UNITED STATES ENVIRONMENTAL PROTECTION AGENCY 

WASHINGTON D.C. 20460 

OFFICE OF THE ADMINISTRATOR 

 SCIENCE ADVISORY BOARD 

November 24, 2009 

EPA-CASAC-10-001 

The Honorable Lisa P. Jackson 

Administrator 

U.S. Environmental Protection Agency 

1200 Pennsylvania Avenue, NW 

Washington, D.C. 20460 

Subject: Review of Integrated Science Assessment for Particulate Matter (Second 

External Review Draft, July 2009)

Dear Administrator Jackson: 

The Clean Air Scientific Advisory Committee (CASAC) Particulate Matter (PM) 

National Ambient Air Quality Standards (NAAQS) Review Panel met on October 5 - 6, 2009 to 

review the Integrated Science Assessment for Particulate Matter (ISA), (Second External Review 

Draft, July 2009). The Panel also held a public teleconference on November 12, 2009 to discuss 

and finalize its draft report. In this letter, CASAC offers general comments on the ISA, followed 

by CASAC’s consensus responses to the Agency’s charge questions. Comments from individual 

panelists are also attached. 

CASAC commends EPA’s National Center for Environmental Assessment for its 

comprehensive effort to address the concerns and comments offered by CASAC in its review of 

the first draft ISA. EPA has improved the document and focused its presentation of a substantial 

body of evidence so that it now more clearly highlights the findings that are relevant to the Risk 

Assessment (RA) and the Policy Assessment (PA). As mentioned in its comments on the charge 

questions, CASAC also commends EPA for the continued evolution of the process for evidence 

evaluation. The five-level classification of strength of evidence for causal inference has been 

systematically applied; this approach has provided transparency and a clear statement of the level 

of confidence with regard to causation, and we recommend its continued use in future ISAs. The 

implementation of the Health & Environmental Research Online (HERO) database greatly 

enhances the ISA and facilitates its evaluation by providing electronic hotlinks to citations and 

study data. We support its further evolution to include abstracted, key findings. 

1
With regard to the approach taken in the ISA, we find EPA’s decision to focus the 

discussion of causality on PM2.5 and PM10-2.5 independently to be appropriate and supported by 

the scientific evidence. As stated in our earlier review of the 1st draft ISA, the handling of PM10

as a separate pollutant was problematic because it is comprised of the fine (PM2.5) and the coarse 

(PM10-2.5) fractions. CASAC also supports EPA’s changes to the causal determinations for longterm exposure to PM2.5 and cardiovascular effects (from “likely causal” to “causal”), for cancer 

and PM2.5 (from “inadequate” to “suggestive”) and for cardiovascular and respiratory effects of 

short-term exposure to ultrafine particulate matter (UFP) (from “inadequate” to “suggestive”). 

CASAC concurs with EPA’s definition of “susceptible subpopulations” as those that have a 

greater likelihood of experiencing health effects related to PM exposure; and we find that the 

ISA offers a careful characterization of the factors that may contribute to increased susceptibility 

to PM-induced health effects. 

In terms of welfare effects, the visibility valuation and preference studies help to 

demonstrate that there are levels of visual air quality which are consistently judged to be 

"unacceptable" at levels well below the current PM NAAQS in a number of different study areas, 

an important finding that is appropriately highlighted. CASAC concurs that Chapter 9 has been 

improved by the additional discussion of optical measurement methods. Added material 

provides further support for the proposed use of a new “PM light extinction” indicator, which 

would be both readily measurable and reflective of the human perception of visibility effects 

caused by PM pollutants. CASAC also concurs that the added discussions on climate forcing 

effects and on ecological effects of PM strengthen the chapter’s coverage of these topics. 

Ultimately, EPA should move toward developing exposure-response relationships for ecological 

endpoints, perhaps in the next review cycle for PM. 

We have two major suggestions for improvement: 

• The ISA could be strengthened by providing more information on the correlations of 

concentrations of PM10 with those of PM2.5 and PM10-2.5, preferably stratified by region of 

the country, in order to better understand PM10 as an indicator of the two subfractions, 

PM2.5 and PM10-2.5. As currently written, the ISA uses PM10 findings to support PM2.5

effects whereas the relevance of PM10 findings for PM10-2.5 effects is left ambiguous. 

Because of the role played by the current PM10 standard, PM10 findings that are 

particularly relevant to PM10-2.5 should also be highlighted. 

• CASAC recommends “upgrading” the causal classification for PM2.5 and total mortality 

to “causal” for both the short-term and long-term time frames. There are epidemiological 

studies showing a positive association of all-cause mortality with PM2.5. We 

acknowledge that the association is weaker for all-cause mortality (in comparison with 

cardiovascular mortality), but cardiovascular deaths are the largest component of total 

2
deaths attributable to PM. If PM2.5 effects for cardiovascular mortality are “causal,” they 

must also be “causal” for total mortality, and the weaker association with all-cause 

mortality would be anticipated. 

CASAC recommends that future assessments more fully consider evidence on the 

compositional differences in PM effects in relation to both health and welfare, especially given 

the emerging view that metals and carbonaceous aerosols, typically referred to as elemental and 

organic carbon, are of greater concern for many endpoints. 

CASAC agrees that the PM ISA will be adequate for rulemaking after EPA incorporates 

our major comments and recommendations as stated above. We thank the Agency for the 

opportunity to provide advice on the PM ISA. 

Sincerely,

/Signed/ 

Dr. Jonathan M. Samet, Chair 

Clean Air Scientific Advisory Committee 

Enclosures: A. CASAC Particulate Matter Review Panel Roster 

 B. CASAC Responses to Charge Questions 

 C. Individual Responses to Charge Questions 

3
Enclosure A

Clean Air Scientific Advisory Committee 

Particulate Matter Review Panel 

CHAIR 

Dr. Jonathan M. Samet, Professor and Chair, Department of Preventive Medicine, University of 

Southern California, Los Angeles, CA 

CASAC MEMBERS (FY 2009) 

Dr. Joseph Brain, Philip Drinker Professor of Environmental Physiology, Department of 

Environmental Health, Harvard School of Public Health, Harvard University, Boston, MA 

Dr. Ellis B. Cowling, University Distinguished Professor At-Large Emeritus, Colleges of Natural 

Resources and Agriculture and Life Sciences, North Carolina State University, Raleigh, NC 

Dr. James Crapo, Professor of Medicine, Department of Medicine, National Jewish Medical and 

Research Center, Denver, CO 

Dr. H. Christopher Frey, Professor, Department of Civil, Construction and Environmental 

Engineering, College of Engineering, North Carolina State University, Raleigh, NC 

Dr. Donna Kenski,∗

 Data Analysis Director, Lake Michigan Air Directors Consortium, 

Rosemont, IL 

Dr. Armistead (Ted) Russell, Professor, Department of Civil and Environmental Engineering, 

Georgia Institute of Technology, Atlanta, GA 

CONSULTANTS 

Dr. Lowell Ashbaugh, Associate Research Ecologist, Crocker Nuclear Lab, University of 

California, Davis, Davis, CA 

Prof. Ed Avol, Professor, Preventive Medicine, Keck School of Medicine, University of 

Southern California, Los Angeles, CA 

Dr. Wayne Cascio, Professor, Medicine, Cardiology, Brody School of Medicine at East Carolina 

University, Greenville, NC 

                                                           

∗ / Unable to participate in this review.   

4
Dr. David Grantz, Director, Botany and Plant Sciences and Air Pollution Research Center, 

Riverside Campus and Kearney Agricultural Center, University of California, Parlier, CA 

Dr. Joseph Helble, Dean and Professor, Thayer School of Engineering, Dartmouth College, 

Hanover, NH 

Dr. Rogene Henderson, Senior Scientist Emeritus, Lovelace Respiratory Research Institute, 

Albuquerque, NM 

Dr. Philip Hopke, Bayard D. Clarkson Distinguished Professor, Department of Chemical 

Engineering, Clarkson University, Potsdam, NY 

Dr. Morton Lippmann, Professor, Nelson Institute of Environmental Medicine, New York 

University School of Medicine, Tuxedo, NY 

Dr. Helen Suh MacIntosh, Associate Professor, Environmental Health, School of Public Health, 

Harvard University, Boston, MA 

Dr. William Malm, Research Physicist, National Park Service Air Resources Division, 

Cooperative Institute for Research in the Atmosphere, Colorado State University, Fort Collins, 

CO 

Mr. Charles Thomas (Tom) Moore, Jr., Air Quality Program Manager, Western Governors' 

Association, Cooperative Institute for Research in the Atmosphere, Colorado State University, 

Fort Collins, CO 

Dr. Robert F. Phalen, Professor, Department of Medicine; Co-Director, Air Pollution Health 

Effects Laboratory; Professor of Occupational & Environmental Health, Center for Occupation 

& Environment Health, University of California Irvine, Irvine, CA 

Dr. Kent Pinkerton, Professor, Regents of the University of California, Center for Health and the 

Environment, University of California, Davis, CA 

Mr. Richard L. Poirot, Environmental Analyst, Air Pollution Control Division, Department of 

Environmental Conservation, Vermont Agency of Natural Resources, Waterbury, VT 

Dr. Frank Speizer, Edward Kass Professor of Medicine, Channing Laboratory, Harvard Medical 

School, Boston, MA 

Dr. Sverre Vedal, Professor, Department of Environmental and Occupational Health Sciences, 

School of Public Health, University of Washington, Seattle, WA 

SCIENCE ADVISORY BOARD STAFF 

Dr. Holly Stallworth, Designated Federal Officer, EPA Science Advisory Board Staff Office, 

Washington, DC 

5
NOTICE 

This report has been written as part of the activities of the EPA's Clean Air Scientific Advisory 

Committee (CASAC), a federal advisory committee independently chartered to provide 

extramural scientific information and advice to the Administrator and other officials of the EPA. 

CASAC provides balanced, expert assessment of scientific matters related to issues and 

problems facing the Agency. This report has not been reviewed for approval by the Agency and, 

hence, the contents of this report do not necessarily represent the views and policies of the EPA, 

nor of other agencies within the Executive Branch of the federal government. In addition, any 

mention of trade names or commercial products does not constitute a recommendation for use. 

CASAC reports are posted on the EPA Web site at: http://www.epa.gov/casac. 

6
Enclosure B 

Integrated Science Assessment for Particulate Matter 

 (Second External Review Draft, July 2009)

CASAC Responses to Agency Charge Questions 

1) Evaluation of the health evidence in Chapters 6 and 7: 

a) In response to the CASAC PM Panel comments about the determinations of 

causality for PM10, we have refocused the evaluation of health effects resulting from 

exposure to PM10. PM10 studies are now included where they provide insights into 

general relationships between PM and its effects, such as concentration-response 

relationships. Separate causality determinations are no longer presented for PM10; 

however, PM10 study results are considered in causality determinations for PM2.5

and PM10-2.5 where appropriate. Please comment on this approach to evaluation of 

evidence from studies of PM10. 

At the April 2009 review of the first PM ISA draft, CASAC noted that findings on PM10, PM2.5 

and PM10-2.5 were often discussed as if these were separate pollutants, even though the PM2.5 and 

PM10-2.5 fractions comprise PM10. This led to inconsistencies in causal determinations, since 

these were provided for each of the three PM indicators independently. In this draft, causal 

determinations are no longer provided for PM10 as they were in the initial draft of the ISA. 

Motivation for dealing with PM10 as a separate entity, at least in the setting of short-term 

exposure, came from the continuation of the 24-hour PM10 standard. Given the different 

sources and the differing chemical compositions of the PM2.5 and PM10-2.5 fractions of PM10, and 

to some extent the evidence for differing toxicity, there is little scientific justification for dealing 

with PM10 as a single entity. The approach taken in the current draft is therefore more in keeping 

with the state of the science. 

Findings pertaining to PM10 in this 2nd draft are discussed alongside those of the two component 

fractions. There was obviously (and understandably) a need to consider the extensive findings 

pertaining to PM10 when evaluating the evidence on PM2.5 and PM10-2.5 since both fractions 

comprise PM10. Findings on PM10 should have some relevance to evaluating evidence on PM2.5

and PM10-2.5. However, the relevance of evidence on PM10 to PM2.5 or to PM10-2.5 likely varies 

across the country. For example, in some regions of the country PM10 is more reflective of PM2.5

whereas elsewhere PM10 is more reflective of PM10-2.5. The charge question states that “PM10

studies are now included where they provide insights into general relationships between PM and 

its effects, such as concentration-response relationships. PM10 study results are considered in 

causality determinations for PM2.5 and PM10-2.5 where appropriate.” For example, Figure 6-6 

(p.6-120) shows a typical concentration-response relationship for short-term PM10 exposures and 

is offered as providing insight into the “PM” concentration response relationship. “PM” is a 

general designation and used without sufficient specificity in this context. 

7
PM10 findings are also used in evaluation of the long-term effects of exposure to specific PM 

fractions (e.g., p. 7-24). For effects of long-term PM exposure on respiratory morbidity, the 

specific finding is made that “studies showing associations only with PM10 were conducted in 

locations where PM was predominantly fine particles, providing support for associations with 

long-term exposure to fine particles” (p. 7-28, line 32; p. 7-60, line 16). PM10 findings are used 

in support of findings on PM2.5. However, in some of the referenced studies, associations were 

found for PM10 only and not for PM2.5 (p. 7-43, line 6), a finding not consistent with the cited 

statement. 

In the respective PM fraction Summary and Causal Determinations sections, there is little 

mention of PM10. However, when findings on PM10 are mentioned in this context, they are only 

offered in regard to PM2.5 (e.g., PM10 findings are cited as strengthening the evidence for PM2.5-

related respiratory effects [p. 6-244] and for mortality effects [p. 6-317]). PM10 evidence is not 

used in support of PM10-2.5 effects. Yet in the discussion of short-term PM exposure mortality 

effects (section 6.5.2), PM10 studies are cited as providing “an underlying basis for the overall 

pattern of associations observed when examining the relationship between PM10-2.5 and PM2.5 and 

mortality.” We urge more consistent handling of the PM10 evidence. 

In order to better interpreting PM10 findings relative to those of PM2.5 and PM10-2.5, it would be 

helpful, perhaps in Chapter 3, to include and/or highlight data on the relationships of PM10 with 

both PM2.5 and PM10-2.5, stratified by region of the country. Also, in consideration of the role of 

the current 24-hour PM10 standard with respect to PM10-2.5, it would be important to better 

document the relevant evidence on the relationship between PM10 and PM10-2.5 across the 

country. 

In summary, the extensive evidence on PM10 is used without specificity or consistency. PM10

evidence is used to support the occurrence of overall effects of PM, but specifically in support of 

effects of PM2.5 but not of PM10-2.5. The current PM10 standard, however, is in place for control 

of PM10-2.5. Nevertheless, providing causality judgments for PM10-2.5 and PM2.5, but not for PM10, 

as in the current draft, is more in line with the current scientific understanding. 

b) In the first draft ISA, causal judgments were made for cardiovascular morbidity, 

respiratory morbidity, and all-cause mortality. In the second draft PM ISA, causal 

judgments were made for cardiovascular effects, and respiratory effects, using 

evidence from both morbidity and mortality. New sections were included within 

cardiovascular and respiratory effects for cause-specific mortality in Chapters 6 

(Sections 6.2.11 and 6.3.9, respectively) and 7 (Sections 7.2.10 and 7.3.8, 

respectively) that draw upon the more complete discussions of this evidence in the 

later mortality sections (Sections 6.5 and 7.6). These latter sections continue to 

present evidence of cause-specific mortality, as it informs the discussions and 

causality determinations for all-cause mortality. Furthermore, important results of 

analyses that examined potential effect modifiers, potential confounding by 

copollutants, PM-mortality concentration-response relationships, and the influence 

of different modeling approaches on the PM-mortality relationship remain in 

Chapter 6, Section 6.5. Considering both mortality and morbidity as part of a suite 

of effects, in addition to the other considerations underlying causality judgments, 

8
In general, CASAC agrees with EPA staff’s decision to link the determination of causal 

judgment to cause-specific cardiovascular and respiratory mortality. In addition, CASAC 

concurs with including cause-specific mortality within the outcomes considered in assessing 

cardiovascular and respiratory effects. New evidence, primarily epidemiological in nature, 

published since the last review cycle, makes such a judgment possible and informative. Because 

much of all-cause mortality is comprised of cardiovascular and respiratory deaths, it is 

appropriate to show these two groupings separately. By showing these two classes of death 

separately, the reader can better appreciate both the magnitude and nature of the deaths 

attributable to PM2.5. 

CASAC finds that the available scientific evidence supports the judgment of a “causal” 

determination for short-term and long-term effects of PM2.5 on cardiovascular effects. CASAC 

also supports the determination of a causal association between short-term and long-term effects 

of PM2.5 exposure and total mortality, based both on the relevant scientific evidence and the 

finding of a causal association for cardiovascular mortality, which makes up a substantial 

proportion of total mortality. Yet, despite strong associations with these cause-specific effects, 

total mortality is less strongly and more variably associated with PM2.5, perhaps because total 

mortality includes a number of categories more weakly linked to PM2.5 or not all associated with 

PM2.5. Consequently, long-term exposure to PM2.5 was judged “likely to be causal” for total 

mortality. This determination might be justified when considered in the context of the 

epidemiological data on all-cause mortality alone, but it is not consistent with the classification 

of cardiovascular mortality as “causal,” given the substantial contribution of cardiovascular 

mortality to all-cause mortality. Specifically, on page 2-18 the ISA states that “a causal” 

relationship exists between long-term exposures to PM2.5 and cardiovascular effects, yet on 7-137 

the ISA states that “the relationship between long-term PM2.5 exposure and mortality is likely to 

be causal.” Because the impact of PM on cardiovascular effects is judged “causal,” and since 

cardiovascular mortality is the largest contributor to total mortality, CASAC believes that the 

association with total mortality should logically be classified as “causal” rather than “likely 

causal.” While cardiovascular mortality is the single greatest contributor to total mortality, other 

causes are less well associated with PM2.5 and some conditions not at all. Because total mortality 

is strongly related to cardiovascular events, consideration should be given to explaining why the 

available studies addressing all-cause mortality appear to be conclusive, by carefully explaining 

the contribution of other less strongly associated conditions. CASAC concurs with the 

conclusion of a “likely to be causal” association between respiratory effects and long-term and 

short-term exposures to PM2.5. 

The added sections included in the ISA are effective in summarizing the recently reported 

evidence and in providing a basis for the causal determinations. As the ISA process matures and 

9
continues to evolve, CASAC recommends that a table be included that lists the previous review 

cycle’s causal judgment determinations directly beside the current cycle determinations, with a 

brief comment about what has changed in the informational database to warrant a change in the 

causal classification. This table would provide the reader with a valuable summary of the 

historical process, and document changes in knowledge and interpretation that form a critical 

part of NAAQS evaluation. 

c) We reexamined the controlled human exposure and toxicological studies of fresh 

diesel and gasoline exhaust and determined that while these exposure atmospheres 

contain relatively high mass concentrations of PM2.5, the particle number count 

distribution was predominantly in the ultrafine size range. Therefore, for the second 

draft ISA, we considered the diesel and gasoline exhaust studies, in addition to the 

other considerations underlying causality judgments, when making our causal 

determinations for ultrafine PM exposure and cardiovascular and respiratory 

effects, resulting in a change from “inadequate” to “suggestive” for both categories. 

Diesel and gasoline exhaust studies also continued to be considered as part of the 

evidence for PM2.5 health effects, as was done for the first draft ISA. With 

consideration of this rationale, please comment on the scope of evidence considered 

in the causal determinations for ultrafine PM. 

CASAC agreed with EPA’s rationale in moving the causal determination for UFP from 

“inadequate” to “suggestive”. Much of the evidence provided from clinical exposures and 

toxicological studies is based on gasoline or diesel exhaust studies, and combustion of these fuels 

generates high levels of -UFP. Epidemiological investigations have been less specific in their 

assignment of health outcomes specifically to UFP, although an increasing number of studies are 

observing effects of exposures proximal to roadsides, reflecting some component of combustion 

exhaust or vehicle operation. While additional research is needed, we concur with changing the 

causal determination for UFP from “inadequate” to “suggestive.” 

d) The CASAC PM Panel recommended that we further consider the evidence related 

to PM exposure and cancer. Section 7.5 (Cancer) was revised to include evaluation 

of epidemiologic studies of both mortality and incidence of cancer with exposure to 

PM, as well as a brief overview of the toxicological evidence conducted using 

intratracheal instillation or dermal routes of exposure to better characterize the role 

of PM in mutagenicity, genotoxicity, and carcinogenicity. As a result of revisions to 

this section, the causal determination for PM2.5 and cancer was changed from 

"inadequate" to "suggestive"; the causal determination for PM10-2.5 remained 

unchanged. Please comment on the expansion of this evaluation to include a 

summary of toxicological studies using routes of exposure other than inhalation, as 

well as consideration of both mortality and incidence studies. 

10
EPA has carefully summarized a complex literature related to both the general and specific 

findings of mutagenicity, genotoxicity and carcinogenicity studies on PM and cancer. The 

charge question has two components. First, publications in toxicological studies to assess 

mutagenicity and genotoxicity on mechanisms for mammalian cancer research have used routes 

of exposure other than inhalation. For some agents, such studies have provided insights on 

potential cancer risks in humans. Thus, such data can be appropriately used for determining the 

degree of certainty with regard to causality. Second, with regard to the recently reported 

findings of epidemiological studies, these have included large, well assessed populations and 

they have shown associations with cardiovascular and respiratory outcomes. The same approach 

has been used for lung cancer, although interpretation is complicated by the possibility of 

potential confounding by smoking. With the exception of one relatively large European study 

that was null, these studies show an association of PM exposure with cancer risk that is robust 

after controlling for smoking. These studies provide support for the “suggestive” classification, 

particularly in the context of other lines of evidence reviewed in the ISA. 

2) Revisions to Chapters 1 (Introduction), 4 (Dosimetry), and 5 (Mode of Action): Changes 

to these chapters included expansion or clarification in a number of areas, as presented 

in more detail in the recent letter from EPA’s Administrator. These included expansion 

or addition of sections on the history of the previous PM NAAQS review in Chapter 1; 

deposition and clearance of particles in Chapter 4; and epigenetics, lung development, 

atherosclerosis and consideration of acute and chronic responses in Chapter 5. Please 

comment on the revisions to these chapters. 

We commend the organizers and authors of this document for providing the CASAC PM Panel 

with well organized and readily readable texts for Chapters 1, 4, and 5 that are, for the most part, 

thorough and accurate in presenting the peer-reviewed literature most relevant to an Introduction 

(Ch. 1), Dosimetry (Ch. 2), and Mode of Action (Ch. 3). The amount of text on UFP could be 

condensed, especially in Chapter 5, where the potential to cause adverse effects is so 

prominently featured, along with the implication that particle number concentration is the most 

important metric for risk. Some additional discussion of still weak evidence in support of this 

hypothesis is warranted. There is inadequate discussion of the usefulness of the limited data on 

ambient air UFP concentrations currently available. The data are essentially limited to particle 

number concentrations, which make no distinction with respect to particle composition. The 

likelihood of effects is likely to differ among UFPs formed as condensation aerosols of sulfuric 

acid droplets, metal oxides, elemental carbon, and organic carbon, and with the changes in 

composition and particle size with residence time in the ambient air. 

3) Evaluation of susceptible population groups in Chapter 8: In response to the CASAC 

PM Panel comments, we have now focused specifically on susceptible subpopulations 

(defined for this ISA as those subpopulations that have a greater likelihood of 

experiencing health effects related to PM exposure) in Chapter 8. The introduction of 

this chapter was revised to include this new definition of susceptible subpopulations, 

recognizing that the terms susceptible and vulnerable have sometimes been used 

interchangeably in the literature, and in other cases have been used to represent two 

different categories (i.e., biological factors [e.g., age gender, etc.] vs. non-biological 

factors [e.g., SES, differential exposure, etc.]), resulting in the lack of a clear and 

consistent definition. The discussion was reorganized to improve the characterization of 

11
factors that may contribute to increased susceptibility to PM-induced health effects. 

Each section was also revised to include the different exposure durations (short- and 

long-term) and PM size fractions examined in the studies discussed within each 

subsection of the chapter. Please comment on the organization and presentation in 

Chapter 8 of evidence regarding susceptible subpopulations. 

The organization and presentation of Chapter 8 is complete, clear and well-organized. The 

authors have been responsive to CASAC’s critique of the first draft of the chapter. The 

definition of "susceptible" is clearly stated with a rather complete listing of how the term has 

been used in the literature in the past. We recommend that the authors consider identifying those 

definitions which are most timely and relevant for the purposes of this chapter. 

Table 8-2 introduces all susceptibility factors that have been evaluated, as well as the particle 

size fraction evaluated and the duration/length of exposures. Table 8-2 is followed by a more 

detailed description of the evaluations that were made. This is a highly appropriate organization 

that could be improved by the addition of a column to the table which briefly summarizes the 

impact of each susceptibility factor on health impacts and/or observed health effects. The title of 

the table "Susceptibility Factors," gives the impression that all factors listed determine 

susceptibility, but some of those listed, such as gender, do not. Therefore, the title could be 

modified to "Susceptibility Factors That Have Been Evaluated" to more accurately reflect the 

contents of this table. The addition of a column to the table to indicate the results of each 

evaluation with a simple plus/minus summary approach would further improve the presentation. 

4) Revisions to Chapter 3 on Source to Exposure: Consistent with revisions made to the 

health effects chapters, Chapter 3 was revised to clarify that PM10 incorporates both 

PM2.5 and PM10-2.5 and reorganized to begin with PM2.5 and PM10-2.5, followed by PM10, 

where applicable. The discussion of measurement techniques and chemistry of PM10-2.5

has been expanded in Sections 3.4 and 3.5, in response to CASAC comments. In 

addition, Section 3.8 on human exposure to PM has been reorganized and expanded to 

better characterize the evidence and provide useful information for interpretation of 

epidemiologic studies. We would appreciate comments from the CASAC PM Panel on 

these revisions. 

The Chapter is a comprehensive summary of the current state of the evidence on PM sources, 

ambient aerosols, monitoring and modeling methods, concentrations and exposures. The 

Chapter generally reflects the state of science in a clear, comprehensive, and well organized 

fashion. Further, the Chapter revision appropriately incorporates comments from the April 

review. Of note, the relationships among PM2.5, PM10-2.5, and PM10 were clarified, although 

some additional information could be pulled forward from the Appendix (see below). The 

inclusion of additional information on UFP, PM components, and PM10-2.5 monitoring methods 

was also an improvement. Similarly, the organization and content of the exposure section was 

greatly improved, and the relevance of exposure findings to interpretation of the results of 

epidemiologic studies was more fully addressed. While significantly improved, further 

improvements could be made to the exposure section to help with the organization, seeming 

overlap with earlier sections, and clarity, as discussed below. 

12
Specific comments: 

• The Chapter would benefit from a more detailed discussion of the relations among 

ambient PM10, PM2.5, and PM10-2.5, particularly for the 15 cities selected for more detailed 

analysis. While this information is in the Appendix, it would be helpful to bring a 

summary of the findings into the main chapter. 

• The distinction between primary and secondary organic aerosols should be expanded to 

discuss the potential for oxidation of primary organic particles which makes them 

become similar to secondary organic aerosol. 

• Standard Reference Materials (page 2-20, line 20): It says “To date, there are few 

standard reference materials ...” This sentence should be reworded to make clear that we 

currently do not have a way to assess mass concentration measurement accuracy, as there 

are no standard reference materials (SRMs) or equivalent standards (to our knowledge) 

that provide a test of accuracy or airborne PM mass. There are, however, SRMs that are 

useful for testing the accuracy of the analytical methods for PM composition. 

• Policy Relevant Background (PRB): The EPA promulgates a health-based standard 

irrespective of the background concentration of particles and thus, the PRB primarily has 

implications for implementation. If the PRB increases because of sources outside of the 

United States, there will be greater difficulty in attaining concentrations that are fully 

protective of public health. The modeling approach to establishing PRB has some 

appeal, but given the inaccuracy of emissions inventories in the US, where substantial 

effort and resources have been expended to develop them, there is little likelihood that we 

can adequately model emissions for the rest of the world. Consequently, the ISA might 

also offer comparisons between the model-based approach and the remote site approach 

to assess the certainty of the model-based estimation of the PRB. 

• Exposure Section: Given the relevance of the measured PM concentrations in the earlier 

sections of the Chapter, and for interpreting the epidemiological studies and the Health 

RA, discussion of exposure measurements should be placed before that for exposure 

modeling. Further, the exposure measurements section should include discussion of new 

methods to measure (1) personal exposures to total PM, (2) PM of outdoor origin, (2) 

ambient concentrations outside individuals’ homes, and (3) indoor PM exposures to total 

PM and to PM of outdoor origin). In this context, studies using tracers of outdoor or 

regional pollution can be introduced. 

o The discussion of each topic should be consolidated into single sections, with 

references to this section made as necessary in later sections. As currently 

written, certain topics, such as spatial variability and particle infiltration, appear 

repeatedly in several subsections. The discussion on these topics would be more 

focused and less confusing if consolidated. 

o In Section 3.8.4.3, it would be helpful to clarify which component of PM is 

discussed. Further, within each subtopic or heading, separate or otherwise distinct 

discussions for PM2.5, PM10-2.5 and the PM components would improve clarity. 

13
o Section 3.8.4 (Exposure Assessment Studies at Different Spatial Scales) and its 

subheadings are misnamed. While the heading titles do provide parallels with 

earlier sections of Chapter 3, they do not accurately describe the contents. For 

example, section 3.8.4.1 does not actually discuss urban scale ambient PM 

exposure, but issues related to exposure error, exposure modeling, and tracers of 

ambient particles. 

o It would be helpful to include a subsection in the beginning of the section, 

perhaps in Section 3.8.1 (General Exposure Concepts) that summarizes the range 

of measured exposures to PM2.5, PM10-2.5, and PM10, their composition, and 

differences by city, susceptible group, and season. 

o Section 3.8.6: Other factors that could affect exposures should be noted, such as 

home ventilation `and activity patterns. 

5) Integrative Synthesis in Chapter 2: The CASAC PM Panel recommended expanding 

Chapter 2 to include all important findings of the PM ISA. The integration of health 

evidence in Chapter 2 was reorganized to focus on effects of PM2.5, PM10-2.5, and 

ultrafine particles, and was expanded to include discussions of effects for which a 

"suggestive" causality determination was drawn. New integration sections were added 

that combine the evidence for health effects of PM2.5, PM10-2.5, and ultrafine PM across 

exposure durations. In addition, these integration discussions incorporated evidence 

related to mode of action, dosimetry, atmospheric chemistry, and exposure assessment 

to the extent possible. When appropriate, figures were added that summarize the 

overall U.S. and Canadian epidemiologic evidence for specific size fractions and 

exposure durations, along with the concentrations reported in the studies or provided 

by study authors. A new section was also added to Chapter 2 that contains policyrelevant considerations, including summaries for the evidence for susceptible 

subpopulations, lag structure of associations in epidemiologic studies, and the PM 

concentration-response relationship. Please comment on these revisions and additions 

to the integration of health effects evidence in Chapter 2. 

Overall, CASAC commends EPA for an excellent draft of Chapter 2. The chapter appropriately 

addresses CASAC’s previous comments from the April review of the 1st draft ISA. The 

revisions as described in the charge questions are appropriate and enhance the content and 

structure of the chapter. 

Although the current draft of Chapter 2 is excellent, it could be strengthened with selected 

revisions. The main technical points that should be addressed in finalizing this chapter are: (a) 

more attention is needed to the role of variability in the composition of PM by size fraction with 

respect to both health and welfare effects; (b) more analysis and discussion of PM effects on 

climate is needed, particularly with regard to the role of PM composition and its implications for 

adverse or beneficial effects; (c) additional synthesis is needed to more clearly tie together 

material related to PM characteristics and impacts on both health and welfare, including strength 

of association, and the implications of uncertainties; (d) there should be more effort to move 

toward exposure-response relationships for ecological effects endpoints; and (e) the conclusion 

regarding only a “likely” causal relationship between long-term exposure to PM2.5 and mortality 

14
should be carefully revisited, since there is evidence that the relationship exists with more weight 

of evidence than conveyed in the document. 

Section 2.3 should have one summary table of all health effects, and the discussion should start 

with those effects for which there is the strongest weight of evidence, moving to those with 

weaker or no weight of evidence (rather than vice versa as in the second draft ISA). Some 

portions of Chapter 2 may be too detailed, such as the text on pages 2-24. There are places 

throughout Chapter 2 (e.g., page 2-13) where citation of later sections of the report would help 

readers in finding more detail to support the summary statements. Although Figures 2.1, 2.2, and 

2.3 are generally very useful, they would be easier to interpret if disaggregated into figure panels, 

each addressing only one outcome. Furthermore, there appears to be an error in the scale at the 

bottom of Figure 2.3. Although there is a lower correlation of PM10 with PM2.5 (Page 2.5, lines 

14-19), the correlation for PM10 is nonetheless remarkably high and should be interpreted more 

appropriately. 

The discussion of PM and climate concludes with an ambiguous summary statement that “a 

causal relationship exists between PM and effects on climate.” This use of the term “effects” is 

inconsistent with causality statements elsewhere in the ISA, where the PM effects being 

considered were consistently and unquestionably adverse. In the case of climate, PM can exert 

both positive and negative climate forcing influences. Some discussion should be offered to 

frame and further clarify this issue, perhaps in Chapter 1. 

CASAC recommends that EPA add more material regarding PM composition, an overall 

synthesis of both health and welfare effects, and a synthesis of the most significant uncertainties 

and their implications for the robustness of conclusions. 

6) Welfare effects evaluation in Chapter 9: Several revisions were made to the evaluation 

of the welfare effects evidence in Chapter 9, in response to the CASAC PM Panel 

comment, to focus further on effects on climate and ecosystems and include further 

evaluation of urban visibility evidence, where possible. In addition, as recommended by 

the CASAC PM Panel, key findings and conclusions from this chapter were 

incorporated in Chapter 2. The discussion of PM effects on climate was increased with 

substantially more detail from recent publications, including discussion of specific 

climate forcing effects from individual PM components and size fractions. The 

discussion of ecological effects was also reorganized to focus on the types of effects and 

effects of individual components. For the effects of PM on visibility, new material was 

added including sections on direct optical measurements and the value of good visual 

air quality. Please comment on the effectiveness of the reorganization and revisions 

regarding welfare effects. 

15
16

CASAC was pleased to note the effective addition of sections on “Ecological and Welfare 

Effects” in the Integrative Overview summary discussion in Chapter 2. CASAC also agreed that 

the revisions to discussions of PM welfare effects in Chapter 9 strengthen the chapter, improve 

its clarity and are directly responsive to previous CASAC comments on the 1st Draft ISA. 

Several minor revisions would be helpful to improve accuracy in some sections (see individual 

panelist comments for detail), but no major revisions are needed. 

Newly added details on climate, ecological and materials effects of PM and its various 

components provide more comprehensive coverage of these important subject areas; however, 

concentration-response functions for climate and ecological endpoints will be needed for future 

ISAs. Information in Chapter 9 on optical measurement methods provides added support for the 

proposed use of a new "PM light extinction" indicator, which is readily measurable and directly 

reflects the human perception of visibility effects caused by PM. The section on night-time 

visibility in Chapter 9 is important and should be brought forward to the summary chapter 

(Chapter 2). The information presented on visibility valuation and preference studies helps to 

demonstrate that visual air quality is consistently judged to be "unacceptable" at levels well 

below the current PM NAAQS in a number of different study areas. The findings in the ISA are 

sufficient to propose levels of PM light extinction above which public welfare is affected 

adversely. Finally, it is important to recognize, as the ISA does, the very substantial welfare 

effects from airborne PM, NOx and SOx are addressed in a separate NAAQS review. 
Enclosure C 

Compendium of Individual Comments 

CASAC Particulate Matter Review Panel 

Integrated Science Assessment for 

Particulate Matter (Second External Review Draft, July 2009) 

Ashbaugh Comments (Dr. Lowell Ashbaugh).............................................................................. 2

Avol Comments (Mr. Ed Avol) ...................................................................................................... 4

Brain Comments (Dr. Joe Brain).................................................................................................. 7

Cascio Comments (Dr. Wayne Cascio) ......................................................................................... 8

Cowling Comments (Dr. Ellis Cowling)...................................................................................... 24

Frey Comments (Dr. Chris Frey)................................................................................................ 25

Grantz Comments (Dr. David Grantz) ........................................................................................ 27

Helble Comments (Dr. Joseph Helble)........................................................................................ 36

Henderson Comments (Dr. Rogene Henderson)........................................................................ 39

Hopke Comments (Dr. Phil Hopke) ............................................................................................ 40

Lippmann Comments (Dr. Mort Lippmann) .............................................................................. 42

Malm Comments (Dr. William Malm)........................................................................................ 47

Pinkerton Comments (Dr. Kent Pinkerton)................................................................................ 49

Phalen Comments (Dr. Robert Phalen) ...................................................................................... 50

Poirot Comments (Mr. Rich Poirot)............................................................................................ 52

Russell Comments (Dr. Armistead (Ted) Russell)...................................................................... 56

Speizer Comments (Dr. Frank Speizer) ...................................................................................... 59

Suh Comments (Dr. Helen Suh).................................................................................................. 63

Vedal Comments (Dr. Sverre Vedal)........................................................................................... 66

1
Ashbaugh Comments (Dr. Lowell Ashbaugh) 

Charge Question 6: 

Several revisions were made to the evaluation of the welfare effects evidence in Chapter 9, in 

response to the CASAC PM Panel comment, to focus further on effects on climate and ecosystems 

and include further evaluation of urban visibility evidence, where possible. In addition, as 

recommended by the CASAC PM Panel, key findings and conclusions from this chapter were 

incorporated in Chapter 2. The discussion of PM effects on climate was increased with substantially 

more detail from recent publications, including discussion of specific climate forcing effects from 

individual PM components and size fractions. The discussion of ecological effects was also 

reorganized to focus on the types of effects and effects of individual components. For the effects of 

PM on visibility, new material was added including sections on direct optical measurements and the 

value of good visual air quality. Please comment on the effectiveness of the reorganization and 

revisions regarding welfare effects. 

The revisions are quite good; the authors have done an excellent job of incorporating comments 

from the earlier review. The integration of welfare effects into Chapter 2 works well. I would 

like to see a short paragraph in Chapter 2 summarizing the effects of PM on nighttime visibility. 

I especially liked the section on nighttime visibility in Chapter 9 on page 9-8. The paragraph on 

lines 22-30 of page 2-37 is not clearly written. Twice in succession it states that the use of a nothreshold log-linear model is supported, but then cites other studies that suggest otherwise. It 

would be good to revise this paragraph to more clearly state – well, I’m not sure what. Probably 

that more research is needed. 

Chapter 9 is also much improved. The organization is good, and small details make it easier to 

read. For example, the spatial contour plots are much easier to compare now that the contour 

scales are similar for related figures. The haze trends figures (9-26 & 9-27) would benefit from 

using a color other than yellow, though, which does not show up clearly. Or perhaps the yellow 

(up) and light green (down) arrows could have a black border. Then they would also be 

distinguishable from the red and dark green when copied in B/W. 

I like Section 9.3.1 but the figures would benefit from better reproduction. Most of the figures 

copied from the CCSP SAP2.3 did not reproduce well (also, the caption for Figure 9-70 contains 

a typo – “Arcic” instead of “Arctic”). Is it possible to obtain the originals? 

The individual components discussion is well organized and easy to read. I’m familiar with one 

reference that could be added to the section on smelters and roadsides (page 9-245). The 

reference is “Resuspension of Soil as a Source of Airborne Lead near Industrial Facilities and 

Highways,” by Thomas M. Young, Deo A. Heeraman, Gorkem Sirin, and Lowell L. Ashbaugh, 

Environmental Science & Technology 2002 36 (11), 2484-2490. It seems to be relevant to the 

discussion. Here’s the abstract: 

Abstract: Geologic materials are an important source of airborne particulate matter less 

than 10 μm aerodynamic diameter (PM10), but the contribution of contaminated soil to 

concentrations of Pb and other trace elements in air has not been documented. To 

examine the potential significance of this mechanism, surface soil samples with a range 

of bulk soil Pb concentrations were obtained near five industrial facilities and along 

2
roadsides and were resuspended in a specially designed laboratory chamber. The 

concentration of Pb and other trace elements was measured in the bulk soil, in soil size 

fractions, and in PM10 generated during resuspension of soils and fractions. Average 

yields of PM10 from dry soils ranged from 0.169 to 0.869 mg of PM10/g of soil. Yields 

declined approximately linearly with increasing geometric mean particle size of the bulk 

soil. The resulting PM10 had average Pb concentrations as high as 2283 mg/kg for 

samples from a secondary Pb smelter. Pb was enriched in PM10 by 5.36-88.7 times as 

compared with uncontaminated California soils. Total production of PM10 bound Pb from 

the soil samples varied between 0.012 and 1.2 mg of Pb/kg of bulk soil. During a 

relatively large erosion event, a contaminated site might contribute approximately 300 

ng/m(3) of PM10-bound Pb to air. Contribution of soil from contaminated sites to airborne 

element balances thus deserves consideration when constructing receptor models for 

source apportionment or attempting to control airborne Pb emissions. 

3
Avol Comments (Mr. Ed Avol) 

1) Evaluation of Chapters 6 & 7 Health Evidence

(a) Evaluation of evidence from PM10 studies (lead discussant, Vedal)

The revised approach is well-presented and understandable. The authors and staff have done a 

commendable job in improving the accessibility of data, readability of the document, and 

documentation of the included information over the previous version. 

 I did not read the entire document (so I am not certain of this), but I did not readily see any 

discussion (or reference to a discussion) announcing, justifying, or explaining this decision to 

“collapse” PM10 into these other categories. For example, this might be justified on a scientific 

basis (high inter-correlation with coarse PM, for example) or possibly even a regulatory one 

(research evolving to smaller particle sizes). Did I miss this somewhere? 

(b) inclusion of cause-specific mortality in the development of causal judgments (lead 

discussant, Cascio)

I agree with the decision to link the determination of causal judgment to cardiovascular and 

respiratory mortality, since these have been very active and productive areas of research since 

the last review cycle. The added sections are effective in summarizing the cumulative recent 

evidence and providing a basis for the causal determinations. As the ISA process mature and 

continue to evolve, it might be worth considering inclusion of a summary table that lists the 

previous review cycle’s causal judgment determinations directly beside the current cycle 

determinations, with a brief comment about what has changed in the informational database to 

warrant a change in causal determination, This would provide the reader, the Staff, and the 

public with a readily trackable means of documenting changes in knowledge and interpretation 

that form a critical part of NAAQS evaluation. 

Response to Charge Question 1c 

(c) Scope of evidence considered in causal determination of UFP (lead discussant, Avol)

I agree with the rationale and thinking of the Staff and authors on moving the causal 

determination for UFP from “inadequate” to “suggestive”. Although there is growing research 

activity in the effects of PM in this size range, there is still much that is not understood, 

appreciated, or being considered. This is complicated by the difficulty in generating and/or 

characterizing “reproducible” or “representative” UFP for study use at ambient exposureappropriate concentrations. Additional concerns include observations that particle surface 

reactivity may be strongly related to fresh combustion and/or new particle formation, and 

observations that smaller particles seem to have increased toxicological properties. 

4
(d) Inclusion of cancer mortality and incidence, additional routes of exposure (lead discussant, 

Speizer)

I agree with the expansion decision for both routes of exposure and consideration of both 

mortality and incidence studies. 

2) Chapters 1 (Introduction),4 (Dosimetry),5 (Mode of Action) revisions

Comments on Chapter 1

(I repeat this comment from 1a, since it is relevant to the Chapter 1 Introduction) 

 I did not read the entire document (so I am not certain of this), but I did not readily see any 

discussion (or reference to a discussion) announcing, justifying, or explaining this decision to 

“collapse” PM10 into these other categories. For example, this might be justified on a scientific 

basis (high inter-correlation with coarse PM, for example) or possibly even a regulatory one 

(research evolving to smaller particle sizes). Did I miss this somewhere? 

P. 1-2, first bullet – Three categories of exposures (short-term, chronic, and peak) are described 

in this carefully crafted opening list of review considerations...but short-term and chronic 

exposures are the focus of the documents. Should some comments, concern, consideration be 

focused on peak exposures, even if just to say we don’t know much about it or need to learn 

more? 

Comments on Chapter 4

P4-2, line 31 – Manufactured nanoparticles are not considered in this chapter (or in the review. 

Presumably manufactured nanoparticles lie somewhere on the continuum from completely 

unrealistic exposures to completely relevant ones...Are manufactured nanoparticles being 

considered as “occupational” exposures? Regardless, some thought should be given to the 

potential for population exposure to these particles, and what might be learnable from these 

engineered exposures (which may not be all that different from laboratory-generated exposures 

of TiO2 or other specifically generated artificial particles that serve an important purpose in 

identification of mechanisms and pathways). Would knowledge and consideration of their 

potential health effects (as a function of their particle size) be an appropriate section in an UFP 

chapter? 

Comments on Chapter 5

I think this chapter was very well done and especially appreciated Section 5.6, which 

summarized new results AND provided references to the appropriate document section to read 

more detail about the individual finding. 

The final text page of the chapter (5-31) “gaps in knowledge” is worthy of a section title or 

tabulation. In a larger document sense, this final summary and assessment of knowledge gaps 

would be useful additions to most every chapter in the ISA. 

General Comments on PM ISA, 2nd Draft, Avol

5
6

In a large, data-rich, and complex document such as this, it would seem helpful to establish a 

consistent presentation paradigm that is followed throughout the relevant chapters, so that the 

reader can move from chapter to chapter, in or out of sequence, and still have some expectation 

of finding a consistent set of validators or signposts with which to review, interpret and integrate 

the presentations. Substantive progress has been made towards that objective in the ISA, but 

there still remain some inconsistencies that provide unnecessary obstacles to the reader. Here are 

two examples of this: 

(1) A consistent PM-size-oriented summary presentation would help to establish a standardized 

format and framework for review. Accordingly, it would be useful if, in each Summary and 

Causal Determinations section of each chapter, health outcome, etc, a paragraph were denoted 

for PM2.5, PM10-2.5, and UFP and a brief summary statement regarding causality judgment -- for 

each size-cut – were made. (This comment motivated by the observation that UFP summary 

statements seem to be sporadically missing, such as in section 7.4.3). 

(2) In Chapter 2 , there is (almost) a developed (and pragmatically useful) standardized listing of 

health outcomes, in five categories (cardiovascular; respiratory; mortality; reproductive and 

developmental; cancer, mutagenicity, and genotoxicity) that could be consistently evaluated 

against each of the pollutants under review for a current judgment of causal determination (from 

not likely to causal). These tabular summaries could then form the basis for guideposts to areas 

of needed future investigations, markers for progress from review to review, etc. 

I suspect there is an error in the listed range of effects estimates in Figure 2-3 (P2-29); it is 

difficult to believe that the effects estimates range from -12 to +32. 

7.2.11 Summary & Causal Determinations (of Cardiovascular and Systemic Effects)– Much 

improved and clearer, providing a basis for what was known prior to the current review, and 

what the new information shows. Summary judgments for PM2.5, PM10-2.5, and UFP all seem 

reasonable, but the supporting comment for UFP (“...due to a few studies being conducted 

without gaseous co-pollutants...” seems unnecessary and inaccurate, since the current breadth of 

studies reporting UFP and health associations is minimal, independent of adjustments for the 

presence or absence of gaseous co-pollutants. There may be some suggestions of effects and a 

valid concern for additional research, but at the time of this review, the cumulative import of 

observed effects in the assembled body of work is unclear and in need of additional 

investigation. 

There still is appears to be an (unnecessary) tendency to discuss study after study after study at a 

level of detail that could be more appropriately placed in the annex. The main section of this 

document would be more useful as an integration of current knowledge, not an exhaustive listing 

of it; additional materials could and should be provided in the annex. 

P7-27, lines 28-29 – “Evidence from these studies alone is inadequate to infer the presence or 

absence of a causal relationship due to a few studies being conducted without gaseous 

pollutants.” This may be true, but can’t the same comment be made for the studies reporting 

effects of PM10, PM2.5, and PM10-2.5? Why make this point for UFP only? 
Brain Comments (Dr. Joe Brain) 

ISA-PM: Charge Question 5: Integrative Synthesis in Chapter 2 

 Overall, chapter 2 is much improved. Especially, making it a synthesis of the entire document 

makes sense. This is consistent with CASAC’s recommendation regarding the first draft of the 

ISA. In particular, I like the delineation of the three critical size ranges of PM: coarse, fine, and 

UFP. These three size ranges are now prominent throughout and adequately discussed in terms 

of exposure and response. The inclusion of welfare considerations and ecological effects is well 

integrated into the chapter as a whole. In toto, this is an extremely valuable component of the 

ISA. It is a section which will be heavily used by policy makers, the scientific community, and 

the lay public. The authors are to be congratulated on producing a summary which is both 

sophisticated as well as accessible. 

 Section 2.4, “Policy Relevant Considerations,” is done well. The role of susceptible populations 

is emphasized. This is important since these individuals make a dominant contribution to the 

observed health effects. 

7
Cascio Comments (Dr. Wayne Cascio) 

Charge Question 1a 

General Comments: 

1) The outstanding effort of the staff at NCEA to address the concerns and comments of the 

CASAC PM panel is very much appreciated, and has improved the document and 

focused the information in such a way as to more clearly justify the message it is 

designed to convey. 

2) As discussed previously by the CASAC PM panel the determination of causality for 

PM10 is problematic as this fraction contains both the fine and coarse (thoracic PM) 

fraction, and its risk appears to be more strongly determined by the fine fraction. 

Consequently, the approach to focus the discussion of causality determination on PM2.5

and PM10-2.5 independently is appropriate, but appears to be at odds with the current PM10

standard. How does EPA intend to reconcile this discontinuity? 

3) Nevertheless, the separation of PM into PM2.5 and PM10-2.5 is strongly supported by 

scientific data. 

4) The concept that the abundant data on PM10 might serve to selectively support the 

causality determinations for PM2.5 and PM10-2.5 is problematic. As described above PM10

contains both fractions and there will always be uncertainty as to whether effects 

measured in response to PM10 are related to the PM2.5 fraction, the PM10-2.5 fraction or 

some combination of the two. 

Charge Question 1c 

General Comments: 

1) The outstanding effort of the staff at NCEA to address the concerns and comments of the 

CASAC PM panel is very much appreciated, and has improved the document and 

focused the information in such a way as to more clearly justify the message it is 

designed to convey. 

2) In Chapters 6 and 7 a comprehensive list of studies reporting health effects, toxicity of 

diesel emission and gasoline emission PM is provided. The rationale to include diesel and 

gasoline emissions as evidence of effects of UFP is reasonable given the strong 

association between PM mass from these source and particle number. Of relevance to this 

question are the results of our recently completed California Freeway Study that showed 

that particle number was most strongly associated with health effects endpoints in 

subjects exposed to traffic related pollutants on two Los Angeles freeways for 2 hours. 

3) Based on the weight of the evidence with the inclusion of diesel and gasoline emission 

data the change in the causal determination for UFP from “inadequate” to “suggestive” is 

appropriate. 

4) The presentation of diesel, gasoline and wood smoke emission data independently 

provides a means to quickly find relevant health effects data linking a specific exposure 

type to health effects. Such an approach was useful in judging the strength of 

associations and determination of causation. 

8
Charge Question 1d 

General Comments: 

1) The outstanding effort of the staff at NCEA to address the concerns and comments of the 

CASAC PM panel is very much appreciated, and has improved the document and 

focused the information in such a way as to more clearly justify the message it is 

designed to convey. 

2) In the 2nd external review draft Section 7.5 provides a more detailed presentation of 

epidemiological and toxicological data. The information is well integrated. This has 

improved the quality of information regarding the association between PM exposure and 

cancer. 

3) In the first ISA the presentation of the possible link between PM exposure and cancer 

was judged as “inadequate”. Now with better integration of epidemiological and 

toxicological data the causal determination has been changed to “suggestive”. This 

change is appropriate based on the presented data. While toxicological studies included in 

this section were conducted with exposure routes other than inhalation these studies are 

important for providing a mechanistic basis to justify the biological plausibility of a 

causal determination. 

Chapter 6 

Specific Comments: 

SEC/PAGE PARA/LINE REVIEW COMMENTS 

6.2.1/2 1. 1 - 5 One can add that decreased HRV may precede some 

clinically important arrhythmias such as atrial 

fibrillation, and SCD in high risk populations. (Chen 

PS, Tan AY. Autonomic nerve activity and atrial 

fibrillation. Heart Rhythm 4(3 Suppl):S61-4, 2007; 

Thong T, Raitt MH. Predicting imminent episodes of 

ventricular tachyarrhythmias using heart rate. Pacing 

Clin Electrophysiol 30:874-84, 2007; Sandercok GR, 

Brodie DA. The role of heart rate variability in 

prognosis for different modes of death in chronic heart 

failure. Pacing Clin Electrophysiol 29:892-904, 2006) 

6.2.1/2 2. 5-7 The sentence, “SDDN generally reflects...” can be 

rewritten, “SDDN generally reflects the overall 

modulation of HR by the autonomic nervous system, 

whereas rMSSD and frequency variations in HR 

9
generally reflect parasympathetic activity”. 

6.2.1/2 2. 7-9 The sentence, “LF is predominately...” can be rewritten 

as “LF is predominately determined by both 

sympathetic and parasympathetic tone and increased 

LF/HF indicates sympathoexcitation,...” 

6.2.1/6 1. 5-6 In the study by Yeatts et al. (2007, 091266) it is true 

that rMSSD but this was not statistically significant. 

P=0.16. Likewise, pNN50 did increase in response to 

PM2.5-10 but this result also did not reach statistical 

significance. P=0.07. 

6.2.1/6 2. 7-9 In the study by Langrish et al. (2009, 191908). Did the 

authors confirm that the facemask did not affect the 

rate or depth of breathing. If not then it is possible that 

the results could have been influenced by the 

facemask. 

6.2.1.2/13 2, 2 Space between “of” and “20” 

6.2.2.1/21 1, 5-7 The sentence, “VPBs are ...” should be rewritten. 

Consider the following, “VPBs are spontaneous beats 

originating from either the right or left ventricles. VT 

refers to 3 or more ventricular beats in succession at a 

rate of 100 beats per minute or greater, while VF is 

characterized by rapid and disorganized ventricular 

electrical activation incapable of generating an 

organized mechanical contraction or cardiac output. 

6-22 1, 10 and 2, 1 The sentence, “Pathophysiologic mechanisms...” 

should be rewritten. Consider the following, 

“Pathophysiologic mechanisms underlying this 

established cause of sudden cardiac death include 

activators and facilitators of arrhythmia such as 

electrolyte abnormalities, modulation of the autonomic 

nervous system, membrane channels, gap junctions, 

oxidant stress, myocardial stretch and ischemia acting 

on myocardium conditioned for arrhythmia by altered 

by cellular and tissue architecture, fibrosis, and 

intracellular calcium handling.” 

10
6-27 1, 7 The sentence, “Such beats...” should include the 

conduction system as a source of arrhythmia. For 

example, “Such beats can arise in the atria, AV node, 

conduction system, or the ventricles. 

6-27 2, 1 “nonsmoking” to “non-smoking” 

6-29 2, section 

heading 

Change “ECG abnormalities indicating arrhythmia” to 

“ECG changes associate the modulation of 

repolarization”. 

6-29 1, 4 A final statement might include, “Alternatively, novel 

non-invasive electrocardiographic telemetry systems 

might be used more effectively to assess the 

relationship between air pollutants and arrhythmia in 

patients with history of arrhythmias or at risk for 

serious arrhythmia.” 

6-34 1, section 

heading 

Change “ECG abnormalities indicating ischemia” to 

“ECG changes suggestive of increased ischemia”. 

6-39 1, 1 Write out “yr” as “year” 

6-39 Write “IHD” as “ischemic heart disease” 

6-40 1, 1 Consider changing the first sentence to “...examine the 

association between 2 measures of vascular reactivity, 

non-endothelium dependent nitroglycerin mediated 

reactivity and endothelium-dependent flow-mediated 

reactivity, and ambient...” 

6-48 1, 1 Write “ET” as “endothelin-1” 

6-62 1, 4 “QA interval” should be defined. 

Table 6-4/65 The closed bracket after m3 is supra-scripted and 

should not be. 

6-69 3, 1-5 Continue “on markers of inflammation...” directly on 

the previous line without indentation. 

6-75 2, 5 Substitute “highway police” for “troopers” 

6-77 2, 1 Write “wood smoke” instead of “WS” 

11
6-81 1, 2 Write “thrombin anti-thrombin complex” instead of 

“TAT” 

6.2.10.5 2, 7 “associate” should be written “associated” 

6-116 2 Consider “Co-pollutant” rather than “Copollutant”. 

6-123 1, 17; 2, 7 Consider “multi-city” rather than “multicity”. 

6-128 2, last line Add to the final sentence such that it would read, “ 

Furthermore, the HRV result...including age and preexiting conditions and genetic polymorphisms 

modulating responses to oxidative stress.” 

6-138 1, last line Consider “co-pollutant” rather than “copollutant”. 

“Copollutant” is used throughout the document. If such 

a change is accepted then other examples should be 

found. 

6-241 1, Consider changing “nonasthmatics” to “nonasthmatics”. 

References 

6-336 Aekplakorn – add Journal title 

Analitis – add Journal title 

Andersen – add Journal title 

Andersen – add Journal title and volume 

6-337 Atiga – add Journal title 

Atkinson - – add Journal title, volume and pages 

6-338 Bastain – add Journal title 

Bell – add Journal title 

12
Berger – add Journal title 

Brauner – add Journal title 

6-339 Brook – add Journal title 

Burnett – add Journal title, volume and pages 

Caligiuri – add reference. “Presented at” ? 

Carlsten – add Journal title 

6-340 Checkoway – add Journal title, volume and pages 

Chevalier – add Journal title 

6-341 Chuang – add Journal title 

Ciencewicki – add Journal title 

D’Ippoliti – add Journal title 

Daniels – add Journal title, volume and pages 

Danielsen – add Journal title 

De Bruin – add Journal title 

De Haar – add Journal title 

6-342 Dockery – add Journal title, volume and pages 

Dominici – add Journal title, volume and pages 

6-343 Dusek – add Journal title 

Fairley – add Journal title, vol. and pages 

Fakhri – get reference 

Farraj – add Journal title 

6-344 Franklin - – add Journal title, vol. and pages 

Gent – add volume 

Gerlofs-Nijland – add volume 

13
Gerlofs-Nijland - – add Journal title 

Gilmour – add Journal title 

6-345 Godleski – add Journal title 

Gong – add Journal title, volume, and pages 

6-346 Hanigan – add Journal title 

Happo – add Journal title 

Harkema – add Journal title, vol. and pages 

Harrod – add Journal title 

Hogervosrt – add Journal title 

Holguin – add Journal title 

6-347 Host – add Journal volume and pages 

Inoue – add Journal volume 

Ito – add Journal title, vol. and pages 

Ito – add Journal title, vol. and pages 

Ito – add Journal title 

Jalaludin – add Journal title 

Janes – add Journal title 

6-348 Johnson – add Journal title 

Katsouyanni – add Journal title, vol. and pages 

Klein-Patel – add Journal title 

Kleinman – add Journal title 

Kleinman – add Journal title 

Klemm – add Journal title, volume and pages 

6-349 Laupacis – add Journal title 

14
6-350 Le Tertre – add Journal title, vol. and pages 

Lee – add Journal title 

Levy – add Journal title 

Li – add Journal title 

6-351 Lin – add Journal title 

Lippmann – add whole reference 

Lippmann – add whole reference 

Lisabeth – add Journal title 

Liu – add Journal title 

Ljungman – add Journal volume and pages 

Low – add Journal title 

6-352 Mar – Epidemiol. Is redundant 

Mar – add Journal title 

Mar – add Journal title, vol. and pages 

Matsumoto – add Journal title 

McCreanor – add Journal title 

Metzger – add Journal title 

6-353 Mills – add Journal title 

Murata – add Journal title 

6-354 Mutlu – add Journal title 

Nadziejko – add Journal title, vol. and pages 

Nadziejko – add Journal title 

O’Connor – add Journal title 

O’Neill – add Journal title 

15
6-355 Okin – add Journal title 

Ostro – add Journal title, vol. and pages 

Park – add Journal title 

Park – add Journal title 

Peel – add Journal title 

Pekkanen – add Journal title 

Peng – add Journal title 

Pennanen – add Journal title 

6-356 Pereira – add Journal title 

Perez – add Journal title 

Peters – add Journal title 

Peters – add Journal title 

Peters – add Journal title 

Piedrahita – form of reference is not consistent with the 

others 

Pope – add Journal title 

6-357 Prystowsky – add Journal title 

6-358 Rodriguez – add Journal title, vol. and pages 

Rundell – add Journal title 

Samet – add Journal title, vol. and pages 

Samet – add Journal title, vol. and pages 

6-359 Sarin – add Journal title 

Schwartz – add Journal title, vol. and pages 

Schwartz – add Journal title 

16
Schwartz – add Journal title 

Seagrave – add Journal title 

6-360 Sheppard – add Journal title 

Sillanpaa – add Journal title 

Smith – add Journal title 

Steinvil – add Journal title 

Stolzel – add Journal title, vol. and pages 

6-361 Sullivan – add Journal title 

Tamagawa – add Journal title 

Tankersley – add Journal title 

Thurston – add Journal title 

6-362 Trenga – add Journal title 

Tsai – add Journal title 

Tunnicliffe – add Journal volume and pages 

Upadhyay – add Journal title 

Van der Werf – add Journal title 

6-363 Vincent – add Journal title, vol. and pages 

Wellenius – add Journal title 

Wellenius – add Journal title 

Whitekus – add Journal title 

6-364 Whitsel – add Journal volume and pages 

Wichmann – add Journal title, volume and pages 

Witten – add Journal title, vol. and pages 

Wong – add Journal title 

17
Yang – add Journal title 

Yue – add Journal title 

6-365 Zabel – add Journal title 

Zanobetti – add Journal title 

Zanobetti – complete reference 

Zanobetti – complete reference 

Zanobetti – add Journal title, vol. and pages 

Zanobetti – add Journal title 

Zhang – add Journal title 

Chapter 7 

Specific Comments: 

SEC/PAGE PARA/LINE REVIEW COMMENTS 

7-2 L. 15-16 Consider “Atherosclerosis is a progressive disease that 

contributes to several adverse outcomes, including acute 

coronary syndromes such as myocardial infarction, 

sudden cardiac death, stroke and vascular aneurysms.” 

7-3 L. 31 Consider starting line 31 with, “CAC represents the 

accumulation of calcium in coronary artery 

macrophages and represents an advanced stage of 

atherosclerosis. As such CAC is a measure of....” 

7-4 L. 3 Replace “AAC” with “Abdomenal aortic calcium 

(AAC)” at least initially when the term is introduced. 

7-5 L. 3-4 Replace “anti-hyperlipidemic drugs” with “lipid 

lowering drugs”. 

7-5 L. 18 Replace “anti-hyperlipidemic drugs” with “lipid 

lowering drugs. 

18
7-5 L. 24 Change font for “in 2002 (the midpoint of the baseline 

exam.). 

7-11 L. 14 “decease” should be “decrease”. 

7-12 L. 14 Replace “TAT” with “Thrombin anti-thrombin complex 

(TAT)” at least initially when the term is introduced. 

For some of these terms that are use very infrequently 

throughout the text it is better to write them out and 

minimize the use of abbreviations. 

7-14 L. 10 “non-statistically” does not meaningful. Consider 

“statistically non-significant”. 

7-14 L. 26 “nonsignificant” should be written as “non-significant”. 

7-14 and 15 L. 32-38 and 

L. 1-4. 

There is no mention of renal function data in the 

Calderon-Garciduenas et al. 2007 paper. Yet, in the 

subsequent paragraph it is mentioned that no mention of 

an assessment of renal function. 

7-19 L. 20 Replace “avg” with “average”. 

7-19 L. 22 Correct font of “respectively”. 

7-19 L. 27 Correct font of “PM2.5”. 

7-20 L. 7 Replace “avg” with “average”. 

7-20 L. 9 Consider “The OR for fatal MI was increased but not 

significantly.” 

7-20 L. 13 and 26 Replace “avg” with “average”. 

7-21 L. 5 Replace “avg” with “average”. 

7-22 L. 17 and 22 Replace “avg” with “average”. 

7-22 L. 28 Write “hospital admissions” rather than “HAs”. 

7-59 L. 20 Change font of “reduction” and “reduced”. 

7-76 L. 16 and 17 Consider the following sequence, “Several age intervals 

have been explored: neonatal (<1 month), infants (<1 

year), and post-neonatal (1 month to 1 year).” rather 

than what is present. Subsequently, on page 7-77 the 

19
order of presentation should follow this order. 

7-77 L. 3-13 Move the paragraph “Infant Mortality and Infant 

Respiratory Mortality, <1 Year” after “Neonatal 

Mortality and Neonatal Respiratory Mortality, < 1 

Month”. “M” in “month” should be capitalized for 

consistency. 

7-121 L. 14 Font of “reduction” and “reduced” should be corrected. 

7-139 Achenbach – Title of journal 

7-140 Arlt – Title of journal 

Baccarelli – Volume and pages 

Binkova – Title of journal 

Bobak – Title of journal 

7-141 Brown – Title of journal 

7-142 Craven – Title of journal 

Dales – Title of journal 

Dinneen – Title of journal 

Dockery – Title of journal 

Dugandzic – Title of journal 

Eftim – Title of journal 

7-143 Fedulov – Title of journal 

Fujimoto – Title of journal 

Gauderman – Title of journal 

Gehring – Title of journal 

Geroulakos – Title of journal 

7-144 Gotschi – Title of journal 

Geenland – Title of journal 

20
Grigg – Reference 

Gabelova – Title of journal 

Gabelova – Title of journal, “Farmer Peter B” should be 

written “Farmer PB”. 

Ha – Title of journal 

Haland – Title of journal 

Hashimoto – Title of journal 

Heinrich – Title of journal 

7-145 Hiramatsu – Title of journal 

Hollander – Title of journal 

Iba – Title of journal 

Ishibara – Title of journal 

Izawa – Title of journal 

Jacobsen – Title of journal 

Jalaludin – Title of journal 

7-146 Janes – Title of journal 

Janssen – Title of journal 

Khattar – Title of journal 

Kizu – Title of journal 

Knobel – Title of journal 

Kunzli – Volumen and pages 

Kunzli – Title of journal 

Lacasana – Title of journal 

7-147 Loomis – Title of journal 

21
Lund – Title of journal 

Maheswaran – Title of journal 

7-148 Matsumoto – Title of journal 

Miller – Title of journal 

Nordling – Title of journal 

7-149 O’Leary – Title of journal 

O’Leary – Title of journal 

O’Neill – Volume and pages 

Oftedal – Title of journal 

Oftedal – Title of journal 

Parker – Title of journal 

Pedersen – Title of journal 

Pignoli – Title of journal 

Pires-Neto – Title of journal 

7-150 Pope – Title of journal 

Pope – Title of journal 

Resnick – Title of journal 

Ritz (2008) – Title of journal 

Ritz (2006) – Title of journal 

Ritz (2000) – Title of journal 

Rogers – Title of journal 

Rojas-Martinez – Title of journal 

7-151 Rosenlund – Title of journal 

Schatz – Title of journal 

22
Schindler – Title of journal 

Sharma – Title of journal 

7-152 Shinkura – Title of journal 

Somers – Title of journal 

Song – Title of journal 

Sorensen – Title of journal 

Sram – Title of journal 

Suh – Title of journal 

Sun – Title of journal 

7-153 US. EPA (2005) – “Just” is hanging. What does this 

mean? 

U.S. EPA (2006) – Correct “AGency”. 

7-155 Yauk (2008) – Reference 

Yauk (1996) - Reference 

Yoshida – Title of journal 

23
Cowling Comments (Dr. Ellis Cowling) 

Charge Question 1:

Welfare effects evaluation in Chapter 9: Several revisions were made to the evaluation of 

the welfare effects evidence in Chapter 9, in response to the CASAC PM Panel comment, 

to focus further on effects on climate and ecosystems and include further evaluation of 

urban visibility evidence, where possible. In addition, as recommended by the CASAC 

PM Panel, key findings and conclusions from this chapter were incorporated in Chapter 

2. The discussion of PM effects on climate was increased with substantially more detail 

from recent publications, including discussion of specific climate forcing effects from 

individual PM components and size fractions. The discussion of ecological effects was 

also reorganized to focus on the types of effects and effects of individual components. 

For the effects of PM on visibility, new material was added including sections on direct 

optical measurements and the value of good visual air quality. Please comment on the 

effectiveness of the reorganization and revisions regarding welfare effects. 

I was pleased with the adjustments in organization that were achieved in this second draft ISA 

for PM and with the statements of key findings with regard to public welfare effects in Chapter 

2. 

I was even more pleased to find that a reasonably very well-balanced distribution of attention 

was given in Chapters 2 and 9 of the PM ISA to three of the four types of welfare effects of PM 

– with visibility effects being covered in the first 83 pages in Chapter 9, climate effects being 

covered in the next 104 pages of Chapter 9, and ecological effects being covered in 43 pages in 

Chapter 9 (recognizing, of course, that the very substantial ecosystems effects the PM forms of 

airborne NOx and SOx on acidification, nutrient enrichments, and methyl-mercury enhancement 

are being handled very thoroughly in the separate integrated NAAQS assessment document for 

public welfare effects of NOx and SOx. 

It was somewhat disappointing, however, to discover that a pretty skimpy 6 pages in Chapter 9 

and only three short paragraphs in Chapter 2 is all the attention that was given to the materials 

damage effects of PM. I would have expected that soiling of exposed textiles and the painted 

and exposed stone and other surfaces of buildings and monuments would have deserved 

somewhat more attention. 

24
Frey Comments (Dr. Chris Frey) 

Charge Question 5: Integrative Synthesis in Chapter 2: The CASAC PM Panel recommended 

expanding Chapter 2 to include all important findings of the PM ISA. The integration of health 

evidence in Chapter 2 was reorganized to focus on effects of PM2.5, PM10-2.5, and ultrafine 

particles, and was expanded to include discussions of effects for which a "suggestive" causality 

determination was drawn. New integration sections were added that combine the evidence for 

health effects of PM2.5, PM10-2.5, and ultrafine PM across exposure durations. In addition, these 

integration discussions incorporated evidence related to mode of action, dosimetry, atmospheric 

chemistry, and exposure assessment to the extent possible. When appropriate, figures were 

added that summarize the overall U.S. and Canadian epidemiologic evidence for specific size 

fractions and exposure durations, along with the concentrations reported in the studies or 

provided by study authors. A new section was also added to Chapter 2 that contains policyrelevant considerations, including summaries for the evidence for susceptible subpopulations, 

lag structure of associations in epidemiologic studies, and the PM concentration-response 

relationship. Please comment on these revisions and additions to the integration of health effects 

evidence in Chapter 2.

Response: The integration of health evidence and its organization with respect to effects of 

PM2.5, PM10-2.5, and UFP is extremely helpful to the reader. The discussion of health effects 

endpoints for which a "suggestive" causality determination was drawn is helpful and 

appropriately fits in this chapter. The material on evidence for health effects of PM2.5, PM10-2.5, 

and UFP for long- and short-term exposure durations is important to the chapter. 

The graphical summary (Figure 2-1, and Figure 2-4) of U.S. and Canadian epidemiologic 

evidence is good. The discussion of policy-relevant considerations is helpful. Overall, the 

structure and content of Chapter 2 is very good. 

A few specific comments are offered. 

Page 2-4, line 8. What averaging time is the basis for these “average” concentrations? 

Page 2-5, line 18. “maintained” is not the right word. Could delete “maintained at” 

Page 2-9, line 7. EGUs are point sources with stacks, so it would be more clear here to refer to 

“non-EGU point sources,” if that is the intended meaning. 

Page 2-10, line 14. Use “such as” rather than “like” 

Page 2-13, lines 5-20. For clarity, should explain why PM10 is not separately considered, just to 

avoid confusion on the part of some readers who might be expecting to see PM2.5 and PM10 as 

the focus, since these are the indicators of the current standard. 

25
Page 2-13 – last half. As a rhetorical device, it is weak to start out with negative findings or 

what is not known. Also, it would help to have just one table that summarizes for each size 

range the list of health effect outcomes and the causality determination. As a reader, I would 

prefer to first see a list of the key outcomes that are the focus of the ISA, followed by a list of 

those for which there is inadequate evidence. 

Page 2-16, line 1. The word “precise” is used here and in a few other places. However, the 

intended meaning might be “statistically significant” rather than “precise.” Either change the 

term here or define what is meant by “precise.” 

Page 2-24: this page seems to go into a lot of detail to a depth that is not consistent with the rest 

of the chapter. Perhaps cut back on this, and just make key points. 

Page 2-25. Similar comment. Reader is wondering what is the “bottom line” here? Details are 

in later chapters. However, the last paragraph on this page is very good. 

Page 2-30, line 14. Delete “It is also important to note that”. More importantly, what are the 

implications of this paragraph? This paragraph is descriptive but it is not explained as to the 

significance or implications of what is being described. 

Page 2-33, line 11, this is awkward. “studies” are inanimate and cannot attempt to do anything. 

This section needs copy editing. 

Page 2-34, line 32-35. “various” might more accurately be replaced with “particular.” The term 

“susceptible” is used here but is not defined. The first time that the terms “susceptible” and 

“vulnerable” are used (either in Chapter 1 or this chapter) they should be defined briefly, with a 

reference to the later section where they are discussed in more detail. 

Page 2-42 - top of the page. Is PM size a factor? 

Page 2-42, lines 15-17. This text refers to “effects” on climate. In the context of all other effects 

discussed throughout the document, the presumption is that they are adverse effects. In this case, 

it is not clearly stated as to whether the “effects” are adverse or beneficial, and hence the policy 

implications of this statement by itself are unclear. 

26
Grantz Comments (Dr. David Grantz) 

ISA for PM, 2nd External Review Draft 

Comments by David Grantz on Charge Question #6—Welfare Effects 

Overall

I was very pleased to read this second draft ISA. The authors have paid close attention to 

the concerns of previous reviews. The resulting two chapters of concern here, Chapters 2 & 9, 

are well organized (few comments below) and provide a useful compendium of available 

knowledge from the previous CD and more recent literature. The current Chapter 2 contributes 

significantly to the presentation. Very few issues of interpretation remain, and these are 

addressed below. 

The increased attention to climate change is appropriate and generally well done. As noted 

below, there is some confusion in the discussion of PM impacts on photosynthetically active 

radiation (PAR). Briefly the issue is that photosynthesis per leaf responds nearly linearly to PAR 

up to some near-saturation flux. At this flux it becomes useful to spread that (excess) radiation 

around to lower leaves which (due to shading of direct beam radiation by upper leaves) are 

generally still on the linear portion of the PAR response curve. Diffusion by PM accomplishes 

this spreading around of PAR. If PM reduces total PAR below saturation for the upper leaves, 

diffusing the flux will have only minimal and second order impacts on total plant photosynthesis. 

Also, once diffuse radiation has become a significant fraction of total PAR, then further increase 

in PM will reduce plant photosynthesis by decreasing total PAR. The current text is unclear and 

seems to imply a conflict or conundrum that does not exist. The issue is important because it 

lends itself very well to the ultimate goal of modeling of response-exposure relationships to PM. 

I remain disappointed that there is little attempt to link ecological endpoints to specific levels of 

ambient PM, with a view towards moving the debate towards response-exposure relationships. In 

several cases cited there are clear endpoints, and exposures are documented. The studies of 

Regoli et al. 2006 with snails and Kuki et al. 2009 with plants, as examples, seem to demonstrate 

causality and at least the beginnings of such relationships. Reference to the study of Nash, 1975 

(page 9-235, line 34) seems to best approximate this goal. Overall, the current organization of 

Chapter 9 by component works very well. 

Specific Comments

Chapter 2--Substantive comments 

page line Comment 

27
2-3 25 It is important to define UFP (ultrafine particles) at first use, with 

respect to size and mode of origin. This might be accomplished by 

moving all of Section 2.1.5 (on PM Formation and Removal) into this 

introductory location, as a way to introduce and define PM.

2-4 

2-5 

2-12 

14 

25 

14-21

The commonly understood more rapid deposition of coarse PM is 

initially stated, but this contrasts with later references to the very 

rapid disappearance of UFP. This should be explained (ie. is UFP 

growing out of the class or depositing out of the atmosphere?)

2-6 14 Is the afternoon peak of UFP also due in part to the collapse of the 

boundary layer as in line 8, just above?

2-6 32 Might want to explain why this logical association between fine PM 

and O3 was not observed in these three cities.

2-6 33 Section 2.1.4 on Measurement Techniques may not be required at all 

in this summary chapter.

2-9 1-4 The implications of this first half of the paragraph are not clear. 

Perhaps this should be merged into Section 2.2.1 

2-11 

2-12 

14, 27-30 

23 

Define first use of “ambient” in this context, is it in opposition to 

regional or to indoor or to personal? 

2-14 

2-26 

2-31 

titles These section headings might better be titled “Effects” rather than 

“Exposure”. Also these sections (especially 2.3.1) may have too 

much detail for this summary chapter. 

2-14 Table 2.1 Seems odd that many of the CV endpoints were death, but CV is 

“causal” and mortality is only “likely to be causal”? 

2-20 

2-28 

2-32 

Sections 

2.3.2 

2.3.4 

2.3.6 

These sections seem redundant in an already ‘overview’ chapter. In 

particular, section 2.3.2 contains much of the information that is 

required in chapter 2. Perhaps these summaries can be blended into 

their preceding sections and condensed. 

2-30 22-23 Text states “is associated” when it was concluded “is suggestive...”. 

These are not equivalent. 

28
2-37 Sect 2.4.3 This entire section is cumbersome and unclear. A figure illustrating 

the no threshold log-linear relationship for some endpoint could be 

placed here (and in section 6.2.10.10 where it is also lacking). 

2-38 7 Add “including NOx and Sox” between “airborne PM” and “on 

visibility”. The distinction between the PM document and the NOxSox document will confuse many readers and should be made very 

clear every time it comes up. 

2-43 5-12 The relationship between crop growth and total intercepted PAR, and 

the role of diffuse PAR when upper leaves are light saturated, is 

poorly conveyed here and in the relevant parts of chapter 9. This is an 

important point, that if properly explained the first time would 

obviate much later discussion and remove the apparent conflict with 

data showing that increasing PM both increases plant growth due to 

light scattering and decreases it. 

Chapter 2--Other comments 

page line Comment 

2-4 5 This summary statement leaves the impression that nothing can be 

known. A more positive concluding sentence here, perhaps 

considering the importance of regional averages, and the existence of 

local hot spots, and more accurately summarizing the subsection, 

would be helpful, particularly for readers who may only read this 

chapter.

2-4 8 Should specify the averaging period (is it as specified at 2-5, 29 or at 

2-14, 5?)

2-5 21 need a summary statement here

2-7 28 “isoprene” seems to be in the wrong place. 

2-8 18 farm equipment may be even more confounded with trucks than are 

locomotives. 

2-9 23 should indent new paragraph 

29
2-14 14 Reference to null findings is unclear and potentially confusing 

2-15 3 Might define “vasomotor” for general readers 

2-20 9-10 Methylation is not a change in the genome 

2-31 4 Typographical error in “cardiovascular” 

2-36 13 Missing word before “children” 

2-36 22 “result(s)” 

2-36 25-26 a priori should be italicized 

2-39 27-29 Is carbonaceous PM largest only in the West, needs to be clarified. 

2-41 7-8 There should be a formal reference to the IPPC AR4. 

2-42 9-14 This run-on sentence is hard to interpret. 

2-43 32-34 The sentence is poorly constructed and factually unclear. Possible 

solution is to insert “which are more often deposited by wet 

deposition” between “fine particles” and “are more likely to contain” 

Chapter 9--Substantive comments—line numbers are approximations

page line Comment 

9-2 21-22 “Biogenic” combustion should be “biomass” combustion. If 

prescribed burns are “natural” from a regulatory perspective then this 

requires a brief explanation. 

9-8 1-31 The level of detail on dark visibility is not necessary here, as it is 

ultimately dismissed. Perhaps this section could be moved to later in 

the chapter, as a suggestion of future concerns. 

9-40 

9-43 

31 

Fig. 9-

22 

The text refers to Puerto Rico values of fine soil, but the figure 

appears to indicate no data for Puerto Rico. 

30
9-46 Fig. 9-

24 

San Joaquin Valley data are unclear. This is a nearly closed airbasin, 

unlike South Coast. Text is needed to explain what is the source of 

regional PM (i.e. what is the region), and where local PM was 

measured (just in urban Fresno?). Given internal gyre based 

circulation in this basin it is not clear that the Valley itself constitutes 

a truly regional source, nor that offshore sources are dominant as 

implied on 9-54, 28 and on 9-55, 1to29. There seems to be a general 

confounding of South Coast and San Joaquin Valley. An explicit 

analysis similar to that provided for the Columbia Gorge (9-57, 1to5) 

would be useful. 

9-93 20 Maximum sight distance of 8 km in Washington DC is outside the 

range of visibilities presented (Table 9-2), does this require some 

explanation? 

9-102 25 on The source of NOx to support the Midwest nitrate bulge has not been 

well discussed to this point, and should be here. Ammonia has been 

dealt with adequately. 

9-210 21 PM effects on precipitation have been omitted from section 9.3.10 

and should be considered here. 

9-213 6-7 The concluding sentence of this paragraph does not summarize the 

paragraph, and may belong with the following paragraph. The 

appropriate concluding sentence here should summarize the 

preceding CD and the material to be excluded from the current ISA. 

9-221 3 There is a distinction made between uptake (or maybe just response?) 

at the air-plant interface, and uptake by above ground tissue. This is 

hard to understand. The authors may want to consider citing a 

description of these processes, and of the leap-frog behavior of SOCs 

discussed later, in the review by Krupa et al., 2008, Journal of Air 

and Waste Management Assoc 58: 986-993. This reference has not 

been cited and perhaps should be consulted. This reference could be 

useful at p. 9-226 mid page, p. 9-256, bottom, and p. 9-259, mid 

page. 

9-221 13 Scavenging by the snowpack implies only dry deposition. There may 

also be wet deposition in the falling snow. 

9-226 7-17 This paragraph takes a generally positive view of biomonitoring 

using mosses etc., which contrasts with conclusions on p. 224-225. 

31
These sections should be more closely aligned with each other. 

9-227 8-15 There are some important concepts contained in the previous CD 

regarding deposition, including specific cation depletion with depth 

and distance into forests, that should be reviewed here. The material 

at top of 9-236 on mosses and lichens should be incorporated into this 

section. These data form the basis for existing models, and for the 

criticism of them posed by Pryor and discussed here. In general, this 

paragraph is hard to understand and should be revised. An entirely 

new idea is introduced with “condensation processes...”. This 

sentence should start a new paragraph, but more importantly should 

be integrated with the overall theme of this section, which has to do 

with the appearance and disappearance of PM in canopies. 

9-227 16-22 This paragraph requires some revision to better communicate that 

biomonitoring and ecosystem impact are different endpoints. The 

sentence “As an ecosystem pool...mosses” could perhaps be moved 

to the end of the paragraph. 

9-231 10 Only near the coast is most salt from sea salt. 

9-231 21-28 This paragraph is out of place. It might be inserted near the beginning 

of 9.4.3.1. The last sentence, “Fine particles...demonstrated” should 

be moved to the bottom of page 9-229. 

9-234 1-8 The material currently in 9.4.5.4 could be included here. Throughout 

the metals section there is some blurring of direct and indirect effects 

that should be clarified. 

9-235 24 It would be useful to explore how S. terebinthifolius avoided stress 

since this would be a useful attribute to look for in other systems. As 

currently written this statement does not communicate much. 

9-246 3-6 The discussion of loss of peat and increase in Hg should be moved to 

or summarized in the section on climate change. 

9-247 24 First paragraph of 9.4.5.5 seems to imply that these are toxicity issues 

(“metals in PM deposition limit phytoplankton growth”), but actually 

they are fertility issues and positive effects. 

9-252 22-25 The dependence of uptake on solubilized Cd is reasonable, but this 

begs the question what determines solubilization (redox, acidity, ?) 

32
9-253 32-36 While the effects of Cu and Ni may be solely attributed to their 

toxicity as statedhere, it was implied previously that these heavy 

metals displace from soil exchange sites the very cations (Mg, Ca and 

Mn) that are reported here to be depleted. Both inhibition of uptake 

and depleted soil stores may be at work. 

9-258 20-24 The greater content of PAH in littoral than pelagic species may 

reflect sequestering in sediment as indicated, or it may (also) reflect 

differences in diet of the two communities. 

9-259 5-8 The role of elevation does not seem to justify use of salmonids as a 

biomonitor. I suspect there was some linkage to prevailing PM 

concentrations (which may have also varied with elevation?) in the 

original publication which could be discussed here. 

9-262 1-10 Again, discussion of PAR and diffuse light requires some attention. 

Also haze has been “modeled” or “calculated” or “measured” rather 

than “estimated” (to diminish visible radiation). 

9-267 4-8 Rust generally applies to iron oxide. Whereas such coatings on 

aluminum do provide some protection against further corrosion, iron 

oxide does not, due to its flaking behavior. 

9-267 16 Is this really dry deposition of gypsum (CaSO4) or is it formation in 

place when sulfuric acid meets limestone or marble? 

Chapter 9--Other comments—line numbers are approximations

page line Comment 

9-1 18 Insert “including NOx and Sox” between “PM” and “on visibility” 

9-13 

9-24 

Eq. 9-1 

Eq. 9-2 

The RH functions shown at top of page 9-14 could be placed within 

equation 9-1, as “where” statements. Analogous RH functions should 

be described for equation 9-2. 

9-49 8-9 The sentence, “Note that the concentration...trend line slope” could 

be moved to the figure legend. 

33
9-61 Fig 9-32 It is unclear what the sulfate and nitrate concentrations in the 

individual figure legends refer to. 

9-64 Fig 9-34 Is top panel average of Class I areas as indicated in figure, or only 

Yellowstone NP as indicated in the legend? 

9-

72,3 

Figs 9-

38,39 

Scale is not technically unitless as indicated in legend (it is %). 

9-96 26-33 The deciview units should be translated into visual range, as was 

done above. 

9-213 29 The reference to Odum 1985 is not complete (p. 9-292) 

9-222 20 The distinction between combustion sources and petrogenic sources 

is unclear. Does combustion source refer to biomass combustion? 

9-235 15-17 Sentence beginning, “A greenhouse study...” is confusing. There is a 

word missing (“under”?) prior to “simulated”. 

9-237 22-26 Second half of paragraph, “Sequential extractions...unavailable” 

could be incorporated into the beginning of this section 9.4.5.2. 

9-242 22 In line beginning with “by increasing” there is a critical typographical 

error, “creasing Cd uptake”. Is is increasing or decreasing? Also at 

beginning of next paragraph “mycorrhizae” is misspelled. 

9-243 8-11 The discussion of shallow-rooted species is not very useful, and 

should be deleted as a distraction. 

9-250 7 MADE should be AMDE. It would be useful to define the reactive 

gaseous Hg species of interest here. 

9-251 7 Should include cement factories as sources of metals, given earlier 

citation of Massicote et al., 2003 to this effect. 

9-252 1-5 It would be useful to describe briefly how isotopes of C and N can 

demonstrate biomagnifications of metals. In the second paragraph, 

the lack of biomagnifications in aquatic systems, if generally true, is 

sufficiently counterintuitive that it should be explained a bit more. 

9-256 25-33 The first 6 lines of this paragraph should be moved to the earlier 

section on deposition. 

34
9-261 18 Ecological effects also include changes in soil microbiology, which 

should be added to the list at the beginning of section 9.4.7. In the 

second paragraph, ions should be added to the list of constituents 

with ecological effects. 

35
Helble Comments (Dr. Joseph Helble)

Charge question 4, ISA 

Revisions to Chapter 3 on Source to Exposure: Consistent with revisions made to the health 

effects chapters, Chapter 3 was revised to clarify that PM10 incorporates both PM2.5 and 

PM10-2.5 and reorganized to begin with PM2.5 and PM10-2.5, followed by PM10, where 

applicable. The discussion of measurement techniques and chemistry of PM10-2.5 has been 

expanded in Sections 3.4 and 3.5, in response to CASAC comments. In addition, Section 3.8 on 

human exposure to PM has been reorganized and expanded to better characterize the evidence 

and provide useful information for interpretation of epidemiologic studies. We would appreciate 

comments from the CASAC PM Panel on these revisions. 

Summary

The expansion and reorganization of Chapter 3 now provide a generally clear, well-organized, 

and comprehensive review of PM2.5, PM10-2.5, and PM10. The sequencing of discussing PM2.5 

followed by the successively larger size fractions provides a logical framework for addressing 

the important differences among these size classes. The revised chapter also does a good job, 

overall, of summarizing areas where studies suggest differing trends, and identifying areas where 

data are sparse and additional research is needed. 

The reorganization and expansion specifically to address deposition in more detail, measurement 

techniques, and diesel emissions were generally clear and well-structured. With regard to 

deposition, a minor suggestion is that Section 3.3.4 page 3-21, the general introduction, be 

expanded to address wet deposition. It is meant to be a general overview of deposition, but only 

discusses dry deposition and ignores wet deposition other than a passing reference in the first 

sentence. Organizationally, if this is to function as the introduction to the sections providing a 

more detailed discussion of both wet and dry deposition, an overview of wet deposition needs to 

be added. 

The importance of particle morphology was clarified in this draft (pages 3-6 to 3-7) as requested 

in the last review, but the discussion remains a general one. There is some limited literature on 

surface area, for example, that could be considered. 

The embedded links to reference documents are a very welcome feature. 

Detail Comments

Lines 19-20, page 3-7, states that “particles in ambient air are generally mixtures or agglomerates 

of particles...from multiple sources...” This statement is true if one is referring to condensed or 

adsorbed species on the surface of nearly all PM, but otherwise, this statement is misleading 

because it is dependent upon particle size and proximity to source. This statement should be 

clarified or, better, removed. 

36
In the discussion of county-based PM spatial distribution in section 3.5.1.1, a slightly expanded 

discussion of the completeness criterion would be helpful in interpreting the results. Counties 

appear in white in the associated figures when they fail to meet the 75% completeness criterion. 

Failing to meet this criterion could, however, be a result of a lack of appropriate monitoring sites 

within the county, or a failure to obtain adequate (complete) data from appropriate monitoring 

sites. Parsing this would be helpful – i.e. how many of the counties failed to meet the criterion 

because existing monitoring sites did not report sufficient data? 

Organizationally, it isn’t clear that the summary in section 3.5.4 is necessary. The individual 

subsections in section 3.5 provide a detailed review of the data, and the summary is essentially 

repeated in section 3.9. Section 3.5.4 therefore adds little. To shorten the document, this subsummary, as well as a few other sub-summaries at the end of individual sections, could be 

deleted, with section 3.9 serving as the overall summary for Chapter 3. 

Page 3-225, line 28 – it seems that two different sentences, and two different ideas, run together 

in this line. The first part of line 28, and the text that precedes it, appears to focus on automobile 

indoor exposure. The remainder of the paragraph, with no transition, addresses school buses. 

Were parts of two different paragraphs truncated? 

Minor / Editorial

Figure 3-2 additional detail needed regarding sampling location and sampling details. 

Lines 10-11, page 3-16 – first sentence in the paragraph confusing. Substitute “being emitted” 

for “emission” to clarify. 

Lines 16 and 17, page 3-31 – impaction-based collection efficiency will decrease, not increase, 

as dp decreases. 

Line 5, page 3-34: “monvolatile” should be changed to “nonvolatile” 

Line 14, page 3-45: change “detect” to “detecting” 

Line 20, page 3-45: change “media” to “medium” 

Tables 3-3:, 3-4, etc. add commas to N values so magnitude of population figures more easily 

seen 

Figure 3-7 and 3-8: display would be enhanced by showing PM2.5 and PM10 monitors on the 

same figure 

Line 6 page 3-59, fix font on PM2.5. Similar comment lines 8 and 9, page 3-60 

Line 31 pg 3-70, insert “per” before cm3

37
Figures 3-12 to 3-14: did EPA consider plotting these figures without using different sizes for 

the different concentrations (i.e., using different colors only)? It might make the figures easier to 

read. 

Figure 3-19 and similar figures – adding state borders would facilitate a quicker understanding of 

monitor locations 

Lines 10 and 11, page 3-135: figure numbers should be changed to 3-52 and 3-52 

Table 3-17 is not adequately explained in the text nor the caption. The parenthetical values in 

column 2 need to be described, and the basis for the data (ng/kg of what? presumably emitted 

PM) stated explicitly. Also, while it is likely that this table came directly from the cited source, 

is EPA certain that 5 significant figures (seen in several of the table entries) are justifiable? 

Line 10, page 3-144: “mighty” should be changed to “might” 

Line 8 page 3-151, “much” should be changed to “must” 

Figure 3-65, page 3-165: caption is incomplete 

Figure 3-68 caption – symbol  is missing. Also missing from title of Table 3-19 page 3-187, 

and from titles of Tables 3-20 through 3-23 

Figure 3-73 page 3-174: caption, change “theem” to “them” 

Line 10, page 3-215: “In this work,” - ? Incomplete sentence 

Line 20, page 3-215: complimentary should be complementary 

Lines 10-11-12 page 3-237, sentence would read better as opening to section. It does not follow 

as a conclusion. 

Page 3-246, Low Angeles should be Los Angeles 

38
Henderson Comments (Dr. Rogene Henderson) 

Reply to Charge Question #3; Susceptible Populations 

I found Chapter 8 to be complete, clear and well-organized. The authors have been 

responsive to the CASAC critique of the first draft of the chapter. Their definition of 

"susceptible" is clearly stated and there is a rather complete listing of how the term has been used 

in the literature in the past. 

 Table 8-2 introduces all of the susceptibility factors that have been evaluated, as well as 

the size fraction evaluated and the length of the exposures. The table is then followed by a more 

detailed description of the evaluations that were made. This is an appropriate organization, with 

one exception. The introductory table 8.2 does not have a column indicating the results of the 

evaluations. Thus if one only looks at the table, which is titled simply "Susceptibility Factors," 

one might get the impression that all of the listed factors showed a susceptibility, when some 

factors, such as gender, did not. I recommend at least expanding the title to "Susceptibility 

Factors That Have Been Evaluated," and if possible add a column that suggests what the results 

of the evaluation were. Maybe just a plus/minus approach could be used. 

1) I found Chapter 8 to be complete, clear and well-organized. The authors have been responsive 

to the CASAC critique of the first draft of the chapter. Their definition of "susceptible" is clearly 

stated and there is a rather complete listing of how the term has been used in the literature in the 

past. 

2) Table 8-2 introduces all of the susceptibility factors that have been evaluated, as well as the 

size fraction evaluated and the length of the exposures. The table is then followed by a more 

detailed description of the evaluations that were made. This is an appropriate organization, with 

one exception. The introductory table 8.2 does not have a column indicating the results of the 

evaluations. Thus if one only looks at the table, which is titled simply "Susceptibility Factors," 

one might get the impression that all of the listed factors showed a susceptibility, when some 

factors, such as gender, did not. I recommend at least expanding the title to "Susceptibility 

Factors That Have Been Evaluated," and if possible add a column that suggests what the results 

of the evaluation were. Maybe just a plus/minus approach could be used. 

39
Hopke Comments (Dr. Phil Hopke) 

Chapter 3 

This chapter is in generally good shape. I think there are some minor changes noted below that 

will improve it. 

There are a number of cases where they talk about “accuracy” with respect to sampling or 

determination of concentrations. In most cases, there is absolutely no knowledge of accuracy 

since there is no way to provide a truly known standard to which the measurement can be 

compared. There may be systems with good precision, but there are no deployed system with 

know accuracy. Thus, there needs to be a careful review of the use of “accurate” with respect to 

the description of any ambient measurement. 

Primary vs secondary organic aerosol: 

I suggest it would be very helpful to clearly distinguish the various types of organic carbon 

species associated with airborne particulate matter. It is too simplistic to just classify the OC 

into primary and secondary. There is also oxidized primary organic matter. The problem is the 

oxidized POM will also be water soluble and have the general characteristics of SOA. 

However, given the sources are different and the chemistry is entirely heterogeneous, it is 

important to clearly distinguish these three different portions of the particulate organic matter. 

The process of forming SOA or oxidized POM leads to the formation of oxidizing species 

(reactive oxygen species). This source of exogenous ROS could be important in the induction of 

adverse health effects. Thus, connecting SOA formation with high concentrations of ROS such 

as seen by Docherty et al. (Docherty, K. S., Wu W., Lim Y. B., Ziemann P. J. (2005) 

Contributions of organic peroxides to secondary aerosol formed from reactions of monoterpenes 

with O3, Environmental Science and Technology 39, 4049-4059). Thus, we can expect ROS to 

be associated with ambient particles and that has been observed by multiple groups (Hung, H-F., 

Wang, C-S.(2002) Experimental determination of reactive oxygen species in Taipei aerosols.

Journal of aerosol science 32, 1201-1211; Hasson A. S., and Paulson S. E. (2003). An 

investigation of the relationship between gas-phase and aerosol-bourne hydroperoxides in urban 

air, J. Aerosol Sci., 34: 459-468.; Venkatachari, P., Hopke, P.K., Brune, W.H., Ren, X., Lesher, 

R., Mao, J., Mitchell, M. (2007) Characterization of wintertime reactive oxygen species 

concentrations in Flushing, New York, Aerosol Science and Technology, 41, 97-111; 

Venkatachari, P., Hopke, P.K. ,Grover, B.D., Eatough, D.J.(2005) Measurement of particlebound reactive oxygen species in Rubidoux aerosols, Journal of atmospheric chemistry, 50, 49-

58). Thus, there needs to be a short paragraph added to point to this pathway to the formation of 

a potentially important class of atmosphere aerosol species that could be directly related to 

observed human health effects. 

Other major issues: 

Although past the cut-off date for inclusion, it may be useful to note Amato F., Pandolfi M., 

Escrig. A., Querol. X., Alastuey A., Pey. J., Perez N. and Hopke P. K., Atmospheric Environ. 43: 

2770-2780 (2009). This paper demonstrates how known source profiles can be included within 

the PMF framework and yield an improved source resolution. 

40
The description of PLS on page 3145 is not fully correct. PLS is in fact a biased regression 

method that is really designed for prediction and not for explication as is the goal of receptor 

modeling. In addition, there is really no basis for choosing PLS over other prediction methods 

like principal components regression (PCR). It is really not a receptor model and it is not clear it 

really belongs in this section. 

There are some minor issues to be resolved. 

On page 3-4, the table uses the term “condensation of gases.” Gases do not condense at normal 

temperatires and pressures. The correct term here is condensation of “vapors.” 

Chapter 5 

The discussion in section 5.1 only focuses on endogeneous ROS. It should be recognized that 

there is exogenous ROS associated with the ambient particulate matter to which we are 

continuously exposed. Even in the evening, there is still significant particle-bound ROS and 

thus, it should be noted as part of the total dose of ROS to the tissue. 

41
Lippmann Comments (Dr. Mort Lippmann) 

Post-Meeting Review Comments 

General Comments: 

1) I commend the organizers and authors of this document for providing the CASAC PM 

Panel with a well organized and readily readable text that is, for the most part, thorough 

and accurate in its presentation of the peer-reviewed literature most relevant to Standard 

setting for PM. 

2) I have one major disagreement with the authors in terms of their characterization of 

Health Effects (Section 2.3). Specifically, in Section 2.3.1.2 on Effects of Long-Term 

Exposure to PM2.5, the conclusion that “a causal relationship is likely to exist between 

long-term exposure to PM2.5 and mortality” is insufficient. It should be changed to “a 

causal relationship exists between long-term exposure to PM2.5 and mortality”. How 

is it possible to conclude that “a causal relationship exists between long-term 

exposure to PM2.5 and cardiovascular effects” (page 2-18, lines 8 & 9), and that the 

strongest support for that causality determination comes from the associations of ambient 

PM2.5 and annual mortality, and then equivocate on the conclusion that PM2.5 causes 

excess mortality. The document amply showed that cardiovascular mortality accounts for 

most of the excess mortality (Pope et al. 2004). The conclusion that I challenge is 

apparently drawn, for the most part, from Section 7.6.5, in which it failed to properly 

consider that chronic PM2.5 exposure studies in mice caused exposure-related aortic 

plague progression. This research provides a toxicological basis for supporting the 

epidemiological findings of excess cardiovascular mortality and a causality conclusion. 

3) I have an important organizational comment on the draft ISA. It is inappropriate to 

include the summary and synthesis on associations of PM sources and components with 

health effects only in Chapter 6 on short-term exposures, since it covers the literature on 

both short-term exposures and long-term exposures, the latter being relevant to Chapter 7. 

This topic should be a separate chapter. If this is not possible, the topic should be covered 

in both Chapters 6 & 7. 

4) There seems to be an overemphasis on UFP, especially in Chapter 5, where the potential 

to cause adverse effects is so prominently featured, along with the implication that 

particle number concentration is the most important metric for risk. Some additional 

discussion of the fact that supporting evidence for this hypothesis remains weak is 

warranted. 

5) Some generic changes that should be made for the final version are: 

a) Use a consistent criterion for “recent”. In the context of this document it should refer 

to papers appearing since the closure on the last PMCD; 

b) Italicize in vivo, in vitro, in situ, a priori, etc. 

42
Specific Comments: 

PAGE LINE REVIEW COMMENTS 

1-3 1 and 2 Two lines of text were left out here 

1-17 9-12 It is inappropriate to include a summary and synthesis 

on associations of sources and components with health 

effects in Chapter 6, since it covers both effects of 

short-term and long-term exposures. It needs to be a 

separate chapter, or divided into parts for Chapter 6 

and parts for Chapter 7. 

1-24 15 Insert “sizes, respiratory parameter and” before 

“branching” 

1-24 34 Citations to the concentrators developed and used by 

the Harvard Group need to be added here 

2-31 5 I don’t agree with the statement: “fresh DE, which is 

typically dominated by UFPs”. It may be true for the 

number concentration, but is usually not true for mass 

concentration due to rapid coagulation of the UFPs 

before they are inhaled. 

3-111 1-14 Cite work of Peltier et al (in press) and Peltier and 

Lippmann (in press) on intra-urban variations in N and 

V in NYC 

4-1 26 Insert “Substantial” before “exposures” 

4-1 30 Change “frequently” to “can” 

4-2 2 Change “Fibers, therefore, deposit largely” to “fibers 

longer than 10 μm can deposit” 

4-2 6 Insert “long” before “fibers” 

4-2 6 Change “prevent” to “affect” 

43
4-3 28 Change “airways” to “respiratory tract” 

4-3 29 Change “airways” to “respiratory tract” 

4-5 2 Change “rats” to “rodents” 

4-6 25 Change “scintigraphic” to “external measurements of 

retained particles having radioactive tracers” 

4-6 25 Change “These” to “Scintigraphic” 

4-14 17 Insert “anatomical and” before “ethical” 

4-15 12 Add “and nasal vs. oral breathing” after “size” 

5-1 18 Insert “with the exception of ultrafine PM” before 

“There” 

5-2 Fig. 5-1 

5-2 Fig. 5-2 

Lowest oval is mis-labeled. It should refer to in-vivo

responses, rather than cellular system assays. 

5-3 21 Insert “soluble” before “metals” 

5-8 13 Change “PM2.5 “ to “accumulation mode PM” 

5-27 15 Delete “ultrafine” 

6-4 12 Change “m” to “ms” 

6-17 7 Change “Tuxedo” to “New York” 

6-17 25 Change “of” to “in” 

6-95 15 Change “NA+” to “Na+” 

6-103 Fig. 6-2 Show vertical line at 0 change 

6-250 Sect. 6.4.1 Chen & Schwartz (2009) does not belong here it is 

clearly a study of chronic exposure and effects 

6-251 Sect. 6.4.3 Cite Veronesi et al (2005) in this section. (See ref. 

listed at end of my comments). 

6-252 Sect. 6.4.3.1 Calderon-Garciduenas et al. (2003) does not belong 

here in the acute exposure section. 

44
6-253 2nd and 3rd para. These studies do not belong in the acute exposure 

section. 

6-320 14 Change “correlation between each” to “correlations 

among the” 

6-320 26 Change “inherently” to “sometimes” 

6-321 16 Insert “and analyzed the concentrations of the 

components therein” after “CAPs” 

6-325 12 Add citation to “Patel et al (in press)”. (See ref. listed 

at end of my comments). 

6-326 6 Insert “of” after “study” 

6-326 3rd para. What about the “Franklin et al (2008)” paper? It needs 

to be cited in this paragraph. 

6-327 3rd para. Line5 Change “similar” to “simultaneous” 

6-327 3rd para. Line7 Cite the “Sama et al (2007)” paper on the effects of 

CAPs on the liver here. (See ref. listed at end of my 

comments). 

6-331 Table 6-17 Add another source category, i.e., “smelter effluent” , 

which is enriched in Ni, Cr, and Fe. 

7-2 14 Cite Veronisi et al (2005) re: nervous system and Tang 

et al (in press) re: hepatic system 

7-6 22a Insert “PM2.5” before “CAPs” 

7-8 12a Change “PM10” to “Ambient Air PM” 

7-10 Sect. 7.2.3 Create a new subsection on Epidemiology that cites 

the study of Chen and Schwartz (2008), using text 

from page 7-11, lines 4-6 

7-25 9 Add at end of sentence: “and with PM2.5- related 

plaque progression in chronically exposed mice” 

7-30 3 “SAPALDIA” is mis-spelled 

7-31 Table 7-3 Add descriptions of “Gent et al (2009) and Patel et al 

45
(in press) to this table 

7-115 5 Add citation to “Xu et al (in press) 

7-131 Table 7-9 Capitalize “New York City” in the table title 

7-137 18 As noted previously, “likely to be” needs to be deleted 

References cited in there Reviewer Comments 

Chen, L.C, Quan, C., Hwang, J.S., Jin, X., Li, Q., Zhong, M., Rajagopalan, S., Sun, Q., 

Atherosclerosis lesion progression during inhalation exposure to environmental tobacco smoke 

in a susceptible animal model, and comparison with that occurring during exposure to 

concentrated ambient air fine particles. Inhal. Toxicol. (in press). 

Lippmann, M. Semi-Continuous Speciation Analyses for Ambient Air Particulate Matter: An 

Urgent Need for Health Effects Studies. . J. Expos. Sci. Environ. Epidemiol. 19:235-247. 

Lippmann, M. and Chen, L.C. Health effects of concentrated ambient air particulate matter 

(CAPs) and its components. Crit. Rev. in Toxicol. 39(10):865-913. 

Patel, M., Hoepner, L.,Garfinkel, R., Chillirud, S., Reyes, A., Perera, F., Millrt, R. (2009). 

Ambient metals and elemental carbon in fine particulate matter predict wheeze and cough in very 

young urban children. Am. J. Respir. Crit. Care Med. (in press). 

Sama, P., Long, T.C., Hester, S., Tajuba, J., Parker, J., Chen, L-C., Veronesi, B. (2007). The 

cellular and genomic response of an immortalized microglia cell line (BV2) to concentrated 

ambient particulate matter. Inhal. Toxicol. 19:1079-1087. 

Tan, H-H., Jinsheng, G., Fiel, M.I., Alvarez, C.E., Chen, L-C., Sun, Q., Friedman, S.I., Odin, 

J.A., Alina, J. Enhancement of fatty liver disease progression and TLR-4-dependent Kupffer cell 

activation by air particulate matter. J. MOLEC. MED, (in press). 

Peltier, R.E., Hsu, S.i., Lall, R., and Lippmann, M. Residual Oil Combustion: A major source of 

airborne nickel in New York City. J. Expos. Sci. Environ. Epidemiol. 19:603-612. 

Peltier, R.E., and Lippmann, M. Residual Oil Combustion: 2. Distribution of airborne nickel and 

vanadium within New York City. J. Expos. Sci. Environ. Epidemiol. (in press). 

Xu, X..

, Kherada, N., Hong, X., Quan, C., Zheng, L., Wang, A., Zhong, M., Lippmann, M. Chen, 

L.C.. Rajagopalan, S., Sun, Q. Diesel exhaust exposure induces angiogenesis. Toxicol. Lett. (in 

press). 

46
Malm Comments (Dr. William Malm) 

Review of Integrated Science Assessment for PM 

Page 9.3: The use of “transparency” is inappropriate here. It usually is reserved for a 

psychophysical reference of the “perceived” transmittance of the atmosphere. One could use 

“transmittance”, but that would also be incorrect because contrast is dependent on other “stuff” 

besides transmittance. I suggest using physiochemical characteristics. 

Page 9.5: The statement in the first paragraph is only true if certain scenic characteristics are 

met! “...regardless of background conditions” seems to say that a percent change in extinction 

exudes a similar perceptual response under all atmospheric conditions, which of course is not 

true. 

Page 9.9: How about using “imperceptible” instead of “unperceivable”? “Achromatic” what? 

Should sentence read “...achromatic contrast and discoloration”? 

Page 9.16: Should include some discussion of the level of uncertainty associated with 

nephelometer measurements of coarse particle scattering. 

Page 9.21: “The resulting underestimation of total light extinction is typically much smaller 

since fine particle light extinction generally exceeds that contributed by coarse particles.” Not 

true – coarse particle fraction of total scattering is often comparable to fine particle scattering. 

Page 9.23: “Among the issues raised is that the algorithm tended to underestimate the light 

extinction for the haziest conditions that occur principally during the summer in the southeastern 

U.S. and overestimate for near pristine conditions that tend to occur most often in the arid 

western U.S.” This statement is not generally true. In the sites where the IMPROVE algorithm 

underestimated extinction for the haziest conditions, it also overestimated extinction for the 

lowest extinction days. Generally, in the West the IMPROVE algorithm tended to work better 

than in the hazier eastern United States. 

Page 9.82: It is well established that current regional scale models underestimate the SOA rather 

substantially. Model limitations should be discussed at some level before presenting modeling 

results. Also, it would be helpful to have a paragraph or two highlighting limitations and 

advantages in the various apportionment approaches. Something along the lines of: 

Transport regression receptor models are based on the association of source signatures 

with measured concentrations. Two different methods were employed in the RoMANS 

study. One method, trajectory mass balance (TrMB), used the residence time over 

defined source regions, estimated from RMNP back trajectories, to estimate the source 

signatures, while a hybrid approach developed source signatures from modeled 

concentrations of conservative tracers released from various source regions. 

In TrMB the model establishes a “scaling” factor between the residence time over a 

source region and the measured concentrations at the receptor site. Average emission, 

dispersion, chemical transformation, and deposition processes are incorporated into this 

one scaling factor. However, all of these processes vary with time, and the source 

apportionments derived from this technique are more accurate on the average than on an 

hourly or episodic basis. A statistical apportionment approach will inherently tend to 

overestimate those source regions where endpoints over the region are better correlated 

with measured concentrations, while underestimating those source regions where 

47
endpoints over that source region show weak-to-little correlation with measured 

concentrations. Furthermore, air often arrives from two or more source regions 

simultaneously, causing the source signatures to be correlated, which increases the 

uncertainties in the analysis. 

In the hybrid modeling approach, the apportionment analysis is more robust in that 

emissions and dispersion are explicitly modeled, and only chemistry and deposition are 

incorporated into the “scaling” factor. In both approaches the scaling factors account for 

possible errors in the models used to develop the source signatures, such as any 

systematic biases in the emissions used in the hybrid approach. Like TrMB, the 

apportionment estimates are more accurate on the average than for an incrementally small 

time period. 

In reading the discussion of sources of ammonia and Nox that contribute to particulate nitrate 

formation, it occurred to me that a discussion of the concept of partial scattering efficiency 

would be helpful, as first proposed by White. The concept being that the only meaningful way to 

look at scattering change response is to explicitly model the change in scattering resulting from a 

change in emissions. Of course, this assumes that the model captures all the complexities 

discussed in the pages presenting the nitrate apportionment work. 

Page 9.89: Here, scattering as a function of emission change is presented. It would be helpful to 

have a discussion, as outlined above, of the concept of partial scattering efficiencies, including 

the limitations and advantages of approaching the apportionment problem in this manner. 

Page 9.103: “Both are a product of incomplete combustion of fuels, including those used in 

internal combustion processes (gasoline and diesel emissions) and open biomass burning (smoke 

from wild and prescribed fire).” EC is more likely to be a product of incomplete combustion 

than OC. I don’t think lumping EC and OC together as in the above statement is accurate. Much 

of measured OC is derived or SOA associated with VOC emissions, which can be natural or 

manmade. 

48
Pinkerton Comments (Dr. Kent Pinkerton) 

Response to Charge Question 3: 

Susceptible Populations, chapter 8 in the Second External Review Draft of the Integrated Science 

Assessment for Particulate Matter, provides an excellent overview and summary of the current 

literature on this topic. 

1) The majority of the definitions provided in Table 8-1 for the terms susceptible and 

vulnerable are appropriate, although it would be good for the authors to make some 

conclusion as to the most timely and relevant definitions for the purposes of this chapter. 

2) The chapter discussion on epidemiologic, controlled human exposure, and toxicological 

studies with inclusion or highlighting of only those studies with stratified results to 

demonstrate susceptible populations is highly appropriate to allow for the comparison of 

subpopulations exposed to similar populations and using the same study design. The 

only concern for such comparisons would be the lack of personal monitoring to arrive at 

the appropriate conclusion of similar exposure conditions. Never-the-less, such 

comparisons of susceptibility based on factors of age, gender, race/ethnicity and preexisting health conditions are critical and extremely helpful for presentation in this 

chapter. 

3) Table 8-2 is a nice list of susceptibility factors along with exposure conditions (i.e. shortterm or long-term) and the PM size fraction evaluated, but no explanation is provided as 

to the outcome and/or consequences of each susceptibility factor in terms of health 

endpoints. The authors should consider the addition of a column to briefly summarize 

the impact of each susceptibility factor on health impacts and/or observed health effects. 

4) Inclusion of the hyperlinks to chapter 8 is a novel and extremely useful feature to the 

document to provide convenient and quick access to the database of scientific literature 

used by the USEPA. How often is this database (HERO) updated in view of the rapidly 

changing literature on PM and health effects? This is a wonderful addition to the REA! 

5) The chapter subsections for each susceptibility factor listed in Table 8-2 are well-written 

and appropriate with corresponding hyperlinks to provide direct access to relevant 

documents under each topic. The authors should be commended for making these 

sections a pleasure to read and to comprehend. 

6) Table 8.3 contains fascinating information on the percent of the US population with preexisting cardiovascular disease (actual numbers are 51.6 million with hypertension, 24.1 

million with heart disease, and 14.1 million with coronary heart disease), respiratory 

disease and diabetes. The table as well as the text for each of these conditions along with 

that of obesity emphasize the increased vulnerability of the US population to potential 

health effects of exposure to PM. It would be nice if the authors could provide some 

overarching conclusions for the relevance of these pre-existing diseases based on type 

and age for this section of the chapter. 

7) Excellent summary for chapter 8. 

49
Phalen Comments (Dr. Robert Phalen) 

Chapter 1 

The revision represents a significant improvement. 

pg. 1-2, line 34: The last sentence is incomplete. 

pg. 1-3, lines 5 to 8: Thank you for mentioning the "non-PM-exposure factor that might 

influence the association..." 

pg. 1-12, lines 16-18: This looks like the cutoff date for cited literature. Is 5/09 a firm date for 

citing publications? 

pg. 1-16, lines 13 to 16: It is good to see that "strength" of the evidence is considered, and also in 

Table 1-2 on "Aspects to aid in judging causality." The more I read on causality, the more I 

believe that the strength of an association is a key indicator of a true causal factor, as opposed to 

a surrogate exposure. When regulations are issued it is critical that the regulated pollutant is a 

true culprit. Much of the controversy, and opposition to PM NAAQS, seems to related to 

concern over whether particle mass is an appropriate indicator for health effects. 

pg. 1-32, lines 5 to 11: There are several garbled words (typos) that need correcting. 

pg. 1-33, line 3: The sentence is garbled. 

pg. 1-33, line 9: Its "express", not "xpress." 

pg. 1-34: Journal title missing from first reference: 

Chapter 4 

pg. 4-1, lines 23-26: Thanks for excluding fibers, nano-objects, etc. Inclusion of such unusual 

particles would expand the chapter unnecessarily. 

pg. 4-3, lines 24 to 25: Please insert "small particles and small" before "aggregates", as large 

aggregates are not characterized by a "thermodynamic-equivalent size." Also, I would replace 

"thermodynamic-equivalent size" with "diffusion-equivalent diameter", in order to clarify and 

avoid confusion with the thermodynamic concepts used in describing granular flows. 

pg. 4-11, line 6: Add "in part" before "because" as mechanisms other than mixing prevent 

particle deposition from being zero. 

pg. 4-12, line 12: True, relatively few coarse particles will pass through the nose in an "average" 

person. However, some people have greater penetration, and even a few coarse particles can 

have appreciable masses. 

50
Accordingly, I suggest adding a sentence at the end of this line, such as: "However some 

individuals have less efficient coarse particle deposition in the ET region, and such particles can 

carry significant mass into the tracheobronchial and alveolar airways." 

pg. 4-13, line 1: Change "between" to "among". 

pg. 4-15, lines 8 and 9: I don't know what "the maximum deposited incremental dose" is. 

Explain or delete the sentence. 

pg. 4-18, line 9: Bennett and Zeman's "children" were age 7-14 years, so the result may not apply 

to young children. Insert "age 7-14 years" before "children". Infants and young children, e.g. 

age under 3-4 years, are very different than adults with respect to particle deposition. We 

must not assume that 7-14 year old children are representative of smaller children. 

pg. 4-22, line 20: Change "humans" to "the average human", variability is significant in particle 

deposition. It is important that we recognize individual differences in dosimetry. 

pg. 4-27, line 11: Change "Stat" to "that". 

pg. 4-27, lines 29-31: Omit this sentence. Long-term TB retention of particles was discovered in 

rodents. The sentence may not be true in all cases. 

pg. 4-28, line 6: Add "average" before "path length". 

pg. 4-37, lines 6 to 7: Delete the sentence starting with "In contrast" as it is not always true. 

pg. 4-44 to 51: Many journal titles are missing from the references. 

Chapter 5 

The chapter is thorough, but speculative, which is ok. The chapter does not address the 

importance of dose very well. This could be stated in the beginning of the chapter. 

pg. 5-11, lines 1 and 3: Add "specific" before "larger", and add "the same mass of" before 

"particles of larger size". 

pg. 5-18, line 12: Add "realistic" before "PM exposure". 

pg. 5-32 to 5-39: Many journal titles are missing.

51
Poirot Comments (Mr. Rich Poirot) 

July 2009 PM Integrated Science Assessment, Charge Question 6: 

Several revisions were made to the evaluation of the welfare effects evidence in Chapter 

9, in response to the CASAC PM Panel comment, to focus further on effects on climate 

and ecosystems and include further evaluation of urban visibility evidence, where 

possible. In addition, as recommended by the CASAC PM Panel, key findings and 

conclusions from this chapter were incorporated in Chapter 2. The discussion of PM 

effects on climate was increased with substantially more detail from recent publications, 

including discussion of specific climate forcing effects from individual PM components 

and size fractions. The discussion of ecological effects was also reorganized to focus on 

the types of effects and effects of individual components. For the effects of PM on 

visibility, new material was added including sections on direct optical measurements and 

the value of good visual air quality. Please comment on the effectiveness of the 

reorganization and revisions regarding welfare effects. 

Generally, the revisions made to Chapter 9 strengthen the chapter, improve its clarity and are 

directly responsive to previous CASAC comments on the 1st Draft ISA. A few minor revisions 

may be warranted, but I don’t think any major revisions are required. The added discussion on 

direct optical measurement methods and on visibility valuation is helpful, although there is 

relatively little presentation or analysis of optical measurement data, and in particular, from 

measurements using combined nephelometer and aethalometer – equipped with various PM (1, 

2.5, or 10 micron or “switching”) size fractioning inlets. Presumably such measurements can be 

shown to agree reasonably well with transmissometers, aerosol reconstruction, etc. Better 

demonstration that there are currently viable, field-tested monitoring techniques to implement the 

proposed optical standard would be helpful in the ISA or should at least be added to the REA. 

Substantial detail has been added on aerosol effects on climate, much of it taken directly from 

recent IPCC documents (which is fine – as these are current, relevant and authoritative). 

Unfortunately the quality of reproduced graphic images is extremely poor – although the fault is 

not with EPA, as the poor graphics appear to come directly from the original IPCC reports. 

While the introduction to section 9-3 indicates that the reproduced CCSP SAP2.3 incorporated 

“significant sections from EPA data and reports related particularly to U.S. emissions and 

measurements”, there is very little reported in the chapter directly relating to emissions from or 

measurements within the US. While a number of causal relationships between emissions, 

aerosol concentrations and climate effects can be identified on global scales, there doesn’t seem 

to be a clear, current basis for establishing specific US secondary PM standards for the purpose 

of ameliorating local or global climate effects. Consequently, I don’t think it would be 

productive for staff to spend time adding to the aerosol/climate section in the current ISA. 

In a similar way, the newly added details on ecological effects of various PM chemical 

components provides a much improved and more comprehensive summary of the subject area, 

but does not suggest that there’s currently a strong justification for setting secondary PM 

standards to protect against adverse ecological effects at the present time, or for expending much 

additional effort on this section of the ISA in the current review cycle. 

52
Specific Comments on PM ISA, Chapter 9: 

p. 9-15, 2nd para, last sentence: Why not name the 5 urban areas with transmissometers? Also, 

this reminds me to suggest that if time allows, possibly the Phoenix hourly transmissometer data 

could be compared with the modeled hourly reconstructed aerosol extinction estimates – to help 

evaluate the quality of those estimates, and/or to suggest ways in which they might be improved. 

p. 9-15, 3rd para, last sentence: A higher resolution (than what’s routinely reported) version of 

the ASOS data is available (and more useful). EPA used to fund STI to routinely access and 

report this higher resolution data, but has discontinued support. 

p. 9-49, 5th line from bottom: This very large (Title IV-related) drop in SO2 emissions from 1994 

to 1995 could be mentioned as a possible explanation for the apparent lack of post-1995 

improvement in clean or hazy days at about half the Eastern IMPROVE sites in figs 9-26 & 9-27. 

p. 9-88, Figure 9-50: The figure caption indicates the right figure includes effects from “nitrate” 

& OMC, while the Y-scale label and above the figure both indicate “Sulfate + OMC”. Change 

“nitrate” to “sulfate” in the figure caption. It might also be noted that the RAIN network 

continuous sulfate data (as measured by Teco 5020) has been shown to be highly correlated with, 

but lower (by factor of 1.3) than collocated IMPROVE filter-based sulfate measurements. If the 

sulfate-associated extinction in left & right sides of Figure 9-50 were increased by 1.3 the slopes 

and R2 would increase. This effect is shown in Figure 5.3 of the referenced NESCAUM report in 

which reconstructed Bsp from OMC + adjusted sulfate = 0.91 Measured Bsp + 4, R2 = 0.94. 

p. 9-95, 2nd para, last line: It would be useful here to also report other aspects (besides just the 

Bext level) of the Denver standard – for example the fixed 8-hour 8 am to 4 pm daylight window, 

4-hour averaging time and <70% RH constraints. 

p. 9-96, 3rd para, last line: As for the Denver standard, why not report other aspects (besides just 

the Bext level) of the Phoenix standard – the daylight window, 4-hour averaging time and <90% 

RH constraint. Also, the Phoenix “standard” is not based on an absolute threshold, but on a 

required improvement across the entire visibility distribution – moving bad days to moderate, 

moderate to good, good to excellent, etc. Discussing this might help emphasize that while there 

appear to be fairly convergent public opinions on levels of poor visibility that are considered 

“unacceptable” in the various studies, there are also adverse welfare effects from reductions in 

the frequencies of periods with moderate, good and excellent visibility, and would be benefits 

from improvements across the whole distribution. Conceivably this might lead toward 

considering a secondary “standard” which would be “progress-based” over fixed future time 

intervals, rather than “threshold-based” with an indeterminately-defined time fuse of “as 

expeditiously as practicable”. 

p. 9-98, last 4 lines: This observation that respondents were often “confused about the role of 

weather and humidity in the different visibility conditions presented in the photos” (even when a 

weather and RH-neutral WinHaze approach was employed) might also lead to a position that a 

good secondary NAAQS should be based on metrics that make as strong a distinction as possible 

53
between effects of pollution and effects of humidity and other weather. Examples include: 

applying an RH filter (I think anything between the 70% used in Denver and 90% used in 

Phoenix could be justified); shortening the daylight window (to exclude the few most humid 

hours), increasing the averaging time (from 1 to 2, 3, or 4 daylight hours); and/or altering the 

form from the xth (90th, 95th or whatever) percentile of the worst 1 hr (or 4hr or 8 hr) in a day 

summed for the year to the xth (90th, 95th or whatever) percentile of the hourly (or 4hr or 8 hr) 

levels in a year or season. Any/all of the above will tend to “dry out” the metric, which would 

reduce differences between the West and the East, spatially and temporally focus regulatory 

efforts more on times and places of maximum pollution rather than maximum humidity, and 

provide the public with as clear a distinction as possible between effects of pollution and effects 

of humidity and other weather. 

p. 9-102, lines 3-11: It might be helpful to include a complementary paragraph describing some 

of the disadvantages an optical measurement-only approach – especially as a basis for a standard. 

For example: cost and difficult siting criteria for transmissometers, similar cost and complex 

operational and data processing issues with nephelometers and aethalometers, absence of 

information on mass, size distribution or composition of pollutants causing the extinction. I 

think these measurement issues can be resolved, but it will require some effort from EPA and the 

states. It might be prudent to start with a small pilot network to find and work out some of the 

bugs. 

p. 9-901, Figure 9-53, and elsewhere in this section: The quality of most of the graphic figures 

copied from the CCSP SAP2.3 is regrettably poor, although I note in checking the original 

reference its not your fault – the original is barely legible. 

p. 9-131: You could add an example here on MODIS AOD vs. AIRNOW PM2.5 from the 

EPA/NASA IDEA site that might be a clearer and more relevant illustration. 

http://www.star.nesdis.noaa.gov/smcd/spb/aq/index.php 

p. 9-194, line 6: Its not clear what “to have a factor of 2” refers to. 

p. 9-208-210: This section (9.3.9.3) is about the only place in section 9.3 that refers to any 

specific effects within the US or resulting directly from emissions from US sources (and which 

therefore might be relevant to consideration of secondary PM standards). Given this, it would 

seem important to be more clear about exactly what the PM causal mechanism(s) is (are). There 

are also indications that urban “heat islands” tend to increase convective precipitation in 

downwind areas (http://www.gsfc.nasa.gov/topstory/20020613urbanrain.html). See also the 

counter arguments presented by Alpert et al. (2008) 

http://www.tau.ac.il/~pinhas/papers/2008/Alpert_et_al_JAMC_2008.pdf Possibly there are 

also other non-aerosol effects of urbanization, such as more rapid runoff and deforestation, that 

would tend to alter downwind precipitation patterns. 

p. 9-210, lines 17-18: This description of “planet brightening when seen from space because 

aerosols scatter most of the visible spectrum light” isn’t quite right. Most aerosol-scattered light 

is ultimately scattered in a forward direction. The “brightening” results only from that (relatively 

54
small, 10-15%) fraction of visible light that is back-scattered in the direction of the hypothetical 

observer in space. 

p. 9-211, 2nd para, line 1: Not clear what you mean by “progress has been made with in-situ and 

remotely sensed aerosols.” 

55
Russell Comments (Dr. Armistead (Ted) Russell) 

First, I note that the word concise was removed from the first sentence, as is appropriate. 

When I showed my air pollution physics and chemistry students the PM ISA, they said “Can’t 

they shorten it?”, to which I replied this is shortened from the old Criteria Document approach, 

and it should demonstrate how active is the field. (I also noted to them how much more is 

known now then when I took the course about 29 years ago when taking a one semester course 

pretty much put you near the front of the field.) On that note, however, I do think that future 

versions (in coming years, not in the revision to this one) should be shortened. I found each 

section to be extremely thorough and providing more information than needed to adequately 

inform the process. This was particularly true for Chapter 3 (and this view may be due, in part, 

to being most familiar with that area), where a part of the material will likely not have much role 

in further review of the NAAQS. It almost appeared as though it was reverting back to the old 

AQCD approach. 

In spite of the call to shorten future versions, overall, I think the ISA has been improved 

significantly. I still view that it does not bring enough attention to compositional differences in 

PM effects (both health and welfare). There is significant information that carbonaceous 

aerosols (typically referred to elemental and organic carbon) are of greater concern for many 

endpoints. The ISA should lay out this information more completely. 

I continue to worry about the treatment of climate. While the inclusion of parts of the 

CCSP provides the foundation for discussing PM impacts on climate, given the importance of 

this issue, and how it could impact how a secondary NAAQS might be formulated, a bit more 

analysis would have been beneficial. Composition and size is very critical here, but is not fully 

transmitted in the synthesis chapter. 

Chapter 2 does a reasonably good job of integrating the findings of the rest of the ISA, 

though a few improvements can be made. The major concern I have, at present, echoes the 

comment above that there is not enough emphasis on compositional differences and their 

implications. I would add to the Section 2.4,” Policy Relevant Considerations” (or possibly a 

new section “2.6. Composition Considerations” since it synthesizes beyond just health effects),a 

subsection on composition that integrates what we understand and suspect about compositional 

differences on health and welfare effects. A particular finding in such a synthesis could be that 

control of organic and elemental carbon (EC/OC) PM from sources such as automobiles and 

biomass burning appears to be more beneficial than controlling other components of PM (or it 

could be couched that a EC/OC has greater deleterious impacts than the same amount of other 

components). 

 I think in prior ISA’s, there was a summary table of those impacts that were causal, likely to be 

causal and suggestive right at the start of the section on effects. This should be followed here. It 

is a bit odd that you find out the “inadequate” relationships first. Thus, add a summary table at 

the beginning of 2.3 of the health effects examined. I find it a bit unnatural to suggest that the 

evidence for the relationship between PM and visibility to be “strong and consistent” in that it is 

well beyond strong and consistent, and if this were not the case it would be in direct 

contradiction to our basic understanding of physics. While such terminology is appropriate for 

the health effects where such a direct linkage is not so established, here it just seems odd. 

56
A final synthesis section might be useful that puts it all together, saying that PM with certain 

characteristics/sources has the following impacts on what aspects of BOTH health and welfare 

(and strength of association). This section would also synthesize uncertainties as to how they 

impact our overall understanding and how to interpret results.. At present the chapter does not 

really synthesize health and welfare and how the various uncertainties impact our overall 

understanding, and ends rather weakly. Might there be a section synthesizing uncertainties 

(possibly in the section discussed above or separately? 

Minor: 

2-7-28: should be .”...oxidation of isoprene, terpenes and...” 

2-8-1 This is still in the research phase and its importance is still being explored. 

2-9-28: Explain the variation in PRB levels. 

2-9-33: Weak beginning of a section.2-11-28/30: I would hesitate to state this as such as it may 

impact the use of such information in other assessments and it is not apparent you are using this 

information in this assessment. 

2-14-10: Font on PM2.5

2-14-14: You might provide a bit of explanation as to why this is consistent with other null 

findings in the West. 

2-19-12 (and related section in the report). In the section above, it appears as though the 

information for this endpoint is very similar to that for acute CVD where the relationship was 

found to be causal. Why the difference? 

2-25-14/29 Much of what this section appears to be trying to explain can be explained by 

compositional/source differences as opposed to the items discussed here, and I think 

compositional differences provide a better explanation. 

Section 2.3.5: It should be noted that UFP effects can not be separated from compositional 

effects. Indeed, there are results that might suggest that sulfate-dominated UFP do not have the 

same effects seen for CAPS and DE. 

2-34-29: Status is not protective... I would say nutritional status can affect response. 

Section 2.4.2: Lag structure is not so important here as the other two, and these parts could be 

integrated in to the appropriate sections discussing the specific health endpoints.. It may be 

important to interpreting the epi studies, and how they were conducted, but as presented this 

section does not have that much to say as to whether the causal/likely causal... decisions were 

appropriate, nor guide what the level of the standard might be chosen to be. For this section to 

stand alone, here, the discussion of lag structure between the endpoints needs to be synthesized. 

Chapter 3 

As noted above, this chapter is very thorough, and is likely more exhaustive than necessary. I 

still might have provided a bit more on the evaluation of exposure models, but if that is done as 

part of the Risk Assessment, that is fine. In general, I found it to be balanced and correct, with a 

few exceptions. 

As an example of where the chapter really goes in to unnecessary detail, and where this leads to 

an error, on page 150, they note that three dimensional CTMs typically use finite difference or 

finite element approaches. This level of detail is not overly informative to reviewing the 

NAAQS. Further, many models use finite volume approaches. Further, the approach used for 

57
deposition is incorrect for particulate deposition (there is no sedimentation velocity in the 

formulation given), and the whole discussion of deposition could be shortened. 

I was a bit taken aback by the paragraph on page 3-225 saying “Clearly there are variations...”, 

concluding that “”too poorly characterized on a broad scale to allow conclusions to be drawn...” 

I thought NARSTO did just that. While there are variations, there are typically consistent 

features as well. This paragraph strikes me as a bit negative. 

The last paragraph on page 3-226 seems out of place, since it is talking about impacts on the 

health effects studies discussed later, and I did not pick this up from the chapter (I may have 

missed it). 

Minor: 

Figure Numbering: It appears as though figures were removed, leading to figure numbers later 

in the document being off. 

3-13-22: You need to be very careful in how you interpret AMS measurements in terms of what 

is secondary or not. They measure spectra and hypothesize what fraction is secondary. 

3-15-8: The 2.8% contribution to OC is a bit misleading in that it represents only the two 

diastereomisomers, and more SOA from isoprene can be present. 

3-18-15: Should just be Maricq. (also line 20) 

3-21-6: (eqn 3-1) This is not truly correct, particularly for particles, and wet deposition is 

usually parameterized differently as well. This section is probably longer than needed here in 

that what is of importance is to note the typical lifetimes and loss processes. 

3-33-21: What is meant by reliable, noting that the prior discussion also suggests it is 

consistently impacted by artifacts? 

3-34-5: nonvolatile. 

3-37-25: “AMS RESULTS did not...” 

3-82-4: Move “only” about 5 words down. 

3-82-21: I would remove “slightly”. 

3-83-5 “...where atmospheric nucleation” 

Figs. 3-42/43: Usually the sizes are given small-big. 

3-186: I would be a bit more tentative about deriving PM10-2.5 from the PM2.5 and PM10 values. 

It is almost assuredly true that there is some correlation in the PRB PM10 and PM2.5 values 

calculated by Trijonis, and the current approach would actually indicate that in some 

circumstances, PM10-2.5 is ~90% of the PM10, which is almost assuredly not true. Use typical 

PM2.5/PM10 ratios for the two regions to get a better estimate of the range in the values. 

Tables 3-19-23...: In many cases, the micro sign is given as a box. 

It is sometimes the case that the rest of the sentence after an equation is given is indented (e.g., 3-

205-14). 

3-223-18: “higher in clear” 

3-223-19: remove the “;” 

3-224-3: Use ~34 times more 

3-225-25: “... 1-h commute...’ 

58
Speizer Comments (Dr. Frank Speizer) 

Chapter 2 

General Comments: 

 EPA Staff are to be commended for doing an excellent job in pulling together and 

presenting in a very readable format the summary of the data contained in the ISA. By placing 

the conclusions here with appropriate documentation of where to find the primary discussed data, 

the whole document becomes more useful. 

Specific Comments: 

Page 2.5, lines 14-19. Although accurate as stated, what seems to be left out in the comparison 

of PM 2.5 to PM10 is that the PM10 correlations in themselves (.70) are really remarkably high and 

suggest, although not quite as consistent as PM2.5 that they can be usefully used to model 

exposure. It might be worth mentioning this. 

Pge 2.6, line 30. Isn’t there also the potential for greater production in the winter of NO2 

(though less efficient winter burning or greater production) to lead to increased quenching of 

O3? 

Page 2.13, lines 21-25 bullets. It might be useful to add to the end of each of these lines the 

specific sections in Chapter 6 or 7 where each topic is discussed. Although I can agree with each 

of the conclusions, I can imagine some “stakeholders” wanting to raise questions and getting 

hung up on not having the specific background data to support the statement. By providing the 

specific paragraph reference it would make documentation easier. 

Page 2.14, Table 2.1. This may be quibbling over semantics. I like putting the summary table 

up front. However, by describing the effects as indicated, the suggestion is that short term 

exposure is causing a chronic condition. These effects are for the most part acute events 

occurring among persons with chronic conditions. (If the table occurred after the descriptions 

that follow there would be no problem). Perhaps a modest change in the Table title or a footnote 

would help. 

Page 2.15, first two paragraphs. I would suggest reversing the order of these paragraph (with 

minor editorial changes). Offering the fresh diesel exhaust data before the PM2.5 data seems to 

be mixing the consistency argument by suggesting that UFP are explaining PM2.5 effect when 

they are really supplementing the findings of the PM2.5 effects reported in the second paragraph. 

Page 2.21 and 2.22, Figures 2.1 and 2.2. Ordering the points in these figures by level of 

exposure estimate has made them less useful. They mix up outcomes that really cannot be 

looked at as a result of gradient of exposure. It would be better if they were divided into small 

figures by specific outcomes, and then look at gradients of exposure. 

Pages 2.26l-2.30, whole section. Not enough emphasis is made of the fact that for each of the 

outcomes discussed there are only a limited number of studies, thus the designation of 

59
suggestive. Again breaking out the kinds of outcomes in Figure 2.3 would be better than 

lumping them all together. 

Page 2.29, Figure 2.3: There is clearly something wrong here. The units in this Figure are 

wildly different from Figure 2.1 and 2.2, and are simply not believeable. I just may be a labeling 

problem, but it needs to be fixed. 

Page 2.33, paragraph beginning on line 14. Some editing needed. The first sentence says 

controlled study effects seen in susceptible subjects with CVD and/or respiratory diseases the 

last sentence says respiratory diseases. Suggest change the last to cardiorespiratory diseases. 

Responses to Charge Questions ( paraphrased and shown in italics) on ISA Draft 2 

1. Evaluation of health evidence in Chapters 6 and 7 

a. The role of the studies of PM10 in consideration in causality determinations for 

PM2.5 and PM10-2.5.

 Although this seems perfectly appropriate, it would seem that leading into this 

argument there should be some material (which I looked for in Chapter 3, but could 

not find, maybe just my inability to find) that could be referenced here or perhaps 

even summarized to justify the correlative nature of the relationships. This would 

help justify using the PM10 studies when neither PM2.5 or PM 10-2.5 were available to 

further assure the consistency of the data. 

b. The inclusion of cause-specific mortality as part of suite of CVD and 

respiratory effects, in the development of causality judgments.

 The use of cause-specific mortality provides a refinement of the data that is 

logical and appropriate. Since the bulk of the mortality is dominated by 

cardiovascular deaths it is appropriate to show these separately, and similarly since 

respiratory deaths are the fourth leading cause of deaths these also provide important 

information. By showing these two classes of death separately and then showing the 

total (which is clearly dominated by these two, but less subject to reporting or disease 

classification error) the reader gets a better understanding of both the magnitude and 

nature of the deaths that are occurring. 

c. Scope of evidence considered in the causality determination for ultrafine PM. 

 The change of the designation from inadequate to suggestive appears to be 

dominated by the interpretation of the relatively greater number of clinical and 

toxicological studies of diesel and gasoline exhaust studies, that are clearly dominated 

by UFP. This is in contrast to the few epidemiological studies, that are for the most 

part null or poorly defined as UFP exposure studies. Thus, the designation of 

suggestive is rational and probably right, but clearly the designation itself will need 

additional work in the future to either sustain or refute the designation. This probably 

should be indicated. 

Charge Question 1d: 

d. With regard to the role of PM in mutagenicity, genotoxicity and carcinogenicity 

comment upon the expansion of this evaluation to include a summary of 

toxicological studies using routes of exposure other than inhalation, as well as 

consideration of both mortality and incidence studies. 

60
Staff has done an excellent job in summarizing a complex literature related to 

both the general and specific associations of using mutagenicity, genotoxicity and 

carcinogenicity studies in assessing the PM effects on cancer. The charge question is 

really in two parts. With regard to using routes of exposure other than inhalation, to 

assess mutagenicity and genotoxicity, these are standard procedures used in the field 

and have formed the basis of much of the general literature basis of mechanistic 

understanding in mammalian cancer research. There are examples where such studies 

have resulted in leads to where to look for cancer risks in humans. Thus it is 

appropriate to use such data in determining where along the spectrum of certainty 

with regard to causality these studies should be considered. Secondly, with regard to 

the population studies that are reported in the last few years, these have been large, 

well assessed groups, in which the same exposure parameters have been used for 

cardiovascular and respiratory findings (that appear to be defined as causal 

associations) with an outcome that is well defined, albeit it dominated by the potential 

confounder of smoking. The relatively consistent finding of lung cancer excesses as 

an exclusively associated cancer, along with the attempts to control for smoking are 

suggestive, and thus the appropriate interpretation and designation appears to have 

been made. 

2. Revisions to Chapters 1, 4, 5. 

Chapter 1, expansion or additions to sections on history of previous PM NAAQS 

reviews. 

 It seems to me this is just about right. There is a slight shift of tone from the early 

historical discussion of setting the NAAQS to a more “legalistic” description of what has 

gone on in the last 10 years or so. I found one issue (described in a separate memo) with 

regard to table 1.2 on page 1.26. The category of Experimental Evidence seems 

inappropriately defined. 

Chapter 4, and 5 I leave to others to comment upon. 

3. Chapter 8 Susceptible populations 

Please comment on the organization and presentation in Chapter 8 of evidence 

regarding susceptible subpopulations

 Although the Chapter summarizes definitions used by others (and EPA) for susceptibility, 

the definitions provided are not very useful. It might have been better to talk about host vs 

environment more formally. In addition, in discussing each of the “susceptibility factors” 

much of what is reported is really not much different that what is contained in Chapters 6 & 

7. However, the discussion is better organized in defining and using susceptibility factors as 

related to PM exposure. What is clearly left out, and perhaps should have a brief discussion 

is a contrast between susceptibility and vulnerability and how these factors play into a 

discussion of risk and margin of safety. 

4. Chapter 3. 

 Comments on revisions 

61
 This chapter read rather well. I leave to others specific comments on Sections 3.4 and 

3.5. In section 3.8 the Staff has reviewed the factors potentially influencing exposure levels 

for health studies. I would suggest a summary table at the end of this chapter that takes all 

the factors and provides qualitative directionality for the potential factor in biasing away or 

toward the null (or not at all). This I think would identify more readily for the reader what 

to worry about and what not to be concerned about. 

5. Chapter 2. 

Please comment on the integration. 

I believe this is an important chapter and I have already submitted comments on this 

chapter separately. I repeat them here simply to put all my comments together. Clearly I 

have done this in greater detail than what I have done to answer other questions. 

62
Suh Comments (Dr. Helen Suh) 

Charge Question 3: 

Revisions to Chapter 3 on Source to Exposure: Consistent with revisions made to the health 

effects chapters, Chapter 3 was revised to clarify that PM10 incorporates both PM2.5 and 

PM10-2.5 and reorganized to begin with PM2.5 and PM10-2.5, followed by PM10, where 

applicable. The discussion of measurement techniques and chemistry of PM10-2.5 has been 

expanded in Sections 3.4 and 3.5, in response to CASAC comments. In addition, Section 3.8 on 

human exposure to PM has been reorganized and expanded to better characterize the evidence 

and provide useful information for interpretation of epidemiologic studies. We would appreciate 

comments from the CASAC PM Panel on these revisions. 

The Chapter is a massive and comprehensive summary of the current state of the PM sources, 

monitoring and modeling methods, concentrations and exposures. The Chapter was generally 

clear, comprehensive, and well organized, which is notable given the amount of information it 

contains. It clearly and appropriately incorporates comments from the April review. Of note, the 

relation among PM2.5, PM10-2.5, and PM10 was greatly clarified and the inclusion of additional 

information on UFP, PM components, and PM10-2.5 monitoring methods was welcomed. 

Similarly, the organization and content of the exposure section was greatly improved, especially 

with regards to the relevance of exposure findings to epidemiologic studies. While significantly 

improved, further improvements could be made to the exposure section to help with the 

organization, seeming overlap with earlier sections, and clarity, as discussed briefly below. 

- Given the importance of measured PM in the earlier sections of the Chapter, in the 

epidemiological studies, and also in the Health REA, it makes sense to place the discussion 

of exposure measurements before that for exposure modeling. Further, the exposure 

measurements section should include discussion of new methods that have been made to 

measure (1) personal exposures to total PM, (2) PM of outdoor origin, (2) outdoor 

concentrations outside individuals’ homes, and (3) indoor PM exposures to total PM and to 

PM of outdoor origin). In this context, studies using tracers of outdoor or regional pollution 

can be introduced. 

- The discussion of each topic should be consolidated into single sections, with references to 

this section made as necessary in later sections. As is currently written, certain topics, such 

as spatial variability and particle infiltration, appear repeatedly in several subsections. The 

discussion on these topics would be more focused and less confusing if their discussions 

were consolidated. 

- In Section 3.8.4.3, it would be helpful to clarify which component of PM is being discussed. 

Further, within each subtopic or heading, separate or otherwise distinct discussions for PM2.5, 

PM10-2.5 and the PM components would help with clarity. 

- Section 3.8.4 (Exposure Assessment Studies at Different Spatial Scales) and its subheadings 

are misnamed. While the heading titles do provide parallels with earlier sections of Chapter 

3, they do not accurately describe their contents. For example, the section 3.8.4.1 does not 

actually discuss urban scale ambient PM exposure, rather issues related to exposure error, 

exposure modeling, and tracers of ambient particles. 

- It would be helpful to include a subsection in the beginning of the section, perhaps in Section 

3.8.1 (General Exposure Concepts) that summarize the range of measured exposures to 

63
PM2.5, PM10-2.5, and PM10, their composition, and differences by city, susceptible group, and 

season. 

- Section 3.8.6: Other factors that could affect exposures are worth noting, such as home 

ventilation patterns and activity patterns. 

-

Response to Charge Question 4 

Charge Question 4: 

Revisions to Chapter 3 on Source to Exposure: Consistent with revisions made to the health 

effects chapters, Chapter 3 was revised to clarify that PM10 incorporates both PM2.5 and 

PM10-2.5 and reorganized to begin with PM2.5 and PM10-2.5, followed by PM10, where 

applicable. The discussion of measurement techniques and chemistry of PM10-2.5 has been 

expanded in Sections 3.4 and 3.5, in response to CASAC comments. In addition, Section 3.8 on 

human exposure to PM has been reorganized and expanded to better characterize the evidence 

and provide useful information for interpretation of epidemiologic studies. We would appreciate 

comments from the CASAC PM Panel on these revisions. 

The Chapter is a comprehensive summary of the current state of the PM sources, ambient 

aerosols, monitoring and modeling methods, concentrations and exposures. The Chapter 

generally reflects the state of science in a clear, comprehensive, and well organized fashion, 

which is notable given the amount of information the Chapter contains. Further, the Chapter 

revision appropriately incorporates comments from the April review. Of note, the relation 

among PM2.5, PM10-2.5, and PM10 was greatly clarified and the inclusion of additional 

information on UFP PM components, and PM10-2.5 monitoring methods was welcomed. 

Similarly, the organization and content of the exposure section was greatly improved, especially 

with regards to the relevance of exposure findings to epidemiologic studies. While significantly 

improved, further improvements could be made to the exposure section to help with the 

organization, seeming overlap with earlier sections, and clarity, as discussed briefly below. 

Specific comments: 

• Standard Reference Materials (page 2-20, line 20): It says “To date, there are few standard 

reference materials ...” 

This sentence should be reworded to make it clear that we currently do not have a way to 

assess mass concentration measurement accuracy, as there are no materials (to our 

knowledge) that provide a test of accuracy or airborne PM mass. There are, however, SRMs 

that are useful for testing the accuracy of the analytical methods for PM composition. 

 

• Policy Relevant Background (PRB) 

There are the usual concerns regarding the policy relevant background (PRB). The EPA has 

to set a health-based standard irrespective of the background concentration of particles and 

thus, the PRB is really an implementation issue and not a regulation setting issue. As the 

PRB increases because of activity outside of the United States, there is decreasing flexibility 

in attaining concentrations that are fully protective of public health. The modeling approach 

has some appeal, but given the problems with the accuracy of the emissions inventories in the 

US where substantial effort and resources are expended to develop them and there are still 

problems, the likelihood that we can adequate model emissions in the rest of the world seems 

very low. It would seem that there could be some comparisons between the model-based 

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approach and the remote site approach to provide some basis for confidence in the model 

estimation of the PRB. 

• Exposure Section 

o Given the importance of measured PM in the earlier sections of the Chapter, in the 

epidemiological studies, and also in the Health REA, it makes sense to place the 

discussion of exposure measurements before that for exposure modeling. Further, the 

exposure measurements section should include discussion of new methods that have been 

made to measure (1) personal exposures to total PM, (2) PM of outdoor origin, (2) 

outdoor concentrations outside individuals’ homes, and (3) indoor PM exposures to total 

PM and to PM of outdoor origin). In this context, studies using tracers of outdoor or 

regional pollution can be introduced. 

o The discussion of each topic should be consolidated into single sections, with references 

to this section made as necessary in later sections. As is currently written, certain topics, 

such as spatial variability and particle infiltration, appear repeatedly in several 

subsections. The discussion on these topics would be more focused and less confusing if 

their discussions were consolidated. 

o In Section 3.8.4.3, it would be helpful to clarify which component of PM is being 

discussed. Further, within each subtopic or heading, separate or otherwise distinct 

discussions for PM2.5, PM10-2.5 and the PM components would help with clarity. 

o Section 3.8.4 (Exposure Assessment Studies at Different Spatial Scales) and its 

subheadings are misnamed. While the heading titles do provide parallels with earlier 

sections of Chapter 3, they do not accurately describe their contents. For example, the 

section 3.8.4.1 does not actually discuss urban scale ambient PM exposure, rather issues 

related to exposure error, exposure modeling, and tracers of ambient particles. 

o It would be helpful to include a subsection in the beginning of the section, perhaps in 

Section 3.8.1 (General Exposure Concepts) that summarize the range of measured 

exposures to PM2.5, PM10-2.5, and PM10, their composition, and differences by city, 

susceptible group, and season. 

o Section 3.8.6: Other factors that could affect exposures are worth noting, such as home 

ventilation patterns and activity patterns. 

65
66

Vedal Comments (Dr. Sverre Vedal) 

1a. Use of PM10. 

Findings pertaining to PM10 in this 2nd draft are discussed in conjunction with two component 

fractions (PM10-2.5 and PM2.5); causal determinations are no longer provided for PM10 itself. 

There is value in this approach, since both fractions comprise PM10. It does not, however, seem 

logical that evidence on PM10 would be equally relevant to both PM2.5 and PM10-2.5. In some 

regions of the country PM10 is more reflective of PM2.5 whereas elsewhere PM10 is more 

reflective of PM10-2.5. 

In the respective PM fraction Summary and Causal Determinations sections, there is little 

mention of PM10. Where PM10 is mentioned in this context, it only comes up in support of PM2.5

(e.g., PM10 evidence is cited as strengthening the evidence for PM2.5-related respiratory effects 

[p. 6-244] and for mortality effects [p. 6-317]). PM10 evidence is not used in specific support of 

PM10-2.5 effects. Yet in the discussion of short-term PM exposure mortality effects (section 

6.5.2), PM10 studies are cited as providing “an underlying basis for the overall pattern of 

associations observed when examining the relationship between PM10-2.5 and PM2.5 and 

mortality.” There is inconsistency then in the way PM10 findings are used. 

PM10 findings are also used in evaluation of long-term PM fraction exposure effects (e.g., p. 7-

24). For respiratory morbidity effects of long-term PM exposure, a more precise argument is 

made that “studies showing associations only with PM10 were conducted in locations where PM 

was predominantly fine particles, providing support for associations with long-term exposure to 

fine particles” (p. 7-28, line 32; p. 7-60, line 16). However, in some studies effects are only seen 

for PM10 and not for PM2.5 (p. 7-43, line 6), which is not consistent with that statement. 

In order to better interpret PM10 findings relative to those of PM2.5 and PM10-2.5, it would have 

been helpful, perhaps in Chapter 3, to include and/or highlight data on the relationship between 

PM10 and both PM2.5 and PM10-2.5, stratified by region of the country. Also, in light of the role of 

the current 24-hour PM10 standard with respect to PM10-2.5, it would be important to bring 

together the evidence relating to PM10 that allows it to be used for this purpose. 

In short, the way in which PM10 is used is vague and inconsistent. PM10 evidence is used 

generally to support overall effects of PM, but specifically only in support of PM2.5 effects. The 

role of the current PM10 standard, however, is in controlling PM10-2.5. Better justification for the 

utility of PM10 findings is needed from a scientific and policy perspective. Nevertheless, 

providing causality judgments for PM10-2.5 and PM2.5, but not for PM10, as is done in the current 

draft, is more in line with the current science.