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37484 Federal Register / Vol. 50, No. 178 / Friday, September 13, 1985 / Rules and Regulations

ENVIRONMENTAL PROTECTION

AGENCY

40 CFR Part 50

[AD-FRL-2866-61

Review of the National Ambient Air

Quality Standards for Carbon

Monoxide

AGENCY: Environmentat Protection

Agency.

ACTION: Final rule.

SUMMARY: In 1971, identical primary and

secondary national ambient air quality

standards (NAAQS) for carbon

monoxide (CO) were promulgated at

levels of 9 parts per million (ppm), 8-

hour average, and 35 ppm, 1-hour

average, neither to be exceeded more than once per year (36 FR 8186). In

accordance with sections 108 and 109 of

the Clean Air Act, EPA has reviewed

and revised the criteria upon which the

existing NAAQS for CO are based, and

has reviewed those standards to

determine if revisions to the standards are appropriate. On August 18, 1980,

EPA proposed certain changes in the

standards based on the scientific

knowledge reported in the revised

criteria document for CO (45 FR 55066).

Today's notice announces EPA's

decision not to revise the existing

primary (health) standards at this time

and revokes the secondary (welfare)

NAAQS for CO. EPA plans to review

several ongoing human health effect

studies upon their completion and, if

warranted, will reexamine this decision

at that time.

EFFECTIVE DATE: This action is effective

October 15, 1985.

ADDRESSES: A docket (Number OAQPS

79-7) containing information relating to

EPA's review of the CO standards, is

available for public inspection and

copying between 8:00 a.m. and 4:00 p.m.,

on weekdays, at EPA's Central Docket

Section, West Tower Lobby, Gallery I,

Waterside Mall, 401 M Street SW.,

Washington, D.C. A reasonable. fee may

be charged for copying.

Availability of Related Information

The final revised criteria document,

"Air Quality Criteria for Carbon

Monoxide" (EPA-600/8-79-022, October

1979; NTIS PB 81-244840, $17.00 paper

and $4.50 microfiche), an addendum to

the criteria document, "Revised

Evaluation of Health Effects Associated

with Carbon Monoxide Exposure"

(EPA-600/8-83-033F, August 1984; NTIS

PB 85-103471, $10.00 paper and $4.50

microfiche) and the final staff paper,

"Review of the NAAQS for Carbon

Monoxide: Reassessment of Scientific

and Technical Information" (EPA-450/

5-84-004, July 1984; NTIS PB 84-231315,

$10.00 paper and $4.50 microfiche) are available from: U.S. Department of

Commerce, National Technical

Information Service (NTIS), 5285 Port

Royal Road, Springfield, Virginia 22161.

FOR FURTHER INFORMATION CONTACT:

Mr. Michael Jones, Strategies and Air

Standards Division (MD-12), Office of

Air Quality Planning and Standards,

U.S. Environmental Protection Agency,

Research Triangle Park, North Carolina

27711, Telephone: (919) 541-5531 (FTS

629-5531).

SUPPLEMENTARY INFORMATION:

Background

Legislative Requirements Affecting This

Action

Two sections of the Clean Air Act

govern the establishment, review, and

revision of NAAQS. Section 108 (42

U.S.C. 7408) directs the Administrator to

identify pollutants which may

reasonably be anticipated to endanger

public health or welfare and to issue air

quality criteria for them. These air

quality criteria are to reflect the latest

scientific information useful in

indicating the kind and extent of all

identifiable effects on public health or

welfare that may be expected from the

presence of the pollutant in the ambient

air.

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

the Administrator to propose and

promulgate "primary" and "secondary"

NAAQS for pollutants identified under

section 108. Section 109(b)(1) defines a primary standard as one the attainment

and maintenance of which in the

judgment of the Administrator, based on the criteria and allowing for an

adequate margin of safety, is requisite to

protect the public health. The 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 the criteria, is requisite to

protect the public welfare from any

known or anticipated adverse effects

associated with the presence of the

pollutant in the ambient air.

The courts have upheld EPA's

interpretation that the requirement for

an adequate margin of safety for

primary standards is intended to

address uncertainties associated with

inconclusive scientific and technical

information available at the time of

standard setting. It is also intended to

provide a reasonable degree of

protection against hazards that research

has not yet identified. Lead Industries

Association v. EPA, 647 F.2d 1130, 1154

(D.C. Cir. 1980), cert. denied, 101 S. Ct.

621 (1980); American Petroleum Institute

v. Costle, 665 F.2d 1176, 1177 (D.C. Cir.

1981), cert. denied, 102 S. Ct. 1737 (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 with an adequate margin of

safety, the Administrator is seeking not

only to prevent pollution levels that

have been clearly demonstrated to be

harmful, but also to prevent lower

pollutant levels that he finds pose an

unacceptable risk of harm, even if that

risk is not precisely identified as to

nature or degree.

In evaluating such risks for the

purpose of providing an adequate

margin of safety, EPA has considered

such factors as the nature and severity

of the health effects involved-, the size of

the sensitive population(s) at risk, and

the kind and degree of the uncertainties

that must be addressed. Given that the "margin of safety" requirement by

definition comes into play where no

conclusive showing of harm exists, such

factors, Which involve unknown,

qualitatively defined, or only partially

quantified risks, have inherent limits as

guides to action. The selection of any

particular approach to providing an

adequate margin of safety is a policy

choice left specifically to the

Administrator's judgment. Lead

Industries Association v. EPA, supra,

647 F.2d at 1161-62.

The courts, however, have endorsed a

reading of the Act that sets strict limits

on the factors EPA may consider in

providing an adequate margin of safety

for primary standards. The leading

judicial decisions state that the

economic and technological feasibility

of attaining primary standards are not to

be relied upon in setting them, even in

the context of a margin of safety. Lead

Industries Association v. EPA, supra,

647 F.2d at 1148-1151; American

Petroleum Institute v. Castle, supra, 665

F.2d at 1185, 1190. Such factors may,

however, be considered to a degree in

the development of State plans to

implement the standards.

Section 109(d) of the Act (42 U.S.C.

7409(d)) requires periodic review and, if

appropriate, revision of existing criteria

and standards. If, in the Administrator's

judgment, the Agency's review and

revision of criteria make appropriate the

proposal of new or revised standards,

such standards are to be revised and

promulgated in accordance with section

109(b). Alternatively, the Administrator

may find that revision of the standards

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is inappropriate and conclude the

review by leaving the existing

standard(s) unchanged. The process by

which EPA has reviewed the original

criteria and standards for carbon

monoxide (CO) under section 109(d) is

described in a later section of this

notice.

States are primarily responsible for

assuring attainment and maintenance of

ambient air quality standards. Under

section 110 of the Act (42 U.S.C. 7410),

States are to submit to EPA for approval

State implementation plans (SIPs) that

provide for the attainment and

maintenance of such standards through

control programs directed to sources of

the pollutants included. Other federal

programs provide for nationwide

reductions in emissions of these and

other air pollutants through the federal

motor vehicle control program, which

involves controls for automobile, truck,

bus, and motorcycle under Title 1I of the

Act (42 U.S.C. 7501 to 7534), and through

the development of new source

performance standards for various

categories of stationary sources under

section 111 (42 U.S.C. 7411).

Original CO Standards, Revision of the

Criteria Document, and Proposed

Revisions of the Standards

Original CO Standards. On April 30,

1971, the Environmental Protection

Agency (EPA) promulgated NAAQS for

CO under section 109 of the Clean Air

Act (36 FR 8186). Identical primary and

secondary standards were set at levels

of 9 ppm, 8-hour average, and 35 ppm, 1-

hour average, neither to be exceeded

more than once per year. The scientific

and medical bases for these standards

are described in the document, "Air

Quality Criteria for Carbon Monoxide"

(DHEW, 1970), published by the U.S.

Department of Health, Education, and

Welfare in March 1970. The primary

standards set in 1971 were based largely

on work by Beard and Wertheim (1967)

suggesting that low-level CO exposures

resulting in carboxyhemoglobin (COHb)

levels of 2 to 3 percent were associated

with impairment of ability to

discriminate time intervals, a central

nervous system effect.

Revision of the Criteria Document. On

December 1, 1978, EPA announced that

it was in the process of reviewing and

updating the 1970 document, "Air

Quality Criteria for Carbon Monoxide,"

and called for information that might be

helpful in revising the document (43 FR

56250). In the process of developing the

revised criteria document, EPA provided

a number of opportunities for review

and comment by organizations and

individuals outside the Agency. Two

successive drafts of a revised criteria

document, prepared by EPA's

Environmental Criteria and Assessment

Office (ECAO), were made available for

external review, and EPA received

approximately 30 written comments on

these drafts. The external review drafts

of the criteria document were also

reviewed by the Clean Air Scientific

Advisory Committee (CASAC)I

Subcommittee on Carbon Monoxide on

January 30-31, 1979 and June 14-15,

1979. These meetings were open to the

public and were attended by individuals

and representatives of organizations

who provided critical reviews and new

information for consideration. A

summary of EPA's responses to the

comments on the two external review

drafts of the criteria document has been

placed in the public docket (Docket No.

ECAO-CD-78-3). Transcripts of the two

CASAC meetings have also been placed

in the docket.

The CASAC prepared a "closure"

memorandum (Hovey, 1979) to the

Administrator indicating its satisfaction

that the final draft of the criteria

document was scientifically adequate

for standard-setting purposes. The

closure memorandum, dated October 9,

1979 also outlines major issues

addressed by the CASAC's and

CASAC's recommendation concerning

those issues. A summary of the issues

raised by CASAC and the general public

prior to proposal is contained in the

proposal notice (45 FR 55080).

On the basis of a careful review of

scientific information contained in the

revised Criteria Document (EPA, 1979a)

EPA's Office of Air Quality Planning

and Standards (OAQPS) prepared a

Staff Paper (EPA, 1979a) in which

several key considerations were

identified as major factors to be

considered in the possible revision of

the CO standards. A draft of the Staff

Paper was provided to the CASAC,

made available to the public, and

reviewed by the CASAC CO

Subcommittee on June 14-15,1979.

Proposed Revisions of the Standards.

The principal findings of the Staff Paper

are summarized in the August 18, 1980

proposal notice (45 FR 55066). As

discussed in this notice and in the

revised Criteria Document, the Beard

and Wertheim (1967) study, the

prinicipal basis for the 1971 primary

standards, is no longer considered a

sound scientific basis for the standards.

However, medical evidence

accumulated since 1970 indicated at the

I CASAC is a standing committee of scientists

and engineers external to the Federal government

established under Section 109 of the Clean Air Act

to advise the Administrator on the scientific basis

for ambient air quality standards.

time of the 1980 proposal that

aggravation of angifia pectoris and other

cardiovascular diseases could occur at

COHb levels as low as 2.7 to 2.9 percent.

Assessment of this and other medical

evidence led EPA to propose: (1)

retaining the 8-hour primary standard

level of 9 ppm, (2) revising the 1-hour

primary standard level from 35 ppm to

25 ppm, (3) revoking the existing

secondary CO standards (since no

adverse welfare effects have been

reported at or near ambient CO levels),

(4) changing the form of the primary

standards from deterministic to

statistical (i.e., EPA proposed to allow

one expected exceedance of each

standard level per year), (5) adopting a

daily interpretation for exceedances of

the primary standards, so that

exceedances would be determined on

the basis of the number of days on

which the 8- or 1-hour average

concentrations are above the standard

levels (45 FR 55066). The proposal notice

set forth in more detail the rationale for

these and other proposed revisions of

the CO NAAQS and background

information related to the proposal.

Developments Subsequent to Proposal

Following proposal, EPA held two

public meetings to receive comments on

the proposed standard revisions.

Meetings were held in Washington, D.C.

on October 2, 1980 and Denver,

Colorado on October 10, 1980;

transcripts are available in the docket

(Docket No. OAQPS 79-7). The CASAC

CO Subcommittee also met on

November 15, 1980 to review the notice

of proposed rulemaking (45 FR 55066)

with EPA officials, and the CASAC met

on November 17, 1981 to hear a status

reporton the regulation. The public was

invited to both CASAC meetings (45 FR

73790 and 46 FR 53210) and transcripts

of the meetings have been placed in the

docket (Docket No. OAQPS 79-7).

On June 18, 1982 EPA announced (47

FR 26407) an additional public comment

period to address several key issues

concerning the 1980 proposal and

technical documents related to the

review of the CO standards. These

issues included: (1) role of the Aronow

(1.981) study, (2) consideration of a

multiple exceedance 8-hour standard,

(3) the technical adequacy of the revised

draft sensitivity analysis on the Coburn

model predictions of blood

carboxyhemoglobin (COHb) levels, and

(4) the technical adequacy of the revised

exposure analysis. The CASAC met on

July 6, 1982 to provide its advice on

these issues. CASAC's

recommendations arising from that

meeting are summarized in an August

37485

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31, 1982 letter to the Administrator

(Friedlander, 1982) which has been

placed in the public docket (Docket No.

OAQPS 79-7, IV-H-41}.

The 1980 proposal was based in part

on the evaluation by EPA staff and

CASAC in 1979 of several health studies

conducted by Dr. Wilbert Aronow. EPA

concluded at that time, based in part on

the Aronow studies, that COHb levels of

2.7-3.0 percent represent a health

concern for individuals with angina and

other types of cardiovascular disease. In

March 1983 EPA learned that the Food

and Drug Administration (FDA) had

raised serious questions regarding the

technical adequacy of several studies

conducted by Dr. Aronow on

experimental drugs, leading FDA to

reject use of the Aronow drug studies

data. While there was then no direct

evidence that similar problems might

exist for Dr. Aronow's CO studies, EPA

concluded that an independent

examination of these studies was

advisable prior in a final decision on the

CO NAAQS.

An expert committee was convened

and met with Dr. Aronow to discuss his

studies and to examine the limited

available data and records from his 1981

CO study. In its report, the Committee

(chaired by Dr. Steven M. Horvath,

Director of the Institute of

Environmental Stress, University of

California-Santa Barbara) concluded

that EPA should not rely on Dr.

Aronow's data due to concerns

regarding the research which

substantially limit the validity and

usefulness of the results (Horvath et al.,

1983). In early June 1983, EPA received a

detailed reply (Aronow, 1983) from Dr.

Aronow disputing, but not effectively

refuting, the major points raised in the

" lorvath Committee" report.

Addendum to the 1979 Criteria

Document and Staff Reassessment. On

August 18, 1983, EPA announced (48 FR

37519] the availability of an external

review draft of a document entitled

"Revised Evaluation of Health Effects

Associated with Carbon Monoxide

Exposure: An Addendum to the 1979 Air

Quality Criteria Document for Carbon

Monoxide" (hereafter cited as

Addendum). The Addendum reevaluates

the scientific data base concerning

health effects associated with exposure

to CO at or near ambient exposure

levels in light of the Horvath

Committee's recommendations

concerning Dr. Aronow's studies and

taking into account new findings

reported beyond those reviewed in the

1979 Criteria Document.

On September 16, 1983 EPA

announced the availability of a draft

staff paper, "Review of the NAAQS for

Carbon Monoxide: 1983 Reassessment

of Scientific and Technical Information"

(hereafter cited as Staff Reassessment]

and solicited public comment on the

draft paper [48 FR 41608). The Staff

Reassessment, prepared by the OAQPS,

provided the staffs assessment of how

the scientific data reviewed in the

Addendum might be used in selection of

final CO standards. CASAC held a

public meeting on September 25, 1983 to

review both the draft Staff

Reassessment. In addition to comments

from CASAC members, representation

of several organizations also provided

critical review of both EPA documents.

A transcript of the CASAC meeting has

been placed in the public docket

(OAQPS 79-7).

The CASAC sent a closure letter to

the Administrator on May 17, 1984

which concluded that both the

Addendum and Staff Reassessment "represent a scientifically balanced and

defensible summary of the current basis

of our knowledge of the health effects

literature for this pollutant" (Lippmann,

1984]. The closure letter, which also

discusses major issues addressed by the

CASAC and CASAC's recommendations

concerning those issues, has been

placed in the public docket (Docket No.

OAQP 79-7, IV-K-25.

On August 9, 1984, EPA announced (49

FR 31923] the availability of the final

Addendum (EPA, 1984b] and final Staff

Reassessment (EPA, 1984a) which were

revised to reflect public and CASAC

comments. Both final documents are

available from the address given earlier

in the Availability of Related

Information Section of this notice.

Where there are differences between the

1979 Criteria Document and 1980

proposal assessment of the health

effects evidence and the more recent

EPA documents, the final Addendum

and final Staff Reassessment

represented the Agency's interpretation

as of their issuance. In the August 9,

1984 notice (49 FR 31923] EPA also

reviewed the basis for EPA's proposal to

revise the CO standards and solicited

additional public comment.

Carbon Monoxide and Human Health

Effects

Control of human exposures to

sources of CO is important because CO,

when inhaled, can enter the

bloodstream and disrupt the delivery of

oxygen to the body's tissues. A

continous and adequate flow of oxygen

to the body's tissues is essential to

maintain normal health. After being

inhaled into the lungs, oxygen normally

enters the bloodstream and is delivered,

via the circulating blood, to the body's

energy-consuming organs, tissues, and

cells. Once in the tissue cells, oxygen

reacts with nutrients to form energy.

This energy is essehtial to the normal

functioning of cells, tissues, and organs.

Humans have specialized molecules

in blood and other tissue cells for

ensuring a large, continuous flow of

oxygen to the tissues. The most

important chemical substance is

"heme," an iron-containing substance

that has a special affinity for oxygen

and that-combines with proteins to form

hemo-proteins. Hemoglobin, a highly

specialized hemo-protein contained in

red blood cells, binds oxygen to the

lungs to form oxyhemoglobin (O2Hb]

and delivers the oxygen to all other

tissues where it is released for use.

Unfortunately, CO can also bind to

hemoglobin, forming

carboxyhemoglobin (COHb), with an

affinity that is 200 to 300 times greater

than that of oxygen. For this reason,

small elevations of CO in ambient air

that enters the lungs can result in a

relatively large displacement of oxygen

from the carrier hemoglobin.

Mechanisms of CO Toxicity

The two principal sources of CO that

contribute to levels of CO in the human

body are: (1) endogenous CO production

from the normal breakdown of

hemoglobin constituents in the body and

(2] inhalation of exogenous CO from

ambient and non-ambient (e.g.,

occupational and indoor) exposures.

2

Endogenous CO production contributes

roughly 0.3 to 0.7 percent of hemoglobin

saturation (0.3 to 0.7 percent COH).

Presently, the most important

mechanism of CO toxicity at low-level

CO exposures is thought to be hypoxia.

This mechanism generally involves

diffusion of exogenous CO through the

lungs into the blood with resultant

formation of COHb. Such an increase in

COHb levels disrupts normal delivery of

oxygen to the tissues in two ways. First,

CO displaces oxygen on the hemoglobin

carrier so that the hemoglobin has a

reduced capacity to carry oxygen

through the blood to the tissues (EPA,

1979b). Second, CO makes it more

difficult for the oxygen that is still

transported by hemoglobin to be

released at the tissue (EPA, 1979b).

Under these conditions, the tissues must

operate at lower than normal levels of

oxygen, a condition known as hypoxia,

and this amount of oxygen may be

inadequate to meet the energy needs of

the tissues. The effects of CO on the

cardiovascular system, central nervous

system, and other systems are thought

2

The contribution of direct smoking to levels of

CO in the body is not a part of this rulemaking.

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to be directly related to this reduction in

the ability of the blood to deliver oxygen

to these systems and thie resultant

oxygen deficiency in the tissues

themselves.

Other possible mechanisms of toxicity

have been discussed (Coburn, 1979;

EPA, 1984b). These alternative

mechanisms involve the binding of CO

to such intracellular hemoproteins as

cytochrome oxidase, myoglobin,

tryptophan deoxygenase, and

tryptophan catalase. Because the

affinity of CO for these proteins is much

less than for hemoglobin, it is unlikely

that they play a major role in CO

hypoxia. However, in tissues with a high

oxygen gradient between blood and

tissue, it is likely that the interaction of

CO with these proteins in these tissues

may play a role in CO toxicity. This is

particularly true of myoglobin in heart

muscle cells. Myoglobin appears to

facilitate the movement of oxygen

through muscle cells and, as a shortterm oxygen reservoir in muscle, it

releases oxygen during sudden

increased metabolic activity. The

affinity of myoglobin for CO is about 40

times greater than the affinity of

myoglobin for oxygen. The ratio of CO

content in heart muscle to CO content in

blood is approximately three. Therefore,

given human exposure to CO,

substantial amounts of CO may be

stored in heart muscle. In situations of

sudden, severe stress or exertion, the

heart muscle's immediate oxygen supply

may be inadequate, even in healthy

persons and particularly in persons with

a history of disease. This mechanism

could provide theoretical support for

experimental evidence of myocardial

ischemia (in which part of the heart

muscle is deprived of oxygen), such as

electrocardiographic irregularities and

decrements in work capacity discussed

later in this notice. It is not known

whether binding of CO to myoglobin is

related to health effects observed at

COHb levels as low as 4-5 percent

(EPA, 1979b).

In summary, disruption of the normal

transport of oxygen by formation of

COHb in the blood appears to be the

primary mechanism of CO toxicity. In

addition, EPA concludes that regardless

of the mechanism of toxicity, COHb

levels provide a meaningful and useful

physiological marker of the body's CO

burden and exposure to exogenous

sources of CO (EPA, 1948b).

Health Effects As A Result of CO

Exposure

Exposure to high levels of exogenous

CO can result in headache, dizziness,

drowiness, nausea, vomiting, collapse,

coma, or death, depehding on how much

the flow of oxygen to the body is

impeded (EPA, 1979b). The most

notorious effects of CO are severe

functional losses and death, which can

result from automobile or truck

emissions trapped in the enclosed

interior of a vehicle or garage. In this

case, so much hemoglobin is bound with

CO that a severely inadequate supply of

oxygen is delivered to the tisses; the

cause of death is severe hypoxia (or

oxygen deficiency). Exposure to lower

levels of CO (i.e., levels closer to

ambient air levels) is associated with

effects on several different organ

systems. Because the cardiovascular

system (including the heart) and the

central nervous system (including the

brain) are always active and have a

continuous need for oxygen, even when

the body is at rest, these organ systems

are particularly sensitive to reduced

supplies of oxygen.

Cardiovascular System. The heart and

blood vessels are critical to human

survival because they pump and carry,

respectively, blood containing oxygen

and essential nutrients to all organs,

tissues, and cells of the body, including

the brain and the heart muscle itself.

Because the heart has almost no ability

to function without oxygen, nor the

ability (except in situations of clear

heart muscle hypoxia) to increase

extraction of oxygen from blood, the

human body has compensatory

mechanisms for ensuring that in lowoxygen situations, the heart continues to

receive whatever oxygen is available

(EPA, 1979b). These compensatory

mechanisms include increasing heart

rate, blood pressure, and blood flow to

maximize the amount of oxygen

available to the muscle (EPA, 1979b).

Although these compensatory changes

have not been associated

experimentally with damage to the

cardiovascular system, it is possible that

the added stress on the body due to the

functioning of the compensatory

mechanisms themselves may result in

damage to the heart muscle or

vasculature (EPA, 1979b). The potential

damage includes those effects

associated with elevated blood pressure,

primarily an increased risk of damage to

the arteries, and elevated heart rate,

which further increases the heart

muscle's demand for oxygen. However,

if the coronary arteries supplying the

heart muscle are unable to compensate

for CO exposure, parts of the heart

muscle may receive amounts of oxygen

inadequate for normal activity.

As a result, EPA is concerned that CO

exposure may increase the risk of the

following effects on the cardiovascular

system:

* Local myocardial ischemia (in

which a part of the heart muscle is

deprived of oxygen);

" Aggravation of angina pectoris;

* Heart attack (myocardial

infarction), including heart attacks

leading to sudden death;

* Reduced exercise and physical

work capacity: and

* Enhanced development of

arteriosclerosis and coronary artery

disease.

Associations between low-level CO

exposure and angina and reduced work

capacity are supported by human

experimental evidence discussed later in

this notice. Angina pectoris (or simply "angina") is a group of symptoms of

pressure and pain in the chest resulting

from a transient episode of insufficient

oxygen supply to a portion of the heart

muscle (EPA, 1948b). The pain probably

results from an accumulation of

unoxygenated metabolic products that

irritate nerve endings in the heart

muscle. The intensity of pain varies from

mild chest discomfort to severe and

incapacitating distress. Although angina,

by definition falls short of inducing

death of part of the heart muscle, it can

cause serious discomfort, and each

attack carries some risk of heart attach.

Acute coronary insufficiency, coronary

failure, and myocardial infarction result

when an episode of ischemia is more

prolonged and severe.

An individual with an underlying

coronary insufficiency is at risk of

having an angina attack under any

condition that places an additional

demand on the heart. CO exposures can

place an added demand on the heart,

and, therefore, would appear to increase

the risk of having an angina attack, and

may increase the risk of a more severe

attack. There is some experimental

evidence of reduced time to onset of

angina attack and increased duration of

angina attack associated with low

COHb levels (Anderson.et al. 1973).

A heart attack is usually a precipitous

and frequently fatal consequence of

coronary heart disease, which usually

results from a sudden reduction or

cessation of a significant portion of the

blood and oxygen flow normally

reaching the heart. Very little is known

about the specific factors which induce

or precipitate heart attack or sudden

death. However, any agent that reduces

the supply of oxygen available to the

heart muscle in an individual with preexisting heart disease is suspect as a

precipitating factor for heart attacks and

sudden death. A relation between

elevated COHb and these cardiac

effects is plausible in light of what is

known about CO toxicity and possible

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pathological mechanisms of heart

disease.

EPA has reviewed the available

epidemiological data relating to

hypotheses of an association between

elevated COflb or CO exposure and the

risk of heart attack, sudden death, and

progression of atherosclerosis and has

found them to be inconclusive (EPA,

1979b). EPA would like to see further

epidemiological research in this area,

although, admittedly, these questions

will be extremely difficult to resolve

with absolute certainty because of the

multitude of experimental confounding

factors, the multitude of risk factors for

heart disease, the variability in human

response, and the technical difficulty in

investigating them.

Nonetheless, from a theoretical

standpoint, associations between CO

and these coronary effects are possible.

For this reason, and because the health

effects in question are very serious, EPA

believes that it is prudent to take early

signs of cardiovascular effects and other

potential, but not well understood,

cardiovascular effects very seriously.

Central Nervous System. Elevated

COllb levels can reduce the oxygen

available to parts of the central nervous

system (CNS), including the brain. It

appears that the body can compensate,

to some extent, by increasing the blood

flow through the brain's vasculature

(EPA, 1979b). However, in some

circumstances compensation may not

always occur, leaving the brain with a

reduced amount of available oxygen. In

addition, or alternatively, prolonged

compensation may damage the brain's

blood vessels (EPA, 1979b).

When elevated COHb reduces the

amount of oxygen delivered to the brain

to a level which is below critical needs,

two types of damage may result. First,

severe acute oxygen deprivation of

sufficient duration and intensity can

result in a stroke (the damage or death

of brain cells (neurons)). Loss of mature

brain cells is irreversible since the CNS

is not thought capable of replacement of

neurons. Depending upon the duration of

oxygen deficit to the brain, the effects

may range from unconsciousness and

convulsions, brain swelling and

protrusion, to death of parts of the brain

or death of the individual. Individuals

who recover often have significant

deficits in brain function. Second,

repeated episodes of impaired oxygen

supply would be expected to damage

the blood-brain barrier and possibly

cause structural damage resulting in the

inability of the CNS to transmit

information.

At lower CO-lb levels there is

evidence of neurobehavioral effects:

impaired learning ability, reduced

vigilance (ability to detect small changes

in a subject's environment), decreased

manual dexterity, impaired performance

of complex tasks, and disturbed sleep

activity (EPA, 1984b). Although the

potential influence of ambient CO levels

on drivers has received only slight

attention, suggestive but not conclusive

evidence has indicated that drivers in

fatal auto accidents often have elevated

COHb levels (Yabroff et al., 1974). There

is no evidence with which to determine

whether these effects at lower CO levels

are associated with pathological

changes to the CNS or with reduced

oxygen tension in the CNS. Due to

redundancy in structure of the CNS,

functional changes (e.g., behavior

changes) may not be observed until the

structural damage is great. Observation

of such effects may be more likely in the

case of a severe reduction in oxygen or

in an individual who has a history of an

impaired oxygen delivery system.

Basis for Decision Not To Revise the

Primary Standards

The current primary NAAQS for CO

are 10 mg/m 3 (9 ppm), 8-hour average

and 40 mg/m 3 (35 ppm), 1-hour average,

neither of which is to be exceeded more

than once per year. As indicated above,

the Act requires review of the existing

criteria and ambient air quality

standards for CO and other pollutants

every five years. During the current

standard review for CO, EPA has

considered whether it should retain the

existing CO primary standards,

repropose the same or different

standards, or promulgate the revisions

proposed in August 1980. For the

reasons discussed below, the

Administrator has concluded that there

is no need to revise the existing primary

CO standards at this time.

As indicated above, section 109(b)(1)

of the Clean Air Act requires EPA to set

primary standards, based on the air

quality criteria which, in the

Administator's judgment, are requisite

to protect the public health with an

adequate margin of safety. The

legislative history of the Act makes

clear the Congressional intent to protect

sensitive persons who in the normal

course of daily activity are exposed to

the ambient environment. Air quality

standards are to be established with

reference to protecting the health of a

represenative, statistically related,

sample of persons comprising the

sensitive group rather than a single

person in such a group.

EPA's objective in reviewing primary

standards, therefore, has been to

determine whether new or revised

standards are appropriate, based on the

existing scientific evidence, assessment

of the uncertainties in this evidence,

understanding of underlying biological

mechanisms, and the need to make a

reasonable provision for scientific and

medical knowledge yet to be acquired.

in order to protect sensitive population

groups with an adequate margin of

safety. As for other ambient standard

pollutants, none of the evidence

presented in the 1979 Criteria Document

or Addendum shows a clear threshold

for adverse health effects of CO. Rather,

there is a continuum, ranging from CO

levels at which health effects are

undisputed, through levels at which

many, but not all scientists generally

agree that health effects have been

convincingly shown, down to levels at

which the indication of health effects

are less certain.and more difficult to

identify. This does not necessarily mean

that there is no threshold, other than

zero, for CO related health effects; it

simply means that no precise threshold

can be identified with certainty based

on existing scientific evidence. Thus, in

setting a standard, EPA is unable to

append an exact margin of safety to a

known threshold effect level. Rather,

setting a standard with an adequate

margin of safety is necessarily a public

health policy judgment that must take

into account both the known continuum

of effects, understanding of the

underlying biological mechanisms of

effects, and any gaps and uncertainties

in the existing scientific data base.

In determining whether revision of the

primary CO standards is appropriate,

EPA has made assessments and

judgments in the following areas:

1. Identification of reported effect

levels and associated exposure duration

that scientific research has linked to

health effects in healthy and sensitive

persons.

2. Characterization of scientific

uncertainties in the health effects

evidence and judgments concerning

which effects are important to consider

in reviewing or setting primary

standards.

3. Description of population groups

believed to be most sensitive to CO and

estimates of the size of those groups.

4. The estimated number of sensitive

persons that would be exposed to

elevated CO levels upon attainment of a

given standard and the uncertainties in

these exposure estimates.

5. The uncertainties in estimating

carboxyhemoglobin (COHb) levels that

result from exposures to CO.

6. Consideration of CO standard

levels and averaging times that provide

an adequate margin of safety based on

CO levels and exposure periods that

may affect sensitive population groups,

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No. 178 / Friday, September 13, 1985 / Rules and Regulations 37489

taking into account the various

uncertainties.

Based on the assessment of relevant

scientific and technical information in

the Criteria Document and the

Addendum, the Staff Reassessment

outlines a number of key factors to be

considered in each of the above areas.

Both the staff and CASAC

recommended that the Administrator

focus consideration on a discrete range

of policy options in each area. In most

respects, the Administrator has adopted

the recommendations and supporting

reasons contained in the Staff

Reassessment, the most recent CASAC

closure letter (Lippmann, 1984) and

applicable portions of the earlier Staff

Paper (EPA, 1979b) and CASAC closure

letters (Hovey, 1979; Friedlander, 1982).

Rather than reiterating those

discussions at length, the following

discussion of the final decision focuses

primarily on those considerations that

were most influential in the

Administrator's selection of a particular

option, or that differ in some respect

from considerations that influenced the

staff and/or CASAC recommendations.

Assessment of Health Effects Evidence

The Staff Reassessment, which has

been placed in the public docket (Docket

No. OAQPS 79-7, IV-A-10), presents an

assessment by OAQPS staff of the key

health effect studies contained in the

1979 Criteria Document and in the

Addendum and other critical scientific

and technical issues relevant to the

review of the existing CO standards.

TABLE 1.-LOWEST OBSERVED EFFECT LEVELS

FOR HUMAN HEALTH EFFECTS ASSOCIATED

WITH Low LEVEL CARBON MONOXIDE ExPoSURE

COHb

Effects concen. References tration

(percent)-

Statistically significant

decreased (-3-7%)

work bme to

exhaustion in

exercising young

healthy men.

Statistically significant

decreased exercise

capacity (i.e.,

shortened duration

of exercise before

onset of pain) in

patients with angina

pectoris.

Statistically significant

decreased maximal

oxygen consumption

and exercise time

during strenuous

exercise in young

healthy men.

No stat~stically

significant vtglance

decrements after

exposure to CO.

2.3-4.3 Horvath et al. 1975.

Drinkwater at al.,

1974. Raven at al..

1974.

2.9-4.5 Anderson al al., 1973.

5-5.5

Below 5

Klein at al., 1980,

Stewart at at.. 1979.

Weiser at al.. 1978.

Haider at al.. 1976.

Winneke. 1974,

Christensen at al..

1977. Benegnus at

al., 1977. Puttz o atl..

1976.

TABLE 1.-LOWEST OBSERVED EFFECT LEVELS

FOR HUMAN HEALTH EFFECTS ASSOCIATED

WITH Low LEVEL CARBON MONOXIDE ExPoSURE-Continued

COHb

Effets concen- References htroion

(percent)'

Statistically significant 5-7.6 Horvath et at. 1971.

impairment of GrolI-Knapp etalt.,

vigilance tasks in 1972. Fodor and

healthy experimental Winneke. 1972. Putz

subjects. et al., 1976.

Statistically significant 5-17 Bender et al., 1971,

diminution of visual Schulte, 1973.

perception, manual O'Donnell et al.,

dexterity. ability to 1971, McFarland el

learn, or al.. 1944, McFarland.

performance in 1973, Putz et al.,

complex 1976. Salvatore.

sensorimotor tasks 1974, Wright et al.,

(such as driving). 1973, Rockwell and

Weir. 1975. Rummo

and Sartanis, 1974,

Putz et al., 1979,

Putz, 1979.

Statistically significant 7-20 Ekblom and Huot.

decreased maximal 1972, Prnay et at.

oxygen consumption 1971, Vogel and

during strenuous Gleser. 1972.

exercise in young

healthy men.

The physiologic norm (i.e., COHb levels resulting from the normal breakdown of hemoglobin and other heme.containing materials) has been estimated to be in the range of 0.3 to 0. 7 percent (Coburn at al., 1963).

Table I is a summary of key clinical

studies reporting human health effects

associated with low-level exposures to

CO. This table is based on evidence

discussed in the 1979 Criteria Document

(EPA, 1979a) and in the Addenum (EPA,

1984b) but excludes a series of studies

by Dr. Aronow for reasons given below.

The table is included primarily as an aid

for the following discussion and should

be used only in conjunction with

qualifying statements made in the 1979

Criteria Document, in the Addenum, in

the Staff Reassessment, or in this notice

regarding the technical merits of each

study.

Cardiovascular Effects. In reviewing

the primary standards, a principal area

of concern to the Administrator has

been evidence linking aggravation of

angina and other cardiovascular

diseases to CO exposures. Angina

patients who have been exposed to low

levels of CO while resting have

subsequently exhibited, during exercise,

reduced time to onset of angina

(Anderson et al., 1973). Increased

duration of angina attacks has also been

reported (Anderson et al., 1973). In

proposing to revise the CO standards,

EPA viewed aggravation of angina, as

reported above, to be an adverse health

effect (45 FR 55066) and CASAC

concurred with EPA's judgment on this

matter.

One controlled human exposure study

(Anderson et al. 1973) reported that

experimental subjects with angina

exhibited statistically significant

reduced time to onset of exerciseinduced angina after exposure to low

levels of CO resulting in mean COHb

levels of 2.9 (range 1.3-3.8 percent) and

4.5 percent (range 2.8-5.4 percent). In the

same study, it was reported that

subjects experienced statistically

significant increases in duration of

angina attacks during exercise at a

mean COHb level of 4.5 percent. Some

concerns have been raised about the

study findings due to ambiguities

regarding the design and conduct of the

study and the small number of subjects

(N=10) examined. However, as

discussed in the Addendum and in a

subsequent section of this notice, a

reevaluation of the Anderson et al.

(1973) study, addressing major points of

concern, found that the study provides

reasonably good evidence for the

hastening of angina occurring in angina

patients at COHb levels of 2.9 to 4.5

percent.

In similar studies Aronow and Isbell

(1973) and Aronow (1981) reported

decreased time to onset of angina for

exercising subjects with reported COHb

levels in the range of 2 to 3 percent. In

addition, Aronow et al. (1974) reported

that subjects with peripheral vascular

disease had reduced time to onset of leg

pain at similar COHb levels. As

discussed earlier in this notice, however,

an expert committee convened to

conduct an independent review of these

CO studies expressed considerable

concern about the validity of the result

reported and concluded that EPA should

not rely on.Dr. Aronow's data (Horvath

et al., 1983.3 As stated earlier in this

notice, Dr. Aronow provided EPA a

detailed reply disputing, but not

effectively refuting, the substance of the

concerns raised by the Committee

(Aronow, 1983). The Committee also

recommended that EPA pursue and

support both current in-house and

independent scientific research to

resolve the issues raised by the

reevaluation of Dr. Aronow's CO

studies. Because EPA shares the

concerns raised by the committee and

by some public comments, the

Administrator has not considered Dr.

Aronow's studies in his decision on the

CO primary standards.

iThe Committee's concerns included (1) apparent

failure to maintain a "double blind" approach as

reported in the publications. (2 raw data were lost

or discarded, (3) available data were of poor

quality. (4) quality control for COHb measurements

was nonexistent or inadequate, and (5) there

appeared to be discrepancies between hospital

record descriptions of patient diagnosis and those

reported in Dr. Aronow's publications [Hlorvath et

a1., 1983).

Federal Register / Vol. 50,

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37490 Federal Register / Vol. 50, No. 178 / Friday, September 13, 1985 / Rules and Regulations

Another cardiovascular effect of

concern is the possible detrimental

effect of increased blood flow that

occurs as a compensatory response to

CO exposure (Ayres et al., 1969; Ayres

et al., 1970; and Ayres et al., 1979). This

effect may be related to coronary

damage or cerebrovascular effects at

very high blood flow rates due to the

added stress on the cardiovascular

system. However, community

epidemiological studies have been

inconclusive. In particular, based on

EPA's evaluation of the Goldsmith and

Landau (1968), Kurt et al. (1978), and

Kurt et al. (1979) epidemiological

studies, the relationship between CO

exposures and effects such as mortality

from myocardial infarction (heart

attack), sudden death due to

arteriosclerotic heart disease, and

cardiorespiratory complaints remains in

question.

Maximum aerobic capacity and

exercise capacity are indirect measures

of cardiovascular capacity which have

been reported to be reduced in several

carefully conducted studies involving

normal healthy adults exposed to CO. A

linear decline in maximum aerobic

capacity for healthy individuals was

reported for COt-lb levels ranging fron

5-20 percent in a series of studies

(Stewart et al., 1978; Weiser et al., 1978;

and Ekblom and Huot, 1972). Hlorvath et

at. (1975) found decreases in maximum

aerobic capacity when COI lb levels

were 4.3 percent and that COHb levels

of 3.3 and 4.3 percent reduced work time

to exhaustion by 4.9 and 7.0 percent,

respectively. The effects of lower CO

exposure levels in healthy individuals

have also been investigated under

conditions of short-term, maximum

exercise duration. In a series of studies

involving different CO exposure levels,

two alternative ambient temperatures

(25°C and 35'C), and two different

healthy adult populations (young and

middle-aged), no statistically significant

reduction in maximum aerobic capacity

was observed for either group when CO

exposures were compared with the

clean air control. However, small (less

than or equal to 5 percent) decreases in

absolute exercise time were consistently

observed in the non-smoking subjects

whose COt lb levels reached 2.3 and 2.5

percent (Drinkwater et al., 1974; Raven

et al., 1974). These effects, while not as

serious as aggravation of angina, are

still a matter of concern since they have

been found to occur in healthy

individuals and such effects might

impair the normal activity of more

sensitive populations. Therefore, these

effects have been considered in judging

which CO standards provide an

adequate margin of safety.

Central Nervous System Effects.

Numerous studies (Putz et al., 1976;

Bender et al., 1971; Schulte, 1973;

O'Donnel et al., 1971; McFarland et al.,

1944; McFarland, 1973; Salvatore, 1974;

Wright et al., 1973; Rockwell and Weir,

1975; and Rummo and Sarlanis, 1974)

have reported effects on the central

nervous system for CO exposures

resulting in COttb levels in the range 5-

17 percent. The range of effects reported

included impairment of vigilance, visual

perception, manual dexterity, learning

ability, and performance of complex

tasks. While one study (Beard and

Grandstaff, 1975) has suggested that

vigilance effects may occur at levels as

low as 1.8 percent COHb, several other

studies (Haider et al., 1976; Winneke,

1976; Christensen et al., 1977; Benignus

et al., 1977; and Putz et al., 1976) have

not found any vigilance decrements

below 5 percent COHb. Measurement

methods used to detect effects may have

been too insensitive to detect changes in

the latter vigilance studies. Based on the

assessment of the above mentioned

studies, the Addendum concluded that,

at least under some conditions, small

decrements in vigilance occur at 5

percent COHb. A series of studies (Putz

et al., 1976; Putz et al., 1979; and Putz

1979) has also found that 5 percent

COHb produced decrements in

compensatory tracking, a hand-eye

coordination task. EPA considers handeye coordination effects as well as

decrements in vigilance to be important

since these functions are components of

more complex tasks, such as driving,

and reduced alertness or visual

sensitivity could lead to increased

vehicular accidents.

Fetal Effects. Based on limited animal

toxicology data, the 1979 Criteria

Document and the Addendum (EPA,

1984b) suggest that CO may produce

effects on the fetus or newborn. CO from

long-term or intermittent exposures is

taken up and eliminated more slowly in

the fetus than in the mother, so that a

maternal exposure can result in mean

fetal COtlb concentrations well above

maternal COHb levels (EPA, 1979b).

Elevated COHb levels may lead to

interference with fetal tissue

oxygenation during development.

Because the fetus may be developing at

or near critical tissue oxygenation

levels, even exposures to moderate

levels of CO may produce deleterious

effects on the fetus such as reduced

birth weight, increased newborn

mortality, and lower behavioral activity

levels (Longo, 1977), although this

remains to be demonstrated along with

pertinent dose-response relationships

(EPA, 1984b). Evidence from smoking

mothers is suggestive of similar fetal

and newborn effects due to CO

exposures (Peterson, 1981). While the

fact that cigarette smoke contains

substances other than CO prevents a

direct quantitative application of the

results of these studies in setting the CO

primary standards, these studies do

suggest the need for caution in

protecting unborn children from such

potentially deleterious effects of CO

exposures.

As discussed in the Addendum and

Staff Reassessment, research on sudden

infant death syndrome (SIDS) recently

has suggested a possible link between

ambient CO levels and increased

incidence of SIDS (Hoppenbrowers et

al., 1981). In response to this study,

Goldstein (1982) has suggested that

indoor sources of CO, as well as other

pollutants (e.g., nitrogen dioxide, lead),

may be at least as important as ambient

CO in causing SIDS and that several

covariates (e.g., seasonal trends) may be

responsible for the associations

reported. Because the number of

potentially confounding factors makes

finding an association between CO and

SIDS extremely difficult, further

confirmation is needed before any

causal relationship can be inferred

(EPA, 1984a; EPA, 1984b).

Sensitive Population Groups

In EPA's judgment, the available

health effects data identify persons with

angina or other types of cardiovascular

disease (e.g., history of heart attack or

peripheral vascular disease) as the

groups at greatest risk from low-level,

ambient exposures to CO. Based on 1980

census data (DOC, 1980) and earlier U.S.

National Health Examination Survey

data (DHEW, 1975), this group is

estimated to number approximately 8.7

million individuals. As discussed

previously, the concern for persons with

cardiovascular disease results from the

fact that their condition is due to an

insufficient oxygen supply to cardiac

tissue, so that persons with this

condition have an inadequate oxygen

reserve capacity and an impaired ability

to compensate for the effects of excess

Co.

The Addendum and Staff

Reassessment also identify several other

groups as likely to be particularly

sensitive to low-level CO exposures

based on EPA's review of the health

effects evidence. These groups include:

(1) persons with chronic respiratory

disease (e.g., bronchitis, emphysema,

and asthma), (2) elderly individuals,

especially those with reduced

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cardiopulmonary function, (3) fetuses

and.young infants, and (4) individuals

suffering from anemia and those with

abnormal hemoglobin types that affect

oxygen carrying capacity or transport in

the blood. In addition, individuals taking

certain medications or drinking

alcoholic beverages may be at greater

risk for CO-induced effects based on

some limited evidence suggesting

interactive effects between CO and

some drugs. Visitors to high altitude

locations are also expected to be more

vulnerable to CO health effects due to

reduced levels of oxygen in the air they

breathe. Finally, individuals with some

combination of the disease states or

conditions listed above (e.g., individuals

with angina visiting a high altitude

location) may be particularly sensitive

to low-level CO exposures, although

there is no experimental evidence to

confirm this hypothesis.

For many of the groups cited above

there is little specific experimental

evidence to clearly demonstrate that

they are indeed at increased risk for

CO-induced health effects. However, it

is reasonable to expect that individuals

with preexisting illnesses or

physiological conditions which limit

oxygen absorption into blood or its

transport to body tissues would be more

susceptible to the hypoxic (i.e., oxygen

deficiency) effects of CO. Since no

human experimental evidence exists

that identifies CO effect levels for these

other groups, however, EPA is

considering the possible effects of CO

on these groups only in its determination

of an adequate margin of safety.

Uncertainty in Estimating COHb Levels

The health effect studies discussed

above report the effects observed at

varying COHb levels. In order to make

decisions about ambient CO standards

based on these studies, it is necessary to

estimate the ambient concentrations of

CO that are likely to result in COHb

levels at or near those observed in the

studies. A model known as the Coburn

equation (Coburn et al., 1965) has been

developed to estimate COHb levels

resulting from CO concentrations as a

function of time and various

physiological factors (e.g., blood volume,

endogenous CO production rate). Table

2 presents "baseline" estimates (using

typical values for the various

physiological parameters) of COHb

levels expected to be reached by adult

nonsmokers exposed to various constant

concentrations of CO for either 1 or 8

hours based on the Coburn model.

TABLE 2.-PREDICTED COHb RESPONSE TO

EXPOSURE TO CONSTANT CO CONCENTRATIONS ASSUMING TYPICAL VALUES FOR

PHYSIOLOGICAL PARAMETERS

(Percent COHb Based on Coburn Equation" Exposure Time

1 hour exposure 8 hours exposure

Intermit- Intermit- I

CO (ppm) tent rest/ Moderate tent rest/ I Moderate

light activity light activity activity activity

TABLE 2.-PREDICTED COHb RESPONSE TO

EXPOSURE TO CONSTANT CO CONCENTRATIONS ASSUMING TYPICAL VALUES FOR

PHYSIOLOGICAL PARAMETERS-Continued

(Percent COHb Based on Coburn Equation, Exposure Time

1 hour exposure 8 hours exposure

Intermit- Intermit- CO (ppm) tent rest/ Moderate tent rest/ Moderate

light activity light activity

activity activity

50.0 2.0 2.7 6.4 6.9

-Assumed parameters for non-smoking adults: alveolar

ventilation rates= 10 liters/mn (intermittent rest/light activity)

and 20 liters/min (moderate activity); hemoglobin= 15 9/100 ml (normal male): ahitude-sea level; initial COHb level=0.5 percent; endogenous CO production rate=O.007 ml/mmo; blood volume=5500 ml. Haldane constant (measure of affini- ty of hemoglobin for CO)=218; lung ditfusivity for CO 30 m!/min/torr.

TABLE 3.-PERCENTAGE OF NON-SMOKING ADULTS WITH CARBOXYHEMOGLOBIN GREATER THAN

OR EQUAL TO SPECIFIED PEAK VALUE WHEN EXPOSED TO AIR QUALITY ASSOCIATED WITH

ALTERNATIVE EIGHT-HOUR CARBON MONOXIDE STANDARDS a.b.C

9 ppm, 8-hr 12 ppm, 8-hr

Mid- MidPeak COHb percent Low range High Low High

pat- rag pat- pat- range

tern tern tern pat- tern tern tern 1

3 .7 .............................................................................................................

......................................... ... < 0.0 1

3 .5 .......................... 1 ........................................................... a ....................................................................... ....................................... ... 0 .0 1 3 .3 .............................................................................................................

............................ 0 .1

3 .1 .............................................................................................................

............... ............... ............... ................ < 0 .0 1 0 .6 2.9 .............................................................................................................

o ................. <0.01 ............... 001 2

2.7 .............................................................................................................

0.02 <0.01 0.2 9

2.5 ..................................................................................................................... <0.01 0.2 0.01 2. 36

2.3 .............................................................................................................

. 0.02 2 0.2 12 84

2.1 .............................................................................................................

<0,01 0.4 10 4 49 100

1.9 .............................................................................................................005 5 53 36 88 100

1.7 .............................................................................................................

3 35 98 91 99 100

1.5 .............................................................................................................

39 88 100 100 100 100

1.3 .............................................................................................................97 100 100 100 100 100

1.1 .............................................................................................................

100 100 100 100 100 . 100

"COHb responses to fluctuating CO concentrations were dynamically evaluated using the Coburn model prediction of the COHb level resulting from one hour's exposure as the initial COHb level for the next hour. The series of 1-hour CO concentrations used were from 20 sets of actual air quality data. Each pattern was proportionally rolled back or up so that-its peak 8-hour average CO concentration equalled the level of the 8-hour standard. Of the 20 selected patterns, results from 3 patterns are presented here. The low pattern tends to give the lowest peak COHb levels, the midrange pattern tends to give a

midrange value, and the high pattern tends to give the highest value. * Haldane constant= 218. Alveolar ventilation rate= 10 liters/min. Altitude =0.0 ft. * The estimation of distributions for each of the physiological parameters used in the Coburn model and the Monte Carlo

procedure used to generate these estimates are discussed in Appendix C of the Sensitivity Analysis (Biller and Richmond,

1982).

There are, however, at least two

uncertainties involved in estimating

COHb levels resulting from exposure to

CO concentrations. First, for each of the

physiological parameters used in the

Coburn model, there is a distribution of

values in the general population. These

variations are sufficient to produce

noticeable deviations from the COHb

levels in Table 2, which as noted above

were predicted using a set of typical

physiological parameter values. Second,

predictions based on exposure to

constant CO concentrations

inadequately represent the responses of

individuals exposed to widely

fluctuating CO concentrations that

typically occur in ambient exposure

situations.

As discussed in the proposal

preamble (45 FR 55066), EPA attempted

to represent these uncertainties in a

draft Sensitivity Analysis (EPA, 1980).

This analysis used the Coburn model to

examine the effects of fluctuating CO

concentrations and variations in

physiological parameters on COHb

estimates. Since proposal, EPA has

revised the Sensitivity Analysis to

address concerns raised in several

public comments and placed the repoit

(Biller and Richmond, 1982) in the

docket (QAQPS 79-7, IV-A-8). Table 3

presents estimates of the distribution of

COHb levels in the adult non-smoking

population based on variations in

physiological parameters upon exposure

to three different patterns of CO levels

which just meet alternative 9 ppm and

12 ppm CO standards. The estimates

given in Table 3 and others contained in

the Sensitivity Analysis report (Biller

and Richmond, 1982) are based on the

assumption that the entire adult

population is exposed to CO levels just

meeting a given standard.

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The impact of fluctuating air quality

levels on COHb uptake can be roughly

estimatdd by comparing the "baseline"

result of a constant 9 ppm exposure for 8

hours (1.4 percent COHb from Table 2)

with selected results shown in Table 3.

For a "typical" (50th percentile) adult

exposed to several different air quality

patterns that result in the same

maximum 8-hour dose (i.e., 9 ppm, 8-

hour average), the results shown in

Table 3 indicate that COHb levels

ranging from approximately 1.4 to 1.9

percent can be reached. A similar

comparison of the results for air quality

with a 12 ppm, 8-hour average peak

exposure indicates that fluctuating CO

levels can increase the peak COHb

value from that observed with a

constant CO exposure by up to 0.7

percent OCHb (i.e., from 1.7 percent

COHb in Table 2 to 2.4 percent COHb

for the 50th percentile in the high pattern

column of Table 3).

The Sensitivity Analysis results in

Table 3 also illustrate the effect of using

distributions of values for each

physiological parameter rather than just

a single representative set of values in

applying the Coburn model. For any

given air quality pattern, the effect of

using the distribution of values for each

physiological parameter is to generate a

distribution of peak COHb levels that

the population would reach. For

example, the results in Table 3 show

that 95 percent of the population is

estimated to be within ±0.3 percent

COHb of the median adult value after

exposure to the midrange pattern with a

peak 9 ppm, 8-hour average. This

variation in COHb levels attained is one

further source of uncertainty that is

being considered in judging which

standards provide an adequate margin

of safety.

Since proposal, EPA has made

considerable improvements in its

exposure analysis methodology which,

unlike the Sensitivity Analysis, treats

movement of people and variation of CO

concentration levels through time and

space. EPA believes that the revised

Exposure Analysis described below,

represents the best available tool for

estimating the percentage of the

population that would reach various CO

concentrations and COHb levels upon

attainment of alternative CO standards.

Since the Exposure Analysis model

simulates the exposure of individuals on

an hourly basis and simulates actual air

quality patterns, the impact of

fluctuating CO levels is largely taken

into account in the Exposure Analysis

results. The results of the revised

Sensitivity Analysis are useful,

however, in characterizing the

uncertainties resulting from variations in

physiological parameters in the

population which at this time are not

fully accounted for in the Exposure

Analysis.

Exposure Analysis Estimates

EPA's revised exposure analysis

report and addendum, "The NAAQS

Exposure Model (NEM) Applied to

Carbon Monoxide," (Johnson and Paul,

1983; Paul and Johnson, 1985) contain

estimates of the numbers and

percentages of urban American adults

that would be exposed to various

ambient CO levels if alternative 8-hour

CO standards were just attained. In

addition, estimates have been made of

the percentage of this population that

would exceed selected COHb levels

each year. These latter estimates were

derived by applying the Coburn model

which relates patterns of CO exposure

to resultant COHb levels, to the

exposure model outputs using a typical

set of physiological parameters for adult

men and a separate set of physiological

parameters for adult women.

In contrast to the Sensitivity Analysis,

the Exposure Analysis simulates

pollutant concentrations and the

activities of people with regard to time,

place, and exercise level. In the

exposure model, the population is

represented by a set of "cohorts" (i.e.

age-occupational groups that tend to

"track together" in time and space). For

each hour of the year each cohort is

located in one of five

"microenvironments." A

microenvironment is a general physical

location such as indoors-at-home or

inside a transportation vehicle.

CO levels in each of the

microenvironments are estimated by the

use of multiplicative "transformation

factors," which relate CO levels

recorded at the nearest monitor to

estimate CO levels for each

microenvironment. This method is used

since attainment of a standard is

defined in terms of the monitoring

system. Values of the multiplicative

transformation factors that would give

the best exposure estimates are

uncertain. The values used for these

factors were estimated making use of

the available literature on (1) indoor and

inside-motor-vehicle air pollution and

(2) statistical analyses of monitoring

data (e.g., how ambient values change

with height and distance from a

monitor). A more detailed description of

the approach, input data, and

assumptions used to derive exposure

estimates appears in the Exposure

Analysis reports (Johnson and Paul,

1983; Paul and Johnson, 1985).

The exposure analysis model

described above was applied to four

urban areas: Chicago, Los Angeles,

Philadelphia, and St. Louis. Exposure

estimates for the adult population living

in urban areas in the United States were

obtained primarily by associating each

urban area in the United States having a

population greater than 200,000 with one

of the four cities mentioned above. The

association was made on the basis of

geographic proximity to one of the base

areas, average wind speed, peak CO

concentrations, observed climate, and

general character of the area.

TABLE 4.-CUMULATIVE PERCENT OF ADULT

POPULATION IN URBAN AREAS WHOSE COHb

Levels Would Exceed Specified COHb Val.

ues Upon Attainment of Alternative 8-Hour

Standards 1..,c

8--our standards

COHb level 12 ppm 15 ppm cee 9 p[pm 1 I

exceeded (percent) expected expected expected

exceedance exceed- exceed-

__________ ance ance

3.0 ................. .. <.01 1.1 2.9 . . ..... .................................... .02 2.5

2.7 ....................................... 0.1 5.9 25.... .... . 0,8 9.7

2.3 .................. <0.1 4.1 14 2.1 ...................... .... 0.1 (<.01)" 8.6 20

.Projected cardiovascular and peripheral vascular disease

population in all urbanized areas in the United States for

1987 is 5.240.000 adults. bThese exposure estimates are based on air quality distributions which have been adjusted to just attain the given standards.

' These exposure estimates are based on best judgments of microenvironment transformation factors. Projections for one urban area based on lower and upper estimates of the

microenvironment transformation factors are provided in the

Exposure Analysis report (Johnson and Paul. 1983). "Exposure estimate for current 9 ppm. 8-hour average deterministic standard.

Table 4 provides estimates for 1987 of

the percentage of the adult population

living in urban areas who would exceed

various COHb levels upon attainment of

three alternative 8-hour standards. For

example, less than 0.01 percent of the

adult population in urban areas is

estimated to exceed 2.1 percent COHb

due to CO exposures associated with

attainment of the current (deterministic)

9 ppm standard, and approximately 20

percent of the adult population is

estimated to exceed 2.1 percent COHb

upon attainment of a 15 ppm standard

with 1 expected exceedance allowed per

year. It should be noted that the

estimates given in Table 4 are based on

air quality distributions which have

been adjusted to just attain the given

standards.

Several factors make the accuracy of

the nationwide exposure estimates

uncertain. They include: (1) the paucity

of information on several of the needed

inputs (e.g., some of the

microenvironment multiplicative

transformation factors) and (2) the fact

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that nationwide estimates were

extrapolated from only four urbanized

areas. In addition, the results of the

Coburn Model Sensitivity Analysis,

discussed previously, suggest that the

use of two representative sets of

physiological parameters (one for men and one for women), rather than the full

distributions of the physiological

parameters for the population, in

applying the Coburn model to derive

COHb estimates introduces some

further uncertainty, although the

uncertainty about such inputs as the

microenvironment multiplicative

transformation factors is much larger.

Exposure Analysis report (Johnson and

Paul, 1983) describes some limited

sensitivity analysis runs for one

urbanized area to give a rough idea of

the range of possible COI-Ib levels that

would be reached.

Decision on the Primary Standards

The Staff Reassessment and 1984

CASAC findings and recommendations

set forth a framework for considering

whether revision of the primary CO

standards is appropriate at this time.

The discussion that follows relies

heavily on that framework and on applicable supporting material in the

1979 Criteria Document, 1984

Addendum, 1979 Staff Paper, and earlier

CASAC closure letters (Hovey, 1979;

Friedlander, 1982).

Based on its assessment of scientific

evidence discussed previously in this

notice, EPA concludes that adverse

health effects clearly occur, even in

healthy individuals, at COHb levels in

the range of 5 to 20 percent. EPA also

remains concerned that adverse health

effects may be experienced by large

numbers of sensitive individuals with

COHb levels in the range 3.0 to 5.0

percent. On this point, CASAC similarly

concluded after reviewing the scientific

literature (not including the Aronow

studies), "that the critical effects level

for NAAQS-setting purposes is

approximately 3 percent COHb (not

including a margin of safety)"

(Lippmann, 1984).

In addition to concurring with EPA

that cardiovascular effects are likely to

occur at approximately 3 percent COHb

(Anderson et al., 1973), the CASAC also

indicated that several studies

(Drinkwater et al., 1974; Raven et al.,

1974; and Davies and Smith, 1980)

reporting physiological effects in the

range 2.3-2.8 percent COHb lend

support to concerns about low level CO

exposures and should be considered in

determining whether a given standard

provides an adequate margin of safety.

As discussed previously, the

Administrator has excluded Dr.

Aronow's studies from consideration in

his decision on the CO primary

standards.

Based on the exposure analysis

results summarized previously in Table

4 of this notice, 8-hour single

exceedance CO standards in the range 9

to 12 ppm are estimated to keep more

than 99 percent of the non-smoking

cardiovascular population below 3.0

percent COHb. Different standards

within this range would, of course,

provide different levels of protection.

For example, the current 9 ppm, 8-hour

average standard is estimated to keep

more than 99.9 percent of the adult

cardiovasular population below 2.1

percent COHb. A 12 ppm, 8-hour

standard is estimated to keep more than

99 percent of the population below 2.5

percent COHb. The 2.5 percent COHb

level is in the range where physiological

effects of concern to EPA and CASAC

have been reported.

In considering whether revision of the

existing primary CO standards is

appropriate at this time, the

Administrator has considered

uncertainties regarding the lowest levels

of COHb at which adverse health effects

may occur, as well as uncertainties

about the levels of COHb likely to result

from CO exposure at the levels

* associated with attainment of

alternative standards. More specifically,

the Administrator considered the

following factors and sources of

uncertainty, discussed in the Staff

Reassessment (EPA, 1984), in his

decision:

1. Human susceptibility to health

effects and the levels at which these

effects occur vary considerably among

individuals, and EPA cannot be certain

that experimental evidence has

accounted for the full range of

susceptibility. In addition, for ethical

reasons, clinical investigators have

generally excluded from their studies

individuals who may be especially

sensitive to CO exposure, such as those

with a history of myocardial infarction

or multiple disease states (e.g., both

angina and anemia). Another factor is

that, once the Aronow et al. studies are

excluded, there are no human exposure

studies investigating effects on individuals with angina at COHb levels

below the 2.9 percent level reported by

Anderson et al. (1973).

2. There is some animal study

evidence indicating that there may be

detrimental effects on fetal development

(e.g., reduced birth weight, increased

newborn mortality, and behavioral

effects) associated with CO exposure.

Similar types of effects have also been

found in studies examining effects of

maternal smoking on human fetuses.

However, it is not possible at this time

to sort out the confounding influence of

other components of tobacco smoke in

causing the effects observed in the

human studies. While human exposureresponse relationships for fetal effects

remain to be determined, these findings

denote a need for caution in evaluating

the margin of safety provided by

alternative CO standards.

3. Other groups that may be affected

by ambient CO exposures but for which

there is little or no experimental

evidence include: anemic individuals

(over 3 million individuals), persons

with chronic respirat6ry diseases (about

14 million individuals), elderly

individuals (over 24.7 million individuals

over 65 years old), visitors to high

altitude locations, and individuals on

certain medications. The levels of COHb

that might produce adverse effects for

each of these groups is uncertain.

However, elevated COHb levels in even

a small percentage of this very large

potentially sensitive population would

translate to a significant number of

individuals. The large size of the

potentially sensitive population, then,

argues for standards providing a greater

margin of safety.

4. There are a number of uncertainties

regarding the uptake of CO, including

those related to the accuracy of the

Coburn equation, in assessing variations

in the population due to differing

physiological parameters and exposure

to varying air quality patterns.

5. Several factors contribute to

uncertainties about the exposure

estimates of the expected number of

individuals achieving various COHb

levels upon attainment of alternative

standards. These factors include: the

paucity of information on several of the

needed inputs, the fact that nationwide

estimates were extrapolated from only

four urbanized areas, and the use of two

representative sets (one for men and one

for women) of physiological parameters

(e.g., blood volume) rather than

distributions of physiological

parameters in applying the Coburn

model to derive COHb estimates in the

exposure analysis. As indicated in the

Staff Reassessment (pp. 18-21), some

individuals with physiological

parameters that maximize uptake of

COHb, if exposed to certain patterns of

air quality attaining a 12 ppm, 8-hour

standard, would likely exceed 3.0

percent COHb. Consequently, the

Agency is concerned that a 12 ppm, 8-

hour standard may not provide an

adequate margin of safety. EPA is

continuing its CO exposure research

efforts, which should lead to future

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improvements in its exposure analysis

and a better capability to assess the

accuracy of the exposure estimates

(Johnson, 1984; Hartwell et al., 1984).

6. There is uncertainty regarding

adverse health effects that may result

from very short duration, high-level CO

exposures (the bolus effect). As

discussed in the proposal notice (45 FR

55077), existing air quality data indicate

that attainment of a 9 ppm, 8-hour

averaging time standard should limit the

magnitude of short-term peak

concentrations.

7. There is some concem about

possible interactions between CO and

other pollutants, although there is little

experimental evidence to document

such interactions at this time.

8. Given the unsettled nature of the

scientific information bearing on the

level of the standard, EPA believes that

there is much to be said for a policy that

would maintain the status quo until the

data become more adequate. That is

particularly so given the absence of the

information indicating with some

assurance that the present standard is

set at an incorrect level. For the reasons

stated elsewhere in this preamble, the

available information falls short of

supporting such finding.

The CASAC concurred with the

ranges of 9 to 12 ppm for the 8-hour and

25 to 35 ppm for the 1-hour primary

standards recommended in the Staff

Reassessment and characterized them

as scientifically defensible standard

ranges. They recommended that the

Administrator consider choosing

standards that maintain approximately

the same level of protection as that

afforded by the current standards

(Lippman, 1984). In making its

recommendation the CASAC cited the

uncertainties associated with the

scientific data base and margin of safety

concerns and its belief" . . . that where

the scientific data, as in this case, are

subject to large uncertainties, it is

desirable for the Administrator to

consider a greater margin of safety than

the numerical values of COHb generated

by the Coburn equation might otherwise

suggest" (Lippmann 1984).

Several ongoing human health effect

studies are being conducted by EPA and

other groups to investigate the effect of

CO on aggravation of angina. Subjects

in these studies are being exposed to CO

levels that result in blood COHb levels

in the range 2.0 to 4,0 percent. One study

is being conducted by EPA, several are

being conducted at the request of EPA

by the Health Effects Institute (HEI), and

another study is being sponsored by the

California Air Resources Board (CARB).

The Health Effects Institute is an

independent organization which

sponsors research on automotive

pollutants and is jointly funded by EPA

and automobile manufacturers. The

peer-reviewed results of these studies

are expected by December 1986. EPA

will be initiating development of a new

criteria document for CO in Fiscal Year

1986. Thus, the Agency should be in a

good position to expeditiously assess

the results from the above health

studies, as well as other scientific

evidence published since completion of

the Addendum.

Given the uncertainty in the current

data base and the fact that new studies

are in progress, the Administrator

considered deferring a final decision on

the CO standards until these new

studies have been completed. While this

might allow the Administrator to base

the decision on better information, the

Clean Air Act appears to require

periodic decisions on NAAQS

notwithstanding any uncertainty in the

data base. Deferring this decision would

imply that the Agency has inadequate

evidence to select an appropriate course

of action at this time. However, both

EPA and the CASAC have concluded

that, even without the Aronow studies, a

sufficient scientific data base exists

upon which to base a decision. Given

these findings, and the concern that a

deferral of the decision could be

perceived as a signal to relax or delay

ongoing control programs, the

Administrator has concluded that final

action now on the CO standards is

warranted and justified.

In reaching a final decision, the

Administrator has focused primarily on

the level of protection the CO standards

should provide. As previously noted,

after reassessing the available scientific

data and EPA staff recommendations,

the CASAC has recommended that the

CO standards provide protection

approximately equal to the current'

standards. Based on EPA's assessment

of the scientific data, the Administrator

concurs with this recommendation.

Retention of the current standards

would, of course, satisfy this objective.

As discussed above, the standards

proposed in August 1980 would also

provide approximately the same level of

protection as that afforded by the

current standards. In addition, these

standards would provide some technical

changes that the Agency believes would

be advantageous. However, the

proposed changes would require some modification in the way attainment of

the standards is determined. Given the

uncertainties in the existing data base

and the possibility that the results of the

new studies in progress might warrant

further revisions within a few years, the

Administrator has concluded that it

would not be prudent to promulgate the

proposed revisions at this time,

particularly when they would alter the

manner in which attainment is

determined.

In short, the Administrator has

concluded that it would not be prudent

to defer a decision on the CO standards

pending the results of the new research

mentioned above, that the standards

should provide approximately the same

level of protection as that afforded by

the current standards, and that

disruption of ongoing control programs

should be minimized. Given these

considerations, the Administrator has

concluded that the best course of action

is not to revise the CO primary

standards at this time. Together with the

Administrator's decision to rescind the

secondary standards (discussed below],

this decision completes the current

review of the NAAQS for CO under

section 109(d). The ongoing studies

conducted by the Agency, by the HEI,

and by the CARB (all discussed above)

will, of course, be considered in the next

5-year review cycle of the CO criteria

and standards. Upon completion of this

series of studies, the Agency plans to

review the results with the CASAC and

assess the need for any revisions in the

primary standards. If revisions in the

standards seem appropriate, the Agency

will act expeditiously to revise the

standards.

Welfare Effects and the Secondary

Standards

Carbon monoxide is a normal

constituent of the plant environment.

Plants can both metabolize and produce

CO. This may explain the fact that

relatively high levels of CO are

necessary before damage occurs to

vegetation. The lowest level for which

significant effects on vegetation have

been reported is 100 ppm for 3 to 35

days. The effect observed in this study

was an inhibition of nitrogen fixation in

legumes. Since CO concentrations of

this magnitude are rarely if ever

observed in the ambient air, it is very

unlikely that any damage to vegetation

will occur from CO air pollution. No

other effects on welfare have been

associated with CO exposures at or near

ambient levels. Because no standards

appear to be requisite to protect the

public welfare from any known or

anticipated adverse effects from

ambient CO exposures, EPA is

rescinding the existing secondary

standards.

Significant Harm Levels

Section 303 of the Clean Air Act

authorizes the Administrator to take

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certain emergency actions if pollution

levels in an area constitute "an

imminent and substantial endangerment

to the health of persons." EPA's

regulations governing adoption and

submittal of SIP's contain a provision

(40 CFR 51.16] that requires the adoption

by States of contingency plans to

prevent ambient pollutant

concentrations from reaching specified

significant harm levels. The existing

significant harm levels for CO were

established in 1971 (36 FR 24002) at the

following levels and averaging times:

50 ppm-8-hour average

75 ppm-4-hour average

125 ppm--hour average

Exposure under these conditions

could result in a widespread blood

COHb concentration of 5 to 10 percent,

the range EPA has determined would

cause significant harm. On the basis of

EPA's reassessment of the earlier data

and assessment of more recent medical

evidence, no modifications are being

made to the existing significant harm

designations. EPA's assessment of the

medical evidence on exposure to higher

CO concentrations that could lead to

significant harm is contained in the 1979

Criteria Document (EPA, 1979b) and in

the Addendum (EPA), 1984b).

Summary of Public Comments and

Agency Responses

Overview of Comments

The following discussion summarizes

in general terms the comments received,

at various times since the 1980 proposal,

from the public and from Federal and

State agencies on the levels of the

primary standards and on the related

issue of multiple exceedance standards.

Significant comments on all aspects of

the CO proposal and Agency responses

to these comments are summarized by

category later in this section. A more

detailed description of individual

comments and Agency responses is

contained in the public docket (OAQPS

79-7).

Comments on 1980 Proposal. Of the

written comments received during the

initial comment period (which closed

November 24, 1980) that expressed some

opinion on the level of the proposed 8-

hour standard, 7 out of 11 favored EPA's

proposed standard or a more stringent

standard. Environmental group

comments endorsed the proposed

standard or recommended tightening of

the standard, industry groups favored

relaxation of the standard, and local

and State agency comments supported

the proposed standard or some

relaxation of the standard.

Several comments were received on

the Agency's proposal to lower the 1-

hour standard to 25 ppm. Of the 18

written comments which expressed an

opinion on the 1-hour standard, 8

comments favored the proposed

standard level, 5 comments urged

retention of the existing 35 ppm

standard level, and 3 comments

recommended revocation of the 1-hour

standard. There also was one comment

favoring further tightening of the 1-hour

standard and one comment favoring a

relaxation of the standard. Those

favoring revocation of the 1-hour

standard argued that the 1-hour

standard was redundant since

attainment of the 8-hour standard would

effectively prevent 1-hour average levels

from exceeding either 25 or 35 ppm.

Comments on the proposed revisions

were received from five Federal

agencies. Four of these agencies neither

supported nor opposed the proposed

standards. The Department of

Commerce urged EPA to maintain the

existing 35 ppm, 1-hour standard. The

Council on Wage and Price Stability

suggested, through the Regulatory

Analysis Review Group, that the

proposed standards should be based on

cost-effectiveness analysis and that if

costs were considered, the proposed

standards might be excessively

stringent.

Comments on Subsequent Notices. As

discussed earlier in this notice, EPA

announced an additional public

comment period on June 18, 1982 to

address several key issues, including the

Agency's consideration of multiple

expected exceedance 8-hour CO

standards (47 FR 26407). Of the

comments that expressed an opinion on

the issue of multiple expected

exceedances, 12 out of 23 favored the

use of the multiple expected

exceedances approach for ambient

standards. While State and local

governments' comments were almost

evenly divided on the question, all

industrial groups supported the concept

and all environmental groups opposed

multiple exceedance standards.

Comments from private citizens were

evenly divided for and against multiple

exceedance standards.

During the period from November 24,

1980 through August 6, 1982 (the close of

the second comment period), of those

commenting on whether the 8-hour

standard should be relaxed, 10 out of 45

favored relaxation. Most of the States

(12 of 14) opposed relaxation, while 3 of

5 local governments favored relaxation.

As in the earlier comment period, all

industry comments favored relaxation

while all environmental groups opposed

relaxation.

Subsequent to the close of the secoid

public comment period, the State and

Territorial Air Pollution Program

Administrators (STAPPA) submitted a

resolution, endorsed by a majority of

State air pollution agencies, which

expressed several reservations about a

multiple exceedance CO standard. The

STAPPA resolution recommended

promulgation of single exceedance CO

standards.

EPA solicited additional public

comment on the draft Staff

Reassessment which evaluated the

scientific data in view of the diminished

value of Dr. Aronow's CO studies on

September 16, 1983 (48 FR 41608). Of the

13 comments received in response to

this notice that expressed an opinion on

the levels of the standards, 7 favored

retaining the current primary standards,

2 favored the proposed standards (i.e., 9

ppm for the 8-hour averaging time and

25 ppm for the 1-hour averaging time),

and 4 favored relaxation of the 8-hour

standard to 12 ppm or higher. Those

supporting the proposed or current

standards included an environmental

group, several State environmental

agencies, two health scientists, and one

local environmental agency. Those

favoring relaxation of the primary 8-

hour standard included two from the

automotive industry and two local

environmental agencies.

On August 9, 1984, EPA summarized

the basis for EPA's proposed revisions

to the CO standards, announced

availability of the final Addendum (EPA,

1984b) and Staff Reassessment (EPA,

1984a), and solicited additional public

comment (49 FR 31923). Of the 7

comments received that expressed an

opinion on the levels of the standards, 2

favored retaining the current primary

standards, 2 favored the proposed

primary standards (i.e., 9 ppm, 8-hour

and 25 ppm, 1-hour, and 3 favored

relaxation of the 8-hour standard to 12

ppm or higher. Two commentors argued

that EPA should defer final action on the

CO standards until the Health Effects

Institute's CO research was completed.

Summary of Significant Comments and

Agency Responses

Significant comments are summarized

and responded to by category below.

I. Health Effects Criteria and Selection

of the Primary Standards

A. Definition of An Adverse Health

Effect

Comment. It is questionable whether a reduction in the time to onset of an

angina attack following exercise is

adverse.

Agency Response: EPA concludes that

aggravation of angina represents an

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adverse health effect. As explained in

the proposal preamble (45 FR 55066),

EPA considers such aggravation of

angina to be an adverse health effect for

several reasons. First, it may result in

cardiovascular damage, which is

unquantifiable using present technology.

Second, aggravation of angina may be

the first in a series of progressively more

serious symptoms that accompany

cardiovascular disease. At low levels of

oxygen deprivation, angina patients

experience symptoms of chest pain

described above. Coronary insufficiency

is a more serious symptom that occurs

at greater levels of oxygen deprivation.

This symptom is sometimes

accompanied by changes in enzyme

levels and electrocardiographic

irregularities. The most serious effect in

this continuum of effects is myocardial

infarction. In addition to longer and

more intense pain, myocardial infarction

is accompanied by irreversible heart

damage (death of myocardial cells) as

indicated by enzyme level changes and

electrocardiographic alterations. Finally,

because aggravation of angina may be

the first in a series of symptoms that

may lead to permanent heart damage,

EPA considers aggravation of angina an

adverse effect and an indicator that

more serious effects may occur in some

individuals at the same COHb levels.

EPA's judgment has been supported by

the CASAC and CASAC CO

Subcommittee (Hovey, 1979; Lippmann,

1984).

Comment: Scientific research on CO

suggests that there is no clear threshold

level at which adverse health effects

begin. Rather, there appears to be an

increase in severity of potential health

effects with increasing levels of CO. The

fact that a no-effects level cannot be

identified may lead to a standard near

zero. The current evidence can support

standards other than those proposed by

EPA.

Agency Response: EPA agrees that

there is a continuum of effects consisting

of COHb levels at which health effects

are certain, through levels at which

scientists can generally agree that

medically significant effects have been

convincingly shown, and down to levels

at which health effects are less certain,

are harder to identify, and the medical

significance of which are typically

disputed. In short, the present scientific

evidence does not permit selection of an

undisputed value for a primary

standard. Rather, the Administrator in

selecting a standard must make a

judgment as to the level of physiological

response that should be considered

adverse and the relative acceptability of

various degrees of uncertainty that any

given level is low enough to prevent

known and possible adverse health

effects.

B. Scientific Validity of the Human

Experimental Studies

Comment: Work of Dr. Wilbert

Aronow is suspect because results are

too consistent, data are not available for

evaluation, the study was not double

blind, and the subjects tested were not a

representative set of angina patients.

The Horvath Committee (Horvath et al.,

1983) recommended that EPA not rely on

Dr. Aronow's studies in setting the CO

standards.

. Agency Response: The Administrator

agrees with the Horvath Committee that

there are very serious technical

questions about the validity of Dr.

Aronow's CO studies and, therefore, is

not considering the results of these

studies in his decision.

Comment: The Anderson et al. (1973)

study should be eliminated from

consideration because Anderson et al.

reported a COHb level of only 4.5

percent after a four hour, 100 ppm CO

exposure, whereas other investigators

have generally reported 8-10 percent

COHb for similar exposures.

Agency Response: During the

Anderson et al. (1973) study, subjects

were allowed breaks and, thus, were

exposed to CO intermittently, not

continuously, for 4 hours. This would

cause COHb levels to be substantially

lower than for the continuous exposure

periods used in other studies.

Comment: The Anderson et al. (1973)

study should not be considered for

drawing conclusions about lowest

observed effect levels because of the (1)

small number of subjects, (2)

questionable double-blind conditions,

(3] missing data for some subjects, (4)

lack of dose-response relationships for

onset and duration of angina in some

subjects, (5) reliance on subjective.

responses, and (6f inadequate

presentation of statistical procedures.

Agency Response: EPA has carefully

reviewed the Anderson et al. (1973)

study and the above criticisms of the

study. A detailed response is contained

in a February 20, 1985 memorandum

prepared by EPA's scientists in the

Office of Research and Development

which has been placed in the public

docket (OAQPS 79-7, IV,-B-2). EPA does

not challenge the proposition that the

Anderson study has limitations that

must be weighed in assessing the

study's value for standard setting. Very

few, if any, studies are perfect and thus

conclusively demonstrate precise

pollutant thresholds for the entire range

of sensitive persons under various

environmental conditions. However, the

Agency does not agree with the

commenters' characterization of the

Anderson study limitations nor with the

commenters' conclusion that those

limitations are grounds for totally

excluding the study from an assessment

of the health risks of CO. After carefully

evaluating the scientific merit of the

study and considering the advice

provided by the CASAC, EPA has

concluded that the Anderson study

should be considered in selecting a CO

standard with an adequate margin of

safety.

EPA's responses to the major points of

concern about the Anderson et al. (1973)

study are briefly summarized below:

1. EPA readily acknowledges that the

subject sample size is small and that the

study would be strengthened if the

number of subjects had been greater.

However, the sample size is adequate to

treat the data statistically and large

enough to use in making statistical

inferences regarding effects and causal

agents. These inferences are routinely

made by clinical investigators

conducting studies with relatively few

subjects and treatment replications. In

addition, even though only a small

number of subjects were tested, they do

represent some portion of the national

population suffering from angina.

2. Because of the explicit precautions

taken by the author to ensure the

integrity of such a protocol, EPA rejects

the speculative assertion that the study

was not double blind. Specifically, a

"double blind" study is one where both

the administering investigator and

patient are unaware of the nature of any

treatment. EPA has contacted the author

(Docket ECAO CD 78-3, IIA-J-3) who

reaffirmed the study protocol which is

consistent with the definition of double

blind. The author cited the published

study which states:

A 5-day, double-blind exposure protocol

was followed-Only the investigator

administering the gas knew which

concentration of CO was being used. The

patient, technician, and the investigator

conducting the'exercise test were all unaware of the exposure condition. A curtain

separated the gas tanks from the patient-On

completion of the five exercise tests for each

subject, the ECG records were assigned a

random code number and interpreted by an

investigator who had not been present and

had no knowledge of the exposure sequence.

3. Because of the explicit double blind

protocol practiced in the study, there is

no basis for concluding that the two

subjects who missed one day of

exposure had in some way gained

knowledge of the exposure conditions

due to their missing one of the exposure

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sessions. EPA rejects this assertion as

illogical and unfounded.

4. The fact that the effects reported

were not dose-related in the Anderson

et al. study is not surprising given the

small range of exposure concentrations,

the fact that the exposures were close to

the lower limits for CO-related effects,

and the small number of subjects.

However, EPA has not used this or any

other study to develop a dose-response

relationship which would show different

levels of subject response over a specific

range of administered CO doses. EPA

has argued that the Anderson study

does suggest an increased risk of

aggravation of angina for sensitive

individuals who have elevated COHb

levels.

5. The fact that the endpoint measured

by Anderson et al., namely time to onset

of angina pian, is subjective in nature is

no basis for ignoring this serious and

important effect as carefully articulated

in the proposal preamble (45 FR 55069):

EPA considers such aggravation of angina

to be an adverse health effect for several reasons. First, it may result in cardiovascular

damage, which is unquantifiable using

present technology. Second, aggravation of

angina may be the first in a series of

progressively more serious symptoms that

accompany cardiovascular disease. At low

levels of oxygen deprivation, angina patients

experience symptoms of chest pain described

above. Coronary insufficiency is a more serious symptom that occurs at greater levels

of oxygen deprivation. This symptom is

sometimes accompanied by changes in

enzyme levels and electrocardiographic

irregularities. The most serious symptom in

this continuum of effects is myocardial

infarction. In addition to longer and more intense pain, myocardial infarction is

accompanied by irreversible heart damage

(death of myocardial cells) as indicated by

enzyme level changes and

electrocardiographic alterations. Finally, because aggravation of angina may be the

first in a series of symptoms that may lead to

permanent heart damage, EPA considers

aggravation of angina an adverse effect and an indicator that more serious effects may occur in some individuals at the same COHb

levels.

6. EPA has reanalyzed the data from

the Anderson et al. study using a more

conservative multivariate analysis

which tests each health endpoint

separately for purposes of inference (see

Appendix A in the Addendum; EPA

1984b). EPA believes that, had Anderson

et al. originally used this technique, the

effect of time to onset of angina would

have been statistically significant

(p=0.014 at the 97.5 percent confidence

level] but that duration of angina

experience would not have been

statistically significant (p=0.11 at the

97.5 percent confidence level).

In conclusion, EPA agrees with the

CASAC statement,

... that it is important to replicate such a study, but the notion that a study has no validity until it's been replicated is flawed.

Based upon its current knowledge of how the

study was conducted, CASAC presumes that

double blind protocols were, in fact, observed

and that discrepancies between observed

and predicted COHb levels are not as great or as serious as originally suggested. In

summary, while CASAC treats the Anderson

et al. study with caution, it can find no substantive reason at this time to dispute the

reported values, and it recommends that the

Agency not disregard its findings (Lippmann.

1984).

The Agency continues to believe that

the Anderson et al. findings can be

appropriately interpreted as providing

reasonably good evidence of

exacerbation of angina symptoms

occurring in some segments of the

population at approximately 2.9 to 4.5

percent COHb.

Comment: Psychological factors

contribute to angina attacks, making it

difficult to reproduce experiments

linking CO and angina.

Agency Response: Although

psychological factors may contribute to

angina attacks, it has been reasonably

shown in the study by Anderson et al.

that exposure to CO does contribute

independently to the aggravation of

angina. Given the double-blind design of

this study, there is no reason to suppose

that the subjects were exposed to

different psychological factors on

experimental CO exposure days than

they were on clean air control days.

C. Margin of Safety

Comment: EPA has proposed CO

standards with an inappropriate margin

of safety. The margin of safety was

criticized as being either inadequate or

excessive.

Agency Response: The decision

regarding an adequate margin of safety

is a judgment which must be made by

the Administrator after weighing all the

medical evidence bearing on the effects

of CO. The factors to be taken into

account include inconclusive evidence

as well as findings from studies that are

considered definitive and not subject to

challenge. The Administrator has

considered uncertainties regarding the

lowest levels of COHb at which adverse

health effects may occur, as well as

uncertainties about the levels of COHb

likely to result from CO exposure at the

levels associated with attainment of

alternative standards. More specifically,

the Administrator considered the factors

and sources of uncertainty, discussed

earlier in the Decision on the Primary

Standards section of this notice and in

the Staff Reassessment (EPA, 1984).

EPA has examined the health

protection afforded by alternatives to

the current CO primary standards. For

example, attainment of a 12 ppm, 8-hour

CO standard is estimated to keep more

than 99 percent of the population below

2.5 percent COHb. The 2.5 percent

COHb level, however, is in the range

where physiological effects of concern

to EPA and CASAC have been reported.

In addition, as indicated in the Staff

Reassessment (pp. 18-21), some

individuals with physiological

parameters that maximize uptake of

COHb if exposed to certain patterns of

air quality attaining a 12 ppm, 8-hour

standard would exceed 3.0 percent

COHb. Consequently, the Administrator

is concerned that a 12 ppm, 8-hour

standard may not provide an adequate

margin of safety. There is no credible

scientific evidence that suggests more

stringent CO primary standards than the

current standards are required to protect

public health with an adequate margin

of safety.

D. Coburn Model Sensitivity Analysis of

COHb Levels

Comment: The term used in the

Coburn model analysis for inspired CO

pressure was mistakenly interpreted as

a pressure in dry ambient air. The term

was intended to refer to CO pressure in

air saturated with water vapor at body

temperature.

Agency Response: EPA agrees with

the comment and has revised all of the

COHb estimates used in this notice and

in the final COHb Sensitivity Analysis

(Biller and Richmond, 1982) to reflect

this change.

Comment: The parameters utilized in

the EPA COHb Sensitivity Analysis

were not representative of the medical

literature. Modeling efforts of this kind'

should choose conservative values for

physiological parameters in order to err

on the side of protecting public health.

Agency Response: The values selected

for the physiological parameters used in

the Sensitivity Analysis were carefully

reviewed with members of the scientific

community and with consultants to the

CASAC and were judged to be

reasonable estimates. EPA does not

agree that the most conservative values

should be selected for the physiological

parameters because this would

introduce an additional margin of safety

into an analysis attempting to estimate

the effects of alternative standards. The

Sensitivity Analysis does use a range of

values for the various physiological

parameters.

Comment: The draft Sensitivity

Analysis does not adequately treat

37497

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differences in physiological parameters

between men and women. Agency Response: In an Appendix to

the revised Sensitivity Analysis (Biller

and Richmond, 1982), men and women

are modelled separately and appropriate

physiological parameters are selected

for each sex based on a review of the

scientific literature.

E. Exposure Estimates for Sensitive

Population Groups

Comm'ent: Various technical factors in

the expobure analysis either

systematically underestimate or

overestimate exposures that would

occur upon attainment of alternative

standards. The exposure analysis should

not be used in selecting the primary

standards until all the recommended

changes are incorporated into the

analysis.

Agency Response: EPA has carefully

reviewed these comments and separated

them into three categories. The first

category includes comments with which

EPA agrees and for which changes have

been made in the exposure analysis. The

revised exposure analysis estimates are

similar in magnitude, after taking these

comments into account, to the original

exposure estimates.

A second category of comments

suggested changes that EPA agrees

would refine the exposure assessment

methodology, but which are not feasible

at this time because of limitations on the

resources and time available for this

standard review. EPA will incorporate

these comments into its plan for

improving its exposure assessment

capability. While the exact impact of

these refinements cannot be clearly

predicted at this time, EPA agrees with

CASAC's conclusion that the exposure

analysis is "acceptable given the current

state-of-the-art of the scientific

community's ability to model

physiological and other parameters

related to this pollutant" (Friedlander,

1982).

A third category consists of comments

where EPA disagrees with the suggested

changes. Detailed responses to these

comments are provided in the docket

(Docket OAQPS 79-7, V-C-I). EPA

recognizes that there is uncertainty

about the accuracy to the exposure

estimates, but it believes that the

revised estimates are reasonable given

the state-of-the-art of exposure

assessment.

While future refinements in the

methodology and availability of

additional data will undoubtedly reduce

the degree of uncertainty in the

exposure estimates, EPA believes that

the current Exposure Analysis provides

a useful tool to estimate the number of

sensitive individuals who would be

exposed to various COHb levels upon

attainment of alternative standards.

II. Form of the Primary Standards

Comment: Some commenters favored

retaining the current deterministic form;

others supported either EPA's 1980

proposal to adopt single-expectedexceedance (statistical form) or the

concept of multiple-expectedexceedances (statistical form) primary

CO standards. Those in favor of

adopting a statistical form argued that it

would minimize the impact of unusual

meteorological events on control

strategies with minimal reductions in

health protection offered by the

standard. Those opposed to a multipleexpected-exceedances standard

expressed concerns about the increased

health risks to the sensitive population

and the ability of the public to

understand the basis for allowing

multiple excursions of the standard

levels.

Agency Response: Given the concerns

expressed by the vast majority of State

air pollution control agencies and others

that a single-exceedance standard,

either deterministic or statistical, more

closely reflects the health basis for the

standard and is more readily

implemented and understood by the

general public, EPA has decided to

retain the single exceedance format for

the primary standards. While EPA

believes that adopting a statistical,

single-exceedance standard would be a

technical improvement, EPA is deferring

any such change in the primary CO

standards until the uncertainties

regarding the health effects basis for the

standards are better resolved.

III. Miscellaneous

A. Natural Background

Comment: It has been reported that

93% of the CO in the atmosphere is

produced by vegetation and the oceans

and, therefore, anthropogenic sources of

CO should be of little concern.

Agency Response: Although much of

the CO produced globally may be of

natural origin, the elevated CO levels

found in urban areas and in rural areas

near roadways are principally a result of

human activities involving the

combustion of fossil fuels.

B. Stating Standards in ppm and Not

mg/m 3

Comment: EPA should state the

revised CO standards solely in parts per

million (ppm) rather than mg/m.

Changing to ppm would (1) avoid

confusion as to the level of the

standards at different altitudes, (2)

provide additional protection for high

altitude areas, and (3) be consistent with

health and monitoring data using the

Federal Reference Methods which are

reported in ppm.

Agency Response: EPA is retaining

both systems of units but is indicating

that ppm is the preferred system of

units. Section 50.3 specifies that

measurements of air quality are to be

corrected to standard conditions (i.e., 25

degrees centigrade and sea level

pressure), the only difference between

ppm and mg/m 3 (at standard conditions)

is a scale factor that does not vary with

altitude. That is, if a measurement is

expressed in ppm units or mg/m3 units

(at standard conditions) the values will

differ by a factor of 0.875 regardless of

altitude. This conversion factor is

specified in Appendix D of 40 CFR Part

50.

Revisions to Part 50 Regulations

Because EPA has decided not to

revise the CO primary standards, there

are no substantive changes to the Part

50 regulations concerning these

standards. EPA is revising the text of the

standards slightly, however, to make

them clearer and more understandable

to the public. EPA is also explicitly

stating several data handling

conventions that have traditionally been

used in EPA's data systems and

guidance. These changes are not

intended to redefine the standard but

simply to reduce potential ambiguity

and to formalize existing data handling

conventions. The specific points are the

75 percent data completeness rule that

EPA has used when computing 8-hour

averages and the number of significant

figures retained when making

comparisons with the levels of the

standard. These changes were discussed

in the proposal notice. EPA is also

changing to ppm units as the preferred

units as discussed in the proposal

notice. Finally, EPA is also rescinding

the secondary standards for CO, as

proposed, because there is no evidence

of welfare related effects at or near

ambient levels.

Part 51 Regulations and SIP

Development

This action does not modify the

existing Part 51 regulations. Current

guidance to State and local air pollution

control agencies on how to interpret air

quality data for purposes of attainment

decisions and SIP development is

contained in "Guidelines for the

Interpretation of Air Quality Standards"

(EPA, 1977).

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Regulatory and Environmental Impacts

Regulatory Impact Analysis

As has been noted, the Clean Air Act

specifically requires that NAAQS be

based on scientific criteria relating to

the level that should be attained to

protect public health and welfare

adequately. The courts haye endorsed a reading of the Act that excludes reliance

on the cost or feasibility of achieving

such a standard in determining the level

of the primary standards. In response to

Executive Order 12291, EPA has

prepared a regulatory impact analysis

(RIA). However, EPA's analysis,

"Regulatory Impact Analysis for Carbon

Monoxide," has not been considered in

determining the standard levels in this

final notice. The document is available

from the address given earlier in the For

Further Information Contact section of

this notice until supplies are exhausted

and from the NTIS whose address is

given in the Addressees section of this

notice.

Both the RIA and this final notice were submitted to the Office of

Management and Budget (OMB) for

review under Executive Order 12291.

Any written comments from OMB and

any written EPA responses to those

comments are available for public

inspection at EPA's Central Docket

Section, Docket No. OAQPS 79-7, West

Tower Lobby, Gallery I, Waterside Mall,

401 M Street SW., Washington, D.C.

Environmental Impacts

Environmental impacts associated

with control of CO emission have been

examined in the Environmental Impact

Statement, which is available in the

docket (OAQPS 79-7, IV-A-13) or from

EPA at the address given earlier in the

For Further Information Contact Section

of this notice. This analysis indicates

that control strategies required to attain

the standards will have minimal adverse

impacts on other environmental media.

Impact on Small Entities

The Regulatory Flexibility Act (5

U.S.C. 601 et seq.) requires that all

federal agencies consider the impacts of

final regulations on small entities, which

are defined to be small businesses,

small organizations, and small

governmental jurisdictions. EPA's

analysis pursuant to this Act is

summarized in a section of the final

report, "Cost and Economic Assessment

of Alternative National Ambient Air

Quality Standards for Carbon

Monoxide" (EPA, 1985). A NAAQS for

CO by itself has no direct impact on

small entities. However, it requires each

State to design and implement control

strategies for those areas not in

attainment. Three possible sources of

impadts on small entities include (1) the

FMVCP for cars and trucks, (2) I&M

programs, and (3) stationary source

control programs. FMVCP requirements

are largely established by statute or by

regulatory provisions not directly

related to the levels of these standards.

In addition, they fall primarily on

automobile manufacturers, none of

which are classified as small businesses.

Additionally, the incremental cost of CO

control, which is passed on to

purchasers of motor vehicles-including

small entities-is a small fraction of the

purchase price and, thus, the impact to

these purchasers should be negligible.

I&M programs for CO control may

have a slight negative economic impact

on small entities, but may also have a

positive economic impact on some small

entities. The estimated pe'r vehicle

average annual cost for the CO portion

of an I&M program is estimated to be

$3.50 for the inspection fee and $19 for

repairs to failed vehicles. (In those few

areas needing an I&M program for CO

only, these estimates would be doubled.)

These costs should not impose a

significant negative economic impact on

small entities. On the other hand, some small entities such as gas stations and

garages will be repairing failed vehicles

resulting in a net increase in receipts

due to a CO I&M program. In addition, if

a decentralized I&M program is

implemented using small businesses to

inspect motor vehicles, then their net

receipts will also increase due to receipt

of the inspection fee, most of which they

retain. (The remainder goes to the

governmental unit sponsoring the areawide I&M program.)

Finally, only the largest stationary

sources of CO appear to need to

implement controls to attain the CO

standards that were analyzed. These

sources are among the largest facilities

within their standard industrial class,

and therefore are not likely to be small

entities.

Based on the analysis summarized

above, EPA concludes that no small

entity group will be significantly

negatively affected due to retention of

the primary CO NAAQS. Therefore,

pursuant to 5 U.S.C. 605(b) the

Administrator certifies that this

regulation will not have a significant

economic impact on a substantial

number of small entities.

Impact on Reporting Requirements

There are no reporting requirements

directly associated with this action.

There are reporting requirements

associated with related sections of the

Act, particularly sections 107, 110, 160,

and 317 (42 U.S.C. 7407, 7410, 7460, and

7617), however, there are no changes in

reporting requirements associated with

this final action since the current

primary standards are being retained.

Federal Reference Method

The measurement principle and

calibration procedure applicable to

reference methods for measuring

ambient CO concentrations to determine

compliance with applicable CO

standards are not affected by this

action. The measurement principle and

the calibration procedure for CO are set

forth in Appendix C of 40 CFR Part 50.

Reference methods, as well as

equivalent methods, for monitoring CO

are designated in accordance with 40

CFR Part 53. A list of all methods

designated by EPA as reference or

equivalent methods for measuring CO is

available from any EPA Regional Office,

or from EPA, Department E (MD-76),

Research Triangle Park, N.C. 27711.

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monotony and on psychomotor capacity.

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Lit of Subjects in 40 CFR Part 50

Air pollution control, Carbon

monoxide, Ozone, Sulfur oxides,

Particulate matter, Nitrogen dioxide,

Lead.

Dated: September 5, 1985.

Lee M. Thomas,

Administrator.

PART 50-NATIONAL PRIMARY AND

SECONDARY AMBIENT AIR QUALITY

STANDARDS

For the reasons set forth in the

preamble, EPA amends Chapter 1, Part

50, of Title 40 of the Code of Federal

Regulations as follows:

1. The authority citation for Part 50

continues to read as follows:

Authority: Sec. 109 and 301(a), Clean Air

Act, as amended (42 U.S.C. 7409, 7601(a)).

2. Section 50.8 is revised to read as

follows:

§ 50.8 National primary ambient air quality

standards for carbon monoxide.

(a) The national primary ambient air

quality standards for carbon monoxide

are:

11) 9 parts per million (10 milligrams

per cubic meter) for an 8-hour average

concentration not to be exceeded more

than once per year and

(2) 35 parts per million (40 milligrams

per cubic meter) for a 1-hour average

concentration not to be exceeded more

than once per year.

(b) The levels of carbon monoxide in

the ambient air shall be measured by:

(1) a reference method based on

Appendix C and designated in

accordance with Part 53 of this chapter,

or .

(2) an equivalent method designated

in accordance with Part 53 of this

chapter.

(c) An 8-hour average shall be

considered valid if at least 75 percent of

the hourly average for the 8-hour period

are available. In the event that only six

(or seven) hourly averages are available,

the 8-hour average shall be computed on

the basis of the hours available using six

(or seven) as the divisor.

(d) When summarizing data for

comparision with the standards,

averages shall be stated to one decimal

place. Comparison of the data with the

levels of the standards in parts per

million shall be nade in terms of

integers with fractional parts of 0.5 or

greater rounding up.

[FR Doc. 85-22025 Filed 9-12-85:8:45 aml

BILLING CODE 6560-50-M

37501

HeinOnline -- 50 Fed. Reg. 37501 1985