# Policy Assessment for the Review of the Carbon Monoxide National Ambient Air Quality StandardsThis page is intentionally blank.EPA 452/R-10-007 October 2010



## Policy Assessment for the Review of the Carbon Monoxide National Ambient Air Quality Standards

U.S. Environmental Protection Agency Office of Air Quality Planning and Standards Health and Environmental Impacts Division Research Triangle Park, North CarolinaThis page is intentionally blankDISCLAIMER

This document has been reviewed by the Office of Air Quality Planning and Standards (OAQPS), U.S. Environmental Protection Agency (EPA), and approved for publication. This OAQPS Policy Assessment contains conclusions of the staff of the OAQPS and does not necessarily reflect the views of the Agency. Mention of trade names or commercial products is
not intended to constitute endorsement or recommendation for use.ACKNOWLEDGEMENTS

This document is the product of the Offi ce of Air Quality Planning and Standards (OAQPS). For the chapter on hea lth effects, dose, exposure/risk, and primary standards, the principal authors include Deirdre Murphy, Ines Pagan, Stephen Graham and Pradeep Rajan. For the chapter on welfare eff ects and consideration of a secondary standard, the principal author is Meredith Lassiter. The principa l contributors of the ambient monitoring information presented in the introductory chapter include Nealson Watkins and Rhonda Thompson. Other staff from OAQPS and staff from other EPA of fices, including the Office of Research and Development, and the Office of General Counsel also pr ovided valuable comments and contributions.
An earlier draft of this do cument was formally reviewed by the Clean Air Scientific Advisory Committee (CASAC) and made available for public comment. This final document has been informed by the expert advice and comments received from CASAC, as well as by public comments.i 

### TABLE OF CONTENTS

List of Figures................................................................................................................

................ ii

List of Tables .................................................................................................................

............... iii

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

1.1 PURPOSE.................................................................................................................... 1-1
1.2 BACKGROUND .........................................................................................................1-2

1.2.1 Legislative Requirements.....................................................................................1-2 1.2.2 Previous Reviews.................................................................................................1-4 1.2.3 The Current Review.............................................................................................1-5 1.3 CURRENT AIR QUALITY ........................................................................................1-6

1.3.1 Sources to Ambient Air .......................................................................................1-6 1.3.2 Ambient Monitoring Network .............................................................................1-8 1.3.3 Ambient Monitoring Concentrations .................................................................1-10
1.4 GENERAL APPROACH AND ORGANI ZATION OF THE DOCUMENT...........1-14
REFERENCES .................................................................................................................... 1 -15

2 REVIEW OF THE PRIMARY STANDA RDS FOR CARBON MONOXIDE ..........2-1

2.1 APPROACH ................................................................................................................2-1

2.1.1 Approach Used in the Previous Review .............................................................. 2-2 2.1.2 Approach for the Current Review........................................................................2-6 2.2 ADEQUACY OF THE CURRENT STANDARD...................................................... 2-8

2.2.1 Evidence-based Considerations ........................................................................... 2-8 2.2.2 Exposure/Risk-based Considerations................................................................. 2-40 2.2.3 CASAC Advice.................................................................................................. 2-56 2.2.4 Staff Conclusions on Adequacy of the Current Standards.................................2-57
2.3 CONSIDERATION OF ALTER NATIVE STANDARDS ....................................... 2-60

2.3.1 Indicator ............................................................................................................. 2-6 0 2.3.2 Averaging Time .................................................................................................2-60 2.3.3 Form and Level..................................................................................................2-62 2.3.3.1 Alternative Forms ........................................................................................2-62 2.3.3.2 Alternative Levels........................................................................................2-65 2.3.4 CASAC Advice.................................................................................................. 2-71 2.3.5 Staff Conclusions on Alternative Standards ...................................................... 2-71
2.4 SUMMARY OF STAFF CONCLUSIONS ON PRIMARY STANDARDS............ 2-76
2.5 KEY UNCERTAINTIES AND AREAS FOR FUTURE RESEARCH AND
DATA COLLECTION .............................................................................................. 2-79
REFERENCES ....................................................................................................................2 -81ii 3 CONSIDERATION OF A SECONDARY STANDARD FOR CARBON MONOXIDE ...................................................................................................3-1

3.1 CONSIDERATION IN PREVIOUS REVIEWS ........................................................3-1
3.2 CONSIDERATION OF EVIDENCE AVAILABLE IN THE CURRENT
REVIEW......................................................................................................................3- 2
3.3 CASAC ADVICE........................................................................................................3-3
3.4 STAFF CONCLUSIONS FOR THE CURRENT REVIEW.......................................3-4
3.5 KEY UNCERTAINTIES AND AREA S FOR FUTURE RESEARCH
AND DATA COLLECTION.......................................................................................3-4
REFERENCES ..................................................................................................................... .3-5

ATTACHMENT: Clean Air Scientific Ad visory Committee Letter (June 8, 2010)

APPENDICES

A. Summary of 2003 NRC Repor t Recommendations........................................................ A-1

B. Air Quality Data from Ambient Monitors Re porting CO Measurements in Geographical Areas of Key Epidemiological Studies During Periods of Study..............................B-1

C. Relationships (Ratios) Between 1-hour and 8-hour CO Concentration Metrics for Counties with CO Monitors (2007-2009) .................................................................C-1

D. Additional REA Estimates from Simulations for Alternative Levels and Forms for the 1-hour and 8-hour Standards ......................................................................................... D-1

E. Predicted Percentage of Counties with a Monitor Not Likely to Meet Alternative Standards and Associated Percentage Population............................................................E-1

LIST OF FIGURES

Figure 1-1. Trends in anthropogenic CO emissi ons in the U.S. by source category for 1990 and 1996-2005........................................................................................................... 1-7 Figure 1-2. Second maximum 8-hour average concen trations of CO at monitors nationally, 2009. ........................................................................................................................ 1 -11 Figure 1-3. Second maximum 1-hour average concen trations of CO at monitors nationally, 2009. ........................................................................................................................ 1 -12 Figure 1-4. Trends in CO concentration (sec ond maximum 8-hour average) in the U.S., 1990-2009................................................................................................................ 1-13 Figure 1-5. Trends in CO concentration (sec ond maximum 1-hour average) in the U.S., 1990-2009................................................................................................................ 1-14

Figure 2-1. A conceptual model of CO source-to-health outcome pathway..............................2-27 Figure 2-2. Components of CO s ource-to-outcome conceptual m odel measured in controlled human exposure and epidemiological studi es discussed in this document. ............2-28iii LIST OF TABLES

Table 2-1. U.S. epidemiological studies for isch emic heart disease, cardiovascular disease and congestive heart failure. ..........................................................................................2-14 Table 2-2. Carboxyhemoglobin levels and report ed effects in CAD patients and healthy adults from short-term CO exposures.. ...................................................................2-25 Table 2-3. Air quality information for geograp hical areas of key U.S. epidemiological studies......................................................................................................................2 -32 Table 2-4. Portion of simulated HD populations with at least one daily maximum end-of-hour COHb level (absolute) at or above indi cated levels under air quality conditions simulated to just meet the current st andard and “as is” conditions. ........................ 2-49 Table 2-5. Portion of simulated CHD population with multiple days of maximum end-of-hour COHb levels (absolute) at or above the indicated levels under air quality conditions simulated to just meet the current st andard and “as is” conditions. ........................ 2-50 Table 2-6. Portion of simulated CHD populatio n with at least one daily maximum ambient contribution to end-of-hour COHb at or a bove the indicated leve ls under air quality conditions simulated to just meet the curre nt standard and “as is” conditions. ......2-51 Table 2-7. Level and form for potential alternative 8-hour and 1- hour standards that would be just met in the REA air quality scenarios simulated with data for the Denver and Los Angeles study areas. ......................................................................................... 2-64 Table 2-8. Percentage of si mulated HD population with dail y maximum end-of-hour COHb levels (absolute) below th e indicated COHb levels unde r alternative levels and forms for the 1-hour and 8-hour standards.............................................................. 2-68iv This page is intentionally blank1-1 

### 1 INTRODUCTION

1.1 PURPOSE The U.S. Environmental Protection Agency (EPA) is presently conducting a review of the carbon monoxide (CO) national ambient air qua lity standards (NAAQS). The overall plan and schedule for this review were presented in the Plan for Review of the National Ambient Air Quality Standards for Carbon Monoxide (IRP; USEPA, 2008b). 1 The IRP identified key policyrelevant issues to be addressed in this review as a series of ques tions that frame our consideration of whether the current NAAQS for CO should be retained or revised. This Policy Assessment (PA), prepared by sta ff in EPA’s Office of Air Quality Planning and Standards (OAQPS), is intended to help “bri dge the gap” between the relevant scientific information and assessments and the judgmen ts required of the EPA Administrator in determining whether, and if s o, how it is appropriate to revi se the NAAQS for CO. This PA presents factors relevant to EP A’s review of the current prim ary (health-based) standards and consideration of a secondary (w elfare-based) standard. It fo cuses on both evidence- and riskbased information in evaluating the adequacy of the current CO NAAQ S and in identifying potential alternative standards for consideration. In this PA, we consid er the scientific and
technical information available in this review as assessed in the Integrated Science Assessment for Carbon Monoxide (henceforth referred to as the ISA, USEPA, 2010a), prepared by EPA’s National Center for Environmental Assessment (NCEA), and the Quantitative Risk and Exposure Assessment for Carbon Monoxide - Amended (henceforth referred to as the Risk and Exposure Assessment document or REA, USEPA, 2010b). In so doing, we focus on information that is most pertinent to evaluating the ba sic elements of NAAQS: indicator, 2 averaging time, form, 3 and level. These elements, which together serv e to define each standard, must be considered collectively in evaluating the health and welfar e protection afforded by the CO standards. While this PA should be of use to all partie s interested in the CO NAAQS review, it is written with an expectation that the reader has some familiarity with the technical discussions contained in the ISA (USEPA, 2010a) and the REA (USEPA, 2010b).

1 As described below in section 1.2.3, the schedule for this review is governed by a court order.

2 The “indicator” of a standard defines the chemical species or mixture that is to be measured in determining whether an area attains the standard.

3 The “form” of a standard defines the air quality statistic that is to be compared to the level of the standard in determining whether an area attains the standard. For example, the form of the annual PM 2.5 NAAQS is the 3- year average of the we ighted annual mean PM 2.5 concentrations, while the form of the current 8-hour CO NAAQS is the second-highest 8-h our average in a year.1-2 1.2 BACKGROUND

1.2.1 Legislative Requirements

Two sections of the Clean Air Act (Act) gove rn the establishment and revision of the NAAQS. Section 108 (42 U.S.C. 74 08) directs the Administrator to identify certain pollutants that meet specified criteria, including emissi ons which “may reasonably be anticipated to endanger public health and we lfare” and whose presence “in the ambient air results from numerous or diverse mobile or stationary sources” and to issue air quality criteria for them. Air quality criteria are to “accurately reflect the late st scientific knowledge useful in indicating the kind and extent of identifiable effects on public h ealth or welfare which may be expected from the presence of [a] pollutant in ambient air . . .” Section 109 (42 U.S.C. 7409) directs the Administrator to propose and promulgate “primary” and “secondary” NAAQS for pollutants li sted under section 10 8. Section 109(b)(1) defines a primary standard as one “the attainment and maintenance of which in the judgment of the Administrator, based on such criteria and allowi ng an adequate margin of safety, are requisite to protect the public health.” 4 A secondary standard, as defi ned in Section 109(b)(2), must “specify a level of air quality the attainment and maintenance of which, in the judgment of the Administrator, based on such crit eria, is requisite to protect the public welfare from any known or anticipated adverse effects asso ciated with the presence of [the ] pollutant in the ambient air.” 5 The requirement that primary standards incl ude an adequate margin of safety was
intended to address uncertainties associated with inconclusive scientific and technical
information available at the time of standard set ting. It was also intended to provide a reasonable degree of protection against hazards th at research has not yet identified. Lead Industries

Association v. EPA , 647 F.2d 1130, 1154 (D.C. Cir 1980), cert. denied, 449 U.S. 1042 (1980);
American Petroleum Institute v. Costle , 665 F.2d 1176, 1186 (D.C. Cir. 1981), cert. denied, 455 U.S. 1034 (1982). Both kinds of uncertainties ar e components of the risk associated with pollution at levels below those at which human health effects can be said to occur with reasonable scientific certainty. T hus, in selecting primary standa rds that include an adequate margin of safety, the Administrator is seeking no t only to prevent pollution levels that have been

4 The legislative history of section 109 indicates that a primary standard is to be set at the “maximum permissible ambient air level...which will protect the health of any [sensitive] group of the population,” and that for this purpose “reference should be made to a representative sample of persons comprising the sensitive group rather than a single person in such group.” S. Rep. No.91-1196, 91 st Cong., Sess. 10 (1970)

5 Welfare effects as defined in section 302(h) (42U.S.C . 7602(h)) include, but are not limited to, “effects in soils, water, crops, vegetation, man-made materials, animals, wildlife, weather, visibility and climate, damage to and deterioration of property, and hazards to transportation, as well as effect on economic values on personal comfort and well-being.”1-3 demonstrated to be harmful but also to prev ent lower pollutant levels that may pose an unacceptable risk of harm, even if the risk is not precisely identified as to nature or degree. In selecting a margin of safety, the EPA consid ers such factors as the nature and severity of the health effects involved, the size of th e sensitive population(s) at risk, and the kind and degree of the uncertainties that must be addresse d. The selection of any particular approach to providing an adequate margin of safety is a policy choice left specifically to the Administrator’s judgment. Lead Industries Association v. EPA , supra, 647 F.2d at 1161-62. In setting standards that are “requisite” to protect public health a nd welfare, as provided in section 109(b), EPA’s task is to establish standards that are neither more nor less stringent than necessary for these purposes. In so doing, EPA may not consider th e costs of implementing the standards. See generally Whitman v. American Trucking Associations , 531 U.S. 457, 465- 472, 475-76 (2001). Section 109(b)(1) of the Act requires that “not later than December 31, 1980, and at 5- year intervals thereafter, the Administrator shall complete a thorough review of the criteria published under section 108 and th e national ambient air quality st andards . . . and shall make
such revisions in such criteri a and standards and promulgate such new standards as may be appropriate . . . .” Section 109(d)(2) requires th at an independent scie ntific review committee “shall complete a review of th e criteria . . . and the national primary and secondary ambient air quality standards . . . and sha ll recommend to the Administrato r any new . . . standards and revisions of existing criteria and standards as ma y be appropriate . . . .” Since the early 1980's, this independent review function has been pe rformed by the Clean Air Scientific Advisory Committee (CASAC) of EPA’s Science Advisory Board.

1.2.2 Previous Reviews

EPA initially established NAAQS for CO, under section 109 of the Act, on April 30, 1971. The primary standards were establishe d to protect agains t the occurrence of carboxyhemoglobin levels in human blood associated with health effects of concern. The standards were set at 9 parts per million (ppm), as an 8-hour average and 35 ppm, as a 1-hour average, neither to be exceeded more than on ce per year (36 FR 8186). In the 1971 decision, the Administrator judged that attain ment of these standards would provide protection of public health with an adequate margin of safety and would also protect against known and anticipated adverse effects on public welfare, and accordingl y set the secondary (welfare-based) standards identical to the primary (health-based) standards. In 1985, EPA concluded its first periodic review of the criteria and standards for CO (50 FR 37484). In that review, EPA updated the sc ientific criteria upon which the initial CO standards were based through the publication of the 1979 Air Quality Criteria Document for1-4 Carbon Monoxide (AQCD; USEPA, 1979a) and prepared a Staff Paper (USEPA, 1979b), which, along with the 1979 AQCD, served as the basis fo r the development of the notice of proposed rulemaking which was published on August 18, 1980 (45 FR 55066). Delays due to uncertainties regarding the scien tific basis for the final decision resulted in EPA’s announcing a second public comment period (47 FR 26407). Fo llowing substantial reexamination of the scientific data, EPA prepared an Addendum to the 1979 AQCD (USEPA, 1984a) and an updated Staff Paper (USEPA, 1984b). Following review by CASAC (McClellan, 1991, 1992), EPA announced its decision not to revise the existing primary standard and to revoke the secondary standard for CO on September 13, 1985, due to a lack of evidence of effects on public welfare at ambient concentrations (50 FR 37484). 6 On August 1, 1994, EPA concluded its second periodic review of the criteria and standards for CO by deciding that revisions to the CO NAAQS we re not warranted at that time (59 FR 38906). This decision reflected EPA's re view of relevant sc ientific information assembled since the last review, as cont ained in the 1991 AQCD (U SEPA, 1991) and the 1992 Staff Paper (USEPA, 1992). Thus, the primary sta ndards were retained at 9 ppm with an 8-hour averaging time, and 35 ppm with a 1-hour averaging time, neither to be exceeded more than once per year (59 FR 38906). EPA initiated the next periodic review in 1997 and held a workshop in September 1998
to review and discuss material to be contai ned in the AQCD. On June 9, 1999, CASAC held a public meeting to review the first draft AQCD an d to provide a consulta tion on a draft exposure analysis methodology document. Comments from CASAC Panel members and the public on the AQCD were considered in a second draft AQCD, which was reviewed at a CASAC meeting, held on November 18, 1999. After revision of the second draft AQCD, the final 2000 AQCD (U.S. EPA, 2000) was released in August 2000. EPA put this review on hold when Congress requested that the National Re search Council (NRC) review th e impact of meteorology and topography on ambient CO concentrations in high al titude and extreme cold regions of the U.S.
The NRC convened the Committee on Carbon M onoxide Episodes in Meteorological and Topographical Problem Areas, which focused on Fairbanks, Alaska as a case-study. A final report, “Managing Carbon Monoxide Pollution in Meteorological and Topographical Problem Areas,” was published in 2003 (NRC, 2003) and offered a wide range of recommendations regarding management of CO air pollution, cold start emissions standards, oxygenated fuels, and CO monitoring (see A ppendix A). Following completion of the NRC report, EPA did not conduct rule making to complete the review.

6 EPA concluded in 1985 that “no standards appear to be requisite to protect the public welfare from any known or anticipated adverse effects from ambient CO exposures” (50 FR 37494).1-5 1.2.3 The Current Review

On September 13, 2007, EPA issued a call for information from the public (72 FR 52369) requesting the submission of recent scientific in formation on specified topics. A workshop was held on January 28–29, 2008 (73 FR 2490) to discu ss policy-relevant scie ntific and technical information to inform EPA’s planning for the CO NAAQS review. Following the workshop, a draft IRP (USEPA, 2008a) was made availabl e in March 2008 for public comment and was discussed by the CASAC via a publicly accessi ble teleconference consultation on April 8, 2008 (73 FR 12998; Henderson, 2008). EPA made the final IRP available in August 2008 (USEPA, 2008b). In preparing the CO ISA, NCEA held an au thors’ teleconference in November 2008 with invited scientific experts to di scuss preliminary draft materials prepared as part of the ongoing development of the CO ISA and its supplementary annexes. The first draft ISA (USEPA, 2009a) was made available for public review on March 12, 2009 (74 FR 10734) and reviewed by CASAC at a meeting held on May 12-13, 2009 (74 FR 15265). A second draft ISA (USEPA, 2009b) was released for CASAC and public re view on September 23, 2009 (74 FR 48536), and it was reviewed by CASAC at a meeting held on November 16-17, 2009 (74 FR 54042). The final ISA was released in January 2010 (USEPA, 2010a). In May 2009, OAQPS released a draft planni ng document, the draft Scope and Methods Plan (USEPA, 2009c), for consultation with CASA C and public review at the CASAC meeting held on May 12-13, 2009. Taking into considerati on comments on the draft Plan from CASAC (Brain, 2009) and the public, OAQPS staff deve loped and released for CASAC review and public comment a first draft REA (USEPA, 2009d) , which was reviewed at the CASAC meeting held on November 16-17, 2009. Subsequent to th at meeting and taking into consideration comments from CASAC (Brain and Samet, 2010a) and public comments on the first draft REA, a second draft REA (USEPA, 2010c) was released for CASAC review and public comment in February 2010, and reviewed at a CASAC mee ting held on March 22-23, 2010. Drawing from
information in the final CO ISA and the sec ond draft REA, a draft PA (USEPA, 2010d) was released in early March for CASAC review and public comment at the same meeting. Taking
into consideration comments on th e second draft REA and the draf t PA from CASAC (Brain and Samet, 2010b, 2010c) and the public, staff complete d the quantitative as sessments which are presented in the final REA (USEPA , 2010b) and discussed in this PA. The schedule for completion of this review is governed by a court order resolving a lawsuit filed in March 2003 by a group of plainti ffs who alleged that EPA had failed to perform its mandatory duty, under section 10 9(d)(1), of completing a revi ew of the CO NAAQS within1-6 the period provided by statute. 7 The court order that governs th is review, entered by the court on November 14, 2008 and amended on August 30, 2010, provides that EPA will sign, for publication, notices of proposed and final rulema king concerning its review of the CO NAAQS no later than January 28, 2011 a nd August 12, 2011, respectively.

1.3 CURRENT AIR QUALITY This section provides a genera l overview of the current air quality conditions to provide
context for this considera tion of the current standard s for carbon monoxide. A more comprehensive discussion of air quality inform ation is provided in the ISA (ISA, sections 3.2 and 3.4), and a more detailed discussion of asp ects particularly relevant to the exposure assessment is provided in the REA (REA, chapter 3).

1.3.1 Sources to Ambient Air

Carbon monoxide in ambient air is formed primarily by the incomplete combustion of carbon-containing fuels and by photochemical reactions in the atmosphere. As a result of the combustion conditions, CO emissions from large fo ssil-fueled power plants are typically very low because optimized fuel consumption conditions make boiler combustion highly efficient. In contrast, internal combustion engines used in many mobile sources have widely varying operating conditions. Therefore, higher and mo re varying CO formation results from the operation of these mobile sources (ISA, section 3.2). As with previ ous reviews of the CO NAAQS, mobile sources continue to be a significant source sector for CO in ambient air, as indicated by national emissi ons estimates from on-road vehicles, which accounted for approximately half of the total CO emissions by individual source sect ors in 2002 (ISA, Figure 3-1). 8 National-scale anthropogenic CO emissions have decreased by approximately 45% between 1990 and 2005 (Figure 1-1), with nearly all of this nati onal-scale reduction coming from
reductions in on-road vehicle emi ssions (ISA, Figure 3-2; 2005 NEI 9 ).

7 Communities for a Better Environment, et al. v. EPA (No. 07-CV-03678, N.D. Cal.).

8 EPA compiles CO emissions estimates for the U.S. in the National Emissions Inventory (NEI). The 2002 NEI provides the most recent publicly available CO emissi ons estimates for the U.S. that meet EPA’s data quality assurance objectives. Estimates come from various sources and different data sources us e different data collection methods, most of which are based on engineering calculations and estimates rather than measurements. Although these estimates are generated using well-established approa ches, uncertainties are inhere nt in the emission factors and models used to represent sources for which emissions have not been directly measured. Uncertainties vary by source category, season and region (ISA, section 3.2.1).

9 The emissions trends information he re and in Figure 1-1are drawn fr om recently availa ble 2005 National Emissions Inventory estimates ( http://www.epa.gov/ttn/chief/net/2005inventory.html , Tier Summaries) and 1990 and other estimates, available at http://www.epa.gov/ttn/chief/net/critsummary.html Figure 3-2 from the ISA provides estimates through 2005.1-7 Figure 1-1. Trends in anthropogenic CO emission s in the U.S. by source category for 1990 and 1996-2005.

The role of mobile source emi ssions is evident in the spatia l and temporal patterns of ambient CO concentrations, which are heavily infl uenced by the patterns associated with mobile source emissions (ISA, chapter 3). In metropolitan areas of the U.S., due to their greater motor vehicle density relative to rural areas, mobile source contribution to all ambient CO emissions was estimated to be as high as 75% in the 2002 National Emissions Inve ntory (ISA, p. 3-2). When considering all mobile sources nationw ide (non-road and on-road combined), the
contribution to total ambient CO emissions natio nally is over 80%. As an example, on-road mobile source emissions in urban Denver County, Colorado are estimated to be about 71% of
total CO emissions and emissions from all mobile sources (on-road and non-road combined) are estimated to contribute about 98% (ISA, section 3.2). In contrast, on-road CO emissions are estimated to be just 20 % of the total for rural Garfield County, Colorado 10 (ISA, section 3, Figure 3-6).

10 The 2002 National Emissions Inventory estimate for on-road emissions in Garfield is 20,000 tons, and the total emissions from all sources is estimated to be 98,831 (99K) tons. Thus, in this example the on-road vehicles accounts for 20.2% of the total emissions (ISA, section 3, figure 3-6).1-8 1.3.2 Ambient Monitoring Network

Ambient CO concentrations are measured by monitoring networks that are operated by state and local monitoring agencies in the U.S., which are typically funded in part by the EPA. The main network providing ambient data for use in comparison to the NAAQS is the State and Local Air Monitoring Stations (SLA MS) network. CO monitors are typically sited to reflect one of the following spatial scales:

 Microscale: Data represent concentrations in air volumes associated with area dimensions ranging from several meters up to 100 meters. Particularly for CO, microscale monitors have hist orically been sited 2 – 10 meters from a roadway. These microscale CO measurements have typical ly represented street canyon and traffic corridors.

 Middle scale: Data represent concentrati ons in air volumes associated with area dimensions ranging from 100 meters to 500 me ters. Such measurements are analogous to CO concentrations representa tive of several city blocks.

 Neighborhood scale: Defines con centrations within some exte nded area of the city that has relatively uniform land use with dime nsions in the 0.5 to 4.0 kilometers range. Such measurements are intended to re present extended portions of a city. Currently, there are no minimum monitori ng requirements for the number of CO monitoring sites, except in the new Nationa l Core (NCore) monitoring network, although continued operation of existing SLAMS CO sites is required until discontinuation is approved by the EPA Regional Administrator. 11 Further, in areas where SLAMS CO monitoring is ongoing,
at least one site must be a maximum concentr ation site for that ar ea under investigation. 12 The complete NCore network, which will be comprised of multi-pollutant monitoring stations throughout the country, is required to be fully implem ented by January 1, 2011. This network will consist of approximately 63 urban and 18 rural stations and will include some existing SLAMS sites that have been modified to include additional measurements. The majority of NCore stations will be sited, however, to represent neighborhood, urban, and regional scales, consistent w ith the NCore network design obj ective of representing exposure expected across urban and rural areas in locations that are not dominated by local sources (ISA, p. 3-21). Although NCore stations are intended to meet multiple monitoring objectives, they also provide data that are suitable for comparison to the NAAQS.

11 Prior to 2006, minimum CO monitoring requirements called for one “peak” concentration site (near a high traffic road or in an urban core) and one area- or community-wide monitor in any urban area over 500,000 population (44 FR 27558). In 2006, monitoring requirements for CO and other NAAQS pollutants were revised with the establishment of the National Core monitoring network (71 FR 61298).

12 40 CFR Appendix D to Part 58, section 4.2. Carbon Monoxide (CO) Design Criteria

.1-9 EPA has established federal reference me thods (FRMs) and methods designated as equivalent (federal equivalent methods, FEMs) for use in ambient air sample collection and analysis to promote uniform enforcement of the air quality standards se t forth under the CAA. Measurements for determinations of NAAQS co mpliance must be made with FRMs or FEMs.
More than 95% of FRM or FEM CO monitors in use in the CO monitoring network during 2005- 2007 had lower detectable limits (LDLs) of 0.5 ppm (ISA, Appendix A, Table A-8). Given the levels of the CO NAAQS (35 ppm, 1-hour; 9 pp m, 8-hour), a lower detectable limit (LDL) on the order of 0.5 ppm is well below the NAAQS levels and is therefore sufficient for demonstration of compliance. 13 However, with ambient CO levels now routinely near or below 1 ppm, however, a large percenta ge of the measurements from the CO monitoring network are below the LDL of conventional CO monitors, cont ributing greater uncertain ty in a larger portion of the distribution of monitoring data (ISA, sect ion 3.4.1). For example, more than half of the dataset of nationally reported hourly data for 2005-2007 analy zed in the ISA fell below the reported LDL of 0.5 ppm (ISA, p. 3-56). To reduce the uncertainty in monitoring data collected at these lower concentrations, a new generation of ambient CO monitors has been designed that provides improved sensitivity for measurements at or below the typical ambient CO levels
measured in most urban and all rural locations. These sensitive, or so-called ‘trace level,’ CO monitors generally have LDLs on the order of 0.04 ppm. The numbe r of active monitors employing such sensitive methods is increasing, pr imarily in association with the implementation
of the NCore network. 14 The extent to which these trace- level monitors or other sensitive reference or equivalent monito ring methods become integrated into non-NCore SLAMS stations, however, will depend on the availability of fundi ng for states to replace existing legacy CO monitors as well as the possibili ty that monitoring requirements for CO might either encourage or require such technolo gical improvements.

13 Among the 13 approved FRMs in use in the SLAMS ne twork for which data were reported to EPA’s Air Quality System (AQS) between 2005 an d 2009, nine are “legacy” methods with a federal method detection limit (MDL) listed as 0.5 ppm.

14 For example, four approved FRMs are newer, more sensitive methods with a federal MDL of 0.02 ppm and a growing body of ambient data from more sensitive CO instruments is becoming available. Testing performed by EPA on several such CO monitors in 2005 and 2006 demonstrated MDLs of approximately 0.017 – 0.018 ppm (17 – 18 ppb), slightly below the stated LDL of 0.02 – 0.04 ppm (ISA, section 3.4.1).1-10 1.3.3 Ambient Monitoring Concentrations

In 2009, approximately 350 ambient monitori ng stations across the U.S. reported continuous hourly averages of CO concen trations to EPA’s Air Quality System. 15 For the most recent period for which air quali ty status relative to the CO NAAQS has been analyzed (2009), all areas of the U.S. meet both CO NAAQS. 16 Although one area of the country (Las Vegas, Nevada) is designated in non-attainment with the CO NAAQS, air quality in that area currently meets the standards. In two of the previ ous three data review periods (2005-2006 and 2006- 2007), one area (Jefferson County, Alabama) has faile d to meet the 8-hour standard. Large CO
emissions sources in this area are associated with an integrated iron and steel facility. As shown in Figures 1-2 and 1-3 below, 2009 concentrations of CO at most currently operating monitors are well below the current standards, with just a few locations having c oncentrations near the controlling 8-hour standard of 9 ppm as a second maximum 8-hour average. 17 . Of the monitoring sites with extensive records 18 for 2007, sites in two countie s reported second-highest 1-hour CO concentrations between 15.1 and 35.0 pp m and sites in five counties reported secondhighest 8-hour CO concentration of 5.0 ppm or higher (ISA, section 3.5.1.1).

15 http://www.epa.gov/ttn/airs/airsaqs/.

16 The air quality status in areas monitored relative to the CO NAAQS is provided at http://www.epa.gov/air/airtrends/values.html.

17 As the form of the CO 8-hour standard is not-to-b e-exceeded more than once per year, the second highest 8-hour average in a year is the design value for this standard. Based on the current rounding convention, the standard is met if the CO concentrations over a year resu lt in a design value at or below 9.4 ppm. More detailed information on CO NAAQS design values is availa ble at http://www.epa.gov/airtrends/values.html.

18 During the period 2005-2007, 291 out of 376 monito rs sited in 243 differ ent counties, cities or municipalities met the following dataset completeness criteria: 75% of the hours in a day, 75% of days in a calendar quarter and 3 complete quarters for 3 years (ISA, section 3.4.2.2). An exception was made for monitors in U.S. EPA Region 10 for which two rather than three complete quarter s were considered to meet the criteria (ISA, p. 3-20).1-11 Figure 1-2. Second maximum 8-hour average concentrations of CO at monitors nationally, 2009.

curr8h09 0 - 2.4 2.5 - 6.4 >= 6.4 0.0-2.4 6.4-9.4 2.5-6.4 >9.4 ppm No. of Counties 176 25 3 01-12 Figure 1-3. Second maximum 1-hour average concentrations of CO at monitors nationally, 2009.

0.0-4.4 9.4-35.4 4.5-9.4 >35.4 ppm
No. of Counties 180 17 7 0 curr1hr09 0 - 4.4 4.5 - 9.4 >= 9.41-13 The current levels of ambient CO across the U.S. reflect the steady declines in ambient concentrations that have occurred over the past several years. Both the second highest 1-hour and 8-hour concentrations have significantly declined since the last review (Figures 1-4 and 1-5).
At the set of sites acros s the U.S. that have been conti nuously monitored since 1990 the average second highest 8-hour and 1-hour concentrations have d eclined by nearly 70%.

Figure 1-4. Trends in CO concentration (second maximum 8-hour average) in the U.S., 1990-2009. The white line indicates average acr oss the sites; ninety percent of sites have concentrations below the top line, while ten percent of sites have concentrations below the bottom line.

0 2 4 6 8 10 12 14 16

1 9 9 0 1 9 9 1 1 9 9 2 1 9 9 3 1 9 9 4 1 9 9 5 1 9 9 6 1 9 9 7 1 9 9 8 1 9 9 9 2 0 0 0 2 0 0 1 2 0 0 2 2 0 0 3 2 0 0 4 2 0 0 5 2 0 0 6 2 0 0 7 2 0 0 8 2 0 0 9 

### CO Air Quality, 1990 - 2009Concentration (ppm)

National Standard 9 ppm (Based on Annual 2nd Maximum 8-hour average)

National Trend Based on 187 sites

90% of sites have concentrations below this line

10% of sites have concentrations below this line Average among all sites1-14 Figure 1-5. Trends in CO concentration (second maximum 1-hour average) in the U.S., 1990-2009. The white line indicates average acro ss the sites; ninety percent of sites have concentrations below the top line, while ten percent of sites have concentrations below the bottom line.

1.4 GENERAL APPROACH AND ORGANI ZATION OF THE DOCUMENT This PA includes staff’s evaluation of the po licy implications of the scientific evidence
reviewed in the ISA and the re sults of quantitative analyses based on that evidence. Taken together, this information informs staff conclusi ons and the identification of a range of policy options for consideration in addressing public hea lth and welfare effects associated with ambient

CO. Following this introductory chapter, chapter 2 focuses on review of the primary standards for CO, presenting background information on th e rationale for previous reviews and the approach followed in the current review. Ch apter 2 discusses the adequacy of the current standards, taking into account evidence- and risk-based consid erations, and includes staff conclusions on adequacy. Chapter 2 also di scusses potential alternative standards for consideration, focusing on indica tor, averaging time, form, an d level, and includes staff
conclusions on alternative standards for consider ation. Finally, chapter 3 discusses information
relevant to staff’s consideration of a secondary standard for CO. 0 5 10 15 20 25 30 35

1 9 9 0 1 9 9 1 1 9 9 2 1 9 9 3 1 9 9 4 1 9 9 5 1 9 9 6 1 9 9 7 1 9 9 8 1 9 9 9 2 0 0 0 2 0 0 1 2 0 0 2 2 0 0 3 2 0 0 4 2 0 0 5 2 0 0 6 2 0 0 7 2 0 0 8 2 0 0 9 

### CO Air Quality, 1990 - 2009Concentration (ppm) National Standard 35 ppm (Based on Annual 2nd Maximum 1-hour average)

National Trend Based on 187 sites

90% of sites have concentrations below this line

10% of sites have concentrations below this line Average among all sites1-15 REFERENCES
Brain, J.D. (2009) Letter from Dr. Joseph Brain to Ad ministrator Lisa Jackson. Re: Consultation on EPA’s Carbon Monoxide National Ambient Air Quality Standards: Sc ope and Methods Plan for Health Risk and Exposure Assessment. CASAC-09-012. July 14, 2009.

Brain, J.D. and Samet, J.M. (2010a) Letter from Drs. J.D. Brain and J.M. Samet to Administrator Lisa Jackson. Re: Review of the Risk and Exposure Assessment to Support the Review of the Carbon Monoxide (CO) Primary National Ambient Air Quality Standards: First External Review Draft . EPA-CASAC-10-006. February 12, 2010.

Brain J.D. and Samet J.M. (2010b) Letter from Drs. J.D. Br ain and J.M. Samet to Administrator Lisa Jackson. Re: Review of the Risk and Exposure Assessment to Support the Review of the Carbon Monoxide (CO) Primary National Ambient Air Quality Standards: Second External Review Draft . EPA-CASAC-10-012. May 19, 2010.

Henderson R. (2008) Letter from Dr. Rogene Henderson, Chairman, Clean Air Scientific Advisory Committee, to Administrator Stephen Johnson. Re: Consultation on EPA’s Draft Plan for Review of the Primary NAAQS for Carbon Monoxide CASAC-08-013. June 12, 2008.

McClellan R.O. (1991) Letter from Dr. Roger McClellan, Chairman, Clean Air Scientif ic Advisory Committee, to William K. Reilly, EPA Administrator, July 17, 1991.

McClellan R.O. (1992) Letter from Dr. Roger McClellan, Chairman, Clean Air Scientif ic Advisory Committee, to William K. Reilly, EPA Administrator, August 1, 1992.

National Research Council. (2003) Managing Carbon Monoxide Pollution in Meteorological and Topographical Problem Areas. The National Academ ies Press, Washington, D.C.

U.S. Environmental Protection Agency. (1979a) Air Quality Criteria for Carbon Monoxide. Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Research Triangle Park, NC. EPA-600/8-79-022.

U.S. Environmental Protection Agency. (1979b) Assessment of Adverse Health Effects from Carbon Monoxide and Implications for Possible Modifications of the Standard

. Office of Air Quality Planning and Standards, Research Triangle Park, NC.

U.S. Environmental Protection Agency. (1984a) Revised Evaluation of Health Effects Associated with Carbon Monoxide Exposure: An Addendum to the 1979 EPA Air Quality Criteria Document for Carbon Monoxide. Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Research Triangle Park, NC. EPA-600/8-83-033F

U.S. Environmental Protection Agency. (1984b) Review of the NAAQS for Carbon Monoxide: Reassessment of Scientific and Technical Information. Office of Ai r Quality Planning and Stan dards, Research Triangle Park. NC. EPA-450/584-904

U.S. Environmental Protection Agency. (1991) Air Quality Criteria for Carbon Monoxide. Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Research Triangle Park, NC. EPA/600/8-90/045F.

U.S. Environmental Protection Agency. (1992) Review of the National Ambient Air Quality Standards for Carbon Monoxide: Assessment of Scientific and Technical In formation, OAQPS Staff Pape r. Office of Air Quality Planning and Standards, Research Triangle Park, NC. EPA/452/R-92-004.1-16 U.S. Environmental Protection Agency. (2000) Air Qua lity Criteria for Carbon Monoxide. National Center for Environmental Assessment, Research Triangle Park, NC. EPA/600/P-99/001F. Available at: http://cfpub.epa.gov/ncea/cfm/r ecordisplay.cfm?deid=18163

U.S. Environmental Protection Agency. (2008a) Draft Pl an for Review of the National Ambient Air Quality Standards for Carbon Monoxide. Also known as Draft Integrated Review Plan . National Center for Environmental Assessment and Office of Air Quality Pl anning and Standards, Research Triangle Park, NC. EPA-452/D-08-001. Available a t: http://www.epa.gov/ttn/naaqs/standards/co/s_co_cr_pd.html.

U.S. Environmental Protection Agency. (2008b) Plan for Re view of the National Ambient Air Quality Standards for Carbon Monoxide. Also known as Integrated Review Plan . National Center for Environmental Assessment and Office of Air Quality Planning and Standards, Research Triangle Park, NC. EPA-452/R-08-005. Available at: http://www.epa.gov/ttn/naa qs/standards/co/s_co_cr_pd.html.

U.S. Environmental Protection Agency. (2009a) Integrated Science Assessment for Carbon Monoxide, First External Review Draft. National Center for Envi ronmental Assessment, Research Triangle Park, NC. EPA/600/R-00/019. Available at: http://www.epa.gov/ttn/naaqs/standards/co/s_co_cr_isa.html

U.S. Environmental Protection Agency. (2009b) Integrated Science Assessment for Carbon Monoxide, Second External Review Draft. National Center for Envi ronmental Assessment, Research Triangle Park, NC. EPA/600/R-09/019B. Available at: http://www.epa.gov/ttn/naaqs/standards/co/s_co_cr_isa.html

U.S. Environmental Protection Agency. (2009c) Carbon Mo noxide National Ambient Air Quality Standards: Scope and Methods Plan for Health Risk and Exposure Asse ssment. Draft. Office of Air Quality Planning and Standards, Research Triangle Park, NC . EPA-452/R-09-004. Available at: http://www.epa.gov/ttn/naaqs/st andards/co/s_co_cr_pd.html

U.S. Environmental Protection Agency. (2009d) Risk and Exposure Assessment to Support the Review of the Carbon Monoxide Primary National Ambient Air Quality Standards, First External Review Draft. Office of Air Quality Planning and Standards, Research Tria ngle Park, NC. EPA-452/P-09-008. Available at: http://www.epa.gov/ttn/naaqs/st andards/co/s_co_cr_rea.html

U.S. Environmental Protection Agency. (2010a) Integrated Science Assessment for Carbon Monoxide. National Center for Environmental Assessment, Research Triangle Park, NC. EPA/600/R-09/019F. Available at: http://www.epa.gov/ttn/naaqs/sta ndards/co/s_co_cr_isa.html

U.S. Environmental Protection Agency. (2010b) Quantitative Risk and Exposure Assessment for Carbon Monoxide - Amended. Office of Air Quality Planning and Stan dards, Research Triangle Park, NC. EPA-452/R-10- 009. Available at: http://www.epa.gov/ttn/naaqs/standards/co/s_co_cr_rea.html

U.S. Environmental Protection Agency. (2010c) Risk and Exposure Assessment to Support the Review of the Carbon Monoxide Primary National Ambient Air Quality Standards, Second Exte rnal Review Draft, U.S Environmental Protection Agency, Research Triangle Park, NC, report no. EPA-452/P-10-004. Available
at: http://www.epa.gov/ttn/naaqs/standards/co/s_co_cr_rea.html

U.S. Environmental Protection Agency. (2010d) Policy Assessment for the Review of the Carbon Monoxide National Ambient Air Quality Standards, External Re view Draft. Office of Air Quality Planning and Standards, Research Triangle Park, NC. EPA-452/P-10-005. Available at: http://www.epa.gov/ttn/naaqs/standards/co/s_co_cr_pa.html2-1 

### 2 REVIEW OF THE PRIMARY STANDARDS FOR CARBON MONOXIDE

This chapter presents staff conclusions for consideration in deciding whether the existing primary standards for carbon monoxide (CO) should be revised and, if so, what revisions are appropriate. The current primary CO standards include a 1-hour and an 8-hour standard to protect public health from exposure to CO. In evaluating the current primary NAAQS we have reviewed, and as appropriate, updat ed, a series of key policy-rele vant issues presented in the Plan for Review of the National Ambient Air Quality Standards for Carbon Monoxide (USEPA, 2008a, section 3.1). The answers to these policy -relevant questions will inform decisions on whether, and if so, how to revise the primary standards for CO. Following a background section regarding consid erations in the previous review, the discussion in this chapter focuses on two central issues related to: (1) the adequacy of the current CO standards and (2) what potentia l alternative standards, if any, should be considered in this review. Within each of these broad areas, a series of questions are addressed. The four basic elements of the NAAQS (indicator, averaging time, level, and form) are co nsidered collectively in evaluating the health protecti on afforded by the current or any potential alterna tive standards.

2.1 APPROACH

For the purposes of this Policy Assessment (P A), staff has drawn from EPA’s assessment and integrated synthesis of the scie ntific evidence presented in the Integrated Science Assessment for Carbon Monoxide (USEPA, 2010a; henceforth referred to as the ISA) and 2000 Air Quality Criteria Document for Carbon Monoxide (USEPA, 2000; henceforth referred to as the 2000 AQCD) and on the analyses presented in th e Risk and Exposure Assessment (USEPA, 2010b; henceforth referred to as the REA). The eviden ce-based discussions pres ented in this chapter draw upon evidence from epidemiologic studie s, controlled human e xposure studies, and toxicological studies evaluating shor t- or long-term exposures to CO , as discussed in chapter 5 of the ISA, with supporting evidence related to dosime try and potential mode of action as presented in chapters 4 and 5 of the ISA, respectively, as well as the integration of evidence across each of these disciplines, as presented in chapter 2 of th e ISA. The exposure/risk-based discussions have drawn from the quantitative hea lth analyses for CO presented in the REA. Together the
evidence-based and risk-based considerations have informed our conclusions related to the adequacy of the current CO standards and al ternative standards th at are supported by the currently available scientific evidence. In presenting a range of primar y standard options for consider ation, we note that the final decision is largely a public hea lth policy judgment. A final d ecision must draw upon scientific2-2 information and analyses about health effects and risks, as well as judgments about how to consider the range and magnitude of uncertainties that are inherent in the scientific evidence and analyses. Our approach to informing these judgm ents, discussed more fully below, is based on the recognition that the available health e ffects evidence generally reflects a continuum, consisting of ambient levels at which scientists generally agree that health effects are likely to occur, through lower levels at which the li kelihood and magnitude of the response become increasingly uncertain. This approach is c onsistent with the requirements of the NAAQS provisions of the Act and with how EPA and the c ourts have historically interpreted the Act. These provisions require the Administrator to establish primary st andards that, in the Administrator’s judgment, are requi site to protect public health with an adequate margin of safety. In so doing, the Administ rator seeks to establish standard s that are neither more nor less stringent than necessary for this purpose. The Ac t does not require that pr imary standards be set at a zero-risk level, but rath er at a level that avoids un acceptable risks to public health. The following subsections include background in formation on the approach used in the previous review of the CO sta ndards (section 2.1.1) and also a di scussion of the approach for the current review (section 2.1.2).

2.1.1 Approach Used in the Previous Review

The current primary standards for CO are se t at 9 parts per million (ppm) as an 8-hour average and 35 ppm as a 1-hour aver age, neither to be exceeded more than once per year. These standards were initially set in 1971to protect against th e occurrence of carboxyhemoglobin (COHb) levels that may be associated with eff ects of concern (36 FR 8186). Reviews of these standards in the 1980s and early 1990s identified additional evid ence regarding ambient CO, CO exposures, COHb levels, and associated he alth effects (USEPA, 1984a, 1984b; USEPA, 1991; USEPA, 1992; McClellan, 1991, 1992). Assessment of the evidence in t hose reviews led the EPA to retain the existing standa rds without revision (59 FR 38906). The 1994 decision to retain the primary st andards without revision was based on the evidence published through 1990 and review ed in the 1991 AQCD (USEPA, 1991), the 1992 Staff Paper assessment of the policy-relevant information containe d in the AQCD and the quantitative exposure assessment (USEPA, 1992) , and the advice and recommendations of CASAC (McClellan 1991, 1992). At that time, as at the time of the prior NAAQS review (50 FR 37484), COHb levels in blood were recognized as the most useful estimates of exogenous CO exposures and to serve as the best biomarker of CO toxicity for ambient-level exposures to CO. Consequently, COHb levels were used as the indicator of health effects in the identification
of health effect levels of concern for CO (59 FR 38909).2-3 In reviewing the standards in 1994 the Admi nistrator first rec ognized the need to determine the COHb levels of concern “taking into account a large and diverse health effects
database.” The more uncertain and less quantifiable ev idence was taken into account to identify the lower end of this range to prov ide an adequate margin of safety for effects of clear concern. To consider ambient CO concentrations likely to result in COHb levels of concern, a model
solution to the Coburn-Forster-Kan e (CFK) differential equation was employed in the analysis of CO exposures expected to occur under air quality scenar ios related to just meeting the current 8- hour CO NAAQS, the contro lling standard (USEPA, 1992). 1 Key considerations in this approach are described below.

Carboxyhemoglobin Levels of Concern and Margin of Safety
The assessment of the science that wa s presented in the 1991 AQCD (USEPA, 1991)
indicated that CO is associated with effects in the cardiovascular system , central nervous system (CNS), and the developing fetus. Additionally, f actors recognized as having potential to alter the effects of CO included exposures to other po llutants, some drugs and some environmental factors, such as altitude. Cardiovascular effect s of CO, as measured by decreased time to onset of angina and to onset of significant elec trocardiogram (ECG) ST-segment depression 2 were judged by the Administrator to be “the health e ffects of greater concern, which clearly had been associated with CO exposures at levels observed in ambient air” (59 FR 38913). Based on the consistent findings of response in patients with coronary artery disease 3

across the controlled human e xposure evidence (Adams et al., 1988; Allred et al., 1989a, 1989b, 1991; Anderson et al., 1973; Kleinman et al., 1989, 1998; Sheps et al., 1987 4 ) and discussions of

1 Air quality analyses of CO levels in the U.S. consistently demonstrate that meeting the 8-hour standard results in 1-hour maximum concentrations well below the corresponding 1-hour standard.

2 The ST-segment is a portion of the electrocardiogram, depression of which is an indication of insufficient oxygen supply to the heart muscle tissue (myocardial ischemia). Myocardial ischemia can result in chest pain (angina pectoris) or such characteristic changes in ECGs or both. In individuals with coronary artery disease, it tends to occur at specific levels of ex ercise. The duration of exercise require d to demonstrate chest pain and/or a 1- mm change in the ST segment of the ECG were key measurem ents in the multicenter study by Allred et al (1989a, 1989b, 1991).

3 Coronary artery disease (CAD), often also called coronary heart disease or ischemic heart disease is a category of cardiovascular disease associ ated with narrowed heart arteries. Individuals with this disease may have myocardial ischemia, which occurs when the heart muscle receives insufficient oxygen delivered by the blood. Exercise-induced angina pectoris (chest pain) occurs in many of them. Among all patients with diagnosed CAD, the predominant type of ischemia, as identified by ST segment de pression, is asymptomatic (i.e., silent). Patients who experience angina typically have additional ischemic epis odes that are asymptomatic (2000 AQCD, section 7.7.2.1). In addition to such chronic conditions, CAD can lead to s udden episodes, such as myo cardial infarction (ISA, p. 5- 24).

4 Statistical analyses of the data from Sheps et al., (1987) by Bissette et al (1986) indicate a significant decrease in time to onset of angina at 4.1% COHb if subjects that did not experience exercise-induced angina during air exposure are also included in the analyses.2-4 adverse health consequences in the 1991 AQCD and the 1992 Staff Paper, at the CASAC meetings and in the July 1991 CA SAC letter, the Administrator concluded that “CO exposures resulting in COHb levels of 2.9- 3.0 percent (CO-Ox) or higher in persons with heart disease have the potential to increase the risk of decreased time to onset of angina pain and ST-segment depression” (59 FR 38913). Two of the five key studies were given par ticular emphasis in the 1991 AQCD to indicate the basis fo r conclusions regarding lowest observed-effect levels of COHb in patients with exercise-induced isch emia, in terms of measured COHb and its representation in terms of increase from baseline COHb on the order of 1.5 to 2.2% (USEPA, 1991, pp. 1-11 to 1-12; Allred et al., 1989a, 1989b, 1991; Anderson et al., 1973). While EPA and CASAC recognized the existe nce of a range of views among health professionals on the clinical signi ficance of the responses observ ed in the clinical studies,
CASAC noted that the dominant vi ew was that they should be c onsidered “adverse or harbinger of adverse effect” (McClellan, 1991) and EPA rec ognized that it was “impor tant that standards be set to appropriately reduce the risk of ambient exposures which produce COHb levels that could induce such potentially adve rse effects” (59 FR 38913) as those occurring at COHb levels of 2.9-3.0% (CO-Ox) representing an increase on the order of 1.5 to 2.2 percent above baseline (59 FR 38913; USEPA, 1991, p. 1-12; USEPA, 1992, pp. 20-22). In further considering
additional results from the cont rolled human exposure evidence as well as other aspects of the available evidence and uncertainties regardi ng modeling estimates of COHb formation and human exposure to COHb levels in the population associated with attainment of a given CO NAAQS, the Administrator recognized the need to extend the range of COHb levels for consideration in evaluating whether the current CO standards provide an adequate margin of safety to those falling between 2.0 to 2.9 (59 FR 38913). Factors considered in recognizing this margin of safety included the following (59 FR 38913).

 Uncertainty regarding the clinical importance of cardiovascular effects associated with exposures to CO that resulted in COHb levels of 2 to 3 percent. Although recognizing the possibility that there is no threshold for these effects even at lower COHb levels, the health significance of the small changes observed for ST-segment depression at 2.0 COHb (Allred et al., 1989a,b) was described as appearing to be “rel atively trivial” (59 FR 38913).

 Findings of short-term reduction in maxi mal work capacity measured in trained athletes exposed to CO at levels resulti ng in COHb levels of 2.3 to 7 percent.

 The potential that the most sensitive indi viduals have not been studied, the limited information regarding the effects of ambien t CO in the developing fetus, and concern about visitors to high altitudes, individuals w ith anemia or respiratory disease, or the elderly.2-5  Potential for short term peak CO exposur es to be responsible for impairments (impairment of visual perception, sensorimot or performance, vigilance or other CNS effects) which could be a matter of concern fo r complex activities such as driving a car, although these effects had not been demonstrated to be caused by CO concentrations in ambient air.

 Concern based on limited evidence for individua ls exposed to CO concurrently with drugs (e.g., alcohol), during heat stress, or co-exposure to other pollutants.

 Uncertainties, described as “l arge,” that remained regard ing modeling COHb formation and estimating human exposure to CO which could lead to overestimation of COHb levels in the population associated with attainment of a given CO NAAQS.

 Uncertainty associated with COHb measur ements made using CO-Ox which may not reflect COHb levels in angina patients studied, thereby creating uncertainty in establishing a lowest effects level for CO. Based on these considerations of the evidence, the Administrator identified a range of COHb levels of concern extending from 2.9% at the upper end down to 2% at the lower end and concluded that “evaluation of the adequacy of the current standard s hould focus on reducing the

number of individuals with car diovascular disease from being exposed to CO levels in the

ambient air that would result in COHb levels of 2.1 percent”. She additionally concluded that standards that “protect against COHb levels at the lower end of the range should provide an adequate margin of safety against effects of un certain occurrence, as well as those of clear

concern that have been associated with COHb levels in the upper-e nd of the range” (59 FR 48914).

Estimation of Population Exposures To estimate CO exposures and resulting COHb levels that might be expected under air quality conditions that just met the current standards, an analys is of exposure and associated
internal dose in terms of COHb levels in the population of interest in the city of Denver, Colorado was performed (59 FR 38906; USEPA, 1992). That analysis indicated that if the 9 ppm 8-hour standard were just met, the proportion of the nonsmoking population with cardiovascular disease experiencing a daily maxi mum 8-hour exposure at or above 9 ppm for 8 hours decreased by an order of magnitude or more as compared to the proportion under thenexisting CO levels, down to less than 0.1 percent of the total person-days in that population. More specifically, upon meeting the 8-hour standa rd, EPA estimated that less than 0.1% of the nonsmoking cardiovascular-disease population would experience a COHb level greater than or equal to 2.1%. A smaller percentage of the at-risk population was estimated to exceed higher2-6 COHb levels. 5 Based on these estimates, the Administrator concluded that “relatively few people of the cardiovascular sensitive population group analyzed will experience COHb levels ≥ 2.1 percent when exposed to CO levels in absenc e of indoor sources when the current standards are attained.” The analysis also took into account that certain i ndoor sources (e.g., passive smoking, gas stove usage) contributed to tota l CO exposure and EPA recognized that such sources may be of concern for such high risk grou ps as individuals with cardiovascular disease, pregnant women, and their unborn children but concluded that “the contribution of indoor sources cannot be effectively mitigated by ambient air quality standards” (59 FR38914).

Decision Regarding Adequacy of the Standards
Based on consideration of the evidence and the quantitative results of the exposure assessment, the Administrator conc luded that revisions of the cu rrent primary standards for CO were not appropriate at that time (59 FR 38914). The Administrator additionally concluded that both averaging times for the primary standards, 1 hour and 8 hours, be retained. The 1-hour and 8-hour averaging times were first chosen when EPA promulgated the primary NAAQS for CO in 1971. The selection of the 8-hour averaging time was based on the following: (a) most individuals’ COHb levels appeared to approach equilibrium after 8 hours of exposure, (b) the 8- hour time period corresponded to the blocks of time when people were often exposed in a particular location or activity (e.g., working or sleeping), and (c) judgment that this provided a good indicator for tracking continuous expos ures during any 24-hour period. The 1-hour averaging time was selected as better represen ting a time period of intere st to short-term CO exposure and providing protection from effects which might be en countered from very short duration peak exposures in the urban environment (59 FR 38914).

2.1.2 Approach for the Current Review

To evaluate whether it is appropriate to consider reta ining the current primary CO standards, or whether considerati on of revisions is appropriate, we adopted an approach in this review that builds upon the general approach used in the last re view and reflects the broader body of evidence and information now available. As summarized above, the Administrator’s decisions in the previous review were based on an integration of information on health effects associated with exposure to ambient CO; expert judgment on the adversity of such effects on individuals; and policy j udgments as to when the standard is requisite to protect public health

5 In the 1992 assessment, the person-days (number of persons multiplied by the number of days per year exposed) and person-hours (number of persons multiplied by the number of hours per year exposed) were the reported exposure metrics. Upon meeting the 8-hour sta ndard, it was estimated that less than 0.1% of the total person-days simulated for the nonsmoking cardiovascular-disease population were associated with a maximum COHb level greater than or equal to 2.1% (USEPA, 1992; Johnson et al., 1992).2-7 with an adequate margin of safety, which were informed by air quality and related analyses, quantitative exposure and risk as sessments when possible, and qua litative assessment of impacts that could not be quantified. In conducting this assessment, we draw on the current evid ence and quantitative assessments of exposure pertaining to the public h ealth risk of ambient CO . In considering the
scientific and technical informati on, we consider both the informati on available at the time of the last review and information newly available sinc e the last review, including the current ISA and the 2000 AQCD (USEPA, 2010; USEPA, 2000), as we ll as current and preceding quantitative exposure/risk assessments (USEPA 2010b; Johnson et al., 2000; USEPA 1992). As was the case at the time of the last review, th e best characterized health effect associated with CO levels of concern is hypoxia (reduced oxyge n availability) induced by incr eased COHb levels in blood (ISA, section 5.1.2). Accordingly, CO exposure is of particular concern for those with impaired cardiovascular systems, and the most compelling ev idence of cardiovascular effects is that from
a series of controlled human exposure studies among exercising i ndividuals with coronary heart disease (CHD) also referred to as coronary ar tery disease (CAD) (ISA, sections 5.2.4 and 5.2.6). Additionally available in this re view are a number of epidemiologi cal studies that investigated
the association of cardiovascular disease-related h ealth outcomes with concentrations of CO at
ambient monitors. To inform our review of the ambient standards, we performed a quantitative exposure and dose modeling analysis that estimated COHb levels associated with different air quality conditions in simulated at-risk populations in two U.S. cities. Thus, in developing
conclusions in this review as di scussed in sections 2.2 and 2.3 below, we have taken into account both evidence-based and exposure/ri sk-based considerations fram ed by a series of key policyrelevant questions.2-8 2.2 ADEQUACY OF THE CURRENT STANDARD

In considering the adequacy of the current CO standards, the overarching question we
consider is:

 Does the currently available scientific evidence- and exposure/risk-based information, as reflected in the ISA a nd REA, support or call into question the adequacy of the protection afforded by the current CO standards? To assist us in interpreting the currently av ailable scientific evidence and the results of recent quantitative exposure/risk analyses to addr ess this question, we have focused on a series of more specific questions, pos ed within sections 2.2.1 and 2.2.2 below. In considering the
scientific and technical informati on, we consider both the informati on available at the time of the last review and information newly available sinc e the last review which has been critically analyzed and characterized in the 2000 AQCD and more recently in the ISA.

2.2.1 Evidence-based Considerations

In considering the evidence with regard to th e issue of adequacy of the current standard, we address a series of questions that focus on policy-relevant as pects of the evidence beginning with the health effects associated with CO expos ure, followed by the use of COHb levels as the indicator of CO exposures and biomarker for ch aracterizing the potential for health effects associated with exposures to ambient CO, and then the identification of the populations most susceptible to the effects of CO. We next consider the evidence regarding the levels of CO in
ambient air associated with health effects and the important uncertainties associated with the
evidence.

 Does the current evidence alter our conc lusions from the previous review regarding the health effects associated with exposure to CO?

The current evidence continue s to support our conclusions from the previous review regarding key health eff ects associated with CO exposure. Th e best characterized effect of CO
continues to be related to the bi nding of CO to blood Hb to form increased levels of COHb (ISA, sections 4.1 and 5.1.2) and the primary focus is on associated cardiov ascular effects (ISA, section 5.2). In the scientific assessment for the current review, a likely causal relationship is judged to exist between relevant CO exposures 6 and cardiovascular eff ects (ISA, section 2.5.1)
which is similar to conclusions in the last review. The evidence for effects on the central nervous system, birth outcomes and developmental e ffects, and respiratory effects, in some cases expanded from that which was availa ble at the time of the last re view, is judged to be suggestive

6 Relevant CO exposures are defined in the ISA as "generally within one or two orders of magnitude of ambient CO concentrations" (ISA, section 2.5).2-9 of a causal relationship with relevant CO expos ures (ISA, section 2.5). These overall findings, additional details of which are described below, are consistent with and extend in some ways
conclusions drawn from the health ef fects evidence in the last review. The long-standing body of evidence that has es tablished many aspects of the biological
effects of CO continues to cont ribute to our understanding of the health effects of ambient CO. Binding to heme proteins and the alteration of their function is the common mechanism underlying biological responses to CO. Upon i nhalation, CO diffuses through the respiratory zone (alveoli) to the blood where it binds to Hb, forming COHb. Accordingly, inhaled CO
elicits various health effects th rough binding to, and associated alteration of the function of, a number of heme-containing molecules, mainly Hb (see e.g., ISA, section 4.1). The best
characterized health effect a ssociated with CO levels of concern is hypoxia (reduced oxygen availability) induced by increased COHb levels in blood and decreased o xygen availability to critical tissues and organs, specifically the he art (ISA, section 5.1.2). Consistent with this,
medical conditions that affect the biological mechanisms to compensate for this effect (e.g., vasodilation and increased coronary blood fl ow with increased oxygen delivery to the myocardium) can contribute to a reduced amount of oxygen available to key body tissues, potentially affecting organ system function a nd limiting exercise capaci ty (2000 AQCD, section 7.1). 7 The dose metric most commonly used as a bi oindicator of exposure and health risk from
CO is the level of COHb in the blood (1991 AQCD, 2000 AQCD, 2010 ISA). The body of health effects evidence for CO has grown considerably since the review completed in 1994 with the addition of numerous epidemiological and toxicological studies (ISA; 2000 AQCD). This evidence provides ad ditional detail and support to our prior understanding of CO effects and population susceptibilit y. For example, the currently available evidence expands on potential nonhy poxic mechanisms for CO effects, although the importance of such mechanisms at environmentally-relevan t CO exposures is uncle ar (ISA, section 5.1.3). Most notably, the current evidence includes much expanded epidemiological evidence that is consistent with previous conclu sions regarding cardiovascular di sease-related susceptibility and may provide indications of air qua lity conditions that may be asso ciated with ambient CO-related risk. In this review, the clearest evidence is available for cardiovasc ular effects. In the ISA, the
evidence is characterized as to likelihood of causal relationships between exposure to ambient CO and specific health effects using an estab lished framework (ISA, ch apter 1). The major conclusion drawn in the ISA regarding the critical analysis of all availabl e data on health effects of CO including the clinical a nd epidemiological evidence is that "Given the consistent and

7 People with peripheral vascular diseases and heart disease patients often have markedly reduced circulatory capacity and reduced ability to compensate for increased circulatory demands during exercise and other stress (2000 AQCD, p. 7-7).2-10 coherent evidence from epidemiologic and human clinical studies, along with biological plausibility provided by CO’s role in limiting oxygen avai lability, it is conc luded that a causal relationship is likely to exist between relevant 8 short-term CO exposures and cardiovascular morbidity" (ISA, p. 2-6, section 2.5.1). Additiona lly, as mentioned above, the ISA judges the evidence to be suggestive of causal relationships between relevant shor t- and long-term CO exposures and CNS effects, birth outcomes a nd developmental effects following long-term exposure, respiratory morbidity following short- term exposure, and mortality following shortterm exposure (ISA, section 2.5, Table 2-1). The IS A concludes there is not likely to be a causal relationship between relevant long-term CO exposures and mortality (ISA, Table 2-1). Similar to the previous re view, results from controlled human exposure studies of individuals with coronary arte ry disease (Adams et al., 1988 ; Allred et al., 1989a, 1989b, 1991; Anderson et al., 1973; Kleinman et al., 1989, 1998; Sheps et al., 1987 9 ) are the “most compelling
evidence of CO-induced effects on the cardiovascul ar system” (ISA, Section 5.2). Additionally,
the use of an internal dose metr ic, COHb, adds to the strength of the findings in these controlled exposure studies. As a group, th ese studies demonstrate the ro le of CO in increasing the susceptibility of people with CAD to incidents of exercise-associated myocardial ischemia. Toxicological studies described in the current review provide evidence of CO effects on the cardiovascular system, including el ectrocardiographic eff ects of 1-hour exposures to 35 ppm CO in a rat strain developed as an animal mode l of cardiac susceptibilit y (ISA, section 5.2.5.3). Further toxicological evidence is identified for other effects (e.g., aortic injury, microvascular permeability, vascular remodeling, ventricular hype rtrophy) occurring at laboratory animal CO exposure levels ranging up to 200 ppm for multiple durations, including much longer than 1 hour (ISA, section 5.2.5). Among the controlled human exposure studies, the ISA places principal emphasis on the study of CAD patients by Allred et al. (1989a, 1989b, 1991) 10 which was key to considerations from the previous review for the following r easons: 1) dose-respons e relationships were observed; 2) effects were obser ved at the lowest COHb levels tested (mean of 2-2.4% COHb 11

8 Relevant CO exposures are defined in the ISA as "generally within one or two orders of magnitude of ambient CO concentrations" (ISA, section 2.5).

9 See footnote 4 above.

10 Other controlled human exposure studies of CAD patients (listed in Table 2-2 below, and discussed in more detail in the 1991 and 2000 AQCDs) similarly provid e evidence of reduced time to exercise-induced angina associated with elevated COHb resulting from controlled sh ort-duration exposure to increased concentrations of CO.

11 These levels and other COHb levels described for this study below are based on GC analysis unless otherwise specified. Based on matched measurements available for CO-oximetry (CO-Ox) and gas chromatography (GC) in this study, staff note that CO-Ox measurements of 2.9 to 3.0 percent COHb appear to correspond to GC measurements on the order of 2% (Allred et al., 1991)2-11 following experimental CO exposure), with no evid ence of a threshold; 3) objective measures of myocardial ischemia (ST-segment depression) we re assessed, as well as the subjective measure of decreased time to induction of angina; 4) measurements were taken both by gas chromatography (GC), which provides a more accurate measurement of COHb blood levels 12

, and by CO-Ox; 5) a large number of study subjects were used; 6) a st rict protocol for selection of study subjects was employed to include only CAD patients with reproducible exercise-induced angina.; and 7) the study was conducted at multiple laboratories around the U.S. This study evaluated changes in time to exercise-induced onse t of markers of myocardial ischemia resulting from two short CO exposures targeted to result in mean study subject C OHb levels of 2% and 4%, respectively (ISA, section 5.2.4). In this st udy, subjects (n=63) on th ree separate occasions underwent an initial graded exercise treadmill test, followed by 50 to 70-minute exposures under resting conditions to room air CO concentrations or CO concentr ations targeted for each subject
to achieve blood COHb levels of 2% and 4%. Th e exposures were to average CO concentrations of 0.7 ppm (room air concentration range 0-2 ppm), 117 ppm (range 42-202 ppm) and 253 ppm (range 143-357 ppm). After the 50- to 70-minute exposures, subjects unde rwent a second graded exercise treadmill test, and the percent change in time to onset of angina and time to ST endpoint
between the first and second exercise tests wa s determined. For the two CO exposures, the average post-exposure COHb concentrations were reported as 2.4% and 4.7%, and the subsequent post-exercise aver age COHb concentrations were reported as 2.0% and 3.9%. 13 Across all subjects, the mean time to angina onset for control (“r oom” air) exposures was approximately 8.5 minutes, and the mean time to ST endpoint was approximately 9.5 minutes (Allred et al., 1989b). Relative to room-air exposure that resu lted in a mean COHb level of 0.6% (post-exercise), exposure to CO resulting in post-exercise mean COHb concentrations of
2.0% and 3.9% were observed to decrease the exercise time required to induce ST-segment depression by 5.1 (p=0.01) and 12.1% (p<0.001) , respectively. These changes were well
correlated with the onset of ex ercise-induced angina, the time to which was shortened by 4.2%

12 As stated in the ISA, the gas chromatographic t echnique for measuring COHb levels “is known to be more accurate than spectrophotometric measurements, particularly for sample s containing COHb concentrations < 5%” (ISA, p. 5-41). CO-oximetry is a spectrophotometric method commonly used to rapidly provide approximate concentrations of COHb during controlled exposures (ISA, p. 5-41). At the low concentrations of COHb (<5%) more relevant to ambient CO exposures, co-oximeters are reported to overestimate C OHb levels compared to GC measurements, while at higher concentrations, this method is reported to produce underestimates (ISA, p.4-18).

13 While the COHb blood level for each subject during the exercise tests was intermediate between the post-exposure and subsequent post-exercise measurements (e.g., mean 2.0-2.4% and 3.9-4.7%), the study authors noted that the measurements at the end of the exercise test represented the COHb concentrations at the approximate time of onset of myocardial ischemia as indicated by angina and ST segment changes. The corresponding ranges ofCO-Ox measurements for the two exposures were 2.7-3.2% and 4.7-5.6%. In this document, we refer to the GCmeasured mean of 2.0% or 2.0-2.4% for the COHb leve ls resulting from the lower experimental CO exposure.2-12 (p=0.027) and 7.1% (p=0.002), respec tively, for the two experimental CO exposures (Allred et al., 1989a, 1989b, 1991). 14 As at the time of the last re view, while ST-segment depression is recognized as an indicator of myocardial isch emia, the exact physiologi cal significance of the observed changes among those with CAD is unclear (ISA, p. 5-48). No human clinical studies have been specifi cally designed to eval uate the effect of controlled short-term exposures to CO resulting in COHb levels lower than a study mean of 2% (ISA, section 5.2.6). However, an important fi nding of the multi-laboratory study was the doseresponse relationship (discussed further in addr essing a subsequent question below) observed between COHb and the markers of myocardial is chemia, with effects observed at the lowest increases in COHb tested, without evidence of a measurable thresh old effect. As reported by the authors, the results comparing “the effects of increasing COHb from baseline levels (0.6%) to 2 and 3.9% COHb showed that each produced fu rther changes in objec tive ECG measures of ischemia” implying that “small increments in CO Hb could adversely affect myocardial function and produce ischemia” (Allred et al., 1989b, 1991). The epidemiological evidence has expanded cons iderably since the la st review including numerous additional studies that are coherent with the evidence on markers of myocardial ischemia from controlled human exposure studie s of CAD patients (ISA, section 2.7). The most recent set of epidemiological studies in the U.S. have evaluated the associations between ambient concentrations of multiple pollutants (i.e. fine particles or PM 2.5 , nitrogen dioxide, sulfur dioxide, ozone, and CO) at fixed-site ambient monitors a nd increases in emergency department visits and hospital admissions for specific cardiovascular h ealth outcomes including ischemic heart disease (IHD), myocardial infarction (MI), congestive heart fail ure (CHF), and cardi ovascular diseases (CVD) as a whole (Bell et al ., 2009; Koken et al., 2003; Linn et al., 2000; Mann et al., 2002; Metzger et al., 2004; Symons et al., 2006; Tolbert et al., 2007; We llenius et al., 2005). Findings of positive associations for these outcomes with metrics of ambient CO concentrations are
coherent with the evidence from controlled hum an exposure studies of myocardial ischemiarelated effects resulting from elevated CO e xposures (ISA, section 2.5.1; ISA, Figure 2-1). Table 2-1 below presents studi es reporting associations of ambient CO concentration
estimates for several U.S. urban areas with hos pital admissions for ischemic heart disease, cardiovascular disease or congestiv e heart failure described in th e ISA (ISA, Figures 5-2, 5-5 and 5-4). Presented first in Table 2-1 are the U.S. studies reporting associations with ischemia-

14 Another indicator measured in the study was the combination of heart rate and systolic blood pressure which provides a clinical index of the work of the heart and myocardial oxygen consumption, since heart rate and blood pressure are major determinants of myocardial oxygen consumption (A llred et al., 1991). A decrease in oxygen to the myocardium would be expected to be paralleled by ischemia at lower heart rate and systolic blood pressure. This heart rate-systolic blood pressure indicator at the time to ST-endpoint was decreased by 4.4% at the 3.9% COHb dose level and by a nonstatistically-significant, smaller amount at the 2.0% COHb dose level.2-13 related health outcomes as the studied outcomes most explicitly consistent with the role of CO in limiting oxygen availability. In th ese studies, the ambient CO concentration averaging time for which health outcomes were analyzed varied from 1 hour to 24 hours, with the air quality metrics based on either a selected central-site monitor for the area or an average for multiple monitors in the area of interest. The study ar eas include the Atlanta, Georgia metropolitan statistical area, the greater Los Angeles, Cali fornia, area and a group of 126 urban counties. Together the individual study periods spanned the years from 1988 through 2005. The risk estimates from these studies presented here indicat e statistically significant positive associations
were observed with ambient CO concentrations based on air quality fo r the day of hospital admission or based on the average of the selected ambient CO concentration metric across that day and 2 or 3 days previous (ISA, Figures 5-2 and 5-5). Many of the studies for these outcomes include same day or next day la g periods, which, as noted in th e ISA “are consistent with the propose mechanism and biological plausibility of these CVD outcomes” (ISA, p. 5-40). Of the
studies for which estimates shown in Table 2-1 are based on multi-day averages (the Atlanta
studies and the California st udy by Mann et al., 2002), the Calif ornia study by Mann et al., (2002) also observed a significant positive asso ciation with same da y CO concentration. Additionally presented in Table 2-1 are the U.S. studies reporting associations with hospital admissions for CHF, a co ndition that affects an individua l’s ability to compensate for reduced oxygen availability. One of the IHD outcome studies cited above also reported a significant association for ambien t CO with hospital admissions for CHF (Linn et al., 2000), as did additional studies in Allegheny County (P ittsburgh) for 1987-1999 study period, and Denver for the months of July-August during 1993-1997 (Koken et al., 2003; Wellenius et al., 2005; ISA, pp. 5-31 to 5-33). The risk estimates presen ted for all three of these studies are based on the 24-hour CO concentration, with the Califor nia and Allegheny Count y studies’ association with same-day air quality, while the associati on shown for the Denver st udy was with ambient CO 3 days prior to health outcome (Table 2-1).2-14Table 2-1.U.S. epidemiological studies for ischemic heart disease, cardiovascular disease and congestive heart failure.Study ReferenceHealthOutcomeARisk EstimateB(confidence interval)Estimates arestandardized withinaveraging times.CO Concentration Metric forRisk Estimated PresentedAssignment ofMonitors to StudySubjectsStudy AreaStudy TimePeriodU.S. studies of hospital admissions for coronary heart disease (ISA, Figure 5-2).Metzger et al., 2004IHD1.016 (0.999-1.034)1-hour daily maximum, average formost recent 3 daysSingle central residentialmonitor20-county Atlanta area 1993-2000IHD 1.0136 (1.0053-1.0220)Mann et al., 2002IHD+CHF 1.0304 (1.0135-1.0475)8-hour daily maximum, average formost recent 4 daysResidence grid centroidinterpolated from 3 closestmonitorsSouth Coast Air Basin,CA1988-1995Linn et al., 2000MI 1.020 (1.011-1.029) 24-hour average, same day Average across all monitors “ 1992-1995U.S. studies of hospital admissions for cardiovascular disease (ISA, Figure 5-5).Bell et al., 2009CVD 65+ 1.0096 (1.0079-1.0112) 1-hour daily maximum, same dayAverage of monitors incounty of residence126 urban counties 1999-2005Tolbert et al., 2007CVD 1.016 (1.008-1.025)1993-2004Metzger et al., 2004CVD 1.017 (1.008–1.027)1-hour daily maximum, average formost recent 3 daysSingle central residentialmonitor20-county Atlanta area1993-2000Linn et al., 2000CVD 1.016 (1.013-1.019) 24-hour average, same day Average across all monitorsSouth Coast Air Basin,CA1992-1995U.S. studies of hospital admissions for congestive heart failure (ISA, Figure 5-4).Linn et al., 2000CHF 1.013 (1.004-1.021) 24-hour average, same day Average across all monitorsSouth Coast Air Basin,CA1992-1995Metzger et al., 2004CHF 1.010 (0.988-1.032)1-hour daily maximum, average formost recent 3 daysSingle central residentialmonitor20-county Atlanta area 1993-2000Symons et al., 2006CHF 1.08 (0.40-2.99)8-hour daily maximum, average formost recent 4 daysSingle central residentialmonitorBaltimore area, MD 2002 (April-Dec)Wellenius et al., 2005CHF 1.0843 (1.0614-1.1077) 24-hour average, same daySingle area-widerepresentation based on 3monitorsAllegheny county, PA 1987-1999Koken et al., 2003CHF 1.181 (1.002-1.393) 24-hour average, 3 days prior Average across all monitors Denver county, CO1993-1997(Jul-Aug)A Hospital admissions for ischemic heartdisease (IHD), myocardial infarction (MI), cardiovascular disease (CVD; Bell 2009 included only subjects 65 yearsold and above), and congestiveheart failure (CHF).B Unadjusted for other pollutants and standardized for 1 ppm increase in CO concentration for 1-hour metric, 0.75 ppm for 8-hour metric and 0.5 ppm for 24-hour metric.2-15 As noted by the ISA, “[s]tudies of hospital admissions and ED visits for IHD provide the strongest [epidemiological] evidence of ambi ent CO being associated with adverse CVD outcomes” (ISA, p. 5-40, section 5.2.3; Linn et al ., 2000; Mann et al., 2002; Metzger et al., 2004). With regard to studies for other measures of cardiovascular morbid ity, the ISA notes that “[t]hough not as consistent as the IHD effects, the effects for all CVD hospital admissions (which include IHD admissions) and CHF hospital admissions also provide evidence for an
association of cardiovascular ou tcomes and ambient CO concentrations” (ISA, section 5.2.3; Bell et al., 2009; Tolbert et al., 2007). While noting the difficulty in determining the extent to which CO is independently associated with CVD outcomes in this group of studies as compared to CO
as a marker for the effects of another traffic- related pollutant or mix of pollutants, the ISA concludes that the epidemiological evidence, pa rticularly when considering the copollutant analyses, provides support to the clinical evidence for a direct effect of short-term ambient CO exposure on CVD morbidity (ISA, pp. 5-40 to 5-41). Additional epidemiological studies have evalua ted associations of am bient CO with other
cardiovascular effects since the last review. For example, preliminary evidence of a link between exposure to CO and alteration of bl ood markers of coagulation and inflammation in individuals with CAD or CVD has been pr ovided by a few well conducted and informative studies (ISA, Table 5-6; Delfino et al., 2008; Liao et al., 2005 ). As noted by the ISA, however, further studies are warranted to investigate the ro le of these markers in prothrombotic events and their possible contribution to th e pathophysiology of CO-induced a ggravation of ischemic heart disease (ISA, section 5.2.1.8). Other epidemiol ogical studies (includi ng field and or panel studies) also provide some evidence of a link betw een CO exposure and heart rate and heart rate variability (ISA, section 5.2.1.1). With regard to the two of three studies reporting a positive
association with heart ra te, the ISA concluded that “further research is warranted” to corroborate the results, while the larger number of studies for heart rate variability parameters is characterized as having mixed associations (ISA , p. 5-15). Additionally, of the two studies of electrocardiogram changes indi cative of ischemic events (IS A, section 5.2.1.2), one found no association and, in the other study, the associa tion with CO did not remain statistically significant in multipollutant mode ls, unlike the association with black carbon in that study (ISA, p. 5-16). A limited number of epidemiological studi es (Bell et al., 2009; Li nn et al., 2000) have investigated hospital admissions for stroke (including both hemorrhagic and ischemic forms) and generally report small or no associations with ambient CO concentra tions (ISA, section 5.2.1.9, Table 5-8 and Figure 5-3).
At the time of the last revi ew, there was evidence for eff ects other than cardiovascular morbidity, including neurological, re spiratory and developmental effe cts. These findings include the following.2-16  With regard to neurological effects, acut e exposures to CO have long been known to induce CNS effects such as those observe d with CO poisoning, although limited and equivocal evidence available at the time of th e last review included indications of some neurobehavioral effects to re sult from CO exposures resu lting in a ra nge of 5-20% COHb (2000 AQCD, section 6.3.2). No additio nal clinical or epidemiological studies are now available that investigated such eff ects of CO at ambient levels (ISA, section 5.3).

 With regard to potential eff ects of CO on birth outcomes and developmental effects, the potential vulnerability of the fetus a nd very young infant to CO was recognized during the 1994 review and in the 2000 AQCD. The CO-spe cific evidence available, however, included limited epidemiological anal yses focused primarily on very high CO exposures associated with maternal smoki ng, and animal studies involving very high CO exposures (USEPA, 1992; 2000 AQCD). The 2000 AQCD concluded that typical ambient CO levels were unlikely to cause increased fetal risk (2000 AQCD, p. 6-44). The current review includes additional ep idemiological and animal toxicological studies. The currently available ev idence includes limited but suggestive epidemiologic evidence for a CO-induced effect on preterm-birth, birth defects, decrease in birth weight, other measures of fetal growth, and infant mortality (ISA, section 5.4.3). The available animal toxi cological studies provide some support and coherence for these birth and developm ental outcomes at higher than ambient
exposures, 15 although a clear understanding of th e mechanisms underlying potential reproductive and developmental effects is still lacking (ISA, section 2.5.3).

 With regard to respiratory effects, th e 2000 AQCD concluded it unlikely that CO has direct effects on lung tissue, except at ex tremely high concentra tions (2000 AQCD, p. 6-45). There is currently lim ited, suggestive evidence of an association between shortterm exposure to CO and respiratory-related outcomes. Only prel iminary evidence is available, however, regarding a mechanism that could provide plausibility for COinduced effects (ISA, section 5.5.5.1). Thus, while there is some additional evidence on neurological, respirat ory and developmental effects, it remains limited. In summary, rather than altering our conclu sions from the previous review, the current evidence provides continued support and some additional strength to our previous conclusions regarding the health effects associated with exposure to CO and continues to indicate cardiovascular effects, particularly effects re lated to the role of CO in limiting oxygen availability, as those of greates t concern at low exposures.

15 The lowest exposures eliciting an effect in the anim al studies were exposures of 22 hours per day over about 14 prenatal days at a concentration of 12 ppm (ISA, Table 5-17).2-17  Does the current evidence continue to support a focus on COHb levels as the most useful indicator of CO exposures and the best biomarker to characterize potential for health effects associated with exposu res to ambient CO? Or does the current evidence provide support for a focus on alt ernate dose indicators to characterize potential for health effects? As discussed in both the 2000 AQCD (USEPA, 2000) and the ISA, the best characterized mechanism of action of CO is tissue hypoxia cau sed by binding of CO to hemoglobin to form COHb. Increasing levels of COHb with subsequent decrease in oxygen availability for organs and tissues are of concern in people with pr e-existing heart disease who have compromised compensatory mechanisms (e.g., lack of capacity to increase blood flow due to the inability of coronary arteries to vasodilate in response to increased CO). Th e integrative review of health
effects of CO indicates that “the clearest eviden ce indicates that indivi duals with CAD are most susceptible to an increase in CO -induced health effects” (ISA, section 5.7.8) and the evidence, including that from clinical studies described in addressing the previous question (regarding health effects associated with exposure to CO), continues to support levels of COHb as the most useful indicator of CO exposure that is related to the health effects of CO of major concern. Apart from the impaired oxygen delivery to tissues related to COHb formation, the evidence also indicates cytotoxic effects in dependent of limited oxygen availability (2000 AQCD, section 5.9; ISA, section 5.1.3). These alternative mechanisms of CO-induced effects are primarily associated with CO’s ability to bind heme-c ontaining proteins other than hemoglobin and myoglobin, and involve a wi de range of molecular targets and CO concentrations, as described in the 2000 AQCD (USEPA, 2000, secti on 5.8) and in the ISA (ISA, section 5.1.3). Older toxicological studies demons trated that exposure to high concentrations of CO resulted in altered functions of heme pr oteins other than myoglobin and hemoglobin, potentially interfering with basic cell and mol ecular processes and leadin g to dysfunction and/or disease. More recent toxicological in vitro and in vivo studies have provi ded evidence of alteration of nitric oxide signa ling, inhibition of cytochrome C oxidase, heme loss from protein, disruption of iron homeostasis and alteration of cellular reduction-oxidati on status (ISA, section 5.1.3.2). The ISA notes that these mechanisms may be interrelated. The evidence for
mechanisms related to alterati on in ion channel activity and modulation of protein kinase signaling pathways is less well understood (ISA, section 5.1.3.2). As noted in the ISA, “CO may be responsib le for a continuum of effects from cell signaling to adaptive responses to cellular injury, depending on intr acellular concentrations of CO, heme proteins and molecules which modulat e CO binding to heme proteins” (ISA, section 5.1.3.3). New research based on this evidence for pa thways other than those related to impaired oxygen delivery to tissues is need ed to further understand these pathways and their linkage to2-18 CO-induced effects in susceptible populations. Th erefore, at this time, the evidence indicates
that COHb continues to be the most useful a nd well-supported indicator of CO exposures and the best biomarker to characterize the potential for health effects associated with exposures to
ambient CO.

 Does the current evidence alter our und erstanding of populations that are particularly susceptible to CO exposu res? Is there new evidence that suggest additional susceptible populations that sh ould be given increased focus in this review? The term susceptibility has been used to recognize populations that have a greater likelihood of experiencing effects related to ambient CO exposure (ISA, section 5.7). Thus, susceptible populations are at greater risk of CO effects and are also referred to as at-risk in the
discussion here. This increased likelihood of response to CO ca n potentially result from many factors, including pre-existing medi cal disorders or disease state, lifestage, gender, lifestyle or increased exposures (ISA, section 5.7). The current evidence, while much expanded in a number of ways, continues to support our conclusions from the previous review re garding susceptible populations for exposure to
ambient CO. In the 1994 review and th e 2000 AQCD, the evidence best supported the identification of patients with CAD as a populatio n at increased risk for low levels of CO (USEPA, 1992; 2000 AQCD). Other groups were also recognized as potent ially susceptible in the 2000 AQCD based on consideration of the clinic al evidence and theoretical work, as well as laboratory animal research (2000 AQCD, p. 7-6) . These include fetuses and young infants; pregnant women; the elderly, es pecially those with compromise d cardiovascular function; people with conditions affecting oxygen absorption, blood flow, oxygen car rying capacity or transport; people using drugs with central nervous system depressant prope rties or exposed to chemical substances that increase endogenous formation of CO; and people who have not adapted to high altitude and are exposed to a combination of high altitude and CO. For these potentially susceptible groups, little empirical evidence was available by which to specify health effects
associated with ambient or near-ambie nt CO exposures (2000 AQCD, p. 7-6).
Based on the evidence from clinical studies also considered in the la st review, with which the now much-expanded epidemiological evidence base is coherent, th e population with preexisting cardiovascular disease associated with limitation in oxygen availability continues to be the best characterized population at risk of adverse CO-induced e ffects, with CAD recognized as “the most important susceptibil ity characteristic for increased risk due to CO exposure” (ISA, section 2.6.1). An important factor determining the increased susceptibilit y of this population is their inability to compensate for the reduction in oxygen levels due to an already compromised cardiovascular system. Individuals with a heal thy cardiovascular system (i.e., with healthy2-19 coronary arteries) have oper ative physiologic compensatory mechanisms (e.g., increased blood flow and oxygen extraction) for CO-induced hypoxia a nd are unlikely to be at increased risk of CO-induced effects (ISA, p. 2-10). 16 In addition, the high oxygen consumption of the heart, together with the inability to compensate for the hypoxic effects of CO ma ke the cardiac muscle of a person suffering with CAD a critical target for the hypoxic effects of CO. In the current review, recognition of suscep tibility of the popula tion with pre-existing cardiovascular disease, such as CAD, is s upported by the expanded epidemiological database, which includes a number of studies reporting si gnificant increases in hospital admissions for IHD, angina and MI in relation to CO exposures (ISA, section 2.7). Further support is provided by epidemiologic studies (Mann et al., 2002; a nd Peel et al., 2007) of increased hospital admissions and emergency department visits for IHD among individu als with secondary diagnoses for other cardiovascular outcomes incl uding arrhythmia and congestive heart failure (ISA, section 5.7), and toxicological studies repo rting altered cardiac outco mes in animal models of cardiovascular disease (ISA, section 5.2.1.9). Cardiovascular disease comprises many type s of medical disorder s, including heart disease, cerebrovascular disease (e.g., stroke), hypertension (hi gh blood pressure), and peripheral vascular diseases. Heart disease, in turn, comprises several types of disorders, including ischemic heart disease (CHD or CAD, myocardial infarction, angina), congestive heart failure, and disturbances in cardiac rhythm (2000 AQC D, section 7.7.2.1). Types of cardiovascular
disease other than those discusse d above may also contribute to increased susceptibility to the
adverse effects of low levels of CO (ISA, section 5.7.1.1). For example, some evidence with regard to other types of cardiova scular disease such as congestiv e heart failure, arrhythmia, and non-specific cardiovascular dis ease, although more limited fo r peripheral vascular and cerebrovascular disease, indicates that “the continuous nature of the progression of CAD and its close relationship with other forms of cardiovasc ular disease suggest th at a larger population than just those individuals with a prior diagnosis of CAD may be suscepti ble to health effects from CO exposure” (ISA, p. 5-117). Although there was little experimental data ava ilable at the time of the last review to adequately characterize specific health effects of CO at ambient levels for other potentially atrisk populations, several other popula tions were identified as being potentially more at risk of
CO-induced effects due to a number of factors. These factors include pre-existing diseases that could inherently decrease oxygen av ailability to tissues, lifestage vulnerabilities (e.g., fetuses,

16 The other well-studied individuals at the time of the last review were healthy male adults that experienced decreased exercise duratio n at similar COHb levels during s hort term maximal exercise. This population was of lesser concern since it represented a sma ller sensitive group, and potentially limited to individuals that would engage in vigorous exercise such as competing athletes (1991 AQCD, section 10.3.2).2-20 young infants or newborns, the elderly), gender, li festyle, medications or alterations in the physical environment (e.g., increased altitude). Th is is consistent with the ISA conclusions in the current review which recognize other populations that may be potentially susceptible to the effects of CO as continuing to include: those with other pre- existing diseases that may have already limited oxygen availability or increased COHb produc tion or levels, such as people with obstructive lung diseases, diabetes and anemia; older adults; fetuse s during critical phases of development and young infants or newborns; commute rs and those living near heavily traveled roadways; visitors to high-altitude locations ; and people ingesting medications and other substances that enhance endogenous or metabolic CO production. Preliminary evidence from epidemiol ogical, controlled human exposure, and toxicological studies suggest that people with obstructive lung di sease (e.g., COPD patients with underlying hypoxia, asthmatics) may be a suscep tible population (ISA, section 5.7.1.2). Overall, the few available epidemiological studies have reported weak, positive associations between ambient CO and CVD hospital admissions for indi viduals with underlying COPD. Additionally, a controlled human exposure study of individuals with COPD reported that two patients experienced COPD exacerbation and a slight anti- inflammatory effect during CO exposures of 100-125 ppm for 2 hours (ISA, section 5.5.1.2). Othe r epidemiological studies (ISA, section 5.5.2.2) have reported weak associations in asthma tics, which constitute another population that can experience exercise-induced ai rflow limitation. Preliminary evidence was also shown in one animal toxicological study (G hio et al., 2008), indicating m ild pulmonary inflammation upon exposure to 50 ppm CO. With regard to other potentially at-risk populat ions, there is also limited epidemiological data regarding the susceptibility of diabetic s (ISA, section 5.7.1.3). Epidemiologic studies (Pereira Filho et al., 2008; Za nobetti and Schwartz, 2001) provide suggestive evidence that CVD patients with diabetes may be at greater risk of emergency department visits and hospital admissions than those without diabetes (ISA, section 5.7.1.3). Inferences may also be drawn from results from panel studies for individuals with metabolic syndrome 17 that observed associations between short-term exposures to CO and changes in heart rate variability parameters (ISA, section 5.2.1.1) and from a toxicological study providing evidence of vascular dysfunction associated with increases in endogenous CO in an animal model of me tabolic syndrome (ISA, section 5.7.1.3). People with anemia who have reduced oxygen-carrying cap acity and/or higher baseline COHb levels are an additional population considered to be potentially susceptible to the hypoxic effects of CO. However, there are no c ontrolled human studies or epidemiological

17 These patients share risk factors with diabetics; see ISA section 5.7.1.3.2-21 studies that have specifically ex amined the CO-related health effects in individuals with anemia (ISA, section 2.6.1, p. 2-11). Older adults (65+) have been considered as a potentially suscep tible population to the effects of CO, primarily due to the increased prevalence of ca rdiovascular disease among this population when compared to all age groups or lifestages. There is limited epidemiologic evidence showing greater positive associations between short-term ambient CO concentrations and IHD or myocardial infarcti on (MI) hospital admissions among ol der adults as compared to all age groups or younger adults. The combination of this limited epidemiological data and the fact that older adults have a higher prevalence of CAD than the general population, indicates that older adults are a potentially susceptible populat ion for increased health effects due to CO exposure (ISA, section 5.7.2.1). The developing fetus and young infants or ne wborns have been considered to be potentially susceptible to CO e xposures due to their altered CO kinetics. Although the effects of
CO on maternal-fetal relationshi ps are not well understood, fetuse s are likely to have higher circulating COHb levels than the mother due to differences in uptake and elimination of CO from fetal Hb (AQCD 2000, section 7.7.1). Newbor n infants are also potentially susceptible to CO-induced effects due to their comparativ ely higher oxygen consumption rate and lower oxygen-transport capacity than thos e of adults, which could pote ntially result in higher COHb levels (AQCD 2000, section 7.7.1). Data from la boratory animal studies on CO developmental toxicity suggest that prolonged exposure to high CO levels (>60 ppm) during gestation may produce reduction in birth weight , transient cardiomegaly and dela yed behavioral development, or may disrupt the normal phys iological roles of endogenous CO in the body (ISA, section 5.4.2.2). Multiple-day prenatal animal exposures to exposures at or above 12 ppm indicated effects on the developing auditory system (ISA, pp. 5-75 to 5-76). Limited epidemiological evidence suggests some associati on of short-term ambient CO e xposure with pre-term birth and birth defects, and weak evidence suggests an asso ciation with reduction in birth weight and fetal growth, and infant mortality (ISA, section 5.7.2.2; 2000 AQCD, section 7.7.1), although a clear understanding of the mechanisms by which CO ma y induce those effects and at what exposure levels is lacking (ISA, section 5.4.3). Gender has also been considered as a possi ble source for susceptib ility. However, the
evidence is inconclusive based on the limited epidemiological data and the gender-specific variability in CO endogenous pr oduction (ISA, section 5.7.3). In creased altitude and physical activity through their eff ect on CO uptake and elimination have also been considered to potentially influence susceptibility. For exam ple, residents of low altitudes visiting high altitudes, especially the elderl y and those with CAD (Leaf and Kleinman, 1996; Kleinman et al., 1998), may be at greater risk from added effects of ambient CO than adapted residents (ISA, p.2-22 2-12). Other less certain susceptibi lity factors have been considere d, such as use of medications that may alter CO production (ISA, p. 2-12). Lastly, people experi encing increased CO exposures, such as those spending relatively gr eater amounts of time in microenvironments with relatively higher levels of ambient CO have beenconsidered to be potentially at risk for COinduced effects (ISA, section 5.7.6). As we recognize the potential susceptibility of the populations identified above, we also note the lack of information on specific COHb levels that may be associated with health effects in these other groups and the nature of those eff ects, as well as a way to relate the specific evidence available for the CAD popula tion to these other populations. In summary, the current evidence continues to support the identific ation of people with cardiovascular disease as having susceptibility to CO-induced hea lth effects (ISA, 2-12), with those having CAD as the populati on with the best char acterized susceptibility to CO-induced health effects (ISA, sections 5.7.1.1 and 5.7.8). 18 An important susceptibility consideration for this population is the inability to compensate for CO-induced hypoxia since individuals with CAD have an already compromised cardiovascu lar system. Included in this susceptible population are those with angina pectoris (cardiac chest pain), those who have experienced a heart attack, and those with silent ischemia or undiagnosed IHD (AHA, 2003). People with other cardiovascular diseases, particularly heart diseases, are also at risk of CO-induced health effects. We also recognize other populations potentially susceptible to CO-induced effects, most particularly those with othe r pre-existing diseas es that may have already limited oxygen availability, increased COHb levels, or in creased endogenous CO production, such as people with obstructive lung diseases, diabetes and anemia; however, information characterizing susceptibility for this population is limited.

18 As recognized in the ISA, “Although the weight of evidence varies depending on the factor being evaluated, the clearest evidence indicates that individuals with CAD are mostsusceptible to an increase in COinduced health effect s” (ISA, p. 2-12).2-23  Does the current evidence alter our conc lusions from the previous review regarding the levels of CO in ambient air associated with health effects? At the time of the last review, EPA’s conc lusions regarding concentrations of CO in ambient air that might be associated with risk of health effects were drawn from the combined
consideration of the evidence of COHb levels for which cardiova scular effects of concern had been reported and the results of an exposure and dose modeling assessment (59 FR 38906). As described in more detail in section 2.1.1 above, th e key effects judged to be associated with CO exposures resulting from concentrations observed in ambient air were cardiovascular effects, as measured by decreased time to onset of exerci se-induced angina and to onset of ECG STsegment depression (59 FR 38913).
Levels of COHb that have been associated with different types of effects in clinical
studies are summarized in Table 2- 2 below. At the time of the last review, decreases in time to onset of exercise-induced angina (a symptom of myo cardial ischemia) had been documented in multiple studies at post-exposure COHb leve ls ranging from 2.9 to 5.9% (CO-Ox), which represented incremental increases of 1.5-4.4% COHb from baseline (Adams et al., 1988; Allred et al., 1989a, 1989b, 1991; Anderson et al., 1973; Kleinman et al., 1989, 1998; Sheps et al.,

1987 19 ). The matched measurements available fr om Allred et al. (1989a, 1989b, 1991) of COOx and gas chromatography, the method generally r ecognized to be the more accurate for COHb levels below 5% (ISA, section 5.2.4), indicate that CO-Ox measurements of 2.9 to 3.0% COHb generally correspond to GC measur ements on the order of 2-2.4%. 20 Evidence of effects in other clinical study groups includes eff ects in subjects with cardiac a rrhythmias and effects on exercise duration and maximal aerobic capacity in health y adults. Among the studies of myocardial ischemia indicators in patients with CAD, the two studies involving the lowest experimental CO exposures (which resulted in average increases in COHb of about 1.5% over pre-exposure baseline) were Anderson et al. (1973) 21 and the more recent Allred et al. (1989a, 1989b, 1991) to which we give primary attention in this review (discussed in more detail above). Neither study provided evidence of a measurable threshold at the lowest experimental CO exposures and associated COHb levels assessed (mean of 2.0- 2.4% COHb, GC). Allr ed et al. (1989a, 1989b, 1991) further reported a dose-response relationshi p between the increased COHb levels and the

19 See footnote 4 above.

20 In the lower CO exposure group, the post-exposure mean COHb was 3.21% by CO-Ox and 2.38% by GC, while the post-exercise mean COHb was 2.65% by CO-Ox and 2.00% by GC (Allred et al., 1989a, 1989b, 1991).

21 The study by Anderson et al. (1973) did not use GC to measure COHb levels, and reported reduced exercise duration due to increased chest pain at CO exposures resulting in 2.9% COHb (CO-Ox), representing a 1.6% increase in average COHb levels over baseline.2-24 response of the assessed indicators of myocar dial ischemia (Allred et al., 1989a, 1989b, 1991).
While this evidence informed our conclusions re garding COHb levels associated with health effects, the CO exposure concentrations employed in the studies to achieve these COHb levels were substantially above ambien t concentrations. Thus, an exposure and dose assessment was performed to consider the COHb levels that might be attained as a result of exposures to ambient CO allowed under the current NAAQS, as described in section 2.1.1 above.2-25 Table 2-2. Carboxyhemoglobin levels and reported effects in CAD patients and healthy adults resulting from short-term CO exposures.

%COHb, mean Study Population Effect

GC CO-Ox %COHb, increase

over baseline, GC (CO-Ox) Study

Reduction in time to exercise-induced onset of myocardial ischemia following ~1-hour exposures

- 5.1% decrease in time to ST- segment change, 4.2% decrease in time to angina

- 12.1% decrease in time to ST- segment change, 7.1% decrease in time to angina 2.0-2.4 B

3.9-4.7 B 2.7-3.2 B

4.7-5.6 B 1.4-1.8 B (1.4-2.0) 3.2-4.0 B (3.5-4.4) Allred et al., 1989a, 1989b, 1991

Reduction in time to exercise-induced angina and/or ST segment changes following exposures of 1-4 hours NA C 2.9-5.9 (1.4-4.2) Adams et al., 1988; Anderson et al., 1973; Kleinman et al., 1989, 1998;Sheps et al,1987 D Patients with

coronary

artery disease A

Exercise-induced arrhythmia following 1-hour exposure NA 5.3 E (3.5) E Sheps et. al., 1990, 1991

Reduction in exercise duration and/or maximal aerobic capacity NA 3 F -20 - Adir et al., 1999; Drinkwater et al., 1974; Ekblom and Huot, 1972; Horvath, 1975; Raven et al., 1974; Weiser et al., 1978 Healthy adults

Inconsistent findings of behavioral effects (hand eye coordination, vigilance, continuous performance of critical tasks) NA 5-20 - Benignus et. al., 1987, 1990; Fodor and Winneke, 1972 ; Horvath et al., 1971; Putz et. al., 1976, 1979

A All studies involved subjects with reproducible exercise-induced angina.

B The values presented correspond to the study subject aver age levels post and pre-exercise (subsequent to CO exposure).

C NA = not available.

D Statistical analyses of the Sheps data by Bi ssette et al (1986) indicate a significant decrease in time to onset of angina at 4.1% COHb if subjects that did not exper ience exercise-induced angina during air ex posure are also included in the analyses.

E Based on mean of pre-and post-exercise measurements for the 6% COHb group and increase from pre-exposure. The difference in COHb from the mean air exposure day level was 3.9%.

F The study of adults aged 40-57 (Raven et al., 1974) reported an effe ct on exercise duration at 2.3% COHb (CO-Ox), while the other studies, which were of adults younger than 35 reported effects at or above 3.3%.

Since the time of the last review, there have been no new controlled human exposure studies specifically designed to evaluate the eff ects of CO exposure in su sceptible populations at COHb levels below 2%. Thus, similar to the la st review, the multilaboratory study by Allred et al. (1989a, 1989b, 1991) continues to be the study that has evaluate d cardiovascular effects of2-26 greatest concern (i.e., reduced time to exercise -induced myocardial ischemia as indicated by ECG ST-segment changes and angina) at the lowest tested COHb levels (ISA, section 2.7). This study is also of particular importance in this re view because it is considered the most rigorous and well designed study, presenting the most sensitive analysis methods (GC used in addition to CO-Ox) to quantify COHb blood levels. Key findings from that study with regard to levels of CO associated with health effects include the following:

 Short (50-70 minute) exposure to increased CO concentrations that resulted in increases in COHb to mean levels of 2.0% and 3.9% from baseline of 0.6% significantly reduced exercise time required to induce markers of myocardial ischemia in CAD patients (by about one half minute in the lower exposure). 22

 The associated dose-response relationship between incremental changes in COHb and change in time to myocardial ischemia in CAD patients indicates a 1.9% and 3.9% reduction in time to onset of exercise-i nduced angina and ST-segment change, respectively, per 1% increase in COHb con centration from average baseline COHb of 0.6% without evidence of a measurable threshold. In considering the clinical study evidence on COHb levels associated with effects to address the question regarding ambient CO concentr ations associated with health effects, we have developed estimates of COHb associated with different air qua lity conditions using quantitative exposure and dose modeling, as was done at the time of the last review. Since the last review, there have been numerous improveme nts to the exposure and COHb models that we use to estimate exposure and dose for the current review. The results of modeling using these improved tools in the current review and our conclusions based on it with regard to the expectation for COHb levels of concern to occur in the at-risk popul ation under differing air quality conditions are descri bed in section 2.2.2 below. As discussed in more detail above, a numb er of epidemiological studies of health
outcome associations with ambient CO have been conducted since the last review. These include studies, identifie d in Table 2-1 above, that have repo rted associations with different ambient CO metrics (e.g., 1-hour and 8-hour aver ages, often as central-site estimates) derived
from CO measurements at fixed-site ambient mon itors in selected urban areas of the U.S. and cardiovascular endpoints other th an stroke, particularly hos pitalizations and emergency

22 Relative to baseline (0.6% mean CO Hb), mean COHb levels of 2.0-2.4% and 3.9-4.7% were associated with decreases in time to onset of exercise-induced ST -segment changes of 5.1% (p=0.01) and 12.1%(p<0.001), respectively. Similarly, the time to onset of exercise-induced angina was shortened by 4.2% (p=0.027) and 7.1% (p=0.002) for these two mean levels of COHb (Allred et al ., 1989a, 1989b.1991). Across all subjects, the mean time to angina onset for baseline or contro l (“clean” air) exposures was approxim ately 8.5 minutes, and the mean time to ST endpoint was approximately 9.5 minutes, with the “time to onset” reductions of the two exposure levels being approximately one half and one minute, respectively for ST-segment change, and slightly less and slightly more than one half minute, respectively, for angina (Allred et al., 1989b).2-27 department visits for specific cardiovascul ar health outcomes incl uding IHD, CHF and CVD (Bell et al., 2009; Koken et al., 2003; Linn et al., 2000; Mann et al., 2002; Metzger et al., 2004; Symons et al., 2006; Tolbert et al., 2007; Wellenius et al., 2005). In general, these studies, many of which were designed to evaluate the effects of a variety of air pollutant s, including CO, report positive associations, a number of which are st atistically significant (ISA, sections 5.2.3 and 5.2.1.9; Table 2-1 above). The long-standing bod y of evidence for CO summarized above, including the well-characterized role of CO in limiting oxygen availability, lends biological plausibility to the ischemia-related health ou tcomes reported in the epidemiological studies, providing coherence between these studies and the clinical eviden ce of short-term exposure to
CO and health effects.
In consideration of the evidence base for CO cardiovascular eff ects, Figure 2-1 below presents a conceptual model of the pathway from CO exposures to these effects. Figure 2-2 separately shows elements of this conceptual model investigated in clinical studies in contrast to those in the epidemiological studies referenced above. As shown in Figure 2-2, the clinical studies document relationships be tween directly measured controlled short-term CO exposures and specific levels of an internal dose metr ic, COHb, which elicited specific myocardial ischemia-related responses in CAD patients. Th ese studies inform our interpretation of the associations we observed in the epidemiological studies. The epidemio logical studies reported
associations between CO levels measured at fixe d-site monitors and emergency department visits and/or hospital admissions for IHD and other card iovascular disease-rela ted outcomes that are plausibly related to the effects on physiological indicators of myocardi al ischemia (e.g., STsegment changes) demonstrated in the controlle d human exposure studies, providing coherence between the two sets of findings (ISA, p. 5-48).

Exposure Internal Dose (e.g., COHb) Nonambient CO Ambient CO Health Outcomes (e.g., hospital admissions) Effects (e.g., markers of myocardial Ischemia) E ndogenous CO

Figure 2-1. A conceptual model of CO source-to-health outcome pathway.2-28 Controlled CO Exposure Internal Dose (COHb) Effects (markers of myocardial Ischemia)

Ambient CO Health Outcomes (e.g., IHD hospital admissions) Epidemiological Studies Clinical Studies (CAD Patients) Baseline CO (endogenous + background)

Figure 2-2. Components of CO source-to-outcome conceptual model measured in controlled human exposure and epidemio logical studies discussed in this document.

We recognize, however, several gaps between the two lines of evidence (clinical and epidemiological) which complicate their integrat ion, particularly with regard to ambient exposures and ambient concentrations associated w ith health effects. These gaps limit our ability to integrate the evidence from these epidemiol ogical studies with our knowledge of CO-related
effects based on the clinical evid ence. Most particularly we lack information on the actual CO exposures and associated internal COHb le vels for the epidemiological study populations, including the relative co ntributions from ambient and nonambient CO. These gaps in our understanding of the role of nonambient CO expo sures and their contribution to COHb levels complicate our ability to discern the ambient concentr ations that may be eliciting health effects. Moreover, it is also unknown how the unmeas ured exposures in epidemiological study populations relate to the exposur e concentrations of the clin ical studies (e.g., 1 hour at approximately 50-200 ppm), which were substan tially higher than current commonly occurring ambient concentrations (ISA, section 2.7). 23,24 We are also limited in our understanding of the

23 As recognized in the ISA in consideration of the epidemiological studies, the known role of CO in limiting oxygen (O 2 ) availability lends biological plausibility to ischemia-related health outcomes following CO exposures, although “it is not clear whether the small changes in COHb as sociated with ambi ent CO exposures results in substantially reduced O 2 delivery to tissues” (ISA, p. 5-48).

24 Experimental studies have not been conducted at COHb levels that might be elicited in response to exposures to lower CO concentrations such as those with in the ranges of current ma ximum ambient concentrations2-29 specific relationship between the changes in indi cators of myocardial ischemia observed in the controlled human exposure studies and the hospita l admissions assessed in the epidemiological studies. Together, these gaps complicate our ability to draw conclusions re garding the levels of
CO in ambient air associated with health e ffects that are based on an integration of the epidemiological evidence into the full body of evidence for CO. In considering these epidemiological studies in the case of CO, we recognize that in
contrast to other traffic-relate d pollutants, CO presents specif ic challenges that complicate the quantitative interpretation with regard to ambi ent concentrations that might be eliciting the reported health outcomes. In particular, a major challenge relates to the difficulty in determining
the extent to which ambient CO is independently associated with cardiovascular effects or if CO at ambient levels is acting as a surrogate for th e effects of another tra ffic-related pollutant or mixture of pollutants (ISA, section 5.2.3). As noted in the ISA, in interpreting the epidemiological evidence for cardiovascular morbid ity “[i]t is difficult to determine from this group of studies the extent to which CO is independently asso ciated with CVD outcomes or
whether CO is a marker for the effects of anothe r traffic-related pollutant or mix of pollutants. As recognized in the ISA, “[o]n-ro ad vehicle exhaust emissions are a nearly ubiquitous source of combustion pollutant mixtures that include CO and can be an im portant contribu tor to CO in near-road locations” (ISA, p. 5-40 – 5-41). We also note CASAC’s recognition of the potential for co-pollutants to serve as confounders to be “p articularly problematic for CO” and the need to give consideration to the possibi lity of CO serving as a surrogate for a mixture of fossil-fuelcombustion-related pollutants (Brain and Samet, 2010a). While recognizing the complications regarding the use of the epidemiological studies in drawing conclusions about ambient CO levels associated with health effects, we have nonetheless considered for our purposes in addressing the question posed here the epidemiological studies in U.S. locations that investigated ischemia-related and CHF outcomes presented in Table 2-3. Among the epidemiological evidence, the studies of hospital admissions for CHD (i.e., IHD and MI) were co nsidered to provide the strongest and most consistent weight
of evidence for short-term eff ects of CO (ISA, Figure 5-2, pp. 5-24 to 5-26), with the U.S. studies for the broader category of all CVD hosp ital admissions also contributing to the ISA’s causality determination (ISA, Figure 5-5, pp. 5-33 to 5-36). In considering the studies in Table 2-3, we recognize that CHF is a chronic condition for which there are multiple causes and for which the evidence regarding the role of CO is less clear than it is for IHD, MI and all CVD

(ISA, section 2.7) or closer to pers onal exposure concentrations more co mmonly expected currently (e.g., ISA, Figure 3-45).2-30 outcomes (which are inclusive of IHD), for which more direct c onceptual linkages can be drawn to the myocardial ischemia effects of the CAD clinical studies. As recognized above, this set of studies prov ides epidemiological evidence for a positive
association between cardiovascul ar outcomes and ambient CO concentrations. With regard to our overarching question as to the adequacy of th e protection afforded by the current standards, however, the studies in which CO concentra tions exceeded the current NAAQS during some portion of the study period are, ac cordingly, less informative. While the full set of these epidemiological studies, includi ng those reporting associations with ambient CO concentrations
under conditions when the current standards were not met, provide support to the previous evidence regarding cardiovascular effects of CO, it is the studies involvin g air quality conditions
in which the current standards were met that ar e most informative to the overarching question of adequacy. Accordingly, in considering these epid emiological studies, we ha ve considered the air quality conditions during the periods of study as described below.
The set of studies listed in Table 2-3 en compasses a range of air quality conditions extending from those that did not meet the curren t 8-hour CO standard down to those that did. 25 As mentioned above, the study areas for the IHD and CVD outcomes (inclusive of IHD) include Atlanta, urban areas of Californi a and a group of 126 urban counties 26 and the multi-year time periods for this set of studies together span the period from 1 988 through 2005 (Table 2-3 below). During the time periods of study, however , only the Atlanta stud ies (Metzger et al., 2004; Tolbert et al., 2007) did not include years in which ambien t CO concentrations exceeded the 8-hour standard (Table 2-3). The CO concentration with whic h an association with hospital
admissions was observed in the Atlanta studie s was the average of daily maximum 1-hour concentrations on the day of and two days prior to hospital admi ssion. Based on data reported to AQS for the general areas studied, ambient CO concentrations during a portion of the time periods studied in the other three of these an alyses exceeded the leve l of the current 8-hour NAAQS (Bell et al., 2007; Linn et al., 2000; Mann et al., 2002) , with the second highest nonoverlapping 8-hour average CO c oncentration in a year (i.e., the design value for the 8-hour standard) ranging up to 24.3 ppm, as compar ed to the 8-hour standard of 9 ppm. 27 In the Atlanta

25 While the 1-hour CO standard was met during the fu ll study period for all of these studies, the 8-hour standard was not (Table 2-3). As in past reviews, the 8-hour standard continues to be the controlling standard.

26 The 126 counties span some 40 states , including the District of Columbia.

27 Staff also note that the national- scale study of 126 urban counties by Bell et al. (2009) included a subset analysis that evaluated associations for a ll cardiovascular outcomes, adjusted for NO 2 , after restricting the dataset to days with a 1-hour daily maximum CO concentration less than 35 ppm, which is the level of the 1-hour standard although its form is the 2 nd maximum in a year. This subset analysis fo und a statistically significant effect estimate identical to the estimated risk with the full data set. Further subset analyses by Bell et al. (2009) using data below cutoff values of 1-10 ppm all found positive, statisti cally significant associations (with adjustment for NO 2 ),2-31 study area, the design value for the 8-hour st andard ranged from 2.6 up to 5.3 ppm over the combined 12 years of study. The study areas for which statistically signi ficant positive associations with CHF were
observed include the area of Ca lifornia described for Linn et al (2000) above, as well as two additional areas (Table 2-3; ISA, pp. 5-31 to 5- 33; Table 2-1 above). The additional study areas were Denver, Colorado, and Allegheny County, Pe nnsylvania (Koken et al ., 2003; Wellenius et al., 2005). While the current 8-hour standard was not met in the Denver or California study areas during the full period of those studies, 28 the current 8-hour standard was just met in the Allegheny County study area, with design values ranging from 3.8 ppm up to 8.8 ppm. This study was focused on 24-hour average CO concentr ations, having analyzed the relationship between hospital admissions for CHF hospital admissions and estim ates of daily county-wide
ambient CO concentrations (Wellenius et al., 2005). 29 We additionally note other positive, though not statistically significant, associations were observed for CHF-related hospitalizations
in the Atlanta and Baltimore studies with the average 1- or 8-hour daily maximum CO
concentrations over the most r ecent 3 or 4 days, respectively. 30

although confidence intervals increased at the lower cutoff values and th e proportion of values near and below the limit of detection grew larger.

28 In the study focused in Denver, a statistically signifi cant association is observed with CO concentrations 3 days prior to the health outcome (Koken et al., 2003)

29 Data from three monitors were used to derive a daily estimate for the study area described by the authors as generally representative of the study area as opposed to being reflective of local conditions near any specific monitor (Zanobetti et al., 2000). The algorithm us ed was described as accounting for monitor-specific measurements and variances (Wellenius et al., 2005).

30 As noted in the ISA, associations with same day or previous day CO concentrations are considered consistent with the mode of action described for CO (ISA, p. 5-40).2-32Table 2-3.Air quality information for geographical areas of key U.S. epidemiological studies.Study Information Ambient Air QualityAStudy-reported COConcentrations,Cinterms of study metric(ppm)Design Valuesfor Current NAAQS,across study years (ppm)StudyAreaStudyTimePeriodStudyReferenceHealthOutcomeBCO ConcentrationMetric Associatedwith HealthOutcomeAssignment ofMonitors to StudySubjectsMean/median*Range1-hourStandard=358-hourStandard=999thpercentile1-hour dailymaximum(ppm)99thpercentile8-hour dailymaximum(ppm)IHD1993-2000Metzger etal., 2004CHFNS1-hour dailymaximum,average for mostrecent 3 daysSingle centralresidential monitor1.80.5 – 3.4(10th- 90thpercentile)4.8 -16.3 3.2 - 5.3 4.4 – 7.9 3.0 – 4.920-countyAtlantaarea1993-2004Tolbert etal., 2007CVD1-hour dailymaximum,Average for mostrecent 3 daysSingle centralresidential monitor1.6 0.1 – 7.7 4.5 -16.3 2.6 - 5.3 3.6 – 7.9 2.4 – 4.9IHD,1988-1995Mann et al.,2002IHD+CHF8-hour dailymaximum,average formost recent 4 daysResidence gridcentroid interpolatedfrom 3 closest monitors2.07 0.30 – 11.8 16.5 - 32 11.6 – 23.4 16.1 – 31.0 11.2 – 19.1MICVDSouthCoast AirBasin, CA1992-1995Linn et al.,2000CHF24-hour average,same dayAverage across allmonitors in basin1.5 0.3 – 5.3 16.5 - 25 11.6 -16.4 16.1 – 21.0 11.2-14.4126 urbancounties1999-2005Bell et al.,2009CVD 65+1-hour dailymaximum, same dayAverage of monitors incounty of residence1.3* 0.05 – 9.7 14.9-33.5 8.2-24.3 10.4 – 31.8 6.7-18.9Baltimore,MD2002(April-Dec)Symons etal., 2006CHFNS8-hour dailymaximum,Average for mostrecent 4 daysSingle centralresidential monitor0.4 0.0 – 2.3 9.2 3.0 4.7 2.8Alleghenycounty, PA1987-1999Welleniuset al., 2005CHF24-hour average,same daySingle area-widerepresentation of 3monitors1.03*0.42 – 2.04(5th- 95thpercentile)5.4-19.4 3.8-8.8 4.3 – 15.9 3.3 – 8.0Denver1993-1997(Jul-Aug)Koken etal., 2003CHF24-hour average,3 days priorAverage across allmonitors0.9 0.3 – 1.6 11.2-18.2A6.4-10.4A9.3 – 16.2 5.8 – 10.4A Air quality information provided here is drawn from monitors reporting to the U.S. Air Quality System, and two monitors reporting to the SouthEastern Aerosol Research and Characterizationstudy database (Appendix B). Design values are CO concentrations for the study area in the statistical form of the standard.Presented is the range of 2nd maximum 1-hour and 8-hour averageconcentrations at highest monitor reporting to AQS in each study area across years of study. For partial-year studies, the values presented reflect full year of data, inclusive of study months.B Hospital admissions for ischemic heart disease (IHD), myocardial infarction (MI), cardiovascular disease (CVD; for Bell et al. [2009] only subjects >65 years old), congestive heart failure (CHF).C Ambient CO concentrations reported in the study.NS Association was not statistically significant.2-33 In summary, although there is no new eviden ce regarding the effects of short-term controlled CO exposures that result in lower C OHb levels, the evidence is much expanded with regard to epidemiological 31 analyses of ambient monitor concentrations, which observed associations between specific and overall ca rdiovascular-related outcomes and ambient CO measurements. With regard to extending our und erstanding of effects occurring below levels of
CO observed in the clinical st udies, however, the epidemiological evidence for CO is somewhat limited. The epidemiological evidence lacks m easurements of COHb or personal exposure
concentrations that would facili tate integration with the clin ical data. Furthermore, the epidemiological evidence base for IHD outco mes or CVD outcomes as a whole includes a number of studies involving condi tions in which the current sta ndard was not met. Though these
studies are informative to consideration of the re lationship of health eff ects to the full range of ambient CO concentrations, they are less usef ul to informing our conclusions regarding adequacy of the current standards. The smalle r set of studies, under conditions where the current standards were met, is considered to better in form our assessment of the adequacy of the
standards or conditions of lowe r ambient concentrations. Among the few studies conducted during conditions in which the current standards were always met, the studies reporting statistical significance for IHD or all CVD outcomes are limited to a single study area (i.e . Atlanta). When the analys es reporting significance for
association with CHF outcomes are also considered, a second study area is identified (Allegheny County, PA) in which the current standard is met throughout the study period. The analyses for
both areas involve the use of central site monito r locations or area-wide average concentrations, which given the significant con centration gradients of CO in urban areas (ISA, section 3.6.8.2), complicates our ability to draw conclusions from them regarding ambient CO concentrations of

concern. Therefore, with regard to this question of CO concentrations, we have primarily focused our consideration of the epidemiological studi es on the extent to which this evidence is consistent with and generally supportive of conc lusions drawn from the combined consideration of the controlled human exposure evidence w ith estimates from the exposure and dose assessment (section 2.2.2 below). As in the previ ous review, we believe the integration of the controlled human exposure evidence with the exposure and dose estimates will be most important to informing conclusions regarding ambient CO concentratio ns of public health concern. This integration, based on the REA for the current review, is considered with regard to the adequacy of the current st andards in section 2.2.2 below.

31 Few epidemiological studies that had investigated the relationship between CO exposure and ischemic heart disease were available at the time of the last completed review (USEPA, 1991, section 10.3.3).2-34  To what extent have important uncertaint ies identified in the last review been reduced and/or have new uncertainties emerged?

Since the time of the last re view, some important uncertainti es have been reduced, some still remain and others associated with newly av ailable evidence have been identified. A range of important uncertainties were identified in a nu mber of areas at the time of the last review (59 FR 38913, USEPA, 1992), including:

 The adverse nature and health significance of the small changes in time to ST-segment depression identified at the lowest COHb leve ls investigated in the controlled human exposure studies, and the magn itude of risk associated wi th such changes for specific health outcomes, such as myocardial infarc tion, or of slight but cumulative myocardial damage, among other possibilities.

 The extent to which COHb measurements made using CO-Ox do not reflect COHb levels in angina patients studi ed and the potential for as ye t unidentified health effects at COHb levels below 2%.

 The potential for short-term peak CO expos ures to contribute to CNS effects which might affect individual’s perf ormance of complex activities su ch as driving a car or to contribute to other effects of concern.

 Effects of ambient CO on potentially sus ceptible populations other than those with cardiovascular disease, incl uding the developing fetus.

 Modeling of COHb formation associated with exposures to ambien t CO under different air quality conditions, includi ng those associated with ju st meeting different NAAQS. As discussed below, some of these uncertainties have been reduced, while some still remain.
The CO-induced effects considered of concern at the time of the last review were reduced time to exercise-induced angina and ST-segment depression in patients suffering from coronary artery disease as a result of increases in COHb associated w ith short CO exposures. These
effects had been well documented in multiple studies, and it was r ecognized that the majority of cardiologists at the time believed that recurrent exercise-induced angina was associated with substantial risk of precipitating myocardial infa rction, fatal arrhythmia, or slight but cumulative myocardial damage (USEPA, 1992, p. 22; 59 FR 38911; Basan, 1990; 1991 AQCD). As at the time of the last review, although ST-segment depr ession is a recognized in dicator of myocardial ischemia, the exact physiological significance of the observed changes among individuals with CAD is unclear (ISA, p. 48). In interpreting the study results at the time of the last review, EPA recognized uncertainty in the COHb measurements made using CO-Ox and associated uncertainty in establishing a lowest effects level for CO (USEPA, 1992, p. 31). A then-recent multicenter study (Allred et al., 1989a, 1989b, 1991) was of great importance at that ti me for several reasons including the large number of subjects used, the rigor ous protocol used for subject selection, the us e of the most2-35 accurate method to measure blood COHb levels and the finding of a dose-response relationship
between COHb levels and the is chemic events evaluated in the study. This study reported changes in post-exercise ST-segment depression and reduced time to onset of exercise-induced angina as a result of increases in COHb from a mean baseline of 0.6% to mean levels of 2% and 3.9% (ISA, section 5.2.4; (Allred et al., 1989a,19 89b, 1991). In the current review of the
evidence related to cardiovascular effects asso ciated with CO exposure, we place primary emphasis on the findings of Allred et al. (1989a , 1989b, 1991) recognizing the superior quality of the study, both in terms of the rigorous study design as well as the sensitivity of the analytical methods used in determining COHb concentratio ns (ISA, Section 2.7). No additional clinical
studies are available that evalua te responses to lower COHb leve ls in the cardiovascular-disease population, and uncertainties still re main in determining specific and quantitative relationships
between the CO-induced effects in these studie s and the increased risk of specific health outcomes. Further, with regard to then-unident ified effects at lower COHb levels, no studies
have identified other effects on the CAD population or on other populations at lower exposures (ISA, sections 5.2.2). The last review recognized a variety of neurobehavioral e ffects associated with CO exposure, including changes in visual perception, hearing, mo tor performance and vigilance among other measures of neurobehavioral perfor mance based on a series of studies conducted from the mid 1960’s through the early 1990’s (1991 AQC D). Since these effects were observed at exposures to CO resulting in COHb levels ranging from 5-20%, and were poorly understood at the time (1991 AQCD), the review focused on card iovascular effects, which had been observed at COHb levels below 5% and consequently fo r which a focus would also provide adequate protection against potential adve rse neurobehavioral effects. No new human clinical studies
have evaluated CNS or behavioral effects of exposure to CO (ISA, section 5.3.1). However, given the drastic reduction in CO ambient concentrations, the o ccurrence of these effects in response to ambient CO would be expected to be rare within the curren t population. Thus, our uncertainty with regard to the pot ential for such effects to be a ssociated with current ambient CO exposures is reduced. Since the 1994 review, the epidemiologic and toxicological evidence of effects on birth and developmental outcomes has expanded, although the available evidence is still considered limited with regard to effects on preterm birth, birth defects, decr eases in birth weight, measures of fetal growth, and infant mortality (ISA, sec tion 5.4). Further, while animal toxicological studies provide support and coherence for those effects, the understandi ng of the mechanisms underlying reproductive and developmental effects is still la cking (ISA, section 5.4.1). Thus, although the evidence continues to “suggest[s] th at critical developmental phases may be characterized by enhanced sensi tivity to CO exposure” (ISA, p. 2-11), evidence is lacking for2-36 adverse developmental or reproductive effects at CO exposure concentrations near those
associated with current levels of ambient CO. Numerous improvements have been made over the last decade that have reduced the
uncertainties associated with the models used to estimate COHb levels resulting from ambient CO exposures under different air qu ality conditions, including those associated with just meeting the current CO NAAQS (REA, section 4.3). This progression in exposure model development has led to the model currently used by the Agen cy (APEX4.3), which has an enhanced capacity to estimate population CO exposures and more accurately predicts COHb levels in persons exposed to CO. Our application of APEX4.3 in this review, usi ng updated data and new algorithms to estimate exposures and doses expe rienced by individuals, better represents the variability in population exposure and COHb dose leve ls than the model version used in previous CO assessments. However, while APEX 4.3 is greatly improved when compared with previously used exposure models, its application is still limited with regard to data to inform our understanding of spatial relationships in ambient CO concentrations and within microenvironments of particular interest. Further informati on regarding model improvements and remaining exposure modeling uncertainties are described in section 2.2.2 below. The much-expanded epidemiologic database in the current review includes studies that
show associations between ambient CO concentra tions and increases in emergency room visits and hospitalizations for disease ev ents plausibly linked to the eff ects observed in the controlled human exposure studies of CA D patients (ISA, section 2.5.1), providing support for our conclusion regarding coronary artery disease as th e most important susceptibility characteristic for increased health risk due to CO exposure (I SA, p. 2-10). However, we recognize aspects of this epidemiological evidence that complicate quantitative interpretation of it with regard to ambient concentrations that might be eliciting the reported health outcomes. As an initial matter, we note the substantially fewer st udies conducted in areas meeting the current CO standards than
is the case for NO 2 and PM (USEPA, 2008c, 2009a), as recognized above. Further, we recognize complicating aspects of the evidence that relate to c onclusions regarding CO as the pollutant eliciting the effect reported in the ep idemiological studies a nd to our understanding of
the ambient CO and nonambient concentrations to which study subjects demonstrating these outcomes are exposed. In considering conclusions regarding CO as the pollutant eliciting the effects in these studies, we note the use of two- pollutant regression models, a co mmonly used statistical method (ISA, section 1.6.3). Although CO associations, in some studies , are slightly attenuated in models that adjusted for other combustion-related pollutants (e.g., PM 2.5 or NO 2 ), they generally2-37 remain robust (ISA, Figures 5-6 and 5-7). 32 In considering these two-pollutant model results, however, we recognize the potential for there to be etiologically releva nt pollutants that are correlated with CO yet absent from the anal ysis. Similarly, CASAC commented that “the problem of co-pollutants serving as potential c onfounders is particularly problematic for CO”. They stated that “consideration needs to be given to the possibility that in some situations CO may be a surrogate for exposure to a mix of po llutants generated by fossil fuel combustion” and “a better understanding of the possi ble role of co-pollutants is relevant to ... the interpretation of epidemiologic studies on the hea lth effects of CO” (Brain and Samet, 2010a). This issue is particularly important in the case of CO in light of the uncertain ty (referenced below) regarding the biological plausibility of CO-related effects at low ambient concentrations and in light of the sizeable portion of ambient CO measurements that are at or below monitor detection limits. Consequently, the extent to which multi-pollutantregression models eff ectively disentangle and quantitatively interpret a CO -specific effect distinct from that of other pollutants remains an area of uncertainty. In considering ambient concentrations that ma y be triggering health outcomes analyzed in the epidemiological studies, we recognize th e uncertainty introduced by exposure error. Exposure error can occur when a surrogate is us ed for the actual ambient exposure experienced by the study population (e.g., ISA, section 3.6.8). There are two aspects to the epidemiological studies in the specific case of CO, as contrasted with the case s of other pollutants such as NO 2 and PM, that may contribute to exposure error in the CO studies. The first relates to the low concentrations of CO considered in the epidem iological studies and monitor detection limits. The second relates to the use in the epidemiologi cal studies of area-wide or central-site monitor CO concentrations (Table 2-3) in light of information about the gradient in CO concentrations
with distance from source locations such as hi ghly-trafficked roadways (e.g., Karner et al., 2010). Uncertainty in the assessment of exposure to ambient CO concentrations is related to the prevalence of ambient monitor CO concentrations at or below det ection limits, which is a greater concern for the more recently available epidemio logical studies in which the study areas have much reduced ambient CO concentrations compared with those in the pa st. For example, the ISA notes that roughly one third of the 1-hour ambient CO measurements reported to AQS for

32 In interpreting the epidemiological evidence for cardiovascular morbidity the ISA notes that it “is difficult to determine from this group of studies the extent to which CO is independently associated with CVD outcomes or if CO is a marker for the effects of another traffic-related pollutant or mix of pollutants. On-road vehicle exhaust emissions are a nearly ubiquitous source of combustion pollutant mixtures that include CO and can be an important contributor to CO in near-road locations. Although this complicates the efforts to disentangle specific CO-related health effects, the evidence indicates that CO associations generally remain robust in copollutant models and supports a direct effect of short-term ambient CO exposure on CVD morbidity.” (ISA, pp. 5-40 to 5-41).2-38 2005-2007 were below the method limit of detection for the monitors analyzed (ISA, p. 3-34). Appendix B additionally indicates a similarly notable proportion of measurements below limit of detection for epidemiological study areas meeting the current standards (e .g., Atlanta, Allegheny County). This complicates our interpretation of specific ambient CO concentrations associated with health effects (ISA, p. 3-91; Brain and Same t, 2010a). In contrast to CO, other combustionrelated criteria pollutants such as PM 2.5 and NO 2 generally occur above levels of detection, providing us with greater confiden ce in quantitative interpretations of epidemiological studies for those pollutants. There are also differences in the sp atial variability associated with PM 2.5 and NO 2 concentrations as compared to CO concentrations that add complexity to the estimation of CO exposures in epidemiological studies. In general, PM 2.5 concentrations tend to be more spatially homogenous across an urban area than CO concentra tions. CO concentrations in urban areas are largely driven by mobile sources, while urban PM 2.5 concentrations s ubstantially reflect contributions from mobile and a variety of statio nary sources. The greater spatial homogeneity
in PM 2.5 concentrations is due in part to the trans port and dispersion of small particles from the multiple sources (USEPA, 2009a, sections 3.5.1.2 a nd 3.9.1.3), as well as to contributions from secondarily formed components “produced by th e oxidation of precursor gases (e.g., sulfur dioxide and nitrogen oxides) and re actions of acidic products with NH 3 and organic compounds” (USEPA, 2009a, p. 3-185), which likely contribute to spatial homogeneity. Similarly, “because

NO 2 in the ambient air is due largely to the atmospheric oxidation of NO emitted from combustion sources (ISA, section 2.2.1), elevated NO 2 concentrations can extend farther away from roadways than the primary pollutants al so emitted by on-road mobile sources” (40 FR 6479, February 9, 2010). In contrast to PM 2.5 and NO 2 , CO is comparatively non-reactive, which may contribute to the steeper CO gradient observed near roadways. Therefore, the misclassification of exposure arising from the u tilization of central site monitors to measure

PM 2.5 and NO 2 exposures is likely to be smaller th an is the case for CO exposures. An additional complication to a comparison of our consideration of the CO epidemiological evidence to that for other traffic-re lated criteria pollutants is that, in contrast to the situation for all other criteria pollutants, th e epidemiological studies for CO use a different exposure/dose metric from that which has been the focus of the broade r health evidence base, and additional information that might be used to bridge this gap is lacking. In the case of CO, the epidemiological studies use air concentration as the exposure/dose metric, while the broader
health effects evidence for CO demonstrates and focuses on an internal biomarker of CO exposure (COHb) which has been considered a critical key to CO toxicity. In the case of the only other criteria pollutant for wh ich the health evidence relies on an internal dose metric – lead2-39 - the epidemiological studies also use that metric. 33 For other criteria pollutants, including PM
and NO 2 , air concentrations are used as the exposure/dose metric in both the epidemiological studies and the other types of health evidence. T hus, there is no comparable aspect in the PM or

NO 2 evidence base. The strong evidence describi ng the role of COHb in CO toxicity is important to consider in interpreting the CO epidemiological studies and contributes to the biological plausibility of the is chemia-related health outcomes that have been associated with ambient CO concentrations. Yet, we do not have information on the COHb levels of epidemiological study subjects that we can evaluate in the context of the COHb levels eliciting
health effects in clinical studies . Further, we lack additional in formation on the CO exposures of the epidemiological study subjects to both ambient and nonambient sources of CO that might be used to estimate their COHb levels and bridge the gap between the two study types. And, as noted in the ISA, “it is not clear whether the sm all changes in COHb associated with ambient CO exposure results in substantially reduced {oxygen} delivery to tissues,” with further investigations needed to investigate potential roles of other mechanisms in CO toxicity (ISA, p. 5-48). Thus, there are uncertainties associat ed with the epidemiological evidence that “complicate the quantitative interpretation of the epidemiologic findings, particularly regarding the biological plausibility of health effects occurr ing at COHb levels resulting from exposures to
the ambient CO concentrations” asse ssed in these studies (ISA, p. 2-17). In summary, some important uncertainties fr om the last review have been reduced, including those associated with concerns for ambien t levels of CO to pose neurobehavioral risks. A variety of uncertainties still remain including the adverse nature and significance of the small changes in time to ST-segment depression identified at the lowest COHb levels investigated, and the magnitude of associated risk of specific heal th outcomes, as well as the potential for as-yetunidentified health effects at COHb levels be low 2%. Our exposure and dose models have improved giving us increased confidence in thei r estimates. Additionally , although the evidence base is somewhat expanded with regard to th e potential for CO effects on the developing fetus, uncertainties remain in our understanding of the potential influence of low, ambient CO exposures on conditions existing in the fetu s and newborn infant and on maternal-fetal relationships. We additionally recognize that the expanded b ody of epidemiological evidence
includes its own set of uncertainties wh ich complicates its interpretation.

33 Another criteria pollutant for which the evidence is strengthened through the existence of an internal biomarker is lead (Pb). In the case of Pb, in contrast to that of CO, the epidemiol ogical evidence is focused on associations of Pb-related health effects with measurements of Pb in blood, providing a direct linkage between the pollutant, via the internal biomarker of dose, and the health effects.2-40 2.2.2 Exposure/Risk-based Considerations

Our consideration of the scientific evidence in the current review, as at the time of the last review (summarized in section 2.1.1 above), is informed by results from a quantitative analysis of estimated population exposure and resulta nt COHb levels. As in our consideration of the evidence in section 2.2.1 above, we have or ganized the discussion that follows here around a set of key questions to assist us in drawing from the assessment of CO exposure and resultant COHb levels for potentially at-risk populations liv ing in two urban areas under current air quality conditions and conditions simulated to just meet the current CO standards. Prior to addressing the series of questions below, we provide a summary of key aspects of the assessment, including the study areas and air quality scenarios investigated, modeling tools used, at-risk populations simulated, and COHb benchm ark levels of interest. We then consider aspects of the questions beginning with the magnitude of COHb levels estimated in the simulated at-risk populations in response to ambient CO exposure, followed by the key uncertainties
associated with our assessment of exposure and dose with regard to drawing conclusions as to the adequacy of the protection afforded by the cu rrent CO standards. Lastly, we consider the exposure and dose estimates from the quantitative a ssessment with regard to the extent to which such estimates may be judged to be important from a public health perspective.
In the assessment conducted for this review, describe d in detail in the REA and summarized here, we have estimated CO exposur e and associated COHb levels in simulated populations in two urban study area s in Denver and Los Angeles, in which current ambient CO
concentrations are below the current standards. We selected these areas because: (1) areas of both cities have been included in prior CO NAAQ S exposure assessments and thus serve as an important connection with past assessments; (2) hi storically, they have generally had the highest ambient CO concentrations among urban areas in the U.S.; and (3) Denver is at high altitude and represents an important risk scen ario due to the potent ial increased susceptibility to CO exposure associated with high altitudes. In addition, of 10 urban areas across the U.S. selected for detailed air quality analysis in the ISA and having ambient monitors meeting a 75% completeness criterion, the two study area locations were ra nked first (Los Angeles) and second (Denver) regarding the percentage of elderly population within 5, 10, and 15 km of mon itor locations, and ranked first (Los Angeles) and fifth (Denver) re garding number of 1- a nd 8-hour daily maximum CO concentration measurements (ISA, section 3.5.1.1). Estimates were developed for exposures associ ated with current “as is” conditions (2006 air quality) and also for higher ambient CO concen trations associated with air quality conditions simulated to just meet th e current 8-hour standard, 34 as well as for air quality conditions

34 As discussed elsewhere, the 8-hour standard is th e controlling standard for ambient CO concentrations.2-41 simulated to just meet alterna tive standards (as discussed in s ection 2.3.3 below). In considering the adequacy of the current standards, it is impor tant to note that over th e last few years, the standards have been met throughout the country with few exceptions. 35 Although we consider it unlikely that air concentrations in many urban ar eas across the U.S. that are currently well below the current standards would increase to just meet the 8-hour standard, we recognize the potential
for CO concentrations in some areas currently below the standard to increase to just meet the standard. Accordingly, we have simulated conditi ons of increased CO concentrations that just
meet the current 8-hour standard in the two st udy areas. In this scen ario, we note there is uncertainty associated with simulating this hypothe tical profile of higher CO concentrations that just meet the current 8-hour standard. To investigate the extent to which the re lationship between 1-hour and 8-hour average
ambient CO concentrations in the REA-simulated air quality datasets reflect those prevalent in the U.S. today, we have considered ratios of 1- hour design values to 8-hour design values for those datasets in light of th e distribution of such ratios for U.S. counties with 2009 CO monitoring data (Appendix C). Under air quality conditions for just meeting the current 8-hour standard and those for just mee ting alternative standards these ra tios for the two study areas fall well within the 2009 national distribution. More sp ecifically, the ratio of the 1-hour design value to the 8-hour design value for the Los Angeles study area corresponds to approximately the 25 th percentile of U.S. counties in 2009 and the ra tio for the Denver study area corresponds to approximately the 75 th percentile of U.S. counties in 2009. Under “as is” conditions the ratios for these two study areas corres pond to approximately the 40 th percentile of the 2009 national
distribution. The exposure and dose modeling, presented in detail in the REA, relied on EPA’s Air Pollutant Exposure model (APEX4.3), which es timates human exposure using a stochastic, event-based microenvironmental approach (REA, chapter 4). This model has a history of application, evaluation, and progressive model development in estimating human exposure and dose for several NAAQS reviews, including CO, ozone (O 3 ), NO 2 , and sulfur dioxide (SO 2 ). As mentioned above, we have made major changes to the exposure modeling approach used in the last CO review. The prior review relied on estimated population expos ure and dose generated from pNEM, a model that 1) employed a cohort-based approach, 36 2) relied on a limited set of

35 As described in section 1.3.3 above, in the most recent period analyzed (2007-2008), all areas of the U.S. met both CO NAAQS. In both of the previous periods (2005-2006 and 2006-2007), one area of the country (Jefferson County, Alabama) did not meet the 8-hour sta ndard. Further, one area of the country (Las Vegas, Nevada) is designated in non-attainment with the CO NAAQ S although air quality in that area has met the standards in the past three periods.

36 When using the cohort approach, each cohort is assumed to contain persons with identical exposures during the specified exposure period. Thus, variability in exposure will be attributed to differences in how the2-42 activity pattern data (approximately 3,600 person-d ays), 3) used four br oadly defined categories to estimate breathing rates (i.e., slow-sleep ing, slow-awake, medium, and fast), and 4) implemented a geodesic distance range methodology to approximate workplace commutes (Johnson et al., 1992; US EPA, 1992). Each of these approaches used by pNEM, while appropriate given the data availa ble at that time, would tend to limit the ability to accurately model expected variability in the popul ation exposure and dose distributions. In contrast, APEX4.3 includes new algorithms to 1) simu late longitudinal activity sequences and exposure profiles for individuals, 2) estimate activity-specific minute-by-minute oxygen consumption and breathing rates, 3) address spatial variability in home and work-tract ambient concentrations for commuters, and 4) estimate event-based microenvironmental
concentrations. APEX also uses additional data available from recent activity pattern surveys (CHAD 37 now has about 34,000 person-days of data) and uses the most recent US census data to represent population demographi cs and home-to-workplace commute s. Modeling the prevalence of exposures or dose in a population of interest (s uch as individuals with coronary heart disease)
has also been enhanced in APEX with the addi tion of output tables pr esenting statistics for identified subpopulations and age groups (or lifest ages). Further, the current model uses the updated census population demographic data and incl udes options for selecting algorithms used
to estimate microenvironmental concentrations. Each of these new model developments (REA, chapter 4) are designed to allow APEX to be tter represent human behavior, human physiology,
and microenvironmental concentrations and to more accurately estimate variability in CO exposures and COHb levels. APEX probabilistically generates a sample of hypothetical indivi duals from an actual population database and simulate s each individual’s movements through time and space (e.g., indoors at home, inside vehicles) to estimate his or her exposure to a pollutant (REA , chapter 4). Population characteristics are taken into accoun t to represent the demographics of each study area. With regard to age and gender demogra phics for the two simulated at-risk populations,
adults with CAD and adults with heart diseases of any type (HD), we augmented the prevalence estimates provided by the Nationa l Health Interview Survey with estimates of undiagnosed ischemia (REA, section 5.5.1). The undiagnosed ischemia estimates were based on two

cohorts are defined, not neces sarily reflecting differe nces in how individuals might be exposed in a population. In the assessment for the review completed in 1994, a total of 420 cohorts were used to estimate population exposure based on selected demographic information (11 groups using age, gender, work status), residential location, work location, and presence of indoor gas stoves (Johnson, et al., 1992; USEPA, 1992).

37 CHAD is EPA’s Comprehensive Human Activity Data base which provides input data for APEX model simulations (REA, sections 4.3 and 4.4).2-43 assumptions: (1) there are 3.5 million persons in U.S. with undiagnosed IHD (AHA, 2003) and (2) persons with undiagnosed IHD are distributed within the population in the same manner as persons with diagnosed IHD (REA, section 5.5.1 ). Based on exposure concentrations, minuteby-minute activity levels, and physiological charact eristics of the simulated person (see REA, chapters 4 and 5), APEX estimates the level of COHb in the blood at the end of each hour based
on a nonlinear solution to the Coburn-Fors ter-Kane equation (REA, section 4.4.7). APEX simulations performed for this review have focused on exposures to ambient CO occurring in eight microenvironments, abse nt any contribution to microenvironment concentrations from indoor (nonambient) CO s ources, although, where present, indoor sources, including gas stoves, attached garages and tobacco smoke, can also be important contributors to total CO exposure (ISA, section 3.6.1). Some as sessments performed previously have included modeling simulations both with and without certain indoor sources, and these assessments provide context for the assessment of ambien t CO exposure and dose. For example, a 2000 exposure/dose assessment indicated that the impact of such s ources can be substantial with regard to the portion of the at-risk population experiencing higher exposures and COHb levels (Johnson et al., 2000). In the last review it wa s noted that while thes e indoor sources were shown to contribute to total CO exposure they w ould not be effectively mitigated by setting more stringent ambient air quality standards (59 FR 38914). While we are limited with regard to information regarding CO emissions from indoor sources today and how they may differ from the time of the 2000 assessment, we note that am bient contributions have notably declined, and
indoor source contributions from some sources ma y also have declined. Thus, we have no firm
basis to conclude a different role for indoor sources today w ith regard to contribution to population CO exposure and COHb levels. We note that the absence of indoor (nonambient) sources 38 in the model simulations for this review is expected to result in somewh at higher estimates of the contribution of shortduration increases in ambient CO exposure to COHb levels than is likely to be the case in situations where the presence of nonambient sources contributes to higher baseline COHb levels in the exposed individuals. The amount by wh ich the ambient contri bution estimates might differ is influenced by the magnitude of nonambie nt-source exposures and associated baseline
COHb levels. One reason for this is that in the presence of indoor sources, baseline COHb levels (i.e., COHb prior to a short-du ration exposure event) will be higher for a given population group than COHb levels for that group arising sole ly from endogenous CO in the absence of any exposure, which is the “baseline” for the REA es timates of ambient cont ribution to COHb (REA,

38 Nonambient sources of CO exposure can include ga s stoves, space heaters, attached garages and tobacco smoke (ISA, pp. 3-76, 3-83).2-44 appendix B.6). As CO uptake depends in part on the amount of CO already present in the blood (and the blood-air CO concentration gradient), in general, a higher baseline COHb, with all other variables unchanged, will lead to relatively lesser uptake of CO from short-duration exposures (ISA, section 4.3; AQCD, section 5.2). Additiona lly, as is indicated by the REA estimates, the attainment of a particular dose level is driven largely by short-term (and often high concentration) exposure events. This is because of the relatively rapid uptake of CO into a person’s blood, as demonstrated by the pattern in the REA time-series of ambient concentrations, microenvironmental exposures, and COHb levels (REA, Appendix B, Figure B-2). For example the time lag for response of an individual’s C OHb levels to variable ambient CO (and hence exposure) concentrations may be only a few hours. As discussed in the previous section (Section 2.2.1), people with cardiovascular disease are the population of primary focus in this review . More specifically, coronary artery disease, also known as coronary heart di sease is the “most important su sceptibility characteristic for increased risk due to CO exposure” (ISA, p. 2- 11). Controlled human exposure studies have provided quantitative COHb dose-response informa tion for this specific population with regard to effects on markers of myocardial ischemia. In identifying COHb levels of interest for at-risk populations simulated in the REA, we have give n primary focus to the multi-laboratory study in which COHb was analyzed by the more accura te GC method (Allred et al., 1989a, 1989b, 1991)
discussed in section 2.2.1 above. Based on the strength of the ev idence and the av ailability of quantitative information from these controlled human exposure studies, the REA focuses on estimates of the percent of the simulated at-risk populations expect ed to experience one or more occurrences of daily maximum end-of-hour COHb levels of interest. Further, based on the current evidence with regard to quantitative info rmation of COHb levels and association with specific health effects, the at-risk populations simulated in the quantitative assessment were (1) adults with CHD (also known as ischemic h eart disease IHD or C AD), both diagnosed and undiagnosed, and (2) adults w ith any heart diseases, incl uding undiagnosed ischemia. 39 Evidence characterizing the nature of specific health effects of CO in other populations is limited and does not include specific COHb levels related to health effect s in those groups. As a result, the quantitative assessment does no t develop separate quantitative dose estimates for populations
other than those with CAD or HD. The REA developed COHb estimates for the si mulated at-risk populations with attention
to both COHb in absolute terms and in terms of the contribution to absolute levels associated with ambient CO exposures. For the REA results described below, absolute COHb refers to

39 As described in section1.2 above, this is the same population group that was the focus of the CO NAAQS exposure/dose assessments conducted previously (e.g., USEPA, 1992; Johnson et al., 2000).2-45 estimates of COHb levels resulting from e ndogenously produced CO and exposure to ambient CO, in the absence of any nonambient sources. The additional REA estimates of ambient CO exposure contribution to COHb levels are calculated by subt racting COHb estimates obtained in the absence of CO exposure - i.e., that due to endogenous CO production alone (see REA, appendix B.6) - from the corresponding end-of-hour absolute COHb estimates for each simulated
individual. The maximum end-of-hour ambient contributions across the simulated year are considered, in addition to the maximum absolute end-of hour COHb levels. In considering these two types of COHb estimates, we note that the lack of nonambient sources is likely to have
resulted in lower baseline COHb levels (levels of COHb prior to an individual’s encounter with elevated ambient exposure concentrations) than if the individuals’ exposure history included
additional CO sources. These REA “baseline” COHb levels would also be expected to be lower than the initial, pre-exposure, COHb levels of subjects in the cont rolled exposure studies. 40 As mentioned above, such a lower baseline contribut es to a relatively greater COHb response to short-duration high-con centration exposures.
In our consideration of the REA dose estima tes with regard to consideration of the adequacy of the current standards, we focus on estimates of the portion of the simulated at-risk populations estimated to experience daily maximu m end-of-hour absolute COHb levels above identified benchmark levels, and also consid er the population estimat es of daily maximum
ambient contribution to end-of- hour COHb levels. The benchm ark levels, described below, assist in our interpretation of the COHb estimates in light of the evidence for ischemia-related effects in CAD patients in the controlled human exposure studies. For purposes of considering estimates of abso lute COHb, we identif ied benchmark levels of 1.5%, 2.0%, 2.5% and 3% COHb. This range incl udes the range of COHb levels identified as levels of concern in the review completed in 1994 (2.0 to 2.9%) and the level given particular focus (2.1%) at that time, as described in section 2.1.1 above (USEPA, 1992; 59 FR 48914). Selection of this range of benchmark levels is based on consideration of the evidence from
controlled human clinical studie s of CAD patients (discussed in section 2.2.1 above), with the lower end of the range extending below the lowe st mean COHb level resulting from controlled exposure to CO in the clinical evidence (e.g., 2.0% post-exercise in Allred et al., 1989b). The extension of this range reflects a number of c onsiderations, including: (1) comments from the CASAC CO panel on the draft Scope and Methods Plan (Brain, 2009); (2) consideration of the

40 REA estimates of endogenously formed COHb averaged about 0.3% across the simulated populations, with slightly higher levels in the higher altitude Denver study area (REA, pp. B-21 to B-22). Levels in the Denver study population ranged from 0.1 to 1.1 % COHb, with an average of 0.31%, while levels for Los Angeles ranged from 0.1 to 0.7% with an average of 0.27% COHb. Initial, pre-exposure COHb levels in the subjects of the Allred et al. study (1989b), which reflect the subjects pre-study exposure history as well as endogenous CO formation, ranged from 0.2 to 1.1%, averaging about 0.6% COHb.2-46 uncertainties regarding the actua l COHb levels experienced in the controlled human exposure studies; (3) that these studies did not include individuals with most severe cardiovascular
disease 41 ; (4) the lack of studies that have evaluated effects of e xperimentally controlled shortterm CO exposures resulting in mean COHb leve ls below 2.0-2.4%; and (5) the lack of evidence
of a threshold at the increased COHb levels ev aluated. We note that CASAC comments on the
first draft REA recommended the addition of a benchmark at 1.0% COHb and results are presented for this COHb level in the REA. Given that this level overlaps with the upper part of the range of endogenous levels in healthy individu als as characterized in the ISA (ISA, p. 2-6), and is within the upper part of the range of baseline COHb levels in the study by Allred et al (1989b, Appendix B), however, we considered that it may not be appropriate to place weight on it as a benchmark level and accordingly have not focused on interpreting absolute COHb
estimates at and below this level in the disc ussion below. Additionally we note the REA estimates indicating that, in th e absence of CO exposure, appr oximately 0.5% to 2% of the simulated at-risk populations in the two study area s were estimated to experience a single daily maximum end-of-hour COHb level, arising sole ly from endogenous CO production, at or above 1% (REA, Appendix B, Figure B-3).
We also consider the evidence from contro lled human exposure studies, discussed in section 2.2.1 above, in our interpretation of th e REA estimates of maximum ambient exposure contributions to end-of-hour COHb levels (des cribed in sections 4.4.7 and 5.10.3 of the REA). As discussed above, the study by Allred et al (1989a, 1989b, 1991) observed reduced time to exercise-induced angina and ST-s egment change in groups of subj ects with pre-existing CAD for which controlled CO exposures increased th eir COHb levels by on average 1.4-1.7% and 3.3-
4.0% COHb from initial COHb levels of on aver age 0.6% COHb (ISA, section 5.2.4; Allred et al., 1989a, 1989b, 1991). The study reported a dose -response relationship in terms of time reduction per 1% increase in COHb concentratio n based on analysis of the full data set across both exposure groups. For purposes of the discussi on in this document, we have presented the percentage of the simulated at-risk populati ons estimated to experience maximum ambient
contribution to end-of-hour COHb levels above and below a range of levels extending from 1.4 to 2.0%. In considering REA results for this me tric, we recognize distinctions between the REA “baseline” (arising from prior ambient exposur e and endogenous CO production) and the preexposure COHb levels in the clinical study (a rising from ambient and nonambient exposure history, as well as from endogenous CO producti on). We also note the impact of “baseline”

41 Although the CAD patients evaluated in the controlled human exposure study by Allred et al. (1989a, 1989b, 1991) are not necessarily representative of the mo st sensitive population, the level of disease in these individuals ranged from moderate to severe, with the majority either having a history of myocardial infarction or having ≥ 70% occlusion of one or more of the coronary arteries (ISA, p. 5-43).2-47 COHb levels on COHb levels occurring in response to short ambient CO exposure events such as
those simulated in the REA as discussed above.

 What is the magnitude of at-risk populat ion COHb levels estimated to occur in areas simulated to just meet the current CO standards? What portion of the atrisk population is estimated to experien ce maximum COHb levels above levels of potential health concern? In addressing this question, we consider the population COHb estimates provided by the REA simulations of exposure to ambient CO (R EA, section 6.2). As in the last review, we recognize that indoor sour ces of CO can be important determ inants of population exposures to CO and to population distributions of daily maxi mum COHb levels, and th at for some portions of the population, these sources may dominate CO exposures and related maximum COHb levels. We additionally take note of the conclu sions drawn in the prev ious review that the
contribution of indoor sources to individual exposures and associ ated COHb levels cannot be effectively mitigated by ambient air quality st andards (e.g., 59 FR 38914) and so focus here on COHb levels resulting from ambient CO exposures . In so doing, however, we also recognize as noted above, that simulations focused solely on exposures associated with ambient CO may overestimate the response of COHb levels to short-duration ambient e xposures (the ambient contribution) as pre-exposure baseline COHb leve ls will necessarily not reflect the contribution
of both nonambient and ambient sources. In considering the REA estimates for curr ent or “as is” air quality conditions and conditions simulated to just meet the current 8-hour standard, we particularly focus on the extent to which the current standards provide protecti on to the simulated at-r isk population from COHb levels of potential concern, by comparing the estimated levels in the population to the
benchmarks described above. As described a bove, the REA presents two sets of COHb
estimates: the first set of absolute estimates refl ect the impact of ambient CO exposures in the absence of exposure to nonambient CO, but in the presence of endogenous CO production, while the second set are estimates of the portion of ab solute COHb estimated to occur in response to the simulated ambient CO exposures, i.e., afte r subtraction of COHb resulting from endogenous CO production (REA, sections 4.4.7 and 5.10.3). In describing the REA results here, we draw from exposure and dose estimates for both th e HD and CHD populations (REA, section 6.2), recognizing that, in term s of percentages of persons expos ed and experiencing daily maximum end-of-hour COHb at or above spec ific levels, the results are sim ilar for the two simulated at-risk populations (HD and CHD). We not e that, in terms of absolute numbers of persons, the results
differ due to differences in the size of the two populations. First, we consider the absolute COHb results, with regard to the percentage of simulated populations experiencing at leas t one day with an end-of hour COHb level above selected2-48 benchmarks (Table 2-4). Another dimension of the analysis, presente d in Table 2-5, is the percentage of simulated populations experiencing multiple days in the simulated year with an
end-of-hour COHb level above the same benc hmarks. These two dimensions of the dose estimates are combined in the metric, person-days , which is presented in Tables 6-15, 6-16, 6-18 and 6-19 of the REA. The metric, person-days, wa s the focus of exposure/dose considerations in the last review for which a previous version of the exposure/dose model was used (59 FR 38914; USEPA, 1992). 42 The person-days metric is a co mmon cumulative measure of population exposure/dose that simultaneously takes into account both numbers of people affected and
numbers of times affected. Under current air quality condi tions, the absolute COHb esti mates are appreciably lower than those for conditions of higher ambient CO concentrations in which the current 8-hour standard is just met (Table 2-4). Under “as is” (2006) conditions in the two study areas, no person in the simulated at-risk popu lations is estimated to experien ce any days in the year with
end-of-hour COHb concentrations at or above 3% COHb, and le ss than 0.1 % of the simulated at-risk populations are estimated to experience at leas t one end-of-hour COHb concentration at or above 2% (Table 2-4). Slightly higher pe rcentages of the simulated populations (1-2%) are estimated to experience a single occurrence of daily maximum COHb at or above 1.5%. Under conditions with higher ambient CO con centrations simulated to just meet the current 8-hour standard, the porti on of the simulated at-risk popul ations estimated to experience daily maximum end-of-hour COHb levels at or a bove benchmarks is great er in both study areas, with somewhat higher percentages for the Denv er study area population (T able 2-4). In both study areas, nonetheless, less than 1% of the simulated at-ris k populations is estimated to experience a single day with a ma ximum end-of hour COHb level at or above 3% (Table 2-4) and no person is estimated to experience more than one such day in a year (Table 2-5). Further, less than 0.1% of simulated populat ions in either study area is estimated to experience a single day with maximum end-of-hour COHb at or abov e 4%. A difference between the study areas is more evident for lower benchmarks, with less than 5% of the simulated at-risk population in the Denver study area and less than 1% of the corresponding population in the Los Angeles study area estimated to experience any days with a ma ximum end-of-hour COHb level at or above 2% (Table 2-4). Appreciably smaller percentages of the simulated at-risk pop ulation were estimated to experience more than one day with such leve ls (Table 2-5). For example, less than 1.5% of the population is estimated to experience more th an one day in a year with a maximum COHb level at or above 2.0%, and less than 0.1% are estimated to experience six or more days such

42 As described above, pNEM, the model used in the last review, employed a cohort-based approach from which person-days were the exposure and dose metrics (USEPA, 1992; Johnson et al., 1992).2-49 days in a year. Additionally, consistent with the findings of the assessment performed for the review completed in 1994, less th an 0.1% of person-days for the simulated at-risk populations
were estimated to have end-of-hour COHb levels at or above 2% COHb (REA, Tables 6-18 and 6-19).

Table 2-4. Portion of simulated HD populations wi th at least one daily maximum end-ofhour COHb level (absolute) at or above indicated levels under air quality conditions simulated to just meet the cu rrent standard and “as is” conditions.

Percentage (%) of Simulated HD Population A

Just Meeting Current 8-hour Sta ndard “As is” (2006) Conditions Daily Maximum End-of-hour COHb (Absolute) Los Angeles (1-hr DV = 11.8 ppm) Denver (1-hr DV = 16.2 ppm) Los Angeles (8-hr DV = 5.6 ppm) (1-hr DV = 8.2 ppm) Denver (8-hr DV = 3.1 ppm) (1-hr DV = 4.6 ppm)

> 4.0% 0 <0.1 B

> 3.0% < 0.1 B 0.3

> 2.5% < 0.1 B 0.9 0 0

> 2.0% 0.6 4.5 < 0.1 B < 0.1 B

> 1.5% 5.0 24.5 1.6 1.2

A Drawn from Tables 6-15 through 6-19 of the REA.

B < 0.1” is used to represent nonzero estimates below 0.1%. Abbreviations: hr = hour, DV = Design Value2-50 Table 2-5. Portion of simulated CHD population with multiple days of maximum end-ofhour COHb levels (absolute) at or ab ove the indicated levels under air quality conditions simulated to just meet the cu rrent standard and “as is” conditions.

Percentage (%) of Simulated CHD Population A Just Meeting Current 8-hour Sta ndard “As is” (2006) Conditions
Los Angeles (1-hr DV = 11.8 ppm) Denver (1-hr DV = 16.2 ppm) Los Angeles (8-hr DV = 5.6 ppm) (1-hr DV = 8.2 ppm) Denver (8-hr DV = 3.1 ppm) (1-hr DV = 4.6 ppm) Maximum

End-ofhour COHb Level (Absolute) > 2 days > 4 days > 6 days > 2 days > 4 days > 6 days > 2 days > 4 days > 6 days > 2 days > 4 days > 6 days

≥ 3.0% 0 0 0 0 0 0 0 0 0 0 0 0

≥ 2.5% < 0.1 B 0 0 < 0.1 B 0 0 0 0 0 0 0 0

≥ 2.0% 0.2 < 0.1 B < 0.1 B 1.4 0.2 < 0.1 0 0 0 < 0.1 B < 0.1 B < 0.1 B

≥ 1.5% 2.2 0.7 0.5 11.2 5.0 3.3 0.5 0.2 0. 1 0.7 0.5 0.4

A These estimates are drawn mainly from Figures 6-5 and 6-6 of the REA and repres ent the percentage of persons experiencing greater than or equal to 2, 4, or 6 days with a maximum end-of-hour COHb (absolute) at or above the selected level.

B < 0.1 is used to represent nonzero estimates below 0.1%.

As described above, the REA also presented estimates of the portion of the absolute COHb levels occurring in response to the simula ted ambient CO exposures (i.e., that not derived from endogenous CO production). The REA refers to these estimates as the ambient CO contribution to (absolute) COHb. Under conditions just meeting the current 8-hour standard in the two study areas, less than 3 percent of the simulated at-risk populations was estimated to experience a daily maximum ambient CO contri bution to end-of-hour COHb level above 2% (Table 2-6), with less than 13 percent of e ither population experiencing maximum ambient
contributions at or above 1.4% COHb. As obs erved with the absolute COHb estimates under conditions just meeting the standard, the resu lts for the Denver study area included larger percentages of the population abov e specified levels than those for the Los Angeles study area, reflecting the study area differen ce in 1-hour peak concentrati ons (Table 2-6). Although estimates of population percentages for multiple occurrences are not available for the ambient contribution estimates, it is expected that simila r to those for absolute COHb, they would be appreciably lower than those shown here for at least one occurrence. Additionally, as mentioned above, somewhat lower ambient contribution estima tes might be expected if other (nonambient) CO sources were present in the simulations.2-51 Table 2-6. Portion of simulated CHD population with at least one daily maximum ambient contribution to end-of-hour COHb at or above the indicated levels under air quality conditions simulated to just meet the current standard and “as is” conditions.

Percentage (%) of Simulated CHD Population A

Just Meeting Current 8-hour Sta ndard “As is” (2006) Conditions Maximum Ambient Contribution

to End-ofhour COHb Los Angeles (1-hr DV = 11.8 ppm) Denver (1-hr DV = 16.2 ppm) Los Angeles (8-hr DV = 5.6 ppm) (1-hr DV = 8.2 ppm) Denver (8-hr DV = 3.1 ppm) (1-hr DV = 4.6 ppm)

≥ 2.0% 0.5 2.7

≥ 1.8% 0.8 3.4 0 0

≥ 1.6% 1.3 6.8

≥ 1.4% 2.0 12.8 0.5 0.2

A Drawn from Tables 6-17 and 6-20 of the REA. Abbreviations: hr = hour, DV = Design Value

In considering the estimates presented here of population occurren ces of daily maximum
COHb levels for REA simulations under conditions just meeting the curre nt 8-hour standard, we note that an important contribu ting factor to the higher percentages estimated for the Denver study area population is the occu rrence of higher 1-hour peak am bient CO concentrations and consequent higher CO exposures than occur in the corresponding Lo s Angeles study area simulation (REA, section 6.1.2, Tables 6-7 and 6-10). The difference in the peak 1-hour ambient concentrations is illustrated by the higher 1-hour design values noted for Denver as compared to Los Angeles in Table 2-4 (16.2 ppm versus 11.8 ppm) . This difference, particularly at the upper percentiles of the air quality distribution, is likely driving the higher population percentages estimated to experience higher 1-hour and 8- hour exposures in the Denver study area as compared to Los Angeles (REA, Tables 6-7 and 6-10). 43 The situation is largely reversed under “as is” conditions, where the Los Angeles st udy area has generally hi gher 1-hour and 8-hour
ambient CO concentrations as il lustrated by the design values for alternative standard forms in Table 2-7 below (as well as Tables 3-1 to 3-6, 5-14 and 5-16 of the REA), and Los Angeles also has higher percentages of people estimated to be exposed to the higher exposure concentrations (REA, Tables 6-1 and 6-4). Thus, we recogni ze the impact on daily maximum COHb levels of

43 Other factors that contribute less to differences in COHb estimates between the two study areas, include altitude, which slightly enhances endogenous CO and C OHb formation and can enhance COHb formation induced by CO exposure under resting conditions (ISA, p. 4-19), and design aspects of the study areas with regard to spatial variation in monitor CO concentrations and population density near these monitors (REA, section 7.2.2.1).2-52 1-hour ambient concentrations separate from th e impact of 8-hour average concentrations, and take note of this in considering the REA results with regard to the ad equacy of the 1-hour standard. Taken together, the REA results indi cate occurrences of C OHb levels above the
benchmarks considered here that are associated with 1-hour ambient concen trations that are not controlled by the current suite of standards.

 What are the key uncertainties associated with our exposure and dose estimates, including those of particular significance with regard to drawing conclusions as to the adequacy of the protection affo rded by the current CO standards? In considering the uncertaintie s associated with the quantitative estimates of exposure and dose from the REA, we relied on an appro ach intended to identify and compare the relative impact that important sources of uncertainty may have on the estim ated potential health effect endpoints (i.e., estimates of the maximum end-o f-hour COHb levels in the simulated at-risk population). The generally qualita tive approach used (as described in section 7.2 of the REA) was developed using guidelines outlining how to conduct a qualitative uncertainty characterization (WHO, 2008) and applied in the most recent NO 2 (USEPA, 2008b) and SO 2 NAAQS reviews (USEPA, 2009). We employed this approach given the extremely limited data available to inform probabilistic analyses. The qualitative approach used varies from that of WHO (2008) in that a greater focus of the ch aracterization performed was placed on evaluating the direction and the magnitude of the uncertainty; that is, qualit atively rating how the source of uncertainty, in the presence of alternative information, may aff ect the estimated exposures and
health risk results. In addition and consistent with the WHO (2008) guidance, we discuss the uncertainty in the knowledge-base (e.g., the accuracy of the data used, acknowledgement of data gaps) and decisions made where possible (e.g., selection of particular model forms), though qualitative ratings were assigned only to uncertainty regarding the knowledge-base. In the characterization of uncertainty for the current analysis, we identified and evaluated sixteen separate sources of uncer tainty associated with four main components of the assessment:

 Ambient monitor CO concentrations

- database quality, spatial and temporal representation, ze ro concentration frequency, and missing data substitution;

 Adjustment of air quality to simulate just meeting the current and potential alternative standards

- historical data used, pro portional approach used;

 APEX inputs and algorithms

- population database, activity pattern data base, longitudinal profile algorithm, meteorological data, microenvironmenta l algorithm and input data, commuting algorithm, prevalence rates for at-risk populations, phys iological factors; and,2-53  Potential health effects benchmark leve ls for the simulated at-risk population. Further, an additional area of uncertainty not di rectly evaluated is the contribution of ambient CO to COHb levels in the presence of nona mbient exposures, although as discussed above, previous assessments indicated that, where presen t, the contribution of nonambient exposures to COHb can be substantial in comparison to ambient exposures. By comparing judgments made regarding the magnitude and direction of influence the identified sources have on estimated exposure concentrations and dose levels and the existing uncertainties in the knowledge-base, we identifie d seven sources (i.e., the spatial and temporal representation of ambient monitoring data, histor ical data used in representing alternative air quality scenarios, activity pattern database, longitudinal profile algor ithm, microenvironmental algorithm and input data, and physiological fact ors) that remain as the most important uncertainties in this assessment. Taking in to consideration improvements in the model algorithms and data since the last review, and having identified and characterized these uncertainties here, we conclude that the estima tes associated with the current analysis, at a minimum, better reflect the full distribution of ex posures and dose as compared to results from the 1992 analysis. We note, however, potentia lly greater uncertainty remaining in our characterization of the upper a nd lower percentiles of the dist ribution of population exposures
and COHb dose levels relative to that of ot her portions of the respect ive distribution. When considering the overall quality of the current e xposure modeling approach , the algorithms, and input data used, alongside the id entified limitations and uncertain ties, we conclude that the quantitative assessment provides reasonable esti mates of CO exposure and COHb dose for the simulated population the assessment is intended to represent (i.e., the popul ation residing within the urban core of each study area). We additionally note the impact on the REA dose estimates for ambient CO contribution
to COHb of the lack of nonambient sources in the model simulations. This aspect of the assessment design may contribute to higher esti mates of the contribution of short-duration ambient CO exposures to total C OHb than would result from simu lations that include the range of commonly encountered CO sources beyond ju st those contributing to ambient air CO concentrations. Although the sp ecific quantitative impact of this on estimates of population percentages discussed in this document is unknow n, consideration of COHb estimates from the 2000 assessment indicates a poten tial for the inclusion of nonamb ient sources to appreciably affect absolute COHb (REA, section 6.3) and a ccordingly implies the potential, where present, for an impact on overall ambient cont ribution to a person’s COHb level.2-54  To what extent are the estimates of at-risk population COHb levels under conditions just meeting the current CO standards important from a public health perspective? In considering the public health implications of the quantitative dose estimates, we first consider the effects identified by the evidence to be associated with COHb levels of a magnitude of the daily maximum end-of-hour levels estimat ed in the REA for conditions just meeting the current suite of standards. For example, as a result of ambient CO exposures occurring under air quality conditions adjusted to just meet the curr ent standard, the REA estimates that 0.6 percent of the Los Angeles and 4.2 percent of the Denver study CHD populations may experience an occurrence of a daily maximum end-of-hour COHb level at or above 2% COHb, the low end of the range of average COHb leve ls experienced by the lower c ontrolled exposure group in the study by Allred et al. (1989a, 1989b, 1991), while 0.2 and 1.4 percent, respectively, of the populations are estimated to experience more than one such occurrence. Additionally, less than 0.1 percent of the simulated populat ions in either study area are es timated to experience a COHb level similar to the higher contro lled exposure group (4% COHb). As discussed in section 2.2.1 above, the study by Allred et al., (1989a, 1989b, 1991)
indicates that increases in blood COHb in response to 1-hour CO exposures on the order of 50 to 200 ppm (and higher) produce evidence of myocar dial ischemia in CAD patients with reproducible exercise-induced angina. At a study group average COHb level of 2%, the statistically significant reduction in the time to ex ercise-induced markers of myocardial ischemia (angina and ECG ST-segment ch ange) in CAD patients was 4-5% on average (approximately 30 seconds), with larger reductions observed at the 4% COHb level. In discussing public health implications of the observed res ponses, the study authors noted th at the response observed at the higher COHb level (~4%) were similar to that c onsidered clinically significant when evaluating medications to treat angina from coronary artery disease. The independe nt review panel for the study further noted that frequent encounters in “everyday life” with increased COHb levels on
the order of those tested in the study might be expected to limit ac tivity and affect quality of life (Allred et al., 1989b, pp. 38, 92- 94; 1991 AQCD, p. 10-35). In the review completed in 1994, the body of ev idence that demonstrated cardiovascular effects in CAD patients exposed to CO was given primary consider ation, with the Administrator recognizing the findings of decreas ed time to onset of ECG change and angina pain as the “health effects of greatest conc ern, which clearly have been asso ciated with CO exposures at levels observed [at that time] in the ambient ai r” (59 FR 38913). We additionally note the doseresponse relationship observed for COHb resulting fr om brief, elevated CO exposures in persons with pre-existing CAD, with no evidence of thre shold, as discussed in section 2.2.1 above (ISA,2-55 section 5.2.4; Allred et al., 1989a, 1989b, 1991). 44 In the current review of the evidence, the ISA describes the physiological significance of the ch anges at the lowest te sted dose level (~2% COHb, Allred et al 1989b) as unc lear, additionally noting that vari ability in severity of disease among individuals with CAD is likely to influenc e the critical level of COHb which leads to adverse cardiovascular effects (ISA, p. 2-6). In the 1994 review decision, less significance was
ascribed to the effects at the lowest COHb le vels assessed in short-term CO exposure studies than effects associated with higher COHb levels (59 FR 38913), with additional weight given to those occurring at dose levels at or above 2.9%, which were described at that time as “effects ... of clear concern” (59 FR 38914). In considering public health implications of the REA estimates, we also consider the size of the at-risk populations simulated. The popula tion with CAD (including undiagnosed cases) is well recognized as susceptible to increased risk of CO-induced health effects (ISA, sections 5.7.1.1 and 5.7.8). The 2007 estimate from the National Health Interview Survey (NHIS) performed by the U.S. Centers for Disease Cont rol of the size of the U.S. population with coronary heart disease, angina pectoris (cardiac chest pain) or who have experienced a heart attack (ISA, Table 5-26) is 13.7 million people (IS A, pp.5-117). Further, there are estimated to be three to four million additional people with silent ischemia or undiagnosed IHD (AHA, 2003). In combination, this represen ts a large population represented by the REA analyses and for which the COHb benchmarks described above (bas ed on studies of CAD patients) are relevant, that is, more susceptible to ambient CO exposur e when compared to the general population (ISA, section 5.7). In addition to the population with diagnos ed and undiagnosed CAD, the REA also simulated ambient CO exposures for the larger HD population, which may also be at increased risk of CO-induced health effects (ISA, section 2.6.1). Within this broader group, implications of CO exposures are more significant for those pe rsons for whom their dis ease state affects their ability to compensate for th e hypoxia-related effects of CO (ISA, section 4.4.4). The NHIS
estimates for 2007 indicate there is a total of a pproximately 25 million people with heart disease of any type (ISA, Table 5-26). Accordingly, whil e the REA estimates in terms of percentages of

44 The dose-response relationship was derived as the average of the regressions of the individual study subject data for changes in time to onset of the monitore d measures of ischemia across their range of COHb levels (from their baseline COHb to their two higher COHb levels resulting from the two experimental CO exposures). The clean-air exposure, post-exercise (baseline) COHb levels in the individual study subjects ranged from 0.2% to 1.1%, their post-exercise COHb levels for the lower experimental CO exposure ranged from 1.0 to 3.0% and their post-exercise COHb levels for the higher experimental CO exposure ranged from 2.3 to 5.1%. The dose-response analysis indicated decreases of roughly 1.9% in time to exercise-induced angina and 3.9% in time to exerciseinduced ST-segment change per 1% increase in COHb concentration (Allred et al., 1989b).2-56 the CAD and HD populations above COHb levels of interest are similar, the estimates in terms
of number of individuals are hi gher for the larger HD population. Other populations potentially sus ceptible to the effects of CO include people with chronic obstructive pulmonary disease, diabetes and anem ia, as well as older adults and fetuses during critical phases of development (as discussed in section 2.2.1 above). In considering potential impacts on such populations, we recognize that the ev idence is limited or lacking with regard to effects of CO at ambient levels, and associat ed exposures and COHb levels, while providing no indication of susceptibility to ambient CO gr eater than that of CHD and HD populations. In summary, while we note the substantial si ze of the population of individuals with CHD
or other heart diseases in the U.S., we recognize that the REA results for conditions just meeting
the current standards indicate a ve ry small portion of this populati on that might be expected to experience more than one occurrence of COHb a bove 2%, with less than 0.1% of this population expected to experience such a leve l on as many as six days in a year or a single occurrence as high as 4%, and 0% of the populat ion expected to experience mo re than one occurrence above 4% COHb. In light of the imp lications of the health evidence discussed above, the public health significance of these REA results and conclusion s regarding the extent to which they are important from a public health perspective depe nds in part on public health policy judgments about the public health signifi cance of effects at the COHb be nchmark levels considered and judgments about the level of public health protec tion with an adequate margin of safety.

2.2.3 CASAC Advice

In our consideration of the adequacy of the cu rrent standards, in a ddition to the evidenceand risk/exposure-based informa tion discussed above, we have al so considered the advice and recommendations of CASAC, based on their review of the ISA, the REA, a nd the earlier draft of this document, as well as comments from the public on earlier drafts of this document and the

REA. 45 The few public comments received on this revi ew to date that have addressed adequacy of the current standards conveyed the view that the curr ent standards are adequate. In support of this view, these commenters disagreed with the REA estimat es of in-vehicle exposure concentrations and argued that little weight should be given to the epidemiological studies. In their comments on the draft PA, the CASAC CO Panel stated overall agreement with staff’s conclusion that the body of evidence and the quantitative exposure and risk assessment provide support for retaining or revising the current 8-hour standard. They additionally,

45 All written comments submitted to the Agency will be av ailable in the docket for this rulemaking, as will be transcripts of the public meetings held in conjunction wi th CASAC’s review of the earlier draft of this document, of drafts of the REA, and of drafts of the ISA.2-57 however, expressed a “preference” for a lower sta ndard and stated that “[i]f the epidemiological evidence is given additional weight, the conclu sion could be drawn that health effects are occurring at levels below the current standard, which would support the tig htening of the current standard.” Taking this into account, the Panel further advised that “rev isions that result in lowering the standard should be cons idered” (Brain and Samet, 2010b).

2.2.4 Staff Conclusions on Adequacy of the Current Standards

In considering the adequacy of the current st andards, staff gives great weight to the longstanding body of evidence for CO, augmented in so me aspects since the last review, that has
established: the common mechan ism of CO health effects as involving binding to reduced iron in heme proteins and the alteration of their functioning; the important role of hypoxia (reduced oxygen availability) induced by increased COHb blood le vels in eliciting hea lth effects; the use
of COHb as the bioindicator and dose metric for evaluating CO exposure and potential for health effects; and, people with cardi ovascular disease as a key popu lation at risk from low CO exposures (ISA; 2000 AQCD; 1991 AQCD). We a dditionally recognize the expansion of the epidemiological evidence that provides logical coherence with our conclusions regarding
cardiovascular disease-re lated susceptibility (IS A, section 5.2.1). As at the time of the last review, we give weight to COHb estimates developed from modeling exposures to ambient CO under conditi ons simulated to just meet the current, controlling, 8-hour standard. We note the different modeling approach in the last review for which the results metric was person-days, and we note similarities between results of the current and past modeling in terms of that metric. In the current modeling, additional metrics for percentage of population with at least one or multip le occurrences of COHb levels of interest are
considered. These absolute COHb estimates an d the incremental contribution to them from ambient CO exposures are considered in light of the evidence from controlled human exposure studies, while recognizing distin ctions between the measurements in those studies and the REA estimates that would be likely to affect the res ponse of COHb levels to elevated ambient CO exposure events. These estimates, which vary be tween the two study areas, indicate that 0.5 to 4.5% of the simulated at-risk populations may experience at least one daily maximum COHb level of a magnitude (at or above 2% COHb) that has been associated with shortened time to exercise-induced appearance of markers of myocar dial ischemia subsequent to 1-hour elevations in CO exposure, and larger portions of the population would experien ce lower COHb levels, below those which have been specifically addr essed in the health effects evidence. In considering the public health signi ficance of such estimates, while recognizing uncer tainty in the health significance associated with the smaller effects observed at the lowest studied COHb levels, we note the substantial size of the at-risk populati on in the U.S. and the existence of other2-58 potentially susceptible populations for which ev idence pertaining to eff ects resulting from CO exposures associated with ambient concentrations is much more limited or lacking. We also take
note of the noticeable variation in the REA e xposure and dose estimates between the two study
areas under conditions simulated to just meet the current 8-hour standard, and its relationship to differences in hourly ambient CO concentrations which fall well below conditions controlled by
the 1-hour standard.
The extent to which the current standards ar e judged to be adequate depends on a variety
of factors inclusive of scien ce policy judgments and public hea lth policy judgments. These factors include public health policy judgments concerning the appropriate COHb benchmark levels on which to place weight, as well as judgm ents on the public health significance of the
effects that have been observed at the lowest levels evaluated, particularly with regard to relatively rare occurrences. The factors relevant to judging the adequacy of the standards also
include consideration of the uncer tainty associated with interp retation of the epidemiological evidence as providing information on ambient CO as distinct from information on the mixture of pollutants associated with traffic, and, give n this uncertainty, the weight to place on interpretations of ambient CO concentrations for the few epidemiological studies available for air quality conditions that did not exceed the current st andards. And, lastly these factors include the interpretation of, and decisions as to the weight to place on, the results of the exposure
assessment for the two areas studied relative to each other and to results from past assessments, recognizing the implementation of an improved m odeling approach and new input data, as well
as distinctions between the REA simulations a nd resulting COHb estimates and the response of COHb levels to experimental CO exposure as re corded in the controlled human exposure studies. We draw conclusions with regard to the ade quacy of the current standards from both the evidence and from the exposure and dose asse ssment, taking into consideration related information, limitations and uncertainties recogni zed above. We conclude that the combined consideration of the body of evidence and the qu antitative exposure and dose estimates provide support for a suite of standards at least as protective as the curren t suite. Further, we recognize that conclusions regarding the ad equacy of the current standards depend in part on public health policy judgments identified above and judgments a bout the level of public health protection with an adequate margin of safety. We additiona lly note the influence that hourly ambient CO
concentrations well below the cu rrent 1-hour standard may have on ambient CO exposures and resultant COHb levels under conditions just m eeting the 8-hour standard, as indicated by the
REA results. We conclude that the REA results indicate the potential for the current controlling
8-hour standard to allow the o ccurrence of 1-hour ambient concen trations that contribute to population estimates of daily maximum COHb leve ls, that depending on public health judgments in the areas identified above, may be considered to call into question the adequacy of the 1-hour2-59 standard and support consideration of revisions of that standard in order to reduce the likelihood of such occurrences in areas just meeting the 8-hour standard. Thus, we conclude that the combined consideration of the evidence and qua ntitative estimates described above may be viewed as providing support for ei ther retaining or re vising the current suite of standards. Staff’s conclusions with regard to elements of revised primary standards for CO that may be appropriate to consider are discussed in the following sections.2-60 2.3 CONSIDERATION OF ALTERNATIVE STANDARDS

To the extent that the information available in this review suggests that revision of the current standards is appropriate to consider, staff has consider ed whether the available body of evidence supports consideration of options that are different from the current standards, as articulated by the following overarching question:

 To what extent does the currently availabl e scientific evidence- and exposure/riskbased information, as reflected in the ISA and REA, support consideration of alternatives to the current CO standard s to provide increased protection from ambient CO exposures? To assist us in interpreting the currently av ailable scientific evidence and the results of recent quantitative exposure/risk analyses to addr ess this question, we have focused on a series of more specific questions in sections 2.3.1, 2.3.2 and 2.3.3 below. In considering the scientific and technical information, we consider both the information available at the time of the last review and information newly available since the last review which has been critically analyzed and characterized in the 2000 AQCD and more recen tly in the ISA. Specifically, we consider how the currently available scient ific evidence informs decisions regarding the basic elements of the NAAQS: indicator, averaging time, level and form . Considerations with regard to indicator and averaging time are presented in sections 2.3.1 and 2.3.2. Form and level are discussed in
section 2.3.3.

2.3.1 Indicator The indicator for CO is CO as measured by the federal reference methods and equivalent methods. Unlike several other criteria pollutants, there are not multiple compounds or size
fractions of CO. Federal refere nce methods are available that can effectively measure CO, and as discussed in section 1.3.2 above, the availabl e federal reference methods include a range of analytical sensitivities to support quantification of CO at ambien t levels. Thus we have not identified any basis for considering an i ndicator other than CO for the standard.

2.3.2 Averaging Time In considering potential averaging times alternative to the current 1- and 8-hour averaging times, we consid er the following question:

 Do health effects evidence and air qualit y/exposure assessments provide support for considering different exposure indices or averaging times? The averaging times for the current standard s are 1 hour (35 ppm) and 8 hours (9 ppm). These averaging times were first chosen when EPA promulgated the primary NAAQS for CO in 1971 (36 FR 8186) and were retained in s ubsequent reviews (1980, 45 FR 55066; 1985, 50 FR2-61 37485; and 1994, 59 FR 38906). The 8-hour averaging time was selected primarily based on the rationale that most individuals appear to a pproach equilibrium blood levels of COHb after approximately 8 hours of continuous CO exposure (USDHEW, 1971; USEPA, 1979; AQCD 2000, section 7.4; ISA, section 4.3.2. 2). Another consideration ha s been that the 8-hour time frame represented a good basis for tracking continuous exposures dur ing any 24-hour period, recognizing that people may be e xposed in approximately 8-hour blocks of time (e.g., working or sleeping) (45 FR 55077). The 1-hour averaging ti me primarily reflected consideration of the potential impact of shorter exposures. Since the establishment of the 1-h our standard, the health effects rationale for that averaging time has been strengthened, with much of the health evidence linked to exposures of 1 hour or somewhat l onger, such as the c ontrolled human studies demonstrating aggravation of myoc ardial ischemia after exposure of individuals with CAD to CO for approximately 1 hour (USEPA, 1984a, 1991; 2000 AQCD; ISA, section 5.2.4). In the last review of the standards, it was recognized that the 1-hour av eraging period provides a better
indicator of short-term health effects of CO (59 FR 38914). Furt her, in considering peak CO concentrations during shorter time periods (eg., hundreds of ppm for several minutes), EPA has recognized that attainment of the 1-hour and 8- hour standards would tend to also limit such short-duration peak concentrations , such as those occurring near busy roadways, to levels below those of concern (45 FR 55077). In considering whether the information availabl e in this review supports consideration for different averaging times for the CO standards, we note that the available information in this review is generally consistent with and supportiv e of the conclusions reached in the previous
reviews to retain the 1- a nd 8-hour averaging times.

 Controlled human exposure studies, with wh ich epidemiological evidence is coherent, provide the clearest evidence of short-term CO-induced eff ects and reflect exposures of 1-2 hours (ISA, sections 5.2, 5.2.6.1).

 Most individuals would be expected to achie ve steady-state levels of blood COHb after 6-8 hours of continuous exposure to a fixed CO concentration. Therefore, 8 hours may reasonably be considered closely represen tative of longer continuous exposures (2000 AQCD, section 7.4).

 Epidemiological studies provide evidence based on analyses of 1-, 8-, and 24-hour averaging times (ISA, section 5.2.6).

 The 1-hour and 8-hour averaging times are c onsidered to provide protection from the occurrence of short-duration elevations in e xposure concentrations of ambient CO that may be encountered in some e nvironments and from COHb levels that may result from such exposures (2000 AQCD, section 7.4; ISA, section 2.4.1).2-62 Taken together, we conclude that the info rmation available in the current review continues to support the 1- and 8-hour averaging times and does not provide support for
consideration of standards with alternative averaging times.

2.3.3 Form and Level In considering forms and levels for potential alternative standards below, we address the following overarching question:

 What is the range of alternative levels and forms for the standard that are supported by the health effects evid ence and air quality/exposure assessments, and what are the uncertainties and limitatio ns in that health effects evidence and air quality/exposure assessments? We focus on general considerations with re gard to form in section 2.3.3.1. We then address specific consider ations for level in combination with form in section 2.3.3.2, with regard
to the 1-hour and 8-hour standards.

2.3.3.1 Alternative Forms

When evaluating potential alternative form s for the CO NAAQS in conjunction with specific levels, staff considers the adequacy of the public health pr otection provided by the
combination of level and form to be the foremost consideration. In additio n, we recognize that it is preferable to have a form that is reasonably stable and relative ly insulated from the impacts of extreme meteorological events or other rare, transitory impacts on air quality. A standard set with a high degree of instability could have the eff ect of reducing public he alth protection because
shifts in and out of attainment could disr upt an area’s ongoing implementation plans and associated control programs. Since the 1971 prom ulgation of the CO NAAQS, this full set of factors have been given weight in revisions to the forms of a number of other NAAQS (e.g., O 3 , PM and NO 2 ). Our consideration of these factors in our evaluation of the form for the CO NAAQS has led us to focus on three aspects which together lead to consid eration of a percentilebased daily maximum statistic av eraged over three years. First, as noted in the review of the O 3 NAAQS (EPA, 2007e), forms that call for averaging of concentrations over three years can better reflect pollutant-associated health risks
than forms based on allowable exceedances. Th is is because such forms give proportionally greater weight to periods of tim e when pollutant concentrations are well above the level of the standard than to times during which the concentra tions are just above the standard, while a form
that allows for one or more exceedances of the standard level would give the same weight to periods of time with concentrations that just exce ed the standard as to times when concentrations greatly exceed the standard level. Additiona lly, averaging concentrations over three years provides greater regulatory stability (e.g., with regard to control programs associated with2-63 attainment status) than a form based on allowing a single exceedance in a year. In considering revision to this aspect of the standard, we not e that while the REA simulations each included only a single year, air quality analyses (e.g., REA, section 3.1.5) may be used to inform consideration of the REA findings with regard to potential revision to a form based on a 3-year average statistic, as well as the approp riate level to accompany such a form. Secondly, a percentile-based statis tic for the form provides for the specification of a more consistent level of air quality among areas of the country having differing numbers of measurements during the time period evaluated. For example, the 90 th percentile of an area with
200 measurements and one with 100 measurem ents would, in both cases, represent the
concentration above which 10% of the measurements in either location are estimated to occur,
while the 3 rd highest concentration in th e first case would be the c oncentration above which 1%
of the concentrations in the location occur and in the second case would be the concentration
above which 2% of the concentrations occur. Lastly, in conjunction with a percentile-ba sed statistic, we have focused on daily maximum concentrations for each averaging time as compared to the maximum across the complete data review period as is the case with the current standard forms of maximum 1-hour average and maximum non-overlapping 8-hour av erage in a year. Daily maximum forms, inherently give greater weight to occurrences on separate days than to multiple occurrences on the same day, and being somewhat less extreme statistics than maximums across a year, may provide for greater regulatory stab ility, thus affording more consis tent air quality protection. In considering specific forms on which to focu s the current review, as shown in Table 2- 7, we note such forms that have been consid ered in other NAAQS reviews, including the 98 th

and 99 th percentile forms. These forms, averaged ove r three years, were c onsidered with regard
to a 24-hour standard for PM and 1-hour standards for NO 2 and SO 2 (USEPA, 2005; USEPA, 2008b; USEPA 2009b). We recognize that at a sp ecific location with measurements taken on every day in a year, a 99 th percentile form for an 8-hour daily maximum standard would correspond to the fourth highest daily maximum 8-hour average con centration in a year, while a

98 th percentile form would corr espond approximately to the 7 th or 8 th highest daily maximum.
We have considered forms of a 99 th percentile (fourth highes t daily maximum) or a 98 th percentile, each averaged over th ree years, as potentia lly providing appropriate balances between limiting peak CO concentrations and providing a stable regulatory targ et. In considering percentile-based statistics for the form of poten tial alternative CO standa rds, however, we focus
on the REA results in section 2.3.3.2 below with regard to a 99 th percentile concentration in recognition of the rapid response of COHb to elevations in CO exposure. When considering results of the REA as they relate to form of the standard presented in section 2.3.3.2 below, we note that a decision on form must be made in conjunction with2-64 selection of a particular standard level. The primary emphasis in such a decision will be on the level of public health protection provided by th e combination of form and level. Table 2-7 presents levels for three standard forms (the current form and two alternatives) for potential
alternative 8-hour and 1-hour standards that would be just met in the five air quality scenarios simulated in the REA based on the air quality da ta sets identified for the two study areas and
described in the REA. The current form of bot h the 8-hour and 1-hour standards is a maximum, not to be exceeded more than once per year. In the section below we consider the results of the
REA for different combinations of level with the alte rnate forms described above in addition to the current “exceeded only once per year” form.

Table 2-7. Level and form for potential alternativ e 8-hour and 1-hour standards that would be just met in the REA air qualit y scenarios simulated with data for the Denver and Los Angeles study areas.

8-hour Averaging Time 1- hour Averaging Time

2

nd

highest maximum a 99 th percentile

daily maximum 98 th percentile

daily maximum 2 nd

highest maximum a 99 th percentile

daily maximum 98 th percentile

daily maximum

------------ ------------ --------- Level (p pm) --------

------------ ------------ Air Quality Scenario Modeled Denver Study Area b

9.4 c 7.2 6.0 16.2 13.3 11.5 Current 8-hour standard (9 ppm)

6.5 5.0 4.2 11.2 9.2 8.0 99 th percentile daily max 8-hr (5.0 ppm)

5.6 4.3 3.6 9.7 8.0 6.9 99 th percentile daily max 1-hr (8.0 ppm)

5.4 c 4.1 3.5 9.3 7.7 6.6 2 nd highest 8-hour average (5 ppm)

3.1 2.8 2.4 4.6 4.5 3.9 As Is (2006) Los Angeles Study Area d

9.4 c 8.2 7.2 11.8 11.6 9.9 Current 8-hour standard (9 ppm)

6.5 5.7 4.9 8.1 8.0 6.8 99 th percentile daily max 1-hr (8.0 ppm)

5.6 5.1 4.8 8.2 7.4 6.7 As Is (2006)

5.7 5.0 4.4 7.2 7.1 6.0 99 th percentile daily max 8-hr (5.0 ppm)

5.4 c 4.7 4.1 6.8 6.7 5.7 2 nd highest 8-hour average (5 ppm) b

Notes:

a This is the form of the current standards.

b For other than As is (2006) scenario, the relationships shown are based on 1995 air quality data proportionally adjusted to just meet the specified air quality scenario.

c Note that the current rounding convention for a standard level for which no decimal places are specified allows for concentrat ions up to the given standard level plus 0.4 ppm.

d For other than As is (2006) scenario, the relationships shown are based on 1997 air quality data proportionally adjusted to just meet the specified air quality scenario.2-65 2.3.3.2 Alternative Levels

In considering alternative standa rd levels with regard to th e potential to provide greater protection than that afforded by the current suite of standards ag ainst CO-related adverse health effects, we have taken into account scient ific evidence from both experimental and epidemiologic studies, as well as the uncertain ties and limitations in that evidence, and the quantitative estimates of exposure and dose provide d by the REA. We note that the scientific evidence and quantitative assessment can provide in sights into alternative standard levels only within the context of specific averaging times and forms. Therefore, this section considers the evidence and quantitative analysis as they relate to alternative levels particular to different forms and averaging times. We believe that the integration of the health effects evidence with the exposure and dose estimates will be particularly important to info rming conclusions regardin g standard levels and forms considered to provide protection of public hea lth with an adequate margin of safety. With regard to the scientific eviden ce, as discussed in section 2.2.1 above, we have given principal emphasis to findings of the multi-laboratory cont rolled human exposure study of individuals with pre-existing CAD (Allred et al., 1989a, 1989b, 1991) . In this study, controlled experimental exposures to CO that resulted in a post-exercise study mean COHb level as low as 2.0% relative to room-air exposures that result ed in a mean baseline COHb leve l of 0.6% (post-exercise) were associated with myocardial ischemia-related eff ects, including, specific ally, reduced time to exercise-induced angina and ST-segment change. 46 Additionally, analysis of the study subjectspecific data indicated a dose-re sponse relationship for these re sponses, with no evidence of a measurable threshold at the controlled exposures evaluated (ISA, secti on 5.2.4; Allred et al., 1989a, 1989b, 1991). For our purposes here, we have also consider ed the epidemiological studies with regard
to the extent to which this evidence is consis tent with and generally supportive of conclusions
drawn from the combined cons ideration of the controlled human exposure evidence with estimates from the exposure and dose assessment. We take note of the epidemiological studies showing positive associations with IHD, CHD a nd CHF health outcomes described in section 2.2.1 above, four of which were based in a study ar ea in which the current standard was met, the associations for three of which (studying two diffe rent areas) were statisti cally significant. In our consideration of the evidence, we recogni ze CASAC advice, both with regard to relative emphasis to give this evidence and with regard to aspects of the epidemiological evidence that

46 The exposure resulting in an average of 2-2.4% COHb reduced the time to these markers by approximately one half minute from the 8.5- to 9.5-minute period without exposure (Allred, et al., 1989b).2-66 are “particularly problematic for CO” and the wei ght to be given to the well-conducted clinical studies (Brain and Samet, 2010a, 2010b). Turning first to the REA results, we consider the absolute COHb estimates for alternative
levels in terms of the current form and of a 99 th percentile daily maximum form in Table 2-8 below. In considering health risk implications for the simulated at-risk population associated with these estimates, we focus on the percentage of simulated at-risk population in each study area estimated to experience daily maximum end-of-hour absolute COHb levels below three benchmark COHb levels: 3.0%, 2.0% and 1.5%. Among the various benchmarks described in section 2.2.2 above, we have iden tified these three specific levels to particularly inform our consideration of the REA estimates in light of different aspects of th e evidence that suggest differing degrees of health signifi cance for each of them. As discu ssed in the sections above, the 3.0% benchmark level is within the range of COHb levels identified in the last review as levels that could induce potentially adverse effects for which it was appropriate that standards provide protection against (59 FR 38913). The 2.0% COHb benchmark level represents the lowest COHb study level resulting from CO exposure at which a resp onse was also observed, although smaller and of less clear health significance. In contrast, the 1.5% benchm ark provides a point of comparison that falls below the levels for which we have evidence of effects. In considering the REA estimates across these three benchmarks, we also recognize a distin ction in public health implications between single and multiple occurrences, particularly with regard to exceedances of
the lower COHb benchmark levels. In considering alternative sta ndard levels, consistent with conclusions reached in section 2.2.4 above, we consider levels for both standard s, while focusing predominantly on the 1-hour
standard. We note the current role of the 8-hour standard in control ling CO concentrations nationally which has led to our greater focus on that standard in desi gning the REA simulations, while recognizing the REA results which indicate the influential role of the 1-hour ambient CO concentrations with regard to magnitude of ambient CO exposures, associated daily maximum end-of-hour COHb levels, and the percentage of the population estimated to experience COHb at or above benchmark levels that may be of concer n. For example, as shown in Table 2-8 below, the REA results for just meeting the current 8- hour standard indicate that the corresponding 1- hour ambient CO level is lower in the Los Angele s study area, and the percentage of the at-risk population exceeding the 2% COHb benchmark is al so lower there than in the Denver study area (Table 2-8, 1st two rows for each form). A mu ch larger difference in population percentages
occurs between these two 1-hour levels at the 1.5 % COHb benchmark level. More specifically, the percentage of the simulated at-risk populati on for whom all daily maximum absolute COHb levels experienced are below 1.5% is estimated to be 95.0% in the Los Angeles study area and2-67 only 75.5% in the Denver study area. At lower altern ative 1-hour standard levels, the differences in population percentage at all COHb benchmarks are much smaller.
We have also considered the REA estimates fo r a series of alternat ive 1-hour standard levels below those associated with just meeti ng the current 8-hour st andard. Based on this information, presented in Table 2-8, we compared REA results for these alte rnative levels to the results for levels just meeting the current 8-hou r standard. For example, in focusing first on estimates for the 3.0% COHb benchmark level, we note that the percentage of the at-risk population for which all daily maximum COHb le vels are below 3.0% COHb ranges from 99.7% of the population under conditions that just meet the current 8-hour standard and for a 1-hour level of 16.2 ppm (2 nd highest form) to >99.9-100% of the population under all alternative 1-hour levels. For the 2.0% COHb benchmark, the corresponding percentage of population avoiding even one such occurrence ranges from 95.5% for the highest 1-hour level to approximately 99% or more of the population for all alternative levels. Lastly, the percentage of population avoiding even one occurrence of a 1.5% daily maximum COHb (the benchmark level below the COHb levels represented in the ev idence) ranges from approximately 75% of the population under conditions that just meet the current 8-hour standard and for a 1-hour level of 16.2 ppm (2 nd highest form) to approximately 90-99% of the population for other standard levels.2-68 Table 2-8. Percentage of simulated HD populatio n with daily maximum end-of-hour COHb levels (absolute) below the i ndicated COHb levels under alternative levels and forms for the 1-hour and 8-hour standards.

Current and Potential Alternative Standards Daily Maximum End-of-hour COHb Level (Absolute)

Level < 3.0 % COHb < 2.0 % COHb < 1.5 % COHb Form 1-hour (ppm) 8-hour (ppm) Los Angeles Denver Los Angeles Denver Los Angeles Denver 8-hour Levels (ppm)

16.2 + 99.7 95.5 75.5 11.8 + 9.4 + >99.9 99.4 95.0 9.4 +

11.2 98.9 90.4 6.5 9.7 93.9 5.6 9.3 >99.9 99.4 94.6 5.4 8.2* 98.4 5.6 * 8.1 98.5 6.5 7.2 99.0 5.7 6.8 5.4–6.5

100 > 99.9

99.2 5.4 Second Highest Non-overlapping

Concentration (Current Form)

4.6* 3.1* 100 >99.9 98.8 3.1 *
13.3 + 99.7 95.5 75.5 7.2 +
11.6 + 7.2-8.2 + >99.9 99.4 95.0 8.2 +
9.2 >99.9 98.9 90.4 5.0
100 > 99.9 98.5 5.7 8.0 93.9 4.3
7.7 >99.9 99.4 94.6 4.1 7.4* 98.4 5.1 *
7.1 99.0 5.0
6.7 4.1– 5.7

100 >99.9

99.2 4.7 99th Percentile of Daily Maximum Concentrations

4.5* 2.8* 100 >99.9 98.8 2.8 * + Plus marks indicate simulations based on air quality conditions just meeting the current 8-hour standard. * Asterisks indicate simulations based on “as is” (2006) air quality co nditions for the two study areas. Drawn from REA tables 6-15 to 6-19 and 6-21 to 6-22, consistent with Table 2-7above.

In addition to consideration of the absolute COHb estimates from the REA, we have also considered the REA population estimates of daily maximum ambient contri bution to end-of-hour (ambient contribution COHb) 47 for the same array of alternativ e levels and forms (Appendix D). In so doing, we recognize additional complexity in interpretations associated with these results,

47 As described in section 2.2.2 above, “ambient contribution COHb” equals “absolute COHb” minus COHb resulting from simulations absent any CO exposu re. The estimates for “absolute COHb” are based on simulations where CO exposure arises only from ambi ent CO sources, in the abse nce of nonambient (indoor) sources. As discussed above, by not considering the contribution of other (nonambient) sources to COHb, the magnitude of the ambient contribution may be overestimated for some persons, affecting these population estimates.2-69 and the lack of information regarding multiple occurrences of specific magnitudes of ambient contribution to COHb. Nonetheless, we observe that all daily maximu m ambient contributions
to end-of-hour COHb estimates are less than 1.5% for more than 90% of the simulated population under all air quality conditions assesse d, and for higher percentages of the population
for somewhat lower standard le vels. In considering this obs ervation, we recognize that the
COHb increase from baseline for the 2% COHb exposure group in the controlled human exposure studies was on the order of 1.5% COHb (Allred et al., 1989b). Taking into account the differences between the simulations for the two study areas, recognizing considerations regard ing absolute COHb benchmarks of 1.5 to 2% and above, the
influence of baseline COHb on COHb level re sponse to exposure even ts, and estimates of
numbers of occurrences of COHb levels of in terest, and being mindful of support provided by the epidemiological studies, we consider th e REA estimates of daily maximum end-of-hour COHb levels with regard to level of protec tion estimated to be pr ovided by the different
alternative levels for the 8-hour and 1-hour standards (Table 2-8) . In further considering the weight to place on this information, we are mi ndful of several key aspects of the evidence (described in more deta il in section 2.2.1 above):

 Uncertainty in the public health significan ce of the effects observed at the lowest exposures in the controlled human exposure studies of CAD patients.

 The lack of evidence for a measurable thresh old effect for the effects observed in the human clinical studies and the lack of studies that have evaluated effects of experimentally controlled short-term CO exposures of individuals with CAD that resulted in study mean COHb levels below 2%.

 Uncertainty associated with interpretation of COHb levels estimated in the quantitative assessment to result from simulated CO exposure concentrations much lower than the experimental CO exposure concentrations used in the controlled human studies to increase subject COHb leve ls to COHb study targets.

 The influence of baseline COHb levels on the impact of short-duration increases in CO exposure concentrations on subsequent COHb levels.

 The lack of studies of COHb levels associat ed with health effects in other potentially susceptible populations.

 Complications associated with quantitativ e interpretation of the epidemiological studies for CO which affect estimation of ambient concentrations that may be triggering health outcomes. We recognize that, just as we concluded in section 2.2.4 above with regard to adequacy of the current suite of standards, the range of alternative standa rds that may be appropriate to consider differs based on the weight placed on diffe rent aspects of the evidence and on different aspects of the quantitative dose estimates, as we ll as on public health policy decisions regarding2-70 the public health significance of the effects considered, the appropriate COHb benchmark on which to focus in considering maximum end-of- hour COHb levels, and th e targeted percentage of the at-risk population. To the extent that consideration is given to revising the 1-hour standard to provide protection against COHb levels associated with elevated 1-hour ambient CO concentrations, in light of the influence of 1-hour CO levels appr eciably below the current 1-hour standard of 35 ppm on population estimates of daily maximum end- of-hour COHb levels, we recognize that the alternative levels appropriate to consider va ry depending on the weight placed on each of the
factors identified above. For exam ple, to the extent that the REA estimates are judged to indicate that the range of 1-hour concentr ations allowed under conditions just meeting the current 8-hour standard may contribute to exposur es of concern in areas of the country with relatively higher 1- hour peaks, it may be appropriate to consider a revised level for the 1-hour standard that would achieve more uniform protection. As one option fo r such a level, alternat ive 1-hour levels that provide generally equivalent prot ection to the current 8-hour sta ndard, nationally, with increased protection for areas with relativ ely higher 1-hour peaks, may be appropriate to consider. Accordingly, we note that the population distribu tion of daily maximum C OHb levels associated with just meeting the current 8-hour standard in the REA simulations are also associated with just meeting a 1-hour level of approximately 12 to 16 ppm, in terms of the current form, and approximately 12 to 13 ppm, in terms of a 99 th percentile daily maximu m form (Table 2-8). Further, depending on judgments with regard to the weight to be placed on the factors identified above, levels for the 1-hour standard appreciably lower than those associated with conditions just meeting the currently controlling 8-hour standard may be appropria te to consider. For example, focusing on the 2.0% absolute COHb benchmark and considering a target for the at-risk population of approximately 99% for at most a single occurrence of daily maximum COHb at such a level would indicate support for 1-hour st andard levels ranging down to approximately 11 or 9 ppm, for the current form or a 99 th percentile daily maximum fo rm, respectively. On the other hand, if one were to place weight on the tw o epidemiological studies finding statistically significant associations in two lo cations in which the current standard was met (and the ambient CO concentrations in those study locations), a nd on the REA estimates for this same population target (e.g., 99% having no occurrences) combined w ith an absolute COHb benchmark as low as 1.5% (a level appreciably below those recognized in the evidence), one might find support for a range extending down to approximately 5 ppm (combined with either form).2-71 2.3.4 CASAC Advice

In our consideration of a lternative standards, in a ddition to the evidence- and risk/exposure-based information discussed above, we have also considered the advice and recommendations of CASAC, based on their review of the ISA, the REA, a nd the earlier draft of this document, as well as comments from the public on earlier drafts of this document and the

REA. 48 As recognized in section 2.3.2 above, no public comments have been received to date in support of revisions to the current standards. In CASAC’s consideration of specific revisions to the standards in their review of the draft Policy Assessment, they suggested that st aff describe example policy options such as retaining an 8-hour standard with “consideration given to levels within the range of 3 to 6 ppm, with no more than a single exceedance or revise the form of the standard to 99th percentile with a concentration range of 3-5 ppm.” With rega rd to the 1-hour standa rd, CASAC suggested the policy option of retainin g a 1-hour standard “to provide pr otection against infrequent acute exposures” and considering “a range of concentra tions from 5 ppm to 15 ppm, combined with a

99 th percentile or fourth highest daily maximum.” The Panel furt her stated that they did not concur with the option of revoking the 1-hour standard (B rain and Samet, 2010b, p. 13).

2.3.5 Staff Conclusions on Alternative Standards Staff’s consideration of alternative primar y CO standards builds on our conclusion from section 2.2.4 above that the body of evidence in co mbination with the results of the REA support standards at least as pr otective as the current standards, a nd, depending on the weight given to different aspects of the evidence and both public health and science policy judgments, it may be interpreted to provide support for alternative, more protective, standards. As an initial matter, we conclude it is appropriate to continue to use measurements of CO in accordance with federal
reference methods as the indicato r to address effects associated with exposure to ambient CO. We additionally conclude that it is appropriate to continue to retain standards with averaging times of 1 and 8 hours. With regard to form a nd level for those standards, we conclude that, depending on public health policy judgments regard ing the protection of pub lic health with an adequate margin of safety, the information avai lable in this review s upports consideration of either retaining the current suite of sta ndards or revising one or both standards. We reach the conclusion that it is appropriate to consider retaining the current suite of
standards without revision based on consideration of the health effects evidence in combination

48 All written comments submitted to the Agency will be av ailable in the docket for this rulemaking, as will be transcripts of the public meetings held in conjunction wi th CASAC’s review of the earlier draft of this document, of drafts of the REA, and of drafts of the ISA.2-72 with the results of the REA (sections 2.2.1, 2.2.2, 2.3.2 and 2.3.3 above) and what may be considered reasonable judgments on the public health implications of the COHb levels estimated to occur under the current standard, the public health significance of the CO effects being considered, the weight to be gi ven to findings in the epidemiol ogical studies in locations where the current standards are met, and advice from CASAC. Such a conclusion takes into account the long-standing body of evidence that supports our understanding of the role of COHb in eliciting effects in susceptible populations, most specifically the evidence for those with cardiovascular disease, and gives particular weig ht to findings of contro lled exposure studies of CAD patients in which sensitive indicators of myo cardial ischemia were associated with COHb levels resulting from short-du ration, high-concentration CO expos ures. This conclusion also
takes into account uncertainties associated with the differing circumstances of ambient air CO exposures from the CO exposures in the contro lled human exposure studies, as well as, the unclear public health significance of the size of effects at the lowest studied exposures. As in the last review, this conclusion gives more weight to the significance of the effects observed in these studies at somewhat higher COHb levels. A dditionally, this conclusi on takes into account judgments in interpreting the public health implications of the REA estimates of COHb associated with ambient exposures based on th e application of our cu rrent exposure modeling tools, and the size of th e at-risk populations estimated to be protected from experiencing daily maximum COHb levels of potential concern by the current standard. Further, this conclusion considers the uncertainties in quantitative interp retations associated with the epidemiological studies to be too great for reliance on info rmation from the few studies where the current
standards were met as a basis for sel ection of alternative standards. In addition to considering re taining the current suite of standards without revision, we
also conclude that it is reasona ble to consider revising the 1-h our standard downward to provide protection from infrequent shor t-duration peak ambient concen trations that may not be adequately provided by the current standards. Wh ile the quantitative analyses for this review focused predominantly on the controlling, 8-hour standard, the analyses have indicated the
influential role of elevated 1-hour concentrations in contributing to daily maximum COHb levels
over benchmark levels. In addition to the REA re sults, we note the health effects evidence from 1-hour controlled exposures, whic h indicates the effects in sus ceptible groups from such short duration exposures. The evidence and REA estim ates indicate support for consideration of a range of 1-hour standard leve ls which would address the pot ential for the current 8-hour standard, as the controlling st andard, to “average away” high s hort-duration exposures that may contribute to exposures of concer n. Consequently, in considering alternative standard levels, we
focus here on the 1-hour standa rd as providing the most direct approach for controlling the likelihood of such occurrences. Additionally, fo llowing consideration of alternative 1-hour2-73 standard levels below, we also c onsider the extent to which it is appropriate, in conjunction with revisions to the 1-hour standard, to consider revising or retaini ng the current 8-hour standard. We have identified a range of 1-hour standa rd levels from 15 to 5 ppm as being an appropriate range for consideration. These levels are in terms of a 99 th percentile daily maximum form, averaged over three years, which we consider to provide increased regulatory stability over the current form. Given the obj ective for the 1-hour standard of providing protection from high ambient CO exposures of dur ation shorter than 8 hours and perhaps much shorter, we suggest the 99 th percentile form for consideration in preference to a 98 th percentile form. We additionally take note of CASAC’s preference for a revision to the standards to provide greater protection and obser ve that the range of 1-hour sta ndard levels discussed here is also the range that the CASA C CO Panel suggested was appr opriate for consideration. We have identified the upper part of the rang e of 1-hour standard levels for consideration (11-15 ppm) based on the objective of providing ge nerally equivalent pr otection, nationally, to that provided by current 8-hour st andard and potentially providing increased protection in some areas, such as those with relatively higher 1-hour peaks that are allowed by the current 8-hour standard. This part of the range is estimat ed to generally correspond to 1-hour CO levels occurring under conditions ju st meeting the current 8-hour standard based on current relationships between 1-hour and 8-hour average concentrations at current U.S. monitoring locations (Appendix C). Specifically, we considered the 25 th and 75 th percentiles of the
distribution of ratios of 1-hour 99 th percentile daily maximum concentrations averaged over three years to 8-hour second maximum concentration for 2009. As a result, this part of the range is represented by levels of about 11 ppm to 15 ppm, with a 99 th percentile daily maximum form, averaged over three years. Sele ction of a 1-hour standard within this upper part of the range would be expected to allow for a somewhat simila r pattern of ambient CO concentrations as the current, controlling 8-hour st andard, although with explicit an d independent control against shorter-duration peak co ncentrations which may contribute to daily maximum COHb levels in those exposed. Consideration of 1- hour standard levels in this part of the range would take into account the factors recognized with regard to the option of retain ing the current standards. But it would additionally recognize the importance of limiting 1-hour concentr ations that are not controlled by the current 8-hour standard but that may contribute to exceedances of relevant
COHb benchmark levels. We have also concluded that, based on th e evidence and REA estimates and judgments that may be considered reasonable regarding appropriate population targ ets for maximum COHb levels induced by ambient CO exposures, it may be appropriate to consider standard levels that provide additional protection than that afforded by the current standards against the occurrence of short-duration peak ambient CO exposures an d associated COHb levels. With this policy2-74 objective in mind, we consider it ap propriate to consider 1-hour st andard levels of 9-10 ppm, which comprise the middle part of the range of 1-hour standard levels suggested for
consideration. We conclude that consideration of standard levels in this part of the range would give greater weight to protecti on of the at-risk population agains t the small decrements in timeto-exercise-induced markers of myocardial ischem ia associated with the lowest COHb levels studied, and provide increased protection for at-risk populations from higher COHb levels. Additionally, this conclusion considers the uncertainties in quantitative interpretations associated with the epidemiological studies to be too great for reliance on information from the few studies
where the current standards were met as a basi s for selection of alte rnative standards. In further considering the evidence, we take note of the expanded epidemiological evidence and suggest that to the ex tent one places weight on the public health significance of the smaller changes in COHb assessed in the REA, gives greater importance to increasing the portion of at-risk populations estimated to keep COHb levels resulting from ambient CO exposures below 1.5% COHb and c oncludes that the epidemiologi cal studies in areas meeting the current standards are reasonably interpreted as indicating that ambient CO is responsible for the health outcomes observed, consideration of levels extending down to the lower levels assessed in the REA and the lower part of the ra nge of CO levels in th e three epidemiological studies may be appropriate. In li ght of this, we have identified 1- hour standard levels of 5-8 ppm as comprising the lower part of the range of 1-hour standard levels for consideration. In considering the relative strength of the evidence supporting each of the 3 parts of the range, we conclude that the upper part of the rang e is most strongly support ed, both with regard to judgments concerning adversity and quantitativ e interpretation of the epidemiological studies with regard to ambient concentrations that may el icit effects. For the lower parts of the range, support provided by the available information is mo re limited, especially for the lowest part of the range. As mentioned above, we also conclude it is a ppropriate to consider retaining a standard with an 8-hour averaging time. As when it wa s established, the 8-hour standard continues to provide protection from multiple-hour ambient CO exposures which may contribute to elevated
COHb levels and associated effects. In c onjunction with considera tion of a revised 1-hour standard to a level in the upper pa rt of the range described above, we conclude it is appropriate to consider either retaining the current 8-hour stan dard or revising the form of the standard to potentially provide greater regula tory stability, with adjustment to level to provide generally equivalent protection as the curr ent 8-hour standard. Based on ai r quality relati onships between
the current form and an alternative form of 99 th percentile daily maximum 8-hour concentration averaged over three years (Appendix C), we concl ude that levels for the revised form that are appropriate to consider are 8 or 9 ppm.2-75 In conjunction with considera tion of a revised 1-hour standard to a level in the middle part of the range described above , we conclude it is appropriat e to consider revising the 8-hour standard to provide additional pr otection from 8-hour average con centrations to a level within the range of 5-7 ppm in terms of a 99 th percentile daily maximum, averaged over three years. Further, in conjunction with cons ideration of a revised 1-hour st andard to a level in the lower part of the range described above, we have also identified 8-hour standard levels of 3-4 ppm, in
terms of a 99 th percentile daily maximum, averaged over three years. In both cases, the considerations leading to identification of these 8-hour standa rd levels are those discussed above with regard to the corresponding parts of the rang e identified for consideration of alternative 1-
hour standard levels. To provide some perspective on the implications of alternative prim ary standards (within the range of levels identified above), staff analyzed ambient CO concentrations for 2007-2009 to estimate the percentage of countie s, and the populations in those counties that likely would not
attain various alternative standards identified ab ove. The analysis, shown in Appendix E was not
considered as a basis for the above staff conclusions.2-76 2.4 SUMMARY OF STAFF CONCLUSIONS ON PRIMARY STANDARDS

Staff conclusions on policy options for the pr imary CO NAAQS that are appropriate for
the Administrator’s considerati on in making decisions on the prim ary standards for CO, together with supporting conclusions from sections 2.2.4 and 2.3.2 above, are briefly summarized below. In reaching conclusions on alternat ive standards to provide requisite protection for health effects associated with ambient CO exposures, staff has c onsidered these standards in terms of the basic elements of the NAAQS: indicator, averaging tim e, form, and level. In drawing these conclusions, we are mindful that the Act requires st andards to be set that, in the Administrator’s judgment, are requisite to protect public health w ith an adequate margin of safety, such that the
standards are to be neither more nor less stringent than necessar y. Thus, the Act does not require that NAAQS be set at zero-risk levels, but rather at levels that avoid un acceptable risks to public
health.

(1) Staff concludes that the combined cons ideration of the body of evidence and the results from the quantitative exposure and dose assessment provide support for standards at least as protective as the current suite of standards to provide appropriate public health protection for susceptible populations, including most particularly individuals with cardiovascular disease, against effects of CO in exacerbating conditions of reduced oxygen avai lability to the heart.
(2) Staff additionally concludes that, depending on public health policy judgments regarding the protection of pub lic health with an adequate margin of safety, the information available in this review suppor ts consideration of either retaining the current suite of standards or revising one or both standards.
(3) With regard to the indicator for the CO standards, staff concludes that it is appropriate to continue to use measurem ents of CO in accordance with federal reference methods as the indicator to addr ess effects associated with exposure to ambient CO.
(4) With regard to averaging times for the CO standards, staff concludes that it is appropriate to continue to retain standards with averag ing times of 1 and 8 hours.
(5) With regard to the levels and forms of the standards, staff concl udes it is appropriate to consider retaining the cu rrent standards, without revi sion, or revising the current suite of standards, with part icular focus on revision of the 1-hour standard to provide protection that is no t adequately provided by the curre nt standards from infrequent, short-duration, peak ambi ent concentrations.
(6) With regard to a revised 1-hour standard, we conclude that it is appropriate to give consideration to a rang e of levels from 15 to 5 ppm, w ith a revised level selected in2-77 combination with a revised form of 99 th percentile (or fourth highest) daily maximum form, averaged over three years. Staff has identified three parts of this range that differ with regard to science and public health policy judgments, and supporting information.

a. To provide additional protection in areas with relatively higher 1-hour peaks that are allowed by the current 8-hour st andard, it is appropriate to consider the upper part of the range, represented by 11-15 ppm. This part of the range would provide generally equivalent pr otection, nationally, to that provided by the current 8-hour standard. Staff conclude s that this part of the range is most strongly supported by th e current information.

b. To the extent it is judged appropriate to provide additional protection against COHb levels at or above 2% in sus ceptible populations, it is appropriate to consider the middle part of the range, represented by 9-10 ppm.

c. To the extent one places greater im portance on COHb levels below 2.0% and concludes that the epidemiological ev idence for areas meeting the current standards is reasonably interpreted as i ndicating ambient CO is responsible for the health outcomes observed, it may be appropriate to consider the lower part of the range (approximately 5 – 8 ppm) to potentially provide a greater degree of additional protection.
(7) In conjunction with a revision to the 1-hour st andard, we conclude it is appropriate to give consideration to the followi ng options for the 8-hour standard:

a. In conjunction with a revision of the 1-hour standard in the upper part of the range, it is appropriate to consider either retaining the current 8-hour standard or revising the form to provide greater re gulatory stability, with adjustment to level to provide generally equivalent protection, nationally, as the current 8- hour standard. For a form of 99 th percentile daily maximum, averaged over three years, a level of 8 or 9 ppm may be appropriate to consider with this option. b. In conjunction with a revision of the 1- hour standard to a level in the middle part of the range, it is also appropriate to consider revising the 8-hour standard to a level from 5-7 ppm (with a 99 th percentile daily maximum form) to provide additional protection from maxi mum COHb levels that may result from 8-hour ambient CO exposures.

c. In conjunction with a revision of the 1- hour standard to a level in the lower part of the range, it is also appropriate to consider revising the 8-hour standard to provide a more precautionary level of protection from 8-hour ambient CO2-78 exposures, giving considerati on to levels of approximately 3 or 4 ppm, with a

99 th percentile daily maximum form.2-79 2.5 KEY UNCERTAINTIES AND AREA S FOR FUTURE RESEARCH AND DATA COLLECTION Staff believes it is important to highlight key uncertainties associated with establishing ambient standards for CO. Such key uncerta inties and recommendations for health-related research, model development, and data gathering ar e outlined below. In some cases, research in these areas can go beyond aiding stan dard setting to aiding in the development of more efficient and effective control strategies. We note, however, that a full set of research recommendations to meet standards implementation and strategy development needs is beyond the scope of this discussion. We have identified the following key un certainties, research que stions and data gaps that have been highlighted in this review of the health-based primary standards.

 A critical aspect of our consideration of the eviden ce and the quantitative dose estimates is our interpretation of the c ontrolled human exposure studies. While additional human exposure studies of this t ype are unlikely to be undertaken, expansion of our understanding of the implications of se veral aspects of this evidence base would reduce uncertainty in our interpretation for purposes of risk characterization.

o Additional information relevant to the likelihood of health effects from shortterm increases in CO exposure that result in COHb levels below 2% in individuals with CAD.

o Additional research to help clarify the physiological significance of the changes in time to sensitive markers of myocardial ischemia observed in controlled human exposure studies of CA D patients at the lowest exposures.

o Research to reduce uncertainty associated with interpretation of COHb levels estimated in the quantitative assessment to result from simulated CO exposure concentrations much lower than the e xperimental CO exposure concentrations used in the controlled human studies to increase subject COHb levels to COHb study targets.

 Further characterization of the physiological and environm ental influences, including characteristics of exposure, on COHb levels , particularly those most influential to COHb levels in today’s population, and th e magnitude of those influences, would benefit future exposure and dose modeling

 Existing clinical data correlate CO-induced effects (i.e., cardiovascular ischemia observed at specific COHb leve ls) to COHb levels resulti ng from short-term, high CO exposure concentrations. However, there is a lack of other studies evaluating effects of CO, in terms of COHb levels, at lower am bient concentrations and/or longer-term exposure periods.

 Further research to characterize CO e ffects for other poten tially susceptible populations, including populations with preexisting di seases other than CAD that limit oxygen availability, such as anemia and obstruc tive respiratory diseases; populations at certain lifestages (i.e., older adults and fetu ses at critical stages of development); and2-80 populations with elevated ba seline COHb due to increased endogenous CO formation, such as individuals with diabet es and visitors to high altitude.

 Our interpretation of the epidemiological ev idence for CO would benefit from a better understanding of the possible role of co- pollutants, and current information on CO concentrations, arising from both ambient and nonambient sources, in different microenvironments, including traffic- or roadway-related microenvironments.

 Our future assessments would benefit from research on studies evaluating effects of CO linked to biomarkers other than C OHb and research on mechanisms of COinduced effects other that thos e associated with limiting oxygen availability at ambient CO levels.2-81 REFERENCES

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Horvath S.M.; Dahms T.E.; O'Hanlon J.F. (1971). Carbon monoxide and human vigilance: A deleterious effect of present urban concentrations. Arch Environ Occup Health, 23: 343-347.

Johnson T.; Capel J.; Paul R.; Wijnberg L. (1992) Estimation of Carbon Monoxide Exposure and associated Carboxyhemoglobin levels in Denver Residents Using a Probabalistic verion of NEM, prepared by International Technology for U.S. EPA, Office of Air Quality Planning and Standards, Durham, NC, Contract No. 68-D0-0062.

Johnson T.; Mihlan G.; LaPointe J.; Fletcher K.; Capel J. (2000) Estimation of Carbon Monoxide Exposures and Associated Carboxyhemoglobin Levels for Residents of Denver and Los Angeles Using pNEM/CO (Version 2.1). Report prepared by ICF Consulting and TRJ Environmental, Inc., under EPA Contract No. 68-D6-0064. U.S. Environmental Protection Agency, Research Triangle Park, North Carolina. Available
at: http://www.epa.gov/ttn/fera/human_related.html . June 2000.

Karner A.A.; Eisinger D.S.; Niemeier D.A. (2010) Near-Roadway Air Quality: Synthesizing the Findings from Real-World Data. Environ Sci Technol 44: 5334-5344.

Kleinman M.T.; Davidson D.M.; Vandagriff R.B.; Caiozzo V.J.; Whittenberger J.L. (1989 ) Effects of short-term exposure to carbon monoxide in subjects with coronary artery disease. Arch. Environ. Health 44:361-369.

Kleinman M.T.; Leaf D.A.; Kelly E.; Caiozzo V.; Osann K.; O'Niell T. (1998) Urban angina in the mountains: effects of carbon monoxide and mild hypoxemia on subjects with chronic stable angina. Arch. Environ.Health 53:388-397.

Koken P.J.M.; Piver W.T.; Ye F.; Elixhauser A.; Olsen L. M.; Portier C.J. (2003) Temp erature, air pollution, and hospitalization for cardiovascular diseases among elderly people in Denver. Environ Health Perspect, 111:1312-1317.

Leaf D.A.; Kleinman M.T. (1996a) Urban ectopy in the mountains: carbon monoxide exposure at high altitude. Arch. Environ. Health 51:283-290.

Linn W.S.; Szlachcic Y.; Gong H. Jr; Kinney P.L.; Berhane K.T. (2000) Air pollution and daily hospital admissions in metropolitan Los Angeles. Environ Health Perspect, 108:427-434.

Longo L.D. (1977) The biological effects of carbon monoxide on the pregnant woman, fetus, and newborn infant. Am. J. Obstet. Gunacol. 129:69-103.2-83 Mann J.K.; Tager I.B.; Lurmann F.; Segal M.; Quesenberr y C.P. Jr; Lugg M.M.; Shan J.; Van den Eeden S.K. (2002) Air pollution and hospital admissions for ischem ic heart disease in pers ons with congestive heart failure or arrhythmia. Environ Health Perspect, 110:1247-1252.

McClellan R.O. (1991) Letter from Dr. Roger O. McClellan, Chairman, Clean Air Scientific Advisory Committee to Administrator William K. Reilly. July 17, 1991.

McClellan R.O. (1992) Letter from Dr. Roger O. McClellan, Chairman, Clean Air Scientific Advisory Committee to Administrator William K. Reilly. August 1, 1992.

Metzger K.B.; Tolbert P.E.; Klein M.; Peel J.L.; Flanders W.D.; Todd K.H.; Mulholland J.A.; Ryan P.B.; Frumkin H. (2004) Ambient air pollution and cardiovascular emergency department visits. Epidemiology, 15:46-56.

Peel J.L.; Metzger K.B.; Klein M.; Flan ders W.D.; Mulholland J.A.; Tolbert P.E. (2007) Ambient air pollution and cardiovascular emergency department visits in potentially sensitive groups. Am J Epidemiol, 165:625-633.

Putz V.R.; Johnson B.L.; Setzer J.V. (1976) Effects of CO on vigilance performance effects of low level carbon monoxide on divided attention, pitch discrimination, and the auditory evoked potential. Cincinnati, OH: U. S. Department of Health, Education, and Welfare Na tional Institute for Occupational Safety and Health; report no. NIOSH-77-124. Available from: NTIS, Springfield, VA; PB-274219.

Putz V.R.; Johnson B.L.; Setzer J.V. (1979) A comparativ e study of the effects of car bon monoxide and methylene chloride on human performance. J. Environ. Pathol. Toxicol. 2:97-112.

Raven P.B.; Drinkwater B.L.; Horvath S.M.; Ruhling R.O. ; Gliner J.A.; Sutton J.C.; Bolduan N.W. (1974) Age, smoking habits, heat stress, and their interactive effects with carbon monoxide and peroxyacetylnitrate on man’s aerobic power. Int. J. Biometeorol. 18:222-232.

Sheps D.S.; Adams K.F. Jr.; Bromberg P.A.; Goldstein G.M.; O'Neil J.J.; Horstman D.; Koch G. (1987) Lack of effect of low levels of carboxyhemoglobin on cardi ovascular function in patients with ischemic heart disease. Arch. Environ. Health 42:108-116.

Sheps D.S.; Herbst M.C.; Hinderliter A.L.; Adams K.F.; Ekelund L.G.; O'Neil J.J.; Goldstein G.M.; Bromberg P.A.; Dalton J.L.; Ballenger M.N.; Davis S.M.; Koch G. G. (1990) Production of arrythmias by elevated carboxyhemoglobin in patients with coronary artery disease. Ann. Intern. Med. 113:343-351.

Symons J.M.; Wang L.; Guallar E.; Howell E.; Dominici F.; Schwab M.; Ange B.A.; Samet J.; Ondov J.; Harrison D.; Geyh A. (2006) A case-crossover study of fine particulate matter air pollution and onset of congestive heart failure symptom exacerbatio n leading to hospitalization. Am J Epidemiol, 164:421-433.

Tolbert P.E.; Klein M.; Peel J.L.; Sarn at S.E.; Sarnat J.A. (2007) Multipollutant modeling issues in a study of ambient air quality and emergency department visits in Atlanta. J Expo Sci Environ Epidemiol, 17:S29- S35.

U.S. Department of Health,Education and Welfare. (1970) Air Quality Criteri a for Carbon Monoxide. National Air Pollution Control Administration, Public Health Service, Washington, DC.

U.S. Environmental Protection Agency. (1979) Air Quality Criteria for Carbon Monoxide. Research Triangle Park, NC: Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office. EPA/600/8-79-022.

U.S. Environmental Protection Agency. (1984a) Revised Evaluation of Health Effects Associated with Carbon Monoxide Exposure: An Addendum to the 1979 EPA Air Quality Criteria Document for Carbon Monoxide. Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Research Triangle Park, NC. EPA-600/8-83-033F.2-84 U.S. Environmental Protection Agency. (1984b) Review of the NAAQS for Carbon Monoxide: Reassessment of Scientific and Technical Information. Office of Ai r Quality Planning and Stan dards, Research Triangle Park. NC. EPA-450/584-904.

U.S. Environmental Protection Agency.. (1991) Air Qua lity Criteria for Carbon Monoxide. Office of Health and Environmental Assessment, Research Triangle Park, NC. EPA/600/8-90/045F. Available at: http://www.epa.gov/ttn/naaqs/standards/co/s_co_pr.html

U.S. Environmental Protection Agency. (1992) Review of the National Ambient Air Quality Standards for Carbon Monoxide: Assessment of Scientific and Technical In formation. OAQPS Staff Pape r. Office of Air Quality Planning and Standards, Research Triangle Park, NC. EPA/452/R-92-004.

U.S. Environmental Protection Agency . (2000) Air Quality Criteria for Ca rbon Monoxide. National Center for Environmental Assessment, Office of Research and Development, Research Triangle Park, NC. EPA/600/P-99/001F. Available at: http://cfpub.e pa.gov/ncea/cfm/recordisplay.cfm?deid=18163.

U.S. Environmental Protection Agency. (2005) Review of the National Ambient Air Quality Standards for Particulate Matter: Policy Assessment of Scientific and Technical Information, OAQPS Staff Paper. Office of Air Quality Planning and Standards, Re search Triangle Park, NC. EPA-452/R-05-005a.

U.S. Environmental Protection Agency. (2007) Review of the National Ambient Air Quality Standards for Ozone: Policy Assessment of Scientific an d Technical Information, OAQPS St aff Paper. Office of Air Quality Planning and Standards, Research Triangle Park, NC. EPA-452/R-07-007.

U.S. Environmental Protection Agency. (2008a) Plan for Re view of the National Ambient Air Quality Standards for Carbon Monoxide. Also known as Integrated Review Plan . Office of Air Quality Planning and Standards, Research Triangle Park, NC. EPA/452R-08-005. Available at: http://www.epa.gov/ttn/naaqs/st andards/co/s_co_cr_pd.html

. U.S. Environmental Protection Agency. (2008b) Risk and Exposure Assessment to Support the Review of the NO2 Primary National Ambient Air Quality Standard. Office of Air Quality Planning and Standards, Research Triangle Park, NC. EPA-452/R-08-008a.

U.S. Environmental Protection Agency. (2008c) Integrated Science Assessment for Oxides of Nitrogen – Health Criteria (Final Report). EPA/600/R-08/071.

U.S. Environmental Protection Agency. (2009a) Integrated Science Assessment for Particulate Matter (Final Report). EPA/600/R-08/139F.

U.S. Environmental Protection Agency. (2009b) Risk and Exposure Assessment to Support the Review of the SO 2 Primary National Ambient Air Quality Standard. Office of Air Quality Planning and Standards, Research Triangle Park, NC. EPA-452/R-09-007. August 2009. Available at http://www.epa.gov/ttn/naaqs/standards/s o2/data/200908SO2REAFinalReport.pdf.

U.S. Environmental Protection Agency. (2010a) Integrated Science Assessment for Carbon Monoxide. National Center for Environmental Assessment, Research Triangle Park, NC. EPA/600/R-09/019F. Available at: http://www.epa.gov/ttn/naaqs/sta ndards/co/s_co_cr_isa.html

U.S. Environmental Protection Agency. (2010b) Quantitative Risk and Exposure Assessment for Carbon Monoxide – Amended. Office of Air Quality Planning and Stan dards, Research Triangle Park, NC. July. EPA-452/R10-009. Available at: http://www.epa.gov/ttn/naaqs/st andards/co/s_co_cr_rea.html

Weiser, P.C.; Morrill, C.G.; Dickey, D.W. ; Kurt, T.L.; Cropp, G.J.A. (1978) E ffects of low-level carbon monoxide exposure on the adaptation of healthy young men to aerobic work at an altitude of 1,610 meters. In2-85 Folinsbee, L.J.; Wagner, J.A.; Borgia , J.F.; Drinkwater, B.L. ; Gliner, J.A.; Bedi, J.F., [eds] Environmental stress: individual human adaptations. New York, NY: Academic Press, Inc.; pp. 101-110.

Wellenius G.A.; Bateson T.F.; Mittlema n M.A.; Schwartz J. (2005) Particul ate air pollution and the rate of hospitalization for congestive heart failure among medicar e beneficiaries in Pittsbu rgh, Pennsylvania. Am J Epidemiol 161:1030-1036.

WHO (2008). Harmonization Project Document No. 6. Part 1: Guidance document on characterizing and communicating uncertainty in exposure assessment. Available at: http://www.who.in t/ipcs/methods/harmonization/areas/exposure/en/.

Zanobetti A.; Schwartz J. and D.W. Dock ery (2000) Airborne par ticles are a risk factor for hospital admissions for heart and lung disease. Environ Health Persp 108(11):1071-1077.

Zanobetti A. and Schwartz J. ( 2001) Are diabetics more susceptible to the h ealth effects of airborne particles? Am J Respir. Crit. Care Med. 164:831-833.3-1 

### 3 CONSIDERATION OF A SECONDARY STANDARD FOR CARBON MONOXIDE

This chapter focuses on the key policy-relevant issues related to th e review of welfarerelated effects of CO. Under Section 109(b) of th e Clean Air Act, a secondary standard is to be established at a level “requisite to protect the public welfare from any known or anticipated
adverse effects associated with the presence of the pollutant in ambient air.” Section 302(h) of the Act defines effects on welfare in part as “e ffects on soils, water, cr ops, vegetation, man-made materials, animals, weather, visibility, and climate.” Specifically, this chapter first summarizes the history of EPA’s consideration of secondary standards for CO. It then discusse s the evidence currently available for welfare
effects to inform decisions in this review as to whether, and if so how, to establish secondary standards for CO based on public welfare consid erations. Staff conclusions are based on the assessment and integrative synthesis of the scientific evidence presented in the ISA (USEPA, 2010), building on the evidence described in the 2000 AQCD (USEPA, 2000).

3.1 CONSIDERATION IN PREVIOUS REVIEWS

With the establishment of the first NAAQS for CO in 1971, secondary standards were set identical to the primary standards. CO was not shown to produce detrimental effects on certain higher plants at levels below 100 ppm. The onl y significant welfare eff ect identified for CO levels possibly approaching those in ambient air was inhibition of nitrogen fixation by microorganisms in the root nodules of legumes a ssociated with CO levels of 100 ppm for one month (U.S. DHEW, 1970). In the first review of the CO NAAQS, which was completed in 1985, the threshold level for plant effects was rec ognized to occur well above ambient CO levels, such that vegetation damage as a result of CO in ambient air was concluded to be very unlikely (50 FR 37494). As a result, EPA concluded that the evidence did not support maintaining a secondary standard for CO, as welfare-related effects had not been documented to occur at ambient concentrations (50 FR 37494). Based on that conclusion, EPA revoked the secondary standard. In the most recent review of CO, which was completed in 1994, EPA again concluded
there was insufficient evidence of welfare effects occurring at or near ambient levels to support setting a secondary NAAQS (59 FR 38906). That review did not consider climate-related
effects.3-2 3.2 CONSIDERATION OF EVIDENCE AVAILABLE IN THE CURRENT REVIEW

To evaluate whether consideration of estab lishment of a secondary standard for CO is appropriate, we adopted an appro ach in this review that builds upon the general approach used in the last review and reflects the broader body of evidence and information now available. In developing conclusions in this review below, staff has taken into account the following overarching question:

 Does the currently available scientif ic information provide support for considering the establishment of a secondary standard for CO? In considering this overarching question, we firs t note that the extensiv e literature search performed for the current review did not identify any evidence of ecological effects of CO unrelated to climate-related effects, at or n ear ambient levels (ISA, section 1.3 and p. 1-3). However, ambient CO has been associated with welfare effects related to climate (ISA, section 3.3). Climate-related effects of CO were consid ered for the first time in the 2000 AQCD. The greater focus on climate in the current ISA re lative to the 2000 AQCD reflects comments from
CASAC and increased attention to the role of CO in climate forcing (Brain and Samet, 2009). Based on the current evidence, the ISA conclude s that “a causal relationship exists between current atmospheric concentrations of CO and effects on climate” (ISA, section 2.2). Accordingly, the following discussion focuses on c limate-related effects of CO in addressing the question posed above. Recently available information does not alter the current well-established understanding of the role of urban and regional CO in continen tal and global-scale chem istry, as outlined in the 2000 AQCD. CO is a weak direct contributo r to greenhouse warming. The most significant effects on climate result indirectly from CO chemistry, related to the role of CO as the major atmospheric sink for hydroxyl groups (OH). Incr eased concentrations of CO can lead to increased concentrations of other gases whose lo ss processes also involve OH chemistry. Some of these gases, such as methane (CH 4 ) and ozone (O 3 ), contribute to the greenhouse effect directly while others deplete stratospheric O 3 (ISA, section 3.3 and p. 3-11). Advances in modeling and measurement have improved our understanding of the relative contribution of CO to climate forcing. CO cont ributes to climate forc ing through both direct radiative forcing (RF) of CO, estimated at 0.024 W/m 2 by Sinha and Toumi (1996), and indirect effects of CO on climate through CH 4 , O 3 and carbon dioxide (CO 2 ) (Forster et al. 2007). The Intergovernmental Panel on Climate Change (IPCC) estimated the combined RF for these
indirect effects of CO to be ~0.2 W/m 2 over the period 1750-2005 (For ster et al., 2007), with more than one-half of the forcing attributed to O 3 formation (ISA, section 3.3 and p. 3-13).3-3 CO is classified as a short-lived climate fo rcing agent, prompting CO emission reductions to be considered as a possible strategy to m itigate effects of global warming. However, it is highly problematic to evaluate the indirect effects of CO on climate due to the spatial and temporal variation in emissions and concentratio ns of CO and due to the localized chemical interdependencies involving CO, CH 4 , and O 3 (ISA section 3.3 and p. 3-12). Most climate
model simulations are based on global-scale scenarios and have a high degree of uncertainty
associated with short-lived climate forcers su ch as CO (ISA, section 3.3 and p. 3-16). These models may fail to consider the local variations in climate forc ing due to emissions sources and local meteorological patterns (ISA, section 3.3 and p. 3-16). It is possible to compute individual contributions to RF of CO from separate em issions sectors, although uncertainty in these estimates has not been quantified (ISA, section 3.3, p. 3-13 and Figure 3-7).
Uncertainties in the estimates of the indirect RF from CO are related to uncertainties in the chemical interdependencies of CO and trace gases, as described above. Large regional
variations in CO concentrations also contribute to the uncertaintie s in the RF from CO and other trace gases (ISA section 3.3 and p. 3-12). A lthough measurement of and techniques for assessing climate forcing are improving, estimates of RF still have ~50% uncertainty (ISA, section 3.3, and p. 3-13).

3.3 CASAC ADVICE

In our consideration of a secondary standard, in addition to the evidence discussed above,
we have also considered the advice and recomm endations of CASAC, ba sed on their review of the ISA, and the earlier draft of this document. 1 In their comments on the draft Policy Assessm ent, CASAC did not disagree with staff’s
initial conclusions that there is insufficient in formation to support consideration of a secondary standard at this time. CASAC did express the view that there is subs tantial evidence that CO
has adverse effects on climate and recommended that staff summarize information that is currently lacking and would assist in consideration of a secondary standard in the future (Brain and Samet 2010). This recommendation is addressed in section 3.5 below.

1 Thus far in this review, no public comments have been received regarding the secondary standard.3-4 3.4 STAFF CONCLUSIONS FOR THE CURRENT REVIEW

In considering whether the currently availabl e scientific information indicates the need for a secondary standard for CO, we ha ve reached the following conclusions:

(1) With respect to non-climate we lfare effects, including eco logical effects and impacts to vegetation, there is no currently availabl e scientific informati on that supports a CO secondary standard.

(2) With respect to climate-related effects, we note that there is evidence of climate forcing effects associated with CO (ISA, s ections 2.2 and 3.3). There are weak direct, and stronger, but highly variable and uncer tain indirect cont inental and regional climate forcing effects from CO. Howeve r, the available information provides no basis for estimating how locali zed changes in the temporal and spatial patterns of ambient CO likely to occur across the US with (or without) a secondary standard would affect local, regional, or nationwide changes in clim ate. Moreover, more than half of the indirect forcing eff ect of CO is attributable to O 3 formation, and welfarerelated effects of O 3 are more appropriately considered in the context of the review of the O 3 NAAQS, rather than in this CO NA AQS review. For these reasons, it is currently not feasible to conduct an anal ysis for the purpose of considering a CO secondary standard based on climate considerations. Based on these considerations, staff concludes there is insufficient in formation at this time to support the consideration of a secondary NAAQS base d on CO effects on climate processes.

3.5 KEY UNCERTAINTIES AND AREA S FOR FUTURE RESEARCH AND DATA COLLECTION Staff believes it is important to highlight key uncertainties associated with considering a secondary standard for CO, including those associ ated with CO effects on climate processes.
Research and model refinements that would redu ce such key uncertainties are outlined below, although we note that a full set of research recommendations is beyond the scope of this document. In summary, to better inform future considerations of a secondary standard for CO, additional information, such as th at described below, is needed.

 More accurate U.S. and global emissions inve ntories to provide sour ce-specific data on CO contributions to cl imate precursors.

 Improved representation and characterization of localized chemical reactions between CO, CH 4 and O 3 in global and regional climate m odels to enable the more accurate prediction of the role of CO in climate a nd local variations in climate forcing due to emissions sources and local meteorological patterns.

 Monitoring designed specifically to improve characterization of the spatial and temporal heterogeneity of the impact of CO emissions and to improve climate modeling capabilities.3-5 REFERENCES

Brain J. and Samet J. (2009) Letter from Drs. J.D. Brain an d J.M. Samet to Administrator Lisa Jackson. Re: Review of EPA's Integrated Science Assessment for Carbon Monoxide (First External Review Draft) EPACASAC-09-011.June 24, 2009..Available at: http://yosemite.epa.gov/sab/sabproduct.nsf/264cb1227d55e02c85257402007446a4/90e1eb5977789a4f8525 746e006275a8!OpenDocument&TableRow=2.3#2

.
Brain J.D. and Samet J.M. (2010) Letter from Drs. J.D. Br ain and J.M. Samet to Administrator Lisa Jackson. Re: Review of the Policy Assessment for the Review of the Carbon Monoxide National Ambient Air Quality Standards (NAAQS): External Review Draft . EPA-CASAC-10-013. June 8, 2010.

Forster P.; Ramaswamy V.; Artaxo P.; Berntsen T.; Betts R.; Fahey D.W.; Ha ywood J.; Lean J.; Lowe D.C.; Myhre G.; Nganga J.; Prinn R.; Raga G.; Schultz M.; Van Do rland R. (2007) Changes in atmospheric constituents and in radiative forcing, Chapter 2. In Solomon S; Qin D; Manning M; Chen Z; Marquis M; Averyt KB; Tignor M; Miller HL (Ed.) IPCC Fourth Assessment Report (AR4): Climate Change 2007: Working Group I Report: The Physical Science Basis. (pp. 129-234). Cambridge, U.K. and New York, NY: Intergovernmental Panel on Climate Change; Cambridge University Press.

Sinha A. and Toumi R. (1996) A comparison of climate forcings due to chloroflurocarbons and carbon monoxide. Geophys Res Lett, 23: 65-68.

U.S. Environmental Protection Agency. (2000) Air Qua lity Criteria for Carbon Monoxide. National Center for Environmental Assessment, Office of Research and Development, Research Triangle Park, NC. EPA/600/P-99/001F. Available at: http://cfpub.e pa.gov/ncea/cfm/recordisplay.cfm?deid=18163.

U.S. Environmental Protection Agency. (2010) Integrated Science Assessment for Carbon Monoxide. National Center for Environmental Assessment, Research Triangle Park, NC. EPA/600/R-09/019F. Available at: http://www.epa.gov/ttn/naaqs/sta ndards/co/s_co_cr_isa.html

. U.S. Department of Health, Education and Welfare. (1970) Air Quality Crite ria for Carbon Monoxide. National Air Pollution Control Administration, Public Health Service, Washington, DC. NAPCA-PUB-AP-62. Available from: NTIS, Springfield VA; PB-190261

### ATTACHMENT

Clean Air Scientific Ad visory Committee Letter (June 8, 2010)UNITED STATES ENVIRONMENTAL PROTECTION AGENCY WASHINGTON D.C. 20460

OFFICE OF THE ADMINISTRATOR SCIENCE ADVISORY BOARD June 8, 2010 EPA-CASAC-10-013

The Honorable Lisa P. Jackson Administrator U.S. Environmental Protection Agency 1200 Pennsylvania Avenue, N.W. Washington, D.C. 20460

Subject: Review of the Policy Assessment for the Review of the Carbon Monoxide National Ambient Air Quality Standards (NAAQS): External Review Draft

Dear Administrator Jackson:

The Clean Air Scientific Advisory Committee (CASAC or Committee) Carbon Monoxide (CO) NAAQS Review Panel me t on March 22-23, 2010, to review EPA’s Policy Assessment for the Review of the Carbon Monox ide National Ambient Air Quality Standards (NAAQS): External Review Draft . The chartered CASAC held a public teleconference on April 19, 2010, to review and approve the report. This letter provides CASAC’s overall comments and evaluation. We highlight the most important issues which need to be addressed as the draft Policy Assessment (PA) is revised and finalized.

CASAC expresses appreciation to EPA staff in regard to the draft PA document. We recognize that limited time was av ailable for its development, give n the court ordered deadline. In this letter, we offer the main suggestions and concerns identified by the Carbon Monoxide Panel and approved by CASAC. The PA needs to be clearer about how th e three main sources of carbon monoxide that contribute to the ca rbon monoxide dose in the body combine and interact. These three primary sources are endogenous production of carbon monoxide, exposure to indoor sources, and ambient outdoor CO expos ure. Ambient CO exposure needs to be considered in the context of these other two sources of the biologically effective dose.

The Panel found that there was too much de pendence on the now classic clinical study conducted by Allred et al. (1989) and funded by the Health Effects Institute (HEI). While agreeing that this seminal study provided impor tant evidence, its findi ngs should not be so emphasized as to ignore more contemporary epidem iologic studies, especial ly those directed at coronary artery disease (CAD) and at cardiovascular diseas e (CVD) more generally. The epidemiologic studies are important because ot her cardiovascular conditions affect a large number of people who are at risk from CO exposure. We support the high level of attention to populations at risk, but continue to be concerned that the Agency is underestimating CO exposure among some vulnerable groups, especially persons with low income status. This is one

1rationale for placing greater empha sis on the findings of the epidemiologic studies versus the controlled clinical studies. As with other crit eria pollutants, the existence of these populations and the extent of their increased susceptibility are essential to promulgating NAAQS that protect the public health. We recommend this greater em phasis of the epidemiol ogic data across all of the CO documents, beginning with the Integrat ed Science Assessment and extending through the PA. There needs to be greater balance in treating the various lines of evidence.

The chartered CASAC feels that, in general, an ideal PA should be far shorter and more focused. Staff and the Administrator can turn to the REA and the ISA for more background regarding CO as necessary. The PA could be reduced in length to present a more concise summary of the evidence and how the evidence re lates to alternative CO standards. A concise description of how the form of the standard is importa nt would also be useful.

It is important to acknowledge the decrease s in ambient CO levels over time; however, this success should not preclude an objective assessment of the poten tial health consequences of exposures at the current CO NAAQS. While me asured concentrations infrequently reach the current NAAQS, evidence indicates that adverse heal th effects could occur at these levels. For that reason, CASAC expresses its preference for a lower standard.

We understand there will not be a subsequent draft before the releas e of the final PA. After EPA incorporates our major comments and recommendations, the PA will be adequate for rulemaking. We look forward to the Agency’s re sponse and the successful completion of the CO NAAQS review. The CASAC and Panel membership s are listed in Enclosure A. The Panel’s responses to EPA’s charge questi ons are presented in Enclosure B. Finally, Enclosure C is a compilation of individual panel member comments.

Sincerely,

/Signed/ /Signed/

Dr. Joseph D. Brain, Chair Dr. Jonathan M. Samet, Chair CASAC CO Review Panel Clean Air Scientific Advisory Committee

Enclosures

2NOTICE

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 of commercial products does not constitute a recommendation for use. CASAC reports are posted on the EPA website at http://www.epa.gov/CASAC.

3Enclosure A

Rosters of the CASAC CO Panel and CASAC



### U.S. Environmental Protection Agency Clean Air Scientific Advisory Committee Carbon Monoxide Review Panel

CHAIR Dr. Joseph Brain , Cecil K. and Philip Drinker Profe ssor of Environmental Physiology, Department of Environmental Health, Harvard School of Public Healt h, Harvard University, Boston, MA

MEMBERS Dr. Paul Blanc , Professor and Chief, Department of Medicine, Endowed Chair, Occupational and Environmental Medicine, Division of Occupa tional and Environmental Medicine, University of California San Francisco, San Francisco, CA

Dr. Thomas Dahms , Professor and Director, Anesthesiol ogy Research, School of Medicine, St. Louis University, St. Louis, MO

Dr. Russell R. Dickerson , Professor and Chair, Department of Meteorology, University of Maryland, College Park, MD

Dr. Laurence Fechter , Senior Career Research Scientist, Department of Veterans Affairs, Loma Linda VA Medical Center, Loma Linda , CA

Dr. H. Christopher Frey , Professor, Department of Civ il, Construction and Environmental Engineering, College of Engineering, No rth Carolina State University, Raleigh, NC

Dr. Milan Hazucha , Professor, Department of Medicine , Center for Environmental Medicine, Asthma and Lung Biology, University of North Carolina - Chapel Hi ll, Chapel Hill, NC

Dr. Joel Kaufman , Director, Occupational and Environmen tal Medicine Program, University of Washington, Seattle, WA

Dr. Michael T. Kleinman , Professor, Department of Medicine, Division of Occupational and Environmental Medicine, University of California, Irvine, Irvine, CA

Dr. Francine Laden , Professor, Channing Laboratory, Harvard University, Boston, MA

Dr. Arthur Penn , Professor LSU School of Veterinary Medicine, Department of Comparative Biomedical Sciences, Louisiana St ate University, Baton Rouge, LA

4Dr. Beate Ritz , Professor, Epidemiology, School of Public Health, University of California at Los Angeles, Los Angeles, CA

Dr. Paul Roberts , Executive Vice President, Sono ma Technology, Inc., Petaluma, CA

Dr. Armistead (Ted) Russell , Professor, Department of Civ il and Environmental Engineering, Georgia Institute of Technology, Atlanta, GA

Dr. Anne Sweeney , Professor of Epidemiology, Department of Epidemiology and Biostatistics, School of Rural Public Health, Texas A&M H ealth Science Center, College Station, TX

Dr. Stephen R. Thom , Professor, Institute for Environmental Medicine, University of Pennsylvania, Philadelphia, PA

SCIENCE ADVISORY BOARD STAFF Ms. Kyndall Barry , Designated Federal Officer, 1200 Pe nnsylvania Avenue, NW, Washington, DC

5

### U.S. Environmental Protection Agency Clean Air Scientific Advisory Committee

CHAIR Dr. Jonathan M. Samet , Professor and Flora L. Thornton Chair, Department of Preventive Medicine, University of Southern California, Los Angeles, CA

MEMBERS Dr. Joseph Brain , Cecil K. and Philip Drinker Profe ssor of Environmental Physiology, Department of Environmental Health, Harvard School of Public Healt h, Harvard University, Boston, MA

Dr. H. Christopher Frey , Professor, Department of Civ il, 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, Department of Civ il and Environmental Engineering, Georgia Institute of Technology, Atlanta, GA

Dr. Helen Suh , Associate Professor, Department of Environmental Health, School of Public Health, Harvard University, Boston, MA

Dr. Kathleen Weathers , Senior Scientist, Cary Institute of Ecosystem Studies, Millbrook, NY

SCIENCE ADVISORY BOARD STAFF Dr. Holly Stallworth , Designated Federal Officer, Washington, DC

6Enclosure B

CASAC’s Consensus Responses to EPA’s Charge Questions

1. Does the Panel find the introductory and bac kground material, includ ing that pertaining to previous reviews of the CO standard, the current review and current air quality, to be clearly communicated and appropriately characterized?

Chapter 1 of the PA does a good job providing bac kground information. There is a brief review of the CAA and provisions to establish primar y and secondary NAAQS; adequate margins of safety; previous reviews; CO sources in ambien t air; the monitoring network; low dose levels; new monitors/NCore network; recent ambient and steady-state decreases in ambient CO; and finally, the “staff’s evaluation of policy implications of scientific evidence in the ISA and results of quantitative analyses based on that evidence.” The PA focuses on the four basic elements of a NAAQS: indicator, averaging time, form and level. None of these elements have been clearly defined in the PA. The Panel recommends including clear definitions of these four elements, consistent with previous CASA C recommendations in the review of other criteria pollutants.

2. Consistent with the revised NAAQS proce ss which includes development of this draft Policy Assessment (PA) document, consideratio ns with regard to the primary standard for CO have been organized around a set of polic y-relevant questions for the review.

a. Does the Panel find the question posed to appropriately reflect the policy relevant questions in the review?

The questions posed raise the major issues, and the information provided in response to these questions provides the essential ev idence required for making policy decisions. It is difficult to make a judgment on the adequacy of protection because there is no estimate of the total population exposed to benchmark CO concentrati ons. Only numbers for test cases in Denver and Los Angeles are provided and additional information is needed on the application of the two case studies’ findings to the whole country.

The increase in scientific evidence on the effect s of environmental CO si nce the last evaluation of CO standards, as documented in the ISA, co mes primarily from epidemiology based studies. A combined consideration of the findings of epidemiological studies and controlled human exposure studies leads to the conclusion that subs tantial numbers of persons experience ambient CO concentrations resulting in lower effective CO doses than the doses used in the controlled human exposures. The document does not appear to give the epidemiologic studies sufficient standing relative to the controlle d human exposure data, even though they may be more realistic.

One question that was not adequately posed is: what are the confounding effects of non-traffic sources of CO (e.g., indoor air)? Numerous st udies have shown that we spend 80-90% of time indoors. For healthy elderly and people with CVD, the time they spend indoors may be even greater. The non-traffic sources of CO are at times substantial a nd may override the ambient CO

7levels in contributing to dose. It is suggested that informa tion from the 2000 criteria document on indoor sources be included.

b. Does the Panel consider the document to pr ovide the appropriate level of detail in addressing these policy-relevant questions?

For the controlled human studies , the Panel found the level of de tail appropriate. However, the opposite is true for the epidemiological studies.

3. The discussion of the health effects evidence (e.g., secti on 2.2.1) draws from the most recent information contained in the final IS A for CO and information from the previous review described in previous Ai r Quality Criteria Documents.

a. Does the draft PA accurately reflect the cu rrently available health effects evidence for CO as characterized in the final ISA and the extent to which it differs from that available at the time of the last review? b. Does the Pane find the presentation to be technically sound, clearly communicated and appropriately balanced?

The description of the data considered by the pr evious EPA reviews is basically sound but too focused on the Allred et al. study. There should be a way to mention key elements of other controlled human studies in this document. The document continues to emphasize the use of %COHb as the optimal dose metric for assessing ri sk associated with CO exposure and its health consequences. However, the discussion of the epidemiological data s hould also consider nonhypoxia mechanisms. Increased COHb is importan t, but may not be the only mechanism for CO health effects.

The last review of CO was halted for several ye ars due to the pending stu dy of the effects of CO at high altitude and extreme cold environments and its subsequent report. The PA should very briefly acknowledge the findings of this report . Without that information, it is difficult to determine to what extent ther e are changes from the last review that commenced in 1999.

In order to facilitate be tter understanding of the cardiovascular effects, particularly myocardial ischemia, we suggest adding to the reported values of changes in % time to angina on page 2-11 (top paragraph), including the actual changes in seconds with the conf idence intervals (CI). Moreover, regarding time to angina endpoint, are there any long-term consequences on repeated exposures, duration of angina, and frequency of occurrence without CO exposure? EPA should address these questions. If data are not available, the PA should st ate this to be the case. This information would seem to be important for the more complete understanding of the uncertainties associated with using these data to support the standards.

4. The discussion of the quantitative analysis of exposure and dose (e.g., section 2.2.2) draws from the analyses described in the second draft Risk and Exposure Assessment (REA).

a. Does this discussion accurately reflect the analyses contained in the draft REA?

8The Panel largely agreed that the discussion in th e PA accurately reflects the analyses contained in the second draft REA. We continue to be concerned with whether increased emphasis could be placed on the increment that ambient CO c ontributes to COHb or whether the emphasis should be on the final resulting %COHb concentra tion itself. We have a related interest in modeling indoor source contribution to C OHb to better understand the total COHB concentrations.

Panel members offered mixed opinion regarding th e decision by the EPA not to pursue the 1% COHb benchmark as suggested by the Panel. Th e staff correctly pointed out that “this level overlaps with the upper part of the range of endogenous levels.” One Panel member supported the agency’s decision, since this complies with th e EPA’s task “to establish standards that are neither more nor less stringent than necessary fo r these purposes”, i.e., public health. However, other members considered that a more adva nced modeling approach could focus on the increment that ambient CO contributes to %COHb, rather than the final resulting COHb concentration itself. The incremental CO analysis would provide a clear co ntext of the full range of benchmarks for policy analysis. Further, if adverse effects are clearl y observed in controlled human exposure studies with a small sample size associated with an increase in the percent COHb of 2%, then it is prudent to consider standards that would use a benchmark of ambient CO-attributable COHb increases as low as 1%. This benchmark would lead to a wider range for a margin of safety, given that a no observable adverse effect level for CO effects among susceptible populations has not been demonstrated.

b. Does the Panel find the presentati on to be technically sound, clearly communicated and appropriately balanced?

Most Panel members agreed that the presenta tion was technically sound and appropriately balanced. However, most of the Panel was concerned that the pres entation unnecessarily diminished the value of epidemiological studies in establishing the underpinnings (if not the details) of the quantitative relatio nship. Despite the fact that th e PA may need to be based on a risk assessment drawn primarily from one partic ularly informative controlled human exposure study (i.e., the multi-center investigation described in Allred, et al.), there would be value in highlighting the supporting role of other studies, in particul ar the body of epidemiological evidence.

The %COHb module of the APEX model, although the most important, also has weaknesses, given that some physiologic data and the range of values for many variables that enter into the model are not transparent. Despite these limitations, however, there seems to be sufficient information for some variables that can be used to refine the estimates generated (e.g., Hb concentrations stratified by race-ethnicity as should be ava ilable from NHANES or other readily accessible sources).

5. Does the document identify and appropriately characterize the important uncertainties associated with the evidence and quantitative anal ysis of CO exposure and dose, particularly those of particular significance in drawing conc lusions as to the adequacy of the current CO standards?

9In general, the uncertainties are dealt with appropriately with one exception. Under the pretext of evaluating the uncertainty rega rding ST segment changes, the cu rrent review suggests that the uncertainty is now greater than in 1991 (p. 2-32). The Allred et al. study used EKG changes in the ST segment to substantiate that the subjective measure of angina was indeed due to ischemia. These two indicators, one subjective and one obj ective, were very high ly correlated and not independent. Therefore, separate analyses of the two indicators should be avoided.

The most thorough clinical studies re main those of Allred et al., Kl einman et al., and Sheps et al. While the effects in these groups are clear, and together thes e subjects may be “the best characterized population,” it is not clear that they re present the “most su sceptible population.” First, these experiments have not been repeated in the past 20 years, and second, other potential susceptible groups have not been exposed to such controlled clinical c onditions. Additionally, the epidemiologic data on cardiovascular (heart ) disease, including congestive heart failure (CHF), suggest that those groups might be at le ast as susceptible to CO -related stress as the coronary artery disease group.

The data available in the PA and the ISA on CO a nd heart failure are instructive. The statement on page 2-14 (lines 16-19) that there are onl y “...small or no associa tions between hospital admissions” and stroke is inaccurate (see next para graph). Of the five studies listed in the footnote at the bottom of that page, four of th e five reported increased hospital admissions for CHF. A close look at Figures 5-2, 5-3, and 5-4 in the ISA suppor t the association of CO with CHF and stroke more than for CAD. If all th e studies for stroke, CHF and CAD were placed on the same x-axis, it could very well demonstrate th e heightened uncertainty in statements of CAD patients being the most suscep tible to CO effects.

Another possible uncertainty rega rds the question of whether CO is a surrogate and whether its effects at low concentrations ca n be separated from those of co- pollutants (p. 2-34, lines 24-34). There are analytical and methodologi cal challenges in disentangling the effects of CO from those of co-pollutants, although the pr oblem does not exist in the contro lled clinical studies of CO alone.

6. This document has integrated health evidence from the final ISA and risk and exposure information from the second draft REA as it relates to reaching conclusions about the adequacy of the current standard and potential alternative standards for consideration.

a. Does the Panel view this integration to be technically sound, clearly communicated, and appropriately characterized?

Although it may be a challenging task, it is important to inte grate the evidence from the epidemiological studies with clin ical studies (p. 2-25). Some of the conclusions are not well supported. In particular, the estimation of popul ation exposures (p. 2-5, lines 27-34, and p. 2-6, lines 1-8) may underestimate exposures of thos e in lower socioeconomic status populations because of their higher likelihood of residing in heavily trafficked areas and an increased probability of exposure to secondhand tobacco sm oke. Inclusion of population prevalence of low income status and smoking prevalence in the simulated populations might shift the distribution of estimated CO e xposures towards higher levels.

10The conclusion that the current evidence supports a primary focus on those with cardiovascular disease is justifiably based on observations from clinical st udies. However, the best characterized and most extensively studied population does not necessarily coincide with the most highly susceptible population. Since the last review, ther e are additional studies with positive findings that assess effects on the fetuses. There is also strong toxicological evidence relevant to the association of prenatal CO e xposure with adverse pregnancy outcomes, such as premature birth and low birth weight. A stronger commentar y on exposure during pregnancy and reproductive outcomes is needed.

b. Does the document appropriately characteri ze the results of th e draft REA, including their significance from a pub lic health perspective?

The conclusion that the current evidence s upports a primary focus on individuals with cardiovascular disease is justif ied by current clinical research . Discussion should be added, however, that the best characterized and most extensively studied population does not necessarily identify the most highly susceptibl e population. In particular, commentary on the fetus as an at-risk group should be added because of newer data describing the effects of CO on the fetus coupled with toxicological evidence for risks associated with prenatal CO exposure.

If the PA is going to use %COHb as the dose me tric, then there has to be a better rationale provided for interpretation of the epid emiological data using this metric.

7. What are the views of the Panel regarding the staff’s disc ussion of considerations related to the adequacy of the current and potential alter native standards?

The staff has provided an extensive analysis of the adequacy of th e current and potential alternative primary CO standards. The current st andards set the levels for 1-hr average and 8-hr average at 35 ppm and 9 ppm, resp ectively. The form of the standard is that those levels are not to be exceeded more than once per year. In re viewing the recent literature, staff has documented that the “much expanded epidemiological eviden ce ... provides support for previous conclusions regarding cardiovascular disease- related susceptibility and indicat ions of air quality conditions that may be associated with ambient CO-related risk” and concluded that a causal relationship is likely to exist between relevant short term exposures to CO and cardiovascular morbidity.

Staff also concludes that th e currently available evidence provides limited but suggestive epidemiologic evidence for CO-induced effect s on preterm births, birth defects, and developmental outcomes. Individuals with condi tions limiting their ability to deliver oxygen to target tissues represent groups susceptible to the adverse effects of CO, in addition to those with coronary artery disease. Based on the analyses of epidemiological studies presented in the PA, there is consensus in the Panel that the current standards may not protect public health with an adequate margin of safety, and therefore revision s that result in lowering the standards should be considered.

While the epidemiologic studies pr ovide evidence that is coherent with the controlled exposure studies, the Staff determined that four of the studies cited in Table 2.1 included years in which

11the ambient CO concentrations exceeded the 8-hr standard. However, Table 2.1 includes three studies of hospitalizations for is chemic heart disease and/or conge stive heart failure from Atlanta for which this was not the case (Tolbert 2007, Peel 2007, Metzger 2007). An additional study of CHF (Wellenius, 2005) also did not include data from years in whic h either the 1-hr or the 8-hr standards were exceeded.

The PA suggests that CHF could have multiple causes, and for that reason it would be problematic to use it as a health effect indicat or. The three studies of ischemic heart disease were consistent, but only the Tolb ert et al. study had clear statistic ally significant results. It should be recognized that new cont rolled exposure studies of some of the sensitive groups (e.g., infants, fetuses, individuals with CHF or MI’s) would be nearly impossibl e to justify ethically. Therefore more reliance needs to be placed on the epidemiologic studies and assessing whether there are causal relationships. Pooling methods, such as quantitativ e meta-analyses, may also be useful for developing exposure-response relationsh ips. The available studies cover periods during which the current NAAQS wa s exceeded as well as studies covering lower ranges. This coverage of a wide range of CO concentrations makes possible a relatively robust estimation of exposure-response relationships. The emphasis s hould be on studies that used a multipollutant model approach to control for potential confounding of CO effects by those of other co-varying pollutants.

While there have been no new controlled human e xposures designed to examine effects of CO at COHb levels below 2%, there have been num erous improvements to the exposure and COHb dosimetry models employed to provide exposure and risk estimates. The Staff analysis indicates that some of the uncertainties identified in previo us reviews of the standard have been reduced. Based on their overall analysis, they conclude that the body of eviden ce and the quantitative exposure and dose estimates provide support for a st andard at least as pr otective as the current standards. I.e. the data provi de support for retaining or revising the current 8-hr standard.

Overall the Panel agrees with this conclusion. If the epid emiological evidence is given additional weight, the conclusion co uld be drawn that health effect s are occurring at levels below the current standard, which would support the tight ening of the current st andard. The PA should include an analysis the number of exceedances that would have occurred if the standard had been based on the epidemiological data.

8. Staff believes that the evid ence presented in the final ISA and the exposure and risk information presented in the second draft REA supports a range of policy options for the CO standards.

The Staff have proposed a range of policy optio ns based on the quantitative risk analyses performed. As a starting point, the Staff indi cates that the evidence is consistent with maintaining standards that are at least as protec tive as the current leve ls. However, given new evidence, primarily epidemiological, that there are many individuals potentially at risk in addition to those with coronary artery diseas e (e.g., fetuses, pregnant women, people with congestive heart disease, and peopl e with anemia of various types) , there is reason to consider reducing the standard below the current level(s).

12The Panel suggests describing ex ample policy options such as:

• 8 hr – retain the 8-hr averaging time with c onsideration given to le vels within the range of 3 to 6 ppm, with no more than a single exceedance or revise the form of the standard to 99 th percentile with a concentra tion range of 3-5 ppm. See also Figure 1 which shows the linear relationship between the 99 th percentile and the design value measured for epidemiologic studies summarized in PA Table 2-1.

• 1 hr – retain the current standa rd to provide protection agains t infrequent acute exposures. Consider a range of concentrations fro m 5 ppm to 15 ppm, combined with a 99 th percentile or fourth-highest daily maximum. The panel does not concur with revoking the 1 hr standard.

Figure 1

a. To what extent does the document provide su fficient rationale to justify this range of options?

The risk models were based on effects in people with coronary artery disease. They were used to estimate the percentages of indivi duals in LA and Denver that would reach benchmark levels of COHb ranging from <1.5% COHb to <2% COHb. These were summarized in Tables 2-6 and 2- 7 in the PA. The overall guidance for the policy was not clearly described and the wide range of options needs better definition. It might be useful to present a ta ble of options with the pros and cons of each respectively. The information is embedded in the RA and PA documents, but the options and their respective adva ntages or disadvantages need to be more clearly summarized.

The Panel concurs with the staff that the 1-hr standard might provide pr otection independent of the type of protection provided by the 8-hr standard (page 2-54, line 14); however, the discussion supporting this statement should be more clearly documented.

13b. Does the Panel have any recommendations regarding additional considerations which should inform characterization of these options for both the 8-hour and 1- hour standards?

In choosing a more stable form of the standard, such as the 99 th percentile, which would allow more days on which the standard can be exceeded in a given year, the level of the standard must be reduced to insure that the degree of health protection is su fficient. EPA should consider conducting an evaluation of the re presentativeness of th e risk analysis to the entire US. Currently, the PA is based on two very different cities. Spatial heteroge neity of CO exposures that increase exposures near major sources, i.e. near and on roadways, should be given more weight since these might drive some of the adverse health effects.

9. What are the Panel’s views regarding the l evel of detail presente d in this chapter?

The PA concludes that there is insufficient informa tion at this time to support the consideration of a secondary standard for CO. In general, the level of discussion detail is ap propriate; however, some additional detail could be added at the end of chapter 3 on what inform ation is missing in order to make a determination regarding a secondary standard.

10. The discussion of the CO-relat ed welfare effects draws from the most recent information contained in the final ISA for CO. a. Does the draft PA accurately reflect the currently available evidence as characterized in the final ISA?

The Panel agrees that the Policy Assessment appropriate ly characterizes the evidence as presented in the ISA. b. Does this discussion effectiv ely summarize the information on climate-related effects of CO?

Yes, but there should be a clear statement, to match a similar assertion in the ISA, that there is some evidence that CO has effects on climat e. It addition, it would be appropria te in the last paragraph of this chapter to summarize what information is missing and thus needed, such as more accurate U.S. and global emissions inventory, monitoring specifically fo r climate rather than just for standards and exposure, and improvements in localized chemical reactions between CO, CH 4 , and O 3 within global models.

11. What are the Panel’s views regarding the appropriateness of staff’s initial conclusions related to considering a secondary standard for CO?

The PA concludes that there is insufficient inform ation at this time to support consideration of a secondary NAAQS. Nonetheless, there is subs tantial evidence that CO has adverse effects on climate. It would be appropria te in the last paragraph of this chapter to summarize what information is missing.

14

### Enclosure C

Review Comments from CASAC CO Panel Members on the Policy Assessment for the Review of the Carbon Monoxide National Ambient Air Quality Standards: External Review Draft

Dr. Paul Blanc ............................................................................................................................... 16 Dr. Thomas Dahms ....................................................................................................................... 17 Dr. Russell Dickerson ................................................................................................................... 21 Dr. Milan Hazucha ........................................................................................................................ 22 Dr. Michael Kleinman .................................................................................................................. 27 Dr. Francine Laden ....................................................................................................................... 30 Dr. Arthur Penn ............................................................................................................................. 31 Dr. Beate Ritz

............................................................................................................................... . 33 Dr. Anne Sweeney ........................................................................................................................ 35 Dr. Stephen Thom ......................................................................................................................... 37

15

### Dr. Paul Blanc

4. The discussion of the quantitative analysis of exposure and dose (e.g., section 2.2.2) draws from the analyses described in the second draft Risk and Exposure Assessment (REA). a. Does this discussion accurately reflect the analyses contained in the draft REA? b. Does the Panel find the presentati on to be technically sound, clearly communicated and appropriately balanced?

The Policy Assessment perpetuates and to a degr ee magnifies the fundamental misunderstanding of the REA in relation to suscep tibility based to narrowly on CAD al one (i.e., past MI or angina) rather than on cardiovascular disease as a group. In both cases this is a misread of the ISA and marks a failure to grasp what the accumulate d epidemiological eviden ce shows. Thus this presentation is unbalanced, in interpreting the ISA through the flawed “lens” of the REA.

6. This document has integrated health evidence from the final ISA and risk and exposure information from the second draft REA as it relates to reaching conclusions about the adequacy of the current standard and potential alternative standards for consideration. a. Does the Panel view this integra tion to be technically sound, clearly communicated, and appropriately characterized? b. Does the document appropriately charac terize the results of the draft REA, including their significance from a public health perspective

It is very difficult to decipher the conclusions of Policy Assessment beyond an unequivocal position that what ever is done th e current standards should not be weakened . I would characterize the conclusion as clearly communi cating a sense of not wishing to communicate something definitive, at this point at least. Th e rationale for not considering how many at risk persons are pushed over a threshold of body bur den of COHb because they have baseline exposures form non-ambient sources seems ill-judged and counter-intuitive in terms of public health protection. Perhaps there are parallels in considerations of ambient lead exposure limits?

16

### Dr. Thomas Dahms

Charge Question 2. Consistent with the revise d NAAQS process which includes development of this draft Policy Assessment (PA) document, considerations with regard to the primary standard for CO have been organized around a set of po licy-relevant questi ons for the review.

a. Does the Panel find the question posed to appropriately reflect the policy relevant questions in the review?

I believe that the questions posed raise the majo r issues and the information provided in response to these questions provides th e essential data re quired for making policy decisions. These questions regarding 1. the adequacy of pr otection by the current standards; 2.does new information alter previous conclu sions regarding health effects; 3. should COHb continue to be the dose indicator for CO exposure; 4. the hea lth effects of ambient CO levels; and 5. any reduction in the uncertainties regarding CO.

Regarding the adequacy of protect ion: it is difficult to make a j udgement in this area for two

reasons. 1. There is no definition presented of what is considered to be an acceptable risk and 2. The number of persons in the at risk groups exposed to criteria levels of CO is not defined for the country. The only description of numbers exposed is for two cities: Los Angeles and Denver with no guidance provided for extrapolation to the whole co untry. For example, if the document is to discuss the numbers of persons in the U.S. with CAD, then the reader needs to have some estimate of how many of these persons woul d reach criteria levels of COHb on an annual basis given the current stan dards. Therefore it is difficult to judge the effectiveness of the current standards in protecting the population

2. The new information in this area all comes from epidemiological studies that are crucial to the interpretation of the mean ing of the controlled human exposures. The adverse health effect of limiting the amount of work a person w ith CAD can perform with doses of CO near the current standard has been clearly establishe d. However it is not clear that the extent of limitation has any further impact on the health of this at risk group. This concern is implied in the discussion regarding the uncertainty a bout the significance of ST segment changes on page 2-32. The epidemiological studies are desi gned to provide one means of determine if low CO doses have measureable impacts on h ealth by correlating CO exposure with hospital based treatment for CV related events. This link between the two types of studies is clear in my mind but I’m not sure that the connecti on is clearly stated in this document.

3. Carbon monoxide is unique among the regula ted air pollutants because it has a clear marker of dose, %COHb. The document indicates that the well established effects of COHb are related to the reduction in oxygen delivery to the tissues. This is in the face of the immerging evidence of effects of the partial pressure of CO, P CO , as a messenger molecule, which could result in various patho-physio logical conditions in combination with CO exposure. What is missing from the REA and ca rried through to the PA is a brief description of the relationship between P CO and %COHb. This could possibly provide some prospective for the reader as to the importance of th e physiological tensions of carbon monoxide in

17tissues of interest. This woul d not distract from the curren t understanding that the dose indicator of %COHb is cu rrently the primary focus for policy assessment.

4. The decreasing ambient levels of CO in the United States makes it ever more difficult to demonstrate health effects of CO based on the concept of sufficient exogenous dose to result in %COHb levels that have been shown to ha ve pathophysiological effe cts. It would appear that the epidemiological effects of CO occur at such low levels of exposure as to result in very little increases in %C OHb. Accepting the premise that the epidemiological results attributed primarily to CO exposure implies that adverse health effect s occur at levels of %COHb considerably below those shown to have statistically significant effects in controlled human exposures. For these effects to be c onsistent with the c ontrolled human exposure data, one would have to accept the statement th at the effects of CO are without threshold (page2-11, Line 9; 2-12, L4; 2-15, L24; 2-16, L2 6; 2-40, L2). Are we to assume that the reason that the epidemiological studies can show significant effects of very low levels of exposure (very small increases in %COHb) is due to the larg e number of subjects being studied. Or is there anothe r hypothesis regarding how th ese effects are mediated?

5. The uncertainties related to CO exposure have not been lessened.

b. Does the Panel consider the document to pr ovide the appropriate level of detail in addressing these policy-relevant questions?

Yes but brief verbiage linking concepts as noted above would be helpful in creating transitions between the types of information.

Charge question 3. The discussion of the health effects evidence (e.g., section 2.2.1) draws from the most recent information cont ained in the final ISA for CO and information from the previous review described in previous Ai r Quality Criteria Documents.

a. Does the draft PA accurately reflect the cu rrently available health effects evidence for CO as characterized in the final ISA and the extent to which it differs from that available at the time of the last review? b. Does the Pane find the presentation to be technically sound, clearly communicated and appropriately balanced?

The description of the current state of knowledge includes su ggestive information regarding cellular processes that can result in regional increases in endogenous levels of CO that could be altered by exogenous exposure. Given the considerable amount of curre nt research in this area, mention of this data should exist in this documen t. The last review of CO was halted for several years due to the pending study and report on the effects of CO at altitude and at extreme cold environments. The document should very briefl y acknowledge the findings of this report. Without that information in the current documen t it is difficult to determine how this report should differ from the last review started in 1999.

18Charge Question 4. The discussion of the quantit ative analysis of exposure and dose (e.g.,section 2.2.2) draws from the analyses described n th e second draft Risk and exposure Assessment (REA).

a. Does this discussion accurately reflect the analyses contained in the draft REA?

The discussion focuses on the detail of one mu lticenter study following brief mention of the supporting studies. I believe that this information could be st rengthened by working in the information that the CO exposures in the ot her studies was very similar with confirming evidence regarding time to angina. This would addr ess the current concern of imbalance in the discussion of the studi es in this area.

b. Does the panel find the presentation to be technically sound, clearly communicated and appropriately balanced? There are some concerns regarding the techni cal soundness of the descriptions given which do make physiological sense.

i. Inaccuracy: page 2-8, line 26. The statement “This binding to reduced iron...” is very misleading. It has been transferred from the REA description of CO binding to hemoglobin. In particular it comes fr om the mathematical fiddle noted in Appendix B of the REA on page B-5 whic h states: “In working with the CFK model it is convenient to expre ss COHb as a percent of [RHb] 0 .” This false concept should not be repeated in the text of the document. The fundamental relationship as described by Haldane cl early indicates that the much higher affinity of hemoglobin for CO vs Oxyge n results in CO displacing O2 from oxygenated hemoglobin. The implication th at CO binds preferentially to only reduced Hb is incorrect a nd needs to be corrected.
ii. Page 2-9, line 1. The statement “...or incr eased cardiac output) is not clear. The preceding sentence is discussing cardiovasc ular disease in the context of CAD. Therefore the normal compensatory mechanis m that exist in healthy individuals is increased myocardial blood flow through vasodilatation, not vasodilatation and increased cardiac output. The current verb iage does not make sense and needs to be changed.

Charge Question 5. Does the document identify and appropriately characterize the important uncertainties associated with the evidence and quantitative analysis of CO exposure and dose, particularly those of particular significance in drawing conclusi ons as to the adequacy of the current CO standards?

Generally the uncertainties are dealt with approp riately with the exception of the item mentioned below.

The current review on page 2-32 under the guis e of evaluating the uncertainty regarding ST segment changes suggests that the uncertainty is now greater than it was in 1991. The policy assessment is based on the adverse health effect s of 2% COHb resulting in reducing the amount of work a person with CAD can perform before ch est pain develops with is due to myocardial ischemia. The Allred et al study used EKG changes in the ST segm ent to substantiate that the

19subject measure of angina was indeed due to is chemia. These two indicators, one subjective and one objective, were very highly correlated and not inde pendent. Therefore the separation of the two indicators (page 2-32, line 25 -28) is a reflection of the revi ewers not understanding the study design. (This should have been corrected through out the ISA, REA and the PA. The statement attributed to the ISA, p.48 –assumed to be 5- 48—on page 2-32 needs to have a line reference otherwise it is difficult to locate th is conclusion in the ISA.) In f act the ever increasing amount of epidemiological data on the effects of CO probabl y reduces the uncertainty of the effects of CO exposure in individuals with cardiovascular disease.

Exposure/Risk-based Considerations Page 2-40 lines 3-10. The rationale for not using the benchmark of 1% COHb is flawed. In the version of the ISA dated January 2010, I cannot find a reference to the range of endogenous levels of %COHb: the source needs to be bett er documented. There is a list of rates of endogenous product provided in the Appendix but there are multiple studies listed. If one of these studies is the source it should be identifi ed. The rationale for re questing the inclusion of this benchmark was the sense that ‘the effects of CO are without threshold (page2-11, Line 9; 2- 12, L4; 2-15, L24; 2-16, L26; 2-40, L2).’ The %COHb da ta that is being used is that of Allred et al cited on page 2-11, line 1 as showing %COHb levels for exposure to 0-2 ppm CO as being 0.6%. The benchmark of 1% does not appreciably ove rlap 0.6% any more than one would expect there to be overlap between 1.5% and 2.0%. What is not stated is th at the Apex model may overestimate the range of values resul ting from no exposure to exogenous CO. Without the 1% COHb benchmark how are the ep idemiologic studies to be interpreted? Are these effects due to the effects of a pollutant that is not measur ed but very highly correlated to atmospheric CO? If the Policy Assessment is going to use %COHb as the dose metric, then there has to be a rationale provided for interpre tation of the epidemiological data using this metric. If the result is a very high number of individuals with CAD having doses of 1%COHb and very few appearing in the ER or being admitted, this point should be discussed.

20

### Dr. Russell Dickerson

The Policy Assessment in Chapter 3 addresse s the issue of a secondary standard.

9. What are the Panel’s views re garding the level of detail?

The detail is a little li ght as indicated below.

10. a. Does the draft PA accurately reflect the currently available evidence?

Within the limits of what is written yes.

b . Does this discussion effectiv ely summarize the information on climate related effects of CO?

See below.

11. What are the Panel’s views re garding the appropriateness of the initial conclusions?

The PA concludes that there is insufficient information at this time to support the consideration of a secondary NAAQS. None-the-less, there is ev idence that CO has adverse effects on climate.

It would be appropriate in the last paragraph of this chapter to summarize what information is missing. For example, U.S. and global emissions inventories must achieve a certain level of accuracy before a secondary standard is established. Is the level of uncer tainty sufficient and if not what would it take? Monito ring was being phased out – should this policy be reconsidered? Representative monitoring to evaluate emissions inventories or models may look different from

monitoring to access exposure. The basic question of what form is needed for regulations or standards should be addressed. A concentr ation-based standard would probably be inappropriate. Emissions standards su ch as are being considered for CO 2 would be more applicable to the issue of how to control CO emissions. The ISA (Figure 3.8) shows nicely how CO is low hanging fruit with resp ect to short term (20- year) climate forcing. The PA may be an

appropriate forum to provide gui dance to how these environmenta l benefits may be realized.

21

### Dr. Milan Hazucha

The first external draft of the document provid es a comprehensive overv iew of the legislative requirements and approaches to policy decision ma king process. The draft presents in a succinct way all aspects of the scientific evidence requir ed for a successful policy assessment. The staff has reviewed and discusses key scientific and techni cal knowledge with clear understanding of health effects associated with CO presence in the ambient air. Various related issues are presented in sufficient detail and clearly communicated. Asking specific questions throughout the document and answering them in a succinct manner has been very helpful in focusing on the cr itical aspect of the policy setting. Answers to charge questions and specific comments: Introduction and Background for the Policy Assessment (Chapter 1)

1. Does the Panel find the introductory and bac kground material, includi ng that pertaining to previous reviews of the CO standard, the curren t review and current air quality, to be clearly communicated and appropria tely characterized?

I find the introductory and background material pertaining to the previous and current reviews to be clearly communicated and appr opriately characterized. All the important factors needed to make an informed judgment are adequately presente d and briefly discussed.

Review of the Primary Standard (Chapter 2)

2. Consistent with the revised NAAQS process wh ich includes developmen t of this draft Policy Assessment (PA) document, considerations with regard to the primary standard for CO have been organized around a set of policy-rele vant questions for the review.

a. Does the Panel find the questions posed to appropriately reflect the policy-relevant questions in this review?

Qualified yes in all respects. One question that was not posed is about the confounding effects of no-traffic sources of CO, e.g., indoor air. Numerous studies have shown that we spend~80% of time indoors. For healthy el derly and people with CVD the time spend indoors may be even longer. The non-traffic sour ces of CO are at times substantial and will override the ambient CO levels.

b. Does the Panel consider the document to provide the appropriate level of detail in addressing these policy-relevant questions?

Yes, in all respects. The PA is well written, providing suffi cient details, and highlighting important factors/concerns so that the polic y relevant questions can be addressed both quantitatively and qualitatively.

223. The discussion of the health effects eviden ce (e.g., section 2.2.1) dr aws from the most recent information contained in the final ISA for CO and information from the previous review described in previous Air Quality Criteria Documents.

a. Does the draft PA accurately reflect the currently available health effects evidence for CO as characterized in the final ISA and the extent to which it differs from that available at the time of the last review?

Yes, in all respects. The currently available sc ientific evidence is evaluated, characterized and presented in a sufficient de tail supporting the adequacy of the protection afforded by the current CO standard. The differences with the last review are clearl y presented. There are no new human laboratory studies or exposure/risk-based evidence that would alter the conclusions. The evidence from new epidemiologi c studies has been pres ented in a balanced way. The PA correctly points out to limitations in integrating the evidence from laboratory and epidemiologic studies.

Based on the current scientific evidence and practical consid erations (e.g. arterial blood draw) venous blood COHb level is the op timal indicator of “CO health.”

b. Does the Panel find the presentation to be technically sound, cl early communicated, and appropriately balanced?

Qualified yes. In order to facilitate be tter understanding of the cardiovascular effects, particularly myocardial ischemia , I suggest to add to the repo rted values of % time changes to angina on p.2-11, top paragraph, the actual changes in seconds w ith the confidence intervals (CI) included as well. For example, the reported 4.2% shorter time to angina from a control ~ 9 min interval amounts to 22 sec, with th e CI=8.7%. Since Allred et al. studies are considered the key studies, it would be very helpful to comment briefly on the clinical significance of the shortened tim e. Moreover, regarding time to angina endpoint, are there any long-term consequences on repeated exposur es, on the duration of angina, and frequency of occurrence without CO exposure? EPA shoul d address these questions and if we do not have respective data the PA should state so. Moreover, the first part of the statemen t in footnote #12 (p. 2-12) commenting on the difficulty determining associa tion of CO with CVD and as a marker for traffic-related pollutants should, because of its importance, be moved from the footnote to the body of respective paragraph. Recently published HEI Special Report #17 (Jan. 2010) entitled:”Traffic-Related Air Pollution: A Criti cal Review of the Literature on Emissions, Exposure, and Health Effects” discusses CO as a marker for another traffic-related pollutants such as PM and NO 2 and not as a major health hazard. The review of the epidemiologic evidence (p.2 -14) accurately reflects the difficulties to establish causal relationship between CO a nd reported effects. Similarly, well reasoned section (p. 2-25) points to difficulties integrating laboratory/clinical findings and epidemiologic observations.

4. The discussion of the quantitative analysis of exposure and dose (e.g., section 2.2.2) draws from the analyses described in the second draf t Risk and Exposure Assessment (REA).

23a. Does this discussion accurately reflect the analyses contained in the draft REA?

Qualified yes. The COHb modul e of the APEX model though the most important is also the weakest, since we do not have sufficient physio logic data or the range of values for many variables that enter into the model. Howeve r, despite this limitation there seems to be sufficient information for some variables that can be used to tune the estimates, e.g. Hb concentration for whites and blacks.

As far 1% COHb benchmark suggested by the Pane l, the staff correctly pointed out that “this level overlaps with the upper part of the range of endogenous levels” and decided not to focus on dose estimates (p.2-40). I support this ap proach since this complies with the EPA’s task “to establish standards that are neither mo re nor less stringent than necessary for these purposes”, .i.e. public health.

b. Does the Panel find the presentation to be technically sound, cl early communicated and appropriately balanced?

Yes, in all respects. Again, because of the impor tance of the statement, the first sentence of the footnote #25 on the difficulty to determ ine association between CO and CVD in interpreting epidemiological evidence s hould be moved to the body of a respective paragraph.

5. Does the document identify and appropriate ly characterize the important uncertainties associated with the evidence a nd quantitative analysis of CO exposure and dose, particularly those of particular significance in drawing conc lusions as to the adequ acy of the current CO standards?

Yes, in all respects; The key uncertainties associated with exposure and dose estimates should, besides traffic, list other sources of CO, such as indoor air, smoking, occupational exposures, to name the main ones (p.2-42, l.31) . A succinct discussion of how these sources can override the protection afforded by the current CO standard would be helpful.

6. This document has integrated health evidence from the fi nal ISA and risk and exposure information from the second draft REA as it rela tes to reaching conclusions about the adequacy of the current standard and potential a lternative standards fo r consideration.

a. Does the Panel view this integration to be technically sound, clearly communicated, and appropriately characterized?

Yes, in all respects

b. Does the document appropriately characte rize the results of the draft REA, including their significance from a pub lic health perspective?

Yes, in all respects

247. What are the views of the Panel regarding the staff’s discussion of considerations related to the adequacy of the current and pot ential alternative standards?

I find the initial staff conclusion “for either retaining or revisi ng the current 8-hour standard” (p. 2-46) based on the available estimates of e xposure ambivalent. Does this mean that EPA is undecided or that the evidence is split 50/50? It is true, as subse quently stated, that a variety of factors will be considered in judgi ng the adequacy of the current standard. But such adequacy should be based primarily on the evidence from laboratory/clinical studies and not on policy and other considerations. The evidence from the epidemiology studies, as commented on in several previous sections of this document, is difficult to evaluate and integrate with clinical evidence (p. 2-25). The CO concentrations reported in epidemiol ogy studies will produce COHb levels within a normal range. From reading interpretation of th ese studies in the latest EPA PM ISA the dominant effects in these studies are due to PM. Since we do not have any measurements of COHb level or other adverse effects that can be specifically associated with CO the studies provide no proof beyond statistics that there is a causal relatio nship. CO is primarily known for its anti-inflammatory effects. However, CO is highly correlated with PM and other pollutants, therefore, it is very likely that CO acts as a surrogate for PM and other pollutants. Thus based strictly on scient ific evidence, I agree with the staff interpretation of epidemiology studies and their leaning towards retaining th e current 8-hour standard. The section 2.3 of the discussion of the averag ing time, the form and level of alternative standard and potential alternative levels is succ inct and well reasoned. What is not clear what form might the alterna tive standard have?

8. Staff believes that the evidence presented in the final ISA and the exposure and risk information presented in the second draft REA supports a range of policy options for the CO standards.

a. To what extent does the document provide sufficient rationale to justify this range of options?

Yes, the staff provides sufficient rationale for di scussion of the range of options, particularly the policy options.

b. Does the Panel have any recommendations regarding additional considerations which should inform characterization of these options for both the 8-hour and 1-hour standards?

There should be a greater emphasis on the evid ence based on laboratory/ clinical studies.

Consideration of a Secondary Standard (Chapter 3)

9. What are the Panel’s views regarding the level of detail presented in this chapter?

The level of detail presented in this chapter is sufficient.

2510. The discussion of the CO-related welfare eff ects draws from the most recent information contained in the final ISA for CO.

a. Does the draft PA accurately reflect the currently available evidence as characterized in the final ISA?

Yes, in all respects

b. Does this discussion effectively summarize the information on climate-related effects of CO?

Yes, in all respects

11. What are the Panel’s views re garding the appropriateness of st aff’s initial conclusions related to considering a secondary standard for CO?

Fully agree with staff conclusions.

26

### Dr. Michael Kleinman

7. What are the views of the Panel regarding the staff’s discussion of considerations related to the adequacy of the current and potential alter native standards?

The staff has provided an extensive analysis of the adequacy of th e current and potential alternative primary CO standards. The current standards include a 1-hr average and an 8-hr average standard of 35 ppm and 9 ppm, respectively. The form of the standard is that those levels are not to be exceeded more than once per year. In reviewi ng the recent literature staff has documented that the “much expanded epidemiol ogical evidence ... provides support for previous conclusions regarding card iovascular disease –related susceptibi lity and indications of air quality conditions that may be associated with ambien t CO-related risk” and concluded that a causal relationship is likely to exist between relevant short term exposures to CO and cardiovascular morbidity. Staff also conclude that the cu rrently available evidence provides limited but suggestive epidemiologic evidence for CO-induced effects on pre-term births, birth defects, developmental outcomes and that individuals with conditions limiting their ability to deliver oxygen to target tissues represent groups susceptible to the adverse effects of CO, in addition to those with coronary artery dise ase. Based on the analyses of epidemiological studies presented in the PA there is a consensus in the panel that the current standards ma y not adequately protect public health with a reasonable margin of safety and therefore revisions that result in reducing the standards should be considered.

While the epidemiologic studies provide evidence of coherence with th e controlled exposure studies, the Staff determined that four of the studies cited in Table 2.1 included years in which the ambient CO concentrations exceeded the 8 hr standard. However Table 2.1 includes 3 studies of hospitalizations for is chemic heart disease and/or conge stive heart failure (CGF) from Atlanta for which this was not the case (T olbert 2007, Peel 2007, Metzger 2007) and one additional study of CGF (Wellenius , 2005) which did not include da ta from years in which the either the 1 hr or the 8 hr standards were exceeded. The PA suggests that CHF could have multiple causes and for that reason it would be problematic to use as a health effect indicator. The 3 IHD studies were consistent but only the Tolbert study had clearly statistically significant results. It should be recognized new controlled exposure studies of some of the sensitive groups (e.g. infants, fetuses, individuals with CHF or MI’s) would be nearly impossible to justify ethically. Therefore more reliance needs to be placed on the epidemiologic studies and uncovering causal relationships may require me thods such as meta-a nalyses to develop exposure-response curves. For this purpose the f act that some studies included periods in which the current standard was exceeded becomes less impor tant because there are also studies at lower levels so that CR relationships can be interpol ated (as opposed to extrapolated). The emphasis should be on studies that used a multipolluta nt model approach to control for potential confounding of CO effects by other co-varying pollutants.

While there have been no new controlled human e xposures that were designed to examine effects of CO at COHb levels below 2%, there have be en numerous improvements to the exposure and COHb dosimetry models employed to provide expos ure and risk estimates. The Staff analysis

27indicates that some of the uncertainties identified in previous reviews of the standard have been reduced and that based on their overall analys is conclude that the body of evidence and the quantitative exposure and dose esti mates provide support for a standa rd at least as protective as the current standards, i.e. the data provide s upport for retaining or revi sing the current 8-hr standard. Overall the panel agrees with this conclusion, at the bare minimum. If the epidemiological evidence is given additional weight, than one might conclude that health effects are accruing at levels below the current standard and therefore the eviden ce might be leaning in the direction of revising the current standard. An issue is that some of the epidemiological studies were under conditions in which the current standard was exceeded at least in some part. More complete details of the degree to which the standard was exceeded should be summarized in the PA document, i.e. some studies covered as many as 7 years; woul d it have been excluded for as little as 1 exceedence in 7 years?

8. Staff believes that the evidence presente d in the final ISA and the exposure and risk information presented in the second draft REA supports a range of policy options for the CO standards.

The Staff have proposed a range of policy optio ns based on the quantitative risk analysis performed. As a starting point the Staff indicates that the evidence is consistent with maintaining standards that are at least as protective as the current levels. However, given the new evidence, primarily epidemiologic, that there are many indivi duals potentially at risk in addition to those with coronary artery disease (e.g. fetuses, pre gnant women, people with congestive heart disease, people with anemia of various type s) there is reason to consider reducing the standard below the current level(s).

The panel suggests example policy options such as: 8 hr – retain the 8h r averaging time with cons ideration given to levels within the range of 3 to 6 ppm, with no more than 1 exceedance or revise the form of the standard to 99 th percentile with a concentration range of 3-5. Note s ee Figure 1 which shows the linear relationship between the 99 th percentile and the design value measured for epidemiologic studies summarized in PA Table 2-1 that showed significant IHD hospitalizations. 1 hr – retain the current sta ndard to provide protection agains t infrequent acute exposures. Consider a range of concentrations fro m 5 ppm to 15 ppm, combined with a 99 th percentile or fourth-highest daily maximum. The panel does not concur with revoking the 1 hr standard..

a. To what extent does the document provide su fficient rationale to justify this range of options?

The risk models were based on coronary artery disease effects and were used to estimate the percents of i ndividuals in LA and Denver that would reach benchmark levels of COHb ranging from <1.5% COHb to <2% COHb. These were summarized in Tables 2-6 and 2-7 in the PA document. The overall guidance for the policy was not very clearly described and the wide rang e of options needs be tter definition. It might be useful to present the options in a table with the pros and cons laid out. The information is embedded in the RA and PA documents but the options and their respective advantages or disadvantages need to be more clearly summarized.

28The panel concurs with the staff that th e 1 hr standard might provide protection independent of the type of protection provided by the 8 hr standard (2-54; L 14), however the discussion supporti ng this statement should be more clearly documented.

b. Does the Panel have any recommendations regarding additional considerations which should inform characterization of these options for both the 8-hour and 1- hour standards? i. In choosing a more stable form of the standard, such as the 99 th percentile, which would allow more days on which the standard can be exceeded in a given year, the level of the standard must be reduced to insure that the degree of health protection is sufficient. ii. A summary of the options and their pros or cons would be more helpful. iii. An evaluation of how representative th e risk analysis which is based on 2 very different cities is with regard to the entire US.
i. Spatial heterogeneity of CO exposures that increase exposures near major sources i.e. near and on roadways shoul d be given some weight since these might drive a lot of the adverse health effects.

Figure 1

29

### Dr. Francine Laden

2. Consistent with the revised NAAQS proce ss which includes development of this draft Policy Assessment (PA) document, consideratio ns with regard to the primary standard for CO have been organized around a set of polic y-relevant questions for the review. a. Does the Panel find the questions posed to appropriately reflect the policy relevant questions in this review?

Yes – the questions appropriately re flect the policy relevant questions.

b. Does the Panel consider the document to prov ide the appropriate leve l of detail in addressing these policy-relevant questions?

Yes – the level of detail is appropriate.

3. The discussion of the health effects evidence (e.g., secti on 2.2.1) draws from the most recent information contained in the final IS A for CO and information from the previous review described in previous Ai r Quality Criteria Documents. a. Does the draft PA accurately reflect the curren tly available health effects evidence for CO as characterized in the final ISA and th e extent to which it differs from that available at the time of the last review?

Yes – the draft PA accurately reflects the curren tly available health eff ects evidence for CO. One minor point: On page 2-9, it is stated that “ it was concluded that there is not likely to be a causal relationship between relevant long-term CO exposures and mortality.” Is EPA confident of this conclusion, or is there not suffici ent data to address this relationship?

b. Does the Panel find the presentation to be technically sound, clearly communicated, and appropriately balanced?

Yes – the presentation is techni cally sound, clearly communicated and appropriately balanced.

30

### Dr. Arthur Penn

1. Does the Panel find the introductory and bac kground material, includ ing that pertaining to previous reviews of the CO standard, the current review and current air quality, to be clearly communicated and appropriately characterized?

Chapter 1 of the PA does a good job, in a limited # of pages, of providing intro/background for the PA. There is a brief review of the CAA and establishment of NAAQS (1 o , 2 o ); adequate margins of safety; previous revi ews; CO sources in ambient ai r; the monitoring network; low dose levels; new monitors/NCore network; recent ambient and steady-state decreases in ambient CO; and finally, the “staff’s evalua tion of policy implications of scientific evidence in the ISA and results of quantitative analyses based on that evidence”.

There is one item on p. 1-1 that could benefit fr om some clarification and possible change of location. Lines 22-25 on that page em phasize that the focus of the PA is on the 4 basic elements of NAAQS: indicator, averaging time, form and le vel. None of these items is explicitly defined in the first 46 pages of the PA. “Indicator ” & “averaging time” both on p. 2-47 are clearly defined. “Level” is not defined explicitly, but its meaning is implicit in Tables 2-6 & 2-7. “Form” (pp. 2-48 & 2-49) is never defined clea rly. “Concentration-based form”, apparently an area of focus, also is not defined. Lines 15-23 on p. 2-49 suggest that “form” = percentile. Is that correct? Is it ever anyt hing else? If it = per centile, why not say so?

If everything in the PA is based on these 4 elements, perhaps they should be defined on p.1.

5. Does the document identify and appropriately characterize the important uncertainties associated with the evidence and quantitativ e analysis of CO exposure and dose, particularly those of particula r significance in drawing conc lusions as to the adequacy of the current CO standards?

2 major uncertainties are listed on pp. 2-26 &2-27. 3 others are list ed on pp. 2-4 & 2-5; + 5 on p. 2-53.

There are a couple of other conclu sions of the PA that have ra ised questions for me. Whether they rise to the level of uncertainty de pends on how other CASAC CO panelists respond. p.2-18: The most thorough clinical studies remain those of Allr ed-Kleinman-Sheps. While the effects in these similar subject groups are clear, and together these subjects may be “the best characterized population” it is not clear that th ey represent the “most susceptible population”. Since a) these experiments have not been repeated in the past 20 years and b) no other groups have been exposed to such controlled clinical cond itions, it’s difficult to conclude that this is the “most susceptible population”. A dditionally, the epidemiologic da ta on congestive heart failure and stroke patients, while minimized in the PA write-up, suggest that those groups might be at least as susceptible to CO-related stress as the coronary hear t disease group.

31The data available in the PA and the ISA on CO/h eart failure are instructive. The statements in the PA, p 2-14, lines 16-19, that there are only “...small or no associations between hospital admissions” and stroke are not a ccurate (see next paragraph). This tone continues on p. 2-27, lines 8-10, where the document states that “...we did not include studies of associations with CHF... for which the evidence is less clear”. Unle ss I’ve misread the data, of the 5 studies listed in the footnote at the bottom of that page, 4/5 reported increased hospital admissions for CHF. A close look at Figures 5-2, 5-3 & 5-4 in the ISA supports the CO association with CHF and stroke more than for CHD. In those 3 figures the range of relative risk ( RR) values on the x-axis varies widely. In Figure 5-2 the range is from 1.0 -1.4, so small changes in RR appear to be larger than they are. On the other hand, the wider ranges of RR values for CHF (1.0-2.20) and for stroke (1.0-4.5) make larger RR va lues in those figures appear sma ller than they really are. In Figure 5-2 (CHD) 27/31 values have a RR< 1.05 a nd only 4/31 with values between 1.10 &1.18. In Figure 5-3 (stroke) at least 6 studies reported a RR of at least 1.25 and one was as high as 2.8. In Figure 5-4 (CHF), 4/10 studies had RR between 1.2-1.75. If all the st udies for stroke, CHF and CHD were placed on the same x-axis, uncer tainty could well be heightened about CHD patients being the most susceptibl e to CO effects. In addition, the mean ambient CO levels (24 hr) reported in 2 of the studies with large increases in RR were ~0.8 ppm, i.e., even lower than the 1 ppm value recommended by the CASAC CO panel at its Nov. 2009 meeting as worthy of attention.

Another possible uncertainty rega rds the question (PA-p. 2-34, lines 24-34) of whether CO is a surrogate and whether its effects at low concen trations can be untangled from those of copollutants. While there may be administrative reasons for focusing on these distinctions, the science justification is not clear. Both CO a nd organic particles in ambient air are largely products of incomplete combustion (PICs). In real-w orld (and in most labor atory) situations it is essentially impossible to genera te, and therefore to breathe, or ganic particle PICs without volatiles, including CO. So, disentan gling CO effects from those of co-pollutants (not a problem in the Allred-Kleinman-Sheps controlled clinical studies) is not only diffi cult, but likely also artificial.

32

### Dr. Beate Ritz

7. What are the views of the P anel regarding the staff’s discussi on of considerations related to the adequacy of the current and pot ential alternati ve standards?

In reviewing the recent literature EPA staff has concluded that a causal re lationship is likely to exist between relevant short term exposures to CO and cardiovascular morbidity based mainly on the coherence between the result s from controlled human chambe r studies and the more recent epidemiologic literature. However, the PA ma kes an argument that epidemiologic studies of IHD and CVD are including some areas with CO concentrations that exceeded the 8-hour standards but also cited and comme nted on 3 studies from Atlanta for which this was not the case (Tolbert 2007, Peel 2007, Metzge r 2007) and stated that 2 of the three stud ies reported nonstatistically significant results.

For the Atlanta studies, first this statement is incorrect, i.e. all 3 studi es from Atlanta reported significant results for CVDs (I checked the original papers and this is also not correct according to the ISA table on page C-25), and second the eff ect estimate sizes are all very comparable (in all three studies) and this is more important th an statistically significan ce testing. Nevertheless, since the 3 Atlanta studies do not use mutually exclusive data a nd the Tolbert study is the most comprehensive one with regard to the time fram e and # of hospitals c overed, this largest study can be considered the most informative of the three. Concerning the studi es covering areas that exceeded the current standards during the study period, it seems not comp letely justified to disregard them because of this fact when assess ing whether or not to use alternate standards, unless these studies can be shown to be less valid in principle or show some kind of threshold effect rather than a dose response and are very different in the estimated effect sizes reported. Thus, altogether Page 2- 27-28 provide an exam ple of a general tenden cy of the PA to misinterpretate and mis-represent epidemiologic stu dy results that is even more evident when it comes to interpreting results for ot her types of health outcomes.

This is very obvious on page 2-33 in the text addressing the available evidence for CO-induced effects on pre-term births, birth defects, deve lopmental outcomes; the PA states that “the epidemiologic evidence ....has somewhat expande d, although the available evidence is still considered limited with regard to effects ..” This, is a misreprese ntation of the large expansion of data on these outcomes in the epidemiologic literature in past decade. The category of limited evidence is not attributable to lit tle or conflicting epidemiologic evidence but rather to the lack or impossibility of human chamber studies and vali d animal models for many of these outcomes and a general tendency of the EPA staff to not attribute causality solely on the basis of epidemiologic evidence alone.

The EPA staff indicates that some of the uncerta inties identified in previous reviews of the standard have been reduced and th ey provide support for a standard at least as protective as the current standards, i.e. the data provide support for retaining or revi sing the current 8-hr standard. In fact if the epidemiological evidence was not down-weighted or outright ignored as much as it

33currently is in this PA, enough evidence has accrued at levels below the current standard to revise them downwards in the inte rest of public health in genera l (not just for CVD outcomes).

8. Staff believes that the ev idence presented in the final ISA and the exposure and risk information presented in the second draft REA supports a range of policy options for the CO standards.

a. To what extent does the document provide sufficient rationale to justify this range of options?

Yes, the sufficient rationale for discussi on of the range of options is provided

b. Does the Panel have any recommendations regarding additional c onsiderations which should inform characterization of these opti ons for both the 8-hour and 1-hour standards?

Spatial heterogeneity of CO exposures that incr ease exposures near major sources i.e. near and on roadways should be given so me weight since these might driv e a lot of the adverse health effects.

34

### Dr. Anne Sweeney

CQ. 7. The discussion of consider ations related to the adequacy of the current and potential alternative standards was comprehensive and clearly established the context for the ensuing discussions. However, some of the conclusi ons reached were not we ll-supported, including:

a. The Estimation of Population Exposures (Page 2-5, lines 27-34, and page 2-6, lines 1-8). The contribution of ambient air CO levels to i ndoor CO levels would be especially relevant among lower socioeconomic status populations . Given environmental justice concerns rendering lower income individuals more likely to reside in heavily trafficked areas, as well as lower income resulting in lack of air conditioning and extended periods of time with windows opened allowing influx of ambient air, and an increased probability of exposure to tobacco smoke, it seems critical to examine th e contribution of indoor CO exposures in the modeling. Inclusion of population prevalence of low income status and smoking prevalence (based on income status) in the simulated popul ations would greatly e nhance the ability to estimate CO exposures.

b. Regarding Evidence-based Considerations (2.2.1): The conclusion that the current evidence supports a primary focus on cardiovascu lar disease (CVD) is justifiably based on the research examining formation of COHb and related CVDs as the most extensively studied adverse health effect supporting an asso ciation with CO. It is stated on Page 2-18, lines 15-18 that “.. the population with pre-ex isting cardiovascular disease associated with limitation in oxygen avai lability continues to be the est characterized popula tion at risk of adverse CO-induced effects ..”. However, the best characteriz ed and most extensively studied population does not necessarily identify th e most highly susceptible population. The expansion of studies with positive findings evaluating effects on fetuses since the previous review, supported by strong toxico logical evidence for the finding of prenatal CO exposure and adverse pregnancy outcomes, warrants more attention to this subpopulation. As stated on Page 2-16, lines 12-18: “ With regard to potential eff ects of CO on birth outcomes and developmental effects, the currently availabl e evidence includes limited but suggestive epidemiologic evidence for a CO-i nduced effect on preterm birth, birth defects, decrease in birth weight, other measures of fetal growth, and infant mort ality (ISA, section 5.4.3). The available animal toxicological studies prov ide some support and coherence for these birth and developmental outcomes, although a clear understanding of the mechanisms underlying potential reproductive and developmental effect s is still lacking (ISA, section 2.5.3).” This reviewer agrees that the number of human studies in these areas is limited, however, the strength of the evidence to da te supports an association of greater concern than the current evaluation bestows.

35CQ. 8.

a. Overall, the range of options recomme nded by the staff support at minimum the continuation of the current CO standards a nd possibly a lowering of those standards to provide increased public health protection (Page 2-56, lines 23 -27). This position is wellsupported chiefly by the review of the effects of ambient CO exposure at levels at or below the current standards and the effects on CVD endpoints.

b. Again, the additive or multiplicat ive effects of ambient and i ndoor CO exposures need to be given more consideration. In assessi ng averaging time (section 2.3.2). the 8-hour averaging time was selected in part because “.. this time-frame represented a good basis for tracking continuous exposures during any 24-hou r period, recognizing that most people may be exposed in approximately 8-hour blocks of time (e.g., working or sleeping).” The comments regarding indoor CO exposures es pecially among lower income populations are relevant here as well.

36

### Dr. Stephen Thom

1. Background/introduction is clear and appropriate.

2. Chapter 2.1 - the approach taken to review primary standards for CO is well organized.

Section 2.2 discusses the adequacy of the current standard by listing key questions. The format involves reiterating much of the ra tionale listed in the REA, sometimes stating the same evidence used in conclusions multiple times ( e.g. the Allred, et al. findings – page 2- 10 lines 4 – 26; page 2-22, lines 17 – 31; page 2-23, lines 7 – 13; page 2-32, line 36 – 37; page 2-33, line 1 – 5). This seems quite redundant.

Of greater concern, there are instances where qu estions are posed but not answered. Therefore, this reviewer feels that some sections are poor ly communicated. For example, section 2-2 poses the question: “Does the curren tly available scien tific evidence and exposure/risk-based information, as reflected in the ISA and draft RE A, support or call into qu estion the adequacy of the protection afforded by the current CO standards?” I cannot find any place in the document where the question is answered. Instead section 2-2 is broken down into other questions in sections 2.2.1 and 2.2.2, some of which are answered and some are not.

3. In section 2.2.1 on page 2-8, line 9 the que stion “Does the current evidence alter our conclusions from the previous re view regarding the health effects associated with exposure to CO” is answered (page 2-16, line 23-27). On page 2-16 the question, “Does the current evidence continue to support a focus on COHb ... or does the current evidence provide support for ... alternate dose indicators ...” is answered (p age 2-17, line 29-31). On page 2-18, line 1 the question “Does the current eviden ce alter our understanding of popula tions that are particularly susceptible to CO exposures?” is answered (pag e 2-21, line 17 – 20). Of note, there is also a second question posed on line 2-19 that is redun dant with that posed on 2-18. The question on page 2-22, line 1, “Does the current evidence alter our conclusions from the previous review regarding the levels of CO in am bient air associated with health effects?” is not answered. The staff reiterates much of the uncer tainty with the current state of CO pathophysiology but never offers a conclusion. Moreover, there are parts of this section that ar e unnecessarily convoluted ( e.g. the paragraph on page 2-27, lines 14 – 22). The question posed on page 2-31, line 29, “To what extent have important uncerta inties identified in the last re view been reduced and/or have new uncertainties emerged?” is answered (page 2-35, line 12-19).

4. In section 2.2.2 the end of the first paragraph has the sentence: “These questions are intended to inform consideration of the following overarc hing question.”, but no ques tion stated. On page 2-40 two questions read, “What is the magnitude of ... COHb levels estimated to occur in areas [that] just meet the current CO standards” a nd “What proportion of the .... population experience maximum COHb levels above levels of poten tial health concern?” The answers to these questions are, for the most part, outlined in table 2-5 but there is no written summary. The question on page 2-42, “What are the key uncertain ties associated with our exposure and dose estimates ... ?” This question is clearly answered in the ensuing paragraph. The question on page 2-43,”To what extent are the estimates of at-risk population COHb levels ....important from a

37public health perspective?” is not answered. Instead, the staff state that the answer depends on public health policy (page 2-44, line 26). This is common sense and does not draw upon the scientific data outlined in the ISA.

To conclude, the section 2.2 starts with a ques tion: “Does the currently available scientific evidence and exposure/risk-based information, as reflected in the ISA and draft REA, support or call into question the adequacy of the protection afforded by the current CO standards?”. This is clearly important but it remains unanswe red in the current policy assessment.

5. Section 2.2.3 is said to offer conclusions on the adequacy of the current standard. The first two paragraphs clearly outline the ratio nal taken by the staff and why th ey give weight to the 8-hour standard (versus the 1-hour standard). The first three sentences of the third paragraph state what appear to be truisms and in the fourth sentence the “conclusion” is that the eight hour standard should be either retained or revi sed. Hence, there is no conclusion.

6. Section 2.3, considerations of alternative standards, is or ganized by posing a series of questions. The first question (page 2-46) is,” To what extent does .... information ... support consideration of alternatives to the current CO standard s ... ?” is broken down into sub-headings and more questions. Section 2.3.1 states the i ndicator for carbon monoxi de is carbon monoxide (not sure this is really necessa ry). Alternatively, you fail to me ntion the issues outlined in ISA chapter 3. Might it be appropriate to mention that CO is an O 3 precursor and there is a localized chemical interdependency of the CO-CH 4 -NO x system, although these a lternative products are not used in estimating local CO production? Secti on 2.3.2 is said to consider alternatives to the current averaging times of 1- and 8-hour exposures. A question (page 2-47) is then posed, “Do health effects ... assessments provide support fo r considering different exposure ... times?”. It seems to me the answer is stated on page 2-24, line 4 (... retain the 1- and 8- hour averaging times) but then the staff back away from this in later sections. A new question is posed on page 2-48, “What is the range of alte rnative levels and forms for th e standard ... ?” The ensuing paragraphs and sections discuss use of a 99 th percentile concentra tion-based form and the ‘exceeded only once per year’ form. Much of the discussion in the REA is recapitulated in the following pages and the ‘conclusions’, summarized in section 2.3.4, are that the standards could be either revised or retaine d. Hence, the document offers no conclusion. A minor comment on the tables 2-6 and 2-7 is uncertainty over the te rm ‘level’ in the second columns. I assume, but am unsure that ‘level’ refers to ppm of CO.

7. I think discussion of current a nd potential alternative standards is adequate. I have one last comment pertaining to the uncertain ties sections of the staff analysis. This relates to the APEX modeling. The discussion in the REA document includes information that most fixed monitors have a 1 ppm CO lower detectable limit so th e modelers added 0.5 ppm CO to all measured values to remove zeros and negati ve numbers thought to be related to monitor drift. It seems to me that this severely weakens estimates of th e at-risk population and thre shold COHb levels and thus contradicts consideration of changes from th e current standards. However, I defer to other Review Panel members with modeling expe rtise on whether my concerns are valid.

3839 8. I do not think the options listed by the staff ar e helpful. They merely state what was obvious before starting the entire review process – that is , the guidelines can be left as they are or they could be changed.

9. Section 3 pertaining to consid eration of a secondary standard for CO concludes, I think justifiably, that the science doe s not support establishing a seconda ry standard. I think the level of detail presented is adequate.A-1 

### Appendix A

Summary of 2003 NRC Repo rt RecommendationsA-2 Summary of NRC Report 1 Recommendations This report was requested to investigate the char acteristics of CO in areas of the country with meteorological and topographical characteristics that exacerbate pollution and to address potential approaches to predicting, assessing, and managing epis odes of high CO concentrations in such areas. A summarized list of the report recommendations is provided here. Vulnerability to Future Violations

 Planning for worst-case combinations of emissions and meteorology, particularly in areas of high population growth and/or high meteorological variability and investigation of how largescale and local meteorological/climatological phenomena can affect the susceptibility of a location to CO buildup in ambient air.

Health Effects:

 Emphasis of ambient CO issues through enhanced public-awareness campaigns. Further study of CO effects on the fetus, on CO effects sep arate from those of copollutants, and on the automobile exhaust mixture is encouraged. Management and Control of CO:

 Federal/state assistance to communities with special CO problems and periodic reassessment of programs implemented to reduce CO emissions . Assessment of the relationship of CO to other pollutants, such as PM 2.5 and air toxics.

 Additional emissions testing of cold-start conditions.

 Targeting of high-emitting vehicles for repair or removal from the fleet and evaluation of the effectiveness of programs to control high-emitting vehicles.

 Review of the oxygenated fuels programs and implementation of cost-effective reductions to help areas in attaining/maintaining compliance with the NAAQS.

 Inclusion of public-health education compone nts in local emissions-reduction programs and regular evaluation of their effectiveness.

CO Assessment

 Use of CO to represent distribution of other mobile-source pollutants, such as in hot spots identification, improvement of model representa tion of relationships between transportation activity and emissions, and approximation of c oncentrations of some motor-vehicle-related pollutants. 2

 Use of several tools to better characterize CO spatial distribution, in particular, to better understand the upper end of the distribution of ambient exposures.

 Support from federal/other sources to continue monitoring operations in areas where CO concentrations are well below the standard.

 Continued model development in c oncert with improved monitoring.

1 Summarized from Managing Carbon Monoxide Pollution in Meteorological and Topographical Problem Areas . National Research Council of the National Acad emies of Science. April 2003. The report should be consulted for complete recommendations in context of the NRC analysis. 2 The committee noted that CO is most useful as an indicator in microscale settings and less reliable in representing regional distributions of these pollutants.B-1 

### Appendix B

Air Quality Data from Ambient Monitors Reporting CO Measurements in Geographical Areas of Key Epidemiological Studies During Periods of StudyB-2 Air quality information provided here is dr awn from monitors reporting to the U.S. Air Quality System (AQS) 1 , and for the Atlanta study, two monito rs reporting to the SouthEastern Aerosol Research and Characterization study (SEARCH) 2 database. Available meta-data from AQS and SEARCH were used to create the monito r description tables for each monitor. Annual design values for each monitor are CO concentrations for the study area in the statistical form of the standards (i.e., second maximum, non-overl apping 8-hour average in a year and second maximum 1-hour average in a year). Annual statistics for each monitor were computed for each study period and area from availa ble 1-hour data and summarized 8-hour daily maximum data. For the 126-county Bell et al (2009) study, the highest annual statisti c reported by any monitor in the county was used.

1 http://www.epa.gov/ttn/airs/airsaqs/

2 The Southeastern Aerosol Research and Charact erization (SEARCH) network data are publically available at the SEARCH website (http://www.atmospheri c-research.com/studies/SEARCH/index.html). This information includes meterological, gaseous, and particle (filter and continuous) measurements from 1998 to the
present.Atlanta - January 1st 1993 to August 31st 200 0 (Study area and time period for Metzger et al., 2004)

Monitor Description

Site ID Street Address Latitude Longitude Time Period Tangent Road Number Traffic Count Tangent Road Name Type Road Year of Traffic Count

130891002 495 N Indian Crk Dr 33.789617 -84.235833 93-00 1 500 Unknown Local St/Hy

- 131210099 4434 Roswell Rd 33.87647278 -84.3802857 8/4/94-00 1 44000 Roswell Rd Maj St/Hy 1992 Search database Jefferson St 33.776 -84.413 8/1/98-8/31/00 - - - - -

B -3Atlanta - January 1st 1993 to August 31st 200 0 (Study area and time period for Metzger et al., 2004)

Design values for current standards

SITE 1993 1994 1995 1996 1997 1998 1999 2000 130891002 6.5 7.1 6.3 5.5 5.4 4.8 6.3 4.6 131210099 6.6 16.3 6.6 5.8 5.0 5.1 4.3 search database 5.6 7.7 4.8

Maxperyear 6.5 7.1 16.3 6.6 5.8 5.6 7.7 4.8 * (of all 8760 possible 1-hr values in each year)

SITE 1993 1994 1995 1996 1997 1998 1999 2000 130891002 4.9 5.3 4.5 3.7 4.3 4.1 4.1 3.2 131210099 4.3 5.2 3.8 3.7 3.1 3.0 2.6 Maxperyear 4.9 5.3 5.2 3.8 4.3 4.1 4.1 3.2 1-hour - 2nd maximum (ppm) per monitor, per year for 1993-2000 (current standard is 35 ppm)

8-hour - 2nd maximum non-overlapping 8-hr average (ppm) per monitor, per year for1993- 2000 (current standard is 9 ppm)

B - 4Atlanta - January 1st 1993 to August 31st 200 0 (Study area and time period for Metzger et al., 2004)

Statistics for Other Metrics

SITE 1993 1994 1995 1996 1997 1998 1999 2000 130891002 6.1 6.3 5.8 5.3 5.0 4.8 5.4 4.1 131210099 6.6 7.9 6.1 5.4 4.9 4.9 3.8 search database 5.6 7.2 4.4

Maxperyear 6.1 6.6 7.9 6.1 5.4 5.6 7.2 4.4 7.9 Total Max Minperyear 6.1 6.3 5.8 5.3 5.0 4.8 4.9 3.8 3.8 Total Min

SITE 1993 1994 1995 1996 1997 1998 1999 2000 130891002 1.7 1.6 1.6 1.5 1.3 1.5 1.2 1.1 131210099 2.8 2.6 2.1 1.9 1.8 1.7 1.6 search database 0.9 1.0 0.8

Maxperyear 1.7 2.8 2.6 2.1 1.9 1.8 1.7 1.6 2.8 Total Max Minperyear 1.7 1.6 1.6 1.5 1.3 0.9 1.0 0.8 0.8 Total Min

SITE 1993 1994 1995 1996 1997 1998 1999 2000 130891002 4.4 4.9 4.3 3.6 4.2 3.9 3.8 3.0 131210099 4.3 4.9 3.5 3.1 2.8 3.0 2.4 Maxperyear 4.4 4.9 4.9 3.6 4.2 3.9 3.8 3.0 4.9 Total Max Minperyear 4.4 4.3 4.3 3.5 3.1 2.8 3.0 2.4 2.4 Total Min

SITE 1993 1994 1995 1996 1997 1998 1999 2000 130891002 1.2 1.2 1.1 1.1 1.0 1.2 0.9 0.7 131210099 2.0 2.0 1.6 1.4 1.3 1.3 1.2 Maxperyear 1.2 2.0 2.0 1.6 1.4 1.3 1.3 1.2 2.0 Total Max Minperyear 1.2 1.2 1.1 1.1 1.0 1.2 0.9 0.7 0.7 Total Min

SITE 1993 1994 1995 1996 1997 1998 1999 2000 130891002 2.4 2.7 2.4 2.0 2.3 2.4 2.0 1.5 131210099 3.3 3.2 2.7 2.4 2.1 2.3 1.8 search database 2.0 2.6 1.5

Maxperyear 2.4 3.3 3.2 2.7 2.4 2.4 2.6 1.8 3.3 Total Max Minperyear 2.4 2.7 2.4 2.0 2.3 2.0 2.0 1.5 1.5 Total Min

SITE 1993 1994 1995 1996 1997 1998 1999 2000 130891002 0.7 0.7 0.6 0.6 0.7 0.8 0.5 0.4 131210099 1.3 1.4 1.1 0.9 0.9 0.8 0.8 search database 0.4 0.4 0.3

Maxperyear 0.7 1.3 1.4 1.1 0.9 0.9 0.8 0.8 1.4 Total Max Minperyear 0.7 0.7 0.6 0.6 0.7 0.4 0.4 0.3 0.3 Total Min 1-hour - 99th percentile daily maximum (of all 365 possible daily maximum 1-hour values)

1-hour - 50th percentile daily maximum (of all 365 possible daily maximum 1-hour values)

8-hour - 99th percentile daily maximum (of all 365 possible daily 8-hour maximum averages)

8-hour -50th percentile daily maximum (of all 365 possible daily 8-hour maximum averages)

24-hou r - 99th percentile (of all 365 possible daily 24-hour averages)

24-hour - 50th percentile (of all 365 possible daily 24-hour averages)

B - 5Atlanta-- January 1st 1993 through December 31st, 2004 (Study area and time period for Tolbert et al., 2007 )

Monitor Description

Site ID Street Address Latitude Longitude Time Period Tangent Road Numbe r Traffic Count Tangent Road Name Type Road Year of Traffic Count

130891002 495 N Indian Crk Dr 33.789617 -84.235833 93-6/30/03 1 500 Unknown Local St/Hy

- 131210099 4434 Roswell Rd 33.87647278 -84.3802857 8/4/94-04 1 44000 Roswell Rd Maj St/Hy 1992 132230003 CRAWFORD ROAD 33.92855 -85.04548 7/16/02-04 1 6 Crawford Rd Local St/Hy 1995

130890002 2390-B Wildcat Road, Decatur GA 33.68808 -84.29018 5/19/03-04 1 9250 Clifton Springs Rd/Wildcat Rd Local St/Hy 2007

Search database Jefferson St 33.776 -84.413 8/1/98-04 - - - - -

B - 6Atlanta-- January 1st 1993 through December 31st, 2004 (Study area and time period for Tolbert et al., 2007 )

Percentage of Measurements below method MDL SITE 1993 1994 1995 1996 1997 1998 1999 2000 2001 2002 2003 2004 130891002 33 38 41 46 34 21 52 64 38 45 64 131210099 16 10 20 24 19 25 26 31 37 25 42 132230003 96 0 14 130890002 3 11

Design values for current standards

SITE 1993 1994 1995 1996 1997 1998 1999 2000 2001 2002 2003 2004 130891002 6.5 7.1 6.3 5.5 5.4 4.8 6.3 4.6 5.3 4.6 2.9 131210099 6.6 16.3 6.6 5.8 5.0 5.1 4.3 4.9 3.7 3.5 4.6 132230003 0.7 0.9 0.9 130890002 3.0 3.7 search database 5.6 7.7 5.7 5.9 5.9 4.5 4.4

Maxperyear 6.5 7.1 16.3 6.6 5.8 5.6 7.7 5.7 5.9 5.9 4.5 4.6 * (of all possible 8760 1-hr values in each year)

SITE 1993 1994 1995 1996 1997 1998 1999 2000 2001 2002 2003 2004 130891002 4.9 5.3 4.5 3.7 4.3 4.1 4.1 3.2 4.1 3.6 2.0 131210099 4.3 5.2 3.8 3.7 3.1 3.0 2.6 3.0 2.3 2.5 2.5 132230003 0.6 0.8 0.5 130890002 2.6 2.6 Maxperyear 4.9 5.3 5.2 3.8 4.3 4.1 4.1 3.2 4.1 3.6 2.6 2.6

Statistics for Other Metrics

SITE 1993 1994 1995 1996 1997 1998 1999 2000 2001 2002 2003 2004 130891002 6.1 6.3 5.8 5.3 5.0 4.8 5.4 4.1 4.3 3.6 2.6 131210099 6.6 7.9 6.1 5.4 4.9 4.9 3.8 4.2 3.5 3.3 2.9 132230003 0.7 0.9 0.7 130890002 2.7 2.7 search database 5.6 7.2 5.0 5.0 4.9 3.6 3.6

Maxperyear 6.1 6.6 7.9 6.1 5.4 5.6 7.2 5.0 5.0 4.9 3.6 3.6 7.9 Total Max Minperyear 6.1 6.3 5.8 5.3 5.0 4.8 4.9 3.8 4.2 0.7 0.9 0.7 0.7 Total Min

SITE 1993 1994 1995 1996 1997 1998 1999 2000 2001 2002 2003 2004 130891002 1.7 1.6 1.6 1.5 1.3 1.5 1.2 1.1 1.3 0.9 0.8 131210099 2.8 2.6 2.1 1.9 1.8 1.7 1.6 1.4 1.2 1.2 1.0 132230003 0.3 0.4 0.3 130890002 1.0 0.9 search database 0.9 1.0 0.9 0.8 0.7 0.7 0.7

Maxperyear 1.7 2.8 2.6 2.1 1.9 1.8 1.7 1.6 1.4 1.2 1.2 1.0 2.8 Total Max Minperyear 1.7 1.6 1.6 1.5 1.3 0.9 1.0 0.9 0.8 0.3 0.4 0.3 0.3 Total Min 1-hour - 2nd maximum (ppm) per monitor, per year for 1993-2004 (current standard is 35 ppm)

8-hour - 2nd maximum non-overlapping 8-hr average (ppm) per monitor, per year for1993-2004 (current standard is 9 ppm)

1-hour - 99th percentile daily maximum (of all 365 possible daily maximum 1-hour values)

1-hour - 50th percentile daily maximum (of all 365 possible daily maximum 1-hour values)

B - 7Atlanta-- January 1st 1993 through December 31st, 2004 (Study area and time period for Tolbert et al., 2007 )

SITE 1993 1994 1995 1996 1997 1998 1999 2000 2001 2002 2003 2004 130891002 4.4 4.9 4.3 3.6 4.2 3.9 3.8 3.0 2.8 2.5 2.0 131210099 4.3 4.9 3.5 3.1 2.8 3.0 2.4 2.3 2.2 2.1 2.0 132230003 0.6 0.7 0.5 130890002 2.5 2.4 Maxperyear 4.4 4.9 4.9 3.6 4.2 3.9 3.8 3.0 2.8 2.5 2.5 2.4 4.9 Total Max Minperyear 4.4 4.3 4.3 3.5 3.1 2.8 3.0 2.4 2.3 0.6 0.7 0.5 0.5 Total Min

SITE 1993 1994 1995 1996 1997 1998 1999 2000 2001 2002 2003 2004 130891002 1.2 1.2 1.1 1.1 1.0 1.2 0.9 0.7 0.9 0.8 0.6 131210099 2.0 2.0 1.6 1.4 1.3 1.3 1.2 1.0 0.9 1.0 0.8 132230003 0.3 0.4 0.3 130890002 0.8 0.7 Maxperyear 1.2 2.0 2.0 1.6 1.4 1.3 1.3 1.2 1.0 0.9 1.0 0.8 2.0 Total Max Minperyear 1.2 1.2 1.1 1.1 1.0 1.2 0.9 0.7 0.9 0.3 0.4 0.3 0.3 Total Min

24-hour - 99th percentile (of all 365 possible daily 24-hour averages) SITE 1993 1994 1995 1996 1997 1998 1999 2000 2001 2002 2003 2004 130891002 2.4 2.7 2.4 2.0 2.3 2.4 2.0 1.5 1.9 1.5 1.2 131210099 3.3 3.2 2.7 2.4 2.1 2.3 1.8 1.8 1.6 1.7 1.5 132230003 0.4 0.7 0.5 130890002 1.6 1.5 search database 2.0 2.6 2.3 1.8 1.6 1.5 1.4

Maxperyear 2.4 3.3 3.2 2.7 2.4 2.4 2.6 2.3 1.9 1.6 1.7 1.5 3.3 Total Max Minperyear 2.4 2.7 2.4 2.0 2.3 2.0 2.0 1.5 1.8 0.4 0.7 0.5 0.4 Total Min

24-hour - 50th percentile (of all 365 possible daily 24-hour averages) SITE 1993 1994 1995 1996 1997 1998 1999 2000 2001 2002 2003 2004 130891002 0.7 0.7 0.6 0.6 0.7 0.8 0.5 0.4 0.6 0.5 0.4 131210099 1.3 1.4 1.1 0.9 0.9 0.8 0.8 0.7 0.6 0.7 0.5 132230003 0.3 0.3 0.3 130890002 0.6 0.5 search database 0.4 0.4 0.4 0.3 0.4 0.3 0.3

Maxperyear 0.7 1.3 1.4 1.1 0.9 0.9 0.8 0.8 0.7 0.6 0.7 0.5 1.4 Total Max Minperyear 0.7 0.7 0.6 0.6 0.7 0.4 0.4 0.4 0.3 0.3 0.3 0.3 0.3 Total Min 8-hour - 99th percentile daily maximum (of all 365 possible daily 8-hour maximum averages)

8-hour -50th percentile daily maximum (of all 365 possible daily 8-hour maximum averages)

B - 8Denver-- January 1st 1993 through December 31st, 1997 (Study area and time period for Koken et al., 2003 )

Monitor Description

Site ID Street Address Latitude Longitude Time Period Tangent Road Number Traffic Count Tangent Road Name Type Road Year of Traffic Count

080310020 935 Colorado Blvd 39.731389 -104.940833 11/01/94-3/31/95 1 50000 Colorado Blvd Maj St/Hy 1992 080310013 14th Ave and Albion St 39.738578 -104.939925 93-97 1 57000 Colorado Blvd Maj St/Hy

- 080310018 1300 Blaje St - Blake side 39.748168 -105.002604 11/18/93-3/16/94 1 500 Blake St Maj St/Hy 1992 080310014 2325 Irving St 39.751761 -105.030681 93-97 1 5000 Unknown Thru St/Hy

- 080310019 1300 Blake St 39.748163 -105.002564 11/18/93-97 1 500 Speer Pkwy Maj St/Hy 1993 080310002 2105 Broadway 39.751184 -104.987625 93-97 1 17200 Broadway Maj St/Hy 1995

B - 9Denver-- January 1st 1993 through December 31st, 1997 (Study area and time period for Koken et al., 2003 )

Percentage of Measurements below method MDL SITE 1993 1994 1995 1996 1997 080310020 6 8 080310013 30 22 12 18 19 080310018 7 5 080310014 43 33 22 29 31 080310019 5 8 8 7 10 080310002 16 11 6 8 9

Design values for current standards

SITE 1993 1994 1995 1996 1997 080310020 11.7 10.3 080310013 14.9 12.2 13.6 9.4 10.6 080310018 15.3 11.6 080310014 12.1 10.9 9.9 8.2 8.4 080310019 16.1 13.4 14.0 12.5 11.2 080310002 18.2 17.1 16.4 16.7 10.0 Maxperyear 18.2 17.1 16.4 16.7 11.2

SITE 1993 1994 1995 1996 1997 080310020 6.8 6.0 080310013 7.8 7.6 6.2 5.2 4.7 080310018 7.7 6.5 080310014 8.2 7.3 5.9 5.7 6.2 080310019 7.7 8.2 7.1 7.0 6.4 080310002 10.4 8.2 9.5 7.3 5.5 Maxperyear 10.4 8.2 9.5 7.3 6.4

Statistics for Other Metrics

SITE 1993 1994 1995 1996 1997 080310020 12.8 11.9 080310013 12.8 11.3 10.1 9.0 7.9 080310018 16.2 12.2 080310014 9.8 9.6 8.1 7.3 7.7 080310019 16.2 13.4 14.0 9.9 9.3 080310002 13.5 13.8 13.1 12.8 8.8 Maxperyear 16.2 13.8 14.0 12.8 9.3 16.2 Total Max Minperyear 9.8 9.6 8.1 7.3 7.7 7.3 Total Min

SITE 1993 1994 1995 1996 1997 080310020 4.9 3.9 080310013 2.7 2.9 2.8 2.5 2.4 080310018 6.3 5.3 080310014 2.2 2.5 2.3 2.2 2.0 080310019 7.5 5.6 4.3 3.6 3.0 080310002 3.2 3.1 2.9 2.7 2.6 Maxperyear 7.5 5.6 4.3 3.6 3.0 7.5 Total Max Minperyear 2.2 2.5 2.3 2.2 2.0 2.0 Total Min 1-hour - 2nd maximum (ppm) per monitor, per year for 1993- 2004 (current standard is 35

8-hour - 2nd maximum nonoverlapping 8-hr average (ppm) per monitor, per year for1993-

1-hour - 99th percentile daily maximum (of all 365 possible daily maximum 1-hour values)

1-hour - 50th percentile daily maximum (of all 365 possible daily maximum 1-hour values)

B - 10Denver-- January 1st 1993 through December 31st, 1997 (Study area and time period for Koken et al., 2003 )

SITE 1993 1994 1995 1996 1997 080310020 7.6 7.4 080310013 6.5 6.7 5.3 5.1 4.7 080310018 10.4 7.8 080310014 6.9 6.2 5.7 5.4 5.6 080310019 10.4 8.6 7.1 7.0 5.8 080310002 8.7 8.2 7.3 7.2 5.1 Maxperyear 10.4 8.6 7.4 7.2 5.8 10.4 Total Max Minperyear 6.5 6.2 5.3 5.1 4.7 4.7 Total Min

SITE 1993 1994 1995 1996 1997 080310020 3.4 2.5 080310013 1.7 1.8 1.9 1.7 1.6 080310018 4.9 3.3 080310014 1.2 1.5 1.5 1.4 1.3 080310019 5.1 3.8 3.0 2.2 2.0 080310002 2.0 1.9 2.0 1.8 1.7 Maxperyear 5.1 3.8 3.0 2.2 2.0 5.1 Total Max Minperyear 1.2 1.5 1.5 1.4 1.3 1.2 Total Min

SITE 1993 1994 1995 1996 1997 080310020 4.9 5.0 080310013 3.6 3.2 3.0 3.0 2.8 080310018 6.0 4.7 080310014 4.0 4.0 3.1 2.9 3.2 080310019 5.5 5.2 4.5 3.6 3.8 080310002 4.8 4.4 3.9 3.6 3.9 Maxperyear 6.0 5.2 5.0 3.6 3.9 6.0 Total Max Minperyear 3.6 3.2 3.0 2.9 2.8 2.8 Total Min

SITE 1993 1994 1995 1996 1997 080310020 2.1 1.6 080310013 0.9 1.1 1.1 1.0 1.0 080310018 2.6 2.0 080310014 0.7 0.8 0.9 0.8 0.8 080310019 2.7 2.1 1.7 1.4 1.3 080310002 1.3 1.3 1.4 1.2 1.2 Maxperyea r 2.7 2.1 1.7 1.4 1.3 2.7 Total Max Minperyear 0.7 0.8 0.9 0.8 0.8 0.7 Total Min 8-hour - 99th percentile daily maximum (of all 365 possible daily 8-hour maximum averages)

8-hour -50th percentile daily maximum (of all 365 possible daily 8-hour maximum averages)

24-hour - 99th percentile ( o f all 365 possible daily 24-hour averages)

24-hour -50th percentile (of all 365 possible daily 24-hour averages)

B - 11Pennsylvania-- January 1st 1987 through November 30th, 1999 (Study area and time period for Wellenius et al., 2005 )

Monitor Description

Site ID Street Address Latitude Longitude Time Period Tangent Road Number Traffic Count Tangent Road Name Type Road Year of Traffic Count

420030003 Harper Rd Evergreen Park Monroeville 40.45 -79.771111 3/16/87-4/30/93 - - - - - 420030010 Carnegie Scienct Center - 1 Allecheney Rd 40.4455765 -80.0161549 11/25/97-99 1 1000 Allegheny Rd Maj St/Hy 1997 420030026 Oakland 4 416 Semple St 40.436667 -79.954722 87-10/26/97 1 2000 Unknown Maj St/Hy

- 420030038 Forbes Ave and Grant St Pgh. PA 15219 40.438889 -79.997222 87-99 1 15000 Unknown Maj St/Hy

- 420030052 Gateway Center Subway Entrance on Roof 40.441389 -80.003333 3/16/87-99 - - - - -

B - 12Allegheny County, PA-- January 1st 1987 through November 30th, 199 9 (Study area and time period for Wellenius et al., 2005 )

Percentage of Measurements below method MDL SITE 1987 1988 1989 1990 1991 1992 1993 1994 1995 1996 1997 1998 1999 420030003 9 43 32 42 45 55 61 420030010 55 54 68 420030026 4 8 4 18 18 16 28 25 38 48 58 420030038 3 7 11 11 9 13 4 9 8 12 17 8 17 420030052 0 7 10 9 4 6 12 31 25 23 22 25 39

Design values for current standards

SITE 1987 1988 1989 1990 1991 1992 1993 1994 1995 1996 1997 1998 1999 420030003 4.5 6.7 5.1 5.3 3.6 5.4 3.3 420030010 4.2 3.5 3.3 420030026 18.0 12.6 9.0 11.0 6.3 9.0 6.1 7.3 6.2 7.0 4.6 420030038 19.4 10.7 11.2 10.5 10.2 8.9 7.6 10.2 8.3 6.8 5.4 7.0 6.0 420030052 15.9 8.3 9.4 9.2 7.9 9.0 6.4 8.2 5.3 5.7 4.2 3.8 4.3 Maxperyear 19.4 12.6 11.2 11.0 10.2 9.0 7.6 10.2 8.3 7.0 5.4 7.0 6.0

SITE 1987 1988 1989 1990 1991 1992 1993 1994 1995 1996 1997 1998 1999 420030003 3.1 2.8 2.8 2.9 2.2 2.6 1.3 420030010 3.2 2.7 2.5 420030026 7.9 7.5 6.1 6.9 4.3 6.3 4.7 4.2 4.2 3.5 2.4 420030038 8.8 6.6 7.8 8.1 5.3 6.9 5.4 7.0 5.9 4.3 3.8 3.8 3.9 420030052 7.9 6.1 6.6 6.0 6.0 5.6 4.7 4.5 3.7 3.9 2.9 3.1 2.6 Maxperyear 8.8 7.5 7.8 8.1 6.0 6.9 5.4 7.0 5.9 4.3 3.8 3.8 3.9

Statistics for Other Metrics

SITE 1987 1988 1989 1990 1991 1992 1993 1994 1995 1996 1997 1998 1999 420030003 4.5 5.3 4.4 4.0 3.4 4.3 3.3 420030010 5.0 3.0 2.9 420030026 10.9 11.1 11.2 8.4 8.0 5.5 6.5 6.0 6.0 5.7 5.9 3.7 420030038 12.7 9.5 10.4 9.9 8.0 8.3 7.5 8.4 7.2 5.8 5.0 4.3 5.6 420030052 15.9 8.0 8.7 7.6 6.5 6.0 5.6 5.5 5.1 4.8 3.7 3.4 3.9 Maxperyear 15.9 11.1 11.2 9.9 8.0 8.3 7.5 8.4 7.2 5.8 5.9 4.3 5.6 15.9 Total Max Minperyear 4.5 5.3 4.4 4.0 3.4 4.3 3.3 5.5 5.1 4.8 3.7 3.0 2.9 2.9 Total Min

SITE 1987 1988 1989 1990 1991 1992 1993 1994 1995 1996 1997 1998 1999 420030003 1.6 1.2 1.1 1.2 1.0 0.8 0.7 420030010 1.0 1.0 0.9 420030026 2.0 2.0 2.0 1.9 1.5 1.5 1.2 1.4 1.2 1.0 0.9 420030038 4.2 3.1 3.0 2.8 2.7 2.6 2.7 2.4 2.3 2.1 1.8 1.9 1.7 420030052 3.1 2.5 2.5 2.4 1.9 1.8 1.7 1.8 1.4 1.4 1.3 1.2 1.1 Maxperyear 4.2 3.1 3.0 2.8 2.7 2.6 2.7 2.4 2.3 2.1 1.8 1.9 1.7 4.2 Total Max Minperyear 1.6 1.2 1.1 1.2 1.0 0.8 0.7 1.4 1.2 1.0 0.9 1.0 0.9 0.7 Total Min 1-hour - 2nd maximum (ppm) per monitor, per year for 1993-2004 (current standard is 35 ppm)

8-hour - 2nd maximum non-overlapping 8-hr average (ppm) per monitor, per year for1993-2004 (current standard is 9 ppm)

1-hour - 99th percentile daily maximum (of all 365 possible daily maximum 1- hour values)

1-hour - 50th percentile daily maximum (of all 365 possible daily maximum 1- hour values)

B - 13Allegheny County, PA-- January 1st 1987 through November 30th, 199 9 (Study area and time period for Wellenius et al., 2005 )

SITE 1987 1988 1989 1990 1991 1992 1993 1994 1995 1996 1997 1998 1999 420030003 3.1 2.6 2.4 2.6 2.0 2.0 1.3 420030010 3.5 2.6 2.2 420030026 7.1 6.0 5.8 6.1 3.9 4.4 4.3 4.2 3.9 3.4 2.3 420030038 8.0 6.1 7.0 5.7 5.2 6.9 5.2 6.9 5.4 4.2 3.7 3.3 3.5 420030052 7.9 5.1 5.6 5.5 4.4 5.5 4.3 4.2 3.7 3.8 2.7 3.0 2.6 Maxperyear 8.0 6.1 7.0 6.1 5.2 6.9 5.2 6.9 5.4 4.2 3.7 3.3 3.5 8.0 Total Max Minperyear 3.1 2.6 2.4 2.6 2.0 2.0 1.3 4.2 3.7 3.4 2.3 2.6 2.2 1.3 Total Min

SITE 1987 1988 1989 1990 1991 1992 1993 1994 1995 1996 1997 1998 1999 420030003 1.3 0.8 0.9 0.8 0.8 0.6 0.5 420030010 0.8 0.8 0.6 420030026 1.5 1.5 1.5 1.4 1.2 1.2 1.0 1.0 0.9 0.8 0.7 420030038 3.1 2.3 2.2 2.1 2.1 1.9 2.0 1.9 1.7 1.7 1.3 1.5 1.3 420030052 2.3 1.8 1.8 1.8 1.5 1.4 1.3 1.2 1.1 1.0 1.0 1.0 0.8 Maxperyear 3.1 2.3 2.2 2.1 2.1 1.9 2.0 1.9 1.7 1.7 1.3 1.5 1.3 3.1 Total Max Minperyear 1.3 0.8 0.9 0.8 0.8 0.6 0.5 1.0 0.9 0.8 0.7 0.8 0.6 0.5 Total Min

24-hour - 99th percentile (of all 365 possible daily 24-hour averages) SITE 1987 1988 1989 1990 1991 1992 1993 1994 1995 1996 1997 1998 1999 420030003 1.9 1.7 1.7 1.9 1.3 1.4 0.9 420030010 2.8 1.5 1.5 420030026 4.1 4.2 3.6 3.3 2.4 2.5 2.6 2.6 2.4 2.0 1.3 420030038 5.5 3.3 4.9 4.2 3.7 4.0 4.0 4.0 3.4 2.8 2.5 2.5 2.3 420030052 5.6 3.0 4.3 3.7 3.4 2.9 3.4 3.3 2.5 2.5 1.9 2.1 1.9 Maxperyear 5.6 4.2 4.9 4.2 3.7 4.0 4.0 4.0 3.4 2.8 2.5 2.5 2.3 5.6 Total Max Minperyear 1.9 1.7 1.7 1.9 1.3 1.4 0.9 2.6 2.4 2.0 1.3 1.5 1.5 0.9 Total Min

SITE 1987 1988 1989 1990 1991 1992 1993 1994 1995 1996 1997 1998 1999 420030003 0.9 0.6 0.6 0.6 0.5 0.4 0.4 420030010 0.4 0.5 0.4 420030026 1.1 1.1 1.1 1.0 0.9 0.8 0.7 0.7 0.6 0.5 0.4 420030038 2.1 1.5 1.4 1.4 1.4 1.2 1.4 1.3 1.2 1.1 0.9 1.1 0.9 420030052 1.7 1.3 1.3 1.3 1.1 1.0 0.9 0.8 0.7 0.8 0.7 0.7 0.6 Maxperyear 2.1 1.5 1.4 1.4 1.4 1.2 1.4 1.3 1.2 1.1 0.9 1.1 0.9 2.1 Total Max Minperyear 0.9 0.6 0.6 0.6 0.5 0.4 0.4 0.7 0.6 0.5 0.4 0.5 0.4 0.4 Total Min 24-hour -50th percentile (of all 365 possible daily 8-hour - 99th percentile daily maximum (of all 365 possible daily 8-hour maximum averages)

8-hour -50th percentile daily maximum (of all 365 possible daily 8-hour maximum averages)

B - 14Baltimore-- April 1st 2002 through December 31st, 2002 (Study area and time period for Symons et al., 2006 )

Monitor Description

Site ID Street Address Latitude Longitude Time Period Tangent Road Number Traffic Count Tangent Road Name Type Road Year of Traffic Count

240053001 600 Dorsey Avenue 39.310833 -76.474444 2002 1 500 Woodward Local St/Hy 1993 245100040 Oldtown Fire Station, 1100 Hillen Street 39.298056 -76.604722 2002 1 15300 Hillen St Thru St/Hy 1990

B - 15Baltimore-- April 1st 2002 through December 31st, 2002 (Study area and time period for Symons et al., 2006 )

Percentage of Measurements below method MDL Baltimore 2002 240053001 61 county 245100040 43 city

Design values for current standards

Baltimore 2002 240053001 9.2 county 245100040 4.4 city

Baltimore 2002 240053001 2.6 county 245100040 3 city

Statistics for Other Metrics

Baltimore 2002 240053001 4.7 county 245100040 3.9 city

Baltimore 2002 240053001 0.9 county 245100040 0.9 city

Baltimore 2002 240053001 2.4 county 245100040 2.8 city

Baltimore 2002 240053001 0.60 county 245100040 0.70 city

Baltimore 2002 240053001 1.46 county 245100040 1.86 city

Baltimore 2002 240053001 0.4 county 245100040 0.5 city 24-hou r -50th percentile (of all 365 possible daily 24-hour averages) 1-hour - 2nd maximum (ppm) per monitor, per year for 1993-2004 (current standard is 35 ppm)

8-hour - 2nd maximum non-overlapping 8-hr average (ppm) per monitor, per year for1993-2004 (current standard is 9 ppm)

1-hour - 99th percentile daily maximum (of all 365 possible daily maximum 1-hour values)

1-hou r - 50th percentile daily maximum (of all 365 possible daily maximum 1-hour values)

8-hour - 99th percentile daily maximum (of all 365 possible daily 8

- hour maximum averages)

8-hou r -50th percentile daily maximum (of all 365 possible daily 8- hour maximum averages)

24-hou r - 99th percentile (of all 365 possible daily 24-hour averages)

B - 16California-- January 1st 1992 through December 31st, 199 5 (Study area and time period for Linn et al., 2000 )

Design values for current standard s

California 1992 1993 1994 1995 Los Angele s 060370002 6.0 6.0 6.4 7.3 060370113 8.0 8.0 7.9 7.4 060371002 13.0 11.0 12.1 12.5 060371103 11.0 9.0 10.7 9.2 060371201 12.0 10.0 12.8 11.8 060371301 25.0 20.0 20.8 16.5 060371601 11.0 8.0 9.9 9.3 060371701 12.0 8.0 9.8 7.7 060372005 11.0 10.0 12.3 11.4 060374002 10.0 9.0 11.5 8.1 060375001 18.0 14.0 13.9 11.1 060376002 8.0 7.0 7.5 6.5 060379002 9.0 8.0 9.0 6.8 Orange 060590001 15.0 15.0 12.0 9.8 060591003 11.0 9.0 9.5 7.5 060592001 9.0 7.0 7.8 6.0 060595001 18.0 14.0 16.1 11.5 Riverside 060650006 5.0 2.0 060651003 10.0 9.0 11.0 9.0 060655001 4.0 4.0 3.5 3.1 060658001 6.0 8.0 7.6 6.7 San Bernadino 060710001 6.0 4.0 3.5 3.1 060710006 2.0 2.0 060710012 3.0 2.0 1.8 1.7 060710014 4.0 3.7 3.1 060710017 5.5 3.3 060714001 5.0 4.0 3.4 3.0 060719004 7.0 7.0 7.5 7.4 Maxperyea r 25.0 20.0 20.8 16.5 1-hou r - 2nd maximum (ppm) per monitor, per year for 1992

- 1995 (current standard is 35 ppm)

B - 17California-- January 1st 1992 through December 31st, 199 5 (Study area and time period for Linn et al., 2000 )

California 1992 1993 1994 1995 Los Angele s 060370002 4.3 4.0 4.4 6.2 060370113 5.7 4.6 5.8 5.6 060371002 9.8 8.1 10.2 11.0 060371103 8.0 6.7 8.4 7.9 060371201 8.1 8.0 9.9 9.4 060371301 16.4 13.8 16.0 11.6 060371601 7.7 6.3 8.4 7.6 060371701 6.9 5.1 6.3 6.0 060372005 7.1 6.3 7.7 8.6 060374002 7.3 6.9 7.6 6.2 060375001 11.3 9.6 11.3 8.7 060376002 3.7 3.8 3.8 3.8 060379002 5.3 5.3 5.1 4.5 Orange 060590001 8.6 6.6 8.1 7.3 060591003 8.3 6.7 7.8 5.3 060592001 5.0 3.9 5.4 3.9 060595001 8.0 6.0 8.0 6.4 Riverside 060650006 3.6 1.8 060651003 6.0 5.8 6.0 5.8 060655001 2.0 1.8 1.7 1.5 060658001 4.6 5.3 5.6 5.2 San Bernadino 060710001 3.3 2.6 2.1 2.1 060710006 2.0 1.9 060710012 1.3 1.3 1.4 1.3 060710014 2.6 2.0 2.4 060710017 2.6 1.8 060714001 3.1 3.0 2.1 2.0 060719004 5.1 5.0 5.5 5.9 Maxperyea r 16.4 13.8 16.0 11.6 8-hour - 2nd maximum non-overlapping 8-hr average (ppm) per monitor, per year for1992-1995 (current standard is 9 ppm)

B - 18California-- January 1st 1992 through December 31st, 199 5 (Study area and time period for Linn et al., 2000 )

Statistics for Other Metric s

California 1992 1993 1994 1995 Los Angele s 060370002 6.0 6.0 5.5 6.9 060370113 7.0 7.0 7.6 6.5 060371002 12.0 10.0 11.4 11.6 060371103 10.0 8.0 10.0 9.0 060371201 12.0 10.0 11.0 10.4 060371301 21.0 19.0 18.0 16.1 060371601 10.0 8.0 9.8 9.2 060371701 10.0 8.0 8.8 7.3 060372005 10.0 9.0 10.9 10.1 060374002 9.0 9.0 9.0 7.4 060375001 15.0 13.0 12.8 11.0 060376002 7.0 7.0 6.9 6.3 060379002 8.0 7.0 7.6 6.1 Orange 060590001 12.0 9.0 11.0 9.0 060591003 10.0 8.0 9.1 7.3 060592001 7.0 7.0 7.1 5.4 060595001 16.0 13.0 14.5 10.7 Riverside 060650006 5.0 2.0 060651003 10.0 9.0 10.0 8.7 060655001 4.0 3.0 2.9 2.9 060658001 6.0 7.0 6.5 6.3 San Bernadino 060710001 5.0 3.0 3.5 2.9 060710006 2.0 2.1 060710012 2.0 2.0 1.7 1.5 060710014 4.0 3.7 3.1 060710017 2.8 3.3 060714001 4.0 3.0 2.9 2.9 060719004 7.0 6.0 6.6 7.1 Maxperyea r 21.0 19.0 18.0 16.1 21.0 Total Ma x Minperyea r 2.0 2.0 1.7 1.5 1.5 Total Mi n 1-hou r - 99th percentile daily maximum (of all 365 possible daily maximum 1-hour values)

B - 19California-- January 1st 1992 through December 31st, 199 5 (Study area and time period for Linn et al., 2000 )

California 1992 1993 1994 1995 Los Angele s 060370002 2.0 2.0 2.1 1.9 060370113 3.0 2.0 2.5 2.0 060371002 3.0 3.0 3.3 3.2 060371103 4.0 3.0 3.8 3.1 060371201 3.0 3.0 3.1 1.9 060371301 4.0 4.0 4.4 3.8 060371601 3.0 3.0 3.1 2.7 060371701 3.0 3.0 3.4 2.8 060372005 3.0 3.0 2.8 2.7 060374002 2.0 2.0 2.3 1.7 060375001 3.0 3.0 3.2 2.6 060376002 2.0 2.0 2.6 2.1 060379002 2.0 2.0 2.0 1.7 Orange 060590001 2.0 2.0 2.3 2.0 060591003 2.0 1.0 1.6 1.1 060592001 2.0 2.0 1.6 1.4 060595001 3.0 3.0 2.9 2.4 Riverside 060650006 1.0 1.0 060651003 3.0 3.0 4.0 3.0 060655001 1.0 1.0 0.9 0.9 060658001 2.0 2.0 2.7 2.3 San Bernadino 060710001 1.0 1.0 0.7 0.9 060710006 1.0 0.9 060710012 1.0 1.0 0.7 0.5 060710014 1.0 1.2 0.9 060710017 0.9 1.3 060714001 2.0 2.0 1.4 1.2 060719004 2.0 2.0 2.0 2.0 Maxperyea r 4.0 4.0 4.4 3.8 4.4 Total Ma x Minperyea r 1.0 1.0 0.7 0.5 0.5 Total Mi n 1-hou r - 50th percentile daily maximum (of all 365 possible daily maximum 1-hour values)

B - 20California-- January 1st 1992 through December 31st, 199 5 (Study area and time period for Linn et al., 2000 )

California 1992 1993 1994 1995 Los Angele s 060370002 4.0 3.9 4.1 5.3 060370113 5.3 4.6 5.3 4.7 060371002 9.4 7.5 9.9 9.5 060371103 7.9 6.3 8.0 7.6 060371201 7.8 7.6 9.5 8.8 060371301 14.4 13.0 14.2 11.2 060371601 7.4 6.0 8.0 7.0 060371701 6.4 5.0 6.3 5.5 060372005 7.0 5.9 7.5 8.4 060374002 6.9 6.7 6.8 5.8 060375001 10.9 9.1 9.8 8.5 060376002 3.3 3.6 3.7 3.8 060379002 5.0 5.1 5.0 4.5 Orange 060590001 8.3 6.0 7.7 6.5 060591003 8.1 6.4 6.7 4.8 060592001 4.3 3.9 4.8 3.8 060595001 7.3 6.0 7.5 6.3 Riverside 060650006 3.5 1.8 060651003 5.8 5.4 5.9 5.6 060655001 2.0 1.5 1.6 1.4 060658001 4.5 4.9 5.4 4.9 San Bernadino 060710001 3.0 2.6 2.1 2.0 060710006 2.0 1.9 060710012 1.1 1.3 1.4 1.3 060710014 2.3 1.9 2.4 060710017 2.3 2.0 060714001 3.1 2.3 2.0 1.9 060719004 4.5 4.9 5.2 5.7 Maxperyea r 14.4 13.0 14.2 11.2 14.4 Total Ma x Minperyea r 1.1 1.3 1.4 1.3 1.1 Total Mi n 8-hour - 99th percentile daily maximum (of all 365 possible daily 8-hour maximum averages)

B - 21California-- January 1st 1992 through December 31st, 199 5 (Study area and time period for Linn et al., 2000 )

California 1992 1993 1994 1995 Los Angele s 060370002 1.6 1.4 1.6 1.5 060370113 1.6 1.7 1.7 1.2 060371002 2.6 2.4 2.6 2.7 060371103 2.9 2.4 2.8 2.4 060371201 2.0 2.0 2.3 1.2 060371301 2.9 2.7 3.0 2.8 060371601 2.1 2.0 2.2 2.0 060371701 2.6 2.4 2.5 1.9 060372005 2.1 2.0 2.2 2.2 060374002 1.7 1.7 1.8 1.3 060375001 2.0 1.8 1.8 1.6 060376002 1.6 1.5 1.8 1.4 060379002 1.4 1.3 1.2 1.1 Orange 060590001 1.7 1.6 1.6 1.5 060591003 1.2 1.0 0.9 0.7 060592001 1.5 1.3 1.1 1.0 060595001 2.0 1.9 2.0 1.7 Riverside 060650006 1.0 1.0 060651003 2.6 2.4 2.6 2.3 060655001 1.0 1.0 0.7 0.7 060658001 1.6 1.4 1.8 1.6 San Bernadino 060710001 1.0 1.0 0.5 0.7 060710006 0.9 0.7 060710012 1.0 0.9 0.6 0.4 060710014 1.0 0.8 0.6 060710017 0.7 1.0 060714001 1.9 1.4 1.0 0.9 060719004 1.4 1.5 1.6 1.5 Maxperyea r 2.9 2.7 3.0 2.8 3.0 Total Ma x Minperyea r 1.0 0.9 0.5 0.4 0.4 Total Mi n 8-hou r -50th percentile daily maximum (of all 365 possible daily 8-hour maximum averages)

B - 22California-- January 1st 1992 through December 31st, 199 5 (Study area and time period for Linn et al., 2000 )

California 1992 1993 1994 1995 Los Angele s 060370002 3.0 3.0 2.9 4.1 060370113 3.1 2.9 3.3 3.3 060371002 5.9 4.9 6.6 6.8 060371103 5.0 4.3 5.4 5.4 060371201 4.6 5.0 5.5 5.7 060371301 9.6 8.0 8.9 7.6 060371601 4.6 4.0 5.3 5.2 060371701 4.2 3.5 4.2 4.2 060372005 3.9 3.5 4.7 4.9 060374002 4.8 4.1 4.7 3.7 060375001 5.9 5.2 5.8 4.9 060376002 2.3 2.3 2.5 2.7 060379002 3.1 2.7 2.6 2.4 Orange 060590001 4.4 3.7 4.8 4.7 060591003 4.8 3.4 4.0 3.4 060592001 3.0 2.7 3.5 2.4 060595001 5.0 3.8 5.4 4.5 Riverside 060650006 2.6 1.2 060651003 4.0 4.0 4.1 4.2 060655001 1.4 1.2 1.0 1.0 060658001 2.7 2.9 3.6 3.5 San Bernadino 060710001 2.1 1.9 1.2 1.2 060710006 1.7 1.8 060710012 1.0 1.1 1.1 1.0 060710014 1.7 1.5 2.1 060710017 1.8 1.5 060714001 2.8 2.0 1.5 1.4 060719004 2.8 3.0 3.3 3.8 Maxperyea r 9.6 8.0 8.9 7.6 9.6 Total Ma x Minperyea r 1.0 1.1 1.0 1.0 1.0 Total Mi n 24-hou r - 99th percentile (of all 365 possible daily 24-hour averages)

B - 23California-- January 1st 1992 through December 31st, 199 5 (Study area and time period for Linn et al., 2000 )

California 1992 1993 1994 1995 Los Angele s 060370002 1.2 1.0 1.2 1.1 060370113 1.0 1.0 0.9 0.7 060371002 1.7 1.7 1.8 1.9 060371103 1.7 1.6 1.9 1.6 060371201 1.4 1.3 1.5 0.8 060371301 1.9 1.9 2.2 2.0 060371601 1.5 1.3 1.5 1.5 060371701 1.7 1.7 1.8 1.2 060372005 1.5 1.5 1.5 1.6 060374002 1.2 1.2 1.2 0.9 060375001 1.1 0.9 0.9 1.0 060376002 1.1 1.0 1.2 1.0 060379002 1.0 0.9 0.8 0.7 Orange 060590001 1.2 1.1 1.1 1.1 060591003 0.8 0.7 0.5 0.4 060592001 1.1 1.0 0.7 0.6 060595001 1.3 1.3 1.3 1.2 Riverside 060650006 0.9 0.6 060651003 1.8 1.7 1.9 1.6 060655001 0.6 0.6 0.4 0.4 060658001 1.0 0.9 1.1 0.9 San Bernadino 060710001 1.0 0.6 0.3 0.4 060710006 0.5 0.6 060710012 0.5 0.5 0.3 0.3 060710014 0.8 0.5 0.4 060710017 0.5 0.7 060714001 1.3 1.1 0.7 0.6 060719004 1.0 1.1 1.2 1.2 Maxperyea r 1.9 1.9 2.2 2.0 2.2 Total Ma x Minperyea r 0.5 0.5 0.3 0.3 0.3 Total Mi n 24-hour -50th percentile (of all 365 possible daily 24-hour averages)

B - 24California-- January 1st 1988 through December 31st, 1995 (Study area and time period for Mann et al., 2002 )

Design values for current standards

California 1988 1989 1990 1991 1992 1993 1994 1995 Los Angeles 060370002 8.0 7.0 7.0 7.0 6.0 6.0 6.4 7.3 060370113 12.0 12.0 11.0 9.0 8.0 8.0 7.9 7.4 060371002 14.0 19.0 15.0 12.0 13.0 11.0 12.1 12.5 060371103 15.0 14.0 13.0 11.0 11.0 9.0 10.7 9.2 060371201 15.0 16.0 18.0 16.0 12.0 10.0 12.8 11.8 060371301 32.0 28.0 23.0 29.0 25.0 20.0 20.8 16.5 060371601 12.0 12.0 11.0 11.0 8.0 9.9 9.3 060371701 11.0 11.0 10.0 12.0 8.0 9.8 7.7 060372005 13.0 15.0 13.0 11.0 10.0 12.3 11.4 060374002 12.0 12.0 10.0 12.0 10.0 9.0 11.5 8.1 060375001 21.0 22.0 17.0 15.0 18.0 14.0 13.9 11.1 060376002 9.0 10.0 8.0 8.0 7.0 7.5 6.5 060379002 10.0 10.0 9.0 8.0 9.0 6.8 Orange 060590001 16.0 17.0 15.0 13.0 15.0 15.0 12.0 9.8 060591002 16.0 13.0 060591003 13.0 10.0 11.0 9.0 9.5 7.5 060592001 9.0 8.0 8.0 8.0 9.0 7.0 7.8 6.0 060595001 20.0 23.0 18.0 16.0 18.0 14.0 16.1 11.5 Riverside 060650006 5.0 5.0 2.0 060651003 11.0 13.0 15.0 12.0 10.0 9.0 11.0 9.0 060655001 6.0 5.0 4.0 4.0 4.0 3.5 3.1 060658001 9.0 12.0 9.0 8.0 6.0 8.0 7.6 6.7 San Bernadino 060710001 9.0 6.0 5.0 10.0 6.0 4.0 3.5 3.1 060710006 2.0 2.0 060710012 8.0 3.0 8.0 2.0 3.0 2.0 1.8 1.7 060710014 4.0 3.7 3.1 060710017 5.5 3.3 060711004 8.0 7.0 8.0 7.0 060712002 8.0 7.0 6.0 5.0 060714001 6.0 6.0 7.0 5.0 5.0 4.0 3.4 3.0 060719004 9.0 10.0 9.0 8.0 7.0 7.0 7.5 7.4 Maxperyea r 32.0 28.0 23.0 29.0 25.0 20.0 20.8 16.5 1-hour - 2nd maximum (ppm) per monitor, per year for 1988- 1995 (current standard is 35 ppm)

B - 25California-- January 1st 1988 through December 31st, 1995 (Study area and time period for Mann et al., 2002 )

California 1988 1989 1990 1991 1992 1993 1994 1995 Los Angeles 060370002 5.4 5.4 5.0 5.3 4.3 4.0 4.4 6.2 060370113 6.7 7.8 6.6 6.0 5.7 4.6 5.8 5.6 060371002 11.7 11.6 11.6 10.6 9.8 8.1 10.2 11.0 060371103 10.4 9.4 8.8 8.7 8.0 6.7 8.4 7.9 060371201 11.9 12.0 13.4 12.3 8.1 8.0 9.9 9.4 060371301 23.4 18.3 15.9 15.7 16.4 13.8 16.0 11.6 060371601 9.3 8.4 8.9 7.7 6.3 8.4 7.6 060371701 7.1 6.4 6.8 6.9 5.1 6.3 6.0 060372005 8.4 8.7 9.4 7.1 6.3 7.7 8.6 060374002 9.4 9.6 8.9 7.8 7.3 6.9 7.6 6.2 060375001 15.6 14.4 12.1 11.1 11.3 9.6 11.3 8.7 060376002 4.9 4.5 4.8 3.7 3.8 3.8 3.8 060379002 6.9 7.0 5.3 5.3 5.1 4.5 Orange 060590001 10.4 10.9 8.7 8.6 8.6 6.6 8.1 7.3 060591002 10.0 9.0 060591003 9.9 7.1 8.3 6.7 7.8 5.3 060592001 4.9 4.8 5.1 4.5 5.0 3.9 5.4 3.9 060595001 9.8 10.3 9.4 7.6 8.0 6.0 8.0 6.4 Riverside 060650006 2.9 3.6 1.8 060651003 7.1 8.1 7.3 6.8 6.0 5.8 6.0 5.8 060655001 2.4 2.0 2.4 2.0 1.8 1.7 1.5 060658001 5.9 7.9 5.9 6.1 4.6 5.3 5.6 5.2 San Bernadino 060710001 3.3 3.6 3.8 8.1 3.3 2.6 2.1 2.1 060710006 2.0 1.9 060710012 3.7 2.0 3.0 2.0 1.3 1.3 1.4 1.3 060710014 2.6 2.0 2.4 060710017 2.6 1.8 060711004 4.9 5.3 5.8 4.3 060712002 4.6 5.6 4.4 4.1 060714001 3.6 3.4 3.1 3.7 3.1 3.0 2.1 2.0 060719004 7.0 8.0 6.0 6.9 5.1 5.0 5.5 5.9 Maxperyea r 23.4 18.3 15.9 15.7 16.4 13.8 16.0 11.6 8-hour - 2nd maximum non-overlapping 8-hr average (ppm) per monitor, per year for1988-1995 (current standard is 9 ppm)

B - 26California-- January 1st 1988 through December 31st, 1995 (Study area and time period for Mann et al., 2002 )

Statistics for Other Metrics

California 1988 1989 1990 1991 1992 1993 1994 1995 Los Angeles 060370002 7.0 7.0 6.0 7.0 6.0 6.0 5.5 6.9 060370113 11.0 10.0 8.0 8.0 7.0 7.0 7.6 6.5 060371002 14.0 18.0 14.0 12.0 12.0 10.0 11.4 11.6 060371103 13.0 13.0 10.0 10.0 10.0 8.0 10.0 9.0 060371201 13.0 14.0 14.0 13.0 12.0 10.0 11.0 10.4 060371301 31.0 25.0 22.0 21.0 21.0 19.0 18.0 16.1 060371601 12.0 11.0 10.0 10.0 8.0 9.8 9.2 060371701 11.0 10.0 10.0 10.0 8.0 8.8 7.3 060372005 12.0 10.0 11.0 10.0 9.0 10.9 10.1 060374002 11.0 12.0 10.0 10.0 9.0 9.0 9.0 7.4 060375001 21.0 19.0 15.0 14.0 15.0 13.0 12.8 11.0 060376002 9.0 9.0 8.0 7.0 7.0 6.9 6.3 060379002 9.0 9.0 8.0 7.0 7.6 6.1 Orange 060590001 15.0 14.0 11.0 12.0 12.0 9.0 11.0 9.0 060591002 12.0 13.0 060591003 11.0 10.0 10.0 8.0 9.1 7.3 060592001 8.0 8.0 8.0 7.0 7.0 7.0 7.1 5.4 060595001 19.0 22.0 18.0 15.0 16.0 13.0 14.5 10.7 Riverside 060650006 5.0 5.0 2.0 060651003 11.0 12.0 13.0 11.0 10.0 9.0 10.0 8.7 060655001 4.0 4.0 4.0 4.0 3.0 2.9 2.9 060658001 9.0 9.0 7.0 8.0 6.0 7.0 6.5 6.3 San Bernadino 060710001 7.0 5.0 5.0 9.0 5.0 3.0 3.5 2.9 060710006 2.0 2.1 060710012 4.0 2.0 5.0 2.0 2.0 2.0 1.7 1.5 060710014 4.0 3.7 3.1 060710017 2.8 3.3 060711004 7.0 7.0 7.0 7.0 060712002 6.0 6.0 6.0 5.0 060714001 5.0 5.0 5.0 5.0 4.0 3.0 2.9 2.9 060719004 9.0 9.0 8.0 7.0 7.0 6.0 6.6 7.1 Maxperyea r 31.0 25.0 22.0 21.0 21.0 19.0 18.0 16.1 31.0 Total Ma x Minperyea r 4.0 2.0 4.0 2.0 2.0 2.0 1.7 1.5 1.5 Total Min 1-hour - 99th percentile daily maximum (of all 365 possible daily maximum 1-hour values)

B - 27California-- January 1st 1988 through December 31st, 1995 (Study area and time period for Mann et al., 2002 )

California 1988 1989 1990 1991 1992 1993 1994 1995 Los Angeles 060370002 2.0 2.0 2.0 2.0 2.0 2.0 2.1 1.9 060370113 3.0 3.0 3.0 2.0 3.0 2.0 2.5 2.0 060371002 4.0 4.0 4.0 3.0 3.0 3.0 3.3 3.2 060371103 4.0 4.0 4.0 4.0 4.0 3.0 3.8 3.1 060371201 3.0 3.0 3.0 3.0 3.0 3.0 3.1 1.9 060371301 5.0 5.0 5.0 4.0 4.0 4.0 4.4 3.8 060371601 3.0 3.0 3.0 3.0 3.0 3.1 2.7 060371701 4.0 4.0 4.0 3.0 3.0 3.4 2.8 060372005 3.0 3.0 3.0 3.0 3.0 2.8 2.7 060374002 2.0 2.0 3.0 2.0 2.0 2.0 2.3 1.7 060375001 3.0 3.0 4.0 3.0 3.0 3.0 3.2 2.6 060376002 3.0 2.0 2.0 2.0 2.0 2.6 2.1 060379002 2.0 2.0 2.0 2.0 2.0 1.7 Orange 060590001 3.0 2.0 3.0 2.0 2.0 2.0 2.3 2.0 060591002 2.0 4.0 060591003 1.0 1.0 2.0 1.0 1.6 1.1 060592001 2.0 2.0 2.0 2.0 2.0 2.0 1.6 1.4 060595001 4.0 4.0 3.0 3.0 3.0 3.0 2.9 2.4 Riverside 060650006 3.0 1.0 1.0 060651003 4.0 4.0 4.0 3.0 3.0 3.0 4.0 3.0 060655001 1.0 1.0 1.0 1.0 1.0 0.9 0.9 060658001 2.0 3.0 3.0 2.0 2.0 2.0 2.7 2.3 San Bernadino 060710001 2.0 1.0 2.0 2.0 1.0 1.0 0.7 0.9 060710006 1.0 0.9 060710012 1.0 1.0 1.0 1.0 1.0 1.0 0.7 0.5 060710014 1.0 1.2 0.9 060710017 0.9 1.3 060711004 3.0 3.0 3.0 3.0 060712002 2.0 2.0 2.0 2.0 060714001 2.0 2.0 2.0 2.0 2.0 2.0 1.4 1.2 060719004 3.0 3.0 3.0 2.0 2.0 2.0 2.0 2.0 Maxperyea r 5.0 5.0 5.0 4.0 4.0 4.0 4.4 3.8 5.0 Total Ma x Minperyea r 1.0 1.0 1.0 1.0 1.0 1.0 0.7 0.5 0.5 Total Min 1-hour - 50th percentile daily maximum (of all 365 possible daily maximum 1-hour values)

B - 28California-- January 1st 1988 through December 31st, 1995 (Study area and time period for Mann et al., 2002 )

California 1988 1989 1990 1991 1992 1993 1994 1995 Los Angeles 060370002 4.5 4.9 4.4 5.1 4.0 3.9 4.1 5.3 060370113 6.6 7.3 6.0 5.6 5.3 4.6 5.3 4.7 060371002 10.9 11.3 11.3 10.4 9.4 7.5 9.9 9.5 060371103 9.8 9.4 8.1 8.6 7.9 6.3 8.0 7.6 060371201 10.7 11.6 12.3 11.9 7.8 7.6 9.5 8.8 060371301 19.1 18.0 15.3 13.6 14.4 13.0 14.2 11.2 060371601 8.9 8.1 8.3 7.4 6.0 8.0 7.0 060371701 7.1 6.1 6.8 6.4 5.0 6.3 5.5 060372005 8.1 7.6 8.6 7.0 5.9 7.5 8.4 060374002 8.9 8.7 8.5 7.1 6.9 6.7 6.8 5.8 060375001 13.8 12.4 11.7 10.3 10.9 9.1 9.8 8.5 060376002 4.5 4.3 4.8 3.3 3.6 3.7 3.8 060379002 6.6 6.5 5.0 5.1 5.0 4.5 Orange 060590001 9.7 10.7 8.6 8.3 8.3 6.0 7.7 6.5 060591002 8.9 9.7 060591003 9.4 7.0 8.1 6.4 6.7 4.8 060592001 4.4 4.5 4.1 4.5 4.3 3.9 4.8 3.8 060595001 9.3 10.0 8.6 7.4 7.3 6.0 7.5 6.3 Riverside 060650006 2.9 3.5 1.8 060651003 6.1 7.8 6.3 6.4 5.8 5.4 5.9 5.6 060655001 2.1 1.9 1.9 2.0 1.5 1.6 1.4 060658001 5.8 7.1 5.3 5.1 4.5 4.9 5.4 4.9 San Bernadino 060710001 3.3 3.5 3.7 7.3 3.0 2.6 2.1 2.0 060710006 2.0 1.9 060710012 2.9 2.0 2.0 2.0 1.1 1.3 1.4 1.3 060710014 2.3 1.9 2.4 060710017 2.3 2.0 060711004 4.8 5.0 4.0 4.4 060712002 4.5 4.9 4.1 4.1 060714001 3.6 3.0 3.1 3.7 3.1 2.3 2.0 1.9 060719004 7.0 7.4 5.8 6.5 4.5 4.9 5.2 5.7 Maxperyea r 19.1 18.0 15.3 13.6 14.4 13.0 14.2 11.2 19.1 Total Ma x Minperyea r 2.9 2.0 1.9 1.9 1.1 1.3 1.4 1.3 1.1 Total Min 8-hour - 99th percentile daily maximum (of all 365 possible daily 8-hour maximum averages)

B - 29California-- January 1st 1988 through December 31st, 1995 (Study area and time period for Mann et al., 2002 )

California 1988 1989 1990 1991 1992 1993 1994 1995 Los Angeles 060370002 1.4 1.8 1.5 1.6 1.6 1.4 1.6 1.5 060370113 2.0 1.8 1.9 1.6 1.6 1.7 1.7 1.2 060371002 3.0 3.1 2.6 2.4 2.6 2.4 2.6 2.7 060371103 3.0 2.9 2.6 2.6 2.9 2.4 2.8 2.4 060371201 2.1 1.9 2.4 2.1 2.0 2.0 2.3 1.2 060371301 3.3 3.0 2.9 2.6 2.9 2.7 3.0 2.8 060371601 2.1 2.1 2.0 2.1 2.0 2.2 2.0 060371701 3.0 2.8 2.7 2.6 2.4 2.5 1.9 060372005 2.6 2.3 2.0 2.1 2.0 2.2 2.2 060374002 1.6 1.3 2.1 1.7 1.7 1.7 1.8 1.3 060375001 1.6 1.6 2.0 1.6 2.0 1.8 1.8 1.6 060376002 1.7 1.6 1.5 1.6 1.5 1.8 1.4 060379002 1.4 1.3 1.4 1.3 1.2 1.1 Orange 060590001 1.9 1.6 2.0 1.7 1.7 1.6 1.6 1.5 060591002 1.1 2.9 060591003 0.8 1.0 1.2 1.0 0.9 0.7 060592001 1.4 1.1 1.4 1.4 1.5 1.3 1.1 1.0 060595001 2.7 2.6 2.1 2.0 2.0 1.9 2.0 1.7 Riverside 060650006 1.9 1.0 1.0 060651003 2.9 2.5 2.6 2.3 2.6 2.4 2.6 2.3 060655001 0.9 0.9 1.0 1.0 1.0 0.7 0.7 060658001 1.7 1.9 1.7 1.4 1.6 1.4 1.8 1.6 San Bernadino 060710001 1.1 1.1 1.7 1.6 1.0 1.0 0.5 0.7 060710006 0.9 0.7 060710012 0.8 1.0 1.0 1.0 1.0 0.9 0.6 0.4 060710014 1.0 0.8 0.6 060710017 0.7 1.0 060711004 2.0 2.0 2.0 1.6 060712002 1.6 1.7 1.7 1.3 060714001 1.7 1.7 1.7 1.9 1.9 1.4 1.0 0.9 060719004 2.3 2.3 2.0 1.8 1.4 1.5 1.6 1.5 Maxperyea r 3.3 3.1 2.9 2.7 2.9 2.7 3.0 2.8 3.3 Total Ma x Minperyea r 0.8 0.9 0.8 1.0 1.0 0.9 0.5 0.4 0.4 Total Min 8-hour -50th percentile daily maximum (of all 365 possible daily 8

- hour maximum averages)

B - 30California-- January 1st 1988 through December 31st, 1995 (Study area and time period for Mann et al., 2002 )

California 1988 1989 1990 1991 1992 1993 1994 1995 Los Angeles 060370002 3.3 3.4 3.4 3.7 3.0 3.0 2.9 4.1 060370113 4.0 4.0 3.9 4.0 3.1 2.9 3.3 3.3 060371002 6.6 7.8 6.7 6.6 5.9 4.9 6.6 6.8 060371103 6.0 6.0 5.5 5.9 5.0 4.3 5.4 5.4 060371201 6.0 6.9 6.6 6.2 4.6 5.0 5.5 5.7 060371301 10.9 9.6 8.7 8.7 9.6 8.0 8.9 7.6 060371601 6.1 5.1 5.7 4.6 4.0 5.3 5.2 060371701 5.0 4.7 4.7 4.2 3.5 4.2 4.2 060372005 4.9 4.8 4.6 3.9 3.5 4.7 4.9 060374002 6.0 6.1 5.4 4.7 4.8 4.1 4.7 3.7 060375001 8.2 6.9 6.1 5.5 5.9 5.2 5.8 4.9 060376002 3.0 2.7 3.0 2.3 2.3 2.5 2.7 060379002 3.6 3.3 3.1 2.7 2.6 2.4 Orange 060590001 6.2 6.4 4.5 5.0 4.4 3.7 4.8 4.7 060591002 6.2 6.9 060591003 5.2 4.7 4.8 3.4 4.0 3.4 060592001 3.2 3.1 3.0 3.0 3.0 2.7 3.5 2.4 060595001 6.2 6.5 5.2 5.0 5.0 3.8 5.4 4.5 Riverside 060650006 2.1 2.6 1.2 060651003 4.6 5.7 4.5 4.3 4.0 4.0 4.1 4.2 060655001 1.4 1.2 1.4 1.4 1.2 1.0 1.0 060658001 3.3 4.5 3.7 3.3 2.7 2.9 3.6 3.5 San Bernadino 060710001 2.1 2.4 3.1 5.3 2.1 1.9 1.2 1.2 060710006 1.7 1.8 060710012 1.2 1.7 1.3 2.0 1.0 1.1 1.1 1.0 060710014 1.7 1.5 2.1 060710017 1.8 1.5 060711004 3.3 3.3 3.0 2.7 060712002 3.0 3.2 2.8 2.7 060714001 3.2 2.5 3.0 3.0 2.8 2.0 1.5 1.4 060719004 4.3 4.5 3.6 3.6 2.8 3.0 3.3 3.8 Maxperyea r 10.9 9.6 8.7 8.7 9.6 8.0 8.9 7.6 10.9 Total Ma x Minperyea r 1.2 1.4 1.2 1.4 1.0 1.1 1.0 1.0 1.0 Total Min 24-hour - 99th percentile (of all 365 possible daily 24-hour averages)

B - 31California-- January 1st 1988 through December 31st, 1995 (Study area and time period for Mann et al., 2002 )

California 1988 1989 1990 1991 1992 1993 1994 1995 Los Angeles 060370002 1.1 1.2 1.1 1.1 1.2 1.0 1.2 1.1 060370113 1.3 1.0 1.2 1.0 1.0 1.0 0.9 0.7 060371002 2.1 2.2 1.8 1.7 1.7 1.7 1.8 1.9 060371103 1.8 1.7 1.6 1.8 1.7 1.6 1.9 1.6 060371201 1.2 1.1 1.5 1.3 1.4 1.3 1.5 0.8 060371301 2.3 2.3 1.9 1.8 1.9 1.9 2.2 2.0 060371601 1.3 1.4 1.5 1.5 1.3 1.5 1.5 060371701 1.9 1.9 1.7 1.7 1.7 1.8 1.2 060372005 2.0 1.6 1.4 1.5 1.5 1.5 1.6 060374002 1.0 0.8 1.6 1.2 1.2 1.2 1.2 0.9 060375001 0.9 0.7 1.0 0.8 1.1 0.9 0.9 1.0 060376002 1.2 1.1 1.0 1.1 1.0 1.2 1.0 060379002 1.0 0.9 1.0 0.9 0.8 0.7 Orange 060590001 1.2 1.1 1.3 1.2 1.2 1.1 1.1 1.1 060591002 0.7 1.5 060591003 0.4 0.5 0.8 0.7 0.5 0.4 060592001 0.9 0.8 1.0 1.0 1.1 1.0 0.7 0.6 060595001 2.0 2.0 1.5 1.3 1.3 1.3 1.3 1.2 Riverside 060650006 1.2 0.9 0.6 060651003 2.0 1.9 1.8 1.5 1.8 1.7 1.9 1.6 060655001 0.5 0.5 0.5 0.6 0.6 0.4 0.4 060658001 1.1 1.1 1.0 1.0 1.0 0.9 1.1 0.9 San Bernadino 060710001 1.0 1.0 1.2 1.1 1.0 0.6 0.3 0.4 060710006 0.5 0.6 060710012 0.4 0.6 0.6 1.0 0.5 0.5 0.3 0.3 060710014 0.8 0.5 0.4 060710017 0.5 0.7 060711004 1.4 1.3 1.3 1.1 060712002 1.1 1.2 1.1 1.0 060714001 1.2 1.3 1.2 1.3 1.3 1.1 0.7 0.6 060719004 1.7 1.6 1.3 1.2 1.0 1.1 1.2 1.2 Maxperyea r 2.3 2.3 1.9 1.8 1.9 1.9 2.2 2.0 2.3 Total Ma x Minperyea r 0.4 0.5 0.4 0.5 0.5 0.5 0.3 0.3 0.3 Total Min 24-hour -50th percentile (of all 365 possible daily 24-hour averages)

B - 32126County-- January 1st 1999 through December 31st, 2005 (Study area and time period for Bell et al., 2009 )

Design values for current standards

STATENAME fips COUNTYNAME fips 1999 2000 2001 2002 2003 2004 2005 A labama 01 Jefferson 073 32.3 23.6 33.5 17.7 9.1 15.0 20.9 A rizona 04 Maricopa 013 13.5 10.5 9.6 7.9 7.3 7.5 7.0 A rizona 04 Pima 019 7.8 7.5 5.7 5.1 9.6 4.7 3.6 A rkansas 05 Pulaski 119 6.0 4.5 4.0 6.1 3.7 2.8 2.6 California 06 Alameda 001 6.1 5.4 5.2 7.6 6.0 3.5 3.3 California 06 Contra Costa 013 6.2 4.2 4.2 5.9 2.9 3.7 3.1 California 06 Fresno 019 10.0 8.2 6.2 6.0 5.0 3.9 4.0 California 06 Kern 029 5.5 8.9 5.8 4.4 4.2 3.3 3.2 California 06 Los Angeles 037 16.0 13.2 11.7 13.6 10.4 8.7 7.2 California 06 Riverside 065 7.1 7.5 5.7 6.0 4.4 3.9 3.7 California 06 Sacramento 067 7.3 7.2 6.7 7.5 4.7 7.1 6.6 California 06 San Bernardino 071 7.4 4.7 4.1 4.0 5.0 3.8 3.3 California 06 San Diego 073 9.2 9.2 8.4 8.0 8.3 6.1 7.4 California 06 San Francisco 075 7.8 4.9 4.7 4.9 5.1 3.4 3.8 California 06 San Joaquin 077 8.9 8.0 7.0 5.2 4.9 3.5 4.2 California 06 San Mateo 081 7.1 8.9 6.9 5.5 5.1 4.3 4.4 California 06 Santa Clara 085 8.8 8.6 7.4 5.9 5.3 3.9 4.0 California 06 Stanislaus 099 10.9 7.8 7.0 5.1 4.6 4.4 3.5 Colorado 08 Adams 001 6.0 4.3 5.8 4.4 5.2 4.0 3.3 Colorado 08 Denver 031 12.1 12.8 9.3 7.5 14.9 8.7 4.3 Connecticut 09 Fairfield 001 5.1 6.0 4.7 4.4 4.0 4.0 3.4 Connecticut 09 Hartford 003 11.9 15.2 7.8 9.5 10.1 9.8 9.9 Connecticut 09 New Haven 009 4.2 4.3 3.5 3.4 2.7 2.8 2.6 Delaware 10 New Castle 003 4.0 3.5 3.7 3.1 3.4 3.4 4.3 District Of 11 District of 001 7.3 6.6 6.3 7.5 8.3 4.0 3.8 Florida 12 Broward 011 7.9 7.5 5.9 6.8 5.3 4.2 4.6 Florida 12 Duval 031 6.3 6.0 5.3 3.9 3.8 3.4 3.2 Florida 12 Hillsborough 057 8.5 5.4 5.1 5.3 5.7 4.4 4.0 Florida 12 Miami-Dade 086 7.1 6.2 7.3 5.1 5.8 9.1 4.1 Florida 12 Orange 095 5.2 7.5 3.8 4.4 3.2 2.7 7.8 Florida 12 Palm Beach 099 5.2 4.9 3.2 3.8 4.2 3.7 3.4 Florida 12 Pinellas 103 4.5 5.3 4.0 3.7 3.6 2.8 2.5 Georgia 13 DeKalb 089 6.3 4.6 5.3 4.6 3.0 3.7 3.2 Georgia 13 Fulton 121 5.1 4.3 4.9 3.7 3.5 4.6 2.6 Hawaii 15 Honolulu 003 3.8 3.8 4.1 3.1 3.0 2.8 2.7 Idaho 16 Ada 001 9.1 7.6 5.3 5.2 4.7 3.9 4.6 Illinois 17 Cook 031 6.4 6.2 5.0 4.9 4.4 4.8 3.5 Illinois 17 Winnebago 201 6.5 4.8 4.9 3.3 3.3 3.2 3.2 Indiana 18 Allen 003 5.5 5.8 4.4 4.8 4.3 4.4 2.8 Indiana 18 Marion 097 4.8 5.7 3.8 14.2 3.8 4.0 4.2 Iowa 19 Polk 153 6.5 16.5 9.0 4.1 3.7 3.8 2.8 Kansas 20 Sedgwick 173 8.6 6.8 6.3 6.3 4.5 4.8 9.7 Kentuck y 21 Jefferson 111 9.1 10.7 5.1 9.9 5.6 4.5 4.0 Louisiana 22 East Baton 033 6.8 6.2 6.5 5.8 4.3 3.8 3.1 Louisiana 22 Orleans 071 6.1 5.7 5.4 5.6 6.5 5.2 2.7 1-hour - 2nd maximum (ppm) per monitor, per year for 1999-2005 (current standard is 35 ppm)

B - 33126County-- January 1st 1999 through December 31st, 2005 (Study area and time period for Bell et al., 2009 ) Maryland 24 Baltimore (City) 510 10.2 4.6 4.4 4.4 3.8 4.8 9.2 Massachusetts 25 Hampden 013 7.9 5.4 4.9 5.5 3.9 4.7 3.3 Massachusetts 25 Middlesex 017 8.4 5.3 4.2 3.6 3.8 2.5 2.6 Massachusetts 25 Suffolk 025 7.0 3.4 4.9 3.7 4.0 2.8 3.6 Massachusetts 25 Worcester 027 6.8 9.0 5.9 4.5 3.6 3.9 3.3 Michigan 26 Kent 081 4.1 4.2 4.3 4.7 3.2 2.8 2.6 Michigan 26 Macomb 099 4.0 5.1 4.0 3.7 3.5 3.3 3.6 Michigan 26 Oakland 125 4.8 4.7 4.5 3.4 3.7 4.0 3.4 Michigan 26 Wayne 163 6.0 7.7 5.4 4.6 4.5 3.9 3.4 Minnesota 27 Dakota 037 1.2 1.7 1.5 1.3 1.2 1.0 0.7 Minnesota 27 Hennepin 053 4.3 5.0 5.6 6.1 4.7 3.2 3.3 Minnesota 27 Ramsey 123 7.6 6.6 11.1 5.8 6.1 5.3 5.6 Minnesota 27 Saint Louis 137 4.6 3.8 4.1 3.2 2.8 2.9 4.2 Mississippi 28 Hinds 049 8.2 4.4 5.3 4.9 4.9 4.2 3.4 Missouri 29 Jackson 095 6.7 6.7 10.1 10.2 3.5 3.4 3.6 Missouri 29 Saint Louis 189 5.0 4.3 4.3 4.5 3.3 2.3 1.7 Missouri 29 St. Louis City 510 6.1 5.6 8.1 8.1 4.5 4.3 4.7 Nevada 32 Clark 003 10.2 8.5 8.7 7.5 6.9 6.5 6.3 Nevada 32 Washoe 031 9.5 7.2 7.1 6.7 6.1 5.8 4.4 New Hampshire 33 Hillsborough 011 12.0 8.0 6.5 5.9 7.5 4.8 6.1 New Jerse y 34 Bergen 003 5.7 4.8 4.5 4.2 5.2 4.1 3.4 New Jerse y 34 Camden 007 5.5 5.3 5.6 3.8 2.9 3.7 3.9 New Jerse y 34 Hudson 017 10.0 8.5 5.1 4.4 4.0 4.1 4.8 New Jerse y 34 Middlesex 023 4.5 4.7 4.8 3.7 3.7 3.5 3.0 New Jerse y 34 Morris 027 5.9 5.1 5.6 4.9 3.6 3.1 2.8 New Jerse y 34 Union 039 8.9 7.2 6.1 6.4 6.0 5.4 4.6 New Mexico 35 Bernalillo 001 7.5 7.0 9.5 6.0 9.6 5.0 4.3 New Yor k 36 Albany 001 2.5 1.8 1.9 2.2 2.9 1.7 1.9 New Yor k 36 Bronx 005 5.7 6.0 4.9 3.7 3.4 2.8 3.5 New Yor k 36 Erie 029 3.9 4.7 3.2 4.0 3.0 2.6 2.5 New Yor k 36 Kings 047 7.3 6.2 5.7 4.9 3.5 3.6 4.1 New Yor k 36 Monroe 055 5.5 4.2 4.3 5.7 2.8 2.8 2.5 New Yor k 36 New York 061 7.1 6.0 6.5 4.5 4.0 3.6 2.2 New Yor k 36 Niagara 063 4.2 3.8 2.3 2.2 2.8 2.5 5.7 New Yor k 36 Onondaga 067 5.6 3.9 3.8 3.4 3.2 3.0 2.8 New Yor k 36 Queens 081 3.4 6.3 3.8 3.5 11.2 3.1 2.4 New Yor k 36 Suffolk 103 3.4 3.4 3.7 2.8 2.9 2.3 North Carolina 37 Forsyth 067 4.8 5.1 6.1 5.7 5.5 4.4 3.1 North Carolina 37 Mecklenburg 119 7.1 10.8 8.8 5.7 4.6 3.5 2.9 North Carolina 37 Wake 183 6.6 6.8 5.4 4.6 4.3 3.4 3.4 Ohio 39 Cuyahoga 035 6.8 11.1 5.5 8.0 5.5 12.8 5.5 Ohio 39 Franklin 049 8.5 4.9 4.7 3.6 4.8 4.4 4.2 Ohio 39 Hamilton 061 4.9 4.9 4.5 5.7 3.0 5.8 3.2 Ohio 39 Lake 085 2.5 2.7 2.4 2.7 2.9 1.7 2.2 Ohio 39 Montgomery 113 4.1 5.0 4.8 3.4 3.7 4.1 2.8 Ohio 39 Stark 151 4.5 3.3 4.0 3.8 5.4 3.6 3.8 Ohio 39 Summit 153 4.7 5.6 5.2 3.6 5.1 3.5 3.1 Oklahoma 40 Oklahoma 109 6.5 5.5 5.6 5.0 4.6 3.4 3.2 Oklahoma 40 Tulsa 143 5.6 6.7 7.5 4.9 4.2 2.6 3.2 Oregon 41 Lane 039 7.8 6.6 5.5 5.6 5.4 6.8 4.9

B - 34126County-- January 1st 1999 through December 31st, 2005 (Study area and time period for Bell et al., 2009 ) Oregon 41 Multnomah 051 10.4 8.4 6.4 5.4 5.2 8.6 4.5 Pennsylvani a 42 Allegheny 003 6.0 5.5 4.2 5.7 5.6 3.5 3.1 Pennsylvani a 42 Berks 011 4.6 3.8 3.8 4.1 3.2 2.7 2.4 Pennsylvani a 42 Dauphin 043 4.9 3.5 4.4 3.6 3.0 2.3 2.0 Pennsylvani a 42 Erie 049 10.6 11.9 7.2 7.5 7.6 1.8 3.1 Pennsylvani a 42 Lackawanna 069 3.5 4.4 2.9 2.7 2.4 2.9 2.6 Pennsylvani a 42 Lancaster 071 3.1 3.0 2.9 3.0 2.7 3.2 2.5 Pennsylvani a 42 Northampton 095 4.4 5.5 3.1 2.3 2.3 2.4 2.5 Pennsylvani a 42 Philadelphia 101 7.4 6.3 7.7 5.0 5.4 5.1 12.1 Pennsylvani a 42 York 133 5.3 3.7 3.8 4.3 2.6 2.8 2.5 Rhode Island 44 Providence 007 7.0 5.4 9.0 3.9 3.7 3.5 7.9 South Carolina 45 Charleston 019 6.4 4.4 5.1 3.5 4.6 3.1 2.1 South Carolina 45 Greenville 045 6.9 5.3 4.7 4.2 4.0 3.4 3.6 South Carolina 45 Richland 079 4.2 4.6 4.6 3.4 2.9 3.0 2.5 Tennessee 47 Davidson 037 7.6 6.7 7.1 6.2 4.9 5.0 4.1 Tennessee 47 Shelby 157 7.6 5.8 6.6 4.9 4.9 8.0 3.8 Texas 48 Bexar 029 6.3 4.6 6.0 4.5 4.6 3.1 3.7 Texas 48 Cameron 061 4.4 3.3 2.7 3.7 3.9 3.9 3.4 Texas 48 Dallas 113 4.3 3.5 3.6 3.3 3.0 2.9 4.1 Texas 48 El Paso 141 14.4 17.0 14.3 13.1 11.7 11.3 11.5 Texas 48 Harris 201 6.3 5.7 5.7 4.4 5.4 3.6 3.8 Texas 48 Tarrant 439 4.8 4.3 4.3 4.0 3.5 2.9 7.5 Texas 48 Travis 453 2.1 1.8 1.7 1.6 2.2 0.9 1.0 Utah 49 Salt Lake 035 9.7 10.0 7.1 6.2 8.2 5.4 5.5 Virginia 51 Fairfax 059 7.0 5.6 4.6 3.3 3.3 3.6 2.5 Virginia 51 Norfolk City 710 9.2 6.9 7.2 6.6 4.6 3.8 2.1 Washington 53 Clark 011 12.9 8.4 8.0 7.2 7.1 6.3 6.9 Washington 53 King 033 15.6 8.6 8.8 7.0 8.7 4.7 5.9 Washington 53 Pierce 053 11.0 7.7 8.4 9.3 10.1 6.4 6.1 Washington 53 Spokane 063 9.3 8.9 7.6 8.6 8.2 7.8 7.4 Wisconsin 55 Milwaukee 079 3.5 3.5 4.2 4.2 5.0 4.9 9.5

Maxperyea r 32.3 23.6 33.5 17.7 14.9 15.0 20.9

B - 35126County-- January 1st 1999 through December 31st, 2005 (Study area and time period for Bell et al., 2009 )

STATENAME fips COUNTYNAME fips 1999 2000 2001 2002 2003 2004 2005 A labama 01 Jefferson 073 19.8 16.3 24.3 11.7 4.5 8.2 8.8 A rizona 04 Maricopa 013 8.1 7.2 6.6 5.5 5.5 5.1 4.8 A rizona 04 Pima 019 3.8 4.7 2.9 2.6 2.7 2.5 2.4 A rkansas 05 Pulaski 119 4.0 2.9 2.2 5.2 2.2 1.8 2.1 California 06 A lameda 001 4.5 3.0 3.9 4.9 4.3 2.4 2.3 California 06 Contra Costa 013 3.3 2.6 2.4 2.5 1.8 1.8 1.7 California 06 Fresno 019 7.6 5.9 4.5 4.3 3.6 2.8 2.8 California 06 Kern 029 4.1 5.2 3.4 2.5 2.2 2.4 2.0 California 06 Los Angeles 037 11.1 9.9 7.2 8.5 7.2 6.1 5.6 California 06 Riverside 065 4.1 4.2 3.6 3.5 3.6 2.8 2.3 California 06 Sacramento 067 6.2 6.2 5.0 4.2 3.8 3.2 3.7 California 06 San Bernardino 071 4.0 3.7 3.2 3.1 3.9 2.9 2.2 California 06 San Diego 073 4.9 4.7 4.7 3.8 4.1 3.9 4.4 California 06 San Francisco 075 4.5 2.8 3.1 2.4 3.2 2.6 2.5 California 06 San Joaquin 077 6.0 6.3 3.6 3.2 3.0 2.3 2.5 California 06 San Mateo 081 3.7 3.6 3.5 2.6 2.3 2.0 2.2 California 06 Santa Clara 085 6.2 6.9 5.0 4.1 3.7 2.9 3.0 California 06 Stanislaus 099 6.3 5.6 4.8 3.7 3.3 2.9 2.5 Colorado 08 A dams 001 3.6 2.9 3.3 2.6 3.0 2.8 2.2 Colorado 08 Denve r 031 5.2 5.4 4.1 3.7 4.5 4.1 2.5 Connecticut 09 Fairfield 001 3.8 3.0 3.1 3.2 2.6 2.2 2.5 Connecticut 09 Hartford 003 5.5 7.3 4.5 5.1 5.2 5.7 4.4 Connecticut 09 New Haven 009 3.1 2.6 2.5 2.3 1.9 2.0 1.9 Delaware 10 New Castle 003 3.0 2.6 2.5 2.2 2.4 2.1 2.0 District Of 11 District of 001 5.6 5.0 4.7 4.5 4.0 3.4 3.2 Florida 12 Broward 011 5.4 3.7 4.2 4.0 3.7 3.4 3.2 Florida 12 Duval 031 4.1 3.8 3.4 2.6 2.4 2.3 2.2 Florida 12 Hillsborough 057 4.7 3.1 3.0 3.8 3.3 2.5 3.0 Florida 12 Miami-Dade 086 4.0 3.4 4.2 3.4 3.6 5.3 2.5 Florida 12 Orange 095 3.3 2.6 2.1 2.5 2.0 1.8 2.6 Florida 12 Palm Beach 099 3.1 2.9 2.2 2.3 1.8 2.1 2.2 Florida 12 Pinellas 103 2.6 2.3 2.4 2.3 1.9 1.7 1.6 Georgia 13 DeKalb 089 4.1 3.2 4.1 3.6 2.6 2.6 2.3 Georgia 13 Fulton 121 3.0 2.6 3.0 2.3 2.5 2.5 1.8 Hawaii 15 Honolulu 003 2.1 2.0 1.9 1.8 2.2 2.0 1.6 Idaho 16 A da 001 4.6 3.1 3.2 3.1 3.2 2.4 2.2 Illinois 17 Cook 031 4.9 4.3 3.8 3.7 3.4 3.2 2.5 Illinois 17 Winnebago 201 3.8 2.9 2.9 2.4 2.4 2.7 2.3 Indiana 18 A llen 003 3.3 3.9 2.6 3.3 2.6 2.6 2.1 Indiana 18 Marion 097 2.6 3.8 2.5 5.0 2.7 2.2 2.4 Iowa 19 Polk 153 3.5 4.9 4.6 2.7 2.3 2.5 2.1 Kansas 20 Sedgwick 173 4.6 6.2 4.1 3.7 3.1 3.3 4.9 Kentuck y 21 Jefferson 111 4.8 4.1 3.9 4.8 3.3 3.3 2.6 Louisiana 22 East Baton 033 4.5 3.6 4.8 3.7 3.1 2.7 2.1 Louisiana 22 Orleans 071 3.3 4.0 3.6 3.6 3.5 3.4 1.7 Maryland 24 Baltimore (City) 510 5.6 3.4 3.3 3.0 2.5 2.9 2.7 8-hour - 2nd maximum non-overlapping 8-hr average (ppm) per monitor, per year for1999-2005 (current standard is 9 ppm)

B - 36126County-- January 1st 1999 through December 31st, 2005 (Study area and time period for Bell et al., 2009 ) Massachusetts 25 Hampden 013 5.6 4.0 3.0 3.6 3.0 3.1 2.6 Massachusetts 25 Middlese x 017 4.2 3.2 2.7 2.4 2.7 1.6 1.8 Massachusetts 25 Suffolk 025 4.2 2.4 2.8 2.2 2.4 1.5 2.3 Massachusetts 25 Worcester 027 3.3 3.3 2.6 2.9 1.7 1.9 2.3 Michigan 26 Ken t 081 3.5 2.6 3.1 2.8 2.0 1.8 1.9 Michigan 26 Macomb 099 2.5 1.4 2.7 2.3 2.2 2.3 2.0 Michigan 26 Oakland 125 2.8 2.6 3.0 2.1 2.5 2.3 2.1 Michigan 26 Wayne 163 4.4 4.5 3.4 3.7 3.0 2.4 2.0 Minnesota 27 Dakota 037 1.0 1.5 1.0 0.9 0.8 0.8 0.4 Minnesota 27 Hennepin 053 2.9 2.7 2.9 3.1 2.3 1.8 1.8 Minnesota 27 Ramsey 123 5.2 5.1 5.1 3.9 4.3 3.2 3.0 Minnesota 27 Saint Louis 137 2.9 2.1 2.5 2.1 1.7 1.5 1.6 Mississippi 28 Hinds 049 5.0 3.2 4.2 3.0 3.3 2.5 2.6 Missouri 29 Jackson 095 3.6 5.2 3.6 3.3 1.8 2.2 2.4 Missouri 29 Saint Louis 189 2.7 3.0 2.6 2.5 2.1 1.6 1.3 Missouri 29 St. Louis Cit y 510 4.1 3.8 4.5 6.9 3.0 2.8 3.0 Nevada 32 Clark 003 8.2 7.1 6.5 5.8 5.3 5.1 5.2 Nevada 32 Washoe 031 7.1 5.2 5.2 4.4 3.8 3.9 3.2 New Hampshire 33 Hillsborough 011 5.3 4.1 4.0 3.7 4.0 2.8 3.2 New Jerse y 34 Bergen 003 4.4 3.4 3.1 3.4 2.4 2.7 2.8 New Jerse y 34 Camden 007 3.7 4.3 3.9 2.1 1.8 2.9 3.0 New Jerse y 34 Hudson 017 6.1 4.8 3.0 2.8 2.9 3.2 2.8 New Jerse y 34 Middlese x 023 3.3 3.3 3.3 2.6 1.9 2.1 1.9 New Jerse y 34 Morris 027 4.1 3.1 3.3 2.4 2.3 1.9 1.8 New Jerse y 34 Union 039 6.6 4.7 4.8 4.4 3.3 3.3 3.4 New Mexico 35 Bernalillo 001 4.6 3.8 4.2 3.9 3.5 3.5 3.1 New Yor k 36 A lban y 001 1.4 1.1 1.2 1.5 1.5 1.1 1.4 New Yor k 36 Bronx 005 4.0 3.5 2.7 2.4 2.1 2.0 2.2 New Yor k 36 Erie 029 2.2 2.0 1.9 1.8 2.4 1.4 1.6 New Yor k 36 Kings 047 4.9 4.3 3.5 3.4 2.6 2.5 2.2 New Yor k 36 Monroe 055 2.6 2.6 1.8 2.2 2.1 1.6 2.0 New Yor k 36 New Yor k 061 4.7 4.2 3.2 3.1 3.0 2.4 1.5 New Yor k 36 Niagara 063 2.5 1.6 1.6 1.7 2.0 1.4 1.8 New Yor k 36 Onondaga 067 3.1 2.4 2.2 2.1 1.8 1.4 1.9 New Yor k 36 Queens 081 2.5 3.3 3.0 2.5 2.6 2.0 1.6 New Yor k 36 Suffolk 103 2.8 2.2 1.9 1.6 1.6 1.5 North Carolina 37 Forsyth 067 3.6 3.7 4.0 4.1 3.7 3.2 2.5 North Carolina 37 Mecklenburg 119 4.3 4.7 4.3 3.2 3.0 3.1 2.3 North Carolina 37 Wake 183 4.9 5.2 3.5 3.1 2.9 2.7 2.4 Ohio 39 Cuyahoga 035 3.9 7.9 3.5 2.2 3.4 5.4 2.9 Ohio 39 Franklin 049 2.5 2.8 2.6 2.5 3.0 2.6 2.0 Ohio 39 Hamilton 061 2.8 2.4 2.9 2.6 1.9 2.8 1.8 Ohio 39 Lake 085 1.4 1.4 1.4 2.4 2.7 1.3 1.3 Ohio 39 Montgomer y 113 2.8 3.1 2.6 1.8 2.5 2.6 1.8 Ohio 39 Stark 151 2.3 2.6 2.6 2.8 2.2 2.6 2.7 Ohio 39 Summit 153 3.1 2.6 2.7 2.1 2.5 2.2 1.7 Oklahoma 40 Oklahoma 109 4.3 4.2 4.0 3.0 2.8 2.2 2.1 Oklahoma 40 Tulsa 143 3.5 3.7 4.1 3.0 2.5 1.7 1.4 Oregon 41 Lane 039 5.0 4.3 4.1 4.2 3.4 3.4 2.7 Oregon 41 Multnomah 051 6.2 4.4 4.1 4.5 4.0 3.9 3.1

B - 37126County-- January 1st 1999 through December 31st, 2005 (Study area and time period for Bell et al., 2009 ) Pennsylvani a 42 A lleghen y 003 3.9 3.2 3.4 2.7 2.3 2.3 2.2 Pennsylvani a 42 Berks 011 2.8 2.1 2.2 2.2 2.0 1.8 1.9 Pennsylvani a 42 Dauphin 043 4.3 2.1 2.8 2.3 2.0 1.3 1.3 Pennsylvani a 42 Erie 049 5.6 6.0 4.4 4.5 3.4 1.3 1.4 Pennsylvani a 42 Lackawanna 069 1.7 2.1 1.8 1.6 1.5 1.8 1.5 Pennsylvani a 42 Lancaster 071 2.1 1.9 2.2 2.2 1.7 1.6 1.5 Pennsylvani a 42 Northampton 095 3.0 2.4 2.4 1.8 1.4 1.7 1.9 Pennsylvani a 42 Philadelphia 101 4.9 4.0 4.7 2.9 3.9 3.4 3.4 Pennsylvani a 42 York 133 2.4 1.8 2.2 2.2 1.7 1.8 1.4 Rhode Island 44 Providence 007 3.9 3.5 3.8 2.7 2.3 2.5 2.5 South Carolina 45 Charleston 019 4.0 2.7 3.0 2.8 2.7 2.1 0.6 South Carolina 45 Greenville 045 4.8 3.7 3.4 3.3 3.1 2.5 2.4 South Carolina 45 Richland 079 3.7 3.6 3.3 2.8 2.2 2.3 2.2 Tennessee 47 Davidson 037 5.4 5.6 5.8 5.1 3.7 3.8 3.3 Tennessee 47 Shelb y 157 5.2 4.4 4.8 3.6 3.3 4.0 2.8 Texas 48 Bexar 029 4.2 2.7 2.7 2.6 2.7 1.9 2.7 Texas 48 Cameron 061 2.6 1.6 1.5 1.9 1.9 2.1 1.7 Texas 48 Dallas 113 3.2 2.2 2.4 2.1 2.0 1.8 2.6 Texas 48 El Paso 141 8.2 9.2 8.8 6.8 6.4 6.4 5.4 Texas 48 Harris 201 4.1 4.2 4.4 3.3 4.2 2.9 2.6 Texas 48 Tarrant 439 2.6 2.2 2.3 2.1 1.6 1.7 2.6 Texas 48 Travis 453 1.2 1.1 0.9 0.9 0.9 0.6 0.6 Utah 49 Salt Lake 035 5.7 5.2 4.1 3.7 4.3 3.7 3.6 Virginia 51 Fairfax 059 3.2 3.5 3.0 2.3 2.7 2.3 1.9 Virginia 51 Norfolk Cit y 710 4.6 4.1 4.2 3.7 2.9 3.0 1.1 Washington 53 Clark 011 6.7 6.2 4.7 5.7 4.5 4.8 4.6 Washington 53 King 033 6.1 6.3 6.5 5.0 5.5 3.3 3.8 Washington 53 Pierce 053 6.6 5.5 5.0 4.5 5.3 4.0 3.9 Washington 53 Spokane 063 5.7 5.6 5.2 5.2 4.6 4.0 5.1 Wisconsin 55 Milwaukee 079 2.2 2.4 2.7 3.1 2.6 3.0 4.5

Maxperyea r 19.8 16.3 24.3 11.7 7.2 8.2 8.8

B - 38126County-- January 1st 1999 through December 31st, 2005 (Study area and time period for Bell et al., 2009 )

Statistics for Other Metrics

STATENAME fips COUNTYNAME fips 1999 2000 2001 2002 2003 2004 2005 A labama 01 Jefferson 073 26.4 18.5 31.8 15.9 7.9 14.1 16.1 A rizona 04 Maricopa 013 13.5 9.8 9.0 7.7 6.9 6.4 6.4 A rizona 04 Pima 019 7.2 7.0 5.5 4.9 5.4 4.4 3.2 A rkansas 05 Pulaski 119 5.4 4.3 3.8 4.9 3.5 2.7 2.5 California 06 A lameda 001 5.5 4.7 5.8 6.2 6.0 2.7 2.9 California 06 Contra Costa 013 5.3 4.0 4.2 4.6 2.5 2.8 2.7 California 06 Fresno 019 9.0 8.2 5.5 5.6 5.0 3.6 3.7 California 06 Kern 029 5.2 6.8 5.3 3.7 3.1 2.9 3.0 California 06 Los Angeles 037 14.5 12.5 10.6 10.4 9.1 8.0 7.1 California 06 Riverside 065 6.8 6.5 5.7 5.6 4.3 3.6 3.4 California 06 Sacramento 067 7.0 6.5 5.3 4.8 4.4 6.1 6.2 California 06 San Bernardino 071 4.9 4.6 3.9 3.7 4.3 3.4 2.9 California 06 San Diego 073 9.1 9.1 7.9 7.7 6.9 6.0 5.8 California 06 San Francisco 075 5.8 3.7 4.2 3.7 4.2 3.2 3.6 California 06 San Joaquin 077 8.4 7.6 5.3 5.0 4.2 3.1 3.4 California 06 San Mateo 081 7.0 6.6 6.8 5.4 4.9 4.0 4.3 California 06 Santa Clara 085 8.4 7.2 7.5 5.7 4.4 3.8 3.8 California 06 Stanislaus 099 7.5 6.5 6.0 4.9 4.4 3.9 3.3 Colorado 08 A dams 001 5.3 4.2 4.7 3.7 3.6 3.4 3.0 Colorado 08 Denve r 031 8.8 8.7 7.2 6.9 6.6 5.9 3.8 Connecticut 09 Fairfield 001 4.5 5.2 4.2 4.2 3.3 2.6 3.2 Connecticut 09 Hartford 003 10.4 11.0 7.5 9.4 9.8 7.8 7.1 Connecticut 09 New Haven 009 3.4 3.3 3.1 3.0 2.5 2.4 2.6 Delaware 10 New Castle 003 4.0 3.1 3.4 2.8 2.9 3.0 2.6

District Of Columbia 11 District of Columbia 001 6.7 6.0 4.7 5.1 5.4 3.7 3.5 Florida 12 Broward 011 6.6 4.7 5.7 5.4 4.7 4.1 3.2 Florida 12 Duval 031 4.6 4.1 4.7 3.3 3.5 3.3 2.8 Florida 12 Hillsborough 057 5.1 4.8 4.1 4.8 4.4 3.8 3.8 Florida 12 Miami-Dade 086 6.7 5.2 5.8 4.4 4.9 6.0 4.1 Florida 12 Orange 095 4.8 4.2 3.5 3.5 2.8 2.1 2.5 Florida 12 Palm Beach 099 5.0 4.4 2.8 3.1 3.4 3.3 2.9 Florida 12 Pinellas 103 3.8 3.8 3.0 3.2 2.8 2.5 2.2 Georgia 13 DeKalb 089 5.4 4.1 4.3 3.6 2.7 2.7 2.6 Georgia 13 Fulton 121 4.9 3.8 4.2 3.5 3.3 2.9 2.4 Hawaii 15 Honolulu 003 3.4 3.4 3.0 2.8 2.8 2.7 2.3 Idaho 16 A da 001 7.8 5.7 4.8 5.0 4.6 3.7 3.5 Illinois 17 Cook 031 5.9 4.9 4.2 4.3 4.0 3.7 2.9 Illinois 17 Winnebago 201 5.6 4.4 3.5 3.2 3.1 2.9 3.0 Indiana 18 A llen 003 4.5 4.6 4.1 4.4 3.7 3.2 2.5 Indiana 18 Marion 097 4.5 4.4 3.7 10.1 3.4 3.0 3.1 Iowa 19 Polk 153 6.5 5.8 5.2 3.9 3.2 3.4 2.8 Kansas 20 Sedgwick 173 6.4 6.5 4.7 4.6 4.3 4.3 3.6 Kentuck y 21 Jefferson 111 9.1 5.5 4.4 7.0 4.5 3.8 3.7 Louisiana 22 East Baton Rouge 033 6.5 5.2 4.8 4.2 3.6 3.5 2.6 Louisiana 22 Orleans 071 5.3 4.7 4.3 4.5 3.4 4.5 2.4 1-hour - 99th percentile daily maximum (of all 365 possible daily maximum 1-hour values)

B - 39126County-- January 1st 1999 through December 31st, 2005 (Study area and time period for Bell et al., 2009 ) Maryland 24 Baltimore (City) 510 14.9 3.8 3.6 3.9 3.1 2.8 9.2 Massachusetts 25 Hampden 013 5.1 5.1 4.0 4.3 4.0 3.5 3.0 Massachusetts 25 Middlesex 017 7.3 4.3 3.9 2.8 3.1 2.4 2.3 Massachusetts 25 Suffolk 025 5.9 3.0 3.5 3.4 2.9 2.0 2.6 Massachusetts 25 Worcester 027 4.5 4.1 4.5 3.8 3.1 2.4 2.9 Michigan 26 Ken t 081 3.8 3.8 4.0 3.4 2.8 2.5 2.3 Michigan 26 Macomb 099 3.5 2.4 2.6 3.3 3.1 2.6 2.6 Michigan 26 Oakland 125 4.0 4.1 3.7 2.8 3.4 3.0 2.5 Michigan 26 Wayne 163 5.3 5.8 4.9 3.6 3.8 3.7 2.9 Minnesota 27 Dakota 037 1.2 1.5 1.3 1.0 0.9 0.8 0.6 Minnesota 27 Hennepin 053 4.1 4.6 4.0 4.0 3.7 2.6 2.9 Minnesota 27 Ramsey 123 6.8 6.4 8.0 4.8 4.9 5.0 4.1 Minnesota 27 Saint Louis 137 3.8 3.4 2.5 2.7 2.4 2.6 2.6 Mississippi 28 Hinds 049 5.9 4.1 4.8 3.8 3.3 3.3 2.9 Missouri 29 Jackson 095 4.8 5.0 7.9 7.5 4.5 2.6 3.1 Missouri 29 Saint Louis 189 4.1 4.1 3.9 3.8 2.6 2.2 1.5 Missouri 29 St. Louis Cit y 510 4.9 5.1 5.6 8.1 3.8 4.1 3.3 Nevada 32 Clark 003 10.0 8.5 7.9 6.6 6.3 6.0 6.0 Nevada 32 Washoe 031 8.6 7.0 6.8 6.3 5.6 5.5 4.0 New Hampshire 33 Hillsborough 011 9.0 6.7 6.0 5.1 4.5 3.4 4.6 New Jerse y 34 Bergen 003 4.9 4.3 4.0 3.9 3.1 3.1 2.7 New Jerse y 34 Camden 007 4.6 4.6 4.5 3.2 2.8 2.7 3.5 New Jerse y 34 Hudson 017 9.1 8.1 4.2 4.2 4.0 3.4 3.6 New Jerse y 34 Middlese x 023 4.4 4.0 4.1 3.5 2.8 2.9 2.7 New Jerse y 34 Morris 027 5.6 4.5 4.4 3.8 3.4 2.5 2.4 New Jerse y 34 Union 039 7.9 6.7 6.0 5.8 5.0 4.5 4.1 New Mexico 35 Bernalillo 001 7.3 5.8 7.7 5.4 4.4 4.3 3.9 New Yor k 36 A lban y 001 1.7 1.6 1.7 1.7 1.5 1.6 1.2 New Yor k 36 Bronx 005 4.8 3.5 3.9 3.4 2.9 2.2 2.5 New Yor k 36 Erie 029 3.3 3.3 2.7 2.7 2.8 2.1 2.1 New Yor k 36 Kings 047 5.8 5.6 4.8 4.5 3.4 3.5 3.4 New Yor k 36 Monroe 055 4.7 3.3 3.5 2.8 2.5 2.8 2.2 New Yor k 36 New Yor k 061 5.3 5.5 4.5 3.9 3.2 2.6 2.0 New Yor k 36 Niagara 063 2.5 2.6 2.1 1.9 2.6 2.2 2.2 New Yor k 36 Onondaga 067 5.0 3.6 2.7 3.0 2.6 2.5 2.4 New Yor k 36 Queens 081 3.3 3.4 3.8 2.8 3.2 2.5 2.1 New Yor k 36 Suffolk 103 3.4 2.9 2.6 2.5 2.1 2.1 North Carolina 37 Forsyth 067 4.6 5.1 5.6 5.5 4.4 3.7 3.0 North Carolina 37 Mecklenburg 119 6.2 7.7 6.7 5.1 3.7 3.3 2.7 North Carolina 37 Wake 183 6.2 6.3 6.2 4.6 4.3 3.4 3.4 Ohio 39 Cuyahoga 035 5.5 5.5 5.3 4.0 4.7 11.6 5.0 Ohio 39 Franklin 049 3.7 4.6 3.4 3.0 3.8 2.7 2.6 Ohio 39 Hamilton 061 3.6 3.9 3.1 3.3 2.8 4.9 2.4 Ohio 39 Lake 085 2.0 2.1 2.0 2.5 2.7 1.6 2.0 Ohio 39 Montgomer y 113 4.0 4.6 3.2 2.6 3.4 3.7 2.3 Ohio 39 Stark 151 3.2 3.2 2.8 3.0 2.8 3.2 3.3 Ohio 39 Summit 153 4.1 4.7 4.2 3.3 3.7 3.2 2.6 Oklahoma 40 Oklahoma 109 5.0 5.1 4.7 3.9 3.4 2.6 2.9 Oklahoma 40 Tulsa 143 5.0 5.2 6.3 4.4 3.6 2.1 1.8 Oregon 41 Lane 039 6.5 6.0 5.4 5.1 4.9 4.5 4.8

B - 40126County-- January 1st 1999 through December 31st, 2005 (Study area and time period for Bell et al., 2009 ) Oregon 41 Multnomah 051 10.4 6.0 6.3 5.4 5.2 5.1 4.5 Pennsylvani a 42 A lleghen y 003 5.6 4.4 4.0 3.9 3.3 2.8 2.5 Pennsylvani a 42 Berks 011 3.8 3.4 3.2 3.2 2.2 2.4 2.3 Pennsylvani a 42 Dauphin 043 3.8 3.1 3.5 3.0 2.2 2.1 1.7 Pennsylvani a 42 Erie 049 9.1 10.1 6.7 6.8 6.3 1.7 2.3 Pennsylvani a 42 Lackawanna 069 2.7 3.1 2.8 2.6 2.3 2.6 2.2 Pennsylvani a 42 Lancaster 071 3.0 2.3 2.6 2.8 2.2 2.4 2.2 Pennsylvani a 42 Northampton 095 3.7 3.3 2.7 2.3 1.9 2.0 2.1 Pennsylvani a 42 Philadelphia 101 6.4 4.7 5.9 4.0 4.7 4.6 3.7 Pennsylvani a 42 York 133 4.1 3.2 3.2 2.8 2.5 2.6 2.4 Rhode Island 44 Providence 007 6.5 4.5 5.2 3.5 3.3 3.2 3.0 South Carolina 45 Charleston 019 5.0 3.9 3.9 3.5 3.0 2.3 2.3 South Carolina 45 Greenville 045 5.5 4.1 4.5 4.0 3.9 3.3 2.7 South Carolina 45 Richland 079 4.2 4.2 3.8 3.3 2.7 2.6 2.4 Tennessee 47 Davidson 037 7.1 6.6 6.6 5.3 4.7 4.2 3.8 Tennessee 47 Shelb y 157 6.6 5.5 5.5 4.7 4.1 4.6 3.6 Texas 48 Bexar 029 5.3 3.7 4.4 3.5 3.5 3.1 3.6 Texas 48 Cameron 061 4.2 2.5 2.2 3.5 2.8 2.5 2.4 Texas 48 Dallas 113 3.8 3.0 3.4 3.2 2.5 2.3 2.7 Texas 48 El Paso 141 14.2 15.6 12.7 12.4 10.4 10.0 10.3 Texas 48 Harris 201 6.0 4.7 7.1 4.2 4.1 3.5 3.0 Texas 48 Tarrant 439 4.5 3.1 3.9 3.3 3.0 2.3 6.3 Texas 48 Travis 453 1.7 1.5 1.4 1.4 1.2 0.9 0.9 Utah 49 Salt Lake 035 9.7 10.0 6.5 6.2 8.2 5.4 5.5 Virginia 51 Fairfax 059 4.5 4.5 4.0 2.9 3.0 2.6 2.5 Virginia 51 Norfolk Cit y 710 5.3 5.8 5.7 5.1 4.3 3.7 2.2 Washington 53 Clark 011 8.8 7.8 7.1 6.6 6.5 5.6 5.9 Washington 53 King 033 7.8 7.8 6.6 6.3 6.9 4.4 5.0 Washington 53 Pierce 053 9.7 6.7 5.9 5.3 6.6 4.9 4.9 Washington 53 Spokane 063 7.8 8.3 6.8 7.1 7.3 5.6 6.2 Wisconsin 55 Milwaukee 079 3.0 3.3 3.6 3.2 3.3 4.2 7.7

Maxperyea r 26.4 18.5 31.8 15.9 10.4 14.1 16.1 31.8 Total Ma x Minperyea r 1.2 1.5 1.3 1.0 0.9 0.8 0.6 0.6 Total Min

B - 41126County-- January 1st 1999 through December 31st, 2005 (Study area and time period for Bell et al., 2009 )

STATENAME fips COUNTYNAME fips 1999 2000 2001 2002 2003 2004 2005 A labama 01 Jefferson 073 2.3 2.4 2.4 1.9 1.3 1.1 1.5 A rizona 04 Maricopa 013 5.9 4.4 3.6 4.5 3.2 2.6 2.1 A rizona 04 Pima 019 3.5 3.2 2.5 2.2 1.8 1.7 1.5 A rkansas 05 Pulaski 119 2.0 1.8 1.3 0.9 0.8 0.6 0.7 California 06 A lameda 001 1.2 1.1 2.0 1.0 1.9 0.7 0.7 California 06 Contra Costa 013 1.0 1.0 0.8 1.2 0.9 0.9 0.6 California 06 Fresno 019 2.8 1.6 1.0 0.9 1.0 0.7 0.7 California 06 Kern 029 1.4 1.4 1.5 1.3 1.1 1.1 1.0 California 06 Los Angeles 037 3.1 2.7 2.2 2.5 2.0 2.4 1.6 California 06 Riverside 065 2.4 2.2 2.0 1.7 1.4 1.3 1.2 California 06 Sacramento 067 1.3 1.3 1.5 1.1 1.4 1.0 1.1 California 06 San Bernardino 071 1.7 1.3 1.4 1.4 1.4 1.2 1.2 California 06 San Diego 073 4.7 1.9 3.4 1.6 1.6 1.6 1.8 California 06 San Francisco 075 1.4 1.3 1.3 1.2 1.2 1.1 1.0 California 06 San Joaquin 077 1.0 1.0 1.0 1.0 1.0 0.7 0.7 California 06 San Mateo 081 1.4 1.5 1.3 1.2 1.1 1.0 1.0 California 06 Santa Clara 085 1.6 1.4 1.8 3.5 1.1 1.0 0.9 California 06 Stanislaus 099 1.0 0.8 0.7 0.7 0.7 0.6 0.6 Colorado 08 A dams 001 1.6 1.3 1.4 1.2 1.1 1.1 1.0 Colorado 08 Denve r 031 2.7 2.3 2.1 1.7 1.5 1.3 1.3 Connecticut 09 Fairfield 001 1.8 1.6 1.5 1.5 1.4 1.1 1.2 Connecticut 09 Hartford 003 2.3 2.3 2.8 2.9 2.8 2.3 2.2 Connecticut 09 New Haven 009 1.1 1.1 1.0 1.0 1.0 0.8 1.2 Delaware 10 New Castle 003 1.0 1.0 0.8 0.7 0.7 0.7 0.7

District Of Columbia 11 District of Columbia 001 1.7 1.7 1.7 1.6 1.4 1.2 1.2 Florida 12 Broward 011 1.8 1.5 1.3 1.3 1.3 1.6 1.1 Florida 12 Duval 031 1.5 1.3 1.4 1.4 1.4 1.2 0.7 Florida 12 Hillsborough 057 2.6 2.3 2.2 1.9 1.9 1.9 1.6 Florida 12 Miami-Dade 086 1.6 1.4 1.2 1.3 2.1 1.9 0.9 Florida 12 Orange 095 1.8 1.4 1.3 1.4 1.3 1.0 0.8 Florida 12 Palm Beach 099 1.7 1.4 0.3 0.5 1.4 1.1 1.0 Florida 12 Pinellas 103 1.7 1.6 1.4 1.3 1.3 1.2 1.0 Georgia 13 DeKalb 089 1.2 1.1 1.3 0.9 1.0 0.9 1.0 Georgia 13 Fulton 121 1.7 1.6 1.4 1.2 1.2 1.0 1.0 Hawaii 15 Honolulu 003 1.3 1.2 1.1 1.6 1.2 1.2 0.9 Idaho 16 A da 001 2.4 2.2 2.1 1.9 1.8 1.6 1.4 Illinois 17 Cook 031 3.1 2.6 2.4 2.4 2.0 2.1 1.4 Illinois 17 Winnebago 201 1.9 1.7 1.6 1.5 1.1 0.9 1.0 Indiana 18 A llen 003 1.5 1.3 1.2 1.3 1.2 1.2 1.0 Indiana 18 Marion 097 1.9 1.7 1.7 1.4 1.3 1.3 1.2 Iowa 19 Polk 153 1.5 1.1 1.3 1.4 1.2 1.1 0.7 Kansas 20 Sedgwick 173 1.3 1.6 1.2 1.2 0.8 0.8 1.1 Kentuck y 21 Jefferson 111 2.4 1.4 1.4 1.5 1.4 1.3 1.1 Louisiana 22 East Baton Rouge 033 1.3 1.1 1.1 1.0 0.9 0.8 0.6 Louisiana 22 Orleans 071 1.6 1.5 1.4 1.1 1.4 1.3 1.2 Maryland 24 Baltimore (City) 510 2.5 0.9 1.0 0.9 0.9 0.9 0.8 Massachusetts 25 Hampden 013 1.7 1.7 1.7 1.5 1.7 0.7 0.6 1-hour - 50th percentile daily maximum (of all 365 possible daily

B - 42126County-- January 1st 1999 through December 31st, 2005 (Study area and time period for Bell et al., 2009 ) Massachusetts 25 Middlesex 017 1.2 1.0 0.8 0.7 0.7 0.5 0.5 Massachusetts 25 Suffolk 025 1.5 1.2 1.0 1.2 0.9 0.6 0.5 Massachusetts 25 Worcester 027 1.1 0.9 1.0 0.9 0.9 0.7 0.8 Michigan 26 Ken t 081 0.9 0.8 0.6 0.6 0.6 0.6 0.6 Michigan 26 Macomb 099 0.7 0.3 0.3 0.3 0.6 0.6 0.7 Michigan 26 Oakland 125 0.7 0.6 0.6 0.3 0.7 0.6 0.5 Michigan 26 Wayne 163 1.4 1.3 0.9 0.8 0.8 0.8 0.7 Minnesota 27 Dakota 037 0.5 0.3 0.3 0.3 0.3 0.3 0.3 Minnesota 27 Hennepin 053 1.5 1.4 1.1 1.1 0.8 0.6 0.6 Minnesota 27 Ramsey 123 2.4 2.0 1.9 1.5 1.3 1.4 1.2 Minnesota 27 Saint Louis 137 1.1 0.9 0.8 0.9 0.8 0.7 0.7 Mississippi 28 Hinds 049 0.5 0.6 0.7 0.6 0.7 0.6 0.6 Missouri 29 Jackson 095 1.6 1.6 1.1 1.2 1.2 0.7 0.8 Missouri 29 Saint Louis 189 1.3 1.0 1.1 1.0 0.9 0.8 0.7 Missouri 29 St. Louis Cit y 510 1.4 1.2 0.9 1.0 1.0 0.8 0.7 Nevada 32 Clark 003 3.4 3.5 2.7 3.2 2.3 2.1 2.0 Nevada 32 Washoe 031 2.8 2.8 2.4 2.5 2.1 1.9 1.6 New Hampshire 33 Hillsborough 011 2.0 1.1 1.2 0.9 1.2 1.2 1.0 New Jerse y 34 Bergen 003 2.4 2.0 2.1 1.7 1.4 1.2 1.1 New Jerse y 34 Camden 007 0.8 0.8 0.9 0.8 0.8 0.7 0.6 New Jerse y 34 Hudson 017 3.4 3.1 1.9 1.9 1.9 1.8 1.7 New Jerse y 34 Middlese x 023 1.9 1.5 1.4 1.5 1.1 0.9 1.0 New Jerse y 34 Morris 027 2.0 1.8 1.5 1.3 1.1 1.0 0.9 New Jerse y 34 Union 039 2.5 2.3 1.9 1.7 1.8 1.5 1.4 New Mexico 35 Bernalillo 001 2.1 1.9 1.9 1.8 1.3 1.2 1.2 New Yor k 36 A lban y 001 0.5 0.6 0.5 0.6 0.7 0.6 0.5 New Yor k 36 Bronx 005 1.0 1.0 1.0 0.9 1.0 0.9 0.8 New Yor k 36 Erie 029 1.0 0.9 0.8 0.7 0.8 0.6 0.6 New Yor k 36 Kings 047 2.5 2.9 1.9 1.7 1.8 1.6 1.4 New Yor k 36 Monroe 055 1.0 0.9 0.8 0.8 0.8 0.7 0.6 New Yor k 36 New Yor k 061 2.8 2.4 2.0 1.5 1.5 1.2 0.9 New Yor k 36 Niagara 063 0.6 0.5 0.5 0.5 0.5 0.3 0.3 New Yor k 36 Onondaga 067 0.9 1.0 0.9 0.9 1.0 0.8 0.8 New Yor k 36 Queens 081 1.0 0.9 1.0 0.9 0.9 0.8 0.8 New Yor k 36 Suffolk 103 0.5 0.3 0.3 0.3 0.3 0.3 North Carolina 37 Forsyth 067 1.7 1.7 1.6 1.4 1.4 1.2 1.2 North Carolina 37 Mecklenburg 119 1.8 1.5 1.2 1.3 0.8 0.8 0.8 North Carolina 37 Wake 183 2.1 2.1 2.4 1.9 1.8 1.7 1.4 Ohio 39 Cuyahoga 035 2.0 1.8 1.8 1.3 1.4 1.3 1.3 Ohio 39 Franklin 049 1.1 1.0 0.9 1.1 1.2 1.0 0.8 Ohio 39 Hamilton 061 1.4 1.3 1.2 1.1 1.0 0.9 0.8 Ohio 39 Lake 085 0.8 0.8 0.8 1.0 1.5 0.7 0.7 Ohio 39 Montgomer y 113 1.0 1.1 1.0 0.9 0.8 1.0 0.6 Ohio 39 Stark 151 1.0 0.7 0.9 0.9 0.3 0.7 1.0 Ohio 39 Summit 153 1.5 1.5 1.5 1.3 1.2 1.0 0.9 Oklahoma 40 Oklahoma 109 1.6 1.4 1.2 1.1 1.1 0.7 0.6 Oklahoma 40 Tulsa 143 1.4 1.2 1.2 1.3 1.3 0.7 0.8 Oregon 41 Lane 039 2.1 2.1 1.9 1.8 1.5 1.5 1.4 Oregon 41 Multnomah 051 3.1 2.9 2.4 2.3 2.2 1.9 1.9 Pennsylvani a 42 A lleghen y 003 1.7 1.6 1.3 0.8 0.8 0.9 0.8

B - 43126County-- January 1st 1999 through December 31st, 2005 (Study area and time period for Bell et al., 2009 ) Pennsylvani a 42 Berks 011 0.8 0.7 0.9 0.8 0.7 0.7 0.8 Pennsylvani a 42 Dauphin 043 0.8 0.8 0.7 0.8 0.7 0.7 0.6 Pennsylvani a 42 Erie 049 1.2 1.4 1.0 0.8 0.8 0.5 0.7 Pennsylvani a 42 Lackawanna 069 0.3 0.8 0.9 0.3 0.3 0.5 0.5 Pennsylvani a 42 Lancaster 071 0.5 0.5 0.7 0.8 0.6 0.6 0.5 Pennsylvani a 42 Northampton 095 0.6 0.7 0.5 0.5 0.3 0.5 0.3 Pennsylvani a 42 Philadelphia 101 1.8 1.6 1.5 1.3 1.4 1.2 1.1 Pennsylvani a 42 York 133 0.6 0.7 0.7 0.6 0.5 0.7 0.3 Rhode Island 44 Providence 007 1.9 1.7 1.5 1.4 1.2 1.1 1.0 South Carolina 45 Charleston 019 1.2 1.0 1.0 0.8 0.8 0.6 1.0 South Carolina 45 Greenville 045 1.3 1.1 1.0 0.9 0.8 0.8 0.5 South Carolina 45 Richland 079 1.7 1.5 1.3 1.2 1.1 0.9 0.9 Tennessee 47 Davidson 037 2.4 1.8 1.7 1.5 1.6 1.4 1.4 Tennessee 47 Shelb y 157 2.0 1.9 1.3 1.3 1.1 1.0 0.8 Texas 48 Bexar 029 1.4 0.9 0.9 0.8 0.9 0.8 0.8 Texas 48 Cameron 061 0.7 0.7 0.6 0.6 0.7 0.5 0.6 Texas 48 Dallas 113 0.6 0.7 0.6 0.6 0.6 0.6 0.6 Texas 48 El Paso 141 4.2 2.5 2.0 1.7 1.6 2.3 1.5 Texas 48 Harris 201 1.4 1.0 1.3 1.0 1.1 0.8 0.8 Texas 48 Tarrant 439 1.2 0.8 0.8 0.6 0.6 0.6 0.6 Texas 48 Travis 453 0.5 0.5 0.5 0.5 0.3 0.3 0.3 Utah 49 Salt Lake 035 3.5 2.9 2.4 2.5 2.1 2.1 1.9 Virginia 51 Fairfax 059 1.2 1.1 1.2 0.8 0.9 0.8 0.9 Virginia 51 Norfolk Cit y 710 1.3 0.9 0.9 0.8 0.7 0.5 1.0 Washington 53 Clark 011 2.2 2.2 2.7 1.8 1.6 1.5 1.5 Washington 53 King 033 3.0 2.8 2.6 2.1 2.1 1.8 1.7 Washington 53 Pierce 053 1.8 2.1 1.8 1.5 1.4 1.4 1.3 Washington 53 Spokane 063 3.5 3.2 2.9 2.8 2.7 2.3 2.1 Wisconsin 55 Milwaukee 079 1.0 0.7 0.9 0.9 0.8 0.8 0.7

Maxperyea r 5.9 4.4 3.6 4.5 3.2 2.6 2.2 5.9 Total Ma x Minperyea r 0.3 0.3 0.3 0.3 0.3 0.3 0.3 0.3 Total Min

B - 44126County-- January 1st 1999 through December 31st, 2005 (Study area and time period for Bell et al., 2009 )

STATENAME fips COUNTYNAME fips 1999 2000 2001 2002 2003 2004 2005 A labama 01 Jefferson 073 15.8 14.5 18.9 10.7 3.9 7.7 8.5 A rizona 04 Maricopa 013 10.0 7.0 5.9 5.5 5.2 4.3 4.6 A rizona 04 Pima 019 3.5 4.1 2.8 3.3 2.8 2.4 2.3 A rkansas 05 Pulaski 119 3.6 2.7 2.2 4.9 2.2 1.6 1.6 California 06 A lameda 001 4.3 2.9 3.4 4.4 4.3 2.3 1.9 California 06 Contra Costa 013 3.0 2.4 2.4 2.4 1.7 1.7 1.6 California 06 Fresno 019 6.9 5.9 4.1 4.0 3.4 2.7 2.7 California 06 Kern 029 3.7 5.1 3.1 2.3 2.2 2.2 2.0 California 06 Los Angeles 037 10.7 9.4 6.8 7.9 6.7 5.3 4.7 California 06 Riverside 065 3.7 4.2 3.5 3.3 2.9 2.6 2.2 California 06 Sacramento 067 6.1 5.6 4.3 4.1 3.7 3.2 3.6 California 06 San Bernardino 071 3.7 3.6 3.0 3.0 3.3 2.5 2.1 California 06 San Diego 073 5.1 4.6 4.5 3.6 4.3 3.6 4.4 California 06 San Francisco 075 4.0 2.6 2.8 2.2 2.3 2.2 2.3 California 06 San Joaquin 077 5.4 5.5 3.4 2.9 3.0 2.2 2.3 California 06 San Mateo 081 3.6 3.3 3.1 2.6 2.2 1.9 2.1 California 06 Santa Clara 085 5.6 5.1 4.7 4.5 3.4 2.8 2.9 California 06 Stanislaus 099 6.1 5.1 4.3 3.4 3.2 2.7 2.5 Colorado 08 A dams 001 3.4 2.8 3.1 2.5 2.8 2.8 2.0 Colorado 08 Denve r 031 4.7 4.6 4.1 3.6 4.0 3.9 2.3 Connecticut 09 Fairfield 001 3.7 2.9 2.9 2.9 2.4 2.2 2.4 Connecticut 09 Hartford 003 4.8 5.6 4.1 5.1 5.0 4.7 3.8 Connecticut 09 New Haven 009 3.1 2.6 2.3 2.1 1.9 1.9 1.9 Delaware 10 New Castle 003 2.8 2.5 2.4 2.0 2.2 2.0 1.9

District Of Columbia 11 District of Columbia 001 5.1 4.2 4.0 3.9 4.0 3.0 3.1 Florida 12 Broward 011 4.5 3.5 3.6 3.4 3.1 2.7 2.7 Florida 12 Duval 031 3.2 3.0 2.7 2.5 2.4 2.2 1.9 Florida 12 Hillsborough 057 3.3 3.1 2.8 3.2 3.1 2.4 2.8 Florida 12 Miami-Dade 086 3.6 2.9 3.8 3.0 3.5 4.7 2.0 Florida 12 Orange 095 2.7 2.4 2.1 2.4 1.9 1.6 1.7 Florida 12 Palm Beach 099 2.5 2.7 1.9 2.0 1.8 2.1 2.1 Florida 12 Pinellas 103 2.5 2.2 2.2 2.2 1.6 1.6 1.5 Georgia 13 DeKalb 089 3.8 3.0 2.8 2.5 2.5 2.4 2.0 Georgia 13 Fulton 121 3.0 2.4 2.3 2.2 2.1 2.0 1.7 Hawaii 15 Honolulu 003 2.1 2.0 1.6 2.1 1.9 1.9 1.5 Idaho 16 Ada 001 4.4 2.9 2.8 3.0 3.1 2.3 2.1 Illinois 17 Cook 031 4.7 4.3 3.6 3.6 3.3 3.1 2.3 Illinois 17 Winnebago 201 3.5 2.8 2.4 2.2 2.1 2.1 1.9 Indiana 18 Allen 003 3.3 3.3 2.6 3.1 2.2 2.4 2.0 Indiana 18 Marion 097 2.6 3.8 2.1 4.4 2.3 1.9 2.0 Iowa 19 Polk 153 3.5 3.6 2.9 2.7 2.2 2.3 2.0 Kansas 20 Sedgwick 173 4.0 6.2 3.6 3.2 2.5 2.8 2.8 Kentucky 21 Jefferson 111 4.8 3.4 3.6 3.9 3.0 3.1 2.5 Louisiana 22 East Baton Rouge 033 4.2 3.4 3.6 2.8 2.4 2.3 1.7 Louisiana 22 Orleans 071 3.0 3.4 3.2 3.3 2.6 3.3 1.7 8-hour - 99th percentile daily maximum (of all 365 possible daily 8-hour maximum averages)

B - 45126County-- January 1st 1999 through December 31st, 2005 (Study area and time period for Bell et al., 2009 ) Maryland 24 Baltimore (City) 510 8.0 3.0 2.9 2.8 2.4 2.5 2.1 Massachusetts 25 Hampden 013 4.0 3.8 2.8 3.4 2.8 2.5 2.5 Massachusetts 25 Middlesex 017 3.7 3.0 2.6 2.2 2.6 1.6 1.5 Massachusetts 25 Suffolk 025 3.8 2.2 2.8 2.0 2.3 1.4 2.1 Massachusetts 25 Worcester 027 2.7 2.4 2.5 2.9 1.7 1.8 2.1 Michigan 26 Kent 081 3.1 2.3 2.6 2.6 2.0 1.6 1.6 Michigan 26 Macomb 099 2.0 0.9 1.9 2.1 2.0 1.9 1.9 Michigan 26 Oakland 125 2.6 2.6 3.0 1.9 2.3 2.1 1.4 Michigan 26 Wayne 163 3.8 3.2 2.9 2.6 2.6 2.3 1.8 Minnesota 27 Dakota 037 1.0 1.3 1.0 0.7 0.7 0.6 0.4 Minnesota 27 Hennepin 053 2.8 2.5 2.4 2.8 1.9 1.6 1.5 Minnesota 27 Ramsey 123 4.8 4.5 4.7 3.6 3.3 2.7 2.4 Minnesota 27 Saint Louis 137 2.4 2.1 1.6 1.8 1.6 1.5 1.5 Mississippi 28 Hinds 049 4.8 2.7 4.0 2.7 2.3 2.3 2.2 Missouri 29 Jackson 095 3.3 2.9 3.4 3.2 2.1 2.1 2.2 Missouri 29 Saint Louis 189 2.6 2.8 2.6 2.2 2.0 1.6 1.2 Missouri 29 St. Louis City 510 3.7 3.8 4.1 7.7 2.5 2.8 2.2 Nevada 32 Clark 003 7.6 6.2 6.2 5.8 5.2 5.0 5.1 Nevada 32 Washoe 031 6.4 4.9 4.9 4.2 3.8 3.6 3.0 New Hampshire 33 Hillsborough 011 4.9 4.0 3.9 3.7 3.9 2.8 3.2 New Jersey 34 Bergen 003 4.0 3.3 2.9 3.3 2.4 2.6 2.1 New Jerse y 34 Camden 007 3.1 3.6 2.8 2.0 1.7 2.3 2.5 New Jerse y 34 Hudson 017 5.8 5.2 2.9 2.7 2.8 2.7 2.6 New Jerse y 34 Middlese x 023 3.4 3.1 2.8 2.6 1.8 2.1 1.9 New Jerse y 34 Morris 027 3.9 3.0 3.1 2.3 2.1 1.7 1.6 New Jerse y 34 Union 039 6.2 4.3 4.4 3.6 3.2 2.9 3.1 New Mexico 35 Bernalillo 001 4.6 3.7 4.0 3.8 3.4 3.3 2.9 New Yor k 36 A lban y 001 1.3 1.1 1.1 1.2 1.3 1.0 0.9 New Yor k 36 Bronx 005 3.6 3.3 2.6 1.9 2.0 1.8 1.7 New Yor k 36 Erie 029 2.1 1.8 1.8 1.6 1.8 1.3 1.5 New Yor k 36 Kings 047 4.7 4.0 3.2 3.3 2.5 2.4 2.2 New Yor k 36 Monroe 055 2.5 2.4 1.8 1.9 1.9 1.6 1.8 New Yor k 36 New Yor k 061 4.4 3.8 3.1 2.9 2.6 2.1 1.5 New Yor k 36 Niagara 063 1.4 1.4 1.3 1.5 1.4 1.3 1.4 New Yor k 36 Onondaga 067 3.0 2.3 2.0 1.8 1.7 1.4 1.8 New Yor k 36 Queens 081 2.4 3.2 3.0 2.3 2.3 1.7 1.6 New Yor k 36 Suffolk 103 2.2 2.1 1.8 1.6 1.6 1.4 North Carolina 37 Forsyth 067 3.4 3.6 4.0 3.9 3.4 2.9 2.4 North Carolina 37 Mecklenburg 119 3.8 4.3 4.2 3.0 2.7 2.5 2.0 North Carolina 37 Wake 183 4.7 5.2 3.7 3.1 2.9 2.7 2.4 Ohio 39 Cuyahoga 035 3.6 6.6 3.0 2.1 2.6 4.7 2.8 Ohio 39 Franklin 049 2.2 2.6 2.4 1.9 2.3 1.9 1.8 Ohio 39 Hamilton 061 2.7 2.3 2.4 2.4 1.8 2.2 1.7 Ohio 39 Lake 085 1.4 1.4 1.4 2.1 2.6 1.2 1.3 Ohio 39 Montgomer y 113 2.6 2.4 2.0 1.7 2.1 3.2 1.7 Ohio 39 Stark 151 2.1 2.4 1.8 2.5 1.9 2.5 2.4 Ohio 39 Summit 153 2.5 2.4 2.3 2.0 2.1 1.9 1.6 Oklahoma 40 Oklahoma 109 4.0 3.8 3.2 2.8 2.6 2.0 2.0 Oklahoma 40 Tulsa 143 3.3 3.3 4.0 2.9 3.0 1.6 1.3 Oregon 41 Lane 039 4.5 4.2 4.0 4.1 3.3 3.4 2.7

B - 46126County-- January 1st 1999 through December 31st, 2005 (Study area and time period for Bell et al., 2009 ) Oregon 41 Multnomah 051 6.2 5.2 4.1 4.5 4.0 4.1 3.1 Pennsylvani a 42 A lleghen y 003 3.5 3.2 2.6 2.6 2.2 2.3 2.0 Pennsylvani a 42 Berks 011 2.5 1.8 1.9 1.9 1.9 1.7 1.7 Pennsylvani a 42 Dauphin 043 2.5 2.1 2.6 2.0 1.5 1.3 1.3 Pennsylvani a 42 Erie 049 5.3 5.2 4.1 3.8 3.2 1.2 1.4 Pennsylvani a 42 Lackawanna 069 1.7 2.0 1.7 1.4 1.4 1.6 1.5 Pennsylvani a 42 Lancaster 071 2.0 1.8 1.8 2.0 1.6 1.5 1.3 Pennsylvani a 42 Northampton 095 2.5 2.3 1.9 1.6 1.3 1.6 1.8 Pennsylvani a 42 Philadelphia 101 4.0 3.4 3.9 2.5 3.8 3.1 3.3 Pennsylvani a 42 York 133 2.2 1.8 1.9 2.1 1.5 1.6 1.2 Rhode Island 44 Providence 007 3.7 3.3 3.1 2.6 2.2 2.2 2.3 South Carolina 45 Charleston 019 3.2 2.6 2.6 2.5 2.3 1.7 1.6 South Carolina 45 Greenville 045 4.1 3.4 3.0 3.1 2.8 2.4 2.1 South Carolina 45 Richland 079 3.3 3.2 3.0 2.5 2.1 2.1 1.9 Tennessee 47 Davidson 037 5.3 5.0 5.6 4.4 3.6 3.6 3.1 Tennessee 47 Shelb y 157 4.7 4.2 4.5 3.5 3.2 3.0 2.5 Texas 48 Bexar 029 3.5 2.6 2.5 2.4 2.3 1.6 2.1 Texas 48 Cameron 061 2.5 1.5 1.2 1.8 1.7 1.2 1.3 Texas 48 Dallas 113 2.4 2.0 2.2 2.0 1.8 1.8 2.2 Texas 48 El Paso 141 8.8 8.8 8.0 6.2 5.9 5.4 5.1 Texas 48 Harris 201 3.5 3.3 3.6 2.9 2.9 2.5 2.5 Texas 48 Tarrant 439 2.6 2.1 2.3 2.0 1.5 1.5 2.5 Texas 48 Travis 453 1.1 1.0 0.9 0.9 0.7 0.5 0.6 Utah 49 Salt Lake 035 5.7 5.2 4.5 3.7 4.3 3.5 3.4 Virginia 51 Fairfax 059 3.0 3.4 2.9 2.0 2.5 2.0 1.8 Virginia 51 Norfolk Cit y 710 3.9 3.8 3.9 3.7 2.4 2.7 1.3 Washington 53 Clark 011 6.0 6.1 4.2 5.3 4.4 4.2 4.5 Washington 53 King 033 6.1 6.1 6.2 4.6 5.8 3.3 3.8 Washington 53 Pierce 053 6.4 5.1 4.4 4.3 4.8 3.3 3.9 Washington 53 Spokane 063 5.3 5.5 4.5 4.9 4.4 3.9 4.5 Wisconsin 55 Milwaukee 079 2.1 2.3 1.8 2.4 2.0 2.1 3.8

Maxperyea r 15.8 14.5 18.9 10.7 6.7 7.7 8.5 18.9 Total Ma x Minperyea r 1.0 0.9 0.9 0.7 0.7 0.5 0.4 0.4 Total Min

B - 47126County-- January 1st 1999 through December 31st, 2005 (Study area and time period for Bell et al., 2009 )

STATENAME fips COUNTYNAME fips 1999 2000 2001 2002 2003 2004 2005 A labama 01 Jefferson 073 1.7 1.7 1.6 1.5 0.8 0.8 0.9 A rizona 04 Maricopa 013 4.2 2.8 2.4 3.1 2.0 1.5 1.3 A rizona 04 Pima 019 2.0 1.8 1.6 1.4 1.2 1.2 1.1 A rkansas 05 Pulaski 119 1.7 1.5 1.1 0.6 0.6 0.5 0.5 California 06 A lameda 001 0.9 0.9 1.2 0.7 1.1 0.5 0.6 California 06 Contra Costa 013 0.7 0.8 0.6 0.9 0.6 0.8 0.4 California 06 Fresno 019 2.2 1.0 0.7 0.7 1.0 0.5 0.5 California 06 Kern 029 0.9 1.0 1.1 0.9 0.8 0.7 0.7 California 06 Los Angeles 037 2.2 2.0 1.6 1.6 1.4 1.6 1.1 California 06 Riverside 065 1.7 1.6 1.4 1.2 1.0 1.0 0.9 California 06 Sacramento 067 1.0 0.9 1.2 0.9 1.1 0.9 0.9 California 06 San Bernardino 071 1.2 1.0 1.0 1.1 1.2 0.9 0.9 California 06 San Diego 073 3.2 1.3 2.3 1.1 1.2 1.2 1.5 California 06 San Francisco 075 1.2 1.0 1.1 0.9 0.9 0.9 0.8 California 06 San Joaquin 077 0.7 0.7 0.6 0.6 0.7 0.6 0.5 California 06 San Mateo 081 0.9 1.0 0.8 0.8 0.7 0.7 0.6 California 06 Santa Clara 085 1.1 1.1 1.0 2.3 0.8 0.7 0.7 California 06 Stanislaus 099 0.7 0.6 0.5 0.5 0.5 0.4 0.4 Colorado 08 A dams 001 1.0 0.8 0.9 0.7 0.7 0.8 0.7 Colorado 08 Denve r 031 1.8 1.6 1.4 1.1 1.0 0.9 0.9 Connecticut 09 Fairfield 001 1.4 1.2 1.2 1.2 1.1 0.9 0.9 Connecticut 09 Hartford 003 1.8 1.7 2.2 2.4 2.2 2.0 1.8 Connecticut 09 New Haven 009 0.9 0.9 0.8 0.8 0.8 0.7 1.1 Delaware 10 New Castle 003 0.7 0.8 0.6 0.6 0.5 0.5 0.6

District Of Columbia 11 District of Columbia 001 1.4 1.4 1.3 1.3 1.2 1.1 1.1 Florida 12 Broward 011 1.2 1.1 0.9 0.8 0.9 1.3 0.9 Florida 12 Duval 031 0.9 0.8 1.0 1.0 1.0 0.8 0.5 Florida 12 Hillsborough 057 1.8 1.6 1.5 1.3 1.3 1.4 1.3 Florida 12 Miami-Dade 086 1.2 1.1 1.0 1.0 1.7 1.6 0.8 Florida 12 Orange 095 1.4 1.0 0.9 1.0 1.0 0.7 0.6 Florida 12 Palm Beach 099 0.8 0.6 0.3 0.3 0.6 0.8 0.9 Florida 12 Pinellas 103 1.2 1.2 1.0 0.9 1.0 0.9 0.8 Georgia 13 DeKalb 089 0.9 0.7 0.9 0.8 0.8 0.7 0.7 Georgia 13 Fulton 121 1.3 1.2 1.0 0.9 1.0 0.8 0.8 Hawaii 15 Honolulu 003 1.0 0.9 0.9 1.3 1.0 1.0 0.7 Idaho 16 Ada 001 1.6 1.5 1.5 1.4 1.3 1.2 1.1 Illinois 17 Cook 031 2.5 2.1 2.0 2.0 1.7 1.7 1.1 Illinois 17 Winnebago 201 1.5 1.3 1.2 1.2 0.9 0.7 0.8 Indiana 18 Allen 003 1.1 1.0 0.9 1.0 1.0 1.1 0.9 Indiana 18 Marion 097 1.4 1.3 1.2 1.1 1.0 0.9 0.9 Iowa 19 Polk 153 1.2 0.9 1.2 1.2 1.0 1.0 0.6 Kansas 20 Sedgwick 173 0.9 1.2 1.0 0.9 0.5 0.5 0.9 Kentucky 21 Jefferson 111 1.8 1.0 1.1 1.3 1.2 1.1 0.9 Louisiana 22 East Baton Rouge 033 1.1 0.9 1.0 0.9 0.8 0.7 0.5 Louisiana 22 Orleans 071 1.1 1.1 1.0 0.8 1.1 1.0 1.0 Maryland 24 Baltimore (City) 510 1.6 0.7 0.7 0.7 0.7 0.7 0.6 8-hour - 50th percentile daily maximum (of all 365 possible daily 8-hour maximum averages)

B - 48126County-- January 1st 1999 through December 31st, 2005 (Study area and time period for Bell et al., 2009 ) Massachusetts 25 Hampden 013 1.3 1.2 1.2 1.2 1.0 0.6 0.4 Massachusetts 25 Middlesex 017 0.9 0.7 0.6 0.5 0.5 0.3 0.3 Massachusetts 25 Suffolk 025 1.2 0.9 0.8 1.0 0.8 0.4 0.4 Massachusetts 25 Worcester 027 0.8 0.7 0.8 0.7 0.7 0.5 0.7 Michigan 26 Kent 081 0.6 0.6 0.4 0.4 0.4 0.4 0.4 Michigan 26 Macomb 099 0.4 0.3 0.3 0.3 0.4 0.4 0.5 Michigan 26 Oakland 125 0.4 0.4 0.4 0.3 0.5 0.4 0.3 Michigan 26 Wayne 163 0.9 0.9 0.5 0.6 0.5 0.6 0.5 Minnesota 27 Dakota 037 0.3 0.3 0.3 0.3 0.3 0.3 0.3 Minnesota 27 Hennepin 053 1.1 1.1 0.8 0.9 0.5 0.4 0.4 Minnesota 27 Ramsey 123 1.8 1.6 1.4 1.1 0.9 0.9 0.8 Minnesota 27 Saint Louis 137 0.8 0.6 0.5 0.7 0.6 0.4 0.5 Mississippi 28 Hinds 049 0.4 0.4 0.4 0.4 0.5 0.4 0.4 Missouri 29 Jackson 095 1.2 1.1 0.8 0.8 0.8 0.6 0.7 Missouri 29 Saint Louis 189 1.0 0.8 0.8 0.8 0.8 0.7 0.6 Missouri 29 St. Louis City 510 1.2 0.9 0.8 0.8 0.8 0.6 0.4 Nevada 32 Clark 003 2.0 2.7 1.6 2.3 1.4 1.3 1.2 Nevada 32 Washoe 031 1.5 1.5 1.5 1.2 1.2 1.0 0.7 New Hampshire 33 Hillsborough 011 1.1 1.0 0.8 0.5 0.9 1.0 0.8 New Jersey 34 Bergen 003 2.0 1.7 1.8 1.4 1.1 1.0 0.9 New Jersey 34 Camden 007 0.6 0.7 0.7 0.6 0.7 0.6 0.5 New Jerse y 34 Hudson 017 2.4 2.2 1.5 1.5 1.5 1.5 1.4 New Jerse y 34 Middlese x 023 1.4 1.1 1.1 1.2 0.8 0.7 0.8 New Jerse y 34 Morris 027 1.5 1.4 1.2 1.0 0.9 0.8 0.7 New Jerse y 34 Union 039 1.9 1.8 1.5 1.3 1.3 1.2 1.1 New Mexico 35 Bernalillo 001 1.3 1.3 1.4 1.2 0.8 0.7 0.8 New Yor k 36 A lban y 001 0.3 0.4 0.4 0.4 0.6 0.5 0.3 New Yor k 36 Bronx 005 0.8 0.8 0.8 0.8 0.9 0.7 0.7 New Yor k 36 Erie 029 0.8 0.7 0.6 0.6 0.6 0.5 0.4 New Yor k 36 Kings 047 2.0 2.2 1.5 1.4 1.4 1.2 1.0 New Yor k 36 Monroe 055 0.8 0.7 0.6 0.6 0.7 0.7 0.5 New Yor k 36 New Yor k 061 2.3 2.0 1.7 1.3 1.3 1.1 0.8 New Yor k 36 Niagara 063 0.4 0.4 0.3 0.3 0.4 0.3 0.3 New Yor k 36 Onondaga 067 0.6 0.8 0.6 0.6 0.8 0.6 0.6 New Yor k 36 Queens 081 0.9 0.7 0.7 0.7 0.8 0.7 0.6 New Yor k 36 Suffolk 103 0.3 0.3 0.3 0.3 0.3 0.3 North Carolina 37 Forsyth 067 1.3 1.1 1.1 1.1 1.1 0.9 1.0 North Carolina 37 Mecklenburg 119 1.3 1.1 0.9 1.1 0.6 0.5 0.7 North Carolina 37 Wake 183 1.4 1.5 1.9 1.6 1.5 1.4 1.1 Ohio 39 Cuyahoga 035 1.5 1.3 1.2 1.0 1.0 0.9 0.9 Ohio 39 Franklin 049 0.8 0.7 0.7 0.6 0.7 0.6 0.6 Ohio 39 Hamilton 061 1.0 1.0 0.9 0.8 0.7 0.7 0.6 Ohio 39 Lake 085 0.6 0.7 0.7 0.8 1.3 0.7 0.5 Ohio 39 Montgomer y 113 0.7 0.8 0.8 0.7 0.6 0.8 0.5 Ohio 39 Stark 151 0.8 0.5 0.7 0.6 0.3 0.6 0.9 Ohio 39 Summit 153 1.0 1.1 1.1 0.9 0.8 0.7 0.6 Oklahoma 40 Oklahoma 109 1.4 1.1 1.0 0.9 0.9 0.6 0.4 Oklahoma 40 Tulsa 143 1.1 0.9 1.1 1.1 1.1 0.5 0.7 Oregon 41 Lane 039 1.6 1.6 1.5 1.4 1.2 1.1 1.1 Oregon 41 Multnomah 051 2.4 2.1 1.9 1.8 1.7 1.6 1.5

B - 49126County-- January 1st 1999 through December 31st, 2005 (Study area and time period for Bell et al., 2009 ) Pennsylvani a 42 A lleghen y 003 1.3 1.3 1.0 0.5 0.6 0.6 0.6 Pennsylvani a 42 Berks 011 0.5 0.5 0.7 0.6 0.4 0.5 0.5 Pennsylvani a 42 Dauphin 043 0.5 0.5 0.4 0.5 0.6 0.5 0.5 Pennsylvani a 42 Erie 049 0.8 0.9 0.8 0.6 0.6 0.4 0.5 Pennsylvani a 42 Lackawanna 069 0.3 0.5 0.6 0.3 0.3 0.3 0.3 Pennsylvani a 42 Lancaster 071 0.3 0.3 0.4 0.6 0.4 0.4 0.3 Pennsylvani a 42 Northampton 095 0.4 0.4 0.3 0.3 0.3 0.3 0.3 Pennsylvani a 42 Philadelphia 101 1.4 1.2 1.2 1.0 1.1 1.0 1.0 Pennsylvani a 42 York 133 0.4 0.4 0.4 0.4 0.4 0.5 0.3 Rhode Island 44 Providence 007 1.4 1.3 1.1 1.0 0.9 0.8 0.8 South Carolina 45 Charleston 019 0.8 0.7 0.6 0.5 0.5 0.3 0.6 South Carolina 45 Greenville 045 0.8 0.8 0.7 0.6 0.6 0.5 0.3 South Carolina 45 Richland 079 1.1 1.1 1.0 0.9 0.8 0.7 0.6 Tennessee 47 Davidson 037 1.8 1.2 1.3 1.2 1.3 1.1 1.1 Tennessee 47 Shelb y 157 1.4 1.4 0.9 1.0 0.9 0.8 0.5 Texas 48 Bexar 029 1.1 0.7 0.7 0.6 0.7 0.6 0.7 Texas 48 Cameron 061 0.4 0.5 0.4 0.4 0.5 0.3 0.3 Texas 48 Dallas 113 0.4 0.4 0.4 0.4 0.5 0.4 0.4 Texas 48 El Paso 141 3.3 1.6 1.3 1.1 1.1 1.6 1.0 Texas 48 Harris 201 1.0 0.7 1.0 0.7 0.8 0.6 0.5 Texas 48 Tarrant 439 1.0 0.7 0.6 0.5 0.5 0.4 0.4 Texas 48 Travis 453 0.3 0.3 0.3 0.3 0.3 0.3 0.3 Utah 49 Salt Lake 035 2.4 1.9 1.7 1.6 1.4 1.4 1.2 Virginia 51 Fairfax 059 1.0 0.9 1.1 0.6 0.8 0.7 0.8 Virginia 51 Norfolk Cit y 710 1.0 0.7 0.7 0.6 0.5 0.3 0.8 Washington 53 Clark 011 1.7 1.7 2.0 1.3 1.2 1.1 1.0 Washington 53 King 033 2.4 2.1 2.0 1.7 1.8 1.4 1.4 Washington 53 Pierce 053 1.3 1.6 1.2 1.1 1.1 1.1 1.0 Washington 53 Spokane 063 2.7 2.4 2.3 2.1 2.0 1.7 1.6 Wisconsin 55 Milwaukee 079 0.8 0.5 0.9 0.7 0.6 0.7 0.5

Maxperyea r 4.2 2.8 2.4 3.1 2.2 2.0 1.8 4.2 Total Ma x Minperyea r 0.3 0.3 0.3 0.3 0.3 0.3 0.3 0.3 Total Min

B - 50126County-- January 1st 1999 through December 31st, 2005 (Study area and time period for Bell et al., 2009 )

STATENAME fips COUNTYNAME fips 1999 2000 2001 2002 2003 2004 2005 A labama 01 Jefferson 073 9.3 6.4 11.0 4.0 2.2 3.7 5.0 A rizona 04 Maricopa 013 5.6 4.1 3.6 4.2 3.5 3.1 3.3 A rizona 04 Pima 019 2.1 2.4 1.9 1.7 1.7 1.3 1.3 A rkansas 05 Pulaski 119 2.7 1.8 1.6 4.0 1.3 0.9 1.0 California 06 A lameda 001 2.9 2.1 2.3 2.6 2.3 1.3 1.4 California 06 Contra Costa 013 1.9 1.7 1.6 1.4 1.1 1.0 1.0 California 06 Fresno 019 3.7 3.3 2.4 2.0 1.9 1.6 1.5 California 06 Kern 029 2.5 3.8 2.1 1.5 1.5 1.3 1.3 California 06 Los Angeles 037 6.8 5.9 4.5 4.4 4.2 3.6 2.9 California 06 Riverside 065 2.8 3.1 2.6 2.3 2.1 1.9 1.7 California 06 Sacramento 067 3.7 3.7 2.2 2.1 2.6 2.0 2.2 California 06 San Bernardino 071 2.4 2.4 2.1 1.9 2.1 1.7 1.4 California 06 San Diego 073 3.3 3.5 2.9 2.5 2.6 2.3 3.9 California 06 San Francisco 075 2.1 1.6 1.8 1.5 1.5 1.3 1.2 California 06 San Joaquin 077 3.1 2.8 1.7 1.6 1.5 1.2 1.3 California 06 San Mateo 081 2.6 2.2 2.1 1.8 1.5 1.2 1.4 California 06 Santa Clara 085 3.7 3.6 3.4 3.3 2.2 1.9 2.0 California 06 Stanislaus 099 2.8 2.2 2.1 1.8 1.5 1.4 1.6 Colorado 08 A dams 001 2.1 1.9 1.9 1.4 1.5 1.7 1.3 Colorado 08 Denve r 031 2.9 3.2 2.6 1.7 2.3 1.8 1.8 Connecticut 09 Fairfield 001 2.3 2.0 2.2 1.9 1.7 1.5 1.6 Connecticut 09 Hartford 003 2.9 3.1 2.8 2.9 2.7 2.5 2.5 Connecticut 09 New Haven 009 1.6 1.6 1.6 1.5 1.3 1.3 1.3 Delaware 10 New Castle 003 1.7 1.5 1.5 1.2 1.2 1.1 1.3

District Of Columbia 11 District of Columbia 001 3.1 2.7 2.7 2.2 2.6 1.7 2.2 Florida 12 Broward 011 2.1 2.0 2.3 1.7 2.4 2.1 1.8 Florida 12 Duval 031 2.1 2.1 1.4 1.7 1.5 1.4 1.8 Florida 12 Hillsborough 057 2.4 2.1 1.8 2.5 2.1 1.9 2.2 Florida 12 Miami-Dade 086 2.0 1.8 1.9 1.7 2.4 2.5 1.3 Florida 12 Orange 095 2.1 1.7 1.5 1.6 1.4 1.2 1.3 Florida 12 Palm Beach 099 1.4 1.3 0.9 0.9 1.1 1.2 1.3 Florida 12 Pinellas 103 1.5 1.5 1.3 1.5 1.3 1.1 1.1 Georgia 13 DeKalb 089 2.0 1.5 1.9 1.5 1.6 1.4 1.2 Georgia 13 Fulton 121 2.3 1.8 1.8 1.6 1.7 1.5 1.2 Hawaii 15 Honolulu 003 1.6 1.4 1.2 1.7 1.4 1.5 1.2 Idaho 16 Ada 001 2.8 2.1 2.0 2.4 2.4 1.7 1.6 Illinois 17 Cook 031 3.4 3.0 3.1 2.7 2.5 2.6 1.6 Illinois 17 Winnebago 201 2.0 1.9 1.7 1.6 1.2 1.0 1.3 Indiana 18 Allen 003 1.8 2.7 1.6 1.7 1.6 1.4 1.2 Indiana 18 Marion 097 1.5 3.2 1.4 2.1 1.3 1.2 1.3 Iowa 19 Polk 153 2.0 1.7 1.7 1.6 1.6 1.3 1.4 Kansas 20 Sedgwick 173 3.0 5.8 1.6 1.3 1.3 1.2 1.6 Kentucky 21 Jefferson 111 3.6 2.1 2.7 2.8 2.4 2.0 1.6 Louisiana 22 East Baton Rouge 033 2.2 1.6 1.8 2.0 1.3 1.3 0.9 Louisiana 22 Orleans 071 1.6 1.6 1.8 1.6 1.6 2.3 1.3 Maryland 24 Baltimore (City) 510 3.9 1.7 1.8 1.9 1.6 1.4 1.4 Massachusetts 25 Hampden 013 2.7 2.0 2.0 2.1 1.7 1.3 1.4 24-hour - 99th percentile daily maximum (of all 365 possible daily 8-hour

B - 51126County-- January 1st 1999 through December 31st, 2005 (Study area and time period for Bell et al., 2009 ) Massachusetts 25 Middlesex 017 2.0 1.4 1.6 1.3 1.5 1.0 1.0 Massachusetts 25 Suffolk 025 2.1 1.5 1.6 1.5 1.4 0.9 1.3 Massachusetts 25 Worcester 027 1.8 1.5 1.6 1.5 1.1 0.9 1.1 Michigan 26 Kent 081 1.5 1.2 1.9 1.4 1.0 0.9 1.0 Michigan 26 Macomb 099 1.0 0.6 1.4 1.0 1.1 1.5 1.3 Michigan 26 Oakland 125 2.4 1.5 1.9 1.4 1.2 1.1 0.9 Michigan 26 Wayne 163 2.2 1.6 1.5 2.5 1.2 1.3 1.0 Minnesota 27 Dakota 037 0.7 1.1 0.8 0.5 0.6 0.5 0.3 Minnesota 27 Hennepin 053 1.6 1.7 1.2 1.3 0.9 0.9 0.7 Minnesota 27 Ramsey 123 2.8 2.4 2.5 1.7 1.5 1.3 1.5 Minnesota 27 Saint Louis 137 1.3 1.2 0.9 1.2 1.0 0.8 0.9 Mississippi 28 Hinds 049 2.2 1.6 1.7 1.2 1.2 1.2 1.1 Missouri 29 Jackson 095 2.3 2.1 1.8 1.3 1.2 1.4 1.6 Missouri 29 Saint Louis 189 1.6 1.4 1.9 1.3 1.2 1.1 1.1 Missouri 29 St. Louis City 510 2.0 2.1 1.8 5.2 1.5 1.2 1.2 Nevada 32 Clark 003 4.9 4.0 3.8 3.3 3.2 3.0 3.1 Nevada 32 Washoe 031 4.1 3.5 3.4 2.6 2.3 2.2 2.1 New Hampshire 33 Hillsborough 011 2.5 2.3 2.3 1.9 2.1 1.6 1.7 New Jersey 34 Bergen 003 2.7 2.3 2.0 1.9 1.6 1.5 1.5 New Jersey 34 Camden 007 1.5 1.6 1.7 1.4 1.2 1.2 1.3 New Jerse y 34 Hudson 017 3.7 3.0 2.0 1.9 2.1 2.2 1.8 New Jerse y 34 Middlese x 023 2.9 1.8 2.0 1.6 1.3 1.3 1.4 New Jerse y 34 Morris 027 2.5 1.9 2.0 1.4 1.3 1.2 1.2 New Jerse y 34 Union 039 3.3 2.8 2.8 2.2 2.1 2.0 2.1 New Mexico 35 Bernalillo 001 2.8 2.3 2.6 2.5 1.8 1.9 1.8 New Yor k 36 A lban y 001 1.1 0.9 0.8 1.0 1.1 0.7 0.7 New Yor k 36 Bronx 005 1.7 1.6 1.5 1.3 1.4 1.2 1.1 New Yor k 36 Erie 029 1.2 1.2 0.9 1.1 1.2 0.8 1.0 New Yor k 36 Kings 047 3.1 2.8 2.3 2.0 2.0 1.7 1.6 New Yor k 36 Monroe 055 1.4 1.2 1.0 1.0 1.0 1.1 1.2 New Yor k 36 New Yor k 061 2.7 2.9 2.2 1.9 1.8 1.5 1.0 New Yor k 36 Niagara 063 0.8 1.0 0.8 1.0 0.8 0.6 0.8 New Yor k 36 Onondaga 067 1.7 1.4 1.3 1.1 1.1 0.9 1.1 New Yor k 36 Queens 081 1.5 1.4 1.6 1.3 1.4 1.4 1.1 New Yor k 36 Suffolk 103 1.0 1.2 0.9 0.7 0.6 0.6 North Carolina 37 Forsyth 067 2.1 2.0 1.9 1.9 1.8 1.8 1.5 North Carolina 37 Mecklenburg 119 2.5 2.2 2.3 1.7 1.5 1.5 1.3 North Carolina 37 Wake 183 2.6 3.0 2.3 2.3 2.4 2.0 1.9 Ohio 39 Cuyahoga 035 2.1 2.4 1.8 1.3 1.6 2.4 1.6 Ohio 39 Franklin 049 1.2 1.4 1.3 1.1 1.2 1.2 1.0 Ohio 39 Hamilton 061 1.9 1.6 1.5 1.2 1.2 1.1 1.2 Ohio 39 Lake 085 1.2 1.0 1.0 2.0 2.5 0.9 1.0 Ohio 39 Montgomer y 113 1.2 1.6 1.3 1.1 1.3 1.8 1.2 Ohio 39 Stark 151 1.3 1.6 1.3 2.2 1.5 1.9 1.8 Ohio 39 Summit 153 1.5 1.5 1.6 1.3 1.3 1.2 1.1 Oklahoma 40 Oklahoma 109 1.8 1.7 1.8 1.3 1.2 1.0 1.1 Oklahoma 40 Tulsa 143 2.0 2.0 2.2 2.1 1.7 1.0 0.9 Oregon 41 Lane 039 2.9 2.3 2.3 2.4 1.9 1.9 1.6 Oregon 41 Multnomah 051 3.6 2.7 2.6 2.8 2.4 2.3 2.1 Pennsylvani a 42 A lleghen y 003 2.3 2.3 1.8 1.5 1.4 1.2 1.4

B - 52126County-- January 1st 1999 through December 31st, 2005 (Study area and time period for Bell et al., 2009 ) Pennsylvani a 42 Berks 011 1.4 1.2 1.2 1.2 1.2 1.1 1.2 Pennsylvani a 42 Dauphin 043 1.1 1.4 1.5 1.1 1.1 0.9 1.0 Pennsylvani a 42 Erie 049 1.9 1.9 1.7 1.6 1.2 0.7 1.2 Pennsylvani a 42 Lackawanna 069 0.8 1.2 1.2 1.0 0.8 1.0 1.1 Pennsylvani a 42 Lancaster 071 1.3 1.3 1.5 1.3 1.0 0.9 0.9 Pennsylvani a 42 Northampton 095 1.6 1.3 1.3 0.9 0.7 1.2 1.2 Pennsylvani a 42 Philadelphia 101 4.0 1.8 1.9 1.6 1.9 1.6 1.6 Pennsylvani a 42 York 133 1.4 1.0 1.2 1.0 0.9 1.1 0.8 Rhode Island 44 Providence 007 2.3 2.1 1.9 1.7 1.5 1.4 1.3 South Carolina 45 Charleston 019 1.7 1.2 1.1 1.1 0.9 0.8 0.8 South Carolina 45 Greenville 045 2.2 1.5 1.5 1.6 1.5 1.2 1.4 South Carolina 45 Richland 079 2.0 2.0 1.8 1.5 1.2 1.1 1.2 Tennessee 47 Davidson 037 3.1 2.4 3.0 2.1 2.3 2.0 1.8 Tennessee 47 Shelb y 157 2.2 2.5 2.3 1.7 1.6 1.6 1.3 Texas 48 Bexar 029 2.0 1.3 1.4 1.1 1.3 0.9 1.2 Texas 48 Cameron 061 1.7 1.0 0.7 0.8 0.8 0.7 0.9 Texas 48 Dallas 113 1.4 1.1 1.1 1.0 0.9 0.9 1.3 Texas 48 El Paso 141 3.8 3.9 3.4 2.8 2.4 2.3 2.2 Texas 48 Harris 201 2.1 1.8 2.3 1.5 1.9 1.4 1.1 Texas 48 Tarrant 439 1.7 0.9 1.2 0.8 0.8 0.8 1.2 Texas 48 Travis 453 0.8 0.5 0.6 0.5 0.5 0.4 0.3 Utah 49 Salt Lake 035 3.7 3.7 2.9 2.5 2.9 2.1 2.4 Virginia 51 Fairfax 059 1.8 2.3 1.8 1.4 1.4 1.2 1.2 Virginia 51 Norfolk Cit y 710 1.8 1.8 1.7 1.7 1.2 1.1 0.9 Washington 53 Clark 011 3.5 3.5 2.8 3.0 2.7 2.8 2.6 Washington 53 King 033 4.0 3.4 3.4 2.8 3.6 2.1 2.0 Washington 53 Pierce 053 3.9 3.4 2.8 2.7 2.8 2.5 2.3 Washington 53 Spokane 063 3.5 3.1 2.8 3.2 2.7 2.3 2.7 Wisconsin 55 Milwaukee 079 1.4 1.3 1.3 1.1 1.3 1.2 1.5

Maxperyea r 9.3 6.4 11.0 5.2 4.2 3.7 5.0 11.0 Total Ma x Minperyea r 0.7 0.5 0.6 0.5 0.5 0.4 0.3 0.3 Total Min

B - 53126County-- January 1st 1999 through December 31st, 2005 (Study area and time period for Bell et al., 2009 )

STATENAME fips COUNTYNAME fips 1999 2000 2001 2002 2003 2004 2005 A labama 01 Jefferson 073 1.1 1.3 1.1 1.1 0.5 0.4 0.6 A rizona 04 Maricopa 013 2.7 1.8 1.5 1.9 1.2 0.9 0.8 A rizona 04 Pima 019 1.1 1.0 0.9 0.8 0.7 0.7 0.7 A rkansas 05 Pulaski 119 1.3 1.2 0.8 0.4 0.4 0.3 0.3 California 06 A lameda 001 0.7 0.7 0.6 0.6 0.6 0.3 0.5 California 06 Contra Costa 013 0.5 0.5 0.4 0.5 0.5 0.6 0.3 California 06 Fresno 019 1.0 0.5 0.4 0.5 0.8 0.3 0.3 California 06 Kern 029 0.7 0.7 0.8 0.5 0.6 0.5 0.5 California 06 Los Angeles 037 1.5 1.4 1.2 1.1 1.1 0.9 0.8 California 06 Riverside 065 1.2 1.2 1.1 0.9 0.8 0.7 0.7 California 06 Sacramento 067 0.6 0.5 0.7 0.6 0.8 0.6 0.7 California 06 San Bernardino 071 0.9 0.8 0.7 0.9 0.9 0.6 0.6 California 06 San Diego 073 2.1 0.9 1.3 0.8 0.9 1.0 1.2 California 06 San Francisco 075 0.9 0.8 0.8 0.7 0.7 0.7 0.6 California 06 San Joaquin 077 0.5 0.4 0.4 0.4 0.5 0.4 0.3 California 06 San Mateo 081 0.6 0.7 0.6 0.5 0.5 0.5 0.4 California 06 Santa Clara 085 0.8 0.7 0.9 1.4 0.5 0.5 0.6 California 06 Stanislaus 099 0.5 0.4 0.3 0.3 0.4 0.3 0.3 Colorado 08 A dams 001 0.6 0.5 0.5 0.4 0.4 0.5 0.5 Colorado 08 Denve r 031 1.1 1.0 1.0 0.7 0.7 0.6 0.6 Connecticut 09 Fairfield 001 0.9 0.9 0.9 0.9 0.9 0.7 0.7 Connecticut 09 Hartford 003 1.2 1.1 1.5 1.5 1.4 1.3 1.2 Connecticut 09 New Haven 009 0.6 0.6 0.6 0.6 0.6 0.5 0.8 Delaware 10 New Castle 003 0.4 0.6 0.4 0.4 0.3 0.3 0.4

District Of Columbia 11 District of Columbia 001 1.0 1.1 1.0 1.1 1.0 0.9 0.9 Florida 12 Broward 011 0.9 0.8 0.6 0.7 0.6 1.1 0.7 Florida 12 Duval 031 0.5 0.5 0.6 0.7 0.6 0.6 0.4 Florida 12 Hillsborough 057 1.3 1.2 1.1 1.0 0.9 1.1 1.0 Florida 12 Miami-Dade 086 0.9 0.9 0.8 0.8 1.4 1.1 0.6 Florida 12 Orange 095 1.0 0.7 0.6 0.7 0.8 0.5 0.5 Florida 12 Palm Beach 099 0.4 0.4 0.3 0.3 0.4 0.7 0.7 Florida 12 Pinellas 103 0.8 0.6 0.6 0.6 0.7 0.6 0.5 Georgia 13 DeKalb 089 0.5 0.4 0.6 0.5 0.6 0.5 0.5 Georgia 13 Fulton 121 0.8 0.8 0.7 0.6 0.7 0.5 0.5 Hawaii 15 Honolulu 003 0.9 0.8 0.8 1.0 0.8 0.8 0.6 Idaho 16 Ada 001 1.1 1.0 1.0 1.0 0.9 0.9 0.8 Illinois 17 Cook 031 1.7 1.5 1.6 1.6 1.2 1.3 0.7 Illinois 17 Winnebago 201 1.0 0.9 0.8 0.8 0.5 0.4 0.5 Indiana 18 Allen 003 0.7 0.6 0.5 0.6 0.6 0.8 0.6 Indiana 18 Marion 097 0.9 0.8 0.8 0.7 0.6 0.6 0.6 Iowa 19 Polk 153 0.9 0.8 0.9 1.0 0.9 0.8 0.4 Kansas 20 Sedgwick 173 0.5 0.8 0.9 0.6 0.3 0.3 0.7 Kentucky 21 Jefferson 111 1.2 0.6 0.7 0.6 0.9 0.9 0.7 Louisiana 22 East Baton Rouge 033 0.9 0.7 0.8 0.7 0.6 0.5 0.4 Louisiana 22 Orleans 071 0.8 0.8 0.8 0.6 0.9 0.8 0.8 Maryland 24 Baltimore (City) 510 1.0 0.5 0.5 0.5 0.5 0.5 0.4 Massachusetts 25 Hampden 013 0.8 0.8 0.8 0.9 0.6 0.4 0.3 24-hour - 50th percentile daily maximum (of all 365 possible daily 8-hour

B - 54126County-- January 1st 1999 through December 31st, 2005 (Study area and time period for Bell et al., 2009 ) Massachusetts 25 Middlesex 017 0.6 0.4 0.4 0.3 0.3 0.3 0.3 Massachusetts 25 Suffolk 025 0.9 0.6 0.5 0.8 0.6 0.3 0.3 Massachusetts 25 Worcester 027 0.6 0.5 0.5 0.5 0.5 0.4 0.5 Michigan 26 Kent 081 0.4 0.4 0.3 0.3 0.3 0.3 0.3 Michigan 26 Macomb 099 0.3 0.3 0.3 0.3 0.3 0.3 0.3 Michigan 26 Oakland 125 0.3 0.3 0.3 0.3 0.3 0.3 0.3 Michigan 26 Wayne 163 0.6 0.5 0.3 0.4 0.3 0.4 0.3 Minnesota 27 Dakota 037 0.3 0.3 0.3 0.3 0.3 0.3 0.3 Minnesota 27 Hennepin 053 0.7 0.7 0.5 0.6 0.3 0.3 0.3 Minnesota 27 Ramsey 123 1.1 1.0 0.8 0.6 0.5 0.5 0.4 Minnesota 27 Saint Louis 137 0.4 0.4 0.3 0.4 0.4 0.3 0.3 Mississippi 28 Hinds 049 0.3 0.3 0.3 0.3 0.3 0.3 0.3 Missouri 29 Jackson 095 0.8 0.8 0.5 0.5 0.5 0.4 0.5 Missouri 29 Saint Louis 189 0.7 0.6 0.5 0.6 0.6 0.6 0.4 Missouri 29 St. Louis City 510 0.9 0.7 0.7 0.7 0.6 0.4 0.3 Nevada 32 Clark 003 1.4 1.2 1.0 1.2 0.7 0.9 0.9 Nevada 32 Washoe 031 1.1 0.8 0.9 0.7 0.7 0.6 0.4 New Hampshire 33 Hillsborough 011 0.8 0.6 0.5 0.3 0.6 0.7 0.6 New Jersey 34 Bergen 003 1.4 1.2 1.3 1.0 0.9 0.7 0.6 New Jersey 34 Camden 007 0.4 0.5 0.5 0.5 0.6 0.5 0.4 New Jersey 34 Hudson 017 1.6 1.5 1.0 1.0 1.0 1.0 1.0 New Jerse y 34 Middlese x 023 1.0 0.8 0.8 0.8 0.6 0.5 0.6 New Jerse y 34 Morris 027 1.0 0.9 0.8 0.7 0.7 0.6 0.5 New Jerse y 34 Union 039 1.2 1.1 0.9 0.9 0.9 0.8 0.7 New Mexico 35 Bernalillo 001 1.0 0.9 1.0 0.8 0.6 0.4 0.5 New Yor k 36 A lban y 001 0.3 0.3 0.3 0.3 0.4 0.3 0.3 New Yor k 36 Bronx 005 0.6 0.6 0.6 0.6 0.7 0.6 0.6 New Yor k 36 Erie 029 0.5 0.5 0.4 0.4 0.4 0.3 0.3 New Yor k 36 Kings 047 1.4 1.7 1.1 1.0 1.1 1.0 0.8 New Yor k 36 Monroe 055 0.6 0.5 0.4 0.5 0.5 0.5 0.4 New Yor k 36 New Yor k 061 1.7 1.5 1.3 1.0 1.0 0.9 0.6 New Yor k 36 Niagara 063 0.3 0.3 0.3 0.3 0.3 0.3 0.3 New Yor k 36 Onondaga 067 0.4 0.5 0.4 0.4 0.6 0.4 0.4 New Yor k 36 Queens 081 0.6 0.5 0.5 0.5 0.6 0.5 0.5 New Yor k 36 Suffolk 103 0.3 0.3 0.3 0.3 0.3 0.3 North Carolina 37 Forsyth 067 0.8 0.8 0.7 0.8 0.7 0.6 0.7 North Carolina 37 Mecklenburg 119 1.0 0.8 0.6 0.8 0.5 0.4 0.5 North Carolina 37 Wake 183 0.9 0.9 1.0 0.9 1.0 1.0 0.8 Ohio 39 Cuyahoga 035 1.0 0.8 0.8 0.6 0.7 0.6 0.6 Ohio 39 Franklin 049 0.5 0.4 0.4 0.4 0.5 0.4 0.4 Ohio 39 Hamilton 061 0.7 0.7 0.7 0.5 0.5 0.4 0.4 Ohio 39 Lake 085 0.4 0.4 0.4 0.6 1.1 0.4 0.3 Ohio 39 Montgomer y 113 0.5 0.6 0.5 0.4 0.4 0.7 0.3 Ohio 39 Stark 151 0.6 0.3 0.6 0.4 0.3 0.4 0.7 Ohio 39 Summit 153 0.7 0.7 0.8 0.6 0.5 0.4 0.4 Oklahoma 40 Oklahoma 109 0.9 0.8 0.7 0.6 0.6 0.4 0.3 Oklahoma 40 Tulsa 143 0.8 0.7 0.9 0.8 0.8 0.3 0.5 Oregon 41 Lane 039 1.0 1.0 1.0 0.9 0.8 0.7 0.7 Oregon 41 Multnomah 051 1.5 1.4 1.2 1.1 1.0 0.9 0.9 Pennsylvani a 42 A lleghen y 003 0.9 0.9 0.7 0.3 0.4 0.4 0.4

B - 55126County-- January 1st 1999 through December 31st, 2005 (Study area and time period for Bell et al., 2009 ) Pennsylvani a 42 Berks 011 0.3 0.3 0.5 0.4 0.3 0.4 0.4 Pennsylvani a 42 Dauphin 043 0.3 0.3 0.3 0.4 0.4 0.3 0.3 Pennsylvani a 42 Erie 049 0.5 0.5 0.5 0.4 0.4 0.3 0.4 Pennsylvani a 42 Lackawanna 069 0.3 0.3 0.4 0.3 0.3 0.3 0.3 Pennsylvani a 42 Lancaster 071 0.3 0.3 0.3 0.4 0.3 0.3 0.3 Pennsylvani a 42 Northampton 095 0.3 0.3 0.3 0.3 0.3 0.3 0.3 Pennsylvani a 42 Philadelphia 101 1.0 0.8 0.8 0.7 0.8 0.7 0.7 Pennsylvani a 42 York 133 0.3 0.3 0.3 0.3 0.3 0.4 0.3 Rhode Island 44 Providence 007 1.0 1.0 0.8 0.7 0.6 0.6 0.6 South Carolina 45 Charleston 019 0.5 0.4 0.4 0.3 0.4 0.3 0.4 South Carolina 45 Greenville 045 0.5 0.4 0.4 0.4 0.4 0.3 0.3 South Carolina 45 Richland 079 0.7 0.7 0.6 0.5 0.5 0.5 0.4 Tennessee 47 Davidson 037 1.3 0.9 0.8 0.8 1.0 0.9 0.9 Tennessee 47 Shelb y 157 0.8 0.9 0.6 0.6 0.5 0.5 0.3 Texas 48 Bexar 029 0.8 0.4 0.5 0.4 0.5 0.4 0.5 Texas 48 Cameron 061 0.3 0.3 0.3 0.3 0.4 0.3 0.3 Texas 48 Dallas 113 0.3 0.3 0.3 0.3 0.3 0.3 0.3 Texas 48 El Paso 141 1.4 0.8 0.7 0.6 0.6 0.8 0.7 Texas 48 Harris 201 0.8 0.5 0.8 0.5 0.6 0.4 0.4 Texas 48 Tarrant 439 0.7 0.5 0.4 0.3 0.3 0.3 0.3 Texas 48 Travis 453 0.3 0.3 0.3 0.3 0.3 0.3 0.3 Utah 49 Salt Lake 035 1.3 1.2 1.0 0.9 0.9 1.0 0.8 Virginia 51 Fairfax 059 0.8 0.8 0.9 0.5 0.6 0.5 0.6 Virginia 51 Norfolk Cit y 710 0.7 0.4 0.4 0.4 0.3 0.3 0.4 Washington 53 Clark 011 1.1 1.2 1.4 0.9 0.8 0.8 0.8 Washington 53 King 033 1.6 1.5 1.5 1.2 1.3 1.0 1.0 Washington 53 Pierce 053 0.7 1.0 0.8 0.7 0.8 0.7 0.7 Washington 53 Spokane 063 1.7 1.6 1.5 1.5 1.3 1.1 1.1 Wisconsin 55 Milwaukee 079 0.6 0.3 0.4 0.5 0.4 0.4 0.3

Maxperyea r 2.7 1.8 1.6 1.9 1.4 1.3 1.2 2.7 Total Ma x Minperyea r 0.3 0.3 0.3 0.3 0.3 0.3 0.3 0.3 Total Min

B - 56Appendix C

Relationships (Ratios) Between 1-hour and 8-hour CO Concentration Metrics For Counties with CO Monitors (2007-2009)In calculating the different metrics analyzed here, different completeness requirements
were followed for the current CO standard CO design values and for the metrics involving averaging over three years. For the current CO standard running 8-hour and 1-hour metrics, there are no completeness requirements other than that each running 8-hour period is required to have 75% (or 6) of the 8 hours in the period. For the current standards, the 2 nd maximum running 8-hour period and the 2 nd maximum 1-hour value for the entire ye ar, regardless of how incomplete the site data was, is compared to the standard. With regard to data completeness for the alternative metrics, past EPA practice for other NAAQS pollutants was followed by requiring that in general at least 75% of the monitoring data that should have resulted from following the planned monitoring schedule in a period must be available for the key air quality sta tistic from that period to be considered valid. The alternative CO metrics presented here are the daily maximum 1-hour and 8-hour concentrations in three successive years. It is important that sampling within a day encompass the period when concentrations are likely to be hi ghest and that all season s of the year are well represented. Hence, in judging data completene ss for derivation of th ese metrics, the 75% requirement is applied at the daily and quarterly levels. Also, because CO has been shown to have seasonal variability, 3 of the 4 quarters are required. And because it is a 3-year average, all 3 years are required. For the metrics derived he re, the largest value is identified from two calculation procedures. Procedure 1 uses the proposed completeness re quirements above and procedure 2 relaxes the daily re quirement of having 75% of the hours in a day but still requires the quarterly and yearly completeness. Because of the differing completeness require ments, when comparing the alternative daily maximum metrics to the cu rrent running 8-hour and 1-hour metrics, different sites are complete for different metrics. To avoid having ra tios of 0 or a division by 0 error, sites that had a design value for the current 8-hour standard were only used if they had 3 years worth of design
values on the site level co mparison tables and the 2 nd maximum 8-hour value for 2009 was used as the design value when comparing at the county level. After the alternative design values were calculated at each site, the county level metric s were created by taking the maximum value among all the sites in the county.Annual 99th percentile daily maximum 1-hour

concentration, averaged over 3

years (ppm) 2nd highest, nonoverlapping, 8-hour average concentration in year (ppm) ratio STATE COUNTY (2007-2009) (2009) UT WEBER CO 12.2 2.9 4.21 WV BROOKE CO 2.5 0.8 3.17 VA NORFOLK 2.1 0.8 2.67 CO DENVER CO 5.4 2.2 2.45 OH HAMILTON CO 2.7 1.1 2.42 IN LAKE CO 5.0 2.2 2.26 TN BLOUNT CO 0.7 0.3 2.24 PR SAN JUAN 5.3 2.5 2.12 AL JEFFERSON CO 14.2 6.7 2.12 IA POLK CO 1.9 0.9 2.08 NV DOUGLAS CO 5.3 2.6 2.05 CA SAN MATEO CO 3.5 1.7 2.04 WV HANCOCK CO 2.2 1.1 2.03 AZ PIMA CO 2.4 1.2 2.00 MT GALLATIN CO 4.6 2.3 2.00 TX CAMERON CO 1.6 0.8 1.96 TX JEFFERSON CO 1.0 0.5 1.95 CT HARTFORD CO 4.8 2.5 1.92 LA EAST BATON ROUGE PAR 2.1 1.1 1.87 CA ORANGE CO 4.5 2.4 1.86 TX WEBB CO 3.0 1.6 1.85 CO BOULDER CO 2.9 1.6 1.83 PA WASHINGTON CO 1.3 0.7 1.81 TX HARRIS CO 3.6 2 1.78 SC CHARLESTON CO 0.5 0.3 1.78 NJ CAMDEN CO 0.7 0.4 1.75 UT SALT LAKE CO 3.9 2.3 1.68 CA NAPA CO 2.3 1.4 1.67 CO EL PASO CO 3.2 1.9 1.67 MO ST LOUIS 2.8 1.7 1.67 MT CASCADE CO 2.7 1.6 1.67 VT RUTLAND CO 2.5 1.5 1.67 CA MARIN CO 1.8 1.1 1.67 CO LARIMER CO 3.0 1.8 1.67 CO WELD CO 3.5 2.1 1.67 MO GREENE CO 2.2 1.3 1.67 TX BEXAR CO 3.0 1.8 1.67 ME AROOSTOOK CO 0.8 0.5 1.65 CA MONTEREY CO 1.5 0.9 1.63 IL SANGAMON CO 1.9 1.2 1.61 TX MC LENNAN CO 0.5 0.3 1.61 KS SEDGWICK CO 2.7 1.7 1.61 NJ MORRIS CO 1.6 1 1.60 FL PINELLAS CO 1.9 1.2 1.58 CA KERN CO 2.4 1.5 1.58 PA ALLEGHENY CO 2.4 1.5 1.58 DE NEW CASTLE CO 2.1 1.3 1.58 MT YELLOWSTONE CO 2.8 1.8 1.57Annual 99th percentile daily maximum 1-hour

concentration, averaged over 3

years (ppm) 2nd highest, nonoverlapping, 8-hour average concentration in year (ppm) ratio STATE COUNTY (2007-2009) (2009)
OH LAKE CO 1.6 1 1.57 NY SCHENECTADY CO 1.9 1.2 1.56 CA SONOMA CO 1.8 1.2 1.53 WI DODGE CO 0.5 0.3 1.51 TX TRAVIS CO 0.6 0.4 1.50 NV WASHOE CO 3.8 2.6 1.47 OR LANE CO 2.3 1.6 1.46 OH STARK CO 2.0 1.4 1.45 CA RIVERSIDE CO 2.6 1.8 1.44 OH FRANKLIN CO 2.2 1.5 1.44 PA DAUPHIN CO 1.3 0.9 1.44 IN MARION CO 3.6 2.5 1.43 CA HUMBOLDT CO 1.6 1.1 1.42 GA PAULDING CO 0.7 0.5 1.42 OR JACKSON CO 3.4 2.4 1.42 OK TULSA CO 1.8 1.3 1.41 CO LA PLATA CO 1.3 0.9 1.41 PA YORK CO 2.0 1.4 1.40 CA STANISLAUS CO 2.8 2 1.40 TX TARRANT CO 1.5 1.1 1.39 TN DAVIDSON CO 2.4 1.7 1.39 MD BALTIMORE CO 2.6 1.9 1.39 CA SANTA BARBARA CO 1.8 1.3 1.38 SC GREENVILLE CO 1.8 1.3 1.38 AZ MARICOPA CO 4.6 3.3 1.38 CA SAN JOAQUIN CO 2.8 2 1.38 TX EL PASO CO 5.5 4 1.38 MO ST LOUIS CO 1.0 0.7 1.38 CT LITCHFIELD CO 1.0 0.7 1.38 CA SAN DIEGO CO 4.1 3 1.38 KS WYANDOTTE CO 2.2 1.6 1.38 NC ROWAN CO 1.1 0.8 1.38 CO ADAMS CO 2.6 1.9 1.37 FL BROWARD CO 2.6 1.9 1.37 CA FRESNO CO 2.7 2 1.37 TN SULLIVAN CO 1.4 1 1.37 NY ERIE CO 1.5 1.1 1.36 NY ONONDAGA CO 1.6 1.2 1.36 NJ MONMOUTH CO 1.9 1.4 1.36 MD BALTIMORE 2.4 1.8 1.35 WA SPOKANE CO 3.7 2.8 1.33 AR PULASKI CO 2.0 1.5 1.33 CA SAN BERNARDINO CO 2.1 1.6 1.33 IL ST CLAIR CO 2.1 1.6 1.33 UT UTAH CO 3.3 2.5 1.32 KY JEFFERSON CO 2.8 2.1 1.32 CA BUTTE CO 2.6 2 1.32 CA IMPERIAL CO 7.2 5.5 1.32Annual 99th percentile daily maximum 1-hour

concentration, averaged over 3

years (ppm) 2nd highest, nonoverlapping, 8-hour average concentration in year (ppm) ratio STATE COUNTY (2007-2009) (2009)
NV CLARK CO 4.1 3.1 1.31 CA CONTRA COSTA CO 1.4 1.1 1.30 FL MIAMI-DADE CO 2.9 2.2 1.30 PA ERIE CO 1.4 1.1 1.30 MT FLATHEAD CO 3.4 2.6 1.29 NC FORSYTH CO 2.2 1.7 1.29 NY ALBANY CO 1.0 0.8 1.29 NJ BURLINGTON CO 1.8 1.4 1.29 NY SUFFOLK CO 1.7 1.3 1.28 NC MECKLENBURG CO 2.2 1.7 1.27 CA SANTA CLARA CO 2.9 2.3 1.27 OR MULTNOMAH CO 2.9 2.3 1.27 MN ST LOUIS CO 1.9 1.5 1.27 MA SUFFOLK CO 1.5 1.2 1.26 CA SOLANO CO 2.8 2.2 1.26 HI HONOLULU CO 1.5 1.2 1.25 IL PEORIA CO 2.5 2 1.25 NJ MIDDLESEX CO 1.7 1.4 1.24 VA ARLINGTON CO 1.6 1.3 1.23 GA FULTON CO 1.8 1.5 1.22 MN STEARNS CO 2.0 1.7 1.20 NY BRONX CO 2.3 1.9 1.19 OH CUYAHOGA CO 7.9 6.6 1.19 OH MONTGOMERY CO 1.9 1.6 1.19 NJ BERGEN CO 2.0 1.7 1.18 VA ROANOKE 2.0 1.7 1.18 NH HILLSBOROUGH CO 2.3 2 1.17 PA LAWRENCE CO 1.2 1 1.17 NY QUEENS CO 1.9 1.6 1.16 MN RAMSEY CO 2.3 2 1.15 IA SCOTT CO 1.0 0.9 1.15 NE LANCASTER CO 3.2 2.8 1.14 NM BERNALILLO CO 2.7 2.4 1.14 PA PHILADELPHIA CO 2.3 2 1.13 RI PROVIDENCE CO 1.5 1.3 1.13 FL DUVAL CO 1.8 1.6 1.13 PA CAMBRIA CO 1.6 1.4 1.12 VA ALEXANDRIA 1.6 1.4 1.12 CA SAN FRANCISCO CO 2.1 1.9 1.11 CA SACRAMENTO CO 3.1 2.8 1.10 NY NIAGARA CO 1.2 1.1 1.09 WY TETON CO 0.9 0.8 1.08 WA KING CO 2.8 2.6 1.08 MA HAMPDEN CO 1.9 1.8 1.07 IL COOK CO 2.5 2.3 1.07 IL WINNEBAGO CO 2.0 1.9 1.07 PA NORTHAMPTON CO 1.8 1.7 1.06 MN HENNEPIN CO 2.0 1.9 1.05Annual 99th percentile daily maximum 1-hour

concentration, averaged over 3

years (ppm) 2nd highest, nonoverlapping, 8-hour average concentration in year (ppm) ratio STATE COUNTY (2007-2009) (2009)
CO MESA CO 2.3 2.2 1.05 MD PRINCE GEORGES CO 0.9 0.9 1.04 TN SHELBY CO 2.1 2 1.03 OH SUMMIT CO 2.1 2.1 1.02 MA WORCESTER CO 1.9 1.9 1.00 NY MONROE CO 1.3 1.3 1.00 VT CHITTENDEN CO 1.6 1.6 1.00 IN ALLEN CO 2.5 2.5 0.99 PA BUCKS CO 2.3 2.3 0.99 CA ALAMEDA CO 1.9 1.9 0.98 MA MIDDLESEX CO 1.6 1.6 0.98 FL ORANGE CO 1.2 1.2 0.97 VA RICHMOND 1.4 1.5 0.93 ME HANCOCK CO 0.3 0.3 0.92 DC WASHINGTON 3.4 3.8 0.89 FL HILLSBOROUGH CO 0.8 1 0.81 CA LOS ANGELES CO 3.3 4.5 0.73 CA SANTA CRUZ CO 2.6 3.8 0.69 MN DAKOTA CO 0.9 1.5 0.61 CT FAIRFIELD CO 1.0 1.8 0.56 NJ HUDSON CO 2.3 8.2 0.28 min 0.28 0.30 0.28 p5 0.81 0.50 0.94 p10 1.02 0.80 1.01 p25 1.57 1.20 1.17 p50 2.13 1.60 1.37

mean 2.44 1.77 1.42 p75 2.77 2.00 1.61 p90 3.79 2.60 1.94 p95 4.93 3.26 2.11

ma x 14.20 8.20 4.212nd highest 1-hour CO concentration in year (ppm) 2nd highest, nonoverlapping, 8-hour average concentration in year (ppm) ratio
STAT COUNTY (2009) (2009) UT WEBER CO 16.2 2.9 5.59 MT FLATHEAD CO 12.8 2.6 4.92 PR SAN JUAN 9.4 2.5 3.76 IN LAKE CO 7.5 2.2 3.41 CO DENVER CO 6.8 2.2 3.09 WI DODGE CO 0.921 0.3 3.07 MD BALTIMORE CO 5.8 1.9 3.05 NJ MONMOUTH CO 4.2 1.4 3.00 NV DOUGLAS CO 7.6 2.6 2.92 ID ADA CO 9.5 3.3 2.88 MO ST LOUIS 4.7 1.7 2.76 OH SUMMIT CO 5.8 2.1 2.76 MT GALLATIN CO 6.2 2.3 2.70 PA BERKS CO 3.2 1.2 2.67 OH CUYAHOGA CO 17.3 6.6 2.62 CA SANTA BARBARA CO 3.4 1.3 2.62 PA ADAMS CO 1 0.4 2.50 OK TULSA CO 3.2 1.3 2.46 MT YELLOWSTONE CO 4.3 1.8 2.39 CA SANTA CRUZ CO 9 3.8 2.37 OK CHEROKEE CO 1.4 0.6 2.33 WY TETON CO 1.8 0.8 2.25 PA LACKAWANNA CO 1.7 0.8 2.13 TX CAMERON CO 1.7 0.8 2.13 RI PROVIDENCE CO 2.7 1.3 2.08 VT RUTLAND CO 3.1 1.5 2.07 ND CASS CO 1.003 0.5 2.01 CA SAN FRANCISCO CO 3.8 1.9 2.00 CO BOULDER CO 3.2 1.6 2.00 IN HENDRICKS CO 1.4 0.7 2.00 NJ CAMDEN CO 0.8 0.4 2.00 NJ MORRIS CO 2 1 2.00 OH MEDINA CO 1.6 0.8 2.00 SC CHARLESTON CO 0.6 0.3 2.00 TX MC LENNAN CO 0.6 0.3 2.00 MA SUFFOLK CO 2.366 1.2 1.97 CA SAN MATEO CO 3.3 1.7 1.94 CA IMPERIAL CO 10.5 5.5 1.91 CO EL PASO CO 3.6 1.9 1.89 AZ PIMA CO 2.2 1.2 1.83 MN STEARNS CO 3.1 1.7 1.82 MT CASCADE CO 2.9 1.6 1.81 TX JEFFERSON CO 0.906 0.5 1.81 LA EAST BATON ROUGE PAR 1.99 1.1 1.81 AL JEFFERSON CO 12.1 6.7 1.81 CT HARTFORD CO 4.5 2.5 1.80 GA FULTON CO 2.7 1.5 1.80 OR MULTNOMAH CO 4.1 2.3 1.782nd highest 1-hour CO concentration in year (ppm) 2nd highest, nonoverlapping, 8-hour average concentration in year (ppm) ratio
STAT COUNTY (2009) (2009)
OK ADAIR CO 0.702 0.4 1.76 IA POLK CO 1.576 0.9 1.75 CA ORANGE CO 4.2 2.4 1.75 FL PINELLAS CO 2.1 1.2 1.75 TX TRAVIS CO 0.7 0.4 1.75 VA NEWPORT NEWS 1.4 0.8 1.75 CA ALAMEDA CO 3.3 1.9 1.74 CA MARIN CO 1.9 1.1 1.73 OH HAMILTON CO 1.9 1.1 1.73 NY QUEENS CO 2.76 1.6 1.73 TX BEXAR CO 3.1 1.8 1.72 PA WASHINGTON CO 1.2 0.7 1.71 PA YORK CO 2.4 1.4 1.71 CO WELD CO 3.6 2.1 1.71 MO GREENE CO 2.2 1.3 1.69 TX WEBB CO 2.7 1.6 1.69 CA SONOMA CO 2 1.2 1.67 IL SANGAMON CO 2 1.2 1.67 OK OKLAHOMA CO 2 1.2 1.67 CA MONTEREY CO 1.5 0.9 1.67 CO LARIMER CO 3 1.8 1.67 PA PHILADELPHIA CO 3.3 2 1.65 KS SEDGWICK CO 2.8 1.7 1.65 CA NAPA CO 2.3 1.4 1.64 NJ MIDDLESEX CO 2.3 1.4 1.64 PA CAMBRIA CO 2.3 1.4 1.64 CA CONTRA COSTA CO 1.8 1.1 1.64 CA HUMBOLDT CO 1.8 1.1 1.64 PA ERIE CO 1.8 1.1 1.64 WV HANCOCK CO 1.8 1.1 1.64 NC ROWAN CO 1.3 0.8 1.63 VA HAMPTON 1.3 0.8 1.63 VA NORFOLK 1.3 0.8 1.63 ME AROOSTOOK CO 0.808 0.5 1.62 DE NEW CASTLE CO 2.1 1.3 1.62 NV WASHOE CO 4.2 2.6 1.62 NY SUFFOLK CO 2.1 1.3 1.62 UT SALT LAKE CO 3.7 2.3 1.61 WA SPOKANE CO 4.5 2.8 1.61 IL PEORIA CO 3.2 2 1.60 IN MARION CO 4 2.5 1.60 NH HILLSBOROUGH CO 3.2 2 1.60 TN SULLIVAN CO 1.6 1 1.60 MN ST LOUIS CO 2.4 1.5 1.60 TX DALLAS CO 2.377 1.5 1.58 FL ORANGE CO 1.9 1.2 1.58 MI WAYNE CO 1.9 1.2 1.58 NY ONONDAGA CO 1.9 1.2 1.582nd highest 1-hour CO concentration in year (ppm) 2nd highest, nonoverlapping, 8-hour average concentration in year (ppm) ratio
STAT COUNTY (2009) (2009)
NJ BURLINGTON CO 2.2 1.4 1.57 IA LINN CO 1.882 1.2 1.57 UT UTAH CO 3.9 2.5 1.56 CO LA PLATA CO 1.4 0.9 1.56 MD BALTIMORE 2.8 1.8 1.56 TX EL PASO CO 6.2 4 1.55 TX HARRIS CO 3.1 2 1.55 WA KING CO 4 2.6 1.54 PA ALLEGHENY CO 2.3 1.5 1.53 NV CLARK CO 4.7 3.1 1.52 AZ MARICOPA CO 5 3.3 1.52 CT FAIRFIELD CO 2.7 1.8 1.50 NM BERNALILLO CO 3.6 2.4 1.50 FL BROWARD CO 2.8 1.9 1.47 NY BRONX CO 2.8 1.9 1.47 CA KERN CO 2.2 1.5 1.47 OH FRANKLIN CO 2.2 1.5 1.47 TX TARRANT CO 1.6 1.1 1.45 AK FAIRBANKS NORTH STAR BOROUGH 4.5 3.1 1.45 CA FRESNO CO 2.9 2 1.45 CA SAN JOAQUIN CO 2.9 2 1.45 CA RIVERSIDE CO 2.6 1.8 1.44 CA SAN BERNARDINO CO 2.3 1.6 1.44 KS WYANDOTTE CO 2.3 1.6 1.44 NC WAKE CO 2.3 1.6 1.44 OH MONTGOMERY CO 2.3 1.6 1.44 CA SAN DIEGO CO 4.3 3 1.43 NJ UNION CO 3 2.1 1.43 IL WINNEBAGO CO 2.7 1.9 1.42 NY SCHENECTADY CO 1.7 1.2 1.42 OR JACKSON CO 3.4 2.4 1.42 IA SCOTT CO 1.271 0.9 1.41 VA ROANOKE 2.4 1.7 1.41 ME CUMBERLAND CO 2.1 1.5 1.40 VA RICHMOND 2.1 1.5 1.40 CA BUTTE CO 2.8 2 1.40 NE LANCASTER CO 3.9 2.8 1.39 VT CHITTENDEN CO 2.2 1.6 1.38 CO ADAMS CO 2.6 1.9 1.37 NY ERIE CO 1.5 1.1 1.36 NC FORSYTH CO 2.3 1.7 1.35 CA STANISLAUS CO 2.7 2 1.35 CT NEW HAVEN CO 1.89 1.4 1.35 TN SHELBY CO 2.7 2 1.35 IL COOK CO 3.1 2.3 1.35 HI HONOLULU CO 1.6 1.2 1.33 NC DURHAM CO 0.8 0.6 1.33 PR BAYAMON 3.2 2.4 1.332nd highest 1-hour CO concentration in year (ppm) 2nd highest, nonoverlapping, 8-hour average concentration in year (ppm) ratio
STAT COUNTY (2009) (2009)
IN VANDERBURGH CO 2.4 1.8 1.33 KY JEFFERSON CO 2.8 2.1 1.33 MA ESSEX CO 0.791 0.6 1.32 IL ST CLAIR CO 2.1 1.6 1.31 MI KENT CO 2.1 1.6 1.31 OR LANE CO 2.1 1.6 1.31 AK ANCHORAGE BOROUGH 7.6 5.8 1.31 VA ARLINGTON CO 1.7 1.3 1.31 VA FAIRFAX CO 1.7 1.3 1.31 NJ ESSEX CO 2.6 2 1.30 CA SANTA CLARA CO 2.98 2.3 1.30 PA NORTHAMPTON CO 2.2 1.7 1.29 TN DAVIDSON CO 2.2 1.7 1.29 MD GARRETT CO 0.387 0.3 1.29 MO ST LOUIS CO 0.9 0.7 1.29 OH STARK CO 1.8 1.4 1.29 NY NEW YORK CO 2.3 1.8 1.28 CA SOLANO CO 2.8 2.2 1.27 NY NIAGARA CO 1.4 1.1 1.27 CT LITCHFIELD CO 0.89 0.7 1.27 AR PULASKI CO 1.9 1.5 1.27 MA WORCESTER CO 2.4 1.9 1.26 MN HENNEPIN CO 2.4 1.9 1.26 NE DOUGLAS CO 2.9 2.3 1.26 FL DUVAL CO 2 1.6 1.25 MN RAMSEY CO 2.5 2 1.25 NY ALBANY CO 1 0.8 1.25 WV BROOKE CO 1 0.8 1.25 MD PRINCE GEORGES CO 1.123 0.9 1.25 MT MISSOULA CO 3.1 2.5 1.24 NC MECKLENBURG CO 2.1 1.7 1.24 NJ BERGEN CO 2.1 1.7 1.24 NJ HUDSON CO 10.1 8.2 1.23 SC GREENVILLE CO 1.6 1.3 1.23 FL MIAMI-DADE CO 2.7 2.2 1.23 CA LOS ANGELES CO 5.5 4.5 1.22 MA HAMPDEN CO 2.2 1.8 1.22 PA DAUPHIN CO 1.1 0.9 1.22 VA ALEXANDRIA 1.7 1.4 1.21 IN ALLEN CO 3 2.5 1.20 OH LAKE CO 1.2 1 1.20 PA LAWRENCE CO 1.2 1 1.20 CA SACRAMENTO CO 3.2 2.8 1.14 TN BLOUNT CO 0.34 0.3 1.13 MA MIDDLESEX CO 1.8 1.6 1.13 DC WASHINGTON 4.2 3.8 1.11 OH ATHENS CO 1.3 1.2 1.08 FL HILLSBOROUGH CO 1.082 1 1.082nd highest 1-hour CO concentration in year (ppm) 2nd highest, nonoverlapping, 8-hour average concentration in year (ppm) ratio
STAT COUNTY (2009) (2009)
NY MONROE CO 1.4 1.3 1.08 CO MESA CO 2.3 2.2 1.05 PA BUCKS CO 2.4 2.3 1.04 WA CLALLAM CO 0.311 0.3 1.04 GA PAULDING CO 0.502 0.5 1.00 MN DAKOTA CO 1.5 1.5 1.00 NY STEUBEN CO 0.29 0.3 0.97 ME HANCOCK CO 0.288 0.3 0.96 KY EDMONSON CO 0.25 0.3 0.83 OK KAY CO 0.25 0.3 0.83 SD UNION CO 0.25 0.3 0.83 WY UINTA CO 0.25 0.3 0.83 min 0.25 0.30 0.83 p5 0.60 0.30 1.05 p10 0.91 0.60 1.20 p25 1.60 1.10 1.31 p50 2.30 1.55 1.55

mean 2.86 1.68 1.65 p75 3.20 2.00 1.75 p90 4.64 2.60 2.31 p95 7.59 3.27 2.76

max 17.30 8.20 5.592nd highest, nonoverlapping, 8-hour average concentration in year (ppm) Annual 99th percentile daily maximum 8-hour average concentration, averaged over 3 years (ppm) ratio STATE COUNTY (2009) (2007-2009) NJ HUDSON CO 8.2 1.7 4.92 CA SANTA CRUZ CO 3.8 1.4 2.65 WY TETON CO 0.8 0.4 2.18 MN HENNEPIN CO 1.9 1.1 1.78 CA LOS ANGELES CO 4.5 2.5 1.78 MN DAKOTA CO 1.5 0.9 1.67 OH SUMMIT CO 2.1 1.3 1.58 OH CUYAHOGA CO 6.6 4.3 1.55 FL HILLSBOROUGH CO 1 0.7 1.50 PA BUCKS CO 2.3 1.6 1.47 CO MESA CO 2.2 1.5 1.47 ID ADA CO 3.3 2.3 1.41 MI KENT CO 1.6 1.1 1.41 VA RICHMOND 1.5 1.1 1.41 MA WORCESTER CO 1.9 1.4 1.36 VT CHITTENDEN CO 1.6 1.2 1.33 FL ORANGE CO 1.2 0.9 1.33 PA BERKS CO 1.2 0.9 1.33 TN SHELBY CO 2 1.5 1.30 MT FLATHEAD CO 2.6 2.0 1.30 NY SUFFOLK CO 1.3 1.0 1.30 RI PROVIDENCE CO 1.3 1.0 1.30 DC WASHINGTON 3.8 2.9 1.30 IA SCOTT CO 0.9 0.7 1.29 IN VANDERBURGH CO 1.8 1.4 1.29 HI HONOLULU CO 1.2 0.9 1.29 ME HANCOCK CO 0.3 0.2 1.29 OK CHEROKEE CO 0.6 0.5 1.29 NJ MIDDLESEX CO 1.4 1.1 1.27 PA YORK CO 1.4 1.1 1.27 UT UTAH CO 2.5 2.0 1.27 NY NIAGARA CO 1.1 0.9 1.27 CA SAN FRANCISCO CO 1.9 1.5 1.27 FL DUVAL CO 1.6 1.3 1.26 MA MIDDLESEX CO 1.6 1.3 1.26 IN ALLEN CO 2.5 2.0 1.25 IL WINNEBAGO CO 1.9 1.5 1.24 IL COOK CO 2.3 1.9 1.23 NY QUEENS CO 1.6 1.3 1.23 FL MIAMI-DADE CO 2.2 1.8 1.22 GA FULTON CO 1.5 1.2 1.22 MN STEARNS CO 1.7 1.4 1.212nd highest, nonoverlapping, 8-hour average concentration in year (ppm) Annual 99th percentile daily maximum 8-hour average concentration, averaged over 3 years (ppm) ratio STATE COUNTY (2009) (2007-2009)
MA HAMPDEN CO 1.8 1.5 1.20 PA PHILADELPHIA CO 2 1.7 1.20 VA ROANOKE 1.7 1.4 1.19 MN ST LOUIS CO 1.5 1.3 1.18 NE LANCASTER CO 2.8 2.4 1.18 MD PRINCE GEORGES CO 0.9 0.8 1.17 TX EL PASO CO 4 3.4 1.17 ME AROOSTOOK CO 0.5 0.4 1.15 PA LAWRENCE CO 1 0.9 1.15 WA SPOKANE CO 2.8 2.4 1.15 NY MONROE CO 1.3 1.1 1.15 NC ROWAN CO 0.8 0.7 1.14 NM BERNALILLO CO 2.4 2.1 1.14 CA ALAMEDA CO 1.9 1.7 1.14 NJ BURLINGTON CO 1.4 1.2 1.14 NH HILLSBOROUGH CO 2 1.8 1.13 CA SACRAMENTO CO 2.8 2.5 1.12 OH MONTGOMERY CO 1.6 1.4 1.12 VA ARLINGTON CO 1.3 1.2 1.11 PA NORTHAMPTON CO 1.7 1.5 1.11 VA ALEXANDRIA 1.4 1.3 1.11 NY ERIE CO 1.1 1.0 1.10 PA ERIE CO 1.1 1.0 1.10 WA KING CO 2.6 2.4 1.10 AR PULASKI CO 1.5 1.4 1.10 TX DALLAS CO 1.5 1.4 1.10 NY BRONX CO 1.9 1.7 1.10 CA IMPERIAL CO 5.5 5.0 1.09 FL PINELLAS CO 1.2 1.1 1.09 MA SUFFOLK CO 1.2 1.1 1.09 PA ADAMS CO 0.4 0.4 1.09 TX TRAVIS CO 0.4 0.4 1.09 NJ UNION CO 2.1 1.9 1.09 NJ BERGEN CO 1.7 1.6 1.09 CA MONTEREY CO 0.9 0.8 1.08 TX BEXAR CO 1.8 1.7 1.08 NE DOUGLAS CO 2.3 2.1 1.08 PA CAMBRIA CO 1.4 1.3 1.08 AZ MARICOPA CO 3.3 3.1 1.08 MD BALTIMORE CO 1.9 1.8 1.08 PA ALLEGHENY CO 1.5 1.4 1.07 MT CASCADE CO 1.6 1.5 1.072nd highest, nonoverlapping, 8-hour average concentration in year (ppm) Annual 99th percentile daily maximum 8-hour average concentration, averaged over 3 years (ppm) ratio STATE COUNTY (2009) (2007-2009)
CA CONTRA COSTA CO 1.1 1.0 1.06 TX TARRANT CO 1.1 1.0 1.06 NC MECKLENBURG CO 1.7 1.6 1.06 MT GALLATIN CO 2.3 2.2 1.06 CA SANTA BARBARA CO 1.3 1.2 1.05 CA SAN JOAQUIN CO 2 1.9 1.05 MN RAMSEY CO 2 1.9 1.05 CT NEW HAVEN CO 1.4 1.3 1.05 AK ANCHORAGE BOROUGH 5.8 5.5 1.05 CA SANTA CLARA CO 2.3 2.2 1.05 IL ST CLAIR CO 1.6 1.5 1.04 CT FAIRFIELD CO 1.8 1.7 1.04 CA BUTTE CO 2 1.9 1.03 CA SOLANO CO 2.2 2.1 1.03 MI WAYNE CO 1.2 1.2 1.03 NJ MONMOUTH CO 1.4 1.4 1.02 CA SAN BERNARDINO CO 1.6 1.6 1.02 CA RIVERSIDE CO 1.8 1.8 1.02 CO EL PASO CO 1.9 1.9 1.02 CA FRESNO CO 2 2.0 1.02 IL PEORIA CO 2 2.0 1.02 KY JEFFERSON CO 2.1 2.1 1.02 CA ORANGE CO 2.4 2.4 1.01 IN MARION CO 2.5 2.5 1.01 CO WELD CO 2.1 2.1 1.00 FL BROWARD CO 1.9 1.9 1.00 MD GARRETT CO 0.3 0.3 1.00 MT YELLOWSTONE CO 1.8 1.8 1.00 NV DOUGLAS CO 2.6 2.6 1.00 NV WASHOE CO 2.6 2.6 1.00 NY ONONDAGA CO 1.2 1.2 1.00 OH FRANKLIN CO 1.5 1.5 1.00 OK KAY CO 0.3 0.3 1.00 SC CHARLESTON CO 0.3 0.3 1.00 SC GREENVILLE CO 1.3 1.3 1.00 TX CAMERON CO 0.8 0.8 1.00 UT SALT LAKE CO 2.3 2.3 1.00 VT RUTLAND CO 1.5 1.5 1.00 CA SAN DIEGO CO 3 3.0 0.99 OR JACKSON CO 2.4 2.4 0.99 CA STANISLAUS CO 2 2.0 0.98 CO ADAMS CO 1.9 1.9 0.982nd highest, nonoverlapping, 8-hour average concentration in year (ppm) Annual 99th percentile daily maximum 8-hour average concentration, averaged over 3 years (ppm) ratio STATE COUNTY (2009) (2007-2009)
MD BALTIMORE 1.8 1.8 0.98 NC FORSYTH CO 1.7 1.7 0.98 KS WYANDOTTE CO 1.6 1.6 0.98 DE NEW CASTLE CO 1.3 1.3 0.98 IL SANGAMON CO 1.2 1.2 0.97 OR MULTNOMAH CO 2.3 2.4 0.97 PA DAUPHIN CO 0.9 0.9 0.96 NY ALBANY CO 0.8 0.8 0.96 MO ST LOUIS CO 0.7 0.7 0.95 PR SAN JUAN 2.5 2.6 0.95 AK FAIRBANKS NORTH STAR BOROUGH 3.1 3.3 0.95 CA SONOMA CO 1.2 1.3 0.95 CA SAN MATEO CO 1.7 1.8 0.94 TN DAVIDSON CO 1.7 1.8 0.94 CA HUMBOLDT CO 1.1 1.2 0.94 CA MARIN CO 1.1 1.2 0.94 NV CLARK CO 3.1 3.3 0.94 CA KERN CO 1.5 1.6 0.94 NJ MORRIS CO 1 1.1 0.94 TN SULLIVAN CO 1 1.1 0.94 VA FAIRFAX CO 1.3 1.4 0.93 AL JEFFERSON CO 6.7 7.2 0.93 NJ CAMDEN CO 0.4 0.4 0.92 OR LANE CO 1.6 1.7 0.92 IN LAKE CO 2.2 2.4 0.92 CT HARTFORD CO 2.5 2.7 0.91 CT LITCHFIELD CO 0.7 0.8 0.91 CO LA PLATA CO 0.9 1.0 0.90 CA NAPA CO 1.4 1.6 0.89 MT MISSOULA CO 2.5 2.8 0.89 MO GREENE CO 1.3 1.5 0.89 OK TULSA CO 1.3 1.5 0.89 TX WEBB CO 1.6 1.8 0.87 MO ST LOUIS 1.7 2.0 0.86 CO BOULDER CO 1.6 1.9 0.86 NC DURHAM CO 0.6 0.7 0.86 IA POLK CO 0.9 1.1 0.84 CO DENVER CO 2.2 2.6 0.84 TX JEFFERSON CO 0.5 0.6 0.83 PA LACKAWANNA CO 0.8 1.0 0.83 VA NORFOLK 0.8 1.0 0.83 OH STARK CO 1.4 1.7 0.822nd highest, nonoverlapping, 8-hour average concentration in year (ppm) Annual 99th percentile daily maximum 8-hour average concentration, averaged over 3 years (ppm) ratio STATE COUNTY (2009) (2007-2009)
KS SEDGWICK CO 1.7 2.1 0.82 TX MC LENNAN CO 0.3 0.4 0.82 NY SCHENECTADY CO 1.2 1.5 0.82 WI DODGE CO 0.3 0.4 0.82 TX HARRIS CO 2 2.5 0.81 NC WAKE CO 1.6 2.0 0.80 AZ PIMA CO 1.2 1.5 0.80 CO LARIMER CO 1.8 2.3 0.79 GA PAULDING CO 0.5 0.6 0.79 VA HAMPTON 0.8 1.0 0.77 LA EAST BATON ROUGE PAR 1.1 1.4 0.77 WV HANCOCK CO 1.1 1.5 0.75 IN HENDRICKS CO 0.7 0.9 0.75 OH LAKE CO 1 1.3 0.75 PA WASHINGTON CO 0.7 1.0 0.70 OH HAMILTON CO 1.1 1.7 0.63 UT WEBER CO 2.9 4.6 0.63 TN BLOUNT CO 0.3 0.5 0.60 WV BROOKE CO 0.8 1.6 0.502nd highest, nonoverlapping, 8-hour average concentration in year (ppm) Annual 99th percentile daily maximum 8-hour average concentration, averaged over 3 years (ppm) ratio STATE COUNTY (2009) (2007-2009)
min 0.30 0.23 0.50 p5 0.43 0.43 0.78 p10 0.76 0.72 0.82 p25 1.10 1.07 0.94 p50 1.60 1.50 1.05

mean 1.75 1.61 1.10 p75 2.05 1.95 1.18 p90 2.60 2.48 1.30 p95 3.30 3.00 1.47

max 8.20 7.23 4.92This page is intentionally blankD-1 Appendix D

Additional REA Estimate s from Simulations for
Alternative Levels and Forms for th e 1-hour and 8-hour Standards.D-2Table D-1.Percentage of simulated HD population with daily maximum end-of-hour COHb levels (absolute) below theindicated COHb levels under alternative levels and forms for the 1-hour and 8-hour standards.Current andPotential Alternative StandardsDaily Maximum End-of-hour COHb Level (Absolute)Level < 3.0 % COHb < 2.5 % COHb < 2.0 % COHb < 1.75 % COHb < 1.5 % COHbForm1-hour(ppm)8-hour(ppm)LosAngelesDenverLosAngelesDenverLosAngelesDenverLosAngelesDenverLosAngelesDenver8-hourLevels(ppm)16.2+99.7 99.1 95.5 88.9 75.511.8+9.4+>99.9 >99.9 99.4 98.3 95.09.4+11.299.898.996.890.46.59.7 98.0 93.95.69.3>99.999.999.498.494.65.48.2* 98.45.6*8.199.598.56.57.2 99.7 99.05.76.85.4–6.5100100> 99.999.899.25.4Second HighestNon-overlappingConcentration(Current Form)4.6* 3.1* 100 100 >99.9 99.7 98.83.1*13.3+99.7 99.1 95.5 88.9 75.57.2+11.6+7.2-8.2+>99.9 >99.9 99.4 98.3 95.08.2+9.2>99.999.898.996.890.45.0100 100 > 99.9 99.5 98.55.78.098.093.94.37.7>99.999.999.498.4 94.64.17.4*99.598.45.1*7.1 99.7 99.05.06.74.1– 5.7100100>99.999.899.24.799th Percentileof DailyMaximumConcentrations4.5* 2.8* 100 100 >99.9 99.7 98.82.8*+ Plus marks indicate simulations based on air quality conditions just meeting the current 8-hour standard.* Asterisks indicate simulations basedon “as is” (2006) air quality conditions for the two study areas.Drawn from REA tables 6-15 to 6-19 and 6-21to 6-22, consistent with Table 2-7above.D-3Table D-2.Percentage of simulated CHD population with maximum ambient contributions to end-of-hour COHb levels belowthe indicated COHb levels under alternative levelsand forms for the 1-hour and 8-hour standards.Current andPotential Alternative StandardsMaximum Ambient Contributionto End-of-hourCOHb LevelLevel< 2.0 % COHb < 1.8 % COHb< 1.6 % COHb < 1.4 % COHbForm1-hour(ppm)8-hour(ppm)LosAngeles DenverLosAngeles DenverLosAngeles DenverLosAngeles Denver8-hourLevel(ppm)16.2+97.396.6 93.287.211.8+9.499.599.2 98.798.09.411.299.899.1 97.396.36.58.2* 100*99.7* 99.5*99.5*5.67.25.6-6.599.799.7 99.799.55.7SecondHighest NonoverlappingConcentration(Current Form)4.6* 3.1 100*100* 99.8*99.8*3.113.3+7.2 97.396.6 93.287.27.211.6+8.2 99.599.2 98.798.08.29.299.899.1 97.396.35.07.4* 100*99.7* 99.5*99.5*5.17.15.0-5.199.799.7 99.799.55.099th Percentileof DailyMaximumConcentrations4.5* 2.8 100*100* 99.8*99.8*2.8+ Plus marks indicate simulations based on air quality conditions just meeting the current 8-hour standard.* Asterisks indicate simulations basedon “as is” (2006) air quality conditions for the two study areas.Drawn from REA tables 6-17, 6-20 and 6-23, consistent withTable 2-7 in chapter 2 of this document above.This page is intentionally blankE-1 

### Appendix E

Predicted Percentage of Counties with a Monitor Not Likely to Meet Alternative Standard s and Associated Percentage PopulationE-2 Data Analysis

Hourly data for CO were pu lled from EPA’s Air Quality Sy stem in July 2010. Daily 1- hour maximums were calculat ed from the hourly data. Past EPA practice for other NAAQS pollutants was followed by requiring th at in general at least 75% of the monitoring data that should have resulted from follo wing the planned monitoring schedule in a period must be available for the key air quality statistic from that period to be considered valid. The ke y air quality statistics are th e daily maximum 1-hour and 8- hour concentrations in three successive years. The 75% requirem ent was applied at the daily and quarterly levels. Also, because CO has been shown to ha ve seasonal variability, 3 of the 4 quarters were required. And because it is a 3-year average, all 3 years were required. For the alternative design values, the larg est value from two calculation procedures is wh at was compared to the potential alternative standards. Procedure 1 uses the complete ness requirements above and pr ocedure 2 relaxes the daily requirement of having 75% of the hours in a day but still requires the quarterly and yearly completeness. After the alternative design valu es in were calculated at each site, the county level design values we re created by taking the maxi mum design value of all the sites in the county. The regions are the same as those used fo r similar analyses in recent NAAQS reviews (e.g., lea d, particulate matter).E-3Appendix E. Predicted percentage of counties with a monitor not likely to meetalternative atandards (based on 2007-2009data) and associated percentage population.Total Counties(population in millions)Northeast SoutheastIndustrialMidwestUpperMidwestSouthwest NorthwestSouthernCaliforniaOutsideRegionsNumber of Countieswith monitors165 (115) 41 26 30 10 9 38 9 2Alternative Levels for aform of 99th percentiledaily 1-hourmaximum,averaged over 3 years15.0 0 0 0 0 0 0 0 0 014.0 .6 (.7) 0 4 0 0 0 0 0 013.0 .6 (.7) 0 4 0 0 0 0 0 012.0 1.2 (.9) 0 4 0 0 0 3 0 011.0 1.2 (.9) 0 4 0 0 0 3 0 010.0 1.2 (.9) 0 4 0 0 0 3 0 09.0 1.2 (.9) 0 4 0 0 0 3 0 08.0 1.2 (.9) 0 4 0 0 0 3 0 07.0 2.4 (2.4) 0 4 3 0 11 3 0 06.0 2.4 (2.4) 0 4 3 0 11 3 0 05.0 4.8 (4.1) 0 4 3 0 22 8 0 50Number of Countieswith monitors187 (125) 48 31 35 11 9 40 9 4Alternative Levels for aform of 99th percentiledaily 8-hourmaximum,averaged over 3 years9.0 0 0 0 0 0 0 0 0 08.0 0 0 0 0 0 0 0 0 07.0 0.5 (.7) 0 3 0 0 0 0 0 06.0 0.5 (.7) 0 3 0 0 0 0 0 05.0 1.1 (.9) 0 3 0 0 0 0 0 254.0 2.7 (2.7) 0 3 3 0 11 3 0 253.0 4.8 (7.9) 0 3 3 0 44 3 0 50** "Outside Regions" includes Alaska, Hawaii, Puerto Rico, and the Virgin Islands.Of counties with a monitor, the percentage not likely to meet stated alternative standard(population - percentage of population in counties with monitors)Of counties with a monitor, the percentage not likely to meet stated alternative standard(population - percentage of population in counties with monitors)United StatesEnvironmental ProtectionAgencyOffice of Air Quality Planning and StandardsHealth and Environmental Impacts DivisionResearch Triangle Park, NCPublication No. EPA-452/R-10-007October 2010