[Federal Register Volume 59, Number 146 (Monday, August 1, 1994)]
[Unknown Section]
[Page 0]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 94-18659]
[[Page Unknown]]
[Federal Register: August 1, 1994]
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ENVIRONMENTAL PROTECTION AGENCY
40 CFR Part 50
[AD-FDL-4735-5]
National Ambient Air Quality Standards for Carbon Monoxide--Final
Decision
AGENCY: U.S. Environmental Protection Agency (U.S. EPA).
ACTION: Final decision.
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SUMMARY: Identical primary (health-based) and secondary (welfare-based)
national ambient air quality standards (NAAQS) for carbon monoxide (CO)
were promulgated in 1971 at 9 parts per million (ppm), 8-hour average,
and 35 ppm, 1-hour average, neither to be exceeded more than one time
per year. In 1985, the EPA announced the decision not to revise the
primary CO NAAQS and at the same time to revoke the secondary CO NAAQS.
In accordance with sections 108 and 109 of the Clean Air Act (Act), the
EPA has reviewed and revised the criteria upon which the existing NAAQS
for CO are based. Based on that review, this document announces the
EPA's final decision under section 109(d)(1) that revisions of the
NAAQS for CO are not appropriate at this time.
ADDRESSES: A docket containing information relating to the EPA's review
of the CO NAAQS (Docket No. A-93-05) is available for public inspection
in the Air and Radiation Docket and Information Center of the U.S.
Environmental Protection Agency, South Conference Center, Room 4, 401 M
Street, SW., Washington, DC. The docket may be inspected between 8 a.m.
and 4 p.m. on weekdays, and a reasonable fee may be charged for
copying. The information in the docket constitutes the complete basis
for the decision announced in this notice. For availability of related
information, see SUPPLEMENTARY INFORMATION.
FOR FURTHER INFORMATION CONTACT: Dr. David J. McKee, Air Quality
Management Division (MD-12), U.S. Environmental Protection Agency,
Research Triangle Park, NC 27711, telephone (919) 541-5288.
SUPPLEMENTARY INFORMATION:
Availability of Related Information
Certain documents are available from: U.S. Department of Commerce,
National Technical Information Service, 5285 Port Royal Road,
Springfield, Virginia 22161. Available documents include: the revised
criteria document, ``Air Quality Criteria for Carbon Monoxide'' (EPA/
600/8-90-045F; NTIS # PB 93-167492, $77.00 paper copy and $27.00
microfiche), and the 1992 staff paper, ``Review of the National Ambient
Air Quality Standards for Carbon Monoxide: Assessment of Scientific and
Technical Information-OAQPS Staff Paper'' (EPA-452/R-92-004, August
1992; NTIS No. PB 93-157717, $19.50 paper copy and $9.00 microfiche).
(Add $3.00 handling charge per order.) Other documents generated in
connection with review of this standard (e.g., exposure analysis) are
available in the EPA Docket No. A-93-05.
The contents of this document are listed in the following outline:
I. Background
A. Legislative Requirements Affecting This Decision
1. Primary and Secondary Standards
2. Related Control Requirements
B. Existing Primary Standards for Carbon Monoxide
C. Review of Air Quality Criteria and Standards for Carbon
Monoxide; Development of the Staff Paper
D. Decision Docket
II. Scientific Basis for This Regulatory Decision
A. Measuring and Assessing Carboxyhemoglobin Levels
B. Health Effects Associated With Carbon Monoxide
1. Mechanisms of Toxicity
2. Cardiovascular Effects
3. Effects on Exercise Capacity and Oxygen Uptake
4. Central Nervous System Effects
5. Developmental Toxicity Effects
6. Environmental Factors, Drugs, and Other Pollutants
C. Populations Potentially at Risk
III. Rationale for This Decision
A. Carboxyhemoglobin Levels of Concern
B. Margin of Safety
C. Relationship Between CO Exposure and COHb Levels
D. Estimating Population Exposure
E. Decision on the Primary Standards
IV. Final Decision Not to Revise the Standards
V. Regulatory Impacts
A. Regulatory Impact Analysis
B. Impact on Small Entities
VI. Other Reviews
References
I. Background
A. Legislative Requirements Affecting This Decision
1. Primary and Secondary Standards
Two sections of the Act govern the establishment and revision of
NAAQS. Section 108 (42 U.S.C. 7408) directs the Administrator to
identify pollutants which may reasonably be anticipated to endanger
public health and welfare and to issue air quality criteria for them.
These air quality criteria are to accurately reflect the latest
scientific knowledge useful in indicating the kind and extent of all
identifiable effects on public health or welfare which may be expected
from the presence of [a] pollutant in the ambient air.
Section 109 (42 U.S.C. 7409) directs the Administrator to propose
and promulgate ``primary'' and ``secondary'' NAAQS for pollutants
identified under section 108. Section 109(b)(1) defines a primary
standard as one the attainment and maintenance of which, in the
judgment of the Administrator, based on the criteria and allowing an
adequate ``margin of safety,'' [is] requisite to protect the public
health. A secondary standard, as defined in section 109(b)(2), must
specify a level of air quality the attainment and maintenance of which,
in the judgment of the Administrator, based on [the] criteria, is
requisite to protect the public welfare from any known or anticipated
adverse effects associated with the presence of [the] pollutant in the
ambient air. Welfare effects as defined in section 302(h) [42 U.S.C.
7602(h)] include, but are not limited to, effects on soils, water,
crops, vegetation, manmade materials, animals, wildlife, weather,
visibility and climate, damage to and deterioration of property, and
hazards to transportation, as well as effects on economic values and on
personal comfort and well-being.
The U.S. Court of Appeals for the District of Columbia Circuit has
held that the requirement for an adequate ``margin of safety'' for
primary standards was intended to address uncertainties associated with
inconclusive scientific and technical information available at the time
of standard setting. It was also intended to provide a reasonable
degree of protection against hazards that research has not yet
identified. [Lead Industries Association v. EPA, 647 F.2d 1130, 1154
(D.C. Cir. 1980), cert. denied, 101 S. Ct. 621 (1980); American
Petroleum Institute v. Costle, 665 F.2d 1176, 1177 (D.C. Cir. 1981),
cert. denied, 102 S. Ct. 1737 (1982)]. Both kinds of uncertainties are
components of the risk associated with pollution at levels below those
at which human health effects can be said to occur with reasonable
scientific certainty. Thus, by selecting primary standards that provide
an adequate ``margin of safety,'' the Administrator is seeking not only
to prevent pollution levels that have been demonstrated to be harmful
but also to prevent lower pollutant levels that she finds may pose an
unacceptable risk of harm, even if the risk is not precisely identified
as to nature or degree.
In selecting a ``margin of safety,'' the EPA considers such factors
as the nature and severity of the health effects involved, the size of
the sensitive population(s) at risk, and the kind and degree of the
uncertainties that must be addressed. Given that the ``margin of
safety'' requirement by definition only comes into play where no
conclusive showing of adverse effects exists, such factors, which
involve unknown or only partially quantified risks, have their inherent
limits as guides to action. The selection of any particular approach to
provide an adequate ``margin of safety'' is a policy choice left
specifically to the Administrator's judgment. [Lead Industries
Association v. EPA, supra, 647 F.2d at 1161-62].
Section 109(d)(1) of the Act requires that not later than December
31, 1980, and at 5-year intervals thereafter, the Administrator shall
complete a thorough review of the criteria published under section 108
and the NAAQS and shall make such revisions in such criteria and
standards as may be appropriate. Section 109(d)(2) (A) and (B) requires
that a scientific review committee be appointed and provides that the
committee shall complete a review of the criteria and the national
primary and secondary ambient air quality standards and shall recommend
to the Administrator any revisions of existing criteria and standards
as may be appropriate. If the EPA decides to revise an existing
standard, the rulemaking procedures of section 307(d) apply.1
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\1\The EPA has also chosen to follow rulemaking procedures in
several NAAQS reviews that did not involve revision of existing
standards. However, the EPA interprets section 307(d) as not
requiring such procedures where the Administrator decides to retain
an existing standard without change; i.e., to maintain the status
quo. Although such a decision is subject to judicial review as a
final action under section 307(b), neither the Act nor its
legislative history evidences any intent to require rulemaking where
the Administrator has not concluded that revision of an existing
NAAQS is appropriate. The Agency's conclusion that rulemaking
procedures are not required to retain an existing NAAQS without
revision is not affected by the Court's brief reference to the use
of rulemaking procedures in Environmental Defense Fund v. Thomas,
870 F.2d 892, 900 (2d Cir.), cert. denied, 110 S.Ct. 537 (1989). As
a practical matter, even without the use of rulemaking procedures,
the process by which the EPA reviews existing criteria and standards
involves substantial opportunities for public and expert comment on
both its assessment of relevant scientific and technical data and
its proposed use of the data for decision making purposes.
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The process by which the EPA has reviewed the existing air quality
criteria and standards for CO under section 109(d) is described in a
later section of this notice.
2. Related Control Requirements
States are primarily responsible for ensuring attainment and
maintenance of ambient air quality standards once the EPA has
established them. Under title I of the Act (42 U.S.C. 7410), States are
to submit, for EPA approval, State implementation plans (SIP's) that
provide for the attainment and maintenance of such standards through
control programs directed to sources of the pollutants involved. The
States, in conjunction with the EPA, also administer the prevention of
significant deterioration program (42 U.S.C. 7470-7479) and the
visibility protection program (42 U.S.C. 7491-7492) for these and other
air pollutants. In addition, Federal programs provide for nationwide
reductions in emissions of air pollutants through the Federal motor
vehicle control program under title II of the Act (42 U.S.C. 7521-
7574), which involves controls for automobile, truck, bus, motorcycle,
and aircraft emissions; the new source performance standards under
section 111 (42 U.S.C. 7411); and the national emission standards for
hazardous air pollutants under section 112 (42 U.S.C. 7412).
B. Existing Primary Standards for Carbon Monoxide
On April 30, 1971, the EPA promulgated NAAQS for CO under section
109 of the Act (36 FR 8186). Identical primary and secondary NAAQS were
set at 9 ppm as an 8-hour average and 35 ppm as a 1-hour average,
neither to be exceeded more than once per year. Scientific and
technical bases for these NAAQS are provided in the document, ``Air
Quality Criteria for Carbon Monoxide'' (U.S. Dept. of Health, Education
and Welfare, 1970). The NAAQS promulgated in 1971 were based largely
upon research by Beard and Wertheim (1967) who reported that CO
exposures which produced carboxyhemoglobin (COHb) levels of 2 to 3
percent were associated with central nervous system (CNS) effects such
as impaired ability to discriminate time intervals.
A revised Air Quality Criteria for Carbon Monoxide (U.S. EPA,
1979a), prepared by the Environmental Criteria and Assessment Office
(ECAO), and a Staff Paper (U.S. EPA, 1979b), prepared by the Office of
Air Quality Planning and Standards (OAQPS), identified several major
factors pertinent to subsequent action taken on the NAAQS for CO. The
Clean Air Scientific Advisory Committee (CASAC) met on June 14-15, 1979
to review drafts of these documents and provide advice on the CO
standards. As discussed in a notice of proposed rulemaking (45 FR
55066) published on August 18, 1980, although the Beard and Wertheim
(1967) study no longer could serve as a basis for the CO NAAQS, other
studies available in 1980 provided alternative evidence of decreased
time to onset of angina attack at COHb levels as low as 2.7 to 3.0
percent. This as well as other scientific evidence served as the basis
for the EPA to propose: (1) Retaining the 8-hour primary standard level
of 9 ppm, (2) revising the 1-hour primary standard level from 35 ppm to
25 ppm, (3) revoking the existing secondary CO NAAQS due to a lack of
evidence of adverse welfare effects at or near ambient CO levels, (4)
changing the form of the standard from deterministic to statistical by
stating allowable exceedances as expected values rather than as
explicit values, and (5) adopting a daily interpretation for
exceedances of the CO NAAQS so exceedances would be determined on the
basis of days on which the 8- or 1-hour average concentrations were
above the standard levels.
On June 18, 1982, the EPA announced (47 FR 26407) that a second
public comment period was necessary to open discussion on several
important issues and additional analyses. These issues included: (1)
The role of the Aronow (1981) study in assessing CO effects; (2)
consideration of a multiple exceedance 8-hour standard for CO; (3)
technical adequacy of the revised draft sensitivity analysis (Biller
and Richmond, 1982) on the Coburn, Forster, and Kane model predictions
of COHb levels; and (4) technical adequacy of the revised exposure
analysis (Johnson and Paul, 1983). The CASAC met on July 6, 1982 to
discuss these issues and provide advice, a summary of which was sent to
the Administrator on August 31, 1982 (Friedlander, 1982).
The 1980 proposal (45 FR 55066) was based in large part on studies
by Dr. Wilbert Aronow (Aronow, 1978; Aronow, et al., 1972, 1973, 1974a,
1974b, 1977; Aronow and Isbell, 1973; Aronow and Cassidy, 1975), which
provided the CASAC and the EPA staff with a basis for concluding that
COHb levels of 2.7-3.0 percent posed a health risk of concern in
individuals with angina and other types of cardiovascular disease. A
subsequent disclosure in March 1983 by the Food and Drug Administration
(FDA) concerning work conducted for the FDA by Dr. Aronow caused the
EPA to question the scientific credibility of Dr. Aronow's research on
CO. As a result, the EPA decided it would be prudent to conduct an
independent review of his CO research prior to making a decision on the
CO standards. A committee of experts was convened and chaired by Dr.
Steven Horvath (University of California, Santa Barbara). Following
meetings with Dr. Aronow and examination of limited data and records
available from his CO studies, the committee concluded in its report
(Horvath et al., 1983) that the EPA should not rely on Dr. Aronow's
studies for a decision on levels of the CO NAAQS due to problems
regarding data collection/analysis.
As a result of this finding, the ECAO prepared a draft Addendum to
the 1979 Air Quality Criteria for Carbon Monoxide. Concurrently, the
OAQPS prepared a draft Review of the NAAQS for Carbon Monoxide:
Reassessment of Scientific and Technical Information. These documents
were prepared to reevaluate the scientific and technical evidence on
health effects of CO at or near ambient levels in consideration of the
reduced usefulness of the Aronow studies. Both documents were reviewed
by the CASAC at a public meeting on September 25, 1983. The CASAC sent
a closure letter to the Administrator on May 17, 1984, which concluded
that the draft Addendum and the draft Staff Paper Reassessment
represented scientifically-balanced and defensible summaries of health
effects literature for CO. On August 9, 1984, the EPA announced (49 FR
31923) availability of the final Addendum (1984b) and final Staff
Reassessment (1984a), both of which had been revised to reflect the
CASAC's and public comments. In the same notice, the EPA reviewed the
basis for the 1980 proposal to revise the CO standards and solicited
additional public comment. In a subsequent Federal Register notice (50
FR 37484) published on September 13, 1985, the EPA announced its final
decision not to revise the existing primary standards and to revoke the
secondary standards for CO. In doing so, the Administrator determined
that the existing 1-hour and 8-hour primary NAAQS provided adequate
protection from exposure to ambient CO.
C. Review of Air Quality Criteria and Standards for Carbon Monoxide;
Development of the Staff Paper
On July 22, 1987, the ECAO published in the Federal Register (52 FR
27580) a call for information to assist in the development of a draft
revised Air Quality Criteria for Carbon Monoxide (Criteria Document).
Notice of availability of the external review draft Criteria Document
was published in the Federal Register (55 FR 14858) on April 19, 1990.
This draft Criteria Document included discussion of several new studies
of effects of CO on angina patients, which had been initiated in light
of the controversy discussed above. The CASAC reviewed the draft
Criteria Document at a public meeting held on April 30, 1991. The EPA
placed a transcript of the CASAC meeting in the docket (ECAO-CD-86-
073). The EPA carefully considered comments received from the public
and the CASAC members in preparing the final Criteria Document (U.S.
EPA, 1991). On July 17, 1991, the CASAC sent to the Administrator a
``closure letter'' (McClellan, 1991) outlining key issues and
recommendations and indicating that the document provides a
scientifically-balanced and defensible summary of current knowledge of
the effects of this pollutant and provides an adequate basis for the
EPA to make a decision as to the appropriate primary NAAQS for CO.
Immediately following the CASAC meeting of April 30, 1991, the
OAQPS began development of the revised draft Staff Paper. This document
was released for public review in February 1992. The CASAC held a
public meeting on March 5, 1992 to review the draft revised Staff
Paper. A copy of the transcript of this meeting has been placed in the
docket (A-93-05). Major issues discussed at the meeting included:
interpretation of new scientific information, the definition of adverse
health effects associated with CO exposure, populations at risk, COHb
levels of concern, and estimates of population exposure. In response to
comments made by the public and the CASAC members, minor revisions to
the Staff Paper were made and briefly reviewed at a public meeting of
the CASAC held on April 28, 1992 prior to preparation of the final
Staff Paper (U.S. EPA, 1992). The CASAC came to closure on its review
of the Staff Paper in a letter to the Administrator dated August 11,
1992. In that ``closure letter'' (McClellan, 1992) the CASAC states
that ``this document is consistent with all aspects of the scientific
evidence presented in the criteria document for carbon monoxide. It has
organized the relevant information in a logical fashion and the
Committee believes that it provides a scientifically adequate basis for
regulatory decisions on carbon monoxide. The staff paper concludes, and
the CASAC concurs, that a standard of the present form and with a
numerical value similar to that of the present standard would be
supported by the present scientific data on health effects of exposure
to carbon monoxide.''
D. Decision Docket
On February 2, 1993, the EPA created a docket (Docket No. A-93-05)
for this decision. The docket incorporated by reference a separate
docket established in 1986 for criteria document revision (Docket No.
ECAO-CD-86-073).
II. Scientific Basis for This Regulatory Decision
A. Measuring and Assessing COHb Levels
As concluded in the Staff Paper (U.S. EPA, 1992, p. 10), blood COHb
level is not only the best indicator of CO exposure but also has been
related to health effects of major concern for CO. In most CO health
effects studies, the co-oximeter (CO-Ox) has been used to measure COHb
at levels in the range of 0 to 5 percent COHb; however, concerns have
been raised regarding accuracy of the CO-Ox.
While CO-Ox measurements are very precise (i.e., replicable),
research has shown that the accuracy (i.e., ability to detect the
actual level) of these optical instruments is not always sufficient to
use alone at levels 5 percent COHb (Allred et al., 1989a,b,
1991). As indicated in the Criteria Document (U.S. EPA, 1991, pp. 8-72
to 8-73), the results from linear regression analyses of comparisons
between CO-Ox instruments and various reference instruments [involving
gas chromatography (GC)] show a fairly linear slope and a wide range of
intercept values, thus suggesting good precision but poor accuracy for
the CO-Ox. In the only health effects study that used both CO-Ox and GC
methods to measure COHb levels in subjects with heart disease,
researchers found that the spread of COHb values was much greater for
the CO-Ox values than for the GC values (Allred et al., 1989a,b, 1991).
In order for optical instruments such as CO-Ox to be used to
measure COHb levels accurately at low levels, they must be calibrated
routinely with an alternative method (U.S. EPA, 1991, p. 8-64). When
properly calibrated, CO-Ox instruments provide useful information on
mean COHb values; however, variation in individual oxyhemoglobin
(O2Hb) levels appears to influence COHb readings (Allred et al.,
1989a,b) and, as noted above, CO-Ox instruments also give a broader
range of COHb values when compared to GC measurements on the same
samples (Allred et al., 1989a,b, 1991). Although the CASAC identified
the GC as the method of choice (McClellan, 1992), the fact that most of
the health effects literature for CO relies on CO-Ox measurements led
to the decision that CO-Ox data would be used in establishing levels of
concern.
B. Health Effects Associated With Carbon Monoxide
Health effects associated with exposure to CO include
cardiovascular system effects, CNS effects, and developmental toxicity
effects, as well as effects of combined exposure to CO and other
pollutants, drugs, and environmental factors. Cardiovascular effects of
CO are directly related to a reduced oxygen (O2) content of the
blood caused by combination of CO with hemoglobin (Hb) to form COHb and
resulting in tissue hypoxia. Most healthy individuals have mechanisms
(e.g., increased blood flow, blood vessel dilation) which compensate
for this reduction in tissue O2 levels, although the effect of
reduced maximal exercise capacity has been reported in healthy persons
even at low COHb levels. Compensatory mechanisms are less effective in
elderly people, pregnant women, small children, and in certain people
with anemia or pulmonary and cardiovascular diseases, thereby
increasing their susceptibility to potential adverse effects of CO
during exercise. Research studies considered most significant to the
establishment of NAAQS for CO are summarized in Table 1 and are
discussed below.
1. Mechanisms of Toxicity
The mechanism of toxicity principally associated with health
effects of greatest concern from CO exposure is hypoxia induced by
elevated COHb levels. The primary exchange route for CO to human
tissues is through the lungs. Although CO is a naturally occurring
chemical in blood being produced endogenously by normal catabolic
processes, blood COHb levels do not often exceed 0.5 to 0.7 percent in
normal individuals unless exogenous CO is breathed. Some individuals
with high endogenous CO production can have COHb levels of 1.0 to 1.5
percent (e.g., anemics). Exogenous CO diffuses through the respiratory
zone (alveoli) to the blood where it binds to Hb to form COHb. The
chemical affinity of CO for Hb is 218 to 250 times greater than that of
O2 (Roughton, 1970; Wyman et al., 1982; Rodkey et al., 1969). This
preferential binding of CO to Hb limits the availability of Hb for
O2 transport to tissues throughout the body. As COHb levels
increase, the dissociation curve for normal human blood is shifted to
the left resulting in more reduced delivery of O2 to tissues and a
greater of CO-induced hypoxia. It is this reduced O2 delivery to
heart muscle tissue which is of great concern for individuals with
ischemic heart disease because their already compromised condition puts
them at increased risk.
Table 1.--Key Health Studies for Establishing NAAQS for Carbon Monoxide
------------------------------------------------------------------------
COHb
concent. Health effects Referencesb
percenta
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2.3-7.0... Decreased short-term Drinkwater et al. (1974), Ekblom
maximal exercise and Huot (1972), Horvath et al.
duration in young (1975), Raven et al. (1974a,b),
healthy men. Weiser et al. (1978).
2.9-5.9... Decreased exercise Adams et al. (1988), Allred et al.
duration due to (1989a,b; 1991), Anderson et al.
increased chest pain (1973), Kleinman et al. (1989),
(angina) in patients Sheps et al. (1987).
with ischemic heart
disease.
5.0-20.0.. Decreased maximal oxygen Ekblom and Huot (1972), Klein et
consumption with short- al. (1980), Pirnay et al. (1971),
term strenuous exercise Stewart et al. (1978), Vogel and
in young healthy men. Gleser (1972), Weiser et al.
(1978).
5.0-20.0.. Equivocal effects on Benignus et al. (1977, 1987,
visual perception, 1990a,b), Bunnell and Horvath
audition, motor and (1988), Christensen et al.
sensorimotor (1977), Gliner et al. (1983),
performance, vigilance, Harbin et al. (1988), Hudnell and
and other measures of Benignus (1989), McFarland (1970,
neurobehavioral 1973), McFarland et al. (1944),
performance. Mihevic et al. (1983), O'Donnell
et al. (1971), Putz et al. (1976)
Putz (1979), Roche et al. (1981),
Rummo and Sarlanis (1974),
Seppannen et al. (1977), Von Post-
Lingen (1964), Winneke (1974).
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aBlood COHb levels determined by optical methods.
bReferences also found in U.S. EPA (1991) and U.S. EPA (1992).
Although several other mechanisms of toxicity are discussed in the
Criteria Document (U.S. EPA, 1991), these are not considered to be as
well understood as COHb hypoxia. Intracellular effects of CO (U.S. EPA,
1991, pp. 9-22 to 9-31) have been associated with CO toxicity.
Preferential binding of CO to myoglobin, cytochrome P-450, and
cytochrome c oxidase has been studied and could lead to impairment of
intracellular oxygen transport to mitochondria. However, mechanisms of
toxicity associated with CO-induced inhibition of these hemoproteins at
relevant CO levels are not well understood at this time and will
require further research.
Based on the review and conclusions drawn in the Criteria Document
(U.S. EPA, 1991), COHb levels provide the most useful estimate of
exogenous CO exposures and serve as the best biomarker of CO toxicity
for ambient-level exposures to CO. Thus, COHb levels are used as the
indicator of health effects and to identify the lowest effects level
for CO.
2. Cardiovascular Effects
The best documented cardiovascular effects of CO in patients with
chronic heart disease are decreased time to onset of chest pain and ST-
segment depression during exercise stress. The commonly accepted
criterion of exercise-induced myocardial ischemia is 1 mm or greater
ST-segment depression. The ST segment is a portion of the
electrocardiogram (ECG), depression of which is an indication of
insufficient O2 supply to heart muscle tissue.
Five key studies on cardiovascular effects of CO (Allred et al.,
1989a,b, 1991; Kleinman et al., 1989; Adams et al., 1988; Sheps et al.,
1987; Anderson et al., 1973) have provided evidence of the potential
for CO to enhance development of exercise-induced myocardial ischemia
in patients who suffer from angina pectoris. (Angina pectoris is a
spasmodic, strangling sensation or heavy chest pain, often radiating to
the arms, especially the left, most often due to lack of O2 to the
heart muscle and precipitated by effort or excitement.) An early study
by Anderson et al. (1973) reported decreased time to onset of angina
pain for COHb levels as low as 2.9 (CO-Ox), representing a 1.6 percent
increase in average COHb levels over baseline. Details of this study
were reported at length in the Addendum (U.S. EPA, 1984b).
More recent controlled exposure studies of angina patients have
provided substantial new evidence of decreased time to early onset of
chest pain. (See discussion in U.S. EPA, 1991, pp. 10-21 to 10-35). A
study which provides strong evidence of the health effects of CO is the
multicenter study of Allred et al. (1989a,b, 1991). There are several
reasons why this particular study is important to the CO NAAQS review:
(1) Dose-response relationships are shown, (2) information on ST-
segment depression of subjects is available, (3) COHb measurements were
taken using both GC and CO-Ox, (4) a large number of subjects was used,
and (5) it was conducted at multiple laboratories around the U.S. This
study involved 63 males (41-75 years of age) with coronary artery
disease living in three different U.S. cities. The objective was to
assess the impact of exposure to CO on time to onset of significant
ischemia during a standard treadmill test. Unusual care was taken to
establish presence of coronary artery disease in all subjects prior to
testing. The protocol for the study was quite similar to that used in
the Aronow studies, i.e., two exercise tests were performed on the same
day separated by a recovery period and a double-blind exposure period.
Subjects were exposed to either clean air, 117 ppm CO, or 253 ppm CO
for 50 to 70 minutes while performing symptom-limited exercise on a
treadmill. Time to onset of angina and time to ST-segment depression
were determined for each test following exposure to both CO levels and
compared to clean air (<2 ppm CO) exposure. After exposure to 117 ppm
and 253 ppm CO, COHb levels measured before the exercise stress test
were 2.4 and 4.7 percent COHb (GC) and 3.2 and 5.6 percent COHb (CO-
Ox), respectively. After the stress test COHb levels were 2.0 and 3.9
percent (GC) and 2.7 and 4.7 percent (CO-Ox). Using the objective
measure of time to ST-segment depression, CO exposure which produced
3.2 percent COHb (CO-Ox, pretest) resulted in a 5.1 percent (p=0.01)
decrease in time to the ST criterion, and 5.6 percent COHb (CO-Ox,
pretest) decreased time to the ST criterion by 12.1 percent (p<0.001)
relative to clean air exposure. Combining slopes for the 62 individuals
yielded a significant (p<0.005) regression which indicates that there
was a 3.9 percent decrease in time to ST criterion for every 1 percent
increase in COHb. Time to onset of angina also was reduced in the same
subjects, and regression analysis yielded a significant relationship
(p<0.025). Both endpoints (time to angina and time to ST change) were
highly correlated.
In another study (Sheps et al., 1987), 30 nonsmokers with ischemic
heart disease (ages 38-75) were exercised during exposure to 100 ppm CO
or air using a 3-day, randomized double blind protocol. Following CO
exposure, average COHb levels were 4.1 percent (CO-Ox), representing a
2.2 percent COHb increase from the initial COHb level. In comparing
results of air-exposed subjects to CO-exposed subjects as a group, no
statistically significant differences were reported in time to onset of
angina, maximal exercise time, maximal ST-segment depression, or time
to significant ST-segment depression. Although the authors concluded
that 4.1 percent COHb did not produce clinically significant effects in
the paired subject group, 3 of 30 patients did experience angina on CO-
exposure days but not on air-exposure days. Further analysis of the 30
person data base from Sheps et al. (1987) of time to onset of angina
that included these three patients indicated a statistically-
significant decrease for CO exposure compared to air exposure (Bissette
et al., 1986). The same group of researchers (Adams et al., 1988)
exposed 30 subjects with obstructive coronary artery disease to either
air or sufficient CO to reach COHb levels of 5.9 percent (CO-Ox),
representing an average increase of 4.2 percent COHb above initial COHb
levels. As in the earlier study, several patients experienced angina on
the CO-exposure day and not on the air-exposure day but never the
reverse. Results of this study provide statistically significant
evidence that exposure to CO induces earlier onset of angina and
ventricular dysfunction as well as poorer exercise performance in
patients with ischemic heart disease. Although the Sheps et al. (1987)
and Adams et al. (1988) studies did not observe statistically-
significant changes in time to onset of angina using conventional
statistical procedures, results of these studies are not incompatible
with the rest of the studies reporting an effect of CO (U.S. EPA, 1991,
p. 10-32).
A separate study of effects of CO exposure was conducted with 26
nonsmoking male, angina patients (Kleinman and Whittenberger, 1985;
Kleinman et al., 1989). One hour of exposure to 100 ppm CO raised COHb
levels to 3.0 percent (CO-Ox), representing an average increase of 1.5
percent COHb over initial COHb level. For the group, CO exposure
resulted in a decrease in time to onset of angina by 6.9 percent
compared to clean air exposure (Kleinman and Whittenberger, 1985). This
was a statistically-significant difference (p=0.03). Reanalysis,
necessitated by dropping two subjects due to inconsistent medical
records, resulted in an average decrease of 5.9 percent (p=0.046) in
time to onset of angina for CO exposure compared to air exposure
(Kleinman et al., 1989). For the eight patients who exhibited
depression in the ST segment of ECG traces during exercise, there was a
decrease of 10 percent (p<0.036) in time to onset of angina and a
decrease of 19 percent (p<0.044) in time to onset of ST-segment
depression.
Allred et al. (1989b, 1991) discuss possible reasons for some
differences in results of the above-cited studies. These studies have
different designs, types of exercise tests, inclusion criteria (e.g.,
patient populations), exposure conditions, and measurement methods for
COHb. Of the studies, only two (Allred et al., 1989a,b, 1991; Anderson
et al., 1973) investigate more than a single target level of COHb, and
of those two, only Allred et al. (1989a,b, 1991) demonstrate a dose-
response effect of COHb on time to onset of angina. Different
measurement methodologies for COHb also may account for some of the
discrepancies between studies. As discussed in Section V.C.1. of the
Staff Paper (U.S. EPA, 1992) and in the Criteria Document (U.S. EPA,
1991, pp. 8-70 to 8-74), only Allred et al. (1989a,b, 1991) used both
the GC and CO-Ox to measure COHb and found the spread of COHb values to
be much greater for the CO-Ox than for the GC. Another difference in
the studies was that Allred et al. (1989a,b, 1991) used more rigorous
subject entry criteria. All subjects were male, were required to have
stable exertional angina and reproducible exercise-induced ST-segment
depression and angina, and were required to have either a previous
myocardial infarction, angiographic disease or a positive thallium
test.
The major conclusion which can be drawn regarding most of the
studies discussed above is that all show a decrease in time to onset of
angina at postexposure COHb levels ranging from 2.9 to 5.9 percent (CO-
Ox). This represents incremental increases of 1.5 to 4.4 percent COHb
from preexposure baseline levels. Therefore, there are clearly
demonstrable effects of low-level CO exposure in patients with ischemic
heart disease (U.S. EPA, 1991, pp. 10-34 to 10-35). Across-study
comparison is depicted in the Criteria Document (U.S. EPA, 1991, p. 10-
33), presented as an adaptation from Allred et al. (1989b, 1991), and
suggests reasonably good consistency. For purposes of comparison, only
optical methods (CO-Ox) were used to avoid confusion.
The adverse nature of the effects described in the five key studies
is uncertain due to the range of professional judgments on the clinical
significance of small performance decrements produced by exercise and
CO exposure. Although some physicians may not be greatly concerned
about decrements in performance occurring around 3.0 percent COHb (CO-
Ox), consistency across studies of response for both decrease in time
to onset of angina and ST-segment depression suggest that the effect
does occur and may limit the activity of persons with ischemic heart
disease. Bassan (1990) indicates that 58 percent of cardiologists
believe that recurrent exercise-induced angina attacks are associated
with substantial risk of precipitating myocardial infarction, fatal
arrhythmia, or slight but cumulative myocardial damage (U.S. EPA, 1991,
p. 10-35). Based on discussions in the Criteria Document (U.S. EPA,
1991) and at the April 30, 1991 and March 5, 1992 CASAC meetings, staff
recommended in the Staff Paper (U.S. EPA, 1992, p. 22) that 2.9 to 3.0
percent COHb (CO-Ox), representing an increase above initial COHb of
1.5 to 2.2 percent COHb, be considered a level of potential adversity
for individuals at risk.
3. Effects on Exercise Capacity and Oxygen Uptake
Maximal oxygen uptake and maximal exercise capacity are direct
measures of cardiovascular capacity and can provide insight into the
impact of CO on the cardiovascular systems of healthy individuals.
Although decreases in these attributes may not be very serious in
healthy persons for CO exposures typically found in the ambient air,
they can be indicative of the extent to which an individual's ability
to function normally may be affected while engaging in activities which
require high levels of sustained exercise.
Numerous researchers have studied the effects of CO on oxygen
uptake and exercise performance in healthy individuals. Several
investigators (Klein et al., 1980; Stewart et al., 1978; Weiser et al.,
1978; Ekblom and Huot, 1972; Vogel and Gleser, 1972; Pirnay et al.,
1971) found statistically-significant decreases (3 to 23 percent) in
maximal oxygen uptake under conditions of short-term maximal exercise
at COHb levels ranging from 5 to 20 percent (CO-Ox). Horvath et al.
(1975) found that the lowest level at which COHb marginally influenced
maximal oxygen uptake (p<0.10) was about 4.3 percent (CO-Ox); COHb
levels of 3.3 percent and 4.3 percent (CO-Ox) reduced work time to
exhaustion by 4.9 percent and 7 percent, respectively. Similar results
were found following exhaustive treadmill exercise at 5 percent COHb
(CO-Ox) (Stewart et al., 1978; Klein et al., 1980). Short-term maximal
exercise duration has been shown to be reduced by 3 to 38 percent at
COHb levels ranging from 2.3 to 7 percent (CO-Ox) (Horvath et al.,
1975; Drinkwater et al., 1974; Raven et al., 1974a,b; Weiser et al.,
1978; Ekblom and Huot, 1972). Since CO has not been shown to impair
submaximal work capacity, changes in short-term maximal exercise should
be of concern mainly for competing athletes (U.S. EPA, 1991, p. 10-73).
4. Central Nervous System Effects
A variety of CNS effects has been found to be associated with CO
exposures which result in COHb levels of 5 to 20 percent (CO-Ox). These
effects include changes in visual perception, hearing, motor
performance, sensorimotor performance, vigilance, and other measures of
neurobehavioral performance.
Of the behaviors studied, the most sensitive to disruption by COHb
are those that require sustained attention or sustained performance.
For example, the group of studies on motor and sensorimotor
performance, which have used a variety of measures (e.g., fine motor
skills, reaction time, and tracking), offer the most consistent
evidence for effects occurring at COHb levels as low as 5 percent.
Although Winneke (1974) found some effects on steadiness and precision
at 10 percent COHb (CO-Ox), several other investigators (Mihevic et
al., 1983; O'Donnell, 1971; Seppanen et al., 1977) reported no CO
effect at COHb levels ranging from 5.5 to 12.7 percent (CO-Ox).
Reaction time was unaffected by COHb levels of 7 and 10 percent (CO-Ox)
(Rummo and Sarlanis, 1974; Winneke, 1974), and the pervasive finding is
that COHb elevation does not affect reaction time for COHb levels as
high as 20 percent (CO-Ox) (U.S. EPA, 1991, p. 10-118). Compensatory
tracking was not significantly affected by COHb levels of 5.8 percent
(CO-Ox) (Gliner et al., 1983) or by levels of 12 to 13 percent (CO-Ox)
(O'Donnell et al., 1971); however, tracking tasks were significantly
affected by COHb levels of 5 percent (CO-Ox) (Putz et al., 1976; Putz,
1979). Results of the Putz et al. (1976) study were confirmed by
Benignus et al. (1987) but not by Benignus et al. (1990a) when
attempting to demonstrate a dose-effect relationship using the same
experimental design. Benignus et al. (1990b) discusses possible reasons
for high variability between studies, and the Criteria Document (U.S.
EPA, 1991, p. 10-121) concludes that COHb elevation produces small
decrements in tracking that are sometimes statistically significant.
Numerous other studies (Benignus et al., 1977; Bunnell and Horvath,
1988; Christensen et al., 1977; Harbin et al., 1988; Hudnell and
Benignus, 1989; McFarland, 1970, 1973; McFarland et al., 1944; Roche et
al., 1981; von Post-Lingen, 1964) provide additional support for
neurobehavioral effects associated with COHb levels above 5 percent.
Even though new information regarding neurobehavioral effects of
COHb levels in the range of 5-20 percent (CO-Ox) has been published
during the past decade, conditions under which these effects occur are
poorly understood (U.S. EPA, 1991, p. 10-143). Because neurobehavioral
effects have not yet been demonstrated at COHb levels below 5 percent
(CO-Ox), the Staff Paper (U.S. EPA, 1992, p. 24) recommended focussing
on the cardiovascular effects which have been reported at lower COHb
levels. Standards which protect sensitive populations from adverse
cardiovascular effects also should provide adequate protection against
adverse neurobehavioral effects of CO occurring in the exposed
population.
5. Developmental Toxicity Effects
Developmental toxicity covers a variety of effects in the
developing organism including fetal death, structural abnormalities,
altered growth and functional deficits. The fetus may be particularly
vulnerable to the toxic effects of CO exposure because fetal
development often occurs at or near critical tissue oxygenation levels
(Longo, 1977). The COHb levels tend to be naturally elevated in the
fetus due to differences in uptake and elimination of CO from fetal
hemoglobin.
Human data on developmental toxicity of CO are very limited for
obvious ethical reasons. Maternal smoking, however, has been associated
with a number of adverse health effects, many of which can be
attributed to very high CO exposures (500-1000 ppm) from cigarette
smoke. These effects include spontaneous abortion and subsequent fetal
death due to depressed birth weight, increased number of hospital
admissions during the first 5 years of life, and poorer than predicted
school performance during the first 11 years of life. These and other
effects of smoking are reviewed in a report to the U.S. Surgeon General
(National Institute of Child Health and Human Development, 1979). Data
(Hoppenbrouwers et al., 1981) supporting a link between environmental
CO exposure and sudden infant death syndrome (SIDS) are suggestive, but
further study is needed before any causal relationship can be inferred.
Finally, animal studies have provided evidence of fetal mortality,
teratogenicity, reduced body weight, morphological changes, altered
cardiovascular development, and neurochemical changes. However, these
studies are often conducted at CO levels much greater than those found
in the ambient air, and extrapolation to human health effects at
ambient CO exposures remains very difficult.
6. Environmental Factors, Drugs, and Other Pollutants
Several additional factors have been investigated for potential
interactions with CO that may alter health effects. Among the more
important are altitude, drugs, coexposure to other pollutants, and heat
stress. Altitude is a matter of concern because of the large
populations exposed to CO while living in cities above 1500 meters.
While there are some data to support the possibility that effects of
inhaling CO and effects of high altitude may be additive (Cooper et
al., 1985; McDonagh et al., 1986), several studies even at 2,000 m to
4,500 m show little or no additivity (McGrath, 1988; Horvath, 1988;
Horvath and Bedi, 1989). Most other studies have been conducted at CO
levels which are too high to be of regulatory use.
There is evidence that interactions of drug effects with CO
toxicity can occur in both directions, i.e., CO toxicity may be
enhanced by drug use, and toxic or other effects of drugs may be
altered by CO exposure. A recent study (Knisely et al., 1989) reported
a large interaction of CO exposure and alcohol in mice, demonstrating
that alcohol doubled the acute toxicity of CO. In the same study, CO
exposure in combination with administration of barbiturates and other
psychoactive drugs produced additive but not synergistic effects.
Combined exposures of CO and other pollutants have been investigated
primarily using animal subjects with only a few human studies being
published. No interaction was observed in humans for CO in combination
with common ambient air pollutants such as nitrogen dioxide, ozone, and
peroxyacetyl nitrate (Raven et al., 1974a,b; Drinkwater et al., 1974;
Gliner et al., 1975), although a greater decrement in exercise
performance was reported in these studies when heat stress was combined
with 50 ppm CO.
The Staff Paper (U.S. EPA, 1992, p. 26) recommended that
information on CO in combination with other pollutant exposures and
environmental stresses be treated as a margin of safety consideration.
C. Populations Potentially at Risk
In the Administrator's judgment, the available health effects data
identify individuals with angina (e.g., history of heart disease) as
the group at greatest risk from low-level, ambient air exposures to CO.
Based on 1989 data of the American Heart Association (AHA, 1989) and
1990 information from the Department of Health and Human Services
(DHHS, 1990), individuals with both diagnosed and undiagnosed ischemic
heart disease total approximately 10 to 11 million or about 4.5 percent
of the U.S. population. As discussed earlier, concern for these
individuals is due to the fact that their condition is due to an
insufficient supply of oxygen to cardiac tissue. Further reduction in
oxygen reserve capacity by exposure to CO increases the probability of
adverse health effects occurring.
Several other groups have been identified in the Criteria Document
(U.S. EPA, 1991) and Staff Paper (U.S. EPA, 1992) as being potentially
at risk of being sensitive to CO exposure. These groups include: (1)
Persons with cerebrovascular disease, (2) those individuals with anemia
or chronic obstructive lung disease, and (3) fetuses and young infants.
In addition, visitors to high altitude locations may be more
susceptible due to lower oxygen content in the air, and those persons
using drugs or alcohol may be at greater risk due to the interactive
health effects of CO with these substances. For a complete list of
probable risk groups, see the Criteria Document (U.S. EPA, 1991, p. 12-
1).
For many of the groups identified above, there is little or no
experimental evidence to demonstrate that they are at increased risk of
CO-induced health effects. However, it is reasonable to expect that
individuals with preexisting illness (e.g., congestive heart failure,
peripheral vascular or cerebrovascular disease, sickle-cell anemia,
hematological disease, chronic obstructive lung disease) which limit
oxygen absorption or oxygen transport to body tissues would be somewhat
more susceptible to hypoxic (i.e., oxygen starvation) effects of CO
(pp. 12-1 and 12-2, U.S. EPA, 1991). Since no human experimental
evidence exists which identifies CO effects levels for these other
groups, the Administrator is considering the possible effects of CO on
these groups only in the determination of what constitutes an adequate
margin of safety.
III. Rationale for This Decision
This decision completes the EPA's review of health effects of CO
assembled over a 5-year period and contained in the Criteria Document
(U.S. EPA, 1991).2 This review includes the evaluation of key
studies published through 1990 incorporated in the Criteria Document
(U.S. EPA, 1991), the Staff Paper (U.S. EPA, 1992) assessment of most
relevant information contained in the Criteria Document (U.S. EPA,
1991), and the advice and recommendations of the CASAC as presented
both in the discussion of these documents at public meetings and in the
CASAC's 1991 (McClellan, 1991) and 1992 (McClellan, 1992) ``closure
letters.''
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\2\ As previously noted, the EPA believes that section 307(d)
does not require rulemaking procedures where the Administrator
concludes that revision of an existing NAAQS is not appropriate.
---------------------------------------------------------------------------
A. Carboxyhemoglobin Levels of Concern
In selecting the appropriate level(s) and averaging time(s) for the
primary NAAQS for CO, the Administrator must first determine the COHb
levels of concern taking into account a large and diverse health
effects data base. The scientific quality and strength of health data
are assessed in the Criteria Document (U.S. EPA, 1991) and in the Staff
Paper (U.S. EPA, 1992). Based on these assessments, judgments are made
here to identify those studies that are most useful in establishing a
range of COHb levels to be considered in standard setting. In addition,
the more uncertain or less quantifiable evidence is reviewed to
determine the lower end of the range that would provide an adequate
margin of safety from effects of clear concern. Those judgments
relevant to the establishment of an appropriate range of COHb levels
are summarized in the discussion below.
The Administrator judges that cardiovascular effects, as measured
by decreased time to onset of angina pain and by decreased time to
onset of significant ECG ST-segment depression, are the health effects
of greatest concern, which clearly have been associated with CO
exposures at levels observed in the ambient air. Decrease in time to
onset of exercise-induced angina pain is well documented in studies of
angina patients whose postexposure COHb levels have been raised to 2.9-
5.9 percent (CO-Ox), which represents incremental increases of 1.5 to
4.4 percent COHb from baseline levels (Allred et al., 1989a,b, 1991;
Kleinman et al., 1989; Adams et al., 1988; Sheps et al., 1987; Anderson
et al., 1973). Time to onset of significant ECG ST-segment change,
which is indicative of myocardial ischemia in patients with documented
coronary artery disease and a more objective indicator of ischemia than
angina pain, provides supportive evidence of health effects occurring
as low as 2.9-3.0 percent COHb (CO-Ox). In light of the above data and
discussions of adverse health consequences in the Criteria Document
(U.S. EPA, 1991, p. 10-35) and Staff Paper (U.S. EPA, 1992, p. 29), at
the April 30, 1991 and March 5, 1992 CASAC meetings, and in the July
17, 1991 letter to the Administrator from the CASAC Chairman
(McClellan, 1991), the Administrator concludes that CO exposures
resulting in COHb levels of 2.9-3.0 percent (CO-Ox) or higher in
persons with heart disease have the potential to increase the risk of
decreased time to onset of angina pain and ST-segment depression. As
stated by McClellan (1991), ``Among health professionals there is a
range of views as to the clinical significance of these changes with
the dominant view being that the changes should be considered as
adverse or a harbinger of adverse effects.'' It is important that
standards be set to appropriately reduce the risk of ambient exposures
which produce COHb levels that could induce such potentially adverse
effects.
Clinical importance of cardiovascular effects associated with
exposures to CO resulting in COHb levels of 2 to 3 percent remains less
certain. One recent study (Allred et al., 1989a,b) provides evidence of
a 5.1 percent decrease in time to ST-segment depression at 2.0 percent
COHb when using the GC to measure COHb levels. Although it is possible
that there is no threshold for these effects even at lower COHb levels,
the health significance of such small changes in ST-segment depression
appears to be relatively trivial. The Administrator, therefore,
concludes that results suggesting cardiovascular effects in angina
patients when COHb levels are between 2.0 and 2.9 percent only be
considered in evaluating whether the current CO standards provide an
adequate margin of safety.
B. Margin of Safety
There are several factors which the Administrator believes should
be considered in evaluating the adequacy of the current CO NAAQS: (a)
short-term reduction in maximal work capacity has been measured in
trained athletes exposed to CO sufficient to produce COHb levels as low
as 2.3 to 7 percent; (b) the wide range of human susceptibility to CO
exposures and ethical considerations in selecting subjects for
experimental purposes together suggest that the most sensitive
individuals have not been studied; (c) animal studies of developmental
toxicity and human studies of the effects of maternal smoking provide
evidence that exposure to high concentrations of CO can be detrimental
to fetal development, although very little is known about the effects
of ambient CO exposures on the developing fetus; (d) though little is
known about effects of CO on potentially sensitive populations other
than those with ischemic heart disease, there is reason for concern
about visitors to high altitudes, individuals with anemia or
respiratory disease, and the elderly; (e) impairment of visual
perception, sensorimotor performance, vigilance or other CNS effects
has not been demonstrated to be caused by CO concentrations commonly
found in the ambient air; however, short-term peak CO exposures may be
responsible for impairments which could be a matter of concern for
complex activities such as driving a car; (f) limited evidence suggests
concern for individuals exposed to CO concurrently with drug use (e.g.,
alcohol) during heat stress, or coexposure to other pollutants; (g)
large uncertainties remain regarding modelling COHb formation and
estimating human exposure to CO which could lead to overestimation or
underestimation of COHb levels in the population associated with
attainment of a given CO NAAQS; and (h) COHb measurements made using
the CO-Ox may not reflect COHb levels in angina patients studied,
thereby creating uncertainty in establishing a lowest effects level for
CO.
In summary, the Administrator concludes that the lowest COHb level
at which adverse effects have been demonstrated in persons with angina
is around 2.9-3.0 percent, representing an increase of 1.5 percent
above baseline when using the CO-Ox to measure COHb. These data serve
to establish the upper end of the range of COHb levels of concern.
Taking into account uncertainties in the data, the less significant
health endpoints, and less quantifiable data on other potentially
sensitive groups, staff recommends that the lower end of the range be
established at 2.0 percent COHb. Below this level, the potential for
public health risk appears to be small. The Administrator, therefore,
concludes that results suggesting cardiovascular effects in angina
patients when COHb levels are between 2.0 and 2.9 percent only be
considered in evaluating whether the current CO standards provide an
adequate margin of safety.
C. Relationship Between CO Exposure and COHb Levels
In order to set ambient CO standards based on an assessment of
health effects at various COHb levels, it is necessary to estimate the
ambient CO concentrations that are likely to result in COHb levels of
concern. The Criteria Document (U.S. EPA, 1991, p. 9-21) concludes that
the best all around model for predicting COHb levels is the Coburn,
Forster, Kane (CFK) differential equation (Coburn et al., 1965). The
CFK model estimates COHb levels resulting from exposure to CO
concentrations as a function of time and various physiological and
environmental factors (e.g., blood volume, endogenous CO production
rate, ventilation rate, altitude).
Over the last 20 years, modelers have developed and evaluated both
linear and nonlinear solutions to the CFK model. The linear CFK model
assumes that O2Hb is constant and does not vary with COHb level.
The nonlinear CFK model incorporates the interdependence between
O2Hb and COHb. At COHb levels below 6 percent, both approaches
give estimates that are within 0.5 percent COHb (Smith, 1990). While
the linear CFK model is easier to solve and gives approximately the
same COHb estimate in the range of interest (i.e., 1 to 5 percent
COHb), the nonlinear solution tends to be more accurate physiologically
(U.S. EPA, 1992, p. 12). With the assumption of a linear relationship
between O2Hb and COHb, there is an analytical solution to the nonlinear
CFK equation (Muller and Barton, 1987).
The Staff Paper (U.S. EPA, 1992, p. 13) provides baseline estimates
(i.e., typical physiological parameters are used) of COHb levels
expected to be reached by nonsmokers exposed to various constant
concentrations of CO for either 1 or 8 hours based on the CFK model.
(Smokers are not included because they have voluntarily exposed
themselves to high CO levels.) There are, however, two major
uncertainties involved in estimating COHb levels resulting from
exposure to CO concentrations. First, among the population with
cardiovascular disease, or any other group of interest, there is a
distribution for each of the physiological parameters used in the CFK
model. Past work (Biller and Richmond, 1982) has shown that these
variations are sufficient to produce noticeable deviations from the
COHb levels. Second, predictions based on exposure to constant CO
concentrations can underestimate or overestimate response of
individuals exposed to widely fluctuating CO levels that typically
occur in the ambient environment (Biller and Richmond, 1992).
D. Estimating Population Exposure
The Agency's review includes an analysis of CO exposures expected
to be experienced by residents of Denver, Colorado, under air quality
scenarios related to the current situation when the 8-hour CO NAAQS is
just attained. (The 8-hour CO NAAQS is modeled because it is the
``controlling standard'' in Denver and in every other U.S.
nonattainment area for CO.) The analysis includes passive smoking and
gas stove CO emissions as indoor sources of CO pollution. However, it
does not include other less-common CO sources (e.g., wood stoves,
fireplaces, and faulty furnaces). Although these sources of exposure
may be of concern for such high risk groups as individuals with
cardiovascular disease, pregnant women, and their unborn children, the
contribution of indoor sources cannot be effectively mitigated by
ambient air quality standards. The exposure analysis is abstracted in
the Staff Paper (U.S. EPA, 1992) and reported in more complete form in
Johnson et al. (1992).
The analysis indicates that if the current 8-hour standard is
attained, the proportion of the nonsmoking population with
cardiovascular disease experiencing exposures at or above 35 ppm for 1
hour and 9 ppm for 8 hours decreases by an order of magnitude or more,
down to less than 1 percent of the total person-days in that
population. Likewise, attaining the current 8-hour standard reduces the
proportion of the nonsmoking cardiovascular-disease population person
days at or above COHb levels of concern by an order of magnitude or
more. At the 8-hour standard, the EPA estimates that fewer than 0.1
percent of the nonsmoking cardiovascular-disease population would
experience a COHb level 2.1 percent (U.S. EPA, 1992, p.
40). A smaller population is estimated to exceed higher COHb
percentages.
E. Decision on the Primary Standards
Based on this assessment, and considering the 1985 review of
similar CO effects and effects levels, the Administrator concludes that
the evaluation of adequacy of the current CO standards should focus on
reducing the number of individuals with cardiovascular disease from
being exposed to CO levels in the ambient air that would result in COHb
levels of 2.1 percent or greater. Standards that protect against COHb
levels at the lower end of the range should provide an adequate margin
of safety against effects of uncertain occurrence, as well as those of
clear concern that have been associated with COHb levels in the upper-
end of the range.
Based on the exposure analysis results described above, the
Administrator concludes that relatively few people of the
cardiovascular sensitive population group analyzed will experience COHb
levels 2.1 percent when exposed to CO levels in the absence
of indoor sources when the current ambient standards are attained. The
analysis also indicates, however, that certain indoor sources (e.g.,
passive smoking, gas stove usage) contribute to total CO exposure. In
addition, other indoor CO sources such as wood stoves and fireplaces
also contribute to total CO exposure, but they were not explicitly
modeled. Although these sources of exposure may be of concern for such
high risk groups as individuals with cardiovascular disease, pregnant
women, and their unborn children, the contribution of indoor sources
cannot be effectively mitigated by ambient air quality standards.
When the EPA promulgated CO primary NAAQS on April 30, 1971 (36 FR
8186), two averaging times--1-hr and 8-hr--were selected. The 8-hr
standard was chosen because most individuals, even at rest, appear to
approach equilibrium levels of COHb after 8 hours of exposure. In
addition the 8-hr period approximates blocks of time for which people
are often exposed in a particular location or activity (e.g., sleeping,
working) and provides a good indicator for tracking continuous
exposures that occur during any 24-hr period. The 1-hr standard was
chosen because a 1-hr averaging period provides a better indicator of
short-term health effects of CO. The 1-hr standard provides reasonable
protection from effects which might be encountered from very short
duration peak (bolus) exposures in the urban environment. Review of
current scientific information in the Criteria Document (U.S. EPA,
1991) indicates that these reasons for choosing averaging times for the
CO standards remain valid and there are no compelling arguments for
selecting new or different averaging times. The Administrator also
considered and concurs with the staff recommendations contained in the
Staff Paper (U.S. EPA, 1992) that both averaging times be retained for
primary CO standards.
For the above reasons, the Administrator determines under section
109(d)(1) that revisions of the current 1-hr (35 ppm) and 8-hr (9 ppm)
primary standards for CO are not appropriate at this time. As discussed
more fully above, this determination is based on and completes the
EPA's review of the health effects information contained in the final
Criteria Document (U.S. EPA, 1991), the assessment in the final Staff
Paper (U.S. EPA, 1992), and comments made by the CASAC (McClellan,
1991, 1992).
IV. Final Decision Not To Revise the Standards
The EPA has completed its review and revision of the air quality
criteria document concerning the national primary and secondary air
quality standards for CO and has made a final decision pursuant to CAA
section 109(d)(1) that no revision of the standards for CO is
appropriate. This decision is a final Agency action based on a
determination of nationwide scope and effect. It is, therefore, subject
to judicial review under CAA section 307(b) exclusively in the U.S.
Court of Appeals for the District of Columbia Circuit. Any petition for
judicial review of this final action must be filed within sixty days
after August 1, 1994.
V. Regulatory Impacts
A. Regulatory Impact Analysis
Under Executive Order 12866 [58 FR 51,735 (October 4, 1993)], the
Agency must determine whether the regulatory action is ``significant''
and, therefore, subject to Office of Management and Budget (OMB) review
and the requirements of the Executive Order. The Order defines
``significant regulatory action'' as one that is likely to result in a
rule that may:
(1) have an annual effect on the economy of $100 million or more or
adversely affect in a material way the economy, a sector of the
economy, productivity, competition, jobs, the environment, public
health or safety, or State, local, or tribal governments or
communities;
(2) create a serious inconsistency or otherwise interfere with an
action taken or planned by another Agency;
(3) materially alter the budgetary impact of entitlements, grants,
user fees, or loan programs or the rights and obligations or recipients
thereof; or
(4) raise novel legal or policy issues arising out of legal
mandates, the President's priorities, or the principles set forth in
the Executive Order.''
Pursuant to the terms of Executive Order 12866, the OMB has
notified the EPA that this action is a ``significant regulatory
action'' within the meaning of the Executive Order. For this reason,
this action was submitted to the OMB for review. Changes made in
response to the OMB suggestions or recommendations will be documented
in the public record.
B. Impact on Small Entities
Under the Regulatory Flexibility Act (RFA), 5 U.S.C. 601 et seq.,
the EPA must prepare initial and final regulatory flexibility analyses
assessing the impact of certain decisions on small entities. These
requirements are inapplicable to rules or other actions for which the
EPA is not required by the Administrative Procedure Act (APA), 5 U.S.C.
551 et seq., or other law to publish a notice of proposed rulemaking
[(5 U.S.C. 603(a), 604(a)]. Under section 307(d) of the Act, as the EPA
interprets it, neither the APA nor the Act requires rulemaking
procedures where the Agency decides to retain existing NAAQS without
change. Accordingly, the EPA has determined that the impact assessment
requirements of the RFA are inapplicable to this final decision.
VI. Other Reviews
This decision was submitted to the OMB for review. Comments from
the OMB and the EPA's responses to these comments are available for
public inspection at the EPA's Air and Radiation Docket Information
Center (Docket No. A-93-05), South Conference Center, Room 4, Waterside
Mall, 401 M Street, S.W., Washington, DC.
List of Subjects in 40 CFR Part 50
Environmental protection, Air pollution control, Carbon monoxide,
Ozone, Sulfur oxides, Particulate matter, Nitrogen dioxide, Lead.
Dated: July 15, 1994.
Carol M. Browner,
Administrator.
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[FR Doc. 94-18659 Filed 7-29-94; 8:45 am]
BILLING CODE 6560-50-P