Policy Assessment for the Review of the 

Carbon Monoxide National Ambient Air 

Quality Standards 
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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 Carolina 
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DISCLAIMER

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 Office of Air Quality Planning and Standards 

(OAQPS). For the chapter on health 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 effects and consideration of a secondary standard, the principal author is 

Meredith Lassiter. The principal 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 offices, including the Office of Research and Development, 

and the Office of General Counsel also provided valuable comments and contributions. 

An earlier draft of this document 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 ORGANIZATION OF THE DOCUMENT...........1-14 

REFERENCES .................................................................................................................... 1-15 

2 REVIEW OF THE PRIMARY STANDARDS 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 ALTERNATIVE STANDARDS ....................................... 2-60 

2.3.1 Indicator ............................................................................................................. 2-60 

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 ....................................................................................................................2-81 
ii

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 AREAS FOR FUTURE RESEARCH 

 AND DATA COLLECTION.......................................................................................3-4 

REFERENCES ......................................................................................................................3-5 

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

APPENDICES 

A. Summary of 2003 NRC Report Recommendations........................................................ A-1 

B. Air Quality Data from Ambient Monitors Reporting 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 emissions in the U.S. by source category for 1990 

 and 1996-2005........................................................................................................... 1-7 

Figure 1-2. Second maximum 8-hour average concentrations of CO at monitors nationally, 

 2009. ........................................................................................................................ 1-11 

Figure 1-3. Second maximum 1-hour average concentrations of CO at monitors nationally, 

 2009. ........................................................................................................................ 1-12 

Figure 1-4. Trends in CO concentration (second maximum 8-hour average) in the U.S., 

 1990-2009................................................................................................................ 1-13 

Figure 1-5. Trends in CO concentration (second 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 source-to-outcome conceptual model measured in controlled 

human exposure and epidemiological studies discussed in this document. ............2-28 
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LIST OF TABLES 

Table 2-1. U.S. epidemiological studies for ischemic heart disease, cardiovascular disease and 

congestive heart failure. ..........................................................................................2-14 

Table 2-2. Carboxyhemoglobin levels and reported effects in CAD patients and healthy 

 adults from short-term CO exposures.. ...................................................................2-25 

Table 2-3. Air quality information for geographical 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 indicated levels under air quality conditions 

simulated to just meet the current standard 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 standard and “as is” conditions. ........................ 2-50 

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. ......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 simulated HD population with daily maximum end-of-hour COHb 

levels (absolute) below the indicated COHb levels under alternative levels and 

 forms for the 1-hour and 8-hour standards.............................................................. 2-68 
iv

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1-1

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 quality 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 questions that frame our consideration 

of whether the current NAAQS for CO should be retained or revised. 

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

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

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

determining whether, and if so, how it is appropriate to revise the NAAQS for CO. This PA 

presents factors relevant to EPA’s review of the current primary (health-based) standards and 

consideration of a secondary (welfare-based) standard. It focuses on both evidence- and riskbased information in evaluating the adequacy of the current CO NAAQS and in identifying 

potential alternative standards for consideration. In this PA, we consider 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 basic elements of NAAQS: indicator,2

 averaging time, form,3

and level. These elements, which together serve to define each standard, must be considered 

collectively in evaluating the health and welfare protection afforded by the CO standards. 

While this PA should be of use to all parties 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 PM2.5 NAAQS is the 3-

year average of the weighted annual mean PM2.5 concentrations, while the form of the current 8-hour CO NAAQS is 

the second-highest 8-hour average in a year. 
1-2

1.2 BACKGROUND 

1.2.1 Legislative Requirements 

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

NAAQS. Section 108 (42 U.S.C. 7408) directs the Administrator to identify certain pollutants 

that meet specified criteria, including emissions which “may reasonably be anticipated to 

endanger public health and welfare” 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 latest scientific knowledge useful in indicating the 

kind and extent of identifiable effects on public health 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 listed under section 108. 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 allowing an adequate margin of safety, are requisite 

to protect the public health.”4

 A secondary standard, as defined 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 criteria, is requisite to protect the public welfare from any known 

or anticipated adverse effects associated with the presence of [the] pollutant in the ambient air.”5

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

intended to address uncertainties associated with inconclusive scientific and technical 

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

degree of protection against hazards that 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 are 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. Thus, in selecting primary standards that include an adequate 

margin of safety, the Administrator is seeking not 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, 91st 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 prevent 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 considers such factors as the nature and severity 

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

degree of the uncertainties that must be addressed. 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 and 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 the 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 the national ambient air quality standards . . . and shall make 

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

appropriate . . . .” Section 109(d)(2) requires that an independent scientific review committee 

“shall complete a review of the criteria . . . and the national primary and secondary ambient air 

quality standards . . . and shall recommend to the Administrator any new . . . standards and 

revisions of existing criteria and standards as may be appropriate . . . .” Since the early 1980's, 

this independent review function has been performed 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 established to protect against 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 once per year (36 FR 8186). In the 1971 decision, the 

Administrator judged that attainment 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 accordingly 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 scientific criteria upon which the initial CO 

standards were based through the publication of the 1979 Air Quality Criteria Document for 
1-4

Carbon Monoxide (AQCD; USEPA, 1979a) and prepared a Staff Paper (USEPA, 1979b), which, 

along with the 1979 AQCD, served as the basis for the development of the notice of proposed 

rulemaking which was published on August 18, 1980 (45 FR 55066). Delays due to 

uncertainties regarding the scientific basis for the final decision resulted in EPA’s announcing a 

second public comment period (47 FR 26407). Following 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 were not warranted at that time 

(59 FR 38906). This decision reflected EPA's review of relevant scientific information 

assembled since the last review, as contained in the 1991 AQCD (USEPA, 1991) and the 1992 

Staff Paper (USEPA, 1992). Thus, the primary standards 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 contained in the AQCD. On June 9, 1999, CASAC held a 

public meeting to review the first draft AQCD and to provide a consultation 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 Research Council (NRC) review the impact of meteorology and 

topography on ambient CO concentrations in high altitude and extreme cold regions of the U.S. 

The NRC convened the Committee on Carbon Monoxide 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 Appendix A). Following completion of the NRC 

report, EPA did not conduct rulemaking 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 information on specified topics. A workshop was 

held on January 28–29, 2008 (73 FR 2490) to discuss policy-relevant scientific and technical 

information to inform EPA’s planning for the CO NAAQS review. Following the workshop, a 

draft IRP (USEPA, 2008a) was made available in March 2008 for public comment and was 

discussed by the CASAC via a publicly accessible 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 authors’ teleconference in November 2008 with 

invited scientific experts to discuss 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 review 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 planning document, the draft Scope and Methods 

Plan (USEPA, 2009c), for consultation with CASAC and public review at the CASAC meeting 

held on May 12-13, 2009. Taking into consideration comments on the draft Plan from CASAC 

(Brain, 2009) and the public, OAQPS staff developed 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 that 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 meeting held on March 22-23, 2010. Drawing from 

information in the final CO ISA and the second 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 the second draft REA and the draft PA from CASAC (Brain and 

Samet, 2010b, 2010c) and the public, staff completed the quantitative assessments 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 plaintiffs who alleged that EPA had failed to perform 

its mandatory duty, under section 109(d)(1), of completing a review of the CO NAAQS within 
1-6

the period provided by statute.7

 The court order that governs this 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 rulemaking concerning its review of the CO NAAQS 

no later than January 28, 2011 and August 12, 2011, respectively. 

1.3 CURRENT AIR QUALITY 

This section provides a general overview of the current air quality conditions to provide 

context for this consideration of the current standards for carbon monoxide. A more 

comprehensive discussion of air quality information is provided in the ISA (ISA, sections 3.2 

and 3.4), and a more detailed discussion of aspects 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 fossil-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 more varying CO formation results from the 

operation of these mobile sources (ISA, section 3.2). As with previous reviews of the CO 

NAAQS, mobile sources continue to be a significant source sector for CO in ambient air, as 

indicated by national emissions estimates from on-road vehicles, which accounted for 

approximately half of the total CO emissions by individual source sectors 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 national-scale reduction coming from 

reductions in on-road vehicle emissions (ISA, Figure 3-2; 2005 NEI9

). 

 

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 emissions estimates for the U.S. that meet EPA’s data quality 

assurance objectives. Estimates come from various sources and different data sources use 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 approaches, uncertainties are inherent 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 here and in Figure 1-1are drawn from recently available 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 emissions in the U.S. by source category for 

1990 and 1996-2005. 

The role of mobile source emissions is evident in the spatial and temporal patterns of 

ambient CO concentrations, which are heavily influenced 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 Inventory (ISA, p. 3-2). 

When considering all mobile sources nationwide (non-road and on-road combined), the 

contribution to total ambient CO emissions nationally 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, Colorado10 (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 (SLAMS) 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 historically been sited 2 – 10 meters from a roadway. These 

microscale CO measurements have typically represented street canyon and traffic 

corridors. 

 Middle scale: Data represent concentrations in air volumes associated with area 

dimensions ranging from 100 meters to 500 meters. Such measurements are analogous 

to CO concentrations representative of several city blocks. 

 Neighborhood scale: Defines concentrations within some extended area of the city that 

has relatively uniform land use with dimensions in the 0.5 to 4.0 kilometers range. 

Such measurements are intended to represent extended portions of a city. 

Currently, there are no minimum monitoring requirements for the number of CO 

monitoring sites, except in the new National 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 concentration site for that area under investigation.12

The complete NCore network, which will be comprised of multi-pollutant monitoring 

stations throughout the country, is required to be fully implemented 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 with the NCore network design objective 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 methods (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 set forth under the CAA. 

Measurements for determinations of NAAQS compliance 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 ppm, 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 percentage of the measurements from the CO monitoring network are 

below the LDL of conventional CO monitors, contributing greater uncertainty in a larger portion 

of the distribution of monitoring data (ISA, section 3.4.1). For example, more than half of the 

dataset of nationally reported hourly data for 2005-2007 analyzed 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 number of active monitors 

employing such sensitive methods is increasing, primarily in association with the implementation 

of the NCore network.14 The extent to which these trace-level monitors or other sensitive 

reference or equivalent monitoring methods become integrated into non-NCore SLAMS stations, 

however, will depend on the availability of funding for states to replace existing legacy CO 

monitors as well as the possibility that monitoring requirements for CO might either encourage 

or require such technological improvements. 

 

13 Among the 13 approved FRMs in use in the SLAMS network for which data were reported to EPA’s Air 

Quality System (AQS) between 2005 and 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 monitoring stations across the U.S. reported 

continuous hourly averages of CO concentrations to EPA’s Air Quality System.15 For the most 

recent period for which air quality 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 previous three data review periods (2005-2006 and 2006-

2007), one area (Jefferson County, Alabama) has failed 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 concentrations near the 

controlling 8-hour standard of 9 ppm as a second maximum 8-hour average.17. Of the 

monitoring sites with extensive records18 for 2007, sites in two counties reported second-highest 

1-hour CO concentrations between 15.1 and 35.0 ppm 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-be-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 result in a design value at or below 9.4 ppm. More detailed 

information on CO NAAQS design values is available at http://www.epa.gov/airtrends/values.html. 

18 During the period 2005-2007, 291 out of 376 monitors sited in 243 different 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 quarters 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. 

ppm curr8h09 0 - 2.4 2.5 - 6.4 >= 6.4 0.0-2.4 6.4-9.4 2.5-6.4 >9.4

No. of Counties 176 25 3 0
1-12

Figure 1-3. Second maximum 1-hour average concentrations of CO at monitors 

nationally, 2009. 

ppm 0.0-4.4 4.5-9.4 >35.4 9.4-35.4

No. of Counties 180 17 7 0

curr1hr09 0 - 4.4 4.5 - 9.4 >= 9.4
1-13

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 across the U.S. that have been continuously monitored since 1990 the average 

second highest 8-hour and 1-hour concentrations have declined 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 across the sites; ninety percent of 

sites have concentrations below the top line, while ten percent of sites have 

concentrations below the bottom line.

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CO Air Quality, 1990 - 2009

Concentration (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 sites
1-14

Figure 1-5. Trends in CO concentration (second maximum 1-hour average) in the U.S., 

1990-2009. The white line indicates average across 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 ORGANIZATION OF THE DOCUMENT 

This PA includes staff’s evaluation of the policy implications of the scientific evidence 

reviewed in the ISA and the results of quantitative analyses based on that evidence. Taken 

together, this information informs staff conclusions and the identification of a range of policy 

options for consideration in addressing public health 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 the rationale for previous reviews and the 

approach followed in the current review. Chapter 2 discusses the adequacy of the current 

standards, taking into account evidence- and risk-based considerations, and includes staff 

conclusions on adequacy. Chapter 2 also discusses potential alternative standards for 

consideration, focusing on indicator, averaging time, form, and level, and includes staff 

conclusions on alternative standards for consideration. Finally, chapter 3 discusses information 

relevant to staff’s consideration of a secondary standard for CO. 

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CO Air Quality, 1990 - 2009

Concentration (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 sites
1-15

REFERENCES 

Brain, J.D. (2009) Letter from Dr. Joseph Brain to Administrator Lisa Jackson. Re: Consultation on EPA’s Carbon 

Monoxide National Ambient Air Quality Standards: Scope 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. 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: 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 Scientific Advisory Committee, to 

William K. Reilly, EPA Administrator, July 17, 1991. 

McClellan R.O. (1992) Letter from Dr. Roger McClellan, Chairman, Clean Air Scientific 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 Academies 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 Air Quality Planning and Standards, 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 Information, OAQPS Staff Paper. 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 Quality 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/recordisplay.cfm?deid=18163 

U.S. Environmental Protection Agency. (2008a) Draft Plan 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 Planning and Standards, Research Triangle Park, NC. 

EPA-452/D-08-001. Available at: http://www.epa.gov/ttn/naaqs/standards/co/s_co_cr_pd.html. 

U.S. Environmental Protection Agency. (2008b) Plan for Review 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/naaqs/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 Environmental 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 Environmental 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 Monoxide National Ambient Air Quality Standards: Scope 

and Methods Plan for Health Risk and Exposure Assessment. 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/standards/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 Triangle Park, NC. EPA-452/P-09-008. Available at: 

http://www.epa.gov/ttn/naaqs/standards/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/standards/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 Standards, 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 External 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 Review 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.html
2-1

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, updated, a series of key policy-relevant 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 considerations 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 potential 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 considered collectively 

in evaluating the health protection afforded by the current or any potential alternative standards. 

2.1 APPROACH 

For the purposes of this Policy Assessment (PA), staff has drawn from EPA’s assessment 

and integrated synthesis of the scientific 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 the Risk and Exposure Assessment (USEPA, 2010b; 

henceforth referred to as the REA). The evidence-based discussions presented in this chapter 

draw upon evidence from epidemiologic studies, controlled human exposure studies, and 

toxicological studies evaluating short- or long-term exposures to CO, as discussed in chapter 5 of 

the ISA, with supporting evidence related to dosimetry 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 the ISA. The exposure/risk-based discussions have 

drawn from the quantitative health 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 alternative standards that are supported by the 

currently available scientific evidence. 

In presenting a range of primary standard options for consideration, we note that the final 

decision is largely a public health policy judgment. A final decision must draw upon scientific 
2-2

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 judgments, discussed more fully below, is based on 

the recognition that the available health effects 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 likelihood and magnitude of the response become 

increasingly uncertain. This approach is consistent with the requirements of the NAAQS 

provisions of the Act and with how EPA and the courts have historically interpreted the Act. 

These provisions require the Administrator to establish primary standards that, in the 

Administrator’s judgment, are requisite to protect public health with an adequate margin of 

safety. In so doing, the Administrator seeks to establish standards that are neither more nor less 

stringent than necessary for this purpose. The Act does not require that primary standards be set 

at a zero-risk level, but rather at a level that avoids unacceptable risks to public health. 

The following subsections include background information on the approach used in the 

previous review of the CO standards (section 2.1.1) and also a discussion 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 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 once per year. These 

standards were initially set in 1971to protect against the occurrence of carboxyhemoglobin 

(COHb) levels that may be associated with effects of concern (36 FR 8186). Reviews of these 

standards in the 1980s and early 1990s identified additional evidence regarding ambient CO, CO 

exposures, COHb levels, and associated health effects (USEPA, 1984a, 1984b; USEPA, 1991; 

USEPA, 1992; McClellan, 1991, 1992). Assessment of the evidence in those reviews led the 

EPA to retain the existing standards without revision (59 FR 38906). 

The 1994 decision to retain the primary standards without revision was based on the 

evidence published through 1990 and reviewed in the 1991 AQCD (USEPA, 1991), the 1992 

Staff Paper assessment of the policy-relevant information contained 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 Administrator first recognized 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 evidence was taken into account to identify 

the lower end of this range to provide 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-Kane (CFK) differential equation was employed in the analysis of 

CO exposures expected to occur under air quality scenarios related to just meeting the current 8-

hour CO NAAQS, the controlling 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 was 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, factors recognized as having potential to alter the 

effects of CO included exposures to other pollutants, some drugs and some environmental 

factors, such as altitude. Cardiovascular effects of CO, as measured by decreased time to onset 

of angina and to onset of significant electrocardiogram (ECG) ST-segment depression2 were 

judged by the Administrator to be “the health effects 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 disease3

across the controlled human exposure evidence (Adams et al., 1988; Allred et al., 1989a, 1989b, 

1991; Anderson et al., 1973; Kleinman et al., 1989, 1998; Sheps et al., 19874) 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 exercise. The duration of exercise required to demonstrate chest pain and/or a 1-

mm change in the ST segment of the ECG were key measurements 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 associated 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 depression, is asymptomatic (i.e., silent). Patients who 

experience angina typically have additional ischemic episodes that are asymptomatic (2000 AQCD, section 7.7.2.1). 

In addition to such chronic conditions, CAD can lead to sudden episodes, such as myocardial 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 CASAC 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 particular emphasis in the 

1991 AQCD to indicate the basis for conclusions regarding lowest observed-effect levels of 

COHb in patients with exercise-induced ischemia, 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 existence of a range of views among health 

professionals on the clinical significance of the responses observed in the clinical studies, 

CASAC noted that the dominant view was that they should be considered “adverse or harbinger 

of adverse effect” (McClellan, 1991) and EPA recognized that it was “important that standards 

be set to appropriately reduce the risk of ambient exposures which produce COHb levels that 

could induce such potentially adverse 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 controlled human exposure evidence as well as other aspects of the 

available evidence and uncertainties regarding 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 “relatively trivial” (59 

FR 38913). 

 Findings of short-term reduction in maximal work capacity measured in trained 

athletes exposed to CO at levels resulting in COHb levels of 2.3 to 7 percent. 

 The potential that the most sensitive individuals have not been studied, the limited 

information regarding the effects of ambient CO in the developing fetus, and concern 

about visitors to high altitudes, individuals with anemia or respiratory disease, or the 

elderly. 
2-5

 Potential for short term peak CO exposures to be responsible for impairments 

(impairment of visual perception, sensorimotor performance, vigilance or other CNS 

effects) which could be a matter of concern for 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 individuals exposed to CO concurrently with 

drugs (e.g., alcohol), during heat stress, or co-exposure to other pollutants. 

 Uncertainties, described as “large,” that remained regarding 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 measurements 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 should focus on reducing the 

number of individuals with cardiovascular 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 uncertain occurrence, as well as those of clear 

concern that have been associated with COHb levels in the upper-end 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 analysis 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 maximum 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 standard, 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 higher 
2-6

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 absence of indoor sources when the current standards 

are attained.” The analysis also took into account that certain indoor sources (e.g., passive 

smoking, gas stove usage) contributed to total CO exposure and EPA recognized that such 

sources may be of concern for such high risk groups 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 concluded that revisions of the current 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 exposures during any 24-hour period. The 1-hour 

averaging time was selected as better representing a time period of interest to short-term CO 

exposure and providing protection from effects which might be encountered 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 retaining the current primary CO 

standards, or whether consideration of revisions is appropriate, we adopted an approach 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. 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 judgments 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 standard, 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 assessments when possible, and qualitative assessment of impacts 

that could not be quantified. 

In conducting this assessment, we draw on the current evidence and quantitative 

assessments of exposure pertaining to the public health risk of ambient CO. 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, including the current ISA and 

the 2000 AQCD (USEPA, 2010; USEPA, 2000), as well 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, the best characterized health effect associated with CO levels of 

concern is hypoxia (reduced oxygen availability) induced by increased 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 evidence of cardiovascular effects is that from 

a series of controlled human exposure studies among exercising individuals with coronary heart 

disease (CHD) also referred to as coronary artery disease (CAD) (ISA, sections 5.2.4 and 5.2.6). 

Additionally available in this review are a number of epidemiological studies that investigated 

the association of cardiovascular disease-related health 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 discussed in sections 2.2 and 2.3 below, we have taken into account 

both evidence-based and exposure/risk-based considerations framed 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 and REA, support or call into question the 

adequacy of the protection afforded by the current CO standards? 

To assist us in interpreting the currently available scientific evidence and the results of 

recent quantitative exposure/risk analyses to address this question, we have focused on a series 

of more specific questions, posed within sections 2.2.1 and 2.2.2 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 recently in the ISA. 

2.2.1 Evidence-based Considerations 

In considering the evidence with regard to the issue of adequacy of the current standard, 

we address a series of questions that focus on policy-relevant aspects of the evidence beginning 

with the health effects associated with CO exposure, followed by the use of COHb levels as the 

indicator of CO exposures and biomarker for characterizing 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 conclusions from the previous review 

regarding the health effects associated with exposure to CO? 

The current evidence continues to support our conclusions from the previous review 

regarding key health effects associated with CO exposure. The best characterized effect of CO 

continues to be related to the binding 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 cardiovascular effects (ISA, 

section 5.2). In the scientific assessment for the current review, a likely causal relationship is 

judged to exist between relevant CO exposures6

 and cardiovascular effects (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 effects, and respiratory effects, in some cases 

expanded from that which was available at the time of the last review, 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 exposures (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 effects evidence in the last review. 

The long-standing body of evidence that has established many aspects of the biological 

effects of CO continues to contribute 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 inhalation, CO diffuses through the respiratory 

zone (alveoli) to the blood where it binds to Hb, forming COHb. Accordingly, inhaled CO 

elicits various health effects through 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 associated with CO levels of concern is hypoxia (reduced oxygen 

availability) induced by increased COHb levels in blood and decreased oxygen availability to 

critical tissues and organs, specifically the heart (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 flow 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 and limiting exercise capacity (2000 AQCD, section 

7.1).7

 The dose metric most commonly used as a bioindicator 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 additional detail and support to our prior 

understanding of CO effects and population susceptibility. For example, the currently available 

evidence expands on potential nonhypoxic mechanisms for CO effects, although the importance 

of such mechanisms at environmentally-relevant CO exposures is unclear (ISA, section 5.1.3). 

Most notably, the current evidence includes much expanded epidemiological evidence that is 

consistent with previous conclusions regarding cardiovascular disease-related susceptibility and 

may provide indications of air quality conditions that may be associated with ambient CO-related 

risk. In this review, the clearest evidence is available for cardiovascular 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 established framework (ISA, chapter 1). The major 

conclusion drawn in the ISA regarding the critical analysis of all available data on health effects 

of CO including the clinical and 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 availability, it is concluded that a causal 

relationship is likely to exist between relevant8

 short-term CO exposures and cardiovascular 

morbidity" (ISA, p. 2-6, section 2.5.1). Additionally, as mentioned above, the ISA judges the 

evidence to be suggestive of causal relationships between relevant short- and long-term CO 

exposures and CNS effects, birth outcomes and 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 ISA 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 review, results from controlled human exposure studies of 

individuals with coronary artery disease (Adams et al., 1988; Allred et al., 1989a, 1989b, 1991; 

Anderson et al., 1973; Kleinman et al., 1989, 1998; Sheps et al., 19879

) are the “most compelling 

evidence of CO-induced effects on the cardiovascular system” (ISA, Section 5.2). Additionally, 

the use of an internal dose metric, COHb, adds to the strength of the findings in these controlled 

exposure studies. As a group, these studies demonstrate the role 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 electrocardiographic effects of 1-hour exposures to 35 ppm CO 

in a rat strain developed as an animal model of cardiac susceptibility (ISA, section 5.2.5.3). 

Further toxicological evidence is identified for other effects (e.g., aortic injury, microvascular 

permeability, vascular remodeling, ventricular hypertrophy) 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 reasons: 1) dose-response relationships were 

observed; 2) effects were observed at the lowest COHb levels tested (mean of 2-2.4% COHb11

 

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 provide evidence of reduced time to exercise-induced angina 

associated with elevated COHb resulting from controlled short-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 evidence of a threshold; 3) objective measures of 

myocardial ischemia (ST-segment depression) were 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 levels12, 

and by CO-Ox; 5) a large number of study subjects were used; 6) a strict 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 onset of markers of myocardial ischemia resulting 

from two short CO exposures targeted to result in mean study subject COHb levels of 2% and 

4%, respectively (ISA, section 5.2.4). In this study, subjects (n=63) on three 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 concentrations targeted for each subject 

to achieve blood COHb levels of 2% and 4%. The 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 underwent 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 was 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 average COHb concentrations were reported as 2.0% and 3.9%.13 

Across all subjects, the mean time to angina onset for control (“room” 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 resulted 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 exercise-induced angina, the time to which was shortened by 4.2% 

 

12 As stated in the ISA, the gas chromatographic technique for measuring COHb levels “is known to be 

more accurate than spectrophotometric measurements, particularly for samples 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 COHb 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 of 

CO-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 levels resulting from the lower experimental CO exposure. 
2-12

(p=0.027) and 7.1% (p=0.002), respectively, for the two experimental CO exposures (Allred et 

al., 1989a, 1989b, 1991).14 As at the time of the last review, while ST-segment depression is 

recognized as an indicator of myocardial ischemia, the exact physiological significance of the 

observed changes among those with CAD is unclear (ISA, p. 5-48). 

No human clinical studies have been specifically designed to evaluate 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 finding of the multi-laboratory study was the doseresponse relationship (discussed further in addressing a subsequent question below) observed 

between COHb and the markers of myocardial ischemia, with effects observed at the lowest 

increases in COHb tested, without evidence of a measurable threshold 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 further changes in objective ECG measures of 

ischemia” implying that “small increments in COHb could adversely affect myocardial function 

and produce ischemia” (Allred et al., 1989b, 1991). 

The epidemiological evidence has expanded considerably since the last review including 

numerous additional studies that are coherent with the evidence on markers of myocardial 

ischemia from controlled human exposure studies 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 PM2.5, nitrogen dioxide, sulfur dioxide, 

ozone, and CO) at fixed-site ambient monitors and increases in emergency department visits and 

hospital admissions for specific cardiovascular health outcomes including ischemic heart disease 

(IHD), myocardial infarction (MI), congestive heart failure (CHF), and cardiovascular 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; Wellenius et al., 2005). Findings 

of positive associations for these outcomes with metrics of ambient CO concentrations are 

coherent with the evidence from controlled human exposure studies of myocardial ischemiarelated effects resulting from elevated CO exposures (ISA, section 2.5.1; ISA, Figure 2-1). 

Table 2-1 below presents studies reporting associations of ambient CO concentration 

estimates for several U.S. urban areas with hospital admissions for ischemic heart disease, 

cardiovascular disease or congestive heart failure described in the 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 (Allred 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 these 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 areas include the Atlanta, Georgia metropolitan 

statistical area, the greater Los Angeles, California, 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 indicate statistically significant positive associations 

were observed with ambient CO concentrations based on air quality for 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 lag periods, which, as noted in the 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 study by Mann et al., 2002), the California study by Mann et al., 

(2002) also observed a significant positive association with same day CO concentration. 

Additionally presented in Table 2-1 are the U.S. studies reporting associations with 

hospital admissions for CHF, a condition that affects an individual’s ability to compensate for 

reduced oxygen availability. One of the IHD outcome studies cited above also reported a 

significant association for ambient CO with hospital admissions for CHF (Linn et al., 2000), as 

did additional studies in Allegheny County (Pittsburgh) 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 presented for all three of these studies are based on 

the 24-hour CO concentration, with the California and Allegheny County studies’ association 

with same-day air quality, while the association shown for the Denver study was with ambient 

CO 3 days prior to health outcome (Table 2-1). 
2-14

Table 2-1. U.S. epidemiological studies for ischemic heart disease, cardiovascular disease and congestive 

Study Reference 

Health 

Outcome

A

Risk EstimateB

(confidence interval) 

Estimates are 

standardized within 

averaging times.

CO Concentration Metric for 

Risk Estimated Presented 

Assignment of 

Monitors to Study 

Subjects 

Study Area 

 U.S. studies of hospital admissions for coronary heart disease (ISA, Figure 5-2). Metzger et al., 2004 IHD 1.016 (0.999-1.034) 1-hour daily maximum, average for most recent 3 days Single central residential monitor 20-county Atlanta 

IHD 1.0136 (1.0053-1.0220) Mann et al., 2002 

IHD+CHF 1.0304 (1.0135-1.0475) 

8-hour daily maximum, average for 

most recent 4 days 

Residence grid centroid 

interpolated from 3 closest 

monitors 

South Coast Air Ba

CA 

Linn et al., 2000 MI 1.020 (1.011-1.029) 24-hour average, same day Average across all monitors “ U.S. studies of hospital admissions for cardiovascular disease (ISA, Figure 5-5). Bell et al., 2009 CVD 65+ 1.0096 (1.0079-1.0112) 1-hour daily maximum, same day Average of monitors in county of residence 126 urban countiTolbert et al., 2007 CVD 1.016 (1.008-1.025) Metzger et al., 2004 CVD 1.017 (1.008–1.027) 

1-hour daily maximum, average for 

most recent 3 days 

Single central residential 

monitor 20-county Atlanta 

Linn et al., 2000 CVD 1.016 (1.013-1.019) 24-hour average, same day Average across all monitors South Coast Air Ba

CA 

U.S. studies of hospital admissions for congestive heart failure (ISA, Figure 5-4).Linn et al., 2000 CHF 1.013 (1.004-1.021) 24-hour average, same day Average across all monitors South Coast Air Ba

CA 

Metzger et al., 2004 CHF 1.010 (0.988-1.032) 1-hour daily maximum, average for most recent 3 days Single central residential monitor 20-county Atlanta Symons et al., 2006 CHF 1.08 (0.40-2.99) 8-hour daily maximum, average for most recent 4 days Single central residential monitor Baltimore area, MWellenius et al., 2005 CHF 1.0843 (1.0614-1.1077) 24-hour average, same day 

Single area-wide 

representation based on 3 

monitors 

Allegheny county, 

Koken et al., 2003 CHF 1.181 (1.002-1.393) 24-hour average, 3 days prior Average across all monitors Denver county, CA Hospital admissions for ischemic heart disease (IHD), myocardial infarction (MI), cardiovascular disease (CVD; Bell 2009 included only subjects 65 years old and above), and coB 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 ambient 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 morbidity, 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 outcomes 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, particularly 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 evaluated associations of ambient CO with other 

cardiovascular effects since the last review. For example, preliminary evidence of a link 

between exposure to CO and alteration of blood markers of coagulation and inflammation in 

individuals with CAD or CVD has been provided 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 role of these markers in prothrombotic events and 

their possible contribution to the pathophysiology of CO-induced aggravation of ischemic heart 

disease (ISA, section 5.2.1.8). Other epidemiological studies (including field and or panel 

studies) also provide some evidence of a link between 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 rate, 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 indicative of ischemic events (ISA, section 5.2.1.2), one found no 

association and, in the other study, the association with CO did not remain statistically 

significant in multipollutant models, unlike the association with black carbon in that study (ISA, 

p. 5-16). A limited number of epidemiological studies (Bell et al., 2009; Linn 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 concentrations (ISA, section 5.2.1.9, 

Table 5-8 and Figure 5-3). 

At the time of the last review, there was evidence for effects other than cardiovascular 

morbidity, including neurological, respiratory and developmental effects. These findings include 

the following. 
 2-16

 With regard to neurological effects, acute exposures to CO have long been known to 

induce CNS effects such as those observed with CO poisoning, although limited and 

equivocal evidence available at the time of the last review included indications of some 

neurobehavioral effects to result from CO exposures resulting in a range of 5-20% 

COHb (2000 AQCD, section 6.3.2). No additional clinical or epidemiological studies 

are now available that investigated such effects of CO at ambient levels (ISA, section 

5.3). 

 With regard to potential effects of CO on birth outcomes and developmental effects, 

the potential vulnerability of the fetus and very young infant to CO was recognized 

during the 1994 review and in the 2000 AQCD. The CO-specific evidence available, 

however, included limited epidemiological analyses focused primarily on very high CO 

exposures associated with maternal smoking, 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 epidemiological and animal toxicological 

studies. The currently available evidence 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 toxicological studies provide some support and 

coherence for these birth and developmental outcomes at higher than ambient 

exposures,15 although a clear understanding of the mechanisms underlying potential 

reproductive and developmental effects is still lacking (ISA, section 2.5.3). 

 With regard to respiratory effects, the 2000 AQCD concluded it unlikely that CO has 

direct effects on lung tissue, except at extremely high concentrations (2000 AQCD, p. 

6-45). There is currently limited, suggestive evidence of an association between shortterm exposure to CO and respiratory-related outcomes. Only preliminary 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, respiratory and developmental 

effects, it remains limited. 

In summary, rather than altering our conclusions 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 related to the role of CO in limiting oxygen 

availability, as those of greatest concern at low exposures. 

 

15 The lowest exposures eliciting an effect in the animal 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 exposures to ambient CO? Or does the current 

evidence provide support for a focus on alternate 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 caused 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 pre-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). The integrative review of health 

effects of CO indicates that “the clearest evidence indicates that individuals 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 independent 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-containing proteins other than 

hemoglobin and myoglobin, and involve a wide range of molecular targets and CO 

concentrations, as described in the 2000 AQCD (USEPA, 2000, section 5.8) and in the ISA (ISA, 

section 5.1.3). Older toxicological studies demonstrated that exposure to high concentrations of 

CO resulted in altered functions of heme proteins other than myoglobin and hemoglobin, 

potentially interfering with basic cell and molecular processes and leading to dysfunction and/or 

disease. More recent toxicological in vitro and in vivo studies have provided evidence of 

alteration of nitric oxide signaling, inhibition of cytochrome C oxidase, heme loss from protein, 

disruption of iron homeostasis and alteration of cellular reduction-oxidation status (ISA, section 

5.1.3.2). The ISA notes that these mechanisms may be interrelated. The evidence for 

mechanisms related to alteration 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 responsible for a continuum of effects from cell 

signaling to adaptive responses to cellular injury, depending on intracellular concentrations of 

CO, heme proteins and molecules which modulate CO binding to heme proteins” (ISA, section 

5.1.3.3). New research based on this evidence for pathways other than those related to impaired 

oxygen delivery to tissues is needed to further understand these pathways and their linkage to 
 2-18

CO-induced effects in susceptible populations. Therefore, at this time, the evidence indicates 

that COHb continues to be the most useful and 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 understanding of populations that are 

particularly susceptible to CO exposures? Is there new evidence that suggest 

additional susceptible populations that should 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 can potentially result from many 

factors, including pre-existing medical 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 regarding susceptible populations for exposure to 

ambient CO. In the 1994 review and the 2000 AQCD, the evidence best supported the 

identification of patients with CAD as a population at increased risk for low levels of CO 

(USEPA, 1992; 2000 AQCD). Other groups were also recognized as potentially susceptible in 

the 2000 AQCD based on consideration of the clinical 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, especially those with compromised cardiovascular function; people 

with conditions affecting oxygen absorption, blood flow, oxygen carrying capacity or transport; 

people using drugs with central nervous system depressant properties 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-ambient CO exposures (2000 AQCD, p. 7-6). 

Based on the evidence from clinical studies also considered in the last review, with which 

the now much-expanded epidemiological evidence base is coherent, the population with preexisting cardiovascular disease associated with limitation in oxygen availability continues to be 

the best characterized population at risk of adverse CO-induced effects, with CAD recognized as 

“the most important susceptibility characteristic for increased risk due to CO exposure” (ISA, 

section 2.6.1). An important factor determining the increased susceptibility of this population is 

their inability to compensate for the reduction in oxygen levels due to an already compromised 

cardiovascular system. Individuals with a healthy cardiovascular system (i.e., with healthy 
 2-19

coronary arteries) have operative physiologic compensatory mechanisms (e.g., increased blood 

flow and oxygen extraction) for CO-induced hypoxia and 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 make the cardiac muscle 

of a person suffering with CAD a critical target for the hypoxic effects of CO. 

In the current review, recognition of susceptibility of the population with pre-existing 

cardiovascular disease, such as CAD, is supported by the expanded epidemiological database, 

which includes a number of studies reporting significant 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; and Peel et al., 2007) of increased hospital 

admissions and emergency department visits for IHD among individuals with secondary 

diagnoses for other cardiovascular outcomes including arrhythmia and congestive heart failure 

(ISA, section 5.7), and toxicological studies reporting altered cardiac outcomes in animal models 

of cardiovascular disease (ISA, section 5.2.1.9). 

Cardiovascular disease comprises many types of medical disorders, including heart 

disease, cerebrovascular disease (e.g., stroke), hypertension (high 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 AQCD, section 7.7.2.1). Types of cardiovascular 

disease other than those discussed 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 cardiovascular disease such as congestive heart failure, arrhythmia, and 

non-specific cardiovascular disease, although more limited for peripheral vascular and 

cerebrovascular disease, indicates that “the continuous nature of the progression of CAD and its 

close relationship with other forms of cardiovascular disease suggest that a larger population 

than just those individuals with a prior diagnosis of CAD may be susceptible to health effects 

from CO exposure” (ISA, p. 5-117). 

Although there was little experimental data available 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 populations 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 availability 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 duration at similar COHb levels during short term maximal exercise. This 

population was of lesser concern since it represented a smaller 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, lifestyle, medications or alterations in the 

physical environment (e.g., increased altitude). This 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 production or levels, such as people with 

obstructive lung diseases, diabetes and anemia; older adults; fetuses during critical phases of 

development and young infants or newborns; commuters 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 epidemiological, controlled human exposure, and 

toxicological studies suggest that people with obstructive lung disease (e.g., COPD patients with 

underlying hypoxia, asthmatics) may be a susceptible 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 individuals 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). Other epidemiological studies (ISA, section 

5.5.2.2) have reported weak associations in asthmatics, which constitute another population that 

can experience exercise-induced airflow limitation. Preliminary evidence was also shown in one 

animal toxicological study (Ghio et al., 2008), indicating mild pulmonary inflammation upon 

exposure to 50 ppm CO. 

With regard to other potentially at-risk populations, there is also limited epidemiological 

data regarding the susceptibility of diabetics (ISA, section 5.7.1.3). Epidemiologic studies 

(Pereira Filho et al., 2008; Zanobetti 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 syndrome17 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 metabolic syndrome (ISA, 

section 5.7.1.3). People with anemia who have reduced oxygen-carrying capacity 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 controlled 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 examined 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 susceptible population to the 

effects of CO, primarily due to the increased prevalence of cardiovascular 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 infarction (MI) hospital admissions among older 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 population for increased health effects due to CO 

exposure (ISA, section 5.7.2.1). 

The developing fetus and young infants or newborns have been considered to be 

potentially susceptible to CO exposures due to their altered CO kinetics. Although the effects of 

CO on maternal-fetal relationships are not well understood, fetuses 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). Newborn infants are also potentially susceptible to 

CO-induced effects due to their comparatively higher oxygen consumption rate and lower 

oxygen-transport capacity than those of adults, which could potentially result in higher COHb 

levels (AQCD 2000, section 7.7.1). Data from laboratory 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 delayed behavioral development, 

or may disrupt the normal physiological 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 association of short-term ambient CO exposure with pre-term birth and 

birth defects, and weak evidence suggests an association 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 may induce those effects and at what exposure 

levels is lacking (ISA, section 5.4.3). 

Gender has also been considered as a possible source for susceptibility. However, the 

evidence is inconclusive based on the limited epidemiological data and the gender-specific 

variability in CO endogenous production (ISA, section 5.7.3). Increased altitude and physical 

activity through their effect on CO uptake and elimination have also been considered to 

potentially influence susceptibility. For example, residents of low altitudes visiting high 

altitudes, especially the elderly 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 susceptibility factors have been considered, such as use of medications 

that may alter CO production (ISA, p. 2-12). Lastly, people experiencing increased CO 

exposures, such as those spending relatively greater amounts of time in microenvironments with 

relatively higher levels of ambient CO have been considered 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 effects, as well as a way to relate the specific 

evidence available for the CAD population to these other populations. 

In summary, the current evidence continues to support the identification of people with 

cardiovascular disease as having susceptibility to CO-induced health effects (ISA, 2-12), with 

those having CAD as the population with the best characterized 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 cardiovascular 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 other pre-existing diseases that may have already limited oxygen

availability, increased COHb levels, or increased 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 most susceptible to an increase in COinduced health effects” (ISA, p. 2-12). 
 2-23

 Does the current evidence alter our conclusions 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 conclusions 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 cardiovascular 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, the 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 exercise-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 myocardial ischemia) had been documented in 

multiple studies at post-exposure COHb levels 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., 

198719). The matched measurements available from Allred et al. (1989a, 1989b, 1991) of COOx and gas chromatography, the method generally recognized 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 measurements on the order of 2-2.4%.20 Evidence of effects in other 

clinical study groups includes effects in subjects with cardiac arrhythmias and effects on exercise 

duration and maximal aerobic capacity in healthy 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). Allred et al. (1989a, 1989b, 

1991) further reported a dose-response relationship 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 myocardial ischemia (Allred et al., 1989a, 1989b, 1991). 

While this evidence informed our conclusions regarding COHb levels associated with health 

effects, the CO exposure concentrations employed in the studies to achieve these COHb levels 

were substantially above ambient 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 

2.0-2.4B

3.9-4.7B

2.7-3.2B

4.7-5.6B

1.4-1.8B

 

(1.4-2.0) 

3.2-4.0B

(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 

NAC

 2.9-5.9 (1.4-4.2) 

Adams et al., 1988; 

Anderson et al., 1973; 

Kleinman et al., 1989, 

1998;Sheps et al,1987D

Patients with 

coronary 

artery 

diseaseA

Exercise-induced arrhythmia following 1-hour 

exposure 

NA 5.3E

 (3.5)E Sheps et. al., 1990, 

1991 

Reduction in exercise duration and/or 

maximal aerobic capacity NA 3F

-20 - 

Adir et al., 1999; 

Drinkwater et al., 1974; 

Ekblom and Huot, 

1972; Horvath, 1975; 

Raven et al., 1974; 

Healthy Weiser et al., 1978 

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 average levels post and pre-exercise (subsequent to CO exposure). C

 NA = not available. 

D

 Statistical analyses of the Sheps data 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. 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 effect 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 effects of CO exposure in susceptible populations at 

COHb levels below 2%. Thus, similar to the last review, the multilaboratory study by Allred et 

al. (1989a, 1989b, 1991) continues to be the study that has evaluated cardiovascular effects of 
 2-26

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 review 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-induced angina and ST-segment change, 

respectively, per 1% increase in COHb concentration 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 concentrations associated with health effects, we 

have developed estimates of COHb associated with different air quality 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 improvements 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 population under differing air 

quality conditions are described in section 2.2.2 below. 

As discussed in more detail above, a number of epidemiological studies of health 

outcome associations with ambient CO have been conducted since the last review. These 

include studies, identified in Table 2-1 above, that have reported associations with different 

ambient CO metrics (e.g., 1-hour and 8-hour averages, often as central-site estimates) derived 

from CO measurements at fixed-site ambient monitors in selected urban areas of the U.S. and 

cardiovascular endpoints other than stroke, particularly hospitalizations and emergency 

 

22 Relative to baseline (0.6% mean COHb), 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 control (“clean” air) exposures was approximately 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 cardiovascular health outcomes including 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 pollutants, including CO, report 

positive associations, a number of which are statistically significant (ISA, sections 5.2.3 and 

5.2.1.9; Table 2-1 above). The long-standing body 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 outcomes reported in the epidemiological studies, 

providing coherence between these studies and the clinical evidence of short-term exposure to 

CO and health effects. 

In consideration of the evidence base for CO cardiovascular effects, 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 between directly measured controlled short-term CO exposures 

and specific levels of an internal dose metric, COHb, which elicited specific myocardial 

ischemia-related responses in CAD patients. These studies inform our interpretation of the 

associations we observed in the epidemiological studies. The epidemiological studies reported 

associations between CO levels measured at fixed-site monitors and emergency department visits 

and/or hospital admissions for IHD and other cardiovascular disease-related outcomes that are 

plausibly related to the effects on physiological indicators of myocardial ischemia (e.g., STsegment changes) demonstrated in the controlled human exposure studies, providing coherence 

between the two sets of findings (ISA, p. 5-48). 

Exposure Internal 

Dose

Nonambient (e.g., COHb)

CO

Ambient CO Health 

Outcomes

(e.g., hospital 

admissions)

Effects 

(e.g., markers 

of myocardial 

Endogenous Ischemia)

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 

Epidemiological Studies admissions)

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 epidemiological studies discussed in this 

document. 

We recognize, however, several gaps between the two lines of evidence (clinical and 

epidemiological) which complicate their integration, particularly with regard to ambient 

exposures and ambient concentrations associated with health effects. These gaps limit our ability 

to integrate the evidence from these epidemiological studies with our knowledge of CO-related 

effects based on the clinical evidence. Most particularly we lack information on the actual CO 

exposures and associated internal COHb levels for the epidemiological study populations, 

including the relative contributions from ambient and nonambient CO. These gaps in our 

understanding of the role of nonambient CO exposures and their contribution to COHb levels 

complicate our ability to discern the ambient concentrations that may be eliciting health effects. 

Moreover, it is also unknown how the unmeasured exposures in epidemiological study 

populations relate to the exposure concentrations of the clinical studies (e.g., 1 hour at 

approximately 50-200 ppm), which were substantially 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 (O2) availability lends biological plausibility to ischemia-related health outcomes following CO 

exposures, although “it is not clear whether the small changes in COHb associated with ambient CO exposures 

results in substantially reduced O2 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 within the ranges of current maximum ambient concentrations 
 2-29

specific relationship between the changes in indicators of myocardial ischemia observed in the 

controlled human exposure studies and the hospital admissions assessed in the epidemiological 

studies. Together, these gaps complicate our ability to draw conclusions regarding the levels of 

CO in ambient air associated with health effects 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-related pollutants, CO presents specific challenges that complicate the 

quantitative interpretation with regard to ambient 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 the effects of another traffic-related pollutant or 

mixture of pollutants (ISA, section 5.2.3). As noted in the ISA, in interpreting the 

epidemiological evidence for cardiovascular morbidity “[i]t is difficult to determine from this 

group of studies the extent to which CO is independently associated with CVD outcomes or 

whether CO is a marker for the effects of another traffic-related pollutant or mix of pollutants. 

As recognized in the ISA, “[o]n-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” (ISA, p. 5-40 – 5-41). We also note CASAC’s recognition of the potential 

for co-pollutants to serve as confounders to be “particularly problematic for CO” and the need to 

give consideration to the possibility 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 considered to provide the strongest and most consistent weight 

of evidence for short-term effects of CO (ISA, Figure 5-2, pp. 5-24 to 5-26), with the U.S. 

studies for the broader category of all CVD hospital 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 personal exposure concentrations more commonly expected currently (e.g., ISA, 

Figure 3-45). 
 2-30

outcomes (which are inclusive of IHD), for which more direct conceptual linkages can be drawn 

to the myocardial ischemia effects of the CAD clinical studies. 

As recognized above, this set of studies provides epidemiological evidence for a positive 

association between cardiovascular outcomes and ambient CO concentrations. With regard to 

our overarching question as to the adequacy of the protection afforded by the current standards, 

however, the studies in which CO concentrations exceeded the current NAAQS during some 

portion of the study period are, accordingly, less informative. While the full set of these 

epidemiological studies, including 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 involving air quality conditions 

in which the current standards were met that are most informative to the overarching question of 

adequacy. Accordingly, in considering these epidemiological studies, we have considered the air 

quality conditions during the periods of study as described below. 

The set of studies listed in Table 2-3 encompasses a range of air quality conditions 

extending from those that did not meet the current 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 California and a group of 126 urban counties26 and the multi-year time 

periods for this set of studies together span the period from 1988 through 2005 (Table 2-3 

below). During the time periods of study, however, only the Atlanta studies (Metzger et al., 

2004; Tolbert et al., 2007) did not include years in which ambient CO concentrations exceeded 

the 8-hour standard (Table 2-3). The CO concentration with which an association with hospital 

admissions was observed in the Atlanta studies was the average of daily maximum 1-hour 

concentrations on the day of and two days prior to hospital admission. 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 analyses exceeded the level 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 concentration in a year (i.e., the design value for the 8-hour 

standard) ranging up to 24.3 ppm, as compared to the 8-hour standard of 9 ppm.27 In the Atlanta 

 

25 While the 1-hour CO standard was met during the full 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 all cardiovascular outcomes, adjusted for NO2, 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 2nd maximum in a year. This subset analysis found 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, statistically significant associations (with adjustment for NO2), 
 2-31

study area, the design value for the 8-hour standard ranged from 2.6 up to 5.3 ppm over the 

combined 12 years of study. 

The study areas for which statistically significant positive associations with CHF were 

observed include the area of California 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, Pennsylvania (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 concentrations, having analyzed the relationship 

between hospital admissions for CHF hospital admissions and estimates 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 recent 3 or 4 days, respectively.30 

 

although confidence intervals increased at the lower cutoff values and the proportion of values near and below the 

limit of detection grew larger. 

28 In the study focused in Denver, a statistically significant 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 used 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). 
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Table 2-3. Air quality information for geographical areas of key U.S. epidemiological studies. 

Study Information Ambient A

Study-reported CO 

Concentrations, C in 

terms of study metric

(ppm)

Design Values 

for Current NAAQS,

across study years (ppm) Study Area Study Time 

Period 

Study 

Reference 

Health 

OutcomeB 

CO Concentration Metric Associated 

with Health 

Outcome 

Assignment of 

Monitors to Study 

Subjects Mean/ 

median* Range 1-hour Standard=35 8-hour Standard=9

IHD 

1993-2000 Metzger et 

al., 2004 CHFNS

1-hour daily 

maximum, 

average for most 

recent 3 days 

Single central 

residential monitor 1.8 

0.5 – 3.4 

 (10th - 90th

percentile) 

4.8 -16.3 3.2 - 5.3 

20-county 

Atlanta 

area 

1993-2004 Tolbert et al., 2007 

CVD 

1-hour daily 

maximum, 

 Average for most 

recent 3 days 

Single central 

residential monitor 1.6 0.1 – 7.7 4.5 -16.3 2.6 - 5.3 

IHD, 1988-1995 Mann et al., 2002 IHD+CHF 8-hour daily maximum, average for most recent 4 days Residence grid centroid interpolated from 3 closest monitors 2.07 0.30 – 11.8 16.5 - 32 11.6 – 23.4 

MI 

CVD 

South 

Coast Air 

Basin, CA 1992-1995 Linn et al., 2000 

CHF 

24-hour average, 

same day 

Average across all 

monitors in basin 1.5 0.3 – 5.3 16.5 - 25 11.6 -16.4 

126 urban 

counties 1999-2005 Bell et al., 2009 CVD 65+ 1-hour daily maximum, same day Average of monitors in county of residence 1.3* 0.05 – 9.7 14.9-33.5 8.2-24.3 

Baltimore, 

MD 

2002 

(April-Dec) 

Symons et al., 2006 

CHFNS

8-hour daily 

maximum, 

 Average for most 

recent 4 days 

Single central 

residential monitor 0.4 0.0 – 2.3 9.2 3.0 

Allegheny 

county, PA 1987-1999 Wellenius et al., 2005 CHF 24-hour average, same day Single area-wide representation of 3 monitors 1.03* 0.42 – 2.04 (5th - 95th percentile) 5.4-19.4 3.8-8.8 

Denver 1993-1997 (Jul-Aug) Koken et al., 2003 CHF 24-hour average, 3 days prior Average across all monitors 0.9 0.3 – 1.6 11.2-18.2A 6.4-10.4A 

A 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 Resestudy 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 concentrations 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, incB Hospital admissions for ischemic heart disease (IHD), myocardial infarction (MI), cardiovascular disease (CVD; for Bell et al. [2009] only subjects >65 years old), co

C Ambient CO concentrations reported in the study. NS Association was not statistically significant. 
 2-33

In summary, although there is no new evidence regarding the effects of short-term 

controlled CO exposures that result in lower COHb levels, the evidence is much expanded with 

regard to epidemiological31 analyses of ambient monitor concentrations, which observed 

associations between specific and overall cardiovascular-related outcomes and ambient CO 

measurements. With regard to extending our understanding of effects occurring below levels of 

CO observed in the clinical studies, however, the epidemiological evidence for CO is somewhat 

limited. The epidemiological evidence lacks measurements of COHb or personal exposure 

concentrations that would facilitate integration with the clinical data. Furthermore, the 

epidemiological evidence base for IHD outcomes or CVD outcomes as a whole includes a 

number of studies involving conditions in which the current standard was not met. Though these 

studies are informative to consideration of the relationship of health effects to the full range of 

ambient CO concentrations, they are less useful to informing our conclusions regarding 

adequacy of the current standards. The smaller set of studies, under conditions where the current 

standards were met, is considered to better inform our assessment of the adequacy of the 

standards or conditions of lower 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 analyses 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 monitor locations or area-wide average concentrations, 

which given the significant concentration 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 studies on the extent to which this evidence is 

consistent with and generally supportive of conclusions drawn from the combined consideration 

of the controlled human exposure evidence with estimates from the exposure and dose 

assessment (section 2.2.2 below). As in the previous 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 concentrations of public health 

concern. This integration, based on the REA for the current review, is considered with regard to 

the adequacy of the current standards 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). 
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 To what extent have important uncertainties identified in the last review been 

reduced and/or have new uncertainties emerged? 

Since the time of the last review, some important uncertainties have been reduced, some 

still remain and others associated with newly available evidence have been identified. A range 

of important uncertainties were identified in a number 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 levels investigated in the controlled human 

exposure studies, and the magnitude of risk associated with such changes for specific 

health outcomes, such as myocardial infarction, 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 studied and the potential for as yet unidentified health effects 

at COHb levels below 2%. 

 The potential for short-term peak CO exposures to contribute to CNS effects which 

might affect individual’s performance of complex activities such as driving a car or to 

contribute to other effects of concern. 

 Effects of ambient CO on potentially susceptible populations other than those with 

cardiovascular disease, including the developing fetus. 

 Modeling of COHb formation associated with exposures to ambient CO under different 

air quality conditions, including those associated with just 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 with short CO exposures. These 

effects had been well documented in multiple studies, and it was recognized that the majority of 

cardiologists at the time believed that recurrent exercise-induced angina was associated with 

substantial risk of precipitating myocardial infarction, 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 depression is a recognized indicator 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 time for several reasons including the large 

number of subjects used, the rigorous protocol used for subject selection, the use of the most 
 2-35

accurate method to measure blood COHb levels and the finding of a dose-response relationship 

between COHb levels and the ischemic 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,1989b, 1991). In the current review of the 

evidence related to cardiovascular effects associated 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 concentrations (ISA, Section 2.7). No additional clinical 

studies are available that evaluate responses to lower COHb levels in the cardiovascular-disease 

population, and uncertainties still remain in determining specific and quantitative relationships 

between the CO-induced effects in these studies and the increased risk of specific health 

outcomes. Further, with regard to then-unidentified 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 effects associated with CO 

exposure, including changes in visual perception, hearing, motor performance and vigilance 

among other measures of neurobehavioral performance based on a series of studies conducted 

from the mid 1960’s through the early 1990’s (1991 AQCD). 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 cardiovascular effects, which had been observed 

at COHb levels below 5% and consequently for which a focus would also provide adequate 

protection against potential adverse 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 occurrence of these effects in 

response to ambient CO would be expected to be rare within the current population. Thus, our 

uncertainty with regard to the potential for such effects to be associated 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, decreases in birth weight, measures 

of fetal growth, and infant mortality (ISA, section 5.4). Further, while animal toxicological 

studies provide support and coherence for those effects, the understanding of the mechanisms 

underlying reproductive and developmental effects is still lacking (ISA, section 5.4.1). Thus, 

although the evidence continues to “suggest[s] that critical developmental phases may be 

characterized by enhanced sensitivity to CO exposure” (ISA, p. 2-11), evidence is lacking for 
 2-36

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 quality 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 Agency (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, using updated data and new 

algorithms to estimate exposures and doses experienced by individuals, better represents the 

variability in population exposure and COHb dose levels 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 information 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 concentrations and increases in emergency room visits 

and hospitalizations for disease events plausibly linked to the effects observed in the controlled 

human exposure studies of CAD patients (ISA, section 2.5.1), providing support for our 

conclusion regarding coronary artery disease as the most important susceptibility characteristic 

for increased health risk due to CO exposure (ISA, 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 studies conducted in areas meeting the current CO standards than 

is the case for NO2 and PM (USEPA, 2008c, 2009a), as recognized above. Further, we 

recognize complicating aspects of the evidence that relate to conclusions regarding CO as the 

pollutant eliciting the effect reported in the epidemiological studies and 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 commonly 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., PM2.5 or NO2), they generally 
 2-37

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 relevant pollutants that are 

correlated with CO yet absent from the analysis. Similarly, CASAC commented that “the 

problem of co-pollutants serving as potential confounders 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 pollutants generated by fossil fuel combustion” and 

“a better understanding of the possible role of co-pollutants is relevant to ... the interpretation of 

epidemiologic studies on the health effects of CO” (Brain and Samet, 2010a). This issue is 

particularly important in the case of CO in light of the uncertainty (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-pollutant regression models effectively disentangle and 

quantitatively interpret a CO-specific effect distinct from that of other pollutants remains an area 

of uncertainty. 

In considering ambient concentrations that may be triggering health outcomes analyzed 

in the epidemiological studies, we recognize the uncertainty introduced by exposure error. 

Exposure error can occur when a surrogate is used 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 cases of other pollutants such as NO2

and PM, that may contribute to exposure error in the CO studies. The first relates to the low 

concentrations of CO considered in the epidemiological studies and monitor detection limits. 

The second relates to the use in the epidemiological 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 highly-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 detection limits, which is a greater 

concern for the more recently available epidemiological studies in which the study areas have 

much reduced ambient CO concentrations compared with those in the past. 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 Samet, 2010a). In contrast to CO, other combustionrelated criteria pollutants such as PM2.5 and NO2 generally occur above levels of detection, 

providing us with greater confidence in quantitative interpretations of epidemiological studies for 

those pollutants. 

There are also differences in the spatial variability associated with PM2.5 and NO2

concentrations as compared to CO concentrations that add complexity to the estimation of CO 

exposures in epidemiological studies. In general, PM2.5 concentrations tend to be more spatially 

homogenous across an urban area than CO concentrations. CO concentrations in urban areas are 

largely driven by mobile sources, while urban PM2.5 concentrations substantially reflect 

contributions from mobile and a variety of stationary sources. The greater spatial homogeneity 

in PM2.5 concentrations is due in part to the transport and dispersion of small particles from the 

multiple sources (USEPA, 2009a, sections 3.5.1.2 and 3.9.1.3), as well as to contributions from 

secondarily formed components “produced by the oxidation of precursor gases (e.g., sulfur 

dioxide and nitrogen oxides) and reactions of acidic products with NH3 and organic compounds” 

(USEPA, 2009a, p. 3-185), which likely contribute to spatial homogeneity. Similarly, “because 

NO2 in the ambient air is due largely to the atmospheric oxidation of NO emitted from 

combustion sources (ISA, section 2.2.1), elevated NO2 concentrations can extend farther away 

from roadways than the primary pollutants also emitted by on-road mobile sources” (40 FR 

6479, February 9, 2010). In contrast to PM2.5 and NO2, CO is comparatively non-reactive, which 

may contribute to the steeper CO gradient observed near roadways. Therefore, the 

misclassification of exposure arising from the utilization of central site monitors to measure 

PM2.5 and NO2 exposures is likely to be smaller than 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-related criteria pollutants is that, in contrast to 

the situation for all other criteria pollutants, the epidemiological studies for CO use a different 

exposure/dose metric from that which has been the focus of the broader 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 which the health evidence relies on an internal dose metric – lead 
 2-39

- the epidemiological studies also use that metric.33 For other criteria pollutants, including PM 

and NO2, air concentrations are used as the exposure/dose metric in both the epidemiological 

studies and the other types of health evidence. Thus, there is no comparable aspect in the PM or 

NO2 evidence base. The strong evidence describing 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 ischemia-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 information 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 small 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 associated with the epidemiological evidence that 

“complicate the quantitative interpretation of the epidemiologic findings, particularly regarding 

the biological plausibility of health effects occurring at COHb levels resulting from exposures to 

the ambient CO concentrations” assessed in these studies (ISA, p. 2-17). 

In summary, some important uncertainties from the last review have been reduced, 

including those associated with concerns for ambient 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 health outcomes, as well as the potential for as-yetunidentified health effects at COHb levels below 2%. Our exposure and dose models have 

improved giving us increased confidence in their estimates. Additionally, although the evidence 

base is somewhat expanded with regard to the 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 fetus and newborn infant and on maternal-fetal 

relationships. We additionally recognize that the expanded body of epidemiological evidence 

includes its own set of uncertainties which 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 epidemiological 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 resultant COHb levels. As in our consideration of 

the evidence in section 2.2.1 above, we have organized 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 living 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 benchmark 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 current CO standards. Lastly, we consider the 

exposure and dose estimates from the quantitative assessment 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, described in detail in the REA and 

summarized here, we have estimated CO exposure and associated COHb levels in simulated 

populations in two urban study areas 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 NAAQS exposure assessments and thus serve as an 

important connection with past assessments; (2) historically, 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 scenario due to the potential 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 ranked first (Los Angeles) and second (Denver) 

regarding the percentage of elderly population within 5, 10, and 15 km of monitor locations, and 

ranked first (Los Angeles) and fifth (Denver) regarding number of 1- and 8-hour daily maximum 

CO concentration measurements (ISA, section 3.5.1.1). 

Estimates were developed for exposures associated with current “as is” conditions (2006 

air quality) and also for higher ambient CO concentrations associated with air quality conditions 

simulated to just meet the current 8-hour standard,34 as well as for air quality conditions 

 

34 As discussed elsewhere, the 8-hour standard is the controlling standard for ambient CO concentrations. 
 2-41

simulated to just meet alternative standards (as discussed in section 2.3.3 below). In considering 

the adequacy of the current standards, it is important to note that over the 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 areas 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 conditions of increased CO concentrations that just 

meet the current 8-hour standard in the two study areas. In this scenario, we note there is 

uncertainty associated with simulating this hypothetical profile of higher CO concentrations that 

just meet the current 8-hour standard. 

To investigate the extent to which the relationship 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 the 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 meeting alternative standards these ratios for the two study areas fall 

well within the 2009 national distribution. More specifically, the ratio of the 1-hour design value 

to the 8-hour design value for the Los Angeles study area corresponds to approximately the 25th

percentile of U.S. counties in 2009 and the ratio for the Denver study area corresponds to 

approximately the 75th percentile of U.S. counties in 2009. Under “as is” conditions the ratios 

for these two study areas correspond to approximately the 40th 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 estimates 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 (O3), NO2, and sulfur dioxide (SO2). 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 exposure 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 standard. Further, one area of the country (Las Vegas, 

Nevada) is designated in non-attainment with the CO NAAQS 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 the 
 2-42

activity pattern data (approximately 3,600 person-days), 3) used four broadly defined categories 

to estimate breathing rates (i.e., slow-sleeping, 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 available at that time, would tend to limit the ability to accurately 

model expected variability in the population exposure and dose distributions. 

In contrast, APEX4.3 includes new algorithms to 1) simulate 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 

(CHAD37 now has about 34,000 person-days of data) and uses the most recent US census data to 

represent population demographics and home-to-workplace commutes. Modeling the prevalence 

of exposures or dose in a population of interest (such as individuals with coronary heart disease) 

has also been enhanced in APEX with the addition of output tables presenting statistics for 

identified subpopulations and age groups (or lifestages). Further, the current model uses the 

updated census population demographic data and includes options for selecting algorithms used 

to estimate microenvironmental concentrations. Each of these new model developments (REA, 

chapter 4) are designed to allow APEX to better 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 individuals from an actual 

population database and simulates 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 account to represent the demographics of each study 

area. With regard to age and gender demographics 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 National 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 necessarily reflecting differences 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 Database 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 characteristics 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-Forster-Kane equation (REA, section 4.4.7). 

APEX simulations performed for this review have focused on exposures to ambient CO 

occurring in eight microenvironments, absent any contribution to microenvironment 

concentrations from indoor (nonambient) CO sources, 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 assessments performed previously have included 

modeling simulations both with and without certain indoor sources, and these assessments 

provide context for the assessment of ambient CO exposure and dose. For example, a 2000 

exposure/dose assessment indicated that the impact of such sources 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 was noted that while these indoor sources were 

shown to contribute to total CO exposure they would 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 ambient contributions have notably declined, and 

indoor source contributions from some sources may also have declined. Thus, we have no firm 

basis to conclude a different role for indoor sources today with regard to contribution to 

population CO exposure and COHb levels. 

We note that the absence of indoor (nonambient) sources38 in the model simulations for 

this review is expected to result in somewhat 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 which the ambient contribution estimates might 

differ is influenced by the magnitude of nonambient-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-duration exposure event) will be higher for a given population group 

than COHb levels for that group arising solely from endogenous CO in the absence of any 

exposure, which is the “baseline” for the REA estimates of ambient contribution to COHb (REA, 

 

38 Nonambient sources of CO exposure can include gas 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). Additionally, 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 COHb 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 disease is the “most important susceptibility characteristic for 

increased risk due to CO exposure” (ISA, p. 2-11). Controlled human exposure studies have 

provided quantitative COHb dose-response information 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 given primary focus to the multi-laboratory study in 

which COHb was analyzed by the more accurate GC method (Allred et al., 1989a, 1989b, 1991) 

discussed in section 2.2.1 above. Based on the strength of the evidence and the availability of 

quantitative information from these controlled human exposure studies, the REA focuses on 

estimates of the percent of the simulated at-risk populations expected 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 information 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 heart disease IHD or CAD), both diagnosed and 

undiagnosed, and (2) adults with any heart diseases, including 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 effects in those groups. As a result, 

the quantitative assessment does not develop separate quantitative dose estimates for populations 

other than those with CAD or HD. 

The REA developed COHb estimates for the simulated 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 endogenously 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 subtracting 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 controlled exposure studies.40 As 

mentioned above, such a lower baseline contributes to a relatively greater COHb response to 

short-duration high-concentration exposures. 

In our consideration of the REA dose estimates 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 maximum end-of-hour absolute COHb levels above 

identified benchmark levels, and also consider the population estimates of daily maximum 

ambient contribution to end-of-hour COHb levels. The benchmark 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 absolute COHb, we identified benchmark levels 

of 1.5%, 2.0%, 2.5% and 3% COHb. This range includes 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 studies of CAD patients (discussed in section 2.2.1 above), with the 

lower end of the range extending below the lowest 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 considerations, 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 actual COHb levels experienced in the controlled human exposure 

studies; (3) that these studies did not include individuals with most severe cardiovascular 

disease41; (4) the lack of studies that have evaluated effects of experimentally controlled shortterm CO exposures resulting in mean COHb levels below 2.0-2.4%; and (5) the lack of evidence 

of a threshold at the increased COHb levels evaluated. 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 individuals 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 discussion below. Additionally we note the REA 

estimates indicating that, in the absence of CO exposure, approximately 0.5% to 2% of the 

simulated at-risk populations in the two study areas were estimated to experience a single daily 

maximum end-of-hour COHb level, arising solely from endogenous CO production, at or above 

1% (REA, Appendix B, Figure B-3). 

We also consider the evidence from controlled human exposure studies, discussed in 

section 2.2.1 above, in our interpretation of the REA estimates of maximum ambient exposure 

contributions to end-of-hour COHb levels (described 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-segment change in groups of subjects with pre-existing CAD for 

which controlled CO exposures increased their COHb levels by on average 1.4-1.7% and 3.3-

4.0% COHb from initial COHb levels of on average 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 concentration based on analysis of the full data set across 

both exposure groups. For purposes of the discussion in this document, we have presented the 

percentage of the simulated at-risk populations 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 metric, we recognize distinctions between the REA 

“baseline” (arising from prior ambient exposure and endogenous CO production) and the preexposure COHb levels in the clinical study (arising from ambient and nonambient exposure 

history, as well as from endogenous CO production). 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 most 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 population COHb levels estimated to occur in 

areas simulated to just meet the current CO standards? What portion of the atrisk population is estimated to experience 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 (REA, section 6.2). As in the last review, we 

recognize that indoor sources of CO can be important determinants of population exposures to 

CO and to population distributions of daily maximum COHb levels, and that for some portions 

of the population, these sources may dominate CO exposures and related maximum COHb 

levels. We additionally take note of the conclusions drawn in the previous review that the 

contribution of indoor sources to individual exposures and associated COHb levels cannot be 

effectively mitigated by ambient air quality standards (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 exposures (the ambient 

contribution) as pre-exposure baseline COHb levels will necessarily not reflect the contribution 

of both nonambient and ambient sources. 

In considering the REA estimates for current 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 protection to the simulated at-risk population from COHb 

levels of potential concern, by comparing the estimated levels in the population to the 

benchmarks described above. As described above, the REA presents two sets of COHb 

estimates: the first set of absolute estimates reflect 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 absolute COHb estimated to occur in response to 

the simulated ambient CO exposures, i.e., after 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 the HD and CHD populations (REA, section 6.2), 

recognizing that, in terms of percentages of persons exposed and experiencing daily maximum 

end-of-hour COHb at or above specific levels, the results are similar for the two simulated at-risk 

populations (HD and CHD). We note 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 least one day with an end-of hour COHb level above selected 
 2-48

benchmarks (Table 2-4). Another dimension of the analysis, presented 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 benchmarks. 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, was 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 common 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 conditions, the absolute COHb estimates 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 populations is estimated to experience any days in the year with 

end-of-hour COHb concentrations at or above 3% COHb, and less than 0.1 % of the simulated 

at-risk populations are estimated to experience at least one end-of-hour COHb concentration at 

or above 2% (Table 2-4). Slightly higher percentages 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 concentrations simulated to just meet the 

current 8-hour standard, the portion of the simulated at-risk populations estimated to experience 

daily maximum end-of-hour COHb levels at or above benchmarks is greater in both study areas, 

with somewhat higher percentages for the Denver study area population (Table 2-4). In both 

study areas, nonetheless, less than 1% of the simulated at-risk populations is estimated to 

experience a single day with a maximum 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 populations in either study area is estimated to experience a single 

day with maximum end-of-hour COHb at or above 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 maximum end-of-hour COHb level at or above 2% 

(Table 2-4). Appreciably smaller percentages of the simulated at-risk population were estimated 

to experience more than one day with such levels (Table 2-5). For example, less than 1.5% of 

the population is estimated to experience more than 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 than 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 with at least one daily maximum end-ofhour COHb level (absolute) at or above indicated levels under air quality 

conditions simulated to just meet the current standard and “as is” conditions. 

Percentage (%) of Simulated HD PopulationA

Just Meeting Current 8-hour Standard “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 <0.1B

> 3.0% < 0.1B 0.3 

> 2.5% < 0.1B 0.9 

0 0 

> 2.0% 0.6 4.5 < 0.1B < 0.1B

> 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 Value
 2-50

Table 2-5. Portion of simulated CHD population with multiple days of maximum end-ofhour COHb levels (absolute) 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 PopulationA

Just Meeting Current 8-hour Standard “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 < 0.1B 0 0 0 0 0 0 0 0 

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

≥ 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 represent 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 simulated 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 contribution to end-of-hour COHb level above 2% 

(Table 2-6), with less than 13 percent of either population experiencing maximum ambient 

contributions at or above 1.4% COHb. As observed with the absolute COHb estimates under 

conditions just meeting the standard, the results for the Denver study area included larger 

percentages of the population above specified levels than those for the Los Angeles study area, 

reflecting the study area difference in 1-hour peak concentrations (Table 2-6). Although 

estimates of population percentages for multiple occurrences are not available for the ambient 

contribution estimates, it is expected that similar 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 estimates 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 PopulationA

Just Meeting Current 8-hour Standard “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 occurrences of daily maximum 

COHb levels for REA simulations under conditions just meeting the current 8-hour standard, we 

note that an important contributing factor to the higher percentages estimated for the Denver 

study area population is the occurrence of higher 1-hour peak ambient CO concentrations and 

consequent higher CO exposures than occur in the corresponding Los 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 study area has generally higher 1-hour and 8-hour 

ambient CO concentrations as illustrated 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 recognize 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 COHb 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 the impact of 8-hour average concentrations, and 

take note of this in considering the REA results with regard to the adequacy of the 1-hour 

standard. Taken together, the REA results indicate occurrences of COHb levels above the 

benchmarks considered here that are associated with 1-hour ambient concentrations 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 afforded by the current CO standards? 

In considering the uncertainties associated with the quantitative estimates of exposure 

and dose from the REA, we relied on an approach intended to identify and compare the relative 

impact that important sources of uncertainty may have on the estimated potential health effect 

endpoints (i.e., estimates of the maximum end-of-hour COHb levels in the simulated at-risk 

population). The generally qualitative 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 NO2 (USEPA, 2008b) and SO2

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 characterization performed was placed on evaluating 

the direction and the magnitude of the uncertainty; that is, qualitatively rating how the source of 

uncertainty, in the presence of alternative information, may affect 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 uncertainty associated with four main components of the assessment: 

 Ambient monitor CO concentrations 

- database quality, spatial and temporal representation, zero concentration 

frequency, and missing data substitution; 

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

standards 

- historical data used, proportional approach used; 

 APEX inputs and algorithms 

- population database, activity pattern database, longitudinal profile algorithm, 

meteorological data, microenvironmental algorithm and input data, commuting 

algorithm, prevalence rates for at-risk populations, physiological factors; and, 
 2-53

 Potential health effects benchmark levels for the simulated at-risk population. 

Further, an additional area of uncertainty not directly evaluated is the contribution of ambient 

CO to COHb levels in the presence of nonambient exposures, although as discussed above, 

previous assessments indicated that, where present, 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 identified seven sources (i.e., the spatial and temporal 

representation of ambient monitoring data, historical data used in representing alternative air 

quality scenarios, activity pattern database, longitudinal profile algorithm, microenvironmental 

algorithm and input data, and physiological factors) that remain as the most important 

uncertainties in this assessment. Taking into consideration improvements in the model 

algorithms and data since the last review, and having identified and characterized these 

uncertainties here, we conclude that the estimates associated with the current analysis, at a 

minimum, better reflect the full distribution of exposures and dose as compared to results from 

the 1992 analysis. We note, however, potentially greater uncertainty remaining in our 

characterization of the upper and lower percentiles of the distribution of population exposures 

and COHb dose levels relative to that of other portions of the respective distribution. When 

considering the overall quality of the current exposure modeling approach, the algorithms, and 

input data used, alongside the identified limitations and uncertainties, we conclude that the 

quantitative assessment provides reasonable estimates of CO exposure and COHb dose for the 

simulated population the assessment is intended to represent (i.e., the population 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 estimates of the contribution of short-duration 

ambient CO exposures to total COHb than would result from simulations that include the range 

of commonly encountered CO sources beyond just those contributing to ambient air CO 

concentrations. Although the specific quantitative impact of this on estimates of population 

percentages discussed in this document is unknown, consideration of COHb estimates from the 

2000 assessment indicates a potential for the inclusion of nonambient sources to appreciably 

affect absolute COHb (REA, section 6.3) and accordingly implies the potential, where present, 

for an impact on overall ambient contribution 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 estimated 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 current 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 levels experienced by the lower controlled 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 populations in either study area are estimated to experience a COHb 

level similar to the higher controlled 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 myocardial 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 exercise-induced markers of myocardial ischemia 

(angina and ECG ST-segment change) 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 responses, the study authors noted that the response observed at the 

higher COHb level (~4%) were similar to that considered clinically significant when evaluating 

medications to treat angina from coronary artery disease. The independent 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 activity 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 evidence that demonstrated cardiovascular 

effects in CAD patients exposed to CO was given primary consideration, with the Administrator 

recognizing the findings of decreased time to onset of ECG change and angina pain as the 

“health effects of greatest concern, which clearly have been associated with CO exposures at 

levels observed [at that time] in the ambient air” (59 FR 38913). We additionally note the doseresponse relationship observed for COHb resulting from brief, elevated CO exposures in persons 

with pre-existing CAD, with no evidence of threshold, as discussed in section 2.2.1 above (ISA, 
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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 changes at the lowest tested dose level (~2% 

COHb, Allred et al 1989b) as unclear, additionally noting that variability in severity of disease 

among individuals with CAD is likely to influence 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 levels 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 population 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 Control 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 (ISA, 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 represents a large population represented by the REA analyses and for 

which the COHb benchmarks described above (based on studies of CAD patients) are relevant, 

that is, more susceptible to ambient CO exposure when compared to the general population (ISA, 

section 5.7). 

In addition to the population with diagnosed 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 persons for whom their disease state affects their 

ability to compensate for the hypoxia-related effects of CO (ISA, section 4.4.4). The NHIS 

estimates for 2007 indicate there is a total of approximately 25 million people with heart disease 

of any type (ISA, Table 5-26). Accordingly, while 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 monitored 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 higher for the larger HD population. 

Other populations potentially susceptible to the effects of CO include people with chronic 

obstructive pulmonary disease, diabetes and anemia, 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 evidence is limited or lacking with regard to 

effects of CO at ambient levels, and associated exposures and COHb levels, while providing no 

indication of susceptibility to ambient CO greater than that of CHD and HD populations. 

In summary, while we note the substantial size 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 very small portion of this population that might be expected to 

experience more than one occurrence of COHb above 2%, with less than 0.1% of this population 

expected to experience such a level on as many as six days in a year or a single occurrence as 

high as 4%, and 0% of the population expected to experience more than one occurrence above 

4% COHb. In light of the implications of the health evidence discussed above, the public health 

significance of these REA results and conclusions regarding the extent to which they are 

important from a public health perspective depends in part on public health policy judgments 

about the public health significance of effects at the COHb benchmark levels considered and 

judgments about the level of public health protection with an adequate margin of safety. 

2.2.3 CASAC Advice 

In our consideration of the adequacy of the current standards, in addition to the evidenceand 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, and 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 review to date that have addressed adequacy 

of the current standards conveyed the view that the current standards are adequate. In support of 

this view, these commenters disagreed with the REA estimates 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 available in the docket for this rulemaking, as will 

be transcripts of the public meetings held in conjunction with CASAC’s review of the earlier draft of this document, 

of drafts of the REA, and of drafts of the ISA. 
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however, expressed a “preference” for a lower standard and stated that “[i]f the epidemiological 

evidence is given additional weight, the conclusion could be drawn that health effects are 

occurring at levels below the current standard, which would support the tightening of the current 

standard.” Taking this into account, the Panel further advised that “revisions that result in 

lowering the standard should be considered” (Brain and Samet, 2010b). 

2.2.4 Staff Conclusions on Adequacy of the Current Standards 

In considering the adequacy of the current standards, staff gives great weight to the longstanding body of evidence for CO, augmented in some aspects since the last review, that has 

established: the common mechanism 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 levels in eliciting health effects; the use 

of COHb as the bioindicator and dose metric for evaluating CO exposure and potential for health 

effects; and, people with cardiovascular disease as a key population at risk from low CO 

exposures (ISA; 2000 AQCD; 1991 AQCD). We additionally recognize the expansion of the 

epidemiological evidence that provides logical coherence with our conclusions regarding 

cardiovascular disease-related susceptibility (ISA, 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 conditions 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 multiple occurrences of COHb levels of interest are 

considered. These absolute COHb estimates and the incremental contribution to them from 

ambient CO exposures are considered in light of the evidence from controlled human exposure 

studies, while recognizing distinctions between the measurements in those studies and the REA 

estimates that would be likely to affect the response of COHb levels to elevated ambient CO 

exposure events. These estimates, which vary between 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 myocardial ischemia subsequent to 1-hour elevations 

in CO exposure, and larger portions of the population would experience lower COHb levels, 

below those which have been specifically addressed in the health effects evidence. In 

considering the public health significance of such estimates, while recognizing uncertainty 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 population in the U.S. and the existence of other 
 2-58

potentially susceptible populations for which evidence pertaining to effects 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 exposure 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 are judged to be adequate depends on a variety 

of factors inclusive of science policy judgments and public health policy judgments. These 

factors include public health policy judgments concerning the appropriate COHb benchmark 

levels on which to place weight, as well as judgments 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 uncertainty associated with interpretation of the epidemiological 

evidence as providing information on ambient CO as distinct from information on the mixture of 

pollutants associated with traffic, and, given 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 standards. 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 modeling approach and new input data, as well 

as distinctions between the REA simulations and resulting COHb estimates and the response of 

COHb levels to experimental CO exposure as recorded in the controlled human exposure studies. 

We draw conclusions with regard to the adequacy of the current standards from both the 

evidence and from the exposure and dose assessment, taking into consideration related 

information, limitations and uncertainties recognized above. We conclude that the combined 

consideration of the body of evidence and the quantitative exposure and dose estimates provide 

support for a suite of standards at least as protective as the current suite. Further, we recognize 

that conclusions regarding the adequacy of the current standards depend in part on public health 

policy judgments identified above and judgments about the level of public health protection with 

an adequate margin of safety. We additionally note the influence that hourly ambient CO 

concentrations well below the current 1-hour standard may have on ambient CO exposures and 

resultant COHb levels under conditions just meeting 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 occurrence of 1-hour ambient concentrations that contribute to 

population estimates of daily maximum COHb levels, that depending on public health judgments 

in the areas identified above, may be considered to call into question the adequacy of the 1-hour 
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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 quantitative estimates described above may be 

viewed as providing support for either retaining or revising 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. 
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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 considered 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 available scientific evidence- and exposure/riskbased information, as reflected in the ISA and REA, support consideration of 

alternatives to the current CO standards to provide increased protection from 

ambient CO exposures? 

To assist us in interpreting the currently available scientific evidence and the results of 

recent quantitative exposure/risk analyses to address 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 recently in the ISA. Specifically, we consider 

how the currently available scientific 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 reference methods are available that can effectively measure CO, and 

as discussed in section 1.3.2 above, the available federal reference methods include a range of 

analytical sensitivities to support quantification of CO at ambient levels. Thus we have not 

identified any basis for considering an indicator 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 consider the following question: 

 Do health effects evidence and air quality/exposure assessments provide support 

for considering different exposure indices or averaging times? 

The averaging times for the current standards 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 subsequent reviews (1980, 45 FR 55066; 1985, 50 FR 
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37485; and 1994, 59 FR 38906). The 8-hour averaging time was selected primarily based on the 

rationale that most individuals appear to approach 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 has been that the 8-hour time 

frame represented a good basis for tracking continuous exposures during any 24-hour period, 

recognizing that people may be exposed in approximately 8-hour blocks of time (e.g., working or 

sleeping) (45 FR 55077). The 1-hour averaging time primarily reflected consideration of the 

potential impact of shorter exposures. Since the establishment of the 1-hour 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 longer, such as the controlled human studies 

demonstrating aggravation of myocardial 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 averaging period provides a better 

indicator of short-term health effects of CO (59 FR 38914). Further, 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 available 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 supportive of the conclusions reached in the previous 

reviews to retain the 1- and 8-hour averaging times. 

 Controlled human exposure studies, with which epidemiological evidence is coherent, 

provide the clearest evidence of short-term CO-induced effects and reflect exposures of 

1-2 hours (ISA, sections 5.2, 5.2.6.1). 

 Most individuals would be expected to achieve 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 representative 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 considered to provide protection from the 

occurrence of short-duration elevations in exposure concentrations of ambient CO that 

may be encountered in some environments and from COHb levels that may result from 

such exposures (2000 AQCD, section 7.4; ISA, section 2.4.1). 
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Taken together, we conclude that the information 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 evidence and air quality/exposure assessments, 

and what are the uncertainties and limitations in that health effects evidence and 

air quality/exposure assessments? 

We focus on general considerations with regard to form in section 2.3.3.1. We then 

address specific considerations 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 forms for the CO NAAQS in conjunction with 

specific levels, staff considers the adequacy of the public health protection provided by the 

combination of level and form to be the foremost consideration. In addition, we recognize that it 

is preferable to have a form that is reasonably stable and relatively 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 effect of reducing public health protection because 

shifts in and out of attainment could disrupt an area’s ongoing implementation plans and 

associated control programs. Since the 1971 promulgation 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., O3, 

PM and NO2). 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 consideration of a percentilebased daily maximum statistic averaged over three years. 

First, as noted in the review of the O3 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. This is because such forms give proportionally 

greater weight to periods of time when pollutant concentrations are well above the level of the 

standard than to times during which the concentrations 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 exceed the standard as to times when concentrations 

greatly exceed the standard level. Additionally, averaging concentrations over three years 

provides greater regulatory stability (e.g., with regard to control programs associated with 
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attainment status) than a form based on allowing a single exceedance in a year. In considering 

revision to this aspect of the standard, we note 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 appropriate level to accompany such a form. 

Secondly, a percentile-based statistic 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 90th percentile of an area with 

200 measurements and one with 100 measurements would, in both cases, represent the 

concentration above which 10% of the measurements in either location are estimated to occur, 

while the 3rd highest concentration in the first case would be the concentration 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-based 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 average 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 stability, thus affording more consistent air quality protection. 

In considering specific forms on which to focus the current review, as shown in Table 2-

7, we note such forms that have been considered in other NAAQS reviews, including the 98th

and 99th percentile forms. These forms, averaged over three years, were considered with regard 

to a 24-hour standard for PM and 1-hour standards for NO2 and SO2 (USEPA, 2005; USEPA, 

2008b; USEPA 2009b). We recognize that at a specific location with measurements taken on 

every day in a year, a 99th percentile form for an 8-hour daily maximum standard would 

correspond to the fourth highest daily maximum 8-hour average concentration in a year, while a 

98th percentile form would correspond approximately to the 7th or 8th highest daily maximum. 

We have considered forms of a 99th percentile (fourth highest daily maximum) or a 98th 

percentile, each averaged over three years, as potentially providing appropriate balances between 

limiting peak CO concentrations and providing a stable regulatory target. In considering 

percentile-based statistics for the form of potential alternative CO standards, however, we focus 

on the REA results in section 2.3.3.2 below with regard to a 99th 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 with 
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selection of a particular standard level. The primary emphasis in such a decision will be on the 

level of public health protection provided by the 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 data sets identified for the two study areas and 

described in the REA. The current form of both 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 alternate forms described above in addition to 

the current “exceeded only once per year” form. 

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. 

8-hour Averaging Time 1- hour Averaging Time 

2nd highest 

maximuma

99th

percentile 

daily 

maximum 

98th

percentile 

daily 

maximum 

2nd highest 

maximuma

99th

percentile 

daily 

maximum 

98th

percentile 

daily 

maximum 

--------------------------------- Level (ppm) -------------------------------- Air Quality Scenario Modeled 

Denver Study Areab

9.4c 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 99th percentile daily max 8-hr (5.0 ppm) 

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

5.4c 4.1 3.5 9.3 7.7 6.6 2nd 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

9.4c 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 99th 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 99th percentile daily max 8-hr (5.0 ppm) 

5.4c 4.7 4.1 6.8 6.7 5.7 2nd 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 concentrations 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. 
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2.3.3.2 Alternative Levels 

In considering alternative standard levels with regard to the potential to provide greater 

protection than that afforded by the current suite of standards against CO-related adverse health 

effects, we have taken into account scientific evidence from both experimental and 

epidemiologic studies, as well as the uncertainties and limitations in that evidence, and the 

quantitative estimates of exposure and dose provided by the REA. We note that the scientific 

evidence and quantitative assessment can provide insights 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 informing conclusions regarding standard levels and 

forms considered to provide protection of public health with an adequate margin of safety. With 

regard to the scientific evidence, as discussed in section 2.2.1 above, we have given principal 

emphasis to findings of the multi-laboratory controlled 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 resulted in a mean baseline COHb level of 0.6% (post-exercise) were 

associated with myocardial ischemia-related effects, including, specifically, reduced time to 

exercise-induced angina and ST-segment change.46 Additionally, analysis of the study subjectspecific data indicated a dose-response relationship for these responses, with no evidence of a 

measurable threshold at the controlled exposures evaluated (ISA, section 5.2.4; Allred et al., 

1989a, 1989b, 1991). 

For our purposes here, we have also considered the epidemiological studies with regard 

to the extent to which this evidence is consistent with and generally supportive of conclusions 

drawn from the combined consideration 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 and CHF health outcomes described in section 

2.2.1 above, four of which were based in a study area in which the current standard was met, the 

associations for three of which (studying two different areas) were statistically significant. In 

our consideration of the evidence, we recognize 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). 
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are “particularly problematic for CO” and the weight 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 99th 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 identified these three specific levels to particularly inform our 

consideration of the REA estimates in light of different aspects of the evidence that suggest 

differing degrees of health significance for each of them. As discussed 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 response was also observed, although 

smaller and of less clear health significance. In contrast, the 1.5% benchmark 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 distinction in public health 

implications between single and multiple occurrences, particularly with regard to exceedances of 

the lower COHb benchmark levels. 

In considering alternative standard levels, consistent with conclusions reached in section 

2.2.4 above, we consider levels for both standards, while focusing predominantly on the 1-hour 

standard. We note the current role of the 8-hour standard in controlling CO concentrations 

nationally which has led to our greater focus on that standard in designing 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 concern. 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 Angeles study area, and the percentage of the at-risk 

population exceeding the 2% COHb benchmark is also lower there than in the Denver study area 

(Table 2-8, 1st two rows for each form). A much 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 population 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 and 
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only 75.5% in the Denver study area. At lower alternative 1-hour standard levels, the differences 

in population percentage at all COHb benchmarks are much smaller. 

We have also considered the REA estimates for a series of alternative 1-hour standard 

levels below those associated with just meeting the current 8-hour standard. Based on this 

information, presented in Table 2-8, we compared REA results for these alternative levels to the 

results for levels just meeting the current 8-hour 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 levels 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 (2nd 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 evidence) 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 (2nd

highest form) to approximately 90-99% of the population for other standard levels. 
 2-68

Table 2-8. Percentage of simulated HD population with daily maximum end-of-hour 

COHb levels (absolute) below the indicated 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 conditions 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 contribution to end-of-hour 

(ambient contribution COHb)47 for the same array of alternative 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 exposure. The estimates for “absolute COHb” are based on 

simulations where CO exposure arises only from ambient CO sources, in the absence 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 maximum 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 assessed, and for higher percentages of the population 

for somewhat lower standard levels. In considering this observation, 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 regarding absolute COHb benchmarks of 1.5 to 2% and above, the 

influence of baseline COHb on COHb level response to exposure events, and estimates of 

numbers of occurrences of COHb levels of interest, and being mindful of support provided by 

the epidemiological studies, we consider the REA estimates of daily maximum end-of-hour 

COHb levels with regard to level of protection estimated to be provided 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 mindful of several key aspects of the evidence 

(described in more detail in section 2.2.1 above): 

 Uncertainty in the public health significance of the effects observed at the lowest 

exposures in the controlled human exposure studies of CAD patients. 

 The lack of evidence for a measurable threshold 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 levels 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 associated with health effects in other potentially 

susceptible populations. 

 Complications associated with quantitative 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 standards that may be appropriate to 

consider differs based on the weight placed on different aspects of the evidence and on different 

aspects of the quantitative dose estimates, as well as on public health policy decisions regarding 
 2-70

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 the 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 appreciably 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 vary depending on the weight placed on each of the 

factors identified above. For example, to the extent that the REA estimates are judged to indicate 

that the range of 1-hour concentrations allowed under conditions just meeting the current 8-hour 

standard may contribute to exposures 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 for such a level, alternative 1-hour levels that 

provide generally equivalent protection to the current 8-hour standard, nationally, with increased 

protection for areas with relatively higher 1-hour peaks, may be appropriate to consider. 

Accordingly, we note that the population distribution of daily maximum COHb 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 99th percentile daily maximum 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 appropriate 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 standard levels ranging down to approximately 11 

or 9 ppm, for the current form or a 99th percentile daily maximum form, respectively. On the 

other hand, if one were to place weight on the two epidemiological studies finding statistically 

significant associations in two locations in which the current standard was met (and the ambient 

CO concentrations in those study locations), and on the REA estimates for this same population 

target (e.g., 99% having no occurrences) combined with 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 alternative standards, in addition 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, and 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 staff 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 regard to the 1-hour standard, CASAC suggested the 

policy option of retaining a 1-hour standard “to provide protection against infrequent acute 

exposures” and considering “a range of concentrations from 5 ppm to 15 ppm, combined with a 

99th percentile or fourth highest daily maximum.” The Panel further stated that they did not 

concur with the option of revoking the 1-hour standard (Brain and Samet, 2010b, p. 13). 

2.3.5 Staff Conclusions on Alternative Standards 

Staff’s consideration of alternative primary CO standards builds on our conclusion from 

section 2.2.4 above that the body of evidence in combination with the results of the REA support 

standards at least as protective as the current standards, and, 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 indicator 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 and level for those standards, we conclude that, 

depending on public health policy judgments regarding the protection of public health with an 

adequate margin of safety, the information available in this review supports consideration of 

either retaining the current suite of standards 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 available in the docket for this rulemaking, as will 

be transcripts of the public meetings held in conjunction with 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 given to findings in the epidemiological 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 weight to findings of controlled exposure studies of 

CAD patients in which sensitive indicators of myocardial ischemia were associated with COHb 

levels resulting from short-duration, high-concentration CO exposures. This conclusion also 

takes into account uncertainties associated with the differing circumstances of ambient air CO 

exposures from the CO exposures in the controlled 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. Additionally, this conclusion takes into account 

judgments in interpreting the public health implications of the REA estimates of COHb 

associated with ambient exposures based on the application of our current exposure modeling 

tools, and the size of the 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 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 basis for selection of alternative standards. 

In addition to considering retaining the current suite of standards without revision, we 

also conclude that it is reasonable to consider revising the 1-hour standard downward to provide 

protection from infrequent short-duration peak ambient concentrations that may not be 

adequately provided by the current standards. While 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 results, we note the health effects evidence from 

1-hour controlled exposures, which indicates the effects in susceptible groups from such short 

duration exposures. The evidence and REA estimates indicate support for consideration of a 

range of 1-hour standard levels which would address the potential for the current 8-hour 

standard, as the controlling standard, to “average away” high short-duration exposures that may 

contribute to exposures of concern. Consequently, in considering alternative standard levels, we 

focus here on the 1-hour standard as providing the most direct approach for controlling the 

likelihood of such occurrences. Additionally, following consideration of alternative 1-hour 
 2-73

standard levels below, we also consider the extent to which it is appropriate, in conjunction with 

revisions to the 1-hour standard, to consider revising or retaining the current 8-hour standard. 

We have identified a range of 1-hour standard levels from 15 to 5 ppm as being an 

appropriate range for consideration. These levels are in terms of a 99th percentile daily 

maximum form, averaged over three years, which we consider to provide increased regulatory 

stability over the current form. Given the objective for the 1-hour standard of providing 

protection from high ambient CO exposures of duration shorter than 8 hours and perhaps much 

shorter, we suggest the 99th percentile form for consideration in preference to a 98th percentile 

form. We additionally take note of CASAC’s preference for a revision to the standards to 

provide greater protection and observe that the range of 1-hour standard levels discussed here is 

also the range that the CASAC CO Panel suggested was appropriate for consideration. 

We have identified the upper part of the range of 1-hour standard levels for consideration 

(11-15 ppm) based on the objective of providing generally equivalent protection, nationally, to 

that provided by current 8-hour standard 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 estimated to generally correspond to 1-hour CO levels 

occurring under conditions just 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 25th and 75th percentiles of the 

distribution of ratios of 1-hour 99th 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 99th percentile daily maximum form, 

averaged over three years. Selection of a 1-hour standard within this upper part of the range 

would be expected to allow for a somewhat similar pattern of ambient CO concentrations as the 

current, controlling 8-hour standard, although with explicit and independent control against 

shorter-duration peak concentrations 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 retaining the current standards. But it 

would additionally recognize the importance of limiting 1-hour concentrations 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 the evidence and REA estimates and judgments 

that may be considered reasonable regarding appropriate population targets 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 and associated COHb levels. With this policy 
 2-74

objective in mind, we consider it appropriate to consider 1-hour standard 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 protection of the at-risk population against the small decrements in timeto-exercise-induced markers of myocardial ischemia 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 basis for selection of alternative standards. 

In further considering the evidence, we take note of the expanded epidemiological 

evidence and suggest that to the extent 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 concludes that the epidemiological 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 range of CO levels in the three epidemiological 

studies may be appropriate. In light 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 range is most strongly supported, both with regard 

to judgments concerning adversity and quantitative interpretation of the epidemiological studies 

with regard to ambient concentrations that may elicit effects. For the lower parts of the range, 

support provided by the available information is more limited, especially for the lowest part of 

the range. 

As mentioned above, we also conclude it is appropriate to consider retaining a standard 

with an 8-hour averaging time. As when it was 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 conjunction with consideration of a revised 1-hour 

standard to a level in the upper part of the range described above, we conclude it is appropriate to 

consider either retaining the current 8-hour standard or revising the form of the standard to 

potentially provide greater regulatory stability, with adjustment to level to provide generally 

equivalent protection as the current 8-hour standard. Based on air quality relationships between 

the current form and an alternative form of 99th percentile daily maximum 8-hour concentration 

averaged over three years (Appendix C), we conclude that levels for the revised form that are 

appropriate to consider are 8 or 9 ppm. 
 2-75

In conjunction with consideration of a revised 1-hour standard to a level in the middle 

part of the range described above, we conclude it is appropriate to consider revising the 8-hour 

standard to provide additional protection from 8-hour average concentrations to a level within 

the range of 5-7 ppm in terms of a 99th percentile daily maximum, averaged over three years. 

Further, in conjunction with consideration of a revised 1-hour standard 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 99th percentile daily maximum, averaged over three years. In both cases, the 

considerations leading to identification of these 8-hour standard levels are those discussed above 

with regard to the corresponding parts of the range identified for consideration of alternative 1-

hour standard levels. 

To provide some perspective on the implications of alternative primary standards (within 

the range of levels identified above), staff analyzed ambient CO concentrations for 2007-2009 to 

estimate the percentage of counties, and the populations in those counties that likely would not 

attain various alternative standards identified above. 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 primary CO NAAQS that are appropriate for 

the Administrator’s consideration in making decisions on the primary 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 alternative standards to provide requisite protection for health effects 

associated with ambient CO exposures, staff has considered these standards in terms of the basic 

elements of the NAAQS: indicator, averaging time, form, and level. In drawing these 

conclusions, we are mindful that the Act requires standards to be set that, in the Administrator’s 

judgment, are requisite to protect public health with an adequate margin of safety, such that the 

standards are to be neither more nor less stringent than necessary. Thus, the Act does not require 

that NAAQS be set at zero-risk levels, but rather at levels that avoid unacceptable risks to public 

health. 

(1) Staff concludes that the combined consideration 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 availability to the heart. 

(2) Staff additionally concludes that, depending on public health policy judgments 

regarding the protection of public health with an adequate margin of safety, the 

information available in this review supports 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 measurements of CO in accordance with federal 

reference methods as the indicator to address 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 averaging times of 1 and 8 hours. 

(5) With regard to the levels and forms of the standards, staff concludes it is appropriate 

to consider retaining the current standards, without revision, or revising the current 

suite of standards, with particular focus on revision of the 1-hour standard to provide 

protection that is not adequately provided by the current standards from infrequent, 

short-duration, peak ambient concentrations. 

(6) With regard to a revised 1-hour standard, we conclude that it is appropriate to give 

consideration to a range of levels from 15 to 5 ppm, with a revised level selected in 
 2-77

combination with a revised form of 99th 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 standard, 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 protection, nationally, to that provided by 

the current 8-hour standard. Staff concludes that this part of the range is most 

strongly supported by the current information. 

b. To the extent it is judged appropriate to provide additional protection against 

COHb levels at or above 2% in susceptible populations, it is appropriate to 

consider the middle part of the range, represented by 9-10 ppm. 

c. To the extent one places greater importance on COHb levels below 2.0% and 

concludes that the epidemiological evidence for areas meeting the current 

standards is reasonably interpreted as indicating 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 standard, we conclude it is appropriate to 

give consideration to the following 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 regulatory stability, with adjustment to 

level to provide generally equivalent protection, nationally, as the current 8-

hour standard. For a form of 99th 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 99th percentile daily maximum form) to 

provide additional protection from maximum 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 CO 
 2-78

exposures, giving consideration to levels of approximately 3 or 4 ppm, with a 

99th percentile daily maximum form. 
 2-79

2.5 KEY UNCERTAINTIES AND AREAS FOR FUTURE RESEARCH AND 

DATA COLLECTION 

Staff believes it is important to highlight key uncertainties associated with establishing 

ambient standards for CO. Such key uncertainties and recommendations for health-related 

research, model development, and data gathering are outlined below. In some cases, research in 

these areas can go beyond aiding standard 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 uncertainties, research questions and data gaps 

that have been highlighted in this review of the health-based primary standards. 

 A critical aspect of our consideration of the evidence and the quantitative dose 

estimates is our interpretation of the controlled human exposure studies. While 

additional human exposure studies of this type are unlikely to be undertaken, expansion 

of our understanding of the implications of several 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 CAD 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 experimental CO exposure concentrations 

used in the controlled human studies to increase subject COHb levels to 

COHb study targets. 

 Further characterization of the physiological and environmental influences, including 

characteristics of exposure, on COHb levels, particularly those most influential to 

COHb levels in today’s population, and the 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 levels) to COHb levels resulting 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 ambient concentrations and/or longer-term 

exposure periods. 

 Further research to characterize CO effects for other potentially susceptible 

populations, including populations with preexisting diseases other than CAD that limit 

oxygen availability, such as anemia and obstructive respiratory diseases; populations at 

certain lifestages (i.e., older adults and fetuses at critical stages of development); and 
 2-80

populations with elevated baseline COHb due to increased endogenous CO formation, 

such as individuals with diabetes and visitors to high altitude. 

 Our interpretation of the epidemiological evidence 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 COHb and research on mechanisms of COinduced effects other that those associated with limiting oxygen availability at ambient 

CO levels. 
 2-81

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 3-1

3 CONSIDERATION OF A SECONDARY STANDARD FOR 

CARBON MONOXIDE 

This chapter focuses on the key policy-relevant issues related to the review of welfarerelated effects of CO. Under Section 109(b) of the 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 “effects on soils, water, crops, 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 discusses 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 considerations. 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 only significant welfare effect identified for CO 

levels possibly approaching those in ambient air was inhibition of nitrogen fixation by 

microorganisms in the root nodules of legumes associated 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 recognized 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 establishment of a secondary standard for CO is 

appropriate, we adopted an approach 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 scientific information provide support for 

considering the establishment of a secondary standard for CO? 

In considering this overarching question, we first note that the extensive literature search 

performed for the current review did not identify any evidence of ecological effects of CO 

unrelated to climate-related effects, at or near 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 considered for the first time in the 2000 AQCD. The 

greater focus on climate in the current ISA relative 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 concludes 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 climate-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 continental and global-scale chemistry, as outlined in the 

2000 AQCD. CO is a weak direct contributor 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). Increased concentrations of CO can lead to 

increased concentrations of other gases whose loss processes also involve OH chemistry. Some 

of these gases, such as methane (CH4) and ozone (O3), contribute to the greenhouse effect 

directly while others deplete stratospheric O3 (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 contributes to climate forcing through both direct 

radiative forcing (RF) of CO, estimated at 0.024 W/m2

 by Sinha and Toumi (1996), and indirect 

effects of CO on climate through CH4, O3 and carbon dioxide (CO2) (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/m2

 over the period 1750-2005 (Forster et al., 2007), with 

more than one-half of the forcing attributed to O3 formation (ISA, section 3.3 and p. 3-13). 
 3-3

CO is classified as a short-lived climate forcing agent, prompting CO emission reductions 

to be considered as a possible strategy to mitigate 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 concentrations of CO and due to the localized chemical 

interdependencies involving CO, CH4, and O3 (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 such as CO (ISA, section 3.3 and p. 3-16). These 

models may fail to consider the local variations in climate forcing 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 emissions 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 uncertainties in the RF from CO and other 

trace gases (ISA section 3.3 and p. 3-12). Although 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 recommendations of CASAC, based on their review of 

the ISA, and the earlier draft of this document.1

 

In their comments on the draft Policy Assessment, CASAC did not disagree with staff’s 

initial conclusions that there is insufficient information to support consideration of a secondary 

standard at this time. CASAC did express the view that there is substantial 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 available scientific information indicates the need 

for a secondary standard for CO, we have reached the following conclusions: 

 

(1) With respect to non-climate welfare effects, including ecological effects and impacts 

to vegetation, there is no currently available scientific information 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, sections 2.2 and 3.3). There are weak direct, 

and stronger, but highly variable and uncertain indirect continental and regional 

climate forcing effects from CO. However, the available information provides no 

basis for estimating how localized 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 climate. Moreover, more than 

half of the indirect forcing effect of CO is attributable to O3 formation, and welfarerelated effects of O3 are more appropriately considered in the context of the review of 

the O3 NAAQS, rather than in this CO NAAQS review. For these reasons, it is 

currently not feasible to conduct an analysis for the purpose of considering a CO 

secondary standard based on climate considerations. Based on these considerations, 

staff concludes there is insufficient information at this time to support the 

consideration of a secondary NAAQS based on CO effects on climate processes. 

3.5 KEY UNCERTAINTIES AND AREAS 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 associated with CO effects on climate processes. 

Research and model refinements that would reduce 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 that described below, is needed. 

 More accurate U.S. and global emissions inventories to provide source-specific data on 

CO contributions to climate precursors. 

 Improved representation and characterization of localized chemical reactions between 

CO, CH4 and O3 in global and regional climate models to enable the more accurate 

prediction of the role of CO in climate and 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 and 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. Brain 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.; Haywood J.; Lean J.; Lowe D.C.; Myhre 

G.; Nganga J.; Prinn R.; Raga G.; Schultz M.; Van Dorland 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 Quality 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.epa.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/standards/co/s_co_cr_isa.html. 

U.S. Department of Health, Education and Welfare. (1970) Air Quality Criteria 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 Advisory 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 met on March 22-23, 2010, to review EPA’s Policy 

Assessment for the Review of the Carbon Monoxide 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 available for its development, given 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 the three main sources 

of carbon monoxide that contribute to the carbon 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 exposure. 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 dependence 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 important evidence, its findings should not be so 

emphasized as to ignore more contemporary epidemiologic studies, especially those directed at 

coronary artery disease (CAD) and at cardiovascular disease (CVD) more generally. The 

epidemiologic studies are important because other 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 

1
rationale for placing greater emphasis on the findings of the epidemiologic studies versus the 

controlled clinical studies. As with other criteria 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 emphasis of the epidemiologic data across all of 

the CO documents, beginning with the Integrated 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 relates to alternative CO standards. A concise 

description of how the form of the standard is important would also be useful. 

It is important to acknowledge the decreases in ambient CO levels over time; however, 

this success should not preclude an objective assessment of the potential health consequences of 

exposures at the current CO NAAQS. While measured concentrations infrequently reach the 

current NAAQS, evidence indicates that adverse health 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 release 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 response and the successful completion of the CO 

NAAQS review. The CASAC and Panel memberships are listed in Enclosure A. The Panel’s 

responses to EPA’s charge questions 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 

2
NOTICE 

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

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

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

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

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

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

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

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

CASAC reports are posted on the EPA website at http://www.epa.gov/CASAC. 

3
Enclosure 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 Professor of Environmental Physiology, 

Department of Environmental Health, Harvard School of Public Health, Harvard University, 

Boston, MA 

MEMBERS 

Dr. Paul Blanc, Professor and Chief, Department of Medicine, Endowed Chair, Occupational 

and Environmental Medicine, Division of Occupational and Environmental Medicine, University 

of California San Francisco, San Francisco, CA 

Dr. Thomas Dahms, Professor and Director, Anesthesiology 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 Civil, Construction and Environmental 

Engineering, College of Engineering, North 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 Hill, Chapel Hill, NC 

Dr. Joel Kaufman, Director, Occupational and Environmental 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 State University, Baton Rouge, LA 

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

Los Angeles, Los Angeles, CA 

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

Dr. Armistead (Ted) Russell, Professor, Department of Civil 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 Health 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 Pennsylvania 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 Professor of Environmental Physiology, 

Department of Environmental Health, Harvard School of Public Health, Harvard University, 

Boston, MA 

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

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

Dr. Donna Kenski, Data Analysis Director, Lake Michigan Air Directors Consortium, 

Rosemont, IL 

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

Georgia Institute of Technology, Atlanta, GA 

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 

6
Enclosure B 

CASAC’s Consensus Responses to EPA’s Charge Questions

1. Does the Panel find the introductory and background material, including 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 background information. There is a brief review 

of the CAA and provisions to establish primary and secondary NAAQS; adequate margins of 

safety; previous reviews; CO sources in ambient 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 CASAC recommendations in the review of other criteria pollutants.

2. Consistent with the revised 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 policy-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 evidence 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 concentrations. 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 effects of environmental CO since the last evaluation 

of CO standards, as documented in the ISA, comes primarily from epidemiology based studies. 

A combined consideration of the findings of epidemiological studies and controlled human 

exposure studies leads to the conclusion that substantial 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 controlled 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 studies 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 and may override the ambient CO 

7
levels in contributing to dose. It is suggested that information from the 2000 criteria document 

on indoor sources be included. 

b. Does the Panel consider the document to provide the appropriate level of detail in 

addressing these policy-relevant questions? 

For the controlled human studies, the Panel found the level of detail appropriate. However, the 

opposite is true for the epidemiological studies. 

3. The discussion of the health effects evidence (e.g., section 2.2.1) draws 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? 

b. Does the Pane find the presentation to be technically sound, clearly communicated 

and appropriately balanced? 

The description of the data considered by the previous 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 risk associated with CO exposure and its health 

consequences. However, the discussion of the epidemiological data should also consider nonhypoxia mechanisms. Increased COHb is important, but may not be the only mechanism for CO 

health effects. 

The last review of CO was halted for several years due to the pending study 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 there are changes from the last review that commenced in 1999. 

In order to facilitate better 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 confidence 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 state 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? 

8
The Panel largely agreed that the discussion in the 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 contributes to COHb or whether the emphasis 

should be on the final resulting %COHb concentration itself. We have a related interest in 

modeling indoor source contribution to COHb to better understand the total COHB 

concentrations. 

Panel members offered mixed opinion regarding the decision by the EPA not to pursue the 1% 

COHb benchmark as suggested by the Panel. The 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 the EPA’s task “to establish standards that are 

neither more nor less stringent than necessary for these purposes”, i.e., public health. However, 

other members considered that a more advanced 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 context of the full range 

of benchmarks for policy analysis. Further, if adverse effects are clearly 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 presentation to be technically sound, clearly 

communicated and appropriately balanced? 

Most Panel members agreed that the presentation was technically sound and appropriately 

balanced. However, most of the Panel was concerned that the presentation unnecessarily 

diminished the value of epidemiological studies in establishing the underpinnings (if not the 

details) of the quantitative relationship. Despite the fact that the PA may need to be based on a 

risk assessment drawn primarily from one particularly 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 particular 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 available from NHANES or other readily 

accessible sources). 

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 conclusions as to the adequacy of the current CO 

standards? 

9
In general, the uncertainties are dealt with appropriately with one exception. Under the pretext 

of evaluating the uncertainty regarding ST segment changes, the current 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 objective, were very highly correlated and not 

independent. Therefore, separate analyses of the two indicators should be avoided. 

The most thorough clinical studies remain those of Allred et al., Kleinman et al., and Sheps et al. 

While the effects in these groups are clear, and together these subjects may be “the best 

characterized population,” it is not clear that they represent the “most susceptible 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 conditions. Additionally, 

the epidemiologic data on cardiovascular (heart) disease, including congestive heart failure 

(CHF), suggest that those groups might be at least as susceptible to CO-related stress as the 

coronary artery disease group. 

The data available in the PA and the ISA on CO and heart failure are instructive. The statement 

on page 2-14 (lines 16-19) that there are only “...small or no associations between hospital 

admissions” and stroke is inaccurate (see next paragraph). Of the five studies listed in the 

footnote at the bottom of that page, four of the five reported increased hospital admissions for 

CHF. A close look at Figures 5-2, 5-3, and 5-4 in the ISA support the association of CO with 

CHF and stroke more than for CAD. If all the studies for stroke, CHF and CAD were placed on 

the same x-axis, it could very well demonstrate the heightened uncertainty in statements of CAD 

patients being the most susceptible to CO effects. 

Another possible uncertainty regards the question of whether CO is a surrogate and whether its 

effects at low concentrations can be separated from those of co-pollutants (p. 2-34, lines 24-34). 

There are analytical and methodological challenges in disentangling the effects of CO from those 

of co-pollutants, although the problem does not exist in the controlled 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 integrate the evidence from the 

epidemiological studies with clinical studies (p. 2-25). Some of the conclusions are not well 

supported. In particular, the estimation of population exposures (p. 2-5, lines 27-34, and p. 2-6, 

lines 1-8) may underestimate exposures of those 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 smoke. Inclusion of population prevalence of 

low income status and smoking prevalence in the simulated populations might shift the 

distribution of estimated CO exposures towards higher levels. 

10
The conclusion that the current evidence supports a primary focus on those with cardiovascular 

disease is justifiably based on observations from clinical studies. However, the best 

characterized and most extensively studied population does not necessarily coincide with the 

most highly susceptible population. Since the last review, there 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 exposure with adverse pregnancy outcomes, such as 

premature birth and low birth weight. A stronger commentary on exposure during pregnancy 

and reproductive outcomes is needed. 

b. Does the document appropriately characterize the results of the draft REA, including 

their significance from a public health perspective? 

The conclusion that the current evidence supports a primary focus on individuals with 

cardiovascular disease is justified 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 susceptible 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 metric, then there has to be a better rationale 

provided for interpretation of the epidemiological data using this metric. 

7. What are the views of the Panel regarding the staff’s discussion of considerations related 

to the adequacy of the current and potential alternative standards? 

The staff has provided an extensive analysis of the adequacy of the current and potential 

alternative primary CO standards. The current standards set the levels for 1-hr average and 8-hr 

average at 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 reviewing the recent literature, staff has documented 

that the “much expanded epidemiological evidence ... provides support for previous conclusions 

regarding cardiovascular disease-related susceptibility and indications 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 the currently available evidence provides limited but suggestive 

epidemiologic evidence for CO-induced effects on preterm births, birth defects, and 

developmental outcomes. 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 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 revisions that result in lowering the standards should be 

considered. 

While the epidemiologic studies provide 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 

11
the ambient CO concentrations exceeded the 8-hr standard. However, Table 2.1 includes three 

studies of hospitalizations for ischemic heart disease and/or congestive 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 which 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 indicator. The three studies of ischemic heart disease 

were consistent, but only the Tolbert et al. study had clear statistically significant results. It 

should be recognized that 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 assessing whether 

there are causal relationships. Pooling methods, such as quantitative meta-analyses, may also be 

useful for developing exposure-response relationships. The available studies cover periods 

during which the current NAAQS was 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 should 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 exposures designed to examine effects of CO at 

COHb levels below 2%, there have been numerous 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 previous reviews of the standard have been reduced. 

Based on their overall analysis, they conclude that the body of evidence and the quantitative 

exposure and dose estimates provide support for a standard at least as protective as the current 

standards. I.e. the data provide support for retaining or revising the current 8-hr standard. 

Overall the Panel agrees with this conclusion. If the epidemiological evidence is given 

additional weight, the conclusion could be drawn that health effects are occurring at levels below 

the current standard, which would support the tightening of the current standard. 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 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. 

The Staff have proposed a range of policy options based on the quantitative risk analyses 

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 new 

evidence, primarily epidemiological, that there are many individuals potentially at risk in 

addition to those with coronary artery disease (e.g., fetuses, pregnant women, people with 

congestive heart disease, and people with anemia of various types), there is reason to consider 

reducing the standard below the current level(s). 

12
The Panel suggests describing example policy options such as: 

• 8 hr – retain the 8-hr averaging time 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. See also Figure 1 which shows the 

linear relationship between the 99th percentile and the design value measured for 

epidemiologic studies summarized in PA Table 2-1. 

• 1 hr – retain the current standard to provide protection against infrequent acute exposures. 

Consider a range of concentrations from 5 ppm to 15 ppm, combined with a 99th

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 sufficient 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 individuals 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 table 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 advantages or disadvantages need to be more clearly summarized. 

The Panel concurs with the staff that the 1-hr standard might provide protection 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. 

13
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? 

In choosing a more stable form of the standard, such as the 99th 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. EPA should consider 

conducting an evaluation of the representativeness of the risk analysis to the entire US. 

Currently, the PA is based on two very different cities. Spatial heterogeneity 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 level of detail presented in this chapter? 

The PA concludes that there is insufficient information at this time to support the consideration of a 

secondary standard for CO. In general, the level of discussion detail is appropriate; however, some 

additional detail could be added at the end of chapter 3 on what information is missing in order to make 

a determination regarding a secondary standard. 

10. The discussion of the CO-related 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 appropriately characterizes the evidence as presented in the 

ISA. 

b. Does this discussion effectively 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 climate. It addition, it would be appropriate 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 for climate rather than just for standards and 

exposure, and improvements in localized chemical reactions between CO, CH4, and O3 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 information at this time to support consideration of a 

secondary NAAQS. Nonetheless, there is substantial evidence that CO has adverse effects on 

climate. It would be appropriate 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 presentation to be technically sound, clearly 

communicated and appropriately balanced? 

The Policy Assessment perpetuates and to a degree magnifies the fundamental misunderstanding 

of the REA in relation to susceptibility based to narrowly on CAD alone (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 accumulated epidemiological evidence 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 integration to be technically sound, clearly 

communicated, and appropriately characterized? 

b. Does the document appropriately characterize 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 the current standards should not be weakened. I would 

characterize the conclusion as clearly communicating a sense of not wishing to communicate 

something definitive, at this point at least. The rationale for not considering how many at risk 

persons are pushed over a threshold of body burden 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 revised 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 policy-relevant questions 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 major issues and the information provided in response 

to these questions provides the essential data required for making policy decisions. These 

questions regarding 1. the adequacy of protection by the current standards; 2.does new 

information alter previous conclusions regarding health effects; 3. should COHb continue to be 

the dose indicator for CO exposure; 4. the health effects of ambient CO levels; and 5. any 

reduction in the uncertainties regarding CO. 

Regarding the adequacy of protection: it is difficult to make a judgement 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 country. 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 would reach criteria levels of COHb on an 

annual basis given the current standards. 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 meaning of the controlled human exposures. The adverse health 

effect of limiting the amount of work a person with CAD can perform with doses of CO near 

the current standard has been clearly established. 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 about the significance of ST segment changes on 

page 2-32. The epidemiological studies are designed to provide one means of determine if 

low CO doses have measureable impacts on health 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 connection is clearly stated in this document. 

3. Carbon monoxide is unique among the regulated 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, PCO, as a messenger molecule, 

which could result in various patho-physiological conditions in combination with CO 

exposure. What is missing from the REA and carried through to the PA is a brief description 

of the relationship between PCO and %COHb. This could possibly provide some prospective 

for the reader as to the importance of the physiological tensions of carbon monoxide in 

17
tissues of interest. This would not distract from the current understanding that the dose 

indicator of %COHb is currently 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 have pathophysiological effects. It would appear 

that the epidemiological effects of CO occur at such low levels of exposure as to result in 

very little increases in %COHb. Accepting the premise that the epidemiological results 

attributed primarily to CO exposure implies that adverse health effects occur at levels of 

%COHb considerably below those shown to have statistically significant effects in controlled 

human exposures. For these effects to be consistent with the controlled human exposure 

data, one would have to accept the statement that the effects of CO are without threshold 

(page2-11, Line 9; 2-12, L4; 2-15, L24; 2-16, L26; 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 large number of subjects being 

studied. Or is there another hypothesis regarding how these effects are mediated? 

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

b. Does the Panel consider the document to provide 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 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? 

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 suggestive 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 current research in this area, 

mention of this data should exist in this document. 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 briefly acknowledge the findings of this report. 

Without that information in the current document it is difficult to determine how this report 

should differ from the last review started in 1999. 

18
Charge Question 4. The discussion of the quantitative analysis of exposure and dose (e.g.,section 

2.2.2) draws from the analyses described n the 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 multicenter study following brief mention of the 

supporting studies. I believe that this information could be strengthened by working in the 

information that the CO exposures in the other studies was very similar with confirming 

evidence regarding time to angina. This would address the current concern of imbalance in the 

discussion of the studies 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 technical 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 from the mathematical fiddle noted in 

Appendix B of the REA on page B-5 which states: “In working with the CFK 

model it is convenient to express 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 clearly indicates that the much higher 

affinity of hemoglobin for CO vs Oxygen results in CO displacing O2 from 

oxygenated hemoglobin. The implication that CO binds preferentially to only 

reduced Hb is incorrect and needs to be corrected. 

ii. Page 2-9, line 1. The statement “...or increased cardiac output) is not clear. The 

preceding sentence is discussing cardiovascular disease in the context of CAD. 

Therefore the normal compensatory mechanism that exist in healthy individuals is 

increased myocardial blood flow through vasodilatation, not vasodilatation and 

increased cardiac output. The current verbiage 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 conclusions as to the adequacy of the 

current CO standards? 

Generally the uncertainties are dealt with appropriately with the exception of the item mentioned 

below. 

The current review on page 2-32 under the guise 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 effects of 2% COHb resulting in reducing the amount 

of work a person with CAD can perform before chest pain develops with is due to myocardial 

ischemia. The Allred et al study used EKG changes in the ST segment to substantiate that the 

19
subject measure of angina was indeed due to ischemia. These two indicators, one subjective and 

one objective, were very highly correlated and not independent. Therefore the separation of the 

two indicators (page 2-32, line 25-28) is a reflection of the reviewers not understanding the study 

design. (This should have been corrected throughout 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 this conclusion in the ISA.) In fact the ever increasing amount of 

epidemiological data on the effects of CO probably 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 better 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 identified. The rationale for requesting 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 data 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 overlap 0.6% any more than one would expect 

there to be overlap between 1.5% and 2.0%. What is not stated is that the Apex model may 

overestimate the range of values resulting from no exposure to exogenous CO. 

Without the 1% COHb benchmark how are the epidemiologic studies to be interpreted? Are 

these effects due to the effects of a pollutant that is not measured 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 interpretation 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 addresses the issue of a secondary standard. 

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

The detail is a little light 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 effectively summarize the information on climate related effects of 

CO? 

See below. 

11. What are the Panel’s views regarding 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 evidence 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 uncertainty sufficient and if 

not what would it take? Monitoring 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 concentration-based standard would probably be 

inappropriate. Emissions standards such as are being considered for CO2 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 respect to short term (20-year) climate forcing. The PA may be an 

appropriate forum to provide guidance to how these environmental benefits may be realized. 

21
Dr. Milan Hazucha

The first external draft of the document provides a comprehensive overview of the legislative 

requirements and approaches to policy decision making process. The draft presents in a succinct 

way all aspects of the scientific evidence required for a successful policy assessment. The staff 

has reviewed and discusses key scientific and technical 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 critical 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 background material, including that pertaining to 

previous reviews of the CO standard, the current review and current air quality, to be clearly 

communicated and appropriately characterized? 

I find the introductory and background material pertaining to the previous and current 

reviews to be clearly communicated and appropriately characterized. All the important 

factors needed to make an informed judgment are adequately presented and briefly discussed. 

Review of the Primary Standard (Chapter 2) 

2. Consistent with the revised 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 policy-relevant 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 elderly and people with CVD the time spend 

indoors may be even longer. The non-traffic sources 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 sufficient details, and highlighting 

important factors/concerns so that the policy relevant questions can be addressed both 

quantitatively and qualitatively. 

22
3. The discussion of the health effects evidence (e.g., section 2.2.1) draws 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 scientific evidence is evaluated, characterized 

and presented in a sufficient detail supporting the adequacy of the protection afforded by the 

current CO standard. The differences with the last review are clearly presented. There are no 

new human laboratory studies or exposure/risk-based evidence that would alter the 

conclusions. The evidence from new epidemiologic studies has been presented 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 considerations (e.g. arterial blood 

draw) venous blood COHb level is the optimal indicator of “CO health.” 

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

appropriately balanced? 

Qualified yes. In order to facilitate better understanding of the cardiovascular effects, 

particularly myocardial ischemia, I suggest to add to the reported values of % time changes 

to angina on p.2-11, top paragraph, the actual changes in seconds with 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 the 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 time. Moreover, regarding time to angina endpoint, are there 

any long-term consequences on repeated exposures, on the duration of angina, and frequency 

of occurrence without CO exposure? EPA should address these questions and if we do not 

have respective data the PA should state so. 

Moreover, the first part of the statement in footnote #12 (p. 2-12) commenting on the 

difficulty determining association 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 Critical Review of the Literature on Emissions, 

Exposure, and Health Effects” discusses CO as a marker for another traffic-related pollutants 

such as PM and NO2 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 and 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 draft Risk and Exposure Assessment (REA). 

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

Qualified yes. The COHb module of the APEX model though the most important is also the 

weakest, since we do not have sufficient physiologic data or the range of values for many 

variables that enter into the model. However, 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 Panel, 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 approach since this complies with the EPA’s 

task “to establish standards that are neither more nor less stringent than necessary for these 

purposes”, .i.e. public health. 

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

appropriately balanced? 

Yes, in all respects. Again, because of the importance of the statement, the first sentence of 

the footnote #25 on the difficulty to determine association between CO and CVD in 

interpreting epidemiological evidence should be moved to the body of a respective 

paragraph. 

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 conclusions as to the adequacy 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 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? 

Yes, in all respects 

 b. Does the document appropriately characterize the results of the draft REA, including 

their significance from a public health perspective? 

Yes, in all respects 

24
7. What are the views of the Panel regarding the staff’s discussion of considerations related to 

the adequacy of the current and potential alternative standards? 

I find the initial staff conclusion “for either retaining or revising the current 8-hour standard” 

(p. 2-46) based on the available estimates of exposure ambivalent. Does this mean that EPA 

is undecided or that the evidence is split 50/50? It is true, as subsequently stated, that a 

variety of factors will be considered in judging 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 epidemiology studies will produce COHb levels within a 

normal range. From reading interpretation of these 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 relationship. 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 scientific evidence, I agree with the staff interpretation of 

epidemiology studies and their leaning towards retaining the current 8-hour standard. 

The section 2.3 of the discussion of the averaging time, the form and level of alternative 

standard and potential alternative levels is succinct and well reasoned. What is not clear what 

form might the alternative 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 discussion 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 evidence 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. 

25
10. The discussion of the CO-related 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? 

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 regarding the appropriateness of staff’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 alternative standards? 

The staff has provided an extensive analysis of the adequacy of the 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 reviewing the recent literature staff has 

documented that the “much expanded epidemiological evidence ... provides support for previous 

conclusions regarding cardiovascular disease –related susceptibility and indications 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 conclude that the currently 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 disease. Based on the analyses of epidemiological studies presented 

in the PA there is a consensus in the panel that the current standards may 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 the 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 ischemic heart disease and/or congestive heart failure (CGF) from 

Atlanta for which this was not the case (Tolbert 2007, Peel 2007, Metzger 2007) and one 

additional study of CGF (Wellenius, 2005) which did not include data 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 methods such as meta-analyses to develop 

exposure-response curves. For this purpose the fact that some studies included periods in which 

the current standard was exceeded becomes less important because there are also studies at lower 

levels so that CR relationships can be interpolated (as opposed to extrapolated). The emphasis 

should be on studies that used a multipollutant model approach to control for potential 

confounding of CO effects by other co-varying pollutants. 

While there have been no new controlled human exposures that were designed to examine effects 

of CO at COHb levels below 2%, there have been numerous improvements to the exposure and 

COHb dosimetry models employed to provide exposure and risk estimates. The Staff analysis 

27
indicates that some of the uncertainties identified in previous reviews of the standard have been 

reduced and that based on their overall analysis conclude that the body of evidence and the 

quantitative exposure and dose estimates provide support for a standard at least as protective as 

the current standards, i.e. the data provide support for retaining or revising 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 evidence 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; would it have been excluded 

for as little as 1 exceedence in 7 years? 

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. 

The Staff have proposed a range of policy options 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 individuals potentially at risk in addition to those 

with coronary artery disease (e.g. fetuses, pregnant women, people with congestive heart disease, 

people with anemia of various types) 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 consideration 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 99th percentile 

with a concentration range of 3-5. Note see Figure 1 which shows the linear relationship 

between the 99th 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 standard to provide protection against infrequent acute exposures. 

Consider a range of concentrations from 5 ppm to 15 ppm, combined with a 99th 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 sufficient 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 individuals 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 range of options needs better 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. 

28
The panel concurs with the staff that the 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 supporting 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 99th 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 the 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 should 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 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 policy-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 reflect the policy relevant questions. 

b. Does the Panel consider the document to provide the appropriate level 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., section 2.2.1) draws 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 – the draft PA accurately reflects the currently available health effects 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 sufficient 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 technically sound, clearly communicated and appropriately balanced. 

30
Dr. Arthur Penn 

1. Does the Panel find the introductory and background material, including 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 (1o, 2o); adequate 

margins of safety; previous reviews; CO sources in ambient 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”. 

There is one item on p. 1-1 that could benefit from some clarification and possible change of 

location. Lines 22-25 on that page emphasize that the focus of the PA is on the 4 basic elements 

of NAAQS: indicator, averaging time, form and level. 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 clearly. “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 anything else? If it = percentile, 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 quantitative analysis of CO exposure and dose, 

particularly those of particular significance in drawing conclusions as to the adequacy of 

the current CO standards? 

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

2-53. 

There are a couple of other conclusions of the PA that have raised questions for me. Whether 

they rise to the level of uncertainty depends on how other CASAC CO panelists respond. 

p.2-18: The most thorough clinical studies remain those of Allred-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 they 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 conditions, it’s difficult to conclude that this is the 

“most susceptible population”. Additionally, the epidemiologic data 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 heart disease group. 

31
The data available in the PA and the ISA on CO/heart 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 accurate (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”. Unless 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 values in those figures appear smaller than they really are. In 

Figure 5-2 (CHD) 27/31 values have a RR< 1.05 and 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 studies for stroke, CHF 

and CHD were placed on the same x-axis, uncertainty could well be heightened about CHD 

patients being the most susceptible 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 regards the question (PA-p. 2-34, lines 24-34) of whether CO is a 

surrogate and whether its effects at low concentrations 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 and organic particles in ambient air are largely 

products of incomplete combustion (PICs). In real-world (and in most laboratory) situations it is 

essentially impossible to generate, and therefore to breathe, organic particle PICs without 

volatiles, including CO. So, disentangling CO effects from those of co-pollutants (not a problem 

in the Allred-Kleinman-Sheps controlled clinical studies) is not only difficult, but likely also 

artificial. 

32
Dr. Beate Ritz 

7. What are the views of the Panel regarding the staff’s discussion of considerations related to 

the adequacy of the current and potential alternative standards? 

In reviewing the recent literature EPA staff has concluded that a causal relationship is likely to 

exist between relevant short term exposures to CO and cardiovascular morbidity based mainly on 

the coherence between the results from controlled human chamber studies and the more recent 

epidemiologic literature. However, the PA makes 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 commented on 3 studies from Atlanta for which this was not the case 

(Tolbert 2007, Peel 2007, Metzger 2007) and stated that 2 of the three studies reported nonstatistically significant results. 

For the Atlanta studies, first this statement is incorrect, i.e. all 3 studies 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 effect estimate sizes are all very comparable (in 

all three studies) and this is more important than statistically significance testing. Nevertheless, 

since the 3 Atlanta studies do not use mutually exclusive data and the Tolbert study is the most 

comprehensive one with regard to the time frame and # of hospitals covered, this largest study 

can be considered the most informative of the three. Concerning the studies covering areas that 

exceeded the current standards during the study period, it seems not completely justified to 

disregard them because of this fact when assessing 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 example of a general tendency of the PA to misinterpretate and mis-represent epidemiologic study results that is even more evident when it 

comes to interpreting results for other 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, developmental outcomes; the PA states that “the 

epidemiologic evidence ....has somewhat expanded, although the available evidence is still 

considered limited with regard to effects ..” This, is a misrepresentation 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 little or conflicting epidemiologic evidence but rather to the lack or 

impossibility of human chamber studies and valid 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 uncertainties identified in previous reviews of the 

standard have been reduced and they provide support for a standard at least as protective as the 

current standards, i.e. the data provide support for retaining or revising the current 8-hr standard. 

In fact if the epidemiological evidence was not down-weighted or outright ignored as much as it 

33
currently is in this PA, enough evidence has accrued at levels below the current standard to 

revise them downwards in the interest of public health in general (not just for CVD outcomes). 

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 sufficient rationale for discussion of the range of options is provided 

 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? 

 Spatial heterogeneity of CO exposures that increase exposures near major sources i.e. near 

and on roadways should be given some weight since these might drive a lot of the adverse health 

effects. 

34
Dr. Anne Sweeney 

CQ. 7. The discussion of considerations 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 conclusions reached were not well-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 indoor 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 the 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 populations would greatly enhance 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 cardiovascular 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 association with CO. It is stated on Page 2-18, 

lines 15-18 that “.. the population with pre-existing cardiovascular disease associated with 

limitation in oxygen availability continues to be the est characterized population at risk of 

adverse CO-induced effects..”. However, the best characterized and most extensively studied 

population does not necessarily identify the most highly susceptible population. The 

expansion of studies with positive findings evaluating effects on fetuses since the previous 

review, supported by strong toxicological 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 effects of CO on birth outcomes and 

developmental effects, the currently available evidence 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 toxicological studies provide some support and coherence for these birth 

and developmental outcomes, although a clear understanding of the mechanisms underlying 

potential reproductive and developmental effects 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 date supports an association of greater concern than the current 

evaluation bestows. 

35
CQ. 8. 

a. Overall, the range of options recommended by the staff support at minimum the 

continuation of the current CO standards and 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 multiplicative effects of ambient and indoor CO exposures need to 

be given more consideration. In assessing 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-hour 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 especially 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 rationale 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 questions are posed but not answered. Therefore, 

this reviewer feels that some sections are poorly communicated. For example, section 2-2 poses 

the question: “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?” 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 question “Does the current evidence alter our 

conclusions from the previous review 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 (page 2-17, line 29-31). On page 2-18, line 1 the 

question “Does the current evidence alter our understanding of populations that are particularly 

susceptible to CO exposures?” is answered (page 2-21, line 17 – 20). Of note, there is also a 

second question posed on line 2-19 that is redundant 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 ambient air associated with health effects?” is not answered. The 

staff reiterates much of the uncertainty with the current state of CO pathophysiology but never 

offers a conclusion. Moreover, there are parts of this section that are 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 uncertainties identified in the last review 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 overarching question.”, but no question 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” and “What proportion of the .... population experience 

maximum COHb levels above levels of potential 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 uncertainties 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 

37
public 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 question: “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 unanswered 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 rational taken by the staff and why they 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 revised. Hence, there is no conclusion. 

6. Section 2.3, considerations of alternative standards, is organized 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 standards ... ?” is broken down into sub-headings 

and more questions. Section 2.3.1 states the indicator for carbon monoxide is carbon monoxide 

(not sure this is really necessary). Alternatively, you fail to mention the issues outlined in ISA 

chapter 3. Might it be appropriate to mention that CO is an O3 precursor and there is a localized 

chemical interdependency of the CO-CH4-NOx system, although these alternative products are 

not used in estimating local CO production? Section 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 for 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 alternative levels and forms for the standard ... ?” The ensuing 

paragraphs and sections discuss use of a 99th percentile concentration-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 retained. Hence, the document offers no conclusion. A minor comment on 

the tables 2-6 and 2-7 is uncertainty over the term ‘level’ in the second columns. I assume, but 

am unsure that ‘level’ refers to ppm of CO. 

7. I think discussion of current and potential alternative standards is adequate. I have one last 

comment pertaining to the uncertainties 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 the modelers added 0.5 ppm CO to all measured 

values to remove zeros and negative numbers thought to be related to monitor drift. It seems to 

me that this severely weakens estimates of the at-risk population and threshold COHb levels and 

thus contradicts consideration of changes from the current standards. However, I defer to other 

Review Panel members with modeling expertise on whether my concerns are valid. 

38
39

8. I do not think the options listed by the staff are 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 consideration of a secondary standard for CO concludes, I think 

justifiably, that the science does not support establishing a secondary standard. I think the level 

of detail presented is adequate. 
A-1 

Appendix A 

Summary of 2003 NRC Report Recommendations 

 

 
A-2 

Summary of NRC Report1 Recommendations

This report was requested to investigate the characteristics 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 episodes 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 separate 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 PM2.5 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 components 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 representation of relationships between transportation 

activity and emissions, and approximation of concentrations 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 concert with improved monitoring. 

1 Summarized from Managing Carbon Monoxide Pollution in Meteorological and Topographical 

Problem Areas. National Research Council of the National Academies 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 Study

 
B-2 

Air quality information provided here is drawn from monitors reporting to the U.S. Air 

Quality System (AQS)1

, and for the Atlanta study, two monitors reporting to the SouthEastern 

Aerosol Research and Characterization study (SEARCH)2 database. Available meta-data from 

AQS and SEARCH were used to create the monitor 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-overlapping 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 available 1-hour data and summarized 8-hour daily maximum data. 

For the 126-county Bell et al (2009) study, the highest annual statistic reported by any monitor in 

the county was used. 

 

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

2

 The Southeastern Aerosol Research and Characterization (SEARCH) network data are publically 

available at the SEARCH website (http://www.atmospheric-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 2000

(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 -3
Atlanta - January 1st 1993 to August 31st 2000

(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 - 4
Atlanta - January 1st 1993 to August 31st 2000

(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-hour - 99th percentile (of all 365 possible 

daily 24-hour averages)

24-hour - 50th percentile (of all 365 possible 

daily 24-hour averages)

B - 5
Atlanta-- 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 

Number

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 - 6
Atlanta-- 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 - 7
Atlanta-- 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 - 8
Denver-- 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 - 9
Denver-- 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 - 10
Denver-- 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

Maxperyear 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 (of all 365 possible daily 

24-hour averages)

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

24-hour averages)

B - 11
Pennsylvania-- 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 - 12
Allegheny County, PA-- January 1st 1987 through November 30th, 1999

(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 - 13
Allegheny County, PA-- January 1st 1987 through November 30th, 1999

(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 - 14
Baltimore-- 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 - 15
Baltimore-- 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-hour -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-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-hour - 99th percentile (of all 365 possible daily 24-hour 

averages)

B - 16
California-- January 1st 1992 through December 31st, 1995

(Study area and time period for Linn et al., 2000 )

Design values for current standards

California 1992 1993 1994 1995

Los Angeles 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

Maxperyear 25.0 20.0 20.8 16.5

1-hour - 2nd maximum (ppm) per monitor, per year for 1992-

1995 (current standard is 35 ppm)

B - 17
California-- January 1st 1992 through December 31st, 1995

(Study area and time period for Linn et al., 2000 )

California 1992 1993 1994 1995

Los Angeles 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

Maxperyear 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 - 18
California-- January 1st 1992 through December 31st, 1995

(Study area and time period for Linn et al., 2000 )

Statistics for Other Metrics

California 1992 1993 1994 1995

Los Angeles 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

Maxperyear 21.0 19.0 18.0 16.1 21.0 Total Max

Minperyear 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 - 19
California-- January 1st 1992 through December 31st, 1995

(Study area and time period for Linn et al., 2000 )

California 1992 1993 1994 1995

Los Angeles 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

Maxperyear 4.0 4.0 4.4 3.8 4.4 Total Max

Minperyear 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 - 20
California-- January 1st 1992 through December 31st, 1995

(Study area and time period for Linn et al., 2000 )

California 1992 1993 1994 1995

Los Angeles 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

Maxperyear 14.4 13.0 14.2 11.2 14.4 Total Max

Minperyear 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 - 21
California-- January 1st 1992 through December 31st, 1995

(Study area and time period for Linn et al., 2000 )

California 1992 1993 1994 1995

Los Angeles 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

Maxperyear 2.9 2.7 3.0 2.8 3.0 Total Max

Minperyear 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 - 22
California-- January 1st 1992 through December 31st, 1995

(Study area and time period for Linn et al., 2000 )

California 1992 1993 1994 1995

Los Angeles 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

Maxperyear 9.6 8.0 8.9 7.6 9.6 Total Max

Minperyear 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 - 23
California-- January 1st 1992 through December 31st, 1995

(Study area and time period for Linn et al., 2000 )

California 1992 1993 1994 1995

Los Angeles 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

Maxperyear 1.9 1.9 2.2 2.0 2.2 Total Max

Minperyear 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 - 24
California-- 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

Maxperyear 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 - 25
California-- 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

Maxperyear 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 - 26
California-- 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

Maxperyear 31.0 25.0 22.0 21.0 21.0 19.0 18.0 16.1 31.0 Total Max

Minperyear 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 - 27
California-- 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

Maxperyear 5.0 5.0 5.0 4.0 4.0 4.0 4.4 3.8 5.0 Total Max

Minperyear 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 - 28
California-- 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

Maxperyear 19.1 18.0 15.3 13.6 14.4 13.0 14.2 11.2 19.1 Total Max

Minperyear 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 - 29
California-- 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

Maxperyear 3.3 3.1 2.9 2.7 2.9 2.7 3.0 2.8 3.3 Total Max

Minperyear 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 - 30
California-- 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

Maxperyear 10.9 9.6 8.7 8.7 9.6 8.0 8.9 7.6 10.9 Total Max

Minperyear 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 - 31
California-- 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

Maxperyear 2.3 2.3 1.9 1.8 1.9 1.9 2.2 2.0 2.3 Total Max

Minperyear 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 - 32
126County-- 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

Alabama 01 Jefferson 073 32.3 23.6 33.5 17.7 9.1 15.0 20.9

Arizona 04 Maricopa 013 13.5 10.5 9.6 7.9 7.3 7.5 7.0

Arizona 04 Pima 019 7.8 7.5 5.7 5.1 9.6 4.7 3.6

Arkansas 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

Kentucky 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 - 33
126County-- 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 Jersey 34 Bergen 003 5.7 4.8 4.5 4.2 5.2 4.1 3.4

New Jersey 34 Camden 007 5.5 5.3 5.6 3.8 2.9 3.7 3.9

New Jersey 34 Hudson 017 10.0 8.5 5.1 4.4 4.0 4.1 4.8

New Jersey 34 Middlesex 023 4.5 4.7 4.8 3.7 3.7 3.5 3.0

New Jersey 34 Morris 027 5.9 5.1 5.6 4.9 3.6 3.1 2.8

New Jersey 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 York 36 Albany 001 2.5 1.8 1.9 2.2 2.9 1.7 1.9

New York 36 Bronx 005 5.7 6.0 4.9 3.7 3.4 2.8 3.5

New York 36 Erie 029 3.9 4.7 3.2 4.0 3.0 2.6 2.5

New York 36 Kings 047 7.3 6.2 5.7 4.9 3.5 3.6 4.1

New York 36 Monroe 055 5.5 4.2 4.3 5.7 2.8 2.8 2.5

New York 36 New York 061 7.1 6.0 6.5 4.5 4.0 3.6 2.2

New York 36 Niagara 063 4.2 3.8 2.3 2.2 2.8 2.5 5.7

New York 36 Onondaga 067 5.6 3.9 3.8 3.4 3.2 3.0 2.8

New York 36 Queens 081 3.4 6.3 3.8 3.5 11.2 3.1 2.4

New York 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 - 34
126County-- 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

Pennsylvania 42 Allegheny 003 6.0 5.5 4.2 5.7 5.6 3.5 3.1

Pennsylvania 42 Berks 011 4.6 3.8 3.8 4.1 3.2 2.7 2.4

Pennsylvania 42 Dauphin 043 4.9 3.5 4.4 3.6 3.0 2.3 2.0

Pennsylvania 42 Erie 049 10.6 11.9 7.2 7.5 7.6 1.8 3.1

Pennsylvania 42 Lackawanna 069 3.5 4.4 2.9 2.7 2.4 2.9 2.6

Pennsylvania 42 Lancaster 071 3.1 3.0 2.9 3.0 2.7 3.2 2.5

Pennsylvania 42 Northampton 095 4.4 5.5 3.1 2.3 2.3 2.4 2.5

Pennsylvania 42 Philadelphia 101 7.4 6.3 7.7 5.0 5.4 5.1 12.1

Pennsylvania 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

Maxperyear 32.3 23.6 33.5 17.7 14.9 15.0 20.9

B - 35
126County-- 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

Alabama 01 Jefferson 073 19.8 16.3 24.3 11.7 4.5 8.2 8.8

Arizona 04 Maricopa 013 8.1 7.2 6.6 5.5 5.5 5.1 4.8

Arizona 04 Pima 019 3.8 4.7 2.9 2.6 2.7 2.5 2.4

Arkansas 05 Pulaski 119 4.0 2.9 2.2 5.2 2.2 1.8 2.1

California 06 Alameda 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 Adams 001 3.6 2.9 3.3 2.6 3.0 2.8 2.2

Colorado 08 Denver 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 Ada 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 Allen 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

Kentucky 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 - 36
126County-- 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 Middlesex 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 Kent 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 City 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 Jersey 34 Bergen 003 4.4 3.4 3.1 3.4 2.4 2.7 2.8

New Jersey 34 Camden 007 3.7 4.3 3.9 2.1 1.8 2.9 3.0

New Jersey 34 Hudson 017 6.1 4.8 3.0 2.8 2.9 3.2 2.8

New Jersey 34 Middlesex 023 3.3 3.3 3.3 2.6 1.9 2.1 1.9

New Jersey 34 Morris 027 4.1 3.1 3.3 2.4 2.3 1.9 1.8

New Jersey 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 York 36 Albany 001 1.4 1.1 1.2 1.5 1.5 1.1 1.4

New York 36 Bronx 005 4.0 3.5 2.7 2.4 2.1 2.0 2.2

New York 36 Erie 029 2.2 2.0 1.9 1.8 2.4 1.4 1.6

New York 36 Kings 047 4.9 4.3 3.5 3.4 2.6 2.5 2.2

New York 36 Monroe 055 2.6 2.6 1.8 2.2 2.1 1.6 2.0

New York 36 New York 061 4.7 4.2 3.2 3.1 3.0 2.4 1.5

New York 36 Niagara 063 2.5 1.6 1.6 1.7 2.0 1.4 1.8

New York 36 Onondaga 067 3.1 2.4 2.2 2.1 1.8 1.4 1.9

New York 36 Queens 081 2.5 3.3 3.0 2.5 2.6 2.0 1.6

New York 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 Montgomery 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 - 37
126County-- January 1st 1999 through December 31st, 2005

(Study area and time period for Bell et al., 2009 )

Pennsylvania 42 Allegheny 003 3.9 3.2 3.4 2.7 2.3 2.3 2.2

Pennsylvania 42 Berks 011 2.8 2.1 2.2 2.2 2.0 1.8 1.9

Pennsylvania 42 Dauphin 043 4.3 2.1 2.8 2.3 2.0 1.3 1.3

Pennsylvania 42 Erie 049 5.6 6.0 4.4 4.5 3.4 1.3 1.4

Pennsylvania 42 Lackawanna 069 1.7 2.1 1.8 1.6 1.5 1.8 1.5

Pennsylvania 42 Lancaster 071 2.1 1.9 2.2 2.2 1.7 1.6 1.5

Pennsylvania 42 Northampton 095 3.0 2.4 2.4 1.8 1.4 1.7 1.9

Pennsylvania 42 Philadelphia 101 4.9 4.0 4.7 2.9 3.9 3.4 3.4

Pennsylvania 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 Shelby 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 City 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

Maxperyear 19.8 16.3 24.3 11.7 7.2 8.2 8.8

B - 38
126County-- 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

Alabama 01 Jefferson 073 26.4 18.5 31.8 15.9 7.9 14.1 16.1

Arizona 04 Maricopa 013 13.5 9.8 9.0 7.7 6.9 6.4 6.4

Arizona 04 Pima 019 7.2 7.0 5.5 4.9 5.4 4.4 3.2

Arkansas 05 Pulaski 119 5.4 4.3 3.8 4.9 3.5 2.7 2.5

California 06 Alameda 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 Adams 001 5.3 4.2 4.7 3.7 3.6 3.4 3.0

Colorado 08 Denver 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 Ada 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 Allen 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

Kentucky 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 - 39
126County-- 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 Kent 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 City 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 Jersey 34 Bergen 003 4.9 4.3 4.0 3.9 3.1 3.1 2.7

New Jersey 34 Camden 007 4.6 4.6 4.5 3.2 2.8 2.7 3.5

New Jersey 34 Hudson 017 9.1 8.1 4.2 4.2 4.0 3.4 3.6

New Jersey 34 Middlesex 023 4.4 4.0 4.1 3.5 2.8 2.9 2.7

New Jersey 34 Morris 027 5.6 4.5 4.4 3.8 3.4 2.5 2.4

New Jersey 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 York 36 Albany 001 1.7 1.6 1.7 1.7 1.5 1.6 1.2

New York 36 Bronx 005 4.8 3.5 3.9 3.4 2.9 2.2 2.5

New York 36 Erie 029 3.3 3.3 2.7 2.7 2.8 2.1 2.1

New York 36 Kings 047 5.8 5.6 4.8 4.5 3.4 3.5 3.4

New York 36 Monroe 055 4.7 3.3 3.5 2.8 2.5 2.8 2.2

New York 36 New York 061 5.3 5.5 4.5 3.9 3.2 2.6 2.0

New York 36 Niagara 063 2.5 2.6 2.1 1.9 2.6 2.2 2.2

New York 36 Onondaga 067 5.0 3.6 2.7 3.0 2.6 2.5 2.4

New York 36 Queens 081 3.3 3.4 3.8 2.8 3.2 2.5 2.1

New York 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 Montgomery 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 - 40
126County-- 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

Pennsylvania 42 Allegheny 003 5.6 4.4 4.0 3.9 3.3 2.8 2.5

Pennsylvania 42 Berks 011 3.8 3.4 3.2 3.2 2.2 2.4 2.3

Pennsylvania 42 Dauphin 043 3.8 3.1 3.5 3.0 2.2 2.1 1.7

Pennsylvania 42 Erie 049 9.1 10.1 6.7 6.8 6.3 1.7 2.3

Pennsylvania 42 Lackawanna 069 2.7 3.1 2.8 2.6 2.3 2.6 2.2

Pennsylvania 42 Lancaster 071 3.0 2.3 2.6 2.8 2.2 2.4 2.2

Pennsylvania 42 Northampton 095 3.7 3.3 2.7 2.3 1.9 2.0 2.1

Pennsylvania 42 Philadelphia 101 6.4 4.7 5.9 4.0 4.7 4.6 3.7

Pennsylvania 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 Shelby 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 City 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

Maxperyear 26.4 18.5 31.8 15.9 10.4 14.1 16.1 31.8 Total Max

Minperyear 1.2 1.5 1.3 1.0 0.9 0.8 0.6 0.6 Total Min

B - 41
126County-- 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

Alabama 01 Jefferson 073 2.3 2.4 2.4 1.9 1.3 1.1 1.5

Arizona 04 Maricopa 013 5.9 4.4 3.6 4.5 3.2 2.6 2.1

Arizona 04 Pima 019 3.5 3.2 2.5 2.2 1.8 1.7 1.5

Arkansas 05 Pulaski 119 2.0 1.8 1.3 0.9 0.8 0.6 0.7

California 06 Alameda 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 Adams 001 1.6 1.3 1.4 1.2 1.1 1.1 1.0

Colorado 08 Denver 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 Ada 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 Allen 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

Kentucky 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 - 42
126County-- 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 Kent 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 City 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 Jersey 34 Bergen 003 2.4 2.0 2.1 1.7 1.4 1.2 1.1

New Jersey 34 Camden 007 0.8 0.8 0.9 0.8 0.8 0.7 0.6

New Jersey 34 Hudson 017 3.4 3.1 1.9 1.9 1.9 1.8 1.7

New Jersey 34 Middlesex 023 1.9 1.5 1.4 1.5 1.1 0.9 1.0

New Jersey 34 Morris 027 2.0 1.8 1.5 1.3 1.1 1.0 0.9

New Jersey 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 York 36 Albany 001 0.5 0.6 0.5 0.6 0.7 0.6 0.5

New York 36 Bronx 005 1.0 1.0 1.0 0.9 1.0 0.9 0.8

New York 36 Erie 029 1.0 0.9 0.8 0.7 0.8 0.6 0.6

New York 36 Kings 047 2.5 2.9 1.9 1.7 1.8 1.6 1.4

New York 36 Monroe 055 1.0 0.9 0.8 0.8 0.8 0.7 0.6

New York 36 New York 061 2.8 2.4 2.0 1.5 1.5 1.2 0.9

New York 36 Niagara 063 0.6 0.5 0.5 0.5 0.5 0.3 0.3

New York 36 Onondaga 067 0.9 1.0 0.9 0.9 1.0 0.8 0.8

New York 36 Queens 081 1.0 0.9 1.0 0.9 0.9 0.8 0.8

New York 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 Montgomery 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

Pennsylvania 42 Allegheny 003 1.7 1.6 1.3 0.8 0.8 0.9 0.8

B - 43
126County-- January 1st 1999 through December 31st, 2005

(Study area and time period for Bell et al., 2009 )

Pennsylvania 42 Berks 011 0.8 0.7 0.9 0.8 0.7 0.7 0.8

Pennsylvania 42 Dauphin 043 0.8 0.8 0.7 0.8 0.7 0.7 0.6

Pennsylvania 42 Erie 049 1.2 1.4 1.0 0.8 0.8 0.5 0.7

Pennsylvania 42 Lackawanna 069 0.3 0.8 0.9 0.3 0.3 0.5 0.5

Pennsylvania 42 Lancaster 071 0.5 0.5 0.7 0.8 0.6 0.6 0.5

Pennsylvania 42 Northampton 095 0.6 0.7 0.5 0.5 0.3 0.5 0.3

Pennsylvania 42 Philadelphia 101 1.8 1.6 1.5 1.3 1.4 1.2 1.1

Pennsylvania 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 Shelby 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 City 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

Maxperyear 5.9 4.4 3.6 4.5 3.2 2.6 2.2 5.9 Total Max

Minperyear 0.3 0.3 0.3 0.3 0.3 0.3 0.3 0.3 Total Min

B - 44
126County-- 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

Alabama 01 Jefferson 073 15.8 14.5 18.9 10.7 3.9 7.7 8.5

Arizona 04 Maricopa 013 10.0 7.0 5.9 5.5 5.2 4.3 4.6

Arizona 04 Pima 019 3.5 4.1 2.8 3.3 2.8 2.4 2.3

Arkansas 05 Pulaski 119 3.6 2.7 2.2 4.9 2.2 1.6 1.6

California 06 Alameda 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 Adams 001 3.4 2.8 3.1 2.5 2.8 2.8 2.0

Colorado 08 Denver 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 - 45
126County-- 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 Jersey 34 Camden 007 3.1 3.6 2.8 2.0 1.7 2.3 2.5

New Jersey 34 Hudson 017 5.8 5.2 2.9 2.7 2.8 2.7 2.6

New Jersey 34 Middlesex 023 3.4 3.1 2.8 2.6 1.8 2.1 1.9

New Jersey 34 Morris 027 3.9 3.0 3.1 2.3 2.1 1.7 1.6

New Jersey 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 York 36 Albany 001 1.3 1.1 1.1 1.2 1.3 1.0 0.9

New York 36 Bronx 005 3.6 3.3 2.6 1.9 2.0 1.8 1.7

New York 36 Erie 029 2.1 1.8 1.8 1.6 1.8 1.3 1.5

New York 36 Kings 047 4.7 4.0 3.2 3.3 2.5 2.4 2.2

New York 36 Monroe 055 2.5 2.4 1.8 1.9 1.9 1.6 1.8

New York 36 New York 061 4.4 3.8 3.1 2.9 2.6 2.1 1.5

New York 36 Niagara 063 1.4 1.4 1.3 1.5 1.4 1.3 1.4

New York 36 Onondaga 067 3.0 2.3 2.0 1.8 1.7 1.4 1.8

New York 36 Queens 081 2.4 3.2 3.0 2.3 2.3 1.7 1.6

New York 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 Montgomery 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 - 46
126County-- 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

Pennsylvania 42 Allegheny 003 3.5 3.2 2.6 2.6 2.2 2.3 2.0

Pennsylvania 42 Berks 011 2.5 1.8 1.9 1.9 1.9 1.7 1.7

Pennsylvania 42 Dauphin 043 2.5 2.1 2.6 2.0 1.5 1.3 1.3

Pennsylvania 42 Erie 049 5.3 5.2 4.1 3.8 3.2 1.2 1.4

Pennsylvania 42 Lackawanna 069 1.7 2.0 1.7 1.4 1.4 1.6 1.5

Pennsylvania 42 Lancaster 071 2.0 1.8 1.8 2.0 1.6 1.5 1.3

Pennsylvania 42 Northampton 095 2.5 2.3 1.9 1.6 1.3 1.6 1.8

Pennsylvania 42 Philadelphia 101 4.0 3.4 3.9 2.5 3.8 3.1 3.3

Pennsylvania 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 Shelby 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 City 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

Maxperyear 15.8 14.5 18.9 10.7 6.7 7.7 8.5 18.9 Total Max

Minperyear 1.0 0.9 0.9 0.7 0.7 0.5 0.4 0.4 Total Min

B - 47
126County-- 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

Alabama 01 Jefferson 073 1.7 1.7 1.6 1.5 0.8 0.8 0.9

Arizona 04 Maricopa 013 4.2 2.8 2.4 3.1 2.0 1.5 1.3

Arizona 04 Pima 019 2.0 1.8 1.6 1.4 1.2 1.2 1.1

Arkansas 05 Pulaski 119 1.7 1.5 1.1 0.6 0.6 0.5 0.5

California 06 Alameda 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 Adams 001 1.0 0.8 0.9 0.7 0.7 0.8 0.7

Colorado 08 Denver 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 - 48
126County-- 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 Jersey 34 Hudson 017 2.4 2.2 1.5 1.5 1.5 1.5 1.4

New Jersey 34 Middlesex 023 1.4 1.1 1.1 1.2 0.8 0.7 0.8

New Jersey 34 Morris 027 1.5 1.4 1.2 1.0 0.9 0.8 0.7

New Jersey 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 York 36 Albany 001 0.3 0.4 0.4 0.4 0.6 0.5 0.3

New York 36 Bronx 005 0.8 0.8 0.8 0.8 0.9 0.7 0.7

New York 36 Erie 029 0.8 0.7 0.6 0.6 0.6 0.5 0.4

New York 36 Kings 047 2.0 2.2 1.5 1.4 1.4 1.2 1.0

New York 36 Monroe 055 0.8 0.7 0.6 0.6 0.7 0.7 0.5

New York 36 New York 061 2.3 2.0 1.7 1.3 1.3 1.1 0.8

New York 36 Niagara 063 0.4 0.4 0.3 0.3 0.4 0.3 0.3

New York 36 Onondaga 067 0.6 0.8 0.6 0.6 0.8 0.6 0.6

New York 36 Queens 081 0.9 0.7 0.7 0.7 0.8 0.7 0.6

New York 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 Montgomery 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 - 49
126County-- January 1st 1999 through December 31st, 2005

(Study area and time period for Bell et al., 2009 )

Pennsylvania 42 Allegheny 003 1.3 1.3 1.0 0.5 0.6 0.6 0.6

Pennsylvania 42 Berks 011 0.5 0.5 0.7 0.6 0.4 0.5 0.5

Pennsylvania 42 Dauphin 043 0.5 0.5 0.4 0.5 0.6 0.5 0.5

Pennsylvania 42 Erie 049 0.8 0.9 0.8 0.6 0.6 0.4 0.5

Pennsylvania 42 Lackawanna 069 0.3 0.5 0.6 0.3 0.3 0.3 0.3

Pennsylvania 42 Lancaster 071 0.3 0.3 0.4 0.6 0.4 0.4 0.3

Pennsylvania 42 Northampton 095 0.4 0.4 0.3 0.3 0.3 0.3 0.3

Pennsylvania 42 Philadelphia 101 1.4 1.2 1.2 1.0 1.1 1.0 1.0

Pennsylvania 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 Shelby 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 City 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

Maxperyear 4.2 2.8 2.4 3.1 2.2 2.0 1.8 4.2 Total Max

Minperyear 0.3 0.3 0.3 0.3 0.3 0.3 0.3 0.3 Total Min

B - 50
126County-- 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

Alabama 01 Jefferson 073 9.3 6.4 11.0 4.0 2.2 3.7 5.0

Arizona 04 Maricopa 013 5.6 4.1 3.6 4.2 3.5 3.1 3.3

Arizona 04 Pima 019 2.1 2.4 1.9 1.7 1.7 1.3 1.3

Arkansas 05 Pulaski 119 2.7 1.8 1.6 4.0 1.3 0.9 1.0

California 06 Alameda 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 Adams 001 2.1 1.9 1.9 1.4 1.5 1.7 1.3

Colorado 08 Denver 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 - 51
126County-- 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 Jersey 34 Hudson 017 3.7 3.0 2.0 1.9 2.1 2.2 1.8

New Jersey 34 Middlesex 023 2.9 1.8 2.0 1.6 1.3 1.3 1.4

New Jersey 34 Morris 027 2.5 1.9 2.0 1.4 1.3 1.2 1.2

New Jersey 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 York 36 Albany 001 1.1 0.9 0.8 1.0 1.1 0.7 0.7

New York 36 Bronx 005 1.7 1.6 1.5 1.3 1.4 1.2 1.1

New York 36 Erie 029 1.2 1.2 0.9 1.1 1.2 0.8 1.0

New York 36 Kings 047 3.1 2.8 2.3 2.0 2.0 1.7 1.6

New York 36 Monroe 055 1.4 1.2 1.0 1.0 1.0 1.1 1.2

New York 36 New York 061 2.7 2.9 2.2 1.9 1.8 1.5 1.0

New York 36 Niagara 063 0.8 1.0 0.8 1.0 0.8 0.6 0.8

New York 36 Onondaga 067 1.7 1.4 1.3 1.1 1.1 0.9 1.1

New York 36 Queens 081 1.5 1.4 1.6 1.3 1.4 1.4 1.1

New York 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 Montgomery 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

Pennsylvania 42 Allegheny 003 2.3 2.3 1.8 1.5 1.4 1.2 1.4

B - 52
126County-- January 1st 1999 through December 31st, 2005

(Study area and time period for Bell et al., 2009 )

Pennsylvania 42 Berks 011 1.4 1.2 1.2 1.2 1.2 1.1 1.2

Pennsylvania 42 Dauphin 043 1.1 1.4 1.5 1.1 1.1 0.9 1.0

Pennsylvania 42 Erie 049 1.9 1.9 1.7 1.6 1.2 0.7 1.2

Pennsylvania 42 Lackawanna 069 0.8 1.2 1.2 1.0 0.8 1.0 1.1

Pennsylvania 42 Lancaster 071 1.3 1.3 1.5 1.3 1.0 0.9 0.9

Pennsylvania 42 Northampton 095 1.6 1.3 1.3 0.9 0.7 1.2 1.2

Pennsylvania 42 Philadelphia 101 4.0 1.8 1.9 1.6 1.9 1.6 1.6

Pennsylvania 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 Shelby 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 City 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

Maxperyear 9.3 6.4 11.0 5.2 4.2 3.7 5.0 11.0 Total Max

Minperyear 0.7 0.5 0.6 0.5 0.5 0.4 0.3 0.3 Total Min

B - 53
126County-- 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

Alabama 01 Jefferson 073 1.1 1.3 1.1 1.1 0.5 0.4 0.6

Arizona 04 Maricopa 013 2.7 1.8 1.5 1.9 1.2 0.9 0.8

Arizona 04 Pima 019 1.1 1.0 0.9 0.8 0.7 0.7 0.7

Arkansas 05 Pulaski 119 1.3 1.2 0.8 0.4 0.4 0.3 0.3

California 06 Alameda 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 Adams 001 0.6 0.5 0.5 0.4 0.4 0.5 0.5

Colorado 08 Denver 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 - 54
126County-- 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 Jersey 34 Middlesex 023 1.0 0.8 0.8 0.8 0.6 0.5 0.6

New Jersey 34 Morris 027 1.0 0.9 0.8 0.7 0.7 0.6 0.5

New Jersey 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 York 36 Albany 001 0.3 0.3 0.3 0.3 0.4 0.3 0.3

New York 36 Bronx 005 0.6 0.6 0.6 0.6 0.7 0.6 0.6

New York 36 Erie 029 0.5 0.5 0.4 0.4 0.4 0.3 0.3

New York 36 Kings 047 1.4 1.7 1.1 1.0 1.1 1.0 0.8

New York 36 Monroe 055 0.6 0.5 0.4 0.5 0.5 0.5 0.4

New York 36 New York 061 1.7 1.5 1.3 1.0 1.0 0.9 0.6

New York 36 Niagara 063 0.3 0.3 0.3 0.3 0.3 0.3 0.3

New York 36 Onondaga 067 0.4 0.5 0.4 0.4 0.6 0.4 0.4

New York 36 Queens 081 0.6 0.5 0.5 0.5 0.6 0.5 0.5

New York 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 Montgomery 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

Pennsylvania 42 Allegheny 003 0.9 0.9 0.7 0.3 0.4 0.4 0.4

B - 55
126County-- January 1st 1999 through December 31st, 2005

(Study area and time period for Bell et al., 2009 )

Pennsylvania 42 Berks 011 0.3 0.3 0.5 0.4 0.3 0.4 0.4

Pennsylvania 42 Dauphin 043 0.3 0.3 0.3 0.4 0.4 0.3 0.3

Pennsylvania 42 Erie 049 0.5 0.5 0.5 0.4 0.4 0.3 0.4

Pennsylvania 42 Lackawanna 069 0.3 0.3 0.4 0.3 0.3 0.3 0.3

Pennsylvania 42 Lancaster 071 0.3 0.3 0.3 0.4 0.3 0.3 0.3

Pennsylvania 42 Northampton 095 0.3 0.3 0.3 0.3 0.3 0.3 0.3

Pennsylvania 42 Philadelphia 101 1.0 0.8 0.8 0.7 0.8 0.7 0.7

Pennsylvania 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 Shelby 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 City 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

Maxperyear 2.7 1.8 1.6 1.9 1.4 1.3 1.2 2.7 Total Max

Minperyear 0.3 0.3 0.3 0.3 0.3 0.3 0.3 0.3 Total Min

B - 56
Appendix C 

Relationships (Ratios) Between 1-hour and 8-hour CO Concentration Metrics 

For Counties with CO Monitors (2007-2009) 

C-1
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 2nd maximum running 8-hour 

period and the 2nd maximum 1-hour value for the entire year, 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 statistic 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 highest and that all seasons of the year are well 

represented. Hence, in judging data completeness for derivation of these 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 here, the largest value is identified from two 

calculation procedures. Procedure 1 uses the proposed completeness requirements above and 

procedure 2 relaxes the daily requirement of having 75% of the hours in a day but still requires 

the quarterly and yearly completeness. 

Because of the differing completeness requirements, when comparing the alternative 

daily maximum metrics to the current running 8-hour and 1-hour metrics, different sites are 

complete for different metrics. To avoid having ratios 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 comparison tables and the 2nd 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 metrics were created by taking the maximum value 

among all the sites in the county. 

C-2
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 1.57

C-3
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)

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 1.32

C-4
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)

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 1.05

C-5
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)

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

max 14.20 8.20 4.21

C-6
2nd 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 1.78

C-7
2nd 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 1.58

C-8
2nd 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 1.33

C-9
2nd 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 1.08

C-10
2nd 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 5.59

C-11
2nd 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 1.21

C-12
2nd 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 1.07

C-13
2nd 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 0.98

C-14
2nd 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 0.82

C-15
2nd 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 0.50

C-16
2nd 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 4.92

C-17
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D-1

Appendix D 

Additional REA Estimates from Simulations for 

Alternative Levels and Forms for the 1-hour and 8-hour Standards. 

 
D-2

Table D-1. Percentage of simulated HD population with daily maximum end-of-hour COHb levels (absolu

indicated 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 < 2.5 % COHb < 2.0 % COHb < 1.75 % COHb < 1.5 % COH

Form 1-hour

(ppm) 

8-hour

(ppm) 

Los 

Angeles Denver

Los 

Angeles Denver

Los 

Angeles Denver 

Los 

Angeles Denver 

Los 

Angeles De

16.2+ 99.7 99.1 95.5 88.9 711.8+

9.4+

>99.9 >99.9 99.4 98.3 95.0 

11.2 99.8 98.9 96.8 9

9.7 98.0 99.3 

>99.9 99.9 99.4 98.4 9

8.2* 98.4 

8.1 99.5 98.5 7.2 99.7 99.0 6.8 

5.4–6.5 

100 100 > 99.9 

99.8 99.2 

Second Highest 

Non-overlapping 

Concentration 

(Current Form) 

4.6* 3.1* 100 100 >99.9 99.7 9

13.3+ 99.7 99.1 95.5 88.9 711.6+

7.2-8.2+

>99.9 >99.9 99.4 98.3 95.0 

9.2 >99.9 99.8 98.9 96.8 9

100 100 > 99.9 99.5 98.5 

8.0 

98.0 9

7.7 

>99.9 99.9 99.4 

 98.4 9

7.4* 99.5 98.4 

7.1 99.7 99.0 6.7 

4.1– 5.7 

100 100 >99.9 

99.8 99.2 

99th Percentile 

of Daily 

Maximum 

Concentrations 

4.5* 2.8* 100 100 >99.9 99.7 9

+ 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 conditions 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.
D-3

Table D-2. Percentage of simulated CHD population with maximum ambient contributions to end-of-hou

the indicated COHb levels under alternative levels and forms for the 1-hour and 8-hour stand

Current and 

Potential Alternative Standards Maximum Ambient Contribution to End-of-hour COHb Level 

Level < 2.0 % COHb < 1.8 % COHb < 1.6 % COHb < 1.4 % COHb 

Form 1-hour 

(ppm)

8-hour 

(ppm)

Los 

Angeles Denver 

Los 

Angeles Denver 

Los 

Angeles Denver 

Los 

Angeles Denver 

8-ho

Leve

(ppm

16.2+ 97.3 96.6 93.2 87.2 11.8+

9.4 

99.5 99.2 98.7 98.0 9.4 

11.2 99.8 99.1 97.3 96.3 6.5 

8.2* 100* 99.7* 99.5* 99.5* 5.6 

7.2 

5.6-6.5 

99.7 99.7 99.7 99.5 5.7 

Second 

Highest Nonoverlapping 

Concentration 

(Current Form) 

4.6* 3.1 100* 100* 99.8* 99.8* 3.1 

13.3+ 7.2 97.3 96.6 93.2 87.2 7.2 11.6+ 8.2 99.5 99.2 98.7 98.0 8.2 

9.2 99.8 99.1 97.3 96.3 5.0 

7.4* 100* 99.7* 99.5* 99.5* 5.1 

7.1 

5.0-5.1 

99.7 99.7 99.7 99.5 5.0 

99th Percentile 

of Daily 

Maximum 

Concentrations

4.5* 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 based on “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.
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E-1

Appendix E 

Predicted Percentage of Counties with a Monitor 

Not Likely to Meet Alternative Standards and Associated Percentage Population 
E-2

Data Analysis

Hourly data for CO were pulled from EPA’s Air Quality System in July 2010. Daily 1-

hour maximums were calculated from the hourly data. 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 statistic from that period to 

be considered valid. The key air quality statistics are the daily maximum 1-hour and 8-

hour concentrations in three successive years. The 75% requirement was applied at the 

daily and quarterly levels. Also, because CO has been shown to have 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 largest value from two 

calculation procedures is what was compared to the potential alternative standards. 

Procedure 1 uses the completeness requirements above and procedure 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 values in were calculated at each site, the 

county level design values were created by taking the maximum design value of all the 

sites in the county. The regions are the same as those used for similar analyses in recent 

NAAQS reviews (e.g., lead, particulate matter).
E-3

Appendix E. Predicted percentage of counties with a monitor not likely to meet alternative atandards (basdata) and associated percentage population. 

Total Counties (population in millions) Northeast Southeast

Industrial Midwest

Upper Midwest Southwest Northwest

Number of Counties with monitors  165 (115) 41 26 30 10 9 38 

Alternative Levels for a 

form of 99th percentile 

daily 1-hour maximum, 

averaged over 3 years 



15.0 0 0 0 0 0 0 0 14.0 .6 (.7) 0 4 0 0 0 0 13.0 .6 (.7) 0 4 0 0 0 0 12.0 1.2 (.9) 0 4 0 0 0 3 11.0 1.2 (.9) 0 4 0 0 0 3 10.0 1.2 (.9) 0 4 0 0 0 3 

9.0 1.2 (.9) 0 4 0 0 0 3 8.0 1.2 (.9) 0 4 0 0 0 3 7.0 2.4 (2.4) 0 4 3 0 11 3 6.0 2.4 (2.4) 0 4 3 0 11 3 5.0 4.8 (4.1) 0 4 3 0 22 8 

Number of Counties with monitors  187 (125) 48 31 35 11 9 40 

Alternative Levels for a 

form of 99th percentile 

daily 8-hour maximum, 

averaged over 3 years 



9.0 0 0 0 0 0 0 0 8.0 0 0 0 0 0 0 0 7.0 0.5 (.7) 0 3 0 0 0 0 6.0 0.5 (.7) 0 3 0 0 0 0 5.0 1.1 (.9) 0 3 0 0 0 0 4.0 2.7 (2.7) 0 3 3 0 11 3 3.0 4.8 (7.9) 0 3 3 0 44 3 

** "Outside Regions" includes Alaska, Hawaii, Puerto Rico, and the Virgin Islands.

Of counties with a monitor, the percentage not likely to meet stated alternative s

(population - percentage of population in counties with monitors)

Of counties with a monitor, the percentage not likely to meet stated alternative s

(population - percentage of population in counties with monitors)
United States 

Environmental Protection Agency 

Office of Air Quality Planning and Standards 

Health and Environmental Impacts Division 

Research Triangle Park, NC 

Publication No. EPA-452/R-10-007 

October 2010