3). 33 Total incidence of short-term exposure-re lated CV mortality attributable for PM 2.5 for the 34 ten study areas where the 24-hour standard is controlling (Baltimore, Detroit, Fresno, Los 35 Angeles, New York, Philadelphia, Pittsburgh, Salt Lake City, St. Louis, and Tacoma), range 36Draft Do Not Quote or Cite March 2010 2-49 from 9 (Salt Lake City) to 106 (S t. Louis) (Table 2-3). The pe rcent of total incidence of CV 1 mortality attributable to PM 2.5 ranges from 0.7% (Tacoma) to 2.1% (New York and Philadelphia) 2 (Table 2-3). Total inciden ce of CV hospital admissions (HA) attributable to PM 2.5 for this group 3 of study areas ranges from 9 (Salt Lake City) to 7 52 (Los Angeles) (Table 2-3), while percent of 4
total incidence attributable to PM 2.5 ranges from 0.4% (Salt Lake City) to 1.3% (St. Louis and 5 Philadelphia) (Table 2-3). 6 As observed with the long-term exposure-re lated mortality, estimates of short-term 7 exposure-related mortality and morbidity risk under the current su ite of standards are 8 significantly more variable for the ten study ar eas where the 24-hour standard is controlling 9 compared with the three study area s where the current annual standa rd is controlling. Again, this 10 notable different in variability re flects the fact that simulation of just meeting the current 24-hour 11 standard (for those study areas where it is controlling) produ ces varying impacts on annual12 average PM 2.5 concentrations and hence on risk. By c ontrast, those study areas where the annual 13 standard is controlling ha ve similar annual-average PM 2.5 levels and consequently similar levels 14 of risk remaining upon simulation of the curren t suite of standards (r ecall that short-term 15 exposure-related risk is driven more by changes in annual-average PM 2.5 then by changes in peak 16 daily PM 2.5 levels). 17 Given increased emphasis placed in this analysis on long-term exposure-related 18 mortality, the uncertainty analyses completed for this health endpoint category are more 19 comprehensive than those conducted for short-te rm exposure-related mortality and morbidity, 20 which to some extent reflects limitations in study data available for addressing uncertainty in the 21 later category. 22

 What roles do the current 24 hour and annua l standards have in simulating the risks 23 remaining upon just meeting the current suite of standards? 24 As note above, of the thirteen urban study ar eas that do not meet the current suite of 25 standards based on 2005-2007 air qual ity data, ten areas have the 24-hour standard controlling, 26 while only 3 areas have the annual standard contro lling. This pattern is generally characteristic of 27 the larger set of urban areas across the U.S. that do not meet the current suite of standards (US 28 EPA, 2010a, section 4.5). 21 29 Estimated risks remaining upon just meeting th e current suite of standards vary across 30 study areas, even when considering risks norma lized for differences in population size and 31 baseline incidence rates. This variability in estim ated risks is a consequence of the variability in 32 the annual-average PM 2.5 concentrations across study areas th at result from simulating just 33

21 Of the 256 urban areas in the U.S. (including a combination of CSA and CBSAs), 67 have ambient PM 2.5 levels exceeding either the 24-hour or annu al standard (or both) based on PM 2.5 monitoring data from 2005-2007. Of these, 51 have the 24-hour standard controlling, while 16 have the annual standard controlling.Draft Do Not Quote or Cite March 2010 2-50 Table 2-3. Estimated Incidence and Percent of Total Annual Incidence Associated with 1 Short-Term PM 2.5 Exposure Based on Simulation of the Current Suite of Standards (CV 2 mortality and hospital admissions based on 2007 PM 2.5 concentrations) 1,2 3 4

5Draft Do Not Quote or Cite March 2010 2-51 meeting the current standards. 22 Variability in annual-average PM 2.5 concentrations is 1 substantially greater in those st udy areas in which the 24-hour sta ndard is controlling. In such 2 areas, the variability acro ss study areas in estimated risks is largest when regional patterns of 3
reductions in PM 2.5 concentrations are simulated (using pr oportional rollback, as was done in the 4 core analyses), with less variability when more localized patterns of PM 2.5 reductions are 5 simulated (using peak shaving rollback, as was done in a sensitivity analysis). 6 In simulating just meeting the current suite of standards for the urban study areas, the 7 resulting annual-average PM 2.5 concentrations range from about 15 μg/m 3 (for the study areas in 8 which the annual standard was controlling) down to as low as about 8 μg/m 3 (for the study areas 9 in which the 24-hour standard was controlling). We note that, for long- term exposure-related 10 mortality, estimates of risk based on annual-average PM 2.5 concentrations approaching the LML 11 of 5.8 μg/m 3 have greater uncertainty than estimates based on annual-average concentrations 12 closer to the mean of the epid emiological study from which the C- R functions are obtained (14 to 13 21 μg/m 3 ). 23 Therefore, we generally have less conf idence in risk estimates generated for study 14
areas where the 24-hour standard is controlling since these tend to have lower annual-average 15

PM 2.5 levels (which can approach the LML) compared with study areas where the annual16 average is controlling. 17 These observations when considered togeth er suggest that, when we simulate PM 2.5 18 concentrations meeting the current suite of stan dards, we find that in study areas where the 19
current 24-hour standard is cont rolling, the degree of public health protection afforded by the 20
current suite of standards is much more variable than in study areas where the annual standard is 21 controlling. Furthermore, we generally have less confidence in the risk estimates generated for 22
urban areas where the current 24-hour standard is controlling due simulated lower annual23 average PM 2.5 concentrations that are in some cases much lower, approaching the LML. 24

 How representative are the risk estimates ge nerated for the urban study areas from a 25 national perspective? 26 As part of the risk assessment, we comple ted several additional analyses intended to 27 place the core risk estimates in the broader natio nal-context by considering the degree to which 28 the 15 urban study areas are represen tative of larger urban areas within the U.S., particularly 29 areas likely to experience elevated risk rela ted to PM exposure. Below we provide brief 30 descriptions of each analysis, along with observa tions results from each analysis regarding the 31

22 As noted earlier, changes in both short-term and long-term exposure-related risk reflect primarily changes in longterm average (annual) PM 2.5 levels.
23 This observation also holds for estimates of risk associated with short-term PM 2.5 although we note that the LML for these studies is below PRB, which allows us to make estimates of risk for lower PM 2.5 levels with greater confidence relative to modeling long-term exposur e-related mortality with its higher LML.Draft Do Not Quote or Cite March 2010 2-52 representativeness of th e urban study areas: 1

 The representativeness analysis (US EPA, 2010a, section 4.4) compared attributes of the 15 2 urban study eras (assessed at the county-level ) against national distri butions for the same 3 attributes. The analysis suggest s that the 15 urban study areas repr esent areas in the U.S. that 4 are among the most densely populated, have re latively higher levels of annual and 24-hour 5 98 th percentile PM 2.5 concentrations, and capture well the range of effect estimates 6 represented by the Zanobetti and Schwartz (2009) study. Together , these factors suggest that 7 the urban study areas should capture well the overall distribution of risk for the nation, with 8 the potential for better characterization of the high end of that distribution. 24 9

 Consideration of the mi x of design values across the 15 urban study areas as contrasted with 10 design values for the broader set of urban study areas in the U.S. suggests that the 15 urban 11 study areas do a good job of capturing the key groupi ngs of urban areas in the U.S. likely to 12 experience elevated risk due to PM (i.e., we ha ve coverage for each of the zones containing 13 urban study areas likely to experi ence risk reductions under the su ites of altern ative standard 14 levels considered – see US EPA,2010a, secti on 4.5.1). Furthermore, this analysis suggested 15 that we have also included study areas likely to experience relatively greater degrees of 16 PM 2.5 -related risk, considering the pattern of design values acro ss urban areas in the U.S. 17

 Consideration of where the 15 urban study area s fell along the distribut ion of U.S. counties 18 included in the national-scale mortality analysis further suggests that we have captured 19 counties likely to experience elevated PM 2.5 -related risk

. As part of the national-scale 20 mortality analysis (see US EPA, 2010a, chapte r 5), we created a cumulative distribution of 21 the percentage of mortality attributable to PM 2.5 based on the county-level estimates for the 22 U.S. 25 We then identified where along this cumulative distribution the 31 counties 23 comprising our 15 urban study areas fell. This analysis suggests that our urban study areas 24 capture the upper end of th e tail with regard to PM 2.5 -attributable risk, with 23 of these 25 counties falling within the upper 5 th percentile of the distributi on. These findings support the 26 assertion based on the other analyses described a bove that the urban stud y areas are likely to 27 capture risk at urban ar eas experiencing relatively elevated levels of PM 2.5- attributable 28 mortality. 29 Our overall assessment of the representati veness of the 15 urban study areas in the 30 national context, based on the three analyses summarized above, is that our study areas do a good 31 job of representing urban areas in the U.S. experiencing elevated leve ls of risk related to ambient 32

PM 2.5 exposure. The results of the national-scale mortality analysis also suggest that, while our 33 15 urban study areas do provide coverage for ur ban areas in the U.S. experiencing elevated 34
levels of PM 2.5 -related risk, there are many additional ar eas (counties) not modeled in the risk 35

24 This analysis also showed that the urban study areas do not capture areas with the highest baseline morality risks or the oldest populations (both of which can result in higher PM 2.5 -related mortality estimates). However, some of the areas with the highest values for th ese attributes have relatively lower PM 2.5 levels (e.g., urban areas in Florida) and consequently failure to include these areas in the set of urban study areas is unlikely to bias the risk estimates in terms of excluding high PM 2.5 -risk locations.
25 Note that by using this risk metric, we avoid influence by difference in overall population size (as would be the case with raw incidence) and focus on a unitized estimate of PM 2.5 -related mortality which reflects differences in (a) baseline mortality incidence, and (b) the annual average PM 2.5 concentrations for each county.Draft Do Not Quote or Cite March 2010 2-53 assessment that experience elevated PM 2.5 -related risk. In other words, it should not be 1
construed that significant PM 2.5 -related risk is limited only to the urban study areas included in 2
the risk assessment. 3

 To what extent are the risks remaining upon simulation of the current suite of 4 standards important from a public health perspective? 5 With respect to considering the results of th e quantitative risk assessment to inform our 6 understanding of risks asso ciated with long-term PM 2.5 exposures, we reach the preliminary 7 conclusion that the long-term exposure-related mo rtality risks remaining upon simulation of just 8 meeting the current suite of PM 2.5 standards can reasonably be j udged to be important from a 9 public health perspective. This preliminary conclu sion is based, in part, on both the nature of the 10 risks (total and cause-specific mortality) as well as the magnit ude of these risks (the total 11 incidence and percen tage of incidence associated with PM 2.5 exposure as presented in Table 2-2). 12 In addition, based on considera tion of both our qualitative a nd quantitative assessments of 13 uncertainty, as well as additional factors consider ed in the risk model (e.g., modeling risk down 14 to LML rather than PRB), we are reasonably confident that we have not overstated the 15 magnitude of risk associated with simulating the current suite of standards. However, we do note 16 that we have greater overall c onfidence in estimates of risk associated with long-term PM 2.5 17 exposure in the subset of urban study areas for which the current annual st andard is controlling, 18
since these locations tend to have higher annual-average PM 2.5 concentrations. In contrast, the 19 urban study areas where the current 24-hour standa rd is controlling tend to have substantially 20 lower annual-average PM 2.5 concentrations, which reduces our overall confidence in these 21
estimates of risks relate d to long-term exposures. 22 With regard to considering th e results of the quantitative risk assessment to inform our 23 understanding of risks associated with short-term PM 2.5 exposures, we reach the preliminary 24 conclusion that short-term exposure-related mort ality and morbidity risks upon simulation of the 25
current suite of PM 2.5 standards can reasonably be judged to be important from a public health 26 perspective. Similar to the discussion of risks associated with long-term PM 2.5 exposure, this 27 preliminary conclusion is based, in part, on both th e nature of the risks (total and cause-specific 28 mortality as well as cause-specific hospital admi ssions) as well as the magnitude of those risks 29 (total incidence and percentage of incidence associated with PM 2.5 exposure as presented in 30 Table 2-3). We note however, that in the case of mortality associated with short-term PM 2.5 31 exposure, the magnitude of these risks is substan tially lower than that as sociated with long-term 32 exposure to PM 2.5 . With regard to our overall confidence in the estimates of risks related to 33
short-term PM 2.5 exposures, while we believe that the co re simulation of risk is based on C-R 34 functions that are well-supported in the literature, we acknowledge that we have not completed 35 as comprehensive an assessment of uncertainty and variability as was done for estimates of 36Draft Do Not Quote or Cite March 2010 2-54 mortality risks related to long-term PM 2.5 exposure. Therefore, our overall confidence that we 1
have not over-stated risk associated with short- term exposure-related mortality and morbidity is 2 not as high as for long-term exposure-related mo rtality, although we have no reason to believe 3
that we have over-stated risk. 4

2.2.3 Preliminary Staff Conclusions on Adequacy of Current Standards 5 Collectively, taking into consideration the responses to specific questions focusing on 6 different ways to address the adeq uacy of the current suite of PM 2.5 standards, we revisit the 7 overarching policy question: does th e currently available scientific evidence and risk-based 8 information support or call into question the ade quacy of the protection afforded by the current 9 suite of fine particle standards? 10 With respect to evidence-based considerati ons, the currently available evidence provides 11 stronger evidence beyond what was available in the last review, that associ ations between short12 and long-term PM 2.5 exposures and a broad range of advers e health effects exist. The newly 13 available information strengthens the associations between PM 2.5 and mortality and 14 cardiovascular and respiratory morbidity effects observed in the last review and expands our 15 understanding of a broader range of health outcomes as well as our understanding of effects in 16 susceptible populations. The newl y available evidence provides support for associations that 17
extend to lower concentrations than what had be en observed in the last review, including at 18
ambient concentrations below the leve ls of the current standards. 19
In relation to risk-based considerations for informing our understand ing of the adequacy 20 of the current fine particle standa rds, we focus on the estimates of PM 2.5 -related mortality and 21 morbidity effects likely to remain upon meeting th e current standards in a number of example 22 urban areas. In considering the core risk es timates together with our understanding of the 23 uncertainties in these estimates based upon ex tensive sensitivity analyses, we reach the 24 preliminary conclusion that the risks estimated to be associated with just meeting the current 25 standards can reasonably be judged to be important from a public health perspective and these 26 estimated risks provide support for consideratio n of standards that w ould provide increased 27 protection beyond that afforded by the current PM 2.5 standards. 28 We recognize that important uncertaintie s and research questions remain when 29 considering both evidence- and risk -based approaches. Nonetheless, we note that much progress 30 has been made in reducing some key uncertainti es since the last revi ew, including important 31 progress in advancing our unde rstanding of potential mech anisms by which ambient PM 2.5 is 32 causally linked with mortality, cardiovascular, an d respiratory effects observed in epidemiologic 33 studies. Additional information continues to emerge for a broader range of health effects 34 including reproductive and development effects a nd more information is available to understand 35Draft Do Not Quote or Cite March 2010 2-55 susceptible populations includi ng children, older adults, and i ndividuals with pre-existing 1 cardiovascular and respiratory disease. As was tr ue in the last review, we recognize that as the 2 body of available evidence has expanded, it has a dded greatly both to our knowledge of health 3 effects associated with fine particle exposures , as well as to the co mplexity inherent in 4 interpreting the evidence in a policy-relevant contex t as a basis for setting appropriate standards. 5 In evaluating both evidence-based and risk-bas ed considerations, along with associated 6 limitations and uncertainties, we reach the prelim inary conclusion that the available information 7 clearly calls into question the ade quacy of the current suite of PM 2.5 standards and provides 8 strong support for giving consideration to revi sing the current standards to provide increased 9 public health protection. 10

2.3 CONSIDERATION OF ALTERNATIVE STANDARDS 11 Having reached the conclusion that the currently available scie ntific evidence calls into 12 question the adequacy of the current suite of PM 2.5 standards, staff considers a second 13 overarching question: 14

What alternative suite(s) of fine particle standards is (are) supported by the currently 15 available scientific evidence and risk-based info rmation, as reflected in the ISA and second 16 draft RA? 17 To inform the answer to this overarching que stion, we have posed a series of more 18 specific questions to aid in consideri ng how the current suite of primary PM 2.5 standards might be 19 revised to provide requis ite public health protection. Specifica lly, we consider how the currently 20
available scientific evidence informs decisions regarding the basic elements of the NAAQS: 21 indicator (section 2.3.1), averagi ng time (section 2.3.2), form (sect ion 2.3.3), and level (sections 22 2.3.4 and 2.3.5). These elements will be consider ed collectively in evaluating the health 23 protection afforded by alternative suites of standards under consid eration. In considering the 24 currently available scie ntific and technical information, we consider both the information 25
available in the last review and information that is newly available since the last review as 26 assessed and presented in the ISA and second dr aft RA prepared for this review (US EPA, 27 2009a; US EPA, 2010a). 28

2.3.1 Indicator 29 In 1997, EPA decided that particles from th e fine and coarse fractions of thoracic 30 particles (PM 10 ) should be defined as separate pollutants. At that time, the Agency established 31

PM 2.5 as the indicator for fine particle, while retaining PM 10 as the indicator for thoracic coarse 32 particles. In determining the indicator for fine particles, the Agency first considered whether the 33
indicator should be based on the mass of a size-diffe rentiated sample of fine particles or one or 34Draft Do Not Quote or Cite March 2010 2-56 more components within the mix of fine particle s. In that review, EPA first concluded it was 1 more appropriate to control fine particles as a group, as opposed to singling out any particular 2 component or class of fine particles. Second, in establishing a size-based indicator, a size cut 3 was selected that would appropria tely distinguish fine particles from particles in the coarse 4 mode. In focusing on a size cut w ithin the size range of 1 to 3 μ m (i.e., the intermodal range 5 between fine and coarse mode particles), EP A recognized that the choice of any specific 6 sampling size cut within this range was largely a policy judgment. In ma king this judgment, the 7 Agency noted that the available epidemiologic st udies of fine particles were based largely on 8

PM 2.5 and also considered monitoring technology that was generally available. In the 9 Administrator’s final decision, the selection of a 2.5 μm size cut reflected the regulatory 10 importance that was placed on defining an indicator that would more comp letely capture fine 11 particles under all conditions like ly to be encountered across th e U.S., especially when fine 12 particle concentrations are likely to be high, while recognizing th at some small coarse particles 13 would also be captured by current methods to monitor PM 2.5 (62 FR 38667 to 38668, July, 18, 14 1997). 15 In reaching the decision to retain PM 2.5 as the indicator for fine particles in the last 16 review, the same considerations continued to appl y for selection of an appropriate indicator for 17 fine particles (71 FR 61162 to 61164, October, 17, 2006). The available epidemiologic studies 18 linking mortality and/or morbidity effects with sh ort- and long-term exposures to fine particles 19 continued to be largely indexed by PM 2.5. While emerging evidence focused on various PM 2.5 20 constituents and provided some evidence related to various components within the mix of fine 21 particles (e.g., sulfates (SO 2 -4 ), nitrates, elemental carbon (EC) , organic compounds, and metals) 22 as well as associations between mortality and par ticles from different sources of fine particles, 23
this evidence was deemed too limited to s upport a distinct standard for a specific PM 2.5 24 component or fine particle source. More spec ifically, the Agency conc luded, there was “not 25
sufficient evidence that would lead toward the se lection of one or more PM components as being 26 primarily responsible for effects as sociated with fine particles, nor is there sufficient evidence to 27 suggest that any component should be eliminated from the indicator for fine particles” (71 FR 28 61163/1). 29 In this review, in considering alternative fine particle standards, we first address the issue 30 of indicator by asking the following question: 31

 Does the currently available evidence provi de support for the continued use of PM 2.5 as 32 the mass-based indicator for fine particles? 33 As noted above, the selection of PM 2.5 to characterize respirab le particles in 1997 was 34 driven mainly by considerations related to meas urement techniques available at the time rather 35 than dosimetry. In this review, the ISA notes, “[c]urrently, cut points other than 2.5 μ m are 36Draft Do Not Quote or Cite March 2010 2-57 attainable and frequently put into use...[m]ost commonly, however, PM 2.5 is used as an indicator 1 of respirable particles” (US EPA, 2009a, p. 3-3). Recently, there has been increasing interest in 2 examining the relationship between the particle numb er concentration by size and health effects. 3 However, several instruments are needed to pr ovide size distribution measurements (number and 4 size) over the several orders of magnitude of particle diameter s of interest (US EPA, 2009a, 5 section 3.4.1.5, p. 3-29). These techniques, while wi dely used in aerosol research, have not yet 6 been widely used in health effects studies. 7 As discussed in section 2.2.1, currently av ailable scientific information providing 8
evidence of associations between fine particles and a broad range of health outcomes has been 9 substantially strengthened in this review. Ep idemiological evidence continues to provide the 10 strongest support for standards to protect public health from long- and short- term fine particle 11 exposures. Measurements from community-based ambient monitors have generally been used 12 for time-series and longitudinal epidemiological studies, and may be used for panel studies as 13 well (US EPA, 2009a, p. 3-176). New epidemiological studies available in this review have 14 considered a much larger set of air quality data than was ava ilable in the last review based 15 primarily on ambient measurement data from the existing PM 2.5 monitoring networks. 26 This 16 includes consideration of air quali ty measurements reported in more recent years. These data 17 have improved our understanding of the spatiotemporal distribution of PM 2.5 (US EPA, 2009a, 18 sections 3.5 and 3.9). 19 As presented in the ISA, epidemiological studies linking cardiovasc ular and respiratory 20 effects as well as mortality with short- and long- term fine particle exposures continue to be 21 largely indexed by PM 2.5 (US EPA, 2009a, chapters 6 and 7). Thus, we reach the preliminary 22
conclusion that it is reasonable to retain PM 2.5 as an indicator for fine particles. We then pose 23 additional questions to aid in c onsidering whether the currently available scientific evidence 24 provides support for supplementing the current PM 2.5 mass-based indicator by considering 25
whether there is sufficient eviden ce to support a standard with a di fferent size fraction or whether 26
there is sufficient evidence to establish distin ct standards focused on regulating specific PM 2.5 27 components or sources of fine particles. 28

 To what extent does the currently ava ilable information provide support for 29 considering a separate indicator for ultrafine pa rticles as a subfraction of fine particles? 30

26 The network of PM 2.5 Federal Reference Methods (FRM) monitors has been operational since 1999. This network currently includes over 900 monitoring stations around the U.S. FRM-like air quality data are available from continuous monitors required in metropolitan statistical ar eas (MSAs) that have an FRM/Federal Equivalent (FEM) monitor. The network of continuous PM 2.5 monitors has grown to over 700 locations throughout the U.S. While PM 2.5 continuous monitors primarily suppor t forecasting and reporting for the Air Quality Index (AQI), they are also used in interpreting the diurnal characterization of PM 2.5.Draft Do Not Quote or Cite March 2010 2-58 In considering whether or not the currently available evid ence provides support for an 1 additional size-based indicator by fo cusing on ultrafine particles (UFPs) 27 , we recognize that a 2
number of studies have focused on UFPs as a subset of PM 2.5 . In the last review, limited 3 evidence was available suggesting th at the ultrafine subset of fine particles (gener ally including 4 particles with a nominal aerodynamic diameter le ss than 0.1 μm) was associated with adverse 5 health effects (US EPA, 2004, pp. 8-66 to 8-68). In this review, the ISA notes that there are 6 many reasons for looking more closely at effects a ssociated with this size fraction including, the 7 particle number and large surface area of UFPs per unit of mass. Particle number is most highly 8 concentrated in the UFP fraction with volume (or mass) most concentrated in the larger size 9 fractions (US EPA, 2009a, p. 3-2) Furthermore, per unit mass, UFPs may have more opportunity 10
to interact with cell surfaces due to their greater surface area a nd their greater particle number 11 compared with larger particles (US EPA, 2009a, p. 5-3). Greater surface area increases the 12 potential for soluble components to adbsorb to UFPs and be transported into the body (US EPA, 13 2009a, p. 6-83). Many studies suggest that the surf ace of particles or subs tances released from 14 the surface (e.g., transition metals, or ganics) interact with biologica l substrates, and that surface15
associated free radicals or free radical-generating systems may be responsible for toxicity, 16 resulting in greater toxic ity of UFPs per particle surface area than larger particles. In addition, 17 evidence available in this review suggests that the ability of particles to enhance allergic 18 sensitization is associated more strongly with particle number and surface area than particle mass 19 (US EPA, 2009a, p. 6-127). Evidence is also ava ilable in this review suggesting that smaller 20 particles may have a greater pote ntial to cross cell membranes a nd epithelial barriers. The ISA 21 notes that, for UFPs, “enhanced translocation to interstitial compartments or to the circultaon 22 may be important sequelae” (US EPA, 2009a, p. 5- 6). More information on possible modes of 23 action for effects associated with UFPs exposures is discussed in sections 5.1 and 5.4 of the ISA. 24 With respect to ambient concentrations of U FPs, at present, there is no national network 25 of UFP samplers, thus, only episodic and/or s ite-specific data sets ex ist (US EPA, 2009a, p. 2- 26 2). 28 Therefore, a national characte rization of concentrations, tem poral and spatial patterns, and 27 trends is not possible, and the av ailability of ambient UFPs data to support health studies are 28 extremely limited. In general, UFP particle number concentrations are highly dependent on 29 monitor location and therefore, more subject to exposure error than accumulation mode particles 30 (US EPA, 2009a, p. 2-22). The UFP number c oncentrations fall off sharply downwind from 31 sources, as UFPs may grow into the accumula tion mode by coagulation or condensation (US 32

27 Ultrafine particles (UFPs) are emitted directly to the atmosphere or are formed by nucleation of gaseous constituents in the atmosphere (US EPA, 2009a, p. 3-3).
28 The ISA contains a review of the current scientific information related to measur ements of UFPs (US EPA, 2009a, sections 3.5.1 and 3.5.2).Draft Do Not Quote or Cite March 2010 2-59 EPA, 2009a, p. 3-89). Limited studies of UFP am bient measurements suggest these particles 1 exhibit a high degree of spatial and temporal heterogeneity driv en primarily by differences in 2 nearby source characteristics (US EPA, 2009a, p. 3-84). Internal combustion engines and 3 therefore, on-road roadways are a notable sour ce of UFPs, so concentr ations of UFPs near 4 roadways can generally be expect ed to be elevated (US EPA, 2009a , p. 2-3). Concentrations of 5 UFPs have been reported to drop off much mo re quickly with distance from roadways than 6 larger particle sizes (US EPA, 2009a, p. 3-84). 7
Additional but still limited health evidence av ailable in this review, primarily from 8 controlled human exposure and toxicological st udies, provide evidence for UFP-induced 9 cardiovascular and respiratory effects. This ev idence is largely related to studies focused on 10 exposure to diesel exhaust (DE), “[a]s a result, it is unc lear if the effects observed are due to 11 UFP, larger particles (i.e., PM 2.5 ), or the gaseous components of DE” (US EPA, 2009a, p. 2-22). 12 The ISA notes uncertainty associated with the co ntrolled human exposure studies as concentrated 13 ambient particle (CAP) systems have been show n to modify the composition of UFPs (US EPA, 14 2009a, p. 2-22, see also section 1.5.3). In additio n, relatively few epidemiologic studies have 15 examined the potential cardiovascular and resp iratory effects associated with short-term 16 exposures to UFPs. These studi es have reported inconsistent and mixed results (US EPA, 2009a, 17 section 2.3.5). 18 In considering the body of scientific evidence available in this revi ew, the ISA concludes 19 that the currently available evid ence is suggestive of a causal association between short-term 20 exposures to UFPs and cardiovascul ar and respiratory effects. Furthermore, the ISA concludes 21 that evidence is inadequate to infer a causal association between short-term exposure to UFPs 22 and mortality as well as long-term exposure to UFPs and all outcomes evaluated (US EPA, 23 2009a, sections 2.3.5, 6.2.12.3, 6.3.10.3, 6.5.3.3, 7.2.11.3, 7.3.9, 7.4.3.3, 7.5.4.3, and 7.6.5.3; 24 Table 2-6). Thus, while new ev idence expands our understanding of effects associated with 25 UFPs, we reach the preliminary conclusion that th is information is still too limited to support a 26
distinct PM standard for UFPs. 27

 To what extent does the currently ava ilable information provide support for 28 considering a separate indicator for a specific PM 2.5 component or source category of 29 fine particles? Conversely, to what extent does the currently available information 30 provide support for eliminating any component or source category from the mix of fine 31 particles included in the PM 2.5 indicator? 32 In the last review, EPA recogni zed the availability of a lim ited number of epidemiologic 33 studies that explored associati ons with various components within the mix of fine particles and 34 adverse effects (US EPA, 2004, section 9.2.2.1.1, Table 9–3) as well as severa l studies that used 35

PM 2.5 speciation data to evaluate the association be tween mortality and particles from different 36Draft Do Not Quote or Cite March 2010 2-60 categories of fine particle sources (US EPA, 2004, section 8.2.2.5). As discussed in the last 1 review, different patterns of associations of various PM 2.5 components (e.g., sulfates, nitrates, 2 metals, organic compounds, elemental carbon (EC)) or source categories of fine particles with 3 total or cardiovascular mortality were observed in various short- term exposure studies (US EPA, 4 2004, section 8.2.2.5. Tables 8-3, 8-4, 9-3). However, as noted in the la st review, “many PM 5 components are correlated with each other and also with PM mass, making it difficult to 6 distinguish effects of the various components. Al so, different PM componen ts or characteristics 7 would be expected to be more closely linked with different h ealth outcomes” (US EPA, 2004, p. 8 9-30). In addition, a limited number of studies evaluated in the last review used PM 2.5 speciation 9
data to assess the effects of air pollutant combinations or mixtures using factor analysis or source 10 apportionment methods to link effects with different PM 2.5 source types (Schwartz, 2003; Mar et 11 al., 2003; and Tsai et al., 2000). These studies reported that fine par ticles from combustion 12 sources, including motor vehicle emissions, coal combustion, oil burning and vegetative burning, 13 were associated with increased mortality. No sign ificant increase in mortality was reported with 14 a source factor representing crus tal material in fine particle s (US EPA, 2004, section 8.2.2.5.3). 15
The EPA concluded that these studi es indicated that exposure to fine particles from combustion 16 sources, but not crustal materi al, was associated with mort ality (US EPA, 2004, p. 8-85; US 17 EPA, 2005, p. 3-16). 18 Overall, EPA concluded in th e last review that the avai lable evidence suggested “that 19 many different chemical components of fine partic les and a variety of di fferent types of source 20 categories are all associated wit h, and probably contribute to, mort ality, either independently or 21 in combinations’’ (US EPA, 2004,p. 9-31). Conversely, scientific evidence av ailable in the last 22 review provided no basis to conclude that any individual fine particle component could not be 23 associated with adverse health effects (US EP A, 2005, p. 5–17). This evidence provided the 24
basis for EPA to reach the final decision that “t here was not sufficient evidence that would lead 25
EPA to select one or more PM 2.5 component as being primarily res ponsible for effects associated 26 with fine particles, nor was there sufficient ev idence to suggest that any component should be 27
eliminated from the indicator for fine particles” (71 FR 61163/1, October 17, 2006). 28 In addressing the issue of pa rticle composition in this review, the ISA concludes that, 29 “[f]rom a mechanistic perspective, it is highly plausible that the chemical composition of PM 30 would be a better predictor of health effects than particle size” (US EPA, 2009a, p. 6-202). 31 Heterogeneity of ambient concentrations of PM 2.5 constituents (e.g., elemental carbon (EC), 32 organic carbon (OC), sulfate (SO 4 2- ), and nitrate) observed in di fferent geographical regions as 33 well as regional heterogeneity in PM 2.5 -related health effects reported in a number of 34 epidemiologic studies are consistent with th is hypothesis (US EPA, 2009a, section 6.6). 35Draft Do Not Quote or Cite March 2010 2-61 With respect to the availability of ambi ent measurement data for fine particle 1 components, we recognize that, in this re view, there are more extensive ambient PM 2.5 speciation 2 measurement data available through th e Chemical Speciation Network (CSN). 29 Data from the 3 CSN monitoring network provide further evidence of spatial a nd seasonal variation in both PM 2.5 4 mass and composition among cities/regions (US EP A, 2009a, pp. 3-50 to 3-60; Figures 3-12 to 5 3-18; Figure 3-47). Some of this variation may be related to “regional differences in 6 meteorology, sources, and topography” (US EPA, 2009a, p. 2-3). While the network of 7 approximately 200 CSN monitoring sites provides va luable data for development and tracking of 8 control strategies, its use for providing PM 2.5 speciation data to support epidemiological studies 9 is somewhat limited. The CSN sites provide meas urement data on a one-in-three or one-in-six 10 day schedule and do not capture data every day. Health researchers ha ve expressed a strong 11 interest in having access to PM 2.5 speciation measurements collected more frequently. 30 12 The currently available epidemiologic, t oxicological, and controlled human exposure 13
studies have evaluated the health effects associated with ambient PM 2.5 constituents and 14 categories of fine particle sources, using a variet y of quantitative methods applied to a broad set 15
of PM 2.5 constituents, rather than selecting a few cons tituents a priori (US EPA, 2009a, p. 2-26). 16 Epidemiological studies have used measured ambient PM 2.5 speciation data, including 17 monitoring data from the CSN, while all of th e controlled human exposure and most of the 18 toxicological studies have used CAPs, and anal yzed the constituents therein (US EPA, 2009a, p. 19 6-203). 31 20

29 The CSN consists of 54 Speciation Trends Network (STN ) sites as well as about 150 SLAMS supplemental sites across the country measuring over 40 chemical species. A limited number of CSN monitors began collecting ambient data in 2000 with the majority of sites collecting data starting in 2001. These sites collect aerosol samples over 24 hours on filters that are analyzed for PM 2.5 mass, trace elements, major ions (e.g., sulfates, nitrates, ammonium), and organic and elemental carbon.
30 As outlined in section 6.6.2.11of th e ISA, some investigators have circumvented the issue of less than daily speciation data by using the PM 2.5 chemical species data in a second stage re gression to explain the heterogeneity in PM 10 or PM 2.5 mortality risk estimates across cities and assuming that the relative contributions of PM 2.5 have remained the same over time (US EPA, 2009a, p. 6-206). In April 2008, EPA co-sponsored a workshop to discuss modifications to the current ambient air quality monitoring networks that would advance our understanding of the impacts of PM exposures on public health/welfare in the most meaningful way, including improving our understanding of components of fine particles. This worksh op was a major step in a series of interactions to foster improved long-term communication between external stakeholders, including air quality monitoring experts and health researchers. A summary of the workshop recommendations, including recommendations for daily PM 2.5 speciation measurements in large urban areas, is available at www.epa.gov/ORD/npd/pdfs/FINAL-April-2008-AQHealth-Research-Worksh op-Summary-Dec-2008.pdf . Follow-up for a number of the workshop recommendations is on-going.
31 Most studies considered between 7 and 20 ambient PM 2.5 constituents, with EC, OC, SO 4 2- , nitrate, and metals most commonly measured. Many of the studies reduced the number of ambient PM 2.5 constituents by grouping them with various factorization or source apportionment techniques to examine the relationship between the grouped PM 2.5 constituents and various hea lth effects. However, not all studies la beled the constituent groupings according to their presumed source and a small number of controlled human exposure and toxicological studies did not apply any kind of grouping to the ambient PM 2.5 speciation data. In addition, there were differences in the type and groupingDraft Do Not Quote or Cite March 2010 2-62 With respect to epidemiological studies evalua ting short-term exposures to fine particle 1 constituents, several new multi-city studies are now available. These studies continue to show an 2 association between mortality and cardiovascular and/or respiratory morbidity effects and short3 term exposures to various PM 2.5 components including nickel (Ni) , vanadium (V), elemental 4 carbon (EC), organic carbon (OC), and sulfates (US EPA, 2009a, sections 6.5.2.5 and 6.6). 5 Lippmann et al. (2006); Domini ci et al. (2007) evaluated the heterogeneity in the PM 10 –mortality 6 association as evaluated in the NMMAPS data by analyzing the PM 2.5 speciation data. Nickel 7 (Ni) and Vanadium (V) were identified as significant pred ictors of variation in PM 10 -related 8 mortality across cities, with Ni levels in New Yo rk City being reported as particularly high (US 9 EPA, 2009a, section 6.5.2.5; Figure 6-31). 32 Bell et al. (2009) and Peng et al. (2009) conducted 10 similar analyses focusing on the variation in PM 2.5 -related cardiovascular and respiratory 11 hospital admissions in older adults. Peng et al . (2009) focused on the components that make up 12 the majority of PM 2.5 mass and found that in multi-polluta nt models only EC and OC were 13 significantly associated with risk of hospitalization for cardiovascular disease. Bell et al. (2009) 14 used data from twenty PM 2.5 components and found that EC, Ni, and V were most positively and 15 significantly associated with the risk of PM 2.5 -related hospitalizations suggesting that the 16
observed associations between PM 2.5 and hospitalizations may be primarily due to particles from 17 oil combustion and traffic (US EPA, 2009a, s ection 6.2.10.1). In a study of 25 U.S. cities, 18 Franklin et al. (2008) focused on a time-seri es regression of mortality related to PM 2.5 mass by 19
season and also examined effect modification due to various PM 2.5 species. They concluded that 20 Al, As, Ni, Si and SO 4 2- were significant eff ect modifiers of PM 2.5 mortality risk estimates, and 21 “simultaneously including Al, Ni, and SO 4 2- together or Al, Ni, and As together further increased 22 explanatory power. Of the species examine d, Al and Ni explained the most residual 23 heterogeneity” (US EPA, 2009a, p. 6-194; Table 6-17). 33 Furthermore, Ostro et al (2006) 24
examined associations between PM 2.5 components and mortality in six California counties and 25
found an association between mort ality, especially cardiovascular- related mortality and several 26

PM 2.5 components including EC, OC, nitrate, Fe, K, and Ti at various lags (US EPA, 2009a, p. 6- 27 195). 28

of PM 2.5 constituent data used in the various studies and analyses conducted resulting in important limitations in interpreting these studies together (US EPA, 2009a, p. 6-203).
32 However, as noted in the ISA, in a sensitivity analysis when selectively removing cities from the overall estimate, the significant association between the PM 10 mortality risk estimate and the PM 2.5 Ni fraction was diminished upon removing New York City from the analysis, which is consistent with the results presented by Dominici et al. (2007) (US EPA, 2009a, section 6.5.2.5; Figure 6-32).
33 Of note, New York City was not included in th e 25 cities examined by Franklin et al. (2008).Draft Do Not Quote or Cite March 2010 2-63 Limited evidence is available to evaluate th e health effects associated with long-term 1 exposures to PM 2.5 components (US EPA, 2009a, section 7.6.2). The most significant new 2 evidence is provided by a study that evaluated multiple PM 2.5 components and an indicator of 3 traffic density in an assessment of health effects related to long-term exposure to PM 2.5 (Lipfert 4 et al., 2006). Using health data from a cohort of U.S. military veterans and PM 2.5 data from 5 EPA’s CSN, Lipfert et al. (2006) reported positive asso ciations between mort ality and long-term 6 exposures to nitrates, EC, Ni and V as well as traffic density and peak O 3 concentrations. 7 Additional evidence from a long-term exposur e study conducted in a Dutch cohort provides 8 supportive evidence that long-term exposure to tr affic-related particles is associated with 9 increased mortality (Breelen et al., 2008). 10 With respect to source categories of fine pa rticles associated with a range of health 11 endpoints, the ISA reports that currently available evidence suggests associat ions between 12 cardiovascular effects and a number of specific PM 2.5 –related source categor ies, specifically oil 13 combustion, wood or biomass burning, motor vehicle emissions, and crustal or road dust sources 14 (US EPA, 2009a, section 6.6; Table 6-18). In add ition, a few studies have evaluated associations 15
between PM 2.5 –related source categories and mortality. Thes e studies included a reported 16 association between mortality and a PM 2.5 coal combustion factor (L aden et al., 2000), while 17 others linked mortality to a secondary SO 4 2– long-range transport PM 2.5 source (Ito et al., 2006; 18 Mar et al., 2006) (US EPA, 2009a, section 6.6.2.1). There is less consistency in associations 19
observed between PM 2.5 sources and respiratory health effects, which may be partially due to the 20
fact that fewer studies have been conducted that evaluated respiratory-related outcomes and 21 measures. However, there is some evidence for associations with secondary SO 4 2– .and 22 decrements in lung function in asthmatic and healthy adults (US EPA, 2009a, p. 6-211; Gong et 23 al., 2005; Lanki et al., 2006). Resp iratory effects relating to the cr ustal/soil/road dust and traffic 24
sources of PM have been observed in asthma tic children and adults (US EPA, 2009a, p. 6-205; 25 Gent et al., 2009; Penttin en et al., 2006). 26 Recent studies have shown that source apportio nment methods have the potential to add 27 useful insights into which sources and/or PM constituents may contribute to different health 28 effects. Of particular inte rest are several epidemiologic studies that compared source 29 apportionment methods and reporte d consistent results across re search groups (US EPA, 2009a, 30 p. 6-211; Hopke et al., 2006; It o et al., 2006; Mar et al., 2006; Thurston et al., 2005). These 31 studies reported associations between total morta lity and secondary sulfate in two cities for two 32 different lag times. The sulfate effect was str onger for total mortality in Washington D.C. and 33 for cardiovascular-related morality in Phoenix (U S EPA, 2009a, p. 6-204). These studies also 34
found some evidence for associations with mort ality and a number of source categories (e.g., 35 biomass/wood combustion, traffic, copper smelter, coal combustion, sea salt) at various lag times 36Draft Do Not Quote or Cite March 2010 2-64 (US EPA, 2009a, p. 6-204). Sarn at et al., (2008) compared thr ee different source apportionment 1 methods and reported consistent associations between ED visits for cardiovascular diseases with 2
mobile sources and biomass combustion as well as increased respiratory-related ED visits 3 associated with secondary sulfate (US EPA, 2009a, pp. 6-204 and 6-211; Sarnat et al., 2008). 4 In summary, in considering the currently ava ilable evidence for health effects associated 5 with chemical components and source categories of PM 2.5 as presented in the ISA, we reach the 6 preliminary conclusion that additional information available in this review continues to provide 7 evidence that many different constituents of the fi ne particle mixture as well as specific source 8 categories of fine particles are li nked to adverse health effects. However, as noted in the ISA, 9 while “[t]here is some evidence for trends and patterns that link particular ambient PM 10 constituents or sources with specific health outcomes...there is insufficient evidence to 11 determine whether these patterns are consis tent or robust” (US EPA, 2009a, p. 6-210). 12 Furthermore, the ISA concludes that “the evidence is not yet sufficient to allow differentiation of 13
those constituents or sources that are more closely related to sp ecific health outcomes” (US EPA, 14 2009a, pp. 2-26 and 6-212). Therefore, we reach th e preliminary conclusion that the currently 15
available evidence is not sufficien t to support consideration of a se parate indicator for a specific 16

PM 2.5 component or source category of fine partic les. Furthermore, we also reach the 17 preliminary conclusion that the evidence is not sufficient to support elim inating any component 18 or source from the mix of fine particles included in the PM 2.5 indicator. 19 We recognize that much research supported by EPA, the Health Effects Institute (HEI), 20
the Electric Power Research Inst itute (EPRI), and others is unde rway to evaluate the role of 21

PM 2.5 components/sources and agree that additional research is needed to improve future 22 understanding of the role of specific fine particle components and/or sources of fine particles. 23 Summary 24 In considering whether curre ntly available evidence pr ovides support for retaining, 25 revising, or supplementing the current PM 2.5 mass-based indicator, we first reach the preliminary 26 conclusion that it is appropriate to retain PM 2.5 as the indicator for fine particles. Secondly, we 27 reach the preliminary conclusion that the cu rrently available evidence does not provide a 28 sufficient basis for supplementing the mass-based PM 2.5 indicator by considering a separate 29 indicator for ultrafine particles as a subfraction of fine particles. Furthermore, we also reach the 30 preliminary conclusion that the currently availabl e evidence is too limited to provide support for 31 considering a separate in dicator for a specific PM 2.5 component or source category of fine 32 particles or for eliminating any individual com ponent or source category from the mix of fine 33 particles included in the PM 2.5 mass-based indicator. 34Draft Do Not Quote or Cite March 2010 2-65 2.3.2 Averaging Times 1 In the last review, EPA rec ognized that the available info rmation related to exposure 2 periods of concern was generally consistent and supportive of th e conclusions reached in the 3 review completed in 1997. In that review, the Agency retained two PM 2.5 standards, based on 4 annual and 24-hour averaging times in order to pr ovide protection for health effects associated 5 with short- and long-term exposure periods ( 71 FR 61164, October 17, 2006). In this review, in 6 evaluating alternative fine particle standards, we first address the element of the standard related 7 to averaging time by asking the following question: 8

 To what extent does the currently available information continue to provide support for 9 the current 24-hour and annual averaging times? 10 In considering whether the information availabl e in this review supports consideration of 11 different averaging times for PM 2.5 standards, we note that the av ailable information is generally 12 consistent with and supportive of the conclusions r eached in the previous re views to set a suite of 13

PM 2.5 standards including standards with bot h annual and 24-hour averaging times. The 14 overwhelming majority of studies conducted since the last review continue to utilize 24-hour and 15 annual averaging times, and largel y contribute to the body of eviden ce for health effects related 16 to both short-term (from less than 1 day to up to several days) and long-term (from a year to 17 several years) measures of PM 2.5 . Consequently, our preliminary conclusion is that the currently 18 available evidence continues to provide suppor t for a 24-hour and annual averaging time. 19 With respect to a standard with an annual averaging time, we rec ognize that an annual 20 standard would provide effective protection ag ainst both annual and multi-year, cumulative 21 exposures that are associated with an array of health effects. W ith regard to providing protection 22 for short-term fine particle exposures, we note that the large majo rity of short-term 23 epidemiologic studies report associations base d on 24-hour averaging times or on multiple-day 24 averages (i.e., distributed lag). Furthermor e, we recognize that a 24-hour standard can 25 effectively protect against episodes lasting severa l days, as well as providing some degree of 26 protection from potential effects associated with shorter duration peak levels of PM 2.5 , and from 27 episodes that result in localized or seasonal PM 2.5 exposures of concern in areas where the 28 highest 24-hour-to-annual mean PM 2.5 ratios are appreciably above the national average. In 29 consideration of the currently available evidence, we have fo cused on evaluating alternative 30 standards in the quantitative ri sk assessment conducted for this review that retained the 31 averaging times of the current standards (i.e , 24-hour and annual averaging times) (US EPA, 32 2010a) 33 In summary, we reach the preliminary conclu sion that there is strong support in this 34 review for retaining the current 24-hour and annual averaging times. We have then considered if 35Draft Do Not Quote or Cite March 2010 2-66 the currently available evidence provides support for supplementing the current averaging times 1 with additional standards focused on subdaily, multi-day, or seasonal exposures by posing two 2 more specific questions. 3

 To what extent does the currently availabl e scientific evidence provide support for 4 considering a standard with an averaging ti me less than 24 hours to address health 5 effects associated with subdaily fine particle exposures? 6 In the last review, we recognized the availability of limited ev idence of effects associated 7 with exposure periods shorter than 24-hours (e .g., one to several hours) (US EPA, 2004, section 8 3.5.5.1) and concluded that, while this evidence was “too limited to serve as the basis for 9 establishing a shorter-than-24-hour fine particle primary standard,” it provided “added weight to 10 the importance of a standard with a 24-hour averaging time” (71 FR 61164/2; US EPA, 2005, 11 section 5.3.3). More specifical ly, the AQCD noted that while fe w epidemiological studies had 12
used ambient PM concentrations averaged over time intervals shorter than 24 hours, several 13 epidemiological studies reported statistically si gnificant associations between 2- to 4-hour PM 2.5 14
concentrations and cardiovascular health e ndpoints, including myo cardial infarction (MI) 15
incidence and heart rate vari ability (HRV) (US EP A 2004, pp. 8-162 to 8-165). In particular, 16 Peters et al (2001) reported effect estimates for MI incidence with PM 2.5 averaged over 2- and 17 24- hours that were similar in magnitude a nd statistically significant (US EPA 2004, p. 8-165). 18 In this review, a much larger body of more recent studies provide additional evidence of 19 cardiovascular effects associated with exposur e periods shorter than 24 hours (US EPA, 2009a, 20 section 6.2). In this review, two studies that assessed sub-daily and daily exposures did not 21
observe an association between PM 2.5 and risk of MI, however no association was evident with 22 24-hour exposures to PM 2.5 as well (US EPA, 2009a, p. 6-67; Sull ivan et al., 2005; Peters et al., 23 2005). One study found a strong posi tive association betw een self-reported e xposure to traffic 24 and the onset of an MI within one hour, alt hough this study did not directly measure traffic25 related pollution (US EPA 2009a, p. 6-67; Peters et al. 2004). For cardi ac arrests witnessed by 26 bystanders, another study found a significant association with PM 2.5 exposure during the hour of 27 the arrest, with even larger risk estimates for older adults (ages 60-75) or those that presented 28 with asystole, a particular form of cardiac arrest when electrical activity in the heart stops (US 29 EPA 2009a, p. 6-77; Rosent hal et al. 2008). 30 With respect to heart rate and HRV, epidem iological studies reporte d effects associated 31 with pollutant concen trations lagged as short as 1 to 2 hours, but more consistently with lags of 32
24 to 48 hours. The results of several new cont rolled human exposure studies provide limited 33 evidence to suggest that acute e xposures (2-hour) to near ambient levels of concentrated ambient 34 particles, or CAPs (PM 2.5 , PM 10-2.5 and ultrafine particle s) may be associated with small changes 35 in HRV (USEPA, 2009a, p. 6-10). Changes in HR V parameters, however, are variable with 36Draft Do Not Quote or Cite March 2010 2-67 some showing increased parasympathetic activity relative to sympathetic activity and others 1 showing the opposite. One study reported advers e associations of 2-hour exposures to PM 10 with 2 implantable cardiac defibrillato r-detected ventricular arryth mias (US EPA, 2009a, p. 6-15; 3 Ljungman et al., 2008). Two panel studies of el derly subjects found electrocardiogram changes 4 typically representative of cardiac ischemia (S-T segment depression) significantly associated 5 with exposures to PM 2.5 of less than 24 hours (US EPA 2009a, p. 6-21; Gold et al., 2005; Lanki 6 et al. 2008). 7 With respect to vasomotor function, the system ic vasculature is likely to be a target 8 organ. Endothelial dysfunction is a factor in many diseases and may contribute to the origin 9 and/or exacerbation of perfusion-li mited diseases, such as MI or ischemic heart disease (IHD), as 10 well as hypertension. Endothelial dysfunction is also a characteristic feature of early and 11
advanced atherosclerosis. Six studies found e ffects of exposures of 2 hours or less on other 12

vasomotor outcomes. 34 The evidence on blood pressure changes is more mixed, with one panel 13 study (Dales et al., 2007; EPA 2009, p. 6-35) finding no association with blood pressure changes 14 with 2-hour exposures to traffic-related PM 2.5 ; while one panel and two controlled human 15 exposure studies (US EPA, p. 6-37; Chuang et al., 2005; Urch et al., 2005 and Fakhri et al., 16 2009) reported changes in blood pressure from 1- to 3-hour exposures to submicrometer 17 particles, and 2-hour exposu res to a combination of O 3 and CAPs, respectively. 18 One panel study that investigated associat ions between ambient PM and markers of 19 systemic inflammation among senior citizens ( ≥ 60 years of age) (US EPA, 2009a, p. 6-41; 20 Dubowsky et al., 2006), found positive associations between daily PM 2.5 levels and measures of 21 C-reactive protein (CRP), interleukin-6 (IL-6), and white blood cells (WBCs). When the 22 analysis was limited to exposures that occurred only on daily bus trip s (2 hours), the effect 23
estimates were similar in direction to the main analysis but were smaller in magnitude, with the 24 authors expressing the view that this was likely du e to greater measurement error. Another panel 25 study assessed the effects of in-vehicle exposure to PM 2.5 of healthy young non-smoking male 26 state troopers working from 3 PM to midnight (U S EPA, 2009a, p. 6-41 and 6-48; Riediker et al., 27 2004). This study concluded that PM 2.5 originating from speed-cha nging traffic modulates the 28 autonomic control of the heart rhythm, increases the frequency of premature supraventricular 29 beats and elicits proinflammatory and pro-th rombotic responses in healthy young men. New 30 studies involving controlled human exposures to various particle types have provided limited and 31
inconsistent evidence of a PM-i nduced increase in markers of sy stemic inflammation (US EPA, 32

34 Two studies (Dales et al. 2007; Rundell et al. 2007; US EPA 2009a, p. 6-25) found reductions in flow mediated dilatation (FMD) with 30-minute and 2-hour exposures to PM 2.5 , respectively. Four other studies (Peretz et al., 2008; Lund et al., 2009; Rundell and Caviston, 2008; and Shah et al., 2008; US EPA 2009a, p. 6-28 to 6-29) found effects of exposures of 2 hours or less on other vasomotor outcomes, including brachial artery diameter (BAD), circulating levels of endothelin-1, and reactive hyperemia, respectively.Draft Do Not Quote or Cite March 2010 2-68 2009a, p. 6-46). New findings for hemostasis, th rombosis and coagulation from controlled 1 human exposure studies have provide d in consistent evidence that short-term exposure to PM at 2 near ambient levels may have small, yet statistically significant effects on hemostatic markers in 3 healthy subjects or people with coronary artery disease (US EPA, 2009a, p. 6-50). 4 With respect to respiratory health outcomes, in the last review, evidence of association 5 between respiratory symptoms and subdaily exposures to PM 10 was available from two US panel 6 studies of symptoms in asthmatic subjects (US EPA 2004, section 8.3.3.1.1). These two studies 7 used 1-hour and 24-hour averag e concentrations. The PM 10 1-hour outcome was larger than the 8 24-hour outcome for lower respiratory illness in one study, but the reverse was true for cough in 9 the other study. 10 In this review, evidence of subdaily PM 2.5 exposures associated with respiratory diseases 11
continues to be limited. The ISA concludes that for several studies of hospital admissions or 12 medical visits for respiratory diseases, the str ongest associations were observed with 24-hour 13 average or longer exposures, not with less then 24-hour exposures (US EPA, 2009a, section 6.3). 14 A study that examined evidence of respirat ory effects associated with subdaily PM 2.5 exposures 15 in two New York City communities by assessin g the association between 24-hour and 1-hour 16
maximum PM 2.5 levels and ED visits. This study re ported an increase in asthma-related ED 17 visits that was similar for the two time periods (New York State Depart ment of Health, 2006). 18
These results were robust to ad justment for copollutants. However, a panel study found an 19 association between a 10 μg/m 3 increase in morning maximum 1-hour mean, but not daily, PM 2.5 20
concentrations and increased likelihood of resc ue medication use in asthmatic children (US EPA 21 2009a, p. 6-90; Rabinovitch et al., 2006). Anothe r study examined the association between a 22 marker for pulmonary inflammation (exhale d nitric oxide, or eNO), and ambient PM 2.5 23 concentrations. Each 10 μg/m 3 increase in 1-hour mean PM 2.5 concentration was associated with 24 a statistically significant increase in e NO among asthmatic children not taking inhaled 25 corticosteroids (US EPA 2009, p. 6-101; Mar et al., 2005). 26 In summary, there is a rapidly growing body of studies that provide evidence for 27 cardiovascular effects associated with subdaily exposure to PM, especially effects related to 28 HRV, cardiac ischemia, and vasomotor function, a nd also of changes in markers of systemic 29 inflammation, hemostasis, thrombosis and coa gulation. Because these studies have used 30 different indicators (e.g., PM 2.5 , PM 10 , PM 10-2.5 , ultrafine particles), av eraging times, and health 31 outcomes, it is difficult to draw conclusions abou t cardiovascular effects associated specifically 32 with subdaily exposures to PM 2.5 . Although there is additional ev idence of respiratory effects 33
associated with PM 2.5 exposure periods shorter than 24-hour s (e.g., one to several hours), this 34 evidence is much sparser than for cardiovascular effects. Considering the currently available 35 evidence, we reach the preliminary conclusion that this information is too unclear, with respect 36Draft Do Not Quote or Cite March 2010 2-69 to the indicator, averaging time and health outcome, to serve as a basis for establishing a shorter1
than-24-hour PM 2.5 primary standard at this time. Howe ver, this evidence does provide added 2 weight to the importance of a st andard with a 24-hour averaging time. We recognize that the 3
assessment of health effects asso ciated with shorter- than-24-hour exposure is an important area 4 of research that could provide a basis for the consideration of a subdaily PM standard in the 5 future. We note that the availability of hourly PM 2.5 concentrations from the PM 2.5 continuous 6 monitors reporting to the AQS s hould provide the basis for a cleare r assessment of the effects of 7 subdaily exposure to PM 2.5 in the future. 8

 To what extent does the currently availabl e scientific evidence provide support for 9 considering separate standards with dist inct averaging times to address effects 10 associated with seasonal fine particle exposures? 11 With regard to health effects associated with PM 2.5 exposure across varying seasons in 12 this review, Bell et al . (2008) reported higher PM 2.5 risk estimates for hospitalization for 13 cardiovascular and respiratory diseases in the wi nter compared to other seasons in a large, 14 national multi-city study. In comparison to the winter season, smaller statistically significant 15 associations were also reported between PM 2.5 and cardiovascular morbidity for spring and 16 autumn, and a positive non-signifi cant association was observed fo r the summer months. In the 17 case of mortality, Zanobetti and Schwartz (2009) reported in their multi-c ity US based study a 4- 18 fold higher effect estimate for PM 2.5 associated mortality for the spring as compared to the 19 winter. These results suggest individuals are at greater risk of dying fr om higher exposures to 20

PM 2.5 in the warmer months, and at greater ri sk of PM associated hospitalization for 21 cardiovascular and respiratory diseases during cold er months of the year. Overall, we observe 22 that there are few studies presently ava ilable to deduce a general pattern in PM 2.5 risk across 23 seasons. In addition, these studies utilized 24-hour exposure periods within each season to assess 24
the PM 2.5 associated health effects, and do not provi de information on health effects associated 25 with a season-long exposure to PM 2.5 . Due to these limitations in the currently available 26 evidence, we reach the preliminary conclusion th at there is no basis to consider a seasonal 27 averaging time separate from a 24-hour averaging time. 28 Summary 29 In summary, we recognize that the currently available evidence informs our understanding of 30 exposure durations of concern and continues to pr ovide strong support for standards that provide 31 protection for both short- and long-term exposures . In considering the possibility of effects 32 associated with subdaily PM 2.5 exposures (i.e., less than 24-hour exposures) we recognize that 33
there is additional evidence available in this re view, primarily focused on cardiovascular effects 34 with more limited evidence for respiratory effects. However, because these studies have used 35
different indicators of PM exposure (e.g., PM 2.5, PM 10 , UFPs), averaging times, and a broad 36Draft Do Not Quote or Cite March 2010 2-70 range of health outcomes, it is difficult to use this evidence to serve as a basis for establishing a 1
standard with a shorter-than-24- hour averaging time. W ith respect to seasonal effects, while we 2 recognize there is some new evidence for PM 2.5- related effects differentiated by season, we reach 3 the preliminary conclusion that this evidence is, at this point, too limited to use as a basis for 4 establishing a PM 2.5 standard with a seasonal averaging time. Based on the above considerations, 5 we initially conclude that the currently available inform ation provides strong support for 6 retaining the current annual and 24-hour av eraging times but does not provide support for 7 alternative averaging times of less than 24-hours or for seasons 8

2.3.3 Forms 9 The “form” of a standard defines the air quality statistic that is to be compared to the 10 level of the standard in determining whether an ar ea attains the standard. In this review, staff are 11 evaluating whether curren tly available information support cons ideration of alternative forms for 12
the annual or 24-hour PM 2.5 standards. 13

2.3.3.1 Form of the Annual Standard 14

In 1997, EPA established the form of the annual PM 2.5 standard as an annual arithmetic 15 mean, averaged over 3 years, from single or multiple community-oriented monitors. This form 16 was intended to represent a relatively stable meas ure of air quality and to characterize area-wide 17

PM 2.5 concentrations. The arithmetic mean served to represent the broad di stribution of daily air 18 quality values, and a 3-year aver age provided a more stable risk reduction target than a single19 year annual average. When set ting the initial fine particle st andards in 1997, the level of the 20
annual PM 2.5 standard was to be compared to measurements made at the community-oriented 21 monitoring site recording the highest leve l, or, if specific constraints were met 35 , measurements 22 from multiple community-oriented monitoring sites could be averaged (62 FR 38671 to 38672, 23 July 18, 1997). The constraints for allowing the use of spatially averaged measurements were 24 intended to limit averaging across poorly correlat ed or widely disparate air quality values to 25 ensure that spatial averaging w ould not result in inequities in th e level of protection provided by 26
the PM 2.5 standards against health effects asso ciated with short- and long-term PM 2.5 exposures 27 (62 FR 38672). This approach was judged to be consistent with the epidemiologic studies on 28
which the PM 2.5 standard was primarily based, in which ai r quality data were generally averaged 29 across multiple monitors in an area or were take n from a single monitor that was selected to 30 represent community-wide exposures , not localized “hot spots.” 31

35 The original criteria for spat ial averaging included: (1) the annual mean concentration at each site shall be within 20 percent of the spatially averaged annual mean, and (2) th e daily values for each monitoring site pair shall yield a correlation coefficient of at l east 0.6 for each calendar quarter.Draft Do Not Quote or Cite March 2010 2-71 In the last review, in consideri ng the form of the primary annual PM 2.5 standard, EPA 1 posed the question as to whether an annual standard that allowed for spatial averag ing, within the 2 original specified or a lternative constraints, would provide ap propriate public health protection. 3 Analyses conducted in the last review , based on a much larger set of PM 2.5 air quality data than 4 was available for the review completed in 1997, assessed both aggregate population risk across 5 an entire urban area and the potential for disp roportionate impacts on potentially vulnerable 6 populations within an area. The results of these analyses prov ided evidence concerning the 7 potential for disproportionate impacts on potentia lly vulnerable populations, noting “the highest 8
concentrations in an area tend to be measured at monitors located in areas where the surrounding 9 population is more likely to have lower educati on and income levels, and higher percentages of 10 minority populations” (71 FR 61166/2, see also US EPA, 2005, section 5.3.6.1; Schmidt et al., 11 2005, Attachment A/Analysis 7). 36 12 In addition, the effect of allowing the use of spatial averaging on aggregate population 13 risk was considered as part of the sensitivity analyses included in the health risk assessment 14 conducted for the last review (US EPA, 2005, secti on 4.2.2). In that analysis, changing the basis 15 of the annual standard design value from the conc entration at the highest monitor to the average 16
concentration across all monitors reduced the air quality adjustment needed to just meet the 17
current or alternative annual standards. As expected, the estimated risks remaining upon 18
attainment of the current annual standard in areas where the annual standards was the 19 “controlling standard” we re greater when spatial averaging was used than when the highest 20 monitor was used (i.e., the estimated reductions in risk associated with ju st attaining the current 21
or alternative annual standards are less when spatia l averaging was used ). The estimated 22 mortality incidence associated w ith long-term exposure in most cases ranged from about 10 to 23 60% higher when spatial averagi ng was used, and estimated mortal ity incidence a ssociated with 24 short-term exposure in most cases ranged from about 5 to 25% higher. In light of these analyses, 25
EPA retained the form of the standard as an a nnual arithmetic mean, averaged over 3 years with 26 modifications that strengthened the standard by tightening the criteria for use of spatial 27 averaging 37 to provide increased protection for vulnerable populations exposed PM 2.5
. 28

36 As summarized in footnote 29 at 71 FR 61166/2, the 2004 AQCD noted that some epidemiologic studies, most notably the ACS study of associations between long-term PM 2.5 exposure and mortality, reported larger effect estimates in the cohort subgroup with lower education levels (US EPA, 2004, p 8-103). The 2004 AQCD also noted that lower education level may be a ma rker for lower socioeconomic status (S ES) that may be related to increased vulnerability to the effects of fine particle exposures, for ex ample, as a result of greater exposure from proximity to sources such as roadways and industry, as well as other fact ors such as poorer health st atus and access to health care (US EPA, 2004, section 9.2.4.5).
37 The current criteria for spatial averaging include: (1) the an nual mean concentration at each site shall be within 10 percent of the spatially averaged annual mean, and (2) the daily values for each monitoring site pair shall yield a correlation coefficient of at leas t 0.9 for each calendar quarter (71 FR 61167/2-3, October 17, 2006).Draft Do Not Quote or Cite March 2010 2-72 In this review, the currently availabl e evidence provides stronger support that 1 socioeconomic status (SES), measured using surrogates such as educational attainment, 2 residential location, and income level, modifies the association between PM and morbidity and 3 mortality outcomes. Thus, as discussed in section 2.2.1, the ISA concludes that susceptible 4 populations include persons with lower SES levels. In light of this information and the analyses 5
conducted for the last review as discussed above , we believe that the existing constraints on 6 spatial averaging, as modified in 2006, may not be adequate to avoid substantially greater 7 exposures in some areas, potentially resulting in disproportionate impacts on persons with lower 8 SES levels. Therefore, we ar e reconsidering the appropriateness of continuing to allow spatial 9 averaging across monitors as part of the form of the annual PM 2.5 standard. Recognizing that it is 10
the link between the form and the level of a standard that determines the degree of public health 11 protection the standard affords, we discuss cons ideration for eliminating the spatial averaging 12 provisions from the form of the annual PM 2.5 standard in conjunction with consideration of 13
alternative levels to address heal th effects related to long-term PM 2.5 exposures in section 2.3.4 14
below. 15

2.3.3.2 Form of the 24-Hour Standard 16

In 1997, EPA established the form of the 24-hour PM 2.5 standard as the 98th percentile of 17 24-hour concentrations at each population-oriented monitor within an area, averaged over three 18 years (62 FR at 38671 to 38674, July 18, 1997). In making that decision, EPA recognized that a 19 concentration-based form gave proportionally greater weight to days when concentrations were 20 well above the level of the standard than to days when the concentrations were just above the 21 standard. Further, a concentration-based fo rm better compensated for missing data and less22 than-every-day monitoring; and, when averaged over 3 years, it had greater stability and, thus, 23 facilitated the development of mo re stable implementation programs. The Agency selected the 24
98 th percentile as an appropriate balance between adequately li miting the occurrence of peak 25 concentrations and providing incr eased stability and robustness. In addition, by basing the form 26
of the standard on concentrations measured at population-oriented monitoring sites, EPA 27 intended to provide protection fo r people residing in or near localized areas of elevated 28
concentrations. 29 In the last review, in conjunction with cons idering alternative 24-hour standard levels, 30 EPA concluded it was appropriate to retain a concentration-based fo rm that was defined in terms 31 of a specific percentile of th e distribution of 24-hour PM 2.5 concentrations at each population32 oriented monitor within an area, averaged over 3 years. In that review, in considering retaining 33
the 98 th percentile form or revi sing the standard to a 99 th percentile from, the Agency evaluated 34 the combination of form and level to provide appropriate public health protection and, in 35Draft Do Not Quote or Cite March 2010 2-73 particular, considered: (1) the relative risk re duction afforded by alternative forms at the same 1 standard level, (2) the relative ye ar-to-year stability of the air quali ty statistic to be used as the 2 basis for the form of a standard, and (3) the implications from a public health communication 3 perspective of the extent to which either form a llows different numbers of days in a year to be 4
above the level of the standard in areas that attain the standar d. Based on these considerations, 5 the Administrator concluded it was appropriate to retain the 98 th percentile form of the 24-hour 6 standard in conjunction with lowe ring the level of the standard. In reaching this final decision, 7 EPA recognized a technical proble m associated with a potential bias in the method used to 8
calculate the 98 th percentile concentration for this form . As such, EPA adjusted the sampling 9 frequency requirement in order to reduce this bi as. Accordingly, the Agency modified the final 10 monitoring requirements such that areas that are within 5 percent of the standards are required to 11 increase the sampling frequency to ever y day (71 FR 61164 to 61165, October 17, 2006). 12 In this first draft PA, we have focuse d consideration of a lternative 24-hour PM 2.5 13
standards on alternative levels only, as discussed in secti on 2.3.5. In the second draft PA, we 14 intend to explore more fully information regard ing peak air quality c oncentrations to better 15 inform our understanding of the implications of retaining or m odifying the current form of the 16
24-hour standard. 17

2.3.4 Alternative Levels to Address Heal th Effects Related to Long-term PM 2.5 Exposures 18 In considering alternative PM 2.5 standards that would provide protection against health 19 effects related to long-term exposures, we have taken into account both ev idence-based and risk20 based considerations. As discussed below, we first evaluate the available evidence from long21
term PM 2.5 exposure studies, as well as the uncertain ties and limitations in that evidence as 22 presented in the ISA, to assess the degree to which alternative annual PM 2.5 standards can be 23 expected to provide protection against effects related to long- term exposures (section 2.3.4.1). 24 Secondly, we have considered the quantitative risk estimates associated with long-term PM 2.5 25 exposure, as discussed in the s econd draft RA, to assess the extent to which alternative standards 26 can be expected to reduce the estimated risk s attributable to long-term exposure to PM 2.5 (section 27 2.3.4.2). With respect to the suite of PM 2.5 standards, our preliminar y integrated conclusions 28 presented in section 2.3.6 are base d in part on the conclusions from this section and in part on 29 preliminary staff conclusions from section 2.3.5, in which alternative PM 2.5 standards to address 30
health effects related to short-term PM 2.5 exposures are discussed. 31

2.3.4.1 Evidence-based Considerations 32

In taking into account eviden ce-based considerations for informing our understanding of 33
alternative levels to address heal th effects related to long-term fi ne particle exposures, we have 34Draft Do Not Quote or Cite March 2010 2-74 initially focused on long-term PM 2.5 exposure studies conducted in the U.S. and Canada and 1 placed the greatest weight on associations that have been judged in the ISA to be causal or likely 2
causal. We have also considered the evidence for a broader range of health outcomes judged in 3 the ISA to have suggestive evidence of a causal a ssociation or that focus on specific susceptible 4 populations to evaluate whether this evidence pr ovides support for considering lower alternative 5 levels. Collectively, we have integrated the curr ently available evidence to address the following 6 question: 7

 To what extent does the currently availabl e evidence provide support for revising the 8 current suite of standards to provide protecti on for long-term fine particle exposures? 9 In looking first at evidence from long-term PM 2.5 exposure studies of mortality (causal 10 association), we note, as discu ssed in section 2.2.1, that the ex tended follow-up analyses of the 11 ACS and Harvard Six Cities studies, have confir med and strengthened evidence of associations 12 reported in the last review at lower air quality le vels. In addition, new cohort studies, including 13 the WHI evaluating cardiovascular-related morta lity in postmenopausal women and analyses of 14 mortality in a Medicare cohort, provide further evidence of eff ects associated with long-term 15

PM 2.5 exposures at air quality levels in the same range as the more recent year s of air quality data 16
evaluated in the ACS and Harvard Six Cities extended follow-up studies. 17 As outlined in Figure 2-1 long-term mean PM 2.5 concentrations across all cities evaluated 18 in each of these studies range from 10.7 to 16.4 μg/m 3

. 38 In looking first at the long-term 19 exposure mortality studies, we not e that the long-term mean PM 2.5 concentration in the extended 20 follow-up of the Harvard Six Cities study was 16.4 μg/m 3 . As noted in section 2.2.1, in focusing 21 on the extended follow-up period (1990-1998), we estimate an aggregate long-term mean PM 2.5 22
concentration across th e six cities of 14.8 μg/m 3 (Laden, 2009). Eftim et al., (2008) evaluated 23 mortality in a Medicare cohort consisting of adults age 65 and older, a susceptible population, 24 within the same six cities using more recent air quality with a long- term mean of 14.1 μg/m 3 . In 25 the extended ACS study, the mean for the more recen t time period used in the analysis (1999 to 26 2000) was 14.0 μg/m 3 . In looking at the association ba sed on the air quality for both time 27 periods, the long-term mean PM 2.5 concentration was 17.1 μg/m 3 (Pope et al., 2004). Analysis of 28 mortality associated with long-term PM 2.5 exposure using a Medica re cohort and the ACS 29 locations using more recent air qua lity reported a long-term mean PM 2.5 concentration of 13.6 30 μg/m 3 (Eftim et al., 2008). Additional evidence of mortality associat ed with long-term PM 2.5 31 exposure in the MCAPS study across a larger nu mber of counties (668 vs. 110 counties) using 32 more extensive air quality data, provides eviden ce of effects in older adults, a susceptible 33 population, at similar levels. This study included effect estimates fo r three geographic areas (i.e., 34

38 We note that Figure 2-1 also includes studi es with substantially higher long-term mean PM 2.5 concentrations.Draft Do Not Quote or Cite March 20102-75Figure 2-2. Distribution ofstudy-specific area mean PM2.5concentrations.12 Concentration (μg/m 3 )(a) Representative Long-Term Exposure Studies(b) Representative Short-Term Exposure StudiesEPACMStudyAuthorEPAmaxEPACMStudyAuthorEPAmaxEPACMStudyAuthorEPAmaxEPACMStudyAuthorEPAmaxEPACMStudyAuthorEPAmaxEPACMStudyAuthorEPAmaxBell Dominici06ZanobettiEftim-ACS KrewskiMiller051015202530Left plots represent the study author results; middle plots represent EPA replication results using a community monitor, CM, (spatial average) approach; andright plots represent EPA replication results using a maximum value approach (max monitor mean for each year averaged over thestudy timeframe). Blackoutlined boxes denote inter-quartile range and medians, stars denote means with cyan rectangles spanning +/- one standard deviation from the mean, and dotsrepresent the minimum and maximum values.3Draft Do Not Quote or Cite March 2010 2-76 eastern, central, western) with long-term median PM 2.5 concentrations ranging from 10.7 to 14.0 1 μg/m 3 (Zeger et al., 2008). In evaluating the air qu ality data considered in this study, we believe 2 it is most appropriate to focus on the long-term median concentration across all cities which was 3 reported as 13.2 μg/m 3 (Zeger et al., 2008). A cystic fibros is cohort study of mortality reported a 4 positive but not statistically significant mortality association with an a ggregate long-term mean 5

PM 2.5 concentration of 13.7 μg/m 3 in a susceptible population (Goss et al., 2004) 6 In considering new evidence for cardiovascul ar effects associated with long-term PM 2.5 7 exposure (causal association), we note the WHI reported positive and stat istically significant 8 effects at a long-term average across cities of 13.5 μg/m 3 (Miller et al, 2007). As noted above in 9 section 2.2.1, this study consid ered the associations betw een long-term exposure to PM 2.5 and 10 cardiovascular-related mortality as well as cardi ovascular morbidity in post-menopausal women 11 with no previous history of cardiac disease. 12 Furthermore, with respect to respirator y effects associated with long-term PM 2.5 exposure 13 (likely causal association), the continued follow-up of the Sout hern California CHS's cohort 14 study provides stronger evidence of decreased lung function growth in ch ildren, a susceptible 15 population, that persisted into earl y adulthood at a long-term mean PM 2.5 concentration across 12 16 communities of 13.8 μg/m 3 . McConnell et al., (2003) also reported a positive and statistically 17 significant effect between long-term PM 2.5 concentrations and bronchitic symptoms as part of the 18
Southern California CHS. These results are s upported by a single-city cross-sectional study of 19 bronchitic symptoms in school-a ged children reported a positiv e and statistically significant 20 association with long-term PM 2.5 concentrations of 12 μg/m 3 (Kim et al., 2004). 21 In considering alternative le vels for an annual standard that would provide protection 22 with an adequate margin of safety, we believe it is also appropriate to take into account evidence 23 of effects for which the reporte d associations provide only sugge stive evidence of a causal 24 association, including, but not limited to, eviden ce of reproductive and developmental effects. 25 With respect to emerging evidence on low birth wei ght and infant mortality, especially related to 26 respiratory causes during the post-neonatal perio d, the ISA concludes that effects become “more 27 precise and consistently positive in locations with mean PM 2.5 concentrations of 15 μg/m 3 and 28 above” (US EPA, 2009a, p. 2-13; section 7.4). In particular, we note a recent study of 29 postneonatal infant mortality which observed a po sitive and statistically significant association 30 with an aggregate long-term mean PM 2.5 concentration of 14.8 μg/m 3 (Woodruff et al., 2008). 31 We recognize that these effects are serious in nature and that data are continuing to emerge 32 related to reproductive and developmental outcomes. At this time, however, the PM 2.5 33 concentrations reported in studies evaluating these effects report am bient levels that are equal to 34 or greater than ambient levels observed in st udies reporting mortality and cardiovascular and 35 respiratory effects. Therefore, in selecting alternative levels, we note that in providing protection 36Draft Do Not Quote or Cite March 2010 2-77 for mortality and cardiovascular and respiratory effects, it is reasonable to anticipate that 1 protection will also be provided for repr oductive and developmental effects. 2 With respect to characteriz ing the concentration-respons e relationship for mortality 3 associated with long-term PM 2.5 exposures, we first note, that in the last review, evidence was 4 available to support a linear rela tionship. Using data from the AC S cohort, Pope et al., (2002) 5 reported that the associations for all-cause, ca rdiovascular, and lung cancer mortality “were not 6 significantly different from linear .” In that study, the confidence intervals began to expand 7 significantly starting around 13 to 12 μg/m 3 , indicating greater uncertainty about the shape of the 8 reported concentration-response re lationship at and below this level (US EPA, 2004, Figure 8-7; 9 US EPA 2005, Figure3-4). In this review, a dditional evidence supports a linear concentration10 response relationship. Schwartz et al. (2008) used a variety of statistical methods and reported 11 “the concentration-response curve was linear, cl early continuing below the level of the current 12 U.S. air quality standard of 15 μg/m 3 ” (US EPA, 2009a, p. 7-92). No new evidence is available 13 in this review to inform our understanding of the confidence interval s around the estimated 14 concentration-response functions. 15 In considering what alternative levels woul d provide protection for effects observed in 16 such long-term PM 2.5 exposure studies, we first recognize that the ISA has concluded that no 17
discernable threshold for an eff ect associated with long-term PM 2.5 exposure can be identified 18 based on the currently available evidence (US EPA 2009a, section 2.4.3). We recognize that 19 health effects may occur over the full range of co ncentrations observed in the studies, however, 20
we believe it is reasonable to conclude the evidence of association is strongest down to 21 somewhat below the aggregated mean concentrat ion, such as down to one standard deviation 22 below the mean or to the lower end of the interq uartile range, which includes the range in which 23 the data in the study are most concentrated. This approach is consistent with considering the 24 serious nature of the observed effects, including, but not limited to, mortality and cardiovascular 25 effects for which there is strong ev idence of a causal asso ciation as well as respiratory effects, 26 for which there is strong evidence of a likely causa l relationship. It also in cludes consideration of 27 the range of long-term average co ncentrations across ci ties and the point where the data become 28 less robust, suggestive of a con centration below which the associ ation becomes appreciably more 29 uncertain. In evaluating the long-term exposure st udies, we recognize that the overall density of 30 air quality concentrations becomes noticeable sp arse below the range of air quality levels 31 represented by the lower interquartile range or on e standard deviation below the mean. In our 32 view, an annual standard set below this range would be highly precautiona ry, giving little weight 33 to the remaining uncertainties in the broader bod y of evidence, including the limited number of 34 cities included in the long-term epidemiologic studies that reported long-term below the lower 35 interquartile range. 36Draft Do Not Quote or Cite March 2010 2-78 As discussed in section 1.2.1, this approach is relevant to info rm judgments about 1 providing an adequate margin of safety to prev ent pollution levels that may pose an unacceptable 2 risk of harm, even if the risk is not precisely identified as to nature or degree. As presented in 3 Figure 2-1, the lower interquartil e range of long-term average concentrations or one standard 4 deviation below study mean air quality levels as reported in the long-term mortality studies for 5 the most recent years evaluated, report air qualit y concentrations in the range from about 10 to 6 11 μg/m 3 . With respect to consideri ng air quality levels reported in the extended follow-up to 7 the Southern California CHS, we recognize that using this appr oach, air quality levels one 8 standard deviation below the mean across communities is significantly lower, about 6 μg/m 3 , and 9 close to or below the LML reported in the majo rity of the long-term mortality studies. 10 In considering not only the level but also the form of the annual standard 39 , we 11 acknowledge that there may be differences between mean PM 2.5 concentrations averaged across 12 monitors within a city/county as is typically c onsidered in epidemiologic studies, compared to 13
the current form of the annual PM 2.5 standard which typically focuses on ambient measurements 14 from the highest reporting comm unity-oriented monitor. As suc h, we requested additional air 15 quality distribution data from authors of specifi c epidemiologic studies in order to effectively 16 place key epidemiologic studies in a policy-releva nt context (Hassett-Sipple and Stanek, 2009). 17
Data were received for some but not all studies for which in formation was requested. To 18 broaden this data base, OAQ PS conducted additional analyses for selected long-term PM 2.5 19 exposure studies to better understand air quality distributions averaged across monitors in 20 comparison to air quality levels focused on th e highest reporting monitors (Schmidt, 2010). 21 These analyses focused on selected long-term mo rtality studies and, as presented in Table 2-4 22 Figure 2-2a, reported composite monitor values close to the long-term mean concentrations 23 reported by the study authors. 40 As was expected, estimated air quality levels for the highest 24 reported monitors, within a range of 14.9 μg/m 3 (Eftim et al., 2008) to 16.8 μg/m 3 (Miller et al, 25 2007), were higher than for the composite m onitor values, within a range of 12.9 μg/m 3 (Miller 26 et al., 2007) to 14.0 μg/m 3 (Krewski et al., 2009),. The most notable difference was reported for 27 the WHI study which assessed only one year of air quality data (2000) for 36 study areas 28

39 As summarized in section 2.3.3, the level of the annual PM 2.5 standard is to be compared to measurements made at the community-oriented monitoring site recording the highest level, or if specific constraints are met, measurements from multiple community-oriented monitoring sites could be averaged (“spatial averaging”).
40 As noted by Schmidt (2010), differences between long-term mean concentrations reported by the study authors and the parallel values in the EPA analyses may be re lated to the EPA assessment only encompassing Federal Reference and Federal Equivalent Method air quality data while the study authors may have included additional (non-reference/equivalent) data. Also, there may be additional differences in the sets of monitoring sites utilized due to uncertainties associated with th e geographical area boundary definitions

.Draft Do Not Quote or Cite March 20102-79Table 2-4. Comparison of Air Quality Data for SelectedEpidemiological Studies – Long-term Mean Concentrations411Author Reported DataEPA Analysis (Schmidt 2010)Composite MonitorMaximum MonitorStudyCiteYearsMean(SD)Mean-1 SDRangeMean(SD)Mean -1SDLowerend ofIQRrange(25%)RangeMean(SD)Mean -1SDLowerend ofIQRrange(25%)RangeLong-term Exposure StudiesACS-extendedfollow-upKrewskiet al 20091999-200014.0(3.0)11.05.8 - 2214.0(3.5)10.510.96-2115.4(4.1)11.312.39-25Medicare-ACSEftim et al20082000-200213.6(2.8)10.8 6-25 13.3(3.1)10.2 10.8 7-20 14.9(3.6)11.3 12.0 9-24Women’sHealthInitiativeMiller etal 2007200013.5(3.3)10.2 3.4 – 28 12.9(3.0)9.9 10.8 5-18 16.8(4.3)12.5 14.2 5-28Short-term Exposure StudiesMCAPS-OriginalDominiciet al 20061999-200213.4(2.9)10.511.3-15.2(IQR)*13.3(2.9)10.411.25-2113.9(3.4)10.511.65-29-Extended Bell et al20081999-200512.9(2.7)10.2 4-20 12.9(2.7)10.2 11.0 4-19 13.4(3.1)10.3 11.4 5-26NationalMortalityStudyZanobetti&Schwartz,20091999-200513.2(2.9)10.3 7-25 13.7(3.0)10.7 11.6 6-26 14.1(3.2)10.9 12.07-26.241All concentrations reported as μg/m3. * IQR = interquartile rangeDraft Do Not Quote or Cite March 2010 2-80 (average across monitors and across cities (composite monitor) of 12.9 μg/m 3 , compared to an 1 average of the highest reporting m onitors across cities of 16.8 μg/m 3 ). When more study areas 2 were considered and/or more y ears of air quality data were ev aluated, the difference between the 3 long-term mean for the composite monitor across cities compared to the long-term mean for the 4 highest reporting monitor acr oss cities was decreased. 5 In considering the currently available eviden ce, we reach the preliminary conclusion that 6 the long-term PM 2.5 exposure studies provide a basis for co nsidering alternative levels for the 7
annual PM 2.5 standard within a range of about 13 μg/m 3 down to about 10 μg/m 3 . A standard in 8 the range of 13 to12 μg/m 3 would reflect placing weight on setting a level somewhat below the 9 long-term mean PM 2.5 concentrations evalua ted in long-term PM 2.5 exposure studies that show 10 associations with mortality and cardiovascular and respiratory morbidity over a lower range of 11 air quality levels than ha d been observed in the studi es available in the last review. A standard in 12 the range of 11 to 10 μg/m 3 would be consistent with a judg ment that, recognizing the serious 13
nature of the effects and that no discernable threshold for these effe cts can be identified, 14 appreciable weight should be accorded to consid ering the lower interquartile range of long-term 15 average concentrations within a study, or a range within one sta ndard deviation around the study 16 mean of either the composite monitor or the highest reporting monitor. 17 Furthermore, recognizing that there is a link between the form and the level of a standard 18 that determines the degree of public health prot ection the standard affords, and in light of 19 stronger evidence available in th is review identifying persons with lower SES levels as a 20 susceptible population as discusse d in section 2.2.1, we recognize that the existing constraints on 21 spatial averaging, as modified in 2006, may not be adequate to avoid substantially greater 22 exposures in some areas, potentially resulting in disproportionate impacts on persons with lower 23 SES levels. Therefore, we reach the preliminary conclusion that it is appropriate to consider a 24
form of the annual PM 2.5 standards that does not allow for the use of spatial averaging across 25
monitors such that the annual PM 2.5 standard would be compared to measurements made at 26 monitoring sites that represent “community-wide air quality” reco rding the highest levels only. 27 We plan to conduct additional air quality analyses to explore this issue to inform the second draft 28
PA. 29

2.3.4.2 Risk-based Considerations 30

Beyond looking directly at the relevant ep idemiologic evidence, staff have also 31
considered the extent to which specific levels of alternative PM 2.5 standards are likely to reduce 32 the estimated mortality risks attri buted to long-term exposure to PM 2.5 and the uncertainties in 33
the estimated risk reductions. We have based this evaluation on the results of the quantitative risk 34 assessment presented in the second draft RA (US EPA, 2010a) and posed a series of questions to 35Draft Do Not Quote or Cite March 2010 2-81 aid in considering how the current suite of PM 2.5 standards might be revise d to provide requisite 1 public health protection. 2

 To what extent do alternative standards re duce estimated risks associated with long3 term PM 2.5 exposure compared to risks associated with simulating air quality to just 4 meet the current standards? What roles do the current 24-hour and annual standards 5 have in simulating the risks remaining upo n just meeting the alternative suites of 6 standards considered in the quantitative risk assessment? What level of confidence is 7 associated with these risk estimates? 8 As noted in section 2.1.1, in summarizing ri sk estimates associat ed with long-term 9 exposure-related mortality, we focus on IHD-relate d mortality due to greater overall support for 10 a causal association with this endpoint. Howe ver, we note that risk estimates were also 11 generated for all-cause, cardiopulmonary and lung cancer-related mortality. In presenting these 12 results, we focus first on the degree of risk reduction (and estimates of risk remaining) upon 13
simulation of the alternative annual standard levels considered in the risk assessment. We then 14 discuss the nature and magnitude of risk reductions associated w ith alternative 24 -hour standard 15 levels. Contrasting the degree of risk reduction provided by the suites of alternative annual and 16
24-hour standards is covered in the overall summa ry discussion presented at the end of this 17
section. 18

Risk reduction associated with alternat ive annual standards (14/35, 13/35, and 12/35) 19
In evaluating alternative standards, we first focused on consideration of different levels 20
for the annual PM 2.5 standard (e.g., 14 μg/m 3 , 13 μg/m 3 , 12 μg/m 3 ) in conjunction with retaining 21 the current level of the 24-hour standard (35 μg/m 3 ). We observed a consistent pattern of 22 increasing risk reduction with d ecreasing alternative a nnual standard levels, both in terms of the 23 number of urban study areas experiencing risk re ductions and the magnitude of those reductions 24 (US EPA, 2010a, section 6.2.2). Specifically, 5 of the 15 urban study areas experienced risk 25
reductions under the alternative a nnual standard level of 14 μg/m 3 , with percent reductions in 26

PM 2.5 -attributable long-term exposure-related mortality (relative to risk unde r the current suite of 27 standards) ranging from 9% (Baltimore) to 12 % (Houston and Birmingham) (Figure 2-3 and US 28 EPA, 2010a, Appendix E, Table E-27). Fo r an annual standard level of 12 μg/m 3 , 12 of the 15 29 urban study areas experience risk reductions, with percent reducti ons (relative to risk under the 30 current suite of standards) ranging from 11% (Phoenix) to 35% (Houston and Birmingham) 31 (Figure 2-3 and US EPA, 2010a, Appendix E, Table E-27). Note, that even in the 12/35 case, 32 three of the urban study areas (Tacoma, Fresno and Salt Lake City) did not experience any 33 decreases in risk, although risk reductions were seen for these three study areas when alternative 34
24-hour standards were consid ered, as discussed below. 35Draft Do Not Quote or Cite March 20102-82Figure 2-3. Percent reduction in long-term exposure-related mortality risk1(alternative standards relative to the current standards) (Note: inset shows PM2.5related incidence and percent of total incidence for IHD mortality under the2current suite of standards)34Atlanta, GABaltimore, MDBirmingham, ALDallas, TXDetroit, MIFresno, CAHouston, TXLos Angeles, CANew York, NYPhiladelphia, PAPhoenix, AZPittsburgh, PASalt Lake City, UTSt. Louis, MOTacoma, WA0%20%40%60%15/35** 14/35 13/35 12/35 13/30 12/25Current and Alternative Standards

Long-Term Exposure-Related Risk: Percent Reduction from Current StandardAtlanta, GA 277 (227 - 324); 16.7% (13.7% - 19.5%)Baltimore, MD 374 (307 - 440); 14.7% (12.1% - 17.3%)Birmingham, AL 165 (135 - 194); 13.8% (11.3% - 16.2%)Dallas, TX 247 (202 - 291); 11.4% (9.3% - 13.4%)Detroit, MI 478 (390 - 563); 11.5% (9.4% - 13.5%)Fresno, CA 98 (80 - 116); 8.5% (7% - 10.1%)Houston, TX 434 (355 - 511); 13.6% (11.1% - 16%)Los Angeles, CA 1094 (890 - 1296); 7.7% (6.3% - 9.1%)New York, NY 2222 (1814 - 2620); 11.8% (9.6% - 13.9%)Philadelphia, PA 330 (270 - 389); 13.2% (10.8% - 15.6%)Phoenix, AZ 402 (327 - 476); 8.5% (6.9% - 10.1%)Pittsburgh, PA 324 (264 - 382); 11.8% (9.6% - 13.9%)Salt Lake City, UT 19 (16 - 23); 3.7% (3% - 4.4%)St. Louis, MO 563 (461 - 662); 14.2% (11.6% - 16.7%)Tacoma, WA 49 (40 - 58); 4.7% (3.8% - 5.6%)567*Based on Krewski et al. (2009), exposure period from 1999 – 2000. The legend contains, for each urban area, the incidence estimate (and 95% CI) and the8estimate of percent of total incidence (and 95% CI) under the current standards.9**The current standards consist of an annual standard of 15 μg/m3and a daily standard of 35 μg/m3. Combinations of an annual standard (n) and a daily standard10(m) are denoted n/m in this figure.11***The percent reductions for Salt Lake City and Tacoma at the 12/25 standard are 100% and 93%, respectively.12Draft Do Not Quote or Cite March 2010 2-83 While there is a consistent pattern of risk reduction across the alternative annual 1
standards with lower standard levels resul ting in more urban st udy areas experiencing 2 increasingly larger risk reductions, there is cons iderable variability in the magnitude of these 3 reductions across urban study areas for a given alternativ e annual standard le vel (e.g., as noted 4 above, for the alternative annual standard level of 12 μg/m 3 , risk reduction ranged from 11% for 5 Phoenix to 35% for Houston). The variability in risk estimates refl ects differing degrees of 6 reduction in annual average PM 2.5 concentrations across the st udy areas. The differences in 7 annual average concentrations result, in part, b ecause the study areas be gin with varying annual8 average PM 2.5 concentrations after simulating just m eeting the current suite of standards. 9 Therefore, even if study areas have similar “ending” annual average PM 2.5 , because the starting 10 point in the calculation (i .e., the annual-average PM 2.5 concentrations upon just meeting the 11 current suite of standards) is often variab le, the overall reducti on in annual-average PM 2.5 12
concentrations across the standards is also variable. 42 13 The sensitivity analysis invol ving application of peak shav ing rollback rev eals that the 14 pattern of reductions in ambient PM 2.5 concentrations upon just meeting the current suite of 15 standards can impact the magnit ude of additional risk reductions estimated for just meeting 16 alternative (lower) annual standard levels. Specifically, for th ose study areas with more peaky 17

PM 2.5 distributions 43 , application of peak shaving rollback will result in higher annual-average 18

PM 2.5 levels remaining upon just meeting the current suite of standards. If proportional rollback 19 is then used to simulate just meeting alternat ive annual standard levels, a greater degree of 20 reduction in annual-average PM 2.5 concentrations will result, si nce the “starting point” for the 21 calculation (annual-average PM 2.5 levels upon just meeting the curr ent suite of standards) will be 22 higher. This translates into larger reductions in risk simulated for alternative annual standards 23 when more localized patterns of PM 2.5 reduction are involved with simulating just meeting the 24
current suite of standards. In instances wh ere an urban study area has relatively peaky PM 2.5 25 concentrations, the difference in projected risk reduction for an alternative annual standard can 26 be substantial. For example, with Los Angeles which has fairly peaky PM 2.5 levels, we predict a 27 13% reduction in long-term exposure -related mortality with the 12 μg/m 3 alternative annual 28 standard (relative to risk under th e current suite of sta ndards) if we assume a regional pattern of 29

PM 2.5 reductions for simulating just meeting the curre nt standard as reflected in the application 30

42 We note that additional variation in the risk estimates, in terms of both risk reduction across standard levels and residual risk for each of the alterna tive annual standard levels, results from differences across study areas in the relationship between the maximum monitor annua l-averages values used in estimating percent reductions under an alternative standard and the composite monitor annual-average values used in estimating long-term exposure-related risk.
43 The term “peaky” as used here, refers to urban study areas with relatively high 24-hour design values and lower annual average design values.Draft Do Not Quote or Cite March 2010 2-84 of proportional rollback. By contrast, we predict a 48% reduction in long- term exposure-related 1 mortality risk if we assume a more lo calized pattern of reduction in ambient PM 2.5 levels, as 2 reflected in the application of peak-sha ving rollback (US EPA 2010a, section 6.2.2). 3 Regarding the magnitude of risk estimated to remain after simulation of alternative 4 annual standards, the four study areas displaying the greatest degree of risk reduction across the 5 range of alternative annual standard levels considered (Atlanta, Baltimore, Birmingham and 6 Houston) have PM 2.5 -related IHD mortality estimates ( under the lowest alternative annual 7 standard of 12/35) ranging from 85-110 (Bir mingham) to 220-280 (Houston) (US EPA, 2010a, 8 Appendix E, Table E-21 and E-30). The two urba n study areas with the greatest degree of PM 2.5 - 9 related risk in absolute terms (Los Angeles a nd New York) do not exhib it significant reductions 10
in risk until the lowest annual standard level of 12/ 35 is considered, with PM 2.5 -related IHD 11 mortality estimated at 750-950 and 1,420-1,800, respect ively under that altern ative standard (US 12 EPA, 2010a, Appendix E, Table E-21 and E-30). In terms of the percentage of long-term 13 mortality attributable to PM 2.5 , we see the following levels for the alternative annual standard 14 levels. For an annual standard level of 14 μg/m 3 , the percent of total incidence of IHD mortality 15
attributable to PM 2.5 in the 5 urban study areas experiencing risk reduc tions ranges from 9-11.3% 16 (Detroit) to 11.8-14.9% (Atlanta) (US EPA 2010a, Appendix E, Tables E-24 and E-33). For an 17 annual standard of 12 μg/m 3 , estimated risk remaining in th e 12 urban study areas experiencing 18 risk reductions ranges from 6-7.6% (Phoeni x) to 9-11.4% (Atlanta), again for PM 2.5 -attributable 19 long-term exposure-related mortality (US EP A 2010a, Appendix E, Tables E-24 and E-33). 20 We note that there is considerably less variab ility in the estimates of risk remaining after 21
simulation of the alternative annual standards le vels, compared with the magnitude of risk 22 reductions across the study areas. This reflects the fact that study ar eas experiencing risk 23
reductions under the alternative annual st andards will have similar annual-average PM 2.5 levels 24 given that this simulation involve s annual standard leve ls that are controlling (i.e., these study 25 areas have their annual-average PM 2.5 levels lowered to meet the sa me annual standard level). 26
Observations made earlier in section 2.1.1 in th e context of the curren t suite of standards 27 regarding uncertainty and its impact on risk estimates apply in this context as well. Specifically, 28 given the results of the sensitivity analysis ex amining the form of the C-R functions for long29 term exposure-related mortality, combined with only modeling risk down to the LML, we have 30
increased confidence that we have not overstated either the magnitude of risk reductions across 31 alternative standard levels, or th e magnitude of risk remaining for a given standard level. 32

Risk reduction associated with altern ative 24-hour standards (13/30 and 12/25) 33
We then focused on evaluating risk s associated with long-term PM 2.5 exposures when 34 varying the level of the 24-hour standard while hold ing the level of the annual standard constant. 35Draft Do Not Quote or Cite March 2010 2-85 Comparing risks associated with just meeting th e 13/35 and 13/30 suites of alternative standards 1 (which reflect a 5 μg/m 3 reduction in the 24-hour standard, while holding the annual fixed at 2 13μg/m 3 ), we see considerable variation in the magnitude of risk reduction across urban study 3 areas. For example, St Louis, under the 13/35 su ite of alternative sta ndards has IHD mortality 4
risk attributable to PM 2.5 reduced by 22% relative to risk under the current suite of standards. 5 Very little additional risk reduction (increasi ng from 22% to 24%) is estimated under the 13/30 6 alternative suite of standards. In contrast, with Salt Lake City, we estimate that the 13/35 suite of 7 alternative standards will produce no risk reducti on relative to the curren t suite of standards, 8 while the 13/30 suite would produ ce a 55% reduction in IHD mortal ity risk relative to risk under 9 the current standard level (see Figure 2-3 and US EPA 2010a, Table E-27 in Appendix E). 10 The additional risk reduction provided by an alternative 24-hour standard is more 11 substantial in comparing the 12/25 and 12/35 altern ative suites of standa rds, although there is 12 also greater variability in th e magnitude of risk reductions across study areas. For example, 13 Atlanta, which had a 32% reducti on in risk under the 12/35 suite of standards (relative to the 14 current standard level) only sees an marginal increase to 34% under the 13/ 25 suite of standards. 15 By contrast, Salt Lake City, which has no reducti on in risk under the 12 /35 suite of standards 16 (relative to the current suite of standards), sees a ~100% reduction in ri sk under the alternative 17 suite of 12/25 (see Figure 2-3 and US EPA, 201 0a, Appendix E, Table E-27). The reduction for 18 Salt Lake City reflects a very high 24-hour desi gn value which, when reduced to meet the 24- 19 hour standard of 25 μg/m3 produced a substantial reduction in the annual design value (given 20 application of the proportional adjustment to simu late rollback), such that the value was very 21 close to 5.8 μg/m3 (the LML below which l ong-term exposure-related mortality is not 22 estimated). The specific pattern of risk reduction reflects whether the 24-hour or annual standard 23 was controlling (see discussion below regarding patte rns of risk reduction). We also note, that 24 under the 12/25 alternative suite of standards, we see that nine of th e study areas (Detroit, 25 Fresno, Los Angeles, New York, Philadelphia, P hoenix, Pittsburgh, Salt Lake City and Tacoma) 26
have reductions in risk that ar e at least twice as large as fo r the 12/35 suite of alternative 27 standards, with some substantially larger (see Figure 2-3 and US EPA, 2010a, Table E-27 in 28 Appendix E). 29 Regarding risk remaining after simulation of the suite of alternative 24-hour standards, 30 the four study areas displaying the greatest degree of reduction across these two alternative suites 31 of standards (Tacoma, St. Louis, Los Angeles and Fresno), have PM 2.5 -related IHD mortality 32 estimates (under the 12/25 case) ranging from 3-4 (Tacoma) to 290-360 (Los Angeles) (US EPA, 33 2010a, Appendix E, Table E-21 and E-30). The other urban study area with the greatest degree 34
of PM 2.5 -related risk in absolute terms besides New York (New York) has PM 2.5 -related all-cause 35 mortality estimated at 820-1,040 under the 12/25 case. In terms of the percentage of long-term 36Draft Do Not Quote or Cite March 2010 2-86 mortality attributable to PM 2.5 , we see that under the 13/30 suite of standards, the percent of total 1 incidence of IHD mortality attributable to PM 2.5 ranges from 1.3 to 1.7% (Salt Lake City ) to 2 10.4 to 3.2% (Atlanta) (US EPA, 2010a, Appendix E, Tables E-24 and E-33). Under the 12/25 3 alternative suite, risks for this metric range from ~0 to 0.3% (Salt Lake City) to 8.8 to 11.1% 4 (Atlanta). 5 The observations presented above highlight va riability both in the magnitude of risk 6 reduction as well as in the risk remaining upon simulation of just meeting alternative 24-hour 7
standards. This reflects the f act that, as noted earlier, altern ative 24-hour standards can produce 8 different degrees of reduction in the annual-average PM 2.5 concentrations, depending on the 9 relationship between 24-hour and an nual design values at a particul ar location. It is these annual10 average PM 2.5 levels that drive changes in long-term exposure-related mortality. Those study 11 areas with relatively peaky PM 2.5 levels, such as Salt Lake City, can see a substantial reduction in 12 annual-average PM 2.5 levels under simulation of alternative 24-hour standards. By contrast, study 13 areas with less peaky PM 2.5 levels, such as St. Louis, see su bstantially smalle r reductions in 14 annual-average PM 2.5 levels under the suite of alternative 24-hour sta ndards and consequently 15 lower degrees of risk reduction. 16 In addition, as noted earlier, in those in stances where alternat ive 24-hour standards 17 produce larger reducti on in annual-average PM 2.5 levels (and consequently greater reductions in 18 risk), often these reductions invol ve relatively low annual-average PM 2.5 levels. In some cases, 19 such as with Salt Lake City, these annual-average PM 2.5 levels can approach the LML, which 20
reduces our overall confidence in estimates of long-term exposure-related mortality for these 21
locations. 22 Observations made earlier regarding the imp act of variability in simulating changes in 23

PM 2.5 distributions using different rollback approaches, and its impact on the degree of risk 24 reduction, also hold for these simulations of altern ative 24-hour standards. Specifically, in those 25
instances where PM 2.5 distributions are more peaky, appl ication of peak shaving rollback 26 (reflecting more localized patterns of ambient PM 2.5 reduction) would result in smaller 27 reductions in annual-average PM 2.5 concentrations and conseque ntly, smaller reductions in 28 estimates of long-term exposure-related mortality. For example, with Salt Lake City, which has a 29 peaky PM 2.5 distribution, under the 12/25 suite of sta ndards application of proportional rollback 30 results in an annual average PM 2.5 concentration of 5.7 μg/m 3

, while application of peak shaving 31 results in an estimate of 8.9 μg/m 3 (as noted earlier, differences in annual-average PM 2.5 levels 32 translate into differences in risk). In contra st, simulation of the 12/25 suite of standards for 33 Baltimore, which has a less peaky PM 2.5 distribution, results in an annual average PM 2.5 34 concentration of 10.7 μg/m 3 for proportional rollback compared to 10.8 μg/m 3 with peak 35Draft Do Not Quote or Cite March 2010 2-87 shaving, implying that there would be little diffe rence in risk (see US EPA, 2010a, Table F-49 in 1 Appendix F). 2 Observations made earlier regarding overall confidence in the estimates of long-term 3 exposure-related mortality also hold for these es timates (i.e., the sensi tivity analysis results 4
combined with the fact that we modeled risk down to LML result in our concluding that it is 5 unlikely we have overstated either the degree of risk reduction or the degree of residual risk). 6
Summary 7

The results discussed above show that simulating just meeti ng alternative annual 8 standard levels in the range of 14 to 12 μg/m 3 can produce substantial re ductions in long-term 9 exposure-related mortality risk (with the magnit ude of risk reduction in creasing as lower annual 10 standards in this range are considered). Furthe rmore, the results suggest that alternative 24-hour 11 standard levels in the range of 30 to 25 μg/m 3 can produce substantial re ductions in estimated 12 risk, beyond that produced by simulations of just meeting lower annual standard level down to 13 12 μg/m 3 (combined with a 24-hour standard of 35 μg/m 3 ). This results from the simulation of 14 the alternative 24-hour standard levels produc ing substantially lower annual-average PM 2.5 15 concentrations, which drive reduc tions in both long-term and shor t-term exposure-related risk. 16 However, the results also show that there can be considerable variability across study areas in the 17 degree to which alternative 24-hour standard levels produce reductions in annual average PM 2.5 18 concentrations and, consequently, reductions in risk. This vari ability depends on the peakiness 19
of the PM 2.5 distribution in an area and on the pattern of reductions in ambient PM 2.5 levels 20 associated with just meeting the current and alte rnative suites of standa rds. Conversely, the 21 analysis also suggests that mo re consistent annual-average PM 2.5 concentrations, and thus more 22
consistent reductions in estimated risk and more uniform levels of public health protection 23 would likely result from simulati ng just meeting alternative annua l standards at levels below 12 24 μg/m 3 (i.e., below the lowest annual standard level considered in this assessment). 25 Furthermore, because the alternative 24-hour standard levels assessed resulted in lower 26 simulated annual-average PM 2.5 levels (often approaching the LML used in modeling risk for 27 long-term exposure-related mortality), we also conclude that there is greater uncertainty 28
associated with risk estimates derived for the alternative 24-hour standa rds, relative to risks 29
estimated for the alternative annual standards. 30

2.3.5 Alternative Levels to Address Heal th Effects Related to Short-term PM 2.5 Exposures 31 In considering alternative PM 2.5 standards that would provide protection against health 32 effects related to short-term exposures, staff has taken into account both ev idence-based and risk33 based considerations. First, as discussed in section 2.1.3, it is our view that the evidence from 34 studies of short-term exposure to PM 2.5 can help inform consideration of the protection afforded 35Draft Do Not Quote or Cite March 2010 2-88 by both a 24-hour and an annual standard (secti on 2.3.5.1). Secondly, we have considered the 1 results of the quantitative risk assessment presented in the se cond draft RA (US EPA, 2010a) to 2
assess the extent to whic h alternative annual and/or 24-hour st andards can be e xpected to reduce 3
the estimated risks attributable to short-term exposure to PM 2.5 (section 2.3.5.2). With respect to 4 considering the protection afforded by the suite of PM 2.5 standards, our preliminary integrated 5 conclusions presented in section 2.3.6 are based in part on the prel iminary staff conclusions from 6 this section and in part on preliminary staff c onclusions from section 2.3.4 in which we discuss 7
alternative standards to address heal th effects related to long-term PM 2.5 exposures. 8

2.3.5.1 Evidence-based Considerations 9

In taking into account evidence-based consid erations for informing our understanding of 10
alternative levels to address h ealth effects related to short-te rm fine particle exposures, we 11 initially focused on short-term multi-city PM 2.5 exposure studies. We observe that multi-city 12
studies assessed PM 2.5 -associated health effects among larger study populations, providing 13 enhanced power to detect PM 2.5 -associated health effects. In addition, short-term multi-city 14

PM 2.5 exposure studies generally pr ovide spatial coverage for different regions across the 15 country, reflecting differences in PM 2.5 sources, composition, and potenti ally other factors which 16 might impact PM 2.5 -related risk. We have also evalua ted short-term single-city PM 2.5 exposure 17 studies that provide additional in sights on associated health eff ects occurring at or below the 18

PM 2.5 concentrations reported in the short-term multi-city PM 2.5 exposure studies, specifically in 19 areas that may have unusually high peak-to-mean ratios of PM 2.5 concentrations, possibly 20 associated with strong local or s easonal sources of fine particles. 21 In considering a range of health outcomes, we place the greatest weight on associations 22 that have been judged in the ISA to be causal or likely causal, while being mindful of evidence 23 that informs our understanding of im pacts on susceptible populations. 44 We have considered a 24 number of factors including: (1) the extent to which these studies report statistically significant 25 and relatively precise relative risk estimates; (2) the extent to which the reported associations are 26 robust to co-pollutant confounding; and (3) the extent to which the studies used relatively 27 reliable air quality data. In pa rticular, we focused on those speci fic studies conducted in the U.S. 28 and Canada, briefly summarized in section 2.2.1 and pr esented in more detail in chapter 6 of the 29 ISA, that provide evidence of associations in areas that would likely have met the current 24- 30

44 In contrast to causal inferences fo r effects associated with long-term PM 2.5 exposures, the ISA has not identified any health outcomes as having evidence suggestive of a causal association with short-term PM 2.5 exposures. Thus, the discussion of evidence-based considerations in this section focuses on those effects for which the ISA has determined there is a causal or likely causal association with short-term PM 2.5 exposures only.Draft Do Not Quote or Cite March 2010 2-89 hour PM 2.5 standards during the time of the study. 45 We believe that th is body of evidence can 1 serve as a basis for considering alternative 24- hour and annual PM 2.5 standards that would 2 provide appropriate protection for health effects associated with short-term PM 2.5 exposures. 3 Collectively, we have considered the evidence to address the following question: 4

 To what extent does the currently availabl e evidence provide support for revising the 5 current suite of standards to provide prot ection from short-term fine particle 6 exposures? 7 In considering what alternative levels woul d provide protection for effects associated 8
with short-term PM 2.5 exposure, we first recognize that the ISA has concluded that no discernable 9 threshold, or lowest-observed-eff ect levels, can be identified based upon the currently available 10 evidence (US EPA, 2009a. section 2.4.3). Bein g mindful of the challenges posed by issues 11 relating to threshold and background concentrat ions, we have considered two alternative 12 approaches for using the evidence from short-term exposures studies to inform preliminary staff 13 conclusions regarding alternative st andard levels. First, in consid ering an approach in which the 14 24-hour standard to set to be the primary mean s for providing protection for health effects 15 associated with short-term exposures to PM 2.5 , we considered evidence from short-term exposure 16 epidemiological studies as a ba sis for an alternative 24-hour PM 2.5 standard. Specifically, we 17 focused on the upper end of the distributions of 24-hour PM 2.5 concentrations, particularly in 18 terms of the highest 98 th percentile values for a location, refl ecting the form of the current 24- 19
hour standard. 20 Alternatively, we have also considered an a pproach in which the annual standard is set to 21 be the primary means for providing protection for e ffects associate with both long and short-term 22

PM 2.5 exposures. This approach rec ognizes that, as noted in previous reviews, much of the risk 23 related to daily exposures, when aggregated on an annual basis, results from the large number of 24 days during which the 24-hour aver age concentrations are in the lo w- to mid-range of the entire 25 distribution. Thus, to reduce the aggregate short- term exposure-related risk, it is necessary to 26
shift the bulk of the distribution to lower concentrations, not just to limit the concentrations on 27 days when the PM 2.5 concentrations are relatively hi gh (US EPA, 2005, p. 4-67, Figure 4-10; 28 Abt, 1996, section 7.1, p.79, Exhibit 7.6). This appr oach reflects consideration for allowing the 29
annual standard to serve in most areas as the target fo r control programs designed to be effective 30 in lowering the broad distribution of PM 2.5 concentrations, thus pr otecting not only against 31 effects associated with long-term exposures but also effects associated with short-term 32

45 As noted in section 2.3.4.1 above, we requested additio nal air quality distribution data from authors of specificepidemiological studies. To inform alternative standard levels to provide protection for effects associated with shortterm PM 2.5 exposures, we were particularly interested in 98 th percentile and long-term mean PM 2.5 concentrations considered in short-term exposure studies. In focusing on the current forms of the 24-h our and annual standards, we were also interested in information re lated to the highest reporting monitors.Draft Do Not Quote or Cite March 2010 2-90 exposures. This judgment reflects the recognition that changes in PM 2.5 air quality designed to 1 meet an annual standard would likely result not only in changes in lower annual average 2 concentration but also in fewer and lower peak 24-hour concentrations . In exploring this 3 alternative approach, we considered the eviden ce from the currently available short-term 4 exposure studies, specifically the long-term mean PM 2.5 concentrations from these studies as a 5 basis to inform preliminary conclusions for alternative levels for an annual PM 2.5 standard. 6 Furthermore, we recognize that if the primary purpose of the annual standard was to provide 7 protection for effects associated with both long- and short-term exposures, the purpose of the 24- 8 hour standard would than shift. In that case, the primary purpose of the 24-hour standard would 9 be to serve to provide supplemental protection to provide additional protection beyond the 10 protection afforded by the annual standard in ar eas with unusually high peak-to-mean ratios of 11

PM 2.5 concentrations, possibly associated w ith strong local or seasonal sources. 12 In first considering the approach of using th e 24-hour standard as the primary means for 13 providing protection for health effects associated with short-term exposures to PM 2.5 , we look to 14
the 98 th percentile air quality valu es for specific short-term e xposure studies to inform our 15 consideration of alternative standard levels (see Figure 2-4). With respect to mortality evidence 16 (causal association) from multi-ci ty short-term exposure studies, we note that, as discussed in 17 section 2.2.1, Zanobetti and Schwar tz (2009) and Burnett et al. (2004) reported a 24-hour 98 th 18 percentile PM 2.5 concentration averaged across a ll cities and all years of 34.3 μg/m 3 and 38.0 19 μg/m 3 , respectively. As presented in the ISA, despite large differences in air quality 20 concentrations, Zanobetti and Schw artz (2009) reported “all-cause mortality risk estimates that 21 were fairly uniform across the climatic re gions, except for the ‘Mediterranean’ region” 46 (US 22 EPA, 2009a, p. 6-178, Figure 6-24). 23 With regard to the evidence from studies assessing short-term exposure to PM 2.5 - 24 associated with cardiovascular (causal associa tion) and respiratory (lik ely causal association) 25 morbidity effects, recent multi-city analysis of MCAPS data by Dominici et al. (2006a) and Bell 26 et al. (2008) reported an overall 24-hour average 98 th percentile PM 2.5 concentration across all 27 cities and all years of 34.8 μg/m 3 and 34.2 μg/m 3 , respectively. As noted in section 2.2.1, an 28 unpublished sub-analysis of Domini ci et al (2006a) restricted to days with 24-hour average 29
concentrations at or belo w the level of the current 24-hour standard (35 μg/m 3 ) indicated that, in 30 spite of a reduced statistical power from a sma ller number of study days, statistically significant 31
associations were still obse rved between short-term PM 2.5 exposure and hospital admissions for 32 cardiovascular and respiratory diseases (Dominici, 2006b). 33

46 The Mediterranean region included cities in OR, CA, and WA.Study Outcome Mean a 98th a Effect Estimate (95% CI) Asthma HA 6.1 Chimonas & Gessner (2007, 093261 ) LRI HA 6.1 Lisabeth et al. (2008, 155939 ) Ischemic Stroke/TIA HA 7.0 e 23.6 f Slaughter et al. (2005, 073854 ) Asthma Exacerbation 7.3 e Rabinovitch et al. (2006, 088031 ) Asthma Medication Use 7.4 17.2 f Chen et al. (2004, 087262 ) COPD HA 7.7 Chen et al. (2005, 087942 ) Respiratory HA 7.7 Fung et al. (2006, 089789 ) Respiratory HA 7.7 Villeneuve et al. (2003, 055051 ) Nonaccidental Mortality 7.9 CVD ED Visits 8.5 27.3 f Stieb et al. (2000, 011675 ) Respiratory ED Visits 8.5 27.3 f Hemhrgc Stroke HA 8.5 24.0 f Ischemic Stroke HA 8.5 24.0 f Villeneuve et al. (2006, 090191 )

TIA HA 8.5 24.0 f Lin et al. (2005, 087828 ) RTI HA 9.6 Respiratory Symptoms (any) 9.8 c 25.8 f Mar et al. (2004, 057309 ) Respiratory Symptoms (any) 9.8 c 25.8 f Rich et al. (2005, 079620 ) Ventricular Arrhythmia 9.8 e Dockery et al. (2005, 078995 ) Ventricular Arrhythmia 10.3 e Rabinovitch et al. (2004, 096753 ) Asthma Exacerbation 10.6 d 29.3 f Pope et al. (2006, 091246 ) IHD HA 10.7 c CVD HA 10.8 29.6 f Slaughter et al. (2005, 073854 ) Respiratory ED Visits 10.8 29.6 f Pope et al. (2008, 191969 ) CHF HA 10.8 44.5 d MI HA 11.1 e Zanobetti and Schwartz (2006, 090195 ) Pneumonia HA 11.1 e Peters et al. (2001, 016546 ) MI 12.1 28.2 f Delfino et al. (1997, 082687 ) Respiratory HA (summer) 12.1 31.2 f Sullivan et al. (2005, 050854 ) MI 12.8 Burnett et al. (2004, 086247 ) Nonaccidental Mortality 12.8 38.0 f Respir HA 12.9 d 34.2 f Bell et al. (2008, 156266 ) CVD HA 12.9 d 34.2 f Wilson et al. (2007, 157149 ) CVD Mortality 13.0 31.6 f Zanobetti & Schwartz (2009, 188462 ) Nonaccidental Mortality 13.2 d 34.3 f Burnett and Goldberg (2003, 042798 ) Nonaccidental Mortality 13.3 38.9 f CBVD HA 13.3 34.8 f PVD HA 13.3 34.8 f IHD HA 13.3 34.8 f Dysrhythmia HA 13.3 34.8 f CHF HA 13.3 34.8 f COPD HA 13.3 34.8 f Dominici et al. (2006, 088398 )

RTI HA 13.3 34.8 f Fairley (2003, 042850 ) Nonaccidental Mortality 13.6 59.0 f Zhang et al. (2009, 191970 ) ST Segment Depression 13.9 j 37.6 f O’Connor et al. (2008, 156818 ) Wheeze/Cough 14.0 c 39.0 g Klemm and Mason (2003, 042801 ) Nonaccidental Mortality 14.7 e,i Franklin et al. (2008, 097426 ) Nonaccidental mortality 14.8 43.0 f NYDOH (2006, 090132 ) Asthma ED Visits 15.0 k Ito et al. (2007, 156594 ) Asthma HA 15.1 39.0 f Franklin et al. (2007, 091257 ) Non-accidental Mortality 15.6 45.8 f Rich et al. (2006, 089814 ) Ventricular Arrhythmia 16.2 e Symons et al. (2006, 091258 ) CHF HA 16.5 d 50.1 f Sheppard (2003, 042826 ) Asthma HA 16.7 46.6 f NYDOH (2006, 090132 ) Asthma ED Visits 16.7 l Respiratory HA (summer) 16.8 47.4 f Burnett et al. (1997, 084194 ) CVD HA (summer) 16.8 47.4 f a μg/m 3 b Study did not present mean; median presented. c Mean estimated from data in study. d Mean value slightly different from those reported in the published study or not reported in the published study; mean was either provided by study authors or calculated from data provided by study authors. e Mean value not reported in study; median presented. f 98th percentile of PM 2.5 distribution was either provided by study authors or calculated from data provided by study authors. g 98th estimated from data in study. h Averaged annual values for years in study from data provided by study author. i Air quality data obtained from original study: Schwartz et al. (1996, 077325). j Mean PM 2.5 concentration reported is for lag 0-2. k Bronx; TEOM data. l Manhattan; TEOM data. m Study does not present an overall effect estimate; the vertical lines represent the effect estimate for each of the areas of Phoenix examined. Relative Risk / Odds Ratio

Figure 2-4. Summary of Effect Estimates (per 10 μg/m 3 ) and Air Quality Distri butions for Short-term Exposure Studies Source: US EPA, 2009a, Figure 2-1.Draft Do Not Quote or Cite March 2010 2-92 In looking at short-term single-city PM 2.5 exposure studies conducte d in areas that would 1
have met the current level of the 24-hour standa rd, we recognize that th ese studies can provide 2 additional insights regarding impacts on susceptible populations and/or on areas with isolated 3 peak concentrations that coul d occur in areas that attain the current 24- hour and annual 4 standards. We first consider studies that repor t positive and statistically significant associations. 5 One short-term single-city PM 2.5 exposure study conducted since the last review reported a 6 positive statistically significant association for short-term PM 2.5 exposures in relation to 7 respiratory symptoms among children in Phoenix with an average 98 th percentile value of 25.8 8 μg/m 3 (Mar et al., 2004). In addition, another short-term single-city PM 2.5 exposure a study 9
noted in the last review also reported a positive statistically significant association between 10 short-term exposure to PM 2.5 and myocardial infarction in Boston with an average 98 th percentile 11 value of 28.2 μg/m 3 (Peters et al., 2001). 12 In also considering short-term single-city PM 2.5 exposure studies that report positive but 13 statistically non-significant associ ations for cardiovascular and resp iratory endpoints in areas that 14
would have met the current 24-hour PM 2.5 standard, we note a number of studies conducted in 15 Montreal (respiratory hospital admissions; Delfi no et al., 1997), Saint John (CVD and respiratory 16 hospital admissions; Steib et al ., 2000), Phoenix (CVD mortality; Wilson et al., 2007), Denver 17 (asthma medication use; Rabinovitch et al., 2006), Edmonton (hemorrhagic and ischemic stroke 18 hospital admissions; Villeneuve et al., 2006), and Nueces County, TX (ischemic stroke/transient 19 ischemic attack; Lisabeth et al., 2008). We note that the 98 th percentile values reported in these 20 studies averaging across m onitors in a city/county range from approximately 17.2 μg/m 3 21 (Rabinovitch et al., 2006) in Denver to 31.6 μg/m 3 (Wilson et al, 2007) in Phoenix. However, 22 other short-term single-city PM 2.5 exposure studies report null findi ngs for health effects noted 23 above (i.e., cardiovascular and respiratory morbid ity) as being positively associated with short24 term exposure to PM 2.5 in areas that would have met the current level of the 24-hour PM 2.5 25 standard, including Phoenix (resp iratory symptoms in adults; Mar et al., 2004); Spokane (CVD 26 hospital admissions and respiratory ED vis its; Slaughter et al . 2005), Denver (asthma 27 exacerbation; Rabinovitch et al., 2004) and Edmont on (ischemic stroke and transient ischemic 28 attack hospital admissions; Villeneuve et al., 2006). 29 In considering information from both multi- and single-city short-term PM 2.5 exposure 30 studies as summarized in Figur e 2-4, we believe that the ra nge of alternative 24-hour PM 2.5 31 standards appropriate for considerati on should extend below the range of 98 th percentile values 32 averaged across cities from the multi-city studies identified above so as to provide protection 33
from effects associated with short-term PM 2.5 exposure. In light of the mixed findings reported 34 in single-city studies, particular ly for studies conducted in areas such as Phoenix, Denver, and 35 Edmonton that report both positive and null findi ngs, we place comparativ ely greater weight on 36Draft Do Not Quote or Cite March 2010 2-93 the results from multi-city studies for the reasons previously noted at the beginning of this 1 section. Specifically, the hei ghtened statistical power of mu lti-city studies to detect PM 2.5 2 associated health effects in aggregated analysis across cities and greater spatial coverage for 3 different regions across the country to account for variations in PM 2.5 composition, sources, and 4 potentially other factors which might impact PM 2.5 -related risk. However, we note that 98 th 5 percentile values reported in single-city studies may provide additional in sights for consideration 6 in identifying alternative standa rds to provide protection for pote ntially susceptible populations. 7 Specifically, as noted above, Mar et al. (2004) provides evidence of a statistically significant 8
association between a 98 th percentile PM 2.5 level of 25.8 μg/m 3 and respiratory symptoms among 9
children. 10 In recognition that the current form of th e 24-hour standard disc ussed in section 2.3.3.2 11 applies to the measurements made at each population-oriented monitor, OAQPS conducted 12 additional air quality analyses for selected multi-city short-term PM 2.5 exposure studies to better 13 understand air quality distributions averaged ac ross monitors by the study investigators in 14 comparison to air quality levels focused on th e highest reporting monitors (Schmidt, 2010). 15 These analyses, as noted in section 2.3.4.1, focu sed on selected mortality and hospitalization 16 studies and, as presented in Tabl e 2-5 and Figure 2-5, yielded com posite monitor values close to 17
the 98 th percentile concentrations reported to the EPA by the study authors (ranging from 34.2 18 μg/m 3 (Bell et al 2008) to 34.8 μg/m 3 (Dominici et al., 2006). 47 As was expected, estimated air 19 quality levels for the highest repo rted monitors, ranging from 35.4 μg/m 3 (Bell et al, 2008) to 20 38.9 μg/m 3 (Dominici et al 2007) were higher than for the composite monitor values, ranging 21 from 33.5 μg/m 3 (Bell et al, 2008) to 36.5 μg/m 3 (Zanobetti and Schwartz, 2009). When more 22 study areas were considered and/or more years of air quality data were evaluated, the difference 23
between the 98 th percentile values for the composite monitor across cities compared to the 98 th 24 percentile for the highest reporting mon itor across cities was decreased. 25 Based on the epidemiological evidence and ai r quality analyses summarized above, in 26 considering the 24-hour standard to be the prim ary means to provide protection for short-term 27

PM 2.5 exposures, we reach the preliminary conclusion th at alternative levels could be considered 28 in the range of approximately 35 to 25 μg/m 3 . A level selected at the upper end of this range 29
would reflect consideration of a level somewhat below the 98 th percentile values for the highest 30 reporting monitors in the multi-city studi es (ranging from about 35 to 39 μg/m 3 ) and just below 31
the 98 th percentile values averaged ac ross all cities and all years in these studies (in the range of 32

47 As noted by Schmidt (2010), differences between 24-hour 98 th percentile and long-term mean concentrations reported by the study authors and the parallel values in the EPA analyses may be related to the EPA assessment only encompassing Federal Reference and Federal Equivalent Method air quality data while the study authors may have included additional (non-reference/equivalent) data. Also, there may be additional differences in the sets of monitoring sites utilized due to uncertainties associated with the geographical area boundary definitions

.Draft Do Not Quote or Cite March 20102-94Table 2-5. Comparison of Air Quality Data for Selected Epidemiological Studies– 98 Percentile Values4812Author Reported DataEPA Analysis (Schmidt 2010)Composite MonitorMaximum MonitorStudyCiteYears98%Range98%Range98%RangeMCAPS-OriginalDominici et al 2006 1999-2002 34.8 10-86 34.5 11-77 36.6 13-92-Extended Bell et al 2008 1999-2005 34.2 9-77 33.5 10-67 35.4 12-79NationalMortalityStudyZanobetti &Schwartz, 20091999-2005 34.318-80 35.6 17-75 36.9 19-79348All concentrations reported as μg/m3.Draft Do Not Quote or Cite March 20102-95Figure 2-5. Distributionof Study-specific 98thPercentile Concentrations12 Concentration (μg/m 3 )Left plots represent the study author results; middle plots represent EPA replication results using a community monitor, CM, (spatial average) approach; andright plots represent EPA replication results using a maximum value approach (max monitor 98thpercentile for each year averaged over the study timeframe).Black outlined boxes denote inter-quartile range and medians, stars denote means with cyan rectangles spanning +/- one standarddeviation from the mean,and dots represent the minimum and maximum values.EPAC MS tu d yA u th o rEPAm axB e llD o m in ic i0 6 Z a n o b e ttiEPAC MS tu d yA u th o rEPAm axEPAC MS tu d yA u th o rEPAm ax051 01 52 02 53 03 54 04 55 05 56 06 57 07 58 08 59 09 51003Draft Do Not Quote or Cite March 2010 2-96 about 34 to 35 μg/m 3 ). A level selected at the lowe r end of this range would reflect 1
consideration of a level just below the lowest 98 th percentile value associated with statistically 2 significant effects in a single-city study reporting effects in child ren, identified as a susceptible 3 population (Mar et al., 2004, 25.8 μg/m 3 ). 4 Alternatively, in considering the approach of using the a nnual standard as the primary 5 means for providing protection for both long- and short-term PM 2.5 exposures, we look to the 6 long-term mean PM 2.5 concentrations from short-term PM 2.5 exposure studies to inform 7
considerations of altern ative annual standard levels. Using this approach, the same short-term 8 multi- and single-city PM 2.5 exposure studies briefly describe d above were evaluated. In 9 focusing on multi-city short-term PM 2.5 exposure studies of cardi ovascular and respiratory 10 mortality, the ISA concludes that associations ar e generally consistent an d precise at long-term 11
mean PM 2.5 concentrations of 12.8 μg/m 3 and above (see Figure 2-4; US EPA, 2009a, pp. 2-9 to 12 2-11). More specifically, with respect to morta lity effects, Zanobetti and Schwartz (2009) report 13
associations with an overall annual av erage across all 112 cities of 13.2 μg/m 3 and Burnett et 14 al.(2004) report associations with an overall annual average acr oss 12 Canadian cities of 12.8 15 μg/m 3 . With regard to cardiovascular effects, Zhang et al. (2009) reported positive statistically 16 non-significant associati on between an average PM 2.5 concentration of 13.9 μg/m 3 and ST 17 segment depression among participants of the Women’s Health Initiative. 18 In considering PM 2.5 -related hospital admissions for cardiovascular and respiratory 19 effects in older adults, an identified suscepti ble population, Dominici et al. (2006a) and Bell et 20 al. (2008) report an overall annual average across 204 and 202 counties of 13.3μg/m 3 and 12.9 21 μg/m 3 , respectively (US EPA, 2009a, Figure 2-1). In looking at short-term single-city PM 2.5 22 exposure studies, similarly to the discussion of the 24-hour standard, Mar et al. (2004) (average 23

PM 2.5 concentration of 9.8 μg/m 3 ) and Peters et al. (2001) (average PM 2.5 concentration of 12.1 24 μg/m 3 ) report statistically significant associations for areas currently meeting the annual PM 2.5 25 standard. Several short-term single-city PM 2.5 exposure studies report positive but non26 statistically significant a ssociations in areas that would have met the current level of the annual 27 standard for respiratory and cardiovascular morb idity and mortality endpoints associated with 28 long-term mean PM 2.5 concentrations ranging from 7.0 μg/m 3 to 13.6 μg/m 3 (Figure 2-4). 29 However, as noted in the discussion of this eviden ce with regard to alternatives levels for the 24- 30 hour standard, investigators also reported null (Slaughter et al. 2005; Rabinovitch et al., 2004) 31 and mixed (Mar et al. 2004, Villeneuve et al., 2006) results for similar endpoints in which 32 positive associations were noted above for ar eas with annual levels ranging from 8.5 μg/m 3 to 33 10.8 μg/m 3 (Figure 2-4). These inconsistent findings suggest the potential for localized events 34 influencing the observed associatio ns in single-city short-term PM 2.5 exposure studies. 35 Consequently, we observe that the results of short-term PM 2.5 exposure studies could potentially 36Draft Do Not Quote or Cite March 2010 2-97 inform judgments on a 24-hour PM 2.5 concentration set at the 98 th percentile that provides 1 adequate protection in areas with unus ually high peak-to-mean ratios of PM 2.5 levels. However, 2 due to the possibility that these studies represent air quality distributions that may be influenced 3 by localized events and not be representative of air quality across the country, we reach the 4 preliminary conclusion that these single-city short-term PM 2.5 exposure studies do not provide 5 support for informing an alternative annual standa rd levels that would apply across the entire 6
U.S. 7 In considering not only the level but also the form of the annual standard, we 8 acknowledge, as was discussed in section 2.3.4.1, that there may be differences between mean 9

PM 2.5 concentrations averaged across monitors within a city/county as is t ypically considered in 10 epidemiological studies, compared to the current form of the annual PM 2.5 standard which 11 typically focuses on ambient measurements fr om the highest reporting community-oriented 12 monitor. As further discussed in section 2.3.4.1, OAQPS conducted additional air quality 13 analyses to better understand air qua lity distributions considered in selected short-term exposure 14 studies to compare long-term mean concentrations averaged across monitors in comparison to air 15 quality levels focused on the highest reporting monitors (Schmidt, 2010). This analysis, as 16 presented in Figure 2-2, reported composite m onitor values close to the long-term mean 17 concentrations reported by the study authors. As was expected, es timated air quality levels for 18 the highest reported monitors we re higher, ranging from 13.4 μg/m 3 (Bell et al.., 2008) to14.8 19 μg/m 3 (Dominici et al., 2007), than for the com posite monitor values, ranging from12.9 μg/m 3 20 (Bell et al.., 2008) to13.7 μg/m 3 (Zanobetti and Schwartz, 2009) . When more study areas were 21 considered and/or more years of air quality data were evaluate d, the difference between the long22 term mean concentrations for the composite mo nitor across cities compared to the long-term 23 mean concentrations for the highest reporting mon itor across cities was decr eased. Of particular 24 interest, is that the difference between the compos ite monitor and the high monitor is even less 25 when focusing on air quality estimates one standa rd deviation below the long-term mean across 26 cities for each of these short-term exposure st udies. With concentrations ranging from 10.2 27 μg/m 3 (Bell et al., 2008) to 10.7 μg/m 3 (Zanobetti and Schwartz, 2009) based one standard 28 deviation below the long-term mean averaged across monitors and across cities/counties and 29 concentrations ranging from 10.3 μg/m 3 (Bell et al., 2008) to 11.0 μg/m 3 (Zanobetti and 30 Schwartz, 2009) based on one standard devia tion below the long-term mean at the highest 31 reporting monitor averaged across cities/counties. 32 In considering the currently available eviden ce, we reach the preliminary conclusion that 33
the short-term PM 2.5 exposure studies provide a basis for co nsidering alternative levels for the 34 annual standard within a range below 13 μg/m 3 down to about 10 μg/m 3 . A standard in the range 35 of 13 to 12 μg/m 3 would reflect placing gr eater weight on setting a le vel somewhat below the 36Draft Do Not Quote or Cite March 2010 2-98 long-term mean concentrations reported in the short-term exposure studies (ranging from12.8 1 μg/m 3 and above). A standard in the range of 11 to 10 μg/m 3 would be consistent with a 2 judgment that, recognizing the serious nature of th e effects and that no discernable threshold for 3 these effects can be identified, appreciable wei ght should be accorded to considering the lower 4 end of the interquartile range of long-term mean concentrations reported in these studies, or a 5 range within one standard deviat ion around the study mean of either the composite or the highest 6 reporting monitor (ranging from about 10 to 11 μg/m 3 ). 7 As recognized above, an annual standard used as the primary means for providing 8 protection for effects associated with both long- and short-term PM 2.5 exposures cannot be 9 expected to offer an adequate margin of sa fety against the effects of all short-term PM 2.5 10 exposures, especially in areas wi th high peak-to-mean ratios of PM 2.5 concentrations, possibly 11 associated with strong local or seasonal sources of fine particles. In considering a basis for 12 setting an alternative standard levels for a 24-hour standard that w ould provide supplemental 13 protection against days with high peak concentra tions associated with lo calized “hotspots” and 14 risk arising from seasonal emissions that mi ght not be well controlled by a national annual 15 standard, we intend to conduct ai r quality analyses of the rela tionships between annual and 24- 16
hour concentrations to incl ude in the second draft PA. 17

2.3.5.2 Risk-based Considerations to Inform Alternative Levels 18

This discussion considers the impact of alterna tive suites of standard levels on short-term 19 exposure-related mortality and morbidity. As suc h, it is intended to address the following policy20 related questions: 21

 To what extent do alternative standards re duce estimated risks associated with short22 term PM 2.5 exposure compared to risks associated with simulating air quality to just 23 meet the current standards? What roles do the current 24 hour and annual standards 24 have in simulating the risks remaining upo n just meeting the alternative suites of 25 standards considered in the risk assessment? Wh at level of confidence is associated with 26 these risk estimates? 27 As was done above for long-term exposure- related mortality, we have divided the 28 discussion of risk for short-term exposure- related mortality and morbidity, between (a) 29
reductions in risk associated with simulation of the three alternative annual standard levels and 30 (b) reductions in risk associated with the two alternative 24-hour standard levels. 31

Risk reduction associated with alternat ive annual standards (14/35, 13/35, and 12/35) 32
Reductions in risk for short-term exposure- related mortality and morbidity exhibits 33 considerable variability across st udy areas for the alternative suite of annual standards (compared 34
with risk under the current suit e of standards) (see section 2.2.1.1). For the 12 urban study areas 35Draft Do Not Quote or Cite March 2010 2-99 experiencing reductions in short-term exposure-re lated CV mortality under the lowest alternative 1 annual standard level assessed (12/35), reductions in risk compared to risk under the current suite 2 of standards ranged from 5% (Phoenix) to 23% (Atlanta and Birmingha m) (see Figure 2-3 and 3 US EPA, 2010a, Appendix E, Ta ble E-90). Estimates of risk reduction for CV-related HA’s 4 exhibited a similar pattern across the study areas for the lowest annual standard level assessed 5 (see Figure 2-6 and US EPA, 2010a, Appendix E, Table E-108). 6 Regarding the magnitude of risk estimated to remain after simulation of the alternative 7 annual standards, the four study areas displaying the greatest degree of reduction across the 8
alternative annual standards (Atlanta, Baltimore, Houston and St. Louis) have PM 2.5 -related CV 9 mortality estimates (under the lowest alternat ive annual standard of 12/35) ranging from 25 10 (Atlanta) to 84 (St. Louis - see US EPA, 2010a , Appendix E, Table E-84). The urban study area 11 with the greatest degree of PM 2.5 -related risk in absolute term s (New York) did not exhibit 12 significant reductions in risk until the lowest annual standard leve l of 12/35 was considered, at 13 which point we estimate a reduction in PM 2.5 -related CV mortality of 424 cases (see US EPA, 14 2010a, Appendix E, Table E-84). In terms of the pe rcentage of mortality attributable to short15
term PM 2.5 exposure, the four study areas experiencing the greatest degree of risk reduction 16
across the four alterna tive annual standard levels had esti mates (for the alternative annual 17 standard of 12 μg/m 3 ) ranging from 0.6% (Atlanta) to 1.3% (Baltimore – US EPA, 2010a, 18 Appendix E, Table E-87). For CV-rela ted HA’s related to short-term PM 2.5 exposure, estimates 19 for this same group of four study areas (for th e lowest alternative annual standard assessed) 20 ranged from 32 (Atlanta) to 142 (St. Louis - RA A ppendix E, Table E-102). This translated into a 21 percentage of CV HA’ s attributable to PM 2.5 ranging from 0.28% (Atlanta) to 1.07% (Baltimore 22 – US EPA, 2010a, Appendix E, Table E-105). 23 As with long-term exposure-related mortalit y, variation in risk reduction across urban 24 study areas for both short-term exposure-related mort ality and morbidity refl ect to a great extent 25 varying degrees of reduction in annual-average PM 2.5 levels. This in turn results from the initial 26
simulation of the current 24-hour standard leve l which can produce varying degrees of reduction 27 in annual-average PM 2.5 levels depending on a number of factors (i.e., peakiness of the PM 2.5 28 monitoring data, specific mix of annual and 24- hour design values for a given location and the 29 spatial pattern of reduction in ambient PM 2.5 levels that is assumed). We note however, that 30 there is greater vari ability in the levels of risk remaining after si mulation of alternative annual 31 standard levels for short-term exposure-relate d health endpoints comp ared with long-term 32 exposure-related mortality. This primarily reflects the fact that we ar e able to specify C-R 33 functions separately by urban area or region fo r short-term exposure related mortality and 34 morbidity endpoints, while a single C-R functi on was used in modeling long-term exposure35 related mortality by endpoint ac ross all urban study areas. 36Draft Do Not Quote or Cite March 20102-100Figure 2-6. Percent Reduction in Short-term Exposure-related Mortality and Morbidity Risk1(alternative standards relativeto the current standards)2(Note: inset shows PM2.5related incidence and percent of total incidence for CV under the currentsuite of standards)3Atlanta, GABaltimore,MDBirmingham, ALDallas, TXDetroit, MIFresno, CAHouston, TXLos Angeles,CANew York,NYPhiladelphia,PAPhoenix, AZPittsburgh, PASalt Lake City, UTSt. Louis, MOTacoma,WA0%5%10%15%20%25%30%35%15/35** 14/35 13/35 12/35 13/30 12/25Recent Air Quality, Current Standard and Alternative Standards

Short-Term Exposure-Related Risk: Percent Reduction from Current StandardAtlanta, GA 32 (-33 - 95); 0.8% (-0.8% - 2.4%)Baltimore, MD 62 (-4 - 126); 1.6% (-0.1% - 3.2%)Birmingham, AL -1 (-42 - 40); 0% (-1.5% - 1.5%)Dallas, TX 29 (-19 - 76); 0.8% (-0.5% - 2.2%)Detroit, MI 60 (-8 - 127); 1% (-0.1% - 2.2%)Fresno, CA 12 (-9 - 33); 0.7% (-0.5% - 2%)Houston, TX 46 (-31 - 122); 0.9% (-0.6% - 2.4%)Los Angeles, CA -30 (-132 - 72); -0.2% (-0.7% - 0.4%)New York, NY 473 (276 - 668); 2.1% (1.2% - 3%)Philadelphia, PA 84 (22 - 145); 2.1% (0.5% - 3.6%)Phoenix, AZ 84 (-4 - 170); 1.3% (-0.1% - 2.7%)Pittsburgh, PA 43 (-9 - 93); 1.1% (-0.2% - 2.3%)Salt Lake City, UT 9 (-2 - 20); 0.8% (-0.2% - 1.7%)St. Louis, MO 106 (24 - 187); 1.9% (0.4% - 3.3%)Tacoma, WA 11 (-6 - 27); 0.7% (-0.4% - 1.8%)`456*Based on Zanobetti and Schwartz(2009). The legend contains,for each urban area, the incidence estimate (and 95% CI) and theestimate of percent of total7incidence (and 95% CI) under the current standards.8**The current standards consist of an annual standard of 15 μg/m3and a daily standard of 35 μg/m3. Combinations of an annual standard (n) and a daily standard9(m) are denoted n/m in this figure.10Draft Do Not Quote or Cite March 2010 2-101 As noted earlier, given increased emphasis pl aced in this analysis on long-term exposure1 related mortality, the uncertainty analyses comp leted for this health endpoint category are 2 somewhat more comprehensive than those conduc ted for short-term exposure-related mortality 3 and morbidity, which to some extent reflects limit ations in study data available for addressing 4 uncertainty in the later category. However, C-R functions used in generating estimates for short5 term exposure-related mortality and morbid ity are well-supported in the literature. 6

Risk reduction associated with altern ative 24-hour standards (13/30 and 12/25) 7
Comparing risks associated with just meeti ng the 13/35 and 13/30 suites of alternative 8 standards (which reflect a 5 μg/m 3 reduction in the 24-hour sta ndard, while holding the annual 9 fixed at 13 μg/m 3 ), we see variation in the magnitude of risk reduction across urban study areas. 10 For example, Baltimore, CV mortality risk attributable to PM 2.5 under the 13/35 suite of 11 alternative standards was reduced by 14% relative to risk under the curren t suite of standards. 12 Very little additional risk reduction (increasi ng from 14% to 15%) is estimated under the 13/30 13 alternative suite of standards. In contrast, with Salt Lake City, we estimate that the 13/35 suite of 14 alternative standards will produce no risk reducti on relative to the curren t suite of standards, 15 while the 13/30 suite would produ ce a 15% reduction in CV mortal ity risk relative to risk under 16 the current standard level (see Figure 2-6 a nd US EPA, 2010a, Table E-90 in Appendix E). 17 The additional risk reduction provided by an alternative 24-hour standard is more 18 substantial in comparing the 12/25 and 12/35 altern ative suites of standa rds, although there is 19 also greater variability in th e magnitude of risk reductions across study areas. For example, 20 Atlanta, which had a 23% reducti on in risk under the 12/35 suite of standards (relative to the 21 current standard level) only sees a marginal in crease to 24% under the 13 /25 suite of standards. 22 By contrast, Salt Lake City, which has no reducti on in risk under the 12 /35 suite of standards 23 (relative to the current suite of standards), sees a 29% reduction in risk un der the alternative suite 24 of 12/25 (see Figure 2-3 and US EPA, 2010a, Appe ndix E, Table E-90). The pattern of risk 25 reduction for CV-related HA’s is very similar to wh at is presented here for CV-related mortality 26 (see Figure 2-6 and US EPA, 2010a, Appendix E, Table E-108). 27
We note that while considerable reductions in risk are seen for short-term exposure28 related mortality across many of the study areas, these are smaller than reductions seen for long29 term exposure-related mortality. This reflects pr imarily the fact that risk is modeled down to 30 PRB for short-term exposure-related mortality, while it is only modeled down to LML for long31 term exposure-related mortality. Therefore, the in cremental reductions in risk associated with 32 short-term exposure-related mortality when we cons ider alternative suites of standards involve a 33 smaller fraction of total risk compared with long-term exposure-related mortality. 34Draft Do Not Quote or Cite March 2010 2-102 Regarding risk remaining after simulation of the suite of alternative 24-hour standards, 1

PM 2.5 -related CV mortality estimates (under the 12/ 25 case) ranging from 6 (Salt Lake City) to 2 336 (New York) (see US EPA, 2010a, Appendix E, Table E-84). Estimates of CV-related HA 3
under the 12/25 suite of standa rds range from 7 (Salt Lake City) to 534 (New York) (see 4 Appendix E, Table E-102). In terms of the percen tage of short-term mortality attributable to 5

PM 2.5 , we see that under the 13/30 su ite of standards, the percen t of total incidence of CV 6 mortality attributable to PM 2.5 ranges from ~0% (Los Angeles, Birmingham) to 1.8% (New 7 York, Philadelphia) (US EPA, 2010a, Appendix E, Table E-87). Under the 12/25 alternative 8 suite, risks for this metric range from ~0% (Bir mingham, Los Angeles) to 1.1% (Baltimore). 9 The observations presented above highlight va riability both in the magnitude of risk 10 reduction as well as in the risk remaining upon simulation of just meeting alternative 24-hour 11
standards. This reflects the f act that, as noted earlier, altern ative 24-hour standards can produce 12 different degrees of reduction in the annual-average PM 2.5 concentrations, depending on the 13 relationship between 24-hour and an nual design values at a particul ar location. As noted before, 14 it is these annual-average PM 2.5 levels that drive changes in long-term exposure-related 15 mortality. In addition, as noted ea rlier, modeling of risk for shor t-term exposure-related mortality 16 and morbidity involves a combination of urban study area- and regional-sp ecific C-R functions, 17 which adds additional variability to risk estimates generated across the study areas. 18 As noted earlier, given increased emphasis pl aced in this analysis on long-term exposure19 related mortality, the uncertainty analyses comp leted for this health endpoint category are 20 somewhat more comprehensive than those conduc ted for short-term exposure-related mortality 21 and morbidity, which to some extent reflects limit ations in study data available for addressing 22 uncertainty in the later category. However, C-R functions used in generating estimates for short23 term exposure-related mortality and morbid ity are well-supported in the literature. 24
Summary 25

The results discussed above show that simulating just meeti ng alternative annual 26 standard levels in the range of 14 to 12 μg/m 3 can produce substantial re ductions in short-term 27 exposure-related mortality and morbidity risk (wit h the magnitude of risk reduction increasing as 28 lower annual standards in this range are consid ered). Furthermore, the results suggest that 29
alternative 24-hour standard leve ls in the range of 30 to 25 μg/m 3 can produce additional 30 reductions in estimated risk, beyond that produced by simulations of just meeting lower annual 31 standard level down to 12 μg/m 3 (combined with a 24-hour standard of 35 μg/m 3 ). However, we 32 note that the magnitude of estimated reductions in short-term exposure-related mortality are 33 substantially lower than estimat es for long-term exposure-related mortality (when comparing 34 risks for the same urban study ar ea and suite of standards). 35Draft Do Not Quote or Cite March 2010 2-103 In addition, while we would expect altern ative 24-hour standa rds to produce more 1 variable reduction in risk estimates and conseq uently in public health protection relative to 2
alternative annual standards (for the same reasons presented earlier for long-term exposure3 related mortality), we see that risk estimates for both annual and 24-hour standards are fairly 4 variable for short-term exposure-re lated health effects categories. Th is reflects in part the fact 5
that we use urban area-differen tiated and regionally-differentia ted C-R functions in modeling 6 short-term exposure-related mortality and morb idity, which introduces additional variability 7 across study areas in terms of both risk reduction and the magnit ude of risks remaining after 8
simulation of alternative suites of standards. 9

2.3.6 Preliminary Staff Conclusions on Alternat ive Levels to Add ress Health Effects 10 Related to Long- and Short-term PM 2.5 Exposures 11 In reaching preliminary staff conclusions on alte rnative standard levels to address health 12
effects related to both long- and short-term PM 2.5 exposures, we have considered the currently 13 available scientific information including: epid emiologic evidence, including evidence of effects 14 in susceptible populations; air qual ity analyses; and estim ates of risk reducti ons associated with 15
alternative annual and/or 24-hour standard leve ls, as well as the related limitations and 16
uncertainties associated with this informa tion as presented in sections 2.3.4 and 2.3.5 and 17 discussed more fully in the ISA and second dr aft RA (US EPA, 2009a; US EPA, 2010a). As 18 outlined in section 2.1.3, we believe it is most appropriate to consider the protection against 19

PM 2.5 -related mortality and morbidity effects, associated with l ong- and short-term exposures, 20 afforded by the annual and 24-hour standards take n together, rather than to consider each 21 standard separately. The extent to which these two standards ar e interrelated in any given area 22 depend in large part on the relative levels of the standards, the peak-to-mean ratios that 23 characterize air quality pa tterns in an area, and whether changes in air quality designed to meet a 24 given suite of standards is of a mo re regional or localized nature. 25 In looking first at the nature of the asso ciations between long- and short-term PM 2.5 26 exposures and a range of health outcomes, we have considered not only the causal inferences 27 presented in the ISA but also at what air quality concentrations th ese effects have been observed. 28 In evaluating these data, we are mindful that th e ISA has concluded that no discernable threshold 29
for an effect associated w ith long- or short-term PM 2.5 exposures can be identified based on the 30 currently available evidence (US EPA, 2009a, section 2.4.3). We ha ve considered a number of 31 different air quality metrics to inform our prel iminary conclusions regard ing alternative levels 32 that should be considered including: 33

 Long-term mean ambient PM 2.5 concentrations reported in long- and short-term 34 exposure studies; 35Draft Do Not Quote or Cite March 2010 2-104  Ambient PM 2.5 concentrations down to one standa rd deviation below the long-term 1 mean concentrations or the lower end of the interquartile range of air quality data 2 evaluated in the long- and short-term exposure studies; 3

 The range of long-term PM 2.5 mean concentrations and the point were the data become 4 more sparse or where the confidence interv al becomes notably wider, suggestive of a 5 concentration below which the association be comes appreciably more uncertain and the 6 possibility that an effects thresh old may exist becomes more likely; 7

 Differences between long-term mean PM 2.5 concentrations averaged across monitors 8 within a city/county as is t ypically considered in epidem iologic studies, compared to 9 the current form of the annual PM 2.5 standard which typically focuses on ambient 10 measurements from the highest re porting community-oriented monitor; 11

 98 th percentile 24-hour ambient PM 2.5 concentrations identified for short-term exposure 12 studies; and 13

 Differences between 98 th percentile 24-hour ambient PM 2.5 concentrations averaged 14 across monitors within a city/county compar ed to the current form of the 24-hour PM 2.5 15 standard which focuses on ambient meas urements from the highest reporting 16 community-oriented monitor 17 In considering the results of quantitative risk assessments conducted for this and previous 18 reviews, specifically the estim ated risk remaining upon simulati on of just meeting alternative 19 suites of standards, we note the following: 20

 Long-term exposure to PM 2.5 has been shown to produce substantially larger mortality 21 risk (in terms of overall inci dence and percent oftotal mortality) compared to short22 term PM 2.5 exposure (section 2.2.2; US EPA, 2010a, p. 6-1). 23 24

 Much of the risk related to daily exposu res, when aggregated on an annual basis, 25 results from the large number of da ys during which the 24-hour average 26 concentrations are in the low- to mid-range of the entire distribution. Thus, to reduce 27 the aggregate short-term exposur e-related risk, it is necessary to shift the bulk of the 28 distribution to lower concentra tions, not just to limit the concentrations on days when 29 the PM 2.5 concentrations are relatively hi gh (US EPA, 2005, p. 4-67, Figure 4-10; 30 Abt, 1996, section 7.1, p.79, Exhibit 7.6). 31 32

 Alternative annual standard levels produced more consistent levels of risk reduction 33 (and consequently public health protection) w ith generally higher levels of confidence 34 when compared with alternative 24-hour st andards. Considerable variability exists 35 across urban study areas with respect to th e degree to which alternative 24-hour 36 standard levels produce reduc tions in annual average PM 2.5 concentrations and, 37 consequently, reductions in risk (section 2.3.4.2). 38 39 Taken together, we believe the best way to provide requisite pr otection for effects 40 associated with both long- and short-term PM 2.5 exposures is to define a suite of standards that 41 will provide generally consistent protection across th e country. In considering the roles that each 42Draft Do Not Quote or Cite March 2010 2-105 standard might be expected to play in the protect ion afforded by alternative suites of standards, 1 we believe it is appropriate to select a policy approach where the annual standard is the 2 “generally controlling” standar d. This approach would reflec t consideration for allowing the 3
annual standard to serve in most areas as the target fo r control programs designed to be effective 4 in lowering the broad distribution of PM 2.5 concentrations, thus pr otecting not only against 5 effects associated with long-term exposures but also effects associated with short-term 6 exposures. This approach reflects the recognition that changes in PM 2.5 air quality designed to 7 meet an annual standard would likely result not only in changes in lower annual average 8
concentrations but also in fewer a nd lower peak 24-hour concentrations. 9 In addition, we recognize that an annual standard cannot be ex pected to offer an adequate 10 margin of safety against the effects of all short-term PM 2.5 exposures, especially in areas with 11 unusually high peak-to-mean ratios of PM 2.5 levels, possibly associat ed with strong local or 12 seasonal sources, or for potential PM 2.5 -related effects that may be a ssociated with shorter-than13 daily exposure periods (noted above in section 2.3.2). As a result, in conjunction with an annual 14 standard that may be adopted as the generally co ntrolling standard, in pa rt to provide protection 15 against effects associated with short-term expos ures, we believe it is a ppropriate to use the 24- 16
hour PM 2.5 standard to provide supplemental pr otection against days with high peak 17 concentrations associated with localized “hotspot s” and risk arising from seasonal emissions that 18 might not be well controlled by a national annual standard. 19 Thus, we reach the preliminary conclusion that it is appropriate to consider defining the 20
annual PM 2.5 standard as the generally controlling standard and the 24-hour PM 2.5 standard as a 21 “backstop” to provide additional protection, wher e needed. We believe selecting a suite of 22 standards using this approach will provide a mo re uniform level of protection across the U.S. 23 compared to using an approach where the 24-hour standard is the generally controlling standard. 24 This preliminary conclusion is consistent with the approach used to set the original PM 2.5 25 standards in 1997 (see section 2.1.1.1). 26 In integrating the preliminary staff co nclusions reached in sections 2.3.4 and 2.3.5 27 regarding alternative levels to provide protection for long- and short-term PM 2.5 exposures, 28 respectively, with the propos ed approach outlined above, we have reached preliminary 29 conclusions regarding alternative levels for bot h the annual and 24-hour st andards. The body of 30 scientific evidence upon which thes e preliminary conclusions are ba sed includes consideration of 31 effects in susceptible populat ions, including evidence of mortality (causal association), 32 cardiovascular effects (causal association) and/or re spiratory effects (likely causal association) in 33 various populations including th e life stages of children and older adults, people with pre34 existing cardiovascular and respir atory disease, and people with lo wer socioeconomic status. As 35 outlined in section 2.3.4.1, in considering alternat ive levels for an annual standard that would 36Draft Do Not Quote or Cite March 2010 2-106 provide protection with an adequate margin of safety, we believe it is also appropriate to take 1
into account evidence of effects for which the IS A has determined the evidence is suggestive of 2 an association with long-term PM 2.5 exposure including reproductive and developmental effects 3 and carcinogencity, mutagenicity, an d genotoxicity. At this time, PM 2.5 concentrations reported 4 in these studies are equal to or greater than ambient concentrations identified in studies reporting 5 associations with mortality, cardiovascular effects, or respiratory effects. Therefore, in selecting 6 alternative levels, we note that, in providing protection for mortality and cardiovascular and 7 respiratory effects, it is reasonable to anticip ate that protection will also be provided for a 8 broader range of health outcomes. 9 Based on the currently availabl e scientific eviden ce, we believe there is support for a 10 “generally controlling” PM 2.5 annual standard in the range of 13 to 10 μg/m 3 to provide 11 protection for effects associated with both long- and short-term PM 2.5 exposures in conjunction 12 with a generally “non-controlling” 24-hour PM 2.5 standard in the range of approximately 30 to 35 13 μg/m 3 to limit peak concentrations in areas with relatively high peak-to-mean PM 2.5 ratios. 14 Selecting a suite of standards with an a nnual standard in the range of 13 to 12 μg/m 3 in 15 conjunction with a 24-hour standard in the range of 35 to 30 μg/m 3 would reflect placing greater 16 weight on setting standard levels just below the PM 2.5 concentrations (long-term mean and 98 th 17 percentile value) reported in the epidemiologic st udies reporting associations with mortality and 18 cardiovascular and respiratory effects. It w ould also recognize cons ideration for setting a 19 standard with an adequate margin of safety by selecting standard levels based on ambient 20 concentrations averaged across monitors as is typically done in epid emiologic studies and 21 applying those levels using the form s of the current annual and 24-hour PM 2.5 standards which 22 generally focus on the ambient c oncentrations reported at the hi ghest reporting monitors. 23 Alternatively, selecting a suite of standards with an annual standard in the range of 11 to 24 10 μg/m 3 in conjunction with a 24-hour standard of 30 to 25 μg/m 3 would reflect a more 25 precautionary approach. This approach would be consistent with a judgment that, recognizing 26
the serious nature of the effects and that no discernable threshold fo r these effects can be 27 identified, appreciable weight should be accorded to recognizing that he alth effects may occur 28 over the full range of concentrations observed in the epidemiologic studies. Using this approach, 29
we believe that it is reasonable to conclude that the evidence of association is strongest down to 30 somewhat further below the aggregate long-term m ean concentrations reported in the long- and 31 short-term exposure studies, such as down to one standard deviation belo w the mean or to the 32 lower end of the interquartile range, which includ es the range in which the data in the study are 33
most concentrated. To serve as an effective “b ackstop” for an alternative annual standard set at 34 the lower end of the preliminary range, we r each the preliminary conclusion that it would be 35Draft Do Not Quote or Cite March 2010 2-107 appropriate to set the level of the 24-hour PM 2.5 standard somewhat lower than the current 1
standard. 2 We recognize that it is the link between the form and the level of the standard that 3 determines the degree of public health protection the standard affords. As discussed in section 4 2.3.3.1, the current form of the annual standard a llows for spatial averaging across monitors 5
within constraints that were narrowed in 2006. In light of the currently available scientific 6 evidence discussed in section 2.2.1 providing stronge r support that socioeconomic status (SES) 49 7
modifies the association between PM and morb idity and morality outcomes, we believe that 8 eliminating the spatial av eraging provisions from the form of the annual PM 2.5 standard in 9 conjunction with consideration of alternative levels for the annual standard discussed above is 10 appropriate for identifying a standa rd that provides requisite protec tion with an adequate margin 11 of safety. In the second draft of this Polic y Assessment, we intend to explore more fully 12 information on the peak to mean air quali ty concentrations re lating the 24-hour 98 th percentile 13

PM 2.5 concentrations relative to the mean annua l concentrations to better inform our 14 understanding of the implications of retaining or modifying th e current form of the annual 15
standard. 16

2.4 PRELIMINARY STAFF CONCLUSIONS ON ALTERNATIVE FINE PARTICLE 17 STANDARDS 18 In reaching preliminary conclusions on potential alternative standards to provide requisite 19 protection for health effects asso ciated with long- and short-term fine particle exposures, staff 20
has considered these standards in terms of th e basic elements of the NAAQS: indicator, 21 averaging time, form, and level. In considering the scientific and technical information, we 22 reflect upon the information available in the last re view integrated with information that is newly 23
available since the last review as assessed and presented in the ISA and second draft RA (US 24 EPA, 2009a; US EPA 2010a) and as summarized in sections 2.2 and 2.3. 25 As outlined in sections 2.1.3 and 2.3.6, in this review, our approach to reaching 26 conclusions about the adequacy of the current suite of PM 2.5 standards and potential alternative 27 standards that are appropriate for consideration is broader and more integr ative than approaches 28 used in past reviews. In appl ying this approach, we recognize that there are various ways to 29 combine the suite of standards to achieve an appr opriate degree of public health protection. Such 30 an approach to standard setting, which inte grates a much expanded body of health effects 31 evidence, more extensive air quality data and an alyses, and a more comprehensive quantitative 32
risk assessment and considers the combined protection afforded by the annual and 24-hour 33 standards, has the potential to result in a more e ffective and efficient suite of standards than an 34

49 Measured using surrogates such as educational a ttainment, residential location, and income level.Draft Do Not Quote or Cite March 2010 2-108 approach that only considers l ong- and short-term exposures ev idence, analyses, and standards 1 independently. 2 In presenting our preliminar y conclusions regarding alternative suites of primary 3 standards and ranges of levels fo r consideration, we summarize conc lusions presented in sections 4 2.3.1 through 2.3.6. We emphasize that these ar e preliminary conclusions that reflect 5
consideration of the scientific and technical in formation assessed and presented in the ISA and 6 second draft RA (US EPA, 2009a; US EPA, 2010a). We note that sta ff conclusions to be 7 presented in the final RA and second draft PA will be based, in part, on input received from 8 CASAC and the public on the second draft RA a nd this first draft PA, as well as additional 9 analyses that we are conducting that will help in form our consideration of alternative forms and 10 levels as noted in sections 2.3.3, 2.3.4, and 2.3.5. 11 We recognize that selecting from among alte rnative standards will necessarily reflect 12 consideration of the qualitative a nd quantitative uncertainties inhe rent in the relevant evidence 13 and in the assumptions that unde rlie the quantitative risk asse ssment. In identifying these 14 alternative suites of primary stan dards and ranges of levels for c onsideration, we are mindful that 15 the Clean Air Act requires standards to be set that are requisite to protect public health with an 16 adequate margin of safety, such that the standard s are to be neither more nor less stringent than 17 necessary. Thus, the Act does not require that the NAAQS be set at zero-risk le vels, but rather at 18 levels that avoid unacceptable risks to public health. 19
20 ( 1) Consideration should be give n to revising the current PM 2.5 primary standards to provide 21 increased public health protection from the e ffects of both long- and short-term exposures 22 to fine particles in the ambient air. This pr eliminary conclusion is ba sed in general on the 23 evaluation in the ISA of the currently availa ble epidemiologic, toxicologic, dosimetric, 24 and exposure-related evidence, and more sp ecifically on the eviden ce of mortality and 25 cardiovascular and respiratory morbidity effects in areas where the current standards 26 were met, together with judgments as to th e public health significance of the estimated 27 incidence of effects upon just meeting the current suite of standards. 28
29 ( 2) The indicator for fine particle st andards should continue to be PM 2.5 . This observation 30 reflects our preliminary conclusions that the available evidence does not provide a 31 sufficient basis for replacing or supplementing the PM 2.5 indicator with an indicator 32 defined in terms of ultrafine particles or for any specific fine particle component or 33 source category of fine particles, nor does it provide a basis for ex cluding any component 34 or source category from the mix of particles included in the PM 2.5 indicator. 35
36Draft Do Not Quote or Cite March 2010 2-109 ( 3) Averaging times for PM 2.5 standards should continue to include annual and 24-hour 1 averages to protect against hea lth effects associated with lo ng-term (seasons to years) and 2 short-term (hours to days) exposure periods. Consideration of ot her averaging times, 3 including an averaging time le ss than 24 hours to address health effects associated with 4 subdaily fine particle exposures or a longer averaging time to address effects associated 5 with seasonal fine partic le exposures, was limited by th e relatively small amount of 6 relevant information availa ble in this review. 7
8 ( 4) Consideration should be given to retaining or revising the fo rm of the annual standard. 9 Consideration should be given to revising the form of the a nnual standard to one based on 10 the highest community-oriented monitor in an area rather than a form that would allow 11 averaging across monitors (e.g., spatial averag ing). The form of the 24-hour standard 12 should continue to be defined in terms of the 98 th percentile of the distribution of 24-hour 13
PM 2.5 concentrations, averaged over three years. 14
15 ( 5) Consideration should be given to alternative suites of PM 2.5 standards to provide 16 protection against effects associ ated with both long- and shor t-term exposures, taking into 17 account both evidence-based and risk-based co nsiderations. Further, we conclude it is 18 appropriate to consider setti ng the levels of the annual and 24-hour standards such that 19 the annual standard would be the “generally controlling” standard to provide protection 20 for both long- and short-term PM 2.5 exposures in conjunction with a 24-hour standard to 21 provide supplemental protection against days with high peak concentrations associated 22 with localized “hotspots” and risk arising fr om seasonal emissions that might not be well 23 controlled by a national annual standard. Integrated preliminary conclusions on ranges 24 of alternative suites of sta ndards that, when considered to gether, would provide requisite 25 protection against effects associated with both long- and short-term exposures include: 26
27 (a) Consideration of a revised annual PM 2.5 standard within the range of 13 to 12 μg/m 3

, 28 together with either retain ing or revising the 24-hour PM 2.5 standard within the range 29 of 35 to 30 μg/m 3

. 30 (b) Consideration of a revised annual PM 2.5 standard, within the range of 11 to 10 μg/m 3

, 31 together with revising the 24-hour PM 2.5 standard within a range of 30 to 25 μg/m 3

. 32
33

2.5 KEY UNCERTAINTIES AND AREAS FOR FUTURE RESEARCH AND DATA 34 COLLECTION 35 [This topic will be discussed in the second draft Policy Assessment.] 36Draft Do Not Quote or Cite March 2010 2-110 2.6 REFERENCES 1
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### 3 REVIEW OF THE PRIMARY STANDARD FOR THORACIC 1 

### COARSE PARTICLES 2

This chapter presents preliminary staff conclu sions with regard to the adequacy of the 3 current primary PM 10 standard, which is intended to protect public health agai nst exposures to 4 thoracic coarse particles (PM 10-2.5 ), and potential alternative prim ary standards for consideration 5
in this review. Our assessment of these issues is framed by a series of key policy-relevant 6 questions, which expand upon those presented in the IRP (US EPA, 2008a) at the outset of this 7 review. The answers to these questions will in form decisions on whether, and if so how, to 8
revise the current PM 10 standard. 9
Staff notes that final decisi ons regarding the primary PM 10 standard will draw upon 10 scientific information about health effects, as we ll as judgments about how to deal with the range 11
of uncertainties that are inherent in the scientific evidence. Ultimately, the final decisions are 12 largely public health policy judgments. Our appr oach to informing these judgments, discussed 13 more fully below, recognizes that the availa ble health effects evid ence reflects a continuum 14 consisting of ambient levels at which scientists generally agree that health effects are likely to 15 occur through lower levels at which the like lihood and magnitude of the response become 16 increasingly uncertain 17 Our current approach for reviewing the primary PM 10 standard is presented in section 3.1. 18 Our preliminary conclusions regardi ng the adequacy of the current PM 10 standard are presented 19 in section 3.2. Section 3.3 presents our prelimin ary considerations and conclusions with respect 20 to potential alternative standards, focusing on each of the basic elements of the standards: 21 pollutant indicator (section 3.3.1), averaging tim e (section 3.3.2), and form and level (section 22 3.3.3). The next draft of this chapter will also include an initial overvie w of key uncertainties 23 and suggested future research areas and data collection efforts. 24

3.1 APPROACH 25 Staff’s approach for reviewing the current primary PM 10 standard builds upon the 26 approaches used in previous PM NAAQS reviews. Our current approach is based on the updated 27
scientific and technical information in the ISA. 1 The past and current approaches described 28 below are all based most fundamentally on usi ng information from epidemiologic studies to 29 inform the selection of PM standards that, in th e Administrator’s judgment, protect public health 30 with an adequate margin of safety. In the case of thoracic coarse particles, such information is in 31

1 As described below, given limitations in the health eff ects data and in the monitoring network, we have not conducted a quantitative risk assessment in this review for thoracic coarse particles.Draft Do Not Quote or Cite March 2010 3-2 the form of PM 10-2.5 and PM 10 air quality distributions over which health effect associations have 1 been reported. In light of limitations in PM 10-2.5 epidemiologic studies, dosimetric and 2 toxicological information also play an important ro le, especially in considerations related to the 3 appropriate indicator for a sta ndard meant to protect against exposures to thoracic coarse 4 particles. Evidence-based appro aches to using information from epidemiologic studies to inform 5 decisions on PM standards are complicated by the recognition that no population threshold, 6
below which it can be concluded with confidence that PM-related effects do not occur, can be 7 discerned from the available evidence. As a result, any approach to reaching decisions on what 8 standards are appropriate require s judgments about how to transl ate the information available 9 from the epidemiologic studies into a basis for appropriate standards, which includes 10 consideration of how to weigh the uncertainties in reported associations across the distributions 11 of PM concentrations in the studies. Such approa ches are consistent with setting standards that 12 are neither more nor less stringe nt than necessary, recognizing that a zero-risk standard is not 13 required by the CAA. 14

3.1.1 Approaches Used in Previous Reviews 15

3.1.1.1 Reviews Completed in 1987 and 1997 16 The PM NAAQS have always included some type of a primary standard to protect 17 against effects associated with exposures to thoracic co arse particles. In 1987, when EPA first 18 revised the PM NAAQS, EPA changed the indicat or for PM from Total Suspended Particles 19 (essentially applicable to particles smaller than 25-45 micrometers) to focus on inhalable 20 particles, those which can pene trate into the trachea, bronchi , and deep lungs (52 FR 24634). 21 EPA changed the PM indicator to PM 10 based on evidence that the ri sk of adverse health effects 22 associated with particles of 10 micrometers or le ss was significantly greater than that associated 23 with larger partic les (52 FR at 24639). 24 In the 1997 review, in conjunction with es tablishing new fine particle (i.e., PM 2.5 ) 25 standards (see above, sections 1.2.3, 2.1.1), EPA c oncluded that continued protection remained 26 warranted against potential effects associated with thoracic coarse particle s in the size range of 27 2.5 to 10 μm. This conclusion was based on par ticle dosimetry, toxicological information, and 28 on limited epidemiologic evidence from studies that measured PM 10 in areas where coarse 29 particles were likely to dominate the dist ribution (62 FR 38677, July 18, 1997). Thus, EPA 30
concluded that the PM 10 standards would provide protection against effects associated with 31 particles in the narrower size range of 2.5 to 10 μm. Although a more narrowly defined indicator 32 was considered in that review (i.e., PM 10-2.5 ), EPA concluded that it wa s more appropriate, based 33 on existing evidence, to continue to use PM 10 as the indicator for sta ndards to control thoracic 34Draft Do Not Quote or Cite March 2010 3-3 coarse particles. This decision was based, in part, on the recognition th at the only studies of 1 clear quantitative relevance to hea lth effects most likely associated with thoracic coarse particles 2
used PM 10 in areas where the coarse fraction was the dominant fraction of PM 10 , namely two 3
studies conducted in areas that su bstantially exceeded the 24-hour PM 10 standard (62 FR 38679). 4 In addition, this decision reflected the fact that there were only very limited ambient air quality 5 data then available specifically for thoracic coarse particles, in contrast to the extensive 6 monitoring network alre ady in place for PM 10, Therefore, it was more administratively feasible 7
to use PM 10 as an indicator. EPA also stated that the PM 10 standards would work in conjunction 8
with the PM 2.5 standards by regulating the portion of particulate pollu tion not regulated by the 9

PM 2.5 standards. 2 10

3.1.1.2 Review Completed in 2006 11 In the review of the PM NAAQS that c oncluded in 2006, EPA considered the growing, 12 but still limited, body of evidence supporting associations between health effects and thoracic 13 coarse particles measured as PM 10-2.5
. 3 The new studies available in the 2006 review included 14 epidemiologic studies that reported associations w ith health effects using direct measurements of 15

PM 10-2.5 , as well as dosimetric and toxicological studies. In light of this growing body of 16 evidence, staff concluded that it was appropriate to revise the PM 10 standards and to base any 17 revised standards principally on available evidence and ai r quality information for PM 10-2.5 . Staff 18 also concluded that it was appropriate to c onsider evidence from studies that measured PM 10 in 19 locations where the majority of PM 10 was in the PM 10-2.5 fraction (US EPA, 2005, section 5.4.1) 20 and that the level of protection afforded by the existing 1987 PM 10 standard remained 21

2 As explained in chapter 1, in May 1998, a three-judge pa nel of the U.S. Court of A ppeals for the District of Columbia Circuit found "ample support" for EPA's decision to regulate coarse particle pollution, but vacated the 1997 PM 10 standards, concluding that EPA had failed to adequately explain its choice of PM 10 as the indicator for thoracic coarse particles pointing to the lack of reason ed explanation for the variable level of allowable concentrations of thoracic coarse particles (varying by levels of PM 2.5 ) and the consequent double regulation of PM 2.5 . American Trucking Associations v. EPA , 175 F. 3d 1027, 1054-56 (D.C. Cir. 1999).. The court also rejected considerations of administrative feasibility as justificatio n for a NAAQS, which are based exclusively on health and welfare considerations. Id. at 1054. Pursuant to the court’s decision, EPA removed the vacated 1997 PM 10 standards from the Code of Federal Regulations (CFR) (69 FR 45592, July 30, 2004) and deleted the regulatory provision [at 40 CFR section 50.6(d)] that controlled the transition from the pre-existing 1987 PM 10 standards to the 1997 PM 10 standards (65 FR 80776, December 22, 2000). The pre- existing 1987 PM 10 standards remained in place.Id. at 80777. As noted in chapter 1 and in more detail above, in the 2006 review of the PM NAAQS, EPA readdressed the appropriateness of using PM 10 as an indicator for a standard m eant to protect against exposures to thoracic coarse particles, and the decision to use PM 10 as the indicator was upheld on judicial review. American Farm Bureau Federation v. EPA , 559 F. 3d 512, 533-38 (D.C. Cir. 2009).
3 The PM Staff Paper (US EPA, 2005) also presents resu lts of a quantitative assessment of health risks for PM 10-2.5 . However, staff concluded that the nature and magnitude of the uncertainties and concerns associated with this risk assessment weighed against its use as a basis for recomme nding specific levels for a thoracic coarse particle standard.Draft Do Not Quote or Cite March 2010 3-4 appropriate (US EPA, 2005, p. 5-67). Responding to CASAC a dvice, staff also recommended 1
that the indicator for thoracic coar se particles be urban coarse pa rticles in the si ze range of 10-2.5 2 micrometer range, thus focusing on those thoracic coarse particles that are generally present in 3 urban environments (US EPA, 2005, p. 5-71). The agency proposed to retain a standard for a 4 subset of thoracic coarse part icles, proposing a qualified PM 10-2.5 indicator to focus on the mix of 5 thoracic coarse particles genera lly present in urban environments . More specifically, the revised 6 thoracic coarse particle standard would have applied only to an ambient mix of PM 10-2.5 that is 7 dominated by resuspended dust from high-density traffic on paved roads a nd/or by industrial and 8
construction sources. The revised standard woul d not have applied to any ambient mix of PM 10- 9

2.5 that is dominated by rural windb lown dust and soils. In additi on, agricultural sources, mining 10 sources, and other similar sources of crustal materi al would not have been subject to control in 11 meeting the standard (71 FR 2667 to 2668, January 17, 2006). 12 The Agency received a large number of comm ents that were overwhelmingly opposed to 13 the proposed qualified PM 10-2.5 indicator (71 FR 61188 to 61197). Af ter careful consideration of 14
the scientific evidence and th e recommendations contained in th e 2005 Staff Paper, the advice 15 and recommendations from CASAC, the public co mments received regarding the appropriate 16 indicator for coarse particles, and after extensiv e evaluation of the alternatives available to the 17 Agency, the Administrator decided it would not be appropriate to adopt a qualified PM 10-2.5 18 indicator. Underlying this determination was the decision that it was requisite to provide 19 protection from exposure to all thoracic coarse PM , regardless of its orig in, rejecting arguments 20
that there are no health effects from community-level exposures to coarse PM in non-urban areas 21 (71 FR 61189). The EPA concluded that dos imetric, toxicologi cal, occupational and 22 epidemiologic evidence supported re tention of a primary standard for short-term exposures that 23 included all thoracic coarse part icles (i.e. both urban and non-urba n), consistent with the Act’s 24 requirement that primary NAAQS provide an ade quate margin of safety. Given the serious 25 potential effects, the large numbers of persons exposed, and the need for a standard to provide an 26 adequate margin of safety, the agency concluded it was appropriate to retain a standard applying 27 to all coarse particles (71 FR 61197). At the same time, the agency concluded that the standard 28 should target protection toward urban areas, wher e the evidence of health effects from exposure 29
to PM 10-2.5 was strongest (71 FR at 61193, 61197). The pr oposed indicator was not suitable for 30 that purpose. Not only did it in appropriately provide no protecti on at all to many areas, but it 31 failed to identify many areas where the ambi ent mix was dominated by coarse particles 32 contaminated with urban/industrial types of coarse particles for which evidence of health effects 33 was strongest (71 FR 61193). 34Draft Do Not Quote or Cite March 2010 3-5 The agency ultimately concluded that the existing indicator, PM 10 , was most consistent 1 with the evidence. Although PM 10 includes both coarse and fine PM, it remained an appropriate 2 indicator for thoracic coarse part icles because fine particle leve ls are generally higher in urban 3 areas and, therefore, a PM 10 standard set at a single unvarying level will generally result in lower 4
allowable concentrations of thor acic coarse particles in urban areas than in non-urban areas. 5 This was considered to be an appropriate targeti ng of protection given that the strongest evidence 6 for effects associated with thoracic coarse pa rticles came from epidemiologic studies conducted 7
in urban areas and that elevated fine particle concentrations in urban areas could result in 8
increased contamination of co arse fraction particles by PM 2.5 , potentially increas ing the toxicity 9 of thoracic coarse particles in urban areas (71 FR 61195-96). Given the evidence that the 10 existing PM 10 standard afforded requisite protection with an ample margin of safety, the Agency 11
retained the level and form of the 24-hour standard. 4 12 The Agency also revoked the annual PM 10 standard, in light of the conclusion in the PM 13 Criteria Document (US EPA, 2004) that the avai lable evidence does not s uggest an association 14 with long-term exposure to PM 10-2.5 and the conclusion in the Sta ff Paper (US EPA, 2005) that 15 there is no quantitative evidence that dire ctly supports an annual standard. 16 In the same rulemaking, EPA also included a new Federal Reference Method (FRM) for 17
the measurement of PM 10-2.5 in the ambient air (71 FR 61212 to 61213). Although the standards 18 for thoracic coarse particles do not use a PM 10-2.5 indicator, the new FRM for PM 10-2.5 was 19 established to provide a basis for approving Federal Equivalent Methods (FEMs) and to promote 20 the gathering of scientific data to suppor t future reviews of the PM NAAQS. 21

3.1.2 Litigation of 2006 Final Rule for thoracic coarse particles 22 A number of groups filed suit in response to the final decisions made in the 2006 review. 23
See American Farm Bureau Federation and th e National Pork Producers Council v. EPA (DC 24 Cir. 2009). Among the petitions for review were challenges from industry groups on the 25
decision to retain the PM 10 indicator and the level of the PM 10 standard and from environmental 26 and public health groups on the decision to revoke the annual PM 10 standard. The court upheld 27 both the daily PM 10 standard and the decision to revoke the annual standard. 28 First, the court upheld EPA’s decision for a standard to cover all thoracic coarse PM,, 29 both of urban and non-urban origi n. The court rejected argument s that the evidence showed 30 there are no risks from exposure to non-urban co arse PM. The court further found that EPA had 31
a reasonable basis not to set se parate standards for urban and non-urban coarse PM, namely the 32

4 Thus, the level of 150 μg/m 3 is met when this level is not exceeded more than once per year on average over a three-year period measured at each monitor within an area.Draft Do Not Quote or Cite March 2010 3-6 inability to reasonably define what ambient mi xes would be included under either ‘urban’ or 1 ‘non-urban;’ and that the eviden ce in the record supported EPA’ s cautious decision to provide 2 “some protection from exposure to thoracic coarse particles... in all areas.” 559 F. 3d at 532-33. 3 Specifically, the court stated, 4
5 Although the evidence of danger from coarse PM is, as EPA recognizes, 6 “inconclusive,” (71 FR 61193, October 17, 2006), the agency need not wait for 7 conclusive findings before regulating a pollutant it reasonably believes may pose 8 a significant risk to public health. The evidence in the record supports the EPA’s 9 cautious decision that “some protection from exposure to thoraci c coarse particles 10 is warranted in all areas.” Id. As the court has consistently reaffirmed, the CAA 11 permits the Administrator to “err on the side of caution” in setting NAAQS

. 12 559 F. 3d at 533. 13 14 The court also upheld EPA’s decision to re tain the level of th e standard at 150 μg/m 3 and 15
to use PM 10 as the indicator for a standa rd meant to protect against exposures to thoracic coarse 16 particles. In upholding the level of the standard, the court referre d to the conclusion in the Staff 17 Paper that there is “little basis for concludi ng that the degree of pr otection afforded by the 18
current PM 10 standards in urban areas is greater than warranted, since potential mortality effects 19 have been associated with air quality levels not allowed by the current 24-hour standard, but 20 have not been associated with air quality levels that would generally m eet that standard, and 21 morbidity effects have been associated with ai r quality levels that exceeded the current 24-hour 22 standard only a few times.” 559 F. 3d at 534. The court also rejected arguments that a PM 10 23 standard established at an unvarying level will re sult in arbitrarily varyin g levels of protection 24 given that the level of coarse PM would vary ba sed on the amount of fine PM present. The court 25 agreed that the variation in allowable coarse PM accorded with the strength of the evidence: 26 typically less coarse PM would be allowed in urban areas (where levels of fine PM are typically 27 higher), in accord with the stronge st evidence of health effects fr om coarse particles. 559 F. 3d 28 at 535-36. In addition, such regulation would not impermissibly double regulate fine particles, 29 since any additional regulation of fine part icles (beyond that afforded by the primary PM 2.5 30 standard) would be for a different purpose; to prevent contaminat ion of coarse particles by fine 31 particles. 559 F. 3d at 535, 536. These same explanations explained the choice of PM 10 as an 32 indicator, and provided the reason ed explanation for that choice lacking in the record for the 33
1997 standard. 559 F. 3d at 536. 34 With regard to the challenge from envir onmental and public health groups, the court 35 upheld EPA’s decision to revoke the annual PM 10 standard. Specifically, the court stated, 36Draft Do Not Quote or Cite March 2010 3-7 The EPA reasonably decided that an annual coarse PM standard is not necessary 1 because, as the Criteria Document and th e Staff Paper make clear, the latest 2 scientific data do not indicat e that long-term exposure to coarse particles poses a 3 health risk. The CASAC also agreed th at an annual coarse PM standard is 4
unnecessary. 5 559 F. 3d at 538-39. 6 7

3.1.3 Approach in the Current Review 8 The staff’s approach in this review is consis tent with the approaches ultimately taken in 9 previous reviews. We have taken into acc ount evidence-based considerations, including 10
consideration of the uncertainties associated with the evidence, to inform our preliminary 11
conclusions related to the adequacy of the current PM 10 standard and potential alternative 12 standards. In so doing, we are seeking to provide as broad an array of options as is supportable 13 by the available evidence, recognizing that the selection of a specific approach to reaching final 14 decisions on the primary PM 10 standard will reflect the judgme nts of the Administrator as to 15 what weight to place on differe nt aspects of the evidence and associated uncertainties. As 16
discussed in more detail in the Quantitative Health Risk Assess ment for Particulate Matter – 17 Second External Review Draft (second draft RA, US EPA, 2010a), we have not conducted a 18 quantitative assessment of health risks associated with PM 10-2.5 . Staff concluded that limitations 19 in the monitoring network and in the health studi es that rely on that monitoring network, which 20 would be the basis for characterizing PM 10-2.5 exposures and risks, would introduce significant 21 uncertainty into a PM 10-2.5 risk assessment such that the risk estimates generated would be of 22 limited utility in informing review of the standard . Therefore, staff conc luded in the second draft 23 RA that a quantitative risk assessment for PM 10-2.5 is not supportable at this time (US EPA, 24 2010a, p. 2-6). 25 For the purposes of this first draft Policy Assessment (PA), we have drawn from the 26 assessment and integration of the studies evaluated in the Integrated Science Assessment for 27 Particulate Matter (Final Report) (ISA, US EPA, 2009a). The discussions presented in this 28 chapter consider evidence from epidemiologic st udies, controlled human exposure studies, and 29 toxicological studies evaluating s hort- or long-term exposures to thoracic coarse particles; as 30 discussed in chapters 6 and 7, re spectively, with supporting inform ation related to dosimetry and 31 potential mode of action (MOA) evidence as presen ted in chapters 4 and 5, respectively, as well 32 as the integration of evidence across disciplin es presented in chapter 2 of the ISA. 33 With respect to these evidence-based considerations, we have considered causal 34
inferences identified in the ISA based on consid eration of the body of scientific evidence for 35 effects related to short- and long-term PM 10-2.5 exposures. In considering these causal inferences, 36Draft Do Not Quote or Cite March 2010 3-8 we take into account evidence of effects for which the reported associations provide suggestive 1
evidence of a causal association. In considering the evidence, we have relied most heavily on the 2 epidemiologic evidence, includ ing our understanding of air quality distributions of PM 10-2.5 and 3

PM 10 present during the times of the studies. While being mindful of the inherent limitations and 4 uncertainties in the currently available evidence , we have developed prel iminary conclusions as 5 to the adequacy of the current 24-hour PM 10 standard to protect against health effects associated 6 with exposure to PM 10-2.5 and the degree to which alternativ e standards could be expected to 7 protect against the reported health effects. 8 In focusing on the key policy-relevant questions by which we have structured the 9 current review, our preliminary conclusions reflect upon our understanding of evidence-based 10
considerations to inform two ove rarching questions rela ted to: (1) the adequa cy of the current 24- 11
hour PM 10 standard to protect against e ffects associated with exposure to thoracic coarse particles 12 and (2) what potential alternative standard(s), if any, should be cons idered in this review. In 13 addressing these broad questions, we have orga nized the discussions below around a series of 14 more specific questions reflecting different aspects of each overarching question. When 15 evaluating the health protection a fforded by the current or any a lternative standards considered, 16
we have taken into account the four basic el ements of the NAAQS (e.g., indicator, averaging 17 time, level, and form). 18 We believe that the approach outlined a bove, when presented in the final PA, will 19 provide a comprehensive basis to help inform the judgments required of the Administrator in 20 reaching decisions about the curren t and potential alternative prim ary standards meant to protect 21 public health against exposures to thoracic coarse particles. 22

3.2 ADEQUACY OF THE EXISTING PM 10 STANDARD 23 In considering the adequacy of the current 24-hour PM 10 standard to protect against 24 effects associated with exposur es to thoracic coarse particles, staff addresses the following 25 overarching question: 26

Does the currently available scientific evidence, as reflected in the ISA, support or call into 27 question the appropriateness of maintaining a st andard to protect against effects associated 28 with exposure to thoracic coarse particles and the adequacy of the protection afforded by 29 the current 24-hour PM 10 standard against those effects? 30

To inform our consideration of this ov erarching question, we consider below the 31 evidence for a link between thoracic coarse partic le exposures and advers e health effects (3.2.1), 32 including the evidence for the link between PM 10-2.5 and mortality and morbidity; impacts on 33 susceptible populations; evidence for PM 10-2.5 -related health effects in locations that meet the 34Draft Do Not Quote or Cite March 2010 3-9 current PM 10 standard; and uncertainties in the evidence. Preliminary staff conclusions 1 regarding the adequacy of the current standard ar e presented in section 3.2.2. In considering the 2 scientific information, we reflect upon both the information available in the last review and 3 information that is newly available since the la st review as assessed and presented in the ISA 4 (US EPA, 2009a). 5

3.2.1 Evidence of Effects Related to Am bient Thoracic Coarse Particles 6 In the 2006 review of the PM NAAQS, th e AQCD (US EPA, 2004, p. 9-48) concluded 7 the following regarding thor acic coarse particles: 8
9
For PM 10‐2.5 , less evidence is available [than for PM 2.5 or PM 10 ], but the 10 studies using short‐term exposure s have reported results that a re of the 11 same magnitude as those for PM 10 and PM 2.5 , though less often statistically 12 significant and thus having less strength, and the associations are generally 13 robust to alternative modeling s trategies or consideration of p otential 14 confounding by co‐pollutants. This evidence is suggestive of as sociations for 15 morbidity with short‐term changes in PM 10‐2.5

. 16 17 In contrast, the AQCD concluded that “[l]ittle evidence is available to allow conclusions 18 to be drawn about long-term PM 10-2.5 exposures and morbidity” (US EPA, 2004, p. 9-46). In 19 considering these conclusions, the Administrator judged that “short-term exposure to thoracic 20 coarse particles can have an important public health impact” and that available evidence 21 “suggests that there is a lack of such effects associated with long-term exposure to thoracic 22 coarse particles” (71 FR 61185/1, October 17, 2006) . As noted above, the Administrator judged 23 that the then-existing bo dy of scientific evidence supported reta ining a standard to protect against 24
health effects associated with s hort-term exposures to all thoracic coarse particles. Specifically, 25 the Administrator noted the following (71 FR 61185/1): 26
27
EPA continues to believe that the health evid ence, including dosimetric, toxicologic, and 28 epidemiologic study findings, supports retaini ng a standard to prot ect against effects 29 associated with short-term exposure to thor acic coarse particles. As noted above and 30 summarized in section III.A of the propos al, there is a growing body of evidence 31 suggesting causal associations between short-term exposure to thoracic coarse particles 32 and morbidity effects, such as respirat ory symptoms and hospital admissions for 33 respiratory diseases, and possibly mortality. 34 35 I n considering the current body of scientific evid ence for health effects of thoracic coarse 36 particles, we have consider ed the following question: 37Draft Do Not Quote or Cite March 2010 3-10  To what extent does the newly available sc ientific evidence a nd related uncertainties 1 strengthen or call into question evidence of associations between ambient thoracic 2 coarse particle exposures and health effects? 3

W e note that since the conclusion of the last review, the Agency has developed a more 4 formal framework for reaching causal inferences from the body of scientific evidence, as 5
discussed above in section 2.2.1. Application of this framewor k draws upon the evaluation and 6 synthesis of evidence from across epidemiologic, controlled human exposure, and toxicological 7
studies. This framework uses a fi ve-level hierarchy that classifies the overall weight of evidence 8 and causality using the following categorizations: causal relations hip, likely to be a causal 9 relationship, suggestive of a causal relationship, inadequate to infer a causal relationship, and not 10 likely to be a causal relationship (ISA, section 1.5, Table 1-3). 11 Applying this framework to thoracic coarse pa rticles, the ISA concludes that the existing 12 evidence is suggestive of a causal relationship between short-term PM 10-2.5 exposures and 13 mortality, cardiovascular effects, and respir atory effects (US EPA, 2009a, section 2.3.3; see 14 Table 3-1 below). Several large multi-city epidemiologic studies, as well as a number of single15 city studies, have been conducted in the U.S. a nd Canada since the last review. These studies 16 have generally reported positive associations between ambient PM 10-2.5 and morbidity and/or 17 mortality (US EPA, 2009a, section 2.3.4). The pl ausibility of associations reported in these 18 epidemiologic studies is supported by some expe rimental evidence, primarily from controlled 19 human exposure studies of heart rate variability and pulmonary inflammation, and by dosimetry 20
studies which show that a la rge proportion of inhaled pa rticles in the 3-6 micron (d ae ) range can 21 reach and deposit in the lower respiratory tract, particularly the tracheobronchial (TB) airways 22 (ISA, Figures 4-3 and 4-4). 23 However, important uncertainties remain with regard to the interpretation of this 24 evidence. For example, experimental support fo r the associations reported in epidemiologic 25
studies has been somewhat limited. Controlled human exposure studies have not reported effects 26 of thoracic coarse particles on pulmonary e ndpoints including lung function or respiratory 27 symptoms. In addition, toxicologi cal studies have not generally assessed inhalation of thoracic 28 coarse particles due to th e technical challenges asso ciated with conducting a PM 10-2.5 inhalation 29 study in rodents. These studies have used intr atracheal instillation and so provide only limited 30 support for the biological plausibility of the asso ciations reported in epidemiologic studies (US 31 EPA, 2009a, section 2.3.4). Beyond the limitations in experimental support, limitations in the 32

PM 10-2.5 monitoring network, uncertainties in the ambient PM 10-2.5 concentrations reported in 33 epidemiologic studies, the relatively small number of epidemiologic studies that have evaluated 34 co-pollutant models to addre ss the potential for conf ounding by co-pollutants, variability in the 35Draft Do Not Quote or Cite March 2010 3-11 chemical and biological composition of PM 10-2.5 , and limited evidence regarding effects of the 1 various components of PM 10-2.5 , are also important sources of uncertainty (US EPA, 2009a, 2 sections 2.3.3, 2.3.4). 3 With respect to effects associated with long-term PM 10-2.5 exposures, the ISA concludes 4
that available evidence is inadequate to infer a causal relationship with all health outcomes 5 evaluated (US EPA, 2009a, secti on 2.3). Specifically, similar to the judgment made in the 6 AQCD (US EPA, 2004), the ISA states, “To date, a sufficient amount of evidence does not exist 7
in order to draw conclusions re garding the health eff ects and outcomes associated with long-term 8 exposure to PM 10-2.5 ” (US EPA, 2009a, section 2.3.4; see Table 3-1 below). 9
10 Table 3-1. Summary of Causality Determinations for PM 10-2.5 11
Exposure Duration Outcome Causal Determination Cardiovascular Effects Suggestive Respiratory Effects Suggestive Mortality Suggestive Short-term Central Nervous System Effects Inadequate Cardiovascular Effects Inadequate Respiratory Effects Inadequate Mortality Inadequate Reproductive and Developmental Effects Inadequate Long-term

Cancer Mutagenicity, Genotoxi city Effects Inadequate
Source: adapted from US EPA, 2009a; Table 2-6 12
13 Therefore, in considering the health evidence more specifically below we have focused on 14 mortality, cardiovascular effects, and respiratory effects associated with short-term exposures to 15 thoracic coarse particles. 16 Mortality 17 We note that, in the last review, a limited num ber of studies, mostly single-city analyses, 18
were evaluated that examined thoracic coarse PM for its association with mortality (US EPA, 19 2004). Of those studies, a small number examined both PM 2.5 and PM 10-2.5 effects, and reported 20
some evidence for PM 10-2.5 effects of the same magnitude as PM 2.5 . Studies conducted in 21 Phoenix (Mar et al., 2003) a nd Coachella Valley (Ostro et al., 2003) reported positive and 22 statistically significant associations between PM 10-2.5 and mortality while other single-city studies 23 reported PM 10-2.5 effect estimates that were positive, but not statistically significant. Multiple 24Draft Do Not Quote or Cite March 2010 3-12 limitations were identified in these studies incl uding measurement and exposure uncertainties for 1

PM 10-2.5 and the correlation between PM 2.5 and PM 10-2.5 . These limitations decreased the 2 precision of effect estimates and increased th e uncertainty surrounding th e concentrations at 3
which PM 10-2.5 -mortality associations were obser ved (US EPA, 2009a, section 6.5.2.3). 4
Evidence that has become ava ilable since the last review provides additional support for 5 the link between exposure to thoracic coarse particles and morta lity, though important 6 uncertainties remain regarding the extent to which PM 10-2.5 itself contributes to reported effects 7 and the thoracic coarse particle concentrations at which associations occur (discussed below in 8 more detail). The ISA assesses several recent st udies that have evaluated associations between 9 mortality and PM 10-2.5 , most of which have reported positiv e, and in some cases, statistically 10 significant PM 10-2.5 effect estimates (US EPA, 2009a, Figur e 6-30). This includes a recent U.S.- 11 based multicity study (Zanobetti a nd Schwartz, 2009) and a Canadi an multi-city study (Burnett 12 et al., 2004), both of which reported positive asso ciations (though in the case of the Canadian 13 study, not statistically significant) between PM 10-2.5 and mortality. In the U.S. study, a 14 significant association with PM 10-2.5 was reported for all-cause, car diovascular, and respiratory 15 mortality (US EPA, 2009a, section 6.5.2.3). The e ffect estimate for all-cause mortality remained 16 “relatively robust” (US EPA, 2009a, p. 6-82) and statistically significant in a two-pollutant 17
model that included PM 2.5 , while the effect estimates for cause-specific mortality remained 18 positive but not statistically significant. When examining the city-specific effect estimates for 19
the 47 cities included in the thoracic coarse particle analysis, statistically significant increases in 20 mortality were associated with PM 10-2.5 in St. Louis, MO; Salt Lake City, UT; Chicago, IL; 21 Pittsburgh, PA; Detroit, MI; and Birmingham, AL. Positive, but not statistically significant, 22 associations were reported for a ll cause and/or cause-sp ecific mortality in the remaining cities 23 (US EPA, 2009a, Figure 6-29). A number of additional studies have also reported positive, but 24 not significant, associations between PM 10-2.5 and mortality (US EPA, 2009a, Figure 6-30). 25 Considered as a whole, the ISA notes that epid emiologic studies that have evaluated thoracic 26 coarse particles have reported consis tent, positive associations between PM 10-2.5 and mortality 27 (US EPA, 2009a, section 6.5.2.3). 28
Cardiovascular effects 29 With regard to cardiovascular morbidit y, we note that the evidence evaluating 30
associations with short-term concentrations of PM 10-2.5 was limited in the last review. Single-city 31 epidemiologic studies found generally positive as sociations, with some reaching statistical 32 significance, between PM 10-2.5 and cardiovascular-related hospital admissions in Toronto 33 (Burnett et al., 1997; 1999) and Detroit, MI (Ito, 2003). In the Detroit study, the PM 10-2.5 effect 34 estimates for ischemic heart disease (IHD) remain ed positive and statistically significant in two- 35Draft Do Not Quote or Cite March 2010 3-13 pollutant models that included gaseous co-pollutants (US EPA, 2009a, Figure 6-5), while effect 1 estimates remained positive and relatively unchanged in magnitude, but not statistically 2 significant, for congestive heart fa ilure (CHF). Effect estimates in the Toronto study (Burnett et 3 al., 1997) were decreased and became non-signifi cant in two-pollutant models that included 4 gaseous co-pollutants (US EPA, 2009a, ISA, Figur e 6-5). In addition, on e study considered in 5 the last review reported a positive, but not signif icant, association between onset of myocardial 6 infarction (MI) and short-term PM 10-2.5 concentrations in Boston (Peters et al., 2001) and, 7 although not a study of PM 10-2.5 specifically, Schwartz et al . (1997) reported a statistically 8 significant association between PM 10 and increased hospitalizations for cardiovascular disease in 9 Tucson, AZ, an urban area where thoracic coarse pa rticles comprise a much greater fraction of 10

PM 10 than fine particles. No controlled human exposure or animal toxi cological studies of PM 10- 11

2.5 and cardiovascular endpoints were pres ented in the 2004 AQCD (US EPA, 2004). 12 In addition to these cardiovascular morbidity studies considered in the last review, the 13 ISA assesses a recent multi-city study evaluatin g hospital admissions and emergency department 14
visits for cardiovascular disease in Medicare patients (Peng et al., 2008). In this study of older 15 adults, the authors reported a positive and statis tically significant association between 24-hour 16

PM 10-2.5 concentrations and cardiovascular disease hos pitalizations in a single pollutant model 17 using air quality data for 108 U.S. coun ties with one or more co-located PM 2.5 and PM 10 18
monitors. The effect estimate was reduced onl y slightly, though it was no longer statistically 19 significant, in two-pollutant models that included PM 2.5 (US EPA, 2009a, sections 2.3.3, 20 6.2.10.9). In addition to this U.S. multi-city stud y, positive associations reported for short-term 21

PM 10-2.5 and cardiovascular morbidity reached stat istical significance in a multi-city study in 22 France (Host et al., 2007) and associations were positive, but often did not reach statistical 23 significance, in several other locat ions (US EPA, 2009a, Figures 6-1 to 6-3, 6-5). In considering 24 the available epidemiologic evidence, the ISA concludes that single- and multi-city 25 epidemiologic studies generally report pos itive associations between short-term PM 10-2.5 26 concentrations and hospital admissions or emergenc y department visits for cardiovascular causes 27 (US EPA, 2009a, section 2.3.3, 6.2.12.2). 28 The generally positive associations between PM 10-2.5 and cardiovascular morbidity 29 reported in these studies are supported by seve ral recent epidemiologic studies that have 30 examined dust storm events and reported incr eases in cardiovascular-related emergency 31 department visits and hospital admissions 5 ; by studies reporting positive associations with 32

5 Such dust storm studies are also important because they pr ovide evidence that cardiovas cular effects are associated with exposures to particles of non-urban origin. As discussed more fully below, this evidence has implications forDraft Do Not Quote or Cite March 2010 3-14 cardiovascular mortality; by reported associations with other cardiovascular health effects 1 including supraventricular ect opy and changes in heart rate va riability; and by a limited number 2 of controlled human exposure studies that have reported alterations in heart rate variability 3 following exposure to PM 10-2.5 (US EPA, 2009a, sections 2.3 .3, 6.2.12.2). As noted above, the 4 few toxicological studies that examined the effect of PM 10-2.5 on cardiovascular health effects 5
used intratracheal instillation and, as a result, provide only li mited evidence on the biological 6 plausibility of PM 10-2.5 induced cardiovascular effects (US EPA, 2009a, sections 2.3.3, 6.2.12.2). 7 Respiratory effects 8 With respect to respiratory effect s associated with short-term PM 10-2.5 exposures, we first 9 note that, in the last review, epidemiologic st udies reported generally positive associations 10
between PM 10-2.5 and respiratory-related hospitalizations or emergency department visits (e.g., 11 for pneumonia, chronic obstructive pulmonary dis ease, and respiratory diseases combined) (US 12 EPA, 2004). Support for these associations came fr om a small number of studies that examined 13 respiratory-related mortality and respiratory symptoms. Experimental evidence for respiratory 14
effects of PM 10-2.5 was limited to a few animal toxico logy studies and no controlled human 15 exposure studies. 16 In the current review, the ISA notes that a number of recent epidemiologic studies have 17 reported consistent, positive associat ions between short-term ambient PM 10-2.5 concentrations and 18 respiratory-related emergency department vi sits and hospital admissions (US EPA, 2009a, 19 section 2.3.3). In a French multi-city study (Host et al., 2008), 24-hour ambient PM 10-2.5 20 concentrations were positively associated w ith respiratory-related hospital admissions among 21 children, with an effect estimate larger than that for PM 2.5 . A U.S. multi-city study of Medicare 22 patients (Peng et al., 2009) reported a positive, but not statistically signifi cant, effect estimate for 23 respiratory-related hospital admissions. A number of additional, mostly single-city, studies have 24 also reported positive, and in some cases statistically significant, PM 10-2.5 effect estimates for 25 respiratory-related hospital admissions and emerge ncy department visits (ISA, Figures 6-10 to 6- 26 15). In epidemiologic studies of respiratory effects, the strongest relationships with PM 10-2.5 27 were observed among children, with less consistent evidence for adults and older adults (i.e., age 28 65 and older) (US EPA, 2009a, section 2.3.3.1). A limited number of epidemiologic studies 29 have focused on specific respiratory morbid ity outcomes and found no evidence of an 30 association with lower respiratory sympto ms, wheeze, and medication use (US EPA, 2009a, 31 sections 2.3.3.1 and 6.3.1.1). While controlled hu man exposure studies have not observed an 32

decisions on the appropriateness of the current PM 10 standard as well as on the ch oice of indicator for thoracic coarse particles.Draft Do Not Quote or Cite March 2010 3-15 effect on lung function or respirat ory symptoms in healthy or asth matic adults in response to 1 short-term exposure to PM 10-2.5 , healthy volunteers have exhibite d an increase in markers of 2 pulmonary inflammation. Toxicologi cal studies using inhalation e xposures are still lacking, but 3 pulmonary injury and inflammation has been obser ved in animals after intratracheal instillation 4 exposure (US EPA, 2009a, section 6.3.5.3) and, in some cases, PM 10-2.5 was found to be more 5 potent than PM 2.5
. 6
Some studies of PM 10-2.5 and respiratory morbidity have investigated potential 7 confounding by co-pollutants through the applicat ion of co-pollutant models (US EPA, 2009a, 8 section 6.3.8.5, Figure 6-15). Several of these st udies have reported posi tive and statistically 9 significant PM 10-2.5 effect estimates in co-pollutant mode ls that included gaseous pollutants (e.g., 10 Lin et al., 2002; Yang et al., 2004; Chen et al., 2005; Lin et al ., 2005). Several other studies 11 report that PM 10-2.5 effect estimates remain positive, though no t always statistically significant, in 12 co-pollutant models that in clude gaseous pollutants or PM 2.5 (US EPA, 2009a, Figure 6-15). 13 Summary 14 In considering the extent to which newly availa ble scientific evidence strengthens or calls 15 into question evidence of associations identified in the last review between ambient thoracic 16 coarse particle concentrations and adverse health effects, we recognize that the available 17 epidemiologic and experimental evidence now in cludes several recent multi-city epidemiologic 18 studies conducted in the U.S., Canada, and Eu rope which have reported associations of PM 10-2.5 19 with cardiovascular and respiratory morbidity and mortality, several studies of dust storm events 20 reporting associations with part icles of non-urban origin, as well as some controlled human 21 exposure studies reporting effects of PM 10-2.5 exposure on heart rate variability and pulmonary 22
inflammation. While uncertainties identified in th e last review remain (see below), these recent 23 studies provide important information not avai lable in that review on the link between PM 10-2.5 24 and mortality and morbidity, and they have br oadened our understandin g of this link with 25 particles from different types of sources and in a variety of locations. Thus, our preliminary 26
conclusion is that there is a dditional support, beyond that ava ilable in the last review, for 27
associations between adverse hea lth effects (mortality, morbidity ) and short-term exposures to 28

PM 10-2.5 from a broad mix of sources and a variety of locations. 29 Having reached this preliminary conclusion, we then consider how the new evidence 30 informs our understanding of susceptible populations by asking the following question: 31

 To what extent does the newly available sc ientific evidence expand our understanding 32 of susceptible populations, including identi fication of new susceptible populations? 33 Our understanding of populations that are more susceptible to PM exposures is discussed 34 above in chapter 2 (section 2.2.1). This includes populations that have a greater likelihood of 35Draft Do Not Quote or Cite March 2010 3-16 experiencing health effects rela ted to exposure to PM due to a variety of factors including, but 1 not limited to, genetic or developmental factors, race, gender, life stage, lifestyle (e.g., smoking 2 status and nutrition), preexist ing disease, or population-level factors that can increase an 3 individual's exposure to PM (e.g., socioeconomic status, reduced access to health care, low 4 educational attainment, residen tial location). Although these studi es have primarily evaluated 5 exposures to PM 2.5 or PM 10 , the available evidence suggests that the identified factors may also 6 enhance susceptibility to PM 10-2.5 (US EPA, 2009a, section 2.4.1). Given this, the discussion in 7 section 2.2.1 of this document, which summarizes the evidence from the ISA as well as staff 8 considerations and conclusions on susceptible po pulations, will not be repeated here. Rather, 9 with regard to PM 10-2.5 , we note the overall conclusion from the ISA that “the epidemiologic, 10 controlled human exposure, and toxi cological studies evaluated in this review provide evidence 11 for increased susceptibility for various populatio ns, including children a nd older adults, people 12 with pre-existing cardiopulmonary diseases, a nd people with lower SES” (US EPA, 2009a, p. 2- 13 24). As discussed in more detail in secti on 2.2.1, these populations, whic h are of particular 14 concern with regard to effects linked to PM e xposures, are similar to the at-risk populations 15
considered in the last re view of the PM NAAQS. 16
We next consider how the available eviden ce informs our understanding of air quality 17 concentrations associated with mortality a nd morbidity by asking the following question: 18

 To what extent does the newly available scie ntific evidence report associations that 19 extend to air quality levels that are lower than had previously been observed or that are 20 observed in areas that wo uld likely meet the current PM 10 standard? 21 As discussed in more detail in chapter 2, th e ISA concluded that there is no evidence to 22 support the existence of a discernable threshol d below which PM-associat ed effects would not 23 occur (US EPA, 2009a, section 2.4.3). Therefore, when considering the level of protection 24 provided by the current 24-hour PM 10 standard against exposures to thoracic coarse particles, we 25
consider whether available evidence provides support fo r associations between PM 10-2.5 and 26 mortality or morbidity in locations with PM 10 concentrations that would be allowed by the 27
current 24-hour PM 10 standard. In this secti on, in considering air quality concentrations at which 28 health effects have been reported, we have focused on effects for which the evidence is 29 suggestive of a causal relationship, as described in the ISA. Where sufficient air quality data are 30 available, we have evaluated air quality concen trations using the form of the current 24-hour 31

PM 10 standard. 6 32

6 The current form of the 24-hour PM 10 standard is one expected exceedance per year, averaged over 3 years.Draft Do Not Quote or Cite March 2010 3-17 In the last review of th e PM NAAQS, the Staff Paper (US EPA, 2005; section 5.4.1) 1 noted that statistically significant associations between thoracic coarse particles and mortality 2 had been reported in studies conducte d in areas that did not meet the PM 10 standard during the 3 time periods of the studies, including Phoenix (Mar et al., 2000, 2003), Coachella Valley, CA 4 (Ostro et al., 2000, 2003), and Steubenville (as part of the Harvard Six Cities study, Schwartz et 5 al., 1996; Klemm et al., 2003). In contrast, the St aff Paper noted that “[i]n areas with lower 6

PM 10-2.5 concentrations, no statistically significant a ssociations were reported with mortality, 7 though many were positive but not statistical ly significant” (US EPA, 2005, p. 5-49). 8 The Staff Paper also noted that epidemiologic studies of PM 10 , in areas where PM 10 is 9 typically dominated by the coarse fraction, provided additional s upportive evidence for 10
associations between coarse frac tion particles and health effects in areas with concentrations 11 generally not meeting the PM 10 standard levels. Th ese studies included re ports of associations 12 with hospitalization for cardiovascular diseases in Tucson, AZ (Schwartz, 1997); hospitalization 13 for chronic obstructive pulmonary disease in Re no/Sparks, NV (Chen et al ., 2000); medical visits 14 for asthma or respiratory diseases in Anchor age, AK (Gordian et al ., 1996; Choudhury et al., 15 1997); and significant associations with mort ality, respiratory hospital admissions, and 16 respiratory symptoms in the Utah Valley area (e.g., Pope et al., 1989; 1991; 1992). 17
We have re-examined the issue of the PM 10 concentrations at which associations between 18

PM 10-2.5 and mortality and morbidity have been reporte d in light of currently available evidence 19 and air quality information. In so doing, we have characterized PM 10 concentrations reported in 20 EPA’s Air Quality System (AQS) 7 from several U.S. study locations (see US EPA, 2009a, 21 Figure 2-3). Specifically, consistent with the form of the current PM 10 standard, we consider the 22 second highest 24-hour average PM 10 concentration for each year of the study, from each 23 monitoring site in the study lo cation. In an attempt to gain insight into whether the PM 10 air 24 quality concentrations in a pa rticular study location were abov e or below those allowed by the 25 current standard, we compare these second highest 24-hour PM 10 concentrations to the level of 26 the standard, 150  g/m 3

. 8 27

PM 10 concentrations from U.S. study locations where positive and statistically significant 28

PM 10-2.5 effect estimates have been reported (e.g., US EPA, 2009a, Figures 2- 3; 6-5; 6-24; 6-30) 29 are presented in Table 3-2 below for Detroit (Lippman, 2000; Ito et al., 2003; Zanobetti and 30 Schwartz, 2009), Phoenix (Mar et al., 2003), Seattle (Sheppard, 2003), Birmingham (Zanobetti 31

7 http://www.epa.gov/ttn/airs/airsaqs/detaildata/downloadaqsdata.htm

8 We recognize that this is not the exact approach taken in making attainment and non-attainment designations for the PM 10 standard, which also involves estimating expected exc eedances for areas with less than daily monitoring, but it does provide important insights into the PM 10 air quality in study areas, and into whether measured PM 10 air quality concentrations would, or would not, be permitted under the current standard.Draft Do Not Quote or Cite March 2010 3-18 and Schwartz, 2009), Coachella Valley (Ostro et al., 2003), Chicago (Zanobetti and Schwartz, 1 2009), Pittsburgh (Zanobetti and Schwartz, 2009), Salt Lake City (Zanobetti and Schwartz, 2 2009), and St. Louis (Zanobe tti and Schwartz, 2009). 9 3
4
5
Table 3-2. PM 10 Concentrations in Cities wi th Statistically Significant PM 10-2.5 Effect 6
Estimates 7
City Second highest 24-hour PM 10 concentration for each study location and study year (  g/m 3 )

Year 1 Year 2 Year 3 Year 4 Year 5 Year 6 Year 7 Year 8 Year 9 Year 10 Birmingham 152 157 130 160 178 166 179

Coachella

Valley 576 278 189 108 91 84 133 155 157 114 Chicago 120 123 124 106 103 84 88

Detroit (Zanobetti and

Schwartz) 126 113 114 96 157 139 87

Detroit (Lippman; Ito) 10 107 113 129

Pittsburgh 120 123 133 107 145 153 142

Phoenix 160 130 301 Salt Lake City 113 117 156 123 209 149 123

Seattle 134 138 140 131 114 119 83

St. Louis 91 92 186 224 161 191 196
8
9 Of these cities for which positive and statistically significant PM 10-2.5 effect estimates 10 have been reported, PM 10 concentrations in Birmingham, Phoenix, and St. Louis were higher 11 than allowed by the current PM 10 standard during most of the st udy periods and concentrations in 12 Coachella Valley were higher than allowed during about half of the study period. In contrast, 13
ambient PM 10 concentrations were below those allowed by the current standard during the entire 14

9 We have evaluated air quality in study locations for whic h single-city effect estimates are presented and for which air quality data during the study period are available. So me important U.S. multi-city st udies (e.g., Peng et al., 2008) are not included in Tabl e 3-2 because they did not present single-city effect estimates. We also note that there are several key studies conducted in Canadian cities; howe ver, we were unable to obtain air quality information for individual monitors in these study locations.
10 These studies in Detroit presented effect estim ates for two separate time frames. Because PM 10 FRM/FEM data is not available prior to 1988, we have focused here on the latter time frame used in the studies (1992-1994).Draft Do Not Quote or Cite March 2010 3-19 study periods for the studies conducted in Chicag o, Detroit, Seattle, and Pittsburgh and during 1 most of the study period in Salt Lake City. 11 2
We also note that two of the studie s included in Table 3-2 evaluated PM 10-2.5 effect 3 estimates in co-pollutant models . Specifically, as discussed a bove, the associations reported by 4 Ito et al. (2003) for PM 10-2.5 and pneumonia hospital admissions in Detroit remained after 5 adjustment for gaseous co-pollutants. In addition, the ISA reported that the overall PM 10-2.5 6 effect estimate for all-cause mortality in th e multi-city study by Zanobetti and Schwartz (2009), 7 which included Chicago, Detroit, Seattle, Pitt sburgh, and Salt Lake City, remained “relatively 8 robust” (US EPA, 2009a, p. 6-82) and statistically significant in a two-pollutant model that 9
included PM 2.5 , though co-pollutant models were not reported for indivi dual cities. As indicated 10 in the ISA (Figure 6-15), seve ral other studies (e.g., those co nducted in Canada) have also 11 reported robust and statistically significant PM 10-2.5 effect estimates in co-pollutant models, 12 however, we were unable to obtain air quality data for these other study lo cations and, therefore, 13 as described above, they were not included in Table 3-2. 14 In addition to the statistically significant resu lts in the cities noted above, several studies 15 have reported positive, but not statistically significant, PM 10-2.5 effect estimates in locations with 16

PM 10 concentrations below those allowed by the cu rrent standard. Specifically, Zanobetti and 17 Schwartz (2009) reported positive PM 10-2.5 effect estimates for mortality in cities with a range of 18

PM 10-2.5 concentrations, even down to the lowest PM 10-2.5 concentrations estimated in the study 19 (ISA, figure 6-29). Many of these cities, wher e positive associations with mortality were 20 reported, attained the current PM 10 standard during the time period of the study. 12 In addition, 21 Fairley et al. (2003) reported a positive, but not statistically significant, association between 22

PM 10-2.5 and mortality in Santa Clar a County, CA (ISA, Figure 6- 30). Though some 24-hour 23

PM 10 concentrations in this location did exceed 150  g/m 3 (i.e., authors report concentrations up 24

to 165  g/m 3 ), an analysis of Santa Clara air qualit y during the study period reveals that the 2 nd 25 highest 24-hour PM 10 concentration did not exceed 150  g/m 3 during any of the study years 26 (range was 58-147  g/m 3 ). Peters et al. (2001) reporte d a positive, but not statistically 27 significant, association between PM 10-2.5 and hospital admissions for myocardial infarction in 28

11 We considered the number of times per year that 24-hour PM 10 concentrations exceeded 150  g/m 3 . For the studies in Chicago, Detroit, Seattle, and Pittsburgh, the average number of days per year with 24-hour PM 10 concentrations above 150  g/m 3 did not exceed 1 for any 3-year period. For Salt Lake City, year 3 of the study had 2 exceedances of 150  g/m 3 and year 5 had 3 exceedances. Therefore, the average number of exceedances over years 3-5 was greater than 1. The average over other 3 year periods during the study did not exceed 1.
12 See http://www.epa.gov/oaqps001/greenbk/pindex.html for information on attainment status of specific locations and http://www.epa.gov/airtrends/values.html for information on design values for PM.Draft Do Not Quote or Cite March 2010 3-20 Boston, a location where the 2 nd highest 24-hour PM 10 concentration did not exceed 150  g/m 3 1 during either of the study years (52 and 80  g/m 3 ). 2
A series of studies conducted in Atlant a have reported mixed results, but none 3 statistically significant, for PM 10-2.5 and mortality and respiratory -related emergency department 4 visits. Specifically, Klemm et al . (2004), Metzger et al. (2004), P eel et al. (2005), and Tolbert et 5 al. (2007) reported both positive and negative PM 10-2.5 effect estimates for mortality and 6 emergency department visits (ISA, Figure 2-3). The 2 nd highest 24-hour PM 10 concentrations in 7 a year over the range of years encompa ssed by these studies did not exceed 150  g/m 3 8 (maximum was 111  g/m 3 ). 9
Summary 10
When viewed as a whole, these U.S. studies provide evidence for associations between 11
ambient PM 10-2.5 concentrations and increased mortality and morbidity in several locations with 12
ambient PM 10 concentrations below those allowed by the current PM 10 standard. Staff’s 13 preliminary conclusions regarding the potential implications of th ese studies for a decision on the 14 adequacy of the current PM 10 standard are discussed below. 15 We next consider the important uncertainti es in the available evidence by asking the 16 following question: 17

 What are the important uncertainties associat ed with the currently available scientific 18 evidence that should be considered in e valuating the adequacy of the current PM 10 19 standard? Have these uncertainties changed or been reduced since the last review? 20 The majority of the health evidence supporting the link between thoracic coarse particle 21 exposures and adverse cardiovascul ar and respiratory effects comes from epidemiologic studies. 22 Staff notes that, while several ne w studies have become available since the last review, little 23 progress has been made in reducing some of the impor tant uncertainties inhere nt in these studies. 24 These uncertainties, and their implications for in terpreting the scientific evidence, are discussed 25
below in more detail. 26 The ISA (sections 2.3.3, 2.3.4) concludes that an important uncertainty in the PM 10-2.5 27 epidemiologic literature is that associated with the air quality estimates used in these studies. 28 Specifically, the ISA concludes that there is greate r error in estimating ambi ent concentrations of 29

PM 10-2.5 than in estimates for PM 2.5 and, therefore, that such uncertain ty is a particularly relevant 30 consideration when interpreting PM 10-2.5 epidemiologic studies. Contri buting to this uncertainty 31 is the relatively limited spatial coverage provided by existing PM 10-2.5 monitors (US EPA, 2009a, 32 sections 2.2.3, 2.3.3, 2.3.4). Currently, a national network to monitor PM 10-2.5 is not in place, 33 limiting the spatial area over which PM 10-2.5 concentrations are measured. Specifically, of the 34Draft Do Not Quote or Cite March 2010 3-21 3,225 counties in the U.S., only 40 (1%), incor porating less than 5% of the population, met 1 completeness and co-location criteria during the years 2005-2007, allowi ng analysis of PM 10-2.5 2 air quality in the ISA (US EPA, 2009a, sect ion 3.5.1.1). In addition, based on the limited 3 available evidence, the ISA concluded that “t here is greater spatial variability in PM 10-2.5 4
concentrations than PM 2.5 concentrations, resulting in increased exposure error for the larger size 5 fraction” (US EPA, 2009a, p. 2-8) and that available measurements do not provide sufficient 6 information to adequately characte rize the spatial di stribution of PM 10-2.5 concentrations (US 7 EPA, 2009a, section 3.5.1.1). As noted in the ISA, these limitations in estimates of ambient 8

PM 10-2.5 concentrations “would tend to increase uncerta inty and make it more difficult to detect 9
effects of PM 10-2.5 in epidemiologic studies” (US EPA 2009a, p. 2-21). 10 Uncertainty also results from the diff erent approaches taken to estimate PM 10-2.5 11 concentrations in epidemiologi c studies. The ISA notes thatambient concentrations of PM 10-2.5 12 are generally determined by the subtraction of PM 2.5 from PM 10 measurements, with different 13 studies using different methods. For example, one important multi-city study (e.g., Peng et al., 14 2008) estimated PM 10-2.5 by taking the difference between collocated PM 10 and PM 2.5 monitors 15 while another important multi-city study (e.g., Zanobe tti and Schwartz, 2009) used the difference 16 between county average PM 10 and PM 2.5 concentrations. A small number of studies have 17 directly measured PM 10-2.5 concentrations with dichotomous samplers (e.g., Burnett et al., 2004; 18 Villeneuve et al., 2003; Klemm et al., 2004) . It is not clear how computed PM 10-2.5 19 measurements, such as those used by Za nobetti and Schwartz, compare with the PM 10-2.5 20
concentrations obtained in other studies eith er by direct measurement with a dichotomous 21 sampler or by calculating the difference using co-located samplers (US EPA, 2009a, section 22 6.5.2.3). 13 Given the use of these differe nt approaches to estimating PM 10-2.5 concentrations 23 across studies, and their inherent limitations, the distributions of thoracic coarse particle 24 concentrations over which reported health ou tcomes occur remain highly uncertain. 25 The ISA also notes that the potential for c onfounding by co-occurring pollutants has been 26 addressed in only a relatively small number of PM 10-2.5 epidemiologic studies, introducing 27 additional uncertainty into the in terpretation of these studies (US EPA, 2009a , section 2.3.3). As 28 discussed above, most studies that have evalua ted co-pollutant models have reported that PM 10- 29

2.5 effect estimates remain positive, but often lose precision and become statistically non30 significant (US EPA, 2009a, Figures 6-5, 6-9, 6- 15). In the U.S. mu lti-city study by Zanobetti 31 and Schwartz (2009) effect estimates for all-cause mortality remained statis tically significant in a 32

13 In addition, when the difference between PM 2.5 and PM 10 is calculated, the potential for differences among operational flow rates and temperatures for PM 10 and PM 2.5 monitors add to the potential for exposure misclassification.Draft Do Not Quote or Cite March 2010 3-22 two-pollutant model that included PM 2.5 while effect estimates for cause-specific mortality 1 remained positive but were not statistically significant. Effect estimates for PM 10-2.5 were also 2 positive, but not statistically significant, in co-pollutant models that included PM 2.5 in the studies 3 by Peng et al. (2008) (car diovascular and respiratory hospital admissions) and Chen et al. (2004) 4 (respiratory hospital admissions). In the Canadi an multi-city study by Burnett et al. (2004) the 5

PM 10-2.5 effect estimates for respiratory-related ho spital admissions remained positive, but not 6 statistically significant, in a co-pol lutant model that also included NO 2 , though the PM 10-2.5 effect 7 estimate remained statistically si gnificant in co-pollutant models with other gaseous pollutants. 8 In other studies (e.g., see Li n et al., 2002; Ito et al., 2003; Chen et al., 2005) PM 10-2.5 effect 9 estimates remained relatively unchanged, and in some cases statistically significant, in co10 pollutant models that incl uded gaseous pollutants. 11
Summary 12
As discussed above, important uncertainties remain in the eviden ce for associations 13
between PM 10-2.5 and mortality and morbidity. In consid ering these uncertainties, we reach the 14 preliminary conclusion that, although a number of studies have been conducted since the last 15 review, the important uncertainties present in that review remain. The implications of these 16 uncertainties for decisions on the adequacy of the PM 10 standard are discussed below. 17

3.2.2 Preliminary Staff Conclusion s on Adequacy of Current PM 10 Standard 18 Collectively, taking into consideration the responses to specific questions focusing on 19 different ways to inform a decision on the adequacy of the current 24-hour PM 10 standard , we 20 revisit the overarching question: 21

 Does the currently available sc ientific evidence, as reflect ed in the ISA, support or 22 call into question the appropriateness of ma intaining a standard to protect against 23 effects associated with exposure to thoracic coarse particles and the adequacy of the 24 protection afforded by the current 24-hour PM 10 standard against those effects? 25 As an initial matter, we note that the current PM 10 standard is meant to protect the public 26 health against effects associat ed with exposures to all PM 10-2.5 . As discussed above, this was 27 judged in the last review to be appropriate given the “growing body of evidence suggesting 28 causal associations between short-term exposur e to thoracic coarse particles and morbidity 29 effects, such as respiratory symptoms and hos pital admissions for respiratory diseases, and 30 possibly mortality” (71 FR 61185, October 17, 2006). In considering the currently available 31
scientific evidence on thoracic co arse particles, we conclude that newly available studies 32
conducted since the last review of the PM NA AQS strengthen this conclusion. As discussed 33Draft Do Not Quote or Cite March 2010 3-23 above, the newly available epidemiologic and expe rimental evidence, combined with evidence 1 available in the last review, includes the following: 2

 Several multi-city epidemiologic studies conducted in the U.S., Canada, and Europe 3 which have reported associations of PM 10-2.5 with cardiovascula r and respiratory 4 morbidity and mortality 5

 Studies that have reported that PM 10-2.5 effect estimates remain positive, and in some 6 cases statistically significant, in co-pollutant models 7

 Studies that have reported positive associations between dust storm events and 8 cardiovascular effects, broadening the avai lable evidence for associations between 9 adverse health effects and particles from a variety of sources, including non-urban 10

sources 11

 Controlled human exposure studies of heart ra te variability and pulmonary inflammation. 12
13
While uncertainties identified in the last revi ew remain, these recent studies support those 14
available in the last review and provide important information on the link between PM 10-2.5 and 15 cardiovascular and respiratory effects, including mortality. In addition, se veral recent dust storm 16 studies provide evidence not available in the last review regarding associ ations between particles 17 of non-urban origin and adverse heal th effects. Therefore, consiste nt with the previous reviews, 18 we judge that it is appropriate to maintain a sta ndard to protect the public health against effects 19 associated with exposures to all thoracic coarse particles. 20 In drawing preliminary conclusions regardi ng the adequacy of the level of protection 21 afforded by the current PM 10 standard, we have considered the ambient PM 10 concentrations in 22 locations where epidemiologic studi es of thoracic coarse particles have been conducted as well 23
as the uncertainties associated with the broader body of scientific eviden ce. Specifically, we 24
note that several recent U.S. studies have re ported generally positive, and in some cases 25 statistically significant, PM 10-2.5 effect estimates in locations with 24-hour PM 10 concentrations 26 below those permitted by the current standard. This includes single-city and multi-city studies, 27 and studies that have reported that PM 10-2.5 effect estimates remain positive, and in some cases 28 robust and statistically significant, in co-pollutant models. As described above, the decision in 29 the last review to retain the existing PM 10 standard was based, in part , on the conclusion that the 30 strongest evidence for the link between PM 10-2.5 and health effects came from studies conducted 31
in locations with PM 10 concentrations above those allowed by the standard. Given that recent 32 epidemiologic studies have repor ted statistically significant PM 10-2.5 effect estimates in several 33
locations with PM 10 concentrations below those allowed by the standard, a similar conclusion 34 would not be supported by the currently available ev idence. Therefore, to the extent that the 35Draft Do Not Quote or Cite March 2010 3-24 approach to considering the adequacy of the curr ent standard in this review is similar to the 1 approach used in the last review, it would be appropriate to conclude that the current 24-hour 2

PM 10 standard does not provide adequa te public health protection and that it should be revised in 3 order to increase protection agai nst effects associated with sh ort-term exposures to thoracic 4 coarse particles. If this appr oach to considering the evidence were adopted, a conclusion that the 5 current standard is not adequate could be supported by the following observations: 6

 A number of epidemiologic studies have reported positive, and in some cases 7 statistically significant, PM 10-2.5 effect estimates for mortality and morbidity in a variety 8 of locations, including in seve ral U.S. cities with 24-hour PM 10 concentrations below 9 those allowed by the current PM 10 standard. 10

 Studies that have evaluate d co-pollutant models have generally reported that PM 10-2.5 11 effect estimates remain robust and, in so me cases, statistically significant when PM 2.5 12 or gaseous co-pollutants ar e added to the model. 13

 Uncertainties in the extent to which ambient PM 10-2.5 concentrations used in 14 epidemiologic studies reflect population expos ures tend to bias the results of those 15 studies toward the null hypothesis. Therefore, given limitations in PM 10-2.5 monitoring, 16 the generally positive PM 10-2.5 effect estimates reported across epidemiologic study 17 locations, even in locations for which eff ect estimates were not significant, provide 18 evidence for associations between PM 10-2.5 and mortality and morbidity. 19

 Controlled human exposure studies and, to a le sser extent, animal toxicological studies 20 have reported cardiovascular and respirator y effects following exposures to thoracic 21 coarse particles, thereby providing some s upport for the biological plausibility of the 22 associations reported in epidemiologic studies. 23

24 However, as discussed above, a decision on th e adequacy of the level of public health 25 protection provided by the current PM 10 standard will be a public health policy judgment in 26 which the Administrator weighs the available ev idence and its inherent uncertainties. Thus, 27 depending on the emphasis placed on different aspects of the evidence and its associated 28 uncertainties, different conclusions could be supported. Specific ally, as discussed above, we 29 note that many of the important uncertainties from the last review remain. In considering the 30 evidence as well as these uncertainties, the ISA c oncluded that the eviden ce is “suggestive” of a 31 causal relationship between short-term PM 10-2.5 exposures and mortality, cardiovascular effects, 32 and respiratory effects. These conclusions c ontrast with those for associations between PM 2.5 33 and health effects, which were judged to be e ither “causal” or “likely causal” for mortality and 34 cardiovascular and respiratory effects a ssociated with short- and long-term PM 2.5 exposures. 35 Among the specific uncertainties noted in the ISA (US EPA, 2009a, sections 2.3.3, 2.3.4) are the 36 following: 37Draft Do Not Quote or Cite March 2010 3-25  Limited monitoring for PM 10-2.5 results in uncertainty in the ambient PM 10-2.5 1 concentrations at which effects reported in epidemiologic studies occur. 2

 The number of epidemiologic studies that have employed co-pollutant models to 3 address the potential for confounding remains re latively limited. Therefore, the extent 4 to which PM 10-2.5 itself contributes to repor ted health effects, rather than one or more 5 co-pollutants, remains uncertain. 6

 Only a limited number of experimental stud ies provide support for the associations 7 reported in epidemiologic studies. 8

 The chemical and biological composition of PM 10-2.5 , and the effects associated with 9 the various components, remains uncertain. 10

11 To the extent a decision on the adequacy of the current PM 10 standard were to emphasize the 12
uncertainties that contributed to the ISA conclu sion that the evidence is “suggestive” of a causal 13 relationship for PM 10-2.5 , rather than indicating a “likely cau sal” or “causal” relationship, it would 14
be reasonable to conclude that the availabl e evidence does not provide a basis for reaching a 15 fundamentally different conclusion from the one r eached in the previous review (i.e., to retain 16
the current 24-hour PM 10 standard). Therefore, our prelimin ary conclusion is that the available 17 evidence could support either revising the current PM 10 standard to increase public health 18 protection against exposures to thoracic coarse particles or retaining the current PM 10 standard, 19 depending on the emphasis placed on different aspects of the evidence and associated 20
uncertainties. 21

3.3 CONSIDERATION OF POTENTIAL ALTERNATIVE STANDARDS 22 Having reached the conclusion that, dependi ng on the approach to considering the 23 available evidence, the adequacy of the current 24-hour PM 10 standard to protect against effects 24 associated with exposures to thoracic coarse particles could be calle d into question, staff 25 considers a second overarching question: 26

What alternative standard(s) to protect against exposures to PM 10-2.5 could be supported by 27 the currently available scie ntific evidence, as reflected in the ISA? 28

To inform the answer to this overarching question, we consider how the currently 29
available scientific evidence could inform decisi ons regarding the basic elements of the NAAQS: 30 indicator (section 3.3.1), averagi ng time (section 3.3.2), and form and level (section 3.3.3). In 31 considering the appropriateness of potential alternative standards, we consider both the evidence 32
available in the last review a nd the evidence that is newly avai lable since the last review, as 33 assessed and presented in the ISA (US EPA, 2009a). 34Draft Do Not Quote or Cite March 2010 3-26 3.3.1 Indicator 1 As noted in section 3.2 of the ISA, unlike gaseous pollutants such as O 3 , SO 2 , and CO, 2 “which are well-defined chemical entities, atmos pheric PM varies in size, shape, and chemical 3 composition” (US EPA, 2009a, p. 3-1). The selection of PM 10 as an indicator of thoracic 4 particles was originally based in large part on dosimetry (U .S. EPA, 1996a) with evidence 5 suggesting that a large proportion of i nhaled coarse particles in the 3-6 μ m (d ae ) range can reach 6 and deposit in the lower respirat ory tract, particularly the trac heobronchial airways, while the 7 fraction deposited decreases as particle size in creases (US EPA, 2009a, Figures 4-3 and 4-4). 8 Currently, it is most common to use PM 10 as an indicator of thoracic particles and PM 10-2.5 as an 9 indicator of the thoracic component of coarse particles, sometimes referred to as thoracic coarse 10 particles. As such, the majority of available he alth evidence for coarse particles links health 11
effects to PM 10-2.5 and/or PM 10 . As discussed in section 3.1.1, in the review of the PM NAAQS 12 completed in 1997, and again in the review comp leted in 2006, EPA concluded that the purpose 13
of the PM 10 standard would be to provide protecti on against effects associated with PM 10-2.5
. 14
This section considers the issue of the appropriate indicator fo r a standard meant to protect 15 against exposures to thoracic coarse particles. Considerations rela ted to indicator in the review 16 completed in 2006 are discussed in section 3.3.1.1; evidence-based considerations to inform our 17 understanding of indicator in th e current review are discussed in section 3.3.1.2; and preliminary 18 staff conclusions regarding indicato r are discussed in section 3.3.1.3. 19

3.3.2 Consideration of Indicator in the Review Completed in 2006 20 In the last review, the Admini strator’s decision on the indicator for a standard meant to 21 protect against exposures to thoracic coarse par ticles took into consider ation the potential for 22 particles originating in different types of envi ronments (i.e., urban versus non-urban), and with 23 different compositions, to possess di fferent degrees of toxicity. At the time, most of the studies 24 supporting the link between exposure to thoracic coar se particles and advers e health effects had 25 been conducted in urban locations. Epidemiologi c studies had reported positive, and in some 26 cases statistically significant, a ssociations between ambient con centrations of thoracic coarse 27 particles and adverse health effect s in studies conducted in cities both inside and outside the U.S. 28 In contrast, very little evidence was available to sugge st that thoracic coar se particles from non29 urban areas posed a threat to human health and a few studies reported th at exposure to crustal 30
material from non-urban locations di d not result in the types of ef fects that had been linked with 31 exposures to urban particles. Specifically, several t oxicological studies reported that volcanic 32 ash from Mt. St. Helens (an exam ple of natural crustal material of geologic origin) caused 33 very little toxicity in animal or in vitro model systems (e.g., see US EPA, 2005, section 5.4.2.1 34Draft Do Not Quote or Cite March 2010 3-27 for discussion).  In addition, an epidemiologic study in Spokan e, WA specifically assessed 1 whether mortality was increased on dust‐storm days using case‐c ontrol analysis methods. 2 The average PM 10 concentration on dust storm days was more than 200 μ g/m 3 higher than on 3 control days; however, the authors reported no ev idence of increased mortality on these specific 4 days (Schwartz et al., 1999). In addition, studie s conducted in several area s in the western U.S. 5 reported that associations between PM 10 and mortality or morbidity remained unchanged or 6 became larger and more precise when days indicative of wind-blown dust were excluded from 7 the analyses (Pope et al., 1999; Schwartz, 1997; Chen et al., 2000; Hefflin et al., 1994). In the 8 last review, this group of studies was interpreted as suggesting that health effects associated 9 with thoracic coarse particles a re not driven by the types of n atural crustal materials that 10 would typically form a major fraction of coarse particles in no n‐urban or rural areas. 14 11 In 2006, the Administrator noted that the apparent differences in toxicity of 12 particles from urban versus non‐urban locations could result from the different contaminants 13 present in urban versus non-urban environmen ts. Specifically, he stated the following 14
15 [T]he observed toxicity of coarse particles in urban and industrial areas comes from the 16 kind of coarse particles found in these environments, for example direct emissions from 17 industrial sources or materials released to ro ad dust from motor ve hicles such as brake 18 and tire wear, as well as from the contaminati on of coarse particles that can occur. This 19 contamination can come from both mobile and st ationary sources. In particular, specific 20 components, such as byproducts of incomplete combustion ( e.g. polycyclic aromatic 21 hydrocarbons) most commonly emitted from mo tor vehicles and other sources in the 22 form of PM 2.5 , as well as metals and other contaminants emitted from other 23 anthropogenic sources, appear in higher levels in urban areas (EPA, 2004a, p. 8–344; 71 24 FR 2665). Many of these contaminants in PM 10–2.5 come originally from fine particles, 25 which may become attached in the atmosphere or be deposited and mixed into coarse 26 materials on the ground. Thus the greater the concentration of PM 2.5 , with higher levels 27 typically found in urban areas, the greater the level of contam ination of coarse particles 28 by fine particles. This contamination increa ses the potential health risk posed by those 29 coarse particles. For that reason, it is logi cal to allow lower levels of coarse particles 30 when fine particle concentrations are high (71 FR 61196, October 17, 2006). 31 32 Given the available evidence and the above c onsiderations, the Administrator judged in 33 the last review that two primary objectives were appropriate to consider when making a decision 34 on the standard indicator. Specifically, give n the preponderance of evidence from studies 35 conducted in urban areas, the Administrator judged it appropriate to have the level of protection 36 reflect the varying degree of pub lic health concern presented by the different ambient mixes of 37

14 Although Ostro (2003) found that rural coarse particles prim arily of crustal origin were associated with mortality effects, as noted by both CASAC and the Administrator (71 FR 61190).Draft Do Not Quote or Cite March 2010 3-28 thoracic coarse particulate matter by allowi ng lower ambient thoracic coarse particle 1
concentrations in locations with higher fine particle concentra tions (e.g., urban areas, where the 2 evidence indicates the public health risks to be significant) and higher concentrations of ambient 3 thoracic coarse particles in locations with lo wer fine particle concen trations (e.g., non-urban 4 areas, where the evidence related to thoracic coar se particles is more limited). In addition, 5 though there was little evidence at the time to sugge st that thoracic coarse particles in non-urban 6 locations posed a threat to huma n health, the Administrator judged that, given uncertainties in the 7 interpretations of some of th e studies of non-urban particles, 15 it was appropriate to take a 8 cautious approach by setting a standard that provides some measure of protection against 9 exposures to all ambient mixes of thoracic coarse partic les, regardless of source of origin or 10 composition (71 FR 61197/3). 11
The Administrator evaluated several differe nt potential indicators by considering the 12
extent to which each would contribute to ac hieving these objectives. Specifically, the 13
Administrator considered a PM 10-2.5 indicator, either qualified so as to exclude some sources and 14 locations (see below) or unqualified with no such exclusions, and a PM 10 indicator, either 15 adjusted to account for the PM 2.5 component of PM 10 or unadjusted. Each of these options, and 16
the Administrator’s consideration of them in the last review, is discussed below. 17 In considering the extent to which a PM 10–2.5 indicator would achieve the objectives for 18 public health protection described above, the Admi nistrator evaluated both a qualified indicator, 19 which would have exempted specific sources (e.g., agricultural and mining sources) and/or 20 locations (e.g., rural areas), and an unqualified indicator. With re gard to the qualif ied indicator, 21
the Administrator concluded that , although it would permit the level of protection to reflect the 22 varying degree of public health concern presente d by the different ambien t mixes of thoracic 23 coarse particles, it would clea rly not meet the goal of providi ng some measure of protection 24 against all ambient mixes of thoracic coarse par ticles for the evident reason that it would have 25 explicitly excluded certain types of sources and locations. In contrast, with regard to the 26 unqualified indicator the Administ rator noted that, though it woul d provide protection against 27 exposures to all ambient mixes of thoracic coarse particle s, “if such an indicator were utilized as 28 part of a standard with a single unvarying level, it would not reflect th e critical difference in 29 evidence regarding the relative publ ic health risks associated w ith urban and non-urban thoracic 30 coarse particles” (71 FR 61195). That is, he concl uded that if the level were selected to provide 31 appropriate protection against eff ects associated with exposure to the ambient mixes typical of 32

15 The final decision in the review completed in 2006 noted that uncertainties in interpreting these and other studies relevant to the consideration of effect s associated with non-urban particles (e .g., changing activity patterns on high dust days in epidemiologic studies) suggested that it remained appropriate to provide some measure of protection against all thoracic coarse particles, even those from non-urban areas.Draft Do Not Quote or Cite March 2010 3-29 urban or industrial areas, the standard could be judged to be more stringe nt than necessary to 1 protect against effects associated with expos ure to the ambient mixes in non-urban areas. 2 Conversely, if a less stringent level were adopted on the grounds that there is less certainty that 3 the ambient mix in non-urban areas poses a health ri sk, then the standard could be judged not to 4 provide sufficient protection from the ambient mix found in urban or industrial areas. In both 5
instances a PM 10-2.5 standard could be judged not to be requisite (i.e

. , ‘‘not lower or higher than is 6 necessary’’ Whitman , 531 U.S. at 476.) to protect the public health with an adequate margin of 7 safety. In considering a potential approach to addressing this issue, the Administrator also 8
concluded that it would not be appropriate to set different PM 10-2.5 standard levels for urban 9 versus non-urban locations given the “lack of evidence to support es tablishing specific 10 quantitative distinctions in le vel based on variations in co arse particle composition and 11 differential toxicity” (71 FR 61195). Given all of these considerati ons, the Administrator 12
concluded that it would not be appropriate to set a standard with a PM 10-2.5 indicator at the time 13
of the last review. 14 In considering the extent to which a PM 10 indicator would achieve the objectives for 15 public health protection described above, the Admini strator evaluated both an adjusted indicator, 16
to account for the PM 2.5 component of PM 10 , and an unadjusted indicator. For the adjusted 17 indicator, the mass of PM 2.5 monitored in excess of the 24-hour standard for PM 2.5 would have 18
been subtracted from monitored PM 10 mass in order to avoid the double regulation of PM 2.5 in 19
the situations where this would have had the mo st regulatory consequence. Under this option, on 20 days when the measured concentration of PM 10 exceeded the level of the standard and the 21
measured concentration of PM 2.5 exceeded the level of the 24-hour PM 2.5 standard, the amount of 22

PM 2.5 in excess of the 24-hour PM 2.5 standard would have been subtracted from the total PM 10 23 mass (71 FR 61197). This option was judged by the Administrator to not be appropriate for two 24 reasons. First, as noted above, the Administra tor had determined that there should be less 25 allowable coarse particulate matter as PM 2.5 levels increase because these are the conditions 26
under which PM 10–2.5 tends to become more contaminated and could become more harmful. 27 Furthermore, this indicator would have inapprop riately relaxed the level of protection afforded 28 by the existing 24-hour PM 10 standard because it would have allowed higher total PM 10 levels on 29 days with high PM 2.5 levels. This indicator was thus di rectionally backwards; it decreased 30 protection when conditions warranted increase d protection. For both of these reasons, the 31 Administrator rejected the adjusted PM 10 indicator. 32
In his final decision in the review completed in 2006, the Administrator judged that the 33
continued use of the una djusted and unqualified PM 10 indicator was appropriate for a standard 34 meant to protect against effects associated with exposures to PM 10-2.5 . In reaching this judgment, 35Draft Do Not Quote or Cite March 2010 3-30 the Administrator concluded that the PM 10 indicator appropriately maintains some protection 1
from all ambient mixes of thoracic coarse particles and provides a le vel of protection that reflects 2 the varying degree of public health concern presented by th e different ambient mixes. 3 Specifically, the Administrator noted that both PM 2.5 and PM 10-2.5 contribute to PM 10 mass. 4 Therefore, he noted that that the PM 10 standard would be expected to allow lower concentrations 5 of thoracic coarse particle s in locations with high er concentrations of PM 2.5 (i.e., urban areas) 6 and higher concentrations of thor acic coarse particles in locations with lower concentrations of 7

PM 2.5 (i.e, non-urban areas). As discussed above , this was judged appropriate because the 8 available evidence indicated the potential for si gnificant public health risks associated with 9 exposures to thoracic coarse part icles in urban areas, which gene rally have higher fine particle 10 concentrations than rural areas, but provided mu ch less certainty regard ing risks in non-urban 11

areas. 12
Given the Administrator’s conclu sion that these elevated fine particle concentrations in 13 urban locations could result in greater fine particle contamination of coarse particles resulting in 14 increased potential health risks posed by coarse particles in urban areas, he noted the following: 15
16 To the extent that use of a PM 10 indicator would result in any reduction in PM 2.5 17 concentrations in an area, this would reduce the pote ntial health risk from coarse particles 18 in the area as well. There is no certainty that the contribution of PM 2.5 to the health risk 19 associated with exposure to contaminated coarse particles woul d be appropriately 20 addressed through the fine particle standards alon e. Thus, to the extent that the inclusion 21 of the PM 2.5 fraction in the PM 10 indicator amounts to double regulation of PM 2.5 , its 22 inclusion is non-duplicative and reasonable (71 FR 61196). 23 24 In reaching these judgments on the standard in dicator, the Administrator recognized that 25 the relationship between allowabl e thoracic coarse particle con centrations and fine particle 26 concentrations is qualitative. That is, the varying coarse part icle concentrati ons allowed under 27
the PM 10 standard do not precisely correspond to the likely variations in toxicity of thoracic 28 coarse particles in different areas. However, the Administrator concluded that, while currently 29 available information does not allow a more pr ecise adjustment for re lative toxicity, the PM 10 30 standard is expected to generally ensure that th e coarse particle levels allowed will appropriately 31 be lower in urban areas and highe r in non-urban areas. Given all of the above considerations, the 32 Administrator judged in th e last review that the unqualified and unadjusted PM 10 indicator was 33 appropriate for a standard meant to protect against exposures to PM 10-2.5
. 16 34

16 As discussed above (section 3.1.2), this decision was upheld on review by the D.C. Circuit, which endorsed every aspect of the Administrator’s rationale in reaching its decision. 559 F. 3d at 533-538.Draft Do Not Quote or Cite March 2010 3-31 3.3.3 Evidence-Based Consideration of Indicator in the Current Review 1 In the current review, in considering potential alternative standards, we have considered 2 the following question with regard to indicator: 3

 To what extent does the currently availabl e information provide support for retaining 4 or revising the current PM 10 indicator? 5 As in the last review, a critical issue in se lecting an appropriate indicator for a standard 6 meant to protect against exposures to thoracic coarse particle s remains the extent to which 7 available evidence supports the appropriateness of a standard that allows lower concentrations of 8

PM 10-2.5 in urban areas than rural areas. In consider ing this issue, we note that the ISA assesses 9 several epidemiologic studies of s hort-term exposures to thoracic co arse particles that have been 10 conducted since the last review (US EPA, 2009a, Ch apter 6). Similar to the studies considered 11 in the previous review, as described above in more detail, most of these more recent studies have 12
been conducted in urban locations in the U.S ., Canada, and Europe. However, a few recent 13 studies have examined the health impacts of dust storm events, where crustal material was 14 generally indicated using PM 10 (US EPA, 2009a, section 6.2.10.1). Specifically, a study of a 15 dust storm in the Gobi desert, which transpor ted PM across the Pacific Ocean reaching the 16 western U.S. in the spring of 1998, reported no excess risk of cardiac or respiratory hospital 17 admissions in the population of British Columb ia’s Lower Fraser Valley despite hourly PM 10 18 concentrations greater than 100 μ g/m 3 and daily average concentra tions several times greater 19
than normal (Bennett et al., 2006). In cont rast, Middleton et al. (2008) re ported that dust storms 20 in Cyprus were associated with a 4.7% ( 95% CI: 0.7-9.0) and 10.4% (95% CI: -4.7 to 27.9) 21 increase in risk of hospitaliza tion for all causes and cardiovascular disease, respectively. PM 10 22 concentrations in this study were much higher than typically reported in non-dust storm studies, 23 with hourly PM 10 concentrations during dust storms frequently approaching 300 to 400  g/m 3 24 and a maximum 24-hour average PM 10 concentration during the study almost 10-fold higher than 25
the level of the current PM 10 standard (i.e., 1,371  g/m 3 ). In addition, Chan et al. (2008) studied 26
the effects of Asian dust storms on cardiovascul ar hospital admissions in Taipei, Taiwan and 27 reported significant adverse effects during 39 Asian dust events. Daily PM 10 concentrations 28
exceeded 150  g/m 3 on several occasions during the st udy period and reached a maximum of 29
between 200 and 250  g/m 3 (see Figure 1 in Chan et al., (2008 )). Bell et al. (2008) analyzed 30 these data independently and conc luded that Asian dust storms we re positively associated with 31 risk of hospitalization for ischemic heart disease. In addition, Yang et al. (2009) reported that 32 hospitalizations for congestive h eart failure were elevated dur ing or immediately following 54 33 Asian dust storm events, though effect estimates we re not statistically si gnificant. Maximum 24- 34Draft Do Not Quote or Cite March 2010 3-32 hour PM 10 concentrations were not reported but th e mean 24-hour concentration due to dust 1

storm events was 112  g/m 3 . In a dust storm study where PM 10-2.5 was specifically evaluated, 2

Perez et al. (2008) tested the hypothesis that outbreak s of Saharan dust exacer bate the effects of 3

PM 10-2.5 on daily mortality in Spain. During Saharan dust days, the PM 10-2.5 effect estimate was 4 larger than on non-dust days, and it became statistically significant whereas it was not 5 statistically significant on non-dust da ys. On Saharan dust days, mean PM 10-2.5 concentrations 6 were about 10% higher than on non-Saharan dust da ys. Several animal toxicological studies 7 have also reported that exposure to PM 2.5 from dust storms increased pulmonary inflammation 8 and blood pressure (Lei et al., 2004; Chang et al., 2007; US EPA, 2009a, sections 6.2.5.3, 9 6.3.3.3). 10 In considering the implications of these studies for a decision on the indicator of a 11 standard meant to protect against exposures to th oracic coarse particles, we first consider the 12 following question: 13

 To what extent is it appropriate to maintain an indicator that provides some measure of 14 protection against all thoracic coarse particles? 15 With regard to this question, we note that, though most of the evidence for associations 16 with morbidity and mortality continues to come from studies conducted in urban areas, 17 17 associations reported in a small number of r ecent dust storm studies suggest that caution is 18 warranted in drawing conclusions about the relative t oxicity of thoracic co arse particles from 19
urban versus non-urban environments. These stud ies of dust storm events , discussed above, raise 20 credible concerns regarding the potential for non-urban pa rticles to cause adverse health effects, 21 though the dust storm-related PM 10 concentrations tend to be higher than those in many locations 22
where recent U.S. and Canadian studie s have reported associations with PM 10-2.5 . At a minimum, 23
these recent dust storm studies indicate that e xposure to relatively high concentrations of non24 urban particles is associated with health effects that are similar to those that, in other studies, 25 have been associated with urban particles. 26 Given the above considerations, as an initia l matter we reach the preliminary conclusion 27 that, for a standard meant to protect against e xposures to thoracic coarse particles, it remains 28 appropriate to provide some m easure of protection ag ainst exposures to al l ambient mixes of 29 thoracic coarse particles, regardless of their source of origin or composition. In drawing this 30 preliminary conclusion, we recognize the results of epidemiologic studie s assessed in the ISA, 31 which have reported positive, and in some cases statistically significant, effect estimates for 32

17 Though in some cases study locations extended into ar eas surrounding urban centers and likely included some non-urban (e.g., suburban) areas.Draft Do Not Quote or Cite March 2010 3-33 thoracic coarse particles in a variety of locations, including st udies of dust storm events where 1 high particle concentrations were due to windblown crustal material. We also recognize that the 2 causality judgments for thoracic coarse pa rticles in the ISA were made for “PM 10-2.5 as a whole 3 regardless of origin, since PM 10-2.5 -related effects have been de monstrated for a number of 4 different environments” (US EPA, 2009a, p. 2-19). Given these considerations, we note that 5
either a PM 10 or a PM 10-2.5 indicator would be expected to pr ovide protection against all ambient 6 mixes of thoracic coarse pa rticles, as long as these indicators were not qualified so as to exclude 7 certain types of sources or locations. 8 In addition, we have considered the follo wing question with regard to indicator: 9

 To what extent does it remain appropriate to draw distinctions between thoracic coarse 10 particles from urban and non-urban enviro nments when making a decision on the 11 indicator for a standard meant to protect against exposures to those particles? 12 In considering this question, we note that r ecent studies do provide some evidence for the 13 toxicity of particles from a va riety of environments, including particles of non-urban origin. 14 Given these studies, it could be judged reasonable to adopt an indicator that does not allow 15 different concentrations of thoracic coarse part icles in urban and rural areas. As discussed 16 above, a PM 10-2.5 indicator would accomplish this. In cont rast, given the generally higher fine 17 particle concentrations in urban ar eas compared to rural areas, a PM 10 indicator would be 18 expected to allow lower PM 10-2.5 concentrations in urban areas than in rural areas. Therefore, to 19 the extent that it is judged appropriate to set a standard that does not allow different 20 concentrations of thoracic coarse particles in different types of e nvironments, it would be 21 appropriate to consider a PM 10-2.5 indicator. 22 However, as discussed above, we also not e that most of the evidence for positive 23
associations between PM 10-2.5 and morbidity and mortality, pa rticularly evidence for these 24 associations at relatively low concentrations of PM 10-2.5 , continues to come from studies 25
conducted in locations where the PM 10-2.5 is expected to be largely of urban origin. While recent 26 studies of dust storm events have provided so me additional informati on on the health effects 27 associated with particles of non-urban origin, the PM 10 concentrations due to dust storm events 28 in these studies are generally highe r, and in at least some cases c onsiderably higher, than those in 29 the U.S. and Canadian cities where positive and statistically significant associations have been 30 reported in recent studies. To the extent that these considerations are emphasized in a decision 31 on the indicator for a standard, a reasonable conc lusion would be that r ecent studies have not 32 fundamentally changed our understanding of the relative toxicity of urban versus non-urban 33 particles, and that avai lable evidence continues to support the conclusion that thoracic coarse 34Draft Do Not Quote or Cite March 2010 3-34 particles of urban origin, where fi ne particle concentrations tend to be highest, are of particular 1

concern. 2 Given this conclusion, it would be reasonable to consider an indicator that focuses control 3 on areas with ambient mixes known with greater certa inty to be associated with adverse health 4 effects (i.e., mixes generally pres ent in urban areas) since such an indicator could provide public 5 health benefits with the greatest degree of certaint y. With regard to this, as discussed in more 6 detail above, we note that the varying levels of thoracic coarse particles allowed by a PM 10 7 indicator would be expected to ta rget protection to thos e locations (i.e., urban or industrial areas) 8 where the strongest evidence has been observed fo r associations between adverse health effects 9 and exposures to thoracic coarse particles. Th erefore, under this approa ch to considering the 10 evidence, a reasonable conclusion would be that a PM 10 indicator remains appropriate for a 11 standard meant to protect against exposures to thor acic coarse particles. Thus, as with a decision 12 on the adequacy of the current standard, different decisions on indicator could be judged to be 13 appropriate, depending on the emphasis placed on different aspects of the evidence and its 14
associated uncertainties. 15

3.3.4 Averaging Time 16 In considering the appropriat e averaging time(s) for the PM 10 standard in the last review, 17 the Administrator considered several epidemiologic studies that had reported statistically 18 significant associations between sh ort-term (24-hour) exposure to PM 10–2.5 and various morbidity 19 effects as well as mortality. Based primarily on these studies, he concl uded that the available 20 evidence continued to support a 24-hour averaging time for a st andard intended to control 21 thoracic coarse particles. In contrast, given the relative lack of studies suppor ting a link between 22 long-term exposures to thoracic coarse partic les and morbidity or mortality, and given the 23 conclusion reached in the AQCD that the avai lable evidence did not suggest a link between 24 morbidity or mortality an d long-term exposure to PM 10–2.5 (US EPA, 2004a, p. 9–79), the 25
Administrator further concluded that an annual coarse particle sta ndard was not warranted at that 26 time. In reaching this decision, the Administrato r also noted that a 24-hour standard would be 27 expected to provide protection against any as yet unidentified potential effects of long-term 28 exposure at ambient concentrations. Thus, in th e 2006 review the Administ rator retained the 24- 29
hour PM 10 standard and revoked the annual PM 10 standard (71 FR 61198-61199). 30 In the current review, we reconsider the exte nt to which the available evidence continues 31 to support these decisions by consid ering the following question: 32

 To what extent does the available evidence continue to support a 24-hour averaging 33 time for a standard meant to protect agai nst effects associat ed with short-term 34 exposures to PM 10-2.5 ? 35Draft Do Not Quote or Cite March 2010 3-35 With regard to this question, we note the c onclusions from the ISA regarding the weight 1 of evidence for different averaging times as we ll as the studies on which those conclusions are 2 based. Specifically, as discussed above (see Table 3-1 above), the ISA concludes that the 3 existing evidence is suggestive of a causal relationship between short-term PM 10-2.5 exposures 4 and mortality, cardiovascular e ffects, and respiratory effect s (ISA, section 2.3.3). This 5 conclusion is based largely on epidemiologi c studies which have primarily evaluated 6
associations between 24-hour PM 10-2.5 concentrations and morbidity and mortality (e.g., see ISA, 7 Figure 2-3), though a smaller number of controlled human exposure studies have reported effects 8 following shorter exposures (i.e., 2-hours) to PM 10-2.5 (e.g., see ISA, sections 6.2.1.2, 6.3.3.2). In 9 contrast, with respect to long-term exposures, the ISA concludes that available evidence is 10 inadequate to infer a causal relationship with all health outcomes evaluated (US EPA, 2009a, 11 section 2.3). Specifically, the ISA states, “To da te, a sufficient amount of evidence does not 12
exist in order to draw conclusi ons regarding the health effect s and outcomes associated with 13 long-term exposure to PM 10-2.5 ” (US EPA, 2009a, section 2.3.4; see Table 3-1 below). 14 In considering the weight of evidence determinations in the ISA, we conclude that, at a 15 minimum, they suggest the importance of having a standard that prot ects against short-term 16 exposures to thoracic coarse part icles. In considering the averag ing times used in the short-term 17 epidemiologic studies, we note that the majo rity of the evidence supporting the link between 18

PM 10-2.5 and morbidity and mortality is based on 24- hour average thoracic coarse particle 19 concentrations. Therefore, our preliminary conc lusion is that the evidence available in this 20 review continues to support the appropri ateness of a 24-hour averaging time for a PM 10 standard 21 meant to protect against short-term exposures to PM 10-2.5 , including potential effects associated 22 with exposures of shorter durati on than 24-hours. We further not e that, given the ISA conclusion 23
that “a sufficient amount of evidence does not ex ist in order to draw conclusions regarding the 24
health effects and outcomes associat ed with long-term exposure to PM 10-2.5 ” (ISA, p. 2-19) the 25 evidence does not support the appr opriateness of an a nnual thoracic coarse pa rticle standard at 26 this time. In reaching this conclusion, we note that, to the extent a short-term standard requires 27 areas to reduce their 24-hour ambient particle concentrations, long-term concentrations would 28 also be expected to decrease. Therefore, a 24-ho ur standard meant to pr otect against short-term 29 exposures to thoracic coarse pa rticles would also be expected to provide protection against any 30 as yet unidentified potential eff ects of long-term exposures at ambient concentrations. 31

3.3.5 Level and Form 32 Given the conclusions above regardin g the adequacy of the current PM 10 standard (i.e., 33 that, depending on the approach to considering the available evidence, the adequacy of the 34Draft Do Not Quote or Cite March 2010 3-36 current 24-hour PM 10 standard to protect agai nst effects associated wi th exposures to thoracic 1 coarse particles could be called into question) and the appropriate indica tor (i.e., that, depending 2 on how the evidence is considered, either a PM 10 or PM 10-2.5 indicator could be judged 3 appropriate), we next consider whether different standard levels and/or forms for a 24-hour PM 10 4
or PM 10-2.5 standard could be supported by the available evidence. To inform our consideration 5 of this issue, we have cons idered the following question: 6

 To what extent does new information suppo rt consideration of an alternative form 7 and/or level? 8 In considering this question, we have taken into account the scientific evidence from studies 9 of the link between short-term exposure to PM 10-2.5 and mortality, cardiovascular morbidity, and 10 respiratory morbidity, as assessed in the ISA, including the uncertainties and limitations in that 11
evidence. 12 In the 2006 review, the Administ rator concluded that “the level of protection afforded by 13
the current 24-hour PM 10 standard of 150 μ g/m 3 , one-expected-exceedance form, continues to be 14 appropriate for the types of thor acic coarse particles typically f ound in urban or industrial areas” 15 (71 FR 61202). In support of this decision, the Administrator noted that “mortality effects 16 observed in epidemiologic studies for [thoracic] coarse particles are generally associated with 17 exposure levels that exceed the current standards, and morbidity effects are generally associated 18 with exposure levels that ex ceeded the current standards on only a few occasions” (71 FR 19 61202). Given this evidence, the Administrator conc luded that the level of protection afforded 20 by the existing PM 10 standard was not greater than warra nted. In addition, the Administrator 21 concluded that uncertainties in population exposures in available morbidity studies 18 suggested 22 that there was little basis for concluding that a greater degree of protection was warranted. 23 Therefore, the Administrator reta ined the existing level of 150 μ g/m 3 for the 24-hour PM 10 24 standard, and the existing one -expected exceedance form. 25 In the sections below, we discuss the appro ach that will be used to identify potential 26 alternative forms and a range of potential alternative levels for a standard meant to protect 27 against exposures to thoracic coar se particles. These potential alternative standard forms and 28 levels will be presented and considered in the second draft PA document. 29

18 Analysis of air quality information in Detroit (Ito, 2003) and Coachella Valley (Ostro et al., 2003) suggested that population exposure concentrations in these areas could be appreciably higher (Detroit) or lower (Coachella Valley) than indicated by the air quality information used in the studies (See US EPA, 2005, pp. 5-64 to 5-66).Draft Do Not Quote or Cite March 2010 3-37 3.3.6 Form 1 As discussed in more detail above, in the 2006 review the Administrator concluded that 2 “the degree of protection affo rded by the current 24-hour PM 10 standard is requisite to protect 3 public health with an adequate margin of sa fety” (71 FR 61201). Given the overall decision in 4 that review to provide the sa me protection as provided by the existing 24-hour standard, the 5
Administrator concluded “it is best to retain bot h the form and the level of the current primary 6
24-hour PM 10 standard” (71 FR 61202). Therefore, the one-expected-exceedance form was 7
retained. 8 This decision is being examined in the curr ent review within the context of the overall 9
decision on whether to retain or revise the current 24-hour PM 10 standard. While the selection of 10 a specific form must be made within the contex t of a decision on the other elements of the 11 standard, EPA generally favors the concentration- based form for short-term standards. In 1997 12
EPA established 98 th percentile form for the 24-hour PM 2.5 standard and, most recently, in 2010 13
EPA established 98 th percentile form for the 1-hour NO 2 standard (62 FR 38671; 75 FR 6474). 14 In making these decisions, EPA judged that, as co mpared to an exceedance-based form, such as 15
that used for the current PM 10 standard, a concentration-based form is more reflective of the 16 health risks posed by elevated pollutant concen trations because it gives proportionally greater 17 weight to days when concentrations are well abov e the level of the standard than to days when 18 the concentrations are just a bove the standard. Further, a concentration-based form better 19 compensates for missing data and less than-daily monitoring. In additi on, when averaged over 3 20 years, it has greater stability than an exceedance-based form a nd, therefore, it facilitates the 21 development of more stable implementation pr ograms. In these previous reviews, after 22 considering different con centration percentiles (95 th to the 99 th for PM 2.5 and 98 th and 99 th for 23
NO 2 ), EPA selected the 98th percentile as an ap propriate balance between adequately limiting 24 the occurrence of peak concentr ations and providing increased stability and robustness. 25 In considering these decisions, our preliminar y conclusion is that a similar logic applies 26
in the case of the 24-hour PM 10 standard. For this reason, to the extent that it is judged 27 appropriate to revise the current 24-hour standard in the current review, we will give preliminary 28 consideration to a rang e of alternative standard options based on 98 th percentile concentrations of 29

PM 10 and/or PM 10-2.5 , as discussed below. 30

3.3.7 Level 31 As noted above, depending on the approach taken in this review to consider the evidence 32 for the adequacy of the current PM 10 standard, it could be judged th at this standard does not 33 provide adequate public health pr otection. If this is judged to be the case, we will consider 34Draft Do Not Quote or Cite March 2010 3-38 potential alternative standard levels for a 24-hour standard that, in conjunction with a 98 th 1 percentile form as described above, would provi de increased public heal th protection against 2 effects associated with exposures to PM 10-2.5 . Given the conclusion abov e that the continued use 3
of the PM 10 indicator could be judged a ppropriate for a standard meant to protect against 4 exposures to PM 10-2.5 , we will consider a range of potential alternative standard levels for a PM 10 5 standard. However, as is also discussed above, a PM 10-2.5 indicator could pot entially be judged 6 appropriate. While the air quality information availa ble to inform the identification of a range of 7 potential alternative standard levels will be more limited for a PM 10-2.5 standard than for a PM 10 8 standard, we recognize that some such information ex ists. Therefore, to the extent that feedback 9 received during the review of this first draft Policy Assessment justifies consideration of a PM 10- 10

2.5 standard, we will discuss potential alternative le vels for such a standard in the second draft 11
document. 12 In considering potential alternative standard levels, staff will consider the available 13
information on PM 10 , and possibly PM 10-2.5 , concentrations in locati ons where health studies 14
have evaluated the link between short-term PM 10-2.5 concentrations and mortality, cardiovascular 15 morbidity, and respiratory morbidity, as well as th e uncertainties and limitations in that evidence. 16 In so doing, we will focus on U.S. studies, as described above in our consideration of the 17 adequacy of the current standard. Specifically, we will consider the extent to which these studies 18 report positive and relatively pr ecise effect estimates; the extent to which the reported 19
associations are robust in co-pollutant models; and the extent to which the studies used relatively 20 reliable air quality data. In particular, we will focus on those specific studies, briefly 21 summarized above and presented in mo re detail in chapter 6 of the ISA, that provide evidence of 22
associations between PM 10-2.5 and mortality and morbidity in areas that would likely have met 23
the current 24-hour PM 10 standard during the time of the study . Staff believes that this body of 24
evidence can serve as a basis for identifying and considering potential alternative 24-hour PM 10 25
and/or PM 10-2.5 standards that would provide increased protection agains t effects related to short26 term exposures to PM 10-2.5
. 27 As an initial matter, we recognize, as disc ussed above, that thes e short-term exposure 28 studies provide no evidence of clear thresholds, or lowest-observed- effects levels, in terms of 24- 29 hour average concentrations. As a consequence, this body of evidence is difficult to translate 30 directly into a specific 24-hour standard that would independen tly protect agai nst all effects 31 associated with short-term exposures. In the absence of an apparent threshold, for purposes 32 of identifying the range of stan dard levels potentially support ed by the epidemiologic 33 evidence, we will focus on the range of PM 10 and/or PM 10-2.5 concentrations that have been 34 measured in locations where key health studies have reported as sociations with PM 10‐2.5

. 35 Specifically, we will focus on the upper end of the distributions of daily PM concentrations, 36Draft Do Not Quote or Cite March 2010 3-39 particularly in terms of the 98 th percentile of the yearly distribution of 24-hour PM 10 and/or 1
PM 10‐2.5 concentrations, reflecting th e considerations above for the appropriate form of the 24- 2 hour standard. As noted above, this analysis of potential alternative sta ndard levels will be 3 presented in the second draft PA document. 4

3.4 KEY UNCERTAINTIES AND AREAS FOR FUTURE RESEARCH AND DATA 5 COLLECTION 6 [This topic will be discussed in the second draft Policy Assessment.] 7

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U.S. EPA. (2009b). Particulate Matter National Ambient Air Quality Standards: Scope and Methods Plan for Health 15 Risk and Exposure Assessment. U.S. Environmental Protection Agency, Research Triangle Park, NC, 16 EPA-452/P-09-002. February 2009. Available: 17 http://www.epa.gov/ttn/naaqs/standards/pm/s_pm_2007_pd.html 18

US EPA (2010a). Quantitative Risk Assessment for Partic ulate Matter – Second External Review Draft. Office of 19 Air Quality Planning and Standards, U.S. Environmental Protection Agency, Research Triangle Park, NC. 20 EPA-452/P-10-001. February 2010. Available: 21 http://www.epa.gov/ttn/naaqs/standards/pm/s_pm_index.html. 22

Yang C-Y; Chen Y-S; Yang C-H; Ho S-C (2004). Relationship between ambient air pollution and hospital 23 admissions for cardiovascular diseases in Kaohsiung, Taiwan. J Toxicol Environ Health A Curr Iss, 67: 24 483-493. 25

Yang CY; Cheng MH; Chen CC (2009). Effects of Asian Du st Storm Events on Hospital Admissions for Congestive 26 Heart Failure in Taipei, Taiwan. J Toxicol Environ Health A Curr Iss, 72: 324-328. 27

Zanobetti A; Schwartz J. (2009). The effect of fine an d coarse particulate air pollution on mortality: A national 28 analysis. Environ Health Perspect, 117: 1-40.(2008). 294-1 Draft – Do Not Quote or Cite March 2010



### 4 REVIEW OF THE SECONDARY STANDARDS FOR VISIBILITY1 

### RELATED EFFECTS 2

This chapter presents preliminary staff conclu sions with regard to the adequacy of the 3 current suite of secondary PM standards to protect against PM-related visibility impairment as 4
well as the alternative se condary PM standards that are appr opriate for consideration in this 5
review. Our assessment of these issues is fram ed by a series of key policy-relevant questions, 6 which expand upon those presented in the Integrat ed Review Plan (IRP) (US EPA, 2008a) at the 7 outset of this review. The answers to these questi ons will inform decisions on whether, and if so 8 how, to revise the current su ite of secondary PM standard s for the purpose of providing 9 appropriate protection from PM-rela ted visibility impairment. 10 In presenting preliminary staff conclusions on alternative secondary standard that are 11 appropriate for consideration, we note that the final decision is largel y a public welfare policy 12 judgment. A final decision must draw upon scie ntific information and analyses about PM13 related visibility impairment a nd related impacts on public welfare, as well as judgments about 14 how to deal with the range of uncertainties th at are inherent in the scientific evidence and 15 analyses. Our approach to informing these judgm ents is discussed more fully below. This 16 approach is consistent with th e requirements of the NAAQS provi sions of the Act and with how 17 EPA and the courts have historically interp reted the Act. These provisions require the 18 Administrator to establish sec ondary standards that, in the Administrator’s judgment, are 19 requisite to protect public welfar e from any known or anticipated a dverse effects associated with 20 the presence of the polluta nt in the ambient air. In so doing, the Administrator seeks to establish 21 standards that are neither more nor less stringent than necessary for this purpose. The Act does 22 not require that secondary standard s be set at a zero-risk level, but rather at a level that avoids 23 unacceptable public welfare impacts. 24 Information on the approaches used to set the secondary PM standards in past reviews as 25 well as our current approach fo r this review are presented in section 4.1. Our preliminary 26 conclusions regarding the adequacy of the current suite of secondary PM standards to protect 27 against PM-related visibility im pairment are presented in sec tion 4.2. Section 4.3 presents our 28 preliminary conclusions with respect to alte rnative PM standards by focusing on each of the 29
basic elements of the standard s: pollutant indica tor (section 4.3.1), averaging time (section 30 4.3.2), and level and form (section 4.3.3). The perfor mance of alternative st andards, with a focus 31 on the uniformity of protection from visibility im pairment afforded by the alternative standards, 32
is evaluated in section 4.3.4. Section 4.4 summa rizes all preliminary st aff conclusions on the 33 secondary PM standards for visibility protection. The next draft of this chapter will conclude 34
with an initial overview of areas of key uncertainties and sugges ted future research areas and 35 data collection efforts (section 4.5) 364-2 Draft – Do Not Quote or Cite March 2010 4.1 APPROACH 1 Staff’s approach for reviewing the curre nt secondary PM st andards builds upon and 2 broadens the approaches used in previous PM NAAQS reviews. We first present a brief 3 summary of the approaches used to establish and review secondary PM standards in the last two 4 reviews of the PM NAAQS (section 4.1.1). Recent litigation on the 2006 st andards has resulted 5
in the remand of the s econdary annual and 24 hour PM 2.5 NAAQS to EPA as discussed in section 6 4.1.2. Our current approach fo r evaluating the secondary PM 2.5 standards using both evidence7 and impact assessment-based considerations is outlined in section 4.1.3. 8

4.1.1 Approaches Used in Previous Reviews 9 The original suite of PM 2.5 standards was established in 1997 and revisions to those 10 standards were made in 2006. The approaches used in making final decisions on secondary 11 standards in those reviews, as well as the curren t review, utilize different ways to consider the 12 underlying body of scientific evidence. They also reflect an evolution in our understanding of 13
the multi-faceted nature of the public welfare visibility effect , from a more narrow focus on 14 Class I area visibility to non-Cl ass I area visibility, including urban areas, and public perception, 15 valuation and impacts on pers onal comfort and well being. 16 4.1.1.1 Review Completed in 1997 17 In 1997, EPA revised the identical primary and secondary PM 10 NAAQS in part by 18 establishing new identical primary and secondary PM 2.5 standards. In revising the secondary 19 standards, EPA recognized that PM produces advers e effects on visibility a nd that impairment of 20 visibility was experienced thr oughout the U.S., in multi-state regi ons, urban areas, and remote 21 mandatory Class I Federal areas alike. Howeve r, in considering an appropriate level for a 22 secondary standard to address adverse effects of PM on visib ility, EPA concluded that the 23 determination of a single national level was co mplicated by regional differences in several 24 factors that influence visibility such as background and current levels of PM, composition of PM, 25 and average relative humidity. Vari ations in these factors could t hus result in situations where 26 attaining even a low concentration of fine pa rticles might or might not provide adequate 27 protection, depending on these factors. The EPA also determined that there was insufficient 28
information at that time to establish a leve l for a national secondary standard that would 29 represent a threshold above whic h visibility conditions would always be adverse and below 30 which visibility conditions would always be acceptable. 31 Based on these considerations, EPA assessed po tential visibility improvements in urban 32 areas and on a regional scale that would result from attainment of the new primary standards for 33

PM 2.5 . The agency concluded that the spatially averaged form of the annual PM 2.5 standard was 34 well suited to the protection of visibility, wh ich involves effects of PM throughout an extended 354-3 Draft – Do Not Quote or Cite March 2010 viewing distance across an urban area. Based on air quality data available at that time, many 1 urban areas in the northeast, midwest, and southeas t, as well as Los Angeles, were expected to 2 see perceptible improvement in visibility if the annual PM 2.5 primary standard was attained. The 3
EPA also concluded that in some areas attainment of the 24-hour PM 2.5 standard would be 4 expected to reduce, to some degree, the number a nd intensity of ‘‘bad visibility’’ days, i.e., the 5 20% of days having the greatest impair ment over the course of a year. 6 Having concluded that attainment of the annual and 24-hour PM 2.5 primary standards 7 would lead to visibility improvements in many eas tern and some western urban areas, EPA also 8
considered whether these sta ndards could provide potential improvements to visibility on a 9 regional scale. Based on information available at the time, EPA conclude d that attainment of 10

PM 2.5 secondary standards set identical to the primar y standards would be expected to result in 11 visibility improvements in the eastern U.S. at both urban and regional sc ales, but little or no 12 change in the western U.S., except in and near certain urban areas. 13 The EPA then considered the potential effec tiveness of a regional haze program, required 14 by sections 169A and 169B of the Act 1 to address the widespread, regionally uniform type of 15 haze caused by a multitude of sources, to address t hose effects of PM on visibility that would not 16 be addressed through attainment of the primary PM 2.5 standards. The structure and requirements 17
of sections 169A and 169B of th e Act provide for visibility protection programs that can be more 18 responsive to the factors contributing to regional differences in visibil ity than can programs 19 addressing a nationally applicable secondary NAAQS . The regional haze visibility goal was 20 more protective than a secondary NAAQS since the goal addresses any man-made impairment 21 rather than just impairment at levels determin ed to be adverse. Thus, an important factor 22
considered in the 1997 review was whether a regional haze program, in conjunction with 23 secondary standards set iden tical to the suite of PM 2.5 primary standards, would provide 24 appropriate protection for visibi lity in non-Class I areas. Th e EPA concluded that the two 25 programs and associated control strategies shou ld provide such protec tion due to the regional 26 approaches needed to manage emissions of pollu tants that impair visibility in many of these 27

areas. 28 For these reasons, EPA concluded that a nati onal regional haze program, combined with a 29 nationally applicable le vel of protection achie ved through secondary PM 2.5 standards set 30 identical to the primary PM 2.5 standards, would be more ef fective in addressing regional 31
variations in the a dverse effects of PM 2.5 on visibility than esta blishing national secondary 32

1 In 1977, Congress established as a national goal ‘‘the prevention of any future, and the remedying of any existing, impairment of visibility in mandatory Class I Federal areas which impairment results from manmade air pollution’’, section 169A(a)(1) of the Act. The EPA is required by section 169A(a)(4) of the Act to promulgate regulations to ensure that ‘‘reasonable progress’’ is ac hieved toward meeting the national goal.4-4 Draft – Do Not Quote or Cite March 2010 standards for PM at lower levels than the primary PM 2.5 standards. The EPA further recognized 1 that people living in certain urban areas may pl ace a high value on unique scenic resources in or 2 near these areas, and as a result might experience visibility problems attri butable to sources that 3 would not necessarily be addressed by the comb ined effects of a regional haze program and 4

PM 2.5 secondary standards. The EPA concluded that in such cases, State or local regulatory 5 approaches, such as past action in Colorado to establish a local visi bility standard for the City of 6 Denver, would be more appropriate and effective in addressing these special situations because 7 of the localized and unique characteristics of th e problems involved. Visibi lity in an urban area 8 located near a mandatory Class I Federal area could also be improved through State 9 implementation of the current visibility regula tions, by which emission limitations can be 10 imposed on a source or group of sources found to be contributing to ‘‘re asonably attributable’’ 11 impairment in the mandatory Class I Federal area. 12
Based on these considerati ons, EPA set secondary PM 2.5 standards identical to the 13 primary PM 2.5 standards, in conjunction with a regional haze program under sections 169A and 14 169B of the Act, as the most appropriate and e ffective means of addre ssing the welfare effects 15 associated with visibility impairment. Toge ther, the two programs and associated control 16 strategies were expected to provi de appropriate protection against the effects of PM on visibility 17 and enable all regions of the country to make reasonable progress toward the national visibility 18 goal. 19 4.1.1.2 Review Completed in 2006 20 In 2006, EPA revised the secondary PM sta ndards by once again making them identical 21 to the revised primary standards. The EPA’s decision to revise the secondary PM standards 22 reflected a number of new developments and sour ces of information that had occurred and/or 23 become available following the 1997 review. Fi rst, EPA promulgated a regional haze program 24 in 1999 (65 FR 35713) which required States to esta blish goals for improving visibility in Class I 25 areas and to adopt control strate gies to achieve these goals. Second, extensive new information 26 from visibility and fine particle monitoring netw orks had become available, allowing for updated 27 characterizations of visibility tr ends and PM levels in urban ar eas, as well as Class I areas. 28
These new data allowed EPA to better characteriz e visibility impairment in urban areas and the 29 relationship between visibility and PM 2.5 concentrations. Finally, addi tional studies in the U.S. 30 and abroad provided the basis for the establis hment of standards and programs to address 31 specific visibility concerns in a number of local areas. These studies (e .g., in Denver, Phoenix, 32 British Columbia) produced reasonably consistent re sults in terms of the visual ranges found to 33 be generally acceptable by the par ticipants in the various studies. These studies utilized 34 photographic representations of visibility impair ment, which were useful in characterizing the 35 nature of particle-induced haze. Based largely on this information, the Administrator concluded 364-5 Draft – Do Not Quote or Cite March 2010 that it was appropriate to revise the secondary PM standards to provide increased protection from 1 visibility impairment principally in urban areas , in conjunction with th e regional haze program 2 for protection of visual air quality in Class I areas. 3 In so doing, the Administrator recognized th at PM-related visibility impairment is 4 principally related to fine particle levels, such that it was appropriate to focus the review on 5 whether the current secondary PM 2.5 standards should be revised. The Administrator also 6 recognized that perception of visibility impairment is most directly re lated to instantaneous 7 levels of visual air quality, such that in c onsidering whether the current suite of secondary 8 standards would provide the appropriate degree of protection, he concluded that it was 9 appropriate to revise ju st the 24-hour secondary PM 2.5 standard to provide requisite protection. 10
The EPA then considered whether PM 2.5 remained the appropriate indicator for a 11 secondary standard to protect visi bility primarily in urban areas. One of the key issues in the 12
1997 review was the extent to which the diffe rences in humidity between East and West 13 complicated the establishmen t of a nationally uniform PM 2.5 secondary standard for urban areas. 14
With the substantial addition to the air quality and visibility da ta made possible by the national 15
urban PM 2.5 monitoring networks, an anal ysis conducted for the 2006 review found that, in urban 16 areas, visibility levels showed far less difference between eas tern and western regions on a 24- 17 hour or shorter time basis than implied by th e largely non-urban data available in the 1997 18 review. In analyzing how well PM 2.5 concentrations correlated with visibility in urban locations 19 across the U.S., the 2005 Staff Paper concluded th at clear correlations existed between 24-hour 20 average PM 2.5 concentrations and reconstructed light ex tinction, which is directly related to 21 visual range. These correlations were similar in the eastern and western regions of the U.S. 22 Particles in the coarse mode ge nerally contributed only marginally to visibility impairment in 23 urban areas. Further, because hygroscopic component s of fine particles, in particular sulfates 24 and nitrates, contribute dispr oportionately to visibility impairment under high humidity 25 conditions, these correlations were less influenc ed by relative humidity and more consistent 26 across regions when PM 2.5 concentrations are averaged over s horter, daylight time periods (e.g., 27 4 to 8 hours) when relative humidity was gene rally lower and less va riable. The 2005 Staff 28 Paper noted that a standa rd set at any specific PM 2.5 concentration would n ecessarily result in 29 visual ranges that vary somewhat in urban areas across the country, reflec ting the variability in 30
the correlations between PM 2.5 concentrations and light extinc tion. Thus, the 2005 Staff Paper 31
concluded that it was appropriate to use PM 2.5 as an indicator for standa rds to address visibility 32 impairment in urban areas, especially when the indicator is defined for a relatively short period 33 (e.g., 4 to 8 hours) of daylight hours. Based on their review of the St aff Paper, most CASAC 34
Panel members also endorsed such a PM 2.5 indicator for a secondary standard to address 35 visibility impairment (Henderson, 2005a). Base d on the above considerations, the Administrator 364-6 Draft – Do Not Quote or Cite March 2010 concluded that PM 2.5 should be retained as the indicator for fine particles as part of a secondary 1 standard to address visibility protection, in conj unction with averaging times from 4 to 24 hours. 2 In considering what level of protection agains t PM-related visibility impairment would be 3 appropriate, the Administrator took into account th e results of the public perception and attitude 4 surveys in the U.S. and Canada, State and local vi sibility standards within the U.S., and visual 5 inspection of photographic representations of se veral urban areas across the U.S. In the 6 Administrator’s judgment, these sources provided useful but still quite limited information on the 7 range of levels appropriate for consideration in setting a national visibility standard primarily for 8 urban areas, given the generally subjective nature of the public welfare effect involved. Based 9 on photographic representations of va rying levels of visual air qua lity, public perception studies, 10 and local and State visibility standards, the 2005 Staff Pa per concluded that 30 to 20 μ g/m 3 PM 2.5 11 represented a reasonable range fo r a national visibility standard primarily for urban areas, based 12 on a sub-daily averaging time. The upper end of this range was below the levels at which 13 illustrative scenic views are significantly obscu red, and the lower end was around the level at 14 which visual air quality genera lly appeared to be good based on observation of the illustrative 15 views. This concentration range generally corr esponded to median visual ranges in urban areas 16 within regions across the U.S. of approximate ly 25 to 35 km, a range which was bounded above 17 by the visual range targets selected in specifi c areas where State or local agencies placed 18 particular emphasis on protecting visual air qualit y. In considering a reasonable range of forms 19
for a PM 2.5 standard within this range of levels , the 2005 Staff Paper concluded that a 20 concentration-based percentile form was appropriate, and that the upper end of the range of 21 concentration percentiles shoul d be consistent with the 98 th percentile used for the primary 22
standard and that the lower e nd of the range should be the 92 nd percentile, which represented the 23
mean of the distribution of the 20 percent most impaired days, as targeted in the regional haze 24 program. While recognizing that it was difficult to select any sp ecific level and form based on 25 then currently available information (Hende rson, 2005a), the CASAC Panel was generally in 26 agreement with the ranges of levels and forms presented in the 2005 Staff Paper. 27
The Administrator also considered the level of protection that would be afforded by the 28 proposed suite of primary PM 2.5 standards (71 FR 2681), on the basis that although significantly 29
more information was available than in the 1997 review concerning the relationship between fine 30 PM levels and visibility across the country, there was still little available information for use in 31 making the relatively subjective value judgment n eeded in selecting the appropriate degree of 32 protection to be afforded by such a standard. In so doing, the Administrator compared the extent 33 to which the proposed suite of primary standa rds would require areas across the country to 34 improve visual air quality with the extent of increased protection likely to be afforded by a 35 standard based on a sub-daily averaging time. Based on such an analysis, the Administrator 364-7 Draft – Do Not Quote or Cite March 2010 observed that the predicted percent of counties with monitors not likely to meet the proposed 1 suite of primary PM 2.5 standards was actually somewhat grea ter than the predicted percent of 2 counties with monitors not likely to meet a sub-da ily secondary standard w ith an averaging time 3 of 4 daylight hours, a level toward the upper e nd of the range recommended in the 2005 Staff 4 Paper, and a form within the recommended range. Based on this comparison, the Administrator 5 concluded that revising the secondary 24-hour PM 2.5 standard to be identical to the proposed 6 revised primary PM 2.5 standard (and retaining the current annual secondary PM 2.5 standard) was a 7 reasonable policy approach to addressing visibi lity protection primarily in urban areas. In 8 proposing this approach, the Administrator also solicited comment on a sub-daily (4- to 8-hour 9 averaging time) secondary PM 2.5 standard (71 FR 2675-2781). 10 In commenting on EPA’s proposal, the CASAC re quested that a sub- daily standard to 11 protect visibility be favora bly reconsidered (Henderson, 200 6). The CASAC noted three 12 cautions regarding the Agency’s proposed reliance on a secondary PM 2.5 standard identical to the 13 proposed 24-hour primary PM 2.5 standard: (1) PM 2.5 mass measurement is a better indicator of 14 visibility impairment during daylight hours, when relative humidity is generally low; the sub15 daily standard more clearly matches the nature of visibility impairment , whose adverse effects 16 are most evident during the daylight hours; using a 24- hour standard as a proxy introduces error 17 and uncertainty in protecting visibility; and s ub-daily standards are used for other NAAQS and 18 should be the focus for visibility; (2) CASAC an d its monitoring subcommittees have repeatedly 19 commended EPA’s initiatives promoting the intr oduction of continuous and near-continuous PM 20 monitoring, and expanded depl oyment of continuous PM 2.5 monitors is consistent with setting a 21 sub-daily standard to protect visibility; (3) The analysis showing a similarity between 22 percentages of counties not likely to meet what they considered to be a lenient 4- to 8-hour 23 secondary standard and a secondary standard id entical to the proposed 24-hour primary standard 24
was a numerical coincidence that was not indi cative of any fundamental relationship between 25 visibility and health. The CASA C Panel further stated that ”visual air quality is substantially 26 impaired at PM 2.5 concentrations of 35 μ g/m 3 ” and that ‘‘it is not reasonable to have the visibility 27 standard tied to the health standard, which may ch ange in ways that make it even less appropriate 28 for visibility concerns.” 29 In reaching a final decision, the Administrato r focused on the limitations in the available 30 hourly air quality data and in the studies of public perception and attitudes regarding the 31 acceptability of various degrees of visibility impairment in urban areas, as well as on the 32 subjective nature of the public welfare judgm ent required. In so doing, the Administrator 33
concluded that caution was warranted in establishing a distinct secondary standard for visibility 34 impairment and that the available information di d not warrant adopting a secondary standard that 354-8 Draft – Do Not Quote or Cite March 2010 would provide either more or less protection agai nst visibility impairment in urban areas than 1 would be provided by secondary standards set equal to the proposed primary PM2.5 standards. 2

4.1.2 Remand of Secondary PM 2.5 Standards 3 Several parties filed petitions for review following promulgation of the revised PM 4 NAAQS in 2006. These petitions challenged severa l aspects of the final rule including EPA’s 5 decision to set the secondary NAAQS for fine PM, which protect the public welfare from 6 adverse visibility effects, at the same level as the primary NAAQS, which protect public health 7 42 U.S.C. 7607(d)(9). 8 On judicial review, the D.C. Circuit rema nded for reconsideration the secondary NAAQS 9 for fine PM to EPA because the Agency’s de cision was unreasonable and contrary to the 10 requirements of 42 U.S. C. section 7409 (b)(2). The petitioners argued that EPA’s decision 11 lacked a reasoned basis. First, they asserted, EPA never determined what level of visibility was 12 “requisite to protect the public welfare” 42 U.S. C. section 7409(b)(2). They argued that EPA 13 unreasonably rejected the target le vel of protection provided by its st aff, while failing to provide 14 a target level of its own. The D. C. Circuit court concurred stating “the EPA’s failure to identify 15 such a level when deciding where to set the level of ai r quality required by the revised secondary 16 fine PM NAAQS is contrary to th e statute and therefore unlawful. Furthermore, the failure to set 17 any target level of visibility pr otection deprived the EPA’s decisionm aking of a reasoned basis.” 18
American Farm Bureau Federation v. EPA, 559 F. 3d 512, (D.C. Cir. 2009). 19 Second, the petitioners challe nged EPA’s method of compar ing the protection expected 20 from potential standards. They contend th at the EPA relied on a meaningless numerical 21 comparison, ignored the effect of humidity on the usefulness of a standard using a daily 22 averaging time, and unreasonably c oncluded that the primary standa rds would achieve a level of 23 visibility roughly equivalent to the level the EPA staff and CASAC deemed “requisite to protect 24 the public welfare.” Again, th e court found that EPA’s equivale ncy analysis failed on its own 25 terms. The same table showing the alternative secondary standa rd used for comparison to the 26 alternative primary to show equivalency al so included six other standards within the 27 recommended CASAC range that would be more “protective” under EPA’s definition than the 28 primary standards. Two thirds of the potential standards within the CASAC’s recommended 29 range would be substantially more protective th an the primary standards. The EPA failed to 30 explain why it looked only at one of the few pot ential standards that would be less protective-and 31 only slightly so- than the prim ary standards. More fundament ally, however, EPA’s equivalency 32 analysis demonstrated nothing ab out the relative protection offere d by the different standards. 33 The tables simply offer no valid information a bout the relative visibility protection provided by 34
the standards. 354-9 Draft – Do Not Quote or Cite March 2010 Finally, the Staff Paper made cl ear that a visibility standard using a daily averaging time 1 will be confounded by regional differences in hu midity. The EPA acknowledged this problem, 2 yet did not address this issue at all in concluding that the primary standards would be sufficiently 3 protective of visibility. Therefore, the court granted the petition for review and remanded for 4 reconsideration the secondary PM NAAQS. Amer ican Farm Bureau Federation, 559 F. 3d at 5
520-24. 6

4.1.3 Current Approach 7 The staff’s approach in this review broadens the general approaches used in the last two 8 PM NAAQS reviews by utilizing, to the extent av ailable, enhanced tools, methods, and data to 9 more comprehensively characterize visibility impact s. As such, staff is taking into account both 10 evidence-based and impact-based considerations to inform staff conclusions related to the 11 adequacy of the current secondary standards and alternative standards th at are appropriate for 12 consideration in this review. In so doing, we are seeking to provide as broad an array of options 13 as is supportable by the available information, recognizing that the sele ction of a specific 14 approach to reaching final decisions on the secondary PM 2.5 standards will reflect the judgments 15 of the Administrator as to what weight to place on the various approaches and types of 16 information presented in the final PA. 17 For the purposes of this first draft Policy Assessment (PA), staff has drawn from the 18 qualitative evaluation of a ll studies evaluated in the Integrated Science Assessment for 19 Particulate Matter (Final Report) (ISA, USEPA, 2009a). The discussions presented in this 20 chapter consider the extensive new air quality and source apportionment information available 21 from the regional planning organizations, long-sta nding evidence of PM eff ects on visibility, and 22 public preference studies from four urban areas, as discussed in chapter 9 of the ISA, as well as 23 the integration of evidence across disciplines presented in chapte r 2 of the ISA. In addition, 24
limited information that has become availabl e regarding the charac terization of public 25 preferences in urban areas has provided some new perspectives on the usefulness of this 26 information in informing the select ion of target levels of urban visibility pr otection. On these 27 bases, we are again focusing our assessments in this review on visibili ty conditions in urban 28

areas. 29 Our preliminary conclusions reflect our understanding of both evidence-based and 30 impact-based considerations to inform two overarc hing questions related to: (1) the adequacy of 31
the current suite of PM 2.5 standards and (2) what potential altern ative standards, if any, should be 32 considered in this review to provide appr opriate protection from PM-related visibility 33 impairment. In addressing these broad questi ons, we have organized the discussions below 34 around a series of more specific questions re flecting different aspects of each overarching 354-10 Draft – Do Not Quote or Cite March 2010 question. When evaluating the visibility protecti on afforded by the current or any alternative 1 standards considered, we have taken into accoun t the four basic elemen ts of the NAAQS (e.g., 2 indicator, averaging time, level, and form). 3 We believe that the approach outlined a bove, when presented in the final PA, will 4 provide a comprehensive basis to help inform the judgments required of the Administrator in 5 reaching decisions about the current and potential alternative secondary PM standards for the 6 purpose of providing appropriate protection from PM-related visibility impairment and in 7 responding to the remand of the 2006 secondary PM 2.5 standards. 8

4.2 ADEQUACY OF CURRENT STANDARDS 9 In considering the adequacy of the current suite of PM 2.5 standards, staff addresses the 10 following overarching question: 11

Does the currently available scientific eviden ce and visibility impact information, as 12 reflected in the ISA and UFVA, support or call into question the adequacy of the visibility 13 protection afforded by the current su ite of fine particle standards? 14 To inform the answer to this overarching que stion, we have posed a series of more 15 specific questions to aid in cons idering the currently available scientific evidence and the results 16 of recent quantitative visibility im pact analyses in a policy-relevant context, as discussed below. 17 In considering the scientific and technical information, we re flect upon both the information 18
available in the last review and information that is newly available since the last review as 19 assessed and presented in the ISA and UF VA (US EPA, 2009a; US EPA, 2010b). 20

4.2.1 Evidence-based Considerations 21 In reviewing the adequacy of the current suite of PM 2.5 standards, we have taken into 22
account evidence-based cons iderations, primarily as presented in the ISA, by considering causal 23 inference, impacts on susceptible populations, and whether visibility effects have been observed 24
in urban areas that would likel y meet the current standards. 25

 To what extent does the newly available sc ientific evidence strengthen or call into 26 question evidence of associations between ambient fine particle exposures and visibility 27 effects? 28 New research conducted by regional planning organizations in support of the Regional 29 Haze Rule, as discussed in chapter 9 of th e ISA, continues to support and refine our 30 understanding of the nature of the PM visibility effect and the sour ce contributions to that effect 31 in rural and remote locations. Additional byprod ucts of this research include new insights 32 regarding the regional source cont ributions to urban visibility a nd better characterization of the 33 urban excess that occurs in many cities above regional background. Ongoing urban PM 2.5 344-11 Draft – Do Not Quote or Cite March 2010 speciated and mass monitoring has produced ne w information that has allowed for updated 1 characterization of visibility trends and current levels in urban areas. Information from both of 2 these sources of PM data, while useful, has not however changed the fundamental and long 3 understood science characterizing the contribution of PM, especially fi ne particles, to visibility 4 impairment from the last review. This science, briefly summarized below, provides the basis for 5 the ISA designation of the relationship between PM and visibility impairment as causal. 6 Visibility impairment is caused by the scat tering and absorption of light by suspended 7 particles and gases in the atmosphere. The combin ed effect of light scattering and absorption by 8 both particles and gases is characterized as light extinction, (i.e. the frac tion of light that is 9 scattered or absorbed per unit of distance in the atmosphere). Light extinction is measured in 10 units of 1/distance, which is often expressed in the technical literature as 1/(million meters) or 11 inverse megameters (abbreviated Mm -1 ). When PM is present in th e air, its contribution to light 12 extinction typically greatly exceeds that of gases. 13 The amount of light extinction contributed by PM depends on the particle size 14 distribution and composition, as well as its concentration. If detail s of the ambient particle size 15 distribution and composition (including the mixi ng of components) are known, Mie theory can 16 be used to accurately calculate PM light ex tinction (ISA chapter 9). However, routine 17 monitoring rarely includes measurements of particle size and composition information with 18
sufficient detail for such calculations. A much si mpler algorithm can be used to estimate light 19 extinction using routinely m onitored fine particle (PM 2.5 ) speciation and coarse particle mass 20 (PM 10 – 2.5 ) data, plus relative humidity information n eeded to estimate the contribution by liquid 21 water in solution with hygroscopic PM componen ts (ISA section 9.2.2.2 and UFVA chapter 3). 22 The concentration of each of the major aerosol components is multiplied by a dry 23 extinction efficiency value and for the hygros copic components (e.g., ammoniated sulfate and 24 ammonium nitrate) an additional multiplicative term to account for the water growth to estimate 25 that components contribution to light extinction. Both the dry extinction efficiency and water 26 growth terms are developed by some combina tion of empirical assessment and theoretical 27 calculation using typical particle size distributions associated with each of the major aerosol 28 components, and they are evaluated by compari ng the algorithm estimates of light extinction 29 with coincident optical measurements. Summin g the contribution of each component gives the 30 estimate of total light extinction. The most co mmonly used of these is referred to as the 31 IMPROVE algorithm because it was developed specifically to use the IMPROVE aerosol 32 monitoring data and was evaluated using IMPROVE optical measurements at the subset of sites 33 that make those measurements (Malm et al., 1994). The formula for th e traditional IMPROVE 34 algorithm is shown below. 35
364-12 Draft – Do Not Quote or Cite March 2010 b ext ≈ 3 x f(RH) x [Sulfate] 1 + 3 x f(RH) x [Nitrate] 2 + 4 x [Organic Mass] 3 + 10 x [Elemental Carbon] 4 + 1 x [Fine Soil] 5 + 0.6 x [Coarse Mass] 6 + 10 7 8 Light extinction ( b ext ) is in units of Mm -1 , the mass concentrations of the components 9
indicated in brackets are in μ g/m 3 , and f(RH) is the unitless water growth term that depends on 10 relative humidity. The dry extinction efficiency for particulate organic mass is larger than those 11 for particulate SO 4 2– and nitrate principally because the density of the dry inorganic compounds 12 is higher than that assumed for the PM orga nic mass components. Since IMPROVE does not 13 include ammonium ion monitoring, th e assumption is made that all SO 4 2– is fully neutralized 14
ammonium sulfate and all nitrate is assumed to be ammonium nitrate. Though often reasonable, 15 neither assumption is always true (see Section 9.2.3.1). In the eastern U.S. during the summer 16 there is insufficient ammonia in the atmosphere to neutralize the SO 4 2– fully. Fine particle 17 nitrates can include sodium or calcium nitrate, which are the fine partic le fraction of generally 18 much coarser particles due to nitric acid interac tions with sea salt at ne ar-coastal areas (sodium 19 nitrate) or nitric acid interacti ons with calcium carbonate in cr ustal aerosol (calcium nitrate). 20 Despite the simplicity of the algorithm, it perfor ms reasonably well and permits the contributions 21 to light extinction from each of the major com ponents (including the water associated with the 22
SO 4 2– and nitrate compounds) to be separately approximated. 23
The f(RH) terms inflate the particulate SO 4 2– and nitrate light scat tering for high relative 24 humidity conditions. For relative humidity below 40% the f(RH) value is 1, but it increases to 2 25 at ~66%, 3 at ~83%, 4 at ~90%, 5 at ~93% and 6 at ~95% relative humidity. The result is that 26 both particulate SO 4 2– and nitrate are more efficient pe r unit mass than any other aerosol 27 component for relative humidity above ~85% wher e its total light extinction efficiency exceeds 28
the 10m 2 /g associated with EC. Based on this algorithm, particulate SO 4 2– and nitrate are 29 estimated to have comparable light extinction efficiencies (i.e., the same dry extinction 30 efficiency and f(RH) water growth terms), so on a per uni t mass concentration basis at any 31 specific relative humidity they are treated as equally effective contributors to visibility effects. 32 Inspection of the PM component-specific term s in the simple algorithm shows that most 33
of the PM 2.5 components contribute 5 times or more light extinction than a similar concentration 34
of PM 10 – 2.5 . We also know that particles with hygr oscopic components (e.g. particulate sulfate 35 and nitrate) contribute mo re light extinction at higher relative humidity than at lower relative 36 humidity because they change size in the atmos phere in response to ambient relative humidity 37 conditions. PM containing elemental or black carbon absorbs light as well as scattering it, 384-13 Draft – Do Not Quote or Cite March 2010 making it the component with the greatest light extinction contributi ons per unit of mass 1 concentration, except for the hygroscopic compon ents under high relative humidity conditions. 2
As a result of better character ization of PM in rural and re mote locations, refinements in 3 the original IMPROVE algorithm have been made to better account for th e aging of the organic 4 aerosols that occurs during transp ort to these more distant areas, and to add a component for sea 5 salt. Since urban areas contain a higher proporti on of newly emitted aerosols that have not aged, 6 the assessments done in support of this review have relied on the original IMPROVE algorithm. 7 As mentioned above, particles are not the only contributor to ambient visibility 8 conditions. Light scattering by ga ses also occurs in ambient ai r. Under pristine atmospheric 9 conditions, naturally occurring gases such as N 2 and O 2 , cause what is known as Rayleigh 10 scattering. Rayleigh scattering, whic h depends on the density of air as a function primarily of the 11 elevation above sea level, can be treated as a si te-dependent constant. Rayleigh contribution to 12 light extinction is only significan t under pristine condi tions. The only other commonly occurring 13 atmospheric gas to appreciably absorb light in the visible spectrum is NO 2 . NO 2 forms in the 14 atmosphere from NO emissions associated w ith combustion processes. These combustion 15 processes also emit PM at levels that generally contribute much higher light extinction than the 16
NO 2 (i.e. NO 2 absorption is generally less than ~ 5% of the light extinction, except where 17 emission controls remove most of the PM pr ior to releasing the remaining gases to the 18 atmosphere). The remainder of this documen t focuses on the contribution of PM, which is 19 typically much greater th an that of gases, to ambient light extinction, unless ot herwise specified. 20

 To what extent does the available evidence inform our understanding of the temporal 21 nature of the PM visibility effect, includi ng relevant exposure periods, associated 22 atmospheric conditions, and diurnal patterns of exposure? 23

Diurnal Periods of Interest 24
Typically, we think of visibi lity associated with day time periods. We recognize, 25 however, that PM light extinction behaves the same at night as during the day, enhancing the scattering 26 of anthropogenic light, contributing to the “skyglow” within and over populated areas, adding to the total 27 sky brightness, and contributing to the reduction in co ntrast of stars against the background. These effects 28 produce the visual result of a reduction of the number of visible stars and the disappearance of diffuse or 29 subtle phenomena such as the Milky Way. The extincti on of starlight is a secondary and minor effect also 30 caused by increased PM scattering and absorption. 31 However, there are significant and important differences between daytime and nighttime visual 32 environments that potentially make the nighttime period inappropriate to address at this time. First, 33 daytime visibility has dominated the attention of th ose who have studied the visibility effects of air 34 pollution. As a result, little research has been c onducted on nighttime visibility and the state of the 35 science is not yet comparable to that associated with daytime visibility impairment. Second, in addition 364-14 Draft – Do Not Quote or Cite March 2010 to air pollution, nighttime visibility is affected by the addition of light into the sight path from numerous 1 sources, including anthropogenic light sources su ch as artificial outdoor lighting, which varies 2 dramatically across space, and natural sources includi ng the Moon, planets, and stars. Light sources and 3 ambient conditions are typically five to seven orders of magnitude dimmer at night than in sunlight. 4 Moonlight, like sunlight, in troduces light throughout an ob server’s sight path at a constant angle. On the 5 other hand, dim starlight emanates from all over th e celestial hemisphere while artificial lights are 6 concentrated in cities and illuminate the atmosphere from below. These different light sources will yield 7 variable changes in visibility as compared to what has been established for the daytime scenario, in which 8 a single source, the sun, is by far the brightest source of light. Third, the human psychophysical response 9 (e.g., how the human eye sees and processes visual stimuli) at night is expected to differ (ISA, section 10 9.2.2). 11 Given the above, we do not believe that the sc ience is available at this time to support 12 adequate characterization of nighttime PM light ex tinction effects. In ad dition, we are not aware 13 of preference or valuation studies providing information on public preferences for nighttime 14 visual air quality (VAQ). Thus, we limit our c onsideration of PM visibility impacts to all 15 daylight hours only. 16
Exposure Durations of Interest 17
Very little is known about the role exposure duration plays in determining the 18 acceptability or unacceptability of a given leve l of VAQ on the public welfare. We do know 19 from preference and/or valuation studies that at mospheric visibility conditions can be quickly 20 assessed and preferences determined. These studie s show that a momentary glance at an image 21 of a scene (i.e. less than a minute) is enough fo r study participants to consistently judge the 22 acceptability or unacceptability of the viewed visual air quality conditions. Outside these 23 controlled settings, we are unaware of any studies that characteri ze the extent to which different 24 frequencies and durations of exposure to visibilit y conditions contribute to the degree of public 25 welfare impact that occurs. 26 In some circumstances, such as infrequent vi sits to scenic vistas in natural or urban 27 environments, people are motivated specifically to take the opport unity to view a valued scene 28 and are likely to do so for many minutes to hours to appreciate various asp ects of the vista they 29 choose to view. In such circumstances, the viewer may consciously evaluate how the VAQ at 30 that time either enhances or diminishes the expe rience/view. However, the public also has many 31 more opportunities to notice visibility conditi ons on a daily basis in settings/surroundings 32 associated with performing daily routines (e .g. during commutes, while walking the dog, or 33 when taking out the recyclables). These scen es, whether iconic or generic, may not be 34 consciously viewed for their scenic value, but their VAQ can still aff ect a person’s sense of 35 wellbeing. Research has demonstrated that peop le are emotionally affected by low VAQ, that 364-15 Draft – Do Not Quote or Cite March 2010 perception of pollution is correlated with stress, annoyance a nd symptoms of depression, and that 1 VAQ is deeply intertwined with a “sense of place, ” affecting peoples sense of the desirability of 2 a neighborhood (ISA section 9.2.4). Though we do not know the extent to which these 3 emotional effects are linked to different periods of exposure to poor VAQ, providing additional 4 protection against even short term exposures to levels of VAQ considered unacceptable would be 5 expected to provide some degree of improvement in the public’s “sense of wellbeing”. 6 Some people have mostly intermittent opportu nities on a daily basis (e.g. during morning 7 and/or afternoon commutes) to e xperience ambient visibility conditions as they spend much of 8
their time indoors without access to windows. For such people a view of poor VAQ during their 9 morning commute may provide thei r perception of the day’s visibi lity conditions until the next 10 time they venture outside during da ylight hours later or perhaps th e next day. Other people have 11 exposure to visibility conditions throughout th e day, so that a day with multiple hours of 12 visibility impairment would likely be judged a having a greater impact on their wellbeing than a 13 day with just one such hour. 14
We have no information or studies on the fr action of the public that has only one or a 15 few opportunities to experience visibility duri ng the day, or information or studies on the 16 duration of the effect on wellbeing from exposure to different durations of poor VAQ conditions. 17 However, it is logical to concl ude that people with limited opportuni ties to experience visibility 18 conditions on a daily basis would receive the entire impact of the day’s VAQ based on the 19 visibility conditions that occur dur ing the short time period when they can see it. On the basis of 20 this rationale, the segment of the population w ith infrequent access to visibility could be 21 characterized as a sensitive subpopulation. Since this group could be aff ected on the basis of 22 observing VAQ conditions for periods as short as one hour or less, we believe it is appropriate to 23 consider characterizing PM visibi lity conditions in terms of the worst or maximum hourly value 24 during daylight hours for each day for purposes of ev aluating the adequacy of the current suite of 25 secondary standards. 26 For another group of observers, those who have access to visibility conditions often or 27 continuously throughout the day, the entire impact of the day’s visibility conditions may be 28 based on the varying visibility conditions they observe throughout the day. For this group, it 29 might be more appropriate to eval uate the adequacy of the current suite of secondary standards in 30 terms of all daylight hours in the day. 31 While both the maximum daily and all hour av eraging times were assessed in the UFVA 32 for the PM light extinction indicator, only the ma ximum daily 1 hour average is assessed for the 33 PM mass concentration indicator (below and Ap pendix A). In looking at the UFVA assessment 34 of PM light extinction, we noticed a close correspondence between th e level of protection 35
afforded for all 15 urban areas in the assessm ent by the maximum daily daylight1-hour with 90 th 364-16 Draft – Do Not Quote or Cite March 2010 percentile and the all day light 1-hour with the 98 th percentile (UFVA s ection 4.1.4). Thus, at 1 these percentiles, either form of the standard provides protecti on of welfare effects to both the 2 fraction of the public with rare opportunities and to those with ample opportunities to experience 3 visibility. For consistency between PM 2.5 mass and PM light extinc tion and because the daily 4 maximum daylight 1-hour is thought to be more protective of those with limited opportunities to 5 experience visibility, only the daily maximu m form results will be displayed here. 6
Temporal Variations of Visibility Impacts 7
While visibility conditions can change quick ly (i.e., less than a minute), atmospheric 8 sight path averaged light extinc tion which is pertinent to visibility impacts generally changes 9 more slowly (i.e. tens of minutes generally). Sub-hourly variations in light extinction 10 determined at any point in the atmosphere are likely the result of small scale spatial pollution 11 features (i.e. plumes) being tr ansported by the wind across that point. At typical wind speeds 12 found in U.S. cities, an hour corresponds to a few te ns of kilometers of air flowing past a point, 13 which is similar to visibility sight path lengths of interest in urban areas. 14 PM concentrations and light extinction in urban environments vary from hour to hour 15 throughout the day due to a combination of diur nal meteorological conditions and systematic 16 changes in emissions activity (e.g. rush hour traffic). Generally low mixing heights at night and 17 during the early morning hour tend to trap locally produced emissi ons, which are diluted as the 18 mixing height increases due to heating during the day. Low te mperatures and high relative 19 humidity at night are conducive to the presences of ammonium nitr ate particles and water growth 20 by hygroscopic particles compared with the generally higher temp eratures and lower relative 21 humidity later in the day. These combine to make early morning the most likely time for peak 22 urban visibility impacts. Superimposed on such sy stematic time of day variations are the effects 23 of synoptic meteorology (i.e., those associated with changing weather) and regional scale air 24 quality that can generate peak visibility im pacts any time of day. The net effects of the 25 systematic urban and larger scale variations are that peak daytime PM light extinction can occur 26 any time of day though more often in early morning hours (UFVA section 3.4.2 and 3.4.3 and 27 shown in Figures 3-9, 3-10 and 3-12). Use of mu lti-hour averaging of PM light extinction would 28 suppress peak hourly conditions that are expect ed to represent peak visibility impacts. 29
Meteorological Causes of Visibility Impacts 30
Visibility is also reduced di rectly by the presence of preci pitation and fog regardless of 31 the presence or absence of PM. A secondary PM NAAQS is not meant to protect against such 32 sources of visibility impairment not related to PM. Therefore, one consideration in the 33 development of alternative standard forms (discu ssed below in section 4.3) was the inclusion of a 344-17 Draft – Do Not Quote or Cite March 2010 relative humidity screen in an effort to avoi d misinterpretation of the direct effect of 1 meteorological conditions on visibility and those caused by PM air quality. 2

 Based on currently available information, what range of levels of visibility impairment 3 is reasonable to consider in reaching judg ments about the adequa cy of the current 4 NAAQS? 5 In order to identify levels of visibility impairment appropriate for consideration in setting 6 secondary PM NAAQS to protect the public welfare, we comprehensively examined information 7 that was available in this review regarding people’s stated prefer ences for acceptable and 8 unacceptable visual air quality. 9 Light extinction is an atmosphe ric property that by itself does not directly translate into a 10 public welfare effect. Instead, li ght extinction becomes meaningful in the context of the impact 11 of visibility on the human observer. This has been studied in terms of the acceptability or 12 unacceptability expressed for it by a human observer. The perception of the visibility impact of 13 a given level of light extinction occurs in conj unction with the associat ed characteristics and 14 lighting conditions of the viewed scene. Thus, a given level of light extin ction may be perceived 15 differently by an observer looking at a different scene or the same scene with different lighting 16 characteristics. Likewise, diffe rent observers looking at the same scene with the same lighting 17 may have different preferences regarding th e associated VAQ. When scene and lighting 18
characteristics are held constant , the perceived appearance of a scene (i.e., how well the scenic 19
features can be seen and the amount of visible haze) depends only on change s in light extinction. 20 This has been demonstrated using the WinHaze m odel that uses image processing technology to 21 apply user-specified changes in light extincti on values to the same base photograph with set 22 scene and lighting characteristics. 23
Much of what we know about th e acceptability of le vels of visibility comes from survey 24 studies in which participants we re asked questions about their pr eference or the value they place 25 on various visibility levels as displayed to them in scenic photographs and/or WinHaze images 26 with a range of known light extinction levels. Ur ban visibility preference studies for four urban 27
areas were reviewed in the UFVA (chapter 2) to assess the light extinction levels judged by the 28 participant to have acceptable visibility. While the results differed among the four urban areas, 29 results from a rating exercise showed that wi thin each preference st udy, survey participants 30 consistently distinguish betw een different levels of light extinction and prefer and value 31 visibility associated with lower light extinction levels among the s cenic images they are shown. 32 The reanalysis included three completed urban visibility preference survey studies plus a 33 pair of smaller focus studies designed to explor e and further develop urban visibility survey 34
instruments. The three western studies included Denver, Colorado (Ely et al., 1991), one in the 35 lower Fraser River valley near Vancouver, Bri tish Columbia (BC), Canada (Pryor, 1996), and 364-18 Draft – Do Not Quote or Cite March 2010 one in Phoenix, Arizona (BBC Research & Consulting, 2003). A pilot focus group study was 1 also conducted for Washington, DC (Abt Associates Inc., 2001). In response to an EPA request 2 for public comment on the Scope and Met hods Plan (74 FR 11580, March 18, 2009), we 3 received comments (Smith, 2009) about the results of a new Wa shington, DC focus group study 4 that had been conducted using methods and appr oaches similar to the method and approach 5 employed in the EPA pilot study (Smith and Howell, 2009). When taken together, these studies 6
from the four different urban areas included a total of 852 individuals, with each individual 7 responding to a series of questi ons answered while viewing a se t of images of various urban 8 VAQ conditions. 9 The approaches used in the four studies are similar and are all derived from the method 10 first developed for the Denver urban visibility study. In particular , the studies all used a similar 11 group interview type of survey to investigate the level of visibility impairment that participants 12 described as “acceptable. While each study asked the basic questi on, “What level of visibility 13 degradation is acceptable?”, th e term “acceptable” was not defined, so that each person’s 14 response was based on his/her own values and pref erences for VAQ. Given the similarities in 15 the approaches used, we concluded that it is reasonable to compare the results to identify overall 16 trends in the study findings and that this comparis on can usefully inform the selection of a range 17
of levels for use in further anal yses. However, variations in the specific materials and methods 18 used in each study introduce uncer tainties that should also be c onsidered when interpreting the 19 results of these comparisons. Key differences betw een the studies include: 1) image presentation 20 methods (e.g., projected slides of actual photos , projected images generated using WinHaze (a 21 significant technical advance in the method of presenting VAQ c onditions), use of computer 22 monitor screen; 2) number of participants in each study; 3) participan t representativeness of the 23 general population of the relevant metropolitan area; and 4) specific wording used to frame the 24 questions used in the group interview process. 25 In the UFVA, each study was evaluated separately and figures developed to display the 26 percentage of participants that rated each photograph as “acceptable ”. The horizontal axis was in 27 terms of light extinction (deciview) and the vertical axis in terms of percent of participants rating 28 “acceptable”. Ely et al. (1991) introduced a “50% acceptability” criteria analysis of the Denver 29 preference study results. The 50% acceptability criteria is designed to identify the VAQ level 30 that best divides the photogra phs into two groups: those with a VAQ rated as acceptable by the 31 majority of the participants, and those rated not acceptable by the majority of participants. We 32 adopted the criteria as a usef ul index for comparison between studies. The results of each 33 individual analysis were then combined graphi cally to allow for visual comparison. Figure 4-1 34 (Figure 2-16 in UFVA) presents the graphical summa ry of the results of the studies in the four 35 cities and draws on results previously presented in Figures 2-3, 2-5, 2-7 and 2-11 of chapter 2 in 364-19 Draft – Do Not Quote or Cite March 2010 the UFVA. Figure 4-1 also contai ns lines at 20 dv and 30 dv that effectively and pragmatically 1 identify a range where the 50% acceptance criteria occur across all four of the urban preference 2 studies. Out of the 114 data points shown in Figure 4-1, only one photograph (or image) with a 3 VAQ below 20 dv was rated as acceptable by less than 50% of the participants who rated that 4 photograph. 2 Similarly, only one image with a VAQ above 30 dv was rated acceptable by more 5 than 50% of the partic ipants who viewed it. 3 6
7 Figure 4-1 Summary of results of urban visibility studies in four cities, showing the identified range of the 50 % acceptance criteria . 4

8 As can be seen in the figure, each urban area has a separate and unique response curve 9 that appears to indicate that it is distinct from the others. These curves are the result of a 10 logistical regression analysis using a logit model of the greater than 19,000 ratings of haze 11 images as acceptable or unacceptable. The mo del results can be us ed to estimate the VAQ 12 deciview values where the estimated response f unctions cross the 50% ac ceptability level, as 13

2 Only 47% of the BC participants ra ted a 19.2 dv photograph as acceptable.
3 In the 2001 Washington, D.C. study, a 30.9 dv image was used as a repeated slide. The first time it was shown 56% of the participants rated it as acceptable, and 11% ra ted it as acceptable the second time it was shown. The same VAQ level was rated as acceptable by 42% of the participants in the 2009 study (Test 1).
4 Top scale shows light extinction in inverse megameter units ; bottom scale in deciviews. Logit analysis estimated response functions are shown as the color-coded curved lines for each of the four urban areas4-20 Draft – Do Not Quote or Cite March 2010 well as any alternative criteria levels. Selected examples of these are shown in Table 4-1 (Table 1 2-4 in UFVA, Chapter 2). These results show that the logit model data also support the upper 2 and lower ends of the range of 50 th percentile acceptabi lity values (e.g. near 20 dv for Denver 3 and near 30 dv for Washington, DC) already identif ied in Figure 4-1 (see Table 2-4 UFVA). 4
5
Table 4-1 Logit model estimated VAQ values corresponding to various percent 6 acceptability values for the four cities. 7 8
Denver British Columbia Phoenix Washington, DC 90% Acceptability criteria 14.21 16.80 24.15 23.03 75% Acceptability criteria 17.05 19.63 21.80 26.03
50% Acceptability Criteria 19.90 22.45 24.15 29.03

25% Acceptability criteria 22.74 25.28 26.51 32.03 10% Acceptability criteria 25.59 28.10 28.87 35.03

9 Based on the composite results and the effective range of 50 th percentile acceptability 10 across the four urban preference studies shown in Figure 4-1 a nd Table 4-1, benchmark levels 11 have been selected in a range from 20 dv to 30 dv (74 Mm -1 to 201 Mm -1 ) for the purpose of 12 provisionally assessing whether visibility cond itions would be consider ed acceptable (i.e., less 13 than the low end of the range), unacceptable (i.e ., greater than the high end of the range) or 14 potentially acceptability (within the range). A midpoint of 25 dv (122 Mm -1 ) was also selected 15 for use in the assessment. This level is also very near to the 50 th percentile criteria value from 16 the Phoenix study (i.e. 24.3 dv), which is by far the be st of the four studies in terms of least noisy 17 preference results and the most representative sel ection of participants. Based on the currently 18 available information, we conclude that the use of 25 dv to represent the middle of the 19
distribution of results seems well supported. 20 These three benchmark values provide a low, middle, and high set of light extinction 21 conditions that are used to provi sionally define daylight hours w ith urban haze conditions that 22 have been judged unacceptable by the participants of these preference studies. As discussed 23 above, PM light extinction is taken to be light extinction minus the Rayl eigh scatter (i.e. light 24 scattering by atmospheric gases which is on average about 10 Mm -1 ), so the low, middle and 25 high levels correspond to PM light extinction levels of about 64 Mm -1 , 112 Mm -1 and 191 Mm -1

. 26 In the UFVA, these three levels were called Cand idate Protection Levels (CPLs). We continue 27 to use this term in this document. However, it is important to note that the degree of protection 284-21 Draft – Do Not Quote or Cite March 2010 provided by a secondary NAAQS is not determined solely by the level of the standard but by all 1 the components (e.g., indicator, form, level, averag ing time) being applied together. Therefore, 2 the reader should keep in mind that the term CPL is meant only to indicate levels within a range 3 that we feel are appropriate for consideration th at could, in conjunction wi th other aspects of the 4 standard, provide an appropriate degree of visibility protection. 5 In characterizing our degree of confidence in each CPL and across th e range, a number of 6 issues were considered. Looking first at the two studies that define the upper and lower bounds 7 of the range, we considered whether they represen t a true regional distinction in preferences for 8 urban visibility conditions between Western an d Eastern U.S.. There is little information 9 available to help sort this out , especially given that we have preference studies in only one 10 Eastern urban area. Smith and Howell (2009) fou nd little difference in preference response to 11 Washington, DC haze photographs between the study participants from Washington, DC and 12 those from Houston, TX. This provides some limited evidence that the value judgment of the 13 public in different areas of the country may not be an important factor in explaining the 14 differences in these study results. 15 In further considering what f actors could explain the observe d differences in preferences 16 across the four urban areas, we noted that th e urban scenes used in each study had different 17 characteristics. For example, each of the We stern urban visibility preference study scenes 18 included mountains in the background while the singl e Eastern urban study did not. It’s also true 19 that each of the Western scenes included objec ts at greater distances from the camera location 20 than in the Washington, DC study. There’s no qu estion that objects at a greater distance have a 21 greater sensitivity to perceived visibility changes as light extinction is changed compared to 22 otherwise similar scenes with obj ects at a shorter range. This alone might explain the difference 23 between the results of the Washington DC, st udy and those from the Western urban studies. 24 Also it’s intuitively likely that people value the views of mountains in the background more than 25 generic distant buildings in the foreground of the Western scenes; just as it seems obvious that 26 the Capital Mall and Washington M onument were the likely objects of greatest interest for the 27 Washington, DC study base photograph. Having s cenes with the object of greatest intrinsic 28 value nearer and hence less sensitive for Washington compared with more distant objects of 29 greatest intrinsic value in the Western urban areas could further expl ain the difference in 30 preference results. 31 Another question that we cons idered was whether the high CP L value that is based on the 32 Washington DC preference results is likely to be generally represen tative of urban areas that do 33
not have associated mountains or other valued objects visible in the di stant background. Such 34
areas would include the middle of the country and many areas in th e eastern US. In order to 35 examine this issue, an effort would have to be ma de to see if scenes in such areas could be found 364-22 Draft – Do Not Quote or Cite March 2010 that would be generally comparable to the western scenes (e.g., contain valued scenic elements at 1
more sensitive distances than that used in th e Washington, DC study). This is only one of a 2 family of issues concerning how exposure to ur ban scenes of varying sensitivity affects public 3 perception, for which no information is currentl y available. Additional urban visibility 4 preference studies employing images selected of potentially more sensit ive scenes could help 5 evaluate whether a lower value for the high CP L is supportable. Othe r investigations to 6
determine how common such scenes are in va rious regions of the country would also be 7 informative. Until such information becomes available, the high end of the CPL range (30 dv) 8 seems to be an appropriate level to consider. 9 With respect to the low end of the range, we considered factors that might further refine 10 our understanding of the robustness of this level. We concluded that additional urban preference 11 studies, especially with a greater variety in types of scenes, in cluding potentially more sensitive 12 Western urban scenes, could help evaluate whether a lower CPL value than the currently selected 13 20 dv is supportable. Further, the reason for the noisiness in data points around the curves 14 apparent in both the Denver and British Columbia results compared to the smoother curve fit of 15 Phoenix study results could be explored. One po ssible explanation that we identified is that 16 these older studies used photogra phs taken at different times of day and on different days to 17 capture the range of light extincti on levels needed for the preference studies. By contrast, the use 18 of WinHaze in the Phoenix (and Washington, DC) st udy, reduced variations in scene appearance 19 that affects preference rating and avoided th e uncertainty inherent in using ambient 20 measurements to represent sight path averaged light extinction values. Reducing these sources 21 of noisiness and uncertainty in th e results of future studies of sensitive urban scenes could 22 provide more certainty in the selection of a low CPL value. 23

 To what extent does the available informatio n demonstrate or suggest that PM-related 24 visibility impairment (within the range of CPLs) is occurring at current ambient 25 conditions or at levels that wo uld meet the current standards? 26 Current Visibility Levels 27
Chapter 3 of the UFVA characterized current visibility conditions in terms of both PM 2.5 28 and light extinction levels for the 15 urban areas selected and compared them to the CPLs 29
identified above. 30 As an initial matter, we note that PM is not necessarily the primary source of visibility 31 impairment during periods with fog or precipit ation. In order to avoid precipitation and fog 32 confounding estimates of PM visibility impairme nt, and as advised by CASAC as part of its 33 comments on the first public review draft of the UFVA, we restrict ed our assessment of visibility 34 conditions to daylight hours with relative humid ity less than or equal to 90% (UFVA section 354-23 Draft – Do Not Quote or Cite March 2010 3.3.5 and Appendix G). However, not all periods with relative humidity above 90% have fog or 1 precipitation. Removing those hours from applica tion of a secondary PM standard involves a 2 tradeoff between the benefits of avoiding ma ny of the hours with me teorological causes of 3 visibility impacts and the cost of not counting some hours with high relative humidity without 4 fog or precipitation, where the growth of hygroscopic PM into large solution droplets results in 5 enhanced PM visibility impacts. For the 11 ur ban areas included in the assessment for which 6 updated meteorological data was obt ained, a 90% relative humidity cutoff criterion is effective in 7 that on average less than 6% of the hours are removed from c onsideration, yet those hours have 8 on average twelve times the likelihood of meteor ological causes of reduced visibility compared 9 with hours with 90% or lower relative humidity. 10 Figure 4-2 (Figure 3-8 in UFVA) presents box-and-whisker plots to illustrate the 11 distributions of the estimates of daylight 1-hour reconstructed PM light ex tinction levels in each 12 area in each year during the 2005-2007 time perio d. The distribution of the daily maximum 1- 13
hour values is shown. The horizontal dashed lines in the plots represent the low, middle, and 14 high CPLs for PM light extinction of 64, 112, and 191 Mm -1 , corresponding to the benchmark 15 VAQ values of 20 dv, 25 dv and 30 dv as discusse d above. Table 4-2 (Table 3-7 in UFVA) 16 provides the percentages of days (across a ll of 2005-2007, unweighted) in which the daily 17 maximum daylight 1-hour PM light extinction le vel was greater than each of the three CPLs 18 (excluding hours with relative hum idity greater than 90 percent). 19 From these displays it can be seen that among the 15 urban areas, those in the East and in 20 California tend to have a higher frequency of vi sibility conditions above the high CPL compared 21 with those in the Western US. Both Figure 4-2 and Table 4-2 indicate that all 15 urban areas 22 have daily maximum hourly PM li ght extinctions that exceed even the highest CPL some of the 23 time. Again, the non-California we stern urban locations have the lowest frequency of maximum 24 hourly PM light extinction with values in exces s of the high CPL for 8 percent or fewer of the 25 days. Except for the two Texas and the non-Calif ornia western urban area s, all of the other 26 urban areas exceed that high CPL from about 20 pe rcent to over 60 percent of the days. Based 27 on these estimated maximum hourly PM light extin ction estimates, all 15 of the urban areas 28 exceed the low CPL for about 40 percent to over 90 percent of the days. Based on all of the 29 above, we conclude that current levels of PM lig ht extinction associated with recent PM air 30 quality exceed levels that could reasonably be considered as protective of the public welfare. 31
32
33
344-24 Draft – Do Not Quote or Cite March 2010 Figure 4-2. Distribution of estimated maximum da ily daylight 1-hour PM light extinction 1 across the 2005-2007 period, by study area (excluding hours with relative 2 humidity greater than 90 percent). (Adapted from Figure 3-8 in UFVA )* 3

* In thel box-and-whisker plot, the box represents the 25 th to 75 th percentile range and the 4 whiskers represent the 10 th and 90 th percentile points of the data; individual data points below the 10 th 5 percentile and above the 90 th percentile are graphed as small circles. The three dashed horizontal lines 6 represent the three CPL levels of 64, 112, and 191 Mm -1

. 74-25 Draft – Do Not Quote or Cite March 2010 1 Table 4-2 Percentage of daily maximum hourly values of daylight PM light extinction 2 exceeding CPLs (excluding hours with relative humidity greater than 90 3 percent). (adapted from Table 3-7 in UFVA) 4 5

Candidate Protection Level 64 Mm -1 112 Mm -1 191 Mm -1
Study Area Number of Days with Estimates (a) Percentage of Daily Maximum Hourly Values Exceeding CPL Tacoma 109 52 22 4

Fresno 324 75 52 30 Los Angeles 300 90 83 62
Phoenix 86 42 7 1 Salt Lake City 306 44 17 8

Dallas 273 80 41 10

Houston 148 79 45 11
St. Louis 289 98 78 40 Birmingham 349 89 65 34

Atlanta 279 91 75 31
Detroit 141 87 68 43 Pittsburgh 277 85 57 26
Baltimore 181 80 50 23 Philadelphia 143 86 64 31

New York 225 83 59 28 Average 229 77 52 26 6
Visibility Levels That Just Meet Current Standards 7

In the second draft of the UFVA, we modeled the “what if ” scenario based on simulating 8 just meeting the current suite of PM 2.5 secondary standards: 15 μg/m 3 annual average PM 2.5 9 concentration and 35 μg/m 3 24-hour average PM 2.5 concentration with a 98 th percentile form, 10 averaged over three years. The steps needed to model the “what if” co nditions involve explicit 11 consideration of changes in PM 2.5 components and are described here. First, we applied 12 proportional rollback to all the PM 2.5 monitoring sites in each st udy area, taking into account 13

PRB PM 2.5 mass, to “just meet” the NAAQS scenario fo r the area as a whole, not just at the 14 visibility assessment study site. The health risk assessment document (EPA 2010a) describes 15 this procedure in detail. Th e degree of rollback is controlle d by the highest annual or 24-hour 16 design value, which in most study areas is from a s ite other than the site us ed in this visibility 17
assessment. The relevant result from this an alysis is the percenta ge reduction in non-PRB PM 2.5 18 mass need to “just meet” the NAAQS scenario, for each study area. These percentage reductions 194-26 Draft – Do Not Quote or Cite March 2010 are shown in Table 4-4 of the UFVA. Note th at Phoenix and Salt Lake City meet the 15/35 1 NAAQS scenario under current cond itions, and require no reduction. PM 2.5 levels in these two 2 cities were not “rolled up.” Second, for each day and hour for each PM 2.5 component, we 3
subtracted the PRB concentrati on from the current conditions concentration, to determine the 4 non-PRB portion of the current c onditions concentration. Third, we applied the percentage 5 reduction from step 1 to the non-P RB portion of each of the five PM 2.5 components and added 6 back the PRB portion of the component. Finally , we re-applied the IMPROVE algorithm, using 7
the reduced PM 2.5 component concentrations, the current conditions PM 10-2.5 concentration for the 8 day and hour, and relative humidity for the day and hour. We then included the term for 9 Rayleigh scattering. 10 Figure 4-3 and Table 4-3 disp lay the results of the rollback procedure as a box and 11 whisker plot of daily maximum daylight 1-hour PM light extinction and th e percentage of daily 12 maximum hourly PM light extinction values exce eding the CPLs when just meeting the current 13

PM 2.5 NAAQS scenario of 15/35 μ g/m 3 (excluding hours with relative humidity greater than 90 14 percent. These displays show that at the curren t PM NAAQS level (i.e., 15 /35) all of the eastern 15 urban areas and Los Angeles exceed the least restrictive CPL more th an 10% of the time and that 16 only Tacoma would not exceed the least restri ctive CPL more than 2% of the time. 174-27 Draft – Do Not Quote or Cite March 2010 1 Figure 4-3. Distribution of daylight 1-hour PM light extinction when rolled back to just 2 meet current PM fine NAAQS across the 2005-2007 period, by study area 3 (excluding hours with relative hu midity greater than 90 percent). * 4 NAAQS Scenario: 15 μ g/m 3 annual; 35 μ g/m 3 24-hour 5 Displayed: Daily Max Daylight Light Ex tinction (excluding hours >90% RH) 6

7 * In thel box-and-whisker plot, the box represents the 25 th to 75 th percentile range and the 8 whiskers represent the 10 th and 90 th percentile points of the data; individual data points below the 10 th 9 percentile and above the 90 th percentile are graphed as small circles. The three dashed horizontal lines 10 represent the three CPL levels of 64, 112, and 191 Mm -1 11 124-28 Draft – Do Not Quote or Cite March 2010 1 Table 4-3 Percentage of daily maximum hourly values of daylight PM light extinction 2 exceeding CPLs when “jus t meeting” the current PM 2.5 NAAQS (15/35 μ g/m 3 ) 3 (excluding hours with relative humidity greater than 90 percent). (Adapted from 4 Table 4-7 in UFVA). 5 6

Candidate Protection Level 64 Mm -1 112 Mm -1 191 Mm -1
Study Area Number of Days with Estimates (a) Percentage of Daily Maximum Hourly Values Exceeding CPL Tacoma 109 43 10 1

Fresno 324 54 30 10 Los Angeles 300 85 69 39
Phoenix 86 44 6 1 Salt Lake City 306 24 9 4

Dallas 273 81 41 10

Houston 148 75 41 11
St. Louis 289 97 74 36 Birmingham 349 84 55 24

Atlanta 279 90 71 25
Detroit 141 80 61 33 Pittsburgh 277 78 48 16
Baltimore 181 78 48 19 Philadelphia 143 85 61 28

New York 225 76 45 19

Average 229 72 45 18

7

4.2.2 Summary 8 In summary, we reach the preliminary conc lusion that the available information in 9 this review, as described above and in the UF VA and ISA, clearly calls into question the 10 adequacy of the current suite of PM 2.5 standards in the c ontext of public welfare protection from 11 unacceptable levels of visibility impairment, prim arily in urban areas, a nd supports consideration 12 of alternative standards to pr ovide appropriate protection. 13 This preliminary conclusion is based first on th e large percentage of days that exceed the 14 range of CPLs identified for consideration unde r both current and just meet PM air quality 15 conditions. In particular, under just meet conditions for the su ite of secondary PM NAAQS (i.e. 16
15/35 μ g/m 3 ) greater than 10% of the days exceed the highest, least pr otective CPL of 191 Mm -1 174-29 Draft – Do Not Quote or Cite March 2010 for 10 of the 15 urban areas. When the middle CPL of 112 Mm -1 is considered, 12 of the 15 1 cities have greater than 10% of their days exceed ing with a range of 30 to 74% of days exceeding 2
this level. At the lowest CPL of 64 Mm -1 , the percentage of days exceeding range from 24 to 3
97% across the 15 urban areas. 4 Second, we have reached the preliminary conc lusion that the averaging times associated 5 with the current suite of PM NAAQS are not well suited to protect against PM-related visibility 6 impairment on the basis that short term exposur es (e.g., 1 hour or less) is sufficient for an 7 unacceptable level of visual air quality to be observed and the associated impacts of that 8 observation to be registered by the observer. Since some portion of the population may only 9 have the opportunity to observe one hour or less of ambient daylight visibility conditions, relying 10 on an averaging time as long as that of the cu rrent 24 hour and annual PM standards would make 11 it difficult to identify a requisite level of pr otection that would translate into appropriate 12 protection against the maximum daily value. In addition, these longer averag ing times also result 13 in the inclusion of nighttime conditions, for whic h the science needed to support identification of 14 appropriate levels of visibility protec tion is not well developed or understood. 15 In reaching the preliminary conclusi on that the current suite of PM 2.5 standards are 16 inadequate to provide the a ppropriate protection of the pub lic welfare from known and/or 17 anticipated adverse effects by calling into question the adequacy of the current levels and 18 averaging times, it also seems reasonable to consider whether the current indicator of PM 2.5 19 remains useful in relating ambient PM to its public welfare effect of visibility impairment. 20
Section 4.3 below discusses these and other considerati ons in its discussion of alternative 21
standards for consideration. 22

4.3 CONSIDERATION OF ALTERNATIVE STANDARDS 23 Having reached the conclusion that ju st meeting the current suite of PM 2.5 standards 24 continues to allow levels of PM visual air qua lity that, based on the scientific evidence and 25 information available in this review, can reasonabl y be considered adverse to the public welfare, 26
this section will discu ss alternative standards that could potentially provide requisite public 27 welfare protection from known and/or anticipated a dverse effects. Any PM standard that results 28 in emissions reductions can be expected to resu lt in visibility improvements, though meeting that 29
standard does not ensure an ad equate or uniform degree of prot ection from adverse visibility 30 conditions. A requisite level of public welfare protection can be facilitate d by adopting a 31 standard specifically designed w ith indicator, averaging time and form that better mimics the 32
characteristics of the e ffect of interest. 334-30 Draft – Do Not Quote or Cite March 2010 4.3.1 Nature of the Indicator 1

 To what extent does information provi de support for considering a different 2 pollution indicator(s) for PM to replace or supplement the PM 2.5 mass based 3 indicator? 4
EPA staff is considering two alternative indicators: PM 2.5 mass and PM light extinction. 5

PM 2.5 mass is taken here to be the same indicator as is used by the current suite of PM NAAQS. 6 PM light extinction is the contributions to light extinction by PM 10 under ambient conditions. 7
EPA staff believes that the use of PM light extinction as an indicator is justified because it is a 8 physically meaningful measure of the PM quantity that is most re levant and directly related to 9 visibility effects. The basis for consid ering each indicator is discussed below. 10
PM Light Extinction Indicator 11
PM light extinction is highly related to light extinction, which is the property of the 12 atmosphere that is most directly related to visibility effects. It differs from light extinction by the 13 nearly constant contributions for Rayleigh (or clean air) light scattering and the minor 14 contributions by NO 2 light absorption. Most importan tly, there are no confounding issues 15 associated with particle size or composition, including PM water. PM light extinction can be 16 directly measured under ambient conditions by several instrumental methods, some of which 17 have been used for decades to routinely mon itor the two components of PM light extinction 18 (light scattering and absorption) or to jointly measure both as total light extinction (from which 19 Rayleigh scattering is subtracted to get PM light extinction). 20 EPA staff also recognizes that while PM 2.5 light extinction can be accurately measured by 21 a number of commercially available instruments, it is technically more challenging to measure 22
the PM 10 – 2.5 component of light extinction. This issu e many not be of concern for many regions 23 of the country where the PM 10 – 2.5 contributions to light extinc tion are minor (see UFVA section 24 3.4.5). However for some regi ons (e.g. Phoenix), the PM 10 – 2.5 contributions to light extinction 25 are substantial and may need to be accounted for by some other methodology (e.g. estimation 26
from PM 10 – 2.5 mass concentration measurements). As an alternative to direct measurements, 27 light extinction can be estimated from PM speciation and relative humidity data (see section 4.2). 28 There are a number of reasons for preferring dir ect measurements to algorithm-estimates of PM 29 light extinction for use in a secondary standar d. These include the grea ter accuracy of direct 30 measurements, the ability to have short averag ing times and the overall simplicity absent when 31 multiple measured parameters need to be processed to generate the indicator for a standard. 32 There currently is no FRM for PM light extin ction monitoring. Development of such an 33 FRM could take one to two years. There is no routinely operated PM light extinction monitoring 34 program in urban areas. Deploying such a network will required time and resources. As a result, 354-31 Draft – Do Not Quote or Cite March 2010 the selection of PM light extinc tion as an indicator could reason ably be expected to extend the 1 time required for promulgation/implemen tation of a secondary PM NAAQS. 2

PM 2.5 Mass Indicator 3

PM 2.5 mass is responsible for most of the visib ility impairment in the majority of urban 4 areas. In these areas, the contribution of PM 10 – 2.5 is a minor contributor to visibility impairment 5 most of the time. However, at some locat ions (see UFVA Figure 3-13 for Phoenix) PM 10 – 2.5 is a 6 major contributor to urban visibility effects. In those cities, a PM 2.5 standard alone may not 7 provide adequate visibility protec tion. In the absence of PM air quality information from a much 8 larger number of urban areas acro ss the country, it is not possible at this time to know how many 9 urban areas fall into this categor y, though it is reasonable to presume that other urban areas in the 10 desert southwestern region of the country may have conditions similar to the conditions shown 11 for Phoenix. A possible solution to this issue would be to add a companion PM 10 – 2.5 standard to 12
control under those circumstances. This latter refine ment has not been developed for this review. 13 PM mass monitoring methods are in wide sp read use, including the Federal Reference 14 Method (FRM) involving the collection of periodic (1 day in 6 and 1 day in 3) 24-hour filter 15 samples. These samples are then subsequently analyzed to determine 24-hour PM fine mass. 16 The Chemical Speciation Network and continuous PM 2.5 monitoring produce hourly average 17 mass concentrations and are conducted at many locations. At a few locations, continuous 18 speciation sampling produces measures some of the major PM 2.5 chemical components. These 19 routine monitoring activities do not include measurement of the water content of the ambient PM 20 that contributes, often significan tly, to visibility impacts. Fu rther, the PM mass concentration 21 monitoring does not provide information on the com position of the PM which also contributes to 22 the variability in the amount of visibility impact associated with any ambient PM mass 23
concentration. 24 The overall performance of PM 2.5 mass as a predictor of visibility effects as indicated by 25 PM light extinction can be seen in scatter plots shown in Figure 4.3-1 for Pittsburgh and 26 Philadelphia, PA (Similar plots for all 15 urban areas are in Appendix D, Figure D-2). These 27 demonstrate the variation in hourly PM light extinction corresponding to any specific level of 28

PM 2.5 mass concentration as well as statistical diffe rences of the average relationships (depected 29 as the best fit lines) between cities. While this degree of variation is an important factor in 30 considering the appr opriateness of a PM 2.5 mass indicator, we note that correctly identifying each 31 hour’s visibility conditions is not required to es timate the extent to which the distribution of 32 visibility conditions may negativ ely impact public welfare. 334-32 Draft – Do Not Quote or Cite March 2010 Figure 4.3-1 Scatter plots of PM light extinction versus PM 2.5 mass concentration of two 1 cities (from UFVA Appendix D, Figure D2). 2

3

4.3.2 Averaging and Applicable Times 4 Consideration of an appropriate averaging ti me and factors with respect to the timing 5 over which a secondary standard should apply were informed by consideration of the nature of 6 PM visibility effects. 7 Nighttime visibility impacts, described in the ISA (section 9.2.2) are significantly 8 different from daytime impacts and not sufficiently well understood to be included at this time. 9 As a result, a secondary standard to protect visibility would best only apply to daylight hours. In 10 the UFVA daylight hours were defined to be those morning hours havi ng no minutes prior to 11 local sunrise and afternoon hours having no minutes after local sunset. This definition ensures 12 the exclusion of periods of time where the sun is not the primary outdoor source of light to 13
illuminate scenic features. 14 PM is not necessarily the primary source of vi sibility impairment during periods with fog 15 or precipitation. By excluding daylight hours with average relative humidity above 90% for 16 inclusion in a secondary PM sta ndard, the likely occurrence of vi sibility effects from fog and 17 precipitation is signif icantly reduced (UFVA section 3.3.5 and Appendix G). However not all 18 periods with relative humidity above 90% have fog or precipitation. So removing those hours 19 from application of a secondary PM standard invo lves a tradeoff between th e benefits if avoiding 20 many of the hours with meteorologi cal causes of visibility imp acts and not counting some hours 21 without fog or precipitation, but where the grow th of hygroscopic PM to large solution droplets 22 results in enhanced PM visibility impacts. Fo r the 11 urban areas included in the assessment for 234-33 Draft – Do Not Quote or Cite March 2010 which updated meteorologi cal data was obtained, 5 a 90% relative humidity cutoff criterion is 1 effective in that on average less than 6% of th e hours are removed from consideration, yet those 2 hours have on average twelve times the likelihood of meteorological causes of reduced visibility 3 compared with hours with 90% or lower relative humidity. 4 As discussed above (section 4.2.1) selection of an appropriate averaging time takes into 5 account both how quickly people experience and judge visibility conditions, as well as the 6 typical rate of change of the path averaged PM light extinc tion over urban areas. While 7 perception of visibility change can occur in less than a minute, meaningful changes to path 8 averaged light extinction occur more slowly a nd can be well represented by hourly averaging. 9 Multi-hour averaging times would have the eff ect of reducing the magnitude of hourly peak 10 visibility impacts which can change significantly from one daylight hour to the next (see UFVA 11 Figure 3-12). Reduction of peak values through multi-hour averaging reduces the ability of the 12 indicator to accurately characterize the visibil ity effects experienced by the segment of the 13 population that has infrequent short- term exposure during peak periods. 14

4.3.3 Alternative Levels/Forms 15

Candidate Protection Levels 16
The results from the visibility preferences st udies conducted in four urban areas define a 17 range of low, middle and high CPLs of 20 dv, 25 dv and 30 dv which are equivalent to PM light 18
extinction of values of 64 Mm -1 , 112 Mm -1 , and 191 Mm -1 (see section 4.2 above). With only the 19 four preference study results, the in dividual low and high CPL are in f act reflective of the results 20 from the Denver and Washington, DC studies in pa rticular, and the middle CPL is very near to 21
the 50 th percentile criteria re sult from Phoenix. 22 Determining PM 2.5 mass concentration values that correspond to the low, middle and 23 high CPL is complicated by the lack of a one-t o-one relationship between PM light extinction 24
and PM 2.5 mass. By considering a range of extincti on efficiency values (i.e., the ratio of PM 25 light extinction to PM 2.5 mass) from 3 m 2 /g to 10 m 2 /g, a range of PM 2.5 concentration levels that 26 crudely corresponds to a low estimate of the low CPL and high estimate of the high CPL values 27 can be determined. The full range is from ~6 μ g/m 3 to ~60 μ g/m 3 . Keeping in mind that there is 28 no exact one-to-one correspondence between PM ma ss concentration and PM light extinction, no 29 individual value in this range of conditions corresponds to the CPL values expressed in terms of 30 PM light extinction, so a number of alternate valu es within the range were selected for assessing 31 their visibility protection performance when co mbined with alternative forms (as described 32

5 Through an oversight, EPA staff did not obtain NWS data for Los Angeles, St. Louis, Houston, and Detroit in time for processing. These data will be added in the final UFVA.4-34 Draft – Do Not Quote or Cite March 2010 below). Five alternative PM 2.5 mass concentration values were selected for this purpose: 10 1

μ g/m 3 , 20 μ g/m 3 , 30 μ g/m 3 , 40 μ g/m 3 and 60 μ g/m 3

. 2

Alternative Forms 3

The form of the current 24-hour PM 2.5 NAAQS entails comparing the level of the 4 standard to the three consecutive year average of the annual 98 th percentile of the measured 5 indicator. The purpose in averaging for three y ears is to provide stability from the occasional 6 effects of inter-annual meteorological variability that can result in unusual high pollution levels 7 for a particular year that is ot herwise typical. The use of a pe rcentile form makes the standard 8 less subject to the possibility of inappropriate violations caused by statistical outlier indicator 9 values. For consistency with the current PM NAAQS and to provide stability from unusual years 10
or outlier indicator data , the secondary PM standard should c onsider incorporat ing the use of a 11 three year average of a specified percentile. 12 The urban visibility preference studies that pr ovided results leading to the range of CPLs 13 being considered in this documen t, offer no information that addr esses the frequency of time that 14 visibility levels should be below those values. Based on this and the natu re of the public welfare 15 effect being one of aesthetics and/ or feelings of wellbeing, we believe that it is not necessary or 16 appropriate to consider eliminating all such exposures and that allowing some number of 17 hours/days with reduced visibility can reason ably be considered. . In the UFVA, 90 th , 95 th and 18
98 th percentile annual values are included in th e PM light extinction NAAQS scenarios (Chapter 19 4). The hourly PM mass concentration scenarios that are described and assessed below and in 20 Appendix A include only the 90 th and 95 th percentile forms. 6 21 Another aspect of the form that needs to be considered is whether to include all daylight 22 hours or only the maximum daily daylight 1-hour. The maximum daily daylight 1-hour form is 23 more appropriate for protecting the welfare of people who have rare intermittent exposure to 24 visibility during the da y (e.g. during commutes), but spend most of their time isolated from 25 outdoor views. For such people a view of poor visibility during their morning commute may 26 represent their perception of the day’s visibil ity conditions until the next time they venture 27 outside during daylight, hours late r or perhaps the next day. Ot her people have exposure to 28 visibility conditions thro ughout the day. For those people it might be more effective to include 29 every daylight hour into assessing compliance wi th a standard, since a day with multiple hours 30 with visibility impairment is likely to be j udged a greater impact on their wellbeing than a day 31 with just one such hour. 32

6 Assessment of the 98 th percentile was thought to be unnecessarily restrictive, so it was not conducted at this time to simply and speed the assessment process.4-35 Draft – Do Not Quote or Cite March 2010 We do not know the fraction of the public that has only one or a few opportunities to 1 experience visibility during the day, nor do we have information or studies on the duration of the 2 effects on wellbeing associated with visibility conditions. However, it is logical that people with 3 limited opportunities to experience visibility conditions on a daily basis would experience the 4 entire impact associated with visibility base d on their short term exposure. The impact of 5 visibility for those who have access to visibility conditions often or continuously during the day 6 may be based on varying conditions throughout th e day. Based on these considerations, the 7 segment of the population with in frequent access to visibility could be characterized as a 8 susceptible population relative to peak visibility impairment, wh ile those with longer exposures 9 are a susceptible population for longe r-term visibility impairment. 10 In light of these considera tions, the UFVA assessment of th e various PM light extinction 11
scenarios included both forms and noticed a close correspondence be tween the level of 12 protection afforded for all 15 urban areas in the assessment by the maximum daily daylight1- 13
hour with 90 th percentile and the all daylight 1-hour with 98 th percentile (UFVA section 4.1.4). 14 In this sense, the reductions in visibility impairme nt required to meet either form of the standard 15 provides protection to both the fraction of the public with rare opportunities and to those with 16 ample opportunities to be affected by PM-related visibility impairment. 17 Both forms are assessed for the PM light extinction indicator (UFVA), but only the 18 maximum daily form is assessed for the PM mass concentration indicator (below and Appendix 19 A). For consistency between the two indicators and because the daily maximum daylight 1-hour 20 is thought to be more protective of those with limite d opportunities to expe rience visibility, only 21 the daily maximum form result s will be displayed here. 22

4.3.4 Performance of Alternative Standards 23

We conducted assessments of alternative standards based both on hourly PM light 24 extinction as the indicator (see Chapter 4 of the UFVA) and on hourly PM mass concentration 25 indicator (see Appendix A in this document). There are nine PM light extinction alternative 26 standards discussed here (i.e., da ily maximum daylight 1-hour PM light extinction at the low, 27 middle and high CPL for each of the 90 th , 95 th and 98 th percentile forms) and there are ten PM 2.5 28 mass concentration alternative standards (i.e., five concentration levels for each of the 90 th and 29
95 th percentile forms). In both cases the assessm ent involves rolling b ack non-policy relevant 30 background (PRB) PM light extinction or PM mass concentration values until these specific 31 alternative standards are just met. 32 In considering the performance of alterna tive standards, we focused on the uniformity 33 across the 15 urban areas of the resulting visibi lity conditions, as measured in terms of light 34 extinction, when the alternative scenarios ar e just met. Because of the one-to-one 354-36 Draft – Do Not Quote or Cite March 2010 correspondence light extincti on and PM light extinction, 7 the PM light extinction indicator based 1 standards should produce visibility conditions exactly as prescribed. The ability to structure a 2 PM light extinction based alternativ e standard to the level of visi bility protection desired is an 3 advantage because it could affords the most unifo rm degree of visibility protection nationwide. 4 Figures similar to 4.3-1 for the other PM light extinction scenarios are shown in 5 Appendix F of the UFVA. Table 4.3-1 shows th e design values for the 9 scenarios based on 6 maximum daily 1-hour PM light exti nction. When an area just meets a scenario, its design value 7 in principle should exactl y equal the NAAQS level, so preparati on of this table serves as a check 8 against calculation errors. Note that the design values in Table 4.3-1, resulting from the rollback 9 steps described in section 4.1.4 of the UFVA, in some cases do not exactly equal the assumed 10 level of the NAAQS, although all are quite clos e. In some cases (e.g. Phoenix for 191 Mm -1 /90 th 11
and 95 th percentile), current conditions already meet the scenar io specifications so no rollback 12 was necessary and current design values are sh own in Table 4.3-1 and reflected in box and 13 whisker plot figures. The minor di fferences between prescribed and assessed design values seen 14 for some applications of the rollback assessmen t are due to hours switching in the PM light 15 extinction frequency distribution that is purely an artifact of the rollback methodology as 16 described in the UFVA (section 4.3). These disc repancies were judged too small to justify 17
iterative rollback that could have been used to eliminate them. 18

7 In this assessment light extinction = PM light extinction + 10Mm -1 , where the last term is Rayleigh or clean air light scattering that in fact can range from about 8Mm -1 to 12Mm -1 depending on average sight path elevation above sea level.4-37 Draft – Do Not Quote or Cite March 2010 1 Figure 4.3-2 Daily maximum daylight 1-hour light extinction after rollba ck to just meet a 2 scenario with daily maximum of 112 Mm -1 for the 90 th percentile excluding 3 hours with relative humidity greater than 90 percent. 4 5
6

74-38 Draft – Do Not Quote or Cite March 2010 1 Table 4.3-1. PM light extinction design values for “just meeting” secondary NAAQS 2 scenarios based on measured PM light extinction (excluding hours with 3 relative humidity greater than 90 percent) 4

Secondary NAAQS Scenarios Based on Daily Maximum

(a) (b) (c) (d) (e) (f) (g) (h) (i)
Level (Mm -1 ) 191 191 191 112 112 112 64 64 64

Percentile

Form 90 th 95 th 98th 90 th 95 th 98th 90 th 95 th 98th
PM light extinction Design Value (based on same percentile form as the NAAQS scenario) Tacoma, WA 140 157 191 112 112 108 66 70 60

Fresno, CA 191 191 191 112 112 112 64 64 64

Los Angeles, CA 191 191 191 112 112 112 65 64 64

Phoenix, AZ 105 144 185 105 112 112 64 64 64

Salt Lake City, UT 164 191 191 112 112 112 64 64 64

Dallas, TX 183 191 191 113 113 112 64 66 66

Houston, TX 191 191 191 115 112 112 67 61 67

St. Louis, IL 191 191 191 113 112 112 65 64 64

Birmingham, AL 191 192 191 113 114 112 64 66 64

Atlanta, GA 191 191 191 112 111 112 64 63 65

Detroit, MI 191 191 191 112 112 112 64 64 65

Pittsburgh, PA 191 191 191 112 112 112 64 64 64

Baltimore, MD 191 191 191 111 112 112 63 64 65

Philadelphia, PA 191 191 191 112 112 112 65 64 64

New York, NY 192 191 191 113 112 112 65 64 64

5
64-39 Draft – Do Not Quote or Cite March 2010 A complete description of th e rollback assessment for the ten maximum daily 1-hour PM 1 mass concentration scenarios is available in Appe ndix A of this document. The process used is 2 very similar to that used in the UFVA for rollbac k of the PM light extinction based scenarios. 3
Since PM mass does not have a one-to-one correspondence to light extinction, the PM 4 light extinction conditions resul ting from just meeting standards based on PM mass are not as 5 uniform as those shown above for PM light extincti on scenarios. This is demonstrated in the box 6 and whisker plot of the maximum daily 1-hour PM light ex tinction for the 30 μ g/m 3 , 90 th 7 percentile scenario shown belo w (Figure 4.3-2), which shows gr eater variation from among the 8 urban areas than the PM light extinction based scenarios. Similar plots for all ten PM mass 9
based scenarios are shown in Appendix A (Figure A-2). 10
11 Figure 4.3-3 Maximum daily daylight 1-hour PM light extinction under "just meet" 12 conditions for a NAAQS scenario based on 1-hour PM 2.5 mass of 30 μ g/m 3

, 13 90th percentile, excluding relative humidity >90%. 14

15 164-40 Draft – Do Not Quote or Cite March 2010 The 90 th percentile PM light extinction de sign values corresponding to the 90 th percentile 1
PM mass concentration based scenarios for the five mass concentration levels are shown in Table 2 4.3-2. Values in the table that exceed each of the CPL values are highlighted using different 3
colors. The values in the table are the same fo r some urban areas for the less restrictive PM mass 4 concentration standard (e.g. Tacoma at 60 μ g/m 3 and 40 μ g/m 3 , or Phoenix at 60 μ g/m 3 , 40 5

μ g/m 3 , 30 μ g/m 3 and 20 μ g/m 3 ), because those areas required no rollback to meet the less 6
restrictive PM mass concentration st andards. In order for most or all urban areas to achieve even 7 the highest CPL at the 90 th percentile, a PM 2.5 mass based standard set below 40 μ g/m 3 would be 8 necessary. The higher PM 2.5 mass levels of 60 μ g/m 3 and 40 μ g/m 3 clearly are not sufficiently 9 protective, since they permit 11 a nd 10 of the 15 areas, respectively, to have design values larger 10
than 191 Mm -1 . At the 20 μ g/m 3 PM 2.5 standard level, all ar eas meet the highest CPL 11 benchmark, except for St. Louis, which doesn’t attain the highest CPL even when a 10 μ g/m 3 12 standard is imposed. We believe that this latter case may have occurred because the coarse mass 13 data in St. Louis may not be representative of the metropolitan area. 8 The 30 μ g/m 3 standard is 14 marginally above the high CPL at three cities and only exceeds it substantially at St. Louis. 15

8 The data set used to determine hourly PM mass and composition data for St. Louis may not be representative of the St. Louis metropolitan areas. See the discussion in the UFVA section 3.2.1.4-41 Draft – Do Not Quote or Cite March 2010 Table 4.3-2 90 th percentile maximum daily 1-hour PM light extinction design values (Mm - 1
1 ) after rollback to meet alternative standard of 60 μ g/m 3 , 40 μ g/m 3 , 30 μ g/m 3 ,20 2
μ g/m 3 and 10 μ g/m 3 maximum daylight 1-hour PM mass concentration for the 3 90th percentile.* 4 5 60 μ g/m 3 40 μ g/m 3 30 μ g/m 3 20 μ g/m 3 10 μ g/m 3
Tacoma, WA 140 Mm -1 140 Mm -1 140 Mm -1 128 Mm -1 82 Mm -1

Fresno, CA 338 Mm -1 248 Mm -1 190 Mm -1 132 Mm -1 74 Mm -1 Los Angeles, CA 403 Mm -1 284 Mm -1 220 Mm -1 156 Mm -1 105 Mm -1
Phoenix, AZ 105 Mm -1 105 Mm -1 105 Mm -1 105 Mm -1 86 Mm -1 Salt Lake City, UT 164 Mm -1 164 Mm -1 153 Mm -1 107 Mm -1 59 Mm -1
Dallas, TX 183 Mm -1 183 Mm -1 183 Mm -1 146 Mm -1 80 Mm -1
Houston, TX 194 Mm -1 194 Mm -1 179 Mm -1 125 Mm -1 73 Mm -1
St. Louis, IL 307 Mm -1 307 Mm -1 277 Mm -1 241 Mm -1 206 Mm -1 Birmingham, AL 357 Mm -1 266 Mm -1 208 Mm -1 152 Mm -1 102 Mm -1
Atlanta, GA 249 Mm -1 249 Mm -1 191 Mm -1 134 Mm -1 76 Mm -1
Detroit, MI 291 Mm -1 202 Mm -1 157 Mm -1 120 Mm -1 88 Mm -1 Pittsburgh, PA 278 Mm -1 243 Mm -1 185 Mm -1 127 Mm -1 69 Mm -1
Baltimore, MD 246 Mm -1 246 Mm -1 201 Mm -1 138 Mm -1 76 Mm -1 Philadelphia, PA 258 Mm -1 175 Mm -1 134 Mm -1 98 Mm -1 63 Mm -1
New York, NY 306 Mm -1 281 Mm -1 212 Mm -1 141 Mm -1 74 Mm -1

6

* Colored highlighting shows which of the C PL levels the values are near, using the 7 following definitions: PM light exti nction equal or above the high CPL > 191 Mm -1 ; above the 8 middle CPL, 112 Mm -1 – 190 Mm -1 ; above the low CPL, 64 Mm -1 – 111 Mm -1 ; below the low 9 CPL, < 64 Mm -1 . Values without color highlighting indi cate no rollback, so no information 10 about the effectiveness of the hourly PM mass based alternative standards 11 12 Aside from St. Louis, the range of 90 th percentile PM light extinction design levels 13 resulting from rollback to just meet a 90 th percentile 20 μ g/m 3 PM mass concentration is from 98 14

Mm -1 for Philadelphia to 156 Mm -1 for Los Angeles with most values near the middle CPL value 15
of 112 Mm -1 . A similar range, excluding St. Louis for the 30 μ g/m 3 PM mass concentration is 16
from 134 Mm -1 to 220 Mm -1 for the same two cities. This de monstrates the amount of variability 17 in visibility conditions that would likely result from usi ng a standard with PM mass 18 concentration instead of PM light extinction as the indicator. Wh ile this degree of variation is 19 not particularly large, it does mean that some areas would be required to further control 20 emissions to meet a secondary st andard though they have visibility conditions that are as good or 21
better than other areas which meet the PM mass ba sed standard. Some measure of the extent to 224-42 Draft – Do Not Quote or Cite March 2010 which this occurs may be gained by comparing th e percent rollback values required to meet the 1
various PM mass and PM li ght extinction values. 2 Based on inspection of the design values shown in Table 4.3-2, among the PM 2.5 mass 3 concentration levels that were assessed, 30 μ g/m 3 provides protection most comparable to the 4 high CPL (191 Mm -1 ), 20 μ g/m 3 provides protection most comparable to the middle CPL (112 5

Mm -1 ) and 10 μ g/m 3 provides protection most comparable to the low CPL (64 Mm -1 ). 6 Care must be taken to avoid misinterpret ation of this suggestion of approximate 7 comparability of protection afforded the va rious urban areas by PM mass at the three 8
concentration levels in term s of the three CPLs. The va lues in Table 4.3-2 are the 90 th percentile 9 values of the PM light extincti on distribution that results from transforming the hourly PM mass 10 and composition values of the rolled back PM distributions for each urban area. Hours with 11
values above the 90 th percentile of PM mass do not necessa rily have PM light extinction above 12
the 90 th percentile and visa versa. As discussed earlier (section 4.3.1) for any individual hourly 13
PM mass concentration there is a substantial range of corresponding PM light extinction values 14 possible. However when used as the indica tor for a secondary PM standard, hourly PM 2.5 mass 15 need only predict the response of the distribution of hourly visi bility conditions to produce 16 requisite levels of protection for visibility welfare effects. 17

4.4 PRELIMINARY STAFF CONCLUSIONS ON ALTERNATIVE SECONDARY PM 18 STANDARDS FOR VISIBILITY-RELATED EFFECTS 19 In reaching preliminary conclusions on pot ential alternative standards to provide 20 requisite protection of PM-related visibility impairment, staff has considered the basic elements 21 of the NAAQS: indicator, averaging time, form and level. In considering the scientific and 22 technical information, we reflect upo n the information available in th e last review integrated with 23 information that is newly available since the last review as assessed and presented in the ISA and 24 the second draft UFVA (US EPA, 2010b) and as summarized in secti ons 4.2, 4.3, and Appendix 25
A. 26 As outlined in section 4.1.3, in this review we emphasize a policy approach that broadens 27 the general approaches used in the last tw o PM NAAQS reviews by utilizing, to the extent 28 available, enhanced tools, methods, and data to more comprehensively characterize visibility 29 impacts. As such, we take into account both evidence-based and impact assessment-based 30
considerations to inform our conclusions related to the adequacy of the current PM 2.5 secondary 31 standards and alternative standards that are approp riate for consideration in this review. In so 32 doing, we are seeking to provide as broad an array of options as is supportable by the available 33 information, recognizing that the selection of a specific approach to reaching final decisions on 34 the secondary PM standards for protection from PM -related visibility impairment will reflect the 354-43 Draft – Do Not Quote or Cite March 2010 judgments of the Administrator as to what weight to place on th e various approaches and types 1 of information presented in the final PA. 2 In presenting our preliminary conclusions regarding alternat ive secondary standards and 3 ranges of levels for consideration, we summari ze conclusions presented in sections 4.3.1 through 4 4.3.4. We emphasize that these are preliminary conclusions that reflect consideration of the 5
scientific and technical inform ation assessed and presented in the ISA and second draft UFVA 6 (US EPA, 2009a; US EPA, 2010b). We note that st aff conclusions to be presented in the final 7
UFVA and second draft PA will be based, in part, on input received from CASAC and the public 8
on the second draft UFVAA and this first draft PA. 9 We recognize that selecting from among alte rnative standards will necessarily reflect 10 consideration of the qualitative a nd quantitative uncertainties inhe rent in the relevant evidence 11 and in the assumptions that under lie the quantitative visibility imp act assessment. In identifying 12
these alternative sec ondary standards and ranges of levels fo r consideration, we are mindful that 13 the Clean Air Act requires standards to be set th at are requisite to prot ect public welfare from 14 any known or anticipated adverse effects, such that the standards are to be neither more nor less 15 stringent than necessary. Thus, the Act does not require that the NAAQS be set at zero-risk 16 levels, but rather at levels that avoi d unacceptable risks to public welfare. 17
18 ( 1) Consideration should be given to revising the current suite of PM 2.5 secondary standards 19 to provide increased public we lfare protection from PM-rela ted visibility impairment, 20 primarily in urban areas. This preliminar y conclusion is based in general on the 21 evaluation in the ISA of the currently availa ble information, including a more extensive 22 characterization of the sources contributing to visibility impairment in both rural and 23 urban locations, a refined understanding of th e contributions of various PM components 24 in such areas, exposure- related evidence supporting a causal relationship between 25 ambient PM and impaired VAQ, and more speci fically, on the evidence that a significant 26 number of days with levels of VAQ that could reasonably be considered unacceptable 27 based on the preference studies would conti nue to occur in areas where the current 28 standards were met, together with judgments as to the public welfar e significance of these 29 occurrences upon just meeti ng the current suite of PM 2.5 standards. 30
31 ( 2) With regard to indicator, consideration shoul d be given to establishing a new PM light 32 extinction indicator; alternatively, consideration can be given to retaining the current 33
PM 2.5 indicator. This preliminary conclusion takes into consideration the available 34 evidence that demonstrates a one-to-one co rrespondence between measured ambient PM 35 light extinction and PM-related visibility impair ment as well as the significant degree of 36 variability in visibility protection across the U.S. allowed by a PM 2.5 indicator, while also 374-44 Draft – Do Not Quote or Cite March 2010 recognizing that either indicator could be used as a basis for a standard that could provide 1 appropriate protection from PM-re lated visibility impairment. 2
3 ( 3) With regard to averaging time, consideration should be given to selecting an alternative 4 averaging time for a secondary PM standa rd to protect against daytime PM-related 5 visibility impairment that take s into account the short term (instantaneous) nature of the 6 perception of visibility impairment, short term variability in PM-related VAQ (partial 7 hour to hourly), and the short-term nature of relevant exposure periods for the viewing 8 public (partial hour to multiple hours). Recognizing that the current 24-hour and annual 9 averaging times do not appropria tely reflect these exposure ch aracteristics, consideration 10 should be given to a one-hour averaging time based on the maximum hour in the daylight 11 period or on all daylight hours. 12
13 ( 4) In conjunction with consideri ng a 1-hour averaging time, c onsideration should be given 14 to a form defined in terms of the 90 th , 95 th or 98 th percentile of the di stribution of 1-hour 15 PM light extinction or PM 2.5 concentrations, averaged over thr ee years. We believe it is 16 appropriate to consider allo wing some number of days/hours with visibility impairment 17 above the target level of protection, such that consideration of the 90 th or 95 th percentile 18 forms is appropriate. In addition, consid eration should be given to applying a 90% 19 relative humidity screen to remove hours in which fog or precipitation is much more 20 likely to contribute to the obs erved visibility impairment. 21
22 ( 5) Consideration should be given to selecting a target level in te rms of PM light extinction. 23 Further, consideration should be given to alternative candidate levels, with a particular 24 focus on a level of 112 Mm -1 as well as levels down to 64 Mm -1 and up to 191 Mm -1 to 25 provide appropriate protection against PM-related visibility impairment. Based on the 26 assessment conducted in this review, we judge that a reasonably consistent 27 correspondence exists between these PM light extincti on benchmark levels and PM 2.5 28 mass concentrations, with a particular focus on a level of 10 μ g/m 3 as well as levels down 29
to 20 μ g/m 3 and up to 30 μ g/m 3. , which would be appropriate to consider in conjunction 30 with consideration of a PM 2.5 indicator. 31
32 ( 6) Consideration should be given to the followi ng alternative secondary PM standards to 33 provide protection against PM -related visibility impairm ent during daylight hours: 34
35 (a) Consideration of a new 1-hour daily maximu m PM light extinction standard set at a 36 level within the range of 64 to 191 Mm -1 (e.g. 20 – 30 deciviews (dv)) with a 90 th or 37
95 th percentile form. 38
394-45 Draft – Do Not Quote or Cite March 2010 (b) Consideration of a revised 1-hour daily maximum PM 2.5 standard set at a level within 1 the range of 10 to 30 μg/m 3 with a 90 th or 95 th percentile form. 2
3 (c) Alternatively, consideration could also be given to a standard based on all daylight 4 hours with either indicator, in conj unction with consideration of a 98 th percentile 5 form. 6
7
8

4.5 REFERENCES 9

ABT (2001). Assessing Public Opinions on Visibility Impairment Due to Air Pollution: Summary Report. 10

BBC Research & Consulting. (2003), Phoenix Area Visibility Survey. Draft Report. . Available: 11 http://www.azdeq.gov/environ/a ir/download/vis_021903f.pdf . Accessed 9/16/2008 12

Henderson, R. (2005a). EPA’s Review of the Nationa l Ambient Air Quality Standards for Particulate Matter 13 (Second Draft PM Staff Paper, January 2005): A review by the Particulate Matter Review Panel of the EPA 14 Clean Air Scientific Advisory Committee. June 6, 2005. Available: http://www.epa.gov/sab/pdf/casac-05- 15 007.pdf

. 16

Henderson, R.; Cowling, E.; Crapo, J.D..; Miller, F. J.; Poirot, R.L.; Speizer, F. ; Zielinska, B. (2006b). Letter from 17 Clean Air Scientific Advisory Committee to the Honorable Stephen L. Johnson, Administrator, US EPA. 18 Clean Air Scientific Advisory Committee Recommendati ons Concerning the Final National Ambient Air 19 Quality Standards for Particulate Matter. September 29, 2006. Available: 20 http://www.epa.gov/sab/pd f/casac-ltr-06-002.pdf 21

Ely DW; Leary JT; Stewart TR; Ross DM (1991). The establishment of the Denver Visibility Standard. Presented at 22 Presented at: 84th annual meeting & exhibition of the Air & Waste Management Association; June; 23 Vancouver, British Columbia. Pittsburgh, PA: Air & Wa ste Management Association; paper no. 91-48.4. 24

Malm, W.C., Sisler, J.F., Huffman, D., El dred, R.A., Cahill, T.A. (1994) Spa tial and Seasonal Trends in Particle 25 Concentration and Optical Extinction in the United Stat es, Journal of Geophysical Research (Atmospheres) 26 99:1347-1370. 27

Pryor SC (1996). Assessing public perception of visibility for standard setting exercises. Atmos Environ, 30: 2705- 28 2716. 29

Smith, A. (2009). Comments on the First External Revi ew Draft of EPA’s “Integra ted Science Assessment for 30 Particulate Matter.” CRA Internation. Washington, DC . March 30. Prepared for the Utility Air Regulatory 31 Group,. Submitted as public comments to the public meeting EPA Clean Air Science Advisory Council. 32 April 2. 33

Smith AE; Howell S (2009). An assessment of the robust ness of visual air quality preference study results. CRA 34 International. Washington, 35 DC.http://yosemite.epa.gov/sab/sabproduct.nsf/ B55911DF9796E5E38525759 2006FB737/$File/CRA+VA 36 Q+Pref+Robustness+Study+3+30+09+final.pdf. 37

US EPA (2005). Review of the National Ambient Air Qua lity Standards for Particulate Matter: Policy Assessment 38 of Scientific and Technical Information, OAQPS Staff Paper. Research Triangle Park, NC 27711: Office 39 of Air Quality Planning and Standa rds; report no. EPA EPA-452/R-05-00 5a. December 2005. Available: 40 http://www.epa.gov/ttn/naaqs/standards/pm/s_pm_cr_sp.html 414-46 Draft – Do Not Quote or Cite March 2010 US EPA (2008a). Integrated Review Plan for the Nationa l Ambient Air Quality Standards for Particulate Matter. 1 National Center for Environmental Assessment and Office of Air Quality Planning and Standards, U.S. 2 Environmental Protection Agency, Research Triangle Park, NC. Report No. EPA 452/R-08-004. March 3 2008. Available at: http://www.epa.gov/ttn/naaqs/standards/pm/s_pm_2007_pd.html

. 4

US EPA (2009a). Integrated Scien ce Assessment for Particulate Matter: Final Report. National Center for 5 Environmental Assessment-RTP Division, Office of Air Quality Planning and Standards, Research 6 Triangle Park, NC. EPA/600/R-08/139F. December 2009. Available: 7 http://www.epa.gov/ttn/naaqs/standards/pm/s_pm_2007_isa.html

. 8

US EPA (2009b). Integrated Science Assessment for Par ticulate Matter: Second External Review Draft. National 9 Center for Environmental Assessment-RTP Division, Office of Air Quality Planning and Standards, 10 Research Triangle Park, NC. EPA/600/R-08/139B. July 2009. Available: 11 http://www.epa.gov/ttn/naaqs/standards/pm/s_pm_2007_isa.html

. 12

US EPA (2009d). Particulate Matter National Ambient Air Quality Standards: Scope and Methods Plan for Urban 13 Visibility Impact Assessment. Office of Air Qua lity Planning and Standards, U.S. Environmental 14 Protection Agency, Research Triangle Park, NC. EPA-452/P-09-001. February 2009. Available: 15 http://www.epa.gov/ttn/naaqs/standards/pm/s_pm_2007_pd.html

. 16

US EPA (2009f). Particulate Matter Ur ban-Focused Visibility Assessment – Exte rnal Review Draft. Office of Air 17 Quality Planning and Standards, U.S. Environmenta l Protection Agency, Research Triangle Park, NC. 18 EPA-452/P-09-005. September 2009. Available: 19 http://www.epa.gov/ttn/naaqs/standards/pm/s_pm_2007_risk.html

. 20

US EPA (2010b). Particulate Matter Urban-Focused Visib ility Assessment – Second External Review Draft. Office 21 of Air Quality Planning and Standards, U.S. Enviro nmental Protection Agency, Research Triangle Park, 22 NC. EPA-452/P-10-002. January 2010. Available: 23 http://www.epa.gov/ttn/naaqs/standards/pm/s_pm_2007_risk.html

. 24Draft – Do Not Quote or Cite A-1 March 2010 

## Appendix A 1

2 

## Information Regarding the 1-hour PM 2.5 

## Mass Indicator 3 4 This Appendix presents inform ation on 2005-2007 levels of 1-hour PM 2.5 mass 5 concentrations in the 15 urban study areas and on the “what if” PM light extinction conditions 6 that would exist if the study areas met each of 10 alternative secondary PM NAAQS scenarios 7 based on a 1-hour PM 2.5 mass indicator. With respect to th e latter subject, this Appendix is 8 therefore similar to Chapter 4 of the Particul ate Matter Urban-Focused Visibility Assessment 9 (UFVA), which presented similar information for 18 secondary PM NAAQS scenarios based on 10 PM light extinction as the indicator, for the current annual and 24-hour PM 2.5 NAAQS, and for a 11 scenario with an annual NAAQS of 12 μg/m 3 and a 24-hour NAAQS of 25 μg/m 3

. 12 13 1.0 Indicator and Monitoring Method 14 15 As in Chapter 4 of the PM UFVA, this Appendix excludes from all NAAQS scenarios and 16 results all non-daylight hours and all daylight hours with re lative humidity greater than 90 17 percent. This applies to both the definition of 10 secondary NAAQS scenarios, and to graphics 18 and tables that characterize ambient conditions . While ambient humidity should not affect 19 conventional measurement approaches for 1-hour PM 2.5 mass, the issue of co-occurrence of high 20 humidity levels with light exti nction due to natural conditions would still apply. See section 3.3.5 21 of the UFVA. The assumed hours of daylight are the same as those used in the UFVA, as shown 22 in Table 3-5 of the UFVA. 23 24 All values for 1-hour PM 2.5 mass concentration in this appendix come from the continuous 25 instruments at the 15 urban study si tes, with no adjustment to make these values consistent with 26 the collocated 24-hour FRM measurement of PM 2.5 mass. Appendix A of the UFVA provides 27 details on the type of continuous instrument at each study site. TEOMs were used at all sites 28 except for beta attenuation instruments in Fresno and Philadelphia, nephelometer instruments in 29 Tacoma and Phoenix, and an FDMS instrument in Salt Lake City. 30 31 For conciseness in this first public review draft, only the daily maximum daylight 1-hour 32 PM 2.5 mass concentration indicator is considered in this Appendix. It would also be possible to 33 construct alternative NAAQS scenarios of an a ll-hours type, which could be analyzed in the 34 same manner as presented in this Appendix. 35 36 2.0 Current Conditions of 1-hour PM 2.5 Mass 37 38 Figure A-1 is a box plot of 2005-2007 daily maximum daylight 1-hour PM 2.5 mass 39 concentrations for the 15 study areas, excludi ng hours with relative hum idity greater than 90 40 percent, to give a sense of the range and centr al tendency of this parameter. The horizontal 41 reference lines are at 10, 20, 30, 40 and 60 μg/m 3

. The relative positions of the 90 percentile 42 concentrations (indicated by the horizontal stroke at the top of the whisker) are generally 43 consistent with the relative ranking of these site s according to their design values for the 24-hour 44Draft – Do Not Quote or Cite A-2 March 2010 PM 2.5 NAAQS (see Table 3-2 of the UFVA); simila rly, the relative positions of the median 1 concentrations are generally consistent with the annual PM 2.5 design values. Table A-1, based on 2 the same data as Figure A-1, presents the pe rcentage of days in 2005-2007 on which the daily 3 maximum daylight 1-hour PM 2.5 concentration exceeded the refe rence levels represented by the 4 horizontal lines in Figure A-1. 5 6 Figure A-1. 2005-2007 daily maximum daylight 1-hour PM 2.5 mass concentrations (μg/m 3 ) 7 for the 15 study areas (excluding hours with relative humidity grea ter than 90 percent) 8

9 10 11 12 13 14 15 16 17 18 19 20 21 22Draft – Do Not Quote or Cite A-3 March 2010 Table A-1. Percentage of days with daily maximum daylight 1-hour PM 2.5 mass 1 concentration exceeding reference levels in 2005-2007 (excluding hour with relative 2 humidity greater than 90 percent) 3 4 1-hour PM 2.5 Mass Reference Level (μg/m 3 ) Study Area Number of Days with Estimates 10 20 30 40 60

Tacoma 109 50 11 1 0 0 Fresno 324 88 62 37 20 8 Los Angeles 300 92 81 67 46 20 Phoenix 86 60 8 1 1 1 Salt Lake City 306 64 20 11 7 2 Dallas 273 75 25 5 0 0 Houston 148 80 42 14 5 0 St. Louis 289 93 47 18 7 2 Birmingham 349 92 60 37 23 8 Atlanta 279 86 56 28 10 1 Detroit 141 92 72 52 36 13 Pittsburgh 277 94 57 28 15 3 Baltimore 181 90 46 22 8 1 Philadelphia 143 99 84 63 45 20 New York 225 75 43 25 13 3 5Draft – Do Not Quote or Cite A-4 March 2010 3.0 Alternative NAAQS Scenar ios Based on 1-hour PM 2.5 Mass as the Indicator 1 2 To ensure examination of a wide enough range of alternative sta ndards based on 1-hour 3 PM 2.5 mass to encompass the range of standards that might be considered as alternatives to the 4 PM light extinction NAAQS scenarios examined in Chapter 4 of the UFVA, we considered 5 levels of 10, 20, 30, 40, and 60 μg/m 3 . Only the daily maximu m daylight hour form was 6 considered. Each level was comb ined with two statistical forms: the three-year average of the 7 annual 90 th percentile value and the three- year average of the annual 95 th percentile value. For 8 ease of reference, these scenarios are designated by letters from “aa” to “jj” and listed in Table 9 A-2. Looking somewhat ahead to results presente d below, the scenarios are arranged in Table 10 A-2 in order of least to most stringent in terms of the reductions in ambient PM 2.5 needed from 11 current levels to meet the current a nd alternative NAAQS levels and forms. 12 13 Table A-2. Alternative NAAQS scenarios base d on daily maximum daylight 1-hour PM 2.5 14 mass, averaged over three years (excluding ho urs with relative humidity greater than 90 15 percent) 16 17 NAAQS Scenario Level (μg/m 3) Statistical Form aa 60 3-year average of 90 th percentile bb 60 3-year average of 95 th percentile cc 40 3-year average of 90 th percentile dd 40 3-year average of 95 th percentile ee 30 3-year average of 90 th percentile ff 30 3-year average of 95 th percentile gg 20 3-year average of 90 th percentile hh 20 3-year average of 95 th percentile ii 10 3-year average of 90 th percentile jj 10 3-year average of 95 th percentile 18 19 4.0 Approach to Modeling “What If” Conditions of PM Light Extinction for Alternative 20 Secondary NAAQS Based on 1-hour PM 2.5 Mass 21 22 Before modeling “what if” conditi ons, we augmented the data se t described in Table 4 of the 23 UFVA in the same manner as described in Section 4.1.4 of the UFVA, to achieve seasonal 24 balance despite the lack of mon itoring data for one quarter in each of Houston and Phoenix. In 25 Tacoma and Phoenix, which had data only for two years in the 2005-2007 period, we averaged 26 the percentile values from the only two available years rather than the th ree years defined for the 27 statistical form of the NAAQS scenarios. 28 29 The modeling of daily ma ximum daylight 1-hour PM 2.5 mass under each of the scenarios 30 listed in Table A-2 used a rollback approach that combined relevant concepts and steps from the 31 rollback methods described in sections 4.1.4 (for PM light extinction scen arios) and 4.2.2 (for 32 scenarios based on annual average and 24-hour average PM 2.5 ) of the UFVA. The following are 33 the steps in the modeling. 34 35 1. Identify the 90 th percentile daily maximum daylight 1-hour PM 2.5 mass value in each of 2005, 36 2006, and 2007 for a study area. Average these to determine the design value for that percentile 37Draft – Do Not Quote or Cite A-5 March 2010 form. Repeat for the 95 th percentile form. These design va lues are presented in Table A-3. 1 They range from 22 to 81 μg/m 3 indicating that some study areas meet some of the NAAQS 2 scenarios under current conditions. In such cases, PM 2.5 concentrations were not adjusted, i.e., 3 there was no “roll up” for any area in any scenario. 4 5 2. Using the same days and hours as contributed by th e three annual 90 th percentile values for 6 actual 1-hour PM 2.5 mass, find the three corresponding va lues of policy relevant background 7 (PRB) 1-hour PM 2.5 mass. Average these three annual values of PRB 1-hour PM 2.5 to obtain the 8 PRB portion of the actual 1-hour PM 2.5 design value for the 90 th percentile form. Repeat for the 9 95 th percentile form. 10 11 In the modeling for the NAAQS scenarios examined in the UF VA, PRB for 1-hour PM 2.5 12 mass was not explicitly calculated because it was not needed in the rollback modeling for the 13 scenarios addressed in the UFVA. Therefore, it was necessary to recons truct this parameter by 14 adding the values for the PRB concentr ations of the five components of PM 2.5 : nitrate, sulfate, 15 elemental carbon, organic carbon material, and so il. The method for estimating PRB for these 16 five components is described in Appendix C of the UFVA.9 17 18 3. Subtract the value from step 2 from the va lue from step 1, to determine the non-PRB portion 19 of the 1-hour PM 2.5 mass design value. 20 21 4. Calculate the percentage reduc tion required in non-PRB 1-hour PM 2.5 mass in order to reduce 22 the design value to the level that defines th e NAAQS scenario, using the following equation: 23 24 Percent reduction required = 1 – (NAAQS level – PRB portion of the design value)/(non-PRB 25 portion of the design value) 26 27 The percentage reductions determined in step 4 are shown in Table A-4. Note that for some 28 combinations of area and scenario no reducti on is required because the 2005-2007 design value 29 already meets the NAAQS scenario. 30 31 5. Turning to the entire set of day/hour-specific actual and PRB daylight 1-hour concentrations 32 of the five PM 2.5 components for the three (or two) y ear period, determine the non-PRB portion 33 of each of the five components in an hour by s ubtracting the PRB value from actual value, 34 reduce it by the percentage determined in step 4, and add ba ck in the PRB 1-hour concentration 35 of the component. 36 37 6. Finally, re-construct PM light ex tinction using the redu ced values of the five components, the 38 original value of 1-hour PM 10-2.5 , and the 1-hour value of f(RH), according to the following 39 equation for PM light extinction (see section 3.2.3 of the UFVA for an explanation of the 40 variables in this equation). 41 42

9 Table C-1 of the UFVA presents the annu al average of all daylight hour PRB PM 2.5 mass. The 90 th and 95 th percentile values of daily maximum PRB PM 2.5 mass were of course higher than shown in that table.Draft – Do Not Quote or Cite A-6 March 2010 b extPM = 3 x f(RH) x [Sulfate] 1 + 3 x f (RH) x [Nitrate] 2 + 4 x [Organic Mass] 3 +10 x [Elemental Carbon] 4 + 1 x [Fine Soil] 5 + 0.6 x [Coarse Mass] 6 7 These steps assume that in order to m eet a PM NAAQS scenario based on 1-hour PM 2.5 as 8 the indicator, each component of PM 2.5 is reduced by an equal percentage, across the five 9 components and across all hours. In actual implementation of such a NAAQS, each state would 10 develop an attainment strategy, which might re sult in unequal percenta ge reductions of the 11 components. If the strategy emphasized reductions in the fine soil component, for example, PM 12 light extinction levels would rema in high relative to those estima ted by these steps, because fine 13 soil is not efficient in terms of reducing visibi lity compared to the other four components on a 14 dry mass-to-mass basis. On the other hand, a strate gy that involves relativel y large reductions in 15 sulfate or nitrate would achieve greater reductions in PM light extinction than estimated by these 16 steps. The uncertainty in how the results of th is rollback method compare to the results of actual 17 attainment strategies should be kept in mind wh en comparing the results of “what if” scenarios 18 for NAAQS based on PM 2.5 mass as the indicator versus scen arios based on PM light extinction. 19 Unlike the effect of humidity va riation between areas, this source of uncertainty is not reflected 20 in any of the results presented in this Appendix and will not be apparent in comparisons of 21 results in this Appendix to results presented in the PM UFVA for NAAQS scenarios based on 22 PM light extinction. 23 24 These steps also assume no change in PM 10-2.5 concentrations between current conditions and 25 “what if” conditions. While reductions in PM 10-2.5 would not be needed to meet a secondary 26 NAAQS based on 1-hour PM 2.5 mass, it is possible that strategies to control PM 2.5 concentrations 27 might also achieve reductions in PM 10-2.5 concentrations because some source emit both and 28 some control methods achieve some reductions in both. However, in most of the 15 study areas, 29 PM 10-2.5 makes a small contribution to estimated PM light extinction, in part because in many of 30 the areas no local data on PM 10-2.5 concentrations were available and the method used to fill this 31 gap (application of a factor to PM 2.5 concentration) simply could not produce a high estimate of 32 PM 10-2.5
. 33Draft – Do Not Quote or Cite A-7 March 2010 Table A-3. 2005-2007 design values for 1-hour PM 2.5 mass (μg/m 3 ) 1 2 Study Area Percentile Form 90th 95th Tacoma 22 27 Fresno 55 66 Los Angeles 72 81 Phoenix 20 24 Salt Lake City 32 45 Dallas 26 29 Houston 33 37 St. Louis 36 44 Birmingham 55 74 Atlanta 40 45 Detroit 64 79 Pittsburgh 46 51 Baltimore 37 43 Philadelphia 67 77 New York 44 55 3 4 Table A-4. Percentage reductions in non-PRB PM 2.5 components required to meet NAAQS 5 scenarios based on 1-hour PM 2.5 mass 6 7 Scenario aa bb cc dd ee ff gg hh ii jj Level (μg/m 3 ) 60 60 40 40 30 30 20 20 10 10 Percentile Form 90 95 90 95 90 95 90 95 90 95 Study Area Percentage Reduction Tacoma 0 0 0 0 0 0 11 27 60 69 Fresno 0 10 28 40 46 55 65 71 83 86 Los Angeles 17 26 45 51 59 64 73 76 87 88 Phoenix 0 0 0 0 0 0 0 15 51 58 Salt Lake City 0 0 0 12 7 34 39 56 70 78 Dallas 0 0 0 0 0 0 23 34 64 69 Houston 0 0 0 0 9 20 40 49 71 78 St. Louis 0 0 0 10 16 33 45 56 74 79 Birmingham 0 19 28 46 46 60 65 74 84 87 Atlanta 0 0 0 12 25 34 51 57 77 80 Detroit 7 24 38 50 54 63 70 75 85 88 Pittsburgh 0 0 13 22 35 42 57 62 79 81 Baltimore 0 0 0 8 19 31 47 55 74 78 Philadelphia 10 22 40 49 55 62 71 75 86 88 New York 0 0 8 28 32 46 55 65 78 83 8 9Draft – Do Not Quote or Cite A-8 March 2010 5.0. 1-hour PM 2.5 Mass Results for “Just Meeting” Alternative Secondary NAAQS 1 Scenarios Based on 1-hour PM 2.5 Mass 2 3 As a check on the reasonableness of the rollb ack method described in section 4.0 and on the 4 accuracy of the code used to implement it, it is of interest to examine the distribution of the 5 levels of 1-hour PM 2.5 that result from the method. Ideall y, after rollback any area that had a 6 non-zero required reduction should have a pos t-rollback design value for 1-hour PM 2.5 mass that 7 is exactly equal to the target design value. Als o, there should be a progres sion of reductions in 1- 8 hour PM 2.5 medians and other percentile points on th e distribution as progressively more 9 stringent scenarios are modeled. 10 11 Table A-5 shows the post-rollback 1-hour PM 2.5 mass design values for the scenarios, with 12 percentile forms matched. Design values for area -scenario combinations for which the required 13 reductions were zero have been omitted, because the current conditions design values for these 14 combinations would not be expected to reflect the target design va lue. It can be seen that the 15 design values progress as expected and are in the vicinity of the target design values, but are not 16 always exactly equal to the targets. EPA staff attr ibutes this to the fact that PRB concentrations 17 of 1-hour PM 2.5 mass vary from hour to hour. It is possible for the daily maximum PM 2.5 mass 18 concentration on a certain day in 2005 with a percentile rank of, for example, 96 th to have a 19 relatively small PRB portion and a large non -PRB portion compared to the daily maximum 20 concentration that ranks 95 th . When an equal reduction is ma de to the non-PRB portion of each 21 total concentration, the two values may sw itch rank positions, and so a new day and hour 22 becomes the 2005 contributor to the rolled back th ree-year design value. Since this day and hour 23 was not used to determine the required percenta ge reduction, the resultin g design value will not 24 exactly meet the target design va lue. It would be possible to iterate with higher and lower 25 percentage reductions until the rolled back design value exactly matched the target design value, 26 but EPA considered this degree of refinement to be unnecessary in order to meet the objectives 27 of the Policy Assessment Document, given other un certainties in the underlying data and in the 28 assumptions used to estimate PM light extinction values. 29 30 EPA staff also generated and examined box plots of daily maximum daylight 1-hour PM 2.5 mass 31 concentrations as a check for conceptual or programming, and found them to match expectations. 32 They are not included here, for conciseness. 33Draft – Do Not Quote or Cite A-9 March 2010 Table A-5. Post-rollback design values for daily maximum 1-hour PM 2.5 mass. Design 1 values are shown only for combinations of stud y area and scenario for which the study area 2 does not meet the scenario under current co nditions, such that reductions were made 3 during the rollback modeling. 4 5 Scenario aa bb cc dd ee ff gg hh ii jj Level (μg/m 3 ) 60 60 40 40 30 30 20 20 10 10 Statistical Form 90th 95th 90th 95th 90th 95th 90th 95th 90th 95th Study Area Corresponding Design Value (μg/m 3 ) (same percentile form as the scenario) Tacoma 20 21 11 12 Fresno 63 40 42 30 31 20 21 10 10 Los Angeles 53 53 35 35 26 26 18 18 9 9 Phoenix 19 10 10 Salt Lake City 38 29 28 19 19 10 10 Dallas 23 23 12 11 Houston 29 27 19 18 10 9 St. Louis 39 31 29 21 19 10 10 Birmingham 58 42 39 32 29 21 20 11 10 Atlanta 36 28 27 19 18 10 10 Detroit 52 59 34 39 26 29 17 20 9 10 Pittsburgh 33 33 24 25 16 17 8 9 Baltimore 38 31 28 21 19 10 10 Philadelphia 46 44 31 30 23 22 16 15 8 8 New York 42 40 32 30 21 20 11 10 6 7 6.0 PM Light Extinction Results for “J ust Meeting” Alternative Secondary NAAQS 8 Scenarios Based on 1-hour PM 2.5 Mass 9 10 The rollback steps described in section 4.0 resulted in estimates of PM light extinction for 11 each day and hour in each study area, for each of the 10 NAAQS scenarios based on 1-hour 12 PM 2.5 mass as the indicator. Two summaries of these conditions are presented here. 13 14 Figure A-2 presents a box plot of daily maxi mum daylight 1-hour PM light extinction for 15 each NAAQS scenario based on 1-hour PM 2.5 mass. These can be compared to Figure 3-8(a) of 16 the UFVA representing pre -rollback daily maximum PM light ex tinction, and to the upper panel 17 of the figures in Appendix F of the UFVA repr esenting the daily maximum PM light extinction 18 levels resulting from the 20 NAAQS scenarios examined in the UFVA (18 scenarios based on 19 PM light extinction as the indicato r, the current annual and 24-hour PM 2.5 NAAQS, and a 20 scenario with an annual NAAQS of 12 μg/m 3 and a 24-hour NAAQS of 25 μg/m 3 ). It can be 21 seen that the distribution of PM 2.5 mass in a given study area shifts downward as the NAAQS 22 scenarios progress from least to most stringent (as indicated by the required percentage 23 reduction) and in most cases become more sim ilar to other areas (once the progression of 24 scenarios begins to require reductions in a given area). St. Louis is an obvious exception, in that 25 it retains many relatively high values even under th e most stringent NAAQS scenario. This is 26 due to the fact that many hours and days in St. Louis have a large estimated PM 10-2.5 27 concentration contribution to estimated PM light extinction, as visualized in the light extinction 28 budgets presented in Figure 3-13 of the UFVA. The rollback approach does not change PM 10-2.5 29 concentrations. Recall from section 3.3.2 and A ppendix A of the UFVA that for St. Louis, PM 10- 30Draft – Do Not Quote or Cite A-10 March 2010 2.5 concentrations were estimated based on a PM 10 instrument located very near a 1 recycling/municipal works yard and a PM 2.5 instrument in another le ss industrial location. As 2 such, those estimated concentrations of PM 10-2.5 may not represent a large portion of the St Louis 3 urban area. 4 5 PM 10-2.5 was also a notable contri butor to the estimated light extinction budgets in Los 6 Angeles on a number of days, although to a lesser degree than in St. Louis. This is reflected in 7 the box plots, which show a number of high values of PM light extinction regardless of the level 8 of the hypothetical PM 2.5 mass NAAQS. Recall from section 3.3.2 and Appendix A of the 9 UFVA that for Los Angeles, PM 10-2.5 concentrations were estimated based on a PM 10 instrument 10 located in Victorville, California which is a considerable distance from the site in Rubidoux, 11 California and is perhaps a dustier area than most of the Los Angeles airshed. 12 13 Table A-6 presents the percentage of da ys in 2005-2007 on which daily maximum 1-hour 14 PM light extinction exceeded each of the CPL, under each of the 10 secondary PM NAAQS 15 scenarios based on 1-hour PM 2.5 mass. These percentages are necessarily based on the days for 16 which data to estimate PM light extinction were available, bu t are best estimates of the 17 percentage of all days in the ye ar given that the days with data were well distributed across the 18 year on either a one-in-three or one-in-six sampling schedule. These percentages can be 19 compared to the same-basis percentages presented in Table 4-7 of the UFVA. 20Draft – Do Not Quote or Cite A-11 March 2010 Figure A-2. Distributions of maximum daily daylight 1-hour PM light extinction under 1 “just meet” conditions for NAAQS scenarios based on 1-hour PM 2.5 mass (excluding hours 2 >90% RH) 3 4 (aa) NAAQS Scenario 5 60 μg/m3 6
90 th percentile 7

8 (bb) NAAQS Scenario 9 60 μg/m3 10 95th percentile 11

12Draft – Do Not Quote or Cite A-12 March 2010 Figure A-2. Distributions of maximum daily daylight 1-hour PM light extinction under 1 “just meet” conditions for NAAQS scenarios based on 1-hour PM 2.5 mass (excluding hours 2 >90% RH) (continued) 3 4 (cc) NAAQS Scenario 5 40 μg/m3 6
90 th percentile 7

8 (dd) NAAQS Scenario 9 40 μg/m3 10
95 th percentile 11

12Draft – Do Not Quote or Cite A-13 March 2010 Figure A-2. Distributions of maximum daily daylight 1-hour PM light extinction under 1 “just meet” conditions for NAAQS scenarios based on 1-hour PM 2.5 mass (excluding hours 2 >90% RH) (continued) 3 4 (ee) NAAQS Scenario 5 30 μg/m3 6
90 th percentile 7

8 (ff) NAAQS Scenario 9 30 μg/m3 10
95 th percentile 11

12Draft – Do Not Quote or Cite A-14 March 2010 Figure A-2. Distributions of maximum daily daylight 1-hour PM light extinction under 1 “just meet” conditions for NAAQS scenarios based on 1-hour PM 2.5 mass (excluding hours 2 >90% RH) (continued) 3 4 (gg) NAAQS Scenario 5 20 μg/m3 6
90 th percentile 7

8 (hh) NAAQS Scenario 9 20 μg/m3 10
95 th percentile 11

12Draft – Do Not Quote or Cite A-15 March 2010 Figure A-2. Distributions of maximum daily daylight 1-hour PM light extinction under 1 “just meet” conditions for NAAQS scenarios based on 1-hour PM 2.5 mass (excluding hours 2 >90% RH) (continued) 3 4 (ii) NAAQS Scenario 5 Daily Max 6 10 μg/m3 7
90 th percentile 8

9 (jj) NAAQS Scenario 10 Daily Max 11 10 μg/m3 12
95 th percentile 13

14Draft Do Not Quote or Cite March 2010A-16Table A-6. Percentage of days across three years (two in the caseof Phoenix and Houston) withmaximum 1-hour daylight PM1light extinction above CPLs when “justmeeting” NAAQS scenarios based on 1-hour PM2.5mass. Blue shading indicates no2reduction required from current conditions.345Days with max hour above64 Mm-1Days with max hour above112 Mm-1Days with max hour above191 Mm-1ScenarioaabbccddeeffgghhiijjaabbccddeeffgghhiijjaabbccddeeffgghhiijjNAAQSLevel(μg/m3)606040403030202010106060404030302020101060604040303020201010NAAQSPercentileForm909590959095909590959095909590959095909590959095909590959095AreaPercentage of daysPercentage of daysPercentage of daysTacoma535353535353 53 53 43 35232323232323 23 23 11 6444444 4 4 1 1Fresno76 73 65 57 69 60 55 44 28 1752 48 37 31 44 32 29 18 9 430 27 17 11 23 12 10 5 1 0Los Angeles89 87 84 81 84 79 74 69 41 30 78 76 65 57 65 53 41 31 11 7 52 46 30 24 30 19 11 6 3 3Phoenix44444444444444 44 37 326666666 6 6 61111111 1 1 1Salt LakeCity454545 37 45 45 45 26 17 10171717 15 17 17 17 11 8 5888 7 8 8 8 5 2 1Dallas818181818181 81 71 41 29414141414141 41 32 8 5101010101010 10 7 0 0Houston79797979 79 79 74 65 32 2744444444 44 44 35 28 6 311111111 11 11 9 6 1 0St. Louis989898 97 98 97 95 89 73 67787878 74 78 75 64 55 34 29404040 36 40 38 27 20 13 13Birmingham89 85 80 68 87 80 72 62 41 3465 56 51 36 58 51 40 30 15 1234 26 21 13 30 20 15 11 4 3Atlanta919191 89 91 89 82 77 47 34757575 68 74 66 51 35 3 3313131 21 31 19 5 3 0 0Detroit84 80 74 72 76 73 65 60 40 33 67 57 51 43 53 48 34 21 9 6 43 28 13 7 14 9 6 4 1 1Pittsburgh8585 81 77 81 77 63 55 27 195757 51 45 52 44 29 22 3 02626 18 14 21 13 6 2 0 0Baltimore818181 76 81 74 64 56 31 20515151 45 51 44 31 23 4 3232323 18 23 16 8 2 1 1Philadelphia84 78 71 62 72 63 55 43 17 10 60 54 33 29 37 31 16 10 3 3 26 17 8 5 8 5 0 0 0 0New York8383 80 71 81 73 63 56 27 196060 56 39 56 40 32 22 6 32929 25 16 25 17 9 5 0 0Average 78 76 74 70 75 71 66 58 36 28 52 49 45 40 47 41 33 25 9 6 24 22 17 13 19 14 9 5 2 2678Draft Do Not Quote or Cite March 2010 5-1 

### 5 REVIEW OF THE SECONDARY STANDARDS FOR OTHER 1 

### WELFARE EFFECTS 2

This chapter presents preliminary staff conclu sions with regard to the current suite of 3 secondary PM standards to protect agains t PM-related welfare effects other than visibility 4 impairment. Specifically, staff has assessed the relevant information re lated to effects of 5 atmospheric PM on the environment, including eff ects on climate, ecological effects, and effects 6 on materials. Our assessment is framed by a series of key policy-re levant questions, which 7 expand upon those presented in the Integrated Revi ew Plan (IRP) (US EPA, 2008a, section 3.2). 8 The answers to these questions will inform decisi ons on whether to retain or revise the current 9 suite of secondary PM standards. 10 In presenting preliminary staff conclusions with regard to the current secondary standards 11 relative to PM-related effects on climate, ecological effects, and materials, we note that the final 12 decision is largely a public welfar e policy judgment. A final deci sion must draw upon scientific 13 information and analyses about non-visibility PM -related effects and related impacts on public 14 welfare, as well as judgments about how to deal with the range of uncertainties that are inherent 15 in the scientific evidence and analyses. Our appr oach to informing these judgments is discussed 16 more fully below. This approach is consiste nt with the requirements of the NAAQS provisions 17
of the Act and with how EPA and the courts ha ve historically interpreted the Act. These 18 provisions require the Administrato r to establish secondary standard s that, in the Administrator’s 19 judgment, are requisite to protect public welfar e from any known or antic ipated adverse effects 20 associated with the presence of the pollutant in the ambient air. In so doing, the Administrator 21
seeks to establish standards that are neither mo re nor less stringent than necessary for this 22 purpose. The Act does not require th at secondary standards be set at a zero-risk level, but rather 23 at a level that avoids unaccepta ble public welfare impacts. 24 Information on the approaches used to set the secondary PM standards in past reviews as 25 well as our current approach for this review are presented in section 5.1. A discussion of the 26 scope of the review as related to non-visibility welfare effects of PM is included in section 5.1.2. 27 This chapter considers each of the non-visibility welfare effects separate ly. The discussion of 28 PM-associated effects on climate (section 5.2), ecological effects (sect ion 5.3), and materials 29 (section 5.4) are each followed by a consideratio n of key uncertainties and areas for future 30
research and data collection. 31Draft Do Not Quote or Cite March 2010 5-2 5.1 APPROACH 1 Background information on the approaches used to establish the PM secondary standards 2
in 1997 and revisions to those standards in 2006 are summarized below. This section also 3 includes a discussion of the ongoing joint review of ecological effects of oxides of nitrogen and 4 sulfur (NOx/SOx secondary review) for clarity, since depositional effect s of PM components of 5 NOx and SOx to ecosystems were historically c onsidered as a component of the PM secondary 6 review. Lastly, there is a disc ussion of the current approach fo r evaluating the effects of PM on 7 climate, ecosystems, and materials using evidence-based considerations to inform our 8 understanding of the key po licy-relevant issues. 9

5.1.1 Approaches Used in Previous Reviews 10

5.1.1.1 Review Completed in 1997 11

In the 1997 review, as discussed in section 2.1.1.1, EPA determined that for the primary 12
standard the fine and coarse fractions of PM 10 should be considered separately and added a suite 13 of new primary standards, using PM 2.5 , as the indicator for fine particles, and retaining PM 10 as 14 the indicator for regulating thoracic coarse particles. The EPA established two new PM 2.5 15 standards: an annual standard of 15 μg/m 3 , based on the 3-year average of annual arithmetic 16
mean PM 2.5 concentrations from single or multiple community-oriented monitors; and a 24-hour 17 standard of 65 μg/m 3 , based on the 3-year average of the 98 th percentile of 24-hour PM 2.5 18 concentrations at each populat ion-oriented monitor within an area (62 FR 38652, July 18, 1997). 19 With respect to the secondary PM standard s, EPA concluded in 1997, that the available 20
evidence on effects of PM on non-vi sibility welfare endpoints wa s not sufficient to warrant a 21 separate secondary standard. Therefore, the se condary standards were set equal to the primary 22

PM 2.5 and PM 10 standards in the final rule to provide protection against eff ects on visibility as 23 well as materials damage and soiling effects rela ted to fine and coarse particles (62 FR 38683). 24

5.1.1.2 Review Completed in 2006 25

In 2006, the Administrator concluded that there was insufficient information to consider a 26 distinct secondary standard ba sed on PM-related impacts to ecos ystems, materials damage and 27 soiling, and climatic and radiative processe s (71 FR 61144, October 17, 2006). Specifically, 28
there was a lack of evidence linki ng various non-visibility welfare e ffects to specific levels of 29 ambient PM. To provide a level of protecti on for welfare-related effects, the secondary 30 standards were set equal to the revised primary standards to directionally improve the level of 31 protection afforded vegetation, ecos ystems and materials (71 FR 61210). 32Draft Do Not Quote or Cite March 2010 5-3 In the last review, the 2004 AQCD concluded that regardless of size fraction, particles 1 containing nitrates and sulfates have the greatest potential for widespread environmental 2 significance (US EPA, 2004, sections 4.2.2 and 4.2.3.1). Considerable supporting evidence was 3
available that indicated a si gnificant role of NOx, SOx, a nd transformation products in 4
acidification and nutrient enrichment of terre strial and aquatic ecosystems (71 FR 61209). The 5 recognition of these ecological eff ects, coupled with other considerations detailed below, led 6 EPA to initiate a joint review of the NO 2 and SO 2 secondary NAAQS that will consider the 7 gaseous and particulate species of NOx and SOx with respect to the ecosystem-related welfare 8 effects that result from the deposition of these pollutants and transformation products. 9

5.1.2 Scope of Current NAAQS Reviews 10 Non-visibility welfare-based e ffects of oxides of nitrogen a nd sulfur are divided between 11 two NAAQS reviews; (1) the PM NAAQS revi ew and, (2) the joint NOx/SOx secondary 12 NAAQS review. The scope of each document and the components of N and S considered in 13
each review are detailed in this se ction and summarized in Table 5-1. 14Draft Do Not Quote or Cite March 20105-412Table 5-1. Scope of the current secondary PM NAAQS review and current NOx/SOx secondary review.3NOx/SOx SecondaryReviewPM SecondaryReviewMaterialsWelfareEffectAcidifyingdeposition,nutrientenrichmentDirect effectsof gas-phaseNOx/SOx onvegetationVisibilityimpairmentClimateForcing effectsEcologicaleffectsDamage SoilingDocumentsISANOx/SOxNOx/SOxPMPMPMPM andNOx/SOxAnnex E PMREANOx/SOx NOx/SOxPM (Urbanfocusedvisibilityassessment)PANOx/SOx NOx/SOx PM PM PM PM PMComponentsDepositedparticulate andgaseous formsof oxides ofnitrogen andsulfur andrelated N and Scontainingcompounds.Gaseous formsof oxides ofnitrogen andsulfur andrelated N and Scontainingcompounds inthe ambient air.All particles10 microns orsmaller in theambient air.Climate-relatedparticles(aerosols) inthe ambient air.Depositedcomponentsof PM,includingmetals andorganics butnot N and Scontainingcompounds.Particles andgasesassociated withambient NOxand SOxincluding NOy,NH3and NHx.Depositedparticles4Draft Do Not Quote or Cite March 2010 5-5 5.1.2.1 Scope of the Current Secondary PM NAAQS Review 1

In reviewing the current suite of secondary PM standards to address visibility impairment 2 (chapter 4), climate forcing eff ects (section 5.2), and other welf are-related effects (sections 5.3 3 and 5.4), all PM-related effects that are not being covered in the NOx/SOx review are 4 considered. With regard to the materials sec tion (5.4), the discussion has been expanded to 5 include particles and gases that are associated with the presence of ambient NOx and SOx, as 6 well as NOy, NH 3 and NH X for completeness. By excludi ng the effects associated with 7 deposited particulate matter components of NOx and SOx and their transformation products 8 which are addressed fully in the NOx/SOx seconda ry review, as outlined below, the discussion 9 of ecological effects of PM has been narrowed to focus on effects associat ed with the deposition 10 of metals and, to a lesser ex tent, organics (section 5.3). 11

5.1.2.2 Scope of the Current NOx/SOx Secondary NAAQS Review 12

This is the first time since the NAAQS were es tablished in 1971 that a joint review of the 13 secondary NAAQS for NOx and SOx

, has been conducted. This review is being conducted 14 because the atmospheric chemistry and environmen tal effects of NOx, SOx, and their associated 15 transformation products are linked, and because the National Research Council (NRC) has 16 recommended that EPA consider multiple pollutants, as appropriate, in forming the scientific 17 basis for the NAAQS. The NOx/SOx secondary revi ew focuses on the welfar e effects associated 18 with exposures from deposited particulate and ga seous forms of oxides of nitrogen and sulfur 19 and related N and S containing compounds and tran sformation products on ecosystem receptors. 20 An assessment of the complex ecological eff ects associated with N deposition requires 21 consideration of multiple forms of N. These include evaluation of data on inorganic reduced 22 forms of N (e.g., ammonia [NH 3 ] and ammonium ion [NH 4 +]), inorganic oxidized forms (e.g., 23 NOx, nitric acid [HNO 3 ], nitrous oxide [N 2 O], nitrate [NO 3

− ]), and organic N compounds (e.g., 24 urea, amines, proteins, nucleic acids). In addi tion to acidification and N-nutrient enrichment, 25
other welfare effects related to deposition of N-and S-containi ng compounds are discussed, such 26 as SOx interactions with mercury (Hg) methyl ation. In addition, the NOx/SOx secondary review 27 includes evidence related to direct ecological eff ects of gas-phase NOx and SOx since the direct 28 effects of gas-phase SOx on vegetation formed a pr imary basis for the initial establishment of the 29 secondary NAAQS for SO 2
. 30 Effects of acidifying deposition associated w ith particulate N and S are covered in the 31

recent Integrated Science Assessmen t for Oxides of Nitrogen and Sulfur-Ecological Criteria 32 ( Final Report (US EPA, 2008c). The Risk and Exposure Assessment for Review of the 33 Secondary National Ambient Air Q uality Standards for Oxides of Nitrogen and Oxides of Sulfur 34Draft Do Not Quote or Cite March 2010 5-6 (Final) (NOx/SOx REA) (US EPA, 2 009h) considers four main targeted ecosystem effects 1 considered in the review of secondary effects of NOx and SOx: (1) aquatic acidification due to N 2 and S, (2) terrestrial acidificat ion due to N and S, (3) aquatic nutrient enrichment, including 3 eutrophication and (4) terrestrial nu trient enrichment. In the draft Policy Assessment for Review 4 of the Secondary National Ambien t Air Quality Standards for Oxides of Nitrogen and Oxides of 5 Sulfur (US EPA 2010c) ecologically-based indicators that link atmospheric concentrations to 6 deposition are being considered. 7

5.1.3 Current Approach 8 The remainder of this chapter summarizes and highlights key aspects of the policy 9 relevant information from the ISA to help info rm the Administrator’s judgments regarding the 10 adequacy of the current suite of secondary PM NAAQS in relation to climate processes, 11 ecological effects, and materials damage. The ISA uses a five-level hierarchy that classifies the 12 weight of evidence for causation, not just asso ciation, into a qualitative statement about the 13 overall weight of evidence and causality (U S EPA, 2009a, section 1.5.5, Table 1-3): causal 14 relationship; likely to be a causa l relationship; suggestiv e of a causal relations hip; inadequate to 15 infer a causal relationship; not likely to be a causal relationship (see US EPA, 2009a, Table 1-3). 16 Staff is evaluating evidence-based consideratio ns primarily by assessing the evidence of 17
associations identified in the ISA. All relations hips between PM and climate, ecological effects, 18 and materials damage effects identified in the ISA are considered to be either “likely causal” or 19 “causal”. The staff’s approach in this review of non-visibility welfare effects of PM is to 20 consider information regarding pa rticulate matter effects on c limate, ecological endpoints and 21
materials. This includes new literature availa ble since the last review as well as existing, 22 relevant information as presented in the ISA (US EPA 2009a). 23

5.2 CLIMATE 24

5.2.1 Scope 25

Information and conclusions about what is currently known about the role of PM in 26 climate is summarized in Chapter 9 of the PM ISA (US EPA, 2009a). The ISA concludes; “that 27 a causal relationship exists between PM and effects on climate, in cluding both direct effects on 28 radiative forcing and indirect effects that involve cloud feedb acks that influence precipitation 29 formation and cloud lifetimes” (US EPA, 2009a, s ection 9.3.10). Material from the climate 30 section of the ISA is principally drawn from the U.S. Climate Change Science Program 31 Synthesis and Assessment Product 2.3, Atmospheric Aerosol Prope rties and Climate Impacts , by 32 Chin et al., (CCSP 2009) and Chapter 2, Changes in Atmospheric Cons tituents and in Radiative 33 Forcing ,(Forster et al., 2007) in the comprehensive Working Group I report in the Fourth 34Draft Do Not Quote or Cite March 2010 5-7 Assessment Report (AR4) from the Intergovernmen tal Panel on Climate Change (IPCC), Climate 1 Change 2007: The Physical Science Basis . Sections 9.3.7 (Fire as a Special Source of PM 2 Welfare Effects), 9.3.9 (Other Special Sources and Effects), 9.3.9.1 (Gla ciers and Snowpack) 3 and 9.3.9.3 (Effects on Local and Regional Climate) of the ISA were written by NCEA staff. 4
This section of the PA summarizes and synthesizes the policy-releva nt science in the ISA for the 5 purpose of helping to inform consideration of clim ate aspects in the review of the secondary PM 6 NAAQS. 7 Atmospheric PM (referred to as aerosols 1 in the remainder of this section to be consistent 8 with the ISA) affects multiple aspects of clim ate. These include absorbing and scattering of 9 incoming solar radiation, alterations in terrestr ial radiation, effects on th e hydrological cycle, and 10 changes in cloud properties (US EPA, 2009a, s ection 9.3.1). Major aerosol components that 11 contribute to climate processes in clude black carbon (BC), organic ca rbon (OC), sulfates, nitrates 12
and mineral dusts. There is a considerable ongoing research effort focused on understanding 13 aerosol contributions to changes in global mean temperature and precip itation patterns. The 14 Climate Change Research Initiative identified re search on atmospheric concentrations and effects 15 of aerosols as a high research priority (Nationa l Research Council, 2001) and the IPCC 2007 16 Summary for Policymakers states that anthropogenic cont ributions to aerosols remain the 17 dominant uncertainty in radiative forcing (IP CC 2007). The current state of the science of 18
climate alterations attributed to PM is in flux as a result of c ontinually updated information. 19

5.2.2 Adequacy of the Current Standard 20 In considering the adequacy of the suite of secondary standards, staff addresses the 21 following overarching question: 22

Does currently available scientific information, as reflected in the ISA, support or call into 23 question the adequacy of the protection for clim ate effects afforded by the current suite of 24 secondary PM standards? 25 To inform the answer to this overarching que stion, staff has posed specific questions to 26 aid in assessing the available scientific eviden ce as related to climate effects attributed to 27 aerosols. In considering the curr ently available scientific and t echnical information, we included 28
both the information available from the last review and information that is newly available since 29 the last review synthesized in Chapter 9 of the ISA (US EPA, 2009). 30

• What new techniques are available to improve our understanding of climate effects of 31 aerosols? 32

1 In the sections of the ISA included from IPCC AR4 and CCSP SAP2.3, ‘aerosols’ is more frequently used than “PM” and that word is retained.Draft Do Not Quote or Cite March 2010 5-8 Global climate change has increasingly been th e focus of intense international research 1 endeavors. Major efforts are underway to unders tand the complexities inherent in atmospheric 2
aerosol interactions and to decrease uncertainties associated with climate estimations. Two recent 3 reports, the US CCSP Product 2.3 and sections of the IPCC AR4 were combined to form the 4 climate discussion in the ISA (CCSP 2009; Forster et al., 2007). A review of the most recently 5 available techniques for assessing climate-aerosol relationships is presented in the ISA. Aerosol 6 measurement capabilities review ed in the ISA include a di scussion of the increasingly 7 sophisticated instrumentation and techniques av ailable for quantifying ae rosols, the enhanced 8 sensing capabilities of satellites , development of remote sensing networks and synergy of 9 measurements with model simulations (US EP A 2009a, section 9.3.2). Advances in measured 10 aerosol properties as related to modeling as well as outstandi ng issues remaining in these 11
measurement-based studies are elaborated in the ISA (US EPA 2009a sections 9.3.3 and 9.3.4). 12 Section 9.3.6 of the ISA, “Global Aerosol Mode ling” considers the capabilities of climate 13 modeling that have developed over the last decade and limitations of the techniques currently in 14 use (US EPA 2009a). 15

• To what extent does newly available eviden ce improve our understanding of the nature 16 and magnitude of climate res ponses to PM (aerosols)? 17

Aerosols have direct and indi rect effects on climate processes. The direct effects of 18 aerosols on climate result mainly from particles scattering light away fr om earth into space, 19 directly altering the radiative ba lance of the Earth-atmosphere sy stem. This reflection of solar 20 radiation back to space decreases the transmission of visible radiation to the surface of the earth 21 and results in a decrease in the heating rate of the surface and the lower atmosphere. At the same 22 time, absorption of either incoming solar radiatio n or outgoing terrestrial radiation by particles, 23 primarily BC, results in an increased heating ra te in the lower atmosphere. Global estimates of 24
aerosol direct radiative forci ng (RF) were recently summarized using a combined model-based 25 estimate (Forster et al., 2007). The overall, model- derived aerosol direct RF was estimated in the 26 IPCC AR4 as -0.5 (-0.9 to -0.1) watts per square meter (W/m 2 ), with an overall level of scientific 27 understanding of this effect as “medium low” (Forster et al., 2007), i ndicating a net cooling 28 effect in contrast to greenhouse gases ( GHGs) which have a warming effect. 29 The contribution of individual aerosol component s to total aerosol dire ct radiative forcing 30 is more uncertain than the globa l average (US EPA, 2009a, section 9.3.6.6). The direct effect of 31 radiative scattering by atmospheri c particles exerts an overall ne t cooling of the atmosphere, 32 while particle absorption of solar radiation leads to warming. For example, the presence of OC 33 and sulfates decrease warming from sunlight by scattering shortwave radia tion back into space. 34 Such a perturbation of incoming radiation by an thropogenic aerosols is designated as aerosol 35 climate forcing, which is distinguished from the aerosol radiative effect of the total aerosol 36Draft Do Not Quote or Cite March 2010 5-9 (natural plus anthropogenic). The aerosol climat e forcing and radiative e ffect are characterized 1 by large spatial and temporal hete rogeneities due to the wide va riety of aerosol sources, the 2 spatial non-uniformity and intermittency of thes e sources, the short atmospheric lifetime of 3 aerosols (relative to that of the greenhouse gases), and processing (chemical and microphysical) 4 that occurs in the atmosphere. For example, OC can be warming (positive forcer) when 5 deposited on or suspended over a highly reflectiv e surface such as snow or ice but, on a global 6 average, is a negative forcer in the atmosphere. 7
More information has also become available on indirect effects of aer osols. Particles in 8 the atmosphere indirectly affect both cloud albe do (reflectivity) and cl oud lifetime by modifying 9 the cloud amount, and microphysical and radiativ e properties (US EPA, 2009a, section 9.3.6.4). 10
The RF due to these indirect e ffects (cloud albedo effect) of aerosols is estimated in the IPCC 11 AR4 to be -0.7(-1.8 to -0.3) W/m 2 with the level of sc ientific understanding of this effect as 12 “low” (Forster et al., 2007). Aerosols act as cloud condensation nuclei (CCN) for cloud 13 formation. Increased particulates in the atmo sphere available as CCN with no change in 14
moisture content of the clouds have resulted in an increase in the number and decrease in the 15 size of cloud droplets in certain clouds that can increase the al bedo of the clouds (the Twomey 16 effect). Smaller partic les slow the onset of precipitation and prolong cloud lifetime. This effect, 17 coupled with changes in cloud albedo, increase the reflection of solar radiation back into space. 18
The altitude of clouds also eff ects cloud radiative forcing. Low clouds reflect incoming sunlight 19 back to space but do not effectively trap outgoin g radiation, thus, cooling the planet, while higher 20 elevation clouds reflect some sunlight but more e ffectively can trap outgoi ng radiation and act to 21 warm the planet (US EPA, 2009a, section 9.3.3.5). 22 The total negative RF due to di rect and indirect effects of aerosols computed from the top 23 of the atmosphere, on a global average, is estimated at -1.3 (-2.2 to -0.5) W/m 2 in contrast to the 24 positive RF of +2.9 (+3.2 to +2.6) W/m 2 for anthropogenic GHGs (IPCC 2007, pg. 200). 25 The understanding of the magnitude of aer osol effects on climate has increased 26 substantially in the last decade. Data on the atmospheric transport and deposition of aerosols 27 indicate a significant role for PM components in multiple aspects of climate. Aerosols can 28 impact glaciers, snowpack, regi onal water supplies, precipitat ion and climate patterns (US EPA 29 2009a section 9.3.9). Aerosols de posited on ice or snow can le ad to melting and subsequent 30 decrease of surface albedo (US EPA 2009a, secti on 9.3.9.2). Aerosols are potentially important 31 agents of climate warming in the Arctic and other locations (US EPA, 2009a, section 9.3.9). 32 Incidental fires and biomass burning are bei ng recognized as having a significant impact on 33

PM 2.5 concentrations and climate forcing. Intermitten t fires can occur at large enough scales to 34 affect hemispheric aerosol concentra tions (US EPA 2009a, section 9.3.7). 35Draft Do Not Quote or Cite March 2010 5-10 A series of studies available since the last review examine the role of aerosols on local 1 and regional scale climate processes (US EP A, 2009a, section 9.3.9.3). Studies on the South 2 Coast Air Basin (SCAB) in California indicate aerosols may reduce near-surface wind speeds, 3 which, in turn reduce evaporation rates and increase cl oud lifetimes. The overall impact can be a 4 reduction in local precipitation (Jacobson and Kaufmann, 2006). Conditions in the SCAB impact 5 ecologically sensitive areas including the Sie rra Nevadas. Precipitation suppression due to 6 aerosols in California (Givati and Rosenfield, 2004) and other similar studies in Utah and 7 Colorado found that orographic precipitation decreased by 15-30% downwind of pollution 8 sources. Evidence of regional-scale impacts of aerosols on meteorological conditions in other 9 regions of the U.S. are lacking. 10

• To what extent does the currently available information provide evidence of association 11 between specific PM constituents (i.e. BC, OC , sulfates) and climat e-related effects? 12 Advances in the understanding of aerosol components and how they contribute to climate 13 change have enabled refined global forcing estimates of individual PM constituents. The global 14 mean radiative effect from individual components of aerosols was estimated for the first time in 15 the IPCC AR4 where they were reported to be (all in W/m 2 units): -0.4 (+ 0.2) for sulfate, -0.05 16 (+ 0.05) for fossil fuel-derived OC, +0.2 (+0.15) for fossil fuel derived BC, +0.03 (+ 0.12) for 17 biomass burning, -0.1 (+ 0.1) for nitrates, and -0.1 (+ 0.2) for mineral dust (US EPA, 2009a, 18 section 9.3.10). Sulfate and fossil fuel-derived OC cause negative forcing whereas BC causes 19 positive forcing because of its highly abso rbing nature (US EPA, 2009a, 9.3.6.3). Although BC 20 comprises only a small fraction of anthropogenic aerosol mass load and aerosol optical depth 21 (AOD), its forcing efficiency (w ith respect to either AOD or ma ss) is an order of magnitude 22 stronger than sulfate and particulate organic ma tter (POM), so its positive shortwave forcing 23 largely offsets the negative direct forcing from sulfate and POM (IPCC, 2007; US EPA 2009a, 24 9.3.6.3). Global loadings for nitrates and anthropo genic dust remain very difficult to estimate, 25 making the radiative forcing estimates for these constituents particularly uncertain (US EPA, 26 2009a, section 9.3.7). 27 Improved estimates of anthropogenic emissions of some aerosols, especially BC and OC, 28 have promoted the development of improved glob al emissions inventorie s and source-specific 29
emissions factors useful in cl imate modeling (Bond et al. 2004). Recent data suggests that BC is 30 one of the largest individual warm ing agents after carbon dioxide (CO 2 ) and perhaps methane 31 (CH 4 ) (Jacobson 2000; Sato et al., 2003; Bond a nd Sun 2005). There are several studies 32 modeling BC effects on climate and/or c onsidering emission reduction measures on 33 anthropogenic warming detailed in section 9.3.9 of the ISA. Fire s release large amounts of BC, 34
CO 2 , CH 4 and OC (US EPA, 2009a, section 9.3.7). 35Draft Do Not Quote or Cite March 2010 5-11 5.2.3 Preliminary Staff Conclusions 1

• Aerosols alter climate processes directly through radiative forc ing and by indirect 2 effects on cloud brightness, changes in pr ecipitation and possibl e changes in cloud 3 lifetimes. 4

• Individual components of aeros ols differ in their reflective properties, and direction of 5 climate forcing. Overall, aerosols have a net climate cooling effect. 6

• Most climate model simulations are based on global scale scenarios. These models 7 may fail to consider the local variations in climate forcing due to emissions sources and 8 local meteorological patterns. 9

• Aerosols that are warming are co-emitted with aerosols that are cooling. The relative 10 mix of these components will vary in areas across the U.S. and over time. 11 Collectively taking into consideration the res ponses to specific que stions regarding the 12 adequacy of the current secondary PM standards for climate effects, we revisit the overarching 13 question: “does available scientif ic information, as reflected in the ISA, support or call into 14 question the adequacy of the pr otection for climate effects affo rded by the current suite of 15 secondary PM standards?” As an initial matter, we considered the appropri ateness of the current 16 secondary standard defined in terms of PM 2.5 and PM 10 indicators, for providing protection 17 against potential climate effects of aerosols. Ne wly available scientific information on climate18 aerosol relationships has improved our understanding of direct and indirect effects of aerosols 19 and aerosol properties. The major aerosol com ponents that contribute to climate processes 20 include BC, OC, sulfate, nitrate and mineral dusts . These components vary in their reflectivity, 21 forcing efficiencies and even in the direction of climat e forcing. The current standards that are 22 defined in terms of aggregate size mass cannot be expected to appropriate ly target controls on 23 components of fine and coarse particles that ar e related to climate forc ing effects. Thus, the 24
current mass-based PM 2.5 and PM 10 secondary standards are not an appropriate or effective 25 means of focusing protection agai nst PM-associated climate effects due to these differences in 26
components. 27 Overall, there is a net climate cooling associ ated with aerosols in the global atmosphere 28 (US EPA, 2009a, section 9.2.10). Staff recognizes that some individual aerosol components, 29 such as BC, are positive climate forcers, wherea s others, such as OC a nd sulfates, are negative 30 climate forcers. However, aerosols that are warming are co-emitted with aerosols that are 31 cooling. The relative mix of components will vary in areas across the U.S. and over time. Due to 32 the spatial and temporal heterogeneity of PM components that contribu te to climate forcing, 33
uncertainties in the measurement of aerosol co mponents, inadequate consideration of aerosol 34 impacts in climate modeling, insufficient data on local and regional microclimate variations and 35 heterogeneity of cloud formations, it is not curre ntly feasible to conduct a quantitative analysis 36 for the purpose of informing revisions of the current NAAQS PM standard based on climate. 37Draft Do Not Quote or Cite March 2010 5-12 Based on these considerations, we reach the pre liminary conclusion that there is insufficient 1
information at this time to base a national ambi ent standard on climate impacts associated with 2
current ambient concentrations of PM or its constituents 2

. 3

5.2.4 Key Uncertainties and Areas for Futu re Research and Data Collection 4 Although considerable progress is being made in estimating aerosol contributions to 5 climate fluctuations, significant uncertainties re main that preclude consideration of climate 6 effects as a basis for establishing a separate NAAQS secondary standard. A major impediment 7 at this time to establishing a secondary standard for PM based on climate is the lack of accurate 8
measurement of aerosol contri butions, specifically quantificat ion of aerosol absorption and 9 inability to separate the anth ropogenic component from total aerosol forcing. Section 9.3.4 of 10
the ISA details the current limitations in aerosol measurement. Most measurement studies focus 11 on the sum of natural and anthropogenic contribu tions under clear sky conditions, however, this 12 scenario is simplistic when effects of cloud cove r and differing reflective properties of land and 13
ocean are considered. Satellite measurements do not currently have the capability to distinguish 14 anthropogenic from natural aerosols. Due to a lack of data on the vertical distribution of aerosols, 15
above-cloud aerosols and profiles of atmospheric radiative heating are poor ly understood (US 16 EPA, 2009a, section 9.3.4). 17 Another uncertainty in consid ering climate effects of PM in the NAAQS review is the 18 spatial and temporal heterogeneity of aerosols. In regions having high concentrations of 19 anthropogenic aerosols, aerosol forcing is greate r than the global average, and can exceed 20 warming by GHGs, locally reversing the sign of the forcing (US EPA, 2009a, section 9.3.1). 21
Emissions of carbonaceous aerosols from interm ittent fires and volcanic activity can further 22 complicate regional climate forcing estimates (US EPA, 2009a, sections 9.3.7 and 9.3.8). 23 Individual components of aerosols may either be positive or negative climate forcers. Airborne 24 PM components may be directly emitted or undergo a variety of physical and chemical 25
interactions and transformations . These result in changes in particle size, structure and 26 composition which alter aerosol reflective prope rties. Aerosols can grow in size in the 27 atmosphere because ambient water vapor c ondenses on individual particles, a phenomenon 28 known as hygroscopic growth (US EPA, 2009a, section 9.3.6.2). Atmosp heric lifetimes of 29 individual aerosol components vary greatly confounding tracking source receptor relationships. 30 Improved representation of aerosols in climat e models is essentia l to more accurately 31 predict the role of PM in climate forcing (US EPA, 2009a, section 9.3.6.7). The influence of 32

2 Given the reasons discussed above, this conclusion would apply for both the secondary (welfare based) and the primary (health based) standards.Draft Do Not Quote or Cite March 2010 5-13 aerosols on climate is not yet adequately take n into account in computer predictions although 1 considerable progress in being made in this ar ea. For example, PM components underrepresented 2 or missing from many models incl ude nitrate aerosols and anthr opogenic secondary aerosols (US 3 EPA, 2009a, section 9.3.6.7). The modeling of aero sol indirect effects and absorption are 4 difficult due to the high level of uncertainty associated with these climate factors. 5
The interaction of PM with clouds remains a large source of uncertainty in climate 6
estimates. The interactions of aerosols with clouds and linkage s between clouds and the overall 7 climate system are complex and limit the feasib ility of conducting quantitative analysis for the 8 purpose of establishing a secondary PM standard based on welfare effects on climate processes. 9

5.3 ECOLOGICAL EFFECTS 10

5.3.1 Scope 11 Information on what is currently known about ecological effects of PM is summarized in 12 Chapter 9 of the ISA (US EPA 2009a). Four main categories of ecological effects are identified 13 in the ISA: direct effects, effect s of PM-altered radiative flux, i ndirect effects of trace metals and 14 indirect effects of organics. Exposure to PM for direct effects occur via deposition (e.g. wet, dry 15 or occult) to vegetation surfaces, while indirect effects occur via deposition to ecosystem soils or 16 surface waters where the deposited constituents of PM then interacts with biological organisms. 17 Both fine and coarse-mode particles may affect plants and other organi sms; however, PM size 18 classes do not necessarily relate to ecological e ffects (U.S. EPA, 1996). More often the chemical 19 constituents drive the ecosystem response to PM (Grantz et al., 2003). The trace metal 20
constituents of PM considered in the ecological effects sectio n of the ISA are cadmium (Cd), 21 copper (Cu), chromium (Cr), mercury (Hg), nickel (Ni) and zinc (Zn). Ecol ogical effects of lead 22 (Pb) in particulate form are covered in the Ai r Quality Criteria Document for Lead (US EPA, 23 2006). The organics included in th e ecological effects s ection of the ISA are persistent organic 24 pollutants (POPs), polyaromatic hydrocarbons (PAHs) and polybromiated diphenyl ethers 25 (PBDEs). 26 Ecological effects of PM include direct eff ects to metabolic processes of plant foliage; 27 contribution to total metal loading resulting in alteration of soil biogeochemistry and 28 microbiology, plant and animal growth and repro duction; and contribution to total organics 29 loading resulting in bioaccumulati on and biomagnification across trophi c levels. It is important 30 to emphasize that the metal and organic constituents of PM contribute to total metal and organic 31 loads in ecosystems. 32 The ISA states that overall, ecological evidence is sufficient to conclude that a causal 33 relationship is likely to exist between depositi on of PM and a variety of effects on individual 34Draft Do Not Quote or Cite March 2010 5-14 organisms and ecosystems based on informati on from the previous review and limited new 1 findings in this review (US EPA 2009a, sectio ns 2.5.3 and 9.4.7). However the ISA also finds, 2 in many cases, it is difficult to characterize the na ture and magnitude of effects and to quantify 3 relationships between ambient co ncentrations of PM and ecosystem response due to significant 4 data gaps and uncertainties as well as considerable variability that exists in the components of 5
PM and their various ecological effects. 6 Ecological effects of PM must then be eval uated to determine if they are known or 7 anticipated to have an adverse impact on public welfare. Characterizi ng a known or anticipated 8 adverse effect to public welf are is an important component of developing any secondary 9 NAAQS. The most recent secondary NAAQS re views have assessed changes in ecosystem 10 structure or processes using a weight-of-evidence approach that uses both quantitative and 11 qualitative data. For example, the 2008 ozone (O 3 ) final rule and 2010 O 3 proposal conclude that 12
a determination of what constitutes an “advers e” welfare effect in th e context of secondary 13 NAAQS review can appropriately occur by consid ering effects at higher ecological levels 14 (populations, communities, ecosystems) as s upported by recent literature. In the 2008 15 rulemaking and current ozone proposa l, the interpretation of what constitutes an adverse effect 16 on vegetation can vary depending on the location a nd intended use of the plant. The degree to 17
which O 3 -related effects are considered adverse depe nds on the intended use of the vegetation 18 and its significance to public welfare (73 FR 16496) . Therefore, effects (e.g. biomass loss, foliar 19 injury, impairment of intended use) may be judged to have a different degree of impact on public 20 welfare depending, for example, on whether that e ffect occurs in a Cla ss I area, a city park, 21 commercial cropland or private land. 22 A paradigm useful in evaluating ecological adversity is the concept of ecosystem 23 services. Ecosystem services identify the varied and numerous ways that ecosystems are 24 important to human welfare. Ecosystems provi de many goods and services that are of vital 25 importance for the functioning of the biosphere an d provide the basis for the delivery of tangible 26 benefits to human society. An EPA initiative to consider how ecosystem structure and function 27 can be interpreted through an ecosystem services approach has resulted in the inclusion of 28 ecosystem services in the NOx/SOx REA (U S EPA, 2009h). The Millennium Ecosystem 29 Assessment (MEA) defines these to include supporting, provisioning, re gulating and cultural 30 services (Hassan et al., 2005): 31

• Supporting services are necessary for the pr oduction of all other ecosystem services. 32 Some examples include biomass pr oduction, production of atmospheric O 2 , soil 33 formation and retention, nutri ent cycling, water cycling, a nd provisioning of habitat. 34 Biodiversity is a supporting serv ice that is increasingly reco gnized to sustain many of 35 the goods and services that humans enjoy from ecosystems. These provide a basis for 36 three higher-level categories of services. 37Draft Do Not Quote or Cite March 2010 5-15 • Provisioning services, such as products (Git ay et al., 2001) i.e., food (including game, 1 roots, seeds, nuts, and other fruit, spices, fodder), fiber (including wood, textiles), and 2 medicinal and cosmetic products (inc luding aromatic plants, pigments). 3

• Regulating services that are of paramount importance for human society such as (a) C 4 sequestration, (b) climate and water regula tion, (c) protection from natural hazards 5 such as floods, avalanches, or rock-fall, (d) water and ai r purification, an d (e) disease 6 and pest regulation. 7

• Cultural services that satisfy human spirit ual and aesthetic appreciation of ecosystems 8 and their components. 9 An important consideration in evaluating biologically advers e effects of PM and linkages 10 to ecosystem services is that many of the ME A categories overlap and any one pollutant may 11 impact multiple services. For example, depos ited PM may alter th e composition of soil12 associated microbial communities, which may affect supporting services such as nutrient 13 cycling. Changes in available soil nutrients coul d result in alterations to provisioning services 14 such as timber yield and regulating services su ch as climate regulation. If enough information is 15 available, these alterations can be quantified based upon economic approaches for estimating the 16 value of ecosystem services. Valuation may be important from a policy perspective because it 17 can be used to compare the benefits of alteri ng versus maintaining an ecosystem. Knowledge 18 about the relationships linking ambient concentra tions and ecosystem services can be used to 19 inform a policy judgment on a known or anti cipated adverse public welfare effect. 20 This review seeks to build upon and focus th is body of science us ing the concept of 21 ecosystem services to qualitatively evaluate linkages between biologically adverse effects and 22 particulate deposition. This approach is similar to that taken in the NOx/SOx REA in which the 23 relationship between air quality indicators, deposition of N and S, ecologically relevant 24
indicators and effects on sensit ive receptors are linked to cha nges in ecosystem structure and 25 services (US EPA, 2009h). This approach consider s the benefits received from the resources and 26 processes that are supplied by ecosystems. Ecos ystem components (e.g. plants, soils, water, 27 wildlife) are impacted by PM air pollution, wh ich may alter the services provided by the 28 ecosystems in question. The goals of this policy assessment are to (1) id entify ecological effects 29 associated with PM deposition that can be li nked to ecosystem services and (2) qualitatively 30 evaluate ecological endpoints when possible. Keeping these goals and guidelines in mind, 31 limited new data on PM effects on plants, soil and nutrient cycling, wildlife and water are 32
evaluated in the context of eco system services to qualitative ly evaluate linkages between 33 biologically adverse effects and particulate deposition for the purpos e of evaluating the adequacy 34
of the current standard. 35Draft Do Not Quote or Cite March 2010 5-16 5.3.2 Adequacy of the Current Standard 1 In considering the adequacy of the suite of secondary standards, staff addresses the 2 following overarching question: 3

Does available scientific informat ion, as reflected in the ISA support or call into question 4 the adequacy of the protection afforded by th e current suite of secondary PM standards for 5 vegetation and ecosystems from the effects of deposited particulate metals and organics? 6 To inform the answer to this overarching que stion, staff has posed specific questions to 7 aid in assessing the available scie ntific evidence as related to ecosy stem effects attributed to PM 8 deposition as presented in the ISA (US EPA, 2009a). 9

• To what extent has key scientific ev idence become availabl e to improve our 10 understanding of the nature and magnitude of ecosystem responses, the variability 11 associated with these responses, and the impact of PM on ecosystem services? 12 Key scientific evidence regarding PM effect s on plants, soil and nut rient cycling, wildlife 13
and water available since the last review is summ arized below to evaluate how this information 14 has improved our understanding of ecosystem responses to PM. 15
Plants 16 As primary producers, plants play a pivotal role in energy flow through ecosystems. 17 Ecosystem services derived from plants incl ude all of the categorie s (supporting, provisioning, 18 regulating, cultural) identified in the MEA (Hassan et al., 20 05). Vegetation supports other 19 ecosystem processes by cycling nu trients through food webs and serving as a source of organic 20
material for soil formation and enrichment. Tree s and plants provide food, wood, fiber, and fuel 21 for human consumption. Flora help to regulate climate by sequestering CO 2 , control flooding by 22 stabilizing soils and cycling water via uptake and evapotranspiration. Plants are significant in 23 aesthetic, spiritual and recreationa l aspects of human interactions. 24 Particulate matter can adversely impact plants and ecosystem services provided by plants 25 by deposition to vegetative surfaces (US EPA, 2009a, section 9.4.3). Par ticulates deposited on 26
the surfaces of leaves and needle s can block light, altering the ra diation received by the plant. 27 PM deposition can obstruct stomata limiting gas exchange, damage leaf cuticles and increase 28 plant temperatures. This level of PM accumulati on is typically observed near sources of heavy 29 deposition such as smelters and mining opera tions (US EPA, 2009a, section 9.4.3). Plants 30 growing on roadsides exhibit impact damage from near-road PM deposition, having higher levels 31 of organics and heavy metals, and accumulate sa lt from road de-icing dur ing winter months (US 32 EPA, section 2009a, sections 9.4.3.1 and 9.4.5.7). 33 In addition to damage to plant surfaces, depos ited PM can be taken up by plants from soil 34 or foliage. The ability of vegetation to take up heavy metals and organics is dependent upon the 35 amount, solubility and chemical composition of the deposited PM. Uptake of PM by plants from 36Draft Do Not Quote or Cite March 2010 5-17 soils and vegetative surfaces can disrupt photosynthesis, alter pigments and mineral content, 1 reduce plant vigor, decrease frost hardiness and impair root developm ent. The ISA indicates that 2
there are little or no effects on foliar processes at ambient leve ls of PM (sections 9.4.3 and 9.4.7) 3 however, damage due to atmospheric pollution ca n occur near point-sources or under conditions 4 where plants are subjected to multiple stressors. 5 Though all heavy metals can be directly toxi c at sufficiently high concentrations, only 6 Cu, Ni, and Zn have been documented as being frequently toxic to pl ants (U.S. EPA, 2004), 7 while toxicity due to Cd, Co, and Pb has b een observed less frequently (Smith, 1990; US EPA 8 2009a, section 9.4.5.3). In general, plant growth is negatively correlated with trace metal and 9 heavy metal concentration in soils and plant tissue (Audet and Charest, 2007). Trace metals, 10 particularly heavy metals, can influence forest growth. Growth suppression of foliar microflora 11 has been shown to result from Fe, Al, and Zn. These three metals can al so inhibit fungal spore 12 formation, as can Cd, Cr, Mg, and Ni (see Sm ith, 1990). Metals cause stress and decreased 13 photosynthesis (Kucera et al., 2008 ) and disrupt numerous enzy mes and metabolic pathways 14 (Strydom et al., 2006). Excessive concentrations of metals result in phyto toxicity through: (i) 15 changes in the permeability of the cell membrane; (i i) reactions of sulfydryl (-SH) groups with 16 cations; (iii) affinity for reacting with phosphate groups and active groups of ADP or ATP; and 17 (iv) replacement of essentia l ions (Patra et al., 2004). 18 New information since the last review provides additional evidence of plant uptake of 19 organics (US EPA, 2009a, sect ion 9.4.6). An area of active study is the impact of PAHs on 20 provisioning ecosystem services due to the poten tial for human and other animal exposure via 21 food consumption (US EPA, 2009a, section 9.4.6 pa ge 9-190). The uptake of PAHs depends on 22 the plant species, site of de position, physical and chemical pr operties of the organic compound 23 and prevailing environmental conditions. It has b een established that most bioaccumulation of 24 PAHs by plants occurs via leaf uptake, and to a lesser extent, thr ough roots. Differences 25 between species in uptake of PAHs confound a ttempts to quantify impacts to ecosystem 26 provisioning services. For example, zucchini ( Cucurbita pepo ) accumulated significantly more 27 PAHs than related plant species (Parrish et al., 2006). 28 Plants as ecosystem regulators can serve as passive monitors of pollution (US EPA, 29 2009a, section 9.4.2.3). Lichens and mosses are sensit ive to pollutants associated with PM and 30
have been used with limited success to show spatial and temporal pa tterns of atmospheric 31 deposition of metals (US EPA, 2009a, section 9.4.2.3). For example, the presence or absence of 32 a specific species of lichen can be used as a bioindicator of me tal or organics contamination. 33
PBDEs detected in moss and lichens in Anta rctica indicate long-ra nge transport of PM 34 components (Yogui and Sericano 2008). In the U. S. Blue Ridge Mountains, a study linked metal 35
concentrations in mosses to elevation and tr ee canopy species at some sites but not with 36Draft Do Not Quote or Cite March 2010 5-18 concentrations of metals in the O horizon of soil (Schilling, 2002). A limitation to employing 1 mosses and lichens to detect for the presence of air pollutants is th e difference in uptake 2
efficiencies of metals between species. The European Moss Biomonitoring Network has been 3 shown to be useful in Europe for estimating general trends in metal concentrations and 4
identification of some sources of trace contaminants, however , quantification of ecological 5 effects is not possible due to the variability of species responses (US EPA, 2009a, section 6 9.4.2.3). 7 A potentially important regulating ecosystem se rvice of plants is their capacity to 8 sequester contaminants (US EPA, 2009a, sect ion 9.4.5.3). Ongoing resear ch on the application 9 of plants to environmental remediation effo rts are yielding some success in removing heavy 10 metals and organics from contaminated sites (phyto remediation) with tolera nt plants such as the 11 willow tree ( Salix spp.) and members of the family Brassicaceae (US EPA, 2009a, section 12 9.4.5.3). Tree canopies can be used in urban locati ons to capture particul ates and improve air 13 quality (Freer-Smith et al., 2004). Plant foliag e is a sink for Hg and other metals and this 14 regulating ecosystem service may be impacted by atmospheric deposition of trace metals. 15 An ecological endpoint (phytochelatin concentrat ion) associated with presence of metals 16
in the environment has been correlated with the ecological effect of tree mortality (Grantz et al., 17 2003). Metal stress may be contributi ng to tree injury and forest de cline in the Northeastern U.S. 18 where red spruce populations are d eclining with increasi ng elevation. Quantitative assessment of 19 PM damage to forests potentially could be conducted by overlaying PM sampling data and 20 elevated phytochelatin levels. However, limite d data on phytochelatin levels in other species 21 currently hinders use of this pep tide as a general biomarker for PM. 22 The presence of PM in the atmosphere affect s ambient radiation as discussed in the ISA 23 which can impact the amount of sunlight rece ived by plants (US EPA, 2009a, section 9.4.4). 24 Atmospheric PM can change the radiation reac hing leaf surfaces th rough attenuation and by 25 converting direct radiation to diffu se radiation. Diffuse radiation is more uniformly distributed in 26 a tree canopy, allowing radiation to reach lower leaves. The net effect of PM on photosynthesis 27 depends on the reduction of photosynthetically ac tive radiation (PAR) a nd the increase in the 28
diffuse fraction of PAR. Decreas es in crop yields (provisioning ecosystem service) have been 29 attributed to regional scale ai r pollution, however, global models suggest that the diffuse light 30 fraction of PAR can increase grow th (US EPA, 2009a, section 9.4.4). 31 Soil and Nutrient Cycling 32 Many of the major indirect pl ant responses to PM depositio n are chiefly soil-mediated 33 and depend on the chemical composition of i ndividual components of deposited PM. Major 34 ecosystem services impacted by PM deposition to soils include support services such as nutrient 35 cycling, products such as crops and regulating flooding and water quality. Upon entering the soil 36Draft Do Not Quote or Cite March 2010 5-19 environment, PM pollutants can alter ecological proce sses of energy flow and nutrient cycling, 1 inhibit nutrient uptake to plants, change microbial community stru cture and, affect biodiversity. 2 Accumulation of heavy metals in soils depends on factors such as local soil characteristics, 3 geologic origin of parent soils, and metal bioavailab ility. It can be difficult to assess the extent 4 to which observed heavy metal concentrations in soil are of anthropogenic origin (US EPA, 5 2009a, section 9.4.5.1). Trace element concentrations are higher in some soils that are remote 6 from air pollution sources due to pare nt material and local geomorphology. 7 Heavy metals such as Zn, Cu, and Cd a nd some pesticides can interfere with 8 microorganisms that are responsible for decompos ition of soil litter, an important regulating 9 ecosystem service that serves as a source of soil nutrients (US EPA, 2009a, sections 9.4.5.1 and 10 9.4.5.2). Surface litter decomposition is reduced in soils having high metal concentrations. Soil 11 communities have associated bacteria, fungi, and i nvertebrates that are esse ntial to soil nutrient 12 cycling processes. Changes to the relative species abundance and community composition can 13 be quantified to measure impacts of deposited PM to soil biota. A mutualistic relationship exists 14 in the rhizophere (plant root zone) between plant roots, f ungi, and microbes. Fungi in 15 association with plant roots form mycorrhizae that are essential for nutrient uptake by plants. 16 The role of mychorrizal fungi in plant uptake of metals from so ils and effects of deposited PM 17
on soil microbes is discussed in section 9.4.5.2 of the ISA. 18
Wildlife 19 Animals play a significant role in ecosyste m function including nutrient cycling and crop 20 production (supporting ecosystem se rvice), and as a source of food (provisioning ecosystem 21 service). Cultural ecosystem services provide d by wildlife include bird and animal watching, 22 recreational hunting and fishing. Impacts on these services are dependent upon the 23 bioavailability of deposited metals and organi cs and their respective toxicities to ecosystem 24 receptors. Pathways of PM exposure to fauna include ingestion, absorption and trophic transfer. 25 Bioindicator species (known as se ntinel organisms) can provide evidence of contamination due 26 to atmospheric pollutants. Use of sentinel spec ies can be of particular value because chemical 27 constituents of deposited PM are difficult to ch aracterize and have vary ing bioavailability (US 28 EPA, 2009a, section 9.4.5.5). Snails readily bioa ccumulate contaminants such as PAHs and 29 trace metals. These organisms have been deploy ed as biomonitors for urban pollution and have 30 quantifiable biomarkers of exposure including growth inhibition, impairment of reproduction, 31 peroxidomal proliferation and induction of metal detoxifying proteins (metallothioneins) 32 (Gomet-de Vaufleury, 2000; Regoli, 2006). Earthw orms have also been used as sensitive 33
indicators of soil metal contamination. 34 Evidence of deposited PM effects on animals is limited (US EPA, 2009a, section 9.4.5.5). 35 Trophic transfer of pollutants of atmospheric orig in has been demonstrated in limited studies. 36Draft Do Not Quote or Cite March 2010 5-20 PM may also be transferred between aquatic a nd terrestrial compartments. There is limited 1 evidence for biomagnifications of heavy metals up the food chain except for Hg which is well 2 known to move readily through environmental compartments (US EPA, 2009a section 9.4.5.6). 3
Bioconcentration of POPs and PBDEs in the Arc tic and deep-water ocea nic food webs indicates 4 the global transport of partic le-associated organics (US EP A, 2009a, section 9.4.6). Salmon 5 migrations are contributing to metal accumula tion in inland aquatic systems, potentially 6 impacting the provisioning and cultural ecosyste m service of fishing (US EPA, 2009a, section 7 9.4.6). Stable isotope analysis can be applied to establish linkages between PM exposure and 8 impacts to food webs, however, the use of this evaluation tool is limited for this ecological 9 endpoint due to the complexity of most troph ic interactions (US EP A 2009a, section 9.4.5.6). 10 Foraging cattle have been used to assess atmos pheric deposition and subs equent bioaccumulation 11 of Hg and trace metals and their impacts on provisioning services (US EPA, 2009a, section 12 9.4.2.3). 13
Water 14 New limited information on impacts of deposite d PM on receiving water bodies indicate 15 that the ecosystem services of primary production , provision of fresh water, regulation of climate 16 and floods, recreational fishing and water purifi cation are adversely impacted by atmospheric 17 inputs of metals and organics (US EPA, 2009a , sections 9.4.2.3 and 9.4.5.4). Deposition of PM 18 to surfaces in urban settings increases the me tal and organic component of storm water runoff 19 (US EPA, 2009a, sections 9.4.2.3). This atmospheri cally-associated pollutant burden can then be 20 toxic to aquatic biota. 21 Atmospheric deposition can be the primary s ource of some organics and metals to 22
watersheds. The contribution of atmospherically deposited PAHs to aquatic food webs was 23 demonstrated in high elevation mountain lakes with no other anthropogenic contaminant sources 24 (US EPA, 2009a, section 9.4.6). Metals associ ated with PM deposition limit phytoplankton 25 growth, impacting aquatic trophic structure. Long-range atmosphe ric transport of 47 pesticides 26 and degradation products to the snowpack in seven national parks in the Western U.S. was 27 recently quantified indicating PM-associated cont aminant inputs to receiving waters during 28 spring snowmelt (Hageman et al., 2006). 29

• What new techniques are available to improve our understanding of ecosystem 30 effects associated with metal and organic components of PM? 31 Regionally-based comprehensive ecological studies 32 The recently completed Western Airborne Contaminants Assessment Project (WACAP) 33 is the most comprehensive database on contaminant transport and PM depositional effects on 34 sensitive ecosystems in the U.S. In this project , the transport, fate, a nd ecological impacts of 35Draft Do Not Quote or Cite March 2010 5-21 anthropogenic contaminants from atmospheric s ources were assessed from 2002 to 2007 in seven 1 ecosystem components (air, snow, water, sedime nt, lichen, conifer needles and fish) in eight 2 core national parks (Landers et al., 2008). The goals of the study were to identify where the 3 pollutants were accumulating, identify ecologi cal indicators for t hose pollutants causing 4 ecological harm, and to determine the source of the air masses most likely to have transported 5 the contaminants to the parks (US EPA, 2009a, s ection 9.4.6). Collected data were analyzed to 6 identify probable local, regional and/or global sources of depo sited PM components and their 7 concurrent effects on ecological receptors. Th e study concluded that bioaccumulation of semi8 volatile organic compounds (SOCs) was observed throughout park ecosystems (Landers et al., 9 2008). Findings from this study included the obs ervation of an elevati onal gradient in PM 10 deposition with greater accumulation at higher altitude areas of the parks. Furthermore, specific 11 ecological indicators were inde ntified in the WACAP that ca n be useful in assessing 12 contamination on larger spatial scales. For exampl e, quantification of con centrations of selected 13 pesticides in second-year coni fer needles served as a method for regional-scale comparison of 14 pollutant distribution (L anders et al., 2008). 15 In the WACAP study, bioaccumulation and biom agnification of airborne contaminants 16 were demonstrated on a regional scale in remo te ecosystems in the Western United States. 17 Contaminants were shown to accumulate geogr aphically based on proximity to individual 18 sources or source areas, primarily agriculture and industry (Lande rs et al., 2008). This finding 19 was counter to the original work ing hypothesis that most of th e contaminants found in western 20 parks would originate from eastern Europe and Asia (Landers et al., 2008 p 6-8). The WACAP 21 study represents an experimental design in whic h ecological effects coul d be correlated to 22 ambient pollutant levels on a regional scale. Although this assessment focuses on chemical 23 species that are components of PM, it does not sp ecifically assess the eff ects of particulates 24 versus gas-phase forms; therefore, in most cases it is difficult to a pply the results to this 25 assessment based on particulate concentration and size fraction (US EPA, 2009a, section 9.4.6). 26 There is a need for ecological modeling of PM components in different environmental 27 compartments to further elucidate links between PM and ecological indicators. 28 Europe and other countries are us ing the critical load approach to assess pollutant effects 29 at the level of the ecosystem. Th is type of assessment requires si te-specific data and information 30 on individual species responses to PM. In re spect to trace metals and organics, there are 31 insufficient data for the vast majority of U.S. ec osystems to calculate critical loads, however, a 32 methodology is being presented in the NOx/SOx Secondary REA (US EPA 2009h) to calculate 33 atmospheric concentrations from deposition that may be applicable to other environmental 34
contaminants. 35Draft Do Not Quote or Cite March 2010 5-22 • Is there currently available information on ambient levels of PM that cause 1 adverse effects on ecosystem components? 2 As reviewed above, there is c onsiderable data on impacts of PM on ecological receptors, 3
but few studies that link ambient PM levels to observ ed effect. This is due, in part, to the nature, 4 deposition, transport and fate of PM in ecosystems. PM is not a single pollutant, but a 5 heterogeneous mixture of particles differing in size, origin and chemical composition (US EPA, 6 2009a, section 9.4.1). The heterogeneity of PM exis ts not only within in dividual particles or 7 samples from individual sites, but to even a greate r extent, between samples from different sites. 8 Since vegetation and other ecosystem components are affected more by particulate chemistry 9 than size fraction, exposure to a given mass concen tration of airborne PM may lead to widely 10 differing plant or ecosystem responses, depending on the particular mix of deposited particles. 11 Many of the PM components bioaccumulat e over time in organisms or plants making 12 correlations to ambient levels of PM impossi ble. For example, in the WACAP study, SOC 13 accumulation in vegetation and air showed differe nt patterns, possibly because each medium 14 absorbs different types of SOCs with vary ing efficiencies (La nders et al., 2008). 15 Bioindicator organisms demonstrated biologi cal effects including growth inhibition, 16 metallothionein induction and repr oductive impairment when exposed to complex mixtures of 17 ambient air pollutants (US EPA 2009a, section 9.4.5.5). Other studie s quantify uptak e of metals 18 and organics by plants or animals. However, due to the difficulty in correlating individual PM 19 components to a specific physiolo gical response, these studies ar e limited. Furthermore, there 20 may be differences in uptake between species such as differing responses to metal uptake 21 observed in mosses and lichens (US EPA 2009a, section 9.4.2.3). PM may also biomagnify 22 across trophic levels confounding efforts to link atmospheric concentrations to physiological 23 endpoints (US EPA, 2009a, section 9.4.5.6). 24
Evidence of PM effects that are linked to a specific ecological endpoint can be observed 25
when ambient levels are exceeded. Most direct ecosystem effects associated with particulate 26 pollution occur in severely polluted areas near in dustrial point sources (quarries, cement kilns, 27 metal smelting) (US EPA, 2009a, sections 9.4.3 a nd 9.4.5.7) . Extensive research on biota near 28 point sources provide some of th e best evidence of ecosystem f unction impacts and demonstrates 29 that deposited PM has the potential to alte r species composition over long time scales. 30 Ecological field studies c onducted in proximity to Cu-Ni smelte r in Harjavalta, Finland indicated 31 ecological structure and community composition are altered in response to PM and these effects 32 decrease with increasing distance from the point source (US EPA 2009a , section 9.4.5.7). The 33 ISA indicates at 4 km distance, species com position of vegetation, insects, birds, and soil 34 microbiota changed, and within 1 km only the mo st resistant organisms were surviving (US 35 EPA, 2009a, section 9.4.5.7). Heavy metal concentr ations were quantified in understory plant 36Draft Do Not Quote or Cite March 2010 5-23 species growing at varying distance from the Ha rjavalta smelter (Salem aa et al., 2004). Heavy 1 metal concentrations were highest in bryophyt es, followed by lichens and were lowest in 2 vascular plants. At the Harjavalta smelter ther e are clear links between PM deposition levels, 3 ecological endpoints and compromised ecosystem st ructure. However, these conditions are not 4
reflective of ambient concentrations of PM in the majority of US ecosystems (US EPA, 2009a, 5 section 9.4.7). 6

5.3.3 Preliminary Staff Conclusions 7

• A number of significant envir onmental effects that either have already occurred or are 8 currently occurring are linked to deposition of chemical constituents found in ambient 9 PM. 10

• Ecosystem services can be adversely impact ed by PM in the environment, including 11 supporting, provisioning, regula ting and cultural services. 12

• The lack of sufficient information to relate specific ambient concentrations of 13 particulate metals and organics to a degr ee of impairment of a specific ecological 14 endpoint hinders our ability to identify a ra nge of appropriate indi cators, levels, forms 15 and averaging times of a dist inct secondary standard to protect against associated 16 effects. 17

• Data from regionally-based ecological studies can be used to establish probable local, 18 regional and/or global sources of depos ited PM components and their concurrent 19 effects on ecological receptors. 20 Collectively taking into consideration the res ponses to specific que stions regarding the 21 adequacy of the current secondary PM standa rds for ecological effects, we revisit the 22 overarching question: “does availabl e scientific information, as re flected in the ISA, support or 23 call into question the adequacy of the protection for ecosystems afforded by the current suite of 24 secondary PM standards?” Staff reaches the preliminary conclusion that the available 25 information is insufficient to assess the adequacy of the protection for ecosystems afforded by 26 the current suite of PM secondary standards. Ecosystem effects linked to PM are difficult to 27 determine because the changes may not be observed until pollutant deposition has occurred for 28 many decades. Because the high levels necessary to cause injury occur only near a few limited 29 point sources and/or on a very lo cal scale, protection against thes e effects alone may not provide 30 sufficient basis for considering a separate sec ondary NAAQS based on the ec ological effects of 31 particulate metals and organics. Data on ecolo gical responses clearly linked with atmospheric 32 PM is not abundant enough to perform a qua ntitative analysis although the WACAP study may 33 represent an opportunity for quantif ication at a regional scale. At this time, we conclude that 34
available evidence is not sufficient for establishi ng a distinct national st andard for ambient PM 35 based on ecosystem effects of particulates not addressed in the NOx/SOx secondary review (e.g. 36 metals, organics). 37Draft Do Not Quote or Cite March 2010 5-24 Staff considered the appropriatene ss of continuing to use the PM 2.5 and PM 10 size 1
fractions as the indicators fo r protection of ecological effect s of PM. Though the chemical 2
constitution of individual particles can be strongly correlated with size, the relationship between 3 particle size and particle compos ition can also be quite complex, making it difficult in most cases 4 to use particle size as a surrogate for chemistry. At this time it remains to be determined as to 5 what extent PM secondary standards focused on a given size fraction woul d result in reductions 6 of the ecologically relevant constituents of PM for any given area. 7

5.3.4 Key Uncertainties and Areas for Futu re Research and Data Collection 8 The above discussions identify linkages between ecological effects of deposited PM and 9 potential impacts to ecosystem services. Un fortunately, our ability to relate ambient 10 concentrations of PM to ecosystem response is hampered by a number of significant data gaps 11 and uncertainties. These limitations include the presence of multiple ecological stressors 12 confounding attempts to link specific ecosystem responses to PM deposition. These stressors 13 can be anthropogenic (e.g. habita t destruction, eutrophicat ion, other pollutants) or natural (e.g. 14 drought, fire, disease). Deposited PM interacts with other stressors to affect ecosystem patterns 15 and processes. Furthermore, the environmental effects of deposited PM are decoupled in space 16 and time from the point of emission confounding efforts to identify ecological perturbations 17 attributed to PM deposition. 18 A second source of uncertainty lies in predic ting the amount of PM deposited to sensitive 19 receptors from measured concentrations of PM in the ambient air. This makes it difficult to 20 relate a given air concentration to a receptor response, an important factor in being able to set a 21 national ambient air quality standard. A multitude of factors such as the mode of deposition 22 (wet, dry and occult), wind speed, surface r oughness or stickiness, elevation, particle 23 characteristics (e.g. size, shape, chemical co mposition), and relative humidity exert varying 24 degrees of influence on the depos ition velocities for different PM components in any point in 25 time. Composition of ambient PM varies in time and space and th e particulate mixture may have 26 synergistic, antagonistic or a dditive effects on ecologi cal receptors depending upon the chemical 27 species present. Furthermore, presence of co-occ urring pollutants make it difficult to attribute 28 observed effects to ecological receptors to PM alone or one component of deposited PM. 29 Third, each ecosystem has developed within a context framed by the topography, 30 underlying bedrock, soils, climate, meteorology, hydrologic regime, natural and land use history, 31 and species composition that make it unique from all others. Sensitivity of ecosystem response 32 is highly variable in space and tim e. Because of this variety and lack of sufficient baseline data 33 on each of these features for most ecosystems, it is currently not possible to extrapolate with 34 confidence any effect from one ecosystem to another. 35Draft Do Not Quote or Cite March 2010 5-25 5.4 MATERIALS 1

5.4.1 Scope 2

Welfare effects on materials associated with deposition of PM include both physical 3 damage (materials damage effects) and impaired aesthetic qualities (soili ng effects). Because the 4 effects of PM are exacerbated by the presence of acidic gases and can be a dditive or synergistic 5 due to the complex mixture of pollutants in the air and surface characteristics of the material, this 6 discussion will also include those particles and ga ses that are associated with the presence of 7 ambient NOx and SOx, as well as NH 3 and NH X for completeness. Building upon the 8 information presented in the last Staff Pape r (US EPA, 2005), and including the limited new 9 information presented in Chapter 9 of the PM ISA (US EPA, 2009a) and Annex E. Effects of 10 NOy, NHx, and SOx on Structures and Material s of the Integrated Science Assessment for 11 Oxides of Nitrogen and Sulfur-Ecological Criteria (NOx/SOx ISA) (US EPA, 2008c) the 12 following sections consider the po licy-relevant aspects of physical damage and aesthetic soiling 13 effects of PM on materials including metal and stone. 14
The ISA concludes that evidence is sufficien t to support a causal relationship between 15 PM and effects on materials (US EPA, 2009a, s ections 2.5.4 and 9.5.4). The deposition of PM 16 can physically affect materials, adding to the effects of natural weat hering processes, by 17 potentially promoting or accelerating the corr osion of metals, by degrading paints and by 18 deteriorating building materials such as stone, concrete and marble (US EPA, 2009a, section 19 9.5). Particles contribute to these physical eff ects because of their electrolytic, hygroscopic and 20 acidic properties, and thei r ability to sorb corrosive gases (principally SO 2 ). In addition, the 21 deposition of ambient PM can reduce the aest hetic appeal of buildings and objects through 22 soiling. Particles consisting primarily of carbonaceous compounds cause soiling of commonly 23 used building materials a nd culturally important items such as statues and works of art. Soiling 24 is the deposition of particles on surfaces by im pingement, and the accumulation of particles on 25 the surface of an exposed material results in degradation of its appearance (US EPA 2009a, 26 section 9.5). Soiling can be remedied by cleaning or washing, and depending on the soiled 27 material, repainting. 28

5.4.2 Adequacy of the Current Standard 29 In considering the adequacy of the suite of secondary standards, staff addresses the 30 following overarching question: 31

Does available scientific informat ion, as reflected in the ISA support or call into question 32 the adequacy of the protection for materials a fforded by the current suite of secondary PM 33 standards? 34Draft Do Not Quote or Cite March 2010 5-26 To inform the answer to this overarching quest ion, staff has posed a specific question to 1 aid in assessing the available scientific evid ence as related to mate rials damage and soiling 2 attributed to PM deposition as pr esented in the ISA (US EPA, 2009a). 3

• What new evidence is available to improve our understanding of effects of PM on 4 materials and linking ambient concentrations to materials damage? 5 The majority of available new studies on mate rials effects of PM are from outside the 6 U.S., however, they provide limited new data fo r consideration of the secondary standard. 7 Metal and stone are susceptible to damage by ambient PM. Considerable research has 8 been conducted on the effects of air pollutants on metal surfaces due to the economic importance 9 of these materials, especially steel, zinc, alum inum, and copper. Chapter 9 of the PM ISA and 10
Annex E of the NOx/SOx ISA summarize the results of a number of studi es on the corrosion of 11 metals (US EPA, 2009a; US EPA, 2008c). Moisture is the single greatest factor promoting metal 12 corrosion, however, deposited PM can have additive, antagonistic or syne rgistic effects. In 13 general, SO 2 is more corrosive than NOx although mixtures of NOx, SO 2 and other particulate 14
matter corrode some metals at a faster rate th an either pollutant al one (US EPA, 2008c, Annex 15 E.5.2). Information from both the PM ISA and NOx /SOx ISA suggest that the extent of damage 16
to metals due to ambient PM is variable a nd dependent upon the type of metal, prevailing 17 environmental conditions, rate of natural weathering and presence or absence of other pollutants. 18
The PM ISA and NOx/SOx ISA summarize the re sults of a number of studies on PM and 19 stone surfaces. While it is clear from the available information that gaseous air pollutants, in 20 particular SO 2 , will promote the deterioration of some types of stones under specific conditions, 21 carbonaceous particles (non-carbonat e carbon) and particles containi ng metal oxides may help to 22 promote the decay process. Studies on metal an d stone summarized in the ISA do not show an 23 association between particle size, chemical composition and frequency of repair. 24
A limited number of new studies available on ma terials damage effects of PM since the 25 last review consider the relationship between pollutants and biodeterior ation of structures 26
associated with microbial communities that colonize monuments and buildings (US EPA 2009a, 27 section 9.5). Presence of air pollutants may syne rgistically enhance mi crobial deterioration 28 processes. The role of heterotr ophic bacteria, fungi and cyanobact eria in biodeteri oration varied 29 by local meterological conditions and pollutant components. In a comparative study of 30 biodeterioration processes on monu ments in Latin America, limest one deterioration at the Mayan 31 site of Uxmal was enhanced by biosolubilizatio n by metabolic acids from bacteria and fungi 32
while destruction of the Cathedra l of La Plata was attributed pr imarily to atmospheric pollutants 33 (Herrera and Videla, 2006). 34 PM deposition onto surfaces such as metal, gl ass, stone and paint can lead to soiling. 35 Soiling results when PM accumulates on an objec t and alters the optical characteristics 36Draft Do Not Quote or Cite March 2010 5-27 (appearance). The reflectivity of a surface may be changed or presence of particulates may alter 1 light transmission. These effects can impact the aesthetic value of a structure or result in 2 reversible or irreversible damage to statues, artwork and architecturally or culturally significant 3 buildings. Due to soiling of building surfaces by PM, the frequency and duration of cleaning 4 may be increased. Soiling affects the aesthetic app eal of painted surfaces. In addition to natural 5 factors, exposure to PM may give painted surfaces a di rty appearance. Pigments in works of art 6 can be degraded or discolored by atmospheric pollutants, especially sulfates (US EPA, 2008c, 7 Annex E-15). 8
Formation of black crusts due to carb onaceous compounds and buildup of microbial 9
biofilms results in discoloration of surfaces. Bl ack crust includes a carbonate component derived 10 from building material and organic carbon (OC) and elemental carbon (EC). In limited new 11 studies quantifying the OC and EC contribution to soiling by black crust, OC predominated over 12 EC at almost all locations (Bonazza et al., 2005). Limited new studies suggest that traffic is the 13 major source of carbon associated with black crust formation (Putaud, 2004) and that soiling of 14 structures in Oxford, UK showed a relationship with traffic and NO 2 concentrations (Viles and 15 Gorbushina, 2003). These findings attempt to link atmospheric concentrations of PM to 16 observed damage. However, no data on rates of damage are available and all studies were 17
conducted outside of the U.S. 18

5.4.3 Preliminary Staff Conclusions 19 Available evidence in regards to material s damage and soiling supports the following 20
observations: 21

• Materials damage and soiling that occur through natural weathe ring processes are 22 enhanced by exposure to atmosphe ric pollutants, most notably SO 2 and particulate 23 sulfates. 24

• While ambient particles play a role in the co rrosion of metals and in the weathering of 25 materials, no quantitative relationships be tween ambient particle concentrations and 26 rates of damage have been established. 27

• While soiling associated with fine and cour se particles can result in increased cleaning 28 frequency and repainting of surfaces, no quant itative relationships between particle 29 characteristics and the frequency of cleani ng or repainting have been established. 30

• Limited new data on the role of microbial colonizers in biodeteri oration processes and 31 contributions of black crust to soiling are not sufficient for quantitative analysis. 32

• While several studies in the PM ISA and NOx/SOx ISA suggest that particles can 33 promote corrosion of metals there remains insufficient evidence to relate corrosive 34 effects to specific particulate levels or to establish a qua ntitative relationship between 35 ambient PM and metal degradation. With respect to damage to calcareous stone, 36Draft Do Not Quote or Cite March 2010 5-28 numerous studies suggest that wet or dry deposition of pa rticles and dry deposition of 1 gypsum particles can enhance na tural weathering processes. 2 Revisiting the overarching policy question as to whether the available scientific evidence 3 supports or calls into question the adequacy of the protection for materials afforded by the 4 current suite of secondary PM standards, we reach the preliminary conclusion that no new 5 evidence in this review calls into question the ad equacy of the protection for materials afforded 6 by the current standard. PM effects on materials can play no quantitative role in considering 7 whether any revisions of the secondary PM NAAQS are appropriate at this time. However, in 8
the absence of information that provides a basis for establishing a different level of control, 9 observations continue to support retaining an appropriate degree of control on both fine and 10 coarse particles to help address material s damage and soiling associated with PM. 11

5.4.4 Key Uncertainties and Areas for Futu re Research and Data Collection 12 Quantitative relationships are needed between particle size, con centration, chemical 13 concentrations and frequency of repainting and repair. Deposition rates of airborne PM to 14 surfaces would provide an indication of rate and degree of damage to surfaces. There is 15 considerable uncertainty with regard to inter action of co-pollutants in regards to materials 16 damage and soiling processes. 17

5.5 REFERENCES 18
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Forster P; Ramaswamy V; Artaxo P; Betss R; Fahey DW; Ha ywood J; Lean J; Lowe DC; Myhre G; Nganga J; Prinn 30 R; Raga G;Schultz M; Van Dorland R. (2007). Changes in atmospheric constituents and in radiative 31 forcing. In Solomon, S.; Qin,D.; Manning, M.; Chen, Z.; Marquis, M.; Averyt, K. B.; Tignor, M.; Miller, 32 H. L. (Ed.),Climate Change 2007: the physical science basis. Contribution of Working Group I to the fourth 33 assessment report of the intergovernmental panel. 34

Freer-Smith PH; El-khatib A; Taylor G. (2004). Capture of particulate pollution by trees: a comparison of species 35 typical of semi-arid areas (Ficus nitida and Eucalyptus globulus) with European and North American 36 species. Water Air Soil Pollut,155: 173-187. 37Draft Do Not Quote or Cite March 2010 5-29 Gitay H; Brown S; Easterling W; Jallow B. (2001). Ecosys tems and their goods and se rvices. In Climate change 1 2001: impacts,adaptation and vulnerability. Contribution of working group II to the third assessment report 2 of the Intergovernmental Panel on Climate Change (pp. 237-342). Cambridge, United Kingdom: 3 Cambridge University Press. 4

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Hageman KJ; Simonich SL; Campbell DH; Wilson GR; Lande rs DH. (2006). Atmospheric deposition of current-use 9 and historic-use pesticides in snow at national parks in the western United States. Environ Sci Technol, 40: 10 3174-3180 11

Hassan R; Scholes R; Ash N. (2005). Ecosystems and human well-being: current state and trends, volume 1. Herrera 12 LK; Videla HA. (2004). The importance of atmospheri c effects on biodeterioration of cultural heritage 13 constructional materials. Int Biodeterior Biodegradation, 54: 125-134. IPCC (2007). Summary for 14 Policymakers. In Climate Change 2007: The Physical Science Basis. Contribution of Working Group I to 15 the Fourth Assessment Report of the Intergovernmental Panel on Climate Change (Solomon, S; Quin D, 16 Manning M, Cehn Z; Marquis M; Averyt KB; Tignor M; and Miller HL (eds.) Cambridge University Press, 17 Cambridge United Kingdom and New York, NY, USA. 18

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