8158 Federal Register / Vol. 76, No. 29 / Friday, February 11, 2011 / Proposed Rules 

ENVIRONMENTAL PROTECTION 

AGENCY 

40 CFR Parts 50, 53 and 58 

[EPA–HQ–OAR–2008–0015; FRL–9261–4; 

2060–AI43] 

National Ambient Air Quality 

Standards for Carbon Monoxide 

AGENCY: Environmental Protection 

Agency (EPA). 

ACTION: Proposed rule. 

SUMMARY: Based on its review of the air 

quality criteria and the national ambient 

air quality standards (NAAQS) for 

carbon monoxide (CO), EPA is 

proposing to retain the current 

standards. EPA is also proposing 

changes to the ambient air monitoring 

requirements for CO including those 

related to network design. 

DATES: Comments must be received on 

or before April 12, 2011. 

Public Hearings: If, by February 18, 

2011, EPA receives a request from a 

member of the public to speak at a 

public hearing concerning the proposed 

regulation, we will hold a public 

hearing on February 28, 2011 in 

Arlington, Virginia. 

ADDRESSES: Submit your comments, 

identified by Docket ID No. EPA–HQ– 

OAR–2008–0015 by one of the following 

methods: 

• http://www.regulations.gov: Follow 

the on-line instructions for submitting 

comments. 

• E-mail: a-and-r-Docket@epa.gov. 

• Fax: 202–566–9744. 

• Mail: Docket No. EPA–HQ–OAR– 

2008–0015, Environmental Protection 

Agency, Mail code 6102T, 1200 

Pennsylvania Ave., NW., Washington, 

DC 20460. Please include a total of two 

copies. 

• Hand Delivery: Docket No. EPA– 

HQ–OAR–2008–0015, Environmental 

Protection Agency, EPA West, Room 

3334, 1301 Constitution Ave., NW., 

Washington, DC. Such deliveries are 

only accepted during the Docket’s 

normal hours of operation, and special 

arrangements should be made for 

deliveries of boxed information. 

Instructions: Direct your comments to 

Docket ID No. EPA–HQ–OAR–2008– 

0015. EPA’s policy is that all comments 

received will be included in the public 

docket without change and may be 

made available online at http:// 

www.regulations.gov, including any 

personal information provided, unless 

the comment includes information 

claimed to be Confidential Business 

Information (CBI) or other information 

whose disclosure is restricted by statute. 

Do not submit information that you 

consider to be CBI or otherwise 

protected through http:// 

www.regulations.gov or e-mail. The 

http://www.regulations.gov Web site is 

an ‘‘anonymous access’’ system, which 

means EPA will not know your identity 

or contact information unless you 

provide it in the body of your comment. 

If you send an e-mail comment directly 

to EPA without going through 

www.regulations.gov your e-mail 

address will be automatically captured 

and included as part of the comment 

that is placed in the public docket and 

made available on the Internet. If you 

submit an electronic comment, EPA 

recommends that you include your 

name and other contact information in 

the body of your comment and with any 

disk or CD–ROM you submit. If EPA 

cannot read your comment due to 

technical difficulties and cannot contact 

you for clarification, EPA may not be 

able to consider your comment. 

Electronic files should avoid the use of 

special characters, any form of 

encryption, and be free of any defects or 

viruses. For additional information 

about EPA’s public docket visit the EPA 

Docket Center homepage at http:// 

www.epa.gov/epahome/dockets.htm. 

Public Hearing. If a public hearing is 

held, it will be held at the U.S. 

Environmental Protection Agency 

Conference Center, First Floor 

Conference Center South, One Potomac 

Yard, 2777 S. Crystal Drive, Arlington, 

VA 22202. All visitors will need to go 

through security and present a valid 

photo identification, such as a driver’s 

license. To request a public hearing or 

information pertaining to a public 

hearing, contact Ms. Jan King, Health 

and Environmental Impacts Division, 

Office of Air Quality Planning and 

Standards (C504–02), Environmental 

Protection Agency, Research Triangle 

Park, North Carolina 27711; telephone 

number (919) 541– 5665; fax number 

(919) 541–2664; e-mail address: 

king.jan@epa.gov. See the 

SUPPLEMENTARY INFORMATION for further 

information about a possible public 

hearing. 

Docket: All documents in the docket 

are listed in the http:// 

www.regulations.gov index. Although 

listed in the index, some information is 

not publicly available, e.g., CBI or other 

information whose disclosure is 

restricted by statute. Certain other 

material, such as copyrighted material, 

will be publicly available only in hard 

copy. Publicly available docket 

materials are available either 

electronically in http:// 

www.regulations.gov or in hard copy at 

the Air and Radiation Docket and 

Information Center, EPA/DC, EPA West, 

Room 3334, 1301 Constitution Ave., 

NW., Washington, DC. The Public 

Reading Room is open from 8:30 a.m. to 

4:30 p.m., Monday through Friday, 

excluding legal holidays. The telephone 

number for the Public Reading Room is 

(202) 566–1744 and the telephone 

number for the Air and Radiation 

Docket and Information Center is (202) 

566–1742. 

FOR FURTHER INFORMATION CONTACT: Dr. 

Deirdre Murphy, Health and 

Environmental Impacts Division, Office 

of Air Quality Planning and Standards, 

U.S. Environmental Protection Agency, 

Mail code C504–06, Research Triangle 

Park, NC 27711; telephone: 919–541– 

0729; fax: 919–541–0237; e-mail: 

murphy.deirdre@epa.gov. For further 

information specifically with regard to 

section IV of this notice, contact Mr. 

Nealson Watkins, Air Quality Analysis 

Division, Office of Air Quality Planning 

and Standards, U.S. Environmental 

Protection Agency, Mail code C304–06, 

Research Triangle Park, NC 27711; 

telephone: 919–541–5522; fax: 919– 

541–1903; e-mail: 

watkins.nealson@epa.gov. To request a 

public hearing or information pertaining 

to a public hearing, contact Ms. Jan 

King, Health and Environmental 

Impacts Division, Office of Air Quality 

Planning and Standards (C504–02), 

Environmental Protection Agency, 

Research Triangle Park, North Carolina 

27711; telephone number (919) 541– 

5665; fax number (919) 541–2664; email address: king.jan@epa.gov. 

SUPPLEMENTARY INFORMATION: 

General Information 

What should I consider as I prepare my 

comments for EPA? 

1. Submitting CBI. Do not submit this 

information to EPA through http:// 

www.regulations.gov or e-mail. Clearly 

mark the part or all of the information 

that you claim to be CBI. For CBI 

information in a disk or CD ROM that 

you mail to EPA, mark the outside of the 

disk or CD ROM as CBI and then 

identify electronically within the disk or 

CD ROM the specific information that is 

claimed as CBI. In addition to one 

complete version of the comment that 

includes information claimed as CBI, a 

copy of the comment that does not 

contain the information claimed as CBI 

must be submitted for inclusion in the 

public docket. Information so marked 

will not be disclosed except in 

accordance with procedures set forth in 

40 CFR part 2. 

2. Tips for Preparing Your Comments. 

When submitting comments, remember 

to: 


jlentini on DSKJ8SOYB1PROD with PROPOSALS4
Federal Register / Vol. 76, No. 29 / Friday, February 11, 2011 / Proposed Rules 8159 

1The legislative history of section 109 indicates 

that a primary standard is to be set at ‘‘the 

maximum permissible ambient air level * * * 

which will protect the health of any [sensitive] 

group of the population,’’ and that for this purpose 

‘‘reference should be made to a representative 

sample of persons comprising the sensitive group 

rather than to a single person in such a group’’ [S. 

Rep. No. 91–1196, 91st Cong., 2d Sess. 10 (1970)]. 

• Identify the rulemaking by docket 

number and other identifying 

information (subject heading, Federal 

Register date and page number). 

• Follow directions—the agency may 

ask you to respond to specific questions 

or organize comments by referencing a 

Code of Federal Regulations (CFR) part 

or section number. 

• Explain why you agree or disagree, 

suggest alternatives, and substitute 

language for your requested changes. 

• Describe any assumptions and 

provide any technical information and/ 

or data that you used. 

• Provide specific examples to 

illustrate your concerns, and suggest 

alternatives. 

• Explain your views as clearly as 

possible, avoiding the use of profanity 

or personal threats. 

• Make sure to submit your 

comments by the comment period 

deadline identified. 

Availability of Related Information 

A number of the documents that are 

relevant to this rulemaking are available 

through EPA’s Office of Air Quality 

Planning and Standards (OAQPS) 

Technology Transfer Network (TTN) 

Web site at http://www.epa.gov/ttn/ 

naaqs/standards/co/s_co_index.html. 

These documents include the Plan for 

Review of the National Ambient Air 

Quality Standards for Carbon Monoxide 

(Integrated Review Plan or IRP, USEPA, 

2008), available at http://www.epa.gov/ 

ttn/naaqs/standards/co/ 

s_co_cr_pd.html, the Integrated Science 

Assessment for Carbon Monoxide 

(USEPA, 2010a), available at http:// 

www.epa.gov/ttn/naaqs/standards/co/ 

s_co_cr_isa.html, the Quantitative Risk 

and Exposure Assessment for Carbon 

Monoxide—Amended (USEPA, 2010b), 

available at http://www.epa.gov/ttn/ 

naaqs/standards/co/s_co_cr_rea.html, 

and the Policy Assessment for the 

Review of the Carbon Monoxide 

National Ambient Air Quality 

Standards (USEPA, 2010c), available at 

http://www.epa.gov/ttn/naaqs/ 

standards/co/s_co_cr_pa.html. These 

and other related documents are also 

available for inspection and copying in 

the EPA docket identified above. 

How can I find information about a 

possible public hearing? 

To request a public hearing or 

information pertaining to a public 

hearing on this document, contact Ms. 

Jan King, Health and Environmental 

Impacts Division, Office of Air Quality 

Planning and Standards (C504–02), 

Environmental Protection Agency, 

Research Triangle Park, North Carolina 

27711; telephone number (919) 541– 

5665; fax number (919) 541–2664; email address: king.jan@epa.gov. If a 

request for a public hearing is received 

by February 18, 2011, information about 

the hearing will be posted prior to the 

hearing on EPA’s Web site for carbon 

monoxide regulatory actions at http:// 

www.epa.gov/airquality/urbanair/co/. 

Table of Contents 

The following topics are discussed in this 

preamble: 

I. Background 

A. Legislative Requirements 

B. Related Carbon Monoxide Control 

Programs 

C. Review of the Air Quality Criteria and 

Standards for Carbon Monoxide 

II. Rationale for Proposed Decisions on the 

Primary Standards 

A. Air Quality Information 

1. Anthropogenic Sources and Emissions of 

Carbon Monoxide 

2. Ambient Concentrations 

B. Health Effects Information 

1. Carboxyhemoglobin as Biomarker and 

Mechanism of Toxicity 

2. Nature of Effects 

3. At-Risk Populations 

4. Potential Impacts on Public Health 

C. Human Exposure and Dose Assessment 

1. Summary of Design Aspects 

2. Key Limitations and Uncertainties 

D. Conclusions on Adequacy of the Current 

Standards 

1. Approach 

2. Evidence-Based and Exposure/DoseBased Considerations in the Policy 

Assessment 

3. CASAC Advice 

4. Administrator’s Proposed Conclusions 

Concerning Adequacy 

E. Summary of Proposed Decisions on 

Primary Standards 

III. Consideration of a Secondary Standard 

A. Background and Considerations in 

Previous Reviews 

B. Evidence-Based Considerations in the 

Policy Assessment 

C. CASAC Advice 

D. Administrator’s Proposed Conclusions 

Concerning a Secondary Standard 

IV. Proposed Amendments to Ambient 

Monitoring Requirements 

A. Monitoring Methods 

1. Proposed Changes to Part 50, Appendix 

C 

2. Proposed Changes to Part 53 

3. Implications for Air Monitoring 

Networks 

B. Network Design 

1. Background 

2. On-Road Mobile Sources 

3. Near-Road Environment 

4. Urban Downtown Areas and Urban 

Street Canyons 

5. Meteorological and Topographical 

Influences 

6. Proposed Changes 

7. Microscale Carbon Monoxide Monitor 

Siting Criteria 

V. Statutory and Executive Order Reviews 

A. Executive Order 12866: Regulatory 

Planning and Review 

B. Paperwork Reduction Act 

C. Regulatory Flexibility Act 

D. Unfunded Mandates Reform Act 

E. Executive Order 13132: Federalism 

F. Executive Order 13175: Consultation 

and Coordination with Indian Tribal 

Governments 

G. Executive Order 13045: Protection of 

Children from Environmental Health and 

Safety Risks 

H. Executive Order 13211: Actions that 

Significantly Affect Energy Supply, 

Distribution or Use 

I. National Technology Transfer and 

Advancement Act 

J. Executive Order 12898: Federal Actions 

to Address Environmental Justice in 

Minority Populations and Low-Income 

Populations References 

I. Background 

A. Legislative Requirements 

Two sections of the Clean Air Act 

(CAA) govern the establishment and 

revision of the NAAQS. Section 108 (42 

U.S.C. 7408) directs the Administrator 

to identify and list ‘‘air pollutant[s]’’ that 

in her ‘‘judgment, cause or contribute to 

air pollution which may reasonably be 

anticipated to endanger public health or 

welfare’’ and satisfy two other criteria, 

including ‘‘whose presence * * * in the 

ambient air results from numerous or 

diverse mobile or stationary sources’’ 

and to issue air quality criteria for those 

that are listed. Air quality criteria are 

intended to ‘‘accurately reflect the latest 

scientific knowledge useful in 

indicating the kind and extent of all 

identifiable effects on public health or 

welfare which may be expected from the 

presence of [a] pollutant in the ambient 

air * * * .’’ 

Section 109 (42 U.S.C. 7409) directs 

the Administrator to propose and 

promulgate ‘‘primary’’ and ‘‘secondary’’ 

NAAQS for pollutants for which air 

quality criteria are issued. 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.’’ 1 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 


jlentini on DSKJ8SOYB1PROD with PROPOSALS4
8160 Federal Register / Vol. 76, No. 29 / Friday, February 11, 2011 / Proposed Rules 

2Welfare effects as defined in section 302(h) (42 

U.S.C. 7602(h)) include, but are not limited to, 

‘‘effects on soils, water, crops, vegetation, man-made 

materials, animals, wildlife, weather, visibility, and 

climate, damage to and deterioration of property, 

and hazards to transportation, as well as effects on 

economic values and on personal comfort and wellbeing.’’ 

associated with the presence of such air 

pollutant in the ambient air.’’ 2

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 

(DC Cir 1980), cert. denied, 449 U.S. 

1042 (1980); American Petroleum 

Institute v. Costle, 665 F.2d 1176, 1186 

(DC 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 demonstrated to be 

harmful but also to prevent lower 

pollution levels that may pose an 

unacceptable risk of harm, even if the 

risk is not precisely identified as to 

nature or degree. The CAA does not 

require the Administrator to establish a 

primary NAAQS at a zero-risk level or 

at background concentration levels, see 

Lead Industries Association v. EPA, 647 

F.2d at 1156 n. 51, but rather at a level 

that reduces risk sufficiently so as to 

protect public health with an adequate 

margin of safety. 

In addressing the requirement for an 

adequate margin of safety, EPA 

considers such factors as the nature and 

severity of the health effects involved, 

the size of the 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, 647 F.2d 

at 1161–62; Whitman v. American 

Trucking Associations, 531 U.S. 457, 

495 (2001). 

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. Whitman 

v. American Trucking Associations, 531 

U.S. 457, 473. In establishing ‘‘requisite’’ 

primary and secondary standards, EPA 

may not consider the costs of 

implementing the standards. Id. at 471. 

Section 109(d)(1) of the CAA requires 

that ‘‘[n]ot 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. * * *’’ This independent 

review function is performed by the 

Clean Air Scientific Advisory 

Committee (CASAC). 

B. Related Carbon Monoxide Control 

Programs 

States are primarily responsible for 

ensuring attainment and maintenance of 

ambient air quality standards once EPA 

has established them. Under section 110 

of the Act, and related provisions, States 

are to submit, for EPA approval, State 

implementation plans (SIPs) that 

provide for the attainment and 

maintenance of such standards through 

control programs directed to sources of 

the pollutants involved. The States, in 

conjunction with EPA, also administer 

the prevention of significant 

deterioration program. See CAA 

sections 160–169. In addition, Federal 

programs provide for nationwide 

reductions in emissions of these and 

other air pollutants through the Federal 

motor vehicle and motor vehicle fuel 

control program under title II of the Act, 

(CAA sections 202–250) which involves 

controls for emissions from moving 

sources and controls for the fuels used 

by these sources; new source 

performance standards under section 

111; and title IV of the Act (CAA 

sections 402–416), which specifically 

provides for major reductions in CO 

emissions. 

C. Review of the Air Quality Criteria and 

Standards for Carbon Monoxide 

EPA initially established NAAQS for 

CO 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 the requisite protection 

of public health with an adequate 

margin of safety and would also provide 

requisite protection 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 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 (Lippmann, 1984), 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). 

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 the final 2000 AQCD (U.S. 

EPA, 2000) was released in August 

2000. After release of the AQCD, 

Congress requested that the National 

Research Council (NRC) review the 


jlentini on DSKJ8SOYB1PROD with PROPOSALS4
Federal Register / Vol. 76, No. 29 / Friday, February 11, 2011 / Proposed Rules 8161 

3As explained below in section IV.A, EPA is 

proposing to repromulgate the Federal reference 

method for CO, as set forth in Appendix C of 40 

CFR part 50. Consistent with EPA’s proposed 

decision to retain the standards, the recodification 

clarifies and updates the text of the FRM, but does 

not make substantive changes to it. 

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. Following 

completion of the NRC report, EPA did 

not conduct rulemaking to complete the 

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 

Integrated Review Plan (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 Integrated Science 

Assessment for Carbon Monoxide (ISA 

or Integrated Science Assessment), EPA 

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 Risk and Exposure 

Assessment (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, 2010d) 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, EPA released a draft 

Policy Assessment (PA) (USEPA, 2010e) 

in early March, 2010 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). Staff 

additionally took into consideration 

those comments and the final REA 

analyses in completing the final Policy 

Assessment (USEPA, 2010c) which was 

released in October, 2010. 

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), to 

complete a review of the CO NAAQS 

within the period provided by statute. 

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. 

This action presents the 

Administrator’s proposed decisions on 

the current CO standards. Throughout 

this preamble a number of conclusions, 

findings, and determinations proposed 

by the Administrator are noted. 

Although they identify the reasoning 

that supports this proposal, they are not 

intended to be final or conclusive in 

nature. The EPA invites general, 

specific, and technical comments on all 

issues involved with this proposal, 

including all such proposed judgments, 

conclusions, findings, and 

determinations. 

II. Rationale for Proposed Decisions on 

the Primary Standards 

This section presents the rationale for 

the Administrator’s proposed decision 

to retain the existing CO primary 

standards.3 As discussed more fully 

below, this rationale is based on a 

thorough review, in the Integrated 

Science Assessment, of the latest 

scientific information, published 

through mid-2009, on human health 

effects associated with the presence of 

CO in the ambient air. This proposal 

also takes into account: (1) Staff 

assessments of the most policy-relevant 

information in the ISA and staff 

analyses of air quality, human exposure 

and health risks presented in the REA 

and the Policy Assessment, upon which 

staff conclusions regarding appropriate 

considerations in this review are based; 

(2) CASAC advice and 

recommendations, as reflected in 

discussions of drafts of the ISA, REA 

and PA at public meetings, in separate 

written comments, and in CASAC’s 

letters to the Administrator; and (3) 

public comments received during the 

development of these documents, either 

in connection with CASAC meetings or 

separately. 

In presenting the rationale and its 

foundations, this section begins with a 

summary of current air quality 

information in section II.A. Section II.B 

summarizes the body of evidence 

supporting this rationale, including key 

health endpoints associated with 

exposure to ambient CO. This rationale 

also draws upon the results of the 

quantitative exposure and risk 

assessments, discussed below in section 

II.C. Evidence- and exposure/dose-based 

considerations that form the basis for 

the Administrator’s proposed decisions 

on the adequacy of the current standard 

are discussed in section II.D.2.a and 

II.D.2.b, respectively. CASAC advice is 

summarized in section II.D.3. The 

Administrator’s proposed conclusions 

are presented in section II.D.4. 

A. Air Quality Information 

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 summarized in 

the Policy Assessment, and a more 

detailed discussion of aspects 

particularly relevant to the exposure 

assessment is provided in the REA 

(REA, chapter 3). 


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4EPA compiles CO emissions estimates for the 

U.S. in the National Emissions Inventory (NEI). 

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). At the time of the ISA 

development, the 2002 NEI was providing the most 

recent publicly available CO emissions estimates for 

the U.S. that meet EPA’s data quality assurance 

objectives. Such estimates are now available from 

the 2005 NEI. 

5The emissions trends information in this 

statement is 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 2002. 

6The 2002 National Emissions Inventory estimate 

for on-road emissions in Garfield County 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). In 

contrast, the 2002 Denver County on-road emissions 

account for 74% of the total for the county which 

is estimated at approximately 180,000 tons. 

7http://www.epa.gov/ttn/airs/airsaqs/. 

8The air quality status in areas monitored relative 

to the CO NAAQS is provided at http:// 

www.epa.gov/air/airtrends/values.html. 

9As the form of the CO 8-hour standard is notto-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. Additional information is 

available at http://www.epa.gov/airtrends/ 

values.html. 

1. Anthropogenic Sources and 

Emissions of Carbon Monoxide 

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).4 Nationalscale anthropogenic CO emissions have 

decreased by approximately 45% 

between 1990 and 2005, with nearly all 

of this national-scale reduction coming 

from reductions in on-road vehicle 

emissions (ISA, Figure 3–2; PA, Figure 

1–1; 2005 NEI 5). 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 some metropolitan areas 

of the U.S., due to their greater motor 

vehicle density relative to rural areas, 

on-road mobile source contribution to 

all ambient CO emissions was estimated 

to be as high as approximately 75%, 

based on the 2002 National Emissions 

Inventory (ISA, p. 3–2). However, the 

mobile source contribution can vary 

widely in specific areas. As an example, 

2002 NEI estimates of on-road mobile 

source emissions in urban Denver 

County, Colorado are about 74% of total 

CO emissions and emissions from all 

mobile sources (on-road and non-road 

combined) are estimated to contribute 

about 98% (ISA, section 3.2.1). In 

contrast, 2002 NEI estimates of on-road 

CO emissions were just 20% of the total 

for rural Garfield County, Colorado6

(ISA, chapter 3, Figure 3–6). 

2. Ambient Concentrations 

As described in section II.A.1 above, 

mobile source emissions are major 

contributors to CO emissions in urban 

areas, with corresponding influence on 

ambient CO concentrations and 

associated concentration gradients, with 

highest ambient concentrations 

occurring on or nearest roadways, 

particularly highly travelled roadways, 

and lowest concentrations in more 

distant locations (ISA, section 3.5.1.3; 

REA, section 3.1.3). For example, as 

described in the ISA CO concentrations 

measured within 20 meters of an 

interstate highway can range from 2 to 

10 times greater than CO concentrations 

measured as far as 300 meters from a 

major road, possibly influenced by wind 

direction and on-road vehicle density 

(ISA, section 3.5.1.3, Figures 3–29 and 

3–30; Zhu et al., 2002; Baldauf et al., 

2008a,b). Additionally, the role of motor 

vehicles in influencing ambient 

concentrations contributes to the 

occurrence of diurnal variation in 

concentrations reflecting rush hour 

patterns (ISA, 3.5.2.2; REA, p. 3–8). The 

influence of motor vehicle emissions on 

ambient concentrations contributes to 

the important role of in-vehicle 

microenvironments in influencing 

short-term ambient CO exposures, as 

described in more detail in the REA and 

summarized in sections II.C.1 and II.D.2 

below. 

In 2009, approximately 350 ambient 

monitoring stations across the U.S. 

reported continuous hourly averages of 

CO concentrations to EPA’s Air Quality 

System.7 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.8 As of September 27, 2010, 

there are no areas designated as 

nonattainment for the CO NAAQS (75 

FR 59090). Since 2005, one area 

(Jefferson County, Alabama) has failed 

to meet the 8-hour standard during 

some periods. Large CO emissions 

sources in this area are associated with 

an integrated iron and steel facility. As 

described in section 1.3.3 of the Policy 

Assessment, 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.9 Of the 

counties with monitoring sites in 2009, 

sites in 3 counties reported second 

maximum 8-hour average 

concentrations at or above 6.4 ppm (PA, 

Figure 1–2). 

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. 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% (PA, section 

1.3.3). 

B. Health Effects Information 

1. Carboxyhemoglobin as Biomarker and 

Mechanism of Toxicity 

As discussed in the Integrated Science 

Assessment, in this review, as in the 

past (e.g., USEPA, 2000; USEPA, 1991), 

the best characterized mechanism of 

action of CO is tissue hypoxia caused by 

binding of CO to hemoglobin to form 

carboxyhemoglobin (COHb). 

Accordingly, COHb level in blood 

continues to be well recognized as an 

important internal dose metric and the 

one most commonly used in evaluating 

CO exposure and the potential for 

health effects (ISA, p. 2–4, sections 4.1, 

4.2, 5.1.1; 1991 AQCD, 2000 AQCD, 

2010 ISA). 

Increasing levels of COHb with 

subsequent decrease in oxygen 

availability for organs and tissues are of 


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10A significant source of nonambient CO long 

recognized as contributing to elevated COHb levels 

is tobacco smoking (e.g., ISA, Figure 4–12). Further, 

baseline COHb levels in active smokers have been 

estimated to range from 3 to 8% for one- to twopack-per-day smokers. As a result of their higher 

baseline COHb levels, smokers may exhale more CO 

into the air than they inhale from the ambient 

environment when not smoking. Tobacco smoking 

can also contribute to increased CO exposures and 

associated COHb levels in nonsmokers (2000 

AQCD, p. 7–4). 11As has been recognized in previous CO NAAQS 

reviews, such sources cannot be effectively 

mitigated by setting more stringent ambient air 

quality standards (59 FR 38914). 

concern in people with pre-existing 

heart disease who have compromised 

compensatory mechanisms (e.g., lack of 

capacity to increase blood flow in 

response to increased CO). The 

integrative review of health effects of 

CO indicates that ‘‘the clearest evidence 

indicates that individuals with 

[coronary artery disease] are most 

susceptible to an increase in COinduced health effects’’ (ISA, section 

5.7.8) and the evidence continues to 

support levels of COHb in the blood as 

the most useful indicator of CO 

exposure that is related to the health 

effects of CO of major concern. 

Carboxyhemoglobin occurs in the 

blood due to endogenous CO production 

from biochemical reactions associated 

with normal breakdown of heme 

proteins, as well as in response to 

inhaled (exogenous) CO exposures (ISA, 

section 4.5). The production of 

endogenous CO and levels of 

endogenous COHb vary with several 

physiological characteristics (e.g., 

slower COHb elimination with 

increasing age), as well as some disease 

states, which can lead to higher 

endogenous levels in some individuals 

(ISA, section 4.5). The amount of COHb 

formed in response to exogenous CO is 

dependent on the CO concentration and 

duration of exposure, exercise (which 

increases the amount of air removed and 

replaced per unit of time for gas 

exchange), the pulmonary diffusing 

capacity for CO, ambient pressure, 

health status, and the specific 

metabolism of the exposed individual 

(ISA, chapter 4; 2000 AQCD, chapter 5). 

The formation of COHb is a reversible 

process, but the high affinity of CO for 

hemoglobin, which affects the 

elimination half-time for COHb, can 

lead to increased COHb levels in some 

circumstances. 

As discussed in the REA, exposure to 

CO in ambient air can occur outdoors as 

well as through infiltration of ambient 

air into indoor locations (REA, section 

2.3). Additionally, indoor sources such 

as gas stoves and tobacco smoke can, 

where present, be important 

contributors to total CO exposure and 

can result in much greater CO exposures 

and associated COHb levels than those 

associated with ambient sources (ISA, 

section 3.6.5.2).10 For example, indoor 

source-related exposures, such as faulty 

furnaces or other combustion 

appliances, have been estimated in the 

past to lead to COHb levels on the order 

of twice as high as those short-term 

exposures to ambient CO considered 

more likely to be encountered by the 

general public (2000 AQCD, p. 7–4). 

Further, some assessments performed 

for previous reviews have included 

modeling simulations both without and 

with indoor sources (gas stoves and 

tobacco smoke) to provide context for 

the assessment of ambient CO exposure 

and dose (e.g., U.S. EPA, 1992; Johnson 

et al., 2000), and these assessments have 

found that nonambient sources have a 

substantially greater impact on the 

highest total exposures experienced by 

the simulated population than do 

ambient sources (Johnson et al., 2000; 

REA, sections 1.2 and 6.3).11. However, 

the focus of this REA, conducted to 

inform the current review of the CO 

NAAQS, is on sources of ambient CO. 

While recognizing this information 

regarding the potential for indoor 

sources, where present, to play a role in 

CO exposures and COHb levels, the 

exposure modeling in the current 

review (described in section II.C below) 

did not include indoor CO sources in 

order to focus on the impact of ambient 

CO sources on population COHb levels. 

Apart from the impaired oxygen 

delivery to tissues related to COHb 

formation, the evidence also indicates 

alternative mechanisms of CO-induced 

effects independent of limited oxygen 

availability (2000 AQCD, section 5.9; 

ISA, section 5.1.3). These mechanisms 

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 5.6) 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 reductionoxidation status (ISA, section 5.1.3.2). 

The ISA notes that these mechanisms 

may be interrelated. The evidence for 

these alternative mechanisms and the 

role they may play in CO-induced 

health effects at concentrations relevant 

to the current NAAQS is not clear. 

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). However, as noted 

in the Policy Assessment, 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 CO-induced effects in 

susceptible populations. Thus, the 

evidence indicates that COHb continues 

to be the most useful and wellsupported indicator of CO exposures 

and the best biomarker to characterize 

the potential for health effects 

associated with exposures to ambient 

CO at this time (PA, section 2.2.1). 

2. Nature of Effects 

As observed in the Policy Assessment, 

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 (PA, 

section 2.2.1). 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 hemoglobin, forming 

COHb. Accordingly, inhaled CO elicits 

various health effects through binding 

to, and associated alteration of the 

function of, a number of hemecontaining molecules, mainly 

hemoglobin (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 


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12For example, 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). 

13Relevant CO exposures are defined in the ISA 

as ‘‘generally within one or two orders of magnitude 

of ambient CO concentrations’’ (ISA, section 2.5). 

14Coronary 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). 

15Statistical 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. 

16Other controlled human exposure studies of 

CAD patients (listed in Table 2–2 of the PA, 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. 

17These levels and other COHb levels described 

for this study below are based on GC analysis 

unless otherwise specified. Matched measurements 

available for CO-oximetry (CO–Ox) and gas 

chromatography (GC) in this study indicate CO–Ox 

measurements of 2.65% (post-exercise mean) and 

3.21% (post-exposure mean) corresponding to the 

GC measurement levels of 2.00% (post-exercise 

mean) to 2.38% (post-exposure mean) for the lower 

exposure level assessed in this study (Allred et al., 

1991). 

18The 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). 

19As 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). COoximetry 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). 

20While 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 2.4–2.0% and 4.7–3.9%), 

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 GC-measured mean of 2.0% or 2.0–2.4% for the 

function and limiting exercise capacity 

(2000 AQCD, section 7.1).12

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. Most notably, 

the current evidence includes much 

expanded epidemiological evidence that 

is consistent with previous conclusions 

regarding cardiovascular disease-related 

susceptibility (ISA, section 5.7; 2000 

AQCD, section 7.7). In this review, the 

clearest evidence for ambient CO-related 

effects is available for cardiovascular 

effects. Using an established framework 

to characterize the evidence as to 

likelihood of causal relationships 

between exposure to ambient CO and 

specific health effects (ISA, chapter 1) 

the ISA states that ‘‘Given the consistent 

and 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 relevant 13 shortterm 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 longterm exposure, respiratory morbidity 

following short-term exposure, and 

mortality following short-term exposure 

(ISA, section 2.5, Table 2–1). 

Similar to the previous review, results 

from controlled human exposure studies 

of individuals with coronary artery 

disease (CAD) 14 (Adams et al., 1988; 

Allred et al., 1989a, 1989b, 1991; 

Anderson et al., 1973; Kleinman et al., 

1989, 1998; Sheps et al., 1987 15) are the 

‘‘most compelling evidence of COinduced 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 short-term CO 

exposures 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). 

Among the controlled human 

exposure studies, the ISA places 

principal emphasis on the study of CAD 

patients by Allred et al. (1989a, 1989b, 

1991) 16 (which was also considered in 

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% COHb 17 following 

experimental CO exposure), with no 

evidence of a threshold; (3) objective 

measures of myocardial ischemia (STsegment depression) 18 were assessed, as 

well as the subjective measure of 

decreased time to induction of angina; 

(4) measurements were taken both by 

CO-oximetry (CO–Ox) and by gas 

chromatography (GC), which provides a 

more accurate measurement of COHb 

blood levels 19; (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 exerciseinduced 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 (approximately 

1-hour) 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%.20


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COHb levels resulting from the lower experimental 

CO exposure. 21Another 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. 

22Of the studies for which risk estimates 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. 

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% (postexercise), 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% (p=0.027) 

and 7.1% (p=0.002), respectively, for 

the two experimental CO exposures 

(Allred et al., 1989a, 1989b, 1991).21 As 

at the time of the last review, while STsegment 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 controlled human exposure 

studies have been specifically designed 

to evaluate the effect of controlled shortterm 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 multilaboratory study was the dose-response 

relationship 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 

ischemia-related effects resulting from 

elevated CO exposures (ISA, section 

2.5.1; ISA, Figure 2–1). 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 for which positive 

associations of these metrics were 

reported with IHD, MI and CVD 

outcomes 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 

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 

proposed mechanism and biological 

plausibility of these CVD outcomes’’ 

(ISA, p. 5–40).22

Additionally, there are U.S. studies 

reporting associations with hospital 

admissions for CHF, a condition that 

affects an individual’s ability to 

compensate for reduced oxygen 

availability. These include one in 

southern California which reported a 

significant association for ambient CO 

with hospital admissions for CHF (Linn 

et al., 2000), as well as studies in 

Allegheny County (Pittsburgh) for 

1987–1999 study period (Wellenius et 

al., 2005), and Denver for the months of 

July-August during 1993–1997 (Koken 

et al., 2003; ISA, pp. 5–31 to 5–33). Risk 

estimates 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 concentration 

three days prior to health outcome (PA, 

Table 2–1). 

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). 

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). 

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). 

As discussed in detail in the ISA, 

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 


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23The 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). 

(ISA, section 5.2.1.8). Other 

epidemiological studies (including field 

and 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. Evidence for 

these effects includes the following. 

• 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,23

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 short-term 

exposure to CO and respiratory-related 

outcomes. Only preliminary evidence is 

available, however, regarding a 

mechanism that could provide 

plausibility for 

CO-induced 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 

conclusions from the previous review, 

the current evidence provides continued 

support and some additional strength to 

the 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. 

3. At-Risk Populations 

In identifying population groups or 

life stages at greatest risk for health risk 

from a specific pollutant, the terms 

susceptibility, vulnerability, sensitivity, 

and at-risk are commonly employed. 

The definition for these terms 

sometimes varies, but in most instances 

‘‘susceptibility’’ refers to biological or 

intrinsic factors (e.g., lifestage, gender) 

while ‘‘vulnerability’’ refers to 

nonbiological or extrinsic factors (e.g., 

visiting a high-altitude location, 

medication use). Additionally, in some 

cases, the terms ‘‘at-risk’’ and sensitive 

have been used to encompass both of 

these concepts. At times, however, 

factors of ‘‘susceptibility’’ and 

‘‘vulnerability’’ are intertwined and are 

difficult to distinguish. In the ISA for 

this review, the term susceptibility has 

been used broadly to recognize 

populations that have a greater 

likelihood of experiencing effects 

related to ambient CO exposure, such 

that use of the term susceptible 

populations in the ISA is defined as 

follows (ISA, section 5.7, p. 5–115): 

Populations that have a greater likelihood 

of experiencing health effects related to 

exposure to an air pollutant (e.g., CO) due to 

a variety of factors including, but not limited 

to: genetic or developmental factors, race, 

gender, lifestage, lifestyle (e.g., smoking 

status and nutrition) or preexisting disease, 

as well as population-level factors that can 

increase an individual’s exposure to an air 

pollutant (e.g., CO) such as socioeconomic 

status [SES], which encompasses reduced 

access to health care, low educational 

attainment, residential location, and other 

factors 

Thus, susceptible populations are at 

greater risk of CO effects and are also 

referred to as at-risk in the 

corresponding discussion in the REA 

and Policy Assessment and the 

summary below. 

The current evidence, while much 

expanded in a number of ways, 

continues to support the conclusions 

from the previous review regarding 

susceptible populations for exposure to 

ambient CO. In the AQCD for the review 

completed in 1994 and in the 2000 

AQCD, the evidence best supported the 

identification of patients with CAD as a 

population at increased risk from 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). 

As summarized in the Policy 

Assessment, based on the evidence from 

controlled human exposure studies also 

considered in the last review, and the 


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24The 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). 

25As 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 CO-induced health effects’’ (ISA, p. 2– 

12). 

now much-expanded epidemiological 

evidence base which is coherent with 

the evidence from these studies, the 

population with pre-existing 

cardiovascular disease associated with 

limitation in oxygen availability 

continues to be the best characterized 

population at risk of adverse COinduced 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 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).24 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 Integrated Science Assessment 

for 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 were 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 

at-risk 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, 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 including: Those with other preexisting 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; those who spend a 

substantial time on or near heavily 

traveled roadways; visitors to highaltitude locations; and people ingesting 

medications and other substances that 

enhance endogenous or metabolic CO 

formation (ISA, section 2.6.1). In 

recognizing the potential susceptibility 

of these populations, the Policy 

Assessment also noted 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 (PA, section 2.2.1). 

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 COinduced health effects (ISA, sections 

5.7.1.1 and 5.7.8).25 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 cause 

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. 

4. Potential Impacts on Public Health 

In light of the evidence described 

above with regard to factors contributing 

to greater susceptibility to health effects 

of ambient CO, this section, drawing 

from the Integrated Science Assessment 

and discussion in the Policy 

Assessment, discusses the health 

significance of the effects occurring with 

the lowest relevant (short-term) 

exposures to ambient CO and the size of 

the at-risk populations in the U.S. These 

considerations are important elements 

in the characterization of potential 

public health impacts associated with 

exposure to ambient CO. 

We first consider the effects identified 

by the evidence at the lowest studied 

short-term exposures. As discussed in 

section II.B.2 above, the study by Allred 

et al., (1989a, 1989b, 1991) indicates 

that increases in blood COHb in 

response to 1-hour CO exposures 


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produce evidence of myocardial 

ischemia in CAD patients with 

reproducible exercise-induced angina. 

At a study group average COHb level of 

2–2.4%, the statistically significant 

reduction in the time to exerciseinduced markers of myocardial 

ischemia in CAD patients was 4–5% on 

average (approximately 30 seconds), 

with larger reductions observed at the 

higher studied COHb level. In 

discussing public health implications of 

the observed responses, the study 

authors noted that the responses 

observed at the studied COHb levels 

were similar to those considered 

clinically significant when evaluating 

medications to treat angina from 

coronary artery disease (Allred et al., 

1989a, 1991). 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 

judging that ‘‘cardiovascular effects, as 

measured by decreased time to onset of 

angina pain and by decreased time to 

onset of significant ST-segment 

depression, are the health effects of 

greatest concern, which clearly have 

been associated with CO exposures at 

levels observed in the ambient air’’ (59 

FR 38913). Additionally, as discussed in 

section II.B.2 above, a dose-response 

relationship has been documented for 

COHb resulting from brief, elevated CO 

exposures in persons with pre-existing 

CAD, with no evidence of threshold (59 

FR 38910; ISA, section 5.2.4; Allred et 

al., 1989a, 1989b, 1991). 

In the 1994 review decision (as 

discussed in section II.D.1.a below), less 

significance was ascribed to the effects 

at the lower COHb level assessed in the 

Allred et al., study (1989a, 1989b, 1991), 

which were described to be of less 

certain clinical importance, than effects 

reported from short-term CO exposure 

studies that assessed higher COHb 

levels (59 FR 38913–38914). In the 

current review of the evidence, the ISA 

describes the physiological significance 

of the changes at the lowest tested dose 

level (e.g., 2% COHb from 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 considering potential public health 

impacts of CO in ambient air, we also 

consider the size of the at-risk 

populations. The population with CAD 

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 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 

ISA notes the size of the larger 

population of people with all types of 

heart disease (HD), 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). 

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 

II.B.3 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. 

C. Human Exposure and Dose 

Assessment 

Our consideration of the scientific 

evidence in the current review, as at the 

time of the last review (summarized in 

section II.D.1 below), is informed by 

results from a quantitative analysis of 

estimated population exposure and 

resultant COHb levels. This analysis 

provides estimates of the percentages of 

simulated at-risk populations expected 

to experience daily maximum COHb 

levels at or above a range of benchmark 

levels under varying air quality 

scenarios (e.g., just meeting the current 

or alternative standards). The 

benchmark COHb levels were identified 

based on consideration of the evidence 

discussed in section II.B above. The 

following subsections summarize the 

design and methods of the quantitative 

assessment (section II.C.1) and the 

important uncertainties associated with 

these analyses (section II.C.2). The 

results of the analyses, as they relate to 

considerations of the adequacy of the 

current standards, are discussed in 

section II.D.2 below. 

1. Summary of Design Aspects 

In this section, we provide a summary 

of key aspects of the assessment 

conducted for this review, including the 

study areas and air quality scenarios 

investigated, modeling tools used, atrisk populations simulated, and COHb 

benchmark levels of interest. The 

assessment is described in detail in the 

REA and summarized in the PA (section 

2.2.2). 

The assessment estimated CO 

exposure and associated COHb levels in 

simulated at-risk 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 continental 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 to ambient CO associated 

with current ‘‘as is’’ conditions (2006 air 

quality) and also for higher ambient CO 

concentrations associated with air 

quality conditions simulated to just 


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26As noted elsewhere, the 8-hour standard is the 

controlling standard for ambient CO concentrations. 

27More 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 (Policy 

Assessment, section 2.2.2). 

28When 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 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). 

29The use of pNEM in the prior review also (1) 

relied on a limited set of activity pattern data 

(approximately 3,600 person-days), (2) used four 

broadly defined categories to estimate breathing 

rates, and (3) implemented a geodesic distance 

range methodology to approximate workplace 

commutes (Johnson et al., 1992; U.S. 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. 

30APEX4.3 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 

(PA, section 2.2.2). 

31CHAD is EPA’s Comprehensive Human 

Activity Database which provides input data for 

APEX model simulations (REA, sections 4.3 and 

4.4). 

32As described in section 1.2 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). 

meet the current 8-hour standard,26 as 

well as for air quality conditions 

simulated to just meet several 

alternative standards. 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. We 

additionally recognize that this 

simulation can provide useful 

information in evaluating the current 

standard. Accordingly, we simulated 

conditions of increased CO 

concentrations that just meet the current 

8-hour standard in the two study areas. 

In so doing, we recognize the 

uncertainty associated with simulating 

this hypothetical profile of higher CO 

concentrations that just meet the current 

8-hour standard. We note, however, that 

an analysis of the ratios of 1-hour to 8- 

hour design value metrics based on 

2009 ambient CO concentrations in U.S. 

locations indicates that the relationships 

between design values for the two study 

areas under the air quality conditions 

simulated to just meet the current 8- 

hour standard fall well within the 2009 

national distribution of such ratios 

(Policy Assessment, section 2.2.2).27

The exposure and dose modeling for 

the assessment, presented in detail in 

the REA, relied on version 4.3 of 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), nitrogen dioxide (NO2), and sulfur 

dioxide (SO2). As described in section 

II.D.1 below, the review of the CO 

standards completed in 1994 relied on 

population exposure and dose estimates 

generated from the probabilistic NAAQS 

exposure model (pNEM), a model that, 

among other differences from the 

current modeling approach with 

APEX4.3, employed a cohort-based 

approach (Johnson et al., 1992; U.S. 

EPA, 1992).28 29 Each of the model 

developments since the use of pNEM in 

that review have been 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 (REA, 

chapter 4).30

As used in the current assessment, 

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 ambient CO (REA, 

chapter 4). The individual’s movements 

are simulated based on data available 

from recent activity pattern surveys 

(CHAD 31 now has about 34,000 persondays of data) and the most recent U.S. 

census data on population 

demographics and home-to-workplace 

commutes. Based on exposure 

concentrations, minute-by-minute 

activity levels, and physiological 

characteristics of the simulated 

individuals (see REA, chapters 4 and 5), 

APEX estimates the level of COHb in the 

blood for each individual at the end of 

each hour based on a nonlinear solution 

to the Coburn-Forster-Kane equation 

(REA, section 4.4.7). These results 

across each simulated individual were 

then summarized in the REA and 

discussed in the Policy Assessment in 

terms of the percent of the simulated atrisk populations expected to experience 

one or more occurrences of daily 

maximum end-of-hour COHb levels of 

interest. 

As discussed in section II.B above, 

people with cardiovascular disease are 

the population of primary focus in this 

review, and more specifically, as 

described in the ISA, 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. Accordingly, 

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.32 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 CHD or HD. 

In representing the two at-risk 

populations and their activity patterns, 

individuals were simulated based on 

age and gender distributions for CHD 

and HD populations. These 

distributions were developed by 

augmenting the prevalence estimates 

provided by the National Health 

Interview Survey for adults with CAD 

and adults with heart diseases of any 

type (HD) with estimates of 

undiagnosed ischemia (as described in 

section 5.5.1 of the REA). The 

undiagnosed ischemia estimates were 

developed based on two 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). 

APEX simulations performed for this 

review focused on exposures to ambient 


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33The 8 microenvironments modeled in the REA 

comprised a range of indoor and outdoor locations 

including residences as well as motor vehiclerelated locations such as inside vehicles, and public 

parking and fueling facilities, where the highest 

exposures were estimated (REA, sections 5.9 and 

6.1). 

34As they result only from endogenous CO 

formation, the REA ‘‘baseline’’ COHb levels would 

also be expected to be, and generally are, lower than 

the initial, pre-exposure, COHb levels of subjects in 

the controlled exposure studies. 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. 

35Although 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). 

CO occurring in eight 

microenvironments,33 absent any 

contribution to microenvironment 

concentrations from indoor 

(nonambient) CO sources. As noted in 

section II.B.1 above, however, where 

present, indoor sources, including gas 

stoves, attached garages and tobacco 

smoke, can also be important 

contributors to total CO exposure (ISA, 

sections 3.6.1 and 3.6.5). Previous 

assessments, that have included 

modeling simulations both with and 

without certain indoor sources, 

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). 

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, as indicated in the Policy 

Assessment, 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. 

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. Absolute COHb 

refers to the REA 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 were 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. Thus, the REA reports 

estimates of the maximum end-of-hour 

ambient contributions across the 

simulated year, in addition to the 

maximum absolute end-of hour COHb 

levels. 

As discussed in the Policy 

Assessment (section 2.2.2), the absence 

of indoor (nonambient) sources in the 

REA simulations is expected to result in 

simulated individuals with somewhat 

higher estimates of the contribution of 

short-duration increases in ambient CO 

exposure to COHb levels (ambient 

contribution) than would be expected 

for individuals in situations where the 

presence of nonambient sources 

contributes to higher baseline COHb 

levels (i.e., COHb prior to a shortduration exposure event). 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 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, appendix B.6).34 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 (e.g., REA, Figure B–2). 

In considering the REA dose estimates 

in the Policy Assessment, as described 

in section II.D.2 below, staff considered 

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 (at least once and on 

multiple occasions), as well as estimates 

of the percentage of population persondays (the only metric available from the 

modeling for the 1994 review), and also 

population estimates of daily maximum 

ambient contribution to end-of-hour 

COHb levels. In identifying COHb 

benchmark levels of interest, primary 

attention was given to the multilaboratory study in which COHb was 

analyzed by the more accurate GC 

method (Allred et al., 1989a, 1989b, 

1991) discussed in section II.B.2 above. 

The REA identified a series of 

benchmark levels for considering 

estimates of absolute COHb: 1.5%, 

2.0%, 2.5% and 3% COHb (REA, 

section 2.6). 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 exposure studies 

of subjects with CAD (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% postexercise 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 

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 disease;35 (4) 

the lack of studies that have evaluated 

effects of experimentally controlled 

short-term 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 


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36APEX4.3 provides estimates for percent of 

population projected to experience a single or 

multiple occurrences of a daily maximum COHb 

level above the various benchmark levels, as well 

as percent of person-days. 

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 endof-hour COHb level, arising solely from 

endogenous CO production, at or above 

1% (REA, Appendix B, Figure B–3). 

The Policy Assessment also 

considered the evidence from controlled 

human exposure studies in interpreting 

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 STsegment change in groups of subjects 

with pre-existing CAD for which 

controlled CO exposures increased their 

COHb levels by on average 1.4–1.8% 

and 3.2–4.0% 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 endof-hour COHb levels above and below a 

range of levels extending from 1.4 to 

2.0%. As noted above, the Policy 

Assessment recognized distinctions 

between the REA ‘‘baseline’’ (arising 

from prior ambient exposure and 

endogenous CO production) and the 

pre-exposure COHb levels in the 

controlled human exposure study 

(arising from ambient and nonambient 

exposure history, as well as from 

endogenous CO production), and also 

noted the impact of ‘‘baseline’’ COHb 

levels on COHb levels occurring in 

response to short ambient CO exposure 

events such as those simulated in the 

REA as discussed above. 

2. Key Limitations and Uncertainties 

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.36 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 

summarized in section 2.2.2 of the 

Policy Assessment and described in 

detail in chapter 7 of the REA. 

The uncertainties associated with the 

quantitative estimates of exposure and 

dose were considered using a generally 

qualitative 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 approach used was 

developed using World Health 

Organization (WHO) guidelines on 

conducting a qualitative uncertainty 

characterization (WHO, 2008) and was 

also applied in the most recent NO2

(USEPA, 2008c) and SO2 NAAQS 

reviews (USEPA, 2009e). A qualitative 

approach was employed given the 

extremely limited data available to 

inform probabilistic uncertainty 

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. Additionally, 

consistent with the WHO (2008) 

guidance, the REA discusses 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. 

Sixteen separate sources of 

uncertainty associated with four main 

components of the assessment were 

identified. By comparing judgments 

made regarding the magnitude and 

direction of influence that the identified 

sources have on estimated exposure 

concentrations and dose levels and the 

existing uncertainties in the knowledge 

base, seven sources of uncertainty (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) 

were identified as the most important 

areas of uncertainty in this assessment 

(PA, section 2.2.2). Taking into 

consideration improvements in the 

model algorithms and data since the last 

review, and having identified and 

characterized these uncertainties here, 

the Policy Assessment concludes 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. As noted in the 

Policy Assessment, however, potentially 

greater uncertainty remains 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, the REA and Policy 

Assessment 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). 

The Policy Assessment additionally 

notes 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 


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37The sensitive population groups identified in a 

NAAQS review may (or may not) be comprised of 

low income or minority groups. Where low income/ 

minority groups are among the sensitive groups, the 

rulemaking decision will be based on providing 

protection for these and other sensitive population 

groups. To the extent that low income/minority 

groups are not among the sensitive groups, a 

decision based on providing protection of the 

sensitive groups would be expected to provide 

protection for the low income/minority groups (as 

well as any other less sensitive population groups). 

38Air 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. 

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. 

D. Conclusions on Adequacy of the 

Current Standards 

The initial issue to be addressed in 

the current review of the primary CO 

standards is whether, in view of the 

advances in scientific knowledge and 

additional information now available, 

the existing standards should be 

retained or revised. In evaluating 

whether it is appropriate to retain or 

revise the current standards, the 

Administrator builds upon the last 

review and reflects the broader body of 

evidence and information now 

available. The Administrator has taken 

into account both evidence-based and 

quantitative exposure- and risk-based 

considerations in developing 

conclusions on the adequacy of the 

current primary CO standards. 

Evidence-based considerations include 

the assessment of evidence from 

controlled human exposure, 

toxicological and epidemiological 

studies evaluating short- or long-term 

exposures to CO, with supporting 

evidence related to dosimetry and 

potential mode of action, as well as the 

integration of evidence across each of 

these disciplines, and with a focus on 

policy-relevant considerations as 

discussed in the PA. The exposure/ 

dose-based considerations draw from 

the results of the quantitative analyses 

presented in the REA and summarized 

in section II.C above, and consideration 

of those results in the PA. More 

specifically, estimates of the magnitude 

of ambient CO-related exposures and 

associated COHb levels associated with 

just meeting the current primary CO 

NAAQS have been considered. Together 

the evidence-based and risk-based 

considerations have informed the 

Administrator’s proposed conclusions 

related to the adequacy of the current 

CO standards in light of the currently 

available scientific evidence. 

1. Approach 

In considering the evidence and 

quantitative exposure and dose 

estimates with regard to judgments on 

the adequacy afforded by the current 

standards, we note that the final 

decision is largely a public health policy 

judgment. A final decision must draw 

upon scientific 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, including the health of sensitive 

groups.37

The following subsections include 

background information on the 

approach used in the previous review of 

the CO standards (section II.D.1.a) and 

also a description of the approach for 

the current review (section II.D.1.b). 

a. Previous Reviews 

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 1971 to 

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, completed in 1985 and 1994, 

led the EPA to retain the existing 

primary standards without revision (50 

FR 37484, 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 first NAAQS review (50 FR 

37484), COHb levels in blood were 

recognized as providing the most useful 

estimate of exogenous CO exposures 

and serving as the best biomarker of CO 

toxicity for ambient-level exposures to 

CO (59 FR 38909). 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). 

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).38 Key 

considerations in this approach are 

described below. 

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 the potential to alter the effects 


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39See footnote 15 above. 

40Based on consideration of the key studies, 

including those two that investigated more than a 

single target COHb level, discussions in the 1991 

AQCD and with CASAC, the 1992 Staff Paper 

recommended that ‘‘2.9–3.0% COHb (CO–Ox), 

representing an increase above initial COHb of 1.5 

to 2.2% COHb, be considered a level of potential 

adversity for individuals at risk’’ (59 FR 38911; 

USEPA, 1992; USEPA, 1991, pp. 1–11 to 1–12; 

Allred et al., 1989a, 1989b, 1991; Anderson et al., 

1973). 

41 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 cardiovasculardisease population were associated with a 

maximum COHb level greater than or equal to 2.1% 

(USEPA, 1992; Johnson et al., 1992). 

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 

depression 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 disease 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., 1987 39) 

and discussions of adverse health 

consequences in the 1991 AQCD and 

the 1992 Staff Paper,40 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). While EPA and CASAC 

recognized the existence of a range of 

views among health professionals on the 

clinical significance of these responses, 

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). 

In further considering additional 

results from the controlled human 

exposure evidence, such as the results 

from Allred et al. (1989a, 1989b) at 2.0% 

COHb (using GC measurement) induced 

by short (approximately 1-hour) CO 

exposure, 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% COHb (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 clinical importance of 

cardiovascular effects associated with 

short (approximately 1-hour) exposures 

to CO resulting in COHb levels as low 

as 2.0% COHb by GC (Allred et al., 

1989a,b) was described as ‘‘less certain’’ 

than effects noted for exposures 

contributing to higher COHb (CO–Ox) 

levels (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. 

• 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 for considering 

margin of safety, extending from 2.9% 

COHb (representing an increase of 1.5% 

above baseline when using CO–Ox 

measurements) at the upper end down 

to 2% at the lower end (59 FR 38913), 

and also 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’’ (59 FR 38914). 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 38914). 

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. Further, 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% and a smaller 

percentage of the at-risk population was 

estimated to exceed higher COHb levels 

(59 FR 38914).41 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 


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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 FR 38914). 

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). 

b. 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 a public 

health policy judgment as to what 

standard is requisite to protect public 

health 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. Similarly, in 

this review, as described in the Policy 

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, here as in the Policy 

Assessment, 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, 2010a; USEPA, 2000), 

as well as current and preceding 

quantitative exposure/dose assessments 

(USEPA 2010b; Johnson et al., 2000; 

USEPA 1992). 

As described earlier, at this time as 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 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, as 

described in detail in the REA and 

summarized in the Policy Assessment 

(PA, section 2.2.2). Thus, in developing 

conclusions with regard to the CO 

NAAQS, EPA has taken into account 

both evidence-based and exposure/dosebased considerations. 

The approach to reaching a decision 

on the adequacy of the current primary 

standards is framed by consideration of 

the following series of key policyrelevant questions. 

• Does the currently available 

scientific evidence- and exposure/dose/ 

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? 

• Does the current evidence alter our 

conclusions from the previous review 

regarding the health effects associated 

with exposure to CO? 

• 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? 

• 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? 

• Does the current evidence alter our 

conclusions from the previous review 

regarding the levels of CO in ambient air 

associated with health effects? 

• To what extent have important 

uncertainties identified in the last 

review been reduced and/or have new 

uncertainties emerged? 

The following sections describe the 

assessment of these issues in the Policy 

Assessment, the advice received from 

CASAC, as well as the comments 

received from various parties, and then 

presents the Administrator’s proposed 

conclusions regarding the adequacy of 

the current primary standards. 

2. Evidence-Based and Exposure/DoseBased Considerations in the Policy 

Assessment 

The Policy Assessment (chapter 2) 

considers the evidence presented in the 

Integrated Science Assessment, and 

preceding AQCDs, as discussed above in 

section II.B as a basis for evaluating the 

adequacy of the current CO standards, 

recognizing that important uncertainties 

remain. The Policy Assessment 

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 (PA, section 

2.4). More specifically, the Policy 

Assessment concludes that the 

combined consideration of the evidence 

and quantitative estimates from the REA 

may be viewed as providing support for 

either retaining or revising the current 

suite of standards (PA, p. 2–59). CASAC 

stated agreement with this conclusion, 

while additionally expressing a 

‘‘preference’’ for revisions to a lower 

standard. Members of the public who 

provided comments on the draft Policy 

Assessment supported retaining the 

current standard without revision. The 

specific considerations on which the 

Policy Assessment conclusions are 

based are described in the subsections 

below. 


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42One new study of this type is available since 

the 1994 review. This study, which focused on a 

target COHb level of 3.9% COHb (CO–Ox) and is 

discussed in the 2000 AQCD is generally consistent 

with the previously available studies (2000 AQCD, 

section 6.2.2; Kleinman et al., 1998). 

43See footnote 15 above. 

44 Gas chromatography is generally recognized to 

be the more accurate method for COHb levels below 

5% (ISA, section 5.2.4). 

45 In the lower CO exposure group, the postexposure 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). 

46The studies by Anderson et al. (1973) and 

Kleinman et al. (1989) did not use GC to measure 

COHb levels, and reported reduced exercise 

duration due to increased chest pain at CO 

exposures resulting in 2.8–3.0% COHb (CO–Ox). 

The COHb levels assessed in these two studies 

represented increase in average COHb levels over 

baseline of 1.4% and 1.6% COHb. 

47Across 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). 

a. Evidence-Based Considerations 

In considering the evidence available 

for the current review of the CO 

NAAQS, the Policy Assessment 

discussed whether or not, or the extent 

to which, the current evidence alters 

conclusions reached in the previous 

review regarding levels of CO in 

ambient air associated with health 

effects and associated judgments on 

adequacy of the current standards. With 

this discussion, the Policy Assessment 

also considered the extent to which 

important uncertainties identified in the 

last review have been reduced or new 

uncertainties have emerged. 

As an initial matter, the Policy 

Assessment recognized that at the time 

of the last review, EPA’s conclusions 

regarding the adequacy of the existing 

CO standards 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 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 exerciseinduced angina and to onset of ECG STsegment depression (59 FR 38913). As at 

the time of the last review, the Policy 

Assessment noted that the evidence 

available in this review includes 

multiple studies that document 

decreases in time to onset of exerciseinduced angina (a symptom of 

myocardial ischemia) in multiple 

studies at post-exposure COHb levels 

ranging from 2.9 to 5.9% (CO–Ox), 

which represent incremental increases 

of approximately 1.4–4.4% COHb from 

baseline (CO–Ox) (PA, Table 2–2; 

Adams et al., 1988; Allred et al., 1989a, 

1989b, 1991; Anderson et al., 1973; 

Kleinman et al., 1989, 1998 42; Sheps et 

al., 1987 43). The study results from 

Allred et al. (1989a, 1989b, 1991) also 

provide evidence for these effects in 

terms of COHb measurements using gas 

chromatography.44 45 Evidence also 

available at the time of the last review 

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, none provide 

evidence of a measurable threshold at 

the lowest experimental CO exposures 

and associated COHb levels assessed 

(e.g., mean of 2.0–2.4% COHb, GC) 

which resulted in average increases in 

COHb of about 1.5% over pre-exposure 

baseline (Anderson et al., 1973; 

Kleinman et al., 1989; Allred et al. 

1989a, 1989b, 1991).46 Allred et al. 

(1989a, 1989b, 1991) further reported a 

dose-response relationship between the 

increased COHb levels and the response 

of the assessed indicators of myocardial 

ischemia (Allred et al., 1989a, 1989b, 

1991). While this evidence informs 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 II.C 

above. 

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 study mean 

COHb levels at or below 2% COHb. 

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 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, as discussed in section II.B.2 

above, 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% (post-exercise) 

from mean a baseline level of 0.6% 

significantly reduced exercise time 

required to induce markers of 

myocardial ischemia in CAD patients. 

For the more objective marker of STsegment change, the lower exposure 

reduced the time to onset by 5.1% 

(approximately one half minute) and the 

higher exposure reduced the time to 

onset by 12.1%.47

• 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. 

As described in section II.B.2 above, 

a number of epidemiological studies of 

health outcome associations with 

ambient CO have been conducted since 

the last review. These include studies 

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 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). The longstanding body of evidence for CO 

summarized above, including the wellcharacterized 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. Thus, 

although there is no new evidence 


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48Few epidemiological studies that had 

investigated the relationship between CO exposure 

and ischemic heart disease were available at the 

time of the last completed review (1991 AQCD, 

section 10.3.3). 

regarding the effects of short-term 

controlled CO exposures that result in 

lower COHb levels, the evidence is 

much expanded with regard to 

epidemiological 48 analyses of ambient 

monitor concentrations, which observed 

associations between specific and 

overall cardiovascular-related outcomes 

and ambient CO measurements. 

The Policy Assessment considered the 

combined evidence base for CO 

cardiovascular effects in the context of 

a conceptual model of the pathway from 

CO exposures to the occurrence of these 

effects (as described in section 2.2.1 of 

the PA). In this context, the Policy 

Assessment noted differences between 

the controlled human exposure and 

epidemiological studies, described 

above, with regard to the elements along 

this pathway that have been 

investigated in those studies. The 

controlled human exposure studies 

document relationships between 

directly measured controlled short-term 

CO exposures and specific levels of an 

internal dose metric, COHb, which 

elicited specific myocardial ischemiarelated 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., ST-segment 

changes) demonstrated in the controlled 

human exposure studies, providing 

coherence between the two sets of 

findings (ISA, p. 5–48). With regard to 

extending our understanding of effects 

occurring below levels of CO evaluated 

in the controlled human exposure 

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 controlled 

human exposure study 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, the Policy 

Assessment indicated that they are less 

useful to informing our conclusions 

regarding adequacy of the current 

standards. 

As discussed in the Policy 

Assessment, the smaller set of 

epidemiological 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, however, 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 areawide 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, the Policy 

Assessment primarily focused 

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, as 

discussed below. The Policy 

Assessment indicated that, as in the 

previous review, 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. 

With regard to areas of uncertainty, 

the Policy Assessment recognized that 

some important uncertainties have been 

reduced since the time of the last 

review, some still remain and others, 

associated with newly available 

evidence, have been identified. This 

range of uncertainties identified at the 

time of the last review (59 FR 38913, 

USEPA, 1992), as well as any newly 

identified uncertainties were considered 

in the Policy Assessment as discussed 

below (PA, section 2.2.1). 

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. 5–48). 

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 

reasons identified above. Similarly, the 

Science and Policy Assessments place 

primary emphasis on the findings from 

this study in the current review of the 

evidence related to cardiovascular 

effects associated with CO exposure, 

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 controlled 

human exposure 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 thenunidentified 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 

uncertainty with regard to the potential 

for short-term CO exposures to 

contribute to CNS effects which might 

affect an individual’s performance of 

complex activities such as driving a car 

or to contribute to other effects of 

concern. It was concluded, however, 

that the focus of the review on 

cardiovascular effects associated with 

COHb levels below 5% also provided 

adequate protection against potential 


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49The evidence available at the time of the last 

review was based on a series of studies conducted 

from the mid 1960’s through the early 1990’s, with 

inconsistent findings of neurological effects at 

exposures to CO resulting in COHb levels ranging 

from 5–20% (1991 AQCD). 

50 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). 

adverse neurobehavioral effects.49 No 

new controlled human exposure 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 Policy Assessment 

concludes that occurrence of these 

effects in response to ambient CO would 

be expected to be rare within the current 

population. Thus, the Policy 

Assessment concludes that uncertainty 

with regard to the potential for such 

effects to be associated with current 

ambient CO exposures is reduced (PA, 

p. 2–35). 

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, the Policy 

Assessment recognizes that 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 adverse developmental or 

reproductive effects at CO exposure 

concentrations near those associated 

with current levels of ambient CO (PA, 

pp. 2–35 to 2–36). 

As described above, the muchexpanded 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 the ISA’s 

conclusion regarding coronary artery 

disease as the most important 

susceptibility characteristic for 

increased health risk due to CO 

exposure (ISA, p. 2–10). However, the 

Policy Assessment recognizes 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, 

the Policy Assessment notes the 

substantially fewer studies conducted in 

areas meeting the current CO standards 

than is the case for NO2 and PM 

(USEPA, 2008d, 2009f). Further, the 

Policy Assessment recognizes 

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. 

With regard to these complications, 

the Policy Assessment first considers 

the extent to which the use of twopollutant regression models, a 

commonly used statistical method (ISA, 

section 1.6.3), inform conclusions 

regarding CO as the pollutant eliciting 

the effects in these studies (PA, pp. 2– 

36 to 2–37). 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 remain 

robust (ISA, Figures 5–6 and 5–7).50 In 

considering these two-pollutant model 

results, however, the Policy Assessment 

recognizes 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, 2010d). This issue is 

particularly important in the case of CO 

in light of uncertainty associated with 

CO-related effects at low ambient 

concentrations (discussed below) 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, 

the Policy Assessment recognizes 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 in light of information 

about the gradient in CO concentrations 

with distance from source locations 

such as highly-trafficked roadways (ISA, 

section 3.5.1.3). 

As discussed in the Policy 

Assessment, uncertainty in the 

assessment of exposure to ambient CO 

concentrations is related to the 

prevalence of ambient CO monitor 

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 (PA, pp. 2–37 to 2–38). For 

example, the ISA notes that roughly one 

third of the 1-hour ambient CO 

measurements reported to AQS for 

2005–2007 were below the method limit 

of detection for the monitors analyzed 

(ISA, p. 3–34). A similarly notable 

proportion of measurements occur 

below the monitor detection limit for 

epidemiological study areas meeting the 

current standards (e.g., Atlanta, 

Allegheny County) (PA, Appendix B). 

This complicates our interpretation of 

specific ambient CO concentrations 

associated with health effects (ISA, p. 3– 

91; Brain and Samet, 2010d). In contrast 

to CO, other combustion-related 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 


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51 In the case of lead (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. Thus, for 

Pb, as compared to the case for CO, we have less 

uncertainty in our interpretations of the 

epidemiological studies with regard to the pollutant 

responsible for the health effects observed. 

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, 2009f, 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, 2009f, 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 onroad mobile sources’’ (40 FR 6479, 

February 9, 2010). In contrast to PM2.5

and NO2, CO is not formed through 

common atmospheric oxidation 

processes, 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 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 is 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—the epidemiological studies also 

use that metric.51 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 the 

controlled human exposure 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. 

Additionally the ISA recognizes that 

the changes in COHb that would likely 

be associated with exposure to the low 

ambient CO concentrations assessed in 

some of the epidemiological studies 

would be smaller than changes 

associated with ‘‘substantially reduced 

{oxygen} delivery to tissues,’’ that might 

plausibly lead to the outcomes observed 

in those studies, with additional 

investigation needed to determine 

whether there may be another 

mechanism of action for CO that 

contributes to the observed outcomes at 

low ambient concentrations (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, the Policy Assessment 

concludes that some important 

uncertainties from the last review have 

been reduced, including those 

associated with concerns for ambient 

levels of CO to pose neurobehavioral 

risks as current concentrations of 

ambient CO are well below those that 

might be expected to result in COHb 

levels as high as those associated with 

these effects. Additionally, our exposure 

and dose models have improved giving 

us increased confidence in their 

estimates. 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-yet-unidentified health 

effects at COHb levels below 2%. 

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, 

particularly with regard to ambient 

concentrations that may be eliciting 

health outcomes. 

b. Exposure/Dose-Based Considerations 

In considering the evidence from 

controlled human exposure studies 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. The current estimates are 

presented in the REA and discussed 

with regard to policy-relevant 

considerations in this review in the 

Policy Assessment (PA, section 2.2.2). 

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 associated 

conclusions in the Policy Assessment 

are described below with regard to the 

expectation for COHb levels of concern 

to occur in the at-risk population under 

air quality conditions associated with 

the current CO standards. 

In considering the results from the 

REA, the Policy Assessment considered 

several questions including those 

concerning the magnitude of COHb 

levels estimated in the simulated at-risk 

populations in response to ambient CO 

exposure, as well as the extent to which 

such estimates may be judged to be 

important from a public health 

perspective. 

In addressing the questions 

concerning the magnitude of at-risk 

population COHb levels estimated to 


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52As described in the REA, the analyses 

providing results for Table 2 were only performed 

for the CHD populations, and so are not available 

for the larger HD population, although as 

mentioned above the results in terms of percentage 

are expected to be similar. 

53As described in section II.C. above, pNEM, the 

model used in the last review, employed a cohortbased approach from which person-days were the 

exposure and dose metrics (USEPA, 1992; Johnson 

et al., 1992). 

occur in areas simulated to just meet the 

current, controlling, 8-hour standard 

and what portion of the at-risk 

population is estimated to experience 

maximum COHb levels above levels of 

potential health concern, the Policy 

Assessment first noted the context for 

the population COHb estimates 

provided by the REA simulations of 

exposure to ambient CO (REA, section 

6.2). As in the last review, the Policy 

Assessment recognized 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. The Policy Assessment 

additionally took 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 focused on COHb levels resulting 

from ambient CO exposures. In so 

doing, however, the Policy Assessment 

also recognized as noted in section II.C 

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. Additionally, these simulations 

may underestimate COHb levels that 

would occur in situations with 

appreciable nonambient exposure. 

As recognized in the Policy 

Assessment and described in detail in 

the REA, estimates for exposure 

concentrations indicated that highest 

ambient CO exposures occurred in invehicle microenvironments, with next 

highest exposures in 

microenvironments where running 

vehicles congregate such as parking 

areas and fueling stations, (REA, section 

6.1). 

In considering the REA estimates for 

current or ‘‘as is’’ air quality conditions 

and conditions simulated to just meet 

the current 8-hour standard, the Policy 

Assessment particularly focused on the 

extent to which the current standards 

provide protection to the simulated atrisk 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, the Policy Assessment 

draws 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 endof-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. 

The Policy Assessment first 

considered 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 benchmarks (Table 

1 includes these results for the HD 

populations). Another dimension of the 

analysis, presented in Table 2 (for the 

CHD populations),52 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).53 The persondays metric, which summarizes 

occurrences across the number of 

persons in the at-risk population 

multiplied by the number of days in the 

year, is a common cumulative measure 

of population exposure/dose that 

simultaneously takes into account both 

the number of people affected and the 

numbers of times each is affected. 

As expected, given that current 

ambient concentrations in the two study 

areas are well below the CO standards, 

the absolute COHb estimates under 

current air quality conditions are 

appreciably lower than the 

corresponding estimates for conditions 

of higher ambient CO concentrations in 

which the current 8-hour standard is 

just met (Table 1). 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 endof-hour COHb concentration at or above 

2% (Table 1). 

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 1). 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 1) and no 

person is estimated to experience more 

than one such day in a year (Table 2). 

Further, less than 0.1% of either 

simulated population 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 1). Appreciably smaller 

percentages of the simulated at-risk 

population were estimated to 

experience more than one day with such 

levels (Table 2). 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 such 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). 


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54Other 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). 

TABLE 1—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

Daily maximum end-of-hour COHb 

(absolute) 

Percentage (%) of simulated HD population A

Just meeting current 8-hour standard 

(8-hr DV = 9.4 ppm) 

‘‘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) 

≥ 4.0% .............................................. 0 B < 0.1 0 0 

≥ 3.0% .............................................. B < 0.1 0.3 

≥ 2.5% .............................................. B < 0.1 0.9 

≥ 2.0% .............................................. 0.6 4.5 B < 0.1 B < 0.1 

≥ 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. 

TABLE 2—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

Maximum end-of-hour 

COHb level (absolute) 

Percentage (%) of simulated CHD population A

Just meeting current 8-hour standard 

(8-hr DV = 9.4 ppm) 

‘‘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) 

≥ 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% .............................. B < 0.1 0 0 B < 0.1 0 0 0 0 0 0 0 0 

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

≥ 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. 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 specific COHb 

ambient contribution levels than those 

for the Los Angeles study area, 

reflecting the study area difference in 

1-hour peak concentrations. 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. 

In considering the estimates of 

population occurrences of daily 

maximum COHb levels for REA 

simulations under conditions just 

meeting the current 8-hour standard 

(presented in Tables 1 and 2 above), the 

Policy Assessment notes 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 value for Denver as 

compared to Los Angeles (16.2 ppm 

versus 11.8 ppm), as noted in Tables 1 

and 2. 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).54 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 as is conditions in 

Tables 1 and 2 above (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, the Policy Assessment 

recognizes the impact on daily 

maximum COHb levels of 1-hour 


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ambient concentrations separate from 

the impact of 8-hour average 

concentrations, and takes note of this in 

considering the REA results with regard 

to the adequacy of the 1-hour standard. 

The Policy Assessment concludes that, 

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 (PA, 

section 2.2.2). 

In considering the public health 

implications of the quantitative dose 

estimates, the Policy Assessment 

considered the daily maximum end-ofhour levels estimated in the REA for 

conditions just meeting the current suite 

of standards in light of the effects 

identified by the evidence at the COHb 

benchmark levels considered. For 

example, as a result of ambient CO 

exposures occurring under air quality 

conditions adjusted to just meet the 

current 8-hour standard, the REA 

estimates that 0.6 percent of the Los 

Angeles and 4.5 percent of the Denver 

study at-risk 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 

simulated at-risk 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 II.B.4 above, the 

Policy Assessment recognized the 

magnitude of the ‘‘time to onset’’ 

reductions observed in the study by 

Allred et al. (1989a, 1989b, 1991), the 

similarity of the study responses to 

responses considered clinically 

significant when evaluating medications 

to treat angina from coronary artery 

disease, and conclusions reached by the 

independent review panel for the study 

regarding the expectation that frequent 

encounters in ‘‘everyday life’’ with 

increased COHb levels on the order of 

those tested in the study might limit 

activity and affect quality of life (Allred 

et al., 1989b, pp. 38, 92–94; 1991 AQCD, 

p. 10–35), as well as considerations in 

the review completed in 1994 and 

assessment of the study findings in the 

current ISA. 

In considering public health 

implications of the REA estimates, the 

Policy Assessment also considered the 

size of the at-risk populations simulated 

as described in section II.B.4 above, 

recognizing that the U.S. population 

with coronary heart disease, angina 

pectoris (cardiac chest pain) or who 

have experienced a heart attack in 

combination with those with silent or 

undiagnosed ischemia comprises 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). The 

Policy Assessment also recognized that 

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), while noting that 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). 

In summary, the Policy Assessment, 

while noting the substantial size of the 

population of individuals with CHD or 

other heart diseases in the U.S., 

recognized 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 in section II.B.4 and 

summarized above, the Policy 

Assessment concluded that 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. 

c. Summary 

With regard to the different elements 

of the current standards, the Policy 

Assessment 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, and that 

it is appropriate to continue to retain 

standards with averaging times of 1 and 

8 hours. With regard to form and level 

for these standards, the Policy 

Assessment concludes that the 

information available in this review 

supports consideration of either 

retaining the current suite of standards 

or revising one or both standards. 

The Policy Assessment concludes that 

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. 

The Policy Assessment conclusions 

with regard to the adequacy of the 

current standards are drawn from both 

the evidence and from the exposure and 

dose assessment, taking into 

consideration related information, 

limitations and uncertainties recognized 

above. The combined consideration of 

the body of evidence and the 

quantitative exposure and dose 

estimates are concluded to provide 

support for a suite of standards at least 

as protective as the current suite. 

Further, the Policy Assessment 

recognizes 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. 


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The Policy Assessment additionally 

notes 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. The REA 

results are concluded to 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 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, 

the Policy Assessment concludes that 

the combined consideration of the 

evidence and quantitative estimates may 

be viewed as providing support for 

either retaining or revising the current 

suite of standards. 

The Policy Assessment conclusion 

that it is appropriate to consider 

retaining the current suite of standards 

without revision is based on 

consideration of the health effects 

evidence in combination with the 

results of the REA (PA, sections 2.2.1, 

2.2.2, 2.3.2 and 2.3.3) 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 shortduration, 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 atrisk 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, the Policy Assessment also 

concludes 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, the Policy Assessment 

notes the health effects evidence from 

1-hour controlled exposures, which 

indicates the effects in susceptible 

groups from such short duration 

exposures. The Policy Assessment 

interpreted the evidence and REA 

estimates to 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, 

the Policy Assessment focuses on the 

1-hour standard as providing the most 

direct approach for controlling the 

likelihood of such occurrences. 

With regard to a revision of the 1-hour 

standard, the Policy Assessment 

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 the 

Policy Assessment considers to provide 

increased regulatory stability over the 

current form. The Policy Assessment 

additionally takes note of CASAC’s 

preference for a revision to the 

standards to provide greater protection 

and observes that the range of 1-hour 

standard levels discussed is also the 

range that the CASAC CO Panel 

suggested was appropriate for 

consideration. 

The Policy Assessment indicates that 

the upper part of the range of 1-hour 

standard levels for consideration (11–15 

ppm) was identified 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 (PA, 

Appendix C). The Policy Assessment 

states that 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 give greater weight to 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. 

The Policy Assessment also 

concluded that, based on the evidence 

and REA estimates and alternative 

judgments 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 objective 

in mind, the Policy Assessment also 

described a rationale for consideration 

of 1-hour standard levels of 9–10 ppm, 

which comprise the middle part of the 

range of 1-hour standard levels 

suggested for consideration (PA, section 

2.3.5). Additionally, the Policy 


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55All written comments submitted to the Agency 

thus far in this review are available in the docket 

for this rulemaking, as are transcripts of the public 

meetings held in conjunction with CASAC’s review 

of the draft PA, of drafts of the REA, and of drafts 

of the ISA. 

Assessment identified 1-hour standard 

levels of 5–8 ppm, in the lower part of 

the range for consideration in light of 

alternative judgments with regard to the 

evidence and REA, including the weight 

to place on public health significance of 

smaller changes in COHb and the small 

number of epidemiological studies in 

areas meeting the current standards (PA, 

section 2.3.5). 

In considering the relative strength of 

the evidence supporting each of the 3 

parts of the range, the Policy 

Assessment concludes 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, 

the Policy Assessment concludes that 

support provided by the available 

information is more limited, especially 

for the lowest part of the range. 

In conjunction with consideration of 

a revised 1-hour standard, the Policy 

Assessment, also concludes it is 

appropriate to consider retaining a 

standard with an 8-hour averaging time, 

recognizing that, 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, the Policy 

Assessment additionally describes 

revision to the 8-hour standard form 

that may be appropriate to consider to 

potentially provide greater regulatory 

stability, with adjustment to level to 

provide generally equivalent protection 

as the current 8-hour standard or as a 

revised 1-hour standard level (PA, 

section 2.3.5). The range of 8-hour levels 

identified in the Policy Assessment is 

inclusive of the range of levels included 

in the example policy option suggested 

by CASAC. 

3. CASAC Advice 

In our consideration of the adequacy 

of the current standards, in addition to 

the evidence- and exposure/dose-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 draft Policy Assessment, as well as 

comments from the public on drafts of 

these documents.55 In these reviews, 

CASAC has provided an array of advice, 

both with regard to interpreting the 

scientific evidence and quantitative 

exposure/dose assessment, as well as 

with regard to consideration of the 

adequacy of the current standards (Brain 

and Samet, 2009, 2010a, 2010b, 2010c, 

2010d). 

In their review of the draft ISA, 

CASAC noted various limitations and 

uncertainties associated with the 

evidence, particularly from the 

epidemiological studies, as noted in 

section II.D.2.1 above. For example, they 

recognized limitations in representation 

of population exposure to ambient CO. 

Further they noted that ‘‘[t]he problem 

of co-pollutants serving as potential 

confounders is particularly problematic 

for CO’’ and that CO may be serving as 

a surrogate for a mixture of pollutants 

generated by fossil fuel combustion 

(Brain and Samet, 2010d) as well as 

noting uncertainty regarding the 

possibility for confounding effects of 

indoor sources of CO (Brain and Samet, 

2010c). 

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, 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, 

2010c). 

As noted in section I.C. above, the 

final Policy Assessment was completed 

with consideration of CASAC comments 

on the draft document, as well as their 

comments on the second draft REA, and 

also public comments. Among the 

revisions made in completing the final 

Policy Assessment were those based on 

additional consideration of the 

epidemiological studies in light of 

CASAC comments. Discussion of these 

studies and the complications with 

regard to their quantitative 

interpretation is described in section 

II.D.2.a above, in addition to other 

evidence-based considerations 

described in the final Policy 

Assessment, and is considered in the 

Administrator’s proposed conclusions 

below. 

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. 

4. Administrator’s Proposed 

Conclusions Concerning Adequacy 

Based on the large body of evidence 

concerning the public health impacts of 

exposure to ambient CO available in this 

review, the Administrator proposes that 

the current primary standards provide 

the requisite protection of public health 

with an adequate margin of safety and 

should be retained. 

In considering the adequacy of the 

current standards, the Administrator has 

carefully considered the available 

evidence and conclusions contained in 

the Integrated Science Assessment; the 

information, exposure/dose assessment, 

rationale and conclusions presented in 

the Policy Assessment; the advice and 

recommendations from CASAC; and 

public comments to date. In the 

discussion below, the Administrator 

considers first the long-standing 

evidence base concerning effects 

associated with exposure to CO, 

including the controlled human 

exposure studies, and the health 

significance of responses observed at the 

2% COHb level induced by 1-hour CO 

exposure, as compared to higher COHb 

levels. As at the time of the review 

completed in 1994, the Administrator 

also takes note of the results for the 

modeling of exposures to ambient CO 

under conditions simulated to just meet 

the current, controlling, 8-hour standard 

in two study areas, as described in the 

REA and Policy Assessment, and the 

public health significance of those 

results. She also considers the newly 

available and much-expanded 

epidemiological evidence, including the 

complexity associated with quantitative 

interpretation of these studies, 

particularly the few studies available in 

areas where the current standards are 

met. Further, the Administrator 

considers the advice of CASAC, 

including both their overall agreement 

with the Policy Assessment conclusion 

that the current evidence and 

quantitative exposure and dose 

estimates provide support for retaining 

the current standard, as well as their 

view that in light of the epidemiological 

studies, revisions to lower the standards 

should be considered and their 

preference for a lower standard. 


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As an initial matter, the Administrator 

takes note of the Policy Assessment’s 

consideration of the long-standing body 

of evidence for CO, augmented in some 

aspects since the last review, as 

summarized in the current Integrated 

Science Assessment. This long-standing 

evidence base has established the 

following key aspects of CO toxicity that 

are relevant to this review as they were 

to the review completed in 1994. The 

common mechanism of CO health 

effects involves binding of CO to 

reduced iron in heme proteins and the 

alteration of their function. Hypoxia 

(reduced oxygen availability) induced 

by increased COHb blood levels plays a 

key role in eliciting CO-related health 

effects. Accordingly, COHb is 

commonly used as the bioindicator and 

dose metric for evaluating CO exposure 

and the potential for health effects. 

Further, people with cardiovascular 

disease are a key population at risk from 

short-term ambient CO exposures. 

With regard to the evidence of health 

effects associated with ambient CO 

exposures relevant to this review, the 

Administrator first recognizes the 

Integrated Science Assessment’s 

conclusion that a causal relationship is 

likely to exist between relevant shortterm exposures to CO and 

cardiovascular morbidity. Further, as at 

the time of the review completed in 

1994, the Administrator takes particular 

note of the evidence from controlled 

human exposure studies that 

demonstrates a reduction in time to 

onset of exercise-induced markers of 

myocardial ischemia in response to 

increased COHb resulting from shortterm CO exposures, and recognizes the 

greater significance accorded both to 

larger reductions in time to myocardial 

ischemia, and to more frequent 

occurrences of myocardial ischemia. 

The Administrator also recognizes the 

uncertain health significance associated 

with the smaller responses to the lowest 

COHb level assessed in the study given 

primary consideration in this review 

(Allred et al., 1989a, 1989b, 1991) and 

with single occurrences of such 

responses. In the study by Allred et al. 

(1989a, 1989b, 1991), a 4–5% reduction 

in time (approximately 30 seconds) to 

the onset of exercise-induced markers of 

myocardial ischemia was associated 

with the 2% COHb level induced by 1- 

hour CO exposure. In considering the 

significance of the magnitude of the 

time decrement to onset of myocardial 

ischemia observed at the 2% COHb 

level induced by short-term CO 

exposure, as well as the potential for 

myocardial ischemia to lead to more 

adverse outcomes, the EPA generally 

places less weight on the health 

significance associated with infrequent 

or rare occurrences of COHb levels at or 

just above 2% as compared to that 

associated with repeated occurrences 

and occurrences of appreciably higher 

COHb levels in response to short-term 

CO exposures. For example, at the 4% 

COHb level, the study by Allred et al., 

(1989a, 1989b, 1991) observed a 7–12% 

reduction in time to the onset of 

exercise-induced markers of myocardial 

ischemia. The Administrator places 

more weight on this greater reduction in 

time to onset of exercise-induced 

markers compared to the reduction in 

time to onset at 2% COHb. The 

Administrator also notes that at the time 

of the 1994 review, an intermediate 

level of approximately 3% COHb was 

identified as a level at which adverse 

effects had been demonstrated in 

persons with angina. Now, as at the time 

of the 1994 review, the Administrator 

primarily considers the 2% COHb level, 

resulting from 1-hour CO exposure, with 

regard to providing a margin of safety 

against effects of concern that have been 

associated with higher COHb levels, 

such as 3–4% COHb. 

As at the time of the last review, the 

Administrator additionally considers 

the exposure and dose modeling results, 

taking note of key limitations and 

uncertainties associated with the 

exposure and dose assessment 

summarized in section II.C.2. above, and 

in light of judgments above regarding 

the health significance of findings from 

the controlled human exposure studies, 

placing less weight on the health 

significance of infrequent or rare 

occurrences of COHb levels at or just 

above 2% and more weight to the 

significance of repeated such 

occurrences, as well as occurrences of 

higher COHb levels. Under air quality 

conditions just meeting the current, 

controlling, 8-hour standard, the 

assessment estimates that, as was the 

case for the assessment conducted for 

the 1994 review, daily maximum COHb 

levels were below 2% COHb for more 

than 99.9% of person-days in the study 

areas evaluated. Further, under these 

conditions, greater than 99.9% of the atrisk populations in the study areas 

evaluated would not be expected to 

experience daily maximum COHb levels 

at or above 4% COHb, and more than 

95% and 98.6% of those populations 

would be expected to avoid single or 

multiple occurrences, respectively, at or 

just above 2% COHb. 

The Administrator additionally takes 

note of the now much-expanded 

evidence base of epidemiological 

studies, including the multiple studies 

that observe positive associations 

between cardiovascular outcomes and 

short-term ambient CO concentrations 

across a range of CO concentrations, 

including conditions above as well as 

below the current NAAQS. She notes 

particularly the Integrated Science 

Assessment finding that these studies 

are logically coherent with the larger, 

long-standing health effects evidence 

base for CO and the conclusions drawn 

from it regarding cardiovascular diseaserelated susceptibility. In further 

considering the epidemiological 

evidence base with regard to the extent 

to which it provides support for 

conclusions regarding adequacy of the 

current standards, the Administrator 

takes note of CASAC’s conclusions 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’’ 

(Brain and Samet, 2010c). Additionally, 

the Administrator places weight on the 

final Policy Assessment consideration of 

aspects that complicate quantitative 

interpretation of the epidemiological 

studies with regard to ambient 

concentrations that might be eliciting 

the reported health outcomes. 

For purposes of evaluating the 

adequacy of the current standards, there 

are multiple complicating features of the 

epidemiological evidence base, as 

described in more detail in the final 

Policy Assessment and in section 

II.D.2.a, above. First, while a number of 

studies observed positive associations of 

cardiovascular disease-related outcomes 

with short-term CO concentrations, very 

few of these studies were conducted in 

areas that met the current standards 

throughout the period of study. In 

addition, CASAC, in their advice 

regarding interpretation of the currently 

available evidence commented that 

‘‘[t]he problem of co-pollutants serving 

as potential confounders is particularly 

problematic for CO’’ and that given the 

currently low ambient CO levels, there 

is a possibility that CO is acting as a 

surrogate for a mix of pollutants 

generated by fossil fuel combustion. 

CASAC further stated that ‘‘[a] better 

understanding of the possible role of copollutants is relevant to regulation’’ 

(Brain and Samet, 2010d). As described 

in the Policy Assessment, there are also 

uncertainties related to representation of 

ambient CO exposures given the steep 

concentration gradient near roadways, 

as well as the prevalence of 

measurements below the method 

detection limit across the database. 

CASAC additionally indicated the need 

to consider the potential for 


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confounding effects of indoor sources of 

CO. As discussed in section II.D.2.a 

above, the interpretation of 

epidemiological studies for CO is 

further complicated because, in contrast 

to the situation for all other criteria 

pollutants, the epidemiological studies 

for CO use an exposure/dose metric (air 

concentration) that differs from the 

metric commonly used in the other key 

CO health studies (COHb). 

Although CASAC expressed a 

preference for a lower standard, CASAC 

also indicated that the current evidence 

provides support for retaining the 

current suite of standards. CASAC’s 

recommendations appear to recognize 

that their preference for a lower 

standard was contingent on a judgment 

as to the weight to be placed on the 

epidemiological evidence. For the 

reasons explained above, after full 

consideration of CASAC’s advice and 

the epidemiological evidence, as well as 

its associated uncertainties and 

limitations, the Administrator judges 

those uncertainties and limitations to be 

too great for the epidemiological 

evidence to provide a basis for revising 

the current standards. 

In considering the adequacy of the 

level of protection provided by the 

current standards, the Administrator 

notes the findings of the exposure and 

dose assessment in light of 

considerations discussed above 

regarding the weight given to different 

COHb levels and their frequency of 

occurrence. The exposure and dose 

assessment results indicate that only a 

very small percentage of the at-risk 

population is estimated to experience a 

single occurrence in a year of daily 

maximum COHb at or above 3.0% 

COHb under conditions just meeting the 

current 8-hour standard in the two 

study areas evaluated, and no multiple 

occurrences are estimated. The 

Administrator also notes the results 

indicating that only a small percentage 

of the at-risk populations are estimated 

to experience a single occurrence of 2% 

COHb in a year under conditions just 

meeting the standard, and still fewer 

estimated to experience multiple such 

occurrences. Taken together, the 

Administrator considers the current 

standard to provide a very high degree 

of protection for the COHb levels and 

associated health effects of concern, as 

indicated by the extremely low 

estimates of occurrences, and provides 

slightly less but a still high degree of 

protection for the effects associated with 

lower COHb levels, the physiological 

significance of which is less clear. 

Additionally, the Administrator 

proposes to conclude that consideration 

of the epidemiological studies does not 

lead her to identify a need for any 

greater protection. Thus, the 

Administrator proposes to conclude that 

the current suite of standards provides 

an adequate margin of safety against 

adverse effects associated with shortterm ambient CO exposures. For these 

and all of the reasons discussed above, 

and recognizing the CASAC conclusion 

that, overall, the current evidence and 

REA results provide support for 

retaining the current standard, the 

Administrator proposes to conclude that 

the current suite of primary CO 

standards are requisite to protect public 

health with an adequate margin of safety 

from effects of ambient CO. 

The Administrator also solicits 

comment on whether it would be 

appropriate to revise the current 

primary standards. The Administrator 

takes note that, while CASAC indicated 

their view that the evidence and 

exposure and dose estimates provide 

support for retaining the current 

NAAQS, they also indicated their 

preference for a lower standard. For 

example, the CASAC CO Panel stated 

that giving additional weight to the 

epidemiological evidence would 

support a tightening of the current 

standard. The Administrator also takes 

note of the Policy Assessment 

conclusions, summarized in section 

II.D.2.c above. Thus, in light of views 

expressed by CASAC, as well as the 

Policy Assessment conclusions, the 

Administrator additionally solicits 

comment on the appropriateness of 

potential revisions to the form and level 

of the standards. Any comments on 

such revisions should include an 

explanation of the basis for the 

commenters’ views. 

E. Summary of Proposed Decisions on 

Primary Standards 

For the reasons discussed above, and 

taking into account information and 

assessments presented in the Integrated 

Science Assessment and Policy 

Assessment, the advice and 

recommendations of CASAC, and the 

public comments to date, the 

Administrator proposes to retain the 

existing suite of primary CO standards. 

Additionally, the Administrator solicits 

comment on the appropriateness of 

revisions to the form and level of the 

standards. 

III. Consideration of a Secondary 

Standard 

This section focuses on the key 

policy-relevant issues related to the 

review of public welfare-related 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.’’ We first summarize the history 

of EPA’s consideration of secondary 

standards for CO in section III.A. In 

section III.B, we then discuss 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 

as presented in the Policy Assessment. 

Advice from CASAC is summarized in 

section III.C. Lastly, the Administrator’s 

proposed conclusions are presented in 

section III.D. 

A. Background and Considerations 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. 

B. Evidence-Based Considerations in the 

Policy Assessment 

To evaluate whether 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 


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56Thus far in this review, no public comments 

have been received regarding the secondary 

standard. 

57This recommendation is addressed in section 

3.5 of the Policy Assessment. 

and information now available. 

Considerations of the evidence available 

in this review in the Policy Assessment 

were organized around 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, the Policy Assessment first 

noted 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). Climaterelated 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; ISA, 

section 3.3). 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. 

As concluded in the Policy 

Assessment, 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 (PA, 

section 3.2). As recognized in the ISA, 

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 radicals. Increased 

concentrations of CO can lead to 

increased concentrations of other gases 

whose loss processes also involve 

hydroxyl radical chemistry. Some of 

these gases, such as methane 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 

(PA, section 3.2). CO contributes to 

climate forcing through both direct 

radiative forcing (RF) of CO, estimated 

at 0.024 watts per square meter (W/m2) 

by Sinha and Toumi (1996), and 

indirect effects of CO on climate 

through methane, O3 and carbon 

dioxide (Forster et al. 2007). The 

Intergovernmental Panel on Climate 

Change 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). 

As discussed in the Policy 

Assessment, CO is classified as a shortlived climate forcing agent, prompting 

CO emission reductions to be 

considered as a possible strategy to 

mitigate effects of global warming (PA, 

section 3.2). However, in considering 

the information presented in the ISA, 

the Policy Assessment notes that 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, 

methane, 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 noted in the 

Policy Assessment to be 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 approximately 

50% uncertainty (ISA, section 3.3, and 

p. 3–13). 

In summary, the Policy Assessment 

drew the following conclusions based 

on the considerations identified above. 

As an initial matter, with respect to nonclimate welfare effects, including 

ecological effects and impacts to 

vegetation, the Policy Assessment 

concluded that there is no currently 

available scientific information that 

supports a CO secondary standard (PA, 

section 3.4). Secondly, with respect to 

climate-related effects, the Policy 

Assessment recognized the evidence of 

climate forcing effects associated with 

CO (ISA, sections 2.2 and 3.3), while 

also noting that 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 U.S. 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 welfare-related effects of 

O3 are more appropriately considered in 

the context of the review of the O3

NAAQS, rather than in this CO NAAQS 

review (PA, section 3.4). For these 

reasons, the Policy Assessment 

concluded that there is insufficient 

information at this time to support the 

consideration of a secondary standard 

based on CO effects on climate 

processes (PA, section 3.4). 

C. CASAC Advice 

In consideration of a secondary 

standard, in addition to the evidence 

discussed above, EPA has also 

considered the advice and 

recommendations of CASAC, based on 

their review of the ISA, and the draft 

Policy Assessment.56

In their comments on the draft Policy 

Assessment, CASAC took note of the 

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 (ISA, 

sections 3.2 and 3.3; Brain and Samet, 

2010c).57 CASAC noted without 

objection or disagreement the staff’s 

conclusions that there is insufficient 

information to support consideration of 

a secondary standard at this time (Brain 

and Samet, 2010c). 

D. Administrator’s Proposed 

Conclusions Concerning a Secondary 

Standard 

The proposed conclusions presented 

here are based on the assessment and 

integrative synthesis of the scientific 

evidence presented in the ISA, building 

on the evidence described in the 2000 

AQCD, as well as staff consideration of 

this evidence in the Policy Assessment 

and CASAC advice. In considering 

whether the currently available 

scientific information supports setting a 

secondary standard for CO, EPA takes 

note of the Policy Assessment 

consideration of the body of available 

evidence (briefly summarized above in 


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section III.B). First, EPA concludes that 

the currently available scientific 

information with respect to non-climate 

welfare effects, including ecological 

effects and impacts to vegetation, does 

not support a CO secondary standard. 

Secondly, with respect to climaterelated effects, the EPA takes note of 

staff considerations in the Policy 

Assessment and concurs with staff 

conclusions that this information is 

insufficient at this time to provide 

support for a CO secondary standard. 

Thus, in considering the evidence, staff 

considerations in the Policy Assessment 

summarized here, as well as the views 

of CASAC, summarized above, the 

Administrator proposes to conclude that 

no secondary standards should be set at 

this time because, as in the past reviews, 

having no standard is requisite to 

protect public welfare from any known 

or anticipated adverse effects from 

ambient CO exposures. 

IV. Proposed Amendments to Ambient 

Monitoring Requirements 

The EPA is proposing changes to the 

ambient air monitoring network design 

requirements to support the NAAQS for 

CO discussed above in section II. 

Because the availability of ambient CO 

monitoring data is an essential element 

of the NAAQS implementation 

framework, EPA is proposing to revise 

the requirements for the ambient CO 

monitoring network to include a 

minimum set of monitors to provide 

data for comparison to the NAAQS (i.e., 

for determining whether areas are 

attaining the standards) in locations 

near roads where CO emissions 

associated with mobile source related 

activity lead to increased ambient 

concentrations. Under such 

requirements, State, local, and Tribal 

monitoring agencies (‘‘monitoring 

agencies’’) collect ambient CO 

monitoring data in accordance with the 

monitoring requirements contained in 

40 CFR parts 50, 53, and 58 for 

comparison to the NAAQS and to meet 

other objectives. 

A. Monitoring Methods 

Ambient air monitoring data are used 

for various purposes, including 

determining compliance with the 

NAAQS. The use of reference methods 

provides uniform, reproducible 

measurements of pollutant 

concentrations in ambient air. 

Equivalent methods allow for the 

introduction of new or alternative 

technologies for the same purpose, 

provided these methods produce 

measurements directly comparable to 

the reference methods. EPA has 

established procedures for determining 

and designating reference and 

equivalent methods, known as Federal 

Reference Methods (FRMs) and Federal 

Equivalent Methods (FEMs), at 40 CFR 

part 53. 

Ambient air monitoring data for CO 

must be obtained using an FRM or an 

FEM, as defined in 40 CFR parts 50 and 

53, for such data to be comparable to the 

NAAQS for CO. All CO monitoring 

methods in use currently by State and 

local monitoring agencies are EPAdesignated FRM analyzers (USEPA, 

2010f). No FEM analyzer, i.e. one using 

an alternative measurement principle, 

has yet been designated by EPA for CO. 

These continuous FRM analyzers have 

been used in monitoring networks for 

many years (USEPA, 2010f) and provide 

CO monitoring data adequate for 

determining CO NAAQS compliance. 

The current list of all approved FRMs 

capable of providing ambient CO data 

for this purpose may be found on the 

EPA Web site, http://www.epa.gov/ttn/ 

amtic/files/ambient/criteria/referenceequivalent-methods-list.pdf. Although 

both the existing CO FRM in 40 CFR 

part 50 and the FRM and FEM 

designation requirements in part 53 

remain adequate to support the CO 

NAAQS, EPA is nevertheless proposing 

editorial revisions to the CO FRM and 

both technical and editorial revisions to 

part 53, as discussed below. 

1. Proposed Changes to Part 50, 

Appendix C 

Reference methods for criteria 

pollutants are described in several 

appendices to 40 CFR part 50; the CO 

FRM is set forth in appendix C of part 

50. A nondispersive infrared 

photometry (NDIR) measurement 

principle is formally prescribed as the 

basis for the CO FRM. Appendix C 

describes the technical nature of the 

NDIR measurement principle stipulated 

for FRM CO analyzers as well as two 

acceptable calibration procedures for 

CO FRM analyzers. It further requires 

that an FRM analyzer must meet 

specific performance, performance 

testing, and other requirements set forth 

in 40 CFR part 53. 

From time to time, as pollutant 

measurement technology advances, EPA 

assesses the FRMs in the 40 CFR part 50 

FRM appendices to determine if they 

are still adequate or if improved or more 

suitable measurement technology has 

become available to better meet current 

FRM needs as well as potential future 

FRM requirements. The CO FRM was 

originally promulgated on April 30, 

1971 (36 FR 8186), in conjunction with 

EPA’s establishment (originally as 42 

CFR part 410) of the first NAAQS for six 

pollutants (including CO) as now set 

forth in 40 CFR part 50. The method 

was amended in 1982 and 1983 (47 FR 

54922; 48 FR 17355) to incorporate 

minor updates, but no substantive 

changes in the fundamental NDIR 

measurement technique have been made 

since its original promulgation. (Those 

updates included clarification that the 

FRM NDIR measurement principle 

encompassed the specific ‘‘gas filter 

correlation’’ measurement technique 

now used by many commercial FRM 

analyzers.). 

In connection with the current review 

of the NAAQS for CO, EPA is proposing 

to again update the existing CO FRM— 

with no substantive changes—as 

explained in further detail below. This 

action is based on the scientific view 

that the CO FRM, as originally 

established and updated in the 1980’s, 

is still fully adequate for FRM purposes 

and is fulfilling that role well. Further, 

the FRM is also well suited for use in 

routine CO monitoring, and several high 

quality FRM analyzer models have been 

available for many years and continue to 

be offered and supported by multiple 

analyzer manufacturers. Finally, EPA 

has determined that no new ambient CO 

measurement technique has become 

available that is superior to the NDIR 

technique specified for the current FRM. 

While EPA believes that the current 

CO FRM is adequate, we also believe 

that the existing CO FRM should be 

improved by implementing updates to 

clarify the language of some provisions, 

to make the format match more closely 

the format of more recently promulgated 

automated FRMs, and to better reflect 

the design and improved performance of 

current, commercially available CO 

FRM analyzers. EPA found that no 

substantive changes were needed to the 

basic NDIR FRM measurement 

principle; therefore, the proposed 

updates are of a very minor, editorial 

nature. However, these proposed 

changes are numerous enough so that 

EPA is proposing to re-promulgate the 

entire CO FRM in appendix C of 40 CFR 

part 50, replacing the existing FRM 

language with revised language. 

2. Proposed Changes to Part 53 

In close association with the proposed 

editorial revision to the CO FRM 

described above, EPA is also proposing 

to update the performance requirements 

for FRM CO analyzers currently 

contained in 40 CFR part 53. These 

requirements were established in the 

1970’s, based primarily on the NDIR CO 

measurement technology available at 

that time. While the fundamental NDIR 

measurement principle, as implemented 

in commercial FRM analyzers, has 

changed little over several decades, 


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FRM analyzer performance has 

improved markedly. Contemporary 

advances in digital electronics, sensor 

technology, and manufacturing 

capabilities have permitted today’s 

NDIR analyzers to exhibit substantially 

improved measurement performance, 

reliability, and operational convenience 

at modest cost. This improved 

instrument performance is not reflected 

in the current performance requirements 

for CO FRM analyzers specified in 40 

CFR part 53, indicating a need for an 

update to reflect that improved 

performance. The updated part 53 

performance requirements would also 

apply to candidate FEM CO analyzers, 

if any new, alternative CO measurement 

technology should be developed. 

As noted previously, the performance 

of FRM analyzers designated under the 

presently specified performance 

requirements of Part 53 is fully adequate 

for current monitoring needs. A review 

of analyzer manufacturers’ 

specifications has determined that all 

existing CO analyzer models currently 

in use in the monitoring network 

already meet the proposed new 

requirements (for the standard 

measurement range). Upgrading the 

analyzer performance requirements to 

be more consistent with the typical 

performance capability available in 

contemporary FRM analyzers would 

ensure that newly designated FRM 

analyzers will have this improved 

measurement performance. Therefore, 

EPA believes that the Part 53 

requirements should be updated to be at 

least commensurate with this typical 

level of CO analyzer performance. In 

addition, this modernization also 

provides for optional, new performance 

requirements applicable to lower, more 

sensitive measurement ranges that 

would support improved monitoring 

data quality in areas of low CO 

concentrations. Accordingly, EPA is 

proposing to amend the performance 

requirements applicable to CO FRMs 

(and any new FEMs) set forth in subpart 

B of 40 CFR part 53, as described in the 

following discussion. 

Subpart B of 40 CFR part 53 

prescribes explicit test procedures to be 

used for testing specified performance 

aspects of candidate FRM and FEM 

analyzers, along with the minimum 

performance requirements that such 

analyzers must meet to qualify for FRM 

or FEM designation. These performance 

requirements are specified in Table B– 

1 of subpart B. Although Table B–1 

covers candidate methods for SO2, O3, 

CO, and NO2, the updates to Table B– 

1 that EPA is now proposing would be 

applicable only to candidate methods 

for CO. 

Some updated performance 

requirements are being proposed for 

candidate CO analyzers that operate on 

the specified ‘‘standard’’ measurement 

range (0 to 50 ppm). This measurement 

range would remain unchanged from 

the existing requirements as it 

appropriately addresses the monitoring 

data needed for assessing attainment. 

However, based on EPA’s review of the 

performance of currently available CO 

FRM analyzers (USEPA, 2010g), EPA is 

proposing revised performance 

requirements for CO analyzers in Table 

B–1, as follows. The measurement noise 

limit would be reduced from 0.5 to 0.2 

ppm, and the lower detectable limit 

would be reduced from 1 to 0.4 ppm. 

Zero drift would be reduced from 1.0 to 

0.5 ppm, and span drift would be 

lowered from 2.5% to 2.0%. The 

existing mid-span drift requirement, 

tested at 20% of the upper range limit 

(URL), would be withdrawn. EPA has 

found that the mid-span drift 

requirement is unnecessary for CO 

instruments because the upper level 

span drift (tested at 80% of the URL) 

completely and much more accurately 

defines analyzer span drift performance. 

EPA proposes to change the lag time 

allowed from 10 to 2 minutes, and the 

rise and fall times from 5 to 2 minutes. 

For precision, EPA proposes to change 

the form of the precision limit 

specifications from an absolute measure 

(ppm) to percent (of the URL) for CO 

analyzers and to set the limit at 1 

percent for both 20% and 80% of the 

URL. One percent is equivalent to the 

existing limit value of 0.5 ppm for 

precision for the standard (50 ppm) 

measurement range. This change in 

units from ppm to percent will make the 

requirement responsive to higher and 

lower measurement ranges (i.e., more 

demanding for lower ranges). 

The interference equivalent limit of 1 

ppm for each interferent would not be 

changed, but EPA proposes to withdraw 

the existing limit requirement for the 

total of all interferents. EPA has found 

that the total interferent limit is 

redundant with the individual 

interferent limit for modern CO 

analyzers. 

These proposed new performance 

requirements would apply only to 

newly designated CO FRM or FEM 

analyzers. Essentially all existing FRM 

analyzers in use today, as noted 

previously, are providing CO 

monitoring data of adequate quality and 

fulfill the proposed requirements. Thus, 

existing FRM analyzers would not be 

required to be re-tested and redesignated under the proposed new 

requirements. All currently designated 

FRM analyzers would retain their 

original FRM designations. 

EPA recognizes that some CO 

monitoring objectives (e.g., area-wide 

monitoring away from major roads and 

rural area surveillance) require 

analyzers with lower, more sensitive 

measurement ranges than the standard 

range used for typical ambient 

monitoring. Part 53 (40 CFR 53.20(b)) 

allows an FRM or FEM designation to 

include lower ranges. To make such 

lower-range measurements more 

meaningful, EPA is proposing a separate 

set of performance requirements that 

would apply specifically to lower ranges 

(i.e., those having a URL of less than 50 

ppm) for CO analyzers. The proposed 

additional, lower-range requirements 

are listed in the proposed revised Table 

B–1. A candidate analyzer that meets 

the Table B–1 requirements for the 

standard measurement range (0 to 50 

ppm) could optionally have one or more 

lower ranges included in its FRM or 

FEM designation by further testing to 

show that it also meets these proposed 

supplemental, lower-range 

requirements. 

Although no substantive changes have 

been determined to be needed to the test 

procedures and associated provisions of 

subpart B for CO, the detailed language 

in many of the subpart B sections is in 

need of significant updates, 

clarifications, refinement, and (in a few 

cases) correction of minor typographical 

errors. EPA believes that these 

provisions should be amended at this 

time in its on-going, pollutant-bypollutant effort to bring the entire 

content of subpart B fully up to date. 

The proposed changes to the subpart 

B text (apart from the changes proposed 

for Table B–1 discussed above) are very 

minor and almost entirely editorial in 

nature, with no changes to the substance 

of the requirements. However, because 

these small changes are quite numerous, 

EPA believes that it is expedient and 

advantageous to propose replacement of 

the subpart B text, in its entirety, with 

the modified text. As discussed 

previously, Table B–1, which sets forth 

the pollutant-specific performance 

limits and was recently amended as 

applicable primarily to SO2 analyzers, 

would be amended at this time only as 

necessary and applicable to CO 

analyzers. EPA intends to amend Table 

B–1 for the remaining pollutant 

methods (O3 and NO2) later, at such 

time as each of those pollutants—along 

with its associated FRM in part 50—is 

addressed specifically. 


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58Spatial scales are defined in 40 CFR part 58 

Appendix D, Section 1.2, where the scales of 

representativeness of most interest for the 

monitoring site types include: 

1. Microscale—Defines the concentration in air 

volumes associated with area dimensions ranging 

from several meters up to about 100 meters. 

2. Middle scale—Defines the concentration 

typical of areas up to several city blocks in size, 

with dimensions ranging from about 100 meters to 

0.5 kilometers. 

3. 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. 

4. Urban scale—Defines concentrations within an 

area of city-like dimensions, on the order of 4 to 50 

kilometers. Within a city, the geographic placement 

of sources may result in there being no single site 

that can be said to represent air quality on an urban 

scale. The neighborhood and urban scales have the 

potential to overlap in applications that concern 

secondarily formed or homogeneously distributed 

air pollutants. 

5. Regional scale—Defines usually a rural area of 

reasonably homogeneous geography without large 

sources, and extends from tens to hundreds of 

kilometers. 

3. Implications for Air Monitoring 

Networks 

As noted previously, existing CO FRM 

analyzers (no CO FEMs are presently 

available) are currently providing 

monitoring data that are adequate for 

the current CO NAAQS. Although EPA 

is proposing to re-promulgate the entire 

CO FRM, the changes are minor, with 

no substantive changes being proposed. 

Thus, this action would have little, if 

any, effect on existing air monitoring 

networks. Similarly, EPA is proposing 

revisions to subpart B of part 53, which 

specifies the testing and performance 

requirements for FRM and FEM 

analyzers. Again, the changes are minor, 

with the exception of the CO analyzer 

performance requirements in Table B–1, 

which EPA is proposing to make more 

consistent with modern CO analyzers 

representative of monitors used in the 

current CO monitoring network. These 

new requirements would be used for 

designation of new CO FRM and FEM 

analyzers. Existing EPA-designated 

FRMs would be unaffected by the 

proposed changes and would continue 

to be designated. As most commercially 

available CO FRM analyzers already 

meet the proposed new performance 

requirements, the cost of new CO 

analyzers that would meet the proposed 

new performance requirements would 

not be increased by the proposed new 

requirements. Therefore, there would be 

no immediate impact on monitoring 

agencies or on their CO monitoring 

networks due to the proposed 

amendments to the CO FRM and the 

associated new performance 

requirements proposed for subpart B. 

In the longer term, the proposed new 

performance requirements would ensure 

that CO network monitors, going 

forward, would maintain their improved 

performance. Monitoring agencies 

would benefit by having greater 

confidence in their CO monitoring data 

quality, particularly at the lower 

ambient levels prevalent in most areas. 

Further, the assurance of increased CO 

data quality in years to come will 

provide better databases to support 

future reviews of the CO NAAQS. 

B. Network Design 

The objectives of an ambient 

monitoring network include the 

collection and dissemination of air 

pollution data to the general public in 

a timely manner, to determine 

compliance with ambient air quality 

standards and the effectiveness of 

emissions control strategies, and to 

provide support for air pollution 

research (40 CFR part 58, appendix D). 

This section on CO network design 

provides background on the monitoring 

network, information on the sources of 

CO, information on factors affecting CO 

emissions, and provides rationale for a 

proposed network design intended to 

support the implementation of the CO 

NAAQS. 

1. Background 

EPA issued the first regulations for 

ambient air quality surveillance, 

codified at 40 CFR part 58, for criteria 

pollutants including CO in 1979 (44 FR 

27558, May 10, 1979). These 1979 

regulations established a monitoring 

network for CO (described in detail in 

the CO Network Review and 

Background document [Watkins and 

Thompson, 2010]) that required two CO 

monitors in urban areas with 500,000 or 

more people. The first of these two 

monitors was a ‘‘peak’’ concentration 

monitor, intended to be located in areas 

‘‘* * * around major traffic arteries and 

near heavily traveled streets in 

downtown areas.’’ The second monitor 

was intended to represent a wider 

geographic area, particularly at 

neighborhood scales ‘‘where 

concentration exposures are significant.’’ 

The 2006 monitoring rule (Revisions to 

Ambient Air Monitoring Regulations, 71 

FR 61236 (October 17, 2006)) removed 

the minimum monitoring requirements 

for the ambient CO monitoring network 

that were promulgated in 1979. 

However, the 2006 monitoring rule 

maintained a requirement that if there 

was ongoing CO monitoring in an area, 

the area must have at least one monitor 

located to measure maximum 

concentration of CO in that area. The 

2006 monitoring rule also included a 

provision requiring the approval of the 

EPA Regional Administrator before any 

existing CO ambient monitors could be 

removed. Finally, the 2006 monitoring 

rule included a requirement for CO 

monitors to be operated at all National 

Core (NCore) multi-pollutant monitoring 

stations; with approximately 80 stations 

projected to have been operational 

nationwide by January 1, 2011 to 

support multi-pollutant monitoring 

objectives. 

An analysis of the available CO 

monitoring network data in the Air 

Quality System (AQS) database shows 

that the network was comprised of 

approximately 345 monitors during 

2009. Information stored in AQS for 

these monitors describes the most 

frequently stated monitor objectives for 

sites in the current CO network as 

assessment of concentrations for general 

population exposure and maximum 

(highest) concentrations at the 

neighborhood scale.58 Approximately 

56 of the monitors operating in 2009 

were at microscale sites, a majority of 

which were likely sites representing 

‘‘peak’’ concentrations which were 

required under the monitoring 

regulations originally promulgated in 

1979, intended to characterize mobile 

source impacts in heavily traveled 

downtown streets or near major arterial 

roads (Watkins and Thompson, 2010). 

The rest of these sites were likely being 

operated to meet objectives including 

NAAQS comparison, to support longterm trend determination, to meet State 

Implementation Plan (SIP) and 

maintenance plan requirements, and to 

support ongoing health studies. 

2. On-Road Mobile Sources 

The REA for this review notes that 

‘‘motor vehicle emissions continue to be 

important contributors to ambient CO 

concentrations’’ (REA, section 2.2). 

Microenvironments influenced by onroad mobile sources are important 

contributors to ambient CO exposures, 

particularly in urban areas (REA, section 

2.7), as indicated by personal exposure 

studies that have generally shown that 

the highest ambient CO exposure levels 

occur while people are in transit in 

motor vehicles (ISA, section 2.3). 

Mobile sources are the primary 

contributors to ambient CO emissions 

because CO is formed by incomplete 

combustion of carbon-containing fossil 

fuels widely used in motor vehicles 

(ISA, section 2.1; REA, section 3.3). 

Further, spark-ignition engines (gasoline 

or light-duty engines) have higher CO 

emission rates than diesel engines 

(heavy-duty engines) because they 

typically operate closer to the 

stoichiometric air-to-fuel ratio, have 


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relatively short residence times at peak 

combustion temperatures, and have very 

rapid cooling of cylinder exhaust gases 

(ISA, section 3.2.1). 

Ambient CO concentrations have 

significantly declined over the past 20 

years, reflecting reductions in on-road 

vehicle emissions, as described in 

section II.A above. Overall, based on the 

2002 National Emissions Inventory 

(NEI), on-road mobile sources account 

for approximately 52% of total CO 

emissions. Based on the more recent 

2005 NEI, the contributions of on-road 

mobile sources has now risen to 

approximately 60% of the total CO 

emissions inventory (not counting 

wildfire emissions) (http:// 

www.epa.gov/ttn/chief/ 

eiinformation.html). As described in 

section II.A above, in some metropolitan 

areas in the U.S., as much as 75% of all 

CO emissions result from on-road 

vehicle exhaust (ISA, section 2.1). 

On-road vehicle CO emission rates 

vary depending on operating conditions, 

such as cold-start conditions and 

operating speed. Under cold start 

conditions, which only last for the first 

minutes of vehicle operation, CO 

emissions are higher due to temporary 

ineffectiveness of vehicle exhaust 

catalysts until they are heated to 

optimal operating temperatures (ISA, 

section 3.2.1; Singer et al., 1999). 

Meanwhile, CO emissions also vary 

based on vehicle operating speeds. 

Increased CO emissions occur under 

conditions of high acceleration, rapid 

speed fluctuations, and heavy vehicle 

loads (ISA, section 3.2.1). Studies have 

found that CO emission rates for tested 

light-duty vehicles are highest for 

accelerating vehicles, second highest for 

vehicles in cruise, third highest for 

vehicles under deceleration, and fourth 

highest (of four operating speed related 

categories) for vehicles at idle (Frey et 

al., 2003). High acceleration and rapid 

speed fluctuations (such as acceleration 

and deceleration occurring over a short 

time period) can be associated with 

congested, stop-and-go traffic 

conditions. 

3. Near-Road Environment 

Information in the ISA and other peerreviewed literature suggest that 

concentrations of mobile source 

pollutants, such as CO, typically display 

peak concentrations on or immediately 

adjacent to roads, typically producing a 

gradient in pollutant concentrations 

where concentrations decrease with 

increasing distance from roads (ISA, 

section 2.3; ISA, section 3.5.1.3; Baldauf 

et al., 2008; Clements et al., 2009; 

Karner et al., 2010; Zhou and Levy, 

2008; Zhu et al., 2002). CO is emitted by 

on-road mobile sources, and is not 

secondarily formed in the near-road 

environment like NO2 (which is both 

primarily emitted and secondarily 

formed in the near-road environment). 

As a result, the near-road gradient for 

CO can be quite steep, where 

concentrations rapidly decay with 

increasing distance away from the road 

when compared to other mobile source 

pollutants such as NO2. Karner et al. 

(2010), synthesized findings from 41 

near-road pollutant monitoring studies 

ranging from 1978 through June 2008 to 

advance the understanding of on-road 

mobile source pollutant dispersion. 

They performed two regression 

analyses, one being a local regression of 

background normalized concentrations 

on distance, and the second being a 

local regression of edge [of road] 

normalized concentrations on distance. 

These analyses found CO to have the 

highest approximate edge-of-road peaks, 

as much as 21 times background 

concentrations, of all pollutants 

analyzed, and also showed CO to have 

one of the fastest decay rates with 

increasing distance from the road, 

showing as much as a 90 percent drop 

in concentration 150 meters from the 

edge of the road. A key reason in the 

difference in decay rate with increasing 

distance from roads between CO and 

NO2 is due to how the two pollutants 

are introduced into the near-road 

environment. CO is a primary emission 

from motor vehicle fuel combustion, 

while NO2 is both emitted as a primary 

emission and secondarily formed in the 

near-road environment. The Integrated 

Science Assessment for Oxides of 

Nitrogen—Health Criteria (NOX ISA; 

USEPA, 2008d) notes that the direct 

emission of NO2 from mobile sources is 

estimated to be only a few percent of the 

total NOX emissions for light duty 

gasoline vehicles, and from less than 10 

percent up to 70 percent of the total 

NOX emission from heavy duty diesel 

vehicles, depending on the engine, the 

use of emission control technologies 

such as catalyzed diesel particulate 

filters (CDPFs), and mode of vehicle 

operation. Although much of the NOX

emissions are initially in the form of 

NO, the rate of conversion of NO to NO2

is generally a rapid process (i.e., on the 

order of a minute) (NOX ISA, section 

2.2.2). Thus, more of the NO2 in the 

near-road environment is a result of 

secondary formation than from primary 

emissions, while CO is almost 

exclusively a result of direct emissions 

from tailpipes. 

Overall, the literature suggests that 

CO concentrations generally return to 

near-background levels within a few 

hundred meters from the road (Karner et 

al., 2010; Zhou and Levy, 2007). The 

actual concentrations of CO, and other 

mobile source pollutants such as NOX

and particulate matter, that occur in the 

near-road environment, and the rate of 

decay of those pollutant concentrations 

with increasing distance from the road, 

are dependent on a number of variables 

including traffic volume, traffic fleet 

mix, roadway type, roadway design, 

surrounding features, topography (or 

terrain), and meteorology (Baldauf et al., 

2009; Baldauf et al., 2008; Clements et 

al., 2009; Hagler et al., 2010; Heist et al., 

2009). EPA notes that these factors were 

taken into account in the requirements 

for the near-road NO2 monitoring 

network, promulgated in February 2010 

(75 FR 6474), which required near-road 

NO2 sites to be selected with 

consideration given to traffic volume 

(via use of Annual Average Daily Traffic 

[AADT] counts), fleet mix, congestion 

patterns, roadway design, terrain, and 

meteorology. 

4. Urban Downtown Areas and Urban 

Street Canyons 

As noted above in section IV.B.2, 

increased CO emissions occur under 

operating conditions of high 

acceleration, rapid speed fluctuations 

(such as acceleration and deceleration 

occurring over a short time period), and 

increased vehicle loads (ISA, section 

3.2.1). High acceleration and rapid 

speed fluctuations can be associated 

with congested traffic conditions, such 

as stop-and-go traffic, which can occur 

on heavily trafficked roads such as 

highways, freeways, and along major 

arterial roads, and also along roads with 

multiple intersections in relatively close 

proximity to each other. Thus, elevated 

CO concentrations, relative to 

surrounding background concentrations, 

can occur not only along heavily 

trafficked roads but also may be found 

in urban downtown areas, where a 

relatively higher number of roads exist 

in an area (high density of roads per 

unit area) and a relatively higher density 

of roadway intersections exist in an area 

(high roadway intersection per unit 

area), which can lead to increased 

occurrences of vehicles operating under 

modes of high acceleration and/or rapid 

speed fluctuations. Even though streets 

in urban downtown areas may not 

individually carry as much traffic as 

larger highways, freeways, or major 

arterials, the impact of many relatively 

smaller streets in close proximity 

carrying traffic experiencing periods of 

high acceleration and/or rapid speed 

fluctuations, or congested traffic, may 

collectively contribute to elevated CO 

concentrations in that downtown area. 


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59A natural canyon may be defined as a ‘‘deep 

narrow valley with steep sides’’ (http:// 

www.merriam-webster.com/dictionary/canyon). 

In addition to traffic undergoing 

periods of high acceleration and/or 

rapid speed fluctuations or experiencing 

general traffic congestion, urban 

downtown areas often have a number of 

relatively tall buildings, typically in 

close proximity to each other. Such 

configurations of tall buildings in 

relatively close proximity often create 

urban features called urban canyons or 

urban street canyons. Although the term 

urban canyon, or urban street canyon, is 

not formally defined, it can generally be 

described as an urban feature, 

resembling a natural canyon 59, where 

streets or roads exist within dense 

blocks of relatively tall buildings. These 

urban features are of interest because, as 

noted in the ISA, recent research by 

Kaur and Nieuwenhuijsen (2009), and 

Carlaw et al. (2007), suggest CO 

concentrations are related to traffic 

volume and fleet mix in the urban street 

canyon environment, which can 

influence potential exposures. EPA has 

had monitoring requirements in the past 

that characterized concentrations of CO 

in heavily trafficked downtown streets, 

i.e. ‘‘urban street canyons,’’ (Watkins and 

Thompson, 2010), and notes such 

locations may have still have relevance 

going forward. 

5. Meteorological and Topographical 

Influences 

In 2003, the National Research 

Council (NRC) of the National 

Academies published a document titled 

Managing Carbon Monoxide Pollution 

in Meteorological and Topographical 

Problem Areas. This report noted how 

drastically ambient CO concentrations 

had dropped across the country from 

the 1970s through the early 2000s, and 

that some of the remaining areas of the 

country that continued to have 

relatively high concentrations tended to 

have meteorological and topographical 

characteristics that exacerbate pollution. 

In particular, meteorological impacts 

can concentrate pollutant build-up in an 

area due to atmospheric inversions and 

cold temperatures. Atmospheric 

inversions essentially prevent pollutant 

emissions in an area from dispersing 

through vertical mixing. As explained 

by the NRC (NRC, 2003), the extent to 

which air mixes vertically depends on 

how the air temperature changes with 

altitude. Warm air is less dense than 

cold air and thus more buoyant, 

allowing surface air to mix upward as 

relatively warmer air rises in the 

atmosphere. However, if the vertical 

temperature profile is such that 

temperatures decrease more slowly than 

normal, or increase with height, vertical 

mixing is inhibited. Inversions can be 

caused by several different specific 

phenomena, including surface based 

cooling (for example, due to snow on 

the ground), due to high altitudes, and 

sometimes due to warm air advection at 

higher altitudes. 

The topographical impacts that can 

lead to pollutant build-up in an area are 

typically due to physical terrain features 

that may aid in trapping pollution in an 

area and/or contribute to meteorological 

related inversions. An example of 

topographical impacts might be an 

urban area within a valley, or 

surrounded on several sides by 

mountain ranges. In such a case, 

pollutant dispersion is inhibited in the 

horizontal, with terrain features 

effectively preventing mixing or 

transport of pollution from a given area. 

Further, in some cases both 

meteorological and topographical 

impacts can combine to exacerbate 

pollutant build-up, such as in an area 

partially surrounded by high terrain 

which is also subject to inversions. 

Although there is available 

information on what can cause 

increased potential for air pollutant 

build-up due to meteorological and 

topographical impacts, there are no 

easily defined or applied criteria that 

could be implemented nationally by 

which all such locations could be 

identified. Identification of such 

locations would require a case-by-case 

approach, where localized and detailed 

information on terrain and meteorology 

would be needed, plus an 

understanding of the types and amounts 

of emission sources in or around any 

particular area. 

6. Proposed Changes 

Although EPA is proposing to retain 

the current 8-hour and 1-hour CO 

NAAQS, as discussed above in section 

II, the Agency is proposing to revise the 

requirements for the ambient CO 

monitoring network to include a 

minimum set of monitors to collect data 

for comparison to the NAAQS in nearroadway locations where CO emissions 

associated with mobile source related 

activity lead to increased ambient 

concentrations. The current network of 

CO monitors, beyond those at NCore 

sites, consists of monitors that were 

established to meet the 1979 monitoring 

rule requirements or which were placed 

by State and local air monitoring 

agencies to meet their own needs or 

objectives. These additional monitors in 

the current network are being operated 

without being required under EPA 

monitoring network regulations and as a 

result, they do not reflect a national 

monitoring network design. In CASAC 

comments on the second draft REA, the 

CASAC panel, aware of the current CO 

monitoring network configuration, 

commented on the need to reconsider 

CO monitoring network designs, stating 

that ‘‘ * * * the approach for siting [CO] 

monitors needs greater consideration. 

More extensive coverage may be 

warranted for areas where 

concentrations may be more elevated, 

such as near roadway locations’’ (Brain 

and Samet, 2010b). Since there is a 

strong relationship between CO 

exposures and mobile source activity, as 

described in the ISA and REA and 

summarized in sections II.D.2 and 

IV.B.2 above, primarily in the near-road 

environment, EPA believes that some 

CO monitors should be located near onroad mobile source activity, where 

ambient concentrations are expected to 

be more elevated, as noted by CASAC. 

Accordingly, EPA is proposing to 

require locating ambient CO monitors 

which would produce data for 

comparison to both the 8-hour and 1- 

hour NAAQS at a subset of near-road 

NO2 monitoring stations, which are 

required under the Primary National 

Ambient Air Quality Standards for 

Nitrogen Dioxide; Final Rule (75 FR 

6474), codified at 40 CFR part 58, 

appendix D. This requirement would 

support the objective of characterizing 

ambient conditions at highly trafficked 

near-road locations where elevated CO 

concentrations (relative to surrounding 

background concentrations) are 

expected to occur. 

The EPA is not proposing to require 

dedicated CO monitoring sites to 

characterize area-wide concentrations 

representing neighborhood and larger 

spatial scales. Based on a recent review 

of the current CO monitoring network 

(Watkins and Thompson, 2010), EPA 

believes that the required NCore sites 

and many of the existing monitoring 

sites in the network provide data 

representative of neighborhood and 

larger spatial scales. These monitors are 

useful in providing relative background 

concentrations that, when compared to 

near-road CO monitors, could aid in the 

quantification of the near-road gradient 

of CO in a given urban area. Between 

the required NCore sites, and an 

expectation based on experience that 

some number of non-required area-wide 

sites will continue to operate in the 

future, we do not believe it is necessary 

to propose a specific area-wide 

monitoring requirement in this 

rulemaking. 

EPA believes that the proposed 

network design which places CO 

monitors at a subset of near-road NO2


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60The EPA’s strategy encouraging multi-pollutant 

monitoring is presented most recently in the 

Ambient Air Monitoring Strategy for State, Local, 

and Tribal Air Agencies document published 

December 2008 (http://www.epa.gov/ttn/amtic/ 

files/ambient/monitorstrat/ 

AAMS%20for%20SLTs%20%20- 

%20FINAL%20Dec%202008.pdf). 

61The near-road NO2 monitoring stations, which 

are proposed to house required CO monitors, shall 

monitoring stations, as described in 

detail in the following sections, will 

require a relatively modest amount of 

new resources by State and local air 

agencies. Recalling that there were 

approximately 345 CO monitors 

operating in 2009, which were largely 

discretionary monitors not operated 

pursuant to Federal network design 

requirements, the Agency believes that 

a large majority of State and local air 

agencies could meet the proposed 

minimum monitoring requirements by 

relocating an existing CO monitor to a 

near-road NO2 monitoring station. In 

some of these cases, the EPA believes 

that the relocation of a CO monitor from 

an existing stand-alone site to a multipollutant near-road NO2 site may also 

result in additional operational cost 

savings as, in some areas, the total 

number of ambient monitoring sites for 

which operational support is needed 

could be reduced. 

The EPA believes that the proposed 

requirement for placing CO monitors at 

some of the forthcoming near-road NO2

monitoring stations would provide an 

important benefit by facilitating the 

implementation of a more targeted 

ambient CO monitoring network that 

provides data for comparison to the 

NAAQS, and is considerably smaller 

than the CO network currently in 

operation. EPA notes that under the 

current regulation, the current CO 

network is subject to a potentially 

significant reduction in size (as detailed 

in Watkins and Thompson, 2010) since 

non-required CO monitoring stations 

can be shut down upon State request, an 

evaluation of historical data to evaluate 

concentrations relative to the NAAQS 

(per 40 CFR 58.14), and EPA Regional 

Administrator approval. The occurrence 

of such a reduction, however, would 

lack the focus and direction needed to 

ensure retention of a network with the 

surveillance aspects essential to 

supporting the implementation of the 

CO NAAQS. In addition to ensuring that 

an effective, modestly sized network 

shall operate in the future, other 

benefits of the proposed approach of colocating required CO monitors at 

required near-road NO2 monitoring 

stations include: ongoing comparison of 

data to the NAAQS (for assessing 

attainment), providing data that can 

support health studies, providing data 

that can be used in verification of 

modeling results, and supporting the 

implementation of the Agency’s multipollutant monitoring objectives.60

a. Monitoring for Carbon Monoxide at 

Required Near-Road Nitrogen Dioxide 

Monitoring Stations 

Traffic volume on urban area roads is 

much greater than in the more rural 

areas of the country, as was noted in the 

preamble to the final rule to the NO2

NAAQS (75 FR 6474). The U.S. 

Department of Transportation Federal 

Highway Administration’s Status of the 

Nation’s Highways, Bridges, and 

Transit: 2008 Conditions and 

Performance document (http:// 

www.fhwa.dot.gov/policy/2008cpr/ 

es.htm#c2b) states that ‘‘while urban 

mileage constitutes only 25.8 percent of 

total (U.S.) mileage, these roads carried 

66.3 percent of the 3 trillion vehicles 

miles travelled (VMT) in the United 

States in 2006.’’ The document also 

states that urban interstate highways 

made up only 0.8 percent of total (U.S.) 

mileage but carried 16.3 percent of total 

VMT. 

The EPA notes that the 2007 

American Housing Survey (http:// 

www.census.gov/hhes/www/housing/ 

ahs/ahs07/ahs07.html) estimates that 

over 20 million housing units are within 

300 feet (∼91 meters) of a 4-lane 

highway, airport, or railroad. Using the 

same survey, and considering that the 

average number of residential occupants 

in a housing unit is approximately 2.25, 

it is estimated that at least 45 million 

American citizens live near 4-lane 

highways, airports, or railroads. Among 

these three transportation facilities, 

roads are the most pervasive of the 

three, suggesting that a significant 

number of people may live near major 

roads. Furthermore, the 2008 American 

Time Use Survey (http://www.bls.gov/ 

tus/) reported that the average U.S. 

civilian spent over 70 minutes traveling 

per day, and as recognized in section 

II.D.2.b, the exposure and dose 

assessment for this review found invehicle microenvironments to be those 

with the highest ambient CO exposures. 

Additionally, as described in the ISA, 

PA and the REA, higher concentrations 

are reported at locations immediately 

near or on roadways as compared to 

monitors somewhat removed from the 

roadways (ISA, section 3.6; PA, section 

2.2.1; REA, section 2.7). These locations 

capture ambient concentrations that 

contribute to ambient exposure 

concentrations occurring in vehicles. 

Accordingly, EPA believes that air 

pollution monitors near major roads 

will provide information pertaining to a 

significant component of ambient CO 

exposure for a large portion of the 

population that would otherwise not be 

available. 

The EPA recognizes the information 

mentioned above regarding the 

dominant role of mobile sources in the 

national CO emission inventory 

(discussed in section IV.B.2 above), 

findings of the substantial near-road 

concentration gradient, with elevated 

CO concentrations in the near-road 

environment compared to relative 

background concentrations (discussed 

in section IV.B.3 above), and the 

importance of on-road mobile sources as 

contributors to ambient CO exposures 

particularly in urban areas (REA, section 

2.7). We also note that (as referenced 

above) CASAC indicated that additional 

monitoring near roadways may be 

warranted, and further stated ‘‘the Panel 

found in some instances current 

networks underestimated carbon 

monoxide levels near roadways. Such 

underestimation is a critical issue 

***’’ (Brain and Samet, 2010b). In 

light of this information, and the fact 

that we generally expect the increased 

levels of ambient CO (and the greatest 

exposure to ambient CO) to occur nearroadways, EPA has determined that it is 

appropriate to propose requiring CO 

monitoring near heavily trafficked roads 

in urban areas. 

EPA additionally notes that near-road 

NO2 monitoring sites will be placed 

near highly trafficked roads in urban 

areas, where elevated CO concentrations 

due to on-road mobile sources are 

known to occur, and that CASAC has 

recommended that EPA establish a nearroad monitoring network that would 

include sites with both NO2 and CO 

monitors (Russell and Samet, 2010). 

Accordingly, the EPA is proposing to 

require CO monitors that will provide 

data for comparison to the NAAQS to 

operate at a subset of required near-road 

NO2 monitoring stations, which are 

required in 40 CFR part 58, appendix D. 

Specifically, the EPA is proposing that 

CO monitors be required in any required 

near-road NO2 monitoring station in a 

core based statistical area (CBSA) with 

a population of 1,000,000 or more 

persons. Based on 2009 U.S. Census 

estimates (http://www.census.gov) and 

Federal Highway Administration data 

(http://www.fhwa.dot.gov/ 

policyinformation/tables/02.cfm) 

applied to near-road NO2 network 

design requirements (noted above), 

there would be approximately 77 CO 

monitoring sites required within nearroad NO2 monitoring stations within 53 

CBSAs (including San Juan, PR).61


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be selected per considerations spelled out in 40 

CFR part 58, Appendix D, section 4.3.2(a)(1), which 

prescribes site selection by ranking all road 

segments in a CBSA by AADT and then identifying 

a location or locations adjacent to those highest 

ranked road segments, considering fleet mix, 

roadway design, congestion patterns, terrain, and 

meteorology. 

In this proposal, EPA concludes that, 

given the strong relationship between 

CO exposures and mobile source 

activity, placing CO monitors at nearroad NO2 monitoring sites (which will 

be near highly trafficked roads in urban 

areas) is needed to fulfill the ambient 

CO monitoring objectives identified in 

section IV.B above. While having two 

monitors within CBSAs of 500,000 or 

more persons was the historical 

monitoring requirement (discussed in 

detail in Watkins and Thompson, 2010), 

with declining ambient levels we 

believe there is less likelihood for high 

CO concentrations in relatively smaller 

(in population) CBSAs. Accordingly, we 

believe that proposing to require CO 

monitoring only in near-road NO2

monitoring stations in CBSAs of 

1,000,000 or more persons is a 

reasonable approach that results in a 

sufficient number of CO monitors near 

highly trafficked roads in urban areas to 

provide data for supporting the NAAQS, 

for use in health studies, for model 

validation, and to support multipollutant monitoring objectives. The 

EPA solicits comment upon the 

proposed requirement to require CO 

monitors to operate within a subset of 

required near-road NO2 monitoring 

stations, specifically those in CBSAs 

with 1,000,000 or more persons. The 

EPA solicits comment on using 

alternative population thresholds within 

which CO monitors might be required to 

operate in near-road NO2 monitoring 

stations, e.g. CBSAs with 750,000 or 

500,000 or more persons (which would 

require approximately 92 and 126 

monitors, respectively), in light of the 

proposal to retain the existing CO 

NAAQS. Finally, the EPA also solicits 

comment on the merits of having any 

minimum near-road monitoring 

requirements for the CO monitoring 

network. 

b. Regional Administrator Authority 

The EPA is proposing to include a 

provision allowing the Regional 

Administrators to have the discretion to 

require monitoring above the minimum 

requirements as necessary to address 

situations where minimum monitoring 

requirements are not sufficient to meet 

monitoring objectives presented above 

in section IV.B.1. The EPA recognizes 

that minimum monitoring requirements 

may not always result in a network 

sufficient to fulfill one or more data 

needs or monitoring objectives for a 

particular area. An example of when an 

EPA Regional Administrator might 

require an additional monitor above the 

minimum requirements is to address a 

situation where data or other 

information suggest that a stationary CO 

source may be contributing to ground 

level concentrations that are 

approaching or exceeding the NAAQS. 

A second example of where an EPA 

Regional Administrator might require 

additional monitoring is in otherwise 

unmonitored urban downtown areas or 

urban street canyons (as discussed 

above in section IV.B.4), where data or 

other information suggest CO 

concentrations may be approaching or 

exceeding the NAAQS. A third example 

of where an EPA Regional 

Administrator might require additional 

monitoring is in unmonitored areas that 

are subject to high ground level CO 

concentrations particularly due to or 

enhanced by topographical and 

meteorological impacts, as discussed in 

section IV.B.5 above. In all cases, the 

Regional Administrator and the 

responsible State or local air monitoring 

agency should work together to design 

and/or maintain the most appropriate 

CO network to service monitoring 

objectives and any particular variety of 

data needs for an area. 

c. Required Network Implementation 

EPA proposes that state and, when 

appropriate, local air monitoring 

agencies provide a plan for deploying 

required CO monitors by July 1, 2012. 

We also propose that the ambient CO 

monitoring network be physically 

established no later than January 1, 

2013. These dates correspond with the 

implementation schedule of the 

required near-road NO2 sites, which are 

the same locations at which CO 

monitors have been proposed to be 

placed. EPA solicits comment on these 

proposed implementation dates. 

7. Microscale Carbon Monoxide Monitor 

Siting Criteria 

Carbon monoxide monitors that are 

proposed to operate at near-road NO2

sites would likely be classified as 

microscale-type sites, per the general 

definition of microscale sites in 40 CFR 

part 58, appendix D, section 1.2. Such 

CO monitors would be paired with NO2

monitors required to have inlet probe 

heights between 2 and 7 meters, and be 

placed within 50 meters of a target road 

segment. However, when the original 

minimum monitoring requirements for 

CO were introduced in the 1979 

monitoring rule (44 FR 27571), the 

siting criteria codified for microscale CO 

sites was specifically intended to 

account for the installation of a nearroad site in street canyon or street 

corridor locations. The specific siting 

criteria for microscale CO sites, 

currently located at 40 CFR part 58, 

appendix E, section 6.2, and listed in 

Table E–4 of appendix E, state that ‘‘the 

inlet probes for microscale carbon 

monoxide monitors that are being used 

to measure concentrations near 

roadways must be between 2.5 and 3.5 

meters above ground level.’’ Likewise, 

criteria currently located at 40 CFR part 

58, appendix E, section 6.2, and listed 

in Table E–4 of appendix E state that 

microscale CO monitors are to be 

between 2 and 10 meters from the edge 

of the nearest traffic lane. These siting 

criteria, originally developed in 1979, 

were for use primarily in the urban 

downtown and urban street canyon 

environment. In that type of urban 

environment, such specific and 

relatively tight siting criteria were, and 

still are, appropriate since there is often 

little space within which ambient air 

monitoring inlets can be accommodated 

due to the typical dense configuration of 

buildings. However, outside of the 

urban downtown and urban street 

canyon environment, such criteria may 

be less applicable, considering site 

placement logistics and site safety for 

monitoring near the major highways, 

freeways, interstates, and major arterials 

that carry so much of today’s urban 

traffic volume. 

As noted above, the intent of existing 

microscale CO siting criteria reflects the 

historical intent of monitoring in urban 

downtown areas and urban street 

canyons. Since EPA is proposing that 

CO monitors be required to operate at a 

subset of near-road NO2 sites to 

characterize roadway pollutant 

concentrations the majority of which are 

not anticipated to be in urban street 

canyons, EPA has revisited the 

appropriateness of the existing 

microscale CO siting requirement, 

particularly for near-road sites that exist 

outside of the downtown urban areas 

and urban street canyons. EPA 

consulted on this issue with the CASAC 

Ambient Air Monitoring and Methods 

Subcommittee (CASAC–AAMMS) in 

September, 2010. Specifically, EPA 

requested feedback on whether it would 

be appropriate to revise existing 

microscale CO siting criteria to match 

those of near-road NO2 monitors and 

microscale PM2.5 monitors. In their 

response to EPA, the CASAC–AAMMS 

recommended ‘‘that sampling criteria for 

CO and other monitors at sites installed 

to monitor [at] near-road NO2 [sites] 

match those for NO2.’’ The CASAC– 


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AAMMS also noted that ‘‘sampling 

configurations of existing microscale CO 

monitors should be assessed in terms of 

their own sampling objectives, and need 

not necessarily conform to those of nearroad NO2 monitors’’ (Russell and Samet, 

2010). 

Based in part on the CASAC–AAMMS 

comments above, EPA believes that it is 

appropriate to revise the existing siting 

criteria for microscale CO monitors to 

encompass both the current criteria, 

which are still appropriate when 

monitoring in the urban downtown and/ 

or urban street canyon environment, as 

well as the criteria for near-road NO2

sites. Therefore, EPA is proposing that 

microscale CO siting criteria for probe 

height and horizontal spacing be 

changed to match those of near-road 

NO2 sites as prescribed in 40 CFR part 

58 appendix E, sections 2, 4(d), 6.4(a), 

and Table E–4. Specifically, EPA 

proposes to allow microscale CO 

monitor inlet probes to be between 2 

and 7 meters above the ground; that CO 

monitor inlet probes be placed so they 

have an unobstructed air flow, where no 

obstacles exist at or above the height of 

the monitor probe, between the monitor 

probe and the outside nearest edge of 

the traffic lanes of the target road 

segment; and that the CO monitor inlet 

probe shall be as near as practicable to 

the outside nearest edge of the traffic 

lanes of the target road segment, but 

shall not be located at a distance greater 

than 50 meters in the horizontal from 

the outside nearest edge of the traffic 

lanes of the target road segment. 

These proposed siting criteria 

encompass, or bracket, the current 

allowable vertical and horizontal 

spacing criteria for microscale CO sites, 

which will allow current microscale CO 

sites to continue to meet siting criteria. 

EPA believes the proposed revision to 

the microscale CO siting criteria 

presented above will allow States to 

meet siting criteria while co-locating 

required microscale CO monitors with 

required near-road NO2 monitors near 

heavily trafficked roads outside of urban 

downtown areas and urban street 

canyons. EPA solicits comment upon 

the revised CO siting requirements 

proposed above. The Agency also 

solicits comment upon whether it 

should create two distinct sets of siting 

criteria for microscale CO monitoring. 

One set of siting criteria would be those 

proposed above, while the second set 

would be the current siting criteria, but 

directed specifically to apply to existing 

or new microscale CO monitoring sites 

located in downtown urban areas and 

urban street canyons. 

V. Statutory and Executive Order 

Reviews 

A. Executive Order 12866: Regulatory 

Planning and Review 

Under Executive Order 12866 (58 FR 

51735, October 4, 1993), this action is a 

‘‘significant regulatory action’’ because it 

was deemed to ‘‘raise novel legal or 

policy issues.’’ Accordingly, EPA 

submitted this action to the Office of 

Management and Budget (OMB) for 

review under Executive Order 12866 

and any changes made in response to 

OMB recommendations have been 

documented in the docket for this 

action. 

B. Paperwork Reduction Act 

The information collection 

requirements in this final rule have been 

submitted for approval to the Office of 

Management and Budget (OMB) under 

the Paperwork Reduction Act, 44 U.S.C. 

3501 et seq. The information collection 

requirements are not enforceable until 

OMB approves them. The Information 

Collection Request (ICR) document 

prepared by EPA for these revisions to 

part 58 has been assigned EPA ICR 

number 0940.23. 

The information collected under 40 

CFR part 53 (e.g., test results, 

monitoring records, instruction manual, 

and other associated information) is 

needed to determine whether a 

candidate method intended for use in 

determining attainment of the National 

Ambient Air Quality Standards 

(NAAQS) in 40 CFR part 50 will meet 

comparability requirements for 

designation as a Federal reference 

method (FRM) or Federal equivalent 

method (FEM). We do not expect the 

number of FRM or FEM determinations 

to increase over the number that is 

currently used to estimate burden 

associated with CO FRM/FEM 

determinations provided in the current 

ICR for 40 CFR part 53 (EPA ICR 

numbers 0940.23). As such, no change 

in the burden estimate for 40 CFR part 

53 has been made as part of this 

rulemaking. 

The information collected and 

reported under 40 CFR part 58 is needed 

to determine compliance with the 

NAAQS, to characterize air quality and 

associated health impacts, to develop 

emissions control strategies, and to 

measure progress for the air pollution 

program. The amendments would revise 

the technical requirements for CO 

monitoring sites, require the relocation 

or siting of ambient CO air monitors, 

and the reporting of the collected 

ambient CO monitoring data to EPA’s 

Air Quality System (AQS). The annual 

average reporting burden for the 

collection under 40 CFR part 58 

(averaged over the first 3 years of this 

ICR) for a network of 311 CO monitors 

is $7,235,483. Burden is defined at 5 

CFR 1320.3(b). State, local, and Tribal 

entities are eligible for State assistance 

grants provided by the Federal 

government under the CAA which can 

be used for monitors and related 

activities. 

An agency may not conduct or 

sponsor, and a person is not required to 

respond to, a collection of information 

unless it displays a currently valid OMB 

control number. The OMB control 

numbers for EPA’s regulations in 40 

CFR are listed in 40 CFR part 9. 

To comment on the Agency’s need for 

this information, the accuracy of the 

provided burden estimates, and any 

suggested methods for minimizing 

respondent burden, EPA has established 

a public docket for this rule, which 

includes this ICR, under Docket ID 

number EPA–HQ–OAR–2008–0015. 

Submit any comments related to the ICR 

to EPA and OMB. See ADDRESSES

section at the beginning of this notice 

for where to submit comments to EPA. 

Send comments to OMB at the Office of 

Information and Regulatory Affairs, 

Office of Management and Budget, 725 

17th Street, NW, Washington, DC 20503, 

Attention: Desk Office for EPA. Since 

OMB is required to make a decision 

concerning the ICR between 30 and 60 

days after February 11, 2011, a comment 

to OMB is best assured of having its full 

effect if OMB receives it March 14, 

2011. The final rule will respond to any 

OMB or public comments on the 

information collection requirements 

contained in this proposal. 

C. Regulatory Flexibility Act 

The Regulatory Flexibility Act (RFA) 

generally requires an agency to prepare 

a regulatory flexibility analysis of any 

rule subject to notice and comment 

rulemaking requirements under the 

Administrative Procedure Act or any 

other statute unless the agency certifies 

that the rule will not have a significant 

economic impact on a substantial 

number of small entities. Small entities 

include small businesses, small 

organizations, and small governmental 

jurisdictions. 

For purposes of assessing the impacts 

of today’s proposed rule on small 

entities, small entity is defined as: (1) A 

small business that is a small industrial 

entity as defined by the Small Business 

Administration’s (SBA) regulations at 13 

CFR 121.201; (2) a small governmental 

jurisdiction that is a government of a 

city, county, town, school district or 

special district with a population of less 

than 50,000; and (3) a small 


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organization that is any not-for-profit 

enterprise which is independently 

owned and operated and is not 

dominant in its field. 

After considering the economic 

impacts of this proposed rule on small 

entities, I certify that this action will not 

have a significant economic impact on 

a substantial number of small entities. 

This proposed rule will not impose any 

requirements on small entities. Rather, 

this rule proposes to retain existing 

national standards for allowable 

concentrations of CO in ambient air as 

required by section 109 of the CAA. See 

also American Trucking Associations v. 

EPA. 175 F. 3d at 1044–45 (NAAQS do 

not have significant impacts upon small 

entities because NAAQS themselves 

impose no regulations upon small 

entities). Similarly, the proposed 

amendments to 40 CFR part 58 address 

the requirements for States to collect 

information and report compliance with 

the NAAQS and will not impose any 

requirements on small entities. We 

continue to be interested in the 

potential impacts of the proposed rule 

on small entities and welcome 

comments on issues related to such 

impacts. 

D. Unfunded Mandates Reform Act 

Title II of the Unfunded Mandates 

Reform Act of 1995 (UMRA), Public 

Law 104–4, establishes requirements for 

Federal agencies to assess the effects of 

their regulatory actions on State, local, 

and Tribal governments and the private 

sector. Unless otherwise prohibited by 

law, under section 202 of the UMRA, 

EPA generally must prepare a written 

statement, including a cost-benefit 

analysis, for proposed and final rules 

with ‘‘Federal mandates’’ that may result 

in expenditures to State, local, and 

Tribal governments, in the aggregate, or 

to the private sector, of $100 million or 

more in any one year (adjusted for 

inflation). Before promulgating an EPA 

rule for which a written statement is 

required under section 202, section 205 

of the UMRA generally requires EPA to 

identify and consider a reasonable 

number of regulatory alternatives and to 

adopt the least costly, most costeffective or least burdensome alternative 

that achieves the objectives of the rule. 

The provisions of section 205 do not 

apply when they are inconsistent with 

applicable law. Moreover, section 205 

allows EPA to adopt an alternative other 

than the least costly, most cost-effective 

or least burdensome alternative if the 

Administrator publishes with the final 

rule an explanation why that alternative 

was not adopted. Before EPA establishes 

any regulatory requirements that may 

significantly or uniquely affect small 

governments, including Tribal 

governments, it must have developed 

under section 203 of the UMRA a small 

government agency plan. The plan must 

provide for notifying potentially 

affected small governments, enabling 

officials of affected small governments 

to have meaningful and timely input in 

the development of EPA regulatory 

proposals with significant Federal 

intergovernmental mandates, and 

informing, educating, and advising 

small governments on compliance with 

the regulatory requirements. 

This action is not subject to the 

requirements of sections 202 and 205 of 

the UMRA. EPA has determined that 

this proposed rule does not contain a 

Federal mandate that may result in 

expenditures of $100 million or more 

for State, local, and Tribal governments, 

in the aggregate, or the private sector in 

any one year (adjusted for inflation). 

This rule proposes to retain existing 

national ambient air quality standards 

for carbon monoxide. The expected 

costs associated with the monitoring 

requirements are described in EPA’s ICR 

document, but those costs are expected 

to be well less than $100 million 

(adjusted for inflation) in the aggregate 

for any year. Furthermore, as indicated 

previously, in setting a NAAQS, EPA 

cannot consider the economic or 

technological feasibility of attaining 

ambient air quality standards. 

EPA has determined that this 

proposed rule contains no regulatory 

requirements that might significantly or 

uniquely affect small governments 

because it imposes no enforceable duty 

on any small governments. Therefore, 

this rule is not subject to the 

requirements of section 203 of the 

UMRA. 

E. Executive Order 13132: Federalism 

This action does not have federalism 

implications. It will not have substantial 

direct effects on the States, on the 

relationship between the national 

government and the States, or on the 

distribution of power and 

responsibilities among the various 

levels of government, as specified in 

Executive Order 13132. The rule does 

not alter the relationship between the 

Federal government and the States 

regarding the establishment and 

implementation of air quality 

improvement programs as codified in 

the CAA. Under section 109 of the CAA, 

EPA is mandated to establish and 

review NAAQS; however, CAA section 

116 preserves the rights of States to 

establish more stringent requirements if 

deemed necessary by a State. 

Furthermore, this proposed rule does 

not impact CAA section 107 which 

establishes that the States have primary 

responsibility for implementation of the 

NAAQS. Finally, as noted in section D 

(above) on UMRA, this rule does not 

impose significant costs on State, local, 

or Tribal governments or the private 

sector. Thus, Executive Order 13132 

does not apply to this rule. 

However, as also noted in section D 

(above) on UMRA, EPA recognizes that 

States will have a substantial interest in 

this rule, including the proposed air 

quality surveillance requirements of 40 

CFR part 58. Therefore, in the spirit of 

Executive Order 13132, and consistent 

with EPA policy to promote 

communications between EPA and State 

and local governments, EPA specifically 

solicits comment on this proposed rule 

from State and local officials. 

F. Executive Order 13175: Consultation 

and Coordination With Indian Tribal 

Governments 

This action does not have Tribal 

implications, as specified in Executive 

Order 13175 (65 FR 67249, November 9, 

2000). It does not have a substantial 

direct effect on one or more Indian 

Tribes, since Tribes are not obligated to 

adopt or implement any NAAQS. Thus, 

Executive Order 13175 does not apply 

to this rule. 

G. Executive Order 13045: Protection of 

Children From Environmental Health 

and Safety Risks 

This action is not subject to EO 13045 

(62 FR 19885, April 23, 1997) because 

it is not economically significant as 

defined in EO 12866, and because the 

Agency does not believe the 

environmental health or safety risks 

addressed by this action present a 

disproportionate risk to children. This 

action’s health and risk assessments are 

described in sections II.C and II.D.2.b. 

The public is invited to submit 

comments or identify peer-reviewed 

studies and data that assess effects of 

early life exposures to CO. 

H. Executive Order 13211: Actions That 

Significantly Affect Energy Supply, 

Distribution or Use 

This action is not a ‘‘significant energy 

action’’ as defined in Executive Order 

13211, (66 FR 28355 (May 22, 2001)) 

because it is not likely to have a 

significant adverse effect on the supply, 

distribution, or use of energy. The rule 

concerns the review of the NAAQS for 

CO. The rule does not prescribe specific 

pollution control strategies by which 

these ambient standards will be met. 

Such strategies are developed by States 

on a case-by-case basis, and EPA cannot 

predict whether the control options 

selected by States will include 


jlentini on DSKJ8SOYB1PROD with PROPOSALS4
8196 Federal Register / Vol. 76, No. 29 / Friday, February 11, 2011 / Proposed Rules 

regulations on energy suppliers, 

distributors, or users. 

I. National Technology Transfer and 

Advancement Act 

Section 12(d) of the National 

Technology Transfer and Advancement 

Act of 1995 (NTTAA), Public Law 104– 

113, section 12(d) (15 U.S.C. 272 note) 

directs EPA to use voluntary consensus 

standards in its regulatory activities 

unless to do so would be inconsistent 

with applicable law or otherwise 

impractical. Voluntary consensus 

standards are technical standards (e.g., 

materials specifications, test methods, 

sampling procedures, and business 

practices) that are developed or adopted 

by voluntary consensus standards 

bodies. The NTTAA directs EPA to 

provide Congress, through OMB, 

explanations when the Agency decides 

not to use available and applicable 

voluntary consensus standards. 

This proposed rulemaking involves 

technical standards with regard to 

ambient monitoring of CO. We have not 

identified any potentially applicable 

voluntary consensus standards that 

would adequately characterize ambient 

CO concentrations for the purposes of 

determining compliance with the CO 

NAAQS and none have been brought to 

our attention. 

EPA welcomes comments on this 

aspect of the proposed rule, and 

specifically invites the public to identify 

potentially applicable voluntary 

consensus standards and to explain why 

such standards should be used in the 

regulation. 

J. Executive Order 12898: Federal 

Actions To Address Environmental 

Justice in Minority Populations and 

Low-Income Populations 

Executive Order 12898 (59 FR 7629 

(Feb. 16, 1994)) establishes Federal 

executive policy on environmental 

justice. Its main provision directs 

Federal agencies, to the greatest extent 

practicable and permitted by law, to 

make environmental justice part of their 

mission by identifying and addressing, 

as appropriate, disproportionately high 

and adverse human health or 

environmental effects of their programs, 

policies, and activities on minority 

populations and low-income 

populations in the United States. 

EPA has determined that this 

proposed rule will not have 

disproportionately high and adverse 

human health or environmental effects 

on minority or low-income populations 

because it does not affect the level of 

protection provided to human health or 

the environment. The action proposed 

in this notice is to retain without 

revision the existing NAAQS for CO. 

Therefore this action will not cause 

increases in source emissions or air 

concentrations. 

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Office of Air Quality Planning and 

Standards, Research Triangle Park, NC. 

EPA–452/R–05–005a. 

U.S. Environmental Protection Agency. 

(2007) Review of the National Ambient Air 

Quality Standards for Ozone: Policy 

Assessment of Scientific and Technical 

Information, OAQPS Staff Paper. Office of 

Air Quality Planning and Standards, 

Research Triangle Park, NC. EPA–452/R– 

07–007. 

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– 


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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. 

(2008c) Risk and Exposure Assessment to 

Support the Review of the NO2 Primary 

National Ambient Air Quality Standard. 

Office of Air Quality Planning and 

Standards, Research Triangle Park, NC. 

EPA–452/R–08–008a. 

U.S. Environmental Protection Agency. 

(2008d) Integrated Science Assessment for 

Oxides of Nitrogen—Health Criteria (Final 

Report). EPA/600/R–08/071. 

U.S. Environmental Protection Agency. 

(2009a) Integrated Science Assessment for 

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. 

(2009e) Risk and Exposure Assessment to 

Support the Review of the SO2 Primary 

National Ambient Air Quality Standard. 

Office of Air Quality Planning and 

Standards, Research Triangle Park, NC. 

EPA–452/R–09–007. August 2009. 

Available at http://www.epa.gov/ttn/naaqs/ 

standards/so2/data/

200908SO2REAFinalReport.pdf. 

U.S. Environmental Protection Agency. 

(2009f) Integrated Science Assessment for 

Particulate Matter (Final Report). National 

Center for Environmental Assessment, 

Research Triangle Park, NC. EPA/600/R– 

08/139F. 

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) Policy Assessment for the Review 

of the Carbon Monoxide National Ambient 

Air Quality Standards. Office of Air 

Quality Planning and Standards, Research 

Triangle Park, NC. EPA 452/R–10–007. 

Available at: http://www.epa.gov/ttn/ 

naaqs/standards/co/s_co_cr_pa.html 

U.S. Environmental Protection Agency. 

(2010d) 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. 

(2010e) 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 

U.S. Environmental Protection Agency. 

(2010f) Analyzer Use in U.S. Monitoring 

Networks. Spreadsheet of air monitoring 

method utilization in U.S. monitoring 

networks by year. Office of Air Quality 

Planning and Standards. 

U.S. Environmental Protection Agency. 

(2010g) Modern CO Instrument 

Performance Data. Spreadsheet of 

performance data for existing FRM 

analyzers. Office of Research and 

Development. 

Watkins N. and Thompson R. (2010) CO 

Monitoring Network Background and 

Review. Memorandum to the Carbon 

Monoxide NAAQS Review Docket. EPA– 

HQ–OAR–2008–0015. 

Wellenius G.A.; Bateson T.F.; Mittleman 

M.A.; Schwartz J. (2005) Particulate air 

pollution and the rate of hospitalization for 

congestive heart failure among Medicare 

beneficiaries in Pittsburgh, Pennsylvania. 

Am J Epidemiol 161:1030–1036. 

WHO (2008). Harmonization Project 

Document No. 6. Part 1: Guidance 

document on characterizing and 

communicating uncertainty in exposure 

assessment. Available at: http:// 

www.who.int/ipcs/methods/

harmonization/areas/exposure/en/. 

Zanobetti A. and Schwartz J. (2001) Are 

diabetics more susceptible to the health 

effects of airborne particles? Am J Respir. 

Crit. Care Med. 164:831–833. 

Zhou, Y and Levy J.I. (2007) Factors 

influencing the spatial extent of mobile 

source air pollution impacts: A metaanalysis. BMC Public Health, 7:89. 

Zhu Y.; Hinds W.C.; Kim S.; Shen S.; Sioutas 

C. (2002) Study of ultrafine particles near 

a major highway with heavy-duty diesel 

traffic. Atmos Environ, 36: 4323–4335. 

List of Subjects 

40 CFR Part 50 

Environmental protection, Air 

pollution control, Carbon monoxide, 

Lead, Nitrogen dioxide, Ozone, 

Particulate matter, Sulfur oxides. 

40 CFR Part 53 

Environmental protection, 

Administrative practice and procedure, 

Air pollution control, Intergovernmental 

relations, Reporting and recordkeeping 

requirements. 

40 CFR Part 58 

Environmental protection, 

Administrative practice and procedure, 

Air pollution control, Intergovernmental 

relations, Reporting and recordkeeping 

requirements. 

Dated: January 28, 2011. 

Lisa P. Jackson, 

Administrator. 

For the reasons stated in the 

preamble, title 40, chapter I of the Code 

of Federal Regulations is proposed to be 

amended as follows: 

PART 50—NATIONAL PRIMARY AND 

SECONDARY AMBIENT AIR QUALITY 

STANDARDS 

1. The authority citation for part 50 

continues to read as follows: 

Authority: 42 U.S.C. 7401, et seq. 

2. Appendix C to Part 50 is revised to 

read as follows: 

Appendix C to Part 50—Measurement 

Principle and Calibration Procedure for 

the Measurement of Carbon Monoxide 

in the Atmosphere (Non-Dispersive 

Infrared Photometry) 

1.0 Applicability 

1.1 This non-dispersive infrared 

photometry (NDIR) Federal Reference 

Method (FRM) provides measurements 

of the concentration of carbon monoxide 

(CO) in ambient air for determining 

compliance with the primary and 

secondary National Ambient Air Quality 

Standards (NAAQS) for CO as specified 

in § 50.8 of this chapter. The method is 

applicable to continuous sampling and 

measurement of ambient CO 

concentrations suitable for determining 

1-hour or longer average measurements. 

The method may also provide 

measurements of shorter averaging 

times, subject to specific analyzer 

performance limitations. Additional CO 


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monitoring quality assurance 

procedures and guidance are provided 

in part 58, appendix A, of this chapter 

and in reference 1 of this appendix C. 

2.0 Measurement Principle 

2.1 Measurements of CO in ambient 

air are based on automated 

measurement of the absorption of 

infrared radiation by CO in an ambient 

air sample drawn into an analyzer 

employing non-wavelength-dispersive, 

infrared photometry (NDIR method). 

Infrared energy from a source in the 

photometer is passed through a cell 

containing the air sample to be 

analyzed, and the quantitative 

absorption of energy by CO in the 

sample cell is measured by a suitable 

detector. The photometer is sensitized 

specifically to CO by employing CO gas 

in a filter cell in the optical path, which, 

when compared to a differential optical 

path without a CO filter cell, limits the 

measured absorption to one or more of 

the characteristic wavelengths at which 

CO strongly absorbs. However, to meet 

measurement performance 

requirements, various optical filters, 

reference cells, rotating gas filter cells, 

dual-beam configurations, moisture 

traps, or other means may also be used 

to further enhance sensitivity and 

stability of the photometer and to 

minimize potential measurement 

interference from water vapor, carbon 

dioxide (CO2), or other species. Also, 

various schemes may be used to provide 

a suitable zero reference for the 

photometer, and optional automatic 

compensation may be provided for the 

actual pressure and temperature of the 

air sample in the measurement cell. The 

measured infrared absorption, converted 

to a digital reading or an electrical 

output signal, indicates the measured 

CO concentration. 

2.2 The measurement system is 

calibrated by referencing the analyzer’s 

CO measurements to CO concentration 

standards traceable to a National 

Institute of Standards and Technology 

(NIST) primary standard for CO, as 

described in the associated calibration 

procedure specified in section 4 of this 

reference method. 

2.3 An analyzer implementing this 

measurement principle will be 

considered a reference method only if it 

has been designated as a reference 

method in accordance with part 53 of 

this chapter. 

2.4 Sampling considerations. The 

use of a particle filter in the sample inlet 

line of a CO FRM analyzer is optional 

and left to the discretion of the user 

unless such a filter is specified or 

recommended by the analyzer 

manufacturer in the analyzer’s 

associated operation or instruction 

manual. 

3.0 Interferences 

3.1 The NDIR measurement 

principle is potentially susceptible to 

interference from water vapor and CO2, 

which have some infrared absorption at 

wavelengths in common with CO and 

normally exist in the atmosphere. 

Various instrumental techniques can be 

used to effectively minimize these 

interferences. 

4.0 Calibration Procedures 

4.1 Principle. Either of two methods 

may be selected for dynamic multipoint 

calibration of FRM CO analyzers, using 

test gases of accurately known CO 

concentrations obtained from one or 

more compressed gas cylinders certified 

as CO transfer standards: 

4.1.1 Dilution method: A single 

certified standard cylinder of CO is 

quantitatively diluted as necessary with 

zero air to obtain the various calibration 

concentration standards needed. 

4.1.2 Multiple-cylinder method: 

Multiple, individually certified standard 

cylinders of CO are used for each of the 

various calibration concentration 

standards needed. 

4.1.3 Additional information on 

calibration may be found in Section 12 

of reference 1. 

4.2 Apparatus. The major 

components and typical configurations 

of the calibration systems for the two 

calibration methods are shown in 

Figures 1 and 2. Either system may be 

made up using common laboratory 

components, or it may be a 

commercially manufactured system. In 

either case, the principal components 

are as follows: 

4.2.1 CO standard gas flow control 

and measurement devices (or a 

combined device) capable of regulating 

and maintaining the standard gas flow 

rate constant to within ± 2 percent and 

measuring the gas flow rate accurate to 

within ± 2 percent, properly calibrated 

to a NIST-traceable standard. 

4.2.2 For the dilution method 

(Figure 1), dilution air flow control and 

measurement devices (or a combined 

device) capable of regulating and 

maintaining the air flow rate constant to 

within ± 2 percent and measuring the 

air flow rate accurate to within ± 2 

percent, properly calibrated to a NISTtraceable standard. 

4.2.3 Standard gas pressure 

regulator(s) for the standard CO 

cylinder(s), suitable for use with a highpressure CO gas cylinder and having a 

non-reactive diaphragm and internal 

parts and a suitable delivery pressure. 

4.2.4 Mixing chamber for the 

dilution method, of an inert material 

and of proper design to provide 

thorough mixing of CO standard gas and 

diluent air streams. 

4.2.5 Output sampling manifold, 

constructed of an inert material and of 

sufficient diameter to ensure an 

insignificant pressure drop at the 

analyzer connection. The system must 

have a vent designed to ensure nearly 

atmospheric pressure at the analyzer 

connection port and to prevent ambient 

air from entering the manifold. 

4.3 Reagents. 

4.3.1 CO gas concentration transfer 

standard(s) of CO in air, containing an 

appropriate concentration of CO 

suitable for the selected operating range 

of the analyzer under calibration and 

traceable to a NIST standard reference 

material (SRM). If the CO analyzer has 

significant sensitivity to CO2, the CO 

standard(s) should also contain 350 to 

400 ppm CO2 to replicate the typical 

CO2 concentration in ambient air. 

However, if the zero air dilution ratio 

used for the dilution method is not less 

than 100:1 and the zero air contains 

ambient levels of CO2, then the CO 

standard may be contained in nitrogen 

and need not contain CO2. 

4.3.2 For the dilution method, clean 

zero air, free of contaminants that could 

cause a detectable response on or a 

change in sensitivity of the CO analyzer. 

The zero air should contain < 0.1 ppm 

CO. 

4.4 Procedure Using the Dilution 

Method. 

4.4.1 Assemble or obtain a suitable 

dynamic dilution calibration system 

such as the one shown schematically in 

Figure 1. Generally, all calibration gases 

including zero air must be introduced 

into the sample inlet of the analyzer. 

However, if the analyzer has special, 

approved zero and span inlets and 

automatic valves to specifically allow 

introduction of calibration standards at 

near atmospheric pressure, such inlets 

may be used for calibration in lieu of the 

sample inlet. For specific operating 

instructions, refer to the manufacturer’s 

manual. 

4.4.2 Ensure that there are no leaks 

in the calibration system and that all 

flowmeters are properly and accurately 

calibrated, under the conditions of use, 

if appropriate, against a reliable volume 

or flow rate standard such as a soapbubble meter or wet-test meter traceable 

to a NIST standard. All volumetric flow 

rates should be corrected to the same 

temperature and pressure such as 

298.15 K (25 °C) and 760 mm Hg (101 

kPa), using a correction formula such as 

the following: 


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Where: 

Fc = corrected flow rate (L/min at 25 °C and 

760 mm Hg), 

Fm = measured flow rate (at temperature Tm

and pressure Pm), 

Pm = measured pressure in mm Hg (absolute), 

and 

Tm = measured temperature in degrees 

Celsius. 

4.4.3 Select the operating range of 

the CO analyzer to be calibrated. 

4.4.4 Connect the inlet of the CO 

analyzer to the output-sampling 

manifold of the calibration system. 

4.4.5 Adjust the calibration system 

to deliver zero air to the output 

manifold. The total air flow must exceed 

the total demand of the analyzer(s) 

connected to the output manifold to 

ensure that no ambient air is pulled into 

the manifold vent. Allow the analyzer to 

sample zero air until a stable response 

is obtained. After the response has 

stabilized, adjust the analyzer zero 

reading. 

4.4.6 Adjust the zero air flow rate 

and the CO gas flow rate from the 

standard CO cylinder to provide a 

diluted CO concentration of 

approximately 80 percent of the 

measurement upper range limit (URL) of 

the operating range of the analyzer. The 

total air flow rate must exceed the total 

demand of the analyzer(s) connected to 

the output manifold to ensure that no 

ambient air is pulled into the manifold 

vent. The exact CO concentration is 

calculated from: 

Where: 

[CO]OUT = diluted CO concentration at the 

output manifold (ppm), 

[CO]STD = concentration of the undiluted CO 

standard (ppm), 

FCO = flow rate of the CO standard (L/min), 

and 

FD = flow rate of the dilution air (L/min). 

Sample this CO concentration until a 

stable response is obtained. Adjust the 

analyzer span control to obtain the 

desired analyzer response reading 

equivalent to the calculated standard 

concentration. If substantial adjustment 

of the analyzer span control is required, 

it may be necessary to recheck the zero 

and span adjustments by repeating steps 

4.4.5 and 4.4.6. Record the CO 

concentration and the analyzer’s final 

response. 

4.4.7 Generate several additional 

concentrations (at least three evenly 

spaced points across the remaining scale 

are suggested to verify linearity) by 

decreasing FCO or increasing FD. Be sure 

the total flow exceeds the analyzer’s 

total flow demand. For each 

concentration generated, calculate the 

exact CO concentration using equation 

(2). Record the concentration and the 

analyzer’s stable response for each 

concentration. Plot the analyzer 

responses (vertical or y-axis) versus the 

corresponding CO concentrations 

(horizontal or x-axis). Calculate the 

linear regression slope and intercept of 

the calibration curve and verify that no 

point deviates from this line by more 

than 2 percent of the highest 

concentration tested. 

4.5 Procedure Using the MultipleCylinder Method. Use the procedure for 

the dilution method with the following 

changes: 

4.5.1 Use a multi-cylinder, dynamic 

calibration system such as the typical 

one shown in Figure 2. 

4.5.2 The flowmeter need not be 

accurately calibrated, provided the flow 

in the output manifold can be verified 

to exceed the analyzer’s flow demand. 

4.5.3 The various CO calibration 

concentrations required in Steps 4.4.5, 

4.4.6, and 4.4.7 are obtained without 

dilution by selecting zero air or the 

appropriate certified standard cylinder. 

4.6 Frequency of Calibration. The 

frequency of calibration, as well as the 

number of points necessary to establish 

the calibration curve and the frequency 

of other performance checking, will vary 

by analyzer. However, the minimum 

frequency, acceptance criteria, and 

subsequent actions are specified in 

reference 1, appendix D, ‘‘Measurement 

Quality Objectives and Validation 

Template for CO’’ (page 5 of 30). The 

user’s quality control program should 

provide guidelines for initial 

establishment of these variables and for 

subsequent alteration as operational 

experience is accumulated. 

Manufacturers of CO analyzers should 

include in their instruction/operation 

manuals information and guidance as to 

these variables and on other matters of 

operation, calibration, routine 

maintenance, and quality control. 

5.0 Reference 

1. QA Handbook for Air Pollution 

Measurement Systems—Volume II. 

Ambient Air Quality Monitoring 

Program. U.S. EPA. EPA–454/B–08–003 

(2008). 

BILLING CODE 6560–50–P 


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BILLING CODE 6560–50–C 

PART 53—AMBIENT AIR QUALITY 

REFERENCE AND EQUIVALENT 

METHODS 

3. The authority citation for part 53 

continues to read as follows: 

Authority: 42 U.S.C. 7401, et seq. 

4. Subpart B of Part 53 is revised to 

read as follows: 

Subpart B—Procedures for Testing 

Performance Characteristics of Automated 

Methods for SO2, CO, O3, and NO2

Sec. 

53.20 General provisions. 

53.21 Test conditions. 

53.22 Generation of test atmospheres. 

53.23 Test procedure. 

Appendix A to Subpart B—Optional Forms 

for Reporting Test Results 

Subpart B—Procedures for Testing 

Performance Characteristics of 

Automated Methods for SO2, CO, O3, 

and NO2

§ 53.20 General provisions. 

(a) The test procedures given in this 

subpart shall be used to test the 

performance of candidate automated 

methods against the performance 

requirement specifications given in 


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table B–1. A test analyzer representative 

of the candidate automated method 

must exhibit performance better than, or 

not outside, the specified limit or limits 

for each such performance parameter 

specified (except range) to satisfy the 

requirements of this subpart. Except as 

provided in paragraph (b) of this 

section, the measurement range of the 

candidate method must be the standard 

range specified in table B–1 to satisfy 

the requirements of this subpart. 

(b) Measurement ranges. For a 

candidate method having more than one 

selectable measurement range, one 

range must be the standard range 

specified in table B–1, and a test 

analyzer representative of the method 

must pass the tests required by this 

subpart while operated in that range. 

(1) Higher ranges. The tests may be 

repeated for one or more higher 

(broader) ranges (i.e., ranges extending 

to higher concentrations) than the 

standard range specified in table B–1, 

provided that the range does not extend 

to concentrations more than four times 

the upper range limit of the standard 

range specified in table B–1. For such 

higher ranges, only the tests for range 

(calibration), noise at 80% of the upper 

range limit, and lag, rise and fall time 

are required to be repeated. For the 

purpose of testing a higher range, the 

test procedure of § 53.23(e) may be 

abridged to include only those 

components needed to test lag, rise and 

fall time. 

(2) Lower ranges. The tests may be 

repeated for one or more lower 

(narrower) ranges (i.e., ones extending 

to lower concentrations) than the 

standard range specified in table B–1. 

For methods for some pollutants, table 

B–1 specifies special performance limit 

requirements for lower ranges. If special 

low-range performance limit 

requirements are not specified in table 

B–1, then the performance limit 

requirements for the standard range 

apply. For lower ranges for any method, 

only the tests for range (calibration), 

noise at 0% of the measurement range, 

lower detectable limit, (and nitric oxide 

interference for SO2 UVF methods) are 

required to be repeated, provided the 

tests for the standard range shows the 

applicable limit specifications are met 

for the other test parameters. 

(3) If the tests are conducted and 

passed only for the specified standard 

range, any FRM or FEM determination 

with respect to the method will be 

limited to that range. If the tests are 

passed for both the specified range and 

one or more higher or lower ranges, any 

such determination will include the 

additional higher or lower range(s) as 

well as the specified standard range. 

Appropriate test data shall be submitted 

for each range sought to be included in 

a FRM or FEM method determination 

under this paragraph (b). 

(c) For each performance parameter 

(except range), the test procedure shall 

be initially repeated seven (7) times to 

yield 7 test results. Each result shall be 

compared with the corresponding 

performance limit specification in table 

B–1; a value higher than or outside the 

specified limit or limits constitutes a 

failure. These 7 results for each 

parameter shall be interpreted as 

follows: 

(1) Zero (0) failures: The candidate 

method passes the test for the 

performance parameter. 

(2) Three (3) or more failures: The 

candidate method fails the test for the 

performance parameter. 

(3) One (1) or two (2) failures: Repeat 

the test procedures for the performance 

parameter eight (8) additional times 

yielding a total of fifteen (15) test 

results. The combined total of 15 test 

results shall then be interpreted as 

follows: 

(i) One (1) or two (2) failures: The 

candidate method passes the test for the 

performance parameter. 

(ii) Three (3) or more failures: The 

candidate method fails the test for the 

performance parameter. 

(d) The tests for zero drift, span drift, 

lag time, rise time, fall time, and 

precision shall be carried out in a single 

integrated procedure conducted at 

various line voltages and ambient 

temperatures specified in § 53.23(e). A 

temperature-controlled environmental 

test chamber large enough to contain the 

test analyzer is recommended for this 

test. The tests for noise, lower detectable 

limit, and interference equivalent shall 

be conducted at any ambient 

temperature between 20 °C and 30 °C, 

at any normal line voltage between 105 

and 125 volts, and shall be conducted 

such that not more than three (3) test 

results for each parameter are obtained 

in any 24-hour period. 

(e) If necessary, all measurement 

response readings to be recorded shall 

be converted to concentration units or 

adjusted according to the calibration 

curve constructed in accordance with 

§ 53.21(b). 

(f) All recorder chart tracings (or 

equivalent data plots), records, test data 

and other documentation obtained from 

or pertinent to these tests shall be 

identified, dated, signed by the analyst 

performing the test, and submitted. 

Note to § 53.20: Suggested formats for 

reporting the test results and calculations are 

provided in Figures B–2, B–3, B–4, B–5, and 

B–6 in appendix A to this subpart. Symbols 

and abbreviations used in this subpart are 

listed in table B–5 of appendix A to this 

subpart. 

TABLE B–1—PERFORMANCE LIMIT SPECIFICATIONS FOR AUTOMATED METHODS

Performance parameter Units 1

SO2 O3

(Std. 

range) 

CO NO2

(Std. 

range) 

Definitions 

and test 

procedures Std. 

range 3

Lower 

range 2 3

Std. 

range 3

Lower 

range 2 3

1. Range ............................................................ ppm .......... 0–0.5 < 0.5 0–0.5 0–50 < 50 0–0.5 Sec. 53.23(a). 

2. Noise .............................................................. ppm .......... 0.001 0.0005 0.005 0.2 0.1 0.005 Sec. 53.23(b). 

3. Lower detectable limit .................................... ppm .......... 0.002 0.001 0.010 0.4 0.2 0.010 Sec. 53.23(c). 

4. Interference equivalent: 

Each interferent .......................................... ppm .......... ± 0.005 4 ± 0.005 ± 0.02 ± 1.0 ± 0.5 ± 0.02 Sec. 53.23(d). 

Total, all interferents ................................... ppm .......... .............. .............. 0.06 .............. .............. 0.04 Sec. 53.23(d). 

5. Zero drift, 12 and 24 hour ............................. ppm .......... ± 0.004 ± 0.002 ± 0.02 ± 0.5 ± 0.3 ± 0.02 Sec. 53.23(e). 

6. Span drift, 24 hour: 

20% of upper range limit ............................ Percent ..... .............. ± 3.0 ± 20.0 .............. ± 2.0 ± 20.0 Sec. 53.23(e). 

80% of upper range limit ............................ Percent ..... ± 3.0 .............. ± 5.0 ± 2.0 .............. ± 5.0 Sec. 53.23(e). 

7. Lag time ......................................................... Minutes ..... 2 2 20 2.0 2.0 20 Sec. 53.23(e). 

8. Rise time ........................................................ Minutes ..... 2 2 15 2.0 2.0 15 Sec. 53.23(e). 

9. Fall time ......................................................... Minutes ..... 2 2 15 2.0 2.0 15 Sec. 53.23(e). 

10. Precision: 

20% of upper range limit ............................ ppm .......... .............. .............. 0.010 .............. .............. 0.020 Sec. 53.23(e). 

Percent ..... 2 2 .............. 1.0 1.0 .............. Sec. 53.23(e). 


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TABLE B–1—PERFORMANCE LIMIT SPECIFICATIONS FOR AUTOMATED METHODS—Continued 

Performance parameter Units 1

SO2 O3

(Std. 

range) 

CO NO2

(Std. 

range) 

Definitions 

and test 

procedures Std. 

range 3

Lower 

range 2 3

Std. 

range 3

Lower 

range 2 3

80% of upper range limit ............................ ppm .......... .............. .............. 0.010 .............. .............. 0.030 Sec. 53.23(e). 

Percent ..... 2 2 .............. 1.0 1.0 .............. Sec. 53.23(e). 

1To convert from parts per million (ppm) to μg/m3 at 25 °C and 760 mm Hg, multiply by M/0.02447, where M is the molecular weight of the 

gas. Percent means percent of the upper measurement range limit. 2Tests for interference equivalent and lag time do not need to be repeated for any lower range provided the test for the standard range shows 

that the lower range specification (if applicable) is met for each of these test parameters. 3For candidate analyzers having automatic or adaptive time constants or smoothing filters, describe their functional nature, and describe and 

conduct suitable tests to demonstrate their function aspects and verify that performances for calibration, noise, lag, rise, fall times, and precision 

are within specifications under all applicable conditions. For candidate analyzers with operator-selectable time constants or smoothing filters, conduct calibration, noise, lag, rise, fall times, and precision tests at the highest and lowest settings that are to be included in the FRM or FEM designation. 4For nitric oxide interference for the SO2 UVF method, interference equivalent is ± 0.0003 ppm for the lower range. 

§ 53.21 Test conditions. 

(a) Set-up and start-up of the test 

analyzer shall be in strict accordance 

with the operating instructions specified 

in the manual referred to in § 53.4(b)(3). 

Allow adequate warm-up or 

stabilization time as indicated in the 

operating instructions before beginning 

the tests. The test procedures assume 

that the test analyzer has a conventional 

analog measurement signal output that 

is connected to a suitable strip chart 

recorder of the servo, null-balance type. 

This recorder shall have a chart width 

of a least 25 centimeters, chart speeds 

up to 10 cm per hour, a response time 

of 1 second or less, a deadband of not 

more than 0.25 percent of full scale, and 

capability either of reading 

measurements at least 5 percent below 

zero or of offsetting the zero by at least 

5 percent. If the test analyzer does not 

have an analog signal output, or if a 

digital or other type of measurement 

data output is used for the tests, an 

alternative measurement data recording 

device (or devices) may be used for 

recording the test data, provided that 

the device is reasonably suited to the 

nature and purposes of the tests, and an 

analog representation of the analyzer 

measurements for each test can be 

plotted or otherwise generated that is 

reasonably similar to the analog 

measurement recordings that would be 

produced by a conventional chart 

recorder connected to a conventional 

analog signal output. 

(b) Calibration of the test analyzer 

shall be carried out prior to conducting 

the tests described in this subpart. The 

calibration shall be as indicated in the 

manual referred to in § 53.4(b)(3) and as 

follows: If the chart recorder or 

alternative data recorder does not have 

below zero capability, adjust either the 

controls of the test analyzer or the chart 

or data recorder to obtain a + 5% offset 

zero reading on the recorder chart to 

facilitate observing negative response or 

drift. If the candidate method is not 

capable of negative response, the test 

analyzer (not the data recorder) shall be 

operated with a similar offset zero. 

Construct and submit a calibration 

curve showing a plot of recorder scale 

readings or other measurement output 

readings (vertical or y-axis) against 

pollutant concentrations presented to 

the analyzer for measurement 

(horizontal or x-axis). If applicable, a 

plot of base analog output units (volts, 

millivolts, milliamps, etc.) against 

pollutant concentrations shall also be 

obtained and submitted. All such 

calibration plots shall consist of at least 

seven (7) approximately equally spaced, 

identifiable points, including 0 and 

90 ± 5 percent of the upper range limit 

(URL). 

(c) Once the test analyzer has been set 

up and calibrated and the tests started, 

manual adjustment or normal periodic 

maintenance is permitted only every 3 

days. Automatic adjustments which the 

test analyzer performs by itself are 

permitted at any time. The submitted 

records shall show clearly when any 

manual adjustment or periodic 

maintenance was made during the tests 

and describe the specific operations 

performed. 

(d) If the test analyzer should 

malfunction during any of the 

performance tests, the tests for that 

parameter shall be repeated. A detailed 

explanation of the malfunction, 

remedial action taken, and whether 

recalibration was necessary (along with 

all pertinent records and charts) shall be 

submitted. If more than one malfunction 

occurs, all performance test procedures 

for all parameters shall be repeated. 

(e) Tests for all performance 

parameters shall be completed on the 

same test analyzer; however, use of 

multiple test analyzers to accelerate 

testing is permissible for testing 

additional ranges of a multi-range 

candidate method. 

§ 53.22 Generation of test atmospheres. 

(a) Table B–2 specifies preferred 

methods for generating test atmospheres 

and suggested methods of verifying their 

concentrations. Only one means of 

establishing the concentration of a test 

atmosphere is normally required, 

provided that that means is adequately 

accurate and credible. If the method of 

generation can produce accurate, 

reproducible concentrations, 

verification is optional. If the method of 

generation is not reproducible or 

reasonably quantifiable, then 

establishment of the concentration by 

some credible verification method is 

required. 

(b) The test atmosphere delivery 

system shall be designed and 

constructed so as not to significantly 

alter the test atmosphere composition or 

concentration during the period of the 

test. The system shall be vented to 

insure that test atmospheres are 

presented to the test analyzer at very 

nearly atmospheric pressure. The 

delivery system shall be fabricated from 

borosilicate glass, FEP Teflon, or other 

material that is inert with regard to the 

gas or gases to be used. 

(c) The output of the test atmosphere 

generation system shall be sufficiently 

stable to obtain stable response readings 

from the test analyzer during the 

required tests. If a permeation device is 

used for generation of a test atmosphere, 

the device, as well as the air passing 

over it, shall be controlled to 0.1 °C. 

(d) All diluent air shall be zero air free 

of contaminants likely to react with the 

test atmospheres or cause a detectable 

response on the test analyzer. 

(e) The concentration of each test 

atmosphere used shall be quantitatively 

established and/or verified before or 

during each series of tests. Samples for 

verifying test concentrations shall be 


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collected from the test atmosphere 

delivery system as close as feasible to 

the sample intake port of the test 

analyzer. 

(f) The accuracy of all flow 

measurements used to calculate test 

atmosphere concentrations shall be 

documented and referenced to a 

primary flow rate or volume standard 

(such as a spirometer, bubble meter, 

etc.). Any corrections shall be clearly 

shown. All flow measurements given in 

volume units shall be standardized to 

25 °C. and 760 mm Hg. 

(g) Schematic drawings, photos, 

descriptions, and other information 

showing complete procedural details of 

the test atmosphere generation, 

verification, and delivery system shall 

be provided. All pertinent calculations 

shall be clearly indicated. 

TABLE B–2—TEST ATMOSPHERES

Test gas Generation Verification 

Ammonia .................. Permeation device. Similar to system described in references 1 and 2.Indophenol method, reference 3. 

Carbon dioxide ......... Cylinder of zero air or nitrogen containing CO2 as required 

to obtain the concentration specified in table B–3.

Use NIST-certified standards whenever possible. If NIST 

standards are not available, obtain 2 standards from 

independent sources which agree within 2 percent, or 

obtain one standard and submit it to an independent laboratory for analysis, which must agree within 2 percent 

of the supplier’s nominal analysis. 

Carbon monoxide ..... Cylinder of zero air or nitrogen containing CO as required 

to obtain the concentration specified in table B–3.

Use an FRM CO analyzer as described in reference 8. 

Ethane ...................... Cylinder of zero air or nitrogen containing ethane as required to obtain the concentration specified in table B–3.Gas chromatography, ASTM D2820, reference 10. Use 

NIST-traceable gaseous methane or propane standards 

for calibration. 

Ethylene ................... Cylinder of pre-purified nitrogen containing ethylene as required to obtain the concentration specified in table B–3.Do. 

Hydrogen chloride .... Cylinder 1 of pre-purified nitrogen containing approximately 

100 ppm of gaseous HCl. Dilute with zero air to concentration specified in table B–3.

Collect samples in bubbler containing distilled water and 

analyze by the mercuric thiocyanate method, ASTM 

(D612), p. 29, reference 4. 

Hydrogen sulfide ...... Permeation device system described in references 1 and 2 Tentative method of analysis for H2S content of the atmosphere, p. 426, reference 5. 

Methane ................... Cylinder of zero air containing methane as required to obtain the concentration specified in table B–3.Gas chromatography ASTM D2820, reference 10. Use 

NIST-traceable methane standards for calibration. 

Nitric oxide ............... Cylinder 1 of pre-purified nitrogen containing approximately 

100 ppm NO. Dilute with zero air to required concentration.

Gas phase titration as described in reference 6, section 

7.1. 

Nitrogen dioxide ....... 1. Gas phase titration as described in reference 6 .............. 1. Use an FRM NO2 analyzer calibrated with a gravimetrically calibrated permeation device. 

2. Permeation device, similar to system described in reference 6.2. Use an FRM NO2 analyzer calibrated by gas-phase titration as described in reference 6. 

Ozone ....................... Calibrated ozone generator as described in reference 9 ..... Use an FEM ozone analyzer calibrated as described in reference 9. 

Sulfur dioxide ........... 1. Permeation device as described in references 1 and 2 ... Use an SO2 FRM or FEM analyzer as described in reference 7. 

2. Dynamic dilution of a cylinder containing approximately 

100 ppm SO2 as described in Reference 7.

Water ........................ Pass zero air through distilled water at a fixed known temperature between 20° and 30° C such that the air stream 

becomes saturated. Dilute with zero air to concentration 

specified in table B–3.

Measure relative humidity by means of a dew-point indicator, calibrated electrolytic or piezo electric hygrometer, 

or wet/dry bulb thermometer. 

Xylene ...................... Cylinder of pre-purified nitrogen containing 100 ppm xylene. Dilute with zero air to concentration specified in 

table B–3.

Use NIST-certified standards whenever possible. If NIST 

standards are not available, obtain 2 standards from 

independent sources which agree within 2 percent, or 

obtain one standard and submit it to an independent laboratory for analysis, which must agree within 2 percent 

of the supplier’s nominal analysis. 

Zero air ..................... 1. Ambient air purified by appropriate scrubbers or other 

devices such that it is free of contaminants likely to 

cause a detectable response on the analyzer.

2. Cylinder of compressed zero air certified by the supplier 

or an independent laboratory to be free of contaminants 

likely to cause a detectable response on the analyzer.

1 Use stainless steel pressure regulator dedicated to the pollutant measured. 

Reference 1. O’Keefe, A. E., and Ortaman, G. C. ‘‘Primary Standards for Trace Gas Analysis,’’ Anal. Chem. 38, 760 (1966). 

Reference 2. Scaringelli, F. P., A. E. Rosenberg, E*, and Bell, J. P., ‘‘Primary Standards for Trace Gas Analysis.’’ Anal. Chem. 42, 871 (1970). 

Reference 3. ‘‘Tentative Method of Analysis for Ammonia in the Atmosphere (Indophenol Method)’’, Health Lab Sciences, vol. 10, No. 2, 115– 

118, April 1973. 

Reference 4. 1973 Annual Book of ASTM Standards, American Society for Testing and Materials, 1916 Race St., Philadelphia, PA. 

Reference 5. Methods for Air Sampling and Analysis, Intersociety Committee, 1972, American Public Health Association, 1015. 

Reference 6. 40 CFR 50 Appendix F, ‘‘Measurement Principle and Calibration Principle for the Measurement of Nitrogen Dioxide in the Atmosphere (Gas Phase Chemiluminescence).’’ 

Reference 7. 40 CFR 50 Appendix A–1, ‘‘Measurement Principle and Calibration Procedure for the Measurement of Sulfur Dioxide in the Atmosphere (Ultraviolet Fluorscence).’’ 

Reference 8. 40 CFR 50 Appendix C, ‘‘Measurement Principle and Calibration Procedure for the Measurement of Carbon Monoxide in the Atmosphere’’ (Non-Dispersive Infrared Photometry)’’. 


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Reference 9. 40 CFR 50 Appendix D, ‘‘Measurement Principle and Calibration Procedure for the Measurement of Ozone in the Atmosphere’’. 

Reference 10. ‘‘Standard Test Method for C, through C5 Hydrocarbons in the Atmosphere by Gas Chromatography’’, D 2820, 1987 Annual 

Book of Aston Standards, vol 11.03, American Society for Testing and Materials, 1916 Race St., Philadelphia, PA 19103. 

§ 53.23 Test procedures. 

(a) Range—(1) Technical definition. 

The nominal minimum and maximum 

concentrations that a method is capable 

of measuring. 

Note to § 53.23(a)(1): The nominal range is 

given as the lower and upper range limits in 

concentration units, for example, 0–0.5 parts 

per million (ppm). 

(2) Test procedure. Determine and 

submit a suitable calibration curve, as 

specified in § 53.21(b), showing the test 

analyzer’s measurement response over 

at least 95 percent of the required or 

indicated measurement range. 

Note to § 53.23(a)(2): A single calibration 

curve for each measurement range for which 

an FRM or FEM designation is sought will 

normally suffice. 

(b) Noise—(1) Technical definition. 

Spontaneous, short duration deviations 

in measurements or measurement signal 

output, about the mean output, that are 

not caused by input concentration 

changes. Measurement noise is 

determined as the standard deviation of 

a series of measurements of a constant 

concentration about the mean and is 

expressed in concentration units. 

(2) Test procedure. (i) Allow sufficient 

time for the test analyzer to warm up 

and stabilize. Determine measurement 

noise at each of two fixed 

concentrations, first using zero air and 

then a pollutant test gas concentration 

as indicated below. The noise limit 

specification in table B–1 shall apply to 

both of these tests. 

(ii) For an analyzer with an analog 

signal output, connect an integratingtype digital meter (DM) suitable for the 

test analyzer’s output and accurate to 

three significant digits, to determine the 

analyzer’s measurement output signal. 

Note to § 53.23(b)(2): Use of a chart 

recorder in addition to the DM is optional. 

(iii) Measure zero air with the test 

analyzer for 60 minutes. During this 60- 

minute interval, record twenty-five (25) 

test analyzer concentration 

measurements or DM readings at 2- 

minute intervals. (See Figure B–2 in 

appendix A of this subpart.) 

(iv) If applicable, convert each DM 

test reading to concentration units 

(ppm) or adjust the test readings (if 

necessary) by reference to the test 

analyzer’s calibration curve as 

determined in § 53.21(b). Label and 

record the test measurements or 

converted DM readings as r1, r2, r3 * * * 

ri * * * r25. 

(v) Calculate measurement noise as 

the standard deviation, S, as follows: 

where i indicates the i-th test measurement 

or DM reading in ppm. 

(vi) Let S at 0 ppm be identified as S0; 

compare S0 to the noise limit 

specification given in table B–1. 

(vii) Repeat steps in Paragraphs 

(b)(2)(iii) through (v) of this section 

using a pollutant test atmosphere 

concentration of 80 ± 5 percent of the 

URL instead of zero air, and let S at 80 

percent of the URL be identified as S80. 

Compare S80 to the noise limit 

specification given in table B–1 of this 

subpart. 

(viii) Both S0 and S80 must be less 

than or equal to the table B–1 noise 

limit specification to pass the test for 

the noise parameter. 

(c) Lower detectable limit—(1) 

Technical definition. The minimum 

pollutant concentration that produces a 

measurement or measurement output 

signal of at least twice the noise level. 

(2) Test procedure. (i) Allow sufficient 

time for the test analyzer to warm up 

and stabilize. Measure zero air and 

record the stable measurement reading 

in ppm as BZ. (See Figure B–3 in 

appendix A of this subpart.) 

(ii) Generate and measure a pollutant 

test concentration equal to the value for 

the lower detectable limit specified in 

table B–1. 

Note to § 53.23(c)(2): If necessary, the test 

concentration may be generated or verified at 

a higher concentration, then quantitatively 

and accurately diluted with zero air to the 

final required test concentration. 

(iii) Record the test analyzer’s stable 

measurement reading, in ppm, as BL. 

(iv) Determine the lower detectable 

limit (LDL) test result as LDL = BL ¥ BZ. 

Compare this LDL value with the noise 

level, S0, determined in § 53.23(b), for 

the 0 concentration test atmosphere. 

LDL must be equal to or higher than 2 

× S0 to pass this test. 

(d) Interference equivalent—(1) 

Technical definition. Positive or 

negative measurement response caused 

by a substance other than the one being 

measured. 

(2) Test procedure. The test analyzer 

shall be tested for all substances likely 

to cause a detectable response. The test 

analyzer shall be challenged, in turn, 

with each potential interfering agent 

(interferent) specified in table B–3. In 

the event that there are substances likely 

to cause a significant interference which 

have not been specified in table B–3, 

these substances shall also be tested, in 

a manner similar to that for the 

specified interferents, at a concentration 

substantially higher than that likely to 

be found in the ambient air. The 

interference may be either positive or 

negative, depending on whether the test 

analyzer’s measurement response is 

increased or decreased by the presence 

of the interferent. Interference 

equivalents shall be determined by 

mixing each interferent, one at a time, 

with the pollutant at an interferent test 

concentration not lower than the test 

concentration specified in table B–3 (or 

as otherwise required for unlisted 

interferents), and comparing the test 

analyzer’s measurement response to the 

response caused by the pollutant alone. 

Known gas-phase reactions that might 

occur between a listed interferent and 

the pollutant are designated by footnote 

3 in table B–3. In these cases, the 

interference equivalent shall be 

determined without mixing with the 

pollutant. 

(i) Allow sufficient time for warm-up 

and stabilization of the test analyzer. 

(ii) For a candidate method using a 

prefilter or scrubber device based upon 

a chemical reaction to derive part of its 

specificity and which device requires 

periodic service or maintenance, the test 

analyzer shall be ‘‘conditioned’’ prior to 

conducting each interference test series. 

This requirement includes conditioning 

for the NO2 converter in 

chemiluminescence NO/NO2/NOX

analyzers and for the ozone scrubber in 

UV-absorption ozone analyzers. 

Conditioning is as follows: 

(A) Service or perform the indicated 

maintenance on the scrubber or prefilter 

device, as if it were due for such 

maintenance, as directed in the manual 

referred to in § 53.4(b)(3). 

(B) Before testing for each potential 

interferent, allow the test analyzer to 

sample through the prefilter or scrubber 

device a test atmosphere containing the 

interferent at a concentration not lower 

than the value specified in table B–3 (or, 

for unlisted potential interferents, at a 

concentration substantially higher than 

likely to be found in ambient air). 

Sampling shall be at the normal flow 

rate and shall be continued for 6 

continuous hours prior to the 

interference test series. Conditioning for 

all applicable interferents prior to any of 


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the interference tests is permissible. 

Also permissible is simultaneous 

conditioning with multiple interferents, 

provided no interferent reactions are 

likely to occur in the conditioning 

system. 

(iii) Generate three test atmosphere 

streams as follows: 

(A) Test atmosphere P: Pollutant test 

concentration. 

(B) Test atmosphere I: Interferent test 

concentration. 

(C) Test atmosphere Z: Zero air. 

(iv) Adjust the individual flow rates 

and the pollutant or interferent 

generators for the three test atmospheres 

as follows: 

(A) The flow rates of test atmospheres 

I and Z shall be equal. 

(B) The concentration of the pollutant 

in test atmosphere P shall be adjusted 

such that when P is mixed (diluted) 

with either test atmosphere I or Z, the 

resulting concentration of pollutant 

shall be as specified in table B–3. 

(C) The concentration of the 

interferent in test atmosphere I shall be 

adjusted such that when I is mixed 

(diluted) with test atmosphere P, the 

resulting concentration of interferent 

shall be not less than the value specified 

in table B–3 (or as otherwise required 

for unlisted potential interferents). 

(D) To minimize concentration errors 

due to flow rate differences between I 

and Z, it is recommended that, when 

possible, the flow rate of P be from 10 

to 20 times larger than the flow rates of 

I and Z. 

(v) Mix test atmospheres P and Z by 

passing the total flow of both 

atmospheres through a (passive) mixing 

component to insure complete mixing of 

the gases. 

(vi) Sample and measure the mixture 

of test atmospheres P and Z with the test 

analyzer. Allow for a stable 

measurement reading, and record the 

reading, in concentration units, as R (see 

Figure B–3). 

(vii) Mix test atmospheres P and I by 

passing the total flow of both 

atmospheres through a (passive) mixing 

component to insure complete mixing of 

the gases. 

(viii) Sample and measure this 

mixture of P and I with the test 

analyzer. Record the stable 

measurement reading, in concentration 

units, as RI. 

(ix) Calculate the interference 

equivalent (IE) test result as: 

IE = RI ¥ R. 

IE must be within the limits (inclusive) 

specified in table B–1 for each 

interferent tested to pass the 

interference equivalent test. 

(x) Follow steps (iii) through (ix) of 

this section, in turn, to determine the 

interference equivalent for each listed 

interferent as well as for any other 

potential interferents identified. 

(xi) For those potential interferents 

which cannot be mixed with the 

pollutant, as indicated by footnote (3) in 

table B–3, adjust the concentration of 

test atmosphere I to the specified value 

without being mixed or diluted by the 

pollutant test atmosphere. Determine IE 

as follows: 

(A) Sample and measure test 

atmosphere Z (zero air). Allow for a 

stable measurement reading and record 

the reading, in concentration units, as R. 

(B) Sample and measure the 

interferent test atmosphere I. If the test 

analyzer is not capable of negative 

readings, adjust the analyzer (not the 

recorder) to give an offset zero. Record 

the stable reading in concentration units 

as RI, extrapolating the calibration 

curve, if necessary, to represent negative 

readings. 

(C) Calculate IE = RI ¥ R. IE must be 

within the limits (inclusive) specified in 

table B–1 for each interferent tested to 

pass the interference equivalent test. 

(xii) Sum the absolute value of all the 

individual interference equivalent test 

results. This sum must be equal to or 

less than the total interferent limit given 

in table B–1 to pass the test. 

BILLING CODE 6560–50–P 


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BILLING CODE 6560–50–C (e) Zero drift, span drift, lag time, rise 

time, fall time, and precision—(1) 

Technical definitions—(i) Zero drift. 

The change in measurement response to 


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zero pollutant concentration over 12- 

and 24-hour periods of continuous 

unadjusted operation. 

(ii) Span drift. The percent change in 

measurement response to an up-scale 

pollutant concentration over a 24-hour 

period of continuous unadjusted 

operation. 

(iii) Lag time. The time interval 

between a step change in input 

concentration and the first observable 

corresponding change in measurement 

response. 

(iv) Rise time. The time interval 

between initial measurement response 

and 95 percent of final response after a 

step increase in input concentration. 

(v) Fall time. The time interval 

between initial measurement response 

and 95 percent of final response after a 

step decrease in input concentration. 

(vi) Precision. Variation about the 

mean of repeated measurements of the 

same pollutant concentration, expressed 

as one standard deviation. 

(2) Tests for these performance 

parameters shall be accomplished over 

a period of seven (7) or fifteen (15) test 

days. During this time, the line voltage 

supplied to the test analyzer and the 

ambient temperature surrounding the 

analyzer shall be changed from day to 

day, as required in paragraph(e)(4) of 

this section. One test result for each 

performance parameter shall be 

obtained each test day, for seven (7) or 

fifteen (15) test days, as determined 

from the test results of the first seven 

days. The tests for each test day are 

performed in a single integrated 

procedure. 

(3) The 24-hour test day may begin at 

any clock hour. The first approximately 

12 hours of each test day are required 

for testing 12-hour zero drift. Tests for 

the other parameters shall be conducted 

any time during the remaining 12 hours. 

(4) Table B–4 of this section specifies 

the line voltage and room temperature 

to be used for each test day. The 

applicant may elect to specify a wider 

temperature range (minimum and 

maximum temperatures) than the range 

specified in table B–4 and to conduct 

these tests over that wider temperature 

range in lieu of the specified 

temperature range. If the test results 

show that all test parameters of this 

section § 53.23(e) are passed over this 

wider temperature range, a subsequent 

FRM or FEM designation for the 

candidate method based in part on this 

test shall indicate approval for operation 

of the method over such wider 

temperature range. The line voltage and 

temperature shall be changed to the 

specified values (or to the alternative, 

wider temperature values, if applicable) 

at the start of each test day (i.e., at the 

start of the 12-hour zero test). Initial 

adjustments (day zero) shall be made at 

a line voltage of 115 volts (rms) and a 

room temperature of 25 °C. 

(5) The tests shall be conducted in 

blocks consisting of 3 test days each 

until 7 (or 15, if necessary) test results 

have been obtained. (The final block 

may contain fewer than three test days.) 

Test days need not be contiguous days, 

but during any idle time between tests 

or test days, the test analyzer must 

operate continuously and measurements 

must be recorded continuously at a low 

chart speed (or equivalent data 

recording) and included with the test 

data. If a test is interrupted by an 

occurrence other than a malfunction of 

the test analyzer, only the block during 

which the interruption occurred shall be 

repeated. 

(6) During each test block, manual 

adjustments to the electronics, gas, or 

reagent flows or periodic maintenance 

shall not be permitted. Automatic 

adjustments that the test analyzer 

performs by itself are permitted at any 

time. 

(7) At least 4 hours prior to the start 

of the first test day of each test block, 

the test analyzer may be adjusted and/ 

or serviced according to the periodic 

maintenance procedures specified in the 

manual referred to in § 53.4(b)(3). If a 

new block is to immediately follow a 

previous block, such adjustments or 

servicing may be done immediately after 

completion of the day’s tests for the last 

day of the previous block and at the 

voltage and temperature specified for 

that day, but only on test days 3, 6, 9, 

and 12. 

Note to § 53.23(e)(7): If necessary, the 

beginning of the test days succeeding such 

maintenance or adjustment may be delayed 

as required to complete the service or 

adjustment operation. 

(8) All measurement response 

readings to be recorded shall be 

converted to concentration units or 

adjusted (if necessary) according to the 

calibration curve. Whenever a test 

atmosphere is to be measured but a 

stable reading is not required, the test 

atmosphere shall be sampled and 

measured long enough to cause a change 

in measurement response of at least 

10% of full scale. Identify all readings 

and other pertinent data on the strip 

chart (or equivalent test data record). 

(See Figure B–1 illustrating the pattern 

of the required readings.) 

TABLE B–4—LINE VOLTAGE AND ROOM TEMPERATURE TEST CONDITIONS

Test day Line voltage,1 rms 

Room temperature,2

°C 

Comments 

0 ................................................................... 115 25 Initial set-up and adjustments. 

1 ................................................................... 125 20 

2 ................................................................... 105 20 

3 ................................................................... 125 30 Adjustments and/or periodic maintenance permitted at end of tests. 

4 ................................................................... 105 30 

5 ................................................................... 125 20 

6 ................................................................... 105 20 Adjustments and/or periodic maintenance permitted at end of tests. 

7 ................................................................... 125 30 Examine test results to ascertain if further testing is required. 

8 ................................................................... 105 30 

9 ................................................................... 125 20 Adjustments and/or periodic maintenance permitted at end of tests. 

10 ................................................................. 105 20 

11 ................................................................. 125 30 

12 ................................................................. 105 30 Adjustments and/or periodic maintenance permitted at end of tests. 

13 ................................................................. 125 20 

14 ................................................................. 105 20 

15 ................................................................. 125 30 

1Voltage specified shall be controlled to ± 1 volt. 2Temperatures shall be controlled to ±1 °C. 


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BILLING CODE 6560–60–P 

BILLING CODE 6560–60–C 

(9) Test procedure. (i) Arrange to 

generate pollutant test atmospheres as 

follows. Test atmospheres A0, A20, and 

A80 shall be maintained consistent 

during the tests and reproducible from 

test day to test day. 

Test 

atmosphere 

Pollutant concentration 

(percent) 

A0 ............. Zero air. 

A20 ........... 20±5 of the upper range limit. 

A30 ........... 30±5 of the upper range limit. 

A80 ........... 80±5 of the upper range limit. 

Test 

atmosphere 

Pollutant concentration 

(percent) 

A90 ........... 90±5 of the upper range limit. 

(ii) For steps within paragraphs 

(e)(9)(xxv) through (e)(9)(xxxi) of this 

section, a chart speed of at least 10 

centimeters per hour (or equivalent 

resolution for a digital representation) 

shall be used to clearly show changes in 

measurement responses. The actual 

chart speed, chart speed changes, and 

time checks shall be clearly marked on 

the chart. 

(iii) Test day 0. Allow sufficient time 

for the test analyzer to warm up and 

stabilize at a line voltage of 115 volts 

and a room temperature of 25 °C. Adjust 

the zero baseline to 5 percent of chart 

(see § 53.21(b)) and recalibrate, if 

necessary. No further adjustments shall 

be made to the analyzer until the end of 

the tests on the third, sixth, ninth, or 

twelfth test day. 

(iv) Measure test atmosphere A0 until 

a stable measurement reading is 

obtained and record this reading (in 


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ppm) as Z’n, where n = 0 (see Figure B– 

4 in appendix A of this subpart). 

(v) [Reserved] 

(vi) Measure test atmosphere A80.

Allow for a stable measurement reading 

and record it as S’n, where n = 0. 

(vii) The above readings for Z’0 and 

S’0 should be taken at least four (4) 

hours prior to the beginning of test day 

1. 

(viii) At the beginning of each test 

day, adjust the line voltage and room 

temperature to the values given in table 

B–4 of this subpart (or to the 

corresponding alternative temperature if 

a wider temperature range is being 

tested). 

(ix) Measure test atmosphere A0

continuously for at least twelve (12) 

continuous hours during each test day. 

(x) After the 12-hour zero drift test 

(step ix) is complete, sample test 

atmosphere A0. A stable reading is not 

required. 

(xi) Measure test atmosphere A20 and 

record the stable reading (in ppm) as P1. 

(See Figure B–4 in appendix A.) 

(xii) Sample test atmosphere A30; a 

stable reading is not required. 

(xiii) Measure test atmosphere A20

and record the stable reading as P2. 

(xiv) Sample test atmosphere A0; a 

stable reading is not required. 

(xv) Measure test atmosphere A20 and 

record the stable reading as P3. 

(xvi) Sample test atmosphere A30; a 

stable reading is not required. 

(xvii) Measure test atmosphere A20

and record the stable reading as P4. 

(xviii) Sample test atmosphere A0; a 

stable reading is not required. 

(xix) Measure test atmosphere A20 and 

record the stable reading as P5. 

(xx) Sample test atmosphere A30; a 

stable reading is not required. 

(xxi) Measure test atmosphere A20 and 

record the stable reading as P6. 

(xxii) Measure test atmosphere A80

and record the stable reading as P7. 

(xxiii) Sample test atmosphere A90; a 

stable reading is not required. 

(xxiv) Measure test atmosphere A80

and record the stable reading as P8. 

Increase the chart speed to at least 10 

centimeters per hour. 

(xxv) Measure test atmosphere A0. 

Record the stable reading as L1. 

(xxvi) Quickly switch the test 

analyzer to measure test atmosphere A80

and mark the recorder chart to show, or 

otherwise record, the exact time when 

the switch occurred. 

(xxvii) Measure test atmosphere A80

and record the stable reading as P9. 

(xxviii) Sample test atmosphere A90; a 

stable reading is not required. 

(xxix) Measure test atmosphere A80

and record the stable reading as P10. 

(xxx) Measure test atmosphere A0 and 

record the stable reading as L2. 

(xxxi) Measure test atmosphere A80

and record the stable reading as P11. 

(xxxii) Sample test atmosphere A90; a 

stable reading is not required. 

(xxxiii) Measure test atmosphere A80

and record the stable reading as P12. 

(xxxiv) Repeat steps within 

paragraphs (e)(9)(viii) through 

(e)(9)(xxxiii) of this section, each test 

day. 

(xxxv) If zero and span adjustments 

are made after the readings are taken on 

test days 3, 6, 9, or 12, complete all 

adjustments; then measure test 

atmospheres A0 and A80. Allow for a 

stable reading on each, and record the 

readings as Z’n and S’n, respectively, 

where n = the test day number (3, 6, 9, 

or 12). These readings must be made at 

least 4 hours prior to the start of the 

next test day. 

(10) Determine the results of each 

day’s tests as follows. Mark the recorder 

chart to show readings and 

determinations. 

(i) Zero drift. (A) Determine the 12- 

hour zero drift by examining the strip 

chart pertaining to the 12-hour 

continuous zero air test. Determine the 

minimum (Cmin.) and maximum (Cmax.) 

measurement readings (in ppm) during 

this period of 12 consecutive hours, 

extrapolating the calibration curve to 

negative concentration units if 

necessary. Calculate the 12-hour zero 

drift (12ZD) as 12ZD = Cmax.—Cmin. (See 

Figure B–5 in appendix A.) 

(B) Calculate the 24-hour zero drift 

(24ZD) for the n-th test day as 24ZDn = 

Zn ¥ Zn-1, or 24ZDn = Zn ¥ Z’n-1 if zero 

adjustment was made on the previous 

test day, where Zn = 1⁄2(L1+L2) for L1 and 

L2 taken on the n-th test day. 

(C) Compare 12ZD and 24ZD to the 

zero drift limit specifications in table B– 

1. Both 12ZD and 24ZD must be within 

the specified limits (inclusive) to pass 

the test for zero drift. 

(ii) Span drift. 

(A) Calculate the span drift (SD) as: 

or if a span adjustment was made on the 

previous test day, 

where 

n indicates the n-th test day, and i indicates 

the i-th measurement reading on the nth test day. 

(B) SD must be within the span drift 

limits (inclusive) specified in table B–1 

to pass the test for span drift. 

(iii) Lag time. Determine, from the 

strip chart (or alternative test data 

record), the elapsed time in minutes 

between the change in test 

concentration (or mark) made in step 

(xxvi) and the first observable (two 

times the noise level) measurement 

response. This time must be equal to or 

less than the lag time limit specified in 

table B–1 to pass the test for lag time. 

(iv) Rise time. Calculate 95 percent of 

measurement reading P9 and determine, 

from the recorder chart (or alternative 

test data record), the elapsed time 

between the first observable (two times 

noise level) measurement response and 

a response equal to 95 percent of the P9

reading. This time must be equal to or 

less than the rise time limit specified in 

table B–1 to pass the test for rise time. 

(v) Fall time. Calculate five percent of 

(P10 ¥ L2) and determine, from the strip 

chart (or alternative test record), the 

elapsed time in minutes between the 

first observable decrease in 

measurement response following 

reading P10 and a response equal to L2

+ five percent of (P10 ¥ L2). This time 

must be equal to or less than the fall 

time limit specification in table B–1 to 

pass the test for fall time. 

(vi) Precision. Calculate precision 

(both P20 and P80) for each test day as 

follows: 

(A) 

(B) 

(C) Both P20 and P80 must be equal to 

or less than the precision limits 

specified in table B–1 to pass the test for 

precision. 

TABLE B–5—SYMBOLS AND

ABBREVIATIONS

BL ........ Analyzer reading at the specified 

LDL test concentration for the 

LDL test. 

Bz ......... Analyzer reading at 0 concentration 

for the LDL test. 

DM ...... Digital meter. 

Cmax. ... Maximum analyzer reading during 

the 12ZD test period. 

Cmin. .... Minimum analyzer reading during 

the 12ZD test period. 

i ........... Subscript indicating the i-th quantity 

in a series. 

IE ......... Interference equivalent. 

L1 ........ First analyzer zero reading for the 

24ZD test. 


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TABLE B–5—SYMBOLS AND

ABBREVIATIONS—Continued 

L2 ........ Second analyzer zero reading for 

the 24ZD test. 

n .......... Subscript indicating the test day 

number. 

P .......... Analyzer reading for the span drift 

and precision tests. 

Pi ......... The i-th analyzer reading for the 

span drift and precision tests. 

P20 ...... Precision at 20 percent of URL. 

P80 ...... Precision at 80 percent of URL. 

ppb ...... Parts per billion of pollutant gas 

(usually in air), by volume. 

ppm ..... Parts per million of pollutant gas 

(usually in air), by volume. 

R ......... Analyzer reading of pollutant alone 

for the IE test. 

TABLE B–5—SYMBOLS AND

ABBREVIATIONS—Continued 

RI ........ Analyzer reading with interferent 

added for the IE test. 

ri .......... The i-th analyzer or DM reading for 

the noise test. 

S .......... Standard deviation of the noise test 

readings. 

S0 ........ Noise value (S) measured at 0 concentration. 

S80 ...... Noise value (S) measured at 80 

percent of the URL. 

Sn ........ Average of P7 * * * P12 for the n-th 

test day of the SD test. 

S′n ....... Adjusted span reading on the n-th 

test day. 

SD ....... Span drift 

URL ..... Upper range limit of the analyzer’s 

measurement range. 

TABLE B–5—SYMBOLS AND

ABBREVIATIONS—Continued 

Z .......... Average of L1 and L2 readings for 

the 24ZD test. 

Zn ........ Average of L1 and L2 readings on 

the n-th test day for the 24ZD 

test. 

Z′n ........ Adjusted analyzer zero reading on 

the n-th test day for the 24ZD 

test. 

ZD ....... Zero drift. 

12ZD ... 12-hour zero drift. 

24ZD ... 24-hour zero drift. 

Appendix A to Subpart B of Part 53— 

Optional Forms for Reporting Test 

Results 

BILLING CODE 6560–50–P 


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BILLING CODE 6560–50–C 

PART 58—AMBIENT AIR QUALITY 

SURVEILLANCE 

5. The authority citation for part 58 

continues to read as follows: 

Authority: 42 U.S.C. 7403, 7410, 7601(a), 

7611, and 7619. 

Subpart B—[Amended] 

6. Section 58.10, is amended by 

adding paragraph (a)(7) to read as 

follows: 

§ 58.10 Annual monitoring network plan 

and periodic network assessment. 

(a) * * * 

(7) A plan for establishing CO 

monitoring sites in accordance with the 

requirements of appendix D to this part 

shall be submitted to the Administrator 

by July 1, 2012. The plan shall provide 

for all required monitoring stations to be 

operational by January 1, 2013. 

* * * * * 

7. Section 58.13 is amended by 

adding paragraph (e) to read as follows: 

§ 58.13 Monitoring network completion. 

* * * * * 

(e) The network of CO monitors must 

be physically established no later than 

January 1, 2013, and at that time, must 

be operating under all of the 

requirements of this part, including the 

requirements of appendices A, C, D, and 

E to this part. 

8. Appendix D to Part 58 is amended 

by revising section 4.2 to read as 

follows: 

Appendix D to Part 58—Network 

Design Criteria for Ambient Air Quality 

Monitoring 

* * * * * 

4.2 Carbon Monoxide (CO) Design 

Criteria. 


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4.2.1 General Requirements. (a) One CO 

monitor is required to operate co-located 

with any required near-road NO2 monitor, as 

required in Section 4.3.2 of this part, in 

CBSAs having a population of 1,000,000 or 

more persons. Continued operation of 

existing, but non-required SLAMS CO sites 

using an FRM or FEM is required until 

discontinuation is approved by the EPA 

Regional Administrator, per section § 58.14 

of this part. 

4.2.2 Regional Administrator Required 

Monitoring. 

(a) The Regional Administrators, in 

collaboration with states, may require 

additional CO monitors above the minimum 

number of monitors required in 4.2.1 of this 

part, where the minimum monitoring 

requirements are not sufficient to meet 

monitoring objectives. The Regional 

Administrator may require, at his/her 

discretion, additional monitors in situations 

where data or other information suggest that 

CO concentrations may be approaching or 

exceeding the NAAQS. Such situations 

include, but are not limited to, (1) 

Characterizing impacts on ground-level 

concentrations due to stationary CO sources, 

(2) characterizing CO concentrations in urban 

downtown areas or urban street canyons, and 

(3) characterizing CO concentrations in areas 

that are subject to high ground level CO 

concentrations particularly due or enhanced 

by topographical and meteorological impacts. 

(b) The Regional Administrator and the 

responsible State or local air monitoring 

agency should work together to design and/ 

or maintain the most appropriate CO network 

to address the data needs for an area, and 

include all monitors under this provision in 

the annual monitoring network plan. 

4.2.3 CO Monitoring Spatial Scales. (a) 

Microscale and middle scale measurements 

are the most useful site classifications for CO 

monitoring sites since most people have the 

potential for exposure on these scales. 

Carbon monoxide maxima occur primarily in 

areas near major roadways and intersections 

with high traffic density and often in areas 

with poor atmospheric ventilation. 

(1) Microscale—Microscale measurements 

typically represent areas in close proximity 

to major roadways, within street canyons, 

over sidewalks, and in some cases, point and 

area sources. Emissions from roadways result 

in high ground level CO concentrations at the 

microscale, where concentration gradients 

generally exhibit a marked decrease with 

increasing downwind distance from major 

roads, or within urban downtown areas 

including urban street canyons. Emissions 

from stationary point and area sources, and 

non-road sources may, under certain plume 

conditions, result in high ground level 

concentrations at the microscale. 

(2) Middle scale—Middle scale 

measurements are intended to represent areas 

with dimensions from 100 meters to 0.5 

kilometer. In certain cases, middle scale 

measurements may apply to areas that have 

a total length of several kilometers, such as 

‘‘line’’ emission source areas. This type of 

emission sources areas would include air 

quality along a commercially developed 

street or shopping plaza, freeway corridors, 

parking lots and feeder streets. 

* * * * * 

9. Appendix E to Part 58 is amended 

by revising sections 2 and 6.2(a), 6.2(b), 

6.2(c), and Table E–4 to read as follows: 

Appendix E to Part 58—Probe and 

Monitoring Path Siting Criteria for 

Ambient Air Quality Monitoring 

* * * * * 

2. Horizontal and Vertical Placement 

The probe or at least 80 percent of the 

monitoring path must be located between 

2 and 15 meters above ground level for all 

ozone and sulfur dioxide monitoring sites, 

and for neighborhood or larger spatial scale 

Pb, PM10, PM10¥2.5, PM2.5, NO2, and carbon 

monoxide sites. Middle scale PM10¥2.5 sites 

are required to have sampler inlets between 

2 and 7 meters above ground level. 

Microscale Pb, PM10, PM10¥2.5, and PM2.5

sites are required to have sampler inlets 

between 2 and 7 meters above ground level. 

Microscale near-road NO2 monitoring sites 

are required to have sampler inlets between 

2 and 7 meters above ground level. The inlet 

probes for microscale carbon monoxide 

monitors that are being used to measure 

concentrations near roadways must be 

between 2 and 7 meters above ground level. 

The probe or at least 90 percent of the 

monitoring path must be at least 1 meter 

vertically or horizontally away from any 

supporting structure, walls, parapets, 

penthouses, etc., and away from dusty or 

dirty areas. If the probe or a significant 

portion of the monitoring path is located near 

the side of a building or wall, then it should 

be located on the windward side of the 

building relative to the prevailing wind 

direction during the season of highest 

concentration potential for the pollutant 

being measured. 

* * * * * 

6. * * * 

6.2 Spacing for Carbon Monoxide Probes 

and Monitoring Paths. (a) Near-road or urban 

street canyon CO monitoring microscale sites 

are intended to provide a measurement of the 

influence of the immediate source on the 

pollution exposure on the adjacent area. In 

order to provide some reasonable consistency 

and comparability in the air quality data from 

microscale sites, the CO monitor probe shall 

be as near as practicable to the outside 

nearest edge of the traffic lanes of the target 

road segment; but shall not be located at a 

distance greater than 50 meters, in the 

horizontal, from the outside nearest edge of 

the traffic lanes of the target road segment. 

(b) Downtown urban area or urban street 

canyon (microscale) CO monitor inlet probes 

must be located at least 

10 meters from an intersection and preferably 

at a midblock location. Midblock locations 

are preferable to intersection locations 

because intersections represent a much 

smaller portion of downtown space than do 

the streets between them. Pedestrian 

exposure is probably also greater in street 

canyon/corridors than at intersections. 

(c) In determining the minimum separation 

between a neighborhood scale monitoring 

site and a specific roadway, the presumption 

is made that measurements should not be 

substantially influenced by any one roadway. 

Computations were made to determine the 

separation distance, and Table E–2 of this 

appendix provides the required minimum 

separation distance between roadways and a 

probe or 

90 percent of a monitoring path. Probes or 

monitoring paths that are located closer to 

roads than this criterion allows should not be 

classified as neighborhood scale, since the 

measurements from such a site would closely 

represent the middle scale. Therefore, sites 

not meeting this criterion should be 

classified as middle scale. 

* * * * * 

TABLE E–4 OF APPENDIX E TO PART 58—SUMMARY OF PROBE AND MONITORING PATH SITING CRITERIA

Pollutant 

Scale (maximum 

monitoring path 

length, meters) 

Height from ground 

to probe, inlet or 

80% of monitoring 

path 1

Horizontal and 

vertical distance 

from supporting 

structures 2 to 

probe, inlet or 90% 

of monitoring path 1

(meters) 

Distance from trees 

to probe, inlet or 

90% of monitoring 

path 1 (meters) 

Distance from roadways to 

probe, inlet or monitoring 

path 1 (meters) 

SO2 3,4,5,6 .................. Middle (300 m) .......

Neighborhood 

Urban, and Regional (1 km).

2–15 >1 >10 N/A. 


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TABLE E–4 OF APPENDIX E TO PART 58—SUMMARY OF PROBE AND MONITORING PATH SITING CRITERIA—Continued 

Pollutant 

Scale (maximum 

monitoring path 

length, meters) 

Height from ground 

to probe, inlet or 

80% of monitoring 

path 1

Horizontal and 

vertical distance 

from supporting 

structures 2 to 

probe, inlet or 90% 

of monitoring path 1

(meters) 

Distance from trees 

to probe, inlet or 

90% of monitoring 

path 1 (meters) 

Distance from roadways to 

probe, inlet or monitoring 

path 1 (meters) 

CO 4,5,7 ..................... Micro, middle (300 

m).

Neighborhood (1 

km).

2–7: 2–15 >1 >10 2–10 for downtown urban 

area or street canyon 

microscale; ≤50 for nearroad microscale; see Table 

E–2 of this appendix for 

middle and neighborhood 

scales. 

O3 3,4,5 ...................... Middle (300 m) .......

Neighborhood, 

Urban, and Regional (1 km).

2–15 >1 >10 See Table E–1 of this appendix for all scales. 

NO2 3,4,5 .................... Micro (Near-road 

[50–300]).

Middle (300m) ........

Neighborhood, 

Urban, and Regional (1 km).

2–7 (micro); 2–15 

(all other scales) 

>1 >10 ≤50 meters for near-road 

microscale; 

See Table E–1 of this appendix for all other scales. 

Ozone precursors 

(for PAMS) 3,4,5.

Neighborhood and 

Urban (1 km).

2–15 >1 >10 See Table E–4 of this appendix for all scales. 

PM,Pb 3,4,5,6,8 ........... Micro: Middle, 

Neighborhood, 

Urban and Regional.

2–7 (micro); 

2–7 (middle 

PM10–2.5); 

2–15 (all other 

scales) 

>2 (all scales, horizontal distance 

only) 

>10 (all scales) 2–10 (micro); see Figure E–1 

of this appendix for all other 

scales. 

N/A—Not applicable. 

1 Monitoring path for open path analyzers is applicable only to middle or neighborhood scale CO monitoring, middle, neighborhood, urban, and 

regional scale NO2 monitoring, and all applicable scales for monitoring SO2,O3, and O3 precursors. 2When probe is located on a rooftop, this separation distance is in reference to walls, parapets, or penthouses located on roof.

3Should be >20 meters from the drip-line of tree(s) and must be 10 meters from the drip-line when the tree(s) act as an obstruction. 4 Distance from sampler, probe, or 90% of monitoring path to obstacle, such as a building, must be at least twice the height the obstacle protrudes above the sampler, probe, or monitoring path. Sites not meeting this criterion may be classified as middle scale (see text). 5 Must have unrestricted airflow 270 degrees around the probe or sampler; 180 degrees if the probe is on the side of a building or a wall. 

6The probe, sampler, or monitoring path should be away from minor sources, such as furnace or incineration flues. The separation distance is 

dependent on the height of the minor source’s emission point (such as a flue), the type of fuel or waste burned, and the quality of the fuel (sulfur, 

ash, or lead content). This criterion is designed to avoid undue influences from minor sources. 7For microscale CO monitoring sites in downtown areas or street canyons (not at near-road NO2 monitoring sites), the probe must be >10 meters from a street intersection and preferably at a midblock location. 8 Collocated monitors must be within 4 meters of each other and at least 2 meters apart for flow rates greater than 200 liters/min or at least 1 

meter apart for samplers having flow rates less than 200 liters/min to preclude airflow interference. 

* * * * * 

[FR Doc. 2011–2404 Filed 2–10–11; 8:45 am] 

BILLING CODE 6560–50–P 


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