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 Comm ittee (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 Particul ate Matter (ISA), (S econd External Review Draft, July 2009) . The Panel also held a public tel econference on November 12, 2009 to discuss and finalize its draft report. In this letter, CA SAC offers general comments on the ISA, followed by CASAC’s consensus responses to the Agency’s charge questi ons. Comments from individual panelists are also attached.

CASAC commends EPA’s Nationa l 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 documen t 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 con tinued evolution of the process for evidence
evaluation. The five-level classi fication of strength of evidence for causal inference has been systematically applied; this appr oach has provided transparency a nd 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 ho tlinks to citations and study data. We support its further evoluti on to include abstracted, key findings.

1With regard to the approach taken in th e ISA, we find EPA’s decision to focus the discussion of causality on PM 2.5 and PM 10-2.5 independently to be appr opriate and supported by
the scientific evidence. As stat ed in our earlier review of the 1 st draft ISA, the handling of PM 10 as a separate pollutant was problematic be cause it is comprised of the fine (PM 2.5 ) and the coarse (PM 10-2.5 ) fractions. CASAC also supports EPA’s changes to the causal determinations for longterm exposure to PM 2.5 and cardiovascular effects (from “lik ely causal” to “causal”), for cancer
and PM 2.5 (from “inadequate” to “sugges tive”) and for cardiovascular and respiratory effects of short-term exposure to ultrafine particulate ma tter (UFP) (from “inadequa te” to “suggestive”).
CASAC concurs with EPA’s definition of “sus ceptible 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 characterizati on of the factors that may contribu te to increased susceptibility
to PM-induced health effects.

In terms of welfare effects, the visibility valuation and prefer ence 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 highlig hted. CASAC concurs that Chapter 9 has been improved by the additional discussion of opti cal 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 pe rception of visibility effects caused by PM pollutants. CASAC also concurs that the added discussions on climate forcing effects and on ecological effects of PM strength en 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 PM 10 with those of PM 2.5 and PM 10-2.5 , preferably stratified by region of the country, in order to better understand PM 10 as an indicator of the two subfractions,

PM 2.5 and PM 10-2.5 . As currently written, the ISA uses PM 10 findings to support PM 2.5 effects whereas the relevance of PM 10 findings for PM 10-2.5 effects is left ambiguous. Because of the role played by the current PM 10 standard, PM 10 findings that are particularly relevant to PM 10-2.5 should also be highlighted.

• CASAC recommends “upgrading” the causal classification for PM 2.5 and total mortality to “causal” for both the short-term and long- term time frames. There are epidemiological studies showing a positive associati on of all-cause mortality with PM 2.5 . We acknowledge that the as sociation is weaker for all-cause mortality (in comparison with cardiovascular mortality), but cardiovascular deaths are the largest component of total

2deaths attributable to PM. If PM 2.5 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 relatio n to both health and welfare, especially given the emerging view that metals and carbonaceous aeros ols, typically referred to as elemental and organic carbon, are of greater concern for many endpoints.

CASAC agrees that the PM ISA will be ade quate for rulemaking after EPA incorporates our major comments and recommendations as st ated 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 Partic ulate Matter Review Panel Roster B. CASAC Responses to Charge Questions C. Individual Responses to Charge Questions

3Enclosure A Clean Air Scientific Advisory Committee Particulate Matter Review Panel

CHAIR

Dr. Jonathan M. Samet, Professor and Chair, Depa rtment of Preventive Me dicine, 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, Ha rvard University, Boston, MA

Dr. Ellis B. Cowling, University Distinguished Pr ofessor At-Large Emeritus, Colleges of Natural Resources and Agriculture and Life Sciences, North Carolina State University, Raleigh, NC

Dr. James Crapo, Professor of Medicine, Departme nt of Medicine, National Jewish Medical and Research Center, Denver, CO

Dr. H. Christopher Frey, Profe ssor, Department of Civil, Construction and Environmental Engineering, College of Engineering, No rth Carolina State University, Raleigh, NC

Dr. Donna Kenski, ∗ Data Analysis Director, Lake Mi chigan Air Directors Consortium, Rosemont, IL

Dr. Armistead (Ted) Russell, Professor, Depart ment of Civil and Envi ronmental Engineering, Georgia Institute of Technology, Atlanta, GA

CONSULTANTS

Dr. Lowell Ashbaugh, Associate Research Ecologi st, Crocker Nuclear Lab, University of California, Davis, Davis, CA

Prof. Ed Avol, Professor, Prev entive Medicine, Keck School of Medicine, University of Southern California, Los Angeles, CA

Dr. Wayne Cascio, Professor, Medicine, Cardio logy, Brody School of Medicine at East Carolina University, Greenville, NC

∗ / Unable to participate in this review.

4Dr. David Grantz, Director, Botany and Plant Sciences and Air Pollution Research Center, Riverside Campus and Kearney Ag ricultural Center, University of California, Parlier, CA

Dr. Joseph Helble, Dean and Professor, Thay er School of Engineer ing, Dartmouth College, Hanover, NH

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

Dr. Philip Hopke, Bayard D. Clarkson Distingu ished Professor, Department of Chemical Engineering, Clarkson University, Potsdam, NY

Dr. Morton Lippmann, Professor, Nelson Instit ute of Environmental Medicine, New York University School of Medicine, Tuxedo, NY

Dr. Helen Suh MacIntosh, Associat e Professor, Environmental Hea lth, School of Public Health, Harvard University, Boston, MA

Dr. William Malm, Research Physicist, Natio nal Park Service Ai r Resources Division, Cooperative Institute for Research in the Atmosp here, Colorado State University, Fort Collins, CO

Mr. Charles Thomas (Tom) Moore, Jr., Air Qu ality 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 Di vision, 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, Universi ty of Washington, Seattle, WA

SCIENCE ADVISORY BOARD STAFF

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

5NOTICE

This report has been written as part of the activ ities of the EPA's Clean Air Scientific Advisory Committee (CASAC), a federal advisory committee independently chartered to provide extramural scientific information and advice to th e 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 b een reviewed for approval by the Agency and, hence, the contents of this report do not necessa rily represent the views and policies of the EPA, nor of other agencies within the Executive Br anch 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 We b site at: http://www.epa.gov/casac.

6Enclosure B

Integrated Science Assessm ent 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 PM 10 , we have refocused the evaluation of health effects resulting from exposure to PM 10 . PM 10 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 PM 10 ; however, PM 10 study results are considered in causality determinations for PM 2.5 and PM 10-2.5 where appropriate. Please comment on this approach to evaluation of evidence from studies of PM 10 .

At the April 2009 review of the first PM ISA draft, CASAC noted that findings on PM 10 , PM 2.5 and PM 10-2.5 were often discussed as if these were separate pollutants, even though the PM 2.5 and
PM 10-2.5 fractions comprise PM 10 . This led to inconsistencies in causal determinations, since these were provided for each of the three PM indi cators independently. In this draft, causal determinations are no longer provided for PM 10 as they were in the initial draft of the ISA.

Motivation for dealing with PM 10 as a separate entity, at least in the setting of short-term exposure, came from the continuation of the 24-hour PM 10 standard. Given the different sources and the differing chemical compositions of the PM 2.5 and PM 10-2.5 fractions of PM 10 , and to some extent the evidence for differing toxicity, th ere is little scientific justification for dealing with PM 10 as a single entity. The appro ach taken in the current draft is therefore more in keeping with the state of the science.

Findings pertaining to PM 10 in this 2nd draft are discussed alongside those of the two component fractions. There was obviously (and understandab ly) a need to consider the extensive findings pertaining to PM 10 when evaluating the evidence on PM 2.5 and PM 10-2.5 since both fractions comprise PM 10 . Findings on PM 10 should have some relevance to evaluating evidence on PM 2.5 and PM 10-2.5 . However, the relevance of evidence on PM 10 to PM 2.5 or to PM 10-2.5 likely varies across the country. For example, in some regions of the country PM 10 is more reflective of PM 2.5 whereas elsewhere PM 10 is more reflective of PM 10-2.5 . The charge questio n states that “PM 10 studies are now included where they provide insi ghts into general relationships between PM and its effects, such as concentration-response relationships. PM 10 study results are considered in causality determinations for PM 2.5 and PM 10-2.5 where appropriate.” For example, Figure 6-6 (p.6-120) shows a typical concentration -response relationship for short-term PM 10 exposures and is offered as providing insight into the “PM” concentration response re lationship. “PM” is a general designation and used without suffici ent specificity in this context.

7PM 10 findings are also used in evaluation of the long-term effects of e xposure to specific PM fractions (e.g., p. 7-24). For e ffects of long-term PM exposure on respiratory morbidity, the specific finding is made that “studies showing associations only with PM 10 were conducted in locations where PM was predominantly fine par ticles, providing support for associations with long-term exposure to fine particles” (p. 7-28, line 32; p. 7-60, line 16). PM 10 findings are used in support of findings on PM 2.5 . However, in some of the referenced studies, associations were found for PM 10 only and not for PM 2.5 (p. 7-43, line 6), a finding not consistent with the cited

statement.

In the respective PM fraction Summary and Caus al Determinations sections, there is little mention of PM 10 . However, when findings on PM 10 are mentioned in this context, they are only offered in regard to PM 2.5 (e.g., PM 10 findings are cited as stre ngthening the evidence for PM 2.5 - related respiratory effects [p. 6-244] a nd for mortality effects [p. 6-317]). PM 10 evidence is not used in support of PM 10-2.5 effects. Yet in the discussion of short-term PM exposure mortality effects (section 6.5.2), PM 10 studies are cited as providing “a n underlying basis for the overall pattern of associations observed when examining the relationship between PM 10-2.5 and PM 2.5 and mortality.” We urge more c onsistent handling of the PM 10 evidence.

In order to better interpreting PM 10 findings relative to those of PM 2.5 and PM 10-2.5 , it would be helpful, perhaps in Chapter 3, to include and/ or highlight data on the relationships of PM 10 with both PM 2.5 and PM 10-2.5 , stratified by region of the country. Al so, in consideration of the role of the current 24-hour PM 10 standard with respect to PM 10-2.5 , it would be important to better document the relevant evidence on the relationship between PM 10 and PM 10-2.5 across the country.

In summary, the extensive evidence on PM 10 is used without specifici ty or consistency. PM 10 evidence is used to support the occurrence of overall effects of PM, but specifically in support of effects of PM 2.5 but not of PM 10-2.5

. The current PM 10 standard, however, is in place for control of PM 10-2.5 . Nevertheless, providing cau sality judgments for PM 10-2.5 and PM 2.5 , but not for PM 10 , as in the current draft, is more in lin e with the current sc ientific understanding.

b) In the first draft ISA, causal judgments were made for cardiovascular morbidity, respiratory morbidity, and all-cause mortalit y. In the second draft PM ISA, causal judgments were made for cardiovascular ef fects, 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, respectivel y) and 7 (Sections 7.2.10 and 7.3.8, respectively) that draw upon the more comple te discussions of this evidence in the later mortality sectio ns (Sections 6.5 and 7.6). These latter sections continue to present evidence of cause-specific mortal ity, as it informs the discussions and causality determinations for all-cause mortal ity. Furthermore, important results of analyses that examined potential effe ct 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 mort ality and morbidity as part of a suite of effects, in addition to the other co nsiderations underlying causality judgments,

8In 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 ev idence, primarily epidemiological in nature, published since the last review cy cle, makes such a judgment possible and informative. Because much of all-cause mortality is comprised of cardiovascular and resp iratory deaths, it is appropriate to show these two groupings separately. By showi ng these two classes of death separately, the reader can be tter appreciate both the magnitude and nature of the deaths attributable to PM 2.5

.

CASAC finds that the availabl e scientific evidence supports the judgment of a “causal” determination for short-term and long-term effects of PM 2.5 on cardiovascular eff ects. CASAC also supports the determination of a causal associ ation between short-term and long-term effects of PM 2.5 exposure and total mortality, based both on the relevant scientific evidence and the finding of a causal association for cardiovasc ular mortality, which makes up a substantial proportion of total mortality. Yet, despite strong a ssociations with these cause-specific effects, total mortality is less strongly and more variably associated with PM 2.5 , perhaps because total mortality includes a number of cat egories more weakly linked to PM 2.5 or not all associated with
PM 2.5 . Consequently, long-term exposure to PM 2.5 was judged “likely to be causal” for total mortality. This determination might be justif ied 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 mortalit y. Specifically, on page 2-18 th e ISA states that “a causal” relationship exists between long-term exposures to PM 2.5 and cardiovascular e ffects, yet on 7-137 the ISA states that “the re lationship between long-term PM 2.5 exposure and mortal ity is likely to be causal.” Because the impact of PM on cardiovascular effects is judged “causal,” and since cardiovascular mortality is the largest contribut or 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 si ngle greatest contributor to total mortality, other causes are less well associated with PM 2.5 and some conditions not at all. Because total mortality is strongly related to cardiovascular events, c onsideration should be give n to explaining why the available studies addressing all-cause mortality ap pear to be conclusive, by carefully explaining the contribution of other less strongly associ ated conditions. CASAC concurs with the conclusion of a “likely to be cau sal” association between respir atory effects and long-term and short-term exposures to PM 2.5

.

The added sections included in the ISA are effective in summarizi ng the recently reported evidence and in providing a basis fo r the causal determinations. As the ISA process matures and

9continues to evolve, CASA C recommends that a table be included that lists the previous review cycle’s causal judgment determinations directly be side the current cycle determinations, with a brief comment about what has changed in the info rmational database to warrant a change in the causal classification. This tabl e would provide the reader with a valuable summary of the historical process, and document changes in kno wledge 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 PM 2.5 , the particle number count distribution was predominantly in the ultraf ine size range. Therefore, for the second draft ISA, we considered the diesel and gasoline exhaust studies, in addition to the other considerations underlying causalit y judgments, when making our causal determinations for ultrafine PM expo sure and cardiovascular and respiratory effects, resulting in a change from “inadequa te” to “suggestive” for both categories. Diesel and gasoline exhaust studies also co ntinued to be considered as part of the evidence for PM 2.5 health effects, as was done for the first draft ISA. With consideration of this rationale, please co mment 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 studie s, and combustion of these fuels generates high levels of -UFP. Epidemiological i nvestigations have been less specific in their assignment of health outcomes specifically to U FP, although an increasing number of studies are observing effects of exposures proximal to road sides, reflecting some component of combustion exhaust or vehicle operation. While additional res earch 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 (Can cer) 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 ca rcinogenicity. As a result of revisions to this section, the causal determination for PM 2.5 and cancer was changed from "inadequate" to "suggestive"; the causal determination for PM 10-2.5 remained unchanged. Please comment on the expans ion of this evaluation to include a summary of toxicological studi es using routes of exposure other than inhalation, as well as consideration of both mortality and incidence studies.

10EPA 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 toxicolo gical studies to assess mutagenicity and genotoxicity on mechanisms fo r mammalian cancer research have used routes of exposure other than inhalation. For some ag ents, 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 re gard to the recently reported findings of epidemiological studies, these have included large, well a ssessed populations and they have shown associations w ith cardiovascular and respiratory outcomes. The same approach has been used for lung cancer, although interp retation is complicated by the possibility of potential confounding by smoking. With the excepti on 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 “s uggestive” classification, particularly in the context of other lines of evidence reviewed in the ISA.

2) Revisions to Chapters 1 (Introduction), 4 (D osimetry), and 5 (Mode of Action): Changes to these chapters included expansion or clarif ication in a number of areas, as presented in more detail in the recent le tter 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 Chap ter 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 read able 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 th e potential to cause adverse effects is so prominently featured, along with the implication th at particle number con centration is the most important metric for risk. Some additional discus sion of still weak evid ence in support of this hypothesis is warranted. There is inadequate discussion of the usefulness of the limited data on ambient air UFP concentrations cu rrently available. The data are essentially limited to particle number concentrations, which make no distinct ion 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 re sidence 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 sp ecifically on susceptible subpopulations (defined for this ISA as those subpopulatio ns that have a grea ter likelihood of experiencing health effects related to PM exposure) in Chapter 8. The introduction of this chapter was revised to include this ne w definition of suscep tible subpopulations, recognizing that the terms susceptible a nd vulnerable have sometimes been used interchangeably in the literature, and in ot her cases have been used to represent two different categories (i.e., biol ogical factors [e.g., age gend er, etc.] vs. non-biological factors [e.g., SES, differential exposure, etc. ]), resulting in the lack of a clear and consistent definition. The discussion was reor ganized to improve the characterization of

11factors that may contribute to increased susceptibility to PM-induced health effects. Each section was also revised to include th e 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 critiq ue 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 r ecommend that the authors consider identifying those definitions which are most timely and relevant for the purposes of this chapter.

Table 8-2 introduces all susceptibi lity factors that have been eval uated, as well as the particle size fraction evaluated and the duration/length of exposures. Ta ble 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 colu mn 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 indica te the results of each evaluation with a simple plus/minus summary a pproach would further imp rove 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 PM 10 incorporates both
PM 2.5 and PM 10-2.5 and reorganized to begin with PM 2.5 and PM 10-2.5 , followed by PM 10 , where applicable. The discussion of measurement techniques and chemistry of PM 10-2.5 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 appreciat e 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 appropr iately incorporates comments from the April review. Of note, the relationships among PM 2.5 , PM 10-2.5 , and PM 10 were clarified, although some additional information could be pulled fo rward from the Appendix (see below). The inclusion of additional informati on on UFP, PM components, and PM 10-2.5 monitoring methods was also an improvement. Similarly, the orga nization 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 addre ssed. While signifi cantly improved, further improvements could be made to the exposure se ction to help with th e organization, seeming overlap with earlier sections, a nd clarity, as discussed below.

12Specific comments:

• The Chapter would benefit from a more de tailed discussion of the relations among ambient PM 10 , PM 2.5 , and PM 10-2.5 , 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 seconda ry organic aerosols should be expanded to discuss the potential for oxidation of prim ary organic particles which makes them become similar to secondary organic aerosol.

• Standard Reference Materials (page 2-20, line 20): It sa ys “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 c oncentration 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. Ther e 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 c oncentration 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 de velop 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-base d approach and the remote site approach to assess the certainty of the model-based estimation of the PRB.

• Exposure Section: Given the relevance of th e measured PM concentr ations in the earlier sections of the Chapter, and for interpreti ng the epidemiological studies and the Health RA, discussion of exposure measurements s hould 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’ ho mes, 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 cons olidated into single sections, with references to this section made as nece ssary in later secti ons. As currently written, certain topics, such as spatial va riability 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 PM 2.5 , PM 10-2.5 and the PM components would improve clarity.

13o Section 3.8.4 (Exposure Assessment Studies at Different Spatial Scales) and its subheadings are misnamed. While the h eading titles do prov ide 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 subs ection in the beginning of the section, perhaps in Section 3.8.1 (General Exposur e Concepts) that su mmarizes the range of measured exposures to PM 2.5 , PM 10-2.5 , and PM 10 , their com position, and differences by city, suscep tible group, and season.

o Section 3.8.6: Other factors that could a ffect exposures should be noted, such as home ventilation `a nd activity patterns.

5) Integrative Synthesis in Chapter 2: Th e 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 reorganiz ed to focus on effects of PM 2.5 , PM 10-2.5 , and ultrafine particles, and was expanded to in clude discussions of effects for which a "suggestive" causality determination was dr awn. New integration sections were added that combine the evidence for health effects of PM 2.5 , PM 10-2.5 , and ultrafine PM across exposure durations. In addition, these inte gration discussions incorporated evidence related to mode of action, dosimetry, a tmospheric chemistry, and exposure assessment to the extent possible. When appropriat e, figures were added that summarize the overall U.S. and Canadian epidemiologic evidence for specific size fractions and exposure durations, along with the concentrat ions reported in the studies or provided by study authors. A new section was also added to Chapter 2 that contains policyrelevant considerations, including summa ries for the evidence for susceptible subpopulations, lag structure of associatio ns 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 1 st 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 Chap ter 2 is excellent, it could be strengthened w ith selected revisions. The main technical poi nts that should be addressed in fi nalizing 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 discus sion of PM effects on climate is needed, particularly with regard to th e 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 impact s on both health and welfar e, including strength of association, and the implications of uncertainties; (d) there s hould be more effort to move toward exposure-response relationships for ecolo gical effects endpoints; and (e) the conclusion regarding only a “likely” causal relationship between long-term exposure to PM 2.5 and mortality

14should be carefully revisited, since there is evidence that the relati onship 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 stronge st weight of evidence, moving to those with weaker or no weight of evidence (rather than vice versa as in the s econd 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 disaggre gated into figure panels, each addressing only one outcome. Furthermore, ther e appears to be an erro r in the scale at the bottom of Figure 2.3. Although there is a lower correlation of PM 10 with PM 2.5 (Page 2.5, lines 14-19), the correlation for PM 10 is nonetheless remarkably high and should be interpreted more appropriately.

The discussion of PM and climate concludes wi th 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 elsewh ere in the ISA, where the PM effects being considered were consistently and unquestionably a dverse. In the case of climate, PM can exert both positive and negative climate forcing influe nces. Some discussion should be offered to frame and further clarify this issue, perhaps in Chapter 1.

CASAC recommends that EPA add more mate rial regarding PM composition, an overall synthesis of both health and welf are effects, and a synthesis of the most significant uncertainties and their implications for th e robustness of conclusions.

6) Welfare effects evaluation in Chapter 9: Se veral revisions were made to the evaluation of the welfare effects evidence in Chapt er 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, wh ere 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 public ations, including discussion of specific climate forcing effects from individual PM components and size fractions. The discussion of ecological effects was also reorg anized 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 effectiv eness of the reorganization and revisions regarding welfare effects.

1516 CASAC was pleased to note the effective addition of secti ons on “Ecological and Welfare Effects” in the Integrative Overview summary di scussion in Chapter 2. CASAC also agreed that the revisions to discussions of PM welfare effect s in Chapter 9 strengthen the chapter, improve its clarity and are directly responsive to pr evious CASAC comments on the 1st Draft ISA. Several minor revisions would be helpful to im prove accuracy in some sections (see individual panelist comments for detail), but no major revisions are needed.

Newly added details on climate, ecological a nd materials effects of PM and its various components provide more comprehensive coverage of these important su bject areas; however, concentration-response functions for climate and ecological endpoint s will be needed for future ISAs. Information in Chapter 9 on optical meas urement methods provides added support for the proposed use of a new "PM light extinction" indicat or, 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 s hould be brought forward to the summary chapter (Chapter 2). The information presented on visi bility valuation and preference studies helps to demonstrate that visual air quality is consistent ly 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 extinc tion 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, NO
x and SO
x 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 Extern al 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

1Ashbaugh 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 disc ussion of specific climate forcing effects from individual PM components and size fractions. Th e discussion of ecological effects was also reorganized to focus on the types of effects and e ffects 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 excellen t job of incorporating comments from the earlier review. The integration of welf are 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 visib ility 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 suppo rted, 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 organizat ion is good, and small details make it easier to read. For example, the spatial contour plots ar e much easier to compare now that the contour scales are similar for related figures. The haze tr ends 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) a rrows could have a black border. Then they would also be distinguishable from the red and da rk green when copied in B/W.

I like Section 9.3.1 but the figures would benefit from better repr oduction. 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 adde d to the section on smelters and roadsides (p age 9-245). The reference is “Resuspension of Soil as a Source of Airborne Lead near I ndustrial Facilities and Highways,” by Thomas M. Young, Deo A. Heer aman, 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 ar e an important source of airb orne particulate matter less than 10 μm aerodynamic diameter (PM 10 ), but the contribution of contaminated soil to concentrations of Pb and ot her 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 obtaine d near five industria l facilities and along

2roadsides and were resuspended in a sp ecially designed laboratory chamber. The concentration of Pb and other trace elements was measured in the bulk soil, in soil size fractions, and in PM 10 generated during resuspension of soils and fractions. Average yields of PM 10 from dry soils ranged from 0.169 to 0.869 mg of PM 10 /g of soil. Yields declined approximately linearly with increa sing geometric mean particle size of the bulk soil. The resulting PM 10 had average Pb concentrations as high as 2283 mg/kg for samples from a secondary Pb smelter. Pb was enriched in PM 10 by 5.36-88.7 times as compared with uncontaminated Calif ornia soils. Total production of PM 10 bound Pb from the soil samples varied between 0.012 a nd 1.2 mg of Pb/kg of bulk soil. During a relatively large erosion event, a contaminat ed site might contribute approximately 300 ng/m(3) of PM 10 -bound Pb to air. Contribution of soil fr om contaminated sites to airborne element balances thus deserves considerat ion when constructing receptor models for source apportionment or attempting to control airborne Pb emissions.

3Avol Comments (Mr. Ed Avol)

1) Evaluation of Chapters 6 & 7 Health Evidence

(a) Evaluation of evidence from PM 10 studies (lead discussant, Vedal)

The revised approach is well-pr esented 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) announci ng, justifying, or explaining this decision to “collapse” PM 10 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 determina tion 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 ar e effective in summarizing the cumulative recent evidence and providing a basis for the causal dete rminations. 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 direc tly 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 docum enting 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 de termination 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 “su ggestive”. 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 co mplicated 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 rela ted 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 d ecision for both routes of exposure and consideration of both mortality and incidence studies.

2) Chapters 1 (Introduction),4 (Dosim etry),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) announci ng, justifying, or explaining this decision to “collapse” PM 10 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 categor ies of exposures (short-term, ch ronic, and peak) are described in this carefully crafted openi ng list of review consideratio ns...but short-term and chronic exposures are the focus of the documents. S hould some comments, concern, consideration be focused on peak exposures, even if just to sa y we don’t know much about it or need to learn
more?

Comments on Chapter 4

P4-2, line 31 – Manufactured nanoparticles are not c onsidered in this chapter (or in the review. Presumably manufactured nanoparticles lie so mewhere on the continuum from completely unrealistic exposures to completely relevant ones...Are manufactured nanoparticles being considered as “occupational” exposures? Rega rdless, some thought should be given to the potential for population exposure to these particles, and what mi ght be learnable from these engineered exposures (which may not be all that different from laborat ory-generated exposures of TiO2 or other specifically generated artifici al particles that serve an important purpose in identification of mechanisms and pathways). Would knowledge and consideration of their potential health effects (as a func tion of their particle size) be an appropriate section in an UFP chapter?

Comments on Chapter 5

I think this chapter was very well done a nd 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) “gap s in knowledge” is worthy of a section title or tabulation. In a larger docume nt sense, this final summary and assessment of knowledge gaps would be useful additions to mo st every chapter in the ISA.

General Comments on PM ISA, 2 nd Draft, Avol

56 In a large, data-rich, and complex document such as this, it would seem helpful to establish a consistent presentation paradigm that is followe d 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 va lidators 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 provi de unnecessary obstacles to the reader. Here are two examples of this:

(1) A consistent PM-size-oriented summary presen tation 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 PM 2.5 , PM 10-2.5 , and UFP and a brief summary statemen t regarding causality judgment -- for each size-cut – were made. (This comment motiv ated by the observation that UFP summary statements seem to be sporadica lly 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 (cardiova scular; respiratory; mortality; reproductive and developmental; cancer, mutagenicity, and genotoxi city) 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 tabu lar summaries could then form th e 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 Ca rdiovascular and Systemic Effects)– Much improved and clearer, providing a basis for what was known prior to the current review, and what the new information show s. Summary judgments for PM 2.5 , PM 10-2.5 , 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, inde pendent 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 th e 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 discu ss study after study after study at a level of detail that could be mo re appropriately placed in the a nnex. The main section of this document would be more useful as an integratio n of current knowledge, not an exhaustive listing of it; additional materials could a nd 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 PM 10 , PM 2.5 , and PM 10-2.5 ? 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. Especial ly, 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 de lineation of the three critical si ze ranges of PM: coarse, fine, and UFP. These three size ranges are now prominen t throughout and adequately discussed in terms of exposure and response. The inclusion of welf are considerations and ec ological 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 pr oducing a summary which is both sophisticated as well as accessible.

Section 2.4, “Policy Relevant C onsiderations,” is done well. Th e role of susceptible populations is emphasized. This is important since these individuals make a dominant contribution to the observed health effects.

7Cascio 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 appreci ated, 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
PM 10 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 PM 2.5 and PM 10-2.5 independently is appropriate, but app ears to be at odds with the current PM 10 standard. How does EPA intend to reconcile this discontinuity? 3) Nevertheless, the separation of PM into PM 2.5 and PM 10-2.5 is strongly supported by scientific data. 4) The concept that the abundant data on PM 10 might serve to selectively support the causality determinations for PM 2.5 and PM 10-2.5 is problematic. As described above PM 10 contains both fractions and th ere will always be uncertainty as to whether effects measured in response to PM 10 are related to the PM 2.5 fraction, the PM 10-2.5 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 appreci ated, 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 st udies reporting health effects, toxicity of diesel emission and gasoline emission PM is pr ovided. The rationale to include diesel and gasoline emissions as evidence of effect s 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 comp leted California Freeway Study that showed that particle number was mo st strongly associated with health effects endpoints in subjects exposed to traffic related pollut ants on two Los Angeles freeways for 2 hours. 3) Based on the weight of the evidence with th e inclusion of diesel and gasoline emission data the change in the causal determination for UFP from “i nadequate” to “suggestive” is appropriate. 4) The presentation of diesel , gasoline and wood smoke em ission data independently provides a means to quickly find relevant hea lth effects data linking a specific exposure type to health effects. Such an appro ach was useful in judging the strength of associations and determination of causation.

8Charge 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 appreci ated, 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 2 nd external review draft Section 7.5 provi des a more detailed presentation of epidemiological and toxicological data. The information is well integrated. This has improved the quality of information regardi ng the association betw een 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 be tter integration of epidemiological and toxicological data the causal determination has been changed to “suggestive”. This change is appropriate based on the presented da ta. While toxicological studies included in this section were conducted with exposure ro utes other than inhala tion 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 hi gh 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 tachyarrhythmia s using heart rate. Pacing Clin Electrophysiol 30 :874-84, 2007; Sandercok GR,
Brodie DA. The role of h eart 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 au tonomic nervous system, whereas rMSSD and frequency variations in HR

9generally 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 Langr ish 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 ri ght 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 inca pable of generating an organized mechanical cont raction 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 s udden cardiac death include
activators and facilitators of arrhythmia such as electrolyte abnormalities, m odulation 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 arch itecture, fibrosis, and intracellular calcium handling.”

106-27 1, 7 The sentence, “Such beats...” should include the conduction system as a source of arrhythmia. For example, “Such beats can ar ise 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 electrocardiogr aphic telemetry systems might be used more effectively to assess the relationship between air pollu tants and arrhythmia in patients with history of a rrhythmias 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 measur es 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 wi thout indentation.

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

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

116-81 1, 2 Write “thrombin anti-th rombin 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-cit y” rather than “multicity”.

6-128 2, last line Add to the final se ntence such that it would read, “ Furthermore, the HRV resu lt...including age and preexiting conditions and genetic polymorphisms modulating responses to oxidative stress.”

6-138 1, last line Consider “co-pollu tant” rather than “copollutant”. “Copollutant” is used thr oughout 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

12Berger – add Journal title

Brauner – add Journal title

6-339 Brook – add Journal title

Burnett – add Journa l 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 Jour nal 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 J ournal title, vol. and pages

Gent – add volume

Gerlofs-Nijland – add volume

13Gerlofs-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

146-350 Le Tertre – add J ournal 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

156-355 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 refere nce is not consistent with the
others

Pope – add Journal title

6-357 Prystowsky – add Journal title

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

Schwartz – add Journal title

16Schwartz – 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 Journa l 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

17Yang – 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 Journa l 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 “Atheroscleros is is a progressive disease that
contributes to several adve rse 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.

187-5 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 bette r to write them out and
minimize the use of abbreviations.

7-14 L. 10 “non-statistically” doe s 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 re nal 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 “PM 2.5 ”.

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 admi ssions” 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: neonat al (<1 month), infants (<1 year), and post-neonatal (1 month to 1 year).” rather than what is present. Su bsequently, on page 7-77 the

19order 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 Re spiratory Mortality, < 1 Month”. “M” in “month” should be capitalized for consistency.

7-121 L. 14 Font of “reduction” a nd “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

20Grigg – 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

21Lund – 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

22Schindler – 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

23Cowling Comments (Dr. Ellis Cowling)

Charge Question 1:

Welfare effects evaluation in Chapter 9: Several revisions we re 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 eco systems 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 eco logical effects was also reorganized to focus on the types of ef fects and effects of i ndividual components.
For the effects of PM on visi bility, new material was adde d including sections on direct optical measurements and the value of good visual air quality. Please comment on the
effectiveness of the reor ganization and revisions re garding welfare effects.

I was pleased with the adjustments in organizati on that were achieved in this second draft ISA for PM and with the statements of key findings w ith regard to public welfare effects in Chapter

2.

I was even more pleased to find that a reasonabl y very well-balanced di stribution of attention was given in Chapters 2 and 9 of the PM ISA to th ree of the four types of welfare effects of PM – with visibility effects being covered in the fi rst 83 pages in Chapter 9, climate effects being covered in the next 104 pages of Chapter 9, and eco logical effects being covered in 43 pages in Chapter 9 (recognizing, of course, that the very s ubstantial ecosystems ef fects the PM forms of
airborne NOx and SOx on acidifi cation, nutrient enrichments, and methyl-mercury enhancement are being handled very thoroughl y in the separate integrated NAAQS assessment document for public welfare effects of NOx and SOx.

It was somewhat disappointing, however, to disc over 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 build ings and monuments would have deserved
somewhat more attention.

24Frey Comments (Dr. Chris Frey)

Charge Question 5 : Integrative Synthesis in Chapter 2: The CASAC PM Panel recommended expanding Chapter 2 to include all im portant findings of the PM IS A. The integration of health evidence in Chapter 2 was reorgani zed to focus on effects of PM 2.5 , PM 10-2.5 , and ultrafine particles, and was expanded to include discussions of effects for which a "suggestive" causality
determination was drawn. New in tegration sections were added that combine the evidence for health effects of PM 2.5 , PM 10-2.5 , and ultrafine PM across exposure durations. In addition, these integration discussions incorporated evidence re lated to mode of acti on, dosimetry, atmospheric chemistry, and exposure assessm ent 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 th e concentrations reporte d 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 su sceptible subpopulations, lag structure of associations in epidemiologi c 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

PM 2.5 , PM 10-2.5 , 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 ma terial on evidence for health effects of PM 2.5 , PM 10-2.5 , and UFP for long- and short-term exposure dur ations 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 th e 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 stac ks, so it would be more clear here to refer to “non-EGU point sources,” if th at is the intended meaning.

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

Page 2-13, lines 5-20. For cl arity, should explain why PM 10 is not separately considered, just to avoid confusion on the part of some r eaders who might be expecting to see PM 2.5 and PM 10 as the focus, since these are the indi cators of the current standard.

25Page 2-13 – last half. As a rhet orical device, it is weak to star t 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 th e causality determination. As a reader, I would prefer to first see a list of the key outcomes that are the focus of the IS A, 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 deta il 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 wonderi ng 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 im portantly, 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” ar e inanimate and cannot attempt to do anything. This section needs copy editing.

Page 2-34, line 32-35. “various” might more accurate ly 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 pa ge. Is PM size a factor?

Page 2-42, lines 15-17. This text refers to “effects” on climate. In the cont ext 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 wh ether the “effects” are adverse or beneficial, and hence the policy implications of this statement by itself are unclear.

26Grantz Comments (Dr. David Grantz)

ISA for PM, 2 nd External Review Draft

Comments by David Grantz on Ch arge 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 review s. The resulting two chapters of concern here, Chapters 2 & 9, are well organized (few comme nts 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 issu es of interpretation remain, and these are
addressed below.

The increased attention to clim ate change is appropriate and generally well done. As noted below, there is some confusion in the disc ussion of PM impacts on photosynthetically active radiation (PAR). Briefly the issu e is that photosynthesis per leaf responds nearly linearly to PAR up to some near-saturation flux. At this flux it beco mes useful to spread th at (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 significan t 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 deba te towards response-exposure relationships. In
several cases cited there are cl ear 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 begi nnings of such relationships. Re ference to the study of Nash, 1975 (page 9-235, line 34) seems to best approximate th is goal. Overall, the current organization of Chapter 9 by component works very well.

Specific Comments

Chapter 2-- Substantive comments

page line Comment

272-3 25 It is important to define UFP (ultraf ine 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 de positing 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 lo gical 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 me rged into Section 2.2.1

2-11

2-12 14, 27-30

23 Define first use of “ambient” in th is 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 onl y “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 mu ch of the information that is required in chapter 2. Perhaps thes e summaries can be blended into their preceding sect ions and condensed.

2-30 22-23 Text states “is associated” when it was concluded “is suggestive...”. These are not equivalent.

282-37 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 betw een 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 uppe r leaves are light saturated, is poorly conveyed here and in the relevant parts of chapter 9. This is an important point, that if properl y explained the first time would
obviate much later discussion and rem ove the apparent conflict with data showing that increasing PM bot h 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 concludi ng sentence here, perhaps considering the importance of region al averages, and the existence of local hot spots, and more accura tely summarizing the subsection, would be helpful, particularly fo r 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

292-14 14 Reference to null findings is unc lear 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 constructe d 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.

309-46 Fig. 9-

24 San Joaquin Valley data are unclear. Th is 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 cl ear 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 Sa n 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 (Tab le 9-2), does this require some explanation?

9-102 25 on The source of NOx to support th e 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 senten ce here should summarize the preceding CD and the material to be excluded from the current ISA.

9-221 3 There is a distinction made be tween uptake (or maybe just response?) at the air-plant interface, and uptak e by above ground tissue. This is
hard to understand. The authors ma y 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 co nsulted. 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 contra sts with conclusions on p. 224-225.

31These sections should be more cl osely aligned with each other.

9-227 8-15 There are some important con cepts contained in the previous CD regarding deposition, including specif ic cation depletion with depth and distance into forests, that shou ld 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 a nd 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 para graph, but more importantly should be integrated with the overall theme of this section, which has to do with the appearance and disa ppearance 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 blu rring 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 attribut e 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, ?)

329-253 32-36 While the effects of Cu and Ni may be solely at tributed to their toxicity as statedhere, it was im plied previously that these heavy metals displace from soil exchange s ites 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 ma y (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 di ffuse 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 ir on oxide. Whereas such coatings on aluminum do provide some protec tion against furthe r 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” statemen ts. 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.

339-61 Fig 9-32 It is unclear what the sulf ate 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 tr anslated into visual range, as was
done above.

9-213 29 The reference to Odum 1 985 is not complete (p. 9-292)

9-222 20 The distinction between combus tion sources and petrogenic sources
is unclear. Does combustion source refer to biomass combustion?

9-235 15-17 Sentence beginning, “A greenhous e study...” is confusing. There is a word missing (“under”?) prior to “simulated”.

9-237 22-26 Second half of paragraph, “Sequential extract ions...unavailable” could be incorporated into the beginning of this section 9.4.5.2.

9-242 22 In line beginning with “by increa sing” there is a cr itical 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-root ed species is not very useful, and
should be deleted as a distraction.

9-250 7 MADE should be AMDE. It woul d 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 descri be briefly how isotopes of C and N can demonstrate biomagnifications of metals. In the second paragraph, the lack of biomagnifications in aqua tic 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 mo ved to the earlier section on deposition.

349-261 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 adde d to the list of constituents with ecological effects.

35Helble Comments (Dr. Joseph Helble)

Charge question 4, ISA

Revisions to Chapter 3 on Source to Exposure: Cons istent with revisions made to the health effects chapters, Chapter 3 was revised to clarify that PM10 inco rporates 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 te chniques 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 PM 2.5 , PM 10-2.5 , and PM 10 . The sequencing of discussing PM2.5 followed by the successively larg er size fractions provides a l ogical framework for addressing the important differences among these size classe s. The revised chapter also does a good job, overall, of summarizing areas wh ere studies suggest differing tre nds, and identifying areas where data are sparse and additiona l research is needed.

The reorganization and expansion specifically to address depositi on in more detail, measurement techniques, and diesel emissions were generally clear and well-st ructured. W ith regard to deposition, a minor suggestion is that Section 3.3.4 page 3-21, the gene ral introduction, be expanded to address wet deposition. It is mean t to be a general overview of deposition, but only discusses dry deposition and ignores wet depositi on other than a passing reference in the first sentence. Organizationally, if this is to functi on as the introduction to the sections providing a more detailed discussion of both wet and dry de position, 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 disc ussion remains a general one. Th ere 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 gene rally mixtures or agglomerates of particles...from multiple sources...” This statem ent 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 prox imity to source. This statement should be clarified or, better, removed.

36In the discussion of county-based PM spatial di stribution 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 th ey fail to meet the 75% completeness criterion. Failing to meet this criterion coul d, however, be a result of a lack of appropriate monitoring sites within the county, or a failure to obtain adequate (complete) da ta 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 lit tle. To shorten the document, this subsummary, as well as a few other sub-summaries at the end of individua l 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 sent ences, 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, ad dresses school buses. Were parts of two differe nt 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 colle ction efficiency will decrease, not increase, as dp decreases.

Line 5, page 3-34: “monvolatile” sh ould 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 co mmas 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. Si milar comment lines 8 and 9, page 3-60

Line 31 pg 3-70, insert “per” before cm 3

37Figures 3-12 to 3-14: did EPA consider plotti ng these figures without us ing 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 facil itate a quicker understanding of monitor locations

Lines 10 and 11, page 3-135: figure numb ers should be changed to 3-52 and 3-52

Table 3-17 is not adequately explained in the te xt nor the caption. The pa renthetical values in column 2 need to be described, and the basis fo r 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: capti on, change “theem” to “them”

Line 10, page 3-215: “In this wor k,” - ? Incomplete sentence

Line 20, page 3-215: complimentary should be complementary

Lines 10-11-12 page 3-237, senten ce would read better as opening to section. It does not follow
as a conclusion.

Page 3-246, Low Angeles should be Los Angeles

38Henderson Comments (Dr. Rogene Henderson)

Reply to Charge Question #3; Susceptible Populations

I found Chapter 8 to be complete, clear a nd 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 fa ctors 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 no t have a column indica ting the results of the evaluations. Thus if one only looks at the table, which is titled simply "Susceptibilit y Factors," one might get the impression that all of the lis ted factors showed a susceptibility, when some factors, such as gender, did not . I recommend at least expandi ng the title to "Susceptibility Factors That Have Been Evaluated," and if possibl e 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 we ll-organized. The authors have been responsive to the CASAC critique of the first draft of the chap ter. Their definition of "susceptible" is clearly stated and there is a rather comple te listing of how the term has b een used in the literature in the past.

2) Table 8-2 introduces all of the susceptibility fa ctors that have been evaluated, as well as the size fraction evaluated and the length of the e xposures. 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 no t have a column indica ting the results of the evaluations. Thus if one only looks at the table, which is titled simply "Susceptibilit y Factors," one might get the impression that all of the lis ted factors showed a susceptibility, when some factors, such as gender, did not . I recommend at least expandi ng the title to "Susceptibility Factors That Have Been Evaluated," and if possibl e add a column that suggests what the results of the evaluation were. Maybe just a plus/minus approach could be used.

39Hopke 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 provi de a truly known standard to which the measurement can be compared. There may be systems with good pr ecision, but there are no deployed system with know accuracy. Thus, there needs to be a careful review of the us e of “accurate” with respect to the description of any ambient measurement.

Primary vs secondary organic aerosol: I suggest it would be very help ful 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 oxidi zed 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 th e chemistry is entirely heterogeneous, it is important to clearly distinguish these three diffe rent portions of the part iculate organic matter. The process of forming SOA or oxidized POM le ads 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 fo rmation 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 O 3 , Environmental Science and Technology 39, 4049-4059). Thus, we can expect ROS to be associated with ambient pa rticles and that has been obser ved 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 relationshi p between gas-phase and aerosol- bourne hydroperoxides in urban air, J. Aerosol Sci. , 34: 459-468.; Venkatachar i, P., Hopke, P.K., Brune, W.H., Ren, X., Lesher, R., Mao, J., Mitchell, M. (2007) Characteriz ation of wintertime r eactive 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 adde d 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 know n source profiles can be included within the PMF framework and yield an improved source resolution.

40The 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 PL S over other prediction methods like principal components regression (PCR). It is r eally 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 “condensatio n of gases.” Gases do not condense at normal temperatires and pressures. The correct te rm here is condensation of “vapors.”

Chapter 5 The discussion in section 5.1 only focuses on endoge neous 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, th ere is still significan t particle-bound ROS and thus, it should be noted as part of the total dose of ROS to the tissue.

41Lippmann 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 th e most part, thorough and accurate in its presentation of the peer-rev iewed 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). Specificall y, in Section 2.3.1.2 on Effects of Long-Term Exposure to PM 2.5 , the conclusion that “a causal relationship is likely to exist between long-term exposure to PM 2.5 and mortality” is insufficient. It should be changed to “a causal relationship exists be tween long-term exposure to PM 2.5 and mortality” . How is it possible to conclude that “a causal relationship exists between long-term exposure to PM 2.5 and cardiovascular effects” (page 2-18, lines 8 & 9), and that the strongest support for that causality determina tion comes from the associations of ambient PM2.5 and annual mortality, and then equivocate on the conclusion that PM 2.5 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 PM 2.5 exposure studies in mice cause d exposure-related aortic plague progression. This research provide s a toxicological basis for supporting the epidemiological findings of excess cardiova scular 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 associ ations of PM sources and components with health effects only in Chapter 6 on short-term exposures, sin ce it covers the literature on both short-term exposures and long-term exposur es, the latter being re levant to Chapter 7. This topic should be a separate chapter. If this is not possibl e, 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 evid ence 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 th e closure on the last PMCD; b) Italicize in vivo, in vitro, in situ, a priori , etc.

42Specific 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 e xposures. It needs to be a separate chapter, or divided into parts for Chapter 6 and parts for Chapter 7.

1-24 15 Insert “sizes, respirat ory parameter and” before “branching”

1-24 34 Citations to the concen trators 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”

434-3 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 “ex ternal measurements of retained particles havi ng 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 exceptio n 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 “PM 2.5 “ 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 vertic al line at 0 change

6-250 Sect. 6.4.1 Chen & Schwartz (2009) does not belong here it is clearly a study of chr onic 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-Garciduena s et al. (2003) does not belong here in the acute exposure section.

446-253 2 nd and 3 rd para. These studies do not belong in the acute exposure
section.

6-320 14 Change “correlation be tween 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 3 rd para. What about the “Franklin et al (2008)” paper? It needs to be cited in this paragraph.

6-327 3 rd para. Line5 Change “similar” to “simultaneous”

6-327 3 rd 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 ca tegory, 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 “PM 2.5 ” before “CAPs”

7-8 12a Change “PM 10 ” to “Ambient Air PM”

7-10 Sect. 7.2.3 Create a new subsection on Epidemiology that cites the study of Chen and Schw artz (2008), using text from page 7-11, lines 4-6

7-25 9 Add at end of sentence: “and with PM 2.5 - related plaque progression in chronically exposed mice”

7-30 3 “SAPALDIA” is mis-spelled

7-31 Table 7-3 Add descriptions of “G ent 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 Yo rk City” in th e table title

7-137 18 As noted previously, “likel y 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 compar ison with that occurri ng 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 pa rticulate 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., Park er, J., Chen, L-C., Veronesi, B. (2007). The cellular and genomic response of an immortali zed 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 di sease progression and TLR-4-dependent Kupffer cell activation by air particulate matter. J. M OLEC

. M ED
, (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 Combus tion: 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 exposu re induces angiogenesis. Toxicol. Lett. (in press).

46Malm Comments (Dr. William Malm)

Review of Integrated Sc ience Assessment for PM
Page 9.3: The use of “transparency” is inappr opriate here. It usually is reserved for a psychophysical reference of the “perceived” tran smittance of the atmosphere. One could use “transmittance”, but that would also be incorrec t 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 sc enic characteristics are met! “...regardless of background conditions” seem s to say that a percent change in extinction exudes a similar perceptual res ponse under all atmospheric conditi ons, which of course is not

true.
Page 9.9: How about using “imperceptible” inst ead of “unperceivable”? “Achromatic” what? Should sentence read “...achromatic contrast and discoloration”?
Page 9.16: Should include some discussion of the level of uncertain ty associated with nephelometer measurements of coarse particle scattering.
Page 9.21: “The resulting underes timation of total light extincti on is typically much smaller since fine particle light extinc tion generally exceeds that contri buted by coarse particles.” Not true – coarse particle fraction of total scattering is often comparab le 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 condition s 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 conditi ons, 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 establis hed that current regional scale m odels 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 ba sed on the association of source signatures with measured concentrations. Two differe nt 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 deve loped source signatures from modeled concentrations of conserva tive 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 concentratio ns at the receptor site. Average emission, dispersion, chemical transformation, and deposit ion processes are inco rporated into this one scaling factor. However, all of thes e processes vary with time, and the source apportionments derived from this technique ar e more accurate on the average than on an hourly or episodic basis. A statistical a pportionment approach will inherently tend to overestimate those source regions where endpo ints over the region ar e better correlated with measured concentrations, while unde restimating those source regions where

47endpoints over that source region show w eak-to-little correla tion 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 apportion ment analysis is more robust in that emissions and dispersion are explicitly m odeled, and only chemistry and deposition are incorporated into the “scaling” factor. In both approaches the scal ing factors account for possible errors in the models used to de velop 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 th e average than for an incrementally small time period.
In reading the discussion of sources of ammonia and N ox 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. Th e concept being that the only meaningful way to look at scattering change response is to explicitly mode l the change in scattering resulting from a change in emissions. Of course, this assume s that the model captures all the complexities discussed in the pages presenting the nitrate apportionment work.
Page 9.89: Here, scattering as a f unction of emission change is presen ted. It would be helpful to have a discussion, as outlined a bove, of the concept of partial scattering efficiencies, including the limitations and advantages of approachi ng the apportionment problem in this manner.
Page 9.103: “Both are a product of incomplete co mbustion of fuels, including those used in internal combustion processes (gasoline and di esel 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 statem ent is accurate. Much of measured OC is derived or SOA associated with VOC emissions, which can be natural or manmade.

48Pinkerton Comments (Dr. Kent Pinkerton)

Response to Charge Question 3:

Susceptible Populations, chapter 8 in the Second External Review Dr aft 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 woul d 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, c ontrolled human exposure, and toxicological studies with inclusion or hi ghlighting of only those studies with stratified results to demonstrate susceptible populati ons is highly appropriate to allow for the comparison of subpopulations exposed to similar populati ons 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 e xposure conditions. Never-the-less, such comparisons of susceptibility based on factor s 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 sus ceptibility factors along with exposure conditions (i.e. shortterm or long-term) and the PM size fraction ev aluated, 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 heal th impacts and/or observed health effects. 4) Inclusion of the hyperlinks to chapter 8 is a novel and extr emely 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 databa se (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 author s should be commended for making these sections a pleasure to read and to comprehend. 6) Table 8.3 contains fascinating information on the percent ofthe 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 th e 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 woul d be nice if the authors could provide some overarching conclusions for the relevance of these pre-existing dis eases based on type and age for this section of the chapter. 7) Excellent summary for chapter 8.

49Phalen Comments (Dr. Robert Phalen)

Chapter 1

The revision represents a significant improvement.

pg. 1-2, line 34: The last se ntence is incomplete.

pg. 1-3, lines 5 to 8: Thank you for mentioni ng 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 eviden ce 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 a ssociation 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, a nd opposition to PM NAAQS, seems to related to concern over whether particle mass is an a ppropriate indicator for health effects.

pg. 1-32, lines 5 to 11: There are several ga rbled words (typos) that need correcting.

pg. 1-33, line 3: The sentence is garbled.

pg. 1-33, line 9: Its "exp ress", not "xpress."

pg. 1-34: Journal title missi ng 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 th e chapter unnecessarily.

pg. 4-3, lines 24 to 25: Please insert "small par ticles and small" before "aggregates", as large aggregates are not characterized by a "thermodyna mic-equivalent size." Also, I would replace "thermodynamic-equivalent size" with "diffusion-e quivalent diameter", in order to clarify and avoid confusion with the thermodynamic concep ts 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.

50Accordingly, I suggest adding a sentence at the end of this line, such as: "However some individuals have less efficient co arse particle deposition in the ET region, and such particles can carry significant mass into the trache obronchial 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 year s, so the result may not apply to young children. Insert "age 7-14 years" be fore "children". Infants and young children, e.g. age under 3-4 years, are very different than adul ts with respect to particle deposition. We must not assume that 7-14 year old child ren 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 re cognize 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 contra st" 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, whic h 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 j ournal titles are missing.

51Poirot Comments (Mr. Rich Poirot)

July 2009 PM Integrated Science Assessment, Charge Question 6: Several revisions were made to the evaluati on of the welfare effects evidence in Chapter 9, in response to the CASAC PM Panel comme nt, to focus further on effects on climate and ecosystems and include further evaluati on of urban visibility evidence, where possible. In addition, as recommended by the CASAC PM Panel, key findings and conclusions from this chapter were incorpor ated in Chapter 2. The discussion of PM effects on climate was increased with substant ially more detail from recent publications, including discussion of specific climate forc ing effects from individual PM components and size fractions. The discussion of ecologica l effects was also reorganized to focus on the types of effects and effe cts 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 streng then the chapter, improve its clarity and are directly responsive to previ ous CASAC comments on the 1 st Draft ISA. A few minor revisions may be warranted, but I don’t th ink any major revisions are re quired. The added discussion on direct optical measurement methods and on visibi lity valuation is helpful, although there is relatively little presentation or analysis of op tical measurement data, a nd 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 transmisso meters, aerosol recons truction, etc. Better demonstration that there are currently viable, fi eld-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 adde d on aerosol effects on climate, mu ch of it taken directly from recent IPCC documents (which is fine – as th ese 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 repro duced CCSP SAP2.3 incorporated “significant sections fr om EPA data and reports related pa rticularly to U.S. emissions and measurements”, there is very litt le reported in the chapter directly relating to emissions from or measurements within the US. While a numbe r of causal relationships between emissions, aerosol concentrations and climat e effects can be identified on global scales, there doesn’t seem to be a clear, current basis for establishing spec ific US secondary PM standards for the purpose of ameliorating local or globa l climate effects. Conseque ntly, 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 se tting secondary PM standards to protect against adve rse ecological effects at the pres ent time, or for expending much additional effort on this section of th e ISA in the current review cycle.

52Specific Comments on PM ISA, Chapter 9: p. 9-15, 2 nd 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 recons tructed 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, 5 th line from bottom: This very large (Title IV-related) drop in SO 2 emissions from 1994 to 1995 could be mentioned as a possible expl anation for the apparent lack of post-1995 improvement in clean or hazy days at about ha lf 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 indicat e “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 IM PROVE filter-based sulfat e measurements. If the sulfate-associated extinction in left & right sides of Figure 9-50 were increased by 1.3 the slopes and R 2 would increase. This effect is shown in Figure 5.3 of the referenced NESCAUM report in which reconstructed B sp from OMC + adjusted sulfate = 0.91 Measured B sp + 4, R 2 = 0.94.

p. 9-95, 2 nd para, last line: It would be useful here to also repor t other aspects (besides just the
B ext level) of the Denver standard – for example th e 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 re port other aspects (besides just the B ext level) of the Phoenix standard – the day light window, 4-hour averaging time and <90% RH constraint. Also, the Phoe nix “standard” is not based on an absolute threshold, but on a required improvement across the entire visibility distribution – moving ba d days to moderate, moderate to good, good to excellent, etc. Discussi ng this might help emphasize that while there appear to be fairly convergent public opinions on levels of poor vi sibility that are considered “unacceptable” in the various studies, there are al so adverse welfare effects from reductions in the frequencies of periods with moderate, good a nd excellent visibility, and would be benefits from improvements across the whole distributi on. Conceivably this might lead toward considering a secondary “standard ” which would be “progress-base d” over fixed future time intervals, rather than “threshol d-based” with an indeterminat ely-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 diffe rent visibility conditions presen ted in the photos” (even when a weather and RH-neutral WinHaze approach was empl oyed) might also lead to a position that a good secondary NAAQS should be based on metrics that make as strong a distinction as possible

53between effects of pollution and effects of hum idity 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 da ylight window (to exclude the few most humid hours), increasing the aver aging time (from 1 to 2, 3, or 4 da ylight hours); and/or altering the form from the xth (90 th , 95 th or whatever) percentile of the wors t 1 hr (or 4hr or 8 hr) in a day summed for the year to the xth (90 th , 95 th or whatever) percentile of the hourly (or 4hr or 8 hr) levels in a year or season. Any/all of the a bove 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 complement ary paragraph describing some of the disadvantages an optical measurement-only a pproach – 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 aetha lometers, absence of information on mass, size distribution or com position 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 sma ll 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 exampl e here on MODIS AOD vs. AIRNOW PM 2.5 from the EPA/NASA IDEA site that might be a cl earer and more rele vant 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 direct ly 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/tops tory/20020613urbanrain.html ). See also the counter arguments presented by Alpert et al. (2008) http://www.tau.ac.il/~pinhas/pap ers/2008/Alpert_et_al_JAMC_2008.pdf Possibly there are also other non-aerosol effects of urbanization, su ch as more rapid runoff and deforestation, that would tend to alter downwind precipitation patterns.

p. 9-210, lines 17-18: This description of “pla net 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 forw ard direction. The “brigh tening” results only from that (relatively

54small, 10-15%) fraction of visible light that is back-scattered in the direction of the hypothetical observer in space.

p. 9-211, 2 nd para, line 1: Not clear what you mean by “progress has been made with in-situ and remotely sensed aerosols.”

55Russell Comments (Dr. Ar mistead (Ted) Russell)

First, I note that the word concise was removed from the first sentence, as is appropriate. When I showed my air pollution ph ysics and chemistry students th e PM ISA, they said “Can’t they shorten it?”, to which I replied this is sh ortened from the old Crit eria Document approach, and it should demonstrate how activ e 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 mo re information than n eeded 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 app eared as though it was reve rting back to the old AQCD approach.

In spite of the call to shorten future versi ons, overall, I think the ISA has been improved significantly. I still view that it does not bri ng enough attention to compositional differences in PM effects (both health and welfare). Ther e 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 c limate. While the incl usion of parts of the CCSP provides the foundation for discussing PM im pacts on climate, given the importance of this issue, and how it could impact how a s econdary NAAQS might be formulated, a bit more analysis would have been benefici al. Composition and size is very critical here, but is not fully transmitted in the synthesis chapter.

Chapter 2 does a reasonably good job of integr ating the findings of the rest of the ISA, though a few improvements can be made. The majo r concern I have, at present, echoes the comment above that there is not enough empha sis 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 e ffects. 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 dele terious 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 “i nadequate” relationships first. Thus, add a summary table at the beginning of 2.3 of the healtheffects examined. I find it a b it unnatural to suggest that the evidence for the relationship between PM and visibi lity 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 physic s. While such terminology is appropriate for the health effects where such a direct linkage is not so estab lished, here it just seems odd.

56A 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 woul d also synthesize uncertainties as to how they impact our overall understanding and how to interp ret results.. At present the chapter does not really synthesize health and we lfare and how the various uncer tainties impact our overall understanding, and ends rather weakly. Migh t there be a section sy nthesizing uncertainties (possibly in the section disc ussed 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 vari ation 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 informa tion in other assessments and it is not apparent you are using this information in this assessment.
2-14-10: Font on PM 2.5 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 s uggest that sulfate-dominat ed UFP do not have the same effects seen for CAPS and DE. 2-34-29: Status is not prot ective... 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 discussi ng the specific health endpoints.. It may be important to interpreting the ep i 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 leve l of the standard might be chosen to be. For this section to stand alone, here, the discussion of lag structure between the e ndpoints 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 evaluati on of exposure models, but if that is done as part of the Risk Assessment, that is fine. In gene ral, 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 th at three dimensional CTMs typi cally use finite difference or finite element approaches. This level of deta il is not overly informative to reviewing the NAAQS. Further, many models use finite volume approaches. Further, the approach used for

57deposition is incorrect for part iculate deposition (there is no sedimentation velocity in the formulation given), and the whole discussi on 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 char acterized on a broad scale to allo w conclusions to be drawn...” I thought NARSTO did just that. While there are variations, there ar e typically consistent features as well. This paragra ph strikes me as a bit negative.

The last paragraph on page 3-226 seems out of pl ace, since it is talking about impacts on the health effects studies discussed later, and I did not pi ck this up from the chapter (I may have missed it).

Minor: Figure Numbering: It appears as though figures were removed, le ading 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 th e typical lifetimes and loss processes. 3-33-21: What is meant by reliable, noting th at 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 PM 10-2.5 from the PM 2.5 and PM 10 values. It is almost assuredly true that there is some correlation in the PRB PM 10 and PM 2.5 values calculated by Trijonis, and the current approa ch would actually indicate that in some circumstances, PM 10-2.5 is ~90% of the PM 10 , which is almost assuredly not true. Use typical
PM 2.5 /PM 10 ratios for the two regions to get a bett er 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 equa tion 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...’

58Speizer 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 documentati on 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 PM 10 is that the PM 10 correlations in themselves (.70) are really remarkably high and suggest, although not quite as consistent as PM 2.5 that they can be us efully 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 “stakehol ders” 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 woul d 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 cond ition. These effects are for the most part acute events occurring among persons with chro nic conditions. (If the table o ccurred after the descriptions that follow there would be no problem). Perhaps a modest change in the Ta ble 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 fr esh diesel exhaust data before the PM 2.5 data seems to be mixing the consistency argument by s uggesting that UFP are explaining PM 2.5 effect when they are really supplemen ting the findings of the PM 2.5 effects reported in th e 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 studi es, thus the designation of

59suggestive. Again breaking out the kinds of outcomes in Fi gure 2.3 would be better than lumping them all together.

Page 2.29, Figure 2.3: There is clearly somethi ng wrong here. The units in this Figure are wildly different from Figure 2.1 and 2.2, and are simply not believeab le. 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 subject s with CVD and/or respiratory diseases the last sentence says respiratory di seases. Suggest change the last to cardiorespiratory diseases.

Responses to Charge Questions ( paraphrased and shown in italics) on ISA Draft 2

1. Evaluation of health evid ence in Chapters 6 and 7

a. The role of the studies of PM 10 in consideration in causality determinations for
PM 2.5 and PM 10-2.5 . Although this seems perfectly appropriate, it would seem that leading into this argument there should be some material (whi ch I looked for in Chapter 3, but could not find, maybe just my inability to find) th at could be referenced here or perhaps even summarized to justify the correlative nature of the relatio nships. This would help justify using the PM 10 studies when neither PM 2.5 or PM 10-2.5 were available to further assure the consistency of the data. b. The inclusion of cause-specific mort ality as part of suite of CVD and respiratory effects, in the devel opment 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 cau se 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 r eader gets a better understandi ng of both the magnitude and nature of the deaths that are occurring.

c. Scope of evidence considered in the ca usality determination for ultrafine PM. The change of the designation from in adequate to suggestive appears to be dominated by the interpretation of the re latively greater numbe r 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 st udies, that are for the most part null or poorly defined as UFP expos ure 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 su stain or refute the designation. This probably should be indicated. Charge Question 1d: d. With regard to the role of PM in mutage nicity, genotoxicity and carcinogenicity comment upon the expansion of this evaluation to include a summary of toxicological studies using routes of e xposure other than inhalation, as well as consideration of both mortal ity and incidence studies.

60Staff has done an excellent job in summa rizing a complex literature related to both the general and specific associations of using mutagenicit y, genotoxicity and carcinogenicity studies in asse ssing the PM effects on cancer . The charge question is really in two parts. With regard to usi ng routes of exposure other than inhalation, to assess mutagenicity and genotoxicity, these ar e standard procedures used in the field and have formed the basis of much of th e general literature ba sis 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 determ ining where along the spectrum of certainty with regard to causality thes e studies should be considere d. Secondly, with regard to the population studies that are re ported in the last few year s, these have been large, well assessed groups, in which the same e xposure parameters have been used for cardiovascular and respiratory findings (t hat appear to be defined as causal associations) with an outcome that is well de fined, albeit it dominated by the potential confounder of smoking. The relatively consis tent finding of lung cancer excesses as an exclusively associated cancer, along with the attempts to control for smoking are suggestive, and thus the appropriate inte rpretation and designation appears to have been made.

2. Revisions to Chapters 1, 4, 5. Chapter 1, expansion or additions to sect ions 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” desc ription 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 categ ory 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 us ed by others (and EPA) for susceptibility, the definitions provided are not ve ry useful. It might have been better to talk about host vs environment more formally. In addition, in di scussing each of the “susceptibility factors” much of what is reported is really not much di fferent that what is contained in Chapters 6 & 7. However, the discussion is better organized in defining and using su sceptibility factors as related to PM exposure. What is clearly left out, and perhaps should have a brief discussion is a contrast between susceptibility and vulne rability and how these factors play into a discussion of risk and margin of safety.

4. Chapter 3. Comments on revisions

61This 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 f actors potentially influenc ing exposure levels for health studies. I would suggest a summary ta ble at the end of this chapter that takes all the factors and provides qualitative directionality for the potentia l 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 th em here simply to put all my comments together. Clearly I have done this in greater detail than wh at I have done to answer other questions.

62Suh Comments (Dr. Helen Suh) Charge Question 3:

Revisions to Chapter 3 on Source to Exposure: Cons istent with revisions made to the health effects chapters, Chapter 3 was revised to clarify that PM10 in corporates 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 te chniques 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 appropria tely incorporates comments from the April review. Of note, the relation among PM 2.5 , PM 10-2.5 , and PM 10 was greatly clarified and the inclusion of additional information on UFP, PM components, and PM 10-2.5 monitoring methods was welcomed. Similarly, the organization and content of the ex posure section was greatly improved, especially with regards to the relevance of exposure findings to epid emiologic studies. While significantly improved, further improvements could be made to the exposure secti on to help with the organization, seeming overlap with earlier sect ions, and clarity, as di scussed briefly below.

- Given the importance of measured PM in the earlier sections of the Chapter, in the epidemiological studies, and also in the Hea lth 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 individua ls’ 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 curren tly written, certain topics, such as spatial variability a nd particle infiltration, a ppear repeatedly in se veral subsections. The discussion on these topics woul d 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, separa te or otherwise distinct discussions for PM 2.5 , PM 10-2.5 and the PM components woul d help with clarity.

- Section 3.8.4 (Exposure Assessment Studies at Di fferent Spatial Scales) and its subheadings are misnamed. While the headi ng 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 ambi ent PM exposure, rath er issues related to exposure error, exposure modeling, and tracers of ambient particles.

- It would be helpful to include a subsection in the beginning of th e section, perhaps in Section 3.8.1 (General Exposure Concepts ) that summarize the range of measured exposures to

63PM 2.5 , PM 10-2.5 , and PM 10 , their composition, and differences by city, susceptible group, and

season.

- Section 3.8.6: Other factors that could aff ect 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: Cons istent with revisions made to the health effects chapters, Chapter 3 was revised to clarify that PM10 in corporates 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 te chniques 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, c oncentrations and exposures. The Chapter generally reflects the state of science in a cl ear, comprehensive, and well organized fashion, which is notable given the amount of informati on the Chapter contains. Further, the Chapter revision appropriately incorporat es comments from the April re view. Of note, the relation among PM 2.5 , PM 10-2.5 , and PM 10 was greatly clarified and the inclusion of additional information on UFP PM components, and PM 10-2.5 monitoring methods was welcomed. Similarly, the organization and content of the ex posure section was greatly improved, especially with regards to the relevance of exposure findings to epid emiologic studies. While significantly improved, further improvements could be made to the exposure secti on to help with the organization, seeming overlap with earlier sect ions, and clarity, as di scussed briefly below.

Specific comments:

• Standard Reference Materials (p age 2-20, line 20): It says “T o 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 accur acy, 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 c oncentration of particles and thus, the PRB is really an implementation issu e and not a regulation setting issue. As the PRB increases because of activity outside of th e United States, there is decreasing flexibility in attaining concentrations that are fully prot ective of public health. The modeling approach has some appeal, but given the problems with th e 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 m odel emissions in the rest of the world seems very low. It would seem that there coul d be some comparisons between the model-based

64approach 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) i ndoor 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 consolidat ed into single sections, with references to this section made as necessary in later sect ions. As is currently written, certain topics, such as spatial variability and particle infiltration, appear repeatedly in several subsections. The discussion on these topics w ould 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 PM 2.5 , PM 10-2.5 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 headi ng titles do provide pa rallels 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 er ror, 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 PM 2.5 , PM 10-2.5 , and PM 10 , their composition, and differences by city, susceptible group, and season.

o Section 3.8.6: Other factors that could aff ect exposures are worth noting, such as home ventilation patterns and activity patterns.

6566 Vedal Comments (Dr. Sverre Vedal) 1a. Use of PM 10 .
Findings pertaining to PM 10 in this 2 nd draft are discussed in c onjunction with two component fractions (PM 10-2.5 and PM 2.5 ); causal determinations are no longer provided for PM 10 itself. There is value in this approach, since both fractions comprise PM 10 . It does not, however, seem logical that evidence on PM 10 would be equally relevant to both PM 2.5 and PM 10-2.5 . In some regions of the country PM 10 is more reflective of PM 2.5 whereas elsewhere PM 10 is more reflective of PM 10-2.5

.
In the respective PM fraction Summary and Caus al Determinations sections, there is little mention of PM 10 . Where PM 10 is mentioned in this context, it only comes up in support of PM 2.5 (e.g., PM 10 evidence is cited as strengthening the evidence for PM 2.5 -related respiratory effects [p. 6-244] and for mortality effects [p. 6-317]). PM 10 evidence is not used in specific support of
PM 10-2.5 effects. Yet in the discussion of short- term PM exposure mortality effects (section 6.5.2), PM 10 studies are cited as providing “an underl ying basis for the overall pattern of associations observed when examin ing the relationship between PM 10-2.5 and PM 2.5 and mortality.” There is incons istency then in the way PM 10 findings are used.

PM 10 findings are also used in evaluation of l ong-term PM fraction e xposure effects (e.g., p. 7- 24). For respiratory morbidity effects of long-te rm PM exposure, a more precise argument is made that “studies showing associations only with PM 10 were conducted in locations where PM was predominantly fine particles, providing support for associati ons 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 PM 10 and not for PM 2.5 (p. 7-43, line 6), which is not c onsistent with that statement.

In order to better interpret PM 10 findings relative to those of PM 2.5 and PM 10-2.5 , it would have been helpful, perhaps in Chapter 3, to include and/or highlight data on the relationship between
PM 10 and both PM 2.5 and PM 10-2.5 , stratified by region of the country. Also, in light of the role of the current 24-hour PM 10 standard with respect to PM 10-2.5 , it would be important to bring together the evidence relating to PM 10 that allows it to be used for this purpose.

In short, the way in which PM 10 is used is vague and inconsistent. PM 10 evidence is used generally to support overall effects of PM , but specifically only in support of PM 2.5 effects. The role of the current PM 10 standard, however, is in controlling PM 10-2.5 . Better justification for the utility of PM 10 findings is needed from a scientific and policy perspective. Nevertheless, providing causality judgments for PM 10-2.5 and PM 2.5 , but not for PM 10 , as is done in the current draft, is more in line with the current science.