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Citation: 50 Fed. Reg. 37484 1985

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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 QualityStandards 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 9parts 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 ifrevisions 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. EPAplans to review several ongoing human health effect studies upon their completion and,if warranted, will reexamine this decision
at thattime. EFFECTIVE DATE: This action is effective October 15, 1985. ADDRESSES: A docket 

### (NumberOAQPS 79-7) containing information relating to EPA's review ofthe CO standards, is available for public inspection and copying between 8:00a.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. Areasonable.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 staffpaper, "Review ofthe NAAQS forCarbon 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 LegislativeRequirementsAffecting This Action

Two sections of the Clean AirAct govern the establishment, review, and revision ofNAAQS. Section 108 (42 U.S.C. 7408) directs the Administrator to identify pollutants which may reasonably be anticipated to endanger public health orwelfare and toissue air quality criteria forthem. These air quality criteria are to reflect thelatest scientific information useful in indicating the kind and extent ofall identifiable effects on public health or welfare that may be expected from the presence ofthe pollutant in the ambient air.

Section 109(a) (42U.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 ofwhich in the judgment ofthe Administrator,based on the criteria and allowing for an adequate margin ofsafety, is requisite to protect the public health. The secondary standard, as defined in section 109(b)(2),
must specify a level ofair quality the attainment andmaintenance ofwhich in the judgment ofthe 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 ofsafety 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 yetidentified. LeadIndustries Associationv.EPA, 647 F.2d 1130, 1154 (D.C. Cir. 1980), cert.denied,101 S. Ct. 621 (1980);AmericanPetroleumInstitute

v. Costle, 665F.2d 1176, 1177 (D.C. Cir. 1981), cert.denied,102 S. Ct. 1737 (1982). Both kinds ofuncertainties 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, theAdministrator is seeking not only to prevent pollution levels that havebeen clearly demonstrated to be harmful, but also to prevent lower pollutant levels thathe finds pose an unacceptable risk ofharm, even ifthat risk is not precisely identified as to nature or degree.

In evaluating such risks for the purpose ofproviding an adequate margin ofsafety, EPAhas considered such factors as the nature and severity ofthe health effects involved-, the size of the sensitive population(s) at risk, and the kind and degree ofthe uncertainties that must be addressed. Given that the "margin of safety" requirement by definition comes into play where no conclusive showing ofharm exists, such factors, Which involve unknown, qualitatively defined, or onlypartially quantified risks,have inherent limits as guides to action. The selection of any particular approach to providing an adequate margin ofsafety is a policy choice left specifically to the Administrator's judgment.Lead Industries Associationv. EPA,supra, 647 F.2d at 1161-62.

The courts,however, have endorsed a reading ofthe Act that sets strict limits

on thefactors EPA may consider in providing an adequate margin ofsafety for primary standards. The leading judicial decisions state that the economic and technological feasibility ofattaining primary standards are not to be relied upon in setting them, even in the context ofa margin of safety.Lead Industries Associationv.EPA, supra, 647F.2d at 1148-1151; American PetroleumInstitutev. Castle,supra,665 F.2d at 1185, 1190. Such factors may, however, be considered to a degree in the development ofState plans to implement the standards.

Section 109(d) ofthe Act (42 U.S.C. 7409(d)) requires periodic review and, if appropriate, revision ofexisting criteria and standards. If,in the Administrator's judgment, the Agency's review and revision of criteriamake appropriate the proposal ofnew or revised standards, such standards are to be revised and promulgated in accordance with section 109(b). Alternatively, the Administrator may find that revision ofthe 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 ofthis notice.

Statesare primarily responsible for assuring attainment and maintenance of ambient air quality standards. Under section 110 of theAct (42 U.S.C. 7410), States are to submit to EPA forapproval State implementation plans (SIPs) that provide for the attainment and maintenance ofsuch standards through control programs directed to sources of the pollutants included. Other federal
programs provide for nationwide reductions in emissions ofthese and other airpollutants through the federal
motor vehicle control program, which involves controls for automobile, truck, bus, and motorcycle under Title 1Iof the Act (42 U.S.C. 7501 to 7534), and through the development ofnew source performance standards forvarious categories ofstationary sources under section 111 (42 U.S.C. 7411). OriginalCOStandards, Revision ofthe Criteria Document,andProposed Revisionsofthe Standards OriginalCOStandards. 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 of9 ppm, 8-hour average, and 35 ppm, 1- houraverage, neither tobe exceeded

more than once per year.The scientific and medical bases for these standards

are described in the document, "Air Quality Criteria for CarbonMonoxide" (DHEW, 1970), published bythe U.S. Department ofHealth, Education, and Welfare in March 1970. Theprimary 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 of2 to 3percent were associated with impairment ofability to discriminate time intervals, a central

nervous system effect.

Revision ofthe Criteria Document.On December 1, 1978, EPA announced that it was in the process ofreviewing and updating the 1970 document, "Air Quality Criteria for CarbonMonoxide," and called for information that might be helpful in revising the document (43 FR 56250). In the process of developing the revised criteria document, EPAprovided

a number ofopportunities forreview and comment by organizations and individuals outside the Agency. Two successive drafts ofa 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 oforganizations who provided critical reviews and new information forconsideration. A
summary ofEPA's responses to the
comments on the two external review drafts ofthe criteria document has been placed in the public docket (Docket No. ECAO-CD-78-3). Transcripts ofthe two CASAC meetings have alsobeen placed in the docket.

The CASAC prepared a "closure" memorandum (Hovey, 1979) to the Administrator indicating its satisfaction that the final draft ofthe criteria document was scientifically adequate for standard-setting purposes. The closure memorandum, dated October 9, 1979 also outlines major issues addressed bythe CASAC's and CASAC's recommendation concerning those issues. A summaryof the issues raised by CASAC and the general public prior to proposal is contained in the proposal notice (45FR 55080).

Onthe basis ofa careful review of scientific information contained in the revised Criteria Document (EPA, 1979a) EPA's Office ofAir Quality Planning and Standards (OAQPS) prepared a StaffPaper (EPA, 1979a) in which several key considerations were identified as major factors tobe considered in thepossible revision of the CO standards. A draft of the Staff Paper was provided to the CASAC, made available to thepublic, and reviewed by the CASAC CO Subcommittee on June 14-15,1979.

Proposed RevisionsoftheStandards. The principal findings ofthe StaffPaper

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 forthe standards. However, medical evidence accumulated since 1970 indicated at the

ICASAC is a standingcommittee ofscientists and engineers external to the Federal government established under Section 109 ofthe Clean Air Act
toadvise the Administrator on thescientific basis forambient air quality standards. time ofthe 1980 proposal that aggravation of angifia pectoris and other cardiovascular diseases could occur at COHb levels as low as 2.7 to 2.9percent. Assessment of this and other medical evidence led EPA to propose: (1) retaining the 8-hour primary standard level of9 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 ornear ambient CO levels), (4) changing the formof the primary standards from deterministic to statistical (i.e., EPAproposed to allow

one expected exceedance ofeach standard level peryear), (5)adopting a daily interpretation for exceedances of the primary standards, so that exceedances would be determined on the basis ofthe number ofdays 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 CONAAQS and background information related to the proposal. DevelopmentsSubsequenttoProposal

Following proposal, EPA held two public meetings to receive comments on the proposed standard revisions. Meetings were held inWashington, 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 ofproposed 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 toboth CASAC meetings (45FR 73790 and 46 FR 53210) and transcripts of the meetings have beenplaced in the docket (Docket No. OAQPS 79-7).

On June 18, 1982EPA announced (47 FR 26407) an additional public comment period to address several keyissues concerning the 1980 proposal and technical documents related to the review ofthe CO standards. These issues included: (1)role ofthe Aronow (1.981) study, (2) consideration ofa multiple exceedance 8-hour standard, (3) the technical adequacy ofthe revised draft sensitivity analysis on the Coburn model predictions ofblood carboxyhemoglobin (COHb)levels, and (4) the technical adequacy of the revised exposure analysis. TheCASAC met on July 6, 1982 to provide its advice on these issues. CASAC's recommendations arising from that meeting are summarized in an August 

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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 ofseveral health studies conducted by Dr.Wilbert Aronow. EPA concluded at that time, based in part on the Aronow studies, thatCOHb 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 ofseveral 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 similarproblems might exist for Dr.Aronow's CO studies,EPA concluded that an independent examination ofthese studies was advisable prior ina final decision on the CONAAQS.

An expert committee was convened and met with Dr. Aronow to discuss his studies and to examine the limited available data and records fromhis 1981 CO study. In its report, the Committee (chaired by Dr. Steven M. Horvath, Director ofthe 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 ofthe results (Horvath et al., 1983). In early June 1983, EPAreceived 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 1979Criteria DocumentandStaff Reassessment.On August 18, 1983, EPA announced (48FR 37519] the availability ofan external review draft ofa document entitled "Revised Evaluation ofHealth Effects Associated with Carbon Monoxide Exposure: An Addendum to the 1979Air Quality Criteria Document for Carbon Monoxide" (hereafter cited as Addendum). TheAddendum reevaluates the scientific data base concerning health effects associated with exposure to CO at ornear ambient exposure levels inlight ofthe 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 ofa draft staffpaper, "Review ofthe NAAQS for Carbon Monoxide: 1983 Reassessment ofScientific and Technical Information" (hereafter cited as StaffReassessment] and solicited public comment on the draft paper [48 FR 41608). The Staff Reassessment, prepared by the OAQPS, provided the staffs assessment ofhow 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 ofseveral organizations also provided critical review ofboth EPA documents. A transcript ofthe 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 ofour knowledge ofthe 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 ofthe final Addendum (EPA, 1984b] and final Staff Reassessment (EPA, 1984a) which were revised to reflect public and CASAC comments. Both final documents are available fromthe address given earlier in the Availability ofRelated Information Section of thisnotice. Where there are differences between the 1979 Criteria Document and 1980 proposal assessment ofthe health effects evidence and the more recent EPA documents, thefinal Addendum and final StaffReassessment represented the Agency's interpretation

as oftheir issuance. In theAugust 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 ofCO is important because CO, when inhaled, can enterthe bloodstream and disrupt the delivery of oxygen to the body's tissues. A continous and adequate flow ofoxygen 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 ofcells,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 isreleased for use.

Unfortunately, COcan also bind to hemoglobin, forming carboxyhemoglobin (COHb), with an affinity that is 200 to 300 times greater than that ofoxygen. Forthis reason, small elevations ofCO in ambient air that enters the lungs can result in a relatively large displacement ofoxygen from the carrier hemoglobin.

MechanismsofCO Toxicity

The two principal sources of CO that contribute to levels ofCO in the human body are: (1)endogenous CO production from the normal breakdown of hemoglobin constituents in thebody and (2] inhalation ofexogenous COfrom ambient and non-ambient (e.g., occupational and indoor) exposures. 2 Endogenous CO production contributes roughly 0.3to 0.7percent ofhemoglobin saturation (0.3 to 0.7percent COH).

Presently, the most important mechanism ofCO toxicity at low-level CO exposures is thought to be hypoxia. This mechanism generally involves diffusion ofexogenous CO through the lungs into theblood with resultant formation ofCOHb. 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 theblood to the tissues (EPA, 1979b). Second, COmakes 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 ofoxygen may be inadequate to meet theenergy needs of the tissues. The effects ofCO on the 

### cardiovascular system, central nervous system, and other systems are thought

2The contributionofdirect smoking tolevels of CO in the body is not a part ofthis rulemaking. 37486 Federal Register / Vol. 50, No. 178 / Friday, September 13, 1985 / Rules and Regulations

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to be directly related to thisreduction in the ability ofthe blood to deliver oxygen to these systems and thie resultant
oxygen deficiency in the tissues themselves.

Other possible mechanisms oftoxicity have been discussed (Coburn, 1979; EPA, 1984b). These alternative mechanisms involve the binding of CO
tosuch intracellular hemoproteins as cytochrome oxidase, myoglobin, tryptophan deoxygenase, and tryptophan catalase. Because the affinity ofCO forthese proteins is much less than forhemoglobin, 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 ofmyoglobin in heart muscle cells. Myoglobin appears to facilitate the movement ofoxygen through muscle cells and, as a shortterm oxygen reservoir in muscle, it releases oxygen during sudden increased metabolic activity. The affinity ofmyoglobin for CO is about 40 times greater than the affinity of myoglobin for oxygen. The ratio ofCO
content in heart muscle to CO content in blood is approximately three. Therefore, given human exposure to CO, substantial amounts ofCO 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 ofdisease. This mechanism could provide theoretical support for experimental evidence of myocardial ischemia (inwhich part ofthe heart muscle is deprived ofoxygen), such as electrocardiographic irregularities and decrements inwork capacity discussed laterin this notice. Itis not known whether binding of COto 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 COHbin the blood appears to be the primary mechanism ofCO toxicity. In addition,EPA concludes that regardless ofthe mechanism oftoxicity, COHb levels provide a meaningful and useful physiological marker ofthe body's CO burden and exposure to exogenous

sources ofCO (EPA, 1948b).

HealthEffectsAsA ResultofCO Exposure

Exposure to high levels of exogenous COcan result inheadache, dizziness, drowiness, nausea, vomiting, collapse,
coma, ordeath, depehding on how much the flow ofoxygen to the body is impeded (EPA, 1979b). The most notorious effects ofCO are severe functional losses and death, which can result from automobile or truck emissions trapped in the enclosed interior ofa 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 ofdeath is severe hypoxia (or oxygen deficiency). Exposure to lower levels ofCO (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 foroxygen, even when the body is at rest,these organ systems

are particularly sensitive to reduced supplies ofoxygen.

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 thebody, 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 ofclear heart muscle hypoxia) to increase extraction ofoxygen fromblood, 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 ofoxygen available to the muscle (EPA, 1979b). Although these compensatory changes have notbeen associated experimentally with damage to the cardiovascular system, it is possible that the added stress onthe 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 ofdamage to the arteries, and elevated heart rate, which further increases theheart muscle's demand for oxygen. However, ifthe coronary arteries supplying the heart muscle are unable to compensate for CO exposure, parts ofthe heart muscle may receive amounts ofoxygen inadequate for normal activity.

As a result, EPAis concerned that CO
exposure may increase the risk ofthe following effects on the cardiovascular system: * Local myocardial ischemia (in which a part ofthe heart muscle is deprived ofoxygen); " Aggravation ofangina 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 (orsimply "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 ofthe heart muscle (EPA, 1948b). The pain probably results from an accumulation of unoxygenated metabolic products that irritate nerve endings in theheart muscle. The intensity ofpain varies from mild chest discomfort to severe and incapacitating distress. Although angina, by definition falls short of inducing death ofpart ofthe heart muscle, it can

cause serious discomfort, and each attack carries some risk ofheart attach. Acute coronary insufficiency, coronary failure, and myocardial infarction result when an episode of ischemia is more prolonged and severe.

Anindividual with an underlying
coronary insufficiency is atrisk of having an angina attack under any condition that places an additional demand on the heart. COexposures can place an added demand on the heart, and, therefore, would appear to increase the risk ofhaving an angina attack, and may increase the risk of a more severe attack.There is some experimental evidence of reduced time to onsetof 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 ofa significant portion ofthe blood and oxygen flow normally reaching the heart. Very little is known about the specific factors which induce

or precipitate heart attack orsudden death. However, any agent that reduces the supply ofoxygen available to the heart muscle inan individual with preexisting heart disease is suspect as a precipitating factor forheart attacks and sudden death.A relation between elevated COHb and these cardiac effects is plausible in light ofwhat is known about CO toxicity and possible 

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pathological mechanisms ofheart disease.

EPA has reviewed the available epidemiological data relating to hypotheses ofan association between elevated COflb orCO exposure and the risk ofheart attack, sudden death, and progression ofatherosclerosis 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 ofexperimental confounding factors, the multitude ofrisk 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 ofcardiovascular 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 ofavailable oxygen. In addition, or alternatively, prolonged compensation may damage the brain's blood vessels (EPA, 1979b).

When elevated COHb reduces the
amount ofoxygen 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 ina stroke (the damage or death ofbrain cells (neurons)). Loss ofmature brain cells is irreversible since the CNS is not thought capable ofreplacement 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 ofparts ofthe brain

or death of the individual. Individuals who recover often have significant deficits in brain function. Second, repeated episodes ofimpaired oxygen supply would be expected to damage the blood-brain barrier and possibly

cause structural damage resulting in the inability ofthe CNS to transmit information.

At lower CO-lb levels there is evidence ofneurobehavioral effects: impaired learning ability, reduced vigilance (ability to detect small changes in a subject's environment), decreased manual dexterity, impaired performance ofcomplex tasks, and disturbed sleep activity (EPA, 1984b). Although the potential influence ofambient 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 (Yabroffet al., 1974). There is no evidence withwhich 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 ofthe CNS, functional changes (e.g., behavior changes) may not be observed until the structural damage isgreat. Observation ofsuch effects may be more likely in the

case ofa severe reduction in oxygen or in an individual who has a history ofan impaired oxygen delivery system.
Basis forDecision Not To Revise the Primary Standards

The current primary NAAQS forCO

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

### and 40 mg/m 3

### (35ppm), 1-hour average, neither ofwhich is tobe exceeded more than once per year. As indicated above, the Act requires review ofthe existing criteria and ambient air quality standards for CO and other pollutants every five years. During the current standard review forCO, EPA has considered whether it should retain the existing CO primary standards,
repropose the same or different standards, orpromulgate 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 Actrequires 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 ofsafety. The legislative history of the Act makes clear the Congressional intent to protect sensitive persons who in the normal

course ofdaily activity are exposed to the ambient environment. Air quality standards are to be established with reference toprotecting the health ofa represenative, statistically related, sample ofpersons 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 

### ofthe uncertainties in this evidence, understanding of underlying biological mechanisms, and the need tomake 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 forother ambient standard pollutants, none ofthe evidence 

### presented in the 1979Criteria Document

or Addendum shows a clear threshold foradverse health effects ofCO. 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 ofhealth effects

are less certain.and more difficult to identify. This does not necessarily mean 

### that there is no threshold, other than
zero, forCO related health effects; it simply means that no precise threshold



### can be identified with certainty based

on existing scientific evidence. Thus, in settinga standard,EPA is unable to append an exact margin of safetyto a known threshold effect level. Rather, settinga standard with an adequate margin ofsafety is necessarily a public 

### health policyjudgment that must take into account both the known continuum ofeffects, understanding ofthe underlying biological mechanisms of 

### effects, and any gaps and uncertainties in the existing scientific data base.

Indetermining whether revision ofthe primary COstandards is appropriate, EPA has made assessments and judgments in the following areas: 1.Identification ofreported effect 

### levels and associated exposure duration that scientific research has linked to health effects in healthy and sensitive persons.

2. Characterization ofscientific 

### uncertainties in thehealth effects evidence andjudgments concerning which effects are important to consider 

### in reviewing or settingprimary standards.

3.Description ofpopulation groups 

### believed to be most sensitive to CO and estimates ofthe size ofthose groups.

4.The estimated number of sensitive persons that would be exposed to elevated CO levels upon attainment ofa 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 ofCO standard levels and averaging times that provide

an adequate margin ofsafety based on CO levels and exposure periods that may affect sensitive population groups,

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taking into account the various uncertainties.

Based on the assessment ofrelevant scientific and technical information in the Criteria Document and the Addendum, the Staff Reassessment outlines a number ofkey factors to be considered in each of the above areas. Both the staffand CASAC recommended that the Administrator focus consideration on a discrete range ofpolicy 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 ofthe earlier Staff Paper (EPA, 1979b) and CASAC closure letters (Hovey, 1979; Friedlander, 1982). Rather thanreiterating those discussions at length, the following discussion ofthe final decision focuses primarily on those considerations that

were mostinfluential in the Administrator's selection ofa particular option, or that differ in some respect from considerations that influenced the staffand/or CASAC recommendations.

Assessmentof HealthEffectsEvidence

The StaffReassessment, which has been placed in the public docket (Docket No. OAQPS 79-7, IV-A-10), presents an assessment by OAQPS staffofthe 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 ofthe 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 atal.. 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

concen- References Effets htroion (percent)'

Statistically significant 5-7.6 Horvath et at. 1971.

impairment of GrolI-Knapp etalt., vigilancetasks 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 ofstudies 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 StaffReassessment, or in this notice regarding the technical merits ofeach study.

Cardiovascular Effects.Inreviewing the primary standards, a principal area ofconcern 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, duringexercise, reduced time to onset ofangina (Anderson etal., 1973). Increased duration ofangina attacks has alsobeen reported (Anderson etal., 1973). In proposing to revise the CO standards, EPA viewed aggravation ofangina, as reported above, to be an adverse health effect (45 FR 55066) and CASAC concurred with EPA'sjudgment on this
matter.

One controlled human exposure study (Anderson et al. 1973) reported that experimental subjects with angina exhibited statistically significant 

### reduced time to onsetof exerciseinduced angina after exposure to low levels of CO resulting in mean COHb levels of2.9 (range 1.3-3.8 percent) and 4.5percent (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 of4.5 percent. Some

concerns have been raised about the study findings due to ambiguities regarding the design and conduct ofthe 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 ofthe Anderson et al. (1973) study, addressing major points of

concern, found that the study provides reasonably good evidence forthe hastening ofangina occurring in angina patients at COHb levels of2.9 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 of2 to 3percent. In addition, Aronow et al. (1974) reported that subjects with peripheral vascular disease hadreduced 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 ofthese CO studies expressed considerable

concern about the validity ofthe result reported and concluded thatEPA 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 thatEPA 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. (2raw data were lost

ordiscarded, (3)availabledata were of poor quality. (4) quality control for COHb measurements
was nonexistentor 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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Another cardiovascular effect of

concern is the possible detrimental effect ofincreased 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 etal. (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 ofcardiovascular 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 inmaximum aerobic capacity when COI lb levels

were 4.3 percent and that COHb levels of3.3 and 4.3 percent reduced work time
to exhaustion by 4.9 and 7.0 percent, respectively. The effects oflower CO exposure levels in healthy individuals have also been investigated under conditions ofshort-term, maximum exercise duration. In a series ofstudies 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 5percent) 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 ofangina, are still a matter ofconcern since they have been found to occur in healthy individuals and such effects might impair the normal activity ofmore sensitive populations. Therefore, these effects have been considered in judging which CO standards provide an adequate margin ofsafety.

CentralNervousSystem Effects. Numerous studies (Putz et al., 1976; Bender et al., 1971; Schulte, 1973; O'Donnel etal., 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 ofeffects reported included impairment ofvigilance, visual perception, manual dexterity, learning ability, and performance ofcomplex 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 5percent COHb. Measurement methods used to detect effects may have been too insensitive todetect 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 5percent 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 ornewborn. 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 ofCO 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 ofthese studies in setting the CO primary standards, these studies do suggest the need forcaution in protecting unborn children from such potentially deleterious effects ofCO exposures.

As discussed in the Addendum and StaffReassessment, research on sudden infant death syndrome (SIDS) recently has suggested a possible link between ambient CO levels and increased incidence ofSIDS (Hoppenbrowers et al., 1981). In response to this study, Goldstein (1982)has suggested that indoor sources ofCO, 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).

SensitivePopulationGroups

In EPA's judgment, the available health effects data identify persons with angina or other types ofcardiovascular 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 forpersons with cardiovascular disease results fromthe 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 ofexcess 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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### Federal Register / Vol. 50, No. 178 / Friday, September 13, 1985 / Rules and Regulations

cardiopulmonary function, (3)fetuses and.young infants, and (4)individuals suffering from anemia and those with abnormal hemoglobin types that affect
oxygen carrying capacity ortransport in the blood. In addition, individuals taking certain medications ordrinking alcoholic beverages may be at greater risk forCO-induced effects based on

some limited evidence suggesting interactive effects between CO and

some drugs. Visitors to high altitude locations are also expected tobe more vulnerable to CO health effects due to reduced levels ofoxygen in the air they breathe. Finally, individuals with some combination ofthe disease states or conditions listed above (e.g., individuals with angina visiting a high altitude location) may be particularly sensitive
to low-level COexposures, although there is no experimental evidence to confirm thishypothesis.

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 intoblood or its transport tobody tissues would be more susceptible to the hypoxic (i.e.,oxygen deficiency) effects ofCO.Since no human experimental evidence exists that identifies CO effect levels for these other groups, however, EPA is considering the possible effects ofCO

on these groups only inits determination of an adequate margin ofsafety.
Uncertainty inEstimatingCOHbLevels

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 ornear those observed in the studies. Amodel known as the Coburn equation (Coburn et al., 1965) has been developed to estimate COHb levels resulting from CO concentrations as a function oftime and various physiological factors (e.g., blood volume, endogenous CO production rate). Table 2 presents "baseline" estimates (using typical values forthe various physiological parameters) ofCOHb levels expected to be reached by adult nonsmokers exposed to various constant concentrations ofCO for either 1or8 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

1hourexposure 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= 159/100 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- tyof 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 ....................................................................... ....................................... ... 0.01 3.3

........................................................................................................................................................................ ............................ 0.1 3.1

......... ............................................................................................................ ............... ............... ............... ................ <0.01 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 ofthe COHb level resulting from one hour's exposure as the initial COHb level forthe 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 upso that-its peak 8-hour average CO concentration equalled the level ofthe 8-hour standard. Of the 20 selected patterns, results from 3 patterns arepresented 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 highestvalue.

*Haldane constant=218. Alveolar ventilation rate= 10 liters/min. Altitude=0.0 ft. *The estimation of distributions for each ofthe physiological parameters used in the Coburn model and the Monte Carlo procedure used to generate these estimates are discussed in Appendix C of the SensitivityAnalysis (Biller and Richmond, 1982).

There are, however, at least two uncertainties involved in estimating COHb levels resulting from exposure to CO concentrations. First, foreach 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

werepredicted using a set oftypical physiological parameter values. Second, predictions based on exposure to constant CO concentrations inadequately represent the responses of individuals exposed to widely fluctuating COconcentrations 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 offluctuating CO concentrations and variations in physiological parameters on COHb estimates. Since proposal, EPAhas 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 ofthe distribution of COHb levels in the adult non-smoking population based on variations in physiological parameters upon exposure to three different patterns ofCO levels which just meet alternative 9 ppm and 12ppm 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 offluctuating air quality levels on COHbuptake canbe roughly estimatdd by comparing the "baseline" result of a constant 9 ppm exposure for8 hours (1.4 percent COHbfrom 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-hourdose (i.e., 9 ppm, 8- hour average), the results shown in Table 3indicate that COHb levels ranging from approximately 1.4to 1.9 percent can be reached. A similar comparison ofthe resultsfor 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 byup to0.7 percent OCHb (i.e., from 1.7 percent COHb in Table 2 to 2.4 percent COHb forthe 50th percentile in the high pattern column ofTable 3).

The Sensitivity Analysis resultsin Table 3 alsoillustrate the effect ofusing distributions ofvalues for each physiological parameter rather thanjust

a single representative set ofvalues in applying the Coburn model. Forany given airquality pattern, the effect of usingthe distribution ofvalues foreach physiological parameter is to generate a distribution ofpeak COHb levels that the population would reach.For example, theresults in Table 3 show that 95 percent of the population is estimated to be within ±0.3 percent COHb ofthe median adultvalue after
exposure to the midrange pattern with a peak 9 ppm, 8-hour average. This variation in COHblevels attained is one further source ofuncertainty that is being considered injudging which standards provide an adequate margin ofsafety.

Sinceproposal, EPA has made considerable improvements in its exposure analysis methodology which, unlike the Sensitivity Analysis, treats movement ofpeople and variation ofCO concentration levels through time and
space. EPA believes that the revised Exposure Analysis described below, represents the best available tool for estimating the percentage ofthe population that would reach various CO concentrations and COHblevels upon attainment of alternative CO standards. Since theExposure Analysis model simulates theexposure ofindividuals on
an hourlybasis and simulates actual air quality patterns, theimpact of fluctuating CO levels is largely taken into account in theExposure Analysis results.The results ofthe 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 theExposure Analysis.
ExposureAnalysisEstimates

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 ofurban American adults that would be exposed to various ambient COlevels ifalternative 8-hour CO standards were just attained. In addition, estimates have been made of the percentage ofthis population that would exceed selected COHblevels each year.These latterestimates were derived by applying the Coburn model which relates patterns ofCO exposure to resultant COHb levels, to the
exposure model outputs using a typical
set ofphysiological parameters for adult

men and a separate set ofphysiological parameters foradult women.

In contrast to the Sensitivity Analysis, the Exposure Analysis simulates pollutant concentrations and the activities ofpeople 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 ofthe year each cohort is located in one offive "microenvironments." A microenvironment is a general physical location such as indoors-at-home or inside a transportation vehicle.

CO levels in each ofthe microenvironments are estimated by the

use ofmultiplicative "transformation factors," which relate CO levels recorded at the nearest monitor to estimate CO levels foreach microenvironment. This method is used since attainment ofa standard is defined in terms ofthe monitoring system. Values ofthe multiplicative transformation factors that would give the best exposure estimates are uncertain. Thevalues usedfor these factors were estimated making use of the available literature on (1)indoor and inside-motor-vehicle airpollution and (2) statistical analyses ofmonitoring data (e.g., how ambient values change with height and distance from a monitor). Amore detailed description of the approach, inputdata, 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 tofour urban areas: Chicago, Los Angeles, Philadelphia, and St. Louis. Exposure estimates for the adultpopulation living in urban areas in the United States were obtained primarily by associating each urban area in theUnited States havinga population greater than 200,000 with one of the fourcities mentioned above. The association was made on thebasis of geographic proximity to one ofthe base
areas,average wind speed,peak CO concentrations, observed climate, and general character ofthe area.

TABLE 4.-CUMULATIVE PERCENT OF ADULT

POPULATION INURBAN 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 9p[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 is5.240.000 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 inthe 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 thepercentage of the adult population living in urban areas who would exceed various COHblevels upon attainment of three alternative 8-hour standards. For example, less than 0.01 percent ofthe adult population in urban areas is estimated to exceed 2.1 percent COHb due to COexposures associated with attainment ofthe current (deterministic) 9 ppm standard, and approximately 20 percent ofthe adult population is estimated to exceed 2.1 percent COHb upon attainment ofa 15 ppm standard with 1expected 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 tojust attain the given standards.

Several factors make the accuracy of the nationwide exposure estimates uncertain. They include: (1)the paucity ofinformation on several ofthe needed inputs (e.g., some ofthe microenvironment multiplicative transformation factors) and (2) the fact

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that nationwide estimates were extrapolated from only foururbanized

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 forwomen), rather than the full distributions ofthe physiological parameters forthe 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 forone urbanized area to give a rough idea of the range of possible COI-Ib levels that would be reached.

Decisionon thePrimary Standards
The StaffReassessment and 1984 CASAC findings and recommendations
set forth a framework forconsidering whether revision ofthe 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 StaffPaper, and earlier CASAC closure letters (Hovey, 1979; Friedlander, 1982).

Based on its assessment ofscientific evidence discussed previously in this notice, EPA concludes that adverse health effects clearly occur, even in healthy individuals, at COHb levels in the range of5 to 20 percent. EPA also remains concerned that adverse health effects may be experienced by large numbers ofsensitive 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 3percent COHb (not including a margin of safety)" (Lippmann, 1984).

In addition to concurring with EPA that cardiovascular effects are likely to

occur at approximately 3percent 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 ofsafety. 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 ofthis notice, 8-hour single exceedance CO standards in the range 9 to 12 ppm are estimated to keep more than 99 percent ofthe non-smoking cardiovascular population below 3.0 percent COHb. Different standards within this range would, ofcourse, provide different levels ofprotection. For example, the current 9ppm, 8-hour
average standard is estimated to keep

more than 99.9percent of the adult cardiovasular population below 2.1 percent COHb. A 12 ppm, 8-hour standard is estimated to keep more than 99percent ofthe 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 ofCOHb 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 EPAcannot 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 toCO exposure, such as those with a history ofmyocardial infarction

ormultiple disease states (e.g., both angina and anemia). Another factoris that, once the Aronow etal. 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 ofeffects have also been found in studies examining effects of maternal smoking on human fetuses. However, itis 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 forfetal effects remain to be determined, these findings denote a need for caution in evaluating the margin ofsafety provided by alternative CO standards.

3.Other groups that may be affected by ambient COexposures but forwhich there is little orno experimental evidence include: anemic individuals (over 3million individuals), persons with chronic respirat6ry diseases (about 14 million individuals), elderly individuals (over24.7 million individuals

over 65 years old), visitors to high altitude locations, and individuals on certain medications. The levels ofCOHb that mightproduce adverse effects for each ofthese groups is uncertain. However, elevated COHb levels ineven
a small percentage ofthis very large potentially sensitive population would translate to a significant number of individuals. The large size ofthe potentially sensitive population, then, argues for standards providing a greater margin of safety.

4. There are a number ofuncertainties regarding the uptake of CO, including those related to the accuracy ofthe Coburn equation, in assessingvariations in thepopulation due to differing physiological parameters and exposure to varying air quality patterns.

5. Several factors contribute to uncertainties about the exposure estimates ofthe expected number of individuals achieving various COHb levels upon attainment ofalternative standards. These factors include: the paucity ofinformation on several ofthe needed inputs, the fact that nationwide estimates were extrapolated from only foururbanized areas, and the use oftwo representative sets (one for men and one forwomen) ofphysiological parameters (e.g., blood volume) rather than distributions ofphysiological parameters in applying the Coburn model to derive COHb estimates in the exposure analysis. As indicated in the StaffReassessment (pp. 18-21), some individuals with physiological parameters that maximize uptake of COHb, ifexposed 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 ofsafety. EPAis continuing its CO exposure research efforts, which should lead to future Federal Register / Vol. 50,

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improvements in its exposure analysis and a better capability to assess the
accuracy ofthe 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 (thebolus effect). As discussed in the proposal notice (45 FR 55077), existing air quality data indicate that attainment of a 9ppm, 8-hour averaging time standard should limit the magnitude ofshort-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 ofthe scientific information bearing on the level ofthe standard, EPAbelieves 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 ofthe 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 of9 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. Theyrecommended that the Administrator consider choosing standards thatmaintain approximately the same level ofprotection 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 ofsafety

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 ofCOHb 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 theeffect of CO on aggravation ofangina. Subjects in these studies are being exposed toCO levels that result in blood COHb levels in the range 2.0 to 4,0percent. One study is being conducted by EPA, several are being conducted at the request ofEPA by the Health Effects Institute (HEI), and another study is being sponsoredby the California AirResources Board (CARB). The Health Effects Institute is an independent organization which sponsors research on automotive pollutants and isjointly funded by EPA and automobile manufacturers. The peer-reviewed results ofthese studies

are expected by December 1986. EPA will be initiating development ofa new criteria document for COin Fiscal Year 1986. Thus, the Agency should be in a good position to expeditiously assess the results fromthe 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 inprogress, theAdministrator considered deferring a final decision on the CO standards until these new studies havebeen 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 thatthe Agency has inadequate evidence to select an appropriate course ofaction at this time. However, both EPA and the CASAChave 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 ofthe decision could be perceived as a signal to relax ordelay ongoing control programs, the Administrator has concluded that final action now on the CO standards is warranted andjustified.

In reaching a final decision, the Administrator has focused primarily on the level ofprotection the CO standards should provide. Aspreviously noted, afterreassessing the available scientific data and EPA staffrecommendations, the CASAC has recommended that the CO standards provide protection approximately equal to the current' standards. Based on EPA's assessment ofthe scientific data, the Administrator

concurs with this recommendation. Retention of thecurrent standards would, ofcourse, 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 theAgency believes would be advantageous. However, the proposed changes would require some modification in theway attainment of the standards is determined. Given the uncertainties in the existing data base and the possibility that the results ofthe

new studies in progress might warrant further revisions within a few years, the Administrator has concluded that it 

### would notbe prudent topromulgate the proposed revisions at this time, particularly when theywould alter the

manner inwhich attainment is determined.

Inshort, the Administrator has concluded thatitwould notbe prudent to defera decision on the CO standards pending the results ofthe newresearch mentioned above,that the standards should provide approximately the same level ofprotection as that afforded by thecurrent standards, and that disruption ofongoing control programs shouldbe minimized. Given these considerations, theAdministrator has concluded that the bestcourse ofaction is not to revise theCO primary standards at this time.Together with the Administrator's decision to rescind the secondary standards (discussed below], this decision completes the current review oftheNAAQS forCO under section 109(d). The ongoing studies conducted bythe Agency,by the HEI, andby the CARB (alldiscussed above) will, ofcourse, be considered inthenext 5-year review cycle ofthe CO criteria and standards. Upon completion ofthis series ofstudies, theAgency plans to review the results with the CASAC and

assess theneed for anyrevisions inthe primary standards. Ifrevisions in the standards seem appropriate, the Agency will act expeditiously to revisethe standards.

Welfare Effects and the Secondary Standards

Carbonmonoxide is a normal constituent oftheplant environment. Plants canbothmetabolize andproduce CO.This may explain the factthat relatively high levels ofCO are necessary before damage occurs to vegetation. Thelowest level forwhich significant effects onvegetation have beenreported is 100ppm for3to 35 days.The effect observed in this study

was an inhibition ofnitrogen fixation in legumes. Since CO concentrations of this magnitude are rarely ifever observed in the ambient air,itis very unlikely that any damage to vegetation will occur from CO airpollution. No other effects onwelfare havebeen associated with CO exposures at or near ambient levels. Because no standards appear tobe requisite toprotect the public welfare from any known or anticipated adverse effects from ambient CO exposures, EPA is rescinding the existing secondary standards. SignificantHarm Levels

Section 303 ofthe CleanAirAct authorizes theAdministrator totake

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certain emergency actions ifpollution levels in an area constitute "an imminent and substantial endangerment
to the health ofpersons." EPA's regulations governing adoption and submittal of SIP's contain a provision (40 CFR 51.16] that requires the adoption by States ofcontingency plans to prevent ambient pollutant concentrations from reaching specified significant harm levels. The existing significant harm levels for CO were established in 1971 (36FR 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 of5to 10 percent, the range EPA has determined would

cause significant harm. On the basis of EPA's reassessment ofthe earlier data and assessment of more recent medical evidence, no modifications are being made to the existing significant harm designations. EPA's assessment ofthe 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

OverviewofComments

The following discussion summarizes ingeneral terms the comments received,
at various times since the 1980 proposal, from the public and fromFederal and State agencies on thelevels ofthe primary standards and on the related issue of multiple exceedance standards. Significant comments on all aspects of the COproposal and Agency responses to these comments are summarized by category later in this section. Amore detailed description of individual
comments and Agency responses is contained in the public docket (OAQPS 79-7).

Commentson 1980Proposal. Ofthe written comments received during the initial commentperiod (which closed November 24, 1980) that expressed some opinion on the level of the proposed 8- hour standard, 7out 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 ofthe standard, and local and State agency comments supported the proposed standard or some relaxation ofthe standard.

Several comments were received on the Agency's proposal to lower the 1- hour standard to 25 ppm. Ofthe 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 3comments recommended revocation ofthe 1-hour standard. There also was one comment favoring further tightening ofthe 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 ofthe 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 ofthese agencies neither supported noropposed 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.

CommentsonSubsequentNotices.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 ofmultiple expected exceedance 8-hourCO standards (47 FR 26407). Ofthe comments that expressed an opinion on the issue ofmultiple expected exceedances, 12 out of23 favored the

use of themultiple 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 forand against multiple exceedance standards.

During the period from November 24, 1980 through August 6, 1982 (the close of the second comment period), ofthose commenting on whether the 8-hour standard shouldbe relaxed, 10 out of45 favored relaxation. Most of the States (12 of 14) opposed relaxation, while 3 of 5 local governments favored relaxation. As inthe earlier comment period, all industry comments favored relaxation while all environmental groups opposed relaxation.

Subsequent to the close ofthe 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 ofthe diminished value ofDr.Aronow's CO studies on September 16, 1983 (48 FR41608). Ofthe 13 comments received in response to this notice that expressed an opinion on the levels ofthe standards, 7favored retaining the current primary standards, 2 favored theproposed standards (i.e., 9 ppm forthe 8-hour averaging time and 25 ppm forthe 1-hour averaging time), and 4 favored relaxation of the 8-hour standard to 12 ppm orhigher. Those supporting theproposed orcurrent standards included an environmental group, several Stateenvironmental agencies, two health scientists, and one local environmental agency. Those favoring relaxation ofthe 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 thefinal Addendum (EPA, 1984b) and StaffReassessment (EPA, 1984a), and solicited additional public
comment (49FR 31923). Ofthe 7
comments received that expressed an opinion on the levels ofthe standards, 2 favored retaining the current primary standards, 2 favored theproposed primary standards (i.e., 9 ppm, 8-hour and 25 ppm, 1-hour, and 3favored relaxation ofthe 8-hour standard to 12
ppm or higher. Two commentors argued that EPA should deferfinal 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 toby category below.

I.HealthEffects CriteriaandSelection ofthePrimary Standards

A. Definition ofAn Adverse Health Effect

Comment.It is questionable whether a reduction in the time to onset ofan angina attack following exercise is adverse.

AgencyResponse: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 ofangina may be the first in a series ofprogressively more serious symptoms that accompany cardiovascular disease. Atlow levels of oxygen deprivation, angina patients experience symptoms ofchest pain described above. Coronary insufficiency is a more serious symptom that occurs at greater levels ofoxygen deprivation. This symptom is sometimes accompanied by changes in enzyme levels and electrocardiographic irregularities. The most serious effect in thiscontinuum ofeffects is myocardial infarction. In addition to longer and

moreintense pain, myocardial infarction is accompanied byirreversible heart damage (death ofmyocardial cells) as indicated byenzyme level changes and electrocardiographic alterations.Finally, because aggravation ofangina maybe the firstin a series ofsymptoms that maylead to permanent heart damage, EPAconsiders aggravation ofangina an adverse effect and an indicator that

more serious effects may occur in some individuals at the same COHb levels. EPA'sjudgment hasbeen supported by theCASAC 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 severityof potential health effects withincreasing levels ofCO.The factthat a no-effects level cannot be identified may lead to a standard near
zero.The current evidence can support standards other than thoseproposed by EPA.

Agency Response:EPA agrees that there is a continuum ofeffects consisting ofCOHb levels at which health effects

are certain, through levels at which scientists can generally agreethat medically significant effects have been convincingly shown, and down to levels at which health effects are less certain,

are harderto identify, and themedical significance ofwhich are typically disputed.In short,the present scientific evidence does not permit selection ofan undisputed value for a primary standard. Rather, theAdministrator in selecting a standard must make a judgment as to the level ofphysiological response that shouldbe considered adverse and the relative acceptability of various degrees ofuncertainty that any given level is low enough to prevent known and possible adverse health effects.

B. Scientific Validity ofthe Human Experimental Studies

Comment:Work ofDr.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 ofangina patients. The Horvath Committee (Horvath et al., 1983) recommended thatEPA not rely on Dr.Aronow's studies in setting the CO standards.

. AgencyResponse:The Administrator
agrees with the Horvath Committee that there are very serious technical questions about the validity ofDr. Aronow's CO studies and, therefore, is
not considering the results ofthese studies inhis decision.

Comment:The Anderson et al. (1973) study shouldbe eliminated from consideration because Anderson etal. reported a COHb level ofonly4.5 percent after a four hour, 100 ppm CO
exposure, whereas other investigators have generally reported 8-10 percent COHb for similar exposures.

AgencyResponse:During the Anderson et al. (1973) study, subjects

were allowed breaks and, thus, were exposed to CO intermittently, not continuously, for4 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) lackof dose-response relationships for
onset and duration ofangina in some subjects, (5)reliance on subjective.
responses, and (6finadequate presentation ofstatistical procedures.

AgencyResponse:EPA has carefully reviewed the Anderson et al. (1973) study and the above criticisms ofthe study. A detailed response is contained in a February 20, 1985 memorandum prepared by EPA's scientists in the Office ofResearch 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, ifany, studies are perfect and thus conclusively demonstrate precise pollutant thresholds for the entire range ofsensitive 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 aregrounds for totally excluding the study from an assessment of the health risks ofCO. After carefully evaluating the scientific merit of the study and considering the advice provided by the CASAC, EPA has concluded that theAnderson study shouldbe 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 ifthe number ofsubjects 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 ofthe national population suffering from angina.

2.Because of the explicit precautions taken by the author to ensure the integrity ofsuch a protocol, EPArejects 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 (DocketECAO CD78-3, IIA-J-3) who reaffirmed the study protocol which is consistent with the definition ofdouble blind. The author cited the published study which states:

A 5-day, double-blind exposure protocol

was followed-Only the investigator administering the gasknew which concentration of CO wasbeing used. The patient, technician, and the investigator conducting the'exercise test were all unaware ofthe exposure condition. Acurtain separated the gas tanks fromthe patient-On completion ofthe five exercise tests for each subject, theECG records were assigned a random code number and interpreted by an investigator who had notbeen present and hadno knowledge ofthe exposure sequence.

3.Because ofthe explicit double blind protocol practiced in the study,there is

no basis forconcluding that the two subjects who missed one day of
exposure had in some way gained knowledge ofthe exposure conditions due to theirmissing one ofthe 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 inthe Anderson
et al. study is not surprising given the smallrange ofexposure concentrations, thefact that the exposures were close to the lower limits for CO-related effects, and the small number ofsubjects. However, EPAhas not used this orany other study to develop a dose-response relationship which would show different levels ofsubject response over a specific range ofadministered CO doses. EPA has argued that the Anderson study does suggest an increased risk of aggravation ofangina for sensitive individuals who have elevated COHb levels.

5.The fact that the endpoint measured byAnderson et al., namely time to onset ofangina pian, is subjective in nature is

no basis forignoring this serious and important effect as carefully articulated in the proposal preamble (45FR 55069):

EPAconsiders such aggravation ofangina to be an adverse health effect for several

reasons. First,it mayresult in cardiovascular damage, which is unquantifiable using present technology. Second, aggravation of angina may bethe first in a series of progressively more serious symptoms that accompany cardiovascular disease.At low levels ofoxygen deprivation, angina patients experience symptomsof chestpain described above. Coronary insufficiency is a more serious symptom that occurs at greater levels ofoxygendeprivation. This symptom is sometimes accompanied by changes in enzyme levels andelectrocardiographic irregularities. The most serious symptom in this continuum ofeffects is myocardial infarction. In addition to longer andmore intense pain,myocardial infarction is accompanied by irreversible heartdamage (death ofmyocardial cells) as indicated by enzyme level changes and electrocardiographic alterations. Finally, because aggravation ofangina maybe the first in a series ofsymptoms that may lead to permanent heart damage, EPA considers aggravation ofangina an adverse effect and

an indicator thatmore serious effects may
occurin some individuals atthe 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 ofinference (see Appendix A in the Addendum; EPA 1984b). EPA believes that, had Anderson
et al. originally used this technique, the effect oftime to onset of angina would have been statistically significant (p=0.014 at the 97.5 percent confidence level] but that duration ofangina 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 notionthat a studyhas no validity until it's been replicated is flawed. Based upon itscurrent knowledge ofhow the studywas conducted,CASAC presumes that double blind protocols were, infact, observed and thatdiscrepancies between observed andpredicted COHblevels arenot as great

oras serious as originally suggested. In summary, whileCASAC treats theAnderson et al. study with caution, it can find no substantive reason atthis timeto dispute the reported values, and it recommendsthat the Agency not disregard its findings (Lippmann. 1984).

TheAgency continues tobelieve that the Anderson et al. findings can be appropriately interpreted as providing reasonably good evidence of exacerbation ofangina symptoms occurring in some segments ofthe 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.

AgencyResponse:Although psychological factors may contribute to angina attacks, it has beenreasonably shown in the study byAnderson et al. that exposure to CO doescontribute 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 ofSafety

Comment:EPA has proposed CO standards with an inappropriate margin ofsafety. The margin ofsafety was criticized as being either inadequate or excessive.

AgencyResponse:The decision regarding an adequate margin ofsafety is ajudgment which mustbe made by the Administrator after weighing all the medical evidence bearing on the effects ofCO. The factors tobe 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 ofCOHb likely to result from COexposure at the levels associated with attainment of alternative standards. More specifically, theAdministrator considered the factors and sources of uncertainty, discussed earlier in the Decision on thePrimary Standards section of thisnotice and in the StaffReassessment (EPA, 1984). EPA has examined the health protection afforded by alternatives to thecurrent CO primary standards. For example, attainment ofa 12 ppm, 8-hour CO standard is estimated to keep more than 99 percent ofthe 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 ifexposed 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 ofsafety.There is no credible scientific evidence that suggests more stringent CO primary standards than the
current standards are required toprotect public health with an adequate margin ofsafety.

D. Coburn Model Sensitivity Analysis of COHb Levels

Comment:The term usedin 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 COpressure in air saturated with water vapor atbody temperature.

AgencyResponse:EPA agrees with the comment and has revised all ofthe COHb estimates used in thisnotice 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 ofthe medical literature. Modeling efforts ofthis kind' should choose conservative values for physiological parameters in order to err

on the side ofprotecting public health.

Agency Response:The values selected for the physiological parameters usedin the Sensitivity Analysis were carefully reviewed with members ofthe scientific community and with consultants to the CASAC and werejudged to be reasonable estimates. EPA does not agree that themost conservative values should beselected forthe physiological parameters because thiswould introduce an additional margin ofsafety intoan analysis attempting toestimate the effects ofalternative standards. The Sensitivity Analysis doesuse arange of values forthe various physiological parameters.

Comment:The draft Sensitivity Analysis does not adequately treat 

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differences in physiological parameters between men and women.

AgencyResponse:In an Appendix to the revised Sensitivity Analysis (Biller and Richmond, 1982), men and women
are modelled separately and appropriate physiological parameters are selected foreach 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 ofalternative standards. Theexposure analysis should
not be used in selecting the primary standards until all the recommended changes are incorporated into the analysis.

AgencyResponse:EPAhas 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 similarin magnitude, after taking these
comments into account, tothe original
exposure estimates.

A second category ofcomments suggested changes that EPA agrees would refine the exposure assessment methodology, but which are not feasible
at this time because oflimitations on the

resources and time available for this standard review. EPA will incorporate these comments into itsplan for improving itsexposure 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 ofthe scientific community's ability to model physiological and otherparameters related to this pollutant" (Friedlander, 1982).

A third category consists of comments where EPA disagrees with the suggested changes. Detailed responses to these
comments areprovided 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 ofuncertainty 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 levelsupon attainment ofalternative standards.

II.FormofthePrimary Standards
Comment:Some commenters favored retaining the current deterministic form; others supported eitherEPA's 1980 proposal to adopt single-expectedexceedance (statistical form) orthe concept ofmultiple-expectedexceedances (statistical form) primary CO standards.Those in favor of adopting a statistical form argued that it would minimize the impact ofunusual meteorological events on control strategies with minimalreductions in health protection offered bythe standard.Those opposed to a multipleexpected-exceedances standard expressed concerns about the increased health risksto the sensitive population and the ability ofthepublic to understand the basis for allowing multiple excursions ofthe standard levels.

AgencyResponse:Given theconcerns expressed bythe vast majority of State airpollution control agencies and others that a single-exceedance standard, either deterministic orstatistical, more closely reflects the health basis for the standard and ismore readily implemented and understood bythe general public, EPA has decided to retain the single exceedance format for theprimary standards. WhileEPA believes that adopting a statistical, single-exceedance standard would be a technical improvement, EPA isdeferring any such change inthe primary CO standards until the uncertainties regarding thehealth effects basis forthe standards are better resolved.

III.Miscellaneous
A. Natural Background

Comment:Ithas beenreported that 93%ofthe COin theatmosphere is produced by vegetation andthe oceans and,therefore, anthropogenic sources of COshould be oflittleconcern.

AgencyResponse:Although much of the CO produced globally maybe of natural origin, the elevated COlevels found in urbanareas and inrural areas
nearroadways are principally a result of human activities involving the combustion offossil fuels.

B.Stating Standards in ppm and Not mg/m 3



### Comment:EPA should state the revised COstandards solely in partsper million (ppm)rather than mg/m. Changing to ppmwould (1)avoid confusion as to thelevel ofthe standards at different altitudes, (2) provide additional protection for high altitude areas, and (3)be consistent with health and monitoring data usingthe Federal Reference Methods which are reported in ppm.

AgencyResponse:EPA is retaining both systems ofunits 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, ifa measurement is expressed in ppm units ormg/m3 units (at standard conditions) the values will differby a factor of0.875 regardless of altitude. This conversion factoris specified in Appendix D of40CFR Part 50.

Revisions to Part50 Regulations

Because EPAhas decided not to revise the CO primary standards, there

are no substantive changes to thePart 50 regulations concerning these standards. EPA is revising the text ofthe standards slightly, however, to make them clearer and more understandable
to the public. EPAis also explicitly stating several data handling conventions that have traditionally been used inEPA'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 ofsignificant figures retained when making comparisons with the levels ofthe standard. These changes were discussed in the proposal notice. EPA is also changing toppm 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 ofwelfare related effects at or near ambient levels.

Part51 Regulations and SIP Development

This action doesnot modify the existing Part 51 regulations. Current guidance to State and local airpollution control agencies on how to interpret air quality data for purposes ofattainment 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 RegulatoryImpactAnalysis

As has been noted, the Clean Air Act specifically requires thatNAAQS be based on scientific criteria relating to the level that shouldbe attained to protect public health and welfare adequately. The courts haye endorsed a reading of the Act that excludes reliance

on the cost orfeasibility of achieving such a standard in determining the level of the primary standards. In response to Executive Order 12291, EPAhas prepared a regulatory impact analysis (RIA). However, EPA'sanalysis, "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 theFor Further Information Contact section of this notice until supplies are exhausted and from the NTIS whose address is given in the Addressees section ofthis 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 ofCO emission have been examined in the Environmental Impact Statement, which is available in the docket (OAQPS 79-7, IV-A-13) or from EPAat the address given earlier in the ForFurther Information Contact Section ofthis notice. This analysis indicates that control strategies required to attain the standards will have minimal adverse impacts on other environmental media. Impacton SmallEntities

The Regulatory FlexibilityAct (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 ofthe final report, "Cost and Economic Assessment of Alternative National Ambient Air Quality Standards forCarbon Monoxide" (EPA, 1985). A NAAQS for CO by itselfhas 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 forcars and trucks, (2) I&M programs, and (3)stationary source control programs. FMVCP requirements

are largely established by statute orby 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 smallbusinesses. Additionally, theincremental cost ofCO control, which is passed on to purchasers ofmotorvehicles-including small entities-is a small fraction ofthe 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 alsohave a positive economic impact on some small entities. Theestimated pe'r vehicle average annual cost for the CO portion ofan 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 forCO only,these estimates would be doubled.) These costs should not impose a significant negative economic impact on small entities. On the otherhand, some smallentities such as gas stations and garages will be repairing failed vehicles resulting ina 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 motorvehicles, then theirnet receipts will also increase due to receipt ofthe inspection fee, most ofwhich they retain. (The remainder goes to the governmental unit sponsoring the areawide I&M program.)

Finally, only thelargest stationary

sources ofCO 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 groupwill be significantly negatively affected due to retention of theprimary 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 ofsmall entities. ImpactonReportingRequirements

There are no reporting requirements directly associated with this action. There are reporting requirements associated with related sections ofthe 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 ReferenceMethod

The measurement principle and calibration procedure applicable to reference methods formeasuring 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 of40CFR Part 50. Reference methods, as well as equivalent methods, for monitoring CO

are designated in accordance with 40 CFR Part 53. Alist ofall methods designated by EPA as reference or equivalent methods for measuring CO is available from any EPA Regional Office,

orfrom EPA, Department E(MD-76), Research Triangle Park, N.C. 27711.
References Anderson, E.W., R.J. Andelman, J.M.Strauch,

N.J. Fortuin, andJ.H. Knelson (1973). Effect oflow-level carbon monoxide exposure on onset and duration ofangina pectoris: A study on 10patients with ischemic heart disease.Ann.Intern.Med.79:46-50. Aronow, W.S., andM.W. Isbell (1973).

Carbon munoxide effect on exerciseinduced angina pectoris.Ann.Intern.Maed. 79:392-395. Aronow, W.S., E.A. Stemmer, and M.W.

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pectoris by 2% carboxyhemoglobin. AmericanHeart Journal101:154-157. Aronow,W.S. (1983). (Letter to Dr.Lester D.

Grant, including Dr.Aronow's replyto Horvath Committeereport.] June 4,1983. Available from: U.S.Environmental Protection Agency,Central Docket Section, Washington, D.C.; Docket No. OAQPS 79- 7,IV-H-59. Ayres, S.M.,.H.S.Mueller, J.J. Gregory, S.

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(1970). Myocardial and systemic responses to carboxyhemoglobin. In:Biological Effects ofCarbon Monoxide, Proceedings ofa Conference, NewYork, Academyof Sciences, NewYork, January 12-14. Ayres, S.M., R.G.Evans, andM.E. Buehler

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and J.A.Wagner (1977). Effects ofthree kinds of hypoxias on vigilance performance.Av. Sp. Env. Aed. 48:491-496. Coburn, R.F., W.S. Blakemore, and R.E.

Forster (1963]. Endogenous carbon monoxide production in man.I. Clin. hIvest.42:1172-1178. Coburn, R.F., R.E. Foster. and P.B. Kane

(1965). Considerations ofthe physiology and variables that determine the blood carboxyhemoglobin concentration in man. 

### J.Clin.Invest. 44:1899-1910. Coburn, R.F. (1979). Mechanisms ofcarbon

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Electrocardiographic changes inhealthy

men during continuous low-level carbon monoxide exposure. Environ. Res.21:9-15. DHEW [U.S. Department of Health,

Education, and Welfare] (1970). Air Quality Criteria for Carbon Monoxide. Washington, D.C. AP-62. DHEW (1975). Public Health Service (PHS).

Coronary Heart Disease inAdults, United States: 1960-1962. Ityatteville, Maryland.
DtIEW Publication No. (PHS) 79-1019. DOC (U.S. Department ofCommercel (1980).

Statistical Abstract ofthe United States, 1980 (101st edition). Bureau ofCensus. Drinkwater,B.L., PB. Raven,S.M.Horvath,

J.A.Gliner, R.O. Ruhling, N.W. Bolduan,' and S, Taguchi (1974). Air pollution, exercise,and heat stress.Arch. Environ. Health28:177-181. EPA [U.S. Environmental Protection Agency]

(1977). Guideline for the Interpretation of Air Quality Standards.Office ofAir Quality Planning and Standards, Research Triangle Park, N.C. Publication No. 1-2- 008. EPA (1979aj. Preliminary Assessment of

Adverse Health Effects from Carbon Monoxide and Implicationsfor Possible Modifications ofthe Standard. (Draft staff
paper presented at the meeting ofthe Clean Air Scientific Advisory Committee, June 14-16, 1979.) EPA (1979b). Air Quality Criteria for Carbon

Monoxide.-Environmental Criteria and Assessment Office,Research Triangle Park. N.C. EPA-600/8-79-022. EPA (1980). Sensitivity Analysis onCoburn

Model Predictions ofCOHb Levels Associated with Alternative CO Standards (Draft). Office ofAir Quality Planning and Standards, ResearchTriangle Park, N.C. EPA (1984a). Review ofthe NAAQS for

Carbon Monoxide: Reassessmentof Scientific andTechnical Information. Office ofAir Quality Planning and Standards, ResearchTriangle Park, N.C. EPA-450/5-84-004. EPA (1984b). Revised Evaluation of Health

Effects Associated withCarbon Monoxide Exposure: An Addendumto the 1979Air Quality Criteria Document for Carbon Monoxide. Environmental Criteria and Assessment Office, ResearchTriangle Park, N.C. EPA-600/8-83-,033f. Ekblom, B., and R.Huot (1972). Responseto

submaximal and maximal exercise at different levels ofcarboxyhemoglobin. Acta Physiol.Scand.86:474-482. Fodor, G.G., and G. Winneke (1972). Effect of

low CO concentrations on resistance to monotony and on psychomotor capacity. Staub Reinhalt.Luft 32:45-54. Friedlander, S.K. (1982). Letter toAnn M.

Gorsuch, EPA Administrator. August 31. Goldsmith,J.R., and S.A. Landau (1968).

Carbon monoxide and human health. Science 162t1352-1359. Goldstein, I. (1982). Letter tothe ed;tor:

Seasonalrelationship ofsudden infant death syndrome and environmental pollutantsAm.

. Epid.116:189-191. Groll-Knapp, E., H. Wagner, H. Hauck, and

M. Haider(1972). Effects of low carbon monoxide concentrations on vigilance and computer-analyzed brain potentials Staub Reinhalt.Luft32:64-68. Haider M., E.Groll-Knapp, H.tIoeller, M.

Neuberger, and H. Stidl (1976). Effects of moderate CO dose on'the central nervous system-electrophysiological and behaviour data and clinical relevance. In: Research Conference, American Medical Association, San Francisco, California, December 5-6, 1974. A.J. Finkel andW.C. Duel, eds., PublishingSciences Group, Inc., ActonMA. pp. 217-232. l lartwell, T. etal. (1984). Study ofCarbon

Monoxide Exposure of Residents of Washington, D.C., and Denver, Colorado. Prepared by ResearchTriangle Institutefor U.S. EPA, Environmental Monitoring Systems Laboratory, Research Triangle Park, N.C. Iloppenbrouwers,T., M. Calub, K. Arakawa,

and J.E. Hodgman (1981). Seasonal relationship of sudden infant death syndrome and environmental pollutants. Am.

. Epid. 113:623-625. Horvath, S.M., T.E. Dahms, and J.F. O'Hanlon

(1971). Carbon monoxide and human vigilance:A deleterious effect ofpresent urban concentrations. Arch. Environ. Health23:343-347. Horvath, S.M., P.B. Raven,T.E. Dahms, and

D.J. Gray (1975). Maximal aerobiccapacity at different levels ofcarboxyhemoglobin.

. Appl.Physiol. 38.300-303. Horvath, S.M., S.M. Ayres, D.S. Sheps, and J.

Ware (1983). [Letter to Dr. Lester D. Grant, includingthe Horvath Committee report on Dr.Aronow's sutdies.] May 25. Available from: U.S. Environmental Protection Agency,Central DocketSection, Washington, D.C.; docketno. OAQPS 79-7, IV-H-58. Hovey, H.H., Jr. (1979). Memorandum to EPA

Administrator from CASAC CO Subcommittee. October 9. Johnson, T. and R.A. Paul (1983). The NAAQS

Exposure Model (NEM) Applied to Carbon Monoxide. Prepared by PEDCo Environmental, Inc.for Office ofAir Quality Planning and Standards, U.S. EPA, Durham, N.C. EPA-450/5-83-W03. Johnson. T.A. (1984). Studyof Personal

Exposure to Carbon Monoxide in Denver, Colorado. Prepared by PEI, Inc., for U.S. EPA, Environmental Monitoring Systems Laboratory, ResearchTriangle Park,N.C. EPA-600/54-84-014. Klein,J.P., H.V. Forster, R.D. Stewart,and A.

Wu (1980). Hemoglobin affinityfor oxygen during short-term exhaustive exercise.j App. Physiol.48:236-242. Kurt, T.L., R.P., Mogielnicki, and I.E.Chandler

(1978).Association ofthefrequency of acute cardiorespiratory complaints with ambient levels ofcarbon monoxide. Chest 74:10-14. Kurt.T.L, R.P., Mogielnicki, andJ.E.

Chandler, and K.Hirst (1979). Ambient carbon monoxide levels and acute cardiorespiratory complaints: an exploratory-study.Am.!. Public Health 69.360-363. Lippmann, M. (1984). CASAC Findings and

Recommendations on the Scientific Basis for aRevised NAAQS for Carbon Monoxide. [Letter to W.D. Ruckelshaus, EPA Administrator]. May 17.Available from: U.S. EPA, Central Docket Section, Washington, D.C.; docket no. OAQPS 79-7, IV-K-25. Longo, L.D. (1977]. The biological effect of

carbon monoxide on thepregnant woman, fetus, and newborn infant. Am.

. Obstet. GynecoL. 1291.69-103. O'Donnell, R.D., P.Mikulka, P.Heinig. andJ.

Theodore (1971). Low level carbon monoxide exposure and human psychomotor performance. Toxicol. Appl. Pharma-col. 18:593-602. McFarland, R.A., F.J.W. Roughton, M.H.

Halperin,and J.I.Niven (1944). The effects ofcarbon monoxide and altitude on visual thresholds./. Aviat.Med .5:381-394. McFarland, RA. (1973). Low level exposure

to carbon monoxide and driving performance. Arch. Environ. Health 27.355- 359. Paul, R.A. andT.Johnson (1985).The NAAQS

Exposure Model (NEM) AppliedtoCarbon Monoxide: An Addendum. Prepared by PEI, Inc. for U.S. EPA, Office ofAir Quality Planning and Standards, Durham, NC. EPA-450/ Peterson, D. (1981). The sudden infant death

syndrome-reassessment ofgrowth retardation inrelation to maternal smoking and the hypoxia hypothesis. Am.1.Epid. 113:583-589. Pirnay, F., J.Dujardin, R. Deroanne, and J.M.

Petit (1971). Muscular exercise during intoxication by carbon monoxide.

.Appl. Physiol.31:573-575. Putz, V.R., B.L. Johnson,and

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-(1976). Effects ofCO on Vigilance Performance. Effects ofLow Level Carbon Monoxide on DividedAttention, Pitch Discrimination, and the Auditory Evoked Potential. U.S. Department ofHealth, Education, and Welfare, National Institute ofOccupational Safety and Health, Cincinnati, OH. DHEW (NIOSH) Publication No. 77-124.

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(1979). A comparative study ofthe effects ofcarbon monoxide and methylene chloride on human performance. In: Proc. 1st.Ann. NIOSHSci.Symp. Chicago: Pathotox Publishing Co. Putz, V.R. (1979). The effects ofcarbon

monoxide on dual-task performance. HumanFactors21:13-24. Raven. P.B., B.L. Drinkwater, S.M. Horvath,

R.O. Ruhling, J.A. Cliner,J.C. Sutton, and N.W. Bolduan (1974). Age, smoking habits, heat stress, and their interactive effects with carbon monoxide and peroxyacetylnitrate on man's aerobic
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Interactive Effects ofCarbon Monoxide and Alcohol on Driving Skills. Ohio State University Research Foundation, Columbus, OH. Rummo, N., and K. Sarlanis (1974). The effect

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.Saf. Res.6:126-130. Salvatore, S. (1974). Performance decrement

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monoxide intoxication.Arch. Environ. Health7:524-530. Stewart, R.D., P.E. Newton, J. Kaufman, HV. Forster, andJ.P. Klein (1978). Effect ofa rapid4 percent carboxyhemoglobin saturation increase on maximal treadmill exercise. CRC-APRAC-CAPM-22-75. Vogel, J.A. and M.A. Gleser (1972). Effects of

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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

Forthe reasons set forth in the preamble, EPA amends Chapter 1,Part 50, ofTitle 40 ofthe Code ofFederal Regulations as follows:

1. The authority citation for Part 50 continues to read as follows:

Authority: Sec. 109and 301(a), Clean Air Act, as amended (42U.S.C. 7409, 7601(a)). 2. Section 50.8 is revised to read as follows:
§50.8 National primary ambient airquality standards for carbon monoxide.

(a) The national primary ambient air quality standards for carbon monoxide

are:

11) 9 parts per million (10milligrams

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 ofcarbon 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 ofthis 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 ofthe 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 ofthe standards in parts per million shall be nade in terms of integers with fractional parts of0.5 or greater rounding up.
[FR Doc. 85-22025 Filed 9-12-85:8:45 aml

BILLING CODE 6560-50-M 37501

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