EPA-600/8-79-0221
October 1979
Special Series
AIR QUALITY CRITERIA
FOR CARBON MONOXIDE
(PREPRINT)
Environmental Criteria and Assessment Office
Office of Health and Environmental Assessment
Office of Research and Development
U.S. Environmental Protection Agency
D.C. 20460
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EPA-600/8-79-022
October 1979
AIR QUALITY CRITERIA
FOR
CARBON MONOXIDE
(Preprint)
U.S. ENVIRONMENTAL PROTECTION AGENCY
Environmental Criteria and Assessment Office
Office of Health and Environmental Assessment
Office of Research and Development
Washington, B.C. 20460
-------
NOTICE
This document is available through the Library Services Office,
MD-35, Environmental Protection Agency, Research Triangle Park, NC, 27711.
It 1s also available from the Superintendent of Documents, U.S. Government
Printing Office, Washington, DC, 20402. Correspondence relating to the
subject matter of the document should be directed to:
Project Officer for Carbon Monoxide
Environmental Criteria and Assessment Office (MD-52)
Environmental Protection Agency
Research Triangle Park, NC 27711
11
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PREFACE
This document has been prepared pursuant to Section 108(c) of the
Clean Air Act, as amended, which requires that the Administrator from
time to time review and, as appropriate, modify and reissue criteria
issued pursuant to Section 108(a). Air quality criteria are required by
Section 108(a) to reflect accurately the latest scientific information
useful in indicating the kind and extent of all identifiable effects on
public health and welfare which may be expected from the presence of a
pollutant in the ambient air, in varying quantities.
The original criteria document for carbon monoxide was issued
in 1970. Since that time new information has been developed, and this
document represents the modification and reissuance of the air quality
criteria for carbon monoxide.
The regulatory purpose of these criteria is to serve as the basis
for national ambient air quality standards promulgated by the Administrator
under Section 109 of the Clean Air Act, as amended. Accordingly, as
provided by Section 109(d), the Administrator has reviewed the national
ambient air quality standards for carbon monoxide based on these revised
criteria and is proposing appropriate action with respect to those
standards concurrently with the issuance of this document.
The Agency is pleased to acknowledge the efforts and contributions
of all persons and groups who have contributed, as participating authors
or reviewers, to this document. In the last analysis, however, the
Environmental Protection Agency is responsible for its content.
iii
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The studies and data cited comprise the best available basis for
specific standards aimed at protecting human health and the environment
from carbon monoxide (CO) in ambient air. Various natural processes
such as forest fires, oxidation of atmospheric methane, and biological
3
activities maintain a CO background concentration of about 0.05 mg/m
(0.044 ppm). Additional CO from urban and industrial sources increases
3
global concentrations to approximately 0.2 mg/m (0.18 ppm) in the
3
northern hemisphere and to approximately 0.06 mg/m (0.05 ppm) in the
southern hemisphere. Within heavily populated areas such as cities,
much higher concentrations of CO are found as a result of the local
combustion of fossil fuels.
Carbon monoxide is a normal constituent of plant life, which both
metabolizes and produces CO. It has been shown that adverse effects of
CO to plants and various microorganisms require relatively high levels,
considerably greater than those required for adverse health effects in
animals and humans.
In mammals, endogenous sources of CO from metabolic activities
result in levels of blood carboxyhemoglobin (COHb) of about 0.5 percent.
Inhalation of CO from the ambient air may increase COHb to toxic levels,
due to the greater affinity of hemoglobin for CO than for oxygen, thus
creating a lowered oxygen concentration in blood and tissues. Reductions
of blood oxygen content caused by 5-10 percent COHb may be critical for
patients suffering from cardiovascular diseases or chronic obstructive
lung disease.
iv
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Experimental animal studies have indicated deleterious effects upon
the central nervous and cardiovascular systems. Adverse behavioral and
central nervous system effects have been demonstrated at levels of
12-20 percent COHb, while adverse cardiovascular effects have been
demonstrated at levels as low as 4-7 percent COHb.
3
Human exposures to concentrations of CO as low as 17-21 mg/m
(15-18 ppm) for eight hours, resulting in 2.5-3.0 percent COHb,
adversely affects cardiovascular systems. Carbon monoxide exposures
of 29-34 mg/m3 (25-30 ppm) for eight hours, resulting in COHb levels
of 4-6 percent, have been shown to affect the central nervous systems of
humans.
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ABSTRACT
This document is an evaluation and assessment of scientific
information relative to determination of health and welfare experts
associated with exposure to various concentrations of carbon monoxide in
ambient air. The document is not intended as a complete, detailed
literature review. It does not cite every published article relating to
carbon monoxide in the environment and their effects. The literature
through 1978 has been reviewed thoroughly for information relative to
criteria. An attempt has been made to identify the major discrepancies
in our current knowledge, again relative to criteria.
Though the emphasis is on presentation of health and welfare effects
data, other scientific data are presented and evaluated in order to
provide a better understanding of the pollutants in the environment.
To this end, separate chapters are included which discuss properties and
principles of formation, emissions, analytical methods of measurement,
observed ambient concentrations, the global cycle, effects on vegetation
and microorganisms, mammalian metabolism, effects on experimental animals,
and effects on humans.
vi
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TABLE OF CONTENTS
LIST OF FIGURES
LIST OF TABLES
LIST OF ABBREVIATIONS AND SYMBOLS
1. SUMMARY AND CONCLUSIONS 1-1
1.1 INTRODUCTION 1-1
,1.2 PROPERTIES AND PRINCIPLES OF FORMATION OF
CARBON MONOXIDE 1-2
1.3 ESTIMATION OF CARBON MONOXIDE EMISSIONS FROM
TECHNOLOGICAL SOURCES 1-2
,1.4 ANALYTICAL METHODS 1-3
,1.5 CARBON MONOXIDE CONCENTRATIONS IN AMBIENT AIR 1-4
1.6 THE GLOBAL CYCLE OF CARBON MONOXIDE 1-6
1.7 EFFECTS OF CARBON MONOXIDE ON VEGETATION AND
CERTAIN MICROORGANISMS 1-7
1.8 METABOLISM OF CARBON MONOXIDE IN MAMMALS 1-8
1.9 EFFECTS OF CARBON MONOXIDE ON EXPERIMENTAL
ANIMALS 1-9
1.10 EFFECTS OF LOW-LEVEL CARBON MONOXIDE EXPOSURE
ON HUMANS 1-10
2. INTRODUCTION 2-1
3. PROPERTIES AND PRINCIPLES OF FORMATION OF
CARBON MONOXIDE 3-1
3.1 INTRODUCTION 3-1
3 2 PHYSICAL PROPERTIES 3-2
3.3 GASEOUS CHEMICAL REACTIONS OF CARBON MONOXIDE 3-3
3.4 PRINCIPLES OF FORMATION^ 3-7
3.4.1 General Combustion Processes 3-10
3.4.2 Combustion Engines 3-11
3.4.2.1 Mobile Combustion Engines 3-11
3.4.2.2 Internal Combustion Engines -
(Gasoline Fueled, Spark-
Ignition Engines) 3-11
3.4.2.3 Internal Combustion Engines -
(Diesel Engines) 3-14
3.4.2.4 Stationary Combustion Sources -
(Steam Boilers) 3-14
3.5 NON-COMBUSTION INDUSTRIAL SOURCES 3-15
4. ESTIMATION OF CARBON MONOXIDE EMISSIONS FROM
TECHNOLOGICAL SOURCES 4-1
4.1 NATIONAL EMISSION LEVELS 4-2
vii
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4.2 EMISSIONS AND EMISSION FACTORS BY SOURCE TYPE 4-6
4.2.1. Mobile Combustion Sources 4-6
4.2.2 Combustion for Power and Heat 4-7
4.2.3 Technological Processes Producing CO 4-8
4.2.4 Solid Waste Combustion 4-8
4.2.5 Miscellaneous Combustion 4-8
4.3 ESTIMATION OF FUTURE EMISSION LEVELS 4-9
5. ANALYTICAL METHODS FOR MEASUREMENT OF CARBON MONOXIDE .. 5-1
5.1 INTRODUCTION 5-1
5.1.1 Overview of Techniques for Measurement
of CO in Air 5-2
5.1.2 Calibration Requirements 5-3
5.2 PREPARATION OF CARBON MONOXIDE GAS STANDARDS 5-3
5.2.1 Gravimetric Method 5-3
5.2.2 Volumetric Gas Dilution Methods 5-5
5.2.3 Other Methods 5-7
5.3 MEASURING CARBON MONOXIDE IN AIR 5-8
5.3.1 Sampling Techniques 5-8
5.3.2 Sampling Schedules 5-16
5.3.3 Recommended Analytical Methods for
CO Measurements 5-18
5.3.4 Continuous Measurement Methods 5-21
5.3.4.1 Nondispersive Infrared Photometry.. 5-21
5.3.4.2 Gas Chromatography - Flame
lonization 5-24
5.3.4.3 Electrochemical Analyzers 5-25
5.3.4.3.1 Controlled-potential
Electrochemical Analysis. 5-25
5.3.4.3.2 Galvanic Analyzer 5-26
5.3.4.3.3 Coulometric Analyzer ... 5-27
5.3.4.4 Mercury Replacement 5-27
5.3.4.5 Dual Isotope Fluorescence 5-29
5.3.4.6 Catalytic Combustion-Thermal
Detection 5-29
5.3.4.7 Second-Derivative Spectrometry 5-30
5.3.4.8 Fourier Transform Spectroscopy 5-30
5.3.4.9 Gas Filter Correlation Spectroscopy. 5-31
5.3.5 Intermittent Analysis 5-32
5.3.5.1 Colorimetric Analysis 5-32
5.3.5.1.1 Colored Silver Sol Method. 5-32
5.3.5.1.2 National Bureau of
Standards Colorimetric
Indicating Gel 5-33
5.3.5.1.3 Length-of-stain Indicator
Tube 5-33
5.3.5.2 Frontal Analysis 5-34
V111
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6.
5.4 MEASURING CARBON MONOXIDE IN BLOOD
5. 4. 1 Other Methods
5.4.1.1 Gasometric
5.4.1.2 Infrared Spectrometry
5.4.1.3 Catalytic Oxidation
5.4.1.4 Electrochemical Sensors
5.4.1.5 Gas Chromatography
5.4.1.6 Colorimetric Palladium Chloride
Reacti on
5.4.2 Equilibrium Methods
OBSERVED CARBON MONOXIDE CONCENTRATIONS
6.1
6.2
6.3
6.4
6.5
6.6
6.7
THE
7.1
7.2
SITE SELECTION
UNITED STATES DATA BASE
TECHNIQUES OF DATA ANALYSIS
6. 3.1 Introduction
6.3.2 Calculation of Population Statistics
6.3.3 Frequency Analysis
6.3.4 Comparing CO Data to National
Ambient Air Quality Standards
6.3.5 Averaging Time Analysis
6. 3.6 Trend Analyses
6.3.7 Special Analyses
URBAN LEVELS OF CARBON MONOXIDE
6.4.1 Comparison to NAAQS
6. 4. 2 Hourly Patterns
6.4.3 Seasonal Patterns
6.4.4 Annual Patterns
SPECIAL CARBON MONOXIDE EXPOSURE SITUATIONS
6.5.1 Variations with Type of Vehicle Traffic
6.5.2 Car Passenger Exposure to Carbon Monoxide ..
6.5.3 Occupational Exposure
6.5.4 Indoor Carbon Monoxide Exposure
EFFECTS OF METEOROLOGY AND TOPOGRAPHY
CARBON MONOXIDE DISPERSION MODELS
GLOBAL CYCLE OF CARBON MONOXIDE
INTRODUCTION
GLOBAL SOURCES
7.2.1 Technological Sources
7.2.2 Natural Sources
7.2.2.1 Forest Fires and Agricultural
Burni ng
7.2.2.2 Carbon Monoxide Production from
Oceans
7.2.2.3 Oxidation of Natural Hydrocarbons .
7.2.2.4 Emission by Plants
5-34
5-35
5-40
5-41
5-41
5-41
5-41
5-42
5-42
6-1
6-1
6-8
6-13
6-13
6-14
6-18
6-18
6-20
6-20
6-22
6-26
6-26
6-28
6-33
6-33
6-46
6-47
6-48
6-49
6-50
6-53
6-61
7-1
7-1
7-2
7-2
7-4
7-4
7-4
7-5
7-5
IX
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7.2.2.5 Methane Oxidation ^7-6
7.2.2.6 Other Natural Sources 7-9
7.3 BACKGROUND LEVELS AND FATE OF CARBON MONOXIDE 7-10
7.3.1 Measured Background Levels of Carbon
Monoxide 7-10
7.3.1.1 Geographic Distribution 7-10
7.3.1.2 Variation with Height 7-12
7.3.1.3 Diurnal and Seasonal Variation .... 7-15
7.3.2 Residence Time and Removal Mechanisms of
Atmospheric CO 7-16
7.3.2.1 Carbon Monoxide Residence Time 7-16
7.3.2.2 Removal Processes for Carbon
Monoxide 7-17
7.3.2.2.1 The Stratosphere as a
Sink for Tropospheric
CO 7-17
7.3.2.2.2 Soil as a Sink 7-18
7.3.2.2.3 Vegetation 7-19
7.3.2.2.4 Reaction with Hydroxyl . 7-20
7.3.2.2.5 Other Removal Processes. 7-22
7.4 SUMMARY 7-22
8. EFFECTS OF CARBON MONOXIDE ON VEGETATION AND
SOIL MICROORGANISMS 8-1
8.1 INTRODUCTION 8-1
8.2 EFFECTS OF CARBON MONOXIDE ON PLANTS 8-2
8.2.1 Visible Symptoms 8-2
8.2.2 Growth, Yield, and Reproduction 8-4
8.2.3 Biochemical and Physiological Processes 8-6
8.2.3.1 Photosynthesis 8-8
8.2.3.2 Nitrogen Fixation 8-8
8.3 REMOVAL OF CO FROM THE ENVIRONMENT 8-10
8.3.1 Plants 8-11
8.3.2 Soil Microorganisms .A 8-13
8.4 PRODUCTION OF CO BY PLANTS 8-14
8.5 SUMMARY 8-16
9. METABOLISM OF CARBON MONOXIDE IN MAMMALS 9-1
9.1 INTRODUCTION 9-1
9.2 THEORETICAL CONSIDERATIONS 9-3
9.3 ABSORPTION, EXCRETION, AND EQUILIBRATION 9-14
9.4 DISTRIBUTION IN BODY TISSUES 9-23
9.5 SUMMARY 9-25
10. EFFECTS OF CO ON EXPERIMENTAL ANIMALS 10-1
10.1 INTRODUCTION 10-1
10.2 SELECTION OF ANIMAL MODELS 10-2
10.3 NERVOUS SYSTEM AND BEHAVIOR 10-4
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10.3.1 General Activity and Sleep 10-4
10.3.2 Learning and Performance 10-5
10.3.3 Electrophysiological Effects 10-7
10.3.4 Cerebral Blood Supply 10-8
10.3.5 CMS Pathology and
Biochemical Alterations 10-9
10.3.6 Summary and Conclusion of Nervous System
and Behavior in Experimental Animals 10-11
10.4 CARDIOVASCULAR SYSTEMS 10-19
10.4.1 Cardiac Performance and Damage 10-20
10.4.2 Cardiac Fibrillation Threshold 10-22
10.4.3 Cholesterol and Sclerosis 10-23
10.4.4 Coronary Blood Flow 10-24
10.4.5 Hemoglobin 10-25
10.4.6 Summary and Conclusion of Cardiovascular
System in Experimental Animals 10-27
10.5 OTHER DEPENDENT VARIABLES 10-35
10.5.1 Feeding, Drinking, and Body Weight 10-35
10.5.2 Biochemical Effects and Drugs 10-36
10.5.3 Miscellaneous 10-37
10.5.4 Summary and Conclusions of Other Dependent
Variables in Experimental Animals 10-37
10.6 INTERACTIONS WITH OTHER POLLUTANTS, DRUGS, AND
OTHER FACTORS 10-41
10.6.1 Other Pollutants 10-42
10.6.2 Drugs 10-43
10.6.3 Halogenated Hydrocarbons 10-44
10.6.4 Other Variables 10-44
10.6.5 Conclusions About Interactions 10-45
10. 7 MECHANISMS r. 10-45
10.7.1 Hypoxic Hypoxia and CO
Hypoxi a 10-46
10.7.2 Elimination of Hemoglobin 10-49
10.7.3 Conclusions About Mechanisms 10-50
10.8 ADAPTATION, HABITUATION, AND/OR COMPENSATORY
MECHANISMS 10-50
10.8.1 Adaptation (Long-term) 10-51
10.8.2 Habituation (Short-term) 10-53
10.9 SUBJECTS OF SPECIAL RISK 10-55
10.9.1 Fetus and Uterine Exposure 10-55
10.9.2 Impaired Groups 10-56
10.9.3 Drugs 10-57
10.9.4 Unadapted Populations 10-58
10.10 SUMMARY 10-58
xi
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Page
11. EFFECTS OF LOW-LEVEL CO EXPOSURE ON HUMANS 11-1
11.1 INTRODUCTION 11-1
11.2 NERVOUS SYSTEM AND BEHAVIOR 11-4
11.2.1 Sleep and Activity 11-5
11.2.2 Vigilance 11-5
11.2.3 Sensory and Time Discriminations 11-8
11.2.4 Complex Sensorimotor Tasks and Driving ... 11-10
11.2.5 Central Nervous System Electrical Activity. 11-13
11.2.6 Conclusions and Discussion of Nervous
System and Behavior in Humans 11-14
11.3 CARDIOVASCULAR SYSTEMS 11-21
11.3.1 Cardiovascular Damage and EKG
Abnormalities 11-21
11.3.2 Blood Flow and Related Variables 11-23
11.3.3 Angina 11-25
11.3.4 Epidemiological Evidence 11-28
11.3.5 Conclusions and Discussion 11-29
11.4 PULMONARY FUNCTION AND EXERCISE 11-34
11.4.1 Maximal Work 11-34
11.4.2 07 Uptake and Heart Rate 11-34
11.4.3 Aerobic Capacity 11-36
11.4.4 Conclusion and Discussion 11-42
11.5 INTERACTIONS WITH OTHER POLLUTANTS AND DRUGS 11-42
11.5.1 Other Air Pollutants 11-42
11.5.2 Other Environmental Parameters 11-48
11.5.3 Alcohol 11-49
11.5.4 Smoking 11-49
11.5.5 Conclusions and Discussion < 11-56
11.6 HIGH ALTITUDES - MECHANISMS 11-58
11.6.1 Physiological Results 11-58
11.6.2 Behavioral and Central Nervous System 11-61
11.6.3 Conclusions and Discussion of Carbon
Monoxide and High Altitude Combinations .. 11-62
11.7 ADAPTATION, HABITUATION AND COMPENSATORY
MECHANISMS 11-63
11.7.1 Adaptation and Other Long-Term Effects ... 11-63
11.7.2 Habituation and Short-Term Effects 11-65
11.8 SPECIAL GROUPS AT RISK 11-66
11.8.1 Fetus 11-66
11.8.2 Impaired Groups 11-69
11.8.3 Drugs 11-72
11.8.4 Unadapted Individuals 11-72
11.8.5 Occupational 11-73
11.9 SUMMARY 11-82
APPENDIX A. Glossary.
xii
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LIST OF FIGURES
Figure Page
3-1 Effect of air-fuel ratio on exhaust gas carbon
monoxide concentrations from three test engines ... 3-13
4-1 Average composite emission factors for carbon
monoxide 4-11
5-1 Loss of carbon monoxide with time in mild steel
cyl i nders 5-6
5-2 Carbon monoxide monitoring system 5-9
5-3 SAROAD hourly data form 5-14
5-4 Schematic diagram of typical nondispersive infrared
CO analyzer 5-22
6-1 Annual average CO levels in Los Angeles 6-12
6-2 Histogram of 1-hour average CO concentrations 6-15
6-3 Cumulative frequency distribution of 1-hour average
CO concentrations 6-16
6-4 Concentration vs. averaging time and frequency for
carbon monoxide from 12/1/63 to 12/1/68 at
site 662, St. Louis 6-21
6-5 Predicted 1-hour average ambient CO concentrations
(mg/m ) in the vicinity of 1-85 in Atlanta,
Georgia, for 1976 6-23
6-6 Measured 8-hour average background CO concentrations
in Memphis, Tennessee 6-24
6-7 Pollution rose for St. Louis, Missouri 6-25
6-8 Status of carbon monoxide levels, 1973 6-27
6-9 Hourly variations of ambient CO concentrations
for Baltimore, MD 6-29
6-10 Hourly variations of ambient CO concentrations
for Denver, CO 6-30
6-11 Hourly variations of ambient CO concentrations
for Los Angel es, CA 6-31
6-12 Hourly variations of traffic volume 6-32
6-13 Seasonal variations of ambient CO concentrations
for Baltimore, MD 6-34
6-14 Seasonal variations of ambient CO concentrations
for Denver, CO 6-35
6-15 Seasonal variations of ambient CO concentrations
for Los Angel es, CA 6-36
6-16 Annual variations of ambient CO concentrations for
Baltimore, MD 6-37
6-17 Annual variations of ambient CO concentrations for
Denver, CO, SAROAD site #060580002 (former CAMP
station) 6-38
xiii
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Figure Page
6-18 Annual variations of ambient CO concentrations for
Los Angeles, CA, SAROAD site #053900001 6-39
6-19 Annual variations of ambient CO concentrations for
Chicago, IL, SAROAD site #141220002 (former CAMP
station) 6-40
6-20 Annual variations of ambient CO concentrations for
Cincinnati, OH, SAROAD site #361220003 (former
CAMP station discontinued in 1973) 6-41
6-21 Annual variations of ambient CO concentrations for
Philadelphia, PA, SAROAD site #397140002 (former
CAMP station) 6-42
6-22 Annual variations of ambient CO concentrations for
St. Louis, MO, SAROAD site #264280002 (former
CAMP station discontinued in 1973) 6-43
6-23 Annual variations of ambient CO concentrations for
Washington, DC, SAROAD site #090020002 moved in
1969 and redesignated #090020003 (former CAMP
station) 6-44
6-24 Effect of terrain roughness on the wind speed
profile 6-55
6-25 Schematic representation of an elevated inversion ... 6-58
6-26 Hourly variations in inversion height and wind speed
for Los Angel es i n summer 6-60
6-27 Area segment scheme for spatial partitioning of
emissions 6-64
6-28 Normalized concentrations versus normal distance
from the road edge for perpendicular wind
conditions for B and E atmospheric stability
category 6-67
6-29 Normalized concentration versus normal distance to
the road edge for parallel wind conditions for
B and E atmospheric stability category 6-68
7-1 Latitude distribution of carbon monoxide 7-11
7-2 Latitudinal profiles of carbon monoxide 7-14
7-3 Carbon monoxide photochemical production and
destruction rates as a function of average OH
concentration 7-21
9-1 Oxygen dissociation curve with and without the
presence of varying concentrations of CO 9-5
9-2 Blood oxygen dissociation curves at various
COHb val ues 9-6
9-3 Exposure duration, ambient carbon monoxide
concentrations (resting individuals) 9-16
9-4 Exposure duration, ambient carbon monoxide
concentrations (exercising individuals) 9-19
xiv
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Figure Page
11-1 The maintenance of requested COHb level 1n a subject
during rest and at various work levels with a
widely ranging ventilatory exchange. Control
level of COHb was 0.6% prior to the administration
of the initial bolus of CO to raise COHb to desired
level; a total of 34.2 ml of CO STPD was given 11-39
11-2 Relationship between COHb and decrement in maximum
aerobic power 11-41
11-3 Pattern of change in COHb in a typical cigarette
smoker 11-53
xv
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LIST OF TABLES
Table Page
3-1 Physical properties of carbon monoxide 3-4
3-2 Reported room temperature rate constants for
the reaction of OH radicals with CO 3-6
3-3 Automobile emission control schedules 3-9
4-1 Summary of National emission estimates, 1970-1977 4-3
4-2 Nationwide emission estimates, 1977 4-4
4-3 Nationwide carbon monoxide emission estimates,
1970-1977 4-5
4-4 Average vehicle emission factors for two selected
highway scenarios 4-10
5-1 Performance specifications for automated analytical
methods for carbon monoxide 5-19
5-2 Comparison of representative techniques for
analysis of CO in blood 5-36
6-1 Recommended criteria for siting monitoring stations .. 6-4
6-2 Specific probe exposure criteria 6-5
6-3 Suggested priorities of carbon monoxide monitoring
sites 6-7
6-4 Status of CO monitoring in 1977 6-12
7-1 Global carbon monoxide source strength estimates 7-8
8-1 Effects of CO on pi ants 8-7
8-2 Carbon monoxide effects on nitrogen fixation by
micro-organi sms 8-9
8-3 Production and utilization of CO by plants and
micro-organisms 8-12
8-4 Soils as a sink for carbon monoxide 8-15
9-1 Percent COHb versus CO pressure 9-23
10-1 Summary of effects of CO on central
nervous system and behavior of animals 10-12
10-2 Summary of effects of carbon monoxide on
cardiovascular systems of animals 10-28
10-3 Summary of CO effects upon metabolism 10-38
11-1 Summary of data on effects of CO on human behavior
and CNS 11-15
11-2 Exercise-induced angina and carbon monoxide 11-27
11-3 Summary of data on effects of CO on human
cardiovascular system 11-30
11-4 Summary of data on effects of CO on human pulmonary
function and exercise 11-43
11-5 Approximate physiologically equivalent altitudes
at equilibrium with ambient CO levels 11-59
xvi
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Table Page
11-6 Carbon monoxide emission estimates - 1968 11-74
11-7 Average percent of carboxyhemoglobin saturation
in smokers and non-smokers in St. Louis 11-75
11-8 Average percent of carboxyhemoglobin saturation 11-75
11-9 Estimated health effects levels for carbon monoxide
exposure 11-85
xv 11
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ABBREVIATIONS AND SYMBOLS
o
*A
*(A-aDn
U
AEROS
A/F
Amthauer's I.S.T.
AQCR
Ar
ASHD
BCG
8C
CAMP
CBF
CFFF
CHA
CHI)
Cm3
cm
CNS
CNV
CO
C09
CORb
COMb
CV
DCM
dl
dm
ECG
EDTA
EKG
PA
H
HCN
He
hg
Hg
HgO
hv
Angstrom
Alveolar-artery pressure difference in Op
Aerometric and Emissions Reporting System
Air to fuel ratio
Amthauer's Intelligence Structure Test
Air Quality Control Regions
Argon
Arteriosclerotic heart disease
Bal1i stocardiogram
Degrees Centigrade (Celsius)
Continuous Air Monitoring Program
Cerebral blood flow; also coronary blood flow
Critical flicker fusion frequency
Methane
Coronary heart disease
Centimeter
Cubic centimeters
Central nervous system
Contingent negative variation
Carbon monoxide
Carbon dioxide
Carboxyhemoglobi n
Carboxymyoglobin
Coefficient of variation; standard deviation divided
by the mean
Dichloromethane; Methylene chloride;
Deciliter
Decimeter
Echocardiogram
Ethylene-diaminetetraacetic acid, often used as
the disodium salt.
Electrocardi ogram
Environmental Protection Agency
Degrees Fahrenheit
Gram
Molecular hydrogen
Hemoglobin
Hydrocyanic acid
Helium
Hectogram (100 g)
Mercury
Mercuric oxide
The product of Planck's constant times the frequency
of radiated energy (v) = quantum of energy (E).
The amount of energy contained in a unitary particle
of light of frequency v.
CH2C1£
xvm
-------
H0
kg
kJ/mol
km
Kr
LDH
M
m
Mb
MetHb
mg/m
ml
N&AQS
NADB
NBS
NDIR
nm
N09
N90
°
09Hb
P
°2
ppb
ppm
psi
REM
SAROAD
SF
Sll
SRM
VER
VMT
*V
0
2 max
A'
*(V/Q)
Water
Iodine pentoxide
Chemical reaction rate constant
Ki 1 ogram
Kilo joules per mole
Ki 1 ometer
Krypton
Lactate dehydrogenase
Haldane constant (in relation to carboxyhemoglobin);
or, in atmospheric chemistry, an inert molecule or
particle which participates in a chemical reaction
Meter
Myoglobin
Methemoglobin
Microgram
Milligrams per cubic meter
Mill iHter
Molecular nitrogen
National Ambient Air Quality Standards
National Aerometric Data Bank
National Bureau of Standards
Non-dispersive infrared photometry
Nanometer
Nitrogen dioxide
Nitrous oxide; "laughing gas"
Molecular oxygen
Ozone
Hydroxyl radical
Oxyhemoglobin
Carbon monoxide partial pressure
Oxygen partial pressure
Parts per billion
Parts per million
Pounds per square inch
Rapid eye movement
Storage and Retrieval of Aerometric Data
Sulfur hexafluoride
State Implementation Plans
Standard Reference Materials
Visual evoked response
Vehicle miles travelled
Maximal aerobic capacity
Ventilation perfusion ratio
2,3-DPG 2,3 - Diphosphoglycerate
"appears in text as: 8, A-aDQ2, PQ2, VQ2 max, and VA/Q
xix
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CONTRIBUTORS AND REVIEWERS
The following persons were contributing authors to the document.
Dr. David J. McKee, Environmental Criteria and Assessment Office,
Environmental Research Center, U. S. Environmental Protection
Agency, Research Triangle Park, North Carolina 27711.
Mr. Ronald E. Bales, Consultant, Informatics, Inc., Rockvllle, Maryland
20852.
Dr. Vernon A. Benlgnus, Clinical Studies Branch, U. S. Environmental
Protection Agency, Building 224H, University of North Carolina,
Chapel H111, North Carolina 27514.
Dr. Jack Fishman, National Center for Atmospheric Research, Boulder,
Colorado 80307, and Colorado State University.
Dr. J. H. B. Garner, Environmental Criteria and Assessment Office,
Environmental Research Center, U. S. Environmental Protection
Agency, Research Triangle Park, North Carolina 27711.
Dr. Steven M. Horvath, Institute of Environmental Stress, University of
California at Santa Barbara, California 93106.
Dr. Terry L. Miller, Enviro-Measure, Inc., Knoxville, Tennessee 37917.
Dr. Robert W. Rogers, Informatics, Inc., Rockvllle, Maryland 20852.
Dr. Martha Sager, Department of Environmental Systems Management,
The American University, Washington, D. C. 20016.
Dr. Alfred Weissler, Consultant, Informatics, Inc., Rockvllle, Maryland
20852.
The following persons served on the EPA task force and/or were responsible
for the review and preparation of this document.
Dr. David J. McKee, Task Force Chairman, Environmental Criteria and
Assessment Office, Environmental Research Center, U. S.
Environmental Protection Agency, Research Triangle Park,
North Carolina 27711.
xx
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Mr. Michael A. Berry, Environmental Criteria and Assessment Office,
Environmental Research Center, U. S. Environmental Protection
Agency, Research Triangle Park, North Carolina 27711.
Dr. Robert M. Bruce, Environmental Criteria and Assessment Office,
Environmental Research Center, U. S. Environmental Protection
Agency, Research Triangle Park, North Carolina 27711.
Mr. Michael Claggett, Envlro-Measure, Inc., Knoxville, Tennessee 37917.
Ms. Josephine Cooper, Environmental Criteria and Assessment Office,
U. S. Environmental Protection Agency, Research Triangle Park,
North Carolina 27711.
Mr. Thomas C. Curran, Office of Air Quaility Planning and Standards,
MDAD, Durham, North Carolina
Ms. Vandy Duffield, Environmental Criteria and Assessment Office,
Environmental Research Center, U. $. Environmental Protection
Agency, Research Triangle Park, North Carolina 27711.
Mr. Warren P. Freas, Office of Air Quaility Planning and Standards,
AMTB, Durham, North Carolina
Mr. Garry Evans, Environmental Monitoring and Support Laboratory,
U. S. Environmental Protection Agency, Research Triangle Park,
North Carolina 27711.
Dr. Lester D. Grant, Environmental Criteria and Assessment Office,
Environmental Research Center, U. S. Environmental Protection
Agency, Research Triangle Park, North Carolina 27711.
Dr. Robert Norton, Health Effects Research Laboratory,
U. S. Environmental Protection Agency, Research Triangle Park,
North Carolina 27711.
Mr. Alan Hoyt, Environmental Criteria and Assessment Office,
Environmental Research Center, U. S. Environmental Protection
Agency, Research Triangle Park, North Carolina 27711.
Mr. Charles Mann, Office of A1r Quality Planning and Standards,
MDAD, Durham, North Carolina
Mr. Justice Manning, Office of Air Quality Planning and Standards,
SASD, U. S. Environmental Protection Agency, Durham, North Carolina.
Mr. Thomas McMullen, Environmental Criteria and Assessment Office,
U. S. Environmental Protection Agency, Research Triangle Park,
North Carolina 27711.
xx i
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Mr. Edwin L. Meyer, Jr., Office of Air Quality Planning and Standards,
AMTB, Durham, North Carolina.
Mr. John O'Connor, Office of Air Quality Planning and Standards,
U. S. Environmental Protection Agency, Durham, North Carolina.
Mr. Kenneth Rehme, Environmental Monitoring and Support Laboratory, U.
S. Environmental Protection Agency, Research Triangle Park, North
Carolina 27711.
Mr. Harvey Richmond, Office of Air Quality Planning and Standards,
SASD, Durham, North Carolina.
Mr. Jerry Romanovsky, Environmental Sciences Research Laboratory,
Environmental Research Center, U. S. Environmental Protection
Agency, Research Triangle Park, North Carolina 27711.
Mr. S. Z. Shariq, Health Effects Research Laboratory, U. S. Environmental
Protection Agency, Research Triangle Park, North Carolina 27711.
Mr. Jacob G. Summers, Office of Air Quality Planning and Standards,
NADB, Durham, North Carolina.
Ms. Beverly Tilton, Environmental Criteria and Assessment Office,
Environmental Research Center, U. S. Environmental Protection
Agency, Research Triangle Park, North Carolina 27711.
The following persons served as consulting contributors and reviewers
in the preparation of this document.
Dr. Wilbert S. Aronow, Chief, Cardiovascular Section, Veterans Adminis-
tration Hospital, Long Beach, California 90822.
Mr. Lucian Chaney, University of Michigan, Ann Arbor, Michigan 48109.
Dr. C. C. Delwiche, LAWR, Hoagland Hall, University of California at
Davis, California 95616.
Dr. Laurence Fechter, Department of Environmental Health Sciences,
Johns Hopkins University School of Hygiene, Baltimore, Maryland 21205.
Dr. Patrick A. Gorman, George Washington University Medical School,
Washington, D. C. 20037.
Dr. Harvey Jeffries, Department of Environmental Science and Engineering,
School of Public Health, University of North Carolina, Chapel Hill,
North Carolina 27514.
xxii
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Dr. James Kaweckl, University of Maryland, College Park, Maryland 20740.
Dr. Thomas L. Kurt, B-130, Division of Cardiology, University of
Colorado Medical Center, Denver, Colorado 80262.
Dr. Kenneth Noll, Department of Environmental Engineering, Illinois
Institute of Technology, Chicago, Illinois 60616.
Dr. Auguste T. Rossano, Air Resources Program, University of Washington,
Seattle, Washington 98195.
Dr. Wolfgang Seller, National Center for Atmospheric Research, Boulder,
Colorado 80307.
Ms. Kathy Seiple, Department of Environmental Science and Engineering,
School of Public Health, University of North Carolina, Chapel Hill,
North Carolina 27514.
Dr. R. P. Stewart, Department of Environmental Medicine, Medical College
of Wisconsin A-B Laboratory, Milwaukee, Wisconsin 53005.
Dr. Leonard Weinsteln, Boyce Thompson Institute, Ithaca, New York.
The following persons from Informatics Inc., Rockville, Maryland, 20852,
provided consulting, word-processing and technical assistance under
contract with the Environmental Criteria and Assessment Office, EPA.
Ms. Ruth H. Ness, Chairman
Dr. W. B. Dockstader
Ms. Joanna CHchton
Mr. Lewis Johnson
Ms. Marge Herridge
xxi 11
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The following persons from the Environmental Criteria and Assessment
Office provided word-processing and technical assistance in the development
of this document.
Ms. Diane Chappell
Mr. Douglas Fennel 1
Ms. Mavis Pope
Ms. Evelynne Rash
Ms. Donna Wicker
xx iv
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1. SUMMARY AND CONCLUSIONS
1.1 INTRODUCTION
Section 109(d) of the Clean Air Act, as amended, requires a thorough
review of the air quality criteria for carbon monoxide (CO) by December 31,
1980, and at five-year intervals thereafter. The Administrator of the
Environmental Protection Agency (EPA) is required to make such revisions
of the criteria as may be appropriate. In addition, the Administrator
may from time to time review, and where appropriate, modify the criteria
under the authority of Section 108(c).
This document is designed to evaluate the scientific information
which will form the basis for the National Ambient Air Quality Standard
(NAAQS) for CO. Major questions addressed in this document, which
covers new research published since the original CO criteria document
was issued, include the following:
(1) At what level of CO exposure do adverse health effects occur?
(2) What are the major health effects from exposure to CO?
(3) What are the special groups at risk to CO exposure?
(4) What are the major sources of CO exposure?
(5) Are there additive effects from CO exposure in combination
with other pollutants and drugs, or at high altitudes?
1-1
-------
(6) Do present monitoring methods adequately reflect human exposure to
CO?
(7) What are the global effects of increased emissions of CO to the
atmosphere?
1.2 PROPERTIES AND PRINCIPLES OF FORMATION OF CARBON MONOXIDE
Natural processes such as forest fires, methane oxidation, and biological
o
activity maintain a CO background concentration of about 0.05 mg/m (0.044 ppm)
Global atmospheric mixing of urban and industrial sources of CO creates levels
3 3
of about 0.2 mg/m (0.18 ppm) in the northern hemisphere and about 0.06 mg/m
(0.05 ppm) in the southern hemisphere. Much higher levels exist in cities as
a result of local combustion of fossil fuels.
On the average, nearly 85 percent of the CO in urban atmospheres is due
to mobile sources. Carbon monoxide emissions from internal combustion engines
can be reduced by improving the efficiency of combustion through changes in
design and operating conditions, or by the use of catalytic reactors in the
exhaust gas stream to oxidize CO to carbon dioxide (CO^). The measurement of
CO in effluent gas is used to indicate the proper and efficient operation of
any combustion process. The reactions of CO with oxygen (0^), ozone (0~), and
nitrogen dioxide (NOp are relatively slow, but the rapid oxidation of CO by
OH radicals is an important factor affecting its abundance in the atmosphere.
1.3 ESTIMATION OF CARBON MONOXIDE EMISSIONS FROM TECHNOLOGICAL SOURCES
Nationwide, the estimated annual emission from man-made sources of CO in
the U.S. rose from 102 million metric tons in 1970 to 104 in 1972.
1-2
-------
These emissions declined to 97 million metric tons in 1975 and increased to
103 million metric tons in 1977. As of 1977, highway vehicles contributed
75.2 percent of the emission total, nonhighway transportation 8.2 percent, and
industrial processes 8.1 percent. Miscellaneous combustion (agricultural
burning, forest fires, structural fires, etc.) accounted for 4.8 percent,
solid waste combustion 2.5 percent, and heat and electric power generation 1.2
percent.
Future emissions will depend on trends in vehicle use, the effectiveness
of pollution control devices on automobiles, and the efficiency of vehicle
operation. By estimating the growth rate of vehicle use and the increased
control of pollution, total CO emissions from automobiles in the U.S. are
expected to decline after 1979. However, this forecast depends on trends
which may change due to increased fuel prices, traffic flow improvements,
conversion to alternate fuels, and maintenance of pollution control equipment.
1.4 ANALYTICAL METHODS
The EPA-approved method for measuring CO levels in ambient air utilizes
non-dispersive infrared photometry (NDIR). NDIR is based on the characteristic
absorption of infrared radiation by CO. The NDIR continuous-monitoring systems
are sensitive over a wide range of concentrations and have short response
times. Because the systems are adversely affected by vibration or shock, they
are unsuitable for mobile use.
The operating range of NDIR systems is up to 50 ppm CO. Very low background
levels of atmospheric CO can be measured using highly sensitive instruments
1-3
-------
such as a gas chromatograph fitted with a flame ionization detector.
Relatively high levels, as found in parking garages, can be measured by
the catalytic oxidation of CO measured by an electrochemical or a
temperature-rise sensor depending on need for accuracy of results.
Blood carboxyhemoglobin (COHb) levels, a good index of CO exposure,
can be measured using several techniques. These include spectrophoto-
metry, gas chromatography or NDIR. Exhaled air also reflects CO
content of the blood if the air sample is collected under special
conditions.
1.5 CARBON MONOXIDE CONCENTRATIONS IN AMBIENT AIR
The selection of monitoring sites is critical for the accurate
assessment of CO exposure. Site selection depends on the monitoring
program: microscale, mesoscale, or macroscale air pollution regimes.
For instance, the microscale regime should include monitoring sites
along urban roadways, an area with high CO concentrations.
Continuous Air Monitoring Program (CAMP) stations have been operated
by the Federal government at downtown sites in some major cities since
1962. Current measurements of CO levels are reported quarterly to EPA
by state, local, and Federal agencies. California has been the major
contributor to the national CO data base, with 59 sites. Measurements
of CO levels disclose that the NAAQS are often exceeded, especially near
major streets in urban areas. In 1977, 211 out of 456 monitors showed
at least one 8-hour NAAQS violation, but only 11 showed 1-hour NAAQS
violations.
1-4
-------
Concentrations of CO vary with time, season, and geographical
location. These variations often follow predictable trends. In most
cities, CO levels peak at 7 to 9 a.m., 4 to 7 p.m., and 10 p.m. to
midnight. The first two peaks arise from automobile traffic coupled
with meteorological conditions. The midnight peak can be primarily
attributed to calm wind conditions which result in a reduced dispersion
of CO emissions. The highest CO levels tend to occur in the fall and
winter.
The dispersion of CO emissions is affected by wind speed, wind
direction, atmospheric stability, vertical mixing height, and ambient
temperature. In addition, this dispersion is affected by topographic
features such as mountains and buildings.
Mathematical models have been proposed to describe CO transport,
dispersion, and chemical transformations in the atmosphere. These
models can be used to predict air quality CO levels on the basis of the
characteristics of the emission sources plus meteorologic and topographic
factors.
Exposure to unusually high ambient levels of CO may result from the
following scenarios: (1) On a big city freeway where traffic has come
3
to a halt, the ambient CO level may exceed 50 mg/m (44 ppm).
(2) Inside a closed auto where cigarettes are being smoked, CO concen-
3
trations may exceed 100 mg/m (87 ppm). (3) In enclosed, unventilated
3
garages, CO levels in excess of 115 mg/m (100 ppm) have been found.
(4) In a heavily-travelled vehicular tunnel, a 1-hour maximum of 250
mg/m (218 ppm) CO was recorded. And (5), for certain occupational
1-5
-------
exposures, such as those encountered by fire fighters and some foundry
workers and miners, high CO levels have been reported.
1.6 THE GLOBAL CYCLE OF CARBON MONOXIDE
Much of the discussion about the global cycle of CO in the atmos-
phere currently centers on the relative importance of the role of anthro-
pogenic activity in the formulation of the global budget of this gas.
Prior to 1970, nearly all CO emissions were thought to originate from
combustion processes. However, in the early 1970's speculation evolved
that a significant natural source of CO existed from the oxidation of
methane in the unpolluted troposphere. The early estimates of the
source strength of CO from methane oxidation indicated that this source
was approximately ten times greater than man's input of CO into the
atmosphere. With the advent of more sophisticated models, a better
understanding of the geographical distribution of CO, and new chemical
kinetics data being made available, more recent calculations in the late
1970's have suggested that methane oxidation is not the dominant source
of CO in the atmosphere and that man's activities are responsible for
the presence of much and possibly most of the CO observed in the
atmosphere, especially in the Northern Hemisphere. If, indeed, anthro-
pogenic sources of CO have perturbed the natural distribution of this
gas in the troposphere, it then seems likely that the abundance, distri-
bution and the global cycles of many other trace constituents in the
atmosphere have also been altered. Some of these studies even imply
that increased CO amounts may have a significant indirect influence on
the chemistry which maintains the stratospheric ozone layer.
1-6
-------
1.7 EFFECTS OF CARBON MONOXIDE ON VEGETATION AND CERTAIN MICROORGANISMS
Carbon monoxide is a normal constituent of the plant environment.
Plants can both metabolize and produce CO. This may explain the rela-
tively high levels of CO necessary to produce detrimental effects.
There are few studies from which thresholds for detrimental or
other effects might be inferred, although defoliation or inhibition of
leaf and flower formation are demonstrable at high CO (above 100 ppm)
concentrations. These studies are of little value in determining effects
at ambient CO levels since the concentrations used were 1000 or more
times greater than the usual atmospheric concentrations.
Microorganisms show a wide range of response to CO, including its
autotrophic oxidation. Thus, any change in global atmospheric concen-
tration might be expected to reflect a corresponding alteration of soil
microbial population distribution. Soil microflora have the capability
of responding to changing environmental conditions. Soil microflora may
be considered to be a buffering system and an eventual sink for CO.
Comparatively low levels of CO in the soil inhibit nitrogen fixation.
3
Concentrations of 113 mg/m (98 ppm) have been shown to reduce nitrogen
fixation, while 572 to 1145 mg/m3 (500 to 1000 ppm) result in nearly
complete inhibition. An estimated consumption rate of 5 x 10 g/yr
indicates that soil microorganisms are a major sink for CO.
High concentrations of CO can induce the formation of adventitious
roots in higher plants as well as stimulate the growth of latent root
primordia. Plants exposed to 11,450 mg/m3 (10,000 ppm) CO exhibit
growth abnormalities including epinasty and hyponasty in leaves, retarded
1-7
-------
stem elongation, smaller and/or deformed leaves, and premature abscission
3
of leaves. Concentrations of CO in the 1145 to 11,450 mg/m (1,000 to
10,000 ppm) range can induce female expression in genetically male
plants of Cannabis sativa. Many species of plants are capable of ab-
sorbing and metabolizing CO photosynthetically. Although it has been
demonstrated that plants absorb CO, they function as net producers,
emitting more CO than they absorb.
1.8 METABOLISM OF CARBON MONOXIDE IN MAMMALS
Carbon monoxide exists in mammals primarily from the inhalation of
ambient air and from the normal catabolism of pyrrole rings. Endogenous
sources of CO result in COHb levels of approximately 0.5 percent. Any
increment above this level is assumed to have resulted from an exogenous
source. Factors which control and determine the final level of COHb are
the concentration of inspired CO, alveolar ventilation, red cell volume,
barometric pressure, and the diffusive capability of the lungs.
The apparent toxicity of CO is related to the strength of the
coordination bond formed with the iron atom in protoheme (C~ J-L«N.04Fe).
Hemoglobin (Hb), a ferrous iron complex of a protoporphyrin combined
with globin, is contained within the erythrocyte (red blood cell).
One of its primary functions is to transport 0^ and C0?. Hb combines
readily with either 0£ (to form 02Hb) or CO (to form COHb). The affinity
of Hb for CO is about 240 times greater than its affinity for 02. The
presence of COHb in blood not only reduces the availability of 0^ to
the body but also inhibits the dissociation of the remaining 0?. Carbon
monoxide also combines reversibly with heme compounds in the body cells.
1-8
-------
A number of conclusions may be derived from Chapter 9. The reduc-
tion in Og-carrying capacity of the blood is proportional to the amount
of COHb present. However, the amount of available 0^ is still further
*
reduced by the inhibitory influence of COHb on the dissociation of any
02Hb still available. Carbon monoxide diffuses more rapidly through
blood and pulmonary and placental tissues than would be predicted from
comparative solubilities of 02 and CO in water. The small reductions in
Q£ content at 5 to 10 percent COHb may be quite critical for patients
suffering from cardiovascular diseases or chronic obstructive lung
disease. It has been suggested that the principle mechanism of CO
toxicity is not hypoxemia, but rather a blocking of the energy flow
on the cellular level through the cytochrome system. The administration
of CO results in chemoreceptor stimulation. The response appears to be
almost linear with the COHb concentration (at least definitely above 8
percent). Available evidence suggests the presence of a biphasic decline
in arterial blood COHb (percent) levels. The distribution phase, which
persists for the first 20 to 30 minutes, is followed by a slower linear
decline (elimination phase). And, although no final judgment has been
made regarding the effects of CO on oxidative transport, experimental
evidence suggests that the cytochromes are affected during CO poisoning.
1.9 EFFECTS OF CARBON MONOXIDE ON EXPERIMENTAL ANIMALS
Animal studies provide information that may be of importance to
human reactions under similar circumstances. Animal data may permit
predictions concerning sensitive human populations, such as those with
existing CNS and cardiovascular defects.
1-9
-------
o
Carbon monoxide exposures of 58 mg/m (50 ppm; 4 to 7 percent COHb)
have produced cardiovascular effects. The minimal concentration of CO
affecting behavior and CNS appears to be 115 mg/m (100 ppm; 12 to 20
percent COHb).
1.10 EFFECTS OF LOW-LEVEL CARBON MONOXIDE EXPOSURE ON HUMANS
As seen in the animal studies, human exposures to low levels of CO
have also resulted in deleterious effects on the CNS and cardiovascular
3
systems. While an 8-hr exposure to 17-21 mg/m (15-18 ppm; 2.5-3
percent COHb) CO affected cardiovascular systems, concentrations of CO
as low as 29-34 mg/m (25-30 ppm; 4-6 percent COHb) affected behavior
and the CNS.
Fetuses, persons with cardiovascular or central nervous system
defects, sickle cell anemics, young children, older persons, persons
living at high altitudes, and those taking drugs comprise groups at
special risk to CO exposure. The current literature offers little
information regarding the high risk groups; however, it is apparent that
exposure for 8 hrs to CO concentrations as low as 15-18 ppm may be
detrimental to the health of persons suffering cardiac impairment.
1-10
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2. INTRODUCTION
This document has been prepared pursuant to Sections 108(c) and
109(d)(l) of the Clean Air Act, as amended. Section 108(c) requires
that the Administrator of the EPA from time to time review and, as
appropriate, modify and reissue criteria published pursuant to Section 108(a)
Section 109(d)(l) requires both that the Administrator complete a thorough
review, and as may be appropriate, make revisions in the criteria by
December 31, 1980, and at five-year intervals thereafter. Air quality
criteria are required by Section 108(a) to identify effects on public
health and welfare caused by varying amounts of pollutants in the air.
These criteria must be supported by the latest available accurate
scientific information.
The original criteria document for carbon monoxide (CO), The
National Air Pollution Control Administration publication No. AP-62, was
issued in 1970. Since that time, new information has been published.
This document summarizes the pertinent information which will be used in
considering whether the present CO standards are adequate or revisions
are advisable or required.
The purpose of these criteria is to identify air pollution effects
and serve as the basis for national ambient air quality standards
2-1
-------
promulgated by the Administrator under Section 109 of the Clean A1r Act,
as amended. This document therefore is concerned with CO as a pollutant
and will present the air quality criteria descriptive of the presently
available scientific data. Specifically, air quality criteria for CO as
a pollutant are intended to reflect accurately the latest scientific
knowledge useful in indicating the kind and extent of all identifiable
effects on public health and welfare which may be expected from its
presence in the ambient air in varying quantities. There are many
factors and interactions which must be considered in developing such a
criteria document.
This document does not cite extensively the literature reporting
excessively high levels of CO, but focuses on this pollutant as it is
found in ambient environments. The intent is to present an updated
comprehensive review of the available scientific information and data on
CO as an air pollutant.
It is essential for understanding the basis of air pollution effects
that the basic chemistry and sources of CO be considered. Furthermore,
it is necessary to consider analytical techniques and methods so proper
assessment can be made of concentration and potential exposure patterns.
The foregoing information precedes the detailed discussion of the effects
of CO on certain plants and microorganisms.
Ambient and experimental levels of CO are expressed in milligrams
3
per cubic meter (mg/m ) followed by a parenthetical expression in parts
per million (ppm). Gas density varies with pressure and temperature so
that accurate expression of concentrations requires cognizance of these
2-2
-------
parameters. The conversion factor, for example, at a constant standard
pressure of 760 mm Hg, at 0°C 1 mg/m equals 0.800 ppm and 1 ppm equals
O _ ^J A
1.250 mg/m ; at 25 C, 1 mg/m equals 0.874 ppm and 1 ppm equals 1.145 mg/m .
There is some indication that the production of CO and its concomi-
tant release into the atmosphere may have significant effects on some
aspects of the global atmosphere. Some attention is directed toward
this as it may eventually affect human health and welfare.
The last three chapters deal with the metabolism of CO by animals
and most importantly the effects it has on animals and man. Much of the
effort and scientific information contained in this document is directed
toward the health and welfare of humans. Carbon monoxide is a pollutant
that has at least one specific reaction product, carboxyhemoglobin
(COHb), in the human system which appears to be equated to exposure and
detrimental effects. Other physiological responses and reactions have
been postulated recently and are expected to aid in the elucidation of
CO toxicity. Much of the physiological information involves the concen-
tration of COHb in the blood resulting from exposure to ambient or
experimental levels of CO.
In the preparation of this document, much use was made of previous
EPA documentation efforts on the subject as well as the monograph prepared
by the National Academy of Sciences which was published late in 1977.
2-3
-------
3. PROPERTIES AND PRINCIPLES OF FORMATION OF CARBON MONOXIDE
Even far from human habitation, carbon monoxide (CO) occurs in air
at an average background concentration of 0.05 mg/m , primarily as a
result of natural processes such as forest fires and the oxidation of
methane. Much higher concentrations occur in cities due to technological
sources such as automobiles and the production of heat and power.
<
Carbon monoxide emissions are increased when the fuel is burned in an
incomplete or inefficient way. The physical and chemical properties of
CO suggest that atmospheric removal of CO occurs primarily by reaction
with hydroxyl (OH) radicals.
3.1 INTRODUCTION
Carbon monoxide was first discovered to be a minor constituent of
21
the earth's atmosphere by Migeotte in 1948. While taking measurements
of the solar spectrum, he observed a strong absorption band in the
1 Q
infrared region at 4.7 urn which he attributed to CO. On the bases of
the belief that the solar contribution to that band was negligible and
of his observation of a strong day-to-day variability in absorption,
Migeotte concluded that an appreciable amount of CO was present in the
terrestrial atmosphere of Columbus, Ohio. In the 1950's many more
9 10 19 99 33 37
observations >''*' of CO were made, with measured concentrations
3-1
-------
ranging from 0.08 to 100 ppm (parts per million). On the basis of these
and other measurements available in 1963, Junge stated that CO appeared
to be the most abundant trace gas, other than carbon dioxide, in the
37
atmosphere. The studies of Shaw indicated higher mixing ratios near the
ground than in the upper atmosphere, implying a source in the biosphere,
but Junge emphasized that knowledge of the sources and sinks of atmospheric
CO was extremely poor. It was not until the late 1960's that concerted
efforts were made to determine the various production and destruction
mechanisms for CO in the atmosphere.
The remainder of this chapter will focus on the physical properties
and formation principles of CO which contribute to its release into the
atmosphere. In Chapter 4, a review of the various factors which deter-
mine the technological emission source strength will be discussed; a
description of other source strength estimates as well as the global
cycle of CO will be presented in Chapter 7.
3.2 PHYSICAL PROPERTIES
«
Carbon monoxide is a tasteless, odorless, colorless diatomic
molecule which exists as a gas in the earth's atmosphere. Radiation in
the visible and near ultraviolet regions of the electromagnetic spectrum
is not absorbed by CO, although the molecule does have weak absorption
bands between 125 and 155 nm. It absorbs radiation in the infrared
region corresponding to the vibrational excitation of its electronic
ground state. Carbon monoxide has a low electric dipole moment (0.10
debye), short interatomic distance (1.23 8), and a high heat of formation
from atoms, or bond strength (2072 kJ/mol), suggesting that the molecule
3-2
-------
Ol
is a resonance hybrid of three structures, which all contribute
nearly equally to the normal ground state. General physical properties
of CO are given in Table 3-1.
3.3 GASEOUS CHEMICAL REACTIONS OF CARBON MONOXIDE
In its review of the gaseous chemical reactions of CO in 1970,
the National Air Pollution Control Administration (later to become
part of the U. S. Environmental Protection Agency) concluded that no
gaseous reactions have been shown to be important scavengers of CO in
the atmosphere. No data since that time indicate that the processes
they considered, which included reactions of CO with 02, H«0, NOp,
and 0-, are of any importance to atmospheric chemistry. However, the
report did speculate that CO reactions with radicals in the atmosphere
could provide an important sink for CO. Subsequent research has
shown that the CO reaction of most importance in the atmosphere is OH
radical attack. Other radicals react with CO much more slowly
15
(Hampson and Garvin):
CO + H0£ T C02 + OH, k = 10"19 cm3/(molecule x sec),
-17 3
and CO + CH30 T products, k = 4 x 10 cm /(molecule x sec).
39 4
Carbon monoxide also reacts with ground state, and metastable,
atomic oxygen. The relative importance of these reactions to the
overall chemistry occurring in the atmosphere is very slight. In the
o
troposphere and stratosphere, 0( P) is much more likely to react with
molecular oxygen, 0?, in a three-body reaction to form ozone, or with
nitrogen dioxide, N02, to produce NO and 02. Since 0( D) is a highly
reactive species, it is more likely to react with water vapor, methane,
or any other molecule which is more abundant than CO in the atmosphere.
3-3
-------
TABLE 3-1. PHYSICAL PROPERTIES OF CARBON MONOXIDE
24
Molecular weight
Critical point
Melting point
Boiling point
Density
at 0 C, 1 atm
at 25 C,l atm
Specific gravity relative to air
Solubility 1n water
at 0°C
at 20°C
at 25°C
Explosive limits in air
Fundamental vibration transition
CO(X'I ,v' = lEv"0)
Conversion factors
at 0 c, 1 atm
at 25°C, 1 atm
28.01
-140°C at 34.5 atm
-199°C
-191.5°C
1.250g/liter
1.145g/liter
0.967
3.54ml/100mjl
(44.3 ppmm)
2.32ml/100ml
(29.0 ppmm)
2.14ml/100ml
(26.8 ppmm)
12.5-74.
2143.3cm
(4-67 urn)
1 mg/m = 0.800 ppia(
1 ppm * 1.250 mg/m
1 mg/m = 0.873 ppm
1 ppm = 1.145 mq/m
aVolume of carbon monoxide is at 0 C, 1 atm (atmospheric pressure at sea
. level = 760 torr).
Parts per million by mass (ppmm = mg 1)
Parts per million by volume.
3-4
-------
Collision of 0( D) with N2 or 0£ is quite likely to bring this excited
atom down to ground state. Thus, with the exception of the OH reaction,
there is no evidence that any reactions involving CO are of any
consequence in the atmosphere.
Many studies of the measurement of the reaction rate governing the
reaction
CO + OH T C0£ + H
have appeared in the literature since the late 1960's (see Table 3-2).
Until 1976, all of the measurements agreed fairly well, ranging between
-13 3 -13 3
1.3 x 10 cm /(molecule x sec) and 1.9 x 10 cm /(molecule x sec);
the National Bureau of Standards review recommended a value of 1.4 x
-13 3
10 cm /(molecule x sec) and did not find any reason to believe that
either a substantial temperature or pressure dependence existed for this
reaction.
6 -13 3
However, Cox et al. reported a rate constant of 2.7 x 10 cm /
(molecule x sec) for this reaction at 760 torr (1 atm) using a mixture
38
of Np and 0« as the diluent gas. Sie et al. likewise showed that the
CO + OH reaction rate increased as the pressure in their reaction chamber
increased when they used molecular hydrogen as a carrier gas. They also
noted that the type of diluent employed for their experiments had an
effect on the rate of reaction. Subsequent research efforts have
38
supported the findings of Sie et al. In general, it appears that
there is no pressure effect if noble gases (e.g., He or Ar) are used as
the carrier gas, but when other gases, which may be more representative
of the real atmosphere, are utilized in these studies the CO + OH reaction
3-5
-------
TABLE 3-2. REPORTED ROOM TEMPERATURE RATE CONSTANTS
FOR THE REACTION OF OH RADICALS WITH CO
fiate~constant
(10 cnr/mol x sec)
Pressure, torr/
diluent gas
Reference
No observed pressure
1.91 ± 0.08
1.48 ± 0.15
1.49 ± 0.05
1.42
1.66 ± 0.50
1.35 ± 0.20
1.33
1.44
1.56 ±0.2
1.59
1.58
1.51 ± 0.08
1.54 ± 0.16
Pressure dependence
1.00 ± 0.14
1.47 ± 0.19
2.98 ± 0.19
3.45 ± 0.22
3.18 ± 0.29
1.19
2.29
3.41
dependence
-v 1 (He or Ar)
100 (Ar)
not reported
100 (He)
0.2-1.0 (Ar or He)
20 (He)
1-3 (He or Ar)
10-20 (He or N90 + H9)
0.3-6 (He, Ar 5r N9r
20 (He) *
20 (N-)
730 (mostly Ar)
25-654 (Ar)
observed
19.9 (H.)
83.4 (H;)
296 (H9r
702 (H;)
774 (754 H9 + 20 H90)
627 (He) * *
569 (SFfi)
627 (SFg)
9
Dixon-Lewis et^al., 1966
Greiner, 1967^ 47
Wilson and O'Donovan, 1967
Greiner, 1969" 23
Mulcahy and Smith, 1921
Stun! and Niki, 1972** 4fi
Westenberg and de Haas,41973
Smith and Zellner, 1973™
Howard and Evenson* 1974
Davis et al., 1974^
Davis et al., 1974° --
Gordon and Mulac, 1975
Atkinson et al. , 1976
Sie et al., 197638
1.37 ± 0.20
2.97 ± 0.16
2.04
3.24
1.50 ± 0.15
1.52 ± 0.15
1.52 ± 0.16
1.62 ± 0.19
1.62 ± 0.24
1.53 ± 0.16
1.93 ± 0.20
2.40 ± 0.24
3.09 ± 0.31
3.43 ± 0.35
100 (air)
700 (air)
59 (He)
200-359 (SFC)
D
25 (Ar)
75 (Ar)
225 (Ar)
406 (Ar)
643 (Ar)
25 (SF,)
76 (SF°)
208 (SF°)
404
Chan et al., 1977'
Overand and Paraskevopoulos, 1977
29
Perry et al., 1977
32
Perry et al., 1977
32
604 (SFH
D
3-6
-------
rate exhibits an important pressure dependence. Table 3-2 summarizes
most of the reported studies of the CO + OH reaction. Most noteworthy
about the recent efforts is the suggestion that the rate of reaction is
at least twice as fast at pressures representative of lower tropospheric
conditions than was previously indicated. This fact has led to important
changes in our understanding of the global CO cycle as well as the
budgets of several other trace gases. These points will be discussed in
more detail in Chapter 7.
3.4 PRINCIPLES OF FORMATION
In all cases, the burning of any carbonaceous fuel produces, among
other lesser products, two primary products -- carbon dioxide (CO^) and
CO. The production of C0« predominates when the air or oxygen supply is
in excess of the stoichiometric needs for complete combustion. If
burning occurs under fuel-rich conditions, with less air or oxygen than
is needed, CO will be produced in abundance. Most of the CO and C0«
formed in past years was simply emitted into the atmosphere.
In recent years, concerted efforts have been directed to reducing
concentrations of potentially harmful materials in ambient air. The CO
?
found in urban air today originates almost entirely from local combustion
processes. The background concentration of CO contributes less than
Q
0.23 mg/m (0.20 ppm) to the ambient air concentration at any given
urban location. As a result of natural processes such as forest fires,
oxidation of methane and biological activity, the background level of CO
o 35
is estimated to be about 0.05 mg/m (0.04 ppm). Global atmospheric
mixing of urban and industrial pollutants probably accounts for a measured
3-7
-------
3
CO background of about 0.20 mg/m (0.18 ppm) in the northern hemisphere
o oc
and about 0.06 mg/m (0.05 ppm) in the southern hemisphere. The
3
global average appears to be about 0.12 mg/m (0.10 ppm) and does not
34
appear to have been increasing substantially in recent years.
Considerable effort has been made to reduce emissions of CO and
other pollutants to the atmosphere. Generally the approach has been
technological: reduction of CO emissions to the atmosphere either by
improving the efficiency of the combustion processes, thereby increasing
the yield of C0« and decreasing the yield of CO; or by applying secondary
catalytic combustion reactors in the waste gas stream to convert CO to
co2.
The development and application of control technology to reduce
emissions of CO from combustion processes has generally been successful
and is continuing to receive deserved attention. However, the 1977
5
amendments to the Clean Air Act postpone meeting the desired automobile
emission control schedules, reflecting in part the apparent difficulty
encountered by the automobile industry in developing and supplying the
required control technology. Since the automobile engine is recognized
to be the major source of CO in most urban areas, special attention is
given to the control of automotive emissions.
Table 3-3 shows the automobile emission control schedules that have
resulted from the 1970 Clean Air Act and later amendments.
3-8
-------
Table 3-3. AUTOMOBILE EMISSION CONTROL SCHEDULES7
(in grams/mile)
1970
Clean Air Act
HC
CO
NO
1976
1.5
15.0
3.1
1977
0.41
3.4
2.0
1978 1979
—
—
0.4
1980 1981 1982
— — — _ T
T
T
As of jfily 1, 1977
1977
HC
CO
NO
Amendments
HC
CO
NOV
X
1.5
15
3.1
1.5
15
3.1
2.0
—
—
2.0
TO. 41 —
T3.4
0.4
_»
--
T
T
TO. 41
T7.0 3.4 T
1.0 T
The problems encountered in mass-producing and marketing effective
control technology for automobile engines are complex, since a number of
simultaneous requirements are involved, i.e., control of multiple air
pollutants, fuel economy and efficiency, durability and quality control
45
of components, and maintenance. Current testing of automobiles having
fuel injection and catalytic emission control systems has indicated that
durability of the controls will be a problem in meeting the 1981 require-
ment of <3.4 g of CO per mile after 50,000 miles. (Emissions will be
less than 3.4 g of CO per mile on new automobiles.)
The following sub-sections present a brief discussion of the general
principles and mechanisms of formation of CO and control of emissions
associated with the many combustion processes. The processes are commonly
classified in two broad types, mobile sources and stationary sources,
since this division does generally separate distinct types of major
combustion devices. Control techniques for CO emissions from mobile and
stationary sources are detailed in references 27 and 28.
3-9
-------
3.4.1 General Combustion Processes
Incomplete combustion of carbon or carbon-containing compounds
creates varying amounts of CO. The chemical and physical processes that
occur during combustion are complex, because they depend not only on the
type of carbon compound reacting with oxygen, but also on the conditions
20 30
existing in the combustion chamber. ' Despite the complexity of the
combustion process, certain general principles regarding the formation
of CO from the combustion of hydrocarbon fuels are widely accepted.
Gaseous or liquid hydrocarbon fuel reacts with molecular oxygen in
a chain of reactions that result in CO. Carbon monoxide then reacts
with hydroxyl radicals to form carbon dioxide (COp). This second
reaction is approximately 10 times slower than the first. In coal
combustion, the reaction of carbon and oxygen to form CO is also one of
the primary reactions, and a large fraction of carbon atoms go through
the monoxide form. Again, the reaction of monoxide to dioxide is much
slower.
Thus, four basic variables control the concentration of CO in all
combustion of hydrocarbon gases. These are: (1) oxygen concentration,
(2) flame temperature, (3) gas residence time at high temperatures, and
(4) combustion chamber turbulence. Oxygen concentration affects the
formation of both CO and COp because oxygen is required in the initial
reactions with the fuel molecule and in the formation of the hydroxyl
radical. As the availability of oxygen increases, more complete
conversion of monoxide to dioxide results. Flame and gas temperature
affects both the formation of monoxide and the conversion of monoxide to
3-10
-------
dioxide because both reaction rates increase exponentially with increasing
temperature. Also, the hydroxyl radical concentration in the combustion
chamber is very temperature-dependent. The conversion of CO to C0? is
also enhanced by longer residence time, because this is a relatively
slow reaction in comparison to CO formation. Increased gas turbulence
in the combustion zones increases the actual reaction rates by increasing
the mixing of the reactants and assisting the relatively slower gaseous
diffusion process, thereby resulting in more complete combustion.
3.4.2 Combustion Engines
3.4.2.1 Mobile Combustion Engines—Most mobile sources of CO are
internal combustion engines of two types: (1) carbureted, spark-
ignition, gasoline-fueled, reciprocating engines, and (2) diesel-fueled
reciprocating engines. The CO emitted from any given engine is the
product of the following factors: (1) concentration of CO in the exhaust
gases, (2) the flow rate of exhaust gases, and (3) the duration of
operation.
3.4.2.2 Internal Combustion Engines (Gasoline-Fueled, Spark-
Ignition Engines)— Exhaust concentrations of CO increase with lower
(richer) air to fuel (A/F) ratios, decrease with higher (leaner) A/F
ratios, but remain relatively constant with ratios above the stoichio-
metric ratio of about 15 to 1. The behavior of gasoline automobile
engines before and after the installation of pollutant control devices
differs considerably. Depending on the mode of driving, the average
uncontrolled engine operates at A/F ratios ranging from about 11 to 1
to a point slightly above the stoichiometric ratio. During the idling
3-11
-------
mode, at low speeds with light load (such as low speed cruise), during
the full-open throttle mode until speed picks up, and during deceleration,
the A/F ratio is low in uncontrolled cars and CO emissions are high. At
higher-speed cruise and during moderate acceleration, the reverse is
true. Cars with exhaust controls generally remain much closer to
stoichiometric A/F ratios in all modes, and thus the CO emissions are
kept lower. The relationship between CO concentrations in engine exhaust
and A/F ratios is shown in Figure 3-1. The exhaust flow rate increases
with increasing engine power output.
Correlations between total emissions of CO in grams per vehicle
mile and average route speed show a decrease in emissions with increasing
38 41 43
average speed. * ' During low-speed conditions (below 32 km/hour or
20 miles/hour average route speed), the greater emissions per unit of
distance traveled are attributable to an increase in the frequency of
acceleration, deceleration, and idling in the driving cycle encountered
by the vehicle in heavy traffic; and the consequent increase in the
operating time per mile driven.
The CO and the unburned hydrocarbon exhaust emissions from an
uncontrolled engine result from incomplete combustion of the fuel-air
mixture. Emission control on new vehicles is being achieved by engine
modifications, improvements in engine design, and changes in engine
operating conditions. Substantial reductions in CO and other pollutant
emissions result from consideration of design and operating factors such
as leaner, uniform mixing of fuel and air during carburetion, controlled
heating of intake air, increased idle speed, retarded spark timing,
3-12
-------
10
co
i
H*
CO
AIR-FUEL RATIO
Figure 3-1. Effect of air-fuel ratio on exhaust gas carbon monoxide concentrations from three test engines.^ (Used with permission of Society of
Automotive Engineers, Inc. Copyright 1964.)
-------
improved cylinder head design, exhaust thermal reactors, oxidizing and
reducing catalysts, secondary air systems, exhaust recycle systems,
electronic fuel injection, A/F ratio feedback controls, and modified
25
ignition systems.
3.4.2.3 Internal Combustion Engines (Diesel Engines)—Diesel engines in
use are primarily the heavy-duty type which power trucks and buses.
Diesel engines allow more complete combustion and use less volatile
fuels than do spark ignition engines. The operating principles are
significantly different from those of the gasoline engine. In diesel
combustion, CO concentrations in the exhaust are relatively low since
high temperature and large excesses of oxygen are involved in normal
operation. The exhaust emissions from diesel engines have the same
general composition as gasoline engine emissions, though the concentra-
tions of different pollutants vary considerably. For example, the
diesel emits larger quantities of NO and polycylic organic particulates
f^.
than gasoline engines; it emits lesser quantities of CO.
3.4.2.4 Stationary Combustion Sources (Steam BoilersV^This section
refers to fuel-burning installations such as coal-, gas-, or oil-fired
heating or power generating plants (external combustion boilers).
In these combustion systems, the formation of CO is lowest at a
ratio near or slightly above the stoichiometric ratio of air to fuel.
At lower than stoichiometric A/F ratios, high CO concentrations reflect
the relatively low oxygen concentration and the possibility of poor
reactant mixing from low turbulence. These two factors can increase
emissions even though flame temperatures and residence time are high.
3-14
-------
At higher than stoichiometric A/F ratios, increased CO emissions result
from decreased flame temperatures and shorter residence times. These
two factors remain predominant even when oxygen concentrations and
turbulence increase. Minimal CO emissions and maximum thermal efficiency
therefore require combustor designs that provide high turbulence,
sufficient residence time, high temperatures, and near stoichiometric
A/F ratios. Combustor design dictates the actual approach to that
minimum. The measurement of CO in effluent gas is therefore used as an
indication of improper and inefficient operating practice for any given
combustor, or of inefficient combustion.
3.5 NON-COMBUSTION INDUSTRIAL SOURCES
There are numerous industrial activities which result in the
44
emission of CO at one or more stages of the process. Manufacturing
pig iron can produce as much as 700 to 1050 kg CO/metric ton of pig iron.
Other methods of producing iron and steel can produce CO at a rate of
9 to 118.5 kg/metric ton. However, most of the CO generated is normally
recovered and used as fuel. Conditions such as "slips" can cause
instantaneous emissions of CO. Slips have been greatly reduced with
modern equipment. Grey-iron foundries can produce 72.5 kg CO/metric ton
of product but an efficient afterburner can reduce the CO emission to
4.5 kg/metric ton.
Charcoal production results in CO emissions of 160 kg/metric ton
with or without the installation of chemical recovery equipment.
Emissions from carbon black manufacture can range from 5 to 3200 kg
CO/metric ton depending on the efficiency and quality of the emission
control systems.
3-15
-------
Some chemical processes such as phthalic anhydride production give
off as little as 6 kg CO/metric ton with proper controls or as much as
200 kg CO/metric ton if there are no controls installed. There are
numerous other chemical processes which produce relatively small CO
emissions per metric ton of product, such as sulfate pulping for paper
at 1 to 30 kg CO/metric ton; lime manufacturing normally runs 1 to 4 kg
CO/metric ton; and CO from adipic acid production is zero or slight with
proper controls. Other industrial chemical processes which cause CO
emissions are the manufacture of terephthalic acid and the synthesis of
methanol and higher alcohols. As a rule most industries find it economi-
cally desirable to install suitable controls to reduce CO emissions.
Even though some of these CO emission rates seem excessively high,
they are in fact only a small part of the total pollutant load. Mention
of these industries is made to emphasize the concern for localized
pollution problems when accidents occur or proper controls are not used.
While the estimated CO emission resulting from forest wildfires in
the United States for 1971 was 4 x 10 metric tons, the estimated total
industrial process CO emission of the U. S. for 1971 was 10.3 x 10
metric tons.
3-16
-------
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of OH radicals with CO and N20. Chem. Phys. Lett. 44:204-208, 1976.
2. Benesh, W., M. Migeotte, and L. Neven. Investigation of atmospheric CO
at the Jungfraujoch. J. Opt. Soc. Am. 43:1119-1123, 1953.
3. Chan, W. H., W. M. Uselman, J. G. Calvert, and J. H. Shaw. The pressure
dependence of the rate constant for the reaction: OH + CO •> H + C00.
Chem. Phys. Lett. 45:240-244, 1977. ^
4. Clerc, M., and F. Barat. Kinetics of CO formation studies by far-uv
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U.S.C. §7409, 1977.
6. Cox, R. A., R, G. Derwent, and P. M. Holt. Relative rate constants for
the reactions of OH radicals with H«, CHA, CO, NO and HONO at atmospheric
pressure and 296°K. J. Chem. Soc. Faraday Trans. I 72:2031-2043, 1976.
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Eighth Annual Report of the Council on Environmental Quality. U.S.
Government Printing Office, Washington, DC, December 1978.
8. Davis, D. D., S. Fisher, and R. Schiff. Flash photolysis-resonance
fluorescence kinetics study: Temperature dependence of the reactions OH
+ CO -» CO, + H and OH + CHA -> H90 + CH7. J. Chem. Phys. 61:2213-2219,
1974. * 4 ^ d
9. Dixon-Lewis, G., W. E. Wilson, and A. A. Westenberg. Studies of hydroxyl
radical kinetics by quantitative ESR. J. Chem. Phys. 44:2877-2884, 1966.
10. Faith, W. L., N. A. Renzetti, and L. H. Rogers. Fifth Technical Progress
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o
11. Gordon, S., and W. A. Mulac. Reaction of OH(X II) radical produced by
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Symposium on Chemical Kinetics Data for the Upper and Lower Atmosphere,
Stanford Research Institute and National Bureau of Standards, Warrenton,
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1975.
12. Greiner, N. R. Hydroxyl radical kinetics by kinetic spectroscopy.
I. Reactions with H«, CO, and CH. at 300°K. J. Chem. Phys. 46:2795-2799,
1967. *
13. Greiner, N. R. Hydroxyl radical kinetics by kinetic spectroscopy.
V. Reactions with H« and CO in the range 300-500 K. J. Chem. Phys.
51:5049-5051, 1969. *
3-17
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14. Hagen, D. F. , and G. W. Holiday. The effects of engine operating and
design variables on exhaust emissions. In: Vehicle Emissions. (Selected
SAE Papers). Technical Progress Series Volume 6, Society of Automotive
Engineers, Inc., New York, 1964. pp. 206-223.
15. Hampson, R. F., Jr., and D. Garvin. Chemical Kinetic and Photochemical
Data for Modeling Atmospheric Chemistry. NBS Technical Note 866, U.S.
Department of Commerce, National Bureau of Standards, June, 1975.
16. Howard, C. J., and K. M. Evenson. Laser magnetic resonance study of the
gas phase reactions of OH with CO, NO, and N0?. J. Chem. Phys. 61:1943-1952,
1974. *
17. Junge, C. E. Air Chemistry and Radioactivity. Academic Press, New York,
1963.
18. Lagemann, R. T. , A. H. Nielsen,..and F. E> Dickey. The infra-red spectrum
and molecular constants of C^0lt? and C1J0 . Phys. Rev. 72:284-289,
1947.
19. Locke, J. L., and L. Herzberg. The absorption due to carbon monoxide in
the infrared solar spectrum. Can. J. Phys. 31:504-516, 1953.
20. Mellor, A. M. Current kinetic modeling techniques for continuous flow
combustors. In: Emissions from Continuous Combustion Systems, Proceedings
of the Symposium on Emissions from Continuous Combustion Systems, General
Motors Research Laboratories, Warren, Michigan, September, 27-28, 1971.
Plenum Press, New York, 1972. pp. 23-53.
21. Migeotte, M. V. The fundamental band of carbon monoxide at 4-7 mm in the
solar spectrum. Phys. Rev. 75:1108-1109, 1949.
22. Migeotte, M. V., and L. Neven. Recent progress in observing the infrared
solar spectrum at the scientific station at Jungfraujoch, Switzerland.
Mem. Soc. R. Sci. Liege 12:165-178, 1952.
23. Mulcahy, M. F. R., and R. H. Smith. Reactions of OH radicals in the
H-NO£ and H-N02-CO systems. J. Chem. Phys. 54:5215-5221, 1971.
24. Committee on Medical Biologic Effects of Environmental Pollutants. Carbon
Monoxide. National Academy Sciences, Washington, DC, 1977.
25. Committee on Motor Vehicle Emissions. Automotive Spark Ignition Engine
Emmission Control Systems to meet the Requirements of the 1970 Clean Air
Act Amendments. National Academy of Sciences, Washington, DC, May 1973.
26. Committee on Challenges of Modern Society. Air Quality Criteria for
Carbon Monoxide. Report No. 10, North Atlantic Treaty Organization,
Brussels, June 1972.
27. National Air Pollution Control Administration. Control Techniques for
Carbon Monoxide Emissions from Stationary Sources. National Air Pollution
Control Administration Publication No. AP-65, U.S. Department of Health,
Education, and Welfare, Washington, DC, March 1970.
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28. National Air Pollution Control Administration. Control Techniques for
Carbon Monoxide, Nitrogen Oxide, and Hydrocarbon Emissions from Mobile
Sources. National Air Pollution Control Administration Publication No.
AP-66, U.S. Department of Health, Education, and Welfare, Washington, DC,
March 1970.
29. Overand, R., and G. Paraskevopoulos. The question of a pressure effect
in the reaction OH + CO at room temperature. Chem. Phys. Lett. 49:109-111,
1977. —
30. Palmer, H. B. Equilibria and chemical kinetics in flames. Combustion
Technology: Some Modern Developments. H. B. Palmer and J. M. Beer,
Academic Press, 1974. pp. 1-33.
31. Pauling, L. The Nature of the Chemical Bond and the Structure of Molecules
and Crystals: An Introduction to Modern Structural Chemistry. Third
Edition. Cornell University Press, Ithaca, NY, 1960 pp. 194-195.
32. Perry, R. A., R. Atkinson, and J. N. Pitts, Jr. Kinetics of the reactions
of OH radicals with C2H£ and CO. J. Chem. Phys. 67:5577-5584, 1977.
33. Renzetti, N. A., (ed.). An Aerometric Survey of the Los Angeles Basin
August-November, 1954. Report No. 9, Air Pollution Foundation, Los
Angeles, CA., 1955.
34. Robbins, R. C., K. M. Borg, and E. Robinson. Carbon monoxide in the
atmosphere. J. Air Pollut. Control Assoc. 18:106-110, 1968.
35. Seiler, W. The cycle of atmospheric CO. Tellus 26:116-135, 1974.
36. Seiler, W., and C. Junge. Carbon monoxide in the atmosphere. J. Geophys.
Res. 75:2217-2226, 1970.
37. Shaw, J. H. A determination of the abundance of nitrous oxide, carbon
monoxide and methane in ground level air at several locations near Columbus,
OH. Scientific Rpt. No. 1, Contract No. AF19 (604)-2259, Air Force
Cambridge Research Center, 38 pp., 1959. PB 143359.
38. Sie, B. K. T., R. Simonaitis, and J. Heicklen. The reaction of OH with
CO. Int. J. Chem. Kin. 8:85-98, 1976.
39. Simonaitis, R., and J. Heicklen. Kinetics and mechanism of the reaction
of 0(3P) with carbon monoxide. J. Chem. Phys. 56:2004-2011, 1972.
40. Smith, I. W. M., and R. Zellner. Rate measurements of reactions of OH by
resonance absorption. Part 2. - Reactions of OH with CO, C«H. and C?H«.
J. Chem. Soc. Faraday Trans. 2. 69:1617-1627, 1973.
41. Starkman, E. S. Fundamental Process in Nitric Oxide and Carbon Monoxide
~~~ Production from Combustion Engines. XII Congress International des
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42. Stuhl, F., and H. Niki. Pulsed vacuum-uv photochemical study of reactions
of OH with H9, D9, and CO using a resonance-fluorescent detection method.
J. Chem. PhyS. 57:3671-3677, 1972.
43. National Air Pollution Control Administration. Air Quality Criteria for
Carbon Monoxide. National Air Pollution Control Administration Publication
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Emission Factors. Parts A and B. Third Edition. AP-42, U.S. Environmental
Protection Agency, Research Triangle Park, NC, August 1977.
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50,000 miles? - Automot. Eng. 86:32-35, 1978.
46. Westenberg, A. A., and N. deHaas. Rates of CO+OH and H2+OH over an
extended temperature range. J. Chem. Phys. 58:4061-4065, 1973.
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reaction rate of OH with itself and CO. J. Chem. Phys. 47:5455-5457,
1967. ~~
3-20
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4. ESTIMATION OF CARBON MONOXIDE EMISSIONS FROM TECHNOLOGICAL SOURCES
The estimated total annual emissions from all man-made, sources in
the U. S. rose from 102 million metric tons in 1970 to 104 in 1972, but
then declined to 97 in 1975 and subsequently increased to 103 million
metric tons in 1977. About 75 percent of the total comes from highway
vehicles, 8.5 percent from railroads, aircraft, and other non-highway
transportation, 8 percent from industrial processes, 5 percent from
miscellaneous combustion (forest fires, agricultural burning, structural
fires, etc.), 2.5 percent from solid waste combustion, and 1 percent
o
from combustion for heating and electric power generation.
Total emission trends and emission rates for specific sources or
source groups derived from calculated emission estimates provide a basis
for assessing the magnitude and pattern of air pollution resulting from
the various sources and allow the development of methods of estimating
future air quality conditions.
The magnitude of future CO emissions will depend primarily upon
increased vehicle use trends, the effectiveness of pollution control
devices on automobiles, and the efficiency of vehicle operation. The
concentrations of CO will generally be highest along congested major
4-1
-------
highways, because of vehicle exhausts. The interplay between the normal
growth rate of vehicle use and the near-term increase in effectiveness
of pollution control devices will probably cause total CO emissions from
highway vehicles in the U. S. to decline after 1979.
4.1 NATIONAL EMISSION LEVELS
Estimates of the annual emissions of CO and other major air
pollutants from all sources in the U. S. are summarized in Table 4-1
for the years 1970 through 1977. It may be noted that 102.2 million
metric tons of CO were discharged to the atmosphere in 1970. An increase
is shown for 1971 and 1972 to 103.8 million metric tons and a subsequent
decrease is shown for each of the years 1973, 1974, and 1975 to a level
of 96.9 million metric tons. In 1976 the emission of CO rose to
102.9 million metric tons and in 1977 to 102.7 million metric tons.
Total nationwide emissions are shown according to the source
Q
categories in Table 4-2. The percentage contributed to the total
national emission of CO by each of the designated source categories is
shown in the last column.
The calculated nationwide annual emissions of CO from various
source categories are compared for the years 1970 through 1977 in Table
o
4-3. The estimations cited in Tables 4-1, 4-2, and 4-3 are the result
of current methodology and refined emission factors and should not be
compared with data reported earlier. These data show that from 1970
through 1977 the CO emissions increased by 0.5 percent. Since these
data are only calculated estimates of total nationwide emissions,
4-2
-------
TABLE 4-1. SUMMARY OF NATIONAL EMISSION ESTIMATES, 1970-1977
(10 metric tons/yr)
8
Year
1970
1971
1972
1973
1974
1975
1976
1977
TSPa
22.2
20.9
19.6
19.2
17.0
13.7
13.2
12.4
S0x
29.8
28.3
29.6
30.2
28.4
26.1
27.2
27.4
N0x
19.6
20.2
21.6
22.3
21.7
21.0
22.8
23.1
VOC
29.5
29.1
29.6
29.7
28.6
26.9
28.7
28.3
CO
102.2
102.5
103.8
103.5
99.7
96.9
102.9
102.7
a) TSP = total suspended particulates
SO = sulfur oxides
/\
NO = nitrogen oxides
/\
VOC = volatile organic compounds
CO = carbon monoxide
4-3
-------
TABLE 4-2. NATIONWIDE EMISSION ESTIMATES, 1977
(10 metric tons/year)
8
Source Category
Transportation
Highway vehicles
Non- highway vehicles
Stationary fuel combustion
Electric Utilities
Industrial
Residential, commercial,
and institutional
Industrial processes
Chemicals
Petroleum refining
Metals
Mineral products
Oil & gas production & marketing
Industrial organic solvent use
Other processes
Solid waste
Miscellaneous
Forest wildfires
Agricultural burning
Coal refuse burning
Structural fires
Miscellaneous organic solvent use
TSP
1.1
0.8
0.3
4.8
3.4
1.2
0.2
5.4
0.2
0.1
1.3
2.7
0
0
1.1
0.4
0.7
0.5
0.1
0
0.1
0
S0x
0.8
0.4
0.4
22.4
17.6
3.2
1.6
4.2
0.2
0.8
2.4
0.6
0.1
0
0.1
0
0
0
0
0
0
0
N0x
9.1
6.7
2.5
13.0
7.1
5.0
0.9
0.7
0.2
0.4
0
0.1
0
0
0
0.1
0.1
0.1
0
0
0
0
VOC
11.5
9.9
1.6
1.5
0.1
1.3
0.1
10.1
2.7
1.1
0.1
0.1
3.1
2.7
0.3
0.7
4.5
0.7
0.1
0
0
3.7
CO
85.7
77.2
8.5
1.2
0.3
0.6
0.3
8.3
2.8
2.4
2.0
0
0
0
1.1
2.6
4.9
4.3
0.5
0
0.1
0
Percentage of
Total CO
83.4
75.2
8.2
1.2
0.3
0.6
0.3
8.1
2.7
2.3
2.0
0
0
0
1.1
2.5
4.8
4.2
0.5
0
0.1
0
TOTAL
12.4
27.4
23.1
28.3
102.7
100 100
NOTE: A zero indicates emissions of less than 50,000 metric tons.
4-4
-------
cn
TABLE 4-3. NATIONWIDE CARBON MONOXIDE EMISSION ESTIMATES, 1970-1977
(10 metric tons/year)
8
Source Category
Transportation
Highway vehicles
Non-highway vehicles
Stationary fuel combustion
Electric utilities
Industrial
Residential, commercial &
institutional
Industrial processes
Chemicals
Petroleum refining
Metals
Mineral products
Oil & gas production & marketing
Industrial organic solvent use
Other processes
Solid waste
Miscellaneous
Forest wildfires
Agricultural burning
Coal refuse burning
Structural fires
Miscellaneous organic solvent use
1970
80.5
70.9
9.6
1.3
0.2
0.6
0.5
8.0
2.9
2.1
1.1
0
0
0
0.9
6.2
6.2
4.3
1.5
0.3
0.1
0
1971
81.1
71.7
9.4
1.4
0.2
0.6
0.6
7.9
2.7
2.1
2.2
0
0
0
0.9
4.7
7.4
5.9
1.2
0.2
0.1
0
1972
85.4
76.1
9.3
1.3
0.2
0.6
0.5
7.9
2.5
2.2
2.3
0
0
0
1.0
4.0
5.2
4.2
0.8
0.1
0.1
0
1973
85.9
76.5
9.4
1.4
0.3
0.6
0.5
8.2
2.7
2.2
2.3
0
0
0
1.0
3.6
4.4
3.5
0.7
0.1
0.1
0
1974
81.7
73.3
8.4
1.3
0.3
0.6
0.4
8.2
2.5
2.3
2.4
0
0
0
1.0
3.2
5.3
4.5
0.6
0.1
0.1
0
1975
82.0
73.8
8.2
1.1
0.3
0.5
0.3
7.3
2.2
2.4
1.8
0
0
0
0.9
2.9
3.6
3.0
0.5
0
0.1
0
1976
85.1
75.6
8.5
1.2
0.3
0.6
0.3
7.8
2.4
2.4
1.9
0
0
0
1.1
2.9
5.9
5.3
0.5
0
0.1
0
1977
85.7
77.2
8.5
1.2
0.3
0.6
0.3
8.3
2.8
2.4
2.0
0
0
0
1.1
2.6
4.9
4.3
0.5
0
0.1
0
TOTAL
102.2
102.5
103.8
103.5
99.7
96.9
102.9
102.7
NOTE: A zero indicates emissions of less than 50,000 metric tons per year.
-------
trends in emissions for local areas may be much different. Nevertheless*
national emission estimates should be indicative of the overall general
trend in the quantities of air pollutants released to the atmosphere.
Overall, carbon monoxide emissions have not changed significantly
during the period 1970-1977. Emissions have been reduced as a result of
less burning of solid waste and agricultural materials. However,
despite controls implemented on highway motor vehicles, total emissions
8
from this source category have increased by about 9 percent, due to
the increase in vehicle miles traveled.
4.2 EMISSIONS AND EMISSION FACTORS BY SOURCE TYPE
4.2.1 Mobile Combustion Sources
Table 4-3 shows the nationwide annual emission estimates for the
"transportation" category which includes emissions from all mobile
sources. Highway vehicles include passenger cars, trucks, and buses.
Non- highway vehicles include aircraft, railroads, vessels, and
miscellaneous mobile engines such as farm equipment, industrial ano!
construction machinery, lawnmowers, and snowmobiles. The estimated
emissions of CO by highway vehicles in 1977 was 77.2 million metric tons
and by non-highway vehicles, 8.5 million metric tons, representing
75.2 percent and 8.2 percent, respectively, of the total national
emissions of CO.
For localized pollutants such as CO, the ability of test procedures
to predict changes in emissions depends on the similarity of the localized
driving pattern and associated operating conditions to those in the test
procedure. The EPA therefore has developed a series of correction
factors to expand upon the light duty vehicle (LDV) and heavy duty
4-6
-------
vehicle (HDV) test procedures and to predict emissions from a large
number of user-specific scenarios. Data required to develop these
correction factors have been generated using carefully designed statis-
tical studies which test consumer-owned vehicles. Composite average
emission factors determined for a number of combinations of operating
conditions and vehicle mixes are available in the literature.
The data collected in the EPA exhaust emission surveillance programs
are analyzed to provide mean emissions by model-year vehicle in each
calendar year, change in emissions with the accumulation of mileage,
change in emissions with the accumulation of age, percentage of vehicles
complying with standards, and effect on emissions of vehicle parameters
(engine displacement, vehicle weight, etc.). These surveillance data,
along with prototype vehicle test data, assembly line test data, and
technical judgment, form the basis for existing and projected mobile
'
source emission factors.
4.2.2 Combustion for Power and Heat
Table 4-3 shows the nationwide annual emission estimates for the
"stationary fuel combustion" category, which includes all stationary
combustion equipment such as boilers and stationary internal combustion
engines.
The specific emission factors for stationary fuel combustors vary
according to the type and size of the installation and the fuel used as
well as the mode of operation. The EPA compilation of air pollutant
emission factors6 provides emission data obtained from source tests,
material balance studies, engineering estimates, etc., for the various
common emission categories.
4-7
-------
4.2.3 Technological Processes Producing CO
Table 4-3 shows the nationwide annual emission estimates for the
"industrial processes" category, which includes the emissions resulting
from the operation of process equipment by industries manufacturing
chemicals, refining petroleum, producing metals and metal products, and
i
by other processing industries (combining the emissions from pulp and
paper, wood products, agricultural, rubber and plastics, and textile
industries).
The specific emission factors for the various applicable processes
used in these manufacturing industries are detailed in the EPA compilation
of air pollution emission factors. Some specific information on the CO
emissions from industries was included in Chapter 3.
4.2.4 Solid Waste Combustion
Table 4-3 shows the nationwide annual emission estimates for the
"solid waste" category, which includes the emissions resulting from the
combustion of wastes in municipal and other incinerators, and from the
open burning of domestic and municipal refuse.
Specific emission factors for the various waste combustion procedures
in use are detailed in the EPA compilation of air pollution emission
factors.
4.2.5 Miscellaneous Combustion
Table 4-3 shows the nationwide annual emission estimates for a
"miscellaneous" category, which includes emissions from combustion of
forest, agricultural, and coal refuse materials and from structural
fires.
4-8
-------
Emission factors specific to the materials combusted and the
methods used are detailed in the EPA compilation of air pollution
emission factors.
4.3 ESTIMATION OF FUTURE EMISSION LEVELS
Future exposure to ambient CO concentrations will clearly depend
upon future amounts of CO emitted into the atmosphere and future CO
emission patterns. Since highest concentrations of CO generally result
>
from auto emissions, substantial research effort has been expended to
characterize those emissions accurately. Recently, the EPA has adminis-
tered a series of exhaust emission surveillance programs in order to
characterize how well vehicles perform in actual.use. Based on these
surveillance data, the EPA has published a method for calculating
existing and projected mobile source emission factors and has tabulated
average highway vehicle emission factors for 21 different combinations
of operating conditions and vehicle mixes,
Table 4-4 presents the estimated vehicle emission factors in units
of grams of CO per vehicle mile and per vehicle kilometer for the years
1970 through 1999 and for two selected highway scenarios. These data
are plotted in Figure 4-1, which illustrates the projected future
decrease in CO emissions per vehicle-kilometer of travel due to the
gradual replacement of vehicles without emission control equipment by
vehicles with control equipment. The rate of yearly decrease in CO
emission factors (i.e., the slope of the curve) is also affected by the
gradual deterioration of emission control equipment with accumulated age
and mileage.
4-9
-------
TABLE 4-4. AVERAGE VEHICLE EMISSION FACTORS
FOR TWO SELECTED HIGHWAY SCENARIOS
AVERAGE EMISSION FACTORS
Condi ti
Grams/mile
86.9
83.9
81.6
80.0
79.0
77.0
74.3
71.4
68.3
65.2
60.6
55.5
50.6
45.7
40.9
36.7
33.0
30.0
27.6
25.6
24.2
23.1
22.2
21.5
21.1
20.7
20.7
20.7
20.7
20.7
on A
Grams/km
54.0
52.1
50.7
49.7
49.1
47.8
46.1
44.3
42.4
40.5
37.6
34.5
31.4
28.4
25.4
22.8
20.5
18,6
17.1
15.9
15.0
14.3
13.8
13.4
13.1
12.9
12.9
12.9
12.9
12.9
Condi ti
Grams/mile
85.6
82.4
80.0
78.2
77.1
75.1
72.5
69.9
67.1
64.3
60.2
55.8
51.6
47.2
42.9
38.9
35.2
32.2
29.5
27.3
25.6
24.1
23.0
22.1
21.4
20.8
20.8
20.8
20.8
20.8
on B
Grams/km
53.2
51.2
49.7
48.6
47.9
46.6
45.0
43.4
41.7
39.9
37.4
34.7
32.0
29.3
26.6
24.2
21.9
20.0
18.3
17.0
15.9
15.0
14.3
13.7
13.3
12.9
12.9
12.9
12.9
12.9
Year
1970
1971
1972
1973
1974
1975
1976
1977
1978
1979
1980
1981
1982
1983
1984
1985
1986
1987
1988
1989
1990
1991
1992
1993
1994
1995
1996
1997
1998
1999
Speed: 19.6 mph (31.6 kph); Temperature: 75° F, % cold start: 20.6%
and % hot start: 27.3%.
Condition A: vehicle miles traveled = 8.3% automobiles,
5.8% for each of the two light truck classes, 4.5% heavy gas trucks,
3.5% heavy duty diesels, and 0.5% motorcycles, approximating national
vehicle miles traveled mix.
Condition B: vehicle miles traveled = 63% automobiles,
16% for each of the two light truck classes, 2.5% heavy gas trucks,
and 2.5% heavy duty diesel vehicles, approximating a mix of vehicle
miles traveled that might be found in a central city area.
4-10
-------
•g
1
«
E
v
"w
CC
O
h-
o
u.
Z
O
c/5
w
;g
UJ
b/
54
51
48
45
42
39
36
33
30
27
24
21
18
15
12
9
6
3
n
I I I I I I I I I I I I I I I
§w A - NATIONAL AVERAGE MIX OF VEHICLES^
_. ^^
^
*x —
\ ""
V
.
r <••
V. -
v. _
* •
— \\ "~
_ »*» —
^«
— x* . —
^^ w
__ "™* ""• •"• *^1™ •"• £!£,
_ ' — -
_
— —
*' 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1
72 74 7678 80828486 88 9092 9496 98 2000 2002
TIME, year
Figure 4-1. Average composite emission factors for carbon
monoxide.
4-11
-------
Total CO emission rates are also reflected by vehicle-use trends. Over
the past 20 years, there has been an increase in vehicle miles of travel
averaging 4.6 percent a year. ' * Vehicle miles of travel (VMT) increased
4.6 percent in 1971 and 1972; 2.4 percent in 1973 and 1974; 3.4 percent in
1975; and 5.9 percent in 1976. Federal Highway Administration projections
indicate that VMT will continue to increase at an annual average rate of 2.2
2 7
percent through 1999. The latest published EPA emission factors suggest
that CO emissions from mobile sources will peak between 1973 and 1979, then
decrease until 1994. After 1994, total CO emissions from automobiles may rise
again with increases in VMT. There are a number of other factors which may
influence future CO emission trends: delay of the clean car performance
standards, inspection and maintenance of pollution control equipment, possible
retrofit of less well-controlled vehicles, conversion to alternate fuels,
traffic flow improvements, motor vehicle use restraints, use of car pools,
increased fuel prices, etc., which cannot be predicted with certainty.
Ambient levels of CO generally improved from 1972 to 1977. There was a
20 percent increase in the number of sites with sufficient data for trends
analysis due to the expansion of State and local monitoring programs. Data
for CO trend analysis were obtained from EPA's National Aerometric Data Bank.
All sites having at least 4,000 annual values during both 1972-1974 and 1975-1977
were designated as trend sites. For carbon monoxide, 243 sites met this
selection criterion, and more than 80 percent of these sites had at least 4
years of data.
During the 1972-77 period, 80 percent of the selected CO sites showed
long-term improvement and this trend was fairly consistent for all 10 EPA
Regions. The median rate of improvement for the 90th percent!le of 8-hour
4-12
-------
values was approximately 6 percent per year. From 1976 to 1977, 70 percent of
the 243 sites improved. Consistent with this downward trend, almost one-third
of these sites reported their lowest values in 1977.
In discussing the relationship between ambient CO levels and CO emissions,
it is important to clarify certain components involved in estimating CO emissions,
Two key factors are the vehicle miles travelled (VMT) and the emissions per
VMT. In its simplest form, total CO emissions may be viewed as merely the
product of emissions per mile multiplied by the number of miles travelled.
Total CO emissions in 1976-77 were higher than in 1974-75. During this time,
the emissions per VMT actually decreased due to emission controls, but this
was more than offset by an even greater increase in VMT. The net effect was
an overall increase in total CO emissions. Translating these emission components
in terms of ambient CO levels, it would be reasonable to expect improvement at
downtown locations that are saturated with traffic because the emissions per
mile reductions would outweight any increase in VMT. On the other hand,
growth areas could record increases in ambient CO levels because increases in
Q
VMT offset the reduction in emissions per VMT.
4-13
-------
TABLE 4-1. SUMMARY OF NATIONAL EMISSION ESTIMATES, 1970-19778
(10 metric tons/yr)
Year
1970
1971
1972
1973
1974
1975
1976
1977
TSPa
22.2
20.9
19.6
19.2
17.0
13.7
13.2
12.4
S0x
29.8
28.3
29.6
30.2
28.4
26.1
27.2
27.4
NOX
19.6
20.2
21.6
22.3
21.7
21.0
22.8
23.1
VOC
29.5
29.1
29.6
29.7
28.6
26.9
28.7
28.3
CO
102.2
102.5
103.8
103.5
99.7
96.9
102.9
102.7
a) TSP = total suspended participates
SO = sulfur oxides
^
NO = nitrogen oxides
s\
VOC = volatile organic compounds
CO = carbon monoxide
4-14
-------
BIBLIOGRAPHY
1. Berens, A. P., and M. Hill. Automobile Exhaust Emission Surveillance
Analysis of the FY 1974 Program. EPA 460/3-76-019, U.S. Environmental
Protection Agency, Ann Arbor, ML, September 1976.
2. Beaton, J. L., E. C. Shirley, and J. B. Skog. Air Quality Manual. Volume
III. Traffic Information Requirements of Highway Impact on Air Quality.
U.S. Department of Transportation, Washington, DC, April 1972.
3. Office of Air Quality Planning and Standards. Complication of Air Pollution
Emission Factors. Parts A and B. Third Edition. AP-42, U.S. Environmental
Protection Agency, Research Triangle Park, NC, August 1977.
4. Highway Research Board. Highway Capacity Manual 1965. Special Report
87, Publication 1328, National Academy of Sciences, Washington, DC, 1966.
5. Office of Transporation and Land Use Policy. Mobile Source Emission
Factors. Final document. EPA-400/9-78-005, U.S. Environmental Protection
Agency, Washington, DC, March 1978.
6. Office of Air Quality Planning and Standards. National Air Quality and
Emissions Trends Report, 1977. EPA-450/2-78-052, U.S. Environmental
Protection Agency, Research Triangle Park, NC, December 1978.
7. Thayer, S. D., and J. D. Cook. Vehicle Behavior in and Around Complex
Sources and Related Complex Source Characteristics. Volume VI-Major
Highways. EPA-450/3-74-003-f, U.S. Environmental Protection Agency,
Research Triangle Park, NC, November 1973.
8. Federal Highway Administration. Highway Travel Forecasts. U.S. Department
of Transporation, Washington, DC, November 1974.
4-15
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5. ANALYTICAL METHODS FOR MEASUREMENT OF CARBON MONOXIDE
It 1s Impossible to monitor and maintain air quality (or even to
study^the health effects of pollutants) without reliable methods for
measuring the amount of carbon monoxide (CO) present. This chapter
contains surveys of the analytical methods for CO in air and in blood,
as well as some comments on sampling techniques.
5.1 INTRODUCTION
To promote uniform enforcement of the air quality standards set
forth under the Clean Air Act as amended, EPA has established provisions
under which analytical methods can be designated as "reference" or
175
"equivalent" methods. A reference method or equivalent method for air
quality measurements is required for acceptance of measurement data by EPA.
At present the reference methods for monitoring CO in the atmosphere
must be based on non-dispersive infrared photometry (NDIR). However,
before a particular NDIR instrument can be used in a reference method,
it must be so designated by EPA in terms of manufacturer, model number,
components, operating range, etc. Several NDIR instruments have been so
designated. No equivalent methods using a measurement principle other
than NDIR have been designated thus far for CO in ambient air.
5-1
-------
o
An operating range of up to 58 mg/m (0 to 50 ppm) CO in air is typical
for the NDIR instruments designated for reference method use. Analytical
i
capability is needed not only for this range but also for a narrower range up
o
to 1 mg/m (0 to 1 ppm) for measuring background levels in unpolluted atmospheres
o
and a wider range up to 1150 mg/m (up to 1000 ppm) for measuring high concen-
trations, such as in vehicular tunnels and parking garages.
There is a recognized need to relate results by other methods (including
those used in health effects and field studies) to those obtained by the NDIR
reference method, but this is difficult because reported information on the
other methods is inadequate as to variations in operator competence and the
effects of experimental conditions.
5.1.1 Overview of Techniques for Measurement of CO in Air
In the past decade, there have been several excellent reviews on the
measurement of CO in the atn)ospnere.43,54,74>87>97,136)145,164>169)170)184
For monitoring, the best technique at present is nondispersive infrared
photometry,49'81'111'112'125'128'148'149'157'158 usually with a Luft-type
102
detector. A more sensitive method, suitable for measuring background
levels, is gas chromatography.19'22'46'130'160'167'168 For high levels, a
useful technique is catalytic oxidation of the CO, using Hopcalite or other
catalysts either with temperature-rise sensors »l"»i4o or ^^ eiectro-
chemical sensors.12'13'19'50'136'144
Other analytical schemes used for CO in air include: infrared gas-
filter correlation, a refinement of HDIR;1'11'24'25'65'68'69'75'187 dual
isotope infrared fluorescence, another technique derived from NpiR;101)107}108
the reaction with hot mercuric oxide to give elemental mercury
5-2
-------
vapor.I*.110,115,123,138 the react1on w1th heated ioc|ine pentoxide to
give elemental iodine;2'113'118*179'186 and color reactions as with
palladium salts or the silver salt of p_-sulfamoylbenzoate.4'15'60'88'92'
GO TOR 1^4. 1 fil
* * ' A classical procedure for many decades was to use
gasometric apparatus such as the Orsat or Haldane44 1n which the CO
present in a gas sample Is absorbed by cuprous chloride solution, and
the decrease 1n volume or pressure 1s measured, but this 1s not sensi-
tive enough for trace amounts. Many of these methods are described 1n
Section 5.3.
For the future, microwave rotational spectroscopy offers promise of
an analytical technique of high specificity. ' Other possible ways
180
to determine CO include: the chemiluminescent reaction with ozone,
fifi QE
X-ray excited optical fluorescence, radiorelease of Kr from the
kryptonates of mercuric oxide or iodine pentoxide, ' and utilization
8 64
of narrow-band infrared laser sources. *
5.1.2 Calibration Requirements
Whichever method or instrument is used, it is essential that the
results be validated by frequent calibration with samples of known
composition similar to the unknowns.42' ' Chemical analyses can be
relied on only after the analyst has achieved acceptable accuracy in the
analysis of such standard samples through an audit program.
5.2 PREPARATION OF CARBON MONOXIDE GAS STANDARDS
5.2.1 Gravimetric Method
A set of reliable gas standards for CO in air certified at levels
of approximately 12, 23, and 46 mg/cm3 (10, 20, and 40 ppm) is
5-3
-------
obtainable from the National Bureau of Standards (NBS), Washington, D.C.
17ft
20234. These NBS Standard Reference Materials (SRMs) are supplied as
compressed gas (at about 1700 psi) in high-strength aluminum cylinders
o
containing 31 ft of gas at standard temperature and pressure, dry (STP)
and are accurate to better than 1 percent of the stated values. Because
of the time and effort required in their preparation, SRMs are not
intended for use as daily working standards, but rather as primary
standards against which transfer standards can be calibrated.
The gravimetric method used by NBS for preparing primary standards
83 84
of CO ' is as follows. An empty gas cylinder is tared on an analytical
balance; then 2 g of pure CO, weighed accurately to ±2 mg, is added from
a high-pressure tank. Next, 100 g of pure air (accurately weighed) is
added from a pressure tank, and the concentration of CO is calculated
from the respective weights added and the molecular weights of the two
gases. Not only the average "molecular weight" of the air, but also the
requisite careful check of purity, is obtained by mass spectrometry and
gas chromatography analyses of the air and the CO. Lower-concentration
primary standards are prepared by serial dilutions (not more than a
factor of 100 for each step) using the same technique.
The commercial suppliers of compressed gases are another source of
3
samples of air containing CO in the mg/m or ppm range. However, the
nominal values for CO concentration supplied by the vendor should be
verified by intercomparison with an SRM or other validated standard
sample. A three-way intercomparison has been made among the NBS SRMs
and commercial gas blends and an extensive set of standard gas mixtures
5-4
-------
prepared by gravimetric blending at the Environmental Protection Agency.124
The results showed that commercial gas blends are within ±2 percent of
the true value represented by a primary standard. Another study on
59
commercial blends found poorer accuracy. To achieve compatible results
1n sample analyses, different laboratories should interchange and compare
their respective working standards at frequent intervals.
83
In making and using standards, many precautions are needed; one
deserves special mention. Large but unpredictable decreases in CO
concentration occur in mixtures prepared in ordinary mild steel gas
cylinders, within a few months, as shown in Figure 5-1. This may be due
to carbonyl formation or oxidation to carbon dioxide. The difficulty
can be avoided by the use of gas cylinders made of stainless steel or
aluminum. A special treatment for aluminum, which includes enhancement
188
of the aluminum oxide surface layer, has been recommended.
In addition to the set of Standard Reference Materials for CO in
air, another set of SRMs is available from NBS for CO in nitrogen, which
covers concentrations from 10 to 957 ppm.
5.2.2 Volumetric Gas Dilution Methods
Standard samples of CO in air can also be prepared by volumetric
pc
gas dilution techniques. In a versatile system designed for this purpose,
air at a pressure of 10 to 100 psi is first purified and dried by
passage through cartridges of charcoal and silica gel, then passed
through a sintered metal filter into a flow control and flowmeter system.
The CO (or a mixture of CO in air which is to be diluted further), also
under pressure, is passed through a similar flow control and flowmeter
system.
5-5
-------
400
Figure 5-1. Loss of carbon monoxide with time in mild steel cylinders.83
(Used with permission of ISA Transactions, Vol. 14, No. 4 Copyright Instrument
Society of America, 1975.)
5-6
-------
Both gas streams are led into a mixing chamber, which is designed
to mix the gas streams rapidly and completely before passage into the
sampling manifold from which the standard samples may be withdrawn.
From the air flow rate, F., and the CO flow rate, F , the concentration
ft CO
of CO in the sample, CCQ, is readily calculated by the expression
C co
Fco+FA
For samples prepared by dilution of a more concentrated bulk mixture,
the concentration is given by
F +F >
where Fb and C. are the values of flow rate and concentration of CO,
respectively, for the bulk mixture.
5.2.3 Other Methods
Permeation tubes have been used for preparing standard mixtures of
119 143
other pollutant gases such as sulfur dioxide and nitrogen dioxide. *
In this technique, a sample of the pure gas under pressure is allowed to
diffuse through a calibrated partition at a defined rate into a diluent
gas stream, to give a standard sample of known composition. Although
permeation tubes for making CO standards are not routinely used at
present in the United States, such tubes are believed to be in use in
Europe.
Another possible way to liberate known amounts of CO into a diluent
gas is by thermal decomposition of nickel tetracarbonyl . However, an
attempt to use this as a gravimetric calibration source showed that the
relation between CO output and weight loss of the Ni(CO)4 is norr
stoichiometric.
5-7
-------
Chemical assay methods such as those noted in Section 5.1.1
can be used to verify the CO concentration in a standard mixture, but
they do not provide greater accuracy or reliability than is attained by
careful preparation of the standard sample, as for example 1n prepara-
tion of an NBS SRM.
5.3 MEASURING CARBON MONOXIDE IN AIR
Ambient CO monitoring is an expensive and time consuming task,
requiring skilled personnel and sophisticated analytical equipment.
This section discusses several important aspects of the continuous and
intermittent measurement of CO in the atmosphere, including sampling
techniques, sampling schedules, and recommended analytical methods for
CO measurement.
5.3.1 Sampling Techniques
Carbon monoxide monitoring requires a sample introduction system,
an analyzer system, and a data recording system, as illustrated in
174
Figure 5-2. While the "heart" of any air pollution monitoring
system is the air pollution analyzer, Figure 5-2 shows that there is
a considerable amount of supportive equipment that is necessary in
order to perform continuous air monitoring.
A sample introduction system consists of a sampling probe, an
intake manifold, tubing, and air movers. This system is needed to
collect the air sample from the atmosphere and to transport it to the
analyzer without altering the original concentration. It may also be
used to introduce known gas concentrations in order to check periodically
the reliability of analyzer output. Construction materials for the
5-8
-------
SAMPLE INTRODUCTION SYSTEM
OS
vo
BLOWER
SAMPLE INTAKE PORT
MFOLD^S.
+ +. JL. ^.\JU ^ &
ANALYZER SYSTEM
FIRST STAGE
PRESSURE v^
GAUGE T?)
CYLINDER
PRESSURE
VALVE
SECOND STAGE
PRESSURE GAUGE
SECOND STAGE
PRESSURE VALVE
CARBON MONOXIDE ANALYZER
MOISTURE
CONTROL
ROTAMETER I-1
PARTICULATE
FILTER
ZERO GAS
SPAN GAS
DATA RECORDING
AND
DISPLAY SYSTEM
AMPLIFIER
I
ANALYZER
INDICATOR
STRIP CHART
RECORDER
DATA
-(ACQUISITION
SYSTEM
Figure 5-2. Carbon monoxide monitoring system.
-------
sampling probe, intake manifold, and tubing should be tested to demon-
strate that the test atmosphere composition or concentration is not
significantly altered. It is recommended that the sample introduction
37
system be fabricated from borosilicate glass or FEP Teflon when
monitoring for all pollutants. However, when sampling for only CO, it
191
has been reported that no measurable pollutant losses were observed
when sampling systems were constructed of tygon, polypropylene,
polyvinylchloride piping, aluminum, or stainless steel. The sample
introduction system should be constructed such that it presents no
pressure drop to the analyzer.
The analyzer system consists of the analyzer itself and any sample
preconditioning components that may be necessary. Sample preconditioning or
optical filters require a moisture control system to help minimize the false
positive response of the analyzer (e.g., the NDIR analyzer) to water
vapor, and a particulate filter to help protect the analyzer from clogging
and possible chemical interference due to particulate buildup in the
sample lines or analyzer inlet. The sample preconditioning system may
also include a flow metering and flow control device in order to control
the sampling rate to the analyzer. As for the analyzer, there are
several analytical methods for the continuous measurement of CO as fully
discussed in Section 5.3.4.
A data recording system is needed to record the output of the
analyzer. Data recording systems range from simple strip chart recorders
to digital magnetic tape recorders to computerized telemetry systems
which transfer data from remote stations to a central location via
telephone lines or radio waves.
5-10
-------
In order to ensure the accuracy and validity of data collected from
the CO monitoring system, a quality assurance program 1s required.
Such a program consists of procedures for calibration, operational and
preventive maintenance, data handling, and auditing, and are fully
documented 1n a quality assurance program manual.
Calibration procedures consist of periodic multipoint primary
calibration and secondary calibration which are prescribed to minimize
systematic error. Primary calibration involves the introduction of test
atmospheres of known concentration to an instrument in its normal mode
of operation for the purpose of producing a calibration curve.
A calibration curve is derived from the analyzer response obtained
by introducing several successive test atmospheres of different known
concentrations. One recommended method for generating CO test atmos-
pheres is by using zero air (containing no CO) and several known concen-
trations of CO 1n air or nitrogen contained in high pressure gas cylinders
175
and verified using NBS-cert1fied SRM wherever possible. The number
of standard gas mixtures (cylinders) necessary to establish a calibration
curve depends on the nature of the analyzer output. A multipoint cali-
bration at five or six different CO concentrations covering the operating
range of the analyzer is recommended by the EPA.1 ' Alternatively,
the multipoint calibration is accomplished by diluting a known high-
concentration CO standard gas with zero gas using a calibrated flow
dilution system.
5-11
-------
Primary calibrations should be performed when the analyzer is first
174
purchased and every 30 days thereafter. Primary calibration is also
recommended after the analyzer has had maintenance which could affect
its response characteristics or when results from the auditing program
174
show that the desired performance standards are not being met.
Secondary calibration consists of a zero and upscale span of the
177
analyzer which is recommended to be performed daily. If the analyzer
response differs (say by greater than ±2 percent) from the certified
concentrations, then the analyzer is adjusted accordingly. Complete
records of secondary calibrations should be kept to aid in data reduction
and for use in the auditing program.
Operational and preventive maintenance procedures consist of
operational checks which are made to insure the proper operation of the
analyzer and a preventive maintenance schedule which is necessary to
prevent unexpected analyzer failure and the associated loss of data.
Operational checks include checks of zero and span control settings,
sample flow rate, gas cylinder pressures, sample cell pressure, shelter
temperature, water vapor control, the particulate filter, the sample
introduction system, the recording system, and the strip chart record.
These checks may indicate the need for corrective/remedial action. They
are usually performed in conjunction with secondary calibrations. In
addition to operational checks, a routine schedule of preventive mainte-
nance should be developed. Maintenance requirements of the analyzer are
usually specified in the manufacturer's instrument manual. Routine
maintenance of supportive equipment (i.e., the sample introduction
5-12
-------
system and the data recording system) is also required. This may include
sample line filter changes, water vapor control changes, sample line cleaning,
leak checks, and chart paper supply changes.
Data handling procedures consist of data generation, data reduction, data
validation, data recording, and data analysis and interpretation. Data generation
is the process of generating raw, unprocessed and unvalidated observations as
recorded on a strip chart record. Data reduction is the conversion of recorder
output as percent of full scale to concentration units with the use of calibration
records. This is usually a manual operation which requires an individual to
scan a stripchart record and visually average the trace over a given time
period (usually one hour). This is a difficult procedure and care should be
taken. Data validation involves final screening of data before it is recorded.
Questionable data "flagged" by the monitoring technician are reviewed at this
point with the aid of daily calibration and operation records to assess their
validity. Specific criteria for data selection and several instrument checks
are outlined in reference 174. Data recording involves the recording of data
in a standard format for data storage, interchange of data with other agencies,
and/or data analysis. The EPA has adopted a standard recording format known
173
as SAROAD (Storage and Retrieval of Aerometric Data). An example of an
hourly SAROAD data form is given in Figure 5-3. Data analysis and interpretation
usually includes a mathematical or statistical analysis of air quality data
and a subsequent effort to interpret results in terms of exposure patterns,
meteorological conditions, characteristics of emission sources, and geographic
and topographic conditions.
5-13
-------
Hourly Data Form
OS
I
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Country
City Name
ENVIRONMENTAL PROTECTION AGENCY
National Aerometric Data Bank
P.O. Box 12055
Research Trianqle Park
North Carolina 27711
Site Address
Paiamrter obsrived
Method
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Units of obs.
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Figure 5-3. SAROAD hourly data form.173
-------
Auditing procedures consist of several quality control checks and
subsequent error analyses in order to determine an estimate of the
accuracy and precision of air quality measurements made. The quality
control checks for CO include a data processing check, a control sample
check, and a water vapor interference check, which should be performed
by a qualified individual independent of the regular operator. The
error analysis is a statistical evaluation of the accuracy and precision
of air quality data. Guidelines have been published by EPA174 for
calculating an overall bias and standard deviation of errors associated
with data processing, measurement of control samples, and water vapor
interference from which the accuracy and precision of CO measurements
can be determined. More recently, EPA has recommended a method for
determining the accuracy and precision of CO measurements based on
primary and secondary calibration records. Accuracy is the agreement of
an observed measurement with an accepted reference or true value and can
be estimated based on multipoint calibration records. Precision is a
measure of repeatability and can be estimated based on secondary
calibration records.
In summary, the data provided by the quality control checks and
subsequent error analyses are sufficient to provide an overall estimate
of data quality and an indication that data quality may be inadequate.
If the data quality is not adequate, the causes of large deviations
should be determined and appropriate action taken to correct the
deficiencies. These actions may include an increased auditing program,
increased frequency of primary calibrations, increased frequency of
preventive maintenance, changes in monitoring procedures, replacement of
analyzer, and/or personnel changes.
5-15
-------
5.3.2 Sampling Schedules
Carbon monoxide concentrations in the atmosphere exhibit large
temporal variations due to changes in the time and rate that CO is
emitted by different sources and due to changes in meteorological conditions
which govern the amount of transport and dilution which take place.
During a 1-year period an urban CO station may monitor hourly concentrations
3
of CO ranging from 0 to as high as 50 mg/m (45 ppm). Violations of the
NAAQS are based on the second highest 1-hr and 8-hr average concentration,
which represents an isolated and "rare" event when compared to the 8760
hours which constitute one year. In order to measure this "rare" event,
the "best" sampling schedule to employ is continuous monitoring 24 hours
per day, 365 days per year. Even so, continuous stations rarely operate
for significant periods without data losses due to malfunctions, upsets,
and routine maintenance. Data losses of 5 to 10 percent are not uncommon,
which represents 438 to 876 hours. As a result, the data must be inter-
preted in terms of the "likelihood" that the NAAQS were attained or
violated. Statistical methods can be employed to interpret the results. '
While continuous monitoring is the "best" sampling schedule,
statistically valid sampling can be performed using random or systematic
schedules. Most investigations of various sampling schedules have been
8fi 1?T T ?7
performed on particulate air pollution data, * ' but the same
sampling schedules could also be used for CO monitoring. However, NDIR
o
instruments do not perform reliably in intermittent sampling. Akland
evaluated six years of particulate data and showed that sampling one day
every two weeks could be used to obtain annual mean suspended particulate
5-16
-------
concentrations within an accuracy of 2.9 percent to 5.8 percent compared
to sampling every day, for systematic and random sampling, respectively.
By collecting samples every three days, the precision was improved to
0.2 percent and 3.9 percent for the systematic and random methods,
respectively. The systematic method uses a regular sampling interval of
any number of days except 7 or multiples of 7. This ensures that all
days of the week are sampled equally. Random selection is more likely
to result in a less precise yearly estimate than systematic sampling due
to the highly heterogeneous nature of the units (daily fluctuations)
o
within the sampling interval. Systematic sampling tends to be more
representative.
For any number of air samples, the expected deviation of the sample
mean from the true population mean can be determined using statistical
142
techniques such as those described by Saltzman. These methods can be
used a priori to determine the desired number of samples to be collected
121
during a study. Ott has shown that annual mean CO concentrations can
3
be measured with an accuracy of ±2.16 mg/m (±1.94 ppm), at 0.99 confi-
dence level, with as few as nine random 1-hr average samples during the
year (based on San Jose data). With 144 random 1-hr samples, the accuracy
3
was improved to ±0.54 mg/m (±0.49 ppm). The annual mean concentration
at this site was 3.93 mg/m3 (3.54 ppm). Using random sampling techniques
and using automatic bag samplers filling one bag each hour, CO measure-
ments can be made at many more locations and at less cost than continuous
monitoring. Ott121 estimates the cost of random sampling at nine sites
^ f
to be 70 percent less expensive than continuous monitoring at the same
sites.
5-17
-------
Short-term studies designed to sample during "worst case" seasons
and/or times of day can provide data needed on maximum 1-hr and 8-hr CO
concentrations for comparison to NAAQS. In other cases, where concentra-
tion trends are not known and where CO concentrations are expected to be
high, a full year of data may be necessary.
5.3.3 Recommended Analytical Methods for CO Measurements
Different analytical methods for CO measurement are required for
different purposes, depending on the concentrations to be measured
and the physical environment to which the analyzer will be exposed
(i.e., temperature, vibration, etc.). When very low global background
concentrations are being monitored, only the most sensitive analytical
methods can be used. However, for monitoring CO in urban atmospheres
for the purpose of determining compliance with National Ambient Air
Quality Standards (NAAQS) an EPA "reference" or "equivalent" method
should be used. Specifications for automated analytical methods for
the measurement of CO have been issued by EPA (see Table 5-1). The
EPA has specified NDIR as the measurement principle for reference
methods for determining compliance with the NAAQS for CO. An "equivalent
method" can be so designated when an analytical method is shown to
produce results that are equivalent to an approved NDIR method.
Presently, several reference methods using the NDIR principle have
been approved for monitoring for NAAQS achievement. No gas chromato-
graphic/flame ionization (GC) methods have been designated as equivalent
methods but some appear to be suitable for such designation.
The I«0c coulometric method is considered to be "unacceptable" due to
5-18
-------
TABLE 5-1. PERFORMANCE SPECIFICATIONS FOR AUTOMATED
ANALYTICAL METHODS FOR CARBON MONOXIDE175
Range
Noise
Lower detectable limit
Interference equivalent
Each interfering substance
Total interfering substances
Zero drift
12 hour
24 hour
Span drift, 24 hour
20 percent of upper range limit
80 percent of upper range limit
Lag time
Rise time
Fall time
Precision
20 percent of upper range limit
80 percent of upper range limit
0 to 57 mg/m^ (0 to 50 ppm)
0.6 mg/m:: (0.50 ppm)
1.2 mg/m (1.0 ppm)
3
±1.2 mg/m3 (±1.0 ppm)
1.7 mg/m (1.5 ppm)
±1.2 mg/m? (±1.0 ppm)
±1.2 mg/m (±1.0 ppm)
±10.0 percent
±2.5 percent
10 min.
5 min.
5 min.
0.6 mg/rru (0.5 ppm)
0.6 mg/m (0.5 ppm)
Definitions:
Range: Nominal minimum and maximum concentrations that a method is
capable of measuring.
Noise: The standard deviation about the mean of short duration
deviations in output that are not caused by input concentration changes.
Lower Detectable Limit: The minimum pollutant concentration that
produces a signal of twice the noise level.
Interference Equivalent: Positive or negative response caused by a
substance other than the one being measured.
Zero Drift: The change in response to zero pollutant concentration
during continuous unadjusted operation.
Span Drift: The percent change in response to an up-scale pollutant
concentration during continuous unadjusted operation.
Lag Time: The time interval between a step change in input concentration
and the first observable corresponding change in response.
Rise Time: The time interval between initial response and 95 percent of
final response.
Fall Time: The time interval between initial response to a step decrease
in concentration and 95 percent of final response.
Precision: Variation about the mean of repeated measurements of the
same pollutant concentration expressed as one standard deviation about
the mean.
5-19
-------
its slow response, sensitivity to temperature, and interferences by
172
mercaptans, hydrogen sulfide, olefins, acetylenes, and water vapor.
All other methods not specifically designated automatically fall under
the "unapproved" category. Current lists of designated reference and
equivalent methods of analysis for air pollutants can be obtained from
EPA regional offices.
Monitoring of CO for purposes other than NAAQS compliance, such as
atmospheric research, industrial hygiene, or stack sampling may employ
other methods which may be more sensitive to low CO concentrations, or
more suitable to the rigors of field studies. Instruments employing the
NDIR method are very sensitive to vibration, which makes them unsuitable
for mobile or even portable use. The physical size and usual construc-
tion of both NDIR and GC instruments limit their application primarily
to laboratory environments.
Portable instruments are commercially available for making CO
measurements in the field using different analytical techniques.
Instruments based on controlled-potential electrochemical analysis have
3 13 20
detection limits of less than 1 mg/m (0.9 ppm). * These instruments
can be employed for portable measurements in mines and hostile working
45
environments, as well as research for commuter "in-car" exposure,
45
indoor worker exposure, or CO measurements taken from aircraft.
Another common technique for obtaining intermittent CO concentration
data is to employ portable pumps and air sampling bags to collect an air
sample which can be later analyzed for CO concentration using an NDIR or
38 120
other method. ' Bags of 2- to 90-liters are typical. Construction
5-20
-------
materials Include Mylar, Tedlar, aluminlzed Scotch-pak, Scotch-pak,
Saran, and Teflon. > The inert properties of CO make it ideal for
bag sampling, since the rate of decay of the sample while in the bag is
slow. However, investigators using the bag sampling technique should
perform their own tests of decay rate as part of their quality assurance
program.
Grab samples from stacks or automobile exhaust pipes where CO
3
concentrations may range from 500 mg/m (450 ppm) to several percent CO
fi OQ
may be analyzed using colored silver sols detection tubes ' or by
Orsat analysis. Bag samples of these exhaust gases can also be taken,
Oft
quantitatively diluted, then analyzed using an NDIR instrument.
5.3.4 Continuous Measurement Methods
5.3.4.1 Nondispersive Infrared Photometry—Carbon monoxide has a
characteristic infrared absorption near 4.6 urn so that the absorption
of infrared radiation by the CO molecule can be used to measure CO
concentration in the presence of other gases. The NDIR method is based
on this principle.
Although the size, shape, sensitivity, and range of NDIR instruments
vary with manufacturer, their basic components and configurations are
similar. Most commercially available instruments include a hot filament
source of infrared radiation, a rotating sector (chopper), a sample
cell, a reference cell, and a detector (see Figure 5-4).
The reference cell contains a non-infrared-absorbing gas while the
sample cell is continuously flushed with the sample atmosphere. The
detector consists of a two-compartment gas cell (both filled with CO
5-21
-------
INFRARED
SOURCE
REFERENCE
CELL
SAMPLE
CELL
RECORDER
SAMPLE IN
O
-------
under pressure) separated by a diaphragm whose movement causes a change
of electrical capacitance in an external circuit and ultimately an
amplified electrical signal which is suitable for input to a servo-type
recorder.
During analyzer operation an optical chopper intermittently exposes
the reference and sample cells to the infrared sources. At the frequency
imposed by the chopper, a constant amount of infrared energy passes
through the reference cell to one compartment of the detector cell while
a varying amount of infrared energy, approximately inversely proportional
to the CO concentration in the sample cell, reaches the other detector
cell compartment. These unequal amounts of residual infrared energy
reaching the two compartments of the detector cell cause unequal expan-
sion of the detector gas, resulting in variation in the detector cell
diaphragm movement, which in turn produces the electrical signal
previously discussed.
•Cx
Because water vapor is the principal interfering substance in
determining CO by NDIR techniques, a moisture control system is particu-
larly important. To reduce water vapor, which gives an erroneously high
value, water can be removed by drying agents or cooling, or its effect
can be reduced by optical filters.
Nondispersive infrared systems have several advantages. They are
not sensitive to flow rate, they require no wet chemicals, they are
reasonably independent of ambient air temperature changes, they are
sensitive over wide concentration ranges, and they have short response
times. Further, NDIR systems may be operated by nontechnical personnel.
5-23
-------
Such systems also have some disadvantages, such as zero drift, span
drift, nonlinearity, and high cost. Some newer instruments have minimum
drift because good-quality thermostats and solid-state electronics are
used in their manufacture. Such instruments also have automatic zeroing,
spanning, and recalibrating capability; they may also be obtained with
essentially linear outputs.
5.3.4.2 Gas Chromatography - Flame Ionization--A gas sampling valve, a
back flush valve, a precolumn, a molecular sieve column, a catalytic
reactor, and a flame ionization detector comprise the gas chromatography-
flame ionization system. In operation, measured volumes of air are
delivered 4 to 12 times per hour to a hydrogen flame ionization detector
that measures the total hydrocarbon content (THC). A portion of the
same air sample, injected into a hydrogen carrier gas stream, is passed
through a column where it is stripped of water, carbon dioxide, and
hydrocarbons other than methane. Methane is then separated from CO by a
gas chromatographic column. The methane, which is eluted first, is
unchanged after passing through a catalytic reduction tube into the
flame ionization detector. The CO eluted into the catalytic reduction
tube is reduced to methane before passing through the flame ionization
130
detector. Between analyses the stripping column is flushed out.
Nonmethane hydrocarbon concentrations are determined by subtracting the
methane value from the total hydrocarbon value.
There are two possible modes of operation. One of these is a
complete chromatographic analysis showing the continuous output from the
detector for each sample injection. In the other, the system is programmed
5-24
-------
for both automatic zero and span settings to display selected elution peaks as
bar graphs. The peak height is then the measure of the concentration. The
first operation is referred to as the chromatographic or "spectro" mode and
the second as the barographic or "normal" mode.
Since measuring CO entails only a small increase in cost, instrument
->
complexity, and analysis time, these instruments are customarily used to
measure three pollutants: methane, total hydrocarbons, and CO.
The instrumental sensitivity for each of these three components is
3
0.023 mg/m (0.02 ppm). The lowest full-scale range available is usually up
3 3
to 2.3 mg/m (0 to 2 ppm) up to 5.7 mg/m (up to 5 ppm), although at least one
o
instrument has up to 1.2 mg/m (up to 1 ppm) range. Because of the complexity
of these instruments, continuous maintenance by skilled technicians is required
to minimize excessive downtime which may be considered a possible disadvantage
of the system.
5.3.4.3 Electrochemical Analyzers
5.3.4.3.1 Control!ed-potential electrochemical analysis. Carbon monoxide is
measured by means of the current produced in aqueous solution by its electro-
oxidation at a catalytically active electrode. The concentration of CO
reaching the electrode is controlled by its rate of diffusion through a membrane.
12 13
This is dependent on its concentration in the sampled atmosphere. ' Proper
selection of both the membrane and such cell characteristics as the nature of
the electrodes and solutions make the technique selective for various pollutants,
194
A similar technique has been reported by Yamate and Inoue.
5-25
-------
The generated current is linearly proportional to the CO concen-
o 3
tration from 0 to 115 mg/m (0 to 100 ppm). A sensitivity of 1.2 mg/m
(1 ppm) and a 10-second response time (90 percent) are claimed for a
currently available commercial instrument.
Acetylene and ethylene are the chief interfering substances:
1 part acetylene responds as 11 parts CO and 1 part ethylene as
0.25 part CO. For hydrogen, ammonia, hydrogen sulfide, nitric oxide,
nitrogen dioxide, sulfur dioxide, natural gas, and gasoline vapor,
interference is less than 0.03 part CO per 1 part interfering substance.
5.3.4.3.2 Galvanic analyzer. Galvanic cells employed in the manner
described by Hersch ' can be used to measure atmospheric CO
continuously. When an air stream containing CO is passed into a
chamber packed with IpO,- and heated to 150°C^ the following reaction
takes place:
. T n (150or, ^ T
The liberated iodine is absorbed by an electrolyte and transferred to
the cathode of a galvanic cell. At the cathode, the iodine is reduced
and the resulting current is measured by a galvanometer. Instruments
using this detection system have been used successfully to measure CO
levels in traffic along freeways.
Mercaptans, hydrogen sulfide, hydrogen, olefins, acetylenes, and
water vapor interfere. Water may be removed by sampling through a
drying column; hydrogen, hydrogen sulfide, acetylene, and olefin inter-
ferences can be minimized by sampling through an absorption tube con-
taining mercuric sulfate on silica gel.
5-26
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5.3.4.3.3 Coulometric analyzer. A coulometric method employing a
modified Hersch-type cell has been used to measure CO In ambient air on
57
a continuous basis. The reaction of I205 with CO liberates iodine,
which is then passed into a Ditte cell, and the current generated is
measured by an electrometer-recorder combination. Interferences are the
same as those discussed above for the galvanic analyzer.
This technique may be used for a minimum detectable concentration
o
of 1.2 mg/m (1 ppm) with good reproducibility and accuracy if flow
rates and temperatures are well controlled. This method requires careful
column preparation and use of filters to remove interferences. Its
relatively slow response time may be an added disadvantage in some work.
5.3.4.4 Mercury Replacement—Mercury vapor formed by the reduction of
mercuric oxide by CO is detected photometrically by its absorption of
ultraviolet light at 253.7 nm. The reaction involved is:
CO + HgO (21Q°C) CQ2 + Hg
It is potentially a much more sensitive method than infrared absorption
because the oscillator strength of mercury at 253.7 nm is 2,000 times
greater than that of CO at 4.6 urn. Hydrogen and hydrocarbons also
reduce mercuric oxide to mercury and there is some thermal decomposition
of the oxide. Operation of the detector at constant temperature results
in a regular background concentration of mercury from thermal decomposition.
The instrument is portable and has a capability for analyzing CO concen-
o
trations of 0.025 to 12 mg/m3 (0.020 to 10.0 ppm). Changes of 0.002 mg/m
(0.002 ppm) are detectable. For this reason, this instrument has been
used to determine global CO levels.
5-27
-------
McCullough et al. * recommended a temperature of 175°C to
minimize hydrogen interference. A commercial instrument employing these
115
principles was made and used during the middle 1950's. The technique
has been recently used for measuring background CO concentrations.
138
Robbins et al. have described an instrument in which the mercuric
oxide chamber is operated at 210°C, and the amount of hydrogen inter-
ference is assessed by periodically introducing a tube of silver oxide
into the intake air stream. At room temperature silver oxide quantita-
tively oxidizes CO but not hydrogen. Thus, the baseline hydrogen
concentration can be determined, Additional minor improvements are
discussed by Seiler and Junge, who gave the detection limit for CO as
0.003 mg/m3 (0.003 ppm).
123
More recently, Palanos described a less sensitive model of this
instrument intended for use in urban monitoring. It has a range of 0 to
3 3
23 mg/m (20 ppm), a sensitivity of about 0.58 mg/m (0.5 ppm) and a
span and zero drift of less than 2 percent per day. As in other similar
instruments, specificity is achieved by removal of the potentially
interfering substances other than hydrogen (which is less than 10 percent)
All of these instruments assume a constant hydrogen concentration.
In unpolluted atmospheres, the hydrogen concentration is roughly
3
46.5 ug/m (0.56 ppm). However, the automobile is not only a source of
CO but also of hydrogen. Therefore, if this technique is used in
polluted areas, it will be necessary to measure the hydrogen
concentration frequently.
5-28
-------
5.3.4.5 Dual Isotope Fluorescence—This instrumental method utilizes
the slight difference in the infrared spectra of isotopes. The sample
is alternately illuminated with the characteristic infrared wavelengths
of carbon monoxide-16 (CO ) and carbon monoxide-18 (CO18). The CO in
the sample that has the normal isotope ratio, nearly 100 percent CO ,
absorbs only the CO wavelengths. Therefore, there is a cyclic varia-
tion in the intensity of the fluorescent light that is dependent on the
CO16 content of the sample.101'107'108
3
Full-scale ranges of 0 to 23 mg/m (0-20 ppm) and up to 0 to
3 3
230 mg/m (0-200 ppm) with a claimed sensitivity of 0.23 mg/m (0.2 ppm)
are available in this instrument. The response time (90 percent) is
25 seconds, but a 1-second response time is also available. An advan-
tage of this technique is that it minimizes the effects of interfering
substances. '
5.3.4.6 Catalytic Combustion-Thermal Detection--Determination of CO by
this method is based on measuring the temperature rise resulting from
catalytic oxidation of the CO in the sample air.
The sample air is first pumped into a furnace that brings it to a
pre-set, regulated temperature and then over the catalyst bed in the
furnace. A thermopile assembly measures the temperature difference
between the air leaving the catalyst bed and the air entering the
catalyst bed. The output of the thermopile, which is calibrated with
known concentrations of CO in air, is read on a strip-chart recorder as
3
parts of CO per million parts of air. The sensitivity is about 1.2 mg/m
(1 ppm). Most hydrocarbons are oxidized by the same catalyst, and will
5-29
-------
interfere unless removed. These systems are widely used in enclosed
spaces; their applicability for ambient air monitoring is limited
because they function best at high ambient concentrations.
5.3.4.7 Second-Derivative Spectrometry—A second-derivative spectrometer
processes the transmission versus wavelength function of an ordinary
spectrometer to produce an output signal proportional to the second
derivative of this function. Ultraviolet light of continuous wavelength
1s collected and focused onto an oscillating entrance slit of a grating
spectrometer. By slowly changing the grating orientation, the existing
light has a slowly scanning center wavelength with sinusoidal wavelength
modulation Created by the oscillating entrance slit. This radiation
passes through a gas sample and is detected with a photomultiplier tube.
The signal is then electronically processed to produce a second-
96
derivative spectrum. This method has the advantage that it can be
used to measure other pollutants as well as CO. Commercial instruments
are being developed.
5.3.4.8 Fourier Transform Spectroscopy—Fourier transform spectroscopy
is an extremely powerful infrared spectroscopic technique which has
developed in the past 20 years and has been applied in the last 10 years
7? 9fi
to air pollution measurement problems. ' The advantages of this
technique over a standard grating or prism spectrometer are that it has
a higher through-put, which means that the available energy is used more
effectively and a much higher resolving power is obtainable. In air
pollution measurements individual absorption lines can be resolved.
5-30
-------
A special advantage for air pollution measurements is that all the
data required to reconstruct the entire absorption spectrum are acquired
at the same time. The spectrum as a function of wavelength is generated
by a built-in computer. This means that several gases can be measured
simultaneously. Several commercial instruments are now available with
resolutions of 0.06/cm or better. These instruments are capable of
clearly defining the spectra of any gaseous pollutant, including carbon
monoxide, and are currently being used for special air pollution studies.
5.3.4.9 Gas Filter Correlation Spectroscopy—A gas filter correlation
25
(GFC) monitor is in essence a modern NDIR monitor, but has not been
defined as such by EPA. It has all the advantages of an NDIR instrument
and the additional advantage of smaller size, no interference from COp,
and very small interference from water vapor. It is not sensitive to
flow rate, requires no wet chemicals, has a very fast response, and is
independent of reasonable ambient temperature changes. There is a
problem with zero drift, but not with span drift. Furthermore, the
instrument has recently been packaged as a portable monitor.
In this instrument, the infrared beam is collimated by a lens
before passing through the gas filter, the interference filter, and the
sample cell. The signal arises from the difference in the amplitude of
the signal which alternately passes through one-half of the filter cell
containing CO and the other half containing a neutral gas such as N2
and a neutral filter. The signal is balanced when no CO remains in the
sample cell. An increase in CO in the sample cell will increase the
difference signal since the portion of the beam which has already passed
5-31
-------
through the CO in the gas filter will be unchanged by the CO in the
sample cell, whereas the beam passing through the neutral half will be
attenuated by the CO in the sample. A prototype version of this monitor
27
had a minimum sensitivity of 50 parts per billion.
5.3.5 Intermittent Analysis
Intermittent samples may be collected in the field and later
analyzed in the laboratory by continuous analyzing techniques described
above. Sample containers may be rigid (glass cylinders or stainless
steel tanks) or they may be non-rigid (plastic bags). Because of
location or cost, intermittent sampling at times may be the only practical
method for air monitoring. Samples can be taken over a few minutes or
accumulated intermittently to obtain, after analysis, either "spot" or
"integrated" results. Additional techniques for analyzing intermittent
samples are described below.
5.3.5.1 Colorimetric Analysis
5.3.5.1.1 Colored silver sol method. Carbon monoxide reacts in an
alkaline solution with the silver salt of p_-sulfamoylbenzoate to form a
3
colored silver sol. Concentrations of 12 to 23,000 mg/m (10 to 20,000 ppm)
28-32 98
CO may be measured by this method. ' The method has been modified
to determine CO concentrations in incinerator effluents. Samples are
collected in an evacuated flask and reacted. The absorbance of the
resulting colloidal solution is measured spectrophotometrically. Acetylene
and formaldehyde interfere, but can be removed by passing the sample
through mercuric sulfate on silica gel. Carbon monoxide concentrations
3
of 5.8 to 20,700 mg/m (5 to 18,000 ppm) may be measured with an accuracy
of 90 to 100 percent of the true value.
5-32
-------
5.3.5.1.2 National Bureau of Standards colorlmetric Indicating gel,
A National Bureau of Standards (NBS) colorimetric indicating gel
(incorporating palladium and molybdenum salts) has been devised to
151 152
measure CO in the laboratory and in the field. ' The laboratory
,r? i
method involves colorimetric comparison with freshly-prepared indicating
V
gels exposed to known concentrations of CO. The methooT has an accuracy
range of 5 to 10 percent of the amount of CO involved, and the minimum
o
detectable concentration is 1.2 mg/m (1 ppm). This technique requires
relatively simple and inexpensive equipment; but oxidizing and reducing
gases interfere, and the preparation of the indicator tube is a tedious
and time-consuming task.
5.3.5.1.3 Length-of-stain indicator tube. An indicator tube method
153
using potassium palladosulfite is a commonly used manual method.
Carbon monoxide reacts with the contents of the tube and .produces a
discoloration.
/
The length of discoloration is an exponential function of the CO
concentration. This method and other indicator tube manual methods are
estimated to be accurate to within ±25 percent of the amount present,
3
particularly at CO concentrations of about 115 mg/m (100 ppm). Such
indicator tube manual methods have been used frequently in air pollution
studies. Ramsey132 used the technique to measure CO at traffic
intersections, and Brice and Roesler21 used color-shade detector tubes
to estimate CO concentrations with an accuracy of ±15 percent.
Colorimetric techniques and length-of-stain discoloration methods
are recommended for use only when the other physicochemical monitoring
5-33
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systems are not available. They may be used in the field for gross
mapping where accuracy is not required and might be of great value
during emergencies.
5.3.5.2 Frontal Analysis—Air is passed over an adsorbent until
equilibrium is established between the concentration of CO in the air
and the concentration of CO on the adsorbent. The CO is then eluted
with hydrogen, reduced to methane on a nickel catalyst at 250 C, and
determined by flame ionization as methane.
3
Concentrations of CO as low as 0.12 mg/m (0.10 ppm) can be measured.
This method does not give instantaneous concentrations but does give
55 56
averages over a 6-minute or longer sampling period. '
5.4 MEASURING CARBON MONOXIDE IN BLOOD
The best index of CO exposure is the carboxyhemoglobin (COHb)
\
percent saturation. Carboxyhemoglobin can be determined satisfactorily
on venous blood since insignificant differences have been found between
venous and arterial concentrations. Venous blood should be collected in
a closed container (vacutainer tubes are adequate) with an anticoagulant
such as dry sodium heparin or sodium ethylene-diaminetetraacetic acid
(EDTA). There must be no air trapped in the syringe or container.
Blood samples may be preserved for several days prior to analysis if
kept in the cold (4°C) and in the dark. Complete mixing of blood must
be performed if CO, as a gas, and hemoglobin (Hb) are measured separately.
This mixing must assure that the normal hematocrit of the sample is
present prior to analysis. Total Hb determination is most conveniently
53
performed by the reaction to form cyanomethemoglobin. A satisfactory
5-34
-------
procedure is to use the reagent of Van Kampen and Zijlstra181 with
precautions to prevent gradual loss of hydrogen cyanide (HCN) from the
acid reagent and to allow sufficient time for total conversion of COHb.
Measurements of CO by elaboration of the gas or by nondestructive
spectrophotometric procedures have been developed (Table 5-2).
Carbon monoxide combines rapidly with Hb to form COHb, which is
much more stable than 02Hb. This decreases the 0« transport capability
of blood, causing 02 deprivation in tissues and, thus, impaired physio-
logic status. Therefore, the chemical analysis of blood for its COHb
content is an important measure of toxic effect, as well as recent
exposure, for CO.
The analytical results are usually expressed as the ratio of the
concentrations of COHb to total Hb. In humans there is a baseline level
of about 0.5 percent of COHb in blood, due to endogenous production of
small amounts of CO by catabolic processes. This basal level can be
higher at certain times in females, individuals with hemolytic disease,
etc. Urban nonsmokers show about 1 percent COHb in blood, while moderate
1 fifi
smokers show about 5 percent. Parking garage employees have shown
133
levels above 10 percent at the end of the workday.
There are several reviews on analytical procedures for CO in
blood;40'52'61'104 these can be grouped into nondestructive, destructive,
and equilibrium methods.
5.4.1 Other Methods
If the COHb concentration is measured as such in solution, the
method is nondestructive; if the complex is destroyed in order to
liberate the CO gas for measurement, the method is destructive.
5-35
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TABLE 5-2. COMPARISON OF REPRESENTATIVE TECHNIQUES
FOR ANALYSIS OF CO IN BLOODa
Reference
GASOMETRIC
Horvath andQ
Roughton
Sc ho lander, and
Roughton1^
OPTICAL
Coburn, Forster
and Kane
Small et al.156
Maas, Hamelink-.Q3
and De Leeuw
CHROMATOGRAPHIC
McCredJeqand
Joseluy
Col lison, Rodkey
and O'Neal^
9
Ayers et al.
47
Dahms & Horvath
Method
Van Slyke
Syringe-
capi llary
Infrared
Spectro-
photometric
CO-Oxi meter
Thermal
conductivity
Flame
ionization
Thermal
conductivity
Thermal
conductivity
Sample
vol ,
ml
1.0
0.5
2.0
0.1
0.4
1.0
0.1
1.0
0.25
Resolution,
ml/dl
0.03
0.02
0.006
0.08
0.10
0.005
0.002
0.001
0.006
Sample
analysis
time,
min
15
30
30
10
3
20d
20
30
6.5
5T
6
2-4
1.8
1.8
1.8
2.0
1.7
a 47
.From Dahms and Horvath modified.
Smallest detectable difference between duplicate
determinations.
Calculated based on samples containing less than
2.0 ml CO per deciliter.
Best estimate.
5-36
-------
The intense color of Hb and its complexes suggests the use of
spectrophotometry as a nondestructive analytical tool. Very strong
Soret absorption peaks in the 410 to 435 nm region, as well as moder-
ately strong peaks in the 520 to 600 nm region, are shown by reduced
Hb, COHb, 02Hb, MetHb, and other Hb derivatives.53»90»131»156 Even
though the spectrophotometric curves are distinctive for each compound,
they overlap so much that it is not possible to quantitate one component
(such as COHb) in a mixture by a simple measurement of absorbance at
a wavelength where it absorbs light and other Hb derivatives do not.
A systematic procedure in such situations is to (1) determine
the absorptivity of each pure compound at each of several carefully
selected wavelengths; (2) measure the absorbance of the unknown
mixture at each of the wavelengths; and (3) separate the contribution
of each pure compound by solving a set of simultaneous equations
which contain coefficients for the individual absorptivities at each
wavelength. A high precision spectrophotometer with excellent
wavelength stability and resolution is needed.
1 'Sfi
An example of this approach is Small's method. After dilution
of blood 1:70 with 0.04 percent ammonia solution, the absorbance is
measured at four wavelengths in the Soret region. From a set of
simultaneous equations containing these measured values, calculations
give the percent COHb, percent MetHb, and percent 02Hb. The stated
error is ±0.6 percent COHb at concentrations of 25 percent COHb or
lower, which provides ample accuracy at high levels, but makes this
method less useful at low levels of around 1 percent COHb or less.
5-37
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105
A related technique is the basis for a commercial instrument, the
CO-Oximeter model 282 (Instrumentation Laboratory, Inc. , Lexington,
Mass.), which uses four wavelengths outside the Soret region and
includes a small computer for performing the calculations, yielding
percentages of total Hb as well as of COHb, 02Hb, and MetHb. CO-
103 122
Oxi meters are used widely, ' but require careful calibration at
COHb concentrations below 5 percent. This comparison was made against
a CO-X model 182 and the discrepancy at low COHb is correct, but it
140
is not known how this related to the Model 282.
5
An earlier method by Amenta is similar in principle and also
uses wavelengths outside the Soret region: 498 nm (an isosbestic
point), 560 nm, and 575 nm. The percent COHb results obtained in the
low concentration range have a precision of only 10 percent.
73 90
Other spectrophotometric methods include some chemical treatments. '
In Klendshoj's procedure, oxalated blood is first diluted 1:100 with
0.4 percent ammonia; then sodium dithionite ("hydrosulfite") is added
and the absorbance is measured at 480 nm and 555 nm. After dithionite
treatment, the only Hb species present are reduced Hb and COHb. These
two have the same absorptivity at 555 nm, but different absorptivities
at 480 nm; the ratio ACr-r-/A/,on decreases with increased COHb concentration.
ODD
A calibration curve is prepared from known standards; certain precautions
193
are needed in making up such standards. Klendshoj's method is simple,
rapid, and accurate enough to measure a 2 percent change in COHb
concentration, but at low levels is less useful.
5-38
-------
Another spectrophotometric method makes use of the fact that 02Hb
is much more readily precipitated than COHb when heated eight minutes
at 57 C. After the solution is filtered and cooled, the change in
absorbance at 555 nm is measured and the COHb content of the blood is
measured by calibrating the method with standard solutions of known
concentration. The procedure is simple but not very sensitive or accurate.
In the differential spectrophotometric technique of Commins and
41
Lawther, an aqueous solution of the blood sample is divided equally
and oxygen is bubbled through one half of the solution for 15 minutes to
convert any COHb into 02Hb. The spectra of the two halves are then
compared and the difference between them (together with a measurement of
Hb in the oxygenated portion) is used to find the COHb content of the
blood. This method is stated as able to detect 0.2 percent COHb in
blood, and has shown good agreement with two different destructive
23
methods for COHb analysis.
Double wavelength spectrophotometry is used in a recently developed
131
rapid method for COHb. Two monochromators in the same instrument
send light beams of different wavelengths alternately through a single
cuvette; the difference in absorbance is measured by the photometer.
The carefully chosen wavelengths are 530.6 nm and 583.0 nm, at which
0?Hb has equal absorptivities, and also at which reduced Hb has equal
absorptivities. Any difference in absorbance found is due to the
presence of COHb, which has unequal absorptivities at the two wavelengths.
As with all such methods, careful calibration with known samples is
required. The procedure has acceptable accuracy at levels of a few
percent of COHb, but MetHb causes interference.
5-39
-------
Infrared spectrophotometry of CO bound to Hb can be performed
directly on blood and other tissues, and holds future promise as a
specific method for COHb analyses. An exploratory study used measure-
ments at 1951 cm in CaF« cells having 0.05 mm optical pathlength.
Other possible spectrometric techniques for COHb analysis include
Mossbauer (which would require a solid sample, such as frozen blood),
carbon-13 nuclear magnetic resonance, and electron spin resonance.
These offer some promise of specificity, but are far from being developed
into usable methods.
A different approach to COHb analysis is to decompose the complex
and measure the amount of CO gas released. Such liberation of CO has
been carried out by addition of various acids (hydrochloric, sulfuric,
phosphoric, acetic, citric, lactic) and/or oxidizing agents such as
potassium ferricyanide or potassium hydrogen iodate. These methods
tend to have the disadvantage of requiring (1) larger samples of
blood than for spectrophotometry, and (2) a separate analysis for
total concentration of Hb, if the percent COHb is needed.
Of the many analytical methods available for gaseous CO, several
are noted briefly below.
80 182 183
5.4.1.1 Gasometric—The Van Slyke method and its modifications ' *
159
measure the volume or the pressure of the CO gas present. Historically
they were macro methods and not of high sensitivity, but successful
141 146
micro procedures have been developed. ' They require considerable
skill and are time-consuming.
5-40
-------
5.4.1.2 Infrared Spectrometry—Carbon monoxide has a characteristic
infrared absorption near 4.6 urn. This is widely used for analysis,
especially with nondispersive instruments as in the EPA reference
method for atmospheric monitoring. In this method, the absorption
due to any CO present is measured by its differential heating effect
and resulting displacement of a flexible diaphragm which is one
element of a capacitance detector. Methods using NDIR for COHb
analysis in blood are available.35>63>189 Water vapor interferes
unless its concentration is carefully controlled.
5.4.1.3 Catalytic Oxidation—Like NDIR, this method has enough sensi-
tivity and accuracy to detect small changes in COHb concentration.
The liberated CO can be oxidized by a catalyst such as Hopcalite and
the temperature rise caused by this exothermic reaction measured with a
thermopile or quartz crystal.100'117'129'163
5.4.1.4 Electrochemical Sensors—Another analytical technique based
on oxidation of CO is electrochemical. In a special electrode, the
gas sample is allowed to diffuse through a Teflon membrane bearing a
thin film of catalytically active metal (such as platinum) on the far
side, in contact with the electrolyte. At a controlled applied
potential, the current flow is determined by the CO concentration in
the gas.13»17»18»20>34»50 A different electrical procedure for analysis
of CO is to measure the change in conductivity it causes when adsorbed
by a semiconductor such as metal oxides. '
5.4.1.5 Gas chromatography—The chromatographic separation of CO from
other blood gases is readily accomplished by a molecular sieve. » » » »
5-41
-------
In order to achieve greater sensitivity than given by a thermal conduc-
tivity detector, a flame ionization detector can be used in the gas
chromatograph if the CO is first catalytically reduced to methane, in-
39 130 139 192
line after its separation by the molecular sieve. ' ' 5
5.4.1.6 Colorimetric palladium chloride reaction—In a Conway micro-
93
diffusion cell, CO released from blood diffuses into a solution of
palladium (II) chloride, which is reduced to metallic palladium.
The excess PdCl« is determined colorimetrically, by conversion to the
4
pinkish iodide complex or by formation of a violet complex with
OQ
promazine. Another col ori metric reagent for CO is a mixture of
92 99
palladium and molybdenum compounds. *
5.4.2 Equilibrium Methods
If equilibrium can be established between blood gases and lung
gases, then analysis of exhaled air will give a measure of COHb blood
levels 26,60,126,134,155,185 Jhe relationship is
[COHb] = M [0£Hb] GP
P02
where ^0^ is the partial pressure of 0« in the pulmonary blood, pCQ is
the measured partial pressure of CO in the exhaled air, the bracketed
quantities are the blood concentrations of COHb and O^Hb, respectively,
and M is the ratio of the stability constant of COHb to that of 0«Hb.
The Haldane constant, M, has a numerical value of about 220 to 250 for
humans at physiological pH and body temperature. '
5-42
-------
The alveolar air method should be used in epidemiological studies
only with extreme care. Hoover and Albrecht,79 in their study of driving
in New York City traffic, reported that CO concentrations in alveolar
air did not correlate acceptably with measurements of COHb. The equi-
librium method cannot be used in people with chronic lung disease,
because their alveolar gas composition can be quite variable. Even
healthy subjects need special training in the method in order to achieve
valid results.
In this method, the main problem is to approach equilibrium condi-
tions even though the composition of lung gas is changing continually
during normal respiration. One solution is breath-holding. When a
subject holds his breath, the alveolar concentration of CO increases
initially as CO diffuses out of the blood toward equilibration.7'19'36'48'89'137
However, as the alveolar 0« content decreases, some of the CO is re-
absorbed Into the blood. The optimum time period for breath-hoi ding was
found to be 20 seconds.
The standard technique is for the subject to expel air from his
lungs maximally, then breathe in as far as possible, hold his breath for
20 seconds, and then exhale as far as possible. The first 500 ml of
expired air is discarded, and the remainder is collected in a gas-tight
bag for CO analysis by a reliable method. A rugged instrument for field
use, as for measuring COHb in firefighters, is the Ecolyzer, which
measures CO by electrochemical oxidation at a Teflon-bonded diffusion
anode.165
5-43
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1. Acton, L. L., M. Griggs, G. D. Hall, C. B. Ludwig, and W. Malkmus.
Remote measurement of carbon monoxide by a gas filter correlation instrument.
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2. Adams, E. G., and N. T. Simmons. The determination of carbon monoxide by
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3. Akland, G. G. Design of sampling schedules. J. Air Pollut. Control
Assoc. 22:264-266, 1972.
4. Allen, T. H., and W. S. Root. An improved palladium chloride method for
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5. Amenta, J. S. The spectrophotometric determination of carbon monoxide in
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Carbon Monoxide Measurements. Environmental Measurements, Inc., San
Francisco, CA, 1977.
*
11. Bartle, E. R., and G. Hall. Airborne HC1 - CO Sensing System. Final
Report, SAI-76-717-LJ, Science Applications, Inc., La Jolla, CA, March
1977.
12. Bay, H. W., K. E. Blurton, H. C. Lieb, and H. G. Oswin. Electrochemical
measurement of carbon monoxide. Am. Lab, 4:57-58, 60-61, 1972.
13. Bay, H. W., K. F. Blurton, J. M. Sedlak, and A. M. Valentine. Electro-
chemical technique for the measurement of carbon monoxide. Anal. Chem.
46:1837-1839, 1974.
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152. Shepherd, M., S. Schuhmann, and M. V. Kilday. Determination of carbon
monoxide in air pollution studies. Anal. Chem. 27:380-383, 1955.
153. Silverman, L., and G. R. Gardner. Potassium pallado sulfite method for
carbon monoxide detection. J. Am. Ind. Hyg. Assoc. 26:97-105, 1965.
154. Simonescu, T. , V. Rusu, and L. Kiss. New analytical application of some
sulfonamide compounds. Kinetic method for the determination of carbon
monoxide in air. Rev. Chim. (Bucharest) 26:75-78, 1975.
155. Sjostrand, T. A method for the determination of carboxyhaemoglobin
concentrations by analysis of the alveolar air. Acta Physiol. Scand.
16:201-211, 1948.
156. Small, K. A., E. P. Radford, J. M. Frazier, F. L. Rodkey, and H. A.
Collison. A rapid method for simultaneous measurement of carboxy- and
methemoglobin in blood. J. Appl. Physiol. 31:154-160, 1971.
157. Smith, F., and A. C. Nelson, Jr. Guidelines for Development of a Quality
Assurance Program. Reference Method for the Continuous Measurement of
Carbon Monoxide in the Atmosphere. EPA-R4-73-028a, U.S. Environmental
Protection Agency, Washington, DC, June 1973.
158. Smith, R. G. Air Quality Standards for Carbon Monoxide. Air Quality
Monograph #69-9, American Petroleum Institute, New York, February 1969.
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159. Smith, R. G, R. J. Bryan, M. Feldstein, D. C. Locke, and P. 0. Warner.
Tentative method for constant pressure volumetric gas analysis for 02,
C02, CO, N2, hydrocarbons. (ORSAT). Health Lab. Sci. 12:177-181, 1975.
160. Smith, R. G, R. J. Bryan, M. Feldstein, D. C. Locke, and P. 0. Warner.
Tentative method for gas chromatographic analysis of 0«, N?, CO, C0« and
CH4. Health Lab. Sci. 12:173-176, 1975.
161.Smith, R. G., R. J. Bryan, M. Feldstein, D. C. Locke, and P. 0. Warner.
Tentative method for the determination of carbon monoxide (detector tube
method). Health Lab. Sci. 12:171-172, 1975.
162. Stedman, D. H., G. Kok, R. Delumyea, and H. H. Alvord. Redundant calibration
of nitric oxide, carbon monoxide, nitrogen dioxide, and ozone air monitors
by chemical and gravimetric techniques. In: Calibration in Air Monitoring,
a Symposium, American Society for Testing and Materials, Boulder, Colorado,
August 5-7, 1975. ASTM Special Technical Publication, 598, American
Society for Testing and Materials, Philadelphia, PA, 1976. pp. 337-344.
163. Stetter, J. R., and K. F. Blurton. Portable high-temperature catalytic
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164. Stevens, R. K., and W. F. Herget. Analytical Methods Applied to Air
Pollution Measurements. Ann Arbor Science Publishers, Inc., Ann Arbor,
MI, 1974.
165. Stewart, R. D., R. S. Stewart, W. Stamm, R. P. Seelen. Rapid estimation
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1976.
166. Stewart, R. D., J. E. Peterson, E. D. Baretta, R. T. Bachard, M. J.
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171. U.S. Environmental Protection Agency. National primary and secondary
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1973.
5-58
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6. OBSERVED CARBON MONOXIDE CONCENTRATIONS
Ambient concentrations of carbon monoxide (CO) in urban communities
exhibit wide temporal and spatial variations. Exposure patterns of CO
are complex, but they can be discerned from ambient air measurements and
the estimates of computer models. This chapter presents some typical
results of continuous air monitoring of CO in order to provide a better
understanding of the CO problem. In addition to a discussion of observed
diurnal, seasonal, and annual patterns of ambient CO levels in urban
areas, this chapter discusses the importance of air monitoring site
selection, of meteorological and geographical effects on CO exposures,
techniques of CO trend analyses, special CO exposure situations, and an
overview of meteorological diffusion models. The CO problem exists
primarily in the urban areas.
6..1 SITE SELECTION
Because of the many variables which must be considered, site
selection is one of the most complex and critical elements in the design
of CO air monitoring programs. If the wrong sites are chosen, or if a
critical site is missed, no amount of accurate data collection will
allow the objective of the monitoring program to be fully realized.
It has been generally recognized that the choice of monitoring sites
cc
depends on the objective of the monitoring to be performed. The EPA
recognizes the following as general objectives for monitoring:
6-1
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1. To judge compliance with and/or progress made toward meeting
ambient air quality standards.
2. To activate emergency control procedures to prevent air
pollution episodes.
3. To observe pollution trends throughout the region including
the nonurban areas. (Information on the nonurban areas is
needed to evaluate whether air quality in the cleaner portions
of a region is deteriorating significantly and to gain knowledge
about background levels.)
4. To provide a data base for application in evaluation of effects;
urban, land use, and transportation planning, development and
evaluation of abatement strategies; and development and validation
of diffusion models.
Ground level concentrations of CO within an urban area vary widely
due to the large number and close proximity of the principal source of
CO, automobiles. Each car in a city contributes to the CO problem, but
it is large numbers of cars contributing collectively which produce high
CO levels in urban areas. The concentration of CO measured at a
monitoring site will depend on the site's location relative to CO sources,
The scale of representativeness of the data will also be dependent on
the proximity of the monitor to CO sources. Monitoring sites located
well-removed from highways can be representative of a fairly large-scale
air mass. Sites located at the edge of a highway measure CO concen-
trations which are representative of a fairly small spatial area. The
80a
EPA has defined six scales of spatial representativeness for CO
monitoring sites: microscale, middle scale, neighborhood scale, urban
scale, regional scale, and national and global scales.
The choice of monitoring site location depends on the monitoring
objective and the scale of -representativeness which meets the objective
requirements. Most CO monitoring conducted in the United States is for
the purpose of determining attainment or nonattainment of air quality
6-2
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standards. Since monitoring resources have been and continue to be
severely limited, sites chosen for monitoring are usually where maximum
CO concentrations are expected to occur. As a result, many CO sites are
located within the close proximity of major highways, arterials, and
downtown street canyons. These locations are where maximum CO levels
occur, but the scale of representativeness is small. Also, the results
relate primarily to pedestrian exposure near the monitoring station.
Monitoring sites located outside the influence of major roadways, but
within highly populated neighborhoods with a high traffic density, may
be more representative of the maximum CO concentrations to which a large
portion of the population of a city may be exposed.
48
Ott has stated the need for standardization in site selection and
has recommended certain siting criteria depending on station type.
Ott's criteria are presented in Table 6-1.
The EPA80a has also published guidelines for CO monitor siting
which deviate somewhat from Ott's criteria primarily in site type
definition and recommended separation distance between the station and
the nearest major highway. In EPA's criteria, the minimum separation
distance is dependent on traffic volume measured in vehicles per day (VPD)
These guidelines are given in Table 6-2.
80
In regard to which sites should be monitored, EPA guidelines give
the highest priority to microscale sites within street canyons and
neighborhood sites where maximum concentrations are expected. Table 6-3
lists EPA80 priorities for various station types.
6-3
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TABLE 6-1. CRITERIA FOR SITING MONITORING STATIONS48
Station Description
Type
TYPE A Downtown Pedestrian Exposure Station. Locate station in the central
business district (CBD) of the urban area on a congested, downtown street
surrounded by buildings--a "canyon" type street—and having many pedestrians
Average daily travel (ADT) on the street must exceed 10,000 vehicles/day,
with average speeds less than 15 miles/hour. Monitoring probe is to be
located 1/2 meter from the curb at a height of 3 ±1/2 meters.
TYPE B Downtown Background Exposure Station. Locate station in the central
business district (CBD) of the urban area but not close to any major
streets. Specifically, no street with average daily travel (ADT)
exceeding 500 vehicles/day can be less than 100 meters from the monitoring
station. Typical locations are parks, malls, or landscaped areas having
no traffic. Probe height is to be 3 ±1/2 meters above the ground surface.
TYPE C Residential Population Exposure Station. Locate station in the midst of
a residential or suburban area but not in the central business district
(CBD). Station must not be less than 100 meters from any street having a
traffic volume in excess of 500 vehicles/day. Station probe height must
be 3 ±1/2 meters.
TYPE D Mesoscale Meteorological Station. Locate station in the urban area at
appropriate height to gather meteorological data and air quality data at
upper elevations. The purpose of this station is not to monitor human
exposure but to gather trend data and meteorological data at various
heights. Typical locations are tall buildings and broadcasting towers.
The height of the probe, along with the nature of the station location,
must be carefully specified along with the data.
TYPE E Nonurban Background Station. Locate station in a remote nonurban area
having no traffic and no industrial activity. The purpose of this station
is to monitor for trend analyses, for nondegradation assessments, and for
large-scale geographical surveys. The location or height must not be
changed during the period over which the trend is examined. The height of
the probe must be specified along with the data. A suitable height is
3 ±1/2 meters.
TYPE F Specialized Source Survey Station. Locate station very near a particular
air pollution source under scrutiny. The purpose of the station is to
determine the impact on air quality, at specified locations, of a particular
emission source of interest. Station probe height should be 3 ±1/2
meters unless special considerations of the survey require a nonuniform
height.
6-4
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TABLE 6-2. SPECIFIC PROBE EXPOSURE CRITERIA
80
Site Type
Height
Above
Ground
Expected
Concentration Separation of
Gradient with Monitor from
Height Influencing
(1-hr. Average) Sources
General Remarks
Street Canyon
Peak Cone.
Average Cone,
cn
Corridor
3 + 1/2 m Z.5 ppm/m
3 + 1/2 m Z.3 ppm/m
Mid-sidewalk or 2 m
from side of building.
On leeward side of
street.
Mid-sidewalk or 2 m
from side of building.
Central Business District.
High density, slow-moving traffic.
Dense multiple-story buildings
lining both sides of street.
J10 m from intersection.
Neighborhood
Peak Cone.
Average Cone.
3 * 1/2 m 5%/m
3 + 1/2 m 5%/m
Setback
3.5 km
1.5 km
200 m
100 m
35 m
25 m
VPD
100,000
50,000
10,000
5,000
1,000
any
Commercial or residential neighbor
This separation criteria limits th
effect of these streets to II ppm.
3 + 1/2 m
F.3 ppm/m
J5%/m
Dependent on traffic Stop and go or limited access
volume, road configura- traffic J50,000 VPD or greatest
tion and setback in area.
distance of commercial
or residential activity.
-------
TABLE 6-2 (Continued)
Site Type
Height
Above
Ground
Expected
Concentration Separation of
Gradient with Monitor from
Height Influencing
(1-hr. Average) Sources
General Remarks
Background
3 to 10 m
2%/m
5 to 6 km;
03,000 VPH max.
400 m; J100 VPD,
35 km downwind in least frequent
wind direction from city,
limit effects to .2 ppm.
cr>
New Source Review
Preconstruction 3 + 1/2 m 5%/m
Post-
Construction
3 + 1/2 m J5%/m to
F.5 ppm
Usually the same as
neighborhood.
Usually the same as
corridor or street
canyon.
Area of lowest concentration in
proposed indirect source location
for background.
Area of maximum concentration in
area of complete area source.
-------
TABLE 6-3. SUGGESTED PRIORITIES OF CARBON MONOXIDE MONITORING SITES80
Site Types Priority
Peak Street Canyon #1
Peak Neighborhood #1
Average Street Canyon #2
Corridor #3
Background #4
Average Neighborhood #5
The variability of CO concentration with height in the vicinity of
a highway is also sufficiently large that the representativeness of
measurements will be strongly affected by variability of the inlet probe
height. It is, therefore, necessary to standardize the height of the
inlet probe so that data collected at one air monitoring station is
comparable to data collected at others. In an effort to characterize
typical human exposure, the sample inlet probe height should ideally be
set at breathing level. However, as a compromise between representation
of breathing height and practical considerations, such as prevention of
vandalism, it is recommended that inlets for most kinds of sampling be
1 5
at a height of 3 ±0.5 m. ' A 1-m minimum separation of the probe from
adjacent structures to avoid the frictional effects of surfaces on the
75
movement of air is also recommended.
The number of monitoring sites required depends on the objectives
of the monitoring effort and on the complexity of the problem under
study. At present, the only guidelines are from the EPA which requires
one site for cities with 100,000 or less population, 1+0.15 sites per
100,000 population up to 5,000,000 people, and 6+0.05 sites per 100,000
population for populations greater than 5,000,000.
6-7
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Site selection for special purpose studies may not follow the
specific criteria which apply to continuous monitoring sites used for
trends analysis and compliance with air quality standards. In fact,
special purpose studies, where CO concentrations are measured at many
locations, provide the Information about the spatial variations of
ambient CO that form the basis for setting siting criteria. Among the
principal types of special purpose monitoring are research studies for
diffusion model development and improvement, and source surveillance
studies. Source surveillance studies may be conducted for highways or
point sources of CO. Diffusion model development studies may be for
71 81
line source models (such as HIWAY or CALINE-2 ) or area source
models (such as APRAC-2 ). For special purpose studies, the criteria
for site selection is a decision for the investigator.
6.2 UNITED STATES DATA BASE
In accordance with requirements of the Clean Air Act and EPA
15
regulations for State Implementation Plans (SIP's), ambient CO data
from state, local, and Federal networks must be reported each calendar
73
quarter to the EPA's Aerometric and Emissions Reporting System (AEROS).
As a result, continuous measurements of ambient CO concentrations from
numerous cities throughout the United States are available from the
U.S. Environmental Protection Agency's National Aerometric Data Bank
(NADB) in standard Storage and Retrieval of Aerometric Data (SAROAD)
73
reporting format.
The nationwide status of CO monitoring activities reporting to the
AEROS in 1977 1s summarized 1n Table 6-4. This table lists, by state,
the number of CO monitors that reported any CO data.
6-8
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TABLE 6-4. STATUS OF CO MONITORING IN 197780b
State
01 Alabama
02 Alaska
03 Arizona
04 Arkansas
05 California
06 Colorado
07 Connecticut'
08 Delaware
09 District of Columbia
10 Florida
11 Georgia
12 Hawaii
13 Idaho
14 Illinois
15 Indiana
16 Iowa
17 Kansas
18 Kentucky
19 Louisiana
20 Maine
21 Maryland
22 Massachusetts
23 Michigan
24 Minnesota
25 Mississippi
26 Missouri
27 Montana
28 Nebraska
29 Nevada
30 New Hampshire
31 New Jersey
32 New Mexico
33 New York
34 North Carolina
35 North Dakota
36 Ohio
37 Oklahoma
38 Oregon
39 Pennsylvania
40 Puerto Rico
41 Rhode Island
42 South Carolina
43 South Dakota
44 Tennessee
45 Texas
46 Utah
47 Vermont
48 Virginia
49 Washington
50 West Virginia
51 Wisconsin
52 Wyomi ng
53 Guam
54 Virgin Islands
Total Number of Monitors
Reporting any Data
4
6
16
0
84
10
9
3
9
12
4
1
1
20
7
5
7
15
0
4
15
9
11
8
0
14
4
3
3
3
22
10
29
1
0
16
4
5
13
0
1
3
0
5
19
6
2
15
7
2
9
0
0
0
TOTAL
456
6-9
-------
The nationwide historical data base for CO is very limited compared
to total suspended participate or sulfur dioxide air pollutant data, but
it continues to expand. In 1973, 212 sites reported CO data to the EPA.
During 1975, 453 sites submitted CO data though much of it was incomplete.
Total numbers of CO monitors reporting during 1976 and 1977 were 448 and
456, respectively. In 1975, 102 sites had three or more years of
data, while in 1976 there were 202 sites with at least three years of
79
data. The State of California with its well-established monitoring
program is the major contributor to the national CO data base with 84
sites.
Among the oldest CO monitoring sites are the Continuous Air
Monitoring Program stations which have been operated by the Federal
government since 1962. Continuous Air Monitoring Program (CAMP) data
have been collected at nine sites, one each in the cities of Los Angeles,
San Francisco, Denver, Chicago, New Orleans, St. Louis, Cincinnati,
Philadelphia, and Washington, D. C. The stations in Chicago, Cincinnati,
Philadelphia, and Washington, D. C. have been part of the program since
its inception. The Washington, D. C. station was moved to a new location
in 1969, interrupting the continuous data record for that site. The
stations in every case are located in the downtown, central business
district of the city- Since a CAMP station constitutes only one sampling
site per city, its data do not necessarily represent air pollution
levels prevailing beyond the immediate vicinity of the station.
An additional problem with CAMP station data is that continuity is
often lacking due to changes in site location or CO monitoring procedures
6-10
-------
which have occurred since the beginning of the program. Specifically,
1n 1970 the original CO instruments (mono-beam NDIR) were replaced with
dual-beam NDIR detectors with integrating chambers added, and in 1971
calibration gases were changed from CO 1n nitrogen to CO in air. These
changes tended to eliminate water vapor interference, smooth out the
concentration plots, and eliminate C02 interference.67 Similar changes
in CO monitoring procedures were first implemented by the Los Angeles
CO
County Pollution Control District in 1968. Figure 6-1 shows the
annual mean CO concentrations measured at three Los Angeles basin sites
before and after the changes were made. A significant decrease in CO
co
levels measured in 1968 and later is apparent.
Computer retrievals of raw data submitted to the AEROS and published
data summaries such as the National Air Quality and Emission Trends
Report67'68'70'74'75*79*8013 or Air Quality Data - 1976 Annual Statistics
are available.
However, state and local air pollution control agencies are not
required to submit all CO data collected from their monitoring network.
These agencies may also conduct special studies for certain "in-house"
purposes. State departments of transportation and local metropolitan
planning commissions are sources of CO data for the preparation of
environmental impact statements for proposed transportation projects
and/or in the preparation of SIP revisions. Air quality impact research
sponsored by the EPA, the Federal Highway Administration, universities,
and private industries also provide sources of CO data.
6-11
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D1961-67 O1968-72
20
E
a
a
z"
O
p
<
cc
I-
z
o
o
_*
o
I I I I
(a) LENNOX
I I I I I I I
D
D
D
62
66
YEAR
70
a
a
*
z
o
K
<
CC
\-
z
LU
O
z
o
u
20
15
o
I I I I I I I
(b) DOWNTOWN L.A.
D
0 °
62
66
YEAR
70
20
E
a
a
H-
<
CC
I-
z
LU
O
z
o
o
o
T III
(c) AZUSA
D D
D
t
62
66
70
YEAR
Figure 6-1. Annual average CO levels In Los Angeles.
(Used with permission of Journal of Air Pollution Control Association,
2500:1129-1136, 1975.)
6-12
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6.3 TECHNIQUES OF DATA ANALYSIS
6.3.1 Introduction
Air quality surveys inherently involve the taking of a limited
number of samples from a highly variable and uncontrolled population
(i.e., the environment). For this reason, air quality data should be
analyzed using statistical methods, which can be used to describe the
behavior of the total population based on a finite number of samples.
,3
In particular, statistical parameters can be calculated to describe the
typical values observed, the maximum or peak values observed, and the
range of values observed.
Although intermittent sampling is an important research tool for
conducting special studies, the majority of CO monitoring instruments in
use today are intended to operate continuously and yield successive
hourly averages. These data are applied to two principal uses:
(1) characterizing environmental conditions by describing short-term
(hourly, daily, seasonal) and long-term (year-to-year) urban CO concen-
tration patterns, and (2) evaluating, for statutory purposes, an area's
status wfth respect to the 1-hour and 8-hour average NAAQS for CO.
At a minimum, an analysis of CO air quality data should include a
comparison of the highest (or second highest) observed pollution concen-
tration to established air quality standards. In addition, an analysis
of CO data may include calculation of population statistics, frequency
analyses, averaging time analyses, trend analyses, and case analysis.
6-13
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6.3.2 Calculation of Population Statistics
Statistical parameters can be calculated to describe the typical CO
values observed, the maximum or peak CO values observed, and the range
of CO values observed. Indicators of typical CO values are the arith-
metic mean, the median, and the geometric mean. When the term "average"
is used, the arithmetic mean is usually implied. The median is the
middle value of the CO data, that is, the value that has half the data
above it and half below it. The median is a convenient statistic that
is not influenced by changes in extremely high or low CO values of the
distribution, as would be the arithmetic mean. The geometric mean* is
probably the least intuitive of the statistics presented. If a distri-
bution is symmetric, such as the normal distribution, the expected value
of the arithmetic mean and median are identical. However, for a lognor-
mally distributed variable (and CO data often have a distribution that
is approximately lognormal), it is the geometric mean that approximates
the median.
The histogram of Figure 6-2 illustrates the relative frequency of
occurrence of 1-hour average CO concentrations. The shape of the
histogram, which is "skewed to the right" is typical for lognormally
distributed data. A more illustrative method of plotting the data is
shown in Figure 6-3. This curve illustrates the cumulative frequency
distribution of the data when plotted on logarithmic versus probability
(log-probability) graph paper. When the cumulative frequency distribution
*-The geometric mean is calculated by taking the logarithm of each
sampled concentration, adding all of them together, dividing by the
number of samples, and taking the antilog.
6-14
-------
40
30
09
*
>
o
UJ
O
UJ
DC
20
10
__ I
2.3
6.9 11.5 16.1
CO CONCENTRATIONS, mg/m3
20.7
Figure 6-2. Histogram of 1-hr average CO concentrations,
Washington, DC (CAMP).46
6-15
-------
CO
~0>
Z*
O
g
Z
UJ
O
u
o
o
100.0
50.0
20.0
10.0
5.0
2.0
1.0
I I I I I I I I I II I I I I II I I I I I
99.9 99.5 98 90 70 50 30 10 2 0.5 0.05 0.01
FREQUENCY, percent
Figure 6-3. Cumulative frequency distribution of 1-hour average CO
concentrations.
6-16
-------
of the data 1s plotted, each point represents the cumulative frequency
of equaling or exceeding the specific CO concentration.
The cumulative frequency distribution leads to some useful statis-
tical applications which allow CO monitoring data to be analyzed to
determine the maximum CO concentration which probably occurred during a
monitoring period, even though the maximum value itself may not have
been recorded. This is especially applicable to sampling programs
designed to collect CO data Intermittently (i.e., every other day, every
third day, or randomly selected days, etc.), which allows for consider-
able chance for maximum CO concentrations not to be sampled. It also
applies to continuous CO monitoring where data are missed due to
calibrations, maintenance, or instrument failure. The assumption of
lognormality of the data allows these "missed" values to be estimated.
The actual days which maximum CO concentrations occurred cannot be
determined, but the frequency of occurrence of high CO concentrations
can.
Maximum CO values may be indicated by listing the maximum and/or
the second highest value. The second highest value is important because
compliance with the short-term air quality standards for CO is determined
by this value. Since the second highest value does not allow for
differences in sample sizes, difficulty would arise if continuous CO
monitoring data were missed due to calibrations, maintenance, or instru-
ment failure; or if CO were sampled intermittently. To allow for
dependence on sample size, various percent!les are sometimes used to
indicate maxima. By using a percentile value rather than an absolute
6-17
-------
count of samples, allowance is made for sampling schedules that differ
from site to site and year to year.
The customary statistics used to indicate the variability of CO
data are the arithmetic standard deviation and the geometric standard
deviation. Ranges or percentiles can also be used as indicators of
spread. These statistics indicate how variable the data collected are
(i.e., a measure of the uniformity of the data).
6.3.3 Frequency Analysis
A number of investigators,1»32'33'34'50'88 primarily Larsen and
34
Zimmer, have shown that short time averaged air pollution concentrations
(from 5-minute to 24-hour averages) sampled over a much longer period of
time (i.e., weeks, months, or years) tend to be lognormally distributed
within the longer sampling interval. Described simply, a lognormal
frequency distribution means that CO data collected frequently exhibit
many low concentrations, a significant number of moderate concentrations,
and a relatively small number of extreme, peak, or maximum concentrations.
While the standard lognormal model is commonly used in evaluating
air pollution data, other investigators continue to search for improved
methods of statistically describing concentration distribution. Examples
of these are the three-parameter lognormal distribution, proposed by
Mage and Ott, and the Wei bull and Gamma distributions studied by Pollack.
6.3.4 Comparing CO Data to National Ambient Air Quality Standards
The NAAQS for CO are currently based on a 1-hour and an 8-hour
averaging time. Carbon monoxide data are most frequently collected
using time averages of one hour. Evaluating compliance with the 1-hour
6-18
-------
standard simply requires rank-ordering 1-hour values for a year and
comparing the second-highest value with the 1-hour standard, which 1s
currently 40 mg/m3 (35 ppm). If the second-highest 1-hour value 1s less
o
than 40 mg/m , the standard has been met.
Evaluating compliance with the 8-hour standard Involves the calcula-
tion of moving 8-hour averages from the 1-hour data set. These 8-hour
averages are also rank-ordered to obtain the second-highest non-overlap-
ping" value for comparison with the 8-hour standard, which 1s currently
3
10 mg/m (9 ppm). For enforcement purposes, only non-overlapping 8-hour
Intervals are counted as violations, as discussed 1n the Guidelines for
qn
the Interpretation of A1r Quality Standards. It has been shown,
however, that the full set of moving 8-hour averages should be examined
for excessive values. Proposed simplifications such as calculating only
three consecutive non-overlapping 8-hour averages per day can easily
result in missing peak 8-hour intervals and may not afford equitable
comparisons among stations with differing diurnal patterns.
For partial data sets, if continuous CO monitoring data were missed
due to calibrations, maintenance, or instrument failure, or if CO were
sampled intermittently, comparing CO data to standards using lognormal
cumulative frequency distribution plots may become a useful guide.
Once the CO data has been plotted on log-probability graph paper, the
frequency of equaling or exceeding any specified CO concentration can
easily be determined. For example, in Figure 6-3 observe that the CO
o
concentration equals or exceeds 10 mg/m 7 percent of the time and
20 mg/m3 for 0.05 percent of the time. The NAAQS for a 1-hour average
6-19
-------
3
concentration of CO is 40.0 mg/m , not to be exceeded more than once
per year. The frequency of occurrence of the second highest concentra-
tion can be expressed as a percentage by dividing two hours by the
number of hours in a year (i.e., 2 r 8,760 = 0.02284 percent).
6.3.5 Averaging Time Analysis
A method which can be used to determine a maximum 8-hour average CO
concentration when only 1-hour average data is available is a mathemati-
33
cal model developed by Larsen known as "Larsen's Transform". Data
fitting this model can be graphed as shown in Figure 6-4 which includes
the maximum, minimum, and frequency of equaling or exceeding specified
CO concentrations for averaging times ranging from one second to one
year. The most useful and important part of the graph, however, is the
annual maximum line which can be used to determine the annual maximum 8-
hour average CO concentration from 1-hour average values.
6.3.6 Trend Analyses
Carbon monoxide concentrations vary considerably from hour to hour,
day to day, season to season, and year to year. These variations are
usually not random but follow fairly predictable temporal patterns
according to season of the year, day of the week, and hour of the day.
Predicted, long-term, statistical variations in CO concentrations are
referred to as trends.
Carbon monoxide trends are best illustrated using graphs which can
show diurnal, daily, seasonal, or yearly CO concentration comparisons.
Examples of the different ways trends can be shown are illustrated later
in this section.
6-20
-------
1.000
100 k-
o>
I
.
«
o
cc
I-
o
u
10
0.1
second
1
AVERAGING TIME
minute, hour 'day
5 1015 30 1 2 4 8 12 1 247
14
month
23 6 12
170.90
149.19
mg/m-*
ppm
I I I I"T
56.3Q
49.15
34.73
30.32
M II f I
23.31 18.93
20.35 16.53
EXPECTED ANNUAL MAXIMUM CONG
10.02
8.75
7.02
6.13
0.01
1
I
GEO. MEAN FOR 1-hr. = 6.36 mg/m3 = 5.552 ppm
STANDARD GEOMETRIC DEVIATION = 1.56
87 percent OF HOURS HAVE DATA AVAILABLE
I
10,000
1,000
100
10
a
a
O
111
u
z
o
o
0.1
0.01
0.0001
0.001
0.01
0.1 1 10
AVERAGING TIME, hours
100
1,000
10,000
Figure 6-4. Concentration vs. averaging time and frequency for carbon monoxide from 12/1/63 to 12/1/68 at site 662, St. Louis.
-------
Carbon monoxide concentrations also follow fairly predictable
spatial patterns. Spatial distributions of CO concentrations can be
illustrated by the use of isopleth maps. Isopleth CO concentration maps
can be prepared illustrating the spatial distribution of average CO
concentrations, maximum CO concentrations, typical CO values during a
particular time of day or season of year, or the CO concentration distri-
bution that typically occurs under specific meteorological conditions
(wind speed, wind direction, atmospheric stability). Isopleth maps are
especially useful for illustrating the size of the geographical area
affected by CO levels. Examples of isopleth maps are illustrated in
Figures 6-5 and 6-6.
6.3.7 Special Analyses
A useful analysis technique not previously presented is the
"pollution rose" as illustrated in Figure 6-7. The pollution rose
presents the joint frequency distribution of wind direction versus
ambient CO concentration. The pollution rose is very helpful in deter-
i
mining the wind direction associated with the highest ambient CO concen-
trations and intuitively the location of sources of high CO emissions.
Another analysis technique is the case analysis which can be used
to characterize the meteorological and/or emission conditions associated
with observed CO concentrations. For example, in order to characterize
the meteorological conditions associated with the occurrence of high CO
levels, meteorological records can be evaluated for the days when highest
CO concentrations were observed concurrently at several monitoring sites
throughout an urban area. The results of the analysis can then be used
6-22
-------
24
15
12
12
12
12
Figure 6-5. Predicted 1-hour average ambient CO concentrations (mg/m3) in vicinity of I-85 in Atlanta, GA,for 1976.18
-------
MISSISSIPPI RIVER
E-H.CRUMPBLVD
Figure 6-6. Measured 8-hour average background CO concentrations in Memphis, TN.62
6-24
-------
NORTH
10%
LEGEND
CO CONC, mg/m:
0-6.8
Figure 6-7. Pollution rose for St. Louis, MO.
6-25
-------
to develop a meteorological scenario for input to a mathematical model
for the purpose of modeling "worst case" CO concentrations.
6.4 URBAN LEVELS OF CARBON MONOXIDE
6.4.1 Comparison to NAAQS
Measurements of CO in U. S. urban areas show that the NAAQS* for CO
is frequently violated. In 1973, 153 of 212 CO monitoring stations
operated in the U. S. (i.e., 72 percent) reported violations of the 8-
hour NAAQS with 24 stations (i.e., 11 percent) exceeding the 1-hour
NAAQS.70 Of the 30 Air Quality Control Regions (AQCR's) which were
Priority I for CO in 1973, 26 reported at least 1 quarter's data and 25
exceeded the 8-hour standard. Also, 34 AQCR's, classified Priority III
in 1973 which were not required to monitor CO, established monitors and
28 reported at least one site where the 8-hour NAAQS was exceeded.
Figure 6-8 shows a map prepared by the EPA of the location of AQCR's
which observed violations of the NAAQS for CO in 1973.
Since 1973, NAAQS violations have continued to occur, although the
percentage of total monitors reporting NAAQS violations have decreased.
In 1974, 211 out of 377 stations (i.e., 56 percent) reported violations
of the 8-hour NAAQS. In 1975, 234 out of 434 monitors (i.e., 54 percent)
76
showed 8-hour NAAQS violations. Of these, 111 sites measured CO
concentrations at least 50 percent greater than the NAAQS. in 1977,
211 out of 456 monitors (i.e., 46 percent) showed 8-hour NAAQS violations.
Carbon monoxide concentrations exceeding the 1-hour NAAQS were observed
*-The NAAQS (National Ambient Air Quality Standard) for CO is 10 mg/m3
3
and 40 mg/m for 8-hour and 1-hour averagin
not to be exceeded more than once per year.
3
and 40 mg/m for 8-hour and 1-hour averaging times, respectively,
6-26
-------
i
ro
8-hour STANDARD EXCEEDED
ALL REPORTED DATA BELOW THE 8-hour STANDARD
NO DATA
Figure 6-8. Status of carbon monoxide levels, 1973.70
-------
at only 27 locations (i.e., 6 percent) in 1975 and at only 11 locations
(i.e. , 2 percent) in 1977.80b
Part of the reason so many NAAQS violations are observed is due to
the fact that most CO monitoring sites are located next to major streets
in urban areas. While the measured concentrations are probably accurate,
the scale of representativeness of these sites is small such that the
number of people exposed to these CO levels may be relatively small.
6.4.2 Hourly Patterns
Ambient CO concentrations may follow regular hourly patterns of
variation which result from nearby vehicular traffic activity and mete-
orological factors affecting the dispersion of the CO. Three examples
are shown in Figures 6-9, 6-10, and 6-11 which Illustrate the annual
average and "worst case day" hourly CO curves based on 1977 data from CO
42 10
monitoring sites in Baltimore, Maryland, Denver, Colorado, and
CO
Los Angeles, California, respectively. (The "worst case day" 1s
defined herein as that day on which the annual maximum 8-hour average CO
concentration was observed.) While the exact shape and magnitude of the
hourly CO curve for these communities is dependent to a large extent on
meteorological factors, two peaks corresponding with the morning and
evening "rush hour" traffic are evident 1n the figures. For comparison,
an example of typical hourly variations in traffic volume 1s given 1n
Figure 6-12. A third peak in CO concentration during the late evening/
early morning hours can also be noted in several of the figures. This
peak is influenced by late night calm meteorological conditions.
6-28
-------
E
I
to"
<
oc
o
o
u
o
u
36
34
32
30 -
28 -
26
24
22
20
18
16
14
12
10
8
6
4
2
BALTIMORE
/
I I
I I I I
/,
M
\
J
T
T
I T
ANNUAL AVERAGE
WORST CASE DAY
\
12 1
6
AM
9 10 11
12 1
NOON
6
PM
10 11 12
TIME OF DAY
Figure 6-9. Hourly variations of ambient CO concentrations for Baltimore, MD.
-------
i
w
o
34
32
30
28
26
24
22
« 20
* «
O
t 16
Ul
O
14
8 12
O
o
10
8
6
DENVER I I I I
—"•— ANNUAL AVERAGE
_ — — - WORST CASE DAY
A
/ \
\
I
I
I
lU
I I I I
12
6
AM
9 10 11 12 1
NOON
TIME OF DAY
6
PM
9 10 11 12
Figure 6-10. Hourly variations of ambient CO concentrations for Denver, CO.
-------
36
LOS ANGELES I I I I 1 I I I I I T
I
CO
O
01
o
O
o
o
o
34
32
30
28
26
24
22
20
18
16
14
12
10
8|
66
4
2
• ANNUAL AVERAGE
WORST CASE DAY
A
X^x
I II I
12
I I I I I I I I I I I I
6
AM
10
11 12 1
NOON
TIME OF DAY
6
PM
9 10 11 12
Figure 6-11. Hourly variations of ambient CO concentrations for Los Angeles, CA.
-------
1—I—I—I—I—I—[
cr>
i
u>
ro
i i r
i—i—i—i r~
•CBD
CENTRAL CITY
SUBURBS
I I i I I I I
I I I 1 I I
0
6
8
10 11 12
13
14 15 16 17 18 19 20 21 22 23 24
TIME, hours
oo
Figure 6-12. Hourly variations of traffic volume.
-------
Carbon monoxide levels 1n most of the cities generally reach their
Initial dally maximum between 7-9 a.m., coincident with heavy morning
automobile traffic and prior to Inversion layer breakup. The second
peak 1s usually reached 1n the late afternoon between 4-7 p.m. The late
evening peak generally occurs between 10 p.m. and 12 midnight. Although
the morning peak 1n CO concentrations 1s generally the highest, Figure 6-
10 Illustrates that the opposite cart occur.
6.4.3 Seasonal Patterns
Ambient CO levels also follow seasonal patterns, which result
primarily from changes 1n meteorological factors. Figures 6-13, 6-14,
and 6-15 show the seasonal arithmetic mean, maximum 8-hour and maximum
1-hour CO concentrations based on 1977 data for Baltimore, Denver,
co
and Los Angeles, respectively. These figures show the highest ambient
CO concentrations during the winter.
In the winter, the tendency toward colder ambient temperatures
results 1n Increased production of CO emissions from cars, 1n addition
to CO emitted from other fuel burning sources. Also, the more stable
atmospheric conditions and low wind speeds which occur during winter
result 1n decreased dispersion of CO emissions and contribute a substan-
tial part to the occurrence of high ground level CO concentrations.
6.4.4 Annual Patterns
Annual trends of CO concentrations are presented 1n Figures 6-16
through 6-23 for Baltimore,41 Denver,10>64>n LOS Angeles,57'58'64
Chicago,70 Cincinnati,70 Philadelphia,70 St. Louis,70 and Washington, DC.70
Plotted are the highest 1-hour average, the highest 8-hour average, and
the annual arithmetic mean CO concentration observed each year.
6-33
-------
CO
cc
H
LU
O
O
O
O
O
34
32
30
28
26
24
22
20
18
16
14
12
10
8
6
4
BALTIMORE
1-hr MAX
•M
8-hr MAX __
SEASONAL,
AVG
WINTER SPRING SUMMER FALL
Figure 6-13. Seasonal variations of ambient CO
concentrations for Baltimore, MD.
42
6-34
-------
o>
E
DC
h-
ui
O
o
u
o
o
40
38
36
34
32
30
28
26
24
22
20
18
16
14
12
10
8
6
4
2
1
DENVER
1-hrMAX
8-hr MAX
SEASONAL
AVERAGE
WINTER SPRING SUMMER FALL
Figure 6-14. Seasonal variations of ambient CO
concentrations for Denver, CO.
10
6-35
-------
CO
^
TO
CO*
z
O
<
cc
H
LU
O
O
O
O
O
40
38
36
34
32
30
28
26
24
22
20
18
16
14
12
10
8
6
4
2
LOS ANGELES
1-hr. MAX
8-hr. MAX
SEASONAL AVERAGE
WINTER SPRING SUMMER FALL
Figure 6-15. Seasonal variations of ambient CO
concentrations for Los Angeles, CA.
58
6-36
-------
.E
I
*,
Z
O
I-
cc
I-
z
LU
O
z
O
O
O
O
56
48
40
32
24
16
8
1 I I T
— 8 hr MAX
68
70
72
YEAR
74
76
Figure 6-16. Annual variations of ambient CO concentrations for
Baltimore, MD.
6-37
-------
at
E
cc
I-
z
UJ
o
z
o
o
o
o
100
90
80
70
60
50
40
30
20
10
1 T
MAX. 1-hr.
MAX. 8-hr.
ARITH.MEAN
I I
I I
62 64 66 68 70 72 74 76 78
YEAR
Figure 6-17. Annual variations of ambient CO concentrations for
Denver, CO.
6-38
-------
z
80
70
60
50
40
z
uu
O
z
o 30
O
o
20
10
- MAX. 1-
MAX. 8-hr
— ARITH.MEAN
68
70
I
72
YEAR
74
76
78
Figure 6-18. Annual variations of ambient CO concentrations for Los
Angeles, CA, SAROAD Site No. 053900001.
6-39
-------
I
cc
I-
LU
O
z
o
o
o
o
70
60
50
40
30
20
62
ARITH.MEAN
I I
64
66
68
70
YEAR
72
74
76
78
Figure 6-19. Annual variations of ambient CO concentration for
Chicago, IL, SAROAD Site No. 141220002 (former CAMP station).
6-40
-------
z
o
40
f 30
20
1-
Z
LU
O
8 10
O
o
MAX. 1-
-MAX. 1-
ARITH. MEAN
I I
62
64
66
68
70
72
74
YEAR
Figure 6-20. Annual variations of ambient CO concentrations for
Cincinnati, OH, SAROAD Site No. 361220003 (former CAMP station
discontinued in 1973).
6-41
-------
CO
oc
h-
Z
UJ
o
z
8
O
O
70
60
50
2 40
30
20
10
MAX. 1-hr.
MAX. 8-hr.
ARITH.MEAN
62
64
66 68
70 72
YEAR
74
76
78
Figure 6-21. Annual variations of ambient CO concentrations for
Philadelphia, PA, SAROAD Site No. 397140002 (former CAMP
station).
6-42
-------
CO
£
LU
O
o
0
o
o
40
30
tt 20
H-
10
MAX. 1-hr.
MAX. 8-hr.
ARITH.MEAN'
62
64
66
68
70
72
74
YEAR
Figure 6-22. Annual variations of ambient CO concentrations for
St. Louis, MO, SAROAD Site No. 264280002 (former CAMP station
discontinued in 1973).
6-43
-------
O)
E
cc
h-
z
UJ
o
2
O
O
o
o
70
60
50
1 40
30
20
10
MAX. 1-hr.
MAX. 8-hr.
ARITH. MEAN
i i i i r
SITE MOVED TO NEW LOCATION
62
64
66
68
70
72
74
76
78
YEAR
Figure 6-23. Annual variations of ambient CO concentrations for
Washington, DC, SAROAD Site No. 090020002 moved in 1969 and
redesignated No. 090020003 (former CAMP station).
6-44
-------
For Baltimore County, monitoring data from 1976 shows a factor of
3.4 decrease in annual maximum 1-hour average CO concentrations and a
similar decrease (i.e., a factor of 3.1) in annual maximum 8-hour average
CO concentrations compared with 1967 levels.
For Denver, a 53 percent and 32 percent decrease in annual maximum
1-hour and 8-hour average CO concentrations, respectively, has been
observed from 1968 to 1977. The annual arithmetic mean CO concentration
has decreased 44 percent from 1968 to 1977. The number of observed
NAAQS violations has also decreased in Denver over a 10-year period.
Eighty-three violations of the 8-hour standard were observed in 1968
with a peak of 153 violations observed in 1972, then decreased to 48
observed violations in 1977. The number of violations of the 1-hour
standard has decreased from six observations in 1968 to one observation
in 1977.
For Los Angeles, a 50 percent and 24 percent decrease in annual
maximum 1-hour and 8-hour average CO concentrations, respectively, has
been observed from 1968 to 1978. A 45 percent decrease in the annual
arithmetic mean CO concentration has been observed from 1968 to 1978.
Although a significant reduction in ambient CO concentrations has been
observed in Los Angeles, the number of observed NAAQS violations still
remains relatively high. Sixty-four violations of the 8-hour standard
were observed in 1977 compared with 172 observed violations in 1968.
A general trend of decreasing ambient CO levels is evident in most
of the curves presented. This trend toward lower ambient CO concentra-
tions is presumably due to the lower CO emissions of later model
automobiles which incorporate air pollution controls. The CO emissions,
although being maintained at a relatively constant level, are decreasing
in urban areas.
6-45
-------
A1r monitoring results have been presented only from selected sites
1n several major U. S. cities. These sites are generally those located
close to major highways and thus measure some of the highest CO
concentrations; however, measurements at the sites are not necessarily
representative of CO concentrations 1n these cities. Monitoring sites
in the same cities located 100-200 meters from any highway would be
expected to record much lower concentrations. More information on CO
levels measured In, U. S. cities 1s published annually in EPA's Air
Quality Trends Reports.67'68'70'74'76'79'80"
6.5 SPECIAL CARBON MONOXIDE EXPOSURE SITUATIONS
There are a number of circumstances where people may be exposed to
unusually high concentrations of CO. Some of these result from the
operation of automobiles 1n areas which are poorly ventilated. These
exposure situations include highway tunnels, urban street canyons, and
underground parking garages. Other high CO exposure situations may
occur where auto emissions are unusually high (due to large traffic
volumes and congested conditions) such as near large arterial inter-
sections, freeway toll booths, shopping centers, sports stadiums, and
roadway repair and construction sites. The commuter may also be exposed
to high CO concentrations either within his car (especially 1f smoking)
or from the ambient air. Exposure to CO emitted by cars on city streets
is a special concern of bicyclists.
Some occupations require working on or very close to automobile
traffic for long periods of time during the work day which may result 1n
unusually high exposures to CO. These occupations include street repair
6-46
-------
crews, street cleaners, street vendors, delivery men, toll collectors,
garage attendants, police, and taxi and bus drivers. There are other
occupations where exposure to CO is due to sources other than automobiles.
Those include fire fighters, certain airport workers, and some miners
and foundry workers.
6.5.1 Variations with Type of Vehicle Traffic
Ambient CO concentrations near city streets were reported as high
3 3
as 57 mg/m (49.6 ppm), 1-hour average and 41.4 mg/m (36.0 ppm), 8-hour
average for the "worst case" New York City site in 1975. Similar
3
measurements in Los Angeles showed CO concentrations of 60 mg/m
3 43
(52.2 ppm), 1-hour average, and 49.7 mg/m (42.6 ppm), 8-hour average.
These measurements represent some of the highest ambient concentrations
of CO reported in the United States near open city streets.
Concentrations of CO in highway tunnels have been reported by
4
several investigators. Ayres et al. have reported 30-day average CO
3
concentrations of 72.5 mg/m (63 ppm) measured at the Queens Midtown
3
Tunnel in New York and a 1-hour maximum of 250 mg/m (217 ppm).
Measurements at the Sumner Tunnel in Boston, Massachusetts show 1-hour
3
average CO concentrations as high as 145.2 mg/m (126.3 ppm) with a 24-
3 45
hour maximum of 58.4 mg/m (50.8 ppm). Miranda et al. reported that
3
many tunnels usually operate below 115 mg/m (100 ppm) CO, employing
3
emergency ventilating fans whenever CO levels exceed 287.5 mg/m (250 ppm)
oc
Wright et al. measured CO concentrations in underground parking
3
garages. They found CO levels in excess of 115 mg/m (100 ppm) in
enclosed, unventilated garages. Similar measurements taken in a
6-47
-------
well-ventilated underground parking facility showed maximum CO
3
concentrations of 49.5 mg/m (43 ppm).
49
In a study conducted by Patterson et al. CO measurements were
made in the vicinity of Liberty Tree Mall, a regional shopping center in
the Boston area. The study was conducted for two weeks prior to
Christmas of 1973. The maximum 1-hour average concentration measured
3 3
was 35.2 mg/m (30.6 ppm); the maximum 8-hour average was 16.3 mg/m
(14.2 ppm).
5
A similar study was conducted by Bach et al. at two sports stadia:
Three Rivers Stadium 1n Pittsburgh, Pennsylvania and Atlanta Stadium
in Atlanta, Georgia. Measurements were made during both day and night
baseball games 1n June and July, 1973. The maximum 1-hour average CO
3
concentration measured was 28.8 mg/m (25 ppm); the 8-hour maximum was
3
9.4 mg/m (8.2 ppm).
In order to determine the CO exposure of bicyclists, Kleiner and
30
Spengler conducted a study in Boston during the summer of 1974.
As expected, CO exposures of bicyclists on city streets were a function
of traffic volume, street configuration, proximity of traffic, and
3
ventilation. Typical Summer exposures were between 12.7 and 17.3 mg/m
(11 and 15 ppm) for trips ranging from 10 to 45 minutes. In no case did
3
the trip-averaged exposure approach 40.3 mg/m (35 ppm).
6.5.2 Car Passenger Exposure to Carbon Monoxide
Carbon monoxide concentrations have also been measured Inside
o
automobiles. Chaney measured CO concentrations within an automobile
6-48
-------
traveling on the Dan Ryan Expressway (1-94) 1n Chicago, and on the
San Diego Freeway (1-405) 1n Los Angeles and found that CO levels varied
with traffic speed. According to Chaney "when the traffic slowed to
3
10 mph (16 kph) the CO concentration usually exceeded 17.3 mg/m (15 ppm);
o
when 1t halted completely, the CO concentration was about 51.8 mg/m
(45 ppm)". Chaney also observed variations 1n pollution concentration
Inside his automobile depending on the type and age of vehicle he was
following. Heavily-loaded vehicles produced the highest results. While
following a truck over the Sierra Nevada mountains, Chaney recorded CO
3
concentrations which reached 57.5 mg/m (50 ppm) on the steepest grade
O QC
and remained over 28.8 mg/m (25 ppm) for 30 minutes. Wright et al.
3
have reported CO concentrations of 104 mg/m (90 ppm) inside an automobile
due primarily to CO from passengers' cigarette smoke.
6.5.3 Occupational Exposure
I
ftfi
Certain occupations necessitate exposure to CO. Xlntaras et al.
have reported CO exposures of six toll collectors working at 1-65 in
Louisville, Kentucky. The maximum 8-hour average concentration measured
3
was 65.6 mg/m (57 ppm). Over the 12 days of the study, the average 8-
3
hour exposure was 26.2 mg/m (22.8 ppm).
•}
Measurements of CO concentrations in foundry air have been made by
83
Virtamo and Tossavalnen. They found that iron cupola exhaust gases
may contain 20 to 30 percent CO. Forty-six measurements of CO concen-
3
tration 1n the vicinity of the cupolas showed an average of 276 mg/m
3
(240 ppm). They also measured an average 127 mg/m (110 ppm) CO in the
3
casting area of foundries (909 samples) and 97.8 mg/m (85 ppm) in the
6-49
-------
breathing zone (61 samples) of foundry workers. Similar measurements in
3
steel foundries showed less than 23 mg/m (20 ppm) of CO in areas
around electric furnaces. Measurements in the melting and casting areas
3
of copper alloy foundries averaged 23 mg/m (20 ppm) of CO.
54
Rodgers measured CO concentrations in phosphate and copper mine
environments resulting from the use of explosives. Carbon monoxide
3
concentrations exceeded 173 mg/m (150 ppm) for 45 minutes and exceeded
3
58 mg/m (50 ppm) for 110 minutes during shot firing of nitroglycerin
explosives within the mine. Ammonium-nltrate-oil and water gel type
explosives tended to produce less CO than equal weights of nitroglycerin
explosives.
Fire fighters can be exposed to very high concentrations of CO due
35 51
to smoke inhalation. Loke et al. and Radford and Levine both report
maximum carboxyhemoglobin (COHb) levels of 10 percent to 14 percent in
the bloodstream of fire fighters after a fire. Carbon monoxide concen-
trations were not reported.
6.5.4 Indoor Carbon Monoxide Exposure
Indoor levels of CO have been studied by the General Electric
Company for two buildings in New York City- One was a high-rise
apartment building straddling the Trans Manhattan Expressway; the other,
a high-rise office building located adjacent to a midtown Manhattan
street canyon. The study showed that indoor CO levels were directly
related to nearby outdoor CO levels. While indoor concentrations
"lagged behind" (in time) outdoor levels there was "no significant
difference in CO levels along the outside walls and inside the two
6-50
-------
structures". The G. E. study typically reported Indoor and outdoor CO
concentrations of from 4.6 to 11.5 ra,g/m3 (4 to 10 ppm).
55
Shaplowsky et al. have reported the results of CO levels Inside
1,820 houses throughout the United States. Their results showed that
16.8 percent had levels above 11.5 mg/m (10 ppm). In a similar study
CO
conducted by Rench and Savage in 80 households 1n Fort Collins,
Colorado, concentrations 1n homes were recorded 1n the kitchen and
family room around the dinner hour. Their measurements showed over
3
6 percent of the households had CO concentrations greater than 11.5 mg/m
3
(10 ppm). The mean CO levels measured were 3.55 mg/m (3.09 ppm) 1n
3
kitchens and 2.01 mg/m (1.75 ppm) in family rooms.
87
In a study conducted by Yocum CO measurements were made inside
domestic buildings. Yocum found that indoor CO levels increased more
slowly than outdoor levels, but, once built up, indoor levels remained
higher for a longer period of time. Thus, domestic premises have a
tendency to entrap gaseous pollutants. Yocum measured typical CO
3
concentrations of 0.87 to 6.92 mg/m (0.76 to 6.02 ppm).
The effect of smoking cigarettes on indoor CO levels has been
c.
investigated by Bridge and Corn who measured CO during two experimental
3 3
"parties". In one 145 m (5120 ft. ) room containing 50 people, 25
people smoked 50 cigarettes and seven cigars in 1 1/2 hours. With a
3
room air exchange rate of seven times per hour, CO averaged 8 mg/m
3 3
(7 ppm). During a second experiment in a 106 m (3750 ft. ) room
containing 73 people, 36 people smoked 63 cigarettes and 10 cigars in
3
1 1/2 hours producing an average CO content of 10 mg/m (9 ppm).
6-51
-------
28 ^
Hoegg conducted experiments in a closed 25 m chamber. He found
that CO levels increased with the number of cigarettes smoked.
3
Concentrations ranged from 11.5 mg/m (10 ppm) for four cigarettes to
3
80 mg/m (69.8 ppm) for 24 cigarettes.
2
Anderson and Dalhamn measured CO concentrations due to smoking in
3
a medium sized (80 m ) meeting room. Fifty cigarettes were smoked in
3
two hours. With six air changes per hour, initial levels were 2.3 mg/m
3
(2 ppm) and average peaks during smoking were 6.9 mg/m (6 ppm).
22
In Harke's experiments, 21 persons smoked two cigarettes each in
3
enclosed office rooms and within 16 to 18 minutes, in a 57 m room, they
3
produced 56.4 mg/m (49 ppm) of CO. Ventilating the room decreased
these concentrations by 80 percent. In the case of one person smoking
3
11 cigarettes in five hours in a 30 m room, the CO concentration was
3
less than 11.5 mg/m (10 ppm).
Smoking in automobiles can produce significant CO concentrations.
23~27
Harke et al. conducted experiments where smoking was done in a car
within a wind tunnel. During the experiment, time spent smoking was
varied, as was wind speed and ventilation. At 0 km/hr, with full
3
ventilation, CO averaged 9.2 to 11.5 mg/m (8 to 10 ppm); when six
cigarettes were smoked intermittently, CO reached a maximum concentration
3
of 34.5 mg/m (30 ppm). When cigarettes were smoked continuously, one
3
after the other, final CO levels were registered at 92 mg/m (80 ppm)
with no wind or ventilation factor. With wind and ventilation, however,
3
CO remained at 5.8 to 6.9 mg/m (5 to 6 ppm), with no increases observed.
6-52
-------
In all cases CO levels returned to base levels, even with no ventilation,
within a few minutes after smoking stopped.
Srch measured CO concentrations produced by cigarettes in a
closed automobile with no ventilation. The test car was parked in an
unventilated garage while two people smoked five cigarettes each in one
3
hour. Carbon monoxide levels reached 104 mg/m (90 ppm) in that time.
Carboxyhemoglobin in smokers rose from 5 to 10 percent and from 2 to
5 percent in the two nonsmokers present.
The U. S. Department of Transportation in 1973 conducted a study of
cigarette-caused pollution on intercity buses. Inside a stationary
Greyhound bus with the engine off, vents open, and blower on, cigarettes
were allowed to burn in the ashtrays. Tests conducted ranged from the
"worst" case, where it was assumed that all 43 passengers smoked half
the time, to the "realistic" case, where only the last 20 percent of the
seats were allotted to smokers. After 30 minutes in the worst case,
3
CO stabilized at 38.0 mg/m (33 ppm), and in the realistic case, CO
3
stabilized at 20.7 mg/m (18 ppm), after 43 minutes, with the outside
3
level 15.1 mg/m (13 ppm).
Many other studies have been performed to determine indoor exposure
levels of pollutants. A summary of results of many experiments has been
prepared by Sterling and Kobayashi and by the EPA.
6.6 EFFECTS OF METEOROLOGY AND TOPOGRAPHY
Meteorology governs the transport and dispersion of CO emissions in
the atmosphere and thus has a strong influence on the ground level CO
concentrations detected at receptor points downwind of the emission
6-53
-------
sources. Meteorological variables that determine CO transport xand
dispersion patterns include wind speed, wind direction, atmospheric
stability, vertical mixing height, and ambient temperature.
Wind speed and direction influence the horizontal dispersion of CO
emissions. Low wind speeds provide little dilution air, allowing CO
emissions to build up, resulting in higher CO concentrations. Conversely,
high wind speeds aid in the dispersion of CO emissions by increasing the
amount of dilution which takes place, thus decreasing CO concentrations.
Wind direction determines the direction of horizontal transport of CO
emissions and consequently the impact that CO emissions from one area
will have on air quality in another area. For wind directions crossing
an urban area, an accumulation of CO emissions will occur in the downwind
direction, such that mesoscale (1-10 km) CO concentrations will be
highest at the downwind edge of the urban area. In the microscale
regime (1-100 m), for a highway line source, wind directions nearly
parallel to the highway will allow for an accumulation of CO emissions
in the downwind direction, resulting in CO concentrations higher than
would be expected for perpendicular winds under the same conditions.
In addition to transporting pollutants, winds produce turbulence in
the atmosphere which enhances the mixing and dispersion of pollutants in
the air. Turbulence is the result of both mechanical forces and thermal
forces in the atmosphere.
The effect of surface roughness (i.e., mountains, buildings, etc.)
on the wind speed profile over several types of topographic features is
illustrated in Figure 6-24. With increased surface roughness, either
6-54
-------
600
500
400
300
200
en
01
01
100
URBAN AREA
GRADIENT WIND
SUBURBS
LEVEL COUNTRY
0 5 10
WIND SPEED, m/sec
10
Figure 6-24. Effect of terrain roughness on the wind speed profile,
-------
natural or man-made, the wind speed profile is decreased and the depth
of the affected layer is increased. The net effect of increased surface
roughness over an urban area is to induce mechanical turbulence which
aids in the dispersion of CO emissions.
y
Radiation and thermal properties of topographic features influence
the heating and cooling of the atmosphere near the ground surface. The
most notable of these effects is the urban "heat island" effect. Heat
sources, including the asphalt and concrete associated with an urban
area, tend to radiate heat, causing a "heat island" compared to the
cooler surrounding terrain. The buoyant effect of warmer air over the
city tends to induce thermal turbulence (i.e., more unstable atmospheric
conditions) which tend to aid in the dispersion of CO emissions, thus
lowering ambient CO concentrations.
Drainage winds, such as sea-land breezes, lake-land breezes, or
mountain-valley winds are caused by the differential heating of
topographic forms. Drainage winds which affect the net transport of CO
emissions may deviate from the prevailing wind direction. These winds
generally flow in one direction during the day, then in the opposite
direction at night. As a result, an urban area can experience "blow-
back" of CO emissions emitted during the day resulting in higher CO
concentrations at night. Also, the boundary region of the drainage
winds sometimes causes the air mass to remain nearly stationary, or
oscillate back and forth for periods up to several hours, and can be the
site of nearly calm conditions or varying winds. This results in the
slow net transport of CO emissions, allowing them to accumulate, and
thus resulting in higher ambient CO concentrations.
6-56
-------
Vertical mixing height affects the total ventilation capacity of
the atmosphere. When the temperature-altitude relationship 1s reversed
from normal, the resulting Increase 1n temperature with Increase 1n
height produces an Inversion or Inversion I1d which limits vertical
mixing, and thus limits the dilution capacity of the atmosphere.
An Important form of Inversion for CO dispersion 1s the surface or
radiation Inversion. It usually occurs at night with light winds and
clear skies, when the loss of heat by long-wave radiation from the
ground surface cools the surface and subsequently the air adjacent to
It. The surface inversion usually persists for hours and because 1t
typifies stable atmospheric conditions, 1t tends to result 1n high
mlcroscale and mesoscale CO concentrations. With the proper relative
humidity, these same conditions will lead to the formation of radiation
fog. The presence of early morning fog 1s often associated with a
surface-based temperature Inversion.
Another type of Inversion 1s the subsidence Inversion. It Is
caused by a gradual descent of air aloft, accompanied by an Increase 1n
pressure which results 1n an adlabatlc warming of the descending layer.
The resulting subsidence Inversion 1s Illustrated 1n Figure 6-25 where
the temperature decreases with height, and then 1s capped by a subsidence
inversion layer, above which there 1s a normal decrease of temperature
with height. The subsidence inversion usually persists on the order of
days and tends to contribute to high urban background CO concentrations.
The subsidence inversion is usually more persistent during the summer
and fall months.
6-57
-------
1000
*
I
CD
500
rn IY~I i i i i r
in r
2nd MIXING LAYER
INVERSION "LID'
1st MIXING LAYER —
II 11 1 1 I \ I
0 10 20
TEMPERATURE, °C
Figure 6-25. Schematic representation of an elevated inversion.
6-58
-------
The shape of typical plots of hourly CO concentrations (See Figures
6-9, 6-10, and 6-11) can be attributed 1n large part to the effect of
changing wind speeds, atmospheric stability and inversion height during
the course of a day. Figure 6-26 shows the average hourly wind speed
63
and Inversion height occurring in Los Angeles during Summer. The
higher wind speeds and inversion height during early afternoon are
typical throughout the continental United States and play a significant
role 1n lowering urban CO concentrations at midday. Figure 6-26 shows
that traffic volumes, and subsequently CO emissions from cars, would
still be expected to be high at this time of day. Around midnight, when
traffic volumes are relatively low, the effect of low wind speeds and
low Inversion heights tend to cause CO concentrations to increase. Many
monitoring stations 1n the United States observe these relatively high
CO concentrations late at night.
In addition to transport and dispersion effects, ambient surface
temperature also has a unique effect on the production rate of CO
emissions from automobiles. Using a variety of automobiles tested at
artificially-controlled ambient temperatures of 20°, 50°, 75°, and
110°F, the EPA found that lowest CO emissions were produced at 75°F.
However, colder temperatures seem to Increase the emission rate of CO
from automobiles resulting in higher ambient CO concentrations. Warmer
temperatures tend to minimize the emission rate of CO from automobiles
resulting in lower ambient CO concentrations.
6-59
-------
10
WIND SPEED
INVERSION HEIGHT
a
E
Q
ui
UJ
a.
CO
O
20
CM
O
I
iu
X
15
12
18
24
TIME, hours
Figure 6-26. Hourly variations in inversions height and wind speed for Los Angeles in summer.
-------
6.7 CARBON MONOXIDE DISPERSION MODELS
A dispersion model relates pollutant emissions to ambient air
quality by providing a mathematical description of the transport,
dispersion, and chemical transformations that occur in the atmosphere.
This ability to relate source emissions to receptor air quality is very
important to air quality maintenance planning and environmental impact
assessment.
Dispersion models vary in complexity from the simple empirical or
statistical relationships to sophisticated multi-source models that
describe the transport and dispersion of CO throughout an urban area.
For estimates of ambient CO concentrations, a line source model is needed
t,
to estimate the CO levels near a single source or group of sources and
an area source model is needed to estimate the background CO levels due to
other sources. The types of models used, therefore, will depend mainly
on the source configuration to be modeled (i.e., area, line, or point
sources).
Model input data consist of parameters such as traffic volume,
vehicle speed, truck mix, and vehicle age (needed to estimate emissions),
?
and wind speed and direction, atmospheric stability class, source charac-
teristics such as road location, road width, number of lanes, median
width, and receptor location, etc. Typically, model output consists of
tabulated results of input data and predicted CO concentrations. Some
models can provide computer plots of results and isopleth maps showing
the calculated spatial variation in CO levels.
6-61
-------
CQ
The rollback model 1s a simple modeling technique which assumes a
linear relationship between ambient air quality and area pollutant
emissions. The use of rollback requires air monitoring data and emission
Inventories. Its main use has been to calculate the percent reduction
of pollutant emissions needed to achieve the ambient air quality standard.
It has also been used to predict future ambient pollutant concentrations
by factoring air monitoring data by a ratio of projected future pollutant
emissions to base year pollutant emissions. Rollback is widely used
because it is simple and easily understood. In order to use the rollback
method, ambient air monitoring is required to establish existing CO
levels. For those areas without available monitoring data, an alternate
modeling scheme would be necessary. Also, the rollback method incor-
porates the assumption that an overall proportional reduction of emissions
in the area is required to meet the ambient air quality standard when,
in some cases, a reduction in emissions at a few specific sources may be
sufficient to meet the standards. Finally, the model provides little or
no spatial resolution of ambient pollutant concentrations.
More sophisticated techniques for modeling background CO concen-
90 91 37
trations include the Hanna-Gifford model, ' and APRAC-2. In the
Hanna-Gifford model, area source emissions are assigned to grid squares
where it is assumed that the area source strength is uniform across each
square. Gifford's "reciprocal plume" concept is employed in order to
estimate the surface concentrations due to area sources upwind of the
receptor grid. The vertical distribution of the pollutant is assumed to
6-62
-------
be Gaussian. The spatial resolution of the model 1s on the order of
kilometers. The authors of the model feel that 1t performs nearly as
well as much more complex models that require the use of digital computers.
Depending on the model application, correlations between predicted and
19
measured pollutant concentrations ranging from 0.60 to 0.95 have been
found.
37
The APRAC-2 dispersion model uses a number of area segments
spaced at logarithmic upwind intervals from a receptor point as shown in
Figure 6-27. This area segment scheme overlaps the coded traffic network
from which traffic links and portions of links falling within each area
segment are identified. The emissions from each individual link are
then calculated and accumulated to determine the average emission rate
for each of the nine area segments. Background CO concentrations are
calculated from two basically different formulations. For sources near
the receptor, a-Gaussian model is used. A simple "box" model is used
under limited vertical mixing conditions, at the point of restricted
vertical dispersion. The spatial resolution of the model is on the
order of tenths of kilometers.
The APRAC-2 model also provides a choice of two special models for
calculating CO concentrations from nearby highway sources: the street
canyon model and the intersection model. The street canyon model is
-in o/r
based on work by Georgli and the San Jose experiment. These studies
showed that because of lower wind speeds and a general helical circulation,
higher CO concentrations on the leeward side of the street result due to
the reverse flow component at ground level. The intersection model
6-63
-------
16km
i
en
RECEPTOR
POINT
EXPANDED VIEW OF
ANNULAR SEGMENTS
WITHIN 1 km OF
RECEPTOR
62
RECEPTOR
POINT
Figure 6-27. Area segment scheme for spatial portioning of emissions.
-------
predicts CO concentrations In the vicinity of an Intersection by
combining a traffic model, a modal emissions model*, and a line source
dispersion model. The line source model 1s based on an Integrated point
source technique.
Field experiments were performed 1n downtown St. Louis 1n 1971 to
89
evaluate the performance of the APRAC-1A model. Carbon monoxide
concentrations were calculated at four locations within street canyons,
and two at roof level. These calculations were compared to about 600
hour-average observations for each location. The observed concentrations
3
of CO were simulated with root-mean-square errors of 3.5 to 4.6 mg/m
(3 to 4 ppm). Median and 90-percentile concentrations were specified
3 89
within 2:3 to 3.5 mg/m (2 to 3 ppm).
The most widely used line source dispersion models are based on the
89
Gaussian plume equations, namely HIWAY --developed and distributed by
~29 84
the Environmental Protection Agency—and CALINE-2 * —developed by the
California Department of Transportation and distributed by the Federal
Highway Administration. The HIWAY model uses an Integrated Gaussian
point source equation to calculate CO concentrations near a highway line
source. The model approximates a Vine source by a finite number of
point sources of emission strength equal to the total line source
emission strength divided by the number of sources used to simulate the
Hne. CALINE-2 uses an Integrated Gaussian point source equation for
the "pure" parallel wind case (I.e., 0° with respect to the highway) and
97
*-Kunselman et al. have developed a model which can be used to
describe air pollution emissions from automobiles as a function of
operating mode (I.e., steady-state, acceleration, and deceleration).
6-65
-------
a Gaussian line source equation for the "pure" crosswlnd case (I.e., 90°
with respect to the highway). For those wind directions which are
neither 0 nor 90 with respect to the highway, the model uses a
trigonometric function to weight the parallel and crosswind terms.
These line source models provide detailed spatial resolution between
0 and 300 meters from the highway.
In addition to the mathematical differences between the two models,
HIWAY uses a virtual source correction providing an initial dispersion
height of 1.5 meters while CALINE-2 assumes initial dispersion from a
theoretical mechanical "mixing cell" at a height of 4 meters. The HIWAY
model also uses dispersion coefficients that differ from the coefficients
used by the CALINE-2 model.
A comparison of HIWAY and CALINE-2 model predictions is presented
in Figures 6-28 and 6-29 for crosswind and parallel wind predictions,
47
respectively. Based on these model predictions, ambient concentrations
near highways tend to be greatest at the roadside edge, decreasing with
distance from the highway: typically, concentrations 300 meters from
the highway may be only 20 percent of roadside edge concentrations.
47
Noll et al. ^flnd, from a comparison of predicted and measured concen-
trations, that HIWAY and CALINE-2 overestimate concentrations for
parallel wind conditions and underestimate concentrations for oblique
47
and crosswind conditions. Noll et al. report typical correlation
coefficients for the models ranging from 0.5 to 0.85. Higher correla-
tions have been reported but for small sample sizes (i.e., less than 20).
6-66
-------
O 0.2
LLI
O
O
O
I
2!
O
01
N L
cc ;
O',
O
EPA HI WAY
CALINE 2
0.02 -
0.01
100
150
200
250
300
X, NORMAL DISTANCE FROM ROAD EDGE, meters
Figure 6-28. Normalized concentrations versus normal distance from the
road edge for perpendicular wind conditions for B and E atmospheric
stability category.
6-67
-------
4.0
3.0
2.0
EPA HIWAY
g
*t
DNCENTR>
U
1-
z
D
i
•wJ
_J
O
O.
O
UJ :
N ;
1 i
NORMAI
O '
3
U
1.0 '^
0.8
0.6
0.5
0.4
A
R*
0.3 h\- \\
P\ E\\
0.2
0.1
0.08
0.06
0.05
0.04
0.03
0.02
0/*1
H v
M V
\\ \\
\\ \
"V \
:\\
XNk\
x\A
Xjs\
>\
\ ^..
\ v\
i i \ i\
0 50 100 150
r
200 250
|r
X, NORMAL DISTANCE FROM ROAD EDGE, meters
Figure 6-29. Normalized concentration versus normal
distance to the road edge for parallel wind conditions
for B and E atmospheric stability category.
6-68
-------
Other line source modeling techniques Include the numerical modeling
approach and turbulent wake theory approach. Numerical models include
52 12 56 40
those proposed by Ragland, Danard, Sklarew, and Maldonado.
14
Turbulent wake theory models Include those proposed by Fay. Some
other Gaussian and pseudo-Gaussian models have been developed and tested
9
for use on highways by General Motors and by the Virginia Highway and
Transportation Research Council.
6-69
-------
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23. Harke, H. P., A. Baars, B. Frahm, H. Peters, and C. Schultz. Passive
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24. Harke, H. P. The problem of passive smoking. I. The influence of
smoking on the CO concentration in office rooms. Int. Arch. Arbeitsmed.
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25. Harke, H. P. The problem of passive smoking: Particulate matter from
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October 1974.
26. Harke, H. P., and H. Peters. The problem of passive smoking. III. The
influence of smoking on the CO concentrations in driving automobiles.
Int. Arch. Arbeitsmed. 33:221-229, 1974.
27. Harke, H. P., W. Liedl, and D. Denker. The problem of passive smoking.
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28. Hoegg, U. R. Cigarette smoke in closed spaces. Environ. Health Perspect.
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30. Kleiner, B. C., and J. D. Spengler. Carbon monoxide exposure of Boston
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31. Kunselman, P., H. T. Adams, C. J. Domke, and M. E. Williams. Automobile
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32. Larsen, R. I. A new mathematical model of air pollutant concentration
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33. Larsen, R. I. A Mathematical Model for Relating Air Quality Measurements
to Air Quality Standards. AP-89, U.S. Environmental Protection Agency,
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35. Loke, J., W. C. Farmer, R. A. Matthay, J. A. Virgulto, and A. Bouhuys.
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37. Ludwig, F. L., P. B. Simon, R. C. Sandys, J. C. Bobick, L. R. Seiders,
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39. Mancuso, R. L., and F. L. Ludwig. User's Manual for the APRAC-1A Urban
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40. Maldonado, C., and J. A. Bullin. Modeling carbon monoxide dispersion
from roadways. Environ. Sci. Technol. 11:1071-1076, 1977.
41. Bureau of Air Quality and Noise Control. Maryland State Yearly Air
Quality Data Report 1976 Revised. BAQNC-DR-77-06, State of Maryland,
Department of Health and Mental Hygiene, Baltimore, MD, September 1978.
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200 E. Road Street, Baltimore, Maryland, February-December 1977.
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43. McMullen, T. B. Interpreting the eight-hour National Ambient Air Quality
Standard for carbon monoxide. J. Air Pollut. Control Assoc. 25:1009-1014,
1975. ~~
44. Miller, T. L., and K. E. Noll. Measured versus predicted air quality
near highways. J. Environ. Eng. Div. Am. Soc. Civ. Eng. 102:627-643,
< 1976.
45. Miranda, J. M., V. J. Konopinski, and R. I. Larsen. Carbon monoxide
control in a high highway tunnel. Arch. Environ. Health 15:16-25, 1967.
46. Noll, K. E., and T. L. Miller. Highway Air Quality. Volume 1. Design
of Air Monitoring Surveys. Implementation Package No. 75-1, U.S. Department
of Transportation, Federal Highway Administration, Washington, DC, March
1975.
47. Noll, K. E., T. L. Miller, and M. Claggett. A comparison of three highway
line source dispersion models. Atmos. Environ. 12:1323-1329, 1978.
48. Ott, W. R. Development of criteria for siting air monitoring stations.
J. Air Pollut. Control Assoc. 27:543-547, 1977.
49. Patterson, R. M., R. M. Bradway, G. A. Gordon, R. G. Orner, R. W. Cass,
and F. A. Record. Validation Study of an Approach for Evaluating the
Impact of a Shopping Center on Ambient Carbon Monoxide Concentrations.
EPA-450/3-74-059, U.S. Environmental Protection Agency, Research Triangle
Park, NC, August 1974.
50. Pollack, R. I. Studies of Pollutant Concentration Frequency Distributions.
EPA-650/4-75-004, U.S. Environmental Protection Agency, Research Triangle
Park, NC, January 1975.
51. Radford, E. P., and M. S. Levine. Occupational exposure to carbon monoxide
in Baltimore firefighters. J. Occup. Med. 18:628-632, 1976.
52. Ragland, K. W., and J. J. Peirce. Boundary layer model for air pollutant
concentrations due to highway traffic. J. Air Pollut. Control Assoc.
25:48-51, 1975.
53. Rench, J. D., and E. P. Savage. Carbon monoxide in the home environment.
A study. J. Environ. Health 39:104-106, 1976.
54. Rodgers, S. J. Analysis of Noncoal Mine Atmospheres: Toxic Fumes from
Explosives. Bureau of Mines Open File Report 10-77, U.S. Department of
the Interior, Bureau of Mines, Washington, DC, May 1976.
55. Schaplowsky, A. F., F. B. Oglesbay, J. H. Morrison, R. E. Gallagher, and
W. Berman, Jr. Carbon monoxide contamination of the living environment.
A national survey of home air and children's blood. J. Environ. Health
36:569-573, 1974.
6-73
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56. Sklarew, R. C., A. J. Fabrick, and J. E. Prager. A Particle-In-Cell
Method for Numerical Solutions of the Atmospheric Diffusion Equation, and
Applications to Air Pollution Problems. Volume 1. APTD-0952, U.S.
Environmental Protection Agency, Research Triangle Park, NC, November
1971.
57. Lunche, R. G., A. Davidson, J. E. Dickinson, and M. F. Brunei!. Air
Quality Trends in Los Angeles County. Southern California Air Pollution
Control District, Los Angeles, CA, December 1975.
58. Southern California Air Pollution Control District. Carbon monoxide
data: Station 076, Los Angeles, California, January-December 1977.
59. Sterling, T. D., and D. M. Kobayashi. Exposure to pollutants in enclosed
"living spaces." Environ. Res. 13:1-35, 1977.
60. Stanford Research Institute. User's Manual for the APRAC-2 Emissions and
Diffusion Model. Menlo Park, CA, June 1977. Dup of 37.
^
61. Srch, M. The significance of carbon monoxide in cigarette smoke in
passenger car interiors. Dtsch. Z. Gesamte Gerichtl. Med. §0:80-89,
1967.
62. Enviro-Measure. Air Quality Analysis of the FA Route 101 Corridor
Transportation Plan, Memphis, Tennessee. Enviro-Measure, Inc., Knoxville,
TN, January 1978.
63. Tiao, G. C., G. E. P. Box, and W. J. Hamming. A statistical analysis of
the Los Angeles ambient carbon monoxide data 1955-1972. J. Air Pollut.
Control Assoc. 25:1129-1136, 1975.
64. Office of Air Quality Planning and Standards. Air Quality Data - 1968
Annual Statistics. EPA-450/2-76-017, U.S. Environmental Protection
Agency, Research Triangle Park, NC, October 1976.
64a. Office of Air Quality Planning and Standards. Air Quality Data - 1969
Annual Statistics. EPA-450/2-76-018, U.S. Environmental Protection
Agency, Research Triangle Park, NC, October 1976.
64b. Office Air Quality Planning and Standards. Air Quality Data - 1970
Annual Statistics. EPA-450/2-76-019, U.S. Environmental Protection
Agency, Research Triangle Park, NC, October 1976.
64c. Office of Air Quality Planning and Standards. Air Quality Data - 1971
Annual Statistics. EPA-450/2-76-020, U.S. Environmental Protection
Agency, Research Triangle Park, NC, October 1976.
64d. Office of Air Quality Planning and Standards. Air Data - 1972 Annual
Statistics. EPA-450/2-74-001, U.S. Environmental Protection Agency,
Research Triangle Park, NC, March 1974.
64e. Office of Air Quality Planning and Standards. Air Quality Data - 1973
Annual Statistics. EPA-450/2-74-015, U.S. Environmental Protection
Agency, Research Triangle Park, NC, November 1974.
6-74
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64f. Office of Air Quality Planning and Standards. Air Quality Data - 1974
Annual Statistics. EPA-450/2-76-011. U.S. Environmental Protection
Agency, Research Triangle Park, NC, August 1976.
64g. Office of Air Quality Planning and Standards. Air Quality Data - 1975
Annual Statistics Including Summaries with Reference to Standards.
EPA-450/2-77-002, U.S. Environmental Protection Agency, Research Triangle,
Park, NC, May 1977.
65. Office of Air Programs. Guidelines: Air Quality Surveillance Networks,
AP-98, U.S. Environmental Protection Agency, Research Triangle Park, NC,
May 1971.
66. Office of Air Programs. User's Manual: SAROAD (Storage and Retrieval of
Aerometric Data). APTD-0663, U.S. Environmental Protection Agency,
Research Triangle Park, NC, July 1971.
67. Office of Air Quality Planning and Standards. The National Air Monitoring
Program: Air Quality and Emissions Trends Annual Report. Volume I.
EPA-450/l-73-Q01-a, U.S. Environmental Protection Agency, Research Triangle
Park, NC, August 1973.
68. Office of Air Quality Planning and Standards. Monitoring and Air Quality
Trends, 1972. EPA-450/1-73-004, U.S. Environmental Protection Agency,
Research Triangle Park, NC, December 1973.
69. Office of Air Quality Planning and Standards. Guidelines for Air Quality
Maintenance Planning and Analysis. Volume 12: Applying Atmospheric
Simulation Models to Air Quality Maintenance Areas. EPA-450/4-74-013,
U.S. Environmental Protection Agency, Research Triangle Park, NC, September
1974.
70. Office of Air Quality Plannig and Standards. Monitoring and Air Quality
Trends Report, 1973. EPA-450/1-74-007, U.S. Environmental Protection
Agency, Research Triangle Park, NC, October 1974.
71. Zimmerman, J. R., and R. S. Thompson. User's Guide for HIWAY, a Highway
Air Pollution Model. EPA-650/4-74-008, U.S. Environmental Protection
Agency, Research Triangle Park, NC, February 1975.
72. Ludwig, F. L., and J. H. S. Kealoha. Selecting Sites for Carbon Monoxide
Monitoring. EPA-450/3-75-077: U.S. Environmental Protection Agency,
Research Triangle Park, NC, September 1975.
73. Office of Air Quality Planning and Standards. AEROS Manual Series Volume
II: AEROS User's Manual. EPA-450/2-76/029. U.S. Environmental Protection
Agency, Research Triangle Park, NC, December 1976.
74. Office of Air Quality Planning and Standards. Monitoring and Air Quality
Trends Report, 1974. EPA-450/1-76-001, U.S. Environmental Protection
Agency, Research Triangle Park, NC, February 1976.
75. Report of the Air Monitoring Siting Workshop, Las Vegas, NV. July 12-16,
1976.
6-75
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76. Office of Air Quality Planning and Standards. National Air Quality and
Emissions Trends Report, 1975. EPA-450/1-76-002, U.S. Environmental
Protection Agency, Research Triangle Park, NC, November 1976.
77. U.S. Environmental Protection Agency. Air Quality Data - 1975 Annual
Statistics. EPA-450/2-77-002, Office of Air and Waste Management, Office
of Air Quality Planning and Standards, Research Triangle Park, NC, May
1977.
78. Geomet Incorporated. The Status of Indoor Air Pollution Research 1976.
Final Report. EPA-600/4-77-029, U.S. Environmental Protection Agency,
Research Triangle Park, NC, May 1977.
79. Office of Air Quality Planning and Standards. National Air Quality and
Emissions Trends Report, 1976. EPA-450/1-77-002, U.S. Environmental
Protection Agency, Research Triangle Park, NC, December 1977.
80a. U.S. Environmental Protection Agency. Air Quality surveillance and data
reporting. Proposed regulatory revisions. Fed. Regist. 43:34892-34934,
August 7, 1978.
80b. Office of Air Quality Planning and Standards. National Air Quality and
Emission Trends Report, 1977. EPA-450/2-78-52, U.S. Environmental Protection
Agency, Research Triangle Park, NC, December 1978.
81. U.S. Federal Highway Administration. A User's Manual for the CALINE-2
Computer Program, Interim Report. FHWA-RD-76-134, August 1976. Duplicate
of-29
82. U.S. Federal Highway Administration. Special Area Analysis Pollution
Model (SAPOLLUT) Urban Planning Division, % Hourly ADT Default Values.
83. Virtamo, M., and A. Tossavainen. Carbon monoxide in foundry air. Scand.
J. Work Environ. Health Suppl. (1):37-41, 1976.
84. Ward, C. E. Air Quality Manual Modification. Environmental Improvement
Branch, Transportation Laboratory of CALTRANS, March 1975.
85. Wright, G. R., S. Jewczyk, J. Ontro, P. Tomlinson, and R. J. Shephard.
Carbon monoxide in the urban atmosphere. Hazards to the pedestrian and
street worker. Arch. Environ. Health 30:123-129, 1975.
86. Xintaras, C., B. L. Johnson, and I. de Groot, eds. Behavioral Toxicology.
Early Detection of Occupational Hazards. Preceedings of a Workshop,
National Institute for Occupational Safety and Health and University of
Cincinnati, Cincinnati, Ohio, June 24-29, 1973. HEW Publication No.
(NIOSH) 74-126, U.S. Department of Health, Education, and Welfare, National
Institute for Occupational Safety and Health, Cincinnati, OH, 1974.
87. Yocum, J. E., W. L. Clink, and W. L. Cote. Indoor/outdoor air quality
relationships. J. Air Pollut. Control Assoc. 21:251-259, 1971.
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88.
89.
. I. Larsen. Calculating air quality and its control
ol Assoc. 15:565-572, 1965.
Zimmer, C. E., and R. I. Larsen. Calculating
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90.
Zimmerman, J. R., and R. S. Thompson. User's Guide for HIWAY, A Highway
Air Pollution Model. EPA-650/4-74-008, U.S. Environmental Protection
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Office of Air Quality Planning and Standards. Guidelines for the Interpretation
of Air Quality Standards. OAQDS No. 1.2-008, U.S. Environmental Protection
Agency, Research Triangle Park, NC, February 1977.
6-77
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7. THE GLOBAL CYCLE OF CARBON MONOXIDE
Although many studies in the last decade have been devoted to the
identification and quantification of the various sources and sinks of
carbon monoxide (CO) in the global atmospheric equation, a wide range of
uncertainty still exists about the magnitude of many of the terms which
compose the global CO budget. The fundamental question centers around
the natural vs. anthropogenic origins of CO in the atmosphere. Research
efforts in the late 1970's suggest that human activities have signifi-
i
cantly altered the background concentration of CO, especially in the
Northern Hemisphere. The effects of such an alteration are complex, but
6 12
most recent theories ' speculate that the increase in CO background
concentrations will have an important impact on the tropospheric and
stratospheric ozone distributions, as well as having an influence on the
global budgets of several other trace gases.
7.1 INTRODUCTION
Prior to 1970, the general picture of the sources of CO was quite
simple and the sources were thought to be well understood. For the most
part, CO was thought to be produced by incomplete combustion of
carbonaceous matter; any other source was thought to be small compared
to production through combustion. However, a new era of speculation
7-1
-------
23
evolved when Levy proposed that the hydroxyl (OH) radical was present
in the unpolluted troposphere in concentrations greater than 10
3
molecules/cm . With this OH number density, the observed clean air
concentration of methane, and the measured rate constant governing the
(CH4 + OH) reaction,14 it could be shown that a substantial quantity of
CO is generated in the clean atmosphere if the methane oxidized by OH is
converted to CO. According to this scheme, the initial estimates of the
methane oxidation source of CO were 10 to 25 times larger than the
estimated combustion source. * Thus, a new philosophy of atmospheric
chemistry that included photochemical processes in the unpolluted
troposphere (OH can be generated only through a photochemical sequence)
developed in the 1970's.
More recent photochemical calculations indicate that methane oxida-
tion probably is not as large a source of CO as indicated by those first
studies. Because of the uncertainties inherent in numerical models of
photochemical processes and because relatively few measurements must be
extrapolated to derive other global source terms for CO, no definite
conclusion can be drawn as to the dominant source of CO in the atmosphere.
A more detailed discussion of CO sources in the following sections will
review many of the previous studies.
7.2 GLOBAL SOURCES
7.2.1 Technological Sources
17 32
The early inventories ' of CO emissions focused on combustion
sources since no significant natural source of any other type had been
positively identified. Estimates of global emissions of CO from fossil
7-2
-------
32 34
fuel combustion differ by more than a factor of two. ' To derive the
values, emissions from technological sources were computed by assessing
the amount of coal and petroleum fuels produced in a given year and then
18
multiplying that figure by previously determined conversion factors.
The emission rates calculated by this method were 2.6 x 10 g/yr by
32
Robinson and Robbins, who used fossil fuel usage data from 1966, and
3.6 x 1014 g/yr by Jaffe,18 who utilized 1970 data. In general, these
investigators concluded that the automobile was the largest technological
source of CO and that emissions increased substantially between the
3
onset of widespread use of the auto and 1970. The study of Robinson
and Robbins showed that mobile sources were responsible for 68 percent
of the CO emissions; Jaffe's estimate was 70 percent.
34
Seiler has presented the most detailed study to date on the
global cycle of atmospheric CO. He contends in his analysis that the
previously estimated CO emission rates are lower limits. He cites the
fact that the home heating source of CO in West Germany was shown to be
30 percent of the automobile source, whereas Jaffe1s calculations used a
relative home heating contribution of less than 1 percent. Furthermore,
Seiler contends that several industrial sources, such as ammonia and
methanol reforming facilities, synthetic gas and organic chemical manu-
facturing plants, and other possible emitters of CO were not considered
34
in previous inventories. Thus, Seiler1s calculation of technological
"i /i
CO emissions is 6.4 x 10 g/yr, about two times greater than Jaffe's
estimate. Subsequently, aircraft data obtained over Munich and extrapo-
lated for the globe suggest a total technological source ranging from
6 x 1014 to 10 x 1014 g/yr.44
7-3
-------
In addition to direct emission of CO, the oxidation of nonmethane
hydrocarbons given off by automobiles may be considered an indirect
technological source of CO. Although no quantitative estimates of this
potential source have been published, it is possible that if most of the
52 53
carbon contained within the hydrocarbons emitted in an urban area '
were converted to CO, it would account for a source strength equal to
nearly half of the direct CO emissions. The mole-to-mole conversion
rate of certain hydrocarbons found in automobile exhaust to CO has been
observed to exceed 0.4 in smog chamber studies. Although the magnitude
\
of this source has never been computed in detail, it may be equivalent to a
sizable fraction of the amount of CO released directly to the atmosphere
in automobile exhaust.
7.2.2 Natural Sources
7.2.2.1 Forest Fires and Agricultural Burning—Because combustion
processes then appeared to be the only mechanism by which CO was produced,
32
the early emission inventory studies of Robinson and Robbins and
18
Jaffe assumed that natural releases of CO, if they occurred, likewise
originated from combustion of carbonaceous matter. To date, however,
forest fires and agricultural burning have not been shown to be signifi-
cant sources of atmospheric CO. The estimated CO emissions from these
natural sources range from 0.1 x 10 g/yr to 1.5 x 10 g/yr.
7.2.2.2 Carbon Monoxide Production from Oceans—Analyses of ocean ,
?ft 41 4? 4.8 4Q Rfi
water '^•i»'^°>H' often indicate supersaturated quantities
of CO. The highest supersaturation factors were found in nutrient-
rich waters and are believed to be a result of microbiological
7-4
-------
activity. Thus, the ocean acts as a source of atmospheric CO; its
14
strength has been estimated to lie between 0.2 x 10 g/yr and 2.0 x
1014 g/yr.27'42'50
7.2.2.3 Oxidation of Natural Hydrocarbons—Carbon monoxide is produced
by photochemical oxidation of naturally occurring hydrocarbons and
chlorophyll. Went pointed out that the apparent lifetime of terpene-
like hydrocarbons in the atmosphere does not appear to be very long.
Concentrations of these compounds range between 2 and 20 ppb (parts per
31 57
billion), from which Went estimated a global emission rate of 10 x
14 32
10 g/yr for such volatile organic compounds. Robinson and Robbins
14
estimated from these data that 0.6 x 10 g/yr of CO could be produced.
Their calculation is based on the assumptions that one molecule of CO is
21
produced from three molecules of organic matter and that the average
organic molecular weight is 150.
More recent studies, however, suggest that oxidation of naturally
emitted hydrocarbons from vegetation results in a global CO source
ranging from 4 x 1014 to 13 x 1014 g/yr.36'62 Derivation of the CO
source strength from this process requires the inclusion of many
assumptions, and, therefore, it is fair to say that the amount of CO
produced from naturally emitted hydrocarbons is not definitely known.
Many more laboratory and field studies are still required to reduce the
uncertainty about the strength of this source.
59
7.2.2.4 Emission by P1ants--Wi1ks reported that green plants grown
in a clean illuminated environment liberate small quantities of CO as
45
well as certain aldehydes. Although Siegel et al. showed that CO
7-5
-------
was given off by plant material in the dark, it could not be ascertained
whether the CO was emitted directly or was formed as a result of
photolysis of the aldehydes. Further investigation of these phenomena
by Seiler et al. showed that plants contribute 0.7 x 10 g/yr to
global CO concentrations. This estimate is obtained from ij} situ meas-
urements observed from four different C~-type plants and was found to
increase as the radiation intensity increased.
23
7.2.2.5 Methane Oxidation- -When Levy proposed that sufficient concen-
tration of the OH radical could exist in the troposphere to produce
quantities of formaldehyde (CHLO) on the order of 2 ppb (v/v) from
methane oxidation, it was easy to show that significant quantities of CO
could be formed through CHJ3 degradation. Every known important homo-
geneous process that removed CH«0 from the troposphere results in direct
formation of CO:
CH20 + hv -» CO + H2,
or CH20 + hv -» H + HCO,
and CH20 + OH -» H20 + HCO,
rapidly followed by HCO + 02 -» CO + H02.
5 61
The oxidation of methane (CH-) in the troposphere may proceed as follows: '
+ OH ->
+ 02 + M -> CH302 + M,
02 + NO -» CH30 + N02,
and CH30 + 02 -> CH£0 + H02.
Once OH attacks a methane molecule, the subsequent reactions proceed
very fast, and thus the limiting factor in the production of CO is the
7-6
-------
initial rate of the (CH4 + OH) reaction. The net result of the above
demands that the amount of methane oxidized in the troposphere is the
same molar quantity as the CO produced from this process.
Table 7-1 summarizes many of the studies which have been conducted
to determine the various source strengths of atmospheric CO. Of primary
importance is the fact that the first estimates of CO production from
24 29 52 61
methane oxidation ' > ' showed that this source was five to 20 times
32
larger than the anthropogenic sources estimated by Robinson and Robbins,
whose study was the only comprehensive CO source inventory available at
the time of the initial methane oxidation calculations. In all the
photochemical studies cited above, globally and diurnally averaged OH
go go
radical number densities ranged between 1 x 10 /cm and 3 x 10 /cm .
Similar calculations were made later by Weinstock and Chang and Wofsy.
However, those studies employed several key reaction rate constants
which were subsequently shown to be quite inaccurate. In particular,
the reaction rate governing the OH radical's attack on CO (which was
4
discussed in detail in Section 3.3) was reported in later studies to be
pressure dependent and to be more than twice as fast at tropospheric
pressures as the rates measured prior to 1976. Since this reaction
dominates all others in determining the destruction frequency of OH in
the troposphere, a factor-of-two increase in its rate results (to a
first approximation) in a factor-of-two decrease in the average amount
of OH calculated by earlier numerical models.
6 11
Crutzen and Fishman and Fishman and Crutzen have presented
numerical analyses which incorporate the more recent chemical kinetic
7-7
-------
TABLE 7-1. GLOBAL CARBON MONOXIDE SOURCE STRENGTH ESTIMATES
Fossil Forest Methane Oxidation of
Reference Fuel Fires Oxidation Hydrocarbons Oceans Plants
Seller, 197434 6.4 0.6a 0.6 1.0
Robinson & Robbins,
1969^ 1p 2.5 0.1 0.6
Jaffe, 1973i^(. 3.2 0.4
Seiler, 1976 4 0.4 0.2-2.0
SeilerA Zankl,
1976^ 6-10
McConnell et al.,
.y 27
Weinstpck & Niki ,
54 50
Wofsy et al., 1972 15
Levy, 1973^ 33
Weinstpck & Chang, .
DD 38
Wofsy, 1976"" 14
Crutzep & Fishman, .
1977b 0.6-4.0°
Fishman,& Crutzen, ,
197831-1 2.9-7.4°
Zimmerman et al. ,
1978 4-13
Stevensfiet al. ,
19724b n 2.0-5.0C
NAS, 1977*™ 0.5
Swinnerton et al. ,
1970"
Linnenbom et al . ,
1973
Liss &9Slater,
1974^
Seiler.& Schmidt,
1974
Seiler^ Giehl,
1977 J/
Seiler,.gt al . ,
1978
Range of
Estimates 2.5-10 0.1-0.6 0.6-50 0.5-13
0.2
2.0
0.4
0.7
0.2-2.0
0.5
0.5-1.0
0.2-2.0
Units are 10 g/yr
^Includes agricultural burning
Global values derived by doubling Northern Hemisphere values reported in
these studies.
cNorthern Hemisphere estimate.
7-8
-------
data. In their reports some of the uncertainties inherent in the deter-
mination of the rates of photochemical production and destruction of CO
and other trace gases are discussed. In the 1977 paper, Crutzen and
Fishman point out that the methane oxidation reaction sequence may be
broken and no CO produced from it if peroxides are formed and then
removed from the atmosphere by a rapid heterogeneous process. Under
14 14
such an assumption, as little as 0.6 x 10 to 4-0 x 10 g/yr of CO
35
would be produced as a result of methane oxidation. Similarly, Seiler
14
calculated a value of 4 x 10 g/yr for methane oxidation. Anthropogenic
O /I O C. O C.
CO source strengths calculated by Seiler ' ' are 2 to 5 times
18 32
higher than previous calculations by Jaffe and Robinson and Robbins.
Thus it now appears that methane oxidation is no longer believed the
dominant source of atmospheric CO as was the case in the early '70's.
47
7.2.2.6 Other Natural Sources—Swinnerton et al. report that very
high supersaturation values of CO have been found in both rainwater and
cloud droplets. Furthermore, rainwater samples in both unpolluted
(Hawaii) and polluted (Washington, D.C.) regions showed excessive amounts
of CO. The mechanism for this phenomenon is not well understood, but
two possible explanations are the dissociation of carbon dioxide by
electrical discharges and the photolysis of aldehydes dissolved in the
droplets. Quantification of this source on a global scale has been
34
attempted by Seiler, but too many uncertainties exist to produce a
number which is accurate to more than several orders of magnitude. This
is probably not a significant source of CO in the atmosphere.
7-9
-------
Other natural CO sources have been found, but to date none of them
is believed to contribute significantly to the global budget. Green
13
et al. showed that CO could be produced by charged-particle deposition
mechanisms and atmospheric discharge phenomena, including cloud corona
discharges, background radioactivity, natural electrostatic discharges,
photoelectrons in the ionosphere, auroral electrons and protons, cosmic
'rays, and solar wind. The decomposition of hemoglobin in animals also
34
results in CO production. A small amount of CO production by volcanoes
has been noted. Above 70 km, photodissociation of carbon dioxide (C02)
is a source of CO.
7.3 BACKGROUND LEVELS AND FATE OF CARBON MONOXIDE
7.3.1 Measured Background Levels of Carbon Monoxide
7.3.1.1 Geographic Distribution--A distinct latitudinal variation in
CO
background concentrations has been observed by both Wilkness et al.-,
34
in measurements over the Pacific Ocean, and Seiler, in measurements
over the Atlantic Ocean. Seiler1s values are shown in Figure 7-1 and
are averages based on- the integrated concentrations during 1969 obtained
between the surface and the tropopause. Integration of these data over
each hemisphere shows that more than twice as much CO is present in the
Northern Hemisphere than in the Southern Hemisphere. Robinson and
33
Robbins report average mixing ratios of 140 ppb for the Northern
Hemisphere and 60 ppb for the Southern Hemisphere, which have since been
reconfirmed by Seiler's later and more extensive work.
34
Seiler points out that the background mixing ratios in the
Southern Hemisphere remain very constant. The standard deviation of CO
7-10
-------
200
150
.o
a
a.
Z
o
g 100
z
o
o
50
ATLANTIC OCEAN (SEILER, 1974)
PACIFIC OCEAN (ROBINSON & BOBBINS, 1970)
\
\
90 80 70 60 50 40 30 20 10 E 10
SOUTH LATITUDE
20 30
40 50
NORTH
60 70 80 90
Figure 7-1. Latitude distribution of carbon monoxide. (Used with permission of Tellus 26:116-135.)
-------
concentrations in a region between 50 and 65° S and 30 and 80° W over a
three-month period was less than 3 percent, approximately equal to the
accuracy of the instrument being used. Carbon monoxide variations are
largest in the North Atlantic and are attributed to the passage of
continental plumes from North America. A relatively sharp difference in
mixing ratios was quite often observed within the Trade Wind inversion
layers on either side of the intertropical convergence zone in both the
Atlantic and the Pacific.34'58
The considerably higher average CO concentration in the Northern
Hemisphere, where 90 percent of the anthropogenic emission sources are
located, does not support the hypothesis that CH. oxidation is the
30
dominant source of CO as was proposed by the National Academy of Sciences.
18
Since CH. is evenly distributed throughout the world, the magnitude of
the CH. oxidation source of CO should be nearly equal in both hemispheres.
Furthermore, if the anthropogenic CO source is only 10 percent of the
30
natural source, such a small difference in the overall source strengths
in the two hemispheres should result in a much smaller interhemispheric
gradient. Although the inclusion of CH. oxidation as a source of CO is
necessary to develop a clear picture of the global CO budget, its
magnitude relative to other sources, on the basis of the current distri-
bution of CO, remains to be assessed.
40
7.3.1.2 Variation with Height—Seiler and Junge and Seiler and
43
Warneck showed that CO mixing ratios decreased sharply above the
tropopause. In their reports, mixing ratios of less than 40 ppb were
measured at an altitude less than 1 km above the tropopause, in contrast
7-12
-------
to values between 130 and 160 ppb measured just below the stratospheric
boundary in the northern midlatitudes. Thus, it appears that there is a
strong atmospheric sink for CO in the stratosphere; the nature of this
sink most likely is the reaction of CO with OH radicals. This belief is
supported by theoretical calculations, which show that OH concentra-
tions increase above the tropopause because of the much larger ozone
concentrations in the stratosphere. The larger ozone concentrations are
significant because OH radical production is initiated by ozone photolysis
03 + hv -> 0( D) + 02, A.O20 nm,
followed by O^D) + H20 -» 2 OH,
O^D) + CH4 -» OH + CH3,
or OC^-D) + H£ -» OH + H.
Within the troposphere, background-level CO profiles vary at dif-
ferent latitudes. Tropospheric profiles at low and middle latitudes of
both hemispheres are depicted in Figure 7-2. The CO concentrations in
the lower troposphere (below 3 km) reflect the strong latitude gradient
jf
depicted in Figure 7-1. The midlatitude profiles (45° N and 45° S)
fall off to typical stratospheric values at 12 km, since this height is
in the stratosphere at these latitudes. The vertical gradient in the
upper troposphere is much stronger in the Northern Hemisphere. The
average CO concentrations in the tropics at an altitude of 12 km are
higher than the midlatitude concentrations at a corresponding altitude
since the average height of the tropopause is greater than 12 km in the
tropics.
7-13
-------
I
o
HI
Q
D
12
11
10
9
8
7
6
5
4
2
1
i r
i i i r
40
80
120
160
45° N
\
200
240
CO MIXING RATIO, ppb
Figure 7-2. Latitudinal profiles of carbon monoxide.
7-14
-------
7.3.1.3 Diurnal and Seasonal Variation—During an ocean cruise to
measure background concentrations of trace constituents in the Pacific
20
in June 1970, Lamontagne et al. reported a consistent diurnal pattern
of CO concentrations both in sea water and in air samples taken just
above the ocean surface. Both sets of data show a maximum concentration
in the afternoon, when concentrations were typically 20-40 ppb higher
than the average concentration of 130 ppb. However, this finding is
inconsistent with our present knowledge of CO fluxes from the ocean into
the atmosphere. Thus, the diurnal amplitudes reported by Lamontagne et
20
al. would imply a global oceanic source strength considerably larger
than that given in Table 7-1. In agreement with the latter hypothesis,
failure to detect a significant diurnal cycle of CO concentration over
ocean surfaces has been reported. *
Using an instrument that monitored CO continuously over a nine-
month period in Hawaii (at Mauna Loa Observatory, elevation 3400 m),
39
Seller et al. detected an average diurnal cycle. A slightly higher
(less than 10 percent) average concentration was observed in the afternoon.
From these data, it appears that this diurnal cycle may be caused by
local sources in combination with local meteorological phenomena, such
as Upslope and downslope winds.
Data which show seasonal variation of CO concentrations are quite
scarce. Although Stevens et al. showed that the isotopic composition
of CO measured in rural Illinois exhibited a seasonal dependence, a
conclusive seasonal variation in the background CO concentrations could
not be established.
7-15
-------
Analysis of data collected by continuous monitoring during 1975 and
*3 f\
1976 at Mauna Loa Observatory in Hawaii (19.5° N) indicates that the
highest seasonal background CO concentrations exist in the spring (March
and April). The highest average values (120-130 ppb) are considerably
greater than those measured in late summer (70-80 ppb). A good explana-
tion of these observations is not readily available, although the
seasonal variation of tropospheric OH concentrations suggests that more
CO scavenging may take place in the summer. However, such an explanation
is speculative and other factors, including seasonal variation of large-
and small-scale meteorological parameters, must be examined to see how
they could influence the Hawaiian measurements.
In the Northern Hemisphere temperate mid-latitude belt, Dianov-
o
Klokov et al. have reported a similar seasonal variation in the total
amount of CO in the U. S. S. R. They also find maximum values in March
and April and minimum values between July and September.
7.3.2 Residence Time and Removal Mechanisms of Atmospheric CO
7.3.2.1 Carbon Monoxide Residence Time--To derive a budget of a trace
gas in the atmosphere, all possible sources and sinks of that species
are examined. If no increasing or decreasing trend is detected for the
concentrations of the gas, then it is assumed that the sum of the sources
equals the sum of the sinks. Under such conditions, a residence time
can be computed by dividing the measured quantity of the gas in the
atmosphere by either the total emission rate or the total destruction
rate.
7-16
-------
An estimate of the atmospheric residence time of CO by Robinson and
32
Robbins was computed by assuming an average atmospheric mixing ratio
14
of 0.1 ppm, which yields a CO mass in the atmosphere of 5.6 x 10 g.
Division of the calculated mass by their estimated source strength at
14 35
3.2 x 10 g/year results in a CO residence time of 1.8 years. Seiler
estimated a residence time of 0.3 year. By using the wide range of
published source strengths summarized in Table 7-1, a CO residence time
ranging from 0.07 to 1.38 years can be computed.
7.3.2.2 Removal Processes for Carbon Monoxide—The mechanisms by which
34
CO is removed from the atmosphere are summarized by Seiler and the
30
National Academy of Sciences; these studies concluded, after con-
sidering the possible CO sinks, that the major destruction term in the
CO budget is oxidation by the OH radical. More recent reaction rates
measured for the (CO + OH) reaction discussed in Section 3.3 indicate
that the magnitude of this sink is probably twice as large as the values
indicated in these two previous reviews if the globally averaged
concentration of OH is the same.
7.3.2.2.1 The Stratosphere as a Sink for Tropospheric CO. As previously
41 43
mentioned, CO mixing ratios decrease sharply above the tropopause. '
From the average concentrations measured on either side of the tropopause,
a theoretical calculation of the CO flux into the stratosphere can be
made if the atmospheric diffusion coefficients in the region are known.
34
Using this methodology, Seiler derived a tropospheric CO loss rate of
14
1.1 x 10 g/year by migration into the stratosphere. Because of the
large difference in the average CO concentrations above and below the
7-17
-------
14
tropopause in the Northern Hemisphere (see Figure 7-2), 0.9 x 10
14
g/year enter the stratosphere north of the equator while only 0.2 x 10
g/year migrate to the upper atmosphere in the Southern Hemisphere.
22
7.3.2.2.2 Soil as a Sink. Levy showed that nonsterile soil rapidly
depleted CO from test atmospheres containing initial concentrations of
100 ppm. The effect of this removal process was enhanced by increasing
the soil temperature but eliminated by sterilizing the soil. The latter
finding suggests that the biological activity of microorganisms in the
soil is responsible for CO removal.
15
Ingersoll et al. likewise found that soil was potentially a major
sink of CO, but their studies showed that the soil uptake rate reached a
maximum at 30°C and decreased at higher and lower temperatures. At 0°C
' o
the uptake rate was negligible, whereas at 50 C the uptake rate was less
than 10 percent of that at 30°C. Seiler indicated that at 50°C, CO
was given off from the soil rather than taken up by it.
22 15
The studies of Levy and Ingersoll et al. concluded that the
magnitude of the soil sink was considerably larger than the anthropo-
34
genie source of CO. However, Seiler points out that the soil uptake
rate is linearly dependent on the concentrations of CO in the atmosphere
directly above the surface, and thus both estimates are too high because
unrealistically high initial CO concentrations were used in the experiments,
Using an initial atmospheric concentration of 0.2 ppm over the continent,
14
Seiler estimated a global CO sink of 4.5 x 10 g/yr due to soil uptake.
26 37
Later studies ' over different types of soil supported the sink
34
strength estimated by Seiler.
7-18
-------
34
Such an estimate, however, is extremely crude because of vari-
ations observed in the CO equilibrium concentrations above the soil, in
the different types of soil, and in soil temperatures. For example,
Inman et al. point out that soils from different locations exhibit an
eight-fold variability in their ability to remove CO under the same
34
laboratory conditions. Seiler even speculates that some soils may act
as sources rather than sinks of CO. It is clear that more research is
needed to quantify the role of soil on the global CO cycle better.
7.3.2.2.3 Vegetation. The role of vegetation in the global CO cycle is
currently not well understood. Some researchers have suggested that
37 45 59
plants are a source of atmospheric CO; ' ' but others have indicated
19
that CO is absorbed by vegetation. For example, Krall and Tolbert
exposed barley leaves to an artificial atmosphere containing CO and
determined that some of it was converted to serine and other compounds.
2
Similarly, Bidwell and Fraser investigated the incorporation of carbon-
14 from an artificial CO atmosphere into plant carbon compounds. Seven
of nine plant species were observed to take up CO. Extrapolation of
these data indicates that plants are a significant sink for atmospheric
14 14
CO, absorbing as much as 7 x 10 to 70 x 10 g/yr.
37 38
More recently, Seiler and Giehl and Seiler et al. concluded
2
that the study of Bidwell and Fraser is not a true measure of the net
CO exchange rate between plants and the atmosphere. They point to the
fact that the Bidwell and Fraser experiment is useful only to detect the
amount of CO going into the plant and note that the large artificial CO
concentrations used in the laboratory environment precluded accurate
7-19
-------
measurement of any CO coming back into the atmosphere. On the other
hand, the method of Seiler and Giehl enables them to detect only the net
influence of plants on atmospheric CO; they cannot distinguish the
production from the uptake rates of the plants. Their findings indicate
14
that vegetation is a net source of about 0.5 x 10 gCO/yr when both
production and uptake processes are taken into account.
7.3.2.2.4 Reaction with Hydroxyl. Estimates of the amount of CO removed
from the atmosphere by reaction with OH indicate that this mechanism is
the primary removal process for atmospheric CO. » » » if the amount
of CO in the atmosphere is known, the global destruction rate as a
function of the OH distribution can easily be computed. Similarly, if
the distribution of CH. in the atmosphere is known, the amount of CO
produced by methane oxidation can be calculated as a dependent variable
of the average amount of OH present in the atmosphere.
Figure 7-3 shows graphically the results of such a simple calculation,
in which the following parameters are assumed: CH. and CO mixing ratios
9
of 1.4 ppm and 0.1 ppm, respectively;
-13 3
^CO+OH = 2.5 x 10 cm /(molecule* sec); and
kru +OH = 4'8 x 10~15cm3/(molecule*sec).
When the above values are used, the ratio of the rate of photochemical
destruction of CO, D(CO), to the rate of photochemical production of CO,
P(CO), is 3.7. This ratio is a lower limit, since it depends on the
assumption that every CH. molecule oxidized results in the production of
a CO molecule. Such a ratio demands that no more than 27 percent of the
CO produced in the atmosphere comes from CH. oxidation. Furthermore,
such a ratio is totally independent of the amount of OH in the atmosphere
7-20
-------
I
Ol
I-
U
co
Ul
O
z
g
o
Q
o
cc
Q.
o
o
CO DESTRUCTION FROM
REACTION WITH OH
CO PRODUCTION FROM METHANE
OXIDATION (UPPER LIMIT)
14
15
OH CONCENTRATION, 105/cm3
Figure 7-3. Carbon monoxide photochemical production and destruction rates as a function of average OH concentration.
-------
Although the D(CO)/P(CO) ratio is not affected by the average OH
concentration, the magnitude of each of these terms clearly is affected
(see Figure 7-3). Since about 90 percent of these terms is derived from
tropospheric photochemical activity, the average OH number density on
the abscissa refers to a tropospheric value. Although previous studies
derived information about the CO budget from calculated OH distributions, '
the simple analysis depicted by Figure 7-3 can provide some useful
35
insights into the global distribution of OH. For example, Seiler's
14
inventory of CO sources shows that 13.2 x 10 g/yr of CO are emitted to
the atmosphere. If it is assumed that the only CO sink is reaction with
5
OH, then an average OH concentration of 3.6 x 10 /cm will destroy CO at
14
a rate of 13.2 x 10 g/yr more than it can produce from methane oxidation.
7.3.2.2.5 Other Removal Processes. Carbon monoxide adsorption onto
25
atmospheric particulate matter has been reported by Liberti. His
analyses indicate that adsorption by dust which is subsequently deposited
on the earth's surface could be an important removal mechanism for
ambient CO. The magnitude of this possible sink is not known. Further
studies are necessary to determine the adsorption efficiency of different
aerosol materials for the varying concentrations of CO found in the
atmosphere.
7.4 SUMMARY
Although many studies in the last decade have been devoted to the
identification and quantification of the various sources and sinks of CO
in the atmosphere, it is clear from this review that a wide range of
uncertainty exists about the magnitude of many of the terms which compose
7-22
-------
the global CO budget. The fundamental question about the global cycle
of CO raised in the 1970' s centers around the natural vs. anthropogenic
origins of CO in the atmosphere. Resolving this issue is very important
if society is to determine whether or not emission controls are necessary
to decrease CO input into the atmosphere. If the CO production from the
natural oxidation of CH. greatly dominates all anthropogenic input
24 29 54
terms, as was suggested by studies in the early 1970' s,J> suppres-
sion of CO emissions should have little effect on the amount of CO in
the atmosphere. However, the reformulation of the CO budget, which
includes photochemical calculations utilizing more recent chemical
kinetic information, shows that ChL oxidation may not be the dominant
fi
source term for CO. ' The verification of these theoretical discus-
sions on photochemical production and destruction rates of CO awaits
more measurement of OH, NO, and N0« in the atmosphere. Until such data
are available, no authoritative conclusion can be drawn.
If, on the other hand, CO is produced primarily by processes which
are directly or indirectly controlled by man, it is important to consider
the consequences. The simple answer is to say that anthropogenic emis-
sions will raise the background concentrations of CO and that no sub-
stantial harm will come until these levels approach a concentration
which is dangerous to man's environment. However, there may be other
consequences of increased CO concentrations which are not so obvious.
For example, since CO is the predominant scavenger of OH in the
troposphere, increased global concentrations of CO will decrease the
tropospheric quantities of OH. In turn, lesser OH concentrations in the
7-23
-------
51
troposphere may allow greater quantities of trace gases such as CH-
and methyl chloroform to enter the stratosphere, since the primary
tropospheric removal mechanism for these gases is reaction with OH.
Thus, it is not impossible that increased CO emissions may have an
important impact on stratospheric photochemistry and the ozone layer.
The fate of CO in the atmosphere may also provide some insight into
12
the budget and distribution of ozone in the troposphere. Along with
CO, a considerable amount of tropospheric ozone may likewise be produced
5 10
from CH. oxidation. ' In addition, photochemical degradation of CO
may produce large quantities of ozone in the troposphere through the
sequence:
CO + OH -» C02 + H,
H + 02 + M -> H02 + M
H02 + NO -> N02 + OH
N02 + hv -» NO + 0
0+02+M +03+M
CO + 202 •* C02 + 03 (net).
12
Fishman and Crutzen speculate, on the basis of the present knowledge
of tropospheric photochemistry, that the above mechanism may be the
largest source of ozone in the troposphere.
The importance of obtaining a better understanding of the global
cycle of CO should not be underestimated. A clearer picture of the
distribution of OH in the troposphere as well as a better understanding
7-24
-------
of the global budgets of methane, tropospheric ozone and other trace
gases will result from a more accurate description of the role of CO.
One hopes that this goal will be realized as more measurements of
ambient atmospheric trace constituents and better laboratory data
are made available.
7-25
-------
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cycle. |n: Environmental Blogeochemistry. Volume l--Carbon, Nitrogen,
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Symposium on Environmental Biochemistry, Canada Centre for Inland Waters,
Hamilton, Ontario, April 8-12, 1975. J. 0. Nriagu, ed., Ann Arbor Science
Publishers, Inc., Ann Arbor, MI, 1977. pp. 25-37.
45. Siegel, S. M., G. Renwick, and L. A. Rosen. Formation of carbon monoxide
during seed germination and seedling growth. Science 137:683-684, 1962.
46. Stevens, C. M., L. Krout, D. Walling, A. Venters, A. Engelkemeir, and
L. E. Ross. The Isotopic composition of atmospheric carbon monoxide.
Earth Planet. Sci. Lett. 16:147-165, 1972.
47. Swinnerton, J. W., R. A. Lamontagne, and V. J. Llnnenbom. Carbon monoxide
1n rainwater. Science 172:943-945, 1971.
48. Swinnerton, J. W., R. A. Lamontagne, and V. J. Linnenbom. Carbon monoxide
in the South Pacific Ocean. Tellus 26:136-142, 1974.
49. Swinnerton, J. W., V. J. Llnnenbom, and C. H. Cheek. Distribution of
methane and carbon monoxide between the atmosphere and natural waters.
Env. Sci. Tech. 3:836-838, 1969.
50. Swinnerton, J. W., V. J. Llnnenbom, and R. A. Lamontagne. The ocean: a
natural source of carbon monoxide. Science 167:984-986, 1970.
51. Sze, N. D. Anthropogenic CO emissions: Implications for the atmospheric
CO-OH-CH4 cycle. Science 195:673-675, 1977.
52. National Air Pollution Control Admi-nistrati on. Air Quality Criteria for
Carbon Monoxide. National Air Pollution Control Administration, Publication
No. AP-62, U.S. Department of Health, Education, and Welfare, Washington,
DC, March 1970.
53. Office of Air Quality Planning and Standards. 1973. National Emissions
Report. National Emissions Data System (NEDS) of the Aerometric and
Emissions Reporting System (AEROS). EPA-450/2-76-007, U.S. Environmental
Protection Agency, Research Triangle Park, NC, May 1976.
54. Weinstock, B., and H. Niki. Carbon monoxide balance in nature. Science
176:290-292, 1972.
55. Weinstock, B., and T. Y. Chang. The steady-state concentration of carbon
monoxide In the troposphere. ITK Environmental Biogeochemistry. Volume
1- Carbon, Nitrogen, Phosphorus, Sulfur and Selenium Cycles, Proceedings
of the 2nd International Symposium on Environmental Biochemistry, Canada
Centre for Inland Waters, Hamilton, Ontario, April 8-12, 1975. J. 0.
Nriagu, ed., Ann Arbor Science Publishers, Inc., Ann Arbor, MI, 1977.
pp. 39-49.
7-29
-------
56. Went, F. W. Organic matter in the atmosphere and its possible relation
to petroleum production. Proc. Nat!. Acad. Sci. U.S.A. 46:212-221, 1960.
57. Went, F. W. On the nature of Aitken condensation nuclei. Tell us 18:549-556,
1966.
58. Wilkness, P. E., R. A. Lamontagne, R. E. Larson, J. W. Swinnerton, and C.
R. Dickson, and T. Thompson. Atmospheric trace gases in the Southern
Hemisphere. Nature (London) Phys. Sci. 245:45-47, 1973.
59. Wilks, S. S. Carbon monoxide in green plants. Science 129:964-966, 1959.
60. Wofsy, S. C. Interactions of CH. and CO in the earth's atmosphere. Ann.
Rev. Earth Planet. Sci. 4:441-469, 1976.
61. Wofsy, S. C., J. C. McConnell, and M. B. McElroy. Atmospheric ChL, CO
and C00. J. Geophys. Res. 77:4477-4493, 1972.
C.
62. Zimmerman, P. R., R. B. Chatfield, J. Fishman, P. J. Crutzen, and P. L.
Hanst. Estimates on the production of CO and H« from the oxidation of
hydrocarbon emissions from vegetation. Geophys. Res. Lett. 5:679-682,
1978.
7-30
-------
8. EFFECTS OF CARBON MONOXIDE ON VEGETATION AND SOIL MICROORGANISMS
8.1 INTRODUCTION
Because of the potential toxicity of CO to living organisms, there
has been much concern over the large quantities (103 million metric tons
in 1977) of carbon monoxide (CO) released into the atmosphere from
anthropogenic sources. While much work has been done on the effects of
CO on man and animals, relatively little research has been done regarding
the influence of CO on plants. Man's health and well-being, however,
are fundamentally and inextricably bound to the success of the plants,
those organisms which transform the sun's radiant energy into the food
and oxygen necessary for habitation of the planet.
There are no known detrimental effects on green plants due to
carbon monoxide at the natural global background concentrations of CO,
3
0.01 to 0.23 mg/m (0.01 to 0.20 ppm). In urban areas, however, CO
concentrations may be much higher and are closely related to motor
traffic density. Carbon monoxide concentrations, therefore, exhibit
variation along well-marked diurnal patterns with peaks corresponding to
morning and evening "rush hours." High traffic density, when combined
with prolonged periods of air stagnation, has resulted in ambient CO
3
levels of over 34 mg/m (30 ppm) for an 8-hour period in Los Angeles and
8-1
-------
3 15
over 412 mg/m (360 ppm) in London. Even discovery of these relatively
high concentrations, however, has not motivated significant levels of
new research into the effects of CO on plants.
Early investigations into plant growth and development as affected
3 42 43
by CO were carried out at high concentrations (>11,450 mg/m or 10,000 ppm), '
and were directed at determining the manifestation of external symptoms
by treated plants. More current research to determine the effects of
CO, at both ambient and higher concentrations, on vegetation and soils
has been conducted in the following areas:
Effects of CO on plants
1. Visible symptom expression
2. Growth, yield, reproduction
3. Biochemical or physiological response
a. Photosynthesis
b. N«-Fixation
c. Other metabolic effects
4. Removal of CO from the environment
a. By plants
b. By soils
c. By soil micro-organisms
5. Production of CO by photosynthesis
8.2 EFFECTS OF CO ON PLANTS
8.2.1 Visible Symptoms
One of the earliest studies on the effect of CO on plants was
20
carried out by Knight and Crocker in 1913. Pea epicotyls were exposed
8-2
-------
to CO derived from potassium ferrocyanide, from oxalic acid, and from
o
sodium formate in concentrations of 6,000 to 24,000 mg/m (5,200 to
20,900 ppm). Reactions exhibited by the pea seedlings included a
pronounced swelling of the epicotyl accompanied by stem declination, as
much as 90 in some cases. Reactions were similar throughout the range
of concentration levels and no correlation between degree of effect and
CO origin was noted.
43
Zimmerman et al. in 1933 performed a series of experiments in
which they observed the reactions of plants exposed to CO. At CO concen-
3
trations of 572 to 572,000 mg/m (500 to 500,000 ppm), stem tissues of
several plant species exhibited initiation and profuse growth of adven-
titious roots; stimulated development of latent root primordia also
42
occurred. In a subsequent study, the same authors found that the
3
exposure of plants to 11,000 mg/m (9,600 ppm) CO for up to 23 days
also: (1) induced epinasty and hyponasty of leaves; (2) retarded stem
elongation; (3) produced smaller and/or deformed leaves; (4) induced
premature abscission of leaves, flowers, and fruits; and (5) produced
foliar lesions that were characterized by a yellowing of older leaves.
26
Premature leaf abscission was also reported by McMillan and Cope when
they exposed seedlings of several geographic variants of Acacia farnesiana
3
to 23,000 mg/m (20,000 ppm) CO for 24 hr. Varying degrees of leaf
abscission including complete defoliation occurred in the species
mentioned, while two other species of Acacia were not as severely
3
affected. Garden pea (Pisum sativum) seedlings exposed to 27 mg/m
c
(24 ppm) CO also exhibited increased abscission of older leaves.
8-3
-------
41
Wolf and Kidd found that the greening response of etiolated wheat
seedlings upon exposure to light was almost completely inhibited by
exposure to CO at levels that are described only as "high concentrations".
Carbon monoxide has found a commercial application in the produce
industry. Carbon monoxide, in combination with other gases, has been
used to prolong post-harvest storage and increase the appearance and
36
consumer acceptability of head lettuce. Stewart and Uota, working in
the Market Quality and Transportation Laboratory, USDA, held head lettuce
3 3
in an atmosphere of 34,000 mg/m (30,000 ppm) Op plus 17,000 mg/m
(15,000 ppm) CO for 7 days at 3.3°C. Each head was evaluated for
appearance disorders endemic to lettuce such as butt discoloration, pink
rib and rusty brown discoloration. In general, lettuce held in the
experimental atmosphere had a better overall appearance than lettuce
exposed to other gas mixtures. Butt discoloration and pink rib were
inhibited by exposure to the C0/0« combination, while rusty brown
discoloration was not affected in any way.
As stated previously, no visible effects have been identified in
3
plants exposed to CO at ambient 0.01 to 0.23 mg/m (0.01 to 0.20 ppm)
concentrations.
8.2.2 Growth, Yield, and Reproduction
Concentrations of CO at levels much higher than those found in the
ambient air have been shown to inhibit stem elongation in many species
42
of plants. Zimmerman et al. exposed a variety of plant species to CO
3 3
at concentrations of 115 mg/m to 11,500 mg/m (100 to 10,000 ppm) for
from 4 to 23 days. While practically no growth retardation was noted in
plants exposed at the lower level, stem growth was inhibited at the
8-4
-------
higher concentration by as much as 100 percent when compared with
controls. The effects varied considerably among the different species
of plants, tobacco being only slightly retarded while others were
affected greatly. Exposure to the higher concentration of CO also had a
significant effect on the formation and development of new leaves. In
many species, new leaves failed to grow as large as normal and had a
tendency to curl down at the edge.
Pea and bean seedlings also exhibited abnormal leaf formation after
3
exposure to CO at 27 mg/m (24 ppm) for several days. Pea seedlings
showed a decrease in the rate of development of new leaves while leaf
formation in bean seedlings was completely inhibited by the 18th day.
There was no effect noted on the relative rates of germination of peas
and beans exposed to the experimental atmosphere as compared with
controls; likewise there was no observable difference in the growth
rates of exposed plants as determined by increased stem length.
Several studies have demonstrated the influence of CO on sex
27
differentiation in plants. Minina and Tylkina exposed different
3 '
varieties of cucumber to CO at concentrations of 1145 mg/m to 11,450 mg/m*
(1000 to 10,000 ppm) for 50 to 200 hours. The results showed that
sexual differentiation was shifted markedly to the expression of female
characteristics under the influence of the gas. Thus, at the highest
;
level and with prolonged exposure, plants formed exclusively female
3
flowers. With exposure to CO concentrations of 3400 to 5700 mg/m
(3000 to 5000 ppni), female flowers developed first with the appearance
of a very few male flowers a week later. Plants treated at the lowest
8-5
-------
3
CO level (1145 mg/m ; 1000 ppm) proceeded with the development of male
flowers, as is normal for the species studied, and then shifted to
female expression at the sixth day. Controls developed males first, and
this continued throughout the course of the experiment.
Similar results were reported by Heslop-Harrison, who studied the
modification of sexual expression in Cannabis sativa by CO. Young
3
plants exposed briefly to CO at 11,450 mg/m (10,000 ppm) modified the
subsequent sexual expression of the dioecious male plants, inducing the
formation of intersexual or even functionally female flowers. The
effect was registered in flower primordia of a particular age; sex of
the older ones was already determined, and younger ones apparently
recover from treatment to develop normally. Basically, the effect of CO
in modifying sexual expression is similar to that induced by auxin
administration, and it is possible that at effective concentrations the
gas upsets auxin metabolism in treated tissues, perhaps by inhibiting
enzyme systems normally responsible for regulating endogenous auxin
levels. The gross effects of CO on plants are summarized in Table 8-1.
8.2.3 Biochemical and Physiological Processes
Biochemical and physiological responses in plants exposed to CO at
above ambient concentrations have been investigated in various species
and on different metabolic systems with conflicting results, especially
with respect to plant uptake and production of CO. The effects of CO
on photosynthesis and nitrogen fixation are discussed below.
8-6
-------
TABLE 8-1. EFFECTS OF CO ON PLANTS
Cone.
Duration
Effects
Author
5000
10,000 ppm
No evidence of swelling in
pea epicotyls.
Swelling of epicotyls
1-2 cm long; declination of
70-90°.
Knight & Crocker
20
20,000 ppm
0.05-50%
by volume
0.01-50%
by volume
0.3-1.0%
by volume
1.0%
by volume
1.5%
by volume
24 ppm
2-15 days
2-30 days
50-200 hrs,
24-48 hrs.
24 hours
unreported
Swelling of epicotyls
1-1.5 cm long; declination
of 80-90°.
Stimulated development of
root and subsequent root
generation. Some alteration
of normal geotropic growth pattern.
Zimmerman et al.
43
Epinasty, hyponasty,
retarded skin elongation,
abnormally small new leaf size,
general loss of sensitivity to
external stimuli, leaf abscission.
Sex differentiation was
shifted markedly towards
females.
Generation of female
flowers from male plants.
Leaf abscission, with
severity of effects being
dependent upon geographical
variant used.
Exposure of seeds to CO
had essentially no effect on
germination. Some reduction of
leaf formation when seedlings
were exposed was noted.
Zimmerman et al.
42
«^
a-PPM CO can be converted to mg/m CO by multiplying
the above concentrations by 1.145 (@STP).
27
Minina & Tylkina
Heslop-Harrison.,&
Heslop-Harrison
McMillan & Cope
26
Chakrabarti
.6
8-7
-------
8.2.3.1 Photosynthesis--There is evidence that CO can be assimilated by
4 3
plants. Bidwell and Fraser and Bidwell and Beebe found that many species
of plants can absorb and metabolize CO photosynthetically.
Bennett and Hill, however, in 1950, found that CO concentrations as
3
high as 91 mg/m (80 ppm) had essentially no effect on C02 uptake in
plants. Kortschak and Nickel! found that sugar cane leaves removed CO from
2 19
the atmosphere at a rate of 0.01 mg/m /hr.
8.2.3.2 Nitrogen Fixation—Carbon monoxide has been shown to affect
23
nitrogen fixation. Lind and Wilson demonstrated as early as 1941 that CO
inhibition of nitrogen fixation in red clover could usually be observed
3
when plants were exposed to 115 mg/m (100 ppm) CO and that complete
3
inhibition occurred at 573 to 1145 mg/m (500 to 1000 ppm). The authors
suggested that the inhibition might be due to carbon monoxide and molecular
nitrogen having the same molecular weight, the same number of valence
electrons and possessing many physical properties which are remarkably
similar. Due to these similarities, inhibition of the uptake of atmospheric
nitrogen by CO might be the result of the competitition of these two gases
for adsorption on the surface of the enzyme responsible for fixation. The
effect appeared to be readily reversible. The same authors also showed
3
that CO at 23 mg/m (20 ppm) inhibited nitrogen fixation by Azobacter
vinelandii, a free-living, nitrogen-fixing bacterium in culture. Table 8-2
summarizes the CO effects on nitrogen fixation.
2
Bergersen and Turner, in 1968, demonstrated that CO inhibition of
nitrogen fixation is both specific and competitive with respect to
nitrogenase activity. Also, there is an obligatory relationship between
8-8
-------
TABLE 8-2. CARBON MONOXIDE EFFECTS ON NITROGEN FIXATION BY MICRO-ORGANISMS
Cone. Duration Effects Author
23
.005-0.3% 3-34 days Inhibition of nitrogen fixation Lind & Wilson
beginning at 0.01% and almost
complete inhibition at 0.05-0.1%.
24
0.05-0.6% 35-45 hrs. Inhibition of nitrogen fixation Lind & Wilson
observed at 0.1-0.2% with almost
complete suppression at 0.5%-0.6%.
PCO of 30 min. 50% inhibition of CphU-reducing Pankhugst &
5+10 Pa activity in nitrogen fixing Sprent
nodules.
4*
a-PPM CO can be converted to mg/m CO by multiplying
the above concentrations by 1.145 (@STP).
8-9
-------
the occurrence of leghemoglobin, an oxygen binding hemeprotein occurring in
the nitrogen fixing root nodules of legumes, and the ability of the nodule
to fix nitrogen. Various workers have demonstrated the great affinity of
29 40 29
leghemoglobin for CO. * Pankhurst and Sprent have shown that this
affinity interferes with oxygen binding, thus limiting the amount of oxygen
that is available to the bacteroids (bacteria) in the interior of the
nodule and consequently limiting the nitrogen-fixing ability of the bacteria.
As further evidence, acetylene-reducing activity, which is used to estimate
the rate of nitrogen fixation, was found to be inhibited by CO in soy bean
nodules.
8.3 REMOVAL OF CO FROM THE ENVIRONMENT
There has been concern over the large amounts of CO that are being
released into the atmosphere by both anthropogenic and natural sources,
with many fearing that ambient global CO concentrations may someday increase
to levels detrimental to plants and animals. Large amounts of CO are
emitted annually to the atmosphere due to man's activities; however, as of
1973, ambient concentrations did not appear to have changed appreciably
over the previous 20 years. It is apparent, then, that something is
happening to CO soon after its liberation. The chemical and photochemical
reactions known to transform CO in the atmosphere were regarded as being
too slow to account for the disappearance of the quantity of CO in question.
Consequently, attention was turned to components of the biosphere as possible
utilizers of CO. The utilization of CO by plant life and soil microorganisms
is considered in the following sections.
8-10
-------
8.3.1 Plants
As previously mentioned, it has been demonstrated that CO can be
assimilated by plants. ' Bidwell and Fraser supplied CO to bean
3
leaves in light or darkness at 174 to 314 mg/m (150 to 270 ppm) in air.
In the presence of light, CO was absorbed and converted mainly to sucrose
14
and proteins. In darkness, CO was absorbed nearly as fast as in light
but was almost completely converted to C0« and released.
Carbon monoxide fixation by a number of species of plants, while
3
illuminated, was measured using 0.87 to 8.7 mg/m (0.75 to 7.5 ppm) in
2
air, with rates varying from 0 to 0.25 umole/dm /hr. Rates were roughly
proportional to CO concentration but were unrelated to rates of photosynthesis,
4
Bidwell and Fraser , using the bean leaf as an intermediate CO
3 2
absorber, at 1.7 mg/m (1.5 ppm) CO with an uptake rate of 0.06 |jmole/dm /hr,
and assuming a leaf area index (area of leaf per unit area of ground)
between 3 and 30, calculated that the rate of CO uptake would be 0.5 to
2 2
5 mg/m ground per hour, or about 12 to 120 kg/km per day.
19
Kortschak and Nickel! found that the leaves of the sugar cane
plant can absorb and metabolize CO, with sucrose as an end product.
These authors, however, found the rates of CO uptake to be in the order
-4 2
of 10 mg/dm /hr, which would be too low to be significant in removing
CO from the atmosphere. Hill,12 in 1971, and Hill and Chamberlain13 in
1976, found that under carefully controlled laboratory conditions,
alfalfa canopies did not significantly remove CO from the atmosphere.
The production and utilization of CO by plant life is summarized in
Table 8-3.
8-11
-------
TABLE 8-3. PRODUCTION AND UTILIZATION OF CO BY PLANTS AND MICRO-ORGANISMS
Cone.
Duration
Effects
Author
Wide variation in data
for different plants
and experimental
conditions.
0-10 ppm
100-120
ppm
200-360
ppm
80% CO
in air.
6 ppm
Not
reported
<0.1-0.6
ppm
1-2 hr.
3 hrs.
15-25 min,
30 days
15-45 min.
Not
reported
24 hrs.
Data suggests significant role
for plants in reducing
atmospheric CO concentrations;
production of CO may exceed
uptake, however.
The amount of CO uptake by
alfalfa was below limits
of detection.
Indigenous soil fungi reduced
atmospheric CO concentration
from 100-120 ppm to 0 in 3 hours.
Delwiche'
Hill
12
Inman & Ingersoll
17
Test plants absorbed CO, Bidwell & Fraser
converting it to organic material
by day and C0« by night.
o
It is indicated that algae are Crespi & Katz
responsible for significant
natural CO emissions.
Nozhevnikgva &
Zavarzin
Bidwell & Beebe*
Shaedle & Oliver32
Decrease in CO content.
Exposed plants absorbed CO
at an average rate of
0.19/|jl/hg fresh weight.
CO incorporation rates varied
from 0.32 n moles/dm -hr to
28.48 n moles/dm -hr. Grasses
tended to have the lowest rate
of fixation.
Air CO within closed box.
Diurnal variation, temperature-
dependent. Glass box over
natural soil surface.
Several micro-organisms produce Radler et al.
trace amounts of CO in the range
of 0.4-2.6 ppm. Media containing
glucose was found to stimulate
CO production.
Seiler
33
31
a-PPM CO can be converted to mg/m CO by multiplying
the above concentrations by 1.145 (@STP).
8-12
-------
8.3.2 Soil Microorganisms
Inman and Ingersoll tested non-sterile potting soil in plastic
o
atmospheric chambers and found that CO concentrations dropped from 105 mg/m
(90 ppm) to 0 within a 3-hour period. No change occurred in CO concentra-
tions occurred over the controls using sterile soil controls. This indicated
that potting soil, at least, had a distinct capacity for CO uptake. Samples
of natural soils when tested comparatively all varied in their ability to
take up CO. Carbon monoxide uptake appeared to be correlated with high
organic matter and low pH.
From the various tests which were conducted, it appeared that the
capacity for CO uptake was mediated either by a biological mechanism, or by
some physical absorptive process which, on the basis of the inactivity of
sterile soil, was labile to steam heat. A series of tests were conducted
to characterize the phenomenon further. The authors found that when 2.8 kg
of autoclaved potting soil was inoculated with 1 g of non-sterile potting
soil, uptake activity increased as a function of time following the
inoculations. Uptake of CO was inhibited by the addition of 50 ml of 10
percent NaCl to 200 g potting soil. Incubation under anaerobic conditions
for 5 days prior to testing also inhibited CO uptake, as did drenching the
soil with 50 ml of an antibiotic solution containing streptomycin,
erythromycin and cyclohexamide.
These results strongly indicated that the uptake of CO was mediated by
a biological rather than physical mechanism. It was suspected that certain
elements of the soil microflora were responsible for CO fixation. Inman
and Ingersoll then attempted to estimate the total capacity of the soil
8-13
-------
to remove CO from the atmosphere. The average activity of the soils tested
2
was 8.44 mg of CO/hr/m of soil, equivalent to 191.1 metric tons per year
per square mile. If it is assumed that this value is representative of the
average capacity of soils in the temperate zone, the capacity of the total
soil surface of the Continental United States to take up CO [2,977,128
2 2
miles (7,792,533 km )] is estimated to be 569 million metric tons per
year.
22
Liebl and Seiler found soil uptake of CO to be not as great as that
reported by Inman and Ingersoll but concurred that the soil must be
recognized as a major natural sink for CO released into the atmosphere.
Microorganisms other than the soil microflora may have a role in atmospheric
39
CO removal. Uffen described a species of Rhodopseudomonas, a species of
photosynthetic bacteria that requires CO as the sole source of carbon and
28
uses it under anaerobic conditions. Also, Nozhevnikova and Zavarzin have
stated that there exist bacteria which have the capability of oxidizing CO
and are capable of growing and developing on a substrate in which CO serves
as the sole source of carbon and energy. These bacteria represent a
potentially powerful factor in eliminating CO from the atmosphere. The
bacteria which oxidize CO to C0« have not been well studied. Table 8-4
summarizes data showing soils as CO sinks.
8.4 PRODUCTION OF CO BY PLANTS
Carbon monoxide evolution by fresh water algae has been shown by
o
Crespi and Katz to be associated with biosynthesis and degradation of
photosynthetic pigments. Their results indicated that plants may be the
O
source of 10 tons or more of CO per year. Production and utilization of
8-14
-------
TABLE 8-4. SOILS AS A SINK FOR CARBON MONOXIDE
Cone.
Duration
Effects
Author
80-130 ppm
in air
2-19 hrs,
5-100 ppm
in air
2 hrs.-
45 days
0-40 ppm
in gas
Not
reported
100 ppm
2-3 hrs.
Results indicated that the Ingersoll
phenomenon of CO uptake by soil
was due to a biological rather
than physical mechanism and that
CO uptake was due primarily to
indigenous soil microflora. Rate of
uptake was also temperature dependent.
The uptake of CO by soils i_n Ingersoll
situ is variable with soils
rangingpfrom 7.5 to 104.0 mg
CO/hr/m . Tropical soils were
most active; desert soils were
least active. CO uptake by soils
was greatest at a concentration of
100 ppm and decreased as the
concentration decreased.
15
14
Removal of CO by the forest Heichel
soil exceeded that of the field
soil at all moisture contents when
the two were compared at the same
CO concentration. Maximum rates of
removal approached 0.20 mg CO/dm hour.
10
Soils of major vegetative
regions of North American were
tested as well as roadside
soils and soils under cultivation.
CO uptake ranged from 7.6-115 mg
CO/h/m with tropical soils showing
greatest activity and desert soils
the least. Roadside soils were
consistently higher in CO uptake
capacity. Natural soils were more
active in CO uptake than sterile soil.
IngersolJR Inman
&r* * i -LO
Fisher
a-PPM CO can be converted to mg/m CO by multiplying
the above concentrations by 1.145 (@STP).
8-15
-------
CO by algae and two higher plants (Zostera man*na and Medicago sativa) have
25
been reported by Loewus and Delwiche. The assimilation and utilization
of CO by a variety of plants proceeds at a significant rate, exceeding
maximum observed rates of production in some cases. Based on laboratory
studies it can be calculated that a field of 100 hectares of alfalfa could
produce approximately 2000 liters of CO in a ten-hr period. The effect of
temperature on the evolution of CO by the soil also still remains to be
learned, although there are data on temperature effects of CO uptake by
soil. Carbon monoxide production rates were found, however, to be light
-13 2
dependent with an average value of 3x10 g/cm /sec of leaf area for a
4 2
radiation intensity of 5x10 ergs/cm sec. The total CO production by
14 34
plants is estimated to be 0.5 to 1.0 x 10 g/year. This estimate
indicates that plants may contribute significantly to the atmospheric CO
cycle with production rates comparable to the total CO production rate in
the oceans.
8.5 SUMMARY
Of the literature dealing with effects of CO on microorganisms and
plants or with the production and utilization of CO by them, most earlier
work was directed toward physiological studies without reference to
atmospheric concentrations. There are few studies from which thresholds of
detrimental (or other) effects might be inferred. Thus, although neither
defoliation nor the inhibition of leaf formation is demonstrable at
3
concentrations of 11,000 mg/m (10,000 ppm) CO or higher, this study
provides little information regarding possible threshold effects since the
concentration used was more than 10,000 times greater than normal
atmospheric levels.
8-16
-------
The few reports of effects at lower concentrations suggest that
influences in the normal atmospheric concentration range for CO are not
great and that a "threshold" as such does not exist. Since plants can both
metabolize (apparently photosynthetically) CO and produce CO, it is
considered a normal constituent of the plant environment.
Microorganisms have a wide range of responses to CO including its
autotrophic oxidation. Thus, any change in atmospheric concentration could
be expected to result in a corresponding alteration of soil microbial
population distribution; however, no studies seem to have been made. This
flexibility in the response of the soil microflora to changing environmental
conditions is a generalized one and the soil can be viewed as a buffering
system and eventual sink for CO.
8-17
-------
BIBLIOGRAPHY
1. Bennett, J. H., and A. C. H111. Inhibition of apparent photosynthesis by
air pollutants. J. Environ. Qua!. 2:526-530, 1973.
2. Bergersen, F. J., and G. L. Turner. Comparative studies of nitrogen
fixation by soybean foot nodules, bacteroid suspensions and cell-free
extracts. J. Gen. Microbiol. 53:205-220, 1968.
3. Bldwell, R. G. S., and G. P. Bebee. Carbon monoxide fixation by plants.
Can. J. Bot. 52:1841-1848, 1974.
4. Bldwell, R. G. S., and D. E. Fraser. Carbon monoxide uptake and metabolism
by leaves. Can. J. Bot. 50:1435-1439, 1972.
5. Bortner, M. H., R. H. Kummler, and L. S. Jaffe. A review of carbon
monoxide sources, sinks, and concentrations in the earth's atmosphere.
NASA CR-2081, National Aeronautics and Space Administration, Washington,
DC, June 1972.
6. Chakrabarti, A. G. Effects of carbon monoxide and nitrogen dioxide on
garden pea and string bean. Bull. Environ. Contam. Toxlcol. 15:214-222,
1976.
7. Chapanis, A. The relevance of laboratory studies to practical situations.
Ergonomics 10:557-577, 1967.
8. Crespi, H. L., D. Huff, H. F. DaBoll, and J. J. Katz. Carbon monoxide in
the Biosphere: CO Emission by Fresh-Water Algae. Argonne National
Laboratory, Argonne, IL, October 1972.
9. Delwlche, C. C. Carbon monoxide production and utilization by higher
plants. Iji: Biological Effects of Carbon Monoxide, Proceedings of a
Conference, New York Academy of Sciences, New York, January 12-14, 1970.
10. Heichel, G. H. Removal of carbon monoxide by field and forest soils. J.
Environ. Qual. 2:419-423, 1973.
11. Heslop-Harrison, J., and Y. Heslop-Harrison. Studies on flowering-plant
growth and organogenesis. II. The modification of sex expression in
Cannabis satlva by carbon monoxide. Proc. R. Soc. Edinburgh Sect. B
66:424-434, 1957.
12. Hill, A. C. Vegetation: a sink for atmospheric pollutants. J. Air
Pollut. Control Assoc. 21:341-346, 1971.
13. Hill, A. C., and E. M. Chamberlain, Jr. The removal of water soluble
gases from the atmosphere by vegetation. In: Atmosphere-Surface Exchange
of Particulate and Gaseous Pollutants (1974), Proceedings of a Symposium,
Battelle Memorial Institute and U.S. Atomic Energy Commission, Richland,
Washington, September 4-6, 1974. ERDA Symosium Series 38, U.S. Energy
Research and Development Administration, Washington, DC, January 1976.
pp. 153-170.
8-18
-------
14. Ingersoll, R. B. The Capacity of the Soil as a Natural Sink for Carbon
Monoxide. Final Report to Coordinating Research Council and Environmental
Protection Agency. Stanford Research Institute, Menlo Park, CA, December
1972.
15. Ingersoll, R. B. Soil as a Sink for Atmospheric Carbon Monoxide. Final
Report to Coordinating Research Council and Environmental Protection
Agency. Stanford Research Institute, Menlo Park, CA, October 1971.
16. Ingersoll, R. B., R. E. Inman, and W. R. Fisher. Soil's potential as a
sink for atmospheric carbon monoxide. Tell us 26:151-159, 1974.
17. Inman, R. E. , andJJ. B. Ingersoll. Note on the uptake of carbon monoxide
by soil fungi. J. Air Pollut. Control Assoc. 21:646-647, 1971.
18. Inman, R. E., R. B. Ingersoll, and E. A. Levy. Soil: a natural sink for
carbon monoxide. Science 172:1229-1231, 1971.
19. Kortschak, H. P., and L. G. Nickel!. Photosynthetic carbon monoxide
metabolism by sugarcane leaves. Plant Sci. Lett. 1:213-216, 1973.
20. Knight, L. I., and W. Crocker. Toxicity of smoke. Bot. Gaz. (Chicago)
55:337-371, 1913.
21. Krall, A. R., and N. E. Tolbert. A comparison of the light dependent
metabolism of carbon monoxide by barley leaves with that of formaldehyde,
formate and carbon dioxide. Plant Physio!. 32:321-326, 1957.
22. Liebl, K. H., and W. Seller. CO and hL destruction at the soil surface.
In: Proceedings of the Symposium on MTcrobial, Production and Utilization
of Gases (I-L, CH-, CO), Akademie der Wlssenschaften, Goettlnger, Germany,
September 1-5, 1975. H. G. Schlegel, G. Gottschalk, and N. Pfennig,
eds., E. Goltze KG, Goettinger, Germany, 1976. pp. 215-229.
23. L1nd, C. J., and P. W. Wilson. Mechanism of biological nitrogen fixation.
VIII. Carbon monoxide as an inhibitor-for nitrogen fixation by red clover.
J. Am. Chem. Soc. 63:3511-3514, 1941.
24. Lind, C. J., and P. W. Wilson. Carbon monoxide inhibition of nitrogen
fixation by Azotobacter. Arch. Biochem. 1:59-72, 1942.
25. Loewus, M. W., and C. C. Delwiche. Carbon monoxide production by algae.
Plant Physio!. 38:371-374, 1963.
26. McMillan, C., and J. M. Cope. Response to carbon monoxide by geographic
variants in Acacia farnesiana. Am. J. Bot. 56:600-602, 1969.
27. Minina, E. G., and L. G. Tylkina. Physiological study of the effect of
gases upon sex differentiation in plants. Dokl. Akad. Nauk SSSR 55:165-168,
1947.
28. Nozhevnikova, A. N., and G. A. Zavarzln. Symbiotic oxidation of carbon
monoxide by bacteria. Mikrobiologiya 42:158-159, 1973.
8-19
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29. Pankhurst, C. E., and J. I. Sprent. Effects of water stress on the
respiratory and nitrogen fixing activity of soybean root nodules.
J. Exp. Bot. 91:287-304, 1975.
30. Quayle, J. R. The metabolism of one-carbon compounds by micro-organisms.
Adv. Mlcrob. Physio!. 7:119-203, 1972.
31. Radler, F., K. D. Greese, R. Bock, and W. Seller. The formation of
traces of carbon monoxide by Saccharomyces cerevlslae and other
microorganisms. Arch. Mlcrobiol. 100:243-252, 1974.
32. Schaedle, M., and D. Oliver. Carbon monoxide fixation by three plant
communities. Plant Physlol. Suppl.:33, 1974.
33. Seller, W. The cycle of atmospheric CO. Tellus 26:116-133, 1974.
34. Seller, W., H. G1ehl, and G. Bunse. The influence of plants on atmospheric
carbon monoxide and dinitrogen oxide. Pure Appl. Geophys. 116:439-451,
1978.
35. Smith, L., Jr., and E. H. C. Sie. Response of luminescent bacteria to
common atmospheric pollutants. Proc. Annu. Tech. Meet. Inst. Environ.
Sci. 15:154-157, 1969.
36. Stewart, J. K., and M. Uota. Market quality of head lettuce as Influenced
by added CO and C0« and by low 0~ during simulated transit. Hort Science
9:274, 1974. * *
37. Stewart, J. K., and M. Uota. Postharvest effect of modified levels of
carbon monoxide, carbon dioxide, and oxygen on disorders and appearance
of head lettuce. J. Am. Soc. Hortic. Sc1. 101:382-384, 1976.
38. Thompson, C. R., 0. C. Taylor, M. D. Thomas, and J. 0. Iv1e. Effects of
air pollutants on apparent photosynthesis and water use by citrus trees.
Environ. Sci. Technol. 1:644-650, 1967.
39. Uffen, R. L. Anaerobic growth of a Rhodopseudomonas species in the dark
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Chem. 247:527-531, 1972.
41. Wolf, F. T., and G. H. Kidd. Effect of various gas atmospheres upon the
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Contrib. Boyce Thompson Inst. 5:1-17, 1933.
8-20
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9. METABOLISM OF CARBON MONOXIDE IN MAMMALS
Adverse health effects of carbon monoxide (CO) are due primarily to
diminished oxygen (Op) transport by the blood and to interference with
biochemical utilization of 02 in tissues. The chemical binding of CO to
hemoglobin (Hb) and other heme compounds in tissues is so much stronger
than the binding of Op to these compounds that Op is excluded in part
from its normal physiological role. The apparent toxicity of CO is
related to the strength of the coordination bond formed with the iron
atom in protoheme (C-.H-pN.O-Fe). Hemoglobin, a ferrous iron complex of
a protoporphyrin combined with globin, is contained within the erythrocyte
(red cell). A small amount of CO is produced within the body by normal
breakdown processes, which result in carboxyhemoglobin (COHb) levels of
about 0.5 percent in blood. Any increase above this level is assumed to
result from outside sources. The excretion of CO in exhaled air appears
to occur in two stages, rapidly at first and then more slowly.
9.1 INTRODUCTION
Mammals obtain CO from two sources: (a) the endogenous one,
normally from the breakdown of Hb, and (b) by inhaling exogenous CO from
the ambient air. The quantity of endogenous CO is small although greater
quantities can be produced in various disease states and by ingestion or
9-1
-------
inhalation of certain drugs and chemicals. Exogenous CO, from inhalation,
increases the concentration of CO in the alveoli of the lung, which
increases its diffusion through the pulmonary and capillary membranes
into the blood. The final, and most important, factor is the great
avidity with which the Hb in the red cell (erythrocyte) combines with
the CO. The changes in the concentration of this combined Hb and CO
(COHb) is finally determined by many factors: the endogenous CO produced,
the concentration of CO inhaled, the volume of inhaled air (which is
related to the degree of physical activity of the individual), body
size, barometric pressure, and the functional capacity of the lung
35
itself. These factors have been briefly summarized by Klocke and
Coburn.
An Op supply adequate to maintain tissue metabolism is provided by
the integrated functioning of the respiratory and cardiovascular systems
to transport Op from the ambient air to the various tissues of the body.
Nearly all of the 0«, except that dissolved in plasma, is bound reversi-
bly to the Hb contained within the erythrocytes. The most significant
chemical characteristic of the air pollutant, CO, is that it is also
reversibly bound by Hb. Therefore, it is a competitor with 0« for the
four binding sites on the Hb molecule. The reduction in the Op-carrying
capacity of the blood is proportional to the amount of COHb present.
A simplistic example is provided by comparing an anemic individual
having 7.5 g percent of Hb with another individual having 15 g percent
but with half of this Hb as COHb, i.e., 50 percent COHb. The Op-carrying
capacity is equivalent in both. However, the amount of available Op is
still further reduced by the inhibitory influence of COHb on the dissocia-
tion of any oxyhemoglobin (OpHb) still available.
9-2
-------
9.2 THEORETICAL CONSIDERATIONS
The equilibrium constant, M (Haldane's constant), expresses the
relative affinity of Hb for CO and 0« under conditions in which the
21
concentration of reduced Hb is minimal. This M is defined by the
following equation:
(COHb)
= M
(0?Hb) " Pn
* 2
where P«Q and PQp represent the equilibrium gas partial pressures:
each pressure being the same in the erythrocytes or Hb solution as in
the equilibrated gas phase; (COHb) and (OpHb)", on the left side of the
equation, are the concentrations of COHb and OJHb, respectively.
The value of M is about 200 plus in most mammalian species (246 in man),
in spite of the fact that CO combines with Hb more slowly than does 0«.
Carboxyhemoglobin dissociates very slowly due to the tight binding of
CO to Hb. Technically, it is not possible to measure the rate of
dissociation of CO from partly saturated Hb. The dissociation velocity
constant has been measured only by a few investigators on sheep and
human Hb fully saturated with CO. The most commonly used values for M
re
in the recent literature have ranged from 210 to 230. Roughton has
presented the most comprehensive analysis of the interaction of CO with
erythrocyte Hb. He reviewed the extensive early literature and presented
new data on several portions of the dissociation curve. Roughton1s data
clearly indicate that a mean value for M is approximately 246, although
it is different for various portions of the dissociation curve. The
attraction by the Hb molecule for CO, compared to that for Op, is thus
9-3
-------
suggested to be some 246 times greater. In fact, this value was the one
21 34
originally suggested by Douglas et al. and confirmed by Joels and Pugh.
Solution of Haldane's equation would give an approximate level
of COHb; e.g., exposure to ambient environments containing 29, 57, or
3
114 mg/m (25, 50, or 99 ppm) CO would lead to COHb saturations of
approximately 4.8, 9.2, and 16.3 percent if arterial 0^ pressure were
80 torr. The CO enters the lungs with each breath and diffuses across
the alveolar-capillary membrane in a manner similar to 0^. If air with
a constant concentration of CO is breathed for hours, the rate of uptake
of CO decreases exponentially (roughly so) until an equilibrium state is
attained in which the partial pressure of CO in the pulmonary capillary
blood is equivalent to that in alveolar air. The half-time for this
process is approximately two hours in a healthy individual engaged in
light physical activity. This process is altered during heavier
physical exercise or in certain disease states.
Transport of 0« in the blood is best described by the O^Hb dissocia-
tion curve (Figure 9-1). This curve, in the presence of COHb, is no
longer classically sigmoid but is shifted to the left so that a lower 0«
pressure is present for the same O^Hb saturation compared to blood with
57 57
COHb (see Figure 9-2). Roughton and Darling pointed out that only
the upper half of the steep portion of the 0« dissociation curve was
operative for Op unloading, with the lower portion serving as a reserve.
When COHb is below 40 percent, 0« uptake is maintained by use of some or
even all of the reserve 0« from undissociated 0«Hb at low tensions.
9-4
-------
i
Z
UJ
H
Z
O
o
CM
O
1 I i I I
1= 0% COHb
2= 5% COHb
3= 10% COHb
4= 20% COHb
10
20
30
40
60
80 100
PO,
Figure 9-1. Oxygen dissociation curve with and without the presence of
varying concentrations of CO.
9-5
-------
0)
o.
o
K
oc
D
CO
100
80
60
40
30
20
10
10
20
pH7.4
I I
30 40
PO,
60 80 100
Figure 9-2. Blood oxygen dissociation curves at various COHb values.
9-6
-------
If COHb exceeds 40 percent, adequate amounts of 0? cannot be delivered
to the tissues. Figure 9-2 illustrates the extent of the Haldane shift
to the left more clearly than the classical curves of Figure 9-1.
42
Mulhausen et al. illustrate this shift by observing that the P™
(half saturation) Op tension shifted from 26.7 to 23.2 torr in their
subjects, who were intermittently exposed to high concentration of
36 16
ambient CO. Ledwith and Collier have presented methods for deter-
mining P,-0 in the presence of COHb and extended theoretical considera-
tions for the computation of PQ2 in the presence of CO. Carbon monoxide
not only diminishes the total amount of Op available by direct replace-
ment of Op (Figure 9-1) but also alters the dissociation of the remaining
Op so that it is held more tenaciously by Hb and released at lower Op
tensions. The OpHb curve in the presence of COHb progressively resembles
the simple Op dissociation curve of myoglobin. Myoglobin is a heme
compound with only one heme unit per molecule and does not exhibit heme-
heme interactions. It is possible that the combination of one or more
of the four heme groups in Hb with CO decreases the heme-heme interac-
tions of the remaining heme units and results in a molecule approaching
32
the behavior of myoglobin. Hlastala et al. have presented data indi-
cating that heme-heme interaction is different for Op than for CO. This
44
decreased heme-heme interaction has been confirmed by Okada et al.
Carbon monoxide poisoning is similar to anemia wherein the Op
capacity of the blood is reduced due to a reduction in the Hb concentration.
The Op dissociation curve of blood obtained from patients with anemia is
shaped like the normal curve but is vertically compressed. However,
9-7
-------
when curves from individuals with a 50 percent reduction in Hb content
are compared to dissociation curves determined in the presence of
50 percent COHb, there are striking differences. Consequently, the
tendency to make such comparisons is likely to lead to erroneous deduc-
5
tions as to effects occurring at the tissue level. Brody and Coburn
have discussed these differences in relation to arterial and venous P
CO
and PQ2 levels.
The possibility that an adaptation to CO (such as in the case of
adaptation to high altitudes) could alter the position of the 0«
dissociation curve as a consequence of extensive exposure to CO appears
42
to have been answered. Mulhausen et al. found no change in the
degree of left shift in the blood of individuals exposed to CO for a
period of 8 days. Unfortunately, the average COHb of 13 percent was
based on large individual variation in COHb and a periodic exposure to
relatively higher inhaled CO concentrations.
Several investigators have sought for evidence of a potential shift
of the curve back to the right. Red cell 2-3-diphosphoglycerate is
increased in individuals with anemia and during residence at high altitude.
2,3-Diphosphoglycerate (2,3-DPG) is a phosphorylated by-product of
glycolysis. In erythrocytes of man and most other mammals, the molar
concentration of 2,3-DPG is roughly equal to that of Hb. It and some
other organic phosphates are bound rather strongly to deoxyhemoglobin
(de-02Hb) but have little affinity for 02Hb. Increases in 2,3-DPG shift
the effective 0« affinity; i.e., a shift of the 0«Hb dissociation curve
3
to the right occurs. Astrup found a small decrease in erythrocyte
9-8
-------
2,3-DPG in human subjects maintained with 20 percent COHb for 24 hours.
on
Dinman et al. conversely found a small increase in 2,3-DPG in human
subjects after 3 hours at approximately 20 percent COHb and in rats
exposed to higher but variable concentrations of CO. A shift of the
dissociation curve does not appear to indicate an important adaptation
to CO exposures of less than a few days. Cameron et al. have reported
that CO has a significantly greater effect upon the position of the 0?
dissociation curve in patients with sickle-cell anemia than in normal
subjects. It is possible that in sickle-cell anemia there is an
increased Hb affinity for CO.
Any consideration of the toxicity of CO must include not only the
decrease in the Op-carrying capacity of Hb but also the interference
4
with Op release at the tissue level. Ayres et al. raised the COHb
concentration to an acute average of 9.0 percent saturation in 26 subjects,
some with and some without heart disease. Mixed venous PQ2 decreased
from 39 to 31 torr, suggesting a decrease in tissue Op pressure since
mixed venous Op pressure must represent, at least roughly, the maximum
values for tissue oxygenation. Arterial Op tension decreased 5 torr
4
from the control level of 81. Ayres et al. also measured the alveolar-
arterial Op gradient. The 9 torr increase in the gradient implies that
the pulmonary arterio-venous shunts became larger, accounting for both
the increased alveolar-arterial Op difference and the decrease in
52
arterial Op tension. Power, however, found that CO diffuses more
rapidly through blood and pulmonary and placental tissues than would be
predicted from comparative solubilities of Op and CO in water. Brody
9-9
-------
5
and Coburn have indicated that if the 0« content of the mixed venous
blood is abnormally low, as in anemia or CO poisoning, the effect of the
shunted blood in lowering arterial PQ2 wil1 be greater than normal• and
a small increase in the alveolar-arterial pressure difference (A-aDQ2)
will result. The change in the shape of the CLHb curve due to the
5
presence of CO will also increase A-aDQ«. Furthermore, Brody and Coburn
also showed that mild increases in COHb concentrations would have little
or no influence on the A-aDQ2 in normal subjects. However, in patients
with large intracardiac right-to-left shunts or with chronic lung disease
and regional variation in the ventilation perfusion ratio (V./Q), the
presence of CO in the blood will increase the A-aDQ?.
The venous P0p values expected to result from various COHb levels can
24 49
be calculated. ' If blood flow and metabolic rate remain constant,
equilibration with an ambient CO of 200 ppm (25 percent COHb) will lower
venous PQ2 from 40 to less than 30 torr. A similar degree of venous
hypoxemia results from an ascent by a normal individual to an altitude
of 3658 m or a 35 percent reduction in 0« capacity in an anemic patient.
It can also be calculated that at 5 percent COHb there will be only a
slight drop in the mixed venous PQp. Even more significant relationships
can be obtained by plotting Op content against the partial pressure
57
of Op. The difference in Op content at various percentages of COHb
from zero to 20 reveal that only a small change occurs in the availability
of Op due to the Haldane effect (Figure 9-1). It was this evaluation
57
which led Roughton and Darling to conclude that COHb concentrations
less than 40 percent produce relatively easily compensated restrictions
9-10
-------
in the amount of 0« available for tissue delivery. This can only be
applied to subjects with normal respiratory and circulatory systems.
The small reductions in Op content at 5 to 10 percent COHb may be quite
critical for patients suffering from cardiovascular diseases or chronic
12
obstructive lung disease. Coburn et al. published a detailed theoreti-
cal analysis of the physiology and variables that determine blood COHb
levels in man. The details of the formulas used in these calculations
49
are presented in section 9.3. Permutt and Fahri have calculated that
when COHb levels are approximately 5 percent, resting coronary blood
flow (CBF) must increase about 20 percent in order to prevent myocardial
ischemia. This theoretical calculation has been confirmed experimentally
1 33
by Adams et al . and Horvath, who demonstrated such approximate
increases in CBF despite having used very different methods to increase
blood COHb levels.
Cerebral function is said to be altered at low COHb levels and it
is of some interest to examine the available data on cerebral
CO
tensions, cerebral blood flow, and cerebral metabolism. Zorn studied
the effects of CO inhalation in vivo on brain and liver Pno using
- - \J£.
platinum electrodes. Tissue PQ2 fell in both organs, even at COHb
concentrations of 2 percent, and the fall was approximately linear to
increases in COHb. Oxygen partial pressure decreased 0.2 to 1.8 torr
for each I percent fall in 0«Hb saturation. These data suggested that
CO had influences other than at the intracellular level, since if it was
limited to this area, tissue P«« would have been expected to increase.
ep
Weiss and Cohen performed similar studies on rat brain and muscle.
9-11
-------
They found a decrease in cerebral cortical PQ2 consequent to inhalation
of low levels of CO. Unfortunately, they did not measure COHb levels in
these rats, although, in a group of sham-operated animals exposed to
similar levels of inhaled CO, COHb had increased to 3.3 percent.
31
Haggendal et al. reported that during progressive CO administration to
dogs, cerebral blood flow did not increase until COHb levels attained
20 percent. Thereafter, cerebral blood flow increased progressively and
was double the control values when COHb reached 50 percent. Paulson et
48
al. measured cerebral blood flow in five human subjects. No changes
were observed at 8 percent COHb but a greater than 20 percent increase
occurred when COHb was 20 percent. Despite the increase in cerebral
blood flow, the PO« of jugular venous blood was reduced by 3.4 torr at
this high level of COHb. Jugular venous PO« was reduced 1 mm when COHb
was 8 percent but no note was made as to whether this was a significant
decline. Arterial and jugular venous lactates were said to be unchanged.
39
McGrath and Martin have presented evidence that CO may have a
direct effect on the heart in addition to its well known Hb-mediated
effect. Carbon monoxide caused a reduction in developed tension and an
increase in resting tension of cardiac muscle. Recovery of muscle
function was also depressed. Chen and McGrath have also reported that
CO has a specific effect on the myocardial conducting system. Carbon
monoxide may have specific effects independent of the reduction in 0?
availability.
Total-body asanguineous, hypothermic perfusion was recently sug-
2
gested as a therapeutic measure in CO poisoning. In an attempt to
9-12
-------
53
explain this beneficial effect, Ramirez et al . compared the survival of
normal dogs given high levels of CO versus acutely anemic dogs transfused with
COHb blood. All normal dogs with COHb levels of 54 to 100 percent died within
0.25 to 10 hours but the transfused animals, having a final mean COHb of
80 percent after transfusion, survived. The authors suggested that hypoxic
anemia was not the principal mechanism of CO toxicity but that the blocking
out of the energy supply on the cellular level governed by the cytochrome
system was heavily involved.
— 9Q
Goldbaum and co-workers have suggested that in order for CO to
affect mitochondrial respiration (particularly through combination with
cytochromes) it must be dissolved first in plasma. They report that if
0.001 ml CO is physically dissolved in the plasma, even though COHb levels
were above 20 percent, this physically dissolved CO combines with the cyto-
chromes, and it is this combination rather than the reduction in 0^- transport
capacity of the blood that appears to be responsible for the toxic effects of
CO. Dogs injected with CO intraperitoneally survived indefinitely even though
45
their COHb levels were as high as 75 percent. Orellano et al . presented
experimental data which suggested that CO injected intraperitoneally into dogs
is nontoxic. The implication of these results suggests that the CO tension in
the blood after inhaling CO is high because the combination of CO with Hb is
not instantaneous. They postulated that blood leaving the lungs has a high CO
tension and this physically dissolved CO is more likely to combine with the
various heme compounds in tissue and so produce a local effect on mitochondrial
metabolism. There may be some questions regarding these observations since the
9-13
-------
kinetics of CO transport would not be completely supportive of the
22
changes observed. Drabkin et al. had reported a similar effect in
1943 and explained the lack of toxicity as the Haldane effect.
o
Chiodi et al». indicated that the respiratory center or arterial
chemoreceptors were not stimulated to elevate the respiratory minute
volume even when COHb levels were as high as 40 percent. Mills and
41
Edwards measured the frequency of electrical impulses in the afferent
nerves from the aortic and carotid chemoreceptors. They showed that CO
administration does result in chemoreceptor stimulation. The response
appeared to be approximately linear with the COHb concentration (at
least definitely above 8 percent). These findings suggest that CO may
stimulate breathing. The failure to observe an increased minute volume
might be explained by considering that, in the presence of CO, the
chemoreceptor stimulation was offset by hypoxic depression of brain
structures that are involved in breathing. There is some evidence that
this balancing between chemoreceptors and central nervous depression is
CO
operative in anemia. The difference in observed responses may be
related to varying sensitivities of the baro- and chemoreceptors to
carbon monoxide and to PQ2. Additional investigations are needed to
clarify this physiological effect of CO inhalation.
9.3 ABSORPTION, EXCRETION, AND EQUILIBRATION
Carbon monoxide in the body is produced endogenously from the
catabolism of the pyrrole rings originating from Hb, myoglobin,
cytochromes, and other heme-containing pigments. The adult's endogenous
production normally amounts to approximately 0.4 ml (STPD) per hour. '
9-14
-------
15
Increased production can occur in hemolytic anemias, during the
18
menstrual cycle in females, and in the induction of liver cytochromes
consequent to administration of drugs such as phenobarbital or
g
diphenylhydantoin. The basal production of endogenous CO of approxi-
mately 0.31 ±0.07 umole/(hr/kg) can be increased in these conditions by
approximately threefold. These increases are of minimum importance in
the elevation of COHb compared to the increases that occur when exogenous
40
CO input is considered. Mercke et al. have found diurnal endogenous
production to be lowest in the morning. Fasting for 24 hours resulted
in increased endogenous production. It should be kept in mind that
there is considerable inter- and intra-individual variation in endogenous
CO production. The primary factors determining the final level of COHb
are inspired CO, minute alveolar ventilation in rest and exercise,
endogenous CO production, blood volume, barometric pressure, and the
relative diffusion capability of the lungs. The rate of diffusion from
the alveoli and the combination of CO with the blood Hb is the step
limiting the rate of uptake into the blood. A special case of CO exposure,
important to a large proportion of the population, is the intake from
tobacco smoking. This is primarily direct exposure for the smoker and
indirect for the nonsmoker, i.e., inhalation from a smoke-filled
environment.
23
The classical absorption curves of Forbes et al. have been
reevaluated for the resting person and are presented in Figure 9-3.
50
Peterson and Stewart exposed human volunteers to a variety of different
CO concentrations for periods ranging from 0.5 to 24 hours. Using
9-15
-------
ABSORPTION OF CARBON MONOXIDE
I
2L
%
O
o
O
-I
CO
z
00
o
o
LJLJ
X
>
X
o
CQ
OC
I ! II I MM
VQQ= 0.007 ml/min
1000 | 2000
24 hours
5000 min
Figure 9-3. Exposure duration, ambient carbon monoxide concentrations
(resting individuals). (Reprinted from Annual Review of Pharmacology, with
the permission of the publisher.)
9-16
-------
regression analysis, they derived the following empirical relationship
for blood COHb as a function of ambient CO concentration and exposure
time:
Log1Q y = (0.85733 log1Q x + 0.62995 Iog10 t) - 2.29519;
where y = % COHb,
x = CO concentration in ppm, and
t = time in minutes.
Although these new data come closer to presenting potential uptake in
individuals exposed to present-day ambient concentrations of CO, they do
not address themselves to the uptake that would occur in an active
46
individual. Ott and Mage have objected to the Peterson and Stewart
presentation as representing a static model. They indicate that the use
of averaging periods as long as 1 hour versus 10 to 15 minutes introduces
an error into recorded urban concentrations by obscuring short-term high
concentrations.
23
The data presented by Forbes et al. have been until recently the
only experimental information available which takes ventilation into
account and, even so, their information is inadequate since the full
range of inspired, ventilatory volumes possible in exercising man were
50
not considered. Peterson and Stewart reported excellent correlation
between the COHb values measured in their volunteer subjects with those
12
predicted by the Coburn et al. equation (see Figure 9-3). Coburn et al.
have developed an equation which permits the calculation of blood
50
COHb as a function of time, considering appropriate physiological and
physical factors. This equation was used to calculate COHb concentrations
9-17
-------
for exercising individuals, as represented in Figure 9-4. In the equation,
0«Hb concentration depends upon COHb in a complex way and, therefore,
solution of the equation requires some special computer techniques
utilizing a second approximation. These have been attempted, and general
12 51
solutions are available. Peterson and Stewart have shown that this
equation appears to predict COHb levels as well for women as it does for
men, even though the female subjects absorbed CO more rapidly than most
male subjects. Exercise sufficient to increase alveolar ventilation
approximately 2.5 times above resting levels was also predictive. The
small number of subjects of each sex that were studied and the relatively
low exercise ventilatory rates limit the application of this prediction
formula and await further experimental verification. Further development
of Coburn's concepts will undoubtedly improve the base on which theo-
retical uptakes can be calculated. Calculations based on the Haldane
formula can be utilized for determining equilibrium COHb concentrations.
There is no excretion of CO unless there is respiration. When air
or 0« is breathed, CO dissociates from Hb, myoglobin, and heme pigments
and diffuses back into the plasma and into the expired air. Carbon
monoxide can be almost completely recovered in the expired air. Some
animal experiments suggest that a small amount is oxidized i_n vivo to
carbon dioxide (C02).
Adequate data are available on the rate of absorption of CO, but
there is considerably less information concerning the rates of CO
egress from the lungs. The same factors which determine how much CO is
taken up by the blood should apply in reverse when one considers clearance
9-18
-------
20 LPM 50 PPM CO
10 LPM 50 PPM CO
20 LPM 20 PPM CO
10 LPM 20 PPM CO
•First observable
CO effects
20 LPM 10 PPM CO
10 LPM 10 PPM CO
Figure 9-4. Exposure duration, ambient carbon monoxide concentrations.
(Exercising individuals)
9-19
-------
of CO from blood. The primary factors involved are the amounts of CO
and 09 present, the magnitude of ventilation, and the quality of the
£- »
diffusion barrier. Age influences the quality of the barrier and it
appears that with advancing age the barrier becomes more dense and there
59
are fewer gas exchange membranes. Sedov et al. presented data on the
elimination of CO at various atmospheric pressures and ambient
temperatures. Neither lower barometric pressures nor high temperatures
47
appreciably altered the rates of elimination. Pace et al. have implied
that a sex difference in elimination may also exist, i.e., females
appear to have a faster rate than males, at least under their experi-
30
mental conditions. Similarly, Goldsmith et al. indicated that men and
women have different COHb excretion rates — men having a half-life of
4 hours and women, 3 hours. They explained these differences as being
related to physiologic differences in blood volume and pulmonary vital
capacity.
Available evidence suggests the presence of a biphasic decline in
OC CT
the percentage of COHb in arterial blood. * There is a rapid,
initial, exponential decline (distribution phase), probably related to
distribution of CO from the circulating blood to splenic blood, myoglobin,
and cytochrome enzymes. Elimination of CO via the lungs also occurs
during this phase. The distribution phase, which persists for the first
20 to 30 minutes, is followed by a slower linear decline (elimination
phase). This phase probably reflects the rates of release of CO from Hb
and myoglobin, pulmonary diffusion, and ventilation, as well as the fact
43
that Prn decreases with time. Myrhe found a similar biphasic excretion
9-20
-------
pattern to occur at an altitude of 1630 meters. However, he noted that
the half-life of COHb was much longer — 5.5 hours. Tiunov and Kustov
found that following continuous exposure to CO for 49 hours, 50 percent
was eliminated in 30 to 180 minutes and 90 percent within 180 to 420
12 40
minutes. Other investigators * have reported exponential COHb
elimination curves over many hours. However, they were unable, because
of inadequate sampling in the early phase of elimination, to observe the
more rapid initial decline. The absolute level of COHb at the beginning
of elimination studies apparently modifies the rate of disappearance of
CO from the blood. Utilizing the simpler linear relationship, it
appears that half-times for COHb levels of 5 to 16 percent and 20 to
43 percent are approximately 190 and 134 minutes, respectively. If the
more accurate exponential (semilogarithmic) relationship is utilized,
the half-times for the above levels of COHb are 226 and 148 minutes,
respectively. These rates must be considered as being approximations,
since considerable individual variability has been observed. In summary,
discharge of CO occurs first at a rapid rate and then becomes slower
with time; and the lower the initial level of COHb, the slower the rate
of disappearance. No studies have apparently been made to determine the
disappearance rates at the low levels of COHb (2 to 4 percent) that
might be present following exposure to ambient concentrations of CO.
9-21
-------
Several procedures have been tried which could accelerate the
excretion of CO from the blood of individuals who have high levels of
47
COHb (40 to 70 percent). Pace et al. reported that treatment of such
individuals in a recompression chamber with an 0« level equivalent to
2.5 atmospheres (partial pressure of 02 equal to 1900 torr or an alveolar
0« pressure of 1801) would facilitate removal of CO. They indicated
that 1 hour in such a chamber would result in the reduction of COHb to
10 to 15 percent, whatever the initial level might have been. Malorny
38
et al. have revived the Henderson and Haggard treatment concept. They
evaluated the influence of breathing different gas mixtures on the
excretion of CO in animals having high COHb levels (60 to 74 percent).
It was determined that in animals, 50 percent could be excreted in
19 minutes if 5 percent C0? and 95 percent 0« were breathed, compared to
28 minutes for 100 percent 02, and 41 minutes for ambient air. Another
2
approach was suggested by Agostini et al. who employed a total-body
asanguineous, hypothermic procedure. The biological half-life of CO in
man under normal conditions is one and one-half hours. This approach to
removal of the body burden of excessive amounts of CO remains to be
fully evaluated in clinical trials.
9-22
-------
The following table (Table 9-1), based on the Haldane relationship
for resting individuals, indicates the equilibrium percentage saturation
of the Hb with CO at various alveolar pressures of CO (alveolar PO« is
assumed to be 98 torr):
Table 9-1. PERCENT COHb VERSUS CO PRESSURE
CO
%COHb
0.87
1.73
3.45
5.05
6.63
8.16
9.63
11.08
12.46
13.80
15.11
16.37
17.60
18.78
19.95
21.05
22.15
23.23
24.26
25.25
26.22
PPm
5
10
20
30
40
50
60
70
80
90
100
110
120
130
140
150
160
170
180
190
200
% Atmosphere
0.0005
0.001
0.002
0.003
0.004
0.005
0.006
0.007
0.008
0.009
0.010
0.011
0.012
0.013
0.014
0.015
0.016
0.017
0.018
0.019
0.020
Torr
0.0038
0.0076
0.0152
0.0248
0.0304
0.0380
0.0456
0.0532
0.0608
0.0684
0.0760
0.0836
0.0912
0.0988
0.1064
0.1140
0.1216
0.1291
0.1368
0.1442
0.1520
9.4 DISTRIBUTION IN BODY TISSUES
When discussing the intracellular effects of CO, consideration must
be given to the interactions of all substances within the tissue cells
which are involved with 0? delivery. Since Hb and myoglobin are struc-
turally related, they react with CO in a similar manner. The function
of myoglobin (in vivo) may be to act as a reservoir for 0« within the
muscle fiber. There are approximately 132 g of myoglobin in the muscles
of a 70-kg man. The turnover rate is on the order of 0.34 mg/day. The
9-23
-------
CO and 0^ equilibria of human myoglobin (in vitro) has been studied and
a hyperbolic 0« dissociation curve established. This curve, unlike
the hemoglobin one, is not affected by the hydrogen ion concentration,
the ionic strength, or the concentration of myoglobin. The relative
affinity constant, M, is approximately 40 but is still sufficient to
induce appreciable formation of carboxymyoglobin (COMb). Coburn et
al. ' as well as Luomanmaki have studied the interrelationships
14
between COHb and COMb. Coburn1s work utilizing CO has shown that
identical CO exposures can produce different degrees of saturation of
Hb, depending upon the partial pressures of 0« in blood and tissue.
13
Coburn and associates determined that the ratio of CO content in
muscle to the content in blood is a function of arterial P02- This
ratio, for skeletal muscle, was found to be approximately 1 but in
myocardial tissue it was 3. When arterial PQ« fell below 40 to 30 torr,
CO disappeared from the blood, presumably entering the muscle. A sub-
stantial amount of extravascular CO stores are located in muscle. The
higher ratio for cardiac tissue may be of considerable significance.
In an individual with a blood COHb level of 10 percent, some 30 percent
13
of cardiac myoglobin may be saturated with CO. Coburn and his associates
were able to estimate the mean PQ2 of skeletal muscle and myocardium,
finding these to be 6 to 8 and 4 to 6 torr, respectively.
Although no final judgment can be made regarding the next lower
step involved in 0« transport, i.e., the role of cytochromes a3 and P-
450, the fact that experimentally they react with CO as do other heme-
containing substances suggests that they may play a role in CO poisoning.
9-24
-------
The evidence available suggests that interactions between CO and cyto-
chrome oxidases are of minor significance at the concentrations of CO
found in community air pollution. All of the data on the cytochromes
have been obtained from i_n vitro experiments. Whether similar events
occur i_n vivo remains uncertain. The most likely oxidase for inhibition
jj] vivo is P-450, but no convincing evidence for this effect is available.
Cooper et al. have reported that the ratio of CO to 0« required for
50 percent inhibition is approximately 1 to 1, in contrast to the similar
54
ratio for cytochrome a~ of between 2.2 and 2.8. Root believes that at
a PpQ compatible with life, only insignificant blocking of the 0«
consumption system occurs. In terms of the total distribution throughout
the body of an inhaled dose of CO, the amounts bound to these hemoproteins
are small compared with the amounts bound to Hb and Mb. Coburn has
presented a diagrammatic representation of the factors influencing body
CO stores. The possible significance of an important role of these
hemoproteins lies in the concept that under conditions where tissue P02
is decreased, the affinity of intracellular hemoproteins for CO may
increase.
9.5 SUMMARY
One of the primary functions of Hb is to provide for the transport
of 02 and C0«. Hemoglobin combines readily with either 0« (to form
02Hb) or CO (to form COHb). The affinity of Hb for CO is some 240 times
greater than its affinity for 0«. The presence of COHb in blood not
only reduces the availability of 0« to the body, but its presence
inhibits the dissociation of the remaining 0«. Carbon monoxide also
combines reversibly with heme compounds in the cell.
9-25
-------
Carbon monoxide is available primarily from two sources —
exogenously from the ambient air and endogenously from the catabolism of
pyrrole rings originating from heme-containing pigments. Endogenous
sources of CO result in COHb levels of approximately 0.5 percent in
normal males. Any increment above this level arises from exogenous
sources. The primary factors determining the final level of COHb are
the concentration of inspired CO, alveolar ventilation, red cell volume,
barometric pressure, and the diffusive capability of the lungs. The
uptake and final equilibrium level have been fairly well characterized,
but the excretion of CO requires further clarification. The excretion
appears to be biphasic — a rapid exponential fall followed by a slower
rate of decline.
9-26
-------
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9-31
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10. EFFECTS OF CO ON EXPERIMENTAL ANIMALS
10.1 INTRODUCTION
Interpretation of comparative data from other species than man must
be carried out in recognition of the fact that there are species differ-
ences in the particular findings. An attempt must be made to generalize
the principles rather than the particulars from other species to man.
For instance, it would not be surprising to learn that the threshold
level for CO effects on the cardiac system would differ in rat and man,
but it would be less likely that the effect in rats would be salutory
while in man deleterious. The non-human data, although it must be
interpreted rather than simply transferred to man, serves the valuable
ends of (1) suggesting studies to be verified in man, (2) exploring the
properties and principles of an effect in a much more thorough and
extensive fashion than is possible in man, (3) protecting human subjects
from unwarranted exposure, (4) permitting a compression of exposure
duration in relation to aging due to the shorter life expectancies of
animals, and (5) obtaining body tissues, organs, and cellular material
more readily, allowing for studies to be carried out at the local tissue
level.
10-1
-------
Fortunately, the influence of CO on biological systems is not
limited to studies on non-human animals. Many direct experiments have
been carried out on humans during the last century. While many reports
describe inadvertent exposures to various levels of CO, there are a
considerable number of precise and delineated studies utilizing human
subjects. Most of these have been conducted exposing young adult males
to concentrations of CO equivalent to those frequently or occasionally
detected during routine surveys conducted at various ambient monitoring
stations.
10.2 SELECTION OF ANIMAL MODELS
Experimental animal studies have provided valuable insights to both
the potentially adverse effects of CO and the basic mechanisms by which
this substance influences physiological processes. However, many studies
have utilized extraordinary levels of CO, i.e., levels rarely found in
ambient air. These studies are not being considered in this chapter
except as parts of dose-response curves or to obtain insight into
processes, since the toxic effects of very high levels of CO have been
well documented for both animals and man. Unfortunately, the oxygen (0«)
dissociation curves of the animals utilized in CO studies are not
equivalent. There are also questions as to the relative affinities of
hemoglobin (Hb) in various animal species for CO. Klemisch et al.
reported that the blood of hamsters has the greatest affinity for CO,
followed by rats, pigs, and rabbits, respectively.
All of the effects reported later have been shown to occur to
some degree in most animals studied (mice, rats, rabbits, dogs, and
10-2
-------
monkeys). Some differences between species have been reported, but no
definitive studies towards elucidating special sensitivities have been
V,
made. Long-term exposures of animals to sufficiently high concentrations
of CO, producing levels of COHb in excess of 20 to 40 percent, can
induce pathological changes in the heart and brain. As in acute high-
level intoxication in man, serious sequelae also develop in animals.
Species differences in response are ideally illustrated in the
22 23 24
studies by DeBias et al. *•»"»*• on dogs and cynomolgus monkeys (Macaca
irus irus). Chronic exposure (23 hours per day) over several months to
o
115 mg/m (100 ppm) CO resulted in COHb levels of 14 and 12.4 percent in
dogs and monkeys, respectively. The dogs remained in clinically good
23
health with no untoward signs that could be interpreted as CO-induced.
Serum enzymes, hematological parameters, and electrocardiograms did not
change significantly. Carbon monoxide exposure of normal monkeys resulted
in myocardial effects. Experimentally infarcted monkeys had greater P-
wave amplitudes and increased evidence of T-wave inversions than
43
normal monkeys similarly exposed. Jones et al. exposed rats, guinea
3
pigs, dogs, and monkeys to 58, 115, or 230 mg/m (50, 100, or 200 ppm)
CO continuously for 90 days. Hematocrit and Hb levels were unchanged at
the lowest level of CO exposure but were significantly elevated at the
94
two higher levels in all animals but the dogs. Theodore et al. have
summarized the extensive data collected at the Aerospace Medical Research.
Laboratory. Rhesus monkeys, baboons, dogs (beagles), rats, and mice
•2
were exposed for 71 days to CO concentrations of 460 mg/m (400 ppm).
Pathological studies of these animals showed that large animals had no
10-3
-------
changes in the central nervous system (CNS) or in the heart. Cardiac
changes in the rat were the only positive findings.
The above studies have been cited as examples of the particular
differences across species, to urge"caution in generalizing these
findings to man. By such interpretation of the findings, the principles,
rather than the particulars, should be generalized.
10.3 NERVOUS SYSTEM AND BEHAVIOR
10.3.1 General Activity and Sleep
Several authors report effects of CO on gross or overall behavior
such as general activity, sleep and motor performance. Colmant found
disturbances in the sleep patterns of rats when exposed to as little as
3
250 ppm for 96 hours or 345 mg/m (300 ppm) for five hours. Lower
levels of exposure did not affect sleep and higher levels produced
3
progressively greater disturbances. Female rats exposed to 174 mg/m
(150 ppm; 15 percent COHb) during the full term of their pregnancy by
33
Fechter and Annau produced offspring which at first showed reduced
33
activity levels and lowered body weights. At 21 days postpartum,
however, no differences existed between offspring of CO-exposed mothers
and controls. Apparently at much higher levels of exposure, neonatal
19
and adult rats develop hyperactivity rather than reduced activity levels.
Levels of exposure of this extent produce brain damage from which
82
neonates but not adults recover. Plevova and Frantik have reported
decreased motor endurance in rats exposed by two different uptake rates
produced by using different CO concentrations for sufficient time to
reach the target and produce COHb concentration of 20 percent. High
10-4
-------
uptake rates, while producing equivalent COHb levels, had significantly
greater effects than low uptake rates. Lewey and Drabkin50 demonstrated
alterations in gait in dogs exposed for 11 weeks to 115 mg/m3 (100 ppm)
CO (20 percent COHb). Mussel man et al.66 showed no effect on rat
o
activity level as a result of 58 mg/m (50 ppm) exposure for three
months.
10.3.2 Learning and Performance
Using a wide variety of behavioral paradigms, a number of investiga-
tors have shown effects of CO upon the acquisition of new behavior
and/or the performance of already learned tasks. Zorn exposed rats
3
to 174 mg/m (150 ppm; 10 percent COHb) for eight hours each night for
2, 4, and 10 weeks and showed that such exposures reduce efficiency of
O£* 1%
shock-escape behavior at all exposure durations. Goldberg and Chappell,
using a continuous food reinforcement schedule in a lever-press task
with rats, showed reductions in response rate at exposure levels of 230
3
to 288 mg/m (200-250 ppm) CO for two hours. They also showed adverse
effects of such exposures on the performance of a variable ratio task.
Xintaras ' showed no effects on the performance of a fixed interval
3
lever press for food reinforcement in rats exposed to 115 mg/m (100 ppm)
CO for two hours.
Using more complicated schedules of reinforcement and/or more
complicated tasks, perhaps involving more "cognitive" behaviors, other
investigators have shown much higher thresholds for CO effects. Merigan
fil 6 87
and Mclntire, Ator et al., and Smith, et al. used a small number of
rats in progressive ratio, differential-reinforcement-of-low-rates, and
10-5
-------
fixed-consecutive-number schedules, respectively. They showed no
3
statistically significant effects below about 690 mg/m (600 ppm) CO but
with the small number of subjects it is possible that effects were
94
hidden by high variability. Using 12 rhesus monkeys, Theodore et al.
report no statistically significant effects on very complicated long-
term, multi-schedule, aversively-controlled performance tests with CO
3
exposures as high as 575 mg/m (500 ppm) for 100 days, even though the
subjects "appeared to be ill." It should be borne in mind that
aversively-controlled task performance is remarkably stable and insensi-
tive to environmental conditions. These investigators also progressively
increased CO level rather than exposing subjects to the high level
initially and so could have induced behavioral adaptation, but no control
42
group was included to test this possibility. Johnson et al., using
only three rhesus monkeys, found no effects from CO levels of up to
3
575 mg/m (500 ppm; 44 percent COHb) for 14 days on a food-reinforced
time discriminations task. McMillan found definite effects at CO
3
levels as high as 1150 mg/m (1000 ppm) for 1.5 hours using a multiple
fixed-ratio/fixed-interval schedule with pigeons. They showed, however,
3
that at about 575 mg/m (500 ppm) CO for 1.5 hours, the response of
pigeons to d-amphetamine was altered with respect to controls. Pigeons,
on such schedules of reinforcement, tend to be very stable responders in
the face of environmental alterations.
14a 3
Carter et al. report that rats exposed to 1150 mg/m (1000 ppm)
CO for 1.5 hours had drastically reduced response rates on a food-
reinforced fixed-ratio schedule task. If, however, carbon dioxide (C0?)
10-6
-------
was added at 2.5, 5.0, and 7.5 percent levels to the CO-containing air,
performance was progressively and substantially improved. This was
apparently due to increased cerebral blood flow initiated by the CO,,;
C02 levels by themselves produced no behavioral effect.
10.3.3 Electrophysiological Effects
It is not unlikely that CNS electrophysiological measures could
29
provide sensitive indices of pollutant effects. Dyer et al. exposed
3
pregnant rats to 174 mg/m (150 ppm; 15 percent COHb) for their full
term. Offspring were tested at 79 days of age, and it was shown that
some components of the cortical visual evoked responses increased in
amplitude in the females but not in the males. Using direct exposures
3
of CO levels from 174 to 1150 mg/m (150 to 1000 ppm) in adult rats,
28
Dyer and Annau showed marginally increased amplitude in some superior
3
colliculus visual-evoked potentials at 575 mg/m (500 ppm) CO or greater.
Clearly increased latencies in all evoked potential components were
shown only at a level of 1150 mg/m (1000 ppm). Xintaras et al. '
reported similar results in superior colliculus preparations in rats
3
exposed to 115 mg/m (100 ppm) for two hours, but due to the lack of
statistical analysis, it is difficult to evaluate these findings.
Xintaras pointed out that increased evoked potentials are similar to
those found under administration of sodium pentobarbitol and those found
80
when the animal is going to sleep. Petajan et al. report that at high
CO levels (2875 mg/m ; 2500 ppm; 60 to 70 percent COHb), cortical visual-
evoked responses are attenuated.
10-7
-------
3
Annau reports that rats which have been trained to lever press for
the reward of an electrical stimulation to the hypothalamus show slightly
3
reduced response rates when exposed to as little as 174 mg/m (150 ppm)
CO for 16 minutes while they were responding. Higher concentrations
produced greater decrements. These decrements represent early effects
of CO, before COHb equilibrium was reached. It was also shown, in
3
another part of the same study, that with an exposure to 1150 mg/m
(1000 ppm) CO the decline in response rates correlates highly with
increase in COHb. They also reported data which indicated that CO had
more temporary and less severe effects than hypoxic hypoxia which reduced
venous PQ2 to equivalent levels.
75
Pankow et al., using rats given subcutaneous injections of CO
sufficient to produce 19 percent and 60 percent COHb in two exposure
levels, showed that both levels decreased sciatic nerve conduction
velocity for a period of up to 28 days following exposure. Grunnet and
37 3
Petajan, using 2875 mg/m (2500 ppm) CO exposures until peroneal or
ventral caudal nerve conduction was lost, showed a deterioration of
86a
Schwann cells which regenerated by 14 to 21 days. Shul'ga showed
effects on motor chronaxie, CMS pathology, and porphyrin levels by CO
3
levels as low as 29 mg/m (25 ppm) for eight hours per day for 10 weeks.
Pathological changes and porphyrin levels were not quantitatively
documented.
10.3.4 Cerebral Blood Supply
114
Zorn measured various parameters of cerebral blood supply in
unanesthetized cats, rats, and rabbits with exposure levels ranging from
10-8
-------
3
115 to 805 mg/m (100 to 700 ppm) CO. In all cases cerebral, subcortical,
and liver PQ2 measures declined as a linear function of COHb, with PQ2
62
recovery lagging behind COHb elimination. Miller and Wood, on the
other hand, using anesthetized and artifically respirated rats exposed
3
to 575 and 1150 mg/m (500 and 1000 ppm), showed about twice the rate of
decline in the liver as in the brain. Their findings in the brain
114 99
were similar to those of Zorn. Traystman using anesthetized dogs
showed that cerebral blood flow increased as a nearly linear function of
COHb. Similar results were shown for unanesthetized goats by Doblan
26
et al. who also showed that 02 delivery to the brain decreased as a
function of COHb and showed no clear threshold. It would appear from
Traystman's and Dob!an's data that PQ2 might not fall as rapidly in
cerebral tissue as in other tissues because of increased cerebral blood
62
supplies. This hypothesis seems to be supported by Miller and Wood's
114 99
data but not by Zorn's. Traystman, "on the other hand, did not
measure blood flows in other body systems in order to test the notion
that there was not simply an overall vasodilatory response. The amount
88
of hypoxia was indirectly assessed by Sokal using rats and measuring
glucose, pyruvate, lactate and blood pH levels in the brain after
3
exposure to either 11,500 mg/m (10,000 ppm) for four minutes or 4,600
3
mg/m (4,000 ppm) for 40 minutes. The slower uptake rates produced more
extreme effects.
10.3.5 CNS Pathology and Biochemical Alterations
Carbon monoxide poisoning studies where CO levels are very high
have commonly produced CNS lesions due to local and widespread anoxia.
10-9
-------
Experimental results using high-level CO exposure have been used to
infer such brain damage as an explanatory mechanism and have demon-
CQ 03
strated ultrastructural evidence for such damage. Preziosi et al.
exposed dogs on varying short-term exposures sufficient to produce COHb
levels of 40 to 50 percent and on various long-term exposure schemes
(six weeks) which produced COHb levels as low as 4-12 percent. Short-
term, high-level exposures produced varying (only qualitatively described)
CNS pathologies ranging from mild microglial reactions to localized
necrotic lesions. Long-term, low-level.exposures produced brain ventricu-
lar dilation but no other pathological signs. From the article it was
difficult to judge the extent or frequency of the control-experimental
differences. Lewey and Drabkin, using dogs exposed for 11 weeks at
3
115 mg/m (100 ppm CO; 20 percent COHb), demonstrated localized CNS
lesions due to anoxia, similar to but much less in extent than those in
OCa
acute CO poisoning. Ginsberg and Myers, using pregnant rhesus monkeys
with short-term CO exposure just before delivery, showed that COHb
levels in offspring ranged between 10 to 20 percent for a few hours,
which was much lower than maternal COHb (60 percent). Neurological
(CNS) damage in the offspring ranged from none to severe and was inverse-
ly correlated with arterial PQ« values present during exposure. All
mothers showed no clinical effects after recovery, despite much higher
94
levels of exposure. Theodore et al. showed no brain pathology in dogs
3
and monkeys after 168 days of exposure to 460 to 575 mg/m (400 to
500 ppm) CO. Histopathological examination of the brains of monkeys
3
exposed to as much as 77.6 mg/m (67.5 ppm) CO for 22 hrs./day for two
10-10
-------
27
years were normal. Dykyk et al. reported no ultrastructural damage in
either mothers or fetuses when mothers were exposed to 100 percent CO
for 60 minutes just before delivery (mother's COHb = 73.3 percent,
fetuses' COHb = 10.3 percent). These investigators did, however, show
increased 02 uptake in CNS giant reticular formation cells in fetuses
but a decreased Op uptake in the same cells in mothers.
"• "U
33 3
Fechter and Annau exposed female rats to 174 mg/m (150 ppm CO;
15 percent COHb) during their entire term of pregnancy and found reduced
go
levels of dopamine and CNS protein in offspring. Miller and Wood,
3 3
using rats exposed to 575 mg/m (500 ppm) and 1150 mg/m (1000 ppm) CO
until COHb equilibrium was reached, showed changes in brain energy J
metabolism; however, the changes were smaller than predictable from
3
theory. At high levels of CO exposure (1150 mg/m ; 1000 ppm; for four
hours) Newby et al. demonstrated decreased dopamine synthesis but no
93
alterations in norepinepherine levels in rats. Szumanska et al.
using 100 percent CO for 20, 60 and 90 minutes did show decreases in
57
norepinepherine and catecholamine levels. Marks and Swiecicki, however,
exposed rats to CO for 120 minutes and showed increased CNS catecholamine
levels.
10.3.6 Summary and Conclusion of Nervous System and Behavior in
Experimental Animals
Table 10-1 shows a summary of all of the reviewed studies pertinent
to experimental animals, CNS, and behavior. From the data we may
conclude that definite effects of CO may be seen in general overt
3 3
behavior at 230 mg/m (200 ppm) and possibly as low as 115 mg/m (100 ppm),
10-11
-------
TABLE 10-1. SUMMARY OF EFFECTS OF CO ON CENTRAL NERVOUS SYSTEM AND BEHAVIOR OF ANIMALS
Reference
Species
Exposure*
COHb
Dependent
Variable
Results
Comment
17
Colmant
Fechtet and
Annau^ "
Culver-, and
Norton
r>oPlevovaand
Franti \
Lewey and
Drabkin u
Musselman
et al.55
114
Zorn
Stupfe
-------
TABLE 10-1 (continued)
Reference
Species
Exposure*
COHb
Dependent
Variable
Results
Comment
Goldberg-
Chappell
no
Rat 200, 250 and
n=16 in 500 ppm, 2 hr.
each of
2 tasks
Rat 100 ppm, 2 hr.
n-10
Smith
et al.
87
?Ator et al.
•—>
co
Merigan and
MeIntire
Theodore
et al.
Johnson-
et al.
Rat
n=4
Rat
n=4
Rat
n=4
Rhesus
Monkey
n=12
200, 400, and 600 ppm,
for 60 min. during
performance
100, 250, 500, 750
ppm, 2 hr.
Lever press, food
reinforcer, contin-
uous and variable
ratio tasks
Fixed interval,
lever press for
food
Fixed consecutive
number schedule,
lever press for
food
22-57% Differential
reinforcement of
low rate. Lever
press for food
155, 330, 520, and
700 ppm, 30 min. pre-
performance plus up
to 1 hr. during per-
formance
400-500 ppm, 168 days 32-38%
Rhesus 150, 200, 250, and
Monkey 500 ppm, 1-8 days
n=3
Progressive ratio
schedule. Lever
press for food
Complicated series
of shock avoidance,
lever press
13-44% Time discrimination
lever press for
food
Reduced rates in
both tasks and all
levels
No effects
No consistent
effect until
600 ppm
No effect until
750 ppm
No effect until
500-700 ppm
No effect
No effect
Also collected
electrophysiological
measures.
Complicated schedule
might not be
affected. Small
number of subjects.
Schedule produces
extremely stable
data. Might not be
affected by COHb.
Small number of
subjects.
Complicated schedule
might not be
affected. Smal1
number of subjects.
Aversive control
of behavior produces
stable results, less
sensitive to environ-
mental effects.
Small number of
subjects.
-------
TABLE 10-1 (continued)
Reference
Species
Exposure3
COHb
Dependent
Variable
Results
Comment
McMillan
60
Carter
et al.
14a
Dyer et al.
Dyer a
,_Annau
29
Pigeon 380, 490, 930, and
n=8 1410 ppm, 1 hr. +
test session
Rat 1000 ppm, 1.5 hr.
n=10 (Also added CO
Rat 150 ppm for full
n=41 pups term of pregnancy
Annau*
Rat
n=8
Rat
n=10
Rat
n=45
Rat
n=12
150, 250, 500, and
1000 ppm, 2 hr.
100 ppm, 2 hr.
15%
(maternal)
15-58%
2500 ppm until
ventral cortical
nerve conduction
stopped
150, 250, 500, and
1000 ppm
60-70%
Pankow
et al.
75
Rat
n=47
Inject CO subcutane- 19% and 60%
ously in two levels
Multiple (fixed
interval, fixed
ratio). Key peck
for food.
Fixed ratio, lever
press for food.
Cortical visual
evoked potentials
No effect lower
than 500 ppm
Severe depression
of rate
Increased amplitude
but only in females
Showed interaction
of CO with d-ampheta-
mine.
Added C02 restores
response rates to
some extent.
Superior colliculus Increased amplitude
visual evoked at 500 ppm, decreas-
potential ed amplitude at 1000
ppm
Superior colliculus Increased ampli-
visual evoked poten- tude, decreased
tial peak latencies
Cortical visual
evoked potentials
and nerve con-
duction velocity
Lever press for
hypothalamic elec-
trical stimulation
(reward)
Measure sciatic
nerve conduction
velocity
Decreased measures
at 60-70% COHb
Measurements made
while lever pressing
on fixed interval
schedule for food.
Very high levels
at high saturation
rates.
Decreased rates
as a function of
CO beginning with
slight effects at
150 ppm
Decreased velocity
at both levels up
to 28 days but back
to normal at 90 days
-------
TABLE 10-1 (continued)
Reference
Species
Exposure
a
COHb
Dependent
Variable
Results
Comment
Grunnet-and
Petajan*3'
Shul'ga86a
2orn
115
o
i
i—»
en
Miller and
Wood52
Traystman
99
DobIan
et al.
Sokal88
26
Rat
Rat
n=24
Cat and
Rat
5-20 per
group
Rat
Dog
n=23
Goat
n=6
Rat
n=27-34
2500 ppm until
ventral nerve
conduction stopped
25 and 2 ppm for
8 hr/day, 10 wks.
100-700 ppm in
unanesthetized
animals
500 and 1000 ppm
in anesthetized
animals for 25 hr.
CO of various
amount to produce
target levels of
venous P^
CO of various
amount to produce
target levels of
venous PQ2
10,000 ppm, 4 min
and 4,000 ppm, 40
min
60-70%
2.5-50%
0-70%
50%
Peripheral nerve
pathology
Motor chronaxie,
CNS pathology, and
porphyrin levels
r02 and COHb in
brain and liver
r02 and COHb
in brain and liver
Degenerated Schwann Very high levels
cell, regenerated at high saturation
14-21 days rates.
25 ppm increased CNS damage and for
chronaxie, depressed
porphyrin and not quantitatively
produced CNS gross documented.
pathology
p
Qy decreased at
a linear function
of COHb at same
rates for brain and
liver
p
Qy decreased more
for liver than brain
Cerebral blood flow Flow increased as
COHb increased
Cerebral blood
flow
Glucose, pyruvate,
lactate and blood
pH levels in brain
Flow increased as
COHb increased
Increases in all
levels except
decrease blood pH
Slow saturation rate
produced more extreme
effects.
-------
TABLE 10-1 (continued)
Reference
Norton ..and
Species
Rat
Exposure3 COHb
1000 ppm until
Dependent
Variable
CNS pathology
Results
Ultrastructural
Comment
Culver"0,
Norton et al.
Dog
Ginsberg and
Myers
o
I
Theodore
et al. *
Dykyk
et al.
Eckardtn
et al . 3U
Fechtec and
3^ 3d
Rhesus
Monkey
n=9
(pregnant
females)
Monkey
n=9
Dog, n=16
Rat, n=136
Mouse, n=8Q
Rat
(Mothers
n=28,
Fetuses
n=32,
Neonates
n=24)
Cynomolgus
Monkey
n=27
Rat
n=16-32
pups
respiration stopped
50-100 ppm, various
times per day
(4-24) up to 6 wks.
3000 ppm to produce
60% COHb. Just
before delivery
400-500 ppm
168 days
7-12%
60%
Mothers exposed
to 100% CO for
60 min at term
32-38%
(dogs and
monkeys only)
Mothers 73.3%
Fetuses 10.3%
20 and 67.5
ppm, 22 hr/day
for 2 yr
150 ppm during full
term of pregnancy
2.0-5.5%
and
4.8-10.0%
15%
(maternal)
CMS pathology
CNS pathology in
offspring
CNS pathology
Qy consumption
by reticular forma-
tion giant cells.
Histology exams
CNS histo-
pathology
Brain chemistry
evidence for
brain damage
Brain lesions of
various types
similar to CO
poisoning but
more localized
Ranged from severe
brain damage to no
effects
No effects
COHb levels lower
than would be ex-
pected from
exposure level.
COHb in fetuses
did not nearly
approach that of
mothers'.
Increased 4-fold in
fetus. Decreased in
mothers. No histo-
logical differences
No effects
Reduced dopamine
and brain protein
COHb varied
unusually widely.
-------
TABLE 10-1 (continued)
Reference
Species
Exposure*
COHb
Dependent
Variable
Results
Comment
Millet and
Wood52
Szumanska
et al.
Rat
Rat
500 and 1000 ppm
for 2.5 hr.
100% CO for 20, 60,
and 90 min.
33-52%
Brain chemistry
Brain chemistry
Reduced energy
metaboli sm
Reduced noradrena-
lin and catechola-
mine levels. Recov-
ered later
Smaller than
predicted from
theory.
Newby
et al.
Rat
1000 ppm, 4 hrs.
Brain chemistry
Popamine synthesis
rate decreased,
noradrenalin did not
I >^ o _
-------
depending on the species and test employed. In learning and performance
the effect of the particular task being performed appears to be critical,
3
with simple tasks affected above 174 mg/m (150 ppm), but more complex
3
or demanding tasks not being affected until 575 to 690 mg/m (500 to
600 ppm). The effects of CO on learning might have varied among studies
as shown in Table 10-1 due to factors other than complexity of task or
contingencies on performance but these seem to be major variables.
Electrophysiological measures in the CNS seem to provide highly variable
data with only two studies by the same group showing consistent effects
below 500 ppm. Methodological differences were very great in electro-
physiological studies and in any event, results are not as clearly
related to function as are behavioral data. Only one study measured
fifia
peripheral nerve activity at very low levels of CO, and that study
should be replicated. Cerebral blood supply measures seem to indicate a
close relationship between tissue PO« and COHb levels despite the fact
that cerebral blood supply is increased by COHb increases. At higher
levels of COHb, brain damage and alterations in brain chemistry are
reported.
The results reviewed in this document would be more easily inter-
pretable if the general quality of experimental procedures, design, and
analysis were improved. In none of the studies for instance was the use
of blind analysis reported. This is important because (1) the handling
of animals can influence the results of some experiments and
(2) unfortunately, the data are sometimes treated only qualitatively.
In some of the studies, appropriate control groups were not run.
Sometimes COHb levels were not reported.
10-18
-------
An almost universal problem was the use of inappropriate statistical
tests such as the use of multiple t-tests where analysis of variance was
appropriate, or the use of univariate analysis where multivariate analysis
should have been used. This kind of misuse of tests usually leads to
underestimated p-values and hence to overestimates of the number of
effects declared significant. From the statistical consideration alone
one would be led to suspect that the effects of CO are less extreme than
reported in the literature but, fortunately, most authors obtained
results which were still significant when conservative corrections were
applied by the reviewer.
For many studies, it is difficult to answer such basic questions as
the number of subjects run, the statistical method used, the exact
experimental designs employed, etc. An effort has been made in this
literature review to interpret the results from a consistent framework.
Despite problems with the literature, the conclusions reached in
this summary are based upon fairly solid ground. Apparently the simpler
behavioral tasks and general activity yield the lowest thresholds for CO
3
effects; these appear at about 115 to 230 mg/m (100 to 200 ppm) for
times long enough to approach saturation.
10.4 CARDIOVASCULAR SYSTEMS
The various tissues of the body must receive 0« at a rate adequate
to maintain their normal function. Carbon monoxide, when present even
at very low partial pressures, can seriously impair the Op transport
system. Experimental studies of animals have provided insights into the
mechanisms by which CO modifies cardiovascular functions. The presence
10-19
-------
of COHb interferes with tissue oxygenation by increasing the concentration
of carboxymyoglobin (COMb). The ratio of COMb to COHb can increase from
1.0 to 2.5 in skeletal muscles and myocardium if the arterial 0^ tension
is 40 torr or lower.
10.4.1 Cardiac Performance and Damage
34
Fusco et al . found abnormal electrocardiograms (EKG) and changes
in ventricular and arterial pressures in dogs exposed to CO. Lewey and
RD
Drabkin and Enrich et al. exposed dogs to 115 mg/m (100 ppm CO; 20
percent COHb) for 11 weeks, 5-3/4 hours per day, and showed EKG
abnormalities, cardiac hypertrophy, muscle degeneration and necrosis.
53 3
Lindenberg et al . exposed dogs to 58 and 115 mg/m (50 and 100 ppm CO;
2.6 and 5.5 percent COHb) CO continuously and intermittently, seven days
a week for six weeks, and observed abnormal EKGs in all dogs and histo-
logical evidence of cardiac muscle degeneration in some subjects.
83
Effects were more pronounced at the higher exposures. Preziosi et al.
3
exposed dogs continuously to 115 mg/m (100 ppm) for six weeks and
reported abnormal EKG, right and left heart dilation, and myocardial
thinning. Histologic examination showed old scarring in some cases and
fatty degeneration of heart muscle in others. Carboxyhemoglobin levels
of 7 to 12 percent were lower than would be predicted from the exposure.
66 3
Musselman et al . exposed their dogs to 58 mg/m (50 ppm) CO for 24
hours a day, seven days a week for three months. No changes in the
electrocardiogram or heart rates were observed. Examination of organs
and tissues revealed no pathological changes after exposure.
10-20
-------
Monkeys (Macaca irus) were exposed to 288 mg/m (250 ppm; 20.6 per-
cent COHb) CO for two weeks by Thomsen. In all animals so exposed,
the coronary arteries showed more or less pronounced widening of the
subendothelial spaces in which cells with or without lipid droplets were
accumulating. He suggested that monkeys were more sensitive to CO than
4 30
the rabbits studied by Astrup et al. Eckardt et al. exposed
cynomolgus monkeys (22 hours a day, seven days a week for two years) to
3
23 or 77.5 mg/m (20 or 67.5 ppm) CO. Carboxyhemoglobin levels showed
considerable variation during the experimental period, from 2.0 to 5.5
percent and 4.8 to 10.2 percent for low and high CO ambient environments,
respectively. No cardiac effects were noted at these low levels.
78 79
Penney et al. ' studied the influence of CO on the development of
cardiac hypertrophy in the rat. Exposure to various CO levels of 115 to
575 mg/m (100 to 500 ppm) for 20 to 46 days, leading to COHb levels of
9.2 to 41 percent, resulted in hypertrophy of both right and left
90
ventricles. Stupfel and Bouley exposed mice and rats for 95 hours per
o
week to 58 mg/m (50 ppm) CO for either one to three months or for their
natural life expectancy of up to two years. They made a large number of
measurements during exposure, in addition to pathological examination
after death. They observed no important effects of the CO exposure on
their animals.
97 3
Thomsen and Kjeldsen exposed rabbits to 58, 115, and 207 mg/m
(50, 100 and 180 ppm; 4.5, 9.0, and 17.0 percent COHb) CO and demonstra-
3
ted aortic focal intimal lesions beginning at exposure levels of 207 mg/m
A C O
(180 ppm) for four hours. Kjeldsen et al., exposing rabbits to 207 mg/m
10-21
-------
(180 ppm) CO for two weeks (16.7 percent COHb), reported degenerative
changes such as contraction bands, myofibrillar disintegration, myelin
body formation, and dehiscence of the intercalated disks. Thomsen and
96
Kjeldsen determined the threshold for such effects to be about
3
115 mg/m (100 ppm) for four hours (8.5 percent COHb).
Cardiac hypertrophy was demonstrated by Tumasonis and Baker in
3
chick embryos which had been exposed to 490 mg/m (425 ppm; 25.4 percent
COHb) for 144 and 168 hours. Using a wide variety of animals exposed to
3
460 to 575 mg/m (400 to 500 ppm) CO (approximately 32 to 38 percent
94
COHb in dogs and monkeys) for 168 days, Theodore et al. was unable to
demonstrate any cardiac abnormalities.
10.4.2 Cardiac Fibrillation Threshold
3
Continuous exposure of cynomolgus monkeys to 115 mg/m (100 ppm;
12.4 percent COHb) CO for three to six months resulted in demonstrable
electrocardiographic effects in both normal monkeys and monkeys with
21 23
myocardial infarction. * These investigations also considered the
22
susceptibility of the ventricles to induced fibrillation. Normal and
3
infarcted monkeys were exposed to 115 mg/m (100 ppm) CO for six hours.
The voltage required to induce fibrillation was highest in monkeys
exposed to normal air and lowest for infarcted animals breathing CO.
Animals with either infarction alone or CO alone each required signifi-
cantly less voltage for fibrillation and when the two were combined, the
effects were additive. In contrast with these findings it has been
3
shown that as a result of intermittent exposure to CO (575 mg/m (500 ppm),
six-minute pulses of CO each hour for 12 hours each day over a period of
10-22
-------
14 months), cynomolgus monkeys fed either a normal or a semipurified
cholesterol diet, did not show myocardial infarctions or electrocardio-
graphic abnormalties. In these animals, blood COHb reached 21.6
percent at the end of the daily period. Aronow et al. observed in a
blind randomized study that 21 dogs with acute myocardial injury had a
o
reduction in ventricular fibrillation threshold after breathing 115 mg/m
(100 ppm) CO for two hours (6.3 percent COHb).
10.4.3 Cholesterol and Sclerosis
4 5
Astrup et al. ' reported data showing increased aortic cholesterol
7 q
accumulation and atheromatosis in rabbits exposed to 196 mg/m (170 ppm)
CO for eight weeks and then to 350 ppm for two more weeks (17 to 33 per-
104
cent COHb). Webster et al., using squirrel monkeys, found no effects
}
on aortic or carotid vessels nor on serum cholesterol, but did note a
greater incidence of coronary atherosclerosis in groups exposed to
115 to 345 mg/m (100 to 300 ppm; 9 to 26 percent COHb) CO on an inter-
mittent schedule for seven months. Essentially identical results as
found by Webster et al. were reported by Davies et al. using rabbits
exposed intermittently for 10 weeks to CO concentrations to produce
cc
20 percent COHb. Mali now et al. reported no aortic or coronary athero-
sclerosis in cynomolgus monkeys exposed on an intermittent schedule for
14 months so as to produce daily accumulations of 21.6 percent COHb.
89
Stender et al., in Astrup's group, attempted to resolve the
apparent conflict in the above studies, regarding aortic atherosclerosis,
o
by exposing rabbits to 230 mg/m (200 ppm) CO continuously for 12 hours
per day for six weeks. Instead of using a constant high cholesterol
10-23
-------
diet for all subjects, the serum cholesterol was held constant by
variations in diet cholesterol. In this case, no aortic cholesterol or
atherosclerotic differences were seen between CO-exposed and control
groups. In reference to earlier results, Astrup et al. now interpret
these data to mean that observed damage in earlier studies was attributa-
ble to greatly increased serum cholesterol in CO groups, although Davies
et al., Webster et al., and Mali now et al. reported no increased
serum cholesterol either. Differences in cholesterol buildup in aortic
tissue (due to CO exposure) might be related to observed differences due
to CO exposure in lactate dehydrogenase (LDH) enzymes in rabbits, as
OO ~JQ ~?Q
observed in the aorta and by Hellung-Larsen et al. Penney et al. '
also reported increased LDH in rats. However, in the most recent studies
by Astrup's group (Hugod et al. a), non-cholesterol-fed rabbits exposed
only to CO (six weeks at 150-200 ppm or for 201-304 minutes at 2000-
4000 ppm) showed no evidence of histotoxic effects on intimal/subintimal
morphology of coronary arteries or aorta. The weight of evidence suggests
that there is doubt as to the relationship between CO exposure and
atherosclerosis.
10.4.4 Coronary Blood Flow
Carboxyhemoglobin increases result in an increased coronary blood
flow (CBF).1'7'8'40'112 This increase in CBF as a function of COHb is
apparently not sufficient to prevent a reduced 0« supply even at COHb
levels as low as 4 percent. a This partly compensatory response is not
affected by autonomic nervous system blockage and is not mediated by
heart rate, but is apparently due to auto-vasodilatory activity.
Increased CBF in response to COHb was no longer observed in atrioven-
tricular-blocked dogs being maintained by a pacemaker (Horvath ).
10-24
-------
10.4.5 Hemoglobin
Carbon monoxide apparently induces increases in Hb which to an
unknown extent compensate for reduced availability of Hb for 02 carrying.
78 79
Penney et al. ' showed increased Hb levels in rats exposed to as
3
little as 115 mg/m (100 ppm; 9.2 percent COHb) CO continuously, which
began early in the exposure period and reached an asymptotic value by
about 30 days of exposure. These results were similar to those reported
VI O /"*/""
by Jones et al. using rats, and by Mussel man et al. using dogs con-
3
tinuously exposed to 58 mg/m (50 ppm) CO for three months. Theodore
94 3
et al. used monkeys and dogs continuously exposed to 460 to 575 mg/m
(400 to 500 ppm) CO for 168 days and showed increased Hb levels which
reached asymptotic values at about 30 days but which began to decline
toward control values at about 140 days. This might represent a failure
of the compensatory Hb increases after very long exposures, but further
41
study is needed to reach such a conclusion. Jaeger and McGrath exposed
3
Japanese quail to 345 to 403 mg/m (300 to 350 ppm; 30 percent COHb) CO
for 28 days and observed increased hematocrit, Hb, plasma volume and
blood volume. They also noted right ventricle hypertrophy. Baker and
Q
Tumasonis reported vascular hypertrophy in chick embryos after 18-day
3
exposure of eggs to 490 mg/m (425 ppm; 6.15 percent COHb) CO.
Apparently, continuous exposure to CO is needed to show increased
83
Hb levels at lower CO exposures. Preziosi et al. using dogs exposed
to 58 and 115 mg/m3 (50 and 100 ppm; 7 to 12 percent COHb) CO on various
intermittent schedules for six weeks, reported no effects. A group of
3
four dogs exposed to 115 mg/m (100 ppm) continuously for six weeks also
10-25
-------
90
did not show effects. Stupfel and Bouley, using rats and mice exposed
3 30
to 58 mg/m (50 ppm) CO intermittently for two years and Eckhart et al.
3
using monkeys exposed intermittently to 23 and 77.5 mg/m (20 and
67.5 ppm; 2 to 10 percent COHb) did not demonstrate any COHb increases.
35 54 84
Gasaskina, Ljublina, and Rylova, using rabbits, guinea pigs, rats
3
and mice exposed for long periods to 58 mg/m (50 ppm) did not find any
43a
blood morphology changes. Kalmaz et al. exposed rabbits to 50 ppm CO
for eight weeks and found no change in Hb concentration. However, they
did find increased fibrinolytic activity consequent to the CO exposure.
The report may be subject to considerable doubt since their animals,
when exposed to ambient air, had COHb levels of approximately 5 percent
and their CO-exposed (50 ppm) animals had unbelievably high COHb levels —
in excess of 30 percent.
Alterations in Hb have been reported for short-term CO exposures as
well as long-term studies. Ogawa et al. report that in dogs a 30-
3
minute exposure to 690 mg/m (600 ppm; 58.2 percent COHb) CO produced a
decrease in plasma volume resulting in hemoconcentration. They attribu-
ted the plasma decrease to an increase in vascular permeability.
92 3
Syvertsen and Harris, using 224 mg/m (195 ppm) CO for 72 hours
(30 percent COHb), also reported increased Hb but attributed their
findings to increased erythropoiesis. The latter study, which used
intermediate durations of exposure, probably suggests early Hb compen-
sation similar to the long-term findings.
10-26
-------
10.4.6 Summary and Conclusion of Cardiovascular System in Experimental
Animals
Table 10-2 shows a summary of all of the reviewed studies pertinent
to experimental animals and cardiovascular systems. From these data it
may be concluded that under most circumstances EKG abnormalities may be
o
noticed after relatively long-term intermittent exposure to 115 mg/m
(100 ppm; 8 to 13 percent COHb) CO and sometimes, depending upon the
3
species, exposure regimen, etc., as low as 58 mg/m (50 ppm; 4 to
7 percent COHb) CO. Various signs of cardiac damage are found at
similar levels.
Decreased thresholds to electrically induced fibrillation have been
3
demonstrated at CO levels as low as 115 mg/m (100 ppm; 6 to 12 percent
COHb) CO in exposures as short as two hours, but these findings are not
universal. It is almost universally demonstrated that when experimental
animals are fed high cholesterol diets, they develop increased coronary
atherosclerotic damage if they are exposed to CO levels as low as 115 to
3
230 mg/m (100 to 200 ppm; 9 to 18 percent COHb). These exposures were
made on long-term, intermittent schedules. Findings of similar increased
damage in the aorta are in greater dispute but have also been reported
3
with exposures to CO as low as 196 mg/m (170 ppm; 17 percent COHb).
Apparently such damage, and perhaps other atherosclerotic findings, are
due to CO- induced alterations in serum cholesterol and LDH alterations.
As reported for CNS structures, coronary blood flow apparently is
increased by vasodilation, when CO is present, but this increased flow
rate is not sufficient to entirely compensate for the reduced 02 supply -
10-27
-------
TABLE 10-2. SUMMARY OF EFFECTS OF CARBON MONOXIDE ON CARDIOVASCULAR SYSTEMS OF ANIMALS
Reference
Species
Exposure*
COHb
Dependent
Variable
Results
Comment
Lewey a
Drabkin
Erich
et al.
31
o
i
ro
00
Lindenberg
et al.
Preziosi
et al.83
Musselgan
6 w 3 I *
Thomsen
95
Dog
n=4-6
Dog
n=12
Dog
n=46
Dog
n=4
Macaca
irus
monkey
n=20
100 ppm for 11 wks. 20%
for 5-3/4 hr./day
EKG and cardiac
pathology
50-100 ppm for 6 wks. 2.6-5.5%
intermittently and
continuously
50-100 ppm for 6 wks. 7-12%
on various daily
schedules
EKG and pathology
EKG and pathology
50 ppm for 3 mo.
continuously
250 ppm
continuously
for 2 wk.
20.6%
EKG, heart rate
Cardiac
pathology
Some subjects
showed abnormal
EKG, most showed
increased heart
size, muscle
degeneration,
necrosis
Abnormal EKG,
changes in right
ventricular and
arterial pressures
Abnormal EKG,
heart dilation,
myocardial thinning,
some subjects
showed scarring and
degeneration in
heart muscle
No effects
Widening of
subendothelial
spaces of coronary
arteries with
accumulation of
cells with and
without lipid
droplets.
COHb levels were
low for exposure
levels used
Very smal1 n
Lipid-laden
cell findings
indicate greater
sensitivity of
monkeys than
in rabbits (22)
-------
TABLE 10-2 (continued)
o
IN3
Reference
Eckhardt
et al.
Penney?ft 7q
et al.78'79
Species Exposure3
Cynomolgus 20 and 67.5
monkey ppm, 22 hr./day
n=27 for 2 yr.
Rat 100 ppm, 46 days
n=32 200 ppm, 30 days
500 ppm, 20-42 days
COHb
2.5 to 5%
and
4.8-10%
9.2%
15.8%
41.1*
Dependent
Variable
Cardiac
fibres is
Heart size
Results
No effects
Hypertrophy of
both left and
right ventricles
Comment
Unusually wide
variation in COHb
Also studied
hypoxic hypoxia
and lactate
dehydrogenase
i sozyme
Stupfelftand
Bouley*u
Thomsen and
Kjeldsen
Tumasonis
and Baker
,m
lul
Rat
n=336,
mouse
n=767
Rabbit
n=61
Kjeldseo
et al.
Thomsen and
Kjeldsen*0
Rabbit
n=16
Rabbit
n=42
Chick
embryo
50 ppm, 95 hr./wk.
whole natural life
expectancy up to
2 yr. (also short
term)
50, 100 and 4.5%
180 ppm for periods 9.0%
ranging from 30 17.0%
min - 24 hr.
180 ppm, 2 wks. 16.7%
50, 100, and 180 4.5%,
ppm for 2-48 hr. 8.5%,
17.0%
425 ppm for 144 25.4%
and 168 hrs.
EKG, organ
weights
No effects
Aortic damage
Myocardial ultra-
structure
Myocardial
ultrastructure
Cardiac size
Increased
focal intimal
lesions at
180 ppm, 4 hrs.
Signs of myocardial
damage
Ultrastructural
damage threshold
of 100 ppm for
4 hr.
Cardiac
hypertrophy
Also showed no
effects on other
variables
Blind study
-------
TABLE 10-2 (continued)
Reference
Theodogg
et al.
Species Exposure3
Monkey 400-500 ppm for
n=9, 168 days
Baboon
n=3,
Dog
n=16,
Rat
n=136,
Mouse
n=80
COHb
32-38%
(dogs and
monkeys
only)
Dependent
Variable
Cardiovascular
damage
Results Comment
No changes except
slight hypertrophy
in rat heart
DeBias
et al.
91
CO
o
Mali now/-
et al.56
Aronow
et al.
3a
Astrup.
et al.
Cynomolgus 100 ppm for 24 wks
Monkey 23 hr. per day
n=52
Cynomolgus 500 ppm, 6 min
Monkey pulses with a
n=26 24 min declining
washout. Pulsed
1/hr., 12 hr./day
for 14 mo.
12.4%
Dog
n=21
100 ppm, 2 hr.
21.6%
at the
end of
12 hr.
period
6.3%
EKG and suscepti-
bility to induced
fibrillation
EKG and fibrilla-
tion threshold
Abnormal EKG and
increased sensiti-
vity to fibrilla-
tion voltage
No effects
Infarcted animals
showed greatest
effect of COHb
on both dependent
variables.
Used subject on
normal and high
cholesterol diets
Rabbit
n=24
170 ppm for
8 wks., then
350 ppm for last
2 wks.
17-33%
Ventricular
fibrillation
threshold in
subjects with
acute myocardial
injury
Cardiovascular
pathology
Reduced
threshold
Conducted blind
study
1. Increased aortic
atheromatosis and
cholesterol
2. Local degenera-
tive signs and
hemorrhages in hearts
-------
TABLE 10-2 (continued)
Reference
Species
Exposure3
COHb
Dependent
Variable
Results
Comment
Astrup,-
et al.
GO
Davies
et al.
9ft
20
Maii nowc
et al.56
Stende£Q
et al.89
Squirrel 100-300 ppm
Monkey 4 hr./day, 5 days/wk.
n=22 for 7 mo. using
a gradually increas-
ing exposure until
3 mo. then reduce to
250 for 4 mo.
Rabbit Low exposure for
n=24 8 wks., higher
exposure for last
2 wks.
Rabbit 4 hr./day,
n=24 7 day/wk.,
10 wks.
9-26%
15%
and 30%
20%
Cynomolgus 500 ppm, 6 min
Monkey pulses with a 24 min
n=26 declining washout,
pulsed 1 per hour,
12 hr./day for 14 mo.
Rabbit 200 ppm continuously
n=30 and 12 hr./day for
6 wks.
21.6%
at end
of 12
hr. period
17%
Atherosclerosis
in various cardiac
structures plus
serum cholesterol
Aortic
cholesterol
Blood cholesterol
and cardiovascular
pathology
Aortic and
coronary
atherosclerosis
Cardiovascular
pathology
Increased coronary
atherosclerosis but
no effects on
serum cholesterol,
aortic and carotid
atherosclerosis
Increased
in CO exposed
groups
Increased
atherosclerosis
in coronary
artery but no
aortic differences
or plasma choles-
terol differences
No effects
No differences
in atherosclerosis
but CO produced
higher serum
cholesterol levels
Subjects were
on high cholesterol
diets.
Study used
cholesterol
animals.
fed
Study disagrees
with Astrup
et al.
This study used
subjects on high
and low choles-
terol diets.
Disagrees with
Astrup et al.
In this study
serum cholesterol
was controlled by
individual adjust-
ments of diet.
Apparently coronary
atherosclerosis in
(17) was caused
by increased
serum cholesterol.
-------
TABLE 10-2 (continued)
Reference
HellungrLarsen
et al . 38
Species
Rabbit
n=16
Exposure3
170 ppm-550 ppm
In ascending
levels for 5-11
COHb
15-35%
Dependent
Variable
Lactate
dehydrogenase
enzymes LDH
Results
LDH increases
In aortic arch
Comment
Penney7ft ,q
et al.78'79
Ayres
et al.
7,8
Rat
n=32
Dog
n=40
o
oo
Horvath
40
Dog
n=5-7
Young., and
StoneAA*
Dog
Adams
et al.
la
Dog
n=10
days
100 ppm 46 days
200 ppm 30 days
500 ppm 20-42 days
50,000 ppm for 30-
120 sec. and
1000 ppm for 8-15
min.
9.2%
15.82%
41.12%
LDH
CBF
Single dose of CO
to produce desired
COHb (3 levels)
6.2-35.6%
CBF
1000 ppm until
saturation reduced
30%
CBF
1500 ppm for
30 min.
CBF
LDH increases
due to CO
exposure
Increased CBF with
COHb
Increased CBF
with COHb
Increased CBF
with COHb even
when heart rate
paced at 150 beats
per min. or with
blocked autonomic
nervous system
CBF increased as
linear function of
COHb
Also studied humans
the results of
which agree with
dogs except dogs
were more resist-
ant to COHb
below 25%.
Atri oventri cular
blocked dogs,
maintained by
pacemaker, did not
show this effect.
CBF increase was
not enough to
compensate for
increased energy
expenditure.
-------
Reference
Jones .0
, 43
et al.
2^78.79
Theodore
et al.
Mussel man
DO
et al.
Preziosi
et al.
Stupfelnand
Bouleyyu
Species
Rat
n=35,
Guinea
pig
n=35,
Monkey
n=9,
Dog
n=6
Rat
n=32
Monkey
n=9,
Dog
n=16
Dog
n=4
Dog
n=46
Rat
n=336,
Mouse
n=767
Exposure3
51, 96 and 200 ppm
for 90 days
,
100 ppm 46 days
200 ppm 30 days
500 ppm 20-42 days
400-500 ppm for
168 days (contin-
uous)
50 ppm for
3 mo. continuous
50 and 100 ppm
for 6 weeks on
various intermittent
daily schedules
50 ppm for
90 hr./wk.
up to 2 yr.
TABLE 10-2
COHb
3.2-6.2%
4.9-12.7%
9.4-20.2%
dependi ng
upon species
9.20%
15.82%
41.12%
32-38%
7-12%
(continued)
Dependent
Variable Results
Hb levels Increases in
rats at both
exposure levels
Increases in
all animals at
200 ppm
Hb levels Increased even
at 100 ppm
levels
Hb levels and Increased Hb
blood volume and blood volume,
slight decrease
toward control
values after 140
days
Hb, hematocrit and Increased
red cell counts
Hb level No effects
Hb level No effects
Comment
Increased Hb in
rats at 96 ppm
was larger than
at 200 ppm.
About 30 days
until Hb
approached
asymptotic values
About 30 days
until Hb
approached
asymptotic values
-------
TABLE 10-2 (continued)
Reference
Eckhardt
et al.
Species
Cynomolgus
Monkey
n=27
Exposure3
20 and 67.5 ppm,
22 hr./day,
for 2 yr.
COHb
2-5.5%
and
4.8-10.0%
Dependent
Variable
Hematocrit, Hb
and erythrocyte
counts
Results
No changes
Comment
Unusually wide
variation in COHb
Ogawa 7,
et al.
Syvertsen and
Harris^
Dog
n=16
Dog
n=12
Jaeger
McGrath
Quai 1
n=40
Baker &
Tumasonis
Chick
embryo
n=90
6000 ppm for 30 min. 58.2%
195 ppm for 72 hr.
~30%
300-350 ppm
for 28 days
continuous
30%
425 ppm during
first 18 incu-
bation days
6.15%
Plasma volume
Hematocrit and Hb
Hematocrit, Hb,
plasma, blood
volume, heart
size fasting
glucose and
carbohydrate
stores
Decreased due to
CO
Increased concen-
trations but
inferred no
increase in plasma
volume
Hematocrit, Hb,
plasma and blood
volumes increased.
Right ventricle
hypertrophy.
Higher fasting
glucose muscular
carbohydrate.
Probably due to
increased vascular
permeability see
Parving et al.
Attributed change
to increased
erythropoiesis
Vascular structure, Vascular hypertrophy,
Lactate dehydrogen- increased lactic
ase & serum albumin dehydrogenase &
serum albumin.
-------
Needless to say, these findings are not as consistent with all investi-
gators as might be desired. It is difficult to resolve the disagreement,
in most cases, because of differences in exposure regimens, experimental
animal species and analytic techniques, to name but a few of the common
problems of comparison. Studies utilizing bolus concentrations represent
"real world" conditions. Animal subjects are at risk to myocardial
effects for several minutes after exposure.
Long-term exposure to continuous low concentrations of CO produces
increased Hb beginning about 72 hours after exposure and maximizing at
3
58 to 115 mg/m (50 to 100 ppm) in about 30 days. Short-term increases
in hemoconcentration are apparently due to reduced plasma volumes.
Despite the problems in the literature and the heterogeneity of
reported results, it seems safe to conclude that cardiovascular damage
can be demonstrated to occur as a result of long-term, intermittent
3
exposure to CO concentrations as low as 58 to 115 mg/m (50 to 100 ppm).
These results contrast with neuro-behavioral data, which were usually
collected from short-term exposures and which demonstrated certain
3
functional deficits which occur at CO levels as low as 115 to 230 mg/m
(100 to 200 ppm). It would seem advisable to design studies that provide
more short-term exposures during cardiovascular tests and more long-term
results in neuro-behavioral data.
10.5 OTHER DEPENDENT VARIABLES
10.5.1 Feeding, drinking, and body weight
Koob et al.47 using two strains of rats exposed to 288, 575, and
1150 mg/m3 (250, 500, and 1000 ppm) CO for 24 hours, showed decreased
10-35
-------
food and water intake and decreased weight gain during the exposure
32 33
period. Fechter and Annau * reported slightly lower weight gains in
3
rats whose mothers had been exposed to 174 mg/m (150 ppm; 15 percent
94
COHb) CO during full term of pregnancy. Theodore et al. noted no
significant body weight effect in rats exposed for 168 days to 460 to
3
575 mg/m (400 to 500 ppm) CO, but the rats were apparently somewhat
47
more mature than those of Koob et al. No significant weight, feeding
or drinking effects were noted in three other studies: (1) Musselman
66 o
et al. using rats, rabbits, and dogs exposed to 58 mg/m (50 ppm) for
three months, (2) Campbell, who exposed rats to 3450 mg/m (3000
90
ppm) for a total of 300 days, and (3) Stupfel and Bouley, using rats
and mice exposed intermittently for periods ranging from one month to
two years. Since the only study which showed marked effects on weight
and intake was a short-term exposure, it is not possible to conclude
that weight gain and intake are affected by CO exposure, except possibly
in the early stages of exposure and possibly only in growing organisms.
10.5.2 Biochemical Effects and Drugs
72 74
Pankow et al. ' injected CO subcutaneously in rats to produce
COHb levels of 40 percent to 50 percent and showed that only the higher
dosage increased leucine aminopeptidase activity in the liver after a
single injection. Forty injections of the dose producing the lower COHb
over a period of 53 days also produced an enlarged liver. Martynjuk and
CO
Dacenko showed increased aspartate and alanine aminotransferase
3 49
activity after only 20 mg/m (17 ppm). Kustov et al. exposed rats to
3
58 mg/m (50 ppm) and showed depressed cytochrome oxidase activity and
10-36
-------
increased succinate dehydrogenase activity in liver. The latter two
studies indicate general hypoxic effects.
91
Sweicicki exposed rats to CO and noted that an increase in
adrenergic system activity produced an increased carbohydrate metabolism.
Such metabolic alterations could explain weight changes if such changes
were verified.
CO o
Montgomery and Rubin exposed rats to 288 to 3450 mg/m (250 to
3000 ppm) CO for 90 minutes in several groups (20 to 60 percent COHb)
and then injected two dissimilar drugs (hexobarbital and zoxazolamine).
3
They showed that CO exposure prolonged zoxazolamine effects at 288 mg/m
(250 ppm) CO and hexobarbital effects at 1150 mg/m3 (1000 ppm) CO.
10.5.3 Miscellaneous
oc o
Schwetz et al. exposed pregnant rabbits and mice to 288 mg/m
(250 ppm) CO for either 7 or 24 hrs./day for days 6 to 18 and 6 to 15 of
gestation. No statistically significant differences in the number or
extent of skeletal birth defects were noted.
10.5.4 Summary and Conclusions of Other Dependent Variables in
Experimental Animals
Table 10-3 presents a summary of findings regarding CO and various
other dependent variables.
The data regarding feeding, drinking, and body weight suggest the
possibility of a short-term effect at 288 mg/m (250 ppm) CO levels but
definitely show no long-term effects. Since only one study showed
short-term weight loss, this finding should be viewed with caution.
Even if verified, short-term (24 hours) alterations in feeding and
10-37
-------
TABLE 10-3. SUMMARY OF CO EFFECTS UPON METABOLISM
'l
Reference Species
Koob
et al. '
Fechtec &,
Annau^'**
,_. Theodore
? et al.94
CO
<»
Musselgan
ex a i .
Campbell145
Rat
n=36
Rat
n=16-32
Rat
N=136
Rat
n=100,
Rabbit
n=40,
Dog
n=4
Rat
N=36-45
Exposure3 COHb
250, 500, and
1000 ppm for 24 hr.
150 ppm during full 15%
term of pregnancy (maternal)
400-500 ppm for
168 days
50 ppm for 3 mo.
Gradually increasing
exposure reaching
Dependent
Variable
Food & water intake
and weight
Body weight
of offspring
Body weight
Body weight
Body weight
Results
Decreased intakes
during exposure,
less weight gained
Nearly same at birth
but gained at
slightly lower rate
CO group had
slightly lower mean
but not significant
No CO effect
Slightly fewer gains
during 1st 100 days
Comment
True for 2
strains of rat.
Related to cate-
cholamine findings
200 g. starting
weight.
Differences
were very small
240 g. Starting
weight
1. No Signifi-
cance tests
3000 ppm at 100 days
intermittent exposures
and then increased
gain in last 200 days differences
and slight
1st 100 days
represented
normal rapid
growth phase.
Stupfelft&
Bouley30
Rat
n=336.
Mouse
50 ppm for 95 hr/wk
for whole natural
life up to 2 yr.
Also 1-3 mo exposure
groups
Body weight,
food & water
intake
No effect due
to CO
-------
TABLE 10-3 (continued)
Reference
Species
Exposure9
COHb
Dependent
Variable
Results
Comment
PanRow
Ponsold
,73
Martynjuk &
Dacenko °
o
i
CO
Kustov
et al.
49
Swiecicki
Pankow &
Ponsold;
Pankow
73
et al.
73a
Rat Subcutaneous injec-
n=20-30 tion of 7.2 and 9.6
mMol/kg, CO.
40 injections in
53 days
Rat
17 ppm
Rat 50 ppm
n=92
Rat CO exposure
combined with 1%
ethanol.
@ 50%
1 hr after
injection
Leucine aminopep- Single 9.6 mMol/kg
tidase activity and injection increased
liver weight enzyme. Repeated
7.6 mMol/kg injections
increased enzyme
and liver wt.
Aspartate and „ Increased during
alanine aminotrans- Exposure
ferase activity
Cytochrome oxidase
and succinate dehy-
drogenase activity
in liver
Adrenergic system
Depressed cytochrome
oxidase
Increased succinate
dehydrogenase
COHb levels
stimulate system
Increased
carbohydrate
metabolism
Montgomery &
Rubin155
Rat
n=10-20
per group
250-3000 ppm in
various groups for
for 90 min.
20-60%
Rates of metabolism
of hexobarbital and
zoxazolamine
Prologed response to
hexobarbital at 1000
ppm and to zoxazolamine
at 250 ppm.
-------
TABLE 10-3 (continued)
Reference Species
Schwetzfi Pregnant
et al . female
Mouse
n=35-48
Pregnant
female
Rabbit
n=20-21
Dependent
Exposure COHb Variable Results Comment
250 ppm for either 7 10-15% Skeletal malfor- No teratogenic
or 24 hr/day on days mations in pups effects due to
6-15 of gestation CO
As above on days
6-18
Conversion of ppm to mg/m :
multiply by 1.15 @ 25C, 760 mm Hg.
o
i
-------
weight maintenance per se are not particularly serious in an applied
sense.
Biochemical findings suggest that enzyme activities, etc., might be
measurably altered at extremely low levels of CO exposure but the impli-
cation of these findings to health effects is not clear, since the
findings in some cases are indicators of hypoxic effects which are known
from other data to exist. By themselves these data do not provide
information about health concerns. Taken in combination with other
findings, these data might be used as supplementary, explanatory results.
Extensions and verification of these findings should provide interesting
interpretive data.
CQ
The findings of slowed drug metabolism might have practical
import in terms of CO exposure of subjects who are also under medical
treatment with drugs or are under the influence of illicit drugs. The
findings in this area are only suggestive; thresholds need to be estab-
lished for a much wider range of drugs and animals.
There is a paucity of data regarding the effects on offspring for
other than cardiac or CNS effects. No skeletal birth defects were noted
at relatively high levels of CO.
10.6 INTERACTIONS WITH OTHER POLLUTANTS, DRUGS AND OTHER FACTORS
Many materials by themselves have no biological effect but if
combined with other substances, levels of exposure that do not by
themselves produce effects become harmful. The effects of CO have been
explored in only a preliminary fashion with respect to such interactions.
Carbon monoxide exposure frequently occurs in the natural environment in
10-41
-------
combination with other pollutants, noise, and drug exposures such as
therapeutic drugs or alcohol. Tobacco smoking raises COHb levels but
also has other effects which could act in combination with CO.
10.6.1 Other Pollutants
12
Busey exposed rats for 52 weeks to various concentrations of
airborne pollutants (N02, SOp, CaSO., PbClBr, and CO), the CO levels of
3
interest being 23 and 77 mg/m (20 and 67 ppm). No consistent pulmonary
function changes were seen in any of the groups exposed to one of these
pollutants alone or in combination with any other single pollutant.
Hematological and biochemical measurements remained within normal limits
13
in all groups. A similar study was made on cynomolgus monkeys which
were exposed continuously for 104 weeks. The CO concentrations were 22
3
and 75 mg/m (19 and 65 ppm). Although some effects were observed with
the CO and N0? combinations, it was reported that no firm conclusion of
3
any interaction was warranted. The combination of S02 (26.2 mg/m ; 10
3
ppm) and CO (17 ppm; 20 mg/m ) resulted in a significantly increased
osmotic fragility of erythrocytes.
Yamamoto exposed mice and rats to combustion products from
gauze-PAN (Polyacylonitrile) which were analyzed and shown to contain
3
between 920 and 17,020 mg/m (800 and 14,800 ppm) CO and between 209 and
435 ppm HCN, depending upon the intensities of exposure. He concluded
that CO and HCN did not have additive or synergistic effects on survival
rates. The effects of CO and CN on the circulation and metabolism of
81
the brain of anesthetized dogs were studied by Pitt et al . Cerebral
blood flow increased 130 and 200 percent when COHb levels were 30 and
10-42
-------
51 percent. Similar increments in flow were observed when blood CN~
concentrations were 1.0 and 1.5 M9/ml. When CO and CN~ were administered
simultaneously, cerebral blood flow increased additively. Cerebral
metabolism increased only at the higher levels of COHb and CN~ but, when
both substances at the lower levels were presented to the animal,
significant decreases in brain 02 consumption were found.
Murphy a demonstrated that COHb was about 5 percent higher after
3
simultaneous exposure to 345 mg/m (300 ppm) CO and 0.75 ppm 03 than
3
after 345 mg/m (300 ppm) CO alone in mice, guinea pigs, and rats
(25 percent vs. 30 percent COHb). Oda et al.70 did not detect any
effect of simultaneous CO and nitric oxide exposures of 460 ppm and
66 ppm, respectively, on the COHb of mice, beyond that expected due to
CO alone.
cc
Murray et al. exposed mice and rabbits to 25 and 70 ppm SOp,
3
respectively and simultaneously, to 288 mg/m (250 ppm) CO. They studied
teratogenic effects on offspring and found no reliable defects due to
exposure to either or both substances.
10.6.2 Drugs
Surprisingly little systematic work has been done on the interactions
of various drugs and CO. Pankow ' a observed that ethanol had additive
effects on some enzymes in combination with CO if COHb levels exceed
50 percent. McMillan60 noted that CO attenuated the behavioral effects
of d- amphetamine in a systematic dose-dependent way for CO levels as low
Q CO
as 575 mg/m (500 ppm). Montgomery and Rubin showed that the effects
10-43
-------
of two dissimilar drugs (hexobarbital and zoxazolamine) were prolonged
by CO exposure in rats.
10.6.3 Halogenated Hydrocarbons
Polybrominated and polychlorinated biphenyls are converted ijn vivo
14 84
to CO * or stimulate a catabolic process(es) that would produce CO.
The production of CO from dichloromethane (CH?C1«) was reported to be
mediated by an enzyme present in the microsomal fraction prepared from
39
hepatic tissue. These studies indicated a direct role of cytochrome
P-450 in this process. These observations are similar to those reported
2 25
by others. ' Dogs were exposed for two hours to 500, 1000, 2000, and
5000 ppm of CHCl. The rise in COHb was logarithmically related to
the CHpClp exposure concentration. Coronary blood flow increased 20 to
3
25 percent during all exposures above 573 mg/m . Arterial pressure and
myocardial contractility (dP/dt) increased with each concentration.
Heart rate was not influenced by CH^CK exposure but predisposed the
heart to arrhythmias. Interestingly, combined exposures to CO and
CHpClp showed that CH?C1« had no effect on the physiologic responses due
to CO, but CO antagonized the responses due to CH^Clp.
10.6.4 Other Variables
Temperature appears to affect the survival time of newly hatched
3
chicks exposed to 11,500 mg/m (10,000 ppm), with cooler temperatures
producing longer survival. No effort was made, however, to determine
whether cool temperatures might simply have slowed down physiologic
processes. Variables relating to body and/or environmental temperature
should be important but have not been systematically studied.
10-44
-------
Variables relating to the method for the administration of CO have
received little systematic attention. The uptake was shown to be
' 82 ^
important by Plevova and Frantik who exposed rats to 230 mg/m (200 ppm)
3
for 30 minutes and to 805 mg/m (700 ppm) for 24 hours. Both exposures
resulted in 20 percent COHb but the longer exposure produced more effect
on motor endurance. This study is not definitive, however, since the
24-hour group would have reached saturation in two to three hours, thus
spending more time at 20 percent COHb.
10.6.5 Conclusions About Interactions
Despite the paucity of data concerning CO and other substances and
conditions, there are enough data to indicate that such interactions
might well be of importance to health effects. Quite possibly some of
the commonly covarying pollutants and some of the commonly used drugs
(either therapeutic or otherwise) mjjjlxt interact additively or syner-
gistically to make extremely low levels of CO dangerous. This possibi-
lity is based not only upon preliminary evidence but is entirely within
the scope of reason on theoretical grounds. In view of the potential
importance of such work, it is surprising that more studies have not
been reported.
10.7 MECHANISMS
It has been generally assumed that the manner in which CO produces
deleterious effects is by reducing the O^carrying capabilities of
the blood. This view has been challenged in several ways, although
evidence is still very incomplete.
10-45
-------
10.7.1 Hypoxic Hypoxia and CO Hypoxia
If the effects of CO are limited to CO hypoxia, then CO effects
should be similar to the effects of hypoxic hypoxia, given that the
severity of the two hypoxias could be equalized. It is easy enough to
calculate 0« arterial blood levels for CO and hypoxic hypoxias and thus
equalize exposures at asymptotic CO saturation levels. It must be borne
in mind, however, that exposure to atmospheres with low 0« concentrations
produces a rapid reduction in arterial blood 0«, whereas with CO hypoxia
the reduction rate is much slower. Attempting to decide the equivalence
of the two hypoxias in short-term exposures is not a trivial task. In
long-term exposures where the equilibration process is a small proportion
of the exposure, equivalences can more easily be made.
92
Syvertsen and Harris exposed dogs to either simulated altitude
(18,000 feet) or to 225 mg/m (195 ppm) CO for 72 hours and showed that
Hb and hematocrit rose to nearly the same values by the end of the
period. These blood measures rose gradually for the high altitude
group, beginning almost immediately, but for the CO group began to rise
only after 48 hours. They also showed that erythropoietic levels
increased almost immediately for high altitude groups but did not begin
to increase until about 24 hours in the CO group. These differences can
probably be explained by (1) the differences in the early levels of
hypoxia being more extreme in the high altitude groups, and (2) the
chemosensory response to the high altitude condition. This is not,
therefore, evidence for some non-hypoxic effect of CO. It does, however,
appear that compensation for CO effects is not as fast as for hypoxic
hypoxia.
10-46
-------
7ft o
Penney et al. exposed groups of rats to 115, 230, and 575 mg/m
(100, 200 and 500 ppm) CO and to 18,000 feet simulated altitude for
periods of several weeks and showed that high altitude produced mainly
increased right ventricle weight, while CO produced overall heart weight
increases. The levels of arterial blood 0« in high altitude subjects,
however, would not have produced equivalent exposures nor were durations
of exposure the same, so that this result is difficult to interpret.
Winston and Winston and Roberts * showed that pre-exposure
of mice to 500 or 1000 ppm CO for four hours resulted in a significant
3
decrease in mortality resulting from a 2875 mg/m (2500 ppm) exposure
24 hours later. They also showed that the short pre-exposure did not
protect animals against hypoxic hypoxia. Their conclusion was that
108
selective redistribution of blood flow was responsible for their results.
3
Annau showed that rats exposed for about two hours to 1000 ppm at
first showed depressed lever press rates in a behavioral study, but
after the fourth day of repeated testing, the decrement in behavior
began to approach pre-exposure levels. In contrast a group of rats
exposed to 8 percent Op (hypoxic hypoxia) for about two hours recovered
to normal by the second day of repeated testing. This more rapid
recovery by hypoxic animals than by CO-exposed animals is at least a
control for possible practice effects.
Koob et al.47 exposed rats for 24 hours to air containing 16, 14,
and 10 percent 02 and to 288, 576, and 1152 mg/m (250, 500, and
1000 ppm) CO. They showed no differences between CO and lowered 02
groups in feeding, drinking and weight gain. This result implies that
10-47
-------
CO has no effects on these variables other than hypoxic effects, but the
dependent variables are rather gross measures.
That CO hypoxia and hypoxic hypoxia are similar in terms of survival
15
effects was suggested by Clark and Otis, who showed that adaptation to
CO produced increased tolerance of high altitude and vice versa. Wilks
et al. reported similar data. It is difficult to evaluate the
equivalence of exposures in these studies, however.
Careful effort to equalize hypoxic hypoxia and CO hypoxia were made
99 100
by Traystman, ' who measured cerebral blood flow in dogs. Since his
subjects were held at constant ventilation, the effects of hypoxia-
induced hyperventilation were eliminated. His data show that for
exposures of up to 40 minutes, with arterial 0« values ranging from 4
percent to 17 percent for both hypoxic hypoxia and CO hypoxia, the CO
hypoxia reduced cerebrovascular resistance significantly more than did
hypoxic hypoxia. The difference between the two forms of hypoxia
diminished as the degree of hypoxia diminished. These data suggest that
CO produces a more extreme compensatory response than hypoxic hypoxia,
if ventilation is controlled.
3
Annau exposed rats to either 14, 12, 10, or 8 percent 0« in "air"
and to 174, 288, 576, or 1152 mg/m3 (150, 250, 500, and 1000 ppm) CO for
daily exposures of 15 to 60 minutes. He showed that brain-stimulation-
reinforced responses were affected by both variables in about the same
way except for certain temporal effects over the course of several days
exposure. Apparently CO-exposed rats recover response rates more slowly
than low-02 exposed rats. It is unlikely that very much adaptation to
10-48
-------
CO would have taken place in the course of a few days of short exposures;
therefore, this result is difficult to interpret. If replicable, these
data imply that CO has some non-hypoxic effect.
10.7.2 Elimination of Hemoglobin
36
Geyer et al. replaced the blood of rats with artificial blood.
Without Hb, these rats survived 17 hours of exposure to 115,000 mg/m3
(100,000 ppm) which killed controls immediately. Although no other than
observation of "normal" behavior was reported, this data imply that CO
has only hypoxic effects.
Most insects do not have Hb and so may provide a source of material
which could be used to assess the question as to whether or not CO has
effects on mammals in addition to those due to combination of CO with
Hb. Haldane observed that a cockroach was unaffected by 18 days exposure
to an environment containing 80 percent CO and 20 percent Op. Baker and
Wright exposed Coccinella septempunctata (the seven-spotted ladybird)
and Carausis morosus (the stick insect) to an environment of approxi-
mately 80 percent CO and 20 percent 0^. All ladybirds survived 10 days
or less of exposure but longer periods under these conditions hastened
death. Ladybirds were less active and ate less food in this environment.
Stick insects lived in an ambient atmosphere containing 20 percent CO, 5
percent 02, and 75 percent air. Growth was arrested, but no deaths
occurred before 14 days; all were dead by day 37. In an 80 percent CO,
20 percent 02 environment, stick insects died between the 2nd and 21st
day of exposure. It was postulated that the respiratory chain of enzymes,
10-49
-------
although not inactivated, were inhibited to such an extent as to inter-
fere with the animals' well-being. These insects also lack myoglobin.
102
Certain bacteria can live and grow in a 100 percent CO environment.
Carbon monoxide-utilizing bacteria may perform an important function in
natural aquatic environments and in soil.
10.7.3 Conclusions About Mechanisms
There is some evidence from comparison of CO and hypoxic hypoxia
that CO has non-hypoxic effects but the evidence is only suggestive at
this stage and may derive from dose and saturation rate parameters.
There is certainly also evidence for CO having only hypoxic effects but
such evidence stems from the measurement of rather gross variables.
Although the evidence is difficult to interpret in terms of mammals,
insects having no Hb are apparently effected by CO but at very high CO
levels.
10.8 ADAPTATION, HABITUATION AND/OR COMPENSATORY MECHANISMS
In this section consideration will be given to the question of
whether animals exposed to CO eventually develop some physiological
responses which tend to offset the deleterious effects. While there is
possibly a temporal continuum in such processes, in this review the term
"adaptation" will be used to refer to long-term phenomena, and the term
"habituation" will refer to short-term processes. Allusions will be
made, where possible, to the physiological chain of events by which
adaptation and habituation come about but extensive reductive explana-
tions will be avoided and teleogical inferences shunned. The term
"compensatory mechanism" will be used to refer to those physiological
10-50
-------
responses which tend to ameliorate deleterious effects, whether in the
long- or short-term case.
10.8.1 Adaptation (Long-Term)
44
Killick exposed mice to successively higher concentrations of CO,
which in a period of 6 to 15 weeks reached levels of 2300 to 3278 mg/m3
(2000 to 2850 ppm) CO (60 to 70 percent COHb), showing that non-adapted
mice exhibited much more extreme symptoms when exposed to such levels.
A control group was used by Killick to partially rule out effects of
selection of CO-resistant individuals. Clark and Otis15 exposed mice to
gradually increasing CO levels over a period of 14 days until a level of
3
1380 mg/m (1200 ppm) was reached. When exposed to a simulated altitude
of 34,000 feet, survival of the CO-adapted groups was much greater than
controls. Similarly Clark and Otis acclimatized mice to a simulated
altitude of 18,000 feet and showed that these altitude-adapted mice
s
survived 2875 mg/m (2500 ppm) CO better than controls. Wilks et al.
reported similar effects in dogs.
34a
Gorbatow and Noro showed that rats given successive daily short-
term exposures could tolerate, without loss of consciousness, longer and
3
longer exposures. Their CO levels were 2,875 to 11,500 mg/m (2,500 to
10,000 ppm). Increases in tolerance to CO began to be evident as early
as the. fourth or fifth day of exposure and were still occurring as late
as the 47th day. Non-exposure for several days eliminated some of the
113
adaptation. Similar results were reported by Zebro et al.
As discussed in Section 10.4.5, Hb increases in animals exposed to
ny
CO after about 48 hours, and continues to increase in the course of
10-51
-------
continued exposure until about 30 days, depending perhaps upon exposure
level. This hemopoietic response to long-term CO exposure is similar to
that shown for long-term hypoxic hypoxia, except that it is slower to
start, and tends to offset CO hypoxic effects.
Most investigators have at least implied that this increased Hb
level is the mechanism by which adaptation occurs. Certainly this
explanation is reasonable for the studies showing increased survival in
3
groups adapted for several days. The study by Annau made no such
inferences, and it is more likely that some behavioral explanation can
be found for his results, such as the possibility that hypoxic hypoxia
is more easily discriminable by the subjects and they more quickly
3
develop state-dependent learning. Annau1s results might also be due to
some mechanism as discussed by Winston and Winston and Roberts '
34a
or related to the effects shown by Gorbatow and Noro.
While much has been written about compensatory Hb increases, little
has been done to elucidate the extent to which such increases offset
deleterious effects of CO. Only survival studies have been done to
unambiguously show adaptation. The probability that some adaptation
occurs is supported theoretically due to Hb increases, and empirically
in the findings of survival studies.
Compensatory increases in Hb are not without deleterious conse-
quences of their own, such as cardiac hypertrophy. The Hb increases are
also not entirely compensatory at all CO levels in view of the fact that
deleterious effects still occur at some CO levels for many physiological
systems. It is possible, however, that without such mechanisms as Hb
10-52
-------
increases, CO effects would be worse and/or would occur at a lower
threshold.
10.8.2 Habituation (Short-term)
Arguments have been made for the possibility that there exist
short-term habituation and/or compensatory mechanisms for CO exposure.
These mechanisms have been hypothesized (1) to account for certain
putative behavioral findings, and (2) based upon physiological evidence.
The behavioral work upon which short-term habituation hypotheses
are predicated are mostly human studies, where CO exposure at very low
levels or at very early exposure times (well before asymptotic saturation)
have shown performance decrements which were not apparent with either
higher exposures and/or longer exposures. Depending upon the particular
j
version, the habituation hypothesis holds that if some short-term
compensatory mechanism were operative, there might exist some threshold
value of CO below which no compensation would be initiated, or that
there might be some sort of time lag in the compensatory mechanism so
that early CO exposures might produce effects which would later drop
out. The question of behavioral data to support this contention will be
reviewed in the context of human research, but in experimental animal
studies, little behavioral evidence for such thresholds or time lags is
extant. Many of the variable results in the literature would be
attributable to such threshold phenomena if independent evidence for
such were to be demonstrated in experimental designs, devised to
specifically test such an hypothesis.
10-53
-------
There is certainly physiological evidence for responses which would
compensate for the deleterious effects of CO in a very short time span.
As discussed in the section on nervous system and behavior, particularly
10.3.4, there has been demonstrated an increased CNS blood supply during
CO exposure which is apparently produced by cerebrovascular dilation.
It has also been shown, however, that the tissue PQ2 values for various
CNS sites fall in proportion to COHb, despite the increased blood flow.
Apparently the PQ2 values would fall considerably more without the
increased blood flow. Although the graphs which were published on these
data did not show very short time intervals, it appears that tissue PQ2
falls immediately and continuously as COHb rises. There is no evidence
for time delays or for threshold effects. It is also noteworthy that
only very high CO levels were employed, so that the saturation rates
were high and time lags or thresholds would be difficult to detect.
As discussed in the section on cardiovascular effects', as COHb
rises, both coronary blood flow and 0« extraction in the peripheral
musculature increase. These, too, are compensatory mechanisms which
have been shown to be only partly effective. None of the studies present
evidence of time lag or threshold effects, since only terminal and near-
asymptotic values were reported.
Increased blood flow and/or 0^ extraction have been demonstrated
for many body systems in response to CO exposure. In some cases it has
been explicitly shown to be only partly compensatory, and by virtue of
the fact that at some CO levels deleterious effects still occur, it is
apparent that compensatory mechanisms are not entirely complete.
10-54
-------
Disregarding time lags and threshold considerations, without the
compensatory mechanisms, CO would apparently have a more deleterious
effect and the threshold for such effects would be lower.
10.9 SUBJECTS AT SPECIAL RISK
From the theoretical and empirical considerations of the foregoing
literature review and from additional data reviewed below, some strong
conclusions may be drawn about sub-groups in the general population of
experimental animal subjects which would be at especially high risk or
especially sensitive to the deleterious effects of CO exposure. What
follows will in some cases be based directly upon studies designed to
test the given question, and in other instances will be deductions or
syntheses based upon extant data or theory.
10.9.1 Fetus and Uterine Exposure
Several studies27'29'32'33'3639'86 have exposed pregnant females
to CO and in general have shown that the mothers have not been affected,
while the offspring have shown deleterious effects. In many cases the
deleterious effects have been shown to disappear by adulthood, but the
inference of deleterious effects in childhood is of concern.
Additionally, impairment during maturation can have effects on learning
and social behavior which would be developing normally. Most of the
studies cited above did not measure COHb in the fetus during long-term
exposure.
Longo and Hill55 studied the uptake and elimination of CO in fetal
3
and maternal sheep. Following exposure to 58 mg/m (50 ppm) CO, steady-
state maternal COHb was 7.2 percent and fetal COHb was 11.3 percent,
10-55
-------
3
while exposure to 115 mg/m (100 ppm) resulted in steady-state COHb
concentration of 12.2 and 19.8 percent, respectively. The increase in
maternal COHb resembled a simple exponential process with a half-time of
1.5 hours. The half-time for the fetus was five hours. The decay curve
for CO elimination showed similar relations with fetal washout occurring
slower than in the mother.
55
The data of Longo and Hill on long-term maternal exposures suggest
that the fetus is at special risk because of higher COHb levels than
those of the mother. Two studies using short-term exposures * also
measured COHb in the fetus and showed that it was much lower in the
fetus than in the mother, probably because of slower COHb rise times.
Since short-term exposures also adversely affected the fetus, these
studies imply that not only is the fetus1 COHb higher than the mothers'
for long-term exposures, but that the fetus is apparently more fragile
and more subject to CO effects even if COHb is controlled.
While the data clearly show that fetuses are especially at risk,
much more information is required regarding dose-response functions,
from which thresholds, extent of effects, and interactions with other
factors may be estimated.
10.9.2 Impaired Groups
There is clear evidence that subjects with impaired cardiovascular
functioning are especially sensitive to CO exposure because of the
already reduced and/or marginal Op supply from the blood. Any additional
loss of Op due to COHb produces local or general hypoxias and deleterious
3a 21-23
effects. This has been demonstrated for cardiac damage ' and for
10-56
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the effects of high cholesterol levels in some cardiovascular structures.4'56
These results should hold for central nervous system structures but have
not been demonstrated.
Subjects with significant pulmonary function impairment might be at
special risk to GO exposure because of the inadequate supply of 02 to
the blood, especially during exercise. Specific data on this subject in
experimental animal research are not available.
There is one large group of subjects in which several of the above
mentioned impairments are commonly found, i.e., the group including aged
individuals. When there is any of one or more impairments such as
cardiac damage, cholesterol buildup in any vascular structures, anemia
and/or pulmonary function impairment, especially during exercise, low
levels of CO could precipitate major adverse health effects. Unfortu-
nately, there is no experimental evidence for deleterious CO effects in
many of these areas other than cardiovascular impairment. Certainly
more data are needed to estimate dose-response curves so that the extent,
threshold, and pattern of those problems can be assessed.
10.9.3 Drugs
Alcohol has already been shown" to have additive effects with CO, '
albeit at high exposure levels. More refined studies with other
dependent variables will very likely show lower-level effects. Sedatives
63
and other drugs are potentiated by CO. Stimulant drugs have been
60
shown to be attenuated by CO; dose-response functions and a wide range
of dependent variables are not known.
10-57
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10.9.4 Unadapted Populations
There is considerable evidence for long-term adaptation to high
altitudes in the form of increased Hb levels. Individuals who have not
had such adaptation and are then simultaneously exposed to high altitude
and high CO concentrations would seem to be at higher risk because of
the simultaneous effects of hypoxic hypoxia and CO hypoxia. Much data
are available, and estimates of threshold and dose-response functions
could be obtained by projecting arterial 0« content from simultaneous
hypoxic and CO conditions.
10.10 SUMMARY
From the foregoing review of the literature pertaining to low-level
CO effects in normal experimental animals, it may be concluded that CO
produces deleterious effects mainly upon the cardiovascular systems and
the CNS. While many particular conclusions are still in dispute, it
seems safe to conclude that cardiovascular effects can be demonstrated
3
with CO exposures as low as 58 mg/m (50 ppm; 4 to 7 percent COHb).
3
Behavioral and CNS effects seem to require a minimum 115 mg/m (100 ppm;
12 to 20 percent COHb) to produce effects.
The particular levels of CO in experimental animal studies are not
as important as the generalizations about the variables (dependent,
independent, and interactive) that are likely to be important in humans.
Such knowledge also permits the prediction of specially sensitive popula-
tions and allows for anticipation of new effects not yet observed, and
sometimes too dangerous to produce, in humans. The particular level at
which such effects become important in man is an empirical matter for
human research.
10-58
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While the foregoing review has discussed thresholds, and in some
cases dose-response functions, it is apparent that there remains a great
deal of ignorance regarding important health problems. Too little is
known about interactions with other pollutants, drugs, or other environ-
mental conditions. Much remains to be specified regarding particularly
sensitive groups. There is the suggestion that CO has other non-hypoxic
effects which in turn suggests that CO might have as-yet-unanticipated
health effects. From this discussion it may be concluded that a great
deal more information about CO is required with respect to interactions,
groups at special risk, and non-hypoxic CO effects.
10-59
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98. Tiunov, L. A., and V. V. Kustov. Toxicology of carbon monoxide. Leningrad,
1969. (In Russian).
99. Traystman, R. J. Effect of carbon monoxide hypoxia and hypoxic hypoxia
on cerebral circulation. Ln: Multi-disciplinary Perspectives in Event-Related
Brain Potential Research, Proceedings of the Fourth International Congress
on Event-Related Slow Potentials of the Brain (EPIC IV), University of
North Carolina and U.S. Environmental Protection Agency, Hendersonville,
North Carolina, April 4-10, 1976, D. A. Otto, ed., EPA-600/9-77-043, U.S.
EPA, RTP, NC, December 1978. pp. 453-457.
100. Traystman, R. J., and R. S. Fitzgerald. Cerebral circulatory responses
to hypoxic hypoxia and carbon monoxide hypoxia in carotid baroreceptor
and chemoreceptor denervated dogs. Acta Neurol. Scand. Suppl. (64):294-295,
1977.
101. Tumasonis, C. F., and F. D. Baker. Influence of carbon monoxide upon
some respiratory enzymes of the chick embryo. Bull. Environ. Contam.
Toxicol. 8:113-119, 1972.
102. Uffen, R. L. Anaerobic growth of a Rhodopseudomonas species in the dark
with carbon monoxide as sole carbon and energy substrate. Proc. Nat!.
Acad. Sci. U.S.A. 73:3298-3302, 1976.
103. Committee on Medical and Biologic Effects of Environmental Pollutants.
Carbon Monoxide. National Academy of Sciences, Washington, DC, 1977.
pp. 68-167.
104. Webster, W. S., T. B. Clarkson, and H. B. Lofland. Carbon monoxide-
aggravated atherosclerosis in the squirrel monkey. Exp. Mol. Pathol.
13:36-50, 1970.
105. Wilks, S. S., J. F. Tomashefski, and R. T. Clark, Jr. Physiological
effects of chronic exposure to carbon monoxide. J. Appl. Physiol. 14:305-310,
1959.
106. Winston, J. M. A Study of the Mechanism of the Alteration of Carbon
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10-68
-------
107. Winston, J. M. , and R. J. Roberts. Influence of carbon monoxide, hypoxic hypoxia
or potassium cyanide pretreatment on acute carbon monoxide and hypoxic
hypoxia lethality. J. Pharmacol. Exp. Ther. 193:713-719, 1975.
108. Winston, J. M., and R. J. Roberts. Glucose catabolism following carbon
monoxide or hypoxic hypoxia exposure. Biochem. Pharmacol. 27:377-380, 1978.
109. Xintaras, C., C. E. Ulrich, M. F. Sobecki, and R. E. Terrill. Brain
potentials studied by computer analysis. Arch. Environ. Health 13:223-232,
1966.
110. Xintaras, C., B. L. Johnson, C. E. Ulrich, R. E. Terrill, and M. F. Sobecki.
Application of the evoked response technique in air pollution toxicology.
Toxicol. Appl. Pharmacol. 8:77-87, 1966.
111. Yamamoto, K. Acute combined effects of HCN and CO, with the use of the
combustion products from PAN (Polyacrylonitrile)-gauze mixtures. 2. Rechtsmed.
78:303-311, 1976.
112. Young, S. H., and H. L. Stone. Effect of a reduction in arterial oxygen
content (carbon monoxide) on coronary flow. Aviat. Space Environ. Med.
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113. Zebro, T., R. J. Littleton, and E. A. Wright. Adaptation of mice to
carbon monoxide and the effect of splenectomy. Virchows Arch. A: 371:35-51,
1976.
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10-69
-------
11. EFFECTS OF LOW-LEVEL CO EXPOSURE ON HUMANS
11.1 INTRODUCTION
Carbon monoxide (CO) poisoning is a common form of poisoning
occurring both accidentally and voluntarily. The potentially serious
effects of overdosage must always be considered by those concerned
with this contaminant. The early history (from the days of Aristotle)
130
of CO and its effects on mammals has been well described by Lewin.
The clinical-pathological effects, especially of large increments in
carboxyhemoglobin (COHb), are adequately documented in several
?ft ~\ ^? 16^ ?0? ??fi
monographs. ' ' ' ' Neurological signs and sequelae as well
as anatomical alterations in various tissues are presented in these
reviews, as are the occurrences of CO intoxication, clinical symptomology,
complications, progressions, and emergency and subsequent treatment.
47
An extensive bibliography of abstracts up to 1966 was compiled by Cooper.
These severe effects of exposure to high concentrations of CO are not
directly germane to the problems of individuals exposed to current
ambient levels of CO but are valuable in that they indicate the potential
effects of accidental overdose.
11-1
-------
Extensive studies have been conducted using various animal species
as subjects. Under the varied experimental protocols employed by
investigators, considerable information has been obtained on the toxicity
of CO, its effects on blood, tissues, metabolism, etc. The effects
observed on experimental animals have provided some insight into the
potential role CO plays in cellular metabolism. A certain degree of
caution must be employed in extrapolating the results obtained from
these data to man. Not only are there questions related to species
differences, but exposure conditions differ markedly in the studies
204
conducted by different investigators.
Human research is especially fraught with methodological problems.
As with the experimental animal literature, there are many methodological
and reporting problems which make the reported research data difficult
to interpret. These include: failure to measure blood COHb levels;
failure to distinguish between the physiological effects of a CO dose of
high concentration or the slow, insidious increment in COHb over time
with lower inhaled CO concentrations; the amount of CO brought to or
removed from the lungs by changes in alveolar ventilatory volumes; and
the small number of subjects. Other factors involve failure to provide
control measures (via double-blind administration), for experimenter
bias and experimenter effects control periods so that task-learning
effects do not mask negative results, homogeneity and the groups labeled
"smokers", control of possible boredom and fatigue effects, and poor or
inadequate statistical treatments.
11-2
-------
An almost universal problem in this area of research is the use of
inappropriate statistical techniques for data analysis. Experimenters
commonly use tests designed for simple two-group designs when analysis
of variance is required, or use several univariate tests when more than
one dependent variable is measured and multivariate tests are appropriate.
Such inappropriate statistics usually yield results in which the p-value
is too small, so that the possibility exists that too many results were
falsely declared to be statistically significant. In this review, an
effort will be made to account for such problems whenever possible by
making appropriate corrections and/or discussing the possible consequences
of such an error in context.
The above problems are not unique to human research data (as dis-
cussed in Chapter 10). A problem that is unique to human research is
that only low levels of CO exposure may be safely and prudently used.
In such instances of low-level exposure, research findings necessarily
deal with near-threshold effects. The so-called "threshold" for an
effect is conceptually defined as a CO level below which no deleterious
effect on the dependent variable occurs and above which an effect is in
evidence. In practice, a threshold must be defined as a CO level above
which an effect upon a dependent variable is produced a certain per-
centage of the time it is administered. Usually, a threshold is defined
in terms of the point where an effect is noted 50 percent of the time,
although many other, possibly better, definitions are in use. When
research is necessarily restricted to such barely-noticeable effects it
may be expected that (1) results will be more variable due to statistical
11-3
-------
sampling fluctuations and (2) other uncontrolled variables which also
effect the dependent variable in question will be of major importance
and will increase the variability of results. For these reasons, human
data, while being of prime interest, will also be of highest variability.
Such high variability must be resolved with (1) large groups of subjects
(2) theoretical interpretation of results using knowledge gained from
experimental animal data, and (3) consideration of consistency of the
data within and across experiments.
This chapter is intended to review data from studies in which
humans have been either accidentally or intentionally exposed to low
levels of CO. The summary and conclusion of each section of this chapter
will integrate the relevant material from studies which have used exper-
imental animals. Unless otherwise stated, all subjects are considered
to be normal (i.e., without debilitating disease).
11.2 NERVOUS SYSTEM AND BEHAVIOR
The demonstrable changes in central nervous system (CNS) function
in individuals who were inadvertently exposed to high levels of ambient
CO in illuminating gas and in automobile exhaust stimulated psychophysi-
ological research. These studies attempted to determine psychomotor and
psychological aberrations in individuals having lower levels of blood
COHb than those observed in CO-poisoned individuals. Reports of the
earlier studies suffer from a number of deficiencies. These deficiencies
are related to inadequate understanding of the significance of behavioral
changes, the inability to distinguish between simple perceptual motor
performance, and the more complex performance involving sustained and/or
11-4
-------
selective attention, short-term memory, and decision-making among the
possible alternatives.
11.2.1 Sleep and Activity
-I CO
O'Donnel et al. sought to determine how overnight exposure to
low levels of CO (COHb levels up to 12.6 percent) affected sleep and
found small but unreliable changes that they interpreted as a possible
86
reduction in central nervous activation. Groll-Knapp et al. and
95
Haider et al. reported a significant reduction of rapid eye movement
3
(REM) sleep in subjects of both sexes exposed for seven hours to 115 mg/m
(100 ppm) CO.
11.2.2 Vigilance
Vigilance is an individual's ability to detect small changes in his
environment that take place at unpredictable times, thus demanding
continuous attention for long periods of time. In monotonous tasks,
subjects miss signals that they would not have missed when starting the
task. Such signals are usually presented visually or aurally.
Fodor and Winneke used an auditory vigilance task in which they
presented short bursts (0.36 second) of white noise at 2-second intervals
as the stimuli. About three out of every hundred of these noises were
slightly less intense and were the signal to which the subjects were to
respond by pressing a button. Twelve non-smokers (male and female) were
3
tested at 0 to 57 mg/m (0 to 50 ppm) CO for 80 minutes prior to the
first of three vigilance experiments. Carboxyhemoglobin was estimated
to be 2.3 and 3.1 percent, at the beginning and the end, respectively,
of the first vigilance test. Subjects were likely to miss more signals
-------
during the initial test than during the next two vigilance tests; COHb
reached an estimated 4.3 percent at the end of 210 minutes of CO exposure.
These data suggested an initial effect, possibly followed by a compen-
satory response. Compensatory mechanisms might not have been operative
during the first test because of either a threshold level of COHb below
which no compensatory response would be initiated or a time lag in
compensatory responses.
oc o
Groll-Knapp et al. exposed subjects to 0, 57, 115, and 172 mg/m
CO (0, 50, 100, and 150 ppm; 0.0, 3.0, 5.4, and 7.6 percent COHb) for
two hours. They used a 90-minute auditory vigilance test which showed
a dose-related decrement due to CO although their statistical documen-
95
tation is absent. The same group (Haider et al. ) was later unable to
23 217
replicate the results of this study. Winneke utilized the same
test in studies which used 0, 57, 115, and 172 mg/m3 (0, 50, 100, 150 ppm)
CO as well as exposure to methylene chloride (CH^CK), a compound which
causes an elevation in COHb. His results from the CO exposures were
negative, in marked contrast to the previous data, despite an estimated
3
COHb level of approximately 9 percent at the end of the 172 mg/m
(150 ppm) exposure. He did find that his subjects, as a consequence of
CH2C12 exposure, exhibited a striking decrement in vigilance.
19 3
Beard and Grandstaff exposed subjects to 0, 57, 200, or 286 mg/m
CO (0, 50, 175, or 250 ppm; 1.8, 5.2, and 7.5 percent COHb estimated
from alveolar breath) for 1.5 hours during which the subjects performed
a visual vigilance task. They reported a statistically significant
decrement in performance at the two lower CO levels but not at the
11-6
-------
highest level. Their data raise again the question of compensatory
23
mechanism thresholds but their statistical procedure is also questionable.
Horvath et al. utilized a visual vigilance test and were the
only group of earlier investigators to measure COHb. They also required
two responses, one for the non-signal stimuli as well as the usual
response to the signals. Their subjects were pre-exposed for one hour
to 0, 29, and 126 mg/m3 (0, 25, and 110 ppm) CO and then continued the
CO exposure during a 1-hour vigilance task. The COHb levels at the
beginning of the vigil were 0.9, 1.6, and 2.2 percent, respectively, and
at the end of the vigil were 0.9, 2.3, and 6.6 percent. They noted no
initial effects of CO but by the end of the vigil the 110 ppm group
3
exposed to 126 mg/m (110 ppm) showed a statistically significant decre-
218
ment in performance. Recently Winneke et al. attempted to replicate
-I QTT 218
the Horvath et al. study without success. Winneke et al. apparently,
however, provided less sensory deprivation in their study and this may
have raised the arousal level of their subjects, keeping them more
39
alert. Horvath's group also attempted to replicate an earlier study
by Horvath et al. using a less isolated (clear plastic) chamber and
failed to observe a statistically significant decrement due to CO, but
their COHb levels were also marginally lower.
23
Bern"gnus et al. utilized a visual numeric monitoring task with
subjects exposed to 0, 115, and 229 mg/m3 CO (0, 100, and 200 ppm CO;
0, 4.6, and 12.6 percent COHb). No CO exposure levels produced any
23
effect on vigilance performance. The task used by Benignus et al. was
a fairly complex task with high probabilities of signals so that the
11-7
-------
subjects might have been more aroused than they would have been on a
simple vigilance task.
Putz et al. used an auditory and visual monitoring task and
3
exposed subjects to 6, 40, or 80 mg/m CO (5, 35, or 70 ppm CO; 1, 3, or
5 percent COHb) for four hours. Their results showed no CO-related
decrements, although they did report electrophysiological effects (to be
discussed later). Their signal rates were also fairly high and the
performance periods were short, so that their subjects, too, might have
been too aroused to show behavioral vigilance decrements.
125
Krotova and Muzyka studied individuals working for about two years
in an environment containing CO. They had approximately 4 percent COHb
after work. Only 11 of the 56 workers reported a loss of vigilance.
11.2.3 Sensory and Time Discriminations
The first demonstrable influences of CO on CNS functions were noted
142
by McFarland et al. in conjunction with their studies on the effects
of altitude and CO on visual thresholds. They observed decrements in
visual sensitivity at COHb levels as low as 5 percent and extrapolation
of their dose-response curve implies that impairment would occur at even
97
lower levels. Hal perin et al. reported that visual function was
impaired at COHb levels as low as 4 percent and that greater impairment
97
occurred at higher COHb levels. Hal perin et al. further noted that
recovery from the detrimental effects on visual function lagged behind
141 143
the elimination of CO. McFarland and McFarland et al. were unable
to demonstrate statistically significant differences in dark adaptation
and glare recovery for COHb levels of 6 to 17 percent. Ramsey *
11-8
-------
was unable to demonstrate any CO effect on visual brightness discrimi-
nation or depth perception.
187b
Seppanen et al. evaluated the effect of increasing COHb on
visuoperceptual and psychomotor performance in smokers and nonsmokers.
Subjects breathed 1100 ppm carbon monoxide intermittently to eventually
reach COHb levels of up to 18 percent. Interspersed between the inhala-
tion of CO were periods breathing air during which the tests were
performed. No effect on perceptual speed and accuracy was observed.
Visual perception as measured by critical flicker frequency was decreased
linearly with increasing COHb. This study was unusual in the methods
utilized to increase COHb and its significant findings open to questions
of technique.
A perceptual test and a standard cortical function test, critical
flicker fusion frequency (CFFF), apparently is not influenced even by
COHb levels of 10 to 12.7 percent.88,170,171,213,217 Guest et al 88
also utilized an auditory analogue of CFFF, the auditory flutter fusion
threshold. This threshold was not affected by COHb levels of 10 percent.
83
Grandstaff et al. have recently reviewed these studies.
18
Studies by Beard and Wertheim suggested an alteration in CNS
function because the ability to discriminate slight temporal differences
in successive short tones was impaired in subjects having estimated COHb
levels of 2 to 3 percent. These data imply an orderly dose-response
function with increasing decrements in performance as CO levels increase.
Although these data represent the lowest levels of COHb to produce a
significant alteration in behavioral performance, considerable questions
11-9
-------
as to the validity of the observations have been raised. Attempts to
replicate these particular findings have been less than satisfac-
tory158'159'193'197 even though the subjects of all of these other
studies attained higher COHb levels. Some of the failures to replicate
may be explained on the basis of differing protocols and the environmental
conditions under which the tests were conducted. Some investigators
designed their experiments to minimize boredom and fatigue while others,
conversely, attempted to minimize external influences and conducted
-I c~l a
their experiments for a relatively long time. Otto et al., however,
made strong efforts to replicate the study accurately and presented a
strong rationale indicating that time discrimination is probably not
affected by low COHb levels.
11.2.4 Complex Sensorimotor Tasks and Driving
A number of investigators have used broad sensory and/or motor
screening batteries in an effort to discover what types of behavior
might be affected by low-level CO exposure. From the standpoint of
experimental and statistical design, such studies are not always easy to
interpret. When many dependent variables are measured, the chance that
one or more of them will erroneously be declared statistically signifi-
cant is increased, and in order to account for this increased probability
of an inferential error more exotic statistical procedures must be used.
Such procedures usually involve multivariate techniques or at least
conservative corrections. Usually an increased number of dependent
variables requires a concomitantly increased number of subjects. In none
of the cases of behavioral screening batteries reported below did
11-10
-------
researchers take appropriate account of this problem. Attempts were
made on the part of the reviewers to account for this problem by the
application of conservative corrections.
1 ftR
Sayers et al. found no significant changes, despite COHb levels
of approximately 20 to 30 percent, in hand-eye coordination and steadiness,
tapping speed, arithmetic (continuous addition), location memory, and
21 22
simple reaction time tests. Bender et al. ' found a decrement in
learning of meaningless syllables and in hand-eye coordination when the
COHb levels of his subjects were about 7 percent. Other tests which
they administered failed to show decrements in performance at these
-IOC O
levels of COHb. Schulte exposed firemen to 115 mg/m (100 ppm) CO
for variable time periods and reported large changes in performance of a
series of complex tasks. In a test where subjects were required to
underline all plural nouns in prose passages, decreased performance was
noted when COHb was approximately 8 percent. The mean time to complete
an arithmetic test significantly increased at similar or slightly lower
COHb levels. This investigator may have underestimated his COHb levels
since his subjects, mostly smokers, had initial measured values close
•I CQ
to zero. 0'Donne!1 et al. studied the ability of four subjects to
perform arithmetic problems without pencil and paper. Their subjects
required a longer time to complete the answers (89.76 versus 98.64 seconds
141 143
when COHb levels 5.9 and 12.7 percent, respectively). McFarland '
tested subjects' performance of complex psychomotor tasks involving
reaction times to central and peripheral stimuli and showed some minimal
effects of CO (11 and 17 percent COHb) on attention to peripheral
11-11
-------
183
stimuli. Salvatore reported increased reaction times to peripheral
stimuli at COHb levels of 4 to 8 percent. Putz et al. reported
decrements in hand-eye coordination, response times during a complex
monitoring task, and tracking accuracy in subjects exposed to 35 and
70 ppm CO (3 and 5 percent COHb).
114 115
Johnson et al. ' studied employees who worked at a U.S.-Mexico
border crossing and toll collectors at a toll highway. They believed
that more valuable information would be obtained from these workers than
from the usual studies on university students. Toll collectors had COHb
levels ranging from 1.5 to 11.7 percent with a mean value of 3.9 percent
and exhibited slowed eye-hand coordination requiring fine motor control
and disruption of performance on two concurrent tasks.
The potential influence of ambient levels of CO on vehicle operators
as well as the additional increments in blood COHb levels has received
minimal attention. Suggestive but not conclusive evidence has been
reported indicating that drivers in fatal accidents have higher levels
220 70
of COHb. In the early studies of Forbes et al. , five subjects were
exposed to CO sufficient to raise COHb levels as high as 30 percent and
their reaction times, coordination, and perceptual skill were determined
within the context of a test of driving skill. They showed no CO effect
219
on skill. Wright et al. used a driving simulator with both smokers
and nonsmokers as subjects (final COHb levels were 5.6 and 7.0 percent,
respectively). They suggested that a 3.4 percent increase in COHb was
sufficient to obviate safe driving. McFarland et al. ' studied
subjects that actually involved driving instrumented automobiles under
11-12
-------
highway conditions while exposed to CO concentrations producing 17 percent
COHb. They concluded that such COHb levels do not seriously affect
driving but they did show statistically significant increases in roadway
viewing time, though no differences occurred in steeering wheel reversals.
Preliminary data from Rockwell and others,175'177'178'215 in studies in
which subjects drove instrumented automobiles while exposed to CO levels
producing 0, 6, and 13 percent COHb, imply that at COHb levels of 6 and
13 percent subjects showed increased variations in automobile speed,
decreased ability to maintain fixed following distances, and decreased
181
steering motions. Rummo and Sarlanis reported that during a 2-hour
vigilance driving-simulator task subjects with 6 to 8 percent COHb were
significantly slower in responding to changes in speed by the lead car.
11.2.5 Central Nervous System Electrical Activity
54
Dinman analyzed evoked photic responses in subjects with 22 and
37 percent COHb and found no changes in latency or voltage following
109
photic stimulation. Hosko reported changes in CO-induced visual
evoked response but only at COHb levels of about 20 percent. Putz
et al. reported an increase in the amplitude of auditory evoked
o
potentials for CO levels of 40 and 80 mg/m CO (35 and 70 ppm CO; 3 and
oc
5 percent COHb). Groll-knapp measured slow-wave brain potentials (the
so-called contingent negative variation or CNV) and noted a diminution
in the voltage reached by the CNV and the extent of the drop seen after
3
response stimulus given consequent to CO exposure 172 mg/m (150 ppm).
Otto et al.,161b in a preliminary report of evoked slow potentials
11-13
-------
o
during vigilance performance at 115 and 229 mg/m CO (100 and 200 ppm
CO; 4.6 and 12 percent COHb), showed that CNV amplitude decreased as
pc
reported by Groll-Knapp and showed that a positive potential with a
latency of about 100 msec increased with CO.
Ikuta evaluated 87 male adults who had suffered from CO poisoning
at an accidental explosion in a coal mine. Older individuals showed the
greatest degree of impairment.
11.2.6 Conclusions and Discussion of Nervous System and Behavior in Humans
Table 11-1 shows a summary of research results concerning the
effects of CO on CNS and behavior.
Experimental animal data point toward disturbed sleep patterns
3
which have also been reported in humans at levels of 115 mg/m (100 ppm) CO.
General activity levels in humans have not been specifically studied.
Effects of CO on vigilance are in considerable dispute but some
evidence suggests that, if relevant variables are controlled, there is a
decrement in vigilance due to CO at threshold level of about 4 to 6 per-
cent COHb. Human and animal studies point toward such factors as arousal,
environmental temperature and humidity, CO dose rate, task variables,
and subject cerebrovascular health as important and usually uncontrolled
variables. Research is required to clear up this confusion.
Apparently, visual system impairment at low illumination levels or
at quickly-changing illumination is affected by CO exposure at levels
approaching zero in a dose-related manner, but these data are old and
should be replicated. Other sensory systems could also be affected but
have not been extensively studied. Time discrimination does not seem to
be affected by low CO levels.
11-14
-------
TABLE 11-1. SUMMARY OF DATA ON EFFECTS OF CO ON HUMAN BEHAVIOR AND CNS
et
Reference
al.
No. of
subjects
4
Exposure
9 hours to
150 ppm dur
a
75 and
ing
COHb
5.9%
12.7%
Dependent variable
Sleep
No
to
Results
Comment
changes large enough
be significant but
Groll-jCnapp
et al.
Haider et al.
95
Fodor and
Winneke
07
Groll-Knapp
et al.
Beard and
Grandstaff
19
Horvath et al.
107
Winneke
217
10
20
20
9
10
18
sleep
100 ppm 7 hours
(2nd experiment)
2-7 hours
(50-150 ppm)
5 hours (50 ppm)
2 hours
(50-100 ppm)
90 minutes
(50, 175 & 250 ppm)
1 - 2 1/2 hours
(26 and 111 ppm)
5 hours (50
and 100 PPM)
2-5%
3-7.6%
1.8-7.5%
Sleep stages
EEC in sleeping
Vigilance
Auditory vigilance
Visual vigilance
2.3 and 6.6% Visual vigilance
5.1 and 10%
respectively
Vigilance, visual
CFFF, and psycho-
motor tasks com-
paring effects of
CO and methylene
chloride.
trends toward deeper
sleep with CO
Altered proportion of
sleep stages.
REM and stage 2 sleep
depressed but greater
amount of deep sleep.
Vigilance at first
decreased, then increased.
Decreased vigilance
performance.
Significant reduction
in vigilance.
Signal identifica-
tion performance
deteriorated and mono-
tony effect was
potentiated.
No impairment of performance
due to CO exposure could
be demonstrated, while CNS
depression was shown after ex-
posure to methylene chloride
for only 3-4 hours at concentra-
tions as low as 300 ppm.
-------
TABLE 11-1 (continued)
No. of
Reference subjects
Exposure*
COHb
Dependent variable
Results
Comment
Benignus and 52
Otto"
Putz et al.167 30
3 1/3 hours
(100 + 200 ppm)
4.61-12.62%
4 hours (5-70 ppm) 1-5%
Vigilance No effect on
performance vigi1ance
(numeric monitoring performance.
task)
Auditory and visual No effects.
monitoring
McFarland et al.
142
Halperin
97
McFarland141 and
McFarland
et al.™
170
Ramsey
Weber et al.
20
20
4 hours 0-11%
(concentrations high
enough to achieve
stated COHb levels)
3-4 hours (at concen- 3-6.2%
trations high enough
to achieve COHb levels
stated)
Exposure time 6-17%
sufficient to
achieve stated blood
concentrations (700 ppm)
Visual sensitivity
Visual sensitivity
to differences in
light intensity
Dark adaptation
and glare recovery
Low COHb levels
were found to
reduce visual
sensitivity.
Reduced sensitivity
Recovery from effects
of CO lags behind
elimination of CO
from the blood.
No statistically signifi-
cant effects were
demonstrated.
45 minutes (300 ppm) 11.28-15.66% Brightness discrimi- No significant
nation depth percep- effects demon-
tion and CFF strated.
3.5 hours (150 ppm) 9-11%
Critical flicker
fusion frequency
Exposure did not
affect CFFF
either in mono-
tonous or activating
situation.
-------
TABLE 11-1 (continued)
Reference
Guest 00
No. of
subjects
8
Exposure3
65 minutes
COHb
10%
Dependent variable
Auditory flutter
Results
No significant
Comment
et al.
217
Winneke
Beard and
Wertheim
~
18
18
(concentrations high
enough to achieve
stated blood level)
5 hours (50 and
100 ppm)
2 1/2 hours
(50-250 ppm)
9 hours to 75 and
150 ppm
5.1 and 10%
respectively
Estimated
2-3%
5.9% and
12.7%
fusion threshold
and critical flicker
fusion frequency
with phenobarbitone
CFF
Discrimination of
short intervals of
time
effects demonstrated.
No impairment could be detected
due to CO exposure.
Performance deterio-
rated increasingly with
progressively higher
concentrations.
Time discrimination No effects.
Not precise
replications of
Beard and Wertheim.
Stewart—
et al.
197
18
4-7 hours
25-100 ppm
Time discrimation
No effects.
Not precise
replications of
Beard and Wertheim.
Otto
et al.
161a
Bender et al.
21
13
42
0, 75 and 150 ppm
for 3 hours
.16, 3.8 and
7.8%
Time discrimination No effects.
3.5 hours (100 ppm) 3.8-8.2% Level of activation, Level of activation and
visual perception
psychomotor per-
formance, learning
and retention,
Amthauer's I.S.T.,
subjective condition
1ST showed no difference.
Performance declined in
visual perception, learning
and memory and in psychomotor
testing.
-------
CD
TABLE 11-1 (continued)
Reference
OMtanna
No. of
subjects
4
Exposure3
9 hours to 75 and
150 ppm
COHb
5.9% and
12.7%
Dependent variable
Mental arithmetic^
Results
No effects.
Comment
Bender et al.
22
42
McFarland141
and McFarland
et al.
Salvatore
183
Putz et al.
Johnson,A
et al.
167
(not
given)
2 1/2-8 hours
(100 ppm)
700 ppm until
COHb level achieved
20 minutes
(800 ppm)
(not given)
8 hours (22.8 ppm)
TWA
7.2%-11.6%
6-17%
4-8%
(not given)
1.5-11.7%
Visual perception
ability to learn,
manual dexterity
Visual perception
was not affected,
manual dexterity
was diminished, learning
performance deteriorated.
Complex psychomotor Only "minimal"
tasks effects.
Visual function
performance
Detection time was
significantly increased.
No other effects were
noted.
Hand-eye coordina- Decrements in all measures.
tion complex monitoring,
tracking
Eye-hand coordina- Eye-hand coordination
tion, time estima- was impaired. Perform-
tion, visual percep- ance on two concurrent
tion, complex arith- tasks was disrupted.
metic, choice reaction
time, CFF, task time
sharing
-------
TABLE 11-1 (continued)
No. of
Reference subjects
Exposure
a
COHb
Dependent variable
Results
Comment
10
8 hours (0-41 ppm) 1.66-2.5%
Forbes et al.
70
VO
jnq
Wright et al. 50
McFarland141
and McFacland
et al.
Ray and
Rockwell
Rockwell and
Weir177
1 hour (90 ppm)
(Duration of
exposure sufficient
to raise COHb levels
by 3.4% (20,000 ppm)
Exposure with
700 ppm to produce
COHb.
4-6 hours
(950 or 1900 ppm
given every 35
minutes in quanti-
ties sufficient to
maintain COHb levels
of 10 or 20% res-
pectively
22.4-47.2%
1.24-6.97%
6-17%
Mental arithmetic,
audio digit moni-
toring, hearing
acuity, divided
attention, choice
reaction time, CFF,
eye-hand coordina-
tion, subjective
feelings
Reaction time,
depth perception,
visual perception,
motor performance
in driving
Hearing acuity and
CFF were decreased.
Choice reaction time
was increased. No
difference was noted
due to CO in mental
arithmetic, divided
attention, digit
monitoring and
subjective feelings.
No impairment of
function up to
30% COHb.
Poor control data.
Simulated driving Impairment of
varying degrees
was demonstrated.
Driving performance No effects.
Poor analysis
of results.
10 and 20% Driving tasks
Increased response Only preliminary
time to distance and analyses.
velocity, decreases in
time estimation, decrease
in driving precision.
-------
TABLE 11-1 (continued)
Reference
No. of
subjects
Exposure*
COHb
Dependent variable
Results
Comment
Weir and
Rockwell
215
Rummo ancL,
Sal amis101
Hosko
109
ro
o
Putz et al.
Groll-
et al.
167
6-12
(for
various
tests)
Ikuta
110
12
30
20
Otto et al.161b 28
87
90 and 120 minutes 7-20%
(100 and and 490 ppm
respectively)
20 minutes (800 ppm) 6-8%
0.5-24 hours
(1-1000 ppm)
(not given)
2 hours (50, 100
and 150 ppm)
2.5 hours
(100 amd 200 ppm)
(unknown)
Max. 33%
(not given)
3-7.6%
4.95 and
12.04%
(unknown)
velocity variance,
Reaction time to
speed changes,
steering reversal
responses
Visual evoked
response (VER)
Auditory evoked
potential
Computer analyzed
brain potentials
Event related
potentials
Mean velocity and No performance decre-
ment with normal
gas and brake pedal driving tasks.
actuations, steer-
ing wheel reversals,
headway, visual
behavior
Significant increase
in reaction time and
fewer steering wheel
reversal responses.
VER alterations
associated with
COHb levels of
20-22%.
.Increased amplitude.
CNV amplitude No significant
reduced proportional test data.
to progressively
higher COHb concen-
trations.
CNV decreased,
P100 increased.
Preliminary data.
Data obtained
3 years after a coal
mine explosion.
al ppm CO = 1.145 mg/m3 CO and 1 mg/m CO = 0.874 ppm CO, at 25°C and 760 mm Hg.
-------
Complex tasks involving large behavioral loads or fine discrimi-
nation are usually not affected by CO, especially if the duration of the
task performance is short; although the data by Putz et al. appear to
show such effects. Vigilance and sensory functions, which are certainly
components of more complex tasks such as driving, appear to be affected;
thus one would expect an effect on the overall task. It is probable
that research in both experimental animals and man has not shown reliable
effects because: (1) the tasks are highly redundant, so that a great
impairment is required before decrements are noticed; (2) performance
measures of end-result behavior are sometimes gross and insensitive;
and/or (3) the tasks' components stimulate the subject with their variety
and thereby keep alertness high. More sophisticated studies are required.
Quantitation of electrical activity of the CNS as affected by CO
has just begun. While alterations have been demonstrated in both exper-
imental animals and man, interpretation of these results still rests on
their correlation with behavioral data because of the lack of general
theoretical data about CNS electrical activity.
11.3 CARDIOVASCULAR SYSTEMS
Experimental animal studies have suggested that one of the principle
effects of CO occurs in the cardiovascular system. This section reviews
cardiovascular data from studies of both healthy and impaired human
subjects exposed to CO.
11.3.1 Cardiovascular Damage and EKG Abnormalities
48
Corya et al. presented the first evidence for left ventricular
abnormality in five cases of non-fatal CO poisoning (20 percent COHb).
11-21
-------
Abnormal left ventricular wall motion was shown by echocardiograph in
three of five cases. A similar number showed mitral valve prolapse.
221
Zenkevic conducted clinical and physiological hemodynamic studies
on two groups of subjects: individuals in constant contact with CO and
individuals having no evidence of chronic CO intoxication. He noted
considerable cardiovascular abnormalities in the CO-exposed group.
57
A study of cast iron workers by Ejam-Berdyev also suggested a larger
frequency of cardiovascular, as well as CMS disturbances, in these
workers that was related to their increased blood COHb content.
Hemp processing in Japanese villages is conducted in small rooms
3
heated by charcoal. Ambient CO concentrations average about 80 mg/m
o
(70 ppm) and reach peak levels of about 344 mg/m (300 ppm). The inci-
dence of myocardosis was found to be excessively high. Deaths from
cardiac failure in these villages was reported to be 6.8 times greater
123a
than the anticipated numbers for the Japanese population.
Only one study has been reported on patients having peripheral
vascular disease. Ten men with angiographically documented occlusive
arterial disease were exercised on a bicycle ergometer until leg pain
3
occurred. These patients then breathed filtered air 0 or 57 mg/m (0 or
50 ppm) CO for a 2-hour period. Exercise after this time showed that
COHb levels of about 2.8 percent significantly decreased the time to
onset of pain compared to controls. Alexieva and Simitrova studied a
3
large group of workers exposed to an ambient CO level of 57 mg/m
(50 ppm) and reported changes in peripheral vessels suggesting impaired
vascular tone.
11-22
-------
25
Bogusz et al. related electrocardiographic changes in blood
lactate levels, and aspartate aminotransferase activity to levels of COHb.
81
Gorski utilized the ballistocardiogram to demonstrate hypoxemia of the
myocardium in similar cases. Goldsmith and Aronow have reviewed the
available evidence relating CO exposure to the rate of development of
arteriosclerotic heart disease (ASHD).
11.3.2 Blood Flow and Related Variables
The heart has a specialized circulatory system in which the primary
response to increased metabolic demands can only be secured by an
increased cardiac blood flow. Even under no-stress conditions (rest)
there is an almost complete extraction, roughly 75 to 80 percent, of the
available 0« supply from the blood. The increased capacity for flow to
compensate for the small benefit obtainable from more complete extraction
from the perfusing blood has been shown to be on the order of several
hundred percent. \
The studies of Ayres et al. on the hemodynamic and respiratory
14 15
responses of man were made during diagnostic cardiac catheterizations. '
3
They gave these subjects a fixed amount of CO, either 1145 mg/m (1000 ppm)
3
for 8 to 15 minutes or 5725 mg/m (5000 ppm) for 30 to 45 seconds.
These procedures induced COHb levels of between 6 to 12 percent. Two
groups of patients, those with and those without coronary heart disease
(CHD), were studied. The normal individuals responded to the presence
of elevated COHb by increasing their cardiac output and minute ventilation,
...... . 4. • i n • Increased extraction of 00 from
but with a decrease in arterial PQ2 2
arterial blood occurred, as evidenced by the increased extraction rates.
11-23
-------
v,Qr,m,c D decreased from 39 to 31 torr, probably as a result of
VcllOUS ' rt o
the left shift of the 00 dissociation curve. Arterial Pn«
These changes and mixed venous PQ2
In contrast to normal subjects, patients with cardiac heart disease
(CHD) did not show an increase in cardiac output. Cardiac blood flow
3
(CBF) increased significantly in all patients given 5725 ug/m (5000 ppm)
CO for 30 to 95 seconds (COHb about 9 percent), but it only increased in
3
the CHD patients when they breathed 1145 mg/m (1000 ppm) CO for 8 to
15 minutes (COHb about 12 percent). It should be noted that most of
these individuals had relatively high initial COHb concentrations. The
myocardial arteriovenous 0« difference decreased in both situations,
with the greatest percentage decrease occurring at the lowest COHb
concentration. In all but two of those patients, coronary sinus PO«
decreased, suggesting that the increase in CBF was insufficient to
compensate for the decreased Op delivery caused by the presence of COHb.
Further evidence of anaerobic myocardial metabolism was suggested by the
decreased lactate extraction, with four patients showing lactate produc-
tion by the myocardium with no lactate extraction. Ayres reported
14 15
similar changes in concurrent studies conducted on dogs. ' These
observations on man suggest that CO inhalation would have a significant
ff + + • n n in patients with lung disease as well as certain
eTTecL on arterial 'no
cardiovascular disorders.
The potential toxicity of CO present in transfused blood has received
120
little attention. Kandall et al. measured COHb concentrations in
donor blood and in relatively healthy infants receiving exchange blood
11-24
-------
transfusions. The mean pre-transfusion COHb in six cases was 1.34 percent.
Donor blood contained 5.17 percent COHb, resulting in a mean value of
4.92 percent COHb in the transfused infant. In one infant transfused
with blood containing 8.87 percent COHb, the resultant COHb value in the
infant was 7.43 percent. Although it was stated that the infants did
not appear to be adversely affected by the COHb levels reached during
exchange transfusion, it should be noted that although measures were
gross, adverse effects at these levels of COHb have been observed.
Furthermore, in individuals whose 0? transport system or cardiovascular
reserve is already compromised, the presence of additional COHb from
transfused blood may result in a further and more potentially dangerous
decrement in arterial, mixed venous, and coronary sinus 02 tensions. It
should be recalled that some blood samples collected from blood donors
had COHb values that exceeded 18 percent.
An additional hazard to patients, especially those undergoing
146
cardiovascular surgery, may develop during anesthesia. Middleton et al.
have reported markedly elevated expired CO levels in patients undergoing
cardiac bypass surgery. This increment would be related in part to the
CO present in transfused blood and/or to the closed-circuit method of
anesthesia which precludes the loss of endogenously produced CO.
11.3.3 Angina
257
Two groups of investigators ' ' reported studies on patients with
angina pectoris. Aronow et al. studied the influence of riding in an
open car on a major Los Angeles freeway. Two trips of 90 minutes duration
were made; on one the patients breathed compressed CO-free air and on
11-25
-------
q
the other the ambient CO concentration averaged 61 mg/m (53 ppm).
Carboxyhemoglobin levels after this ride averaged 0.65 percent, in contrast to
the 5.08 percent observed in the trip in the open car. Exercise time, on a
bicycle ergometer, to the onset of angina, was determined prior to and after
the completion of the exposure. Although no changes in time of exercise to
onset of anginal pain were noted from the ride while breathing compressed air,
a significant reduction from a mean time of 249 to 174 seconds was found when
COHb was elevated. Ischemic ST-segment depression of at least 1 mm after
exercise-induced angina pectoris occurred earlier, after less exercise.
V
p
Anderson et al. conducted a study in which patients with stable angina walked
on a treadmill. They then breathed, while at rest, air containing 57 or
3
114 mg/m (50 or 100 ppm) intermittently over a period of four hours, raising
their COHb levels to 2.9 and 4.5 percent, respectively. The repeat exercise
tests clearly demonstrated a reduction in walking time to onset of angina. No
differences in time of angina onset were observed at the two induced COHb
levels although the duration of the pain was longer at the higher COHb levels.
Five of the ten patients had deeper ST-segment depression after CO exposure.
Other measures of cardiac function--systolic time intervals, left ventricular
ejection time, pre-ejection period index, and pre-ejection peak to ejection
time ratio—remained within normal limits.
5
Another study by Aronow and Isbell was somewhat similar to the
2 5
work performed by Anderson et al. Aronow and Isbell exposed patients
o
(nonsmokers at the time of the test) to 57 mg/m (50 ppm) CO, resulting
s
in a COHb concentration of 2.68 percent. This study was also conducted
11-26
-------
as a double-blind random trial in which subjects breathed CO on two days and
compressed CO-free air on two other days. All patients had their angina
pectoris documented by history and coronary angiography. A 16 percent
reduction in exercise time (bicycle) resulted following the CO exposures.
Ischemic ST-segment depression after exercise-induced angina occurred earlier
after less exercise and at a lower product of systolic blood pressure times
heart rate at the onset of angina after the patients breathed CO. Plotting of
the data suggests that there was a linear relationship between COHb levels and
the decrease in time to angina. Table 11-2 summarizes the above data.
TABLE 11-2. EXERCISE-INDUCED ANGINA AND CARBON MONOXIDE
(Each Study had 10 Subjects)
Carboxyhemoglobin Ambient3CO
Investigator percent (mg/m )
Initial
Aronow et al. 1.12
5
Aronow and Isbell 1.07
2
Anderson et al. 1.40
Einal
5.08 61*
2.68 57**
2f\r\ r*"7^^*fc
VI II t* / /\ /S /\
* -J\J
-------
while they sat in ventilated or unventilated rooms with other individuals
who were smoking cigarettes. It is possible that in addition to carbon
monoxide and nicotine, other components of tobacco smoke, including
oxides of nitrogen and hydrogen cyanide, and possibly psychological
factors, may have contributed to the decrease in exercise performance.
11.3.4 Epidemiological Evidence
Epidemiologic studies ' ' in the Los Angeles area have suggested
the possibility of increased mortality from myocardial infarction, associated
with high atmospheric levels of CO. Some differences of opinion have
been raised concerning interpretation of these data. A study similar in
128
design has been completed in Baltimore. The Baltimore data indicated
no apparent relation between either the incidence of myocardial infarction
or sudden death due to ASHD and the average 24-hour ambient CO
concentrations. Neither group of investigators was able to detect any
relation between postmortem COHb levels and causes of sudden death. The
Baltimore study was superior in that the diagnoses of disease state were
more precise and the population base more clearly defined than in the
other studies. The ambient levels of CO in Baltimore appeared to be
103
considerably lower than those reported for Los Angeles County.
During a 92-day seasonally excessive period of ambient CO, Kurt et al.
identified cardiorespiratory complaints (CRC) of a non-traumatic origin
from each of 8556 patient encounters at the Emergency Room of Colorado
General Hospital. Excessive numbers of CRC were seen above a threshold
3 3
limit of 6 mg/m (5 ppm) for the 24-hour mean and for the 13 mg/m
(11 ppm) one-hour mean maximum ambient CO.
11-28
-------
Whether this incidence is partially or totally related to CO exposure
and high altitude at which these observations were made needs further
-JCO
investigation. Radford evaluated patients admitted to the myocardial
infarction research unit at Johns Hopkins Hospital. While their diagnoses
were consistent with both an acute and chronic effect on the myocardium of
long term exposure to CO, the effects observed clearly could not be related
to that factor. Therefore, the possibility of an association between CO
levels in ambient air and incidence of myocardial infarction or sudden
deaths remains in question. It is apparent that more comprehensive and
extensive epidemiological studies need to be conducted in order to
clarify this issue.
11.3.5 Conclusions and Discussion
Table 11-3 summarizes the data on cardiovascular effects of CO
exposure. While the data are extremely limited due to the lack of
research on human exposures, it is possible that cardiac damage may result
o 123a
from chronic exposure to CO at levels as low as 80 mg/m (70 ppm).
Since more extensive data from animal studies show that such damage is
systematically observed in chronic exposures, the results of human
studies are not unexpected. The particular threshold level for cardiac
damage in humans has not been reliably determined, however, inasmuch as
o
only one study reports a level as low as 80 mg/m (70 ppm). Studies
utilizing bolus concentrations represent "real world" conditions.
Animal subjects are at risk to myocardial effects for several minutes
after exposure.
11-29
-------
TABLE 11-3. SUMMARY OF DATA ON EFFECTS OF CO ON HUMAN CARDIOVASCULAR SYSTEM
Reference
No. of
subjects
Exposure3
COHb
Dependent variable
Results
Comment
Corya et al.
48
CO
o
Aronow,
et al.
Alexieva and
Simitrova
Bogusz et al.
10
25
47
Ayres et al.
15
26
Ayres et al.14 26
and
15
(unknown)
16-25%
2 hours
(50 ppm)
2.77%
1-6 hours (mean
1 hour 20 min.)
5 hrs 30 min. mean
average
35%
average
17%
8-15 min
(1,000 ppm)
30-45 sees
(5,000 ppm)
(time sufficient to
produce stated COHb
(5,000 ppm 5%)
8-15 minutes
(1,000 ppm - 0.1%)
mean
8.96%
5-25%
Echocardiographic
findings after acute
CO poisoning
Symptoms of inter-
mittent claudication
Aspartate amino-
transferase (AspAT),
lactic acid dehydro-
genase activity,
and lactate level
in lighting-gas com-
pared to coal-stove
poisonings.
Systemic and myocar-
dial hemodynamic
responses
Myocardial and
systemic responses
Echocardiographic
(ECG) findings in
4 of the 5 cases
indicated prolapse
of the mitral valve,
suggesting that
myocardial damage
may occur in cases of
non-fatal CO poisoning.
Patients were ad-
mitted to a hospital
the same day they
suffered acute CO
poisoning due to a
faulty water heater.
Intermittent claudication
was significantly aggra-
vated due to CO exposure.
Enzymatic changes increase
with length of exposure.
Changes enzyme activity and^
lactate level parallel ECG and
clinical changes AspAT activity
was increased even without ECG
or clinical changes.
Coronary blood flow increased,
and extraction ratios decreased.
Systemic oxygen extraction was
increased.
Increased cardiac output and
coronary blood flow. Signs
suggesting myocardial hypoxia
were observed in patients with
coronary artery disease.
-------
TABLE 11-3 (continued)
Reference
No. of
subjects
Exposure*
COHb
Dependent variable
Results
Comment
Randal
et al.
15
(none)
Middletpn
et al145
22
Aronow.
et al.'
oo
Anderson et al.
10
10
Aronow ,
and Isbell
Kuller et al.
128
10
1397
1 1/2 hours
(20-210 ppm)
90 minutes
(42-63 ppm)
4 hours
(50 and 100 ppm)
2 hours
(50 ppm)
7.7-14 ppm
mean Change in COHb with
1.34-4.92% exchange blood
transfusions
(not known) Carbon monoxide
accumulation in
closed circle anes-
thesia systems.
3.8-1
mean
2.9% and
4.5%
mean
2.68%
Symptoms of angina
pectoris.
Onset and duration
of angina pectoris.
Exerci se-i nduced
angina pectoris.
0.9 to 9.9% Relationship between
exposure and heart
attacks\.
Elevations in COHb due to
receiving transfused blood
could not be shown to have
any adverse effect on the
recipient.
Closed system anesthetic
techniques allow the accumu-
lation of endogenous and ex-
ogenous CO, producing minimal
decremental effects.
Angina pectoris developed sooner
after less work, following ex-
posure to highway air.
Exposure to low concentrations
of CO produced anginal pain
of greater duration after less
exercise.
Exposure to CO produced
symptoms of angina sooner and
after less cardiac work.
No relationship was
established between
ambient CO levels
and onset of sudden
death and myocardial
infarction.
This study covers a
two-year period and
involves deaths due
to coronary disease
occurring in the
Baltimore area.
-------
Hexter andft~
Goldsmith1^
TABLE 11-3 (continued).
Reference
No. of
subjects
Exposure
COHb
Dependent variable
Results
Comment
(not
given)
7.3-20.2 ppm
8-17%
Community air
pollution and
mortality—total
number of deaths,
day of occurrence,
maximum temperature,
average CO concentration.
A greater number of
deaths was shown to
have occurred when
ambient CO concen-
trations were
This study covers
a period of 4 yrs
in Los Angeles
County.
higher.
al ppm CO = 1.145 mg/m3 CO and
mg/m3 CO = 0.874 ppm CO, at 25°C and 760 mm Hg.
GO
PO
-------
Certainly the alterations in blood flow observed in man agree with
those observed in experimental animals. Human data have been reported
which show that such compensatory changes do not occur as readily or
extensively, however, in cases of cardiac pathology.
The limited studies on patients having cardiovascular disease
suggest that the critical level of COHb is 2.5 to 3.0 percent. Additional
and confirmatory studies are definitely needed to determine the lowest
concentration of COHb at which no alterations in performance can be
detected. The available studies on patients do not give much information
about the role of CO in the development of the disease but do give some
indication of their dose-response relationship. The validity of these
data is strongly reinforced by complementary experimental animal studies
which show very similar dose-response curves.
The U.S. National Health Survey Examination reported that there
were 3,125,000 adults, ages 18 to 79 years, with definite coronary heart
disease and another 2,410,000 with suspected heart disease. Many of
these individuals, as well as others in the general population, have
COHb levels equal to or above 2.5 percent. It would be rash even to
suggest that the above-mentioned studies implicate CO as a factor in
determining the natural history of heart disease in a community. The
necessary epidemiological evidence for an association between frequency
of episodes of angina pectoris and community ambient CO levels is lacking; /
however, it is not presumptuous to state that individuals with cardiac
-"- - •-- ~^.,,.,_._ — ^ .
P
ailments are especially at risk to CO exposures sufficient to produce
2.5 to 3.0 percent COHb.
11-33
-------
11.4 PULMONARY FUNCTION AND EXERCISE
Maximal exercise can increase the 0« uptake of the whole body in
excess of 20 or more times the resting uptake and will stress the 0«
transport system maximally. Any impairment of 0« transport, such as
could occur when COHb is present, could limit maximal aerobic capacity
). In fact, it has been appreciated for some time that individ-
02 max
uals having a large burden of CO experience difficulty in performing
work.
180
Roughton and Darling suggested, on theoretical grounds, that
work capacity would be reduced to zero when COHb approached 50 percent.
11.4.1 Maximal Work
oc
Chiodi et al . in 1951 showed that subjects were unable to perform
tasks requiring only low levels of physical exertion when their blood
COHb reached 40 to 50 percent. Several collapsed while attempting to
37
perform routine laboratory tasks. Chihaia et al. have reported that
heavy physical work at low ambient CO levels can induce states of CO
74
poisoning. Goldsmith reported that competitive swimmers have impaired
performance when competitive events are conducted in atmospheres con-
3
tain ing 34 mg/m (30 ppm) CO originating from traffic.
11.4.2 0« Uptake and Heart Rate
In studies using submaximal exercise for short durations (5 to
60 minutes) it appears that 0« uptakes during work were unchanged despite
the presence of coHb.31'35'59-60'73.89'155-165-207'208 The only clear
indication of physiological load appeared to be a slight increase in
qc 1 pq
heart rate. Chevalier et al . and Klein et al . , studying men working
11-34
-------
at a light work load for a period of five minutes, reported that while
the Op uptake was not affected when COHb levels were approximately
4 percent (estimated Values), there was a significant increase in Op
debt when this was related to the total Op uptake. Nobody has yet
replicated these results on Op debt. Five subjects studied by Pi may
-I CC
et al. performed work for 15 minutes at an Op uptake of 1.5 liters
per minute. No differences in Op uptake were found, even though COHb
reached 15 percent. In a rather involved study in which COHb fluctuated
122
between 5 and 17 percent, Klausen et al. found no differences related
to CO in energy expenditure when subjects exercised for 15 minutes at
50 percent of their Vno ' Vogel et a1-208 and Vogel and Gleser207
\j£. max
and Pirnay et al. reported consistently higher heart rates for given
selected submaximal work loads, and increased ventilatory volume
exchange per unit of Op uptake, with COHb levels of 15 to 20 percent.
73
Gliner et al. studied the responses of two groups of 10 men each
(mean age 23.0 and 48.4 years, respectively), one-half of each group
, . , A • n -i * oc 4. vi was selected (untrained
being smokers. A work load of 35 percent Vn9 max/ v
\jtL iTIaX
men can work at this level for approximately eight hours with minimum
physiological changes), and the men worked for four hours in an environ-
o
ment containing 57 mg/m (50 ppm) CO. Final COHb's were 10.3 and
13.2 percent, respectively, for nonsmokers and smokers. Ambient temper-
atures were 25°C and 35°C, with relative humidities of 30 percent. The
only significant change was a higher heart rate in the CO environment
irrespective of age of subjects, confirming observations previously
11-35
-------
reported. Since cardiac index remained constant at approximately
2 3
6 liters/minute'm in both filtered air and 57 mg/m (50 ppm) or up to
3
115 mg/m (100 ppm) CO, stroke output was decreased. The full signifi-
cance of this change in long-term performance in co-polluted environments
is not apparent at this time.
Despite the wide variability in experimental conditions—duration
and magnitude of exercise, level of COHb, methods for giving CO to the
subjects, small number of subjects exposed, and their limited age range—
the results from all studies were essentially similar.
11.4.3 Aerobic Capacity
In short-term maximal exercise of several minutes' duration, where
capacity for effort is dependent mainly on aerobic metabolism, it is
anticipated that maximal aerobic capacity would be diminished approxi-
mately in proportion to the level of COHb present in the blood. Such
... .. . „ when COHb is between 7 and 33 percent has been
diminution in Vfto
02 max
conclusively observed by a number of investigators.
In the majority of these studies, exercise bouts ranged from 2 to 6 min-
utes and CO was administered either by breathing relatively high concen-
trations of this gas or by breathing a fixed amount with additional CO
to maintain the desired levels of COHb. Subjects were not always iden-
tified as to their smoking habits.
187a
Seppanen determined the physical work capacity of cigarette
smokers (20 cigarettes/day) following either smoking or inhalation
of CO. A progressive bicycle test to max was conducted after breathing
room air (2.8 percent COHb), after smoking (9.1 percent COHb), and after
11-36
-------
bolus breathing of 1100 ppm CO (9.1 percent COHb). The physical work
capacities at heart rates of 130, 150, and 170 beats per minute decreased
after both CO inhalation and cigarette smoking. The greatest decrease
in calculated maximal work was observed after CO inhalation.
In the above-mentioned studies, the levels of COHb were considerably
in excess of those occurring in men exposed to the outdoor air of certain
metropolitan areas. The initial studies by Horvath's group '*
o
were made on subjects breathing 57 mg/m (50 ppm) CO at either of two
thermal ambients, namely 25°C or 35°C, with a relative humidity of
20 percent. They utilized a walking test (requiring some 15 to 24 min-
utes to complete) with progressively increasing grade in order to measure
v . The two populations consisted of 20 young (24+ years) and
02 max
16 middle-aged (48+ years) subjects, both smokers and nonsmokers. The
middle-aged subjects demonstrated the anticipated decrease in .nv
associated with advancing age. However, the middle-aged nonsmokers had
v some 27 percent greater than that of smokers of the same age.
a V02 max
During the progress of the test, COHb levels in nonsmokers increased
from 0.7 to approximately 2.8 percent, while levels in smokers rose from
2.6 to 3.2 percent to 4.1 to 4.5 percent. Control studies conducted on
these subjects while they breathed filtered air indicated that COHb
decreased in both smokers and nonsmokers. The results from these
studies56'73'173'174 failed to demonstrate any reduction in VQ2 max*
The decrement in Vno „
02 max
the hot environment was greater than the changes that occurred from
breathing CO. Other cardiovascular, respiratory, metabolic, and
11-37
-------
temperature measurements made concurrently with the 0« uptake studies
also failed to show any decrements associated with the CO exposure. The
only significant effect related to CO was a decrease in absolute exercise
time. This was consistently observed in the nonsmoking subjects but not
in the smokers. These observations confirmed those found earlier by
59
Ekblom and Huot who, however, reported a surprisingly large decrease
3
(38 percent) in work time at 7 percent COHb. Aronow and Cassidy found
a slight decrease in work time during a maximal exercise test on 10
middle-aged (50.7 years) subjects. Their reported levels of 4.0 percent
3
COHb in subjects who had breathed 115 mg/m (100 ppm) CO for one hour is
what would be expected with initial control levels of 1.67 percent. One
of ten subjects developed ischemic ST-segment depression after maximal
exercise following CO exposure. No electrocardiographic changes were
observed in the subjects studied by Horvath's group. ' ' '
155
Nielsen found that subjects exercising under a CO load developed
higher internal body temperatures. Reductions in skin conductance
suggested a redistribution of the circulation to the working muscle and
away from the skin.
Horvath and coworkers ' ' ' had some concern about the
changes in COHb levels in their smokers and nonsmokers as well as the
, , f . . „ under the ambient and exercise conditions
lack of change in Vn/,
M 02 max
previously employed. They developed a more precise method to regulate
50
relatively low levels of COHb (Figure 11-1). It is of some importance
that they found that a low ambient level of CO can be quite effective in
maintaining a previously produced high blood COHb concentration. These
11-38
-------
C -15 -10 -50
5 10 15
TIME, minutes
Figure 11-1. The maintenance of requested COHb level in a subject during rest and at^various work levels with a widely ranging
ventilatory exchange. Control level of COHb was 0.6% prior to the administration of the initial bolus of CO to raise COHb to
desired level; a total of 34.2 mlof CCTSTPDI was given. (Used with permission of The American Physiological Society 38:366-368,1975.)
11-39
-------
data suggest that the ambient level of CO may have little to do with the
absolute level of COHb present in an individual. In these experiments a
double-blind study was again utilized in which subjects breathed either
filtered air, or air with CO which resulted in stable levels of COHb.
The data obtained clearly indicate that a threshold level of COHb must
be present before significant physiological alterations can be demon-
were noted when
strated. Statistically significant decreases in V v
max
COHb levels exceeded 4.3 percent. Although this was a double-blind,
randomized study in which neither the investigators nor the subjects
knew the composition of the air breathed, it was subsequently determined
that all subjects correctly identified the experiment in which they had
been exposed to the highest level of ambient CO. In all instances they
noted a heaviness of the lower extremities and greater difficulty in the
task. Ekblom et al . , utilizing a similar technique, raised COHb to
15 percent. The reduction in VQ2 max was e*Pected- Maxl'mal cardiac
output was decreased, however, due to a decreased stroke volume. Mean
, .. n was found by Clark and Coburn40 . . .
myoglobin P "to decrease during exercise
. T/ During exhaustive exercise, Pn increased, suggesting
at V02 max U2
facilitation of Op offloading; but when a COHb level of 5 percent was
present during exercise, P5Q decreased. Though the experiment was
conducted in Denver (1700 m altitude), subjects having a burden of
5 percent COHb exhibited a decrement in maximum performance similar to
that observed by others in subjects at sea level.
The data obtained by Horvath's group and others are summarized in
Figure 11-2. .There is a linear decline in Vn, mav when COHb 1eve1s
lllct/\
11-40
-------
40
30
0)
a
*
X
<
UJ
CO
<
UJ
DC
O
UJ
Q
20
10
SMOKERS
I I
15 25
PERCENT COHb
35
Figure 11-2. Relationship between COHb and decrement in maximum aerobic
power.
11-41
-------
range from 4 to 33 percent COHb. This can be expressed as: percent
decrease in V =0.91 (percent COHb) + 2.2. It should be noted
02 max
that this does not apply to smokers in Horvath's series, who had COHb
levels considerably in excess of 4 to 5 percent with no decrement in
their respective VQ2 ^ values'
11.4.4 Conclusions and Discussion
Table 11-4 summarizes the studies regarding pulmonary function and
exercise and the effects of CO exposure. There is some evidence that
3 205
work capacity is affected at CO levels as low as 34 mg/m (30 ppm),
but the study yielding those results was poorly controlled, since ambient
CO levels were used rather than systematic exposures.
Oxygen uptake during short exposures and submaximal work are
apparently not affected even when COHb levels are 15 to 20 percent.
These studies were usually done on healthy individuals and, frequently,
too few subjects were run for the study to be definitive.
The most carefully executed and extensive studies are those
involving aerobic capacity. Obviously, CO can modify these physiological
responses. The level of blood COHb required to induce these effects
appears to be approximately 5 percent. The concentration of CO in the
blood may be the most sensitive indicator of effect rather than the
ambient levels of this pollutant.
11.5 INTERACTIONS WITH OTHER POLLUTANTS AND DRUGS
11.5.1 Other Air Pollutants
There are many other compounds in polluted atmospheres that have
been demonstrated to have deleterious effects on physiological functions.
11-42
-------
TABLE 11-4. SUMMARY OF DATA ON EFFECTS OF CO ON HUMAN PULMONARY FUNCTION AND EXERCISE
Reference
No. of
subjects
Exposure*
COHb
Dependent variable
Results
Comment
Chiodi et al.
36
dogs
n=2
men
n=4
CO
Chihaia et al.
37
Goldsmith
74
(not
given)
Chevali
et al.
Pirnay
et al.
er
10
>70 minutes
(0.15-0.35%)
16-52%
Job exposure
Up to 2 hours
(11-30 ppm)
up to
50%
2%-3% minutes
(0.5%)
(not stated)
3.95%
15%
Pulmonary ventila-
tion, cardiac output
and plasma pH. Res-
piratory response
to high CO.
Physical work
(not given) Performance of
competitive swimmers
Oxygen uptake
Muscular exercise
during CO intoxica-
tion.
No hyperpnea observable during
rest with acute and severe CO
poisoning.
Arterial pCO? increased and pH
became acidic. In severe
poisoning, respiratory center
was depressed. Cardiac output
was increased slightly with COHb
up to 30%, increased as much as
1/2, up to 50% COHb. The direct
action on the respiratory center
of acute hypoxemia produced by CO
poisoning that is severe while
being still compatible with life
is purely depressive in nature.
Unable to perform low-
oxidation level work after
40 to 50% COHb
It was found that COHb was established
exposure to ambient by measuring expired-
CO raised COHb air CO samples.
levels to compare
with inhaled cigarette
smoke and affected
performance of swimmers.
Greater oxygen debt per
greater oxygen uptake when
compared with nonsmokers.
Maximal 0~ consumption lowered.
Greater ventilation was induced
during exercise. 02 uptake
not affected.
-------
TABLE 11-4 (continued)
Reference
No. of
subjects
Exposure*
COHb
Dependent variable
Results
Comment
Ekblom
and Huot
59
10
Horvat
et al.
Neil sen
155
(not
given)
Pirnay165
et al.
Drinkwater
et al.56
20
15 minutes (in quan-
tity theoretically
determined to obtain
stated blood values)
7 and 20%
Build-up and main-
tenance dose
(75 and 100 ppm) for
a period 15 min +
exercise time
(not given)
2.7, 4.5
and 5.2%
Response to maximal
and submaximal work
load at different
COHb levels
Maximal aerobic
capacity at dif-
ferent levels of
COHb.
(not given) Thermoregulation
and work
(not stated)
15%
50 ppm
3.17%
Muscular exercise
during CO intoxica-
tion.
Exercise and heat
stress
Maximal physical performance
was reduced with increasing
levels of COHb, as was VQ2
. Highest heart rate
aicVeased at 20% COHb during
maximal work and increased
during submaximal work at both
7% and 20% levels. There was
a more significant change in
Oy deficit at 20% COHb than
at 7% COHb.
VAO lower for COHb levels
02 max
of 4% or greater. Ventilatory
volumes were significantly
lower with COHb 3.2-3.4%.
Equilibrium body temperature
was higher. Acute exposure to
altitude left temperature level
unchanged.
Maximal 0? consumption was
lowered. Greater ventilation
was induced during exercise.
02 uptake not affected.
Exposure effectively reduced
work time of nonsmokers and
elicited changes in respiratory
patterns of both smokers and
nonsmokers.
-------
TABLE 11-4 (continued)
Reference
No. of
subjects
Exposure*
COHb
Dependent variable
Results
Comment
Raven
et al.
174
16
50 ppm
2.31-5.54%
Aronow and
Cassidy^
Raven
et al.
173
10
16
en
Ekblom
et al.
60
Clark
and Coburn
40
21
1 hour
100 ppm
(no exposure
time given)
50 ppm
15 minutes
(repeated once)
levels to produce
stated COHb
(not given)
3.95%
Increased
(14% for
smokers)
200% for
for non-
smokers
Age, smoking habits,
heat stress, & CO on
body temperature,
cardi orespi ratory
and metabolic
responses.
Maximal treadmill
exercise
Body temperature,
cardi orespi ratory
and metabolic
responses during
tests of maximal
aerobic power under
2 temperature condi-
tions (25o
12.8-15.8%
Changes in arterial
0« content in rela-
tion to circulation
and physical
performance.
(not given) Mean myoglobin oxy-
gen tension during
exercise at maximal
oxygen uptake
Total working time reduced with
exposure to CO at lower (25 C)
temperature. Older nonsmokers
V
had a decrement in 02 max*
Mean exercise time significantly
reduced.
No significant change in maximum
aerobic power. Total working time
was decreased in 25 C ambient
temperature. Older nonsmokers
w
showed decrement in 02 max*
Older smokers showed no change.
Regardless of ambient conditions,
smokers had a significantly lower
aerobic power than nonsmokers.
Aerobic power of older smokers
was 26% lower than that of younger
smokers.
Maximal physical performance de-
creased after CO exposure. Lower
cardiac output during CO-induced
hypoxia. Maximum heart rate was
significantly lower in 1 subject
at levels >13%.
During exercise of max 0? con-
sumption, CO shifted out of the
vascular compartment. It was
implied that the CO was taken up by
muscle tissue containing myoglobin.
-------
TABLE 11-4 (continued).
Reference
Klausen99
et al.
No. of
subjects
8
Exposure
(not given)
COHb
(not given)
Dependent variable
Circulation, metabo-
lism, ventilation
Results Comment
No change in ventilation at
rest, but changes present
in work.
Vogel
and Gleser
207
16
8
Gliner et al.
73
19
Collier.
et al.
1 hour
225 ppm
225 ppm
4 hours
50 ppm
Loading dose:
10,000 ppm to
produce mean COHb
of 8.9% maintenance
dose: 60-70 ppm for
5 mins (to produce
mean of 7.8%).
17-18% Physical work
capacity
18-20% Effect on 02 trans-
port during exer-
cise, compared with
hypobaric hypoxia
4.6 to Physiologic response
6.8% to long-term work
and thermal stress
8.9% and Physiological adapt-
7.8% ations and exercise
in normal healthy
males.
No impairment in ability to
do heavy work as a result of
elevated COHb was observed.
No significant differences in
0~ transport were detected,
tnough with CO hypoxia a lack
of cardiovascular response at
rest and a lesser ventilation
with exercise was apparent.
Decrement of stroke volume
which increased with higher
ambient temperature was
observed. Heart rate was
increased in CO.
CO produced minute volume +
breathing frequency increased
only during exercise, 0?
consumption and arteriovenous
00 content difference during
">
exercise. Venous 0« content
and venous PO? was Decreased
with exercise and at rest.
-------
TABLE 11-4 (continued)
Reference
Klein ^
et al.
No. of
subjects
4
Exposure3
(not given)
V
COHb
4-12%
Dependent variable
Hemoglobin affinity
for oxygen in rela-
Results Comment
Maximal exercise induces
a change facilitating 0«
tion to exercise and
chronic elevation
of COHb
offloading, but the mecnanisms
and significance of the change
remains to be established. Re-
duction of Ca02 during moderate
elevation of COHb does not in-
duce compensatory changes in P_Q
to facilitate tissue oxygenation.
al ppm CO * 1.145 mg/m3 CO and 1
mg/m CO = 0.674 ppm CO, at 25°C and 760 mm Hg.
-------
Horvath and his group » 3»173»174 have shown that combinations of
3 3
57 mg/m (50 ppm) CO and 1.33 mg/m (0.21 ppm) peroxyacetylnitrate (PAN)
exerted no greater effect on work capacity of healthy men--young and
middle-aged, smokers and nonsmokers—than that of CO alone. However, it
appeared that slightly greater concentrations of either component could
92 93
have led to significant differences in response. Hackney et al. *
found no consistent changes (synergistic or additive) in pulmonary
functions in a 2-hour exposure of young male subjects to a combination
3
of three pollutants - S02, 03, and CO (34 mg/m ; 30 ppm). It has been
139
reported by Mamacasvili, who exposed human volunteers to low concen-
trations of CO and S0«, that each component produced independent delete-
rious visual effects on light and color sensitivity. An 8-hour exposure
to mean ambient concentrations of CO and ammonia resulted in insignifi-
202
cant physiological and biochemical effects on young healthy nonsmokers.
An additive effect was observed by Elfinova et al. for a combination,
at low concentrations, of CO, phenol, and dust.
90
Gzegocskij reported that the presence of CO and nitrogen oxides
in dust-laden air could reinforce the toxic effect of silicon dioxide
and hasten the development of silicosis.
11.5.2 Other Environmental Parameters
The organisms' response to the presence of CO may well be modified
by the presence of other environmental factors such as ambient temperature,
124
relative humidity, and barometric pressure. Korenevskaja indicated
that high ambient temperatures reinforce the toxic effect of CO and that
the presence of CO lowers the body's resistance to overheating. Men
11-48
-------
working for four hours in an ambient temperature of 35°C and 20 percent
relative humidity and exposed to a CO concentration of 57 mg/m3 (50 ppm)
failed to demonstrate synergistic effect. * Horvath's group
reported reduced working time with CO at 25°C but not at 35°C.
Experimental animal studies have shown the importance of temperature
effects on survival at high CO exposure levels.
11.5.3 Alcohol
Rockwell and Weir evaluated the interactive effects of CO and
alcohol on highway driving performance using four young, nonsmoking
college students. Carboxyhemoglobin levels were 0, 2, 8 and 12 percent
and blood alcohol was 0.05 percent. Perceptual narrowing and decreased
visual activity were noted under increasing COHb levels but there was an
alcohol-CO synergistic interaction only in curve negotiation tasks at
the 12 percent COHb level.
Stewart's group has recently evaluated behavioral functions in
relation to the hypothesis that alcohol ingestion (59 mg percent blood
level) would potentiate any deleterious CO effects. Neither the presence
of COHb levels of 8.8 percent or the blood alcohol levels produced
deleterious performances.
11.5.4 Smoking
A common source of CO for the general population comes from tobacco
smoking, with other primary sources arising from the environment.
Exposure to smoking primarily affects the COHb level of the smoker
himself119'129 but in some circumstances, such as in poorly ventilated
space, smokers provide a source that may affect other occupants. In
11-49
-------
addition to CO, other products inhaled by the smoker may produce subtle
physiological and biochemical effects on both the smoker and those
individuals breathing either the pre-inhaled materials or the smokers'
182 191
exhaled products. ' The possible interaction of CO and other
constituents of smoke which may occur in the lungs and other tissues and
so induce pathological changes remains to be elucidated.
Those interested in the problems related to smoking tobacco, i.e.,
carcinogenesis, and cardiovascular and pulmonary disease, should refer
to documents specifically concerned with these matters. ' *
Prospective and retrospective epidemiological studies have identified
cigarette smoking as one of the major factors in the development of
coronary heart disease (CHD). The risk of developing CHD for pipe and
cigar smokers is apparently much less than it is for cigarette smokers
but more than it is for nonsmokers. Tobacco smoking may contribute to
the development and aggravation of CHD through the action of several
independent or complementary mechanisms, one of which is the formation
of significant levels of COHb.168
In the report of their epidemiological study in Baltimore, Kuller
128
et al. have stated that if there is an association between CO and
heart attacks, the significant exposures are probably related to micro-
environmental factors and cigarette smoking rather than community air
pollution. They did note that relatively few heart attacks occur while
11
an individual is smoking a cigarette. Astrup has suggested that
intermittent exposure to CO may be regarded as putting smokers at a much
higher risk than nonsmokers for the development of arterial diseases.
Wald et al. and Ball and Turner have come to similar conclusions.
11-50
-------
Smoking of cigarettes has been found to result in higher COHb
04. TOO
levels than exposure to street air levels of CO. ' Manual workers
had lower COHb levels than sedentary workers (both smokers), probably
related to the increased ventilation required in the occupations of the
34 184 191
manual workers. ' Srch performed tests on two smokers and two
nonsmokers in a small car. Before entering the car the smokers and
nonsmokers had COHb levels of 5 and 2 percent, respectively. Each
smoker smoked five cigarettes with the windows and doors closed. At the
end of the 60-minute test, the respective COHb in the smokers and non-
smokers had increased to 10 and 5 percent. Other studies have reported
essentially similar patterns of accumulation in nonsmoking individuals
exposed to smokers in other closed spaces. The pattern of accumulating
49 113 214
CO (as well as other products) in closed spaces has been reported. ' '
A mathematical model for calculating the build-up of CO and the resultant
118
COHb levels has been developed.
The quantity of CO actually entering the lung depends upon the form
in which tobacco is smoked, the pattern of smoking, and the depth of
inhalation. Very little CO is absorbed in the mouth and larynx
(approximately 5 percent), so that most of the CO available for transfer
to Hb must reach the alveoli in order to raise the level of COHb present
in the blood stream. Cigarette smokers inhale more than cigar smokers,
and the latter less than pipe smokers; but individual differences in
this pattern are quite marked. Heavy cigarette smokers have COHb levels
as high as 15 to 17 percent. The CO concentration in cigarette smoke is
approximately 4.5 percent. 65»"»100»2l0a it has been estimated that the
11-51
-------
o
cigarette smoker may be exposed to 458 to 572 mg/m (400 to 500 ppm) CO
for the approximately six minutes utilized to smoke a cigarette.
129
Landaw noted that a smoker's COHb level increased 1 to 9 percent
during periods of active smoking. He also presented data suggesting
that the half-time of CO elimination in smokers was approximately
188 189
291 minutes. Smith and Landaw ' reported that smokers (mean COHb
of 11.6 percent) had an increased red-cell volume or a reduced plasma
-I CO
volume (or both). Pankow et al. have raised the question as to
whether or not these changes represent an adaptive response. Figure 11-
3 illustrates the pattern of change in COHb in a typical heavy cigarette
129
smoker. An indwelling venous catheter permitted the frequent sampling
of this smoker's blood. The subject smoked only during his working
hours. When he began to smoke the next day, he still had a body burden
of 1.7 percent COHb. Cigarette smokers generally are excreting CO into
the air rather than inhaling it from the ambient environment.
Low-toxicity cigarettes produce significantly smaller amounts of
CO. However, the smoking pattern of the individual markedly .alters the
absolute amount of CO inhaled.
Frankenhaeuser et al. have reported another response to cigarette
smoking that may have important consequences to the smoker. They observed
a progressive increase in adrenaline (epinephrine) excretion with number
of cigarettes smoked. These investigators have also found that certain
psychophysical performance measures did not deteriorate if moderate
smokers smoked during the testing in contrast to the decrement observed
when they did not smoke during testing.
11-52
-------
.0
X
o
u
UJ
o
cc
LU
Q.
3 -
SMOKING
29CIG. @1/14MIN
I
1
10
15
HOURS
20
(05:18)
25
Figure 11^3. Pattern of change in COHb in a typical cigarette
11-53
-------
p
Aronow et al. studied eight angina patients who smoked cigarettes
or were given CO to breathe so that the final COHb levels were approxi-
mately equivalent (3.90 and 3.86 percent). These patients were smokers,
and their initial COHb levels were above 2 percent. Catheterization of
both left and right ventricles permitted an evaluation of the functions
of the myocardium. The major differences observed under the two condi-
tions were as follows: (1) cardiac output decreased with CO inhalation
and did not change with smoking; (2) systolic and diastolic arterial
pressures did not change with CO but increased with smoking; (3) left
ventricular change in pressure with time (dp/dt) decreased with CO but
did not change with smoking; (4) left ventricular end diastolic pressure
increased in both situations; and, (5) the partial pressure of Op in
arterial, mixed venous, and coronary sinus blood decreased with CO
exposure and with smoking. Furthermore, CO causes a negative inotropic
effect on the myocardium; which decreases left ventricular dp/dt,
decreases stroke index, decreases cardiac index, and increases left
ventricular end diastolic pressure. These divergent effects need to be
P
further evaluated. Aronow et al. stated that the increased systemic
blood pressure and heart rates that are observed following cigarette
smoking were related to the nicotine in the cigarette.
A critical problem arises in attempts to separate the CO effects of
cigarette smoking from the effects of other substances present in the
9
inhaled cigarette smoke. Aronow et al. had male angina patients smoke
lettuce leaf, non-nicotine cigarettes, which resulted in blood COHb
levels of 7.8 percent. Heart rate and blood pressure were unaffected by
11-54
-------
this smoking but again angina, on effort, occurred earlier. These data
may suggest that the presence of COHb following smoking of cigarettes
may be the major factor in the development of angina pectoris during
exercise. Chest pain and electrocardiographic changes have been associ-
ated with acute CO poisoning. Wald and Howard have stated in their
overall review on smoking, CO, and arterial disease:
"There is at present only indirect evidence that CO may be a cause
of atheroma in man and for the present, however, it is necessary to
reserve judgment on whether CO is a cause of arterial disease,
while at the same time suspecting that it may be the principal
agent in tobacco smoke."
5 2
Aronow and coworkers, as well as Anderson et al., have shown that
in patients with ischemic heart disease, exercise-induced angina occurs
earlier when the patients are exposed to low levels of CO. Carbon
monoxide exposure also exacerbates and prolongs the pain of intermittent
claudication in patients with this disease. The potential deleterious
influence of cigarette smoking and/or CO exposure on the pregnant woman,
fetus, and neonate will be considered elsewhere. The only direct evidence
that CO adversely influences fetal development was derived from studies
conducted on rabbits and rats. '
A number of studies have suggested that cigarette smoking reduces
work capacity,733'1243'206 in direct relation to the level of COHb
present in the working subject. In young smokers, 21 to 30 years of
age, no differences in maximal aerobic power were observed despite
173
reductions in vital capacity and maximum breathing capacities. Older
smokers (40 to 57 years of age) had significantly lower (27 percent)
174
aerobic power than comparably aged nonsmokers. Younger smokers had
11-55
-------
only a 6 percent lower aerobic power than nonsmokers of similar age.
144
McHenry et al . found that the duration of maximal exercise and maximal
heart rate was significantly shorter in smokers and former smokers than
in nonsmokers. Maximal systolic blood pressure during exercise was
•
greater in smokers. Tobacco smoking decreased Vn9 even in ^ ^
max
moderate smokers. The effect of passive smoking (i.e., exposure to
three individuals smoking five cigarettes each) on nonsmoking patients
"y\\
with exercise-induced angina has been reported. Their exercise time
to the onset of angina was decreased 22 and 38 percent, respectively,
from exposure in a well ventilated versus an unventilated room. Blood
COHb levels were 1.77 and 2.28 percent, respectively, in these patients.
There still remains some question as to the role of other materials in
cigarette smoke in producing this reduced performance.
Smokers may have early closure of small airways, especially when
supine. The diffusing capacity for CO in young smokers as well as
older smokers is impaired. ' Other physiological changes have also
been reported. The potential hazard of rapid smoking utilized in the
stimulus-satiation method to help smokers break the smoking habit has
147
been identified by Miller et al. Carboxyhemoglobin levels above
22 percent can occur.
11.5.5 Conclusions and Discussion
While it is important from the point of view of general and theo-
retical information to know how CO alone affects various physiological
and behavioral systems; CO does not occur by itself in the actual
environment. The data relating CO to other pollutants is so sparse,
11-56
-------
however, that almost no pattern can be discerned. Both human and labora-
tory animal studies suggest cases in which CO either additively or
synergistically combines with other airborne pollutants to produce
increased effects; but there is usually only one study per pollutant
combination and even those do not give parametric data from which dose-
response curves or thresholds might be estimated. There is a definite
need to obtain in a systematic manner information about real-life combi-
nations of other pollutants with CO.
In both human and experimental animal studies, the data regarding
alcohol in combination with CO are only suggestive. This frequently
occurring combination is of such import as to urgently require further
research, especially with regard to behavior and psychomotor performance.
Other drugs (both therapeutic and illicit) which would be expected to
interact with CO have not been studied. It would seem to be of paramount
importance to know the combined effect of CO and such drugs as
tranquilizers, sedatives and illicit psychotropic drugs. Data from
experimental animal studies strongly indicate that the effects of such
drugs are potentiated and/or altered by CO exposure. The possibility
that CO may potentiate or counteract the effects of drugs designed to
alleviate cardiovascular or pulmonary conditions is quite important in
view of COHb levels attributable to environmental sources and smoking.
Smoking is both another source of CO to the smoker and others as
well as a source of other chemicals with which environmental CO levels
could interact. Available data strongly suggest that chronic CO exposure
via smoking produces cardiopulmonary damage, but the interaction with
11-57
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other products of smoking confounds the results. Data on the effects of
environmental CO increments in addition to COHb built up due to smoking
have produced results which in some cases imply additive effects and in
other instances imply adaptation to COHb. There is need for further
systematic and parametric research to descry these relationships.
11.6 HIGH/ALTITUDES - MECHANISMS
Precise data on the potential scope of the problems attributable to
CO for high altitude residents and visitors are not available.
Approximately 2.2 million people live at altitudes (land elevations)
above 1524 meters in the United States. These figures do not present a
complete picture of potential numbers of individuals who may be subjected
to CO at these altitudes because the tourist population in these areas
is high in both summer and winter. Furthermore, proper tuning of automo-
biles for high altitude traveling is uncommon, and the influx of visitors
and cars with their greater emissions of CO and other contaminants may
prove to be an important factor in raising pollution exposure to an
unacceptable point. At 1540 meters, each cubic meter of air contains
approximately 18 percent less oxygen than at sea level. Therefore,
concentrations of carbbn monoxide in air in a city like Denver will be
3
22 percent higher than at sea level (i.e., a 10 mg/m , 8-hour average is
3
equivalent to 11.8 mg/m at Denver's altitude).
11.6.1 Physiological Results
Carbon monoxide exposure may aggravate the Op deficiency present at
high altitudes. When high altitude and CO exposures are combined
(Table 11-5), the effects on 0« availability in blood are apparently
11-58
-------
additive. It should be noted, however, that each of these, decreased
PQ2 in the air and increased COHb, produce different physiologic responses,
They have different effects on blood PQ2, on the affinity of CL for Hb,
on the extent of 02Hb saturation (CO hypoxemia shifts the OJHb dissoci-
ation curve to the left, and a decrease in PAQ2 shifts it to the right),
and on ventilatory drive.
TABLE 11-5. APPROXIMATE PHYSIOLOGICALLY EQUIVALENT ALTITUDES
AT EQUILIBRIUM WITH AMBIENT CO LEVELS
——•.—-.—-.———————_________ _ _ ______ «._....___...__i.,.._—__..________.. _.. ____ _______
Ambient Actual Altitude (meters)
CO concentration 0 (sea level) 1524 3048
mg/m ppm
Physiologically Equivalent
0
28.6
57.3
114.5
0
25
50
100
0 (sea level)
1829
3048
3749
1524
2530
3658
4663
Altitudes with COHb
3048
3962
4694
5486
69
Forbes et al. reported that during light activity at an altitude
of 4875 meters, CO uptake was increased, probably because of the hyper-
ventilation at altitude caused by the respiratory stimulus of decreased
Pn?. Evidence that CO elimination was similar at sea level and at
80 187
altitudes up to 10,000 meters was obtained by several investigators. *
Increased ambient temperatures up to 35°C and hard physical work increased
the rate of elimination. Pitts and Pace stated that every 1 per-
cent increase in COHb (up tp 13 percent) was equivalent to a 109-meter
rise in altitude if the subjects were at altitudes of 2100 to 3070 meters.
Their observations were based on changes in the heart rate response to
work. Subjects who may have been smokers were not identified.
11-59
-------
Two groups of investigators have presented data comparing the
physiologic responses of subjects to altitude and CO where the hypoxemia
due to altitude and the presence of COHb were approximately equivalent.
23
In one study the COHb varied around 12 percent (although the mode of
presentation of CO was such that COHb ranged during the CO exposures
from 5 to 20 percent) and the altitude study was conducted at 3977 meters,
187
The second study compared responses of subjects at altitudes of
4000 meters and a COHb content of 20 percent. In both studies, COHb
content was in excess of that anticipated for typical ambient pollution.
However, it was suggested that the effects attributable to CO and to
209a
altitude were equivalent. Wagner et al. studied smokers and non-
smokers who exercised at 53 percent of their Vno and at 760 and
02 max
523 torr. Carboxyhemoglobin levels were raised to 4.2 percent. While
at altitude and in an altitude chamber with elevated COHb levels, non-
smokers increased their cardiac output and decreased their arterial-
mixed venous 0« difference. Smokers did not respond in similar manner.
Smokers may have developed some degree of adaptation to altitude.
Parving exposed humans to CO to produce 20 percent COHb and to
simulated high altitude sufficient to produce an equivalent arterial
blood oxygen saturation. Exposure times were three to five hours. The
results showed increased capillary permeability for proteins during
exposure to CO but not during exposure to simulated high altitude. It
was also shown that plasma volume decreased significantly during the
simulated high altitude exposure but not during CO exposure. The plasma
volume was explained as due to hypoxia-induced hyperventilation but the
11-60
-------
effect on capillary wall permeability appears to be unique to CO and
therefore apparently represents a non-hypoxic short-term effect.
It was recommended on theoretical grounds that the ambient CO in
tunnels being constructed at 3859 meters should not exceed 29 mg/m
149
(25 ppm). The maximal aerobic capacity is reduced approximately
20 percent in individuals exposed to an altitude of 3085 meters. Weiser
216
et al. reported that max VQ2 was significantly impaired in subjects
living at 1700 meters when their COHb levels were 5 percent. However,
this decrement is similar to that seen in sea level residents. No data
29
are available for higher altitudes. Brewer et al. conducted a study
on residents of Leadville, Colorado (3085 meters). The mean COHb level
in smokers at altitude was higher than that of smokers at sea level.
This increased degree of hypoxemia may have contributed to the elevated
red cell mass observed since individuals who stopped smoking demonstrated
128a
a reduction in their red cell mass. Kurt et al. demonstrated that
ambient CO levels in Denver, Colorado had a significant, low-level
association with a number of patients with acute morbid cardiorespiratory
complaints presenting themselves in an emergency room.
11.6.2 Behavioral and Central Nervous System
The most supportive information on the additive nature of CO hypoxia
and hypoxic hypoxia originates from psychophysiologic studies and even
24
these are not as persuasive as one would desire^ Blackmore analyzed
the cause of aircraft accidents in Britain, finding that COHb levels
provided valuable information relative to altitude and CO sources. The
relatively high levels found could be attributed to equipment failure,
11-61
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smoking, and fires. No data are available on the effects of CO on
native inhabitants of high altitudes or on the reactions of these natives
when they are suddenly removed to sea level and possible high ambient CO
concentrations.
142
McFarland et al. showed that changes in visual threshold occurred
209
at a simulated altitude of approximately 2425 meters. Vollmer et al.
studied the effects of CO at simulated altitudes of 3070 and 4555 meters
and reported that there were no additive effects of CO and altitude.
They suggested that the effects of CO were masked by some compensatory
mechanisms. The data presented were not convincing. Lilienthal and
133
Fugitt indicated that a combination of altitude (1540 meters) and
5 to 9 percent COHb induced a decrease in flicker fusion frequency,
although either one alone had no effect. They also reported that the
presence of 8 to 10 percent COHb was effective in reducing altitude
tolerance by some 1215 meters.
11.6.3 Conclusions and Discussion of Carbon Monoxide and High Altitude
Combinations
Data from both physiologic and behavioral studies on humans seem to
indicate a simple additive effect of CO and high altitudes. They both
reduce 0? availability, and there are data which allow estimation of
their common effect on 0« levels.
It would be erroneous to infer that CO hypoxia and hypoxic hypoxia
are equivalent states or produce equivalent results. They apparently do
at equilibrium states, but CO uptake and elimination produce a slower
rate of 0« change than hypoxic hypoxia. Hypoxic hypoxia also produces
hyperventilation; CO hypoxia does not.
11-62
-------
Data from experimental animal studies imply that for some physiolog-
ical functions, CO has additional non-hypoxic effects which might act to
impair functioning of some systems. Although such additional impairment
might represent unanticipated, more-than-additive effects of CO and high
altitude, data from human studies on this are lacking.
11.7 ADAPTATION, HABITUATION, AND COMPENSATORY MECHANISMS
Extensive discussion of these topics was given in Chapter 10.
There, for purely logistical reasons, the term "adaptation" was used to
refer to long-term effects, and the term "habituation" was used to refer
to short term effects. This convention will be continued here.
In Section 10.8, discussion was made of experimental animal data
showing that COHb levels produced physiological responses which by their
nature tended to offset other deleterious effects of CO. Such responses
were: (1) increased coronary blood flow, (2) increased cerebral blood
flow, (3) increased hemoglobin via increased hemopoeisis, and
(4) increased 0? consumption in muscle. Where possible, an evaluation
of the completeness of such so-called compensatory responses was made
and, in general, the compensation appeared to be only partial in nature.
There was also some evidence that such compensation on a long-term basis
might have undesirable side effects.
11.7.1 Adaptation and Other Long-Term Effects
The presence of a clinical state of chronic CO poisoning with the
implication that adaptation to CO occurs in humans has not been verified.
If it existed, such a state should have been identified by studies on
long-term heavy smokers or on individuals exposed to environmental
11-63
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sources of CO. Early concern in England and Scandinavia with CO intoxi-
87 121
cation led to studies suggesting the possibility of such a condition. *
However, problems regarding the employment of high levels of inspired CO
(several hundred parts per million) and inadequate experimental methods
have resulted in some skepticism of the conclusions presented.
121
Killick, using herself as a subject, reported that she developed
acclimatization as evidenced by diminished symptoms, slower heart rate,
and the attainment of a lower COHb equilibrium level following exposure
to a given inspired CO concentration. Interestingly, Haldane and
96
Priestly had earlier reported a similar finding as to the attainment
of a different COHb equilibrium following exposure to a fixed level of
CO in the ambient air. Additional information on other possible adap-
tation effects in the pre-1940 literature can be found in KiHick's
review.
The mechanism by which long-term adaptation is assumed to occur, if
it could be demonstrated in humans, is an increased Hb concentration via
a several-day increase in hemopoeisis. If, in fact, such data from
human studies were available, the question of the completeness of the
adaptation would be very important as would the question of the undesir-
able chronic side effects of the compensation. If an appreciable amount
of compensation occurs in man, then it may be inferred that in subjects
with impaired compensatory mechanisms, CO effects might be much more
extreme.
11-64
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11.7.2 Habituation and Short-Term Effects
The only evidence for short-term COHb compensation in man is indirect.
From experimental animal studies it is known that coronary blood flow is
increased with COHb, and from human studies it is known that subjects
with impaired cardiac functioning have the lowest threshold to CO-
induced decrements. The implication is that in some cases of cardiac
impairment, the short-term compensatory mechanism is impaired and thus
the threshold is lowered.
In a few instances of behavioral testing, it has appeared that
decrements due to CO have occurred only at very low levels or at early
exposure times and have, in the same studies, not appeared at higher or
longer exposures. This has led to the hypothesis that there might be
some threshold or time lag in a compensatory mechanism, such as increased
cerebral blood flow (CBF). Not only is there no direct physiological
evidence from human or experimental animal studies for such a threshold
or time lag, but it would appear to be more conservative to assume that
the behavioral effects which were observed were due to possible non-
random sampling.
The idea of a threshold or a time lag in compensatory mechanisms
should not be rejected. There simply is no direct evidence. Studies
should be performed which (1) measure CBF and tissue PQ2 with low COHb
levels at various saturation rates to determine early and low level
effects accurately and (2) design behavioral studies where threshold
effects or time lags are factors in the experimental design that can be
explicitly studied.
11-65
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11.8 SPECIAL GROUPS AT RISK
As discussed in Chapter 10, it is known from both theoretical and
empirical experimental animal research that certain groups in the popu-
lation are at a higher than normal risk of detrimental effects of CO
exposure. The list of such groups from Chapter 10 included the fetus,
subjects with health impairments, subjects who are under the influence
of drugs, and subjects who have not been adapted to high altitude and
are then exposed to a combination of high altitude and CO. Even in
laboratory animals, there is too little information about CO effects in
these special risk groups so that an assessment of the extent of the
increased risk and the circumstances under which it might occur is
difficult. In this section, human studies will be reviewed in an attempt
to deduce the extent of the problem which has been described in
experimental animals.
11.8.1 Fetus
It has been shown in experimental animals that short-term maternal
CO exposure results in lower COHb levels in the fetus than in the mother,
but has greater detrimental effects in the fetus than in the mother.
Long-term maternal CO exposure has been shown to lead to higher fetal
than maternal COHb. Fetal uptake and elimination of CO has been shown
to be slower than maternal. These data are reviewed in Chapter 10.
Pregnant mothers and their fetuses may be exposed acutely or chron-
ically to CO either by maternal smoking or by environmental pollution.
The biologic effects of CO exposure on fetal tissues during intrauterine
development or during the newborn period require clarification. Of the
11-66
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several mechanisms that may account for the influence of CO on developing
tissue, the most important is the interference with tissue oxygenation.
Carbon monoxide decreases the capacity of Hb to transport 0? and shifts
the 02 saturation curve to the left. The normal arterial PQ2 supplying
fetal tissue is approximately 28 torr. This additional shift to the
left will tend to decrease further the Op gradient from maternal to
fetal blood across the placenta! tissue. The decreased PQ2 and the
diminished 02 transport due to the presence of COHb may also produce
undesired influences on the fetus.
One of the possible mechanisms by which CO or other components of
tobacco smoke may adversely influence fetal development is through
interference with the metabolic function of placental cells. These
cells have a role in hormone metabolism, as well as in the transport of
vitamins, carbohydrates, ami no acids, and other substances, through
201
their energy-dependent processes. Tanaka reported that the 02
uptake of placenta tissue slices from smoking mothers varied inversely
with maternal carboxyhemoglobin (COIIb), being markedly reduced when
CO Hb was greater than 7.0 percent. The preponderance of evidence
concerning CO Hb levels, along with fetal and perinatal exposure, tends
to warrant the minimization of exogenous CO sources to which this group
T36
might be exposed. Longo has reviewed the pertinent literature up to
inc
1977 and Hill et al. have provided a mathematical model for the
exchange of CO between the fetus and the mother.
Another factor that may produce differential effects on the fetus
is related to the endogenous production of CO by pregnant women.
11-67
-------
135
Longo indicates that nonsmoking pregnant women produce 0.9 ml CO/hr;
137
non-pregnant women produce 0.39 ml CO/hr. Fetal endogenous CO production
accounts for 3 percent of the total COHb present in the blood of a nonsmoking
normal pregnant woman. The source of the remainder is unknown although it may
be partly accounted for by the increased red cell mass of the pregnant woman.
Even though the hyperventilation of pregnancy may partially compensate for the
increased CO production in the absence of exogenous exposure, the CO Hb still
135
remains at about 13 percent above that which is in nonpregnant women. It
should be noted that post-partum (24 hours) females may be producing three
times as much CO as a near-term nonsmoking pregnant woman. Hemolytic disease
of newborn infants (physiological jaundice) produces a high level COHb
resulting from endogenous production and so provides a further stress to the
infant.161'154
Smoking mothers have been reported to have from 2 to 14 percent COHb,
while COHb levels in the fetuses ranged from 2.4 to 9.8 percent. These values
may not represent conditions present during pregnancy, since these data were
obtained just prior to birth. The newborn are also subject to ambient levels
20
of CO. Berhman et al. measured COHb in 16 relatively normal newborns in a
downtown Chicago nursery. Carboxyhemoglobin was found to be as high as 6.98
percent. These investigators indicated that the absolute COHb levels were
related to ambient levels of CO. Some doubts as to this conclusion exist
since the monitoring reference site was some 1.5 miles from the nursery. The
investigators reported no untoward clinical effects from these levels of COHb.
11-68
-------
However, the high levels of COHb in neonates are of some concern and
warrant further investigation.
13 138
Several studies * have demonstrated that babies delivered of
mothers who smoke cigarettes weigh less than those delivered of non-
smoking mothers. Relative maternal, fetal, or placenta! hypoxia may be
responsible, as suggested by the observation that infants born at higher
l ^1
altitudes also weigh less than those born at sea level. The New Mexico
Department of Health (1975) has provided additional confirmation of the
relationship between altitude and birth weight.
Maternal smoking probably constitutes the most frequent source of
fetal exposure to CO. There is some question as to the relationship of
fetal deaths to maternal smoking but there is no doubt that such smoking
results in higher than normal fetal COHb. * Gennser et al.
found that maternal cigarette smoking abruptly decreased the proportion
of time that the fetus made breathing movements. The relation to CO is
not clear. The effect of maternal smoking on surviving children is not
-1 OC
well known. Discussion of this point is available from Longo. There
remain a considerable number of unanswered questions as to the influence
which various levels of COHb have on the mother and on the fetus.
11.8.2 Impaired Groups
As pointed out in the section on cardiovascular effects, the lowest-
effects level of CO (about 2.5 to 3 percent COHb) has been shown in
subjects with cardiovascular damage. Such impairments produce low CO
thresholds because there is already sufficient hypoxia of cardiac tissue
to produce impairment, so that there is no reserve or compensatory
capacity.
11-69
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Another group which also has impaired Op delivery is composed of
individuals with impaired cerebrovasculature. This group consists
mainly of persons with obstructed vasculature due to cholesterol buildup
and to previous cerebrovascular injury. While on theoretical grounds it
is probable that subjects with impaired cerebrovasculature would have
very low thresholds for detrimental effects of CO exposure, there are no
direct experimental data on the subject in either humans or laboratory
animals. The possible effects of reduced 02 supply to the CNS range
from all of the behavioral effects reported to be caused by CO, to the
possibility of precipitation of motor seizures or cerebrovascular
accidents.
Subjects whose blood has reduced 0« carrying capability because of
either dietary or pathological anemia should also be at special risk to
CO exposure. Unfortunately, the effects of CO on anemic patients or
experimental animals have not been adequately studied. It can be assumed,
a priori, that anemic persons could be at greater risk than normal
persons because the capacity of the 0« transport system is reduced.
Tissue oxygenation may be initially compromised due to the anemic state
since mixed venous PQ2 accompanying a particular COHb value is somewhat
greater in anemic than in normal subjects. In patients with hemolytic
fi?
anemia and sickle cell disease, the rate of endogenous CO production
from heme catabolism is increased. Normal subjects produce approximately
18 moles CO/hr, resulting in COHb levels of 0.5 to 0.8 percent. Carbon
41 134
monoxide production in anemic patients ' has been reported to vary
from 31 to 158 moles/hr, producing COHb levels of 1.3 to 5.2 percent.
11-70
-------
Anemic individuals approach equilibrium levels of COHb more rapidly
than those with normal Hb levels at any given exposure to CO. Exposure
3
to 21.9 mg/m (25 ppm) CO for approximately four hours in an individual
with 7 g percent of Hb could result in 4 to 5 percent COHb, compared to
an anticipated level of 2.5 percent for normal individuals. Exogenous
CO exposure of anemic individuals could result, in conjunction with
higher endogenous production, in critical levels of COHb. Subjects
whose blood has low 02 carrying capabilities due to anemia would be
expected to be more sensitive to the effects of CO exposure because of
the already marginal Op delivery system. While dietary anemias are not
as great a problem as in former times, anemias resulting from various
pathological conditions are still major health problems and low levels
of CO exposure could pose a health threat to such groups.
Patients with chronic obstructive pulmonary disease are probably at
high risk although few studies on them have been reported. Any increase
in hypoxia could result in respiratory failure or other effects due to
reduced 0« supply. However, these individuals may absorb less CO due to
their disease and may have compensated for their hypoxia by increased
erythropoiesis and a shift of the Op dissociation curve to the right.
Ogawa et al. have presented evidence on the development of pulmonary
edema and discussed possible mechanisms of the role of CO in the disorder.
-i qrj
Sofoluwe has described the potential further irritation of the lungs
of children having bronchiolitis and bronchopneumonia by their exposure
4
to CO derived from wood fires used for cooking purposes. Aronow et al.
studied 10 patients with chronic obstructive pulmonary disease who had
11-71
-------
been exposed for one hour to CO which raised the COHb level to 4.1 percent.
When they exercised on a bicycle ergometer, dyspnea occurred within
146.6 seconds. However, 218.5 seconds elapsed before dyspnea occurred
when they exercised with COHb levels at 1.48 percent. The investigators'
conclusion was that their limited exercise performance was probably a
cardiovascular limitation rather than a respiratory one.
11.8.3 Drugs
Drugs such as alcohol, tobacco smoke, therapeutic drugs, and illicit
drugs as they interact with CO exposure have been discussed in Section 11.5
on interactions with other pollutants and drugs. Although there is
little empirical data on these interactions in either man or animals,
the little evidence and the theoretical expectations strongly indicate
that individuals taking various drugs would be at special risk. The
group of people under the influence of some form of drugs at any given
time is so large as to include a very major part of the general population.
Since interactions could be serious and the potential for them appears
to be ubiquitous, it is imperative that further research be done on this
subject.
11.8.4 Unadapted Individuals
Adaptation in humans has been discussed extensively in Section 11.6
on high altitudes, and on animals in Sections 10.7 and 10.8. The prepon-
derance of evidence to indicate that people who have not adapted to high
altitudes and are then exposed to both high altitude and CO simultaneously
are at greater risk.
11-72
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11.8.5 Occupational
Certain occupational groups are at special risk because of the
especially high exposures to CO peculiar to their work. These groups
include garage personnel, traffic policemen, steelworkers, firefighters,
and workers in petroleum and chemical industries. The presence of
chronic low-level CO poisoning may have significant influences on the
health and efficiency of these workers but this awaits further study.
Many other occupational exposures occur, but most studies of such exposure
are complicated by the unknown or unreported smoking habits of the
87
workers under study. Table 11-6 illustrates the potential emission
rates of CO for certain industries.
A study of blood COHb in the U.S. general public was carried out by
198 199
Stewart and his associates, * who sampled blood drawn at blood
donor mobile units in 17 urban areas and in some small towns in
52 119 212
New Hampshire and Vermont. Kahn and his associates ' ' evaluated
COHb levels in metropolitan St. Louis, where a total of 45,649 donors
provided blood for analysis. Stewart had 29,000 individuals (1,018 from
St. Louis) and Kahn had 16,649 (all from St. Louis) in their respective
199
samples. It should be noted that Stewart et al.'s subjects were
119
studied in March 1971 and Kahn et al.'s* y during October 1971 to
October 1972. The highest COHb values were 13.0 and 18.2 percent,
respectively, in Stewart et al.'s and Kahn et al.'s samples. Tables 11-
7 and 11-8 present Horvath's summary of the findings of these two
1 QQ
groups. Stewart et al. concluded that 35 percent of the nonsmoking
donors in St. Louis were exposed to ambient CO which led to COHb levels
11-73
-------
TABLE 11-6. NATIONWIDE EMISSION ESTIMATES, 1977
(10 metric tons/year)
223
Source Category
Transportation
Highway vehicles
Non- highway vehicles
Stationary fuel combustion
Electric Utilities
Industrial
Residential, commercial,
and institutional
Industrial processes
Chemicals
Petroleum refining
Metals
Mineral products
Oil & gas production & marketing
Industrial organic solvent use
Other processes
Solid waste
Miscellaneous
Forest wildfires
Agricultural burning
Coal refuse burning
Structural fires
Miscellaneous organic solvent use
TOTAL
TSP
1.1
0.8
0.3
4.8
3.4
1.2
0.2
5.4
0.2
0.1
1.3
2.7
0
0
1.1
0.4
0.7
0.5
0.1
0
0.1
0
12.4
S0x
0.8
0.4
0.4
22.4
17.6
3.2
1.6
4.2
0.2
0.8
2.4
0.6
0.1
0
0.1
0
0
0
0
0
0
0
27.4
N0x
9.1
6.7
2.5
13.0
7.1
5.0
0.9
0.7
0.2
0.4
0
0.1
0
0
0
0.1
0.1
0.1
0
0
0
0
23.1
VOC
11.5
9.9
1.6
1.5
0.1
1.3
0.1
10.1
2.7
1.1
0.1
0.1
3.1
2.7
0.3
0.7
4.5
0.7
0.1
0
0
3.7
28.3
CO
85.7
77.2
8.5
1.2
0.3
0.6
0.3
8.3
2.8
2.4
2.0
0
0
0
1.1
2.6
4.9
4.3
0.5
0
0.1
0
102.7
Percentage of
Total CO
83.4
75.2
8.2
1.2
0.3
0.6
0.3
8.1
2.7
2.3
2.0
0
0
0
1.1
2.5
4.8
4.2
0.5
0
0.1
0
100 100
NOTE: A zero indicates emissions of less than 50,000 metric tons.
-------
TABLE 11-7. AVERAGE PERCENT OF CARBOXYHEMOGLOBIN SATURATION
IN SMOKERS AND NON-SMOKERS IN ST. LOUIS1Ub
Non-smokers
Kahn et al.119
199
Stewart et al . L
No.
of donors
10,157
673
Mean
0.85
1.35
Smokers
No.
of donors
6,492
345
Mean
4.58
5.47
TABLE 11-8. AVERAGE PERCENT OF CARBOXYHEMOGLOBIN SATURATION106
Non-smokers
Kahn et
(St.
Stewart
(U.S.
al . 119
Louis)
. , 199
et al .
A.)
No.
of donors
10,157
16,036
Mean
0.85
1.43
Smokers
No.
of donors
6,492
11,289
Mean
4.58
5.21
11-75
-------
119
greater than 1.5 percent, while Kahn's group reported that 15.3 per-
cent of their St. Louis nonsmoking blood donors had levels above
1.5 percent. Kahn's group also stated that 21.9 percent of their donors
who were nonsmoking industrial workers had COHb levels of 2 percent or
more and only 5.7 percent of the remainder of the nonsmoking sample had
194
levels of 2 percent or more. Stewart et al. have compared COHb
levels found in subjects in Chicago in 1970 and 1974. They reported a
substantial reduction in COHb levels in blood donors over this time
frame, and suggested that the reduction was caused by a decrease in
ambient CO levels.
199
Stewart et al. concluded that there were significant differences
between the COHb saturations of the occupational groups studied.
Students and housewives had the lowest COHb concentrations. Other low
COHb groups included those associated with mental health services,
education, library science, religion, art, road paving, and entertainment.
The vehicle-related occupational groups had higher COHb saturations than
most groups. Other high COHb groups included those associated with
metal processing, chemical processing, stone and glass processing,
printing, welding, electrical assembly and repair, and graphic arts.
They concluded that a significant percentage of the population studied
was continuously exposed to ambient CO concentrations in excess of those
permitted by U.S. air quality standards.
119
On the other hand, Kahn and coworkers concluded that ambient CO
exposure was responsible for only very small increases in COHb levels in
their sample. They suggest that their data indicate two major sources
11-76
-------
of COHb in their subjects: smoking and work-related exposure. They
stated that almost 20 percent of their sample population were industrial
workers who carried an added COHb burden of 1.15 percent compared with
non-industrial workers. They attributed higher COHb levels not to
ambient atmospheric CO but, overwhelmingly, to smoking and occupation.
Most individuals with 2 percent COHb or more were industrial workers or
smokers or both. A similar conclusion was reached by Torbati et al.
38
Chovin has provided some of the most complete information on
Paris policemen, illustrating some of the concerns related to this
occupational group. Similar information is provided by the studies of
Balabaeva and Kalpaznov on traffic policemen in four large towns in
82
Bulgaria. Gothe et al. found relatively low levels of COHb in Swedish
traffic policemen.
T69
Ramsey reported a rise in COHb from 1.5 to 7.3 percent in
14 nonsmoking parking garage employees exposed to an average working-day
3
ambient CO level of 68 mg/m . He also noted that smokers exposed to the
above environment had an initial average COHb level of 2.9 and an average
COHb level of 9.3 percent at the end of the day. Nonsmokers exposed to
this environment had final levels of only 3.9 percent. Ramsey stated
that occupational exposure was more important than smoking in increasing
32
COHb levels. A contrary opinion was expressed by Buchwald, who report-
ed that cigarette smoking was a more significant contributor to the high
levels of COHb which he found in Canadian garage and service workers.
Of the smokers, 70 percent had levels in excess of 5 percent, while only
30 percent of the nonsmokers had such levels. A study of employees of
11-77
-------
the Triborough Bridge and Tunnel Authority, New York City, indicated
that methemoglobin was slightly, although statistically, increased in
these workers occupationally exposed to automobile exhaust. The role of
cigarette smoking was not clarified. Fristedt and Akesson found a
slight increase in COHb in workers employed in service installations of
enclosed parking areas, but attributed the discomfort that the workers
experienced to other components of automobile exhaust.
30
Breysse and Bovee used expired air samples to determine the
exposure to CO of stevedores, gasoline-powered lift-truck drivers, and
winch operators. Of some 700 estimates of COHb in these workers, almost
6 percent (5.7) of the workers exceeded COHb levels of 10 percent.
Levels of COHb greater than 10 percent were found in 7 percent of the
stevedores and 18 percent of the lift-truck operators. Smoking contributed
164
substantially to the attainment of the high levels of COHb. Petrov
also studied dock workers and found COHb levels as high as 10 percent.
74
Goldsmith's study of longshoremen suggested that the alveolar concen-
trations of CO were age-related regardless of smoking history. Pack-a-
day smokers in the 45-to-54-year age bracket had alveolar values of
3 3
31 mg/m , while 75-to-84-year-olds' alveolar values were only 16 mg/m .
Nonsmokers did not exhibit this age-related pattern, since even in
subjects up to 84 years of age, alveolar concentrations remained at the
same level.
Inspectors at U.S.-Mexico border crossing stations are exposed to
3 43
, ambient levels of CO that fluctuate between 6 and 195 mg/m .
Carboxyhemoglobin levels of smokers and nonsmokers prior to their duty
11-78
-------
as inspectors were 4.0 and 1.4, rising to 7.6 and 3.8 percent, respectively.
114
Johnson et al. studied six fare collectors working at a toll highway.
3
Ambient CO levels were 26 mg/m (8-hour time-weighted average for 12 days).
On three days ambient CO exceeded 40 mg/m . Post-shift COHb ranged from
1.8 to 8.6 percent, with a high of 11.7 percent.
Nonsmoking British steelworkers had end-of-shift values of 4.9 percent.
Non-exposed, nonsmoking controls reached 1.5 percent. Smokers had
higher values, reaching levels of 7.4 percent. The highest COHb value
reported was 14.9 percent.
Another major source of CO is the internal combustion engine, which
may in some cases be considered an occupational source since it provides
many forms of transportation. Community CO levels in ambient air follow
a regular diurnal pattern of variation, however, and different
112
concentrations have been measured at different sites. Jech and Ubl
measured alveolar concentrations of CO in individuals during a 2-hour
stay on a busy street and reported a considerable increase in expired CO
levels during that period. Likewise, the passenger compartment of
vehicles provides a potentially hazardous occupational area. Carbon
monoxide may enter this compartment from faulty or damaged exhaust
systems or from the air surrounding roadway traffic. Carbon monoxide
levels in the compartment may be higher than those found outside the
vehicle. Haagen-Smit found average concentrations in a vehicular
3
passenger compartment to be 42 mg/m on a Los Angeles freeway during
3
rush hour traffic (higher concentrations up to 80 mg/m have been report-
ed recently). It has been reported that concentrations in excess of
3
115 mg/m occur in some vehicle interiors.
11-79
-------
Direct measurement of COHb in firefighters engaged in fighting
fires of extremely long duration indicated that 10 percent of these
78
individuals had COHb values in excess of 10 percent. Sammons and
184
Coleman reported that firefighters had changes in those enzymes
related to myocardial damage and that these changes were related to
their COHb levels. However, the high levels of COHb in their control
(non-firefighters) and test (firefighters) groups make their conclusions
somewhat suspect.
Besides contributing to exposure of employees to CO, industry also
contributes to the pollution of the surrounding atmosphere. Gas generator
plants,157 smelters,150 steelworks,33'117'140 plastic works,23 electric
power generating plants, and mines have all been suggested as
sources of environmental CO pollution. Workers in a cast iron foundry
were also found to have high COHb levels associated with various CNS and
co
cardiovascular disorders. Hernberg et al. evaluated 1000 foundry
workers who were exposed to CO, heat, and strenuous physical work. The
presence of angina pectoris showed a clear dose-response relation with
regard to CO exposure from either occupation or smoking, or both.
Rural work establishments, especially those involving intensified
livestock production facilities, can produce high ambient levels of CO.
3
Carbon monoxide concentrations up to 229 mg/m have been found in these
facilities, with both the animals and workers having high levels of
153
COHb. Recreational facilities may also be problem areas. Excessive
levels of CO were found in ice-skating arenas where ice- resurfacing
3
machines were used. Levels as high as 348 mg/m (400 ppm) CO were found
11-80
-------
in such an arena after complaints of illness in children skating there
were reported to the local health department. Johnson et al.116a
reported on eight school children who became sick from CO while in a
school bus. Subsequent testing for ambient CO concentrations in school
buses showed that 36 percent of bus interiors tested had levels of CO in 7
excess of EPA standards for an 8-hour exposure. Improperly regulated
space heaters in enclosed areas can also produce high concentrations of
?fi
CO. Bondi et al . reported that on a submarine patrol of 40 days the
COHb levels of subjects were 2.1 and 1.7 percent at the beginning and
end of the patrol .
The belated discovery that at least one chemical substance utilized
in industry and commerce is degraded within the body to CO has potentially
significant epidemiological and clinical implications. Halogenated
hydrocarbons have been widely utilized as organic solvents, replacing
195
carbon tetrachloride. A chance observation indicated that the inha-
lation of one of these, dichloromethane (methyl ene di chloride,
was followed by a sustained elevation of COHb concentration. Inhalation
of 500 to 1000 ppm of CH^CK (Industrial Threshold Limit Value is 500 ppm)
for one or two hours resulted in COHb levels exceeding 14 percent.
This elevation of COHb continued beyond the time of exposure and gradually
returned to normal during the next 24 hours. Fodor and Roscovanu
exposed human volunteers to 500 ppm CH2C12. After eight hours of exposure,
COHb levels were approximately 12 percent. Exposure to 100 ppm resulted
in raising COHb levels to 5 percent. Elimination of CO was slow, so
that 24 to 26 hours were required to reestablish the control COHb levels.
11-81
-------
Residual alterations in pulmonary function were still noted three months
later.
Several investigators have studied the influence of CHpClp on
physiological function. Astrand et al. examined the effects of ChLClp
on work performance. Central nervous system depression was observed in
196 217
some subjects. Winneke compared the effects of exposure to
3
ambient CO (up to 115 mg/m ) and CHCl on vigilance performance.
Although he noted no effects related to CO, he found a striking decre-
ment in vigilance consequent to ChLClp exposure. A potentially more
dangerous complication of CHpCK exposure has been indicated by Stewart
192
and Hake: ^
"... because it is so sustained following exposure, the cardio-
vascular stress produced by elevated COHb levels, derived from
CH2C12 metabolism, is greater than that resulting from equally high
CORb levels derived from CO."
They report on an individual who experienced three episodes of myocardial
infarction, each following the use of a paint remover. About 80 percent
of CH2C12 is metabolized to Co;55»68>127»148»172»179 the mechanism
179
remains to be elucidated. Roth et al . have noted that animals rarely
succumb to CHpClp (11,520 ppm), possibly because of saturation of the
pathways by ChLClp metabolism and/or rates of CO excretion.
The possible detrimental health effects of chemical compounds that
may be metabolized to CO deserve further investigation.
11.9 SUMMARY
From the foregoing review of the literature pertaining to the
effects of low- level CO exposures of humans and experimental animals,
11-82
-------
it may be concluded that CO deleteriously affects mainly the cardiovascular
and central nervous systems. While many data are ambiguous, poorly
documented, and often in dispute, it still seems safe to conclude that
cardiovascular effects can be demonstrated with CO exposures as low as 17 to
o ' '"
21 mg/m CO (15 t^JJB ppm CO for an 8-hour exposure; 2.5 to 3.0 percent COHb).
For behavioral and CNS effects, a minimum of 29 to 34 mg/m3 CO (25 to 30 ppm
CO; 4 to 6 percent COHb) seems to be required. Visual sensitivity might be
affected as a continuous dose-response function without an obvious CO
threshold, but such data are presently tenuous.
There are important data to be acquired before an appraisal can be made
of the general health effects of CO. Fragments of data seem to point to the
importance of CO and its interactions with other pollutants with which it
commonly occurs. Far too little information exists regarding the effects of
exposures to CO in combination with other pollutants, as opposed to the
effects of CO by itself.
There are suggestions that CO might interact with drugs in a significant
way. Apparently fetuses, health-impaired individuals, individuals under the
influence of drugs, and persons not previously adapted to high altitudes or CO
exposures are at special risk, but the nature of the risk, much less its
magnitude, cannot even be estimated from the present literature.
3
It appears that acute CO exposures to 17 to 21 mg/m (15 to 18 ppm)
may^be adverse to human health. This range of values represents the
level at which the first detectable effect occurs in persons with
11-83
-------
cardiac impairment. The question of the significance of this and other
findings is a matter of general dose-response functions. While only
preliminary information is available on this subject, as discussed
above, the findings in the present literature may be summarized in
Table 11-9. These data are of little use, however, if drugs and other
pollutants alter the responses of individuals who have multiple
impairments. It represents a minimum known set of effects which could
under some circumstances be much worse or which could occur at lower
thresholds. Further data are urgently needed.
11-84
-------
TABLE 11-9. ESTIMATED HEALTH EFFECTS LEVELS FOR CARBON MONOXIDE EXPOSURE*
Effects
Approximate Ambient
CO levels to produce
COHb concen- stated COHb, mg/m
tration, % in resting individuals Reference
Ref.
No.
1-hour
8-hour
Physiologic norm
Passive smoking**
aggravates angina
pectoris
0.30-0.7
1.8-2.3
0 0 Coburn, et al., 1969 222.
(29-70 ppm) (6-15 ppm) Aronow, 1978 2b.
Decreased excercise 2.5-3.0
capacity in patients
with angina pectoris,
intermittent claudi-
cation, or peripheral
arteriosclerosis
Impairment of vigi- 3.0-6.5
lance tasks in
healthy experimental
subjects
Increased angina***
attacks for freeway
travel
Impairment of myocardial**
function in patients with
coronary heart disease
Decreased exercise
performance in normal
persons
Decreased exercise
performance in
patients with chronic
obstructive pulmonary
disease
Linear relationship 5-20
between COHb and
decreasing maximal
oxygen consumption
during strenuous
exercise in young
healthy men
Statistically signi-
ficant diminution of
visual perception,
manual dexterity or
ability to learn
79-97
(70-85 ppm)
97-239
(85-207 ppm)
17-21 Aronow and Rokaw, 1971 9.
(15-18 ppm) Anderson et al., 1973 2.
Aronow and Isbell,1973 5.
Aronow et al., 1974 6.
21-52 Horvath et al., 1971 107.
(18-45 ppm) Groll-Knapp et al., 85.
1972
Fodor et al., 1972 67.
Aronow et al., 1972 7.
Aronow et al., 1974 8.
Aronow and Cassidy, 1975
Aronow et al., 1977 4.
176-887 38-193 Ekblom et al., 1972 59.
(155-175 ppm) (33-170 ppm) Horvath, et al., 1975 108.
*Ayres, Papers 14,15
Bender et al., 1971 22.
**
***
High variability in COHb levels is found between individuals exposed to similar CO levels.
Partial effects may be due to other pollutants found in cigarette smoke.
Partial effects may be due to other pollutants found in automotive exhaust and
the ambient air.
11-85
-------
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187. Sedov, A. V., L. I. Zhukova, and G. E. Mazneva. Carbon monoxide excretion
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199. Stewart, R. D., E. D. Baretta, L. R. Platte, E. B. Stewart, J. H.
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APPENDIX A: GLOSSARY
Abscissa: The horizontal or x axis of a graph.
Abscission: The process of cutting off, as in the dropping of leaves.
Absorbance: The ability of a layer of a substance to absorb light
or other radiation, expressed mathematically as the negative
logarithm of the fraction of light intensity transmitted.
Absorptivity: The absorbance of a solution of unit concentration in a
layer of unit thickness.
Adiabatic: A process occurring without loss or gain of heat.
Adrenaline: British name for epinephrine, a potent stimulator of the
autonomic nervous system.
Adsorption: The adhesion of molecules in an extremely thin layer to
the surfaces of solids or liquids with which they are in
contact.
Alveolar: Pertaining to the alveoli or small air pockets of the lungs.
Alveolar-arterial pressure difference (A-aDQp): Difference in oxygen
pressure between the lung alveoli and the arterial blood.
Ambient air: The surrounding, well-mixed air.
Aminotransferase: Any of a class of enzymes that catalyzes the transfer
of an ami no group from one molecule to another, typically
from an alpha-ami no acid to an alpha-keto acid.
d-Amphetamine: A central nervous system stimulant.
Anaerobic: Living, or active, in the absence of free oxygen.
Anemia: A reduction below normal in the number of erythrocytes
(red blood cells) per cubic millimeter, in the quantity of hemoglobin,
or in the volume of packed red cells per 100 mi 11ilHers of blood.
Angina pectoris: A paroxysmal thoracic pain, with a feeling of
suffocation and impending death, due usually to anoxia of the
heart muscle, and precipitated by effort or excitement.
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Angiogram: An Xray picture of a blood vessel filled with a contrast
medium.
Angstrom: A unit of wavelength of light, equal to one ten-billionth
of a meter, or 10 cm.
Anoxia: Absence or lack of oxygen; reduction of oxygen in body
tissues below physiologic levels.
Anthropogenic: Relating to the impact of man and his activities on
the natural world.
Aortic intima: Innermost lining of the aorta (main trunk from which
the body arteries proceed).
Arteriosclerotic heart disease (ASHD): Sclerosis and thickening of
the walls of small arteries (arterioles) of the heart.
Asanguineous: Bloodless; the blood is replaced by another fluid.
Atheroma: A mass of plaque of degenerated, thickened arterial lining
occurring in atherosclerosis.
Atheromatosis: The process involving fatty degeneration of the inner
coat of an artery.
Autonomic nervous system: The portion of the nervous system concerned
with regulation of the activity of the heart muscle, the smooth
muscle, and the glands; self-regulatory.
Autotrophic: Needing only carbon dioxide or carbonates as a source
of carbon, and a simple inorganic nitrogen compound for metabolic
synthesis.
Auxin: Plant "hormone" that promotes growth in plant cells and tissues.
Bacteroids: Enlarged, branched bacteria found in the nodules of
leguminous plants.
Ballistocardiogram (BCG): Tracing from the apparatus for recording
the movements of the body due to the heartbeat.
Biosphere: The part of the world in which life can exist.
C3 type plant: A type of plant in which the first stable product of
photosynthesis is a compound containing three carbon atoms, namely
phosphoglyceric acid.
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Cannabis sativa: Hemp; contains cannabinol, an hallucinogenic
variously called bhang, ganja, hashish, or marihuana.
Carboxyhemoglobin (COHb): The compound formed by the combination of
carbon monoxide with hemoglobin.
Carboxymyoglobin (COMb): The compound formed by the combination of
carbon monoxide with myoglobin.
Carcinogenesis: The development of a carcinoma, a malignant new
growth of epithelial cells.
Cardiac index: The rate of blood pumping by the heart, divided by
the surface area of the body; expressed in units of liters per
minute per square meter.
Cardiovascular: Pertaining to heart and blood vessels.
Catecholamine: One of a group of compounds having a sympathomimetic
action such as norephinephrine, epinephrine, and dopamine.
Catheter: a tubular, flexible surgical instrument for withdrawing
fluids from, or introducing fluids into, a cavity of the body.
Central nervous system (CNS): Brain and spinal cord together.
Cerebral blood flow (CBF): Blood flow through the cerebrum or main
portion of the brain.
Cerebral cortex: Outer layer of the brain.
Cerebrovascular: Refers to blood vessels of the brain.
Chemical kinetics: The study of the rate or speed at which one
chemical substance is converted into another.
Chemiluminescence: Light emitted during a chemical reaction.
Chemoreceptor: Specialized cells adapted for excitation by chemical
substances, such as found in the senses of smell and of taste.
Chronaxie: The minimum time an electric current must flow at a voltage
twice the minimal potential necessary for stimulation for the muscle
to contract.
Claudication: Limping or lameness; a complex of symptoms frequently
associated with occlusive arterial diseases of the limbs.
Colorimetric: A type of chemical analysis in which the amount of a
chemical substance present is found by measuring the light
absorption due to its intrinsic color or the color of another
substance into which it can be completely converted.
Contingent negative variation (CNV): Slow-wave brain potentials
evoked by a stimulus.
Coronary: Pertaining to the arteries and veins of the heart.
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Coulometric: A type of chemical analysis in which the amount of a
substance present is determined by causing it to undergo an
electrochemical reaction and measuring the amount of electricity
needed to carry the reaction to completion.
Critical flicker fusion frequency (CFEF): The frequency at which
intermittent flashes of light appear as a steady or continuous
light.
Cynomolgus: Monkeys of the genus Macaca, particularly the species
M. irus, used in laboratory research.
Cytochrome: Iron-containing respiratory pigment for intracellular
oxidation.
Cytochrome oxidase: A blood protein enzyme found in cells, usually
attached to mitochondria (rod-shaped organelles), associated
with copper.
-18
Debye: A unit of electric moment equal to 10 stat coulomb-
centimeter; a measure of the electrical asymmetry of a molecule.
Diastole: The dilatation of the heart, filling the ventricles with
blood.
Diffusion: The process by which particles of gases, liquids, or
solids intermingle as a result of their spontaneous movement
caused by thermal agitation, and move from a region of higher
concentration to a region of lower concentration.
Diurnal: Having a daily cycle.
Dyspnea: Difficulty of breathing; labored breathing.
Electrocardiogram (EKG): A tracing made by an electrocardiograph
which measures changes of electrical potential occurring during
the heartbeat.
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Elution: The release or removal of a substance by a solvent, from
a material which had retained the substance for a time.
Endogenous: Originating within the organism.
Epicotyl: The upper portion of an plant embryo or seedling.
Epidemiology: The study of the relationships of the various factors
determining the frequency and distribution of diseases in a
human community.
Epinasty: The downward curling or curving of a foliage leaf.
Equivalent Method: A method of sampling and analyzing air for a
pollutant that has been officially designated as an equivalent
method by the Environmental Protection Agency. It must have a
consistent relationship to a reference method when both methods
are used to measure the concentration of the pollutant in a
real atmosphere.
Ergometer: An apparatus measuring the work performed by a group of
muscles.
Erythrocyte: Red blood cell (corpuscle).
Erythropoiesis: The formation of erythrocytes (red blood cells).
Erythropoietin: Substances regulating the production of red blood
cells.
Ethanol: Ethyl alcohol.
Etiolation: Paleness due to the exclusion of light.
Etiology: Pertaining to the factors that cause disease and the method
of their introduction to the host; the sum of knowledge regarding
causes.
Exogenous: Originating from outside the organism.
Exothermic reaction: A chemical transformation in which heat or other
energy is liberated.
Fibrillation (cardiac): Rapid, irregular contractions of the muscle
fibers of the heart.
Fourier transform spectroscopy: An improved method for obtaining
absorption spectra of high quality. All of the available radiant
energy is sent continuously through the sample (in contrast to
conventional instruments in which only a very narrow band of
wavelengths is used at any moment, the remainder being discarded)
and the absorption spectrum is reconstructed by optical and
mathematical processing.
A-5
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Gas chromatography: A method of chemical analysis in which a mixture
of gases or vapors is separated into its components by passage
(in an inert carrier gas) through a column of material which
interacts more or less strongly with the individual components,
retaining them for longer or shorter times before release into
the effluent gas stream.
Gaussian distribution: Synonymous with normal distribution.
Globin: The protein constituent of hemoglobin.
Glycolysis: The breakdown of glycogen or glucose into lactic acid.
Haldane constant: Ratio of the stability constant for carboxyhemoglobin
to that for oxyhemoglobin; a measure of the relative affinity of
hemoglobin for carbon monoxide as compared to its affinity for
oxygen.
Half-time: The time required for the concentration, or amount, of
a substance to decrease to half its initial value.
Hectare: A metric measure of area containing 10,000 square meters
(2.471 acres).
Hematocrit: The volume percentage of erythrocytes (red blood cells)
in whole blood.
Hemoglobin (Hb): Iron-containing protein respiratory pigments
occurring in the red blood cells of vertebrates and transporting
oxygen to the tissues and carbon dioxide from the tissues.
Hemopoiesis: Hematopoiesis, the formation and development of
blood cells.
Hexobarbital: A sedative and an hypnotic.
Histopathology: Pertaining to diseased tissues of the body.
Hopcalite: A catalyst for converting carbon monoxide to carbon
dioxide, which consists of a mixture of oxides of copper, cobalt,
manganese, and silver.
Hydrocyanic acid (HCN): An aqueous solution of hydrogen cyanide; a
poisonous liquid used chiefly in fumigating and in organic syntheses
Hydroxyl radical: Unstable, electrically neutral fragment of a
molecule containing one oxygen atom and one hydrogen atom. It
is formed by disruption of a water (or other hydroxyl-containing)
molecule, as a result of exposure to far ultraviolet light or
other high-energy radiation such as Xrays.
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Hyperpnea: Abnormal increase in the depth and rate of the respiratory
movements; heavy or labored breathing.
Hypertrophy: The enlargement or overgrowth of an organ or part due
to an increase in size of its constituent cells.
Hypobaric hypoxia: Deficiency of oxygen due to less than normal pressure.
Hyponasty: The upward curling or curving of a foliage leaf.
Hypothalamus: Part of the brain; has many functions, e.g., regulation
of water balance, body temperature, sleep, food intake, and
development of secondary sex characteristics.
Hypothermia: Abnormally low temperature.
Hypoxemia: Deficient oxygenation of the blood; hypoxia.
Hypoxia: Low oxygen content or tension. Anemic hypoxia is due to
reduction of the oxygen-carrying capacity of the blood as a result
of a decrease in the total hemoglobin or an alteration of the
hemoglobin constituents.
Hypoxic hypoxia: A term used to denote hypoxia due to low oxygen tension
to distinguish it from that due to carboxyhemoglobin in which CO
replaces 02-
Intercalated disks: Short lines or V-shaped stripes extending across
the fibers of heart muscle.
Intraperitoneal: Within the body cavity.
In vitro: Outside the living organism.
Jn vivo: Within the living organism.
Ischemia: Deficiency of blood: myocardial ischemia, deficiency of
blood supply to the heart muscle.
Isopleth: On a map, a line connecting points at which a particular
variable has a specified constant value.
Lactate dehydrogenase (LDH): An enzyme that catalyzes the dehydrogenation
of alpha hydroxy acids to alpha keto acids; in certain cases,
specifically restricted to lactate.
Leghemoglobin: A pigment found in leguminous root nodules.
A-7
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Leucine aminopeptidase: A proteolytic enzyme that catalyzes the hydrolysis
of peptide linkage involving the ami no acid, leucine.
Lipids: Various substances including fats, waxes, phosphatids,
cerebrosides and related or derived compounds.
Lognormal: A type of statistical distribution in which the logarithm
of a variable has a normal distribution, in contrast to the
familiar case in which the variable itself has a normal distribution.
Methylene chloride (Dichloromethane; CH^CK): A compound which causes
an elevation of carboxyhemoglobin; a commercial solvent.
Microflora: Microscopic plant life; bacteria.
Microglial: Pertaining to the microglia, small non-neural, interstitial
cells that form part of the supporting structure of the central
nervous system.
Microwave rotational spectroscopy: A method for chemical analysis
of gases by measuring the absorption of electromagnetic radiation
in the centimeter wavelength region, which is based on the
characteristic rotational frequency of the specific gas molecule.
o
Milligrams per cubic meter (mg/m ): A measure of concentration of a
substance. In this instance, the weight in milligrams of CO
contained in one cubic meter of the ambient air, which may be
converted to "parts per million" at one atmosphere by
multiplication by the factor 0.873 at 25 C, or by the factor 0.800
at 0 C. At pressures other than one atmosphere (760 torr) such a
factor should be multiplied by an additional factor of 760/p,
where p is the ambient pressure in torr.
Mitochondria: Small organelles found in the cytoplasm of the cell
and which are concerned with cellular metabolism.
Mixing ratio: The ratio of the mass of a substance (such as water
vapor) in an air sample, to the total mass of all the other
substances in the same air sample.
Mole: Gram molecular weight. The amount of a substance represented
by writing "grams" after its molecular weight (the sum of the
atomic weights of all the elements in its formula). One mole
of any substance contains 6.02 x 10 molecules.
A-8
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Mossbauer spectroscopy: A method for chemical analysis and structure
studies, based on small variations (due to chemical and physical
factors) in the energy of gamma rays emitted by radioactive atoms.
Myelin: A lipid substance forming a sheath around some nerves.
Myocardial infarction: A necrotic (dead) area of the heart muscle.
Myocardium: Muscle of the heart.
Myocardosis: Disorder of the middle, thick muscle layer of the
heart wal1.
Myoglobin: A protein found in muscle fibers, which is similar to
hemoglobin in its reversible binding of oxygen.
Necrosis: Localized death of living tissue.
Neonate: A new-born infant.
Normal distribution: A type of statistical distribution in which the
set of values obtained in a large number of independent repetitions
of a measurement can be represented by a symmetrical bell-shaped
curve.
Nuclear magnetic resonance: A type of radiofrequency spectroscopy
used for chemical analysis and molecular probes, based on small
changes (caused by nearby electrons) in the magnetic energy levels
shown by certain atomic nuclei.
Orsat: An apparatus or method for chemical analysis of gas mixtures,
in which each gas successively is removed from the sample by an
appropriate chemical reagent, and the decrease in volume or
pressure is measured after each step.
Oxygen partial pressure (P02): The amount of pressure exerted by
oxygen as one component of a mixture of gases, equal to the
pressure it would exert if it were alone in the same container.
The total pressure of a gas mixture is the sum of the partial
pressures of the individual gases.
Oxyhemoglobin: The compound formed by the combination of oxygen with
hemoglobin.
Oxymyoglobin: The compound formed by the combination of oxygen with
myoglobin.
Paradigm: An example or pattern.
A-9
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Parts per million (ppm): A measure of concentration of a substance. In
this instance, the volume in liters of CO contained in 1,000,000
liters of the ambient air, which may be converted to "milligrams
per cubic meter" by multiplication by the factor 1.145 at 25 C,
or by the factor 1.250 at 0 C. At pressures other than one
atmosphere (760 torr) such a factor should be multiplied by an
additional factor of p/760, where p is the ambient pressure in
torr.
Pathology: Study of the structural and functional changes produced
by diseases, e.g., abnormalities.
Photic: Pertaining to light.
Photochemistry: Study of the effects of light, ultraviolet rays,
or other radiant energy in causing conversion of one chemical
substance into another.
Photolysis: Disruption of a molecule caused by exposure to ultraviolet
or other radiation energy.
Photometry: Measurement of light intensity; can be used for chemical
analysis by measuring the intensity change caused by characteristic
absorption or emission of radiant energy due to a chemical compound.
Planck's Radiation Law (hv = E): Planck's constant (h) times the
frequency of radiated energy (v) equals quanta of energy (E).
Plume: An elongated mobile column, as of smoke or exhaust gases.
Porphyrin: Iron-free pyrrole derivatives which form the basis for
respiratory pigments.
Postpartum: Following parturition or giving birth to offspring.
Primordia (flower): Earliest stage in the development of the flower.
Protoporphyrin: An iron-free derivative of hematin,
which together with globin forms hemoglobin.
Psychomotor: Pertaining to motor effects of cerebral or psychic
activity.
Psychotropic: Exerting an effect upon the mind; usually applied to
drugs that affect the mental state.
Pyrrole: A liquid, weakly basic, cyclic substance (CJH-NH) obtained
in the destructive distillation of various animal substances.
A-10
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Radicals: Unstable fragments of molecules which have an unpaired
electron and tend to react or change rapidly into more stable
substances.
Rapid eye movement (REM): An indication that the sleeping subject
has entered one of several "stages" characteristic of normal
sleep.
Reference method: The method of sampling and chemical analysis for a
pollutant substance which has been officially designated as
acceptable by the Environmental Protection Agency; includes a
specific instrument which must be used in such analysis.
Scavenger: A chemical substance which removes radicals by a rapid
reaction, converting them to more stable substances.
Second derivative spectrometer: An instrument for detecting weak
absorption peaks by electronic processing of spectral intensity
measurements, to yield the rate of change of the slope of the
absorption spectrum plotted as a function of wavelength. This makes
the peaks much more visible.
Sequela (ae): A lesion or affection following or caused by an
attack of disease.
Sickle-cell anemia: A disease marked by anemia and by ulcers and
characterized by the red blood cells of the patient acquiring
a sickle-like or crescentic shape i_n vitro; the disease is
apparently confined to the negro race and it is hereditary.
Sigmoid: Shaped like the letter S.
Sink: An absorber of a substance, or a process which acts as a
removal or dissipation mechanism.
Soret: Intense peaks of light absorption shown by hemoglobin and
related compounds, in the spectral region of about 400 to 440
nanometers; named for the discoverer.
Spectrophotometer: An instrument for measuring the relative light
intensities (or absorption of light) at different wavelengths
in a spectrum; used for chemical analysis of substances which
have characteristic colors or absorption spectra.
Stoichiometric: The amount of a chemical substance theoretically
needed to react with, or produced by a reaction from, a specified
amount of another substance, as expressed quantitatively by the
chemical equation for the reaction.
A-ll
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Stratosphere: An upper region of the earth's atmosphere, above about
10 to 16 kilometers, in which clouds are rare and there is little
change of temperature with altitude.
Superior colliculus: A portion of the brain primarily concerned
with visual responses.
Synergism: The joint action of agents so that their combined effect
is greater than the algebraic sum of their individual effects.
Systole: Contraction of the heart, forcing the blood out through the
arteries.
Teratology: Science that deals with abnormal development of the fetus,
and congenital malformations.
Terpene: A type of hydrocarbon found in plant oils, resins, and balsams,
such as those produced by pine or other conifers.
Torr: A unit of pressure equal to 1/760 of an atmosphere, roughly equal
to one millimeter of mercury in the Torr i eel li barometer, or 1333
dynes per square centimeter.
Tropopause: The region of the earth's atmosphere which marks the
transition from the troposphere below to the stratosphere above,
at an altitude of about 10 to 16 kilometers, depending on latitude,
season, and weather.
Troposphere: The portion of the earth's atmosphere which extends from
the surface out to an altitude of about 7 to 10 miles or 10 to 16
kilometers.
Valence electrons: The electrons in the outmost shell of the atom
which determine the extent to which an atom may combine with
other atoms.
Vascular: Of or pertaining to the blood vessels.
Vasodilation: Dilation of a blood vessel, increasing the blood flow.
Vigilance: A stage of alertness requiring continuous attention over
long periods of time.
A-12
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Virtual Source: A point from which divergent beams seem to emanate
but do not actually do so.
Visual evoked response (VER): Reaction to a visual stimulus.
White noise: A heterogeneous mixture of sound waves extending over
a wide frequency range.
Zoxazolamine: Skeletal muscle relaxant; promotes excretion of uric
acid in the urine.
A-13
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TECHNICAL REPORT DATA
(Please read Instructions on the reverse before completing)
1. REPORT NO.
EPA-600/8-79-022
3. RECIPIENT'S ACCESSION NO.
4. TITLE ANDSUBTITLE
AIR QUALITY CRITERIA FOR CARBON MONOXIDE
5. REPORT DATE
October 1979
6. PERFORMING ORGANIZATION CODE
7. AUTHOR(S)
Informatics, Inc. and others listed in the
document as "Contributors and Reviewers"
8. PERFORMING ORGANIZATION REPORT NO.
9. PERFORMING ORGANIZATION NAME AND ADDRESS
Informatics, Inc.
6011 Executive Blvd.
Rockville, MD. 20852
10. PROGRAM ELEMENT NO.
11. CONTRACT/GRANT NO.
68-02-2799
12. SPONSORING AGENCY NAME AND ADDRESS
13. TYPE OF REPORT AND PERIOD COVERED
Environmental Criteria and Assessment Office
Office of Research and Development
U.S. Environmental Protection Agency
Research Triangle Park, N.C. 27711
14. SPONSORING AGENCY CODE
EPA/600/00
15. SUPPLEMENTARY NOTES
16. ABSTRACT
This document summarizes current scientific information regarding carbon
monoxide (CO) as a component of the ambient atmosphere and the effects of CO upon man
and the environment. The observed effects, as presented herein, constitute the basis
for the criteria upon which the U.S. Environmental Protection Agency (EPA) will review
the National Ambient Air Quality Standard (NAAQS) for CO. In the CO criteria document
the following questions have been addressed: At what level of CO in the ambient air
do detectable adverse health effects occur? What are these adverse health effects?
What are the major sources of CO? Are there synergistic effects from CO exposure in
combination with other pollutants and drugs? How do ambient concentrations of CO affect
humans living at high altitudes? Are present monitoring methods adequate to determine
human exposure to CO? What are the global effects of increased CO emission into the
atmosphere? It is in response to these and related questions that this document has
been prepared.
17.
KEY WORDS AND DOCUMENT ANALYSIS
a.
DESCRIPTORS
b.IDENTIFIERS/OPEN ENDED TERMS
altitude centra I nervous system
carbon monoxide internal combustion engines
air pollution embryos
human health effects angina pectoris
atmospheric composition nitrogen fixation
cardiovascular diseases plant metabolism
sickle cell anemia
carboxyhemoglobin
nonhypoxic effects
Denver, Colorado
New York, New York
Baltimore, Maryland
Washington, D.C.
CNS effects
claudication
c. COS AT I Field/Group
02A 06T
04B 07C
06A 08A
06C 13B
06E
06F
06P
Q6S
lypoxia
18. DISTRIBUTION STATEMENT
RELEASE TO PUBLIC
19. SECURITY CLASS (This Report)
UNCLASSIFIED
21. NO. OF PAGES
20. SECURITY CLASS (This page)
UNCLASSIFIED
22. PRICE
EPA Form 2220-1 (Rev. 4-77) PREVIOUS EDITION is OBSOLETE
A-14
. GOVERNMENT PRINTING OFFICE: 1979 -640 - 0 1 3/ 3931 REGION NO. 4
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