Policy Assessment 

for the Review of the Particulate Matter 

National Ambient Air Quality Standards 

First External Review Draft 

March 2010 
 

DISCLAIMER

 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 those 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 Advisory 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 27711 
This 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DRAFT DO NOT QUOTE OR CITE i MARCH 2010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 ORGANIZATION OF THIS DOCUMENT........ 1-12 

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

2 REVIEW OF THE PRIMARY STANDARDS 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 PM2.5 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 Adequacy of Current Standards...............2-55 

2.3 CONSIDERATION OF ALTERNATIVE 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 Health Effects Related to Long-term PM2.5 

Exposures ........................................................................................................2-74 

2.3.4.1 Evidence-based Considerations .................................................... 2-74 

2.3.4.2 Risk-based Considerations............................................................ 2-81 
DRAFT DO NOT QUOTE OR CITE ii MARCH 2010

2.3.5 Alternative Levels to Address Health Effects Related to Short-term PM2.5 

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 Alternative Levels to Address Health Effects 

Related to Long- and Short-term PM2.5 Exposures ....................................... 2-104 

2.4 PRELIMINARY STAFF CONCLUSIONS ON ALTERNATIVE FINE PARTICLE 

STANDARDS........................................................................................................ 2-108 

2.5 KEY UNCERTAINTIES AND AREAS FOR FUTURE RESEARCH AND DATA 

COLLECTION ...................................................................................................... 2-110 

2.6 REFERENCES ...................................................................................................... 2-111 

3 REVIEW OF THE PRIMARY STANDARD 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 PM10 STANDARD .......................................... 3-8 

3.2.1 Evidence of Effects Related to Ambient Thoracic Coarse Particles ...............3-9 

3.2.2 Preliminary Staff Conclusions on Adequacy of Current PM10 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 Indicator 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 FOR FUTURE RESEARCH AND DATA 

COLLECTION .................................................................................................................... 3-39 

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

4 REVIEW OF THE SECONDARY STANDARDS FOR VISIBILITY-RELATED 

EFFECTS..............................................................................................................................4-1
DRAFT 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 PM2.5 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 ALTERNATIVE 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 CONCLUSIONS 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 STANDARDS 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.......................................................................5-23 
DRAFT 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 
1 LIST OF TABLES 

2 

3 Table 1-1. Summary of National Ambient Air Quality Standards Promulgated for Particulate 

4 Matter 1971-2006 ...................................................................................................... 1-6 

5 Table 2-1. Summary of Causality Determinations for PM2.5.................................................... 2-16 

6 Table 2-2. Estimated Incidence and Percent of Total Annual Incidence Associated with 

7 Long-term PM2.5 Exposure Based on Simulation of the Current Suite of Standards 

(for IHD mortality based on 2007 PM2.5 Concentrations)1,2 8 ...................................2-46 

9 Table 2-3. Estimated Incidence and Percent of Total Annual Incidence Associated with Short10 Term PM2.5 Exposure Based on Simulation of the Current Suite of Standards (CV 

mortality and hospital admissions based on 2007 PM2.5 concentrations)1,2 11 ............2-50 

12 Table 2-4. Comparison of Air Quality Data for Selected Epidemiological Studies – 

13 Long-term Mean Concentrations.............................................................................2-79 

14 Table 2-5. Comparison of Air Quality Data for Selected Epidemiological Studies– 98 Percentile 

15 Values...................................................................................................................... 2-94 

16 Table 3-1. Summary of Causality Determinations for PM10-2.5 ................................................ 3-11 

17 Table 3-2. PM10 Concentrations in Cities with Statistically Significant PM10-2.5 Effect 

18 Estimates......................................................................................3-18 

19 Table 4-1 Logit model estimated VAQ values corresponding to various percent acceptability 

20 values for the four cities. .........................................................................................4-20 

21 Table 4-2 Percentage of daily maximum hourly values of daylight PM light extinction 

22 exceeding CPLs (excluding hours with relative humidity greater than 90 percent). 

23 (adapted from Table 3-7 in UFVA)......................................................................... 4-25 

24 Table 4-3 Percentage of daily maximum hourly values of daylight PM light extinction 

 exceeding CPLs when “just meeting” the current PM2.5 NAAQS (15/35 μg/m3 25 ) 

26 (excluding hours with relative humidity greater than 90 percent). 

27 (Adapted from Table 4-7 in UFVA)........................................................................ 4-28 

28 Table 4.3 1. PM light extinction design values for “just meeting” secondary NAAQS scenarios 

29 based on measured PM light extinction (excluding hours with relative humidity 

30 greater than 90 percent)........................................................................................... 4-38 

31 Table 4.3-2 90th percentile maximum daily 1-hour PM light extinction design values (Mm-1) 

32 after rollback to meet alternative standard of 60 μg/m3, 40 μg/m3, 30 μg/m3,20 

33 μg/m3 and 10 μg/m3 maximum daylight 1-hour PM mass concentration 

34 for the 90th percentile.*...........................................................................................4-41 

35 Table A-1. Percentage of days with daily maximum daylight 1-hour PM2.5 mass concentration 

36 exceeding reference levels in 2005-2007 (excluding hour with relative humidity 

37 greater than 90 percent)............................................................................................ A-3 

38 Table A-2. Alternative NAAQS scenarios based on daily maximum daylight 1-hour PM2.5 

39 mass, averaged over three years (excluding hours with relative humidity greater than 

40 90 percent)................................................................................................................ A-4 

41 Table A-3. 2005-2007 design values for 1-hour PM2.5 mass (μg/m3 ).................................... A-7 

42 Table A-4. Percentage reductions in non-PRB PM2.5 components required to meet NAAQS 

43 scenarios based on 1-hour PM2.5 mass.................................................................... A-7 
1 Table A-5. Post-rollback design values for daily maximum 1-hour PM2.5 mass. Design 

2 values are shown only for combinations of study area and scenario for which the 

3 study area does not meet the scenario under current conditions, such that reductions 

4 were made during the rollback modeling................................................................. A-9 

5 Table A-6. Percentage of days across three years (two in the case of Phoenix and Houston) 

6 with maximum 1-hour daylight PM light extinction above CPLs when “just meeting” 

7 NAAQS scenarios based on 1-hour PM2.5 mass. Blue shading indicates no 

8 reduction required from current conditions............................................................ A-16 

9 Table 5-1. Scope of the current secondary PM NAAQS review and current NOx/SOx secondary 

10 review. ....................................................................................................................... 5-4 

11 

12 LIST OF FIGURES 

13 

Figure 2-1. Summary of Effect Estimates (per 10 μg/m3 14 ) and Air Quality Distributions for 

15 Long-term Exposure Studies ...................................................................................2-23 

16 Figure 2-2. Distribution of study-specific area mean PM2.5 concentrations. ............................ 2-75 

17 Figure 2-3. Percent reduction in long-term exposure-related mortality risk ............................ 2-82 

Figure 2-4 Summary of Effect Estimates (per 10 μg/m3 18 ) – Short-term Exposure Studies........2-91 

Figure 2-5. Distribution of Study-specific 98th 19 Percentile Concentrations................................ 2-95 

20 Figure 2-6. Percent Reduction in Short-term Exposure-related Mortality and 

21 Morbidity Risk ......................................................................................................2-100 

22 Figure 4-1 Summary of results of urban visibility studies in four cities, showing the identified 

23 range of the 50% acceptance criteria ....................................................................4-19 

24 Figure 4 2. Distribution of estimated maximum daily daylight 1-hour PM light extinction across 

25 the 2005-2007 period, by study area (excluding hours with relative humidity greater 

26 than 90 percent). (Adapted from Figure 3-8 in UFVA)* ........................................4-24 

27 Figure 4 3. Distribution of daylight 1-hour PM light extinction when rolled back to just meet 

28 current PM fine NAAQS across the 2005-2007 period, by study area (excluding 

29 hours with relative humidity greater than 90 percent). ...........................................4-27 

30 Figure 4.3-1 Scatter plots of PM light extinction versus PM2.5 mass concentration of two cities 

31 (from UFVA Appendix D, Figure D2)....................................................................4-32 

32 Figure 4.3-2 Daily maximum daylight 1-hour light extinction after rollback to just meet a 

scenario with daily maximum of 112 Mm-1 for the 90th 33 percentile excluding hours 

34 with relative humidity greater than 90 percent........................................................4-37 

35 Figure 4.3-3 Maximum daily daylight 1-hour PM light extinction under "just meet" conditions 

for a NAAQS scenario based on 1-hour PM2.5 mass of 30 μg/m3 36 , 90th percentile, 

37 excluding relative humidity >90%. .........................................................................4-39 

38 Figure A-1. 2005-2007 daily maximum daylight 1-hour PM2.5 mass concentrations (μg/m3) 

39 for the 15 study areas (excluding hours with relative humidity greater than 90 

40 percent)..................................................................................................................... A-2 

41 Figure A-2. Distributions of maximum daily daylight 1-hour PM light extinction under “just 

42 meet” conditions for NAAQS scenarios based on 1-hour PM2.5 mass (excluding 

43 hours >90% RH)..................................................................................................... A-11 
1 LIST OF ACRONYMS/ABBREVIATIONS 

2 

3 ACS American Cancer Society 

4 AHR Airway Hyperesponsiveness 

5 AHSMOG California Seventh Day Adventist Study 

6 ANS Autonomic nervous system 

7 AQCD Air Quality Criteria Document 

8 AQS EPA’s Air Quality System 

9 AR4 Fourth Assessment Report of the Intergovernmental Panel on Climate 

10 Change 

11 BC Black carbon 

12 BenMAP Benefits Mapping Analysis Program 

13 BP Blood pressure 

14 C Carbon 

15 Ca Calcium 

16 CAA Clean Air Act 

17 CAPs Concentrated Ambient Particles

18 CARB California Air Resources Board 

19 CASAC Clean Air Scientific Advisory Committee 

20 CBSA Consolidated Business Statistical Area 

21 CBVD Cerebrovascular disease 

22 CCN Cloud Condensation Nuclei 

23 CCSP US Climate Change Science Program 

24 Cd Cadmium 

25 CHD Coronary Heart disease 

26 CHF Congestive heart failure 

27 CHS Childrens Health Study 

28 CO Carbon Monoxide 

29 COPD Chronic obstructive pulmonary disease 

30 C-R Concentration-response relationship 

31 CRP C-reactive protein 

32 CSN Chemical Speciation Network 

33 CTM Chemical transport models 

34 Cu Copper 
1 CV Cardiovascular 

2 CVD Cardiovascular disease 

3 DE Diesel Exhaust 

4 DEP Diesel Exhaust Particles 

5 dv deciview 

6 DVT Deep Vein Thrombosis 

7 EC Elemental Carbon 

8 ECG Electrocardiogram 

9 ED Emergency department 

10 EPA Environmental Protection Agency 

11 FEM Federal Equivalent Method 

12 FEV1 Change in forced expiratory volume in one second 

13 FRM Federal Reference Method 

14 GAMs Generalized additive models 

15 GEOS Global Scale Air Circulation Model 

16 GHG Greenhouse Gas 

17 GI Group Interviews 

18 GLMs Generalized linear models 

19 GSH Glutathione 

20 GST Glutathione-S-transferase 

21 HA Hospital admissions 

22 HEI Health Effects Institute 

23 Hg Mercury 

24 HR Heart rate 

25 HRV Heart rate variability 

26 ICD International Classification of Disease 

27 ICR Information Collection Request 

28 IFG Investigative Focus Groups 

29 IHD Ischemic heart disease 

30 IMPROVE Interagency Monitoring of Protected Visual Environment 

31 IPCC Intergovernmental Panel on Climate Change 

32 IRP Integrated Review Plan 

33 ISA Integrated Science Assessment 

34 IT Intratracheal 
1 Km Kilometer 

2 Lag Time between one event and another 

3 Lag 0 Same day as the death, test, hospital, ED, clinic, physician visit; 

4 that occurs on the same day as the exposure to the pollutant(s) 

5 Lag 0-x All the deaths test, hospital, ED, clinic, physician visit; that occurs 

6 on the same day as the exposure to the pollutant(s) and the x days 

7 following the day of exposure 

8 MCAPS Medicare Air Pollution Study 

9 MEA Millennium Ecosystem Assessment 

10 MENTOR Modeling ENvironment for TOtal Risk 

11 MI Myocardial infarction 

12 Mm Megameter 

13 MOA Mode(s) or mechanism(s) of action 

14 MSA Metropolitan Statistical Area 

15 N Nitrogen 

16 NAAQS National Ambient Air Quality Standards 

17 NCEA National Center for Environmental Assessment 

18 NCore National Core Monitoring Network 

19 Ni Nickel 

20 NMMAPS National Morbidity, Mortality, and Air Pollution Study 

21 NO Nitric Oxide 

22 NO2 Nitrogen dioxide 

NO3

- 23 Nitrate 

24 NOx Nitrogen oxides 

25 NPS National Park Service 

26 NRC National Research Council 

27 NWS National Weather Service 

28 O3 Ozone 

29 OAQPS Office of Air Quality Planning and Standards 

30 OAR Office of Air and Radiation 

31 OC Organic Carbon 

32 OR Odds Ratio 

33 ORD Office of Research and Development 

34 OS Observational Study 

35 PA Policy Assessment 
1 PA Pulmonary arterial 

2 PAH Polyaromatic Hydrocarbon 

3 Pb Lead 

4 PEF Peak Expiratory Flow L/min 

5 PM Particulate matter 

6 PM10 Particles with an upper 50% cut-point of 10± 0.5 μm aerodynamic 

7 diameter and a penetration curve as specified in the Code of 

8 Federal Regulations. 

9 PM10-2.5 Particles with an upper 50% cut-point of 10 μm aerodynamic 

10 diameter and a lower 50% cut-point of 2.5 μm aerodynamic 

11 diameter. 

12 

13 PM2.5 Particles with an upper 50% cut-point of 2.5 μm aerodynamic 

14 diameter and a penetration curve as specified in the Code of 

15 Federal Regulations. 

16 

17 PMX The legal definition for PMX, as defined in the Code of Federal 

18 Regulations, includes both a 50% cut-point and a penetration 

19 curve. A 50% cut-point of X μm diameter means that 50% of 

20 particles with aerodynamic diameter of X are removed by the inlet 

21 and 50% pass through the inlet and are collected on the filter. 

22 Depending on the specific penetration curve specified, particles 

23 larger than X μm aerodynamic diameter are collected with an 

24 efficiently than decreases rapidly for particles larger than X while 

25 the collection efficiency for particles smaller than X increases 

26 rapidly with decreasing size until 100 % efficiency is reached. 

27 PRB Policy-Relevant Background 

28 PSAS The French National Program on Air Pollution Health Effects 

29 PT Prothrombin Time 

30 PTT Partial Thomboplastin Time 

31 QA Quality assurance 

32 QT Time for depolarization and repolarization of the ventricles 

33 RA Risk Assessment 

34 REA Risk and Exposure Assessment 

35 RF Radiative forcing 

36 RH Relative humidity 

37 RNS Reactive Nitrogen Species 

38 ROS Reactive Oxygen Species 

39 RR Relative risk 
1 SAB Science Advisory Board 

2 SANDWICH Sulfate, Adjusted Nitrate, Derived Water, Inferred Carbonaceous 

3 mass approach 

4 SAP Synthesis and Assessment Product 

5 SBP Systolic Blood Pressure 

6 SD Standard deviation 

7 SEARCH Southeastern Aerosol Research and Characterization Study 

8 SEDD State Emergency Department Databases 

9 SES Socioeconomic Status 

10 Si Silicon 

11 SID State Inpatient Database 

12 SMOKE Sparse Matrix Operator Kernal Emissions 

13 S Sulfur 

14 SO2 Sulfur Dioxide 

SO4

2- 15 Sulfate 

16 SOx Sulfur Oxides 

17 SOPHIA Study of Particulates and Health in Atlanta 

18 STP Standard Temperature and Pressure 

19 TB Tracheobronchial 

20 TSP Total suspended particulate 

21 UFPs Ultrafine particles 

22 UFVA Urban-Focused Visibility Assessment 

23 V Vanadium 

24 VAQ Visual Air Quality 

25 VOC Volatile organic compounds 

26 WACAP Western Airborne Contaminants Assessment Project 

27 WHI Women’s Health Initiative 

28 Zn Zinc 
1 

2 This page intentionally left blank. 
Draft Do Not Quote or Cite 1-1 March 2010

1 1. INTRODUCTION 

2 1.1 PURPOSE 

3 The U.S. Environmental Protection Agency (EPA) is presently conducting a review of 

4 the national ambient air quality standards (NAAQS) for particulate matter (PM). The overall 

5 plan and schedule for this review were presented in the Integrated Review Plan for the National 

6 Ambient Air Quality Standards for Particulate Matter (IRP; US EPA, 2008a). The IRP 

7 identified key policy-relevant issues to be addressed in this review as a series of questions that 

8 frame our consideration of whether the current NAAQS for PM should be retained or revised. 

9 This Policy Assessment (PA), prepared by staff in the EPA’s Office of Air Quality 

10 Planning and Standards (OAQPS), is intended to help “bridge the gap” between the relevant 

11 scientific information and assessments and the judgments required of the EPA Administrator in 

determining whether, and if so, how, it is appropriate to revise the NAAQS for PM.1 12 This first 

13 draft PA presents factors relevant to EPA’s review of the primary (health-based) and secondary 

14 (welfare-based) PM NAAQS. It focuses on both evidence- and risk-based information in 

15 evaluating the adequacy of the current PM NAAQS and in identifying potential alternative 

16 standards for consideration. In this first draft PA, we consider the scientific and technical 

17 information available in this review as assessed in the Integrated Science Assessment for 

18 Particulate Matter (Final Report) (ISA, US EPA, 2009a), the Quantitative Health Risk 

19 Assessment for Particulate Matter – Second External Review Draft (US EPA, 2010a) and the 

20 Particulate Matter Urban-Focused Visibility Assessment – Second External Review Draft (US 

21 EPA, 2010b). In so doing, we focus on information that is most pertinent to evaluating the basic 

elements of NAAQS: indicator2

, averaging time, form,3 22 and level. These elements, which 

23 together serve to define each standard, must be considered collectively in evaluating the health 

24 and welfare protection afforded by the PM standards. 

25 We also recognize that part of the definition of the NAAQS includes specifying 

26 allowable monitoring methods by which the indicator is to be measured as well as minimum 

27 requirements for monitoring, such as monitor siting criteria. Such monitoring issues were 

28 identified in the IRP (US EPA, 2008a, chapter 7) and we plan to include a discussion of them in 

29 the second draft PA. 

 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 defines 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 air quality statistic that is to be compared to the level of the standard in 

determining whether an area attains the standard. 
Draft Do Not Quote or Cite 1-2 March 2010

1 Although this first draft PA should be of use to all parties interested in this PM NAAQS 

2 review, it is written with an expectation that the reader has familiarity with the technical 

3 discussions contained in the ISA (US EPA, 2009a) and in the draft quantitative risk and visibility 

4 assessment documents (US EPA, 2010a,b). 

5 1.2 BACKGROUND 

6 1.2.1 Legislative Requirements 

7 Two sections of the Clean Air Act (Act) govern the establishment and revision of the 

8 NAAQS. Section 108 (42 U.S.C. section 7408) directs the Administrator to identify and list air 

9 pollutants that meet three specified criteria, including air pollutants “emissions of which, in his 

10 judgment, cause or contribute to air pollution which may reasonably be anticipated to endanger 

11 public health and welfare” and whose “presence . . . in the ambient air results from numerous or 

12 diverse mobile or stationary sources” and to issue air quality criteria for those that are listed. Air 

13 quality criteria are to “accurately reflect the latest scientific knowledge useful in indicating the 

14 kind and extent of all identifiable effects on public health or welfare which may be expected 

15 from the presence of [a] pollutant in the ambient air . . .” 42 U.S.C. § 7408(b). 

16 Section 109 (42 U.S.C. section 7409) directs the Administrator to propose and 

17 promulgate “primary” and “secondary” NAAQS for pollutants for which air quality criteria are 

18 issued. Section 109(b)(1) defines a primary standard as one “the attainment and maintenance of 

19 which in the judgment of the Administrator, based on [air quality] criteria and allowing an 

adequate margin of safety, are requisite to protect the public health.”4 20 A secondary standard, as 

21 defined in Section 109(b)(2), must “specify a level of air quality the attainment and maintenance 

22 of which, in the judgment of the Administrator, based on such [air quality] criteria, is requisite to 

23 protect the public welfare from any known or anticipated adverse effects associated with the 

presence of [the] pollutant in the ambient air.”5 24 

25 The requirement that primary standards include an adequate margin of safety was 

26 intended to address uncertainties associated with inconclusive scientific and technical 

27 information available at the time of standard setting. It was also intended to provide a reasonable 

28 degree of protection against hazards that research has not yet identified. Lead Industries 

 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 any [sensitive] group of the population,” and that for this 

purpose “reference should be made to a representative sample of persons comprising the sensitive group rather than 

to a single person in such a group.” S. Rep. No. 91-1196, 91st 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.” 
Draft Do Not Quote or Cite 1-3 March 2010

1 Association v. EPA, 647 F.2d 1130, 1154 (D.C. Cir 1980), cert. denied, 449 U.S. 1042 (1980);

2 American Petroleum Institute v. Costle, 665 F.2d 1176, 1186 (D.C. Cir. 1981), cert. denied, 455 

3 U.S. 1034 (1982); American Farm Bureau Federation v. EPA, 559 F. 3d 512, 533 (D.C. Cir. 

4 2009). Both kinds of uncertainties are components of the risk associated with pollution at levels 

5 below those at which human health effects can be said to occur with reasonable scientific 

6 certainty. Thus, in selecting primary standards that include an adequate margin of safety, the 

7 Administrator is seeking not only to prevent pollution levels that have been demonstrated to be 

8 harmful but also to prevent lower pollutant levels that may pose an unacceptable risk of harm, 

9 even if the risk is not precisely identified as to nature or degree. 

10 In selecting a margin of safety, EPA considers such factors as the nature and severity of 

11 the health effects involved, the size of the susceptible population(s) at risk, and the kind and 

12 degree of the uncertainties that must be addressed. The selection of any particular approach to 

13 providing an adequate margin of safety is a policy choice left specifically to the Administrator’s 

14 judgment. Lead Industries Association v. EPA, supra, 647 F.2d at 1161-62. 

15 In setting standards that are “requisite” to protect public health and welfare, as provided 

16 in section 109(b), EPA’s task is to establish standards that are neither more nor less stringent 

17 than necessary for these purposes. In so doing, EPA may not consider the costs of implementing 

18 the standards. See generally Whitman v. American Trucking Associations, 531 U.S. 457, 471, 

19 475-76 (2001). 

20 Section 109(d) (1) of the Act requires that “not later than December 31, 1980, and at 5-

21 year intervals thereafter, the Administrator shall complete a thorough review of the criteria 

22 published under section 108 and the national ambient air quality standards . . . and shall make 

23 such revisions in such criteria and standards and promulgate such new standards as may be 

24 appropriate in accordance with section [108]... and subsection (b) . . .” 42 U.S.C. § 7409(d)(1). 

25 Section 109(d)(2) requires that an independent scientific review committee “shall complete a 

26 review of the criteria . . . and the national primary and secondary ambient air quality standards . . 

27 . and shall recommend to the Administrator any new . . . standards and revisions of existing 

28 criteria and standards as may be appropriate . . .” 42 U.S.C. § 7409(d)(2). Since the early 

29 1980's, this independent review function has been performed by the Clean Air Scientific 

30 Advisory Committee (CASAC). 

31 1.2.2 Overview of the NAAQS Review Process 

32 Since completion of the last PM NAAQS review, the Agency has made a number of 

33 changes to the process for reviewing the NAAQS. In making these changes, the Agency 

34 consulted with CASAC and the public. This revised process contains four major components: 

35 planning, science assessment, risk/exposure assessment, and policy assessment/rulemaking. 
Draft Do Not Quote or Cite 1-4 March 2010

1 The planning phase begins with a “kick-off” workshop to get input from external and 

2 internal experts and the public regarding policy-relevant issues from the last review and others 

3 that have more recently emerged. The workshop discussions help inform the preparation of an 

4 IRP jointly by OAQPS and Office of Research and Development/National Center for 

5 Environmental Assessment (ORD/NCEA) staff. A draft IRP is presented for consultation with 

6 CASAC and for public comment. A final IRP reflects consideration of CASAC and public 

7 comments together with early guidance from Agency management. The IRP presents the policy8 relevant questions that will frame the review, the review process and schedule, and descriptions 

9 of the purpose, contents, and approach for developing each of the key documents. 

10 The science assessment phase involves the preparation of an ISA by NCEA staff. The 

11 ISA provides a concise evaluation and integration of the policy-relevant science, including key 

12 science judgments that are important to inform the design and scope of the risk and exposure 

13 assessments. The ISA and its supporting annexes provide a comprehensive assessment of the 

14 current scientific literature pertaining to known and anticipated effects on public health and 

15 welfare associated with the presence of the pollutant in the ambient air, emphasizing information 

16 that has become available since the last review. The process generally includes production of a 

17 first and second draft ISA, which undergo CASAC and public review prior to completion of the 

18 final ISA. 

19 In the risk/exposure assessment phase, OAQPS staff draws upon information and 

20 conclusions presented in the ISA to develop quantitative estimates of the risks/exposures for 

21 health and/or welfare effects associated with current ambient levels of PM, with levels that just 

22 meet the current standards, and with levels that just meet potential alternative standards. The 

23 REAs present methods, key results, observations, and related uncertainties. These assessments 

24 begin with preparation of a planning document that discusses the scope and methods planned for 

25 use in conducting the quantitative assessments. Scope and Methods Plans are generally prepared 

26 in conjunction with the first draft ISA and presented for consultation with CASAC and for public 

27 comment. Comments received on the Scope and Methods Plans are considered by EPA staff in 

28 conducting the analyses and preparing draft REAs. The process generally includes production of 

29 first and second draft REAs, which undergo CASAC and public review prior to completion of 

30 final REAs. 

31 The review process ends with a policy assessment/rulemaking phase. Recent revisions to 

32 process have reinstated the preparation of a Policy Assessment (PA). The PA, like the previous 

33 Staff Paper, integrates and interprets the information from the ISA and REAs to provide a 

34 transparent staff analysis of the scientific basis for alternative policy options for consideration by 

35 the Administrator prior to the issuance of proposed and final rules (Jackson, 2009). One or more 

36 drafts of the PA undergo CASAC and public review prior to completion of the final PA. The PA 
Draft Do Not Quote or Cite 1-5 March 2010

1 is intended to facilitate CASAC’s advice and recommendations to the Administrator on any new 

2 standards or revisions to existing standards as may be appropriate, as provided for in the CAA. 

3 Following issuance of the final PA, the Agency publishes a proposed rule, followed by a public 

4 comment period. Taking into account comments received on the proposed rule, the Agency 

5 issues a final rule to complete the rulemaking process. 

6 1.2.3 History of PM NAAQS Reviews 

7 The NAAQS for PM that have been promulgated to date are summarized in Table 1-1 

8 and briefly discussed below. Particulate matter is the generic term for a broad class of 

9 chemically and physically diverse substances that exist as discrete particles (liquid droplets or 

10 solids) over a wide range of sizes, such that the indicator for a PM NAAQS has historically been 

11 defined in terms of particle size ranges. 

12 The EPA first established NAAQS for PM in 1971 (36 FR 8186), based on the original 

13 air quality criteria document (DHEW, 1969). The reference method specified for determining 

14 attainment of the original standards was the high-volume sampler, which collects PM up to a 

15 nominal size of 25 to 45 micrometers (μm) (referred to as total suspended particles or TSP). The 

primary standards (measured by the indicator TSP) were 260 μg/m3 16 , 24-hour average, not to be 

exceeded more than once per year, and 75 μg/m3 17 , annual geometric mean. The secondary 

standard was 150 μg/m3 18 , 24-hour average, not to be exceeded more than once per year. 

19 In October 1979, EPA announced the first periodic review of the criteria and NAAQS for PM, 

20 and significant revisions to the original standards were promulgated in 1987 (52 FR 24634, July 

21 1, 1987). In that decision, EPA changed the indicator for PM from TSP to PM10, the latter 

including particles with a median aerodynamic diameter6 22 less than or equal to 10 μm, which 

23 delineates thoracic particles (i.e., that subset of inhalable particles small enough to penetrate 

24 beyond the larynx to the thoracic region of the respiratory tract). The EPA also revised the 

25 primary standards by: (1) replacing the 24-hour TSP standard with a 24-hour PM10 standard of 

150 μg/m3 26 with no more than one expected exceedance per year; and (2) replacing the annual 

TSP standard with a PM10 standard of 50 μg/m3 27 , annual arithmetic mean. The secondary 

28 standard was revised by replacing it with 24-hour and annual standards identical in all respects to 

29 the primary standards. The revisions also included a new reference method for the measurement 

30 of PM10 in the ambient air and rules for determining attainment of the new standards. On 

 6

 The more precise term is 50 percent cutpoint or 50 percent diameter (D50). 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 decreasing efficiency and smaller particles are collected with increasing (up to 

100 percent) efficiency. 
Draft Do Not Quote or Cite 1-6 March 2010

1 Table 1-1. Summary of National Ambient Air Quality Standards Promulgated for 

Particulate Matter 1971-20067 2 

3 

Final Rule Indicator Ave. Time Level Form

24-hour

260 μg/m3

(primary) 

150 μg/m3

(secondary) 

Not to be exceeded more than once 

per year 

1971 

(36 FR 8186 

April 30, 1971)

TSP

Annual 75 μg/m3

(primary) 

Annual average 

24-hour 150 μg/m3 Not to be exceeded more than once 

per year on average over a 3-year 

period 

1987 

(52 FR 24634; 

July 1, 1987)

PM10

Annual 50 μg/m3 Annual arithmetic mean, averaged 

over 3 years 

24-hour 65 μg/m3 98th percentile, averaged over 3 years

PM2.5 Annual 15 μg/m3 Annual arithmetic mean, averaged 

over 3 years8

24-hour 150 μg/m3

Initially promulgated 99th 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) PM10

Annual 50 μg/m3 Annual arithmetic mean, averaged 

over 3 years 

24-hour 35 μg/m3 98th percentile, averaged over 3 years

PM2.5 Annual 15 μg/m3 Annual arithmetic mean, averaged 

over 3 years9

2006 

(71 FR 61144 

October 17, 2006)

PM10 24-hour 150 μg/m3

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 measurements 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 tightened by further limiting the conditions under which some 

areas may average measurements from multiple community-oriented monitors to determine compliance (see 71 FR 

61165-61167). 
Draft Do Not Quote or Cite 1-7 March 2010

1 In April 1994, EPA announced its plans for the second periodic review of the criteria and 

2 NAAQS for PM, and promulgated significant revisions to the NAAQS in 1997 (62 FR 38652, 

3 judicial review, the revised standards were upheld in all respects. Natural Resources Defense 

4 Council v. EPA, 902 F. 2d 962 (D.C. Cir. 1990), cert. denied, 498 U.S. 1082 (1991). July 18, 

5 1997). Most significantly, EPA determined that although the PM NAAQS should continue to 

6 focus on particles less than or equal to 10 μm in diameter, the fine and coarse fractions of PM10

7 should be considered separately. New standards were added, using PM2.5, referring to particles 

8 with a nominal median aerodynamic diameter less than or equal to 2.5 μm, as the indicator for 

9 fine particles. The PM10 standards were retained for the purpose of regulating the coarse fraction 

10 of PM10 (referred to as thoracic coarse particles or coarse-fraction particles; generally including 

11 particles with a nominal median aerodynamic diameter greater than 2.5 μm and less than or 

12 equal to 10 μm, or PM10-2.5). The EPA established two new PM2.5 standards: an annual standard 

of 15 μg/m3 13 , based on the 3-year average of annual arithmetic mean PM2.5 concentrations from 

14 single or multiple monitors sited to represent community-wide air quality; and a 24-hour 

standard of 65 μg/m3 15 , based on the 3-year average of the 98th percentile of 24-hour PM2.5

16 concentrations at each population-oriented monitor within an area. Also, EPA established a new 

17 reference method for the measurement of PM2.5 in the ambient air and rules for determining 

18 attainment of the new standards. To continue to address thoracic coarse particles, the annual 

19 PM10 standard was retained, while the form, but not the level, of the 24-hour PM10 standard was 

revised to be based on the 99th 20 percentile of 24-hour PM10 concentrations at each monitor in an 

21 area. The EPA revised the secondary standards by making them identical in all respects to the 

22 primary standards. 

23 Following promulgation of the revised PM NAAQS in 1997, petitions for review were 

24 filed by a large number of parties, addressing a broad range of issues. In May 1998, a three25 judge panel of the U.S. Court of Appeals for the District of Columbia Circuit issued an initial 

26 decision that upheld EPA’s decision to establish fine particle standards, holding that "the 

27 growing empirical evidence demonstrating a relationship between fine particle pollution and 

28 adverse health effects amply justifies establishment of new fine particle standards." American 

29 Trucking Associations v. EPA , 175 F. 3d 1027, 1055-56 (D.C. Cir. 1999) (rehearing granted in 

30 part and denied in part, 195 F. 3d 4 (D.C. Cir. 1999), affirmed in part and reversed in part, 

31 Whitman v. American Trucking Associations, 531 U.S. 457 (2001). The panel also found "ample 

32 support" for EPA's decision to regulate coarse particle pollution, but vacated the 1997 PM10

33 standards, concluding in part that PM10 is a "poorly matched indicator for coarse particulate 

34 pollution" because it includes fine particles. Id. at 1053-55. Pursuant to the court’s decision, 

35 EPA removed the vacated 1997 PM10 standards from the Code of Federal Regulations (CFR) (69 

36 FR 45592, July 30, 2004) and deleted the regulatory provision [at 40 CFR section 50.6(d)] that 
Draft Do Not Quote or Cite 1-8 March 2010

1 controlled the transition from the pre-existing 1987 PM10 standards to the 1997 PM10 standards. 

2 The pre-existing 1987 PM10 standards remained in place (65 FR 80776, December 22, 2000). 

3 The Court also upheld EPA’s determination not to establish more stringent secondary standards 

4 for fine particles to address effects on visibility (175 F. 3d at 1027). 

5 More generally, the panel held (over a strong dissent) that EPA’s approach to 

6 establishing the level of the standards in 1997, both for the PM and for the ozone (O3) NAAQS 

7 promulgated on the same day, effected “an unconstitutional delegation of legislative authority.” 

8 Id. at 1034-40. Although the panel stated that “the factors EPA uses in determining the degree of 

9 public health concern associated with different levels of ozone and PM are reasonable,” it 

10 remanded the rule to EPA, stating that when EPA considers these factors for potential non11 threshold pollutants “what EPA lacks is any determinate criterion for drawing lines” to 

12 determine where the standards should be set. Consistent with EPA’s long-standing interpretation 

13 and D.C. Circuit precedent, the panel also reaffirmed its prior holdings that in setting NAAQS 

14 EPA is “not permitted to consider the cost of implementing those standards” Id. at 1040-41. 

15 On EPA’s petition for rehearing, the panel adhered to its position on these points. 

16 American Trucking Associations v. EPA, 195 F. 3d 4 (D.C. Cir. 1999). The full Court of 

17 Appeals denied EPA’s request for rehearing en banc, with five judges dissenting. Id. at 13. Both 

18 sides filed cross appeals on these issues to the United States Supreme Court, which granted 

19 certiorari. In February 2001, the Supreme Court issued a unanimous decision upholding EPA’s 

20 position on both the constitutional and cost issues. Whitman v. American Trucking Associations, 

21 531 U.S. 457, 464, 475-76. On the constitutional issue, the Court held that the statutory 

22 requirement that NAAQS be “requisite” to protect public health with an adequate margin of 

23 safety sufficiently cabined EPA’s discretion, affirming EPA’s approach of setting standards that 

24 are neither more nor less stringent than necessary. The Supreme Court remanded the case to the 

25 Court of Appeals for resolution of any remaining issues that had not been addressed in that 

26 court’s earlier rulings. Id. at 475-76. In March 2002, the Court of Appeals rejected all 

27 remaining challenges to the standards, holding under the traditional standard of review that 

28 EPA’s PM2.5 standards were reasonably supported by the administrative record and were not 

29 “arbitrary and capricious.” American Trucking Associations v. EPA, 283 F. 3d 355, 369-72 (D.C. 

30 Cir. 2002). 

31 In October 1997, EPA published its plans for the next periodic review of the air quality 

32 criteria and NAAQS for PM (62 FR 55201, October 23, 1997), including the 1997 PM2.5 

33 standards and the 1987 PM10 standards. After CASAC and public review of several drafts, 

34 NCEA finalized the Air Quality Criteria Document for Particulate Matter (henceforth, AQCD or 

35 the "Criteria Document") in October 2004 (U.S. EPA, 2004) and OAQPS finalized an 

36 assessment document, Particulate Matter Health Risk Assessment for Selected Urban Areas 
Draft Do Not Quote or Cite 1-9 March 2010

1 (Abt, 2005), and a “Staff Paper,” Review of the National Ambient Air Quality Standards for 

2 Particulate Matter: Policy Assessment of Scientific and Technical Information, in December 

3 2005 (U.S. EPA, 2005). In conjunction with their review of the Staff Paper, CASAC provided 

4 advice to the Adminstrator on revisions to the PM NAAQS (Henderson, 2005a). In particular, 

5 most CASAC PM Panel members favored revising the level of the 24-hour PM2.5 primary 

standard in the range of 35 to 30 μg/m3 with a 98th 6 percentile form, in concert with revising the 

level of the annual PM2.5 standard in the range of 14 to 13 μg/m3 7 (Henderson, 2005a, p.7). For 

8 thoracic coarse particles, the Panel had reservations in recommending a 24-hour PM10-2.5 primary 

9 standard, and agreed that there was a need for more research on the health effects of thoracic 

10 coarse particles (Henderson, 2005b). With regard to secondary standards, most Panel members 

11 strongly supported establishing a new, distinct secondary PM2.5 standard to protect urban 

12 visibility (Henderson, 2005a, p. 9). 

13 On January 17, 2006, EPA proposed to revise the primary and secondary NAAQS for PM 

14 (71 FR 2620) and solicited comment on a broad range of options. Proposed revisions included: 

revising the level of the 24-hour PM2.5 primary standard to 35 μg/m3 15 ; revising the form, but not 

16 the level, of the annual PM2.5 primary standard by tightening the constraints on the use of spatial 

17 averaging; replacing the 24-hour PM10 primary standard with a 24-hour standard defined in 

terms of a new indicator, PM10-2.5

10 set at a level of 70 μg/m3 18 ; revoking the annual PM10 primary 

19 standard; and revising the secondary standards by making them identical in all respects to the 

proposed suite of primary standards for fine and coarse particles.11 20 Subsequent to the proposal, 

21 CASAC provided additional advice to EPA in a letter to the Administrator requesting 

22 reconsideration of CASAC’s recommendations for both the primary and secondary PM2.5

23 standards as well as the standards for thoracic coarse particles (Henderson, 2006a). 

24 On October 17, 2006, EPA promulgated revisions to the PM NAAQS to provide 

25 increased protection of public health and welfare (71 FR 61144). With regard to the primary and 

26 secondary standards for fine particles, EPA revised the level of the 24-hour PM2.5 standard to 35 

μg/m3

, retained the level of the annual PM2.5 standard at 15 μg/m3 27 , and revised the form of the 

28 annual PM2.5 standard by adding further constraints on the optional use of spatial averaging. The 

29 EPA revised the secondary standards for fine particles by making them identical in all respects to 

30 the primary standards. With regard to the primary and secondary standards for thoracic coarse 

 10 This proposed indicator was qualified so as to include any ambient mix of PM10-2.5 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 PM2.5 standard to address visibility 

impairment, within the range of 20 to 30 μg/m3

 and with a form within the range of the 92nd to 98th percentile (71 FR 

2685). 
Draft Do Not Quote or Cite 1-10 March 2010

1 particles, EPA retained the level and form of the 24-hour PM10 standard (such that the standard 

remained at a level of 150 μg/m3 2 with a one expected exceedance form), and revoked the annual 

3 PM10 standard. The EPA also established a new Federal Reference Method (FRM) for the 

4 measurement of PM10-2.5 in the ambient air (71 FR 61212-13). Although the standards for 

5 thoracic coarse particles were not defined in terms of a PM10-2.5 indicator, the new FRM for 

6 PM10-2.5 was established to provide a basis for approving Federal Equivalent Methods (FEMs) 

7 and to promote gathering scientific data to support future reviews of the PM NAAQS. 

8 Following issuance of the final rule, CASAC articulated its concern that “EPA’s final 

9 rule on the NAAQS for PM does not reflect several important aspects of the CASAC’s advice” 

10 (Henderson et al, 2006b). With regard to the PM2.5 annual primary standard, CASAC expressed 

serious concerns regarding the decision to retain the level of the standard at 15 μg/m3 11 . With 

12 regard to EPA’s final decision to retain the 24-hour PM10 standard for thoracic coarse particles, 

13 CASAC acknowledged concerns associated with retaining this standard while recognizing the 

14 need to have a standard in place to protect against effects associated with short-term exposures to 

15 thoracic coarse particles. With regard to EPA’s final decision to revise the secondary PM2.5

16 standards to be identical in all respects to the revised primary PM2.5 standards, CASAC 

17 expressed concernsthat CASAC’s advice to establish a distinct secondary standard for fine 

18 particles to address visibility impairment was not followed. 

19 1.2.4 Litigation Related to the 2006 PM Standards 

20 Several parties filed petitions for review following promulgation of the revised PM 

21 NAAQS in 2006. These petitions addressed the following issues: (1) selecting the level of the 

22 primary annual PM2.5 standard; (2) retaining PM10 as the indicator of a standard for thoracic 

23 coarse particles, retaining the level and form of the 24-hour PM10 standard, and revoking the 

24 PM10 annual standard; and (3) setting the secondary PM2.5 standards identical to the primary 

25 standards. On February 24, 2009, the U.S. Court of Appeals for the District of Columbia Circuit 

26 issued its opinion in the case American Farm Bureau Federation v. EPA, 559 F. 3d 512 (D.C. 

27 Cir. 2009). The court remanded the primary annual PM2.5 NAAQS to EPA because EPA failed 

28 to adequately explain why the standard provided the requisite protection from both short- and 

29 long-term exposures to fine particles, including protection for at-risk populations. American 

30 Farm Bureau Federation v. EPA, 559 F. 3d 512, (D.C. Cir. 2009). With regard to the standards 

31 for PM10, the court upheld EPA’s decisions to retain the 24-hour PM10 standard to provide 

32 protection from thoracic coarse particle exposures and to revoke the annual PM10. standard. 

33 American Farm Bureau Federation at 533-38. With regard to the secondary PM2.5 standards, the 

34 court remanded the standards to EPA because the Agency failed to adequately explain why 
Draft Do Not Quote or Cite 1-11 March 2010

1 setting the secondary PM standards identical to the primary standards provided the required 

2 protection for public welfare, including protection from visibility impairment. 

3 The decisions of the court with regard to these three issues are discussed in chapters 2, 3 

4 and 4, respectively. The EPA is responding to the court’s remands as part of the current review 

5 of the PM NAAQS. 

6 1.2.5 Current PM NAAQS Review 

7 The EPA initiated the current review of the air quality criteria for PM in June 2007 with a 

8 general call for information (72 FR 35462, June 28, 2007). In July 2007, EPA held two “kick9 off” workshops on the primary and secondary PM NAAQS, respectively (72 FR 34003 and 

34005, June 20, 2007).12 10 These workshops provided an opportunity for the participants to 

11 discuss the key policy-relevant issues around which EPA would structure this PM NAAQS 

12 review and the most meaningful new science that would be available to inform our 

13 understanding of these issues. 

14 Based in part on the workshop discussions, EPA developed a draft IRP outlining the 

15 schedule, process, and key policy-relevant questions that would guide the evaluation of the air 

16 quality criteria for PM and the review of the primary and secondary PM NAAQS. On November 

30, 2007, EPA held a consultation with CASAC13 17 on the draft IRP (72 FR 63177, November 8, 

18 2007), which included the opportunity for public comment. The final IRP (US EPA, 2008a) 

19 incorporated comments from CASAC and the public on the draft plan as well as input from 

20 senior Agency managers. 

21 As part of the process of preparing the PM ISA, NCEA hosted a peer review workshop in 

22 June 2008 on preliminary drafts of key ISA chapters (73 FR 30391, May 27, 2008). The first 

23 external review draft ISA (US EPA, 2008b) was reviewed by CASAC and the public at a 

24 meeting held in April 2009 (74 FR 2688, February 19, 2009). Based on CASAC and public 

25 comments, NCEA prepared a second draft ISA (US EPA, 2009b), which was reviewed by 

26 CASAC and the public at a meeting held on October 5-6, 2009 (74 FR 46586, September 10, 

27 2009). Based on CASAC and public comments, NCEA prepared the final ISA (US EPA, 

28 2009a; 74 FR 66353, December 15, 2009). 

29 In preparing the REA documents that build on the scientific evidence presented in the 

30 ISA, OAQPS released two planning documents: Particulate Matter National Ambient Air 

 12 See workshop materials http://www.regulations.gov/search/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. For more information on the CASAC PM Panel, see 

http://yosemite.epa.gov/sab/sabpeople.nsf/WebCommitteesSubcommittees/CASAC%20Particulate%20Matter%20R

eview%20Panel. 
Draft Do Not Quote or Cite 1-12 March 2010

1 Quality Standards: Scope and Methods Plan for Health Risk and Exposure Assessment and 

2 Particulate Matter National Ambient Air Quality Standards: Scope and Methods Plan for Urban 

3 Visibility Impact Assessment (henceforth, Scope and Methods Plans, US EPA, 2009c,d). These 

4 planning documents outlined the scope and approaches that staff planned to use in conducting 

5 quantitative assessments as well as key issues that would be addressed as part of the assessments. 

6 In designing and conducting the initial health risk and visibility impact assessments, we 

7 considered CASAC comments (Samet 2009a,b) on the Scope and Methods Plans made during an 

8 April 2009 consultation (74 FR 11580, March 18, 2009) as well as public comments.. Two draft 

9 assessment documents, Risk Assessment to Support the Review of the PM2.5 Primary National 

10 Ambient Air Quality Standards: External Review Draft - September 2009 (US EPA 2009e) and 

11 Particulate Matter Urban-Focused Visibility Assessment - External Review Draft - September 

12 2009 (US EPA, 2009f) were reviewed by CASAC and the public at a meeting held on October 5-

13 6, 2009. Based on CASAC (Samet 2009c,d) and public comments, OAQPS staff revised these 

14 draft documents and released second draft assessment documents (US EPA, 2010a,b) in January 

15 and February 2010 (75 FR 4067, January 26, 2010) for CASAC and public review at an 

16 upcoming meeting to be held on March 10-11, 2010. 

17 A preliminary draft PA (US EPA, 2009g) was released in September 2009 for 

18 informational purposes and to facilitate discussion with CASAC at the October 5-6, 2009 

19 meeting on the overall structure, areas of focus, and level of detail to be included in the PA. This 

20 first draft PA reflects consideration of CASAC’s comments on the preliminary draft that 

21 encouraged the development of a document focused on the key policy-relevant issues that draws 

22 from and is not repetitive of information in the ISA and REAs. This first draft PA draws from 

23 the information presented in the final ISA and the two second draft assessment documents. We 

24 plan to present an overview of this document at the upcoming CASAC meeting on March 10-11, 

25 2010, and CASAC and public review of this document will occur during an upcoming 

26 teleconference to be held on April 8-9, 2010 (75 FR 8062, February 23, 2010). We will consider 

27 CASAC and public comments on this first draft PA and on the two draft REAs in preparing a 

28 second draft PA, which will be released for CASAC and public review.

29 1.3 GENERAL APPROACH AND ORGANIZATION OF THIS DOCUMENT 

30 This first draft PA includes staff’s preliminary evaluation of the policy implications of 

31 the scientific assessment of the evidence presented in the ISA and the results of quantitative 

32 assessments based on that evidence presented in the second draft REAs. Taken together, this 

33 information informs preliminary staff conclusions and the identification of policy options for 

34 consideration in addressing public health and welfare effects associated with exposure to ambient 

35 PM. 
Draft Do Not Quote or Cite 1-13 March 2010

1 Since the last review, much new information is now available on PM air quality and 

2 human health effects directly in terms of PM2.5 and, to a much more limited degree, PM10-2.5 and 

3 ultrafine particles (UFPs). Since the purpose of this review is to evaluate the adequacy of the 

4 current standards, which separately address fine and thoracic coarse particles, staff is focusing 

5 this policy assessment and associated quantitative analyses primarily on the evidence related 

6 directly to PM2.5 and PM10-2.5. In so doing, we are considering PM10-related evidence primarily 

7 to help inform our understanding of key issues and to help interpret and provide context for 

8 understanding the public health and welfare impacts of ambient fine and coarse particles. We are 

9 also considering the currently available evidence related to UFPs as well as PM2.5 components to 

10 aid in considering whether or not there is support to consider standards with a different size 

11 fraction and/or distinct standards focused on regulating specific PM2.5 components or categories 

12 of fine particle sources. 

13 Following this introductory chapter, this document is organized into two main parts: 

14 review of the primary PM NAAQS (chapters 2 and 3) and review of the secondary PM NAAQS 

15 (chapters 4 and 5). Chapters 2 and 3 present staff observations and preliminary conclusions 

16 related to review of the primary standards for fine and thoracic coarse particles, respectively. 

17 Each chapter begins with a discussion of policy assessment approaches and focuses on both 

18 evidence-based and quantitative risk-based considerations. Preliminary staff conclusions are 

19 presented with regard to the adequacy of the current primary standards and potential alternative 

20 primary standards for consideration, in terms of indicators, averaging times, forms, and levels. 

21 Chapter 4 focuses on PM-related visibility impairment, and presents staff observations and 

22 preliminary conclusions with regard to the adequacy of the current standards and potential 

23 distinct secondary standards for consideration, in terms of alternative indicators, averaging times, 

24 forms, and levels. Chapter 5 focuses on other PM-related welfare effects, including effects on 

25 climate, ecological effects, and effects on materials, and presents staff observations and 

26 preliminary conclusions with regard to the adequacy of the current standards and the extent to 

27 which information is available to support consideration of alternative standards. 
Draft Do Not Quote or Cite 1-14 March 2010

1 1.4 REFERENCES 

2 Abt Associates (2005). Particulate Matter Health Risk Assessment for Selected Urban Areas. Final Report. 

3 Bethesda, MD. Prepared for the Office of Air Quality Planning and Standards, U.S. Environmental 

4 Protection Agency, Contract No. 68-D-03-002. EPA 452/R-05-007A. Available: 0 

5 Henderson, R. (2005a). EPA’s Review of the National Ambient Air Quality Standards for Particulate Matter 

6 (Second Draft PM Staff Paper, January 2005): A review by the Particulate Matter Review Panel of the EPA 

7 Clean Air Scientific Advisory Committee. June 6, 2005. Available: http://www.epa.gov/sab/pdf/casac-05-

8 007.pdf. 

9 Henderson, R. (2005b). Clean Air Scientific Advisory Committee (CASAC) Review of the EPA Staff 

10 Recommendations Concerning a Potential Thoracic Coarse PM Standard in the Review of the National 

11 Ambient Air Quality Standards for Particulate Matter: Policy Assessment of Scientific and Technical 

12 Information (Final PM OAQPS Staff Paper, EPA-452/R-05-005). September 15, 2005. Available: 

13 http://www.epa.gov/sab/panels/casacpmpanel.html. 

14 Henderson, R. (2006a). Letter from Dr. Rogene Henderson, Chair, Clean Air Scientific Advisory Committee to the 

15 Honorable Stephen L. Johnson, Administrator, US EPA. Clean Air Scientific Advisory Committee 

16 Recommendations Concerning the Proposed National Ambient Air Quality Standards for Particulate 

17 Matter. March 21, 2006. Available: http://www.epa.gov/sab/pdf/casac-ltr-06-002.pdf 

18 Henderson, R.; Cowling, E.; Crapo, J.D..; Miller, F. J.; Poirot, R.L.; Speizer, F.; Zielinska, B. (2006b). Letter from 

19 Clean Air Scientific Advisory Committee to the Honorable Stephen L. Johnson, Administrator, US EPA. 

20 Clean Air Scientific Advisory Committee Recommendations Concerning the Final National Ambient Air 

21 Quality Standards for Particulate Matter. September 29, 2006. Available: 

22 http://www.epa.gov/sab/pdf/casac-ltr-06-002.pdf 

23 Jackson (2009). Memo from Administrator Lisa P. Jackson to Elizabeth Craig, Acting Assistant Administrator for 

24 OAR and Lek Kadeli, Acting Assistant Administrator for ORD. Process for Reviewing the National 

25 Ambient Air Quality Standards. May 21, 2009. Available: 

26 http://www.epa.gov/ttn/naaqs/pdfs/NAAQSReviewProcessMemo52109.pdf. 

27 Samet, J. (2009a). Letter from Clean Air Scientific Advisory Committee to the Honorable Lisa P. Jackson, 

28 Administrator, US EPA. Consultation on EPA’s Particulate Matter National Ambient Air Quality 

29 Standards: Scope and Methods Plan for Health Risk and Exposure Assessment. May 21, 2009. Available: 

30 http://yosemite.epa.gov/sab/sabproduct.nsf/723FE644C5D758DF852575BD00763A32/$File/EPA31 CASAC-09-009-unsigned.pdf

32 Samet, J. (2009b). Letter from Clean Air Scientific Advisory Committee to the Honorable Lisa P. Jackson, 

33 Administrator, US EPA. Consultation on EPA’s Particulate Matter National Ambient Air Quality 

34 Standards: Scope and Methods Plan for Urban Visibility Impact Assessment. May 21, 2009. Available: 

35 http://yosemite.epa.gov/sab/sabproduct.nsf/0F63D7995F5850D5852575BD0077869C/$File/EPA-CASAC36 09-010-unsigned.pdf 

37 Samet, J. (2009c). Letter from Clean Air Scientific Advisory Committee to the Honorable Lisa P. Jackson, 

38 Administrator, US EPA. Review of the Risk Assessment to Support the Review of the Particulate Matter 

39 (PM) Primary National Ambient Air Quality Standards – External Review Draft (September 2009). 

40 November 24, 2009. Available: 

41 http://yosemite.epa.gov/sab/sabproduct.nsf/BC1ECC5D539EF72385257678006D5754/$File/EPA42 CASAC-10-003-unsigned.pdf

43 Samet, J. (2009d). Letter from Clean Air Scientific Advisory Committee to the Honorable Lisa P. Jackson, 

44 Administrator, US EPA. Review of Particulate Matter Urban-Focused Visibility Assessment (External 
Draft Do Not Quote or Cite 1-15 March 2010

1 Review Draft, September 2009). November 24, 2009. Available: 

2 http://yosemite.epa.gov/sab/sabproduct.nsf/15872217938041F685257678006A26E3/$File/EPA-CASAC3 10-002-unsigned.pdf 

4 US Department of Health, Education and Welfare (DHEW). (1969). Air Quality Criteria for Particulate Matter. 

5 U.S. Government Printing Office, Washington DC, AP-49. 

6 US EPA (2004). Air Quality Criteria for Particulate Matter. National Center for Environmental Assessment, Office 

7 of Research and Development, U.S. Environmental Protection Agency, Research Triangle Park, NC 27711; 

8 report no. EPA/600/P-99/002aF and EPA/600/P-99/002bF. October 2004. Available: 

9 http://www.epa.gov/ttn/naaqs/standards/pm/s_pm_cr_cd.html

10 US EPA (2005). Review of the National Ambient Air Quality Standards for Particulate Matter: Policy Assessment 

11 of Scientific and Technical Information, OAQPS Staff Paper. Research Triangle Park, NC 27711: Office 

12 of Air Quality Planning and Standards; report no. EPA EPA-452/R-05-005a. December 2005. Available: 

13 http://www.epa.gov/ttn/naaqs/standards/pm/s_pm_cr_sp.html

14 US EPA (2008a). Integrated Review Plan for the National Ambient Air Quality Standards for Particulate Matter. 

15 National Center for Environmental Assessment and Office of Air Quality Planning and Standards, U.S. 

16 Environmental Protection Agency, Research Triangle Park, NC. Report No. EPA 452/R-08-004. March 

17 2008. Available at: http://www.epa.gov/ttn/naaqs/standards/pm/s_pm_2007_pd.html. 

18 US EPA (2008b). Integrated Science Assessment for Particulate Matter: First External Review Draft. National 

19 Center for Environmental Assessment-RTP Division, Office of Air Quality Planning and Standards, 

20 Research Triangle Park, NC. EPA/600/R-08/139 and 139A. December 2008. Available: 

21 http://www.epa.gov/ttn/naaqs/standards/pm/s_pm_2007_isa.html. 

22 US EPA (2009a). Integrated Science Assessment for Particulate Matter: Final Report. National Center for 

23 Environmental Assessment-RTP Division, Office of Air Quality Planning and Standards, Research 

24 Triangle Park, NC. EPA/600/R-08/139F. December 2009. Available: 

25 http://www.epa.gov/ttn/naaqs/standards/pm/s_pm_2007_isa.html. 

26 US EPA (2009b). Integrated Science Assessment for Particulate Matter: Second External Review Draft. National 

27 Center for Environmental Assessment-RTP Division, Office of Air Quality Planning and Standards, 

28 Research Triangle Park, NC. EPA/600/R-08/139B. July 2009. Available: 

29 http://www.epa.gov/ttn/naaqs/standards/pm/s_pm_2007_isa.html. 

30 US EPA (2009c). Particulate Matter National Ambient Air Quality Standards: Scope and Methods Plan for Health 

31 Risk and Exposure Assessment. Office of Air Quality Planning and Standards, U.S. Environmental 

32 Protection Agency, Research Triangle Park, NC. EPA-452/P-09-002. February 2009. Available: 

33 http://www.epa.gov/ttn/naaqs/standards/pm/s_pm_2007_pd.html. 

34 US EPA (2009d). Particulate Matter National Ambient Air Quality Standards: Scope and Methods Plan for Urban 

35 Visibility Impact Assessment. Office of Air Quality Planning and Standards, U.S. Environmental 

36 Protection Agency, Research Triangle Park, NC. EPA-452/P-09-001. February 2009. Available: 

37 http://www.epa.gov/ttn/naaqs/standards/pm/s_pm_2007_pd.html. 

38 US EPA (2009e). Risk Assessment to Support the Review of the PM Primary National Ambient Air Quality 

39 Standards - External Review Draft. Office of Air Quality Planning and Standards, U.S. Environmental 

40 Protection Agency, Research Triangle Park, NC. EPA-452/P-09-006. September 2009. Available: 

41 http://www.epa.gov/ttn/naaqs/standards/pm/s_pm_2007_risk.html. 

42 US EPA (2009f). Particulate Matter Urban-Focused Visibility Assessment – External Review Draft. Office of Air 

43 Quality Planning and Standards, U.S. Environmental Protection Agency, Research Triangle Park, NC. 
Draft Do Not Quote or Cite 1-16 March 2010

1 EPA-452/P-09-005. September 2009. Available: 

2 http://www.epa.gov/ttn/naaqs/standards/pm/s_pm_2007_risk.html. 

3 US EPA (2009g). Policy Assessment for the Review of the Particulate Matter National Ambient Air Quality 

4 Standards – Preliminary Draft. Office of Air Quality Planning and Standards, U.S. Environmental 

5 Protection Agency, Research Triangle Park, NC. EPA-452/P-09-007. September 2009. Available: 

6 http://www.epa.gov/ttn/naaqs/standards/pm/s_pm_2007_pa.html. 

7 US EPA (2010a). Quantitative Risk Assessment for Particulate Matter – Second External Review Draft. Office of 

8 Air Quality Planning and Standards, U.S. Environmental Protection Agency, Research Triangle Park, NC. 

9 EPA-452/P-10-001. February 2010. Available: 

10 http://www.epa.gov/ttn/naaqs/standards/pm/s_pm_2007_risk.html. 

11 US EPA (2010b). Particulate Matter Urban-Focused Visibility Assessment – Second External Review Draft. Office 

12 of Air Quality Planning and Standards, U.S. Environmental Protection Agency, Research Triangle Park, 

13 NC. EPA-452/P-10-002. January 2010. Available: 

14 http://www.epa.gov/ttn/naaqs/standards/pm/s_pm_2007_risk.html. 
Draft Do Not Quote or Cite March 2010 2-1

1 2 REVIEW OF THE PRIMARY STANDARDS FOR FINE PARTICLES 

2 This chapter presents preliminary staff conclusions with regard to the adequacy of the 

3 current suite of primary PM2.5 standards and the alternative primary standards for fine particles 

4 that are appropriate for consideration in this review. Our assessment of these issues is framed by 

5 a series of key policy-relevant questions, which expand upon those presented in the Integrated 

6 Review Plan (IRP) (US EPA, 2008a) at the outset of this review. The answers to these questions 

7 will inform decisions on whether, and if so how, to revise the current suite of primary fine 

8 particle standards. 

9 Staff notes that final decisions regarding the primary standards must draw upon scientific 

10 information and analyses about health effects and risks, as well as judgments about how to deal 

11 with the range of uncertainties that are inherent in the scientific evidence and analyses. 

12 Ultimately, the final decisions are largely public health policy judgments. Our approach to 

13 informing these judgments, discussed more fully below, recognizes that the available health 

14 effects evidence generally reflects a continuum consisting of ambient levels at which scientists 

15 generally agree that health effects are likely to occur through lower levels at which the likelihood 

16 and magnitude of the response become increasingly uncertain 

17 Our current approach for reviewing the primary standards for fine particles is presented 

18 in section 2.1. Our preliminary conclusions regarding the adequacy of the current suite of 

19 primary PM2.5 standards are presented in section 2.2, focusing on both evidence-based and 

20 quantitative risk-based considerations. Section 2.3 presents our initial conclusions with respect 

21 to alternative fine particle standards, focusing on each of the basic elements of the standards: 

22 pollutant indicator (section 2.3.1), averaging time (section 2.3.2), form (section 2.3.3), and level. 

23 We have evaluated separately the protection that a suite of PM2.5 standards with alternative levels 

24 would likely provide against effects associated with long-term exposures (section 2.3.4) and 

25 short-term exposures (section 2.3.5). These separate evaluations provide the basis for 

26 preliminary integrated conclusions on alternative suites of standards that would appropriately 

27 protect against effects associated with both long- and short-term exposures to fine particles 

28 (section 2.3.6) Section 2.4 summarizes all preliminary staff conclusions on the primary fine 

29 particle standards. The next draft of this chapter will conclude with an initial overview of key 

30 uncertainties and suggested future research areas and data collection efforts (section 2.5). 

31 2.1 APPROACH 

32 Staff’s approach for reviewing the current primary PM2.5 standards builds upon and 

33 broadens the approaches used in previous PM NAAQS reviews. Our current approach is based 

34 on the updated scientific and technical information presented in the Integrated Science 
Draft Do Not Quote or Cite March 2010 2-2

1 Assessment (ISA) and second draft quantitative risk assessment (RA). These assessments take 

2 into consideration the currently available scientific information as well as enhanced tools and 

3 methods for informing the current review. 

4 The past and current approaches described below are all based most fundamentally on 

5 using information from epidemiological studies to inform the selection of PM standards that, in 

6 the Administrator’s judgment, protect public health with an adequate margin of safety. Such 

7 information can be in the form of air quality distributions over which health effect associations 

8 have been observed, or in the form of concentration-response functions that support quantitative 

9 risk assessment. However, evidence- and risk-based approaches using information from 

10 epidemiological studies to inform decisions on PM standards are complicated by the recognition 

11 that no population threshold, below which it can be concluded with confidence that PM-related 

12 effects do not occur, can be discerned from the available evidence. As a result, any approach to 

13 reaching decisions on what standards are appropriate necessarily requires judgments about how 

14 to translate the information available from the epidemiological studies into a basis for 

15 appropriate standards, which includes consideration of how to weigh the uncertainties in reported 

16 associations across the distributions of PM concentrations in the studies or in quantitative 

17 estimates of risk. Such approaches are consistent with setting standards that are neither more nor 

18 less stringent than necessary, recognizing that a zero-risk standard is not required by the CAA. 

19 2.1.1 Approaches Used in Previous Reviews 

20 Staff has considered policy assessment approaches used in past reviews to inform the 

21 approach we are using in this review to reach preliminary conclusions regarding the adequacy of 

22 the current standard and alternative standards that are appropriate to consider in this review. We 

23 begin this section with a review of the approach used to set the original fine particle standards in 

24 1997 (section 2.1.1.1). The approach used to review and ultimately support revisions to these 

25 standards in 2006 is discussed in section 2.1.1.2. Litigation related to the standards finalized in 

26 2006, including the remand of the primary PM2.5 annual standard are then discussed in section 

27 2.1.1.3. 

28 2.1.1.1 Review Completed in 1997 

29 In setting the 1997 primary PM2.5 annual and 24-hour standards, the Agency relied 

30 primarily on an evidence-based approach that focused on epidemiological evidence, especially 

31 from short-term exposure studies of fine particles judged to be the strongest evidence at that 

32 time. The EPA did not place much weight on quantitative risk estimates from the very limited 

33 risk assessment conducted, but did conclude that the assessment results confirmed the general 

34 conclusions drawn from the epidemiological evidence that a serious public health problem was 
Draft Do Not Quote or Cite March 2010 2-3

1 associated with ambient PM levels allowed under the then current PM10 standards (62 FR 

2 38665/1, July 18, 1997). 

3 The EPA considered the epidemiological evidence and data on air quality relationships 

4 to set an annual PM2.5 standard that was intended to be the “generally controlling” standard; i.e., 

the primary means of lowering both long- and short-term ambient concentrations of PM2.5.

1 5 In 

6 conjunction with the annual standard, EPA also established a 24-hour PM2.5 standard to provide 

7 supplemental protection against days with high peak concentrations, localized “hotspots,” and 

8 risks arising from seasonal emissions that might not be well controlled by a national annual 

9 standard. (62 FR 38669/3). Recognizing that there are various ways to combine two standards to 

10 achieve an appropriate degree of public health protection, such as an approach that only 

11 considered short- and long-term exposure evidence, analyses, and standards independently, EPA 

12 concluded that the selected approach based on a generally controlling annual standard was the 

13 most effective and efficient approach. This conclusion was based in part on one of the key 

14 observations from the quantitative risk assessment, that much if not most of the aggregate annual 

15 risk associated with short-term exposures results from the large number of days during which the 

16 24-hour average concentrations are in the low- to mid-range, below the peak 24-hour 

17 concentrations. As a result, lowering a wide range of ambient 24-hour PM2.5 concentrations by 

18 means of a generally controlling annual standard, as opposed to focusing on control of peak 24-

19 hour concentrations, was determined to be the most effective and efficient way to reduce total 

20 population risk (62 FR 38670 to 38671). 

21 In setting the level of the annual standard in 1997, EPA first determined a level for the 

22 annual standard based on the short-term exposure studies, and then considered whether the key 

23 long-term exposure studies suggested the need for a lower level. While recognizing that health 

24 effects may occur over the full range of concentrations observed in the studies, EPA concluded 

25 that the strongest evidence for short-term PM2.5-related effects occurs at concentrations near the 

26 long-term (e.g., annual) average in the short-term exposure studies. Given the serious nature of 

27 the potential effects, EPA selected a level for the annual standard at or below the long-term mean 

28 concentrations in studies providing evidence of associations with short-term exposures, placing 

29 greatest weight on those short-term exposure studies that reported clearly statistically significant 

30 associations with mortality and morbidity effects (62 FR 38676/1). Further consideration of the 

 1

 In so doing, EPA noted that an annual standard would focus control programs on annual average PM2.5

concentrations, 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 situations where the daily peaks and annual averages are not 

consistently correlated (62 FR 38669). 
Draft Do Not Quote or Cite March 2010 2-4

1 average PM2.5 concentrations across the cities in the key long-term exposure studies of mortality 

2 and respiratory effects in children did not provide a basis for establishing a lower annual 

3 standard level. Because the annual standard level selected was below the range of annual 

4 concentrations most strongly associated with both short- and long-term exposure effects, and 

5 because even small changes in annual means in this concentration range could make significant 

6 difference in overall risk reduction and total population exposures, EPA concluded that this 

7 standard would provide an adequate margin of safety against effects observed in these 

8 epidemiological studies (62 FR 68676/3). 

9 The selection of the level of the annual standard was done in conjunction with having 

10 first selected the form of the annual standard to be based on the concentration measured at a 

11 single monitor sited to represent community-wide air quality, or a value resulting from an 

12 average of measurements from multiple community-wide air quality monitoring sites that met 

13 specific criteria and constraints (“spatial averaging”). This decision emphasized consistency 

14 with the types of air quality measurements that were used in the relevant epidemiological studies. 

15 In reaching this decision, EPA recognized the importance of ensuring that spatial averaging 

16 would not result in inequities in the level of protection provided by the PM2.5 standards in some 

17 areas. Because the annual standard, defined in terms of single or averaged community-wide air 

18 quality monitoring sites, could not be expected to offer an adequate margin of safety against the 

19 effects of all potential short-term exposures in areas with strong local or seasonal sources that 

20 could not be directly evaluated in the epidemiological studies, EPA set the level of the 24-hour 

21 standard to supplement the control afforded by the annual standard based on air quality 

22 relationships between annual and 24-hour concentrations. This approach was intended to 

23 provide an adequate margin of safety against infrequent or isolated peak concentrations that 

24 could occur in areas that attain the annual standard (62 FR 38677). 

25 2.1.1.2 Review Completed in 2006 

26 In 2006, EPA used a different evidence-based approach to assess the appropriateness of 

27 the levels of the 24-hour and annual PM2.5 standards. Based on an expanded body of 

28 epidemiological evidence that was stronger and more robust, including both short- and long-term 

29 exposure studies, the Administrator decided that using evidence of effects associated with 

30 periods of exposure that were most closely matched to the averaging time of each standard was 

31 the most appropriate public health policy approach for evaluating the scientific evidence to 

32 inform selecting the level of each standard. Thus, the Administrator relied upon evidence from 

33 the short-term exposure studies as the principal basis for selecting the level of the 24-hour PM2.5 

34 standard, with the 24-hour standard designed to protect against effects associated with short-term 

35 exposures. The Administrator relied upon evidence from long-term exposure studies as the 
Draft Do Not Quote or Cite March 2010 2-5

1 principal basis for selecting the level of the annual PM2.5 standard, with the annual standard 

2 designed to protect against effects associated with long-term exposures. 

3 With respect to quantitative risk-based considerations, the Administrator recognized that 

4 the analyses conducted for this review were based on “a more extensive body of data and [was] 

5 more comprehensive in scope than the assessment conducted in the last review, but was mindful 

6 that significant uncertainties continue[d] to underlie the resulting risk estimates” (71 FR 61168/2, 

October 17, 2006).2 7 The Administrator determined that the estimates of risks likely to remain 

8 upon attainment of the 1997 suite of PM2.5 standards were indicative of risks that could be 

9 reasonably judged important from a public health perspective, and, thus, supported revision of 

10 the standards. However, the Administrator judged that the quantitative risk assessment had 

11 important limitations and did not provide an appropriate basis for selecting either the level of the 

12 24-hour or annual PM2.5 standard (71 FR 61174/1-2). The Administrator more heavily weighed 

13 the implications of the uncertainties associated with the quantitative risk assessment than the 

14 Clean Air Scientific Advisory Committee (CASAC) apparently did in their comments on the 

15 proposed rulemaking, where CASAC stated, “[w]hile the risk assessment is subject to 

16 uncertainties, most of the PM Panel found EPA’s risk assessment to be of sufficient quality to 

17 inform its recommendations...The risk analyses indicated that the uncertainties would increase 

rapidly below an annual level of 13 μg/m3 18 – and that was the basis for the PM Panel’s 

recommendation of 13 μg/m3 19 as the lower bound for the annual PM2.5 standard level” 

20 (Henderson, 2006a, p.3). 

21 With regard to final decisions on the primary annual PM2.5 standard, the Administrator 

22 placed the greatest weight for determining the level of the annual standard on the long-term 

23 means of the concentrations associated with mortality effects in the two key long-term exposure 

24 studies in the record, the American Cancer Society (ACS) and Harvard Six Cities studies (71 FR 

25 at 61172 to 61177). Important validation and reanalyses of the original ACS and Harvard Six 

26 Cities studies provided “evidence of generally robust associations and provide[d] a basis for 

27 greater confidence in the reported associations than in the last review, for example, in the extent 

28 to which they have made progress in understanding the importance of issues related to co29 pollutant confounding and the specification of statistical models.” Furthermore, the extended 

30 ACS study provided “new evidence of mortality related to lung cancer and further 

 2

 Uncertainties identified in the quantitative risk assessment were 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 PM2.5 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 

PM2.5 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

1 substantiate[d] the statistically significant associations with cardiorespiratory-related mortality 

2 observed in the original studies” (71 FR 61172/1-2). The Administrator also recognized the 

3 availability of long-term exposure studies that provided evidence of respiratory morbidity, 

4 including changes in lung function measurements and decreased growth in lung function as 

5 reported in the 24-Cities study and the Southern California Children’s Health Study, 

respectively. In retaining the level of the annual standard at 15 μg/m3 6 , the Administrator selected 

7 a level that was “appreciably below” the long-term average concentrations reported in the key 

8 long-term mortality studies and “basically at the same level” as the long-term average 

9 concentrations in the key long-term respiratory morbidity studies. In the judgment of the 

10 Administrator, the two long-term respiratory morbidity studies provided an uncertain basis for 

11 setting the level of a national standard, and therefore, did “not warrant setting a lower level for 

12 the annual standard than the level warranted based on the key mortality studies” (71 FR 

13 61176/3). 

14 In considering the form of the primary annual PM2.5 standard, the Administrator retained 

15 the form of the standard as an annual arithmetic mean, averaged over 3 years with modifications 

16 that strengthen the standard by tightening the criteria for use of spatial averaging. Specifically, 

17 the Administrator narrowed the circumstances under which spatial averaging may be utilized. 

18 Analyses conducted in the review completed in 2006, based on a much larger set of PM2.5 air 

19 quality data than was available for the review completed in 1997, provided evidence concerning 

20 the potential for disproportionate impacts on potentially vulnerable subpopulations. Specifically, 

21 the results of the analyses suggested that “the highest concentrations in an area tend to be 

22 measured at monitors located in areas where the surrounding population [was] more likely to 

23 have lower education and income levels, and higher percentages of minority populations” (71 FR 

24 61166/2, see also US EPA, 2005, section 5.3.6.1; Schmidt et al., 2005, Attachment A/Analysis 

7).3 25 

In deciding to revise the level of the 24-hour PM2.5 standard from 65 μg/m3 to 35 μg/m3 26 , 

27 the Administrator placed the greatest weight on the much expanded body of evidence from short28 term exposure studies, with a focus on U.S. and Canadian studies that had been reanalyzed, as 

29 appropriate, to address statistical modeling issues and that used relatively reliable air quality 

30 data. A comprehensive evaluation considered and weighed a variety of evidence, including 

 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 PM2.5 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 marker for lower socioeconomic status (SES) that may be related to increased 

vulnerability to the effects of fine particle exposures, for example, as a result of greater exposure from proximity to 

sources such as roadways and industry, as well as other factors such as poorer health status and access to health care 

(US EPA, 2004, section 9.2.4.5). 
Draft Do Not Quote or Cite March 2010 2-7

1 biological plausibility of associations between various pollutants and health outcomes, and 

2 focused on the stability of the size of the effect estimates in time-series studies using both single3 and multi-pollutant models, rather than just looking at statistical significance in a large number 

4 of alternative models to simplistically delineate between real and suspect associations (71 FR 

5 61170/2). Emphasis was placed on those studies that provided evidence of statistically 

6 significant associations in areas that would have met the then current annual and 24-hour PM2.5 

7 standards during the time of the study. The Administrator recognized that these studies provided 

8 no evidence of clear effect thresholds or lowest-observed effect levels. Nonetheless, in focusing 

on the 98th 9 percentile air quality values in these studies, the Administrator sought to establish a 

10 standard level that would require improvements in air quality generally in areas in which the 

11 distribution of daily short-term exposure to PM2.5 could reasonably be expected to be associated 

12 with serious health effects. The Administrator recognized that although future air quality 

13 improvement strategies in any particular area were not yet defined, most such strategies were 

14 likely to move a broad distribution of PM2.5 air quality values in an area lower, resulting in 

15 reductions in risk associated with exposures to PM2.5 levels across a wide range of concentrations 

and not just at the 98th 16 percentile concentrations (71 FR 61168/3). 

17 2.1.2 Remand of Primary Annual PM2.5 Standard 

18 As noted above in section1.2.4, several parties filed petitions for review following 

19 promulgation of the revised PM NAAQS in 2006. These petitions challenged several aspects of 

20 the final rule including the selection of the level of the primary PM2.5 annual standard. More 

21 specifically, petitioners representing environmental groups (American Lung Association, 

22 Environmental Defense, and the National Parks Conservation Association) and several states and 

23 state agencies argued that the decision to retain the level of the annual PM2.5 standard at 15 

μg/m3 24 was “arbitrary, capricious, an abuse of discretion, or otherwise not in accordance with 

25 law.” 42 U.S.C. 7607(d)(9). The primary 24-hour PM2.5 standard was not challenged by any of 

26 the litigants and, thus, not considered in the court’s review and final decision. 

27 On judicial review, the D.C. Circuit remanded the primary annual PM2.5 NAAQS to EPA 

28 because the Agency failed to adequately explain why the annual standard provided the requisite 

29 protection from both short- and long-term exposures to fine particles including protection for 

30 susceptible populations. American Farm Bureau Federation v. EPA, 559 F. 3d 512 (D.C. Cir. 

31 2009). With respect to human health protection from short-term PM2.5 exposures, the court 

32 considered the different approaches used by EPA in the 1997 and 2006 PM NAAQS decisions as 

33 summarized above. The court found that EPA failed to adequately explain why a 24-hour PM2.5 

34 standard by itself would provide the protection needed from short-term exposures and remanded 

35 the annual PM2.5 standard to EPA “for further consideration of whether it is set at a level 
Draft Do Not Quote or Cite March 2010 2-8

1 requisite to protect the public health while providing an adequate margin of safety from the risk 

2 of short-term exposures to PM2.5.” American Farm Bureau Federation, 559 F. 3d at 520-24. 

3 With respect to protection from long-term exposure to fine particles, the court found that 

4 EPA failed to adequately explain how the current primary annual PM2.5 standard provided an 

5 adequate margin of safety for children and other susceptible populations. The court found that 

6 EPA did not provide a reasonable explanation of why certain morbidity studies, including a 

7 study of children in Southern California showing lung damage associated with long-term PM2.5 

8 exposure (Gauderman et.al, 2000) and a multi-city study (24-Cities Study) evaluating decreased 

9 lung function in children associated with long-term PM2.5 exposures (Raizenne et al., 1996), did 

10 not call for a more stringent annual PM2.5 standard. Id. at 522-23. Specifically, the court found 

11 that: 

12 

13 EPA was unreasonably confident that, even though it relied solely upon long-term 

14 mortality studies, the revised standard would provide an adequate margin of safety with 

15 respect to morbidity among children. Notably absent from the final rule, moreover, is 

16 any indication of how the standard will adequately reduce risk to the elderly or to those 

17 with certain heart or lung diseases despite (a) the EPA’s determination in its proposed 

18 rule that those subpopulations are at greater risk from exposure to fine particles and (b) 

19 the evidence in the record supporting that determination. Id. at 525. 

20 

21 Petitioners also objected to the EPA analysis of the long-term exposure studies arguing 

22 that the EPA “unreasonably focused” upon the long-term mean ambient concentrations of PM2.5 

in the ACS (17.7 μg/m3) and the Harvard Six Cities Study (18 μg/m3 23 ) and then set a level below 

24 those concentrations for the annual PM2.5 standard. Specifically, these petitioners claimed that 

25 “this approach violates the requirement of the Clean Air Act (CAA) that the NAAQS provide ‘an 

26 adequate margin of safety’ which requires that EPA ‘err on the side of caution’” and argued that 

27 the level of the annual standard should be revised lower because the most recent data from these 

28 studies “showed adverse health effects in years when the mean ambient concentration of PM2.5 

was below 15 μg/m3 29 .” Id. at 526. The court rejected these arguments stating: “The EPA, 

30 mindful of its obligation to set a standard ‘not lower or higher than is necessary...to protect 

31 public health,’ Whitman, 531 U.S. at 475-76, reasonably decided to address long-term mean 

32 concentrations in the ACS and Six Cities studies...We approved a similar approach to assuring 

33 an adequate margin of safety in ATAIII and we do so again here.” Id. at 527. 

34 Petitioners also challenged the Agency’s decision not to rely upon the quantitative risk 

35 assessment in making final decisions on the level of the primary annual PM2.5 standard. More 

36 specifically, these petitioners argued that “[b]oth CASAC and EPA staff concluded that the 

37 Agency’s risk assessment ... was of sufficient quality to deserve consideration in determining 

38 the level of the annual standard necessary to provide an adequate margin of safety” and that, in 
Draft Do Not Quote or Cite March 2010 2-9

retaining the level of the annual standard at 15 μg/m3 1 significant public health impacts remained 

2 (State brief, pp. 22 to 23). The court rejected arguments that EPA was compelled to use a risk3 based approach to determine the level of the standards, or otherwise compelled to use the risk 

4 assessment quantitatively in the standard-setting process, concluding that EPA “reasonably 

5 analyzed the risk assessment,” and deferred to the EPA’s assessment of “scientific data within its 

6 technical expertise.” Id at 529-530. 

7 In remanding the primary annual standard for reconsideration, the court did not vacate the 

8 annual standard. Id. at 530. 

9 2.1.3 Current Approach 

10 Staff’s approach in this review is founded on a much expanded body of epidemiological 

11 evidence, more extensive air quality data and analyses, and a more comprehensive risk 

12 assessment relative to the information available in past reviews. As a result, our approach to 

13 reaching conclusions about the adequacy of the current suite of PM2.5 standards and potential 

14 alternative standards that are appropriate for consideration is broader and more integrative than 

15 in past reviews. Our approach takes into account both evidence-based and risk-based 

16 considerations, and the uncertainties related to both types of information, to inform the 

17 preliminary conclusions presented in this first draft Policy Assessment (PA). In so doing, we are 

18 seeking to provide as broad an array of options as is supportable by the available information, 

19 recognizing that the selection of a specific approach to reaching final decisions on the primary 

20 PM2.5 standards will reflect the judgments of the Administrator as to what weight to place on the 

21 various approaches and types of information presented in the final PA. 

22 As an initial matter, we believe it is most appropriate to consider the protection against 

23 PM2.5-related mortality and morbidity effects, associated with both long- and short-term 

24 exposures, afforded by the annual and 24-hour standards taken together, rather than to consider 

25 each standard separately. In so doing, we look at the types of evidence that can inform each 

26 standard, then integrate the results of those considerations to reach preliminary conclusions about 

27 the current and alternative suites of standards. This approach reflects the recognition that 

28 changes in PM2.5 air quality designed to meet an annual standard would likely result not only in 

29 lower annual average concentrations but also in fewer and lower peak 24-hour concentrations. 

30 Conversely, we recognize that changes designed to meet a 24-hour standard would result not 

31 only in fewer and lower peak 24-hour concentrations but also in lower annual average 

32 concentrations, especially to the extent that changes of a more regional, rather than local, nature 

33 occur. The extent to which these two standards are interrelated in any given area depends in 

34 large part on the relative levels of the standards, the peak-to-mean ratios that characterize air 
Draft Do Not Quote or Cite March 2010 2-10

1 quality patterns in an area, and whether changes in air quality designed to meet a given suite of 

2 standards is of a more regional or more localized nature. 

3 Our consideration of the protection afforded by the current and alternative suites of 

4 standards focuses first on PM2.5-related health effects associated with long-term exposures, for 

5 which quantitative estimates of risks to public health are appreciably larger; we then also focus 

6 on effects associated with short-term exposures. In both cases, we place greatest weight on 

7 associations that have been judged in the ISA to be causal and likely causal, while also 

8 considering associations judged to be suggestive of a causal relationship or that focus on specific 

9 susceptible populations. We focus on studies conducted in the U.S. and Canada and place 

10 relatively greater weight on statistically significant associations that yield relatively more precise 

11 effect estimates and that are judged to be robust to confounding by other air pollutants. In the 

12 case of short-term exposure studies, we place greatest weight on large multi-city studies, while 

13 also considering associations in single-city studies. 

14 As part of our evidence-based approach, we first evaluate the evidence from long-term 

15 exposure studies, as well as the uncertainties and limitations in that evidence, to assess the 

16 degree to which the current and alternative suites of standards can be expected to protect against 

17 effects related to long-term exposures. As in past reviews, we believe this evidence can most 

18 directly help inform consideration of the protection afforded by an annual PM2.5 standard. In 

19 evaluating the long-term exposure evidence, we look at the aggregate long-term mean PM2.5

20 concentration in each study, the range of long-term mean PM2.5 concentrations across cities, and 

21 the distribution of city-specific means in terms of the standard deviation or interquartile range, to 

22 the extent such data are available. In considering the adequacy of the current suite of PM2.5

23 standards in protecting against long-term exposure-related effects, we consider whether 

24 associations from long-term exposure studies have been reported across areas in which the 

25 aggregate long-term study mean concentrations are at or below the level of the current annual 

26 standard. We conclude that such long-term exposure studies can reasonably be viewed as calling 

27 into question the adequacy of the current annual standard. 

28 In considering what alternative standards would be protective against effects observed in 

29 such long-term exposure studies, we first note the absence of any discernable threshold within 

30 the range of long-term mean concentrations reported in the long-term exposure studies. While 

31 recognizing that health effects may occur over the full range of concentrations observed in the 

32 studies, we believe that it is reasonable to conclude that the evidence of association is strongest 

33 down to somewhat below the aggregate mean concentration, such as down to one standard 

34 deviation below the mean or to the lower end of the interquartile range, which includes the range 

35 in which the data in the study are most concentrated. We also believe it is appropriate to 

36 consider the long-term mean concentration at the point where the confidence interval becomes 
Draft Do Not Quote or Cite March 2010 2-11

1 notably wider, suggestive of a concentration below which the association becomes appreciably 

2 more uncertain and the possibility that an effects threshold may exist becomes more likely. 

3 Based on these considerations, we identify a range of alternative annual standard levels that we 

4 judge to be appropriate to consider for protecting against PM2.5-related long-term exposure 

5 effects based on the evidence available in this review. 

6 We next evaluate the evidence from short-term exposure studies, as well as the 

7 uncertainties and limitations in that evidence, to assess the degree to which the current and 

8 alternative suites of standards can be expected to protect against effects related to short-term 

9 exposures. As in past reviews, it is staff’s view that this evidence can help inform consideration 

of the protection afforded by both an annual and 24-hour standard.4 10 In evaluating the short-term 

11 exposure evidence, we look both at the aggregate long-term mean PM2.5 concentrations in key 

studies as well as the distributions of 24-hour PM2.5 concentrations, with a focus on the 98th 12 

13 percentile concentrations to match the form of the current 24-hour standard, to the extent such 

14 data are available. In evaluating the short-term exposure studies to help inform consideration of 

15 the protection afforded by an annual PM2.5 standard, we observe, based on quantitative risk 

16 assessments conducted in past reviews, that much of the risk related to daily exposures, when 

17 aggregated on an annual basis, results from the large number of days during which the 24-hour 

18 average concentrations are in the low- to mid-range of the entire distribution. Thus, to reduce the 

19 aggregate short-term exposure-related risk, it is necessary to shift the bulk of the air quality 

20 distribution to lower levels, not just to limit the concentrations on days when the PM2.5

21 concentrations are relatively high. 

22 While shifting the distribution can be accomplished through control strategies aimed at 

23 meeting either an annual or 24-hour standard, we have seen in quantitative risk assessments 

24 conducted in this and past reviews that more consistent aggregated risk reductions across study 

25 areas are likely to be accomplished through strategies aimed at meeting an annual standard. 

26 Thus, in considering the adequacy of the current suite of standards in protecting against effects 

27 associated with short-term exposures, we consider whether associations in short-term exposure 

28 studies have been reported in areas in which the aggregate long-term study mean concentrations 

29 are at or below the level of the current annual standard, as well as by considering whether the 

98th 30 percentile PM2.5 concentrations in such studies are at or below the level of the current 24-

31 hour standard. We conclude that such short-term exposure studies can reasonably be viewed as 

32 calling into question the adequacy of the current annual and/or 24-hour standards. 

 4

 While this view is consistent with that 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

1 In considering what alternative standards would be protective against effects observed in 

2 such short-term exposure studies, we first note the absence of any discernable threshold within 

3 the distribution of 24-hour average concentrations in the short-term exposure studies. While 

4 recognizing that health effects may occur over the full range of 24-hour concentrations observed 

5 in the studies, as with the long-term exposure studies, we believe that it is reasonable to conclude 

6 that the evidence of association is strongest down to somewhat below the mean 24-hour average 

7 concentration, such as down to one standard deviation below the mean or to the lower end of the 

8 interquartile range, where the data in the study are most concentrated. We also believe it is 

9 appropriate to consider whether, and if so, where in the distribution of 24-hour average 

10 concentrations the confidence interval becomes notably wider, suggestive of a concentration 

11 below which the association becomes appreciably more uncertain and the possibility that an 

12 effects threshold may exist becomes more likely. Based on these considerations, we identify a 

13 range of alternative annual standard levels that we conclude are appropriate to consider for 

14 protecting against PM2.5-related short-term exposure effects based on the evidence available in 

15 this review. We also recognize that it is unlikely that an annual standard could effectively 

16 protect against short-term exposure-related effects in all areas across the country, especially in 

17 areas with relatively high peak-to-mean ratios in PM2.5 concentrations or in areas that are 

18 strongly affected by localized “hotspots” or by seasonal exposures that may not be well 

19 controlled by an annual standard. Thus, we also identify a range of alternative 24-hour standard 

20 levels that we judge to be appropriate to consider for protecting against PM2.5-related short-term 

21 exposure effects, in conjunction with a range of alternative annual standards, based on the 

22 evidence available in this review. 

23 Based on the evidence-based considerations outlined above, we then develop integrated 

24 preliminary conclusions with regard to alternative suites of standards, including both annual and 

25 24-hour standards, that we believe are appropriate for consideration in this review based on the 

26 currently available evidence. In so doing, we discuss the roles that each standard might be 

27 expected to play in the protection afforded by alternative suites of standards. 

28 Beyond these evidence-based considerations, we also consider the quantitative risk 

29 estimates and the key observations presented in the second draft quantitative risk assessment 

30 (RA). This assessment included an evaluation of 15 urban case study areas and estimated risk 

31 associated with a number of health endpoints associated with long-term and short-term PM2.5

32 exposures (US EPA, 2010a). As part of our risk-based considerations, we have considered 

33 estimates of the magnitude of PM2.5-related risks associated with recent air quality levels and air 

34 quality simulated to just meet the current and alternative suites of standards using alternative 

35 simulation approaches. We have also characterized the risk reductions, relative to the risks 

36 remaining upon just meeting the current standards, associated with just meeting alternative suites 
Draft Do Not Quote or Cite March 2010 2-13

1 of standards. In so doing, we recognize the uncertainties inherent in such risk estimates, and 

2 have taken such uncertainties into account by considering the sensitivity of the “core” risk 

3 estimates to alternative assumptions and methods likely to have substantial impact on the 

4 estimates. In addition, we have conducted additional analyses to characterize the 

5 representativeness of the urban study areas within a broader national context. We have 

6 considered this risk-based information to help inform our preliminary conclusions on the 

7 adequacy of the current suite of standards, potential alternative suites of standards that are 

8 appropriate for consideration in this review, and on the roles that the annual and 24-hour 

9 standards may play in affording protection against effects related to both long- and short-term 

10 PM2.5 exposures. 

11 Our preliminary conclusions reflect our understanding of both evidence-based and risk12 based considerations to inform two overarching questions related to: (1) the adequacy of the 

13 current suite of PM2.5 standards and (2) what potential alternative standards, if any, should be 

14 considered in this review to provide appropriate protection from the effects associated with both 

15 long- and short-term exposures to fine particles. In addressing these broad questions, we have 

16 organized the discussions below around a series of more specific questions reflecting different 

17 aspects of each overarching question. When evaluating the health protection afforded by the 

18 current or any alternative suites of standards considered, we have taken into account the four 

19 basic elements of the NAAQS (e.g., indicator, averaging time, form, and level). 

20 We believe that the approach outlined above, when presented in the final PA, will 

21 provide a comprehensive basis to help inform the judgments required of the Administrator in 

22 reaching decisions about the current and potential alternative primary PM2.5 standards and in 

23 responding to the remand of the 2006 annual PM2.5 standard. 

24 2.2 ADEQUACY OF CURRENT STANDARDS 

25 In considering the adequacy of the current suite of PM2.5 standards, staff addresses the 

26 following overarching question: 

27 Does the currently available scientific evidence and risk-based information, as reflected in 

28 the ISA and RA, support or call into question the adequacy of the protection afforded by 

29 the current suite of fine particle standards? 

30 To inform the answer to this broad question, we have posed a series of more specific 

31 questions to aid in considering the currently available scientific evidence and the results of recent 

32 quantitative risk analyses in a policy-relevant context, as discussed below. In considering the 

33 scientific and technical information, we reflect upon both the information available in the last 

34 review and information that is newly available since the last review as assessed and presented in 

35 the ISA and second draft RA (US EPA, 2009a; US EPA, 2010a). 
Draft Do Not Quote or Cite March 2010 2-14

1 2.2.1 Evidence-based Considerations 

2 In reviewing the adequacy of the current suite of PM2.5 standards, we have taken into 

3 account evidence-based considerations primarily by assessing the currently available evidence as 

4 presented in the ISA. Our review of the adequacy of the current standards begins by considering 

5 causal inference, impacts on susceptible populations, and whether health effects have been 

6 observed in areas where the air quality concentrations extend to levels lower than previously 

7 reported. 

8  To what extent does the newly available scientific evidence and related uncertainties 

9 strengthen or call into question evidence of associations between ambient fine particle 

10 exposures and health effects? 

11 In considering the strength of the associations between short- and long-term exposures to 

12 PM2.5 and health effects, we first recognize that, in the last review, EPA concluded that there was 

13 “strong epidemiological evidence” for PM2.5 linking short-term exposures with cardiovascular 

14 and respiratory mortality and morbidity, and long-term exposures with cardiovascular and lung 

15 cancer mortality and respiratory morbidity (US EPA, 2004, p. 9-46; US EPA, 2005, p. 5-4). 

16 Overall, the epidemiological evidence supported “likely causal associations” between PM2.5 and 

17 both mortality and morbidity from cardiovascular and respiratory diseases, based on “an 

18 assessment of strength, robustness, and consistency in results” (US EPA, 2004, p. 9-48). 

19 In looking across the extensive new scientific evidence available in this review, our 

20 overall understanding of health effects associated with fine particle exposures has been greatly 

21 expanded. The currently available evidence is stronger in comparison to evidence available in 

22 the last review because of its breadth and the substantiation of previously observed health effects 

23 (US EPA, 2009a, section 2.3.1). A number of large multi-city epidemiological studies have been 

24 conducted throughout the U.S. including extended analyses of studies that were important to 

25 inform decisionmaking in the last review. These studies have reported consistent increases in 

26 morbidity and/or mortality related to ambient PM2.5 concentrations, with the strongest evidence 

27 reported for cardiovascular-related effects. In addition, the findings of new toxicological and 

28 controlled human exposure studies provide stronger support for a number of potential biologic 

29 mechanisms or pathways for PM-related cardiovascular and respiratory effects (US EPA, 2009a, 

30 chapter 5; Figures 5-4 and 5-5). In summary, the ISA concludes, “[t]he new evidence ... greatly 

31 expands upon the evidence available in the 2004 PM AQCD particularly in providing greater 

32 understanding of the underlying mechanisms for PM2.5 induced cardiovascular and respiratory 

33 effects for both short- and long-term exposures” (US EPA, 2009a, p. 2-17). 

34 As an initial matter, we note that since the conclusion of the last PM NAAQS review, the 

35 Agency has developed a more formal framework for reaching causal inferences from the body of 

36 scientific evidence drawing upon the evaluation and synthesis of evidence from across 
Draft Do Not Quote or Cite March 2010 2-15

1 epidemiological, controlled human exposure, and toxicological studies. This framework uses a 

2 five-level hierarchy that classifies the overall weight of evidence and causality using the 

3 following categorizations: causal relationship, likely to be a causal relationship, suggestive of a 

4 causal relationship, inadequate to infer a causal relationship, and not likely to be a causal 

5 relationship (US EPA, 2009a, Table 1-3). 

6 In reaching causal inferences, EPA has considered uncertainties that bear on our 

7 understanding of the body of currently available scientific evidence (US EPA, 2009a, section 

8 1.5). For example, in epidemiological studies the potential for confounding bias remains an 

9 important source of uncertainty in evaluating the health effects associated with one pollutant that 

10 is part of a larger, complex mixture of pollutants. Epidemiological studies attempt to disentangle 

11 the effects of the air pollution mixture and identify the health effects associated with a specific 

12 pollutant, such as PM2.5, using multivariate regression models to control for the potential 

confounding effects by other pollutants (e.g., gaseous co-pollutants5 13 ) for which measurements 

14 are available. However, there are several statistical issues influencing results generated using co15 pollutant models that lead to uncertainty in the quantitative interpretation of these results. In this 

16 review, the uncertainties associated with the evaluation of the body of scientific evidence for 

17 PM2.5-associated health effects remain largely the same as in previous reviews (e.g., co-pollutant 

18 confounding, exposure misclassification) and have been considered in reaching causality 

19 determinations as discussed in the ISA. 

20 Looking broadly to integrate epidemiological evidence with that from controlled human 

21 exposure studies and toxicologic studies and using this causal framework, the ISA concludes that 

22 the collective evidence is largely consistent with past studies and substantially strengthens what 

23 was known in the last review to reach the conclusion that a causal relationship exists between 

24 both short- and long-term exposures to PM2.5 and mortality and cardiovascular effects. 

25 Furthermore, the ISA concludes that the collective evidence continues to support likely causal

26 associations between short- and long-term PM2.5 exposures and respiratory effects. Additional 

27 evidence is suggestive of a causal relationship between long-term PM2.5 exposures and other 

28 health effects, including developmental and reproductive effects (e.g., low birth weight) and 

29 carcinogenic, mutagenic, and genotoxic (e.g., lung cancer mortality) effects. Table 2-1 

30 summarizes the causal determinations for health outcomes associated with short- and long-term 

31 exposures to PM2.5 (US EPA, 2009a, sections 2.3.1 and 2.6). 

32 

 5

 A gaseous co-pollutant (e.g., O3, CO, SO2, NO2) meets the criteria for potential confounding in PM2.5-related 

effects if: (1) it is a potential risk factor for the health effect under study; (2) it is correlated with PM2.5 and (3) it 

does not act as an intermediate step in the pathway between PM2.5 exposure and the health effect under study (US 

EPA, 2004, p. 8-10).
Draft Do Not Quote or Cite March 2010 2-16

1 Table 2-1. Summary of Causality Determinations for PM2.5

Exposure 

Duration Outcome 

Causality 

Determination 

Mortality Causal 

Cardiovascular Effects Causal 

Respiratory Effects Likely to be Causal 

Reproductive and Developmental Effects Suggestive 

Long-term 

Cancer, Mutagenicity, Genotoxicity Effects Suggestive 

Mortality Causal 

Cardiovascular Effects Causal 

Short-term Respiratory Effects Likely to be Causal 

Central Nervous System Effects Inadequate 

2 Source: adapted from US EPA, 2009, Table 2-6. 

3 Health Effects Associated with Long-term PM2.5 Exposure

4 With regard to mortality associated with long-term PM2.5 exposures, the ISA concludes 

5 that newly available evidence significantly strengthens the evidence linking long-term exposure 

6 to PM2.5 and mortality, while providing indications that the magnitude of the PM2.5-mortality 

7 association may be larger than previously estimated (US EPA, 2009a, sections 7.2.10, 7.2.11, 

8 7.6.1; Figures 7-6 and 7-7). A number of large U.S. cohort studies have been published since the 

9 last review. This evidence includes new analyses and insights from extended analyses of the 

10 American Cancer Society (ACS) and Harvard Six Cities studies (US EPA, 2009a, pp 7-84 to 7-

11 85; Figure 7-6; Krewski et al., 2009; Pope et al., 2004; Jerrett et al., 2005; Laden et al., 2006). In 

12 addition, new long-term PM2.5 exposure studies evaluating mortality impacts in additional 

13 cohorts are now available. The Women’s Health Initiative has investigated the effects of PM2.5 

14 on cardiovascular-related mortality in post-menopausal women with no previous history of 

15 cardiac disease (US EPA, 2009a, p. 7-87; Miller et al., 2007). Mortality impacts in older adults 

16 using Medicare data have been reported by a number of investigators (US EPA, 2009a, pp. 7-87 

17 to 7-89; Eftim et al., 2008; Zeger et al., 2007, 2008). We note that other long-term PM2.5

18 exposure studies provide additional evidence of mortality associated with long-term PM2.5 

19 exposures as discussed more fully in section 7.6 of the ISA. Collectively, these long-term PM2.5

20 exposure studies, along with the evidence available in the last review, provide us with consistent 

21 and stronger evidence of associations between long-term exposure to PM2.5 and mortality (U.S. 

22 EPA, 2009a, sections 2.3.1 and 7.6). 
Draft Do Not Quote or Cite March 2010 2-17

1 When integrating the mortality evidence, EPA considered impacts on all-cause or non2 accidental mortality as well as cause-specific mortality (e.g., cardiovascular-related mortality, 

3 respiratory-related mortality, lung cancer mortality) and reached the conclusion that there is a 

4 causal association between mortality and long-term PM2.5 exposure (US EPA, 2009a, pp. 2-12 

5 and 7-96). The strongest evidence indicates an association between long-term PM2.5 exposures 

6 and mortality due to cardiovascular disease, with additional evidence supporting an association 

7 between PM2.5 and mortality related to lung cancer (US EPA, 2009a, pp. 2-12, 7-81, and 7-95 to 

8 7-96; Figure 7-7). We note that fewer long-term PM2.5 exposure studies have evaluated the 

9 respiratory component of cardiopulmonary mortality, and the evidence to support an association 

10 with long-term exposure to PM2.5 and respiratory mortality is, therefore, much more limited (US 

11 EPA 2009a, p. 2-12; Figure 7-7). The strength of associations for cause-specific mortality is 

12 coherent with cardiovascular-related morbidity endpoints as discussed below. The most recent 

13 evidence for cardiovascular-related mortality in post-menopausal women indicates that the 

14 evidence of association with long-term exposure to PM2.5 in this population is “particularly 

15 strong” (US EPA, 2009a, p. 7-96). 

16 In addition, the strength of the causal association between long-term PM2.5 exposure and 

17 mortality builds upon new studies providing evidence of improvement in community health 

18 following reduction in ambient fine particle concentrations. Pope et al. (2009) have documented 

19 the population health benefits of reducing ambient air pollution by correlating past reductions in 

20 ambient PM2.5 concentrations with increased life expectancy. These investigators report that 

21 reductions in fine particle ambient concentrations that occurred during the 1980s and 1990s 

22 account for as much as 15 percent of the overall improvement in life expectancy in 51 U.S. 

23 metropolitan areas also analyzed in the ACS study. The decrease in fine particle exposure was 

24 reported to be associated with an estimated increase in mean life expectancy of approximately 5 

25 to 9 months (US EPA, 2009a, p. 7-95; Pope et al., 2009). An extended analysis of the Harvard 

26 Six Cities study found that as cities cleaned up their air, locations with the largest reductions in 

27 PM2.5 saw the largest improvements in reduced mortality rates, while those with the smallest 

28 decreases in PM2.5 concentrations saw the smallest improvements in reduced mortality rates 

29 (Laden et al., 2006). Reduced mortality risk observed in this extended follow-up study was 

30 related to deaths due to cardiovascular and respiratory-related disease, but not from lung cancer 

31 (US EPA, 2009a, p. 7-84). An additional extended follow-up to the Harvard Six Cities study 

32 investigated the delay between changes in exposure and changes in mortality. Schwartz et al. 

33 (2008) reported that the effects of changes in PM2.5 exposures were seen within the 2 years prior 

34 to death (US EPA, 2009a, p. 7-92; Figure 7-9). 

35 With regard to cardiovascular effects associated with fine particle exposures, the ISA 

36 includes consideration of both cardiovascular-related mortality as well as morbidity effects and 
Draft Do Not Quote or Cite March 2010 2-18

1 concludes that a causal association exists between long-term PM2.5 exposure and cardiovascular 

2 effects (US EPA, 2009a, pp. 2-12 and 7-19). Recent studies have provided new evidence linking 

3 long-term exposure to PM2.5 with cardiovascular outcomes that has “expanded upon the 

4 continuum of effects ranging from the more subtle subclinical measures to cardiopulmonary 

5 mortality” (US EPA, 2009a, p. 2-17). Several new epidemiologic studies have examined the 

6 association between cardiovascular effects and long-term PM2.5 exposures in multi-city studies 

7 conducted in the U.S. and Europe. The ISA concludes that the strongest evidence of 

8 cardiovascular effects related to long-term exposure to PM2.5 has been reported in recent studies 

9 investigating cardiovascular-related mortality. This includes evidence from a number of large, 

10 multi-city U.S. long-term cohort studies including extended follow-up analyses of the ACS and 

11 Harvard Six Cities studies as well as the WHI as outlined above (US EPA, 2009a, sections 7.2.10 

12 and 7.6.1; Krewski et al., 2009; Pope et al., 2004; Laden et al., 2006; Miller et al., 2007). Pope 

13 et al. (2004) report a positive association between mortality and long-term PM2.5 exposure for a 

14 number of specific cardiovascular diseases, including ischemic heart disease (IHD), 

15 dysrhythmia, heart failure, and cardiac arrest (US EPA, 2009a, p. 7-84; Figure 7-7). Krewski et 

16 al. (2009) provides further evidence and precision for IHD-related mortality associated with 

17 long-term PM2.5 exposure (US EPA, 2009a, p. 7-84, Figure 7-7). 

18 Epidemiologic studies examining cardiovascular morbidity associated with long-term 

19 PM2.5 exposures were not available in the previous PM reviews. In the current review, studies 

20 are now available that evaluated a number of endpoints ranging from subtle indicators of 

21 cardiovascular health to serious clinical events associated with coronary heart disease (CHD) and 

22 cerebrovascular disease (CVD) including myocardial infarction (MI), coronary artery 

23 revascularization (e.g., bypass graft, angioplasty, stent, atherectomy), congestive heart failure 

24 (CHF), and stroke. The most significant new evidence comes from the WHI study which 

25 provides evidence of nonfatal cardiovascular events including both coronary and cerebrovascular 

26 events in a cohort of post-menopausal women with no previous history of cardiac disease (Miller 

27 et al., 2007; US EPA, 2009a, sections 7.2.9 and 7.6.1). 

28 As noted in the ISA, there may be multiple mechanisms related to the observed 

29 associations between PM2.5 and cardiovascular effects, and these processes may be interlinked 

30 (US EPA, 2009a, sections 5.2, 5.3, 5.5, 5.6, 5.7). For example, myocardial ischemia and MI may 

31 occur as a result the proposed effects of PM on atherosclerosis, plaque instability, plaque rupture, 

32 thrombosis, and/or altered vasoreactivity of coronary vessels. Myocardial ischemia and MI may 

33 alter the conduction and depolarization properties of the heart and lead to arrhythmic events. In 

34 addition, thrombosis may lead to stroke and/or thromboembolic disease. The ISA notes that “it 

35 is not clear at this time whether PM initiates cardiovascular disease or whether it perturbs 

36 existing disease” (US EPA, 2009a, p. 5-18). 
Draft Do Not Quote or Cite March 2010 2-19

1 Toxicological studies provide evidence that the cardiovascular morbidity effects observed 

2 in epidemiological studies are biologically plausible and coherent with studies of cardiovascular3 related mortality observed in long-term exposures as well as with studies of cardiovascular4 related morbidity and mortality associated with short-term exposures to PM2.5 as described below 

5 (US EPA, 2009a, p 7-19). For example, it has been hypothesized that that exposure to PM2.5 can 

6 lead to myocardial ischemia through an effect on the autonomic nervous system or by altering 

7 vasomotor function. Furthermore, PM-induced systemic inflammation and oxidative stress may 

8 contribute to altered vasomotor function which has been demonstrated as altered microvascular 

reactivity, altered vessel tone, and reduced blood flow during ischemia. 6 9 Toxicological studies 

10 demonstrating increased right ventricular pressure and diminished cardiac contractility also 

11 provide biological plausibility for the associations observed between PM2.5 and CHF in 

12 epidemiological studies (US EPA, 2009a, p. 2-15). Additional evidence of cardiovascular13 related morbidity and mortality associated with long-term PM2.5 exposures is discussed more 

14 fully in section 7.2 of the ISA. Additional evidence discussing potential mechanisms underlying 

15 cardiovascular effects are discussed more fully in sections 5.2 through 5.6 of the ISA. 

16 The ISA notes extended analyses of studies available in the last review as well as new 

17 epidemiologic studies conducted in the U.S. and abroad provide stronger evidence of respiratory18 related morbidity associated with long-term PM2.5 exposure. As mentioned above, more limited 

19 data are available for respiratory-related mortality effects. Considering morbidity and mortality 

20 effect collectively, the ISA has concluded that there is continued support for a likely causal 

21 association between long-term PM2.5 exposures and respiratory effects. The strongest evidence 

22 for respiratory-related effects available in this review is from studies that have evaluated 

23 decrements in lung function growth, increased respiratory symptoms, and asthma development 

(U.S. EPA, 2009a, sections 2.3.1.2, 7.3.1.1, and 7.3.2.1).7 24 Specifically, extended analyses of the 

25 Southern California Children’s Health Study (CHS) provide evidence that clinically important 

deficits in lung function8 26 associated with long-term exposure to PM2.5 persisted into early 

 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 compartmentalization, (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 well 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 observed associations between long-term exposure to PM10 and an 

increase in respiratory symptoms and reductions in lung function grown in areas where PM10 is dominated by PM2.5” 

(US EPA, 2009a, p. 2-12). 8 Clinical significance was defined as a FEV1 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

1 adulthood (U.S., EPA, 2009a, p. 7-27; Gauderman et al., 2004). Additional analyses of the CHS 

2 cohort report an association between long-term PM2.5 exposure and bronchitic symptoms (US 

3 EPA, 2009a, p. 7-24; McConnell et al., 2003) and a strong modifying effect on the association 

4 between lung function with asthma incidence (US EPA, 2009, 7-25; Islam et al., 2007). The 

5 strength and robustness of the outcomes observed in these more recent reports from the Southern 

6 California CHS, including evaluation of a broader range of endpoints than previous CHS studies 

7 with shorter follow-up periods, were larger in magnitude and more precise. Supporting these 

8 results are new longitudinal cohort studies conducted by other researchers in varying locations 

9 using different methods (U.S. EPA, 2009a, section 7.3.9.1). New evidence from a U.S. cohort of 

10 cystic fibrosis (CF) patients provides evidence of association between long-term PM2.5 exposures 

11 and exacerbations of respiratory symptoms resulting in hospital admissions or use of home 

12 intravenous antibiotics (US EPA, 2009a, p. 7-25; Goss et al., 2004). 

13 Toxicological studies provide coherence and biological plausibility for the respiratory 

14 effects observed in epidemiological studies (US EPA, 2009a, p. 7-42). For example, pre- and 

15 postnatal exposure to ambient levels of urban particles has been found to affect lung 

16 development in an animal model (US EPA, 2009a, section 7.3.2.2; p. 7-43). This finding is 

17 important because impaired lung development is one mechanism by which PM exposure may 

18 decrease lung function growth in children (US EPA, 2009a, p. 2-12; section 7.3). Subchronic 

19 and chronic toxicological studies of concentrated ambient particles (CAPs) as well as evaluations 

20 of specific sources of fine particles including, diesel exhaust (DE), roadway air, and woodsmoke 

21 provide some evidence for altered pulmonary function, mild inflammation, oxidative responses, 

22 immune suppression, and histopathologic changes. In addition, exacerbated allergic responses 

23 have been observed in animals exposed to DE and wood smoke (US EPA, 2009a, p. 2-12, 

24 section 7.3). 

25 With respect to respiratory-related mortality associated with long-term PM2.5 exposure, 

26 evidence is “limited and inconclusive” (US EPA, 2009a, p. 7-41). The extended follow-up of the 

27 Harvard Six Cities study reports a positive but non-statistically significant association between 

28 long-term PM2.5 exposure and respiratory-related mortality (Laden et al., 2006). Pope et al. 

29 (2004) found no association with long-term PM2.5 exposure and respiratory-related mortality (US 

30 EPA, 2009a, p. 7-84). There is emerging but limited evidence for an association between long31 term PM2.5 exposure and respiratory mortality in post-neonatal infants where long-term exposure 

32 was considered as approximately one month to one year (US EPA, 2009a, pp. 7-54 to 7-55). 

33 Emerging evidence of short- and long-term exposure to PM2.5 and respiratory morbidity effects 

34 and infant mortality are coherent with the weak respiratory mortality effects observed. 

35 Beyond effects considered to have causal or likely causal associations with long-term 

36 PM2.5 exposure as discussed above, the ISA also notes health outcomes classified as having 
Draft Do Not Quote or Cite March 2010 2-21

1 evidence suggestive of a causal association with long-term PM2.5 exposure. This includes two 

2 broad categories of health outcomes: (1) reproductive and developmental effects and (2) cancer, 

3 mutagenicity, and genotoxicity effects (US EPA, 2009a, Table 2-6). With respect to 

4 reproductive and developmental effects, the ISA notes, “[e]vidence is accumulating for PM2.5 

5 effects on low birth weight and infant mortality, especially due to respiratory causes during the 

6 post-neonatal period” (US EPA, 2009a, section 2.3.1.2). New evidence available in this review 

7 reports a significant association between exposure to PM2.5 during pregnancy and lower birth 

8 weight, pre-term birth, and intrauterine growth restriction, respectively, and post-natal exposure 

9 to PM2.5 associated with an increased risk of infant mortality (US EPA, 2009a, section 7.4). The 

10 ISA further notes that “[i]nfants and fetal development processes may be particularly vulnerable 

11 to PM exposure, and although the physical mechanisms are not fully understood, several 

12 hypotheses have been proposed involving direct effects on fetal health, altered placenta function, 

13 or indirect effects on the mother’s health” (US EPA, 2009a, section 7.4.1). However, 

14 toxicological studies provide some evidence which is coherent with an association between long15 term PM2.5 exposure and adverse reproductive and developmental outcomes, but provide “little 

16 mechanistic information or biological plausibility for an association between long-term PM 

17 exposure and adverse birth outcomes (e.g., low birth weight or infant mortality)” (US EPA, 

18 2009a, p. 2-13). 

19 With respect to cancer, mutagenic and genotoxic effects, “[m]ultiple epidemiologic 

20 studies have shown a consistent positive association between PM2.5 and lung cancer mortality, 

21 but studies have generally not reported associations between PM2.5 and lung cancer incidence” 

22 (US EPA, 2009a, sections 2.3.1.2 and 7.5; Table 7-7; Figures 7-6 and 7-7). The extended 

23 follow-up to the ACS study reported an association between long-term PM2.5 exposure and lung 

24 cancer mortality (US EPA, 2009a, p. 7-71; Krewski et al., 2009). The extended follow-up of the 

25 Harvard Six Cities study also evaluated lung cancer mortality and reported a positive association 

26 when considering the entire 25-year follow-up period. However, estimated decreases in average 

27 PM2.5 concentrations between the first and second follow-up periods were not associated with 

28 reduced lung cancer mortality (US EPA, 2009a, p. 7-71; Laden et al, 2006). Epidemiological 

29 evidence is not currently available to evaluate cancer in organs or systems other than the lung 

30 related to long-term exposure to PM2.5 (US EPA, 2009a, p. 7-81). There is some evidence, 

31 primarily from in vitro studies, providing biological plausibility for the PM-lung cancer 

32 relationships observed in epidemiological studies (US EPA, 2009a, p. 7-80). Toxicological 

33 studies providing evidence of carcinogenicity, mutagenicity, and genotoxicity reported mixed 

34 results as discussed in section 7.5 of the ISA. 

35 Health Effects Associated with Short-term PM2.5 Exposure
Draft Do Not Quote or Cite March 2010 2-22

1 In considering effects associated with short-term PM2.5 exposure, the body of currently 

2 available scientific evidence has been expanded greatly by the publication of a number of new 

3 multi-city time-series studies that have used uniform methodologies to investigate the effects of 

4 short-term fine particle exposures on public health. This body of evidence provides a more 

5 expansive data base and considers multiple locations representing varying regions and seasons 

6 that provide evidence on the influence of climate and air pollution mixes on PM2.5-associated 

7 health effects. These studies provide more precise estimates of the magnitude of effects 

8 associated with short-term PM2.5 exposure than most smaller-scale single-city studies that were 

9 more commonly available in the last review (U.S. EPA 2009a, chapter 6). 

10 With regard to mortality effects, looking broadly across all of the available scientific 

11 evidence, the ISA concludes that a causal association exists between short-term PM2.5 exposure 

12 and premature death. Extended and expanded analyses of multi-city studies available in the last 

13 review as well as a large number of new U.S. multi-city and single-city short-term PM2.5

14 exposure studies have found generally consistent positive associations between short-term PM2.5 

15 exposures and cardiovascular- and respiratory-related mortality as well as all-cause (non16 accidental) mortality (US EPA, 2009a, sections 2.3.1.1, 6.2.11 and 6.5.2.2; Figures 6-26, 6-27, 

17 and 6-28). These newly published U.S. multi-city short-term PM2.5 exposure studies provide a 

18 much larger body of evidence since the last review. In an analysis of National Morbidity, 

19 Mortality, and Air Pollution Study (NMMAPS) data, Dominici et al. (2007) reported 

20 associations between fine particle exposures and all-cause and cardio-respiratory mortality (US 

21 EPA, 2009a, p. 6-175, Figure 6-26). A Canadian multi-city study available in the last review 

22 was expanded from 8 to 12 cities (Burnett and Goldberg, 2003; Burnett et al., 2004). The results 

23 of this expanded analysis were consistent with the earlier findings of a positive and statistically 

24 significant association between short-term PM2.5 exposure and mortality (US EPA, 2009a, p 6-

25 182, Figure 2-1). However, the influence of NO2 and limited PM2.5 data for several years during 

26 the study period somewhat diminish these findings and underscore the need for additional data 

27 on the co-pollutants in relation to the PM2.5-mortality association. Zanobetti and Schwartz 

28 (2009) reported positive (99%) and frequently statistically significant (55%) associations across 

29 most of the 112 cities between short-term PM2.5 exposure and total, cardiovascular-related, and 

30 respiratory-related mortality (US EPA, 2009a, pp 6-176 to 6-179; Figures 6-23 and 6-24). 

31 Collectively, these studies provide generally consistent and much stronger evidence than the 

32 evidence available in the last review. 

33 With respect to cardiovascular effects, the ISA considers both cardiovascular-related 

34 mortality as well as cardiovascular morbidity effects in reaching the conclusion that there is a 

35 causal association between short-term PM2.5 exposure and cardiovascular effects. New multi36 city as well as single-city short-term PM2.5 exposure studies conducted since the prior review 
Figure 2-1. Summary of Effect Estimates (per 10 μg/m3) and Air Quality Distributions for Long-term Exposure Studies 

Study Outcome Mean 

(SD)

Mean 

– 1SD Lower IQR Range Effect Estimate (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 – 28.3 Eftim et al. (2008) All-Cause Mortality, ACS Sites 13.6 (2.8) 10.8 6.0-25.1 Goss et al. (2004) All-Cause Mortality 13.7 (4.2) 9.5 11.8 11.8-15.9 McConnell et al. (2003) Bronchitis (Children) 13.8 (7.7) 6.1 6-29 Zeger 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 5.8-22 Eftim et al. (2008) All-Cause Mortality, Harv 6-Cities 14.1 (3.1) 11.0 9.6-19.1 Lipfert 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 5.8-20.7 Woodruff et al. (2008) Infant Mortality (Respiratory) 14.9**** 12.0 Laden et al. (2006) All-Cause Mortality 16.4 (5.6)* 10.8 10-22 Woodruff et al. (2006) Infant Mortality (Respiratory) 19.2 Enstrom (2005) All-Cause Mortality 23.4 Chen et al. (2005) CHD Mortality, Females 29.0 

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 Ratio 

Modified from Figure 2-2, US EPA, 2009a. 
Draft Do Not Quote or Cite March 2010 2-24

1 support a largely positive and frequently statistically significant relationship between short-term 

2 exposure to PM2.5 and cardiovascular-related disease, substantiating prior findings of a positive 

3 relation between exposure to fine particles and cardiovascular morbidity. For example, short4 term exposure to PM2.5 in association with cardiovascular and respiratory effects was evaluated 

5 among a multi-city cohort of older adults participating in the Medicare Air Pollution Study 

6 (MCAPS) (US EPA, 2009a, pp. 6-57 to 58; Dominici et al, 2006a; Bell et al, 2008). Overall, 

7 short-term PM2.5 exposure studies available in the current review provide consistent evidence of 

8 a positive association between short-term PM2.5 exposures and hospital admissions (HA) or 

9 emergency department (ED) visits as well as premature mortality related to cardiovascular 

10 outcomes. The strongest evidence has been observed for cardiovascular morbidity effects 

11 predominately associated with HA and ED visits reported for ischemic heart disease (IHD) and 

12 congestive heart failure (CHF) and cardiovascular-related mortality (US EPA, 2009a, Figure 2-1, 

13 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 

14 et al., 2007; Zanobetti and Schwartz, 2009). Furthermore, these findings are supported by a 

15 recent study of a multi-city cohort of women participating in the Women’s Health Initiative that 

16 reported a non-significantly association between short-term exposure to PM2.5 and myocardial 

17 ischemia (Zhang et al., 2009). 

18 In focusing on respiratory effects, the ISA integrates evidence of respiratory-related 

19 mortality with respiratory morbidity effects to reach the conclusion that there is a likely causal 

20 association between short-PM2.5 exposure and respiratory effects. The strongest evidence from 

21 short-term PM2.5 exposure studies has been observed for respiratory-related ED visits and HAs 

22 for chronic obstructive pulmonary disease (COPD) and respiratory infections (U.S. EPA, 2009a, 

23 sections 2.3.1.1 and 6.3.8.3; Figures 2-1 and 6-13; Dominici et al., 2006a;). Evidence for PM2.5-

24 related respiratory effects has also been observed in panel studies, which indicate associations 

25 with respiratory symptoms, pulmonary function, and pulmonary inflammation among asthmatic 

26 children. Although not consistently observed, some controlled human exposure studies have 

27 reported small decrements in various measures of pulmonary function following controlled 

28 exposures to PM2.5 (US EPA, 20009a, p. 2-10). Furthermore, the comparatively larger body of 

29 toxicological evidence since the last review is coherent with short-term exposures to PM2.5 and 

30 respiratory effects (US EPA 2009a, section 6.3.10.1). 

31 

32 Summary

33 In considering the extent to which newly available scientific evidence strengthens or calls 

34 into question evidence of associations identified in the last review between ambient fine particle 

35 exposures and health effects, we recognize that much progress has been made in assessing some 

36 key uncertainties related to our understanding of health effects associated with short- and long-
Draft Do Not Quote or Cite March 2010 2-25

1 term exposure to PM2.5. As briefly discussed above as well as in the more complete discussion of 

2 the evidence as assessed in the ISA, we note that the newly available information combined with 

3 information available in the last review provides substantially stronger confidence in a causal 

4 association between short- and long-term exposures to PM2.5 and mortality and cardiovascular 

5 effects. In addition, the newly available evidence reinforces and expands the evidence 

6 supporting the likely causal nature of the associations between short- and long-term exposure to 

7 PM2.5 and respiratory effects. Causal inferences, as discussed in the ISA, are based not only on 

8 the more expansive epidemiological evidence available in this review but also reflects 

9 consideration of important progress that has been made to advance our understanding of a 

10 number of potential biologic modes of actions or pathways for PM-related cardiovascular and 

11 respiratory effects (US EPA 2009a, chapter 5). With respect to suggestive evidence for a 

12 broader range of effects, the body of scientific evidence is somewhat expanded but is still limited 

13 with respect to associations between long-term PM2.5 exposures and developmental and 

14 reproductive effects as well as cancer, mutagenic, and genotoxic effects. Thus, we reach the 

15 preliminary conclusion that there is stronger and more consistent and coherent support for 

16 associations between short- and long-term PM2.5 exposure and a broader range of health 

17 outcomes than was available in the last review, providing the basis for fine particles at least as 

18 protective as the current PM2.5 standards. 

19 Having reached this initial conclusion, we then consider how the new evidence informs 

20 our understanding of susceptible populations by asking the following question: 

21  To what extent does the newly available scientific evidence expand our understanding 

22 of susceptible populations, including identification of new susceptible populations? 

23 As an initial matter, interindividual variation in human responses to air pollutants 

24 indicates that some population groups are at increased risk for the detrimental effects of ambient 

exposure to PM.9 25 To facilitate the identification of populations at greatest risk for PM-related 

26 health effects, studies have evaluated factors that contribute to the susceptibility or vulnerability 

27 of an individual to PM. The definition for both of these terms has been found to vary across 

28 studies, but in most instances susceptibility refers to biological or intrinsic factors (e.g., lifestage, 

29 gender) while vulnerability refers to non-biological or extrinsic factors (e.g., socioeconomic 

30 status [SES]) (see US EPA, 2009a, Table 8-1). However, in many cases a factor identified that 

31 increases an individual's risk for morbidity or mortality effects from exposure to an air pollutant 

32 (e.g., PM) cannot be easily categorized as a susceptibility or vulnerability factor. At times, the 

33 terms susceptibility and vulnerability cannot be distinguished from one another. As it has been 

 9

 Although studies have primarily used exposures to PM10 or PM2.5, the available evidence suggests that the 

identified factors also increase risk from PM10-2.5 (US EPA, 2009a, section 8.1.8). 
Draft Do Not Quote or Cite March 2010 2-26

1 defined in the ISA (US EPA, 2009a, p. 8-1), the term “susceptible” encompasses both these 

2 concepts. This document maintains that definition. 

3 The 2004 AQCD noted that the existence of heart and lung disease was clearly linked 

4 with increased susceptibility to effects from PM exposure, based on epidemiological and 

5 toxicological studies along with dosimetric evidence. The epidemiological evidence for 

6 increased susceptibility to PM in this population was primarily derived from studies of short7 term exposure. Long-term exposure studies suggested that PM may result in chronic respiratory 

8 disease or decreased lung function growth, thereby increasing susceptibility to short-term 

9 changes in PM. It was also noted that studies available at that time supported considering older 

10 adults and children, including possibly infants, as susceptible groups, recognizing that there is 

11 likely overlap between age categories and the preexistence of cardiopulmonary diseases. 

12 Emerging evidence indicated that people of lower (SES) or people who have particularly 

13 elevated exposures, due to factors such as residential location, may be at greater risk of PM14 related effects. The evidence available at that time did not generally allow distinctions to be 

15 drawn between the PM indicators, in terms of which groups might be more susceptible to PM2.5

16 and/or PM10-2.5. 

17 As discussed below, the ISA concludes that the epidemiological, controlled human 

18 exposure and toxicological studies continue to provide evidence of increased risk for various 

19 populations, including people at certain life stages, in this case children and older adults, people 

20 with pre-existing cardiovascular and respiratory diseases (e.g., asthma), and people with lower 

21 SES (US EPA, 2009a, section 2.4.1, chapter 8). This section expands on the discussion in the 

22 ISA of susceptible populations in that it also considers supporting evidence for increased risk in 

23 these populations from studies that examined only one susceptible population. However it does 

24 not contain information from the ISA for potentially susceptible populations for which there was 

25 not sufficient evidence to it to draw conclusions about increased susceptibility (e.g., people with 

26 diseases that involve chronic inflammation, such as diabetes, or with genetic susceptibility). 

27 Children and Older Adults 

28 Childhood represents a life stage that has generally been considered susceptible to 

29 exposure to PM due to the following factors: children spend more time outdoors; children have 

30 greater activity levels than adults; children have exposures resulting in higher doses per body 

31 weight and lung surface area; and also because of the potential for irreversible effects on the 

32 developing lung (US EPA, 2009a, section 8.1.1.2). Recent studies of long-term exposure to 

33 PM2.5 have greatly expanded the evidence for effects on lung development in children. The 

34 extended follow-up for the Southern California CHS includes several new studies that report 

35 positive associations between long-term exposure to PM2.5 and respiratory morbidity, 

36 particularly for such endpoints as lung function growth, respiratory symptoms (i.e., bronchitic 
Draft Do Not Quote or Cite March 2010 2-27

1 symptoms), and respiratory disease incidence (US EPA, 2009a, section 7.3; Gauderman et al., 

2 2004). New analyses have been conducted that include longer follow-up periods of the CHS 

3 cohort through 18 years of age, provide evidence that effects from exposure to PM2.5 persist into 

4 early adulthood and are more robust and larger in magnitude than reported for shorter follow-up 

5 periods available in 2004. Supporting these results are new cohort studies conducted by other 

6 researchers in other locations with different methods that provide enhanced evidence for 

7 respiratory effects related to long-term exposures to PM10 that is dominated by PM2.5 (US EPA, 

8 2009a, section 7.3). New studies provide positive associations from Mexico City, Sweden, and a 

9 national cystic fibrosis cohort in the U.S. A natural experiment in Switzerland reported that 

10 improving PM air quality may slow the annual rate of decline in lung function in adulthood, 

11 indicating benefits to public health. In addition, investigators of the CHS suggest PM2.5 may also 

12 act as a modifier of the association between lung function and asthma, inducing declines in lung 

13 function and a concomitant increase in new onset asthma (Islam et al 2007). Thus, the ISA (US 

14 EPA, 2009a, section 7.3.9.1) concludes that the data for respiratory morbidity in children are 

15 consistent and coherent across several study designs, locations, and researchers. Preliminary 

16 evidence from toxicological studies provides some coherence and biological plausibility for the 

17 observed associations with lung function decrements (US EPA, 2009a, section 7.3.2.2). 

18 With respect to short-term exposures to PM, the 2004 AQCD found that studies which 

19 stratified results by age typically reported associations between short-term exposures to PM and 

20 respiratory-related health effects in children with asthma (US EPA, 2004, section 8.4.9). This 

21 body of evidence has been strengthened by newly available epidemiological studies that provide 

22 evidence of reductions in lung function (FEV1) and an increase in respiratory symptoms and 

23 medication use associated with PM exposure among asthmatic children (US EPA, 2009a, 

24 sections 6.3.1 and 6.3.2.1). These include two large, longitudinal studies in urban areas of the 

25 US, as well as a number of smaller panel studies conducted in the U.S. (US EPA, 2009a, section 

26 6.3.1). 

27 No epidemiologic studies of pulmonary inflammation were described in the 2004 AQCD. 

28 Several new panel studies of children, using exhaled NO (eNO) as a biomarker of airway 

29 inflammation, found generally positive associations between PM exposure and eNO levels in 

30 asthmatic children who did not use inhaled corticosteroids (US EPA, 2009a, section 6.3.3.1). 

31 With respect to short-term increases in PM concentrations associated with respiratory32 related hospitalizations and ED visits, the epidemiologic evidence presented in the 2004 AQCD 

33 was consistent across studies (US EPA, 2004, section 8.3.2.5). Newly available evidence 

34 provides further support for this relationship, with larger effect estimates observed among 

35 children and older adults. However, effect estimates are clearly heterogeneous and sensitive to 
Draft Do Not Quote or Cite March 2010 2-28

1 choice of lag, with evidence of both regional and seasonal differences (US EPA, 2009a, sections 

2 6.3.8 and 6.3.10). 

3 Two recent toxicological studies, presented in the ISA (US EPA, 2009a, section 8.1.1.2), 

4 provide biological plausibility for the increase in PM-related respiratory effects in children 

5 observed in the epidemiological studies. These studies include effects on lung function, 

6 pulmonary injury and evidence suggesting that the developing lung is more susceptible to PM. 

7 The ISA (US EPA, 2009a, p. 8-5) concludes that the evidence from epidemiological studies that 

8 have examined the health effects associated with all size fractions of PM and toxicological 

9 studies that have examined individual PM components provide support for the hypothesis that 

10 children are at greater risk of respiratory effects from exposure to PM. 

11 With respect to older adults, the 2004 AQCD (US EPA, 2004, section 9.2.4.2) concluded 

12 that people aged 65+ years appear to be at somewhat higher risk for PM exacerbation of 

13 cardiovascular-related disease effects and, perhaps, tend to experience higher PM-related total 

14 (nonaccidental) mortality risk, as well. The higher prevalence of pre-existing cardiovascular and 

15 respiratory diseases found in this age range compared to younger age groups increases risk, 

16 primarily due to the gradual decline in physiological processes as part of the aging process (US 

17 EPA, 2009a, section 8.1.1.1). Therefore, some overlap exists between this life stage and the 

18 group of people with pre-existing diseases. 

19 Newly available evidence for PM-related health effects in the older adult life stage spans 

20 epidemiologic, controlled human exposure, and toxicological studies (US EPA, 2009a, section 

21 8.1.1.1). One new large epidemiologic study (US EPA, 2009a, section 7.2.9; Miller et al., 2007) 

22 of post-menopausal female residents of 36 U.S. metropolitan areas (age range = 50-79 yr) found 

increases in PM2.5-related risk of MI, coronary revascularization,10 23 and their combination with 

24 CHD-related death for participants free of CVD at baseline. While recent epidemiological 

25 evidence for cardiovascular morbidity effects in older adults in response to short-term exposure 

26 to PM2.5 and PM10-2.5 is limited, when taken together with evidence from studies of PM10, 

27 support is found for increased risk of cardiovascular morbidity in older adults. With regard to 

28 respiratory morbidity, while some epidemiologic studies have reported an increase in respiratory 

29 hospital admissions in individuals 65 years of age and older, consistent associations have not 

30 been observed across all such studies. 

31 With respect to mortality, recent epidemiologic studies have also found that individuals 

32 greater than 65 years old are at greater risk of all-cause (non-accidental) mortality upon short33 term exposure to both PM2.5 and PM10, consistent with the findings of the 2004 AQCD. 

34 Epidemiological studies that examined the association between mortality and long-term exposure 

 10 Coronary revascularization includes percutaneous coronary interventions, such as angioplasty. 
Draft Do Not Quote or Cite March 2010 2-29

1 to PM2.5 and stratified the results by age (i.e., less than 65 year of age compared to aged 65 and 

2 older) reported results that are consistent with the short-term exposure studies. However, in 

3 sensitivity analyses studies have found evidence that risk declines with age starting at age 60 

4 until there is no evidence of an association among people age 85 and older. 

5 Controlled human exposure and dosimetry studies provide additional evidence for an 

6 increase in cardiovascular and respiratory effects among older adults. Healthy older subjects 

7 exposed to PM2.5 concentrated ambient particles (CAPs) experienced significant decreases in 

8 HRV (both in time and frequency) immediately following exposure, when compared to healthy 

9 young subjects and to older adults with COPD (US EPA, 2009a, section 8.1.1.1). Dosimetry 

10 studies have shown a depression of fine and coarse PM clearance in all regions of the respiratory 

11 tract with increasing age beyond young adulthood. These results suggest that older adults are at 

12 greater risk of PM-related respiratory health effects (US EPA, 2009a, section 8.1.1).

13 Animal toxicological studies have attempted to characterize the relationship between age 

14 and PM-related health effects through the development of models that mimic the physiologic 

15 conditions associated with older people. For example, arrhythmias have been observed in older, 

16 but not younger, rats exposed to PM2.5 CAPs. In addition, studies that used a mouse model of 

17 terminal senescence observed various cardiovascular-related responses. Overall, these studies 

18 provide biological plausibility for the increase in cardiovascular effects in older adults observed 

19 in the controlled human exposure and epidemiologic studies (US EPA, 2009a, section 8.1.1). 

20 In summary, the ISA concludes that evidence from epidemiological, controlled human 

21 exposure, and toxicological studies provide coherence and biological plausibility for the 

22 association between short-term exposure to PM and cardiovascular morbidity in older adults (US 

23 EPA, 2009a, section 8.1.1.1). Additional evidence from epidemiological studies that focus on 

24 mortality and respiratory morbidity in response to short-term exposure to PM also indicate that 

25 older adults represent a susceptible life stage. 

26 Pre-existing Cardiovascular or Respiratory Diseases

27 With regard to the risk from PM exposure to people with pre-existing cardiovascular or 

28 respiratory diseases, the 2004 AQCD (US EPA, 2004, section 9.2.4.1) noted that a number of 

29 time-series epidemiological studies reported increased risk in study subsets of individuals with 

30 preexisting heart or lung diseases. Toxicological studies using animal models of 

31 cardiopulmonary disease provided evidence suggestive of enhanced susceptibility to inhaled PM 

32 in “compromised” hosts. Human dosimetry studies of subjects with COPD and asthma indicated 

33 that airways disease leads to very heterogeneous distributions of PM deposited within the lung. 

34 These studies have shown up to 10-fold higher than normal deposition at airway bifurcations, 

35 thus creating “hot-spots” that may have biological implications. 
Draft Do Not Quote or Cite March 2010 2-30

1 The ISA notes that more recent epidemiological and controlled human exposure studies 

2 have directly examined the effect of PM on individuals with pre-existing diseases and 

3 toxicological studies have employed disease models to identify whether exposure to PM 

4 disproportionately effects certain populations (US EPA, 2009a, section 8.1.6). 

5 The potential effect of underlying cardiovascular diseases on PM-related health responses 

6 has been examined using epidemiological studies that stratify effect estimates by underlying 

7 conditions or secondary diagnoses, and toxicological studies that use animal models to mimic the 

8 pathophysiological conditions associated with various cardiovascular diseases (e.g., MI, 

9 ischemia, and atherosclerosis). A limited number of controlled human exposure studies have 

10 also examined the potential relationship between cardiovascular diseases and exposure to PM in 

11 individuals with underlying cardiovascular conditions, but these studies have provided somewhat 

12 inconsistent evidence for these associations. 

13 One epidemiological study (US EPA, 2009a, section 7.2.9; Zanobetti and Schwartz, 

14 2007) investigated associations between long-term exposure to PM10 and the progression of 

15 disease or reduced survival in a 21-city study of people discharged following an acute 

16 myocardial infarction (MI). The study found significant associations for mortality, CHF and 

17 new hospitalization for MI. This is the first long-term study showing a significant association 

18 between particle exposure and adverse post-MI outcomes in people who survived an MI. A few 

19 toxicological studies examined potential effect modification of pre-existing cardiovascular 

20 conditions on effects of long-term exposure to PM. In studies that focused on the cardiovascular 

effects following subchronic exposure to PM in ApoE-/- 21 mice, pathophysiological effects were 

22 observed that included a decreasing trend in heart rate, physical activity, and temperature along 

23 with responses in HRV; enhanced size of early atherosclerotic lesions was observed consistently 

24 across studies. 

25 The majority of the epidemiological literature that examined associations between short26 term exposure to PM and cardiovascular outcomes focuses on cardiovascular-related hospital 

27 admissions (HA) and emergency department (ED) visits. Hypertension is the pre-existing 

28 condition that has been considered to the greatest extent when examining the association 

29 between short-term exposure to PM and cardiovascular-related HAs and ED visits. The results 

30 of these studies have been mixed. There is also some new evidence from epidemiological 

31 studies that individuals with pre-existing IHD are at greater risk from PM exposure, with 

32 evidence from a toxicological study implicating impaired myocardial blood flow in the response. 

33 Additional studies have examined the effects of PM on cardiac function in individuals with 

34 dysrhythmia with mixed results. Limited and inconclusive evidence is available from 

35 epidemiological studies that examined other pre-existing cardiovascular conditions, such as CHF 

36 and MI. Toxicological studies have provided some additional evidence for the cardiovascular 
Draft Do Not Quote or Cite March 2010 2-31

1 health effects associated with exposure to PM in rodent models of underlying MI, but the 

2 evidence is also inconclusive. Controlled human exposure studies that examined the effect of 

3 pre-existing diseases on cardiovascular outcomes with exposure to PM are less consistent and 

4 difficult to interpret in the context of the results from the epidemiological and toxicological 

5 studies. 

6 A few new studies have also examined effect modification in mortality associations. 

7 These studies have found evidence of an increase in risk estimates for associations between PM10

8 and mortality in individuals with underlying stroke, and effect modification of the PM-mortality 

9 association in individuals with CHF. 

10 In summary, the newly available evidence from epidemiological and toxicological, and to 

11 a lesser extent, controlled human exposure studies indicates increased susceptibility of 

12 individuals with underlying cardiovascular diseases to PM exposure. Although the evidence for 

13 some outcomes was inconsistent across epidemiological and toxicological studies, this could be 

14 due to a variety of issues including the PM size fraction used in the study, along with the study 

15 location. 

16 With regard to pre-existing respiratory illnesses, studies evaluated in the ISA have 

17 examined the effect of these illnesses on multiple health outcomes (e.g., mortality, asthma 

18 symptoms) in response to exposure to ambient concentrations of PM (US EPA, 2009a, section 

19 8.1.6.2). Epidemiological studies have examined the effect of short-term exposure to PM on the 

20 respiratory health of asthmatic individuals finding an increase in medication use and respiratory 

21 symptoms (i.e., asthma symptoms, cough, shortness of breath, and chest tightness) with short22 term exposure to PM2.5, and morning symptoms and asthma attacks with short-term exposure to 

23 PM10. Toxicological studies provide evidence that PM exposure results in allergic sensitization, 

24 and that individuals with allergic airways conditions are at greater risk of allergic airways 

25 responses upon exposure to PM2.5. Further, there is much more limited evidence which suggests 

26 that non-allergic respiratory morbidities may also increase the susceptibility of an individual to 

27 PM-related respiratory effects. 

28 The results from the epidemiological and toxicological studies that focused on underlying 

29 allergic airways disease are supported by a series of controlled human exposure studies which 

30 have shown that exposure to diesel exhaust particles (DEPs) increases the allergic inflammatory 

31 response in atopic individuals. However, other studies reported that healthy and asthmatic 

32 subjects exposed to coarse, fine and ultrafine CAPs, exhibited similar respiratory responses, 

33 although these studies excluded moderate and severe asthmatics that would be expected to show 

34 increased susceptibility to PM exposure. 

35 With respect of pre-existing COPD, the results of epidemiological studies have been 

36 mixed. A few controlled human exposure studies examined the effects of exposure to PM2.5 
Draft Do Not Quote or Cite March 2010 2-32

1 CAPs on healthy and COPD subjects and found no significant difference in respiratory effects. 

2 However, the results from dosimetric studies have shown that COPD patients have increased 

3 dose rates and impaired mucociliary clearance relative to age-matched healthy subjects, 

4 suggesting that individuals with COPD are potentially at a greater risk of PM-related health 

5 effects (US EPA, 2009a, section 3.2.1). 

6 A few epidemiological studies examined the effect of underlying respiratory illnesses on 

7 the association between short- and long-term exposure to PM and mortality. Using different 

8 pre-existing respiratory illnesses, two studies found that short-term exposure to PM10 increased 

9 the risk of non-accidental mortality in individuals with a secondary diagnosis of pneumonia and 

10 circulatory mortality in individuals with a secondary diagnosis of a respiratory illnesses. Another 

11 study observed an association between long-term exposure to PM10 and mortality in individuals 

12 that had previously been hospitalized for COPD. Together, these studies show the potential 

13 effect of underlying respiratory illnesses on the PM-mortality relationship (US EPA, 2009a, p. 8-

14 13). 

15 In summary, with respect to the potential for increased risk from PM exposure to people 

16 with respiratory disease, overall, the controlled human exposure and toxicological studies 

17 evaluated in the ISA provide biological plausibility for the increased risk of health effects 

18 observed in epidemiological studies among asthmatic individuals in response to PM exposure 

19 (US EPA, 2009a, section 8.1.6.2). The evidence from studies that examined associations 

20 between PM and health effects in individuals with COPD is inconsistent. 

21 Socioeconomic Status

22 Socioeconomic status is a composite measure that usually consists of economic status, 

23 measured by income; social status measured by education; and work status measured by 

24 occupation. Based on data from the U.S. Census Bureau in 2006, from among commonly-used 

25 indicators of SES, about 12% of individuals and 11% of families are below the poverty line (US 

26 EPA, 2009a, section 8.1.7). Within the U.S. approximately 16% of the population does not have 

27 a high school degree and only 27% have a bachelor’s degree or higher level of education (US 

28 Census, 2009). Educational attainment generally coincides with an individual’s income level, 

29 which is correlated to other surrogates of SES, such as residential environment. Additionally, 

30 low SES individuals have been found to have a higher prevalence of pre-existing diseases; 

31 limited access to medical treatment; and limited access to fresh foods leading to a reduced intake 

32 of antioxidants, polyunsaturated fatty acids and vitamins, which can increase this population 

33 group’s risk from PM. Low SES and surrogates of SES such as educational attainment, 

34 residential location and nutritional status have been shown in some studies to modify health 

35 outcomes of PM exposure for a population. 
Draft Do Not Quote or Cite March 2010 2-33

1 The 2004 AQCD concluded there is effect modification of long-term PM exposures2 mortality associations due to socioeconomic factors. In the ACS and Harvard Six Cities cohort 

3 analyses on mortality risk with long-term exposure to PM2.5, there was clear evidence of greater 

4 effects being reported in the cohort subgroups with lower education levels (US EPA 2004, 

5 section 9.2.4.5). The ISA concludes that this is further supported by a reanalysis of the ACS 

6 cohort (Krewski et al., 2009), which found moderate evidence for increased lung cancer 

7 mortality in individuals with a high school education or less in response to long-term exposure to 

8 PM2.5 (US EPA, 2009a, section 8.1.7). Another study examined whether long-term exposure to 

9 traffic-related pollutants varied by SES at the block group level. The authors found higher 

10 concentrations of NO2 associated with lower SES areas, which suggests that lower SES 

11 individuals are disproportionately exposed to traffic-related pollutants, including PM. 

12 Among the studies of short-term PM exposure, the 2004 CD concluded that the evidence 

13 was mixed regarding SES and PM-related health risks. New studies evaluated in the ISA 

14 indicate that evidence of the influence of SES on health outcomes related to short-term exposures 

15 is stronger (US EPA, 2009a, section 8.1.7). These include an increased risk in mortality 

16 associated with short-term exposure to PM2.5 and its components. Jerrett et al. (2004) examined 

17 the modification of short-term mortality effects due to particulate air pollution exposure by 

18 residential location in Hamilton, Canada. The authors found that the area of the city with the 

19 highest SES characteristics (measured using the surrogate educational attainment) displayed no 

20 evidence of effect modification while the area with the lowest SES characteristics had the largest 

21 health effects. Another study noted an increased risk in mortality associated with short-term 

22 exposure to PM2.5 and its components for individuals with low SES, while additional analyses 

23 stratified by education level have also observed consistent trends of increased mortality for PM2.5

24 and PM2.5 species for individuals with low educational attainment (US EPA 2009a, section 

25 8.1.7). 

26 Nutritional deficiencies have been associated with increased susceptibility to a variety of 

27 infectious diseases and chronic health effects. Low SES may decrease access to fresh food, 

28 thereby nutritional deficiencies could increase susceptibility to PM-related health effects. One 

29 study that examined the association between exposure to PM2.5 and HRV in individuals with 

30 genetic polymorphisms associated with increased risk of CVD, found that when individuals with 

31 these genetic polymorphisms increased their intake of B6, B12, or methionine, no PM2.5 effect on 

32 HRV was observed. 

33 The ISA concludes that there is evidence that SES, measured using surrogates such as 

34 educational attainment or residential location, modifies the association between PM and 

35 morbidity and mortality outcomes (US EPA, 2009a, section 8.1.8). In addition, nutritional 
Draft Do Not Quote or Cite March 2010 2-34

1 status, another surrogate of SES, has been shown to have protective effects against PM exposure 

2 in individuals that have a higher intake of some vitamins and nutrients. 

3 Summary

4 In summary, we reach the preliminary conclusion that there are several population groups 

5 that are likely to be susceptible to PM-related effects. These groups include the life stages of 

6 children and older adults, those with preexisting heart and lung diseases, and those of lower SES. 

7 We also preliminarily conclude that the available evidence does not generally allow distinctions 

8 to be drawn between the PM indicators, in terms of which groups might have greater 

9 susceptibility to PM2.5 and PM10-2.5. 

10  To what extent does the newly available scientific evidence report associations that 

11 extend to air quality concentrations that are lower than had previously been observed 

12 or that are observed in areas that would likely meet the current suite of PM2.5 

13 standards? 

14 We now focus our attention on addressing the question of whether the available evidence 

15 supports consideration of standards that are more protective than the current suite of PM2.5

16 standards. In addressing this question, we first recognize that the ISA concludes there is no 

17 evidence to support the existence of a discernable threshold below which effects would not occur 

18 (US EPA, 2009a, section 2.4.3). We consider whether new evidence provides information for 

19 health effects associated with air quality levels that are lower than had previously been observed, 

in particular to levels at or below the level of the current annual standard (15 μg/m3 20 ) and/or to 

levels at or below the level of the current 24-hour standard (35 μg/m3 21 ). As an initial matter, we 

22 first focus on levels at which effects classified as having a causal or likely causal association 

23 with PM2.5 exposure have been observed. We consider effects classified as having suggestive 

24 associations with PM2.5 exposure in section 2.3 when considering the margin of safety provided 

25 by alternative suites of standards. We have evaluated the air quality data using the forms of the 

current PM2.5 standards.11 26 

27 Associations with Long-term PM2.5 Exposure

28 With regard to mortality associated with long-term PM2.5 exposure, in the last review, the 

29 2004 AQCD placed greatest weight on the reanalyses and extensions of two prospective cohort 

30 studies, the ACS and the Harvard Six Cities studies, finding that these studies provided “strong 

31 evidence” for associations with fine particles and confirmed and strengthened the evidence 

32 available in the review completed in 1997 (US EPA, 2004, p. 9-33; Krewski et al., 2000). In the 

 11 The current form of the annual PM2.5 standard is the annual arithmetic mean, averaged over 3 years with limited 

conditions allowing spatial averaging. The current form of the 24-hour PM2.5 standard is the 98th percentile, 

averaged over 3 years. 
Draft Do Not Quote or Cite March 2010 2-35

1 current review, as stated above, staff notes that newly available extended follow-up analyses of 

2 the ACS and Harvard Six Cities studies provide consistent and stronger evidence of a causal 

3 association with mortality at lower air quality distributions of PM2.5. 

4 In considering studies of the ACS cohort, in the last review, the original and reanalysis 

5 studies reported significant associations between fine particles and mortality (US EPA, 2004, 

6 8.2.3.2.1; Pope et al., 1995; Krewski et al., 2000). In addition, an extended analysis using the 

7 ACS cohort also available in the last review doubled the original follow-up period to more than 

8 16 years. This study continued to report statistically significant associations with long-term 

9 PM2.5 exposure with the inclusion of more recent PM2.5 air quality data and triple the number of 

10 deaths (US EPA, 2004, 8.2.3.2.2; Pope et al., 2002). As with the original ACS cohort study, no 

11 evidence of a threshold was observed in the relationships with total, cardiovascular-related, and 

12 lung cancer mortality reported in this extended study. A recent extended analysis of the ACS 

13 cohort available in this review lengthens the follow-up of this important study to 18 years (1982 

14 to 2000) (US EPA, 2009a, pp. 7-84 to 7-85; Figure 7-6; Krewski et al., 2009). This extended 

15 analysis has “confirmed with remarkable consistency the association of mortality and exposure 

16 to PM2.5 reported in previous studies of the ACS data starting 15 years ago... and added 

17 precision, especially for the evidence that ischemic heart disease is a cause of death particularly 

18 affected by exposure” to PM2.5 (HEI, 2009, p. 135). We note the decline in ambient PM2.5 

19 concentrations over 18 years, from an aggregate long-term mean in 58 metropolitan statistical 

areas (MSAs) of 21.2 (4.6)12 μg/m3

 (ranging from approximately 9 to 34 μg/m3 20 across cities) in 

21 the original monitoring period (1979 to 1983) declining to air quality distributions reported for 

22 the most recent years evaluated (1999-2000) for 116 MSAs with an aggregate long-term mean 

PM2.5 concentration of 14.0 (3.0) μg/m3 (ranging from approximately 6 to 22 μg/m3 23 across cities) 

to an overall average across all year of 17.1 (3.7) μg/m3 24 (ranging from about 7.5 to 30 

μg/m3 25 )(US EPA, 2009a, Figure 7-6; Krewski et al, 2009; Pope et. al, 2004). In addition, Eftim et 

26 al., (2008) assessed the ACS sites using an ecological cross-sectional study design of a Medicare 

27 cohort, incorporating more recent air quality (2000-2002) with an aggregate long-term mean 

PM2.5 concentration of 13.6 (2.8) μg/m3

 (ranging from approximately 6 to 25 μg/m3 28 ). This study 

29 reported somewhat higher effect estimates than those reported by the original investigators. The 

30 ISA concludes there may be several possible explanations for this apparent increase, especially 

31 that this is an older population or more likely because of the lack of personal confounder 

32 information (e.g., past personal smoking information) that “led to an insufficient control for the 

33 effects of these other variables’ effects on mortality, inflating the pollution effect estimates 

 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

1 somewhat, similar to what has been found in the ACS analyses when only ecological-level 

2 control variables were included” (US EPA, 2009a, pp. 7-87 to 7-88; Figures 7-6 and 7-7). 

3 With respect to a the Harvard Six Cities study, Laden et al (2006) have extended 

4 mortality follow-up for an additional eight years during a period of “reduced air pollution 

5 concentrations” lengthening the follow-up period to 25 years. These investigators reported 

6 statistically significant associations between long-term exposure to PM2.5 and mortality for air 

7 quality data for the original study period (1974 to 1989) as well as the extended follow-up period 

8 (1990-1998). As noted in the ISA, this study provides evidence of a statistically significant 

9 reduction in mortality risk with decreasing long-term PM2.5 concentrations (US EPA, 2009a, p. 

10 7-84). Evidence from the original and reanalysis of the Harvard Six Cities study available in the 

last review reported an aggregate long-term mean PM2.5 concentration of 18 μg/m3 11 (ranging from 

approximately 11 to 30 μg/m3 12 across cities) (US EPA, 2004, p. x.x; Dockery et al., 1993; 

13 Krewski et al., 2000). In the extended follow-up period, an aggregate long-term mean PM2.5 

concentration of 14.8 (4.2) μg/m3

 (ranging from approximately 10 to 22 μg/m3 14 across cities) with 

an overall aggregate mean across both study periods of 16.4 (5.6) μg/m3 15 (ranging from 

approximately 11 to 25 μg/m3 16 ) (US EPA, 2009a, Figure 7-6; Laden et al., 2006; Laden, 2009). 

17 This reduction was observed for total mortality as well as cardiovascular-related and respiratory18 related mortality but not deaths related to lung cancer, “a disease with a longer latency period 

19 and less reversibility” (Laden et al, 2006). The ISA notes that “a statistically significant 

20 reduction in mortality risk [was] reported with reduced long-term PM2.5 concentrations” (US 

21 EPA, 2009a, p. 7-84). These findings suggest that the mortality effects of long-term air pollution 

22 may be at least partially reversible over periods of a decade” (Laden et al., 2006; Table 3). In an 

23 additional analysis of the extended follow-up of the Harvard Six Cities cohort study, 

24 investigators reported the concentration-response relationship was linear and “clearly continuing 

25 below the level” of the current annual standard (US EPA, 2009a, p. 7-92; Schwartz et al., 2008). 

26 Eftim et al. (2008) also analyzed the Harvard Six Cities study sites using a Medicare cohort with 

27 more recent air quality data (2000-2002) and reported consistent but somewhat higher effect 

28 estimates with relation to the extended follow-up of this study conducted by Laden et al. (2006) 

29 (US EPA, 2009a, pp. 77-87-7-88, Figures 7-6 and 7-7). The aggregate long-term mean reported 

in this study was 14.1(3.1) μg/m3

 (ranging from about 10 to 19 μg/m3 30 ) (Eftim et al., 2008). 

31 In addition to extended follow-up analyses of the ACS and Harvard Six Cities studies, 

32 new evidence is available in this review from two new U.S. long-term cohort studies. The 

33 Women’s Health Initiative (WHI) provides evidence of association between long-term PM2.5 

34 exposure and cardiovascular morbidity and mortality effects. This study reported results 

35 consistent with the ACS and Harvard Six Cities studies while identifying much larger relative 

risk estimates per μg/m3 36 . This study represents an important new cohort of postmenopausal 
Draft Do Not Quote or Cite March 2010 2-37

1 women with no previous history of pre-existing cardiac disease, potentially a “healthier cohort 

2 population” than that considered by the ACS and Harvard Six Cities studies (US EPA, 2009a, p. 

3 7-87). The ISA notes, that the “PM2.5 impacts may yield higher relative risk estimates in the 

4 WHI population because the PM2.5 risk is being compared to a much lower prevailing risk of 

5 cardiovascular death in this select study population” (US EPA, 2009a, p. 7-87). The overall 

PM2.5 concentration averaged across cities reported in this study was 13.5(3.3) μg/m3 6 (ranging 

from about 3.4 to 28 μg/m3 7 ) (Miller et al., 2007). 

8 A new retrospective cohort study, the Medicare Cohort Air Pollution Study (MCAPS) 

9 has evaluated long-term PM2.5 exposure and mortality risk in older adults (65 years of age and 

10 older) within 3 geographic regions. Zeger et al. (2007) reported that long-term exposure to PM2.5

11 was significantly associated with an increase in mortality among Medicare participants, and 

12 stronger associations were observed in eastern counties compared to a national estimate, and no 

13 association was observed among Western counties. However, effect estimates decreased by 50% 

14 with adjustment for spatial confounding. In a subsequent retrospective cohort study (MCAPS), 

15 Zeger et al. (2008), reported that average 6-year exposure to PM2.5 was significantly associated 

with increased risk of mortality in the eastern and central regions.13 16 In addition, the results 

17 indicated that risk declined with increasing age, and similar to their earlier study, no association 

18 was observed between PM2.5 and mortality in the western region. Moreover, risk estimates were 

19 similar to effect estimates reported in the ACS and Harvard Six Cities study, providing 

20 coherence across prospective studies for an association between long-term exposure to PM2.5 and 

21 mortality. This study reported associations between long-term PM2.5 exposure and mortality for 

22 the eastern and central regions that were qualitatively similar to those reported in the ACS and 

23 Harvard Six Cities studies. The long-term aggregate PM2.5 median concentration reported 

across all cities was 13.2 μg/m3 (with an interquartile range from about 11 to 15 μg/m3 24 ) (US 

EPA, 2009a, p. 7-88; Zeger et al., 2008).14 25 

26 With respect to respiratory morbidity effects associated with long-term PM2.5 exposure, 

27 the 2004 AQCD concluded that new studies of a cohort of children in Southern California had 

28 built upon earlier limited evidence to provide evidence that long-term exposure to fine particles 

29 was associated with development of chronic respiratory disease and reduced lung function 

30 growth (US EPA, 2004, p. 9-33). The across-city mean of 2-week average PM2.5 concentrations 

31 reported in the initial Southern California Children’s Health Study was approximately 15.1 

 13 The Zeger et al. (2008) analysis included COPD as a proxy for smoking status. The investigators 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 PM2.5 exposure for three U.S. 

regions. Median (IQR) PM2.5 concentrations reported by region were: Eastern region - 14.0 μg/m3 (12.3-15.3); 

Central region – 10.7 μg/m3

 (9.8-12.2); Western region – 13.1 μg/m3 (10.4-18.5).
Draft Do Not Quote or Cite March 2010 2-38

μg/m3 (ranging from approximately 7 to 32 μg/m3 1 ) (Peters et al., 1999). These results were found 

2 to be consistent with results of cross-sectional analyses of the 24-City study by Dockery et al. 

3 (1996) and Raizenne et al. (1996) which reported a long-term cross-city mean PM2.5 

concentration of 14.5(4.2) μg/m3 (ranging from approximately 6 to 21 μg/m3 4 ). Gauderman et al. 

5 (2004) have now extended the analysis of the Southern California Children’s Health Study to 8 

6 years, following the children between the ages of 10 and 18, “a period of rapid lung 

7 development” and reported that the “pollution-related deficits in the average growth in lung 

8 function over the 8-year period resulted in clinically important deficits in attained lung function 

at the age of 18” (US EPA, 2009a, p. 7-27). The four year cross-city mean was 13.8 (7.7) μg/m3 9 

(ranging from approximately 6 to 29 μg/m3 10 ) across the 12 study communities (McConnell et al., 

11 2003). 

12 In summary, newly available scientific evidence provides support for associations 

13 between long-term PM2.5 exposure and mortality and morbidity effects that extend to air quality 

14 levels that are lower than had previously been observed. These studies evaluate a broader range 

15 of health outcomes than were considered in the last review and include extended follow-up for 

16 prospective epidemiological studies that were important in the last review as well as additional 

17 evidence in important new cohorts. In looking across the body of scientific evidence and 

18 focusing on the most recent years of air quality data considered in these studies, we observe 

19 effects occurring below the level of the current annual PM2.5 standard (US EPA, 2009a, chapter 

20 7; Figures 2-2 and 7-7).

21 Associations with Short-term PM2.5 Exposure

22 In the last review, in selecting the level of the 24-hour PM2.5 standard, emphasis was 

placed on short-term exposure studies and their 98th 23 percentile air quality values that provided 

24 evidence of associated health effects in areas that would have met the then current annual and 

24-hour PM2.5 standards during the time of the study. In focusing on the 98th 25 percentile value in 

26 these studies the Administrator recognized that these studies did not provide evidence of clear 

27 effect thresholds or lowest-observed levels. Therefore, the Administrator sought to establish a 

28 standard level that would require improvements in air quality generally in areas in which the 

29 distribution of daily short-term exposure to PM2.5 can reasonably be expected to be associated 

30 with serious health outcomes (i.e., mortality, respiratory and cardiovascular morbidity). In the 

31 prior review, we noted an overall pattern of statistically significant associations observed in 

32 studies of short-term exposure to PM2.5 across a wide range of 24-hour average 98th percentile 

33 values in predominately single-city studies as well as a limited number of multi-city studies. A 

predominance of studies with 98th percentile values down to approximately 39 μg/m3 34 (Burnett 

35 and Goldberg, 2003) reported statistically significant associations with mortality, hospital 
Draft Do Not Quote or Cite March 2010 2-39

admissions, and respiratory symptoms. Within the range of 24-hour average 98th 1 percentile 

PM2.5 concentrations of about 35 to 30 μg/m3 2 , we did not observe a preponderance of statistically 

significant results. Furthermore, the limited number of studies in which the 98th 3 percentile values 

4 were below this range did not provide a basis for reaching conclusions about associations at such 

5 levels (71 FR 61168/3 – 61169/2, October 17, 2006). 

6 As discussed in section 2.1.3, our current approach to reaching preliminary conclusions 

7 about the adequacy of the current suite of PM2.5 standards is more integrative than the approach 

8 used in the last review. In this review, in considering the adequacy of the current suite of 

9 standards, in evaluating the currently available evidence from short-term PM2.5 exposure studies, 

10 we look both at the aggregate long-term mean PM2.5 concentration in key studies as well as the 

distributions of 24-hour PM2.5 concentrations, with a focus on the 98th 11 percentile concentrations 

12 to match the form of the current 24-hour standard, to the extent such data are available. 

13 A number of new multi-city and single-city short-term PM2.5 exposure studies and 

14 additional analysis of a previously existing cohort study available in this review examine the 

15 association between short-term exposure to PM2.5 and mortality and a broader range of 

16 cardiovascular and respiratory morbidity endpoints. Multi-city studies support a largely positive 

17 and frequently statistically significant relationship between short-term exposure to PM2.5 and 

18 increased risk of mortality. In a multi-city time-series analysis of 112 U.S. cities, Zanobetti and 

Schwartz (2009) reported that an overall 24-hour average15 19 PM2.5 level across all years of 34.3 

(8.8) μg/m3 (ranging from 17.9 to 80.3 μg/m3 20 ) (US EPA, 2009a, Figure 6-24) from lag 0-1 days 

21 were positively and significantly associated with all-cause, cardiovascular-related (e.g., 

22 myocardial infarction, stroke), and respiratory-related mortality. Furthermore, city-specific 

23 effect estimates included in Figure 6-24 of the ISA indicate the association between short-term 

24 exposure to PM2.5 and total mortality and cardiovascular mortality and respiratory mortality 

25 endpoints is consistently positive for an overwhelming majority (99%) of the 112 cities across a 

26 wide range of air quality concentrations (US EPA, 2009a, p. 6-178 to 179). In addition, the 

27 authors report that for all-cause mortality city-specific effect estimates were statistically 

significant for 55% of the 112 cities, with 24-hour PM2.5 levels ranging from 18.4 to 64.9 μg/m3 28 . 

29 In the current review of evidence on mortality associated with short-term exposure to 

30 PM2.5, we note that an expansion of the multi-city Canadian study from 8 (Burnett and Goldberg, 

31 2003) to 12 Cities (Burnett et al 2004) yielded results consistent with prior findings of a positive 

32 and statistically significant association between an average 1-day lag 24-hour PM2.5 exposure 

across all years of 38.1 μg/m3

(extending from 25 to 50 μg/m3 33 ) and daily mortality (US EPA, 

34 2009a, Figure 2-1). However, the influence of NO2 and limited PM2.5 data for several years 

 15 Concentrations reported for short-term studies are mean 98th percentile (standard deviation, SD) 
Draft Do Not Quote or Cite March 2010 2-40

1 during the study period somewhat diminish these findings and underscore the need for more 

2 frequent PM2.5 measurements and additional data on co-pollutants to inform our understanding of 

3 the PM2.5-mortality association. In general, as can be seen in Figure 6-27 of the ISA, effect 

4 estimates for associations between mortality and short-term exposure to PM2.5 are positive and a 

5 number are statistically significant (ISA, US EPA, 2009a, p. 6-184). Larger effect estimates 

6 were reported in some studies for associations with respiratory mortality in comparison to 

7 cardiovascular and all-cause mortality, but these effect estimate include larger confidence 

8 intervals (i.e. less precision) since respiratory deaths comprise only a small proportion of total 

9 deaths. 

10 With regard to cardiovascular and respiratory morbidity effects, in the first analysis of the 

11 MCAPS cohort conducted by Dominici et al (2006a) across 204 US counties, investigators 

12 reported a statistically significant association between an average 24-hour PM2.5 concentration 

across all years of 34.8 μg/m3 (extending from 10.4 to 85.6 μg/m3 13 ) and hospitalizations for 

14 cardiovascular and respiratory diseases. Furthermore, a sub-analysis restricted to days with 24-

hour average concentrations of PM2.5 at or below 35 μg/m3 15 indicated that, in spite of a reduced 

16 statistical power from a smaller number of study days, statistically significant associations were 

17 still observed between short-term exposure to PM2.5 and hospital admissions for cardiovascular 

and respiratory diseases (Dominici, 2006b16 18 )). These results along with the observation that 

19 approximately 50% of PM2.5 levels across the 204 counties across all years were below the 24-

20 hour standard suggests that the overall health effects observed across the U.S. are not primarily 

21 driven by the higher end of the PM2.5 air quality distribution (Cite Docket # for AQ provided by 

22 authors). In an extended analysis of the MCAPS study, Bell et al (2008) reported a positive and 

23 statistically significant increase in cardiovascular hospitalizations associated with and average0-

day lag PM2.5 concentration across all years of 34.2 (8.5) μg/m3 24 (extending from 9.4 to 77.0 

μg/m3 25 ). In addition, significant increases in respiratory disease hospitalizations were associated 

26 with mean PM2.5 at lag 2. Furthermore, several single-city short-term PM2.5 exposure studies 

with average 98th percentile PM2.5 exposures below 35 μg/m3 27 substantiate findings from the 

28 aforementioned multi-city studies generally reporting positive statistically significant and non29 significant associations for PM2.5 exposures in relation to mortality, cardiovascular and 

30 respiratory hospitalizations and ED visits (Figure 2-4). Consequently, these short-term studies 

31 provide evidence of PM2.5 associated mortality and morbidity effects occurring at and below the 

32 level of the current 24-hour standard. 

 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

1 In considering long-term average ambient concentrations from short-term PM2.5 exposure 

2 studies, we recognize that in the last review, several U.S. and Canadian studies provided 

3 evidence of associations between short-term exposure to PM2.5 and serious health effects in areas 

with PM2.5 levels at and above the level of the current annual PM2.5 standard (15 μg/m3 4 ). 

5 Moreover, a few short-term PM2.5 exposure studies (Figure 2-4) available in that review provided 

6 evidence of statistically significant associations with PM2.5 in relation to cardiovascular and 

7 respiratory effects for areas in which long-term average PM2.5 concentrations ranged between 12 

and 14 μg/m3 and 98th percentile 24-hour concentrations ranged between 31 and 59 μg/m3 8 (US 

9 EPA, 2005, p. 5-7). 

10 Similarly, in this review, many short-term PM2.5 exposure studies, and in particular those 

11 conducted across multiple cities, report statistically significant effects with mean concentrations 

12 below the level of the current annual standard. Dominici et al. (2006a) and Bell et al. (2008) 

report 24-hour average PM2.5 levels across all years of 13.4 (2.9) μg/m3 13 (extending from 4.4 to 

22.7 μg/m3

) and 12.9 (2.7) μg/m3(extending from 4.3 to 20.4 μg/m3 14 ), respectively (US EPA, 

15 2009a, Figure 2-1). Likewise, Zanobetti and Schwartz (2009) report city annual averages across 

all years of 13.2 () μg/m3

 (extending from 6.6 μg/m3 to 24.7 μg/m3 16 ) (Figures 2-1 and 6-24, US 

17 EPA, 2009a). In addition, Burnett et al. 2004, reports city annual averages across all years of 

12.8 μg/m3 (extending 8.1 to 16.7 μg/m3 18 ) (Figure 2-1, ISA – US EPA, 2009a). Based on the 

19 findings from these multi-city short-term PM2.5 exposure studies, the ISA concludes that overall, 

20 consistent positive associations have been reported for a range of mortality and cardiovascular 

and respiratory morbidity effects for mean 24-hour PM2.5 concentrations at and above 12.8 μg/m3 21 

22 (US EPA, section 2.3.1.1). 

23 Taken together, these findings from single- and multi-city epidemiological studies of 

24 short-term PM2.5 exposure in relation to mortality and cardiovascular and respiratory morbidity 

25 provide evidence of short-term PM2.5 associated health effects occurring at or below the current 

26 levels of the 24-hour standard (Figure 2-1, US EPA, 2009a, p. 2-14). These findings are 

27 bolstered by evidence of statistically significant PM2.5 associated health effects occurring in 

analyses restricted to days in which 24-hour average PM2.5 levels were below 35 μg/m3 28 

29 (Dominici, 2006b). Multi-city short-term studies conducted since the prior review (Burnett et al. 

30 2004; Dominici et al. 2006a; Bell et al. 2008; Zanobetti and Schwartz, 2009) also provide 

31 supportive evidence for short-term PM2.5 exposure associated health effects occurring at levels at 

32 and below the annual standard. 

33 Summary 

34 In evaluating the currently available scientific evidence, we reach the preliminary 

35 conclusion that the evidence from long and short-term PM2.5 exposure studies, and in particular 

36 those studies conducted across multiple U.S. cities calls into question whether the current suite of 
Draft Do Not Quote or Cite March 2010 2-42

1 PM2.5 primary standards protects public health with an adequate margin of safety from effects 

2 associated with long- and short-term exposures to PM2.5. We also reach the preliminary 

3 conclusion that this evidence provides strong support for considering fine particle standards that 

4 would impart increased protection beyond that afforded by the current annual and 24-hour PM2.5 

5 standards. More protective standards would reflect the substantially stronger and broader body 

6 of evidence for mortality and cardiovascular and respiratory morbidity effects now available in 

7 this review both at lower levels of air quality than had previously been observed and at levels 

below the current annual (15 μg/m3

) and 24-hr (35 μg/m3 8 ) PM2.5 standards.

9 2.2.2 Risk-based Considerations 

10 Looking beyond evidence-based considerations, staff also has considered the extent to 

11 which health risks estimated to occur upon just meeting the current suite of PM2.5 standards may 

12 be judged to be important from a public health perspective, taking into account key uncertainties 

13 associated with the estimated risks. 

14 The quantitative risk assessment conducted in this review (US EPA, 2010a) builds upon 

15 and expands upon the analyses conducted for the previous review (US EPA, 2005, chapter 4; 

16 Abt, 2005). As an initial matter, we recognize that the previous quantitative risk assessment 

17 incorporated alternative assumed cutpoints as surrogates for potential population thresholds. In 

18 the current review, the ISA examined the available epidemiologic evidence to characterize the 

19 shape of the concentration-response (C-R) relationship and assess possible PM “thresholds” (i.e., 

20 levels which PM2.5 concentrations must exceed in order to elicit a health response). Overall, 

21 based on limited evidence primarily focusing on cardiovascular-related hospital admissions and 

22 emergency department visits associated with short-term exposures to PM10 and mortality 

23 associated with long-term exposure to PM2.5, using a variety of methods and models, the ISA 

24 concludes the currently available evidence supports the use of a no-threshold, log-linear model 

25 (US EPA, 2009a, p. 2-25). Therefore, the quantitative risk assessment conducted for this review 

26 did not include assumed cutpoints as surrogates for potential population thresholds. We 

concluded that is was more appropriate to focus on alternative rollback strategies.17 27 

28 The assessment of uncertainty and variability completed for this analysis is more 

29 comprehensive than had been done for previous risk assessments. This reflects, in part, the 

30 development of methods by EPA staff to address potentially important sources of variability and 

 17 While we have not included cutpoints in the risk assessment for the reasons cited, in the case of long-term 

exposure-related mortality, we have limited estimation of risk to ambient PM2.5 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, section 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 PM2.5 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

1 uncertainty. For example, to more fully explore potential variability in the patterns of reductions 

2 in ambient PM2.5 that may occur upon just meeting the current and alternative standards, we 

3 incorporated as part of the sensitivity analysis, two additional rollback approaches (hybrid and 

4 peak shaving) in addition to the proportional rollback used in the core analysis. In addition, 

5 recently published literature has allowed us to more rigorously examine the impact of uncertainty 

6 related to specifying C-R functions for long-term exposure-related mortality through a series of 

7 sensitivity analyses (i.e., Krewski et al. (2009) provided extensive analysis of alternative model 

8 specifications for mortality which could be readily incorporated into our sensitivity analysis). 

9 For this review, we have estimated risk for a set of health effects endpoints that reflected 

10 consideration of the degree of support in the literature for a causal relationship between PM2.5

11 exposure and the health effect of interest as assessed in the ISA, together with consideration of 

the health significance of the endpoint.18 12 Specifically, we have estimated risks for (a) all-cause, 

13 IHD, cardiopulmonary and lung cancer mortality related to long-term PM2.5 exposure, (b) non14 accidental, cardiovascular (CV) and respiratory mortality related to short-term PM2.5 exposure, 

15 and (c) cardiovascular-related and respiratory-related hospital admissions (HA) and asthma16 related emergency department visits associated with short-term PM2.5 exposure. While we have 

17 modeled risk for a selection of long-term and short-term exposure-related endpoints, in the 

18 discussion of risk estimates presented below, we focus on cardiovascular-related endpoints, since 

19 the causal association for these endpoints based on available literature is assessed in the ISA to 

20 be the strongest of the endpoints considered. 

21 In considering the health risks estimated in selected urban study areas to occur upon just 

22 meeting the current suite of PM2.5 standards, we focused on a core (primary) set of risk results 

23 based on the application of modeling element choices (e.g., concentration-response functions, lag 

24 periods) that have the greatest overall support in the literature (hereafter referred to as the “core” 

25 results). In addition, to gain insights into which sources of uncertainty may have the greatest 

26 impact on risk estimates when acting alone, or in combination with other sources of uncertainty, 

27 as noted above, we conducted a series of single-element and multi-element sensitivity analyses to 

28 generate a broader set of reasonable alternative risk estimates that allowed us to place the results 

29 of the core analysis in context with regard to uncertainty. We also conducted additional analyses 

30 to place the results of the urban study area analysis into a broader context for characterizing 

31 potential national risks. While the core risk estimates receive primary focus in the discussion of 

32 risk estimates presented below, we do references the results of these additional supplemental 

 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

1 analyses in addressing overall confidence associated with the core risk estimates and in placing 

2 the core risk estimates in a broader national-context. 

3 An important factor to consider in interpreting risk results is that the magnitude of both 

4 long- and short-term exposure-related risk depends primarily on annual-average PM2.5

5 concentrations. Furthermore, reductions in both categories of risk, as we consider simulating just 

6 meeting current and alternative suites of standards, also depend primarily on changes in annual7 average PM2.5 concentrations. 

8 The role of annual-average ambient PM2.5 concentrations in driving long-term exposure9 related risk is intuitive given that this risk category is modeled using the annual-average air 

quality metric.19 10 The fact that short-term exposure-related risk is also driven by changes in long11 term average PM2.5 concentrations is less intuitive, since changes in average daily PM2.5

concentrations are used to estimate changes in risk for this category.20 12 Analyses in previous PM 

13 NAAQS risk assessments have shown that short-term exposure-related risks are not primarily 

14 driven by the small number of days with PM2.5 concentrations in the upper tail of the air quality 

15 distribution, but rather by the large number of days with PM2.5 concentrations at and around the 

16 mean of the distribution. Consequently, consideration for changes in annual-average PM2.5

17 concentrations will explain to a large extent changes in short-term exposure-related risk. 

18 Therefore, in interpreting patterns of long-term exposure-related risk, and the similar patterns we 

19 observe in short-term exposure-related risk, we consider how simulating just meeting specific 

20 suites of PM2.5 standards impacts the annual-average PM2.5 concentration for the study areas. 

21 We have considered a series of questions to inform our understanding of the adequacy of 

22 the current suite of fine particle standards based on the insights obtained from the quantitative 

23 risk assessment. The remainder of the discussion is organized around these questions. 

24  What is the nature and magnitude of the long-term exposure-related risks remaining 

25 upon just meeting the current suite of PM2.5 standards? What level of confidence is 

26 associated with these risk estimates? 

27 Of the fifteen study areas included in the risk assessment, thirteen are simulated to 

28 experience risk reductions upon meeting the current suite of standards. Of these thirteen study 

 19 As noted in section 3.2.1 of the second draft RA, estimates of long-term exposure-related mortality are actually 

based on an average annual PM2.5 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 design value) determines the percent reduction in PM2.5 levels 

required to attain a particular standard. Both types of air 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 PM2.5. 

concentrations. However, similar to the case with long-term exposure-related mortality, it is the maximum monitor 

98th percentile 24-hour concentration (the 24-hour design value) 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

1 areas, three areas (Atlanta, Birmingham and Houston) have design values which resulted in the 

2 current annual standard controlling. Therefore, in assessing the level of long-term exposure3 related mortality risk remaining upon just meeting the current annual standard, we focus on risk 

4 estimates for these three study areas. Total incidence of PM2.5-related mortality ranges from 

5 131-165 (Birmingham) to 344-434 (Houston) (Table 2-2). The percent of total incidence of IHD 

6 mortality attributable to PM2.5 ranges from 10.7-13.6% (Houston) to 13.2-16.7% (Atlanta) (Table 

7 2-2). Total incidence estimates for all-cause and cardiopulmonary mortality related to PM2.5

8 exposure for these study areas are larger than for IHD, while total PM2.5-attributable incidence 

9 estimates for lung-cancer are lower. However, the percent of total incidence attributable to PM2.5

10 exposure is larger for IHD than for the other mortality categories assessed. 

11 The remaining ten study areas that would experience reductions in risk under the current 

12 suite of standards (relative to risk under recent conditions) have design values which result in the 

13 current 24-hour standard controlling. These study areas include: Baltimore, Detroit, Fresno, Los 

14 Angeles, New York, Philadelphia, Pittsburgh, Salt Lake City, St. Louis, and Tacoma. Therefore, 

15 we consider risk estimates for these study areas in assessing the degree of risk associated with 

16 just meeting the current 24-hour standard. Total incidence of PM2.5-related mortality ranges 

17 from 15-19 (Salt Lake City) to 1,755-2,222 (New York City) (Table 2-2). The percent of total 

18 incidence of IHD mortality attributable to PM2.5 ranges from 2.9-3.7 (Salt Lake City) to 11.2-

19 14.2% (St. Louis) (Table 2-2). Total incidence estimates for all-cause and cardiopulmonary 

20 mortality related to PM2.5 exposure for these study areas are larger than for IHD, while total 

21 PM2.5-attributable incidence estimates for lung-cancer are lower. However, the percent of total 

22 incidence attributable to PM2.5exposure is larger for IHD than for the other mortality categories 

23 assessed. 

24 Estimates of risk under the current suite of standards is significantly more variable for the 

25 ten study areas where the 24-hour standard is controlling compared with the three study areas 

26 where the current annual standard is controlling. This notable difference in variability reflects the 

27 fact that simulation of just meeting the current 24-hour standard (for those study areas where it is 

28 controlling) produces varying impacts on annual-average PM2.5 concentrations. By contrast, 

29 simulation of just meeting the annual standard results in similar annual-average PM2.5

30 concentrations for those study areas where the annual standard is controlling. Because annual31 average PM2.5 concentrations are one of the primary determinants of the level of long-term 

32 exposure-related mortality risk, variation in this statistic translates into greater variation in risk 

33 remaining upon simulation of the current suite of standards for the ten study areas where the 24-

34 hour level is controlling. 

35 A related point, which has bearing on the level of confidence associated with our risk 

36 estimates, is the observation that several of the study areas where the 24-hour standard was 
Draft Do Not Quote or Cite March 2010 2-46

1 Table 2-2. Estimated Incidence and Percent of Total Annual Incidence Associated with 

2 Long-term PM2.5 Exposure Based on Simulation of the Current Suite of Standards (for 

IHD mortality based on 2007 PM2.5 Concentrations)1,2 3 

4 

5 
Draft Do Not Quote or Cite March 2010 2-47

1 controlling have annual-average PM2.5 concentrations that are well below the level of the current 

2 annual standard and in some instances, approaching the lowest measured level (LML) of 5.8 

μg/m3 3 used as the lower bound for risk estimation. Although we are not able to quantify the 

4 degree of increased uncertainty, we do have reduced confidence in risk estimates involving 

5 annual-average PM2.5 concentrations that are substantially below the mean annual PM2.5

concentrations reported by Krewski et al. (2009) (14-21 μg/m3 6 – see Table 1 in the study) and 

approaching the LML of 5.8 μg/m3 7 identified for that study. This reflects the fact that, while 

8 available literature does not support a PM2.5-related threshold for health effects, we do have 

9 increased uncertainty in characterizing the nature of the C-R function as we move away from the 

10 central mass of observations in the epidemiological study from which the C-R functions was 

11 obtained and towards the LML. Study areas with relatively low annual-average PM2.5

concentrations less than the level of the current standard include: Tacoma (8.4 μg/m3 12 ), Salt Lake 

City (7.7 μg/m3), and Fresno (9.9 μg/m3 13 ) (note, that the current 24-hour standard is controlling 

14 for all of these study areas – see US EPA, 2010a, Appendix F, Table F-49). Conversely, we note 

15 that we would have greater confidence in applying C-R functions in the risk assessment for those 

16 study areas with annual-average PM2.5 levels under the current suite of standards near the range 

of 14-21 μg/m3 17 . Study areas in this category include: Atlanta, Birmingham and Houston (where 

18 the annual standard is controlling) and Baltimore, Detroit, Philadelphia, St. Louis, New York 

19 (where the 24-hour standard is controlling). 

20 Consideration of variability in the spatial pattern of PM2.5 reductions associated with 

21 simulation of the current suite of standards suggests that this factor can impact risk estimates, 

22 particularly in those instances where the 24-hour standard is controlling. For example, 

23 consideration of a more localized pattern of reduction in PM2.5 concentrations (as reflected in the 

24 peak shaving rollback method), resulted in risk estimates for the 10 study areas where the 24-

25 hour standard is controlling that are from ~0 to 53% higher than those estimated assuming a 

26 more regionalized pattern of PM2.5 reductions (as reflected in the proportional rollback method 

27 used in the core analysis). 

28 Additional sensitivity analyses considering sources of uncertainty impacting the core risk 

29 estimates focused on specification of the C-R function for long-term PM2.5 exposure-related 

30 mortality. This analysis suggested that most of the alternative model specifications supported by 

31 available literature would produce risk estimates that were higher (by up to a factor of 2 to 3) 

32 than the core risk estimates. These findings would apply both to estimates of PM2.5-attributable 

33 IHD mortality incidence, as well as to estimates of the percent of total IHD mortality incidence 

34 attributable to PM2.5 exposure. 

35 Taken together, the sensitivity analyses completed for this risk assessment, including 

36 those considering variability in rollback methods as well as uncertainty in the form of C-R 
Draft Do Not Quote or Cite March 2010 2-48

1 functions, suggest that the set of alternative risk model specifications that we identified generally 

2 produced risk estimates that are higher than the core risk estimates. Furthermore, our decision to 

3 model risk down to the LML (rather than to lower policy-relevant background (PRB) 

4 concentrations) for long-term PM2.5 exposure-related mortality, despite the lack of evidence for a 

5 threshold, results in lower estimates of risk that would have resulted from modeling risk down to 

6 PRB. These considerations increase our overall confidence that we did not over-state risks with 

7 the core risk estimates. However, as noted above, there are different levels of confidence 

8 associated with risk estimates reflecting the annual-average PM2.5 concentrations associated 

9 with the risk estimates (with lower confidence associated with annual-average PM2.5

concentrations closer to the LML of 5.8 μg/m3 10 ). 

11  What is the nature and magnitude of the short-term exposure-related risks remaining 

12 upon just meeting the current suite of PM2.5 standards? What level of confidence is 

13 associated with these risk estimates? 

14 As noted earlier, changes in annual-average PM2.5 levels drive reductions in both long15 term and short-term exposure-related risk. Consequently, patterns of risk reduction for long-term 

16 exposure-related mortality associated with the suite of annual standard levels generally hold for 

17 short-term exposure-related mortality and morbidity (although absolute levels of risk will differ). 

18 As was done above for long-term exposure-related mortality, we have divided the discussion of 

19 risk for short-term exposure-related mortality and morbidity, between (a) the three study areas 

20 where the current annual standard was driving and (b) the ten study areas where the 24-hour 

21 standard was controlling. Again, this reflects the fact that these two groups of study areas had 

22 different patterns of risk reduction under the current suite of standards, reflecting differences in 

23 the way the two standard levels effected annual-average PM2.5 levels (i.e., fairly similar annual24 average PM2.5 levels for study areas where the annual standard controls and more variable 

25 annual-average PM2.5 levels for study areas where the 24-hour standard controls). 

26 Total incidence of short-term exposure-related CV mortality attributable for PM2.5 for the 

27 three study areas where the current annual standard controls (Atlanta, Birmingham and Houston) 

28 ranges from 32 (Atlanta) to 46 (Houston) (Table 2-3). The percent of total CV mortality 

29 incidence attributable to PM2.5 for this subset of study areas ranges from 0.8% (Atlanta) to 0.9% 

30 (Houston) (Table 2-3). Total incidence of CV hospital admissions (HA) attributable to PM2.5 for 

31 this group of study areas ranges from 16 (Birmingham) to 56 (Houston) (Table 2-3), while 

32 percent of total incidence attributable to PM2.5 ranges from 0.3% (Birmingham) to 0.4% 

33 (Atlanta) (Table 2-3). 

34 Total incidence of short-term exposure-related CV mortality attributable for PM2.5 for the 

35 ten study areas where the 24-hour standard is controlling (Baltimore, Detroit, Fresno, Los 

36 Angeles, New York, Philadelphia, Pittsburgh, Salt Lake City, St. Louis, and Tacoma), range 
Draft Do Not Quote or Cite March 2010 2-49

1 from 9 (Salt Lake City) to 106 (St. Louis) (Table 2-3). The percent of total incidence of CV 

2 mortality attributable to PM2.5 ranges from 0.7% (Tacoma) to 2.1% (New York and Philadelphia) 

3 (Table 2-3). Total incidence of CV hospital admissions (HA) attributable to PM2.5 for this group 

4 of study areas ranges from 9 (Salt Lake City) to 752 (Los Angeles) (Table 2-3), while percent of 

5 total incidence attributable to PM2.5 ranges from 0.4% (Salt Lake City) to 1.3% (St. Louis and 

6 Philadelphia) (Table 2-3). 

7 As observed with the long-term exposure-related mortality, estimates of short-term 

8 exposure-related mortality and morbidity risk under the current suite of standards are 

9 significantly more variable for the ten study areas where the 24-hour standard is controlling 

10 compared with the three study areas where the current annual standard is controlling. Again, this 

11 notable different in variability reflects the fact that simulation of just meeting the current 24-hour 

12 standard (for those study areas where it is controlling) produces varying impacts on annual13 average PM2.5 concentrations and hence on risk. By contrast, those study areas where the annual 

14 standard is controlling have similar annual-average PM2.5 levels and consequently similar levels 

15 of risk remaining upon simulation of the current suite of standards (recall that short-term 

16 exposure-related risk is driven more by changes in annual-average PM2.5 then by changes in peak 

17 daily PM2.5 levels). 

18 Given increased emphasis placed in this analysis on long-term exposure-related 

19 mortality, the uncertainty analyses completed for this health endpoint category are more 

20 comprehensive than those conducted for short-term exposure-related mortality and morbidity, 

21 which to some extent reflects limitations in study data available for addressing uncertainty in the 

22 later category. 

23  What roles do the current 24 hour and annual standards have in simulating the risks 

24 remaining upon just meeting the current suite of standards? 

25 As note above, of the thirteen urban study areas that do not meet the current suite of 

26 standards based on 2005-2007 air quality data, ten areas have the 24-hour standard controlling, 

27 while only 3 areas have the annual standard controlling. This pattern is generally characteristic of 

28 the larger set of urban areas across the U.S. that do not meet the current suite of standards (US 

EPA, 2010a, section 4.5).21 29 

30 Estimated risks remaining upon just meeting the current suite of standards vary across 

31 study areas, even when considering risks normalized for differences in population size and 

32 baseline incidence rates. This variability in estimated risks is a consequence of the variability in 

33 the annual-average PM2.5 concentrations across study areas that result from simulating just 

 21 Of the 256 urban areas in the U.S. (including a combination of CSA and CBSAs), 67 have ambient PM2.5 levels 

exceeding either the 24-hour or annual standard (or both) based on PM2.5 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

1 Table 2-3. Estimated Incidence and Percent of Total Annual Incidence Associated with 

2 Short-Term PM2.5 Exposure Based on Simulation of the Current Suite of Standards (CV 

mortality and hospital admissions based on 2007 PM2.5 concentrations)1,2 3 

4 

5 
Draft Do Not Quote or Cite March 2010 2-51

meeting the current standards.22 1 Variability in annual-average PM2.5 concentrations is 

2 substantially greater in those study areas in which the 24-hour standard is controlling. In such 

3 areas, the variability across study areas in estimated risks is largest when regional patterns of 

4 reductions in PM2.5 concentrations are simulated (using proportional rollback, as was done in the 

5 core analyses), with less variability when more localized patterns of PM2.5 reductions are 

6 simulated (using peak shaving rollback, as was done in a sensitivity analysis). 

7 In simulating just meeting the current suite of standards for the urban study areas, the 

resulting annual-average PM2.5 concentrations range from about 15 μg/m3 8 (for the study areas in 

which the annual standard was controlling) down to as low as about 8 μg/m3 9 (for the study areas 

10 in which the 24-hour standard was controlling). We note that, for long-term exposure-related 

11 mortality, estimates of risk based on annual-average PM2.5 concentrations approaching the LML 

of 5.8 μg/m3 12 have greater uncertainty than estimates based on annual-average concentrations 

13 closer to the mean of the epidemiological study from which the C-R functions are obtained (14 to 

21 μg/m3

).23 14 Therefore, we generally have less confidence in risk estimates generated for study 

15 areas where the 24-hour standard is controlling since these tend to have lower annual-average 

16 PM2.5 levels (which can approach the LML) compared with study areas where the annual17 average is controlling. 

18 These observations when considered together suggest that, when we simulate PM2.5

19 concentrations meeting the current suite of standards, we find that in study areas where the 

20 current 24-hour standard is controlling, the degree of public health protection afforded by the 

21 current suite of standards is much more variable than in study areas where the annual standard is 

22 controlling. Furthermore, we generally have less confidence in the risk estimates generated for 

23 urban areas where the current 24-hour standard is controlling due simulated lower annual24 average PM2.5 concentrations that are in some cases much lower, approaching the LML. 

25  How representative are the risk estimates generated for the urban study areas from a 

26 national perspective? 

27 As part of the risk assessment, we completed several additional analyses intended to 

28 place the core risk estimates in the broader national-context by considering the degree to which 

29 the 15 urban study areas are representative of larger urban areas within the U.S., particularly 

30 areas likely to experience elevated risk related to PM exposure. Below we provide brief 

31 descriptions of each analysis, along with observations results from each analysis regarding the 

 22 As noted earlier, changes in both short-term and long-term exposure-related risk reflect primarily changes in longterm average (annual) PM2.5 levels. 23 This observation also holds for estimates of risk associated with short-term PM2.5 although we note that the LML 

for these studies is below PRB, which allows us to make estimates of risk for lower PM2.5 levels with greater 

confidence relative to modeling long-term exposure-related mortality with its higher LML. 
Draft Do Not Quote or Cite March 2010 2-52

1 representativeness of the urban study areas: 

2  The representativeness analysis (US EPA, 2010a, section 4.4) compared attributes of the 15 

3 urban study eras (assessed at the county-level) against national distributions for the same 

4 attributes. The analysis suggests that the 15 urban study areas represent areas in the U.S. that 

5 are among the most densely populated, have relatively higher levels of annual and 24-hour 

98th 6 percentile PM2.5 concentrations, and capture well the range of effect estimates 

7 represented by the Zanobetti and Schwartz (2009) study. Together, these factors suggest that 

8 the urban study areas should capture well the overall distribution of risk for the nation, with 

the potential for better characterization of the high end of that distribution.24 9 

10  Consideration of the mix of design values across the 15 urban study areas as contrasted with 

11 design values for the broader set of urban study areas in the U.S. suggests that the 15 urban 

12 study areas do a good job of capturing the key groupings of urban areas in the U.S. likely to 

13 experience elevated risk due to PM (i.e., we have coverage for each of the zones containing 

14 urban study areas likely to experience risk reductions under the suites of alternative standard 

15 levels considered – see US EPA,2010a, section 4.5.1). Furthermore, this analysis suggested 

16 that we have also included study areas likely to experience relatively greater degrees of 

17 PM2.5-related risk, considering the pattern of design values across urban areas in the U.S. 

18  Consideration of where the 15 urban study areas fell along the distribution of U.S. counties 

19 included in the national-scale mortality analysis further suggests that we have captured 

20 counties likely to experience elevated PM2.5-related risk. As part of the national-scale 

21 mortality analysis (see US EPA, 2010a, chapter 5), we created a cumulative distribution of 

22 the percentage of mortality attributable to PM2.5 based on the county-level estimates for the 

U.S.25 23 We then identified where along this cumulative distribution the 31 counties 

24 comprising our 15 urban study areas fell. This analysis suggests that our urban study areas 

25 capture the upper end of the tail with regard to PM2.5-attributable risk, with 23 of these 

counties falling within the upper 5th 26 percentile of the distribution. These findings support the 

27 assertion based on the other analyses described above that the urban study areas are likely to 

28 capture risk at urban areas experiencing relatively elevated levels of PM2.5-attributable 

29 mortality. 

30 Our overall assessment of the representativeness of the 15 urban study areas in the 

31 national context, based on the three analyses summarized above, is that our study areas do a good 

32 job of representing urban areas in the U.S. experiencing elevated levels of risk related to ambient 

33 PM2.5 exposure. The results of the national-scale mortality analysis also suggest that, while our 

34 15 urban study areas do provide coverage for urban areas in the U.S. experiencing elevated 

35 levels of PM2.5-related risk, there are many additional areas (counties) not modeled in the risk 

 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 PM2.5-related mortality estimates). However, some of 

the areas with the highest values for these attributes have relatively lower PM2.5 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 PM2.5-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 PM2.5-related mortality which reflects differences in (a) 

baseline mortality incidence, and (b) the annual average PM2.5 concentrations for each county. 
Draft Do Not Quote or Cite March 2010 2-53

1 assessment that experience elevated PM2.5-related risk. In other words, it should not be 

2 construed that significant PM2.5-related risk is limited only to the urban study areas included in 

3 the risk assessment.

4  To what extent are the risks remaining upon simulation of the current suite of 

5 standards important from a public health perspective? 

6 With respect to considering the results of the quantitative risk assessment to inform our 

7 understanding of risks associated with long-term PM2.5 exposures, we reach the preliminary 

8 conclusion that the long-term exposure-related mortality risks remaining upon simulation of just 

9 meeting the current suite of PM2.5 standards can reasonably be judged to be important from a 

10 public health perspective. This preliminary conclusion is based, in part, on both the nature of the 

11 risks (total and cause-specific mortality) as well as the magnitude of these risks (the total 

12 incidence and percentage of incidence associated with PM2.5 exposure as presented in Table 2-2). 

13 In addition, based on consideration of both our qualitative and quantitative assessments of 

14 uncertainty, as well as additional factors considered in the risk model (e.g., modeling risk down 

15 to LML rather than PRB), we are reasonably confident that we have not overstated the 

16 magnitude of risk associated with simulating the current suite of standards. However, we do note 

17 that we have greater overall confidence in estimates of risk associated with long-term PM2.5 

18 exposure in the subset of urban study areas for which the current annual standard is controlling, 

19 since these locations tend to have higher annual-average PM2.5 concentrations. In contrast, the 

20 urban study areas where the current 24-hour standard is controlling tend to have substantially 

21 lower annual-average PM2.5 concentrations, which reduces our overall confidence in these 

22 estimates of risks related to long-term exposures.

23 With regard to considering the results of the quantitative risk assessment to inform our 

24 understanding of risks associated with short-term PM2.5 exposures, we reach the preliminary 

25 conclusion that short-term exposure-related mortality and morbidity risks upon simulation of the 

26 current suite of PM2.5 standards can reasonably be judged to be important from a public health 

27 perspective. Similar to the discussion of risks associated with long-term PM2.5 exposure, this 

28 preliminary conclusion is based, in part, on both the nature of the risks (total and cause-specific 

29 mortality as well as cause-specific hospital admissions) as well as the magnitude of those risks 

30 (total incidence and percentage of incidence associated with PM2.5 exposure as presented in 

31 Table 2-3). We note however, that in the case of mortality associated with short-term PM2.5 

32 exposure, the magnitude of these risks is substantially lower than that associated with long-term 

33 exposure to PM2.5. With regard to our overall confidence in the estimates of risks related to 

34 short-term PM2.5 exposures, while we believe that the core simulation of risk is based on C-R 

35 functions that are well-supported in the literature, we acknowledge that we have not completed 

36 as comprehensive an assessment of uncertainty and variability as was done for estimates of 
Draft Do Not Quote or Cite March 2010 2-54

1 mortality risks related to long-term PM2.5 exposure. Therefore, our overall confidence that we 

2 have not over-stated risk associated with short-term exposure-related mortality and morbidity is 

3 not as high as for long-term exposure-related mortality, although we have no reason to believe 

4 that we have over-stated risk. 

5 2.2.3 Preliminary Staff Conclusions on Adequacy of Current Standards 

6 Collectively, taking into consideration the responses to specific questions focusing on 

7 different ways to address the adequacy of the current suite of PM2.5 standards, we revisit the 

8 overarching policy question: does the currently available scientific evidence and risk-based 

9 information support or call into question the adequacy of the protection afforded by the current 

10 suite of fine particle standards? 

11 With respect to evidence-based considerations, the currently available evidence provides 

12 stronger evidence beyond what was available in the last review, that associations between short13 and long-term PM2.5 exposures and a broad range of adverse health effects exist. The newly 

14 available information strengthens the associations between PM2.5 and mortality and 

15 cardiovascular and respiratory morbidity effects observed in the last review and expands our 

16 understanding of a broader range of health outcomes as well as our understanding of effects in 

17 susceptible populations. The newly available evidence provides support for associations that 

18 extend to lower concentrations than what had been observed in the last review, including at 

19 ambient concentrations below the levels of the current standards. 

20 In relation to risk-based considerations for informing our understanding of the adequacy 

21 of the current fine particle standards, we focus on the estimates of PM2.5-related mortality and 

22 morbidity effects likely to remain upon meeting the current standards in a number of example 

23 urban areas. In considering the core risk estimates together with our understanding of the 

24 uncertainties in these estimates based upon extensive sensitivity analyses, we reach the 

25 preliminary conclusion that the risks estimated to be associated with just meeting the current 

26 standards can reasonably be judged to be important from a public health perspective and these 

27 estimated risks provide support for consideration of standards that would provide increased 

28 protection beyond that afforded by the current PM2.5 standards. 

29 We recognize that important uncertainties and research questions remain when 

30 considering both evidence- and risk-based approaches. Nonetheless, we note that much progress 

31 has been made in reducing some key uncertainties since the last review, including important 

32 progress in advancing our understanding of potential mechanisms by which ambient PM2.5 is 

33 causally linked with mortality, cardiovascular, and respiratory effects observed in epidemiologic 

34 studies. Additional information continues to emerge for a broader range of health effects 

35 including reproductive and development effects and more information is available to understand 
Draft Do Not Quote or Cite March 2010 2-55

1 susceptible populations including children, older adults, and individuals with pre-existing 

2 cardiovascular and respiratory disease. As was true in the last review, we recognize that as the 

3 body of available evidence has expanded, it has added greatly both to our knowledge of health 

4 effects associated with fine particle exposures, as well as to the complexity inherent in 

5 interpreting the evidence in a policy-relevant context as a basis for setting appropriate standards. 

6 In evaluating both evidence-based and risk-based considerations, along with associated 

7 limitations and uncertainties, we reach the preliminary conclusion that the available information 

8 clearly calls into question the adequacy of the current suite of PM2.5 standards and provides 

9 strong support for giving consideration to revising the current standards to provide increased 

10 public health protection. 

11 2.3 CONSIDERATION OF ALTERNATIVE STANDARDS 

12 Having reached the conclusion that the currently available scientific evidence calls into 

13 question the adequacy of the current suite of PM2.5 standards, staff considers a second 

14 overarching question: 

15 What alternative suite(s) of fine particle standards is (are) supported by the currently 

16 available scientific evidence and risk-based information, as reflected in the ISA and second 

17 draft RA? 

18 To inform the answer to this overarching question, we have posed a series of more 

19 specific questions to aid in considering how the current suite of primary PM2.5 standards might be 

20 revised to provide requisite public health protection. Specifically, we consider how the currently 

21 available scientific evidence informs decisions regarding the basic elements of the NAAQS: 

22 indicator (section 2.3.1), averaging time (section 2.3.2), form (section 2.3.3), and level (sections 

23 2.3.4 and 2.3.5). These elements will be considered collectively in evaluating the health 

24 protection afforded by alternative suites of standards under consideration. In considering the 

25 currently available scientific and technical information, we consider both the information 

26 available in the last review and information that is newly available since the last review as 

27 assessed and presented in the ISA and second draft RA prepared for this review (US EPA, 

28 2009a; US EPA, 2010a). 

29 2.3.1 Indicator 

30 In 1997, EPA decided that particles from the fine and coarse fractions of thoracic 

31 particles (PM10) should be defined as separate pollutants. At that time, the Agency established 

32 PM2.5 as the indicator for fine particle, while retaining PM10 as the indicator for thoracic coarse 

33 particles. In determining the indicator for fine particles, the Agency first considered whether the 

34 indicator should be based on the mass of a size-differentiated sample of fine particles or one or 
Draft Do Not Quote or Cite March 2010 2-56

1 more components within the mix of fine particles. In that review, EPA first concluded it was 

2 more appropriate to control fine particles as a group, as opposed to singling out any particular 

3 component or class of fine particles. Second, in establishing a size-based indicator, a size cut 

4 was selected that would appropriately distinguish fine particles from particles in the coarse 

5 mode. In focusing on a size cut within the size range of 1 to 3 μm (i.e., the intermodal range 

6 between fine and coarse mode particles), EPA recognized that the choice of any specific 

7 sampling size cut within this range was largely a policy judgment. In making this judgment, the 

8 Agency noted that the available epidemiologic studies of fine particles were based largely on 

9 PM2.5 and also considered monitoring technology that was generally available. In the 

10 Administrator’s final decision, the selection of a 2.5 μm size cut reflected the regulatory 

11 importance that was placed on defining an indicator that would more completely capture fine 

12 particles under all conditions likely to be encountered across the U.S., especially when fine 

13 particle concentrations are likely to be high, while recognizing that some small coarse particles 

14 would also be captured by current methods to monitor PM2.5 (62 FR 38667 to 38668, July, 18, 

15 1997). 

16 In reaching the decision to retain PM2.5 as the indicator for fine particles in the last 

17 review, the same considerations continued to apply for selection of an appropriate indicator for 

18 fine particles (71 FR 61162 to 61164, October, 17, 2006). The available epidemiologic studies 

19 linking mortality and/or morbidity effects with short- and long-term exposures to fine particles 

20 continued to be largely indexed by PM2.5. While emerging evidence focused on various PM2.5 

21 constituents and provided some evidence related to various components within the mix of fine 

particles (e.g., sulfates (SO2

-4 22 ), nitrates, elemental carbon (EC), organic compounds, and metals) 

23 as well as associations between mortality and particles from different sources of fine particles, 

24 this evidence was deemed too limited to support a distinct standard for a specific PM2.5 

25 component or fine particle source. More specifically, the Agency concluded, there was “not 

26 sufficient evidence that would lead toward the selection of one or more PM components as being 

27 primarily responsible for effects associated with fine particles, nor is there sufficient evidence to 

28 suggest that any component should be eliminated from the indicator for fine particles” (71 FR 

29 61163/1). 

30 In this review, in considering alternative fine particle standards, we first address the issue 

31 of indicator by asking the following question: 

32  Does the currently available evidence provide support for the continued use of PM2.5 as 

33 the mass-based indicator for fine particles? 

34 As noted above, the selection of PM2.5 to characterize respirable particles in 1997 was 

35 driven mainly by considerations related to measurement techniques available at the time rather 

36 than dosimetry. In this review, the ISA notes, “[c]urrently, cut points other than 2.5 μm are 
Draft Do Not Quote or Cite March 2010 2-57

1 attainable and frequently put into use...[m]ost commonly, however, PM2.5 is used as an indicator 

2 of respirable particles” (US EPA, 2009a, p. 3-3). Recently, there has been increasing interest in 

3 examining the relationship between the particle number concentration by size and health effects. 

4 However, several instruments are needed to provide size distribution measurements (number and 

5 size) over the several orders of magnitude of particle diameters of interest (US EPA, 2009a, 

6 section 3.4.1.5, p. 3-29). These techniques, while widely used in aerosol research, have not yet 

7 been widely used in health effects studies. 

8 As discussed in section 2.2.1, currently available scientific information providing 

9 evidence of associations between fine particles and a broad range of health outcomes has been 

10 substantially strengthened in this review. Epidemiological evidence continues to provide the 

11 strongest support for standards to protect public health from long- and short- term fine particle 

12 exposures. Measurements from community-based ambient monitors have generally been used 

13 for time-series and longitudinal epidemiological studies, and may be used for panel studies as 

14 well (US EPA, 2009a, p. 3-176). New epidemiological studies available in this review have 

15 considered a much larger set of air quality data than was available in the last review based 

primarily on ambient measurement data from the existing PM2.5 monitoring networks.26 16 This 

17 includes consideration of air quality measurements reported in more recent years. These data 

18 have improved our understanding of the spatiotemporal distribution of PM2.5 (US EPA, 2009a, 

19 sections 3.5 and 3.9). 

20 As presented in the ISA, epidemiological studies linking cardiovascular and respiratory 

21 effects as well as mortality with short- and long-term fine particle exposures continue to be 

22 largely indexed by PM2.5 (US EPA, 2009a, chapters 6 and 7). Thus, we reach the preliminary 

23 conclusion that it is reasonable to retain PM2.5 as an indicator for fine particles. We then pose 

24 additional questions to aid in considering whether the currently available scientific evidence 

25 provides support for supplementing the current PM2.5 mass-based indicator by considering 

26 whether there is sufficient evidence to support a standard with a different size fraction or whether 

27 there is sufficient evidence to establish distinct standards focused on regulating specific PM2.5 

28 components or sources of fine particles. 

29  To what extent does the currently available information provide support for 

30 considering a separate indicator for ultrafine particles as a subfraction of fine particles? 

 26 The network of PM2.5 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 areas (MSAs) that have an FRM/Federal Equivalent (FEM) 

monitor. The network of continuous PM2.5 monitors has grown to over 700 locations throughout the U.S. While 

PM2.5 continuous monitors primarily support forecasting and reporting for the Air Quality Index (AQI), they are also 

used in interpreting the diurnal characterization of PM2.5. 
Draft Do Not Quote or Cite March 2010 2-58

1 In considering whether or not the currently available evidence provides support for an 

additional size-based indicator by focusing on ultrafine particles (UFPs)27 2 , we recognize that a 

3 number of studies have focused on UFPs as a subset of PM2.5. In the last review, limited 

4 evidence was available suggesting that the ultrafine subset of fine particles (generally including 

5 particles with a nominal aerodynamic diameter less than 0.1 μm) was associated with adverse 

6 health effects (US EPA, 2004, pp. 8-66 to 8-68). In this review, the ISA notes that there are 

7 many reasons for looking more closely at effects associated with this size fraction including, the 

8 particle number and large surface area of UFPs per unit of mass. Particle number is most highly 

9 concentrated in the UFP fraction with volume (or mass) most concentrated in the larger size 

10 fractions (US EPA, 2009a, p. 3-2) Furthermore, per unit mass, UFPs may have more opportunity 

11 to interact with cell surfaces due to their greater surface area and their greater particle number 

12 compared with larger particles (US EPA, 2009a, p. 5-3). Greater surface area increases the 

13 potential for soluble components to adbsorb to UFPs and be transported into the body (US EPA, 

14 2009a, p. 6-83). Many studies suggest that the surface of particles or substances released from 

15 the surface (e.g., transition metals, organics) interact with biological substrates, and that surface16 associated free radicals or free radical-generating systems may be responsible for toxicity, 

17 resulting in greater toxicity of UFPs per particle surface area than larger particles. In addition, 

18 evidence available in this review suggests that the ability of particles to enhance allergic 

19 sensitization is associated more strongly with particle number and surface area than particle mass 

20 (US EPA, 2009a, p. 6-127). Evidence is also available in this review suggesting that smaller 

21 particles may have a greater potential to cross cell membranes and epithelial barriers. The ISA 

22 notes that, for UFPs, “enhanced translocation to interstitial compartments or to the circultaon 

23 may be important sequelae” (US EPA, 2009a, p. 5-6). More information on possible modes of 

24 action for effects associated with UFPs exposures is discussed in sections 5.1 and 5.4 of the ISA. 

25 With respect to ambient concentrations of UFPs, at present, there is no national network 

26 of UFP samplers, thus, only episodic and/or site-specific data sets exist (US EPA, 2009a, p. 2-

2).28 27 Therefore, a national characterization of concentrations, temporal and spatial patterns, and 

28 trends is not possible, and the availability of ambient UFPs data to support health studies are 

29 extremely limited. In general, UFP particle number concentrations are highly dependent on 

30 monitor location and therefore, more subject to exposure error than accumulation mode particles 

31 (US EPA, 2009a, p. 2-22). The UFP number concentrations fall off sharply downwind from 

32 sources, as UFPs may grow into the accumulation mode by coagulation or condensation (US 

 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 measurements of UFPs (US EPA, 

2009a, sections 3.5.1 and 3.5.2). 
Draft Do Not Quote or Cite March 2010 2-59

1 EPA, 2009a, p. 3-89). Limited studies of UFP ambient measurements suggest these particles 

2 exhibit a high degree of spatial and temporal heterogeneity driven primarily by differences in 

3 nearby source characteristics (US EPA, 2009a, p. 3-84). Internal combustion engines and 

4 therefore, on-road roadways are a notable source of UFPs, so concentrations of UFPs near 

5 roadways can generally be expected to be elevated (US EPA, 2009a, p. 2-3). Concentrations of 

6 UFPs have been reported to drop off much more quickly with distance from roadways than 

7 larger particle sizes (US EPA, 2009a, p. 3-84). 

8 Additional but still limited health evidence available in this review, primarily from 

9 controlled human exposure and toxicological studies, provide evidence for UFP-induced 

10 cardiovascular and respiratory effects. This evidence is largely related to studies focused on 

11 exposure to diesel exhaust (DE), “[a]s a result, it is unclear if the effects observed are due to 

12 UFP, larger particles (i.e., PM2.5), or the gaseous components of DE” (US EPA, 2009a, p. 2-22). 

13 The ISA notes uncertainty associated with the controlled human exposure studies as concentrated 

14 ambient particle (CAP) systems have been shown to modify the composition of UFPs (US EPA, 

15 2009a, p. 2-22, see also section 1.5.3). In addition, relatively few epidemiologic studies have 

16 examined the potential cardiovascular and respiratory effects associated with short-term 

17 exposures to UFPs. These studies have reported inconsistent and mixed results (US EPA, 2009a, 

18 section 2.3.5). 

19 In considering the body of scientific evidence available in this review, the ISA concludes 

20 that the currently available evidence is suggestive of a causal association between short-term 

21 exposures to UFPs and cardiovascular and respiratory effects. Furthermore, the ISA concludes 

22 that evidence is inadequate to infer a causal association between short-term exposure to UFPs 

23 and mortality as well as long-term exposure to UFPs and all outcomes evaluated (US EPA, 

24 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; 

25 Table 2-6). Thus, while new evidence expands our understanding of effects associated with 

26 UFPs, we reach the preliminary conclusion that this information is still too limited to support a 

27 distinct PM standard for UFPs. 

28  To what extent does the currently available information provide support for 

29 considering a separate indicator for a specific PM2.5 component or source category of 

30 fine particles? Conversely, to what extent does the currently available information 

31 provide support for eliminating any component or source category from the mix of fine 

32 particles included in the PM2.5 indicator? 

33 In the last review, EPA recognized the availability of a limited number of epidemiologic 

34 studies that explored associations with various components within the mix of fine particles and 

35 adverse effects (US EPA, 2004, section 9.2.2.1.1, Table 9–3) as well as several studies that used 

36 PM2.5 speciation data to evaluate the association between mortality and particles from different 
Draft Do Not Quote or Cite March 2010 2-60

1 categories of fine particle sources (US EPA, 2004, section 8.2.2.5). As discussed in the last 

2 review, different patterns of associations of various PM2.5 components (e.g., sulfates, nitrates, 

3 metals, organic compounds, elemental carbon (EC)) or source categories of fine particles with 

4 total or cardiovascular mortality were observed in various short-term exposure studies (US EPA, 

5 2004, section 8.2.2.5. Tables 8-3, 8-4, 9-3). However, as noted in the last review, “many PM 

6 components are correlated with each other and also with PM mass, making it difficult to 

7 distinguish effects of the various components. Also, different PM components or characteristics 

8 would be expected to be more closely linked with different health outcomes” (US EPA, 2004, p. 

9 9-30). In addition, a limited number of studies evaluated in the last review used PM2.5 speciation 

10 data to assess the effects of air pollutant combinations or mixtures using factor analysis or source 

11 apportionment methods to link effects with different PM2.5 source types (Schwartz, 2003; Mar et 

12 al., 2003; and Tsai et al., 2000). These studies reported that fine particles from combustion 

13 sources, including motor vehicle emissions, coal combustion, oil burning and vegetative burning, 

14 were associated with increased mortality. No significant increase in mortality was reported with 

15 a source factor representing crustal material in fine particles (US EPA, 2004, section 8.2.2.5.3). 

16 The EPA concluded that these studies indicated that exposure to fine particles from combustion 

17 sources, but not crustal material, was associated with mortality (US EPA, 2004, p. 8-85; US 

18 EPA, 2005, p. 3-16). 

19 Overall, EPA concluded in the last review that the available evidence suggested “that 

20 many different chemical components of fine particles and a variety of different types of source 

21 categories are all associated with, and probably contribute to, mortality, either independently or 

22 in combinations’’ (US EPA, 2004,p. 9-31). Conversely, scientific evidence available in the last 

23 review provided no basis to conclude that any individual fine particle component could not be 

24 associated with adverse health effects (US EPA, 2005, p. 5–17). This evidence provided the 

25 basis for EPA to reach the final decision that “there was not sufficient evidence that would lead 

26 EPA to select one or more PM2.5 component as being primarily responsible for effects associated 

27 with fine particles, nor was there sufficient evidence to suggest that any component should be 

28 eliminated from the indicator for fine particles” (71 FR 61163/1, October 17, 2006). 

29 In addressing the issue of particle composition in this review, the ISA concludes that, 

30 “[f]rom a mechanistic perspective, it is highly plausible that the chemical composition of PM 

31 would be a better predictor of health effects than particle size” (US EPA, 2009a, p. 6-202). 

32 Heterogeneity of ambient concentrations of PM2.5 constituents (e.g., elemental carbon (EC), 

organic carbon (OC), sulfate (SO4

2- 33 ), and nitrate) observed in different geographical regions as 

34 well as regional heterogeneity in PM2.5-related health effects reported in a number of 

35 epidemiologic studies are consistent with this hypothesis (US EPA, 2009a, section 6.6). 
Draft Do Not Quote or Cite March 2010 2-61

1 With respect to the availability of ambient measurement data for fine particle 

2 components, we recognize that, in this review, there are more extensive ambient PM2.5 speciation 

measurement data available through the Chemical Speciation Network (CSN). 29 3 Data from the 

4 CSN monitoring network provide further evidence of spatial and seasonal variation in both PM2.5 

5 mass and composition among cities/regions (US EPA, 2009a, pp. 3-50 to 3-60; Figures 3-12 to 

6 3-18; Figure 3-47). Some of this variation may be related to “regional differences in 

7 meteorology, sources, and topography” (US EPA, 2009a, p. 2-3). While the network of 

8 approximately 200 CSN monitoring sites provides valuable data for development and tracking of 

9 control strategies, its use for providing PM2.5 speciation data to support epidemiological studies 

10 is somewhat limited. The CSN sites provide measurement data on a one-in-three or one-in-six 

11 day schedule and do not capture data every day. Health researchers have expressed a strong 

interest in having access to PM2.5 speciation measurements collected more frequently.30 12 

13 The currently available epidemiologic, toxicological, and controlled human exposure 

14 studies have evaluated the health effects associated with ambient PM2.5 constituents and 

15 categories of fine particle sources, using a variety of quantitative methods applied to a broad set 

16 of PM2.5 constituents, rather than selecting a few constituents a priori (US EPA, 2009a, p. 2-26). 

17 Epidemiological studies have used measured ambient PM2.5 speciation data, including 

18 monitoring data from the CSN, while all of the controlled human exposure and most of the 

19 toxicological studies have used CAPs, and analyzed the constituents therein (US EPA, 2009a, p. 

6-203).31 20 

 29The 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 PM2.5 mass, trace elements, major ions (e.g., sulfates, nitrates, 

ammonium), and organic and elemental carbon. 

30 As outlined in section 6.6.2.11of the ISA, some investigators have circumvented the issue of less than daily 

speciation data by using the PM2.5 chemical species data in a second stage regression to explain the heterogeneity in 

PM10 or PM2.5 mortality risk estimates across cities and assuming that the relative contributions of PM2.5 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 workshop 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 PM2.5 

speciation measurements in large urban areas, is available at www.epa.gov/ORD/npd/pdfs/FINAL-April-2008-AQHealth-Research-Workshop-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 PM2.5 constituents, with EC, OC, SO4

2-, nitrate, and metals 

most commonly measured. Many of the studies reduced the number of ambient PM2.5 constituents by grouping them 

with various factorization or source apportionment techniques to examine the relationship between the grouped 

PM2.5 constituents and various health effects. However, not all studies labeled 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 PM2.5 speciation data. In addition, there were differences in the type and grouping 
Draft Do Not Quote or Cite March 2010 2-62

1 With respect to epidemiological studies evaluating short-term exposures to fine particle 

2 constituents, several new multi-city studies are now available. These studies continue to show an 

3 association between mortality and cardiovascular and/or respiratory morbidity effects and short4 term exposures to various PM2.5 components including nickel (Ni), vanadium (V), elemental 

5 carbon (EC), organic carbon (OC), and sulfates (US EPA, 2009a, sections 6.5.2.5 and 6.6). 

6 Lippmann et al. (2006); Dominici et al. (2007) evaluated the heterogeneity in the PM10–mortality 

7 association as evaluated in the NMMAPS data by analyzing the PM2.5 speciation data. Nickel 

8 (Ni) and Vanadium (V) were identified as significant predictors of variation in PM10-related 

9 mortality across cities, with Ni levels in New York City being reported as particularly high (US 

EPA, 2009a, section 6.5.2.5; Figure 6-31).32 10 Bell et al. (2009) and Peng et al. (2009) conducted 

11 similar analyses focusing on the variation in PM2.5-related cardiovascular and respiratory 

12 hospital admissions in older adults. Peng et al. (2009) focused on the components that make up 

13 the majority of PM2.5 mass and found that in multi-pollutant models only EC and OC were 

14 significantly associated with risk of hospitalization for cardiovascular disease. Bell et al. (2009) 

15 used data from twenty PM2.5 components and found that EC, Ni, and V were most positively and 

16 significantly associated with the risk of PM2.5-related hospitalizations suggesting that the 

17 observed associations between PM2.5 and hospitalizations may be primarily due to particles from 

18 oil combustion and traffic (US EPA, 2009a, section 6.2.10.1). In a study of 25 U.S. cities, 

19 Franklin et al. (2008) focused on a time-series regression of mortality related to PM2.5 mass by 

20 season and also examined effect modification due to various PM2.5 species. They concluded that 

Al, As, Ni, Si and SO4

2- 21 were significant effect modifiers of PM2.5 mortality risk estimates, and 

“simultaneously including Al, Ni, and SO4

2- 22 together or Al, Ni, and As together further increased 

23 explanatory power. Of the species examined, Al and Ni explained the most residual 

heterogeneity” (US EPA, 2009a, p. 6-194; Table 6-17).33 24 Furthermore, Ostro et al (2006) 

25 examined associations between PM2.5 components and mortality in six California counties and 

26 found an association between mortality, especially cardiovascular-related mortality and several 

27 PM2.5 components including EC, OC, nitrate, Fe, K, and Ti at various lags (US EPA, 2009a, p. 6-

28 195).

 

of PM2.5 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 PM10 mortality risk estimate and the PM2.5 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 the 25 cities examined by Franklin et al. (2008). 
Draft Do Not Quote or Cite March 2010 2-63

1 Limited evidence is available to evaluate the health effects associated with long-term 

2 exposures to PM2.5 components (US EPA, 2009a, section 7.6.2). The most significant new 

3 evidence is provided by a study that evaluated multiple PM2.5 components and an indicator of 

4 traffic density in an assessment of health effects related to long-term exposure to PM2.5 (Lipfert 

5 et al., 2006). Using health data from a cohort of U.S. military veterans and PM2.5 data from 

6 EPA’s CSN, Lipfert et al. (2006) reported positive associations between mortality and long-term 

7 exposures to nitrates, EC, Ni and V as well as traffic density and peak O3 concentrations. 

8 Additional evidence from a long-term exposure study conducted in a Dutch cohort provides 

9 supportive evidence that long-term exposure to traffic-related particles is associated with 

10 increased mortality (Breelen et al., 2008). 

11 With respect to source categories of fine particles associated with a range of health 

12 endpoints, the ISA reports that currently available evidence suggests associations between 

13 cardiovascular effects and a number of specific PM2.5 –related source categories, specifically oil 

14 combustion, wood or biomass burning, motor vehicle emissions, and crustal or road dust sources 

15 (US EPA, 2009a, section 6.6; Table 6-18). In addition, a few studies have evaluated associations 

16 between PM2.5–related source categories and mortality. These studies included a reported 

17 association between mortality and a PM2.5 coal combustion factor (Laden et al., 2000), while 

others linked mortality to a secondary SO4

2– 18 long-range transport PM2.5 source (Ito et al., 2006; 

19 Mar et al., 2006) (US EPA, 2009a, section 6.6.2.1). There is less consistency in associations 

20 observed between PM2.5 sources and respiratory health effects, which may be partially due to the 

21 fact that fewer studies have been conducted that evaluated respiratory-related outcomes and 

measures. However, there is some evidence for associations with secondary SO4

2– 22 .and 

23 decrements in lung function in asthmatic and healthy adults(US EPA, 2009a, p. 6-211; Gong et 

24 al., 2005; Lanki et al., 2006). Respiratory effects relating to the crustal/soil/road dust and traffic 

25 sources of PM have been observed in asthmatic children and adults (US EPA, 2009a, p. 6-205; 

26 Gent et al., 2009; Penttinen et al., 2006). 

27 Recent studies have shown that source apportionment methods have the potential to add 

28 useful insights into which sources and/or PM constituents may contribute to different health 

29 effects. Of particular interest are several epidemiologic studies that compared source 

30 apportionment methods and reported consistent results across research groups (US EPA, 2009a, 

31 p. 6-211; Hopke et al., 2006; Ito et al., 2006; Mar et al., 2006; Thurston et al., 2005). These 

32 studies reported associations between total mortality and secondary sulfate in two cities for two 

33 different lag times. The sulfate effect was stronger for total mortality in Washington D.C. and 

34 for cardiovascular-related morality in Phoenix (US EPA, 2009a, p. 6-204). These studies also 

35 found some evidence for associations with mortality and a number of source categories (e.g., 

36 biomass/wood combustion, traffic, copper smelter, coal combustion, sea salt) at various lag times 
Draft Do Not Quote or Cite March 2010 2-64

1 (US EPA, 2009a, p. 6-204). Sarnat et al., (2008) compared three different source apportionment 

2 methods and reported consistent associations between ED visits for cardiovascular diseases with 

3 mobile sources and biomass combustion as well as increased respiratory-related ED visits 

4 associated with secondary sulfate (US EPA, 2009a, pp. 6-204 and 6-211; Sarnat et al., 2008). 

5 In summary, in considering the currently available evidence for health effects associated 

6 with chemical components and source categories of PM2.5 as presented in the ISA, we reach the 

7 preliminary conclusion that additional information available in this review continues to provide 

8 evidence that many different constituents of the fine particle mixture as well as specific source 

9 categories of fine particles are linked to adverse health effects. However, as noted in the ISA, 

10 while “[t]here is some evidence for trends and patterns that link particular ambient PM 

11 constituents or sources with specific health outcomes...there is insufficient evidence to 

12 determine whether these patterns are consistent or robust” (US EPA, 2009a, p. 6-210). 

13 Furthermore, the ISA concludes that “the evidence is not yet sufficient to allow differentiation of 

14 those constituents or sources that are more closely related to specific health outcomes” (US EPA, 

15 2009a, pp. 2-26 and 6-212). Therefore, we reach the preliminary conclusion that the currently 

16 available evidence is not sufficient to support consideration of a separate indicator for a specific 

17 PM2.5 component or source category of fine particles. Furthermore, we also reach the 

18 preliminary conclusion that the evidence is not sufficient to support eliminating any component 

19 or source from the mix of fine particles included in the PM2.5 indicator.

20 We recognize that much research supported by EPA, the Health Effects Institute (HEI), 

21 the Electric Power Research Institute (EPRI), and others is underway to evaluate the role of 

22 PM2.5 components/sources and agree that additional research is needed to improve future 

23 understanding of the role of specific fine particle components and/or sources of fine particles. 

24 Summary 

25 In considering whether currently available evidence provides support for retaining, 

26 revising, or supplementing the current PM2.5 mass-based indicator, we first reach the preliminary 

27 conclusion that it is appropriate to retain PM2.5 as the indicator for fine particles. Secondly, we 

28 reach the preliminary conclusion that the currently available evidence does not provide a 

29 sufficient basis for supplementing the mass-based PM2.5 indicator by considering a separate 

30 indicator for ultrafine particles as a subfraction of fine particles. Furthermore, we also reach the 

31 preliminary conclusion that the currently available evidence is too limited to provide support for 

32 considering a separate indicator for a specific PM2.5 component or source category of fine 

33 particles or for eliminating any individual component or source category from the mix of fine 

34 particles included in the PM2.5 mass-based indicator. 
Draft Do Not Quote or Cite March 2010 2-65

1 2.3.2 Averaging Times 

2 In the last review, EPA recognized that the available information related to exposure 

3 periods of concern was generally consistent and supportive of the conclusions reached in the 

4 review completed in 1997. In that review, the Agency retained two PM2.5 standards, based on 

5 annual and 24-hour averaging times in order to provide protection for health effects associated 

6 with short- and long-term exposure periods (71 FR 61164, October 17, 2006). In this review, in 

7 evaluating alternative fine particle standards, we first address the element of the standard related 

8 to averaging time by asking the following question: 

9  To what extent does the currently available information continue to provide support for 

10 the current 24-hour and annual averaging times? 

11 In considering whether the information available in this review supports consideration of 

12 different averaging times for PM2.5 standards, we note that the available information is generally 

13 consistent with and supportive of the conclusions reached in the previous reviews to set a suite of 

14 PM2.5 standards including standards with both annual and 24-hour averaging times. The 

15 overwhelming majority of studies conducted since the last review continue to utilize 24-hour and 

16 annual averaging times, and largely contribute to the body of evidence for health effects related 

17 to both short-term (from less than 1 day to up to several days) and long-term (from a year to 

18 several years) measures of PM2.5. Consequently, our preliminary conclusion is that the currently 

19 available evidence continues to provide support for a 24-hour and annual averaging time. 

20 With respect to a standard with an annual averaging time, we recognize that an annual 

21 standard would provide effective protection against both annual and multi-year, cumulative 

22 exposures that are associated with an array of health effects. With regard to providing protection 

23 for short-term fine particle exposures, we note that the large majority of short-term 

24 epidemiologic studies report associations based on 24-hour averaging times or on multiple-day 

25 averages (i.e., distributed lag). Furthermore, we recognize that a 24-hour standard can 

26 effectively protect against episodes lasting several days, as well as providing some degree of 

27 protection from potential effects associated with shorter duration peak levels of PM2.5, and from 

28 episodes that result in localized or seasonal PM2.5 exposures of concern in areas where the 

29 highest 24-hour-to-annual mean PM2.5 ratios are appreciably above the national average. In 

30 consideration of the currently available evidence, we have focused on evaluating alternative 

31 standards in the quantitative risk assessment conducted for this review that retained the 

32 averaging times of the current standards (i.e, 24-hour and annual averaging times) (US EPA, 

33 2010a) 

34 In summary, we reach the preliminary conclusion that there is strong support in this 

35 review for retaining the current 24-hour and annual averaging times. We have then considered if 
Draft Do Not Quote or Cite March 2010 2-66

1 the currently available evidence provides support for supplementing the current averaging times 

2 with additional standards focused on subdaily, multi-day, or seasonal exposures by posing two 

3 more specific questions. 

4  To what extent does the currently available scientific evidence provide support for 

5 considering a standard with an averaging time less than 24 hours to address health 

6 effects associated with subdaily fine particle exposures? 

7 In the last review, we recognized the availability of limited evidence of effects associated 

8 with exposure periods shorter than 24-hours (e.g., one to several hours) (US EPA, 2004, section 

9 3.5.5.1) and concluded that, while this evidence was “too limited to serve as the basis for 

10 establishing a shorter-than-24-hour fine particle primary standard,” it provided “added weight to 

11 the importance of a standard with a 24-hour averaging time” (71 FR 61164/2; US EPA, 2005, 

12 section 5.3.3). More specifically, the AQCD noted that while few epidemiological studies had 

13 used ambient PM concentrations averaged over time intervals shorter than 24 hours, several 

14 epidemiological studies reported statistically significant associations between 2- to 4-hour PM2.5

15 concentrations and cardiovascular health endpoints, including myocardial infarction (MI) 

16 incidence and heart rate variability (HRV) (US EPA 2004, pp. 8-162 to 8-165). In particular, 

17 Peters et al (2001) reported effect estimates for MI incidence with PM2.5 averaged over 2- and 

18 24- hours that were similar in magnitude and statistically significant (US EPA 2004, p. 8-165). 

19 In this review, a much larger body of more recent studies provide additional evidence of 

20 cardiovascular effects associated with exposure periods shorter than 24 hours (US EPA, 2009a, 

21 section 6.2). In this review, two studies that assessed sub-daily and daily exposures did not 

22 observe an association between PM2.5 and risk of MI, however no association was evident with 

23 24-hour exposures to PM2.5 as well (US EPA, 2009a, p. 6-67; Sullivan et al., 2005; Peters et al., 

24 2005). One study found a strong positive association between self-reported exposure to traffic 

25 and the onset of an MI within one hour, although this study did not directly measure traffic26 related pollution (US EPA 2009a, p. 6-67; Peters et al. 2004). For cardiac arrests witnessed by 

27 bystanders, another study found a significant association with PM2.5 exposure during the hour of 

28 the arrest, with even larger risk estimates for older adults (ages 60-75) or those that presented 

29 with asystole, a particular form of cardiac arrest when electrical activity in the heart stops (US 

30 EPA 2009a, p. 6-77; Rosenthal et al. 2008). 

31 With respect to heart rate and HRV, epidemiological studies reported effects associated 

32 with pollutant concentrations lagged as short as 1 to 2 hours, but more consistently with lags of 

33 24 to 48 hours. The results of several new controlled human exposure studies provide limited 

34 evidence to suggest that acute exposures (2-hour) to near ambient levels of concentrated ambient 

35 particles, or CAPs (PM2.5, PM10-2.5 and ultrafine particles) may be associated with small changes 

36 in HRV (USEPA, 2009a, p. 6-10). Changes in HRV parameters, however, are variable with 
Draft Do Not Quote or Cite March 2010 2-67

1 some showing increased parasympathetic activity relative to sympathetic activity and others 

2 showing the opposite. One study reported adverse associations of 2-hour exposures to PM10 with 

3 implantable cardiac defibrillator-detected ventricular arrythmias (US EPA, 2009a, p. 6-15; 

4 Ljungman et al., 2008). Two panel studies of elderly subjects found electrocardiogram changes 

5 typically representative of cardiac ischemia (S-T segment depression) significantly associated 

6 with exposures to PM2.5 of less than 24 hours (US EPA 2009a, p. 6-21; Gold et al., 2005; Lanki 

7 et al. 2008). 

8 With respect to vasomotor function, the systemic vasculature is likely to be a target 

9 organ. Endothelial dysfunction is a factor in many diseases and may contribute to the origin 

10 and/or exacerbation of perfusion-limited diseases, such as MI or ischemic heart disease (IHD), as 

11 well as hypertension. Endothelial dysfunction is also a characteristic feature of early and 

12 advanced atherosclerosis. Six studies found effects of exposures of 2 hours or less on other 

vasomotor outcomes.34 13 The evidence on blood pressure changes is more mixed, with one panel 

14 study (Dales et al., 2007; EPA 2009, p. 6-35) finding no association with blood pressure changes 

15 with 2-hour exposures to traffic-related PM2.5; while one panel and two controlled human 

16 exposure studies (US EPA, p. 6-37; Chuang et al., 2005; Urch et al., 2005 and Fakhri et al., 

17 2009) reported changes in blood pressure from 1- to 3-hour exposures to submicrometer 

18 particles, and 2-hour exposures to a combination of O3 and CAPs, respectively. 

19 One panel study that investigated associations between ambient PM and markers of 

20 systemic inflammation among senior citizens (≥ 60 years of age) (US EPA, 2009a, p. 6-41; 

21 Dubowsky et al., 2006), found positive associations between daily PM2.5 levels and measures of 

22 C-reactive protein (CRP), interleukin-6 (IL-6), and white blood cells (WBCs). When the 

23 analysis was limited to exposures that occurred only on daily bus trips (2 hours), the effect 

24 estimates were similar in direction to the main analysis but were smaller in magnitude, with the 

25 authors expressing the view that this was likely due to greater measurement error. Another panel 

26 study assessed the effects of in-vehicle exposure to PM2.5 of healthy young non-smoking male 

27 state troopers working from 3 PM to midnight (US EPA, 2009a, p. 6-41 and 6-48; Riediker et al., 

28 2004). This study concluded that PM2.5 originating from speed-changing traffic modulates the 

29 autonomic control of the heart rhythm, increases the frequency of premature supraventricular 

30 beats and elicits proinflammatory and pro-thrombotic responses in healthy young men. New 

31 studies involving controlled human exposures to various particle types have provided limited and 

32 inconsistent evidence of a PM-induced increase in markers of systemic inflammation (US EPA, 

 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 PM2.5, 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

1 2009a, p. 6-46). New findings for hemostasis, thrombosis and coagulation from controlled 

2 human exposure studies have provided in consistent evidence that short-term exposure to PM at 

3 near ambient levels may have small, yet statistically significant effects on hemostatic markers in 

4 healthy subjects or people with coronary artery disease (US EPA, 2009a, p. 6-50). 

5 With respect to respiratory health outcomes, in the last review, evidence of association 

6 between respiratory symptoms and subdaily exposures to PM10 was available from two US panel 

7 studies of symptoms in asthmatic subjects (US EPA 2004, section 8.3.3.1.1). These two studies 

8 used 1-hour and 24-hour average concentrations. The PM10 1-hour outcome was larger than the 

9 24-hour outcome for lower respiratory illness in one study, but the reverse was true for cough in 

10 the other study. 

11 In this review, evidence of subdaily PM2.5 exposures associated with respiratory diseases 

12 continues to be limited. The ISA concludes that for several studies of hospital admissions or 

13 medical visits for respiratory diseases, the strongest associations were observed with 24-hour 

14 average or longer exposures, not with less then 24-hour exposures (US EPA, 2009a, section 6.3). 

15 A study that examined evidence of respiratory effects associated with subdaily PM2.5 exposures 

16 in two New York City communities by assessing the association between 24-hour and 1-hour 

17 maximum PM2.5 levels and ED visits. This study reported an increase in asthma-related ED 

18 visits that was similar for the two time periods (New York State Department of Health, 2006). 

19 These results were robust to adjustment for copollutants. However, a panel study found an 

association between a 10 μg/m3 20 increase in morning maximum 1-hour mean, but not daily, PM2.5

21 concentrations and increased likelihood of rescue medication use in asthmatic children (US EPA 

22 2009a, p. 6-90; Rabinovitch et al., 2006). Another study examined the association between a 

23 marker for pulmonary inflammation (exhaled nitric oxide, or eNO), and ambient PM2.5

concentrations. Each 10 μg/m3 24 increase in 1-hour mean PM2.5 concentration was associated with 

25 a statistically significant increase in eNO among asthmatic children not taking inhaled 

26 corticosteroids (US EPA 2009, p. 6-101; Mar et al., 2005). 

27 In summary, there is a rapidly growing body of studies that provide evidence for 

28 cardiovascular effects associated with subdaily exposure to PM, especially effects related to 

29 HRV, cardiac ischemia, and vasomotor function, and also of changes in markers of systemic 

30 inflammation, hemostasis, thrombosis and coagulation. Because these studies have used 

31 different indicators (e.g., PM2.5, PM10, PM10-2.5, ultrafine particles), averaging times, and health 

32 outcomes, it is difficult to draw conclusions about cardiovascular effects associated specifically 

33 with subdaily exposures to PM2.5. Although there is additional evidence of respiratory effects 

34 associated with PM2.5 exposure periods shorter than 24-hours (e.g., one to several hours), this 

35 evidence is much sparser than for cardiovascular effects. Considering the currently available 

36 evidence, we reach the preliminary conclusion that this information is too unclear, with respect 
Draft Do Not Quote or Cite March 2010 2-69

1 to the indicator, averaging time and health outcome, to serve as a basis for establishing a shorter2 than-24-hour PM2.5 primary standard at this time. However, this evidence does provide added 

3 weight to the importance of a standard with a 24-hour averaging time. We recognize that the 

4 assessment of health effects associated with shorter-than-24-hour exposure is an important area 

5 of research that could provide a basis for the consideration of a subdaily PM standard in the 

6 future. We note that the availability of hourly PM2.5 concentrations from the PM2.5 continuous 

7 monitors reporting to the AQS should provide the basis for a clearer assessment of the effects of 

8 subdaily exposure to PM2.5 in the future. 

9  To what extent does the currently available scientific evidence provide support for 

10 considering separate standards with distinct averaging times to address effects 

11 associated with seasonal fine particle exposures? 

12 With regard to health effects associated with PM2.5 exposure across varying seasons in 

13 this review, Bell et al. (2008) reported higher PM2.5 risk estimates for hospitalization for 

14 cardiovascular and respiratory diseases in the winter compared to other seasons in a large, 

15 national multi-city study. In comparison to the winter season, smaller statistically significant 

16 associations were also reported between PM2.5 and cardiovascular morbidity for spring and 

17 autumn, and a positive non-significant association was observed for the summer months. In the 

18 case of mortality, Zanobetti and Schwartz (2009) reported in their multi-city US based study a 4-

19 fold higher effect estimate for PM2.5 associated mortality for the spring as compared to the 

20 winter. These results suggest individuals are at greater risk of dying from higher exposures to 

21 PM2.5 in the warmer months, and at greater risk of PM associated hospitalization for 

22 cardiovascular and respiratory diseases during colder months of the year. Overall, we observe 

23 that there are few studies presently available to deduce a general pattern in PM2.5 risk across 

24 seasons. In addition, these studies utilized 24-hour exposure periods within each season to assess 

25 the PM2.5 associated health effects, and do not provide information on health effects associated 

26 with a season-long exposure to PM2.5. Due to these limitations in the currently available 

27 evidence, we reach the preliminary conclusion that there is no basis to consider a seasonal 

28 averaging time separate from a 24-hour averaging time. 

29 Summary

30 In summary, we recognize that the currently available evidence informs our understanding of 

31 exposure durations of concern and continues to provide strong support for standards that provide 

32 protection for both short- and long-term exposures. In considering the possibility of effects 

33 associated with subdaily PM2.5 exposures (i.e., less than 24-hour exposures) we recognize that 

34 there is additional evidence available in this review, primarily focused on cardiovascular effects 

35 with more limited evidence for respiratory effects. However, because these studies have used 

36 different indicators of PM exposure (e.g., PM2.5, PM10, UFPs), averaging times, and a broad 
Draft Do Not Quote or Cite March 2010 2-70

1 range of health outcomes, it is difficult to use this evidence to serve as a basis for establishing a 

2 standard with a shorter-than-24-hour averaging time. With respect to seasonal effects, while we 

3 recognize there is some new evidence for PM2.5- related effects differentiated by season, we reach 

4 the preliminary conclusion that this evidence is, at this point, too limited to use as a basis for 

5 establishing a PM2.5 standard with a seasonal averaging time. Based on the above considerations, 

6 we initially conclude that the currently available information provides strong support for 

7 retaining the current annual and 24-hour averaging times but does not provide support for 

8 alternative averaging times of less than 24-hours or for seasons 

9 2.3.3 Forms 

10 The “form” of a standard defines the air quality statistic that is to be compared to the 

11 level of the standard in determining whether an area attains the standard. In this review, staff are 

12 evaluating whether currently available information support consideration of alternative forms for 

13 the annual or 24-hour PM2.5 standards. 

14 2.3.3.1 Form of the Annual Standard 

15 In 1997, EPA established the form of the annual PM2.5 standard as an annual arithmetic 

16 mean, averaged over 3 years, from single or multiple community-oriented monitors. This form 

17 was intended to represent a relatively stable measure of air quality and to characterize area-wide 

18 PM2.5 concentrations. The arithmetic mean served to represent the broad distribution of daily air 

19 quality values, and a 3-year average provided a more stable risk reduction target than a single20 year annual average. When setting the initial fine particle standards in 1997, the level of the 

21 annual PM2.5 standard was to be compared to measurements made at the community-oriented 

monitoring site recording the highest level, or, if specific constraints were met35 22 , measurements 

23 from multiple community-oriented monitoring sites could be averaged (62 FR 38671 to 38672, 

24 July 18, 1997). The constraints for allowing the use of spatially averaged measurements were 

25 intended to limit averaging across poorly correlated or widely disparate air quality values to 

26 ensure that spatial averaging would not result in inequities in the level of protection provided by 

27 the PM2.5 standards against health effects associated with short- and long-term PM2.5 exposures 

28 (62 FR 38672). This approach was judged to be consistent with the epidemiologic studies on 

29 which the PM2.5 standard was primarily based, in which air quality data were generally averaged 

30 across multiple monitors in an area or were taken from a single monitor that was selected to 

31 represent community-wide exposures, not localized “hot spots.”

 35 The original criteria for spatial averaging included: (1) the annual mean concentration at each site shall be within 

20 percent of the spatially averaged annual mean, and (2) the daily values for each monitoring site pair shall yield a 

correlation coefficient of at least 0.6 for each calendar quarter. 
Draft Do Not Quote or Cite March 2010 2-71

1 In the last review, in considering the form of the primary annual PM2.5 standard, EPA 

2 posed the question as to whether an annual standard that allowed for spatial averaging, within the 

3 original specified or alternative constraints, would provide appropriate public health protection. 

4 Analyses conducted in the last review, based on a much larger set of PM2.5 air quality data than 

5 was available for the review completed in 1997, assessed both aggregate population risk across 

6 an entire urban area and the potential for disproportionate impacts on potentially vulnerable 

7 populations within an area. The results of these analyses provided evidence concerning the 

8 potential for disproportionate impacts on potentially vulnerable populations, noting “the highest 

9 concentrations in an area tend to be measured at monitors located in areas where the surrounding 

10 population is more likely to have lower education and income levels, and higher percentages of 

11 minority populations” (71 FR 61166/2, see also US EPA, 2005, section 5.3.6.1; Schmidt et al., 

2005, Attachment A/Analysis 7).36 12 

13 In addition, the effect of allowing the use of spatial averaging on aggregate population 

14 risk was considered as part of the sensitivity analyses included in the health risk assessment 

15 conducted for the last review (US EPA, 2005, section 4.2.2). In that analysis, changing the basis 

16 of the annual standard design value from the concentration at the highest monitor to the average 

17 concentration across all monitors reduced the air quality adjustment needed to just meet the 

18 current or alternative annual standards. As expected, the estimated risks remaining upon 

19 attainment of the current annual standard in areas where the annual standards was the 

20 “controlling standard” were greater when spatial averaging was used than when the highest 

21 monitor was used (i.e., the estimated reductions in risk associated with just attaining the current 

22 or alternative annual standards are less when spatial averaging was used). The estimated 

23 mortality incidence associated with long-term exposure in most cases ranged from about 10 to 

24 60% higher when spatial averaging was used, and estimated mortality incidence associated with 

25 short-term exposure in most cases ranged from about 5 to 25% higher. In light of these analyses, 

26 EPA retained the form of the standard as an annual arithmetic mean, averaged over 3 years with 

27 modifications that strengthened the standard by tightening the criteria for use of spatial 

averaging37 28 to provide increased protection for vulnerable populations exposed PM2.5. 

 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 PM2.5 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 marker for lower socioeconomic status (SES) that may be related to increased 

vulnerability to the effects of fine particle exposures, for example, as a result of greater exposure from proximity to 

sources such as roadways and industry, as well as other factors such as poorer health status and access to health care 

(US EPA, 2004, section 9.2.4.5). 

37 The current criteria for spatial averaging include: (1) the annual 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 least 0.9 for each calendar quarter (71 FR 61167/2-3, October 17, 2006). 
Draft Do Not Quote or Cite March 2010 2-72

1 In this review, the currently available evidence provides stronger support that 

2 socioeconomic status (SES), measured using surrogates such as educational attainment, 

3 residential location, and income level, modifies the association between PM and morbidity and 

4 mortality outcomes. Thus, as discussed in section 2.2.1, the ISA concludes that susceptible 

5 populations include persons with lower SES levels. In light of this information and the analyses 

6 conducted for the last review as discussed above, we believe that the existing constraints on 

7 spatial averaging, as modified in 2006, may not be adequate to avoid substantially greater 

8 exposures in some areas, potentially resulting in disproportionate impacts on persons with lower 

9 SES levels. Therefore, we are reconsidering the appropriateness of continuing to allow spatial 

10 averaging across monitors as part of the form of the annual PM2.5 standard. Recognizing that it is 

11 the link between the form and the level of a standard that determines the degree of public health 

12 protection the standard affords, we discuss consideration for eliminating the spatial averaging 

13 provisions from the form of the annual PM2.5 standard in conjunction with consideration of 

14 alternative levels to address health effects related to long-term PM2.5 exposures in section 2.3.4 

15 below.

16 2.3.3.2 Form of the 24-Hour Standard 

17 In 1997, EPA established the form of the 24-hour PM2.5 standard as the 98th percentile of 

18 24-hour concentrations at each population-oriented monitor within an area, averaged over three 

19 years (62 FR at 38671 to 38674, July 18, 1997). In making that decision, EPA recognized that a 

20 concentration-based form gave proportionally greater weight to days when concentrations were 

21 well above the level of the standard than to days when the concentrations were just above the 

22 standard. Further, a concentration-based form better compensated for missing data and less23 than-every-day monitoring; and, when averaged over 3 years, it had greater stability and, thus, 

24 facilitated the development of more stable implementation programs. The Agency selected the 

98th 25 percentile as an appropriate balance between adequately limiting the occurrence of peak 

26 concentrations and providing increased stability and robustness. In addition, by basing the form 

27 of the standard on concentrations measured at population-oriented monitoring sites, EPA 

28 intended to provide protection for people residing in or near localized areas of elevated 

29 concentrations. 

30 In the last review, in conjunction with considering alternative 24-hour standard levels, 

31 EPA concluded it was appropriate to retain a concentration-based form that was defined in terms 

32 of a specific percentile of the distribution of 24-hour PM2.5 concentrations at each population33 oriented monitor within an area, averaged over 3 years. In that review, in considering retaining 

the 98th percentile form or revising the standard to a 99th 34 percentile from, the Agency evaluated 

35 the combination of form and level to provide appropriate public health protection and, in 
Draft Do Not Quote or Cite March 2010 2-73

1 particular, considered: (1) the relative risk reduction afforded by alternative forms at the same 

2 standard level, (2) the relative year-to-year stability of the air quality statistic to be used as the 

3 basis for the form of a standard, and (3) the implications from a public health communication 

4 perspective of the extent to which either form allows different numbers of days in a year to be 

5 above the level of the standard in areas that attain the standard. Based on these considerations, 

the Administrator concluded it was appropriate to retain the 98th 6 percentile form of the 24-hour 

7 standard in conjunction with lowering the level of the standard. In reaching this final decision, 

8 EPA recognized a technical problem associated with a potential bias in the method used to 

calculate the 98th 9 percentile concentration for this form. As such, EPA adjusted the sampling 

10 frequency requirement in order to reduce this bias. Accordingly, the Agency modified the final 

11 monitoring requirements such that areas that are within 5 percent of the standards are required to 

12 increase the sampling frequency to every day (71 FR 61164 to 61165, October 17, 2006). 

13 In this first draft PA, we have focused consideration of alternative 24-hour PM2.5 

14 standards on alternative levels only, as discussed in section 2.3.5. In the second draft PA, we 

15 intend to explore more fully information regarding peak air quality concentrations to better 

16 inform our understanding of the implications of retaining or modifying the current form of the 

17 24-hour standard. 

18 2.3.4 Alternative Levels to Address Health Effects Related to Long-term PM2.5 Exposures 

19 In considering alternative PM2.5 standards that would provide protection against health 

20 effects related to long-term exposures, we have taken into account both evidence-based and risk21 based considerations. As discussed below, we first evaluate the available evidence from long22 term PM2.5 exposure studies, as well as the uncertainties and limitations in that evidence as 

23 presented in the ISA, to assess the degree to which alternative annual PM2.5 standards can be 

24 expected to provide protection against effects related to long-term exposures (section 2.3.4.1). 

25 Secondly, we have considered the quantitative risk estimates associated with long-term PM2.5

26 exposure, as discussed in the second draft RA, to assess the extent to which alternative standards 

27 can be expected to reduce the estimated risks attributable to long-term exposure to PM2.5 (section 

28 2.3.4.2). With respect to the suite of PM2.5 standards, our preliminary integrated conclusions 

29 presented in section 2.3.6 are based in part on the conclusions from this section and in part on 

30 preliminary staff conclusions from section 2.3.5, in which alternative PM2.5 standards to address 

31 health effects related to short-term PM2.5 exposures are discussed. 

32 2.3.4.1 Evidence-based Considerations 

33 In taking into account evidence-based considerations for informing our understanding of 

34 alternative levels to address health effects related to long-term fine particle exposures, we have 
Draft Do Not Quote or Cite March 2010 2-74

1 initially focused on long-term PM2.5 exposure studies conducted in the U.S. and Canada and 

2 placed the greatest weight on associations that have been judged in the ISA to be causal or likely 

3 causal. We have also considered the evidence for a broader range of health outcomes judged in 

4 the ISA to have suggestive evidence of a causal association or that focus on specific susceptible 

5 populations to evaluate whether this evidence provides support for considering lower alternative 

6 levels. Collectively, we have integrated the currently available evidence to address the following 

7 question: 

8  To what extent does the currently available evidence provide support for revising the 

9 current suite of standards to provide protection for long-term fine particle exposures? 

10 In looking first at evidence from long-term PM2.5 exposure studies of mortality (causal 

11 association), we note, as discussed in section 2.2.1, that the extended follow-up analyses of the 

12 ACS and Harvard Six Cities studies, have confirmed and strengthened evidence of associations 

13 reported in the last review at lower air quality levels. In addition, new cohort studies, including 

14 the WHI evaluating cardiovascular-related mortality in postmenopausal women and analyses of 

15 mortality in a Medicare cohort, provide further evidence of effects associated with long-term 

16 PM2.5 exposures at air quality levels in the same range as the more recent years of air quality data 

17 evaluated in the ACS and Harvard Six Cities extended follow-up studies. 

18 As outlined in Figure 2-1 long-term mean PM2.5 concentrations across all cities evaluated 

in each of these studies range from 10.7 to 16.4 μg/m3.

38 19 In looking first at the long-term 

20 exposure mortality studies, we note that the long-term mean PM2.5 concentration in the extended 

follow-up of the Harvard Six Cities study was 16.4 μg/m3 21 . As noted in section 2.2.1, in focusing 

22 on the extended follow-up period (1990-1998), we estimate an aggregate long-term mean PM2.5 

concentration across the six cities of 14.8 μg/m3 23 (Laden, 2009). Eftim et al., (2008) evaluated 

24 mortality in a Medicare cohort consisting of adults age 65 and older, a susceptible population, 

within the same six cities using more recent air quality with a long-term mean of 14.1 μg/m3 25 . In 

26 the extended ACS study, the mean for the more recent time period used in the analysis (1999 to 

2000) was 14.0 μg/m3 27 . In looking at the association based on the air quality for both time 

periods, the long-term mean PM2.5 concentration was 17.1 μg/m3 28 (Pope et al., 2004). Analysis of 

29 mortality associated with long-term PM2.5 exposure using a Medicare cohort and the ACS 

30 locations using more recent air quality reported a long-term mean PM2.5 concentration of 13.6 

μg/m3 31 (Eftim et al., 2008). Additional evidence of mortality associated with long-term PM2.5 

32 exposure in the MCAPS study across a larger number of counties (668 vs. 110 counties) using 

33 more extensive air quality data, provides evidence of effects in older adults, a susceptible 

34 population, at similar levels. This study included effect estimates for three geographic areas (i.e., 

 38 We note that Figure 2-1 also includes studies with substantially higher long-term mean PM2.5 concentrations.
Draft Do Not Quote or Cite March 2010 2-75

1 Figure 2-2. Distribution of study-specific area mean PM2.5 concentrations. 2 

Concentration (μg/m3)

(a) Representative Long-Term Exposure Studies (b) Representative Short-Term Exposure Studies

EPA 

CM

Study

Author

EPA 

max

EPA 

CM

Study

Author

EPA 

max

EPA 

CM

Study

Author

EPA 

max

EPA 

CM

Study

Author

EPA 

max

EPA 

CM

Study

Author

EPA 

max

EPA 

CM

Study

Author

EPA 

max

Eftim-ACS Krewski Miller Bell Dominici06 Zanobetti

05

1015202530

Left plots represent the study author results; middle plots represent EPA replication results using a community monitor, CM, (spatial average) approach; and right plots represent EPA replication results using a maximum value approach (max monitor mean 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 standard deviation from the mean, and dots represent the minimum and maximum values.

3 
Draft Do Not Quote or Cite March 2010 2-76

1 eastern, central, western) with long-term median PM2.5 concentrations ranging from 10.7 to 14.0 

μg/m3 2 (Zeger et al., 2008). In evaluating the air quality data considered in this study, we believe 

3 it is most appropriate to focus on the long-term median concentration across all cities which was 

reported as 13.2 μg/m3 4 (Zeger et al., 2008). A cystic fibrosis cohort study of mortality reported a 

5 positive but not statistically significant mortality association with an aggregate long-term mean 

PM2.5 concentration of 13.7 μg/m3 6 in a susceptible population (Goss et al., 2004)

7 In considering new evidence for cardiovascular effects associated with long-term PM2.5 

8 exposure (causal association), we note the WHI reported positive and statistically significant 

effects at a long-term average across cities of 13.5 μg/m3 9 (Miller et al, 2007). As noted above in 

10 section 2.2.1, this study considered the associations between long-term exposure to PM2.5 and 

11 cardiovascular-related mortality as well as cardiovascular morbidity in post-menopausal women 

12 with no previous history of cardiac disease. 

13 Furthermore, with respect to respiratory effects associated with long-term PM2.5 exposure 

14 (likely causal association), the continued follow-up of the Southern California CHS's cohort 

15 study provides stronger evidence of decreased lung function growth in children, a susceptible 

16 population, that persisted into early adulthood at a long-term mean PM2.5 concentration across 12 

communities of 13.8 μg/m3 17 . McConnell et al., (2003) also reported a positive and statistically 

18 significant effect between long-term PM2.5 concentrations and bronchitic symptoms as part of the 

19 Southern California CHS. These results are supported by a single-city cross-sectional study of 

20 bronchitic symptoms in school-aged children reported a positive and statistically significant 

association with long-term PM2.5 concentrations of 12 μg/m3 21 (Kim et al., 2004). 

22 In considering alternative levels for an annual standard that would provide protection 

23 with an adequate margin of safety, we believe it is also appropriate to take into account evidence 

24 of effects for which the reported associations provide only suggestive evidence of a causal 

25 association, including, but not limited to, evidence of reproductive and developmental effects. 

26 With respect to emerging evidence on low birth weight and infant mortality, especially related to 

27 respiratory causes during the post-neonatal period, the ISA concludes that effects become “more 

precise and consistently positive in locations with mean PM2.5 concentrations of 15 μg/m3 28 and 

29 above” (US EPA, 2009a, p. 2-13; section 7.4). In particular, we note a recent study of 

30 postneonatal infant mortality which observed a positive and statistically significant association 

with an aggregate long-term mean PM2.5 concentration of 14.8 μg/m3 31 (Woodruff et al., 2008). 

32 We recognize that these effects are serious in nature and that data are continuing to emerge 

33 related to reproductive and developmental outcomes. At this time, however, the PM2.5 

34 concentrations reported in studies evaluating these effects report ambient levels that are equal to 

35 or greater than ambient levels observed in studies reporting mortality and cardiovascular and 

36 respiratory effects. Therefore, in selecting alternative levels, we note that in providing protection 
Draft Do Not Quote or Cite March 2010 2-77

1 for mortality and cardiovascular and respiratory effects, it is reasonable to anticipate that 

2 protection will also be provided for reproductive and developmental effects. 

3 With respect to characterizing the concentration-response relationship for mortality 

4 associated with long-term PM2.5 exposures, we first note, that in the last review, evidence was 

5 available to support a linear relationship. Using data from the ACS cohort, Pope et al., (2002) 

6 reported that the associations for all-cause, cardiovascular, and lung cancer mortality “were not 

7 significantly different from linear.” In that study, the confidence intervals began to expand 

significantly starting around 13 to 12 μg/m3 8 , indicating greater uncertainty about the shape of the 

9 reported concentration-response relationship at and below this level (US EPA, 2004, Figure 8-7; 

10 US EPA 2005, Figure3-4). In this review, additional evidence supports a linear concentration11 response relationship. Schwartz et al. (2008) used a variety of statistical methods and reported 

12 “the concentration-response curve was linear, clearly continuing below the level of the current 

U.S. air quality standard of 15 μg/m3 13 ” (US EPA, 2009a, p. 7-92). No new evidence is available 

14 in this review to inform our understanding of the confidence intervals around the estimated 

15 concentration-response functions. 

16 In considering what alternative levels would provide protection for effects observed in 

17 such long-term PM2.5 exposure studies, we first recognize that the ISA has concluded that no 

18 discernable threshold for an effect associated with long-term PM2.5 exposure can be identified 

19 based on the currently available evidence (US EPA 2009a, section 2.4.3). We recognize that 

20 health effects may occur over the full range of concentrations observed in the studies, however, 

21 we believe it is reasonable to conclude the evidence of association is strongest down to 

22 somewhat below the aggregated mean concentration, such as down to one standard deviation 

23 below the mean or to the lower end of the interquartile range, which includes the range in which 

24 the data in the study are most concentrated. This approach is consistent with considering the 

25 serious nature of the observed effects, including, but not limited to, mortality and cardiovascular 

26 effects for which there is strong evidence of a causal association as well as respiratory effects, 

27 for which there is strong evidence of a likely causal relationship. It also includes consideration of 

28 the range of long-term average concentrations across cities and the point where the data become 

29 less robust, suggestive of a concentration below which the association becomes appreciably more 

30 uncertain. In evaluating the long-term exposure studies, we recognize that the overall density of 

31 air quality concentrations becomes noticeable sparse below the range of air quality levels 

32 represented by the lower interquartile range or one standard deviation below the mean. In our 

33 view, an annual standard set below this range would be highly precautionary, giving little weight 

34 to the remaining uncertainties in the broader body of evidence, including the limited number of 

35 cities included in the long-term epidemiologic studies that reported long-term below the lower 

36 interquartile range. 
Draft Do Not Quote or Cite March 2010 2-78

1 As discussed in section 1.2.1, this approach is relevant to inform judgments about 

2 providing an adequate margin of safety to prevent pollution levels that may pose an unacceptable 

3 risk of harm, even if the risk is not precisely identified as to nature or degree. As presented in 

4 Figure 2-1, the lower interquartile range of long-term average concentrations or one standard 

5 deviation below study mean air quality levels as reported in the long-term mortality studies for 

6 the most recent years evaluated, report air quality concentrations in the range from about 10 to 

11 μg/m3 7 . With respect to considering air quality levels reported in the extended follow-up to 

8 the Southern California CHS, we recognize that using this approach, air quality levels one 

standard deviation below the mean across communities is significantly lower, about 6 μg/m3 9 , and 

10 close to or below the LML reported in the majority of the long-term mortality studies. 

In considering not only the level but also the form of the annual standard39 11 , we 

12 acknowledge that there may be differences between mean PM2.5 concentrations averaged across 

13 monitors within a city/county as is typically considered in epidemiologic studies, compared to 

14 the current form of the annual PM2.5 standard which typically focuses on ambient measurements 

15 from the highest reporting community-oriented monitor. As such, we requested additional air 

16 quality distribution data from authors of specific epidemiologic studies in order to effectively 

17 place key epidemiologic studies in a policy-relevant context (Hassett-Sipple and Stanek, 2009). 

18 Data were received for some but not all studies for which information was requested. To 

19 broaden this data base, OAQPS conducted additional analyses for selected long-term PM2.5 

20 exposure studies to better understand air quality distributions averaged across monitors in 

21 comparison to air quality levels focused on the highest reporting monitors (Schmidt, 2010). 

22 These analyses focused on selected long-term mortality studies and, as presented in Table 2-4 

23 Figure 2-2a, reported composite monitor values close to the long-term mean concentrations 

reported by the study authors.40 24 As was expected, estimated air quality levels for the highest 

reported monitors, within a range of 14.9 μg/m3 (Eftim et al., 2008) to 16.8 μg/m3 25 (Miller et al, 

2007), were higher than for the composite monitor values, within a range of 12.9 μg/m3 26 (Miller 

et al., 2007) to 14.0 μg/m3 27 (Krewski et al., 2009),. The most notable difference was reported for 

28 the WHI study which assessed only one year of air quality data (2000) for 36 study areas 

 39 As summarized in section 2.3.3, the level of the annual PM2.5 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 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 2010 2-79

Table 2-4. Comparison of Air Quality Data for Selected Epidemiological Studies – Long-term Mea

1 

Author Reported Data EPA Analysis (Schmidt 2010) 

Composite Monitor Maximu

Study Cite Years Mean 

(SD)

Mean 

-1 SD

Range Mean 

(SD) 

Mean - 

1SD 

Lower 

end of 

IQR 

range 

(25%) 

Range Mean 

(SD) 

Mean - 

1SD 

Long-term Exposure Studies

ACS - extended follow-up 

Krewski et al 2009 

1999-

2000 

14.0 

(3.0) 

11.0 5.8 - 22 14.0 

(3.5) 

10.5 10.9 6-21 15.4 

(4.1) 

11.3 

Medicare-ACS 

Eftim et al 2008 

2000-

2002 

13.6 

(2.8) 

10.8 6-25 13.3 

(3.1) 

10.2 10.8 7-20 14.9 

(3.6) 

11.3 

Women’s Health Initiative 

Miller et al 2007 

2000 13.5 

(3.3) 

10.2 3.4 – 28 12.9 

(3.0) 

9.9 10.8 5-18 16.8 

(4.3) 

12.5 

Short-term Exposure Studies

MCAPS -Original

Dominici et al 2006 

1999-

2002

13.4 

(2.9)

10.5 11.3-

15.2 

(IQR)*

13.3 

(2.9)

10.4 11.2 5-21 13.9 

(3.4)

10.5 

-Extended Bell et al 

2008 

1999-

2005 

12.9 

(2.7) 

10.2 4-20 12.9 

(2.7) 

10.2 11.0 4-19 13.4 

(3.1) 

10.3 

National Mortality Study 

Zanobetti & Schwartz, 2009 

1999-

2005 

13.2 

(2.9) 

10.3 7-25 13.7 

(3.0) 

10.7 11.6 6-26 14.1 

(3.2) 

10.9 

2 .

41 All concentrations reported as μg/m3. * IQR = interquartile range 
Draft Do Not Quote or Cite March 2010 2-80

(average across monitors and across cities (composite monitor) of 12.9 μg/m3 1 , compared to an 

average of the highest reporting monitors across cities of 16.8 μg/m3 2 ). When more study areas 

3 were considered and/or more years of air quality data were evaluated, the difference between the 

4 long-term mean for the composite monitor across cities compared to the long-term mean for the 

5 highest reporting monitor across cities was decreased. 

6 In considering the currently available evidence, we reach the preliminary conclusion that 

7 the long-term PM2.5 exposure studies provide a basis for considering alternative levels for the 

annual PM2.5 standard within a range of about 13 μg/m3 down to about 10 μg/m3 8 . A standard in 

the range of 13 to12 μg/m3 9 would reflect placing weight on setting a level somewhat below the 

10 long-term mean PM2.5 concentrations evaluated in long-term PM2.5 exposure studies that show 

11 associations with mortality and cardiovascular and respiratory morbidity over a lower range of 

12 air quality levels than had been observed in the studies available in the last review. A standard in 

the range of 11 to 10 μg/m3 13 would be consistent with a judgment that, recognizing the serious 

14 nature of the effects and that no discernable threshold for these effects can be identified, 

15 appreciable weight should be accorded to considering the lower interquartile range of long-term 

16 average concentrations within a study, or a range within one standard deviation around the study 

17 mean of either the composite monitor or the highest reporting monitor. 

18 Furthermore, recognizing that there is a link between the form and the level of a standard 

19 that determines the degree of public health protection the standard affords, and in light of 

20 stronger evidence available in this review identifying persons with lower SES levels as a 

21 susceptible population as discussed in section 2.2.1, we recognize that the existing constraints on 

22 spatial averaging, as modified in 2006, may not be adequate to avoid substantially greater 

23 exposures in some areas, potentially resulting in disproportionate impacts on persons with lower 

24 SES levels. Therefore, we reach the preliminary conclusion that it is appropriate to consider a 

25 form of the annual PM2.5 standards that does not allow for the use of spatial averaging across 

26 monitors such that the annual PM2.5 standard would be compared to measurements made at 

27 monitoring sites that represent “community-wide air quality” recording the highest levels only. 

28 We plan to conduct additional air quality analyses to explore this issue to inform the second draft 

29 PA.

30 2.3.4.2 Risk-based Considerations 

31 Beyond looking directly at the relevant epidemiologic evidence, staff have also 

32 considered the extent to which specific levels of alternative PM2.5 standards are likely to reduce 

33 the estimated mortality risks attributed to long-term exposure to PM2.5 and the uncertainties in 

34 the estimated risk reductions. We have based this evaluation on the results of the quantitative risk 

35 assessment presented in the second draft RA (US EPA, 2010a) and posed a series of questions to 
Draft Do Not Quote or Cite March 2010 2-81

1 aid in considering how the current suite of PM2.5 standards might be revised to provide requisite 

2 public health protection.

3  To what extent do alternative standards reduce estimated risks associated with long4 term PM2.5 exposure compared to risks associated with simulating air quality to just 

5 meet the current standards? What roles do the current 24-hour and annual standards 

6 have in simulating the risks remaining upon just meeting the alternative suites of 

7 standards considered in the quantitative risk assessment? What level of confidence is 

8 associated with these risk estimates?

9 As noted in section 2.1.1, in summarizing risk estimates associated with long-term 

10 exposure-related mortality, we focus on IHD-related mortality due to greater overall support for 

11 a causal association with this endpoint. However, we note that risk estimates were also 

12 generated for all-cause, cardiopulmonary and lung cancer-related mortality. In presenting these 

13 results, we focus first on the degree of risk reduction (and estimates of risk remaining) upon 

14 simulation of the alternative annual standard levels considered in the risk assessment. We then 

15 discuss the nature and magnitude of risk reductions associated with alternative 24-hour standard 

16 levels. Contrasting the degree of risk reduction provided by the suites of alternative annual and 

17 24-hour standards is covered in the overall summary discussion presented at the end of this 

18 section. 

19 Risk reduction associated with alternative annual standards (14/35, 13/35, and 12/35)

20 In evaluating alternative standards, we first focused on consideration of different levels 

for the annual PM2.5 standard (e.g., 14 μg/m3

, 13 μg/m3, 12 μg/m3 21 ) in conjunction with retaining 

the current level of the 24-hour standard (35 μg/m3 22 ). We observed a consistent pattern of 

23 increasing risk reduction with decreasing alternative annual standard levels, both in terms of the 

24 number of urban study areas experiencing risk reductions and the magnitude of those reductions 

25 (US EPA, 2010a, section 6.2.2). Specifically, 5 of the 15 urban study areas experienced risk 

reductions under the alternative annual standard level of 14 μg/m3 26 , with percent reductions in 

27 PM2.5-attributable long-term exposure-related mortality (relative to risk under the current suite of 

28 standards) ranging from 9% (Baltimore) to 12% (Houston and Birmingham) (Figure 2-3 and US 

EPA, 2010a, Appendix E, Table E-27). For an annual standard level of 12 μg/m3 29 , 12 of the 15 

30 urban study areas experience risk reductions, with percent reductions (relative to risk under the 

31 current suite of standards) ranging from 11% (Phoenix) to 35% (Houston and Birmingham) 

32 (Figure 2-3 and US EPA, 2010a, Appendix E, Table E-27). Note, that even in the 12/35 case, 

33 three of the urban study areas (Tacoma, Fresno and Salt Lake City) did not experience any 

34 decreases in risk, although risk reductions were seen for these three study areas when alternative 

35 24-hour standards were considered, as discussed below.
Draft Do Not Quote or Cite March 2010 2-82

1 Figure 2-3. Percent reduction in long-term exposure-related mortality risk 2 (alternative standards relative to the current standards) (Note: inset shows PM2.5 related incidence and percent of total incidence for I

3 current suite of standards)4 

Atlanta, G

 Baltimore

 Birmingha

Dallas, T

 Detroit, MI

 Fresno, C

Houston

Los Angeles, 

 New York, NY

 Philadelphia, PA

 Phoenix, AZ

Pittsburgh

 Salt Lake City, UT

 St. Louis, 

Tacoma, WA 

0%

20%40%60%

15/35** 14/35 13/35 12/35 13/30 12/25

Current and Alternative Standards

Long-Term Exposure-Related Risk: 

Percent Reduction from Current Standard

 Atlanta, 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%)

5 

6 7 8 *Based on Krewski et al. (2009), exposure period from 1999 – 2000. The legend contains, for each urban area, the incidence estimate (9 estimate of percent of total incidence (and 95% CI) under the current standards. 

**The current standards consist of an annual standard of 15 μg/m3 and a daily standard of 35 μg/m3 10 . Combinations of an annual standar

11 (m) are denoted n/m in this figure. 12 ***The percent reductions for Salt Lake City and Tacoma at the 12/25 standard are 100% and 93%, respectively. 
Draft Do Not Quote or Cite March 2010 2-83

1 While there is a consistent pattern of risk reduction across the alternative annual 

2 standards with lower standard levels resulting in more urban study areas experiencing 

3 increasingly larger risk reductions, there is considerable variability in the magnitude of these 

4 reductions across urban study areas for a given alternative annual standard level (e.g., as noted 

above, for the alternative annual standard level of 12 μg/m3 5 , risk reduction ranged from 11% for 

6 Phoenix to 35% for Houston). The variability in risk estimates reflects differing degrees of 

7 reduction in annual average PM2.5 concentrations across the study areas. The differences in 

8 annual average concentrations result, in part, because the study areas begin with varying annual9 average PM2.5 concentrations after simulating just meeting the current suite of standards. 

10 Therefore, even if study areas have similar “ending” annual average PM2.5, because the starting 

11 point in the calculation (i.e., the annual-average PM2.5 concentrations upon just meeting the 

12 current suite of standards) is often variable, the overall reduction in annual-average PM2.5

concentrations across the standards is also variable.42 13 

14 The sensitivity analysis involving application of peak shaving rollback reveals that the 

15 pattern of reductions in ambient PM2.5 concentrations upon just meeting the current suite of 

16 standards can impact the magnitude of additional risk reductions estimated for just meeting 

17 alternative (lower) annual standard levels. Specifically, for those study areas with more peaky 

PM2.5 distributions43 18 , application of peak shaving rollback will result in higher annual-average 

19 PM2.5 levels remaining upon just meeting the current suite of standards. If proportional rollback 

20 is then used to simulate just meeting alternative annual standard levels, a greater degree of 

21 reduction in annual-average PM2.5 concentrations will result, since the “starting point” for the 

22 calculation (annual-average PM2.5 levels upon just meeting the current suite of standards) will be 

23 higher. This translates into larger reductions in risk simulated for alternative annual standards 

24 when more localized patterns of PM2.5 reduction are involved with simulating just meeting the 

25 current suite of standards. In instances where an urban study area has relatively peaky PM2.5

26 concentrations, the difference in projected risk reduction for an alternative annual standard can 

27 be substantial. For example, with Los Angeles which has fairly peaky PM2.5 levels, we predict a 

13% reduction in long-term exposure-related mortality with the 12 μg/m3 28 alternative annual 

29 standard (relative to risk under the current suite of standards) if we assume a regional pattern of 

30 PM2.5 reductions for simulating just meeting the current standard as reflected in the application 

 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 alternative annual standard levels, results from differences across study areas in the 

relationship between the maximum monitor annual-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

1 of proportional rollback. By contrast, we predict a 48% reduction in long-term exposure-related 

2 mortality risk if we assume a more localized pattern of reduction in ambient PM2.5 levels, as 

3 reflected in the application of peak-shaving rollback (US EPA 2010a, section 6.2.2). 

4 Regarding the magnitude of risk estimated to remain after simulation of alternative 

5 annual standards, the four study areas displaying the greatest degree of risk reduction across the 

6 range of alternative annual standard levels considered (Atlanta, Baltimore, Birmingham and 

7 Houston) have PM2.5-related IHD mortality estimates (under the lowest alternative annual 

8 standard of 12/35) ranging from 85-110 (Birmingham) to 220-280 (Houston) (US EPA, 2010a, 

9 Appendix E, Table E-21 and E-30). The two urban study areas with the greatest degree of PM2.5-

10 related risk in absolute terms (Los Angeles and New York) do not exhibit significant reductions 

11 in risk until the lowest annual standard level of 12/35 is considered, with PM2.5-related IHD 

12 mortality estimated at 750-950 and 1,420-1,800, respectively under that alternative standard (US 

13 EPA, 2010a, Appendix E, Table E-21 and E-30). In terms of the percentage of long-term 

14 mortality attributable to PM2.5, we see the following levels for the alternative annual standard 

levels. For an annual standard level of 14 μg/m3 15 , the percent of total incidence of IHD mortality 

16 attributable to PM2.5 in the 5 urban study areas experiencing risk reductions ranges from 9-11.3% 

17 (Detroit) to 11.8-14.9% (Atlanta) (US EPA 2010a, Appendix E, Tables E-24 and E-33). For an 

annual standard of 12 μg/m3 18 , estimated risk remaining in the 12 urban study areas experiencing 

19 risk reductions ranges from 6-7.6% (Phoenix) to 9-11.4% (Atlanta), again for PM2.5-attributable 

20 long-term exposure-related mortality (US EPA 2010a, Appendix E, Tables E-24 and E-33). 

21 We note that there is considerably less variability in the estimates of risk remaining after 

22 simulation of the alternative annual standards levels, compared with the magnitude of risk 

23 reductions across the study areas. This reflects the fact that study areas experiencing risk 

24 reductions under the alternative annual standards will have similar annual-average PM2.5 levels 

25 given that this simulation involves annual standard levels that are controlling (i.e., these study 

26 areas have their annual-average PM2.5 levels lowered to meet the same annual standard level). 

27 Observations made earlier in section 2.1.1 in the context of the current suite of standards 

28 regarding uncertainty and its impact on risk estimates apply in this context as well. Specifically, 

29 given the results of the sensitivity analysis examining the form of the C-R functions for long30 term exposure-related mortality, combined with only modeling risk down to the LML, we have 

31 increased confidence that we have not overstated either the magnitude of risk reductions across 

32 alternative standard levels, or the magnitude of risk remaining for a given standard level. 

33 Risk reduction associated with alternative 24-hour standards (13/30 and 12/25)

34 We then focused on evaluating risks associated with long-term PM2.5 exposures when 

35 varying the level of the 24-hour standard while holding the level of the annual standard constant. 
Draft Do Not Quote or Cite March 2010 2-85

1 Comparing risks associated with just meeting the 13/35 and 13/30 suites of alternative standards 

(which reflect a 5 μg/m3 2 reduction in the 24-hour standard, while holding the annual fixed at 

13μg/m3 3 ), we see considerable variation in the magnitude of risk reduction across urban study 

4 areas. For example, St Louis, under the 13/35 suite of alternative standards has IHD mortality 

5 risk attributable to PM2.5 reduced by 22% relative to risk under the current suite of standards. 

6 Very little additional risk reduction (increasing from 22% to 24%) is estimated under the 13/30 

7 alternative suite of standards. In contrast, with Salt Lake City, we estimate that the 13/35 suite of 

8 alternative standards will produce no risk reduction relative to the current suite of standards, 

9 while the 13/30 suite would produce a 55% reduction in IHD mortality risk relative to risk under 

10 the current standard level (see Figure 2-3 and US EPA 2010a, Table E-27 in Appendix E). 

11 The additional risk reduction provided by an alternative 24-hour standard is more 

12 substantial in comparing the 12/25 and 12/35 alternative suites of standards, although there is 

13 also greater variability in the magnitude of risk reductions across study areas. For example, 

14 Atlanta, which had a 32% reduction in risk under the 12/35 suite of standards (relative to the 

15 current standard level) only sees an marginal increase to 34% under the 13/25 suite of standards. 

16 By contrast, Salt Lake City, which has no reduction in risk under the 12/35 suite of standards 

17 (relative to the current suite of standards), sees a ~100% reduction in risk under the alternative 

18 suite of 12/25 (see Figure 2-3 and US EPA, 2010a, Appendix E, Table E-27). The reduction for 

19 Salt Lake City reflects a very high 24-hour design value which, when reduced to meet the 24-

20 hour standard of 25 μg/m3 produced a substantial reduction in the annual design value (given 

21 application of the proportional adjustment to simulate rollback), such that the value was very 

22 close to 5.8 μg/m3 (the LML below which long-term exposure-related mortality is not 

23 estimated). The specific pattern of risk reduction reflects whether the 24-hour or annual standard 

24 was controlling (see discussion below regarding patterns of risk reduction). We also note, that 

25 under the 12/25 alternative suite of standards, we see that nine of the study areas (Detroit, 

26 Fresno, Los Angeles, New York, Philadelphia, Phoenix, Pittsburgh, Salt Lake City and Tacoma) 

27 have reductions in risk that are at least twice as large as for the 12/35 suite of alternative 

28 standards, with some substantially larger (see Figure 2-3 and US EPA, 2010a, Table E-27 in 

29 Appendix E). 

30 Regarding risk remaining after simulation of the suite of alternative 24-hour standards, 

31 the four study areas displaying the greatest degree of reduction across these two alternative suites 

32 of standards (Tacoma, St. Louis, Los Angeles and Fresno), have PM2.5-related IHD mortality 

33 estimates (under the 12/25 case) ranging from 3-4 (Tacoma) to 290-360 (Los Angeles) (US EPA, 

34 2010a, Appendix E, Table E-21 and E-30). The other urban study area with the greatest degree 

35 of PM2.5-related risk in absolute terms besides New York (New York) has PM2.5-related all-cause 

36 mortality estimated at 820-1,040 under the 12/25 case. In terms of the percentage of long-term 
Draft Do Not Quote or Cite March 2010 2-86

1 mortality attributable to PM2.5, we see that under the 13/30 suite of standards, the percent of total 

2 incidence of IHD mortality attributable to PM2.5 ranges from 1.3 to 1.7% (Salt Lake City ) to 

3 10.4 to 3.2% (Atlanta) (US EPA, 2010a, Appendix E, Tables E-24 and E-33). Under the 12/25 

4 alternative suite, risks for this metric range from ~0 to 0.3% (Salt Lake City) to 8.8 to 11.1% 

5 (Atlanta). 

6 The observations presented above highlight variability both in the magnitude of risk 

7 reduction as well as in the risk remaining upon simulation of just meeting alternative 24-hour 

8 standards. This reflects the fact that, as noted earlier, alternative 24-hour standards can produce 

9 different degrees of reduction in the annual-average PM2.5 concentrations, depending on the 

10 relationship between 24-hour and annual design values at a particular location. It is these annual11 average PM2.5 levels that drive changes in long-term exposure-related mortality. Those study 

12 areas with relatively peaky PM2.5 levels, such as Salt Lake City, can see a substantial reduction in 

13 annual-average PM2.5 levels under simulation of alternative 24-hour standards. By contrast, study 

14 areas with less peaky PM2.5 levels, such as St. Louis, see substantially smaller reductions in 

15 annual-average PM2.5 levels under the suite of alternative 24-hour standards and consequently 

16 lower degrees of risk reduction. 

17 In addition, as noted earlier, in those instances where alternative 24-hour standards 

18 produce larger reduction in annual-average PM2.5 levels (and consequently greater reductions in 

19 risk), often these reductions involve relatively low annual-average PM2.5 levels. In some cases, 

20 such as with Salt Lake City, these annual-average PM2.5 levels can approach the LML, which 

21 reduces our overall confidence in estimates of long-term exposure-related mortality for these 

22 locations. 

23 Observations made earlier regarding the impact of variability in simulating changes in 

24 PM2.5 distributions using different rollback approaches, and its impact on the degree of risk 

25 reduction, also hold for these simulations of alternative 24-hour standards. Specifically, in those 

26 instances where PM2.5 distributions are more peaky, application of peak shaving rollback 

27 (reflecting more localized patterns of ambient PM2.5 reduction) would result in smaller 

28 reductions in annual-average PM2.5 concentrations and consequently, smaller reductions in 

29 estimates of long-term exposure-related mortality. For example, with Salt Lake City, which has a 

30 peaky PM2.5 distribution, under the 12/25 suite of standards application of proportional rollback 

results in an annual average PM2.5 concentration of 5.7 μg/m3 31 , while application of peak shaving 

results in an estimate of 8.9 μg/m3 32 (as noted earlier, differences in annual-average PM2.5 levels 

33 translate into differences in risk). In contrast, simulation of the 12/25 suite of standards for 

34 Baltimore, which has a less peaky PM2.5 distribution, results in an annual average PM2.5

concentration of 10.7 μg/m3 for proportional rollback compared to 10.8 μg/m3 35 with peak 
Draft Do Not Quote or Cite March 2010 2-87

1 shaving, implying that there would be little difference in risk (see US EPA, 2010a, Table F-49 in 

2 Appendix F). 

3 Observations made earlier regarding overall confidence in the estimates of long-term 

4 exposure-related mortality also hold for these estimates (i.e., the sensitivity analysis results 

5 combined with the fact that we modeled risk down to LML result in our concluding that it is 

6 unlikely we have overstated either the degree of risk reduction or the degree of residual risk). 

7 Summary

8 The results discussed above show that simulating just meeting alternative annual 

standard levels in the range of 14 to 12 μg/m3 9 can produce substantial reductions in long-term 

10 exposure-related mortality risk (with the magnitude of risk reduction increasing as lower annual 

11 standards in this range are considered). Furthermore, the results suggest that alternative 24-hour 

standard levels in the range of 30 to 25 μg/m3 12 can produce substantial reductions in estimated 

13 risk, beyond that produced by simulations of just meeting lower annual standard level down to 

12 μg/m3

 (combined with a 24-hour standard of 35 μg/m3 14 ). This results from the simulation of 

15 the alternative 24-hour standard levels producing substantially lower annual-average PM2.5

16 concentrations, which drive reductions in both long-term and short-term exposure-related risk. 

17 However, the results also show that there can be considerable variability across study areas in the 

18 degree to which alternative 24-hour standard levels produce reductions in annual average PM2.5

19 concentrations and, consequently, reductions in risk. This variability depends on the peakiness 

20 of the PM2.5 distribution in an area and on the pattern of reductions in ambient PM2.5 levels 

21 associated with just meeting the current and alternative suites of standards. Conversely, the 

22 analysis also suggests that more consistent annual-average PM2.5 concentrations, and thus more 

23 consistent reductions in estimated risk and more uniform levels of public health protection 

24 would likely result from simulating just meeting alternative annual standards at levels below 12 

μg/m3 25 (i.e., below the lowest annual standard level considered in this assessment). 

26 Furthermore, because the alternative 24-hour standard levels assessed resulted in lower 

27 simulated annual-average PM2.5 levels (often approaching the LML used in modeling risk for 

28 long-term exposure-related mortality), we also conclude that there is greater uncertainty 

29 associated with risk estimates derived for the alternative 24-hour standards, relative to risks 

30 estimated for the alternative annual standards. 

31 2.3.5 Alternative Levels to Address Health Effects Related to Short-term PM2.5 Exposures 

32 In considering alternative PM2.5 standards that would provide protection against health 

33 effects related to short-term exposures, staff has taken into account both evidence-based and risk34 based considerations. First, as discussed in section 2.1.3, it is our view that the evidence from 

35 studies of short-term exposure to PM2.5 can help inform consideration of the protection afforded 
Draft Do Not Quote or Cite March 2010 2-88

1 by both a 24-hour and an annual standard (section 2.3.5.1). Secondly, we have considered the 

2 results of the quantitative risk assessment presented in the second draft RA (US EPA, 2010a) to 

3 assess the extent to which alternative annual and/or 24-hour standards can be expected to reduce 

4 the estimated risks attributable to short-term exposure to PM2.5 (section 2.3.5.2). With respect to 

5 considering the protection afforded by the suite of PM2.5 standards, our preliminary integrated 

6 conclusions presented in section 2.3.6 are based in part on the preliminary staff conclusions from 

7 this section and in part on preliminary staff conclusions from section 2.3.4 in which we discuss 

8 alternative standards to address health effects related to long-term PM2.5 exposures. 

9 2.3.5.1 Evidence-based Considerations 

10 In taking into account evidence-based considerations for informing our understanding of 

11 alternative levels to address health effects related to short-term fine particle exposures, we 

12 initially focused on short-term multi-city PM2.5 exposure studies. We observe that multi-city 

13 studies assessed PM2.5-associated health effects among larger study populations, providing 

14 enhanced power to detect PM2.5-associated health effects. In addition, short-term multi-city 

15 PM2.5 exposure studies generally provide spatial coverage for different regions across the 

16 country, reflecting differences in PM2.5 sources, composition, and potentially other factors which 

17 might impact PM2.5-related risk. We have also evaluated short-term single-city PM2.5 exposure 

18 studies that provide additional insights on associated health effects occurring at or below the 

19 PM2.5 concentrations reported in the short-term multi-city PM2.5 exposure studies, specifically in 

20 areas that may have unusually high peak-to-mean ratios of PM2.5 concentrations, possibly 

21 associated with strong local or seasonal sources of fine particles.

22 In considering a range of health outcomes, we place the greatest weight on associations 

23 that have been judged in the ISA to be causal or likely causal, while being mindful of evidence 

that informs our understanding of impacts on susceptible populations.44 24 We have considered a 

25 number of factors including: (1) the extent to which these studies report statistically significant 

26 and relatively precise relative risk estimates; (2) the extent to which the reported associations are 

27 robust to co-pollutant confounding; and (3) the extent to which the studies used relatively 

28 reliable air quality data. In particular, we focused on those specific studies conducted in the U.S. 

29 and Canada, briefly summarized in section 2.2.1 and presented in more detail in chapter 6 of the 

30 ISA, that provide evidence of associations in areas that would likely have met the current 24-

 44 In contrast to causal inferences for effects associated with long-term PM2.5 exposures, the ISA has not identified 

any health outcomes as having evidence suggestive of a causal association with short-term PM2.5 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 PM2.5 exposures only. 
Draft Do Not Quote or Cite March 2010 2-89

hour PM2.5 standards during the time of the study.45 1 We believe that this body of evidence can 

2 serve as a basis for considering alternative 24-hour and annual PM2.5 standards that would 

3 provide appropriate protection for health effects associated with short-term PM2.5 exposures. 

4 Collectively, we have considered the evidence to address the following question:

5  To what extent does the currently available evidence provide support for revising the 

6 current suite of standards to provide protection from short-term fine particle 

7 exposures? 

8 In considering what alternative levels would provide protection for effects associated 

9 with short-term PM2.5 exposure, we first recognize that the ISA has concluded that no discernable 

10 threshold, or lowest-observed-effect levels, can be identified based upon the currently available 

11 evidence (US EPA, 2009a. section 2.4.3). Being mindful of the challenges posed by issues 

12 relating to threshold and background concentrations, we have considered two alternative 

13 approaches for using the evidence from short-term exposures studies to inform preliminary staff 

14 conclusions regarding alternative standard levels. First, in considering an approach in which the 

15 24-hour standard to set to be the primary means for providing protection for health effects 

16 associated with short-term exposures to PM2.5, we considered evidence from short-term exposure 

17 epidemiological studies as a basis for an alternative 24-hour PM2.5 standard. Specifically, we 

18 focused on the upper end of the distributions of 24-hour PM2.5 concentrations, particularly in 

terms of the highest 98th 19 percentile values for a location, reflecting the form of the current 24-

20 hour standard. 

21 Alternatively, we have also considered an approach in which the annual standard is set to 

22 be the primary means for providing protection for effects associate with both long and short-term 

23 PM2.5 exposures. This approach recognizes that, as noted in previous reviews, much of the risk 

24 related to daily exposures, when aggregated on an annual basis, results from the large number of 

25 days during which the 24-hour average concentrations are in the low- to mid-range of the entire 

26 distribution. Thus, to reduce the aggregate short-term exposure-related risk, it is necessary to 

27 shift the bulk of the distribution to lower concentrations, not just to limit the concentrations on 

28 days when the PM2.5 concentrations are relatively high (US EPA, 2005, p. 4-67, Figure 4-10; 

29 Abt, 1996, section 7.1, p.79, Exhibit 7.6). This approach reflects consideration for allowing the 

30 annual standard to serve in most areas as the target for control programs designed to be effective 

31 in lowering the broad distribution of PM2.5 concentrations, thus protecting not only against 

32 effects associated with long-term exposures but also effects associated with short-term 

 45 As noted in section 2.3.4.1 above, we requested additional air quality distribution data from authors of specific 

epidemiological studies. To inform alternative standard levels to provide protection for effects associated with shortterm PM2.5 exposures, we were particularly interested in 98th percentile and long-term mean PM2.5 concentrations 

considered in short-term exposure studies. In focusing on the current forms of the 24-hour and annual standards, we 

were also interested in information related to the highest reporting monitors.
Draft Do Not Quote or Cite March 2010 2-90

1 exposures. This judgment reflects the recognition that changes in PM2.5 air quality designed to 

2 meet an annual standard would likely result not only in changes in lower annual average 

3 concentration but also in fewer and lower peak 24-hour concentrations. In exploring this 

4 alternative approach, we considered the evidence from the currently available short-term 

5 exposure studies, specifically the long-term mean PM2.5 concentrations from these studies as a 

6 basis to inform preliminary conclusions for alternative levels for an annual PM2.5 standard. 

7 Furthermore, we recognize that if the primary purpose of the annual standard was to provide 

8 protection for effects associated with both long- and short-term exposures, the purpose of the 24-

9 hour standard would than shift. In that case, the primary purpose of the 24-hour standard would 

10 be to serve to provide supplemental protection to provide additional protection beyond the 

11 protection afforded by the annual standard in areas with unusually high peak-to-mean ratios of 

12 PM2.5 concentrations, possibly associated with strong local or seasonal sources. 

13 In first considering the approach of using the 24-hour standard as the primary means for 

14 providing protection for health effects associated with short-term exposures to PM2.5, we look to 

the 98th 15 percentile air quality values for specific short-term exposure studies to inform our 

16 consideration of alternative standard levels (see Figure 2-4). With respect to mortality evidence 

17 (causal association) from multi-city short-term exposure studies, we note that, as discussed in 

section 2.2.1, Zanobetti and Schwartz (2009) and Burnett et al. (2004) reported a 24-hour 98th 18 

percentile PM2.5 concentration averaged across all cities and all years of 34.3 μg/m3 19 and 38.0 

μg/m3 20 , respectively. As presented in the ISA, despite large differences in air quality 

21 concentrations, Zanobetti and Schwartz (2009) reported “all-cause mortality risk estimates that 

were fairly uniform across the climatic regions, except for the ‘Mediterranean’ region”46 22 (US 

23 EPA, 2009a, p. 6-178, Figure 6-24). 

24 With regard to the evidence from studies assessing short-term exposure to PM2.5-

25 associated with cardiovascular (causal association) and respiratory (likely causal association) 

26 morbidity effects, recent multi-city analysis of MCAPS data by Dominici et al. (2006a) and Bell 

et al. (2008) reported an overall 24-hour average 98th 27 percentile PM2.5 concentration across all 

cities and all years of 34.8 μg/m3 and 34.2 μg/m3 28 , respectively. As noted in section 2.2.1, an 

29 unpublished sub-analysis of Dominici et al (2006a) restricted to days with 24-hour average 

concentrations at or below the level of the current 24-hour standard (35 μg/m3 30 ) indicated that, in 

31 spite of a reduced statistical power from a smaller number of study days, statistically significant 

32 associations were still observed between short-term PM2.5 exposure and hospital admissions for 

33 cardiovascular and respiratory diseases (Dominici, 2006b).

 46 The Mediterranean region included cities in OR, CA, and WA. 
Study Outcome Meana 98tha Effect Estimate (95% CI) 

Chimonas & Gessner (2007, 093261) Asthma HA 6.1 

LRI HA 6.1 

Lisabeth et al. (2008, 155939) Ischemic Stroke/TIA HA 7.0e 23.6f 

Slaughter et al. (2005, 073854) Asthma Exacerbation 7.3e 

Rabinovitch et al. (2006, 088031) Asthma Medication Use 7.4 17.2f 

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 27.3f Stieb et al. (2000, 011675) 

Respiratory ED Visits 8.5 27.3f

 

Hemhrgc Stroke HA 8.5 24.0f 

Ischemic Stroke HA 8.5 24.0f 

Villeneuve et al. (2006, 090191) 

TIA HA 8.5 24.0f

 

Lin et al. (2005, 087828) RTI HA 9.6 

Respiratory Symptoms (any) 9.8c 25.8f Mar et al. (2004, 057309) 

Respiratory Symptoms (any) 9.8c

 25.8f 

Rich et al. (2005, 079620) Ventricular Arrhythmia 9.8e 

Dockery et al. (2005, 078995) Ventricular Arrhythmia 10.3e 

Rabinovitch et al. (2004, 096753) Asthma Exacerbation 10.6d 29.3f 

Pope et al. (2006, 091246) IHD HA 10.7c 

CVD HA 10.8 29.6f Slaughter et al. (2005, 073854) 

Respiratory ED Visits 10.8 29.6f

 

Pope et al. (2008, 191969) CHF HA 10.8 44.5d 

MI HA 11.1e Zanobetti and Schwartz (2006, 090195) 

Pneumonia HA 11.1e

 

Peters et al. (2001, 016546) MI 12.1 28.2f 

Delfino et al. (1997, 082687) Respiratory HA (summer) 12.1 31.2f 

Sullivan et al. (2005, 050854) MI 12.8 

Burnett et al. (2004, 086247) Nonaccidental Mortality 12.8 38.0f 

Respir HA 12.9d 34.2f Bell et al. (2008, 156266) 

CVD HA 12.9d

 34.2f 

Wilson et al. (2007, 157149) CVD Mortality 13.0 31.6f 

Zanobetti & Schwartz (2009, 188462) Nonaccidental Mortality 13.2d 34.3f 

Burnett and Goldberg (2003, 042798) Nonaccidental Mortality 13.3 38.9f 

CBVD HA 13.3 34.8f 

PVD HA 13.3 34.8f 

IHD HA 13.3 34.8f 

Dysrhythmia HA 13.3 34.8f 

CHF HA 13.3 34.8f 

COPD HA 13.3 34.8f 

Dominici et al. (2006, 088398) 

RTI HA 13.3 34.8f

 

Fairley (2003, 042850) Nonaccidental Mortality 13.6 59.0f 

Zhang et al. (2009, 191970) ST Segment Depression 13.9j 37.6f 

O’Connor et al. (2008, 156818) Wheeze/Cough 14.0c 39.0g 

Klemm and Mason (2003, 042801) Nonaccidental Mortality 14.7e,i 

Franklin et al. (2008, 097426) Nonaccidental mortality 14.8 43.0f 

NYDOH (2006, 090132) Asthma ED Visits 15.0k 

Ito et al. (2007, 156594) Asthma HA 15.1 39.0f 

Franklin et al. (2007, 091257) Non-accidental Mortality 15.6 45.8f 

Rich et al. (2006, 089814) Ventricular Arrhythmia 16.2e 

Symons et al. (2006, 091258) CHF HA 16.5d 50.1f 

Sheppard (2003, 042826) Asthma HA 16.7 46.6f 

NYDOH (2006, 090132) Asthma ED Visits 16.7l 

Respiratory HA (summer) 16.8 47.4f Burnett et al. (1997, 084194) 

CVD HA (summer) 16.8 47.4f

 

 a μg/m3

 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 PM2.5 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 PM2.5 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/m3) and Air Quality Distributions for Short-term 

Exposure Studies 

Source: US EPA, 2009a, Figure 2-1. 
Draft Do Not Quote or Cite March 2010 2-92

1 In looking at short-term single-city PM2.5 exposure studies conducted in areas that would 

2 have met the current level of the 24-hour standard, we recognize that these studies can provide 

3 additional insights regarding impacts on susceptible populations and/or on areas with isolated 

4 peak concentrations that could occur in areas that attain the current 24-hour and annual 

5 standards. We first consider studies that report positive and statistically significant associations. 

6 One short-term single-city PM2.5 exposure study conducted since the last review reported a 

7 positive statistically significant association for short-term PM2.5 exposures in relation to 

respiratory symptoms among children in Phoenix with an average 98th 8 percentile value of 25.8 

μg/m3 9 (Mar et al., 2004). In addition, another short-term single-city PM2.5 exposure a study 

10 noted in the last review also reported a positive statistically significant association between 

short-term exposure to PM2.5 and myocardial infarction in Boston with an average 98th 11 percentile 

value of 28.2 μg/m3 12 (Peters et al., 2001). 

13 In also considering short-term single-city PM2.5 exposure studies that report positive but 

14 statistically non-significant associations for cardiovascular and respiratory endpoints in areas that 

15 would have met the current 24-hour PM2.5 standard, we note a number of studies conducted in 

16 Montreal (respiratory hospital admissions; Delfino et al., 1997), Saint John (CVD and respiratory 

17 hospital admissions; Steib et al., 2000), Phoenix (CVD mortality; Wilson et al., 2007), Denver 

18 (asthma medication use; Rabinovitch et al., 2006), Edmonton (hemorrhagic and ischemic stroke 

19 hospital admissions; Villeneuve et al., 2006), and Nueces County, TX (ischemic stroke/transient 

ischemic attack; Lisabeth et al., 2008). We note that the 98th 20 percentile values reported in these 

studies averaging across monitors in a city/county range from approximately 17.2 μg/m3 21 

(Rabinovitch et al., 2006) in Denver to 31.6 μg/m3 22 (Wilson et al, 2007) in Phoenix. However, 

23 other short-term single-city PM2.5 exposure studies report null findings for health effects noted 

24 above (i.e., cardiovascular and respiratory morbidity) as being positively associated with short25 term exposure to PM2.5 in areas that would have met the current level of the 24-hour PM2.5

26 standard, including Phoenix (respiratory symptoms in adults; Mar et al., 2004); Spokane (CVD 

27 hospital admissions and respiratory ED visits; Slaughter et al. 2005), Denver (asthma 

28 exacerbation; Rabinovitch et al., 2004) and Edmonton (ischemic stroke and transient ischemic 

29 attack hospital admissions; Villeneuve et al., 2006). 

30 In considering information from both multi- and single-city short-term PM2.5 exposure 

31 studies as summarized in Figure 2-4, we believe that the range of alternative 24-hour PM2.5

standards appropriate for consideration should extend below the range of 98th 32 percentile values 

33 averaged across cities from the multi-city studies identified above so as to provide protection 

34 from effects associated with short-term PM2.5 exposure. In light of the mixed findings reported 

35 in single-city studies, particularly for studies conducted in areas such as Phoenix, Denver, and 

36 Edmonton that report both positive and null findings, we place comparatively greater weight on 
Draft Do Not Quote or Cite March 2010 2-93

1 the results from multi-city studies for the reasons previously noted at the beginning of this 

2 section. Specifically, the heightened statistical power of multi-city studies to detect PM2.5

3 associated health effects in aggregated analysis across cities and greater spatial coverage for 

4 different regions across the country to account for variations in PM2.5 composition, sources, and 

potentially other factors which might impact PM2.5-related risk. However, we note that 98th 5 

6 percentile values reported in single-city studies may provide additional insights for consideration 

7 in identifying alternative standards to provide protection for potentially susceptible populations. 

8 Specifically, as noted above, Mar et al. (2004) provides evidence of a statistically significant 

association between a 98th percentile PM2.5 level of 25.8 μg/m3 9 and respiratory symptoms among 

10 children. 

11 In recognition that the current form of the 24-hour standard discussed in section 2.3.3.2 

12 applies to the measurements made at each population-oriented monitor, OAQPS conducted 

13 additional air quality analyses for selected multi-city short-term PM2.5 exposure studies to better 

14 understand air quality distributions averaged across monitors by the study investigators in 

15 comparison to air quality levels focused on the highest reporting monitors (Schmidt, 2010). 

16 These analyses, as noted in section 2.3.4.1, focused on selected mortality and hospitalization 

17 studies and, as presented in Table 2-5 and Figure 2-5, yielded composite monitor values close to 

the 98th 18 percentile concentrations reported to the EPA by the study authors (ranging from 34.2 

μg/m3

 (Bell et al 2008) to 34.8 μg/m3 (Dominici et al., 2006).47 19 As was expected, estimated air 

quality levels for the highest reported monitors, ranging from 35.4 μg/m3 20 (Bell et al, 2008) to 

38.9 μg/m3 21 (Dominici et al 2007) were higher than for the composite monitor values, ranging 

from 33.5 μg/m3 (Bell et al, 2008) to 36.5 μg/m3 22 (Zanobetti and Schwartz, 2009). When more 

23 study areas were considered and/or more years of air quality data were evaluated, the difference 

between the 98th percentile values for the composite monitor across cities compared to the 98th 24 

25 percentile for the highest reporting monitor across cities was decreased. 

26 Based on the epidemiological evidence and air quality analyses summarized above, in 

27 considering the 24-hour standard to be the primary means to provide protection for short-term 

28 PM2.5 exposures, we reach the preliminary conclusion that alternative levels could be considered 

in the range of approximately 35 to 25 μg/m3 29 . A level selected at the upper end of this range 

would reflect consideration of a level somewhat below the 98th 30 percentile values for the highest 

reporting monitors in the multi-city studies (ranging from about 35 to 39 μg/m3 31 ) and just below 

the 98th 32 percentile values averaged across all cities and all years in these studies (in the range of 

 47 As noted by Schmidt (2010), differences between 24-hour 98th 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 2010 2-94

Table 2-5. Comparison of Air Quality Data for Selected Epidemiological Studies– 98 Percentil

1 2 

Author Reported Data EPA Analysis (Sch

Composite Monitor 

Study Cite Years 98% Range 98% Range 

MCAPS -Original

Dominici et al 2006 1999-2002 34.8 10-86 34.5 11-77 

-Extended Bell et al 2008 1999-2005 34.2 9-77 33.5 10-67 National Mortality Study 

Zanobetti & Schwartz, 2009 

1999-2005 34.3 18-80 35.6 17-75 

3 

48 All concentrations reported as μg/m3. 
Draft Do Not Quote or Cite March 2010 2-95

Figure 2-5. Distribution of Study-specific 98th 1 Percentile Concentrations 

2 

Concentration (μg/m3)

Left plots represent the study author results; middle plots represent EPA replication results using a community monitor, CM, (spatial average) approach; and right plots represent EPA replication results using a maximum value approach (max monitor 98th percentile 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 standard deviation from the mean, 

and dots represent the minimum and maximum values.

EPA 

C M

S tu d y

A u th o r

EPA 

m ax

B e ll D o m in ic i0 6 Z a n o b e tti

EPA 

C M

S tu d y

A u th o r

EPA 

m ax

EPA 

C M

S tu d y

A u th o r

EPA 

m ax

05

1 01 52 02 53 03 54 04 55 05 56 06 57 07 58 08 59 09 5

100

3 
Draft Do Not Quote or Cite March 2010 2-96

about 34 to 35 μg/m3 1 ). A level selected at the lower end of this range would reflect 

consideration of a level just below the lowest 98th 2 percentile value associated with statistically 

3 significant effects in a single-city study reporting effects in children, identified as a susceptible 

population (Mar et al., 2004, 25.8 μg/m3 4 ).

5 Alternatively, in considering the approach of using the annual standard as the primary 

6 means for providing protection for both long- and short-term PM2.5 exposures, we look to the 

7 long-term mean PM2.5 concentrations from short-term PM2.5 exposure studies to inform 

8 considerations of alternative annual standard levels. Using this approach, the same short-term 

9 multi- and single-city PM2.5 exposure studies briefly described above were evaluated. In 

10 focusing on multi-city short-term PM2.5 exposure studies of cardiovascular and respiratory 

11 mortality, the ISA concludes that associations are generally consistent and precise at long-term 

mean PM2.5 concentrations of 12.8 μg/m3 12 and above (see Figure 2-4; US EPA, 2009a, pp. 2-9 to 

13 2-11). More specifically, with respect to mortality effects, Zanobetti and Schwartz (2009) report 

associations with an overall annual average across all 112 cities of 13.2 μg/m3 14 and Burnett et 

15 al.(2004) report associations with an overall annual average across 12 Canadian cities of 12.8 

μg/m3 16 . With regard to cardiovascular effects, Zhang et al. (2009) reported positive statistically 

non-significant association between an average PM2.5 concentration of 13.9 μg/m3 17 and ST 

18 segment depression among participants of the Women’s Health Initiative. 

19 In considering PM2.5-related hospital admissions for cardiovascular and respiratory 

20 effects in older adults, an identified susceptible population, Dominici et al. (2006a) and Bell et 

al. (2008) report an overall annual average across 204 and 202 counties of 13.3μg/m3 21 and 12.9 

μg/m3 22 , respectively (US EPA, 2009a, Figure 2-1). In looking at short-term single-city PM2.5

23 exposure studies, similarly to the discussion of the 24-hour standard, Mar et al. (2004) (average 

PM2.5 concentration of 9.8 μg/m3 24 ) and Peters et al. (2001) (average PM2.5 concentration of 12.1 

μg/m3 25 ) report statistically significant associations for areas currently meeting the annual PM2.5

26 standard. Several short-term single-city PM2.5 exposure studies report positive but non27 statistically significant associations in areas that would have met the current level of the annual 

28 standard for respiratory and cardiovascular morbidity and mortality endpoints associated with 

long-term mean PM2.5 concentrations ranging from 7.0 μg/m3

 to 13.6 μg/m3 29 (Figure 2-4). 

30 However, as noted in the discussion of this evidence with regard to alternatives levels for the 24-

31 hour standard, investigators also reported null (Slaughter et al. 2005; Rabinovitch et al., 2004) 

32 and mixed (Mar et al. 2004, Villeneuve et al., 2006) results for similar endpoints in which 

positive associations were noted above for areas with annual levels ranging from 8.5 μg/m3 33 to 

10.8 μg/m3 34 (Figure 2-4). These inconsistent findings suggest the potential for localized events 

35 influencing the observed associations in single-city short-term PM2.5 exposure studies. 

36 Consequently, we observe that the results of short-term PM2.5 exposure studies could potentially 
Draft Do Not Quote or Cite March 2010 2-97

inform judgments on a 24-hour PM2.5 concentration set at the 98th 1 percentile that provides 

2 adequate protection in areas with unusually high peak-to-mean ratios of PM2.5 levels. However, 

3 due to the possibility that these studies represent air quality distributions that may be influenced 

4 by localized events and not be representative of air quality across the country, we reach the 

5 preliminary conclusion that these single-city short-term PM2.5 exposure studies do not provide 

6 support for informing an alternative annual standard levels that would apply across the entire 

7 U.S. 

8 In considering not only the level but also the form of the annual standard, we 

9 acknowledge, as was discussed in section 2.3.4.1, that there may be differences between mean 

10 PM2.5 concentrations averaged across monitors within a city/county as is typically considered in 

11 epidemiological studies, compared to the current form of the annual PM2.5 standard which 

12 typically focuses on ambient measurements from the highest reporting community-oriented 

13 monitor. As further discussed in section 2.3.4.1, OAQPS conducted additional air quality 

14 analyses to better understand air quality distributions considered in selected short-term exposure 

15 studies to compare long-term mean concentrations averaged across monitors in comparison to air 

16 quality levels focused on the highest reporting monitors (Schmidt, 2010). This analysis, as 

17 presented in Figure 2-2, reported composite monitor values close to the long-term mean 

18 concentrations reported by the study authors. As was expected, estimated air quality levels for 

the highest reported monitors were higher, ranging from 13.4 μg/m3 19 (Bell et al.., 2008) to14.8 

μg/m3 (Dominici et al., 2007), than for the composite monitor values, ranging from12.9 μg/m3 20 

(Bell et al.., 2008) to13.7 μg/m3 21 (Zanobetti and Schwartz, 2009). When more study areas were 

22 considered and/or more years of air quality data were evaluated, the difference between the long23 term mean concentrations for the composite monitor across cities compared to the long-term 

24 mean concentrations for the highest reporting monitor across cities was decreased. Of particular 

25 interest, is that the difference between the composite monitor and the high monitor is even less 

26 when focusing on air quality estimates one standard deviation below the long-term mean across 

27 cities for each of these short-term exposure studies. With concentrations ranging from 10.2 

μg/m3 (Bell et al., 2008) to 10.7 μg/m3 28 (Zanobetti and Schwartz, 2009) based one standard 

29 deviation below the long-term mean averaged across monitors and across cities/counties and 

concentrations ranging from 10.3 μg/m3

 (Bell et al., 2008) to 11.0 μg/m3 30 (Zanobetti and 

31 Schwartz, 2009) based on one standard deviation below the long-term mean at the highest 

32 reporting monitor averaged across cities/counties. 

33 In considering the currently available evidence, we reach the preliminary conclusion that 

34 the short-term PM2.5 exposure studies provide a basis for considering alternative levels for the 

annual standard within a range below 13 μg/m3 down to about 10 μg/m3 35 . A standard in the range 

of 13 to 12 μg/m3 36 would reflect placing greater weight on setting a level somewhat below the 
Draft Do Not Quote or Cite March 2010 2-98

1 long-term mean concentrations reported in the short-term exposure studies (ranging from12.8 

μg/m3 and above). A standard in the range of 11 to 10 μg/m3 2 would be consistent with a 

3 judgment that, recognizing the serious nature of the effects and that no discernable threshold for 

4 these effects can be identified, appreciable weight should be accorded to considering the lower 

5 end of the interquartile range of long-term mean concentrations reported in these studies, or a 

6 range within one standard deviation around the study mean of either the composite or the highest 

reporting monitor (ranging from about 10 to 11 μg/m3 7 ). 

8 As recognized above, an annual standard used as the primary means for providing 

9 protection for effects associated with both long- and short-term PM2.5 exposures cannot be 

10 expected to offer an adequate margin of safety against the effects of all short-term PM2.5 

11 exposures, especially in areas with high peak-to-mean ratios of PM2.5 concentrations, possibly 

12 associated with strong local or seasonal sources of fine particles. In considering a basis for 

13 setting an alternative standard levels for a 24-hour standard that would provide supplemental 

14 protection against days with high peak concentrations associated with localized “hotspots” and 

15 risk arising from seasonal emissions that might not be well controlled by a national annual 

16 standard, we intend to conduct air quality analyses of the relationships between annual and 24-

17 hour concentrations to include in the second draft PA. 

18 2.3.5.2 Risk-based Considerations to Inform Alternative Levels 

19 This discussion considers the impact of alternative suites of standard levels on short-term 

20 exposure-related mortality and morbidity. As such, it is intended to address the following policy21 related questions: 

22  To what extent do alternative standards reduce estimated risks associated with short23 term PM2.5 exposure compared to risks associated with simulating air quality to just 

24 meet the current standards? What roles do the current 24 hour and annual standards 

25 have in simulating the risks remaining upon just meeting the alternative suites of 

26 standards considered in the risk assessment? What level of confidence is associated with 

27 these risk estimates? 

28 As was done above for long-term exposure-related mortality, we have divided the 

29 discussion of risk for short-term exposure-related mortality and morbidity, between (a) 

30 reductions in risk associated with simulation of the three alternative annual standard levels and 

31 (b) reductions in risk associated with the two alternative 24-hour standard levels. 

32 Risk reduction associated with alternative annual standards (14/35, 13/35, and 12/35)

33 Reductions in risk for short-term exposure-related mortality and morbidity exhibits 

34 considerable variability across study areas for the alternative suite of annual standards (compared 

35 with risk under the current suite of standards) (see section 2.2.1.1). For the 12 urban study areas 
Draft Do Not Quote or Cite March 2010 2-99

1 experiencing reductions in short-term exposure-related CV mortality under the lowest alternative 

2 annual standard level assessed (12/35), reductions in risk compared to risk under the current suite 

3 of standards ranged from 5% (Phoenix) to 23% (Atlanta and Birmingham) (see Figure 2-3 and 

4 US EPA, 2010a, Appendix E, Table E-90). Estimates of risk reduction for CV-related HA’s 

5 exhibited a similar pattern across the study areas for the lowest annual standard level assessed 

6 (see Figure 2-6 and US EPA, 2010a, Appendix E, Table E-108). 

7 Regarding the magnitude of risk estimated to remain after simulation of the alternative 

8 annual standards, the four study areas displaying the greatest degree of reduction across the 

9 alternative annual standards (Atlanta, Baltimore, Houston and St. Louis) have PM2.5-related CV 

10 mortality estimates (under the lowest alternative annual standard of 12/35) ranging from 25 

11 (Atlanta) to 84 (St. Louis - see US EPA, 2010a, Appendix E, Table E-84). The urban study area 

12 with the greatest degree of PM2.5-related risk in absolute terms (New York) did not exhibit 

13 significant reductions in risk until the lowest annual standard level of 12/35 was considered, at 

14 which point we estimate a reduction in PM2.5-related CV mortality of 424 cases (see US EPA, 

15 2010a, Appendix E, Table E-84). In terms of the percentage of mortality attributable to short16 term PM2.5 exposure, the four study areas experiencing the greatest degree of risk reduction 

17 across the four alternative annual standard levels had estimates (for the alternative annual 

standard of 12 μg/m3 18 ) ranging from 0.6% (Atlanta) to 1.3% (Baltimore – US EPA, 2010a, 

19 Appendix E, Table E-87). For CV-related HA’s related to short-term PM2.5 exposure, estimates 

20 for this same group of four study areas (for the lowest alternative annual standard assessed) 

21 ranged from 32 (Atlanta) to 142 (St. Louis - RA Appendix E, Table E-102). This translated into a 

22 percentage of CV HA’s attributable to PM2.5 ranging from 0.28% (Atlanta) to 1.07% (Baltimore 

23 – US EPA, 2010a, Appendix E, Table E-105).

24 As with long-term exposure-related mortality, variation in risk reduction across urban 

25 study areas for both short-term exposure-related mortality and morbidity reflect to a great extent 

26 varying degrees of reduction in annual-average PM2.5 levels. This in turn results from the initial 

27 simulation of the current 24-hour standard level which can produce varying degrees of reduction 

28 in annual-average PM2.5 levels depending on a number of factors (i.e., peakiness of the PM2.5 

29 monitoring data, specific mix of annual and 24-hour design values for a given location and the 

30 spatial pattern of reduction in ambient PM2.5 levels that is assumed). We note however, that 

31 there is greater variability in the levels of risk remaining after simulation of alternative annual 

32 standard levels for short-term exposure-related health endpoints compared with long-term 

33 exposure-related mortality. This primarily reflects the fact that we are able to specify C-R 

34 functions separately by urban area or region for short-term exposure related mortality and 

35 morbidity endpoints, while a single C-R function was used in modeling long-term exposure36 related mortality by endpoint across all urban study areas. 
Draft Do Not Quote or Cite March 2010 2-100

1 Figure 2-6. Percent Reduction in Short-term Exposure-related Mortality and Morbidity R2 (alternative standards relative to the current standards) 

3 (Note: inset shows PM2.5 related incidence and percent of total incidence for CV under the current suite 

A

 Baltimore,

 MD

 Birmingham, AL

D

Detroit, MI 

 Fresno, CA 

 Houston, TX 

Lo

 New York,

 NY

 Philadelphia,

PA

 Pittsburgh, PA Phoenix, AZ 

Salt Lake City, UT 

St. Louis, MO 

 Tacoma,

 WA

0%5%

10%15%20%25%30%35

%

15/35** 14/35 13/35 12/35 13/30 12/2

Recent Air Quality, Current Standard and Alternative Standards

Short-Term Exposure-Related Risk: 

Percent Reduction from Current Standard

 Atlanta, 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%)

`

4 5 

6 7 *Based on Zanobetti and Schwartz (2009). The legend contains, for each urban area, the incidence estimate (and 95% CI) and the estim8 incidence (and 95% CI) under the current standards. 

**The current standards consist of an annual standard of 15 μg/m3 and a daily standard of 35 μg/m3 9 . Combinations of an annual standar

10 (m) are denoted n/m in this figure.
Draft Do Not Quote or Cite March 2010 2-101

1 As noted earlier, given increased emphasis placed in this analysis on long-term exposure2 related mortality, the uncertainty analyses completed for this health endpoint category are 

3 somewhat more comprehensive than those conducted for short-term exposure-related mortality 

4 and morbidity, which to some extent reflects limitations in study data available for addressing 

5 uncertainty in the later category. However, C-R functions used in generating estimates for short6 term exposure-related mortality and morbidity are well-supported in the literature.

7 Risk reduction associated with alternative 24-hour standards (13/30 and 12/25)

8 Comparing risks associated with just meeting the 13/35 and 13/30 suites of alternative 

standards (which reflect a 5 μg/m3 9 reduction in the 24-hour standard, while holding the annual 

fixed at 13 μg/m3 10 ), we see variation in the magnitude of risk reduction across urban study areas. 

11 For example, Baltimore, CV mortality risk attributable to PM2.5 under the 13/35 suite of 

12 alternative standards was reduced by 14% relative to risk under the current suite of standards. 

13 Very little additional risk reduction (increasing from 14% to 15%) is estimated under the 13/30 

14 alternative suite of standards. In contrast, with Salt Lake City, we estimate that the 13/35 suite of 

15 alternative standards will produce no risk reduction relative to the current suite of standards, 

16 while the 13/30 suite would produce a 15% reduction in CV mortality risk relative to risk under 

17 the current standard level (see Figure 2-6 and US EPA, 2010a, Table E-90 in Appendix E). 

18 The additional risk reduction provided by an alternative 24-hour standard is more 

19 substantial in comparing the 12/25 and 12/35 alternative suites of standards, although there is 

20 also greater variability in the magnitude of risk reductions across study areas. For example, 

21 Atlanta, which had a 23% reduction in risk under the 12/35 suite of standards (relative to the 

22 current standard level) only sees a marginal increase to 24% under the 13/25 suite of standards. 

23 By contrast, Salt Lake City, which has no reduction in risk under the 12/35 suite of standards 

24 (relative to the current suite of standards), sees a 29% reduction in risk under the alternative suite 

25 of 12/25 (see Figure 2-3 and US EPA, 2010a, Appendix E, Table E-90). The pattern of risk 

26 reduction for CV-related HA’s is very similar to what is presented here for CV-related mortality 

27 (see Figure 2-6 and US EPA, 2010a, Appendix E, Table E-108). 

28 We note that while considerable reductions in risk are seen for short-term exposure29 related mortality across many of the study areas, these are smaller than reductions seen for long30 term exposure-related mortality. This reflects primarily the fact that risk is modeled down to 

31 PRB for short-term exposure-related mortality, while it is only modeled down to LML for long32 term exposure-related mortality. Therefore, the incremental reductions in risk associated with 

33 short-term exposure-related mortality when we consider alternative suites of standards involve a 

34 smaller fraction of total risk compared with long-term exposure-related mortality. 
Draft Do Not Quote or Cite March 2010 2-102

1 Regarding risk remaining after simulation of the suite of alternative 24-hour standards, 

2 PM2.5-related CV mortality estimates (under the 12/25 case) ranging from 6 (Salt Lake City) to 

3 336 (New York) (see US EPA, 2010a, Appendix E, Table E-84). Estimates of CV-related HA 

4 under the 12/25 suite of standards range from 7 (Salt Lake City) to 534 (New York) (see 

5 Appendix E, Table E-102). In terms of the percentage of short-term mortality attributable to 

6 PM2.5, we see that under the 13/30 suite of standards, the percent of total incidence of CV 

7 mortality attributable to PM2.5 ranges from ~0% (Los Angeles, Birmingham) to 1.8% (New 

8 York, Philadelphia) (US EPA, 2010a, Appendix E, Table E-87). Under the 12/25 alternative 

9 suite, risks for this metric range from ~0% (Birmingham, Los Angeles) to 1.1% (Baltimore). 

10 The observations presented above highlight variability both in the magnitude of risk 

11 reduction as well as in the risk remaining upon simulation of just meeting alternative 24-hour 

12 standards. This reflects the fact that, as noted earlier, alternative 24-hour standards can produce 

13 different degrees of reduction in the annual-average PM2.5 concentrations, depending on the 

14 relationship between 24-hour and annual design values at a particular location. As noted before, 

15 it is these annual-average PM2.5 levels that drive changes in long-term exposure-related 

16 mortality. In addition, as noted earlier, modeling of risk for short-term exposure-related mortality 

17 and morbidity involves a combination of urban study area- and regional-specific C-R functions, 

18 which adds additional variability to risk estimates generated across the study areas. 

19 As noted earlier, given increased emphasis placed in this analysis on long-term exposure20 related mortality, the uncertainty analyses completed for this health endpoint category are 

21 somewhat more comprehensive than those conducted for short-term exposure-related mortality 

22 and morbidity, which to some extent reflects limitations in study data available for addressing 

23 uncertainty in the later category. However, C-R functions used in generating estimates for short24 term exposure-related mortality and morbidity are well-supported in the literature.

25 Summary

26 The results discussed above show that simulating just meeting alternative annual 

standard levels in the range of 14 to 12 μg/m3 27 can produce substantial reductions in short-term 

28 exposure-related mortality and morbidity risk (with the magnitude of risk reduction increasing as 

29 lower annual standards in this range are considered). Furthermore, the results suggest that 

alternative 24-hour standard levels in the range of 30 to 25 μg/m3 30 can produce additional 

31 reductions in estimated risk, beyond that produced by simulations of just meeting lower annual 

standard level down to 12 μg/m3

 (combined with a 24-hour standard of 35 μg/m3 32 ). However, we 

33 note that the magnitude of estimated reductions in short-term exposure-related mortality are 

34 substantially lower than estimates for long-term exposure-related mortality (when comparing 

35 risks for the same urban study area and suite of standards). 
Draft Do Not Quote or Cite March 2010 2-103

1 In addition, while we would expect alternative 24-hour standards to produce more 

2 variable reduction in risk estimates and consequently in public health protection relative to 

3 alternative annual standards (for the same reasons presented earlier for long-term exposure4 related mortality), we see that risk estimates for both annual and 24-hour standards are fairly 

5 variable for short-term exposure-related health effects categories. This reflects in part the fact 

6 that we use urban area-differentiated and regionally-differentiated C-R functions in modeling 

7 short-term exposure-related mortality and morbidity, which introduces additional variability 

8 across study areas in terms of both risk reduction and the magnitude of risks remaining after 

9 simulation of alternative suites of standards. 

10 2.3.6 Preliminary Staff Conclusions on Alternative Levels to Address Health Effects 

11 Related to Long- and Short-term PM2.5 Exposures 

12 In reaching preliminary staff conclusions on alternative standard levels to address health 

13 effects related to both long- and short-term PM2.5 exposures, we have considered the currently 

14 available scientific information including: epidemiologic evidence, including evidence of effects 

15 in susceptible populations; air quality analyses; and estimates of risk reductions associated with 

16 alternative annual and/or 24-hour standard levels, as well as the related limitations and 

17 uncertainties associated with this information as presented in sections 2.3.4 and 2.3.5 and 

18 discussed more fully in the ISA and second draft RA (US EPA, 2009a; US EPA, 2010a). As 

19 outlined in section 2.1.3, we believe it is most appropriate to consider the protection against 

20 PM2.5-related mortality and morbidity effects, associated with long- and short-term exposures, 

21 afforded by the annual and 24-hour standards taken together, rather than to consider each 

22 standard separately. The extent to which these two standards are interrelated in any given area 

23 depend in large part on the relative levels of the standards, the peak-to-mean ratios that 

24 characterize air quality patterns in an area, and whether changes in air quality designed to meet a 

25 given suite of standards is of a more regional or localized nature. 

26 In looking first at the nature of the associations between long- and short-term PM2.5 

27 exposures and a range of health outcomes, we have considered not only the causal inferences 

28 presented in the ISA but also at what air quality concentrations these effects have been observed. 

29 In evaluating these data, we are mindful that the ISA has concluded that no discernable threshold 

30 for an effect associated with long- or short-term PM2.5 exposures can be identified based on the 

31 currently available evidence (US EPA, 2009a, section 2.4.3). We have considered a number of 

32 different air quality metrics to inform our preliminary conclusions regarding alternative levels 

33 that should be considered including:

34  Long-term mean ambient PM2.5 concentrations reported in long- and short-term 

35 exposure studies; 
Draft Do Not Quote or Cite March 2010 2-104

1  Ambient PM2.5 concentrations down to one standard deviation below the long-term 

2 mean concentrations or the lower end of the interquartile range of air quality data 

3 evaluated in the long- and short-term exposure studies; 

4  The range of long-term PM2.5 mean concentrations and the point were the data become 

5 more sparse or where the confidence interval becomes notably wider, suggestive of a 

6 concentration below which the association becomes appreciably more uncertain and the 

7 possibility that an effects threshold may exist becomes more likely; 

8  Differences between long-term mean PM2.5 concentrations averaged across monitors 

9 within a city/county as is typically considered in epidemiologic studies, compared to 

10 the current form of the annual PM2.5 standard which typically focuses on ambient 

11 measurements from the highest reporting community-oriented monitor; 

 98th 12 percentile 24-hour ambient PM2.5 concentrations identified for short-term exposure 

13 studies; and 

 Differences between 98th 14 percentile 24-hour ambient PM2.5 concentrations averaged 

15 across monitors within a city/county compared to the current form of the 24-hour PM2.5 

16 standard which focuses on ambient measurements from the highest reporting 

17 community-oriented monitor 

18 In considering the results of quantitative risk assessments conducted for this and previous 

19 reviews, specifically the estimated risk remaining upon simulation of just meeting alternative 

20 suites of standards, we note the following: 

21  Long-term exposure to PM2.5 has been shown to produce substantially larger mortality 

22 risk (in terms of overall incidence and percent of total mortality) compared to short23 term PM2.5 exposure (section 2.2.2; US EPA, 2010a, p. 6-1). 

24 

25  Much of the risk related to daily exposures, when aggregated on an annual basis, 

26 results from the large number of days during which the 24-hour average 

27 concentrations are in the low- to mid-range of the entire distribution. Thus, to reduce 

28 the aggregate short-term exposure-related risk, it is necessary to shift the bulk of the 

29 distribution to lower concentrations, not just to limit the concentrations on days when 

30 the PM2.5 concentrations are relatively high (US EPA, 2005, p. 4-67, Figure 4-10; 

31 Abt, 1996, section 7.1, p.79, Exhibit 7.6). 

32 

33  Alternative annual standard levels produced more consistent levels of risk reduction 

34 (and consequently public health protection) with generally higher levels of confidence 

35 when compared with alternative 24-hour standards. Considerable variability exists 

36 across urban study areas with respect to the degree to which alternative 24-hour 

37 standard levels produce reductions in annual average PM2.5 concentrations and, 

38 consequently, reductions in risk (section 2.3.4.2). 

39 

40 Taken together, we believe the best way to provide requisite protection for effects 

41 associated with both long- and short-term PM2.5 exposures is to define a suite of standards that 

42 will provide generally consistent protection across the country. In considering the roles that each 
Draft Do Not Quote or Cite March 2010 2-105

1 standard might be expected to play in the protection afforded by alternative suites of standards, 

2 we believe it is appropriate to select a policy approach where the annual standard is the 

3 “generally controlling” standard. This approach would reflect consideration for allowing the 

4 annual standard to serve in most areas as the target for control programs designed to be effective 

5 in lowering the broad distribution of PM2.5 concentrations, thus protecting not only against 

6 effects associated with long-term exposures but also effects associated with short-term 

7 exposures. This approach reflects the recognition that changes in PM2.5 air quality designed to 

8 meet an annual standard would likely result not only in changes in lower annual average 

9 concentrations but also in fewer and lower peak 24-hour concentrations. 

10 In addition, we recognize that an annual standard cannot be expected to offer an adequate 

11 margin of safety against the effects of all short-term PM2.5 exposures, especially in areas with 

12 unusually high peak-to-mean ratios of PM2.5 levels, possibly associated with strong local or 

13 seasonal sources, or for potential PM2.5-related effects that may be associated with shorter-than14 daily exposure periods (noted above in section 2.3.2). As a result, in conjunction with an annual 

15 standard that may be adopted as the generally controlling standard, in part to provide protection 

16 against effects associated with short-term exposures, we believe it is appropriate to use the 24-

17 hour PM2.5 standard to provide supplemental protection against days with high peak 

18 concentrations associated with localized “hotspots” and risk arising from seasonal emissions that 

19 might not be well controlled by a national annual standard. 

20 Thus, we reach the preliminary conclusion that it is appropriate to consider defining the 

21 annual PM2.5 standard as the generally controlling standard and the 24-hour PM2.5 standard as a 

22 “backstop” to provide additional protection, where needed. We believe selecting a suite of 

23 standards using this approach will provide a more uniform level of protection across the U.S. 

24 compared to using an approach where the 24-hour standard is the generally controlling standard. 

25 This preliminary conclusion is consistent with the approach used to set the original PM2.5 

26 standards in 1997 (see section 2.1.1.1).

27 In integrating the preliminary staff conclusions reached in sections 2.3.4 and 2.3.5 

28 regarding alternative levels to provide protection for long- and short-term PM2.5 exposures, 

29 respectively, with the proposed approach outlined above, we have reached preliminary 

30 conclusions regarding alternative levels for both the annual and 24-hour standards. The body of 

31 scientific evidence upon which these preliminary conclusions are based includes consideration of 

32 effects in susceptible populations, including evidence of mortality (causal association), 

33 cardiovascular effects (causal association) and/or respiratory effects (likely causal association) in 

34 various populations including the life stages of children and older adults, people with pre35 existing cardiovascular and respiratory disease, and people with lower socioeconomic status. As 

36 outlined in section 2.3.4.1, in considering alternative levels for an annual standard that would 
Draft Do Not Quote or Cite March 2010 2-106

1 provide protection with an adequate margin of safety, we believe it is also appropriate to take 

2 into account evidence of effects for which the ISA has determined the evidence is suggestive of 

3 an association with long-term PM2.5 exposure including reproductive and developmental effects 

4 and carcinogencity, mutagenicity, and genotoxicity. At this time, PM2.5 concentrations reported 

5 in these studies are equal to or greater than ambient concentrations identified in studies reporting 

6 associations with mortality, cardiovascular effects, or respiratory effects. Therefore, in selecting 

7 alternative levels, we note that, in providing protection for mortality and cardiovascular and 

8 respiratory effects, it is reasonable to anticipate that protection will also be provided for a 

9 broader range of health outcomes. 

10 Based on the currently available scientific evidence, we believe there is support for a 

“generally controlling” PM2.5 annual standard in the range of 13 to 10 μg/m3 11 to provide 

12 protection for effects associated with both long- and short-term PM2.5 exposures in conjunction 

13 with a generally “non-controlling” 24-hour PM2.5 standard in the range of approximately 30 to 35 

μg/m3 14 to limit peak concentrations in areas with relatively high peak-to-mean PM2.5 ratios. 

Selecting a suite of standards with an annual standard in the range of 13 to 12 μg/m3 15 in 

conjunction with a 24-hour standard in the range of 35 to 30 μg/m3 16 would reflect placing greater 

weight on setting standard levels just below the PM2.5 concentrations (long-term mean and 98th 17 

18 percentile value) reported in the epidemiologic studies reporting associations with mortality and 

19 cardiovascular and respiratory effects. It would also recognize consideration for setting a 

20 standard with an adequate margin of safety by selecting standard levels based on ambient 

21 concentrations averaged across monitors as is typically done in epidemiologic studies and 

22 applying those levels using the forms of the current annual and 24-hour PM2.5 standards which 

23 generally focus on the ambient concentrations reported at the highest reporting monitors. 

24 Alternatively, selecting a suite of standards with an annual standard in the range of 11 to 

10 μg/m3

 in conjunction with a 24-hour standard of 30 to 25 μg/m3 25 would reflect a more 

26 precautionary approach. This approach would be consistent with a judgment that, recognizing 

27 the serious nature of the effects and that no discernable threshold for these effects can be 

28 identified, appreciable weight should be accorded to recognizing that health effects may occur 

29 over the full range of concentrations observed in the epidemiologic studies. Using this approach, 

30 we believe that it is reasonable to conclude that the evidence of association is strongest down to 

31 somewhat further below the aggregate long-term mean concentrations reported in the long- and 

32 short-term exposure studies, such as down to one standard deviation below the mean or to the 

33 lower end of the interquartile range, which includes the range in which the data in the study are 

34 most concentrated. To serve as an effective “backstop” for an alternative annual standard set at 

35 the lower end of the preliminary range, we reach the preliminary conclusion that it would be 
Draft Do Not Quote or Cite March 2010 2-107

1 appropriate to set the level of the 24-hour PM2.5 standard somewhat lower than the current 

2 standard. 

3 We recognize that it is the link between the form and the level of the standard that 

4 determines the degree of public health protection the standard affords. As discussed in section 

5 2.3.3.1, the current form of the annual standard allows for spatial averaging across monitors 

6 within constraints that were narrowed in 2006. In light of the currently available scientific 

evidence discussed in section 2.2.1 providing stronger support that socioeconomic status (SES)49 7 

8 modifies the association between PM and morbidity and morality outcomes, we believe that 

9 eliminating the spatial averaging provisions from the form of the annual PM2.5 standard in 

10 conjunction with consideration of alternative levels for the annual standard discussed above is 

11 appropriate for identifying a standard that provides requisite protection with an adequate margin 

12 of safety. In the second draft of this Policy Assessment, we intend to explore more fully 

information on the peak to mean air quality concentrations relating the 24-hour 98th 13 percentile 

14 PM2.5 concentrations relative to the mean annual concentrations to better inform our 

15 understanding of the implications of retaining or modifying the current form of the annual 

16 standard. 

17 2.4 PRELIMINARY STAFF CONCLUSIONS ON ALTERNATIVE FINE PARTICLE 

18 STANDARDS 

19 In reaching preliminary conclusions on potential alternative standards to provide requisite 

20 protection for health effects associated with long- and short-term fine particle exposures, staff 

21 has considered these standards in terms of the basic elements of the NAAQS: indicator, 

22 averaging time, form, and level. In considering the scientific and technical information, we 

23 reflect upon the information available in the last review integrated with information that is newly 

24 available since the last review as assessed and presented in the ISA and second draft RA (US 

25 EPA, 2009a; US EPA 2010a) and as summarized in sections 2.2 and 2.3. 

26 As outlined in sections 2.1.3 and 2.3.6, in this review, our approach to reaching 

27 conclusions about the adequacy of the current suite of PM2.5 standards and potential alternative 

28 standards that are appropriate for consideration is broader and more integrative than approaches 

29 used in past reviews. In applying this approach, we recognize that there are various ways to 

30 combine the suite of standards to achieve an appropriate degree of public health protection. Such 

31 an approach to standard setting, which integrates a much expanded body of health effects 

32 evidence, more extensive air quality data and analyses, and a more comprehensive quantitative 

33 risk assessment and considers the combined protection afforded by the annual and 24-hour 

34 standards, has the potential to result in a more effective and efficient suite of standards than an 

 49 Measured using surrogates such as educational attainment, residential location, and income level. 
Draft Do Not Quote or Cite March 2010 2-108

1 approach that only considers long- and short-term exposures evidence, analyses, and standards 

2 independently. 

3 In presenting our preliminary conclusions regarding alternative suites of primary 

4 standards and ranges of levels for consideration, we summarize conclusions presented in sections 

5 2.3.1 through 2.3.6. We emphasize that these are preliminary conclusions that reflect 

6 consideration of the scientific and technical information assessed and presented in the ISA and 

7 second draft RA (US EPA, 2009a; US EPA, 2010a). We note that staff conclusions to be 

8 presented in the final RA and second draft PA will be based, in part, on input received from 

9 CASAC and the public on the second draft RA and this first draft PA, as well as additional 

10 analyses that we are conducting that will help inform our consideration of alternative forms and 

11 levels as noted in sections 2.3.3, 2.3.4, and 2.3.5. 

12 We recognize that selecting from among alternative standards will necessarily reflect 

13 consideration of the qualitative and quantitative uncertainties inherent in the relevant evidence 

14 and in the assumptions that underlie the quantitative risk assessment. In identifying these 

15 alternative suites of primary standards and ranges of levels for consideration, we are mindful that 

16 the Clean Air Act requires standards to be set that are requisite to protect public health with an 

17 adequate margin of safety, such that the standards are to be neither more nor less stringent than 

18 necessary. Thus, the Act does not require that the NAAQS be set at zero-risk levels, but rather at 

19 levels that avoid unacceptable risks to public health. 

20 

21 ( 1)Consideration should be given to revising the current PM2.5 primary standards to provide 

22 increased public health protection from the effects of both long- and short-term exposures 

23 to fine particles in the ambient air. This preliminary conclusion is based in general on the 

24 evaluation in the ISA of the currently available epidemiologic, toxicologic, dosimetric, 

25 and exposure-related evidence, and more specifically on the evidence of mortality and 

26 cardiovascular and respiratory morbidity effects in areas where the current standards 

27 were met, together with judgments as to the public health significance of the estimated 

28 incidence of effects upon just meeting the current suite of standards. 

29 

30 ( 2)The indicator for fine particle standards should continue to be PM2.5. This observation 

31 reflects our preliminary conclusions that the available evidence does not provide a 

32 sufficient basis for replacing or supplementing the PM2.5 indicator with an indicator 

33 defined in terms of ultrafine particles or for any specific fine particle component or 

34 source category of fine particles, nor does it provide a basis for excluding any component 

35 or source category from the mix of particles included in the PM2.5 indicator. 

36 
Draft Do Not Quote or Cite March 2010 2-109

1 ( 3)Averaging times for PM2.5 standards should continue to include annual and 24-hour 

2 averages to protect against health effects associated with long-term (seasons to years) and 

3 short-term (hours to days) exposure periods. Consideration of other averaging times, 

4 including an averaging time less than 24 hours to address health effects associated with 

5 subdaily fine particle exposures or a longer averaging time to address effects associated 

6 with seasonal fine particle exposures, was limited by the relatively small amount of 

7 relevant information available in this review. 

8 

9 ( 4)Consideration should be given to retaining or revising the form of the annual standard. 

10 Consideration should be given to revising the form of the annual standard to one based on 

11 the highest community-oriented monitor in an area rather than a form that would allow 

12 averaging across monitors (e.g., spatial averaging). The form of the 24-hour standard 

should continue to be defined in terms of the 98th 13 percentile of the distribution of 24-hour 

14 PM2.5 concentrations, averaged over three years. 

15 

16 ( 5)Consideration should be given to alternative suites of PM2.5 standards to provide 

17 protection against effects associated with both long- and short-term exposures, taking into 

18 account both evidence-based and risk-based considerations. Further, we conclude it is 

19 appropriate to consider setting the levels of the annual and 24-hour standards such that 

20 the annual standard would be the “generally controlling” standard to provide protection 

21 for both long- and short-term PM2.5 exposures in conjunction with a 24-hour standard to 

22 provide supplemental protection against days with high peak concentrations associated 

23 with localized “hotspots” and risk arising from seasonal emissions that might not be well 

24 controlled by a national annual standard. Integrated preliminary conclusions on ranges 

25 of alternative suites of standards that, when considered together, would provide requisite 

26 protection against effects associated with both long- and short-term exposures include: 

27 

(a) Consideration of a revised annual PM2.5 standard within the range of 13 to 12 μg/m3 28 , 

29 together with either retaining or revising the 24-hour PM2.5 standard within the range 

of 35 to 30 μg/m3 30 . 

(b) Consideration of a revised annual PM2.5 standard, within the range of 11 to 10 μg/m3 31 , 

together with revising the 24-hour PM2.5 standard within a range of 30 to 25 μg/m3 32 . 

33 

34 2.5 KEY UNCERTAINTIES AND AREAS FOR FUTURE RESEARCH AND DATA 

35 COLLECTION 

36 [This topic will be discussed in the second draft Policy Assessment.] 
Draft Do Not Quote or Cite March 2010 2-110

1 2.6 REFERENCES 

2 Abt (1996). A Particulate Matter Risk Assessment for Philadelphia and Los Angeles. Abt Associates. Bethesda, 

3 MD. Update of July 3, 1996 (November 1996). Supplement to November 1996 Report (December 1996). 

4 Prepared for the Office of Air Quality Planning and Standards, U.S. Environmental Protection Agency, 

5 Contract No 68-W4-0029. Available: http://www.epa.gov/ttn/naaqs/standards/pm/s_pm_pr_td.html. 

6 Abt (2005). Particulate Matter Health Risk Assessment for Selected Urban Areas. Abt Associates. Final Report. 

7 Bethesda, MD. Prepared for the Office of Air Quality Planning and Standards, U.S. Environmental 

8 Protection Agency, Contract No. 68-D-03-002. EPA 452/R-05-007A. Available: 

9 http://www.epa.gov/ttn/naaqs/standards/pm/s_pm_cr_td.html. 

10 ATSDR (2006). A study of ambient air contaminants and asthma in New York City: Part A and B. Agency for 

11 Toxic Substances and Disease Registry; Public Health Service; U.S. Department of Health and Human 

12 Services. Atlanta, GA. 

13 http://permanent.access.gpo.gov/lps88357/ASTHMA_BRONX_FINAL_REPORT.pdf. 

14 Bell ML, Ebisu K, Peng RD, Walker J, Samet JM, Zeger SL, Dominic F. (2008). Seasonal and regional short-term 

15 effects of fine particles on hospital admissions in 202 U.S. counties, 1999-2005. Am J Epidemiol, 168: 

16 1301-1310. 

17 Bell ML, Ebisu K, Peng R, Samet J, Dominici F. (2009). Hospital Admissions and Chemical Composition of Fine 

18 Particle Air Pollution. Am J Respir Crit Care Med, 179: 1115-1120. 

19 Beelen R, Hoek G, van den Brandt PA, Goldbohm RA, Fischer P, Schouten LJ, Jerrett M, Hughes E, Armstrong B, 

20 Brunekreef B (2008). Long-term effects of traffic-related air pollution on mortality in a Dutch cohort 

21 (NLCS-AIR study). Environ Health Perspect, 116: 196-202. 

22 Burnett RT, Goldberg MS. (2003) Size-fractionated particulate mass and daily mortality in eight Canadian cities. In: 

23 Revised analyses of time-series studies of air pollution and health. Special report. Boston, MA: Health 

24 Effects Institute; pp. 85-90. Available: http://www.healtheffects.org/news.htm [16 May, 2003]. 

25 Burnett RT, Stieb D, Brook JR, Cakmak S, Dales R, Raizenne M, Vincent R, Dann T. (2004). Associations between 

26 short-term changes in nitrogen dioxide and mortality in Canadian cities. Arch Environ Occup Health, 59: 

27 228-236. 

28 Chen Y, Yang Q, Krewski D, Shi Y, Burnett RT, McGrail K (2004). Influence of relatively low level of particulate 

29 air pollution on hospitalization for COPD in elderly people. Inhal Toxicol, 16: 21-25. 

30 Chen LH, Knutsen SF, Shavlik D, Beeson WL, Petersen F, Ghamsary M, Abbey D. (2005). The association between 

31 fatal coronary heart disease and ambient particulate air pollution: Are females at greater risk? Environ 

32 Health Perspect, 113: 1723-1729. 

33 Chuang KJ, Chan CC, Shiao GM, Su TC (2005). Associations between submicrometer particles exposures and 

34 blood pressure and heart rate in patients with lung function impairments. J Occup Environ Med, 47: 1093-

35 1098. 

36 Dales R, Liu L, Szyszkowicz M, Dalipaj M, Willey J, Kulka R, Ruddy TD (2007). Particulate air pollution and 

37 vascular reactivity: the bus stop study. Int Arch Occup Environ Health, 81: 159-164. 

38 Delfino RJ, Murphy-Moulton AM, Burnett RT, Brook JR, Becklake MR (1997). Effects of air pollution on 

39 emergency room visits for respiratory illnesses in Montreal, Quebec. Am J Respir Crit Care Med, 155: 568-

40 576. 

41 Dockery DW, Pope CA III, Xu X, Spengler JD, Ware JH, Fay ME, Ferris BG Jr, Speizer FE. (1993). An association 

42 between air pollution and mortality in six US cities. NEJM 329: 1753-1759. 
Draft Do Not Quote or Cite March 2010 2-111

1 Dockery DW, Cunningham J, Damokosh AI, Neas LM, Spengler JD, Koutrakis P, Ware JH, Raizenne M, Speizer 

2 FE. (1996). Health effects of acid aerosols on North American children: respiratory symptoms. Environ 

3 Health Perspect. 104(5):500-5. 

4 Dockery DW, Luttmann-Gibson H, Rich DQ, Link MS, Mittleman MA, Gold DR, Koutrakis P, Schwartz JD, 

5 Verrier RL (2005). Association of air pollution with increased incidence of ventricular tachyarrhythmias 

6 recorded by implanted cardioverter defibrillators. Environ Health Perspect, 113: 670-674. 

7 Dominici F, Peng RD, Bell ML, Pham L, McDermott A, Zeger SL, Samet JL. (2006a). Fine particulate air pollution 

8 and hospital admission for cardiovascular and respiratory diseases. JAMA, 295: 1127-1134. 

9 Dominic F. (2006b). Letter from Francesca Dominici, Associate Professor of Biostatistics, Bloomberg School of 

10 Public Health, Johns Hopkins University, comments to the proposed rule. Docket No. OAR-2001-0017-

11 0988. March 21, 2006. 

12 Dominici F, Peng RD, Zeger SL, White RH, Samet JM. (2007). Particulate air pollution and mortality in the United 

13 States: did the risks change from 1987 to 2000? Am J Epidemiol, 166: 880-8. 

14 Dominici F, Peng RD, Ebisu K, Zeger SL, Samet JM, Bell ML (2007). Does the effect of PM10 on mortality depend 

15 on PM nickel and vanadium content? A reanalysis of the NMMAPS data. Environ Health Perspect, 115: 

16 1701-1703. 

17 Dubowsky SD, Suh H, Schwartz J, Coull BA, Gold DR (2006). Diabetes, obesity, and hypertension may enhance 

18 associations between air pollution and markers of systemic inflammation. Environ Health Perspect, 114: 

19 992-998. 

20 Eftim SE, Samet JM, Janes H, McDermott A, Dominici F. (2008). Fine Particulate Matter and Mortality: A 

21 Comparison of the Six Cities and American Cancer Society Cohorts With a Medicare Cohort. 

22 Epidemiology, 19: 209- 216. 

23 Enstrom JE. (2005). Fine particulate air pollution and total mortality among elderly Californians, 1973-2002. Inhal 

24 Toxicol, 17: 803-816. 

25 Fairley D (2003). Mortality and air pollution for Santa Clara County, California, 1989-1996, In: Revised analyses of 

26 time-series studies of air pollution and health. Special report. Health Effects Institute. Boston, MA. 

27 http://www.healtheffects.org/Pubs/TimeSeries.pdf. 

28 Fakhri AA, Ilic LM, Wellenius GA, Urch B, Silverman F, Gold DR, Mittleman MA (2009). Autonomic effects of 

29 controlled fine particulate exposure in young healthy adults: Effect modification by ozone. Environ Health 

30 Perspect, 117: 1287-1292. 

31 Gauderman WJ., McConnell R, Gilliland F, London S, Thomas D, Avol E, Vora H., Berhane K., Rappaport EB., 

32 Lurmann F, Margolis HG, Peters J. (2000). Association between air pollution and lung function growth in 

33 southern California children. Am. J. Respir. Crit. Care Med. 162: 1383-1390. 

34 Gauderman WJ, Gilliland GF, Vora H, Avol E, Stram D, McConnell R, Thomas D, Lurmann F, Margolis HG, 

35 Rappaport, E. B., Berhane, K., Peters, J. M. (2002). Association between air pollution and lung function 

36 growth in southern California children: results from a second cohort. Am. J. Respir. Crit. Care Med. 166: 

37 76-84. 

38 Gauderman W.J, Avol, E., Gilliland, F., Vora, H., Thomas, D., Berhane, K., McConnell, R., Kuenzli, N., Lurmann, 

39 F., Rappaport, E., Margolis, H., Bates, D., Peters, J.(2004). The effect of air pollution on lung development 

40 from 10 to 18 years of age. NEJM 351:1057-67. 
Draft Do Not Quote or Cite March 2010 2-112

1 Gent JF, Koutrakis P, Belanger K, Triche E, Holford TR, Bracken MB, Leaderer BP. (2009) Symptoms and 

2 medication use in children with asthma and traffic-related sources of fine particle pollution. Environ 

3 Health Perspect. 117:1168-74. 

4 Gold DR, Litonjua AA, Zanobetti A, Coull BA, Schwartz J, MacCallum G, Verrier RL, Nearing BD, Canner MJ, 

5 Suh H, Stone PH (2005). Air pollution and ST-segment depression in elderly subjects. Environ Health 

6 Perspect 113: 883-887. 

7 Gong H Jr, Linn WS, Clark KW, Anderson KR, Geller MD, Sioutas C. (2005) Respiratory responses to exposures 

8 with fine particulates and nitrogen dioxide in the elderly with and without COPD. Inhal Toxicol. 

9 17(3):123-32. 

10 Goss CH: Newsom SA, Schildcrout JS, Sheppard L, Kaufman JD. (2004). Effect of ambient air pollution on 

11 pulmonary exacerbations and lung function in cystic fibrosis. Am J Respir Crit Care Med, 169: 816-821. 

12 Hassett-Sipple B and Stanek L (2009) Particulate Matter Air Quality Data Requested from Epidemiologic Study 

13 Authors. Memorandum to PM NAAQS review docket EPA-HQ-OAR-2007-0492. 

14 HEI (2009). Health Effects Institute Health Review Committee Commentary for Research Report No. 140, 

15 Extended Follow-up and Spatial Analysis of the American Cancer Society Study Linking Particulate Air 

16 Pollution and Mortality. HEI Research Report 140. Health Effects Institute, Boston , MA. pp. 115-136. 

17 Available: http://pubs.healtheffects.org/view.php?id=315. 

18 Henderson, R. (2006a). Letter from Dr. Rogene Henderson, Chair, Clean Air Scientific Advisory Committee to the 

19 Honorable Stephen L. Johnson, Administrator, US EPA. Clean Air Scientific Advisory Committee 

20 Recommendations Concerning the Proposed National Ambient Air Quality Standards for Particulate 

21 Matter. March 21, 2006. Available: http://www.epa.gov/sab/pdf/casac-ltr-06-002.pdf

22 Henderson R., Cowling, E., Crapo, J.D.., Miller, F. J., Poirot, R.L., Speizer, F., Zielinska, B. (2006b). Letter from 

23 Clean Air Scientific Advisory Committee to the Honorable Stephen L. Johnson, Administrator, US EPA. 

24 Clean Air Scientific Advisory Committee Recommendations Concerning the Final National Ambient Air 

25 Quality Standards for Particulate Matter. September 29, 2006. Available: 

26 http://www.epa.gov/sab/pdf/casac-ltr-06-002.pdf

27 Hopke PK, Ito K, Mar T, Christensen WF, Eatough DJ, Henry RC, Kim E, Laden F, Lall R, Larson TV, Liu H, Neas 

28 L, Pinto J, Stolzel M, Suh H, Paatero P, Thurston GD (2006). PM source apportionment and health effects: 

29 1 Intercomparison of source apportionment results. J Expo Sci Environ Epidemiol, 16: 275-286. 

30 Islam T, Gauderman WJ, Berhane K, McConnell R, Avol E, Peters JM, Gilliland FD. (2007). The relationship 

31 between air pollution, lung function and asthma in adolescents. Thorax, 62: 957-963. 

32 Ito K, Christensen WF, Eatough DJ, Henry RC, Kim E, Laden F, Lall R, Larson TV, Neas L, Hopke PK, Thurston 

33 GD (2006). PM source apportionment and health effects: 2 An investigation of intermethod variability in 

34 associations between source-apportioned fine particle mass and daily mortality in Washington, DC. J Expo 

35 Sci Environ Epidemiol, 16: 300-310. 

36 Jerret M, Burnett RT, Ma R: Pope CA, Kreski D, Newbold KB, Thurston G, Shi Y, Finkelstein N, Calle N, Thun 

37 MJ. (2005) Spatial analysis of air pollution and mortality in Los Angeles. Epidemiology, 16: 727-36. 

38 Kim JJ, Smorodinsky S, Lipsett M, Singer BC, Hodgson AT, Ostro B. (2004). Traffic-related air pollution near busy 

39 roads: the East Bay children's Respiratory Health Study. Am J Respir Crit Care Med, 170: 520-526. 

40 Krewski, D., Burnett, R. T., Goldberg, M. S., Hoover, K., Siemiatycki, J,, Jerrett, M., Abrahamowicz, M., White, W. 

41 H. (2000). Reanalysis of the Harvard Six Cities Study and the American Cancer Society Study of 
Draft Do Not Quote or Cite March 2010 2-113

1 particulate air pollution and mortality. A special report of the Institute’s particle epidemiology reanalysis 

2 project. Cambridge, MA: Health Effects Institute. http://pubs.healtheffects.org/view.php?id=6

3 Krewski D, Jerrett M, Burnett RT, Ma R, Hughes E, Shi Y, Turner MC, Pope AC III, Thurston G, Calle EE, Thun 

4 MJ. (2009). Extended Follow-Up and Spatial Analysis of the American Cancer Society Study Linking 

5 Particulate Air Pollution and Mortality. HEI Research Report 140, Health Effects Institute, Boston, MA. 

6 Available: http://pubs.healtheffects.org/view.php?id=315. 

7 Kunzli N, Medina S, Kaiser R, et al. (2001). Assessment of deaths attributable to air pollution: should we use risk 

8 estimates based on time series or on cohort studies? Am J Epidemiol 153:1050 –1055. 

9 Laden F, Neas LM, Dockery DW, Schwartz J. (2000). Association of fine particulate matter from different sources 

10 with daily mortality in six US cities. Environ Health Perspect, 108: 941-947. 

11 Laden F, Schwartz J, Speizer FE, Dockery DW. (2006). Reduction in fine particulate air pollution and mortality: 

12 extended follow-up of the Harvard Six Cities Study. Am. J. Respir. Crit. Care. Med. 173: 667-672. 

13 Laden F. (2009). Personal communication with Dr. Francine Laden: Annual PM2.5 levels used in the update of the 

14 Harvard Six Cities Study. May 21, 2009. Docket EPA-HQ-OAR-2007-0492 

15 Lanki T, Hoek G, Timonen K, Peters A, Tiittanen P, Vanninen E, Pekkanen J (2008). Hourly variation in fine 

16 particle exposure is associated with transiently increased risk of ST segment depression. Br Med J, 65: 782-

17 786. 

18 Lin M, Stieb DM, Chen Y (2005). Coarse particulate matter and hospitalization for respiratory infections in children 

19 younger than 15 years in Toronto: a case-crossover analysis. Pediatrics, 116: 235-240. 

20 Lipfert FW, Baty JD, Miller JP, Wyzga RE. (2006). PM2.5 constituents and related air quality variables as predictors 

21 of survival in a cohort of U.S. military veterans. Inhal Toxicol, 18: 645-657. 

22 Lippmann M, Ito K, Hwang JS, Maciejczyk P, Chen LC (2006). Cardiovascular effects of nickel in ambient air. 

23 Environ Health Perspect, 114: 1662-1669. 

24 Lisabeth LD, Escobar JD, Dvonch JT, Sanchez BN, Majersik JJ, Brown DL, Smith MA, Morgenstern LB (2008). 

25 Ambient air pollution and risk for ischemic stroke and transient ischemic attack. Ann Neurol, 64: 53-59. 

26 Ljungman PLS, Berglind N, Holmgren C, Gadler F, Edvardsson N, Pershagen G, Rosenqvist M, Sjögren B, 

27 Bellander T (2008). Rapid effects of air pollution on ventricular arrhythmias. Eur Heart J, 29: 2894-2901. 

28 Lund AK, Lucero J, Lucas S, Madden MC, McDonald JD, Seagrave JC, Knuckles TL, Campen MJ (2009). 

29 Vehicular emissions induce vascular MMP-9 expression and activity associated with endothelin-1 mediated 

30 pathways. Arterioscler Thromb Vasc Biol, 29: 511-517. 

31 Mar TF., Norris GA., Larson TV., Wilson, W. E., Koenig, J. Q. (2003) Air pollution and cardiovascular mortality in 

32 Phoenix, 1995-1997. In: Revised analyses of time-series studies of air pollution and health. Special report. 

33 Boston, MA: Health Effects Institute, pp. 177-182. Available: http://www.healtheffects.org/news.htm [16 

34 May, 2003]. 

35 Mar TF, Larson TV, Stier RA, Claiborn C, Koenig JQ (2004). An analysis of the association between respiratory 

36 symptoms in subjects with asthma and daily air pollution in Spokane, Washington. Inhal Toxicol, 16: 809-

37 815. 

38 Mar TF, Ito K, Koenig JQ, Larson TV, Eatough DJ, Henry RC, Kim E, Laden F, Lall R, Neas L, Stölzel M, Paatero 

39 P, Hopke PK, Thurston GD.(2006) PM source apportionment and health effects. 3. Investigation of inter-
Draft Do Not Quote or Cite March 2010 2-114

1 method variations in associations between estimated source contributions of PM2.5 and daily mortality in 

2 Phoenix, AZ. J Expo Sci Environ Epidemiol. 16:311-20 

3 Mar TF, Jansen K, Shepherd K, Lumley T, Larson TV, Koenig JQ (2005). Exhaled nitric oxide in children with 

4 asthma and short-term PM25 exposure in Seattle. Environ Health Perspect, 113: 1791-1794. 

5 McConnell R, Berhane K, Gilliland F, Molitor J, Thomas D, Lurmann F, Avol E, Gauderman WJ, Peters JM. 

6 (2003). Prospective study of air pollution and bronchitic symptoms in children with asthma. Am J Respir 

7 Crit Care Med, 168: 790-797. 

8 Metzger KB, Tolbert PE, Klein M, Peel JL, Flanders WD, Todd KH, Mulholland JA, Ryan PB, Frumkin H. (2004). 

9 Ambient air pollution and cardiovascular emergency department visits. Epidemiology, 15: 46-56. 

10 Metzger KB, Klein M, Flanders WD, Peel JL, Mulholland JA, Langberg JJ, Tolbert PE. (2007). Ambient air 

11 pollution and cardiac arrhythmias in patients with implantable defibrillators. Epidemiology, 18: 585-592. 

12 Miller KA, Siscovick DS, Sheppard L, Shepherd K, Sullivan JH, Anderson GL, Kaufman JD. (2007). Long-term 

13 exposure to air pollution and incidence of cardiovascular events in women. N Engl J Med, 356: 447-458. 

14 Ostro B.D., Broadwin, R., Green, S., Feng, W., Lipsett, M.(2006). Fine particulate air pollution and mortality in 

15 nine California counties: results from CALFINE. Env. Health Perspect. 114: 29-33. 

16 Peel JL, Tolbert PE, Klein M, Metzger KB, Flanders WD, Knox T, Mulholland JA, Ryan PB, Frumkin H. (2005). 

17 Ambient air pollution and respiratory emergency department visits. Epidemiology, 16: 164-174. 

18 Peel JL, Metzger KB, Klein M, Flanders WD, Mulholland JA, Tolbert PE. (2007). Ambient air pollution and 

19 cardiovascular emergency department visits in potentially sensitive groups. Am J Epidemiol, 165: 625-633. 

20 Peng RD, Bell ML, Geyh AS, McDermott A, Zeger SL, Samet JM, Dominici F (2009). Emergency admissions for 

21 cardiovascular and respiratory diseases and the chemical composition of fine particle air pollution. Environ 

22 Health Perspect. 117:957-63. 

23 Penttinen P, Vallius M, Tiittanen P, Ruuskanen J, Pekkanen J (2006). Source-specific fine particles in urban air and 

24 respiratory function among adult asthmatics. Inhal Toxicol, 18: 191-198. 

25 Peretz A, Kaufman JD, Trenga CA, Allen J, Carlsten C, Aulet MR, Adar SD, Sullivan JH (2008). Effects of diesel 

26 exhaust inhalation on heart rate variability in human volunteers. Environ Res, 107: 178-184. 

27 Peters A., Dockery, D. W., Muller, J. E., Mittleman, M. A. (2001). Increased particulate air pollution and the 

28 triggering of myocardial infarction. Circulation 103:2810-2815. 

29 Pope CA 3rd, Thun, M.J., Namboodiri, M.M., Dockery, D.W., Evans, J.S., Speizer, F.E., Heath,, C.W. (1995). 

30 Particulate air pollution as a predictor of mortality in a prospective study of U.S. adults. Am J Respir Crit 

31 Care Med. 151: 669-674. 

32 Pope CA 3rd, Burnett, R. T., Thun, M. J., Calle, E. E., Krewski, D., Ito, K., Thurston, G. D. (2002). Lung cancer, 

33 cardiopulmonary mortality, and long-term exposure to fine particulate air pollution. J. Am. Med. Assoc. 

34 287:1132-1141. 

35 Pope CA 3rd, Burnett RT, Thurston GD, Thun MJ, Calle EE, Krewski D, Godleski JJ (2004). Cardiovascular 

36 mortality and long-term exposure to particulate air pollution: epidemiological evidence of general 

37 pathophysiological pathways of disease. Circulation, 109: 71-77. 

38 Pope CA 3rd, Ezzati M, Dockery DW. (2009). Fine-particulate air pollution and life expectancy in the United States. 

39 N Engl J Med, 360: 376-386. 
Draft Do Not Quote or Cite March 2010 2-115

1 Rabinovitch N, Zhang LN, Murphy JR, Vedal S, Dutton SJ, Gelfand EW (2004). Effects of wintertime ambient air 

2 pollutants on asthma exacerbations in urban minority children with moderate to severe disease. J Allergy 

3 Clin Immunol, 114: 1131-1137. 

4 Rabinovitch N, Strand M, Gelfand EW (2006). Particulate levels are associated with early asthma worsening in 

5 children with persistent disease. Am J Respir Crit Care Med, 173: 1098-1105. 

6 Rabl A. (2003) Interpretation of air pollution mortality: number of deaths or years of life lost? J Air Waste Manag 

7 Assoc., 53:41–50. 

8 Raizenne M, Neas LM, Damokosh AI, Dockery DW, Spengler JD, Koutrakis P, Ware JH, Speizer FE. (1996). 

9 Health effects of acid aerosols on North American children: pulmonary function. Environ Health Perspect, 

10 104: 506-514. 

11 Rich DQ, Schwartz J, Mittleman MA, Link M, Luttmann-Gibson H, Catalano PJ, Speizer FE, Dockery DW (2005). 

12 Association of short-term ambient air pollution concentrations and ventricular arrhythmias. Am J 

13 Epidemiol, 161: 1123-1132. 

14 Riediker M, Cascio WE, Griggs TR, Herbst MC, Bromberg PA, Neas L, Williams RW, Devlin RB (2004). 

15 Particulate matter exposure in cars is associated with cardiovascular effects in healthy young men. Am J 

16 Respir Crit Care Med, 169: 934-940. 

17 Rosenthal FS, Carney JP, Olinger ML (2008). Out-of-hospital cardiac arrest and airborne fine particulate matter: a 

18 case-crossover analysis of emergency medical services data in Indianapolis, Indiana. Environ Health 

19 Perspect, 116: 631-636. 

20 Ross M, Langstaff, J. (2005). Updated statistical information on air quality data from epidemiologic studies. 

21 Memorandum to PM NAAQS review docket EPA-HQ-OAR-2001-0017. Docket No. OAR-2001-0017-

22 0261. January 31, 2005. 

23 Ross M, Langstaff, J. (2006). Statistical information on air quality data from additional epidemiologic studies. 

24 Memorandum to PM NAAQS review docket EPA-HQ-OAR-2001-0017. Docket ID No. OAR-2001-0017-

25 1409. April 5, 2006. 

26 Rundell KW, Hoffman JR, Caviston R, Bulbulian R, Hollenbach AM (2007). Inhalation of ultrafine and fine 

27 particulate matter disrupts systemic vascular function. Inhal Toxicol, 19: 133-140. 

28 Rundell KW, Caviston R (2008). Ultrafine and fine particulate matter inhalation decreases exercise performance in 

29 healthy subjects. J Strength Cond Res, 22: 2-5. 

30 Schmidt M, Frank, N., Mintz, D., Rao, T., McCluney, L. (2005). Analyses of particulate matter (PM) data for the 

31 PM NAAQS review. Memorandum to PM NAAQS review docket EPA-HQ-OAR-2001-0017. June 30, 

32 2005. 

33 Schmidt M (2010). Analyses of PM2.5 data for the PM NAAQS review. Memorandum to PM NAAQS review 

34 docket EPA-HQ-OAR-2007-0492. 

35 Schwartz J (2003). Daily deaths associated with air pollution in six US cities and short-term mortality displacement 

36 in Boston. From Revised Analyses of Time-Series Studies of Air Pollution and Health, Health Effects 

37 Institute Special Report, May 2003. 

38 Schwartz J, Coull B, Laden F, Ryan L (2008). The effect of dose and timing of dose on the association between 

39 airborne particles and survival. Environ Health Perspect, 116: 64-69. 
Draft Do Not Quote or Cite March 2010 2-116

1 Shah AP, Pietropaoli AP, Frasier LM, Speers DM, Chalupa DC, Delehanty JM, Huang LS, Utell MJ, Frampton MW 

2 (2008). Effect of inhaled carbon ultrafine particles on reactive hyperemia in healthy human subjects. 

3 Environ Health Perspect, 116: 375-380. 

4 Slaughter JC, Lumley T, Sheppard L, Koenig JQ, Shapiro GG. (2003). Effects of ambient air pollution on symptom 

5 severity and medication use in children with asthma. Ann Allergy Asthma Immunol, 91: 346-353. 

6 Slaughter JC, Kim E, Sheppard L, Sullivan JH, Larson TV, Claiborn C (2005). Association between particulate 

7 matter and emergency room visits, hospital admissions and mortality in Spokane, Washington. J Expo Sci 

8 Environ Epidemiol, 15: 153-159. 

9 Stieb DM, Beveridge RC, Brook JR, Smith-Doiron M, Burnett RT, Dales RE, Beaulieu S, Judek S, Mamedov A 

10 (2000). Air pollution, aeroallergens and cardiorespiratory emergency department visits in Saint John, 

11 Canada. J Expo Sci Environ Epidemiol, 10: 461-477. 

12 Sullivan J, Sheppard L, Schreuder A, Ishikawa N, Siscovick D, Kaufman J (2005). Relation between short-term 

13 fine-particulate matter exposure and onset of myocardial infarction. Epidemiology, 16: 41-48. 

14 Thurston G, Ito K, Mar T, Christensen WF, Eatough DJ, Henry RC, Kim E, Laden F, Lall R, Larson TV, Liu H, 

15 Neas L, Pinto J, Stolzel M, Suh H, Hopke PK (2005). Results and implications of the workshop on the 

16 source apportionment of PM health effects. Epidemiology, 16: S134-S135. 

17 Tolbert PE, Klein M, Peel JL, Sarnat SE, Sarnat JA. (2007). Multipollutant modeling issues in a study of ambient air 

18 quality and emergency department visits in Atlanta. J Expo Sci Environ Epidemiol, 24: 938-945. 

19 Tsai FC, Apte MG, Daisey JM (2000). An exploratory analysis of the relationship between mortality and the 

20 chemical composition of airborne particulate matter. Inhal Toxicol, 12: 121-135. 

21 Urch B, Silverman F, Corey P, Brook JR, Lukic KZ, Rajagopalan S, Brook RD (2005). Acute blood pressure 

22 responses in healthy adults during controlled air pollution exposures. Environ Health Perspect, 113: 1052-

23 1055. 

24 US EPA (1996a). Air Quality Criteria for Particulate Matter. Research Triangle Park, NC: National Center for 

25 Environmental Assessment-RTP Office, report no. EPA/600/P-95/001. 3v. Available: 

26 http://www.epa.gov/ttn/naaqs/standards/pm/s_pm_pr_cd.html. 

27 US EPA (1996b). Review of the National Ambient Air Quality Standards for Particulate Matter: Policy Assessment 

28 of Scientific and Technical Information, OAQPS Staff Paper. Research Triangle Park, NC 27711: Office 

29 of Air Quality Planning and Standards, report no. EPA-452\R-96-013. Available: 

30 http://www.epa.gov/ttn/naaqs/standards/pm/s_pm_pr_sp.html. 

31 US EPA (2004). Air Quality Criteria for Particulate Matter. National Center for Environmental Assessment, Office 

32 of Research and Development, U.S. Environmental Protection Agency, Research Triangle Park, NC 27711, 

33 report no. EPA/600/P-99/002aF and EPA/600/P-99/002bF. October 2004. Available: 

34 http://www.epa.gov/ttn/naaqs/standards/pm/s_pm_cr_cd.html

35 US EPA (2005). Review of the National Ambient Air Quality Standards for Particulate Matter: Policy Assessment 

36 of Scientific and Technical Information, OAQPS Staff Paper. Research Triangle Park, NC 27711: Office 

37 of Air Quality Planning and Standards, report no. EPA EPA-452/R-05-005a. December 2005.

38 Available: http://www.epa.gov/ttn/naaqs/standards/pm/s_pm_cr_sp.html

39 US EPA (2008a). Integrated Review Plan for the National Ambient Air Quality Standards fro Particulate Matter. 

40 National Center for Environmental Assessment and Office of Air Quality Planning and Standards, U.S. 

41 Environmental Protection Agency, Research Triangle Park, NC. Report No. EPA 452/R-08-004. March 
Draft Do Not Quote or Cite March 2010 2-117

1 2008. Available at: 

2 http://www.epa.gov/ttn/naaqs/standards/pm/data/2008_03_final_integrated_review_plan.pdf

3 US EPA (2009a). Integrated Science Assessment for Particulate Matter (Final Report). U.S. Environmental 

4 Protection Agency, Washington, DC, EPA/600/R-08/139F, December 2009. Available: 

5 http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=216546

6 US EPA (2010a). Quantitative Risk Assessment for Particulate 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-09-001. February 2010. Available: 

9 http://www.epa.gov/ttn/naaqs/standards/pm/s_pm_index.html. 

10 Villeneuve PJ, Chen L, Stieb D, Rowe BH (2006). Associations between outdoor air pollution and emergency 

11 department visits for stroke in Edmonton, Canada. Eur J Epidemiol, 21: 689-700. 

12 Woodruff TJ, Darrow LA, Parker JD (2008). Air pollution and postneonatal infant mortality in the United States, 

13 1999-2002. Environ Health Perspect, 116: 110-115. 

14 Zanobetti A, Schwartz J. (2009). The effect of fine and coarse particulate air pollution on mortality: A national 

15 analysis. Environ Health Perspect, 117: 1-40. 

16 Zhang Z, Whitsel E, Quibrera P, Smith R, Liao D, Anderson G, Prineas R (2009). Ambient fine particulate matter 

17 exposure and myocardial ischemia in the Environmental Epidemiology of Arrhythmogenesis in the 

18 Women's Health Initiative (EEAWHI) study. Environ Health Perspect, 117: 751-756. 

19 Zeger S, McDermott A, Dominicit F, Samet J. (2007). Mortality in the Medicare population and chronic exposure 

20 to fine particulate air pollution. Johns Hopkins University. Baltimore. 

21 http://www.bepress.com/jhubiostat/paper133. 

22 Zeger S, Dominici F, McDermott A, Samet J. (2008). Mortality in the Medicare population and chronic exposure to 

23 fine particulate air pollution in urban centers (2000-2005). Environ Health Perspect, 116: 1614. 
Draft Do Not Quote or Cite March 2010 

 

3-1

1 3 REVIEW OF THE PRIMARY STANDARD FOR THORACIC 

2 COARSE PARTICLES 

3 This chapter presents preliminary staff conclusions with regard to the adequacy of the 

4 current primary PM10 standard, which is intended to protect public health against exposures to 

5 thoracic coarse particles (PM10-2.5), and potential alternative primary standards for consideration 

6 in this review. Our assessment of these issues is framed by a series of key policy-relevant 

7 questions, which expand upon those presented in the IRP (US EPA, 2008a) at the outset of this 

8 review. The answers to these questions will inform decisions on whether, and if so how, to 

9 revise the current PM10 standard. 

10 Staff notes that final decisions regarding the primary PM10 standard will draw upon 

11 scientific information about health effects, as well as judgments about how to deal with the range 

12 of uncertainties that are inherent in the scientific evidence. Ultimately, the final decisions are 

13 largely public health policy judgments. Our approach to informing these judgments, discussed 

14 more fully below, recognizes that the available health effects evidence reflects a continuum 

15 consisting of ambient levels at which scientists generally agree that health effects are likely to 

16 occur through lower levels at which the likelihood and magnitude of the response become 

17 increasingly uncertain 

18 Our current approach for reviewing the primary PM10 standard is presented in section 3.1. 

19 Our preliminary conclusions regarding the adequacy of the current PM10 standard are presented 

20 in section 3.2. Section 3.3 presents our preliminary considerations and conclusions with respect 

21 to potential alternative standards, focusing on each of the basic elements of the standards: 

22 pollutant indicator (section 3.3.1), averaging time (section 3.3.2), and form and level (section 

23 3.3.3). The next draft of this chapter will also include an initial overview of key uncertainties 

24 and suggested future research areas and data collection efforts. 

25 3.1 APPROACH 

26 Staff’s approach for reviewing the current primary PM10 standard builds upon the 

27 approaches used in previous PM NAAQS reviews. Our current approach is based on the updated 

scientific and technical information in the ISA.1 28 The past and current approaches described 

29 below are all based most fundamentally on using information from epidemiologic studies to 

30 inform the selection of PM standards that, in the Administrator’s judgment, protect public health 

31 with an adequate margin of safety. In the case of thoracic coarse particles, such information is in 

 1

As described below, given limitations in the health effects 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

1 the form of PM10-2.5 and PM10 air quality distributions over which health effect associations have 

2 been reported. In light of limitations in PM10-2.5 epidemiologic studies, dosimetric and 

3 toxicological information also play an important role, especially in considerations related to the 

4 appropriate indicator for a standard meant to protect against exposures to thoracic coarse 

5 particles. Evidence-based approaches to using information from epidemiologic studies to inform 

6 decisions on PM standards are complicated by the recognition that no population threshold, 

7 below which it can be concluded with confidence that PM-related effects do not occur, can be 

8 discerned from the available evidence. As a result, any approach to reaching decisions on what 

9 standards are appropriate requires judgments about how to translate the information available 

10 from the epidemiologic studies into a basis for appropriate standards, which includes 

11 consideration of how to weigh the uncertainties in reported associations across the distributions 

12 of PM concentrations in the studies. Such approaches are consistent with setting standards that 

13 are neither more nor less stringent than necessary, recognizing that a zero-risk standard is not 

14 required by the CAA. 

15 3.1.1 Approaches Used in Previous Reviews 

16 3.1.1.1 Reviews Completed in 1987 and 1997 

17 The PM NAAQS have always included some type of a primary standard to protect 

18 against effects associated with exposures to thoracic coarse particles. In 1987, when EPA first 

19 revised the PM NAAQS, EPA changed the indicator for PM from Total Suspended Particles 

20 (essentially applicable to particles smaller than 25-45 micrometers) to focus on inhalable 

21 particles, those which can penetrate into the trachea, bronchi, and deep lungs (52 FR 24634). 

22 EPA changed the PM indicator to PM10 based on evidence that the risk of adverse health effects 

23 associated with particles of 10 micrometers or less was significantly greater than that associated 

24 with larger particles (52 FR at 24639). 

25 In the 1997 review, in conjunction with establishing new fine particle (i.e., PM2.5)

26 standards (see above, sections 1.2.3, 2.1.1), EPA concluded that continued protection remained 

27 warranted against potential effects associated with thoracic coarse particles in the size range of 

28 2.5 to 10 μm. This conclusion was based on particle dosimetry, toxicological information, and 

29 on limited epidemiologic evidence from studies that measured PM10 in areas where coarse 

30 particles were likely to dominate the distribution (62 FR 38677, July 18, 1997). Thus, EPA 

31 concluded that the PM10 standards would provide protection against effects associated with 

32 particles in the narrower size range of 2.5 to 10 μm. Although a more narrowly defined indicator 

33 was considered in that review (i.e., PM10-2.5), EPA concluded that it was more appropriate, based 

34 on existing evidence, to continue to use PM10 as the indicator for standards to control thoracic 
Draft Do Not Quote or Cite March 2010 

 

3-3

1 coarse particles. This decision was based, in part, on the recognition that the only studies of 

2 clear quantitative relevance to health effects most likely associated with thoracic coarse particles 

3 used PM10 in areas where the coarse fraction was the dominant fraction of PM10, namely two 

4 studies conducted in areas that substantially exceeded the 24-hour PM10 standard (62 FR 38679). 

5 In addition, this decision reflected the fact that there were only very limited ambient air quality 

6 data then available specifically for thoracic coarse particles, in contrast to the extensive 

7 monitoring network already in place for PM10, Therefore, it was more administratively feasible 

8 to use PM10 as an indicator. EPA also stated that the PM10 standards would work in conjunction 

9 with the PM2.5 standards by regulating the portion of particulate pollution not regulated by the 

PM2.5 standards.2 10 

11 3.1.1.2 Review Completed in 2006 

12 In the review of the PM NAAQS that concluded in 2006, EPA considered the growing, 

13 but still limited, body of evidence supporting associations between health effects and thoracic 

coarse particles measured as PM10-2.5.

3 14 The new studies available in the 2006 review included 

15 epidemiologic studies that reported associations with health effects using direct measurements of 

16 PM10-2.5, as well as dosimetric and toxicological studies. In light of this growing body of 

17 evidence, staff concluded that it was appropriate to revise the PM10 standards and to base any 

18 revised standards principally on available evidence and air quality information for PM10-2.5. Staff 

19 also concluded that it was appropriate to consider evidence from studies that measured PM10 in 

20 locations where the majority of PM10 was in the PM10-2.5 fraction (US EPA, 2005, section 5.4.1) 

21 and that the level of protection afforded by the existing 1987 PM10 standard remained 

 2

As explained in chapter 1, in May 1998, a three-judge panel of the U.S. Court of Appeals for the District of 

Columbia Circuit found "ample support" for EPA's decision to regulate coarse particle pollution, but vacated the 

1997 PM10 standards, concluding that EPA had failed to adequately explain its choice of PM10 as the indicator for 

thoracic coarse particles pointing to the lack of reasoned explanation for the variable level of allowable 

concentrations of thoracic coarse particles (varying by levels of PM2.5) and the consequent double regulation of 

PM2.5. American Trucking Associations v. EPA , 175 F. 3d 1027, 1054-56 (D.C. Cir. 1999).. The court also rejected 

considerations of administrative feasibility as justification 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 PM10

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 PM10 standards to the 

1997 PM10 standards (65 FR 80776, December 22, 2000). The pre-existing 1987 PM10 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 PM10 as an indicator for a standard meant to protect against exposures to 

thoracic coarse particles, and the decision to use PM10 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 results of a quantitative assessment of health risks for PM10-2.5. 

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 recommending specific levels for a thoracic coarse particle 

standard.
Draft Do Not Quote or Cite March 2010 

 

3-4

1 appropriate (US EPA, 2005, p. 5-67). Responding to CASAC advice, staff also recommended 

2 that the indicator for thoracic coarse particles be urban coarse particles in the size range of 10-2.5 

3 micrometer range, thus focusing on those thoracic coarse particles that are generally present in 

4 urban environments (US EPA, 2005, p. 5-71). The agency proposed to retain a standard for a 

5 subset of thoracic coarse particles, proposing a qualified PM10-2.5 indicator to focus on the mix of 

6 thoracic coarse particles generally present in urban environments. More specifically, the revised 

7 thoracic coarse particle standard would have applied only to an ambient mix of PM10-2.5 that is 

8 dominated by resuspended dust from high-density traffic on paved roads and/or by industrial and 

9 construction sources. The revised standard would not have applied to any ambient mix of PM10-

10 2.5 that is dominated by rural windblown dust and soils. In addition, agricultural sources, mining 

11 sources, and other similar sources of crustal material would not have been subject to control in 

12 meeting the standard (71 FR 2667 to 2668, January 17, 2006). 

13 The Agency received a large number of comments that were overwhelmingly opposed to 

14 the proposed qualified PM10-2.5 indicator (71 FR 61188 to 61197). After careful consideration of 

15 the scientific evidence and the recommendations contained in the 2005 Staff Paper, the advice 

16 and recommendations from CASAC, the public comments received regarding the appropriate 

17 indicator for coarse particles, and after extensive evaluation of the alternatives available to the 

18 Agency, the Administrator decided it would not be appropriate to adopt a qualified PM10-2.5 

19 indicator. Underlying this determination was the decision that it was requisite to provide 

20 protection from exposure to all thoracic coarse PM, regardless of its origin, rejecting arguments 

21 that there are no health effects from community-level exposures to coarse PM in non-urban areas 

22 (71 FR 61189). The EPA concluded that dosimetric, toxicological, occupational and 

23 epidemiologic evidence supported retention of a primary standard for short-term exposures that 

24 included all thoracic coarse particles (i.e. both urban and non-urban), consistent with the Act’s 

25 requirement that primary NAAQS provide an adequate margin of safety. Given the serious 

26 potential effects, the large numbers of persons exposed, and the need for a standard to provide an 

27 adequate margin of safety, the agency concluded it was appropriate to retain a standard applying 

28 to all coarse particles (71 FR 61197). At the same time, the agency concluded that the standard 

29 should target protection toward urban areas, where the evidence of health effects from exposure 

30 to PM10-2.5 was strongest (71 FR at 61193, 61197). The proposed indicator was not suitable for 

31 that purpose. Not only did it inappropriately provide no protection at all to many areas, but it 

32 failed to identify many areas where the ambient mix was dominated by coarse particles 

33 contaminated with urban/industrial types of coarse particles for which evidence of health effects 

34 was strongest (71 FR 61193). 
Draft Do Not Quote or Cite March 2010 

 

3-5

1 The agency ultimately concluded that the existing indicator, PM10, was most consistent 

2 with the evidence. Although PM10 includes both coarse and fine PM, it remained an appropriate 

3 indicator for thoracic coarse particles because fine particle levels are generally higher in urban 

4 areas and, therefore, a PM10 standard set at a single unvarying level will generally result in lower 

5 allowable concentrations of thoracic coarse particles in urban areas than in non-urban areas. 

6 This was considered to be an appropriate targeting of protection given that the strongest evidence 

7 for effects associated with thoracic coarse particles came from epidemiologic studies conducted 

8 in urban areas and that elevated fine particle concentrations in urban areas could result in 

9 increased contamination of coarse fraction particles by PM2.5, potentially increasing the toxicity 

10 of thoracic coarse particles in urban areas (71 FR 61195-96). Given the evidence that the 

11 existing PM10 standard afforded requisite protection with an ample margin of safety, the Agency 

retained the level and form of the 24-hour standard.4 12 

13 The Agency also revoked the annual PM10 standard, in light of the conclusion in the PM 

14 Criteria Document (US EPA, 2004) that the available evidence does not suggest an association 

15 with long-term exposure to PM10-2.5 and the conclusion in the Staff Paper (US EPA, 2005) that 

16 there is no quantitative evidence that directly supports an annual standard. 

17 In the same rulemaking, EPA also included a new Federal Reference Method (FRM) for 

18 the measurement of PM10-2.5 in the ambient air (71 FR 61212 to 61213). Although the standards 

19 for thoracic coarse particles do not use a PM10-2.5 indicator, the new FRM for PM10-2.5 was 

20 established to provide a basis for approving Federal Equivalent Methods (FEMs) and to promote 

21 the gathering of scientific data to support future reviews of the PM NAAQS. 

22 3.1.2 Litigation of 2006 Final Rule for thoracic coarse particles 

23 A number of groups filed suit in response to the final decisions made in the 2006 review. 

24 See American Farm Bureau Federation and the National Pork Producers Council v. EPA (DC 

25 Cir. 2009). Among the petitions for review were challenges from industry groups on the 

26 decision to retain the PM10 indicator and the level of the PM10 standard and from environmental 

27 and public health groups on the decision to revoke the annual PM10 standard. The court upheld 

28 both the daily PM10 standard and the decision to revoke the annual standard. 

29 First, the court upheld EPA’s decision for a standard to cover all thoracic coarse PM,, 

30 both of urban and non-urban origin. The court rejected arguments that the evidence showed 

31 there are no risks from exposure to non-urban coarse PM. The court further found that EPA had 

32 a reasonable basis not to set separate standards for urban and non-urban coarse PM, namely the 

 4

 Thus, the level of 150 μg/m3 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

1 inability to reasonably define what ambient mixes would be included under either ‘urban’ or 

2 ‘non-urban;’ and that the evidence in the record supported EPA’s cautious decision to provide 

3 “some protection from exposure to thoracic coarse particles... in all areas.” 559 F. 3d at 532-33. 

4 Specifically, the court stated, 

5 

6 Although the evidence of danger from coarse PM is, as EPA recognizes, 

7 “inconclusive,” (71 FR 61193, October 17, 2006), the agency need not wait for 

8 conclusive findings before regulating a pollutant it reasonably believes may pose 

9 a significant risk to public health. The evidence in the record supports the EPA’s 

10 cautious decision that “some protection from exposure to thoracic coarse particles 

11 is warranted in all areas.” Id. As the court has consistently reaffirmed, the CAA 

12 permits the Administrator to “err on the side of caution” in setting NAAQS.

13 559 F. 3d at 533. 

14 

The court also upheld EPA’s decision to retain the level of the standard at 150 μg/m3 15 and 

16 to use PM10 as the indicator for a standard meant to protect against exposures to thoracic coarse 

17 particles. In upholding the level of the standard, the court referred to the conclusion in the Staff 

18 Paper that there is “little basis for concluding that the degree of protection afforded by the 

19 current PM10 standards in urban areas is greater than warranted, since potential mortality effects 

20 have been associated with air quality levels not allowed by the current 24-hour standard, but 

21 have not been associated with air quality levels that would generally meet that standard, and 

22 morbidity effects have been associated with air quality levels that exceeded the current 24-hour 

23 standard only a few times.” 559 F. 3d at 534. The court also rejected arguments that a PM10

24 standard established at an unvarying level will result in arbitrarily varying levels of protection 

25 given that the level of coarse PM would vary based on the amount of fine PM present. The court 

26 agreed that the variation in allowable coarse PM accorded with the strength of the evidence: 

27 typically less coarse PM would be allowed in urban areas (where levels of fine PM are typically 

28 higher), in accord with the strongest evidence of health effects from coarse particles. 559 F. 3d 

29 at 535-36. In addition, such regulation would not impermissibly double regulate fine particles, 

30 since any additional regulation of fine particles (beyond that afforded by the primary PM2.5 

31 standard) would be for a different purpose; to prevent contamination of coarse particles by fine 

32 particles. 559 F. 3d at 535, 536. These same explanations explained the choice of PM10 as an 

33 indicator, and provided the reasoned explanation for that choice lacking in the record for the 

34 1997 standard. 559 F. 3d at 536. 

35 With regard to the challenge from environmental and public health groups, the court 

36 upheld EPA’s decision to revoke the annual PM10 standard. Specifically, the court stated, 
Draft Do Not Quote or Cite March 2010 

 

3-7

1 The EPA reasonably decided that an annual coarse PM standard is not necessary 

2 because, as the Criteria Document and the Staff Paper make clear, the latest 

3 scientific data do not indicate that long-term exposure to coarse particles poses a 

4 health risk. The CASAC also agreed that an annual coarse PM standard is 

5 unnecessary. 

6 559 F. 3d at 538-39. 

7 

8 3.1.3 Approach in the Current Review 

9 The staff’s approach in this review is consistent with the approaches ultimately taken in 

10 previous reviews. We have taken into account evidence-based considerations, including 

11 consideration of the uncertainties associated with the evidence, to inform our preliminary 

12 conclusions related to the adequacy of the current PM10 standard and potential alternative 

13 standards. In so doing, we are seeking to provide as broad an array of options as is supportable 

14 by the available evidence, recognizing that the selection of a specific approach to reaching final 

15 decisions on the primary PM10 standard will reflect the judgments of the Administrator as to 

16 what weight to place on different aspects of the evidence and associated uncertainties. As 

17 discussed in more detail in the Quantitative Health Risk Assessment for Particulate Matter – 

18 Second External Review Draft (second draft RA, US EPA, 2010a), we have not conducted a 

19 quantitative assessment of health risks associated with PM10-2.5. Staff concluded that limitations 

20 in the monitoring network and in the health studies that rely on that monitoring network, which 

21 would be the basis for characterizing PM10-2.5 exposures and risks, would introduce significant 

22 uncertainty into a PM10-2.5 risk assessment such that the risk estimates generated would be of 

23 limited utility in informing review of the standard. Therefore, staff concluded in the second draft 

24 RA that a quantitative risk assessment for PM10-2.5 is not supportable at this time (US EPA, 

25 2010a, p. 2-6). 

26 For the purposes of this first draft Policy Assessment (PA), we have drawn from the 

27 assessment and integration of the studies evaluated in the Integrated Science Assessment for 

28 Particulate Matter (Final Report) (ISA, US EPA, 2009a). The discussions presented in this 

29 chapter consider evidence from epidemiologic studies, controlled human exposure studies, and 

30 toxicological studies evaluating short- or long-term exposures to thoracic coarse particles; as 

31 discussed in chapters 6 and 7, respectively, with supporting information related to dosimetry and 

32 potential mode of action (MOA) evidence as presented in chapters 4 and 5, respectively, as well 

33 as the integration of evidence across disciplines presented in chapter 2 of the ISA. 

34 With respect to these evidence-based considerations, we have considered causal 

35 inferences identified in the ISA based on consideration of the body of scientific evidence for 

36 effects related to short- and long-term PM10-2.5 exposures. In considering these causal inferences, 
Draft Do Not Quote or Cite March 2010 

 

3-8

1 we take into account evidence of effects for which the reported associations provide suggestive 

2 evidence of a causal association. In considering the evidence, we have relied most heavily on the 

3 epidemiologic evidence, including our understanding of air quality distributions of PM10-2.5 and 

4 PM10 present during the times of the studies. While being mindful of the inherent limitations and 

5 uncertainties in the currently available evidence, we have developed preliminary conclusions as 

6 to the adequacy of the current 24-hour PM10 standard to protect against health effects associated 

7 with exposure to PM10-2.5 and the degree to which alternative standards could be expected to 

8 protect against the reported health effects. 

9 In focusing on the key policy-relevant questions by which we have structured the 

10 current review, our preliminary conclusions reflect upon our understanding of evidence-based 

11 considerations to inform two overarching questions related to: (1) the adequacy of the current 24-

12 hour PM10 standard to protect against effects associated with exposure to thoracic coarse particles 

13 and (2) what potential alternative standard(s), if any, should be considered in this review. In 

14 addressing these broad questions, we have organized the discussions below around a series of 

15 more specific questions reflecting different aspects of each overarching question. When 

16 evaluating the health protection afforded by the current or any alternative standards considered, 

17 we have taken into account the four basic elements of the NAAQS (e.g., indicator, averaging 

18 time, level, and form). 

19 We believe that the approach outlined above, 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 standards meant to protect 

22 public health against exposures to thoracic coarse particles. 

23 3.2 ADEQUACY OF THE EXISTING PM10 STANDARD 

24 In considering the adequacy of the current 24-hour PM10 standard to protect against 

25 effects associated with exposures to thoracic coarse particles, staff addresses the following 

26 overarching question: 

27 Does the currently available scientific evidence, as reflected in the ISA, support or call into 

28 question the appropriateness of maintaining a standard to protect against effects associated 

29 with exposure to thoracic coarse particles and the adequacy of the protection afforded by 

30 the current 24-hour PM10 standard against those effects? 

31 To inform our consideration of this overarching question, we consider below the 

32 evidence for a link between thoracic coarse particle exposures and adverse health effects (3.2.1), 

33 including the evidence for the link between PM10-2.5 and mortality and morbidity; impacts on 

34 susceptible populations; evidence for PM10-2.5-related health effects in locations that meet the 
Draft Do Not Quote or Cite March 2010 

 

3-9

1 current PM10 standard; and uncertainties in the evidence. Preliminary staff conclusions 

2 regarding the adequacy of the current standard are presented in section 3.2.2. In considering the 

3 scientific information, we reflect upon both the information available in the last review and 

4 information that is newly available since the last review as assessed and presented in the ISA 

5 (US EPA, 2009a). 

6 3.2.1 Evidence of Effects Related to Ambient Thoracic Coarse Particles 

7 In the 2006 review of the PM NAAQS, the AQCD (US EPA, 2004, p. 9-48) concluded 

8 the following regarding thoracic coarse particles: 

9 

10 For PM10‐2.5, less evidence is available [than for PM2.5 or PM10], but the 

11 studies using short‐term exposures have reported results that are of the 

12 same magnitude as those for PM10 and PM2.5, though less often statistically 

13 significant and thus having less strength, and the associations are generally 

14 robust to alternative modeling strategies or consideration of potential 

15 confounding by co‐pollutants. This evidence is suggestive of associations for 

16 morbidity with short‐term changes in PM10‐2.5.  

17 

18 In contrast, the AQCD concluded that “[l]ittle evidence is available to allow conclusions 

19 to be drawn about long-term PM10-2.5 exposures and morbidity” (US EPA, 2004, p. 9-46). In 

20 considering these conclusions, the Administrator judged that “short-term exposure to thoracic 

21 coarse particles can have an important public health impact” and that available evidence 

22 “suggests that there is a lack of such effects associated with long-term exposure to thoracic 

23 coarse particles” (71 FR 61185/1, October 17, 2006). As noted above, the Administrator judged 

24 that the then-existing body of scientific evidence supported retaining a standard to protect against 

25 health effects associated with short-term exposures to all thoracic coarse particles. Specifically, 

26 the Administrator noted the following (71 FR 61185/1): 

27 

28 EPA continues to believe that the health evidence, including dosimetric, toxicologic, and 

29 epidemiologic study findings, supports retaining a standard to protect against effects 

30 associated with short-term exposure to thoracic coarse particles. As noted above and 

31 summarized in section III.A of the proposal, there is a growing body of evidence 

32 suggesting causal associations between short-term exposure to thoracic coarse particles 

33 and morbidity effects, such as respiratory symptoms and hospital admissions for 

34 respiratory diseases, and possibly mortality. 

35 

36 In considering the current body of scientific evidence for health effects of thoracic coarse 

37 particles, we have considered the following question: 
Draft Do Not Quote or Cite March 2010 

 

3-10

1  To what extent does the newly available scientific evidence and related uncertainties 

2 strengthen or call into question evidence of associations between ambient thoracic 

3 coarse particle exposures and health effects? 

4   We note that since the conclusion of the last review, the Agency has developed a more 

5 formal framework for reaching causal inferences from the body of scientific evidence, as 

6 discussed above in section 2.2.1. Application of this framework draws upon the evaluation and 

7 synthesis of evidence from across epidemiologic, controlled human exposure, and toxicological 

8 studies. This framework uses a five-level hierarchy that classifies the overall weight of evidence 

9 and causality using the following categorizations: causal relationship, likely to be a causal 

10 relationship, suggestive of a causal relationship, inadequate to infer a causal relationship, and not 

11 likely to be a causal relationship (ISA, section 1.5, Table 1-3). 

12 Applying this framework to thoracic coarse particles, the ISA concludes that the existing 

13 evidence is suggestive of a causal relationship between short-term PM10-2.5 exposures and 

14 mortality, cardiovascular effects, and respiratory effects (US EPA, 2009a, section 2.3.3; see 

15 Table 3-1 below). Several large multi-city epidemiologic studies, as well as a number of single16 city studies, have been conducted in the U.S. and Canada since the last review. These studies 

17 have generally reported positive associations between ambient PM10-2.5 and morbidity and/or 

18 mortality (US EPA, 2009a, section 2.3.4). The plausibility of associations reported in these 

19 epidemiologic studies is supported by some experimental evidence, primarily from controlled 

20 human exposure studies of heart rate variability and pulmonary inflammation, and by dosimetry 

21 studies which show that a large proportion of inhaled particles in the 3-6 micron (dae) range can 

22 reach and deposit in the lower respiratory tract, particularly the tracheobronchial (TB) airways 

23 (ISA, Figures 4-3 and 4-4). 

24 However, important uncertainties remain with regard to the interpretation of this 

25 evidence. For example, experimental support for the associations reported in epidemiologic 

26 studies has been somewhat limited. Controlled human exposure studies have not reported effects 

27 of thoracic coarse particles on pulmonary endpoints including lung function or respiratory 

28 symptoms. In addition, toxicological studies have not generally assessed inhalation of thoracic 

29 coarse particles due to the technical challenges associated with conducting a PM10-2.5 inhalation 

30 study in rodents. These studies have used intratracheal instillation and so provide only limited 

31 support for the biological plausibility of the associations reported in epidemiologic studies (US 

32 EPA, 2009a, section 2.3.4). Beyond the limitations in experimental support, limitations in the 

33 PM10-2.5 monitoring network, uncertainties in the ambient PM10-2.5 concentrations reported in 

34 epidemiologic studies, the relatively small number of epidemiologic studies that have evaluated 

35 co-pollutant models to address the potential for confounding by co-pollutants, variability in the 
Draft Do Not Quote or Cite March 2010 

 

3-11

1 chemical and biological composition of PM10-2.5, and limited evidence regarding effects of the 

2 various components of PM10-2.5, are also important sources of uncertainty (US EPA, 2009a, 

3 sections 2.3.3, 2.3.4). 

4 With respect to effects associated with long-term PM10-2.5 exposures, the ISA concludes 

5 that available evidence is inadequate to infer a causal relationship with all health outcomes 

6 evaluated (US EPA, 2009a, section 2.3). Specifically, similar to the judgment made in the 

7 AQCD (US EPA, 2004), the ISA states, “To date, a sufficient amount of evidence does not exist 

8 in order to draw conclusions regarding the health effects and outcomes associated with long-term 

9 exposure to PM10-2.5” (US EPA, 2009a, section 2.3.4; see Table 3-1 below). 

10 

11 Table 3-1. Summary of Causality Determinations for PM10-2.5

Exposure Duration Outcome Causal Determination

Cardiovascular Effects Suggestive 

Respiratory Effects Suggestive 

Short-term Mortality Suggestive 

Central Nervous System Effects Inadequate 

Cardiovascular Effects Inadequate 

Respiratory Effects Inadequate 

Mortality Inadequate 

Reproductive and Developmental Effects Inadequate 

Long-term 

Cancer Mutagenicity, Genotoxicity Effects Inadequate 

12 Source: adapted from US EPA, 2009a; Table 2-6 

13 

14 Therefore, in considering the health evidence more specifically below we have focused on 

15 mortality, cardiovascular effects, and respiratory effects associated with short-term exposures to 

16 thoracic coarse particles. 

17 Mortality

18 We note that, in the last review, a limited number of studies, mostly single-city analyses, 

19 were evaluated that examined thoracic coarse PM for its association with mortality (US EPA, 

20 2004). Of those studies, a small number examined both PM2.5 and PM10-2.5 effects, and reported 

21 some evidence for PM10-2.5 effects of the same magnitude as PM2.5. Studies conducted in 

22 Phoenix (Mar et al., 2003) and Coachella Valley (Ostro et al., 2003) reported positive and 

23 statistically significant associations between PM10-2.5 and mortality while other single-city studies 

24 reported PM10-2.5 effect estimates that were positive, but not statistically significant. Multiple 
Draft Do Not Quote or Cite March 2010 

 

3-12

1 limitations were identified in these studies including measurement and exposure uncertainties for 

2 PM10-2.5 and the correlation between PM2.5 and PM10-2.5. These limitations decreased the 

3 precision of effect estimates and increased the uncertainty surrounding the concentrations at 

4 which PM10-2.5-mortality associations were observed (US EPA, 2009a, section 6.5.2.3). 

5 Evidence that has become available since the last review provides additional support for 

6 the link between exposure to thoracic coarse particles and mortality, though important 

7 uncertainties remain regarding the extent to which PM10-2.5 itself contributes to reported effects 

8 and the thoracic coarse particle concentrations at which associations occur (discussed below in 

9 more detail). The ISA assesses several recent studies that have evaluated associations between 

10 mortality and PM10-2.5, most of which have reported positive, and in some cases, statistically 

11 significant PM10-2.5 effect estimates (US EPA, 2009a, Figure 6-30). This includes a recent U.S.-

12 based multicity study (Zanobetti and Schwartz, 2009) and a Canadian multi-city study (Burnett 

13 et al., 2004), both of which reported positive associations (though in the case of the Canadian 

14 study, not statistically significant) between PM10-2.5 and mortality. In the U.S. study, a 

15 significant association with PM10-2.5 was reported for all-cause, cardiovascular, and respiratory 

16 mortality (US EPA, 2009a, section 6.5.2.3). The effect estimate for all-cause mortality remained 

17 “relatively robust” (US EPA, 2009a, p. 6-82) and statistically significant in a two-pollutant 

18 model that included PM2.5, while the effect estimates for cause-specific mortality remained 

19 positive but not statistically significant. When examining the city-specific effect estimates for 

20 the 47 cities included in the thoracic coarse particle analysis, statistically significant increases in 

21 mortality were associated with PM10-2.5 in St. Louis, MO; Salt Lake City, UT; Chicago, IL; 

22 Pittsburgh, PA; Detroit, MI; and Birmingham, AL. Positive, but not statistically significant, 

23 associations were reported for all cause and/or cause-specific mortality in the remaining cities 

24 (US EPA, 2009a, Figure 6-29). A number of additional studies have also reported positive, but 

25 not significant, associations between PM10-2.5 and mortality (US EPA, 2009a, Figure 6-30). 

26 Considered as a whole, the ISA notes that epidemiologic studies that have evaluated thoracic 

27 coarse particles have reported consistent, positive associations between PM10-2.5 and mortality 

28 (US EPA, 2009a, section 6.5.2.3). 

29 Cardiovascular effects 

30 With regard to cardiovascular morbidity, we note that the evidence evaluating 

31 associations with short-term concentrations of PM10-2.5 was limited in the last review. Single-city 

32 epidemiologic studies found generally positive associations, with some reaching statistical 

33 significance, between PM10-2.5 and cardiovascular-related hospital admissions in Toronto 

34 (Burnett et al., 1997; 1999) and Detroit, MI (Ito, 2003). In the Detroit study, the PM10-2.5 effect 

35 estimates for ischemic heart disease (IHD) remained positive and statistically significant in two-
Draft Do Not Quote or Cite March 2010 

 

3-13

1 pollutant models that included gaseous co-pollutants (US EPA, 2009a, Figure 6-5), while effect 

2 estimates remained positive and relatively unchanged in magnitude, but not statistically 

3 significant, for congestive heart failure (CHF). Effect estimates in the Toronto study (Burnett et 

4 al., 1997) were decreased and became non-significant in two-pollutant models that included 

5 gaseous co-pollutants (US EPA, 2009a, ISA, Figure 6-5). In addition, one study considered in 

6 the last review reported a positive, but not significant, association between onset of myocardial 

7 infarction (MI) and short-term PM10-2.5 concentrations in Boston (Peters et al., 2001) and, 

8 although not a study of PM10-2.5 specifically, Schwartz et al. (1997) reported a statistically 

9 significant association between PM10 and increased hospitalizations for cardiovascular disease in 

10 Tucson, AZ, an urban area where thoracic coarse particles comprise a much greater fraction of 

11 PM10 than fine particles. No controlled human exposure or animal toxicological studies of PM10-

12 2.5 and cardiovascular endpoints were presented in the 2004 AQCD (US EPA, 2004). 

13 In addition to these cardiovascular morbidity studies considered in the last review, the 

14 ISA assesses a recent multi-city study evaluating hospital admissions and emergency department 

15 visits for cardiovascular disease in Medicare patients (Peng et al., 2008). In this study of older 

16 adults, the authors reported a positive and statistically significant association between 24-hour 

17 PM10-2.5 concentrations and cardiovascular disease hospitalizations in a single pollutant model 

18 using air quality data for 108 U.S. counties with one or more co-located PM2.5 and PM10

19 monitors. The effect estimate was reduced only slightly, though it was no longer statistically 

20 significant, in two-pollutant models that included PM2.5 (US EPA, 2009a, sections 2.3.3, 

21 6.2.10.9). In addition to this U.S. multi-city study, positive associations reported for short-term 

22 PM10-2.5 and cardiovascular morbidity reached statistical significance in a multi-city study in 

23 France (Host et al., 2007) and associations were positive, but often did not reach statistical 

24 significance, in several other locations (US EPA, 2009a, Figures 6-1 to 6-3, 6-5). In considering 

25 the available epidemiologic evidence, the ISA concludes that single- and multi-city 

26 epidemiologic studies generally report positive associations between short-term PM10-2.5

27 concentrations and hospital admissions or emergency department visits for cardiovascular causes 

28 (US EPA, 2009a, section 2.3.3, 6.2.12.2). 

29 The generally positive associations between PM10-2.5 and cardiovascular morbidity 

30 reported in these studies are supported by several recent epidemiologic studies that have 

31 examined dust storm events and reported increases in cardiovascular-related emergency 

department visits and hospital admissions5 32 ; by studies reporting positive associations with 

 5

Such dust storm studies are also important because they provide evidence that cardiovascular effects are associated 

with exposures to particles of non-urban origin. As discussed more fully below, this evidence has implications for 
Draft Do Not Quote or Cite March 2010 

 

3-14

1 cardiovascular mortality; by reported associations with other cardiovascular health effects 

2 including supraventricular ectopy and changes in heart rate variability; and by a limited number 

3 of controlled human exposure studies that have reported alterations in heart rate variability 

4 following exposure to PM10-2.5 (US EPA, 2009a, sections 2.3.3, 6.2.12.2). As noted above, the 

5 few toxicological studies that examined the effect of PM10-2.5 on cardiovascular health effects 

6 used intratracheal instillation and, as a result, provide only limited evidence on the biological 

7 plausibility of PM10-2.5 induced cardiovascular effects (US EPA, 2009a, sections 2.3.3, 6.2.12.2). 

8 Respiratory effects

9 With respect to respiratory effects associated with short-term PM10-2.5 exposures, we first 

10 note that, in the last review, epidemiologic studies reported generally positive associations 

11 between PM10-2.5 and respiratory-related hospitalizations or emergency department visits (e.g., 

12 for pneumonia, chronic obstructive pulmonary disease, and respiratory diseases combined) (US 

13 EPA, 2004). Support for these associations came from a small number of studies that examined 

14 respiratory-related mortality and respiratory symptoms. Experimental evidence for respiratory 

15 effects of PM10-2.5 was limited to a few animal toxicology studies and no controlled human 

16 exposure studies. 

17 In the current review, the ISA notes that a number of recent epidemiologic studies have 

18 reported consistent, positive associations between short-term ambient PM10-2.5 concentrations and 

19 respiratory-related emergency department visits and hospital admissions (US EPA, 2009a, 

20 section 2.3.3). In a French multi-city study (Host et al., 2008), 24-hour ambient PM10-2.5

21 concentrations were positively associated with respiratory-related hospital admissions among 

22 children, with an effect estimate larger than that for PM2.5. A U.S. multi-city study of Medicare 

23 patients (Peng et al., 2009) reported a positive, but not statistically significant, effect estimate for 

24 respiratory-related hospital admissions. A number of additional, mostly single-city, studies have 

25 also reported positive, and in some cases statistically significant, PM10-2.5 effect estimates for 

26 respiratory-related hospital admissions and emergency department visits (ISA, Figures 6-10 to 6-

27 15). In epidemiologic studies of respiratory effects, the strongest relationships with PM10-2.5

28 were observed among children, with less consistent evidence for adults and older adults (i.e., age 

29 65 and older) (US EPA, 2009a, section 2.3.3.1). A limited number of epidemiologic studies 

30 have focused on specific respiratory morbidity outcomes and found no evidence of an 

31 association with lower respiratory symptoms, wheeze, and medication use (US EPA, 2009a, 

32 sections 2.3.3.1 and 6.3.1.1). While controlled human exposure studies have not observed an 

 

decisions on the appropriateness of the current PM10 standard as well as on the choice of indicator for thoracic 

coarse particles. 
Draft Do Not Quote or Cite March 2010 

 

3-15

1 effect on lung function or respiratory symptoms in healthy or asthmatic adults in response to 

2 short-term exposure to PM10-2.5, healthy volunteers have exhibited an increase in markers of 

3 pulmonary inflammation. Toxicological studies using inhalation exposures are still lacking, but 

4 pulmonary injury and inflammation has been observed in animals after intratracheal instillation 

5 exposure (US EPA, 2009a, section 6.3.5.3) and, in some cases, PM10-2.5 was found to be more 

6 potent than PM2.5. 

7 Some studies of PM10-2.5 and respiratory morbidity have investigated potential 

8 confounding by co-pollutants through the application of co-pollutant models (US EPA, 2009a, 

9 section 6.3.8.5, Figure 6-15). Several of these studies have reported positive and statistically 

10 significant PM10-2.5 effect estimates in co-pollutant models that included gaseous pollutants (e.g., 

11 Lin et al., 2002; Yang et al., 2004; Chen et al., 2005; Lin et al., 2005). Several other studies 

12 report that PM10-2.5 effect estimates remain positive, though not always statistically significant, in 

13 co-pollutant models that include gaseous pollutants or PM2.5 (US EPA, 2009a, Figure 6-15). 

14 Summary

15 In considering the extent to which newly available scientific evidence strengthens or calls 

16 into question evidence of associations identified in the last review between ambient thoracic 

17 coarse particle concentrations and adverse health effects, we recognize that the available 

18 epidemiologic and experimental evidence now includes several recent multi-city epidemiologic 

19 studies conducted in the U.S., Canada, and Europe which have reported associations of PM10-2.5 

20 with cardiovascular and respiratory morbidity and mortality, several studies of dust storm events 

21 reporting associations with particles of non-urban origin, as well as some controlled human 

22 exposure studies reporting effects of PM10-2.5 exposure on heart rate variability and pulmonary 

23 inflammation. While uncertainties identified in the last review remain (see below), these recent 

24 studies provide important information not available in that review on the link between PM10-2.5 

25 and mortality and morbidity, and they have broadened our understanding of this link with 

26 particles from different types of sources and in a variety of locations. Thus, our preliminary 

27 conclusion is that there is additional support, beyond that available in the last review, for 

28 associations between adverse health effects (mortality, morbidity) and short-term exposures to 

29 PM10-2.5 from a broad mix of sources and a variety of locations. 

30 Having reached this preliminary conclusion, we then consider how the new evidence 

31 informs our understanding of susceptible populations by asking the following question: 

32  To what extent does the newly available scientific evidence expand our understanding 

33 of susceptible populations, including identification of new susceptible populations?

34 Our understanding of populations that are more susceptible to PM exposures is discussed 

35 above in chapter 2 (section 2.2.1). This includes populations that have a greater likelihood of 
Draft Do Not Quote or Cite March 2010 

 

3-16

1 experiencing health effects related to exposure to PM due to a variety of factors including, but 

2 not limited to, genetic or developmental factors, race, gender, life stage, lifestyle (e.g., smoking 

3 status and nutrition), preexisting disease, or population-level factors that can increase an 

4 individual's exposure to PM (e.g., socioeconomic status, reduced access to health care, low 

5 educational attainment, residential location). Although these studies have primarily evaluated 

6 exposures to PM2.5 or PM10, the available evidence suggests that the identified factors may also 

7 enhance susceptibility to PM10-2.5 (US EPA, 2009a, section 2.4.1). Given this, the discussion in 

8 section 2.2.1 of this document, which summarizes the evidence from the ISA as well as staff 

9 considerations and conclusions on susceptible populations, will not be repeated here. Rather, 

10 with regard to PM10-2.5, we note the overall conclusion from the ISA that “the epidemiologic, 

11 controlled human exposure, and toxicological studies evaluated in this review provide evidence 

12 for increased susceptibility for various populations, including children and older adults, people 

13 with pre-existing cardiopulmonary diseases, and people with lower SES” (US EPA, 2009a, p. 2-

14 24). As discussed in more detail in section 2.2.1, these populations, which are of particular 

15 concern with regard to effects linked to PM exposures, are similar to the at-risk populations 

16 considered in the last review of the PM NAAQS. 

17 We next consider how the available evidence informs our understanding of air quality 

18 concentrations associated with mortality and morbidity by asking the following question: 

19  To what extent does the newly available scientific evidence report associations that 

20 extend to air quality levels that are lower than had previously been observed or that are 

21 observed in areas that would likely meet the current PM10 standard? 

22 As discussed in more detail in chapter 2, the ISA concluded that there is no evidence to 

23 support the existence of a discernable threshold below which PM-associated effects would not 

24 occur (US EPA, 2009a, section 2.4.3). Therefore, when considering the level of protection 

25 provided by the current 24-hour PM10 standard against exposures to thoracic coarse particles, we 

26 consider whether available evidence provides support for associations between PM10-2.5 and 

27 mortality or morbidity in locations with PM10 concentrations that would be allowed by the 

28 current 24-hour PM10 standard. In this section, in considering air quality concentrations at which 

29 health effects have been reported, we have focused on effects for which the evidence is 

30 suggestive of a causal relationship, as described in the ISA. Where sufficient air quality data are 

31 available, we have evaluated air quality concentrations using the form of the current 24-hour 

PM10 standard.6 32 

 

6 The current form of the 24-hour PM10 standard is one expected exceedance per year, averaged over 3 years. 
Draft Do Not Quote or Cite March 2010 

 

3-17

1 In the last review of the PM NAAQS, the Staff Paper (US EPA, 2005; section 5.4.1) 

2 noted that statistically significant associations between thoracic coarse particles and mortality 

3 had been reported in studies conducted in areas that did not meet the PM10 standard during the 

4 time periods of the studies, including Phoenix (Mar et al., 2000, 2003), Coachella Valley, CA 

5 (Ostro et al., 2000, 2003), and Steubenville (as part of the Harvard Six Cities study, Schwartz et 

6 al., 1996; Klemm et al., 2003). In contrast, the Staff Paper noted that “[i]n areas with lower 

7 PM10-2.5 concentrations, no statistically significant associations were reported with mortality, 

8 though many were positive but not statistically significant” (US EPA, 2005, p. 5-49). 

9 The Staff Paper also noted that epidemiologic studies of PM10, in areas where PM10 is 

10 typically dominated by the coarse fraction, provided additional supportive evidence for 

11 associations between coarse fraction particles and health effects in areas with concentrations 

12 generally not meeting the PM10 standard levels. These studies included reports of associations 

13 with hospitalization for cardiovascular diseases in Tucson, AZ (Schwartz, 1997); hospitalization 

14 for chronic obstructive pulmonary disease in Reno/Sparks, NV (Chen et al., 2000); medical visits 

15 for asthma or respiratory diseases in Anchorage, AK (Gordian et al., 1996; Choudhury et al., 

16 1997); and significant associations with mortality, respiratory hospital admissions, and 

17 respiratory symptoms in the Utah Valley area (e.g., Pope et al., 1989; 1991; 1992). 

18 We have re-examined the issue of the PM10 concentrations at which associations between 

19 PM10-2.5 and mortality and morbidity have been reported in light of currently available evidence 

20 and air quality information. In so doing, we have characterized PM10 concentrations reported in 

EPA’s Air Quality System (AQS)7 21 from several U.S. study locations (see US EPA, 2009a, 

22 Figure 2-3). Specifically, consistent with the form of the current PM10 standard, we consider the 

23 second highest 24-hour average PM10 concentration for each year of the study, from each 

24 monitoring site in the study location. In an attempt to gain insight into whether the PM10 air 

25 quality concentrations in a particular study location were above or below those allowed by the 

26 current standard, we compare these second highest 24-hour PM10 concentrations to the level of 

the standard, 150 g/m3

.

8 27 

28 PM10 concentrations from U.S. study locations where positive and statistically significant 

29 PM10-2.5 effect estimates have been reported (e.g., US EPA, 2009a, Figures 2-3; 6-5; 6-24; 6-30) 

30 are presented in Table 3-2 below for Detroit (Lippman, 2000; Ito et al., 2003; Zanobetti and 

31 Schwartz, 2009), Phoenix (Mar et al., 2003), Seattle (Sheppard, 2003), Birmingham (Zanobetti 

 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 

PM10 standard, which also involves estimating expected exceedances for areas with less than daily monitoring, but it 

does provide important insights into the PM10 air quality in study areas, and into whether measured PM10 air quality 

concentrations would, or would not, be permitted under the current standard. 
Draft Do Not Quote or Cite March 2010 

 

3-18

1 and Schwartz, 2009), Coachella Valley (Ostro et al., 2003), Chicago (Zanobetti and Schwartz, 

2 2009), Pittsburgh (Zanobetti and Schwartz, 2009), Salt Lake City (Zanobetti and Schwartz, 

2009), and St. Louis (Zanobetti and Schwartz, 2009).9 3 

4 

5 

6 Table 3-2. PM10 Concentrations in Cities with Statistically Significant PM10-2.5 Effect 

7 Estimates 

City Second highest 24-hour PM10 concentration for each study location and study year 

(g/m3

) 

 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 

10 Of these cities for which positive and statistically significant PM10-2.5 effect estimates 

11 have been reported, PM10 concentrations in Birmingham, Phoenix, and St. Louis were higher 

12 than allowed by the current PM10 standard during most of the study periods and concentrations in 

13 Coachella Valley were higher than allowed during about half of the study period. In contrast, 

14 ambient PM10 concentrations were below those allowed by the current standard during the entire 

 9

We have evaluated air quality in study locations for which single-city effect estimates are presented and for which 

air quality data during the study period are available. Some important U.S. multi-city studies (e.g., Peng et al., 

2008) are not included in Table 3-2 because they did not present single-city effect estimates. We also note that there 

are several key studies conducted in Canadian cities; however, we were unable to obtain air quality information for 

individual monitors in these study locations. 

10These studies in Detroit presented effect estimates for two separate time frames. Because PM10 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

1 study periods for the studies conducted in Chicago, Detroit, Seattle, and Pittsburgh and during 

most of the study period in Salt Lake City.11 2 

3 We also note that two of the studies included in Table 3-2 evaluated PM10-2.5 effect 

4 estimates in co-pollutant models. Specifically, as discussed above, the associations reported by 

5 Ito et al. (2003) for PM10-2.5 and pneumonia hospital admissions in Detroit remained after 

6 adjustment for gaseous co-pollutants. In addition, the ISA reported that the overall PM10-2.5 

7 effect estimate for all-cause mortality in the multi-city study by Zanobetti and Schwartz (2009), 

8 which included Chicago, Detroit, Seattle, Pittsburgh, and Salt Lake City, remained “relatively 

9 robust” (US EPA, 2009a, p. 6-82) and statistically significant in a two-pollutant model that 

10 included PM2.5, though co-pollutant models were not reported for individual cities. As indicated 

11 in the ISA (Figure 6-15), several other studies (e.g., those conducted in Canada) have also 

12 reported robust and statistically significant PM10-2.5 effect estimates in co-pollutant models, 

13 however, we were unable to obtain air quality data for these other study locations and, therefore, 

14 as described above, they were not included in Table 3-2. 

15 In addition to the statistically significant results in the cities noted above, several studies 

16 have reported positive, but not statistically significant, PM10-2.5 effect estimates in locations with 

17 PM10 concentrations below those allowed by the current standard. Specifically, Zanobetti and 

18 Schwartz (2009) reported positive PM10-2.5 effect estimates for mortality in cities with a range of 

19 PM10-2.5 concentrations, even down to the lowest PM10-2.5 concentrations estimated in the study 

20 (ISA, figure 6-29). Many of these cities, where positive associations with mortality were 

reported, attained the current PM10 standard during the time period of the study.12 21 In addition, 

22 Fairley et al. (2003) reported a positive, but not statistically significant, association between 

23 PM10-2.5 and mortality in Santa Clara County, CA (ISA, Figure 6-30). Though some 24-hour 

PM10 concentrations in this location did exceed 150 g/m3 24 (i.e., authors report concentrations up 

to 165 g/m3

), an analysis of Santa Clara air quality during the study period reveals that the 2nd 25 

highest 24-hour PM10 concentration did not exceed 150 g/m3 26 during any of the study years 

(range was 58-147 g/m3 27 ). Peters et al. (2001) reported a positive, but not statistically 

28 significant, association between PM10-2.5 and hospital admissions for myocardial infarction in 

 

11We considered the number of times per year that 24-hour PM10 concentrations exceeded 150 g/m3

. For the 

studies in Chicago, Detroit, Seattle, and Pittsburgh, the average number of days per year with 24-hour PM10

concentrations above 150 g/m3

 did not exceed 1 for any 3-year period. For Salt Lake City, year 3 of the study had 

2 exceedances of 150 g/m3

 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 2nd highest 24-hour PM10 concentration did not exceed 150 g/m3 1 

during either of the study years (52 and 80 g/m3 2 ). 

3 A series of studies conducted in Atlanta have reported mixed results, but none 

4 statistically significant, for PM10-2.5 and mortality and respiratory-related emergency department 

5 visits. Specifically, Klemm et al. (2004), Metzger et al. (2004), Peel et al. (2005), and Tolbert et 

6 al. (2007) reported both positive and negative PM10-2.5 effect estimates for mortality and 

emergency department visits (ISA, Figure 2-3). The 2nd 7 highest 24-hour PM10 concentrations in 

a year over the range of years encompassed by these studies did not exceed 150 g/m3 8 

(maximum was 111 g/m3 9 ). 

10 Summary 

11 When viewed as a whole, these U.S. studies provide evidence for associations between 

12 ambient PM10-2.5 concentrations and increased mortality and morbidity in several locations with 

13 ambient PM10 concentrations below those allowed by the current PM10 standard. Staff’s 

14 preliminary conclusions regarding the potential implications of these studies for a decision on the 

15 adequacy of the current PM10 standard are discussed below. 

16 We next consider the important uncertainties in the available evidence by asking the 

17 following question: 

18  What are the important uncertainties associated with the currently available scientific 

19 evidence that should be considered in evaluating the adequacy of the current PM10 

20 standard? Have these uncertainties changed or been reduced since the last review? 

21 The majority of the health evidence supporting the link between thoracic coarse particle 

22 exposures and adverse cardiovascular and respiratory effects comes from epidemiologic studies. 

23 Staff notes that, while several new studies have become available since the last review, little 

24 progress has been made in reducing some of the important uncertainties inherent in these studies. 

25 These uncertainties, and their implications for interpreting the scientific evidence, are discussed 

26 below in more detail. 

27 The ISA (sections 2.3.3, 2.3.4) concludes that an important uncertainty in the PM10-2.5

28 epidemiologic literature is that associated with the air quality estimates used in these studies. 

29 Specifically, the ISA concludes that there is greater error in estimating ambient concentrations of 

30 PM10-2.5 than in estimates for PM2.5 and, therefore, that such uncertainty is a particularly relevant 

31 consideration when interpreting PM10-2.5 epidemiologic studies. Contributing to this uncertainty 

32 is the relatively limited spatial coverage provided by existing PM10-2.5 monitors (US EPA, 2009a, 

33 sections 2.2.3, 2.3.3, 2.3.4). Currently, a national network to monitor PM10-2.5 is not in place, 

34 limiting the spatial area over which PM10-2.5 concentrations are measured. Specifically, of the 
Draft Do Not Quote or Cite March 2010 

 

3-21

1 3,225 counties in the U.S., only 40 (1%), incorporating less than 5% of the population, met 

2 completeness and co-location criteria during the years 2005-2007, allowing analysis of PM10-2.5 

3 air quality in the ISA (US EPA, 2009a, section 3.5.1.1). In addition, based on the limited 

4 available evidence, the ISA concluded that “there is greater spatial variability in PM10-2.5 

5 concentrations than PM2.5 concentrations, resulting in increased exposure error for the larger size 

6 fraction” (US EPA, 2009a, p. 2-8) and that available measurements do not provide sufficient 

7 information to adequately characterize the spatial distribution of PM10-2.5 concentrations (US 

8 EPA, 2009a, section 3.5.1.1). As noted in the ISA, these limitations in estimates of ambient 

9 PM10-2.5 concentrations “would tend to increase uncertainty and make it more difficult to detect 

10 effects of PM10-2.5 in epidemiologic studies” (US EPA 2009a, p. 2-21). 

11 Uncertainty also results from the different approaches taken to estimate PM10-2.5 

12 concentrations in epidemiologic studies. The ISA notes that ambient concentrations of PM10-2.5

13 are generally determined by the subtraction of PM2.5 from PM10 measurements, with different 

14 studies using different methods. For example, one important multi-city study (e.g., Peng et al., 

15 2008) estimated PM10-2.5 by taking the difference between collocated PM10 and PM2.5 monitors 

16 while another important multi-city study (e.g., Zanobetti and Schwartz, 2009) used the difference 

17 between county average PM10 and PM2.5 concentrations. A small number of studies have 

18 directly measured PM10-2.5 concentrations with dichotomous samplers (e.g., Burnett et al., 2004; 

19 Villeneuve et al., 2003; Klemm et al., 2004). It is not clear how computed PM10-2.5

20 measurements, such as those used by Zanobetti and Schwartz, compare with the PM10-2.5

21 concentrations obtained in other studies either by direct measurement with a dichotomous 

22 sampler or by calculating the difference using co-located samplers (US EPA, 2009a, section 

6.5.2.3).13 23 Given the use of these different approaches to estimating PM10-2.5 concentrations 

24 across studies, and their inherent limitations, the distributions of thoracic coarse particle 

25 concentrations over which reported health outcomes occur remain highly uncertain. 

26 The ISA also notes that the potential for confounding by co-occurring pollutants has been 

27 addressed in only a relatively small number of PM10-2.5 epidemiologic studies, introducing 

28 additional uncertainty into the interpretation of these studies (US EPA, 2009a, section 2.3.3). As 

29 discussed above, most studies that have evaluated co-pollutant models have reported that PM10-

30 2.5 effect estimates remain positive, but often lose precision and become statistically non31 significant (US EPA, 2009a, Figures 6-5, 6-9, 6-15). In the U.S. multi-city study by Zanobetti 

32 and Schwartz (2009) effect estimates for all-cause mortality remained statistically significant in a 

 13In addition, when the difference between PM2.5 and PM10 is calculated, the potential for differences among 

operational flow rates and temperatures for PM10 and PM2.5 monitors add to the potential for exposure 

misclassification. 
Draft Do Not Quote or Cite March 2010 

 

3-22

1 two-pollutant model that included PM2.5 while effect estimates for cause-specific mortality 

2 remained positive but were not statistically significant. Effect estimates for PM10-2.5 were also 

3 positive, but not statistically significant, in co-pollutant models that included PM2.5 in the studies 

4 by Peng et al. (2008) (cardiovascular and respiratory hospital admissions) and Chen et al. (2004) 

5 (respiratory hospital admissions). In the Canadian multi-city study by Burnett et al. (2004) the 

6 PM10-2.5 effect estimates for respiratory-related hospital admissions remained positive, but not 

7 statistically significant, in a co-pollutant model that also included NO2, though the PM10-2.5 effect 

8 estimate remained statistically significant in co-pollutant models with other gaseous pollutants. 

9 In other studies (e.g., see Lin et al., 2002; Ito et al., 2003; Chen et al., 2005) PM10-2.5 effect 

10 estimates remained relatively unchanged, and in some cases statistically significant, in co11 pollutant models that included gaseous pollutants. 

12 Summary 

13 As discussed above, important uncertainties remain in the evidence for associations 

14 between PM10-2.5 and mortality and morbidity. In considering these uncertainties, we reach the 

15 preliminary conclusion that, although a number of studies have been conducted since the last 

16 review, the important uncertainties present in that review remain. The implications of these 

17 uncertainties for decisions on the adequacy of the PM10 standard are discussed below. 

18 3.2.2 Preliminary Staff Conclusions on Adequacy of Current PM10 Standard 

19 Collectively, taking into consideration the responses to specific questions focusing on 

20 different ways to inform a decision on the adequacy of the current 24-hour PM10 standard , we 

21 revisit the overarching question: 

22  Does the currently available scientific evidence, as reflected in the ISA, support or 

23 call into question the appropriateness of maintaining a standard to protect against 

24 effects associated with exposure to thoracic coarse particles and the adequacy of the 

25 protection afforded by the current 24-hour PM10 standard against those effects? 

26 As an initial matter, we note that the current PM10 standard is meant to protect the public 

27 health against effects associated with exposures to all PM10-2.5. As discussed above, this was 

28 judged in the last review to be appropriate given the “growing body of evidence suggesting 

29 causal associations between short-term exposure to thoracic coarse particles and morbidity 

30 effects, such as respiratory symptoms and hospital admissions for respiratory diseases, and 

31 possibly mortality” (71 FR 61185, October 17, 2006). In considering the currently available 

32 scientific evidence on thoracic coarse particles, we conclude that newly available studies 

33 conducted since the last review of the PM NAAQS strengthen this conclusion. As discussed 
Draft Do Not Quote or Cite March 2010 

 

3-23

1 above, the newly available epidemiologic and experimental evidence, combined with evidence 

2 available in the last review, includes the following: 

3  Several multi-city epidemiologic studies conducted in the U.S., Canada, and Europe 

4 which have reported associations of PM10-2.5 with cardiovascular and respiratory 

5 morbidity and mortality 

6  Studies that have reported that PM10-2.5 effect estimates remain positive, and in some 

7 cases statistically significant, in co-pollutant models 

8  Studies that have reported positive associations between dust storm events and 

9 cardiovascular effects, broadening the available evidence for associations between 

10 adverse health effects and particles from a variety of sources, including non-urban 

11 sources 

12  Controlled human exposure studies of heart rate variability and pulmonary inflammation. 

13 

14 While uncertainties identified in the last review remain, these recent studies support those 

15 available in the last review and provide important information on the link between PM10-2.5 and 

16 cardiovascular and respiratory effects, including mortality. In addition, several recent dust storm 

17 studies provide evidence not available in the last review regarding associations between particles 

18 of non-urban origin and adverse health effects. Therefore, consistent with the previous reviews, 

19 we judge that it is appropriate to maintain a standard to protect the public health against effects 

20 associated with exposures to all thoracic coarse particles. 

21 In drawing preliminary conclusions regarding the adequacy of the level of protection 

22 afforded by the current PM10 standard, we have considered the ambient PM10 concentrations in 

23 locations where epidemiologic studies of thoracic coarse particles have been conducted as well 

24 as the uncertainties associated with the broader body of scientific evidence. Specifically, we 

25 note that several recent U.S. studies have reported generally positive, and in some cases 

26 statistically significant, PM10-2.5 effect estimates in locations with 24-hour PM10 concentrations 

27 below those permitted by the current standard. This includes single-city and multi-city studies, 

28 and studies that have reported that PM10-2.5 effect estimates remain positive, and in some cases 

29 robust and statistically significant, in co-pollutant models. As described above, the decision in 

30 the last review to retain the existing PM10 standard was based, in part, on the conclusion that the 

31 strongest evidence for the link between PM10-2.5 and health effects came from studies conducted 

32 in locations with PM10 concentrations above those allowed by the standard. Given that recent 

33 epidemiologic studies have reported statistically significant PM10-2.5 effect estimates in several 

34 locations with PM10 concentrations below those allowed by the standard, a similar conclusion 

35 would not be supported by the currently available evidence. Therefore, to the extent that the 
Draft Do Not Quote or Cite March 2010 

 

3-24

1 approach to considering the adequacy of the current standard in this review is similar to the 

2 approach used in the last review, it would be appropriate to conclude that the current 24-hour 

3 PM10 standard does not provide adequate public health protection and that it should be revised in 

4 order to increase protection against effects associated with short-term exposures to thoracic 

5 coarse particles. If this approach to considering the evidence were adopted, a conclusion that the 

6 current standard is not adequate could be supported by the following observations: 

7  A number of epidemiologic studies have reported positive, and in some cases 

8 statistically significant, PM10-2.5 effect estimates for mortality and morbidity in a variety 

9 of locations, including in several U.S. cities with 24-hour PM10 concentrations below 

10 those allowed by the current PM10 standard. 

11  Studies that have evaluated co-pollutant models have generally reported that PM10-2.5 

12 effect estimates remain robust and, in some cases, statistically significant when PM2.5 

13 or gaseous co-pollutants are added to the model. 

14  Uncertainties in the extent to which ambient PM10-2.5 concentrations used in 

15 epidemiologic studies reflect population exposures tend to bias the results of those 

16 studies toward the null hypothesis. Therefore, given limitations in PM10-2.5 monitoring, 

17 the generally positive PM10-2.5 effect estimates reported across epidemiologic study 

18 locations, even in locations for which effect estimates were not significant, provide 

19 evidence for associations between PM10-2.5 and mortality and morbidity. 

20  Controlled human exposure studies and, to a lesser extent, animal toxicological studies 

21 have reported cardiovascular and respiratory effects following exposures to thoracic 

22 coarse particles, thereby providing some support for the biological plausibility of the 

23 associations reported in epidemiologic studies. 

24 

25 However, as discussed above, a decision on the adequacy of the level of public health 

26 protection provided by the current PM10 standard will be a public health policy judgment in 

27 which the Administrator weighs the available evidence and its inherent uncertainties. Thus, 

28 depending on the emphasis placed on different aspects of the evidence and its associated 

29 uncertainties, different conclusions could be supported. Specifically, as discussed above, we 

30 note that many of the important uncertainties from the last review remain. In considering the 

31 evidence as well as these uncertainties, the ISA concluded that the evidence is “suggestive” of a 

32 causal relationship between short-term PM10-2.5 exposures and mortality, cardiovascular effects, 

33 and respiratory effects. These conclusions contrast with those for associations between PM2.5

34 and health effects, which were judged to be either “causal” or “likely causal” for mortality and 

35 cardiovascular and respiratory effects associated with short- and long-term PM2.5 exposures. 

36 Among the specific uncertainties noted in the ISA (US EPA, 2009a, sections 2.3.3, 2.3.4) are the 

37 following: 
Draft Do Not Quote or Cite March 2010 

 

3-25

1  Limited monitoring for PM10-2.5 results in uncertainty in the ambient PM10-2.5 

2 concentrations at which effects reported in epidemiologic studies occur. 

3  The number of epidemiologic studies that have employed co-pollutant models to 

4 address the potential for confounding remains relatively limited. Therefore, the extent 

5 to which PM10-2.5 itself contributes to reported health effects, rather than one or more 

6 co-pollutants, remains uncertain. 

7  Only a limited number of experimental studies provide support for the associations 

8 reported in epidemiologic studies. 

9  The chemical and biological composition of PM10-2.5, and the effects associated with 

10 the various components, remains uncertain. 

11 

12 To the extent a decision on the adequacy of the current PM10 standard were to emphasize the 

13 uncertainties that contributed to the ISA conclusion that the evidence is “suggestive” of a causal 

14 relationship for PM10-2.5, rather than indicating a “likely causal” or “causal” relationship, it would 

15 be reasonable to conclude that the available evidence does not provide a basis for reaching a 

16 fundamentally different conclusion from the one reached in the previous review (i.e., to retain 

17 the current 24-hour PM10 standard). Therefore, our preliminary conclusion is that the available 

18 evidence could support either revising the current PM10 standard to increase public health 

19 protection against exposures to thoracic coarse particles or retaining the current PM10 standard, 

20 depending on the emphasis placed on different aspects of the evidence and associated 

21 uncertainties. 

22 3.3 CONSIDERATION OF POTENTIAL ALTERNATIVE STANDARDS 

23 Having reached the conclusion that, depending on the approach to considering the 

24 available evidence, the adequacy of the current 24-hour PM10 standard to protect against effects 

25 associated with exposures to thoracic coarse particles could be called into question, staff 

26 considers a second overarching question: 

27 What alternative standard(s) to protect against exposures to PM10-2.5 could be supported by 

28 the currently available scientific evidence, as reflected in the ISA? 

29 To inform the answer to this overarching question, we consider how the currently 

30 available scientific evidence could inform decisions regarding the basic elements of the NAAQS: 

31 indicator (section 3.3.1), averaging time (section 3.3.2), and form and level (section 3.3.3). In 

32 considering the appropriateness of potential alternative standards, we consider both the evidence 

33 available in the last review and the evidence that is newly available since the last review, as 

34 assessed and presented in the ISA (US EPA, 2009a). 
Draft Do Not Quote or Cite March 2010 

 

3-26

1 3.3.1 Indicator 

2 As noted in section 3.2 of the ISA, unlike gaseous pollutants such as O3, SO2, and CO, 

3 “which are well-defined chemical entities, atmospheric PM varies in size, shape, and chemical 

4 composition” (US EPA, 2009a, p. 3-1). The selection of PM10 as an indicator of thoracic 

5 particles was originally based in large part on dosimetry (U.S. EPA, 1996a) with evidence 

6 suggesting that a large proportion of inhaled coarse particles in the 3-6 μm (dae) range can reach 

7 and deposit in the lower respiratory tract, particularly the tracheobronchial airways, while the 

8 fraction deposited decreases as particle size increases (US EPA, 2009a, Figures 4-3 and 4-4). 

9 Currently, it is most common to use PM10 as an indicator of thoracic particles and PM10-2.5 as an 

10 indicator of the thoracic component of coarse particles, sometimes referred to as thoracic coarse 

11 particles. As such, the majority of available health evidence for coarse particles links health 

12 effects to PM10-2.5 and/or PM10. As discussed in section 3.1.1, in the review of the PM NAAQS 

13 completed in 1997, and again in the review completed in 2006, EPA concluded that the purpose 

14 of the PM10 standard would be to provide protection against effects associated with PM10-2.5. 

15 This section considers the issue of the appropriate indicator for a standard meant to protect 

16 against exposures to thoracic coarse particles. Considerations related to indicator in the review 

17 completed in 2006 are discussed in section 3.3.1.1; evidence-based considerations to inform our 

18 understanding of indicator in the current review are discussed in section 3.3.1.2; and preliminary 

19 staff conclusions regarding indicator are discussed in section 3.3.1.3. 

20 3.3.2 Consideration of Indicator in the Review Completed in 2006 

21 In the last review, the Administrator’s decision on the indicator for a standard meant to 

22 protect against exposures to thoracic coarse particles took into consideration the potential for 

23 particles originating in different types of environments (i.e., urban versus non-urban), and with 

24 different compositions, to possess different degrees of toxicity. At the time, most of the studies 

25 supporting the link between exposure to thoracic coarse particles and adverse health effects had 

26 been conducted in urban locations. Epidemiologic studies had reported positive, and in some 

27 cases statistically significant, associations between ambient concentrations of thoracic coarse 

28 particles and adverse health effects in studies conducted in cities both inside and outside the U.S.  

29 In contrast, very little evidence was available to suggest that thoracic coarse particles from non30 urban areas posed a threat to human health and a few studies reported that exposure to crustal 

31 material from non-urban locations did not result in the types of effects that had been linked with 

32 exposures to urban particles. Specifically, several toxicological studies reported that volcanic 

33 ash from Mt. St. Helens (an example of natural crustal material of geologic origin) caused 

34 very little toxicity in animal or in vitro model systems (e.g., see US EPA, 2005, section 5.4.2.1 
Draft Do Not Quote or Cite March 2010 

 

3-27

1 for discussion).  In addition, an epidemiologic study in Spokane, WA specifically assessed 

2 whether mortality was increased on dust‐storm days using case‐control analysis methods.  

The average PM10 concentration on dust storm days was more than 200 μg/m3 3 higher than on 

4 control days; however, the authors reported no evidence of increased mortality on these specific 

5 days (Schwartz et al., 1999). In addition, studies conducted in several areas in the western U.S. 

6 reported that associations between PM10 and mortality or morbidity remained unchanged or 

7 became larger and more precise when days indicative of wind-blown dust were excluded from 

8 the analyses (Pope et al., 1999; Schwartz, 1997; Chen et al., 2000; Hefflin et al., 1994). In the 

9 last review, this group of studies was interpreted as suggesting that health effects associated 

10 with thoracic coarse particles are not driven by the types of natural crustal materials that 

would typically form a major fraction of coarse particles in non‐urban or rural areas.14 11    

12 In 2006, the Administrator noted that the apparent differences in toxicity of 

13 particles from urban versus non‐urban locations could result from the different contaminants 

14 present in urban versus non-urban environments. Specifically, he stated the following 

15 

16 [T]he observed toxicity of coarse particles in urban and industrial areas comes from the 

17 kind of coarse particles found in these environments, for example direct emissions from 

18 industrial sources or materials released to road dust from motor vehicles such as brake 

19 and tire wear, as well as from the contamination of coarse particles that can occur. This 

20 contamination can come from both mobile and stationary sources. In particular, specific 

21 components, such as byproducts of incomplete combustion (e.g. polycyclic aromatic 

22 hydrocarbons) most commonly emitted from motor vehicles and other sources in the 

23 form of PM2.5, as well as metals and other contaminants emitted from other 

24 anthropogenic sources, appear in higher levels in urban areas (EPA, 2004a, p. 8–344; 71 

25 FR 2665). Many of these contaminants in PM10–2.5 come originally from fine particles, 

26 which may become attached in the atmosphere or be deposited and mixed into coarse 

27 materials on the ground. Thus the greater the concentration of PM2.5, with higher levels 

28 typically found in urban areas, the greater the level of contamination of coarse particles 

29 by fine particles. This contamination increases the potential health risk posed by those 

30 coarse particles. For that reason, it is logical to allow lower levels of coarse particles 

31 when fine particle concentrations are high (71 FR 61196, October 17, 2006). 

32 

33 Given the available evidence and the above considerations, the Administrator judged in 

34 the last review that two primary objectives were appropriate to consider when making a decision 

35 on the standard indicator. Specifically, given the preponderance of evidence from studies 

36 conducted in urban areas, the Administrator judged it appropriate to have the level of protection 

37 reflect the varying degree of public health concern presented by the different ambient mixes of 

 14Although Ostro (2003) found that rural coarse particles primarily 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

1 thoracic coarse particulate matter by allowing lower ambient thoracic coarse particle 

2 concentrations in locations with higher fine particle concentrations (e.g., urban areas, where the 

3 evidence indicates the public health risks to be significant) and higher concentrations of ambient 

4 thoracic coarse particles in locations with lower fine particle concentrations (e.g., non-urban 

5 areas, where the evidence related to thoracic coarse particles is more limited). In addition, 

6 though there was little evidence at the time to suggest that thoracic coarse particles in non-urban 

7 locations posed a threat to human health, the Administrator judged that, given uncertainties in the 

interpretations of some of the studies of non-urban particles,15 8 it was appropriate to take a 

9 cautious approach by setting a standard that provides some measure of protection against 

10 exposures to all ambient mixes of thoracic coarse particles, regardless of source of origin or 

11 composition (71 FR 61197/3). 

12 The Administrator evaluated several different potential indicators by considering the 

13 extent to which each would contribute to achieving these objectives. Specifically, the 

14 Administrator considered a PM10-2.5 indicator, either qualified so as to exclude some sources and 

15 locations (see below) or unqualified with no such exclusions, and a PM10 indicator, either 

16 adjusted to account for the PM2.5 component of PM10 or unadjusted. Each of these options, and 

17 the Administrator’s consideration of them in the last review, is discussed below. 

18 In considering the extent to which a PM10–2.5 indicator would achieve the objectives for 

19 public health protection described above, the Administrator evaluated both a qualified indicator, 

20 which would have exempted specific sources (e.g., agricultural and mining sources) and/or 

21 locations (e.g., rural areas), and an unqualified indicator. With regard to the qualified indicator, 

22 the Administrator concluded that, although it would permit the level of protection to reflect the 

23 varying degree of public health concern presented by the different ambient mixes of thoracic 

24 coarse particles, it would clearly not meet the goal of providing some measure of protection 

25 against all ambient mixes of thoracic coarse particles for the evident reason that it would have 

26 explicitly excluded certain types of sources and locations. In contrast, with regard to the 

27 unqualified indicator the Administrator noted that, though it would provide protection against 

28 exposures to all ambient mixes of thoracic coarse particles, “if such an indicator were utilized as 

29 part of a standard with a single unvarying level, it would not reflect the critical difference in 

30 evidence regarding the relative public health risks associated with urban and non-urban thoracic 

31 coarse particles” (71 FR 61195). That is, he concluded that if the level were selected to provide 

32 appropriate protection against effects associated with exposure to the ambient mixes typical of 

 15 The final decision in the review completed in 2006 noted that uncertainties in interpreting these and other studies 

relevant to the consideration of effects 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

1 urban or industrial areas, the standard could be judged to be more stringent than necessary to 

2 protect against effects associated with exposure to the ambient mixes in non-urban areas. 

3 Conversely, if a less stringent level were adopted on the grounds that there is less certainty that 

4 the ambient mix in non-urban areas poses a health risk, then the standard could be judged not to 

5 provide sufficient protection from the ambient mix found in urban or industrial areas. In both 

6 instances a PM10-2.5 standard could be judged not to be requisite (i.e., ‘‘not lower or higher than is 

7 necessary’’ Whitman, 531 U.S. at 476.) to protect the public health with an adequate margin of 

8 safety. In considering a potential approach to addressing this issue, the Administrator also 

9 concluded that it would not be appropriate to set different PM10-2.5 standard levels for urban 

10 versus non-urban locations given the “lack of evidence to support establishing specific 

11 quantitative distinctions in level based on variations in coarse particle composition and 

12 differential toxicity” (71 FR 61195). Given all of these considerations, the Administrator 

13 concluded that it would not be appropriate to set a standard with a PM10-2.5 indicator at the time 

14 of the last review. 

15 In considering the extent to which a PM10 indicator would achieve the objectives for 

16 public health protection described above, the Administrator evaluated both an adjusted indicator, 

17 to account for the PM2.5 component of PM10, and an unadjusted indicator. For the adjusted 

18 indicator, the mass of PM2.5 monitored in excess of the 24-hour standard for PM2.5 would have 

19 been subtracted from monitored PM10 mass in order to avoid the double regulation of PM2.5 in 

20 the situations where this would have had the most regulatory consequence. Under this option, on 

21 days when the measured concentration of PM10 exceeded the level of the standard and the 

22 measured concentration of PM2.5 exceeded the level of the 24-hour PM2.5 standard, the amount of 

23 PM2.5 in excess of the 24-hour PM2.5 standard would have been subtracted from the total PM10

24 mass (71 FR 61197). This option was judged by the Administrator to not be appropriate for two 

25 reasons. First, as noted above, the Administrator had determined that there should be less 

26 allowable coarse particulate matter as PM2.5 levels increase because these are the conditions 

27 under which PM10–2.5 tends to become more contaminated and could become more harmful. 

28 Furthermore, this indicator would have inappropriately relaxed the level of protection afforded 

29 by the existing 24-hour PM10 standard because it would have allowed higher total PM10 levels on 

30 days with high PM2.5 levels. This indicator was thus directionally backwards; it decreased 

31 protection when conditions warranted increased protection. For both of these reasons, the 

32 Administrator rejected the adjusted PM10 indicator. 

33 In his final decision in the review completed in 2006, the Administrator judged that the 

34 continued use of the unadjusted and unqualified PM10 indicator was appropriate for a standard 

35 meant to protect against effects associated with exposures to PM10-2.5. In reaching this judgment, 
Draft Do Not Quote or Cite March 2010 

 

3-30

1 the Administrator concluded that the PM10 indicator appropriately maintains some protection 

2 from all ambient mixes of thoracic coarse particles and provides a level of protection that reflects 

3 the varying degree of public health concern presented by the different ambient mixes. 

4 Specifically, the Administrator noted that both PM2.5 and PM10-2.5 contribute to PM10 mass. 

5 Therefore, he noted that that the PM10 standard would be expected to allow lower concentrations 

6 of thoracic coarse particles in locations with higher concentrations of PM2.5 (i.e., urban areas) 

7 and higher concentrations of thoracic coarse particles in locations with lower concentrations of 

8 PM2.5 (i.e, non-urban areas). As discussed above, this was judged appropriate because the 

9 available evidence indicated the potential for significant public health risks associated with 

10 exposures to thoracic coarse particles in urban areas, which generally have higher fine particle 

11 concentrations than rural areas, but provided much less certainty regarding risks in non-urban 

12 areas. 

13 Given the Administrator’s conclusion that these elevated fine particle concentrations in 

14 urban locations could result in greater fine particle contamination of coarse particles resulting in 

15 increased potential health risks posed by coarse particles in urban areas, he noted the following: 

16 

17 To the extent that use of a PM10 indicator would result in any reduction in PM2.5 

18 concentrations in an area, this would reduce the potential health risk from coarse particles 

19 in the area as well. There is no certainty that the contribution of PM2.5 to the health risk 

20 associated with exposure to contaminated coarse particles would be appropriately 

21 addressed through the fine particle standards alone. Thus, to the extent that the inclusion 

22 of the PM2.5 fraction in the PM10 indicator amounts to double regulation of PM2.5, its 

23 inclusion is non-duplicative and reasonable (71 FR 61196). 

24 

25 In reaching these judgments on the standard indicator, the Administrator recognized that 

26 the relationship between allowable thoracic coarse particle concentrations and fine particle 

27 concentrations is qualitative. That is, the varying coarse particle concentrations allowed under 

28 the PM10 standard do not precisely correspond to the likely variations in toxicity of thoracic 

29 coarse particles in different areas. However, the Administrator concluded that, while currently 

30 available information does not allow a more precise adjustment for relative toxicity, the PM10

31 standard is expected to generally ensure that the coarse particle levels allowed will appropriately 

32 be lower in urban areas and higher in non-urban areas. Given all of the above considerations, the 

33 Administrator judged in the last review that the unqualified and unadjusted PM10 indicator was 

appropriate for a standard meant to protect against exposures to PM10-2.5.

16 34 

 16As 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

1 3.3.3 Evidence-Based Consideration of Indicator in the Current Review 

2 In the current review, in considering potential alternative standards, we have considered 

3 the following question with regard to indicator: 

4  To what extent does the currently available information provide support for retaining 

5 or revising the current PM10 indicator?

6 As in the last review, a critical issue in selecting an appropriate indicator for a standard 

7 meant to protect against exposures to thoracic coarse particles remains the extent to which 

8 available evidence supports the appropriateness of a standard that allows lower concentrations of 

9 PM10-2.5 in urban areas than rural areas. In considering this issue, we note that the ISA assesses 

10 several epidemiologic studies of short-term exposures to thoracic coarse particles that have been 

11 conducted since the last review (US EPA, 2009a, Chapter 6). Similar to the studies considered 

12 in the previous review, as described above in more detail, most of these more recent studies have 

13 been conducted in urban locations in the U.S., Canada, and Europe. However, a few recent 

14 studies have examined the health impacts of dust storm events, where crustal material was 

15 generally indicated using PM10 (US EPA, 2009a, section 6.2.10.1). Specifically, a study of a 

16 dust storm in the Gobi desert, which transported PM across the Pacific Ocean reaching the 

17 western U.S. in the spring of 1998, reported no excess risk of cardiac or respiratory hospital 

18 admissions in the population of British Columbia’s Lower Fraser Valley despite hourly PM10

concentrations greater than 100 μg/m3 19 and daily average concentrations several times greater 

20 than normal (Bennett et al., 2006). In contrast, Middleton et al. (2008) reported that dust storms 

21 in Cyprus were associated with a 4.7% (95% CI: 0.7-9.0) and 10.4% (95% CI: -4.7 to 27.9) 

22 increase in risk of hospitalization for all causes and cardiovascular disease, respectively. PM10

23 concentrations in this study were much higher than typically reported in non-dust storm studies, 

with hourly PM10 concentrations during dust storms frequently approaching 300 to 400 g/m3 24 

25 and a maximum 24-hour average PM10 concentration during the study almost 10-fold higher than 

the level of the current PM10 standard (i.e., 1,371 g/m3 26 ). In addition, Chan et al. (2008) studied 

27 the effects of Asian dust storms on cardiovascular hospital admissions in Taipei, Taiwan and 

28 reported significant adverse effects during 39 Asian dust events. Daily PM10 concentrations 

exceeded 150 g/m3 29 on several occasions during the study period and reached a maximum of 

between 200 and 250 g/m3 30 (see Figure 1 in Chan et al., (2008)). Bell et al. (2008) analyzed 

31 these data independently and concluded that Asian dust storms were positively associated with 

32 risk of hospitalization for ischemic heart disease. In addition, Yang et al. (2009) reported that 

33 hospitalizations for congestive heart failure were elevated during or immediately following 54 

34 Asian dust storm events, though effect estimates were not statistically significant. Maximum 24-
Draft Do Not Quote or Cite March 2010 

 

3-32

1 hour PM10 concentrations were not reported but the mean 24-hour concentration due to dust 

storm events was 112 g/m3 2 . In a dust storm study where PM10-2.5 was specifically evaluated, 

3 Perez et al. (2008) tested the hypothesis that outbreaks of Saharan dust exacerbate the effects of 

4 PM10-2.5 on daily mortality in Spain. During Saharan dust days, the PM10-2.5 effect estimate was 

5 larger than on non-dust days, and it became statistically significant whereas it was not 

6 statistically significant on non-dust days. On Saharan dust days, mean PM10-2.5 concentrations 

7 were about 10% higher than on non-Saharan dust days. Several animal toxicological studies 

8 have also reported that exposure to PM2.5 from dust storms increased pulmonary inflammation 

9 and blood pressure (Lei et al., 2004; Chang et al., 2007; US EPA, 2009a, sections 6.2.5.3, 

10 6.3.3.3). 

11 In considering the implications of these studies for a decision on the indicator of a 

12 standard meant to protect against exposures to thoracic coarse particles, we first consider the 

13 following question: 

14  To what extent is it appropriate to maintain an indicator that provides some measure of 

15 protection against all thoracic coarse particles? 

16 With regard to this question, we note that, though most of the evidence for associations 

with morbidity and mortality continues to come from studies conducted in urban areas,17 17 

18 associations reported in a small number of recent dust storm studies suggest that caution is 

19 warranted in drawing conclusions about the relative toxicity of thoracic coarse particles from 

20 urban versus non-urban environments. These studies of dust storm events, discussed above, raise 

21 credible concerns regarding the potential for non-urban particles to cause adverse health effects, 

22 though the dust storm-related PM10 concentrations tend to be higher than those in many locations 

23 where recent U.S. and Canadian studies have reported associations with PM10-2.5. At a minimum, 

24 these recent dust storm studies indicate that exposure to relatively high concentrations of non25 urban particles is associated with health effects that are similar to those that, in other studies, 

26 have been associated with urban particles. 

27 Given the above considerations, as an initial matter we reach the preliminary conclusion 

28 that, for a standard meant to protect against exposures to thoracic coarse particles, it remains 

29 appropriate to provide some measure of protection against exposures to all ambient mixes of 

30 thoracic coarse particles, regardless of their source of origin or composition. In drawing this 

31 preliminary conclusion, we recognize the results of epidemiologic studies assessed in the ISA, 

32 which have reported positive, and in some cases statistically significant, effect estimates for 

 17Though in some cases study locations extended into areas surrounding urban centers and likely included some 

non-urban (e.g., suburban) areas. 
Draft Do Not Quote or Cite March 2010 

 

3-33

1 thoracic coarse particles in a variety of locations, including studies of dust storm events where 

2 high particle concentrations were due to windblown crustal material. We also recognize that the 

3 causality judgments for thoracic coarse particles in the ISA were made for “PM10-2.5 as a whole 

4 regardless of origin, since PM10-2.5-related effects have been demonstrated for a number of 

5 different environments” (US EPA, 2009a, p. 2-19). Given these considerations, we note that 

6 either a PM10 or a PM10-2.5 indicator would be expected to provide protection against all ambient 

7 mixes of thoracic coarse particles, as long as these indicators were not qualified so as to exclude 

8 certain types of sources or locations. 

9 In addition, we have considered the following question with regard to indicator: 

10  To what extent does it remain appropriate to draw distinctions between thoracic coarse 

11 particles from urban and non-urban environments when making a decision on the 

12 indicator for a standard meant to protect against exposures to those particles? 

13 In considering this question, we note that recent studies do provide some evidence for the 

14 toxicity of particles from a variety of environments, including particles of non-urban origin. 

15 Given these studies, it could be judged reasonable to adopt an indicator that does not allow 

16 different concentrations of thoracic coarse particles in urban and rural areas. As discussed 

17 above, a PM10-2.5 indicator would accomplish this. In contrast, given the generally higher fine 

18 particle concentrations in urban areas compared to rural areas, a PM10 indicator would be 

19 expected to allow lower PM10-2.5 concentrations in urban areas than in rural areas. Therefore, to 

20 the extent that it is judged appropriate to set a standard that does not allow different 

21 concentrations of thoracic coarse particles in different types of environments, it would be 

22 appropriate to consider a PM10-2.5 indicator. 

23 However, as discussed above, we also note that most of the evidence for positive 

24 associations between PM10-2.5 and morbidity and mortality, particularly evidence for these 

25 associations at relatively low concentrations of PM10-2.5, continues to come from studies 

26 conducted in locations where the PM10-2.5 is expected to be largely of urban origin. While recent 

27 studies of dust storm events have provided some additional information on the health effects 

28 associated with particles of non-urban origin, the PM10 concentrations due to dust storm events 

29 in these studies are generally higher, and in at least some cases considerably higher, than those in 

30 the U.S. and Canadian cities where positive and statistically significant associations have been 

31 reported in recent studies. To the extent that these considerations are emphasized in a decision 

32 on the indicator for a standard, a reasonable conclusion would be that recent studies have not 

33 fundamentally changed our understanding of the relative toxicity of urban versus non-urban 

34 particles, and that available evidence continues to support the conclusion that thoracic coarse 
Draft Do Not Quote or Cite March 2010 

 

3-34

1 particles of urban origin, where fine particle concentrations tend to be highest, are of particular 

2 concern. 

3 Given this conclusion, it would be reasonable to consider an indicator that focuses control 

4 on areas with ambient mixes known with greater certainty to be associated with adverse health 

5 effects (i.e., mixes generally present in urban areas) since such an indicator could provide public 

6 health benefits with the greatest degree of certainty. With regard to this, as discussed in more 

7 detail above, we note that the varying levels of thoracic coarse particles allowed by a PM10

8 indicator would be expected to target protection to those locations (i.e., urban or industrial areas) 

9 where the strongest evidence has been observed for associations between adverse health effects 

10 and exposures to thoracic coarse particles. Therefore, under this approach to considering the 

11 evidence, a reasonable conclusion would be that a PM10 indicator remains appropriate for a 

12 standard meant to protect against exposures to thoracic coarse particles. Thus, as with a decision 

13 on the adequacy of the current standard, different decisions on indicator could be judged to be 

14 appropriate, depending on the emphasis placed on different aspects of the evidence and its 

15 associated uncertainties. 

16 3.3.4 Averaging Time 

17 In considering the appropriate averaging time(s) for the PM10 standard in the last review, 

18 the Administrator considered several epidemiologic studies that had reported statistically 

19 significant associations between short-term (24-hour) exposure to PM10–2.5 and various morbidity 

20 effects as well as mortality. Based primarily on these studies, he concluded that the available 

21 evidence continued to support a 24-hour averaging time for a standard intended to control 

22 thoracic coarse particles. In contrast, given the relative lack of studies supporting a link between 

23 long-term exposures to thoracic coarse particles and morbidity or mortality, and given the 

24 conclusion reached in the AQCD that the available evidence did not suggest a link between 

25 morbidity or mortality and long-term exposure to PM10–2.5 (US EPA, 2004a, p. 9–79), the 

26 Administrator further concluded that an annual coarse particle standard was not warranted at that 

27 time. In reaching this decision, the Administrator also noted that a 24-hour standard would be 

28 expected to provide protection against any as yet unidentified potential effects of long-term 

29 exposure at ambient concentrations. Thus, in the 2006 review the Administrator retained the 24-

30 hour PM10 standard and revoked the annual PM10 standard (71 FR 61198-61199). 

31 In the current review, we reconsider the extent to which the available evidence continues 

32 to support these decisions by considering the following question: 

33  To what extent does the available evidence continue to support a 24-hour averaging 

34 time for a standard meant to protect against effects associated with short-term 

35 exposures to PM10-2.5? 
Draft Do Not Quote or Cite March 2010 

 

3-35

1 With regard to this question, we note the conclusions from the ISA regarding the weight 

2 of evidence for different averaging times as well as the studies on which those conclusions are 

3 based. Specifically, as discussed above (see Table 3-1 above), the ISA concludes that the 

4 existing evidence is suggestive of a causal relationship between short-term PM10-2.5 exposures 

5 and mortality, cardiovascular effects, and respiratory effects (ISA, section 2.3.3). This 

6 conclusion is based largely on epidemiologic studies which have primarily evaluated 

7 associations between 24-hour PM10-2.5 concentrations and morbidity and mortality (e.g., see ISA, 

8 Figure 2-3), though a smaller number of controlled human exposure studies have reported effects 

9 following shorter exposures (i.e., 2-hours) to PM10-2.5 (e.g., see ISA, sections 6.2.1.2, 6.3.3.2). In 

10 contrast, with respect to long-term exposures, the ISA concludes that available evidence is 

11 inadequate to infer a causal relationship with all health outcomes evaluated (US EPA, 2009a, 

12 section 2.3). Specifically, the ISA states, “To date, a sufficient amount of evidence does not 

13 exist in order to draw conclusions regarding the health effects and outcomes associated with 

14 long-term exposure to PM10-2.5” (US EPA, 2009a, section 2.3.4; see Table 3-1 below). 

15 In considering the weight of evidence determinations in the ISA, we conclude that, at a 

16 minimum, they suggest the importance of having a standard that protects against short-term 

17 exposures to thoracic coarse particles. In considering the averaging times used in the short-term 

18 epidemiologic studies, we note that the majority of the evidence supporting the link between 

19 PM10-2.5 and morbidity and mortality is based on 24-hour average thoracic coarse particle 

20 concentrations. Therefore, our preliminary conclusion is that the evidence available in this 

21 review continues to support the appropriateness of a 24-hour averaging time for a PM10 standard 

22 meant to protect against short-term exposures to PM10-2.5, including potential effects associated 

23 with exposures of shorter duration than 24-hours. We further note that, given the ISA conclusion 

24 that “a sufficient amount of evidence does not exist in order to draw conclusions regarding the 

25 health effects and outcomes associated with long-term exposure to PM10-2.5” (ISA, p. 2-19) the 

26 evidence does not support the appropriateness of an annual thoracic coarse particle standard at 

27 this time. In reaching this conclusion, we note that, to the extent a short-term standard requires 

28 areas to reduce their 24-hour ambient particle concentrations, long-term concentrations would 

29 also be expected to decrease. Therefore, a 24-hour standard meant to protect against short-term 

30 exposures to thoracic coarse particles would also be expected to provide protection against any 

31 as yet unidentified potential effects of long-term exposures at ambient concentrations. 

32 3.3.5 Level and Form 

33 Given the conclusions above regarding the adequacy of the current PM10 standard (i.e., 

34 that, depending on the approach to considering the available evidence, the adequacy of the 
Draft Do Not Quote or Cite March 2010 

 

3-36

1 current 24-hour PM10 standard to protect against effects associated with exposures to thoracic 

2 coarse particles could be called into question) and the appropriate indicator (i.e., that, depending 

3 on how the evidence is considered, either a PM10 or PM10-2.5 indicator could be judged 

4 appropriate), we next consider whether different standard levels and/or forms for a 24-hour PM10

5 or PM10-2.5 standard could be supported by the available evidence. To inform our consideration 

6 of this issue, we have considered the following question: 

7  To what extent does new information support consideration of an alternative form 

8 and/or level? 

9 In considering this question, we have taken into account the scientific evidence from studies 

10 of the link between short-term exposure to PM10-2.5 and mortality, cardiovascular morbidity, and 

11 respiratory morbidity, as assessed in the ISA, including the uncertainties and limitations in that 

12 evidence. 

13 In the 2006 review, the Administrator concluded that “the level of protection afforded by 

the current 24-hour PM10 standard of 150 μg/m3 14 , one-expected-exceedance form, continues to be 

15 appropriate for the types of thoracic coarse particles typically found in urban or industrial areas” 

16 (71 FR 61202). In support of this decision, the Administrator noted that “mortality effects 

17 observed in epidemiologic studies for [thoracic] coarse particles are generally associated with 

18 exposure levels that exceed the current standards, and morbidity effects are generally associated 

19 with exposure levels that exceeded the current standards on only a few occasions” (71 FR 

20 61202). Given this evidence, the Administrator concluded that the level of protection afforded 

21 by the existing PM10 standard was not greater than warranted. In addition, the Administrator 

concluded that uncertainties in population exposures in available morbidity studies18 22 suggested 

23 that there was little basis for concluding that a greater degree of protection was warranted. 

Therefore, the Administrator retained the existing level of 150 μg/m3 24 for the 24-hour PM10

25 standard, and the existing one-expected exceedance form. 

26 In the sections below, we discuss the approach that will be used to identify potential 

27 alternative forms and a range of potential alternative levels for a standard meant to protect 

28 against exposures to thoracic coarse particles. These potential alternative standard forms and 

29 levels will be presented and considered in the second draft PA document. 

 18Analysis 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

1 3.3.6 Form 

2 As discussed in more detail above, in the 2006 review the Administrator concluded that 

3 “the degree of protection afforded by the current 24-hour PM10 standard is requisite to protect 

4 public health with an adequate margin of safety” (71 FR 61201). Given the overall decision in 

5 that review to provide the same protection as provided by the existing 24-hour standard, the 

6 Administrator concluded “it is best to retain both the form and the level of the current primary 

7 24-hour PM10 standard” (71 FR 61202). Therefore, the one-expected-exceedance form was 

8 retained. 

9 This decision is being examined in the current review within the context of the overall 

10 decision on whether to retain or revise the current 24-hour PM10 standard. While the selection of 

11 a specific form must be made within the context of a decision on the other elements of the 

12 standard, EPA generally favors the concentration-based form for short-term standards. In 1997 

EPA established 98th 13 percentile form for the 24-hour PM2.5 standard and, most recently, in 2010 

EPA established 98th 14 percentile form for the 1-hour NO2 standard (62 FR 38671; 75 FR 6474). 

15 In making these decisions, EPA judged that, as compared to an exceedance-based form, such as 

16 that used for the current PM10 standard, a concentration-based form is more reflective of the 

17 health risks posed by elevated pollutant concentrations because it gives proportionally greater 

18 weight to days when concentrations are well above the level of the standard than to days when 

19 the concentrations are just above the standard. Further, a concentration-based form better 

20 compensates for missing data and less than-daily monitoring. In addition, when averaged over 3 

21 years, it has greater stability than an exceedance-based form and, therefore, it facilitates the 

22 development of more stable implementation programs. In these previous reviews, after 

considering different concentration percentiles (95th to the 99th for PM2.5 and 98th and 99th 23 for 

24 NO2), EPA selected the 98th percentile as an appropriate balance between adequately limiting 

25 the occurrence of peak concentrations and providing increased stability and robustness. 

26 In considering these decisions, our preliminary conclusion is that a similar logic applies 

27 in the case of the 24-hour PM10 standard. For this reason, to the extent that it is judged 

28 appropriate to revise the current 24-hour standard in the current review, we will give preliminary 

consideration to a range of alternative standard options based on 98th 29 percentile concentrations of 

30 PM10 and/or PM10-2.5, as discussed below. 

31 3.3.7 Level 

32 As noted above, depending on the approach taken in this review to consider the evidence 

33 for the adequacy of the current PM10 standard, it could be judged that this standard does not 

34 provide adequate public health protection. If this is judged to be the case, we will consider 
Draft Do Not Quote or Cite March 2010 

 

3-38

potential alternative standard levels for a 24-hour standard that, in conjunction with a 98th 1 

2 percentile form as described above, would provide increased public health protection against 

3 effects associated with exposures to PM10-2.5. Given the conclusion above that the continued use 

4 of the PM10 indicator could be judged appropriate for a standard meant to protect against 

5 exposures to PM10-2.5, we will consider a range of potential alternative standard levels for a PM10

6 standard. However, as is also discussed above, a PM10-2.5 indicator could potentially be judged 

7 appropriate. While the air quality information available to inform the identification of a range of 

8 potential alternative standard levels will be more limited for a PM10-2.5 standard than for a PM10

9 standard, we recognize that some such information exists. Therefore, to the extent that feedback 

10 received during the review of this first draft Policy Assessment justifies consideration of a PM10-

11 2.5 standard, we will discuss potential alternative levels for such a standard in the second draft 

12 document. 

13 In considering potential alternative standard levels, staff will consider the available 

14 information on PM10, and possibly PM10-2.5, concentrations in locations where health studies 

15 have evaluated the link between short-term PM10-2.5 concentrations and mortality, cardiovascular 

16 morbidity, and respiratory morbidity, as well as the uncertainties and limitations in that evidence. 

17 In so doing, we will focus on U.S. studies, as described above in our consideration of the 

18 adequacy of the current standard. Specifically, we will consider the extent to which these studies 

19 report positive and relatively precise effect estimates; the extent to which the reported 

20 associations are robust in co-pollutant models; and the extent to which the studies used relatively 

21 reliable air quality data. In particular, we will focus on those specific studies, briefly 

22 summarized above and presented in more detail in chapter 6 of the ISA, that provide evidence of 

23 associations between PM10-2.5 and mortality and morbidity in areas that would likely have met 

24 the current 24-hour PM10 standard during the time of the study. Staff believes that this body of 

25 evidence can serve as a basis for identifying and considering potential alternative 24-hour PM10

26 and/or PM10-2.5 standards that would provide increased protection against effects related to short27 term exposures to PM10-2.5. 

28 As an initial matter, we recognize, as discussed above, that these short-term exposure 

29 studies provide no evidence of clear thresholds, or lowest-observed-effects levels, in terms of 24-

30 hour average concentrations. As a consequence, this body of evidence is difficult to translate 

31 directly into a specific 24-hour standard that would independently protect against all effects 

32 associated with short-term exposures. In the absence of an apparent threshold, for purposes 

33 of identifying the range of standard levels potentially supported by the epidemiologic 

34 evidence, we will focus on the range of PM10 and/or PM10-2.5 concentrations that have been 

35 measured in locations where key health studies have reported associations with PM10‐2.5.  

36 Specifically, we will focus on the upper end of the distributions of daily PM concentrations, 
Draft Do Not Quote or Cite March 2010 

 

3-39

particularly in terms of the 98th 1 percentile of the yearly distribution of 24-hour PM10 and/or 

2 PM10‐2.5 concentrations, reflecting the considerations above for the appropriate form of the 24-

3 hour standard. As noted above, this analysis of potential alternative standard levels will be 

4 presented in the second draft PA document. 

5 3.4 KEY UNCERTAINTIES AND AREAS FOR FUTURE RESEARCH AND DATA 

6 COLLECTION 

7 [This topic will be discussed in the second draft Policy Assessment.] 

8 3.5 REFERENCES 

9 Bell ML; Ebisu K; Peng RD; Walker J; Samet JM; Zeger SL; Dominic F (2008). Seasonal and regional short-term 

10 effects of fine particles on hospital admissions in 202 U.S. counties, 1999-2005. Am J Epidemiol, 168: 

11 1301-1310. 

12 Bennett CM; McKendry IG; Kelly S; Denike K; Koch T (2006). Impact of the 1998 Gobi dust event on hospital 

13 admissions in the Lower Fraser Valley, British Columbia. Sci Total Environ, 366: 918-925. 

14 Burnett RT; Cakmak S; Brook JR; Krewski D (1997). The role of particulate size and chemistry in the association 

15 between summertime ambient air pollution and hospitalization for cardiorespiratory diseases. Environ 

16 Health Perspect, 105: 614-620. 

17 Burnett RT; Stieb D; Brook JR; Cakmak S; Dales R; Raizenne M; Vincent R; Dann T (2004). Associations between 

18 short-term changes in nitrogen dioxide and mortality in Canadian cities. Arch Environ Occup Health, 59: 

19 228-236. 

20 Chan CC; Chuang KJ; Chen WJ; Chang WT; Lee CT; Peng CM (2008). Increasing cardiopulmonary emergency 

21 visits by long-range transported Asian dust storms in Taiwan. Environ Res, 106: 393-400. 

22 Chang C-C; Hwang J-S; Chan C-C; Wang P-Y; Cheng T-J (2007). Effects of concentrated ambient particles on 

23 heart rate, blood pressure, and cardiac contractility in spontaneously hypertensive rats during a dust storm 

24 event. Inhal Toxicol, 19: 973-978. 

25 Chen L; Yang W; Jennison BL; Omaye ST (2000). Air particulate pollution and hospital admissions for chronic 

26 obstructive pulmonary disease in Reno, Nevada. Inhal Toxicol, 12: 281-298. 

27 Chen Y; Yang Q; Krewski D; Shi Y; Burnett RT; McGrail K (2004). Influence of relatively low level of particulate 

28 air pollution on hospitalization for COPD in elderly people. Inhal Toxicol, 16: 21-25. 

29 Chen Y; Yang Q; Krewski D; Burnett RT; Shi Y; McGrail KM (2005). The effect of coarse ambient particulate 

30 matter on first, second, and overall hospital admissions for respiratory disease among the elderly. Inhal 

31 Toxicol, 17: 649-655. 

32 Choudhury, A. H.; Gordian, M. E.; Morris, S. S. (1997) Associations between respiratory illness and PM10 air 

33 pollution. Arch. Environ. Health 52: 113-117. 

34 Fairley D (2003). Mortality and air pollution for Santa Clara County, California, 1989-1996, In: Revised analyses of 

35 time-series studies of air pollution and health. Special report. Health Effects Institute. Boston, 

36 MA.http://www.healtheffects.org/Pubs/TimeSeries.pdf . 
Draft Do Not Quote or Cite March 2010 

 

3-40

1 Gordian ME; Ozkaynak H; Xue J; Morris SS; Spengler JD (1996). Particulate air pollution and respiratory disease in 

2 Anchorage, Alaska. Environ Health Perspect, 104: 290-297. 

3 Hefflin BJ; Jalaludin B; McClure E; Cobb N; Johnson CA; Jecha L; Etzel RA (1994). Surveillance for dust storms 

4 and respiratory diseases in Washington State, 1991. Arch Environ Occup Health, 49: 170-174. 

5 Host S; Larrieu S; Pascal L; Blanchard M; Declercq C; Fabre P; Jusot JF; Chardon B; Le Tertre A; Wagner V; 

6 Prouvost H; Lefranc A (2007). Short-term Associations between Fine and Coarse Particles and 

7 Cardiorespiratory Hospitalizations in Six French Cities. Occup Environ Med, 18: S107-S108. 

8 Host S; Larrieu S; Pascal L; Blanchard M; Declercq C; Fabre P; Jusot JF; Chardon B; Le Tertre A; Wagner V; 

9 Prouvost H; Lefranc A (2008). Short-term associations between fine and coarse particles and hospital 

10 admissions for cardiorespiratory diseases in six French cities. Occup Environ Med, 65: 544-551. 

11 Ito K (2003). Associations of particulate matter components with daily mortality and morbidity in Detroit, 

12 Michigan, In: Revised analyses of time-series studies of air pollution and health. Special report. Health 

13 Effects Institute. Boston, MA. R828112. http: //www.healtheffects.org/Pubs/TimeSeries.pdf . 

14 Klemm RJ; Mason R (2003). Replication of reanalysis of Harvard Six-City mortality study. In HEI Special Report: 

15 Revised Analyses of Time-Series Studies of Air Pollution and Health, Part II (pp. 165-172). Boston, MA: 

16 Health Effects Institute. 

17 Klemm RJ; Lipfert FW; Wyzga RE; Gust C (2004). Daily mortality and air pollution in Atlanta: two years of data 

18 from ARIES. Inhal Toxicol, 16 Suppl 1: 131-141. 

19 Lei Y-C; Chan C-C; Wang P-Y; Lee C-T; Cheng T-J (2004). Effects of Asian dust event particles on inflammation 

20 markers in peripheral blood and bronchoalveolar lavage in pulmonary hypertensive rats. Environ Res, 95: 

21 71-76. 

22 Lei YC; Chen MC; Chan CC; Wang PY; Lee CT; Cheng TJ (2004). Effects of concentrated ambient particles on 

23 airway responsiveness and pulmonary inflammation in pulmonary hypertensive rats. Inhal Toxicol, 16: 

24 785-792. 

25 Lin M; Chen Y; Burnett RT; Villeneuve PJ; Krewski D (2002). The influence of ambient coarse particulate matter 

26 on asthma hospitalization in children: case-crossover and time-series analyses. Environ Health Perspect, 

27 110: 575-581. 

28 Lippmann M; Ito K; Nadas A; Burnett RT (2000). Association of particulate matter components with daily mortality 

29 and morbidity in urban populations. Health Effects Institute. Cambridge, MA. 

30 Mar TF; Norris GA; Koenig JQ; Larson TV (2000). Associations between air pollution and mortality in Phoenix, 

31 1995-1997. Environ Health Perspect, 108: 347-353. 

32 Mar, T. F.; Norris, G. A.; Larson, T. V.; Wilson, W. E.; Koenig, J. Q. (2003). Air pollution and cardiovascular 

33 mortality in Phoenix, 1995-1997. In: Revised analyses of time-series studies of air pollution and health. 

34 Special report. Boston, MA: Health Effects Institute; pp. 177-182. Available: 

35 http://www.healtheffects.org/Pubs/TimeSeries.pdf. October 18, 2004. 

36 Metzger KB; Tolbert PE; Klein M; Peel JL; Flanders WD; Todd KH; Mulholland JA; Ryan PB; Frumkin H (2004). 

37 Ambient air pollution and cardiovascular emergency department visits. Epidemiology, 15: 46-56. 

38 Middleton N; Yiallouros P; Kleanthous S; Kolokotroni O; Schwartz J; Dockery DW; Demokritou P; Koutrakis P 

39 (2008). A 10-year time-series analysis of respiratory and cardiovascular morbidity in Nicosia, Cyprus: the 

40 effect of short-term changes in air pollution and dust storms. Environ Health, 7: 39. 
Draft Do Not Quote or Cite March 2010 

 

3-41

1 Miller, F.J; Gardner, D.E.; Graham, J.A.; Lee, R.E.; Wilson, W.E.; Bachmann, J.D. (1979). Size considerations for 

2 establishing a standard for inhalable particles. J Air Pollution Control Assoc. 29:610-615. 

3 Ostro, B. D.; Broadwin, R.; Lipsett, M. J. (2000) Coarse and fine particles and daily mortality in the Coachella 

4 Valley, California: a follow-up study. J. Exposure Anal. Environ. Epidemiol. 10: 412-419. 

5 Ostro, B. D.; Broadwin, R.; Lipsett, M. J. (2003). Coarse particles and daily mortality in Coachella Valley, 

6 California. In: Revised analyses of time-series studies of air pollution and health. Special report. Boston, 

7 MA: Health Effects Institute; pp. 199-204. Available: http://www.healtheffects.org/Pubs/TimeSeries.pdf. 

8 October 18, 2004. 

9 Peel JL; Tolbert PE; Klein M; Metzger KB; Flanders WD; Knox T; Mulholland JA; Ryan PB; Frumkin H (2005). 

10 Ambient air pollution and respiratory emergency department visits. Epidemiology, 16: 164-174. 

11 Peng RD; Chang HH; Bell ML; McDermott A; Zeger SL; Samet JM; Dominici F. (2008). Coarse particulate matter 

12 air pollution and hospital admissions for cardiovascular and respiratory diseases among Medicare patients. 

13 JAMA, 299: 2172-2179. 

14 Peng R; Bell M; Geyh A; McDermott A; Zeger S; Samet J; Dominici F (2009). Emergency admissions for 

15 cardiovascular and respiratory diseases and the chemical composition of fine particle air pollution. Environ 

16 Health Perspect, 117: 957-963. 

17 Peters A; Dockery DW; Muller JE; Mittleman MA (2001). Increased particulate air pollution and the triggering of 

18 myocardial infarction. Circulation, 103: 2810-2815. 

19 Pope CA III (1989). Respiratory disease associated with community air pollution and a steel mill, Utah Valley. Am J 

20 Public Health, 79: 623-628. 

21 Pope CA III; Dockery DW; Spengler JD; Raizenne ME (1991). Respiratory health and PM10 pollution: a daily time 

22 series analysis. Am J Respir Crit Care Med, 144: 668-674. 

23 Pope, C. A., III; Schwartz, J.; Ransom, M. R. (1992) Daily mortality and PM10 pollution in Utah valley. Arch. 

24 Environ. Health 47: 211-217. 

25 Pope, C. A., III; Hill, R. W.; Villegas, G. M. (1999) Particulate air pollution and daily mortality on Utah's Wasatch 

26 Front. Environ. Health Perspect.: 107: 567-573. 

27 Schwartz, J.; Dockery, D. W.; Neas, L. M. (1996) Is daily mortality associated specifically with fine particles? J. Air 

28 Waste Manage. Assoc. 46: 927-939. 

29 Schwartz J (1997). Air pollution and hospital admissions for cardiovascular disease in Tucson. Epidemiology, 8: 

30 371-377. 

31 Schwartz J; Norris G; Larson T; Sheppard L; Claiborne C; Koenig J (1999). Episodes of high coarse particle 

32 concentrations are not associated with increased mortality. Environ Health Perspect, 107: 339-342. 

33 Sheppard L; Levy D; Norris G; Larson TV; Koenig JQ (2003). Effects of ambient air pollution and nonelderly 

34 asthma hospital admissions in Seattle, Washington, 1987-1994. Epidemiology, 10: 23-30. 

35 Tolbert PE; Klein M; Peel JL; Sarnat SE; Sarnat JA (2007). Multipollutant modeling issues in a study of ambient air 

36 quality and emergency department visits in Atlanta. J Expo Sci Environ Epidemiol, 17: S29-S35. 

37 US EPA (2004). Air Quality Criteria for Particulate Matter. National Center for Environmental Assessment, Office 

38 of Research and Development, U.S. Environmental Protection Agency, Research Triangle Park, NC 27711; 
Draft Do Not Quote or Cite March 2010 

 

3-42

1 report no. EPA/600/P-99/002aF and EPA/600/P-99/002bF. October 2004. Available: 

2 http://www.epa.gov/ttn/naaqs/standards/pm/s_pm_cr_cd.html 

3 US EPA (2005). Review of the National Ambient Air Quality Standards for Particulate Matter: Policy Assessment 

4 of Scientific and Technical Information, OAQPS Staff Paper. Research Triangle Park, NC 27711: Office 

5 of Air Quality Planning and Standards; report no. EPA EPA-452/R-05-005a. December 2005. Available: 

6 http://www.epa.gov/ttn/naaqs/standards/pm/s_pm_cr_sp.html 

7 US EPA (2008a). Integrated Review Plan for the National Ambient Air Quality Standards for Particulate Matter. 

8 National Center for Environmental Assessment and Office of Air Quality Planning and Standards, U.S. 

9 Environmental Protection Agency, Research Triangle Park, NC. Report No. EPA 452/R-08-004. March 

10 2008. Available at: 

11 http://www.epa.gov/ttn/naaqs/standards/pm/data/2008_03_final_integrated_review_plan.pdf 

12 US EPA (2009a). Integrated Science Assessment for Particulate Matter (Final Report). U.S. Environmental 

13 Protection Agency, Washington, DC, EPA/600/R-08/139F, December 2009. Available: 

14 http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=216546 

15 U.S. EPA. (2009b). Particulate Matter National Ambient Air Quality Standards: Scope and Methods Plan for Health 

16 Risk and Exposure Assessment. U.S. Environmental Protection Agency, Research Triangle Park, NC, 

17 EPA-452/P-09-002. February 2009. Available: 

18 http://www.epa.gov/ttn/naaqs/standards/pm/s_pm_2007_pd.html 

19 US EPA (2010a). Quantitative Risk Assessment for Particulate Matter – Second External Review Draft. Office of 

20 Air Quality Planning and Standards, U.S. Environmental Protection Agency, Research Triangle Park, NC. 

21 EPA-452/P-10-001. February 2010. Available: 

22 http://www.epa.gov/ttn/naaqs/standards/pm/s_pm_index.html. 

23 Yang C-Y; Chen Y-S; Yang C-H; Ho S-C (2004). Relationship between ambient air pollution and hospital 

24 admissions for cardiovascular diseases in Kaohsiung, Taiwan. J Toxicol Environ Health A Curr Iss, 67: 

25 483-493. 

26 Yang CY; Cheng MH; Chen CC (2009). Effects of Asian Dust Storm Events on Hospital Admissions for Congestive 

27 Heart Failure in Taipei, Taiwan. J Toxicol Environ Health A Curr Iss, 72: 324-328. 

28 Zanobetti A; Schwartz J. (2009). The effect of fine and coarse particulate air pollution on mortality: A national 

29 analysis. Environ Health Perspect, 117: 1-40.(2008). 
4-1 

Draft – Do Not Quote or Cite March 2010 

1 4 REVIEW OF THE SECONDARY STANDARDS FOR VISIBILITY2 RELATED EFFECTS 

3 This chapter presents preliminary staff conclusions with regard to the adequacy of the 

4 current suite of secondary PM standards to protect against PM-related visibility impairment as 

5 well as the alternative secondary PM standards that are appropriate for consideration in this 

6 review. Our assessment of these issues is framed by a series of key policy-relevant questions, 

7 which expand upon those presented in the Integrated Review Plan (IRP) (US EPA, 2008a) at the 

8 outset of this review. The answers to these questions will inform decisions on whether, and if so 

9 how, to revise the current suite of secondary PM standards for the purpose of providing 

10 appropriate protection from PM-related visibility impairment. 

11 In presenting preliminary staff conclusions on alternative secondary standard that are 

12 appropriate for consideration, we note that the final decision is largely a public welfare policy 

13 judgment. A final decision must draw upon scientific information and analyses about PM14 related visibility impairment and related impacts on public welfare, as well as judgments about 

15 how to deal with the range of uncertainties that are inherent in the scientific evidence and 

16 analyses. Our approach to informing these judgments is discussed more fully below. This 

17 approach is consistent with the requirements of the NAAQS provisions of the Act and with how 

18 EPA and the courts have historically interpreted the Act. These provisions require the 

19 Administrator to establish secondary standards that, in the Administrator’s judgment, are 

20 requisite to protect public welfare from any known or anticipated adverse effects associated with 

21 the presence of the pollutant in the ambient air. In so doing, the Administrator seeks to establish 

22 standards that are neither more nor less stringent than necessary for this purpose. The Act does 

23 not require that secondary standards be set at a zero-risk level, but rather at a level that avoids 

24 unacceptable public welfare impacts. 

25 Information on the approaches used to set the secondary PM standards in past reviews as 

26 well as our current approach for this review are presented in section 4.1. Our preliminary 

27 conclusions regarding the adequacy of the current suite of secondary PM standards to protect 

28 against PM-related visibility impairment are presented in section 4.2. Section 4.3 presents our 

29 preliminary conclusions with respect to alternative PM standards by focusing on each of the 

30 basic elements of the standards: pollutant indicator (section 4.3.1), averaging time (section 

31 4.3.2), and level and form (section 4.3.3). The performance of alternative standards, with a focus 

32 on the uniformity of protection from visibility impairment afforded by the alternative standards, 

33 is evaluated in section 4.3.4. Section 4.4 summarizes all preliminary staff conclusions on the 

34 secondary PM standards for visibility protection. The next draft of this chapter will conclude 

35 with an initial overview of areas of key uncertainties and suggested future research areas and 

36 data collection efforts (section 4.5) 
4-2 

Draft – Do Not Quote or Cite March 2010 

1 4.1 APPROACH 

2 Staff’s approach for reviewing the current secondary PM standards builds upon and 

3 broadens the approaches used in previous PM NAAQS reviews. We first present a brief 

4 summary of the approaches used to establish and review secondary PM standards in the last two 

5 reviews of the PM NAAQS (section 4.1.1). Recent litigation on the 2006 standards has resulted 

6 in the remand of the secondary annual and 24 hour PM2.5 NAAQS to EPA as discussed in section 

7 4.1.2. Our current approach for evaluating the secondary PM2.5 standards using both evidence8 and impact assessment-based considerations is outlined in section 4.1.3. 

9 4.1.1 Approaches Used in Previous Reviews 

10 The original suite of PM2.5 standards was established in 1997 and revisions to those 

11 standards were made in 2006. The approaches used in making final decisions on secondary 

12 standards in those reviews, as well as the current review, utilize different ways to consider the 

13 underlying body of scientific evidence. They also reflect an evolution in our understanding of 

14 the multi-faceted nature of the public welfare visibility effect, from a more narrow focus on 

15 Class I area visibility to non-Class I area visibility, including urban areas, and public perception, 

16 valuation and impacts on personal comfort and well being. 

17 4.1.1.1 Review Completed in 1997 

18 In 1997, EPA revised the identical primary and secondary PM10 NAAQS in part by 

19 establishing new identical primary and secondary PM2.5 standards. In revising the secondary 

20 standards, EPA recognized that PM produces adverse effects on visibility and that impairment of 

21 visibility was experienced throughout the U.S., in multi-state regions, urban areas, and remote 

22 mandatory Class I Federal areas alike. However, in considering an appropriate level for a 

23 secondary standard to address adverse effects of PM on visibility, EPA concluded that the 

24 determination of a single national level was complicated by regional differences in several 

25 factors that influence visibility such as background and current levels of PM, composition of PM, 

26 and average relative humidity. Variations in these factors could thus result in situations where 

27 attaining even a low concentration of fine particles might or might not provide adequate 

28 protection, depending on these factors. The EPA also determined that there was insufficient 

29 information at that time to establish a level for a national secondary standard that would 

30 represent a threshold above which visibility conditions would always be adverse and below 

31 which visibility conditions would always be acceptable. 

32 Based on these considerations, EPA assessed potential visibility improvements in urban 

33 areas and on a regional scale that would result from attainment of the new primary standards for 

34 PM2.5. The agency concluded that the spatially averaged form of the annual PM2.5 standard was 

35 well suited to the protection of visibility, which involves effects of PM throughout an extended 
4-3 

Draft – Do Not Quote or Cite March 2010 

1 viewing distance across an urban area. Based on air quality data available at that time, many 

2 urban areas in the northeast, midwest, and southeast, as well as Los Angeles, were expected to 

3 see perceptible improvement in visibility if the annual PM2.5 primary standard was attained. The 

4 EPA also concluded that in some areas attainment of the 24-hour PM2.5 standard would be 

5 expected to reduce, to some degree, the number and intensity of ‘‘bad visibility’’ days, i.e., the 

6 20% of days having the greatest impairment over the course of a year. 

7 Having concluded that attainment of the annual and 24-hour PM2.5 primary standards 

8 would lead to visibility improvements in many eastern and some western urban areas, EPA also 

9 considered whether these standards could provide potential improvements to visibility on a 

10 regional scale. Based on information available at the time, EPA concluded that attainment of 

11 PM2.5 secondary standards set identical to the primary standards would be expected to result in 

12 visibility improvements in the eastern U.S. at both urban and regional scales, but little or no 

13 change in the western U.S., except in and near certain urban areas. 

14 The EPA then considered the potential effectiveness of a regional haze program, required 

by sections 169A and 169B of the Act1 15 to address the widespread, regionally uniform type of 

16 haze caused by a multitude of sources, to address those effects of PM on visibility that would not 

17 be addressed through attainment of the primary PM2.5 standards. The structure and requirements 

18 of sections 169A and 169B of the Act provide for visibility protection programs that can be more 

19 responsive to the factors contributing to regional differences in visibility than can programs 

20 addressing a nationally applicable secondary NAAQS. The regional haze visibility goal was 

21 more protective than a secondary NAAQS since the goal addresses any man-made impairment 

22 rather than just impairment at levels determined to be adverse. Thus, an important factor 

23 considered in the 1997 review was whether a regional haze program, in conjunction with 

24 secondary standards set identical to the suite of PM2.5 primary standards, would provide 

25 appropriate protection for visibility in non-Class I areas. The EPA concluded that the two 

26 programs and associated control strategies should provide such protection due to the regional 

27 approaches needed to manage emissions of pollutants that impair visibility in many of these 

28 areas. 

29 For these reasons, EPA concluded that a national regional haze program, combined with a 

30 nationally applicable level of protection achieved through secondary PM2.5 standards set 

31 identical to the primary PM2.5 standards, would be more effective in addressing regional 

32 variations in the adverse effects of PM2.5 on visibility than establishing national secondary 

 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 achieved toward meeting the national goal. 
4-4 

Draft – Do Not Quote or Cite March 2010 

1 standards for PM at lower levels than the primary PM2.5 standards. The EPA further recognized 

2 that people living in certain urban areas may place a high value on unique scenic resources in or 

3 near these areas, and as a result might experience visibility problems attributable to sources that 

4 would not necessarily be addressed by the combined effects of a regional haze program and 

5 PM2.5 secondary standards. The EPA concluded that in such cases, State or local regulatory 

6 approaches, such as past action in Colorado to establish a local visibility standard for the City of 

7 Denver, would be more appropriate and effective in addressing these special situations because 

8 of the localized and unique characteristics of the problems involved. Visibility in an urban area 

9 located near a mandatory Class I Federal area could also be improved through State 

10 implementation of the current visibility regulations, by which emission limitations can be 

11 imposed on a source or group of sources found to be contributing to ‘‘reasonably attributable’’ 

12 impairment in the mandatory Class I Federal area. 

13 Based on these considerations, EPA set secondary PM2.5 standards identical to the 

14 primary PM2.5 standards, in conjunction with a regional haze program under sections 169A and 

15 169B of the Act, as the most appropriate and effective means of addressing the welfare effects 

16 associated with visibility impairment. Together, the two programs and associated control 

17 strategies were expected to provide appropriate protection against the effects of PM on visibility 

18 and enable all regions of the country to make reasonable progress toward the national visibility 

19 goal. 

20 4.1.1.2 Review Completed in 2006 

21 In 2006, EPA revised the secondary PM standards by once again making them identical 

22 to the revised primary standards. The EPA’s decision to revise the secondary PM standards 

23 reflected a number of new developments and sources of information that had occurred and/or 

24 become available following the 1997 review. First, EPA promulgated a regional haze program 

25 in 1999 (65 FR 35713) which required States to establish goals for improving visibility in Class I 

26 areas and to adopt control strategies to achieve these goals. Second, extensive new information 

27 from visibility and fine particle monitoring networks had become available, allowing for updated 

28 characterizations of visibility trends and PM levels in urban areas, as well as Class I areas. 

29 These new data allowed EPA to better characterize visibility impairment in urban areas and the 

30 relationship between visibility and PM2.5 concentrations. Finally, additional studies in the U.S. 

31 and abroad provided the basis for the establishment of standards and programs to address 

32 specific visibility concerns in a number of local areas. These studies (e.g., in Denver, Phoenix, 

33 British Columbia) produced reasonably consistent results in terms of the visual ranges found to 

34 be generally acceptable by the participants in the various studies. These studies utilized 

35 photographic representations of visibility impairment, which were useful in characterizing the 

36 nature of particle-induced haze. Based largely on this information, the Administrator concluded 
4-5 

Draft – Do Not Quote or Cite March 2010 

1 that it was appropriate to revise the secondary PM standards to provide increased protection from 

2 visibility impairment principally in urban areas, in conjunction with the regional haze program 

3 for protection of visual air quality in Class I areas. 

4 In so doing, the Administrator recognized that PM-related visibility impairment is 

5 principally related to fine particle levels, such that it was appropriate to focus the review on 

6 whether the current secondary PM2.5 standards should be revised. The Administrator also 

7 recognized that perception of visibility impairment is most directly related to instantaneous 

8 levels of visual air quality, such that in considering whether the current suite of secondary 

9 standards would provide the appropriate degree of protection, he concluded that it was 

10 appropriate to revise just the 24-hour secondary PM2.5 standard to provide requisite protection. 

11 The EPA then considered whether PM2.5 remained the appropriate indicator for a 

12 secondary standard to protect visibility primarily in urban areas. One of the key issues in the 

13 1997 review was the extent to which the differences in humidity between East and West 

14 complicated the establishment of a nationally uniform PM2.5 secondary standard for urban areas. 

15 With the substantial addition to the air quality and visibility data made possible by the national 

16 urban PM2.5 monitoring networks, an analysis conducted for the 2006 review found that, in urban 

17 areas, visibility levels showed far less difference between eastern and western regions on a 24-

18 hour or shorter time basis than implied by the largely non-urban data available in the 1997 

19 review. In analyzing how well PM2.5 concentrations correlated with visibility in urban locations 

20 across the U.S., the 2005 Staff Paper concluded that clear correlations existed between 24-hour 

21 average PM2.5 concentrations and reconstructed light extinction, which is directly related to 

22 visual range. These correlations were similar in the eastern and western regions of the U.S. 

23 Particles in the coarse mode generally contributed only marginally to visibility impairment in 

24 urban areas. Further, because hygroscopic components of fine particles, in particular sulfates 

25 and nitrates, contribute disproportionately to visibility impairment under high humidity 

26 conditions, these correlations were less influenced by relative humidity and more consistent 

27 across regions when PM2.5 concentrations are averaged over shorter, daylight time periods (e.g., 

28 4 to 8 hours) when relative humidity was generally lower and less variable. The 2005 Staff 

29 Paper noted that a standard set at any specific PM2.5 concentration would necessarily result in 

30 visual ranges that vary somewhat in urban areas across the country, reflecting the variability in 

31 the correlations between PM2.5 concentrations and light extinction. Thus, the 2005 Staff Paper 

32 concluded that it was appropriate to use PM2.5 as an indicator for standards to address visibility 

33 impairment in urban areas, especially when the indicator is defined for a relatively short period 

34 (e.g., 4 to 8 hours) of daylight hours. Based on their review of the Staff Paper, most CASAC 

35 Panel members also endorsed such a PM2.5 indicator for a secondary standard to address 

36 visibility impairment (Henderson, 2005a). Based on the above considerations, the Administrator 
4-6 

Draft – Do Not Quote or Cite March 2010 

1 concluded that PM2.5 should be retained as the indicator for fine particles as part of a secondary 

2 standard to address visibility protection, in conjunction with averaging times from 4 to 24 hours. 

3 In considering what level of protection against PM-related visibility impairment would be 

4 appropriate, the Administrator took into account the results of the public perception and attitude 

5 surveys in the U.S. and Canada, State and local visibility standards within the U.S., and visual 

6 inspection of photographic representations of several urban areas across the U.S. In the 

7 Administrator’s judgment, these sources provided useful but still quite limited information on the 

8 range of levels appropriate for consideration in setting a national visibility standard primarily for 

9 urban areas, given the generally subjective nature of the public welfare effect involved. Based 

10 on photographic representations of varying levels of visual air quality, public perception studies, 

and local and State visibility standards, the 2005 Staff Paper concluded that 30 to 20 μg/m3 11 PM2.5 

12 represented a reasonable range for a national visibility standard primarily for urban areas, based 

13 on a sub-daily averaging time. The upper end of this range was below the levels at which 

14 illustrative scenic views are significantly obscured, and the lower end was around the level at 

15 which visual air quality generally appeared to be good based on observation of the illustrative 

16 views. This concentration range generally corresponded to median visual ranges in urban areas 

17 within regions across the U.S. of approximately 25 to 35 km, a range which was bounded above 

18 by the visual range targets selected in specific areas where State or local agencies placed 

19 particular emphasis on protecting visual air quality. In considering a reasonable range of forms 

20 for a PM2.5 standard within this range of levels, the 2005 Staff Paper concluded that a 

21 concentration-based percentile form was appropriate, and that the upper end of the range of 

concentration percentiles should be consistent with the 98th 22 percentile used for the primary 

standard and that the lower end of the range should be the 92nd 23 percentile, which represented the 

24 mean of the distribution of the 20 percent most impaired days, as targeted in the regional haze 

25 program. While recognizing that it was difficult to select any specific level and form based on 

26 then currently available information (Henderson, 2005a), the CASAC Panel was generally in 

27 agreement with the ranges of levels and forms presented in the 2005 Staff Paper. 

28 The Administrator also considered the level of protection that would be afforded by the 

29 proposed suite of primary PM2.5 standards (71 FR 2681), on the basis that although significantly 

30 more information was available than in the 1997 review concerning the relationship between fine 

31 PM levels and visibility across the country, there was still little available information for use in 

32 making the relatively subjective value judgment needed in selecting the appropriate degree of 

33 protection to be afforded by such a standard. In so doing, the Administrator compared the extent 

34 to which the proposed suite of primary standards would require areas across the country to 

35 improve visual air quality with the extent of increased protection likely to be afforded by a 

36 standard based on a sub-daily averaging time. Based on such an analysis, the Administrator 
4-7 

Draft – Do Not Quote or Cite March 2010 

1 observed that the predicted percent of counties with monitors not likely to meet the proposed 

2 suite of primary PM2.5 standards was actually somewhat greater than the predicted percent of 

3 counties with monitors not likely to meet a sub-daily secondary standard with an averaging time 

4 of 4 daylight hours, a level toward the upper end of the range recommended in the 2005 Staff 

5 Paper, and a form within the recommended range. Based on this comparison, the Administrator 

6 concluded that revising the secondary 24-hour PM2.5 standard to be identical to the proposed 

7 revised primary PM2.5 standard (and retaining the current annual secondary PM2.5 standard) was a 

8 reasonable policy approach to addressing visibility protection primarily in urban areas. In 

9 proposing this approach, the Administrator also solicited comment on a sub-daily (4- to 8-hour 

10 averaging time) secondary PM2.5 standard (71 FR 2675-2781). 

11 In commenting on EPA’s proposal, the CASAC requested that a sub-daily standard to 

12 protect visibility be favorably reconsidered (Henderson, 2006). The CASAC noted three 

13 cautions regarding the Agency’s proposed reliance on a secondary PM2.5 standard identical to the 

14 proposed 24-hour primary PM2.5 standard: (1) PM2.5 mass measurement is a better indicator of 

15 visibility impairment during daylight hours, when relative humidity is generally low; the sub16 daily standard more clearly matches the nature of visibility impairment, whose adverse effects 

17 are most evident during the daylight hours; using a 24- hour standard as a proxy introduces error 

18 and uncertainty in protecting visibility; and sub-daily standards are used for other NAAQS and 

19 should be the focus for visibility; (2) CASAC and its monitoring subcommittees have repeatedly 

20 commended EPA’s initiatives promoting the introduction of continuous and near-continuous PM 

21 monitoring, and expanded deployment of continuous PM2.5 monitors is consistent with setting a 

22 sub-daily standard to protect visibility; (3) The analysis showing a similarity between 

23 percentages of counties not likely to meet what they considered to be a lenient 4- to 8-hour 

24 secondary standard and a secondary standard identical to the proposed 24-hour primary standard 

25 was a numerical coincidence that was not indicative of any fundamental relationship between 

26 visibility and health. The CASAC Panel further stated that ”visual air quality is substantially 

impaired at PM2.5 concentrations of 35 μg/m3 27 ” and that ‘‘it is not reasonable to have the visibility 

28 standard tied to the health standard, which may change in ways that make it even less appropriate 

29 for visibility concerns.” 

30 In reaching a final decision, the Administrator focused on the limitations in the available 

31 hourly air quality data and in the studies of public perception and attitudes regarding the 

32 acceptability of various degrees of visibility impairment in urban areas, as well as on the 

33 subjective nature of the public welfare judgment required. In so doing, the Administrator 

34 concluded that caution was warranted in establishing a distinct secondary standard for visibility 

35 impairment and that the available information did not warrant adopting a secondary standard that 
4-8 

Draft – Do Not Quote or Cite March 2010 

1 would provide either more or less protection against visibility impairment in urban areas than 

2 would be provided by secondary standards set equal to the proposed primary PM2.5 standards. 

3 4.1.2 Remand of Secondary PM2.5 Standards 

4 Several parties filed petitions for review following promulgation of the revised PM 

5 NAAQS in 2006. These petitions challenged several aspects of the final rule including EPA’s 

6 decision to set the secondary NAAQS for fine PM, which protect the public welfare from 

7 adverse visibility effects, at the same level as the primary NAAQS, which protect public health 

8 42 U.S.C. 7607(d)(9). 

9 On judicial review, the D.C. Circuit remanded for reconsideration the secondary NAAQS 

10 for fine PM to EPA because the Agency’s decision was unreasonable and contrary to the 

11 requirements of 42 U.S. C. section 7409 (b)(2). The petitioners argued that EPA’s decision 

12 lacked a reasoned basis. First, they asserted, EPA never determined what level of visibility was 

13 “requisite to protect the public welfare” 42 U.S.C. section 7409(b)(2). They argued that EPA 

14 unreasonably rejected the target level of protection provided by its staff, while failing to provide 

15 a target level of its own. The D.C. Circuit court concurred stating “the EPA’s failure to identify 

16 such a level when deciding where to set the level of air quality required by the revised secondary 

17 fine PM NAAQS is contrary to the statute and therefore unlawful. Furthermore, the failure to set 

18 any target level of visibility protection deprived the EPA’s decisionmaking of a reasoned basis.” 

19 American Farm Bureau Federation v. EPA, 559 F. 3d 512, (D.C. Cir. 2009). 

20 Second, the petitioners challenged EPA’s method of comparing the protection expected 

21 from potential standards. They contend that the EPA relied on a meaningless numerical 

22 comparison, ignored the effect of humidity on the usefulness of a standard using a daily 

23 averaging time, and unreasonably concluded that the primary standards would achieve a level of 

24 visibility roughly equivalent to the level the EPA staff and CASAC deemed “requisite to protect 

25 the public welfare.” Again, the court found that EPA’s equivalency analysis failed on its own 

26 terms. The same table showing the alternative secondary standard used for comparison to the 

27 alternative primary to show equivalency also included six other standards within the 

28 recommended CASAC range that would be more “protective” under EPA’s definition than the 

29 primary standards. Two thirds of the potential standards within the CASAC’s recommended 

30 range would be substantially more protective than the primary standards. The EPA failed to 

31 explain why it looked only at one of the few potential standards that would be less protective-and 

32 only slightly so- than the primary standards. More fundamentally, however, EPA’s equivalency 

33 analysis demonstrated nothing about the relative protection offered by the different standards. 

34 The tables simply offer no valid information about the relative visibility protection provided by 

35 the standards. 
4-9 

Draft – Do Not Quote or Cite March 2010 

1 Finally, the Staff Paper made clear that a visibility standard using a daily averaging time 

2 will be confounded by regional differences in humidity. The EPA acknowledged this problem, 

3 yet did not address this issue at all in concluding that the primary standards would be sufficiently 

4 protective of visibility. Therefore, the court granted the petition for review and remanded for 

5 reconsideration the secondary PM NAAQS. American Farm Bureau Federation, 559 F. 3d at 

6 520-24. 

7 4.1.3 Current Approach 

8 The staff’s approach in this review broadens the general approaches used in the last two 

9 PM NAAQS reviews by utilizing, to the extent available, enhanced tools, methods, and data to 

10 more comprehensively characterize visibility impacts. As such, staff is taking into account both 

11 evidence-based and impact-based considerations to inform staff conclusions related to the 

12 adequacy of the current secondary standards and alternative standards that are appropriate for 

13 consideration in this review. In so doing, we are seeking to provide as broad an array of options 

14 as is supportable by the available information, recognizing that the selection of a specific 

15 approach to reaching final decisions on the secondary PM2.5 standards will reflect the judgments 

16 of the Administrator as to what weight to place on the various approaches and types of 

17 information presented in the final PA. 

18 For the purposes of this first draft Policy Assessment (PA), staff has drawn from the 

19 qualitative evaluation of all studies evaluated in the Integrated Science Assessment for 

20 Particulate Matter (Final Report) (ISA, USEPA, 2009a). The discussions presented in this 

21 chapter consider the extensive new air quality and source apportionment information available 

22 from the regional planning organizations, long-standing evidence of PM effects on visibility, and 

23 public preference studies from four urban areas, as discussed in chapter 9 of the ISA, as well as 

24 the integration of evidence across disciplines presented in chapter 2 of the ISA. In addition, 

25 limited information that has become available regarding the characterization of public 

26 preferences in urban areas has provided some new perspectives on the usefulness of this 

27 information in informing the selection of target levels of urban visibility protection. On these 

28 bases, we are again focusing our assessments in this review on visibility conditions in urban 

29 areas. 

30 Our preliminary conclusions reflect our understanding of both evidence-based and 

31 impact-based considerations to inform two overarching questions related to: (1) the adequacy of 

32 the current suite of PM2.5 standards and (2) what potential alternative standards, if any, should be 

33 considered in this review to provide appropriate protection from PM-related visibility 

34 impairment. In addressing these broad questions, we have organized the discussions below 

35 around a series of more specific questions reflecting different aspects of each overarching 
4-10 

Draft – Do Not Quote or Cite March 2010 

1 question. When evaluating the visibility protection afforded by the current or any alternative 

2 standards considered, we have taken into account the four basic elements of the NAAQS (e.g., 

3 indicator, averaging time, level, and form). 

4 We believe that the approach outlined above, when presented in the final PA, will 

5 provide a comprehensive basis to help inform the judgments required of the Administrator in 

6 reaching decisions about the current and potential alternative secondary PM standards for the 

7 purpose of providing appropriate protection from PM-related visibility impairment and in 

8 responding to the remand of the 2006 secondary PM2.5 standards. 

9 4.2 ADEQUACY OF CURRENT STANDARDS 

10 In considering the adequacy of the current suite of PM2.5 standards, staff addresses the 

11 following overarching question: 

12 Does the currently available scientific evidence and visibility impact information, as 

13 reflected in the ISA and UFVA, support or call into question the adequacy of the visibility 

14 protection afforded by the current suite of fine particle standards? 

15 To inform the answer to this overarching question, we have posed a series of more 

16 specific questions to aid in considering the currently available scientific evidence and the results 

17 of recent quantitative visibility impact analyses in a policy-relevant context, as discussed below. 

18 In considering the scientific and technical information, we reflect upon both the information 

19 available in the last review and information that is newly available since the last review as 

20 assessed and presented in the ISA and UFVA (US EPA, 2009a; US EPA, 2010b). 

21 4.2.1 Evidence-based Considerations 

22 In reviewing the adequacy of the current suite of PM2.5 standards, we have taken into 

23 account evidence-based considerations, primarily as presented in the ISA, by considering causal 

24 inference, impacts on susceptible populations, and whether visibility effects have been observed 

25 in urban areas that would likely meet the current standards. 

26  To what extent does the newly available scientific evidence strengthen or call into 

27 question evidence of associations between ambient fine particle exposures and visibility 

28 effects? 

29 New research conducted by regional planning organizations in support of the Regional 

30 Haze Rule, as discussed in chapter 9 of the ISA, continues to support and refine our 

31 understanding of the nature of the PM visibility effect and the source contributions to that effect 

32 in rural and remote locations. Additional byproducts of this research include new insights 

33 regarding the regional source contributions to urban visibility and better characterization of the 

34 urban excess that occurs in many cities above regional background. Ongoing urban PM2.5
4-11 

Draft – Do Not Quote or Cite March 2010 

1 speciated and mass monitoring has produced new information that has allowed for updated 

2 characterization of visibility trends and current levels in urban areas. Information from both of 

3 these sources of PM data, while useful, has not however changed the fundamental and long 

4 understood science characterizing the contribution of PM, especially fine particles, to visibility 

5 impairment from the last review. This science, briefly summarized below, provides the basis for 

6 the ISA designation of the relationship between PM and visibility impairment as causal. 

7 Visibility impairment is caused by the scattering and absorption of light by suspended 

8 particles and gases in the atmosphere. The combined effect of light scattering and absorption by 

9 both particles and gases is characterized as light extinction, (i.e. the fraction of light that is 

10 scattered or absorbed per unit of distance in the atmosphere). Light extinction is measured in 

11 units of 1/distance, which is often expressed in the technical literature as 1/(million meters) or 

inverse megameters (abbreviated Mm-1 12 ). When PM is present in the air, its contribution to light 

13 extinction typically greatly exceeds that of gases. 

14 The amount of light extinction contributed by PM depends on the particle size 

15 distribution and composition, as well as its concentration. If details of the ambient particle size 

16 distribution and composition (including the mixing of components) are known, Mie theory can 

17 be used to accurately calculate PM light extinction (ISA chapter 9). However, routine 

18 monitoring rarely includes measurements of particle size and composition information with 

19 sufficient detail for such calculations. A much simpler algorithm can be used to estimate light 

20 extinction using routinely monitored fine particle (PM2.5) speciation and coarse particle mass 

21 (PM10 – 2.5) data, plus relative humidity information needed to estimate the contribution by liquid 

22 water in solution with hygroscopic PM components (ISA section 9.2.2.2 and UFVA chapter 3). 

23 The concentration of each of the major aerosol components is multiplied by a dry 

24 extinction efficiency value and for the hygroscopic components (e.g., ammoniated sulfate and 

25 ammonium nitrate) an additional multiplicative term to account for the water growth to estimate 

26 that components contribution to light extinction. Both the dry extinction efficiency and water 

27 growth terms are developed by some combination of empirical assessment and theoretical 

28 calculation using typical particle size distributions associated with each of the major aerosol 

29 components, and they are evaluated by comparing the algorithm estimates of light extinction 

30 with coincident optical measurements. Summing the contribution of each component gives the 

31 estimate of total light extinction. The most commonly used of these is referred to as the 

32 IMPROVE algorithm because it was developed specifically to use the IMPROVE aerosol 

33 monitoring data and was evaluated using IMPROVE optical measurements at the subset of sites 

34 that make those measurements (Malm et al., 1994). The formula for the traditional IMPROVE 

35 algorithm is shown below. 

36 
4-12 

Draft – Do Not Quote or Cite March 2010 

1 bext ≈ 3 x f(RH) x [Sulfate] 

2 + 3 x f(RH) x [Nitrate] 

3 + 4 x [Organic Mass] 

4 + 10 x [Elemental Carbon] 

5 + 1 x [Fine Soil] 

6 + 0.6 x [Coarse Mass] 

7 + 10 

8 

Light extinction (bext) is in units of Mm-1 9 , the mass concentrations of the components 

indicated in brackets are in μg/m3 10 , and f(RH) is the unitless water growth term that depends on 

11 relative humidity. The dry extinction efficiency for particulate organic mass is larger than those 

for particulate SO4

2– 12 and nitrate principally because the density of the dry inorganic compounds 

13 is higher than that assumed for the PM organic mass components. Since IMPROVE does not 

include ammonium ion monitoring, the assumption is made that all SO4

2– 14 is fully neutralized 

15 ammonium sulfate and all nitrate is assumed to be ammonium nitrate. Though often reasonable, 

16 neither assumption is always true (see Section 9.2.3.1). In the eastern U.S. during the summer 

there is insufficient ammonia in the atmosphere to neutralize the SO4

2– 17 fully. Fine particle 

18 nitrates can include sodium or calcium nitrate, which are the fine particle fraction of generally 

19 much coarser particles due to nitric acid interactions with sea salt at near-coastal areas (sodium 

20 nitrate) or nitric acid interactions with calcium carbonate in crustal aerosol (calcium nitrate). 

21 Despite the simplicity of the algorithm, it performs reasonably well and permits the contributions 

22 to light extinction from each of the major components (including the water associated with the 

SO4

2– 23 and nitrate compounds) to be separately approximated. 

The f(RH) terms inflate the particulate SO4

2– 24 and nitrate light scattering for high relative 

25 humidity conditions. For relative humidity below 40% the f(RH) value is 1, but it increases to 2 

26 at ~66%, 3 at ~83%, 4 at ~90%, 5 at ~93% and 6 at ~95% relative humidity. The result is that 

both particulate SO4

2– 27 and nitrate are more efficient per unit mass than any other aerosol 

28 component for relative humidity above ~85% where its total light extinction efficiency exceeds 

the 10m2

/g associated with EC. Based on this algorithm, particulate SO4

2– 29 and nitrate are 

30 estimated to have comparable light extinction efficiencies (i.e., the same dry extinction 

31 efficiency and f(RH) water growth terms), so on a per unit mass concentration basis at any 

32 specific relative humidity they are treated as equally effective contributors to visibility effects. 

33 Inspection of the PM component-specific terms in the simple algorithm shows that most 

34 of the PM2.5 components contribute 5 times or more light extinction than a similar concentration 

35 of PM10 – 2.5. We also know that particles with hygroscopic components (e.g. particulate sulfate 

36 and nitrate) contribute more light extinction at higher relative humidity than at lower relative 

37 humidity because they change size in the atmosphere in response to ambient relative humidity 

38 conditions. PM containing elemental or black carbon absorbs light as well as scattering it, 
4-13 

Draft – Do Not Quote or Cite March 2010 

1 making it the component with the greatest light extinction contributions per unit of mass 

2 concentration, except for the hygroscopic components under high relative humidity conditions. 

3 As a result of better characterization of PM in rural and remote locations, refinements in 

4 the original IMPROVE algorithm have been made to better account for the aging of the organic 

5 aerosols that occurs during transport to these more distant areas, and to add a component for sea 

6 salt. Since urban areas contain a higher proportion of newly emitted aerosols that have not aged, 

7 the assessments done in support of this review have relied on the original IMPROVE algorithm. 

8 As mentioned above, particles are not the only contributor to ambient visibility 

9 conditions. Light scattering by gases also occurs in ambient air. Under pristine atmospheric 

10 conditions, naturally occurring gases such as N2 and O2, cause what is known as Rayleigh 

11 scattering. Rayleigh scattering, which depends on the density of air as a function primarily of the 

12 elevation above sea level, can be treated as a site-dependent constant. Rayleigh contribution to 

13 light extinction is only significant under pristine conditions. The only other commonly occurring 

14 atmospheric gas to appreciably absorb light in the visible spectrum is NO2. NO2 forms in the 

15 atmosphere from NO emissions associated with combustion processes. These combustion 

16 processes also emit PM at levels that generally contribute much higher light extinction than the 

17 NO2 (i.e. NO2 absorption is generally less than ~ 5% of the light extinction, except where 

18 emission controls remove most of the PM prior to releasing the remaining gases to the 

19 atmosphere). The remainder of this document focuses on the contribution of PM, which is 

20 typically much greater than that of gases, to ambient light extinction, unless otherwise specified. 

21  To what extent does the available evidence inform our understanding of the temporal 

22 nature of the PM visibility effect, including relevant exposure periods, associated 

23 atmospheric conditions, and diurnal patterns of exposure? 

24 Diurnal Periods of Interest 

25 Typically, we think of visibility associated with daytime periods. We recognize, 

26 however, that PM light extinction behaves the same at night as during the day, enhancing the scattering 

27 of anthropogenic light, contributing to the “skyglow” within and over populated areas, adding to the total 

28 sky brightness, and contributing to the reduction in contrast of stars against the background. These effects 

29 produce the visual result of a reduction of the number of visible stars and the disappearance of diffuse or 

30 subtle phenomena such as the Milky Way. The extinction of starlight is a secondary and minor effect also 

31 caused by increased PM scattering and absorption. 

32 However, there are significant and important differences between daytime and nighttime visual 

33 environments that potentially make the nighttime period inappropriate to address at this time. First, 

34 daytime visibility has dominated the attention of those who have studied the visibility effects of air 

35 pollution. As a result, little research has been conducted on nighttime visibility and the state of the 

36 science is not yet comparable to that associated with daytime visibility impairment. Second, in addition 
4-14 

Draft – Do Not Quote or Cite March 2010 

1 to air pollution, nighttime visibility is affected by the addition of light into the sight path from numerous 

2 sources, including anthropogenic light sources such as artificial outdoor lighting, which varies 

3 dramatically across space, and natural sources including the Moon, planets, and stars. Light sources and 

4 ambient conditions are typically five to seven orders of magnitude dimmer at night than in sunlight. 

5 Moonlight, like sunlight, introduces light throughout an observer’s sight path at a constant angle. On the 

6 other hand, dim starlight emanates from all over the celestial hemisphere while artificial lights are 

7 concentrated in cities and illuminate the atmosphere from below. These different light sources will yield 

8 variable changes in visibility as compared to what has been established for the daytime scenario, in which 

9 a single source, the sun, is by far the brightest source of light. Third, the human psychophysical response 

10 (e.g., how the human eye sees and processes visual stimuli) at night is expected to differ (ISA, section 

11 9.2.2). 

12 Given the above, we do not believe that the science is available at this time to support 

13 adequate characterization of nighttime PM light extinction effects. In addition, we are not aware 

14 of preference or valuation studies providing information on public preferences for nighttime 

15 visual air quality (VAQ). Thus, we limit our consideration of PM visibility impacts to all 

16 daylight hours only. 

17 Exposure Durations of Interest

18 Very little is known about the role exposure duration plays in determining the 

19 acceptability or unacceptability of a given level of VAQ on the public welfare. We do know 

20 from preference and/or valuation studies that atmospheric visibility conditions can be quickly 

21 assessed and preferences determined. These studies show that a momentary glance at an image 

22 of a scene (i.e. less than a minute) is enough for study participants to consistently judge the 

23 acceptability or unacceptability of the viewed visual air quality conditions. Outside these 

24 controlled settings, we are unaware of any studies that characterize the extent to which different 

25 frequencies and durations of exposure to visibility conditions contribute to the degree of public 

26 welfare impact that occurs. 

27 In some circumstances, such as infrequent visits to scenic vistas in natural or urban 

28 environments, people are motivated specifically to take the opportunity to view a valued scene 

29 and are likely to do so for many minutes to hours to appreciate various aspects of the vista they 

30 choose to view. In such circumstances, the viewer may consciously evaluate how the VAQ at 

31 that time either enhances or diminishes the experience/view. However, the public also has many 

32 more opportunities to notice visibility conditions on a daily basis in settings/surroundings 

33 associated with performing daily routines (e.g. during commutes, while walking the dog, or 

34 when taking out the recyclables). These scenes, whether iconic or generic, may not be 

35 consciously viewed for their scenic value, but their VAQ can still affect a person’s sense of 

36 wellbeing. Research has demonstrated that people are emotionally affected by low VAQ, that 
4-15 

Draft – Do Not Quote or Cite March 2010 

1 perception of pollution is correlated with stress, annoyance and symptoms of depression, and that 

2 VAQ is deeply intertwined with a “sense of place,” affecting peoples sense of the desirability of 

3 a neighborhood (ISA section 9.2.4). Though we do not know the extent to which these 

4 emotional effects are linked to different periods of exposure to poor VAQ, providing additional 

5 protection against even short term exposures to levels of VAQ considered unacceptable would be 

6 expected to provide some degree of improvement in the public’s “sense of wellbeing”. 

7 Some people have mostly intermittent opportunities on a daily basis (e.g. during morning 

8 and/or afternoon commutes) to experience ambient visibility conditions as they spend much of 

9 their time indoors without access to windows. For such people a view of poor VAQ during their 

10 morning commute may provide their perception of the day’s visibility conditions until the next 

11 time they venture outside during daylight hours later or perhaps the next day. Other people have 

12 exposure to visibility conditions throughout the day, so that a day with multiple hours of 

13 visibility impairment would likely be judged a having a greater impact on their wellbeing than a 

14 day with just one such hour. 

15 We have no information or studies on the fraction of the public that has only one or a 

16 few opportunities to experience visibility during the day, or information or studies on the 

17 duration of the effect on wellbeing from exposure to different durations of poor VAQ conditions. 

18 However, it is logical to conclude that people with limited opportunities to experience visibility 

19 conditions on a daily basis would receive the entire impact of the day’s VAQ based on the 

20 visibility conditions that occur during the short time period when they can see it. On the basis of 

21 this rationale, the segment of the population with infrequent access to visibility could be 

22 characterized as a sensitive subpopulation. Since this group could be affected on the basis of 

23 observing VAQ conditions for periods as short as one hour or less, we believe it is appropriate to 

24 consider characterizing PM visibility conditions in terms of the worst or maximum hourly value 

25 during daylight hours for each day for purposes of evaluating the adequacy of the current suite of 

26 secondary standards. 

27 For another group of observers, those who have access to visibility conditions often or 

28 continuously throughout the day, the entire impact of the day’s visibility conditions may be 

29 based on the varying visibility conditions they observe throughout the day. For this group, it 

30 might be more appropriate to evaluate the adequacy of the current suite of secondary standards in 

31 terms of all daylight hours in the day. 

32 While both the maximum daily and all hour averaging times were assessed in the UFVA 

33 for the PM light extinction indicator, only the maximum daily 1 hour average is assessed for the 

34 PM mass concentration indicator (below and Appendix A). In looking at the UFVA assessment 

35 of PM light extinction, we noticed a close correspondence between the level of protection 

afforded for all 15 urban areas in the assessment by the maximum daily daylight1-hour with 90th 36 
4-16 

Draft – Do Not Quote or Cite March 2010 

percentile and the all daylight 1-hour with the 98th 1 percentile (UFVA section 4.1.4). Thus, at 

2 these percentiles, either form of the standard provides protection of welfare effects to both the 

3 fraction of the public with rare opportunities and to those with ample opportunities to experience 

4 visibility. For consistency between PM2.5 mass and PM light extinction and because the daily 

5 maximum daylight 1-hour is thought to be more protective of those with limited opportunities to 

6 experience visibility, only the daily maximum form results will be displayed here. 

7 Temporal Variations of Visibility Impacts

8 While visibility conditions can change quickly (i.e., less than a minute), atmospheric 

9 sight path averaged light extinction which is pertinent to visibility impacts generally changes 

10 more slowly (i.e. tens of minutes generally). Sub-hourly variations in light extinction 

11 determined at any point in the atmosphere are likely the result of small scale spatial pollution 

12 features (i.e. plumes) being transported by the wind across that point. At typical wind speeds 

13 found in U.S. cities, an hour corresponds to a few tens of kilometers of air flowing past a point, 

14 which is similar to visibility sight path lengths of interest in urban areas. 

15 PM concentrations and light extinction in urban environments vary from hour to hour 

16 throughout the day due to a combination of diurnal meteorological conditions and systematic 

17 changes in emissions activity (e.g. rush hour traffic). Generally low mixing heights at night and 

18 during the early morning hour tend to trap locally produced emissions, which are diluted as the 

19 mixing height increases due to heating during the day. Low temperatures and high relative 

20 humidity at night are conducive to the presences of ammonium nitrate particles and water growth 

21 by hygroscopic particles compared with the generally higher temperatures and lower relative 

22 humidity later in the day. These combine to make early morning the most likely time for peak 

23 urban visibility impacts. Superimposed on such systematic time of day variations are the effects 

24 of synoptic meteorology (i.e., those associated with changing weather) and regional scale air 

25 quality that can generate peak visibility impacts any time of day. The net effects of the 

26 systematic urban and larger scale variations are that peak daytime PM light extinction can occur 

27 any time of day though more often in early morning hours (UFVA section 3.4.2 and 3.4.3 and 

28 shown in Figures 3-9, 3-10 and 3-12). Use of multi-hour averaging of PM light extinction would 

29 suppress peak hourly conditions that are expected to represent peak visibility impacts. 

30 Meteorological Causes of Visibility Impacts 

31 Visibility is also reduced directly by the presence of precipitation and fog regardless of 

32 the presence or absence of PM. A secondary PM NAAQS is not meant to protect against such 

33 sources of visibility impairment not related to PM. Therefore, one consideration in the 

34 development of alternative standard forms (discussed below in section 4.3) was the inclusion of a 
4-17 

Draft – Do Not Quote or Cite March 2010 

1 relative humidity screen in an effort to avoid misinterpretation of the direct effect of 

2 meteorological conditions on visibility and those caused by PM air quality. 

3  Based on currently available information, what range of levels of visibility impairment 

4 is reasonable to consider in reaching judgments about the adequacy of the current 

5 NAAQS? 

6 In order to identify levels of visibility impairment appropriate for consideration in setting 

7 secondary PM NAAQS to protect the public welfare, we comprehensively examined information 

8 that was available in this review regarding people’s stated preferences for acceptable and 

9 unacceptable visual air quality. 

10 Light extinction is an atmospheric property that by itself does not directly translate into a 

11 public welfare effect. Instead, light extinction becomes meaningful in the context of the impact 

12 of visibility on the human observer. This has been studied in terms of the acceptability or 

13 unacceptability expressed for it by a human observer. The perception of the visibility impact of 

14 a given level of light extinction occurs in conjunction with the associated characteristics and 

15 lighting conditions of the viewed scene. Thus, a given level of light extinction may be perceived 

16 differently by an observer looking at a different scene or the same scene with different lighting 

17 characteristics. Likewise, different observers looking at the same scene with the same lighting 

18 may have different preferences regarding the associated VAQ. When scene and lighting 

19 characteristics are held constant, the perceived appearance of a scene (i.e., how well the scenic 

20 features can be seen and the amount of visible haze) depends only on changes in light extinction. 

21 This has been demonstrated using the WinHaze model that uses image processing technology to 

22 apply user-specified changes in light extinction values to the same base photograph with set 

23 scene and lighting characteristics. 

24 Much of what we know about the acceptability of levels of visibility comes from survey 

25 studies in which participants were asked questions about their preference or the value they place 

26 on various visibility levels as displayed to them in scenic photographs and/or WinHaze images 

27 with a range of known light extinction levels. Urban visibility preference studies for four urban 

28 areas were reviewed in the UFVA (chapter 2) to assess the light extinction levels judged by the 

29 participant to have acceptable visibility. While the results differed among the four urban areas, 

30 results from a rating exercise showed that within each preference study, survey participants 

31 consistently distinguish between different levels of light extinction and prefer and value 

32 visibility associated with lower light extinction levels among the scenic images they are shown. 

33 The reanalysis included three completed urban visibility preference survey studies plus a 

34 pair of smaller focus studies designed to explore and further develop urban visibility survey 

35 instruments. The three western studies included Denver, Colorado (Ely et al., 1991), one in the 

36 lower Fraser River valley near Vancouver, British Columbia (BC), Canada (Pryor, 1996), and 
4-18 

Draft – Do Not Quote or Cite March 2010 

1 one in Phoenix, Arizona (BBC Research & Consulting, 2003). A pilot focus group study was 

2 also conducted for Washington, DC (Abt Associates Inc., 2001). In response to an EPA request 

3 for public comment on the Scope and Methods Plan (74 FR 11580, March 18, 2009), we 

4 received comments (Smith, 2009) about the results of a new Washington, DC focus group study 

5 that had been conducted using methods and approaches similar to the method and approach 

6 employed in the EPA pilot study (Smith and Howell, 2009). When taken together, these studies 

7 from the four different urban areas included a total of 852 individuals, with each individual 

8 responding to a series of questions answered while viewing a set of images of various urban 

9 VAQ conditions. 

10 The approaches used in the four studies are similar and are all derived from the method 

11 first developed for the Denver urban visibility study. In particular, the studies all used a similar 

12 group interview type of survey to investigate the level of visibility impairment that participants 

13 described as “acceptable. While each study asked the basic question, “What level of visibility 

14 degradation is acceptable?”, the term “acceptable” was not defined, so that each person’s 

15 response was based on his/her own values and preferences for VAQ. Given the similarities in 

16 the approaches used, we concluded that it is reasonable to compare the results to identify overall 

17 trends in the study findings and that this comparison can usefully inform the selection of a range 

18 of levels for use in further analyses. However, variations in the specific materials and methods 

19 used in each study introduce uncertainties that should also be considered when interpreting the 

20 results of these comparisons. Key differences between the studies include: 1) image presentation 

21 methods (e.g., projected slides of actual photos, projected images generated using WinHaze (a 

22 significant technical advance in the method of presenting VAQ conditions), use of computer 

23 monitor screen; 2) number of participants in each study; 3) participant representativeness of the 

24 general population of the relevant metropolitan area; and 4) specific wording used to frame the 

25 questions used in the group interview process. 

26 In the UFVA, each study was evaluated separately and figures developed to display the 

27 percentage of participants that rated each photograph as “acceptable”. The horizontal axis was in 

28 terms of light extinction (deciview) and the vertical axis in terms of percent of participants rating 

29 “acceptable”. Ely et al. (1991) introduced a “50% acceptability” criteria analysis of the Denver 

30 preference study results. The 50% acceptability criteria is designed to identify the VAQ level 

31 that best divides the photographs into two groups: those with a VAQ rated as acceptable by the 

32 majority of the participants, and those rated not acceptable by the majority of participants. We 

33 adopted the criteria as a useful index for comparison between studies. The results of each 

34 individual analysis were then combined graphically to allow for visual comparison. Figure 4-1 

35 (Figure 2-16 in UFVA) presents the graphical summary of the results of the studies in the four 

36 cities and draws on results previously presented in Figures 2-3, 2-5, 2-7 and 2-11 of chapter 2 in 
4-19 

Draft – Do Not Quote or Cite March 2010 

1 the UFVA. Figure 4-1 also contains lines at 20 dv and 30 dv that effectively and pragmatically 

2 identify a range where the 50% acceptance criteria occur across all four of the urban preference 

3 studies. Out of the 114 data points shown in Figure 4-1, only one photograph (or image) with a 

4 VAQ below 20 dv was rated as acceptable by less than 50% of the participants who rated that 

photograph.2 5 Similarly, only one image with a VAQ above 30 dv was rated acceptable by more 

than 50% of the participants 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 

9 As can be seen in the figure, each urban area has a separate and unique response curve 

10 that appears to indicate that it is distinct from the others. These curves are the result of a 

11 logistical regression analysis using a logit model of the greater than 19,000 ratings of haze 

12 images as acceptable or unacceptable. The model results can be used to estimate the VAQ 

13 deciview values where the estimated response functions cross the 50% acceptability level, as 

 2

 Only 47% of the BC participants rated 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% rated 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 areas 
4-20 

Draft – Do Not Quote or Cite March 2010 

1 well as any alternative criteria levels. Selected examples of these are shown in Table 4-1 (Table 

2 2-4 in UFVA, Chapter 2). These results show that the logit model data also support the upper 

and lower ends of the range of 50th 3 percentile acceptability values (e.g. near 20 dv for Denver 

4 and near 30 dv for Washington, DC) already identified in Figure 4-1 (see Table 2-4 UFVA). 

5 

6 Table 4-1 Logit model estimated VAQ values corresponding to various percent 

7 acceptability values for the four cities. 

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 50th 10 percentile acceptability 

11 across the four urban preference studies shown in Figure 4-1 and Table 4-1, benchmark levels 

have been selected in a range from 20 dv to 30 dv (74 Mm-1 to 201 Mm-1 12 ) for the purpose of 

13 provisionally assessing whether visibility conditions would be considered acceptable (i.e., less 

14 than the low end of the range), unacceptable (i.e., greater than the high end of the range) or 

potentially acceptability (within the range). A midpoint of 25 dv (122 Mm-1 15 ) was also selected 

for use in the assessment. This level is also very near to the 50th 16 percentile criteria value from 

17 the Phoenix study (i.e. 24.3 dv), which is by far the best of the four studies in terms of least noisy 

18 preference results and the most representative selection of participants. Based on the currently 

19 available information, we conclude that the use of 25 dv to represent the middle of the 

20 distribution of results seems well supported. 

21 These three benchmark values provide a low, middle, and high set of light extinction 

22 conditions that are used to provisionally define daylight hours with urban haze conditions that 

23 have been judged unacceptable by the participants of these preference studies. As discussed 

24 above, PM light extinction is taken to be light extinction minus the Rayleigh scatter (i.e. light 

scattering by atmospheric gases which is on average about 10 Mm-1 25 ), so the low, middle and 

high levels correspond to PM light extinction levels of about 64 Mm-1, 112 Mm-1 and 191 Mm-1 26 . 

27 In the UFVA, these three levels were called Candidate Protection Levels (CPLs). We continue 

28 to use this term in this document. However, it is important to note that the degree of protection 
4-21 

Draft – Do Not Quote or Cite March 2010 

1 provided by a secondary NAAQS is not determined solely by the level of the standard but by all 

2 the components (e.g., indicator, form, level, averaging time) being applied together. Therefore, 

3 the reader should keep in mind that the term CPL is meant only to indicate levels within a range 

4 that we feel are appropriate for consideration that could, in conjunction with other aspects of the 

5 standard, provide an appropriate degree of visibility protection. 

6 In characterizing our degree of confidence in each CPL and across the range, a number of 

7 issues were considered. Looking first at the two studies that define the upper and lower bounds 

8 of the range, we considered whether they represent a true regional distinction in preferences for 

9 urban visibility conditions between Western and Eastern U.S.. There is little information 

10 available to help sort this out, especially given that we have preference studies in only one 

11 Eastern urban area. Smith and Howell (2009) found little difference in preference response to 

12 Washington, DC haze photographs between the study participants from Washington, DC and 

13 those from Houston, TX. This provides some limited evidence that the value judgment of the 

14 public in different areas of the country may not be an important factor in explaining the 

15 differences in these study results. 

16 In further considering what factors could explain the observed differences in preferences 

17 across the four urban areas, we noted that the urban scenes used in each study had different 

18 characteristics. For example, each of the Western urban visibility preference study scenes 

19 included mountains in the background while the single Eastern urban study did not. It’s also true 

20 that each of the Western scenes included objects at greater distances from the camera location 

21 than in the Washington, DC study. There’s no question that objects at a greater distance have a 

22 greater sensitivity to perceived visibility changes as light extinction is changed compared to 

23 otherwise similar scenes with objects at a shorter range. This alone might explain the difference 

24 between the results of the Washington DC, study and those from the Western urban studies. 

25 Also it’s intuitively likely that people value the views of mountains in the background more than 

26 generic distant buildings in the foreground of the Western scenes; just as it seems obvious that 

27 the Capital Mall and Washington Monument were the likely objects of greatest interest for the 

28 Washington, DC study base photograph. Having scenes with the object of greatest intrinsic 

29 value nearer and hence less sensitive for Washington compared with more distant objects of 

30 greatest intrinsic value in the Western urban areas could further explain the difference in 

31 preference results. 

32 Another question that we considered was whether the high CPL value that is based on the 

33 Washington DC preference results is likely to be generally representative of urban areas that do 

34 not have associated mountains or other valued objects visible in the distant background. Such 

35 areas would include the middle of the country and many areas in the eastern US. In order to 

36 examine this issue, an effort would have to be made to see if scenes in such areas could be found 
4-22 

Draft – Do Not Quote or Cite March 2010 

1 that would be generally comparable to the western scenes (e.g., contain valued scenic elements at 

2 more sensitive distances than that used in the Washington, DC study). This is only one of a 

3 family of issues concerning how exposure to urban scenes of varying sensitivity affects public 

4 perception, for which no information is currently available. Additional urban visibility 

5 preference studies employing images selected of potentially more sensitive scenes could help 

6 evaluate whether a lower value for the high CPL is supportable. Other investigations to 

7 determine how common such scenes are in various regions of the country would also be 

8 informative. Until such information becomes available, the high end of the CPL range (30 dv) 

9 seems to be an appropriate level to consider. 

10 With respect to the low end of the range, we considered factors that might further refine 

11 our understanding of the robustness of this level. We concluded that additional urban preference 

12 studies, especially with a greater variety in types of scenes, including potentially more sensitive 

13 Western urban scenes, could help evaluate whether a lower CPL value than the currently selected 

14 20 dv is supportable. Further, the reason for the noisiness in data points around the curves 

15 apparent in both the Denver and British Columbia results compared to the smoother curve fit of 

16 Phoenix study results could be explored. One possible explanation that we identified is that 

17 these older studies used photographs taken at different times of day and on different days to 

18 capture the range of light extinction levels needed for the preference studies. By contrast, the use 

19 of WinHaze in the Phoenix (and Washington, DC) study, reduced variations in scene appearance 

20 that affects preference rating and avoided the uncertainty inherent in using ambient 

21 measurements to represent sight path averaged light extinction values. Reducing these sources 

22 of noisiness and uncertainty in the results of future studies of sensitive urban scenes could 

23 provide more certainty in the selection of a low CPL value. 

24  To what extent does the available information demonstrate or suggest that PM-related 

25 visibility impairment (within the range of CPLs) is occurring at current ambient 

26 conditions or at levels that would meet the current standards? 

27 Current Visibility Levels

28 Chapter 3 of the UFVA characterized current visibility conditions in terms of both PM2.5 

29 and light extinction levels for the 15 urban areas selected and compared them to the CPLs 

30 identified above. 

31 As an initial matter, we note that PM is not necessarily the primary source of visibility 

32 impairment during periods with fog or precipitation. In order to avoid precipitation and fog 

33 confounding estimates of PM visibility impairment, and as advised by CASAC as part of its 

34 comments on the first public review draft of the UFVA, we restricted our assessment of visibility 

35 conditions to daylight hours with relative humidity less than or equal to 90% (UFVA section 
4-23 

Draft – Do Not Quote or Cite March 2010 

1 3.3.5 and Appendix G). However, not all periods with relative humidity above 90% have fog or 

2 precipitation. Removing those hours from application of a secondary PM standard involves a 

3 tradeoff between the benefits of avoiding many of the hours with meteorological causes of 

4 visibility impacts and the cost of not counting some hours with high relative humidity without 

5 fog or precipitation, where the growth of hygroscopic PM into large solution droplets results in 

6 enhanced PM visibility impacts. For the 11 urban areas included in the assessment for which 

7 updated meteorological data was obtained, a 90% relative humidity cutoff criterion is effective in 

8 that on average less than 6% of the hours are removed from consideration, yet those hours have 

9 on average twelve times the likelihood of meteorological causes of reduced visibility compared 

10 with hours with 90% or lower relative humidity. 

11 Figure 4-2 (Figure 3-8 in UFVA) presents box-and-whisker plots to illustrate the 

12 distributions of the estimates of daylight 1-hour reconstructed PM light extinction levels in each 

13 area in each year during the 2005-2007 time period. The distribution of the daily maximum 1-

14 hour values is shown. The horizontal dashed lines in the plots represent the low, middle, and 

high CPLs for PM light extinction of 64, 112, and 191 Mm-1 15 , corresponding to the benchmark 

16 VAQ values of 20 dv, 25 dv and 30 dv as discussed above. Table 4-2 (Table 3-7 in UFVA) 

17 provides the percentages of days (across all of 2005-2007, unweighted) in which the daily 

18 maximum daylight 1-hour PM light extinction level was greater than each of the three CPLs 

19 (excluding hours with relative humidity greater than 90 percent). 

20 From these displays it can be seen that among the 15 urban areas, those in the East and in 

21 California tend to have a higher frequency of visibility conditions above the high CPL compared 

22 with those in the Western US. Both Figure 4-2 and Table 4-2 indicate that all 15 urban areas 

23 have daily maximum hourly PM light extinctions that exceed even the highest CPL some of the 

24 time. Again, the non-California western urban locations have the lowest frequency of maximum 

25 hourly PM light extinction with values in excess of the high CPL for 8 percent or fewer of the 

26 days. Except for the two Texas and the non-California western urban areas, all of the other 

27 urban areas exceed that high CPL from about 20 percent to over 60 percent of the days. Based 

28 on these estimated maximum hourly PM light extinction estimates, all 15 of the urban areas 

29 exceed the low CPL for about 40 percent to over 90 percent of the days. Based on all of the 

30 above, we conclude that current levels of PM light extinction associated with recent PM air 

31 quality exceed levels that could reasonably be considered as protective of the public welfare. 

32 

33 

34 
4-24 

Draft – Do Not Quote or Cite March 2010 

1 Figure 4-2. Distribution of estimated maximum daily daylight 1-hour PM light extinction 

2 across the 2005-2007 period, by study area (excluding hours with relative 

3 humidity greater than 90 percent). (Adapted from Figure 3-8 in UFVA)* 

*In thel box-and-whisker plot, the box represents the 25th to 75th 4 percentile range and the 

whiskers represent the 10th and 90th percentile points of the data; individual data points below the 10th 5 

percentile and above the 90th 6 percentile are graphed as small circles. The three dashed horizontal lines 

represent the three CPL levels of 64, 112, and 191 Mm-1 7 . 
4-25 

Draft – Do Not Quote or Cite March 2010 

1 

2 Table 4-2 Percentage of daily maximum hourly values of daylight PM light extinction 

3 exceeding CPLs (excluding hours with relative humidity greater than 90 

4 percent). (adapted from Table 3-7 in UFVA) 

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 

7 Visibility Levels That Just Meet Current Standards

8 In the second draft of the UFVA, we modeled the “what if” scenario based on simulating 

just meeting the current suite of PM2.5 secondary standards: 15 μg/m3 9 annual average PM2.5 

concentration and 35 μg/m3

 24-hour average PM2.5 concentration with a 98th 10 percentile form, 

11 averaged over three years. The steps needed to model the “what if” conditions involve explicit 

12 consideration of changes in PM2.5 components and are described here. First, we applied 

13 proportional rollback to all the PM2.5 monitoring sites in each study area, taking into account 

14 PRB PM2.5 mass, to “just meet” the NAAQS scenario for the area as a whole, not just at the 

15 visibility assessment study site. The health risk assessment document (EPA 2010a) describes 

16 this procedure in detail. The degree of rollback is controlled by the highest annual or 24-hour 

17 design value, which in most study areas is from a site other than the site used in this visibility 

18 assessment. The relevant result from this analysis is the percentage reduction in non-PRB PM2.5 

19 mass need to “just meet” the NAAQS scenario, for each study area. These percentage reductions 
4-26 

Draft – Do Not Quote or Cite March 2010 

1 are shown in Table 4-4 of the UFVA. Note that Phoenix and Salt Lake City meet the 15/35 

2 NAAQS scenario under current conditions, and require no reduction. PM2.5 levels in these two 

3 cities were not “rolled up.” Second, for each day and hour for each PM2.5 component, we 

4 subtracted the PRB concentration from the current conditions concentration, to determine the 

5 non-PRB portion of the current conditions concentration. Third, we applied the percentage 

6 reduction from step 1 to the non-PRB portion of each of the five PM2.5 components and added 

7 back the PRB portion of the component. Finally, we re-applied the IMPROVE algorithm, using 

8 the reduced PM2.5 component concentrations, the current conditions PM10-2.5 concentration for the 

9 day and hour, and relative humidity for the day and hour. We then included the term for 

10 Rayleigh scattering. 

11 Figure 4-3 and Table 4-3 display the results of the rollback procedure as a box and 

12 whisker plot of daily maximum daylight 1-hour PM light extinction and the percentage of daily 

13 maximum hourly PM light extinction values exceeding the CPLs when just meeting the current 

PM2.5 NAAQS scenario of 15/35 μg/m3 14 (excluding hours with relative humidity greater than 90 

15 percent. These displays show that at the current PM NAAQS level (i.e., 15/35) all of the eastern 

16 urban areas and Los Angeles exceed the least restrictive CPL more than 10% of the time and that 

17 only Tacoma would not exceed the least restrictive CPL more than 2% of the time. 
4-27 

Draft – Do Not Quote or Cite March 2010 

1 

2 Figure 4-3. Distribution of daylight 1-hour PM light extinction when rolled back to just 

3 meet current PM fine NAAQS across the 2005-2007 period, by study area 

4 (excluding hours with relative humidity greater than 90 percent). * 

NAAQS Scenario: 15 μg/m3 annual; 35 μg/m3 5 24-hour 

6 Displayed: Daily Max Daylight Light Extinction (excluding hours >90% RH) 

7 

 * In thel box-and-whisker plot, the box represents the 25th to 75th 8 percentile range and the 

whiskers represent the 10th and 90th percentile points of the data; individual data points below the 10th 9 

percentile and above the 90th 10 percentile are graphed as small circles. The three dashed horizontal lines 

represent the three CPL levels of 64, 112, and 191 Mm-1 11 

12 
4-28 

Draft – Do Not Quote or Cite March 2010 

1 

2 Table 4-3 Percentage of daily maximum hourly values of daylight PM light extinction 

exceeding CPLs when “just meeting” the current PM2.5 NAAQS (15/35 μg/m3 3 ) 

4 (excluding hours with relative humidity greater than 90 percent). (Adapted from 

5 Table 4-7 in UFVA). 

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 

8 4.2.2 Summary 

9 In summary, we reach the preliminary conclusion that the available information in 

10 this review, as described above and in the UFVA and ISA, clearly calls into question the 

11 adequacy of the current suite of PM2.5 standards in the context of public welfare protection from 

12 unacceptable levels of visibility impairment, primarily in urban areas, and supports consideration 

13 of alternative standards to provide appropriate protection. 

14 This preliminary conclusion is based first on the large percentage of days that exceed the 

15 range of CPLs identified for consideration under both current and just meet PM air quality 

16 conditions. In particular, under just meet conditions for the suite of secondary PM NAAQS (i.e. 

15/35 μg/m3

) greater than 10% of the days exceed the highest, least protective CPL of 191 Mm-1 17 
4-29 

Draft – Do Not Quote or Cite March 2010 

for 10 of the 15 urban areas. When the middle CPL of 112 Mm-1 1 is considered, 12 of the 15 

2 cities have greater than 10% of their days exceeding with a range of 30 to 74% of days exceeding 

this level. At the lowest CPL of 64 Mm-1 3 , the percentage of days exceeding range from 24 to 

4 97% across the 15 urban areas. 

5 Second, we have reached the preliminary conclusion that the averaging times associated 

6 with the current suite of PM NAAQS are not well suited to protect against PM-related visibility 

7 impairment on the basis that short term exposures (e.g., 1 hour or less) is sufficient for an 

8 unacceptable level of visual air quality to be observed and the associated impacts of that 

9 observation to be registered by the observer. Since some portion of the population may only 

10 have the opportunity to observe one hour or less of ambient daylight visibility conditions, relying 

11 on an averaging time as long as that of the current 24 hour and annual PM standards would make 

12 it difficult to identify a requisite level of protection that would translate into appropriate 

13 protection against the maximum daily value. In addition, these longer averaging times also result 

14 in the inclusion of nighttime conditions, for which the science needed to support identification of 

15 appropriate levels of visibility protection is not well developed or understood. 

16 In reaching the preliminary conclusion that the current suite of PM2.5 standards are 

17 inadequate to provide the appropriate protection of the public welfare from known and/or 

18 anticipated adverse effects by calling into question the adequacy of the current levels and 

19 averaging times, it also seems reasonable to consider whether the current indicator of PM2.5

20 remains useful in relating ambient PM to its public welfare effect of visibility impairment. 

21 Section 4.3 below discusses these and other considerations in its discussion of alternative 

22 standards for consideration. 

23 4.3 CONSIDERATION OF ALTERNATIVE STANDARDS 

24 Having reached the conclusion that just meeting the current suite of PM2.5 standards 

25 continues to allow levels of PM visual air quality that, based on the scientific evidence and 

26 information available in this review, can reasonably be considered adverse to the public welfare, 

27 this section will discuss alternative standards that could potentially provide requisite public 

28 welfare protection from known and/or anticipated adverse effects. Any PM standard that results 

29 in emissions reductions can be expected to result in visibility improvements, though meeting that 

30 standard does not ensure an adequate or uniform degree of protection from adverse visibility 

31 conditions. A requisite level of public welfare protection can be facilitated by adopting a 

32 standard specifically designed with indicator, averaging time and form that better mimics the 

33 characteristics of the effect of interest. 
4-30 

Draft – Do Not Quote or Cite March 2010 

1 4.3.1 Nature of the Indicator 

2  To what extent does information provide support for considering a different 

3 pollution indicator(s) for PM to replace or supplement the PM2.5 mass based 

4 indicator? 

5 EPA staff is considering two alternative indicators: PM2.5 mass and PM light extinction. 

6 PM2.5 mass is taken here to be the same indicator as is used by the current suite of PM NAAQS. 

7 PM light extinction is the contributions to light extinction by PM10 under ambient conditions. 

8 EPA staff believes that the use of PM light extinction as an indicator is justified because it is a 

9 physically meaningful measure of the PM quantity that is most relevant and directly related to 

10 visibility effects. The basis for considering each indicator is discussed below. 

11 PM Light Extinction Indicator

12 PM light extinction is highly related to light extinction, which is the property of the 

13 atmosphere that is most directly related to visibility effects. It differs from light extinction by the 

14 nearly constant contributions for Rayleigh (or clean air) light scattering and the minor 

15 contributions by NO2 light absorption. Most importantly, there are no confounding issues 

16 associated with particle size or composition, including PM water. PM light extinction can be 

17 directly measured under ambient conditions by several instrumental methods, some of which 

18 have been used for decades to routinely monitor the two components of PM light extinction 

19 (light scattering and absorption) or to jointly measure both as total light extinction (from which 

20 Rayleigh scattering is subtracted to get PM light extinction). 

21 EPA staff also recognizes that while PM2.5 light extinction can be accurately measured by 

22 a number of commercially available instruments, it is technically more challenging to measure 

23 the PM10 – 2.5 component of light extinction. This issue many not be of concern for many regions 

24 of the country where the PM10 – 2.5 contributions to light extinction are minor (see UFVA section 

25 3.4.5). However for some regions (e.g. Phoenix), the PM10 – 2.5 contributions to light extinction 

26 are substantial and may need to be accounted for by some other methodology (e.g. estimation 

27 from PM10 – 2.5 mass concentration measurements). As an alternative to direct measurements, 

28 light extinction can be estimated from PM speciation and relative humidity data (see section 4.2). 

29 There are a number of reasons for preferring direct measurements to algorithm-estimates of PM 

30 light extinction for use in a secondary standard. These include the greater accuracy of direct 

31 measurements, the ability to have short averaging times and the overall simplicity absent when 

32 multiple measured parameters need to be processed to generate the indicator for a standard. 

33 There currently is no FRM for PM light extinction monitoring. Development of such an 

34 FRM could take one to two years. There is no routinely operated PM light extinction monitoring 

35 program in urban areas. Deploying such a network will required time and resources. As a result, 
4-31 

Draft – Do Not Quote or Cite March 2010 

1 the selection of PM light extinction as an indicator could reasonably be expected to extend the 

2 time required for promulgation/implementation of a secondary PM NAAQS. 

3 PM2.5 Mass Indicator

4 PM2.5 mass is responsible for most of the visibility impairment in the majority of urban 

5 areas. In these areas, the contribution of PM10 – 2.5 is a minor contributor to visibility impairment 

6 most of the time. However, at some locations (see UFVA Figure 3-13 for Phoenix) PM10 – 2.5 is a 

7 major contributor to urban visibility effects. In those cities, a PM2.5 standard alone may not 

8 provide adequate visibility protection. In the absence of PM air quality information from a much 

9 larger number of urban areas across the country, it is not possible at this time to know how many 

10 urban areas fall into this category, though it is reasonable to presume that other urban areas in the 

11 desert southwestern region of the country may have conditions similar to the conditions shown 

12 for Phoenix. A possible solution to this issue would be to add a companion PM10 – 2.5 standard to 

13 control under those circumstances. This latter refinement has not been developed for this review. 

14 PM mass monitoring methods are in wide spread use, including the Federal Reference 

15 Method (FRM) involving the collection of periodic (1 day in 6 and 1 day in 3) 24-hour filter 

16 samples. These samples are then subsequently analyzed to determine 24-hour PM fine mass. 

17 The Chemical Speciation Network and continuous PM2.5 monitoring produce hourly average 

18 mass concentrations and are conducted at many locations. At a few locations, continuous 

19 speciation sampling produces measures some of the major PM2.5 chemical components. These 

20 routine monitoring activities do not include measurement of the water content of the ambient PM 

21 that contributes, often significantly, to visibility impacts. Further, the PM mass concentration 

22 monitoring does not provide information on the composition of the PM which also contributes to 

23 the variability in the amount of visibility impact associated with any ambient PM mass 

24 concentration. 

25 The overall performance of PM2.5 mass as a predictor of visibility effects as indicated by 

26 PM light extinction can be seen in scatter plots shown in Figure 4.3-1 for Pittsburgh and 

27 Philadelphia, PA (Similar plots for all 15 urban areas are in Appendix D, Figure D-2). These 

28 demonstrate the variation in hourly PM light extinction corresponding to any specific level of 

29 PM2.5 mass concentration as well as statistical differences of the average relationships (depected 

30 as the best fit lines) between cities. While this degree of variation is an important factor in 

31 considering the appropriateness of a PM2.5 mass indicator, we note that correctly identifying each 

32 hour’s visibility conditions is not required to estimate the extent to which the distribution of 

33 visibility conditions may negatively impact public welfare. 
4-32 

Draft – Do Not Quote or Cite March 2010 

1 Figure 4.3-1 Scatter plots of PM light extinction versus PM2.5 mass concentration of two 

2 cities (from UFVA Appendix D, Figure D2). 

3 

4 4.3.2 Averaging and Applicable Times 

5 Consideration of an appropriate averaging time and factors with respect to the timing 

6 over which a secondary standard should apply were informed by consideration of the nature of 

7 PM visibility effects. 

8 Nighttime visibility impacts, described in the ISA (section 9.2.2) are significantly 

9 different from daytime impacts and not sufficiently well understood to be included at this time. 

10 As a result, a secondary standard to protect visibility would best only apply to daylight hours. In 

11 the UFVA daylight hours were defined to be those morning hours having no minutes prior to 

12 local sunrise and afternoon hours having no minutes after local sunset. This definition ensures 

13 the exclusion of periods of time where the sun is not the primary outdoor source of light to 

14 illuminate scenic features. 

15 PM is not necessarily the primary source of visibility impairment during periods with fog 

16 or precipitation. By excluding daylight hours with average relative humidity above 90% for 

17 inclusion in a secondary PM standard, the likely occurrence of visibility effects from fog and 

18 precipitation is significantly reduced (UFVA section 3.3.5 and Appendix G). However not all 

19 periods with relative humidity above 90% have fog or precipitation. So removing those hours 

20 from application of a secondary PM standard involves a tradeoff between the benefits if avoiding 

21 many of the hours with meteorological causes of visibility impacts and not counting some hours 

22 without fog or precipitation, but where the growth of hygroscopic PM to large solution droplets 

23 results in enhanced PM visibility impacts. For the 11 urban areas included in the assessment for 
4-33 

Draft – Do Not Quote or Cite March 2010 

which updated meteorological data was obtained,5 1 a 90% relative humidity cutoff criterion is 

2 effective in that on average less than 6% of the hours are removed from consideration, yet those 

3 hours have on average twelve times the likelihood of meteorological causes of reduced visibility 

4 compared with hours with 90% or lower relative humidity. 

5 As discussed above (section 4.2.1) selection of an appropriate averaging time takes into 

6 account both how quickly people experience and judge visibility conditions, as well as the 

7 typical rate of change of the path averaged PM light extinction over urban areas. While 

8 perception of visibility change can occur in less than a minute, meaningful changes to path 

9 averaged light extinction occur more slowly and can be well represented by hourly averaging. 

10 Multi-hour averaging times would have the effect of reducing the magnitude of hourly peak 

11 visibility impacts which can change significantly from one daylight hour to the next (see UFVA 

12 Figure 3-12). Reduction of peak values through multi-hour averaging reduces the ability of the 

13 indicator to accurately characterize the visibility effects experienced by the segment of the 

14 population that has infrequent short-term exposure during peak periods. 

15 4.3.3 Alternative Levels/Forms 

16 Candidate Protection Levels

17 The results from the visibility preferences studies conducted in four urban areas define a 

18 range of low, middle and high CPLs of 20 dv, 25 dv and 30 dv which are equivalent to PM light 

extinction of values of 64 Mm-1, 112 Mm-1, and 191 Mm-1 19 (see section 4.2 above). With only the 

20 four preference study results, the individual low and high CPL are in fact reflective of the results 

21 from the Denver and Washington, DC studies in particular, and the middle CPL is very near to 

the 50th 22 percentile criteria result from Phoenix. 

23 Determining PM2.5 mass concentration values that correspond to the low, middle and 

24 high CPL is complicated by the lack of a one-to-one relationship between PM light extinction 

25 and PM2.5 mass. By considering a range of extinction efficiency values (i.e., the ratio of PM 

light extinction to PM2.5 mass) from 3 m2/g to 10 m2 26 /g, a range of PM2.5 concentration levels that 

27 crudely corresponds to a low estimate of the low CPL and high estimate of the high CPL values 

can be determined. The full range is from ~6 μg/m3 to ~60 μg/m3 28 . Keeping in mind that there is 

29 no exact one-to-one correspondence between PM mass concentration and PM light extinction, no 

30 individual value in this range of conditions corresponds to the CPL values expressed in terms of 

31 PM light extinction, so a number of alternate values within the range were selected for assessing 

32 their visibility protection performance when combined with alternative forms (as described 

 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 

1 below). Five alternative PM2.5 mass concentration values were selected for this purpose: 10 

μg/m3, 20 μg/m3, 30 μg/m3, 40 μg/m3 and 60 μg/m3 2 . 

3 Alternative Forms

4 The form of the current 24-hour PM2.5 NAAQS entails comparing the level of the 

standard to the three consecutive year average of the annual 98th 5 percentile of the measured 

6 indicator. The purpose in averaging for three years is to provide stability from the occasional 

7 effects of inter-annual meteorological variability that can result in unusual high pollution levels 

8 for a particular year that is otherwise typical. The use of a percentile form makes the standard 

9 less subject to the possibility of inappropriate violations caused by statistical outlier indicator 

10 values. For consistency with the current PM NAAQS and to provide stability from unusual years 

11 or outlier indicator data, the secondary PM standard should consider incorporating the use of a 

12 three year average of a specified percentile. 

13 The urban visibility preference studies that provided results leading to the range of CPLs 

14 being considered in this document, offer no information that addresses the frequency of time that 

15 visibility levels should be below those values. Based on this and the nature of the public welfare 

16 effect being one of aesthetics and/or feelings of wellbeing, we believe that it is not necessary or 

17 appropriate to consider eliminating all such exposures and that allowing some number of 

hours/days with reduced visibility can reasonably be considered. . In the UFVA, 90th, 95th 18 and 

98th 19 percentile annual values are included in the PM light extinction NAAQS scenarios (Chapter 

20 4). The hourly PM mass concentration scenarios that are described and assessed below and in 

Appendix A include only the 90th and 95th percentile forms.6 21 

22 Another aspect of the form that needs to be considered is whether to include all daylight 

23 hours or only the maximum daily daylight 1-hour. The maximum daily daylight 1-hour form is 

24 more appropriate for protecting the welfare of people who have rare intermittent exposure to 

25 visibility during the day (e.g. during commutes), but spend most of their time isolated from 

26 outdoor views. For such people a view of poor visibility during their morning commute may 

27 represent their perception of the day’s visibility conditions until the next time they venture 

28 outside during daylight, hours later or perhaps the next day. Other people have exposure to 

29 visibility conditions throughout the day. For those people it might be more effective to include 

30 every daylight hour into assessing compliance with a standard, since a day with multiple hours 

31 with visibility impairment is likely to be judged a greater impact on their wellbeing than a day 

32 with just one such hour. 

 6

 Assessment of the 98th 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 

1 We do not know the fraction of the public that has only one or a few opportunities to 

2 experience visibility during the day, nor do we have information or studies on the duration of the 

3 effects on wellbeing associated with visibility conditions. However, it is logical that people with 

4 limited opportunities to experience visibility conditions on a daily basis would experience the 

5 entire impact associated with visibility based on their short term exposure. The impact of 

6 visibility for those who have access to visibility conditions often or continuously during the day 

7 may be based on varying conditions throughout the day. Based on these considerations, the 

8 segment of the population with infrequent access to visibility could be characterized as a 

9 susceptible population relative to peak visibility impairment, while those with longer exposures 

10 are a susceptible population for longer-term visibility impairment. 

11 In light of these considerations, the UFVA assessment of the various PM light extinction 

12 scenarios included both forms and noticed a close correspondence between the level of 

13 protection afforded for all 15 urban areas in the assessment by the maximum daily daylight1-

hour with 90th percentile and the all daylight 1-hour with 98th 14 percentile (UFVA section 4.1.4). 

15 In this sense, the reductions in visibility impairment required to meet either form of the standard 

16 provides protection to both the fraction of the public with rare opportunities and to those with 

17 ample opportunities to be affected by PM-related visibility impairment. 

18 Both forms are assessed for the PM light extinction indicator (UFVA), but only the 

19 maximum daily form is assessed for the PM mass concentration indicator (below and Appendix 

20 A). For consistency between the two indicators and because the daily maximum daylight 1-hour 

21 is thought to be more protective of those with limited opportunities to experience visibility, only 

22 the daily maximum form results will be displayed here. 

23 4.3.4 Performance of Alternative Standards 

24 We conducted assessments of alternative standards based both on hourly PM light 

25 extinction as the indicator (see Chapter 4 of the UFVA) and on hourly PM mass concentration 

26 indicator (see Appendix A in this document). There are nine PM light extinction alternative 

27 standards discussed here (i.e., daily maximum daylight 1-hour PM light extinction at the low, 

middle and high CPL for each of the 90th, 95th and 98th 28 percentile forms) and there are ten PM2.5

mass concentration alternative standards (i.e., five concentration levels for each of the 90th 29 and 

95th 30 percentile forms). In both cases the assessment involves rolling back non-policy relevant 

31 background (PRB) PM light extinction or PM mass concentration values until these specific 

32 alternative standards are just met. 

33 In considering the performance of alternative standards, we focused on the uniformity 

34 across the 15 urban areas of the resulting visibility conditions, as measured in terms of light 

35 extinction, when the alternative scenarios are just met. Because of the one-to-one 
4-36 

Draft – Do Not Quote or Cite March 2010 

correspondence light extinction and PM light extinction,7 1 the PM light extinction indicator based 

2 standards should produce visibility conditions exactly as prescribed. The ability to structure a 

3 PM light extinction based alternative standard to the level of visibility protection desired is an 

4 advantage because it could affords the most uniform degree of visibility protection nationwide. 

5 Figures similar to 4.3-1 for the other PM light extinction scenarios are shown in 

6 Appendix F of the UFVA. Table 4.3-1 shows the design values for the 9 scenarios based on 

7 maximum daily 1-hour PM light extinction. When an area just meets a scenario, its design value 

8 in principle should exactly equal the NAAQS level, so preparation of this table serves as a check 

9 against calculation errors. Note that the design values in Table 4.3-1, resulting from the rollback 

10 steps described in section 4.1.4 of the UFVA, in some cases do not exactly equal the assumed 

level of the NAAQS, although all are quite close. In some cases (e.g. Phoenix for 191 Mm-1/90th 11 

and 95th 12 percentile), current conditions already meet the scenario specifications so no rollback 

13 was necessary and current design values are shown in Table 4.3-1 and reflected in box and 

14 whisker plot figures. The minor differences between prescribed and assessed design values seen 

15 for some applications of the rollback assessment are due to hours switching in the PM light 

16 extinction frequency distribution that is purely an artifact of the rollback methodology as 

17 described in the UFVA (section 4.3). These discrepancies were judged too small to justify 

18 iterative rollback that could have been used to eliminate them. 

 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 

2 Figure 4.3-2 Daily maximum daylight 1-hour light extinction after rollback to just meet a 

scenario with daily maximum of 112 Mm-1 for the 90th 3 percentile excluding 

4 hours with relative humidity greater than 90 percent. 

5 

6 

7 
4-38 

Draft – Do Not Quote or Cite March 2010 

1 

2 Table 4.3-1. PM light extinction design values for “just meeting” secondary NAAQS 

3 scenarios based on measured PM light extinction (excluding hours with 

4 relative humidity greater than 90 percent) 

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 90th 95th 98th 90th 95th 98th 90th 95th 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 

6 
4-39 

Draft – Do Not Quote or Cite March 2010 

1 A complete description of the rollback assessment for the ten maximum daily 1-hour PM 

2 mass concentration scenarios is available in Appendix A of this document. The process used is 

3 very similar to that used in the UFVA for rollback of the PM light extinction based scenarios. 

4 Since PM mass does not have a one-to-one correspondence to light extinction, the PM 

5 light extinction conditions resulting from just meeting standards based on PM mass are not as 

6 uniform as those shown above for PM light extinction scenarios. This is demonstrated in the box 

and whisker plot of the maximum daily 1-hour PM light extinction for the 30 μg/m3

, 90th 7 

8 percentile scenario shown below (Figure 4.3-2), which shows greater variation from among the 

9 urban areas than the PM light extinction based scenarios. Similar plots for all ten PM mass 

10 based scenarios are shown in Appendix A (Figure A-2). 

11 

12 Figure 4.3-3 Maximum daily daylight 1-hour PM light extinction under "just meet" 

conditions for a NAAQS scenario based on 1-hour PM2.5 mass of 30 μg/m3 13 , 

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

15 

16 
4-40 

Draft – Do Not Quote or Cite March 2010 

The 90th percentile PM light extinction design values corresponding to the 90th 1 percentile 

2 PM mass concentration based scenarios for the five mass concentration levels are shown in Table 

3 4.3-2. Values in the table that exceed each of the CPL values are highlighted using different 

4 colors. The values in the table are the same for some urban areas for the less restrictive PM mass 

concentration standard (e.g. Tacoma at 60 μg/m3 and 40 μg/m3, or Phoenix at 60 μg/m3 5 , 40 

μg/m3, 30 μg/m3 and 20 μg/m3 6 ), because those areas required no rollback to meet the less 

7 restrictive PM mass concentration standards. In order for most or all urban areas to achieve even 

the highest CPL at the 90th percentile, a PM2.5 mass based standard set below 40 μg/m3 8 would be 

necessary. The higher PM2.5 mass levels of 60 μg/m3 and 40 μg/m3 9 clearly are not sufficiently 

10 protective, since they permit 11 and 10 of the 15 areas, respectively, to have design values larger 

than 191 Mm-1. At the 20 μg/m3 11 PM2.5 standard level, all areas meet the highest CPL 

benchmark, except for St. Louis, which doesn’t attain the highest CPL even when a 10 μg/m3 12 

13 standard is imposed. We believe that this latter case may have occurred because the coarse mass 

data in St. Louis may not be representative of the metropolitan area.8

 The 30 μg/m3 14 standard is 

15 marginally above the high CPL at three cities and only exceeds it substantially at St. Louis. 

 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 90th percentile maximum daily 1-hour PM light extinction design values (Mm- 1 

1

) after rollback to meet alternative standard of 60 μg/m3, 40 μg/m3, 30 μg/m3 2 ,20 

μg/m3 and 10 μg/m3 3 maximum daylight 1-hour PM mass concentration for the 

4 90th percentile.* 

5 

60 μg/m3 40 μg/m3 30 μg/m3 20 μg/m3 10 μg/m3

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 

7 *Colored highlighting shows which of the CPL levels the values are near, using the 

following definitions: PM light extinction equal or above the high CPL >191 Mm-1 8 ; above the 

middle CPL, 112 Mm-1 – 190 Mm-1; above the low CPL, 64 Mm-1 – 111 Mm-1 9 ; below the low 

CPL, < 64 Mm-1 10 . Values without color highlighting indicate no rollback, so no information 

11 about the effectiveness of the hourly PM mass based alternative standards

12 

Aside from St. Louis, the range of 90th 13 percentile PM light extinction design levels 

resulting from rollback to just meet a 90th percentile 20 μg/m3 14 PM mass concentration is from 98 

Mm-1 for Philadelphia to 156 Mm-1 15 for Los Angeles with most values near the middle CPL value 

of 112 Mm-1. A similar range, excluding St. Louis for the 30 μg/m3 16 PM mass concentration is 

from 134 Mm-1 to 220 Mm-1 17 for the same two cities. This demonstrates the amount of variability 

18 in visibility conditions that would likely result from using a standard with PM mass 

19 concentration instead of PM light extinction as the indicator. While this degree of variation is 

20 not particularly large, it does mean that some areas would be required to further control 

21 emissions to meet a secondary standard though they have visibility conditions that are as good or 

22 better than other areas which meet the PM mass based standard. Some measure of the extent to 
4-42 

Draft – Do Not Quote or Cite March 2010 

1 which this occurs may be gained by comparing the percent rollback values required to meet the 

2 various PM mass and PM light extinction values. 

3 Based on inspection of the design values shown in Table 4.3-2, among the PM2.5 mass 

concentration levels that were assessed, 30 μg/m3 4 provides protection most comparable to the 

high CPL (191 Mm-1), 20 μg/m3 5 provides protection most comparable to the middle CPL (112 

Mm-1) and 10 μg/m3 provides protection most comparable to the low CPL (64 Mm-1 6 ). 

7 Care must be taken to avoid misinterpretation of this suggestion of approximate 

8 comparability of protection afforded the various urban areas by PM mass at the three 

concentration levels in terms of the three CPLs. The values in Table 4.3-2 are the 90th 9 percentile 

10 values of the PM light extinction distribution that results from transforming the hourly PM mass 

11 and composition values of the rolled back PM distributions for each urban area. Hours with 

values above the 90th 12 percentile of PM mass do not necessarily have PM light extinction above 

the 90th 13 percentile and visa versa. As discussed earlier (section 4.3.1) for any individual hourly 

14 PM mass concentration there is a substantial range of corresponding PM light extinction values 

15 possible. However when used as the indicator for a secondary PM standard, hourly PM2.5 mass 

16 need only predict the response of the distribution of hourly visibility conditions to produce 

17 requisite levels of protection for visibility welfare effects.

18 4.4 PRELIMINARY STAFF CONCLUSIONS ON ALTERNATIVE SECONDARY PM 

19 STANDARDS FOR VISIBILITY-RELATED EFFECTS 

20 In reaching preliminary conclusions on potential alternative standards to provide 

21 requisite protection of PM-related visibility impairment, staff has considered the basic elements 

22 of the NAAQS: indicator, averaging time, form and level. In considering the scientific and 

23 technical information, we reflect upon the information available in the last review integrated with 

24 information that is newly available since the last review as assessed and presented in the ISA and 

25 the second draft UFVA (US EPA, 2010b) and as summarized in sections 4.2, 4.3, and Appendix 

26 A. 

27 As outlined in section 4.1.3, in this review we emphasize a policy approach that broadens 

28 the general approaches used in the last two PM NAAQS reviews by utilizing, to the extent 

29 available, enhanced tools, methods, and data to more comprehensively characterize visibility 

30 impacts. As such, we take into account both evidence-based and impact assessment-based 

31 considerations to inform our conclusions related to the adequacy of the current PM2.5 secondary 

32 standards and alternative standards that are appropriate for consideration in this review. In so 

33 doing, we are seeking to provide as broad an array of options as is supportable by the available 

34 information, recognizing that the selection of a specific approach to reaching final decisions on 

35 the secondary PM standards for protection from PM-related visibility impairment will reflect the 
4-43 

Draft – Do Not Quote or Cite March 2010 

1 judgments of the Administrator as to what weight to place on the various approaches and types 

2 of information presented in the final PA. 

3 In presenting our preliminary conclusions regarding alternative secondary standards and 

4 ranges of levels for consideration, we summarize conclusions presented in sections 4.3.1 through 

5 4.3.4. We emphasize that these are preliminary conclusions that reflect consideration of the 

6 scientific and technical information assessed and presented in the ISA and second draft UFVA 

7 (US EPA, 2009a; US EPA, 2010b). We note that staff conclusions to be presented in the final 

8 UFVA and second draft PA will be based, in part, on input received from CASAC and the public 

9 on the second draft UFVAA and this first draft PA. 

10 We recognize that selecting from among alternative standards will necessarily reflect 

11 consideration of the qualitative and quantitative uncertainties inherent in the relevant evidence 

12 and in the assumptions that underlie the quantitative visibility impact assessment. In identifying 

13 these alternative secondary standards and ranges of levels for consideration, we are mindful that 

14 the Clean Air Act requires standards to be set that are requisite to protect public welfare from 

15 any known or anticipated adverse effects, such that the standards are to be neither more nor less 

16 stringent than necessary. Thus, the Act does not require that the NAAQS be set at zero-risk 

17 levels, but rather at levels that avoid unacceptable risks to public welfare. 

18 

19 ( 1)Consideration should be given to revising the current suite of PM2.5 secondary standards 

20 to provide increased public welfare protection from PM-related visibility impairment, 

21 primarily in urban areas. This preliminary conclusion is based in general on the 

22 evaluation in the ISA of the currently available information, including a more extensive 

23 characterization of the sources contributing to visibility impairment in both rural and 

24 urban locations, a refined understanding of the contributions of various PM components 

25 in such areas, exposure-related evidence supporting a causal relationship between 

26 ambient PM and impaired VAQ, and more specifically, on the evidence that a significant 

27 number of days with levels of VAQ that could reasonably be considered unacceptable 

28 based on the preference studies would continue to occur in areas where the current 

29 standards were met, together with judgments as to the public welfare significance of these 

30 occurrences upon just meeting the current suite of PM2.5 standards. 

31 

32 ( 2)With regard to indicator, consideration should be given to establishing a new PM light 

33 extinction indicator; alternatively, consideration can be given to retaining the current 

34 PM2.5 indicator. This preliminary conclusion takes into consideration the available 

35 evidence that demonstrates a one-to-one correspondence between measured ambient PM 

36 light extinction and PM-related visibility impairment as well as the significant degree of 

37 variability in visibility protection across the U.S. allowed by a PM2.5 indicator, while also 
4-44 

Draft – Do Not Quote or Cite March 2010 

1 recognizing that either indicator could be used as a basis for a standard that could provide 

2 appropriate protection from PM-related visibility impairment. 

3 

4 ( 3)With regard to averaging time, consideration should be given to selecting an alternative 

5 averaging time for a secondary PM standard to protect against daytime PM-related 

6 visibility impairment that takes into account the short term (instantaneous) nature of the 

7 perception of visibility impairment, short term variability in PM-related VAQ (partial 

8 hour to hourly), and the short-term nature of relevant exposure periods for the viewing 

9 public (partial hour to multiple hours). Recognizing that the current 24-hour and annual 

10 averaging times do not appropriately reflect these exposure characteristics, consideration 

11 should be given to a one-hour averaging time based on the maximum hour in the daylight 

12 period or on all daylight hours. 

13 

14 ( 4)In conjunction with considering a 1-hour averaging time, consideration should be given 

to a form defined in terms of the 90th, 95th or 98th 15 percentile of the distribution of 1-hour 

16 PM light extinction or PM2.5 concentrations, averaged over three years. We believe it is 

17 appropriate to consider allowing some number of days/hours with visibility impairment 

above the target level of protection, such that consideration of the 90th or 95th 18 percentile 

19 forms is appropriate. In addition, consideration should be given to applying a 90% 

20 relative humidity screen to remove hours in which fog or precipitation is much more 

21 likely to contribute to the observed visibility impairment. 

22 

23 ( 5)Consideration should be given to selecting a target level in terms of PM light extinction. 

24 Further, consideration should be given to alternative candidate levels, with a particular 

focus on a level of 112 Mm-1 as well as levels down to 64 Mm-1 and up to 191 Mm-1 25 to 

26 provide appropriate protection against PM-related visibility impairment. Based on the 

27 assessment conducted in this review, we judge that a reasonably consistent 

28 correspondence exists between these PM light extinction benchmark levels and PM2.5

mass concentrations, with a particular focus on a level of 10 μg/m3 29 as well as levels down 

to 20 μg/m3 and up to 30 μg/m3. 30 , which would be appropriate to consider in conjunction 

31 with consideration of a PM2.5 indicator. 

32 

33 ( 6)Consideration should be given to the following alternative secondary PM standards to 

34 provide protection against PM-related visibility impairment during daylight hours: 

35 

36 (a) Consideration of a new 1-hour daily maximum PM light extinction standard set at a 

level within the range of 64 to 191 Mm-1 (e.g. 20 – 30 deciviews (dv)) with a 90th 37 or 

95th 38 percentile form. 

39 
4-45 

Draft – Do Not Quote or Cite March 2010 

1 (b) Consideration of a revised 1-hour daily maximum PM2.5 standard set at a level within 

the range of 10 to 30 μg/m3 with a 90th or 95th 2 percentile form. 

3 

4 (c) Alternatively, consideration could also be given to a standard based on all daylight 

hours with either indicator, in conjunction with consideration of a 98th 5 percentile 

6 form. 

7 

8 

9 4.5 REFERENCES 

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

11 BBC Research & Consulting. (2003), Phoenix Area Visibility Survey. Draft Report.. Available: 

12 http://www.azdeq.gov/environ/air/download/vis_021903f.pdf. Accessed 9/16/2008 

13 Henderson, R. (2005a). EPA’s Review of the National Ambient Air Quality Standards for Particulate Matter 

14 (Second Draft PM Staff Paper, January 2005): A review by the Particulate Matter Review Panel of the EPA 

15 Clean Air Scientific Advisory Committee. June 6, 2005. Available: http://www.epa.gov/sab/pdf/casac-05-

16 007.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 Recommendations Concerning the Final National Ambient Air 

20 Quality Standards for Particulate Matter. September 29, 2006. Available: 

21 http://www.epa.gov/sab/pdf/casac-ltr-06-002.pdf

22 Ely DW; Leary JT; Stewart TR; Ross DM (1991). The establishment of the Denver Visibility Standard. Presented at 

23 Presented at: 84th annual meeting & exhibition of the Air & Waste Management Association; June; 

24 Vancouver, British Columbia. Pittsburgh, PA: Air & Waste Management Association; paper no. 91-48.4. 

25 Malm, W.C., Sisler, J.F., Huffman, D., Eldred, R.A., Cahill, T.A. (1994) Spatial and Seasonal Trends in Particle 

26 Concentration and Optical Extinction in the United States, Journal of Geophysical Research (Atmospheres) 

27 99:1347-1370. 

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

29 2716. 

30 Smith, A. (2009). Comments on the First External Review Draft of EPA’s “Integrated Science Assessment for 

31 Particulate Matter.” CRA Internation. Washington, DC. March 30. Prepared for the Utility Air Regulatory 

32 Group,. Submitted as public comments to the public meeting EPA Clean Air Science Advisory Council. 

33 April 2. 

34 Smith AE; Howell S (2009). An assessment of the robustness of visual air quality preference study results. CRA 

35 International. Washington, 

36 DC.http://yosemite.epa.gov/sab/sabproduct.nsf/B55911DF9796E5E385257592006FB737/$File/CRA+VA

37 Q+Pref+Robustness+Study+3+30+09+final.pdf. 

38 US EPA (2005). Review of the National Ambient Air Quality Standards for Particulate Matter: Policy Assessment 

39 of Scientific and Technical Information, OAQPS Staff Paper. Research Triangle Park, NC 27711: Office 

40 of Air Quality Planning and Standards; report no. EPA EPA-452/R-05-005a. December 2005. Available: 

41 http://www.epa.gov/ttn/naaqs/standards/pm/s_pm_cr_sp.html
4-46 

Draft – Do Not Quote or Cite March 2010 

1 US EPA (2008a). Integrated Review Plan for the National Ambient Air Quality Standards for Particulate Matter. 

2 National Center for Environmental Assessment and Office of Air Quality Planning and Standards, U.S. 

3 Environmental Protection Agency, Research Triangle Park, NC. Report No. EPA 452/R-08-004. March 

4 2008. Available at: http://www.epa.gov/ttn/naaqs/standards/pm/s_pm_2007_pd.html. 

5 US EPA (2009a). Integrated Science Assessment for Particulate Matter: Final Report. National Center for 

6 Environmental Assessment-RTP Division, Office of Air Quality Planning and Standards, Research 

7 Triangle Park, NC. EPA/600/R-08/139F. December 2009. Available: 

8 http://www.epa.gov/ttn/naaqs/standards/pm/s_pm_2007_isa.html. 

9 US EPA (2009b). Integrated Science Assessment for Particulate Matter: Second External Review Draft. National 

10 Center for Environmental Assessment-RTP Division, Office of Air Quality Planning and Standards, 

11 Research Triangle Park, NC. EPA/600/R-08/139B. July 2009. Available: 

12 http://www.epa.gov/ttn/naaqs/standards/pm/s_pm_2007_isa.html. 

13 US EPA (2009d). Particulate Matter National Ambient Air Quality Standards: Scope and Methods Plan for Urban 

14 Visibility Impact Assessment. Office of Air Quality Planning and Standards, U.S. Environmental 

15 Protection Agency, Research Triangle Park, NC. EPA-452/P-09-001. February 2009. Available: 

16 http://www.epa.gov/ttn/naaqs/standards/pm/s_pm_2007_pd.html. 

17 US EPA (2009f). Particulate Matter Urban-Focused Visibility Assessment – External Review Draft. Office of Air 

18 Quality Planning and Standards, U.S. Environmental Protection Agency, Research Triangle Park, NC. 

19 EPA-452/P-09-005. September 2009. Available: 

20 http://www.epa.gov/ttn/naaqs/standards/pm/s_pm_2007_risk.html. 

21 US EPA (2010b). Particulate Matter Urban-Focused Visibility Assessment – Second External Review Draft. Office 

22 of Air Quality Planning and Standards, U.S. Environmental Protection Agency, Research Triangle Park, 

23 NC. EPA-452/P-10-002. January 2010. Available: 

24 http://www.epa.gov/ttn/naaqs/standards/pm/s_pm_2007_risk.html.
Draft – Do Not Quote or Cite A-1 March 2010 

1 Appendix A

2 

3 Information Regarding the 1-hour PM2.5 Mass Indicator 

4 

5 This Appendix presents information on 2005-2007 levels of 1-hour PM2.5 mass 

6 concentrations in the 15 urban study areas and on the “what if” PM light extinction conditions 

7 that would exist if the study areas met each of 10 alternative secondary PM NAAQS scenarios 

8 based on a 1-hour PM2.5 mass indicator. With respect to the latter subject, this Appendix is 

9 therefore similar to Chapter 4 of the Particulate Matter Urban-Focused Visibility Assessment 

10 (UFVA), which presented similar information for 18 secondary PM NAAQS scenarios based on 

11 PM light extinction as the indicator, for the current annual and 24-hour PM2.5 NAAQS, and for a 

scenario with an annual NAAQS of 12 μg/m3

 and a 24-hour NAAQS of 25 μg/m3 12 . 

13 

14 1.0 Indicator and Monitoring Method 

15 

16 As in Chapter 4 of the PM UFVA, this Appendix excludes from all NAAQS scenarios and 

17 results all non-daylight hours and all daylight hours with relative humidity greater than 90 

18 percent. This applies to both the definition of 10 secondary NAAQS scenarios, and to graphics 

19 and tables that characterize ambient conditions. While ambient humidity should not affect 

20 conventional measurement approaches for 1-hour PM2.5 mass, the issue of co-occurrence of high 

21 humidity levels with light extinction due to natural conditions would still apply. See section 3.3.5 

22 of the UFVA. The assumed hours of daylight are the same as those used in the UFVA, as shown 

23 in Table 3-5 of the UFVA. 

24 

25 All values for 1-hour PM2.5 mass concentration in this appendix come from the continuous 

26 instruments at the 15 urban study sites, with no adjustment to make these values consistent with 

27 the collocated 24-hour FRM measurement of PM2.5 mass. Appendix A of the UFVA provides 

28 details on the type of continuous instrument at each study site. TEOMs were used at all sites 

29 except for beta attenuation instruments in Fresno and Philadelphia, nephelometer instruments in 

30 Tacoma and Phoenix, and an FDMS instrument in Salt Lake City. 

31 

32 For conciseness in this first public review draft, only the daily maximum daylight 1-hour 

33 PM2.5 mass concentration indicator is considered in this Appendix. It would also be possible to 

34 construct alternative NAAQS scenarios of an all-hours type, which could be analyzed in the 

35 same manner as presented in this Appendix. 

36 

37 2.0 Current Conditions of 1-hour PM2.5 Mass 

38 

39 Figure A-1 is a box plot of 2005-2007 daily maximum daylight 1-hour PM2.5 mass 

40 concentrations for the 15 study areas, excluding hours with relative humidity greater than 90 

41 percent, to give a sense of the range and central tendency of this parameter. The horizontal 

reference lines are at 10, 20, 30, 40 and 60 μg/m3

.

 42 The relative positions of the 90 percentile 

43 concentrations (indicated by the horizontal stroke at the top of the whisker) are generally 

44 consistent with the relative ranking of these sites according to their design values for the 24-hour 
Draft – Do Not Quote or Cite A-2 March 2010 

1 PM2.5 NAAQS (see Table 3-2 of the UFVA); similarly, the relative positions of the median 

2 concentrations are generally consistent with the annual PM2.5 design values. Table A-1, based on 

3 the same data as Figure A-1, presents the percentage of days in 2005-2007 on which the daily 

4 maximum daylight 1-hour PM2.5 concentration exceeded the reference levels represented by the 

5 horizontal lines in Figure A-1. 

6 

Figure A-1. 2005-2007 daily maximum daylight 1-hour PM2.5 mass concentrations (μg/m3 7 ) 

8 for the 15 study areas (excluding hours with relative humidity greater than 90 percent) 

9 

10 

11 

12 

13 

14 

15 

16 

17 

18 

19 

20 

21 

22 
Draft – Do Not Quote or Cite A-3 March 2010 

1 Table A-1. Percentage of days with daily maximum daylight 1-hour PM2.5 mass 

2 concentration exceeding reference levels in 2005-2007 (excluding hour with relative 

3 humidity greater than 90 percent) 

4 

1-hour PM2.5 Mass Reference Level (μg/m3) 

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 

5 
Draft – Do Not Quote or Cite A-4 March 2010 

1 3.0 Alternative NAAQS Scenarios Based on 1-hour PM2.5 Mass as the Indicator 

2 

3 To ensure examination of a wide enough range of alternative standards based on 1-hour 

4 PM2.5 mass to encompass the range of standards that might be considered as alternatives to the 

5 PM light extinction NAAQS scenarios examined in Chapter 4 of the UFVA, we considered 

levels of 10, 20, 30, 40, and 60 μg/m3 6 . Only the daily maximum daylight hour form was 

7 considered. Each level was combined with two statistical forms: the three-year average of the 

annual 90th percentile value and the three-year average of the annual 95th 8 percentile value. For 

9 ease of reference, these scenarios are designated by letters from “aa” to “jj” and listed in Table 

10 A-2. Looking somewhat ahead to results presented below, the scenarios are arranged in Table 

11 A-2 in order of least to most stringent in terms of the reductions in ambient PM2.5 needed from 

12 current levels to meet the current and alternative NAAQS levels and forms. 

13 

14 Table A-2. Alternative NAAQS scenarios based on daily maximum daylight 1-hour PM2.5

15 mass, averaged over three years (excluding hours with relative humidity greater than 90 

16 percent) 

17 

NAAQS Scenario Level (μg/m3) Statistical Form 

aa 60 3-year average of 90th percentile 

bb 60 3-year average of 95th percentile 

cc 40 3-year average of 90th percentile 

dd 40 3-year average of 95th percentile 

ee 30 3-year average of 90th percentile 

ff 30 3-year average of 95th percentile 

gg 20 3-year average of 90th percentile 

hh 20 3-year average of 95th percentile 

ii 10 3-year average of 90th percentile 

jj 10 3-year average of 95th percentile 

18 

19 

20 4.0 Approach to Modeling “What If” Conditions of PM Light Extinction for Alternative 

21 Secondary NAAQS Based on 1-hour PM2.5 Mass 

22 

23 Before modeling “what if” conditions, we augmented the data set described in Table 4 of the 

24 UFVA in the same manner as described in Section 4.1.4 of the UFVA, to achieve seasonal 

25 balance despite the lack of monitoring data for one quarter in each of Houston and Phoenix. In 

26 Tacoma and Phoenix, which had data only for two years in the 2005-2007 period, we averaged 

27 the percentile values from the only two available years rather than the three years defined for the 

28 statistical form of the NAAQS scenarios. 

29 

30 The modeling of daily maximum daylight 1-hour PM2.5 mass under each of the scenarios 

31 listed in Table A-2 used a rollback approach that combined relevant concepts and steps from the 

32 rollback methods described in sections 4.1.4 (for PM light extinction scenarios) and 4.2.2 (for 

33 scenarios based on annual average and 24-hour average PM2.5) of the UFVA. The following are 

34 the steps in the modeling. 

35 

1. Identify the 90th 36 percentile daily maximum daylight 1-hour PM2.5 mass value in each of 2005, 

37 2006, and 2007 for a study area. Average these to determine the design value for that percentile 
Draft – Do Not Quote or Cite A-5 March 2010 

form. Repeat for the 95th 1 percentile form. These design values are presented in Table A-3. 

They range from 22 to 81 μg/m3 2 indicating that some study areas meet some of the NAAQS 

3 scenarios under current conditions. In such cases, PM2.5 concentrations were not adjusted, i.e., 

4 there was no “roll up” for any area in any scenario. 

5 

2. Using the same days and hours as contributed by the three annual 90th 6 percentile values for 

7 actual 1-hour PM2.5 mass, find the three corresponding values of policy relevant background 

8 (PRB) 1-hour PM2.5 mass. Average these three annual values of PRB 1-hour PM2.5 to obtain the 

PRB portion of the actual 1-hour PM2.5 design value for the 90th 9 percentile form. Repeat for the 

95th 10 percentile form. 

11 

12 In the modeling for the NAAQS scenarios examined in the UFVA, PRB for 1-hour PM2.5

13 mass was not explicitly calculated because it was not needed in the rollback modeling for the 

14 scenarios addressed in the UFVA. Therefore, it was necessary to reconstruct this parameter by 

15 adding the values for the PRB concentrations of the five components of PM2.5: nitrate, sulfate, 

16 elemental carbon, organic carbon material, and soil. The method for estimating PRB for these 

17 five components is described in Appendix C of the UFVA.9 

18 

19 3. Subtract the value from step 2 from the value from step 1, to determine the non-PRB portion 

20 of the 1-hour PM2.5 mass design value. 

21 

22 4. Calculate the percentage reduction required in non-PRB 1-hour PM2.5 mass in order to reduce 

23 the design value to the level that defines the NAAQS scenario, using the following equation: 

24 

25 Percent reduction required = 1 – (NAAQS level – PRB portion of the design value)/(non-PRB 

26 portion of the design value) 

27 

28 The percentage reductions determined in step 4 are shown in Table A-4. Note that for some 

29 combinations of area and scenario no reduction is required because the 2005-2007 design value 

30 already meets the NAAQS scenario. 

31 

32 5. Turning to the entire set of day/hour-specific actual and PRB daylight 1-hour concentrations 

33 of the five PM2.5 components for the three (or two) year period, determine the non-PRB portion 

34 of each of the five components in an hour by subtracting the PRB value from actual value, 

35 reduce it by the percentage determined in step 4, and add back in the PRB 1-hour concentration 

36 of the component. 

37 

38 6. Finally, re-construct PM light extinction using the reduced values of the five components, the 

39 original value of 1-hour PM10-2.5, and the 1-hour value of f(RH), according to the following 

40 equation for PM light extinction (see section 3.2.3 of the UFVA for an explanation of the 

41 variables in this equation). 

42 

 9

 Table C-1 of the UFVA presents the annual average of all daylight hour PRB PM2.5 mass. The 90th and 95th

percentile values of daily maximum PRB PM2.5 mass were of course higher than shown in that table. 
Draft – Do Not Quote or Cite A-6 March 2010 

1 bextPM = 3 x f(RH) x [Sulfate] 

2 + 3 x f (RH) x [Nitrate] 

3 + 4 x [Organic Mass] 

4 +10 x [Elemental Carbon] 

5 + 1 x [Fine Soil] 

6 + 0.6 x [Coarse Mass] 

7 

8 These steps assume that in order to meet a PM NAAQS scenario based on 1-hour PM2.5 as 

9 the indicator, each component of PM2.5 is reduced by an equal percentage, across the five 

10 components and across all hours. In actual implementation of such a NAAQS, each state would 

11 develop an attainment strategy, which might result in unequal percentage reductions of the 

12 components. If the strategy emphasized reductions in the fine soil component, for example, PM 

13 light extinction levels would remain high relative to those estimated by these steps, because fine 

14 soil is not efficient in terms of reducing visibility compared to the other four components on a 

15 dry mass-to-mass basis. On the other hand, a strategy that involves relatively large reductions in 

16 sulfate or nitrate would achieve greater reductions in PM light extinction than estimated by these 

17 steps. The uncertainty in how the results of this rollback method compare to the results of actual 

18 attainment strategies should be kept in mind when comparing the results of “what if” scenarios 

19 for NAAQS based on PM2.5 mass as the indicator versus scenarios based on PM light extinction. 

20 Unlike the effect of humidity variation between areas, this source of uncertainty is not reflected 

21 in any of the results presented in this Appendix and will not be apparent in comparisons of 

22 results in this Appendix to results presented in the PM UFVA for NAAQS scenarios based on 

23 PM light extinction. 

24 

25 These steps also assume no change in PM10-2.5 concentrations between current conditions and 

26 “what if” conditions. While reductions in PM10-2.5 would not be needed to meet a secondary 

27 NAAQS based on 1-hour PM2.5 mass, it is possible that strategies to control PM2.5 concentrations 

28 might also achieve reductions in PM10-2.5 concentrations because some source emit both and 

29 some control methods achieve some reductions in both. However, in most of the 15 study areas, 

30 PM10-2.5 makes a small contribution to estimated PM light extinction, in part because in many of 

31 the areas no local data on PM10-2.5 concentrations were available and the method used to fill this 

32 gap (application of a factor to PM2.5 concentration) simply could not produce a high estimate of 

33 PM10-2.5. 
Draft – Do Not Quote or Cite A-7 March 2010 

Table A-3. 2005-2007 design values for 1-hour PM2.5 mass (μg/m3 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 

5 Table A-4. Percentage reductions in non-PRB PM2.5 components required to meet NAAQS 

6 scenarios based on 1-hour PM2.5 mass 

7 

Scenario aa bb cc dd ee ff gg hh ii jj 

Level (μg/m3 ) 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 

9 
Draft – Do Not Quote or Cite A-8 March 2010 

1 5.0. 1-hour PM2.5 Mass Results for “Just Meeting” Alternative Secondary NAAQS 

2 Scenarios Based on 1-hour PM2.5 Mass 

3 

4 As a check on the reasonableness of the rollback method described in section 4.0 and on the 

5 accuracy of the code used to implement it, it is of interest to examine the distribution of the 

6 levels of 1-hour PM2.5 that result from the method. Ideally, after rollback any area that had a 

7 non-zero required reduction should have a post-rollback design value for 1-hour PM2.5 mass that 

8 is exactly equal to the target design value. Also, there should be a progression of reductions in 1-

9 hour PM2.5 medians and other percentile points on the distribution as progressively more 

10 stringent scenarios are modeled. 

11 

12 Table A-5 shows the post-rollback 1-hour PM2.5 mass design values for the scenarios, with 

13 percentile forms matched. Design values for area-scenario combinations for which the required 

14 reductions were zero have been omitted, because the current conditions design values for these 

15 combinations would not be expected to reflect the target design value. It can be seen that the 

16 design values progress as expected and are in the vicinity of the target design values, but are not 

17 always exactly equal to the targets. EPA staff attributes this to the fact that PRB concentrations 

18 of 1-hour PM2.5 mass vary from hour to hour. It is possible for the daily maximum PM2.5 mass 

concentration on a certain day in 2005 with a percentile rank of, for example, 96th 19 to have a 

20 relatively small PRB portion and a large non-PRB portion compared to the daily maximum 

concentration that ranks 95th 21 . When an equal reduction is made to the non-PRB portion of each 

22 total concentration, the two values may switch rank positions, and so a new day and hour 

23 becomes the 2005 contributor to the rolled back three-year design value. Since this day and hour 

24 was not used to determine the required percentage reduction, the resulting design value will not 

25 exactly meet the target design value. It would be possible to iterate with higher and lower 

26 percentage reductions until the rolled back design value exactly matched the target design value, 

27 but EPA considered this degree of refinement to be unnecessary in order to meet the objectives 

28 of the Policy Assessment Document, given other uncertainties in the underlying data and in the 

29 assumptions used to estimate PM light extinction values. 

30 

31 EPA staff also generated and examined box plots of daily maximum daylight 1-hour PM2.5 mass 

32 concentrations as a check for conceptual or programming, and found them to match expectations. 

33 They are not included here, for conciseness.
Draft – Do Not Quote or Cite A-9 March 2010 

1 Table A-5. Post-rollback design values for daily maximum 1-hour PM2.5 mass. Design 

2 values are shown only for combinations of study area and scenario for which the study area 

3 does not meet the scenario under current conditions, such that reductions were made 

4 during the rollback modeling.

5 

Scenario aa bb cc dd ee ff gg hh ii jj 

Level (μg/m3 ) 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/m3 ) (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 

8 6.0 PM Light Extinction Results for “Just Meeting” Alternative Secondary NAAQS 

9 Scenarios Based on 1-hour PM2.5 Mass 

10 

11 The rollback steps described in section 4.0 resulted in estimates of PM light extinction for 

12 each day and hour in each study area, for each of the 10 NAAQS scenarios based on 1-hour 

13 PM2.5 mass as the indicator. Two summaries of these conditions are presented here. 

14 

15 Figure A-2 presents a box plot of daily maximum daylight 1-hour PM light extinction for 

16 each NAAQS scenario based on 1-hour PM2.5 mass. These can be compared to Figure 3-8(a) of 

17 the UFVA representing pre-rollback daily maximum PM light extinction, and to the upper panel 

18 of the figures in Appendix F of the UFVA representing the daily maximum PM light extinction 

19 levels resulting from the 20 NAAQS scenarios examined in the UFVA (18 scenarios based on 

20 PM light extinction as the indicator, the current annual and 24-hour PM2.5 NAAQS, and a 

scenario with an annual NAAQS of 12 μg/m3

 and a 24-hour NAAQS of 25 μg/m3 21 ). It can be 

22 seen that the distribution of PM2.5 mass in a given study area shifts downward as the NAAQS 

23 scenarios progress from least to most stringent (as indicated by the required percentage 

24 reduction) and in most cases become more similar to other areas (once the progression of 

25 scenarios begins to require reductions in a given area). St. Louis is an obvious exception, in that 

26 it retains many relatively high values even under the most stringent NAAQS scenario. This is 

27 due to the fact that many hours and days in St. Louis have a large estimated PM10-2.5

28 concentration contribution to estimated PM light extinction, as visualized in the light extinction 

29 budgets presented in Figure 3-13 of the UFVA. The rollback approach does not change PM10-2.5

30 concentrations. Recall from section 3.3.2 and Appendix A of the UFVA that for St. Louis, PM10-
Draft – Do Not Quote or Cite A-10 March 2010 

1 2.5 concentrations were estimated based on a PM10 instrument located very near a 

2 recycling/municipal works yard and a PM2.5 instrument in another less industrial location. As 

3 such, those estimated concentrations of PM10-2.5 may not represent a large portion of the St Louis 

4 urban area. 

5 

6 PM10-2.5 was also a notable contributor to the estimated light extinction budgets in Los 

7 Angeles on a number of days, although to a lesser degree than in St. Louis. This is reflected in 

8 the box plots, which show a number of high values of PM light extinction regardless of the level 

9 of the hypothetical PM2.5 mass NAAQS. Recall from section 3.3.2 and Appendix A of the 

10 UFVA that for Los Angeles, PM10-2.5 concentrations were estimated based on a PM10 instrument 

11 located in Victorville, California which is a considerable distance from the site in Rubidoux, 

12 California and is perhaps a dustier area than most of the Los Angeles airshed. 

13 

14 Table A-6 presents the percentage of days in 2005-2007 on which daily maximum 1-hour 

15 PM light extinction exceeded each of the CPL, under each of the 10 secondary PM NAAQS 

16 scenarios based on 1-hour PM2.5 mass. These percentages are necessarily based on the days for 

17 which data to estimate PM light extinction were available, but are best estimates of the 

18 percentage of all days in the year given that the days with data were well distributed across the 

19 year on either a one-in-three or one-in-six sampling schedule. These percentages can be 

20 compared to the same-basis percentages presented in Table 4-7 of the UFVA.
Draft – Do Not Quote or Cite A-11 March 2010 

1 Figure A-2. Distributions of maximum daily daylight 1-hour PM light extinction under 

2 “just meet” conditions for NAAQS scenarios based on 1-hour PM2.5 mass (excluding hours 

3 >90% RH)

4 

5 (aa) NAAQS Scenario 

6 60 μg/m3 

 90th 7 percentile

8 

9 (bb) NAAQS Scenario 

10 60 μg/m3 

11 95th percentile 

12 
Draft – Do Not Quote or Cite A-12 March 2010 

1 Figure A-2. Distributions of maximum daily daylight 1-hour PM light extinction under 

2 “just meet” conditions for NAAQS scenarios based on 1-hour PM2.5 mass (excluding hours 

3 >90% RH) (continued)

4 

5 (cc) NAAQS Scenario 

6 40 μg/m3 

 90th 7 percentile 

8 

9 (dd) NAAQS Scenario 

10 40 μg/m3 

 95th 11 percentile 

12 
Draft – Do Not Quote or Cite A-13 March 2010 

1 Figure A-2. Distributions of maximum daily daylight 1-hour PM light extinction under 

2 “just meet” conditions for NAAQS scenarios based on 1-hour PM2.5 mass (excluding hours 

3 >90% RH) (continued)

4 

5 (ee) NAAQS Scenario 

6 30 μg/m3 

 90th 7 percentile

8 

9 (ff) NAAQS Scenario 

10 30 μg/m3 

 95th 11 percentile 

12 
Draft – Do Not Quote or Cite A-14 March 2010 

1 Figure A-2. Distributions of maximum daily daylight 1-hour PM light extinction under 

2 “just meet” conditions for NAAQS scenarios based on 1-hour PM2.5 mass (excluding hours 

3 >90% RH) (continued) 

4 

5 (gg) NAAQS Scenario 

6 20 μg/m3 

 90th 7 percentile 

8 

9 (hh) NAAQS Scenario 

10 20 μg/m3 

 95th 11 percentile 

12 
Draft – Do Not Quote or Cite A-15 March 2010 

1 Figure A-2. Distributions of maximum daily daylight 1-hour PM light extinction under 

2 “just meet” conditions for NAAQS scenarios based on 1-hour PM2.5 mass (excluding hours 

3 >90% RH) (continued) 

4 

5 (ii) NAAQS Scenario 

6 Daily Max 

7 10 μg/m3 

 90th 8 percentile

9 

10 (jj) NAAQS Scenario 

11 Daily Max 

12 10 μg/m3 

 95th 13 percentile 

14 
Draft Do Not Quote or Cite March 2010 A-16

1 Table A-6. Percentage of days across three years (two in the case of Phoenix and Houston) with maximum 

2 light extinction above CPLs when “just meeting” NAAQS scenarios based on 1-hour PM2.5 mass. Blue sha3 reduction required from current conditions. 4 5 

Days with max hour above 

64 Mm-1

Days with max hour above 

112 Mm-1

Days wi

Scenario aa bb cc dd ee ff gg hh ii jj aa bb cc dd ee ff gg hh ii jj aa bb cc dd 

NAAQS 

Level 

(μg/m3) 60 60 40 40 30 30 20 20 10 10 60 60 40 40 30 30 20 20 10 10 60 60 40 40 

NAAQS 

Percentile 

Form 90 95 90 95 90 95 90 95 90 95 90 95 90 95 90 95 90 95 90 95 90 95 90 95 

Area Percentage of days Percentage of days Per

Tacoma 53 53 53 53 53 53 53 53 43 35 23 23 23 23 23 23 23 23 11 6 4 4 4 4 

Fresno 76 73 65 57 69 60 55 44 28 17 52 48 37 31 44 32 29 18 9 4 30 27 17 11 

Los Angeles 89 87 84 81 84 79 74 69 41 30 78 76 65 57 65 53 41 31 11 7 52 46 30 24 

Phoenix 44 44 44 44 44 44 44 44 37 32 6 6 6 6 6 6 6 6 6 6 1 1 1 1 

Salt Lake 

City 45 45 45 37 45 45 45 26 17 10 17 17 17 15 17 17 17 11 8 5 8 8 8 7 

Dallas 81 81 81 81 81 81 81 71 41 29 41 41 41 41 41 41 41 32 8 5 10 10 10 10 

Houston 79 79 79 79 79 79 74 65 32 27 44 44 44 44 44 44 35 28 6 3 11 11 11 11 

St. Louis 98 98 98 97 98 97 95 89 73 67 78 78 78 74 78 75 64 55 34 29 40 40 40 36 

Birmingham 89 85 80 68 87 80 72 62 41 34 65 56 51 36 58 51 40 30 15 12 34 26 21 13 

Atlanta 91 91 91 89 91 89 82 77 47 34 75 75 75 68 74 66 51 35 3 3 31 31 31 21 

Detroit 84 80 74 72 76 73 65 60 40 33 67 57 51 43 53 48 34 21 9 6 43 28 13 7 

Pittsburgh 85 85 81 77 81 77 63 55 27 19 57 57 51 45 52 44 29 22 3 0 26 26 18 14 

Baltimore 81 81 81 76 81 74 64 56 31 20 51 51 51 45 51 44 31 23 4 3 23 23 23 18 

Philadelphia 84 78 71 62 72 63 55 43 17 10 60 54 33 29 37 31 16 10 3 3 26 17 8 5 

New York 83 83 80 71 81 73 63 56 27 19 60 60 56 39 56 40 32 22 6 3 29 29 25 16 

Average 78 76 74 70 75 71 66 58 36 28 52 49 45 40 47 41 33 25 9 6 24 22 17 13 

6 7 8 
 

Draft Do Not Quote or Cite March 2010

5-1

1 5 REVIEW OF THE SECONDARY STANDARDS FOR OTHER 

2 WELFARE EFFECTS 

3 This chapter presents preliminary staff conclusions with regard to the current suite of 

4 secondary PM standards to protect against PM-related welfare effects other than visibility 

5 impairment. Specifically, staff has assessed the relevant information related to effects of 

6 atmospheric PM on the environment, including effects on climate, ecological effects, and effects 

7 on materials. Our assessment is framed by a series of key policy-relevant questions, which 

8 expand upon those presented in the Integrated Review Plan (IRP) (US EPA, 2008a, section 3.2). 

9 The answers to these questions will inform decisions on whether to retain or revise the current 

10 suite of secondary PM standards. 

11 In presenting preliminary staff conclusions with regard to the current secondary standards 

12 relative to PM-related effects on climate, ecological effects, and materials, we note that the final 

13 decision is largely a public welfare policy judgment. A final decision must draw upon scientific 

14 information and analyses about non-visibility PM-related effects and related impacts on public 

15 welfare, as well as judgments about how to deal with the range of uncertainties that are inherent 

16 in the scientific evidence and analyses. Our approach to informing these judgments is discussed 

17 more fully below. This approach is consistent with the requirements of the NAAQS provisions 

18 of the Act and with how EPA and the courts have historically interpreted the Act. These 

19 provisions require the Administrator to establish secondary standards that, in the Administrator’s 

20 judgment, are requisite to protect public welfare from any known or anticipated adverse effects 

21 associated with the presence of the pollutant in the ambient air. In so doing, the Administrator 

22 seeks to establish standards that are neither more nor less stringent than necessary for this 

23 purpose. The Act does not require that secondary standards be set at a zero-risk level, but rather 

24 at a level that avoids unacceptable public welfare impacts. 

25 Information on the approaches used to set the secondary PM standards in past reviews as 

26 well as our current approach for this review are presented in section 5.1. A discussion of the 

27 scope of the review as related to non-visibility welfare effects of PM is included in section 5.1.2. 

28 This chapter considers each of the non-visibility welfare effects separately. The discussion of 

29 PM-associated effects on climate (section 5.2), ecological effects (section 5.3), and materials 

30 (section 5.4) are each followed by a consideration of key uncertainties and areas for future 

31 research and data collection. 
 

Draft Do Not Quote or Cite March 2010

5-2

1 5.1 APPROACH 

2 Background information on the approaches used to establish the PM secondary standards 

3 in 1997 and revisions to those standards in 2006 are summarized below. This section also 

4 includes a discussion of the ongoing joint review of ecological effects of oxides of nitrogen and 

5 sulfur (NOx/SOx secondary review) for clarity, since depositional effects of PM components of 

6 NOx and SOx to ecosystems were historically considered as a component of the PM secondary 

7 review. Lastly, there is a discussion of the current approach for evaluating the effects of PM on 

8 climate, ecosystems, and materials using evidence-based considerations to inform our 

9 understanding of the key policy-relevant issues. 

10 5.1.1 Approaches Used in Previous Reviews 

11 5.1.1.1 Review Completed in 1997 

12 In the 1997 review, as discussed in section 2.1.1.1, EPA determined that for the primary 

13 standard the fine and coarse fractions of PM10 should be considered separately and added a suite 

14 of new primary standards, using PM2.5, as the indicator for fine particles, and retaining PM10 as 

15 the indicator for regulating thoracic coarse particles. The EPA established two new PM2.5 

standards: an annual standard of 15 μg/m3 16 , based on the 3-year average of annual arithmetic 

17 mean PM2.5 concentrations from single or multiple community-oriented monitors; and a 24-hour 

standard of 65 μg/m3, based on the 3-year average of the 98th 18 percentile of 24-hour PM2.5 

19 concentrations at each population-oriented monitor within an area (62 FR 38652, July 18, 1997). 

20 With respect to the secondary PM standards, EPA concluded in 1997, that the available 

21 evidence on effects of PM on non-visibility welfare endpoints was not sufficient to warrant a 

22 separate secondary standard. Therefore, the secondary standards were set equal to the primary 

23 PM2.5 and PM10 standards in the final rule to provide protection against effects on visibility as 

24 well as materials damage and soiling effects related to fine and coarse particles (62 FR 38683). 

25 5.1.1.2 Review Completed in 2006 

26 In 2006, the Administrator concluded that there was insufficient information to consider a 

27 distinct secondary standard based on PM-related impacts to ecosystems, materials damage and 

28 soiling, and climatic and radiative processes (71 FR 61144, October 17, 2006). Specifically, 

29 there was a lack of evidence linking various non-visibility welfare effects to specific levels of 

30 ambient PM. To provide a level of protection for welfare-related effects, the secondary 

31 standards were set equal to the revised primary standards to directionally improve the level of 

32 protection afforded vegetation, ecosystems and materials (71 FR 61210). 
 

Draft Do Not Quote or Cite March 2010

5-3

1 In the last review, the 2004 AQCD concluded that regardless of size fraction, particles 

2 containing nitrates and sulfates have the greatest potential for widespread environmental 

3 significance (US EPA, 2004, sections 4.2.2 and 4.2.3.1). Considerable supporting evidence was 

4 available that indicated a significant role of NOx, SOx, and transformation products in 

5 acidification and nutrient enrichment of terrestrial and aquatic ecosystems (71 FR 61209). The 

6 recognition of these ecological effects, coupled with other considerations detailed below, led 

7 EPA to initiate a joint review of the NO2 and SO2 secondary NAAQS that will consider the 

8 gaseous and particulate species of NOx and SOx with respect to the ecosystem-related welfare 

9 effects that result from the deposition of these pollutants and transformation products. 

10 5.1.2 Scope of Current NAAQS Reviews 

11 Non-visibility welfare-based effects of oxides of nitrogen and sulfur are divided between 

12 two NAAQS reviews; (1) the PM NAAQS review and, (2) the joint NOx/SOx secondary 

13 NAAQS review. The scope of each document and the components of N and S considered in 

14 each review are detailed in this section and summarized in Table 5-1.
Draft Do Not Quote or Cite March 2010

5-4

1 2 3 Table 5-1. Scope of the current secondary PM NAAQS review and current NOx/SOx secondary review. 

 NOx/SOx Secondary 

Review 

PM Secondary Review

 Materials 

Welfare Effect 

Acidifying deposition, nutrient enrichment 

Direct effects of gas-phase NOx/SOx on vegetation 

Visibility impairment 

Climate Forcing effects 

Ecological effects Damage 

Documents  ISA NOx/SOx NOx/SOx PM PM PM 

PM and NOx/SOx Annex E 

 REA NOx/SOx NOx/SOx 

PM (Urban focused visibility assessment) 

 PA NOx/SOx NOx/SOx PM PM PM PM Components 

Deposited particulate and gaseous forms of oxides of nitrogen and sulfur and related N and S containing compounds. 

Gaseous forms of oxides of nitrogen and sulfur and related N and S containing compounds in the ambient air. 

All particles 10 microns or smaller in the ambient air. 

Climate-related particles (aerosols) in the ambient air. 

Deposited components of PM, including metals and organics but not N and S containing compounds. 

Particles and gases associated with ambient NOx and SOx including NOy, NH3 and NHx. 

4 
 

Draft Do Not Quote or Cite March 2010

5-5

1 5.1.2.1 Scope of the Current Secondary PM NAAQS Review 

2 In reviewing the current suite of secondary PM standards to address visibility impairment 

3 (chapter 4), climate forcing effects (section 5.2), and other welfare-related effects (sections 5.3 

4 and 5.4), all PM-related effects that are not being covered in the NOx/SOx review are 

5 considered. With regard to the materials section (5.4), the discussion has been expanded to 

6 include particles and gases that are associated with the presence of ambient NOx and SOx, as 

7 well as NOy, NH3 and NHX for completeness. By excluding the effects associated with 

8 deposited particulate matter components of NOx and SOx and their transformation products 

9 which are addressed fully in the NOx/SOx secondary review, as outlined below, the discussion 

10 of ecological effects of PM has been narrowed to focus on effects associated with the deposition 

11 of metals and, to a lesser extent, organics (section 5.3). 

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

13 This is the first time since the NAAQS were established in 1971 that a joint review of the 

14 secondary NAAQS for NOx and SOx, has been conducted. This review is being conducted 

15 because the atmospheric chemistry and environmental effects of NOx, SOx, and their associated 

16 transformation products are linked, and because the National Research Council (NRC) has 

17 recommended that EPA consider multiple pollutants, as appropriate, in forming the scientific 

18 basis for the NAAQS. The NOx/SOx secondary review focuses on the welfare effects associated 

19 with exposures from deposited particulate and gaseous forms of oxides of nitrogen and sulfur 

20 and related N and S containing compounds and transformation products on ecosystem receptors. 

21 An assessment of the complex ecological effects associated with N deposition requires 

22 consideration of multiple forms of N. These include evaluation of data on inorganic reduced 

forms of N (e.g., ammonia [NH3] and ammonium ion [NH4 23 +]), inorganic oxidized forms (e.g., 

NOx, nitric acid [HNO3], nitrous oxide [N2O], nitrate [NO3 24 −]), and organic N compounds (e.g., 

25 urea, amines, proteins, nucleic acids). In addition to acidification and N-nutrient enrichment, 

26 other welfare effects related to deposition of N-and S-containing compounds are discussed, such 

27 as SOx interactions with mercury (Hg) methylation. In addition, the NOx/SOx secondary review 

28 includes evidence related to direct ecological effects of gas-phase NOx and SOx since the direct 

29 effects of gas-phase SOx on vegetation formed a primary basis for the initial establishment of the 

30 secondary NAAQS for SO2. 

31 Effects of acidifying deposition associated with particulate N and S are covered in the 

32 recent Integrated Science Assessment for Oxides of Nitrogen and Sulfur-Ecological Criteria

33 (Final Report (US EPA, 2008c). The Risk and Exposure Assessment for Review of the 

34 Secondary National Ambient Air Quality Standards for Oxides of Nitrogen and Oxides of Sulfur 
 

Draft Do Not Quote or Cite March 2010

5-6

1 (Final)(NOx/SOx REA) (US EPA, 2009h) considers four main targeted ecosystem effects 

2 considered in the review of secondary effects of NOx and SOx: (1) aquatic acidification due to N 

3 and S, (2) terrestrial acidification due to N and S, (3) aquatic nutrient enrichment, including 

4 eutrophication and (4) terrestrial nutrient enrichment. In the draft Policy Assessment for Review 

5 of the Secondary National Ambient Air Quality Standards for Oxides of Nitrogen and Oxides of 

6 Sulfur (US EPA 2010c) ecologically-based indicators that link atmospheric concentrations to 

7 deposition are being considered. 

8 5.1.3 Current Approach 

9 The remainder of this chapter summarizes and highlights key aspects of the policy 

10 relevant information from the ISA to help inform the Administrator’s judgments regarding the 

11 adequacy of the current suite of secondary PM NAAQS in relation to climate processes, 

12 ecological effects, and materials damage. The ISA uses a five-level hierarchy that classifies the 

13 weight of evidence for causation, not just association, into a qualitative statement about the 

14 overall weight of evidence and causality (US EPA, 2009a, section 1.5.5, Table 1-3): causal 

15 relationship; likely to be a causal relationship; suggestive of a causal relationship; inadequate to 

16 infer a causal relationship; not likely to be a causal relationship (see US EPA, 2009a, Table 1-3). 

17 Staff is evaluating evidence-based considerations primarily by assessing the evidence of 

18 associations identified in the ISA. All relationships between PM and climate, ecological effects, 

19 and materials damage effects identified in the ISA are considered to be either “likely causal” or 

20 “causal”. The staff’s approach in this review of non-visibility welfare effects of PM is to 

21 consider information regarding particulate matter effects on climate, ecological endpoints and 

22 materials. This includes new literature available since the last review as well as existing, 

23 relevant information as presented in the ISA (US EPA 2009a). 

24 5.2 CLIMATE 

25 5.2.1 Scope 

26 Information and conclusions about what is currently known about the role of PM in 

27 climate is summarized in Chapter 9 of the PM ISA (US EPA, 2009a). The ISA concludes; “that 

28 a causal relationship exists between PM and effects on climate, including both direct effects on 

29 radiative forcing and indirect effects that involve cloud feedbacks that influence precipitation 

30 formation and cloud lifetimes” (US EPA, 2009a, section 9.3.10). Material from the climate 

31 section of the ISA is principally drawn from the U.S. Climate Change Science Program 

32 Synthesis and Assessment Product 2.3, Atmospheric Aerosol Properties and Climate Impacts, by 

33 Chin et al., (CCSP 2009) and Chapter 2, Changes in Atmospheric Constituents and in Radiative 

34 Forcing,(Forster et al., 2007) in the comprehensive Working Group I report in the Fourth 
 

Draft Do Not Quote or Cite March 2010

5-7

1 Assessment Report (AR4) from the Intergovernmental Panel on Climate Change (IPCC), Climate 

2 Change 2007: The Physical Science Basis. Sections 9.3.7 (Fire as a Special Source of PM 

3 Welfare Effects), 9.3.9 (Other Special Sources and Effects), 9.3.9.1 (Glaciers and Snowpack) 

4 and 9.3.9.3 (Effects on Local and Regional Climate) of the ISA were written by NCEA staff. 

5 This section of the PA summarizes and synthesizes the policy-relevant science in the ISA for the 

6 purpose of helping to inform consideration of climate aspects in the review of the secondary PM 

7 NAAQS. 

Atmospheric PM (referred to as aerosols1 8 in the remainder of this section to be consistent 

9 with the ISA) affects multiple aspects of climate. These include absorbing and scattering of 

10 incoming solar radiation, alterations in terrestrial radiation, effects on the hydrological cycle, and 

11 changes in cloud properties (US EPA, 2009a, section 9.3.1). Major aerosol components that 

12 contribute to climate processes include black carbon (BC), organic carbon (OC), sulfates, nitrates 

13 and mineral dusts. There is a considerable ongoing research effort focused on understanding 

14 aerosol contributions to changes in global mean temperature and precipitation patterns. The 

15 Climate Change Research Initiative identified research on atmospheric concentrations and effects 

16 of aerosols as a high research priority (National Research Council, 2001) and the IPCC 2007 

17 Summary for Policymakers states that anthropogenic contributions to aerosols remain the 

18 dominant uncertainty in radiative forcing (IPCC 2007). The current state of the science of 

19 climate alterations attributed to PM is in flux as a result of continually updated information. 

20 5.2.2 Adequacy of the Current Standard 

21 In considering the adequacy of the suite of secondary standards, staff addresses the 

22 following overarching question: 

23 Does currently available scientific information, as reflected in the ISA, support or call into 

24 question the adequacy of the protection for climate effects afforded by the current suite of 

25 secondary PM standards? 

26 To inform the answer to this overarching question, staff has posed specific questions to 

27 aid in assessing the available scientific evidence as related to climate effects attributed to 

28 aerosols. In considering the currently available scientific and technical information, we included 

29 both the information available from the last review and information that is newly available since 

30 the last review synthesized in Chapter 9 of the ISA (US EPA, 2009). 

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

32 aerosols? 

 

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

1 Global climate change has increasingly been the focus of intense international research 

2 endeavors. Major efforts are underway to understand the complexities inherent in atmospheric 

3 aerosol interactions and to decrease uncertainties associated with climate estimations. Two recent 

4 reports, the US CCSP Product 2.3 and sections of the IPCC AR4 were combined to form the 

5 climate discussion in the ISA (CCSP 2009; Forster et al., 2007). A review of the most recently 

6 available techniques for assessing climate-aerosol relationships is presented in the ISA. Aerosol 

7 measurement capabilities reviewed in the ISA include a discussion of the increasingly 

8 sophisticated instrumentation and techniques available for quantifying aerosols, the enhanced 

9 sensing capabilities of satellites, development of remote sensing networks and synergy of 

10 measurements with model simulations (US EPA 2009a, section 9.3.2). Advances in measured 

11 aerosol properties as related to modeling as well as outstanding issues remaining in these 

12 measurement-based studies are elaborated in the ISA (US EPA 2009a sections 9.3.3 and 9.3.4). 

13 Section 9.3.6 of the ISA, “Global Aerosol Modeling” considers the capabilities of climate 

14 modeling that have developed over the last decade and limitations of the techniques currently in 

15 use (US EPA 2009a). 

16 • To what extent does newly available evidence improve our understanding of the nature 

17 and magnitude of climate responses to PM (aerosols)? 

18 Aerosols have direct and indirect effects on climate processes. The direct effects of 

19 aerosols on climate result mainly from particles scattering light away from earth into space, 

20 directly altering the radiative balance of the Earth-atmosphere system. This reflection of solar 

21 radiation back to space decreases the transmission of visible radiation to the surface of the earth 

22 and results in a decrease in the heating rate of the surface and the lower atmosphere. At the same 

23 time, absorption of either incoming solar radiation or outgoing terrestrial radiation by particles, 

24 primarily BC, results in an increased heating rate in the lower atmosphere. Global estimates of 

25 aerosol direct radiative forcing (RF) were recently summarized using a combined model-based 

26 estimate (Forster et al., 2007). The overall, model-derived aerosol direct RF was estimated in the 

IPCC AR4 as -0.5 (-0.9 to -0.1) watts per square meter (W/m2 27 ), with an overall level of scientific 

28 understanding of this effect as “medium low” (Forster et al., 2007), indicating a net cooling 

29 effect in contrast to greenhouse gases (GHGs) which have a warming effect. 

30 The contribution of individual aerosol components to total aerosol direct radiative forcing 

31 is more uncertain than the global average (US EPA, 2009a, section 9.3.6.6). The direct effect of 

32 radiative scattering by atmospheric particles exerts an overall net cooling of the atmosphere, 

33 while particle absorption of solar radiation leads to warming. For example, the presence of OC 

34 and sulfates decrease warming from sunlight by scattering shortwave radiation back into space. 

35 Such a perturbation of incoming radiation by anthropogenic aerosols is designated as aerosol 

36 climate forcing, which is distinguished from the aerosol radiative effect of the total aerosol 
 

Draft Do Not Quote or Cite March 2010

5-9

1 (natural plus anthropogenic). The aerosol climate forcing and radiative effect are characterized 

2 by large spatial and temporal heterogeneities due to the wide variety of aerosol sources, the 

3 spatial non-uniformity and intermittency of these sources, the short atmospheric lifetime of 

4 aerosols (relative to that of the greenhouse gases), and processing (chemical and microphysical) 

5 that occurs in the atmosphere. For example, OC can be warming (positive forcer) when 

6 deposited on or suspended over a highly reflective surface such as snow or ice but, on a global 

7 average, is a negative forcer in the atmosphere. 

8 More information has also become available on indirect effects of aerosols. Particles in 

9 the atmosphere indirectly affect both cloud albedo (reflectivity) and cloud lifetime by modifying 

10 the cloud amount, and microphysical and radiative properties (US EPA, 2009a, section 9.3.6.4). 

11 The RF due to these indirect effects (cloud albedo effect) of aerosols is estimated in the IPCC 

AR4 to be -0.7(-1.8 to -0.3) W/m2 12 with the level of scientific understanding of this effect as 

13 “low” (Forster et al., 2007). Aerosols act as cloud condensation nuclei (CCN) for cloud 

14 formation. Increased particulates in the atmosphere available as CCN with no change in 

15 moisture content of the clouds have resulted in an increase in the number and decrease in the 

16 size of cloud droplets in certain clouds that can increase the albedo of the clouds (the Twomey 

17 effect). Smaller particles slow the onset of precipitation and prolong cloud lifetime. This effect, 

18 coupled with changes in cloud albedo, increase the reflection of solar radiation back into space. 

19 The altitude of clouds also effects cloud radiative forcing. Low clouds reflect incoming sunlight 

20 back to space but do not effectively trap outgoing radiation, thus, cooling the planet, while higher 

21 elevation clouds reflect some sunlight but more effectively can trap outgoing radiation and act to 

22 warm the planet (US EPA, 2009a, section 9.3.3.5). 

23 The total negative RF due to direct and indirect effects of aerosols computed from the top 

of the atmosphere, on a global average, is estimated at -1.3 (-2.2 to -0.5) W/m2 24 in contrast to the 

positive RF of +2.9 (+3.2 to +2.6) W/m2 25 for anthropogenic GHGs (IPCC 2007, pg. 200). 

26 The understanding of the magnitude of aerosol effects on climate has increased 

27 substantially in the last decade. Data on the atmospheric transport and deposition of aerosols 

28 indicate a significant role for PM components in multiple aspects of climate. Aerosols can 

29 impact glaciers, snowpack, regional water supplies, precipitation and climate patterns (US EPA 

30 2009a section 9.3.9). Aerosols deposited on ice or snow can lead to melting and subsequent 

31 decrease of surface albedo (US EPA 2009a, section 9.3.9.2). Aerosols are potentially important 

32 agents of climate warming in the Arctic and other locations (US EPA, 2009a, section 9.3.9). 

33 Incidental fires and biomass burning are being recognized as having a significant impact on 

34 PM2.5 concentrations and climate forcing. Intermittent fires can occur at large enough scales to 

35 affect hemispheric aerosol concentrations (US EPA 2009a, section 9.3.7). 
 

Draft Do Not Quote or Cite March 2010

5-10

1 A series of studies available since the last review examine the role of aerosols on local 

2 and regional scale climate processes (US EPA, 2009a, section 9.3.9.3). Studies on the South 

3 Coast Air Basin (SCAB) in California indicate aerosols may reduce near-surface wind speeds, 

4 which, in turn reduce evaporation rates and increase cloud lifetimes. The overall impact can be a 

5 reduction in local precipitation (Jacobson and Kaufmann, 2006). Conditions in the SCAB impact 

6 ecologically sensitive areas including the Sierra Nevadas. Precipitation suppression due to 

7 aerosols in California (Givati and Rosenfield, 2004) and other similar studies in Utah and 

8 Colorado found that orographic precipitation decreased by 15-30% downwind of pollution 

9 sources. Evidence of regional-scale impacts of aerosols on meteorological conditions in other 

10 regions of the U.S. are lacking. 

11 • To what extent does the currently available information provide evidence of association 

12 between specific PM constituents (i.e. BC, OC, sulfates) and climate-related effects? 

13 Advances in the understanding of aerosol components and how they contribute to climate 

14 change have enabled refined global forcing estimates of individual PM constituents. The global 

15 mean radiative effect from individual components of aerosols was estimated for the first time in 

the IPCC AR4 where they were reported to be (all in W/m2 16 units): -0.4 (+0.2) for sulfate, -0.05 

17 (+0.05) for fossil fuel-derived OC, +0.2 (+0.15) for fossil fuel derived BC, +0.03 (+0.12) for 

18 biomass burning, -0.1 (+0.1) for nitrates, and -0.1 (+0.2) for mineral dust (US EPA, 2009a, 

19 section 9.3.10). Sulfate and fossil fuel-derived OC cause negative forcing whereas BC causes 

20 positive forcing because of its highly absorbing nature (US EPA, 2009a, 9.3.6.3). Although BC 

21 comprises only a small fraction of anthropogenic aerosol mass load and aerosol optical depth 

22 (AOD), its forcing efficiency (with respect to either AOD or mass) is an order of magnitude 

23 stronger than sulfate and particulate organic matter (POM), so its positive shortwave forcing 

24 largely offsets the negative direct forcing from sulfate and POM (IPCC, 2007; US EPA 2009a, 

25 9.3.6.3). Global loadings for nitrates and anthropogenic dust remain very difficult to estimate, 

26 making the radiative forcing estimates for these constituents particularly uncertain (US EPA, 

27 2009a, section 9.3.7). 

28 Improved estimates of anthropogenic emissions of some aerosols, especially BC and OC, 

29 have promoted the development of improved global emissions inventories and source-specific 

30 emissions factors useful in climate modeling (Bond et al. 2004). Recent data suggests that BC is 

31 one of the largest individual warming agents after carbon dioxide (CO2) and perhaps methane 

32 (CH4) (Jacobson 2000; Sato et al., 2003; Bond and Sun 2005). There are several studies 

33 modeling BC effects on climate and/or considering emission reduction measures on 

34 anthropogenic warming detailed in section 9.3.9 of the ISA. Fires release large amounts of BC, 

35 CO2, CH4 and OC (US EPA, 2009a, section 9.3.7). 
 

Draft Do Not Quote or Cite March 2010

5-11

1 5.2.3 Preliminary Staff Conclusions 

2 • Aerosols alter climate processes directly through radiative forcing and by indirect 

3 effects on cloud brightness, changes in precipitation and possible changes in cloud 

4 lifetimes. 

5 • Individual components of aerosols differ in their reflective properties, and direction of 

6 climate forcing. Overall, aerosols have a net climate cooling effect. 

7 • Most climate model simulations are based on global scale scenarios. These models 

8 may fail to consider the local variations in climate forcing due to emissions sources and 

9 local meteorological patterns. 

10 • Aerosols that are warming are co-emitted with aerosols that are cooling. The relative 

11 mix of these components will vary in areas across the U.S. and over time. 

12 Collectively taking into consideration the responses to specific questions regarding the 

13 adequacy of the current secondary PM standards for climate effects, we revisit the overarching 

14 question: “does available scientific information, as reflected in the ISA, support or call into 

15 question the adequacy of the protection for climate effects afforded by the current suite of 

16 secondary PM standards?” As an initial matter, we considered the appropriateness of the current 

17 secondary standard defined in terms of PM2.5 and PM10 indicators, for providing protection 

18 against potential climate effects of aerosols. Newly available scientific information on climate19 aerosol relationships has improved our understanding of direct and indirect effects of aerosols 

20 and aerosol properties. The major aerosol components that contribute to climate processes 

21 include BC, OC, sulfate, nitrate and mineral dusts. These components vary in their reflectivity, 

22 forcing efficiencies and even in the direction of climate forcing. The current standards that are 

23 defined in terms of aggregate size mass cannot be expected to appropriately target controls on 

24 components of fine and coarse particles that are related to climate forcing effects. Thus, the 

25 current mass-based PM2.5 and PM10 secondary standards are not an appropriate or effective 

26 means of focusing protection against PM-associated climate effects due to these differences in 

27 components. 

28 Overall, there is a net climate cooling associated with aerosols in the global atmosphere 

29 (US EPA, 2009a, section 9.2.10). Staff recognizes that some individual aerosol components, 

30 such as BC, are positive climate forcers, whereas others, such as OC and sulfates, are negative 

31 climate forcers. However, aerosols that are warming are co-emitted with aerosols that are 

32 cooling. The relative mix of components will vary in areas across the U.S. and over time. Due to 

33 the spatial and temporal heterogeneity of PM components that contribute to climate forcing, 

34 uncertainties in the measurement of aerosol components, inadequate consideration of aerosol 

35 impacts in climate modeling, insufficient data on local and regional microclimate variations and 

36 heterogeneity of cloud formations, it is not currently feasible to conduct a quantitative analysis 

37 for the purpose of informing revisions of the current NAAQS PM standard based on climate. 
 

Draft Do Not Quote or Cite March 2010

5-12

1 Based on these considerations, we reach the preliminary conclusion that there is insufficient 

2 information at this time to base a national ambient standard on climate impacts associated with 

current ambient concentrations of PM or its constituents2 3 . 

4 5.2.4 Key Uncertainties and Areas for Future Research and Data Collection 

5 Although considerable progress is being made in estimating aerosol contributions to 

6 climate fluctuations, significant uncertainties remain that preclude consideration of climate 

7 effects as a basis for establishing a separate NAAQS secondary standard. A major impediment 

8 at this time to establishing a secondary standard for PM based on climate is the lack of accurate 

9 measurement of aerosol contributions, specifically quantification of aerosol absorption and 

10 inability to separate the anthropogenic component from total aerosol forcing. Section 9.3.4 of 

11 the ISA details the current limitations in aerosol measurement. Most measurement studies focus 

12 on the sum of natural and anthropogenic contributions under clear sky conditions, however, this 

13 scenario is simplistic when effects of cloud cover and differing reflective properties of land and 

14 ocean are considered. Satellite measurements do not currently have the capability to distinguish 

15 anthropogenic from natural aerosols. Due to a lack of data on the vertical distribution of aerosols, 

16 above-cloud aerosols and profiles of atmospheric radiative heating are poorly understood (US 

17 EPA, 2009a, section 9.3.4). 

18 Another uncertainty in considering climate effects of PM in the NAAQS review is the 

19 spatial and temporal heterogeneity of aerosols. In regions having high concentrations of 

20 anthropogenic aerosols, aerosol forcing is greater than the global average, and can exceed 

21 warming by GHGs, locally reversing the sign of the forcing (US EPA, 2009a, section 9.3.1). 

22 Emissions of carbonaceous aerosols from intermittent fires and volcanic activity can further 

23 complicate regional climate forcing estimates (US EPA, 2009a, sections 9.3.7 and 9.3.8). 

24 Individual components of aerosols may either be positive or negative climate forcers. Airborne 

25 PM components may be directly emitted or undergo a variety of physical and chemical 

26 interactions and transformations. These result in changes in particle size, structure and 

27 composition which alter aerosol reflective properties. Aerosols can grow in size in the 

28 atmosphere because ambient water vapor condenses on individual particles, a phenomenon 

29 known as hygroscopic growth (US EPA, 2009a, section 9.3.6.2). Atmospheric lifetimes of 

30 individual aerosol components vary greatly confounding tracking source receptor relationships. 

31 Improved representation of aerosols in climate models is essential to more accurately 

32 predict the role of PM in climate forcing (US EPA, 2009a, section 9.3.6.7). The influence of 

 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

1 aerosols on climate is not yet adequately taken into account in computer predictions although 

2 considerable progress in being made in this area. For example, PM components underrepresented 

3 or missing from many models include nitrate aerosols and anthropogenic secondary aerosols (US 

4 EPA, 2009a, section 9.3.6.7). The modeling of aerosol indirect effects and absorption are 

5 difficult due to the high level of uncertainty associated with these climate factors. 

6 The interaction of PM with clouds remains a large source of uncertainty in climate 

7 estimates. The interactions of aerosols with clouds and linkages between clouds and the overall 

8 climate system are complex and limit the feasibility of conducting quantitative analysis for the

9 purpose of establishing a secondary PM standard based on welfare effects on climate processes. 

10 5.3 ECOLOGICAL EFFECTS 

11 5.3.1 Scope 

12 Information on what is currently known about ecological effects of PM is summarized in 

13 Chapter 9 of the ISA (US EPA 2009a). Four main categories of ecological effects are identified 

14 in the ISA: direct effects, effects of PM-altered radiative flux, indirect effects of trace metals and 

15 indirect effects of organics. Exposure to PM for direct effects occur via deposition (e.g. wet, dry 

16 or occult) to vegetation surfaces, while indirect effects occur via deposition to ecosystem soils or 

17 surface waters where the deposited constituents of PM then interacts with biological organisms. 

18 Both fine and coarse-mode particles may affect plants and other organisms; however, PM size 

19 classes do not necessarily relate to ecological effects (U.S. EPA, 1996). More often the chemical 

20 constituents drive the ecosystem response to PM (Grantz et al., 2003). The trace metal 

21 constituents of PM considered in the ecological effects section of the ISA are cadmium (Cd), 

22 copper (Cu), chromium (Cr), mercury (Hg), nickel (Ni) and zinc (Zn). Ecological effects of lead 

23 (Pb) in particulate form are covered in the Air Quality Criteria Document for Lead (US EPA, 

24 2006). The organics included in the ecological effects section of the ISA are persistent organic 

25 pollutants (POPs), polyaromatic hydrocarbons (PAHs) and polybromiated diphenyl ethers 

26 (PBDEs). 

27 Ecological effects of PM include direct effects to metabolic processes of plant foliage; 

28 contribution to total metal loading resulting in alteration of soil biogeochemistry and 

29 microbiology, plant and animal growth and reproduction; and contribution to total organics 

30 loading resulting in bioaccumulation and biomagnification across trophic levels. It is important 

31 to emphasize that the metal and organic constituents of PM contribute to total metal and organic 

32 loads in ecosystems. 

33 The ISA states that overall, ecological evidence is sufficient to conclude that a causal 

34 relationship is likely to exist between deposition of PM and a variety of effects on individual 
 

Draft Do Not Quote or Cite March 2010

5-14

1 organisms and ecosystems based on information from the previous review and limited new 

2 findings in this review (US EPA 2009a, sections 2.5.3 and 9.4.7). However the ISA also finds, 

3 in many cases, it is difficult to characterize the nature and magnitude of effects and to quantify 

4 relationships between ambient concentrations of PM and ecosystem response due to significant 

5 data gaps and uncertainties as well as considerable variability that exists in the components of 

6 PM and their various ecological effects. 

7 Ecological effects of PM must then be evaluated to determine if they are known or 

8 anticipated to have an adverse impact on public welfare. Characterizing a known or anticipated 

9 adverse effect to public welfare is an important component of developing any secondary 

10 NAAQS. The most recent secondary NAAQS reviews have assessed changes in ecosystem 

11 structure or processes using a weight-of-evidence approach that uses both quantitative and 

12 qualitative data. For example, the 2008 ozone (O3) final rule and 2010 O3 proposal conclude that 

13 a determination of what constitutes an “adverse” welfare effect in the context of secondary 

14 NAAQS review can appropriately occur by considering effects at higher ecological levels 

15 (populations, communities, ecosystems) as supported by recent literature. In the 2008 

16 rulemaking and current ozone proposal, the interpretation of what constitutes an adverse effect 

17 on vegetation can vary depending on the location and intended use of the plant. The degree to 

18 which O3-related effects are considered adverse depends on the intended use of the vegetation 

19 and its significance to public welfare (73 FR 16496). Therefore, effects (e.g. biomass loss, foliar 

20 injury, impairment of intended use) may be judged to have a different degree of impact on public 

21 welfare depending, for example, on whether that effect occurs in a Class I area, a city park, 

22 commercial cropland or private land. 

23 A paradigm useful in evaluating ecological adversity is the concept of ecosystem 

24 services. Ecosystem services identify the varied and numerous ways that ecosystems are 

25 important to human welfare. Ecosystems provide many goods and services that are of vital 

26 importance for the functioning of the biosphere and provide the basis for the delivery of tangible 

27 benefits to human society. An EPA initiative to consider how ecosystem structure and function 

28 can be interpreted through an ecosystem services approach has resulted in the inclusion of 

29 ecosystem services in the NOx/SOx REA (US EPA, 2009h). The Millennium Ecosystem 

30 Assessment (MEA) defines these to include supporting, provisioning, regulating and cultural 

31 services (Hassan et al., 2005): 

32 • Supporting services are necessary for the production of all other ecosystem services. 

33 Some examples include biomass production, production of atmospheric O2, soil 

34 formation and retention, nutrient cycling, water cycling, and provisioning of habitat. 

35 Biodiversity is a supporting service that is increasingly recognized to sustain many of 

36 the goods and services that humans enjoy from ecosystems. These provide a basis for 

37 three higher-level categories of services. 
 

Draft Do Not Quote or Cite March 2010

5-15

1 • Provisioning services, such as products (Gitay et al., 2001) i.e., food (including game, 

2 roots, seeds, nuts, and other fruit, spices, fodder), fiber (including wood, textiles), and 

3 medicinal and cosmetic products (including aromatic plants, pigments). 

4 • Regulating services that are of paramount importance for human society such as (a) C 

5 sequestration, (b) climate and water regulation, (c) protection from natural hazards 

6 such as floods, avalanches, or rock-fall, (d) water and air purification, and (e) disease 

7 and pest regulation. 

8 • Cultural services that satisfy human spiritual and aesthetic appreciation of ecosystems 

9 and their components. 

10 An important consideration in evaluating biologically adverse effects of PM and linkages 

11 to ecosystem services is that many of the MEA categories overlap and any one pollutant may 

12 impact multiple services. For example, deposited PM may alter the composition of soil13 associated microbial communities, which may affect supporting services such as nutrient 

14 cycling. Changes in available soil nutrients could result in alterations to provisioning services 

15 such as timber yield and regulating services such as climate regulation. If enough information is 

16 available, these alterations can be quantified based upon economic approaches for estimating the 

17 value of ecosystem services. Valuation may be important from a policy perspective because it 

18 can be used to compare the benefits of altering versus maintaining an ecosystem. Knowledge 

19 about the relationships linking ambient concentrations and ecosystem services can be used to 

20 inform a policy judgment on a known or anticipated adverse public welfare effect. 

21 This review seeks to build upon and focus this body of science using the concept of 

22 ecosystem services to qualitatively evaluate linkages between biologically adverse effects and 

23 particulate deposition. This approach is similar to that taken in the NOx/SOx REA in which the 

24 relationship between air quality indicators, deposition of N and S, ecologically relevant 

25 indicators and effects on sensitive receptors are linked to changes in ecosystem structure and 

26 services (US EPA, 2009h). This approach considers the benefits received from the resources and 

27 processes that are supplied by ecosystems. Ecosystem components (e.g. plants, soils, water, 

28 wildlife) are impacted by PM air pollution, which may alter the services provided by the 

29 ecosystems in question. The goals of this policy assessment are to (1) identify ecological effects 

30 associated with PM deposition that can be linked to ecosystem services and (2) qualitatively 

31 evaluate ecological endpoints when possible. Keeping these goals and guidelines in mind, 

32 limited new data on PM effects on plants, soil and nutrient cycling, wildlife and water are 

33 evaluated in the context of ecosystem services to qualitatively evaluate linkages between 

34 biologically adverse effects and particulate deposition for the purpose of evaluating the adequacy 

35 of the current standard. 
 

Draft Do Not Quote or Cite March 2010

5-16

1 5.3.2 Adequacy of the Current Standard 

2 In considering the adequacy of the suite of secondary standards, staff addresses the 

3 following overarching question: 

4 Does available scientific information, as reflected in the ISA support or call into question 

5 the adequacy of the protection afforded by the current suite of secondary PM standards for 

6 vegetation and ecosystems from the effects of deposited particulate metals and organics? 

7 To inform the answer to this overarching question, staff has posed specific questions to 

8 aid in assessing the available scientific evidence as related to ecosystem effects attributed to PM 

9 deposition as presented in the ISA (US EPA, 2009a). 

10 • To what extent has key scientific evidence become available to improve our 

11 understanding of the nature and magnitude of ecosystem responses, the variability 

12 associated with these responses, and the impact of PM on ecosystem services? 

13 Key scientific evidence regarding PM effects on plants, soil and nutrient cycling, wildlife 

14 and water available since the last review is summarized below to evaluate how this information 

15 has improved our understanding of ecosystem responses to PM. 

16 Plants

17 As primary producers, plants play a pivotal role in energy flow through ecosystems. 

18 Ecosystem services derived from plants include all of the categories (supporting, provisioning, 

19 regulating, cultural) identified in the MEA (Hassan et al., 2005). Vegetation supports other 

20 ecosystem processes by cycling nutrients through food webs and serving as a source of organic 

21 material for soil formation and enrichment. Trees and plants provide food, wood, fiber, and fuel 

22 for human consumption. Flora help to regulate climate by sequestering CO2, control flooding by 

23 stabilizing soils and cycling water via uptake and evapotranspiration. Plants are significant in 

24 aesthetic, spiritual and recreational aspects of human interactions. 

25 Particulate matter can adversely impact plants and ecosystem services provided by plants 

26 by deposition to vegetative surfaces (US EPA, 2009a, section 9.4.3). Particulates deposited on 

27 the surfaces of leaves and needles can block light, altering the radiation received by the plant. 

28 PM deposition can obstruct stomata limiting gas exchange, damage leaf cuticles and increase 

29 plant temperatures. This level of PM accumulation is typically observed near sources of heavy 

30 deposition such as smelters and mining operations (US EPA, 2009a, section 9.4.3). Plants 

31 growing on roadsides exhibit impact damage from near-road PM deposition, having higher levels 

32 of organics and heavy metals, and accumulate salt from road de-icing during winter months (US 

33 EPA, section 2009a, sections 9.4.3.1 and 9.4.5.7). 

34 In addition to damage to plant surfaces, deposited PM can be taken up by plants from soil 

35 or foliage. The ability of vegetation to take up heavy metals and organics is dependent upon the 

36 amount, solubility and chemical composition of the deposited PM. Uptake of PM by plants from 
 

Draft Do Not Quote or Cite March 2010

5-17

1 soils and vegetative surfaces can disrupt photosynthesis, alter pigments and mineral content, 

2 reduce plant vigor, decrease frost hardiness and impair root development. The ISA indicates that 

3 there are little or no effects on foliar processes at ambient levels of PM (sections 9.4.3 and 9.4.7) 

4 however, damage due to atmospheric pollution can occur near point-sources or under conditions 

5 where plants are subjected to multiple stressors. 

6 Though all heavy metals can be directly toxic at sufficiently high concentrations, only 

7 Cu, Ni, and Zn have been documented as being frequently toxic to plants (U.S. EPA, 2004), 

8 while toxicity due to Cd, Co, and Pb has been observed less frequently (Smith, 1990; US EPA 

9 2009a, section 9.4.5.3). In general, plant growth is negatively correlated with trace metal and 

10 heavy metal concentration in soils and plant tissue (Audet and Charest, 2007). Trace metals, 

11 particularly heavy metals, can influence forest growth. Growth suppression of foliar microflora 

12 has been shown to result from Fe, Al, and Zn. These three metals can also inhibit fungal spore 

13 formation, as can Cd, Cr, Mg, and Ni (see Smith, 1990). Metals cause stress and decreased 

14 photosynthesis (Kucera et al., 2008) and disrupt numerous enzymes and metabolic pathways 

15 (Strydom et al., 2006). Excessive concentrations of metals result in phytotoxicity through: (i) 

16 changes in the permeability of the cell membrane; (ii) reactions of sulfydryl (-SH) groups with 

17 cations; (iii) affinity for reacting with phosphate groups and active groups of ADP or ATP; and 

18 (iv) replacement of essential ions (Patra et al., 2004). 

19 New information since the last review provides additional evidence of plant uptake of 

20 organics (US EPA, 2009a, section 9.4.6). An area of active study is the impact of PAHs on 

21 provisioning ecosystem services due to the potential for human and other animal exposure via 

22 food consumption (US EPA, 2009a, section 9.4.6 page 9-190). The uptake of PAHs depends on 

23 the plant species, site of deposition, physical and chemical properties of the organic compound 

24 and prevailing environmental conditions. It has been established that most bioaccumulation of 

25 PAHs by plants occurs via leaf uptake, and to a lesser extent, through roots. Differences 

26 between species in uptake of PAHs confound attempts to quantify impacts to ecosystem 

27 provisioning services. For example, zucchini (Cucurbita pepo) accumulated significantly more 

28 PAHs than related plant species (Parrish et al., 2006). 

29 Plants as ecosystem regulators can serve as passive monitors of pollution (US EPA, 

30 2009a, section 9.4.2.3). Lichens and mosses are sensitive to pollutants associated with PM and 

31 have been used with limited success to show spatial and temporal patterns of atmospheric 

32 deposition of metals (US EPA, 2009a, section 9.4.2.3). For example, the presence or absence of 

33 a specific species of lichen can be used as a bioindicator of metal or organics contamination. 

34 PBDEs detected in moss and lichens in Antarctica indicate long-range transport of PM 

35 components (Yogui and Sericano 2008). In the U.S. Blue Ridge Mountains, a study linked metal 

36 concentrations in mosses to elevation and tree canopy species at some sites but not with 
 

Draft Do Not Quote or Cite March 2010

5-18

1 concentrations of metals in the O horizon of soil (Schilling, 2002). A limitation to employing 

2 mosses and lichens to detect for the presence of air pollutants is the difference in uptake 

3 efficiencies of metals between species. The European Moss Biomonitoring Network has been 

4 shown to be useful in Europe for estimating general trends in metal concentrations and 

5 identification of some sources of trace contaminants, however, quantification of ecological 

6 effects is not possible due to the variability of species responses (US EPA, 2009a, section 

7 9.4.2.3). 

8 A potentially important regulating ecosystem service of plants is their capacity to 

9 sequester contaminants (US EPA, 2009a, section 9.4.5.3). Ongoing research on the application 

10 of plants to environmental remediation efforts are yielding some success in removing heavy 

11 metals and organics from contaminated sites (phytoremediation) with tolerant plants such as the 

12 willow tree (Salix spp.) and members of the family Brassicaceae (US EPA, 2009a, section 

13 9.4.5.3). Tree canopies can be used in urban locations to capture particulates and improve air 

14 quality (Freer-Smith et al., 2004). Plant foliage is a sink for Hg and other metals and this 

15 regulating ecosystem service may be impacted by atmospheric deposition of trace metals. 

16 An ecological endpoint (phytochelatin concentration) associated with presence of metals 

17 in the environment has been correlated with the ecological effect of tree mortality (Grantz et al., 

18 2003). Metal stress may be contributing to tree injury and forest decline in the Northeastern U.S. 

19 where red spruce populations are declining with increasing elevation. Quantitative assessment of 

20 PM damage to forests potentially could be conducted by overlaying PM sampling data and 

21 elevated phytochelatin levels. However, limited data on phytochelatin levels in other species 

22 currently hinders use of this peptide as a general biomarker for PM. 

23 The presence of PM in the atmosphere affects ambient radiation as discussed in the ISA 

24 which can impact the amount of sunlight received by plants (US EPA, 2009a, section 9.4.4). 

25 Atmospheric PM can change the radiation reaching leaf surfaces through attenuation and by 

26 converting direct radiation to diffuse radiation. Diffuse radiation is more uniformly distributed in 

27 a tree canopy, allowing radiation to reach lower leaves. The net effect of PM on photosynthesis 

28 depends on the reduction of photosynthetically active radiation (PAR) and the increase in the 

29 diffuse fraction of PAR. Decreases in crop yields (provisioning ecosystem service) have been 

30 attributed to regional scale air pollution, however, global models suggest that the diffuse light 

31 fraction of PAR can increase growth (US EPA, 2009a, section 9.4.4). 

32 Soil and Nutrient Cycling

33 Many of the major indirect plant responses to PM deposition are chiefly soil-mediated 

34 and depend on the chemical composition of individual components of deposited PM. Major 

35 ecosystem services impacted by PM deposition to soils include support services such as nutrient 

36 cycling, products such as crops and regulating flooding and water quality. Upon entering the soil 
 

Draft Do Not Quote or Cite March 2010

5-19

1 environment, PM pollutants can alter ecological processes of energy flow and nutrient cycling, 

2 inhibit nutrient uptake to plants, change microbial community structure and, affect biodiversity. 

3 Accumulation of heavy metals in soils depends on factors such as local soil characteristics, 

4 geologic origin of parent soils, and metal bioavailability. It can be difficult to assess the extent 

5 to which observed heavy metal concentrations in soil are of anthropogenic origin (US EPA, 

6 2009a, section 9.4.5.1). Trace element concentrations are higher in some soils that are remote 

7 from air pollution sources due to parent material and local geomorphology. 

8 Heavy metals such as Zn, Cu, and Cd and some pesticides can interfere with 

9 microorganisms that are responsible for decomposition of soil litter, an important regulating 

10 ecosystem service that serves as a source of soil nutrients (US EPA, 2009a, sections 9.4.5.1 and 

11 9.4.5.2). Surface litter decomposition is reduced in soils having high metal concentrations. Soil 

12 communities have associated bacteria, fungi, and invertebrates that are essential to soil nutrient 

13 cycling processes. Changes to the relative species abundance and community composition can 

14 be quantified to measure impacts of deposited PM to soil biota. A mutualistic relationship exists 

15 in the rhizophere (plant root zone) between plant roots, fungi, and microbes. Fungi in 

16 association with plant roots form mycorrhizae that are essential for nutrient uptake by plants. 

17 The role of mychorrizal fungi in plant uptake of metals from soils and effects of deposited PM 

18 on soil microbes is discussed in section 9.4.5.2 of the ISA. 

19 Wildlife

20 Animals play a significant role in ecosystem function including nutrient cycling and crop 

21 production (supporting ecosystem service), and as a source of food (provisioning ecosystem 

22 service). Cultural ecosystem services provided by wildlife include bird and animal watching, 

23 recreational hunting and fishing. Impacts on these services are dependent upon the 

24 bioavailability of deposited metals and organics and their respective toxicities to ecosystem 

25 receptors. Pathways of PM exposure to fauna include ingestion, absorption and trophic transfer. 

26 Bioindicator species (known as sentinel organisms) can provide evidence of contamination due 

27 to atmospheric pollutants. Use of sentinel species can be of particular value because chemical 

28 constituents of deposited PM are difficult to characterize and have varying bioavailability (US 

29 EPA, 2009a, section 9.4.5.5). Snails readily bioaccumulate contaminants such as PAHs and 

30 trace metals. These organisms have been deployed as biomonitors for urban pollution and have 

31 quantifiable biomarkers of exposure including growth inhibition, impairment of reproduction, 

32 peroxidomal proliferation and induction of metal detoxifying proteins (metallothioneins) 

33 (Gomet-de Vaufleury, 2000; Regoli, 2006). Earthworms have also been used as sensitive 

34 indicators of soil metal contamination. 

35 Evidence of deposited PM effects on animals is limited (US EPA, 2009a, section 9.4.5.5). 

36 Trophic transfer of pollutants of atmospheric origin has been demonstrated in limited studies. 
 

Draft Do Not Quote or Cite March 2010

5-20

1 PM may also be transferred between aquatic and terrestrial compartments. There is limited 

2 evidence for biomagnifications of heavy metals up the food chain except for Hg which is well 

3 known to move readily through environmental compartments (US EPA, 2009a section 9.4.5.6). 

4 Bioconcentration of POPs and PBDEs in the Arctic and deep-water oceanic food webs indicates 

5 the global transport of particle-associated organics (US EPA, 2009a, section 9.4.6). Salmon 

6 migrations are contributing to metal accumulation in inland aquatic systems, potentially 

7 impacting the provisioning and cultural ecosystem service of fishing (US EPA, 2009a, section 

8 9.4.6). Stable isotope analysis can be applied to establish linkages between PM exposure and 

9 impacts to food webs, however, the use of this evaluation tool is limited for this ecological 

10 endpoint due to the complexity of most trophic interactions (US EPA 2009a, section 9.4.5.6). 

11 Foraging cattle have been used to assess atmospheric deposition and subsequent bioaccumulation 

12 of Hg and trace metals and their impacts on provisioning services (US EPA, 2009a, section 

13 9.4.2.3). 

14 Water

15 New limited information on impacts of deposited PM on receiving water bodies indicate 

16 that the ecosystem services of primary production, provision of fresh water, regulation of climate 

17 and floods, recreational fishing and water purification are adversely impacted by atmospheric 

18 inputs of metals and organics (US EPA, 2009a, sections 9.4.2.3 and 9.4.5.4). Deposition of PM 

19 to surfaces in urban settings increases the metal and organic component of storm water runoff 

20 (US EPA, 2009a, sections 9.4.2.3). This atmospherically-associated pollutant burden can then be 

21 toxic to aquatic biota. 

22 Atmospheric deposition can be the primary source of some organics and metals to 

23 watersheds. The contribution of atmospherically deposited PAHs to aquatic food webs was 

24 demonstrated in high elevation mountain lakes with no other anthropogenic contaminant sources 

25 (US EPA, 2009a, section 9.4.6). Metals associated with PM deposition limit phytoplankton 

26 growth, impacting aquatic trophic structure. Long-range atmospheric transport of 47 pesticides 

27 and degradation products to the snowpack in seven national parks in the Western U.S. was 

28 recently quantified indicating PM-associated contaminant inputs to receiving waters during 

29 spring snowmelt (Hageman et al., 2006). 

30 • What new techniques are available to improve our understanding of ecosystem 

31 effects associated with metal and organic components of PM? 

32 Regionally-based comprehensive ecological studies

33 The recently completed Western Airborne Contaminants Assessment Project (WACAP) 

34 is the most comprehensive database on contaminant transport and PM depositional effects on 

35 sensitive ecosystems in the U.S. In this project, the transport, fate, and ecological impacts of 
 

Draft Do Not Quote or Cite March 2010

5-21

1 anthropogenic contaminants from atmospheric sources were assessed from 2002 to 2007 in seven 

2 ecosystem components (air, snow, water, sediment, lichen, conifer needles and fish) in eight 

3 core national parks (Landers et al., 2008). The goals of the study were to identify where the 

4 pollutants were accumulating, identify ecological indicators for those pollutants causing 

5 ecological harm, and to determine the source of the air masses most likely to have transported 

6 the contaminants to the parks (US EPA, 2009a, section 9.4.6). Collected data were analyzed to 

7 identify probable local, regional and/or global sources of deposited PM components and their 

8 concurrent effects on ecological receptors. The study concluded that bioaccumulation of semi9 volatile organic compounds (SOCs) was observed throughout park ecosystems (Landers et al., 

10 2008). Findings from this study included the observation of an elevational gradient in PM 

11 deposition with greater accumulation at higher altitude areas of the parks. Furthermore, specific 

12 ecological indicators were indentified in the WACAP that can be useful in assessing 

13 contamination on larger spatial scales. For example, quantification of concentrations of selected 

14 pesticides in second-year conifer needles served as a method for regional-scale comparison of 

15 pollutant distribution (Landers et al., 2008). 

16 In the WACAP study, bioaccumulation and biomagnification of airborne contaminants 

17 were demonstrated on a regional scale in remote ecosystems in the Western United States. 

18 Contaminants were shown to accumulate geographically based on proximity to individual 

19 sources or source areas, primarily agriculture and industry (Landers et al., 2008). This finding 

20 was counter to the original working hypothesis that most of the contaminants found in western 

21 parks would originate from eastern Europe and Asia (Landers et al., 2008 p 6-8). The WACAP 

22 study represents an experimental design in which ecological effects could be correlated to 

23 ambient pollutant levels on a regional scale. Although this assessment focuses on chemical 

24 species that are components of PM, it does not specifically assess the effects of particulates 

25 versus gas-phase forms; therefore, in most cases it is difficult to apply the results to this 

26 assessment based on particulate concentration and size fraction (US EPA, 2009a, section 9.4.6). 

27 There is a need for ecological modeling of PM components in different environmental 

28 compartments to further elucidate links between PM and ecological indicators. 

29 Europe and other countries are using the critical load approach to assess pollutant effects 

30 at the level of the ecosystem. This type of assessment requires site-specific data and information 

31 on individual species responses to PM. In respect to trace metals and organics, there are 

32 insufficient data for the vast majority of U.S. ecosystems to calculate critical loads, however, a 

33 methodology is being presented in the NOx/SOx Secondary REA (US EPA 2009h) to calculate 

34 atmospheric concentrations from deposition that may be applicable to other environmental 

35 contaminants. 
 

Draft Do Not Quote or Cite March 2010

5-22

1 • Is there currently available information on ambient levels of PM that cause 

2 adverse effects on ecosystem components? 

3 As reviewed above, there is considerable data on impacts of PM on ecological receptors, 

4 but few studies that link ambient PM levels to observed effect. This is due, in part, to the nature, 

5 deposition, transport and fate of PM in ecosystems. PM is not a single pollutant, but a 

6 heterogeneous mixture of particles differing in size, origin and chemical composition (US EPA, 

7 2009a, section 9.4.1). The heterogeneity of PM exists not only within individual particles or 

8 samples from individual sites, but to even a greater extent, between samples from different sites. 

9 Since vegetation and other ecosystem components are affected more by particulate chemistry 

10 than size fraction, exposure to a given mass concentration of airborne PM may lead to widely 

11 differing plant or ecosystem responses, depending on the particular mix of deposited particles. 

12 Many of the PM components bioaccumulate over time in organisms or plants making 

13 correlations to ambient levels of PM impossible. For example, in the WACAP study, SOC 

14 accumulation in vegetation and air showed different patterns, possibly because each medium 

15 absorbs different types of SOCs with varying efficiencies (Landers et al., 2008). 

16 Bioindicator organisms demonstrated biological effects including growth inhibition, 

17 metallothionein induction and reproductive impairment when exposed to complex mixtures of 

18 ambient air pollutants (US EPA 2009a, section 9.4.5.5). Other studies quantify uptake of metals 

19 and organics by plants or animals. However, due to the difficulty in correlating individual PM 

20 components to a specific physiological response, these studies are limited. Furthermore, there 

21 may be differences in uptake between species such as differing responses to metal uptake 

22 observed in mosses and lichens (US EPA 2009a, section 9.4.2.3). PM may also biomagnify 

23 across trophic levels confounding efforts to link atmospheric concentrations to physiological 

24 endpoints (US EPA, 2009a, section 9.4.5.6). 

25 Evidence of PM effects that are linked to a specific ecological endpoint can be observed 

26 when ambient levels are exceeded. Most direct ecosystem effects associated with particulate 

27 pollution occur in severely polluted areas near industrial point sources (quarries, cement kilns, 

28 metal smelting) (US EPA, 2009a, sections 9.4.3 and 9.4.5.7) . Extensive research on biota near 

29 point sources provide some of the best evidence of ecosystem function impacts and demonstrates 

30 that deposited PM has the potential to alter species composition over long time scales. 

31 Ecological field studies conducted in proximity to Cu-Ni smelter in Harjavalta, Finland indicated 

32 ecological structure and community composition are altered in response to PM and these effects 

33 decrease with increasing distance from the point source (US EPA 2009a, section 9.4.5.7). The 

34 ISA indicates at 4 km distance, species composition of vegetation, insects, birds, and soil 

35 microbiota changed, and within 1 km only the most resistant organisms were surviving (US 

36 EPA, 2009a, section 9.4.5.7). Heavy metal concentrations were quantified in understory plant 
 

Draft Do Not Quote or Cite March 2010

5-23

1 species growing at varying distance from the Harjavalta smelter (Salemaa et al., 2004). Heavy 

2 metal concentrations were highest in bryophytes, followed by lichens and were lowest in 

3 vascular plants. At the Harjavalta smelter there are clear links between PM deposition levels, 

4 ecological endpoints and compromised ecosystem structure. However, these conditions are not 

5 reflective of ambient concentrations of PM in the majority of US ecosystems (US EPA, 2009a, 

6 section 9.4.7). 

7 5.3.3 Preliminary Staff Conclusions 

8 • A number of significant environmental effects that either have already occurred or are 

9 currently occurring are linked to deposition of chemical constituents found in ambient 

10 PM. 

11 • Ecosystem services can be adversely impacted by PM in the environment, including 

12 supporting, provisioning, regulating and cultural services. 

13 • The lack of sufficient information to relate specific ambient concentrations of 

14 particulate metals and organics to a degree of impairment of a specific ecological 

15 endpoint hinders our ability to identify a range of appropriate indicators, levels, forms 

16 and averaging times of a distinct secondary standard to protect against associated 

17 effects. 

18 • Data from regionally-based ecological studies can be used to establish probable local, 

19 regional and/or global sources of deposited PM components and their concurrent 

20 effects on ecological receptors. 

21 Collectively taking into consideration the responses to specific questions regarding the 

22 adequacy of the current secondary PM standards for ecological effects, we revisit the 

23 overarching question: “does available scientific information, as reflected in the ISA, support or 

24 call into question the adequacy of the protection for ecosystems afforded by the current suite of 

25 secondary PM standards?” Staff reaches the preliminary conclusion that the available 

26 information is insufficient to assess the adequacy of the protection for ecosystems afforded by 

27 the current suite of PM secondary standards. Ecosystem effects linked to PM are difficult to 

28 determine because the changes may not be observed until pollutant deposition has occurred for 

29 many decades. Because the high levels necessary to cause injury occur only near a few limited 

30 point sources and/or on a very local scale, protection against these effects alone may not provide 

31 sufficient basis for considering a separate secondary NAAQS based on the ecological effects of 

32 particulate metals and organics. Data on ecological responses clearly linked with atmospheric 

33 PM is not abundant enough to perform a quantitative analysis although the WACAP study may 

34 represent an opportunity for quantification at a regional scale. At this time, we conclude that 

35 available evidence is not sufficient for establishing a distinct national standard for ambient PM 

36 based on ecosystem effects of particulates not addressed in the NOx/SOx secondary review (e.g. 

37 metals, organics). 
 

Draft Do Not Quote or Cite March 2010

5-24

1 Staff considered the appropriateness of continuing to use the PM2.5 and PM10 size 

2 fractions as the indicators for protection of ecological effects of PM. Though the chemical 

3 constitution of individual particles can be strongly correlated with size, the relationship between 

4 particle size and particle composition can also be quite complex, making it difficult in most cases 

5 to use particle size as a surrogate for chemistry. At this time it remains to be determined as to 

6 what extent PM secondary standards focused on a given size fraction would result in reductions 

7 of the ecologically relevant constituents of PM for any given area. 

8 5.3.4 Key Uncertainties and Areas for Future Research and Data Collection 

9 The above discussions identify linkages between ecological effects of deposited PM and 

10 potential impacts to ecosystem services. Unfortunately, our ability to relate ambient 

11 concentrations of PM to ecosystem response is hampered by a number of significant data gaps 

12 and uncertainties. These limitations include the presence of multiple ecological stressors 

13 confounding attempts to link specific ecosystem responses to PM deposition. These stressors 

14 can be anthropogenic (e.g. habitat destruction, eutrophication, other pollutants) or natural (e.g. 

15 drought, fire, disease). Deposited PM interacts with other stressors to affect ecosystem patterns 

16 and processes. Furthermore, the environmental effects of deposited PM are decoupled in space 

17 and time from the point of emission confounding efforts to identify ecological perturbations 

18 attributed to PM deposition. 

19 A second source of uncertainty lies in predicting the amount of PM deposited to sensitive 

20 receptors from measured concentrations of PM in the ambient air. This makes it difficult to 

21 relate a given air concentration to a receptor response, an important factor in being able to set a 

22 national ambient air quality standard. A multitude of factors such as the mode of deposition 

23 (wet, dry and occult), wind speed, surface roughness or stickiness, elevation, particle 

24 characteristics (e.g. size, shape, chemical composition), and relative humidity exert varying 

25 degrees of influence on the deposition velocities for different PM components in any point in 

26 time. Composition of ambient PM varies in time and space and the particulate mixture may have 

27 synergistic, antagonistic or additive effects on ecological receptors depending upon the chemical 

28 species present. Furthermore, presence of co-occurring pollutants make it difficult to attribute 

29 observed effects to ecological receptors to PM alone or one component of deposited PM. 

30 Third, each ecosystem has developed within a context framed by the topography, 

31 underlying bedrock, soils, climate, meteorology, hydrologic regime, natural and land use history, 

32 and species composition that make it unique from all others. Sensitivity of ecosystem response 

33 is highly variable in space and time. Because of this variety and lack of sufficient baseline data 

34 on each of these features for most ecosystems, it is currently not possible to extrapolate with 

35 confidence any effect from one ecosystem to another. 
 

Draft Do Not Quote or Cite March 2010

5-25

1 5.4 MATERIALS 

2 5.4.1 Scope 

3 Welfare effects on materials associated with deposition of PM include both physical 

4 damage (materials damage effects) and impaired aesthetic qualities (soiling effects). Because the 

5 effects of PM are exacerbated by the presence of acidic gases and can be additive or synergistic 

6 due to the complex mixture of pollutants in the air and surface characteristics of the material, this 

7 discussion will also include those particles and gases that are associated with the presence of 

8 ambient NOx and SOx, as well as NH3 and NHX for completeness. Building upon the 

9 information presented in the last Staff Paper (US EPA, 2005), and including the limited new 

10 information presented in Chapter 9 of the PM ISA (US EPA, 2009a) and Annex E. Effects of 

11 NOy, NHx, and SOx on Structures and Materials of the Integrated Science Assessment for 

12 Oxides of Nitrogen and Sulfur-Ecological Criteria (NOx/SOx ISA) (US EPA, 2008c) the 

13 following sections consider the policy-relevant aspects of physical damage and aesthetic soiling 

14 effects of PM on materials including metal and stone. 

15 The ISA concludes that evidence is sufficient to support a causal relationship between 

16 PM and effects on materials (US EPA, 2009a, sections 2.5.4 and 9.5.4). The deposition of PM 

17 can physically affect materials, adding to the effects of natural weathering processes, by 

18 potentially promoting or accelerating the corrosion of metals, by degrading paints and by 

19 deteriorating building materials such as stone, concrete and marble (US EPA, 2009a, section 

20 9.5). Particles contribute to these physical effects because of their electrolytic, hygroscopic and 

21 acidic properties, and their ability to sorb corrosive gases (principally SO2). In addition, the 

22 deposition of ambient PM can reduce the aesthetic appeal of buildings and objects through 

23 soiling. Particles consisting primarily of carbonaceous compounds cause soiling of commonly 

24 used building materials and culturally important items such as statues and works of art. Soiling 

25 is the deposition of particles on surfaces by impingement, and the accumulation of particles on 

26 the surface of an exposed material results in degradation of its appearance (US EPA 2009a, 

27 section 9.5). Soiling can be remedied by cleaning or washing, and depending on the soiled 

28 material, repainting. 

29 5.4.2 Adequacy of the Current Standard 

30 In considering the adequacy of the suite of secondary standards, staff addresses the 

31 following overarching question: 

32 Does available scientific information, as reflected in the ISA support or call into question 

33 the adequacy of the protection for materials afforded by the current suite of secondary PM 

34 standards? 
 

Draft Do Not Quote or Cite March 2010

5-26

1 To inform the answer to this overarching question, staff has posed a specific question to 

2 aid in assessing the available scientific evidence as related to materials damage and soiling 

3 attributed to PM deposition as presented in the ISA (US EPA, 2009a).

4 • What new evidence is available to improve our understanding of effects of PM on 

5 materials and linking ambient concentrations to materials damage? 

6 The majority of available new studies on materials effects of PM are from outside the 

7 U.S., however, they provide limited new data for consideration of the secondary standard. 

8 Metal and stone are susceptible to damage by ambient PM. Considerable research has 

9 been conducted on the effects of air pollutants on metal surfaces due to the economic importance 

10 of these materials, especially steel, zinc, aluminum, and copper. Chapter 9 of the PM ISA and 

11 Annex E of the NOx/SOx ISA summarize the results of a number of studies on the corrosion of 

12 metals (US EPA, 2009a; US EPA, 2008c). Moisture is the single greatest factor promoting metal 

13 corrosion, however, deposited PM can have additive, antagonistic or synergistic effects. In 

14 general, SO2 is more corrosive than NOx although mixtures of NOx, SO2 and other particulate 

15 matter corrode some metals at a faster rate than either pollutant alone (US EPA, 2008c, Annex 

16 E.5.2). Information from both the PM ISA and NOx/SOx ISA suggest that the extent of damage 

17 to metals due to ambient PM is variable and dependent upon the type of metal, prevailing 

18 environmental conditions, rate of natural weathering and presence or absence of other pollutants. 

19 The PM ISA and NOx/SOx ISA summarize the results of a number of studies on PM and 

20 stone surfaces. While it is clear from the available information that gaseous air pollutants, in 

21 particular SO2, will promote the deterioration of some types of stones under specific conditions, 

22 carbonaceous particles (non-carbonate carbon) and particles containing metal oxides may help to 

23 promote the decay process. Studies on metal and stone summarized in the ISA do not show an 

24 association between particle size, chemical composition and frequency of repair. 

25 A limited number of new studies available on materials damage effects of PM since the 

26 last review consider the relationship between pollutants and biodeterioration of structures 

27 associated with microbial communities that colonize monuments and buildings (US EPA 2009a, 

28 section 9.5). Presence of air pollutants may synergistically enhance microbial deterioration 

29 processes. The role of heterotrophic bacteria, fungi and cyanobacteria in biodeterioration varied 

30 by local meterological conditions and pollutant components. In a comparative study of 

31 biodeterioration processes on monuments in Latin America, limestone deterioration at the Mayan 

32 site of Uxmal was enhanced by biosolubilization by metabolic acids from bacteria and fungi 

33 while destruction of the Cathedral of La Plata was attributed primarily to atmospheric pollutants 

34 (Herrera and Videla, 2006). 

35 PM deposition onto surfaces such as metal, glass, stone and paint can lead to soiling. 

36 Soiling results when PM accumulates on an object and alters the optical characteristics 
 

Draft Do Not Quote or Cite March 2010

5-27

1 (appearance). The reflectivity of a surface may be changed or presence of particulates may alter 

2 light transmission. These effects can impact the aesthetic value of a structure or result in 

3 reversible or irreversible damage to statues, artwork and architecturally or culturally significant 

4 buildings. Due to soiling of building surfaces by PM, the frequency and duration of cleaning 

5 may be increased. Soiling affects the aesthetic appeal of painted surfaces. In addition to natural 

6 factors, exposure to PM may give painted surfaces a dirty appearance. Pigments in works of art 

7 can be degraded or discolored by atmospheric pollutants, especially sulfates (US EPA, 2008c, 

8 Annex E-15). 

9 Formation of black crusts due to carbonaceous compounds and buildup of microbial 

10 biofilms results in discoloration of surfaces. Black crust includes a carbonate component derived 

11 from building material and organic carbon (OC) and elemental carbon (EC). In limited new 

12 studies quantifying the OC and EC contribution to soiling by black crust, OC predominated over 

13 EC at almost all locations (Bonazza et al., 2005). Limited new studies suggest that traffic is the 

14 major source of carbon associated with black crust formation (Putaud, 2004) and that soiling of 

15 structures in Oxford, UK showed a relationship with traffic and NO2 concentrations (Viles and 

16 Gorbushina, 2003). These findings attempt to link atmospheric concentrations of PM to 

17 observed damage. However, no data on rates of damage are available and all studies were 

18 conducted outside of the U.S. 

19 5.4.3 Preliminary Staff Conclusions 

20 Available evidence in regards to materials damage and soiling supports the following 

21 observations: 

22 • Materials damage and soiling that occur through natural weathering processes are 

23 enhanced by exposure to atmospheric pollutants, most notably SO2 and particulate 

24 sulfates. 

25 • While ambient particles play a role in the corrosion of metals and in the weathering of 

26 materials, no quantitative relationships between ambient particle concentrations and 

27 rates of damage have been established. 

28 • While soiling associated with fine and course particles can result in increased cleaning 

29 frequency and repainting of surfaces, no quantitative relationships between particle 

30 characteristics and the frequency of cleaning or repainting have been established. 

31 • Limited new data on the role of microbial colonizers in biodeterioration processes and 

32 contributions of black crust to soiling are not sufficient for quantitative analysis. 

33 • While several studies in the PM ISA and NOx/SOx ISA suggest that particles can 

34 promote corrosion of metals there remains insufficient evidence to relate corrosive 

35 effects to specific particulate levels or to establish a quantitative relationship between 

36 ambient PM and metal degradation. With respect to damage to calcareous stone, 
 

Draft Do Not Quote or Cite March 2010

5-28

1 numerous studies suggest that wet or dry deposition of particles and dry deposition of 

2 gypsum particles can enhance natural weathering processes. 

3 Revisiting the overarching policy question as to whether the available scientific evidence 

4 supports or calls into question the adequacy of the protection for materials afforded by the 

5 current suite of secondary PM standards, we reach the preliminary conclusion that no new 

6 evidence in this review calls into question the adequacy of the protection for materials afforded 

7 by the current standard. PM effects on materials can play no quantitative role in considering 

8 whether any revisions of the secondary PM NAAQS are appropriate at this time. However, in 

9 the absence of information that provides a basis for establishing a different level of control, 

10 observations continue to support retaining an appropriate degree of control on both fine and 

11 coarse particles to help address materials damage and soiling associated with PM. 

12 5.4.4 Key Uncertainties and Areas for Future Research and Data Collection 

13 Quantitative relationships are needed between particle size, concentration, chemical 

14 concentrations and frequency of repainting and repair. Deposition rates of airborne PM to 

15 surfaces would provide an indication of rate and degree of damage to surfaces. There is 

16 considerable uncertainty with regard to interaction of co-pollutants in regards to materials 

17 damage and soiling processes. 

18 5.5 REFERENCES 

19 Audet P; Charest C (2007). Heavy metal phytoremediation from a meta-analytical perspective. Environ Pollut, 147: 

20 231-237. 

21 Bonazza A; Sabbioni C; Ghedini N. (2005). Quantitative data on carbon fractions in interpretation of black crusts 

22 and soiling on European built heritage. Atmos Environ, 39: 2607-2618. 

23 Bond TC; Streets DG; Yarber KF; Nelson SM; Woo J-H; Klimont Z. (2004). A technology-based global inventory 

24 of black and organic carbon emissions from combustion. J Geophys Res, 109. 

25 Bond TC; Sun H. (2005). Can reducing black carbon emissions counteract global warming?. Environ Sci Technol, 

26 39: 5921-5926. 

27 CCSP (2009). Atmospheric Aerosol Properties and Climate Impacts, A Report by the U.S. Climate Change Science 

28 Program and the Subcommittee on Global Change Research. [Mian Chin, Ralph A. Kahn, and Stephen E. 

29 Schwartz (eds.)]. National Aeronautics and Space Administration, Washington, D.C., USA. 

30 Forster P; Ramaswamy V; Artaxo P; Betss R; Fahey DW; Haywood J; Lean J; Lowe DC; Myhre G; Nganga J; Prinn 

31 R; Raga G;Schultz M; Van Dorland R. (2007). Changes in atmospheric constituents and in radiative 

32 forcing. In Solomon, S.; Qin,D.; Manning, M.; Chen, Z.; Marquis, M.; Averyt, K. B.; Tignor, M.; Miller, 

33 H. L. (Ed.),Climate Change 2007: the physical science basis. Contribution of Working Group I to the fourth 

34 assessment report of the intergovernmental panel. 

35 Freer-Smith PH; El-khatib A; Taylor G. (2004). Capture of particulate pollution by trees: a comparison of species 

36 typical of semi-arid areas (Ficus nitida and Eucalyptus globulus) with European and North American 

37 species. Water Air Soil Pollut,155: 173-187. 
 

Draft Do Not Quote or Cite March 2010

5-29

1 Gitay H; Brown S; Easterling W; Jallow B. (2001). Ecosystems and their goods and services. In Climate change 

2 2001: impacts,adaptation and vulnerability. Contribution of working group II to the third assessment report 

3 of the Intergovernmental Panel on Climate Change (pp. 237-342). Cambridge, United Kingdom: 

4 Cambridge University Press. 

5 Givati A; Rosenfeld D. (2004). Quantifying precipitation suppression due to air pollution. , 43: 1038-1056. 

6 Gomot-De Vaufleury A; Pihan F. (2002). Methods for toxicity assessment of contaminated soil by oral or dermal 

7 uptake in land snails: Metal bioavailability and bioaccumulation. Environ Toxicol Chem, 21: 820-827. 

8 Grantz DA; Garner JHB; Johnson DW. (2003). Ecological effects of particulate matter. Environ Int, 29: 213-239. 

9 Hageman KJ; Simonich SL; Campbell DH; Wilson GR; Landers DH. (2006). Atmospheric deposition of current-use 

10 and historic-use pesticides in snow at national parks in the western United States. Environ Sci Technol, 40: 

11 3174-3180 

12 Hassan R; Scholes R; Ash N. (2005). Ecosystems and human well-being: current state and trends, volume 1. Herrera 

13 LK; Videla HA. (2004). The importance of atmospheric effects on biodeterioration of cultural heritage 

14 constructional materials. Int Biodeterior Biodegradation, 54: 125-134. IPCC (2007). Summary for 

15 Policymakers. In Climate Change 2007: The Physical Science Basis. Contribution of Working Group I to 

16 the Fourth Assessment Report of the Intergovernmental Panel on Climate Change (Solomon, S; Quin D, 

17 Manning M, Cehn Z; Marquis M; Averyt KB; Tignor M; and Miller HL (eds.) Cambridge University Press, 

18 Cambridge United Kingdom and New York, NY, USA. 

19 Herrera LK; Videla HA. (2004). The importance of atmospheric effects on biodeterioration of cultural heritage 

20 constructional materials. Int Biodeterior Biodegradation, 54: 125-134. 

21 IPCC (2007): Summary for Policymakers. In: Climate Change 2007: The Physical Science Basis. Contribution of 

22 Working Group I to the Fourth Assessment Report of the Intergovernmental Panel on Climate Change 

23 [Solomon, S., D. Qin, M. Manning, Z. Chen, M. Marquis, K.B. Averyt, M.Tignor and H.L. Miller (eds.)]. 

24 Cambridge University Press, Cambridge, United Kingdom and New York, NY, USA. 

25 Jacobson MZ. (2000). A physically-based treatment of elemental carbon optics: implications for global direct 

26 forcing of aerosols. Geophys Res Lett, 27: 217-220. 

27 Jacobson MZ; Kaufman YJ. (2006). Wind reduction by aerosol particles. Geophys Res Lett, 33. 

28 Kucera T; Horakova H; Sonska A (2008). Toxic metal ions in photoautotrophic organisms. Photosynthetica, 46: 

29 481-489. 

30 Landers DH; Simonich SL; Jaffe DA; Geiser LH; Campbell DH; Schwindt AR; Schreck CB; Kent ML; Hafner WD; 

31 Taylor HE; Hageman KJ; Usenko S; Ackerman LK; Schrlau JE; Rose NL; Blett TF; Erway MM. (2008). 

32 The Fate, Transport and Ecological Impacts of Airborne Contaminants in Western National Parks (USA). 

33 U.S. Environmental Protection Agency, Office of Research and Development, NHEERL, Western Ecology 

34 Division. Corvallis, Oregon. EPA/600/R-07/138

35 National Research Council. (2001). Climate change science: an analysis of some key questions. National Research 

36 Council. National Academy Press. Washington, DC. 

37 Parrish ZD; White JC; Isleyen M; Gent MPN; Iannucci-Berger W; Eitzer BD; Kelsey JW; Mattina MI. (2006). 

38 Accumulation of weathered polycyclic aromatic hydrocarbons (PAHs) by plant and earthworm species. 

39 Chemosphere, 64: 609-618. 
 

Draft Do Not Quote or Cite March 2010

5-30

1 Patra M; Bhowmik N; Bandopadhyay B; Sharma A (2004). Comparison of mercury, lead and arsenic with respect to 

2 genotoxic effects on plant systems and the development of genetic tolerance. Environ Exp Bot, 52: 199-

3 223. 

4 Putaud J-P; Raes F; Van Dengenen R; Bruggemann E; Facchini M-C; Decesari S; Fuzzi S; Gehrig R; Huglin C; Laj 

5 P; Lorbeer G; Maenhaut W; Mihalopoulos N; Muller K; Querol X; Rodriguez S; Schneider J; Spindler G; 

6 ten Brink H; Torseth K; Wiedensohler A. (2004). A European aerosol phenomenology--2: chemical 

7 characteristics of particulate matter at kerbside, urban, rural and background sites in Europe. Atmos 

8 Environ, 38: 2579-2595. 

9 Regoli F; Gorbi S; Fattorini D; Tedesco S; Notti A; Machella N; Bocchetti R; Benedetti M; Piva F. (2006). Use of 

10 the land snail Helix aspersa sentinel organism for monitoring ecotoxicologic effects of urban pollution: An 

11 integrated approach. , 114:63-69. 

12 Salemaa M; Derome J; Helmisaari HS; Nieminen T; Vanha-Majamaa I. (2004). Element accumulation in boreal 

13 bryophytes,lichens and vascular plants exposed to heavy metal and sulfur deposition in Finland. Sci Total 

14 Environ, 324: 141-160. 

15 Sato M; Hansen J; Koch D; Lucis A; Ruedy R; Dubovik O; Holben B; Chin M; Novakov T. (2003). Global 

16 atmospheric black carbon inferred from AAEONET. Presented at Proceedings of the National Academy of 

17 Science. 

18 Schilling JS; Lehman ME. (2002). Bioindication of atmospheric heavy metal deposition in the Southeastern US 

19 using the moss Thuidium delicatulum. Atmos Environ, 36: 1611-1618. 

20 Smith WH (1990). Forest nutrient cycling: toxic ions. In Air pollution and forests: interactions between air 

21 contaminants and forest ecosystemsNew York, NY: Springer-Verlag. 

22 Strydom C; Robinson C; Pretorius E; Whitcutt JM; Marx J; Bornman MS (2006). The effect of selected metals on 

23 the central metabolic pathways in biology: A review. WaterSA, 32: 543-554. 

24 U.S. EPA (1996). Air quality criteria for particulate matter. U.S. Environmental Protection Agency. Research 

25 Triangle Park, NC. EPA/600/P-95/001aF-cF.

26 US EPA (2004). Air Quality Criteria for Particulate Matter. National Center for Environmental Assessment, Office 

27 of Research and Development, U.S. Environmental Protection Agency, Research Triangle Park, NC 27711; 

28 report no. EPA/600/P-99/002aF and EPA/600/P-99/002bF. October 2004. Available: 

29 http://www.epa.gov/ttn/naaqs/standards/pm/s_pm_cr_cd.html

30 US EPA (2005). Review of the National Ambient Air Quality Standards for Particulate Matter: Policy Assessment 

31 of Scientific and Technical Information, OAQPS Staff Paper. Research Triangle Park, NC 27711: Office 

32 of Air Quality Planning and Standards; report no. EPA EPA-452/R-05-005a. December 2005.

33 Available: http://www.epa.gov/ttn/naaqs/standards/pm/s_pm_cr_sp.html

34 U.S. EPA. (2006). Air Quality Criteria for Lead Final Report. U.S. Environmental Protection Agency, Washington, 

35 DC, EPA/600/R-05/144aF-bF, 2006. 

36 US EPA (2008a). Integrated Review Plan for the National Ambient Air Quality Standards for Particulate Matter. 

37 National Center for Environmental Assessment and Office of Air Quality Planning and Standards, U.S. 

38 Environmental Protection Agency, Research Triangle Park, NC. Report No. EPA 452/R-08-004. March 

39 2008. Available at: 

40 http://www.epa.gov/ttn/naaqs/standards/pm/data/2008_03_final_integrated_review_plan.pdf
 

Draft Do Not Quote or Cite March 2010

5-31

1 US EPA (2008c). U.S. EPA. Integrated Science Assessment (ISA) for Oxides of Nitrogen and Sulfur Ecological 

2 Criteria (Final Report). U.S. Environmental Protection Agency, Washington, D.C., EPA/600/R-08/082F, 

3 2008. 

4 US EPA (2009a). U.S. EPA. Integrated Science Assessment for Particulate Matter (Final Report). US. 

5 Environmental Protection Agency, Washington, DC, EPA/600/R-08/139F, 2009. 

6 US EPA (2009h) Risk and Exposure Assessment for Review of the Secondary National Ambient Air Quality 

7 Standards for Oxides of Nitrogen and Oxides of Sulfur. (Final Report). US Environmental Protection 

8 Agency, Research Triangle Park, NC, EPA-452/R-09-008a 

9 US EPA (2010c) Policy Assessment for the Review of the Secondary National Ambient Air Quality Standards for 

10 NOx and SOx, First External Review Draft. US Environmental Protection Agency, Research Triangle Park, 

11 NC, EPA-452/P-10-006 

12 Viles HA; Gorbushina AA. (2003). Soiling and microbial colonisation on urban roadside limestone: A three year 

13 study in Oxford, England. , 38: 1217-1224. 

14 Yogui G; Sericano J. (2008). Polybrominated diphenyl ether flame retardants in lichens and mosses from King 

15 George Island, maritime Antarctica. Chemosphere, 73: 1589-1593. 
United States 

Environmental Protection Agency 

Office of Air Quality Planning and Standards 

Health and Environmental Impacts Division 

Research Triangle Park, NC 

Publication N