37484 federal register vol. no. friday, september 13, 1985 ......the final revised criteria...

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

ENVIRONMENTAL PROTECTIONAGENCY

40 CFR Part 50

[AD-FRL-2866-61

Review of the National Ambient AirQuality Standards for CarbonMonoxide

AGENCY: Environmentat ProtectionAgency.ACTION: Final rule.

SUMMARY: In 1971, identical primary andsecondary national ambient air qualitystandards (NAAQS) for carbonmonoxide (CO) were promulgated atlevels of 9 parts per million (ppm), 8-hour average, and 35 ppm, 1-houraverage, neither to be exceeded morethan once per year (36 FR 8186). Inaccordance with sections 108 and 109 ofthe Clean Air Act, EPA has reviewedand revised the criteria upon which theexisting NAAQS for CO are based, andhas reviewed those standards todetermine if revisions to the standardsare appropriate. On August 18, 1980,EPA proposed certain changes in thestandards based on the scientificknowledge reported in the revisedcriteria document for CO (45 FR 55066).Today's notice announces EPA'sdecision not to revise the existingprimary (health) standards at this timeand revokes the secondary (welfare)NAAQS for CO. EPA plans to reviewseveral ongoing human health effectstudies upon their completion and, ifwarranted, will reexamine this decisionat that time.EFFECTIVE DATE: This action is effectiveOctober 15, 1985.ADDRESSES: A docket (Number OAQPS79-7) containing information relating toEPA's review of the CO standards, isavailable for public inspection andcopying between 8:00 a.m. and 4:00 p.m.,on weekdays, at EPA's Central DocketSection, West Tower Lobby, Gallery I,Waterside Mall, 401 M Street SW.,Washington, D.C. A reasonable. fee maybe charged for copying.

Availability of Related Information

The final revised criteria document,"Air Quality Criteria for CarbonMonoxide" (EPA-600/8-79-022, October1979; NTIS PB 81-244840, $17.00 paperand $4.50 microfiche), an addendum tothe criteria document, "RevisedEvaluation of Health Effects Associatedwith Carbon Monoxide Exposure"(EPA-600/8-83-033F, August 1984; NTISPB 85-103471, $10.00 paper and $4.50microfiche) and the final staff paper,"Review of the NAAQS for Carbon

Monoxide: Reassessment of Scientificand Technical Information" (EPA-450/5-84-004, July 1984; NTIS PB 84-231315,$10.00 paper and $4.50 microfiche) areavailable from: U.S. Department ofCommerce, National TechnicalInformation Service (NTIS), 5285 PortRoyal Road, Springfield, Virginia 22161.FOR FURTHER INFORMATION CONTACT:Mr. Michael Jones, Strategies and AirStandards Division (MD-12), Office ofAir Quality Planning and Standards,U.S. Environmental Protection Agency,Research Triangle Park, North Carolina27711, Telephone: (919) 541-5531 (FTS629-5531).SUPPLEMENTARY INFORMATION:

Background

Legislative Requirements Affecting ThisAction

Two sections of the Clean Air Actgovern the establishment, review, andrevision of NAAQS. Section 108 (42U.S.C. 7408) directs the Administrator toidentify pollutants which mayreasonably be anticipated to endangerpublic health or welfare and to issue airquality criteria for them. These airquality criteria are to reflect the latestscientific information useful inindicating the kind and extent of allidentifiable effects on public health orwelfare that may be expected from thepresence of the pollutant in the ambientair.

Section 109(a) (42 U.S.C. 7409) directsthe Administrator to propose andpromulgate "primary" and "secondary"NAAQS for pollutants identified undersection 108. Section 109(b)(1) defines aprimary standard as one the attainmentand maintenance of which in thejudgment of the Administrator, based onthe criteria and allowing for anadequate margin of safety, is requisite toprotect the public health. The secondarystandard, as defined in section 109(b)(2),must specify a level of air quality theattainment and maintenance of which inthe judgment of the Administrator,based on the criteria, is requisite toprotect the public welfare from anyknown or anticipated adverse effectsassociated with the presence of thepollutant in the ambient air.

The courts have upheld EPA'sinterpretation that the requirement foran adequate margin of safety forprimary standards is intended toaddress uncertainties associated withinconclusive scientific and technicalinformation available at the time ofstandard setting. It is also intended toprovide a reasonable degree ofprotection against hazards that researchhas not yet identified. Lead IndustriesAssociation v. EPA, 647 F.2d 1130, 1154

(D.C. Cir. 1980), cert. denied, 101 S. Ct.621 (1980); American Petroleum Institutev. Costle, 665 F.2d 1176, 1177 (D.C. Cir.1981), cert. denied, 102 S. Ct. 1737 (1982).Both kinds of uncertainties arecomponents of the risk associated withpollution at levels below those at whichhuman health effects can be said tooccur with reasonable scientificcertainty. Thus, in selecting primarystandards with an adequate margin ofsafety, the Administrator is seeking notonly to prevent pollution levels thathave been clearly demonstrated to beharmful, but also to prevent lowerpollutant levels that he finds pose anunacceptable risk of harm, even if thatrisk is not precisely identified as tonature or degree.

In evaluating such risks for thepurpose of providing an adequatemargin of safety, EPA has consideredsuch factors as the nature and severityof the health effects involved-, the size ofthe sensitive population(s) at risk, andthe kind and degree of the uncertaintiesthat must be addressed. Given that the"margin of safety" requirement bydefinition comes into play where noconclusive showing of harm exists, suchfactors, Which involve unknown,qualitatively defined, or only partiallyquantified risks, have inherent limits asguides to action. The selection of anyparticular approach to providing anadequate margin of safety is a policychoice left specifically to theAdministrator's judgment. LeadIndustries Association v. EPA, supra,647 F.2d at 1161-62.

The courts, however, have endorsed areading of the Act that sets strict limitson the factors EPA may consider inproviding an adequate margin of safetyfor primary standards. The leadingjudicial decisions state that theeconomic and technological feasibilityof attaining primary standards are not tobe relied upon in setting them, even inthe context of a margin of safety. LeadIndustries Association v. EPA, supra,647 F.2d at 1148-1151; AmericanPetroleum Institute v. Castle, supra, 665F.2d at 1185, 1190. Such factors may,however, be considered to a degree inthe development of State plans toimplement the standards.

Section 109(d) of the Act (42 U.S.C.7409(d)) requires periodic review and, ifappropriate, revision of existing criteriaand standards. If, in the Administrator'sjudgment, the Agency's review andrevision of criteria make appropriate theproposal of new or revised standards,such standards are to be revised andpromulgated in accordance with section109(b). Alternatively, the Administratormay find that revision of the standards

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

is inappropriate and conclude thereview by leaving the existingstandard(s) unchanged. The process bywhich EPA has reviewed the originalcriteria and standards for carbonmonoxide (CO) under section 109(d) isdescribed in a later section of thisnotice.

States are primarily responsible forassuring attainment and maintenance ofambient air quality standards. Undersection 110 of the Act (42 U.S.C. 7410),States are to submit to EPA for approvalState implementation plans (SIPs) thatprovide for the attainment andmaintenance of such standards throughcontrol programs directed to sources ofthe pollutants included. Other federalprograms provide for nationwidereductions in emissions of these andother air pollutants through the federalmotor vehicle control program, whichinvolves controls for automobile, truck,bus, and motorcycle under Title 1I of theAct (42 U.S.C. 7501 to 7534), and throughthe development of new sourceperformance standards for variouscategories of stationary sources undersection 111 (42 U.S.C. 7411).

Original CO Standards, Revision of theCriteria Document, and ProposedRevisions of the Standards

Original CO Standards. On April 30,1971, the Environmental ProtectionAgency (EPA) promulgated NAAQS forCO under section 109 of the Clean AirAct (36 FR 8186). Identical primary andsecondary standards were set at levelsof 9 ppm, 8-hour average, and 35 ppm, 1-hour average, neither to be exceededmore than once per year. The scientificand medical bases for these standardsare described in the document, "AirQuality Criteria for Carbon Monoxide"(DHEW, 1970), published by the U.S.Department of Health, Education, andWelfare in March 1970. The primarystandards set in 1971 were based largelyon work by Beard and Wertheim (1967)suggesting that low-level CO exposuresresulting in carboxyhemoglobin (COHb)levels of 2 to 3 percent were associatedwith impairment of ability todiscriminate time intervals, a centralnervous system effect.

Revision of the Criteria Document. OnDecember 1, 1978, EPA announced thatit was in the process of reviewing andupdating the 1970 document, "AirQuality Criteria for Carbon Monoxide,"and called for information that might behelpful in revising the document (43 FR56250). In the process of developing therevised criteria document, EPA provideda number of opportunities for reviewand comment by organizations andindividuals outside the Agency. Twosuccessive drafts of a revised criteria

document, prepared by EPA'sEnvironmental Criteria and AssessmentOffice (ECAO), were made available forexternal review, and EPA receivedapproximately 30 written comments onthese drafts. The external review draftsof the criteria document were alsoreviewed by the Clean Air ScientificAdvisory Committee (CASAC)ISubcommittee on Carbon Monoxide onJanuary 30-31, 1979 and June 14-15,1979. These meetings were open to thepublic and were attended by individualsand representatives of organizationswho provided critical reviews and newinformation for consideration. Asummary of EPA's responses to thecomments on the two external reviewdrafts of the criteria document has beenplaced in the public docket (Docket No.ECAO-CD-78-3). Transcripts of the twoCASAC meetings have also been placedin the docket.

The CASAC prepared a "closure"memorandum (Hovey, 1979) to theAdministrator indicating its satisfactionthat the final draft of the criteriadocument was scientifically adequatefor standard-setting purposes. Theclosure memorandum, dated October 9,1979 also outlines major issuesaddressed by the CASAC's andCASAC's recommendation concerningthose issues. A summary of the issuesraised by CASAC and the general publicprior to proposal is contained in theproposal notice (45 FR 55080).

On the basis of a careful review ofscientific information contained in therevised Criteria Document (EPA, 1979a)EPA's Office of Air Quality Planningand Standards (OAQPS) prepared aStaff Paper (EPA, 1979a) in whichseveral key considerations wereidentified as major factors to beconsidered in the possible revision ofthe CO standards. A draft of the StaffPaper was provided to the CASAC,made available to the public, andreviewed by the CASAC COSubcommittee on June 14-15,1979.

Proposed Revisions of the Standards.The principal findings of the Staff Paperare summarized in the August 18, 1980proposal notice (45 FR 55066). Asdiscussed in this notice and in therevised Criteria Document, the Beardand Wertheim (1967) study, theprinicipal basis for the 1971 primarystandards, is no longer considered asound scientific basis for the standards.However, medical evidenceaccumulated since 1970 indicated at the

I CASAC is a standing committee of scientistsand engineers external to the Federal governmentestablished under Section 109 of the Clean Air Actto advise the Administrator on the scientific basisfor ambient air quality standards.

time of the 1980 proposal thataggravation of angifia pectoris and othercardiovascular diseases could occur atCOHb levels as low as 2.7 to 2.9 percent.Assessment of this and other medicalevidence led EPA to propose: (1)retaining the 8-hour primary standardlevel of 9 ppm, (2) revising the 1-hourprimary standard level from 35 ppm to25 ppm, (3) revoking the existingsecondary CO standards (since noadverse welfare effects have beenreported at or near ambient CO levels),(4) changing the form of the primarystandards from deterministic tostatistical (i.e., EPA proposed to allowone expected exceedance of eachstandard level per year), (5) adopting adaily interpretation for exceedances ofthe primary standards, so thatexceedances would be determined onthe basis of the number of days onwhich the 8- or 1-hour averageconcentrations are above the standardlevels (45 FR 55066). The proposal noticeset forth in more detail the rationale forthese and other proposed revisions ofthe CO NAAQS and backgroundinformation related to the proposal.

Developments Subsequent to Proposal

Following proposal, EPA held twopublic meetings to receive comments onthe proposed standard revisions.Meetings were held in Washington, D.C.on October 2, 1980 and Denver,Colorado on October 10, 1980;transcripts are available in the docket(Docket No. OAQPS 79-7). The CASACCO Subcommittee also met onNovember 15, 1980 to review the noticeof proposed rulemaking (45 FR 55066)with EPA officials, and the CASAC meton November 17, 1981 to hear a statusreporton the regulation. The public wasinvited to both CASAC meetings (45 FR73790 and 46 FR 53210) and transcriptsof the meetings have been placed in thedocket (Docket No. OAQPS 79-7).

On June 18, 1982 EPA announced (47FR 26407) an additional public commentperiod to address several key issuesconcerning the 1980 proposal andtechnical documents related to thereview of the CO standards. Theseissues included: (1) role of the Aronow(1.981) study, (2) consideration of amultiple exceedance 8-hour standard,(3) the technical adequacy of the reviseddraft sensitivity analysis on the Coburnmodel predictions of bloodcarboxyhemoglobin (COHb) levels, and(4) the technical adequacy of the revisedexposure analysis. The CASAC met onJuly 6, 1982 to provide its advice onthese issues. CASAC'srecommendations arising from thatmeeting are summarized in an August

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31, 1982 letter to the Administrator(Friedlander, 1982) which has beenplaced in the public docket (Docket No.OAQPS 79-7, IV-H-41}.

The 1980 proposal was based in parton the evaluation by EPA staff andCASAC in 1979 of several health studiesconducted by Dr. Wilbert Aronow. EPAconcluded at that time, based in part onthe Aronow studies, that COHb levels of2.7-3.0 percent represent a healthconcern for individuals with angina andother types of cardiovascular disease. InMarch 1983 EPA learned that the Foodand Drug Administration (FDA) hadraised serious questions regarding thetechnical adequacy of several studiesconducted by Dr. Aronow onexperimental drugs, leading FDA toreject use of the Aronow drug studiesdata. While there was then no directevidence that similar problems mightexist for Dr. Aronow's CO studies, EPAconcluded that an independentexamination of these studies wasadvisable prior in a final decision on theCO NAAQS.

An expert committee was convenedand met with Dr. Aronow to discuss hisstudies and to examine the limitedavailable data and records from his 1981CO study. In its report, the Committee(chaired by Dr. Steven M. Horvath,Director of the Institute ofEnvironmental Stress, University ofCalifornia-Santa Barbara) concludedthat EPA should not rely on Dr.Aronow's data due to concernsregarding the research whichsubstantially limit the validity andusefulness of the results (Horvath et al.,1983). In early June 1983, EPA received adetailed reply (Aronow, 1983) from Dr.Aronow disputing, but not effectivelyrefuting, the major points raised in the" lorvath Committee" report.

Addendum to the 1979 CriteriaDocument and Staff Reassessment. OnAugust 18, 1983, EPA announced (48 FR37519] the availability of an externalreview draft of a document entitled"Revised Evaluation of Health EffectsAssociated with Carbon MonoxideExposure: An Addendum to the 1979 AirQuality Criteria Document for CarbonMonoxide" (hereafter cited asAddendum). The Addendum reevaluatesthe scientific data base concerninghealth effects associated with exposureto CO at or near ambient exposurelevels in light of the HorvathCommittee's recommendationsconcerning Dr. Aronow's studies andtaking into account new findingsreported beyond those reviewed in the1979 Criteria Document.

On September 16, 1983 EPAannounced the availability of a draftstaff paper, "Review of the NAAQS for

Carbon Monoxide: 1983 Reassessmentof Scientific and Technical Information"(hereafter cited as Staff Reassessment]and solicited public comment on thedraft paper [48 FR 41608). The StaffReassessment, prepared by the OAQPS,provided the staffs assessment of howthe scientific data reviewed in theAddendum might be used in selection offinal CO standards. CASAC held apublic meeting on September 25, 1983 toreview both the draft StaffReassessment. In addition to commentsfrom CASAC members, representationof several organizations also providedcritical review of both EPA documents.A transcript of the CASAC meeting hasbeen placed in the public docket(OAQPS 79-7).

The CASAC sent a closure letter tothe Administrator on May 17, 1984which concluded that both theAddendum and Staff Reassessment"represent a scientifically balanced anddefensible summary of the current basisof our knowledge of the health effectsliterature for this pollutant" (Lippmann,1984]. The closure letter, which alsodiscusses major issues addressed by theCASAC and CASAC's recommendationsconcerning those issues, has beenplaced in the public docket (Docket No.OAQP 79-7, IV-K-25.

On August 9, 1984, EPA announced (49FR 31923] the availability of the finalAddendum (EPA, 1984b] and final StaffReassessment (EPA, 1984a) which wererevised to reflect public and CASACcomments. Both final documents areavailable from the address given earlierin the Availability of RelatedInformation Section of this notice.Where there are differences between the1979 Criteria Document and 1980proposal assessment of the healtheffects evidence and the more recentEPA documents, the final Addendumand final Staff Reassessmentrepresented the Agency's interpretationas of their issuance. In the August 9,1984 notice (49 FR 31923] EPA alsoreviewed the basis for EPA's proposal torevise the CO standards and solicitedadditional public comment.

Carbon Monoxide and Human HealthEffects

Control of human exposures tosources of CO is important because CO,when inhaled, can enter thebloodstream and disrupt the delivery ofoxygen to the body's tissues. Acontinous and adequate flow of oxygento the body's tissues is essential tomaintain normal health. After beinginhaled into the lungs, oxygen normallyenters the bloodstream and is delivered,via the circulating blood, to the body'senergy-consuming organs, tissues, and

cells. Once in the tissue cells, oxygenreacts with nutrients to form energy.This energy is essehtial to the normalfunctioning of cells, tissues, and organs.

Humans have specialized moleculesin blood and other tissue cells forensuring a large, continuous flow ofoxygen to the tissues. The mostimportant chemical substance is"heme," an iron-containing substancethat has a special affinity for oxygenand that-combines with proteins to formhemo-proteins. Hemoglobin, a highlyspecialized hemo-protein contained inred blood cells, binds oxygen to thelungs to form oxyhemoglobin (O2Hb]and delivers the oxygen to all othertissues where it is released for use.

Unfortunately, CO can also bind tohemoglobin, formingcarboxyhemoglobin (COHb), with anaffinity that is 200 to 300 times greaterthan that of oxygen. For this reason,small elevations of CO in ambient airthat enters the lungs can result in arelatively large displacement of oxygenfrom the carrier hemoglobin.

Mechanisms of CO Toxicity

The two principal sources of CO thatcontribute to levels of CO in the humanbody are: (1) endogenous CO productionfrom the normal breakdown ofhemoglobin constituents in the body and(2] inhalation of exogenous CO fromambient and non-ambient (e.g.,occupational and indoor) exposures. 2

Endogenous CO production contributesroughly 0.3 to 0.7 percent of hemoglobinsaturation (0.3 to 0.7 percent COH).

Presently, the most importantmechanism of CO toxicity at low-levelCO exposures is thought to be hypoxia.This mechanism generally involvesdiffusion of exogenous CO through thelungs into the blood with resultantformation of COHb. Such an increase inCOHb levels disrupts normal delivery ofoxygen to the tissues in two ways. First,CO displaces oxygen on the hemoglobincarrier so that the hemoglobin has areduced capacity to carry oxygenthrough the blood to the tissues (EPA,1979b). Second, CO makes it moredifficult for the oxygen that is stilltransported by hemoglobin to bereleased at the tissue (EPA, 1979b).Under these conditions, the tissues mustoperate at lower than normal levels ofoxygen, a condition known as hypoxia,and this amount of oxygen may beinadequate to meet the energy needs ofthe tissues. The effects of CO on thecardiovascular system, central nervoussystem, and other systems are thought

2The contribution of direct smoking to levels of

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



to be directly related to this reduction inthe ability of the blood to deliver oxygento these systems and thie resultantoxygen deficiency in the tissuesthemselves.

Other possible mechanisms of toxicityhave been discussed (Coburn, 1979;EPA, 1984b). These alternativemechanisms involve the binding of COto such intracellular hemoproteins ascytochrome oxidase, myoglobin,tryptophan deoxygenase, andtryptophan catalase. Because theaffinity of CO for these proteins is muchless than for hemoglobin, it is unlikelythat they play a major role in COhypoxia. However, in tissues with a highoxygen gradient between blood andtissue, it is likely that the interaction ofCO with these proteins in these tissuesmay play a role in CO toxicity. This isparticularly true of myoglobin in heartmuscle cells. Myoglobin appears tofacilitate the movement of oxygenthrough muscle cells and, as a short-term oxygen reservoir in muscle, itreleases oxygen during suddenincreased metabolic activity. Theaffinity of myoglobin for CO is about 40times greater than the affinity ofmyoglobin for oxygen. The ratio of COcontent in heart muscle to CO content inblood is approximately three. Therefore,given human exposure to CO,substantial amounts of CO may bestored in heart muscle. In situations ofsudden, severe stress or exertion, theheart muscle's immediate oxygen supplymay be inadequate, even in healthypersons and particularly in persons witha history of disease. This mechanismcould provide theoretical support forexperimental evidence of myocardialischemia (in which part of the heartmuscle is deprived of oxygen), such aselectrocardiographic irregularities anddecrements in work capacity discussedlater in this notice. It is not knownwhether binding of CO to myoglobin isrelated to health effects observed atCOHb levels as low as 4-5 percent(EPA, 1979b).

In summary, disruption of the normaltransport of oxygen by formation ofCOHb in the blood appears to be theprimary mechanism of CO toxicity. Inaddition, EPA concludes that regardlessof the mechanism of toxicity, COHblevels provide a meaningful and usefulphysiological marker of the body's COburden and exposure to exogenoussources of CO (EPA, 1948b).

Health Effects As A Result of COExposure

Exposure to high levels of exogenousCO can result in headache, dizziness,drowiness, nausea, vomiting, collapse,coma, or death, depehding on how much

the flow of oxygen to the body isimpeded (EPA, 1979b). The mostnotorious effects of CO are severefunctional losses and death, which canresult from automobile or truckemissions trapped in the enclosedinterior of a vehicle or garage. In thiscase, so much hemoglobin is bound withCO that a severely inadequate supply ofoxygen is delivered to the tisses; thecause of death is severe hypoxia (oroxygen deficiency). Exposure to lowerlevels of CO (i.e., levels closer toambient air levels) is associated witheffects on several different organsystems. Because the cardiovascularsystem (including the heart) and thecentral nervous system (including thebrain) are always active and have acontinuous need for oxygen, even whenthe body is at rest, these organ systemsare particularly sensitive to reducedsupplies of oxygen.

Cardiovascular System. The heart andblood vessels are critical to humansurvival because they pump and carry,respectively, blood containing oxygenand essential nutrients to all organs,tissues, and cells of the body, includingthe brain and the heart muscle itself.Because the heart has almost no abilityto function without oxygen, nor theability (except in situations of clearheart muscle hypoxia) to increaseextraction of oxygen from blood, thehuman body has compensatorymechanisms for ensuring that in low-oxygen situations, the heart continues toreceive whatever oxygen is available(EPA, 1979b). These compensatorymechanisms include increasing heartrate, blood pressure, and blood flow tomaximize the amount of oxygenavailable to the muscle (EPA, 1979b).Although these compensatory changeshave not been associatedexperimentally with damage to thecardiovascular system, it is possible thatthe added stress on the body due to thefunctioning of the compensatorymechanisms themselves may result indamage to the heart muscle orvasculature (EPA, 1979b). The potentialdamage includes those effectsassociated with elevated blood pressure,primarily an increased risk of damage tothe arteries, and elevated heart rate,which further increases the heartmuscle's demand for oxygen. However,if the coronary arteries supplying theheart muscle are unable to compensatefor CO exposure, parts of the heartmuscle may receive amounts of oxygeninadequate for normal activity.

As a result, EPA is concerned that COexposure may increase the risk of thefollowing effects on the cardiovascularsystem:

* Local myocardial ischemia (inwhich a part of the heart muscle isdeprived of oxygen);

" Aggravation of angina pectoris;* Heart attack (myocardial

infarction), including heart attacksleading to sudden death;

* Reduced exercise and physicalwork capacity: and

* Enhanced development ofarteriosclerosis and coronary arterydisease.

Associations between low-level COexposure and angina and reduced workcapacity are supported by humanexperimental evidence discussed later inthis notice. Angina pectoris (or simply"angina") is a group of symptoms ofpressure and pain in the chest resultingfrom a transient episode of insufficientoxygen supply to a portion of the heartmuscle (EPA, 1948b). The pain probablyresults from an accumulation ofunoxygenated metabolic products thatirritate nerve endings in the heartmuscle. The intensity of pain varies frommild chest discomfort to severe andincapacitating distress. Although angina,by definition falls short of inducingdeath of part of the heart muscle, it cancause serious discomfort, and eachattack carries some risk of heart attach.Acute coronary insufficiency, coronaryfailure, and myocardial infarction resultwhen an episode of ischemia is moreprolonged and severe.

An individual with an underlyingcoronary insufficiency is at risk ofhaving an angina attack under anycondition that places an additionaldemand on the heart. CO exposures canplace an added demand on the heart,and, therefore, would appear to increasethe risk of having an angina attack, andmay increase the risk of a more severeattack. There is some experimentalevidence of reduced time to onset ofangina attack and increased duration ofangina attack associated with lowCOHb levels (Anderson.et al. 1973).

A heart attack is usually a precipitousand frequently fatal consequence ofcoronary heart disease, which usuallyresults from a sudden reduction orcessation of a significant portion of theblood and oxygen flow normallyreaching the heart. Very little is knownabout the specific factors which induceor precipitate heart attack or suddendeath. However, any agent that reducesthe supply of oxygen available to theheart muscle in an individual with pre-existing heart disease is suspect as aprecipitating factor for heart attacks andsudden death. A relation betweenelevated COHb and these cardiaceffects is plausible in light of what isknown about CO toxicity and possible

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pathological mechanisms of heartdisease.

EPA has reviewed the availableepidemiological data relating tohypotheses of an association betweenelevated COflb or CO exposure and therisk of heart attack, sudden death, andprogression of atherosclerosis and hasfound them to be inconclusive (EPA,1979b). EPA would like to see furtherepidemiological research in this area,although, admittedly, these questionswill be extremely difficult to resolvewith absolute certainty because of themultitude of experimental confoundingfactors, the multitude of risk factors forheart disease, the variability in humanresponse, and the technical difficulty ininvestigating them.

Nonetheless, from a theoreticalstandpoint, associations between COand these coronary effects are possible.For this reason, and because the healtheffects in question are very serious, EPAbelieves that it is prudent to take earlysigns of cardiovascular effects and otherpotential, but not well understood,cardiovascular effects very seriously.

Central Nervous System. ElevatedCOllb levels can reduce the oxygenavailable to parts of the central nervoussystem (CNS), including the brain. Itappears that the body can compensate,to some extent, by increasing the bloodflow through the brain's vasculature(EPA, 1979b). However, in somecircumstances compensation may notalways occur, leaving the brain with areduced amount of available oxygen. Inaddition, or alternatively, prolongedcompensation may damage the brain'sblood vessels (EPA, 1979b).

When elevated COHb reduces theamount of oxygen delivered to the brainto a level which is below critical needs,two types of damage may result. First,severe acute oxygen deprivation ofsufficient duration and intensity canresult in a stroke (the damage or deathof brain cells (neurons)). Loss of maturebrain cells is irreversible since the CNSis not thought capable of replacement ofneurons. Depending upon the duration ofoxygen deficit to the brain, the effectsmay range from unconsciousness andconvulsions, brain swelling andprotrusion, to death of parts of the brainor death of the individual. Individualswho recover often have significantdeficits in brain function. Second,repeated episodes of impaired oxygensupply would be expected to damagethe blood-brain barrier and possiblycause structural damage resulting in theinability of the CNS to transmitinformation.

At lower CO-lb levels there isevidence of neurobehavioral effects:impaired learning ability, reduced

vigilance (ability to detect small changesin a subject's environment), decreasedmanual dexterity, impaired performanceof complex tasks, and disturbed sleepactivity (EPA, 1984b). Although thepotential influence of ambient CO levelson drivers has received only slightattention, suggestive but not conclusiveevidence has indicated that drivers infatal auto accidents often have elevatedCOHb levels (Yabroff et al., 1974). Thereis no evidence with which to determinewhether these effects at lower CO levelsare associated with pathologicalchanges to the CNS or with reducedoxygen tension in the CNS. Due toredundancy in structure of the CNS,functional changes (e.g., behaviorchanges) may not be observed until thestructural damage is great. Observationof such effects may be more likely in thecase of a severe reduction in oxygen orin an individual who has a history of animpaired oxygen delivery system.

Basis for Decision Not To Revise thePrimary Standards

The current primary NAAQS for COare 10 mg/m 3 (9 ppm), 8-hour averageand 40 mg/m 3 (35 ppm), 1-hour average,neither of which is to be exceeded morethan once per year. As indicated above,the Act requires review of the existingcriteria and ambient air qualitystandards for CO and other pollutantsevery five years. During the currentstandard review for CO, EPA hasconsidered whether it should retain theexisting CO primary standards,repropose the same or differentstandards, or promulgate the revisionsproposed in August 1980. For thereasons discussed below, theAdministrator has concluded that thereis no need to revise the existing primaryCO standards at this time.

As indicated above, section 109(b)(1)of the Clean Air Act requires EPA to setprimary standards, based on the airquality criteria which, in theAdministator's judgment, are requisiteto protect the public health with anadequate margin of safety. Thelegislative history of the Act makesclear the Congressional intent to protectsensitive persons who in the normalcourse of daily activity are exposed tothe ambient environment. Air qualitystandards are to be established withreference to protecting the health of arepresenative, statistically related,sample of persons comprising thesensitive group rather than a singleperson in such a group.

EPA's objective in reviewing primarystandards, therefore, has been todetermine whether new or revisedstandards are appropriate, based on theexisting scientific evidence, assessment

of the uncertainties in this evidence,understanding of underlying biologicalmechanisms, and the need to make areasonable provision for scientific andmedical knowledge yet to be acquired.in order to protect sensitive populationgroups with an adequate margin ofsafety. As for other ambient standardpollutants, none of the evidencepresented in the 1979 Criteria Documentor Addendum shows a clear thresholdfor adverse health effects of CO. Rather,there is a continuum, ranging from COlevels at which health effects areundisputed, through levels at whichmany, but not all scientists generallyagree that health effects have beenconvincingly shown, down to levels atwhich the indication of health effectsare less certain.and more difficult toidentify. This does not necessarily meanthat there is no threshold, other thanzero, for CO related health effects; itsimply means that no precise thresholdcan be identified with certainty basedon existing scientific evidence. Thus, insetting a standard, EPA is unable toappend an exact margin of safety to aknown threshold effect level. Rather,setting a standard with an adequatemargin of safety is necessarily a publichealth policy judgment that must takeinto account both the known continuumof effects, understanding of theunderlying biological mechanisms ofeffects, and any gaps and uncertaintiesin the existing scientific data base.

In determining whether revision of theprimary CO standards is appropriate,EPA has made assessments andjudgments in the following areas:

1. Identification of reported effectlevels and associated exposure durationthat scientific research has linked tohealth effects in healthy and sensitivepersons.

2. Characterization of scientificuncertainties in the health effectsevidence and judgments concerningwhich effects are important to considerin reviewing or setting primarystandards.

3. Description of population groupsbelieved to be most sensitive to CO andestimates of the size of those groups.

4. The estimated number of sensitivepersons that would be exposed toelevated CO levels upon attainment of agiven standard and the uncertainties inthese exposure estimates.

5. The uncertainties in estimatingcarboxyhemoglobin (COHb) levels thatresult from exposures to CO.

6. Consideration of CO standardlevels and averaging times that providean adequate margin of safety based onCO levels and exposure periods thatmay affect sensitive population groups,

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

taking into account the variousuncertainties.

Based on the assessment of relevantscientific and technical information inthe Criteria Document and theAddendum, the Staff Reassessmentoutlines a number of key factors to beconsidered in each of the above areas.Both the staff and CASACrecommended that the Administratorfocus consideration on a discrete rangeof policy options in each area. In mostrespects, the Administrator has adoptedthe recommendations and supportingreasons contained in the StaffReassessment, the most recent CASACclosure letter (Lippmann, 1984) andapplicable portions of the earlier StaffPaper (EPA, 1979b) and CASAC closureletters (Hovey, 1979; Friedlander, 1982).Rather than reiterating thosediscussions at length, the followingdiscussion of the final decision focusesprimarily on those considerations thatwere most influential in theAdministrator's selection of a particularoption, or that differ in some respectfrom considerations that influenced thestaff and/or CASAC recommendations.

Assessment of Health Effects Evidence

The Staff Reassessment, which hasbeen placed in the public docket (DocketNo. OAQPS 79-7, IV-A-10), presents anassessment by OAQPS staff of the keyhealth effect studies contained in the1979 Criteria Document and in theAddendum and other critical scientificand technical issues relevant to thereview of the existing CO standards.

TABLE 1.-LOWEST OBSERVED EFFECT LEVELSFOR HUMAN HEALTH EFFECTS ASSOCIATED

WITH Low LEVEL CARBON MONOXIDE ExPo-

SURE

COHbEffects concen. References

tration(percent)-

Statistically significantdecreased (-3-7%)work bme toexhaustion inexercising younghealthy men.

Statistically significantdecreased exercisecapacity (i.e.,shortened durationof exercise beforeonset of pain) inpatients with anginapectoris.

Statistically significantdecreased maximaloxygen consumptionand exercise timeduring strenuousexercise in younghealthy men.

No stat~sticallysignificant vtglancedecrements afterexposure to CO.

2.3-4.3 Horvath et al. 1975.Drinkwater at al.,1974. Raven at al..1974.

2.9-4.5 Anderson al al., 1973.

5-5.5

Below 5

Klein at al., 1980,Stewart at at.. 1979.Weiser at al.. 1978.

Haider at al.. 1976.Winneke. 1974,Christensen at al..1977. Benegnus atal., 1977. Puttz o atl..1976.

TABLE 1.-LOWEST OBSERVED EFFECT LEVELS

FOR HUMAN HEALTH EFFECTS ASSOCIATED

WITH Low LEVEL CARBON MONOXIDE ExPo-

SURE-Continued

COHbconcen- ReferencesEffets htroion

(percent)'

Statistically significant 5-7.6 Horvath et at. 1971.impairment of GrolI-Knapp etalt.,vigilance tasks in 1972. Fodor andhealthy experimental Winneke. 1972. Putzsubjects. 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 ellearn, 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. Rummoand 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 andduring strenuous Gleser. 1972.exercise in younghealthy men.

The physiologic norm (i.e., COHb levels resulting from thenormal breakdown of hemoglobin and other heme.containingmaterials) has been estimated to be in the range of 0.3 to0. 7 percent (Coburn at al., 1963).

Table I is a summary of key clinicalstudies reporting human health effectsassociated with low-level exposures toCO. This table is based on evidencediscussed in the 1979 Criteria Document(EPA, 1979a) and in the Addenum (EPA,1984b) but excludes a series of studiesby Dr. Aronow for reasons given below.The table is included primarily as an aidfor the following discussion and shouldbe used only in conjunction withqualifying statements made in the 1979Criteria Document, in the Addenum, inthe Staff Reassessment, or in this noticeregarding the technical merits of eachstudy.

Cardiovascular Effects. In reviewingthe primary standards, a principal areaof concern to the Administrator hasbeen evidence linking aggravation ofangina and other cardiovasculardiseases to CO exposures. Anginapatients who have been exposed to lowlevels of CO while resting havesubsequently exhibited, during exercise,reduced time to onset of angina(Anderson et al., 1973). Increasedduration of angina attacks has also beenreported (Anderson et al., 1973). Inproposing to revise the CO standards,EPA viewed aggravation of angina, asreported above, to be an adverse healtheffect (45 FR 55066) and CASACconcurred with EPA's judgment on thismatter.

One controlled human exposure study(Anderson et al. 1973) reported thatexperimental subjects with anginaexhibited statistically significant

reduced time to onset of exercise-induced angina after exposure to lowlevels of CO resulting in mean COHblevels of 2.9 (range 1.3-3.8 percent) and4.5 percent (range 2.8-5.4 percent). In thesame study, it was reported thatsubjects experienced statisticallysignificant increases in duration ofangina attacks during exercise at amean COHb level of 4.5 percent. Someconcerns have been raised about thestudy findings due to ambiguitiesregarding the design and conduct of thestudy and the small number of subjects(N=10) examined. However, asdiscussed in the Addendum and in asubsequent section of this notice, areevaluation of the Anderson et al.(1973) study, addressing major points ofconcern, found that the study providesreasonably good evidence for thehastening of angina occurring in anginapatients at COHb levels of 2.9 to 4.5percent.

In similar studies Aronow and Isbell(1973) and Aronow (1981) reporteddecreased time to onset of angina forexercising subjects with reported COHblevels in the range of 2 to 3 percent. Inaddition, Aronow et al. (1974) reportedthat subjects with peripheral vasculardisease had reduced time to onset of legpain at similar COHb levels. Asdiscussed earlier in this notice, however,an expert committee convened toconduct an independent review of theseCO studies expressed considerableconcern about the validity of the resultreported and concluded that EPA shouldnot rely on.Dr. Aronow's data (Horvathet al., 1983.3 As stated earlier in thisnotice, Dr. Aronow provided EPA adetailed reply disputing, but noteffectively refuting, the substance of theconcerns raised by the Committee(Aronow, 1983). The Committee alsorecommended that EPA pursue andsupport both current in-house andindependent scientific research toresolve the issues raised by thereevaluation of Dr. Aronow's COstudies. Because EPA shares theconcerns raised by the committee andby some public comments, theAdministrator has not considered Dr.Aronow's studies in his decision on theCO primary standards.

iThe Committee's concerns included (1) apparentfailure to maintain a "double blind" approach asreported in the publications. (2 raw data were lostor discarded, (3) available data were of poorquality. (4) quality control for COHb measurementswas nonexistent or inadequate, and (5) thereappeared to be discrepancies between hospitalrecord descriptions of patient diagnosis and thosereported in Dr. Aronow's publications [Hlorvath eta1., 1983).

Federal Register / Vol. 50,


Another cardiovascular effect ofconcern is the possible detrimentaleffect of increased blood flow thatoccurs as a compensatory response toCO exposure (Ayres et al., 1969; Ayreset al., 1970; and Ayres et al., 1979). Thiseffect may be related to coronarydamage or cerebrovascular effects atvery high blood flow rates due to theadded stress on the cardiovascularsystem. However, communityepidemiological studies have beeninconclusive. In particular, based onEPA's evaluation of the Goldsmith andLandau (1968), Kurt et al. (1978), andKurt et al. (1979) epidemiologicalstudies, the relationship between COexposures and effects such as mortalityfrom myocardial infarction (heartattack), sudden death due toarteriosclerotic heart disease, andcardiorespiratory complaints remains inquestion.

Maximum aerobic capacity andexercise capacity are indirect measuresof cardiovascular capacity which havebeen reported to be reduced in severalcarefully conducted studies involvingnormal healthy adults exposed to CO. Alinear decline in maximum aerobiccapacity for healthy individuals wasreported for COt-lb levels ranging fron5-20 percent in a series of studies(Stewart et al., 1978; Weiser et al., 1978;and Ekblom and Huot, 1972). Hlorvath etat. (1975) found decreases in maximumaerobic capacity when COI lb levelswere 4.3 percent and that COHb levelsof 3.3 and 4.3 percent reduced work timeto exhaustion by 4.9 and 7.0 percent,respectively. The effects of lower COexposure levels in healthy individualshave also been investigated underconditions of short-term, maximumexercise duration. In a series of studiesinvolving different CO exposure levels,two alternative ambient temperatures(25°C and 35'C), and two differenthealthy adult populations (young andmiddle-aged), no statistically significantreduction in maximum aerobic capacitywas observed for either group when COexposures were compared with theclean air control. However, small (lessthan or equal to 5 percent) decreases inabsolute exercise time were consistentlyobserved in the non-smoking subjectswhose COt lb levels reached 2.3 and 2.5percent (Drinkwater et al., 1974; Ravenet al., 1974). These effects, while not asserious as aggravation of angina, arestill a matter of concern since they havebeen found to occur in healthyindividuals and such effects mightimpair the normal activity of moresensitive populations. Therefore, theseeffects have been considered in judging

which CO standards provide anadequate margin of safety.

Central Nervous System Effects.Numerous studies (Putz et al., 1976;Bender et al., 1971; Schulte, 1973;O'Donnel et al., 1971; McFarland et al.,1944; McFarland, 1973; Salvatore, 1974;Wright et al., 1973; Rockwell and Weir,1975; and Rummo and Sarlanis, 1974)have reported effects on the centralnervous system for CO exposuresresulting in COttb levels in the range 5-17 percent. The range of effects reportedincluded impairment of vigilance, visualperception, manual dexterity, learningability, and performance of complextasks. While one study (Beard andGrandstaff, 1975) has suggested thatvigilance effects may occur at levels aslow as 1.8 percent COHb, several otherstudies (Haider et al., 1976; Winneke,1976; Christensen et al., 1977; Benignuset al., 1977; and Putz et al., 1976) havenot found any vigilance decrementsbelow 5 percent COHb. Measurementmethods used to detect effects may havebeen too insensitive to detect changes inthe latter vigilance studies. Based on theassessment of the above mentionedstudies, the Addendum concluded that,at least under some conditions, smalldecrements in vigilance occur at 5percent COHb. A series of studies (Putzet al., 1976; Putz et al., 1979; and Putz1979) has also found that 5 percentCOHb produced decrements incompensatory tracking, a hand-eyecoordination task. EPA considers hand-eye coordination effects as well asdecrements in vigilance to be importantsince these functions are components ofmore complex tasks, such as driving,and reduced alertness or visualsensitivity could lead to increasedvehicular accidents.

Fetal Effects. Based on limited animaltoxicology data, the 1979 CriteriaDocument and the Addendum (EPA,1984b) suggest that CO may produceeffects on the fetus or newborn. CO fromlong-term or intermittent exposures istaken up and eliminated more slowly inthe fetus than in the mother, so that amaternal exposure can result in meanfetal COtlb concentrations well abovematernal COHb levels (EPA, 1979b).Elevated COHb levels may lead tointerference with fetal tissueoxygenation during development.Because the fetus may be developing ator near critical tissue oxygenationlevels, even exposures to moderatelevels of CO may produce deleteriouseffects on the fetus such as reducedbirth weight, increased newbornmortality, and lower behavioral activitylevels (Longo, 1977), although thisremains to be demonstrated along with

pertinent dose-response relationships(EPA, 1984b). Evidence from smokingmothers is suggestive of similar fetaland newborn effects due to COexposures (Peterson, 1981). While thefact that cigarette smoke containssubstances other than CO prevents adirect quantitative application of theresults of these studies in setting the COprimary standards, these studies dosuggest the need for caution inprotecting unborn children from suchpotentially deleterious effects of COexposures.

As discussed in the Addendum andStaff Reassessment, research on suddeninfant death syndrome (SIDS) recentlyhas suggested a possible link betweenambient CO levels and increasedincidence of SIDS (Hoppenbrowers etal., 1981). In response to this study,Goldstein (1982) has suggested thatindoor sources of CO, as well as otherpollutants (e.g., nitrogen dioxide, lead),may be at least as important as ambientCO in causing SIDS and that severalcovariates (e.g., seasonal trends) may beresponsible for the associationsreported. Because the number ofpotentially confounding factors makesfinding an association between CO andSIDS extremely difficult, furtherconfirmation is needed before anycausal relationship can be inferred(EPA, 1984a; EPA, 1984b).

Sensitive Population Groups

In EPA's judgment, the availablehealth effects data identify persons withangina or other types of cardiovasculardisease (e.g., history of heart attack orperipheral vascular disease) as thegroups at greatest risk from low-level,ambient exposures to CO. Based on 1980census data (DOC, 1980) and earlier U.S.National Health Examination Surveydata (DHEW, 1975), this group isestimated to number approximately 8.7million individuals. As discussedpreviously, the concern for persons withcardiovascular disease results from thefact that their condition is due to aninsufficient oxygen supply to cardiactissue, so that persons with thiscondition have an inadequate oxygenreserve capacity and an impaired abilityto compensate for the effects of excessCo.

The Addendum and StaffReassessment also identify several othergroups as likely to be particularlysensitive to low-level CO exposuresbased on EPA's review of the healtheffects evidence. These groups include:(1) persons with chronic respiratorydisease (e.g., bronchitis, emphysema,and asthma), (2) elderly individuals,especially those with reduced


cardiopulmonary function, (3) fetusesand.young infants, and (4) individualssuffering from anemia and those withabnormal hemoglobin types that affectoxygen carrying capacity or transport inthe blood. In addition, individuals takingcertain medications or drinkingalcoholic beverages may be at greaterrisk for CO-induced effects based onsome limited evidence suggestinginteractive effects between CO andsome drugs. Visitors to high altitudelocations are also expected to be morevulnerable to CO health effects due toreduced levels of oxygen in the air theybreathe. Finally, individuals with somecombination of the disease states orconditions listed above (e.g., individualswith angina visiting a high altitudelocation) may be particularly sensitiveto low-level CO exposures, althoughthere is no experimental evidence toconfirm this hypothesis.

For many of the groups cited abovethere is little specific experimentalevidence to clearly demonstrate thatthey are indeed at increased risk forCO-induced health effects. However, itis reasonable to expect that individualswith preexisting illnesses orphysiological conditions which limitoxygen absorption into blood or itstransport to body tissues would be moresusceptible to the hypoxic (i.e., oxygendeficiency) effects of CO. Since nohuman experimental evidence existsthat identifies CO effect levels for theseother groups, however, EPA isconsidering the possible effects of COon these groups only in its determinationof an adequate margin of safety.

Uncertainty in Estimating COHb Levels

The health effect studies discussedabove report the effects observed atvarying COHb levels. In order to makedecisions about ambient CO standardsbased on these studies, it is necessary toestimate the ambient concentrations ofCO that are likely to result in COHblevels at or near those observed in thestudies. A model known as the Coburnequation (Coburn et al., 1965) has beendeveloped to estimate COHb levelsresulting from CO concentrations as afunction of time and variousphysiological factors (e.g., blood volume,endogenous CO production rate). Table2 presents "baseline" estimates (usingtypical values for the variousphysiological parameters) of COHblevels expected to be reached by adultnonsmokers exposed to various constantconcentrations of CO for either 1 or 8hours based on the Coburn model.

TABLE 2.-PREDICTED COHb RESPONSE TOEXPOSURE TO CONSTANT CO CONCENTRA-TIONS ASSUMING TYPICAL VALUES FORPHYSIOLOGICAL PARAMETERS

(Percent COHb Based on Coburn Equation" Exposure Time

1 hour exposure 8 hours exposureIntermit- Intermit- I

CO (ppm) tent rest/ Moderate tent rest/ I Moderatelight activity light activity

activity activity

TABLE 2.-PREDICTED COHb RESPONSE TO

EXPOSURE TO CONSTANT CO CONCENTRA-

TIONS 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/ Moderatelight activity light activity

activity activity

50.0 2.0 2.7 6.4 6.9

-Assumed parameters for non-smoking adults: alveolarventilation rates= 10 liters/mn (intermittent rest/light activity)and 20 liters/min (moderate activity); hemoglobin= 15 9/100ml (normal male): ahitude-sea level; initial COHb level=0.5percent; endogenous CO production rate=O.007 ml/mmo;blood volume=5500 ml. Haldane constant (measure of affini-ty of hemoglobin for CO)=218; lung ditfusivity for CO 30m!/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-hrMid- Mid-

Peak COHb percent Low range High Low Highpat- rag pat- pat- rangetern tern tern pat- terntern tern 1

3 .7 ........................................................................................................................................................ ......................................... ... < 0.0 13 .5 .......................... 1 ........................................................... a ....................................................................... ....................................... ... 0 .0 13 .3 ........................................................................................................................................................................ ............................ 0 .13 .1 ......... ................................................................................................................. ............... ............... ............... ................ < 0 .0 1 0 .62.9 ..................................................................................................................................... o ................. <0.01 ............... 0.01 2

2.7 ........................................................................................................................................................ 0.02 <0.01 0.2 92.5 ............................................................................................................................ ........ <0.01 0.2 0.01 2. 362.3 ........................................................................................................................................... . 0.02 2 0.2 12 842.1 .......................................................................................................................... <0,01 0.4 10 4 49 1001.9 ........................................................................................................................... 005 5 53 36 88 1001.7 ........................................................................................................................... 3 35 98 91 99 1001.5 ........................................................................................................................... 39 88 100 100 100 1001.3 ........................................................................................................................... 97 100 100 100 100 1001.1 ........................................................................................................................... 100 100 100 100 100 . 100

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

* Haldane constant= 218. Alveolar ventilation rate= 10 liters/min. Altitude =0.0 ft.* The estimation of distributions for each of the physiological parameters used in the Coburn model and the Monte Carlo

procedure used to generate these estimates are discussed in Appendix C of the Sensitivity Analysis (Biller and Richmond,1982).

There are, however, at least twouncertainties involved in estimatingCOHb levels resulting from exposure toCO concentrations. First, for each of thephysiological parameters used in theCoburn model, there is a distribution ofvalues in the general population. Thesevariations are sufficient to producenoticeable deviations from the COHblevels in Table 2, which as noted abovewere predicted using a set of typicalphysiological parameter values. Second,predictions based on exposure toconstant CO concentrationsinadequately represent the responses ofindividuals exposed to widelyfluctuating CO concentrations thattypically occur in ambient exposuresituations.

As discussed in the proposalpreamble (45 FR 55066), EPA attemptedto represent these uncertainties in adraft Sensitivity Analysis (EPA, 1980).

This analysis used the Coburn model toexamine the effects of fluctuating COconcentrations and variations inphysiological parameters on COHbestimates. Since proposal, EPA hasrevised the Sensitivity Analysis toaddress concerns raised in severalpublic comments and placed the repoit(Biller and Richmond, 1982) in thedocket (QAQPS 79-7, IV-A-8). Table 3presents estimates of the distribution ofCOHb levels in the adult non-smokingpopulation based on variations inphysiological parameters upon exposureto three different patterns of CO levelswhich just meet alternative 9 ppm and12 ppm CO standards. The estimatesgiven in Table 3 and others contained inthe Sensitivity Analysis report (Billerand Richmond, 1982) are based on theassumption that the entire adultpopulation is exposed to CO levels justmeeting a given standard.

37491


The impact of fluctuating air qualitylevels on COHb uptake can be roughlyestimatdd by comparing the "baseline"result of a constant 9 ppm exposure for 8hours (1.4 percent COHb from Table 2)with selected results shown in Table 3.For a "typical" (50th percentile) adultexposed to several different air qualitypatterns that result in the samemaximum 8-hour dose (i.e., 9 ppm, 8-hour average), the results shown inTable 3 indicate that COHb levelsranging from approximately 1.4 to 1.9percent can be reached. A similarcomparison of the results for air qualitywith a 12 ppm, 8-hour average peakexposure indicates that fluctuating COlevels can increase the peak COHbvalue from that observed with aconstant CO exposure by up to 0.7percent OCHb (i.e., from 1.7 percentCOHb in Table 2 to 2.4 percent COHbfor the 50th percentile in the high patterncolumn of Table 3).

The Sensitivity Analysis results inTable 3 also illustrate the effect of usingdistributions of values for eachphysiological parameter rather than justa single representative set of values inapplying the Coburn model. For anygiven air quality pattern, the effect ofusing the distribution of values for eachphysiological parameter is to generate adistribution of peak COHb levels thatthe population would reach. Forexample, the results in Table 3 showthat 95 percent of the population isestimated to be within ±0.3 percentCOHb of the median adult value afterexposure to the midrange pattern with apeak 9 ppm, 8-hour average. Thisvariation in COHb levels attained is onefurther source of uncertainty that isbeing considered in judging whichstandards provide an adequate marginof safety.

Since proposal, EPA has madeconsiderable improvements in itsexposure analysis methodology which,unlike the Sensitivity Analysis, treatsmovement of people and variation of COconcentration levels through time andspace. EPA believes that the revisedExposure Analysis described below,represents the best available tool forestimating the percentage of thepopulation that would reach various COconcentrations and COHb levels uponattainment of alternative CO standards.Since the Exposure Analysis modelsimulates the exposure of individuals onan hourly basis and simulates actual airquality patterns, the impact offluctuating CO levels is largely takeninto account in the Exposure Analysisresults. The results of the revisedSensitivity Analysis are useful,however, in characterizing the

uncertainties resulting from variations inphysiological parameters in thepopulation which at this time are notfully accounted for in the ExposureAnalysis.

Exposure Analysis Estimates

EPA's revised exposure analysisreport and addendum, "The NAAQSExposure Model (NEM) Applied toCarbon Monoxide," (Johnson and Paul,1983; Paul and Johnson, 1985) containestimates of the numbers andpercentages of urban American adultsthat would be exposed to variousambient CO levels if alternative 8-hourCO standards were just attained. Inaddition, estimates have been made ofthe percentage of this population thatwould exceed selected COHb levelseach year. These latter estimates werederived by applying the Coburn modelwhich relates patterns of CO exposureto resultant COHb levels, to theexposure model outputs using a typicalset of physiological parameters for adultmen and a separate set of physiologicalparameters for adult women.

In contrast to the Sensitivity Analysis,the Exposure Analysis simulatespollutant concentrations and theactivities of people with regard to time,place, and exercise level. In theexposure model, the population isrepresented by a set of "cohorts" (i.e.age-occupational groups that tend to"track together" in time and space). Foreach hour of the year each cohort islocated in one of five"microenvironments." Amicroenvironment is a general physicallocation such as indoors-at-home orinside a transportation vehicle.

CO levels in each of themicroenvironments are estimated by theuse of multiplicative "transformationfactors," which relate CO levelsrecorded at the nearest monitor toestimate CO levels for eachmicroenvironment. This method is usedsince attainment of a standard isdefined in terms of the monitoringsystem. Values of the multiplicativetransformation factors that would givethe best exposure estimates areuncertain. The values used for thesefactors were estimated making use ofthe available literature on (1) indoor andinside-motor-vehicle air pollution and(2) statistical analyses of monitoringdata (e.g., how ambient values changewith height and distance from amonitor). A more detailed description ofthe approach, input data, andassumptions used to derive exposureestimates appears in the ExposureAnalysis reports (Johnson and Paul,1983; Paul and Johnson, 1985).

The exposure analysis modeldescribed above was applied to foururban areas: Chicago, Los Angeles,Philadelphia, and St. Louis. Exposureestimates for the adult population livingin urban areas in the United States wereobtained primarily by associating eachurban area in the United States having apopulation greater than 200,000 with oneof the four cities mentioned above. Theassociation was made on the basis ofgeographic proximity to one of the baseareas, average wind speed, peak COconcentrations, observed climate, andgeneral character of the area.

TABLE 4.-CUMULATIVE PERCENT OF ADULTPOPULATION IN URBAN AREAS WHOSE COHbLevels Would Exceed Specified COHb Val.ues Upon Attainment of Alternative 8-HourStandards 1..,c

8--our standards

COHb level 12 ppm 15 ppmcee 9 p[pm 1 Iexceeded (percent) expected expected expected

exceedance exceed- exceed-__________ ance ance

3.0 ................. .. <.01 1.12.9 . . ..... .................................... .02 2.52.7 ....................................... 0.1 5.925.... .... . 0,8 9.72.3 .................. <0.1 4.1 142.1 ...................... .... 0.1 (<.01)" 8.6 20

.Projected cardiovascular and peripheral vascular diseasepopulation in all urbanized areas in the United States for1987 is 5.240.000 adults.

bThese exposure estimates are based on air quality distri-butions which have been adjusted to just attain the givenstandards.

' These exposure estimates are based on best judgmentsof microenvironment transformation factors. Projections forone urban area based on lower and upper estimates of themicroenvironment transformation factors are provided in theExposure Analysis report (Johnson and Paul. 1983).

"Exposure estimate for current 9 ppm. 8-hour averagedeterministic standard.

Table 4 provides estimates for 1987 ofthe percentage of the adult populationliving in urban areas who would exceedvarious COHb levels upon attainment ofthree alternative 8-hour standards. Forexample, less than 0.01 percent of theadult population in urban areas isestimated to exceed 2.1 percent COHbdue to CO exposures associated withattainment of the current (deterministic)9 ppm standard, and approximately 20percent of the adult population isestimated to exceed 2.1 percent COHbupon attainment of a 15 ppm standardwith 1 expected exceedance allowed peryear. It should be noted that theestimates given in Table 4 are based onair quality distributions which havebeen adjusted to just attain the givenstandards.

Several factors make the accuracy ofthe nationwide exposure estimatesuncertain. They include: (1) the paucityof information on several of the neededinputs (e.g., some of themicroenvironment multiplicativetransformation factors) and (2) the fact

No. 178 / Friday, September 13, 1985 / Rules and Regulations - 37493

that nationwide estimates wereextrapolated from only four urbanizedareas. In addition, the results of theCoburn Model Sensitivity Analysis,discussed previously, suggest that theuse of two representative sets ofphysiological parameters (one for menand one for women), rather than the fulldistributions of the physiologicalparameters for the population, inapplying the Coburn model to deriveCOHb estimates introduces somefurther uncertainty, although theuncertainty about such inputs as themicroenvironment multiplicativetransformation factors is much larger.Exposure Analysis report (Johnson andPaul, 1983) describes some limitedsensitivity analysis runs for oneurbanized area to give a rough idea ofthe range of possible COI-Ib levels thatwould be reached.

Decision on the Primary Standards

The Staff Reassessment and 1984CASAC findings and recommendationsset forth a framework for consideringwhether revision of the primary COstandards is appropriate at this time.The discussion that follows reliesheavily on that framework and onapplicable supporting material in the1979 Criteria Document, 1984Addendum, 1979 Staff Paper, and earlierCASAC closure letters (Hovey, 1979;Friedlander, 1982).

Based on its assessment of scientificevidence discussed previously in thisnotice, EPA concludes that adversehealth effects clearly occur, even inhealthy individuals, at COHb levels inthe range of 5 to 20 percent. EPA alsoremains concerned that adverse healtheffects may be experienced by largenumbers of sensitive individuals withCOHb levels in the range 3.0 to 5.0percent. On this point, CASAC similarlyconcluded after reviewing the scientificliterature (not including the Aronowstudies), "that the critical effects levelfor NAAQS-setting purposes isapproximately 3 percent COHb (notincluding a margin of safety)"(Lippmann, 1984).

In addition to concurring with EPAthat cardiovascular effects are likely tooccur at approximately 3 percent COHb(Anderson et al., 1973), the CASAC alsoindicated that several studies(Drinkwater et al., 1974; Raven et al.,1974; and Davies and Smith, 1980)reporting physiological effects in therange 2.3-2.8 percent COHb lendsupport to concerns about low level COexposures and should be considered indetermining whether a given standardprovides an adequate margin of safety.As discussed previously, theAdministrator has excluded Dr.

Aronow's studies from consideration inhis decision on the CO primarystandards.

Based on the exposure analysisresults summarized previously in Table4 of this notice, 8-hour singleexceedance CO standards in the range 9to 12 ppm are estimated to keep morethan 99 percent of the non-smokingcardiovascular population below 3.0percent COHb. Different standardswithin this range would, of course,provide different levels of protection.For example, the current 9 ppm, 8-houraverage standard is estimated to keepmore than 99.9 percent of the adultcardiovasular population below 2.1percent COHb. A 12 ppm, 8-hourstandard is estimated to keep more than99 percent of the population below 2.5percent COHb. The 2.5 percent COHblevel is in the range where physiologicaleffects of concern to EPA and CASAChave been reported.

In considering whether revision of theexisting primary CO standards isappropriate at this time, theAdministrator has considereduncertainties regarding the lowest levelsof COHb at which adverse health effectsmay occur, as well as uncertaintiesabout the levels of COHb likely to resultfrom CO exposure at the levels

* associated with attainment ofalternative standards. More specifically,the Administrator considered thefollowing factors and sources ofuncertainty, discussed in the StaffReassessment (EPA, 1984), in hisdecision:

1. Human susceptibility to healtheffects and the levels at which theseeffects occur vary considerably amongindividuals, and EPA cannot be certainthat experimental evidence hasaccounted for the full range ofsusceptibility. In addition, for ethicalreasons, clinical investigators havegenerally excluded from their studiesindividuals who may be especiallysensitive to CO exposure, such as thosewith a history of myocardial infarctionor multiple disease states (e.g., bothangina and anemia). Another factor isthat, once the Aronow et al. studies areexcluded, there are no human exposurestudies investigating effects onindividuals with angina at COHb levelsbelow the 2.9 percent level reported byAnderson et al. (1973).

2. There is some animal studyevidence indicating that there may bedetrimental effects on fetal development(e.g., reduced birth weight, increasednewborn mortality, and behavioraleffects) associated with CO exposure.Similar types of effects have also beenfound in studies examining effects of

maternal smoking on human fetuses.However, it is not possible at this timeto sort out the confounding influence ofother components of tobacco smoke incausing the effects observed in thehuman studies. While human exposure-response relationships for fetal effectsremain to be determined, these findingsdenote a need for caution in evaluatingthe margin of safety provided byalternative CO standards.

3. Other groups that may be affectedby ambient CO exposures but for whichthere is little or no experimentalevidence include: anemic individuals(over 3 million individuals), personswith chronic respirat6ry diseases (about14 million individuals), elderlyindividuals (over 24.7 million individualsover 65 years old), visitors to highaltitude locations, and individuals oncertain medications. The levels of COHbthat might produce adverse effects foreach of these groups is uncertain.However, elevated COHb levels in evena small percentage of this very largepotentially sensitive population wouldtranslate to a significant number ofindividuals. The large size of thepotentially sensitive population, then,argues for standards providing a greatermargin of safety.

4. There are a number of uncertaintiesregarding the uptake of CO, includingthose related to the accuracy of theCoburn equation, in assessing variationsin the population due to differingphysiological parameters and exposureto varying air quality patterns.

5. Several factors contribute touncertainties about the exposureestimates of the expected number ofindividuals achieving various COHblevels upon attainment of alternativestandards. These factors include: thepaucity of information on several of theneeded inputs, the fact that nationwideestimates were extrapolated from onlyfour urbanized areas, and the use of tworepresentative sets (one for men and onefor women) of physiological parameters(e.g., blood volume) rather thandistributions of physiologicalparameters in applying the Coburnmodel to derive COHb estimates in theexposure analysis. As indicated in theStaff Reassessment (pp. 18-21), someindividuals with physiologicalparameters that maximize uptake ofCOHb, if exposed to certain patterns ofair quality attaining a 12 ppm, 8-hourstandard, would likely exceed 3.0percent COHb. Consequently, theAgency is concerned that a 12 ppm, 8-hour standard may not provide anadequate margin of safety. EPA iscontinuing its CO exposure researchefforts, which should lead to future

Federal Register / Vol. 50,


improvements in its exposure analysisand a better capability to assess theaccuracy of the exposure estimates(Johnson, 1984; Hartwell et al., 1984).

6. There is uncertainty regardingadverse health effects that may resultfrom very short duration, high-level COexposures (the bolus effect). Asdiscussed in the proposal notice (45 FR55077), existing air quality data indicatethat attainment of a 9 ppm, 8-houraveraging time standard should limit themagnitude of short-term peakconcentrations.

7. There is some concem aboutpossible interactions between CO andother pollutants, although there is littleexperimental evidence to documentsuch interactions at this time.

8. Given the unsettled nature of thescientific information bearing on thelevel of the standard, EPA believes thatthere is much to be said for a policy thatwould maintain the status quo until thedata become more adequate. That isparticularly so given the absence of theinformation indicating with someassurance that the present standard isset at an incorrect level. For the reasonsstated elsewhere in this preamble, theavailable information falls short ofsupporting such finding.

The CASAC concurred with theranges of 9 to 12 ppm for the 8-hour and25 to 35 ppm for the 1-hour primarystandards recommended in the StaffReassessment and characterized themas scientifically defensible standardranges. They recommended that theAdministrator consider choosingstandards that maintain approximatelythe same level of protection as thatafforded by the current standards(Lippman, 1984). In making itsrecommendation the CASAC cited theuncertainties associated with thescientific data base and margin of safetyconcerns and its belief" . . . that wherethe scientific data, as in this case, aresubject to large uncertainties, it isdesirable for the Administrator toconsider a greater margin of safety thanthe numerical values of COHb generatedby the Coburn equation might otherwisesuggest" (Lippmann 1984).

Several ongoing human health effectstudies are being conducted by EPA andother groups to investigate the effect ofCO on aggravation of angina. Subjectsin these studies are being exposed to COlevels that result in blood COHb levelsin the range 2.0 to 4,0 percent. One studyis being conducted by EPA, several arebeing conducted at the request of EPAby the Health Effects Institute (HEI), andanother study is being sponsored by theCalifornia Air Resources Board (CARB).The Health Effects Institute is anindependent organization which

sponsors research on automotivepollutants and is jointly funded by EPAand automobile manufacturers. Thepeer-reviewed results of these studiesare expected by December 1986. EPAwill be initiating development of a newcriteria document for CO in Fiscal Year1986. Thus, the Agency should be in agood position to expeditiously assessthe results from the above healthstudies, as well as other scientificevidence published since completion ofthe Addendum.

Given the uncertainty in the currentdata base and the fact that new studiesare in progress, the Administratorconsidered deferring a final decision onthe CO standards until these newstudies have been completed. While thismight allow the Administrator to basethe decision on better information, theClean Air Act appears to requireperiodic decisions on NAAQSnotwithstanding any uncertainty in thedata base. Deferring this decision wouldimply that the Agency has inadequateevidence to select an appropriate courseof action at this time. However, bothEPA and the CASAC have concludedthat, even without the Aronow studies, asufficient scientific data base existsupon which to base a decision. Giventhese findings, and the concern that adeferral of the decision could beperceived as a signal to relax or delayongoing control programs, theAdministrator has concluded that finalaction now on the CO standards iswarranted and justified.

In reaching a final decision, theAdministrator has focused primarily onthe level of protection the CO standardsshould provide. As previously noted,after reassessing the available scientificdata and EPA staff recommendations,the CASAC has recommended that theCO standards provide protectionapproximately equal to the current'standards. Based on EPA's assessmentof the scientific data, the Administratorconcurs with this recommendation.Retention of the current standardswould, of course, satisfy this objective.

As discussed above, the standardsproposed in August 1980 would alsoprovide approximately the same level ofprotection as that afforded by thecurrent standards. In addition, thesestandards would provide some technicalchanges that the Agency believes wouldbe advantageous. However, theproposed changes would require somemodification in the way attainment ofthe standards is determined. Given theuncertainties in the existing data baseand the possibility that the results of thenew studies in progress might warrantfurther revisions within a few years, theAdministrator has concluded that it

would not be prudent to promulgate theproposed revisions at this time,particularly when they would alter themanner in which attainment isdetermined.

In short, the Administrator hasconcluded that it would not be prudentto defer a decision on the CO standardspending the results of the new researchmentioned above, that the standardsshould provide approximately the samelevel of protection as that afforded bythe current standards, and thatdisruption of ongoing control programsshould be minimized. Given theseconsiderations, the Administrator hasconcluded that the best course of actionis not to revise the CO primarystandards at this time. Together with theAdministrator's decision to rescind thesecondary standards (discussed below],this decision completes the currentreview of the NAAQS for CO undersection 109(d). The ongoing studiesconducted by the Agency, by the HEI,and by the CARB (all discussed above)will, of course, be considered in the next5-year review cycle of the CO criteriaand standards. Upon completion of thisseries of studies, the Agency plans toreview the results with the CASAC andassess the need for any revisions in theprimary standards. If revisions in thestandards seem appropriate, the Agencywill act expeditiously to revise thestandards.

Welfare Effects and the SecondaryStandards

Carbon monoxide is a normalconstituent of the plant environment.Plants can both metabolize and produceCO. This may explain the fact thatrelatively high levels of CO arenecessary before damage occurs tovegetation. The lowest level for whichsignificant effects on vegetation havebeen reported is 100 ppm for 3 to 35days. The effect observed in this studywas an inhibition of nitrogen fixation inlegumes. Since CO concentrations ofthis magnitude are rarely if everobserved in the ambient air, it is veryunlikely that any damage to vegetationwill occur from CO air pollution. Noother effects on welfare have beenassociated with CO exposures at or nearambient levels. Because no standardsappear to be requisite to protect thepublic welfare from any known oranticipated adverse effects fromambient CO exposures, EPA isrescinding the existing secondarystandards.

Significant Harm Levels

Section 303 of the Clean Air Actauthorizes the Administrator to take


certain emergency actions if pollutionlevels in an area constitute "animminent and substantial endangermentto the health of persons." EPA'sregulations governing adoption andsubmittal of SIP's contain a provision(40 CFR 51.16] that requires the adoptionby States of contingency plans toprevent ambient pollutantconcentrations from reaching specifiedsignificant harm levels. The existingsignificant harm levels for CO wereestablished in 1971 (36 FR 24002) at thefollowing levels and averaging times:50 ppm-8-hour average75 ppm-4-hour average

125 ppm--hour averageExposure under these conditions

could result in a widespread bloodCOHb concentration of 5 to 10 percent,the range EPA has determined wouldcause significant harm. On the basis ofEPA's reassessment of the earlier dataand assessment of more recent medicalevidence, no modifications are beingmade to the existing significant harmdesignations. EPA's assessment of themedical evidence on exposure to higherCO concentrations that could lead tosignificant harm is contained in the 1979Criteria Document (EPA, 1979b) and inthe Addendum (EPA), 1984b).

Summary of Public Comments andAgency Responses

Overview of Comments

The following discussion summarizesin general terms the comments received,at various times since the 1980 proposal,from the public and from Federal andState agencies on the levels of theprimary standards and on the relatedissue of multiple exceedance standards.Significant comments on all aspects ofthe CO proposal and Agency responsesto these comments are summarized bycategory later in this section. A moredetailed description of individualcomments and Agency responses iscontained in the public docket (OAQPS79-7).

Comments on 1980 Proposal. Of thewritten comments received during theinitial comment period (which closedNovember 24, 1980) that expressed someopinion on the level of the proposed 8-hour standard, 7 out of 11 favored EPA'sproposed standard or a more stringentstandard. Environmental groupcomments endorsed the proposedstandard or recommended tightening ofthe standard, industry groups favoredrelaxation of the standard, and localand State agency comments supportedthe proposed standard or somerelaxation of the standard.

Several comments were received onthe Agency's proposal to lower the 1-

hour standard to 25 ppm. Of the 18written comments which expressed anopinion on the 1-hour standard, 8comments favored the proposedstandard level, 5 comments urgedretention of the existing 35 ppmstandard level, and 3 commentsrecommended revocation of the 1-hourstandard. There also was one commentfavoring further tightening of the 1-hourstandard and one comment favoring arelaxation of the standard. Thosefavoring revocation of the 1-hourstandard argued that the 1-hourstandard was redundant sinceattainment of the 8-hour standard wouldeffectively prevent 1-hour average levelsfrom exceeding either 25 or 35 ppm.

Comments on the proposed revisionswere received from five Federalagencies. Four of these agencies neithersupported nor opposed the proposedstandards. The Department ofCommerce urged EPA to maintain theexisting 35 ppm, 1-hour standard. TheCouncil on Wage and Price Stabilitysuggested, through the RegulatoryAnalysis Review Group, that theproposed standards should be based oncost-effectiveness analysis and that ifcosts were considered, the proposedstandards might be excessivelystringent.

Comments on Subsequent Notices. Asdiscussed earlier in this notice, EPAannounced an additional publiccomment period on June 18, 1982 toaddress several key issues, including theAgency's consideration of multipleexpected exceedance 8-hour COstandards (47 FR 26407). Of thecomments that expressed an opinion onthe issue of multiple expectedexceedances, 12 out of 23 favored theuse of the multiple expectedexceedances approach for ambientstandards. While State and localgovernments' comments were almostevenly divided on the question, allindustrial groups supported the conceptand all environmental groups opposedmultiple exceedance standards.Comments from private citizens wereevenly divided for and against multipleexceedance standards.

During the period from November 24,1980 through August 6, 1982 (the close ofthe second comment period), of thosecommenting on whether the 8-hourstandard should be relaxed, 10 out of 45favored relaxation. Most of the States(12 of 14) opposed relaxation, while 3 of5 local governments favored relaxation.As in the earlier comment period, allindustry comments favored relaxationwhile all environmental groups opposedrelaxation.

Subsequent to the close of the secoidpublic comment period, the State and

Territorial Air Pollution ProgramAdministrators (STAPPA) submitted aresolution, endorsed by a majority ofState air pollution agencies, whichexpressed several reservations about amultiple exceedance CO standard. TheSTAPPA resolution recommendedpromulgation of single exceedance COstandards.

EPA solicited additional publiccomment on the draft StaffReassessment which evaluated thescientific data in view of the diminishedvalue of Dr. Aronow's CO studies onSeptember 16, 1983 (48 FR 41608). Of the13 comments received in response tothis notice that expressed an opinion onthe levels of the standards, 7 favoredretaining the current primary standards,2 favored the proposed standards (i.e., 9ppm for the 8-hour averaging time and25 ppm for the 1-hour averaging time),and 4 favored relaxation of the 8-hourstandard to 12 ppm or higher. Thosesupporting the proposed or currentstandards included an environmentalgroup, several State environmentalagencies, two health scientists, and onelocal environmental agency. Thosefavoring relaxation of the primary 8-hour standard included two from theautomotive industry and two localenvironmental agencies.

On August 9, 1984, EPA summarizedthe basis for EPA's proposed revisionsto the CO standards, announcedavailability of the final Addendum (EPA,1984b) and Staff Reassessment (EPA,1984a), and solicited additional publiccomment (49 FR 31923). Of the 7comments received that expressed anopinion on the levels of the standards, 2favored retaining the current primarystandards, 2 favored the proposedprimary standards (i.e., 9 ppm, 8-hourand 25 ppm, 1-hour, and 3 favoredrelaxation of the 8-hour standard to 12ppm or higher. Two commentors arguedthat EPA should defer final action on theCO standards until the Health EffectsInstitute's CO research was completed.

Summary of Significant Comments andAgency Responses

Significant comments are summarizedand responded to by category below.

I. Health Effects Criteria and Selectionof the Primary Standards

A. Definition of An Adverse HealthEffect

Comment. It is questionable whether areduction in the time to onset of anangina attack following exercise isadverse.

Agency Response: EPA concludes thataggravation of angina represents an

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adverse health effect. As explained inthe proposal preamble (45 FR 55066),EPA considers such aggravation ofangina to be an adverse health effect forseveral reasons. First, it may result incardiovascular damage, which isunquantifiable using present technology.Second, aggravation of angina may bethe first in a series of progressively moreserious symptoms that accompanycardiovascular disease. At low levels ofoxygen deprivation, angina patientsexperience symptoms of chest paindescribed above. Coronary insufficiencyis a more serious symptom that occursat greater levels of oxygen deprivation.This symptom is sometimesaccompanied by changes in enzymelevels and electrocardiographicirregularities. The most serious effect inthis continuum of effects is myocardialinfarction. In addition to longer andmore intense pain, myocardial infarctionis accompanied by irreversible heartdamage (death of myocardial cells) asindicated by enzyme level changes andelectrocardiographic alterations. Finally,because aggravation of angina may bethe first in a series of symptoms thatmay lead to permanent heart damage,EPA considers aggravation of angina anadverse effect and an indicator thatmore serious effects may occur in someindividuals at the same COHb levels.EPA's judgment has been supported bythe CASAC and CASAC COSubcommittee (Hovey, 1979; Lippmann,1984).

Comment: Scientific research on COsuggests that there is no clear thresholdlevel at which adverse health effectsbegin. Rather, there appears to be anincrease in severity of potential healtheffects with increasing levels of CO. Thefact that a no-effects level cannot beidentified may lead to a standard nearzero. The current evidence can supportstandards other than those proposed byEPA.

Agency Response: EPA agrees thatthere is a continuum of effects consistingof COHb levels at which health effectsare certain, through levels at whichscientists can generally agree thatmedically significant effects have beenconvincingly shown, and down to levelsat which health effects are less certain,are harder to identify, and the medicalsignificance of which are typicallydisputed. In short, the present scientificevidence does not permit selection of anundisputed value for a primarystandard. Rather, the Administrator inselecting a standard must make ajudgment as to the level of physiologicalresponse that should be consideredadverse and the relative acceptability ofvarious degrees of uncertainty that any

given level is low enough to preventknown and possible adverse healtheffects.

B. Scientific Validity of the HumanExperimental Studies

Comment: Work of Dr. WilbertAronow is suspect because results aretoo consistent, data are not available forevaluation, the study was not doubleblind, and the subjects tested were not arepresentative set of angina patients.The Horvath Committee (Horvath et al.,1983) recommended that EPA not rely onDr. Aronow's studies in setting the COstandards.. Agency Response: The Administratoragrees with the Horvath Committee thatthere are very serious technicalquestions about the validity of Dr.Aronow's CO studies and, therefore, isnot considering the results of thesestudies in his decision.

Comment: The Anderson et al. (1973)study should be eliminated fromconsideration because Anderson et al.reported a COHb level of only 4.5percent after a four hour, 100 ppm COexposure, whereas other investigatorshave generally reported 8-10 percentCOHb for similar exposures.

Agency Response: During theAnderson et al. (1973) study, subjectswere allowed breaks and, thus, wereexposed to CO intermittently, notcontinuously, for 4 hours. This wouldcause COHb levels to be substantiallylower than for the continuous exposureperiods used in other studies.

Comment: The Anderson et al. (1973)study should not be considered fordrawing conclusions about lowestobserved effect levels because of the (1)small number of subjects, (2)questionable double-blind conditions,(3] missing data for some subjects, (4)lack of dose-response relationships foronset and duration of angina in somesubjects, (5) reliance on subjective.responses, and (6f inadequatepresentation of statistical procedures.

Agency Response: EPA has carefullyreviewed the Anderson et al. (1973)study and the above criticisms of thestudy. A detailed response is containedin a February 20, 1985 memorandumprepared by EPA's scientists in theOffice of Research and Developmentwhich has been placed in the publicdocket (OAQPS 79-7, IV,-B-2). EPA doesnot challenge the proposition that theAnderson study has limitations thatmust be weighed in assessing thestudy's value for standard setting. Veryfew, if any, studies are perfect and thusconclusively demonstrate precisepollutant thresholds for the entire rangeof sensitive persons under variousenvironmental conditions. However, the

Agency does not agree with thecommenters' characterization of theAnderson study limitations nor with thecommenters' conclusion that thoselimitations are grounds for totallyexcluding the study from an assessmentof the health risks of CO. After carefullyevaluating the scientific merit of thestudy and considering the adviceprovided by the CASAC, EPA hasconcluded that the Anderson studyshould be considered in selecting a COstandard with an adequate margin ofsafety.

EPA's responses to the major points ofconcern about the Anderson et al. (1973)study are briefly summarized below:

1. EPA readily acknowledges that thesubject sample size is small and that thestudy would be strengthened if thenumber of subjects had been greater.However, the sample size is adequate totreat the data statistically and largeenough to use in making statisticalinferences regarding effects and causalagents. These inferences are routinelymade by clinical investigatorsconducting studies with relatively fewsubjects and treatment replications. Inaddition, even though only a smallnumber of subjects were tested, they dorepresent some portion of the nationalpopulation suffering from angina.

2. Because of the explicit precautionstaken by the author to ensure theintegrity of such a protocol, EPA rejectsthe speculative assertion that the studywas not double blind. Specifically, a"double blind" study is one where boththe administering investigator andpatient are unaware of the nature of anytreatment. EPA has contacted the author(Docket ECAO CD 78-3, IIA-J-3) whoreaffirmed the study protocol which isconsistent with the definition of doubleblind. The author cited the publishedstudy which states:

A 5-day, double-blind exposure protocolwas followed-Only the investigatoradministering the gas knew whichconcentration of CO was being used. Thepatient, technician, and the investigatorconducting the'exercise test were all unawareof the exposure condition. A curtainseparated the gas tanks from the patient-Oncompletion of the five exercise tests for eachsubject, the ECG records were assigned arandom code number and interpreted by aninvestigator who had not been present andhad no knowledge of the exposure sequence.

3. Because of the explicit double blindprotocol practiced in the study, there isno basis for concluding that the twosubjects who missed one day ofexposure had in some way gainedknowledge of the exposure conditionsdue to their missing one of the exposure


sessions. EPA rejects this assertion asillogical and unfounded.

4. The fact that the effects reportedwere not dose-related in the Andersonet al. study is not surprising given thesmall range of exposure concentrations,the fact that the exposures were close tothe lower limits for CO-related effects,and the small number of subjects.However, EPA has not used this or anyother study to develop a dose-responserelationship which would show differentlevels of subject response over a specificrange of administered CO doses. EPAhas argued that the Anderson studydoes suggest an increased risk ofaggravation of angina for sensitiveindividuals who have elevated COHblevels.

5. The fact that the endpoint measuredby Anderson et al., namely time to onsetof angina pian, is subjective in nature isno basis for ignoring this serious andimportant effect as carefully articulatedin the proposal preamble (45 FR 55069):

EPA considers such aggravation of anginato be an adverse health effect for severalreasons. First, it may result in cardiovasculardamage, which is unquantifiable usingpresent technology. Second, aggravation ofangina may be the first in a series ofprogressively more serious symptoms thataccompany cardiovascular disease. At lowlevels of oxygen deprivation, angina patientsexperience symptoms of chest pain describedabove. Coronary insufficiency is a moreserious symptom that occurs at greater levelsof oxygen deprivation. This symptom issometimes accompanied by changes inenzyme levels and electrocardiographicirregularities. The most serious symptom inthis continuum of effects is myocardialinfarction. In addition to longer and moreintense pain, myocardial infarction isaccompanied by irreversible heart damage(death of myocardial cells) as indicated byenzyme level changes andelectrocardiographic alterations. Finally,because aggravation of angina may be thefirst in a series of symptoms that may lead topermanent heart damage, EPA considersaggravation of angina an adverse effect andan indicator that more serious effects mayoccur in some individuals at the same COHblevels.

6. EPA has reanalyzed the data fromthe Anderson et al. study using a moreconservative multivariate analysiswhich tests each health endpointseparately for purposes of inference (seeAppendix A in the Addendum; EPA1984b). EPA believes that, had Andersonet al. originally used this technique, theeffect of time to onset of angina wouldhave been statistically significant(p=0.014 at the 97.5 percent confidencelevel] but that duration of anginaexperience would not have beenstatistically significant (p=0.11 at the97.5 percent confidence level).

In conclusion, EPA agrees with theCASAC statement,... that it is important to replicate such astudy, but the notion that a study has novalidity until it's been replicated is flawed.Based upon its current knowledge of how thestudy was conducted, CASAC presumes thatdouble blind protocols were, in fact, observedand that discrepancies between observedand predicted COHb levels are not as greator as serious as originally suggested. Insummary, while CASAC treats the Andersonet al. study with caution, it can find nosubstantive reason at this time to dispute thereported values, and it recommends that theAgency not disregard its findings (Lippmann.1984).

The Agency continues to believe thatthe Anderson et al. findings can beappropriately interpreted as providingreasonably good evidence ofexacerbation of angina symptomsoccurring in some segments of thepopulation at approximately 2.9 to 4.5percent COHb.

Comment: Psychological factorscontribute to angina attacks, making itdifficult to reproduce experimentslinking CO and angina.

Agency Response: Althoughpsychological factors may contribute toangina attacks, it has been reasonablyshown in the study by Anderson et al.that exposure to CO does contributeindependently to the aggravation ofangina. Given the double-blind design ofthis study, there is no reason to supposethat the subjects were exposed todifferent psychological factors onexperimental CO exposure days thanthey were on clean air control days.

C. Margin of Safety

Comment: EPA has proposed COstandards with an inappropriate marginof safety. The margin of safety wascriticized as being either inadequate orexcessive.

Agency Response: The decisionregarding an adequate margin of safetyis a judgment which must be made bythe Administrator after weighing all themedical evidence bearing on the effectsof CO. The factors to be taken intoaccount include inconclusive evidenceas well as findings from studies that areconsidered definitive and not subject tochallenge. The Administrator hasconsidered uncertainties regarding thelowest levels of COHb at which adversehealth effects may occur, as well asuncertainties about the levels of COHblikely to result from CO exposure at thelevels associated with attainment ofalternative standards. More specifically,the Administrator considered the factorsand sources of uncertainty, discussedearlier in the Decision on the PrimaryStandards section of this notice and inthe Staff Reassessment (EPA, 1984).

EPA has examined the healthprotection afforded by alternatives tothe current CO primary standards. Forexample, attainment of a 12 ppm, 8-hourCO standard is estimated to keep morethan 99 percent of the population below2.5 percent COHb. The 2.5 percentCOHb level, however, is in the rangewhere physiological effects of concernto EPA and CASAC have been reported.In addition, as indicated in the StaffReassessment (pp. 18-21), someindividuals with physiologicalparameters that maximize uptake ofCOHb if exposed to certain patterns ofair quality attaining a 12 ppm, 8-hourstandard would exceed 3.0 percentCOHb. Consequently, the Administratoris concerned that a 12 ppm, 8-hourstandard may not provide an adequatemargin of safety. There is no crediblescientific evidence that suggests morestringent CO primary standards than thecurrent standards are required to protectpublic health with an adequate marginof safety.

D. Coburn Model Sensitivity Analysis ofCOHb Levels

Comment: The term used in theCoburn model analysis for inspired COpressure was mistakenly interpreted asa pressure in dry ambient air. The termwas intended to refer to CO pressure inair saturated with water vapor at bodytemperature.

Agency Response: EPA agrees withthe comment and has revised all of theCOHb estimates used in this notice andin the final COHb Sensitivity Analysis(Biller and Richmond, 1982) to reflectthis change.

Comment: The parameters utilized inthe EPA COHb Sensitivity Analysiswere not representative of the medicalliterature. Modeling efforts of this kind'should choose conservative values forphysiological parameters in order to erron the side of protecting public health.

Agency Response: The values selectedfor the physiological parameters used inthe Sensitivity Analysis were carefullyreviewed with members of the scientificcommunity and with consultants to theCASAC and were judged to bereasonable estimates. EPA does notagree that the most conservative valuesshould be selected for the physiologicalparameters because this wouldintroduce an additional margin of safetyinto an analysis attempting to estimatethe effects of alternative standards. TheSensitivity Analysis does use a range ofvalues for the various physiologicalparameters.

Comment: The draft SensitivityAnalysis does not adequately treat

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differences in physiological parametersbetween men and women.

Agency Response: In an Appendix tothe revised Sensitivity Analysis (Billerand Richmond, 1982), men and womenare modelled separately and appropriatephysiological parameters are selectedfor each sex based on a review of thescientific literature.

E. Exposure Estimates for SensitivePopulation Groups

Comm'ent: Various technical factors inthe expobure analysis eithersystematically underestimate oroverestimate exposures that wouldoccur upon attainment of alternativestandards. The exposure analysis shouldnot be used in selecting the primarystandards until all the recommendedchanges are incorporated into theanalysis.

Agency Response: EPA has carefullyreviewed these comments and separatedthem into three categories. The firstcategory includes comments with whichEPA agrees and for which changes havebeen made in the exposure analysis. Therevised exposure analysis estimates aresimilar in magnitude, after taking thesecomments into account, to the originalexposure estimates.

A second category of commentssuggested changes that EPA agreeswould refine the exposure assessmentmethodology, but which are not feasibleat this time because of limitations on theresources and time available for thisstandard review. EPA will incorporatethese comments into its plan forimproving its exposure assessmentcapability. While the exact impact ofthese refinements cannot be clearlypredicted at this time, EPA agrees withCASAC's conclusion that the exposureanalysis is "acceptable given the currentstate-of-the-art of the scientificcommunity's ability to modelphysiological and other parametersrelated to this pollutant" (Friedlander,1982).

A third category consists of commentswhere EPA disagrees with the suggestedchanges. Detailed responses to thesecomments are provided in the docket(Docket OAQPS 79-7, V-C-I). EPArecognizes that there is uncertaintyabout the accuracy to the exposureestimates, but it believes that therevised estimates are reasonable giventhe state-of-the-art of exposureassessment.

While future refinements in themethodology and availability ofadditional data will undoubtedly reducethe degree of uncertainty in theexposure estimates, EPA believes thatthe current Exposure Analysis providesa useful tool to estimate the number of

sensitive individuals who would beexposed to various COHb levels uponattainment of alternative standards.

II. Form of the Primary StandardsComment: Some commenters favored

retaining the current deterministic form;others supported either EPA's 1980proposal to adopt single-expected-exceedance (statistical form) or theconcept of multiple-expected-exceedances (statistical form) primaryCO standards. Those in favor ofadopting a statistical form argued that itwould minimize the impact of unusualmeteorological events on controlstrategies with minimal reductions inhealth protection offered by thestandard. Those opposed to a multiple-expected-exceedances standardexpressed concerns about the increasedhealth risks to the sensitive populationand the ability of the public tounderstand the basis for allowingmultiple excursions of the standardlevels.

Agency Response: Given the concernsexpressed by the vast majority of Stateair pollution control agencies and othersthat a single-exceedance standard,either deterministic or statistical, moreclosely reflects the health basis for thestandard and is more readilyimplemented and understood by thegeneral public, EPA has decided toretain the single exceedance format forthe primary standards. While EPAbelieves that adopting a statistical,single-exceedance standard would be atechnical improvement, EPA is deferringany such change in the primary COstandards until the uncertaintiesregarding the health effects basis for thestandards are better resolved.

III. Miscellaneous

A. Natural Background

Comment: It has been reported that93% of the CO in the atmosphere isproduced by vegetation and the oceansand, therefore, anthropogenic sources ofCO should be of little concern.

Agency Response: Although much ofthe CO produced globally may be ofnatural origin, the elevated CO levelsfound in urban areas and in rural areasnear roadways are principally a result ofhuman activities involving thecombustion of fossil fuels.

B. Stating Standards in ppm and Notmg/m

3

Comment: EPA should state therevised CO standards solely in parts permillion (ppm) rather than mg/m.Changing to ppm would (1) avoidconfusion as to the level of thestandards at different altitudes, (2)

provide additional protection for highaltitude areas, and (3) be consistent withhealth and monitoring data using theFederal Reference Methods which arereported in ppm.

Agency Response: EPA is retainingboth systems of units but is indicatingthat ppm is the preferred system ofunits. Section 50.3 specifies thatmeasurements of air quality are to becorrected to standard conditions (i.e., 25degrees centigrade and sea levelpressure), the only difference betweenppm and mg/m 3 (at standard conditions)is a scale factor that does not vary withaltitude. That is, if a measurement isexpressed in ppm units or mg/m3 units(at standard conditions) the values willdiffer by a factor of 0.875 regardless ofaltitude. This conversion factor isspecified in Appendix D of 40 CFR Part50.

Revisions to Part 50 Regulations

Because EPA has decided not torevise the CO primary standards, thereare no substantive changes to the Part50 regulations concerning thesestandards. EPA is revising the text of thestandards slightly, however, to makethem clearer and more understandableto the public. EPA is also explicitlystating several data handlingconventions that have traditionally beenused in EPA's data systems andguidance. These changes are notintended to redefine the standard butsimply to reduce potential ambiguityand to formalize existing data handlingconventions. The specific points are the75 percent data completeness rule thatEPA has used when computing 8-houraverages and the number of significantfigures retained when makingcomparisons with the levels of thestandard. These changes were discussedin the proposal notice. EPA is alsochanging to ppm units as the preferredunits as discussed in the proposalnotice. Finally, EPA is also rescindingthe secondary standards for CO, asproposed, because there is no evidenceof welfare related effects at or nearambient levels.

Part 51 Regulations and SIPDevelopment

This action does not modify theexisting Part 51 regulations. Currentguidance to State and local air pollutioncontrol agencies on how to interpret airquality data for purposes of attainmentdecisions and SIP development iscontained in "Guidelines for theInterpretation of Air Quality Standards"(EPA, 1977).

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Regulatory and Environmental Impacts

Regulatory Impact Analysis

As has been noted, the Clean Air Actspecifically requires that NAAQS bebased on scientific criteria relating tothe level that should be attained toprotect public health and welfareadequately. The courts haye endorsed areading of the Act that excludes relianceon the cost or feasibility of achievingsuch a standard in determining the levelof the primary standards. In response toExecutive Order 12291, EPA hasprepared a regulatory impact analysis(RIA). However, EPA's analysis,"Regulatory Impact Analysis for CarbonMonoxide," has not been considered indetermining the standard levels in thisfinal notice. The document is availablefrom the address given earlier in the ForFurther Information Contact section ofthis notice until supplies are exhaustedand from the NTIS whose address isgiven in the Addressees section of thisnotice.

Both the RIA and this final noticewere submitted to the Office ofManagement and Budget (OMB) forreview under Executive Order 12291.Any written comments from OMB andany written EPA responses to thosecomments are available for publicinspection at EPA's Central DocketSection, Docket No. OAQPS 79-7, WestTower Lobby, Gallery I, Waterside Mall,401 M Street SW., Washington, D.C.

Environmental Impacts

Environmental impacts associatedwith control of CO emission have beenexamined in the Environmental ImpactStatement, which is available in thedocket (OAQPS 79-7, IV-A-13) or fromEPA at the address given earlier in theFor Further Information Contact Sectionof this notice. This analysis indicatesthat control strategies required to attainthe standards will have minimal adverseimpacts on other environmental media.

Impact on Small Entities

The Regulatory Flexibility Act (5U.S.C. 601 et seq.) requires that allfederal agencies consider the impacts offinal regulations on small entities, whichare defined to be small businesses,small organizations, and smallgovernmental jurisdictions. EPA'sanalysis pursuant to this Act issummarized in a section of the finalreport, "Cost and Economic Assessmentof Alternative National Ambient AirQuality Standards for CarbonMonoxide" (EPA, 1985). A NAAQS forCO by itself has no direct impact onsmall entities. However, it requires eachState to design and implement controlstrategies for those areas not in

attainment. Three possible sources ofimpadts on small entities include (1) theFMVCP for cars and trucks, (2) I&Mprograms, and (3) stationary sourcecontrol programs. FMVCP requirementsare largely established by statute or byregulatory provisions not directlyrelated to the levels of these standards.In addition, they fall primarily onautomobile manufacturers, none ofwhich are classified as small businesses.Additionally, the incremental cost of COcontrol, which is passed on topurchasers of motor vehicles-includingsmall entities-is a small fraction of thepurchase price and, thus, the impact tothese purchasers should be negligible.

I&M programs for CO control mayhave a slight negative economic impacton small entities, but may also have apositive economic impact on some smallentities. The estimated pe'r vehicleaverage annual cost for the CO portionof an I&M program is estimated to be$3.50 for the inspection fee and $19 forrepairs to failed vehicles. (In those fewareas needing an I&M program for COonly, these estimates would be doubled.)These costs should not impose asignificant negative economic impact onsmall entities. On the other hand, somesmall entities such as gas stations andgarages will be repairing failed vehiclesresulting in a net increase in receiptsdue to a CO I&M program. In addition, ifa decentralized I&M program isimplemented using small businesses toinspect motor vehicles, then their netreceipts will also increase due to receiptof the inspection fee, most of which theyretain. (The remainder goes to thegovernmental unit sponsoring the area-wide I&M program.)

Finally, only the largest stationarysources of CO appear to need toimplement controls to attain the COstandards that were analyzed. Thesesources are among the largest facilitieswithin their standard industrial class,and therefore are not likely to be smallentities.

Based on the analysis summarizedabove, EPA concludes that no smallentity group will be significantlynegatively affected due to retention ofthe primary CO NAAQS. Therefore,pursuant to 5 U.S.C. 605(b) theAdministrator certifies that thisregulation will not have a significanteconomic impact on a substantialnumber of small entities.

Impact on Reporting Requirements

There are no reporting requirementsdirectly associated with this action.There are reporting requirementsassociated with related sections of theAct, particularly sections 107, 110, 160,and 317 (42 U.S.C. 7407, 7410, 7460, and

7617), however, there are no changes inreporting requirements associated withthis final action since the currentprimary standards are being retained.

Federal Reference Method

The measurement principle andcalibration procedure applicable toreference methods for measuringambient CO concentrations to determinecompliance with applicable COstandards are not affected by thisaction. The measurement principle andthe calibration procedure for CO are setforth in Appendix C of 40 CFR Part 50.Reference methods, as well asequivalent methods, for monitoring COare designated in accordance with 40CFR Part 53. A list of all methodsdesignated by EPA as reference orequivalent methods for measuring CO isavailable from any EPA Regional Office,or from EPA, Department E (MD-76),Research Triangle Park, N.C. 27711.

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Goldstein, I. (1982). Letter to the ed;tor:Seasonal relationship of sudden infantdeath syndrome and environmentalpollutants Am. . Epid. 116:189-191.

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Lit of Subjects in 40 CFR Part 50

Air pollution control, Carbonmonoxide, Ozone, Sulfur oxides,Particulate matter, Nitrogen dioxide,Lead.

Dated: September 5, 1985.Lee M. Thomas,Administrator.

PART 50-NATIONAL PRIMARY ANDSECONDARY AMBIENT AIR QUALITYSTANDARDS

For the reasons set forth in thepreamble, EPA amends Chapter 1, Part50, of Title 40 of the Code of FederalRegulations as follows:

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

Authority: Sec. 109 and 301(a), Clean AirAct, as amended (42 U.S.C. 7409, 7601(a)).

2. Section 50.8 is revised to read asfollows:

§ 50.8 National primary ambient air qualitystandards for carbon monoxide.

(a) The national primary ambient airquality standards for carbon monoxideare:

11) 9 parts per million (10 milligramsper cubic meter) for an 8-hour averageconcentration not to be exceeded morethan once per year and

(2) 35 parts per million (40 milligramsper cubic meter) for a 1-hour averageconcentration not to be exceeded morethan once per year.

(b) The levels of carbon monoxide inthe ambient air shall be measured by:

(1) a reference method based onAppendix C and designated inaccordance with Part 53 of this chapter,or .

(2) an equivalent method designatedin accordance with Part 53 of thischapter.

(c) An 8-hour average shall beconsidered valid if at least 75 percent ofthe hourly average for the 8-hour periodare available. In the event that only six(or seven) hourly averages are available,the 8-hour average shall be computed onthe basis of the hours available using six(or seven) as the divisor.

(d) When summarizing data forcomparision with the standards,averages shall be stated to one decimalplace. Comparison of the data with thelevels of the standards in parts permillion shall be nade in terms ofintegers with fractional parts of 0.5 orgreater rounding up.

[FR Doc. 85-22025 Filed 9-12-85:8:45 amlBILLING CODE 6560-50-M

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37484 federal register vol. no. friday, september 13, 1985 ......the final revised criteria...

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